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Epi Mix > Epi Mix F 1001-1200 > Flashcards

Epi Mix F 1001-1200 Flashcards

1
Q

Tetanus is only seen in horse

A

F

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2
Q

Over-eating can predispose animals to Tetanus

A

F

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3
Q

The agent of Tetanus needs oxygen to replicate

A

F

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4
Q

Anatoxin vaccines are available for the prevention of tetanus

A

T

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5
Q

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

A

F

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6
Q

Spasms are typical clinical signs of tetanus

A

T

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7
Q

Tetanus is a zoonosis

A

F

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8
Q

xoid vaccines can be used for the prevention of tetanus

A

T

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9
Q

Dogs are resistant to tetanus

A

F

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10
Q

The clinical signs of tetanus are inducible

A

T

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11
Q

Tetanus toxin cleaves synaptobrevin

A

T

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12
Q

For tetanus we use vaccines which contain toxoid

A

T

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13
Q

Tetanus cannot be prevented with vaccination

A

F

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14
Q

Tetanus is caused by Clostridium tetani

A

T

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15
Q

The agent of tetanus causes septicaemia

A

F

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16
Q

Tetanus can be diagnosed on the basis of post mortem lesions

A

F

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17
Q

Clostridium tetani produced endotoxin

A

F

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18
Q

C. tetani needs anaerobic conditions for propagation

A

T

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19
Q

Dogs are susceptible to tetanus

A

T

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20
Q

Tetanus can be prevented with vaccines containing inactivated bacteria

A

F

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21
Q

Tetanus can cause spasms

A

T

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22
Q

Horses are resistant to tetanus

A

F

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23
Q

Tetanus can only develop after deep wounds

A

F ?

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24
Q

Wounds can predispose to tetanus

A

T

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25
Q

The paralysis usually starts at the place of the wound

A

F

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26
Q

Clostridium tetani toxin is produced in the feed

A

F

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27
Q

Horses are most sensitive to tetanus

A

T

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28
Q

Tetanus can be prevented by anatoxin vaccination

A

T

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29
Q

Tetanus causes rigid paralysis

A

T

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30
Q

There is no vaccine for tetanus

A

F

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31
Q

Dogs have high resistance to tetanus

A

T

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32
Q

Clostridium tetani produces neurotoxins

A

T

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33
Q

The toxin of clostridium botulinum causes flaccid paralysis

A

T

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34
Q

Clostridium botulinum generally causes wound infection

A

F

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35
Q

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

A

F

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36
Q

The toxin of Clostridium botulinum has irreversible effect

A

T

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37
Q

Botulism can be seen as a result of a wound infection

A

F

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38
Q

Flaccid paralysis is the main clinical sign of botulism

A

T

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39
Q

Birds are resistant to botulism

A

F

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40
Q

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

A

F

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41
Q

Generally wounds predispose animals to botulism

A

F

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42
Q

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

A

F

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43
Q

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

A

F

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44
Q

Clostridium botulinum can produce toxins outside the hosts

A

T

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45
Q

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

A

T

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46
Q

Botulism doesn’t occur in Europe

A

F

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47
Q

Clostridium botulinum cannot tolerate air at all

A

T

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48
Q

Botulism usually develops following a wound infection

A

F

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49
Q

Clostridium botulinum propagates in rotten materials

A

T

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50
Q

In Hungary, botulism is seen most commonly in birds

A

T

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51
Q

Clostridium botulinum spores are extremely resistant to heat

A

T

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52
Q

In Hungary, botulism occurs in winter and early spring

A

F

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53
Q

Botulism is eradicated in Europe

A

F

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54
Q

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

A

T

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55
Q

Botulism is seen mainly during summer

A

T

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56
Q

Spasms are the typical clinical sign of botulism

A

F

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57
Q

Paralysis is the main sign of botulism

A

T

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58
Q

Toxins of botulism are produced generally in the food

A

T

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59
Q

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

A

T

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60
Q

Transmissible encephalopathies can be diagnosed by detecting infective prions in the brain

A

T

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61
Q

In the case of transmissible encephalopathies lesions can only be seen in the central nervous system

A

F

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62
Q

Prion diseases can be diagnosed by detecting the antibodies with ELISA.

A

T

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63
Q

There are major differences in the amino acid sequence of the normal and infective prions

A

F

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64
Q

Spongiform encephalopathies of animals occur worldwide except Australia and New Zealand

A

F

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65
Q

Prions can become infective prions as a result of a mutation

A

T

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66
Q

In the case of transmissible encephalopathies always degenerative lesions can be seen

A

T

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67
Q

In the case of transmissible encephalopathies meningoencephalitis is a typical postmortem lesion

A

F

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68
Q

Infective prions are resistant against the usual concentration of disinfectants

A

T

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69
Q

Agents of transmissible encephalopathies are most frequently detected with PCR

A

F

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70
Q

Weight loss is a clinical sign of Transmissible encephalopathies

A

T

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71
Q

ELISA can be used for the detection of infective prions in the brain

A

T

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72
Q

The folding of normal and the infective prion is different

A

T

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73
Q

Infective prions are resistant against proteases

A

T

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74
Q

Infective prions can survive 100 °C

A

T

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75
Q

Prions consist of protein and DNA

A

F

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76
Q

Chronic prion has no nucleic acid inside

A

T

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77
Q

Chronic prion is inactivated by boiling

A

F

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78
Q

Chronic prion form has other form than normal prions

A

T

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79
Q

Prions contain protein and DNA

A

F

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80
Q

Infection with infective prions generally happens per os

A

T

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81
Q

Transmissible encephalopathies are slow diseases

A

T

82
Q

In the case of transmissible encephalopathies encephalitis can be seen in the grey material of the brain

A

F

83
Q

Transmissible encephalopathies are caused by prions

A

T

84
Q

PCR is used to the detection of prions

A

F

85
Q

Prions always cause viraemia in the infected hosts

A

F

86
Q

Prions are spreading in the host along the nerves

A

T

87
Q

Normal prions are essential components of the cell membrane of the hosts

A

T

88
Q

Infective prions replicate in the cytoplasm of the neurons

A

T

89
Q

Infective prions are taken per os.

A

T

90
Q

Encephalitis is typical in the case of transmissible encephalopathies

A

F

91
Q

Protease breaks down prions

A

F

92
Q

Transmissible encephalopathies are acute or per-acute diseases

A

F

93
Q

Antibodies to prions cannot be detected in the case of transmissible encephalopathies

A

T

94
Q

Allergy tests are widely used to diagnose transmissible encephalopathies

A

F

95
Q

Scrapie has genetic predisposition

A

T

96
Q

Scrapie prion is shed in discharges of the infected animals

A

T

97
Q

The EU is free from Scrapie

A

F

98
Q

Scrapie is a zoonotic disease

A

F

99
Q

Atypical scrapie strains are not shed by the infected animals

A

T

100
Q

Scrapie prion is detected with PCR

A

F

101
Q

Scrapie is a disease of sheep, goats, and cattle

A

F

102
Q

Scrapie is mainly seen in sheep between 1.5 and 5 years of age

A

T

103
Q

Itching is a frequent sign of scrapie

A

T

104
Q

Both typical and atypical scrapie strains can cause itching

A

F

105
Q

Scrapie has more clinical signs in lambs than adult sheep

A

F

106
Q

Certain genotypes of sheep are resistant against Scrapie prion

A

T

107
Q

Scrapie is spreading with per os infection

A

T

108
Q

Genetic predisposition is needed for scrapie to develop

A

T

109
Q

Atypical scrapie strains can cause the same clinical signs as typical scrapie

A

F

110
Q

Scrapie can be prevented with live vaccines

A

F

111
Q

Scrapie sensitivity depends on genotype of sheep

A

T

112
Q

Scrapie can be transmitted between sheep in a flock

A

T

113
Q

Itching is always a clinical sign of scrapie

A

F

114
Q

In scrapie we can observe lameness

A

F

115
Q

Scrapie occurs only in Britain and Ireland

A

F

116
Q

Sheep cannot shed the scrapie prion

A

F

117
Q

Clinical signs of scrapie are most frequent in animals between 6 and 12 months of age

A

F

118
Q

Scrapie is seen only in adult sheep

A

F

119
Q

Scrapie is seen in sheep and goats

A

T

120
Q

Goat are resistant to scrapie

A

F

121
Q

Scrapie is spread within the flock from animal to animal

A

T

122
Q

Scrapie prion can infect susceptible animals per os

A

T

123
Q

Itching can be seen in the case of typical scrapie

A

T

124
Q

Itching can be seen in the case of atypical scrapie

A

F

125
Q

Certain sheep can be resistant to scrapie

A

T

126
Q

Scrapie can be prevented with inactivated vaccines

A

F

127
Q

Scrapie prion is shed by the infected animals

A

T

128
Q

Scrapie can be prevented by using attenuated vaccines

A

F

129
Q

There is a per os infection in the case of transmissible mink encephalopathy

A

T

130
Q

The behaviour of the animals is changed in the case of transmissible mink encephalopathy

A

T

131
Q

Transmissible Mink encephalopathy can be transmitted by eating infected meat.

A

T

132
Q

Transmissible Mink encephalopathy symptoms: being anxious

A

T

133
Q

Minks are infected with transmissible mink encephalopathy prion per os

A

T

134
Q

Minks shed the transmissible mink encephalopathy prion in the faeces

A

F (no shedding at all!!!!)

135
Q

Movement disorders are typical signs of transmissible mink encephalopathy

A

T

136
Q

Aggressiveness is a clinical sign of BSE

A

T

137
Q

BSE prion causes meningoencephalitis

A

F

138
Q

Clinical signs of BSE appear in cattle slowly

A

T

139
Q

Movement disorders are typical clinical signs of BSE

A

T

140
Q

BSE prion is shed in milk in large amount

A

F

141
Q

BSE prion generally infects cattle in aerosol

A

F

142
Q

BSE prion travels along the nerves from the gut to the brain

A

T

143
Q

BSE infects animals per os

A

T

144
Q

Enteritis and haemorrhages can be seen postmortem in BSE cattle

A

F

145
Q

Hyperaesthesia is a clinical sign of BSE

A

T

146
Q

Calves of cows infected with BSE are frequently infected, they have to be destroyed

A

F

147
Q

There is no vaccine for the prevention of BSE

A

T

148
Q

Ataxia is a clinical sign of BSE

A

T

149
Q

BSE is a zoonotic disease

A

T

150
Q

BSE is spreading fast in the infected herd

A

F

151
Q

Clinical signs of BSE can be seen mainly in 1-1.5 years old cattle

A

F

152
Q

For Bovine spongiform encephalopathy laboratory examination, we use ELISA

A

T

153
Q

In Bovine spongiform encephalopathy the meat contains high number of prions

A

T

154
Q

Creutzfeldt Jakob syndrome is a new type of Bovine spongiform encephalopathy in humans

A

T

155
Q

BSE prions are shed in the faeces and it is transmitted to other cattle in the herd

A

F

156
Q

The incubation time of BSE is 3-5 years

A

T

157
Q

Only a few animals show clinical signs of BSE in an infected herd

A

T

158
Q

Bovine spongiform encephalopathy is widespread in Europe; it is common in most European countries

A

F

159
Q

BSE is not spreading from animal to animal

A

T

160
Q

In the case of BSE polioencephalitis is the main post mortem lesion

A

F

161
Q

BSE prion is mainly detected with PCR

A

F

162
Q

The agent of bovine spongiform encephalopathy is not shed by the infected animals

A

T

163
Q

Antibodies against bovine spongiform encephalopathy are detected with ELISA

A

F

164
Q

The agent of bovine spongiform encephalopathy is spreading along the nerves in the infected animals

A

T

165
Q

The agent of bovine spongiform encephalopathy is shed in large number in the milk

A

F

166
Q

Changed behaviour is a typical sign of bovine spongiform encephalopathy

A

T

167
Q

In case of spongiform encephalopathies micro abscesses are in the brain stem

A

F

168
Q

Spongiform encephalopathies are mainly acute diseases

A

F

169
Q

In the case of spongiform encephalopathies there is encephalitis

A

F

170
Q

Spongiform encephalopathies can be diagnosed by detecting circulating antibodies

A

F

171
Q

In the case of spongiform encephalopathies the behaviour of the animal is generally changed

A

T

172
Q

In the case of spongiform encephalopathies encephalitis is the main post mortem lesion

A

F

173
Q

In the case of spongiform encephalopathies high levels of antibodies is produced

A

F

174
Q

Spongiform encephalopathies are caused by prions

A

T

175
Q

Bovine spongiform encephalopathy cannot infect humans

A

F

176
Q

Bovine spongiform encephalopathy causes aggression

A

T

177
Q

You can diagnose bovine spongiform encephalopathy with ELISA

A

T

178
Q

Bovine spongiform encephalopathy causes an immune response

A

F

179
Q

Bovine spongiform encephalopathy is a contact infection

A

F

180
Q

BSE can be seen in calves from the age of 6 months

A

F

181
Q

Hypersensitivity is a clinical sign of BSE

A

T

182
Q

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

A

F

183
Q

2-6 months old calves having BSE are frequently aggressive

A

F

184
Q

Bovine spongiform encephalopathy is seen only in beef cows

A

F

185
Q

Cattle with bovine spongiform encephalopathy have movement difficulties

A

T

186
Q

Steptococcus dysgalactiae and streptococcus agalactiae can cause mastitis in cows

A

T

187
Q

The capsule is a virulence factor of Streptococcus equi

A

T

188
Q

Streptococcus can be divided according to their antigens

A

T

189
Q

Streptococcus are epiphytes

A

T

190
Q

Streptococcus are obligate aerobic

A

F

191
Q

Steptococcus suis can cause encephalitis of humans

A

T

192
Q

Streptococcus suis can cause generalised septicemia in 1-4 week old piglets

A

T

193
Q

Diarrhoea is a frequent clinical sign of streptococcosis of pigs

A

F

194
Q

Iron deficiency can predispose to porcine streptococcosis

A

T

195
Q

Porcine streptococcosis can be prevented with inactivated vaccines

A

T

196
Q

Porcine streptococcosis is treated with penicillins

A

T

197
Q

Arthritis is a frequent clinical sign of streptococcosis of pigs

A

T

198
Q

Generalised porcine streptococcosis can mainly be seen in piglets till 5 weeks of age

A

T

199
Q

Purulent menigoencephalitis can be a postmortem lesion of porcine streptococcosis

A

T

200
Q

Calcium deficiency can predispose suckling piglets to streptococcosis

A

F

Epi Mix (35 decks)

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