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21.3: Viral Infections of the Skin and Eyes - Biology

21.3: Viral Infections of the Skin and Eyes - Biology


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Learning Objectives

  • Identify the most common viruses associated with infections of the skin and eyes
  • Compare the major characteristics of specific viral diseases affecting the skin and eyes

Until recently, it was thought that the normal microbiota of the body consisted primarily of bacteria and some fungi. However, in addition to bacteria, the skin is colonized by viruses, and recent studies suggest that Papillomaviridae, Polyomaviridae and Circoviridae also contribute to the normal skin microbiota. However, some viruses associated with skin are pathogenic, and these viruses can cause diseases with a wide variety of presentations.

Numerous types of viral infections cause rashes or lesions on the skin; however, in many cases these skin conditions result from infections that originate in other body systems. In this chapter, we will limit the discussion to viral skin infections that use the skin as a portal of entry. Later chapters will discuss viral infections such as chickenpox, measles, and rubella—diseases that cause skin rashes but invade the body through portals of entry other than the skin.

Papillomas

Papillomas (warts) are the expression of common skin infections by human papillomavirus (HPV) and are transmitted by direct contact. There are many types of HPV, and they lead to a variety of different presentations, such as common warts, plantar warts, flat warts, and filiform warts. HPV can also cause sexually-transmitted genital warts, which will be discussed in Urogenital System Infections. Vaccination is available for some strains of HPV.

Common warts tend to develop on fingers, the backs of hands, and around nails in areas with broken skin. In contrast, plantar warts (also called foot warts) develop on the sole of the foot and can grow inwards, causing pain and pressure during walking. Flat warts can develop anywhere on the body, are often numerous, and are relatively smooth and small compared with other wart types. Filiform warts are long, threadlike warts that grow quickly.

In some cases, the immune system may be strong enough to prevent warts from forming or to eradicate established warts. However, treatment of established warts is typically required. There are many available treatments for warts, and their effectiveness varies. Common warts can be frozen off with liquid nitrogen. Topical applications of salicylic acidmay also be effective. Other options are electrosurgery (burning), curettage (cutting), excision, painting with cantharidin (which causes the wart to die so it can more easily be removed), laser treatments, treatment with bleomycin, chemical peels, and immunotherapy (Figure (PageIndex{1})).

Oral Herpes

Another common skin virus is herpes simplex virus (HSV). HSV has historically been divided into two types, HSV-1 and HSV-2. HSV-1 is typically transmitted by direct oral contact between individuals, and is usually associated with oral herpes. HSV-2 is usually transmitted sexually and is typically associated with genital herpes. However, both HSV-1 and HSV-2 are capable of infecting any mucous membrane, and the incidence of genital HSV-1 and oral HSV-2 infections has been increasing in recent years. In this chapter, we will limit our discussion to infections caused by HSV-1; HSV-2 and genital herpes will be discussed in Urogenital System Infections.

Infection by HSV-1 commonly manifests as cold sores or fever blisters, usually on or around the lips (Figure (PageIndex{2})). HSV-1 is highly contagious, with some studies suggesting that up to 65% of the US population is infected; however, many infected individuals are asymptomatic.1 Moreover, the virus can be latent for long periods, residing in the trigeminal nerve ganglia between recurring bouts of symptoms. Recurrence can be triggered by stress or environmental conditions (systemic or affecting the skin). When lesions are present, they may blister, break open, and crust. The virus can be spread through direct contact, even when a patient is asymptomatic.

While the lips, mouth, and face are the most common sites for HSV-1 infections, lesions can spread to other areas of the body. Wrestlers and other athletes involved in contact sports may develop lesions on the neck, shoulders, and trunk. This condition is often called herpes gladiatorum. Herpes lesions that develop on the fingers are often called herpetic whitlow.

HSV-1 infections are commonly diagnosed from their appearance, although laboratory testing can confirm the diagnosis. There is no cure, but antiviral medications such as acyclovir, penciclovir, famciclovir, and valacyclovir are used to reduce symptoms and risk of transmission. Topical medications, such as creams with n-docosanol and penciclovir, can also be used to reduce symptoms such as itching, burning, and tingling.

Exercise (PageIndex{1})

What are the most common sites for the appearance of herpetic lesions?

Roseola and Fifth Disease

The viral diseases roseola and fifth disease are somewhat similar in terms of their presentation, but they are caused by different viruses. Roseola, sometimes called roseola infantum or exanthem subitum (“sudden rash”), is a mild viral infection usually caused by human herpesvirus-6 (HHV-6) and occasionally by HHV-7. It is spread via direct contact with the saliva or respiratory secretions of an infected individual, often through droplet aerosols. Roseola is very common in children, with symptoms including a runny nose, a sore throat, and a cough, along with (or followed by) a high fever (39.4 ºC). About three to five days after the fever subsides, a rash may begin to appear on the chest and abdomen. The rash, which does not cause discomfort, initially forms characteristic macules that are flat or papules that are firm and slightly raised; some macules or papules may be surrounded by a white ring. The rash may eventually spread to the neck and arms, and sometimes continues to spread to the face and legs. The diagnosis is generally made based upon observation of the symptoms. However, it is possible to perform serological tests to confirm the diagnosis. While treatment may be recommended to control the fever, the disease usually resolves without treatment within a week after the fever develops. For individuals at particular risk, such as those who are immunocompromised, the antiviral medication ganciclovir may be used.

Fifth disease (also known as erythema infectiosum) is another common, highly contagious illness that causes a distinct rash that is critical to diagnosis. Fifth disease is caused by parvovirus B19, and is transmitted by contact with respiratory secretions from an infected individual. Infection is more common in children than adults. While approximately 20% of individuals will be asymptomatic during infection,2 others will exhibit cold-like symptoms (headache, fever, and upset stomach) during the early stages when the illness is most infectious. Several days later, a distinct red facial rash appears, often called “slapped cheek” rash (Figure (PageIndex{3})). Within a few days, a second rash may appear on the arms, legs, chest, back, or buttocks. The rash may come and go for several weeks, but usually disappears within seven to twenty-one days, gradually becoming lacy in appearance as it recedes.

In children, the disease usually resolves on its own without medical treatment beyond symptom relief as needed. Adults may experience different and possibly more serious symptoms. Many adults with fifth disease do not develop any rash, but may experience joint pain and swelling that lasts several weeks or months. Immunocompromised individuals can develop severe anemia and may need blood transfusions or immune globulin injections. While the rash is the most important component of diagnosis (especially in children), the symptoms of fifth disease are not always consistent. Serological testing can be conducted for confirmation.

Exercise (PageIndex{2})

Identify at least one similarity and one difference between roseola and fifth disease.

Viral Conjunctivitis

Like bacterial conjunctivitis viral infections of the eye can cause inflammation of the conjunctiva and discharge from the eye. However, viral conjunctivitis tends to produce a discharge that is more watery than the thick discharge associated with bacterial conjunctivitis. The infection is contagious and can easily spread from one eye to the other or to other individuals through contact with eye discharge.

Viral conjunctivitis is commonly associated with colds caused by adenoviruses; however, other viruses can also cause conjunctivitis. If the causative agent is uncertain, eye discharge can be tested to aid in diagnosis. Antibiotic treatment of viral conjunctivitis is ineffective, and symptoms usually resolve without treatment within a week or two.

Herpes Keratitis

Herpes infections caused by HSV-1 can sometimes spread to the eye from other areas of the body, which may result in keratoconjunctivitis. This condition, generally called herpes keratitis or herpetic keratitis, affects the conjunctiva and cornea, causing irritation, excess tears, and sensitivity to light. Deep lesions in the cornea may eventually form, leading to blindness. Because keratitis can have numerous causes, laboratory testing is necessary to confirm the diagnosis when HSV-1 is suspected; once confirmed, antiviral medications may be prescribed.

VIRAL INFECTIONS OF THE SKIN AND EYES

A number of viruses can cause infections via direct contact with skin and eyes, causing signs and symptoms ranging from rashes and lesions to warts and conjunctivitis. All of these viral diseases are contagious, and while some are more common in children (fifth disease and roseola), others are prevalent in people of all ages (oral herpes, viral conjunctivitis, papillomas). In general, the best means of prevention is avoiding contact with infected individuals. Treatment may require antiviral medications; however, several of these conditions are mild and typically resolve without treatment. Figure (PageIndex{4}) summarizes the characteristics of some common viral infections of the skin and eyes.

Key Concepts and Summary

  • Papillomas (warts) are caused by human papillomaviruses.
  • Herpes simplex virus (especially HSV-1) mainly causes oral herpes, but lesions can appear on other areas of the skin and mucous membranes.
  • Roseola and fifth disease are common viral illnesses that cause skin rashes; roseola is caused by HHV-6 and HHV-7 while fifth disease is caused by parvovirus 19.
  • Viral conjunctivitis is often caused by adenoviruses and may be associated with the common cold. Herpes keratitis is caused by herpesviruses that spread to the eye.

Footnotes

  1. 1 Wald, A., and Corey, L. “Persistence in the Population: Epidemiology, Transmission.” In: A. Arvin, G. Campadelli-Fiume, E. Mocarski et al. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press, 2007. www.ncbi.nlm.nih.gov/books/NBK47447/. Accessed Sept 14, 2016.
  2. 2 Centers for Disease Control and Prevention. “Fifth Disease.” http://www.cdc.gov/parvovirusb19/fifth-disease.html. Accessed Sept 14, 2016.

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)


What is meant by skin infection?

Skin is the most important and largest organ of our body. The main function of the skin is to safeguard the body from infection. In certain cases, the skin becomes infected. There are several reasons for skin infections. It is caused due to a wide range of germs and the symptoms of infection differ from minor to serious. It is possible to treat minor skin infections by taking over the counter medicines as well as home remedies. But certain serious infections need immediate medical attention.


Biology of Zika Virus Infection in Human Skin Cells

Zika virus (ZIKV) is an emerging arbovirus of the Flaviviridae family, which includes dengue, West Nile, yellow fever, and Japanese encephalitis viruses, that causes a mosquito-borne disease transmitted by the Aedes genus, with recent outbreaks in the South Pacific. Here we examine the importance of human skin in the entry of ZIKV and its contribution to the induction of antiviral immune responses. We show that human dermal fibroblasts, epidermal keratinocytes, and immature dendritic cells are permissive to the most recent ZIKV isolate, responsible for the epidemic in French Polynesia. Several entry and/or adhesion factors, including DC-SIGN, AXL, Tyro3, and, to a lesser extent, TIM-1, permitted ZIKV entry, with a major role for the TAM receptor AXL. The ZIKV permissiveness of human skin fibroblasts was confirmed by the use of a neutralizing antibody and specific RNA silencing. ZIKV induced the transcription of Toll-like receptor 3 (TLR3), RIG-I, and MDA5, as well as several interferon-stimulated genes, including OAS2, ISG15, and MX1, characterized by strongly enhanced beta interferon gene expression. ZIKV was found to be sensitive to the antiviral effects of both type I and type II interferons. Finally, infection of skin fibroblasts resulted in the formation of autophagosomes, whose presence was associated with enhanced viral replication, as shown by the use of Torin 1, a chemical inducer of autophagy, and the specific autophagy inhibitor 3-methyladenine. The results presented herein permit us to gain further insight into the biology of ZIKV and to devise strategies aiming to interfere with the pathology caused by this emerging flavivirus.

Importance: Zika virus (ZIKV) is an arbovirus belonging to the Flaviviridae family. Vector-mediated transmission of ZIKV is initiated when a blood-feeding female Aedes mosquito injects the virus into the skin of its mammalian host, followed by infection of permissive cells via specific receptors. Indeed, skin immune cells, including dermal fibroblasts, epidermal keratinocytes, and immature dendritic cells, were all found to be permissive to ZIKV infection. The results also show a major role for the phosphatidylserine receptor AXL as a ZIKV entry receptor and for cellular autophagy in enhancing ZIKV replication in permissive cells. ZIKV replication leads to activation of an antiviral innate immune response and the production of type I interferons in infected cells. Taken together, these results provide the first general insights into the interaction between ZIKV and its mammalian host.

Copyright © 2015, American Society for Microbiology. All Rights Reserved.

Figures

Primary human fibroblasts are susceptible…

Primary human fibroblasts are susceptible to ZIKV. (A) Primary fibroblasts infected with ZIKV…

ZIKV infects human keratinocytes and…

ZIKV infects human keratinocytes and induces morphological changes in human skin biopsy specimens.…

Dendritic cells are permissive to…

Dendritic cells are permissive to ZIKV and DENV. Human immature dendritic cells were…

Entry receptors involved in ZIKV…

Entry receptors involved in ZIKV infection. (A) Expression profiles of HEK293T cells stably…

Involvement of AXL and TIM-1…

Involvement of AXL and TIM-1 in ZIKV infection of A549 cells. (A) Cell…

Expression of AXL permits ZIKV…

Expression of AXL permits ZIKV infection of skin fibroblasts. (A) Cell surface expression…

ZIKV induces an innate antiviral…

ZIKV induces an innate antiviral response in primary human skin fibroblasts. (A) Primary…

Effects of PRR silencing on…

Effects of PRR silencing on ZIKV replication and IFN expression. (A to D)…

IFNs inhibit ZIKV infection. Primary…

IFNs inhibit ZIKV infection. Primary skin fibroblasts were pretreated with different concentrations of…

Electron microscopic imaging of ZIKV-infected…

Electron microscopic imaging of ZIKV-infected primary fibroblasts. (A) Membrane vesicles with sizes between…

ZIKV induces autophagy in infected…

ZIKV induces autophagy in infected skin fibroblasts. (A) Visualization of autophagosome formation by…


22.3 Viral Infections of the Respiratory Tract

Viruses are the most frequent cause of respiratory tract infections. Unlike the bacterial pathogens, we have few effective therapies to combat viral respiratory infections. Fortunately, many of these diseases are mild and self-limiting. A few respiratory infections manifest their primary symptoms at other locations in the body.

The Common Cold

The common cold is a generic term for a variety of mild viral infections of the nasal cavity. More than 200 different viruses are known to cause the common cold. The most common groups of cold viruses include rhinovirus es, coronavirus es, and adenovirus es. These infections are widely disseminated in the human population and are transmitted through direct contact and droplet transmission. Coughing and sneezing efficiently produce infectious aerosols, and rhinoviruses are known to persist on environmental surfaces for up to a week. 17

Viral contact with the nasal mucosa or eyes can lead to infection. Rhinoviruses tend to replicate best between 33 °C (91.4 °F) and 35 °C (95 °F), somewhat below normal body temperature (37 °C [98.6 °F]). As a consequence, they tend to infect the cooler tissues of the nasal cavities. Colds are marked by an irritation of the mucosa that leads to an inflammatory response. This produces common signs and symptoms such as nasal excess nasal secretions (runny nose), congestion, sore throat, coughing, and sneezing. The absence of high fever is typically used to differentiate common colds from other viral infections, like influenza. Some colds may progress to cause otitis media, pharyngitis, or laryngitis, and patients may also experience headaches and body aches. The disease, however, is self-limiting and typically resolves within 1–2 weeks.

There are no effective antiviral treatments for the common cold and antibacterial drugs should not be prescribed unless secondary bacterial infections have been established. Many of the viruses that cause colds are related, so immunity develops throughout life. Given the number of viruses that cause colds, however, individuals are never likely to develop immunity to all causes of the common cold.

Check Your Understanding

Clinical Focus

Part 3

Since antibiotic treatment had proven ineffective, John’s doctor suspects that a viral or fungal pathogen may be the culprit behind John’s case of pneumonia. Another possibility is that John could have an antibiotic-resistant bacterial infection that will require a different antibiotic or combination of antibiotics to clear.

The RIDT tests both came back negative for type A and type B influenza. However, the diagnostic laboratory identified the sputum isolate as Legionella pneumophila. The doctor ordered tests of John’s urine and, on the second day after his admission, results of an enzyme immunoassay (EIA) were positive for the Legionella antigen. John’s doctor added levofloxacin to his antibiotic therapy and continued to monitor him. The doctor also began to ask John where he had been over the past 10 to 14 days.

  • Do negative RIDT results absolutely rule out influenza virus as the etiologic agent? Why or why not?
  • What is John’s prognosis?

Jump to the next Clinical Focus box. Go back to the previous Clinical Focus box.

Influenza

Commonly known as the flu, influenza is a common viral disease caused by an orthomyxovirus that primarily affects the upper respiratory tract but can also extend into the lower respiratory tract. Influenza is pervasive worldwide and causes 3,000–50,000 deaths each year in the United States. The annual mortality rate can vary greatly depending on the virulence of the strain(s) responsible for seasonal epidemics. 18

Influenza infections are most typically characterized by fever, chills, and body aches. This is followed by symptoms similar to the common cold that may last a week or more. Table 22.2 compares the signs and symptoms of influenza and the common cold.

Comparing the Common Cold and Influenza
Sign/Symptom Common Cold Influenza
Fever Low (37.2 °C [99 °F]) High (39 °C [102.2 °F])
Headache Common Common
Aches and pains Mild Severe
Fatigue Slight Severe
Nasal congestion Common Rare
Sneezing Common Rare

In general, influenza is self-limiting. However, serious cases can lead to pneumonia and other complications that can be fatal. Such cases are more common in the very young and the elderly however, certain strains of influenza virus (like the 1918–1919 variant discussed later in this chapter) are more lethal to young adults than to the very young or old. Strains that affect young adults are believed to involve a cytokine storm —a positive feedback loop that forms between cytokine production and leukocytes. This cytokine storm produces an acute inflammatory response that leads to rapid fluid accumulation in the lungs, culminating in pulmonary failure. In such cases, the ability to mount a vigorous immune response is actually detrimental to the patient. The very young and very old are less susceptible to this effect because their immune systems are less robust.

A complication of influenza that occurs primarily in children and teenagers is Reye syndrome . This sequela causes swelling in the liver and brain, and may progress to neurological damage, coma, or death. Reye syndrome may follow other viral infections, like chickenpox, and has been associated with the use of aspirin. For this reason, the CDC and other agencies recommend that aspirin and products containing aspirin never be used to treat viral illnesses in children younger than age 19 years. 19

The influenza virus is primarily transmitted by direct contact and inhalation of aerosols. The RNA genome of this virus exists as seven or eight segments, each coated with ribonucleoprotein and encoding one or two specific viral proteins. The influenza virus is surrounded by a lipid membrane envelope, and two of the main antigens of the influenza virus are the spike proteins hemagglutinin (H) and neuraminidase (N), as shown in Figure 22.17. These spike proteins play important roles in the viral infectious cycle.

Following inhalation, the influenza virus uses the hemagglutinin protein to bind to sialic acid receptor s on host respiratory epithelial cells. This facilitates endocytosis of the viral particle. Once inside the host cell, the negative strand viral RNA is replicated by the viral RNA polymerase to form mRNA, which is translated by the host to produce viral proteins. Additional viral RNA molecules are transcribed to produce viral genomic RNA, which assemble with viral proteins to form mature virions. Release of the virions from the host cell is facilitated by viral neuraminidase , which cleaves sialic-acid receptors to allow progeny viruses to make a clean exit when budding from an infected cell.

There are three genetically related influenza viruses, called A, B, and C. The influenza A viruses have different subtypes based on the structure of their hemagglutinin and neuraminidase proteins. There are currently 18 known subtypes of hemagglutinin and 11 known subtypes of neuraminidase. Influenza viruses are serologically characterized by the type of H and N proteins that they possess. Of the nearly 200 different combinations of H and N, only a few, such as the H1N1 strain, are associated with human disease. The influenza viruses A, B, and C make up three of the five major groups of orthomyxoviruses. The differences between the three types of influenza are summarized in Table 22.3. The most virulent group is the influenza A virus es, which cause seasonal pandemics of influenza each year. Influenza A virus can infect a variety of animals, including pigs, horses, pigs, and even whales and dolphins. Influenza B virus is less virulent and is sometimes associated with epidemic outbreaks. Influenza C virus generally produces the mildest disease symptoms and is rarely connected with epidemics. Neither influenza B virus nor influenza C virus has significant animal reservoirs.

The Three Major Groups of Influenza Viruses
Influenza A virus Influenza B virus Influenza C virus
Severity Severe Moderate Mild
Animal reservoir Yes No No
Genome segments 8 8 7
Population spread Epidemic and pandemic Epidemic Sporadic
Antigenic variation Shift/drift Drift Drift

Influenza virus infections elicit a strong immune response, particularly to the hemagglutinin protein, which would protect the individual if they encountered the same virus. Unfortunately, the antigenic properties of the virus change relatively rapidly, so new strains are evolving that immune systems previously challenged by influenza virus cannot recognize. When an influenza virus gains a new hemagglutinin or neuraminidase type, it is able to evade the host’s immune response and be successfully transmitted, often leading to an epidemic.

There are two mechanisms by which these evolutionary changes may occur. The mechanisms of antigen drift and antigenic shift for influenza virus have been described in Virulence Factors of Bacterial and Viral Pathogens. Of these two genetic processes, it is viruses produced by antigenic shift that have the potential to be extremely virulent because individuals previously infected by other strains are unlikely to produce any protective immune response against these novel variants.

The most lethal influenza pandemic in recorded history occurred from 1918 through 1919. Near the end of World War I, an antigenic shift involving the recombination of avian and human viruses is thought to have produced a new H1N1 virus. This strain rapidly spread worldwide and is commonly claimed to have killed as many as 40 million to 50 million people—more than double the number killed in the war. Although referred to as the Spanish flu , this disease is thought to have originated in the United States. Regardless of its source, the conditions of World War I greatly contributed to the spread of this disease. Crowding, poor sanitation, and rapid mobilization of large numbers of personnel and animals facilitated the dissemination of the new virus once it appeared.

Several of the most important influenza pandemics of modern times have been associated with antigenic shifts. A few of these are summarized in Table 22.4.

Historical Influenza Outbreaks 20 21 22
Years Common Name Serotype Estimated Number of Deaths
1918–1919 Spanish flu H1N1 20,000,000–40,000,000
1957–1958 Asian flu N2N2 1,000,000–2,000,000
1968–1969 Hong Kong flu H3N2 1,000,000–3,000,000
2009–2010 Swine flu H1N1/09 152,000–575,000

Laboratory diagnosis of influenza is typically performed using a variety of RIDTs. These tests are inoculated by point-of-care personnel and give results within 15–20 minutes. Unfortunately, these tests have variable sensitivity and commonly yield false-negative results. Other tests include hemagglutination of erythrocytes (due to hemagglutinin action) or complement fixation. Patient serum antibodies against influenza viruses can also be detected in blood samples. Because influenza is self-limiting disease, diagnosis through these more time-consuming and expensive methods is not typically used.

Three drugs that inhibit influenza neuraminidase activity are available: inhaled zanamivir , oral oseltamivir , and intravenous peramivir . If taken at the onset of symptoms, these drugs can shorten the course of the disease. These drugs are thought to impair the ability of the virus to efficiently exit infected host cells. A more effective means of controlling influenza outbreaks, though, is vaccination. Every year, new influenza vaccine s are developed to be effective against the strains expected to be predominant. This is determined in February by a review of the dominant strains around the world from a network of reporting sites their reports are used to generate a recommendation for the vaccine combination for the following winter in the northern hemisphere. In September, a similar recommendation is made for the winter in the southern hemisphere. 23 These recommendations are used by vaccine manufacturers to formulate each year’s vaccine. In most cases, three or four viruses are selected—the two most prevalent influenza A strains and one or two influenza B strains. The chosen strains are typically cultivated in eggs and used to produce either an inactivated or a live attenuated vaccine (e.g., FluMist). For individuals 18 years or older with an allergy to egg products, a recombinant egg-free trivalent vaccine is available. Most of the influenza vaccines over the past decade have had an effectiveness of about 50%. 24

Case in Point

Flu Pandemic

During the spring of 2013, a new strain of H7N9 influenza was reported in China. A total of 132 people were infected. Of those infected, 44 (33%) died. A genetic analysis of the virus suggested that this strain arose from the reassortment of three different influenza viruses: a domestic duck H7N3 virus, a wild bird H7N9 virus, and a domestic poultry H9N2 virus. The virus was detected in the Chinese domestic bird flocks and contact with this reservoir is thought to have been the primary source of infection. This strain of influenza was not able to spread from person to person. Therefore, the disease did not become a global problem. This case does, though, illustrate the potential threat that influenza still represents. If a strain like the H7N9 virus were to undergo another antigenic shift, it could become more communicable in the human population. With a mortality rate of 33%, such a pandemic would be disastrous. For this reason, organizations like the World Health Organization and the Centers for Disease Control and Prevention keep all known influenza outbreaks under constant surveillance.

Check Your Understanding

  • Compare the severity of the three types of influenza viruses.
  • Why must new influenza vaccines be developed each year?

Viral Pneumonia

Viruses cause fewer cases of pneumonia than bacteria however, several viruses can lead to pneumonia in children and the elderly. The most common sources of viral pneumonia are adenovirus es, influenza virus es, parainfluenza virus es, and respiratory syncytial virus es. The signs and symptoms produced by these viruses can range from mild cold-like symptoms to severe cases of pneumonia, depending on the virulence of the virus strain and the strength of the host defenses of the infected individual. Occasionally, infections can result in otitis media.

Respiratory syncytial virus (RSV) infections are fairly common in infants most people have been infected by the age of 2 years. During infection, a viral surface protein causes host cells to fuse and form multinucleated giant cells called syncytia . There are no specific antiviral therapies or vaccines available for viral pneumonia. In adults, these infections are self-limiting, resemble the common cold, and tend to resolve uneventfully within 1 or 2 weeks. Infections in infants, however, can be life-threatening. RSV is highly contagious and can be spread through respiratory droplets from coughing and sneezing. RSV can also survive for a long time on environmental surfaces and, thus, be transmitted indirectly via fomites.

Check Your Understanding

  • Who is most likely to contract viral pneumonia?
  • What is the recommended treatment for viral pneumonia?

SARS and MERS

Severe acute respiratory syndrome ( SARS ) and Middle East respiratory syndrome ( MERS ) are two acute respiratory infections caused by coronavirus es. In both cases, these are thought to be zoonotic infections. Bats and civet cats are thought to have been the reservoirs for SARS camels seem to be the reservoir for MERS.

SARS originated in southern China in the winter of 2002 and rapidly spread to 37 countries. Within about 1 year, more than 8,000 people experienced influenza-like symptoms and nearly 800 people died. The rapid spread and severity of these infections caused grave concern at the time. However, the outbreak was controlled in 2003 and no further cases of SARS have been recorded since 2004. 25 Signs and symptoms of SARS include high fever, headache, body aches, and cough, and most patients will develop pneumonia.

MERS was first reported in Saudi Arabia in 2013. Although some infected individuals will be asymptomatic or have mild cold-like symptoms, most will develop a high fever, aches, cough and a severe respiratory infection that can progress to pneumonia. As of 2015, over 1,300 people in 27 countries have been infected. About 500 people have died. There are no specific treatments for either MERS or SARS. In addition, no vaccines are currently available. Several recombinant vaccines, however, are being developed.

Check Your Understanding

Viral Respiratory Diseases Causing Skin Rashes

Measles, rubella (German measles), and chickenpox are three important viral diseases often associated with skin rashes. However, their symptoms are systemic, and because their portal of entry is the respiratory tract, they can be considered respiratory infections.

Measles (Rubeola)

The measles virus (MeV) causes the highly contagious disease measles , also known as rubeola, which is a major cause of childhood mortality worldwide. Although vaccination efforts have greatly reduced the incidence of measles in much of the world, epidemics are still common in unvaccinated populations in certain countries. 26

The measles virus is a single-stranded, negative-strand RNA virus and, like the influenza virus, it possesses an envelope with spikes of embedded hemagglutinin. The infection is spread by direct contact with infectious secretions or inhalation of airborne droplets spread by breathing, coughing, or sneezing. Measles is initially characterized by a high fever, conjunctivitis, and a sore throat. The virus then moves systemically through the bloodstream and causes a characteristic rash. The measles rash initially forms on the face and later spreads to the extremities. The red, raised macular rash will eventually become confluent and can last for several days. At the same time, extremely high fevers (higher than 40.6 °C [105 °F]) can occur. Another diagnostic sign of measles infections is Koplik’s spots , white spots that form on the inner lining of inflamed cheek tissues (Figure 22.18).

Although measles is usually self-limiting, it can lead to pneumonia, encephalitis , and death. In addition, the inhibition of immune system cells by the measles virus predisposes patients to secondary infections. In severe infections with highly virulent strains, measles fatality rates can be as high as 10% to 15%. There were more than 145,000 measles deaths (mostly young children) worldwide in 2013. 27

The preliminary diagnosis of measles is typically based on the appearance of the rash and Koplik’s spots. Hemagglutination inhibition tests and serological tests may be used to confirm measles infections in low-prevalence settings.

There are no effective treatments for measles. Vaccination is widespread in developed countries as part of the measles, mumps, and rubella ( MMR ) vaccine. As a result, there are typically fewer than 200 cases of measles in the United States annually. 28 When it is seen, it is often associated with children who have not been vaccinated.

Micro Connections

Preventable Measles Outbreaks

In December 2014, a measles epidemic began at Disneyland in southern California. Within just 4 months, this outbreak affected 134 people in 24 states. 29 Characterization of the virus suggests that an unidentified infected individual brought the disease to the United States from the Philippines, where a similar virus had sickened more than 58,000 people and killed 110. 30 Measles is highly communicable, and its spread at Disneyland may have been facilitated by the low vaccination rate in some communities in California. 31

Several factors could conceivably lead to a strong comeback of measles in the U.S. Measles is still an epidemic disease in many locations worldwide. Air travel enables infected individuals to rapidly translocate these infections globally. Compounding this problem, low vaccination rates in some local areas in the United States (such as in Amish communities) provide populations of susceptible hosts for the virus to establish itself. Finally, measles has been a low-prevalence infection in the U.S. for some time. As a consequence, physicians are not as likely to recognize the initial symptoms and make accurate diagnoses. Until vaccination rates become high enough to ensure herd immunity, measles is likely to be an ongoing problem in the United States.

Rubella (German Measles)

Rubella, or the German measles , is a relatively mild viral disease that produces a rash somewhat like that caused by the measles, even though the two diseases are unrelated. The rubella virus is an enveloped RNA virus that can be found in the respiratory tract. It is transmitted from person to person in aerosols produced by coughing or sneezing. Nearly half of all infected people remain asymptomatic. However, the virus is shed and spread by asymptomatic carriers. Like rubeola, rubella begins with a facial rash that spreads to the extremities (Figure 22.19). However, the rash is less intense, shorter lived (2–3 days), not associated with Koplik’s spots, and the resulting fever is lower (101 °F [38.3 °C]).

Congenital rubella syndrome is the most severe clinical complication of the German measles. This occurs if a woman is infected with rubella during pregnancy . The rubella virus is teratogenic , meaning it can cause developmental defects if it crosses the placenta during pregnancy. There is a very high incidence of stillbirth, spontaneous abortion, or congenital birth defects if the mother is infected before 11 weeks of pregnancy and 35% if she is infected between weeks 13–16 after this time the incidence is low. 32 For this reason, prenatal screening for rubella is commonly practiced in the United States. Postnatal infections are usually self-limiting and rarely cause severe complications.

Like measles, the preliminary diagnosis of rubella is based on the patient’s history, vaccination records, and the appearance of the rash. The diagnosis can be confirmed by hemagglutinin inhibition assays and a variety of other immunological techniques. There are no antiviral therapies for rubella, but an effective vaccine ( MMR ) is widely available. Vaccination efforts have essentially eliminated rubella in the United States fewer than a dozen cases are reported in a typical year.

Chickenpox and Shingles

Chickenpox, also known as varicella , was once a common viral childhood disease. The causative agent of chickenpox , the varicella-zoster virus , is a member of the herpesvirus family. In children, the disease is mild and self-limiting, and is easily transmitted by direct contact or inhalation of material from the skin lesions. In adults, however, chickenpox infections can be much more severe and can lead to pneumonia and birth defects in the case of infected pregnant women. Reye syndrome , mentioned earlier in this chapter, is also a serious complication associated with chickenpox, generally in children.

Once infected, most individuals acquire a lifetime immunity to future chickenpox outbreaks. For this reason, parents once held “chickenpox parties” for their children. At these events, uninfected children were intentionally exposed to an infected individual so they would contract the disease earlier in life, when the incidence of complications is very low, rather than risk a more severe infection later.

After the initial viral exposure, chickenpox has an incubation period of about 2 weeks. The initial infection of the respiratory tract leads to viremia and eventually produces fever and chills. A pustular rash then develops on the face, progresses to the trunk, and then the extremities, although most form on the trunk (Figure 22.20). Eventually, the lesions burst and form a crusty scab. Individuals with chickenpox are infectious from about 2 days before the outbreak of the rash until all the lesions have scabbed over.

Like other herpesviruses, the varicella-zoster virus can become dormant in nerve cells. While the pustular vesicles are developing, the virus moves along sensory nerves to the dorsal ganglia in the spinal cord. Once there, the varicella-zoster virus can remain latent for decades. These dormant viruses may be reactivated later in life by a variety of stimuli, including stress, aging, and immunosuppression. Once reactivated, the virus moves along sensory nerves to the skin of the face or trunk. This results in the production of the painful lesions in a condition known as shingles (Figure 22.21). These symptoms generally last for 2–6 weeks, and may recur more than once. Postherpetic neuralgia, pain signals sent from damaged nerves long after the other symptoms have subsided, is also possible. In addition, the virus can spread to other organs in immunocompromised individuals. A person with shingles lesions can transmit the virus to a nonimmune contact, and the newly infected individual would develop chickenpox as the primary infection. Shingles cannot be transmitted from one person to another.

The primary diagnosis of chickenpox in children is mainly based on the presentation of a pustular rash of the trunk. Serological and PCR-based tests are available to confirm the initial diagnosis. Treatment for chickenpox infections in children is usually not required. In patients with shingles, acyclovir treatment can often reduce the severity and length of symptoms, and diminish the risk of postherpetic neuralgia. An effective vaccine is now available for chickenpox. A vaccine is also available for adults older than 60 years who were infected with chickenpox in their youth. This vaccine reduces the likelihood of a shingles outbreak by boosting the immune defenses that are keeping the latent infection in check and preventing reactivation.

Check Your Understanding

  • Why does measles often lead to secondary infections?
  • What signs or symptoms would distinguish rubella and measles?
  • Why can chickenpox lead to shingles later in life?

Eye on Ethics

Smallpox Stockpiles

Smallpox has probably killed more humans than any other infectious disease, with the possible exception of tuberculosis. This disease, caused by the variola major virus, is transmitted by inhalation of viral particles shed from lesions in the throat. The smallpox virus spreads systemically in the bloodstream and produces a pustular skin rash. Historical epidemics of smallpox had fatality rates of 50% or greater in susceptible populations. Concerted worldwide vaccination efforts eradicated smallpox from the general population in 1977. This was the first microbial disease in history to be eradicated, a feat made possible by the fact that the only reservoir for the smallpox virus is infected humans.

Although the virus is no longer present in the wild, laboratory samples of the virus still exist in the United States and Russia. 33 The question is, why do these samples still exist? Some claim that these stocks should be maintained for research purposes. Should the smallpox virus ever reappear, they say, we would need access to such stocks for development of vaccines and treatments. Concerns about a re-emergence of the virus are not totally unfounded. Although there are no living reservoirs of the virus, there is always the possibility that smallpox could re-emerge from mummified human bodies or human remains preserved in permafrost. It is also possible that there are as-yet undiscovered samples of the virus in other locations around the world. An example of such "lost" samples was discovered in a drawer in a Food and Drug Administration lab in Maryland. 34 If an outbreak from such a source were to occur, it could lead to uncontrolled epidemics, since the population is largely unvaccinated now.

Critics of this argument, including many research scientists and the World Health Organization, claim that there is no longer any rational argument for keeping the samples. They view the “re-emergence scenarios” as a thinly veiled pretense for harboring biological weapons. These scenarios, they say, are less probable than an intentional reintroduction of the virus from militarized stocks by humans. Furthermore, they point out that if we needed to research smallpox in the future, we could rebuild the virus from its DNA sequence.

What do you think? Are there legitimate arguments for maintaining stockpiles of smallpox, or should all forms of this deadly disease be eradicated?

Disease Profile

Viral Infections of the Respiratory Tract

Many viruses are capable of entering and causing disease in the respiratory system, and a number are able to spread beyond the respiratory system to cause systemic infections. Most of these infections are highly contagious and, with a few exceptions, antimicrobial drugs are not effective for treatment. Although some of these infections are self-limiting, others can have serious or fatal complications. Effective vaccines have been developed for several of these diseases, as summarized in Figure 22.22.

Footnotes

    AG L’Huillier et al. “Survival of Rhinoviruses on Human Fingers.” Clinical Microbiology and Infection 21, no. 4 (2015):381–385. Centers for Disease Control and Prevention. “Estimating Seasonal Influenza-Associated Deaths in the United States: CDC Study Confirms Variability of Flu.” 2016. http://www.cdc.gov/flu/about/disease/us_flu-related_deaths.htm. Accessed July 6, 2016. ED Belay et al. “Reye’s Syndrome in the United States From 1981 Through 1997.” New England Journal of Medicine 340 no. 18 (1999):1377–1382. CE Mills et al. “Transmissibility of 1918 Pandemic Influenza.” Nature 432, no. 7019 (2004):904–906. E. Tognotti. “Influenza Pandemics: A Historical Retrospect.” Journal of Infection in Developing Countries 3, no. 5 (2009):331–334. FS Dawood et al. “Estimated Global Mortality Associated with the First 12 Months of 2009 Pandemic Influenza A H1N1 Virus Circulation: A Modelling Study.” The Lancet Infectious Diseases 12, no. 9 (2012):687–695. World Health Organization. “WHO Report on Global Surveillance of Epidemic-Prone Infectious Diseases.” 2000. http://www.who.int/csr/resources/publications/surveillance/Influenza.pdf. Accessed July 6, 2016. Centers of Disease Control and Prevention. “Vaccine Effectiveness - How Well Does the Flu Vaccine Work?” 2016. http://www.cdc.gov/flu/about/qa/vaccineeffect.htm. Accessed July 6, 2016. Y. Huang. “The SARS Epidemic and Its Aftermath in China: A Political Perspective.” In Learning from SARS: Preparing for the Next Disease Outbreak. Edited by S. Knobler et al. Washington, DC: National Academies Press 2004. Available at: http://www.ncbi.nlm.nih.gov/books/NBK92479/ Centers for Disease Control and Prevention. “Global Health - Measles, Rubella, and CRS, Eliminating Measles, Rubella & Congenital Rubella Syndrome (CRS) Worldwide.” 2015. http://www.cdc.gov/globalhealth/measles/. Accessed July 7, 2016. World Health Organization. “Measles Factsheet.” 2016. http://www.who.int/mediacentre/factsheets/fs286/en/. Accessed July 7, 2016. Centers for Disease Control and Prevention. “Measles Cases and Outbreaks.” 2016. http://www.cdc.gov/measles/cases-outbreaks.html. Accessed July 7, 2016. Ibid. World Health Organization. “Measles-Rubella Bulletin.” Manila, Philippines Expanded Programme on Immunization Regional Office for the Western Pacific World Health Organization 9 no. 1 (2015). http://www.wpro.who.int/immunization/documents/mrbulletinvol9issue1.pdf M. Bloch et al. “Vaccination Rates for Every Kindergartener in California.” The New York Times February 6, 2015. http://www.nytimes.com/interactive/2015/02/06/us/california-measles-vaccines-map.html?_r=1. Accessed July 7, 2016. E. Miller et al. “Consequences of Confirmed Maternal Rubella at Successive Stages of Pregnancy.” The Lancet 320, no. 8302 (1982):781–784. Centers for Disease Control and Prevention. “CDC Media Statement on Newly Discovered Smallpox Specimens.” July 8, 2014. http://www.cdc.gov/media/releases/2014/s0708-nih.html. Accessed on July 7, 2016. Ibid.

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