Clostridia Flashcards
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
5
Q
Clostridium perfringens is an obligate pathogenic bacterium
A
F
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
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
Enterotoxaemia of young animals foals and piglets
14
Q
Clostridium difficile is seen in foal and piglets
A
T
15
Q
Many Clostridium species have flagella
A
F
Only clostridium dificcile has peritrichous flagellae
je giafto troi metronitazoli :)
16
Q
Clostridium species are only found in the subtropics
A
F
17
Q
Clostridium can cause severe contagious diseases
A
F
18
Q
Clostridium are obligate pathogens
A
F
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
22
Q
Malignant oedema is generally endogenous in cattle
A
F
malignant odema = wound only
Black leg =swce sheep wound cattle endogenous
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
DDx : Blackleg
27
Malignant oedema is caused due to wound infection
T
28
Malignant oedema is only in ruminants
F
mainly horses also mammals and birds
29
Malignant oedema, one of the clinical signs is lameness/movement problems
T
30
Malignant oedema, attenuated vaccine for prevention
F
Anatoxin anaculture which are inactivated toxin and agent
31
Clostridium channel is the agent of malignant oedema
F
32
Clostridium septicum is an agent of malignant oedema
T
33
Clostridium histolyticum can cause malignant oedema
T
34
Agents of malignant oedema can be detected by bacterium culture
T
35
There are no vaccines for the prevention of malignant oedema
F
36
Malignant oedema occurs in _ruminants and pigs_
T
Mammals and birds
37
Malignant oedema is an acute fatal disease
T
Acute for sure 1-2days ip fatal yes because a lot of pathology
38
Malignant oedema can be treated with antibiotics
F
too late
39
Malignant oedema can occur in any warm-blooded animal
F
40
Once an area is infected with gas gangrene re-occurrence is common
T
41
Malignant oedema cannot occur in swine
F
42
Malignant oedema usually develop following an endogenous infection
F
Strictly wound
43
Malignant oedema is well treated with long-term antibiotics therapy
F
44
Malignant oedema can be treated with polymyxin
F
45
Malignant oedema can be well treated with antibiotics over a long period
F
46
gas gangrene (malignant oedema) is a regional illness
F
Worldwide
47
The lesions of malignant oedema are mainly seen in the lungs
F
48
Blackleg is caused by Clostridium septicum
F
49
Lesions of blackleg are mainly seen on the claws
F
50
Lameness is a clinical sign of blackleg
T
51
Blackleg is a frequent disease in pigs
F
52
Generally attenuated vaccines are used for the prevention of blackleg
F
53
Anaculture or anatoxin vaccines are used for the prevention of blackleg
T
54
Blackleg occurs only in tropical and subtropical countries
F
55
Blackleg generally occurs in endemic
T
Endemic regions
56
Blackleg occurs most frequently in pigs
F
57
Blackleg is a gas gangrene disease
T
58
Blackleg is generally endogenous in sheep
F
Swce
59
Blackleg is generally endogenous in cattle
T
60
Movement disorders and lameness can be clinical signs of Blackleg
T
61
Clostridium chauvoei can produce acids and gas from carbohydrates
T
62
Blackleg occurs mainly in ruminants
T
63
Oedema is a typical clinical sign of blackleg
T
64
Live vaccines are used for the prevention of blackleg
F
65
Blackleg infects ovine through wounds
T
66
In Blackleg disease we use attenuated vaccine
F
67
In the case of sheep, blackleg is generally consequence of a wound infection
T
68
Blackleg is caused by Clostridium chauvoei
T
69
Severe diarrhoea is the main clinical sign of blackleg
F
70
Blackleg occurs in cattle and sheep
T
71
If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is generally successful
F
72
Blackleg disease occurs **only** in ruminants
F
Rarely other species
73
Blackleg can usually be treated with antibiotics successfully
F
74
Blackleg in cattle is mainly endogenous between 6 months-3 years old
F
75
The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep
T
76
The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle
T
77
Blackleg has four toxins
T
78
Blackleg can be prevented by using vaccine
T
79
We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei
F
80
Blackleg in cattle is mainly endogenous between 2 months-2 years old
T
swce
81
Blackleg in bovine is caused by wound infections
F
82
Classical swine fever is a frequent predisposing factor of bradsot
F
83
Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot
T
rennet = abomasum
84
Bradsot is caused by Clostridium chauvoei
F
85
Bradsot occurs mainly in tropical and subtropical countries
F
north europe kriada frozen potato and turnip
86
Soil contaminated frozen feed is a frequent predisposing factor of bradsot
T
87
Frozen food is a predisposing factor of bradsot
T
88
Bradsot occurs mainly late autumn and winter
T
89
Overeating can predispose the animals to bradsot
F
90
Thickening of and oedema in the stomach wall are typical lesions of bradsot
T
91
Aminoglycosides are successfully used for treatment in the case of bradsot
F
92
Bradsot is caused by Clostridium septicum
T
93
Severe pneumonia is a typical clinical sign of bradsot
F
94
Bradsot has a very fast course
T
95
Bradsot occurs only in suckling lambs
F
96
Bradsot is typically a chronic disease
F
97
Bradsot is common in the summer out on the pasture
F
98
Bradsot is an acute disease resulting in sudden death in many cases
T
99
We can use anaculture strain vaccine against Bradsot
T
100
Bradsot causes oedema of the legs and necrosis
F
101
Post mortem lesions of bradsot can be seen in the stomach (rennet).
T
102
Köves disease is an indicator disease
T
Indicator of a primary disease theat caused ulceration haemorrhages on the git.
103
CSF is a predisposing factor of koves disease
T
104
Köves disease can be seen in pigs.
T
105
Köves disease is caused by Clostridium chavoei
F
106
Infectious necrotic hepatitis is mainly seen in pigs
F
107
Infectious necrotic hepatitis can be prevented by using anatoxin vaccines
T
108
Liver fluke can predispose animals to infectious necrotic hepatitis
T
109
In sheep, Clostridium septicum causes necrotic liver infection
F
110
Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver
T
111
There is no vaccine to prevent infectious necrotic hepatitis
F
112
Infectious necrotic hepatitis is caused by Clostridium septicum
F
113
Infectious necrotic hepatitis is mainly seen in suckling lambs
F
114
Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis
T
115
Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis
T
116
Anatoxin vaccines can be used for the prevention of infectious necrotic hepatitis
T
117
Infectious necrotic hepatitis is caused by Clostridium novyi
T
118
Infectious necrotic hepatitis is spread by tick
F
119
Infectious necrotic hepatitis is caused by Clostridium novyi type B
T
120
Infectious necrotic hepatitis is found worldwide
T
121
Infectious necrotic hepatitis can be transmitted by liver flukes
F
122
**Infectious necrotic hepatitis** occurs mostly in ** young sheep**
F
Mainly sheep also cattle
1-4 years old? is this young
123
There is intravascular haemolysis in the case of bacillary haemoglobinuria
T
124
Bacillary haemoglobinuria is caused by Clostridium haemolyticum
T
125
There are no vaccines for the prevention of bacillary hemoglobinuria
F
126
Phospholipidase C is a virulence factor of the agent of bacillary hemoglobinuria
T
127
Bacillary haemoglobinuria is mainly seen in cattle
T
Black disease SC
Bac haemo CS
128
Bacillary haemoglobinuria is caused by Clostridium septicum
F
129
Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria
T
130
Red urine is a typical clinical sign of bacillary hemoglobinuria
T
131
Bacillary haemoglobinuria is a slow, chronic disease
F
sudden onset all histolytic clostridia and (enterotoxaemic clostridia?)
132
Bacillary hemoglobinuria can frequently be seen in horses
F
133
Clostridium novyi is the causative agent of bacillary hemoglobinuria
F
134
Bacillary hemoglobinuria causes severe haemorrhages
T
135
Bacillary hemoglobinuria are caused by infection from the soil
T
mainly endogenous but also infection from the soil
136
Lamb dysentery occurs in a week old animal
T
137
Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery
F
138
Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery
F
139
Lesions of lamb dysentery are generally seen in the large intestine
F
140
Lesions of lamb dysentery can be seen in the small intestine
T
141
Lamb dysentery is caused by Clostridium perfringens B
T
142
Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery
F
Ewes
143
Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery
F
144
Pregnant ewes have to be vaccinated in order to prevent lamb dysentery
T
145
Haemorrhagic diarrhoea is a clinical sign of lamb dysentery
T
146
Lamb dysentery can be seen in lambs around weaning
F
147
Lamb dysentery is found in 3-4-week-old lambs.
F
148
Pathological lesions of Lamb dysentery starts in the colon
F
149
We can culture the pathogen of Lamb dysentery from the intestines
T
150
Lamb dysentery is caused by Clostridium dysenteriae
F
151
Lamb dysentery can be seen in lambs after weaning
F
152
There is no vaccine for the prevention of lamb dysentery
F
153
Lamb dysentery occurs in 2-6 weeks old lambs
F
154
For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine
T
lamb dysentery no bacterium isolation from the gut but microscopy culture is okay
155
Pathological symptoms of lamb dysentery can be found in the large intestines
F
156
Lamb dysentery can be prevented by vaccinating pregnant ewes
T
157
Lamb dysentery can be successfully treated with penicillin when clinical signs appear
F
158
Lamb dysentery occurs in a week-old animal
T
159
Lamb dysentery can be diagnosed by culturing the bacteria
T
160
Newborn lambs have to be vaccinated in order to prevent lamb dysentery
F
161
Toxoid vaccines can be used in the prevention of the disease
T
162
Infection of lamb by secretion in the milk
F
163
Lamb dysentery occurs in 1-2 weeks old lambs
T
164
Struck is caused by Clostridium perfringens C.
T
165
Overeating is a predisposing factor of struck
T
166
Struck can be seen mainly in **lambs** younger than 2 weeks
F
167
Struck is an acute disease in horses
F
168
Struck is a zoonotic disease
F
169
Struck is a slow disease of older sheep
F
Fast course sudden onset
170
Struck is a worldwide common disease with great economic impact
F
171
Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life
T
2-4d so 1st week
172
The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large intestine
F
173
Maternal protection is important in the case of Infectious necrotic enteritis of piglets
T
174
There is no vaccination for the prevention of Infectious necrotic enteritis of piglets
F
175
Pig enterotoxaemia can be prevented by vaccinating the pregnant sows
T
176
Pig enterotoxaemia is caused by Clostridium perfringens C
T
177
Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics immediately
F
Too late
Penicillins to sows
178
Lesions of pig enterotoxaemia can be seen in the small intestine
T
179
Pig enterotoxaemia is more frequent in the litter of young than old sows
T
180
Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets
T
181
Pig enterotoxaemia can be generally seen in weaned piglets
F
182
Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia
T
183
Clostridium enterotoxaemia of piglets is caused by C. perfringens
T
184
Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows
T
185
Clostridium perfringens C causes infectious necrotic enteritis of piglets
T
186
Infectious necrotic enteritis of piglets occurs in piglets after weaning
F
187
The lesions of infectious necrotic enteritis of piglets can be seen generally in the small intestine
T
188
Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin
T
189
Pig enterotoxaemia has to be diagnosed by detecting **antibodies** in the piglets
F
direct detection
190
Pig enterotoxaemia causes abdominal contractions in sows
F
191
Mesenteric lymph node is congested in case of pig enterotoxaemia
F
192
Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut
T
193
Enteritis in piglets are caused by Clostridium perfringens D.
F
194
Enteritis in piglets can be avoided by anatoxin vaccination
T
195
Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology
F
196
Pig enterotoxaemia is caused by β-toxin production in 1st week of life.
T
197
Pig enterotoxaemia can cause a high mortality
T
198
Necrotic enteritis of piglets **cannot** be diagnosed by isolating the agent from the gut
T
Epidi en na evris c.perfringes C pou kami jalla disease??
culture smear microscopy no isolation
199
Pig enterotoxaemia is not present in Europe
F
200
Pig enterotoxaemia cannot be prevented by using vaccines
F
201
Pulpy kidney disease is caused by Clostridium perf. D
T
202
Overeating is a predisposing factor to pulpy kidney disease
T
203
The toxin of the agent of pulpy kidney disease is sensitive to trypsin
T
D(α, ε=trypsin act)
204
Pulpy Kidney Diseases is caused by Clostridium chauvoei
F
205
Pulpy kidney disease generally occurs in 1-2week old lambs
F
206
Pulpy kidney disease can occur at any age
F
207
Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes
F
208
Sudden change the diet is a predisposing factor to pulpy kidney disease
T
209
The toxin damages the endothelial cells in the case of pulpy kidney disease
T
210
Neurological signs are typical in the case of pulpy kidney disease
T
211
Isolation of the agent is necessary to the diagnosis of pulpy kidney disease
F
212
Pulpy kidney disease is typically seen in lambs below 2 weeks of age
F
213
Inactivated vaccines are used for the prevention of pulpy kidney disease
T
214
Pulpy kidney disease is seen in piglets in the first week of life
F
215
Pulpy kidney disease is a worldwide common disease
T
216
Enterotoxaemia of sheep is also called pulpy kidney disease
T
217
Cattle are not susceptible to this disease
T
218
Vaccination are possible against pulpy kidney disease
T
219
Coccidiosis is a predisposing factor of ulcerative enteritis in poultry
T
220
Ulcerative enteritis of chicken is caused by Clostridium colinum
T
221
Ulcerative enteritis is frequently seen in day old chicken
F
222
Ulcers sometimes covered with pseudomembranes are frequent post mortem lesions of ulcerative enteritis of chicken
T
223
Ulcerative enteritis can occur in 4-12-week-old chickens
T
do not confuse with Necrotic enteritis of Chicken caused by C. perfringes A
Broiler 2-5w, turkeys 7-12w
224
Clostridium perfringens is the causative agent of ulcerative enteritis in poultry
F
225
Ulcerative enteritis of poultry is generally prevented with vaccination
F
226
Lesions of ulcerative enteritis are mostly seen in the small intestines
T
First small intestine then upper large intestine
227
Ulcerative enteritis is a common disease in large scale farms
T
228
Prevention of coccidiosis can help lower the incidence of ulcerative enteritis
T
229
Coccidiosis is a predisposing factor of necrotic enteritis of chicken
T
230
Foamy, brownish-red faeces is a clinical sign of necrotic enteritis of chicken
T
231
Lesions of **necrotic** enteritis of chicken are typically occur in the large intestine
F
jejunum and ileum =SI
232
Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis
F
233
Necrotic enteritis mostly occurs in chicken
T
Thus the name necrotic enteritis of chicken
Also turkeys
234
Waterfowl are not susceptible to necrotic enteritis
F
They are
235
Necrotic enteritis occurs in 1-3 weeks of age
F
236
Tyzzer’s disease is caused by Clostridium piliforme
T
237
Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A
T
238
Gangrenous dermatitis is caused by obligate pathogens
F
239
Gangrenous dermatitis causes muscle oedema
T
240
Vaccines are the primary way of prevention of gangrenous dermatitis
F
241
Flaccid paralysis is a frequent clinical sign of tetanus
F
242
The agent of tetanus is strictly anaerobic
T
243
The agent of tetanus can enter the host through wounds
T
244
Tetanus is only seen in horse
F
245
Over-eating can predispose animals to Tetanus
F
246
The agent of Tetanus needs oxygen to replicate
F
247
Anatoxin vaccines are available for the prevention of tetanus
T
248
Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus
F
249
Spasms are typical clinical signs of tetanus
T
250
Tetanus is a zoonosis
F
251
xoid vaccines can be used for the prevention of tetanus
T
252
Dogs are resistant to tetanus
F
253
The clinical signs of tetanus are inducible
T
254
Tetanus toxin cleaves synaptobrevin
T
255
For tetanus we use vaccines which contain toxoid
T
256
Tetanus cannot be prevented with vaccination
F
257
Tetanus is caused by Clostridium tetani
T
258
The agent of tetanus causes septicaemia
**F**
The bacterium never enters the bloodstream. Only the toxins released after the autolysis of the vegetative bacterium. Necrotic anaerobic conditions at entry site initiate spore germination.
259
Tetanus can be diagnosed on the basis of post mortem lesions
F
260
Clostridium tetani produced endotoxin
F
Endotoxins= membrane compounds of gram negative bacteria
Exotoxins = are proteinoid substances released
261
C. tetani needs anaerobic conditions for propagation
T
262
Dogs are susceptible to tetanus
T
263
Tetanus can be prevented with vaccines containing **inactivated bacteria**
F
inactivated toxoid = Anatoxin
264
Tetanus can cause spasms
T
265
Horses are resistant to tetanus
F
266
Tetanus can only develop after deep wounds
F
Not deep only, even navel infection, teeth of foals, and ear tagging
267
Wounds can predispose to tetanus
T
268
The paralysis usually starts at the place of the wound
F
Spasms begin from the head
269
Clostridium tetani toxin is produced in the feed
F
270
Horses are most sensitive to tetanus
T
271
Tetanus can be prevented by anatoxin vaccination
T
272
Tetanus causes rigid paralysis
T
273
There is no vaccine for tetanus
F
274
Dogs have high resistance to tetanus
T
have natural resistance to the toxin
275
Clostridium tetani produces neurotoxins
T
276
The toxin of clostridium botulinum causes flaccid paralysis
T
277
Clostridium botulinum generally causes wound infection
F
278
Focal necrosis in the liver is a typical post mortem lesion of Botulism
F
279
The toxin of Clostridium botulinum has irreversible effect
T
280
Botulism can be seen as a result of a wound infection
F
281
Flaccid paralysis is the main clinical sign of botulism
T
282
Birds are resistant to botulism
F
283
Necrotic foci in the liver are typical post mortem lesions of botulism
F
284
Generally wounds predispose animals to botulism
F
285
The agent of botulism generally produces toxin at the site of entry
F
286
Botulism is diagnosed on the basis of the typical post mortem lesions
F
287
Clostridium botulinum can produce toxins outside the hosts
T
288
No characteristic post mortem lesions can be seen in the case of botulism
T
289
Botulism doesn’t occur in Europe
F
290
Clostridium botulinum cannot tolerate air at all
T
291
Botulism usually develops following a wound infection
F
292
Clostridium botulinum propagates in rotten materials
T
293
In Hungary, botulism is seen most commonly in birds
T
294
Clostridium botulinum spores are extremely resistant to heat
T
295
In Hungary, botulism occurs in winter and early spring
F
warmer climate summer
296
Botulism is eradicated in Europe
F
297
Clostridium botulinum can produce toxin, some of which are activated by proteases
T
298
Botulism is seen mainly during summer
T
299
Spasms are the typical clinical sign of botulism
F
300
Paralysis is the main sign of botulism
T
301
Toxins of botulism are produced generally in the food
T
302
Animals are mostly sensitive to C and D types of Clostridium botulinum
T
