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57 terms

micro bacterial skin infections

STUDY
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staphylococcus aureus characteristics
1. g(+) aerobic clusters

2. possess catalase and coagulase → helps localize lesion

3. β hemolytic

4. toxins: α-toxin, TSST-1, exfoliatins

5. extracellular products: hemolysins, hyraluronidase, nuclease, lipase, protease

6. normal flora of skin and vagina

7. supf. and deep skin/ tissue infec., toxic shock, staph. pneumonia
s. aureus α-toxin
insertion of pores → causes membrane leakage → necrosis
s. aureus pyrogenic exotoxin
1. similar to GA strep pyrogenic toxin

2. stim. enhanced T-lymphoyte responses → release of cytokines
toxic shock syndrome
1. caused by pyrogenic exotoxin toxic shock syndrome toxin 1 (TSST-1)

2. stim. release of cytokines → rapid death

3. direct toxic effect on endothelial cells

4. high fever, vomiting, diarrhea, sore throat, and muscle pain → shock w/in 48hrs

5. skin rash and strawberry tongue

6. desquam. of skin deeper than scalded skin syn.
s. aureus exfoliatins
only some strains

splits stratum spinosum and stratum granulosum by disrupting intercellular jxns → sunburn effect

staph. scalded skin syndrome and bullous impetigo
cellulitis
staph., strep. pyogenes

1. infec. of skin and soft tissue

2. alt. btwn walling off and rapid extention of infec.
furnuncle
staph. aureus

localized boils devo in hair follicles

carbuncle = spread to multi hair follicles and adjacent tissues
chronic furunculosis
chronic furuncles due to hypersensitivity to staph. products → inflamm. and necrosis
impetigo
staph. aureus and GA strept.

1. small vesicles w/ erythema → pustular → honey colored crust

2. glomerulonephritis is a complication
scalded skin syndrome
exfoliatin absorbed into bloodstream → erythema and intraepidermal desquamation

staph. aureus not in desquamated sites
therapy for s. aureus
1. most strains susceptible to penicillin G → methicillin

2. methicillin resistant strains = MRSA

3. community acquired and health care assoc. MRSA → may need IV vancomycin

4. isolation of vancomycin resistant strains

5. VISA and hVISA are hard to detect
coagulase negative staphylococci
1. normal commensals: skin, nares, ear canals, mucous membranes

2. not β hemolytic

3. s. lugdunensis, s. epidermidis

4. must collect deep invasive samples to avoid normal flora contamination → must be present in multi cultures; multi colonies >15; (+) gram stain
s. lugdunensis
1. has some characteristics of s. aureus

2. abscess formation

3. must collect deep invasive samples to avoid normal flora contamination → must be present in multi cultures; multi colonies > 15; (+) gram stain
s. epidermidis
1. coagulase (-) staph.

2. forms biofilm on catheters, artificial heart valves, CSF shunts, hip replacements → protected form phagocytosis and antibiotics

3. must collect deep invasive samples to avoid normal flora contamination → must be present in multi cultures; multi colonies > 15; (+) gram stain
streptococci characteristics
1. g(+) chains

2. normal flora of oral cavity, GI, and genital tract

3. β hemolytic

4. GA = strep. pyogenes

5. GB = strep. agalactiae
group A toxin
1. pyrogenic exotoxin (SPE)

2. stim. release of cytokines

3. red rash on skin as seen in scarlet fever
pharyngitis
1. caused by GA strep. (may also be caused by GC or GG strep)

2. spread by aerosols or direct contact

3. carrier up to 1-4 wks after infec.
scarlet fever
1. caused by GA strep.

2. sore throat w/ rash

3. deep red cheeks, temples, buccal mucosa, strawberry tongue

4. sandpaper rash on trunk, arms, and legs

5. punctate hemorrhages on palate
acute rheumatic fever
poststreptococcal sequelae

1. inflamm. → fever, carditis, subcutaneous nodules, migratory polyarthritis

2. heart valve damage → murmurs, cardiac enlargement
acute glomerulonephritis
poststreptococcal sequelae

ds of childhood
1. lesions of glomeruli → 10 days after resp. infec. → recover after wks. or months

2. Ag-Ab complexes in kidney
erysipelas
1. GA strep infec. of skin and subcut. tissues

2. erythema and edema → rapidly spreading edges

3. pain, fever, lymphadenopathy

4. ususally on face

5. may be deadly if not treated
toxic shock like syndrome
1. strep. pyrogenes exotoxin

2. shock, diarrhea, rash, renal impairment, respiratory failure

3. multi organ
group B streptococci characteristics
strep. agalactiae

1. 30% women have GBS in normal vaginal flora

2. neonates can acquire through birth canal → lethargy, fever, sepsis, meningitis, resp. distress

3. older children and adults → fever before delivery, skin and soft tissue infec
viridans streptococci characterisitcs
1. α strep. that were rules not strep. pneumoniae

2. α hemolytic

3. normal flora of mouth, gut, and moist skin

4. treat w/ penicillin G
what are some examples of viridans streptococci species?
1. s. milleri → deep tissue abscess

2. s. mutans → dental caries and subacute endocarditis

3. s. mitis and s. salivarius → endocarditis
abiotrophia species
1. nutritionally deficient strep.

2. wont grow on blood agar w/o supplemental nutrients or vitamins

3. colonies resemble viridans or nonhemolytic strep.

4. causes endocarditis
enterococcus characteristics
1. g(+) cocci chains

2. GD strep. → nonhemolytic

3. normal flora in gut
what are the major species of enterococcus?
1. e. faecalis (is sensitive)

2. e. faecium (ultra mean) → resistant to ampicillin; more likely to be resistant to vancomycin than e. faecalis
what are some examples of enterococcus disease?
1. opportunistic infec.

2. endocarditis

3. urinary tract infec.

4. wound infec. in ICU mixed w/ e.coli or anaerobes
corynebacterium characteristics
1. g(+) rods → coccobacilli or irreg. rods

2. diptheria

3. corynebac. ulcerans → skin infec.

4. corynebac. jeikeium → nosocomial bloodstream and wound infec.
corynebacterium diptheriae
1. diptheria

2. impetigo like skin lesions
- common in tropics and native americans

3. blood agar for colony
- Tellurite and Loeffler's agars
erysipelothrix rhusiopathiae
1. g(+) rod

2. catalase negative

3. blood agar for colony

4. causes erysipeloid
erysipeloid
1. caused by erysipelothrix rhusiopathiae

2. painful slowly spreading skin infec.

3. treat w/ penicillin or erythromycin
where is there normal anaerobic flora?
1. predom. in stool

2. mouth, throat, GI, vaginal tract, skin (sebaceous gland)
what are the acceptable specimens for anaerobic culture?
1. abscess fluid aspirates

2. surgically removed tissue

3. blood cultures → 2 to 3 sets w/ 2 sticks each

4. supf. specimens from skin and wounds is NOT ACCEPTABLE
clostridium perfringens characteristics
1. g(+) spore forming rod → spores not seen in stains of tissue

2. fast growing anaerobic fermenter → produces ↑ H2 and CO2 → stormy litmus milk culture

3. encapsulated and not motile

4. found in colon and soil
what kinds of toxins does clostridium perfringens have?
1. α toxin: main pathogenic factor → ↑ necrotic growth

2. θ toxin → toxic to heart muscle and capillaries
- similar to streptolysin O (hemolytic toxin) in β strep.

3. enterotoxin → food poisoning
what are some mechanisms of pathogenesis of clostridium perfrigens?
1. toxins

2. fermentation of muscle carbohydrate → palpable gas → crepitation

3. destructive extracellular enzymes: collagenase, DNAse, hyaluronidase → spreading enzyme, protease
gas gangrene
1. c. perfringens

2. severe traumatic wounds → contaminated with dirt or feces → GSW or gallbladder surgery

3. rapidly life threatening → detect gas in infec. tissue

4. treated w/ surgical debridement and/or drain wound

5. 2° tx: hyperbaric chamber; penicillin
anaerobic cellullitis
1. clostridial infec. of wounds and surrounding subcut. tissue

2. gas formation

3. no gas gangrene toxicity → less pain and swelling
what are some non-spore forming g(+) anaerobic rods?
1. actinomyces

2. propionibacterium

3. mobiluncus

4. lactobacillus

5. eubacterium

6. rothia
lactobacillus characteristics
1. non-spore forming g(+) anaerobic rod

2. normal vaginal flora

3. if lactobacillus is replaced w/ mobiluncus → vaginitis
actinomyces characteristics
1. non-spore forming g(+) anaerobic rod

2. a. israelii is most common

3. can cause serious chronic infection: uterus w/ device; aspiration of pneumonia; abscesses in neck or head

4. may see pus in granules in infec. → sulphur granules
propionibacterium characteristics
1. non-spore forming g(+) anaerobic rod

2. normal skin flora

3. common blood culture contaminant

4. infec.: acne, prosthetic devices, part of mixed anaerobic infec.
bacteroides fragilis characterisitcs
1. g(-) anaerobic rod

2. most common

3. 10 species are penicillin resistant

4. capsule w/ antiphagocytic fxn
rickettsia characteristics
1. g(-) rod

2. insect vector transmission

3. infect vascular endothelium → RBC leaks from cells → fever w/ rash

4. manifestations: fever, headache, external rash and internal focal lesions, endotoxin like shock
how is rickettsial diagnosed?
1. culture is diff. and hazardous

2. PCR is the BEST method

3. enzyme immuno assays for Ab prdxn after infec. → look for rise in Ig

4. make clinical diagnosis for RMSF and treat immediately
rocky mountain spotted fever (RMSF)
1. caused by rickettsia ricketsii

2. occurs in warmer months; mostly by tick bite

3. incub. 2 - 14 days → RASH (palms and soles are key) on 2nd or 3rd day → fever, headache, confusion, myalgia
what is the treatment therapy for RMSF?
1. chloramphenicol for serious illness and in children < 8 YO

2. tetracyclin is a 2nd choice
rickettsiapox
1. urban ds caused by r. akari

2. transmitted by house mouse mite bite

3. benign self limiting illness

4. papulovesicle → fever → rash

5. tetracycline for tx
scrub typhus
1. caused by r. trutsugamushi

2. transmitted by rodent mites

3. lesions → maculopapular rash, eschar, splenomegaly, lymph
Louse-Borne typhys fever
epidemic typhus

1. caused by rickettsia prowazeki

2. transmitter to host via body louse

3. can cause gangrene due to compromised circulation
typhus fever
1. symptoms start 1 - 2 wks after louse bite → fever, headache, malaise, mylagia, rash

2. complications: CNS and heart

3. tx: tetracycline and chloramphenicol
recrudescent typhus
Brill's disease

1. relapse of louse borne typhus

2. 10 - 40 years after first infec.

3. rickettsiae remain dormant in reticuloendothelias cells

4. fading immunity of old age allows fading immunity of old age allows organism to attack again
borrelia burgdorferi
1. large spirochete

2. has toxic lipipolysaccharide

3. lyme ds
what are the clinical manisfestation of lyme?
1. 1° lesion °→ 3 - 30 days after tick bite → erthema chronicum migrans (ECM)

2. 2° → spirochetemia + systemic symptoms

3. late stage → few organs w/ immunological mediated damage
how is borrelia burgdorferi diagnosed?
1. organisms are present in low numbers in tissue

2. EIA for antibody plus western blot

3. PCR on if joint fluid