MT3- 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 (obligate anaerobic)
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
extracellular enzymes
toxins (can be converted to anatoxin)
8
Q
There are no vaccines for the prevention of diseases caused by clostridia
A
F
(inactivated bacterium culture (anaculture)
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
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 (obligate anaerobic)
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
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
Is gas gangrene (malignant oedema) 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 - NOT FREQUENT
ruminants (sometimes pigs and 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
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
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 (sheep)
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
82
The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep
T
83
The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle.
T
84
Blackleg has four toxins
T
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
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 caused by Clostridium novyi type B
T
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 (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
small intestine
147
Lesions of lamb dysentery can be seen in the small intestine
T
148
Lamb dysentery is caused by Clostridium perfringens
T
Clostridium perfringens B
149
Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery
F
Prevention :
- improving hygiene
- ewes: penicillin
- vaccine: pregnant ewes are vaccinated twice, yearly booster
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
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 the disease
T
169
Infection of lamb 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
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
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
180
Maternal protection is important in the case of Infectious necrotic enteritis of piglets
T, F??
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
185
Lesions of pig enterotoxaemia can be seen in the small intestine
T
186
Lesions of pig enterotoxaemia can be seen in the large intestine
F
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
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 C
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. (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
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, kids
- 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 this disease
T
???idk
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)
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
ENTEROTOXAEMIA DISEASES
237
Ulcerative enteritis of poultry is generally prevented with vaccination.
F
* hygiene
* optimal management
* elimination of predisposing factors
238
Lesions of ulcerative enteritis are mostly seen in the small intestines
T
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
247
Necrotic enteritis occurs in 1-3 weeks of age
F
broiler 2–5-week-old
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
251
Gangrenous dermatitis causes muscle oedema
T
* muscles: oedema, reddish, crepitation
252
Vaccines are the primary way of prevention of gangrenous dermatitis
F
* antibiotics p.o.
* elimination of predisposing effects
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
predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria
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
anaerobic conditions
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
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
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
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
285
There is no vaccine for tetanus
F
anatoxin vaccination
286
Clostridium tetani produces neurotoxins
T
287
Dogs have high resistance to tetanus
T
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
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
- birds
- horse
- mink
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
