14 – Clostridium & Clostridioides Flashcards
Microbiological characteristics
- Biocontainment level 2 (biocontainment level 3: C. botulinum)
- Gram positive, spore forming rods (not all stain well)
- Anaerobes: variably tolerant of O2
- Famous for toxin production
Clostridium perfringens: morphology
- Gram-positive rod
- boxcar
- 2 zones of hemolysis: 2nd zone when put back in the fridge
Clostridium tetani: morphology
- Presence of terminal spores
- drumstick
Natural host or habitat
- Wide distribution
- Found in environment (water and soil)
- Many species part of normal microbiota (found in feces)
Virulence factors
- TOXINS
Clostridium tetani: tetanus
- Soil (especially with feces)=natural habitat
- Organism enter body through breaches in skin
o Ex. stepping on rusty nail, fecal contamination of umbilicus - Organism multiples in necrotic tissue (if you find it, culture!)
Clostridium tetani: opisthotonos
- Production of toxins: disseminate form focus of infection
o Tentanolysin
o Tentanospasmin - Treatment: high dose of penicillin + tetanus anti-toxin
- *spasmodic paralysis
- *toxin causes EXTREME muscle stiffness
Clostridium tetani: opisthotonos, tentanolysin
- Enhances tissue invasion
Clostridium tetani: opisthotonos, tentanospasmin
- Neurotoxin which causes spasms of both flexor and extensor muscles
Clostridium tenani: risus sardonicus
- Muscle spasm in face ‘lockjaw’
- *sardonic smile
- *facial expression with raised eyebrows and grinning distortion of the face
Clostridium botulinum: botulism
- Widely distributed in soils and aquatic environments
- Toxin production when spores GERMINATE in ANAERBOIC environments
- Spores are EXTREMELY RESISTANT
- Disease from extremely potent toxin (1mg can kill 120M mice)
Clostridium botulinum: botulism, spores are extremely resistant
- Survive boiling, pressure canner recommended from home canning!
- Exposure through ingestion
Clostridium botulinum: botulism toxin
- Prevents release of ACh at neuromuscular junction
o *FLACCID PARALYSIS
Clostridium botulinum: botulism, 7 different toxin types
- Associated with different species (don’t need to know it all)
Clostridium botulinum: ruminants
- Source: poultry litter
- Contaminated litter used as feed or fertilizer on pasture
- Sign: drooping tongue
Clostridium botulinum: cattle and horses
- Source: forage
o Anaerobic conditions within large round bales of hay=growth of organism - Initial contamination resulting of nestling birds/rodents scooped up with hay or carrion contaminated plant material
Clostridium botulinum: fish
- Source: feed
- Feed containing C. botulinum type E which germinate
Clostridium botulinum: humans
- Source: food
- Improperly preserved canned foods, meat or vegetables
Clostridium botulinum: waterfowl:
- Sources: invertebrates, detritus
1. C. botulinum spores on lake bottom
2. Birds eat detritus or invertebrates from lake bottom
3. Become intoxicated
4. Droopy necks=drown or respiratory failure
5. Carcasses eaten by maggots
6. Toxin laden maggots eaten by birds->leads to more cases
5 forms of botulism in humans
- Foodborne (ex. home grown foods)
- Wound botulism (ex. IV drug users)
- Infant botulism
- Adult intestinal toxemia
- Iatrogenic botulism: OPPS! (medical procedures)
Infant botulism
- Similar to shaker foals
- Replication of C. botulinum in intestines and release of toxin
o Don’t feed babies HONEY!
Treatment options for Clostridium botulinum
- Antibiotics
- Antitoxin
- Supportive therapy
- Vaccination possible: horses
Antibiotics for Clostridium botulinum
- Cases where animals have infection (ex. shaker foal)
- Not when animals are simply intoxicated
Supportive therapy for Clostridium botulinum
- *Companion animals
- Stoll softeners
- Soft bedding to prevent decubital sores
- Possibly ventilation if muscles of respiration affected
Clostridium chauvoei (cattle, sheep):
- BLACK LEG
- Common in environment and feces
- Ingested endospores typically pass though body without incident
o May occasionally lodge in tissues (hindquarters, cardiac muscle) - Disease occurs when spores stimulated to germinant
- *acute febrile disease
Inciting factor of Clostridium chauvoei no understood
- Perhaps injury: vaccination, bumping into something
o Results in damage with a locally anaerobic environment
Acute febrile disease: Clostridium chauvoei
- Lameness
- Sudden death (necrotizing myositis+systemic toxemia)
- Often find with affected leg up
Black leg: ‘clinical signs’
- May fell crepitation (due to production of gas)
- Muscle is dark red: black and spongy with rancid odour
Black leg treatment
- Typically not practical or possible
- Penicillin + surgical debridement of affected tissues
Control of black leg
- Vaccination
Clostridium septicum: malignant edema
- Primarily large animals of all ages
- Typically from soil
- Infection typically occurs following deep puncture + trauma
- Acute fetal toxemia
- Lesion at site of infection and edema at other body sites
Infection of clostridium septicum following deep puncture and trauma
- Vaccination, surgery, through umbilicus
- *outbreaks can occur following group procedures (sheering, tail, docking)
Acute fetal toxemia: Clostridium septicum
- Production of ‘necrotoxins’ which cause extensive edema and gangrene
Treatment of Clostridium septicum
- High dose penicillin systemically and injected around primary lesion
- Antitoxin: $$$
Control of Clostridium septicum
- Hygiene when performing invasive procedures (docking, etc.)
- Vaccination
In people C. septicum is INFREQUENTLY isolated
- Rare infections are often fatal
- Associated with colon carcinoma
Clostridium novyi Type B (sheep, cattle) (rarely in pigs and horses)
- Acquired from environment
o fecal contamination by carrier of pasture=important - disease is acute, necrotic hepatitis
o animals usually found dead - occurs in well-nourished adult sheep
- spores reach liver hematogenously, germinate with necrotic insult and release alpha-toxin
o disease associated with liver flukes (Fasciola hepatica or liver trauma)
Treatment of C. novyi Type B
- no effective treatment available
Control of C. novyi Type B
- vaccination
- control of possible inciting causes (liver fluke)
Type A (C. perfringens)
- most widespread toxinotype
- found in guts of healthy AND diseased animals
o enteric disease (role hard to demonstrate, Koch’s postulates) - associated with non-enteric syndromes
o gas gangrene
o emphysematous abomasitis
Lamb dysentery (Type B, C. perfringens)
- high morbidity and mortality, sudden death
- predisposed by abrupt change in diet
- seen in young
o colostrum contains anti-trypsin substances which prevent toxin degradation
Hemorrhagic enteritis in piglets (Type C, C. perfringens)
- often see outbreaks of entire litters
- acute onset
- high mortality, death within 24 hours
- can also see infections in calves, foals, lambs
- Trypsin susceptibility of toxin explains disease predilection for NEONATES
Necrotic enteritis in chickens (Type G, C. perfringens)
- Acute enterotoxemia
- Anorexia, depression, dehydrations, ruffled feathers
- Sudden death: necrosis of small intestine
Pulpy kidney disease (Type D, C. perfringens)
- *over-eating disease
- High starch content stimulates overgrowth of C. perfringens
o Excess toxin production leads to toxemia - Acute disease
- Kidney=soft
- Control by managing diet
C. perfingens, Type A – NetF producing: dogs
- Hemorrhagic diarrhea syndrome
- Poorly characterized disease
o Rapid onset
o +/- necrotic lesions and frank blood in feces
o Mortality rate undetermined
C. perfingens, Type A – NetF producing: horses
- enterocolitis in young foals (less than 3 days of age)
C. perfringens (humans, type F)
- Food and water borne
- 2nd most common cause of bacterial foodborne illness
- Can cause necrotizing intestinal disease (“fire bowels”)
o Associated with foods containing trypsin inhibitors: peanuts, sweet potatoes, casava) - (Turkey, look for 0 C. perfringens on food packets)
C. pilliforme: Tyzzer’s disease in horse
- Most commonly seen in apparently thriving foals (also seen in rabbits)
- Animals often found dead or comatose
- Disease: multifocal hepatic necrosis
o May also find lesions in heart or intestine
C. difficile (pigs)
- early onset of scours
- sudden death
- mesocolonic edema=classical pathological finding
- *important differential diagnosis for edema disease (E. coli)
- Production of 2 enterotoxins (A, B)
- *not all strains are toxigenic
Toxin A (C. difficile)
- Enterotoxin
- Causes fluid accumulation
Toxin B (C. difficile)
- Potent cytotoxin
C. difficile (small animals)
- Very little evidence
- Found in healthy and sick dogs
- Be careful with interpretations
- Reservoir for people?
C. difficile (humans): ‘sharting disease’
- Disease is debilitating
- Antibiotic associated diarrhea
- Community infections increasingly recognized
- Treatment: challenging and unrewarding
- Vancomycin, metronidazole
- Fecal transplants: oral or suppository
C. tetani: sample collecting and handling
- Drumstick organism on gram-stained smears
- Serum from affect animals injected into mouse to ID circulating neurotoxin
C. botulinum: sample collecting and handling
- Toxicity studies: inject mice with serum or filtrate of rumen contents
C. chauvoei, septicum and novyi: sample collecting and handling
- Culture possible: collect large chunk of tissue
- Fixed tissues for histology
- Fluorescent antibody test
C. perfringens: sample collecting and handling
- Culture feces (diarrhea), renal tissues (pulpy kidney disease)
- Gram stain: box car cells
- ID of toxin by PCR
- Tissues for histopathology
C. difficile: sample collecting and handling
- culture feces
- ID of toxin by PCR
Lab ID
- Variety of options available
- Talk to lab about how to interpret
- Some species NOT cultureable (C. piliforme)
Zoonotic/interspecies transmission
- C. perfringens common foodborne illness
o Behind Salmonell and S. aureus
o Associated with contaminated meat products - C. difficile may be aquired from pigs
- *direct transmission is uncommon of other C. species
