Anaerobic Infections

Question 1

1. 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

Answer 1

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

Question 2

2. Discuss the clinical syndromes caused by the anaerobes present in mouth head and neck.

Answer 2

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)

Question 3

3. Explain the concept of the anaerobic microenvironment and cite examples.

Answer 3

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

Question 4

4. Discuss the mechanism by which anaerobic bacteria cause human illness.

Answer 4

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)

Question 5

5. Discuss the general principles of diagnosis and treatment of anaerobic bacterial infections.

Answer 5

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

Question 6

6. Recognize the clinical scenarios that should prompt the clinician to consider anaerobes as pathogens.

Answer 6

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

Question 7

Rate the best drugs for treating anaerobic infections

Answer 7

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

Question 8

Describe risk factors for anaerobic infection.

Answer 8

occlusion of airway or vasculature

malignancy
diabetes
trauma
immune compromise (chemo)
foreign bodies
antibodies (select out anaerobes)

Question 9

2. Discuss the clinical syndromes caused by Bacteroides.

Answer 9

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

Question 10

2. Discuss the clinical syndromes caused by Fusobacterium.

Answer 10

F. necrophorum (long thin rods)
mouth and gingival flora, causing much disease due to poor dentition
major virulence factor is their active endotoxin

Question 11

2. Discuss the clinical syndromes caused by Peptostreptococcus.

Answer 11

(#2 most common) located in mouth, GI and GU tracts; nearly always with mixed flora

virulence factors are poorly understood

Question 12

Describe the pathogenesis of Ludwig’s angina and Lemierre’s syndrome.

Answer 12

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

Question 13

Name clinically relevant anaerobes in the oral cavity.

Answer 13

Peptostreptococcus
Provotella
Fusobacterium
Bacteriodes spp. (non B. fagilis)
Actionmyces

Question 14

Name common anaerobes of the GI tract.

Answer 14

Bacteriodes fragilis
Peptostreptococcus
Fusobacterium
Clostridia

(aerobes: E.coli, Klebsiella, Enterobacter, Staph, strep, enterococci)

Question 15

2. Discuss the clinical syndromes caused by the anaerobes present GI tract

Answer 15

peritonitis: primary (infection of ascitic fluid), secondary peritonitis (bacterial contamination of peritoneal cavity after breach of GI)
intra-abdominal abscess
liver abscess

Question 16

Name organisms of GU tract.

Answer 16

Prevotella
Peptostreptococcus
Bacteriodes fragilis group
Clostridia

Question 17

2. Discuss the clinical syndromes caused by the anaerobes present GU (GYN) tract

Answer 17

endometritis (C. perfringens)
tuboovarian abscesses and PID
bacterial vaginosis (decline in Lactobacilli and other normal flora)

Question 18

Discuss clinically relevant SSTI and their associated orgs.

Answer 18

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)

Question 19

____ ___ is the most frequently isolated anaerobe from blood cultures, its most common sources being GI, female, GU, lung or soft tissue.

Answer 19

B. fragilis group

Question 20

List the key characteristics of Clostridia.

Answer 20

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

Question 21

Discuss pathogenesis and tx. of tetanus.

Answer 21

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)

Question 22

Discuss pathogenesis and tx. of botulism.

Answer 22

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)

Question 23

Discuss pathogenesis and tx. of gas gangrene.

Answer 23

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)

Question 24

Discuss pathogenesis and tx. of C. difficile.

Answer 24

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

Question 25

Endotoxin is also known as what?

Answer 25

LPS- lipopolysaccharide

Question 26

Discuss pathogenesis and tx. of food poisoning by C. perfingens.

Answer 26

food borne illness due to improper temp control of foods prepared ahead of time (meats, poultry, gravy)

produce toxin in-vivo (8-16hrs) causes abdominal cramps, diarrhea, ending in 24hrs, vomitting is rare