Epi Mix F 1001-1200 Flashcards
1
Q
Tetanus is only seen in horse
A
F
2
Q
Over-eating can predispose animals to Tetanus
A
F
3
Q
The agent of Tetanus needs oxygen to replicate
A
F
4
Q
Anatoxin vaccines are available for the prevention of tetanus
A
T
5
Q
Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus
A
F
6
Q
Spasms are typical clinical signs of tetanus
A
T
7
Q
Tetanus is a zoonosis
A
F
8
Q
xoid vaccines can be used for the prevention of tetanus
A
T
9
Q
Dogs are resistant to tetanus
A
F
10
Q
The clinical signs of tetanus are inducible
A
T
11
Q
Tetanus toxin cleaves synaptobrevin
A
T
12
Q
For tetanus we use vaccines which contain toxoid
A
T
13
Q
Tetanus cannot be prevented with vaccination
A
F
14
Q
Tetanus is caused by Clostridium tetani
A
T
15
Q
The agent of tetanus causes septicaemia
A
F
16
Q
Tetanus can be diagnosed on the basis of post mortem lesions
A
F
17
Q
Clostridium tetani produced endotoxin
A
F
18
Q
C. tetani needs anaerobic conditions for propagation
A
T
19
Q
Dogs are susceptible to tetanus
A
T
20
Q
Tetanus can be prevented with vaccines containing inactivated bacteria
A
F
21
Q
Tetanus can cause spasms
A
T
22
Q
Horses are resistant to tetanus
A
F
23
Q
Tetanus can only develop after deep wounds
A
F ?
24
Q
Wounds can predispose to tetanus
A
T
25
The paralysis usually starts at the place of the wound
F
26
Clostridium tetani toxin is produced in the feed
F
27
Horses are most sensitive to tetanus
T
28
Tetanus can be prevented by anatoxin vaccination
T
29
Tetanus causes rigid paralysis
T
30
There is no vaccine for tetanus
F
31
Dogs have high resistance to tetanus
T
32
Clostridium tetani produces neurotoxins
T
33
The toxin of clostridium botulinum causes flaccid paralysis
T
34
Clostridium botulinum generally causes wound infection
F
35
Focal necrosis in the liver is a typical post mortem lesion of Botulism
F
36
The toxin of Clostridium botulinum has irreversible effect
T
37
Botulism can be seen as a result of a wound infection
F
38
Flaccid paralysis is the main clinical sign of botulism
T
39
Birds are resistant to botulism
F
40
Necrotic foci in the liver are typical post mortem lesions of botulism
F
41
Generally wounds predispose animals to botulism
F
42
The agent of botulism generally produces toxin at the site of entry
F
43
Botulism is diagnosed on the basis of the typical post mortem lesions
F
44
Clostridium botulinum can produce toxins outside the hosts
T
45
No characteristic post mortem lesions can be seen in the case of botulism
T
46
Botulism doesn’t occur in Europe
F
47
Clostridium botulinum cannot tolerate air at all
T
48
Botulism usually develops following a wound infection
F
49
Clostridium botulinum propagates in rotten materials
T
50
In Hungary, botulism is seen most commonly in birds
T
51
Clostridium botulinum spores are extremely resistant to heat
T
52
In Hungary, botulism occurs in winter and early spring
F
53
Botulism is eradicated in Europe
F
54
Clostridium botulinum can produce toxin, some of which are activated by proteases
T
55
Botulism is seen mainly during summer
T
56
Spasms are the typical clinical sign of botulism
F
57
Paralysis is the main sign of botulism
T
58
Toxins of botulism are produced generally in the food
T
59
Animals are mostly sensitive to C and D types of Clostridium botulinum
T
60
Transmissible encephalopathies can be diagnosed by detecting infective prions in the brain
T
61
In the case of transmissible encephalopathies lesions can only be seen in the central nervous system
F
62
Prion diseases can be diagnosed by detecting the antibodies with ELISA.
T
63
There are major differences in the amino acid sequence of the normal and infective prions
F
64
Spongiform encephalopathies of animals occur worldwide except Australia and New Zealand
F
65
Prions can become infective prions as a result of a mutation
T
66
In the case of transmissible encephalopathies always degenerative lesions can be seen
T
67
In the case of transmissible encephalopathies meningoencephalitis is a typical postmortem lesion
F
68
Infective prions are resistant against the usual concentration of disinfectants
T
69
Agents of transmissible encephalopathies are most frequently detected with PCR
F
70
Weight loss is a clinical sign of Transmissible encephalopathies
T
71
ELISA can be used for the detection of infective prions in the brain
T
72
The folding of normal and the infective prion is different
T
73
Infective prions are resistant against proteases
T
74
Infective prions can survive 100 °C
T
75
Prions consist of protein and DNA
F
76
Chronic prion has no nucleic acid inside
T
77
Chronic prion is inactivated by boiling
F
78
Chronic prion form has other form than normal prions
T
79
Prions contain protein and DNA
F
80
Infection with infective prions generally happens per os
T
81
Transmissible encephalopathies are slow diseases
T
82
In the case of transmissible encephalopathies encephalitis can be seen in the grey material of the brain
F
83
Transmissible encephalopathies are caused by prions
T
84
PCR is used to the detection of prions
F
85
Prions always cause viraemia in the infected hosts
F
86
Prions are spreading in the host along the nerves
T
87
Normal prions are essential components of the cell membrane of the hosts
T
88
Infective prions replicate in the cytoplasm of the neurons
T
89
Infective prions are taken per os.
T
90
Encephalitis is typical in the case of transmissible encephalopathies
F
91
Protease breaks down prions
F
92
Transmissible encephalopathies are acute or per-acute diseases
F
93
Antibodies to prions cannot be detected in the case of transmissible encephalopathies
T
94
Allergy tests are widely used to diagnose transmissible encephalopathies
F
95
Scrapie has genetic predisposition
T
96
Scrapie prion is shed in discharges of the infected animals
T
97
The EU is free from Scrapie
F
98
Scrapie is a zoonotic disease
F
99
Atypical scrapie strains are not shed by the infected animals
T
100
Scrapie prion is detected with PCR
F
101
Scrapie is a disease of sheep, goats, and cattle
F
102
Scrapie is mainly seen in sheep between 1.5 and 5 years of age
T
103
Itching is a frequent sign of scrapie
T
104
Both typical and atypical scrapie strains can cause itching
F
105
Scrapie has more clinical signs in lambs than adult sheep
F
106
Certain genotypes of sheep are resistant against Scrapie prion
T
107
Scrapie is spreading with per os infection
T
108
Genetic predisposition is needed for scrapie to develop
T
109
Atypical scrapie strains can cause the same clinical signs as typical scrapie
F
110
Scrapie can be prevented with live vaccines
F
111
Scrapie sensitivity depends on genotype of sheep
T
112
Scrapie can be transmitted between sheep in a flock
T
113
Itching is always a clinical sign of scrapie
F
114
In scrapie we can observe lameness
F
115
Scrapie occurs only in Britain and Ireland
F
116
Sheep cannot shed the scrapie prion
F
117
Clinical signs of scrapie are most frequent in animals between 6 and 12 months of age
F
118
Scrapie is seen only in adult sheep
F
119
Scrapie is seen in sheep and goats
T
120
Goat are resistant to scrapie
F
121
Scrapie is spread within the flock from animal to animal
T
122
Scrapie prion can infect susceptible animals per os
T
123
Itching can be seen in the case of typical scrapie
T
124
Itching can be seen in the case of atypical scrapie
F
125
Certain sheep can be resistant to scrapie
T
126
Scrapie can be prevented with inactivated vaccines
F
127
Scrapie prion is shed by the infected animals
T
128
Scrapie can be prevented by using attenuated vaccines
F
129
There is a per os infection in the case of transmissible mink encephalopathy
T
130
The behaviour of the animals is changed in the case of transmissible mink encephalopathy
T
131
Transmissible Mink encephalopathy can be transmitted by eating infected meat.
T
132
Transmissible Mink encephalopathy symptoms: being anxious
T
133
Minks are infected with transmissible mink encephalopathy prion per os
T
134
Minks shed the transmissible mink encephalopathy prion in the faeces
F (no shedding at all!!!!)
135
Movement disorders are typical signs of transmissible mink encephalopathy
T
136
Aggressiveness is a clinical sign of BSE
T
137
BSE prion causes meningoencephalitis
F
138
Clinical signs of BSE appear in cattle slowly
T
139
Movement disorders are typical clinical signs of BSE
T
140
BSE prion is shed in milk in large amount
F
141
BSE prion generally infects cattle in aerosol
F
142
BSE prion travels along the nerves from the gut to the brain
T
143
BSE infects animals per os
T
144
Enteritis and haemorrhages can be seen postmortem in BSE cattle
F
145
Hyperaesthesia is a clinical sign of BSE
T
146
Calves of cows infected with BSE are frequently infected, they have to be destroyed
F
147
There is no vaccine for the prevention of BSE
T
148
Ataxia is a clinical sign of BSE
T
149
BSE is a zoonotic disease
T
150
BSE is spreading fast in the infected herd
F
151
Clinical signs of BSE can be seen mainly in 1-1.5 years old cattle
F
152
For Bovine spongiform encephalopathy laboratory examination, we use ELISA
T
153
In Bovine spongiform encephalopathy the meat contains high number of prions
T
154
Creutzfeldt Jakob syndrome is a new type of Bovine spongiform encephalopathy in humans
T
155
BSE prions are shed in the faeces and it is transmitted to other cattle in the herd
F
156
The incubation time of BSE is 3-5 years
T
157
Only a few animals show clinical signs of BSE in an infected herd
T
158
Bovine spongiform encephalopathy is widespread in Europe; it is common in most European countries
F
159
BSE is not spreading from animal to animal
T
160
In the case of BSE polioencephalitis is the main post mortem lesion
F
161
BSE prion is mainly detected with PCR
F
162
The agent of bovine spongiform encephalopathy is not shed by the infected animals
T
163
Antibodies against bovine spongiform encephalopathy are detected with ELISA
F
164
The agent of bovine spongiform encephalopathy is spreading along the nerves in the infected animals
T
165
The agent of bovine spongiform encephalopathy is shed in large number in the milk
F
166
Changed behaviour is a typical sign of bovine spongiform encephalopathy
T
167
In case of spongiform encephalopathies micro abscesses are in the brain stem
F
168
Spongiform encephalopathies are mainly acute diseases
F
169
In the case of spongiform encephalopathies there is encephalitis
F
170
Spongiform encephalopathies can be diagnosed by detecting circulating antibodies
F
171
In the case of spongiform encephalopathies the behaviour of the animal is generally changed
T
172
In the case of spongiform encephalopathies encephalitis is the main post mortem lesion
F
173
In the case of spongiform encephalopathies high levels of antibodies is produced
F
174
Spongiform encephalopathies are caused by prions
T
175
Bovine spongiform encephalopathy cannot infect humans
F
176
Bovine spongiform encephalopathy causes aggression
T
177
You can diagnose bovine spongiform encephalopathy with ELISA
T
178
Bovine spongiform encephalopathy causes an immune response
F
179
Bovine spongiform encephalopathy is a contact infection
F
180
BSE can be seen in calves from the age of 6 months
F
181
Hypersensitivity is a clinical sign of BSE
T
182
Focal necrosis in the liver is a typical post mortem lesion of BSE
F
183
2-6 months old calves having BSE are frequently aggressive
F
184
Bovine spongiform encephalopathy is seen only in beef cows
F
185
Cattle with bovine spongiform encephalopathy have movement difficulties
T
186
Steptococcus dysgalactiae and streptococcus agalactiae can cause mastitis in cows
T
187
The capsule is a virulence factor of Streptococcus equi
T
188
Streptococcus can be divided according to their antigens
T
189
Streptococcus are epiphytes
T
190
Streptococcus are obligate aerobic
F
191
Steptococcus suis can cause encephalitis of humans
T
192
Streptococcus suis can cause generalised septicemia in 1-4 week old piglets
T
193
Diarrhoea is a frequent clinical sign of streptococcosis of pigs
F
194
Iron deficiency can predispose to porcine streptococcosis
T
195
Porcine streptococcosis can be prevented with inactivated vaccines
T
196
Porcine streptococcosis is treated with penicillins
T
197
Arthritis is a frequent clinical sign of streptococcosis of pigs
T
198
Generalised porcine streptococcosis can mainly be seen in piglets till 5 weeks of age
T
199
Purulent menigoencephalitis can be a postmortem lesion of porcine streptococcosis
T
200
Calcium deficiency can predispose suckling piglets to streptococcosis
F
