Clostridium Clostridioides Flashcards
Characteristics
-biocontainment level 2 (except C. botulinum is level 3 where lab work can generate aerosols)
-gram positive, spore forming rods (not all species stain well)
-anaerobes (variably tolerant of O2)
-produce toxins!
Strict anaerobes
Clostridium haemolyticum and Clostridium novyi
Less fussy anaerobes
Clostridioides difficile, Clostridium perfringens
Clostrodium perfingens appearance
-gram positive, boxcar morphology
-2 zones of hemolysis on blood agar
Clostridium tetani appearance
-Presence of terminal spores= drumstick
-long flagella under special staining
Natural host or habitat of Clostridium and Clostridioides
-wide distribution
-found in environment (water and soil)
-many species part of normal microbiota such as in feces
Taxonomy of C. tetani
Differentiated from other species because of the presence of terminal spores
Virulence factors
TOXINS
Neurotoxic species
- Clostridium tetani= tetanus
- Clostridium botulinum= botulism (flaccid paralysis)
Histotoxic species
- Clostridium chauvoei= cattle- blackleg
- Clostridium septicum= large animals- malignant edema
- Clostridium novyi= sheep/cattle- necrotic hepatitis
- Clostridium perfringens= gangrene
Enterotoxin species
- Clostridium perfringens
-Bloody diarrhea in lambs, pigs, chickens, humans
-pulpy kidney disease in sheep
-Acute hemorrhagic diarrhea syndrome in dogs and horses - Clostridium piliforme- Tyzzer’s disease in horses
- Clostridium spiroforme in rabbits= antibiotic induced typhlocolitis
- C. difficile
-pigs= scours, mesocolonic diarrhea
-humans- natibiotis associated diarrhea
Clostridium tetani
Natural habitat: soil contaminated with feces
-Organisms enter through breaks in skin (stepping on rusty nail, fecal contamination of umbilicus, tail docking) Then organism will multiply in necrotic tissues
C. tetani presentation
- Production of toxins which disseminate from focus of infection
-Tetanolysin enhances tissue invasion
-Tetanospasmin causes spasms of both flexor and extensor muscles - Results in spasmodic paralysis. Toxin causes extreme muscle stiffness
-ex. Lockjaw; risus sardonicus (sardonic smile)
Treatment for tetanus
High dose penicillin and tetanus anti-toxin
Clostridium botulinum in environment
-widely present in soils and aquatic environment
-Botulism toxin is produced when spores germinate in anaerobic environments
-Toxin prevents the release of Ach at neuromuscular junction= flaccid paralysis
Clostridium botulinum spores
Extremely resistant
-survive boiling
-recommended to use pressure canner (autoclave) for home canning
Exposure: ingestion
Steps of C. botulinum in birds
- Spores on lake bottom
- Birds eat detritus or invertebrates from lake bottom
- Become intoxicated
- Results in droopy necks= drowning or respiratory failure
- Carcasses eaten by maggots
- Toxin laden maggots eaten by birds
Five forms of botulism
- Foodborne- eat foods with toxin (home canned food)
- Wound botulism-infection; occurs in IV drug users
- Infant botulism-replication of toxin in intestines and release of toxin (no honey for babies)
- Adult intestinal toxemia- colonization of gut similar to infant
- Latrogenic botulism- used in medical procedures and accidentally goes elsewhere
Treatment of C. botulinum
- Antibiotics used when animals have infection , not when they are intoxicated
- Can give antitoxin
- Supportive therapy
- Respiratory ventilation
-stool softeners, soft bedding to prevent bed sores - Vaccination possible (horses)
Clostridium chauvoei
-causes blackleg
-organism is common in the environment and feces
-cattle or sheep ingest endospores which pass through body without incident but sometimes get stuck into hindquarters and cardiac muscle
-Disease occurs when spores germinate due to low O2 levels
Why does sporulation occur in C. chauvoei?
Relatively unknown
-could be due to injury (vaccination, bumping into something) which causes damage and results in locally anaerobic environment
Acute febrile disease
-lameness
-sudden death (necrotizing myositis and systemic toxemia)
>crepitation (due to gas production), dark red muscle (black, spongy, rancid)
-often find with affected leg up
Treatment of C chauvoei
**typically not practical or possible
Can try penicillin and surgical debridement of affected tissues
C. septicum
-typically from soil
-affects large animals of all ages and causes malignant edema
C. septicum presentation
- Infection occurs following a deep puncture + trauma
-outbreaks may occur after group procedures (ie. tail docking)
2.May result in acute fatal toxemia
-production of necrotoxins causing edema and gangrene
- Lesion at site of infection, edema at other body sites
Treatment of C. septicum
-high dose penicillin systemically and injected around primary lesion
-Can also use antitoxin but very expensive
Control of C. septicum
- Hygiene when performing invasive procedures (ex.docking)
- vaccination
C. septicum in people
-Rare
-infections are fatal
-associated with colon carcinoma
C. novyi type B
-occurs in sheep (well nourished), cattle, and rarely in pigs and horses
-acquired from environment, fecal contamination by carrier of pasture plays a role
-causes acute, necrotic hepatitis (animals are usually found dead)
Mechanism of C. novyi type B
Spores reach liver hematogenously, germinate with necrotic insult and release alpha toxin
»disease associated with liver flukes (Fasciola hepatica) or liver trauma
Treatment and control of C. novyi type B
Treatment: none
Control: Vaccination and control of inciting causes such as liver fluke
TOXIN SLIDE??
Type A C. perfringens
-most widespread toxinotype
-found in the guts of both healthy and diseased animals
-Causes enteric diseases, and gas gangrene, and emphysematous abomasitis
Type B C. perfringens
Lamb dysentery
-high morbidity and mortality, sudden death
-predisposed by abrupt change in diet
-Seen in young because colostrum contains anti-trypsin substances which prevent toxin degradation
Type C C. perfringens
-causes hemorrhagic enteritis in piglets, and sometimes in calves, foals, lambs
>outbreaks in entire litters
>acute onset, high mortality, death within 24 hrs
-trypsin susceptibility of toxin explains disease predilection for neonates
Type G C. perfringens
Causes necrotic enteritis in chickens
-acute enterotoxemia
-anorexia, depression, dehydration, ruffled feathers
-sudden death, necrosis of small intestine
Type D C. perfringens
Over eating disease- associated with gorging on grain or lush pasture
-high starch content stimulates overgrowth of C. perfringens, and the increase in toxin production leads to toxemia
-Results in acute disease in otherwise healthy lambs= pulpy kidney (autolysis resulting in soft renal cortex)
**control by managing diet
Type A C. perfringens
-NetF producing
-occurs in dogs and horses
Dogs:
-Acute hemorrhagic diarrhea syndrome
-rapid onset
-may include necrotic lesions and frank blood in feces
-mortality rate unknown because diarrhea causes not often brought into vet
Horses:
-Enterocolitis in young foals under 3 days of age
Type F C. perfringens
-food and water borne; 2nd most common cause of bacterial foodborne illness
-can cause necrotizing intestinal disease= Fire bowels
>associated with foods containing trypsin inhibitors (peanuts, sweet potatoes, casava)
C. piliforme
-commonly seen in apparently thriving foals and in some rabbits
-animals often found dead or comatose
-disease classically described as multifocal hepatic necrosis, and can find lesions in heart and intestines
C. difficile
-results in early onset scours, sudden death, mesocolonic edema in pigs
**important differential diagnosis for edema disease from E.coli
Enterotoxins from C. difficile
- Toxin A-enterotoxin, causing fluid accumulation
- Toxin B- potent cytotoxin
Results in Colonic dysregulation and cellular death; not all strains are toxigenic (pathogenic)
C. difficile in dogs and cats
Very little evidence of association with disease in small animals (found in healthy and diarrheic animals)
C. difficile in humans
Debilitating disease
-antibiotic associated diarrhea
Treatment challenging
-Vancomycin, metronidazole
-Fecal transplants (oral or suppository)
Sample collection and handling for C. tetani
-gram stained smears revealing drumstick organisms
-classically, serum from affected animal was injected into a mouse to ID circulating neurotoxin
sample collection and handling for C. botulinum
-Toxicity studies, injecting mice with serum or filtrate of rumen contents
Sample collection and handling for C. chauvoei, septicum, and novyi
-Culture possible (collect large chunk of tissue to maintain anaerobic center)
-fixed tissues for histology
-fluorescent antibody test for C. chauvoei
Sample collection and handling of C. perfringens
- Culture feces (diarrhea), renal tissue (pulpy kidney disease)
- Gram stain= box car cells
- ID toxin by PCR
- Tissues for histopathology
Sample collection and handling for C. difficile
- Culture feces
- ID of toxin by PCR (on fecal samples or on pure cultures)
Lab ID
-Variety of ID diagnostic available
-Ask lab about how to interpret findings. Ex. Does positive culture indicate an infection or just colonization??
-C. piliforme is not cultureable
Zoonosis of C. perfringens
-common cause of foodborne illness
Zoonosis of C. difficile
-can be zoonotically acquired from pigs
