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viro2
| Question | Answer |
|---|---|
| The poxvirus complex is what shape | Brick shaped |
| Replication of the pox virus takes place where on the cell | Cytoplasm |
| Which pox virus is an important pathogen in humans | Small pox |
| What is another name for the contagious pustular dermatitis virus of sheep and goats | Orf |
| How is orf transmitted | Direct contact, contamination of feeding troughs, fomites |
| What is the appearance of an orf lesion | Papule than becomes a pustule and thickens to a crust |
| Where do the orf lesions tend to occur | Muzzle and lips, young lambs may have lesions on mouth m gum and tongue |
| Lesions can also occur on the teat interfering with what | Prevent lambs from suckling |
| What is the mortality of Orf | Low |
| Diagnosis of Orf would include visualizing the virus using what method | Electron microscope |
| The isolation of the Orf virus for identicfication takes place in which cells | Sheep cell culture |
| What is seen histopathologically in a skin lesion of Orf | Cytoplasmic inclusions |
| Orf can be prevented by vaccinating ewes at what timeframe | Several weeks before lambing |
| How is the vaccine created | Derived from infected scabs or propogated in cell culture |
| Orf is zoonotic, how do humans acquire the virus | Contact with infected animals or carcasses or fomites |
| Which groups of people are more likely to acquire Orf | Shepherds, vets, farmers who bottle feed young lambsButchers and eat porters from handling infected carcass |
| What is the pathogmnoemnic lesion of Orf in humans | Solitary lesion on the dorsum of the index finger |
| By what other methods can Poxvirus be transmitted | Aerosol, arthropods |
| Histopathlogy of an Orf lesion in a human would show what | Marked pseudoepitheliomatous hyperplasia of epidermis,Intracytoplasmic inclusion bodies |
| Swine pox causes what type of lesions | Generalized skin disease in swine that appears to be localized to epithelial cells and draining lymph nodes |
| How are the neutralizing antibodies detected | Usually aren’t |
| Mechanical transmission of swine pox is thought to occur through which arthropod | Lice |
| Is swinepox zoonotic | No |
| How widespread is swinepox in the US | It’s not, rarely seen |
| Is the swinepox vaccine modified live or DNA | There isn’t one |
| Sheep and goat pox is in which genus | Capripoxvirus |
| Where do lesions occur on sheep | Muzzle and tail |
| Sheep pox and goat pox are notifiable. Is a vaccine available | Yes, used in endemic areas for prevention |
| Herpesvirus replicates where in the cell | Nucleus |
| What is another name for Pseudorabies | Aujeszky’s disease |
| The primary host for Aujeszky’s disease is which species, Secondary host | Primary = swine, secondary= catlle, horse, sheep, goat, dog, cat |
| How does pseudorabies infection occur | Direct nose to nose contact, by ingestion |
| What is the dominant clinical sign of infection in cattle | Intense pruritis on flanks or hind limbs |
| In swine, where is the virus carried | On the tonsils |
| What condition can re-activate the virus in a carrier pig | Stress |
| What nervous signs can be seen in infected piglets | Stop suckling, tremble, become incoordinated and have convulsions, walk in circles |
| 1-2 days after the onset of nervous, mortality of Aujeszky’s disease can be how high | 100% |
| What are the clinical signs of pseudorabies in weaned pigs | High fever, pneumonia, nervous signs, death (10% mortality) |
| The clinical signs associated with pseudorabies vary depending on what | Variations in the virulence of the strain and immune status of the pig |
| Virus isolation of pseudorabies is best from which tissue samples | Nasal swabs, brain, tonsils |
| What other diagnostic techniques are used | Histopath, immunofl, elisa, PCR, RFLP |
| In pregnant sows, what effect can pseudorabies have | Abortion |
| What purpose does a vaccine sere in PRV | -protects swine from clinical disease, duration of virus excretion id reduced |
| Can the virus be transmitted via vaccine | Yes, when using a live vaccine |
| Which is more virulent….equine herpes virus 1 or 4 | 1 |
| EHV 4 produces an upper respiratory tract disease called what | Equine rhinopneumonitis |
| In additional to respiratory infections, EHV 1 invades other organ systems that can result in what | Neonatal fetal death, abortion |
| How is equine herpes virus transmitted | Direct contact, aerosol (respiratory secretions), fomites |
| What environmental condtions can contribute to the transmission of EHV | Over crowding, poor nutrition, extreme climates, dense population |
| EHV 1 &4 persist in latently infected carrier horses. Where does the virus reside | In the sensory neurons of the trigeminal ganglia |
| Reactivation of the virus from the latent stage is attributed to what | Stress: surgery, prolonged transport, weaning, lactation, inclement weather |
| What are the primary clinical signs of EHV | Respiratory disease, fever, rhinitis & pharyngitis, nasal discharge, conjunctivitis |
| What neuro signs might develop in a EHV1 infection | Incoordination, inability to stand, urinate and defecate |
| What types of inclusion bodies help identify EHV | Intranuclear inclusion bodies |
| The HPV virus can be isolated from which samples | Pharyngeal secretions, blood leucocytes |
| What type of vaccine is used for the prevention of EHV | Combined inactive EHV 1 and EHV2 vaccine |
| Equine coital exanthema is caused by what virus | EHV 3 |
| How is EHV 3 transmitted | Directly through sexual contact, contaminated supplies and instruments |
| What are the clinical signs of EHV 3 | Pustules and ulcerations of vagina, penis, prepuce, perineum |
| Lesions may also be seen on lips and teats | |
| What effect does EHV 3 have on the fertility of stallions & mares | None |
| How do you prevent the spread of EHV3 | Stop natural mating and let disease run its course…10-14 days |
| How can EHV 3 carrier horses be identified | Sometimes they have spots of pigment loss on black skin in genital region |
| What technique is used to demonstrate the presence of the viral particles | EM |
| Briefly explain what a reverse transcribing virus is | Reverse transcription of a virion RNA in double stranded DNA |
| Caprine arthritis encephalitis is caused by what virus | Lentivirus, a retorvirus |
| What closely related lentivirus causes disease in sheep | Maedi-visna or ovine progressive pneumonia of sheep |
| What does Maedi-visna mean | Maedi- labored breathing (interstitial pneumonitis)Visna- shrinkage or wasting (paralyzing menigoencephalitis) |
| What are the cellular vectors that spread the disease to target cells within the animal | Macrophages and monocytes |
| What is a source of horizontal transmission of CAEV | Colostrum or milk |
| What clinical signs are seen in joints from a CAEV infection | Arthritis |
| What clinical signs are seen in the brain from a CAEV infection | Encephalitis |
| What clinical signs are seen in the mammary glands | Mastitis |
| What clinical signs are seen in the lungs | Interstitial pneumonia |
| In an CAEV infection, what clinical signs are seen in kids 2-6 months age | Encephalomyelitis, posterior paresis progressing to paralysis |
| Kids that recover from the neurological disease develop what condition as an adult | The arthritis that is common in adults progresses to the gradual swelling of which joint, leading to lameness |
| What microscopic sign of infection is seen in the brain | Perivascular cuffing |
| What microscopic changes are seen in the arthritic joints of CAEV | Marked hyperplasia of synovial membranes & villosites was well as mineralization and fibrosis of soft tissue |
| Ovine progressive pneumonia can result in what condition related to the udder | Hard bag |
| Which immune response eliminates the viral organism- humoral or cellular | Neither |
| Are vaccines effective against lentiviruses | No |
| The betaretrovirus that causes ovine pulmonary adenomatosis is also called what | Jaagsiekte sheep retrovirus |
| Ovine pulmonary adenomatosis cause progressive respiratory distress,The severity of signs is dependent on what | Depends upon the tumor development in lungs |
| What is another name for ovine pulmonary adenomatosis | Ovine pulmonary adenocarcinoma |
| What other clinical signs can be seen | Accumulation of fluid in the respiratory tract, rales, weight loss, bacterial pneumonia, death |
| The lesions associated with ovine pulmonary adenomatosis are confined to which ares | The lungs |
| What is the appearance of the affected lungs | Enlarged and heavier than normal due to extensive nodular lesions |
| What is the appearance of the tumors | Solid, grey or light purple with a shiney translucent sheen |
| Microscopically, the proliferation of what type of cells can be seen in an OPA infection | Type II pneumocytes |
| The cuboidal or columnar cells are replace by what type of cells | Normal thin alveolar cells |
| What method is used to isolate the OPA virus | There is none currently |
| What is Scrapie | A naturally occurring neurodegenerative disease of sheep and goats |
| What type of organism causes scrapie | A transmiss bale agent, prion |
| Scrapie is a member of what group of encephalopathies | Transmissible spongiform encephalopathy |
| What type of changes does scrapie cause | Behavioral and locomotive changes, degeneration of CNS and death |
| What clinical signs would you expect to see | Behavioral abnormalities, neuro signs, pruritis, incoordination, loss of body condition, death |
| What is a common lesion seen with scrapie | Loss of wool over neck and back |
| What type of microscopic changes are seen in the CNS | Vacuolar or spongy changes, bilateral or symmetrical |
| Where can the prion be detected long before clinical signs are seen | In some lymphoid tissues |
| A diagnostic MAB assay is carried out on what type of sample to diagnose scrapie | Small piece of lymphoid tissue from nictitating membrane |
| What gene is responsible , in sheep, for affecting scrapie susceptibility | Prion protein genes (PRNP) |
| African Horse Sickness is a virus in which family | Reoviridae |
| AHS affects which species | Horses, donkeys, mules |
| In which species is mortality the highest | Horse |
| What is the biological vector for the transmission of AHS | Culicoides |
| Is AHS contagious | No, infectious |
| AHS may occur in what 4 forms | Peracute (pulmnonary), subacute edematous (cardiac), acute (mixed) , or horse sickness fever |
| The peracur (pulmonary) form has clinical signs that include fever, respiratory distress and coughingWhat type of nasal discharge is seen | Forthy serofibrinous |
| How soon does death occur after the onset of clinical signs | A few hours |
| The pulmonary form is seen in animals with highly virulent strains of the virus or animals that have done what | Been worked during the febrile stage |
| How often do animals recover from the peracute form | Rarely |
| Does the subacute, edematous or cardiac, form of AHS have high or low virulence | Low |
| In the edematous form of infection, where does selling occur | Neck, thorax, brisket, shoulders, suprorbital fossa, eyelids, facial tissues |
| In the subacute form, death can occur between 4-8 days after febrile reaction, and is caused by what | Cardiac failure |
| The acute or mixed form of AHS shows signs of both pulmonary and cardiac forms of the disease. In what order are the signs seen | Pulmonary signs followed by edematous swelling of head and neck |
| What is the mildest form of the disease | Horse sickness fever |
| What are some of the clinical signs of horse sickness fever | Intermittent fever, anorexia, depression, slight congestion of conjunctiva |
| In the peracute form of AHS, what lesions are seen on organs | Edema of lungs or hydrothorax, subcapsular hemorrhage in spleen. Comgestion of renal cortex, edema and emlargement of lymph nodes |
| What type of lesions are seen on the epicardium and endocardium in the cardiac form of the disease | Petechial and ecchymotic hemorrhages |
| From which tissues can the AHS virus be isolated | Blood (during febrile stage), from lung, lymph node, spleen during necropsy |
| Diagnosis can also be made by cell culture or inoculation of what | 2-6 day old mice |
| Are vaccines available for the prevention of AHS | Yes |
| Is AHS zoonotic | Yes but rarely |
| Blue tongue primarily affects which species | Sheep |
| Blue tongue is a reo virus that replicates where in the cell | Cytoplasm |
| Blue tongue is tranmistted by what vector | Culicoides |
| What are the primary clinical signs of blur tongue | Purple-blue discoloration of the tongue, coronary band hemorrhage |
| What are the morbidity and mortality levels of blue tongue | High |
| Surviving animals grow poorly with what 2 conditions | Alopecia and sterility |
| What post mortem lesions might be seen in a case of blue tongue | Cardiac hemorrhages, enlarged lymph nodes, splenomegaly, hepatomegaly, muscles reveal swelling and necrosis |
| For diagnosis, the blue tongue virus is isolated from what type of sample | Buffy coat |
| The virus is cultured in what type of cells for identification | Chicken embryos |
| Attenuated vaccines are available for the control of blue tongue. What type of vaccine reactions have been seen | Fetal death and cerebral abnormalities |
| Eastern Equine Enecphalitis, WEE and VEE viruses are of which genus | Togoviridae |
| Which species are the susceptible host for EEE, WEE, VEE | Horses and humans |
| Horses and humans are dead end host. How is the virus transmitted. | |
| Between a mosquito and a vertebrate host (bird), the mosquito infecting the hores or human | |
| Which of the 3 diseases has the highest mortality rate | EEE |
| In the host, where does the virus replicate | At the site of entry, in lymph nodes, muscle, connective tissue, the reticuloendothelial system and CNS |
| Give 3 clinical signs of Equine encephalitis | Subclinical, fever, anorexia, depression, drowsiness, incoordination, impaired vision, photophobia, inability to rise, inability to swallow, teeth grinding, circling, paralysis, occasional convulsion and death |
| Microscopic lesions of the CNS include | Perivascular & interstitial mononuclear cell infiltration, diffuse and focal gliosis, neuronal degeneration with neuronophagia, interstitial edema |
| Which is the tissue of choice for virus isolation and identification | Brain tissue |
| What technique is used to detect the viral antigen | Immunofluorescence |
| What is the fate of animals with mild EEE, WEE or VEE infections | Recover with neurological sequeal (dullness and dementia) (“dummies”) |
| How are susceptible horses protected | Inactivated vaccines |
| Is equine encephalitis zoonotic | Yes |
| West nile virus is of which family | flaviviridae |
| West Nile Virus is spread by being passed back and forth between what 2 biological vectors | Birds and mosquitos |
| Do horse infected with WNV transmit the virus t other horses | No |
| To detect the WNV viral genome, PCR is used that is specific to what primers | E gene specific |
| What new type of vaccine has been developed for the prevention of WNV | DNA vaccine |
| Japanese encephalitis is another mosquito born virus that affects horses and humans. Which species is the amplifying host of the virus | Swine |
| What effect can the Japanese encephalitis virus have on pigs | Can cause abortion |
| What steps have been taken in Japan to reduce the spread of Japanese encephalitis | Draining of rice paddies during mosquito breeding season, remove swine for areas inhabited by humans, vaccination |
| The influenza virus is of which family | Orhtomyxoviridae |
| The influenza virions are pleomorphic, which means what | They are spherical and filamentous |
| In the host, where does the virus replicate | Nucleus and cytoplasm |
| Type A influenza viruses are divided into subtypes based on the antigenic nature of their surface glycoproteins. How many different hemagglutinins (HA’s) and neuraminidases (NA’s) are there | HA = 15, NA =9 |
| Which species is a natural reservoir for the influenza virus | Duck, waterfowl |
| Equine influenza has how many subtypes | 2, equine influenza 1 (H7N7) and equine influenza 2 (H3N8) |
| What is a main clinical feature of equine incluenza | High morbidity, highly contagious-rapid spread |
| How is equine influenza transmitted | Respiratoyr route, close contact, aerosol exudates, contaminated equipment, transport vehicles, clothing of stable personnel |
| In which cells of the host does the virus multiply | Epithelial cells of the upper respiratory tract |
| What clinical signs are seen from this infection | Inflammatory changes result in serous nasal discharge, laryhgitis, tracheitis, bronchitis, bronchiolitis, intertstitial pneumonia |
| Prolonged fever, as a result of influenza, may cause what condition in mares | Abortion |
| Isolation of the virus is performed from what type of samples | Nasal mucus or lung tissue at necropsy |
| The virus is best cultured in what type of media | 9 -10 day old chicken embryo |
| Once cultured, what is the most accurate method of detecting the influenza virus | Detection of hemagglutination activity in the amniotic or allantoic fluid of the infected embryo |
| Another method to detect the virus is to add rbc’s to the cell culture and check for the response of the virus. This technique is called what | Hemadsorption |
| Several methods are available to detect the viral antigen including immunoflruorescence, Elisa and PCR. How does the hemagglutination inhibition (HI) method work | Paired serum samples are test, one taken during the acute phase, one 3-4 weeks later, results are compared to demonstrate the increase in antibody titer |
| Swine influenza usually peaks during what time of year | Colder months |
| Why is swine influenza zoonotic | Pigs have receptors for both human and avian viruses |
| Why are pigs considered a “mixing vessel” for viruses | They can acquire both human and avian viruses and are a site for genetic reassortment |
| Porcine reproductive and respiratory disease syndrome is caused by what virus | Equine arteritis virus |
| Porcine reproductive and respiratory disease syndrome is caused by a virus of which family | Arterivirus |
| Why is PRRS of concern | Largest economically significant disease of swine in US and worldwide |
| Where in the host does the virus replicate | Macrophages |
| How is the PRRS virus transmitted | Direct contact |
| Where n the body does the virus reside | Respiratory tract and tonsils, in some cases in semen |
| What are some of the clinical signs of PRRS | Lethargy, anorexia, fever, abortion, embryonic death, infertility, decreased fertility, delayed estrous, decreased farrowing rates, stillbirths |
| The virus selectively kills which cells | Lung macrophages |
| The majority of clinical signs and post mortem changes are related to what | Secondary infections |
| What is the pathognomonic lesion of PRRS | Collapsed lung, no air space |
| What effect do vaccines have on the PRRS virus | Killed vaccine reduce excretion of the virus and clinical signsMLV are variable , reduce excretion of virus |
| How is the equine arteritis virus transmitted | Respiratory predominates, venereal from carrier stallion |
| What is the typical lesion of equine viral arteritis | Urticarial rash over the neck and shoulders |
| What other signs might be seen | Hind limb edema, periorbital edema and pink eye, scrotal and preputial edema |
| What main post mortem lesions are seen in EVA | Excessive fluid in the body cavities and interlobular interstitial pneumonia |
| The differential diagnoses for EVA include which diseases | Equine influenza, equine herpes virus 1 & 4, equine infectious anemia, African horse sickness |
| What type of samples are submitted for virus isolation | Nasal secretions, blood, semen, placenta, post mortem tissues |
| How are carrier stallions identified | Virus isolation from semen |
| How is EVA prevented | Vaccination, separate vaccinated animals from noninfected animals |
| Porcine parvo is in which virus family | Parvoviridae |
| Where in the host cell does the parvo virus replicate | Nucleus |
| Procine parvo is associated with what types of clinical signs and lesions in pigs | Respiratory and vesicular disease |
| Infected adults are typically subclinical in signs, what effect can the virus have on the fetus | Fetal death (transplacental infection leading to death and mummification) |
| Equine infectious anemia is a retrovirus in which genus | Lentivirus |
| The lentivirus can persist in the host and cause chronic illness. What other long term effect can the virus have | Immunodeficiency |
| What are the 2 biological vectors of equine infectious anemia | Stable flies (stomoxys) and culicoides |
| How does transmission occur | Interrupted feeding of bloodcuking horsefly on a clinically ill horse, and then on a susceptible horse |
| In what other ways can the virus be transmitted | Contaminated needles, in-utero infection of fetus |
| Onc einfected, how long does it take for the infection to clear from the blood | It doesn’t, blood remains infectious for life |
| Initially, which cells are infected | Macrophages and then lymphocytes |
| The infection cause what type of erythrocyte destruction | Automimmune destruction |
| What clinical signs are seen in EIA | Recurrent fever, thrombocytopenia, anemia, rapid weight loss, edema of lower body, death |
| What gross changes are seen in lymph nodes, spleen and liver | Enlargement |
| Microscopically, the lymph nodes, spleen and liver are infiltrated with what types of cells | Nests of immature lymphocytes and plasma cells |
| What diagnostic test is performed to identify EIA | Coggins (immunodiffusion) |
| Is EIA a contagious disease | Yes can spread horse to horse by body fluids, or mosquitos |
| Acute equine respiratory syndrome is caused by an infection of what virus | Equine morbillivirus |
| The equine mobillivirus is of what family | Paramyxoviridae |
| How is the morbillivirus transmitted | Direct contact with saliva or nasal secretions |
| Along with respiratory signs, what other clinical sign can be seen with a morbillivirus infection | Head pressing |
| Morbillivirus is a naturally occurring disease in which species | Horses and humans |
| Gross lesions of morbillivirus include sever edema and congestion of the lungs. What is seen microscopically | Large endothelial syncytial cells |
| Pest de Petit Ruminants affects which species | Sheep and goat |
| PPR produces respiratory signs (pneumonia, coughing, rales)as well as what lesions of the oral cavity | Stomatitis and gingivitis |
| What is the mortality rate of PPR | Higher in goats (95%) tan in sheep |
| Lesions can run from the mouth to where | Reticulo-rumen junction |
| What other lesion might be seen | Necrotic or hemorrhagic enteritis, necrotic lesions in the spleen, enlarged lymph nodes, apical pneumonia |
| Virus isolation for identification takes place in what tyope of cells | Lamb kindey cells |
| Vaccinations for PPR have been carried out using what other virus | Rinderpest in tissue cultures |
| Foot and Mouth disease is a highly contagious infection that is in which virus family | Picornaviridae |
| How many serotypes of FMD are there | 7 |
| Clinically, FMD cannot be differentiated from what other diseases | Swime vesicular disease, vesicular stomatitis,vesicular exanthema |
| Which species are the hosts of FMD | Cattle, sheep, goats, swine, wild mammals |
| How is FMD transmitted | Ingestion of infected food, mainly pigs |
| Where in the body does FMD replicate | Respiratory tract |
| How does FMD spread rapidly | Movement of infected animals to market, mechanical transmission (clothes, shoes, instruments) |
| Vesicles (blisters) develop where on the body | Lips, tongue, gums, nostril, coronary bands, interdigital space, teats |
| What is the predominant clinical sign in FMD | Lamness |
| Where in the cell does the FMD virus replicate | Cytoplasm |
| Is FMD zoonotic | Yes and reportable |
| Which species is resistant to FMD | Horses |
| The virus causing swim vesicular disease is in which family | Picornaviridae |
| How does the swine vesicular virus gain entry | Damaged skin or by eating garbage |
| With the onset of viremia, the virus is excreted from where | Feces |
| What clinical signs would you seen in an infection of swimvesicular disease | Lameness in several animals in a herd, fever, lesions on snout, lips, tongue, vesicles between heel and coronary band, encephalomyelitits (ataxia, circling, convulsions) |
| What type of cells are used for virus isolation | Swine kidney cells |
| Swine vesicular disease is a notifiable disease. Is there a vaccine to prevent the disease | No |
| The virus causing vesicular stomatitis is in which family | Rhabdoviridae |
| Which species are naturally susceptible to the disease | Horses, cattle, pigs |
| What 2 biological vectors are involved in the transmission of the virus | Sand fly and black fly |
| How does the virus enter the body | Break in the mucosa or skin |
| Vesicular stomatitis is a zoonotic disease. Which people are at risk | Farmers and vets |
| Vesicular exanthema of swine is caused by a virus of which family | Caliciviridae |
| Why did we learn this virus | Don’t know…it’s extinct |
| What are the four corna viral diseases in swine | Transmissible gastroenteritis, respiratory disease, porcine epidemic diarrhea, vomiting and wasting disease |
| How is the cornavirus transmitted in transmissible gastroenteritis | Contact exposure, aerosol |
| Which cells does the virus affect | Destruction of the villous epithelial cells of jejunum and ileim |
| The virus enters by ingestion, where are piglets more susceptible | Gastric secretions not as acidic as adults, virus protected from gastric acid by buffering action of milk, virus infects villous enterocytes of small intestines |
| In piglets under 7 days of age, mortality is almost 100% What causes their death | Severe dehydration and electrolyte imbalance |
| Weaners and growers are affected with watery diarrhea, vomiting and dehydration. What is the mortality level of this age group | Low |
| Which provides better immunity from TGE, IgA of IgG antibodies | Iga antibodies |
| How effective have vaccines been at protection against TGE | Not very effective |
| Porcine respiratory corona virus arises from the TGE virus from a deletion of which part of the virion | S glycoprotein deletion |
| What is the difference between TGE and porcine epidemic diarrhea | Disease spreads slower |
| Porcine vomiting and wasting disease is caused by what condition | Porcine hemagglutinating encephalomyelitis virus disease |
| Vomiting and wasting disease affects piglets of what age | Under 2 weeks of age |
| What clinical sign is NOT seen | Diarrhea |
| The virus first replicates in the nasal mucosa, tonsils, lungs and small intestines. How does it spread to the CNS | Via peripheral nerves |
| Vomiting is caused by virus replication where | Ganglion distale vagi (distal vagus ganglion) |
| What is the wasting attributed to | Neurological disturbances of the vomition center |
| What common infection of the small intestine in nursing or post weaning pigs | Rota viral enteritis |
| Rota virus infects and destroys the villous enterocytes of the small intestine leading to what conditions | Malabsorption and osmotic diarrhea |
| What is the appearance of the infected pig | Gaunt and rough haired |
| Neonatal pigs may potentially have protection form rotavirus enteritis from where | Colostrum |
| What lesions of the intestines are seen post mortem | Small intestine appears thin walled, Cecum and colon contain liquid feces |
| How might passive protection be achieved | Vaccination of sows |
| What clinical signs are seen in a foal with rotavirus induced enteritis | Diarrhea, depression, anorexia, profuse malodorous feces |
| What steps can be taken to prevent a rotavirus infection in foals | Isolation of arriving horses and foals for 7 days, vacc of pregnant mare to induce colostral antibodies |
| Hog cholera is caused by a virus of which family | Flaviviradae |
| Which route is the common route for transmission of hog cholera | Oral |
| Clinical signs of hog cholera include fiver and conjunctivitis, what posture will you see | Arched back, staggering gait |
| There may be purple discoloration of the skin in what areas | Abdomen and inner aspect of the thighs |
| What is the status of a pig that has recovered from an acute infection of hog cholera | Chronic carried, grow poorly have an arched back |
| What affect does the disease have on pregnant sows | Increased number of abortions, mummified and stillborns |
| What post mortem lesion is pathognomonic for hog cholera | Infarction of the spleen |
| What effect can hog cholera have on the lymphoid system | Exhaustion of the lymphoid system, atrophy of the thymus and germinal centers in the spleen and lymph nodes |
| African swine fever is caused by a virus of which family | Asfarviridae |
| How is AFS transmitted | Pig to pig contact, mechanical or ticks |
| In pigs, where does the virus replicate | In the cells of the reticuloendotheliel system and causes severe leucopenia |
| Which test is performed to differentiate African swine fever from hog cholera | Hemadsorption |
| Rift valley fever virus is in which family | Bunyaviridae |
| RVF causes severe disease in which species | Cattles, sheep, camels and goats |
| What is the abortion rate in ewes with an infection of RVF | 100%, first signal of the start of an epidemic |
| The mortality of lambs is over 90% whereas the mortality of adult sheep can be what | 10% |
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