Genus Clostridium Flashcards
(129 cards)
1
Q
What are the general characteristics of Clostridium organisms?
A
Large, gram + rods; obligate anaerobes; produce endospores (terminal or subterminal).
2
Q
Describe the habitat of Clostridium.
A
Soil, intestines, etc.
3
Q
Clostridial exotoxins are produced by _____ pathogenic clostridia.
A
All.
4
Q
What are the classifications of clostridial toxins?
A
Extracellular; protoplasmic; sporulation.
5
Q
What are the two activity classifications of clostridial toxins?
A
Prototoxins (precursors); active toxins.
6
Q
How are clostridial toxins detected?
A
Mouse neutralization test.
7
Q
What are the immunization products for clostridial toxins?
A
Antitoxins; toxoids; bacterins.
8
Q
Describe neurotoxic clostridia.
A
Toxin forming noninvasive bacteria; little to no ability to invade tissues.
9
Q
How do neurotoxic clostridia produce disease?
A
Create neurological signs and damage by absorption of preformed or locally produced toxins.
10
Q
Describe the appearance of C. tetani.
A
Drumstick appearance due to terminal endospore.
11
Q
What is the habitat of C. tetani?
A
Soil and intestines of horses and ruminants.
12
Q
Describe the species susceptibility of C. tetani.
A
Seen in horses, humans, pigs, cattle, sheep; rare in dogs; cats and chickens are more resistant.
13
Q
What are the exotoxins of C. tetani?
A
Tetanospasmin: protoplasmic and prototoxin; tetanolysin: hemolytic and necrotizing toxin.
14
Q
What is toxin neutralization?
A
Antibody blocks binding of toxin to cellular receptor, thus inhibiting the pathological effect of the toxin.
15
Q
Describe the mechanisms of transmission of tetanus.
A
Puncture wounds; via the umbilicus (T neo-natorum); via the uterus (puerperal tetanus).
16
Q
What are the characteristics of the pathogenesis of tetanus?
A
Anaerobic environment for germination of endospores; release and activation of tetanospasmin; intra-axonal transport to CNS.
17
Q
What is the mode of action of tetanospasmin?
A
Blocks the release of inhibitory transmitters causing continuous stimulation by excitatory transmitters.
18
Q
What are the signs of equine tetanus?
A
Erect ears, prolapsed third eyelid, open nostrils; stiff, stilted gait; tail head elevation; ‘sawhorse’ stance.
19
Q
What is opisthotonus?
A
Extensor rigidity of neck, limbs, trunk, and tail as seen with tetanus.
20
Q
Describe the treatment and prevention methods of tetanus.
A
Tetanus immune globulin: prophylactic and therapeutic use; active immunization.
21
Q
Is tetanus zoonotic?
A
Yes, it results in facial spasm, risus sardonicus, and opisthotonus.
22
Q
C. botulinum toxins are produced under what conditions?
A
Anaerobic conditions.
23
Q
What species are the most susceptible to C. botulinum?
A
Humans, poultry, and waterfowl; ruminants, horses, pigs, dogs, and cats are more resistant.
24
Q
Describe the transmission of C. botulinum.
A
Intoxication in foods (preformed toxins); wound contamination; infant botulism.
25
What is the common source of botulinum intoxication in ruminants?
Contaminated poultry litter used as feed or fertilizer on pasture.
26
What is the common source of botulinum intoxication in cattle and horses?
Forage; anaerobic conditions within large round bales of hay allows the growth of organisms after initial contamination resulting from nestling birds/rodents scooped up with hay or contaminated plant material.
27
What is the common source of botulinum intoxication in fish?
Feed containing C. botulinum Type E which germinates.
28
What is the common source of botulinum intoxication in humans?
Improperly preserved canned foods, meat, or veggies.
29
What is the common source of botulinum intoxication in waterfowl?
Detritus from invertebrates.
30
Give a clinical example of pathogenesis of C. botulinum in waterfowl.
C. botulinum toxins on lake bottom germinate and birds eat detritus or invertebrates from the lake; become intoxicated which causes droopy neck, resulting in drowning or respiratory failure; carcasses are eaten by maggots which are then eaten by birds.
31
What are the CDC 5 forms of botulism?
Food-borne: eating contaminated foods commonly seen in at-home canning; wound botulism: common in IV drug users; infant botulism: replication and release of toxin in intestines; similar to shaker foals; adult intestinal toxemia: colonization of gut; Iatrogenic botulism: needles.
32
Infant botulism is a reason to not feed what kind of food to babies?
Honey.
33
Describe the pathogenesis of botulism.
Ingestion of preformed toxin, big bale silage, fruit or vegetable wastes, or contact of infected carcasses in feeds; toxin dissemination in blood to NMJ; inhibition of release of acetylcholine, causing flaccid paralysis.
34
How does flaccid paralysis due to botulism present?
Initially with restlessness, uncoordinated movements, difficulty swallowing, and muscle weakness; leads to respiratory failure, circulatory failure, and death.
35
Animal may be __________ as a result of a botulism infection.
Slaughtered on humane grounds.
36
What are the results of toxicoinfectious botulism?
Floppy baby syndrome; shaker foal syndrome.
37
What is the method of action of C. botulinum?
Toxin blocks the release of ACh, and therefore the stimulation of muscles is blocked.
38
What is limberneck?
Type C botulism in wild and domestic poultry.
39
In what species is forage poisoning botulism seen?
Horses, cattle, and sheep.
40
What is Lamziekte?
Loin disease; pica (P deficiency).
41
Describe histotoxic clostridia.
Generalized invaders of high pathogenicity; primarily affecting muscle, liver, and intestines.
42
C. chauvoie causes what condition?
Blackleg in cattle, sheep, and goats.
43
What is the habitat of C. chauvoie?
Soil and intestinal tract.
44
What are the toxins of C. chauvoie?
Alpha, beta, delta, and gamma toxins.
45
Describe the transmission of blackleg.
Via exposure to bacterial spores in the soil and forage contamination in young stock 6 months-2 years often at grass; endogenous in cattle and exogenous in sheep and goats.
46
Describe the pathogenesis of blackleg.
Germination of endospore in damaged muscle causing necrosis of skeletal muscles, systemic toxicity, and lymphadenopathy.
47
What parts of cattle are typically affected by blackleg?
Muscles of the leg and back but also the tongue and heart due to muscle damage from poor handling (crush, bulling).
48
How is blackleg commonly caused in sheep?
Through shearing, injuries, poor hygiene during manual lambing, and naval infection in lambs.
49
What are the most common signs of blackleg?
Cold noticeable swelling with gas and rancid smell, unwilling to stand, poor appetite, depression, coma, and death.
50
What are the neurotoxic Clostridium species?
C. tetani (tetanus) and C. botulinum (botulism).
51
What are the histotoxic species of Clostridium?
C. chauvoie: blackleg in cattle; C. septicum: malignant edema in large animals; C. novyi: necrotic hepatitis in sheep and cattle; C. perfringens: gangrene.
52
What is Clostridium septicum?
Malignant edema seen in cattle, sheep, pigs, and horses.
53
What are the toxins of C. septicum?
Alpha, beta, gamma, and delta toxins that destroy endothelial cells, RBCs, etc.
54
How is C. septicum transmitted?
Wound infections from fights in rams, dirty IM injections, or castration.
55
Describe the pathogenesis of C. septicum.
Toxemia; necrotic cellulitis accompanied by edema; little or no gas.
56
What are the signs of C. septicum?
Severe swelling at the infection site, skin darkened, high fever, and death within 24-36 hrs; swelling of head and neck as well as depression in sheep followed by rapid death.
57
What is C. novyi type B?
Infectious necrotic hepatitis (black disease) in sheep and cattle; occasionally in pigs and horses.
58
What are the toxins of C. novyi type B?
Alpha toxin: hepatic necrosis and toxemia; beta toxin: membranolytic.
59
What is the predisposing factor to infectious hepatic necrosis (black disease)?
Hepatic damage due to migrating metacercariae.
60
Describe the pathogenesis of C. novyi type B.
Ingestion of endospores; latency infection of liver; hepatic injury resulting in germination of endospores and toxin production; toxemia, endothelial damage, etc.
61
Describe the clinical signs of C. novyi in cattle.
Affects cattle of all ages and most infected are found dead; illness may last 48 hours with depression, high fever, reluctance to move, and death.
62
Describe the clinical signs of C. novyi in sheep.
Depression, rapid breathing, sudden quiet death wherein skin darkens quickly afterwards (thus the name black disease).
63
C. hemolyticum is the causative agent of what?
Bacillary hemoglobinuria (bacterial red water) of cattle and sheep.
64
How is C. hemolyticum transmitted?
Soil-borne spores in wet, swampy land with snail host of liver fluke.
65
What triggers an infection of C. hemolyticum?
Pre-existing liver fluke infection of liver damage.
66
Describe the toxins of C. hemolyticum.
Necrotizing, hemolytic, etc.; causes hepatic necrosis, IV hemolysis, and increased vascular permeability.
67
Describe the pathogenesis of C. hemolyticum.
Same as black disease: anemia; hepatic infarcts; port-wine colored urine.
68
What are the signs of C. hemolyticum?
Stop feeding, ruminating, and dung passing; lactation may stop suddenly; anemia, dark red urine, and rapid death; sheep may have discolored fleece due to urine and dies within 48 hrs.
69
What is enterotoxemia?
A frequently severe disease of sheep and goats of all ages that is caused by either type C or D C. perfringens; as the organism grows it releases very potent toxins that harm the animal.
70
What is the habitat of C. perfringens?
Soil and intestinal tract.
71
What accounts for the pathophysiology of enterotoxemia?
Multiple toxins and enzymes.
72
Diseases due to C. perfringens are usually characterized by what?
Sudden deaths in affected animals.
73
C. perfringens type A produces what toxins?
Just alpha.
74
C. perfringens type B produces what toxins?
Alpha, beta, and epsilon.
75
C. perfringens type C produces what toxins?
alpha and beta
76
C. perfringens type D produces what toxins?
alpha and epsilon
77
C. perfringens type E produces what toxins?
alpha and iota
78
The only strain of C. perfringens not found in the USA is ____.
type B
79
What diseases does C. perfringens type A cause?
gangrenous infections, hemorrhagic/necrotizing gastroenteritis
80
What diseases does C. perfringens type B cause?
lamb dysentery
81
What diseases does C. perfringens type C cause?
neonatal hemorrhagic/necrotizing enteritis
82
What diseases does C. perfringens type D cause?
ovine enterotoxemia (over-eating disease)
83
What diseases does C. perfringens type E cause?
bovine hemorrhagic gastroenteritis
84
What diseases does C. perfringens type F cause?
food-borne illness in people
85
What diseases does C. perfringens type G cause?
avian necrotic enteritis
86
What symptoms do we see with C. perfringens in lambs, pigs, chickens, and humans?
bloody diarrhea
87
What symptoms do we see with C. perfringens in sheep?
pulpy kidney disease
88
What symptoms do we see with C. perfringens in dogs and horses?
acute hemorrhagic diarrhea syndrome
89
What symptoms do we see with C. piliforme in horses?
Tyzzer's disease
90
What symptoms do we see with C. spiroforme in rabbits?
antibiotic-induced typhlocolitis
91
What symptoms do we see with C. difficile in pigs?
scours, mesocolonic edema
92
What symptoms do we see with C. difficile in humans?
antibiotic associated diarrhea
93
What are the characteristics of Type A Enterotoxemia?
- alpha toxin and enterotoxin (food poisoning)
- causes 'yellow lamb disease', hemorrhagic diarrhea in dogs, and foal enterotoxemia
- rapid death, weakness, convulsions, and abdominal pain
94
What are the symptoms of 'yellow lamb disease'?
rare severe hemolysis and jaundice
95
What are the symptoms of hemorrhagic diarrhea in dogs?
vomiting, anorexia, lethargy, and abdominal pain
96
What are the symptoms of foal enterotoxemia?
colic, foul-smelling and hemorrhagic diarrhea, abdominal distention, and death
97
Sudden death in young animals on full speed suspect what?
enterotoxemia
98
What does Type A enterotoxemia cause in humans?
- wound contamination: gas gangrene
- food poisoning
99
Which toxin is the most important and produced by all subtypes?
alpha toxin (phospholipase C)
100
What is the pathophysiology of alpha toxin (phospholipase C)?
- destroys leukocytes, RBCs, endothelium, and platelets
- anemia, hemorrhage, organ dysfunction, etc.
101
What is the pathophysiology of beta toxin?
destroys enterocytes and increases capillary permeability
102
What is the pathophysiology of epsilon toxin?
destroys enterocytes and increases vascular permeability
103
Which toxins are prototoxins?
epsilon (precursor toxin) and iota
104
What is the pathophysiology of iota toxin?
necrotizing activity and increases vascular permeability
105
Enterotoxemia is a disease of what parts of the body?
small and large intestine
106
What is the major predisposing factor to enterotoxemia?
high concentrate diet which promotes rapid growth of the organisms of the intestine
107
The toxins that cause enterotoxemia cause what conditions to occur?
- necrotizing enteritis with loss of mucosa
- multiple organ dysfunction
108
What are the characteristics of type C enterotoxemia?
- beta toxin
- commonly fatal disease that occurs in calves and lambs
- infects young animals less than 3 weeks old
- animals stop nursing, listlessness, fetid, blood tinged diarrhea, and death
109
Type C enterotoxemia causes ___________ in neonatal lambs, calves, foals, piglets, and kids.
hemorrhagic enteritis
110
Type C enterotoxemia causes ___________ in poultry.
necrotic enteritis
111
Describe Type C necrotic enteritis in avian species.
- acute to chronic disease in chickens, turkeys, and ducks worldwide
- cause depression, ruffled feathers, inappetence, dark colored diarrhea, and death in good condition
112
Describe type D enterotoxemia.
- epsilon toxin
- 'Overeating disease' of feedlot lambs
- pulpy kidney disease
- characterized by effects on digestive system, CNS, and kidneys
113
Pulpy kidney disease is a major killer of what?
lambs from shortly after birth throughout the entire feeding period
114
What is the first sign of pulpy kidney in sheep?
death within 2 hours of onset after roughage and high energy diet
115
What are the digestive system signs of pulpy kidney in sheep?
colic, muscle tremors, or convulsions
116
What are the CNS signs of pulpy kidney in sheep?
grinding of teeth, oscillation of eyes, etc.
117
Pulpy kidney is common in what kind of lambs?
vigorous, healthy, and rapidly growing ones
118
What are the C. perfringens immunization products?
- antitoxin (passive immunity)
- toxoid vaccine
119
What are the characteristics of C. piliforme?
- gram +, filamentous intracellular bacteria
- does not grow on artificial medium
- orally infects foals 6 weeks or less
120
What is the pathology of C. piliforme?
extensive liver necrosis
121
What disease does C. piliforme cause?
Tyzzer's disease in which many patients are seen comatose or dead; causes depression, fever, anorexia, jaundice, and diarrhea
122
Describe the treatment of Tyzzer's disease.
supportive and nonspecific; success rate is usually very low
123
How is Tyzzer's disease diagnosed?
based on analysis of gross and microscopic lesions and/or PCR assay for C. piliforme
124
Describe the sample collection and handling of C. tetani.
- gram-stained smears revealing 'drumstick' organisms
- classically, serum from affected animal was injected into a mouse to identify circulating neurotoxin
125
Describe the sample collection and handling of C. botulinum.
toxicity studies, injecting mice with serum or filtrate of rumen contents
126
Describe the sample collection and handling of C. chauvoie, septicum, and novyi.
- culture possible by collecting a large chunk of tissue and maintaining an anaerobic center
- fixed tissues for histology
- fluorescent Ab test (C. chauvoie)
127
Describe the sample collection and handling of C. perfringens.
- culture feces, renal tissue
- gram stain to reveal box car cells
- ID toxin via PCR
- tissues for histopathology
128
Describe the sample collection and handling of C. difficile.
- culture feces
- ID toxin via PCR on fecal samples or on pure cultures
129
Which clostridium species is not cultureable?
C. piliforme
