Anaerobes Flashcards
Factors that affect anaerobic growth?
low oxidation reduction potential
absence of oxygen
Oxidation-reduction potential (Eh) related to anatomic site?
- 50 periodontal pocket
- 200 dental plaque
- 300 colon
Anaerobes lack certain enzymes?
superoxide dismutase, catalase, peroxidase
inability to remove oxygen radicals, radicals kill the bacteria
General considerations about anaerobes?
prominant GI normal flora
most infections are ploymicrobic
not communicable
Clinical findings of anaerobic infections?
foul smelling discharge necrotic tissue with gas block discolor of blood contain exudate oragnsisms seen on Gram stain fail to grow aerobic proximal to mucosal surface vascular insufficiency infections follow human/animal bites infections follow sever trauma
Incidence of anaerobes in infections?
60-100% intraabdominal pelvic abscess
50-100% dental, chronic sinusitis
60-90% brain abcess
20-50% aspiration pneumonia
Lab diagnosis?
collect specimen
aspirate pus with a needle and syringe
swabs- obtain specimen and immediately immerse in a reduced transport medium
if contaminated with aerobic flora, unacceptable for culture
Gram stain?
pleomorphic or have distinctive morphology
Culture?
requires special media -Kanamycin-vanco agar -reduced anaerobic blood agar -thioglycerate broth anaerobic conditions (N 85%, H 10%, CO2 5%) most are slow growing
Bacteroides fragilis?
light stain, gram neg rods, pleomorphic
grow relatively rapidly, stimulated by bile
human gut, female genital tract
capsule
extracellular enzymes- collagesnase, hylauronidase
weak or no endotoxin
infections- GI abscess, pelvic inflammatory disease, cellulitis
Prevotella melaninogenicus?
gram neg coccobacilli to short rods
brick red fluoursecence under wood lamp
distinctive black colonial apperance on agar
oral flora
low number in GI tract
oral and brain abscesses, lung abscess, female genital tract abcess
Treatment Prevotella melaninogenicus?
Debiedment and drainage (cellulitis and severe abscesses)
metronidazole (DOC)
clindamycin
Metronidazole moa?
targets DNA synthesis
disrupts DNA helical structure under anaerobic conditions
Fuscobacterium nucleatum?
gram neg, long, slender filaments and fusiform rods
oral cavity, occasional stool
head, neck, chest infections
-syngerizes with oral spirochetes to form trench mouth or Vincent’s angina
Peptostreptococcus and other anerobic streptococci?
normal habitat-mouth or stool
infections cause syndergistic infections with S. aureus and Bacteroides sp.
brain abscesses, head infections
Actinomyces israelii?
only one that is anaerobic
gram pos branching rods
produce sulfer granules in abscesses and culture
Clostriduium perfringens?
gram pos rods
forms spores
most path due to toxins
requires low Eh potential
Clostriduium perfringens habitat?
soil, GI tract
Clostriduium perfringens clinical?
severe cellulitis and myonecrosis (gas gangrene) associated with high mortality
food poisoning
Clostriduium perfringens virulence factors?
exotoxins
- alpha
- theta
alpha toxin?
degrades mamalian cell membranes
theta toxin?
pore forming cytotoxin causes lecukocyte destruction and vascular damage
Myonecrosis (gas gangrene)?
C. prefringes infects soft tissue following severe trauma- organism multiply, toxins, utilize glycogen– gas, edema, impair cirulation- vascular destruction and lactic acid buildup lowers redox potential- cellulitis- myonecrosis- shock and renal failure
Lower redox potential in myonecrosis?
greater the damage
lab diagnosis Clostriduium perfringens?
gram stain; gram pos box car like rods
culture: distinctive double zone of hemolysis
Treatment Clostriduium perfringens?
cellulitis and myonecrosis
-debride wound
DOC- penicillin and clindamycin
Food poisoning- self limiting without treatment
Clostridium difficile cause?
pseudomembranous colitis
Clostridium difficile virulence factors?
toxin A (enterotoxin)- fluid production and mucosal damage
Toxin-B (cytotoxin)- kills mucosal cells
Lab diagnosis Clostridium difficile?
Clostridium difficile toxin assay
Treatment Clostridium difficile?
metronidazole (vancomycin)
