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BACTERIOLOGY > 14 – Clostridium & Clostridioides > Flashcards

14 – Clostridium & Clostridioides Flashcards

1
Q

Microbiological characteristics

A
  • 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
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2
Q

Clostridium perfringens: morphology

A
  • Gram-positive rod
  • boxcar
  • 2 zones of hemolysis: 2nd zone when put back in the fridge
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3
Q

Clostridium tetani: morphology

A
  • Presence of terminal spores
  • drumstick
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4
Q

Natural host or habitat

A
  • Wide distribution
  • Found in environment (water and soil)
  • Many species part of normal microbiota (found in feces)
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5
Q

Virulence factors

A
  • TOXINS
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6
Q

Clostridium tetani: tetanus

A
  • 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!)
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7
Q

Clostridium tetani: opisthotonos

A
  • 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
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8
Q

Clostridium tetani: opisthotonos, tentanolysin

A
  • Enhances tissue invasion
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9
Q

Clostridium tetani: opisthotonos, tentanospasmin

A
  • Neurotoxin which causes spasms of both flexor and extensor muscles
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10
Q

Clostridium tenani: risus sardonicus

A
  • Muscle spasm in face ‘lockjaw’
  • *sardonic smile
  • *facial expression with raised eyebrows and grinning distortion of the face
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11
Q

Clostridium botulinum: botulism

A
  • 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)
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12
Q

Clostridium botulinum: botulism, spores are extremely resistant

A
  • Survive boiling, pressure canner recommended from home canning!
  • Exposure through ingestion
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13
Q

Clostridium botulinum: botulism toxin

A
  • Prevents release of ACh at neuromuscular junction
    o *FLACCID PARALYSIS
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14
Q

Clostridium botulinum: botulism, 7 different toxin types

A
  • Associated with different species (don’t need to know it all)
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15
Q

Clostridium botulinum: ruminants

A
  • Source: poultry litter
  • Contaminated litter used as feed or fertilizer on pasture
  • Sign: drooping tongue
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16
Q

Clostridium botulinum: cattle and horses

A
  • 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
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17
Q

Clostridium botulinum: fish

A
  • Source: feed
  • Feed containing C. botulinum type E which germinate
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18
Q

Clostridium botulinum: humans

A
  • Source: food
  • Improperly preserved canned foods, meat or vegetables
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19
Q

Clostridium botulinum: waterfowl:

A
  • 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
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20
Q

5 forms of botulism in humans

A
  1. Foodborne (ex. home grown foods)
  2. Wound botulism (ex. IV drug users)
  3. Infant botulism
  4. Adult intestinal toxemia
  5. Iatrogenic botulism: OPPS! (medical procedures)
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21
Q

Infant botulism

A
  • Similar to shaker foals
  • Replication of C. botulinum in intestines and release of toxin
    o Don’t feed babies HONEY!
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22
Q

Treatment options for Clostridium botulinum

A
  • Antibiotics
  • Antitoxin
  • Supportive therapy
  • Vaccination possible: horses
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23
Q

Antibiotics for Clostridium botulinum

A
  • Cases where animals have infection (ex. shaker foal)
  • Not when animals are simply intoxicated
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24
Q

Supportive therapy for Clostridium botulinum

A
  • *Companion animals
  • Stoll softeners
  • Soft bedding to prevent decubital sores
  • Possibly ventilation if muscles of respiration affected
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25
Q

Clostridium chauvoei (cattle, sheep):

A
  • 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
26
Q

Inciting factor of Clostridium chauvoei no understood

A
  • Perhaps injury: vaccination, bumping into something
    o Results in damage with a locally anaerobic environment
27
Q

Acute febrile disease: Clostridium chauvoei

A
  • Lameness
  • Sudden death (necrotizing myositis+systemic toxemia)
  • Often find with affected leg up
28
Q

Black leg: ‘clinical signs’

A
  • May fell crepitation (due to production of gas)
  • Muscle is dark red: black and spongy with rancid odour
29
Q

Black leg treatment

A
  • Typically not practical or possible
  • Penicillin + surgical debridement of affected tissues
30
Q

Control of black leg

A
  • Vaccination
31
Q

Clostridium septicum: malignant edema

A
  • 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
32
Q

Infection of clostridium septicum following deep puncture and trauma

A
  • Vaccination, surgery, through umbilicus
  • *outbreaks can occur following group procedures (sheering, tail, docking)
33
Q

Acute fetal toxemia: Clostridium septicum

A
  • Production of ‘necrotoxins’ which cause extensive edema and gangrene
34
Q

Treatment of Clostridium septicum

A
  • High dose penicillin systemically and injected around primary lesion
  • Antitoxin: $$$
35
Q

Control of Clostridium septicum

A
  • Hygiene when performing invasive procedures (docking, etc.)
  • Vaccination
36
Q

In people C. septicum is INFREQUENTLY isolated

A
  • Rare infections are often fatal
  • Associated with colon carcinoma
37
Q

Clostridium novyi Type B (sheep, cattle) (rarely in pigs and horses)

A
  • 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)
38
Q

Treatment of C. novyi Type B

A
  • no effective treatment available
39
Q

Control of C. novyi Type B

A
  • vaccination
  • control of possible inciting causes (liver fluke)
40
Q

Type A (C. perfringens)

A
  • 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
41
Q

Lamb dysentery (Type B, C. perfringens)

A
  • 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
42
Q

Hemorrhagic enteritis in piglets (Type C, C. perfringens)

A
  • 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
43
Q

Necrotic enteritis in chickens (Type G, C. perfringens)

A
  • Acute enterotoxemia
  • Anorexia, depression, dehydrations, ruffled feathers
  • Sudden death: necrosis of small intestine
44
Q

Pulpy kidney disease (Type D, C. perfringens)

A
  • *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
45
Q

C. perfingens, Type A – NetF producing: dogs

A
  • Hemorrhagic diarrhea syndrome
  • Poorly characterized disease
    o Rapid onset
    o +/- necrotic lesions and frank blood in feces
    o Mortality rate undetermined
46
Q

C. perfingens, Type A – NetF producing: horses

A
  • enterocolitis in young foals (less than 3 days of age)
47
Q

C. perfringens (humans, type F)

A
  • 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)
48
Q

C. pilliforme: Tyzzer’s disease in horse

A
  • 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
49
Q

C. difficile (pigs)

A
  • 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
50
Q

Toxin A (C. difficile)

A
  • Enterotoxin
  • Causes fluid accumulation
51
Q

Toxin B (C. difficile)

A
  • Potent cytotoxin
52
Q

C. difficile (small animals)

A
  • Very little evidence
  • Found in healthy and sick dogs
  • Be careful with interpretations
  • Reservoir for people?
53
Q

C. difficile (humans): ‘sharting disease’

A
  • Disease is debilitating
  • Antibiotic associated diarrhea
  • Community infections increasingly recognized
  • Treatment: challenging and unrewarding
  • Vancomycin, metronidazole
  • Fecal transplants: oral or suppository
54
Q

C. tetani: sample collecting and handling

A
  • Drumstick organism on gram-stained smears
  • Serum from affect animals injected into mouse to ID circulating neurotoxin
55
Q

C. botulinum: sample collecting and handling

A
  • Toxicity studies: inject mice with serum or filtrate of rumen contents
56
Q

C. chauvoei, septicum and novyi: sample collecting and handling

A
  • Culture possible: collect large chunk of tissue
  • Fixed tissues for histology
  • Fluorescent antibody test
57
Q

C. perfringens: sample collecting and handling

A
  • Culture feces (diarrhea), renal tissues (pulpy kidney disease)
  • Gram stain: box car cells
  • ID of toxin by PCR
  • Tissues for histopathology
58
Q

C. difficile: sample collecting and handling

A
  • culture feces
  • ID of toxin by PCR
59
Q

Lab ID

A
  • Variety of options available
  • Talk to lab about how to interpret
  • Some species NOT cultureable (C. piliforme)
60
Q

Zoonotic/interspecies transmission

A
  • 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

BACTERIOLOGY (19 decks)

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