Anatomy and Normal Microbiota of the Skin

Human skin is an important part of the innate immune system. In addition to serving a wide range of other functions, the skin serves as an important barrier to microbial invasion. Not only is it a physical barrier to penetration of deeper tissues by potential pathogens, but it also provides an inhospitable environment for the growth of many pathogens.

The Skin

Layers of the Skin

Human skin is made up of several layers and sublayers. The two main layers are the epidermis and the dermis. These layers cover a third layer of tissue called the hypodermis, which consists of fibrous and adipose connective tissue (Figure 21.2).

The epidermis is the outermost layer of the skin, and it is relatively thin. The exterior surface of the epidermis, called the stratum corneum, primarily consists of dead skin cells. This layer of dead cells limits direct contact between the outside world and live cells. The stratum corneum is rich in keratin, a tough, fibrous protein that is also found in hair and nails. Keratin helps make the outer surface of the skin relatively tough and waterproof. It also helps to keep the surface of the skin dry, which reduces microbial growth. However, some microbes are still able to live on the surface of the skin, and some of these can be shed with dead skin cells in the process of desquamation, which is the shedding and peeling of skin that occurs as a normal process but that may be accelerated when infection is present.

Beneath the epidermis lies a thicker skin layer called the dermis. The dermis contains connective tissue and embedded structures such as blood vessels, nerves, and muscles. Structures called hair follicles (from which hair grows) are located within the dermis, even though much of their structure consists of epidermal tissue. The dermis also contains the two major types of glands found in human skin: sweat glands (tubular glands that produce sweat) and sebaceous glands (which are associated with hair follicles and produce sebum, a lipid-rich substance containing proteins and minerals).

Perspiration (sweat) provides some moisture to the epidermis, which can increase the potential for microbial growth. For this reason, more microbes are found on the regions of the skin that produce the most sweat, such as the skin of the underarms and groin. However, in addition to water, sweat also contains substances that inhibit microbial growth, such as salts, lysozyme, and antimicrobial peptides. Sebum also serves to protect the skin and reduce water loss. Although some of the lipids and fatty acids in sebum inhibit microbial growth, sebum contains compounds that provide nutrition for certain microbes.

Figure 21.2 (a) A micrograph of a section through human skin shows the epidermis and dermis. (b) The major layers of human skin are the epidermis, dermis, and hypodermis. (credit b: modification of work by National Cancer Institute)

Normal Microbiota of the Skin

The skin is home to a wide variety of normal microbiota, consisting of commensal organisms that derive nutrition from skin cells and secretions such as sweat and sebum. The normal microbiota of skin tends to inhibit transient-microbe colonization by producing antimicrobial substances and outcompeting other microbes that land on the surface of the skin. This helps to protect the skin from pathogenic infection.

The skin’s properties differ from one region of the body to another, as does the composition of the skin’s microbiota. The availability of nutrients and moisture partly dictates which microorganisms will thrive in a particular region of the skin. Relatively moist skin, such as that of the nares (nostrils) and underarms, has a much different microbiota than the dryer skin on the arms, legs, hands, and top of the feet. Some areas of the skin have higher densities of sebaceous glands. These sebum-rich areas, which include the back, the folds at the side of the nose, and the back of the neck, harbor distinct microbial communities that are less diverse than those found on other parts of the body.

Different types of bacteria dominate the dry, moist, and sebum-rich regions of the skin. The most abundant microbes typically found in the dry and sebaceous regions are Betaproteobacteria and Propionibacteria, respectively. In the moist regions, Corynebacterium and Staphylococcus are most commonly found (Figure 21.3). Viruses and fungi are also found on the skin, with Malassezia being the most common type of fungus found as part of the normal microbiota. The role and populations of viruses in the microbiota, known as viromes, are still not well understood, and there are limitations to the techniques used to identify them. However, CircoviridaePapillomaviridae, and Polyomaviridae appear to be the most common residents in the healthy skin virome.

Figure 21.3 The normal microbiota varies on different regions of the skin, especially in dry versus moist areas. The figure shows the major organisms commonly found in different locations of a healthy individual’s skin and external mucosa. Note that there is significant variation among individuals. (credit: modification of work by National Human Genome Research Institute)

Infections of the Skin

While the microbiota of the skin can play a protective role, it can also cause harm in certain cases. Often, an opportunistic pathogen residing in the skin microbiota of one individual may be transmitted to another individual more susceptible to an infection. For example, methicillin-resistant Staphylococcus aureus (MRSA) can often take up residence in the nares of health care workers and hospital patients; though harmless on intact, healthy skin, MRSA can cause infections if introduced into other parts of the body, as might occur during surgery or via a post-surgical incision or wound. This is one reason why clean surgical sites are so important.

Injury or damage to the skin can allow microbes to enter deeper tissues, where nutrients are more abundant and the environment is more conducive to bacterial growth. Wound infections are common after a puncture or laceration that damages the physical barrier of the skin. Microbes may infect structures in the dermis, such as hair follicles and glands, causing a localized infection, or they may reach the bloodstream, which can lead to a systemic infection.

In some cases, infectious microbes can cause a variety of rashes or lesions that differ in their physical characteristics. These rashes can be the result of inflammation reactions or direct responses to toxins produced by the microbes. Table 21.1 lists some of the medical terminology used to describe skin lesions and rashes based on their characteristics; Figure 21.4 and Figure 21.5 illustrate some of the various types of skin lesions. It is important to note that many different diseases can lead to skin conditions of very similar appearance; thus the terms used in the table are generally not exclusive to a particular type of infection or disease.

Some Medical Terms Associated with Skin Lesions and Rashes
Term Definition
abscess localized collection of pus
bulla (pl., bullae) fluid-filled blister no more than 5 mm in diameter
carbuncle deep, pus-filled abscess generally formed from multiple furuncles
crust dried fluids from a lesion on the surface of the skin
cyst encapsulated sac filled with fluid, semi-solid matter, or gas, typically located just below the upper layers of skin
folliculitis a localized rash due to inflammation of hair follicles
furuncle (boil) pus-filled abscess due to infection of a hair follicle
macules smooth spots of discoloration on the skin
papules small raised bumps on the skin
pseudocyst lesion that resembles a cyst but with a less defined boundary
purulent pus-producing; suppurative
pustules fluid- or pus-filled bumps on the skin
pyoderma any suppurative (pus-producing) infection of the skin
suppurative producing pus; purulent
ulcer break in the skin; open sore
vesicle small, fluid-filled lesion
wheal swollen, inflamed skin that itches or burns, such as from an insect bite
Table 21.1

Figure 21.4 (a) Acne is a bacterial infection of the skin that manifests as a rash of inflamed hair follicles (folliculitis). The large whitehead near the center of the cheek is an infected hair follicle that has become purulent (or suppurative), leading to the formation of a furuncle. (b) An abscess is a pus-filled lesion. (credit b: modification of work by Bruce Blaus)

Figure 21.5 Numerous causes can lead to skin lesions of various types, some of which are very similar in appearance. (credit: modification of work by Bruce Blaus)


Infections of the Skin

Bacterial Infections of the Skin and Eyes

Despite the skin’s protective functions, infections are common. Gram-positive Staphylococcus spp. and Streptococcus spp. are responsible for many of the most common skin infections. However, many skin conditions are not strictly associated with a single pathogen. Opportunistic pathogens of many types may infect skin wounds, and individual cases with identical symptoms may result from different pathogens or combinations of pathogens.

In this section, we will examine some of the most important bacterial infections of the skin and eyes and discuss how biofilms can contribute to and exacerbate such infections. Key features of bacterial skin and eye infections are also summarized in the Disease Profile boxes throughout this section.

Staphylococcal Infections of the Skin

Staphylococcus species are commonly found on the skin, with S. epidermidis and S. hominis being prevalent in the normal microbiota. S. aureus is also commonly found in the nasal passages and on healthy skin, but pathogenic strains are often the cause of a broad range of infections of the skin and other body systems.

S. aureus is quite contagious. It is spread easily through skin-to-skin contact, and because many people are chronic nasal carriers (asymptomatic individuals who carry S. aureus in their nares), the bacteria can easily be transferred from the nose to the hands and then to fomites or other individuals. Because it is so contagious, S. aureus is prevalent in most community settings. This prevalence is particularly problematic in hospitals, where antibiotic-resistant strains of the bacteria may be present, and where immunocompromised patients may be more susceptible to infection. Resistant strains include methicillin-resistant S. aureus (MRSA), which can be acquired through health-care settings (hospital-acquired MRSA, or HA-MRSA) or in the community (community-acquired MRSA, or CA-MRSA). Hospital patients often arrive at health-care facilities already colonized with antibiotic-resistant strains of S. aureus that can be transferred to health-care providers and other patients. Some hospitals have attempted to detect these individuals in order to institute prophylactic measures, but they have had mixed success.

When a staphylococcal infection develops, choice of medication is important. As discussed above, many staphylococci (such as MRSA) are resistant to some or many antibiotics. Thus, antibiotic sensitivity is measured to identify the most suitable antibiotic. However, even before receiving the results of sensitivity analysis, suspected S. aureus infections are often initially treated with drugs known to be effective against MRSA, such as trimethoprim-sulfamethoxazole (TMP/SMZ), clindamycin, a tetracycline (doxycycline or minocycline), or linezolid.

The pathogenicity of staphylococcal infections is often enhanced by characteristic chemicals secreted by some strains. Staphylococcal virulence factors include hemolysins called staphylolysins, which are cytotoxic for many types of cells, including skin cells and white blood cells. Virulent strains of S. aureus are also coagulase-positive, meaning they produce coagulase, a plasma-clotting protein that is involved in abscess formation. They may also produce leukocidins, which kill white blood cells and can contribute to the production of pus and Protein A, which inhibits phagocytosis by binding to the constant region of antibodies. Some virulent strains of S. aureus also produce other toxins, such as toxic shock syndrome toxin-1.

To confirm the causative agent of a suspected staphylococcal skin infection, samples from the wound are cultured. Under the microscope, gram-positive Staphylococcus species have cellular arrangements that form grapelike clusters; when grown on blood agar, colonies have a unique pigmentation ranging from opaque white to cream. A catalase test is used to distinguish Staphylococcus from Streptococcus, which is also a genus of gram-positive cocci and a common cause of skin infections. Staphylococcus species are catalase-positive while Streptococcus species are catalase-negative.

Other tests are performed on samples from the wound in order to distinguish coagulase-positive species of Staphylococcus (CoPS) such as S. aureus from common coagulase-negative species (CoNS) such as S. epidermidis. Although CoNS are less likely than CoPS to cause human disease, they can cause infections when they enter the body, as can sometimes occur via catheters, indwelling medical devices, and wounds. Passive agglutination testing can be used to distinguish CoPS from CoNS. If the sample is coagulase-positive, the sample is generally presumed to contain S. aureus. Additional genetic testing would be necessary to identify the particular strain of S. aureus.

Another way to distinguish CoPS from CoNS is by culturing the sample on mannitol salt agar (MSA)Staphylococcus species readily grow on this medium because they are tolerant of the high concentration of sodium chloride (7.5% NaCl). However, CoPS such as S. aureus ferment mannitol (which will be evident on a MSA plate), whereas CoNS such as S. epidermidis do not ferment mannitol but can be distinguished by the fermentation of other sugars such as lactose, malonate, and raffinose (Figure 21.9).

a) An agar plate with 2 regions of growth. One region has a yellow background, the other has a pink background. B) A micrograph of clusters of round cells. Each cell is just under 1 µm in diameter.
Figure 21.9 (a) A mannitol salt agar plate is used to distinguish different species of staphylococci. In this plate, S. aureus is on the left and S. epidermidis is in the right. Because S. aureus is capable of fermenting mannitol, it produces acids that cause the color to change to yellow. (b) This scanning electron micrograph shows the characteristic grapelike clusters of S. aureus. (credit a: modification of work by “ScienceProfOnline”/YouTube; credit b: modification of work by Centers for Disease Control and Prevention)

Eye On Ethics

Screening Patients for MRSA

According to the CDC, 86% of invasive MRSA infections are associated in some way with healthcare, as opposed to being community-acquired. In hospitals and clinics, asymptomatic patients who harbor MRSA may spread the bacteria to individuals who are more susceptible to serious illness.

In an attempt to control the spread of MRSA, hospitals have tried screening patients for MRSA. If patients test positive following a nasal swab test, they can undergo decolonization using chlorhexidine washes or intranasal mupirocin. Some studies have reported substantial reductions in MRSA disease following implementation of these protocols, while others have not. This is partly because there is no standard protocol for these procedures. Several different MRSA identification tests may be used, some involving slower culturing techniques and others rapid testing. Other factors, such as the effectiveness of general hand-washing protocols, may also play a role in helping to prevent MRSA transmission. There are still other questions that need to be addressed: How frequently should patients be screened? Which individuals should be tested? From where on the body should samples be collected? Will increased resistance develop from the decolonization procedures?

Even if identification and decolonization procedures are perfected, ethical questions will remain. Should patients have the right to decline testing? Should a patient who tests positive for MRSA have the right to decline the decolonization procedure, and if so, should hospitals have the right to refuse treatment to the patient? How do we balance the individual’s right to receive care with the rights of other patients who could be exposed to disease as a result?

Superficial Staphylococcal Infections

S. aureus is often associated with pyoderma, skin infections that are purulent. Pus formation occurs because many strains of S. aureus produce leukocidins, which kill white blood cells. These purulent skin infections may initially manifest as folliculitis, but can lead to furuncles or deeper abscesses called carbuncles.

Folliculitis generally presents as bumps and pimples that may be itchy, red, and/or pus-filled. In some cases, folliculitis is self-limiting, but if it continues for more than a few days, worsens, or returns repeatedly, it may require medical treatment. Sweat, skin injuries, ingrown hairs, tight clothing, irritation from shaving, and skin conditions can all contribute to folliculitis. Avoidance of tight clothing and skin irritation can help to prevent infection, but topical antibiotics (and sometimes other treatments) may also help. Folliculitis can be identified by skin inspection; treatment is generally started without first culturing and identifying the causative agent.

In contrast, furuncles (boils) are deeper infections (Figure 21.10). They are most common in those individuals (especially young adults and teenagers) who play contact sports, share athletic equipment, have poor nutrition, live in close quarters, or have weakened immune systems. Good hygiene and skin care can often help to prevent furuncles from becoming more infective, and they generally resolve on their own. However, if furuncles spread, increase in number or size, or lead to systemic symptoms such as fever and chills, then medical care is needed. They may sometimes need to be drained (at which time the pathogens can be cultured) and treated with antibiotics.

When multiple boils develop into a deeper lesion, it is called a carbuncle (Figure 21.10). Because carbuncles are deeper, they are more commonly associated with systemic symptoms and a general feeling of illness. Larger, recurrent, or worsening carbuncles require medical treatment, as do those associated with signs of illness such as fever. Carbuncles generally need to be drained and treated with antibiotics. While carbuncles are relatively easy to identify visually, culturing and laboratory analysis of the wound may be recommended for some infections because antibiotic resistance is relatively common.

Proper hygiene is important to prevent these types of skin infections or to prevent the progression of existing infections.

Figure 21.10 Furuncles (boils) and carbuncles are infections of the skin often caused by Staphylococcus bacteria. (a) A furuncle contains pus and exhibits swelling. (b) A carbuncle is a pus-filled lesion that is typically deeper than the furuncle. It often forms from multiple furuncles. (credit a: modification of work by “Mahdouch”/Wikimedia Commons; credit b: modification of work by “Drvgaikwad”/Wikimedia Commons)

Staphylococcal scalded skin syndrome (SSSS) is another superficial infection caused by S. aureus that is most commonly seen in young children, especially infants. Bacterial exotoxins first produce erythema (redness of the skin) and then severe peeling of the skin, as might occur after scalding (Figure 21.11). SSSS is diagnosed by examining characteristics of the skin (which may rub off easily), using blood tests to check for elevated white blood cell counts, culturing, and other methods. Intravenous antibiotics and fluid therapy are used as treatment.

Figure 21.11 A newborn with staphylococcal scalded skin syndrome (SSSS), which results in large regions of peeling, dead skin. (credit: modification of work by D Jeyakumari, R Gopal, M Eswaran, and C MaheshKumar)


The skin infection impetigo causes the formation of vesicles, pustules, and possibly bullae, often around the nose and mouth. Bullae are large, fluid-filled blisters that measure at least 5 mm in diameter. Impetigo can be diagnosed as either nonbullous or bullous. In nonbullous impetigo, vesicles and pustules rupture and become encrusted sores. Typically the crust is yellowish, often with exudate draining from the base of the lesion. In bullous impetigo, the bullae fill and rupture, resulting in larger, draining, encrusted lesions (Figure 21.12).

Especially common in children, impetigo is particularly concerning because it is highly contagious. Impetigo can be caused by S. aureus alone, by Streptococcus pyogenes alone, or by coinfection of S. aureus and S. pyogenes. Impetigo is often diagnosed through observation of its characteristic appearance, although culture and susceptibility testing may also be used.

Topical or oral antibiotic treatment is typically effective in treating most cases of impetigo. However, cases caused by S. pyogenes can lead to serious sequelae (pathological conditions resulting from infection, disease, injury, therapy, or other trauma) such as acute glomerulonephritis (AGN), which is severe inflammation in the kidneys.

Figure 21.12 Impetigo is characterized by vesicles, pustules, or bullae that rupture, producing encrusted sores. (credit: modification of work by FDA)

Nosocomial S. epidermidis Infections

Though not as virulent as S. aureus, the staphylococcus S. epidermidis can cause serious opportunistic infections. Such infections usually occur only in hospital settings. S. epidermidis is usually a harmless resident of the normal skin microbiota. However, health-care workers can inadvertently transfer S. epidermidis to medical devices that are inserted into the body, such as catheters, prostheses, and indwelling medical devices. Once it has bypassed the skin barrier, S. epidermidis can cause infections inside the body that can be difficult to treat. Like S. aureusS. epidermidis is resistant to many antibiotics, and localized infections can become systemic if not treated quickly. To reduce the risk of nosocomial (hospital-acquired) S. epidermidis, health-care workers must follow strict procedures for handling and sterilizing medical devices before and during surgical procedures.

Streptococcal Infections of the Skin

Streptococcus are gram-positive cocci with a microscopic morphology that resembles chains of bacteria. Colonies are typically small (1–2 mm in diameter), translucent, entire edge, with a slightly raised elevation that can be either nonhemolytic, alpha-hemolytic, or beta-hemolytic when grown on blood agar (Figure 21.13). Additionally, they are facultative anaerobes that are catalase-negative.

Figure 21.13 Streptococcus pyogenes forms chains of cocci. (credit: modification of work by Centers for Disease Control and Prevention)

The genus Streptococcus includes important pathogens that are categorized in serological Lancefield groups based on the distinguishing characteristics of their surface carbohydrates. The most clinically important streptococcal species in humans is S. pyogenes, also known as group A streptococcus (GAS)S. pyogenes produces a variety of extracellular enzymes, including streptolysins O and S, hyaluronidase, and streptokinase. These enzymes can aid in transmission and contribute to the inflammatory response. S. pyogenes also produces a capsule and M protein, a streptococcal cell wall protein. These virulence factors help the bacteria to avoid phagocytosis while provoking a substantial immune response that contributes to symptoms associated with streptococcal infections.

S. pyogenes causes a wide variety of diseases not only in the skin, but in other organ systems as well. Examples of diseases elsewhere in the body include pharyngitis and scarlet fever, which will be covered in later chapters.

Cellulitis, Erysipelas, and Erythema Nosodum

Common streptococcal conditions of the skin include cellulitis, erysipelas, and erythema nodosum. An infection that develops in the dermis or hypodermis can cause cellulitis, which presents as a reddened area of the skin that is warm to the touch and painful. The causative agent is often S. pyogenes, which may breach the epidermis through a cut or abrasion, although cellulitis may also be caused by staphylococci. S. pyogenes can also cause erysipelas, a condition that presents as a large, intensely inflamed patch of skin involving the dermis (often on the legs or face). These infections can be suppurative, which results in a bullous form of erysipelas. Streptococcal and other pathogens may also cause a condition called erythema nodosum, characterized by inflammation in the subcutaneous fat cells of the hypodermis. It sometimes results from a streptococcal infection, though other pathogens can also cause the condition. It is not suppurative, but leads to red nodules on the skin, most frequently on the shins (Figure 21.14).

In general, streptococcal infections are best treated through identification of the specific pathogen followed by treatment based upon that particular pathogen’s susceptibility to different antibiotics. Many immunological tests, including agglutination reactions and ELISAs, can be used to detect streptococci. Penicillin is commonly prescribed for treatment of cellulitis and erysipelas because resistance is not widespread in streptococci at this time. In most patients, erythema nodosum is self-limiting and is not treated with antimicrobial drugs. Recommended treatments may include nonsteroidal anti-inflammatory drugs (NSAIDs), cool wet compresses, elevation, and bed rest.

Figure 21.14 S. pyogenes can cause a variety of skin conditions once it breaches the skin barrier through a cut or wound. (a) Cellulitis presents as a painful, red rash. (b) Erysipelas presents as a raised rash, usually with clear borders. (c) Erythema nodosum is characterized by red lumps or nodules, typically on the lower legs. (credit a: modification of work by “Bassukas ID, Gaitanis G, Zioga A, Boboyianni C, Stergiopoulou C; credit b: modification of work by Centers for Disease Control and Prevention; credit c: modification of work by Dean C, Crow WT)

Necrotizing Fasciitis

Streptococcal infections that start in the skin can sometimes spread elsewhere, resulting in a rare but potentially life-threatening condition called necrotizing fasciitis, sometimes referred to as flesh-eating bacterial syndromeS. pyogenes is one of several species that can cause this rare but potentially-fatal condition; others include KlebsiellaClostridiumEscherichia coliS. aureus, and Aeromonas hydrophila.

Necrotizing fasciitis occurs when the fascia, a thin layer of connective tissue between the skin and muscle, becomes infected. Severe invasive necrotizing fasciitis due to Streptococcus pyogenes occurs when virulence factors that are responsible for adhesion and invasion overcome host defenses. S. pyogenes invasins allow bacterial cells to adhere to tissues and establish infection. Bacterial proteases unique to S. pyogenes aggressively infiltrate and destroy host tissues, inactivate complement, and prevent neutrophil migration to the site of infection. The infection and resulting tissue death can spread very rapidly, as large areas of skin become detached and die. Treatment generally requires debridement (surgical removal of dead or infected tissue) or amputation of infected limbs to stop the spread of the infection; surgical treatment is supplemented with intravenous antibiotics and other therapies (Figure 21.15).

Necrotizing fasciitis does not always originate from a skin infection; in some cases there is no known portal of entry. Some studies have suggested that experiencing a blunt force trauma can increase the risk of developing streptococcal necrotizing fasciitis.

Figure 21.15 (a) The left leg of this patient shows the clinical features of necrotizing fasciitis. (b) The same patient’s leg is surgically debrided to remove the infection. (credit a, b: modification of work by Piotr Smuszkiewicz, Iwona Trojanowska, and Hanna Tomczak)

Pseudomonas Infections of the Skin

Another important skin pathogen is Pseudomonas aeruginosa, a gram-negative, oxidase-positive, aerobic bacillus that is commonly found in water and soil as well as on human skin. P. aeruginosa is a common cause of opportunistic infections of wounds and burns. It can also cause hot tub rash, a condition characterized by folliculitis that frequently afflicts users of pools and hot tubs. P. aeruginosa is also the cause of otitis externa (swimmer’s ear), an infection of the ear canal that causes itching, redness, and discomfort, and can progress to fever, pain, and swelling (Figure 21.16).

Figure 21.16 (a) Hot tub folliculitis presents as an itchy red rash. It is typically caused by P. aeruginosa, a bacterium that thrives in wet, warm environments such as hot tubs. (b) Otitis externa (swimmer’s ear) may also be caused by P. aeruginosa or other bacteria commonly found in water. Inflammation of the outer ear and ear canal can lead to painful swelling. (credit b: modification of work by Klaus D. Peter)

Wounds infected with P. aeruginosa have a distinctive odor resembling grape soda or fresh corn tortillas. This odor is caused by the 2-aminoacetophenone that is used by P. aeruginosa in quorum sensing and contributes to its pathogenicity. Wounds infected with certain strains of P. aeruginosa also produce a blue-green pus due to the pigments pyocyanin and pyoverdin, which also contribute to its virulence. Pyocyanin and pyoverdin are siderophores that help P. aeruginosa survive in low-iron environments by enhancing iron uptake. P. aeruginosa also produces several other virulence factors, including phospholipase C (a hemolysin capable of breaking down red blood cells), exoenzyme S (involved in adherence to epithelial cells), and exotoxin A (capable of causing tissue necrosis). Other virulence factors include a slime that allows the bacterium to avoid being phagocytized, fimbriae for adherence, and proteases that cause tissue damage. P. aeruginosa can be detected through the use of cetrimide agar, which is selective for Pseudomonas species (Figure 21.17).

Figure 21.17 (a) These P. aeruginosa colonies are growing on xylose lysine sodium deoxycholate (XLD) agar. (b) Pseudomonas spp. can produce a variety of blue-green pigments. (c) Pseudomonas spp. may produce fluorescein, which fluoresces green under ultraviolet light under the right conditions. (credit a: modification of work by Centers for Disease Control and Prevention)

Pseudomonas spp. tend to be resistant to most antibiotics. They often produce β-lactamases, may have mutations affecting porins (small cell wall channels) that affect antibiotic uptake, and may pump some antibiotics out of the cell, contributing to this resistance. Polymyxin B and gentamicin are effective, as are some fluoroquinolones. Otitis externa is typically treated with ear drops containing acetic acid, antibacterials, and/or steroids to reduce inflammation; ear drops may also include antifungals because fungi can sometimes cause or contribute to otitis externa. Wound infections caused by Pseudomonas spp. may be treated with topical antibiofilm agents that disrupt the formation of biofilms.


One of the most ubiquitous skin conditions is acne. Acne afflicts nearly 80% of teenagers and young adults, but it can be found in individuals of all ages. Higher incidence among adolescents is due to hormonal changes that can result in overproduction of sebum.

Acne occurs when hair follicles become clogged by shed skin cells and sebum, causing non-inflammatory lesions called comedones. Comedones (singular “comedo”) can take the form of whitehead and blackhead pimples. Whiteheads are covered by skin, whereas blackhead pimples are not; the black color occurs when lipids in the clogged follicle become exposed to the air and oxidize (Figure 21.18).

Figure 21.18 (a) Acne is characterized by whitehead and blackhead comedones that result from clogged hair follicles. (b) Blackheads, visible as black spots on the skin, have a dark appearance due to the oxidation of lipids in sebum via exposure to the air. (credit a: modification of work by Bruce Blaus)

Often comedones lead to infection by Propionibacterium acnes, a gram-positive, non-spore-forming, aerotolerant anaerobic bacillus found on skin that consumes components of sebum. P. acnes secretes enzymes that damage the hair follicle, causing inflammatory lesions that may include papulespustulesnodules, or pseudocysts, depending on their size and severity.

Treatment of acne depends on the severity of the case. There are multiple ways to grade acne severity, but three levels are usually considered based on the number of comedones, the number of inflammatory lesions, and the types of lesions. Mild acne is treated with topical agents that may include salicylic acid (which helps to remove old skin cells) or retinoids (which have multiple mechanisms, including the reduction of inflammation). Moderate acne may be treated with antibiotics (erythromycinclindamycin), acne creams (e.g., benzoyl peroxide), and hormones. Severe acne may require treatment using strong medications such as isotretinoin (a retinoid that reduces oil buildup, among other effects, but that also has serious side effects such as photosensitivity). Other treatments, such as phototherapy and laser therapy to kill bacteria and possibly reduce oil production, are also sometimes used.



The zoonotic disease anthrax is caused by Bacillusanthracis, a gram-positive, endospore-forming, facultative anaerobe. Anthrax mainly affects animals such as sheep, goats, cattle, and deer, but can be found in humans as well. Sometimes called wool sorter’s disease, it is often transmitted to humans through contact with infected animals or animal products, such as wool or hides. However, exposure to B. anthracis can occur by other means, as the endospores are widespread in soils and can survive for long periods of time, sometimes for hundreds of years.

The vast majority of anthrax cases (95–99%) occur when anthrax endospores enter the body through abrasions of the skin. This form of the disease is called cutaneous anthrax. It is characterized by the formation of a nodule on the skin; the cells within the nodule die, forming a black eschar, a mass of dead skin tissue (Figure 21.19). The localized infection can eventually lead to bacteremia and septicemia. If untreated, cutaneous anthrax can cause death in 20% of patients. Once in the skin tissues, B. anthracis endospores germinate and produce a capsule, which prevents the bacteria from being phagocytized, and two binary exotoxins that cause edema and tissue damage. The first of the two exotoxins consists of a combination of protective antigen (PA) and an enzymatic lethal factor (LF), forming lethal toxin (LeTX). The second consists of protective antigen (PA) and an edema factor (EF), forming edema toxin (EdTX).

Figure 21.19 (a) Cutaneous anthrax is an infection of the skin by B. anthracis, which produces tissue-damaging exotoxins. Dead tissues accumulating in this nodule have produced a small black eschar. (b) Colonies of B. anthracis grown on sheep’s blood agar. (credit a, b: modification of work by Centers for Disease Control and Prevention)

Less commonly, anthrax infections can be initiated through other portals of entry such as the digestive tract (gastrointestinal anthrax) or respiratory tract (pulmonary anthrax or inhalation anthrax). Typically, cases of noncutaneous anthrax are more difficult to treat than the cutaneous form. The mortality rate for gastrointestinal anthrax can be up to 40%, even with treatment. Inhalation anthrax, which occurs when anthrax spores are inhaled, initially causes influenza-like symptoms, but mortality rates are approximately 45% in treated individuals and 85% in those not treated. A relatively new form of the disease, injection anthrax, has been reported in Europe in intravenous drug users; it occurs when drugs are contaminated with B. anthracis. Patients with injection anthrax show signs and symptoms of severe soft tissue infection that differ clinically from cutaneous anthrax. This often delays diagnosis and treatment, and leads to a high mortality rate.

B. anthracis colonies on blood agar have a rough texture and serrated edges that eventually form an undulating band (Figure 21.19). Broad spectrum antibiotics such as penicillinerythromycin, and tetracycline are often effective treatments.

Unfortunately, B. anthracis has been used as a biological weapon and remains on the United Nations’ list of potential agents of bioterrorism. Over a period of several months in 2001, a number of letters were mailed to members of the news media and the United States Congress. As a result, 11 individuals developed cutaneous anthrax and another 11 developed inhalation anthrax. Those infected included recipients of the letters, postal workers, and two other individuals. Five of those infected with pulmonary anthrax died. The anthrax spores had been carefully prepared to aerosolize, showing that the perpetrator had a high level of expertise in microbiology.

A vaccine is available to protect individuals from anthrax. However, unlike most routine vaccines, the current anthrax vaccine is unique in both its formulation and the protocols dictating who receives it. The vaccine is administered through five intramuscular injections over a period of 18 months, followed by annual boosters. The US Food and Drug Administration (FDA) has only approved administration of the vaccine prior to exposure for at-risk adults, such as individuals who work with anthrax in a laboratory, some individuals who handle animals or animal products (e.g., some veterinarians), and some members of the United States military. The vaccine protects against cutaneous and inhalation anthrax using cell-free filtrates of microaerophilic cultures of an avirulent, nonencapsulated strain of B. anthracis. The FDA has not approved the vaccine for routine use after exposure to anthrax, but if there were ever an anthrax emergency in the United States, patients could be given anthrax vaccine after exposure to help prevent disease.

Disease Profile

Bacterial Infections of the Skin

Bacterial infections of the skin can cause a wide range of symptoms and syndromes, ranging from the superficial and relatively harmless to the severe and even fatal. Most bacterial skin infections can be diagnosed by culturing the bacteria and treated with antibiotics. Antimicrobial susceptibility testing is also often necessary because many strains of bacteria have developed antibiotic resistance. Figure 21.20 summarizes the characteristics of some common bacterial skin infections.

Figure 21.20


Viral Infections of the Skin

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 PapillomaviridaePolyomaviridae 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 primarily discuss viral skin infections that use the skin as a portal of entry. Furthermore, we 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. See also ‘Table 21.4 Important infectious childhood exanthems’ at the end of this section for an overview.


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.

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).

Figure 22.18 (a) Measles typically presents as a raised macular rash that begins on the face and spreads to the extremities. (b) Koplik’s spots on the oral mucosa are also characteristic of measles. (c) A thin-section transmission electron micrograph of a measles virion. (credit a, b, c: modification of work by Centers for Disease Control and Prevention)


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.

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. 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. 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. Measles is highly communicable, and its spread at Disneyland may have been facilitated by the low vaccination rate in some communities in California.

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. 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.

Figure 22.19 (a) This photograph shows the appearance of the German measles (rubella) rash. Note that this is less intense than the rash of measles and the lesions are not confluent. (b) This transmission electron micrograph shows rubella virus virions just budding from a host cell. (credit a, b: modification of work by Centers for Disease Control and Prevention)

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.

Figure 22.20 (a) The characteristic appearance of the pustular chickenpox rash is concentrated on the trunk region. (b) This transmission electron micrograph shows a viroid of human herpesvirus 3, the virus that causes chickenpox in children and shingles when it is reactivated in adults. (credit b: modification of work by Centers for Disease Control and Prevention)

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.

Figure 22.21 (a) An individual suffering from shingles. (b) The rash is formed because of the reactivation of a varicella-zoster infection that was initially contracted in childhood. (credit a: modification of work by National Institute of Allergy and Infectious Diseases (NIAID); credit b: modification of work by Centers for Disease Control and Prevention)

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. 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. 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?

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, 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 21.25). 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.

Figure 21.25 (a) Roseola, a mild viral infection common in young children, generally begins with symptoms similar to a cold, followed by a pink, patchy rash that starts on the trunk and spreads outward. (b) Fifth disease exhibits similar symptoms in children, except for the distinctive “slapped cheek” rash that originates on the face.


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 wartsplantar wartsflat 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 acid may 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 21.26).

Figure 21.26 Warts can vary in shape and in location. (a) Multiple plantar warts have grown on this toe. (b) A filiform wart has grown on this eyelid.

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 21.27). 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. 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 acyclovirpenciclovirfamciclovir, 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.

Figure 21.27 A cold sore caused by HSV-1. (credit: Centers for Disease Control and Prevention)
Disease Pathogen Age Incubation period Infectious period Prodromal phase Exanthema Enanthema At risk populations
Measles (rubeola) morbillivirus 0,5 – 4 y/o 7 – 14 days 4 days pre until 4 days post presentation of exanthema conjunctivitis, rhinitis, dry cough, high fever (40.6 °C / 105 °F not unusual) rough feeling, red, raised macular rash will eventually become confluent, starts in the face, spreads to extremities, later centrifugal expansion Koplik’s spots (white spots that form on the inner lining of inflamed cheek tissues) about 48 hours pre exanthema children < 1 year old, especially newborns from non-immune mothers
Scarlet fever group-A-streptococcus (GAS) 2 – 10 y/o 2 – 7 days uncomplicated and untreated in 10 – 21 days, in case of antibiotics after 24 – 48 hours verlies eetlust, koorts (tot 40 °C / 104 °F), keelpijn, braken diffuse redness with small papules (goose pimples), sandpaper texture, starts at the flexion of a.o. the elbow, then trunk and extremities. Face flushed, most in cheeks with ring of paleness around mouth. After the rash spreads, more pronounced in creases in the skin, such as the skin folds in the inguinal and axillary regions. Within 1 week of onset the rash begins to fade followed by weeks of desquamation. inflamed pharynx, tonsil debris, strawberry tongue children with anatomical deviations in the ENT area (e.g. Down syndrome)
Rubella rubellavirus 6-12 y/o 12-23 days 10 days pre to 7 days post exanthema similar to upper airway infection, and lymphadenopathy retroauriculary and neck like rubeola, rubella begins with a facial rash that spreads to the extremities, but the rash is less intense, shorter lived (2–3 days), not associated with Koplik’s spots, and the resulting fever is lower (38.3 °C / 101 °F) small red spots on the palate pregnant women in first trimester with primo-infection
Fifth disease (erythema infectiosum) parvovirus B19 4-10 y/o 7-21 days week pre symptoms several days aspecifical symptoms, mild fever rash, butterfly shaped exanthema in face (apple / slapped cheeks), nose unaffected, red lacy rash on stretch-side of extremities, sharp borders followed by confluency and central whitening none pregnant women before 20th week with primo-infection
Roseola (exanthema subitum) herpesvirus type 6 3 months to 3 years 5-14 days unknown, possible lifelong several days of high fever after fever subsides rash on chest and abdomen, characteristic macules that are flat or papules that are firm and slightly raised; some macules or papules may be surrounded by a white ring, may eventually spread to the neck and arms, and sometimes face and legs none none
Chickenpox varicella-zoster virus 0-4 years 10-21 days 2 days pre skin lesions and after all vesicles have dryed up fever rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs (often all stages present simulateously), 5% bacterial superinfection vesicles or ulcers mouth in adults, chickenpox infections can be much more severe and can lead to pneumonia and birth defects in the case of infected pregnant women infected in week 13-20. Reye syndrome, mentioned earlier in this chapter, is also a serious complication associated with chickenpox, generally in children.

Table 21.4 Important infectious childhood exanthems


Mycoses of the Skin


Many fungal infections of the skin involve fungi that are found in the normal skin microbiota. Some of these fungi can cause infection when they gain entry through a wound; others mainly cause opportunistic infections in immunocompromised patients. Other fungal pathogens primarily cause infection in unusually moist environments that promote fungal growth; for example, sweaty shoes, communal showers, and locker rooms provide excellent breeding grounds that promote the growth and transmission of fungal pathogens.

Fungal infections, also called mycoses, can be divided into classes based on their invasiveness. Mycoses that cause superficial infections of the epidermis, hair, and nails, are called cutaneous mycoses. Mycoses that penetrate the epidermis and the dermis to infect deeper tissues are called subcutaneous mycoses. Mycoses that spread throughout the body are called systemic mycoses.


A group of cutaneous mycoses called tineas are caused by dermatophytes, fungal molds that require keratin, a protein found in skin, hair, and nails, for growth. There are three genera of dermatophytes, all of which can cause cutaneous mycoses: TrichophytonEpidermophyton, and Microsporum. Tineas on most areas of the body are generally called ringworm, but tineas in specific locations may have distinctive names and symptoms (see Table 21.4 and Figure 21.29). Keep in mind that these names—even though they are Latinized—refer to locations on the body, not causative organisms. Tineas can be caused by different dermatophytes in most areas of the body.

Some Common Tineas and Location on the Body
Tinea corporis (ringworm) Body
Tinea capitis (ringworm) Scalp
Tinea pedis (athlete’s foot) Feet
Tinea barbae (barber’s itch) Beard
Tinea cruris (jock itch) Groin
Tinea unguium (onychomycosis) Toenails, fingernails
Table 21.4

Figure 21.29 Tineas are superficial cutaneous mycoses and are common. (a) Tinea barbae (barber’s itch) occurs on the lower face. (b) Tinea pedis (athlete’s foot) occurs on the feet, causing itching, burning, and dry, cracked skin between the toes. (c) A close-up view of tinea corporis (ringworm) caused by Trichophyton mentagrophytes. (credit a, c: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G)

Dermatophytes are commonly found in the environment and in soils and are frequently transferred to the skin via contact with other humans and animals. Fungal spores can also spread on hair. Many dermatophytes grow well in moist, dark environments. For example, tinea pedis (athlete’s foot) commonly spreads in public showers, and the causative fungi grow well in the dark, moist confines of sweaty shoes and socks. Likewise, tinea cruris (jock itch) often spreads in communal living environments and thrives in warm, moist undergarments.

Tineas on the body (tinea corporis) often produce lesions that grow radially and heal towards the center. This causes the formation of a red ring, leading to the misleading name of ringworm.

Several approaches may be used to diagnose tineas. A Wood’s lamp (also called a black lamp) with a wavelength of 365 nm is often used. When directed on a tinea, the ultraviolet light emitted from the Wood’s lamp causes the fungal elements (spores and hyphae) to fluoresce. Direct microscopic evaluation of specimens from skin scrapings, hair, or nails can also be used to detect fungi. Generally, these specimens are prepared in a wet mount using a potassium hydroxide solution (10%–20% aqueous KOH), which dissolves the keratin in hair, nails, and skin cells to allow for visualization of the hyphae and fungal spores. The specimens may be grown on Sabouraud dextrose CC (chloramphenicol/cyclohexamide), a selective agar that supports dermatophyte growth while inhibiting the growth of bacteria and saprophytic fungi (Figure 21.30). Macroscopic colony morphology is often used to initially identify the genus of the dermatophyte; identification can be further confirmed by visualizing the microscopic morphology using either a slide culture or a sticky tape prep stained with lactophenol cotton blue.

Various antifungal treatments can be effective against tineas. Allylamine ointments that include terbinafine are commonly used; miconazole and clotrimazole are also available for topical treatment, and griseofulvin is used orally.

Figure 21.30 To diagnose tineas, the dermatophytes may be grown on a Sabouraud dextrose CC agar plate. This culture contains a strain of Trichophyton rubrum, one of the most common causes of tineas on various parts of the body. (credit: Centers for Disease Control and Prevention)

Cutaneous Aspergillosis

Another cause of cutaneous mycoses is Aspergillus, a genus consisting of molds of many different species, some of which cause a condition called aspergillosis. Primary cutaneous aspergillosis, in which the infection begins in the skin, is rare but does occur. More common is secondary cutaneous aspergillosis, in which the infection begins in the respiratory system and disseminates systemically. Both primary and secondary cutaneous aspergillosis result in distinctive eschars that form at the site or sites of infection (Figure 21.31). Pulmonary aspergillosis will be discussed more thoroughly in Respiratory Mycoses).

Figure 21.31 (a) Eschar on a patient with secondary cutaneous aspergillosis. (b) Micrograph showing a conidiophore of Aspergillus. (credit a: modification of work by Santiago M, Martinez JH, Palermo C, Figueroa C, Torres O, Trinidad R, Gonzalez E, Miranda Mde L, Garcia M, Villamarzo G; credit b: modification of work by U.S. Department of Health and Human Services)

Primary cutaneous aspergillosis usually occurs at the site of an injury and is most often caused by Aspergillus fumigatus or Aspergillus flavus. It is usually reported in patients who have had an injury while working in an agricultural or outdoor environment. However, opportunistic infections can also occur in health-care settings, often at the site of intravenous catheters, venipuncture wounds, or in association with burns, surgical wounds, or occlusive dressing. After candidiasis, aspergillosis is the second most common hospital-acquired fungal infection and often occurs in immunocompromised patients, who are more vulnerable to opportunistic infections.

Cutaneous aspergillosis is diagnosed using patient history, culturing, histopathology using a skin biopsy. Treatment involves the use of antifungal medications such as voriconazole (preferred for invasive aspergillosis), itraconazole, and amphotericin B if itraconazole is not effective. For immunosuppressed individuals or burn patients, medication may be used and surgical or immunotherapy treatments may be needed.

Candidiasis of the Skin and Nails

Candida albicans and other yeasts in the genus Candida can cause skin infections referred to as cutaneous candidiasis. Candida spp. are sometimes responsible for intertrigo, a general term for a rash that occurs in a skin fold, or other localized rashes on the skin. Candida can also infect the nails, causing them to become yellow and harden (Figure 21.32).

Figure 21.32 (a) This red, itchy rash is the result of cutaneous candidiasis, an opportunistic infection of the skin caused by the yeast Candida albicans. (b) Fungal infections of the nail (tinea unguium) can be caused by dermatophytes or Candida spp. The nail becomes yellow, brittle, and prone to breaking. This condition is relatively common among adults. (c) C. albicans growing on Sabouraud dextrose agar. (credit a: modification of work by U.S. Department of Veterans Affairs; credit c: modification of work by Centers for Disease Control and Prevention)

Candidiasis of the skin and nails is diagnosed through clinical observation and through culture, Gram stain, and KOH wet mounts. Susceptibility testing for anti-fungal agents can also be done. Cutaneous candidiasis can be treated with topical or systemic azole antifungal medications. Because candidiasis can become invasive, patients suffering from HIV/AIDS, cancer, or other conditions that compromise the immune system may benefit from preventive treatment. Azoles, such as clotrimazoleeconazolefluconazoleketoconazole, and miconazolenystatinterbinafine; and naftifine may be used for treatment. Long-term treatment with medications such as itraconazole or ketoconazole may be used for chronic infections. Repeat infections often occur, but this risk can be reduced by carefully following treatment recommendations, avoiding excessive moisture, maintaining good health, practicing good hygiene, and having appropriate clothing (including footwear).

Candida also causes infections in other parts of the body besides the skin. These include vaginal yeast infections and oral thrush.


Whereas cutaneous mycoses are superficial, subcutaneous mycoses can spread from the skin to deeper tissues. In temperate regions, the most common subcutaneous mycosis is a condition called sporotrichosis, caused by the fungus Sporothrixschenkii and commonly known as rose gardener’s disease or rose thorn disease. Sporotrichosis is often contracted after working with soil, plants, or timber, as the fungus can gain entry through a small wound such as a thorn-prick or splinter. Sporotrichosis can generally be avoided by wearing gloves and protective clothing while gardening and promptly cleaning and disinfecting any wounds sustained during outdoor activities.

Sporothrix infections initially present as small ulcers in the skin, but the fungus can spread to the lymphatic system and sometimes beyond. When the infection spreads, nodules appear, become necrotic, and may ulcerate. As more lymph nodes become affected, abscesses and ulceration may develop over a larger area (often on one arm or hand). In severe cases, the infection may spread more widely throughout the body, although this is relatively uncommon.

Sporothrix infection can be diagnosed based upon histologic examination of the affected tissue. Its macroscopic morphology can be observed by culturing the mold on potato dextrose agar, and its microscopic morphology can be observed by staining a slide culture with lactophenol cotton blue. Treatment with itraconazole is generally recommended.

Disease profile

Mycoses of the Skin

Cutaneous mycoses are typically opportunistic, only able to cause infection when the skin barrier is breached through a wound. Tineas are the exception, as the dermatophytes responsible for tineas are able to grow on skin, hair, and nails, especially in moist conditions. Most mycoses of the skin can be avoided through good hygiene and proper wound care. Treatment requires antifungal medications. Figure 21.33 summarizes the characteristics of some common fungal infections of the skin.

Figure 21.33



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This part contains content from OpenStax College, Microbiology. OpenStax CNX. Access for free at

Chapters and sections were borrowed and adapted from the above existing OER textbook. Without these foundational texts, a lot more work would have been required to complete this project. Thank you to those who shared before us.

SA Bos, M.D.

Lead Author