Clostridium Flashcards

1
Q

Most clostridia have low invasive capacity

A

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2
Q

Spores of clostridia are generally very resistant against heat

A

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3
Q

The habitat of clostridia is the gut and the soil

A

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4
Q

Clostridia are obligate aerobic bacteria

A

F

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5
Q

Clostridium perfringens is an obligate pathogenic bacterium

A

F

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6
Q

Clostridium perfringens can produce main and auxillary toxins

A

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7
Q

Extracellular enzymes and toxins are virulence factors of clostridia

A

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8
Q

There are no vaccines for the prevention of diseases caused by clostridia

A

F

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9
Q

There are no vaccines for the prevention of diseases caused by clostridia

A

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10
Q

Clostridium bacteria is not in the environment, because it cannot tolerate oxygen

A

F

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11
Q

Clostridium spreads usually rapid in a herd

A

F

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12
Q

Clostridium spread mostly with insecticides

A

F

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13
Q

Clostridium difficile can be treated with metronidazole

A

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14
Q

Clostridium difficile is seen in foal and piglets

A

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15
Q

Many Clostridium species have flagella

A

F

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16
Q

Clostridium species are only found in the subtropics

A

F

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17
Q

Clostridium can cause severe contagious diseases

A

F

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18
Q

Clostridium are obligate pathogens

A

F

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19
Q

Anaculture or anatoxin vaccines are used for the prevention of malignant oedema

A

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20
Q

Cl. chauvoei is the agent of malignant oedema

A

F

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21
Q

Lesions of malignant oedema are mainly seen in the large muscles

A

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22
Q

Malignant oedema is generally a consequence of wound infection

A

F

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23
Q

Malignant oedema is generally a consequence of wound infection

A

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24
Q

Movement difficulties are frequently seen in the case of malignant oedema

A

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25
Q

Clostridium novyi can cause malignant oedema

A

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26
Q

Malignant oedema can be diagnosed based on clinical signs

A

F

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27
Q

Malignant oedema is caused due to wound infection

A

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28
Q

Malignant oedema is only in ruminants

A

F

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29
Q

Malignant oedema, one of the clinical signs is lameness/movement problems

A

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30
Q

Malignant oedema, attenuated vaccine for prevention

A

F

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31
Q

Clostridium channel is the agent of malignant oedema

A

F

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32
Q

Malignant oedema is generally a consequence of a wound infection

A

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33
Q

Clostridium histolyticum can cause malignant oedema

A

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34
Q

Clostridium histolyticum can cause malignant oedema

A

F

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35
Q

Clostridium histolyticum can cause malignant oedema

A

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36
Q

Agents of malignant oedema can be detected by bacterium culture

A

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37
Q

There are no vaccines for the prevention of malignant oedema.

A

F

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38
Q

Malignant oedema occurs in ruminants and pigs

A

T

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39
Q

Malignant oedema is an acute fatal disease

A

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40
Q

Malignant oedema can be treated with antibiotics

A

F

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41
Q

Malignant oedema can occur in any warm-blooded animal.

A

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42
Q

Once an area is infected with gas gangrene re-occurrence is common

A

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43
Q

Malignant oedema cannot occur in swine

A

F

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44
Q

Malignant oedema usually develop following an endogenous infection

A

F

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45
Q

Malignant oedema is well treated with long-term antibiotics therapy

A

F

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46
Q

Malignant oedema can be treated with polymyxin

A

F

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47
Q

Malignant oedema can be well treated with antibiotics over a long period

A

F

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48
Q

Is gas gangrene (malignant oedema) a regional illness

A

F

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49
Q

The lesions of malignant oedema are mainly seen in the lungs

A

F

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50
Q

Blackleg is caused by Clostridium septicum

A

F

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51
Q

Lesions of blackleg are mainly seen on the claws

A

F

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52
Q

Lameness is a clinical sign of blackleg

A

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53
Q

Blackleg is a frequent disease in pigs

A

F

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54
Q

Generally attenuated vaccines are used for the prevention of blackleg

A

F

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55
Q

Anaculture or anatoxin vaccines are used for the prevention of blackleg

A

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56
Q

Blackleg occurs only in tropical and subtropical countries

A

F

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57
Q

Generally attenuated vaccines are used for the prevention of blackleg

A

F

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58
Q

Blackleg generally occurs in endemic form

A

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59
Q

Blackleg occurs most frequently in pigs

A

F

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60
Q

Blackleg is a gas gangrene disease

A

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61
Q

Blackleg is generally endogenous in sheep

A

F

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62
Q

Blackleg is generally endogenous in cattle

A

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63
Q

Movement disorders and lameness can be clinical signs of Blackleg

A

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64
Q

Clostridium chauvoei can produce acids and gas from carbohydrates

A

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65
Q

Blackleg occurs mainly in ruminants

A

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66
Q

Oedema is a typical clinical sign of blackleg

A

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67
Q

Live vaccines are used for the prevention of blackleg

A

F

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68
Q

Blackleg infects ovine through wounds

A

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69
Q

In Blackleg disease we use attenuated vaccine

A

F

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70
Q

In the case of sheep, blackleg is generally consequence of a wound infection

A

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71
Q

Oedema in the muscles is a typical clinical sign of blackleg

A

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72
Q

Attenuated vaccines are used for the prevention of blackleg

A

F

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73
Q

Blackleg is caused by Clostridium chauvoei

A

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74
Q

Severe diarrhoea is the main clinical sign of blackleg

A

F

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75
Q

Blackleg is caused by Clostridium septicum

A

F

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76
Q

Blackleg occurs in cattle and sheep.

A

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77
Q

Blackleg occurs in cattle and sheep.

A

F

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78
Q

Attenuated vaccines are used for the prevention of blackleg

A

F

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79
Q

Blackleg disease occurs only in ruminants

A

F

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80
Q

Blackleg can usually be treated with antibiotics successfully

A

F

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81
Q

Blackleg in cattle is mainly endogenous between 6 months-3 years old

A

F

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82
Q

The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep

A

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83
Q

The disease caused by Clostridium chauvoei is primarily the result of endogenous infection
in cattle.

A

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84
Q

Blackleg has four toxins

A

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85
Q

Blackleg can be prevented by using vaccine

A

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86
Q

We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei

A

F

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87
Q

Blackleg in cattle is mainly endogenous between 2 months-2 years old

A

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88
Q

Blackleg in bovine is caused by wound infections

A

F

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89
Q

Blackleg in bovine is caused by wound infections

A

F

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90
Q

Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot

A

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91
Q

Bradsot is caused by Clostridium chauvoei

A

F

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92
Q

Bradsot is caused by Clostridium chauvoei

A

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93
Q

Soil contaminated frozen feed is a frequent predisposing factor of bradsot

A

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94
Q

Frozen food is a predisposing factor of bradsot

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95
Q

Bradsot occurs mainly late autumn and winter

A

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96
Q

Overeating can predispose the animals to bradsot

A

F

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97
Q

Thickening of and oedema in the stomach wall are typical lesions of bradsot

A

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98
Q

Aminoglycosides are successfully used for treatment in the case of bradsot

A

F

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99
Q

Bradsot is mainly seen in late autumn and winter

A

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100
Q

Bradsot is mainly seen in late autumn and winter

A

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101
Q

Severe pneumonia is a typical clinical sign of bradsot

A

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102
Q

Bradsot has a very fast course

A

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103
Q

Bradsot occurs only in suckling lambs

A

F

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104
Q

Bradsot is typically a chronic disease

A

F

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105
Q

Bradsot is common in the summer out on the pasture

A

F

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106
Q

Bradsot is an acute disease resulting in sudden death in many cases

A

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107
Q

We can use anaculture strain vaccine against Bradsot

A

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108
Q

Bradsot causes oedema of the legs and necrosis

A

F

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109
Q

Post mortem lesions of bradsot can be seen in the stomach (rennet)

A

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110
Q

Koves disease is an indicator disease

A

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111
Q

CSF is a predisposing factor of koves disease

A

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112
Q

Koves disease can be seen in pigs

A

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113
Q

Koves disease is caused by Clostridium chavoei

A

F

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114
Q

Infectious necrotic hepatitis is mainly seen in pigs

A

F

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115
Q

Infectious necrotic hepatitis can be prevented by using anatoxin vaccines

A

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116
Q

Liver fluke can predispose animals to infectious necrotic hepatitis

A

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117
Q

In sheep, Clostridium septicum causes necrotic liver infection

A

F

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118
Q

Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver

A

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119
Q

There is no vaccine to prevent infectious necrotic hepatitis

A

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120
Q

Infectious necrotic hepatitis is caused by Clostridium septicum

A

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121
Q

Infectious necrotic hepatitis is mainly seen in suckling lambs

A

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122
Q

Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis

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123
Q

Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis

A

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124
Q

Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis

A

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125
Q

Infectious necrotic hepatitis is caused by Clostridium septicum

A

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126
Q

Infectious necrotic hepatitis is caused by Clostridium novyi

A

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127
Q

Infectious necrotic hepatitis is spread by tick

A

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128
Q

Infectious necrotic hepatitis is caused by Clostridium novyi type B

129
Q

Infectious necrotic hepatitis is caused by Clostridium novyi type B

130
Q

Infectious necrotic hepatitis can be transmitted by liver flukes

131
Q

Infectious necrotic hepatitis occurs mostly in young sheep

132
Q

There is intravascular haemolysis in the case of bacillary haemoglobinuria

133
Q

Bacillary haemoglobinuria is caused by Clostridium haemolyticum

134
Q

There are no vaccines for the prevention of bacillary hemoglobinuria

135
Q

Phospholipase C is a virulence factor of the agent of bacillary hemoglobinuria

136
Q

Bacillary haemoglobinuria is mainly seen in cattle

137
Q

Bacillary haemoglobinuria is caused by Clostridium septicum

138
Q

Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria

139
Q

Red urine is a typical clinical sign of bacillary hemoglobinuria

140
Q

Bacillary hemoglobinuria is a slow, chronic disease

141
Q

Bacillary hemoglobinuria can frequently be seen in horses

142
Q

Clostridium novyi is the causative agent of bacillary hemoglobinuria.

143
Q

Bacillary hemoglobinuria causes severe haemorrhages

144
Q

Bacillary hemoglobinuria are caused by infection from the soil

145
Q

Lamb dysentery occurs in a week old animal

146
Q

Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery

147
Q

Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery

148
Q

Lesions of lamb dysentery are generally seen in the large intestine

149
Q

Lesions of lamb dysentery can be seen in the small intestine

150
Q

Lamb dysentery is caused by Clostridium perfringens

151
Q

Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery

152
Q

Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery

153
Q

Pregnant ewes have to be vaccinated in order to prevent lamb dysentery

154
Q

Haemorrhagic diarrhoea is a clinical sign of lamb dysentery

155
Q

Lamb dysentery can be seen in lambs around weaning

156
Q

Lamb dysentery is found in 3-4-week-old lambs

157
Q

Pathological lesions of Lamb dysentery starts in the colon

158
Q

We can culture the pathogen of Lamb dysentery from the intestines

159
Q

Lamb dysentery is caused by Clostridium dysenteriae

160
Q

Lamb dysentery can be seen in lambs after weaning

161
Q

There is no vaccine for the prevention of lamb dysentery

162
Q

Lamb dysentery occurs in 2-6 weeks old lambs

163
Q

For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine

164
Q

Pathological symptoms of lamb dysentery can be found in the large intestines

165
Q

Lamb dysentery can be prevented by vaccinating pregnant ewes

166
Q

Lamb dysentery can be successfully treated with penicillin when clinical signs appear

167
Q

Lamb dysentery occurs in a week-old animal.

168
Q

Lamb dysentery can be diagnosed by culturing the bacteria

169
Q

Newborn lambs have to be vaccinated in order to prevent lamb dysentery.

170
Q

Toxoid vaccines can be used in the prevention of the disease

171
Q

Infection of lamb by secretion in the milk

172
Q

Lamb dysentery occurs in 1-2 weeks old lambs.

173
Q

Struck is caused by Clostridium perfringens

174
Q

Overeating is a predisposing factor of struck

175
Q

Struck can be seen mainly in lambs younger than 2 weeks

176
Q

Struck is an acute disease in horses

177
Q

Struck is a zoonotic disease

178
Q

Struck is a slow disease of older sheep

179
Q

Struck is a worldwide common disease with great economic impact

180
Q

Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life

181
Q

The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large
intestine

182
Q

Maternal protection is important in the case of Infectious necrotic enteritis of piglets

183
Q

There is no vaccination for the prevention of Infectious necrotic enteritis of piglets

184
Q

Pig enterotoxaemia can be prevented by vaccinating the pregnant sows.

185
Q

Pig enterotoxaemia is caused by Clostridium perfringens C

186
Q

Pig enterotoxaemia is caused by Clostridium perfringens C

187
Q

Lesions of pig enterotoxaemia can be seen in the small intestine

188
Q

Lesions of pig enterotoxaemia can be seen in the large intestine

189
Q

Lesions of pig enterotoxaemia can be seen in the large intestine

190
Q

Lesions of pig enterotoxaemia can be seen in the large intestine

191
Q

Pig enterotoxaemia can be generally seen in weaned piglets

192
Q

Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia

193
Q

Clostridium enterotoxaemia of piglets is caused by C. perfringens

194
Q

Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows

195
Q

Clostridium perfringens C causes infectious necrotic enteritis of piglets

196
Q

Infectious necrotic enteritis of piglets occurs in piglets after weaning

197
Q

The lesions of infectious necrotic enteritis of piglets can be seen generally in the small
intestine

198
Q

Infectious necrotic enteritis of piglets can be prevented by vaccinating the pregnant sows

199
Q

Necrotic enteritis of piglets is seen in piglets around weaning

200
Q

Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin

201
Q

Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets

202
Q

Pig enterotoxaemia causes abdominal contractions in sows

203
Q

Mesenteric lymph node is congested in case of pig enterotoxaemia

204
Q

Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut

205
Q

Enteritis in piglets are caused by Clostridium perfringens D

206
Q

Enteritis in piglets can be avoided by anatoxin vaccination

207
Q

Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology

208
Q

Pig enterotoxaemia is caused by β-toxin production in 1st week of life

209
Q

Pig enterotoxaemia can cause a high mortality

210
Q

Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut

211
Q

Enterotoxaemia is mainly seen in piglets after weaning

212
Q

Pig enterotoxaemia is not present in Europe

213
Q

Pig enterotoxaemia cannot be prevented by using vaccines

214
Q

Pulpy kidney disease is caused by Clostridium perf. D

215
Q

Overeating is a predisposing factor to pulpy kidney disease

216
Q

The toxin of the agent of pulpy kidney disease is sensitive to trypsin

217
Q

Pulpy kidney disease is caused by Clostridium perfringens D

218
Q

Pulpy Kidney Diseases is caused by Clostridium chauvoei.

219
Q

Pulpy kidney disease generally occurs in 1-2week old lambs

220
Q

Pulpy kidney disease can occur at any age

221
Q

Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes

222
Q

Sudden change the diet is a predisposing factor to pulpy kidney disease

223
Q

The toxin damages the endothelial cells in the case of pulpy kidney disease

224
Q

Neurological signs are typical in the case of pulpy kidney disease

225
Q

Isolation of the agent is necessary to the diagnosis of pulpy kidney disease

226
Q

Pulpy kidney disease is typically seen in lambs below 2 weeks of age

227
Q

Inactivated vaccines are used for the prevention of pulpy kidney disease

228
Q

Pulpy kidney disease is seen in piglets in the first week of life

229
Q

Pulpy kidney disease is a worldwide common disease.

230
Q

Enterotoxaemia of sheep is also called pulpy kidney disease.

231
Q

Pulpy kidney disease is caused by Clostridium perfringens D.

232
Q

Cattle are not susceptible to this disease

233
Q

Vaccination are possible against pulpy kidney disease

234
Q

Coccidiosis is a predisposing factor of ulcerative enteritis in poultry

235
Q

Ulcerative enteritis of chicken is caused by Clostridium colinum.Ulcerative enteritis of chicken is caused by Clostridium colinum.

236
Q

Ulcerative enteritis is frequently seen in day old chicken

237
Q

Ulcers sometimes covered with pseudomembranes are frequent post mortem lesions of
ulcerative enteritis of chicken

238
Q

Ulcerative enteritis can occur in 4-12-week-old chickens

239
Q

Clostridium perfringens is the causative agent of ulcerative enteritis in poultry

240
Q

Ulcerative enteritis of poultry is generally prevented with vaccination.

241
Q

Lesions of ulcerative enteritis are mostly seen in the small intestines

242
Q

Lesions of ulcerative enteritis are mostly seen in the small intestines

243
Q

Prevention of coccidiosis can help lower the incidence of ulcerative enteritis

244
Q

Coccidiosis is a predisposing factor of necrotic enteritis of chicken

245
Q

Foamy, brownish-red faeces is a clinical sign of necrotic enteritis of chicken

246
Q

Lesions of necrotic enteritis of chicken are typically occur in the large intestine

247
Q

Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis

248
Q

Necrotic enteritis mostly occurs in chicken

249
Q

Waterfowl are not susceptible to necrotic enteritis

250
Q

Necrotic enteritis occurs in 1-3 weeks of age

251
Q

Tyzzer’s disease is caused by Clostridium piliforme

252
Q

Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A

253
Q

Gangrenous dermatitis is caused by obligate pathogens

254
Q

Gangrenous dermatitis causes muscle oedema

255
Q

Vaccines are the primary way of prevention of gangrenous dermatitis

256
Q

Flaccid paralysis is a frequent clinical sign of tetanus

257
Q

The agent of tetanus is strictly anaerobic

258
Q

The agent of tetanus can enter the host through wounds

259
Q

Tetanus is only seen in horse

260
Q

Over-eating can predispose animals to Tetanus

261
Q

The agent of Tetanus needs oxygen to replicate

262
Q

Anatoxin vaccines are available for the prevention of tetanus

263
Q

Haemorrhages under the serous membranes and enlargement of parenchymal organs are
typical postmortem lesions of tetanus

264
Q

Spasms are typical clinical signs of tetanus

265
Q

Tetanus is a zoonosis

266
Q

Toxoid vaccines can be used for the prevention of tetanus.

267
Q

Dogs are resistant to tetanus

268
Q

The clinical signs of tetanus are inducible

269
Q

Tetanus toxin cleaves synaptobrevin

270
Q

For tetanus we use vaccines which contain toxoid

271
Q

Tetanus cannot be prevented with vaccination.

272
Q

Tetanus is caused by Clostridium tetani

273
Q

The agent of tetanus causes septicaemia.

274
Q

Tetanus can be diagnosed on the basis of post mortem lesions

275
Q

Clostridium tetani produced endotoxin

276
Q

C. tetani needs anaerobic conditions for propagation

277
Q

Dogs are susceptible to tetanus

278
Q

Tetanus can be prevented with vaccines containing inactivated bacteria

279
Q

Tetanus can cause spasms

280
Q

Horses are resistant to tetanus

281
Q

Tetanus can only develop after deep wounds

282
Q

Wounds can predispose to tetanus

283
Q

The paralysis usually starts at the place of the wound

284
Q

Clostridium tetani toxin is produced in the feed

285
Q

Horses are most sensitive to tetanus

286
Q

Tetanus can be prevented by anatoxin vaccination

287
Q

Tetanus causes rigid paralysis

288
Q

There is no vaccine for tetanus

289
Q

Dogs have high resistance to tetanus

290
Q

Dogs have high resistance to tetanus

291
Q

The toxin of clostridium botulinum causes flaccid paralysis

292
Q

Clostridium botulinum generally causes wound infection

293
Q

Focal necrosis in the liver is a typical post mortem lesion of Botulism

294
Q

The toxin of Clostridium botulinum has irreversible effect

295
Q

Botulism can be seen as a result of a wound infection

296
Q

Flaccid paralysis is the main clinical sign of botulism

297
Q

Birds are resistant to botulism

298
Q

Necrotic foci in the liver are typical post mortem lesions of botulism

299
Q

Generally wounds predispose animals to botulism

300
Q

The agent of botulism generally produces toxin at the site of entry

301
Q

Botulism is diagnosed on the basis of the typical post mortem lesions

302
Q

Clostridium botulinum can produce toxins outside the hosts.

303
Q

No characteristic post mortem lesions can be seen in the case of botulism

304
Q

Botulism doesn’t occur in Europe

305
Q

Clostridium botulinum cannot tolerate air at all

306
Q

Botulism usually develops following a wound infection

307
Q

Clostridium botulinum propagates in rotten materials.

308
Q

In Hungary, botulism is seen most commonly in birds

309
Q

In Hungary, botulism is seen most commonly in birds

310
Q

In Hungary, botulism occurs in winter and early spring.

311
Q

Botulism is eradicated in Europe

312
Q

Clostridium botulinum can produce toxin, some of which are activated by proteases

313
Q

Botulism is seen mainly during summer

314
Q

Spasms are the typical clinical sign of botulism

315
Q

Paralysis is the main sign of botulism

316
Q

Toxins of botulism are produced generally in the food.

317
Q

Botulism happen generally through wound infection

318
Q

Animals are mostly sensitive to C and D types of Clostridium botulinum.