anaerobes Flashcards
3 “diseases” associated with Clostridium perfringens
- gas gangrene (toxin)
- intra-abdominal infections (toxin or vegetative)
- Food poisoning (toxin)
Clostridium perfringens structure/identifying characteristics
Gram positive Non-motile Encapsulated Forms spores Double zone hemolysis
Gas Gangrene from Clostridium perfringens
• Pathogenesis
- Trauma with devitalized tissue/muscle
(usually a deep wound like a puncture by farm equipment)
- Spores of C. perfringens, C. novyi, C. septicum, C. ramosum germinate quickly
- Extremities, endometrium, abdominal wall
• Typing A-E – based upon combination of toxins produced by organism
(type A most common in US)
Clostridium perfringens toxins
** α toxin –lecithinase (phospholipase C), lysis of inflammatory cells, tissue destruction (muscle) –keeps the bacteria protected from the immune system (drain the bullae the organism will be present by no WBC)
β-toxin- enteritis necroticans (pig bel)
i – necrosis and vascular permeability
-ε toxin- Systemic, vascular permeability
Θ toxin -Cardiotoxic
clinical presentation of gas gangrene
Rapid onset (6 - 72 hr) necrosis of muscle (myonecrosis), skin tense edema bullae formation ** gas formation (fermentation) (=crepitus)
Systemic
shock
hyper or hypothermia
gas gangrene treatment
- debridement, debridement, debridement
- antibiotics (penicillin, B-lactam/inhibitor)
clindamycin (stops toxin production)
very susceptible to pcn but the devitalized tissue has no blood flow therefore must be amputated
Clostridium perfringens food poisioning
• Heat resistant spores survive gravy, soups • enterotoxin- produced following germination of large numbers of organisms (different than toxins involved in gas gangrene) • Clinical 8 - 24 hr after ingestion nausea, abdominal pain, diarrhea • self-limiting/ usually not treated
Clostridium tetani spread
puncture wounds
burns
umbilicus
local germination without necrosis
Tetanospasmin
neurotoxin (plasmid borne)
blocks postsynaptic inhibition spinal motor reflexes (GABA)
Spasmotic contractions (uninhibited reflexes)
Clostridium tetani symptoms
- trismus (lockjaw)
- risus sardonicus (increased tone orbicularis oris)
- **opisthotonus (arm flexion, leg extension)- classic rigid appearance
- Respiratory (obstruction, diaphragm)
Treatment of tetnus
- Human tetanus immunoglobulin (HTIG) (will bind any unbound toxin but cannot reverse what has already bound)
- Sedation
- Control of spasms
- supportive (airway)
Clostridium botulinum most commonly comes from
Home canning fruits/vegetables, fish
preformed toxin from contaminated food
spores in honey (infants)
12 - 36 hrs after ingestion
spores are very very heat resistant (needs pressure + heat to kill the spores)
Clostridium botulinum toxin
large single polypeptide (150-165 Da) cleaved by bacterial protease most potent toxin in nature blocks acetylcholine no transmitter release = paralysis synapse permanently damaged can travel axons heat labile (toxin is killed by boiling 10min)
causes permanent damage therefore synapses must be remade
clinical symptoms of botulism
• GI (nausea, dry mouth, diarrhea)
• descending** paralysis (flaccid) cranial (III, IV, VI) (begins with eyes and moves down the body) symmetric neurologic effects afebrile patient conscious heart rate normal no sensory deficits
• Wound botulism
Prevention/Treatment of botulism
avoid contaminated food
heating of food (boiling)
antitoxin (equine serum to A,B,E)
supportive
how is Clostridium difficile aquired
Rare normal flora
spores acquired in hospital
antibiotic therapy usually precedes disease
can be spread person to person or environment to person but does not cause illness until something triggers it… often receiving antibiotics
Clostridium difficile toxins
Toxin A - enterotoxin, inflammatory response, major toxin
Toxin B - cytotoxic
Clostridium difficile clinical symptoms
pseudomembranous colitis** classic presentation diarrhea (watery, severe, bloody) abdominal pain leukocytosis** fever toxic megacolon (risk of perforation)
BI (Nap1) strain of Clostridium difficile
Increased Toxin A production
Higher mortality, especially elderly
Up to 50% of isolates in the US
- been here for a long time but has some how become more virulent
C. difficile diagnosis
• Detection of toxin A in stool
- ELISA
85 - 90% sensitivity (single assay)
95% sensitive (two assay)
• *PCR- New standard-amplifies toxin region
90+ % sensitivity, 98% specificity
• Culture
not routinely recommended
• Sigmoidoscopy/colonoscopy (risk of perforating the colon)
C. difficile treatment
Stop antibiotics if possible
Metronidazole (oral preferred)
** Vancomycin (oral only, expensive)
main drug
colon resection
Lactobacillus, fecal enema (transplant) - very good success with relapsing C. diff
Propionobacterium acnes
Slow growing anaerobe
Contaminant in blood cultures
Cause of infection:
Prosthetic devices or hardware
Opportunistic infections
Acne
Treatment – if indicated
Penicillin as well as many other agents except metronidazole!!
Peptostreptococcus
• Normal flora of mouth, GI tract, pelvis
• Contiguous infections (usually mixed)
Intra-abdominal, endometritis, pulmonary
• Brain abscess
• Diagnosis –culture only gram positive cocci anaerobe
• Treatment – debridement and penicillin, metronidazole, cabapenems, clindamycin
B. fragilis group characteristics
mixed infections - usually dominant anaerobe Non-spore forming, non-motile Requires enriched media to grow Normal inhabitant of GI tract (colon) Provide protection from invasion (?)
hallmark of B. fragilis infection
abscess formation
- Inflammatory response to infection
- Encapsulated “pus”
- PMN’s
- Fibrin, fibrinogen
- Debris, necrotic tissue
Almost always mixed infections (aerobes and anaerobes
main virulence factor of B. fragilis
polysaccharide capsule
- adherence to peritoneal cavity
- Resists phagocytosis
- Resistance to T cell and humoral immunity
virulence factors of B. fragilis
Polysaccharide capsule
Oxygen tolerance
Super oxide dismutase
Catalase
Toxins : Defective endotoxin – not associated with sepsis (same toxin as E. coli)
Prevotella spp characteristics
Residents of mouth, GI tract, and Pelvis Gram negative strict anaerobes Require enriched media (blood containing) Non-motile Non-encapsulated Virulence – unknown
Prevotella pathogensis
abscess formation
Female genital tract infections
Oral, pleuropulmonary
Oral cavity, urogenital, GI tract
most active drugs for bacteroides
metronidazole chloramphenicol ampicillin/sulbactam piperacillin/tazobactam carbapenems
