Anaerobes 1: Neurotoxic & Histotoxic Clostridium

Question 1

Describe the key bacterial characteristics of anaerobes.

Answer 1

-present in GIT
-gram pos & neg *
>gram pos = spore forming: clostridium spp
>gram neg = non spore forming: fusobacterium n, dichelobacter n, porphyromonas spp, prevotella spp
-require anaerobic environ or devitalized tissue for growth *
-anaerobic transport
-cause abscess, wound inf, aspiration pneumonia, intra ab inf, bacteremia, enteric inf, toxemia
-localized: oral, GIT
-spread via mucosal surface
>transient bacteremia & 2ndary localization
-polymicrobial inf & synergistic
-anaerobic inf = endogenous origin *

Question 2

Describe Clostridium key bacterial characteristics.

Answer 2

-gram pos rod
-anaerobic
-motile via flagella
-rapid multiplication
-endospore
-in soil, GIT, feces *
-powerful toxin producers
-epsilon toxin from C. Perfringens = bioterrorism

Question 3

Describe species of vet IMP.

Answer 3

Question 4

Describe virulence factors & pathogenesis of Clostridium.

Answer 4

Question 5

Describe clostridium tetani tetanus etiology.

Answer 5

-acute, potentially fatal intoxication w neurotoxic clostridia = spastic paralysis
-reservoir: soil & feces
-microscope: gram pos drum stick shaped robs w terminal endospores

Question 6

Describe clostridium tetani pathogenesis of tetanus.

Answer 6

binding of the toxin is irreversible = revert requires the gen of new axon terminals
1. Ascending tetanus (dogs & cats) = less sus
-toxin travels from regional motor nerve in limb -> other parts
2. Descending tetanus (humans & horses)
-toxin in blood stream affect motor nerve in head & neck -> spread to limbs

Question 7

Describe clostridium tetani diagnosis.

Answer 7

-incubation period = 5-10d
-latent = when wound at site of inf is healed
-CS: stiffness, lock jaw, localized spasms, alt HR & respiratory rates, dysphagia
-diagnosis: history & CS, culture
-animals that recover = not immune bc toxin could be below threshold required to stim prod of neutralizing antibodies

Question 8

Describe clostridium tetani treatment.

Answer 8

-antitoxin = neutralize unbound toxin -> quick & short term protection
-anti tetanus equine serum
-toxoid = inactive vaccine to promote active IR
-pen = kill toxin producing vegetative cells of c tetani in lesions
-surgical debridement of wounds & flush w H2O2 = aerobic conditions
-supportive care: dec ext stim, sedative, muscle relaxant

Question 9

Describe tetanus control of clostridium tetani.

Answer 9

-toxoid immunization
-post exposure prophylaxis via toxoid booster
-wound management & antimicrobial therapy
-aseptic technique in surgery + sterilization of instruments *
-IMP surveillance = tetanus is vaccine preventable so the poss of failure to vaccinate investigated in every case
-promote awareness

Question 10

Describe clostridium botulinum - botulism etiology.

Answer 10

-serious, potentially fatal intoxication by ingestion of pre formed neurotoxin (food) causing flaccid paralysis
-reservoir: germination of endospores w growth of vegetative cells & toxin production in rotting carcass, decaying vegetation, contaminated canned food, meat, fish, invertebrates

Question 11

Describe clostridium botulinum - botulism pathogenesis.

Answer 11

binding of toxin is irreversible to presynaptic membrane = slowly releases -> nerve damage heals within wks to months

Question 12

Describe botulism in humans.

Answer 12

-food born
-wound (needles)
-infant (spore contaminated honey)
-inhalation

Question 13

Describe clostridium botulinum - diagnosis.

Answer 13

-CS in 3-17d after ingestion of toxin
>dilated pupils, dry MM & dec salivation, tongue flaccid & dysphagia, paralysis of respiratory muscles -> ab breathing
-toxin in serum & food *
-c botulinum & toxin = select agents *

Question 14

Describe botulism T & P.

Answer 14

-T: hydration via electrolytes & antitoxin
-P:
>toxoid vaccine in endemic regions
>routine vaccine
>destroy contaminated foodstuffs
>prepare & preserve feed & food *
>high qual feed & prevent water & soil contamination *

Question 15

Describe clostridium chavoei.

Answer 15

‘Blackleg’
-sheep (any age) & cattle (3mo - 2yr)
-acute exogenous inf w necrotizing myositis caused by histotoxic clostridia c. Chauvoei
-exogenous inf via wounds -> anaerobic environ -> deposition of endospores, germination, multiplication -> toxin cause tissue destruction *
-fermentation of muscle glycogen -> gas accumulation -> metabolic end prod w smell *
-death w toxemia & bacteremia in 24h
-affect lg muscle mass
-acute, febrile, highly fatal w emphysematous swelling & necrotizing myositis (100% fatality) *
-edematous swelling w crepitation due to gas
-lameness
-myocardium & diaphragm also affected

Question 16

Describe clostridium novyi.

Answer 16

-malignant edema, gas gangrene
-exogenous, necrotizing, soft tissue wound inf by histotoxic clostridia C novyi type A, type B c hemolyticum
-gas formation & toxemia
-SQ crepitation
-prevention: surgical treatment of wound to remove necrotizing muscle tissue & promote drainage
>prophylaxis w pen

Question 17

Describe clostridium septicum.

Answer 17

‘Braxy’ = abomasitis of sheep by exotoxin
-malignant edema = exogenous inf thru wounds or endogenous thru dormant spores in muscle
-risk factor: IM inj, shearing, docking, lambing, parturition, castration
-local exotoxin -> inflam & myositis -> edema, necrosis, gangrene

Question 18

Describe histoxoic clostridia diagnosis, T & P.

Answer 18

Diagnosis: fluorescent antibody staining test
>anaerobic culture = time consuming, not easy or rewarding *
Treatment: pen
Prevention: routine vaccine

Question 19

SUMMARY.

Answer 19