PQS - Clostridium Flashcards
(317 cards)
1
Q
Most clostridia have low invasive capacity
A
T
2
Q
Spores of clostridia are generally very resistant against heat
A
T
3
Q
The habitat of clostridia is the gut and the soil
A
T
4
Q
Clostridia are obligate aerobic bacteria
A
F
obligate ANaerobic
5
Q
Clostridium perfringens is an obligate pathogenic bacterium
A
F
facultative pathogens
6
Q
Clostridium perfringens can produce main and auxillary toxins
A
T
7
Q
Extracellular enzymes and toxins are virulence factors of clostridia
A
T
8
Q
There are no vaccines for the prevention of diseases caused by clostridia
A
F
inactivated bacterium culture
9
Q
Clostridium is anaerobe spore forming bacteria
A
T
10
Q
Clostridium bacteria is not in the environment, because it cannot tolerate oxygen
A
F
11
Q
Clostridium spreads usually rapid in a herd
A
F
No animal – to animal transmission
12
Q
Clostridium spread mostly with insecticides
A
F
13
Q
Clostridium difficile can be treated with metronidazole
A
T
14
Q
Clostridium difficile is seen in foal and piglets
A
T
15
Q
Many Clostridium species have flagella
A
F
16
Q
Clostridium species are only found in the subtropics
A
F
tropical and subtropical area
17
Q
Clostridium can cause severe contagious diseases
A
F
18
Q
Clostridium are obligate pathogens
A
F
facultative pathogens
19
Q
Anaculture or anatoxin vaccines are used for the prevention of malignant oedema
A
T
20
Q
Cl. chauvoei is the agent of malignant oedema
A
F
21
Q
Lesions of malignant oedema are mainly seen in the large muscles
A
T
- oedema, swelling
- wound infection
22
Q
Malignant oedema is generally endogenous in cattle
A
F
23
Q
Malignant oedema is generally a consequence of wound infection
A
T
24
Q
Movement difficulties are frequently seen in the case of malignant oedema
A
T
25
Clostridium novyi can cause malignant oedema
T
26
Malignant oedema can be diagnosed based on clinical signs
F
27
Malignant oedema is caused due to wound infection
T
28
Malignant oedema is only in ruminants
F
29
Malignant oedema, one of the clinical signs is lameness/movement problems
T
30
Malignant oedema, attenuated vaccine for prevention
F
inactivated bacterium culture (anaculture)
31
Clostridium channel is the agent of malignant oedema
F
32
Attenuated vaccines are used for the prevention of malignant oedema
F
33
Clostridium septicum is an agent of malignant oedema
T
**septicum, novyi, histolyticum and sordelli are causative agents**
34
Malignant oedema is generally a consequence of a wound infection
T
35
Clostridium histolyticum can cause malignant oedema
T
-C. Septicum
-C. Novyi
- C. Histolyticum
- C. Sordelli
36
Agents of malignant oedema can be detected by bacterium culture
T
37
There are no vaccines for the prevention of malignant oedema.
F
inactivated bacterium culture (anaculture)
38
Malignant oedema occurs in ruminants and pigs
T
39
Malignant oedema is an acute fatal disease
T
40
Malignant oedema can be treated with antibiotics
F
difficult, limited (fast course, toxic effects)
41
Malignant oedema can occur in any warm-blooded animal.
T
42
Once an area is infected with gas gangrene re-occurrence is common
T
43
Malignant oedema cannot occur in swine
F
44
Malignant oedema usually develop following an endogenous infection
F
45
Malignant oedema is well treated with long-term antibiotics therapy
F
46
Malignant oedema can be treated with polymyxin
F
47
Malignant oedema can be well treated with antibiotics over a long period
F
48
Gas gangrene (malignant oedema) is a regional illness
F
49
The lesions of malignant oedema are mainly seen in the lungs
F
50
Blackleg is caused by Clostridium septicum
F.
**C. chauvoei**
51
Lesions of blackleg are mainly seen on the claws
F
52
Lameness is a clinical sign of blackleg
T
53
Blackleg is a frequent disease in pigs
F
**Mainly seen in cattle and sheep, rarely in other species**
54
Generally attenuated vaccines are used for the prevention of blackleg
F
55
Anaculture or anatoxin vaccines are used for the prevention of blackleg
T
- anaculture, anatoxin
- combined vaccines
56
Blackleg occurs only in tropical and subtropical countries
F
**worldwide**
57
Generally attenuated vaccines are used for the prevention of blackleg
F
58
Blackleg generally occurs in endemic form
T
59
Blackleg occurs most frequently in pigs
F
ruminants (sometimes pigs and other species)
60
Blackleg is a gas gangrene disease
T
61
Blackleg is generally endogenous in sheep
F
**iatrogenic in sheep,endogenous in cattle**
62
Blackleg is generally endogenous in cattle
T
63
Movement disorders and lameness can be clinical signs of Blackleg
T
64
Clostridium chauvoei can produce acids and gas from carbohydrates
T
active carbohydrate fermentation (production of acid and gas)
65
Blackleg occurs mainly in ruminants
T
66
Oedema is a typical clinical sign of blackleg
T
67
Live vaccines are used for the prevention of blackleg
F
68
Blackleg infects ovine through wounds
T
69
In Blackleg disease we use attenuated vaccine
F
70
In the case of sheep, blackleg is generally consequence of a wound infection
T
71
Oedema in the muscles is a typical clinical sign of blackleg
T
72
Attenuated vaccines are used for the prevention of blackleg
F
73
Blackleg is caused by Clostridium chauvoei
T
74
Severe diarrhoea is the main clinical sign of blackleg
F
75
Blackleg is caused by Clostridium septicum
F
C. chauvoei
76
Blackleg occurs in cattle and sheep.
T
77
If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is generally successful
F
78
Attenuated vaccines are used for the prevention of blackleg
F
79
Blackleg disease occurs only in ruminants
F
80
Blackleg can usually be treated with antibiotics successfully
F
81
Blackleg in cattle is mainly endogenous between 6 months-3 years old
F
**Frequent in cattle between 2 months and 2 years**
82
The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep
T
**Causing by blackleg**
83
The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle.
T
84
Blackleg has four toxins
T
**toxins: a, b, g, d**
85
Blackleg can be prevented by using vaccine
T
86
We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei
F
87
Blackleg in cattle is mainly endogenous between 2 months-2 years old
T
88
Blackleg in bovine is caused by wound infections
F
Soil infection: mainly on pastures of poor quality
-sheep: wound infection
89
Classical swine fever is a frequent predisposing factor of bradsot
F
90
Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot
T
91
Bradsot is caused by Clostridium chauvoei
F
**C. septicum**
92
Soil contaminated frozen feed is a frequent predisposing factor of bradsot
T
* after driving the animals to winter pasture
* frozen feed contaminated with soil (potato, turnip, grass)
93
Frozen food is a predisposing factor of bradsot
T
94
Bradsot occurs mainly late autumn and winter
T
late autumn, winter, frost
95
Overeating can predispose the animals to bradsot
F
after driving the animals to winter pasture
* frozen feed contaminated with soil (potato, turnip, grass)
96
Thickening of and oedema in the stomach wall are typical lesions of bradsot
T (rennet)
97
Aminoglycosides are successfully used for treatment in the case of bradsot
F
98
Bradsot is mainly seen in late autumn and winter
T
99
Bradsot is mainly seen in late autumn and winter
T
late autumn, winter, frost
100
Bradsot is caused by Clostridium septicum
T
101
Severe pneumonia is a typical clinical sign of bradsot
F
102
Bradsot has a very fast course
T
103
Bradsot occurs only in suckling lambs
F
104
Bradsot is typically a chronic disease
F
105
Bradsot is common in the summer out on the pasture
F
late autumn, winter, frost
106
Bradsot is an acute disease resulting in sudden death in many cases
T
107
We can use anaculture strain vaccine against Bradsot
T, f ??
108
Bradsot causes oedema of the legs and necrosis
F
109
Post mortem lesions of bradsot can be seen in the stomach (rennet)
T
110
Koves disease is an indicator disease
T
indicator (haemorrhages in the stomach, erosions)
111
CSF is a predisposing factor of koves disease
T
112
Koves disease can be seen in pigs
T
113
Koves disease is caused by Clostridium chavoei
F
**C. septicum**
114
Infectious necrotic hepatitis is mainly seen in pigs
F
**Sheep 1-4 years**
115
Infectious necrotic hepatitis can be prevented by using anatoxin vaccines
T
(anaculture, anatoxin)
116
Liver fluke can predispose animals to infectious necrotic hepatitis
T
117
In sheep, Clostridium septicum causes necrotic liver infection
F
**C. novyi B**
118
Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver
T
119
There is no vaccine to prevent infectious necrotic hepatitis
F
vaccine (anaculture, anatoxin)
120
Infectious necrotic hepatitis is caused by Clostridium septicum
F
C. novyi B
121
Infectious necrotic hepatitis is mainly seen in suckling lambs
F
sheep 1-4 years (sometimes cattle, other)
122
Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis
T
parasite infection (liver flukes)
123
Anatoxin vaccines can be used for the prevention of infectious necrotic hepatitis.
T
124
Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis.
T
125
Infectious necrotic hepatitis is caused by Clostridium novyi
T
126
Infectious necrotic hepatitis is spread by tick
F
127
Infectious necrotic hepatitis is found worldwide
T
128
Infectious necrotic hepatitis can be transmitted by liver flukes
T
129
Infectious necrotic hepatitis occurs mostly in young sheep
F
sheep 1-4 year
130
There is intravascular haemolysis in the case of bacillary haemoglobinuria
T
131
Bacillary haemoglobinuria is caused by Clostridium haemolyticum
T
132
There are no vaccines for the prevention of bacillary hemoglobinuria
F
vaccine (6-month-long protection)
133
Phospholipase C is a virulence factor of the agent of bacillary hemoglobinuria
T
134
Bacillary haemoglobinuria is mainly seen in cattle
T
**cattle, mainly beef cattle (sometimes sheep)**
135
Bacillary haemoglobinuria is caused by Clostridium septicum
F
C. haemolyticum
136
Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria
T
- sudden onset
- fever, depression
- haemoglobinuri
- jaundice
- anaemia
- increased heart and breath rate
137
Red urine is a typical clinical sign of bacillary hemoglobinuria
T
138
Bacillary hemoglobinuria is a slow, chronic disease
F
139
Bacillary hemoglobinuria can frequently be seen in horses
F
cattle (sometimes sheep)
140
Clostridium novyi is the causative agent of bacillary hemoglobinuria.
F
C. haemolyticum
141
Bacillary hemoglobinuria causes severe haemorrhages
T
142
Bacillary hemoglobinuria are caused by infection from the soil
T
habitat: gut, soil
143
Lamb dysentery occurs in a week old animal
T
**1–2-week-old lambs**
144
Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery
F
145
Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery
F
146
Lesions of lamb dysentery are generally seen in the large intestine
F
**In the small intestine**
147
Lesions of lamb dysentery can be seen in the small intestine
T
148
Lamb dysentery is caused by Clostridium perfringens
T
149
Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery
F
**pregnant ewes are vaccinated**
150
Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery
F
Prevention :
- improving hygiene
- ewes: penicillin
- vaccine: pregnant ewes are vaccinated twice, yearly booster
151
Pregnant ewes have to be vaccinated in order to prevent lamb dysentery
T
pregnant ewes are vaccinated twice, yearly booster
152
Haemorrhagic diarrhoea is a clinical sign of lamb dysentery
T
153
Lamb dysentery can be seen in lambs around weaning
F
1–2-week-old lambs
154
Lamb dysentery is found in 3-4-week-old lambs
F
1–2-week-old lambs
155
Pathological lesions of Lamb dysentery starts in the colon
F
**Small intestine**
156
We can culture the pathogen of Lamb dysentery from the intestines
T
157
Lamb dysentery is caused by Clostridium dysenteriae
F
C. perfringens B
158
Lamb dysentery can be seen in lambs after weaning
F
1–2-week-old lambs
159
There is no vaccine for the prevention of lamb dysentery
F
Vaccine: pregnant ewes are vaccinated twice, yearly booster
160
Lamb dysentery occurs in 2-6 weeks old lambs
F
1–2-week-old lambs
161
For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine
T
162
Pathological symptoms of lamb dysentery can be found in the large intestines
F
small intestine
163
Lamb dysentery can be prevented by vaccinating pregnant ewes
T
pregnant ewes are vaccinated twice, yearly booster
164
Lamb dysentery can be successfully treated with penicillin when clinical signs appear
F
**treatment is generally not possible**
165
Lamb dysentery occurs in a week-old animal.
T
1–2-week-old lambs
166
Lamb dysentery can be diagnosed by culturing the bacteria
T
167
Newborn lambs have to be vaccinated in order to prevent lamb dysentery.
F
168
Toxoid vaccines can be used in the prevention of lamb dysentery
T
169
Infection of lamb dysentery by secretion in the milk
F
170
Lamb dysentery occurs in 1-2 weeks old lambs.
T
171
Struck is caused by Clostridium perfringens
T
Clostridium perfringens C
172
Overeating is a predisposing factor of struck
T
- overeating
- high protein and carbohydrate content
- change of the diet
173
Struck can be seen mainly in lambs younger than 2 weeks
F
**In grower, adult sheep**
174
Struck is an acute disease in horses
F
175
Struck is a zoonotic disease
F
176
Struck is a slow disease of older sheep
F
**very fast course**
177
Struck is a worldwide common disease with great economic impact
F
it is worldwide, but not great economic impact
178
Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life
F
**2–4-day-old piglets**
179
The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large intestine
F
**small intestine, jejunum**
180
Maternal protection is important in the case of Infectious necrotic enteritis of piglets
T
181
There is no vaccination for the prevention of Infectious necrotic enteritis of piglets
F
**vaccination of pregnant sows**
182
Pig enterotoxaemia can be prevented by vaccinating the pregnant sows.
T
PIG ENTEROTOXAEMIA (INFECTIOUS NECROTIC ENTERITIS OF PIGLETS)
183
Pig enterotoxaemia is caused by Clostridium perfringens C
T
184
Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics
immediately
F
**Fast course ,no time for treatment**
185
Lesions of pig enterotoxaemia can be seen in the small intestine
T
186
Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets
T
187
Pig enterotoxaemia is more frequent in the litter of young than old sows
T
**Older sows give protection through colostrum**
188
Pig enterotoxaemia can be generally seen in weaned piglets
F
2–4-day-old piglets
189
Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia
T
190
Clostridium enterotoxaemia of piglets is caused by C. perfringens
T
C. perfringens C
191
Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows
T
192
Clostridium perfringens C causes infectious necrotic enteritis of piglets
T
193
Infectious necrotic enteritis of piglets occurs in piglets after weaning
F
194
The lesions of infectious necrotic enteritis of piglets can be seen generally in the small intestine
T
195
Infectious necrotic enteritis of piglets can be prevented by vaccinating the pregnant sows
T
196
Necrotic enteritis of piglets is seen in piglets around weaning
F
197
Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin
T
198
Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets
F
detection of the agent
199
Pig enterotoxaemia causes abdominal contractions in sows
F
200
Mesenteric lymph node is congested in case of pig enterotoxaemia
F
201
Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut
T
202
Enteritis in piglets are caused by Clostridium perfringens D
F
**Clostridium perfringens D causes pulpy kidney disease**
203
Enteritis in piglets can be avoided by anatoxin vaccination
T
204
Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology
F
205
Pig enterotoxaemia is caused by β-toxin production in 1st week of life
T
a and b toxin (b toxin is trypsin sensitive)
206
Pig enterotoxaemia can cause a high mortality
T.
**Mortality = 20-100%**
207
Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut
F
208
Enterotoxaemia is mainly seen in piglets after weaning
F
209
Pig enterotoxaemia is not present in Europe
F
**worldwide**
210
Pig enterotoxaemia cannot be prevented by using vaccines
F
vaccination of pregnant sows
211
Pulpy kidney disease is caused by Clostridium perf. D
T
212
Overeating is a predisposing factor to pulpy kidney disease
T
- overaating
- sudden change of the diet
213
The toxin of the agent of pulpy kidney disease is sensitive to trypsin
F
**activated by trypsin**
214
Pulpy kidney disease is caused by Clostridium perfringens D
T
215
Pulpy Kidney Diseases is caused by Clostridium chauvoei.
F
Clostridium perfringens D
216
Pulpy kidney disease generally occurs in 1-2 week old lambs
F
**most frequent in 6-12-month-old lambs, but sometimes 1-2 months old**
217
Pulpy kidney disease can occur at any age
F
- most frequent in 6-12-month-old lambs, kids
- sometimes 1-2 months old
218
Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes
F
219
Sudden change the diet is a predisposing factor to pulpy kidney disease
T
- overeating
- sudden change of the diet
220
The toxin damages the endothelial cells in the case of pulpy kidney disease
T
221
Neurological signs are typical in the case of pulpy kidney disease
T
* neurological signs
* abdominal pain
* diarrhoea
* glucosuria
222
Isolation of the agent is necessary to the diagnosis of pulpy kidney disease
F
223
Pulpy kidney disease is typically seen in lambs below 2 weeks of age
F
* most frequent in 6-12-month-old lambs, kids
* sometimes 1-2 months old
224
Inactivated vaccines are used for the prevention of pulpy kidney disease
T
225
Pulpy kidney disease is seen in piglets in the first week of life
F
* most frequent in 6-12-month-old lambs, kids
* sometimes 1-2 months old
226
Pulpy kidney disease is a worldwide common disease.
T
227
Enterotoxaemia of sheep is also called pulpy kidney disease.
T
228
Pulpy kidney disease is caused by Clostridium perfringens D.
T
229
Cattle are not susceptible to pulpy kidney disease
T
**Sheep an goat**
230
Vaccination are possible against pulpy kidney disease
T
231
Coccidiosis is a predisposing factor of ulcerative enteritis in poultry
T
Predisposing factor:
- coccidiosis
- infectious bursitis
- chicken anaemia
- overcrowding
- nutritional problems
- old litter
232
Ulcerative enteritis of chicken is caused by Clostridium colinum.
T
233
Ulcerative enteritis is frequently seen in day old chicken
F
**4–12-week-old chicken and 3–8-week-old turkey**
234
Ulcers sometimes covered with pseudomembranes are frequent post mortem lesions of ulcerative enteritis of chicken
T
235
Ulcerative enteritis can occur in 4-12-week-old chickens
T
236
Clostridium perfringens is the causative agent of ulcerative enteritis in poultry
F
**It is C. colinum**
237
Ulcerative enteritis of poultry is generally prevented with vaccination.
F
**With hygiene, optimal management and elimination of predisposing factors**
238
Lesions of ulcerative enteritis are mostly seen in the small intestines
F
239
Ulcerative enteritis is a common disease in large scale farms
T
240
Prevention of coccidiosis can help lower the incidence of ulcerative enteritis
T
241
Coccidiosis is a predisposing factor of necrotic enteritis of chicken
T
predisposing factors:
- coccidiosis, mycotoxicosis
- feed: wheat, fishmeal
- poorly digestible feed
- alteration of the intestinal flora
- damage of the mucosa
242
Foamy, brownish-red faeces is a clinical sign of necrotic enteritis of chicken
T
243
Lesions of necrotic enteritis of chicken are typically occur in the large intestine
F
**small intestine - jejunum and ileum**
244
Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis
F
245
Necrotic enteritis mostly occurs in chicken
T
246
Waterfowl are not susceptible to necrotic enteritis
F
**seen in chickens, turkeys and ducks worldwide**
247
Necrotic enteritis occurs in 1-3 weeks of age
F
**In broiler 2–5-week-old, and turkey 7–12-week-old**
248
Tyzzer’s disease is caused by Clostridium piliforme
T
249
Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A
T
* C. septicum
* C. perfringens A
* Staphylococcus aureus
* facultative pathogenic bacteria
250
Gangrenous dermatitis is caused by obligate pathogens
F
**facultative pathogens**
251
Gangrenous dermatitis causes muscle oedema
T
* muscles: oedema, reddish, crepitation
252
Vaccines are the primary way of prevention of gangrenous dermatitis
F
**No vaccines are available**
253
Flaccid paralysis is a frequent clinical sign of tetanus
F
254
The agent of tetanus is strictly anaerobic
T
255
The agent of tetanus can enter the host through wounds
T
256
Tetanus is only seen in horse
F
**horse, sheep, cattle, swine, dog**
257
Over-eating can predispose animals to Tetanus
F
predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria
258
The agent of Tetanus needs oxygen to replicate
F
**cannot survive in the presence of oxygen !!**
259
Anatoxin vaccines are available for the prevention of tetanus
T
260
Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus
F
**No gross lesions**
261
Spasms are typical clinical signs of tetanus
T
horse, sheep:
* spasms, stiffness, tonic contractions
* lockjaw, „saw-horse”
* ears stand up, third eyelid, nares are wide
262
Tetanus is a zoonosis
F
263
Toxoid vaccines can be used for the prevention of tetanus.
T
264
Dogs are resistant to tetanus
F
265
The clinical signs of tetanus are inducible
T
**= capable of being induced**
266
Tetanus toxin cleaves synaptobrevin
T
267
For tetanus we use vaccines which contain toxoid
T
268
Tetanus cannot be prevented with vaccination.
F
269
Tetanus is caused by Clostridium tetani
T
270
The agent of tetanus causes septicaemia.
F
271
Tetanus can be diagnosed on the basis of post mortem lesions
F
272
Clostridium tetani produced endotoxin
F
273
C. tetani needs anaerobic conditions for propagation
T
274
Dogs are susceptible to tetanus
T
275
Tetanus can be prevented with vaccines containing inactivated bacteria
F
276
Tetanus can cause spasms
T
277
Horses are resistant to tetanus
F
278
Tetanus can only develop after deep wounds
F
279
Wounds can predispose to tetanus
T
predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria
280
The paralysis usually starts at the place of the wound
F
**Spasms begin at the site of entry, in the LOCAL form**
281
Clostridium tetani toxin is produced in the feed
F
282
Horses are most sensitive to tetanus
T
283
Tetanus can be prevented by anatoxin vaccination
T
284
Tetanus causes rigid paralysis
T
**Causing spastic or rigid muscle paralysis**
285
There is no vaccine for tetanus
F
anatoxin vaccination
286
Clostridium tetani produces neurotoxins
T
287
Dogs have high resistance to tetanus
T
**Tetanus is a relatively uncommon disease in dogs and cats because of their natural resistance to the toxin**
288
The toxin of clostridium botulinum causes flaccid paralysis
T
289
Clostridium botulinum generally causes wound infection
F
290
Focal necrosis in the liver is a typical post mortem lesion of Botulism
F
**Pathological lesions are not characteristic**
291
The toxin of Clostridium botulinum has irreversible effect
T
292
Botulism can be seen as a result of a wound infection
F
293
Flaccid paralysis is the main clinical sign of botulism
T
294
Birds are resistant to botulism
F
**Most frequent = mink, fox, duck, geese, pheasant**
295
Necrotic foci in the liver are typical post mortem lesions of botulism
F
Pathology:
* not characteristic
* hyperaemic organs
* oedema in the lungs
296
Generally wounds predispose animals to botulism
F
297
The agent of botulism generally produces toxin at the site of entry
F
298
Botulism is diagnosed on the basis of the typical post mortem lesions
F
299
Clostridium botulinum can produce toxins outside the hosts.
T
300
No characteristic post mortem lesions can be seen in the case of botulism
T
Pathology
* not characteristic
* hyperaemic organs
* oedema in the lungs
301
Botulism doesn’t occur in Europe
F
**worldwide – warmer climate**
302
Clostridium botulinum cannot tolerate air at all
T
**anaerobic bacterium, meaning it cannot survive in the presence of oxygen. Exposure to air can inhibit its growth and toxin production**
303
Botulism usually develops following a wound infection
F
304
Clostridium botulinum propagates in rotten materials.
T
305
In Hungary, botulism is seen most commonly in birds
T
306
Clostridium botulinum spores are extremely resistant to heat
T
307
In Hungary, botulism occurs in winter and early spring.
F
**worldwide – warmer climate**
308
Botulism is eradicated in Europe
F
worldwide – warmer climate
309
Clostridium botulinum can produce toxin, some of which are activated by proteases
T
310
Botulism is seen mainly during summer
T
worldwide – warmer climate
311
Spasms are the typical clinical sign of botulism
F
312
Paralysis is the main sign of botulism
T
313
Toxins of botulism are produced generally in the food.
T
314
Botulism happen generally through wound infection
F
315
Animals are mostly sensitive to C and D types of Clostridium botulinum.
T
**A, B, E, F = Humans**
316
Lesions of pig enterotoxaemia can be seen in the large intestine
F
**Jejunum**
317
Infectious necrotic hepatitis is caused by Clostridium novyi type B
T
