MIdterm S2, 1st (part 2) Flashcards
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
T
Prion diseases can be diagnosed by detecting the antibodies with ELISA
F
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
T
Prions can become infective prions as a result of a mutation
T
In the case of transmissible encephalopathies always degenerative lesions can be seen
F
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
Transmissible encephalopathies can be diagnosed by detecting infective prions in the brain
T
Weight loss is a clinical sign of Transmissible encephalopathies
T
Prion diseases can be diagnosed by detecting antibodies with ELISA
F
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
Infective prions are resistant against proteases
T
Infective prions are resistant against the usual concentration of disinfectants
T
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
Mutations can result infective prions
T
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.
F
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
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
BSE prion generally infects cattle in aerosol
F
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
Bovine spongiform encephalopathy is spreading fast in the infected herd
F
Clinical signs of BSE can be seen mainly in 1-1.5 years old cattle
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
Antibodies to BSE can be detected with ELISA in infected animals.
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
Animals showing clinical signs of anthrax have to be killed, treatment is not allowed
F
The agent of anthrax is spreading in the herd very fast from animal to animal
F
Anthrax is frequently a peracute disease in cattle
T
Anthrax is caused by Clostridium anthracis.
F
Enlargement of the spleen is a frequent postmortem lesion of anthrax
T
Anthrax can occur only in ruminants
F
Anthrax can be diagnosed by staining blood smear
T
Anthrax is zoonosis
T
Incomplete blood clotting is a typical postmortem finding in the case of anthrax
T
Animals are infected with the agent of anthrax mainly per os
T
There are no vaccines for the prevention of Anthrax
F
Animals are infected with the agent of anthrax mainly per os
T
Anthrax can cause clinical signs in pigs
T
Horses are resistant to Anthrax
F
Generally live vaccines are used for the prevention of anthrax
T
There is a metachromatic staining in the case of Bacillus Anthracis
T
Capsule and oedema factor are virulence factors of Bacillus anthracis
T
Carbon dioxide is needed to the spore production of Bacillus Anthracis
F
Capsule is a virulence factor of the agent of anthrax
T
CO2 is needed for the spore formation of the agent of anthrax
F
Pigs are more susceptible to anthrax than sheep
F
Oedema factor is a virulence factor of the agent of anthrax
T
Human anthrax cannot be treated with antibiotics
F
Inactivated vaccines are used for the prevention of Anthrax
F
Only herbivorous animals can show clinical signs of Anthrax
F
The spore of Bacillus anthracis can survive several decades in the soil
T
Bacillus Anthracis cannot produce spores in the infected animals
T
Dogs are more susceptible to Bacillus Anthracis than sheep
F
Europe is already free from anthrax
F
Anthrax cannot be seen in Europe anymore
F
Capsule is a virulence factor of B. anthracis
T
Cattle are infected with B. anthracis mainly from the soil
T
Pigs are more susceptible to anthracis than sheep
F
Anthrax is a per-acute or acute diseases in cattle
T
Colic is a typical clinical sign of anthrax in horses
T
Anthrax can be diagnosed with microscopic examination of blood
T
Inactivated vaccines are used for the prevention of anthrax
F
Bacillus anthracis main virulence factor is in the capsule
T
The oedema factor is an important virulence factor in bacillus anthracis
T
Bacillus anthracis spores: after 1 hour of boiling they are still alive
T
Bacillus anthracis makes spores only without oxygen
F
Anthrax important symptom is high fever
T
If the animals have Anthrax and they have a fever, you have to vaccinate them immediately.
F
For anthrax we use inactive vaccine
F
Humans infected with Anthrax, primarily per os
F
Bacillus anthracis, herbivores are especially susceptible
T
Bacillus anthracis is not in pig
F
Anthrax spreads rapidly in a herd
F
Bacillus anthracis is in the soil.
T
In anthrax, tracheitis common in carnivores
F
Anthrax causes necrotic foci in liver
F
Anthrax diagnosis with blood/staining
T
Anthrax cannot occur in dogs and cats
F
The agent of anthrax can infect only herbivorous animals
F
The agent of anthrax is not spreading from animal to animal
T
There is a septicaemia in cattle in the case of anthrax
T
Anthrax is caused by Bacillus bovine
F
The capsule of the agent of anthrax is polypeptide
T
Anaerobic conditions are needed to the spore formation of the agent of anthrax
F
Pigs are the most susceptible animals to the agent of anthrax
F
Animals showing clinical signs of anthrax are not allowed to be treated with antibiotics
F
Only capsulated strains of Bacillus anthracis can cause anthrax
T
Oedema factor and lethal factor are important virulence factors of Bacillus anthracis
T
The clinical signs of anthrax in pigs are more severe than in cattle
F
Dogs and cats are resistant against the agent of anthrax
F
Only capsulated strain of B. anthracis is virulent
T
Toxin is a virulence factor of B. anthracis
T
Lethal factor is a virulence factor of B. anthracis
T
Cell wall antigen is a virulence factor of B. anthracis
F
Oxygen is needed to the spore production of B. anthracis
T
Spore is a virulence factor of B. anthracis
F
B. anthracis can cause blackleg
F
Anthrax is generally seen as a chronic disease in cattle
F
In case of anthrax, febrile animals have to be separated and vaccinated
F
Animals with anthrax can be treated with penicillin
T
Anthrax spreads rapidly in a herd from animal to animal
F
B. anthracis can only be diagnosed by bacterial culture
F
B. anthracis can only be diagnosed by Ascoli test
F
Animals suspected of being infected with anthrax should be vaccinated
F
Animals infected with anthrax should be treated with antibiotics
T
Virulence factors of anthrax: capsule, toxin, protective antigen
T
Virulence factors of anthrax: capsule, toxin, cilia
F
Virulence factors of anthrax: capsule, toxin, oedema factor
T
Virulence factors of anthrax: capsule, toxin, cell wall antigen
F
Anthrax is an epidemic disease that rapidly develops
F
Anthrax is a quickly spreading, contagious infectious disease
F
For lab examination of Anthrax you always have to send a spleen sample
F
Animals can only be infected by anthrax on the pasture
F
Sheep, cattle, and goats are the most sensitive animals to anthrax infection
T
Flagella is a virulence factor of B. anthracis
F
Anthrax spore is a virulence factor
F
The source of anthrax infection on animals is generally the soil
T
Anthrax appears generally in the form of a local infection in pigs
T
Fever is a typical sign of acute anthrax
T
Anthrax can be prevented by using a live vaccine
T
Europe is free from Anthrax
F
Anthrax is caused by Clostridium chauvoei
F
Anthrax is not spreading from animal to animal.
T
Horses are resistant to anthrax
T
Anthrax is an epidemic disease that rapidly develops
F
Ruminants are the most sensitive to anthrax
T
Animals suffering from anthrax should be treated with antibiotics and hyperimmune sera,
they should not be slaughtered
T
Causative agent of anthrax is spore-forming bacterium in air
T
Anthrax spreads in a herd by direct contact
F
In order to diagnose anthrax all carcasses have to be dissected
F
Anthrax is an acute disease in cattle with high fever
T
Swine is highly susceptible in anthrax
F
Splenic fever causes suffocation
T
Splenic fever in cattle is a per-acute/acute disease
T
Splenic fever is similar in every species
F
Swine anthrax is generally seen in the form of local lesions
T
Carnivorous animals are resistant to Bacillus anthracis
F
Incomplete clotting of the blood is a post mortem lesion of anthrax
T
Fibrinous pneumonia is a common post mortem lesion of anthrax
F
Animals showing clinical signs of anthrax have to be treated with antibiotics immediately
T
Horses are more susceptible to Bacillus anthracis than pigs
T
Only vaccinated animals are allowed to graze on pastures infected with Bacillus anthracis
F
Gastric juice can kill Bacillus anthracis in the meat, so per os infection does not occur in
humans
F
Most clostridia have low invasive capacity
T
Spores of clostridia are generally very resistant against heat
T
The habitat of clostridia is the gut and the soil
T
Clostridia are obligate aerobic bacteria
F
Clostridium perfringens is an obligate pathogenic bacterium.
F
Clostridium perfringens can produce main and auxillary toxins
T
Extracellular enzymes and toxins are virulence factors of clostridia
T
There are no vaccines for the prevention of diseases caused by clostridia
F
Clostridium is anaerobe spore forming bacteria
T
Clostridium bacteria is not in the environment, because it cannot tolerate oxygen
F
Clostridium spreads usually rapid in a herd
F
Clostridium spread mostly with insecticides
F
Clostridium difficile can be treated with metronidazole
T
Clostridium difficile is seen in foal and piglets
T
Many Clostridium species have flagella
F
Clostridium species are only found in the subtropics
F
Clostridium can cause severe contagious diseases
F
Clostridium are obligate pathogens
F
Anaculture or anatoxin vaccines are used for the prevention of malignant oedema
T
Cl. chauvoei is the agent of malignant oedema
F
Lesions of malignant oedema are mainly seen in the large muscles
T
Malignant oedema is generally endogenous in cattle
F
Malignant oedema is generally a consequence of wound infection
T
Movement difficulties are frequently seen in the case of malignant oedema
T
Clostridium novyi can cause malignant oedema
T
Malignant oedema can be diagnosed based on clinical signs
F
Malignant oedema is caused due to wound infection
T
Malignant oedema is only in ruminants
F
Malignant oedema, one of the clinical signs is lameness/movement problems
T
Malignant oedema, attenuated vaccine for prevention
F
Clostridium channel is the agent of malignant oedema
F
Malignant oedema is generally a consequence of a wound infection
T
Clostridium septicum is an agent of malignant oedema
T
Attenuated vaccines are used for the prevention of malignant oedema
F
Clostridium histolyticum can cause malignant oedema
T
Agents of malignant oedema can be detected by bacterium culture
T
There are no vaccines for the prevention of malignant oedema
F
Malignant oedema occurs in ruminants and pigs
T
Malignant oedema is an acute fatal disease
T
Malignant oedema can be treated with antibiotics
F
Malignant oedema can occur in any warm-blooded animal
T
Once an area is infected with gas gangrene re-occurrence is common
T
Malignant oedema cannot occur in swine
F
Malignant oedema usually develop following an endogenous infection
F
Malignant oedema is well treated with long-term antibiotics therapy
F
Malignant oedema can be treated with polymyxin
F
Malignant oedema can be well treated with antibiotics over a long period
F
Is gas gangrene (malignant oedema) a regional illness
F
The lesions of malignant oedema are mainly seen in the lungs
F
Blackleg is caused by Clostridium septicum
F
Lesions of blackleg are mainly seen on the claws
F
Lameness is a clinical sign of blackleg
T
Blackleg is a frequent disease in pigs
F
Generally attenuated vaccines are used for the prevention of blackleg
F
Anaculture or anatoxin vaccines are used for the prevention of blackleg
T
Blackleg occurs only in tropical and subtropical countries
F
Generally attenuated vaccines are used for the prevention of blackleg
F
Blackleg generally occurs in endemic form
T
Blackleg occurs most frequently in pigs
F
Blackleg is a gas gangrene disease
T
Blackleg is generally endogenous in sheep
F
Blackleg is generally endogenous in cattle
T
Movement disorders and lameness can be clinical signs of Blackleg
T
Clostridium chauvoei can produce acids and gas from carbohydrates
T
Blackleg occurs mainly in ruminants
T
Oedema is a typical clinical sign of blackleg
T
Live vaccines are used for the prevention of blackleg
F
Blackleg infects ovine through wounds
T
In Blackleg disease we use attenuated vaccine
F
In the case of sheep, blackleg is generally consequence of a wound infection
T
Oedema in the muscles is a typical clinical sign of blackleg
T
Attenuated vaccines are used for the prevention of blackleg
F
Blackleg is caused by Clostridium chauvoei
T
Severe diarrhoea is the main clinical sign of blackleg
F
Blackleg is caused by Clostridium septicum
F
Blackleg occurs in cattle and sheep
T
If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is
generally successful
F
Attenuated vaccines are used for the prevention of blackleg
F
Blackleg disease occurs only in ruminants
F
Blackleg can usually be treated with antibiotics successfully
F
Blackleg in cattle is mainly endogenous between 6 months-3 years old
F
The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep
T
The disease caused by Clostridium chauvoei is primarily the result of endogenous infection
in cattle
T
Blackleg has four toxins
T
Blackleg can be prevented by using vaccine
T
We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei
F
Blackleg in cattle is mainly endogenous between 2 months-2 years old
T
Blackleg in bovine is caused by wound infections
F
Classical swine fever is a frequent predisposing factor of bradsot
F
Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot
T
Bradsot is caused by Clostridium chauvoei
F
Bradsot occurs mainly in tropical and subtropical countries
F
Soil contaminated frozen feed is a frequent predisposing factor of bradsot
T
Frozen food is a predisposing factor of bradsot
T
Bradsot occurs mainly late autumn and winter
T
Overeating can predispose the animals to bradsot
F
Thickening of and oedema in the stomach wall are typical lesions of bradsot
T
Aminoglycosides are successfully used for treatment in the case of bradsot
F
Bradsot is mainly seen in late autumn and winter
T
Bradsot is caused by Clostridium septicum
T
Severe pneumonia is a typical clinical sign of bradsot
F
Bradsot has a very fast course
T
Bradsot occurs only in suckling lambs
F
Bradsot is typically a chronic disease
F
Bradsot is common in the summer out on the pasture
F
Bradsot is an acute disease resulting in sudden death in many cases
T
We can use anaculture strain vaccine against Bradsot
T
Bradsot causes oedema of the legs and necrosis
F
Post mortem lesions of bradsot can be seen in the stomach (rennet)
T
Köves disease is an indicator disease
T
CSF is a predisposing factor of koves disease
T
Köves disease can be seen in pigs
T
Köves disease is caused by Clostridium chavoei
F
Infectious necrotic hepatitis is mainly seen in pigs
F
Infectious necrotic hepatitis can be prevented by using anatoxin vaccines
T
Liver fluke can predispose animals to infectious necrotic hepatitis
T
In sheep, Clostridium septicum causes necrotic liver infection
F
Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver
T
There is no vaccine to prevent infectious necrotic hepatitis
F
Infectious necrotic hepatitis is caused by Clostridium septicum
F
Infectious necrotic hepatitis is mainly seen in suckling lambs
F
Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis
T
Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis
T
Anatoxin vaccines can be used for the prevention of infectious necrotic hepatitis
T
Infectious necrotic hepatitis is caused by Clostridium septicum
F
Infectious necrotic hepatitis is caused by Clostridium novyi
T
Infectious necrotic hepatitis is spread by tick
F
Infectious necrotic hepatitis is caused by Clostridium novyi type B
T
Infectious necrotic hepatitis is found worldwide
T
Infectious necrotic hepatitis can be transmitted by liver flukes
F
Infectious necrotic hepatitis occurs mostly in young sheep
F
There is intravascular haemolysis in the case of bacillary haemoglobinuria
T
Bacillary haemoglobinuria is caused by Clostridium haemolyticum
T
There are no vaccines for the prevention of bacillary hemoglobinuria
F
Phospholipase C is a virulence factor of the agent of bacillary hemoglobinuria
T
Bacillary haemoglobinuria is mainly seen in cattle
T
Bacillary haemoglobinuria is caused by Clostridium septicum
F
Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria
T
Red urine is a typical clinical sign of bacillary hemoglobinuria
T
Bacillary hemoglobinuria is a slow, chronic disease
F
Bacillary hemoglobinuria can frequently be seen in horses
F
Clostridium novyi is the causative agent of bacillary hemoglobinuria
F
Bacillary hemoglobinuria causes severe haemorrhages
T
Bacillary hemoglobinuria are caused by infection from the soil
T
Lamb dysentery occurs in a week old animal.
T
Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery
F
Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery.
F
Lesions of lamb dysentery are generally seen in the large intestine
F
Lesions of lamb dysentery can be seen in the small intestine
T
Lamb dysentery is caused by Clostridium perfringens B
T
Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery
F
Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery
F
Pregnant ewes have to be vaccinated in order to prevent lamb dysentery
T
Haemorrhagic diarrhoea is a clinical sign of lamb dysentery
T
Lamb dysentery can be seen in lambs around weaning
F
Lamb dysentery is found in 3-4-week-old lambs.
F
Pathological lesions of Lamb dysentery starts in the colon
F
We can culture the pathogen of Lamb dysentery from the intestines
T
Lamb dysentery is caused by Clostridium dysenteriae
F
Lamb dysentery can be seen in lambs after weaning
F
There is no vaccine for the prevention of lamb dysentery
F
Lamb dysentery occurs in 2-6 weeks old lambs
F
For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine
T
Pathological symptoms of lamb dysentery can be found in the large intestines
F
Lamb dysentery can be prevented by vaccinating pregnant ewes
T
Lamb dysentery can be successfully treated with penicillin when clinical signs appear
F
Lamb dysentery occurs in a week-old animal.
T
Lamb dysentery can be diagnosed by culturing the bacteria
T
Newborn lambs have to be vaccinated in order to prevent lamb dysentery
F
Toxoid vaccines can be used in the prevention of the disease
T
Infection of lamb by secretion in the milk
F
Lamb dysentery occurs in 1-2 weeks old lambs
T
Struck is caused by Clostridium perfringens C
T
Overeating is a predisposing factor of struck
T
Struck can be seen mainly in lambs younger than 2 weeks
F
Struck is an acute disease in horses
F
Struck is a zoonotic disease
F
Struck is a slow disease of older sheep
F
Struck is a worldwide common disease with great economic impact
F
Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life
T
The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large
intestine
F
Maternal protection is important in the case of Infectious necrotic enteritis of piglets
T
There is no vaccination for the prevention of Infectious necrotic enteritis of piglets
F
Pig enterotoxaemia can be prevented by vaccinating the pregnant sows
T
Pig enterotoxaemia is caused by Clostridium perfringens C
T
Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics
immediately
F
Lesions of pig enterotoxaemia can be seen in the small intestine
T
Lesions of pig enterotoxaemia can be seen in the large intestine
F
Pig enterotoxaemia is more frequent in the litter of young than old sows
T
Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets
T
Pig enterotoxaemia can be generally seen in weaned piglets
F
Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia
T
Clostridium enterotoxaemia of piglets is caused by C. perfringens
T
Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows
T
Clostridium perfringens C causes infectious necrotic enteritis of piglets
T
Infectious necrotic enteritis of piglets occurs in piglets after weaning
F
The lesions of infectious necrotic enteritis of piglets can be seen generally in the small
intestine
T
Infectious necrotic enteritis of piglets can be prevented by vaccinating the pregnant sows.
T
Necrotic enteritis of piglets is seen in piglets around weaning
F
Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin
T
Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets
F
Pig enterotoxaemia causes abdominal contractions in sow
F
Mesenteric lymph node is congested in case of pig enterotoxaemia
F
Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut
T
Enteritis in piglets are caused by Clostridium perfringens D.
F
