Infectious disease of Skin

Structure and function of skin Salt inhibits microbes Lysozyme hydrolyzes peptidoglycan Fatty acids inhibit some pathogens

Microbial Diseases of the Skin Rashes and lesions on the skin do not necessarily indicate an infection of the skin; in fact, many diseases manifested by skin lesions are actually systemic diseases affecting internal organs. Variations in these lesions are often useful in describing the symptoms of the disease. For example, small, fluid-filled lesions are vesicles (Figure 21.2a). Vesicles larger than about 1 cm in diameter are termed bullae (Figure 21.2b). Flat, reddened lesions are known as macules (Figure 21.2c). Raised lesions are called papules or, when they contain pus, pustules (Figure 21.2d). Although the focus of infection is often elsewhere in the body, it is convenient to classify these diseases by the organ most obviously affected: the skin. A skin rash that arises from disease conditions is called an exanthem; on mucous membranes, such as the interior of the mouth, such a rash is called an enanthem.

Microbial Diseases of the Skin Figure 21.2

Staphylococcal skin disease Staphylococci are spherical gram-positive bacteria that form irregular clusters like grapes. For almost all clinical purposes, these bacteria can be divided into those that produce coagulase, an enzyme that coagulates(clots) fibrin in blood, and those that do not. Coagulase-negative strains, such as Staphylococccus epidermidis, are very common on the skin, where they may represent 90% of the normal microbiota. They are generally pathogenic only when the skin barrier is broken or is invaded by medical procedures, such as the insertion and removal of catheters into veins. On the surface of the catheter, the bacteria are surrounded by a slime layer of capsular material, that protects them from desiccation and disinfectants.

Staphylococcal skin disease Staphylococcus aureus is the most pathogenic staphylococci. Almost all pathogenic strains of S. aureus are coagulase- positive. Fibrin clots may protect the bacteria from phagocytosis and isolate them from other defenses. There is a high correlation between the bacterium's ability to form coagulase and its production of damaging toxins, several of which facilitate the spread of the organism in tissue, damage tissue, or are lethal to host defenses. In addition, some strains can cause life-threatening sepsis. Staphylococci produce:  Leukocidin- destroys phagocytic leukocytes.  Exfoliative toxin-responsible for scalded skin syndrome

Coagulase negative staphylococci

Staphylococcal skin disease Because this organism is so commonly present in human nasal passages, it is often transported from there to the skin. There it can enter the body through natural openings in the skin barrier, such as the hair follicle. Such infections, or folliculitis, often occur as pimples. The infected follicle of an eyelash is called a sty. A more serious hair follicle infection is the furuncle (boil), which is a type of abscess, a localized region of pus surrounded by inflamed tissue. Antibiotics do not penetrate well into abscesses, and the infection is therefore difficult to treat. Draining pus from the abscess is frequently a preliminary step to successful treatment. When the body fails to wall off a furuncle, neighboring tissue can be progressively invaded. The extensive damage is called a carbuncle, a hard, round deep inflammation of tissue under the skin. At this stage of infection, the patient usually exhibits the symptoms of generalized illness with fever.

Furuncle and Curbuncle

Staphylococcal skin disease (Impetigo) Staphylococci are the most important causative organism of impetigo. This is a highly contagious skin infection mostly affecting children 2 to 5 years of age, among whom it is spread by direct contact. Impetigo: painless, fluid filled blisters. The skin around the blister is usually red and itchy and become yellow brown crust. The other type of impetigo, bullous impetigo, is caused by a staphylococcal toxin and is a localized form of staphylococcal scalded skin syndrome (SSS). Actually, there are two serotypes of the toxin; toxin A, which remains localized, causes bullous impetigo, and toxin B, which circulates to distant sites, causes scalded skin syndrome. Both toxins cause a separation of the skin layers, exfoliation. Exfoliative toxin is an epidermolytic exotoxin which causes detachment within the epidermal layer.

Impetigo

Scalded Skin Syndrome Staphylococcal infections always carry the risk that the underlying tissue will become infected or that the infection will enter the bloodstream. The circulation of toxin, is called toxemia. One such toxin, which is produed by staphylococi lysogenized by certain phage types, causes Scalded Skin syndrome (SSS). This condition is first apparent as a lesion around the nose and mouth, which rapidly develops into bright red area and spreads. Within 48 hours, the skin of affected areas peel off in sheets when it is touched. SSS is frequently observed in children under age 2, especially in newborns, as a complication of staphylococcal infections.

Scalded Skin Syndrome

Streptococcal Skin Infections Streptococci are gram-positive spherical bacteria. Unlike staphylococci, streptococcal cells usually grow in chains. As streptococci grow, they secrete toxins and enzymes, virulence factors that vary with the different streptococcal species. Among these toxins are hemolysins, which lyse red blood cells. Depending on the hemolysin they produce, streptococci are categorized as alpha-hemolytic, beta-hemolytic, and gamma hemolytic (actually non hemolytic) streptococci. Hemolysins can lyse not only red blood cells, but almost any type of cell. It is uncertain, though, just what part they play in streptococcal pathogenicity. Beta-hemolytic streptococci are often associated with human disease.

Streptococcal Skin Infections The group A streptococci (GAS), which are synonymous with the species Streptococcus pyogenes, are the most important of the beta-hemolytic streptococci. They are among the most common human pathogens and are responsible for a number of human diseases- some of them deadly. Two important virulent properties are:  M protein-This protein is external to the cell wall on a fuzzy layerof fibrils. The M protein prevents the activation of complement and allows the microbe to evade phagocytosis and killing by neutrophils.  Hyaluronic acid-capsule of hyaluronic acid. Exceptionally virulent strains have a mucoid appearance on blood-agar plates from heavy encapsulation and are rich in M protein. Hyaluronic acid is poorly immunogenic (it resembles human connective tissue) and few antibodies against the capsule are produced.

M protein of Group A Streptococci

Streptococcal Skin Infections The GAS produce substances that promote the rapid spread of infection through tissue and by liquefying pus. Among these are streptokinases (enzymes that dissolve blood clots), hyaluronidase (an enzyme that dissolves the hyaluronic acid in the connective tissue, where it serves to cement the cells together), and deoxyribonucleases (enzymes that degrade DNA). These streptococci also produce certain enzymes, called streptolysins, that lyse red blood cells and are toxic to neutrophis.

Necrotizing fasciitis Some 15,000 cases of invasive group A streptococcal infection, caused by the "flesh-eating bacteria;' occur each year in the United States. The infection may be precipitated by minor breaks in the skin. and early symptoms are often unrecognized, delaying diagnosis and treatment- with serious consequences. Once established, necrotizing fasciitis, may destroy tissue as rapidly as a surgeon can remove it, and mortality rates from systemic toxicity can exceed 40%. Streptococci are considered the most common causative organism, although other bacteria cause similar conditions. An important factor is an exotoxin produced by certain streptococcal M- protein types, exotoxin A, which acts as a superantigen, causing the immune system to contribute to the damage. Broad-spectrum antibiotics are usually prescribed because of the possibility that multiple bacterial pathogens are present.

Necrotizing fasciitis Necrotizing fasciitis is often associated with streptococcal toxic shock syndrome (streptococcal TSS). In cases of streptococcal TSS, a rash is less likely to be present, but bacteremia is more likely to occur. M proteins shed from the surfaces of these streptococci form a complex with fibrinogen that binds to neutrophils. This causes the activation of the neutrophils, precipitating the release of damaging enzymes and consequent shock and organ damage.

Necrotizing fasciitis

Fungal disease of skin and nail Any fungal infection in the body is called mycosis. Cutaneous Mycoses: Fungi that colonize the hair, nails, and the outer layer (stratum corneum) of the epidermis are called dermatophytes. The dermatophytes secrete keratinase, an enzyme that degrade keratin and grow on the keratin present in those locations. Termed dermatomycoses, these fungal infections are more informally known as tineas or riugworm.

Fungal disease of skin and nail Tmea capitis, or ringworm of the scalp, is fairly common among elementary school children and can result in bald patches. This characteristic led the Romans to adopt the name tinea, Latin for clothes moth, because the infection resembles the holes left by the wormlike larvae of the moth in wool clothing. The infections tend to expand circularly, hence the term riugworm.

Dermatomycoses