Epi Mix F 1001-1200 Flashcards
Tetanus is only seen in horse
F
Over-eating can predispose animals to Tetanus
F
The agent of Tetanus needs oxygen to replicate
F
Anatoxin vaccines are available for the prevention of tetanus
T
Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus
F
Spasms are typical clinical signs of tetanus
T
Tetanus is a zoonosis
F
xoid vaccines can be used for the prevention of tetanus
T
Dogs are resistant to tetanus
F
The clinical signs of tetanus are inducible
T
Tetanus toxin cleaves synaptobrevin
T
For tetanus we use vaccines which contain toxoid
T
Tetanus cannot be prevented with vaccination
F
Tetanus is caused by Clostridium tetani
T
The agent of tetanus causes septicaemia
F
Tetanus can be diagnosed on the basis of post mortem lesions
F
Clostridium tetani produced endotoxin
F
C. tetani needs anaerobic conditions for propagation
T
Dogs are susceptible to tetanus
T
Tetanus can be prevented with vaccines containing inactivated bacteria
F
Tetanus can cause spasms
T
Horses are resistant to tetanus
F
Tetanus can only develop after deep wounds
F ?
Wounds can predispose to tetanus
T
The paralysis usually starts at the place of the wound
F
Clostridium tetani toxin is produced in the feed
F
Horses are most sensitive to tetanus
T
Tetanus can be prevented by anatoxin vaccination
T
Tetanus causes rigid paralysis
T
There is no vaccine for tetanus
F
Dogs have high resistance to tetanus
T
Clostridium tetani produces neurotoxins
T
The toxin of clostridium botulinum causes flaccid paralysis
T
Clostridium botulinum generally causes wound infection
F
Focal necrosis in the liver is a typical post mortem lesion of Botulism
F
The toxin of Clostridium botulinum has irreversible effect
T
Botulism can be seen as a result of a wound infection
F
Flaccid paralysis is the main clinical sign of botulism
T
Birds are resistant to botulism
F
Necrotic foci in the liver are typical post mortem lesions of botulism
F
Generally wounds predispose animals to botulism
F
The agent of botulism generally produces toxin at the site of entry
F
Botulism is diagnosed on the basis of the typical post mortem lesions
F
Clostridium botulinum can produce toxins outside the hosts
T
No characteristic post mortem lesions can be seen in the case of botulism
T
Botulism doesn’t occur in Europe
F
Clostridium botulinum cannot tolerate air at all
T
Botulism usually develops following a wound infection
F
Clostridium botulinum propagates in rotten materials
T
In Hungary, botulism is seen most commonly in birds
T
Clostridium botulinum spores are extremely resistant to heat
T
In Hungary, botulism occurs in winter and early spring
F
Botulism is eradicated in Europe
F
Clostridium botulinum can produce toxin, some of which are activated by proteases
T
Botulism is seen mainly during summer
T
Spasms are the typical clinical sign of botulism
F
Paralysis is the main sign of botulism
T
Toxins of botulism are produced generally in the food
T
Animals are mostly sensitive to C and D types of Clostridium botulinum
T
Transmissible encephalopathies can be diagnosed by detecting infective prions in the brain
T
In the case of transmissible encephalopathies lesions can only be seen in the central nervous system
F
Prion diseases can be diagnosed by detecting the antibodies with ELISA.
T
There are major differences in the amino acid sequence of the normal and infective prions
F
Spongiform encephalopathies of animals occur worldwide except Australia and New Zealand
F
Prions can become infective prions as a result of a mutation
T
In the case of transmissible encephalopathies always degenerative lesions can be seen
T
In the case of transmissible encephalopathies meningoencephalitis is a typical postmortem lesion
F
Infective prions are resistant against the usual concentration of disinfectants
T
Agents of transmissible encephalopathies are most frequently detected with PCR
F
Weight loss is a clinical sign of Transmissible encephalopathies
T
ELISA can be used for the detection of infective prions in the brain
T
The folding of normal and the infective prion is different
T
Infective prions are resistant against proteases
T
Infective prions can survive 100 °C
T
Prions consist of protein and DNA
F
Chronic prion has no nucleic acid inside
T
Chronic prion is inactivated by boiling
F
Chronic prion form has other form than normal prions
T
Prions contain protein and DNA
F
Infection with infective prions generally happens per os
T
Transmissible encephalopathies are slow diseases
T
In the case of transmissible encephalopathies encephalitis can be seen in the grey material of the brain
F
Transmissible encephalopathies are caused by prions
T
PCR is used to the detection of prions
F
Prions always cause viraemia in the infected hosts
F
Prions are spreading in the host along the nerves
T
Normal prions are essential components of the cell membrane of the hosts
T
Infective prions replicate in the cytoplasm of the neurons
T
Infective prions are taken per os.
T
Encephalitis is typical in the case of transmissible encephalopathies
F
Protease breaks down prions
F
Transmissible encephalopathies are acute or per-acute diseases
F
Antibodies to prions cannot be detected in the case of transmissible encephalopathies
T
Allergy tests are widely used to diagnose transmissible encephalopathies
F
Scrapie has genetic predisposition
T
Scrapie prion is shed in discharges of the infected animals
T
The EU is free from Scrapie
F
Scrapie is a zoonotic disease
F
Atypical scrapie strains are not shed by the infected animals
T
Scrapie prion is detected with PCR
F
Scrapie is a disease of sheep, goats, and cattle
F
Scrapie is mainly seen in sheep between 1.5 and 5 years of age
T
Itching is a frequent sign of scrapie
T
Both typical and atypical scrapie strains can cause itching
F
Scrapie has more clinical signs in lambs than adult sheep
F
Certain genotypes of sheep are resistant against Scrapie prion
T
Scrapie is spreading with per os infection
T
Genetic predisposition is needed for scrapie to develop
T
Atypical scrapie strains can cause the same clinical signs as typical scrapie
F
Scrapie can be prevented with live vaccines
F
Scrapie sensitivity depends on genotype of sheep
T
Scrapie can be transmitted between sheep in a flock
T
Itching is always a clinical sign of scrapie
F
In scrapie we can observe lameness
F
Scrapie occurs only in Britain and Ireland
F
Sheep cannot shed the scrapie prion
F
Clinical signs of scrapie are most frequent in animals between 6 and 12 months of age
F
Scrapie is seen only in adult sheep
F
Scrapie is seen in sheep and goats
T
Goat are resistant to scrapie
F
Scrapie is spread within the flock from animal to animal
T
Scrapie prion can infect susceptible animals per os
T
Itching can be seen in the case of typical scrapie
T
Itching can be seen in the case of atypical scrapie
F
Certain sheep can be resistant to scrapie
T
Scrapie can be prevented with inactivated vaccines
F
Scrapie prion is shed by the infected animals
T
Scrapie can be prevented by using attenuated vaccines
F
There is a per os infection in the case of transmissible mink encephalopathy
T
The behaviour of the animals is changed in the case of transmissible mink encephalopathy
T
Transmissible Mink encephalopathy can be transmitted by eating infected meat.
T
Transmissible Mink encephalopathy symptoms: being anxious
T
Minks are infected with transmissible mink encephalopathy prion per os
T
Minks shed the transmissible mink encephalopathy prion in the faeces
F (no shedding at all!!!!)
Movement disorders are typical signs of transmissible mink encephalopathy
T
Aggressiveness is a clinical sign of BSE
T
BSE prion causes meningoencephalitis
F
Clinical signs of BSE appear in cattle slowly
T
Movement disorders are typical clinical signs of BSE
T
BSE prion is shed in milk in large amount
F
BSE prion generally infects cattle in aerosol
F
BSE prion travels along the nerves from the gut to the brain
T
BSE infects animals per os
T
Enteritis and haemorrhages can be seen postmortem in BSE cattle
F
Hyperaesthesia is a clinical sign of BSE
T
Calves of cows infected with BSE are frequently infected, they have to be destroyed
F
There is no vaccine for the prevention of BSE
T
Ataxia is a clinical sign of BSE
T
BSE is a zoonotic disease
T
BSE is spreading fast in the infected herd
F
Clinical signs of BSE can be seen mainly in 1-1.5 years old cattle
F
For Bovine spongiform encephalopathy laboratory examination, we use ELISA
T
In Bovine spongiform encephalopathy the meat contains high number of prions
T
Creutzfeldt Jakob syndrome is a new type of Bovine spongiform encephalopathy in humans
T
BSE prions are shed in the faeces and it is transmitted to other cattle in the herd
F
The incubation time of BSE is 3-5 years
T
Only a few animals show clinical signs of BSE in an infected herd
T
Bovine spongiform encephalopathy is widespread in Europe; it is common in most European countries
F
BSE is not spreading from animal to animal
T
In the case of BSE polioencephalitis is the main post mortem lesion
F
BSE prion is mainly detected with PCR
F
The agent of bovine spongiform encephalopathy is not shed by the infected animals
T
Antibodies against bovine spongiform encephalopathy are detected with ELISA
F
The agent of bovine spongiform encephalopathy is spreading along the nerves in the infected animals
T
The agent of bovine spongiform encephalopathy is shed in large number in the milk
F
Changed behaviour is a typical sign of bovine spongiform encephalopathy
T
In case of spongiform encephalopathies micro abscesses are in the brain stem
F
Spongiform encephalopathies are mainly acute diseases
F
In the case of spongiform encephalopathies there is encephalitis
F
Spongiform encephalopathies can be diagnosed by detecting circulating antibodies
F
In the case of spongiform encephalopathies the behaviour of the animal is generally changed
T
In the case of spongiform encephalopathies encephalitis is the main post mortem lesion
F
In the case of spongiform encephalopathies high levels of antibodies is produced
F
Spongiform encephalopathies are caused by prions
T
Bovine spongiform encephalopathy cannot infect humans
F
Bovine spongiform encephalopathy causes aggression
T
You can diagnose bovine spongiform encephalopathy with ELISA
T
Bovine spongiform encephalopathy causes an immune response
F
Bovine spongiform encephalopathy is a contact infection
F
BSE can be seen in calves from the age of 6 months
F
Hypersensitivity is a clinical sign of BSE
T
Focal necrosis in the liver is a typical post mortem lesion of BSE
F
2-6 months old calves having BSE are frequently aggressive
F
Bovine spongiform encephalopathy is seen only in beef cows
F
Cattle with bovine spongiform encephalopathy have movement difficulties
T
Steptococcus dysgalactiae and streptococcus agalactiae can cause mastitis in cows
T
The capsule is a virulence factor of Streptococcus equi
T
Streptococcus can be divided according to their antigens
T
Streptococcus are epiphytes
T
Streptococcus are obligate aerobic
F
Steptococcus suis can cause encephalitis of humans
T
Streptococcus suis can cause generalised septicemia in 1-4 week old piglets
T
Diarrhoea is a frequent clinical sign of streptococcosis of pigs
F
Iron deficiency can predispose to porcine streptococcosis
T
Porcine streptococcosis can be prevented with inactivated vaccines
T
Porcine streptococcosis is treated with penicillins
T
Arthritis is a frequent clinical sign of streptococcosis of pigs
T
Generalised porcine streptococcosis can mainly be seen in piglets till 5 weeks of age
T
Purulent menigoencephalitis can be a postmortem lesion of porcine streptococcosis
T
Calcium deficiency can predispose suckling piglets to streptococcosis
F
