Anaerobic Infections Flashcards
- Name the major genera and (where applicable) the principle species of each microbe responsible for most human ANaerobic bacterial infections caused by Gram (-) rods, gram (+) cocci and gram (+) baccili
anaerobes reside on mucus membranes and in anaerobic micro environments (i.e. synergy with aerobic)
Gram negative rods: Bacteroides spp. Fusobacterium spp. Prevotella spp. Porphyromonas spp.
Gram positive cocci:
Peptostreptococcus spp.
Gram positive rods
Clostridia spp. (spore forming)
Actinomyces spp.
Propionibacterium
- Discuss the clinical syndromes caused by the anaerobes present in mouth head and neck.
periodontal disease and gingivitis
necrotizing gingivitis (immunocomp)
deep tissue infection (Ludwig’s and Lemierre’s)
chronic sinusitis and chronic OM
aspiration pneumonia (thick fetid sputum)
lung abscess (fetid sputum)
empyema (infection of the pleural space)
- Explain the concept of the anaerobic microenvironment and cite examples.
a small area where oxygen does not readily reach like a gingival creases with poor dentition or created by the metabolism of aerobic and facultative bacteria
- Discuss the mechanism by which anaerobic bacteria cause human illness.
they are a normal part of flora
reside primarily on mucus membranes and can lead to barrier disruption
can cause infection in devitalized tissue
toxin mediated (Clostridia and endotoxin mediated tetanus, botulism and pseudomembranous colitis)
- Discuss the general principles of diagnosis and treatment of anaerobic bacterial infections.
diagnosis: ‘sterile pus,’ anaerobes are fastidious and require appropriate handling and processing
treatment: requires source control and debridement along with antibiotics with anaerobic activity
some toxin mediated disease require active or passive immunization
- Recognize the clinical scenarios that should prompt the clinician to consider anaerobes as pathogens.
infectious disease syndrome with likelihood of having anaerobic bacteria(intra-abdominal abscess, brain abscess, diabetic foot infection)
syndrome recognition (ie. botulinum)
sites close to mucosal surfaces (GI, GU, oral)
clostridia toxin-mediated diseases
failure to respond to antibiotics that did not cover anaerobes
sterile pus- especially with mixed bacteria on gram stain and a negative culture
Rate the best drugs for treating anaerobic infections
excellent: metronidazole, carbapenems, B-lactamase inhibitor combos, tigecycline, moxifloxacin
clindamycin best for anaerobes above the diaphragm
vancomycin and penicillin for gram positive only
cefoxitine: moderate activity
Describe risk factors for anaerobic infection.
occlusion of airway or vasculature
malignancy diabetes trauma immune compromise (chemo) foreign bodies antibodies (select out anaerobes)
- Discuss the clinical syndromes caused by Bacteroides.
gram negative rod
B. fagillis: (most common with increasing drug resistance through B-lactamases to B lactams and clindamycin) causes abscess formation, more GI specific
Other: mouth and GU tract
- Discuss the clinical syndromes caused by Fusobacterium.
F. necrophorum (long thin rods)
mouth and gingival flora, causing much disease due to poor dentition
major virulence factor is their active endotoxin
- Discuss the clinical syndromes caused by Peptostreptococcus.
(#2 most common) located in mouth, GI and GU tracts; nearly always with mixed flora
virulence factors are poorly understood
Describe the pathogenesis of Ludwig’s angina and Lemierre’s syndrome.
Ludwig’s: ST infection of submandibular and sublingual spaces that can lead to respiratory compromise by elevating floor of mouth and pushing tongue posteriorly
Lemierre’s syndrome: ST infection of the lateral pharyngeal space with suppurative thrombophlebitis of the jugular vein leading to septic pulmonary emboli and bacteremia with Fusobacterium necrophorum
Name clinically relevant anaerobes in the oral cavity.
Peptostreptococcus Provotella Fusobacterium Bacteriodes spp. (non B. fagilis) Actionmyces
Name common anaerobes of the GI tract.
Bacteriodes fragilis
Peptostreptococcus
Fusobacterium
Clostridia
(aerobes: E.coli, Klebsiella, Enterobacter, Staph, strep, enterococci)
- Discuss the clinical syndromes caused by the anaerobes present GI tract
peritonitis: primary (infection of ascitic fluid), secondary peritonitis (bacterial contamination of peritoneal cavity after breach of GI)
intra-abdominal abscess
liver abscess
Name organisms of GU tract.
Prevotella
Peptostreptococcus
Bacteriodes fragilis group
Clostridia
- Discuss the clinical syndromes caused by the anaerobes present GU (GYN) tract
endometritis (C. perfringens) tuboovarian abscesses and PID bacterial vaginosis (decline in Lactobacilli and other normal flora)
Discuss clinically relevant SSTI and their associated orgs.
common pathogens: Bacteriodies, Peptostreptococci, Clostridia
causing
diabetic foot infections
pressure ulcers
necrotizing faciitis (classically Founier’s gangrene)
bite wounds
contiguous ostomyelitis (ie. extension of diabetic foot infection)
____ ___ is the most frequently isolated anaerobe from blood cultures, its most common sources being GI, female, GU, lung or soft tissue.
B. fragilis group
List the key characteristics of Clostridia.
large boxy Gram positive rods that produce spores which are able to survive long periods of time in the environment and GI tracts of many animals
well known for producing toxins
Discuss pathogenesis and tx. of tetanus.
Clostridium tetanus gram positive rod (tennis racket) found in soil that produces potent toxin (tetanospasmin- travels retrograde to CNS to terminals of inhibitory cells) that prevents release of inhibitor neurotransmitters (truisms- lockjaw, increased body temp)
tx. includes IC supportive care, esp. for the airway/ventilation, benzos for spasm control and human tetanus immune globulin (less commonly metronidazole and wound debridement) requires weeks to months treatment
Complications include laryngospasms, fractures, autonomic hyperactivity, pulmonary embolism, aspiration pneumonia)
Discuss pathogenesis and tx. of botulism.
C. botulinum is a gram positive rod (soil and marine) with large spore distribution producing a very potent neurotoxin preventing pre-synaptic release of acetylcholine leading to weakness and flaccid paralysis (cranial nerve abnormalities first)
food borne (15%) ingestion of preformed toxin infant (65%): ingestion of spores germinate in colon wound botulism (20%) (longer time course) inhalation botulism (biowarfare)
sym. acute bilateral cranial nerve dysfunction, descending motor weakness, afebrile
tx. supportive care and trivalent antitoxin (danger of hypersensitivity), human botulinum immune globulin used in infant botulism
wound debridement and antibiotics (penicillin)
Discuss pathogenesis and tx. of gas gangrene.
C. perfringens us a gram-positive rod (boxcar) responsible for most cases of ST infection gas gangrene and also GI tract illness
produces lethicinase (a toxin) and hemolysi (Φ toxin) and is often associated with foreign body trauma (lesser extent colon cancer)
signs include rapid evolution of crepitus with magenta or bronze appearance, hemorrhagic bullae and thin dirty brown wound discharge
tx. with early aggressive surgical debridement along with antibiotics (penicillin plus clindamycin)
Discuss pathogenesis and tx. of C. difficile.
most common cause of nosocomial diarrhea, toxigenic disease produced by organisms that reside as spores in the environment or colon
germinate under antibiotic use often and produce exotoxins A and B that cause mucosal damage and diarrheal illness (including pseudomenbranous colitis
dx. via PCR for toxin in stool
tx. contact isolation, stop all unnecessary antibiotics to allow repopulation of colonic flora, antibiotics (oral/ IV metronidazole, oral/rectal vancomycin) IVIG and lastly colectomy
relapses in individuals that lack IgG to toxins: avoid unnecessary antibiotics, retreat with oral vancomycin, probiotics, rifaximin, fidaxomicin and fecal transplantation
