Bacteriology - Clostridium Flashcards
is clostridium aerobic or anaerobic
anaerobic
is clostridium gram positive or negative
positive
is clostridium rods or cocci
rods
how do clostridium cause disease
release of toxins
enterotoxemia
toxins that are generated in the intestines and absorbed into circulation to act on distant organs
is C. perfringens endogenous
yes - most have C. perf in gut without causing disease
culturing it does NOT always indicate disease - requires typing or toxin ID
C. perfringens type A
alpha toxin only
- produced in all clostridial types; does not cause disease in most animals
can C. perfringens type A cause disease
yes but rarely; caused by over production of alpha toxin leading to intravascular hemolysis
Yellow Lamb disease
- anemia, icterus, depression, diarrhea
how to diagnose C. perfringens type A disease
culture w/ typing AND colony count - must be >10^6 CFUs/gram
C. perfringens type B
alpha + beta + epsilon toxins
causes Lamb Dysentery - rarely diagnosed in US
C. perfringens type C - toxins & signalment
alpha + beta toxins
occurs in NEONATAL ruminants, horses, pigs, humans
beta toxin
highly necrotizing - causes necrotizing enteritis
inactivated by TRYPSIN
pathogenesis of C. perfringens type C
- ingestion of C. perfringens type C
- proliferates in intestines
- lack of trypsin (ex. neonates - colostrum inactivates trypsin)
- beta toxin remains active
- necrotic enteritis
clinical signs of C. perfringens type C
hemorrhagic diarrhea
neurologic signs
sudden death
diagnostics for C. perfringens type C
toxin ELISA for beta toxin
culture w/ typing, histology, clinical signs are all suggestive but not diagnostic
C. perfringens type D - toxins and signalment
alpha + epsilon toxins
occurs in ADULT sheep and goats
epsilon toxin
increases vascular permeability
activated by TRYPSIN
pathogenesis of C. perfringens type D
- excess carbohydrate ingestion
- carbohydrates do not get fermented in rumen
- starch enters directly into SI
- promotes C. perf type D growth
- production of epsilon toxin
- travels to brain, heart, lungs, etc
clinical signs of C. perfringens type D
sheep: neurologic disease, respiratory difficulty
- NO diarrhea
goats: neurologic disease, alimentary disease, or BOTH
- can have diarrhea
diagnosis of C. perfringens type D
toxin ELISA for epsilon toxin
culture w/ typing, clinical signs are suggestive
C. perfringens type E
alpha + iota toxins
not a significant cause of disease in animals
C. perfringens type F
alpha + CPE (CP enterotoxin)
causes food poisoning in humans
- not a significant cause of disease in animals
C. perfringens type G - toxin and signalment
alpha + NetB toxins
occurs in poultry
NetB toxin
causes necrotizing enteritis
main predisposing factor is coccidiosis (Eimeria)
clinical signs of C. perfringens type G
- loss of production
- depression
- diarrhea
- sudden death
diagnosis of C. perfringens type G
combination of clinical signs, histology, and culture w/ typing
NO toxin test for NetB
C. difficile toxins and signalment
toxin A, toxin B, CDT
occurs in horses, pigs, rabbits, hamsters
- horses: all ages
- pigs: neonates
what is the main predisposing factor for C. difficile
antibiotic therapy +/- hospitalization
clinical signs of C. difficile
horses: diarrhea +/- hemorrhage, colic
pigs: diarrhea +/- hemorrhage, colic, mesocolonic edema
diagnosis of C. difficile
toxin ELISA for toxins A, B, or both
culture w/ typing, histology, and clinical signs are suggestive
C. piliforme signalment
horses, rabbits, rats, hamsters, cats, others
clinical signs of C. piliforme
Tyzzer Disease - ‘triad of lesions’
- intestines (colitis)
- liver (hepatitis)
- heart (myocarditis)
can cause neurologic signs from hepatic encephalopathy
diagnosis of C. piliforme
histology, PCR
paeniclostridium sordelli clinical signs
hemorrhagic and necrotizing enteritis
paeniclostridium sordelli diagnosis
rule out other causes of enteric disease, then:
- culture
- PCR
- IHC
C. colinum
Quail Disease
causes ulcerative colitis
C. spiroforme
Rabbit Enterotoxemia
causes hemorrhagic cecum
what causes Black Leg
clostridium chauvoei
Black Leg species affected
cattle
sheep (rare)
Black Leg toxins
C. chauvoei toxin A (CctA)
pathogenesis of Black Leg
ENDOGENOUS infection - does not require a cut
- spores ingested in soil and absorbed in intestines
- enters circulation and travels to muscle
- engulfed by muscle macrophages
- spores remain dormant in muscle
- blunt trauma occurs and reduces O2 causing spores to germinate
- produces CctA toxins
- muscular necrosis, toxemia, shock
lesions in Black Leg
muscle necrosis of skeletal AND cardiac muscle
what causes gas gangrene
C. septicum, chauvoei, novae, perfringens, and Paeniclostridium sordelli
Gas Gangrene species affected
sheep, goats, cattle, horses, pigs
pathogenesis of Gas Gangrene
EXOGENOUS infection - requires a cut
- spores or bacteria in soil enter through external wound
- reduction in O2 induces spore germination
- release of toxins
- muscle or SQ necrosis, toxemia, shock
lesions of Gas Gangrene
muscle or SQ necrosis
- NO cardiac muscle; skeletal only
diagnosis of gas gangrene
culture, PCR, FAT, IHC
what clostridium species cause hepatitis
C. novyi and C. haemolyticum
hepatitis type B - disease and species
infectious necrotic hepatitis in sheep
can occur in cattle and horses
hepatitis type D - disease and species
bacillary hemoglobinuria in cattle
can occur in sheep and horses
what are the toxins produced by C. novyi and C. haemolytica
C. novyi - alpha + beta toxin
C. haemolytica - beta toxin only
pathogenesis of Clostridial hepatitis
- spores ingested from soil and absorbed in intestines
- travels in circulation to liver
- engulfed by hepatic macrophages
- spores remain dormant in liver
- liver damage causes reduced O2
- spores germinate and release toxins
- hepatic necrosis, toxemia, shock
what is the predisposing factor for clostridial hepatitis
fasciola hepatica
clinical signs of clostridial hepatitis
- depression
- sudden death
- hemoglobinuria and icterus (type D only)
diagnosis of clostridial hepatitis
culture, PCR, FAT, IHC
