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Ch.19 L.3 (Staphylococcal Scalded Skin Syndrome (Epidemiology (Primarily a…
Ch.19 L.3
Staphylococcal Scalded Skin Syndrome
Pathogen and virulence factors
5% of strains of Staphylococcus aureus secrete one or two distinct exfoliative toxins which cause SSSS
Both of these toxins affect keratinized cells of the epidermis
Diagnosis
made by the distinctive sloughing of the skin
Epidemiology
Primarily a disease of infants and children under the age of 5.
It can affect the elderly, immunosuppressed patients, like those with AIDS
Transmission is by person to person spread of the bacterium onto skin surfaces and then the pathogen will penetrate cuts and abrasions.
Treatment
IV drugs like semisynthetic nafcillin or oxacillin that do not let β-lactamase to bind (remember that β-lactamase deactivates many drugs in the PCN class)
Pathogenesis
No scarring because the epidermis is unaffected by the toxin. The body restores the lost epidermis within 7-10 days.
The blood carries these toxins from the site of infection throughout the body. This circulation of toxins in blood is called toxemia
Mortality (death) is rare but if one does die, it is from a secondary infection of skinless areas by yeast like Candida albicans or by a bacteria like Pseudomonas aeruginosa
Prevention
Little can be done to prevent SSSS because S. aureus is normally on the skin
What is it?
What happens is cells of the outer epidermis separate from one another and from the underlying tissues.
Signs and Symptoms
Reddening and wrinkling of the skin usually near the mouth, spreads over entire body
Large blisters that have clear fluid (no bacteria)
Within 2 days skin peels off in sheets (flesh having been dipped into boiling water)
Impetigo (Pyoderma and Erysipelas)
Epidemiology
Both Staph & Strep spread by person to person contact or via fomites (toys, clothing, bedding, towels, or hairbrushes)
Epidemics of impetigo in nurseries are of concern
Erysipelas occurs most commonly in children and elderly
Children ages 2-5 are most likely to get/develop impetigo
Diagnosis
Vesicles of impetigo
Pathogenesis
Some strains of S. pyogenes may spread from impetigo or erysipelas into the blood (bacteremia) and then to the kidneys, where acute glomerulonephritis can result
Bacteria occasionally colonize the skin and then invade through scratches , abrasions, cold sores or other wounds
Children are often infected just below the nose(frequent wiping will abrade the skin
Treatment
oral and topical antimicrobials(mupirocin, oral clindamycin, doxycycline)and careful cleaning of infected areas
Pathogen and virulence factors
Most cases are caused by S. aureus in 80% of cases
20% of cases involve S. pyogenes alone or with S. aureus (both together is group A Strep.
Virulence factors add to impetigo
Hyaluronic acid
serves as a camouflage for the bacteria, hiding it from phagocytosis
Pyrogenic toxins proteins
stimulate macrophages and helper T-lymphocytes to release cytokines that will in turn stimulate fever, widespread rash, and shock
M protein
cytoplasmic membrane that destabilizes complement and interferes with phagocytosis
Prevention
proper hygiene and cleanliness
Signs and Symptoms
Vesicles are oozing, puss filled on a red base. They eventually break and form a thick sticky crust that is attached to the skin and cause intense itching
Small, flattened, red patches appear on the face and limbs
End up with numerous vesicles at different stages of development because bacteria will spread to other areas
erysipelas
When the infection spread into surrounding lymph nodes and triggers pain and inflammation the condition is called