Final Exam PQ (p1-90) Flashcards
Arthropod borne infections are direct infections
F
Drinking water cannot transmit infective agents since it is hypoosmotic
F
Aerogenic infection is a form of direct infection
F
Infective agents cannot survive in the soil, so soil cannot be a source of infection.
F
Direct infection happens when infected animals pass the infection with water.
F
I f the arthropod is a true vector, if it brings the pathogen into a susceptible animal
F
The arthropod is a true vector, if it can take the pathogen to a further distance.
F
Infection cannot happen through water since bacteria and viruses are inactivated in
water.
F
Meat is never involved in transmission of infections since fermentation of meat kills
agents.
F
Germinative infection is very frequent in mammals
F
New-born animals cannot be infected from the milk thanks to the colostral antibodies.
F
Vertical infection does not occur in mammals
F
Horizontally infections happen only in birds
F
Germinative infection is frequent in mammals, it will result in malformation of the
foetuses.
F
Galactogen infection cannot happen when the animals receive colostrum, since the
antibodies in the colostrum prevent it.
F
Galactogen infection is a form of horizontal infections.
F
) If the dam infects newborn animals, we speak about horizontal infection.
F
Germinative infection can occur mainly in mammals.
F
Horizontal infection does not occur in mammals. F
Vertical infection does not occur in mammals. F
Germinative infection does not occur in mammals. F
Galactogen infection does not occur in mammals F
In germinative infection, the placenta is infected by the mother during pregnancy.F
Germinative infection is a rare form of horizontal infection. F
In germinative infection, the newborn is infected through the milk. F
In the case of cyclozoonoses arthropods are responsible for maintaining the infections F
If humans infect animals we speak about metazoonoses. F
In case of secondary infection, a new pathogen infects an already cured animal. F
In case of secondary infection, two pathogens infect the host simultaneously. F
In case of secondary infection, one of the agents is always a virus. F
Stenoxen agents have a wide host range. F
There is no minimum number of agents necessary to infection, because they can replicate in the host F
The amount of the agent does not influence the outcome of the infection, since it can replicate in the host. F
Virulence is a stable characteristic of an agent. F
Species specific resistance can be overcome by increasing the number of agents. F
Within a pathogenic species no avirulent strains can occur. F
Foetuses do not have immune reactions F
Fetuses have no active immune response F
T he normal microflora of the gut is essential for animals; they cannot live without it F
Foetuses have no immune response; they appear only in 2-4 week old animals F
The age of the animals does not influence their susceptibility to a certain agent F
From 2nd trimester of pregnancy, the foetus produces an immune response against any antigen. F
There is no immune response in the foetus, only from 4 weeks after birth. F
Fetuses cannot be infested since the placenta completely isolates them. F
The incubation time is the time between the appearance of the clinical signs and death of the animal F
Subacute diseases last one or 2 days. F
Intra uterine infections does not occur in mammals since the agents cannot penetrate the placenta. F
In the case of generalised infections the placenta prevents the infection of the foetus. F
The agent does not replicate in dead end hosts F
Dead end hosts do not show clinical signs, they die without signs F
In the case of latent infection the agents are continuously shed F
In the case of latent infections, the agents are continually shed F
Abortion is the main clinical sign of abortive infections F
The animals do not carry the agent after recovery from an infectious disease because the immune system eliminates it. F
Tolerated infections result in high level of immune reaction. F
Infected animals have a high level of antibodies in the case of tolerated infections F
The agent is not shed in the case of inapparent infections. F
When the clinical signs disappear, shedding the agent is finished F
In the case of an abortive infection no clinical signs will be seen F
) In the case of latent infection only mild clinical signs will be seen F
Only animals showing clinical signs can shed infective agents. F
Latent infection is common in the case of Gram-positive bacteria. F
Inapparent infections cannot be detected in laboratory examinations. F
In case of abortive infection, the animal always aborts. F
Tolerated infection can be demonstrated only by serology.F
During a tolerated infection the animals are seropositive. F
) In the case of latent infection no clinical signs can be seen. F
Asymptomatic infections cannot be manifest. F
Animals do not carry the agents after recovery from an infectious disease. F
Mortality show what proportion of the diseased animals die. F
Morbidity shows the percentage of dead animals compared to the size of the herd F
Lethality shows the number of died animals compared to the total number of the herd. F
Prevalence shows the number of diseased animals compared to the total number of the
herd. F
Mortality shows the proportion of dead animals compared to the number of diseases ones. F
Epidemic diseases are fast spreading; they are fast transmitted between continents F
Pandemic diseases have no tendency to spread. F
Lethality shows the ratio of dead animals and the total stock. F
Hemagglutination inhibition test is used for the detection of antigens of certain agents. F
Antigens of certain agents can be detected using PCR F
Surface antigens of certain agents are detected with ELIZA or PCR F
Infective agents can be detected 2-3days after infection using serological tests F
Virus Neutralisation test is used for the detection of antigens of the virus F
MATSA is a form of disease F
Microscopic detection of agents is not used in diagnostic work anymore F
If an animal is infected laboratory tests always detect the agent. F
Polymerase chain reaction is used for the detection of antigens of the agent. F
Microscopic examination of samples is not used in the diagnosis of infectious diseases any more. F
Antibacterial treatment is forbidden in the EU in the case of viral diseases. F
No aetiological treatment is available in the case of viral diseases F
Mass treatment using antibiotics is not allowed in the EU. F
All bacterial agents can be eradicated with antibiotic treatment F
Use of antibiotics in the case of diseases caused by viruses is not allowed because of antibiotic resistance. F
In case of viral diseases, no antibiotics are given. F
Antibiotics may be used only until the disappearance of the clinical signs. F
Only diseased animals have to be treated with antibiotics to prevent resistance. F
There is no anti-viral therapy. F
In case of import of animals into a farm, animals in the quarantine must only be observed, there is nothing to do with them if they do not show clinical signs F
Eggs of different species can be hatched together; they cannot infect each other thanks to the different hatching time. F
Isolated keeping of different age groups of the same species cannot prevent spreading of infectious diseases since all animals of the same species are susceptible to the same
agents. F
Day-old birds cannot be infected in the hatchery because they are protected by yolk Immunity. F
There is no maternal protection in birds. F
Maternal protection occurs only in mammals. F
Animals having epitheliochorial placenta receive maternal antibodies only through the placenta F
The protein and antibody content of the colostrum is stable in the first week after calving F
Absorption of maternal antibodies from the colostrum in the first three days is not changing F
Colostrum is not important in protection of calves since the antibodies can go through the placenta F
The immunoglobulin content of the colostrum is not changed in the first week after birth. F
New-born animals cannot be infected from the milk thanks to the colostral antibodies. F
The protein content of the colostrum remains high for the first two weeks after giving birth. F
The immune globulin content of the colostrum remains high for the first week after giving birth. F
The enteral absorption of immunoglobulins is about the same for a week after birth. F
The endotheliochorial placenta prevents to transport of immunoglobulins to the foetus F
Homologous hyperimmune serum can provide about a year-long protection. F
Adjuvants in vaccines increase the shelf life of vaccines F
The method of vaccination has no effect on the efficacy of the vaccination F
Deletion vaccines can only be used as live vaccines. F
The colostral immunoglobulins have no effect on the vaccination of the new born animals F
DIVA principle can only be used if the animals are vaccinated with deletion vaccines F
For safety reasons only inactivated vaccines are used F
Live vaccines always contain avirulent agents. F
Live vaccines are less effective than the inactivated ones. F
Live vaccines are dangerous, they are not on the market any more. F
Live vaccines are not used in Europe any more. F
Live vaccines do not provide good immunity. F
Marker vaccines are used to mark the site of vaccination. F
It is not allowed to use inactivated deletion vaccines in the EU. F
Marker vaccines are marked with dyes.F
The immune response produced by an attenuated vaccine is low. F
Vaccines containing attenuated strains are not used anymore.F
The amount of antigen in the vaccine has no effect on the efficacy of the vaccine. F
Eradication with selection method is not done nowadays F
Eradication with generation shift cannot be used if the level of infection is high in the herd F
Eradication using generation shift method is mainly used in Poultry F
Implantation of washed embryos from a non infected dam into infected one is a way of eradication F
Eradication using the generation shift method is mainly used in pig herds. F
In the case of generation shift the infected animals must be slaughtered at the beginning of the eradication procedure. F
Caesarean section is the only way of birth when eradication is carried out using the SPF method F
Herd replacement is the cheapest way of eradication of a disease F
Embryo transfer cannot be used for eradication, since the embryo can be infected. F
The selection method cannot be combined vaccination. F
If eradication is made by selection method, vaccination is forbidden.F
Generation shift is a frequently used eradication method in swine. F
In eradication by selective breeding, only the animals shedding the bacteria are eliminated. F
In eradication by selective breeding, vaccination cannot be used. F
Eradication by selective breeding is not used anymore. F
Selection (test and remove) is not used to eradicate a disease anymore. F
There is no neutralizing epitope of parvoviruses. F
SMEDI is caused by goose circovirus. F
SMEDI is caused by porcine circovirus F
If 75-day-old swine foetuses are infected with parvovirus respiratory clinical signs can be seen in the piglets. F
If 100-day-old swine foetuses are infected with parvovirus, respiratory clinical signs can be seen. F
If 100-day-old swine fetuses are infected with parvovirus, dermatitis is a clinical sign F
If 15 day old swine foetuses are infected with parvovirus myoclonia congenital is a
clinical sign F
If 100-day-old swine fetuses are infected with parvovirus, respiratory clinical signs can
be seen F
) If 75 day old swine foetuses are infected with parvovirus abortion can be seen F
If 15 day old swine foetuses are infected with parvovirus mummification can be seen F
The porcine parvovirus 1 causes renal disorders in adults F
PCR is used for the detection of antibodies against porcine parvovirus 1 F
Porcine SMEDI can only be induced by parvoviruses. F
PPV-1 induces diarrhoea in suckling piglets. F
Neurological disorders are frequent in Porcine parvovirus infections. F
Swine parvovirus maternal antibodies can exist up to 6 to 12 months of age. F
Porcine parvovirus can cause neurological signs in sows. F
Porcine parvovirus frequently causes diarrhoea in piglets. F
Porcine parvoviruses are genetically uniform. F
PPV-1 vaccination must be started at 4-6 weeks of age. F
Vaccination against canine parvovirus 2 is independent from maternal antibodies F
The parvovirus enteritis of dogs is caused by canine parvovirus 1 F
The parvoviral enteritis of dogs is type 3 hypersensitivity F
Maternal antibodies against canine parvovirus can protect dogs for about 2 years F
The replication of canine parvovirus 2 is in the crypt cells of large intestine F
Maternal antibodies of dogs protect not longer than 2 weeks in the case of parvoviral enteritis of dogs F
Canine parvoviruses do not infect cats F
Dog parvovirus enteritis is nowadays very rare. F
Dog parvovirus can be detected directly from Sera, Saliva. Foetus. F
Maternal antibodies usually protect for 2-3 weeks against Canine parvovirus disease. F
Canine parvoviruses form a single antigenic group. F
Maternal antibodies against cat parvovirus protect only till 2 weeks age. F
Hyperimmune serum can be used for the treatment of feline panleukopenia F
Feline panleukopenia virus infection of dogs may cause acute diarrhea F
Feline panleukopenia viruses may infect dogs F
Cat panleukopenia virus can infect only cats. F
Cat panleukopenia virus causes disease only in cats.F
To cat panleukopenia virus only cats are susceptible. F
Europe is free of Feline panleukopenia. F
The mink enteritis is a type 2 hypersensitivity F
Aleutian mink disease and mink enteritis are caused by the same virus. F
Aleutian mink disease is caused by protoparvovirus, like cat parvovirus F
Aleutian mink disease virus causes enteritis. F
Vaccines are available against Aleutian mink disease. F
Vaccines are used to prevent Aleutian Mink Disease F
Aleutian mink disease is caused by cat parvovirus F
Aleutian mink disease is a type IV hypersensitivity F
Aleutian mink disease is a type I hypersensitivity F
Attenuated vaccines can be used against Aleutian mink disease F
Inactivated vaccines are used against Aleutian mink disease F
Live vaccines are used against Aleutian Mink Disease. F
Aleutian mink disease virus induces enteritis in older minks F
The Aleutian Mink Disease is usually acute. F
Aleutian Mink Disease occurs only in the US. F
Enteritis is a clinical sign of Aleutian Mink Disease. F
The Derzsy’s disease virus causes pneumonia. F
The Derzsy’s disease virus can infect ducks. F
Derszys disease is caused by a polyomavirus F
The Derzsy’s disease virus causes conjunctivitis F
Derzsy ́ s disease virus does not infect the egg. F
The Derzsy’s disease virus can infect ducks. F
The duck parvovirus can infect goose.
F
The circovirus is too small so it’s a bad antigen F
Circovirus can easily be cultured in different homologous cell lines. F
Circoviruses can be cultured easily in many cell lines. F
Resistance of circovirus is very low, in the environment they are inactivated within a day. F
Only causes the depletion of B-lymphocytes. F
The circovirus has circular RNA in its genome. F
The Derzsy’s disease virus causes pneumonia. F
The Derzsy’s disease virus can infect ducks. F
Derszys disease is caused by a polyomavirus F
The Derzsy’s disease virus causes conjunctivitis F
Derzsy ́ s disease virus does not infect the egg. F
The Derzsy’s disease virus can infect ducks. F
The circovirus is too small so it’s a bad antigen F
Circovirus can easily be cultured in different homologous cell lines. F
Circoviruses can be cultured easily in many cell lines. F
Resistance of circovirus is very low, in the environment they are inactivated within a day. F
The circovirus has circular RNA in its genome. F
Detection of PCV2’s DNA is enough for the correct diagnosis. F
In pigs the porcine circovirus 2 can cause BFD. F
Porcine circovirus 2 always causes clinical signs in pigs F
Porcine circovirus 2 always causes clinical signs in cattle F
There is no efficient vaccine against PCV2 F
Porcine circoviruses cannot be responsible for reproductive disorders F
Porcine circoviruses are genetically and antigenically uniform. F
For prevention of Swine circovirus disease only general hygienic measures can be used. F
Swine circovirus causes only respiratory signs. F
Incubation period of porcine circovirus disease is short, some days. F
Predisposing factors for Porcine Circovirus associated disease can be Food management. F
Porcine circovirus-1 may damage the foetus. F
Porcine circoviruses cannot be responsible for reproductive disorders. F
Reproductive disorders caused by Porcine circoviruses are only significant in North America. F
PMWS is a type 3 hypersensitivity F
PMWS is a type 4 hypersensitivity F
One of the most common pathological signs of PMWS is glomerulonephritis F
A clinical sign of PMWS can be haemorrhages in the skin F
In pigs the porcine circovirus 1 can cause PMWS F
PDNS is a type IV hypersensitivity F
Porcine dermatitis nephropathy can only be caused by circoviruses. F
Porcine dermatitis and nephropathy syndrome are only caused by PCV-2. F
PDNS is only caused by PCV-1. F
PDNS does not occur in Hungary. F
PDNS is caused by both PCV-1 and PCV-2. F
PDNS is not caused by PCV F
PDNS is a rare infection causing clinical signs only in piglets before weaning. F
Prevention of PDNS is with live attenuated vaccines. F
In pigs the porcine circovirus 2 can cause BFD. F
Avian circovirus causes clinical signs similar to those seen in PDNS. F
The pigeon circovirus is not an important disease because the virus causes feather and beak deformities F
The beak and feather diseases causes typically neurological signs F
In parrots porcine circovirus 2 causes the psittacine beak and feather disease F
Pigeon circoviruses are antigenically uniform. F
Avian circoviruses do not cause clinical signs in domestic birds. F
Avian circoviruses do not cause disease in wild birds. F
Inactivated vaccines are used against pigeon circovirus infections. F
Pigeon circovirus infections do not occur in Hungary, the disease is prevented by vaccination. F
Vaccines are available for Pigeon Circoviruses. F
Clinical signs of PBFDV (Psittacine Beak and Feather Disease Virus) are only seen at time of moulting. F
The chicken infectious anaemia virus is also commonly detected in goose. F
The chicken infectious anaemia virus causes only anaemia F
The chicken anaemia virus does not replicate in lymphoid progenitors F
The chicken infectious anaemia causes clinical signs similar to those seen in PDNS F
Vertical infectious is not possible in chicken infectious anaemia F
The chicken infectious anaemia is a disease of hens F
Infectious Chicken anaemia virus can cause clinical signs only in layer hens. F
Chicken anaemia virus infection can result in high mortality of chickens over 3 weeks of age. F
There is no vaccine available against papillomaviruses F
Bovine papillomavirus is malign. F
The sarcoid is caused by equine papillomavirus F
The sarcoid is the disease of cattle F
Papillomaviruses replicates in the kidney F
Bovine papillomavirus can cause metastasis in horse F
Papillomaviruses cause cervical cancer in dogs F
Papillomaviruses can be cultured in epithelial cell lines. F
Treatment of haemorrhagic nephritis enteritis virus can be effective with vaccine against circovirus. F
The haemorrhagic nephritis enteritis virus causes glomerulonephritis F
The primary replication of haemorrhagic nephritis enteritis virus is in small intestine F
Polyomavirus never infects mammals F
Goose haemorrhagic enteritis and nephritis is frequent in ducks F
Haemorrhagic enteritis and nephritis of geese is only prevalent in France F
Haemorrhagic nephritis and enteritis of geese is caused by herpes viruses. F
Goose polyomavirus causes haemorrhagic nephritis and enteritis in all age groups. F
Haemorrhagic nephritis and enteritis of geese is caused by a Herpesvirus. F
Adenoviruses are enveloped viruses, therefore they are sensitive to detergents F
Adenoviruses are arboviruses. F
Adenoviruses are not too resistant enveloped viruses. F
Adenoviruses have mostly a broad host spectrum (euryxen pathogens) F
Adenoviruses are poor antigens F
There is no cross reactivity and cross protection among adenoviruses within genera F
There are no serological cross-reactions between different adenovirus species. F
Adenovirus infections always result in severe disease F
Several adenoviruses of domestic animals are zoonotic agents F
Adenoviruses usually cause central nervous diseases with high lethality. F
Only attenuated vaccines can be applied for immunization against adenoviruses. F
Adenoviruses infect only mammalian hosts. F
Adenoviruses usually cause central nervous diseases with high lethality. F
The hepatitis-hydropericardium syndrome can be caused by siadenoviruses F
Only attenuated vaccines can be applied for immunization against adenoviruses. F
Adenoviruses are zoonotic agents. F
Cholelithiasis is frequently seen in ovine adenovirus 4 infections of rams F
Adenoviruses can cause purulent bronchoalveolar pneumonia in calves and lambs F
Infertility and abortions are the most significant signs of bovine adenovirus infections F
No long-term carrier stage is seen in canine adenovirus serotype 1 infections. F
Lymphocyte cell count is not changed during Canine adenovirus 1 infection. F
Canine Adenovirus 1 infection doesn’t cause viraemia F
The canine adenovirus causes disease only in dogs F
Canine adenovirus infects only dogs F
Only inactivated vaccines are available against infectious canine hepatitis infections F
Glaucoma is a frequent sign of peracute canine infectious hepatitis F
Dogs carry Canine adenovirus serotype-1 usually in the spleen. F
The Canine adenovirus-1 can cause disease only in dogs. F
Infectious Canine Hepatitis is usually seen in elderly dogs. F
Causative agent of Rubarth ́s disease is CAdV-2. F
Canine infectious hepatitis is caused by several adenovirus serotypes. F
Canine adenovirus is characterized by hepatitis and abortion. F
CAdV-2 causes CNS disease in puppies. F
Rubarth’s disease is caused by CAdV-2. F
Rubarth’s disease is a disease of older cats. F
Adenoviruses frequently cause encephalitis in chicken F
Chicken adenoviruses are species-specific. F
Antibiotic therapy is forbidden in turkey haemorrhagic enteritis F
Marble Spleen Disease virus causes lymphatic tumours in geese. F
Egg drop syndrome virus causes cloaca paralysis F
Egg drop syndrome virus causes severe inflammation of the ovaries in hens F
The egg drop syndrome is mostly transmitted by arthropods F
The postmortem lesions of egg drop syndrome virus and polyoma virus in goose are the same F
The pathological lesions of egg drop syndrome virus and polyoma virus in goose are the same F
The egg drop syndrome virus may cause respiratory disease in young geese F
Egg drop syndrome usually appears in the beginning of the laying season F
The Egg Drop Syndrome virus causes hepatitis and hydropericardium in young geese. F
The Egg Drop Syndrome virus is mainly transmitted by arthropods. F
The Egg Drop Syndrome virus damages the oviduct of day-old chicken. F
Egg Drop Syndrome is a disease of chickens of all age groups. F
Adenoviruses of birds, is characteristic with mild diarrhoea and rough, hard eggshell. F
Egg Drop Syndrome is caused by an Aviadenovirus. F
Herpesviruses are good antigens. F
Alphaherpesviruses are host specific slowly multiplying (>24hrs) viruses F
Herpes viruses are resistant to detergents F
Herpesviruses are strong antigens, therefore single vaccinations provide lifelong protection F
There are no serological cross-reactions between different herpesvirus species. F
Because the genome of herpesvnruses is very stable, no attenuated mutant vaccine strains are available. F
Infectious bovine vulvovaginitis virus strains cause abortions and foetal deformities F
The infectious bovine rhinotracheitis virus (IBRV) causes haemorrhagic gastroenteritis. F
Infectious bovine rhinotracheitis virus also causes mastitis in cows F
Infectious bovine rhinotracheitis virus is transmitted by arthropods F
Infectious Bovine Rhinotracheitis virus frequently causes encephalitis in old cow and bulls F
Infectious Bovine Rhinotracheitis virus frequently causes encephalitis in old sow and bulls F
Attenuated vaccines are used in pregnant cows against Infectious Bovine Rhinotracheitis virus. F
Pregnant cows can be immunized against IBRV only with attenuated vaccines. F
Because Bovine herpesvirus l causes latent infections; it is not possible to eradicate it from a cattle population. F
Only inactivated vaccines are available against Bovine herpesvirus l. F
Seropositive cattle cannot be carriers of the Infections Rhinotracheitis virus. F
Infectious Bovine Rhinotracheitis virus (IBRV) can be transmitted through vectors. F
The IBR virus causes nephritis in calves usually in the age between one and six months. F
Infectious Bovine Rhinotracheitis (IBR) cause serous nasal discharge. F
Infectious Bovine Rhinotracheitis in cattle 6 months of age can cause encephalitis. F
Infectious Bovine Rhinotracheitis is rapidly spread within the herd. F
Infectious Bovine Rhinotracheitis is no longer present in Hungary. F
The respiratory form of Infectious Bovine Rhinotracheitis is often followed by genital symptoms. F
We can see characteristic clinical signs of Infectious Bovine Rhinotracheitis in day-old calves.F
Infectious Bovine Rhinotracheitis virus mainly cause encephalitis in cattle older than 6 months. F
Infectious Bovine Rhinotracheitis is rare, BHV-1 only affects cattle. F
In the transmission IBRV, the most important route is the germinative route. F
Genital form of IBR is often followed by abortion. F
Bovine Herpes virus 2 frequently causes abortion F
Bovine herpes mamillitis virus can cause mastitis in cows F
The bovine herpes mamillitis virus causes lesions on the skin of the milkers, therefore it is a zoonotic agent. F
Bovine herpesvirus 2 is the most frequent primary cause of mastitis in cattle F
Bovine Herpes Mammillitis virus causes milkers’ nodules in humans. F
Inclusion body rhinitis is predisposing to fatal respiratory disease in pigs F
Malignant catarrhal fever is mostly fatal in sheep. F
Malignant catarrhal fever is an alphaherpesvirus causing latent infection in ganglia. F
Malignant catarrhal fever develops only in suckling calves up to two weeks of age. F
Malignant catarrhal fever can be seen only in calves younger than one month. F
Malignant catarrhal fever causes only mild respiratory disease in sheep F
Sheep should be immunised against malignant catarrhal fever virus F
Malignant catarrhal fever is frequently seen in cats F
Cattle should be vaccinated against malignant catarrhal fever F
Goats are the reservoir hosts of the malignant catarrhal fever virus F
The incubation period of malignant catarrhal fever is less than one week F
Malignant catarrhal fever is quickly spreading from cattle to cattle. F
Cattle should be vaccinated against malignant catarrhal fever in every six months. F
The malignant catarrhal fever is caused by Bovine Herpes virus-2 F
Rodents are the reservoir hosts of the Malignant Catarrhal Fever virus. F
Swine are the reservoir host of the Malignant Catarrhal Fever virus. F
The Malignant Catarrhal Fever is caused by Bovine herpesvirus-2. F
We vaccinate calves 2 times against Malignant Catarrhal Fever.F
Malignant Catarrhal Fever does not occur in Europe. F
Malignant Catarrhal Fever spreads slowly within a cattle herd. F
Malignant Catarrhal Fever does not occur in Hungary. F
The Aujeszy’s disease virus is stenoxen. F
Wild boars are not susceptible to Aujeszy’s disease virus. F
Dogs should be vaccinated against Aujeszys disease F
Carnivores are the reservoir hosts of the Aujeszky’s disease virus F
The Aujeszys disease in cats is usually a mild respiratory disease with quick recovery F
The natural reservoir hosts of the Aujeszys disease virus are rodents F
The Aujeszy disease causes fatal pneumonia in Ruminants and Carnivores F
The Aujeszy disease is zoonosis F
The Aujeszy disease virus is stenoxen F
Rats are the reservoir hosts of the Aujeszky’s disease. F
Rodents are are the natural reservoir hosts of the Aujeszky’s disease F
The Suid herpesvirus 1 frequently causes encephalitis in humans. F
In adult swine the most frequent manifestation of Aujeszky’s disease is encephalitis F
Cattle should be vaccinated against Malignant Catarrhal Fever. F
Aujeszky disease causes pneumonia in susceptible piglets. F
Aujeszky disease doesn’t cause clinical signs in susceptible piglets. F
Aujeszky disease causes pruritus in susceptible piglets. F
Aujeszky disease causes 20-30% mortality in susceptible piglets. F
Older pigs are more frequently affected by Aujeszky ́s. F
Equine rhinopneumonitis virus is transmitted by arthropods. F
For immunisation against equine rhinopneumonitis virus mostly marker vaccines are used. F
Equine rhinopneumonitis virus causes cytoplasmic inclusion bodies in the foetal hepatocytes. F
Equid herpesvirus 4 more frequently causes encephalitis than Equid herpesvirus 1 F
Equine rhinopneumonitis virus can cause purulent metritis F
Only equine herpesvirus 4 can cause abortion F
Pregnant mares abort usually in the acute phase of equine rhinopneumonitis F
After EHV1 infection pregnant mares abort in the acute febrile stage F
Immunisation against equine rhinopneumonitis virus provides life long protection F
Equine rhinopneumonitis virus is present only in North America F
Vaccinated horses cannot get infected with Equid herpesvirus 1 F
Equid herpesvirus 1 associated abortions are always sporadic F
Only pregnant mares should be immunized against Equid herpesvirus-1 infection. F
A single vaccination against Equid herpesvirus-1 provides life-long protection. F
Equine rhinopneumonitis virus can cause only respiratory problems. F
For immunisation against Equine rhinopneumonitis virus mostly marker vaccines are used. F
A single vaccination of a horse against EHV-1 induces protection for several years. F 27) Equine herpesvirus-4 primarily causes abortion in horses F
Vaccination containing Equine herpesvirus-1 also provides protection against EHV-4. F
Equine herpesvirus-1 primarily causes respiratory symptoms in horses. F
One vaccination is enough to prevent Equine herpesvirus-1. F
Horses should be vaccinated against Equine herpesvirus-1 every six months. F
Equid herpesvirus 5 causes encephalitis in foals F
Equine herpesvirus-2 and 5 causes pustular vulvovaginitis F
Equid herpesvirus-2 may cause Coital Exanthemas in horse. F
Equid herpesvirus-2 and 5 cause diarrhoea and hepatitis in foals. F
It is enough to vaccinate mares 2 times against Equine herpesvirus-2. F
Abortion is frequent complication of coital exanthema in mares F
Coital exanthema virus frequently causes abortion. F
Equine Coital Exanthema can cause abortion storms in studs. F
Equine herpesvirus-3 cause abortion storms. F
Feline herpesvirus infects dogs as well. F
Canine herpesvirus infection can cause blue eye disease. F
Herpesvirus infection of dogs is most severe in 3-6 months old puppies. F
Felid herpesvirus does not cause viraemia and abortion. F
Abortion is uncommon in feline rhinotracheitis of pregnant animals. F
Abortion is rare in rhinotracheitis infected pregnant cats. F
Feline herpesvirus does not cause respiratory signs, only viraemia and abortion F
Felid herpesvirus 1 spreads slowly in cat populations F
Ulcerations of the oral mucosa are frequent signs of Feline Rhinotracheitis. F
Feline Infectious Rhinotracheitis occurs in summer because Felid herpesvirus-1 is transmitted by mosquitoes. F
Feline herpesvirus-1 is mainly transmitted by mosquitoes. F
Felid herpesvirus-1 is moderately contagious: spreads slowly in cat populations.F
Feline Infectious Rhinotracheitis virus is transmitted mainly through the air. F
The infectious laryngotracheitis is seen only in young chickens. F
Diarrhoea is frequent in infectious laryngotracheitis of chickens. F
Encephalitis is a frequent complication in Infectious Laryngotracheitis of chickens F
Ducks are the most susceptible to infectious laryngotracheitis virus F
Chickens above 6 weeks of age are not susceptible to infectious laryngotracheitis F
The infectious laryngotracheitis can cause viraemia and pneumonia in young.. F
Infectious laryngotracheitis virus is typically transmitted by the germinative route F
Infectious laryngotracheitis is most frequently seen in day-old chickens F
Infectious laryngotracheitis virus is shed mainly with faeces F
Infectious Laryngotracheitis virus replicates in the liver of cats. F
Germinative route is the most important factor in the transmission of the Infectious Laryngotracheitis virus. F
Infectious Laryngotracheitis is most frequently seen in day-old turkey. F
Infectious Laryngotracheitis usually occurs clinically under 6 weeks of age. F
Infectious Laryngotracheitis virus invades the kidneys after viraemia. F
Infectious Laryngotracheitis of poultry spreads germinatively. F
Infectious Laryngotracheitis causes eggshell deformation. F
Infectious Laryngotracheitis frequently damages the oviduct of hen. F
The vaccines of Marek’s disease are not efficient. F
Lymphoproliferative form of Marek’s disease can be present in hens (older age). F
Lymphoproliferative form of Mareks disease is a chronic disease F
The duck herpesvirus causes cross immunity against Marek disease F
The free virions spread to organs independent of cells in the case of Marek disease F
Transient paralysis form of Mareks disease can be present in hens F
Neurological form of Mareks disease can be present in 4 week old chicken. F
There is in ovo vaccine against Mareks disease F
Intake of GaHV2 happens most frequently per os. F
Germinative infection does occur in Mareks disease F
In case of viraemia the GaHV2 spreads to fowl’s organs in red blood cells F
Marek disease is usually seen in chickens below 2 weeks of age. F
Marek disease virus is shed with faeces in high titres F
Marek disease is caused by turkey herpesvirus F
Transient paralysis by Marek’s disease usually ends in full recovery F
The chronic form of Marek disease is due to circuses of higher virulence F
Transient paralysis by Marek disease usually ends in full recovery. F
Marek’s disease is most frequently seen in geese and ducks. F
Humoral immunity plays the central role in the host’s defence against the Marek’s disease virus. F
The neurological form of the Marek’s disease is seen only in day-old chicks. F
Conjunctivitis is a frequent sign of acute Marek’s disease. F
Marek ́s disease virus can ́t be prevented by vaccination, because it ́s immunosuppressive. F
The neurological form of Marek ́s disease has a mass appearance. F
The incubation time of acute Marek ́s disease is 1-2 days. F
The neurological form of Marek ́s disease leads to significant liver degeneration. F
Both serotypes of the Marek ́s virus cause disease in geese. F
North America is free of Marek ́s disease. F
Marek’s disease virus is shed mainly via the faeces. F
Marek ́s disease in the blood multiplies in the endothelial cells. F
Marek ́ s disease is a beta herpes virus. F
Marek’s disease primarily targets day old chickens. F
The neoplastic form of Marek’s is caused by low virulence strains. F
Prevention against Marek ́s: no measures needed as the disease remains mostly symptomless. F
No vaccination is needed against Marek’s disease. F
Marek’s disease viruses are uniform in their virulence. F
Only sporadic clinical cases of duck viral enteritis are seen in an affected flock F
Duck plaque (viral enteritis) can’t cause high mortality without secondary bacterial infection F
Duck viral enteritis is seldom fatal F
Treatment is the most effective control method for duck viral enteritis. F
Duck plague is more sever in wild birds than in domestic ducks. F
Duck plague only affects young ducklings F
Duck plague is only seen in day old ducklings F
Duck viral enteritis is usually mild, osmotic diarrhoea. F
Duck plague infects exclusively domestic and wild ducks. F
Antibiotic treatment is the most effective control method for Duck Viral Enteritis. F
Duck plague infects exclusively domestic and wild ducks. F
Beak deformity is a typical sign of Duck Plague. F
Muscovy duck are resistant to the Duck Viral Enteritis. F
Duck Plague/Duck viral Enteritis cause high mortality in all ages. F
Duck Plague/Duck viral Enteritis clinical signs in young ducks are only seen in birds up to 4 weeks of age. F
Duck Plague/Duck viral Enteritis vaccination is not needed as clinical signs are mild. F
Duck Plague only causes hepatitis in young ducks. F
Duck Plague only causes disease in ducks and geese. F
Duck Plague virus causes high mortality in both old and young birds. F
Duck Plague is a disease of young ducks only. F
In most cases the Duck Plague disease remain symptomless. F
Duck Plague is more severe in wild birds than domestic ducks. F
Pigeon herpesvirus mainly causes encephalitis in adult pigeons. F
Pigeon herpesvirus infections usually result a haemorrhagic deadly disease. F
Pigeon herpesvirus kills mostly day old pigeons F
Pigeon herpesvirus infection causes feather development problems F
Pigeon herpesvirus mainly causes encephalitis in adult pigeons F
Pigeon herpesvirus has the highest mortality in day-old pigeons. F
The eradication of monkeypox was successful F
Poxviruses cause inclusion body in the nucleus F
Pox viruses cause lesions in 4 stradia at the site of primer replication F
Parapox viruses cause long lasting immunity F
Poxvirus never cause viraemia and generalized infection. F
Poxvirus are a strong antigens, except for Orthopoxvirus F
Parapoxviruses are strong antigens. F
Avipox viruses can cause fever and rash in children (chickenpox). F
Cowpox causes a pockmark after Infection F
Cowpox virus frequently causes abortions and encephalitis of calves. F
Cowpox virus frequently cause transplacental infection and immunotolerance. F
The Cowpox virus infection is prevented by regular vaccination in endemic countries. F
In cattle the Cowpox infection is mostly fatal F
Recovering from Cowpox leaves lifelong immunity. F
Pseudocowpox virus is closely related to smallpox virus. F
Pseudocowpox virus can infect cats F
Pseudocowpox spreads slowly on a farm F
Pseudocowpox virus usually causes nodules on face of infected cats F
Pseudocowpox causes a pockmark after infection F
Pseudocowpox virus usually causes itchy red nodules on the face of infected person F
Pseudocowpox does not cause a milkers nodule F
Pseudocowpox infections result a long lasting immunity F
Pseudo-cowpox can cause Pseudo-lumpy skin disease in cats. F
Recovering from Pseudo-cowpox leaves/results in lifelong immunity. F
Pseudo-cowpox virus only infects cloven-hoofed animals. F
Bovine papular stomatitis virus can frequently cause coinfection with herpes mamillitis virus F
Vaccination against bovine popular stomatitis provides life-long immunity F
Bovine Papular Stomatitis virus causes vesicles in the oral cavity and hoofs of cattle. F
Calves should be vaccinated against Bovine Papular Stomatitis. F
The mortality of lumpy skin disease is high (above 80%). F
In lumpy skin disease the fertility is good. F
In lumpy skin disease the direct contact is very important. F
The mortality of lumpy skin disease is less than 30% F
The milk production is increased in lumpy skin disease F
The lumpy skin disease is only present in Africa F
Lumpy skin disease causes high mortality in cattle F
Lumpy skin disease is present only in Asia F
Lumpy Skin Disease results high mortality. F
Lumpy Skin Disease is caused by Parapoxviruses. F
Generalization is frequent in lumpy skin disease virus infections. F
The contagious pustular dermatitis can cause pneumonia. F
The contagious pustular dermatitis virus is related to goatpox virus F
Contagious pustular dermatitis virus can infect cows F
The orf virus is same as pseudocowpox F
Contagious pustular dermatitis (orf) virus causes skin lesions in pigs F
Contagious pustular dermatitis is often deadly at any age F
Vaccination against contagious pustular dermatitis virus provides lifelong protection. F
Contagious Pustular Dermatitis can only be seen on the teats of ewes. F
Inactivated vaccines are used against Contagious Pustular Dermatitis. F
Orf is a rare disease of sheep flocks and cattle herds. F
Sheep pox virus is a zoonotic agent. F
A clinical sign of sheeppox can be horseshoe shaped pockmarks on the wool covered body F
Vaccines against sheep poxvirus are widely used in Europe. F
The sheep and goatpox occurs worldwide. F
Sheep and goat poxviruses are mainly taken through the oral route F
The sheep and goat poxvirus is mainly spread by mosquitos F
Clinical signs of sheep and goatpox are seen only at site of the primer replication F
Goat pox virus is a zoonotic agent F
Sheep pox virus can cause skin lesions in humans F
Arthropods play an important role in the transmission of sheeppox virus F
Sheep and goat pox are endemic in Europe. F
Sheep – and goat pox are enzootic in Europe. F
Sheep – and goat pox virus is transmitted only vertically. F
Swinepox virus can infect cattle. F
The swinepox is always generalised F
Swinepox virus is a zoonotic agent F
Swine Pox is frequently generalized in adult pigs. F
Swine pox virus frequently causes interstitial pneumonia. F
Swine pox virus can cause respiratory signs and abortion. F
Swine pox is frequently generalized in adult pigs. F
The swinepox virus causes high economic losses. F
Myxomatosis is a zoonotic disease. F
Myxomatosis causes frequently serious clinical signs and high losses in Lepus europeus. F
A clinical sign of myxomatosis is the swollen belly F
Myxomatosis is not present in America F
Mosquito net can always prevent the myxomatosis F
Late summer is the best period to vaccinate rabbits against myxomatosis F
The attenuated myxomatosis virus has replaced the virulent virus in France F
Myxomatosis causes serious clinical signs in cotton tailed Rabbits F
Myxomatosis is only found in Australia F
There are no vaccines available against Myxomatosis. F
Virulent strains of the myxoma virus are only present in Australia. F
Myxomatosis virus causes high morbidity and mortality in hares. F
Tumour formation in the parenchymal organs is typical of Myxomatosis. F
Myxomatosis virus spread out to the world from China. F
Only domestic rabbits are susceptible to Myxomatosis. F
Avian poxviruses always cause cross immunity. F
Fowlpox is a zoonotic disease. F
The serious form of the fowlpox is the cutaneous form F
Fowlpox virus cause long lasting immunity F
Fowlpox virus can infection only chicken F
The diphtheritic form of fowlpox is usually less severe than the cutaneous F
Heterologous viruses of avian pox frequently cause generalization F
Fowl pox viruses cause generalized diseases in seals. F
The mucosal form of Fowl pox is benign. F
Only inactivated vaccines can be used for prevention against fowl pox. F
Fowlpox is eradicated from most of the European countries. F
Attenuated vaccines are forbidden to be used against Fowlpox. F
Avian pox viruses are species specific. F
ASF virus is shed in the urine of the infected animals F
The leading clinical sign in African swine fever is excess salivation F
The African swine fever virus genome codes only 2 proteins F
The African swine fever virus infects the swine by air F
In African swine fever cases of abortion are never observed F
The primary replication site of African swine fever virus is the oronasal mucosa. F
Vaccines are available in EU to be used in the control of African swine fever F
Vaccines are available to be used in the control of ASF F
In Europe the main route of infection is the transmission of the African swine fever by ticks F
ASF is always a peracute disease F
The African swine fever virus replicated in lymphocytes F
Wild boars may be chronically infected with African swine fever virus F
The resistance of the African swine fever virus is very low F
African swine fever is generally transmitted by mosquitoes F
African swine fever can cause disease in humans F
African swine fever virus can be inactivated by irradiation T
African Swine Fever virus infects every cloven hoofed animal F
African Swine Fever does not occur in Europe.F
Only activated vaccines are used for the prevention of African Swine Fever. F
In ASF cases abortion is never observed F
Attenuated vaccines are used for the prevention of African swine fever. F
African Swine Fever virus has a low resistance. F
The clinical signs of African Swine Fever are more severe in wild boars than in farmed pigs. F
There is a widespread vaccination in endemic areas to prevent African Swine Fever. F
In Europe the ticks are the most important means in the transmission of the ASF virus. F
The moderately virulent ASF virus does not cause fever. F
In case of infection by highly virulent ASF virus we can see skin necrosis as clinical sign. F
The main tool against African Swine Fever is vaccination. F
Vaccination is used for prevention of African Swine Fever. F
African Swine Fever is endemic in Central Europe. F
African Swine Fever virus infects pigs and ruminants. F
African Swine Fever is caused by any arbovirus. F
Virus neutralization is the most important tool for African Swine Fever diagnosis. F
African Swine Fever infection of humans leads to cold like symptoms. F
The ASF virus can be detected by hemagglutination test F
The boutons in the intestines are characteristic pathological findings in case of ASF. F
Picornaviridae are enveloped viruses F
The resistance of Picornaviridae is low, they cannot survive in the environment F
Just State Vet medical steps and general preventative measures are used for prevention for Picornavirus. F
Cardioviruses have a narrow host range F
Picornavirus is characterized by encephalitis and severe diarrhoea. F
There is widespread vaccination to control teschovirus encephalomyelitis F
Teschovirus encephalomyelitis virus is transmitted by arthropods F
There is widespread vaccination using inactivated vaccines to prevent teschovirus encephalomyelitis. F
Porcine teschovirus encephalomyelitis virus is maintained by rodents.F
Porcine teschovirus encephalomyelitis virus can infect pigs and cattle.F
Porcine teschovirus encephalomyelitis virus cannot survive in the environment. F
Dogs and cats can be infected with Teschen disease virus. F
The main clinical sign of Teschen disease in sheep is pneumonia F
Teschen disease occurs in cattle, sheep and pigs F
Enteritis and pneumonia are frequent postmortem lesions of Teschen disease F
Enlargement of the spleen and haemorrhages are typical postmortem lesions of Teschen
disease F
Haemorrhages are typical postmortem lesions of Teschen disease F
Teschen disease is frequent all over the world F
Diarrhoea is a typical clinical sign of Teschen disease. F
Dogs and cats can be infected with Teschen disease virus. F
Teschen disease is endemic in Brazil. F
Teschen is caused by Enterovirus. F
Teschen disease causes diarrhoea in piglets. F
Inactivated vaccines are widely used in Europe to prevent Talfan disease F
There is widespread vaccination in Europe for prevention of Talfan disease F
The clinical signs of Talfan disease are more severe than that of Teschen disease F
Talfan disease occurs in any age groups F
Haemorrhages are typical postmortem lesions of Talfan disease F
Pigs and ruminants are susceptible to the agent of Talfan disease. F
The agent of Talfan disease is shed lifelong after the infections. F
Talfan infects piglets older than 4 months. F
Vesicles can be seen in the liver in the case of swine vesicular disease F
Swine vesicular disease virus cannot cause viraemia F
The resistance of swine vesicular disease virus is very low; it cannot survive in the environment F
Haemorrhages in the serous membranes can be frequently seen postmotem in the case of swine vesicular disease F
Haemorrhages can be seen post mortem in the case of swine vesicular disease F
The mortality of swine vesicular disease is 40-50% F
The mortality of swine vesicular disease is very high, it can be 50-60% F
Swine vesicular disease is frequently seen in Europe F
Only pigs are susceptible to swine vesicular disease virus. F
Swine vesicular disease is frequent among pigs F
Swine vesicular disease occurs only in Africa, it never occurred in Europe F
Swine vesicular disease virus can infect only pigs F
Swine Vesicular Disease virus can infect swine and ruminants. F
Swine Vesicular Disease virus does not cause viraemia, only local lesions can be seen. F
Swine vesicular disease virus cannot survive in the environment. F
Swine Vesicular Disease cause skin lesions in bovids. F
Swine Vesicular Disease is present only in Italy. F
Swine Vesicular Disease is present only in Hong Kong. F
Swine Vesicular Disease has been present in all European countries, but now only present in South-East Asia. F
Swine Vesicular Disease causes skin lesions in cattle. F
Swine Vesicular Disease is frequent among pigs. F
Haemorrhages in the parenchymal organs are frequent postmortem lesions of avian encephalomyelitis F
Haemorrhages are frequent postmortem lesions of avian encephalomyelitis. F
There is no germinative infection in the case of avian encephalomyelitis F
Avian encephalomyelitis is not transmitted germinatively. F
Avian Encephalomyelitis is not transmitted through the egg. F
Avian encephalomyelitis is caused by a double stranded DNA virus. F
Avian encephalomyelitis is caused by enterovirus. T
Avian encephalomyelitis is caused by a hepatovirus. F
Avian encephalomyelitis is not transmitted germinatively. F
Avian encephalomyelitis virus kills the embryo.F
Avian encephalomyelitis is present only in chickens. F
Avian encephalomyelitis virus is killed at hatching temperature. F
Infection via eggs does not occur in Avian encephalomyelitis.F
Avian encephalomyelitis is not transmitted through the egg. F
Germinative infection can happen in the case of duck hepatitis F
Duck hepatitis cannot be prevented with vaccination F
Duck hepatitis A virus does not cause viraemia. F
Duck hepatitis A virus can cause germinative infection. F
Clinical signs of duck hepatitis can be seen mainly in laying ducks. F
Germinative infection is the primary way of infection with Duck hepatitis A Virus. F
There are no vaccines for the prevention of Duck hepatitis. F
Clinical signs of duck hepatitis can be seen in all age groups. F
Duck Viral Hepatitis is present in Hungary on a large scale. F
Duck Viral Hepatitis is caused by type 1 and 2 coronavirus. F
Duck Viral Hepatitis causes haemorrhagic enteritis in older ducks.F
Encephalomyocarditis infections are rare. F
Encephalomyocarditis virus can infect only pigs. F
Encephalomyocarditis virus has a narrow host range.F
FMD is a chronic disease F
FMD spreads slowly within the herd F
Foot and mouth disease is serologically uniform F
Foot and mouth disease virus is uniform, there are no serotype or subtypes of it F
FMD ulcers are usually sharp edged and regular round shaped F
The primary replication site for FMD is the tongue mucosa F
The peracut form of FMD causes severe haemorrhages and death by shock F
The chronic form of FMD means arthritis F
FMD is transmitted by insect vectors F
The SAT-1,2 and 3 serotypes of FMD virus are present in Africa and Arabia. F
The main host (reservoir) of foot and mouth disease virus is swine F
There are no neutralizing antibodies produced against foot and mouth disease virus F
For laboratory tests FMD samples should be submitted frozen F
The resistance of foot and mouth disease virus is low F
In Europe supportive therapy is applied in the treatment of FMD F
Frothy and sticky nasal discharge is the characteristic sign of FMD F
All serotypes of foot and mouth disease can be detected worldwide F
The FMD virus is enveloped T
FMD virus cannot be propagated in cell culture F
FMD virus cannot be isolated in cell culture F
The FMD mortality is nearly 100% F
The mortality of foot and mouth disease is very high in all age groups F
The FMD suspected sample should be sent to lab by post (in mail) F
The primary replication sites of foot and mouth disease are the lymph nodes F
The primary replication sites of foot and mouth disease is the bone marrow F
Horses are susceptible to foot and mouth disease F
Cattle shed foot and mouth disease virus for a shorter time comparing to swine F
The foot and mouth disease virus is very sensitive to the environmental conditions F
Foot and mouth disease is transmitted by insect vectors F
We can observe the most severe foot and mouth disease signs on sheep F
In the control of foot and mouth disease vaccines are used in Europe F
Vaccination using attenuated vaccines is the main way of control of foot and mouth in Europe F
Foot and mouth disease virus can only infect animals F
Water buffalos are not susceptible for FMD. F
Serological examinations are important in diagnosis of FMD. F
The resistance of FMD virus is rather low, in the environment it is inactivated within days. F
Resistance of FMD virus is low, in the environment, they are inactivated within days. F
FMD virus is genetically and serologically uniform.F
Vaccination against FMD can prevent the infection. F
Genotype C of FMD virus is the most frequently detected worldwide. F
Shedding of FMD virus starts 3 days after the infection. F
Europe is endemically infected with Foot and Mouth disease. F
Pigs are not susceptible to Foot and Mouth disease. F
Vaccination is currently used against Foot and Mouth disease in Europe.F
Foot and Mouth disease virus can only infect ruminants. F
Foot and Mouth disease is caused by enteroviruses.F
Foot and Mouth disease is not present in South America. F
Foot and mouth disease are endemic in Europe. F.
Foot and mouth disease is clinically more severe in pigs than in cattle. F
Foot and mouth disease is caused by F2 viruses.F
In the Asian serotype of FMD there are 3 subtypes, Asia 1, 2 and 3. F
FMD causes most severe symptoms in pigs. F
In sheep, clinical signs are usually more severe than in cattle. F
Only the live attenuated strains can provide good immunity. F
Vaccination of cattle herds is permitted everywhere. F
The replication time of FMD virus is over one day F
VES is more contagious than FMD F
Vaccines are ideally used for the prevention against swine vesicular exanthema F
Swine vesicular exanthema virus is present worldwide F
The Vesicular Exanthema of swine virus infects only pigs. F
VES causes the highest mortality in pregnant sows F
VES can be easily differentiated from FMD by the character of the vesicles. F
We can differentiate VES from FMD by the lack of lameness. F
Rodents are the reservoir hosts of Vesicular Exanthema of Swine virus. F
Midges are the main vectors of the Vesicular exanthema of swine virus. F
Cat queens frequently abort in the acute phase of Feline Calici virus infection. F
Feline caliciviruses cause haemorrhagic enteritis F
Virulent systemic feline calicivirus causes more severe symptom in kittens. T
RHD induces clinical signs mostly in animals younger than 2 months F
RHD virus can be propagated in cell culture F
Vaccines against RHDV-1 induce protection against RHDV-2 too F
Encephalitis is a frequent sign of the rabbit haemorrhagic disease F
Rabbit haemorrhagic disease virus is transmitted by mosquitoes F
Australia is free of rabbit haemorrhagic disease F
Rabbit haemorrhagic disease virus usually causes death in 1-3 weeks old rabbits F
There are no vaccines available against rabbit haemorrhagic disease F
The incubation time of rabbit haemorrhagic disease is usually over 3 weeks F
The Rabbit Haemorrhagic Disease is present only in Australia. F
Rabbit Haemorrhagic Disease virus usually causes death in 1-3 weeks old rabbits. F
There are no vaccines available against Rabbit Haemorrhagic Disease. F
The Rabbit Haemorrhagic Disease is a chronic illness with low morbidity. F
The avian hepatitis E is a zoonotic disease F
Hepatitis E virus causes characteristic clinical symptoms in swine. F
Broilers are regularly vaccinated against avian nephritis virus F
Avian nephritis is more frequent in waterfowl than in chicken F
Avian nephritis virus caused by a picornavirus F
Avian nephritis virus is transmitted by rodents F
Avian nephritis virus caused by a picornavirus. F
Attenuated vaccines are used for the prevention of chicken from avian nephritis virus. F
Togaviruses are strongly resistant to the environmental conditions F
Togaviruses cause airborne infection F
Togaviruses cause encephalomyelitis in horses in East-Asia and in Australia only F
No vaccines are available against togaviruses F
Horse encephalomyelitis viruses are transmitted by ticks F
Abortion is the main clinical sign of togavirus infection results in abortion of horses F
The leading clinical sign of togavirus infection is the frothy nasal discharge F
Togavirus infection in horses results in hepatitis F
Rodents serve as reservoirs for Venezuelan horse encephalomyelitis virus F
Horses encephalomyelitis vaccines defend against African horse sickness (cross protection) F
Horse encephalomyelitis viruses are transmitted by ticks F
Birds serve as reservoirs for Venezuelan horse encephalomyelitis virus. F
Western equine encephalitis causes the highest mortality. F
Equine encephalitis can be diagnosed easily by gross pathology. F
Recovery from equine horse encephalitis induces immunity that lasts only 1 year F
Equine encephalitis vaccines are available only for humans F
Eastern equine encephalomyelitis virus infects only horses F
Ticks are involved in the transmission cycle of EEE. F
Viral equine encephalomyelitis is usually diagnosed on the basis of clinical signs F
The Eastern Equine Encephalitis is present in Japan and Korea. F
Togaviruses caused encephalomyelitis of horses occurs frequently worldwide. F
Humans are not susceptible to horse encephalomyelitis togaviruses. F
Vaccines cannot be used to prevent Togaviruses caused encephalomyelitis of horse. F
Mainly ticks are the vectors of Equine encephalomyelitis viruses. F
Equine encephalomyelitis viruses cause disease in horse populations worldwide. F
Togavirus infections can unambiguously be diagnosed based on clinical signs and pathology.
F
In Europe vaccination of horses against equine encephalomyelitis is compulsory. F
Togavirus infection results in abortion of horses F
Flavivirus from distinct serotypes without serological cross-reactions F
Pestiviruses are zoonotic F
Pestiviruses are arboviruses F
Flaviviruses are resistant to lipid solvents. F
Louping ill is seen in cattle in North America F
The louping ill was introduced to Australia to control rabbit population F
The louping ill is seen in cattle in Great Britain and Scandinavia F
The principle vector of the Louping ill virus is Rhipicephalus appendiculatus F
Louping ill is present only in tropical and subtropical countries. F
Abortion and foetal malformations are the most typical signs of louping ill in sheep F
The Louping Ill is seen in rabbits in Australia. F
Louping ill is usually seen in rabbits. F
Louping-Ill is a disease of swine.F
Louping ill occurs in the Far-East. F
Louping ill is transmitted by mosquitoes and midges F
The main vectors of tick borne encephalitis virus are sylvatic mammalian species F
The Tick-borne encephalitis is widespread in North America F
The main vectors of the tick-borne encephalitis virus are sylvatic mammalian species F
The main vectors of the tick-borne encephalitis virus are Hyalomma and Dermocentor species F
The tick-borne encephalitis virus is resistant to detergents F
Mainly birds develop tick-borne encephalitis F
Tick-borne encephalitis viruses are present only in tropical regions. F
The tick-borne encephalitis is widespread in North America. F
Ruminants are long term carries of tick-borne encephalomyelitis virus. F
Tick-borne encephalomyelitis most frequently is seen clinically in ruminants. F
The West Nile Fever can be diagnosed unambiguously by the clinical signs F
The West Nile Fever virus infects mostly swine and cattle F
WNV typically causes reproductive problems in cattle F
West Nile fever can be unambiguously diagnosed on the basis of clinical signs F
Fomites play the most significant role in the transmission of WNV F
West Nile Virus is only present in Africa F
WNV causes central nervous signs in 80-90% of the infections F
WNV cannot be isolated in cell cultures F
Horses are the reservoirs host of WNV F
The weather does not influence the occurrence of WNV outbreaks F
West-Nile fever practically is restricted to Africa. F
Humans are not susceptible to West Nile disease virus. F
The West Nile Virus is genetically uniform, but at least 15 serotypes are known. F
Fomites play the most significant role in the transmission of the West Nile Virus. F
West Nile Virus typically causes reproductive problems in cattle. F
The principal vectors of the West Nile Virus are midges.F
West Nile Virus mainly causes diarrhoea in sheep. F
West Nile Virus causes central nervous signs in 80-90% of the infections. F
West Nile Virus cannot be isolated in cell cultures. F
West Nile Virus is the only known zoonotic flavivirus. F
BVD virus is particularly resistant to disinfectants F
Rodents play a central role in the maintenance of BVD virus in the environment F
Non cytopathic strains of Bovine viral diarrhoea virus (BVDV) can cause hydrocephalus and cerebellar hypoplasia F
In utero infection with cytopathic BVDV strain results immunotolerant calves F
Swine are not susceptible to BVD F
Two serotypes of the BVD virus are known so far, serotype 2 is more virulent. F
Cytopathic strains of Bovine Viral diarrhoea (BVDV) alone can cause mucosal disease F
Non cytopathic strains of Bovine Viral Diarrhoea virus (BVDV) do not cause transplacental infection F
Intrauterine BVD virus infection always causes abortion F
BVD virus cannot be transmitted via artificial insemination F
BVD virus cannot be propagated in cell cultures F
Mucosal disease usually emerges in cattle farms as explosive outbreaks with high morbidity
F
The only efficient way of BVD eradication is the replacement of all animals on the farm F
Bovine neonatal pancytopenia (BNP) is an immunopathy observed in immunotolerant, BVDV infected calves F
Bovine neonatal pancytopenia (BNP) is caused by a bovine viral diarrhea F
Wild birds are the natural hosts of the BVDV. F
Only inactivated vaccines can be used for the prevention against BVD F
The BVD virus genotype 2 is less virulent than genotype 1.F
The BVD virus cannot be transmitted via artificial insemination. F
Only cattle is susceptible to BVD virus. F
BVD virus exists in several serotypes. F
BVDV cannot be propagated in cell cultures. F
Rodents play a central role in the maintenance of BVD virus in the environment. F
Bovine Viral Diarrhoea cannot be transmitted with AI. F
Mucosal Disease, only inactivated vaccines can be used for the prevention against BVD. F
Because Europe is free from BVD, it is forbidden to use vaccines against it. F
Because IBDV is an immunosuppressive virus, no vaccines available against it F
The Border disease virus causes pneumonia in sheep F
The border disease is present only in the United Kingdom F
The border disease virus frequently causes encephalitis in ewes F
Border disease in most frequently seen in horses F
The Border disease is a haemorrhagic, respiratory syndrome in sheep F
Border disease is a respiratory and enteric disease of lambs. F
The CSFV causes central nervous signs only in suckling piglets F
Classical swine fever infection in the second half of the pregnancy leads to foetal development problems F
Shedding of Classical swine fever virus starts 1 week after the infection F
In Europe it is obligatory to vaccinate against Classical swine fever F
All wild type strains of classical swine fever virus are highly virulent F
Six distinct serotypes of CSF virus are recognized so far F
CSF virus is an arbovirus F
CSF virus is a zoonotic agent F
Pigs shed CSF virus only during the clinical stage of the disease F
Based on pathology and clinical signs, chronic classical swine fever is easy to diagnose F
Fomites do not play a role in the transmission of the Classical Swine Fever Virus. F
Swine shed CSFV only in the terminal phase of the disease.F
Europe is free from CSFV . F
Classical Swine Fever is always an acute disease with high mortality in wild boars. F
The large intestine are the earliest lesions in Classical Swine Fever.F
The diagnosis of Classical Swine Fever is based on paired serum investigations. F
The clinical signs of African Swine Fever and Classical Swine Fever are very different. F
All known strains of the Classical Swine Fever virus are of highly virulence. F
Classical swine fever virus is shed with faces, when boutons appear in the intestines. F
Classical swine fever can be eradicated from wild boar populations by oral vaccination. F
Classical swine fever virus is rarely complicated by secondary infections. F
Classical swine fever can be diagnosed easily by the characteristic symptoms and lesions. F
Classical swine fever virus doesn’t induce neutralizing antibody production. F
Classical swine fever virus is inactivated in chilled meat at -20°C.F
.Only DIVA vaccines should be used to prevent classical swine fever in swine stocks. F
Classical swine fever virus causes lympho-histiocytic encephalitis in carnivores. F
Classical swine fever Virus spreads slowly in the host and causes mainly chronic disease. F
Complicated forms of the Classical swine fever are rarely seen. F
Classical swine fever can unambiguously diagnosed by the clinical signs and pathology. F
Piglets of sows vaccinated against CSF are vaccinated at 6-12 months. F
To prevent CSF, we vaccinate pigs older than 6 months of age with live vaccine. F
To prevent CSF we use inactivated vaccines made from the Chinese strain. F
Shedding may start 2-3 days after first clinical signs. F
CSF can be prevented by inactivated vaccines. F
CSF always causes abortion in pigs.F
Hungary does not have to make any preventative action against CSF. F
First symptom of CSF is drooping ears.F
Classical swine fever virus (CSFV) is mainly transmitted by mosquitoes. F
The presence of CSFV in a herd does not influence reproduction parameters. F
Central nervous signs are never seen in CSF. F
Serological cross reactions my occur between BVD virus and CSFV. F
It is a disease of domestic swine and wild boars, but several other species are also suceptible. F
For prevention state medical steps and vaccination are used in Europe. F
Boutons in the large intestine are the earliest lesions in CSF. F
In Europe vaccination of domestic pigs against Classical swine fever is common. F
In Europe vaccination of domestic swine populations against CSF is compulsory. F
Classical swine fever virus strains are classified into several serotypes F
Orbiviruses spread by droplet (aerosol) infection F
Orbiviruses are serologically uniform F
Reoviruses are sensitive to lipid solvents and detergents. F
Orthoreoviruses frequently cause tenosynovitis of horses F
Avian orthoreoviruses cause mainly nephritis and encephalitis F
Mammalian orthoreoviruses can cause pneumoenteritis only in suckling animals F
Orthoreovirus can cause tenosynovitis in pigs F
Avian orthoreoviruses usually cause disease in adult birds F
Yolk immunity does not influence the efficacy of vaccination against avian orthoreovirus F
Horses usually develop lethal hemorrhagic enteritis in Orthoreovirus infections. F
Orthoreoviruses can cause encephalitis in cattle.F
Avian orthoreoviruses infect only via inhalation and parenterally.F
Avian orthoreoviruses only infect via PO infections.F
Tenosynovitis is caused by only one Orthoreovirus. F
Rotaviruses are sensitive to environmental conditions F
Rotavirus infection is sporadic within the herd F
Rotavirus only infects mammals F
Clinical signs of rotavirus infection are usually seen in animals older than 2 weeks of age F
Swine is not susceptible to rotavirus infection F
Rotavirus infection results in high mortality F
Avian rotaviruses are transmitted by germinative infection F
Clinical signs of rotavirus infection are usually seen in animals older than 2 weeks of age F
Rotaviruses damage the mucosa of the large intestines F
Rotaviruses are serologically uniform F
Avian rotaviruses can cause tenosynovitis. F
Rotaviruses can cause chronic enteritis and persistent infection. F
Rotaviruses cause mainly respiratory signs in cattle. F
Rotaviruses mainly cause respiratory disease in older animals. F
Rotaviruses typically cause respiratory disease in 3-6 month old calves. F
Rotavirus is species specific. F
Rotaviruses frequently cause tenosynovitis in birds.F
Bluetongue is present only in tropical areas F
Rodents serve as reservoirs of bluetongue F
Ibaraki disease virus can be used to immunize cattle against bluetongue F
Wild birds play the most important role in the distribution of bluetongue F
Bluetongue occurs only in Africa and Australia F
Bluetongue is transmitted by ticks F
Bluetongue virus is typically vectored by ticks F
Goats are not susceptible to bluetongue virus F
Bluetongue disease occurs only in Africa F
Bluetongue virus infects also horses and dogs F
Sheep are less sensitive to Bluetongue than swine. F
Bluetongue causes transient infection in cattle. F
Bluetongue is named after the pseudo-melanosis of the tongue. F
Bluetongue infects also horses and dogs. F
Ibaraki disease virus immunizes against bluetongue. F
Bluetongue disease is present only in tropical and sub-tropical countries. F
Wild birds are the natural reservoir host of the Bluetongue virus. F
The most severe clinical manifestation of Bluetongue disease is usually seen in goats. F
Bluetongue has 24 known serotypes. F
Bluetongue is an enteral disease of turkeys. F
Bluetongue causes symptoms mostly in sheep and goat. F
Bluetongue is not present in Europe. F
Bluetongue also infects pigs.F
No long-term carrier stage is observed in Bluetongue virus infections. F
Ruminants and swine are the most important hosts of the Bluetongue virus. F
Serological cross protection exists between 25 known serotypes of Bluetongue virus. F
The serotype 8 strain of the bluetongue virus, which emerged in Western Europe, does not cause clinical signs in cattle. F
Epizootic haemorrhagic disease was described only in Australia so far F
African horse sickness is mostly a peracute disease F
African horse sickness virus is endemic in Russia since 2008 F
African horse sickness is spread by ticks F
African horse sickness is zoonotic F
Encephalitis is the most frequent sign of African horse sickness F
Acute form of African horse sickness occurs mainly in zebras and horses F
Zebras are not susceptible to African horse sickness F
Wild birds play the most important role in the spreading of African horse sickness F
In the pathogenesis of African horse sickness, viraemia lasts longer in horse than in zebras. F
The African horse sickness is endemic in Europe and in the USA.F
African horse sickness was transported to Europe by migratory birds. F
African horse sickness can cause encephalitis. F
African Horse Sickness is a frequent disease, distributed worldwide. F
The differential diagnosis of African Horse Sickness and Tetanus is rather complicated. F
African Horse Sickness is spread primarily by “small mosquitos”. F
African Horse Sickness is caused by an arbovirus. F
Reservoir for African Horse Sickness is zebras and donkeys. F
African Horse Sickness is presented mainly per-acutely in donkeys.F
African Horse Sickness virus only infect horses. F
Haemorrhagic meningoencephalitis is the most frequent sign of the African Horse Sickness. F
African horse sickness is a world-wide distributed and frequent disease. F
Equine encephalosis causes the most severe clinical signs in Zebras F
Horse encephalosis occurs only in America F
Equine encephalosis causes high mortality F
Attenuated and inactivated vaccines are available against equine encephalosis. F
Horse encephalosis appeared several times in Europe between 2006 and 2009 F
Meat type hybrids are more sensitive to Gumboro disease than layers F
Clinical signs of Gumboro disease can be seen in chickens older than 8 weeks F
Clinical signs of Gumboro disease can be seen in chickens younger than 8 weeks F
Clinical signs of Gumboro disease can be seen in chickens younger than 8 days F
Bursitis virus causes the highest mortality in day old chicks F
The bursitis virus is very sensitive to the environmental conditions F
Bursitis virus causes disease only in chicken F
Both serotypes of bursitis virus are pathogenic F
In Europe only low virulence strains of infectious bursitis virus can be found F
Pigeons are the most susceptible to IBDV F
Both serotypes of bursitis virus are pathogenic F
The bursitis virus mostly causes germinative infection F
IBDV type 2 is used for immunization of chicken against infectious bursal disease F
Ibdv is a zoonotic virus F
The infectious bursal disease virus is transmitted only vertically F
Only inactivated vaccines can be used against infectious bursal disease F
The infectious bursal disease virus is very sensitive to detergents F
In Europe only low virulence strains of Infectious Bursal Disease Virus (IBDV) can be found. F
Young chicken can be immunized only with inactivated IBDV vaccines. F
Vaccines provide high level of protection against all IBDV strains. F
IBDV serotype 2 is used for immunization of chicken against Infectious Bursal Disease. F
Moderately attenuated (“hot”) IBDV vaccines are used for the immunization of young chicken without yolk immunity. F
There is no vaccine available against infectious bursitis virus. F
The infectious bursitis virus spreads by mosquitoes. F
Infectious bursal disease causes severe illness, mainly in waterfowl. F
The most frequent sign of infectious bursal disease is lameness.F
Only attenuated live vaccines are effective against infectious bursal disease. F
The most frequent sign of infectious bursal disease is lameness due to the inflammation of the subtendinal bursae. F
The infectious bursitis virus is inactivated within 1-2 days in the environment. F
A frequent sign of the infectious bursitis is encephalitis. F
The infectious bursitis virus does not cause any damage in chickens under the age of two weeks. F
Bats have an important role in the epidemiology of influenza F
Influenza viruses are classified into genera by their HA and NA proteins F
Influenza causes persistent infection in donkey F
The main host of influenza is the swine F
Influenza viruses are classified into genera by their HA and NA proteins F
Cat is susceptible to human seasonal influenza F
HPAI strains belong into a certain haemagglutinin types F
Influenzas Causes enteric symptoms in human. F
Anti-neuraminidase drugs inhibit the decapsidation of influenza viruses F
The HPAI causes skin haemorrhages in swine F
Swine influenza outbreaks occur usually during summer F
The mortality of swine influenza is high F
Swine influenza is easily transmitted to people F
In swine all influenza variants can be detected F
In a horse influenza outbreak all infected horses must be killed F
Racehorses should be vaccinated before the influenza season F
Breeding mares should be vaccinated before the influenza season F
Influenza causes persistent infection in horses F
The HPAI infection can be unambiguously differentiated from Newcastle disease by the clinical signs F
Influenza viruses are shed by birds exclusively in the nasal discharge F
Avian influenza can switch directly to human and cause epidemics with high case numbers as result of human to human transmission F
Avian influenza virus is primarily spread through bronchial discharge and aerogenic route F
All Bunyaviruses are transmitted by mosquitoes F
Bunyaviruses cause oral infection F
All bunyaviruses are vectored by insects F
Akabane virus is zoonotic F
Akabane virus causes foetal damages in dogs F
The Akabane disease is mainly seen in geese F
Akabane occurs in South-West Africa and is a disease of swine.F
Schmallenberg virus causes disease only in Suffolk sheep breed F
Schallenberg virus causes foetal damages in humans F
Schmallenberg virus is present worldwide F
Schmallenberg virus causes foetal damages in pigs F
The Schmallenberg virus causes severe disease in humans F
The Schmallenberg virus is a zoonotic agent. F
Ticks are reservoirs and vectors of the Schmallenberg virus. F
Schmallenberg virus was transported to Europe from South-America. F
Wild rabbits are reservoirs of Rift valley fever virus F
Rift valley fever is a human only disease F
The rift valley fever virus causes foetal damages in sheep F
The principle vectors of the rift valley disease are gnats. F
Rift valley fever outbreaks are most frequently seen in horses. F
The most frequent sign of the Nairobi sheep disease is encephalitis. F
The leading symptom of Nairobi disease is renal insufficiency. F
Nairobi sheep disease primarily causes pathological changes in the kidney (renal insufficiency)
. F
Hantaviruses cause hemorrhagic fevers in rodents. F
In domestic animals Hanta viruses typically cause liver dystrophy. F
Hanta viruses cause encephalitis in horses. F
Serological tests can NOT be used for laboratory detection of equine viral arteritis. F
Red blood cells can be used for laboratory detection of equine viral arteritis virus. F
Equine arteritis virus is very resistant to physical damages F
Equine viral arteritis is usually asymptomatic F
Vaccine against Equine Viral Arteritis is never used in Europe F
The Equine Viral Arteritis is caused by retrovirus. F
The equine viral arteritis virus cannot damage the wall of blood vessels F
The equine viral arteritis virus rarely causes asymptomatic infection F
The equine viral arteritis virus always causes clinical symptoms F
EVA is spread by insect vectors. F
Equine viral arteritis in mare is reactivated in pregnancy. F
Equine viral arteritis, aborted embryos have degenerated liver. F
Mares are frequently life-long carriers of the Equine arteritis virus. F
Equine viral arteritis is diagnosed by agarose-gel immunodiffusion (Coggins test). F
Equine viral arteritis virus can infect only by arthropods. F
Equine arteritis virus is very resistant to physical damages. F
Lameness due to inflammatory joints is the most typical sign of Equine infectious arteritis. F
Equine infectious arteritis is a notifiable disease; therefore vaccinations are forbidden. F
PRRS is caused by a coronavirus F
Isolation of PRRS in cell culture can be easily performed in any laboratory F
PRRS has only highly pathogenic variants F
Respiratory signs of PRRS occur just in sows F
PRRS virus replicates in T-lymphocytes F
The pathological signs of PRRS is typical because the lymph nodes are never enlarged F
PRRS cause digestive sign in adult. F
PRRS cause respiratory sign in adult. F
Target cells of PRRSV are alveolar epithelial cells F
PRRS can only be isolated in porcine kidney cells. F
PRRS causes immune suppression in prolonged cases F
PRRS virus causes severe intestinal problems in adult pigs F
PRRS is characterized by respiratory disease in adult pigs F
For PRRS prevention we can get a very good immunization with inactivated vaccines. F
Only inactivated vaccines can be used for the prevention against PRRSV. F
Porcine reproductive and respiratory virus (PRRSV) is a zoonotic agent. F
Porcine reproductive and respiratory vines (PRRSV) does not cause clinical signs in boars. F
Porcine reproductive and respiratory syndrome virus cannot cause abortion, only infertility of the sows. F
There are no vaccines for the prevention of Porcine reproductive and respiratory syndrome.
F
The blue ear disease is caused by dog coronavirus. F
The blue ear disease is caused by FIP. F
The blue ear disease is caused by chicken coronavirus. F
Does PRRS virus have 3 genotypes. F
PRRS is deadly in adult animals. F
Target cells of PRRSV are alveolar epithelial cells. F
PRRS virus can only be isolated in porcine kidney cell culture. F
The Porcine reproductive and respiratory syndrome (PRRS) is only present in North-America. F
Human coronavirus was not known before 2020 F
Recombination between coronaviruses is rare F
Human coronaviruses usually cause death. F
IBV can cause haemagglutination. F
PDCoV can cause haemagglutination. F
CCoV can cause haemagglutination. F
TGEV can cause haemagglutination. F
FIPV can cause haemagglutination. F
PEDV can cause haemagglutination. F
Coronaviruses can survive for months in the environment. F
In the case of transmissible encephalopathies meningoencephalitis is a typical postmortem lesion F
TGE virus does not reach the mammary gland. F
TGE virus can cause haemagglutination in vitro F
TGE virus causes respiratory signs in piglets. F
TGE virus does not cause dehydration F
The pathognomonic sign of TGE is necrosis in the large intestine. F
Porcine transmissible gastroenteritis (TGE) is completely eradicated in Europe. F
TGE causes 100% mortality in sows. F
The incubation time of TGE is usually 5-7 days. F
TGEV is widespread and fully replaced porcine epidemic diarrhoea (PED) virus. F
Porcine respiratory coronavirus induces cross-protection against PED. F
TGE infects only swine. F
The mortality caused by transmissible gastroenteritis of swine is the highest among old sows. F
Transmissible gastroenteritis of swine is a widespread disease, causing high losses in Europe.
F
Transmissible gastroenteritis of pigs is more frequent in the tropical countries that the moderate climate. F
There is no cross protection between transmissible gastroenteritis vines and the pulmonary coronavirus of pigs. F
TGE mainly cause croupous pneumonia. F
TGE replaces the respiratory corona virus. F
Porcine transmissible gastroenteritis is completely eradicated in Europe. F
Only pigs are susceptible to TGE infection. F
TGE is completely eradicated in Europe. F
Transmissible gastroenteritis virus can cause clinical signs in dogs. F
TGE infection is devastating at any age. F
The incubation period of TGE can be as short as 8 hours. F
Pigs has only alphacoronavirus F
The antibodies against porcine respiratory coronavirus protect the pigs against porcine epidemic diarrhoea virus F
Mutations and recombinations do not occur in swine coronaviruses F
PRCoV usually causes pneumonia. F
Porcine respiratory coronavirus causes acute pneumonia in susceptible piglets F
Porcine respiratory coronavirus reduced the prevalence of porcine epidemic diarrhoea. F
Swine pulmonary corona virus has a high mortality by pneumonia. F
Porcine respiratory coronavirus is a modification of the Hemagglutinating encephalomyelitis virus. F
Porcine respiratory coronavirus causes acute pneumonia in susceptible piglets. F
The porcine epidemic diarrhoea virus causes disease in calf F
Porcine epidemic diarrhoea virus can cause disease in humans. F
The virus causing porcine epidemic diarrhoea can replicate in the heart muscle of the foetus
F
Porcine epidemic diarrhoea virus causes more severe symptoms in adult than in young piglets .F
Porcine epidemic diarrhoea is present only in Africa and in the Middle East. F
Porcine epidemic diarrhoea can be transmitted by infected dogs and cats. F
Porcine epidemic diarrhoea frequently occurs in Europe. F
PHEV causes diarrhoea F
Hemagglutinating encephalomyelitis virus is typically vectored by mosquitoes. F
Hemagglutinating coronavirus can cause severe diarrhoea in sows. F
Hemagglutinating coronavirus of pigs is frequently causing malabsorption in sows. F
The hemagglutinating encephalomyelitis virus multiplicate in hematopoietic stem cells of the bone marrow
F
Deltacoronavirus of pigs is a bat virus. F
Bovine coronavirus is generally spreading in summer F
The bovine coronavirus is of avian origin F
Bovine coronavirus is alphacoronavirus F
Bovine coronavirus does not cause haemagglutination in vitro F
Bovine coronavirus remains at the place of the primary replication, and it does not cause viraemia
F
Certain bovine coronaviruses can cause diarrhoea in children. F
Bovine corona virus causes diarrhoea in adult animals mainly in summer. F
Bovine coronavirus can infect humans. F
Certain bovine coronaviruses can affect humans causing clinical signs. F
Coronaviruses mainly cause central nervous disease in cattle. F
Bovine coronaviruses can cause diarrhoea only in calves up to one month of age. F
Calf coronavirus diarrhoea is characterized by several respiratory signs. F
Mortality of calf respiratory coronavirus is high. F
There are no vaccines for the prevention of coronaviral diarrhoea in cattle. F
Winter dysentery causes symptoms in younger age (up to 6 months of age). F
Dogs have only one type of coronavirus. F
The canine coronavirus is a zoonotic agent. F
Canine coronavirus can always cause enteral disease F
Canine coronaviruses frequently cause encephalitis and hepatitis in puppies. F
Canine coronavirus are only present in North America. F
Canine coronavirus vaccines effectively protect from any Canine coronavirus infection. F
CCoV-IIa infections are endemic worldwide F
Canine enteral coronavirus and porcine coronavirus are genetically closely relative F
There are no protective vaccines available against Canine enteric coronavirus. F
Canine pantropic coronavirus is an agent of kennel cough. F
Canine pantropic coronavirus causes subnormal temperature F
Canine pantropic coronaviruses damage only the mucous membranes F
Pantropic canine coronavirus infections are endemic worldwide. F
Pantropic canine coronavirus causes a mild respiratory disease in suckling dogs. F
Canine respiratory coronavirus and human coronaviruses are genetically very distant relatives in all cases F
Canine respiratory coronavirus infection results cross-protection against CCOV-I. F
In suckling dogs CCoV-II infection causes respiratory disease. F
Almost all cat vaccines contain antibodies against FIP. F
The wet form of FIP is II. type of hypersensitivity. F
The dry form of FIP is I. type of hypersensitivity. F
FIP is caused by jackal coronavirus. F
FIP responds well to antibiotic treatment. F
Most animals infected with feline coronavirus develop FIP F
The dry form of FIP is I. type of hypersensitivity F
The feline coronavirus causes viraemia only in FIP. F
The feline coronavirus is a zoonotic agent F
Feline enteric coronaviruses may infect dogs. F
Feline infectious peritonitis viruses form a single serotype. F
Feline enteric coronavirus infection usually causes sudden death of queens. F
FIP causes infection only in cats younger than 1 year of age. F
Feline corona virus does not have a long infection/carrier time. F
Feline infectious peritonitis (FIP) develops only in adult cats (over 1 year of age). F
Feline enteric coronavirus usually causes severe, haemorrhagic enteritis in kittens. F
Feline infectious peritonitis is an acute disease, it appears after a 2-3 days long incubation. F
Feline infectious peritonitis viruses from a single serotype. T
Feline enteric coronavirus infection usually causes sudden death of queens. F
Vaccine effectively protects from feline infectious peritonitis. F
FECoV infection usually causes acute haemorrhagic enteritis. F
FIP forms because of immunotolerance. F
Avian coronaviruses provide long lasting yolk-immunity F
IBV, the most important route is the germinative route. F
IBV, cause stunting growth when embryonated egg is infected. F
IBV is an arterivirus. F
Mortality of IBV is high every ages. F
IBV cannot cause viraemia F
The Infectious Bursitis Virus IBDV is inactivated within 1-2 days in the environment. F
Infectious bronchitis viruses belong into 3 distinct serotypes. F
Infectious bronchitis virus damages the ovaries only in hens. F
Infections bronchitis virus vaccines are used against turkey enteritis. F
Infectious bronchitis can spread very slowly in the flock causing chronic disease. F
There are no vaccines for the prevention of infectious bronchitis of chicken. F
Infectious bronchitis virus of chicken is a uniform virus without any types of variants. F
Germinative route is the most important in the transmission of infectious bronchitis. F
Infectious bronchitis viruses form 2 distinct serotypes. F
Turkey corona virus does not cause strong diarrhoea and causes no necrosis. F
Vaccination of turkey breeding flocks against Turkey enteritis virus is mandatory. F
Paramyxoviruses are bad immunogens F
Paramyxoviruses cannot cause strong cytopathogenic effect in cell cultures F
Parainfluenza viruses are highly host specific F
There are no vaccines on the market against canine parainfluenza 2 virus. F
Canine parainfluenza virus 2 frequently causes encephalitis in old dogs. F
Parainfluenza virus 2 infection is frequent in the aetiology of kennel cough. F
Rinderpest virus can infect cattle F
Rinderpest virus replicated only in the lungs F
Rinderpest virus is resistant; it can survive in the environment for several weeks F
Vesicle formation on the mucous membranes is typical in the case of rinderpest F
Enteral clinical signs are not typical in Rinderpest F
Attenuated viruses are widely used for the prevention of Rinderpest in Africa F
Rinderpest occurs in large number in Africa. F
Wild mammals are asymptomatic carriers of Rinderpest F
It is mandatory to vaccinate cattle against Rinderpest. F
Nowadays Rinderpest virus is used as heterologous vaccine against the PPR virus. F
Rinderpest virus survives for years in nature. F
Only cattle are susceptible to Rinderpest infections. F
Rinderpest is carried by animals for a long time F
Rinderpest commonly occurs in Africa and in Latin America. F
Rinderpest virus is carried by animals for several years. F
Cattle are infected with rinderpest virus mainly per os. F
Rinderpest virus can survive in the environment for several months. F
Peste des pest ruminants virus is resistant, it can survive in the environment for several months F
Peste des petits ruminants is a widespread disease in Europe F
Peste des petit ruminants is a frequently diagnosed disease in America. F
Peste de petits ruminants is a zoonotic disease F
The Peste des petits ruminants are endemic in North- and South America. F
The world is free of Peste des petites ruminants. F
Distemper can be prevented only with the attenuated but not inactivated vaccines F
Distemper is zoonosis F
Canine distemper has six serotypes F
Neurological signs are not typical signs of canine distemper. F
Distemper can be prevented only with attenuated but not inactivated vaccines. F
The dog is the only species which is susceptible to canine distemper virus. F
Ataxia and paralysis are the main clinical signs of distemper in cats F
Distemper virus infects only dogs. F
Dogs infected with Canine distemper virus usually become life-long carriers and shedders. F
Distemper virus infects only species belonging to Canidae. F
Distemper virus spreads mainly by arthropod vectors. F
Distemper is a notifiable disease. F
The dominant clinical sign of Canine distemper is diarrhoea. F
Canine distemper virus only infects Canidae. F
Surviving distemper does not result in protection. F
Vaccinations against distemper at half years of age. F
Hendra virus can infect mainly swine and human. F
Hendra virus can cause enteritis in the small intestine. F
Diseases caused by Nipah virus occur worldwide. F
Wild birds may be reservoir hosts of the Nipah-viruses. F
Nipah virus is transmitted mainly by arthropod vectors. F
Bovine respiratory syncytial virus causes viraemia F
Disease caused by bovine respiratory syncytial virus cannot be prevented with vaccination. F
Bovine respiratory syncytial virus causes low morbidity and high mortality F
Bovine parainfluenza virus causes central nervous clinical signs in calves. F
Disease caused by bovine parainfluenza-3 virus is very rare. F
Parainfluenza 3 virus of cattle spreads mainly by arthropod vectors. F
Parainfluenza-3 virus of cattle can cause thromboembolic meningoencephalitis. F
The main clinical sign of a parainfluenza-3 infection is diarrhoea. F
Velogenic strains of Newcastle disease virus (NDV) cause an acute septicemia F
Apathogenic trains of NDV are used for vaccination F
ND is caused by virulent strains of the APMV-1 serogroup F
Members of every APMV serogroup can cause Newcastle disease F
A usual 1st symptom of neurotropic-vNDV infection is diarrhea F
An acute, nervous form of Newcastle disease can frequently be seen in ducks F
An acute, nervous form of Newcastle disease can frequently be seen in dogs F
Newcastle Disease ND viruses cause dwarfism in embryonated chicken eggs F
There are no vaccines for the prevention of Newcastle disease. F
Only faeces of the infected birds contains Newcastle disease virus F
Newcastle disease virus can infect only chicken F
Eurasia is free from Newcastle disease F
Humans are resistant against Newcastle disease virus F
Lentogenic Newcastle disease virus cause severe fatal infection. F
Germinative infection is an important way of transmission of Newcastle disease virus F
Lentogenic Newcastle disease virus cause severe fatal infection F
Lentogenic Newcastle disease virus can cause high morbidity and mortality in poultry flocks
F
Lentogenic Newcastle disease virus is more virulent than velogenic F
Only inactivated vaccines may be used for the prevention of Newcastle disease F
Newcastle disease virus cannot survive long in the environment. F
Newcastle disease virus is typically vectored by ticks. F
Lentogenic strains of Newcastle disease virus can cause high morbidity and mortality. F
Velogenic viscerotrop strains of Newcastle disease virus can be used for vaccine production.
F
Lentogenic strains of Newcastle disease virus do not cause clinical signs. F
Wild boars may transmit Newcastle disease virus. F
Any member of the avian paramyxovirus serogroups may cause Newcastle disease. F
Newcastle disease could easily be differentiated from avian influenza. F
Using vaccines of velogenic strains of Newcastle disease virus good protection can be reached. F
Avian metapneumovirus infection occurs only in America F
Rhabdoviruses can survive in the environment for several months. F
Vesicular stomatitis virus has a narrow host range. F
Vesicular stomatitis is a frequent disease in Africa. F
Vesicular stomatitis is a widespread disease all over the world F
The mortality of vesicular stomatitis is very high. F
Vesicular stomatitis causes large number of vesicles in humans F
The clinical signs of foot and mouth disease and vesicular stomatitis cannot be differentiated in horses F
Vesicular stomatitis can be transmitted only by arthropods F
Vesicular stomatitis virus does not cause viraemia only local lesions F
Vesicular stomatitis virus is found all over the world. F
Vesicular stomatitis virus: horse is sensitive. F
Vesicular stomatitis virus spreads with insects. F
After recovery of VSV there will be a permanent immunity. F
The host range of vesicular stomatitis and foot and mouth disease is the same. F
In the case of vesicular stomatitis vesicles are formed only at the place of entry of the virus.
F
Vesicular stomatitis cannot be prevented with vaccines. F
The vesicular stomatitis virus is uniform, there are no serotypes, variants etc. F
Vesicular stomatitis virus infects only swine. F
Cattle are not susceptible to vesicular stomatitis virus. F
There are no vaccines for the prevention of vesicular stomatitis. F
Vesicular stomatitis virus can cause severe disease in humans. F
Direct contact is the main way of transmission of ephemeral fever virus F
Ephemeral fever is a frequent disease all over the world F
Ephemeral fever is a zoonotic disease F
Ephemeral fever virus is shed in large amount in the saliva. F
Ephemeral fever occurs only in America. F
Inhalation of the tracheal discharge is the main way of infection with ephemeral fever virus.
F
The clinical signs of ephemeral fever are more severe in horses than cattle. F
In the case of silent rabies rabid dogs cannot bark. F
There is a high level of cross protection between phylogroups of rabies viruses F
Rabies virus is uniform without serotypes, genotypes etc. F
Puppies have to be vaccinated against rabies at the age of 6 weeks. F
Bats infected with European bat lyssaviruses frequently attack animals F
The incubation time of rabies is generally 24-72 hours; however, exceptions can occur F
The host range of rabies is very narrow, mainly dogs and foxes are susceptible F
Only carnivorous animals are susceptible to rabies virus F
Rabies virus appears in the saliva 2-3 days after the onset of the clinical signs F
Rabies can be diagnosed by detection of antibodies in paired sera F
Antibodies against rabies detected with ELISA confirm the diagnosis of rabies F
Rabies virus replicates in the lymphocytes F
Rabies occurs only in tropical countries F
Urban rabies has been eradicated from the Earth. F
Postmortem examination of rabid animals is forbidden F
Haemorrhages of the serous membranes are typical postmortem lesions of rabies F
Rabies can be diagnosed only by using PCR. F
Rabies virus does not penetrate the blood vessels. F
When an animal which is infected with rabies virus attacks another dog, it should be vaccinated immediately F
Rabies is a uniform virus. F
Rabies is a resistant virus. F
Rabies can be transmitted only by saliva. F
The incubation of rabies is generally less than one week. F
The rabies virus is a uniform virus without serotypes, genotypes, subtypes etc. F
Only carnivorous animals are susceptible to rabies virus .F
The causative agent of rabies is a uniform virus, without different types or groups. F
The resistance of the rabies virus is good, it retains infectivity for several months in the environment .F
Humans can be infected with rabies, only by being bitten by rabid animals. F
Rabies virus is shed in the saliva only after the appearance of the clinical signs. F
Focal necrosis in the liver is a typical lesion of rabies. F
Always the furious form of rabies can be seen in dogs. F
Only the classical rabies virus can cause clinical signs, the other genotypes not. F
Rabies virus causes viraemia soon after infection. F
Humans are not susceptible to European bat lyssaviruses. F
There is no haematogenic spreading of the rabies virus. F
Dogs have to be vaccinated against rabies in the first week of life. F
Only the classical rabies virus is present in Europe. F
Urban form of rabies is maintained by the fox in Europe. F
Rabies virus is highly resistant. F
Rabies virus cannot be cultured. F
Presence of antibodies to rabies virus confirms the diagnosis of rabies. F
Detection of Negri bodies is more sensitive than immunofluorescence test, in the case of
rabies. F
Virus isolation is the most widely used way of diagnosis of rabies. F
Rabies virus is replicating in the lymphoid cells and causes viraemia before the appearance of the clinical signs. F
Rabid animals have to be vaccinated immediately. F
Rabies has been eradicated in Europe. F
Rabies spread through venereal. F
The high-titre of virus neutralizing antibodies confirms the diagnosis of rabies. F
Rabies symptoms appear only after CNS signs .F
Rabies virus can only be found in the nervous system. F
Borna disease occurs in Africa, Asia and South America, but Europe is free F
Dyspnoea is the main clinical sign of borna disease F
Only horses are susceptible to Borna disease virus. F
The lethality of Borna disease is low. F
Borna disease is widespread all over the world. F
Pneumonia is the main clinical sign of Borna disease. F
Horse is the reservoir species of Borna disease virus. F
Dyspnoea, nasal discharge and cough are the main signs of Borna disease. F
Borna disease occurs mainly in the Far East. F
Borna disease can be seen all over the world. F
Respiratory signs are the most typical ones in the case of Borna disease. F
Only ruminants are susceptible to Borna disease virus. F
Proventricular disease is a zoonosis F
The reverse transcriptase transforms DNA of the retroviruses to mRNA F
Retroviruses are stable viruses; genetic changes are rare. F
Retroviruses are euryxemic agents F
Mutation of retroviruses is very rare F
Retroviruses replicate mainly in the endothelial cells. F
Retroviruses are generally resistant, they can survive in the environment for several weeks. F
Retroviruses are generally stable viruses, mutations are very rare. F
Retrovirus has a wide host spectrum. F
Retroviruses are generally not carried for more than a month. F
Retroviruses are generally genetically very stable. F
The resistance of retroviruses is generally good, they survive in the environment well. F
Retroviruses are generally very stable viruses, mutations are exceptional in them. F
Retroviruses have a tegument or rind. F
You cannot multiply retrovirus artificially. F
Retroviruses cannot spread from animal to animal. F
Retroviruses replicate mainly in endothelium cell. F
Antibodies against enzootic bovine leukosis virus can be detected only for 1-2 months after infection F
Maternal Antibodies against enzootic bovine leukosis virus can be detected only for 1-2 months F
Generation shift is the only way of eradication of enzootic bovine leukosis F
Enzootic bovine leukosis virus does not spread from animal to animal. F
Mild clinical signs can be seen in the incubation phase of enzootic bovine leukosis. F
Enzootic bovine leukosis virus is not shed in the colostrum F
Enzootic bovine leukosis virus can spread from cattle to sheep, goats , and other ruminants F
In the case of Enzootic bovine leukosis the clinical signs appear at the age of 6-8 months F
Enzootic bovine leukosis occurs only in Holstein Friesian cattles F
Enzootic bovine leukosis virus has several serotypes and subtypes. F
Enzootic bovine leukosis virus cannot result tumour formation. F
Serological examinations cannot be used to the diagnosis of enzootic bovine leukosis. F
Selection cannot be used for eradication of enzootic bovine. F
Bovine enzootic leukosis infect only bovine. F
Bovine enzootic leukosis does not spread with excretion. F
Enzootic bovine leukosis the pre-tumour phase usually in 6-10 months old animals. F
The target cells of the bovine enzootic leukosis virus are the T-lymphocytes. F
The typical signs of bovine enzootic leukosis can be seen in cattle under 1 year of age. F
Selection (test and slaughter) method cannot be used to eradicate enzootic bovine leukosis virus. F
Generation shift method cannot be used to eradicate enzootic bovine leukosis virus. F
Enzootic bovine leukosis virus cannot infect foetuses. F
Enzootic bovine leukosis virus is passed to newborn calves mainly with colostrum in endemically infected herds. F
Tumours can be seen in about 90% of the animals infected with enzootic bovine leukosis virus. F
Tumours caused by enzootic leukosis virus generally appear at the age of 6 months. F
Enzootic bovine leukosis virus is zoonotic. F
Enzootic bovine leukosis virus cannot cause intrauterine infection. F
Enzootic bovine leukosis virus is not shed by the infected animals. F
Clinical signs of enzootic bovine leukosis are seen mainly in 6-8-month-old calves. F
Enzootic bovine leukosis virus has several serotypes and subtypes. F
Enzootic bovine leukosis virus can not result in tumour formation. F
The tumours in the case of bovine enzootic leucosis can be seen from the age of 6 months. F
Bovine enzootic leucosis virus has several serotypes. F
There is no horizontal spread in the case of bovine enzootic leucosis. F
Enzootic bovine leucosis occurs in all ruminant species. F
Enzootic bovine leukosis virus can infect cattle, pigs and horses. F
Enzootic bovine leucosis is spreading very fast in infected herds. F
Enzootic bovine leucosis only infects cattle. F
Enzootic bovine leukosis occurs only in Holstein-Frisian cattle, other cattle races are resistant
F
The most severe clinical signs of ovine pulmonary adenomatosis can be seen in lambs younger than 6 months. F
Antibodies of animals infected with ovine pulmonary adenomatosis virus can be detected with ELISA. F
Ovine pulmonary adenomatosis virus can be transmitted with contaminated objects to other farms F
Ovine pulmonary adenomatosis virus can infect sheep, goats, and cattle. F
The most severe clinical signs of ovine pulmonary adenomatosis can be seen in lambs younger than 6 months. F
Ovine pulmonary adenomatosis virus replicates in lymphoid cells and causes viraemia. F
Ovine pulmonary adenomatosis occurs only in South Africa. F
Ovine pulmonary adenomatosis is prevented with inactivated vaccines. F
The primary replication site of OPA is in the mucosal cells of the intestines. F
Metastasis are frequently seen in parenchymal in the case of OPA.F
Ovine pulmonary adenomatosis virus is found in 2-4 months old lambs. F
Tumours can frequently be seen in the liver and the spleen in the case of ovine pulmonary adenomatosis. F
In the case of ovine pulmonary adenomatosis lesions are common in the liver. F
Ovine pulmonary andenomatosis can be diagnosed by detecting antibodies with ELISA.F
Ovine pulmonary adenomatosis virus causes interstitial pneumonia. F
Lung adenomatosis causes usually dry cough. F
Lung adenomatosis causes a lot of metastasis. F
Ovine pulmonary adenomatosis virus results in malignant transformation of macrophages. F
Europe is free from ovine pulmonary adenomatosis. F
Faces of infected animals contain large amount of ovine pulmonary adenomatosis virus. F
Jaagsiekte affects lambs of 3-6 months. F
Jaagsiekte virus can transform human cells. F
Jaagsiekte is only present in Africa. F
Jaagsiekte causes metastatic abscess formation all over the body F
Feline leukosis virus will be shed lifelong by infected cats. F
There are no vaccines for the prevention of feline leukosis F
FOCMA antigen is a typical surface antigen of feline leukosis viruses F
Feline leukosis virus can only be transmitted with saliva. F
Cats remain infected with feline leukosis virus lifelong. F
Feline leukosis virus is uniform. F
There is no vaccine against Feline leukosis virus. F
Feline leukosis can infect dogs and cats. F
Asymptomatic infection cannot happen in the case of Feline leukosis. F
Feline leukosis virus can infect dogs, cats and wild living carnivorous animals. F
Feline leukosis is a very rare disease. F
FeLV is a uniform virus. F
Infection with feline leukosis virus always appears in clinical signs. F
Inactivated vaccines are used for the prevention of avian leukosis. F
Avian leukosis viruses a resistant, they can survive in the bedding for several weeks F
Avian leukosis virus occurs only in tropical and subtropical countries F
Avian leuKosis virus can cause only lymphoid leukosis F
Clinical signs of avian leukosis can be seen typically in broiler chicken. F
Avian Leukosis virus is uniform. F
Avian leukosis virus cannot infect by germinative way. F
Clinical signs of avian leukosis generally appear in day old chicken. F
The main way of prevention of avian leukosis is vaccination using attenuated strains. F
There is no germinative infection in the case of avian leukosis viruses. F
In a flock infected with avian leukosis virus generally 50-60% of the animals have tumours. F
Avian leukosis is seen during the first week of life in chicken. F
Inactivated vaccines are widely used in order to prevent avian leukosis. F
Reticuloendotheliosis is caused by J type of avian leukosis virus. F
Reticuloendotheliosis is prevented by vaccination of the parent animals. F
Wide vaccination is used to prevent Reticuloendotheliosis. F
Pneumonia is a typical lesion of reticuloendotheliosis. F
Clinical signs of maedi visna are more severe in young animals than in adults F
Heavy nasal discharge is a clinical sign of maedi F
The maedi virus and the visna virus are related but they can be differentiated with PCR. F
Interstitial pneumonia is the main postmortem lesion of visna. F
Inactivated and attenuated vaccines are widely used for the prevention of maedi-visna F
Maedi-visna can occur in sheep, goats, and cattle F
Europe is already free from maedi-visna F
Large amount of mucoid nasal discharge is typical in the case of maedi. F
Clinical sign of maedi/visna appear from the age of 6-8 months F
Meadi/visna most important clinical sign is profuse diarrhoea. F
Maedi/visna virus is shed only in tracheal discharge. F
Clinical signs of maedi are mainly seen in lambs below half a year of age. F
Wet cough and intensive nasal discharge are typical signs of maedi. F
Attenuated vaccines are widely used to prevent maedi/visn F
Maedi is spreading fast. F
In order to eradicate maedi/visna infected ewes have to be culled with their lambs. F
Clinical sign of maedi/visna appear from the age of 6 months. F
Maedi/visna is spreading fast in the flock. F
Maedi/visna virus is shed only in the tracheal discharge. F
Sheep are resistant against caprine arthritis encephalitis virus F
Arthritis caused by caprine arthritis encephalitis virus is mainly seen in lambs F
There is intensive vaccination against Caprine arthritis encephalitis in endemic countries F
In the case of caprine arthritis encephalitis, arthritis is less frequent than encephalitis. F
Arthritis caused by caprine arthritis-encephalitis virus is typically seen in kids below half a year of age. F
Caprine arthritis encephalitis virus replicates in the intestinal tract. F
Mosquitoes are the main vectors of equine infectious anaemia virus; the virus can replicate in them F
Equine infectious anaemia is an acute disease; it does not have a chronic form F
Equine infectious anaemia virus disappears from animals after the viraemia F
Ticks are vectors of equine infectious anaemia virus. F
There is no immune reaction in the case of equine infectious anaemia. F
Equine infectious anaemia is zoonotic. F
There is no immune reaction in horses against equine infectious anaemia virus. F
Equine infectious anaemia has a weak resistance. F
You cannot diagnose Equine infectious anaemia with serology. F
The resistance of equine infectious anaemia is very low. F
Horses and cattle are susceptible to equine infectious anaemia virus. F
In the case of equine infectious anaemia, haemorrhages cannot be seen. F
Equine infectious anaemia virus is mainly transmitted with tracheal discharge. F
Attenuated vaccines are used for the prevention of equine infectious anaemia. F
In the case of transmissible encephalopathies lesions can only be seen in the central nervous system F
Prion diseases can be diagnosed by detecting the antibodies with ELISA. F
There are major differences in the amino acid sequence of the normal and infective prions. F
In the case of transmissible encephalopathies meningoencephalitis is a typical postmortem lesion F
Agents of transmissible encephalopathies are most frequently detected with PCR. F
Prion diseases can be diagnosed by detecting antibodies with ELISA F
Chronic prion is inactivated by boiling. F
Prions contain protein and DNA. F
Mutations can result infective prions. F
Infection with infective prions generally happens per os. F
In the case of transmissible encephalopathies encephalitis can be seen in the grey material of the brain. F
PCR is used to the detection of prions. F
Prions always cause viraemia in the infected hosts. F
Normal prions are essential components of the cell membrane of the hosts. F
Encephalitis is typical in the case of transmissible encephalopathies. F
Protease breaks down prions. F
Transmissible encephalopathies are acute or per-acute diseases .F
Allergy tests are widely used to diagnose transmissible encephalopathies. F
The EU is free from Scrapie F
Scrapie is a zoonotic disease. F
Scrapie prion is detected with PCR F
Scrapie is a disease of sheep, goats, and cattle F
Both typical and atypical scrapie strains can cause itching F
Scrapie has more clinical signs in lambs than adult sheep F
Atypical scrapie strains can cause the same clinical signs as typical scrapie. F
Scrapie can be prevented with live vaccines. F
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
Goat are resistant to scrapie. F
Itching can be seen in the case of atypical scrapie. F
Scrapie can be prevented with inactivated vaccines. F
Scrapie can be prevented by using attenuated vaccines. F
Minks shed the transmissible mink encephalopathy prion in the faeces. F
BSE prion causes meningoencephalitis. F
BSE prion is shed in milk in large amount. F
BSE prion generally infects cattle in aerosol F
Enteritis and haemorrhages can be seen postmortem in BSE cattle F
Calves of cows infected with BSE are frequently infected, they have to be destroyed F
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
BSE prions are shed in the faeces and it is transmitted to other cattle in the herd. F
Bovine spongiform encephalopathy is widespread in Europe; it is common in most European countries. F
In the case of BSE polioencephalitis is the main post mortem lesion. F
BSE prion is mainly detected with PCR. F
Antibodies against bovine spongiform encephalopathy are detected with ELISA. F
The agent of bovine spongiform encephalopathy is shed in large number in the milk. F
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 high levels of antibodies is produced. F
Bovine spongiform encephalopathy cannot infect humans. F
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
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
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 caused by Clostridium anthracis. F
Anthrax can occur only in ruminants F
There are no vaccines for the prevention of Anthrax. F
Horses are resistant to Anthrax. F
Carbon dioxide is needed to the spore production of Bacillus Anthracis F
CO2 is needed for the spore formation of the agent of anthrax F
Pigs are more susceptible to anthrax than sheep F
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
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
Pigs are more susceptible to anthracis than sheep. F
Inactivated vaccines are used for the prevention of anthrax. F
Bacillus anthracis makes spores only without oxygen. F
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 is not in pig. F
Anthrax spreads rapidly in a herd. F
In anthrax, tracheitis common in carnivores. F
Anthrax causes necrotic foci in liver. F
Anthrax cannot occur in dogs and cats. F
The agent of anthrax can infect only herbivorous animals. F
Anthrax is caused by Bacillus bovin F
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
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
Cell wall antigen is a virulence factor of B. anthracis. F
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
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
Virulence factors of anthrax: capsule, toxin, cilia. F
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
Flagella is a virulence factor of B. anthracis. F
Anthrax spore is a virulence factor. F
Europe is free from Anthrax. F
Anthrax is caused by Clostridium chauvoei. F
Horses are resistant to anthrax. F
Anthrax is an epidemic disease that rapidly develops. F
Anthrax spreads in a herd by direct contact. F
In order to diagnose anthrax all carcasses have to be dissected. F
Swine is highly susceptible in anthrax. F
Splenic fever is similar in every species. F
Carnivorous animals are resistant to Bacillus anthracis. F
Fibrinous pneumonia is a common post mortem lesion of anthrax. F
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
Clostridia are obligate aerobic bacteria F
Clostridium perfringens is an obligate pathogenic bacterium. F
There are no vaccines for the prevention of diseases caused by clostridia F
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
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
Cl. chauvoei is the agent of malignant oedema F
Malignant oedema is generally endogenous in cattle. F
Malignant oedema can be diagnosed based on clinical signs F
Malignant oedema is only in ruminants. F
Malignant oedema, attenuated vaccine for prevention. F
Clostridium channel is the agent of malignant oedema .F
Attenuated vaccines are used for the prevention of malignant oedema. F
There are no vaccines for the prevention of malignant oedema. F
Malignant oedema can be treated with antibiotics. F
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
Blackleg is a frequent disease in pigs F
Generally attenuated vaccines are used for the prevention of blackleg. F
Blackleg occurs only in tropical and subtropical countries F
Generally attenuated vaccines are used for the prevention of blackleg. F
Blackleg occurs most frequently in pigs. F
Blackleg is generally endogenous in sheep. F
Live vaccines are used for the prevention of blackleg. F
In Blackleg disease we use attenuated vaccine. F
Attenuated vaccines are used for the prevention of blackleg. F
Severe diarrhoea is the main clinical sign of blackleg. F
Blackleg is caused by Clostridium septicum. F
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
We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei. F
Blackleg in bovine is caused by wound infections. F
Classical swine fever is a frequent predisposing factor of bradsot. F
Bradsot is caused by Clostridium chauvoei F
Bradsot occurs mainly in tropical and subtropical countries F
Overeating can predispose the animals to bradsot. F
Aminoglycosides are successfully used for treatment in the case of bradsot. F
Severe pneumonia is a typical clinical sign of bradsot F
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 causes oedema of the legs and necrosis. F
Köves disease is caused by Clostridium chavoei. F
Infectious necrotic hepatitis is mainly seen in pigs F
In sheep, Clostridium septicum causes necrotic liver infection. F
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
Infectious necrotic hepatitis is caused by Clostridium septicum. F
Infectious necrotic hepatitis is caused by Clostridium novyi. F
Infectious necrotic hepatitis is spread by tick. F
Infectious necrotic hepatitis can be transmitted by liver flukes. F
Infectious necrotic hepatitis occurs mostly in young sheep. F
There are no vaccines for the prevention of bacillary hemoglobinuria F
Bacillary haemoglobinuria is caused by Clostridium septicum. F
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
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
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
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
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
Pathological symptoms of lamb dysentery can be found in the large intestines. F
Lamb dysentery can be successfully treated with penicillin when clinical signs appear. F
Newborn lambs have to be vaccinated in order to prevent lamb dysentery. F
Infection of lamb by secretion in the milk. F
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
The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large
intestine. F
There is no vaccination for the prevention of Infectious necrotic enteritis of piglets. F
Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics
immediately F
Lesions of pig enterotoxaemia can be seen in the large intestine F
Pig enterotoxaemia can be generally seen in weaned piglets. F
Infectious necrotic enteritis of piglets occurs in piglets after weaning. F
Necrotic enteritis of piglets is seen in piglets around weaning. F
Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets. F
Pig enterotoxaemia causes abdominal contractions in sows. F
Mesenteric lymph node is congested in case of pig enterotoxaemia. F
Enteritis in piglets are caused by Clostridium perfringens D. F
Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology. F
Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut. F
Enterotoxaemia is mainly seen in piglets after weaning. F
Pig enterotoxaemia is not present in Europe .F
Pig enterotoxaemia cannot be prevented by using vaccines. F
The toxin of the agent of pulpy kidney disease is sensitive to trypsin F
Pulpy Kidney Diseases is caused by Clostridium chauvoei. F
Pulpy kidney disease generally occurs in 1-2week old lambs F
Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes F
Isolation of the agent is necessary to the diagnosis of pulpy kidney disease. F
Pulpy kidney disease is typically seen in lambs below 2 weeks of age. F
Inactivated vaccines are used for the prevention of pulpy kidney disease. T
Pulpy kidney disease is seen in piglets in the first week of life. F
Ulcerative enteritis is frequently seen in day old chicken. F
Clostridium perfringens is the causative agent of ulcerative enteritis in poultry. F
Ulcerative enteritis of poultry is generally prevented with vaccination. F
Lesions of ulcerative enteritis are mostly seen in the small intestines. F
Lesions of necrotic enteritis of chicken are typically occur in the large intestine. F
Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis. F
Waterfowl are not susceptible to necrotic enteritis. F
Necrotic enteritis occurs in 1-3 weeks of age. F
Gangrenous dermatitis is caused by obligate pathogens. F
Vaccines are the primary way of prevention of gangrenous dermatitis. F
Flaccid paralysis is a frequent clinical sign of tetanus F
Tetanus is only seen in horse F
Over-eating can predispose animals to Tetanus. F
The agent of Tetanus needs oxygen to replicate F
Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus F
Tetanus is a zoonosis F
Dogs are resistant to tetanus F
Tetanus cannot be prevented with vaccination. F
The agent of tetanus causes septicaemia. F
Tetanus can be diagnosed on the basis of post mortem lesions. F
Clostridium tetani produced endotoxin. F
Tetanus can be prevented with vaccines containing inactivated bacteria. F
Horses are resistant to tetanus. F
Tetanus can only develop after deep wounds. F
The paralysis usually starts at the place of the wound. F
Clostridium tetani toxin is produced in the feed. F
There is no vaccine for tetanus. F
Clostridium botulinum generally causes wound infection. F
Focal necrosis in the liver is a typical post mortem lesion of Botulism F
Botulism can be seen as a result of a wound infection. F
Birds are resistant to botulism. F
Necrotic foci in the liver are typical post mortem lesions of botulism. F
Generally wounds predispose animals to botulism. F
The agent of botulism generally produces toxin at the site of entry. F
Botulism is diagnosed on the basis of the typical post mortem lesions. F
Botulism doesn’t occur in Europe. F
Botulism usually develops following a wound infection. F
In Hungary, botulism occurs in winter and early spring. F
Botulism is eradicated in Europe. F
Spasms are the typical clinical sign of botulism. F
Botulism happen generally through wound infection. F
Haemolysins cause haematuria in the case of staphylococcus F
Endotoxins are virulence factors of Staphylococci F
Some species of Staphylococcus are obligate pathogens. F
Staphylococcus are epiphytes. F
Staphylococcus are gram negative cocci. F
Coagulase positive Staphylococcus species are less pathogenic than Coagulase negative. F
Morels disease id caused by Staphylococcus aureus subsp aureus F
Morel’s disease is an acute, fast courses disease F
Morel’s disease occurs mainly in cattle, small ruminants and pigs F
Interstitial pneumonia is the main postmortem lesion of Morel’s disease. F
Morel’s disease is caused by Staphylococcus aureus subsp. Aureus F
Morel’s disease is mainly seen in suckling lambs. F
Diarrhoea is the main clinical sign of Morel’s disease. F
Morel’s disease can mainly be seen in suckling animals. F
Morel’s disease is caused by Streptococcus pyogenes. F
Methicillin resistant Staphylococcus aureus is generally not passed from animals to humans
F
Methicillin resistant Staphylococcus aureus strains are obligate pathogens F
Methicillin resistant Staphylococcus aureus strains are more virulent than the methicillin sensitive ones F
Lesions of Rabbit staphylococcosis are limited to the lungs. F
Rabbit staphylococcosis is caused by Staphylococcus cuniculi F
Rabbit staphylococcosis can be prevented by vaccinating the pregnant rabbits with attenuated vaccine F
Staphylococcus in rabbits typically occurs in newborn rabbits F
Staphylococcosis in rabbits typically occurs in newborn rabbits. F
Staphylococcosis of rabbits is caused by Staphylococcus hyicus. F
Rabbit Staphylococcus can be prevented/treated by vaccination. F
Rabbit staphylococcus are caused by S. aureus subsp. piriformes. F
Rabbit staphylococcus is an obligate pathogen. F
Rabbit staphylococcosis typically occurs in suckling rabbits. F
Staphylococcus aureus subsp. anaerobius is the causative agent of rabbit staphylococcosis. F
Purulent pneumonia can be seen frequently as a clinical sign of staphylococcosis in grower chickens. F
Staphylococci can cause disease only in day-old birds but not in growers or adults. F
Pneumonia is a common clinical form of avian staphylococcosis F
Staphylococcus aureus subsp. aureus can cause frequent pneumonia in chicken. F
Poultry staphylococcus is a rare disease nowadays. F
Exudative dermatitis of pigs is caused by Staphylococcus aureus subsp. Anaerobius F
Necrosis of the skin is the main clinical sign of exudative dermatitis. F
The lesions of exudative dermatitis are itching very much F
Exudative dermatitis is caused by Staphylococcus aureus. F
Exudative dermatitis has high mortality. F
Staphylococcus aureus subsp. aureus is the causative agent of exudative dermatitis in pigs. F
Exudative dermatitis is generally seen in fattening pigs. F
Exudative dermatitis can be prevented by attenuated vaccines. F
Exudative dermatitis of pigs is caused by Streptococcus hyicus. F
Itching is the major clinical sign of exudative dermatitis in pigs. F
Vaccination is widely used in order to prevent exudative dermatitis. F
Exudative skin inflammation is caused by Staphylococcus aureus. F
Exudative dermatitis cannot occur in adult pigs. F
Exudative dermatitis can be spread by lice and ticks. F
Streptococcus are obligate aerobic. F
Diarrhoea is a frequent clinical sign of streptococcosis of pigs F
Calcium deficiency can predispose suckling piglets to streptococcosis. F
Porcine streptococcosis is more frequent among adult animals than among young piglets.. F
Streptococcus pyogenes is the main agent of porcine streptococcosis. F
Streptococcosis of pigs can be seen generally among fattening pigs. F
Streptococcus equi subsp. Equi is a zoonotic agent F
The agent of strangles is carried on the tonsils of most horses. F
Strangles is mainly seen in foals till the age of 4 months of age F
The mortality of strangles is high F
The toxin of the agent is responsible for the lesions of strangles F
Haemorrhagic diarrhoea can be a clinical sign of strangles F
Strangles is caused by Staphylococcus aureus subsp. aureus. F
Strangles is treated with polymyxins. F
When abscesses develop in strangles, the prognosis is poor. F
The causative agent of strangles is obligate pathogen .T
Strangles has disappeared, due to extensive vaccination of the foals. F
Mortality of strangles is high .F
Strangles disappeared because of widespread vaccination of the foals. F
Carriage of the agent of strangles can be confirmed by isolation from the tonsils. F
Strangles pathogen is usually present on mucous membranes. F
The causative agent of strangles are an epiphyte. F
Prognosis of strangles is bad if an abscess rupture. F
The causative agent of strangles is present in all horses. F
The agent of strangles is carried by the majority of horses on the mucous membranes. F
Diarrhoea is a typical sign of strangles. F
Animals with strangles generally do not have fever. F
The agent of swine erysipelas is Erysipelothrix Suis F
Swine erysipelas can mainly be seen in winter after introduction of carrier animals. F
Swine erysipelas can mainly be seen in winter after introduction of carrier animal F
Sheep are generally infected with the agent of swine erysipelas per os F
Vaccines against swine erysipelas give only serotype specific protection F
Swine erysipelas cannot be treated with antibiotics because the course of the disease is very fast. F
Swine erysipelas cannot be prevented with vaccinations. F
There are no vaccines for the prevention of swine erysipelas. F
The agent of swine erysipelas can infect only pigs. F
Vaccines against swine erysipelas give only serotype specific protection. F
Humans can be infected with the agent of swine erysipelas by eating meat of infected pigs. F
Vaccines against swine erysipelas give only serotype specific protection. F
In the case chronic swine erysipelas pneumonia is a frequent clinical sign. F
The agent of swine erysipelas can frequently cause fibrinous pneumonia F
Erysipelas can be seen only in pigs. F
Polymyxins are used for the treatment of erysipelas. F
Erysipelas affects only pigs. F
Only pigs can be infected with Erysipelothrix rhusiopathiae.F
Purulent pneumonia is a typical clinical form of acute erysipelas. F
There is a serotype-specific protection against swine erysipelas. F
The swine erysipelas bacterium is an obligate pathogen. F
Acute erysipelas causes moderate fever. F
Endocarditis is seen in acute erysipelas. F
Erysipelothrix rhusiopathiae is not resistant, it cannot survive in the environment. F
The causative agent of swine erysipelas is an epiphyte. F
“Strong” erysipelas comes together with mild fever. F
There is a serotype specific protection in case of erysipelas. F
Diarrhoea is a frequent clinical sign of listeriosis in sheep F
Diarrhoea is a frequent sign of listeriosis in sheep F
Clinical signs of listeriosis generally seen in the summer F
Listeriae do not cause bacteraemia or septicaemia; they travel only along the nerves F
Listeriosis has very severe clinical signs in pigs F
Listeriosis is prevented by widespread vaccination using attenuated vaccines F
Listeriosis spread very fast in an infected herd from animal to animal. F
Abortion is the most frequent clinical sign of listeriosis in sheep F
Listeria ovis is the agent of listeriosis. F
Listeria are spreading fast from animal to animal. F
Listeriosis spreads from animal to animal and causes high mortality. F
Listeriosis can only be seen in sheep. F
Aerogen infection is the most important form of infection with Listeria in sheep. F
Listeria can be found only in infected animals, they cannot survive in the environment. F
Listeria are transmitted from animal to animal very fast in the infected flock. F
There is widespread vaccination for the prevention of listeriosis. F
The main clinical sign of listeriosis in sheep is pneumonia. F
Vaccination of sheep against listeriosis with inactivated vaccines is widely done in Europe. F
Listeria are not resistant, they cannot survive in the environment. F
Pneumonia is a frequent clinical sign of listeriosis. F
Listeriosis is the most common neurological disease in cattle .F
Listeriosis occurs more frequently during the summer, at time of silage-making. F
In the case of listeriosis of cattle, signs of the nervous system are the most frequently seen.
F
Listeriosis occurs only in tropical areas. F
Neurological symptoms are the most common clinical sign of listeriosis in cow. F
Listeriosis occurs in the summer. F
Listeriosis occurs only in ruminants. F
Corynebacterium pseudotuberculosis can be transmitted between goats and horses. F
Pseudotuberculosis does not occur in Hungary. F
In pseudotuberculosis, only submandibular lymph nodes of sheep are affected. F
Caseous lymphadenitis of sheep occurs in tropical countries but not in Europe F
The agent of Caseous lymphadenitis of sheep can be transmitted to horses and it will cause ulcerative lymphangitis F
Caseous lymphadenitis does not occur in goats and cattle F
Caseous lymphadenitis of sheep is an acute disease F
Clinical signs of caseous lymphadenitis can only be seen in sheep F
Caseous Lymphadenitis of sheep is mainly seen in suckling lambs F
Lesions of caseous lymphadenitis of sheep can be seen only in the lymph nodes. F
Caseous lymphadenitis can occur only in sheep. F
Caseous lymphadenitis is caused by nitrate positive strains of Corynebacterium pseudotuberculosis. F
Caseous lymphadenitis is only seen in suckling lambs .F
Antibiotics cannot be used for the treatment of caseous lymphadenitis. F
Caseous lymphadenitis of sheep occur only in the tropics. F
Caseous lymphangitis is seen mostly in sheep. F
Caseous lymphangitis does not occur in Hungary. F
Caseous lymphangitis can cause abortion in waves. F
Caseous lymphadenitis is caused by Corynebacterium equi. F
Sheep with caseous lymphadenitis can infect horses. F
Ulcerative lymphangitis of horses is caused by Corynebacterium equi F
Ulcerative lymphangitis of horses is caused by Corynebacterium equi F
Ulcerative lymphangitis of horses is caused by nitrate negative strains of Corynebacterium pseudotuberculosis. F
Ulcerative lymphangitis of horses is typically an acute disease. F
Ulcerative lymphangitis of horses is caused by Corynebacterium equi. F
Clinical signs of ulcerative lymphangitis can be mainly seen in suckling horses. F
Equine ulcerative lymphadenitis is an acute disease with high fever. F
Equine ulcerative lymphadenitis occurs only in tropical countries. F
Ulcerative lymphangitis is caused by nitrate negative C. pseudotuberculosis. F
Ulcerative lymphangitis does not occur in Hungary. F
Animals with clinical signs of ulcerative lymphangitis have good prognosis. F
Best way of prevention for ulcerative lymphangitis is toxoid vaccine. F
Corynebacterium renale causes septicaemia in cattle. F
Bovine pyelonephritis can be mainly seen in young calves F
Bovine purulent nephritis is mainly seen in suckling calves. F
Corynebacterium bovis is the causative agent of bovine pyelonephritis. F
Bovine pyelonephritis can mainly be seen in young calves under half a year of age. F
Pyelonephritis mostly occurs in horses. F
Bovine purulent nephritis is mainly seen in suckling calves. F
Facultative pathogenic mycobacteria can colonise only cold-blooded animals. F
Saprophytic and facultative pathogenic mycobacteria cannot colonise warm blooded animals. False
Facultative pathogenic Mycobacteria can only reproduce in the environment. F
Facultative pathogenic Mycobacteria can only colonize in warm-blooded animals. F
There is no antigen connection between facultative and obligate pathogenic mycobacteria f
Pigs are resistant against Mycobacterium tuberculosis. F
Lympho-haematogenous spread of mycobacteria can be seen in the post primary phase of tuberculosis. F
Mycobacterium bovis can cause tuberculosis only in ruminants F
Tuberculin is the toxin produced by mycobacteria. F
Antibodies against mycobacteria are detected in the tuberculin test F
Facultative pathogenic mycobacteria cannot cause tuberculosis F
Mycobacteria cannot be stained F
All mycobacteria species are obligate pathogenic. F
The resistance of mycobacteria is low, they die in the environment soon. F
Fresh tuberculosis lesions in the lymph nodes are common in the post primary phase F
Pigs are resistant against Mycobacterium tuberculosis F
Mycobacterium caprae can infect only goats. F
The habitat of the obligate pathogenic Mycobacteria is the environment. F
Only Mycobacterium tuberculosis can cause tuberculosis in humans. F
Neutrophil granulocytes can be typically found in tubercles. F
The tuberculin contains lipopolysaccharide (LPS) antigens. F
Mycobacterium tuberculosis causes generalized tuberculosis in badgers. F
Mycobacterium tuberculosis causes tuberculosis in poultry. F
The tuberculin contains lipopolysaccharide (LPS) antigens. F
All mycobacteria can replicate in the environment. F
If the increase of the thickness of the skin fold in the tuberculin test is 1.9 mm the reaction is positive. F
Mycobacteria can survive in the environment only for a few days. F
Saprophytic, facultative pathogenic mycobacteria cannot cause tuberculosis. F
Only cattle maintain bovine tuberculosis. F
Mycobacteria are not resistant, they can survive in the environment for maximum of two days. F
Mycobacterium suis is the most frequent agent of tuberculosis of pigs. F
Mycobacteria cannot be cultured. F
Köster staining is a special staining for Mycobacteria. F
In the phase of early generalization Mycobacteria do not replicate in the lymph node. F
Chronic tuberculosis causes changes in the lymph node. F
Tuberculosis can be diagnosed with certainty serology. F
M. tuberculosis is a common mycobacterium infection of pig. F
Facultative pathogenic mycobacteria can cause generalized tuberculosis in pigs. F
The habitat of pathogenic mycobacteria is the soil. F
The habitat of facultative pathogenic mycobacteria is the soil. F
Only cattle are susceptible to Mycobacterium bovis. F
Mainly proliferative lesions can be seen in the late generalization phase of bovine tuberculosis. F
If the tuberculin test is negative, it has to be repeated immediately. F
The tuberculin test in cattle can be false negative if the animal is infected with facultative pathogenic mycobacteria. F
The tuberculin test in cattle can be false negative if the animal is infected with Mycobacterium tuberculosis. F
If the resistance of the animal is high, mainly exudative lesions of tuberculosis can be seen. F
In the case of bovine tuberculosis always exudative lesions can be seen. F
Europe is free from bovine tuberculosis; bovine tuberculosis does not occur in Europe at all. F
Rifampicin is frequently used for the treatment of bovine tuberculosis. F
In case of infection with mycobacterium bovis the reaction against bovine and avian tuberculin is about the same in cattle: F
The incubation time of bovine tuberculosis is 1-2 weeks
F
Dermatitis nodosa is caused by mycobacterium bovis:
F
The skin intradermal tuberculin test can be repeated within a week if necessary. F
The tuberculin test is inconclusive if the increase of the thickness of the skin fold is 3.2 mm and it is painful. F
Cattle are vaccinated every year in order to prevent tuberculosis. F
If the increase of thickness of the skin fold in the tuberculin test is 4.1 mm, the reaction is inconclusive. F
Intestinal tuberculosis has no clinical signs in cattle. F
Vaccines are widely used to prevent bovine tuberculosis. F
Mycobacterium bovis cannot cause tuberculosis in pigs. F
Parallergy lasts lifelong in the case of cattle. F
Parallergy results in false negative reaction in the tuberculin test. F
If the thickness of the skin is increased with 3.4 mm in the tuberculin test and local lesions are present, test is inconclusive. F
Tuberculotic cattle are treated with antibiotics for at least three weeks. F
If the intradermal tuberculin test is inconclusive, it has to be repeated within a week. F
At most cases bovine tuberculosis has a rapid, acute progression. F
Bovine tuberculosis shows clinical signs mainly under the age of 6 months. F
The main pathogen causing bovine tuberculosis is Mycobacterium tuberculosis. F
Bovine tuberculosis only affects the lungs. F
Tuberculosis cannot infect cattle per os.F
Tuberculosis in cattle occurs especially in young animals. F
Cattle tuberculosis can be diagnosed by serological methods. F
Cattle tuberculosis is always generalized. F
Tuberculosis in cattle is prevented with frequent vaccinations. F
Cattle are infected with M. bovis mainly per os and enteric tuberculosis is most frequent.
F
Cattle infected with M. bovis will carry the bacterium for a maximum of 1 year. F
Vaccination of 6-month-old calves with BCG vaccine will result eradication of tuberculosis. F
In cattle extrapulmonary tuberculosis does not occur. F
Late generalization is characterized by productive processes. F
The skin intradermal tuberculin test is negative if the thickness of the skin increased by 4.5 mm. F
Tuberculin test can detect about 50% of the infected animals. F
The skin intradermal tuberculin test is negative if the thickness of the skin increased by 4.1 mm. F
During the general tuberculin test we give the tuberculin SC or IV. F
In case of para-allergic reaction we perform a test-cut.F
In the case of avian tuberculosis, no tubercles are formed. F
Avian tuberculosis is caused by Mycobacterium gallinarum. F
The most severe form of avian tuberculosis can be seen in 1-4 week old chicken: F
Mycobacterium avium subsp avium causes tuberculosis in humans: F
Poultry are widely vaccinated for the prevention of avian tuberculsosis F
Avian tuberculosis is very frequent in large scale poultry farms. F
Avian tuberculosis is mainly seen in chicken below 2 months of age. F
Avian tuberculosis is treated with penicillin and tetracyclines. F
Only Mycobacterium avium subsp. Avium can infect birds. F
Avian tuberculosis has been eradicated in Europe. F
Avian tuberculosis can be typically seen in old, adult birds .F
The agent of avian tuberculosis cannot survive in the environment, its resistance is low F
Avian tuberculosis usually occurs at 6-8 weeks of age. F
Avian tuberculosis result in local processes. F
Avian tuberculosis is a common disease in large scale farms causing high economic losses. F
Waterfowl are more susceptible to avian tuberculosis. F
Crepitation during liver transection is characteristic for avian tuberculosis. F
The resistance of the agent of paratuberculosis is low, it cannot survive in the environment.
F
Paratuberculosis occurs most frequently in pigs: F
Fibrinous pneumonia is a typical lesion of paratuberculosis: F
The agent of paratuberculosis is shed only after the appearance of the clinical signs: F
The most severe clinical signs of Paratuberculosis can be seen in suckling calves F
Lesions are seen in the lungs of animals infected with paratuberculosis F
Paratuberculosis has been eradicated from Europe. F
The clinical signs of paratuberculosis is more severe in calves than in adults. F
Dyspnoea and nasal discharge are the main clinical signs of paratuberculosis. F
Paratuberculosis occurs mainly in the tropical and subtropical countries. F
The clinical signs of paratuberculosis are more severe in sheep than cattle. F
Paratuberculosis is seen in young calves. F
In the case of paratuberculosis tuberculi can be seen in the anterior lobes of the lungs. F
Paratuberculosis can be treated with polymyxins. F
Lesions of the paratuberculosis are localized in the small and large intestine. F
In paratuberculosis, the nodules are seen primarily in the large intestine. F
Young animals are resistant to paratuberculosis. F
he disease paratuberculosis can develop in animals above 2 months. F
In Paratuberculosis, nodules can be found in intestinum crassum. F
Young animals are more susceptible to paratuberculosis. F
Foot rot is more severe in cattle than in sheep. F
Foot rot occurs only in sheep: F
the main virulence factors of dichelobacter nodosus are toxins: F
Foot Rot cannot be prevented by vaccination F
Morbidity of foot rot is very low, 1-5%. F
Foot rot cannot be prevented with vaccination. F
Foot rot has more severe clinical signs in goats than sheep. F
Exotoxins of the causative agent are responsible for the lesions of foot rot. F
Toxins are the main virulence factors of Dichelobacter nodosus. F
Foot rot is a very rare disease in Europe. F
Dichelobacter causes Necrobacillosis. F
The causative agent of foot root can produce exotoxins. F
Aerosol infection is a common form of transmission of the agent of necrobacillosis. F
Abortion is a frequent clinical sign of necrobacillosis:
F
calf diphtheria is caused by Dichelobacter nodosus:
F
Fusobacterium necrophorum subsp. funduliforme is the agent Necrobacillosis in lambs. F
Pulmonary necrosis is a frequent lesion of necrobacillosis of lambs. F
Fusobacterium funduliforme is the causative agent of Necrobacillosis. F
Focal necrosis in the kidney is a frequent post mortem lesion of Necrobacillosis. F
Necrobacillosis is prevented with wide vaccination. F
Necrobacillosis can only be seen in lambs. F
In the case of Necrobacillosis, aerogenic infection is common. F
Fusobacteria are highly resistant, they remain viable in the environment for several weeks. F
Necrobacillosis is a generalized disease with high fever and depression. F
Vaccines containing attenuated agents are widely used to prevent Necrobacillosis. F
Necrobacillosis is caused by Dichelobacter nodosus. F
Foot rot is the main sign of Necrobacillosis. F
The lesions in Necrobacillosis are restricted to the mouth. F
Necrobacillosis occurs mainly in young animals. F
There is no treatment for Necrobacillosis. F
You can find liver abscesses in case of Necrobacillosis. F
Bovine actinomycosis is typically a generalised disease. False
Actinomycosis is a notifiable disease. F
actinomyces species can cause diseases mainly in birds: F
Actinomyces species can be found mainly in the northern hemisphere. F
Arthritis is the most frequent clinical sign of canine actinomycosis F
Clinical signs and pathological findings of canine actinomycosis and nocardiosis are generalized. F
Actinomyces bovis is the causative agent of wooden tongue, it generally attacks soft tissues.
F
Wooden tongue is caused by Actinomyces bovis in cattle. F
Bovine actinomycosis is caused by Actinomyces lignieresii. F
Distortion of the mandibula or maxilla are the typical sessions of swine actinomycosis. F
Canine actinomycosis is caused by Actinomycosis canis. F
Prolonged antibiotic therapy is needed to the treatment of actinomycosis. F
Use of attenuated vaccines against actinomycosis is widespread. F
Actinomycosis is prevented with wide vaccination. F
In the case of bovine actinomycosis the lesions are localized in the udder. F
Actinomycosis is mainly an acute disease. F
In bovine actinomycosis, the first changes are seen in the udder. F
Actinomyces causes a generalized infection. F
Dogs are resistant to actinomycosis. F
Actinomyces viscosus can infect the udder of sow. F
A. israelii is the causative agent if canine actinomycosis. F
Actinomycosis bovis can cause udder infection in horses. F
Dogs can be infected by Actinomyces bovis. F
Vaccines in cattle can be efficient for prevention of the actinomycosis disease. F
Actinomycosis is a gram-negative bacterium. F
Horses are most sensitive to Actinomyces israelii. F
Lumpy jaw is a frequently seen disease in cattle herds with high morbidity. F
Pneumonia is a frequently seen pathological finding in bovine nocardiosis. F
Nocardia species are really fastidious bacteria which can grow on mucous membranes only.
F
Nocardia bacteria can cause inflammation of the lymphatic vessels. F
Nocardia species are Gram negative coccoid rod shaped bacteria: F
Most susceptible species to Nocardiosis are dog and horse. F
Disseminated Nocardiosis in dog occurs after 1 year of age. F
Nocardiosis will cause acute mastitis in cattle. F
Nocardia is a facultative aerobic bacterium. F
Rhodococcus equi causes mainly metritis and urinary tract infections. F
Only moderately virulent Rhodococcus equi strains can cause disease in foals. F
Rhodococcus equi can cause a disease mainly in swine: F
Rhodococcus equi infection is a notifiable disease. F
Rhodococcus equi can cause pneumonia and lymphadenitis in 6 to 18 months-old foals. F
Rhodococcus equi mainly causes CNS clinical signs in 1-4-month-old foals. F
Rhodococcus equi can cause lesions only in horses. F
Rhodococcus equi can generally cause disease in foals above 6 months of age. F
There is widespread vaccination to prevent diseases caused by Rhodococcus equi. F
Rhodococcus equi can cause pneumonia in 1-3 years old foals. F
Interstitial pneumonia is the main lesion caused by Rhodococcus equi in foals. F
Pneumonia caused by Rhodococcus equi can be successfully treated with colistin. F
Rhodococcus equi causes interstitial pneumonia in foals. F
Rhodococcus equi can cause only pneumonia in foals. F
Rhodococcus equi can cause pneumonia in foals of 5-6 months of age. F
Serous pneumonia is caused by Rhodococcus Equi. F
Pneumonia caused by Rhodococcus equi is treated with penicillin. F
R. equi causes pneumonia in foals aged 6-8 months. F
R. equi pneumonia is transmitted from foal to foal. F
R. equi causes severe catarrhal pneumonia. F
Pneumonia caused by R. equi can be treated with rifampicin and erythromycin for 4-5 days.
F
R. equi is an obligate anaerobic bacterium. F
Rhodococcus equi is usually seen during the winter. F
Foals suffering from Rhodococcus equi can be treated with any antibiotic. F
Pneumonia caused by R. equi is a fast spreading acute disease. F
The agents of dermatophilosis cannot survive in the environment, they are mainly transmitted by arthropods. F
dermatophilus hyicus causes exudative dermatitis in piglets: F
Treatment is not allowed in the case of dermatophilosis, eradication of the disease is our primary aim. F
Treatment of dermatophilosis is based on antifungal agents. F
The most susceptible animal species which shows clinical signs of dermatophilosis is the dog.
F
Dermatophilosis is caused by Dermatophilus bovis. F
Dermatophilosis occurs only in tropical and subtropical regions. F
The agent of dermatophilosis is not resistant, it cannot survive in environment. F
Focal necrosis in the parenchymal organs is a typical lesion of dermatophilosis. F
Dermatophilus bovis causes dermatophilosis. F
At dermatophilosis in the parenchymal organs inflammatory-necrotic nodules can be observed. F
Dermatophilosis can be generalized. F
Dermatophilosis can affects also birds and plants. F
Dermatophilosis occurs only in Africa. F
Focal inflammation in the liver is a typical lesion of dermatophilosis. F
Enterotoxigenic Escherichia coli strains are responsible for oedema disease. F
The enterotoxins of E. coli inhibit the protein synthesis. F
The verotoxigenic E. coli strains cause septicaemia of calves. F
Verotoxins are the virulence factors of enterotoxic E. coli strains. F
Fimbria is the virulence factor of enteropathogenic E. coli strains. F
E. coli strains always cause generalized infections in animals. F
Enterotoxins of E. coli cause severe inflammation in the small intestines. F
Enteropathogenic Escherichia coli strains cause neonatal diarrhoea in calves and piglets. F
Verotoxigenic Escherichia coli strains frequently cause septicaemia in chicken. F
Verotoxins are virulence factors of septicemic Escherichia coli strains. F
Enterotoxins are virulence factor enteropathogenic Escherichia coli strains. F
The enterotoxic E. coli strain produces verotoxins. F
The enterotoxic E. coli strains cause oedema disease. F
Enterotoxic E. coli strains attach to enterotoxins. F
Enterotoxin cause enteritis in the large intestine. F
High fever is a common clinical sign of neonatal coli diarrhoea of calves. F
Lack of umbilical disinfection can be a predisposing factor for coli- diarrhoea of calves. F
Bovine coli septicaemia is caused by verotoxigenic Escherichia coli strains F
Severe necrotic enteritis occurs in the case of coli diarrhoea of new-born calves. F
E. coli strains which cause calf diarrhoea harbour F4, F6 or F18 fimbrial-antigens.F
E. coli strains that cause coli-diarrhoea of new-born piglets have F17 fimbrial antigens: F
Coli septicaemia of calves can be diagnosed by isolation of E. coli from the small intestine: F
calves are vaccinated with inactivated vaccines in order to prevent coli septicaemia: F
E. coli O157:H7 strains can cause haemorrhagic enteritis in cattle: F
peroral antibacterial treatment of calves is advisable for treatment of coli-septicaemic calves: F
Coli septicaemia of calves is seen most frequently after weaning: F
Calves have to be vaccinated at the age of 2 and 4 weeks for the prevention of coli diarrhoea. F
Severe diarrhea is a typical clinical signs of Bovine coli septicaemia. F
Severe watery diarrhoea is a clinical sign of coli septicaemia of calves. F
Coli diarrhoea of calves is typically seen in 3-4-week-old calves. F
Enteritis in the large intestine is a typical post mortem sign of coli-diarrhoea of calves. f
Enterotoxigenic E. coli strains are the causative agents of E. coli septicaemia of calves. F
In the case of E. coli septicaemia in calves, diarrhoea generally cannot be seen. f
High fever is a typical sign of coli diarrhoea of calves. F
Severe inflammation in the small intestine can be seen in the case of coli diarrhoea of calves.
F
Verotoxins are responsible for the clinical signs of coli septicaemia of calves. F
Severe watery diarrhoea is a typical sign of coli septicaemia of calves. F
Coli diarrhoea of calves typically occurs after weaning. F
There are no vaccines for the prevention of coli diarrhoea. F
At coli septicaemia of calves, the clinical signs are caused by the enterotoxins. F
Coli septicaemia of calves can be diagnosed by measuring antibodies. F
Coli-septicaemia of cattle can occur at any age. F
Coli-diarrhoea of calves is caused by verotoxic E. coli strains. F
Coli-diarrhoea of calves is caused by E. coli strains equipped with fimbriae. F
In coli-diarrhoea of calves we can see severe inflammation of the colon. F
Coli-diarrhoea of the calf is characterised by a severe inflammation of the large intestine. F
Transport is the most important predisposing factor in coli-diarrhoea. F
Coli-septicaemia is a disease of weaned calves. F
Coli-septicaemia causes severe haemorrhagic diarrhoea. F
Transportation is an important predisposing factor of coli-septicaemia. F
Pneumonia is an important clinical sign of coli-septicaemia in calves. F
Calf dysentery is caused by enterotoxigenic E. coli strains. F
In the case of calf dysentery, not only calves but cows also show severe diarrhoea. F
Calf dysentery is caused by enteropathogenic E. coli strains. F
Morbidity and mortality of calf dysentery are very high. F
Oedema disease of weaned piglets is caused by enterotoxigenic E. coli strains. F
Oedema disease occurs most frequently in calves. F
High fever is a typical clinical sign of coli diarrhoea of new-born piglets. F
E. coli strains that cause coli-diarrhoea of new-born piglets have F17 fimbrial antigens. F
Coli-diarrhoea of new-born piglets are caused by enteroinvasive E.coli strains. F
Verotoxigenic Escherichia coli strains cause neonatal coli diarrhoea of pigs. False
Verotoxigenic E.coli strains can cause disease in 2-8-day-old piglets False
Inflammations of the large intestine is a post mortem lesion of coli diarrhoea of neonatal piglets F
animals showing clinical signs of oedema disease are recommended to be treated with penicillin: F
enterotoxigenic Escherichia coli strains are responsible for oedema disease: F
There is widespread vaccination for the prevention of oedema disease: F
diarrhoea with yellowish faeces is a characteristic clinical sign of oedema diseases of weaned piglets: F
Oedema disease is caused by enteropathogenic Escherichia coli strains: F
In case of coli diarrhoea of new-born piglets, septicaemia is frequent: F
Vero-toxins produced by E. coli strains cause diarrhoea in pigs. F
Haemorrhagic diarrhoea is typical in the case of coli diarrhoea of newborn piglets. F
There are no vaccines to prevent coli diarrhoea of newborn piglets. f
Oedema disease occurs in pigs and calves. F
Oedema disease is caused by enteropathogenic E. coli strains. F
Severe diarrhoea is a typical clinical sign of oedema disease. F
Clinical cases of oedema disease can be successfully treated with parenteral penicillin injections. F
Oedema disease typically occurs in 2-3-week-old piglets. F
Oedema disease can occur at any age. F
Severe diarrhoea is a frequent sign of oedema disease. F
Vaccination of the sows is widely used in order to prevent oedema disease. F
Mainly viral infections predispose weaned piglets to coli-diarrhoea. F
Oedema formation is the main clinical sign of coli-diarrhoea of weaned piglets. F
E. coli diarrhoea in swine occurs in sows in their first pregnancy. F
There are no vaccines to prevent coli-diarrhoea of newborn piglets. F
Less colostrum is a predisposing factor for coli-diarrhoea in weaned pigs. F
Coli-diarrhoea of weaned piglets is generally prevented by vaccinating sows . F
Verotoxins are involved in the pathogenesis of coli-diarrhoea in suckling piglets. F
Oedema disease of swine occurs before weaning. F
Oedema disease is seen mainly in large scale farms with poor hygiene. F
n oedema disease, antibiotics are used to treat diseased piglets F
Oedema disease occurs in the first week of life. F
Verotoxins cause diarrhoea in young piglets. F
Oedema disease of swine occurs at 1-2 weeks old. F
Insufficient colostrum is an important predisposing factor for oedema disease. F
Germinative infection does not occur in the case of e. coli diseases of poultry. F
Enterotoxigenic Escherichia coli strains are responsible for coli-disease of poultry F
Enterotoxigenic e.coli causes death in young chicks. F
E. coli strains cannot cause germinative infection in chicken. F
E. coli can cause clinical signs only in chicken below of 2 weeks of age. F
E. coli disease of poultry is zoonotic. F
Isolation of Escherichia coli from the faeces confirms diagnosis of coli septicaemia of poultry.
F
Escherichia coli can cause only local lessons in chicken, it cannot be generalized. F
Enterotoxigenic E. coli strains can cause septicaemia in day old chicken. F
Enterotoxigenic E. coli causes death in young chicks. F
E. coli disease in poultry mostly occurs in layers at beginning of egg-laying period. F
E. coli disease in poultry causes severe encephalitis in septicaemic form. F
Vaccines can be used for the prevention of E. coli disease in poultry. F
Retarded absorption of the yolk sack is a post mortem lesion in coli-septicaemia in chickens.
F
Verotoxigenic Escherichia coli strains cause coli-diarrhoea of rabbits. F
Coli-diarrhoea of rabbits is typically seen in suckling animals. False
Enterotoxigenic E. coli strains are the causative agents of E. coli diarrhoea in rabbits. F
There is widespread vaccination in order to prevent E. coli diarrhea in rabbits. F
Coli diarrhoea of rabbits is mainly seen in the first week of life. F
Coli diarrhoea is prevented by widespread vaccination of the mothers. F
Insufficient amount of milk predisposes rabbits to coli-diarrhoea. F
Salmonella typhi is a zoonotic agent: F
Salmonella abortion of ewes can be diagnosed by detecting the agent from the faeces of ewes: F
Salmonella enterica subsp. Arizonae strains mainly cause salmonelloisis in pigs. F
Asymptomatic carriage of salmonellae does not occur in animals. F
In the case of generalized salmonellosis, the agent has to be isolated from the faces. F
After antibiotic treatment, no salmonella carriers remain in the flock. F
Sexual transmission is common in the case of certain salmonella diseases. F
Salmonella diseases are always limited to the gut. F
Salmonella Typhi is an obligate pathogen, it is the causative agent of fowl typhoid. F
Only per os infection occurs in the case of salmonellosis. F
Salmonella diseases are always acute in animals. F
After recovering from a salmonella disease, animals do not shed the bacterium any more F
All Salmonella species are zoonotic. F
Salmonella are generally resistant bacteria. F
Exotoxins are important virulence factors of salmonella. F
An allergic test can confirm salmonellosis. F
Septicaemia is always seen in salmonellosis. F
Abortion is the main clinical form of human salmonellosis. F
All serotypes of salmonellae can cause salmonellosis in humans. F
Abortion is the main clinical form of human salmonellosis F
All salmonella serotypes are zoonotic. F
Human salmonellosis is always limited to the gastrointestinal tract. F
In the case of diarrhoea caused by salmonella in humans, penicillin treatment is recommended. F
Septicaemia is the most common presentation of human salmonellosis. F
We use tetracyclines in the treatment of human gastroenteritis caused by Salmonella spp. F
All Salmonella serotypes can infect humans. F
Salmonella Typhi is a zoonotic agent. F
The agent of swine typhoid mainly replicates in the small intestine. F
The agent of swine typhoid can cause lesions only in the gut. F
Swine typhoid mainly occurs in suckling piglets. F
salmonella choleraesuis is the causative agent of swine typhoid: F
the agent of swine typhoid replicates only in the gut, it cannot get into the blood: FALSE
swine typhoid is a very frequent disease in Europe nowadays: F
Swine typhoid is an acute disease: F
Lesions of swine typhoid are always limited to the intestine. F
Swine typhoid is an acute disease; it is spreading fast in the herd F
Infection caused by S. Typhisuis is limited to the intestine. F
Swine typhoid is caused by Salmonella Choleraesuis. F
Salmonella Choleraesuis is an obligate pathogen. F
Swine typhoid is treated with penicillin. F
Swine typhoid is limited to the intestine, it cannot cause bacteremia. F
Lesions of swine typhoid can be seen in the small intestine. F
Swine typhoid is an acute disease of swine. F
Salmonella typhisuis can infect ruminants and swine. F
Swine typhoid occurs only in piglets between 2-5 months. F
Swine typhoid is a frequent disease on large scale farms. F
The agent of swine typhoid can only replicate in the gut. F
Salmonella typhisuis is widespread in different animal species. F
Salmonella typhisuis can cause a fast spreading infection in the herd. F
Swine typhus causes significant economic losses in larger farms. F
Salmonella enteritidis causes swine typhus. F
Swine typhus is usually an acute disease. F
Swine typhus only affects the intestines. F
Salmonella typhisuis causes paratyphoid in swine. F
Swine typhoid is a frequent disease in Europe causing high losses. F
Killed vaccines are used to prevent swine typhoid. F
Swine typhoid is spread by rodents. F
In swine typhoid transport is an important predisposing factor. F
Swine typhoid are mostly seen in 2-3-week-old piglets. F
Serology is an important tool to identify S. Typhisuis. F
In swine typhoid, pathological changes are seen in the whole intestines. F
Swine typhoid is caused by S. typhi. F
Swine paratyphoid is mainly seen in suckling piglets. F
The agent of swine typhoid can infect pigs, dogs, cats and humans. F
Antibiotic treatment isn’t allowed in the case of swine paratyphoid: F
swine paratyphoid is caused by obligate pathogenic bacteria: F
swine paratyphoid has been eradicated from Europe: F
Swine paratyphoid generally occurs in all age groups. F
Only Salmonella Typhimurium can cause swine paratyphoid. F
Antibiotics are not used for the treatment of swine paratyphoid. F
Salmonella Choleraesuis is the only agent of swine paratyphoid. F
Salmonella Choleraesuis is an obligate pathogenic bacterium. f
Swine paratyphoid typically occurs in neonatal piglets, in the first week of life. F
Swine paratyphoid is a sporadic rare disease. F
Swine paratyphoid occurs in piglets between 2-5 weeks of age. F
Swine paratyphoid is caused by S. typhisuis. F
Hyperemic enlargement of the spleen is typical in the case of swine paratyphoid. F
In case of swine paratyphoid, it is easy to diagnose in the faeces. F
The lesions of typhlocolitis can be seen in the small intestines. F
In the case of Typhlocolitis swine the agent can be isolated from the liver in large number. F
Swine typhlocolitis is a common disease with high mortality. F
High fever is an important clinical sign in case of swine typhlocolitis. F
The enterotoxins of the agents are responsible for the clinical signs and lesions of salmonellosis of cattle. F
Treatment of bovine salmonellosis with antibiotics is not recommended. F
Agents of bovine salmonellosis do not infect humans. F
There are no vaccines for the prevention of bovine salmonellosis. F
Salmonella bovis is the causative agent of bovine salmonellosis F
Bovine salmonellosis is always limited to the gut: F
salmonellosis of cattle occurs mainly in day-old calves: F
Salmonella is seen in the large intestine of cattle F
Lack of appropriate provision of colostrum can predispose calves to salmonellosis. F
Salmonella Typhi is a frequent agent of salmonellosis of calves. F
There are no vaccines against salmonellosis of calves. F
Salmonellosis of calves is seen mainly in the first week of life. F
Humans cannot be infected with salmonellae from calves. F
Salmonellae do not enter the blood stream in calves. F
Salmonellosis does not occur in cattle in Europe anymore because of successful eradication.
F
Salmonellosis in calves typically occurs in 1-2-week-old calves. F
Salmonella Paratyphi can cause salmonellosis of calves. F
Salmonellosis does not occur in sheep. F
Salmonella typhimurium is obligate pathogenic bacterium. F
Salmonella bovis is the most frequent causative agent of bovine salmonellosis. f
Salmonellosis of calves only effects the intestines. F
Salmonellosis in cattle is mainly cause by Salmonella bovis strains. F
Salmonellosis in cattle is spread mainly in aerogenic way. F
Diarrhoea without fever is a typical clinical sign of bovine salmonellosis. F
Salmonellosis in cattle, lesions are mostly seen in the stomach. F
S. abortusovis can cause sporadic abortions in cattle. F
Salmonella in calves can be treated successfully with penicillin. F
We can use isolation or ELISA for detection of Salmonellosis in cattle. F
Salmonella is seen in the large intestine of cattle. F
Viral diseases (bluetongue, border disease etc.) frequently predispose sheep to salmonellosis. F
Salmonella Ovis is the main agent of ovine salmonellosis. F
salmonella abortusovis can cause abortion in sheep, goats and cow F
salmonella abortion of ewes can be diagnosed by detecting the agent from the faeces of ewes: F
Sheep are widely vaccinated for the prevention of abortion cause by Salmonellae spp. F
Salmonella Abortusovis can cause epididymitis and orchitis in rams. F
Sexual transmission is the main way of infection with Salmonella Abortusovis. F
Salmonella abortusovis is mainly transmitted at mating. F
Abortions caused by Salmonella abortusovis are prevented with widespread vaccination. F
Abortion caused by S. abortusovis is very common in goats. F
Venereal infection is the primary mode of infection in case of S. abortusovis. F
Vaccination is the best way to prevent S. abortusovis. F
Salmonella abortion of sheep occurs mainly in older ewes. F
Pregnant mares abort in the acute phase of salmonellosis. F
Salmonellosis of horses is limited to the gut; the agent cannot get into the bloodstream. F
salmonella abortion of mares happens always a few days before the expected birth F
Salmonellosis of horses occurs only in foals in the first month of life. F
Horses are regularly vaccinated in order to prevent salmonellosis. F
Foals are aborted in the febrile phase of salmonellosis. F
Mares are regularly vaccination with vaccine containing Salmonella typhimurium. F
Salmonellosis of horses occurs only in acute form. F
Salmonellosis of horses are always limited to gut. F
Vaccination against Salmonella abortusequi is widespread to prevent losses. F
Salmonella Equi is the main agent of equine salmonellosis. F
Diarrhoea is the only clinical sign of equine salmonellosis. F
Foal septicaemia in case of salmonellosis is highly age-related. F
Abortion caused by S. abortusequi occurs a few days after the infection. F
Salmonellosis of horses in abortive form, most often occurs in older mares. F
Abortion caused by S. abortusequi most often occurs in the 2nd trimester. F
Salmonella reduction programs aim the reduction only for S. Enteritidis and S. Typhimurium in breeding poultry flocks. F
In the salmonella reduction programs ELISA tests are used to recognize the carrier animals. F
Fowl typhoid occurs nowadays mainly in large scale farms. F
Fowl typhoid is caused by Salmonella Avium. F
The agent of fowl typhoid does not kill the embryo. F
No postmortem lesions can be seen in the case of fowl typhoid. F
Lesions of fowl typhoid is limited to the gut: F
fowl typhoid can be seen sporadically in zoo birds in Europe: F
The lesions of fowl typhoid are limited to the gut F
Fowl typhoid can be spread by aerogenic infection. F
Fowl typhoid is more frequent in water fowl than hens. F
The susceptibility to fowl typhoid is increasing with age. F
Fowl typhoid has no effect on hatching %. F
Fowl typhoid is a frequent disease in large scale farms. F
Fowl typhoid is caused by Salmonella Enteritidis. F
No post mortem lesions can be seen in the case of fowl typhoid. F
After recovery from fowl typhoid the animals do not remain carriers. F
Salmonella avium is the causative agent of fowl typhoid. F
Fowl typhoid is mainly seen in large scale poultry farms. F
In case of fowl typhoid, the death curve peak at age 5-6 weeks. F
Fowl typhoid can’t spread in a germinative manner. F
Fowl typhoid is caused by Salmonella avium. F
Fowl typhoid have an exponential loss curve. F
Fowl typhoid is caused by facultative pathogenic Salmonella. F
Rotting eggs are an important clinical sign of fowl typhoid. F
Fowl typhoid can be seen only in adult birds. F
Diarrhoea is not a typical clinical sign of fowl cholera. F
Fowl typhoid is more frequent in water fowl than hens. F
Fowl typhoid is usually a disease of waterfowl. F
The highest infection rate of fowl typhoid is between days 8-10. F
The susceptibility to fowl typhoid increases with age. F
Fowl paratyphoid is limited to the gut, there is no septicaemia. F
Fowl paratyphoid has been eradicated in Europe. F
salmonella avium is the main aetiological agent of fowl paratyphoid: F
Fowl paratyphoid is caused by Salmonella Gallinarum/Pullorum. F
Fowl paratyphoid alone occurs at any age. F
Salmonella gallinarum is the causative agent of fowl paratyphoid. F
Fowl paratyphoid cannot be seen in the European poultry flocks anymore. F
Lesions of fowl paratyphoid occur only in the intestinal tract. F
Fowl paratyphoid occurs typically in 2-5 months old poultry. F
Germinative infection does not occur in the case of fowl paratyphoid. F
There are no vaccines to prevent fowl paratyphoid. F
Salmonella derby is a frequent agent of fowl paratyphoid. F
Clinical signs of fowl paratyphoid are mainly seen in adult birds. F
Germinative infection does not occur in the case of fowl paratyphoid. F
Antibiotic treatment can prevent the carriage of salmonella, after fowl paratyphoid. F
Paratyphoid of poultry only affects the intestines. F
Paratyphoid of poultry affects adult animals mainly. F
The clinical signs of fowl paratyphoid can be seen mainly in adult hens. F
Fowl paratyphoid is a rare and sporadic disease. F
Fowl paratyphoid causes disease mainly in water fowl. F
We can certify “Salmonella-free” status of poultry stocks with serological tests. F
Yersinia enterocolitica does not infect humans. F
Lesions caused by Yersinia pseudotuberculosis are always limited to the gut. F
Only rodents are susceptible to Yersinia pseudotuberculosis. F
Yersinia pestis is endemic in certain countries of Europe. F
Yersinia pseudotuberculosis mainly causes respiratory clinical signs in cattle: F
yersinia pestis has been eradicated from earth: F
diseases caused by yersinia pseudotuberculosis occur only in tropical areas: F
Yersinia pestis has been eradicated from Earth: F
The Earth is free from plague. F
Only rats are susceptible to plague. F
Farm animals are regularly vaccinated to prevent infection caused by Yersinia pseudotuberculosis. F
Plague is caused by Yersinia pseudotuberculosis. F
Yersinia pseudotuberculosis is not a zoonotic agent. F
Yersinia enterocolitica can cause diarrhoea only in rodents. F
Only humans are susceptible to the agent of plague. F
Yersinia enterocolitica can infect only swine. F
Yersinia pseudotuberculosis cause tuberculosis in wild living animals F
Yersinia pseudotuberculosis can infect only rodents. F
Infection with Yersinia pseudotuberculosis is limited to the gut. F
Yersinia pseudotuberculosis can cause disease only in rodents. F
Yersinia pseudotuberculosis usually appears in tropical regions. F
Yersinia enterocolitica does not infect humans. F
The agent of yersiniosis cannot be cultured, PCR is the only way of its detection. F
Yersinia pseudotuberculosis can cause severe pleuropneumonia in rodents. F
Infection caused by Yersinia pseudotuberculosis is always limited to the gut. F
Y. enterocolitica has a narrow host range. F
Chronic lesions caused by Y. enterocolitica resemble the lesions of tuberculosis. F
Hare and chinchilla are most susceptible to Y. enterocolitica. F
Lesions are most often seen in the small intestines in case of Y. pseudotuberculosis. F
Y. pseudotuberculosis is normally present in rodents. F
Pasteurella multocida is highly resistant; it can survive in the environment for several months. F
Primary pasteurellosis disease have no predisposing factors. F
The dermonecrotoxin of Pasteurella multocida damages the osteoclast cells: F
Primary pasteurellosis diseases are caused by obligate pathogenic Pasteurella bacteria: F
Dermonecrotoxin of pasteurella multocida causes lesions in the nasal cavity and on the skin of pigs F
Enterotoxins are virulence factors of Pasteurella multocida: F
The agent of acute systemic pasteurellosis is zoonotic: F
Pasteurella ovis can cause pasteurellosis in small ruminants F
Leukotoxin is produced by the majority of Pasteurella multocida. F
Pasteurella multocida can cause disease only in ruminants.F
Pasteurellaceae are resistant bacteria, they remain viable for a long time in the soil. F
Pasteurella are very resistant in the environment. F
Pasteurella are obligate pathogens. F
Pasteurella bovis can cause pasteurellosis in cattle. F
Diarrhoea is the main clinical sign of bovine pasteurellosis. F
The lesions of respiratory pasteurellosis of calves are generally in the diaphragmatic lobes. F
Dermonecrotoxin of the agents is responsible for the clinical signs of respiratory pasteurellosis of cattle. F
Primary pasteurellosis diseases are caused by obligate pathogenic Pasteurella bacteria. F
Respiratory pasteurellosis occurs only among cattle above 6 months of age. F
The lesions of respiratory pasteurellosis of calves are generally in the diaphragmatic lobes. F
Interstitial pneumonia is a frequent post mortem lesion of pulmonary pasteurellosis of cattle. F
The pneumonic lesions in the case of pulmonary pasteurellosis of cattle can be seen mainly in the diaphragmatic lobe. F
Salmonellosis can predispose cattle to pasteurellosis. F
Bovine pasteurellosis cannot be prevented with vaccination. F
Respiratory pasteurellosis has been already eradicated in Europe. F
There are no vaccines for the prevention of respiratory pasteurellosis of cattle. F
The lesions of bovine respiratory pasteurellosis are generally seen in the diaphragmatic lobes. F
Respiratory pasturellosis of cattle are mostly seen in the tropics. F
Haemorrhagic septicaemia of cattle is generally a chronic disease. F
Bleeding from the nose is a frequent clinical sign of haemorrhagic septicaemia of cattle. F
Haemorrhagic septicaemia occurs most frequently among 2-3 month old calves in endemic areas. F
Haemorrhagic septicaemia is mainly seen in pigs and horses. F
After recovering from haemorrhagic septicaemia the animals do not shed the agent. F
Exotoxins are responsible for haemorrhagic septicaemia. F
Haemorrhagic septicaemia cannot be prevented with vaccines. F
Haemorrhagic septicaemia is mainly seen in pigs. F
Haemorrhagic septicaemia is endemic in several European countries. F
The lesions of haemorrhagic septicaemia are caused by the exotoxin of the agent. F
Haemorrhagic septicaemia is caused by Mannheimia haemolytica. F
The leukotoxin of the agent is responsible for the lesions of haemorrhagic septicaemia. F
Haemorrhagic septicaemia occurs only in tropical and subtropical countries. F
There are no vaccines for the prevention of haemorrhagic septicaemia. F
Re-convalescent animals do not carry the agent of haemorrhagic septicaemia after recovery.
F
The exotoxin of the causative agent is responsible for the lesions in haemorrhagic septicaemia. F
There is no functioning vaccine to prevent haemorrhagic septicaemia of cattle. F
The clinical signs of haemorrhagic septicaemia are caused by the dermonecrotoxin of the agent. F
Haemorrhagic septicaemia is mainly seen in 1-2 months old animals. F
Bleeding is the most typical clinical sign of haemorrhagic septicaemia. F
Haemorrhagic septicaemia infected animals carry the bacteria for 1 year. F
Haemorrhagic septicaemia is a slow and chronic disease. F
Haemorrhagic septicaemia of cattle occurs only in tropical countries. F
Secondary infection can occur with haemorrhagic septicaemia of cattle. F
Haemorrhagic septicaemia is mainly seen in sheep and horses. F
Septicaemic ovine pasteurellosis is mainly seen in pregnant animals. F
Pasteurella ovis can cause pasteurellosis in small ruminants. F
Acute systemic pasteurellosis is caused by Pasteurella multocida. False
septicemic pasteurellosis doesn’t occur in goats only in sheep: F
ewes have to be culled after mastitis caused by mannheimia haemolytica because the udder cannot regenerate: F
Enteritis is a frequent clinical sign of ovine pasteurellosis F
The agent of Acute Systemic Pasteurellosis is zoonotic. F
Respiratory pasteurellosis of sheep cannot be prevented with vaccines. F
Acute systemic pasteurellosis occurs in lambs that are younger than 3 months.F
Acute systemic pasteurellosis is caused by Mannheimia haemolytica. F
Acute systemic pasteurellosis occurs in sheep but not goats. F
Respiratory form of ovine pasteurellosis can be seen only in suckling lambs. F
Acute systemic pasteurellosis is caused by Pasteurella multocida. F
Lesions of ovine respiratory pasteurellosis are typically seen in the diaphragmatic lobe of the lungs. F
Mannheimia haemolytica can cause acute systemic pasteurellosis in sheep. F
Mannheimia haemolytica can produce dermonecrotoxin. F
Acute systemic pasteurellosis occurs in sucking lambs and kids. F
Nasal discharge and coughing for a week are the main clinical signs of acute systemic pasteurellosis. F
Acute systemic pasteurellosis is caused by type A and D of Pasteurella multocida. F
Respiratory pasteurellosis in sheep cannot be prevented with vaccination. F
Mannheimia haemolytica ́s endotoxin causes respiratory pasteurellosis in sheep. F
In respiratory pasteurellosis in sheep the cranial lung lobes are affected. F
Pasteurellosis does not cause septicaemia. F
Fibrinous pneumonia is the main post mortem lesion of acute systemic pasteurellosis. F
Serology is widely used to diagnose Pasteurella in sheep. F
The septicaemic form of pasteurellosis is most common in sheep above 1 year. F
You can see croupus pneumonia in case of ovine systemic pasteurellosis. F
Systemic pasturellosis is seen in 2-4-week-old lambs.F
In suckling lambs, acute systemic pasteurellosis may occur. F
Pasteurellosis in the sheep may cause interstitial pneumonia. F
Ιn the respiratory form of ovine pasteurellosis, haemorrhagic pneumonia is seen. F
Pulmonary pasteurellosis is more frequent in suckling piglets than in adults. F
Bordetella bronchiseptica predisposes pigs to pulmonary pasteurellosis F
Pulmonary pasteurellosis of pigs is mainly caused by Mannheimia hemolytica: F
respiratory pasteurellosis of pigs is generally an acute, generalized disease: F
Vaccines can prevent pneumonia of swine caused by pasteurella. F
Europe is free from atrophic rhinitis. F
The dermonecrotoxin of Pasteurella multocida damages the osteoclast cells. F
The most severe clinical signs of atrophic rhinitis can be seen in suckling piglets. F
The mortality and the economic impact of atrophic rhinitis are high: F
The endotoxin of the agent is responsible for the clinical signs and lesions of atrophic rhinitis
F
Atrophic rhinitis in fattening pigs is caused by Bordetella bronchiseptica. F
In 4-6 months old pigs B. bronchiseptica strains cause severe pneumonia. F
Atrophic rhinitis cannot be prevented with vaccination. F
The dermonecrotoxin of P. multocida inhibits the activity of the osteoclast cells. F
Atrophic rhinitis can be prevented by vaccinating the day-old piglets. F
Isolation of the causative agent from the nose confirm the diagnosis of atrophic rhinitis. F
The effects of the dermonecrotoxin produced by Pasteurella multocida are reversible. F
The mortality of atrophic rhinitis can be 50-60%. F
The lesions of atrophic rhinitis are caused by an endotoxin. F
Atrophic rhinitis cannot be prevented with vaccination. F
Hungary is free from atrophic rhinitis of swine. F
The clinical form of atrophic rhinitis can be seen if the piglets were few weeks old when infected F
The dermonecrotoxin of Pasteurella multocida damage the osteoclasts. F
Isolating Pasteurella multocida from pigs’ noses proves atrophic rhinitis. F
The endotoxin of the agent is responsible for the clinical signs and lesions of atrophic rhinitis
F
Atrophic rhinitis can be prevented with toxoid vaccine given at weaning. F
Atrophic rhinitis is examined PM by a longitudinal section of the nose. F
Animals showing signs of atrophic rhinitis remain carriers. F
Atrophic rhinitis cause disease in swine and calves. F
B. bronchiseptica can cause immunosuppression. F
B. bronchiseptica strains producing toxins causing serious lesions. F
The typical PM lesions of atrophic rhinitis are caused by B. bronchiseptica strain. F
Atrophic rhinitis is a common disease that causes severe losses. F
Atrophic rhinitis is proven by isolating P. multocida. F
Clinical signs of pasteurellosis in rabbits are most severe in new-born animals. F
Rabbit pasteurellosis causes only respiratory clinical signs. F
Mannheimia haemolytica causes rabbit pasteurellosis: F
Pasteurellosis is limited to the respiratory tract in rabbits. F
Bibersteinia trehalosi is the causative agent pasteurellosis of rabbits. F
Serous pneumonia is typical in the case of pasteurellosis of rabbits. F
Pasteurellosis is limited to the respiratory track in rabbits. F
Pasteurellosis is common in suckling rabbits. F
Fowl cholera is caused by Pasteurella gallinarum. F
The mortality of fowl cholera is low. F
Fowl cholera occurs mainly in the winter in Europe. False
The most severe form of fowl cholera occurs in day-old birds. False
The agent of fowl cholera is an obligate pathogenic bacterium: F
Antibiotics cannot be used for the treatment of fowl cholera: F
the exotoxin of the agent is responsible for the clinical signs of fowl cholera: F
inflammation of the wattle is a clinical sign of acute fowl cholera: F
Europe is free from fowl cholera: F
Fowl cholera is always an acute disease: F
Parent birds have to be vaccinated just before laying in order to prevent fowl cholera. F
Geese is resistant to fowl cholera F
Fowl cholera cannot be prevented by vaccination F
Hemorrhages generally cannot be seen as post mortem signs of fowl cholera. F
After recovering from fowl cholera the animals do not carry the agent any more. F
Fowl cholera occurs only in hens. F
The agent of fowl cholera is an obligate pathogen. F
Germinative infection is common in the case of fowl cholera. F
Fowl cholera occurs only in chicken. F
Fowl cholera is typically seen in day-old birds. F
Germinative infection is important in the epidemiology of fowl cholera. F
Fowl cholera is caused by Riemerella anatipestifer. F
Fowl cholera has always an acute course. F.
Fowl cholera is the most severe among day-old chicken.F
Vaccines against fowl cholera are not available. F
Fowl cholera may cause high mortality in water birds. F
Turkeys are not sensitive to fowl cholera. F
Fowl cholera occurs mainly at the end of the winter. F
Germinative infection is the primary way of spreading fowl cholera. F
Fowl cholera can cause high losses among day-old chicken. F
Fowl cholera is caused by leukotoxin-producing Pasteurella (Mannheimia) haemolytica. F
Fowl cholera has higher mortality in young broiler stocks. F
Fowl cholera has high mortality in water poultry. F
Turkeys are not susceptible for fowl cholera. F
Fowl cholera is caused by Pasteurella haemolytica. F
Wild birds are very susceptible to fowl cholera. F
Susceptibility in hens decrease with age in case of fowl cholera. F
The clinical signs of anatipestifer disease are more severe in hens than in ducks. F
Anatipestifer disease is a zoonosis. F
Nervous signs are frequently seen in the case of ornithobacteriosis. F
The agent of anatipestifer disease is an obligate pathogenic bacterium .F
Clinical signs of anatipestifer disease are limited to the respiratory tract. F
germinative transmission is important in the case of anatipestifer disease: F
Generally laying flocks are vaccinated in order to prevent ornithobacteriosis: F
Arthritis is a frequent clinical sign of ornithobacteriosis: F
Pasteurella antaipestifer is the aetioligcal agent of Anatipestifer disease F
Anatipestifer disease mostly occurs in small backyard flocks. F
Anatipestifer disease only shows clinical signs in ducks. F
Anatipestifer disease mostly affects older birds. F
Ornithobacterium rhinotracheale most commonly occurs in 3-4-week-old turkeys. F
Thick, fibrinous nasal discharge is the most striking clinical signs in case of Ornithobacterium rhinotracheale. F
Ornithobacterium rhinotracheale. is most commonly infected via the germinative route F
Anatipestifer disease is caused by Pasteurella multocida. F
The clinical signs of Anatipestifer disease are more severe in Turkey than water fowl. F
Germinative infection is important in the case of Ornithobacterium rhinotracheale. F
Ornithobacterium rhinotracheale can cause disease mainly in water fowl. F
Europe is free from Brucella ovis. False
Brucella species are serologically uniform. F
Brucella species are not zoonotic agents. F
There is a close antigenic relationship between B. ovis and B. melitensis. F
Brucella are Gram-positive and Köster-positive bacteria. F
The antigens of Brucella are uniform. F
Brucella are not fastidious bacteria, they can be cultured on simple nutrient agar. F
There is a serological relationship among B. abortus, B. melitensis and B. ovis, because of the same surface polysaccharides. F
There are no brucellosis-free countries in the world. F
There is close antigenic relationship between Brucella bovis and Brucella ovis. F
Brucella species are not fastidious bacteria, we can use nutrient agar in diagnostic work. F
All of the Brucella species are zoonotic agents. F
Rev I. is an inactivated vaccine strain. F
Sheep and goat are the reservoirs for Brucella. F
Humans are resistant to Brucella melitensis. F
Hungary is Brucella free. F
An attenuated vaccine is used in Hungary for prevention of B. melitensis. F
Wild boars can be the carrier of Brucella melitensis. False
Brucella suis can infect only pigs: F
Swine brucellosis does not occur in Europe. F
Rev-1 strain is an attenuated live B. suis strain. F
Brucella suis can cause severe abortion in cattle. F
Brucella bovis can infect brown hares. F
Farmed pigs are regularly vaccinated against brucellosis in Europe in order to prevent infection from wild boars. F
Swine brucellosis is an exotic disease in Europe, we can see this disease in South-East Asia only. F
Pneumonia and nasal discharge are characteristic clinical findings in swine brucellosis. F
Swine brucellosis can be treated successfully with antibiotics. F
With the help of the appropriate antibiotics we can eradicate B. suis from a swine herd. F
Humans are not susceptible to the causative agent of swine brucellosis. F
Wild hare is an important reservoir of Brucella abortus biotype 2 in Europe. F
Brucella suis was isolated by Sir David Bruce as a first time in 1886 in Malta Island. F
In the case of swine brucellosis, no clinical signs can be seen in boars. F
Hungary is free from Brucella suis. F
Maintaining host of swine brucellosis are reindeer, hare and small rodents. F
Boars are asymptomatic in case of brucellosis infection. F
Abortion occurs due to liver lesions in the piglets in case of brucellosis. F
Antibiotics are widely used to treat swine brucellosis. F
Diarrhoea is a frequent clinical sign of porcine brucellosis. F
Fluoroquinolones are the first choice for treatment of bovine brucellosis. F
Calves can be infected with brucellae during pregnancy if the cow is infected. F
Bovine brucellosis is caused by Brucella bovis. F
Brucella abortus can colonise only pregnant cows or heifers F
Bovine brucellosis has to be treated 4-6 weeks long with penicillins F
Brucella abortus can colonise only cattle F
Bovine Brucellosis has to be treated 4-6 weeks long with Penicllins F
Cattle cannot infect humans with Brucellae F
The maintaining host of Bruecella abortus is the goat and the sheep F
Calves can be born with Brucella F
Brucellosis of cattle is mainly limited to the genital tract F
Bovine brucellosis is caused by Brucella bovis. F
The S19 strain is an inactivated B. melitensis strain, which can be used for brucellosis. F
Nervous clinical signs are frequent in the case of bovine brucellosis. F
Bovine brucellosis can be diagnosed using the tuberculin test. F
Bovine brucellosis was described for the first time by Sir David Bruce in 1886. F
Bovine brucellosis is not a notifiable disease. F
Bovine brucellosis can be treated well with penicillin. F
In ABR (Abortus bang ring/Brucella milk ring) test, we detect brucella antigens in the milk. F
Fluoroquinolone treatment can cease shedding of Brucella. F
An early antibiotic therapy is really important in the treatment of bovine brucellosis. F
In case of bovine abortion we must send only fetal fluid to the diagnostic laboratory, because is enough for the diagnosis. F
In the ABR test we detect Brucella abortus bacteria in the cattle milk. F
Icterus is a frequently seen clinical signs of bovine brucellosis. F
ABR test is a human serological test for the detection of antibodies in human blood serum sample. F
Most important clinical sings of bovine brucellosis are icterus and CNS signs. F
Bulls are resistant to Brucella infection. F
Bovine brucellosis is always an acute disease. F
Bovine brucellosis is widespread within the EU. F
ABR test is used to detect Brucella in milk. F
Brucella abortus causes no disease in bulls. F
Brucella abortus can colonize only cattle. F
Cattle are mainly infected with Brucella sexually. F
Brucellosis of cattle is mainly limited to the genital tract only. F
Male calves may be vaccinated with vaccines containing live attenuated strains, without any side effects. F
Brucellosis of bovine cannot be shed in the milk. F
Bovine brucellosis is primarily caused by venereal infection. F
Calves shows clinical sign after weaning when infected young with brucellosis. F
Calves can be born infected with brucellosis. F
Bovine brucellosis is seen in most European countries. F
Cattle recovered from brucellosis do not remain carriers. F
Brucella abortus infects only cattle. F
Bovine brucellosis is only endemic in Hungary. F
The biggest economic damage to bovine brucellosis is orchitis in bulls.F
Brucella abortus infects only cattle. F
Brucella ovis can cause an acute abortion outbreak in a cattle herd. F
Brucella ovis can cause septicaemia in cattle. F
Brucella ovis can infect humans. F
Wild hares can be the carrier of Brucella ovis. F
Brucella ovis mainly causes abortion, clinical signs in males are rare. F
Brucella ovis is a zoonotic agent. F
The most frequently seen clinical sign of B. ovis infection is abortion of ewes. F
Humans can be infected with Brucella ovis from raw sheep or goat milk, are common clinical signs of the disease. F
Ovine brucellosis caused by B. ovis is zoonosis. F
The Rev-I vaccine strain is an attenuated, live B. ovis strain. F
Brucella ovis can cause epididymitis and orchitis also in men. F
Brucella ovis has been eradicated from Europe. F
Sheep, goats, cattle are susceptible for Brucella ovis. F
Brucella ovis infects humans as well. F
Brucellosis of sheep caused by B. ovis is generally treated with tetracyclines. F
B. ovis has a wide host range. F
B. ovis will cause high fever. F
Ewes are lifelong carriers of Brucella ovis. F
You can get B. ovis free only with stock exchange. F
Humans are very susceptible to B. ovis .F
There is no B. ovis in Hungary. F
Humans can be infected with Brucella ovis from raw sheep and goat milk. F
Herd replacement is the only method of eradication of B. melitensis in a goat herd. F
Brucella melitensis can infection only goats and sheep. F
B. melitensis infection is common in most EU countries. F
Brucella melitensis is sporadic in Hungary. F
Brucella melitensis can infect only goats. F
Antibodies against Brucella melitensis can be detected in small ruminants all over Europe. F
melitensis is mostly affecting the northern part of Europe. F
Caprine brucellosis cannot be prevented with vaccination .F
Caprine brucellosis is caused by B. ovis. F
B. melitensis occurs sporadically in sheep flocks in Hungary. F
Brucella canis cannot cause abortion in dogs, it causes only orchitis in males. F
Canine brucellosis does not occur in Europe. F
Rev I. is a live vaccine strain of B. canis. F
For the prevention of canine brucellosis vaccination is a frequently used method in Europe. F
Canine brucellosis has no clinical sign in male dogs. F
Canine brucellosis is a zoonotic disease. F
Sheep, foxes and cats are secondary carriers. F
Attenuated vaccines are widely used for the prevention of canine brucellosis. F
Strong self-limitation can be seen in the case of canine brucellosis. F
Horses are infected by goats in case of brucellosis. F
Hares are susceptible to B. abortus. F
Reindeers are important in maintaining and infecting swine herds with B. suis. F
Clinical signs of tularaemia are mainly seen in cattle. F
Tularaemia can be found mainly on the southern hemisphere. F
Slide agglutination test cannot be used in the serodiagnostics od Tularaemia: F
Clinical signs of tularaemia can be seen only in hares: F
Francisella tularensis is a soil microorganism: F
Europe is free from Tularaemia F
Tularaemia can occur only in hares F
Only hares are suscpetible to the agent of Tularaemia F
Tularaemia affects only sheep in Hungary. F
Tularemia occurs only in America. F
Francisella tularensis ssp. holartica is highly virulent. F
Encephalitis is the main clinical sign of tularemia in humans. F
Francisella tularensis subsp. tularensis is in Europe. F
Hares spread the bacteria Francisella with urine. F
Only hares are susceptible to the agent of tularaemia. F
Tularaemia is not a zoonosis. F
The agent of tularaemia is transmitted only by ticks. F
Farm animals in Europe are widely vaccinated against tularaemia. F
Francisella tularensis subsp. tularensis is the most frequent subspecies of the agent in
Europe. F
Tularaemia can be frequently seen in cattle in Europe. F
Viral agents frequently predispose cattle to actinobacillosis. F
Antibiotics cannot be used successfully for treatment of actinobacillosis. F
Equine actinobacillosis has clinical signs only in foals. F
Foals cannot stand because of encephalitis in the case of actinobacillosis. F
Equine actinobacillosis is caused by Actinobacillus lignieresii. F
horses are regularly vaccinated in order to prevent actinobacillosis of foals: FALSE
Timber tongue is caused by actinobacillus in foals. F
Clinical signs of the central nervous system are typical in the case of actinobacillosis of foals.
F
Wooden tongue is a typical clinical sign of equine actinobacillosis. F
Young foals are regularly vaccinated in order to prevent actinobacillosis. F
Central nervous clinical signs are typical in the case of actinobacillosis of foals. F
Actinobacillosis can cause lameness due to encephalitis in foal. F
Animals will not move due to high fever and encephalitis in case of Actinobacillosis in horses.
F
Tetracyclines can cure the disease at any time in case of Actinobacillosis in horses. F
A. equuli is a common disease in some areas of the world. F
Bovine actinobacillosis is prevented by widespread vaccination with inactivated vaccines. F
Actinobacillosis seminis generally causes septicaemia in sheep and goats. F
Actinobacillosis of cattle is caused by actinobacillus bovis: F
Lesions of bovine actinobacillosis can be found in the maxilla or mandibula: F
Actinobacillosis of cattle is mainly a generalised disease F
Actinobacillosis is a fast, acute disease in cattle. F
Vaccination is the primary way of prevention of actinobacillosis in cattle. F
Actinobacillosis bovis is the causative agent of bovine actinobacillosis.F
Bovine actinobacillosis is a generalized disease with high fever. F
Bovine actinobacillosis affects mainly suckling calves. F
Bovine actinobacillosis is an acute or per-acute disease. F
Bovine actinobacillosis is a zoonosis. F
Actinobacillus pleuropneumonia of pigs: rare, sporadic disease mainly in tropical or subtropical countries. F
Mainly attenuated vaccines are used for the prevention of actinobacillus pleuropneumonia
of swine. F
Actinobacillus pleuropneumonia of pigs is generally a septicaemic disease F
The lesions of actinobacillus pleuropneumonia of swine are mainly located in the anterior lung lobes F
Fibrinous pneumonia is a post mortem lesion of Actinobacillus pleuropneumonia of pigs F
By APP the lesions are primarily found in the cranial lobes of the lung. F
APP causes focal inflammation-necrosis in the liver. F
Actinobacillus pleuropneumonia of swine is caused by Actinobacillus suis. F
Only live attenuated vaccines are used for the prevention of porcine actinobacillosis. F
Biotype 2 causes more severe disease in case of actinobacillosis in swine. F
Actinobacillus pleuropneumonia is caused by an obligate pathogen. F
A. pleuropneumonia strains can cause pneumonia in swine and cattle. F
A. pleuropneumonia type 2 biotype strain widely cause disease. F
The 2nd biotype of APP strains cause disease in large number of animals. F
Purulent nasal discharge can be seen in case of APP in swine. F
Actinobacillus pleuropneumonia can be introduced by rodents into the pig farm. F
Actinobacillus seminis generally causes septicaemia in sheep and goats. F
Glässer’s disease is caused by actinobacillus suis: F
Glasser’s Disease is caused by Actinobacillus suis F
Porcine polyserositis (Haemophilus parasuis) occurs in suckling piglets. F
Polyserositis affects many piglets and the mortality is high. F
Polyserositis of pigs is seen in the first week of life. F
Polyserositis of pigs is caused by Actinobacillus suis. F
Polyserositis of pigs is caused by Haematophilus parasuis. F
Glässer ́s disease causes severe purulent serositis. F
Glässer’s disease is a common disease, and mortality is high. F
Porcine polyserositis is caused by Haemophilus suis. F
Glässer’s disease is mainly seen in finishing pigs. F
Glässer’s disease cannot be prevented with using vaccines F
Actinobacillus suis is the causative agent of Glässer’s disease. F
Histophilus ovis can cause mainly pneumonia in sheep F
Histophilus somni can be venereal infection cause generalized disease F
The Histophilus somni is an obligatory pathogen. F
Histophilus somni can by venereal infection, cause a generalized disease. F
Toxoid vaccines can be used to prevent the Histophilus somni disease. F
Histophilus somni will only cause localized respiratory disease. F
Histophilus somni causes diarrhoea and dehydration in calves. F
Haemophilus somni can frequently cause pneumonia in sheep. F
Germinative infection is common in the case of infectious coryza. F
Infectious coryza is a generalized disease. F
Infectious coryza spreads slowly in the flock. F
Day-old chicks are most susceptible to infectious coryza. F
There is a watery nasal discharge and swelling of the head in case of infectious coryza. F
Infectious coryza usually generalizes. F
Elimination of predisposing factors is important in prevention of infectious coryza. F
In the case of infectious coryza in day-old ducklings, high fever is typical. F
Day-old chicken show severe clinical signs of infectious coryza. F
Infectious coryza causes big losses in broiler flocks. F
Germinative infection is important in the pathogenesis of infectious coryza. F
Infectious coryza is mainly seen in 1-2-week-old chicken. F
Germinative infection is the main way of infection. F
Clinical sign of infectious coryza are more severe in day-old than adult. F
Infectious coryza of poultry can infect all kinds of birds. F
Germinative infection is an important route of spreading for infectious coryza. F
Infectious coryza generalizes and causes fever. F
Mares cannot carry the agent of contagious equine metritis for more than a few weeks. F
The agent of contagious equine metritis generally causes septicaemia in horses. F
Orchitis in stallions is a frequent clinical sign of contagious equine metritis: F
Abortion is frequent in the case of contagious equine metritis: F
The agent of contagious equine metritis can only be transmitted by mating: F
Contagious equine metritis is seen in cattle, too. F
Taylorella equigenitalis mainly causes septicaemia in horses. F
Clinical signs caused by Taylorella equigenitalis can mainly be seen in young foals. F
The clinical signs of Taylorella equigenitalis infection are more severe in males than females.
F
Contagious equine metritis occurs widely in Hungarian thoroughbred studs. F
Contagious equine metritis causes decreased semen quality in stallions. F
We can diagnose Taylorella equigenitalis carrier mares with agglutination probe or ELISA. F
Taylorella equigenitalis is a widespread and common disease. F
The causative agent of contagious equine metritis is Histophilus equi. F
The causative agent of contagious equine metritis is an obligate pathogen. F
Taylorella equigenitalis can spread via feed and water. F
Contagious equine metritis causes high fever in the mare. F
There will be large amount of purulent smelly vaginal discharge in case of contagious equine metritis. F
The agent of contagious equine metritis can infect horses per os. F
After recovery from contagious equine metritis mares become infective for the rest of their life. F
Bordetella pertussis can sometimes infect small ruminants. F
To the isolation of B. avium V-factor, CO2, and chocolate agar are needed. F
The normal habitat of Bordetella species is the mucous membranes of genital tract of animals. F
Bordetella occur mainly on the mucous membranes of the genitals of mammals. F
Bordetella are very fastidious bacteria, cysteine, cystin and chocolate agar are needed to the culture. F
Bordetella canis is an agent of kennel cough of dogs F
Bordetella bronchiseptica can cause kennel cough on its own. F
Toxin-producing B. bronchiseptica strains cause severe clinical signs on their own. F
The causative agent of avian bordetellosis is Bordetella bronchiseptica F
Bordetella bronchiseptica is the causative agent of Turkey Coryza F
Turkey Coryza is an acute septicemia. F
Avian bordetelliosis, chickens are most susceptible. F
Avian bordetelliosis has a relatively low resistance. F
High mortality and morbidity is typical for avian bordetelliosis. F
Avian bordetellosis is a generalized disease with high fever. F
Avian bordetelliosis are resistant to heat and disinfectants. F
Turkey coryza is caused by Bordetella bronchiseptica. F
Moraxella ovis can cause keratoconjunctivitis only in sheep and goats F
The clinical signs of glanders are more severe in horses than in donkeys F
Attenuated vaccines are widely used for the prevention of glanders F
Inactivated vaccines are used for the prevention of glanders F
Contact animals are treated with penicillin in the case of glanders F
Glanders is mainly an acute disease in horses F
Glanders occurs only in horses. F
The agent of bovine genital campylobacteriosis is Campylobacter fetus subsp. bovis. F
Inflammation of the prepuce is a common clinical sign of bovine genital campylobacteriosis.
F
Blood never appears in the faces in the case of enteric campylobacteriosis. F
Campylobacter are obligate anaerobic bacteria. F
Campylobacter jejuni can cause hepatitis in humans. F
There are widespread vaccinations to prevent diseases caused by Campylobacter jejuni in humans. F
Campylobacter species are Gram-positive curved and motile rods. F
Bovine genital campylobacteriosis is caused C. fetus ssp. fetus. F
Campylobacter hepatitis of hens is caused C. fetus ssp. fetus. F
Bovine genital campylobacteriosis is an acute septicemic disease. F
Infertility of the bulls is a clinical sign of bovine genital campylobacteriosis. F
Campylobacter jejuni can cause septicaemia in young dogs. F
Proliferative enteropathies are caused by Campylobacter hyointestinalis F
Haemorrhages under the serous membranes are typically postmortem lesions of swine dysentery F
Leptospirosis of suckling piglets is a frequent acute disease. F
Generally attenuated vaccines are used for the prevention of leptospirosis of pigs. F
Leptospira bacteria are transmitted by ticks. F
Abortion is the main clinical sign of leptospirosis in dogs F
Leptospirosis of young dogs is mainly caused by Leptospira canis F
Majority of the mycoplasmas cannot be cultured on media F
Serous-purulent pneumonia is the typical lesion of contagious bovine pleuropneumonia. F
Animal pathogenic chlamydia species do not cause disease in humans. F
