MIdterm S2, 1st (part 2) Flashcards by Silje Terland

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

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

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Prion diseases can be diagnosed by detecting the antibodies with ELISA

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

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Spongiform encephalopathies of animals occur worldwide except Australia and New Zealand

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Prions can become infective prions as a result of a mutation

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

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

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Infective prions are resistant against the usual concentration of disinfectants

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Agents of transmissible encephalopathies are most frequently detected with PCR

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

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Weight loss is a clinical sign of Transmissible encephalopathies

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Prion diseases can be diagnosed by detecting antibodies with ELISA

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

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The folding of normal and the infective prion is different

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Infective prions are resistant against proteases

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Infective prions can survive 100 °C

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Prions consist of protein and DNA

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Infective prions are resistant against proteases

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Infective prions are resistant against the usual concentration of disinfectants

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Chronic prion has no nucleic acid inside

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Chronic prion is inactivated by boiling

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Chronic prion form has other form than normal prions

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Prions contain protein and DNA

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Mutations can result infective prions

Infection with infective prions generally happens per os

Transmissible encephalopathies are slow diseases

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

Transmissible encephalopathies are caused by prions

PCR is used to the detection of prions

Prions always cause viraemia in the infected hosts

Prions are spreading in the host along the nerves

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

Infective prions replicate in the cytoplasm of the neurons

Infective prions are taken per os

Encephalitis is typical in the case of transmissible encephalopathies

Protease breaks down prions

Transmissible encephalopathies are acute or per-acute diseases

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

Allergy tests are widely used to diagnose transmissible encephalopathies

Scrapie has genetic predisposition

Scrapie prion is shed in discharges of the infected animals

The EU is free from Scrapie

Scrapie is a zoonotic disease

Atypical scrapie strains are not shed by the infected animals

Scrapie prion is detected with PCR

Scrapie is a disease of sheep, goats, and cattle

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

Itching is a frequent sign of scrapie

Both typical and atypical scrapie strains can cause itching

Scrapie has more clinical signs in lambs than adult sheep

Certain genotypes of sheep are resistant against Scrapie prion

Scrapie is spreading with per os infection

Genetic predisposition is needed for scrapie to develop

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

Scrapie can be prevented with live vaccines

Scrapie sensitivity depends on genotype of sheep

Scrapie can be transmitted between sheep in a flock

Itching is always a clinical sign of scrapie

In scrapie we can observe lameness

Scrapie occurs only in Britain and Ireland

Sheep cannot shed the scrapie prion

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

Scrapie is seen only in adult sheep

Scrapie is seen in sheep and goats

Goat are resistant to scrapie

Scrapie is spread within the flock from animal to animal

Scrapie prion can infect susceptible animals per os

Itching can be seen in the case of typical scrapie

Itching can be seen in the case of atypical scrapie

Certain sheep can be resistant to scrapie

Scrapie can be prevented with inactivated vaccines

Scrapie prion is shed by the infected animals

Scrapie can be prevented by using attenuated vaccines

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

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

Transmissible Mink encephalopathy can be transmitted by eating infected meat

Transmissible Mink encephalopathy symptoms: being anxious

Minks are infected with transmissible mink encephalopathy prion per os

Minks shed the transmissible mink encephalopathy prion in the faeces

Movement disorders are typical signs of transmissible mink encephalopathy

Aggressiveness is a clinical sign of BSE

BSE prion causes meningoencephalitis

Clinical signs of BSE appear in cattle slowly

Movement disorders are typical clinical signs of BSE

BSE prion is shed in milk in large amount

BSE prion generally infects cattle in aerosol

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

BSE infects animals per os

BSE prion generally infects cattle in aerosol

Enteritis and haemorrhages can be seen postmortem in BSE cattle

Hyperaesthesia is a clinical sign of BSE

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

There is no vaccine for the prevention of BSE

Ataxia is a clinical sign of BSE

BSE is a zoonotic disease

BSE is spreading fast in the infected herd

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

For Bovine spongiform encephalopathy laboratory examination, we use ELISA

In Bovine spongiform encephalopathy the meat contains high number of prions

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

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

The incubation time of BSE is 3-5 years

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

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

BSE is not spreading from animal to animal.

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

BSE prion is mainly detected with PCR.

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

Antibodies against bovine spongiform encephalopathy are detected with ELISA

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

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

Changed behaviour is a typical sign of bovine spongiform encephalopathy

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

Spongiform encephalopathies are mainly acute diseases

In the case of spongiform encephalopathies there is encephalitis

Spongiform encephalopathies can be diagnosed by detecting circulating antibodies

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

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

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

Spongiform encephalopathies are caused by prions

Bovine spongiform encephalopathy cannot infect humans

Bovine spongiform encephalopathy causes aggression

You can diagnose bovine spongiform encephalopathy with ELISA

Bovine spongiform encephalopathy causes an immune response

Bovine spongiform encephalopathy is a contact infection

Bovine spongiform encephalopathy is spreading fast in the infected herd

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

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

Hypersensitivity is a clinical sign of BSE

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

Antibodies to BSE can be detected with ELISA in infected animals.

2-6 months old calves having BSE are frequently aggressive

Bovine spongiform encephalopathy is seen only in beef cows

Cattle with bovine spongiform encephalopathy have movement difficulties

Animals showing clinical signs of anthrax have to be killed, treatment is not allowed

The agent of anthrax is spreading in the herd very fast from animal to animal

Anthrax is frequently a peracute disease in cattle

Anthrax is caused by Clostridium anthracis.

Enlargement of the spleen is a frequent postmortem lesion of anthrax

Anthrax can occur only in ruminants

Anthrax can be diagnosed by staining blood smear

Anthrax is zoonosis

Incomplete blood clotting is a typical postmortem finding in the case of anthrax

Animals are infected with the agent of anthrax mainly per os

There are no vaccines for the prevention of Anthrax

Animals are infected with the agent of anthrax mainly per os

Anthrax can cause clinical signs in pigs

Horses are resistant to Anthrax

Generally live vaccines are used for the prevention of anthrax

There is a metachromatic staining in the case of Bacillus Anthracis

Capsule and oedema factor are virulence factors of Bacillus anthracis

Carbon dioxide is needed to the spore production of Bacillus Anthracis

Capsule is a virulence factor of the agent of anthrax

CO2 is needed for the spore formation of the agent of anthrax

Pigs are more susceptible to anthrax than sheep

Oedema factor is a virulence factor of the agent of anthrax

Human anthrax cannot be treated with antibiotics

Inactivated vaccines are used for the prevention of Anthrax

Only herbivorous animals can show clinical signs of Anthrax

The spore of Bacillus anthracis can survive several decades in the soil

Bacillus Anthracis cannot produce spores in the infected animals

Dogs are more susceptible to Bacillus Anthracis than sheep

Europe is already free from anthrax

Anthrax cannot be seen in Europe anymore

Capsule is a virulence factor of B. anthracis

Cattle are infected with B. anthracis mainly from the soil

Pigs are more susceptible to anthracis than sheep

Anthrax is a per-acute or acute diseases in cattle

Colic is a typical clinical sign of anthrax in horses

Anthrax can be diagnosed with microscopic examination of blood

Inactivated vaccines are used for the prevention of anthrax

Bacillus anthracis main virulence factor is in the capsule

The oedema factor is an important virulence factor in bacillus anthracis

Bacillus anthracis spores: after 1 hour of boiling they are still alive

Bacillus anthracis makes spores only without oxygen

Anthrax important symptom is high fever

If the animals have Anthrax and they have a fever, you have to vaccinate them immediately.

For anthrax we use inactive vaccine

Humans infected with Anthrax, primarily per os

Bacillus anthracis, herbivores are especially susceptible

Bacillus anthracis is not in pig

Anthrax spreads rapidly in a herd

Bacillus anthracis is in the soil.

In anthrax, tracheitis common in carnivores

Anthrax causes necrotic foci in liver

Anthrax diagnosis with blood/staining

Anthrax cannot occur in dogs and cats

The agent of anthrax can infect only herbivorous animals

The agent of anthrax is not spreading from animal to animal

There is a septicaemia in cattle in the case of anthrax

Anthrax is caused by Bacillus bovine

The capsule of the agent of anthrax is polypeptide

Anaerobic conditions are needed to the spore formation of the agent of anthrax

Pigs are the most susceptible animals to the agent of anthrax

Animals showing clinical signs of anthrax are not allowed to be treated with antibiotics

Only capsulated strains of Bacillus anthracis can cause anthrax

Oedema factor and lethal factor are important virulence factors of Bacillus anthracis

The clinical signs of anthrax in pigs are more severe than in cattle

Dogs and cats are resistant against the agent of anthrax

Only capsulated strain of B. anthracis is virulent

Toxin is a virulence factor of B. anthracis

Lethal factor is a virulence factor of B. anthracis

Cell wall antigen is a virulence factor of B. anthracis

Oxygen is needed to the spore production of B. anthracis

Spore is a virulence factor of B. anthracis

B. anthracis can cause blackleg

Anthrax is generally seen as a chronic disease in cattle

In case of anthrax, febrile animals have to be separated and vaccinated

Animals with anthrax can be treated with penicillin

Anthrax spreads rapidly in a herd from animal to animal

B. anthracis can only be diagnosed by bacterial culture

B. anthracis can only be diagnosed by Ascoli test

Animals suspected of being infected with anthrax should be vaccinated

Animals infected with anthrax should be treated with antibiotics

Virulence factors of anthrax: capsule, toxin, protective antigen

Virulence factors of anthrax: capsule, toxin, cilia

Virulence factors of anthrax: capsule, toxin, oedema factor

Virulence factors of anthrax: capsule, toxin, cell wall antigen

Anthrax is an epidemic disease that rapidly develops

Anthrax is a quickly spreading, contagious infectious disease

For lab examination of Anthrax you always have to send a spleen sample

Animals can only be infected by anthrax on the pasture

Sheep, cattle, and goats are the most sensitive animals to anthrax infection

Flagella is a virulence factor of B. anthracis

Anthrax spore is a virulence factor

The source of anthrax infection on animals is generally the soil

Anthrax appears generally in the form of a local infection in pigs

Fever is a typical sign of acute anthrax

Anthrax can be prevented by using a live vaccine

Europe is free from Anthrax

Anthrax is caused by Clostridium chauvoei

Anthrax is not spreading from animal to animal.

Horses are resistant to anthrax

Anthrax is an epidemic disease that rapidly develops

Ruminants are the most sensitive to anthrax

Animals suffering from anthrax should be treated with antibiotics and hyperimmune sera, they should not be slaughtered

Causative agent of anthrax is spore-forming bacterium in air

Anthrax spreads in a herd by direct contact

In order to diagnose anthrax all carcasses have to be dissected

Anthrax is an acute disease in cattle with high fever

Swine is highly susceptible in anthrax

Splenic fever causes suffocation

Splenic fever in cattle is a per-acute/acute disease

Splenic fever is similar in every species

Swine anthrax is generally seen in the form of local lesions

Carnivorous animals are resistant to Bacillus anthracis

Incomplete clotting of the blood is a post mortem lesion of anthrax

Fibrinous pneumonia is a common post mortem lesion of anthrax

Animals showing clinical signs of anthrax have to be treated with antibiotics immediately

Horses are more susceptible to Bacillus anthracis than pigs

Only vaccinated animals are allowed to graze on pastures infected with Bacillus anthracis

Gastric juice can kill Bacillus anthracis in the meat, so per os infection does not occur in humans

Most clostridia have low invasive capacity

Spores of clostridia are generally very resistant against heat

The habitat of clostridia is the gut and the soil

Clostridia are obligate aerobic bacteria

Clostridium perfringens is an obligate pathogenic bacterium.

Clostridium perfringens can produce main and auxillary toxins

Extracellular enzymes and toxins are virulence factors of clostridia

There are no vaccines for the prevention of diseases caused by clostridia

Clostridium is anaerobe spore forming bacteria

Clostridium bacteria is not in the environment, because it cannot tolerate oxygen

Clostridium spreads usually rapid in a herd

Clostridium spread mostly with insecticides

Clostridium difficile can be treated with metronidazole

Clostridium difficile is seen in foal and piglets

Many Clostridium species have flagella

Clostridium species are only found in the subtropics

Clostridium can cause severe contagious diseases

Clostridium are obligate pathogens

Anaculture or anatoxin vaccines are used for the prevention of malignant oedema

Cl. chauvoei is the agent of malignant oedema

Lesions of malignant oedema are mainly seen in the large muscles

Malignant oedema is generally endogenous in cattle

Malignant oedema is generally a consequence of wound infection

Movement difficulties are frequently seen in the case of malignant oedema

Clostridium novyi can cause malignant oedema

Malignant oedema can be diagnosed based on clinical signs

Malignant oedema is caused due to wound infection

Malignant oedema is only in ruminants

Malignant oedema, one of the clinical signs is lameness/movement problems

Malignant oedema, attenuated vaccine for prevention

Clostridium channel is the agent of malignant oedema

Malignant oedema is generally a consequence of a wound infection

Clostridium septicum is an agent of malignant oedema

Attenuated vaccines are used for the prevention of malignant oedema

Clostridium histolyticum can cause malignant oedema

Agents of malignant oedema can be detected by bacterium culture

There are no vaccines for the prevention of malignant oedema

Malignant oedema occurs in ruminants and pigs

Malignant oedema is an acute fatal disease

Malignant oedema can be treated with antibiotics

Malignant oedema can occur in any warm-blooded animal

Once an area is infected with gas gangrene re-occurrence is common

Malignant oedema cannot occur in swine

Malignant oedema usually develop following an endogenous infection

Malignant oedema is well treated with long-term antibiotics therapy

Malignant oedema can be treated with polymyxin

Malignant oedema can be well treated with antibiotics over a long period

Is gas gangrene (malignant oedema) a regional illness

The lesions of malignant oedema are mainly seen in the lungs

Blackleg is caused by Clostridium septicum

Lesions of blackleg are mainly seen on the claws

Lameness is a clinical sign of blackleg

Blackleg is a frequent disease in pigs

Generally attenuated vaccines are used for the prevention of blackleg

Anaculture or anatoxin vaccines are used for the prevention of blackleg

Blackleg occurs only in tropical and subtropical countries

Generally attenuated vaccines are used for the prevention of blackleg

Blackleg generally occurs in endemic form

Blackleg occurs most frequently in pigs

Blackleg is a gas gangrene disease

Blackleg is generally endogenous in sheep

Blackleg is generally endogenous in cattle

Movement disorders and lameness can be clinical signs of Blackleg

Clostridium chauvoei can produce acids and gas from carbohydrates

Blackleg occurs mainly in ruminants

Oedema is a typical clinical sign of blackleg

Live vaccines are used for the prevention of blackleg

Blackleg infects ovine through wounds

In Blackleg disease we use attenuated vaccine

In the case of sheep, blackleg is generally consequence of a wound infection

Oedema in the muscles is a typical clinical sign of blackleg

Attenuated vaccines are used for the prevention of blackleg

Blackleg is caused by Clostridium chauvoei

Severe diarrhoea is the main clinical sign of blackleg

Blackleg is caused by Clostridium septicum

Blackleg occurs in cattle and sheep

If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is generally successful

Attenuated vaccines are used for the prevention of blackleg

Blackleg disease occurs only in ruminants

Blackleg can usually be treated with antibiotics successfully

Blackleg in cattle is mainly endogenous between 6 months-3 years old

The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep

The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle

Blackleg has four toxins

Blackleg can be prevented by using vaccine

We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei

Blackleg in cattle is mainly endogenous between 2 months-2 years old

Blackleg in bovine is caused by wound infections

Classical swine fever is a frequent predisposing factor of bradsot

Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot

Bradsot is caused by Clostridium chauvoei

Bradsot occurs mainly in tropical and subtropical countries

Soil contaminated frozen feed is a frequent predisposing factor of bradsot

Frozen food is a predisposing factor of bradsot

Bradsot occurs mainly late autumn and winter

Overeating can predispose the animals to bradsot

Thickening of and oedema in the stomach wall are typical lesions of bradsot

Aminoglycosides are successfully used for treatment in the case of bradsot

Bradsot is mainly seen in late autumn and winter

Bradsot is caused by Clostridium septicum

Severe pneumonia is a typical clinical sign of bradsot

Bradsot has a very fast course

Bradsot occurs only in suckling lambs

Bradsot is typically a chronic disease

Bradsot is common in the summer out on the pasture

Bradsot is an acute disease resulting in sudden death in many cases

We can use anaculture strain vaccine against Bradsot

Bradsot causes oedema of the legs and necrosis

Post mortem lesions of bradsot can be seen in the stomach (rennet)

Köves disease is an indicator disease

CSF is a predisposing factor of koves disease

Köves disease can be seen in pigs

Köves disease is caused by Clostridium chavoei

Infectious necrotic hepatitis is mainly seen in pigs

Infectious necrotic hepatitis can be prevented by using anatoxin vaccines

Liver fluke can predispose animals to infectious necrotic hepatitis

In sheep, Clostridium septicum causes necrotic liver infection

Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver

There is no vaccine to prevent infectious necrotic hepatitis

Infectious necrotic hepatitis is caused by Clostridium septicum

Infectious necrotic hepatitis is mainly seen in suckling lambs

Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis

Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis

Anatoxin vaccines can be used for the prevention of infectious necrotic hepatitis

Infectious necrotic hepatitis is caused by Clostridium septicum

Infectious necrotic hepatitis is caused by Clostridium novyi

Infectious necrotic hepatitis is spread by tick

Infectious necrotic hepatitis is caused by Clostridium novyi type B

Infectious necrotic hepatitis is found worldwide

Infectious necrotic hepatitis can be transmitted by liver flukes

Infectious necrotic hepatitis occurs mostly in young sheep

There is intravascular haemolysis in the case of bacillary haemoglobinuria

Bacillary haemoglobinuria is caused by Clostridium haemolyticum

There are no vaccines for the prevention of bacillary hemoglobinuria

Phospholipase C is a virulence factor of the agent of bacillary hemoglobinuria

Bacillary haemoglobinuria is mainly seen in cattle

Bacillary haemoglobinuria is caused by Clostridium septicum

Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria

Red urine is a typical clinical sign of bacillary hemoglobinuria

Bacillary hemoglobinuria is a slow, chronic disease

Bacillary hemoglobinuria can frequently be seen in horses

Clostridium novyi is the causative agent of bacillary hemoglobinuria

Bacillary hemoglobinuria causes severe haemorrhages

Bacillary hemoglobinuria are caused by infection from the soil

Lamb dysentery occurs in a week old animal.

Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery

Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery.

Lesions of lamb dysentery are generally seen in the large intestine

Lesions of lamb dysentery can be seen in the small intestine

Lamb dysentery is caused by Clostridium perfringens B

Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery

Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery

Pregnant ewes have to be vaccinated in order to prevent lamb dysentery

Haemorrhagic diarrhoea is a clinical sign of lamb dysentery

Lamb dysentery can be seen in lambs around weaning

Lamb dysentery is found in 3-4-week-old lambs.

Pathological lesions of Lamb dysentery starts in the colon

We can culture the pathogen of Lamb dysentery from the intestines

Lamb dysentery is caused by Clostridium dysenteriae

Lamb dysentery can be seen in lambs after weaning

There is no vaccine for the prevention of lamb dysentery

Lamb dysentery occurs in 2-6 weeks old lambs

For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine

Pathological symptoms of lamb dysentery can be found in the large intestines

Lamb dysentery can be prevented by vaccinating pregnant ewes

Lamb dysentery can be successfully treated with penicillin when clinical signs appear

Lamb dysentery occurs in a week-old animal.

Lamb dysentery can be diagnosed by culturing the bacteria

Newborn lambs have to be vaccinated in order to prevent lamb dysentery

Toxoid vaccines can be used in the prevention of the disease

Infection of lamb by secretion in the milk

Lamb dysentery occurs in 1-2 weeks old lambs

Struck is caused by Clostridium perfringens C

Overeating is a predisposing factor of struck

Struck can be seen mainly in lambs younger than 2 weeks

Struck is an acute disease in horses

Struck is a zoonotic disease

Struck is a slow disease of older sheep

Struck is a worldwide common disease with great economic impact

Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life

The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large intestine

Maternal protection is important in the case of Infectious necrotic enteritis of piglets

There is no vaccination for the prevention of Infectious necrotic enteritis of piglets

Pig enterotoxaemia can be prevented by vaccinating the pregnant sows

Pig enterotoxaemia is caused by Clostridium perfringens C

Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics immediately

Lesions of pig enterotoxaemia can be seen in the small intestine

Lesions of pig enterotoxaemia can be seen in the large intestine

Pig enterotoxaemia is more frequent in the litter of young than old sows

Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets

Pig enterotoxaemia can be generally seen in weaned piglets

Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia

Clostridium enterotoxaemia of piglets is caused by C. perfringens

Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows

Clostridium perfringens C causes infectious necrotic enteritis of piglets

Infectious necrotic enteritis of piglets occurs in piglets after weaning

The lesions of infectious necrotic enteritis of piglets can be seen generally in the small intestine

Infectious necrotic enteritis of piglets can be prevented by vaccinating the pregnant sows.

Necrotic enteritis of piglets is seen in piglets around weaning

Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin

Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets

Pig enterotoxaemia causes abdominal contractions in sow

Mesenteric lymph node is congested in case of pig enterotoxaemia

Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut

Enteritis in piglets are caused by Clostridium perfringens D.

Enteritis in piglets can be avoided by anatoxin vaccination

Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology

Pig enterotoxaemia is caused by β-toxin production in 1st week of life

Pig enterotoxaemia can cause a high mortality

Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut

Enterotoxaemia is mainly seen in piglets after weaning

Pig enterotoxaemia is not present in Europe

Pig enterotoxaemia cannot be prevented by using vaccines

Pulpy kidney disease is caused by Clostridium perf. D

Overeating is a predisposing factor to pulpy kidney disease

The toxin of the agent of pulpy kidney disease is sensitive to trypsin

Pulpy kidney disease is caused by Clostridium perfringens D

Pulpy Kidney Diseases is caused by Clostridium chauvoei

Pulpy kidney disease generally occurs in 1-2week old lambs

Pulpy kidney disease can occur at any age

Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes

Sudden change the diet is a predisposing factor to pulpy kidney disease

The toxin damages the endothelial cells in the case of pulpy kidney disease

Neurological signs are typical in the case of pulpy kidney disease

Isolation of the agent is necessary to the diagnosis of pulpy kidney disease

Pulpy kidney disease is typically seen in lambs below 2 weeks of age

Inactivated vaccines are used for the prevention of pulpy kidney disease

Pulpy kidney disease is seen in piglets in the first week of life

Pulpy kidney disease is a worldwide common disease.

Enterotoxaemia of sheep is also called pulpy kidney disease.

Pulpy kidney disease is caused by Clostridium perfringens D

Cattle are not susceptible to this disease

Vaccination are possible against pulpy kidney disease

Coccidiosis is a predisposing factor of ulcerative enteritis in poultry

Ulcerative enteritis of chicken is caused by Clostridium colinum

Ulcerative enteritis is frequently seen in day old chicken

Ulcers sometimes covered with pseudomembranes are frequent post mortem lesions of ulcerative enteritis of chicken

Ulcerative enteritis can occur in 4-12-week-old chickens

Clostridium perfringens is the causative agent of ulcerative enteritis in poultry

Ulcerative enteritis of poultry is generally prevented with vaccination

Lesions of ulcerative enteritis are mostly seen in the small intestines

Ulcerative enteritis is a common disease in large scale farms

Prevention of coccidiosis can help lower the incidence of ulcerative enteritis

Coccidiosis is a predisposing factor of necrotic enteritis of chicken

Foamy, brownish-red faeces is a clinical sign of necrotic enteritis of chicken

Lesions of necrotic enteritis of chicken are typically occur in the large intestine

Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis

Necrotic enteritis mostly occurs in chicken

Waterfowl are not susceptible to necrotic enteritis

Necrotic enteritis occurs in 1-3 weeks of age

Tyzzer’s disease is caused by Clostridium piliforme

Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A

Gangrenous dermatitis is caused by obligate pathogens

Gangrenous dermatitis causes muscle oedema.

Vaccines are the primary way of prevention of gangrenous dermatitis

Flaccid paralysis is a frequent clinical sign of tetanus

The agent of tetanus is strictly anaerobic

The agent of tetanus can enter the host through wounds

Tetanus is only seen in horse

Over-eating can predispose animals to Tetanus

The agent of Tetanus needs oxygen to replicate

Anatoxin vaccines are available for the prevention of tetanus.

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

Spasms are typical clinical signs of tetanus

Tetanus is a zoonosis

Toxoid vaccines can be used for the prevention of tetanus

Dogs are resistant to tetanus

The clinical signs of tetanus are inducible

Tetanus toxin cleaves synaptobrevin

For tetanus we use vaccines which contain toxoid

Tetanus cannot be prevented with vaccination

Tetanus is caused by Clostridium tetani

The agent of tetanus causes septicaemia

Tetanus can be diagnosed on the basis of post mortem lesions

Clostridium tetani produced endotoxin

C. tetani needs anaerobic conditions for propagation

Dogs are susceptible to tetanus

Tetanus can be prevented with vaccines containing inactivated bacteria

Tetanus can cause spasms

Horses are resistant to tetanus

Tetanus can only develop after deep wounds

Wounds can predispose to tetanus

The paralysis usually starts at the place of the wound

Clostridium tetani toxin is produced in the feed

Horses are most sensitive to tetanus

Tetanus can be prevented by anatoxin vaccination

Tetanus causes rigid paralysis

There is no vaccine for tetanus

Dogs have high resistance to tetanus

Clostridium tetani produces neurotoxins

The toxin of clostridium botulinum causes flaccid paralysis

Clostridium botulinum generally causes wound infection

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

The toxin of Clostridium botulinum has irreversible effect

Botulism can be seen as a result of a wound infection

Flaccid paralysis is the main clinical sign of botulism

Birds are resistant to botulism

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

Generally wounds predispose animals to botulism

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

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

Clostridium botulinum can produce toxins outside the hosts

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

Botulism doesn’t occur in Europe

Clostridium botulinum cannot tolerate air at all.

Botulism usually develops following a wound infection

Clostridium botulinum propagates in rotten materials

In Hungary, botulism is seen most commonly in birds

Clostridium botulinum spores are extremely resistant to heat

In Hungary, botulism occurs in winter and early spring

Botulism is eradicated in Europe

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

Botulism is seen mainly during summer

Spasms are the typical clinical sign of botulism

Paralysis is the main sign of botulism

Toxins of botulism are produced generally in the food

Botulism happen generally through wound infection

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

Haemolysins cause haematuria in the case of staphylococcus

Leucocidins produced by staphylococci damage white blood cells

Coagulase production is a virulence factor of Staphylococcus aureus

Some extracellular enzymes are virulence factors of Staphylococci

Haemolysins are virulence factors of Staphylococci

Endotoxins are virulence factors of Staphylococci

Protein A is a virulence factor of Staphylococci.

Extracellular enzymes are important virulence factors of pathogenic Staphylococci

Haemolysins and leucocidins are important virulence factors of Staphylococci

Some species of Staphylococcus are obligate pathogens

Staphylococcus are epiphytes.

Staphylococcus can produce EC enzymes.

Staphylococcus can be found on healthy animals’ mucous membranes

Staphylococcus are gram negative cocci

Coagulase positive Staphylococcus species are less pathogenic than Coagulase negative

Abscessation of lymph nodes is a typical sign of Morel’s disease

Morels disease id caused by Staphylococcus aureus subsp aureus

Clinical signs of Morels disease are mainly see above half a year of ag

Morel’s disease is an acute, fast courses disease

Morel’s disease occurs mainly in cattle, small ruminants and pigs

Interstitial pneumonia is the main postmortem lesion of Morel’s disease

Morels disease can be diagnosed by detecting the agent from the lesions

Morel’s disease is caused by Staphylococcus aureus subsp. Aureus

Morel's disease is mainly seen in suckling lambs

In Morel's disease we find abscesses in the subcutis

Diarrhoea is the main clinical sign of Morel's disease

Isolation of the agent from lesions of Morel's disease confirms the diagnosis

Morel's disease can be seen in sheep and goats

Morel's disease can mainly be seen in suckling animals

Abscesses and purulent inflammation are the typical lesions in the case of Morel's disease

Morel's disease is caused by Streptococcus pyogenes

Abscesses in the lymph nodes and in the subcutaneous tissue are typical in Morel's disease

Morel’s disease is seen mainly seen in cattle

Abscess formation is the main clinical sign of Morel’s disease

Morel’s disease affects only lymph nodes in the head

Morel ́s disease is caused by Streptococcus zooepidemicus

In case of several clinical sign in Morel ́s disease, antibiotics should be given through drinking water

Morel disease causes lymph node enlargement

Morel disease is not a zoonosis

Morel’s disease is caused by Staphylococcus hyicus

Ataxia is an important sign of the Morel ́s disease.

In the case of Morel disease per oral antibiotic treatment is used

Morel's disease causes subcutaneous abscesses

Methicillin resistant Staphylococcus aureus is generally not passed from animals to humans

Methicillin resistant Staphylococcus aureus strains are obligate pathogens

Methicillin resistant Staphylococcus aureus strains are more virulent than the methicillin sensitive ones

Methicillin-resistant Staphylococcus aureus (MRSA) is resistant against beta-lactam antibiotics

Methicillin-resistant Staphylococcus aureus (MRSA) can be asymptomatically carried

Methicillin-resistant Staphylococcus aureus (MRSA) can infect humans

Pneumonia is a frequent clinical sign of rabbit staphylococcosis

High ammonia concentration is a predisposing factor of rabbit staphylococcosis

Middle ear infection can happen in the case of rabbit staphylococcosis

Rabbit staphylococcosis is mainly seen in weaned and young rabbits

Rabbit staphylococcosis occurs more frequently in young than in adult animals

Over-crowding and poor ventilation are predisposing factors of Rabbit staphylococcosis

Lesions of Rabbit staphylococcosis are limited to the lungs

Bronchopneunomia is a typical post-mortem lesion of Rabbit staphylococcosis

Rabbit staphylococcosis is caused by Staphylococcus aureus subsp. aureus

Rabbit staphylococcosis is caused by Staphylococcus cuniculi

Subcutaneous abscesses are frequent lesions of rabbit staphylococcosis

Middle ear infection can happen in the case of rabbit staphylococcosis

Rabbit staphylococcosis can be prevented by vaccinating the pregnant rabbits with attenuated vaccine

Staphylococcus in rabbits typically occurs in newborn rabbits

Aerogenic infection is common in the case of staph in rabbits

Arthritis can be a clinical sign of staphylococcus infection in rabbits

If the ammonia level in the air is high it increases the susceptibility of rabbits to staphylococcus

In rabbit staphylococcosis: one symptom is otitis

Staphylococcosis in rabbits typically occurs in newborn rabbits

Abscess formation can be a clinical sign of staphylococcosis of rabbits

Overcrowding is a predisposing factor of rabbit staphylococcosis

Bronchopneumonia is a frequent clinical sign of rabbit staphylococcosis

Staphylococcosis of rabbits is caused by Staphylococcus hyicus

Rabbit Staphylococcus can be prevented/treated by vaccination

Rabbit staphylococcus occurs in 4-16 weeks old rabbits

Rabbit staphylococcus are caused by S. aureus subsp. piriformes

Rabbit staphylococcus causes severe respiratory signs in rabbits

We can use antibiotic treatment to cure rabbit staphylococcus

Rabbit staphylococcus is an obligate pathogen

Rabbit staphylococcosis typically occurs in suckling rabbits

Pneumonia is a typical sign of rabbit staphylococcosis

Staphylococcus aureus subsp. anaerobius is the causative agent of rabbit staphylococcosis

Purulent pneumonia can be seen frequently as a clinical sign of staphylococcosis in grower chickens

Gumboro disease can predispose chicken to staphylococcosis

Staphylococcus aureus subsp. aureus can cause septicemia in day old chicken

Staphylococcus aureus subsp. aureus can cause dermatitis in growers and hens

Staphylococci can cause disease only in day-old birds but not in growers or adults

Marek-disease can predispose poultry to staphylococcosis

Omphalitis is a clinical sign of avian staphylococcosis

Staphylococcus aureus subsp. aureus can kill the chicken embryo

Arthritis is a common clinical sign of avian staphylococcosis

Pneumonia is a common clinical form of avian staphylococcosis

Dermatitis is a common clinical sign of avian staphylococcosis

Staphylococcus aureus subsp. aureus can cause arthritis in poultry

Staphylococcus aureus subsp. aureus can cause frequent pneumonia in chicken

Staphylococcus aureus subsp. aureus can cause dermatitis in poultry

Poultry staphylococcus is caused by S. aureus

In poultry staphylococcus there is a septicaemic form, giving generalized disease

Poultry staphylococcus can infect eggs.

Poultry staphylococcus is a rare disease nowadays

Exudative dermatitis of pigs is caused by Staphylococcus aureus subsp. Anaerobius

Vesicles are formed in the case of exudative Dermatitis

Necrosis of the skin is the main clinical sign of exudative dermatitis

The agent of exudative dermatitis of pigs produces exfoliative toxin.

The agent of exudative dermatitis enters the host through wounds

The agent of exudative dermatitis can be passed from piglets to sows

The lesions of exudative dermatitis are itching very much

Exudative dermatitis can be seen in suckling piglets.

Exudative dermatitis is caused by Staphylococcus aureus

Exudative dermatitis is characterized by crust formation

Exudative dermatitis has high mortality

Staphylococcus aureus subsp. aureus is the causative agent of exudative dermatitis in pigs.

Vesicles are formed in the case of exudative dermatitis in pigs

Exudative dermatitis is generally seen in fattening pigs

Exudative dermatitis can be prevented by attenuated vaccines

Exudative dermatitis is sometimes seen on the udder of sows

Exudative dermatitis of pigs is caused by Staphylococcus hyicus

Exudative dermatitis of pigs is caused by Streptococcus hyicus

Itching is the major clinical sign of exudative dermatitis in pigs

Exudative skin inflammation occur usually in pigs 1-4-week-old

Exudative dermatitis can be treated with antibiotics

Vaccination is widely used in order to prevent exudative dermatitis

Exudative skin inflammation is caused by Staphylococcus aureus

Exudative dermatitis cannot occur in adult pigs

Exudative dermatitis can be spread by lice and ticks

Steptococcus dysgalactiae and streptococcus agalactiae can cause mastitis in cows

The capsule is a virulence factor of Streptococcus equi

Streptococcus can be divided according to their antigens

Streptococcus are epiphytes

Streptococcus are obligate aerobic

Steptococcus suis can cause encephalitis of humans

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

Diarrhoea is a frequent clinical sign of streptococcosis of pigs

Iron deficiency can predispose to porcine streptococcosis

Porcine streptococcosis can be prevented with inactivated vaccines

Porcine streptococcosis is treated with penicillins

Arthritis is a frequent clinical sign of streptococcosis of pigs

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

Purulent meningo-encephalitis can be a postmortem lesion of porcine streptococcosis

Calcium deficiency can predispose suckling piglets to streptococcosis.

Neurological signs are frequent in the case of porcine streptococcosis

Abscesses in the liver frequently seen in the case of porcine streptococcosis

Streptococcus suis is the main agent of porcine streptococcosis

Porcine streptococcosis is more frequent among adult animals than among young piglets

Streptococcus pyogenes is the main agent of porcine streptococcosis

Streptococcosis of pigs can be seen generally among fattening pigs

Streptococcus in swine can be caused by S. suis serotype II

Streptococcus in swine can cause acute purulent encephalomyelitis

All ages are susceptible in case of S. suis

S. porcinus can cause disease and is an epiphyte

S. porcinus is a contagious disease

Streptococcus equi subsp. Equi can sometimes cause arthritis

Streptococcus equi subsp. Equi is a zoonotic agent

Strangles can be diagnosed by staining abscess content

Colic can be a clinical sign of strangles

In endemic studs strangles is generally seen in horses that are older than 6 months

The agent of strangles is carried on the tonsils of most horses

Strangles is mainly seen in foals till the age of 4 months of age

The agent of strangles is spreading very fast among horses

Recovered animals carry the agent of strangles for a certain time

Horses with strangles are treated with penicillin

The mortality of strangles is high

The toxin of the agent is responsible for the lesions of strangles

Abscessation of the lymph nodes is a clinical sign of strangles

Carriers of agent of strangles can detected with PCR

In endemic studs strangles is generally seen in horses that are older than 6 months

Carriers of agent of strangles can detected with bacterium culture

Haemorrhagic diarrhoea can be a clinical sign of strangles

Strangles is caused by Staphylococcus aureus subsp. aureus

The morbidity of strangles is high, but the mortality is low

Abscesses are the typical clinical signs of strangles

The causative agent of strangles is Streptococcus equi subsp. equi

The causative agent of strangles has to be introduced in the herd

Strangles is treated with polymyxins

Strangles can be successfully treated with penicillin

When abscesses develop in strangles, the prognosis is poor

The causative agent of strangles is obligate pathogen

In strangles, morbidity is high

Fever is an important sign of strangles

Strangles has disappeared, due to extensive vaccination of the foals

Mortality of strangles is high

Strangles disappeared because of widespread vaccination of the foals

Carriage of the agent of strangles can be confirmed by isolation from the tonsils

Strangles has a morbidity of 100 %

Strangles pathogen is usually present on mucous membranes

The causative agent of strangles are an epiphyte.

Prognosis of strangles is bad if an abscess rupture

Strangles can be treated with penicillin

For the occurrence of strangles, predisposing factors are needed

Strangles can be diagnosed by serology

The causative agent of strangles is present in all horses

Strangles is mainly seen in horses aged 6 months-21⁄2 years

Penicillin is an effective antibiotic for the treatment of strangles

The agent of strangles is carried by the majority of horses on the mucous membranes

Diarrhoea is a typical sign of strangles

Animals with strangles generally do not have fever

The agent of swine erysipelas is Erysipelothrix Suis

The agent of swine erysipelas is carried by asymptomatic pigs in the tonsil

Swine erysipelas can mainly be seen in winter after introduction of carrier animals

Swine erysipelas can be an acute septicaemia in pigs

Diamond skin disease is a clinical form of swine erysipelas

The agent of swine erysipelas can survive in the environment for a few months

The agent of swine erysipelas can be present in the environment

Swine erysipelas can mainly be seen in winter after introduction of carrier animal

Warm weather is a predisposing factor of swine erysipelas

Hyperaemic spleen is a typical postmortem lesion of swine erysipelas

Sheep are generally infected with the agent of swine erysipelas per os

Vaccines against swine erysipelas give only serotype specific protection

High fever is a clinical sign of acute swine erysipelas

Fever is a frequent clinical sign of Swine erysipelas

Endocarditis can be a post-mortem lesion of Swine erysipelas

Swine erysipelas cannot be treated with antibiotics because the course of the disease is very fast

Swine erysipelas cannot be prevented with vaccinations

There are no vaccines for the prevention of swine erysipelas

The agent of swine erysipelas can infect only pigs

Vaccines against swine erysipelas give only serotype specific protection

Humans can be infected with the agent of swine erysipelas by eating meat of infected pigs

Humans can be infected with Erysipelas Rhusiopathie from fishes

Humans are generally infected with the agent of swine erysipelas through wounds

Vaccines against swine erysipelas give only serotype specific protection.

In the case chronic swine erysipelas pneumonia is a frequent clinical sign

The agent of swine erysipelas can frequently cause fibrinous pneumonia

Erysipelas can be seen only in pigs

Neuraminidase is a virulence factor of the agent of erysipelas

Polymyxins are used for the treatment of erysipelas

In Erysipelas the toxin is the virulence factor.

Diamond skin disease is caused by Erysipelothrix rhusiopathiae

Erysipelas affects only pigs

Chronic form of erysipelas can cause skin necrosis

Erysipelothrix rhusiopathiae can be carried and shed by asymptomatic pigs

Only pigs can be infected with Erysipelothrix rhusiopathiae

Purulent pneumonia is a typical clinical form of acute erysipelas

The agent of porcine erysipelas is carried by asymptomatic pigs

Warm weather and overcrowding can predispose to erysipelas of swine

Diamond skin disease is a subacute form of erysipelas of swine

Overcrowding is a predisposing factor of erysipelas of swine

The agent of swine erysipelas can cause septicaemia

Arthritis can be a clinical sign of erysipelas

Erysipelothrix rhusiopathiae is facultative pathogen

Turkeys are susceptible to Erysipelothrix rhusiopathiae

There is a serotype-specific protection against swine erysipelas

Erysipelas often appears in a septicaemia form

Erysipelas has to be introduced into a herd.

In erysipelas, small vessels in the skin become inflamed, causing erythema

Erysipelothrix rhusiopathiae is a facultative pathogenic bacterium

In the case of acute erysipelas high fever is an important sign

The swine erysipelas bacterium is an obligate pathogen

Erysipelas can be prevented by inactivated vaccine

The main sign in acute erysipelas is fever

Geese are susceptible to Erysipelothrix rhusiopathiae

Acute erysipelas causes moderate fever

Endocarditis is seen in acute erysipelas

Erysipelothrix rhusiopathiae is not resistant, it cannot survive in the environment

Some extracellular enzymes are virulence factors of Erysipelothrix rhusiopathiae

Erysipelas can be well treated by penicillin.

Warm weather can predispose pigs to erysipelas

The causative agent of swine erysipelas is an epiphyte

“Strong” erysipelas comes together with mild fever

There is a serotype specific protection in case of erysipelas

Listeriae can cause mastitis

Listeriae is zoonotic

Listeriosis is zoonosis

Haemolysin is a virulence factor of Listeriae

Diarrhoea is a frequent clinical sign of listeriosis in sheep

Listeriae can cause septicaemia in suckling lambs

Encephalitis is a frequent clinical sign of listeriosis in sheep

Diarrhoea is a frequent sign of listeriosis in sheep

Clinical signs of listeriosis generally seen in the summer

Listeriae do not cause bacteraemia or septicaemia; they travel only along the nerves

Not properly prepared silage can be source of listeria

Listeriosis has very severe clinical signs in pigs

The agent of listeriosis can travel along the nerves

Unpasteurized milk or milk products can be source of Listeria in the case of human listeriosis

Listeriosis is prevented by widespread vaccination using attenuated vaccines

Circling is a typical sign of ovine listeriosis

Listeriosis have very severe clinical signs in pigs

Listeriosis spread very fast in an infected herd from animal to animal

Abortion is a clinical sign of listeriosis

Abortion is the most frequent clinical sign of listeriosis in sheep

Listeria ovis is the agent of listeriosis

Listeriae can survive in pools and poodles

Listeria are soil bacteria

Listeriae are facultative intracellular bacteria

Listeriae can cause micro abscesses in the brain

Encephalitis is a frequent clinical sign of listeriosis in sheep

Infected silage can be the source of listeria.

Listeria are spreading fast from animal to animal.

Listeria ivanovii causes listeriosis in animals

Listeriosis spreads from animal to animal and causes high mortality

Listeriosis causes neurological symptoms in sheep

Listeriosis can infect rodents

Listeriosis can only be seen in sheep

Aerogen infection is the most important form of infection with Listeria in sheep

Listeria can be found only in infected animals, they cannot survive in the environment

Listeria are transmitted from animal to animal very fast in the infected flock

The most frequent sign of bovine listeriosis is abortion

There is widespread vaccination for the prevention of listeriosis

The agent of listeriosis is an intracellular bacterium

The main clinical sign of listeriosis in sheep is pneumonia

Vaccination of sheep against listeriosis with inactivated vaccines is widely done in Europe

Listeriosis causes septicaemia in lambs

Listeriosis mainly occurs at the end of winter

Listeriosis causes mainly abortion in cattle

Listeriosis can be isolated from the brain stem

Overcrowding is a predisposing factor of listeriosis

Listeria can be found in soil

Abortion is the most frequent clinical sign in bovine listeriosis

Listeria are not resistant, they cannot survive in the environment

Listeriosis can be a septicaemic disease

Pneumonia is a frequent clinical sign of listeriosis

Encephalitis is the most frequent clinical sign of listeriosis in sheep

Listeriosis is the most common neurological disease in cattle

Listeriosis occurs more frequently during the summer, at time of silage-making

In the case of listeriosis of cattle, signs of the nervous system are the most frequently seen

Listeriosis occurs only in tropical areas

Neurological symptoms are the most common clinical sign of listeriosis in cow

Listeriosis occurs in the summer

Listeriosis occurs only in ruminants

Main symptoms of listeriosis in sheep is encephalitis, abortion and septicaemia

In cases with encephalitis, abscesses can be found in the medulla oblongata

Phospholipase D is a virulence factor of C. pseudo tuberculosis

In Corynebacterium pseudotuberculosis oedema of the chest is common

Corynebacterium pseudotuberculosis can be transmitted between goats and horses

Pseudotuberculosis does not occur in Hungary

In pseudotuberculosis, only submandibular lymph nodes of sheep are affected.

In pseudotuberculosis oedema of the limbs is common

Corynebacterium pseudotuberculosis causes caseous lymphadenitis

Corynebacterium pseudotuberculosis forms due to dipping of sheep

The agent of caseous lymphadenitis can cause generalised infection in sheep

Caseous lymphadenitis of sheep occurs in tropical countries but not in Europe

Arthritis can be a clinical sign of caseous lymphadenitis of sheep

Caseous lymphadenitis of sheep is caused by Corynebacterium pseudotuberculosis

Corynebacterium pseudotuberculosis produces phospholipase D toxin

The agent of Caseous lymphadenitis of sheep can be transmitted to horses and it will cause ulcerative lymphangitis

Caseous lymphadenitis does not occur in goats and cattle

Caseous lymphadenitis of sheep is an acute disease

Clinical signs f caseous lymphadenitis of sheep can be seen only above 3-4 months

Clinical signs of caseous lymphadenitis can only be seen in sheep

Caseous Lymphadenitis of sheep is mainly seen in suckling lambs

Mycolic acid and lipoids in the cells wall of Corynebacterium pseudotuberculosis contribute to the virulence of the bacterium

Lesions of caseous lymphadenitis of sheep can be seen only in the lymph nodes

Caseous lymphadenitis can occur only in sheep

Caseous lymphadenitis is caused by nitrate positive strains of Corynebacterium pseudotuberculosis

Caseous lymphadenitis is only seen in suckling lambs

Arthritis can be a clinical sign of caseous lymphadenitis

Vaccination can be used for the prevention of caseous lymphadenitis

Caseous lymphadenitis is caused by nitrate-negative Corynebacterium pseudotuberculosis strains

Wound infection can predispose to caseous lymphadenitis

Caseous lymphadenitis can be generalized in sheep

Antibiotics cannot be used for the treatment of caseous lymphadenitis

Phospholipase D is an important virulence factor of the agent of caseous lymphadenitis

Abscesses in the lymph nodes are typical lesions of caseous lymphadenitis

Caseous lymphangitis is nitrate negative

Corynebacterium pseudotuberculosis causes caseous lymphadenitis in goat

Abortion can be a clinical sign of caseous lymphangitis

Caseous lymphadenitis of sheep occur only in the tropics

Caseous lymphangitis is seen mostly in sheep

Caseous lymphangitis does not occur in Hungary

Cross section of the lymph node with caseous lymphangitis shows an onion-like pattern

Caseous lymphangitis can cause abortion in waves

Vaccination can be used in prevention against caseous lymphangitis

Abscess formation in the lymph nodes is typical in the case of caseous lymphadenitis in goats

Caseous lymphadenitis is caused by Corynebacterium equi

Sheep with caseous lymphadenitis can infect horses

The agent of caseous lymphadenitis causes bacteraemia

Ulcerative lymphangitis of horses can be a result of a navel infection

The agent of ulcerative lymphangitis frequently enters the hosts through wounds

Ulcerative lymphangitis of horses is caused by Corynebacterium equi

Ulcerative lymphangitis of horses is caused by nitrate negative strains of Corynebacterium pseudotuberculosis

Ulcerative lymphangitis of horses can be a consequence of umbilical infection

Abscess formation can be seen in the case of ulcerative lymphangitis of horses

Ulcerative lymphangitis of horses is typically an acute disease

Ulcerative lymphangitis is caused by Corynebacterium pseudotuberculosis

Ulcerative lymphangitis of horses is caused by Corynebacterium equi.

Clinical signs of ulcerative lymphangitis can be mainly seen in suckling horses

Purulent inflammation of the lymphatic vessels is typical in the case of ulcerative lymphangitis

The agent of ulcerative lymphangitis can be detected by microscopic examination

Equine ulcerative lymphadenitis is an acute disease with high fever

Equine ulcerative lymphadenitis occurs only in tropical countries

Ulcerative lymphangitis is caused by nitrate negative C. pseudotuberculosis

Ulcerative lymphangitis does not occur in Hungary

Symptoms of ulcerative lymphangitis in horses are seen in pectoral region, legs and ventral abdomen

Ulcerative lymphangitis may evolve during navel infection

Animals with clinical signs of ulcerative lymphangitis have good prognosis

Best way of prevention for ulcerative lymphangitis is toxoid vaccine

Clinical signs of equine ulcerative lymphangitis can be seen in the lymphatic vessels

Equine ulcerative lymphangitis is a chronic disease of horses

Equine ulcerative lymphangitis is not zoonotic

Corynebacterium renale causes septicaemia in cattle

Corynebacterium renale can cause bovine pyelonephritis

Bovine pyelonephritis occurs in adult animals

Bovine pyelonephritis can be mainly seen in young calves

Penicillin can be used for the treatment of Bovine pyelonephritis

Bovine purulent nephritis is mainly seen in suckling calves

Haematuria can happen in the case of bovine purulent nephritis

Corynebacterium bovis is the causative agent of bovine pyelonephritis

Clinical signs of bovine pyelonephritis generally appear after calving

Frequent, painful urination is common clinical sign of bovine pyelonephritis

Bovine pyelonephritis can mainly be seen in young calves under half a year of age

Bovine pyelonephritis is seen as a result of an ascending infection

Pyelonephritis is caused by C. renale, C. pilosum, C. cystiditis

Pyelonephritis mostly occurs in horses.

Pyelonephritis occurs mostly some weeks after parturition

Pyelonephritis can cause positive pain probes of skin area above spine

Corynebacterium renale is the causative agent of bovine purulent nephritis.

Penicillin is used for the treatment of bovine purulent nephritis.

Haematuria can occur in bovine purulent nephritis

Bovine purulent nephritis is mainly seen in suckling calves

Rough, hard feed can predispose cattle to actinomycosis

Actinomyces species can cause diseases mainly in cattle, swine and dogs

Bovine actinomycosis is typically a generalised disease.

Actinomyces species are fastidious bacteria which can be found on mucous membranes

Lumpy jaw is the clinical form of bovine actinomycosis

Actinomyces hordeovulneris can cause actinomycosis of dogs

Actinomyces bovis is the causative agent of bovine actinomycosis

Actinomycosis is a notifiable disease.

Subcutaneous pyogranuloma can be seen in the case of canine actinomycosis

Actinomyces species can cause diseases mainly in birds

Respiratory distress is a clinical sign of canine actinomycosis

Actinomyces species can be found mainly in the northern hemisphere

Arthritis is the most frequent clinical sign of canine actinomycosis

A. hordeovulneris and A. viscosus can cause pleuritis, peritonitis and pericarditis

Clinical signs and pathological findings of canine actinomycosis and nocardiosis are generalized.

Actinomyces bovis is the causative agent of wooden tongue, it generally attacks soft tissues

Wooden tongue is caused by Actinomyces bovis in cattle

Bovine actinomycosis is caused by Actinomyces lignieresii.

Abrasions on the mucous membrane of the oral cavity can predispose to actinomycosis

In the case of actinomycosis sulphur granules can be found in the lesions.

Lumpy jaw is a common clinical sign of bovine actinomycosis

Actinomyces bovis is the causative agent of lumpy jaw

Rough feed and tooth eruption can predispose to lumpy jaw

Actinomyces bovis can cause actinomycosis in swine

Distortion of the mandibula or maxilla are the typical sessions of swine actinomycosis

Canine actinomycosis is caused by Actinomycosis canis

Prolonged antibiotic therapy is needed to the treatment of actinomycosis

Changing teeth is a predisposing factor in actinomycosis

Use of attenuated vaccines against actinomycosis is widespread

The pathological lesions of actinomycosis in pigs are seen in the udder

Sulphur granules are seen in the lesions of actinomycosis

Actinomycosis is prevented with wide vaccination

Hard, stinging feed predisposes cattle to actinomycosis

In the case of bovine actinomycosis the lesions are localized in the udder

Wounds on the udder predispose swine to actinomycosis

Actinomycosis is mainly an acute disease

In the case of bovine actinomycosis lesions can be seen in the mandible or maxilla

Bovine actinomycosis causes changes in the upper and lower jaw

In bovine actinomycosis, the first changes are seen in the udder

Actinomyces causes a generalized infection

In the case of actinomycosis in pigs the lesions are seen in the udder

Dogs are resistant to actinomycosis

Sulphur granules are typical lesions of actinomycosis

Actinomyces viscosus can infect the udder of sow

Actinomyces can affect the retropharyngeal lymph nodes

In dogs, grass awns can be a predisposing factor for actinomycosis infection

A. israelii is the causative agent if canine actinomycosis

Swine actinomycosis is caused by Actinomycosis bovis

Actinomyces species are epiphytes

Actinomycosis bovis can cause udder infection in horses

Dogs can be infected by Actinomyces bovis

Vaccines in cattle can be efficient for prevention of the actinomycosis disease

Wound infection is the primary route of actinomycosis infection

Actinomycosis is a gram-negative bacterium

Horses are most sensitive to Actinomyces israelii

Lumpy jaw is a frequently seen disease in cattle herds with high morbidity

Mastitis is a common clinical sign of bovine nocardiosis

Nocardia species cause lymphadenitis in different animals

Nocardia asteroides can cause mastitis in cattle

Pneumonia is a frequently seen pathological finding in bovine nocardiosis

Nocardia asteroides causes bovine nocardiosis.

Nocardia species are really fastidious bacteria which can grow on mucous membranes only

Nocardia bacteria can cause inflammation of the lymphatic vessels

Cattle are infected with nocardia bacteria from the soil

Nocardia species are Gram negative coccoid rod shaped bacteria

Carnivores and cattle are susceptible to nocardia species

Nocardia are gram positive branching filaments

Nocardia asteroides can cause generalized infection in dogs

Nocardiosis is a chronic infection with granuloma formation

Norcardia species are soil organisms

Nocardia asteroides is a soil microorganism

Nocardia asteroides generally causes mastitis in cattle, which can be an iatrogenic infection

Nocardia asteroides can cause granulomatous lesions of tissues under the skin in cattle

Canine nocardiosis is caused by Nocardia asteroides

Nocardiosis causes chronic mastitis in cows

Nocardia asteroides can cause generalized disease in dogs

Nocardia spp. in cattle primarily causes mastitis

Most susceptible species to Nocardiosis are dog and horse

N. asteroides causes cutaneous pyogranulomas in dog

Nocardia asteroides is zoonotic

Disseminated Nocardiosis in dog occurs after 1 year of age

Nocardiosis will cause acute mastitis in cattle

Bovine farcy causes chronic lesions in the superficial lymph nodes and vessels

Nocardiosis are found mostly in tropical and subtropical regions

Nocardia is a facultative aerobic bacterium

Rhodococcus equi causes mainly metritis and urinary tract infections

Only moderately virulent Rhodococcus equi strains can cause disease in foals

Immunocompromised humans are susceptible to Rhodococcus equi

Rhodococcus equi can cause aseptic arthritis in young foals

Rhodococcus equi can cause a disease mainly in swine

Pneumonia of young foals caused by Rhodococcus equi can mainly be seen in summer time

1 to 3 months old foals acquire Rhodococcus equi from the dust, so the main route of infection is the inhalation of the dust contaminated with the causative agent

Rhodococcus equi infection is a notifiable disease

Rhodococcus equi can cause pneumonia and lymphadenitis in 6 to 18 months-old foals

Rhodococcus equi mainly causes CNS clinical signs in 1-4-month-old foals

Rhodococcus equi can cause abscesses

Rhodococcus equi can cause lesions only in horses

Rhodococcus equi can generally cause disease in foals above 6 months of age

Tetracyclines are the primary antibiotics for the treatment of diseases caused by Rhodococcus equi

Rhodococcus equi can cause pneumonia in horses

Rhodococcus equi can cause disease mainly in foals between 1 and 4 months of age

Rhodococcus equi can cause lesions in the gut

There is widespread vaccination to prevent diseases caused by Rhodococcus equi

Rhodococcus equi can cause pneumonia in 1-3 years old foals

Interstitial pneumonia is the main lesion caused by Rhodococcus equi in foals

Pneumonia caused by Rhodococcus equi can be successfully treated with colistin

Rhodococcus equi can cause lesions in humans

Pneumonia caused by Rhodococcus equi is typically seen in 1-4 months old foals

Rhodococcus equi causes interstitial pneumonia in foals

Rhodococcus equi can cause only pneumonia in foals

Equine herpesvirus-2 can predispose horses to pneumonia caused by Rhodococcus equi

Rhodococcus equi can cause suppurative bronchopneumonia in foals

Bronchopneumonia caused by R. equi is typically seen in foals between 1 and 4 months of age

Combination of Rifampicin and Macrolides antibiotics is used for the treatment of bronchopneumonia caused by R. equi.

Rhodococcus equi can cause pneumonia in foals of 5-6 months of age

Pneumonia caused by Rhodococcus equi is a chronic disease

Serous pneumonia is caused by Rhodococcus Equi

Pneumonia caused by Rhodococcus equi is treated with penicillin

Rhodococcus equi can cause clinical signs in humans

R. equi causes pneumonia in foals aged 6-8 months

R. equi pneumonia is transmitted from foal to foal

R. equi causes severe catarrhal pneumonia

Pneumonia caused by R. equi can be treated with rifampicin and erythromycin for 4-5 days

R. equi is an obligate anaerobic bacterium

R. equi causes high mortality in infected foals

R. equi can cause ulcerative enteritis

Rhodococcus equi is usually seen during the winter

R. equi causes pneumonia with large abscesses

R. equi pneumonia can be treated with rifampicin and erythromycin for 4-10 weeks

Foals suffering from Rhodococcus equi can be treated with any antibiotic

Pneumonia caused by R. equi is a fast spreading acute disease

Many of the clinically sick animals recover after treatment for R. equi infection

R. equi pneumonia is transmitted by inhalation of contaminated dust

R. equi cause purulent pneumonia

Dermatophilus congolensis is the agent of dermatophilosis

Dermatophilus congolensis causes ulcerative dermatitis in sheep

Dermatophilus congolensis can cause metritis in horses

Skin lesions have important role in the pathogenesis of dermatophilosis

Dermatophilus congolensis is mainly a human pathogen

The agents of dermatophilosis cannot survive in the environment, they are mainly transmitted by arthropods

Examination of skin scraping under the microscope is important diagnostic method for the diagnosis of dermatophilosis

Dermatophilus hyicus causes exudative dermatitis in piglets

Heavy rain and wet skin surfaces are important predisposing factors in case of dermatophilosis

Treatment is not allowed in the case of dermatophilosis, eradication of the disease is our primary aim

Treatment of dermatophilosis is based on antifungal agents

The most susceptible animal species which shows clinical signs of dermatophilosis is the dog

Dermatophilosis is more frequent in the tropical areas than in moderate climate

Dermatophilosis is caused by Dermatophilus bovis

The agent of dermatophilosis is resistant, it remains viable for several months in the environment.

Serous dermatitis can be seen in the case of dermatophilosis

Dermatophilosis occurs only in tropical and subtropical regions

Dermatophilosis congolensis is the causative agent of dermatophilosis

The agent of dermatophilosis is not resistant, it cannot survive in environment

Focal necrosis in the parenchymal organs is a typical lesion of dermatophilosis

Dermatophilosis is more common in the tropical environment than in moderate climates

Dermatophilus bovis causes dermatophilosis

Serous dermatitis is the main clinical sign of dermatophilosis

At dermatophilosis in the parenchymal organs inflammatory-necrotic nodules can be observed

The agent of Dermatophilosis can survive in the environment.

Dermatophilosis can be diagnosed by staining a direct smear from the lesions

Dermatophilosis can be diagnosed by microscopic examination

Dermatophilosis can be generalized

Dermatophilosis can affects also birds and plants

Dermatophilosis occurs only in Africa

Focal inflammation in the liver is a typical lesion of dermatophilosis

Dermatophilosis is predisposed by wet skin