Transmissible encephalopathies Flashcards

1
Q

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

A

T

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2
Q

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

A

T

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3
Q

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

A

F

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4
Q

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

A

F

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5
Q

Spongiform encephalopathies of animals occur worldwide except Australia and New Zealand

A

T

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6
Q

Prions can become infective prions as a result of a mutation.

A

T

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7
Q

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

A

F

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8
Q

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

A

F

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9
Q

Infective prions are resistant against the usual concentration of disinfectants.

A

T

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10
Q

Agents of transmissible encephalopathies are most frequently detected with PCR.

A

F

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11
Q

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

A

T

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12
Q

Weight loss is a clinical sign of Transmissible encephalopathies

A

T

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13
Q

Prion diseases can be diagnosed by detecting antibodies with ELISA

A

F

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14
Q

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

A

T

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15
Q

The folding of normal and the infective prion is different

A

T

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16
Q

Infective prions are resistant against proteases

A

T

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17
Q

Infective prions can survive 100 °C.

A

T

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18
Q

Prions consist of protein and DNA.

A

F

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19
Q

Infective prions are resistant against proteases.

A

T

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20
Q

Infective prions are resistant against the usual concentration of disinfectants

A

T

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21
Q

Chronic prion has no nucleic acid inside.

A

T

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22
Q

Chronic prion is inactivated by boiling.

A

F

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23
Q

Chronic prion form has other form than normal prions.

A

T

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24
Q

Prions contain protein and DNA.

A

F

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25
Q

Mutations can result infective prions.

A

T

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26
Q

Infection with infective prions generally happens per os.

A

T

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27
Q

Transmissible encephalopathies are slow diseases.

A

T

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28
Q

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

A

F

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29
Q

Transmissible encephalopathies are caused by prions.

A

T

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30
Q

PCR is used to the detection of prions.

A

F

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31
Q

Prions always cause viraemia in the infected hosts.

A

F

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32
Q

Prions are spreading in the host along the nerves.

A

T

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33
Q

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

A

F

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34
Q

Infective prions replicate in the cytoplasm of the neurons.

A

T

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35
Q

Infective prions are taken per os.

A

T

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36
Q

Encephalitis is typical in the case of transmissible encephalopathies.

A

F

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37
Q

Protease breaks down prions.

A

F

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38
Q

Transmissible encephalopathies are acute or per-acute diseases .

A

F

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39
Q

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

A

T

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40
Q

Allergy tests are widely used to diagnose transmissible encephalopathies.

A

F

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41
Q

Scrapie has genetic predisposition.

A

T

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42
Q

Scrapie prion is shed in discharges of the infected animals.

A

T

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43
Q

The EU is free from Scrapie

A

F

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44
Q

Scrapie is a zoonotic disease

A

F

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45
Q

Atypical scrapie strains are not shed by the infected animals

A

T

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46
Q

Scrapie prion is detected with PCR

A

F

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47
Q

Scrapie is a disease of sheep, goats, and cattle

A

F

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48
Q

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

A

T

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49
Q

Itching is a frequent sign of scrapie

A

T

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50
Q

Both typical and atypical scrapie strains can cause itching

A

F

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51
Q

Scrapie has more clinical signs in lambs than adult sheep

A

F

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52
Q

Certain genotypes of sheep are resistant against Scrapie prion

A

T

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53
Q

13) Scrapie is spreading with per os infection.

A

T

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54
Q

Genetic predisposition is needed for scrapie to develop.

A

T

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55
Q

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

A

F

56
Q

Scrapie can be prevented with live vaccines.

A

F

57
Q

Scrapie sensitivity depends on genotype of sheep.

A

T

58
Q

Scrapie can be transmitted between sheep in a flock.

A

T

59
Q

Itching is always a clinical sign of scrapie.

A

F

60
Q

In scrapie we can observe lameness.

A

F

61
Q

Scrapie occurs only in Britain and Ireland.

A

F

62
Q

Sheep cannot shed the scrapie prion

A

F

63
Q

Clinical signs of scrapie are most frequent in animals between 6 and 12 months of age prevented with inactivated vaccines.

A

F

64
Q

Scrapie is seen only in adult sheep.

A

F

65
Q

Scrapie is seen in sheep and goats.

A

T

66
Q

Goat are resistant to scrapie.

A

F

67
Q

Scrapie is spread within the flock from animal to animal.

A

T

68
Q

Scrapie prion can infect susceptible animals per os.

A

T

69
Q

Itching can be seen in the case of typical scrapie.

A

T

70
Q

Itching can be seen in the case of atypical scrapie.

A

F

71
Q

Certain sheep can be resistant to scrapie.

A

T

72
Q

Scrapie can be prevented with inactivated vaccines

A

F

73
Q

Scrapie prion is shed by the infected animals

A

T

74
Q

Scrapie can be prevented by using attenuated vaccines

A

F

75
Q

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

A

T

76
Q

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

A

T

77
Q

Transmissible Mink encephalopathy can be transmitted by eating infected meat

A

T

78
Q

Transmissible Mink encephalopathy symptoms: being anxious.

A

T

79
Q

Minks are infected with transmissible mink encephalopathy prion per os

A

T

80
Q

Minks shed the transmissible mink encephalopathy prion in the faeces

A

F

81
Q

Movement disorders are typical signs of transmissible mink encephalopathy

A

T

82
Q

Aggressiveness is a clinical sign of BSE

A

T

83
Q

BSE prion causes meningoencephalitis

A

F

84
Q

Clinical signs of BSE appear in cattle slowly

A

T

85
Q

Movement disorders are typical clinical signs of BSE

A

T

86
Q

BSE prion is shed in milk in large amount

A

F

87
Q

BSE prion generally infects cattle in aeroso

A

F

88
Q

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

A

T

89
Q

BSE infects animals per os

A

T

90
Q

BSE prion generally infects cattle in aerosol

A

F

91
Q

Enteritis and haemorrhages can be seen postmortem in BSE cattle

A

F

92
Q

Hyperaesthesia is a clinical sign of BSE

A

T

93
Q

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

A

F

94
Q

There is no vaccine for the prevention of BSE

A

T

95
Q

Ataxia is a clinical sign of BSE

A

T

96
Q

Ataxia is a clinical sign of BSE

A

T

97
Q

BSE is spreading fast in the infected herd

A

F

98
Q

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

A

F

99
Q

For Bovine spongiform encephalopathy laboratory examination, we use ELISA

A

T

100
Q

In Bovine spongiform encephalopathy the meat contains high number of prions

A

T

101
Q

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

A

T

102
Q

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

A

F

103
Q

The incubation time of BSE is 3-5 years

A

T

104
Q

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

A

T

105
Q

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

A

F

106
Q

BSE is not spreading from animal to animal

A

T

107
Q

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

A

F

108
Q

BSE prion is mainly detected with PCR

A

F

109
Q

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

A

T

110
Q

Antibodies against bovine spongiform encephalopathy are detected with ELISA

A

F

111
Q

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

A

T

112
Q

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

A

F

113
Q

Changed behaviour is a typical sign of bovine spongiform encephalopathy

A

T

114
Q

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

A

F

115
Q

Spongiform encephalopathies are mainly acute diseases

A

F

116
Q

In the case of spongiform encephalopathies there is encephalitis

A

F

117
Q

Spongiform encephalopathies can be diagnosed by detecting circulating antibodies

A

F

118
Q

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

A

T

119
Q

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

A

F

120
Q

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

A

F

121
Q

Spongiform encephalopathies are caused by prions

A

T

122
Q

Bovine spongiform encephalopathy cannot infect humans

A

F

123
Q

Bovine spongiform encephalopathy causes aggression

A

T

124
Q

You can diagnose bovine spongiform encephalopathy with ELISA

A

T

125
Q

Bovine spongiform encephalopathy causes an immune response

A

F

126
Q

Bovine spongiform encephalopathy is a contact infection

A

F

127
Q

Bovine spongiform encephalopathy is spreading fast in the infected herd

A

F

128
Q

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

A

F

129
Q

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

A

F

130
Q

Hypersensitivity is a clinical sign of BSE

A

T

131
Q

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

A

F

132
Q

Antibodies to BSE can be detected with ELISA in infected animals

A

F

133
Q

2-6 months old calves having BSE are frequently aggressive

A

F

134
Q

Bovine spongiform encephalopathy is seen only in beef cows

A

F

135
Q

Cattle with bovine spongiform encephalopathy have movement difficulties

A

T