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Infectious Disease

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Any disease caused by bacteria or viruses invading our body tissues are called infectious diseases. As always, every single bit of information that you can share about this topic to the medical community is welcome. With this template, you'll get a dark-colored design with some irregular shapes that have gradients. There are some layouts that you could use in your presentation, for example, to talk about risk factors, prevention or treatment.

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Introduction to Infectious Diseases

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Infectious diseases are disorders that are caused by organisms, usually microscopic in size, such as bacteria, viruses, fungi, or parasites that are passed, directly or indirectly, from one person to another. Humans can also become infected following exposure to an infected animal that harbors a pathogenic organism that is capable of infecting humans.

Infectious diseases are a leading cause of death worldwide, particularly in low-income countries, especially in young children.

In 2019, two infectious diseases - lower respiratory infections and diarrheal diseases - were ranked in the top ten causes of death worldwide by the World Health Organization (WHO). Both of these diseases can be caused by a variety of infectious agents.

Deaths from the infectious diseases  HIV/AIDS  and  tuberculosis  have fallen significantly in recent years, and they no longer appear on the list of top ten causes of death globally. However, these diseases are still a leading cause of death in low-income countries. Malaria is another infectious disease that is a top cause of death in low-income countries. These three diseases are due to single infectious agents. 

A newly emerged infectious disease, COVID-19 , caused by the virus SARS-CoV-2, became a top cause of death in 2020. According to data analyzed by the Centers for Disease Control and Prevention (CDC), COVID-19 was listed as the third leading cause of death during 2020 in the United States, behind heart disease and cancer.

Source; WHO

Agents that Cause Infectious Diseases

Scanning electron micrograph image depicting numerous clumps of methicillin-resistant Staphylococcus aureus bacteria; Magnified 9560x.

Infectious diseases can be caused by several different classes of pathogenic organisms (commonly called germs). These are viruses , bacteria , protozoa, and fungi. Almost all of these organisms are microscopic in size and are often referred to as microbes or microorganisms .

Although microbes can be agents of infection, most microbes do not cause disease in humans. In fact, humans are inhabited by a collection of microbes, known as the microbiome , that plays important and beneficial roles in our bodies.

The majority of agents that cause disease in humans are viruses or bacteria, although the parasite that causes malaria is a notable example of a protozoan.

Examples of diseases caused by viruses are COVID-19 ,  influenza , HIV/AIDS , Ebola ,  diarrheal diseases , hepatitis, and West Nile. Diseases caused by bacteria include anthrax , tuberculosis , salmonella, and respiratory and diarrheal diseases.

Transmission of Infectious Diseases

There are a number of different routes by which a person can become infected with an infectious agent. For some agents, humans must come in direct contact with a source of infection, such as contaminated food, water, fecal material, body fluids or animal products. With other agents, infection can be transmitted through the air.

The route of transmission of infectious agents is clearly an important factor in how quickly an infectious agent can spread through a population. An agent that can spread through the air has greater potential for infecting a larger number of individuals than an agent that is spread through direct contact.

Another important factor in transmission is the survival time of the infectious agent in the environment. An agent that survives only a few seconds between hosts will not be able to infect as many people as an agent that can survive in the environment for hours, days, or even longer. These factors are important considerations when evaluating the risks of potential bioterrorism agents.

Impact of Infectious Diseases on Society

Transmission electron micrograph of Middle East Respiratory Syndrome Coronavirus particles, colorized in yellow.

Infectious diseases have plagued humans throughout history, and in fact have even shaped history on some occasions. The plagues of biblical times, the Black Death of the Middle Ages, and the “Spanish flu” pandemic of 1918 are but a few examples. The 1918 flu pandemic killed more than a half million people in the United States and up to 50 million people worldwide and is thought to have played a contributing role in ending World War I. 

Epidemics and pandemics have always had major social and economic impacts on affected populations, but in our current interconnected world, the impacts are truly global. This has been clearly demonstrated by the COVID-19 pandemic that began in 2020. Infections in one region can easily spread to another. Until the virus can be contained globally, a surge in cases in one area can cause a resurgence of cases in other areas around the world. 

Coronaviruses

Consider the SARS outbreak of early 2003. This epidemic demonstrated that new infectious diseases are just a plane trip away. The virus, SARS-CoV, which caused a severe, and sometimes fatal, respiratory illness emerged in China. Air travelers rapidly spread the disease to Canada, the United States, and Europe. Even though the SARS outbreak was relatively short-lived and geographically contained, the economic loss to Asian countries was estimated at $18 billion as fear inspired by the epidemic led to travel restrictions and the closing of schools, stores, factories, and airports. 

About a decade later, a new SARS-like virus emerged in Saudi Arabia. Named MERS-CoV, the virus causes Middle East respiratory syndrome, or MERS , a severe and often fatal respiratory disease. Infection occurs through direct contact with an infected animal (camel) or person. Even though MERS did not spread easily from person to person, the virus spread to 27 countries in the Middle East, Europe, Asia, and North America, including the United States.

The most recent coronavirus to emerge is named SARS-CoV-2. It causes the disease known as COVID-19 . The effects of COVID-19 pandemic have been felt around the worldwide, with schools and businesses closing, travel restricted, and in some cases even limitations on people leaving their homes. The pandemic has caused major economic hardships, stressed healthcare systems, and impacted mental health. Disagreements within and between countries have arisen in how to respond to the crisis and how to allocate scarce supplies of drugs and vaccines. 

The HIV/AIDS epidemic, particularly in sub-Saharan Africa, illustrates the economic and social impacts of a prolonged and widespread infection. The disproportionate loss of the most economically-productive individuals has reduced workforces and economic growth rates of affected countries, especially those with high infection rates. This impacts the health care, education, and political stability of these nations.

In southern Africa where the infection rate is highest, life expectancy plummeted in a mere decade from 62 years in 1990 -1995 to 48 years in 2000 – 2005. The existence of approximately 18 million children worldwide under that age of 18 that have been orphaned by HIV/AIDS highlights the impact of infectious diseases on families and societies.

Historically, there have been about three to four influenza pandemics each century. The  influenza virus is notable for its ability to change its genetic information. When a new version of the influenza virus arises that has either never circulated in the human population or has not circulated for a very long time (so that most people do not have immunity against the virus), a pandemic can occur. 

There were three influenza pandemics in the 20th century – the “Spanish” flu of 1918-19, the “Asian” flu of 1957-58, and the “Hong Kong” flu of 1968-69 – and one in the 21th century, so far – the 2009 H1N1 “swine flu” pandemic. 

Other influenza variants have emerged in recent decades including the avian H5N1 influenza (or “bird flu”) in 2005 and the H7N9 virus in 2013. The H5N1 virus caused concern because it was so deadly (more than half of the cases were fatal), but it did not spread easily from person to person. Additional novel versions will continue to emerge. The greatest danger would come from a version of the flu virus that is very deadly but is also transmitted readily from one individual to another.

Challenges in Infectious Disease Research

Despite significant advances in infectious disease research and treatment, the control and eradication of these diseases faces major challenges.

A WHO report released in 2007 warns that infectious diseases are spreading more rapidly than ever before and that new infectious diseases are being discovered at a higher rate than at any time in history. In just the past five years, the WHO has identified over 1000 epidemics of infectious diseases including avian flu, swine flu, polio, and cholera.

With greatly increased human mobility, infectious diseases have the potential to swiftly become global epidemics and pandemics.

Some of the reasons for the difficulty in combating infectious diseases are:

  • New infectious diseases continue to emerge
  • Old infectious diseases increase in incidence or geographical distribution
  • Old infectious diseases previously under control begin to re-emerge
  • Potential for intentional introduction of infectious agents by bioterrorists
  • Increasing resistance of pathogens to current antimicrobial drugs
  • Breakdowns in public health systems and communication between nations

The sections on Emerging Infectious Diseases and Bioterrorism Agents further explore these challenges.

For More Information

  • Information about infectious diseases from the National Institutes of Health (NIH)
  • Information about infectious diseases, from the Centers for Disease Control and Prevention (CDC)
  • Information about infectious diseases from the World Health Organization (WHO)
  • Listing of the top ten causes of death compiled by the WHO

Learn more about some of the technical terms found on this page by visiting our glossary of terms.

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Infectious diseases

On this page, when to see a doctor, risk factors, complications, infectious diseases care at mayo clinic.

Our caring teams of professionals offer expert care to people with infectious diseases, injuries and illnesses.

Infectious diseases are disorders caused by organisms — such as bacteria, viruses, fungi or parasites. Many organisms live in and on our bodies. They're normally harmless or even helpful. But under certain conditions, some organisms may cause disease.

Some infectious diseases can be passed from person to person. Some are transmitted by insects or other animals. And you may get others by consuming contaminated food or water or being exposed to organisms in the environment.

Signs and symptoms vary depending on the organism causing the infection, but often include fever and fatigue. Mild infections may respond to rest and home remedies, while some life-threatening infections may need hospitalization.

Many infectious diseases, such as measles and chickenpox, can be prevented by vaccines. Frequent and thorough hand-washing also helps protect you from most infectious diseases.

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  • A Book: Endemic - A Post-Pandemic Playbook
  • A Book: Mayo Clinic Family Health Book, 5th Edition
  • Newsletter: Mayo Clinic Health Letter — Digital Edition

Each infectious disease has its own specific signs and symptoms. General signs and symptoms common to a number of infectious diseases include:

  • Muscle aches

Seek medical attention if you:

  • Have been bitten by an animal
  • Are having trouble breathing
  • Have been coughing for more than a week
  • Have severe headache with fever
  • Experience a rash or swelling
  • Have unexplained or prolonged fever
  • Have sudden vision problems

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Infectious diseases can be caused by:

  • Bacteria. These one-cell organisms are responsible for illnesses such as strep throat, urinary tract infections and tuberculosis.
  • Viruses. Even smaller than bacteria, viruses cause a multitude of diseases ranging from the common cold to AIDS.
  • Fungi. Many skin diseases, such as ringworm and athlete's foot, are caused by fungi. Other types of fungi can infect your lungs or nervous system.
  • Parasites. Malaria is caused by a tiny parasite that is transmitted by a mosquito bite. Other parasites may be transmitted to humans from animal feces.

Direct contact

An easy way to catch most infectious diseases is by coming in contact with a person or an animal with the infection. Infectious diseases can be spread through direct contact such as:

Person to person. Infectious diseases commonly spread through the direct transfer of bacteria, viruses or other germs from one person to another. This can happen when an individual with the bacterium or virus touches, kisses, or coughs or sneezes on someone who isn't infected.

These germs can also spread through the exchange of body fluids from sexual contact. The person who passes the germ may have no symptoms of the disease, but may simply be a carrier.

  • Animal to person. Being bitten or scratched by an infected animal — even a pet — can make you sick and, in extreme circumstances, can be fatal. Handling animal waste can be hazardous, too. For example, you can get a toxoplasmosis infection by scooping your cat's litter box.
  • Mother to unborn child. A pregnant woman may pass germs that cause infectious diseases to her unborn baby. Some germs can pass through the placenta or through breast milk. Germs in the vagina can also be transmitted to the baby during birth.

Indirect contact

Disease-causing organisms also can be passed by indirect contact. Many germs can linger on an inanimate object, such as a tabletop, doorknob or faucet handle.

When you touch a doorknob handled by someone ill with the flu or a cold, for example, you can pick up the germs he or she left behind. If you then touch your eyes, mouth or nose before washing your hands, you may become infected.

Insect bites

Some germs rely on insect carriers — such as mosquitoes, fleas, lice or ticks — to move from host to host. These carriers are known as vectors. Mosquitoes can carry the malaria parasite or West Nile virus. Deer ticks may carry the bacterium that causes Lyme disease.

Food contamination

Disease-causing germs can also infect you through contaminated food and water. This mechanism of transmission allows germs to be spread to many people through a single source. Escherichia coli (E. coli), for example, is a bacterium present in or on certain foods — such as undercooked hamburger or unpasteurized fruit juice.

More Information

  • Ebola transmission: Can Ebola spread through the air?
  • Mayo Clinic Minute: What is the Asian longhorned tick?

While anyone can catch infectious diseases, you may be more likely to get sick if your immune system isn't working properly. This may occur if:

  • You're taking steroids or other medications that suppress your immune system, such as anti-rejection drugs for a transplanted organ
  • You have HIV or AIDS
  • You have certain types of cancer or other disorders that affect your immune system

In addition, certain other medical conditions may predispose you to infection, including implanted medical devices, malnutrition and extremes of age, among others.

Most infectious diseases have only minor complications. But some infections — such as pneumonia, AIDS and meningitis — can become life-threatening. A few types of infections have been linked to a long-term increased risk of cancer:

  • Human papillomavirus is linked to cervical cancer
  • Helicobacter pylori is linked to stomach cancer and peptic ulcers
  • Hepatitis B and C have been linked to liver cancer

In addition, some infectious diseases may become silent, only to appear again in the future — sometimes even decades later. For example, someone who's had chickenpox may develop shingles much later in life.

Follow these tips to decrease the risk of infection:

  • Wash your hands. This is especially important before and after preparing food, before eating, and after using the toilet. And try not to touch your eyes, nose or mouth with your hands, as that's a common way germs enter the body.
  • Get vaccinated. Vaccination can drastically reduce your chances of contracting many diseases. Make sure to keep up to date on your recommended vaccinations, as well as your children's.
  • Stay home when ill. Don't go to work if you are vomiting, have diarrhea or have a fever. Don't send your child to school if he or she has these signs, either.

Prepare food safely. Keep counters and other kitchen surfaces clean when preparing meals. Cook foods to the proper temperature, using a food thermometer to check for doneness. For ground meats, that means at least 160 F (71 C); for poultry, 165 F (74 C); and for most other meats, at least 145 F (63 C).

Also promptly refrigerate leftovers — don't let cooked foods remain at room temperature for long periods of time.

  • Practice safe sex. Always use condoms if you or your partner has a history of sexually transmitted infections or high-risk behavior.
  • Don't share personal items. Use your own toothbrush, comb and razor. Avoid sharing drinking glasses or dining utensils.
  • Travel wisely. If you're traveling out of the country, talk to your doctor about any special vaccinations — such as yellow fever, cholera, hepatitis A or B, or typhoid fever — you may need.
  • Vaccine guidance from Mayo Clinic
  • Enterovirus D68 and parechovirus: How can I protect my child?
  • What are superbugs and how can I protect myself from infection?

Feb 18, 2022

  • Facts about infectious disease. Infectious Disease Society of America. https://www.idsociety.org/public-health/facts-about-id/. Accessed May 29, 2019.
  • Jameson JL, et al., eds. Approach to the patient with an infectious disease. In: Harrison's Principles of Internal Medicine. 20th ed. New York, N.Y.: The McGraw-Hill Companies; 2018. https://accessmedicine.mhmedical.com. Accessed May 29, 2019.
  • Clean hands count for safe health care. Centers for Disease Control and Prevention. https://www.cdc.gov/features/handhygiene/index.html. Accessed May 29, 2019.
  • Kumar P, et al., eds. Infectious diseases and tropical medicine. In: Kumar and Clark's Clinical Medicine. 11th ed. Philadelphia, Pa.: Elsevier; 2017. https://www.clinicalkey.com. Accessed May 29, 2019.
  • LaRocque R, et al. Causes of infectious diarrhea and other foodborne illnesses in resource-rich settings. https://www.uptodate.com/contents/search. Accessed May 29, 2019.
  • Ryan KJ, ed. Infectious diseases: Syndromes and etiologies. In: Sherris Medical Microbiology. 7th ed. New York, N.Y.: McGraw-Hill Education; 2018. https://accessmedicine.mhmedical.com. Accessed May 29, 2019.
  • File TM, et al. Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults. https://www.uptodate.com/contents/search. Accessed May 29. 2019.
  • DeClerq E, et al. Approved antiviral drugs over the past 50 years. Clinical Microbiology Reviews. 2016;29:695.
  • Mousa HAL. Prevention and treatment of influenza, influenza-like illness and common cold by herbal, complementary, and natural therapies. Journal of Evidence-Based Complementary & Alternative Medicine. 2017;22:166.
  • Caring for someone sick. Centers for Disease Control and Prevention. https://www.cdc.gov/flu/treatment/caring-for-someone.htm. Accessed May 29, 2019.
  • Diseases & Conditions
  • Infectious diseases symptoms & causes

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12.2: Characteristics and Steps of Infectious Diseases

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  • Page ID 31850

Learning Objectives

  • Distinguish between signs and symptoms of disease
  • Explain the difference between a communicable disease and a noncommunicable disease
  • Identify and describe the stages of an acute infectious disease in terms of number of pathogens present and severity of signs and symptoms
  • Explain the concept of pathogenicity (virulence) in terms of infectious and lethal dose
  • Distinguish between primary and opportunistic pathogens and identify specific examples of each
  • Summarize the stages of pathogenesis
  • Explain the roles of portals of entry and exit in the transmission of disease and identify specific examples of these portals

A disease is any condition in which the normal structure or functions of the body are damaged or impaired. Physical injuries or disabilities are not classified as disease, but there can be several causes for disease, including infection by a pathogen, genetics (as in many cancers or deficiencies), noninfectious environmental causes, or inappropriate immune responses. Our focus in this chapter will be on infectious diseases, although when diagnosing infectious diseases, it is always important to consider possible noninfectious causes.

Signs and Symptoms of Disease

An infection is the successful colonization of a host by a microorganism. Microorganisms that can cause disease are known as pathogens. Infections can lead to disease, which causes signs and symptoms resulting in a deviation from the normal structure or functioning of the host. The signs of disease are objective and measurable, and can be directly observed by a clinician. Vital signs, which are used to measure the body’s basic functions, include body temperature (normally 37 °C [98.6 °F]), heart rate (normally 60–100 beats per minute), breathing rate (normally 12–18 breaths per minute), and blood pressure (normally between 90/60 and 120/80 mm Hg). Changes in any of the body’s vital signs may be indicative of disease. For example, having a fever (a body temperature significantly higher than 37 °C or 98.6 °F) is a sign of disease because it can be measured.

In addition to changes in vital signs, other observable conditions may be considered signs of disease. For example, the presence of antibodies in a patient’s serum (the liquid portion of blood that lacks clotting factors) can be observed and measured through blood tests and, therefore, can be considered a sign. However, it is important to note that the presence of antibodies is not always a sign of an active disease. Antibodies can remain in the body long after an infection has resolved; also, they may develop in response to a pathogen that is in the body but not currently causing disease.

Unlike signs, symptoms of disease are subjective. Symptoms are felt or experienced by the patient, but they cannot be clinically confirmed or objectively measured. Examples of symptoms include nausea, loss of appetite, and pain. Such symptoms are important to consider when diagnosing disease, but they are subject to memory bias and are difficult to measure precisely. Some clinicians attempt to quantify symptoms by asking patients to assign a numerical value to their symptoms. For example, the Wong-Baker Faces pain-rating scale asks patients to rate their pain on a scale of 0–10. An alternative method of quantifying pain is measuring skin conductance fluctuations. These fluctuations reflect sweating due to skin sympathetic nerve activity resulting from the stressor of pain. 1

A specific group of signs and symptoms characteristic of a particular disease is called a syndrome. Many syndromes are named using a nomenclature based on signs and symptoms or the location of the disease. Table \(\PageIndex{1}\) lists some of the prefixes and suffixes commonly used in naming syndromes.

Clinicians must rely on signs and on asking questions about symptoms, medical history, and the patient’s recent activities to identify a particular disease and the potential causative agent. Diagnosis is complicated by the fact that different microorganisms can cause similar signs and symptoms in a patient. For example, an individual presenting with symptoms of diarrhea may have been infected by one of a wide variety of pathogenic microorganisms. Bacterial pathogens associated with diarrheal disease include Vibrio cholerae , Listeria monocytogenes , Campylobacter jejuni , and enteropathogenic Escherichia coli (EPEC). Viral pathogens associated with diarrheal disease include norovirus and rotavirus. Parasitic pathogens associated with diarrhea include Giardia lamblia and Cryptosporidium parvum . Likewise, fever is indicative of many types of infection, from the common cold to the deadly Ebola hemorrhagic fever.

Finally, some diseases may be asymptomatic or subclinical, meaning they do not present any noticeable signs or symptoms. For example, most individual infected with herpes simplex virus remain asymptomatic and are unaware that they have been infected.

Exercise \(\PageIndex{1}\)

Explain the difference between signs and symptoms.

Periods of Disease

A graph titled “Periods of Disease” with time on the X axis and two separate Y-axes: number of pathogen particles (red) and severity of symptoms (blue). Both of these lines mirror each other and have a general bell shape. The first stage is incubation period when there are few pathogens and symptoms are mild. The next stage is prodromal period when the number of pathogens is increasing and symptoms are becoming more severe. The next stage is period of illness where numbers of pathogens and symptoms both continue to increase. The next stage is period of decline in infection where the number of pathogens is decreasing and symptoms are becoming less severe. The final stage is period of convalescence when symptoms go away and the number of pathogens decrease. Note that there are still pathogens present even after there are no more symptoms of the disease.

The five periods of disease (sometimes referred to as stages or phases) include the incubation, prodromal, illness, decline, and convalescence periods (Figure \(\PageIndex{1}\)). The incubation period occurs in an acute disease after the initial entry of the pathogen into the host (patient). It is during this time the pathogen begins multiplying in the host. However, there are insufficient numbers of pathogen particles (cells or viruses) present to cause signs and symptoms of disease. Incubation periods can vary from a day or two in acute disease to months or years in chronic disease, depending upon the pathogen. Factors involved in determining the length of the incubation period are diverse, and can include strength of the pathogen, strength of the host immune defenses, site of infection, type of infection, and the size infectious dose received. During this incubation period, the patient is unaware that a disease is beginning to develop.

The prodromal period occurs after the incubation period. During this phase, the pathogen continues to multiply and the host begins to experience general signs and symptoms of illness, which typically result from activation of the immune system, such as fever, pain, soreness, swelling, or inflammation. Usually, such signs and symptoms are too general to indicate a particular disease. Following the prodromal period is the period of illness, during which the signs and symptoms of disease are most obvious, specific and severe.

The period of illness is followed by the period of decline, during which the number of pathogen particles begins to decrease, and the signs and symptoms of illness begin to decline. However, during the decline period, patients may become susceptible to developing secondary infections because their immune systems have been weakened by the primary infection. The final period is known as the period of convalescence. During this stage, the patient generally returns to normal functions, although some diseases may inflict permanent damage that the body cannot fully repair.

Infectious diseases can be contagious during all five of the periods of disease. Which periods of disease are more likely to associated with transmissibility of an infection depends upon the disease, the pathogen, and the mechanisms by which the disease develops and progresses. For example, with meningitis (infection of the lining of brain), the periods of infectivity depend on the type of pathogen causing the infection. Patients with bacterial meningitis are contagious during the incubation period for up to a week before the onset of the prodromal period, whereas patients with viral meningitis become contagious when the first signs and symptoms of the prodromal period appear. With many viral diseases associated with rashes (e.g., chickenpox, measles, rubella, roseola), patients are contagious during the incubation period up to a week before the rash develops. In contrast, with many respiratory infections (e.g., colds, influenza, diphtheria, strep throat, and pertussis) the patient becomes contagious with the onset of the prodromal period. Depending upon the pathogen, the disease, and the individual infected, transmission can still occur during the periods of decline, convalescence, and even long after signs and symptoms of the disease disappear. For example, an individual recovering from a diarrheal disease may continue to carry and shed the pathogen in feces for some time, posing a risk of transmission to others through direct contact or indirect contact (e.g., through contaminated objects or food).

Exercise \(\PageIndex{2}\)

Name some of the factors that can affect the length of the incubation period of a particular disease.

Acute and Chronic Diseases

The duration of the period of illness can vary greatly, depending on the pathogen, effectiveness of the immune response in the host, and any medical treatment received. For an acute disease, pathologic changes occur over a relatively short time (e.g., hours, days, or a few weeks) and involve a rapid onset of disease conditions. For example, influenza (caused by Influenzavirus) is considered an acute disease because the incubation period is approximately 1–2 days. Infected individuals can spread influenza to others for approximately 5 days after becoming ill. After approximately 1 week, individuals enter the period of decline.

For a chronic disease, pathologic changes can occur over longer time spans (e.g., months, years, or a lifetime). For example, chronic gastritis (inflammation of the lining of the stomach) is caused by the gram-negative bacterium Helicobacter pylori . H. pylori is able to colonize the stomach and persist in its highly acidic environment by producing the enzyme urease, which modifies the local acidity, allowing the bacteria to survive indefinitely. 2 Consequently, H. pylori infections can recur indefinitely unless the infection is cleared using antibiotics. 3 Hepatitis B virus can cause a chronic infection in some patients who do not eliminate the virus after the acute illness. A chronic infection with hepatitis B virus is characterized by the continued production of infectious virus for 6 months or longer after the acute infection, as measured by the presence of viral antigen in blood samples.

In latent diseases, as opposed to chronic infections, the causal pathogen goes dormant for extended periods of time with no active replication. Examples of diseases that go into a latent state after the acute infection include herpes (herpes simplex viruses [HSV-1 and HSV-2]), chickenpox (varicella-zoster virus [VZV]), and mononucleosis (Epstein-Barr virus [EBV]). HSV-1, HSV-2, and VZV evade the host immune system by residing in a latent form within cells of the nervous system for long periods of time, but they can reactivate to become active infections during times of stress and immunosuppression. For example, an initial infection by VZV may result in a case of childhood chickenpox, followed by a long period of latency. The virus may reactivate decades later, causing episodes of shingles in adulthood. EBV goes into latency in B cells of the immune system and possibly epithelial cells; it can reactivate years later to produce B-cell lymphoma.

Exercise \(\PageIndex{3}\)

Explain the difference between latent disease and chronic disease.

Pathogenicity and Virulence

The ability of a microbial agent to cause disease is called pathogenicity, and the degree to which an organism is pathogenic is called virulence. Virulence is a continuum. On one end of the spectrum are organisms that are avirulent (not harmful) and on the other are organisms that are highly virulent. Highly virulent pathogens will almost always lead to a disease state when introduced to the body, and some may even cause multi-organ and body system failure in healthy individuals. Less virulent pathogens may cause an initial infection, but may not always cause severe illness. Pathogens with low virulence would more likely result in mild signs and symptoms of disease, such as low-grade fever, headache, or muscle aches. Some individuals might even be asymptomatic.

An example of a highly virulent microorganism is Bacillus anthracis , the pathogen responsible for anthrax. B. anthracis can produce different forms of disease, depending on the route of transmission (e.g., cutaneous injection, inhalation, ingestion). The most serious form of anthrax is inhalation anthrax. After B. anthracis spores are inhaled, they germinate. An active infection develops and the bacteria release potent toxins that cause edema (fluid buildup in tissues), hypoxia (a condition preventing oxygen from reaching tissues), and necrosis (cell death and inflammation). Signs and symptoms of inhalation anthrax include high fever, difficulty breathing, vomiting and coughing up blood, and severe chest pains suggestive of a heart attack. With inhalation anthrax, the toxins and bacteria enter the bloodstream, which can lead to multi-organ failure and death of the patient. If a gene (or genes) involved in pathogenesis is inactivated, the bacteria become less virulent or nonpathogenic.

A graph with “number of pathogenic agents (cells or virions)” on the X axis and Percent mortality in experimental group on the Y axis. The graph begins at 0,0 and increases until there is nearly 100% death at 10 to the 5. The line then plateaus at 100%.  A 50% death rate occurs at 10 to the 4. This is the LD 50.

Virulence of a pathogen can be quantified using controlled experiments with laboratory animals. Two important indicators of virulence are the median infectious dose (ID 50 ) and the median lethal dose (LD 50 ), both of which are typically determined experimentally using animal models. The ID 50 is the number of pathogen cells or virions required to cause active infection in 50% of inoculated animals. The LD 50 is the number of pathogenic cells, virions, or amount of toxin required to kill 50% of infected animals. To calculate these values, each group of animals is inoculated with one of a range of known numbers of pathogen cells or virions. In graphs like the one shown in Figure \(\PageIndex{2}\), the percentage of animals that have been infected (for ID 50 ) or killed (for LD 50 ) is plotted against the concentration of pathogen inoculated. Figure \(\PageIndex{2}\) represents data graphed from a hypothetical experiment measuring the LD 50 of a pathogen. Interpretation of the data from this graph indicates that the LD 50 of the pathogen for the test animals is 10 4 pathogen cells or virions (depending upon the pathogen studied).

Table \(\PageIndex{2}\) lists selected foodborne pathogens and their ID 50 values in humans (as determined from epidemiologic data and studies on human volunteers). Keep in mind that these are median values. The actual infective dose for an individual can vary widely, depending on factors such as route of entry; the age, health, and immune status of the host; and environmental and pathogen-specific factors such as susceptibility to the acidic pH of the stomach. It is also important to note that a pathogen’s infective dose does not necessarily correlate with disease severity. For example, just a single cell of Salmonella enterica serotype typhimurium can result in an active infection. The resultant disease, Salmonella gastroenteritis or salmonellosis, can cause nausea, vomiting, and diarrhea, but has a mortality rate of less than 1% in healthy adults. In contrast, S. enterica serotype Typhi has a much higher ID 50 , typically requiring as many as 1,000 cells to produce infection. However, this serotype causes typhoid fever, a much more systemic and severe disease that has a mortality rate as high as 10% in untreated individuals.

Exercise \(\PageIndex{4}\)

  • What is the difference between a pathogen’s infective dose and lethal dose?
  • Which is more closely related to the severity of a disease?

Primary Pathogens versus Opportunistic Pathogens

Pathogens can be classified as either primary pathogens or opportunistic pathogens. A primary pathogen can cause disease in a host regardless of the host’s resident microbiota or immune system. An opportunistic pathogen, by contrast, can only cause disease in situations that compromise the host’s defenses, such as the body’s protective barriers, immune system, or normal microbiota. Individuals susceptible to opportunistic infections include the very young, the elderly, women who are pregnant, patients undergoing chemotherapy, people with immunodeficiencies (such as acquired immunodeficiency syndrome [AIDS]), patients who are recovering from surgery, and those who have had a breach of protective barriers (such as a severe wound or burn).

An example of a primary pathogen is enterohemorrhagic E. coli (EHEC), which produces a virulence factor known as Shiga toxin. This toxin inhibits protein synthesis, leading to severe and bloody diarrhea, inflammation, and renal failure, even in patients with healthy immune systems. Staphylococcus epidermidis , on the other hand, is an opportunistic pathogen that is among the most frequent causes of nosocomial disease. 6 S. epidermidis is a member of the normal microbiota of the skin, where it is generally avirulent. However, in hospitals, it can also grow in biofilms that form on catheters, implants, or other devices that are inserted into the body during surgical procedures. Once inside the body, S. epidermidis can cause serious infections such as endocarditis, and it produces virulence factors that promote the persistence of such infections.

Other members of the normal microbiota can also cause opportunistic infections under certain conditions. This often occurs when microbes that reside harmlessly in one body location end up in a different body system, where they cause disease. For example, E. coli normally found in the large intestine can cause a urinary tract infection if it enters the bladder. This is the leading cause of urinary tract infections among women.

Members of the normal microbiota may also cause disease when a shift in the environment of the body leads to overgrowth of a particular microorganism. For example, the yeast Candida is part of the normal microbiota of the skin, mouth, intestine, and vagina, but its population is kept in check by other organisms of the microbiota. If an individual is taking antibacterial medications, however, bacteria that would normally inhibit the growth of Candida can be killed off, leading to a sudden growth in the population of Candida , which is not affected by antibacterial medications because it is a fungus. An overgrowth of Candida can manifest as oral thrush (growth on mouth, throat, and tongue), a vaginal yeast infection, or cutaneous candidiasis. Other scenarios can also provide opportunities for Candida infections. Untreated diabetes can result in a high concentration of glucose in the saliva, which provides an optimal environment for the growth of Candida, resulting in thrush. Immunodeficiencies such as those seen in patients with HIV, AIDS, and cancer also lead to higher incidence of thrush. Vaginal yeast infections can result from decreases in estrogen levels during the menstruation or menopause. The amount of glycogen available to lactobacilli in the vagina is controlled by levels of estrogen; when estrogen levels are low, lactobacilli produce less lactic acid. The resultant increase in vaginal pH allows overgrowth of Candida in the vagina.

Exercise \(\PageIndex{5}\)

  • Explain the difference between a primary pathogen and an opportunistic pathogen.
  • Describe some conditions under which an opportunistic infection can occur.

Stages of Pathogenesis

To cause disease, a pathogen must successfully achieve four steps or stages of pathogenesis: exposure (contact), adhesion (colonization), invasion, and infection. The pathogen must be able to gain entry to the host, travel to the location where it can establish an infection, evade or overcome the host’s immune response, and cause damage (i.e., disease) to the host. In many cases, the cycle is completed when the pathogen exits the host and is transmitted to a new host.

An encounter with a potential pathogen is known as exposure or contact. The food we eat and the objects we handle are all ways that we can come into contact with potential pathogens. Yet, not all contacts result in infection and disease. For a pathogen to cause disease, it needs to be able to gain access into host tissue. An anatomic site through which pathogens can pass into host tissue is called a portal of entry. These are locations where the host cells are in direct contact with the external environment. Major portals of entry are identified in Figure \(\PageIndex{3}\) and include the skin, mucous membranes, and parenteral routes.

Portals of entry: eye (conjunctiva), nose, mouth, ear, needle, broken skin, insect bite, urethra, vagina, anus, placenta (portal of entry for fetus).

Mucosal surfaces are the most important portals of entry for microbes; these include the mucous membranes of the respiratory tract, the gastrointestinal tract, and the genitourinary tract. Although most mucosal surfaces are in the interior of the body, some are contiguous with the external skin at various body openings, including the eyes, nose, mouth, urethra, and anus.

Most pathogens are suited to a particular portal of entry. A pathogen’s portal specificity is determined by the organism’s environmental adaptions and by the enzymes and toxins they secrete. The respiratory and gastrointestinal tracts are particularly vulnerable portals of entry because particles that include microorganisms are constantly inhaled or ingested, respectively.

Pathogens can also enter through a breach in the protective barriers of the skin and mucous membranes. Pathogens that enter the body in this way are said to enter by the parenteral route. For example, the skin is a good natural barrier to pathogens, but breaks in the skin (e.g., wounds, insect bites, animal bites, needle pricks) can provide a parenteral portal of entry for microorganisms.

In pregnant women, the placenta normally prevents microorganisms from passing from the mother to the fetus. However, a few pathogens are capable of crossing the blood-placental barrier. The gram-positive bacterium Listeria monocytogenes , which causes the foodborne disease listeriosis, is one example that poses a serious risk to the fetus and can sometimes lead to spontaneous abortion. Other pathogens that can pass the placental barrier to infect the fetus are known collectively by the acronym TORCH (Table \(\PageIndex{3}\)).

Transmission of infectious diseases from mother to baby is also a concern at the time of birth when the baby passes through the birth canal. Babies whose mothers have active chlamydia or gonorrhea infections may be exposed to the causative pathogens in the vagina, which can result in eye infections that lead to blindness. To prevent this, it is standard practice to administer antibiotic drops to infants’ eyes shortly after birth.

Table \(\PageIndex{3}\): Pathogens Capable of Crossing the Placental Barrier (TORCH Infections)

Clinical Focus: part 2

At the clinic, a physician takes down Michael’s medical history and asks about his activities and diet over the past week. Upon learning that Michael became sick the day after the party, the physician orders a blood test to check for pathogens associated with foodborne diseases. After tests confirm that presence of a gram-positive rod in Michael’s blood, he is given an injection of a broad-spectrum antibiotic and sent to a nearby hospital, where he is admitted as a patient. There he is to receive additional intravenous antibiotic therapy and fluids.

Exercise \(\PageIndex{6}\)

  • Is this bacterium in Michael’s blood part of normal microbiota?
  • What portal of entry did the bacteria use to cause this infection?

Following the initial exposure, the pathogen adheres at the portal of entry. The term adhesion refers to the capability of pathogenic microbes to attach to the cells of the body using adhesion factors, and different pathogens use various mechanisms to adhere to the cells of host tissues.

Molecules (either proteins or carbohydrates) called adhesins are found on the surface of certain pathogens and bind to specific receptors (glycoproteins) on host cells. Adhesins are present on the fimbriae and flagella of bacteria, the cilia of protozoa, and the capsids or membranes of viruses. Protozoans can also use hooks and barbs for adhesion; spike proteins on viruses also enhance viral adhesion. The production of glycocalyces (slime layers and capsules) (Figure \(\PageIndex{4}\)), with their high sugar and protein content, can also allow certain bacterial pathogens to attach to cells.

Biofilm growth can also act as an adhesion factor. A biofilm is a community of bacteria that produce a glycocalyx, which contributes to the extrapolymeric substances (EPS) that allows the biofilm to attach to a surface. Persistent Pseudomonas aeruginosa infections are common in patients suffering from cystic fibrosis, burn wounds, and middle-ear infections (otitis media) because P. aeruginosa produces a biofilm. The EPS allows the microbe to adhere to the host cells and makes it harder for the host to physically remove the pathogen. The EPS not only allows for attachment but provides protection against the immune system and antibiotic or antimicrobial treatments, preventing the medications from reaching the cells within the biofilm. In addition, not all bacteria in a biofilm are rapidly growing; some are in stationary phase. Since antibiotics are most effective against rapidly growing bacteria, portions of bacteria in a biofilm are protected against antibiotics. 8

clipboard_e90a6ea9f14f14b935006d2e2e4378a88.png

Once adhesion is successful, invasion can proceed. Invasion involves the dissemination of a pathogen throughout local tissues or the body. Pathogens may produce exoenzymes or toxins, which serve as virulence factors that allow them to colonize and damage host tissues as they spread deeper into the body. Pathogens may also produce virulence factors that protect them against immune system defenses. A pathogen’s specific virulence factors determine the degree of tissue damage that occurs. Figure \(\PageIndex{5}\) shows the invasion of H. pylori into the tissues of the stomach, causing damage as it progresses.

Diagram of H. pylori invading the lining of the stomach. In the first image the H. pylori (an oval cell with 3 flagella is not able to penetrate the gastric mucin gel on top of the epithelial cells. Contact with stomach acid keeps the mucin lining the epithelial cell layer in a spongy gel-like state. This consistency is impermeable to the bacterium H. pylori. The second image shows the bacterium entering the lining. The bacterium releases urease, which neutralizes the stomach acid. This causes the mucin to liquefy and the bacterium can swim right through it.

Intracellular pathogens achieve invasion by entering the host’s cells and reproducing. Some are obligate intracellular pathogens (meaning they can only reproduce inside of host cells) and others are facultative intracellular pathogens (meaning they can reproduce either inside or outside of host cells). By entering the host cells, intracellular pathogens are able to evade some mechanisms of the immune system while also exploiting the nutrients in the host cell.

Entry to a cell can occur by endocytosis. For most kinds of host cells, pathogens use one of two different mechanisms for endocytosis and entry. One mechanism relies on effector proteins secreted by the pathogen; these effector proteins trigger entry into the host cell. This is the method that Salmonella and Shigella use when invading intestinal epithelial cells. When these pathogens come in contact with epithelial cells in the intestine, they secrete effector molecules that cause protrusions of membrane ruffles that bring the bacterial cell in. This process is called membrane ruffling. The second mechanism relies on surface proteins expressed on the pathogen that bind to receptors on the host cell, resulting in entry. For example, Yersinia pseudotuberculosis produces a surface protein known as invasin that binds to beta-1 integrins expressed on the surface of host cells.

Some host cells, such as white blood cells and other phagocytes of the immune system, actively endocytose pathogens in a process called phagocytosis. Although phagocytosis allows the pathogen to gain entry to the host cell, in most cases, the host cell kills and degrades the pathogen by using digestive enzymes. Normally, when a pathogen is ingested by a phagocyte, it is enclosed within a phagosome in the cytoplasm; the phagosome fuses with a lysosome to form a phagolysosome, where digestive enzymes kill the pathogen. However, some intracellular pathogens have the ability to survive and multiply within phagocytes. Examples include Listeria monocytogenes and Shigella ; these bacteria produce proteins that lyse the phagosome before it fuses with the lysosome, allowing the bacteria to escape into the phagocyte’s cytoplasm where they can multiply. Bacteria such as Mycobacterium tuberculosis , Legionella pneumophila , and Salmonella species use a slightly different mechanism to evade being digested by the phagocyte. These bacteria prevent the fusion of the phagosome with the lysosome, thus remaining alive and dividing within the phagosome.

Following invasion, successful multiplication of the pathogen leads to infection. Infections can be described as local, focal, or systemic, depending on the extent of the infection. A local infection is confined to a small area of the body, typically near the portal of entry. For example, a hair follicle infected by Staphylococcus aureus infection may result in a boil around the site of infection, but the bacterium is largely contained to this small location. Other examples of local infections that involve more extensive tissue involvement include urinary tract infections confined to the bladder or pneumonia confined to the lungs.

In a focal infection, a localized pathogen, or the toxins it produces, can spread to a secondary location. For example, a dental hygienist nicking the gum with a sharp tool can lead to a local infection in the gum by Streptococcus bacteria of the normal oral microbiota. These Streptococcus spp. may then gain access to the bloodstream and make their way to other locations in the body, resulting in a secondary infection.

When an infection becomes disseminated throughout the body, we call it a systemic infection. For example, infection by the varicella-zoster virus typically gains entry through a mucous membrane of the upper respiratory system. It then spreads throughout the body, resulting in the classic red skin lesions associated with chickenpox. Since these lesions are not sites of initial infection, they are signs of a systemic infection.

Sometimes a primary infection, the initial infection caused by one pathogen, can lead to a secondary infection by another pathogen. For example, the immune system of a patient with a primary infection by HIV becomes compromised, making the patient more susceptible to secondary diseases like oral thrush and others caused by opportunistic pathogens. Similarly, a primary infection by Influenzavirus damages and decreases the defense mechanisms of the lungs, making patients more susceptible to a secondary pneumonia by a bacterial pathogen like Haemophilus influenzae or Streptococcus pneumoniae . Some secondary infections can even develop as a result of treatment for a primary infection. Antibiotic therapy targeting the primary pathogen can cause collateral damage to the normal microbiota, creating an opening for opportunistic pathogens (see Case in Point: A Secondary Yeast Infection below).

A Secondary Yeast Infection

Anita, a 36-year-old mother of three, goes to an urgent care center complaining of pelvic pressure, frequent and painful urination, abdominal cramps, and occasional blood-tinged urine. Suspecting a urinary tract infection (UTI), the physician requests a urine sample and sends it to the lab for a urinalysis. Since it will take approximately 24 hours to get the results of the culturing, the physician immediately starts Anita on the antibiotic ciprofloxacin. The next day, the microbiology lab confirms the presence of E. coli in Anita’s urine, which is consistent with the presumptive diagnosis. However, the antimicrobial susceptibility test indicates that ciprofloxacin would not effectively treat Anita’s UTI, so the physician prescribes a different antibiotic.

After taking her antibiotics for 1 week, Anita returns to the clinic complaining that the prescription is not working. Although the painful urination has subsided, she is now experiencing vaginal itching, burning, and discharge. After a brief examination, the physician explains to Anita that the antibiotics were likely successful in killing the E. coli responsible for her UTI; however, in the process, they also wiped out many of the “good” bacteria in Anita’s normal microbiota. The new symptoms that Anita has reported are consistent with a secondary yeast infection by Candida albicans , an opportunistic fungus that normally resides in the vagina but is inhibited by the bacteria that normally reside in the same environment.

To confirm this diagnosis, a microscope slide of a direct vaginal smear is prepared from the discharge to check for the presence of yeast. A sample of the discharge accompanies this slide to the microbiology lab to determine if there has been an increase in the population of yeast causing vaginitis. After the microbiology lab confirms the diagnosis, the physician prescribes an antifungal drug for Anita to use to eliminate her secondary yeast infection.

Exercise \(\PageIndex{7}\)

  • Why was Candida not killed by the antibiotics prescribed for the UTI?
  • List three conditions that could lead to a secondary infection.

Transmission of Disease

For a pathogen to persist, it must put itself in a position to be transmitted to a new host, leaving the infected host through a portal of exit (Figure \(\PageIndex{6}\)). As with portals of entry, many pathogens are adapted to use a particular portal of exit. Similar to portals of entry, the most common portals of exit include the skin and the respiratory, urogenital, and gastrointestinal tracts. Coughing and sneezing can expel pathogens from the respiratory tract. A single sneeze can send thousands of virus particles into the air. Secretions and excretions can transport pathogens out of other portals of exit. Feces, urine, semen, vaginal secretions, tears, sweat, and shed skin cells can all serve as vehicles for a pathogen to leave the body. Pathogens that rely on insect vectors for transmission exit the body in the blood extracted by a biting insect. Similarly, some pathogens exit the body in blood extracted by needles.

Portals of exit: eye (tears), needle,  mammary glands (milk, secretions), placenta (transmission to fetus), vagina (secretions, blood), urethra (urine), broken skin,  broken skin (blood), skin (flakes), nose (secretions), mouth (saliva, sputum), ear (earwax), urethra (urine, semen, secretions), anus (feces).

Key Concepts and Summary

  • In an infection , a microorganism enters a host and begins to multiply. Some infections cause disease , which is any deviation from the normal function or structure of the host.
  • Signs of a disease are objective and are measured. Symptoms of a disease are subjective and are reported by the patient.
  • Diseases can either be noninfectious (due to genetics and environment) or infectious (due to pathogens). Some infectious diseases are communicable (transmissible between individuals) or contagious (easily transmissible between individuals); others are noncommunicable , but may be contracted via contact with environmental reservoirs or animals ( zoonoses )
  • Nosocomial diseases are contracted in hospital settings, whereas iatrogenic disease are the direct result of a medical procedure
  • An acute disease is short in duration, whereas a chronic disease lasts for months or years. Latent diseases last for years, but are distinguished from chronic diseases by the lack of active replication during extended dormant periods.
  • The periods of disease include the incubation period , the prodromal period , the period of illness , the period of decline , and the period of convalescence . These periods are marked by changes in the number of infectious agents and the severity of signs and symptoms.
  • Virulence , the degree to which a pathogen can cause disease, can be quantified by calculating either the ID 50 or LD 50 of a pathogen on a given population.
  • Primary pathogens are capable of causing pathological changes associated with disease in a healthy individual, whereas opportunistic pathogens can only cause disease when the individual is compromised by a break in protective barriers or immunosuppression.
  • Infections and disease can be caused by pathogens in the environment or microbes in an individual’s resident microbiota .
  • Infections can be classified as local , focal , or systemic depending on the extent to which the pathogen spreads in the body.
  • A secondary infection can sometimes occur after the host’s defenses or normal microbiota are compromised by a primary infection or antibiotic treatment.
  • Pathogens enter the body through portals of entry and leave through portals of exit . The stages of pathogenesis include exposure , adhesion , invasion , infection , and transmission .
  • F. Savino et al. “Pain Assessment in Children Undergoing Venipuncture: The Wong–Baker Faces Scale Versus Skin Conductance Fluctuations.” PeerJ 1 (2013):e37; https://peerj.com/articles/37/
  • J.G. Kusters et al. Pathogenesis of Helicobacter pylori Infection. Clinical Microbiology Reviews 19 no. 3 (2006):449–490.
  • N.R. Salama et al. “Life in the Human Stomach: Persistence Strategies of the Bacterial Pathogen Helicobacter pylori .” Nature Reviews Microbiology 11 (2013):385–399.
  • C. Owens. “ P. aeruginosa survives in sinks 10 years after hospital outbreak.” 2015. www.healio.com/infectious-dis...pital-outbreak
  • Food and Drug Administration. “Bad Bug Book, Foodborne Pathogenic Microorganisms and Natural Toxins.” 2nd ed. Silver Spring, MD: US Food and Drug Administration; 2012.
  • M. Otto. “ Staphylococcus epidermidis --The ‘Accidental’ Pathogen.” Nature Reviews Microbiology 7 no. 8 (2009):555–567.
  • The O in TORCH stands for “other.”
  • D. Davies. “Understanding Biofilm Resistance to Antibacterial Agents.” Nature Reviews Drug Discovery 2 (2003):114–122.

Contributor

Nina Parker, (Shenandoah University), Mark Schneegurt (Wichita State University), Anh-Hue Thi Tu (Georgia Southwestern State University), Philip Lister (Central New Mexico Community College), and Brian M. Forster (Saint Joseph’s University) with many contributing authors. Original content via Openstax (CC BY 4.0; Access for free at  https://openstax.org/books/microbiology/pages/1-introduction )

Introduction to Epidemiology

Available materials.

Epidemiology is the “study of distribution and determinants of health-related states among specified populations and the application of that study to the control of health problems.” — A Dictionary of Epidemiology

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  • Key concepts and terms
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Suggested Citation:

Centers for Disease Control and Prevention (CDC). Introduction to Public Health. In: Public Health 101 Series. Atlanta, GA: U.S. Department of Health and Human Services, CDC; 2014. Available at: https://www.cdc.gov/publichealth101/epidemiology.html .

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Infectious Diseases

Chapter objectives.

The objectives of this chapter are to provide a brief understanding of the following:

  • 1. Clinical evaluation of infectious diseases and altered immune disorders, including physical examination and laboratory studies
  • 2. Various infectious disease processes, including etiology, pathogenesis, clinical presentation, and management
  • 3. Commonly encountered altered immune disorders, including etiology, clinical presentation, and management
  • 4. Precautions and guidelines that a physical therapist should implement when treating a patient with an infectious disease process or altered immunity

Preferred Practice Patterns

The most relevant practice patterns for the diagnoses discussed in this chapter, based on the American Physical Therapy Association's Guide to Physical Therapist Practice , second edition, are as follows:

  • • Health Care–Associated or Nosocomial Infections ( Escherichia coli , Staphylococcus aureus , Enterococcus faecalis , Pseudomonas aeruginosa , Candida albicans , and Coagulase-Negative Staphylococci): 6B, 7A
  • • Antibiotic-Resistant Infections: Methicillin-Resistant Staphylococcus aureus , Vancomycin-Resistant Enterococci, Multi-Drug Resistant Acinetobacter baumannii : 6B, 7A
  • • Upper Respiratory Tract Infections (Rhinitis, Sinusitis, Influenza, Pertussis): 6B, 6F, 6G
  • • Lower Respiratory Tract Infections (Tuberculosis, Histoplasmosis, Legionellosis, Severe Acute Respiratory Syndrome [SARS]): 6B, 7C, 7D
  • • Cardiac Infections: Pericarditis, Myocarditis, Left-Sided Endocarditis, Acute Rheumatic Fever, Rheumatic Heart Disease. See Chapter 3: 6B, 6D
  • • Neurological Diseases: Poliomyelitis, Postpoliomyelitis Syndrome, Meningitis, and Encephalitis: 4A, 5C, 5D, 5G, 6E, 5H, 7A
  • • Musculoskeletal Infections: Osteomyelitis and Its Variations: 4G, 4H, 5H
  • • Skin Infections: Cellulitis, groups A and G Streptococcus, and Staphylococcus aureus : 4E, 6H, 7B, 7C, 7D, 7E
  • • Gastrointestinal Infections: Gastroenteritis, Escherichia coli , Shigella , Clostridium difficile , Salmonella , Rotavirus, Norovirus, Adenovirus, and Astrovirus: Please refer to Chapter 8
  • • Immune System Infections: HIV, Mononucleosis, Cytomegalovirus Infection, and Toxoplasmosis: 4C, 6B
  • • Sepsis: Bacteremia, Septicemia, and Shock Syndrome (or Septic Shock): 5C, 6F, 6H

Please refer to Appendix A for a complete list of the preferred practice patterns, as individual patient conditions are highly variable and other practice patterns may be applicable.

Definition of Terms

To facilitate the understanding of infectious disease processes, terminology that is commonly used when referring to these processes is presented in Table 13-1 . 3 , 4 , 5 , 6

Terminology Associated with Infectious Disease Processes

Body Structure and Function

A person's immune system is composed of many complex, yet synergistic, components that defend against pathogens ( Table 13-2 ). 3 Any defect in this system may lead to the development of active infection. Patients in the acute care setting often present with acquired factors that can create some or most of these defects, which can ultimately affect their immune system ( Box 13-1 ). 4 Congenital factors such as lymphocyte deficiency occur rarely.

Components of the Immune System

Factors Affecting the Immune System

  • • Pregnancy
  • • Preexisting infections
  • • Malignancies (Hodgkin's disease, acute or chronic leukemia, nonlymphoid malignancy, or myeloma)
  • • Stress (emotional or surgical—anesthesia)
  • • Malnutrition (insufficiency of calories, protein, iron, and zinc)
  • • Age
  • • Chronic diseases (diabetes, alcoholic cirrhosis, sickle cell anemia)
  • • Lymph node dissection
  • • Immunosuppressive treatment (corticosteroids, chemotherapy, or radiation therapy)
  • • Indwelling lines and tubes

When an infectious disease process is suspected, a thorough patient interview (history) and physical examination are performed to serve as a screening tool for the differential diagnosis and to help determine which laboratory tests are further required to identify a specific pathogen. 7

Potential contributing factors of the infection are sought out, such as immunocompromise, immunosuppression, recent exposure to infectious individuals, or recent travel to foreign countries. Also, a qualitative description of the symptomatology is discerned, such as onset or nature of symptoms (e.g., a nonproductive versus productive cough over the past days or weeks).

Physical Examination

Observation.

Clinical presentation of infectious diseases is highly variable according to the specific system that is involved. However, common physical findings that occur with infection include sweating and inflammation, both of which are related to the metabolic response of the body to the antigen. The classic signs of inflammation (redness [rubor], and swelling [tumor]) in certain areas of the body can help delineate the source, location(s), or both of infection. Delineating the source of infection is crucial to the diagnostic process.

The presence of warmth (calor) and possible pain (dolor) or tenderness is another typical classic sign of inflammation that may be consistent with active infection. Lymphoid organs (lymph nodes and spleen) can also be swollen and tender with infection, because lymphocytes (processed in these organs) are multiplying in response to the antigen. Inflammation and tenderness in these or other areas of the body can further help to delineate the infectious process.

Vital Signs

Heart rate, blood pressure, and respiratory rate..

Measurement of vital signs helps in determining whether an infectious process is occurring. (Infections result in an increased metabolic rate, which presents as an increased heart rate and respiratory rate.) Blood pressure may also be elevated when metabolism is increased, or blood pressure can be decreased secondary to vasodilation from inflammatory responses in the body.

Temperature.

Monitoring the patient's temperature over time (both throughout the day and daily) provides information regarding the progression (a rise in temperature) or a regression (a fall in temperature) of the infectious process. With an infectious process, some of the bacteria and extracts from normal leukocytes are pyrogenic, causing the thermostat in the hypothalamus to rise, resulting in an elevated body temperature. 8 A fall in body temperature from a relatively elevated temperature may also signify a response to a medication.

 Clinical Tip

An afebrile status is not always indicative of the absence of infection. If a patient is on antipyretics, the fever symptoms may be controlled. Check the medication list and ask about the administration schedule. A patient must be afebrile for at least 24 hours before being discharged from an inpatient setting.

Auscultation

Heart and lung sounds determine whether infectious processes are a direct result from these areas or are indirectly affecting these areas. Refer to Chapters 3 and 4, respectively, for more information on heart and lung auscultation.

Laboratory Studies

Most of the evaluation process for diagnosing an infectious disease is based on laboratory studies. These studies are performed to (1) isolate the microorganisms from various body fluids or sites; (2) directly examine specimens by microscopic, immunologic, or genetic techniques; or (3) assess specific antibody responses to the pathogen. 9 This diagnostic process is essential to prescribing the most specific medical regimen possible for the patient.

During hematologic studies, a sample of blood is taken and analyzed to assist in determining the presence of an infectious process or organism. Hematologic procedures used to diagnose infection include leukocyte count, differential white blood cell (WBC) count, and antibody measurement. 10

Leukocyte Count.

Leukocyte, or WBC, count is measured to determine whether an infectious process is present and should range between 5000 and 10,000 cells/mm 3 . 3 An increase in the number of WBCs, termed leukocytosis , is required for phagocytosis (cellular destruction of microorganisms) and can indicate the presence of an acute infectious process. 11 Leukocytosis can also be present with inflammation and may occur after a surgery with postoperative inflammation. 8 A decreased WBC count from baseline, termed leukopenia , can indicate altered immunity or the presence of an infection that exhausts supplies of certain WBCs. 11 A decreased WBC count relative to a previously high count (i.e., becoming more within normal limits) may indicate the resolution of an infectious process. 11

Differential White Blood Cell Count.

Five types of WBCs exist: lymphocytes, monocytes, neutrophils, basophils, and eosinophils. Specific types of infectious processes can trigger alterations in the values of one or more of these cells. Detection of these changes can assist in identification of the type of infection present. For example, an infection caused by bacteria can result in a higher percentage of neutrophils, which have a normal range of 2.0 to 7.5 × 10 9 /liter. In contrast, a parasitic infection will result in increased eosinophils, which have a normal count of 0.0 to 0.45 × 10 9 /liter. 11

Antibody Measurement.

Antibodies develop in response to the invasion of antigens from new infectious agents. Identifying the presence and concentration of specific antibodies helps in determining past and present exposure to infectious organisms. 12

Microbiology

In microbiology studies, specimens from suspected sources of infection (e.g., sputum, urine, feces, wounds, and cerebrospinal fluid) are collected by sterile technique and analyzed by staining, culture, or sensitivity or resistance testing, or a combination of all of these.

Staining allows for morphologic examination of organisms under a microscope. Two types of staining techniques are available: simple staining and the more advanced differential staining. Many types of each technique exist, but the differential Gram's stain is the most common. 12

Gram's stain is used to differentiate similar organisms by categorizing them as gram-positive or gram-negative. This separation assists in determining subsequent measures to be taken for eventual identification of the organism. A specimen is placed on a microscope slide, and a series of steps are performed. 13 A red specimen at completion indicates a gram-negative organism, whereas a violet specimen indicates a gram-positive organism. 13

The purpose of a culture is to identify and produce isolated colonies of organisms found within a collected specimen. Cells of the organism are isolated and mixed with specific media that provide the proper nourishment and environment (e.g., pH level, oxygen content) needed for the organism to reproduce into colonies. Once this has taken place, the resultant infectious agent is observed for size, shape, elevation, texture, marginal appearance, and color to assist with identification. 13

Sensitivity and Resistance.

When an organism has been isolated from a specimen, its sensitivity (susceptibility) to antimicrobial agents or antibiotics is tested. An infectious agent is sensitive to an antibiotic when the organism's growth is inhibited under safe dose concentrations. Conversely, an agent is resistant to an antibiotic when its growth is not inhibited by safe dose concentrations. Because of a number of factors, such as mutations, an organism's sensitivity, resistance, or both to antibiotics are constantly changing. 14

Cytology is a complex method of studying cellular structures, functions, origins, and formations. Cytology assists in differentiating between an infectious process and a malignancy and in determining the type and severity of a present infectious process by examining cellular characteristics. 12 , 15 It is beyond the scope of this book, however, to describe all of the processes involved in studying cellular structure dysfunction.

Body Fluid Examination

Pleural tap..

A pleural tap, or thoracentesis, is the process by which a needle is inserted through the chest wall into the pleural cavity to collect pleural fluid for examination of possible malignancy, infection, inflammation, or any combination of these. A thoracentesis may also be performed to drain excessive pleural fluid in large pleural effusions. 16

Pericardiocentesis.

Pericardiocentesis is a procedure that involves accessing the pericardial space around the heart with a needle or cannula to aspirate fluid for drainage, analysis, or both. It is primarily used to assist in diagnosing infections, inflammation, and malignancies and to relieve effusions built up by these disorders. 17

Synovial Fluid Analysis.

Synovial fluid analysis, or arthrocentesis, involves aspirating synovial fluid from a joint capsule. The fluid is then analyzed and used to assist in diagnosing infections, rheumatic diseases, and osteoarthritis, all of which can produce increased fluid production within the joint. 18

Gastric Lavage.

A gastric lavage is the suctioning of gastric contents through a nasogastric tube to examine the contents for the presence of sputum in patients suspected of having tuberculosis. The assumption is that patients swallow sputum while they sleep. If sputum is found in the gastric contents, the appropriate sputum analysis should be performed to help confirm the diagnosis of tuberculosis. 16 , 19 Historically, gastric lavage has also been administered as a medical intervention to prevent absorption of ingested toxins in the acutely poisoned patient, although its use for this purpose is now rarely recommended. 20

Peritoneal Fluid Analysis.

Peritoneal fluid analysis, or paracentesis, is the aspiration of peritoneal fluid with a needle. It is performed to (1) drain excess fluid, or ascites, from the peritoneal cavity, which can be caused by infectious diseases, such as tuberculosis; (2) assist in the diagnosis of hepatic or systemic malfunctions, diseases, infection such as spontaneous bacterial peritonitis (SBP), or malignancies; and (3) help detect the presence of abdominal trauma. 16 , 19 , 21

Other Studies

Imaging with plain x-rays, computed tomography scans, positron emission tomography, and magnetic resonance imaging scans can also help identify areas with infectious lesions. 22 , 23 Minuscule amounts of pathogens can be detected by using the molecular biology techniques of enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA), and polymerase chain reaction (PCR). 24 , 25 In addition, the following diagnostic studies can also be performed to help with the differential diagnosis of the infectious process. For a description of these studies, refer to the sections and chapters indicated below:

  • • Sputum analysis (see Chapter 4)
  • • Cerebrospinal fluid (see Chapter 6)
  • • Urinalysis (see Chapter 9)
  • • Wound cultures (Chapter 12)

Health Conditions

Various infectious disease processes, which are commonly encountered in the acute care setting, are described in the following sections. Certain disease processes that are not included in this section are described in other chapters. Please consult the index for assistance.

Health Care–Associated or Nosocomial Infections

Nosocomial infection is an older general term that refers to an infection that is acquired in the hospital setting. Since 2008 the Centers for Disease Control and Prevention (CDC) has used the generic term health care–associated infections instead of nosocomial . 6 Many pathogens can cause an HAI, but the most commonly reported bacteria in past years have been Escherichia coli , Staphylococcus aureus , Enterococcus faecalis , Pseudomonas aeruginosa , Candida albicans , and coagulase-negative staphyloccoci. 26 , 27 Patients who are at risk for developing HAIs are those who present with 28 :

  • 1. Age: the very young or the very old
  • 2. Immunodeficiency: chronic diseases (cancer, chronic renal disease, chronic obstructive pulmonary disease, diabetes, or acquired immunodeficiency syndrome [AIDS])
  • 3. Immunosuppression: chemotherapy, radiation therapy, or corticosteroids
  • 4. Misuse of antibiotics: overprescription of antibiotics or use of broad-spectrum antibiotics, leading to the elimination of a patient's normal flora, which allows for the colonization of pathogens and development of drug-resistant organisms
  • 5. Use of invasive diagnostic and therapeutic procedures: indwelling urinary catheters, monitoring devices, intravenous (IV) catheters, and mechanical ventilation with intubation
  • 6. Agitation: Resulting in removal of medical equipment such as central venous catheters or self-extubation of artificial airways
  • 7. Surgery: incisions provide access to pathogens
  • 8. Burns: disrupt the first line of defense
  • 9. Length of hospitalization: increases the exposure to pathogens and medical intervention

The mode of transmission for pathogens that cause HAIs can vary from contact to airborne. Pathogens can also become opportunistic in patients who are immunocompromised or immunosuppressed. Common sites for HAIs are in the urinary tract, surgical wounds, joints, and the lower respiratory tract (e.g., pneumonia). Clinical manifestations and management of HAIs vary according to the type of pathogen and the organ system involved. However, the primary management strategy for HAIs is prevention by following the standard and specific precautions outlined in Table 13-3 . 9 , 26 , 29 , 30

Prevention or minimizing the risk of developing a pneumonia in patients who have been on bed rest and/or on mechanical intervention can be achieved through chest physical therapy and increased mobility. (Refer to Table 4-12, Dean's Hierarchy for Treatment of Patients with Impaired Oxygen Transport.)

Summary of Precautions to Prevent Infection

Antibiotic-Resistant Infections

The number of antibiotic-resistance infections is growing in health care facilities. Approximately 50% of antibiotic use in hospitals is unnecessary or inappropriate. In response to this problem, the CDC has launched a program called “Get Smart for Healthcare” whose goals include reducing unnecessary antibiotic use (resulting in less antimicrobial resistance), decreasing health care costs, and improving patient outcomes in hospitals and long-term care facilities. 31

Microbial experts from the European Centre for Disease Prevention and Control and in the United States from the CDC have recently developed interim standard terminology to describe this resistance. 32 They developed three major definitions for resistance: multidrug-resistant (MDR), extensively drug-resistant (XDR), and pandrug-resistant (PDR) bacteria. The agreed-on definitions are MDR as acquired nonsusceptibility to at least one agent in three or more antimicrobial categories, XDR as nonsusceptibility to at least one agent in all but two or fewer antimicrobial categories (i.e., remaining susceptible to only one or two categories), and PDR as nonsusceptibility to all agents in all antimicrobial categories.

Methicillin-Resistant Staphylococcus aureus Infection.

Methicillin-resistant S. aureus (MRSA) is a strain of Staphylococcus that is resistant to methicillin or similar agents, such as oxacillin and nafcillin. Methicillin is a synthetic form of penicillin and was developed because S. aureus developed resistance to penicillin, which was originally the treatment choice for S. aureus infection. However, since the early 1980s, this particular strain of S. aureus has become increasingly resistant to methicillin. The contributing factor that is suggested to have a primary role in the increased incidence of this HAI is the indiscriminate use of antibiotic therapy. 30 , 33

In addition, patients who are at risk for developing MRSA infection in the hospital are patients who 33 , 34 , 35 :

  • • Are debilitated, elderly, or both
  • • Are hospitalized for prolonged time periods
  • • Have multiple surgical or invasive procedures, an indwelling cannula, or both
  • • Are taking multiple antibiotics, antimicrobial treatments, or both
  • • Are undergoing treatment in critical care units

MRSA is generally transmitted by person-to-person contact or person-to-object-to-person contact. MRSA can survive for prolonged periods of time on inanimate objects, such as telephones, bed rails, and tray tables, unless such objects are properly sanitized. Hospital personnel can be primary carriers of MRSA, as the bacterium can be colonized in healthy adults. MRSA infections can be diagnosed via nasal swabs. 36

Management of MRSA is difficult and may consist of combining local and systemic antibiotics, increasing antibiotic dosages, and applying whole-body antiseptic solutions. In recent years, vancomycin has become the treatment of choice for MRSA; however, evidence has shown that patients with this strain of S. aureus are also developing resistance to vancomycin (vancomycin intermediate S. aureus —VISA). 30 Therefore prevention of MRSA infection is the primary treatment strategy and includes the following 26 , 33 , 34 , 35 :

  • • Placing patients with MRSA infection on isolation or contact precautions
  • • Strict hand-washing regulations before and after patient care using proper disinfecting agent
  • • Use of gloves, gowns (if soiling is likely), or both
  • • Disinfection of all contaminated objects

Vancomycin-Resistant Enterococci Infection.

Vanco­­mycin-resistant enterococci (VRE) infection is another HAI that has become resistant to vancomycin, aminoglycosides, and ampicillin. The infection can develop as endogenous enterococci (normally found in the gastrointestinal or the female reproductive tract) become opportunistic in patient populations similar to those mentioned earlier with MRSA. VRE infections can be diagnosed via rectal swab. 26 , 30 , 37 , 38

Transmission of the infection can also occur by (1) direct patient-to-patient contact, (2) indirect contact through asymptomatic hospital personnel who can carry the opportunistic strain of the microorganism, or (3) contact with contaminated equipment or environmental surfaces.

Management of VRE infection is difficult, as the enterococcus can withstand harsh environments and easily survive on the hands of health care workers and on hospital objects. Treatment options are very limited for patients with VRE, and the best intervention plan is to prevent the spread of the infectious process. 30 Strategies for preventing VRE infections include the following 37 :

  • • The controlled use of vancomycin
  • • Timely communication between the microbiology laboratory and appropriate personnel to initiate contact precautions as soon as VRE is detected
  • • Implementation of screening procedures to detect VRE infection in hospitals where VRE has not yet been detected (i.e., randomly culturing potentially infected items or patients)
  • • Preventing the transmission of VRE by placing patients in isolation or grouping patients with VRE together, wearing gown and gloves (which need to be removed inside the patient's room), and washing hands immediately after working with an infected patient
  • • Designating commonly used items, such as stethoscopes and rectal thermometers, to be used only with VRE patients
  • • Disinfecting any item that has been in contact with VRE patients with the hospital's approved cleaning agent

Multidrug-Resistant Acinetobacter baumannii .

Over the past decade Acinetobacter baumannii (AB) has become one of the most difficult pathogens to effectively treat because it easily acquires a wide spectrum of antimicrobial resistance, resulting in the commonly found MDR and the much more serious but fortunately rarer PDR forms. It is a gram-negative coccobacillus that has become one of the most important pathogens, particularly in the intensive care unit (ICU). AB infections in the hospital can cause serious complications such as ventilator-associated pneumonia (VAP), bloodstream infection, wound infections, and nosocomial meningitis. 39 , 40

AB is remarkable in that it is ubiquitous, exists in diverse habitats (e.g., human skin), can survive for long periods of time on dry inanimate surfaces (e.g., hospital bed rails) and as already mentioned can acquire antimicrobial resistance extremely rapidly. These factors combined, especially the latter two, greatly facilitate MDR-AB outbreaks in the ICU, in physical therapy wound clinics and even multi-facility outbreaks. 41 , 42 Fortunately, strict infection-control measures (e.g., contact isolation precautions outlined in Table 13-3 and in guidelines for physical therapy intervention at the end of the chapter) can decrease health care staff and environmental colonization and/or contamination. 43 MDR-AB and PDR-AB infections can also be prevented by following the previously mentioned guidelines effective against MRSA and VRE.

Equipment used during physical therapy treatments for patients with antibiotic-resistant bacteria (e.g., MRSA, VRE, or MDR-AB), such as assistive devices, gait belts, cuff weights, or goniometers, should be left in the patient's room and not be taken out until the infection is resolved. If there is an equipment shortage, thorough cleaning of the equipment is necessary before using the equipment with other patients. Linens, hospital curtains, and laboratory coats also need to be properly cleaned to avoid transmission of infection.

Respiratory Tract Infections

Infections of the respiratory tract can be categorized as upper or lower respiratory tract infections. Upper respiratory tract infections that are discussed in this section consist of allergic and viral rhinitis, sinusitis, influenza, and pertussis. Lower respiratory tract infections that are discussed in this section consist of tuberculosis, histoplasmosis, legionellosis, and severe acute respiratory syndrome. Pneumonia is the most common lower respiratory tract infection and is discussed under Health Conditions in Chapter 4.

Upper Respiratory Tract Infections

Rhinitis is the inflammation of the nasal mucous membranes and can result from an allergic reaction or viral infection. Allergic rhinitis is commonly a seasonal reaction from allergens, such as pollen, or a perennial reaction from environmental triggers, such as pet dander or smoke. Viral rhinitis, sometimes referred to as the common cold, is caused by a wide variety of viruses that can be transmitted by airborne particles or by contact.

Clinical manifestations of allergic and viral rhinitis include nasal congestion; sneezing; watery, itchy eyes and nose; altered sense of smell; and thin, watery nasal discharge. In addition to these, clinical manifestations of viral rhinitis include fever, malaise, headache, and thicker nasal discharge.

Management of allergic rhinitis includes antihistamines, decongestants, nasal corticosteroid sprays, and allergen avoidance. Management of viral rhinitis includes rest, fluids, antipyretics, and analgesics. 44 , 45 , 46

Sinusitis is the inflammation or hypertrophy of the mucosal lining of any or all of the facial sinuses (frontal, ethmoid, sphenoid, and maxillary). This inflammation can result from bacterial, viral, or fungal infection.

Clinical manifestations of sinusitis include pain over the affected sinus, purulent nasal drainage, nasal obstruction, congestion, fever, and malaise.

Management of sinusitis includes antibiotics (as appropriate), decongestants or expectorants, and nasal corticosteroids. 45

Despite the benign nature of rhinitis and sinusitis, the manifestations (especially nasal drainage and sinus pain) of these infections can be very disturbing to the patient and therapist during the therapy session and may lower the tolerance of the patient for a given activity. The therapist should be sympathetic to the patient's symptoms and adjust the activity accordingly.

Influenza (the flu) is caused by any of the influenza viruses (A, B, or C and their mutagenic strains) that are transmitted by aerosolized mucous droplets. These viruses have the ability to change over time and are the reason why a great number of patients are at risk for developing this infection. Influenza B is the most likely virus to cause an outbreak within a community. Health care workers should be vaccinated against the influenza virus to decrease the risk of transmission.

Clinical manifestations of influenza include (1) a severe cough, (2) abrupt onset of fever and chills, (3) headache, (4) backache, (5) myalgia, (6) prostration (exhaustion), (7) coryza (nasal inflammation with profuse discharge), and (8) mild sore throat. Gastrointestinal signs and symptoms of nausea, vomiting, abdominal pain, and diarrhea can also present in certain cases. The disease is usually self-limiting in uncomplicated cases, with symptoms resolving in 7 to 10 days. A complication of influenza infection is pneumonia, especially in the elderly and chronically diseased individuals. 3 , 4 , 16 , 45

A rapid flu nasal swab can diagnose influenza. If results have not come back or they are positive, wear a simple face mask to prevent transmission.

If management of influenza is necessary, it may include the following 3 , 4 , 16 , 45 :

  • • Antiinfective agents
  • • Antipyretic agents
  • • Adrenergic agents
  • • Antitussive agents
  • • Active immunization by vaccines
  • • Supportive care with IV fluids and supplemental oxygen, as needed

Pertussis, or whooping cough, is an acute bacterial infection of the mucous membranes of the tracheobronchial tree, and recently the number of cases has been increasing in the United States. 47 It occurs most commonly in children younger than 1 year and in children and adults of lower socioeconomic populations. The defining characteristics are violent cough spasms that end with an inspiratory “whoop,” followed by the expulsion of clear tenacious secretions. Symptoms may last 1 to 2 months. Pertussis is transmitted through airborne particles and is highly contagious. 48

Management of pertussis may include any of the following 16 , 48 :

  • • Antiinfective and antiinflammatory medications
  • • Bronchopulmonary hygiene with endotracheal suctioning, as needed
  • • Supplemental oxygen, assisted ventilation, or both
  • • Fluid and electrolyte replacement
  • • Respiratory isolation for 3 weeks after the onset of coughing spasms or 7 days after antimicrobial therapy

Lower Respiratory Tract Infections

Tuberculosis..

Tuberculosis (TB) is a chronic pulmonary and extrapulmonary infectious disease caused by the tubercle bacillus. It is transmitted through airborne Mycobacterium tuberculosis particles, which are expelled into the air when an individual with pulmonary or laryngeal TB coughs or sneezes. 49 When M. tuberculosis reaches the alveolar surface of a new host, it is attacked by macrophages, and one of two outcomes can result: Macrophages kill the particles, terminating the infectious process, or the particles multiply within the WBCs, eventually causing them to burst. This cycle is then repeated for a variable time frame between 2 and 12 weeks, after which time the individual is considered to be infected with TB and will test positive on tuberculin skin tests, such as the Mantoux test, which uses tuberculin-purified protein derivative, * or the multiple puncture test, which uses tuberculin. At this point, the infection enters a latent period (most common) or develops into active TB. 49 , 50

A six-category classification system has been devised by the American Thoracic Society and the Centers for Disease Control and Prevention (CDC) to describe the TB status of an individual. 49 , 51

  • 1. No TB exposure, not infected
  • 2. TB exposure, no evidence of infection
  • 3. Latent TB infection, no disease
  • 4. TB, clinically active
  • 5. TB, not clinically active
  • 6. TB suspect (diagnosis pending)

Patients with TB are placed, if available, in negative-pressure isolation rooms. This results in air flowing into, but not out, of the isolation room, thus preventing the escape of contaminated air into the rest of the building. Patients who are suspected of TB, but have not been diagnosed with it, are generally placed on “rule-out TB” protocol, in which case respiratory precautions should be observed.

Populations at high risk for acquiring TB include (1) the elderly; (2) Native Americans, Eskimos, and African-Americans (in par­ticular if they are homeless or economically disadvantaged); (3) incarcerated individuals; (4) immigrants from Southeast Asia, Ethiopia, Mexico, and Latin America; (5) malnourished individuals; (6) infants and children younger than 5 years of age; (7) those with decreased immunity (e.g., from AIDS or leukemia, or after chemotherapy); (8) those with diabetes mellitus, end-stage renal disease, or both; (9) those with silicosis; and (10) those in close contact with individuals with active TB. 5 , 49

Persons with normal immune function do not normally develop active TB after acquisition and are therefore not considered contagious. Risk factors for the development of active TB after infection include age (children younger than 8 years and adolescents are at greatest risk), low weight, and immunosupression. 52

When active TB does develop, its associated signs and symptoms include (1) fever, (2) an initial nonproductive cough, (3) mucopurulent secretions that present later, and (4) hemoptysis, dyspnea at rest or with exertion, adventitious breath sounds at lung apices, pleuritic chest pain, hoarseness, and dysphagia, all of which may occur in the later stages. Chest films also show abnormalities, such as atelectasis or cavitation involving the apical and posterior segments of the right upper lobe, the apical-posterior segment of the left upper lobe, or both. 49

Extrapulmonary TB occurs with less frequency than pulmonary TB but affects up to 70% of human immunodeficiency virus (HIV)-positive individuals diagnosed with TB. 53 Organs affected include the meninges, brain, blood vessels, kidneys, bones, joints, larynx, skin, intestines, lymph nodes, peritoneum, and eyes. When multiple organ systems are affected, the term disseminated, or miliary , TB is used. 53 Signs and symptoms that manifest are dependent on the particular organ system or systems involved.

Because of the high prevalence of TB in HIV-positive individuals (up to 60% in some states), 53 it should be noted that the areas of involvement and clinical features of the disease in this population differ from those normally seen, particularly in cases of advanced immunosuppression. Brain abscesses, lymph node involvement, lower lung involvement, pericarditis, gastric TB, and scrotal TB are all more common in HIV-positive individuals. HIV also increases the likelihood that TB infection will progress to active TB by impairing the body's ability to suppress new and latent infections. 53

Management of TB may include the following 3 , 4 , 16 :

  • • Antiinfective agents (see Chapter 19, Table 19-36, Antitubercular Agents)
  • • Corticosteroids
  • • Surgical intervention to remove cavitary lesions (rare) and areas of the lung with extensive disease or to correct hemoptysis, spontaneous pneumothorax, abscesses, intestinal obstruction, ureteral stricture, or any combination of these
  • • Respiratory isolation until antimicrobial therapy is initiated
  • • Blood and body fluid precautions if extrapulmonary disease is present
  • • Skin testing (i.e., Mantoux test and multiple puncture test)
  • • Vaccination for prevention

In recent years, new strains of M. tuberculosis that are resistant to antitubercular drugs (e.g., isoniazid, rifampin, and pyrazinamide) have emerged. These multidrug-resistant TB strains are associated with fatality rates as high as 89% and are common in HIV-infected individuals. Treatment includes the use of direct observational therapy (DOT) and direct observational therapy, short-course (DOTS). These programs designate health care workers to observe individuals to ensure that they take their medications for the entire treatment regimen or for a brief period, respectively, in hopes of minimizing resistance. 53

Facilities should provide health care workers personal protective equipment (PPE) effective against TB such as either specialized masks (e.g., N-95) or powered air-purifying respirators (PAPR) to wear around patients on respiratory precautions. These types of PPE are protective against the airborne TB mycobacterium. Always verify with the nursing staff or physician before working with these patients to determine which type of PPE to wear.

Histoplasmosis.

Histoplasmosis is a pulmonary and systemic infection that is caused by infective spores (fungi), most commonly found in the soil of the central and eastern United States. Histoplasmosis is transmitted by inhalation of dust from the soil or bird and bat feces. The spores form lesions within the lung parenchyma that can be spread to other tissues. The incidence of fungal infection is rising, particularly in immunocompromised, immunosuppressed, and chronically debilitated individuals who may also be receiving corticosteroid, antineoplastic, and multiple antibiotic therapy. 54 , 55

Different clinical forms of histoplasmosis are (1) acute, benign respiratory disease, which results in flulike illness and pneumonia; (2) acute disseminated disease, which can result in septic-type fever; (3) chronic disseminated disease, which involves lesions in the bone marrow, spleen, and lungs and can result in immunodeficiency; and (4) chronic pulmonary disease, which manifests as progressive emphysema.

Management of histoplasmosis may include the following 16 , 54 , 56 , 57 :

  • • Antihistamines
  • • Antifungal therapy (see Chapter 19, Table 19-35, Antifungal Agents)
  • • Supportive care appropriate for affected areas in the various forms of histoplasmosis

Legionellosis.

Legionellosis is commonly referred to as Legionnaire's disease after a pneumonia outbreak in people who attended an American Legion Convention in Philadelphia in 1976. It is an acute bacterial infection primarily resulting in high fever and pneumonia (patchy or confluent consolidation). Legionella pneumophila causes more than 80% of all cases of legionellosis. However, organs beside the lungs may also become involved, especially in the immunocompromised patient. Other risk factors include underlying chronic pulmonary disease, smoking history, and age greater than 50 years. Legionellosis is transmitted by inhalation of aerosolized organisms from infected water sources, such as air-conditioning cooling towers for large buildings including hospitals. Additional examples of infected hospital water sources have included shower heads, tap water from respiratory devices, ice machines, decorative fountains, and even distilled water. 3 , 58 , 59 , 60

Primary clinical manifestations include high fever, pneumonia, malaise, myalgia, headache, and nonproductive cough. Other manifestations can also include diarrhea, confusion and other gastrointestinal symptoms. The disease is rapidly progressive during the first 4 to 6 days of illness, with complications that may include renal failure, bacteremic shock, and respiratory failure. 3 , 59

Management of legionellosis may consist of the following 3 :

  • • Supplemental oxygen with or without assisted ventilation
  • • Temporary renal dialysis
  • • IV fluid and electrolyte replacement

Severe Acute Respiratory Syndrome.

The single-stranded RNA coronavirus is responsible for severe acute respiratory syndrome (SARS), which affects the epithelial cells of the lower respiratory tract. Pathogenesis is not limited to the lungs but often includes mucosal cells of the intestines, tubular epithelial cells of the kidneys, and brain neurons. This new disease was first identified in China in late 2002, and then spread into the rest of the world in the spring and summer of 2003, resulting in the first pandemic of the twenty-first century. Of the approximately 8000 worldwide cases that occurred during this pandemic, about 25% of patients required mechanical ventilation in the ICU and about 10% of infected patients died.

SARS has flulike symptoms of fever, chills, cough, and malaise along with frequent shortness of breath. A common cause of death during this pandemic was diffuse alveolar damage (DAD). In addition, SARS typically compromises the immune response, which increases lung injury.

The 2003-2004 SARS pandemic showed that a prompt, coordinated worldwide response could help contain the disease. Although SARS was rapidly spread throughout the world by international air travelers, the virus itself was not transmitted through the air. Thus adherence to the basic infection control practice of thorough hand washing, implemented with droplet precautions, was able to ultimately stop this particular SARS pandemic. 61 , 62

Cardiac Infections

Infections of the cardiac system can involve any layer of the heart (endocardium, myocardium, or pericardium) and generally result in acute or chronic depression of the patient's cardiac output. Infections that result in chronic cardiomyopathy most likely require cardiac transplantation. Refer to Chapters 3 and 14 for a discussion of cardiomyopathy and cardiac transplantation, respectively. This section focuses on rheumatic fever and resultant rheumatic heart disease.

Acute rheumatic fever is a clinical sequela occurring in up to 3% of patients with group A and β-streptococcal infection of the upper respiratory tract. It occurs primarily in children who are between the ages of 6 and 15 years. Rheumatic fever is characterized by nonsuppurative inflammatory lesions occurring in any or all of the connective tissues of the heart, joints, subcutaneous tissues, and central nervous system. An altered immune reaction to the infection is suspected as the cause of resultant damage to these areas, but the definitive etiology is unknown. Rheumatic heart disease is the term used to describe the resultant damage to the heart from the inflammatory process of rheumatic fever. 16 , 34 , 63 , 64

Cardiac manifestations can include pericarditis, myocarditis, left-sided endocarditis, and valvular stenosis and insufficiency with resultant organic heart murmurs, as well as congestive heart failure. If not managed properly, all of these conditions can lead to significant morbidity or death. 16 , 34 , 63

Management of rheumatic fever follows the treatment for streptococcal infection. The secondary complications mentioned previously are then managed specifically. The general intervention scheme may include the following 16 , 34 , 63 :

  • • Prevention of streptococcal infection
  • • Bed rest
  • • IV fluids (as needed)

Neurologic Infections

Poliomyelitis.

Poliomyelitis is an acute systemic viral disease that affects the central nervous system and fortunately is in rapid decline, with global eradication a distinct possibility. 65 Polioviruses are a type of enterovirus that multiply in the oropharynx and intestinal tract. 16 , 66

Poliomyelitis is usually transmitted directly by the fecal-oral route from person to person but can also be transmitted indirectly by consumption of contaminated water sources. 66

Clinical presentation can range from subclinical infection, to afebrile illness (24 to 36 hours), to aseptic meningitis, to paralysis (after 4 days), and, possibly, to death. If paralysis does occur, it is generally associated with fever and muscle pain. The paralysis is usually asymmetric and involves muscles of respiration, swallowing, and the lower extremities. Paralysis can resolve completely, leave residual deficits, or be fatal. 16 , 66

Management of poliomyelitis primarily consists of prevention with inactivated poliovirus vaccine (IPV) given as four doses to children from the ages of 2 to 6 years of age. 66 If a patient does develop active poliomyelitis, then other management strategies may include the following 16 :

  • • Analgesics and antipyretics
  • • Bronchopulmonary hygiene
  • • Bed rest with contracture prevention with positioning and range of motion

Postpoliomyelitis Syndrome.

Postpoliomyelitis syndrome, also known as postpolio syndrome, occurs 30 to 40 years after an episode of childhood paralytic poliomyelitis. The syndrome results from overuse or premature aging of motor units that were originally affected by the polio virus. It results in muscle fatigue, pain, and decreased endurance. Muscle atrophy and fasciculations may also be present. Patients who are older or critically ill, who have had a previous diagnosis of paralytic poliomyelitis, and who are female are at greater risk for development of this syndrome. 66 , 67 , 68

Meningitis is an inflammation of the meninges that cover the brain and spinal cord, which results from acute infection by bacteria, viruses, fungi, or parasitic worms, or from chemical irritation. The route of transmission is primarily inhalation of infected airborne mucus droplets released by infected individuals, or through the bloodstream via open wounds or invasive procedures. 69 , 70

The more common types of meningitis are (1) meningococcal meningitis, which is bacterial in origin and occurs in epidemic form; (2) Haemophilus meningitis, which is the most common form of bacterial meningitis; (3) pneumococcal meningitis, which occurs as an extension of a primary bacterial upper respiratory tract infection; and (4) viral (aseptic or serous) meningitis, which is generally benign and self-limiting.

Bacterial meningitis is more severe than viral meningitis and affects the pia mater, arachnoid and subarachnoid space, ventricular system, and cerebrospinal fluid. The primary complications of bacterial meningitis include an increase in intracranial pressure, resulting in hydrocephalus. This process frequently results in severe headache and nuchal rigidity (resistance to neck flexion). Other complications of meningitis include arthritis, myocarditis, pericarditis, neuromotor and intellectual deficits, and blindness and deafness from cranial nerve (III, IV, VI, VII, or VIII) dysfunction. 69 , 70

Management of any form of meningitis may include the following 16 , 69 , 71 :

  • • Antimicrobial therapy, antiinfective agents, or immunologic agents
  • • Analgesics
  • • Mechanical ventilation (as needed)
  • • Blood pressure maintenance with IV fluids and vasopressors (e.g., dopamine)
  • • Intracranial pressure control

Encephalitis

Encephalitis is an inflammation of the tissues of the brain and spinal cord, commonly resulting from viral or amebic infection. Types of encephalitis include infectious viral en­­cephalitis, mosquito-borne viral encephalitis, and amebic meningoencephalitis.

Infectious viral encephalitis is transmitted by direct contact with droplets from respiratory passages or other infected excretions and is most commonly associated with the herpes simplex type 1 virus. Viral encephalitis can also occur as a complication of systemic viral infections, such as poliomyelitis, rabies, mononucleosis, measles, mumps, rubella, and chickenpox. Manifestations of viral encephalitis can be mild to severe, with herpes simplex virus encephalitis having the highest mortality rate among all types of encephalitides. 16 , 69 , 70

Mosquito-borne viral encephalitis is transmitted by infectious mosquito bites and cannot be transmitted from person to person. The incidence of this type of encephalitis can be epidemic and typically varies according to geographic regions and seasons. 16 , 69 , 70

Amebic meningoencephalitis is transmitted in water and can enter a person's nasal passages while he or she is swimming. Amebic meningoencephalitis cannot be transmitted from person to person.

General clinical presentation of encephalitis may include the following 16 , 69 , 70 :

  • • Fever
  • • Signs of meningeal irritation from increased intracranial pressure (e.g., severe frontal headache, nausea, vomiting, dizziness, nuchal rigidity)
  • • Altered level of consciousness, irritability, bizarre behaviors (if the temporal lobe is involved)
  • • Seizures (mostly in infants)
  • • Aphasia
  • • Focal neurologic signs
  • • Weakness
  • • Altered deep tendon reflexes
  • • Ataxia, spasticity, tremors, or flaccidity
  • • Hyperthermia
  • • Alteration in antidiuretic hormone secretion

Management of encephalitis may include the following 16 :

  • • Intracranial pressure management
  • • Mechanical ventilation, with or without tracheostomy (as indicated)
  • • Sedation
  • • IV fluids and electrolyte replacement
  • • Nasogastric tube feedings

Musculoskeletal Infections

Osteomyelitis is an acute infection of the bone that can occur from direct or indirect invasion by a pathogen. Direct invasion is also referred to as exogenous or acute contagious osteomyelitis and can occur any time there is an open wound in the body. Indirect invasion is also referred to as endogenous or acute hematogenous osteomyelitis and usually occurs from the spread of systemic infection. Both of these types can potentially progress to subacute and chronic osteomyelitis. Acute osteomyelitis typically refers to an infection of less than 1 month's duration, whereas chronic osteomyelitis refers to infection that lasts longer than 4 weeks. 72 , 73

Acute contagious osteomyelitis is an extension of the concurrent infection in adjacent soft tissues to the bony area. Trauma resulting in compound fractures and tissue infections is a common example. Prolonged orthopedic surgery, wound drainage, and chronic illnesses, such as diabetes or alcoholism, also predispose patients to acute contagious osteomyelitis. 73 , 74

Acute hematogenous osteomyelitis is a blood-borne infection that generally results from S. aureus infection (80%) 3 and occurs mostly in infants; children (in the metaphysis of growing long bones); or patients undergoing long-term IV therapy, hyperalimentation, hemodialysis, or corticosteroid or antibiotic therapy. Patients who are malnourished, obese, or diabetic, or who have chronic joint disease, are also susceptible to acute hematogenous osteomyelitis. 72 , 73

Clinical presentation of both types of acute osteomyelitis includes (1) delayed onset of pain, (2) tenderness, (3) swelling, and (4) warmth in the affected area. Fever is present with hematogenous osteomyelitis. The general treatment course for acute osteomyelitis is early and aggressive administration of the appropriate antibiotics to prevent or limit bone destruction. 3 , 56 , 72 , 73

Chronic osteomyelitis is an extension of the acute cases just discussed. It results in marked bone destruction, draining sinus tracts, pain, deformity, and the potential for limb loss. Chronic osteomyelitis can also result from infected surgical prostheses or infected fractures. Debridement of dense formations (sequestra) may be a necessary adjunct to the antibiotic therapy. If the infection has spread to the surrounding soft tissue and skin regions, then grafting, after debridement, may be necessary. Good treatment results have also been shown with hyperbaric oxygen therapy for chronic osteomyelitis. 72 , 73

Clarify weight-bearing orders with the physician when performing gait training with patients who have any form of osteomyelitis. Both upper and lower extremities can be involved; therefore choosing the appropriate assistive device is essential to preventing pathologic fracture.

Skin Infections

Cellulitis, or erysipelas, is an infection of the dermis and the subcutaneous tissue that can remain localized or be disseminated into the bloodstream, resulting in bacteremia (rare). Cellulitis occurs most commonly on the face, neck, and legs and is associated with an increased incidence of lymphedema. 75

Groups A and G Streptococcus and Staphylococcus aureus are the usual causative agents for cellulitis and generally gain entry into the skin layers when there are open wounds (surgical or ulcers). Patients who are at most risk for developing cellulitis include those who are postsurgical and immunocompromised from chronic diseases or medical treatment.

The primary manifestations of cellulitis are fever with an abrupt onset of hot, stinging, and itchy skin and painful, red, thickened lesions that have firm, raised palpable borders in the affected areas. Identifying the causative agent is often difficult through blood cultures; therefore localized cultures, if possible collected from open wounds, may be more sensitive in helping to delineate the appropriate antibiotic treatment. 74 , 76 , 77

Gastrointestinal Infections

Gastroenteritis is a global term used for the inflammation of the digestive tract that is typically a result of infection. Bacterial sources of gastroenteritis are often caused by Escherichia coli, Shigella (which causes bacterial dysentery), Clostridium difficile, or Salmonella . However, most cases of gastroenteritis are caused by viruses. Rotavirus and norovirus are by far the most frequent cause of gastroenteritis; adenovirus and astrovirus also commonly cause gastroenteritis, especially in children. Transmission of both bacterial and viral gastroenteritis is usually through the ingestion of contaminated food, water, or both or by direct and indirect fecal-oral transmission.

Strict contact and enteric precautions should be observed with patients who have a diagnosis of C. difficile (whose spores can persist on fomites and environmental surfaces for months) and norovirus infection because these pathogens are relatively resistant to waterless alcohol-based antiseptics, and they have been associated with frequent surface contamination in hospital rooms and the hands of health care workers.

Of these aforementioned organisms, rotavirus (a double-stranded RNA virus) infection is the most important cause of severe diarrheal disease in young children. Historically, rotavirus has caused 500,000 childhood deaths annually in the world in less-developed countries. In the United States, 50% of gastroenteritis pediatric cases requiring hospitalization or emergency room visits are caused by rotavirus, and the total health and societal costs of rotavirus infections are estimated to exceed $1 billion per year. Fortunately, the annual pediatric death rate in the United States is relatively low (20 to 60 deaths). Rotavirus is very contagious in that the virus can survive on dry surfaces for up to 10 days and on human hands for up to 4 hours. It also has a low infectious dose (10 or fewer particles) and the infected stool can contain up to 10 11 particles per gram that are present before and up to 2 weeks after the onset of symptoms. Because of its highly contagious nature, it is estimated that for every 4 children admitted to the hospital with a rotavirus infection, 1 additional child acquires it as an HAI. Rotavirus infections also may be transmitted to adults who are around infected children, immunocompromised individuals, and older adults in nursing homes. Fortunately, the newly developed second-generation rotavirus vaccines have proven to be effective and have fewer serious side effects (e.g., intussusception [intestinal invagination]). 78 , 79 , 80 , 81

Norovirus (formally known as Norwalk virus, calicivirus, or small round-structured viruses) is a single-stranded positive sense RNA virus and is the most common cause of nonbacterial gastroenteritis worldwide. These outbreaks occur where groups of individuals gather, including nursing homes, hospitals, restaurants, and cruise ships. Like the rotavirus, norovirus is very contagious (<10 particles can cause infection) and can survive for up to 4 weeks in a dried state at room temperature. In hospitals the most common contaminated sites include toilet tops, door handles, and telephone receivers, and contaminated fingers can spread the norovirus to up to seven clean surfaces.

Norovirus and rotavirus can be transmitted through aerosolization, so health care workers should wear a mask when disposing of infected vomit and feces.

Research has shown that 1 minute of hand washing with soap and water followed by rinsing the hands for 20 seconds, then drying them with a disposable towel completely removes norovirus from hands contaminated with infected stools. Unlike for rotavirus, there is no fully developed vaccine for norovirus, although vaccines for norovirus are in early stages of development. 82 , 83 , 84

The primary manifestations of any form of gastroenteritis are crampy abdominal pain, nausea, vomiting, and diarrhea, all of which vary in severity and duration according to the type of infection. Gastroenteritis is generally a self-limiting infection, with resolution occurring in 3 to 4 days. However, patients in the hospital setting with reduced immunity can have longer periods of recovery, with dehydration being a primary concern. 16 , 56 , 85

Management of acute gastroenteritis may include the following 16 , 56 :

  • • Antiemetic agents (if nausea and vomiting occur)

Immune System Infections

Human immunodeficiency virus infection.

Two types of HIV exist: HIV-1 and HIV-2, with HIV-1 being the more prevalent and the one discussed here. It is a retrovirus, occurring in pandemic proportions, that primarily affects the function of the immune system. Eventually, however, all systems of the body become affected directly, such as the immune system, or indirectly, as in the cardiac system, or through both methods, as occurs in the nervous system. The virus is transmitted in blood, semen, vaginal secretions, and breast milk through sexual, perinatal, and blood or blood-product contact. Proteins on the surface of the virus attach to CD4+ receptors, found primarily on T4 lymphocytes. 86 Other types of cells found to house the virus include monocytes, macrophages, uterine cervical cells, epithelial cells of the gastrointestinal tract, and microglia cells. 86

On entering the cell, the viral and cellular DNA combine, making the virus a part of the cell. The exact pathogenesis of cellular destruction caused by HIV is not completely understood, and several methods of destruction may be entailed. It is known that immediately after initial infection, HIV enters a latent period, or asymptomatic stage, in which viral replication is minimal, but CD4+ T cell counts begin to decline. 86 Continued reduction results in decreasing immunity, eventually leading to symptomatic HIV, in which diseases associated with the virus begin to appear. 86 This eventually leads to the onset of AIDS, which the CDC defines as occurring when the CD4+ T-lymphocyte count falls below 200 cells/µl (reference = 1000 cells/µl) or below 14%; when 1 of 26 specific AIDS-defining disorders is contracted, most of which are opportunistic infections; or a combination of these factors. 87 , 88

Six laboratory tests are available to detect HIV infection 89 , 90 , 91 , 92 :

  • 1. ELISA or enzyme immunoassay test. This procedure tests for the presence of antibodies to HIV proteins in the patient's serum. A sample of the patient's blood is exposed to HIV antigens in the test reagent. If HIV antibodies are identified, it is inferred that the virus is present within the patient.
  • 2. Western blot test. This test detects the presence of antibodies in the blood of two types of HIV viral proteins and is therefore a more specific HIV test. It is an expensive test to perform and is used as a confirmatory tool for a positive ELISA test.
  • 3. Immunofluorescence assay. In this test, the patient's blood is diluted and placed on a slide containing HIV antigens. The slide is then treated with anti-human globulin mixed with a fluorescent dye that will bind to antigen-antibody complexes. If fluorescence is visible when the specimen is placed under a microscope, then HIV antibodies are present in the patient's blood.
  • 4. p24 antigen assay. This test analyzes blood cells for the presence of the p24 antigen located on HIV virions. It can be used to diagnose acute infection, to screen blood for HIV antigens, to determine HIV infection in difficult diagnostic cases, or to evaluate the treatment effects of antiviral agents.
  • 5. PCR for HIV nucleic acid. This highly specific and extremely sensitive test detects viral DNA molecule in lymphocyte nuclei by amplifying the viral DNA. It is used to detect HIV in neonates and when antibody tests are inconclusive.
  • 6. Rapid HIV testing. This highly sensitive and specific test requires a sample of blood, serum, plasma, or oral fluid to detect HIV antibodies. This test can be complete in 20 minutes.

Any clinician who sustains a needle-stick injury when working with a patient with a suspected HIV infection should have an HIV test. A false-negative HIV test can occur if an individual has not yet developed HIV antibodies. If an individual has had exposure to HIV, he or she should have a repeat HIV test to ensure a true negative result. 93

Once HIV has been detected, it can be classified in a number of ways. The Walter Reed staging system has six categories grouped according to the quantity of helper T cells and characteristic signs, such as the presence of an HIV antigen or antibody. 94 However, a more commonly used classification system was devised by the CDC and was last updated in 1993. In this system, infection is divided into three categories, depending on CD4+ T-lymphocyte counts:

  • 1. Category 1 consists of CD4+ T-lymphocyte counts greater than or equal to 500 cells/µl.
  • 2. Category 2 consists of counts ranging between 200 and 499 cells/µl.
  • 3. Category 3 contains cell counts less than 200 cells/µl.

These groups are then subdivided into A, B, and C, according to the presence of specific diseases. 87

A major advancement in the medical treatment of HIV has been antiretroviral therapy. This therapy consists of four classes of medications (see Chapter 19, Table 19-37) 94 :

  • 1. Nucleoside analog reverse transcriptase inhibitors, otherwise known as nucleoside analogs
  • 2. Protease inhibitors
  • 3. Nonnucleoside reverse transcriptase inhibitors
  • 4. Fusion inhibitor

Each of these therapies assists in limiting HIV progression by helping to prevent viral replication. This prevention is further increased when the drugs are used in combination in a treatment technique termed highly active antiretroviral therapy or HAART. 94

There is a significant need for more effective and cost-efficient preventions for HIV. The HIV Vaccine Trials Network (HVTN) is an international collaboration working to develop HIV preventive vaccines. 95

As HIV progresses and immunity decreases, the risk for and severity of infections not normally seen in healthy immune systems increase. These opportunistic infections, combined with disorders that result directly from the virus, often result in multiple diagnoses and medically complex patients. These manifestations of HIV can affect every system of the body and present with a wide array of signs and symptoms, many of which are appropriate for physical therapy intervention. Table 13-4 lists common manifestations and complications of HIV and AIDS and the medications generally used in their management.

Common Complications from HIV and AIDS, and Associated Medical Treatment

AIDS , Acquired immunodeficiency syndrome; HIV, human immunodeficiency virus; IV , intravenous.

Disorders affecting the nervous system include HIV-associated dementia complex, progressive multifocal leukoencephalopathy, primary central nervous system lymphoma, toxoplasmosis, and neuropathies. These manifestations may cause paresis, decreased sensation, ataxia, aphagia, spasticity, altered mental status, and visual deficits. 96 In the pulmonary system, TB, cytomegalovirus (CMV) and pneumonia can result in cough, dyspnea, sputum production, and wheezing. 97 In the cardiac system, cardiomyopathy, arrhythmias, and congestive heart failure can cause chest pain, dyspnea, tachycardia, tachypnea, hypotension, fatigue, peripheral edema, syncope, dizziness, and palpitations. 98

Physical therapy intervention can assist in minimizing the effect of these deficits on functional ability, therefore helping to maximize the independence and quality of life of the individual. However, the course of rehabilitation in HIV-affected individuals can often be difficult owing to coinciding opportunistic infections, an often-rapid downhill disease course, low energy states, and frequent hospitalizations.

Mononucleosis

Mononucleosis is an acute viral disease that has been primarily linked to the Epstein-Barr virus and less commonly to CMV. Mononucleosis is transmitted generally through saliva from symptomatic or asymptomatic carriers (the Epstein-Barr virus can remain infective for 18 months in the saliva). 16 , 99

The disease is characterized by fever, lymphadenopathy (lymph node hyperplasia), and exudative pharyngitis. Splenomegaly, hepatitis, pneumonitis, and central nervous system involvement may occur as rare complications from mononucleosis. The infection is generally self-limiting in healthy individuals, with resolution in approximately 3 weeks without any specific treatment. 16 , 99

If management of mononucleosis is necessary, it may include the following 16 , 99 , 100 :

  • • Corticosteroids in cases of severe pharyngitis
  • • Adequate hydration
  • • Bed rest during the acute stage
  • • Saline throat gargle
  • • Aspirin or acetaminophen for sore throat and fever

Cytomegalovirus Infection

CMV is a member of the herpesvirus group that can be found in all body secretions, including saliva, blood, urine, feces, semen, cervical secretions, and breast milk. CMV infection is a common viral infection that is asymptomatic or symptomatic. CMV infection can remain latent after the initial introduction into the body and can become opportunistic at a later point.

If CMV infection is symptomatic, clinical presentation may be a relatively benign mononucleosis in adults, or in patients with HIV infection, manifestations such as pneumonia, hepatitis, encephalitis, esophagitis, colitis, and retinitis can occur.

CMV is usually transmitted by prolonged contact with infected body secretions, as well as congenitally or perinatally. 16 , 101

Management of CMV infection may include the following 16 , 101 :

  • • Antiviral agents
  • • Immune globulins
  • • Blood transfusions for anemia or thrombocytopenia
  • • Antipyretics

Toxoplasmosis

Toxoplasmosis is a systemic protozoan infection caused by the parasite Toxoplasma gondii , which is primarily found in cat feces. Transmission can occur from three mechanisms: (1) eating raw or inadequately cooked infected meat or eating uncooked foods that have come in contact with contaminated meat; (2) inadvertently ingesting oocysts that cats have passed in their feces, either in a cat litter box or outdoors in soil (e.g., soil from gardening or unwashed fruits or vegetables); and (3) transmission of the infection from a woman to her unborn fetus. Fetal transmission of T. gondii can result in mental retardation, blindness, and epilepsy. 102

Clinical manifestations can range from subclinical infection to severe generalized infection, particularly in immunocompromised individuals, and to death.

The primary way to treat toxoplasmosis is through prevention by safe eating habits (thoroughly cooking meats, peeling and washing fruits and vegetables) and minimizing contact with cat feces when pregnant, along with keeping the cat indoors to prevent contamination. 102

Sepsis is a general term that describes three progressive infectious conditions: bacteremia, septicemia, and shock syndrome (or septic shock). 16

Bacteremia is a generally asymptomatic condition that results from bacterial invasion of blood from contaminated needles, catheters, monitoring transducers, or perfusion fluid. Bacteremia can also occur from a preexisting infection from another body site. Patients with prosthetic heart valves may need to take prophylactic antibiotics for dental surgery because the bacteremia may progress to endocarditis. Bacteremia can resolve spontaneously or progress to septicemia.

Septicemia is a symptomatic extension of bacteremia throughout the body, with clinical presentations that are representative of the infective pathogen and the organ system(s) involved. Sites commonly affected are the brain, endocardium, kidneys, bones, and joints. Renal failure and endocarditis may also occur.

Shock syndrome is a critical condition of systemic tissue hypoperfusion that results from microcirculatory failure (i.e., decreased blood pressure or perfusion). Bacterial damage of the peripheral vascular system is the primary cause of the tissue hypoperfusion.

Management of sepsis may include any of the following 16 :

  • • Removal of suspected infective sources (e.g., lines or tubes)
  • • Blood pressure maintenance with adrenergic agents and corticosteroids
  • • IV fluids
  • • Blood transfusions
  • • Cardiac glycosides
  • • Supplemental oxygen, mechanical ventilation, or both
  • • Anticoagulation

Medical Intervention

Management of the various infectious diseases discussed in this chapter is described in the specific sections of respective disorders. Chapter 19 (Table 19-34, Antibiotics; Table 19-35, Antifungal Agents; Table 19-36, Antitubercular Agents; Table 19-37, Antiretroviral Medications; and Table 19-38, Antiviral Medications) also lists common antiinfective agents used in treating infectious diseases.

Lifestyle Management

The critical importance of encouraging healthy lifestyles to combat disease is indicated by the National Prevention and Health Promotion Strategy that was announced in the summer of 2011. The objective of this strategy is to “move the nation away from a health care system focused on sickness and disease to one focused on wellness and prevention.” 103 The American Physical Therapy Association's president has encouraged physical therapists to support this national prevention initiative by “expanding quality preventative services in both clinical and community settings, empowering people to make healthful choices, and eliminating health disparities” and to become “leaders in their communities to advance these directions and priorities.” 104 Although the physical therapist may have limited treatment options emphasizing prevention and wellness during the acute care stay, he or she has greater opportunities to effect meaningful lifestyle change in other settings such as in nursing homes and home health. At a minimum, the physical therapist can play a key role in all health care settings in helping patients understand the link between lifestyle and infectious disease. These important links, which may be poorly understood by the typical patient, are discussed in this section.

Many of the same lifestyle and nutrition factors that can delay wound healing (see Chapter 12) also affect the immune system and the infection rate. To have an optimally functioning immune system, one should eat plenty of fresh fruits and vegetables as well as foods rich in fiber. Also, it is important to obtain adequate amounts of the micronutrients zinc, selenium, iron, copper, vitamins A, C, E, and B 6 , and folic acid. Vitamin D, which is produced by exposure to sunlight, is known to activate one's innate immunity (i.e., regulatory T cells) by the production of antimicrobial peptides. Excess sugar also decreases the ability of white blood cells to destroy bacteria (leukocytic phagocytosis). Moreover, a healthy immune system is promoted by not only eating proper foods, but also by staying well hydrated, which is a key consideration in combating septic shock. 105 , 106 , 107 , 108 , 109 , 110 , 111

Exposure to fresh and unpolluted air benefits the immune system. It is a well-studied fact that the higher the ventilation rate (amount of outdoor air circulated per unit time), the lower the infection rate of airborne diseases such as measles, TB, influenza, and SARS. The cross-infection problem of the 2002-2003 SARS epidemic was particularly evident where people congregated, such as in airplanes, buses, and hospitals. This would imply a strong benefit for exposing patients to as much fresh air as medically prudent, which is reminiscent of the philosophy behind the “open-air treatment” TB hospitals of the last century. 112 , 113

When one obtains the proper balance of exercise and rest, it helps the immune system fight off infection. Exercise and adequate rest are key factors in promoting a healthy psychological state, which also reduces the negative effects of stress (e.g., high levels of cortisol) on the immune system. However, it should be mentioned that the beneficial effects of resistive exercise (as opposed to cardiovascular exercise) on immunity are less clear, though excessive cardiovascular exercise may lead to immunosuppression. The key role that the crucial rest-promoting hormone melatonin plays in influencing our circadian rhythm (sleep-wake cycle) and immune system (specifically T cell populations) is still being unraveled. Melatonin's peak production occurs at night, which is the inverse of another key immunoregulatory hormone, vitamin D. In order to maximize melatonin levels, which promote sleep efficiency and restfulness, one should exercise regularly, be exposed to natural light (sunlight) especially early in the day, minimize exposure to artificial light at night, and go to bed 2 to 3 hours before midnight in a completely dark room. It is important to follow this advice every day because melatonin has a short half-life and thus must be produced every 24 hours. 110 , 114 , 115 , 116 , 117 , 118 , 119

Alcohol exposure has a well-known immunosuppression effect, which includes negative impacts on lymphocyte activation, cytokine production by macrophages and T cells, and neutrophil function. This results in increased susceptibility to infection and reduces the body's ability to heal after injury. People who smoke and those who are exposed (especially children) to passive or environmental tobacco smoke (ETS) are at greater risk of impairing their immune system, which can cause infections such as influenza and TB for adults and serious respiratory tract infection and pneumonia for children. Caffeine is largely antiinflammatory in nature and thus has an overall negative effect on the immune system. Specifically, caffeine suppresses lymphocyte function, antibody production, and neutrophil and monocyte chemotaxis. Illicit drug users also have well-documented higher infection rates involving bacteria, viruses, fungi, and protozoans. These rates are even higher in injection drug users. 120 , 121 , 122 , 123

Finally, obesity has now been associated with increased infection risk. Increased infection has been observed in obese patients with conditions as diverse as urinary tract infection (UTI), influenza, hepatitis C, and a history of total hip arthroplasty. With obesity rates increasing throughout the world, the exact mechanism of the link between obesity and infection warrants more study. 124 , 125 , 126 , 127

Physical Therapy Intervention

The following are general physical therapy goals and guidelines to be used when working with patients who have infectious disease processes, as well as disorders of altered immunity. These guidelines should be adapted to a patient's specific needs.

The primary physical therapy goals in this patient population are similar to those of patient populations in the acute care setting: (1) to optimize the patient's functional mobility, (2) to maximize the patient's tolerance and endurance, (3) to maximize ventilation and gas exchange in the patient who has pulmonary involvement, and, when appropriate, (4) to educate the patient in proper lifestyle management (see previous section).

Guidelines for Physical Therapy Intervention

General physical therapy guidelines include, but are not limited to, the following:

  • a. Facilities' warning or labeling systems for biohazards and infectious materials may vary slightly.
  • b. Be sure to check the patient's medical record or signs posted on doors and doorways for indicated precautions.
  • c. Table 13-3 provides an outline of the types of personal protective equipment that should be worn with specific precautions.

Proper Hand-Washing Technique

Hand washing with soap and water is the best method to remove pathogens, including highly contagious pathogens (e.g., norovirus, Clostridium difficile spores), from your hands.

  • 1. Wet your hands with clean running water (warm or cold) and apply soap.
  • 2. Rub your hands together to make a lather and scrub them well. Be sure to scrub the backs of your hands, between your fingers, and under your nails.
  • 3. Continue rubbing your hands for at least 20 seconds (as previously mentioned, some pathogens such as norovirus require a longer time of at least 60 seconds to remove stool contamination from hands).
  • 4. Rinse your hands well under running water (stool-contaminated norovirus hands should be rinsed for at least 20 seconds).
  • 5. Dry your hands using a clean disposable towel or air dry.

If soap and water are not available, use an alcohol-based hand sanitizer that contains at least 60% alcohol (continue to rub the sanitizer over all hand and finger surfaces until dry). Alcohol-based hand sanitizers can quickly reduce the number of pathogens, but do not remove all pathogen types (e.g., norovirus, Clostridium difficile spores).

  • a. Cover the mouth and nose with a tissue when coughing or sneezing.
  • b. Put the used tissue in a waste basket.
  • c. If no tissue is available, cough or sneeze into the upper sleeve and not into the hands.
  • d. Wash the hands after coughing or sneezing (see Box 13-2 on previous page).
  • a. Flushing the toilet (even with the lid down) causes aerosolization of pathogens that is greatest with the first flush, and then diminishes with each subsequent flush.
  • b. Aerosolization danger is greatest when the patient has diarrhea (as contrasted to a normal stool) and/or vomits into the toilet.
  • c. Gastroenteritis viral pathogens are especially easy to spread in the foregoing manner because each gram of feces can contain up to 10 11 virus particles.
  • d. Pulsatile lavage is a common wound physical therapy modality that can cause aerosolization of pathogens.
  • e. In addition to the therapist wearing appropriate PPE during pulsatile lavage, patients receiving treatment should wear surgical masks, and all IV lines and other wounds should be covered during treatment. The procedure should be performed in a private room, with minimal equipment and supplies. The room should be thoroughly cleaned and disinfected after each procedure.
  • a. Patients with infectious processes will also be prone to orthostatic hypotension, hypotension with functional activities, or both as a result of the vasodilation occurring from the inflammation associated with infection.
  • b. Therefore slow changes in positions, especially from recumbent to upright positions, and frequent blood pressure monitoring are essential to promoting tolerance for functional activities.
  • a. During an exacerbation or progression of an infection process, rest may be indicated.
  • b. Clarification with the physician or nurse regarding the type of intended physical therapy intervention is helpful in making this decision.

Appendix 13A. Disorders of Altered Immunity

Systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease with strong genetic predisposition. There is also evidence suggesting risk factors that can trigger the onset of this disease, such as physical or emotional stress, pregnancy, sulfa antibiotics, and environmental factors, such as sun exposure. Women who are African-American, Asian, or Native American, ages 20 to 40 years, are more susceptible than men in acquiring this disease. SLE is characterized by a systemic, remitting-and-relapsing clinical presentation. 1 , 2 , 3 , 4

The primary laboratory test for diagnosis of SLE is as antinuclear antibody titer. 5 Diagnosis of SLE is confirmed if a patient has 4 of the following 11 manifestations of SLE: malar rash, discoid rash (individual round lesions), photosensitivity, oral ulcers, arthritis, serositis, renal disorder, neurologic disorder, hematologic disorder, immunologic disorder, and the presence of antinuclear antibodies. 3

Prognosis for 10-year survival after diagnosis is 90%. The most common cause of death in SLE is renal failure, and the second most common is central nervous system dysfunction. 1 , 2 , 3

Clinical presentation of SLE may include the following 1 , 2 , 3 , 4 :

  • • Arthritis or arthralgias (stiffness and pain in hands, feet, and large joints)
  • • Red, warm, and tender joints
  • • Butterfly (malar) rash on face
  • • Fever, fatigue, anorexia, and weight loss
  • • Pleurisy, pericarditis
  • • Headache, seizures
  • • Hemolytic anemia, thrombocytopenia, leukopenia
  • • Renal disease or failure

Management of SLE may consist of nonsteroidal antiin­flammatory drugs; glucocorticoids; immunosuppressive agents (cyclophosphamide); dialysis; and renal transplantation in severe cases. 1 , 2 , 4 , 6

Sarcoidosis

Sarcoidosis is a systemic granulomatous disorder that primarily affects women and nonwhite adults in the third decade of their life. The definitive etiology is unknown, although an autoimmune process that is environmentally triggered is the generally agreed-on hypothesis. Sarcoidosis may present as acute or chronic and have periods of progression and remission. 6 , 7 , 8 , 9 , 10

Multiple body systems may be affected by sarcoidosis. The lungs are the primary organs affected, with dyspnea, dry cough, and chest pain being common symptoms. Pulmonary involvement can be staged according to the following radiographic evidence 7 , 8 :

  • • Stage 0: No radiographic abnormalities
  • • Stage I: Bilateral hilar lymphadenopathy
  • • Stage II: Bilateral hilar adenopathy and parenchymal infiltration
  • • Stage III: Parenchymal infiltration without hilar adenopathy
  • • Stage IV: Advanced fibrosis with evidence of honeycombing, hilar retraction, bullae, cysts, and emphysema

Other systems of the body can be affected as well, with symptoms including the following:

  • • Eye and skin lesions
  • • Fever, fatigue, and weight loss
  • • Hepatosplenomegaly
  • • Hypercalcemia, anemia, and leukopenia
  • • Arthralgia, arthritis

Management of sarcoidosis usually consists of corticosteroid therapy, ranging from topical to oral administration. In addition, cytotoxic agents (methotrexate and azathioprine), antimalarial agents (chloroquine and hydroxychloroquine), and nonsteroidal antiinflammatory drugs may be used. In severe cases of pulmonary disease, single and double lung transplantation may be performed. 6 , 7 , 8

Amyloidosis

Amyloidosis is a group of disorders characterized by deposition of amyloid (a type of protein) in various tissues and organs. Amyloidosis is classified according to protein type and tissue distribution and affects men more than women, between the ages of 60 and 70 years. 11 Clinical signs and symptoms are representative of the affected areas, with common manifestations including 11 :

  • • Fatigue
  • • Shortness of breath
  • • Edema
  • • Paresthesia
  • • Weight loss
  • • Diarrhea
  • • Peripheral neuropathy

In general, the deposition of protein in these areas will result in firmer, less distensible tissues that compromise organ function. Management of amyloidosis consists of controlling any primary disease process that may promote deposition of amyloid into the tissues. 11

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is an autoimmune disease characterized by uncontrolled proliferation of synovial tissue. 12 It is a chronic disease involving systemic inflammation, with periods of exacerbation and remission. 13 The etiology is not fully understood, but it is believed there is a correlation between environmental and genetic factors. Females have an increased risk of developing RA, as do individuals with a positive family history, silicate exposure, or smoking history. 12

There are two forms of RA: juvenile idiopathic arthritis (JIA) and adult RA. JIA occurs most often during the toddler and early adolescent developmental phases, whereas adult RA has a peak onset in the third and fourth decades of life. Both forms of RA have an inflammatory component in disease development and have similar medical management strategies. 13

With RA, an interaction between autoantibodies (rheumatoid factors) and immunoglobulins initiates the inflammatory process, which involves an increased infiltration of leukocytes from the peripheral circulation into the synovial joint. Pannus—a destructive granulation tissue that dissolves periarticular tissues—can develop, ultimately leading to joint destruction. 13

Clinical manifestations of RA can include articular and extra-articular symptoms. Most body systems may be involved, including pulmonary, cardiovascular, neurologic, and gastrointestinal. 13 The joints most commonly affected by RA are those with the highest ratio of synovium compared to articular cartilage, including the wrist, proximal interphalangeal, and metacarpophalangeal joints. 12 Common deformities associated with RA are ulnar drift, swan-neck, and boutonniere deformities. 13 Other symptoms include anorexia, low-grade fever, fatigue, and malaise. 12 Osteoarthritis (OA), also called degenerative joint disease, may result in joint changes and deformation. Table 13A-1 compares OA and RA. 13

TABLE 13A-1

Comparison of Osteoarthritis and Rheumatoid Arthritis

ESR, Erythrocyte sedimentation rate.

Diagnosis of rheumatoid arthritis can be made through the following seven criteria established by the American Rheumatism Association 12 :

  • 1. Morning stiffness
  • 2. Arthritis of three or more joint areas
  • 3. Hand joint involvement
  • 4. Symmetric arthritis
  • 5. Rheumatoid nodules
  • 6. Serum rheumatoid factor positive
  • 7. Radiographic changes of the wrist and hand joints

Laboratory diagnostic tests include a complete blood cell count with differential, rheumatoid factor, and erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP). 11

Management of RA may include the following 12 , 13 :

  • • Nonsteroidal antiinflammatory drugs
  • • Glucocorticoids
  • • Disease-modifying antirheumatic drugs (DMARDs) (Chapter 19, Table 19-13)
  • • Pain management
  • • Joint protection
  • • Control of systemic complications

Modification of an assistive device may be necessary based on the patient's wrist and hand function. For example, a platform walker may more appropriate than a standard walker, and Lofstrand crutches may be more appropriate than axillary crutches.

A patient may be admitted to the hospital setting with an infectious disease process acquired in the community or may develop one as a complication from the hospital environment. The current terminology is to call this type of infection a health care–associated infection (HAI). In 2002, the estimated number of HAIs in U.S. hospitals was 1.7 million, resulting in about 99,000 deaths. 1 The major source of HAI is likely the patient's endogenous flora, but up to 40% of HAIs can be caused by cross infection via the hands of health care workers. 2 An infectious disease process generally has a primary site of origin; however, it may result in diffuse systemic effects that may limit the patient's functional mobility and activity tolerance. Therefore a basic understanding of these infectious disease processes is useful in designing, implementing, and modifying physical therapy treatment programs. The physical therapist may also provide treatment for patients who have disorders resulting from altered immunity. These disorders are mentioned in this chapter because immune system reactions can be similar to those of infectious disease processes (see Appendix 13-A for a discussion of four common disorders of altered immunity: systemic lupus erythematosus, sarcoidosis, amyloidosis, and rheumatoid arthritis).

* A person who has been exposed to the tubercle bacillus will demonstrate a raised and reddened area 2 to 3 days after being injected with the protein derivative of the bacilli.

  • ID Grand Rounds Case Presentations

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Below are a few examples of the fantastic cases and case presentations our first-year fellows are engaged with:

October 3, 2023.

Case 1: An 8-year old boy with fever and maculopapular rash Case 2: A 67-year-old woman with one week of fevers, abdominal pain, and diarrhea

September 13, 2023

Case 1: A 37-year-old man with painful neck swelling Case 2: A 44-year-old woman with Crohn’s disease and acute-onset fever, headache, and myalgia

September 27, 2022

Case 1: “Forging Ahead” Case 2: An 82-year-old diabetic man with 6 weeks of lower extremity pain

September 21, 2022

Case 1: “Mimikers” Case 2: A MISCdirection

September 13, 2022

Case 1: “Eye Heart ID” Case 2: A patient with rheumatoid arthritis, fever, and altered mental status.

October 20, 2020

Case 1: A seventeen-month-old girl who refuses to walk. Case 2: A fifteen-year-old boy with aplastic anemia, neutropenia, and a necrotic nasopharyngeal mass.

September 22, 2020

Case 1:  A 33 year old woman with a shoulder mass Case 2:  A 58 year old man with AML and subcutaneous nodules

September 15, 2020

Case 1:  A 5 year old boy with new onset intractable seizures  Case 2:  A 28 year old man with HIV and diffuse large B cell lymphoma, who presents with a new headache and gait imbalance.

September 8, 2020

Part One:  A man with lung cancer and a brain lesion; a woman with an acute severe headache

Part Two:  A woman with an acute headache

August 4, 2020

Case 1:  A 7 year old girl with new onset seizures Case 2:  A 67 year old man with AML and nausea, vomiting, and diarrhea

August 11, 2020

Case 1:   A man with AIDS, subacute pancytopenia, several weeks of weight loss, and one week of fevers Case 2:   A man with one year of weakness, fatigue, and skin lesions found to have brisk hypercalcemia

July 28, 2020

A 30 year old man with headaches, transient right hand weakness/numbness, and world finding difficulty

June 30, 2020

Case 1:  A man with 4 days of progressive headache culminating in septic shock Case 2:  A man with progressive neurologic dysfunction and nodular spinal cord enhancement

June 16, 2020

Case 1:  A 77 year old man from South America with chronic diarrhea Case 2:  A 4 year old boy with neck stiffness

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infectious diseases

Infectious Diseases

Jul 18, 2014

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Infectious Diseases. Prevention and Treatment. For teacher’s reference. Curriculum Links : Course: SBI 3C Unit: ( C) Microbiology Expectation: 3.5 - describe how different viruses, bacteria, and fungi can affect host organisms, and how

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Infectious Diseases Prevention and Treatment

For teacher’s reference Curriculum Links: Course: SBI 3C Unit: (C) Microbiology Expectation: 3.5 - describe how different viruses, bacteria, and fungi can affect host organisms, and how those effects are normally treated or prevented (e.g., hepatitis viruses can damage the liver, but vaccinations can prevent infections; streptococcus bacteria can cause respiratory infections, which are treated with antibiotics; ringworm is a fungal infection of the skin, treated with fungicides

Misconceptions Antibiotics can cure all types of infectious diseases Antibiotics can be taken to prevent infections Colds and Flu are caused by bacteria (or general confusion over which illnesses are caused by viruses vs. bacteria) You can get the flu from the flu shot Viruses are living organisms

Agenda Infectious Diseases Bacteria, Viruses, Fungi, and Protists that cause Infectious Diseases Transmission of Diseases Prevention of Diseases Treatment of Diseases

Infectious disease • Defined as: • A disease caused by a microscopic pathogen such as bacteria, viruses, fungi, and parasites • These diseases can be transmitted from person to person

Bacteria and Disease • Bacteria cause disease when they build up in large numbers in an affected area of the body. • The toxins from the bacteria “overload” a person’s immune system and it’s ability to remove these poisons • This can have varying effects on the host (depending on bacteria/disease) • decrease function of cells and tissues • destroying cells and tissues

Examples Adapted from Nelson Biology 11 College Preparation

Viruses and Disease • Viruses depend on host cells to survive and reproduce • Through the process of reproduction, viruses attack host cells • This is what causes the symptoms of the disease • Viral Infections are often difficult to treat Why do you think this is?

Examples How do Viruses compare to Bacteria size wise?

Protists and Disease • Protists which are single celled eukaryotes (examples include amoeba, paramecium) • Protists can be parasitic, causing harm to the host organism • What is meant by parasitic?

Fungi and Disease Fungi are responsible for many human diseases. These diseases are referred to as mycoses Most are simply bothersome Some can be life threatening

Examples • Amanita phalloides(a.k.a Dead cap) world’s most dangerous mushroom. Eating one or two can be fatal

Disease Transmission Infectious diseases can spread easily from person to person in five different ways 1._______________________________ 2._______________________________ 3._______________________________ 4._______________________________ 5._______________________________

Disease Transmission Infectious diseases can spread easily from person to person in five different ways 1. Air 2. Food 3. Water 4. Person to Person contact (direct or indirect) 5. Animal bites

Examples of Transmission Methods Adapted from Modern Biology (2002)

Prevention • Vaccinations • Immune System • Specific • Non-Specific – Body’s “first line of defense” for preventing pathogens from entering the body

Non-Specific Immunity • Skin – keratin shield acts as a barrier • Sweat, oils, and waxes released by skin – toxic to many bacteria and fungi • Mucus membranes – Barrier secretes mucus which traps pathogens • Stomach Acid – destroys most swallowed pathogens • Inflammatory Response – Injured cells send a chemical signal as pathogens enter (through a cut for example). Chemical signal attracts phagocytes to destroy foreign pathogen • Fever – Body’s response to infection

Specific Immunity – The Immune System • Include several organs within the body working together to identify pathogens and kill them • Bone marrow • Thymus • Lymph Nodes • Tonsils • Adenoids • Spleen A great animated video to describe the immune system

Vaccinations • Vaccines contain pathogens or toxins that have been modified so they can no longer cause disease • They contain antigens that stimulate an immune response  this produces memory cells • Some diseases that have been controlled through vaccines: • Polio, Measles, Mumps, Tetanus, Diphtheria,

Treatment Different depending on the pathogen causing the disease

Case Study Activity Jessica’s Case Measles Suzie’s Case Malaria Tim’s Case Giardiasis Jack’s Case Cholera

Teaching Strategies/Ideas Graphic organizers (to divide Bacteria, Virus, Protist, and Fungi) Diagnostic activities HIV simulation lab activity Use current/recent events (e.g. H1N1, cholera outbreak in Haiti, SARS) in lessons Incorporate Social Justice (e.g. AIDS awareness, “buy a net” malaria prevention charity)

References http://emedicine.medscape.com/infectious_diseases http://www.microbiologyprocedure.com/infection-and-diseases/diseases-caused-by-bacteria.htm http://www.ehow.com/about_5139239_diseases-do-protists-cause.html http://science.education.nih.gov/supplements/nih1/diseases/guide/understanding1.htm http://www.fungi4schools.org/Documentation/03World-of-Fungi/WF05_Fungi_and_Disease.pdf http://www.phac-aspc.gc.ca/media/nr-rp/2005/2005_3bk1-eng.php

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  • Section 5 - Viral Hemorrhagic Fevers
  • Section 5 - Zika

Yellow Fever

Cdc yellow book 2024.

Author(s): Mark Gershman, J. Erin Staples

Infectious Agent

Transmission, epidemiology, risk for travelers, clinical presentation, international certificate of vaccination or prophylaxis, vaccine requirements versus recommendations.

INFECTIOUS AGENT: Yellow fever virus

Sub-Saharan Africa

Tropical South America

TRAVELER CATEGORIES AT GREATEST RISK FOR EXPOSURE & INFECTION

PREVENTION METHODS

Avoid insect bites

Yellow fever is a vaccine-preventable disease

DIAGNOSTIC SUPPORT

Yellow fever (YF) virus is a single-stranded RNA virus that belongs to the genus Flavivirus .

Vectorborne transmission of YF virus occurs via the bite of an infected mosquito, primarily Aedes or Haemagogus spp. Nonhuman primates and humans are the main reservoirs of the virus, and anthroponotic (human-to-vector-to-human) transmission occurs. YF virus has 3 transmission cycles: sylvatic (jungle), intermediate (savannah), and urban.

The sylvatic (jungle) cycle involves transmission of virus between nonhuman primates and mosquito species found in forest canopies. Virus is transmitted from monkeys to humans via mosquitoes when occupational or recreational activities encroach into the jungle. In Africa, an intermediate (savannah) cycle involves transmission of YF virus from tree hole–breeding Aedes spp. to humans in jungle border areas. YF virus can be transmitted from monkeys to humans or from human to human via these mosquitoes. The urban cycle involves transmission of virus between humans and peridomestic mosquitoes, primarily Ae. aegypti .

Humans infected with YF virus experience the highest levels of viremia shortly before onset of fever and for the first 3–5 days of illness, during which time they can transmit the virus to mosquitoes. Because of the high level of viremia, bloodborne transmission theoretically can occur via transfusion or needlesticks. One case of perinatal transmission of wild-type YF virus from a woman who developed symptoms of YF 3 days prior to delivery has been documented; the infant subsequently tested positive for YF viral RNA and died of fulminant YF on the 12th day of life.

YF occurs in sub-Saharan Africa and tropical South America, where it is endemic and intermittently epidemic (see Table 5-22 and Table 5-23 for lists of countries with risk of YF virus transmission). Most YF disease in humans is due to sylvatic or intermediate transmission cycles. Urban YF occurs periodically in Africa and sporadically in the Americas. In areas of Africa with persistent circulation of YF virus, natural immunity accumulates with age; consequently, infants and children are at greatest risk for disease. In South America, YF occurs most frequently in unimmunized young people exposed to mosquito vectors through their work in forested areas.

Table 5-22 Countries with risk for yellow fever (YF) virus transmission 1

1 Current as of November 2022. Defined by the World Health Organization (WHO) as countries or areas where YF “has been reported currently or in the past and vectors and animal reservoirs currently exist.” See www.who.int/publications/m/item/countries-with-risk-of-yellow-fever-transmission-and-countries-requiring-yellow-fever-vaccination-(november-2022) .

2 These countries are not holoendemic (only a portion of the country has risk of YF virus + transmission). For details, see Map 5-10 , Map 5-11 , and YF vaccine recommendations (Sec. 2, Ch. 5, Yellow Fever Vaccine & Malaria Prevention Information, by Country ).

Table 5-23 Countries with low potential for exposure to yellow fever (YF) virus 1

1 The countries on this list have low potential for exposure to YF virus and are not included on the World Health Organization list of countries with risk for YF virus transmission ( Table 5-22 ). Unless a country requires proof of YF vaccination from all arriving travelers ( Table 5-25 ), or specifies otherwise, proof of YF vaccination should not be required for travelers arriving from the countries on this list.

2 Classified as “low potential for exposure to YF virus” only in some areas; remaining areas are classified as having no risk of exposure to YF virus.

A traveler’s risk for acquiring YF is determined by their immunization status as well as destination-specific (e.g., local rate of virus transmission) and travel-associated (e.g., exposure duration, occupational and recreational activities, season) factors. Reported cases of human disease are the principal but crude indicator of disease risk. Case reports from a destination might be absent because of a low level of transmission, a high level of immunity in the population (e.g., due to vaccination), or failure of local surveillance systems to detect cases. Because “epidemiologic silence” does not mean absence of risk, travelers should not go into endemic areas without taking protective measures.

YF virus transmission in rural West Africa is seasonal; a period of elevated risk occurs at the end of the rainy season and the beginning of the dry season, usually July–October. In East Africa, YF virus transmission is generally less predictable because long periods (years) often pass between virus activity in this region; when YF virus transmission occurs in East Africa, seasonality is similar to that in West Africa.

The risk for infection by sylvatic vectors in South America is greatest during the rainy season (January–May, with a peak incidence during February and March). Ae. aegypti can transmit YF virus episodically, however—even during the dry season—in both rural and densely settled urban areas.

During 1970–2015, 11 cases of YF were reported in people from the United States and Europe who traveled to West Africa (6 cases) or South America (5 cases); 8 (73%) died. Only 1 traveler had a documented history of YF vaccination; that traveler survived. Starting in 2016, the number of travel-associated YF cases increased substantially, primarily because of outbreaks in Angola and Brazil. During 2016–mid-2021, >37 travel-associated cases were reported in unvaccinated travelers who were residents of nonendemic areas or countries, including ≥15 European travelers and 1 American traveler to Peru.

The risk of acquiring YF during travel is difficult to predict because of variations in ecologic determinants of virus transmission. For a 2-week stay, the estimated risk for illness and for death due to YF for an unvaccinated traveler visiting an endemic area are as follows: for West Africa, risk for illness is 50 per 100,000 and risk for death is 10 per 100,000; for South America, risk for illness is 5 per 100,000 and risk for death is 1 per 100,000. These estimates are based on the risk to resident populations, often during peak transmission season, and might not accurately reflect the risk to travelers who have a different immunity profile, follow mosquito bite precautions, have less outdoor exposure, or who travel during off-peak periods. A traveler’s risk for becoming infected is likely greater when outbreaks are occurring at their destination.

Most people infected with YF virus have minimal or no symptoms and are unlikely to seek medical attention. For those who develop symptomatic illness, the incubation period is typically 3–6 days. The initial illness is nonspecific: backache, chills, fever, headache, myalgia, nausea and vomiting, and prostration. Most improve after the initial presentation. After a brief remission of ≤48 hours, ≈12% of infected patients progress to a more serious form of the disease, characterized by hemorrhagic symptoms, jaundice, and eventually shock and multisystem organ failure. The case-fatality rate for severe cases is 30%–60%.

YF is a nationally notifiable disease. A preliminary diagnosis is based on clinical presentation and exposure details. Laboratory diagnosis is best performed by virus isolation or nucleic acid amplification tests (e.g., reverse transcription PCR [RT-PCR]) or by serologic assays. Perform virus isolation or nucleic acid amplification tests for YF virus or YF viral RNA early in the course of the illness. By the time more overt symptoms are recognized, the virus or viral RNA might no longer be detectable; thus, virus isolation and nucleic acid amplification testing should not be used to rule out a diagnosis of YF.

Serologic assays can be used to detect virus-specific IgM and IgG antibodies. Because of the possibility of cross-reactivity between antibodies against other flaviviruses, however, more specific antibody testing (e.g., a plaque reduction neutralization test) should be performed to confirm the infection. Contact your state or local health department or call the Centers for Disease Control and Prevention (CDC) Arboviral Diseases Branch at 970-221-6400 for assistance with diagnostic testing for YF virus infections.

No specific medications are available to treat YF virus infections; treatment is directed at symptomatic relief or life-saving interventions. Fluids, rest, and use of analgesics and antipyretics might relieve symptoms of aching and fever. Avoid prescribing medications than can increase the risk for bleeding (e.g., aspirin or other nonsteroidal anti-inflammatory drugs). During the first few days of illness, protect infected people from further mosquito exposure by keeping them indoors or under a mosquito net, so they do not contribute to the transmission cycle.

Personal Protective Measures

The best way to prevent mosquito-borne diseases, including YF, is to avoid mosquito bites (see Sec. 4, Ch. 6, Mosquitoes, Ticks & Other Arthropods ).

YF is preventable by a relatively safe, effective vaccine. All YF vaccines currently manufactured are live attenuated viral vaccines. Only one YF vaccine (YF-VAX, Sanofi Pasteur) is licensed for use in the United States ( Table 5-24 ). Periodically in the United States, shortages of YF-VAX have occurred due to production issues, including one that lasted from late 2015 until early 2021. To address this most recent shortage, Sanofi Pasteur collaborated with the CDC and the US Food and Drug Administration (FDA) to import and distribute Stamaril (a YF vaccine comparable to YF-VAX, manufactured at the company’s facility in France) under an expanded-access investigational new drug protocol.

The different YF vaccine products, including those manufactured outside the United States, have no substantial differences in reactogenicity or immunogenicity. Consider people who receive YF vaccines licensed in other countries but not approved by the FDA to be protected against YF. For the most current information on YF vaccine availability, check the CDC Travelers’ Health website.

Table 5-24 Vaccine to prevent yellow fever (YF)

TRADE NAME (MANU- FACTURER)

TRADE NAME (MANUFACTURER)

YF-VAX (Sanofi Pasteur)

≥9 months 1

Sub-cutaneous

Not recommended for most people 3

1 Ages 6–8 months and ≥60 years are precautions, and age <6 months is a contraindication to receiving YF vaccine.

2 YF-VAX is available in single-dose and multiple-dose (5-dose) vials.

3 For further details regarding revaccination, see Prevention: Vaccine: Booster Doses, in this chapter.

Indications for Use

YF vaccine is recommended for people aged ≥9 months who are living in or traveling to areas with risk for YF virus transmission in Africa or South America. In addition, some countries require proof of YF vaccination for entry. For country-specific YF vaccination recommendations and requirements, see Sec. 2, Ch. 5, Yellow Fever Vaccine & Malaria Prevention Information, by Country .

Because of the risk for serious adverse events after YF vaccination, clinicians should only vaccinate people at risk for YF virus exposure or who require proof of vaccination to enter a country. To further minimize the risk for serious adverse events, carefully observe the contraindications and consider vaccination precautions before administering YF vaccine ( Box 5-09 ). For additional information, refer to the YF vaccine recommendations of the Advisory Committee on Immunization Practices (ACIP).

Box 5-09 Yellow fever vaccine contraindications & precautions

Contraindications.

  • Age <6 months
  • Allergy to vaccine component 1
  • HIV infection (symptomatic) or CD4 T lymphocyte counts <200/mL (or <15% of total lymphocytes in children aged <6 years) 2,3
  • Primary immunodeficiencies
  • Immunosuppressive and immunomodulatory therapies
  • Malignant neoplasms
  • Thymus disorder associated with abnormal immune cell function
  • Transplantation

PRECAUTIONS

  • Age 6–8 months
  • Age ≥60 years

Breastfeeding

  • HIV infection (asymptomatic) and CD4 T lymphocyte counts 200–499/mL (or 15%–24% of total lymphocytes in children aged <6 years) 2,3

1 If considering vaccination, desensitization can be performed under direct supervision of a physician experienced in the management of anaphylaxis.

2 Symptoms of HIV are classified in Centers for Disease Control and Prevention. 1993 Revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. MMWR Recomm Rep 1992;41(RR-17). Available from: www.cdc.gov/mmwr/preview/mmwrhtml/00018871.htm (see Table 1 Adults and Adolescents); and Panel on Antiretroviral Therapy and Medical Management of HIV-Infected Children. Guidelines for the use of antiretroviral agents in pediatric HIV infection 2010. pp. 20–2. Available from: www.hopkinsmedicine.org/som/faculty/appointments/_documents/_ppc_documents/portfolios/Hutton/Hutton-Portfolio-Samples/guidelines-for-the-use-of-antiretroviral-agents-in-pediatric-hiv-infection.pdf  [PDF].

3 In 2010, the Advisory Committee on Immunization Practices (ACIP) used this clinical classification of levels of immunosuppression among HIV-infected people to inform yellow fever vaccine recommendations (see Staples et al., Yellow fever vaccine: recommendations of the Advisory Committee on Immunization Practices). A revised surveillance case definition for HIV infection was published in 2014. To date, ACIP has not updated YF vaccine recommendations for people infected with HIV.

Administration

For all eligible people, subcutaneously administer a single 0.5 mL injection of reconstituted vaccine, which is the standard dose.

Coadministration With Other Vaccines

Inactivated vaccines.

No evidence exists that inactivated vaccines interfere with the immune response to YF vaccine. Therefore, inactivated vaccines can be administered either simultaneously or at any time before or after YF vaccination.

Live Attenuated Viral Vaccines

ACIP recommends that YF vaccine be given at the same time as other live viral vaccines. If simultaneous administration is not possible, wait 30 days between vaccinations, because the immune response to a live viral vaccine could be impaired if it is administered within 30 days of another live viral vaccine. One study demonstrated that coadministration of YF vaccine and measles-mumps-rubella (MMR) vaccine decreased the seroconversion ratios to all antigens, except measles. Two more recent studies also showed a less robust antibody concentration in people who seroconverted after vaccine coadministration. These studies suggest that whenever possible, it is best to give YF and MMR vaccines 30 days apart. Of greater importance, however, is ensuring that travelers are vaccinated appropriately before travel; coadministration of YF and MMR vaccines is therefore acceptable.

No data are available on the immune response to nasally administered live attenuated influenza vaccine given simultaneously with YF vaccine.

Live Bacterial Vaccines

Data suggest that oral Ty21a typhoid vaccine (Vivotif), a live bacterial vaccine, can be administered simultaneously or at any interval before or after YF vaccine. No data are available on the immune response to live attenuated oral cholera vaccine (Vaxchora) administered simultaneously with YF vaccine.

Fractional Dosing

In recent years, several countries have extended vaccine supplies during large YF outbreaks by administering partial vaccine doses, usually 0.1 mL, a practice known as fractional dosing. Limited study data have demonstrated immunogenicity of fractional dosing is comparable to that of full-dose YF vaccination at 1 month and ≤1 year after subcutaneous administration; knowledge gaps regarding fractional dosing remain, however.

In the United States, FDA has not approved fractional dosing of YF vaccine. Furthermore, WHO notes that fractional dosing does not meet YF vaccination requirements under the International Health Regulations (IHR); proof of vaccination for international travel cannot be issued to a person who has received only a fractional dose.

Booster Doses

In 2014, the WHO Strategic Advisory Group of Experts on Immunization concluded that a single primary dose of YF vaccine provides sustained immunity and lifelong protection against YF disease and that revaccination (a booster dose) is not needed. In 2016, the IHR were officially amended to specify that a completed International Certificate of Vaccination or Prophylaxis (ICVP or “yellow card”) is valid for the lifetime of the vaccinee, and countries cannot require proof of revaccination against YF as a condition of entry, even if the last vaccination was >10 years prior.

ACIP also has stated that a single dose of YF vaccine provides long-lasting protection and is adequate for most travelers. ACIP guidelines do differ slightly from those of WHO, however, by specifying that additional doses of YF vaccine are recommended for the following groups of travelers: people who were pregnant when they received their initial dose of vaccine (administer 1 additional dose before they are next at risk for YF); people who received a hematopoietic stem cell transplant after receiving a dose of YF vaccine (revaccinate before they are next at risk for YF as long as they are sufficiently immunocompetent); people infected with HIV when they received their last dose of YF vaccine (administer a dose every 10 years if they continue to be at risk for YF).

Consider administering a booster dose to travelers who received their last dose of YF vaccine ≥10 years previously if they will be going to higher-risk settings based on activities, duration of travel, location, and season. This consideration applies to travelers planning prolonged stays in endemic areas, those traveling to endemic areas (e.g., rural West Africa) during peak transmission season, or travelers visiting areas with ongoing outbreaks.

Although booster doses of YF vaccine are not recommended for most travelers, and despite the 2016 changes to the IHR, clinicians and travelers should nonetheless review the entry requirements for destination countries. For more information on country-specific recommendations and requirements, see Sec. 2, Ch. 5, Yellow Fever Vaccine & Malaria Prevention Information, by Country .

Adverse Events

Common adverse reactions.

Reactions to YF vaccine are generally mild; 10%–30% of vaccinees report mild systemic symptoms, including headache, low-grade fever, and myalgia, that begin within days after vaccination and last 5–10 days.

Serious Adverse Reactions

Hypersensitivity reactions.

Immediate hypersensitivity reactions, characterized by bronchospasm, rash, or urticaria, are uncommon. Anaphylaxis after YF vaccine is reported to occur at a rate of 1.3 cases per 100,000 doses administered.

Yellow Fever Vaccine–Associated Neurologic Disease

Yellow fever vaccine–associated neurologic disease (YEL-AND) represents a collection of clinical syndromes, including acute disseminated encephalomyelitis, Guillain-Barré syndrome, meningoencephalitis, and, rarely, cranial nerve palsies. Historically, YEL-AND was diagnosed primarily among infants as encephalitis, although more recent case reports have described various neurological syndromes among people of most age groups. YEL-AND is rarely fatal.

Almost all cases of YEL-AND reported globally occur in first-time vaccine recipients. The onset of illness for documented cases in the United States is 2–56 days after vaccination. The incidence of YEL-AND in the United States is 0.8 per 100,000 doses administered, but is greater (2.2 per 100,000 doses) in people aged ≥60 years.

Yellow Fever Vaccine–Associated Viscerotropic Disease

Yellow fever vaccine–associated viscerotropic disease (YEL-AVD) is a severe illness similar to wild-type YF disease, in which vaccine virus proliferates in multiple organs, often leading to multiorgan dysfunction or failure and occasionally death. Since 2001, >100 confirmed and suspected cases of YEL-AVD have been reported throughout the world.

YEL-AVD has been reported to occur only after the first dose of YF vaccine; no laboratory-confirmed YEL-AVD has been reported after booster doses. For YEL-AVD cases reported in the United States, the median time from YF vaccination until symptom onset is 4 days (range 1–18 days). The case-fatality ratio is ≈48% and the incidence is 0.3 cases per 100,000 doses of vaccine administered. The incidence of YEL-AVD is greater for people aged ≥60 years (1.2 per 100,000 doses) and greater still for people aged ≥70 years.

Contraindications

Contraindications to receiving YF vaccine include age <6 months; various forms of altered immunity, including symptomatic HIV infection or HIV infection with severe immunosuppression; and hypersensitivity to vaccine components.

A person who has an absolute YF vaccine contraindication should not be vaccinated, because they have a condition that increases their risk for having a serious adverse event following vaccination. Encourage these people to consider alternative travel plans. If they cannot avoid travel to a YF-endemic area, provide them with a medical waiver (see below for details), emphasize the importance of strict adherence to protective measures against mosquito bites, and discuss risks associated with being unvaccinated.

Age Younger than 6 Months

YF vaccine is contraindicated in infants aged <6 months because the rate of YEL-AND is high, 50–400 cases per 100,000 infants vaccinated. The mechanism of increased neurovirulence in infants is unknown, but could be due to the immaturity of the blood–brain barrier, an increased or more prolonged viremia, or immune system immaturity. Travel to YF-endemic countries for children aged <6 months should be postponed or avoided.

Altered Immune Status

Hiv infection.

YF vaccine is contraindicated in people with AIDS or other clinical manifestations of HIV infection, including those with CD4 T lymphocyte counts <200/mL, or <15% of total lymphocytes for children <6 years old. This contraindication is based on the potential increased risk for encephalitis in this population. See the section on Precautions (later in this chapter) for guidance regarding HIV-infected people who do not meet the above criteria.

Thymus Disorder

YF vaccine is contraindicated in people with a thymus disorder associated with abnormal immune cell function (e.g., myasthenia gravis, thymoma). There is no evidence of immune dysfunction or increased risk for YF vaccine–associated serious adverse events in people who have undergone incidental thymectomy or who have had indirect radiation therapy in the distant past; these people can be vaccinated.

Other Immunodeficiencies

YF vaccine is contraindicated in people who are immunodeficient or immunosuppressed, whether due to an underlying (primary) disorder or medical treatment. Organ transplant recipients and patients with malignant neoplasms are among those for whom YF vaccine is contraindicated (see Sec. 3, Ch. 1, Immunocompromised Travelers ).

Immunosuppressive & Immunomodulatory Therapies

YF vaccine is contraindicated in people whose immunologic response is either suppressed or modulated by current or recent radiation therapy or drugs. Drugs with known immunosuppressive or immunomodulatory properties ( Table 3-04 ) include, but are not limited to, alkylating agents, antimetabolites, high-dose systemic corticosteroids, interleukin blocking agents (e.g., anakinra, tocilizumab), monoclonal antibodies targeting immune cells (e.g., alemtuzumab, rituximab), or tumor necrosis factor-α inhibitors (e.g., etanercept).

People receiving therapies such as those listed above are presumed to be at increased risk for YF vaccine–associated serious adverse events; administration of live attenuated vaccines is contraindicated in the package insert for most of these drugs (see Sec. 3, Ch. 1, Immunocompromised Travelers ). Even among people who have discontinued immunosuppressive or immunomodulatory therapies, defer administration of live viral vaccines until their immune function has improved. Family members of people with altered immune status who themselves have no contraindications can receive YF vaccine.

Hypersensitivity

YF vaccine is contraindicated in people with a history of acute hypersensitivity reaction to a previous dose of the vaccine or to any of the vaccine components, including chicken proteins, eggs, egg products, or gelatin. If vaccination of a person with a questionable history of hypersensitivity to a vaccine component is considered essential, skin testing and, if indicated, desensitization should be performed by an experienced clinician according to instructions provided in the manufacturer’s vaccine prescribing information  [PDF].

Precautions

A person with a precaution (relative contraindication) to YF vaccine has a condition that might increase their risk for having a serious adverse event following vaccination, or that could interfere with the ability of the vaccine to produce immunity. YF vaccination precautions include age 6–8 months, age ≥60 years, asymptomatic HIV infection with moderate immunosuppression, pregnancy, and breastfeeding.

Discussing the benefits and risks of YF vaccination with all patients—but particularly those with underlying precautions—is an essential part of the pretravel consultation. If travel to a YF risk area is unavoidable for a person with a vaccine precaution, the discussion about vaccination should balance the risk for YF virus exposure against the risk for having a serious post-vaccination adverse event.

Solicit information from the traveler about their risk tolerance level, and include this in the shared decision making about whether to administer YF vaccine. If the decision is made not to vaccinate the traveler, provide a medical waiver, emphasize the critical importance of adhering to insect bite precautions, and discuss risks associated with being unvaccinated. When no risk for YF exists in the itinerary, but international travel requirements are in effect in the traveler’s destination(s), the vaccine risk outweighs the disease; avoiding vaccination and issuing a medical waiver to fulfill health regulations is reasonable, but this decision should be made in deliberation with the patient.

Age 6–8 Months

Two cases of YEL-AND have been reported in infants aged 6–8 months. By 9 months of age, risk for YEL-AND is believed to be substantially lower. ACIP recommends that, whenever possible, travel to YF-endemic countries for children aged 6–8 months should be postponed or avoided.

Age ≥60 Years

The rate of reported serious adverse events after YF vaccination in people aged ≥60 years is 7.7 per 100,000 doses distributed, compared with 3.8 per 100,000 for all YF vaccine recipients. The risks for YEL-AND and YEL-AVD are increased in this age group. Because YEL-AVD has been reported exclusively, and YEL-AND almost exclusively, in primary vaccine recipients, carefully consider the risks and benefits of vaccinating older travelers against YF vaccine for the first time.

HIV Infection

Combined studies of >500 asymptomatic HIV-infected people classified as having moderate immune suppression, defined as CD4 T lymphocyte counts of 200–499/mL for people ≥6 years old (or 15%–24% of total lymphocytes for children aged <6 years) identified no serious adverse events after receipt of YF vaccine. HIV infection has, however, been associated with a reduced immunologic response to YF vaccine, and this diminished immune response has been correlated with HIV RNA levels and CD4 T cell counts.

If an asymptomatic HIV-infected person has no evidence of immune suppression based on CD4 counts (CD4 T lymphocyte counts ≥500/mL for people ≥6 years old or ≥25% of total lymphocytes for children aged <6 years), YF vaccine can be administered. Because YF vaccination might be less effective in eliciting an immune response in asymptomatic HIV-infected people, consider measuring their neutralizing antibody response to vaccination before travel. Contact your state health department or the CDC Arboviral Diseases Branch (970-221-6400) to discuss serologic testing.

Safety of YF vaccination during pregnancy has not been studied in any large prospective trials. In 2 observational studies of people vaccinated against YF during pregnancy, a slightly increased risk for minor congenital abnormalities (mainly pigmented nevi) was detected in one study, and a higher rate of spontaneous abortions was reported in the other. Neither finding was substantiated by subsequent studies.

If possible, pregnant people should avoid travel to YF risk areas. If travel is unavoidable and the risk for YF virus exposure is felt to outweigh the vaccination risk, recommending vaccination is appropriate. By contrast, if the vaccine risk is believed to outweigh the risk for YF virus exposure, suggest or offer a medical waiver to the traveler to fulfill health regulations.

The proportion of people vaccinated during pregnancy who develop a YF virus–specific IgG antibody response is variable depending on the study (39% or 98%) and might be correlated with the trimester when they received the vaccine. Because pregnancy can reduce immunologic responsiveness, consider serologic testing to document a protective immune response to the vaccine. Although no specific data are available, ACIP recommends that a person wait 4 weeks after receiving the YF vaccine before conceiving.

At least 3 YEL-AND cases have been reported in exclusively breastfed infants whose mothers were vaccinated with YF vaccine. All 3 infants were <1 month old at the time of exposure, and encephalitis was diagnosed in all 3 infants. Until specific research data are available, avoid vaccinating breastfeeding people against YF. When a person who is nursing cannot avoid or postpone travel to YF-endemic areas, however, recommend vaccination. Although no data are available to support the practice, some experts recommend that breastfeeding people should pump and discard their breast milk for ≥2 weeks after YF vaccination before resuming breastfeeding.

Other Considerations

No data are available regarding possible increased occurrence of adverse events or decreased vaccine efficacy after YF vaccine administration in people with other chronic medical conditions that can affect immune response (e.g., diabetes mellitus, liver disease [including hepatitis C virus infection], or renal disease). Limited data suggest that autoimmune disease, either by itself or in conjunction with other risk factors, including immunosuppressive medication, could increase the risk for YEL-AVD. Therefore, use caution if considering vaccination of such patients. Factors to consider when assessing a patient’s general level of immune competence include clinical stability, comorbidities, complications, disease severity and duration, and which medications they are taking.

The IHR permit countries to require proof of YF vaccination documented on an ICVP ( Figure 5-02 ) as a condition of entry for travelers arriving from certain countries, even if only in transit, to prevent YF virus importation and transmission in the destination country. Some countries require evidence of vaccination from all entering travelers, including those arriving directly from the United States ( Table 5-25 ).

People with YF vaccine contraindications who must travel to destinations that require proof of vaccination should receive a medical waiver from a YF vaccine provider before their departure; see Medical Waivers (Exemptions) below. Travelers without proof of vaccination or a medical waiver arriving to destinations that require this documentation for entry could be denied entry or face mandatory quarantine (up to 6 days) or vaccination on site.

Figure 5-02 International Certificate of Vaccination or Prophylaxis (ICVP): instructions for completion 1,2

Figure 5-02 International Certificate of Vaccination or  Prophylaxis (ICVP): instructions for completion

View Larger Figure

1 Clinics offering yellow fever vaccine can purchase ICVP (Form CDC 731; formerly PHS 731), from the US Government Publishing Office website or by phone (866-512-1800).

2 Instructions for ICVP completion (1) Print the traveler’s name exactly as it appears in their passport. (2, 5, 7) Enter all dates in the format shown: day (in numerals), month (spelled in letters), year. In the example above, the patient’s date of birth is correctly entered as 22 March 1960. (3) Space reserved for the patient’s signature. (4) For yellow fever (YF) vaccination, print “Yellow Fever” in both spaces. If the ICVP is used to document proof of another required vaccination or prophylaxis (following an amendment to the International Health Regulations or by recommendation of the World Health Organization), write the disease or condition name in this space. Other vaccinations may be listed on the other side of the ICVP booklet. (5) Enter the date of vaccine administration, as shown. (6) The health care provider should enter their handwritten signature, as shown. A signature stamp is not acceptable. For yellow fever vaccine, the health care provider signing the ICVP may be the stamp owner, or another health care provider authorized by the stamp holder to administer or supervise the administration of the vaccine. (7) The ICVP is valid beginning 10 days after the date of primary YF vaccination. Add that date to this box along with the suggested wording “life of person vaccinated,” as shown. (8) Imprint the Uniform Stamp of the vaccinating center in this box.

Table 5-25 Countries that require proof of yellow fever (YF) vaccination from all arriving travelers 1

1 Current as of January 2023. Country requirements for YF vaccination are subject to change at any time; check with the destination country’s embassy or consulate before departure.

ICVP Validation

Anyone who received YF vaccination after December 15, 2007, must provide proof of vaccination on the new ICVP. If the person received the vaccine before December 15, 2007, their original International Certificate of Vaccination against Yellow Fever (ICV) card is still valid as proof of vaccination. Vaccinees should receive a completed ICVP, signed by the vaccine provider and validated with the stamp of the center where the vaccine was given. Failure to secure validations can cause a traveler to be denied entry, quarantined, or possibly revaccinated at the point of entry to a country.

A properly completed ICVP is valid beginning 10 days after the date of primary vaccination. As of July 2016, the YF vaccine booster requirement was eliminated in the IHR, and a completed ICVP is considered valid for the lifetime of the vaccinee. Clinics offering YF vaccine can purchase ICVPs (Form CDC 731; formerly PHS 731) from the US Government Publishing Office website or by phone (866-512-1800).

Designated Yellow Fever Vaccination Centers & Providers

The ICVP must bear the original signature of a YF vaccine provider, who can be a physician or other authorized licensed health care professional who supervises the administration of the vaccine. A signature stamp is not acceptable. YF vaccination must be given at a designated center that possesses an official “uniform stamp,” which must be used to validate the ICVP. In the United States, state and territorial health departments are responsible for designating nonfederal YF vaccination centers and issuing uniform stamps to YF vaccine providers. Information about the location and hours of YF vaccination centers is available from the CDC Travelers’ Health website.

Medical Waivers (Exemptions)

A YF vaccine provider issuing a medical waiver for YF vaccine should complete and sign the Medical Contraindications to Vaccination section of the ICVP ( Figure 5-03 ). Reasons other than medical contraindications are not acceptable for exemption from vaccination. The YF vaccine provider should also provide the traveler with a signed and dated exemption letter on letterhead stationery, clearly stating the contraindications to vaccination and bearing the imprint of the uniform stamp used by the YF vaccination center to validate the ICVP. Risks associated with not being vaccinated should be discussed, and the importance of strict adherence to mosquito bite prevention measures emphasized.

Medical waivers might not be accepted by the destination country. To improve the likelihood that a border official will grant a waiver holder entry to their intended destination, recommend that travelers contact the local embassy or consulate of the country or countries well in advance of travel to obtain specific and authoritative advice regarding waiver documentation requirements. All information provided should be kept with the completed Medical Contraindications to Vaccination and waiver letter.

Figure 5-03 International Certificate of Vaccination or Prophylaxis (ICVP): Medical Contraindication to Vaccination section

Figure 5-03 International Certificate of Vaccination or  Prophylaxis (ICVP): Medical Contraindication to Vaccination section

Country entry requirements for proof of YF vaccination under the IHR differ from CDC’s recommendations. Countries are permitted to establish YF vaccine entry requirements to prevent the YF virus importation and transmission within their borders. Unless issued a medical waiver by a YF vaccine provider, travelers must comply with these requirements to enter the country.

Certain countries require vaccination from travelers arriving from all countries ( Table 5-25 ); others require vaccination only for travelers above a certain age coming from countries with risk for YF virus transmission (see Sec. 2, Ch. 5, Yellow Fever Vaccine & Malaria Prevention Information, by Country ). The WHO defines areas with risk for YF virus transmission as places where YF virus activity has been reported currently or in the past, and where vectors and animal reservoirs exist. Countries that contain areas with only low potential for YF virus exposure ( Table 5-23 ) are not included on the official WHO list of countries with risk for YF virus transmission ( Table 5-22 ). Unless a country requires proof of YF vaccination from all arriving travelers, proof of YF vaccination should not be required of travelers coming from countries identified as having low potential for YF virus exposure. Because country entry requirements are subject to change at any time, CDC encourages travelers and their health care providers to check with the relevant embassy or consulate before departure.

To make its recommendations for preventing travel-associated YF virus infections, CDC uses a destination-specific risk classification for YF virus transmission: endemic, transitional, low potential for exposure, and no risk. CDC recommends YF vaccination for travel to endemic or transitional areas ( Map 5-10 and Map 5-11 ). Recommendations are subject to revision at any time because of changes in YF virus circulation; before departure, check the CDC Travelers’ Health website destination pages for current vaccine information and relevant Travel Health Notices .

CDC website: www.cdc.gov/yellowfever

Map 5-10 Yellow fever vaccine recommendations for Africa 1,2

Map 5-10 Yellow fever vaccine recommendations for Africa1,2

1 Current as of November 2022. This map is an updated version of the 2010 map created by the Informal WHO Working Group on the Geographic Risk of Yellow Fever.

2 Yellow fever (YF) vaccination is generally not recommended for travel to areas where the potential for YF virus exposure is low. Vaccination might be considered, however, for a small subset of travelers going to these areas who are at increased risk for exposure to YF virus due to prolonged travel, heavy exposure to mosquitoes, or inability to avoid mosquito bites. Factors to consider when deciding whether to vaccinate a traveler include destination-specific and travel-associated risks for YF virus infection; individual, underlying risk factors for having a serious YF vaccine-associated adverse event; and country entry requirements.

Map 5-11 Yellow fever vaccine recommendations for the Americas 1,2,3

Map 5-11 Yellow fever vaccine recommendations for the Americas

2 In 2017, the Centers for Disease Control and Prevention (CDC) expanded its yellow fever vaccine recommendations for travelers going to Brazil because of a large outbreak in multiple states in that country. For more information and updated recommendations, refer to the CDC Travelers’ Health website.

3 Yellow fever (YF) vaccination is generally not recommended for travel to areas where the potential for YF virus exposure is low. Vaccination might be considered, however, for a small subset of travelers going to these areas who are at increased risk for exposure to YF virus due to prolonged travel, heavy exposure to mosquitoes, or inability to avoid mosquito bites. Factors to consider when deciding whether to vaccinate a traveler include destination-specific and travel-associated risks for YF virus infection; individual, underlying risk factors for having a serious YF vaccine-associated adverse event; and country entry requirements.

The following authors contributed to the previous version of this chapter: Mark D. Gershman, J. Erin Staples

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Jentes ES, Poumerol G, Gershman MD, Hill DR, Lemarchand J, Lewis RF, et al. The revised global yellow fever risk map and recommendations for vaccination, 2010: consensus of the Informal WHO Working Group on Geographic Risk for Yellow Fever. Lancet Infect Dis. 2011;11(8):622–32.

Lindsey NP, Rabe IB, Miller ER, Fischer M, Staples JE. Adverse event reports following yellow fever vaccination, 2007–13. J Travel Med. 2016;23(5):taw045.

Monath TP, Cetron MS. Prevention of yellow fever in persons traveling to the tropics. Clin Infect Dis. 2002;34(10):1369–78.

Staples JE, Barrett ADT, Wilder-Smith A, Hombach J. Review of data and knowledge gaps regarding yellow fever vaccine-induced immunity and duration of protection. NPJ Vaccines. 2020;5(1):54.

Staples JE, Bocchini JA Jr, Rubin L, Fischer M. Yellow fever vaccine booster doses: recommendations of the Advisory Committee on Immunization Practices, 2015. MMWR Morb Mortal Wkly Rep. 20159;64(23):647–50.

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Staples JE, Monath TP, Gershman MD, Barrett ADT. Yellow fever vaccine. In: Plotkin SA, Orenstein WA, Offit PA, editors. Vaccines, 7th edition. Philadelphia: Elsevier; 2018. pp. 1181–265.

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CDC plans to drop five-day covid isolation guidelines

infectious diseases presentation

Americans who test positive for the coronavirus no longer need to routinely stay home from work and school for five days under new guidance planned by the Centers for Disease Control and Prevention.

The agency is loosening its covid isolation recommendations for the first time since 2021 to align it with guidance on how to avoid transmitting flu and RSV, according to four agency officials and an expert familiar with the discussions.

CDC officials acknowledged in internal discussions and in a briefing last week with state health officials how much the covid-19 landscape has changed since the virus emerged four years ago, killing nearly 1.2 million people in the United States and shuttering businesses and schools. The new reality — with most people having developed a level of immunity to the virus because of prior infection or vaccination — warrants a shift to a more practical approach, experts and health officials say.

“Public health has to be realistic,” said Michael T. Osterholm, an infectious-disease expert at the University of Minnesota. “In making recommendations to the public today, we have to try to get the most out of what people are willing to do. … You can be absolutely right in the science and yet accomplish nothing because no one will listen to you.”

The CDC plans to recommend that people who test positive for the coronavirus use clinical symptoms to determine when to end isolation. Under the new approach, people would no longer need to stay home if they have been fever-free for at least 24 hours without the aid of medication and their symptoms are mild and improving, according to three agency officials who spoke on the condition of anonymity to share internal discussions.

Here is the current CDC guidance on isolation and precautions for people with covid-19

The federal recommendations follow similar moves by Oregon and California . The White House has yet to sign off on the guidance that the agency is expected to release in April for public feedback, officials said. One agency official said the timing could “move around a bit” until the guidance is finalized.

Work on revising isolation guidance has been underway since last August but was paused in the fall as covid cases rose. CDC director Mandy Cohen sent staff a memo in January that listed “Pan-resp guidance-April” as a bullet point for the agency’s 2024 priorities.

Officials said they recognized the need to give the public more practical guidelines for covid-19, acknowledging that few people are following isolation guidance that hasn’t been updated since December 2021. Back then, health officials cut the recommended isolation period for people with asymptomatic coronavirus from 10 days to five because they worried essential services would be hobbled as the highly transmissible omicron variant sent infections surging. The decision was hailed by business groups and slammed by some union leaders and health experts.

Covid is here to stay. How will we know when it stops being special?

The plan to further loosen isolation guidance when the science around infectiousness has not changed is likely to prompt strong negative reaction from vulnerable groups, including people older than 65, those with weak immune systems and long-covid patients, CDC officials and experts said.

Doing so “sweeps this serious illness under the rug,” said Lara Jirmanus, a clinical instructor at Harvard Medical School and a member of the People’s CDC, a coalition of health-care workers, scientists and advocates focused on reducing the harmful effects of covid-19.

Public health officials should treat covid differently from other respiratory viruses, she said, because it’s deadlier than the flu and increases the risk of developing long-term complications . As many as 7 percent of Americans report having suffered from a slew of lingering covid symptoms, including fatigue, difficulty breathing, brain fog, joint pain and ongoing loss of taste and smell, according to the CDC.

The new isolation recommendations would not apply to hospitals and other health-care settings with more vulnerable populations, CDC officials said.

While the coronavirus continues to cause serious illness, especially among the most vulnerable people, vaccines and effective treatments such as Paxlovid are available. The latest versions of coronavirus vaccines were 54 percent effective at preventing symptomatic infection in adults, according to data released Feb. 1, the first U.S. study to assess how well the shots work against the most recent coronavirus variant. But CDC data shows only 22 percent of adults and 12 percent of children had received the updated vaccine as of Feb. 9, despite data showing the vaccines provide robust protection against serious illness .

Coronavirus levels in wastewater i ndicate that symptomatic and asymptomatic infections remain high. About 20,000 people are still hospitalized — and about 2,300 are dying — every week, CDC data show. But the numbers are falling and are much lower than when deaths peaked in January 2021 when almost 26,000 people died of covid each week and about 115,000 were hospitalized.

The lower rates of hospitalizations were among the reasons California shortened its five-day isolation recommendation last month , urging people to stay home until they are fever-free for 24 hours and their symptoms are mild and improving. Oregon made a similar move last May.

California’s state epidemiologist Erica Pan said the societal disruptions that resulted from strict isolation guidelines also helped spur the change. Workers without sick leave and those who can’t work from home if they or their children test positive and are required to isolate bore a disproportionate burden. Strict isolation requirements can act as a disincentive to test when testing should be encouraged so people at risk for serious illness can get treatment, she said.

Giving people symptom-based guidance, similar to what is already recommended for flu, is a better way to prioritize those most at risk and balance the potential for disruptive impacts on schools and workplaces, Pan said. After Oregon made its change, the state has not experienced any disproportionate increases in community transmission or severity, according to data shared last month with the national association representing state health officials.

California still recommends people with covid wear masks indoors when they are around others for 10 days after testing positive — even if they have no symptoms — or becoming sick. “You may remove your mask sooner than 10 days if you have two sequential negative tests at least one day apart,” the California guidance states.

It’s not clear whether the updated CDC guidance will continue to recommend masking for 10 days.

Health officials from other states told the CDC last week that they are already moving toward isolation guidelines that would treat the coronavirus the same as flu and RSV, with additional precautions for people at high risk, said Anne Zink, an emergency room physician and Alaska’s chief medical officer.

Many other countries, including the United Kingdom, Denmark, Finland, Norway and Australia, made changes to isolation recommendations in 2022. Of 16 countries whose policies California officials reviewed, only Germany and Ireland still recommend isolation for five days, according to a presentation the California public health department gave health officials from other states in January. The Singapore ministry of health, in updated guidance late last year, said residents could “return to normal activities” once coronavirus symptoms resolve.

Even before the Biden administration ended the public health emergency last May, much of the public had moved on from covid-19, with many people having long given up testing and masking, much less isolating when they come down with covid symptoms.

Doctors say the best way for sick people to protect their communities is to mask or avoid unnecessary trips outside the home.

“You see a lot of people with symptoms — you don’t know if they have covid or influenza or RSV — but in all three of those cases, they probably shouldn’t be at Target, coughing, and looking sick,” said Eli Perencevich, an internal medicine professor at the University of Iowa.

Coronavirus: What you need to know

Covid isolation guidelines: Americans who test positive for the coronavirus no longer need to routinely stay home from work and school for five days under new guidance planned by the Centers for Disease Control and Prevention. The change has raised concerns among medically vulnerable people .

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infectious diseases presentation

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Case report: atypical presentation of mpox with massive hematochezia and prolonged viral shedding despite tecovirimat treatment

  • Sung Un Shin 1 ,
  • Younggon Jung 2 ,
  • Seong Eun Kim 1 &
  • Dong Min Kim 3  

BMC Infectious Diseases volume  24 , Article number:  183 ( 2024 ) Cite this article

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The outbreak of mpox that occurred between 2022 and 2023 is primarily being transmitted through sexual contact. As of now, there is no consensus on the recommended duration of isolation to prevent sexual transmission of the virus. Moreover, this particular mpox outbreak has presented with distinct complications in comparison to previous occurrences. In this report, we present a case involving severe rectal bleeding from an ulcer in a mpox patient with a history of engaging in receptive sexual contact.

Case presentation

A 30-year-old Korean man presented at the hospital with complaints of fever, multiple skin lesions, and anal pain. Monkeypox virus polymerase chain reaction (PCR) results were positive for skin lesions on the penis and wrist. The patient received a 12-day course of tecovirimat due to anal symptoms and perianal skin lesions. Following isolation for 12 days and after all skin scabs had naturally fallen off, with no new skin lesions emerging for a consecutive 48 hours—conforming to the criteria of the Korean Disease Control and Prevention Agency—the patient was discharged. However, 1 day after discharge, the patient returned to the hospital due to hematochezia. His hemoglobin level had significantly dropped from 14.0 g/dL to 8.2 g/dL. Sigmoidoscopy unveiled a sizable rectal ulceration with exposed blood vessels, prompting the application of hemostasis through metal clipping. Subsequent monkeypox virus real-time PCR conducted on rectal tissue and swabs yielded positive results (with cycle threshold values of 28.48 and 31.23, respectively). An abdominal CT scan exposed a perirectal abscess, for which ampicillin-sulbactam was administered.

This case underscores the importance of monitoring for bleeding complications and confirming the resolution of rectal lesions before discharging patients from isolation, particularly in cases where patients have a history of engaging in receptive sexual contact with men or are presenting with anal symptoms.

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Mpox (formerly denominated monkeypox) is a zoonotic disease that caused by monkeypox virus of the Poxviridae family and Orthopoxvirus genus. Its human transmission was first recognized in 1970 and mpox predominantly manifested as an endemic disease in Central and West Africa until the 2022 outbreaks. The outbreak reached a turning point in May 2022 when Europe recorded its first mpox case. This incident was quickly followed by an uptick in cases from countries previously considered non-endemic. As of August 18, 2023, the outbreak, characterized by a surge in cases among young gay, bisexual, and other men who have sex with men (GBMSM), had registered 89,385 confirmed infections [ 1 ]. Although isolation in healthcare settings is widely recommended to prevent transmission of mpox, guidelines generally advocate for isolation until the patient’s scabs have fallen off and no new lesions appear, thereby preventing direct skin-to-skin transmission. However, the 2022–2023 mpox outbreak is primarily transmitted through sexual contact, and to date, there is no consensus on the duration of isolation to prevent sexual transmission especially in the GBMSM population, where mpox is primarily transmitted. In addition, the 2022–2023 monkeypox outbreak is presenting with distinct complications compared to previous outbreaks [ 2 ].

We report a case of major bleeding from rectal ulcer in men who have sex with men (MSM) with a history of receptive sexual contact and demonstrate that monkeypox virus DNA shedding from rectal tissue can occur for a longer period even after the skin lesions were all healed.

A 30-year-old male living in South Korea visited a secondary general hospital (hospital A, as follows), complaining of multiple skin lesions that had started 1 week prior. He was also experiencing lower abdominal discomfort and a yellowish discharge from the anus that had begun 2 days prior. The skin lesions were present throughout his body, including the hands, feet, and anogenital area. Inguinal tender lymphadenopathy was also noted during the physical examination. The skin lesions consisted of ulcers, umbilicated pustules, and erythematous plaques with central erosion. He had no travel history to mpox endemic countries, such as Central or West Africa, nor to recent outbreak countries in Europe or the United States within 3 weeks before symptom onset. He reported having had receptive sexual intercourse with an anonymous male partner 1 week before the symptoms initiated. A polymerase chain reaction (PCR) test result was positive, with a cycle threshold (Ct) value of 24.23, obtained from a penile ulcer and left wrist pustules.

He was transferred to a university-affiliated tertiary hospital (hospital B, as follows) for isolation and treatment for mpox and this is Hospital Day (HD) 0. Some of the skin lesions had formed scabs at the time of hospital admission. Human Immunodeficiency Virus (HIV) antibody testing was negative, and all routine laboratory tests were normal except for an elevated C-reactive protein level of 6.59 mg/dL (normal range: 0–0.3 mg/dL). Tecovirimat was administered orally at a dose of 600 mg every 12 hours due to the infection site being the anal area, and because he complained of anal pain. On HD6, scabs formed on most skin lesions, and the anal pain improved. On HD8, scabs formed on skin lesions, and by HD11 all skin lesions had lost their scabs. After ensuring the absence of new lesions for over 48 hours, the patient was discharged on HD12. Tecovirimat was administered for 12 days during the first hospitalization. A diagram of the patient’s clinical course is shown in Fig.  1 . One day after discharge (HD13), the patient experienced massive hematochezia and revisited the emergency room of hospital A which was he had initially visited when his symptoms appeared. On sigmoidoscopy, spurting bleeding was observed 3 cm above the anus, and hemostatic clipping was performed on the lesion (Fig.  2 A). He was transferred to hospital B after initial hemostasis for further treatment. After transfer, real-time PCR tests were conducted for both monkeypox virus and herpes virus using rectal swab specimens (HD15) as well as rectal tissue obtained through follow-up colonoscopy (Fig. 2 B, HD17). The results were positive for monkeypox virus with Ct values of 31.23 and 28.48, respectively, but negative for herpes simplex virus 1 and 2. From HD15 to HD26, the patient presented with intermittent episodes of hematochezia, and the lowest hemoglobin level recorded was 8.2 g/dL. Abdominal angiographic computed tomography (CT) on HD15 showed proctocolitis and a perirectal abscess without contrast extravasation (Fig.  3 ). The perirectal abscess size was 4.8 cm × 1.6 cm. Intravenous administration of ampicillin/sulbactam was initiated from HD16 to HD28. Same dose of tecovirimat was reintroduced for 7 days after a positive monkeypox virus PCR result was reported from the rectal tissue.

figure 1

Clinical course of the patient

figure 2

( A ) First sigmoidoscopy on hospital day 13 ( B ) Third sigmoidoscopy on hospital day 17

figure 3

Abdominal computed tomography on hospital day 15

After HD26, the patient did not experience any additional signs of bleeding, such as hematochezia or decreasing hemoglobin levels. Follow-up sigmoidoscopy and abdominal CT showed improvement in the several linear ulcers in the distal rectum and a decreased abscess size compared to the previous examination on HD26 and HD27. Antibiotics were switched to oral amoxicillin/sulbactam from HD28, and the patient was discharged on HD30.

Discussion and conclusions

The 2022–23 mpox outbreak has shown different complications compared to previous outbreaks. Earlier outbreaks primarily involved secondary bacterial skin infections or pneumonia, whereas recent reports indicate rectal pain, proctitis, penile edema, and tonsillar or pharyngeal ulceration with associated swallowing difficulties [ 2 ]. This increase in unique complications is thought to be associated with transmission of the virus through direct sexual contact among MSM. Recent studies have reported proctitis in mpox patients ranging from 14 to 31% [ 3 , 4 ]. Another study reported a significantly higher rate of proctitis in MSM who engage in anal receptive sex compared to MSM who do not engage in anal receptive sex (38% vs. 7%) [ 5 ]. It can be inferred that MSM history of receptive sex is associated with the development of proctitis in this patient. In addition to proctitis, rectal bleeding has been reported in 4–11% of mpox patients [ 6 , 7 ]. However, we could not find any reports of major bleeding causing a decrease in hemoglobin as seen in present case. This case demonstrates that major bleeding can occur in mpox patients with rectal ulcer.

Previously, mpox was known to be transmitted through direct skin-to-skin contact, but a study of epidemiologic and clinical data from the 2022 mpox outbreak confirmed that sexual contact is more effective than casual skin-to-skin contact [ 8 ]. To prevent transmission through sexual contact, it is necessary to determine the duration for which viral shedding occurs in the semen, rectum, and vagina. In a previous study, mpox viral DNA was detectable by quantitative PCR for a median time of 16 days (IQR 13–23 days) in the rectum from symptom onset in immunocompetent mild mpox patients [ 4 ]. And there is a study suggested that a Ct value of ≥ 35 corresponds with non or marginal infectivity [ 9 ]. In another study, a significant difference was observed between the median Ct value of samples that grew in viral culture (Ct 22; range 16–36) compared to samples that did not grow (Ct 33; range 26–40) ( p  < 0.001) [ 10 ]. In present case, the Ct value of rectal tissue monkeypox real time PCR was 28.48 on day 24 from symptom onset, suggesting prolonged viral presence compared to usual mpox patients. This suggests that severe complicated mpox patient with rectal ulcer could have prolonged viral shedding and longer isolation period should be considered.

In 2018, the U.S. FDA approved tecovirimat for the treatment of smallpox in children and adults, based on its efficacy in rabbitpox infection in non-human primates. However, the safety and efficacy of tecovirimat in mpox patients have not been established. In the present case, despite the use of tecovirimat for 12 days from the first hospitalization, worsening of the rectal lesion and bleeding occurred, and a positive rectal tissue monkeypox PCR result was confirmed on the second hospitalization. This case suggests a low efficacy of tecovirimat treatment in patients with mpox. This case suggests the need for further clinical studies on the efficacy of tecovirimat in patients with mpox.

This case report illustrates the severe complications, including major rectal bleeding, that can arise in patients with mpox, particularly among those with a history of receptive sexual contact. The prolonged viral shedding observed in our patient, despite treatment with tecovirimat, underscores the potential for persistent infectivity. This raises significant questions regarding the optimal duration of patient isolation and the effectiveness of tecovirimat treatment for mpox. Given the unpredictability and severity of the clinical course of mpox, as evidenced by this patient, vigilant monitoring is paramount, even after the resolution of skin lesions and after isolation termination. This case strongly advocates for the development of rigorous protocols for the evaluation of mucosal and internal lesions, in addition to skin lesions, and for the management of potential bleeding complications, particularly in patients with a history of receptive sexual contact. Further research is necessary to identify the most effective treatment strategies for mpox, to delineate the natural history of viral shedding in various body compartments, and to refine isolation criteria to reduce the risk of ongoing transmission and complications.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.

Abbreviations

Polymerase chain reaction

Gay, bisexual, and other men who have sex with men

Cycle threshold

Human immunodeficiency virus

Hospital day

Computed tomography

Men who have sex with men

Interquartile range

Food and drug administration

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Department of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea

Sung Un Shin & Seong Eun Kim

Department of Internal Medicine, St. Carollo Hospital, Suncheon, South Korea

Younggon Jung

Department of Internal Medicine, College of Medicine, Chosun University, Gwangju, South Korea

Dong Min Kim

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SUS wrote the original draft. YJ collected data. DMK performed the real-time PCR tests. SEK conceived the manuscript and made a revision of it. All authors read and approved the final manuscript.

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Correspondence to Seong Eun Kim .

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Shin, S.U., Jung, Y., Kim, S.E. et al. Case report: atypical presentation of mpox with massive hematochezia and prolonged viral shedding despite tecovirimat treatment. BMC Infect Dis 24 , 183 (2024). https://doi.org/10.1186/s12879-024-09098-2

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  • Rectal ulceration
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BMC Infectious Diseases

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