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33 Cards in this Set
- Front
- Back
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WHAT IS AN ANAEROBE?
Which can grow in the presence or absence of air? Predominant bacterial flora of mucocutaneous surfaces? Most infections are a result of ? |
Bacteria that grow in the absence of oxygen and fail to grow in 10% CO2 in air ( 18% O2)
Facultative anaerobes can grow in the presence or absence of air Anaerobes are the predominant bacterial flora of mucocutaneous surfaces Most infections are a result of breakdown of a mucosal barrier, leakage of flora into sterile sites |
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ROLE OF ANAEROBES IN NORMAL FLORA
What are the major reservoirs? Which are found in the mouth? Relative number in stomach/upper intestine? Relative presence of aerobes:anaerobes in the colon? Relative presence in the vaginal flora? |
Mucosal surfaces are major reservoirs– mouth, GI tract, female genital tract. There are 300-400 different anaerobic species in the human GI tract
In the mouth, 107 - 1011/ml anaerobes – prevotella, fusobacterium, porphyromonas, peptostrep Low numbers in stomach, upper intestine - 104/ml In the colon, anaerobes predominate 1000:1 over aerobes- 1012 anaerobes/g of feces. Bacteroides, fusobacterium, clostridium, peptostreptococcus Normal vaginal flora has 108 aerobes, 109 anaerobes - prevotella, bacteroides, clostridium, fusobacterium |
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KEY POINTS ECOLOGY, DISEASES
Grow in presence of? Major flora of __________ surfaces? Mouth? Lung? Colon? Vagina? CNS? Skin? |
Grow in absence of oxygen
Major flora of mucocutaneous surfaces Mouth 107( prevotella, fusobacterium, peptostrep)- sinusitis, otitis, dental abscess, spread to neck spaces Lung – abscess, emyema from oral aspiration Colon 1012(bacteroides fragilis, clostridium) – peritonitis, appendicitis, intrabdominal abscess Vagina 108(prevotella – PID, tuboovarian abscess, bacterial vaginosis, septic abortion CNS – solitary brain abscess, from otitis, sinusitis Skin – propionibacter, peptostreptococcus; necrotizing fasciitis, gas gangrene, diabetic ulcer |
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ANAEROBES - PATHOGENESIS
hallmarks: anaerobes cause? Acute/Chronic? What predisoposes to anerobic infection? |
Hallmarks – anaerobes cause suppuration, abscess formation, thrombophlebitis, tissue destruction with gas formation
Most infections are chronic, polymicrobial Lowered blood supply predisposes to anaerobic infection – especially trauma, shock, surgery, foreign body , vascular disease |
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ANAEROBES - VIRULENCE
Name them (4) 1/4: what inhibit phagocytosis, release chemokines, promote abscess formation; esp Bacteroides fragilis ? |
Synergy - anaerobic infections are frequently polymicrobial; facultative organisms lower O2, facilitate growth of anaerobes
Capsular polysaccharides inhibit phagocytosis, release chemokines, promote abscess formation; esp Bacteroides fragilis Exotoxins – produced in C. difficile diarrhea, tetanus, botulism, gas gangrene Beta lactamase production - bacteroides |
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KEY POINTS PATHOGENESIS
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Pus formation, abscess, gas in tissues
Most polymicrobial, chronic Decreased blood supply predisposes Synergy – many organisms isolated Virulence factors – exotoxins ( clostridia), capsular polysaccharides, beta lactamase (bacteroides fragilis) |
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ANAEROBIC INFECTIONS
Mouth/Head/Neck: |
chronic otitis media, chronic sinusitis, periodontitis, dental abscess, septic thrombophlebitis
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ANAEROBIC INFECTIONS
CNS |
brain abscess, subdural empyema
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ANAEROBIC INFECTIONS
Thoracic Cavity |
aspiration pneumonia, lung abscess, some empyemas
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ANAEROBIC INFECTIONS
Abdominal Cavity |
peritonitis, intrabdominal abscess, appendicitis, wound infection
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ANAEROBIC INFECTIONS
Pelvic Cavity |
PID, tuboovarian, vaginal abscess
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ANAEROBIC INFECTIONS
Skin/Soft Tissue |
gas gangrene, necrotizing fasciitis, bites, diabetic foot and decubitus ulcers
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Aerobic vs. anaerobic bacterial infections
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AEROBIC
S. pyogenes, H. influenzae Isolation, identification are easy Focal infections (lung, skin, injury sites) Easily cultivated Susceptibility tests routine Many antibiotics available for treatment ANAEROBIC B. fragilis, C. perfringens Special environments and media are required Mucosal sites (oral, intestinal, vaginal etc.) Harder to grow in culture No routine susceptibility testing Fewer effective antibiotics |
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Isolation of anaerobic bacteria
Appropriate specimens? Expel what? Antibiotic susceptibility testing? |
Appropriate specimens – blood, aspirates, pus, deep tissue. No swabs!
Expel air, cap syringe Anaerobic transport medium Anaerobic blood culture bottles Anaerobic sample processing , incubation environments Antibiotic susceptibility testing NOT` routinely performed on anaerobic bacterial isolates. Therefore, Rx must be empirical |
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CLINICAL SIGNS OF ANAEROBIC INFECTION
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Infection adjacent to mucosal surface
Foul smelling discharge Necrotic gangrenous tissue, abscess formation Free gas in tissue!! Bacteremia, endocarditis with no growth in aerobic blood cultures Infection related to tumors, destructive process Predisposing clinical conditions – bowel perforation, amnionitis, aspiration of oral flora Polymicrobial gram stain, but cultures fail to grow |
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KEY POINTS CLINICAL, DIAGNOSIS
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Foul smelling discharge, gas in tissues
Polymicrobial Gram stain, cultures negative Necrotic tissues, abscesses Leakage from mucosal surface ( perforation, aspiration) Culture blood, pus, aspirates, not swabs Anaerobic transport media, blood culture bottles, incubation environment Antibiotic susceptibility not done |
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KEY POINTS MANAGEMENT
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Anaerobic antibiotics – beta lactam inhibitor combinations, carbapenems, cefoxitin, metronidazole, clindamycin
Empirical antibiotic use, as isolation difficult and susceptibility not done Surgical drainage, debridement of necrotic tissue is essential |
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KEY POINTS CLOSTRIDIAL INFECTIONS
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Gram positive bacilli, produce toxins
C difficile spores spread in hospitals, cause antibiotic associated diarrhea, colitis Pseudomembranes; perforation, complications Diagnosis by stool toxin assay Treatment oral vancomycin, metronidazole C perfringens produces gas gangrene; aggressive debridement; Penicillin + clindamycin C tetani – spasms; toxoid booster for prevention C botulinum – descending paralysis ( food, wound) |
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HEAD AND NECK INFECTION
Most dental infections involve? Gingivitis and abscess can spread to? Severe cellulitis of sublingual, submandibular space is called? |
Most dental infections involve anaerobes
Cause gingivitis, abscess; can spread to mandible, deep neck spaces Ludwig’s angina- severe cellulitis of sublingual, submandibular space Prevotella, peptostrep, fusobacteria Amp/clav, clindamycin |
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CNS INFECTION
What kind of brain abscess do anerobes cause? Spreads FROM what usually? Treatment? What do you do if abscess is large? |
Solitary brain abscess is usually anaerobic
Spread from chronic otitis, mastoiditis, sinusitis Metronidazole plus ceftriaxone ( or penicillin) Drainage if large |
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PULMONARY INFECTION
If you suspect aspiration of oral flora, look for what? Usually affects which segments of lungs? Treatment? which do you NOT use? why? |
Aspiration of oral flora – look for gingivitis
Necrotizing pneumonia, lung abscess, empyema Dependent segments Mouth anaerobes Clindamycin, not penicillin ( beta lactamase production) |
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INTRAABDOMINAL INFECTION
Surgery? Treatment? |
Peritonitis, intra abdominal abscess
Perforated appendix, diverticulitis, surgery Rebound tenderness Polymicrobial SURGERY Abx combinations – cefepime or cipro + metronidazole, cefoxitin, pip/tazo, imipenem |
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PELVIC INFECTION
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PID, tuboovarian abscess, bacterial vaginosis, septic abortion, GYN surgery
Actinomycosis with IUD Polymicrobial; look for GC, chlamydia Drainage, anaerobic abx ( cefoxitin) plus doxycycline |
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SKIN AND SOFT TISSUE INFECTION
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Gas gangrene, bites, necrotizing fasciitis, diabetic ulcer
Look for deeper tissue involvement Polymicrobial ; gram positive anaerobes In genital infection, diabetes, aerobic gram negatives also Aggressive debridement, antibiotics |
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BACTEROIDES FRAGILIS
What kind of organism? |
Nonspore gram-negative bacilli
Produces beta lactamase Predominant colon flora Major part of intra-abdominal infections, forms abscess Use anaerobic antibiotics |
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FUSOBACTERIUM
What kind of organism? Where is it found? Resistance? Causes what syndrome? |
Long, thin anaerobic gram negative bacilli
Oral, lung, brain infection Resistance to penicillin – beta lactamase Lemierre syndrome is a lateral pharyngeal space infection associated with septic thrombophlebitis of the jugular vein |
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CLOSTRIDIUM DIFFICLE
What kind of organism? How does it manifest? How is it spread/transmitted? Spores pass through ______, multiply in _________? Disruption of normal by ___________, and ____________, can increase propensity of these to infect Occurs ________ days after antibiotic treatment? (range:??) Which antibiotics has it been seen with? Where is it found? Resistance? Causes what syndrome? |
Gram positive spore forming anaerobic bacillus
Causes 20-30% of antibiotic associated diarrhea, 50-75% of antibiotic associated colitis, >90% of pseudomembanous colitis Hospital environment contaminated with spores; spread by poor hand hygiene from HCW to pts Spores pass through stomach unscathed, multiply in colon Disruption of normal flora by antibiotics, chemotherapy Occurs 5-10 days after abx (1 day – 10 weeks) Cephalosporins, ampicillin, clindamycin – although any antibiotic can be involved |
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CLOSTRIDIUM DIFFICILE - 2
What toxins mediate pathogenesis? What does colonic mucosa look like? How does it affect infants? why? How do you diagnose? How useful is culture? Endotoxin shows? |
Toxin A, B – potent toxins, lead to cytoskeleton disruption, mucosal injury, fluid secretion
Colonic mucosa is studded with white and yellow plaques (pseudomembranes) Infants are protected ( lack toxin receptors) Diagnosis – assay for toxin ( cytotoxicity or EIA) Culture not useful – some nontoxigenic strains Endoscopy shows pseudomembranes |
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CLOSTRIDIUM DIFFICILE - 3
Complications? Treatment? Recurrence? |
Complications – fulminant colitis, perforation, toxic megacolon; may require surgery
Rx–metronidazole effective, cheap; oral vanco (for severe illness) Recurrence is a common problem |
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CLOSTRIDIUM PERFRINGENS
Causes? Normally found in? Produces? Associated with what other comorbidities? Treatment? what do you add (binds toxin)? Can it cause food poisoning? |
Gas gangrene, necrotizing fasciitis, myonecrosis
Ubiquitous in soil and stool Produces toxins, some lethal Gas (H2, N2) production Seen with trauma, surgery, septic abortion, vascular insufficiency, cancer Aggressive debridement Penicillin + clindamycin (binds toxin) Enterotoxin - food poisoning |
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CLOSTRIDIUM TETANI
(inexcusable disease: should not see this) |
Toxin is tetanospasmin
Enters CNS, induces failure of neuromuscular transmission; no inhibition of motor neurons - spasms Tetanus is preventable in almost all patients- give toxoid booster every 10 years Thus, “the inexcusable disease” |
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CLOSTRIDIUM BOTULINUM
How many neurotoxins? that cause what? how? Treatment? |
7 potent neurotoxins
Prevent ACH release, causes paralysis Foodborne (preformed toxin), infant (GI tract), wound (colonization), inhalation (aerosol) Descending paralysis Supportive care, antitoxin |
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ACTINOMYCOSIS (Actinomyces israelii )
Normal flora? Gram? shape? acid-fast? _______ granules in tissues (clumped organisms) Course of infection? What can it cause? What does it do to tissue planes? Treatment? confused with nocardia (acid fast+) |
Normal oral, GI flora
Gram + branching bacilli, not acid - fast Sulfur granules in tissues (clumped organisms) Indolent infection Cervicofacial, lung, abdominal, pelvic (IUD) Extends through tissue planes, like malignancy (eats through tissue planes) Penicillin (for long time since this is a chronic infection) or doxycycline, clindamycin |
