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Multisystem Micro (Final) > Anaerobic Bacteria > Flashcards

Anaerobic Bacteria Flashcards

1
Q

General characteristics of anaerobic bacteria

A

Lack SOD

Generally lack catalase

Ferment

Cannot use O2 as terminal e- acceptor

Facultative = enterobacter

Obligate = ABC (Actinomyces, Bacteroides, Clostridium)

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2
Q

Where is anaerobic bacteria predominant within the body?

A

On ALL mucocutaneous surfaces

Orgal cavity, skin, GI, GU (female)

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3
Q

What “opportunity” does anerobic bacteria require before they cause an infection?

A

Tissue injury

+

Poor perfusion

Usually polymicrobial b/c other organisms help reduce O2 levels

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4
Q

Endogenous vs Exogenous infections

A

Greater amount of endogenous infections (trauma displaces anaerobes into places they are not normally found/deeper sites)

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5
Q

Tx for Anaerobic Bacteria

A

Surgical Debridement

Tissue drainage

Broad spectrum abx (clindamycin, cefazolin, etc.)

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6
Q

Gram (+), spore-forming rod

Obligate anaerobe

Non-motile

A

Clostridium perfringens

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7
Q

Most common invasive obligate anerobe

A

C. perfringens

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8
Q

Clinical presentation:

Cellulitis or

Gas gangrene or

Food poisoning

A

Clostridium

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9
Q

Pathobiology of gas gangrene

A

Spores in soil, introduced via deep muscle laceration (military wounds, automobile accidents, crude abortions, etc.), grows in anaerobic environment, and releases:

  • Alpha toxin (lecithinase) = muscle cell necrosis
    • Type of phospholipase that acts on lecithin
  • Degradative enzymes = subcutaneous bubbles (crepitus)

Look for tissue necrosis with NO PMNs

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10
Q

Gram (+)

Beaded Filaments

Not acid fast

Obligate anaerobe

A

Actinomyces israelii

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11
Q

Clinical presentation:

Abscesses (mouth, lung, GI tract, GU tract)

Draining sinus tracts

A

Actinomyces israelii

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12
Q

Pathobiology of actinomyces

A

NO PERSON-PERSON TRANSMISSION

(normal flora of oral cavity, GI tract, female GU tract)

Trauma/surgery disrupts mucosal barrier, local infection and inflammation, yellow sulfur granules develop (filamentous bacteria lined by proteinaceous coat) surrounded by PMNs, forms pus-filled abscess

Slow expansion to contiguous tissue (sinus tracts form, possible hematogenous spread)

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13
Q

Risk factors for actinomyces

A

Poor oral hygiene

Recent dental surgery (i.e., lumpy jaw after tooth infection)

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14
Q

Tx of actinomyces

A

Penicillin G

Surgical drainage of abscesses

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15
Q

“Most misdiagnosed disease”

A

Actinomyces is often confused with neoplasms

Forms long, branching filaments that resemble hyphae or fungi

Males 3x more likely to develop actinomycosis; for women, IUDs are a risk factor

Distiniguishing b/w Nocardia (only A. israelii forms sulfur granules and only Nocardia is acid-fast)

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16
Q

Gram (-)

Strict anaerobe

A

Bacteroides fragilis

17
Q

Clinical presentation:

peritonitis

GI or pelvic abscesses (“below the diaphragm”)

A

B. fragilis

Typically seen after a bout of appendicitis or diverticulitis

18
Q

Pathobiology of B. fragilis

A

Normal GI flora, ruptured intestinal mucosa (trauma, surgery, perforation), spills into peritoneum along with GI facultative anaerobes, survives oxygen environment via catalase and SOD, facultative anaerobes eventually deplete all oxygen, organism thrives and becomes numerically dominant

Local inflammation, purulent abscess formation (abscess serves as reservoir for organisms, which may spread causing shock)

19
Q

Can B. fragilis cause DIC?

(Disseminated Intravascular Coagulation)

A

No

It lacks typical Gram (-) endotoxin (i.e., LPS)

Only gram (-) without typical endotoxin, similar to how listeria is the only gram (+) with endotoxin

20
Q

Normally makes vitamin K for host (within GI flora)

A

Bacteroides species

21
Q

Anti-phagocytic polysaccharide capsule

B-lactamase producing

Can grow in bile

A

B. fragilis

22
Q

Prevotella melaninogenica (previously known as Bacteriodes melaninogenicus)

A

gram (-) rod anaerobe (along with Fusobacterium nucleatium)

Found in the upper airways and can cause pulmonary abscesses (Tx = penicillin G)

23
Q

Tx of B. fragilis

A

Drain abscess

Repair lesions

Abx (metronidazole, clindamycin)

24
Q

Thrombophlebitis of the jugular vein caused by

gram (-) rod anaerobes

Septic Emboli + Metastatic Infection

A

Lemierre’s syndrome (specifically caused by Fusobacterium species, which are indigenous to the oral cavity)

Occurs in young patients by progression from pharyngitis or dental infections and can be treated w/ ampicillin-sulbactam

25
Q

If a patient presents with Lemierre’s syndrome (or was recently infected with Fusobacterium nucleatum) what disease might you be worried about in the future?

A

Linked to COLON CANCER

26
Q

Antimicrobial tx of wounds (in the military) has lead to the emergence of what type of infections later on?

A

Invasive fungal infections

27
Q

Above waist anaerobic infection

A

Most likely dental origin (e.g., recent tooth infection)

Gram + : Peptostreptococcus, Proprionobacterium, Actinomyces

Gram - : Porphyromonas, Prevotella

Organisms typically sensitive to Abx

28
Q

Below waist anaerobic infection

A

Endogenous origin from GI (and GU for females)

Gram + : Peptostreptococcus, Clostridium species

Gram - : Bacteroides

29
Q

C. tetani

A

Produces tetanus toxin (tetanospasmin)

Neurotoxin that cleaves SNARE proteins (specifically synaptobrevin), preventing the release of GABA and glycine, which are inhibitor neurotransmitters

Result = sustained muscle contraction (i.e., tetany)

30
Q

C. botulinum

A

Produces botulism exotoxin (heat labile A-B neurotoxin)

Targets SNARE protein (specifically SNAP25), which prevents the release of acetylcholine. Symptoms include paralysis and respiratory compromise.

At risk population: consumption of improperly canned foods, traumatic injury, or babies ingest spores from honey (floppy baby syndrome)

Treatment = antitoxin and supportive therapy

31
Q

Is there natural immunity to C. tetani or C. botulinum?

A

No, they are too potent

Multisystem Micro (Final) (11 decks)

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