Skin Infections: Chapter 23- Normal Microbiota of the Skino large numbers of microorganisms live on/in the skino numbers depend upon location and moisture contento skin flora are opportunistic pathogenso most in 3 major groups: diphtheroids staphylococci yeastso Diphtheroids named for resemblance to Corynebacterium diphtheriae Gram-positive bacteria with variable shape (often club) low virulence, no toxins responsible for body odor due to bacterial break-down of sweat common skin diphtheroid = Propionibacterium acnes in acne feed on trapped sebum in blocked hair follicleso Staphylococci Gram-positive, salt-tolerant principle species = Staphylococcus epidermidis prevent colonization of pathogenic flora on skin Maintains balance among microbial skin florao Fungi (yeasts) eukaryotes tiny lipophilic (feed on lipids) yeast on normal skin from late childhood throughout life very common and generally harmless in some can cause skin conditions such as scaly rash, dandruff or tinea versicoloro Tinea versicolor- Hair Follicle Infections o Folliculitis small red bump or pimple often hair can be pulled => infectionresolves if infection spreads from follicle toadjacent tissues => a furuncle or boil =>localized redness, swelling, tenderness o Furuncles pus often drains from the lesion with aplug of inflammatory cells and deadtissue numerous furuncle lesions produce a carbuncleo Carbuncles large areas of redness, swelling,tenderness – often fever, etc numerous sites of draining pus usually develop in areas where skin is thick Ex. back of the necko Causative Agent- most hair follicle infections caused by Staphylococcus aureus- spreading to subcutaneous tissue => larger abcess- systemic spread can lead to infection of the heart, bones and brain- more virulent than more common staphylococci on the skin, in nostrils- a very significant pathogen responsible for numerous medical conditions Staphylococcus aureus – two important virulence factors among many- coagulase - not an enzymeo coagulase + prothrombin => staphylothrombin converts fibrinogen -> fibrin => blood clotso some coagulase on Staph aureus surface => coated with fibrin = protection from phagocytosis- clumping factoro attaches Staph aureus to fibrinogen and fibrin in woundso catheters, etc become fibrinogen-coated quickly after insertion => aids Staph. aureus colonization there- Scalded Skin Syndromeo Staphylococcal scalded skin syndrome (SSSS) primarily in infants potentially fatalo Causative Agent Staphylococcus aureus- Disease due to production of toxin exfoliatin toxin destroys integral layers of the outer epidermis tox genes either on plasmid or on the chromosomeo Symptoms skin appears burned (scalded) first: generalized redness other symptoms: malaise, irritability, fever nose, mouth and genitalia may be painful before other indicators become apparent within 48 hours, - skin becomes red, wrinkled- large fluid-filled blisters form- skin is tender to the touch, may feel rougho Pathogenesis toxin released at - even a small - infection  spreads to larger areas of skin toxin => splits the epidermis just below dead keratinized outer layer outer layer of skin detaches => marked body fluid loss susceptibility to secondary infection such as Candida, Pseudomonas Mortality rates can reach 40% depends on prompt diagnosis, prompt treatment, patient age and overall healtho Epidemiology 5% of S. aureus strains produce exfoliatins SSSS in any age group- mainly infants, the elderly and immuno-compromised Transmission person-to-person- cases usually isolated; small epidemics can occur in nurserieso Prevention  protective patient isolation- limits spread of infection and exposure to potential secondary pathogenso Treatment penicillinase-resistant penicillin removal of dead skin to prevent secondary infection- Lyme Diseaseo recognized in mid-1970’s in Lyme, Connecticuto Symptoms First Stage- erythema migrans (skin rash)- swollen lymph nodes- rash: small red spot at the site of tick bite slowly enlarges- other symptoms are influenza-like (malaise, chills, fever, headache, stiff neck, joint andmuscle pain and backache) Second Stage- 2 to 8 weeks post-rash- Involves heart and nervous systemo electrical conduction in heart impaired => dizziness, faintingo paralysis of facial muscleso impaired concentration, emotional upset Third Stage- arthritiso usually large joints such as kneeo develops in 60% of untreatedo within 6 months after rasho slow disappearance over years- chronic nervous system impairment may occur, depressiono Causative Agent Borrelia burgdorferi- large (10 x 25 um)microaerophilic spirochete- Lyme’s is a zoonosis introduced into skin through bite of infected tick- humans are accidental hostso in skin, bacteria migrate outward in radial fashiono inflammation causes an expanding rasho Epidemiology disease is a zoonosis widespread in USA several tick species implicated as vectors- most important is black-legged tick, Ixodes scapularis- nymph stage seeking blood mealn is mainly responsible for transmitting diseaseo Prevention check for ticks!o Treatment antibiotics relatively effective in early stage less effective in late disease probably because bacteria are not actively multiplying prolonged IV ampicillinViral Skin Disease- Varicella Chicken Pox popular name for varicella very common rash among children incidence declined due to vaccination produces a latent infection that becomes reactivated after recovery of initial illness reactivated disease = shingleso Symptoms - most cases mild, recovery uncomplicated more severe symptoms in older children and adults 20% of adults develop pneumonia rash - appears on back of head, face, mouth- rash is diagnostic- lesions progress: red spots (macules) -> small bumps (papuales) -> small blisters (vesicles) -> pus filled blisters (pustules)- lesions itch and appear at different times- healing begins after pustules break and crust over major threat to newborn- can lead to Congenital Varicella Syndrome if mother develops disease in few days before and after birth- high mortality / severe birth defectso Sequellae include Shingles (= herpes zoster)- reactivation of dormant virus- most commonly rash around waist Reye’s Syndrome- vomiting and coma- especially in children ages 5-15- liver