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162 Cards in this Set
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- Back
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Describe Mucosal Immunity in TGE |
1. Secretory IgA- 2 IgA molecules linked together by a 'secretory piece' wrapped around the dimer. The secretory piece gives protection against intestinal proteases in the body so that it survives in the lumen of the small intestine 2. It is synthesized in the lamina propria by plasma cells and them dimerizes 3. The plasma cells migrate so that if a pregnant sow gets exposed to TGE, an immune response is mounted and the plasma cells get into the mammary gland and the submandibular salivary gland 4. Once there, they start to secrete the sIgA (both mammary and salivary) 5. When they are in the mammary gland, they then pass immunity onto the future baby pigs when they are born. crucial for the passive immunity for the baby pigs, giving them the right antibody for TGE. 5. It is crucial that the baby pigs nurse regularly to get a continuous supply of the SIgA in order to have a continuous immunity |
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If a piglet that was nursing to get TGE immunity is then put on milk replacer and exposed to TGE, what happens? |
The baby pigs will die as fast as fully susceptible pigs. Without the constant flow of immunity from the sow, the pigs have no lasting immunity and will die. *the small intestine becomes susceptible immediately |
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What vaccines are available for TGE? |
MLV vaccine, given IM~Induces IgG antibodies so you only get a limited protection MLV vaccine, given orally~better than IM but does not replicate as much as the field strain so, you get less sIgA levels than with the field strain |
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If you don't vaccinate a pig for TGE, what other prevention protocol can you try? |
Planned exposure to field virus- infect a couple of baby pigs, collect the small intestine and blend it up. Then give this to the other pigs to give them the infection and make the sIgA needed. *best method of prevention |
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What is the mortality rate in baby pigs for Porcine Epidemic diarrhea? What other virus is this virus very similar to? |
90-95% (looks like TGE grossly) Genome of TGE is like PEDV 96.6% to 99.5% |
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PEDV belongs to what viral family? |
Coronavirus |
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What are the most common subtypes of swine influenza? |
H1N1, H1N2, H3N2 *new strain of H1N1 spread from pigs to humans and has now caused cases in pigs, turkeys, ferrets and cats *can spread from swine to pigs, most in the fair season |
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Describe the transmission of Porcine influenza |
1. Aerosolized respiratory secretions 2. Fomites Incubation period of 1-3 days Shedding of virus begins within 24 hours of infection and sheds for 7-10 days *comes fast, goes fast is the rule, Carrier state can last for up to 3 months (exception) |
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What is unique about the cell surface receptors for influenza in pigs? |
They can bind to swine, human and avian influenza so they are quite susceptible to influenza infections Two or more viruses can infect a swine at the same time (called mixing vessels), resulting in reassortment- "antigenic shift" |
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What is the clinical signs of importance seen in swine influenza? |
(typical respiratory signs) Abortions can happen due to high fevers but this virus does not go viremic (secondary effect) *Economic loss in gain is more important with this virus *pigs will recover in 5-7 days with no complications *Morbidity 100%, mortality 1-3% |
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The key diagnostic to find swine influenza is what? |
RT-PCR HI for serum to find antibody levels |
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Porcine reproductive and respiratory syndrome: Enveloped or non-enveloped? RNA/DNA Virus? Family of? Important components of the genome? |
Enveloped RNA Arteriviridae Cluster of glycoproteins 2,3 and 4 that help attach to the host and Glycoprotein 5 is important for sequencing between the different strains of influenza |
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PRRS virus is infecting what cell in the body? |
The alveolar macrophage - helped identify what the target cell was for this virus in initial isolation of this virus |
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What is the transmission for PRRS? |
Aerosol, urine, feces, airborne, fomites, semen, subclinically infected pigs, and persistent carrier pigs |
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Describe the clinical signs seen in the initial phase of PRRS. |
Lasts 1-3 weeks High fever (up to 106) "rolling inappetence"- up to 1 week progressing slowly through the herd When you approach them, they don't move- lethargic, depressed, thumping- rapid abdominal breathing. Abortions in this phase are only occasional- not the rule |
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How would you classify the pneumonia caused by PRRS virus in pigs? |
Interstitial pneumonia |
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What are the clinical signs associated with the climax phase of PRRS virus? |
*most significant economic losses "bankruptcy disease" *abortions seen and virus is able to cross the placenta ONLY in the last third of the pregnancy Premature farrowing- 5-30% of sows Stillbirths 3 weeks into this phase ~with swelling and hemorrhage in the umbilical cords Mummified fetuses Weak pigs born with respiratory signs, susceptible to other diseases and a mortality rate of 30-50% before weaning. In the nursery and growing pigs, mortality is doubled |
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What are the clinical signs seen in the final phase of PRRS virus? |
Most problems seen in nursery and grower-finisher Respiratory signs, secondary infections Weaning of 15% |
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What are the other agents in the PRDC (disease complex?) |
Strep. Suis M. Hyopneumoniae Swine influenza virus Actinobacillus Pleuropneumoniae |
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When boars are infected with PRRS virus, what clinical signs do they show? |
Lethargy Inappetence Mild Fever Loss of libido Longterm shedding- 90 days as determined by RT-PCR |
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What is the pathogenesis of PRRS? |
1. Transmission by inhalation, ingestion, coitus, skin damage, fomites 2. Replication in mucosal, pulmonary and regional macrophages 3. Regional lymph nodes and viremia seen in 12 hours, can last up to 8 weeks *long term viremia means that it can be tested for in serum for a long time 4. Distribution to monunuclear cells and tissue macrophages 5. Subclinical disease or clinical disease results (see clinical signs) |
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How do you make a diagnosis of PRRS virus? |
Clinical signs, gross lesions Virus isolation RT-PCR ELISA for antibody levels FA/immunohistochemistry |
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How do you control PRRS from getting into a farm that doesn't currently have PRRS? |
~Introduce boars/gilts from uninfected farms ~Quarantine and test if the farm of origin is unsure ~If they are from an infected farm, a 4 week quarantine period off-site |
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How do you control PRRS on a farm that is infected? |
Introduce gilts and boars together 1-2 months before breeding In the nursery- partial depopulation, off-site weaning, all-in,all-out, longer interval before groups |
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What vaccinations are available for PRRS virus? |
MLV vaccine *best Inactivated Given to growing pigs |
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Porcine Circovirus-2: Envelopes/Non-enveloped? DNA/RNA virus? Family? Anything special about its genome? |
Non-enveloped DNA virus Circoviridae Circular Genome, smallest virus out there |
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What is the pathogenesis of porcine circovirus-2? |
1. Infects pigs lymph nodes and depletes lymphoid cells (with histiocytic replacement when the lymphoid cells get too low) 2. Can either then have high viremia or low viremia depending on host factors/immunity 3a. with low viremia= seroconversion, infection cleared, subclinical 3b. with high viremia= +/- seroconversion, systemic spread, clinical signs 70-80% mortality 4a. as a result of subclinical infection = reduced vaccine efficacy, reduced growth performance, increased susceptibility to other pathogens |
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What gross lesions are seen with an infection from porcine circovirus-2? |
Edema- interstitial and emphysema of the lungs Areas of necrosis in the kidneys |
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What is the second, not as common form of porcine circovirus-2? |
Porcine dermatitis and nephropathy syndrome |
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What is the most important viral disease in cattle? |
Bovine Viral Diarrhea virus (BVDV) |
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BVDV: Enveloped or non-enveloped? DNA/RNA? Family? Important features of it's genome? |
Enveloped- Lasts only in the environment for 2 weeks RNA Flaviviridae *Other important diseases of the same species: BVDV-1 and 2, Border disease virus, Swine fever virus Genome- E1, E2 enclode glycoproteins, NS2-3, (nonstructural) is the difference between a cytopathic and non-cytopathic strains. If NS2 and NS3 are split, you have a cytopathic strain *virulence of a BVDV strain is not linked to biotype OR genotype |
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What is the predominant stain of BVDV? |
The Non-cytopathic strain. (NS2-3 or p125) |
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Where do you find the cytopathic strains of BVDV? |
1. Mucosal Disease *look for oral ulcerations 2. In vaccines *keep in mind that the genotypes (either Ia or 1b or IIa or 2b) is important for vaccines |
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How is BVDV transmitted? |
Horizontal transmission- persistently infected animals- high, long shedding, fomites, PI fetus in a pregnant animal, most efficient- direct contact with fluids from a PI calf, semen Transplacental- very efficient 90% chance it will pass through the placenta, can lead to a persistently infected calf |
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What clinical signs are seen in an ACUTE BVD with a SUBCLINICAL infection? |
Mild fever, leukopenia, 70-90% will show nothing Will develop neutralizing antibodies |
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What clinical signs are seen in an ACUTE BVD in a NEONATE? |
Enteritis and pneumonia Due to failure of passive transfer |
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What clinical signs are seen in an ACUTE BVD in a CALF OF 6-24 MONTHS OLD? |
Primary or transient BVDV Incubation period of 5-7 days Fever, leukopenia, depression, anorexia, diarreha, decreased milk production Viremia will last 2-5 days, up to 2 weeks virus shedding is lower compared to a persistently infected animal |
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In the acute, severe form of BVD, what is unique about the antibodies formed? |
The high levels of virus neutralizing antibodies for genotype I were cross protective for infections with genotype II *look for hemorrhagic peyer's patches in the severe acute form |
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What clinical signs are seen in an ACUTE BVD in HEMORRHAGIC SYNDROME? |
Severe thrombocytopenia, causing decreased megakaryocytes and necrosis Bloody diarrhea, epistaxis, bleeding from injection sites, pyrexia, leukopenia results *highly fatal |
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BVDV is a _____________ virus and, because of that, it is also _________________. |
Lymphotropic virus, causing immunosuppression |
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If a bull is infected with BVDV, what does that mean for the possibility of spreading this virus venereally? |
A persistently infected bull can pass on the virus in semen (so can an acutely infected bull but, just in less amounts) |
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If a just pregnant cow or a cow that will soon be bred gets infected with BVDV, what does that mean for the rest of the pregnancy? |
Fetal resorption and the need to repeat the breeding in those cows. The farm's fertility rate goes down. Can also cause this when a cow gets bred with infected semen After the acute infection, there is a period of changes in the ovarian tissue that affects ovarian function |
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If a cow is within 50-100 days of gestation and gets infected with BVD, what happens? |
Abortion anywhere from days to months after infection *anywhere during stage of gestation *before day 150, the calf cannot mount an immune response Main goal of vaccination against BVD is to prevent the transplacental infections |
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If a cow is within 100-150 days of gestation and gets infected with BVD, what happens to the calf? |
The calf will be born alive but will show signs of birth defects- wide stance and ataxia, cerebellar hypoplasia, microphtalmia, cataracts, retinal atrophy, hypotrichosis, hypomyelogenesis, thymus, kidney lesions |
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When is a calf in utero going to be infected with a persistent infection of BVD? |
If the calf is between days 50 and 150 and is infected with a ncp strain, they will be persistent shedders of the virus for life in all secretions and excretions. *shedding is higher than any acute infection *these are the main source of BVD for other animals. Identify these ASAP and eliminate from the herd. Death rate is 50% in the first year of life, only some will be smaller an poor-doers If these get bred, the infection will be passed to the fetus |
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if a pregnant cow is after day 150 of gestation, what happens to the fetus? |
The fetus is immunocompetent so they fight off the infection and are born normal Antibodies against the disease would be found in the cord blood before the calf ingests colostrum, suggesting that the calf indeed does fight off the infection. |
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What is the mechanism of BVD mucosal disease? |
Calf must be infected in utero between 50-125 days of gestation with a non cytopathic strain. Also, a cytopathic strain that is antigenically close to the original non-cytopathic strain has to be there as well. This can happen either by being exposed to a cytopathic strain vaccine (this is NOT common) or this can happen when a endogenous mutation takes place to the non-cytopathic original strain making a cytopathic strain. |
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What are the clinical signs associated with the acute mucosal disease form of BVD? |
Highly fatal disease with fever, anorexia, tachycardia, decreased milk production, bloody diarrhea *oral ulcers, esophageal, abomasum, intestine, **tongue Secondary infections with pneumonia, mastitis, metritis and lymphoid depletion |
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What are the clinical signs associated with chronic mucosal disease of BVD? |
Maybe caused because the non-cytopathic and cytopathic strains aren't closely related? (true cause is unknown) Lameness, interdigital skin lesions, immunologically compromised, usually fatal |
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How do you diagnose Acute BVD? |
Nasal swabs for RT-PCR within 1-2 weeks of infection Virus Neutralization with paired serum, 3 weeks apart- watch for 4x increase in titers between the two samples. Submit aborted fetus for testing with RT-PCR |
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How do you diagnose a persistently infected case of BVD? |
In <3mo old, whole blood sample looking for antibody complexes OR Ear notch- most common diagnostic sample for RT-PCR *if positive, try to quarantine and then re-test a second time 3 weeks later. If acutely infected, the infection will be gone in three weeks In >3mo old, serum sample for virus isolation (whole blood can't be used because passive immunity is gone), Ear notch for RT-PCR, ELISA RT-PCR does not differentiate between acute and persistent infection Can also be a positive result 3-10 weeks after vaccination for BVD *will NOT be positive after vaccination if you test ear notches, only blood Can be used on pooled samples of milk, blood, ear notches If you get a positive pooled sample, you have to then separate and do FA with the ear notch samples to find truly positive animals. |
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How do you prevent a case of BVD from being introduced to the farm? |
Isolation and testing of cattle entered the farm (isolate for 3 weeks) Vaccinate 1, MLV- best but only use ones safe for pregnancy in pregnant animals 2, Inactivated |
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Bovine Enteric Viruses: Enveloped/Non-enveloped? RNA/DNA? Family? Special parts of genome? |
Non-enveloped RNA *DOUBLE-STRANDED (11 segments) Reoviridae VP6- capsid protein that determines the subtype (type A is the most common) and is involved in cell-mediated immunity (you can run the RNA directly with electrophenotypying to get the different genome segments) VP4 and 7- help into entry into the host and induces neutralization of the host. VP7 mediates the G type and 4 mediates the P type. Together, these G and P make up the genomic combinations. |
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Describe the transmission of Bovine Rotavirus |
Ingestion of the virus containing material The shedding in feces is very high, up to 1 billion particles/gram of feces |
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What is the pathogenesis of bovine rotavirus? |
1. Virus is ingested 2. Virus gets through the stomach with no problems 3. It infects the epithelial cells lining the small intestine (resistant to lipases) 4. Increases intracellular Ca messing with the tight junctions and cytoskeleton of the cells 5. Viral toxins NSP4 is made and induces secretory diarrhea 6. Virus irritates nerve endings, increasing diarrhea 7. You get malabsorption, fluid accumulation and electrolyte imbalances due to the villous atrophy and the cells falling apart 8. Result- diarrhea (malapsorptive and secretory), dehydration and mortality up to 30% if left untreated (recovered calves takes a few weeks to get them back to normal) |
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What kind of host defenses can be mounted against an infection of bovine rotavirus? |
1. They can have secretory IgA against the virus and the virus can't get into the intestine at all 2. If an immune response is mounted, the damage that the virus can do decreases ~The making of dimeric IgA and T cells can be specific for VP6, decreasing the secretory process |
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What clinical signs are seen in calves when infected with bovine rotavirus? |
Clinical signs are only seen when infection took place in first few weeks of life, seen 2-3 days after exposure There is 4-5 days of protection from colostrum Anorexia, depression, yellowish/pasty/watery diarrhea |
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When infected with bovine rotavirus, what other infections could be going on simultaneously and would determine how bad the clinical signs are? |
Cryptospordium parvum Bovine coronavirus Bovine enteric caliciviruses E. coli C. perfringens, type C |
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How do you diagnose bovine rotavirus? |
Clinical Signs ELISA RT-PCR w/ or w/out genotyping (best for post-clinical phase of disease) Immunomigration- gold particles with antibody to the rotavirus attaches to the sample and migrates by capillary action to the result line. Meets an anti-rotavirus antibody at the result line, resulting in a positive result seen. |
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What are the two most common viruses in neonatal calf diarrhea? |
Rotavirus & Cyptosporidium (rotavirus is the most prevalent by itself) (With Coronavirus and Salmonella being the other common ones) |
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How do you prevent/control an infection of bovine rotavirus? |
Induce lactogenic immunity by allowing calves to nurse (like TGE) Vaccination of he pregnant heifers/cows to ensure that the calves get the right amount of antibodies in the colostrum |
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What aged calves are affected by bovine coronavirus? |
causes respiratory disease OR enteric disease in calves 5-14 days of age (typically) but can affect calves up to 3-4 weeks of age Shedding goes beyond the clinical phase |
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How is bovine coronavirus transmitted? |
Fecal-oral transmission, affecting both the small and large intestines, causing more severe villous atrophy than rotavirus and involve the crypts as well *this is a worse infection then rotavirus! |
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What are the clinical signs associated with an infection of bovine coronavirus? |
Enteric infection- watery or hemorrhagic diarrhea for 2-6 days (malabsorptive and secretory), anorexia, pyrexia, dehydration *morbidity and mortality is high Respiratory infection- mild or sub-clinical. Can see sneezing/coughing in calves 2-16 weeks old. *can lead to more severe bacterial infections *Still SHED high numbers of virus in secretions and this can lead to either respiratory or enteric disease |
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What are the clinical signs associated with "winter dysentery" |
Caused by bovine coronavirus, seen most prevelant in winter months high morbidity, low mortality in adult cows, causes severe watery diarrhea When they recover, they remain immune from this disease for 1-5 years Lesions seen in the spiral colon in the crypt epithelium |
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Bovine Norovirus RNA/DNA? Family? |
RNA viruses Caliciviridae (out there but won't kill calves on the farms) |
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Bovine Torovirus Enveloped/Non-enveloped? RNA/DNA? |
Enveloped RNA |
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What is the pathogenesis of Bovine Torovirus? |
Virus replication is in the small and large intestine If a calf doesn't get sufficient colostrum, calves will consistently develop diarrhea within 72 hours of infection (same for both serotypes) |
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BRSV: Enveloped/Non-enveloped? DNA/RNA? Family? Special parts of its genome? |
Enveloped *VERY labile virus RNA Paramyxoviridae F glycoprotein "fusion"- makes the giant cells G glycoprotein- mediates attachment Non-structural protein 1 and 2 (not actually part of the virus)- interfere with the host interference system |
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What is the transmission of BRSV? Where is the target location for this virus in the host? |
Respiratory route transmission Target location- both upper and lower respiratory tract |
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What is the pathogenesis of the severe form of BRSV? |
1. Aerosol exposure 2. Infection of cilliated and non-cilliated epithelia in the respiratory tract 3. Necrotizing broncholitis and bronchiolitis obliterans results 4. Clinical signs- dyspnea, forced expiration, lung emphysema, fever, crackling lung sounds. (viremia and abortions not prevalent in this disease) 5. Death can happen acutely |
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What clinical signs are associated with the mild form of BRSV? |
Dry coughing, mild nasal discharge, fever, animals typically recover in a week. |
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What gross lesions are associated with BRSV? Histo lesions? |
Pulmonary edema and emphysema Lungs don't collapse when you open the chest Secondary pneumonia Consolidation of lung lobes Enlargement of bronchial and mediastinal lymph nodes histo- Bronchiolitis, alveolar edema and emphyema, multinucleated giant cells, suppurative/fibrinous bronchopneumonia |
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How do you diagnose a case of BRSV? |
RT-PCR, serology on PAIRED sera ELISA IHC FA Clinical signs Gross/histologic lesions |
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What is the immune response seen against BRSV? |
Passive immunity reduces clinical signs but doesn't protect against infection CMI CD8+ plays a role in clearance of the virus. On day 10, the only class of calves that were shedding virus still were those that were depleted in CD8+ |
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What vaccinations are available for BRSV? |
MLV vaccines* 2 doses, 3 week interval, safe for pregnant cattle Induce antibodies for the F protein specifically (and G less so as well), they induce CD8+ and CD4+ Boosters needed as the immunity doesn't last long (inactivated vaccines do not induce any CD8+ cells, making the immunity less effective) |
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How can you treat a case of BRSV? |
Antimicrobials NSAIDS Corticosteroids Antihistamines Antivirals? IBR-PI3 IN vaccine |
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Bovine Herpesvirus: Enveloped/Non-enveloped? DNA/RNA? Family? |
Enveloped DNA Herpesviriridae |
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What are the different subtypes of bovine herpesvirus-1? What are their disease patterns? |
BHV 1.1- Mainly respiratory, abortion BHV 1.2- Genital BHV 1.2b- Genital Classification based on genetic differences |
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What are all of the different herpesviruses that affect cattle? |
BHV 1- Infectious bovine rhinotracheitis BHV 2- Bovine mammilitis, pseudo lumpy skin disease (psuedo cowpox) BHV 4- May be associated with metritis? BHV 5- most neurotropic of all of them, bovine herpesvirus encephalitis AIHV-1- malignant catarrhal fever OHV-2 (last two cattle are not the natural host) |
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Describe how BHV gets into and replicates within a host cell |
1. low affinity binding first, then a more stable binding 2. viral penetration follows fusion between virus and membrane 3. cytoplasmic transport toward the nucleus, viral DNA is released. VP16 is a tegument protein that is released. These proteins are important for transactivation of other proteins. 4. Replication then happens in the nucleus in three stages. IE- proteins for regulation of cell cycle. E- proteins for viral replication L- proteins made into the virions 5. Viral envelope is then made in two parts- primary envelope is acquired as it exits the nucleus. the mature envelope is made by budding into a golgi apparatus compartment *know that this is a two step process, both in and out of the nucleus |
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What is the importance of latency in BHV? |
Latency is important because this reactivated easily. Any small amount of corticosteroids or stress can lead to reactivation. They will lie in latency in the Sensory Nerves at sensory nerve endings, in the ganglia A very small portion of the genome is active during latency, called the latency-related transcript- responsible for inhibition of apoptosis |
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Describe the pathogenesis of BHV |
1. Virus enters and establishes infection at mucous membranes and conjunctiva through direct contact, aerosol transmission, direct contact during copulation 2. Replication at portal of entry causes lysis of the cells that they infect, they're cytopathic 3. They cause necrosis of cells around them while avoiding the immune system 4. They will rapidly spread locally and systemically by cell-associated viremia. 5. They infect the neurons at the end of the olfactory and trigeminal. *BHV-5 more neurovirulent |
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How does the immune system respond to BHV? |
1. innate- cytokine secretion and killing of virus-infected cells 2. Cell-mediated immunity- peaks 7-10 days after infection, clinical signs subside 3. Humoral- begins at day 10, neutralization of free virus, protects against reactivation Immune evasion strategies- complement, type I interferon, chemokines, MHC-1 associated antigen presentation |
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Describe the importance of BHV in the Bovine respiratory disease complex |
Damages the epithelium Decreases ciliary activity and mucus secretion Decreases the activity of alveolar macrophages and neutrophils |
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Describe the clinical manifestation of BHV- infectious bovine rhinotracheitis (IBR) |
1. Animals are 6 months old or older 2. Transmission = close contact 3. Occurs in feedlots usually 2-3 weeks following arrival 4. Clinical signs = fever, nasal secretions, pink muzzle, anorexia, reddening of the conjuntivae, formation of plaques on mucosae, keratitis, corneal opacity, disease in the trachea starts as hyperemia and then gets filled with plaques and major necrosis 5. Cows usually recover in 1-2 weeks unless complications |
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Describe the clinical manifestation of BHV- infectious pustular vulvovaginitis |
Clinical signs- fever, small pustules on vulva and caudal vagina, tail wagging, painful urination infection at the time of service- reduced fertility, chronic endometritis, oophoritis Infection later in the oestrus cycle- decreased conception rate Infection later in the pregnancy- abortion, mummification, stillbirth and birth of a calf which will die shortly after birth Becomes asymptomatic after 2 weeks and does shed for these 2 weeks |
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Describe the clinical manifestation of BHV- infectious balanoposthitis |
1. Acquired during natural breeding 2. Affects penis and prepuce for up to 4 weeks- causes painful lesions and unwillingness to breed 3. The virus is then excreted in semen for 14-22 days 4. This is a lifelong latent infection with potential for reactivation |
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Describe the abortions associated with BHV |
~BHV-1.1 and 1.2 are involved ~4-7 months of gestation ~There is a large time lapse between clinical signs and when the abortions actually happen ~Abortion is a result of cell associated viremia, the virus passes through the placenta |
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How do you diagnose a case of BHV? |
PCR Virus neutralization test |
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What vaccines are available for BHV? |
1. Modified-Live vaccines, IM- use only when approved for pregnant animals, limited shedding, potential to revert to the virulent strain 2. MLV, IN vaccine- less convenient, rapid protection, *induction of an immune response is important, virus is shed, there is a potential for reversion. This does have a latent period but, this is better than the IM vaccine 3. Inactivated IM- No shedding, no latency, no protection against field virus latency, shorter duration of immunity, slower induction of protective titers |
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What is the vaccination protocol for BHV? |
Feedlot- first dose 5-6 months, 2nd dose at arrival at feedlot Dairy farm- first dose 6 months, 2nd dose 2-3 weeks pre-breeding, re-vaccination at 1-2 year intervals Bulls- don't get vaccinated if they are going to an AI Station |
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Bovine Leukemia Virus: (sporadic and enzootic) Enveloped/Non-enveloped? DNA/RNA? Family? What are the important enzymes carried by BLV? |
Enveloped RNA Retroviridae Reverse transcriptase enzyme, and integrase enzyme |
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What is the prevelance of BLV in cow-calf operations? Dairy operations? |
Cow-calf, 39%. Dairy operations, 83% In the '60s and '70s, the US and Canada decided that the control of BLV was not cost-effective *No issue was seen with immune suppression that this causes |
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What is the transmission of BLV? |
Target cells are B lymphocytes. Iatrogenic (dehorning, needles, calving, bloood transfusions, vaccinations) Insects, colostrum, vaginal secretions/placentas (all not that important) |
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What is the pathogenesis of BLV? |
The viral envelope glycoprotein attaches attaches to the B lymphocytes Reverse transcriptase happens in order to incorporate the viral DNA into the host DNA Then, the stages of infection are the primary infection, persistent infections, persistent lymphocytosis, tumoral |
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Is BLV Silent? How does the virus replicate? Is BLV inhibiting apoptosis? |
Viral expression may take place in a subpopulation of infected cells Expansion of integrated provirus by mitosis of the host cell, known as clonal expansion Yes when BLV-infected cells are cultured in vitro, unknown in vivo |
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How are the lymph nodes involved in BLV? What are the clinical signs of peracute BLV? Subacute/chronic? |
Superficial lymph node enlargement, visceral lymph node enlargement, spread to the peritoneum and pelvic viscera, exophthalmos Peracute- sudden death, internal hemorrhage Subacute/chronic- loss of body condition, anorexia, muscle weakness, fatal 2-3 weeks after lymphosarcoma develops |
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How do you diagnose BLV? |
Clinical signs, gross path, histopathology Cytology ELISA PCR AGID |
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w do you control/prevent BLV? |
Control- separate the dams from calves prior to colostrum intake, one animal = one needle, one animal = one OB sleeve, wash and disinfect, electrocautery in dehorning, place calves in individual pens, colostrum from BLV-negative cows, feed frozen colostrum that was from a postive animal (the lymphocytes will be destroyed from freezing and the antibodies will still be there), put seropositive cows and seronegative cows in different groups (always examining the negative ones first) |
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Bluetongue:
Enveloped/Non-enveloped? DNA/RNA? Family? Special Genome characteristics? |
Non-enveloped RNA Reoviridae *segmented genome, 24 serotypes worldwide, in the US- BTV-2, 10, 13, 17 are the endemic serotypes, there are several other nonendemic serotypes *REPORTABLE, potential bioterrorism |
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What is the natural distribution of bluetongue? |
Primarily a disease of sheep, white-tailed deer (have their own cousin and susceptible to bluetongue), antelope, cattle, goats, elk, elephants, camels are all potential reservoirs Disease that is primarily seasonal, based on vectors |
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What is the pathogenesis of bluetongue? |
1. Culicoides (midge) bites 2. Replicatess in regional lymph nodes 3. Gets into circulation 4. Disseminates to lymphoid organs 5. Secondary replication occurs in mononuclear phagocytic and endothelial cells 6. viremia is extended (found on RBCs), up to 60 days 7. Vascular injury and pulmonary edema results |
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What are all of the ways that bluetongue can be transmitted? |
Culicoides midge* Biological vector Ticks or sheep keds- mechanical vectors Fomites (Semen and transplacental transmission) Blood meal is taken from infected animal, virus amplifies in vector for 2 weeks, midge then bites a susceptible animal |
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What is the morbidity/mortality of bluetongue in the following species:
Sheep Cattle/Goats/Elk Whitetail deer and pronghorn antelope |
Sheep- morbidity 100%, mortality 0-50% Cattle/goat/elk- morbidity 5%, mortality rare Whitetail deer and pronghorn antelope- morbidity 100%, mortality 80-80% *most susceptible |
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What are the clinical signs of bluetongue in sheep? In deer? |
In sheep- nasal discharge, depression, fever, emaciation, edema/hyperemia of muzzle ears and eyes, inflammation and ulceration of mucosal surfaces, severe swelling of the tongue (occasionally), lameness (coronary band hyperemia), fetal resorption or abortion, birth of "dummy lambs" (from hydrancephaly), **Hemorrhage at the base of the pulmonary artery, recovery takes a while, not completely normal right away In Deer- fulminating hemorrhagic disease, sudden death possible |
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What are the clinical signs of bluetongue seen in cattle? |
Most are clinically unapparent When clinical, you see erosions, hyperesthesia (sensitive to touch), erect hair, skin thickening, reproductive failure, breaks in the hoofs (necrosis and ulcers), nose and teat hyperemia, coronitis, conjunctivitis, hyperemia of the muzzle, nasal discharge |
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What is the vaccine available for bluetongue?
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MLV
Serotype in the vaccine must match that of field virus Can cause reproductive problems in sheep |
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What is the family for Malignant Catarrhal Fever |
Herpesviridae |
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Alcelaphine Herpes virus-1. Is it a part of malignant catarrhal fever? Natural Host? Clinically susceptible hosts? Alcelpahine Herpesvirus-2? |
Type 1: Yes, Wildebeast, Cattle/Deer Type 2: Yes, Hartebeast (subclinical), Bison |
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Ovine herpesvirus-2 affects many species. Which of these species are the most susceptible? Least Susceptible? |
Most- Bison, white-tailed deer, axis deer and bali cattle (middle)- Rabbits, pigs, cattle (in that order) Least- sheep |
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Describe the pathogenesis of Malignant Catarrhal Fever |
1. Sheep 9-11 months old gets infected- first replicates in the lung. This is lytic replication 2. Tropism switch to lymphoid tissue 3. Second phase- latency in lymphocytes and tissues 4. Virus in the turbinates get reactivated which then start shedding the virus, for a very short time *infectious virus is the exception, not the rule- level of the replication in the buffalo is higher than in the sheep In the buffalo, there is two peaks of viral levels, the immune response is not as big as the sheep, MCF symptoms are seen but no shedding of the infectious virus is happening. (shedding only comes from the sheep, buffalo has to be exposed to sheep) |
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What is the transmission of AHV-1? OHV-1? |
Direct contact, aerosols, vertical transmission
Infected calves at one or two months of age (antibodies develop at 3-4 months) shed the infectious virus, both in nasal and ocular secretions OHV-1: nasal shedding only in 6-9 month old lambs |
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What are the clinical signs seen in cattle when they develop MCF? (regardless of infectious agent) |
Peracute disease- depression, weakness, diarrhea or dysentery, rapid progression to death (*bison typically die of peraute disease) Acute form- fever, bilateral corneal opacity, oculonasal discharge, muzzle/nares are encrusted, Hyperemic oral mucosa, multifocal/diffuse necrosis, erythematous/ulcerated skin Chronic infection (skin lesions) or recovery is possible |
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What post-mortem changes would you see with MCF? |
Inflammation, epithelial necrosis Lymphoproliferation, enlarged lymph nodes Infiltration by lymphoid cells Vasculitis in kidney, intestine, respiratory, urinary bladder, smallarteries Fibrinous polyarthritis Hemorrhagic enterocolitis in those that die suddenly In less severe cases- muzzle, nasal mucosa, hair and skin ulcers |
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How do you make a clinical diagnosis of MCF? |
Any animal with sudden death, fever, erosions, nasal/lacrimal discharge, corneal opacity, especially if the animals have been exposed to sheep *reportable disease PCR- spleen, lymph nodes, adrenal glands |
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What vaccines are available for MCF? |
No vaccine available |
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A prion is a what? |
A proteinaceous infectious particle The NORMAL protein is PrPc (found normally in neuronal cells) The ABNORMAL protein, for scrapie is PrPSc *normal structure is the same, secondary structure is different (more beta sheets) *VERY hard to get rid of, very resistant |
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What is the transmission of BSE? Scrapie? |
BSE- having carcasses in cattle feed with the disease in it. Maternal transmission (at low levels) Scrapie- spread from ewe to offspring through placenta and placental fluids (vertical transmission only) |
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What age sheep are affected with Scrapie? Goats? |
Sheep- 2-5 years old Goats- 2-8 years old |
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What clinical signs are associated with scrapie in sheep and goats? |
Depends on strain of prion, genotype and/or breed (suffolk more susceptible) Hyperexcitable, gait abnormalities, ataxia, incoordination, blindness, trembling, convulsion, pruritis (pruritis is less in goats) Die 2-6 weeks after the onset of symptoms |
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What ante-mortem tests can you do to find scrapie? |
Third eye-lid test and doing immunological tests for antibodies for prion Small piece of rectal mucosa- immunohistochemistry *post-mortem, obex must be obtained in the brain |
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What prevention/control programs exist for scrapie? |
Scrapie Flock certification program- *voluntary National accelerated Scrapie Eradication program |
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When you genetically test sheep for Scrapie and put the coding on their backs, what coding is the best outcome? Worse? |
QQ- worst. Double coding for Glutamine RR- best. Double coding for Arginine |
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If humans consume cattle with BSE what can develop? |
vCJD |
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What are the clinical signs associated with vCJD? |
Depression and schizophrenia Unsteadiness, difficulty walking, involuntary muscle movements Becoming completely immobile and mute |
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What clinical signs of TSEs are seen in mink? |
Initial- nest soiling, dispersal of droppings in cage Progressing to excitability, arching of the tail, incoordination, chewing of the tail, clenching of the jaw |
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What is the diagnosis of BSE? |
Brain tissue examination Tonsilar biopsy, time consuming 3rd eyelid test Rectal mucosa test |
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Avian Influenza: Enveloped/Non-enveloped? DNA/RNA? Family? Classifications? |
Enveloped, RNA, Orthomyxoviridae Nonpathogenic AI, low-pathogenic AI, highly pathogenic AI *classification is based upon the ability to kill chickens when put in IV *typical high path strains are H5 and H7 *can switch overnight to a different strain |
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How many different influenza viruses can you have? |
144- 16 different H combinations 9 different N combinations |
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Besides classifying high pathogenic strains of avian influenza with H and N, what other way can we attempt to identify the type of strain? |
The HA is shielded by glycosylation of amino acid 13 and there is an arginine at the carboxyterminus of the HA1. If these are changed, the isolate can be cleaved and the spectrum of the hosts is increased. (not 100% accurate) |
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What is the native horse of avian influenza? |
Water fowl- they are JUST a reservoir and do not exhibit any clinical signs |
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Why is it that not all strains of avian influenza can just easily pass from one specie to the next? |
Each virus has a different receptor for their specific target site, depending on the strain of virus. |
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What are the clinical signs associated with avian influenza? |
*mortality and morbidity reaches up to 100% Clinical signs- High path- death suddenly Others- respiratory signs, nervous signs, diarrhea, drop in egg production |
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hat gross lesions are seen with avian influenza? |
Cyanotic combs, facial edema, comb blisters, blood in trachea, esophagus, proventriculus, cecal tonsils, hemorrhage on heart and small intestines, fibrinous airsacculitis |
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How do you diagnose avian influenza? |
AGID serology- blood screening test HA and HI VIrus isolation ELISA RT-PCR *done at MSU to detect H5 and H7 only, no test for N (no treatment, quarantine and eradication) |
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Newcastle disease "pneumoencephalitis" Enveloped/Non-enveloped? DNA/RNA? Family? |
Enveloped RNA Paramyxoviridae (1 is the most prominent) ~2,3,6 in turkeys Causes disease in pet birds, chickens and turkeys *Reportable |
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What are the classifications of newcastle disease? |
Lentogenic- mild pathogenicity Mesogenic- moderate pathogenicity Velogenic- very pathogenic (not in the US) Classified on the ability of the virus to kill chicken embryos at 1 day old or chicks at 6 weeks old |
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What clinical signs are associated with each strain with newcastle disease? |
Lentogenic- In young: mild respiratory disease (same with turkeys) In adults: mild to no respiratory disease, deformed eggs Mesogenic (young)- marked respiratory disease, neck paralysis and death Adult: depression, respiratory signs, CNS sign, halted egg production Turkeys, mild respiratory disease Velogenic (young)- faster onset and 50-100% death Adult: dypsnea, diarrhea, face swelling, morbidity and mortality up to 100% |
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hat gross lesions are seen with Newcastle disease? |
Lentogenic and mesogenic strains- reddening of the trachea, conjunctivitis, airsacculitis Velogenic- hemorrhages in the trachea, esophagus, proventriculus, ventriculus, intestine and and cecal tonsils |
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How do you diagnose newcastle disease? Prevention? |
RT-PCR Virus isolation with phenotyping ELISA, HA, HI, VN Prevention- vaccination MLV and pox-vectored vaccine, most made from a lentogenic strain |
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Marek's disease (range paralysis, neural lymphatosis, skin leukosis) Enveloped/Non-enveloped? RNA/DNA? Family? Serotypes? |
Enveloped DNA Herpesviridae Gallid herpesvirus 2- (serotype 1)-avirulent to oncogenic, found in chickens Gallid herpesvirus 3 (serotype 2)- nononcogenic, found in chickens Meleagrid herpesvirus 1 (serotype 3)- nononcogenic, found in turkeys |
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hat clinical signs are associated with marek's disease? Gross lesions? |
Nervous form: ~Paralysis, dropped leg, wing or twisted neck ~enlarged nerves with loss of cross striation, small irregular pupil Skin form: ~increased condemnation at slaughter ~enlarged feather follicles Tumors: ~increased condemnation, increased daily mortality, thin birds ~White masses on any internal organ |
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ow do you diagnose Marek's disease? Prevention? |
Histopath of brain and lesions, tumors often without bursal involvement Effective cleaning of the environment- virus can remain infective up to 8 months in bird dander MLV vaccines available, liquid nitrogen needed *vaccinate young birds |
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Fowl pox (pox or avian pox): Enveloped/Non-enveloped? DNA/RNA? Family? Strains? |
Enveloped DNA, double strand Poxviridae family Strains- fowl pox, turkey, pigeon, quail, canary, mynah, psittacine |
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What are the two forms of fowl pox? pathogenesis? |
Dry- cutaneous form Wet- diphtheritic form, affecting mucous membranes Transmitted by biting insects and needles Stay viable for months to years in scabs and crusts |
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What are the clinical signs associated with fowl pox? |
Decreased production parameters- dry form Increased mortality and difficulty breathing- wet form Dry scabs and crusts, white to yellow masses and plaques on mough and trachea |
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How do you diagnose and treat fowl pox? |
Histopath, isolation of viruses No treatment but you can vaccinate! MLV in wing web or leg of chickens, leg of turkeys only (due to them sleeping under their wing) ~check for "takes" (scabs) 8-10 days after vaccination- you want 90-95% takes |
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Infectious laryngotracheitis: (ILT, LT, laryngotracheitis) Enveloped/nonenveloped? RNA?DNA? Family? |
enveloped Double stranded DNA Gallid herpesvirus-1 Disease of chickens, pheasants and peafowl *high morbidity and mortality in naive birds Young > old *reportable |
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t clinical signs are associated with infectious laryngotracheitis? |
Death with or without clinical signs, conjunctivitis, cough, head shaking, blood on external nares "pump handle breathing" and abnormal vocalization Spreads easily from bird to bird via fomites Viral shedding lasts up to 15 mouths |
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hat gross lesions are seen with infectious laryngotracheitis? |
Conjunctivitis, blood on nares, mouth, feathers and in trachea (cranial 1/2) Laryngeal and tracheal exudate of blood, blood with mucous, fibrin |
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How do you diagnose infectious laryngotracheitis? Treatment? Prevention? |
Diagnosis- microscopic lesions with intranuclear inclusions, virus isolation in 9-11 day embryonated eggs, PCR
Treatment- none Prevention- vaccination MLV via eye drop, water or spray. Embyro and cell culture derived vaccines, vectored vaccines (use for fairs) *Use MLV in outbreaks |
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Proventricular Dilatation Syndrome (Macaw wasting syndrome, myenteric ganglioneuritis, neuropathic gastric dilitation) What is the etiology? |
Avian bornavirus seen in hook billed birds and canada geese |
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What is the history associated with a bird infected with proventricular dilation syndrome? Gross lesions? |
Chronic weight loss, vomiting, passing undigested seeds in the feces Gross lesions- dilated and thin-walled proventriculus, easily torn, emaciation |
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How do you diagnose proventricular dilitation syndrome? Treatment? Prevention? |
Histopath- infiltration of myenteric plexuses by a pleomorphic population of lymphocytes RT-PCR No treatment, no prevention |
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Pacheco's Parrot disease: Etiology? History? Gross lesions? |
Herpesvirus Acute death- when introduced to other birds, the other birds die and that bird lives Multisystemic viremia, large swollen mottled liver |
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How do you diagnose Pacheco's parrot disease? Treatment? Prevention? |
Diagnose- histopathology with IN inclusions and synsytia No treatment, no vaccine Prevention- make sure you have a quarantine pen for 3 weeks. Then introduce them to a few of your birds to see which die, if any. |
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Polyomavirus (Budgerigar fledging disease) What is the etiology of this disease? Clinical signs? Gross lesions? |
Papovaviridae, genera polyomavirus Found in psittacines, finches, canaries Clinical signs- acute death of young, survivors may have feather dystrophies Gross lesions- hydropericardium, epicardialetechiation, hepatic necrosis |
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How do you diagnose polyomavirus? Treatment? Prevention? |
Diagnose- histopath- looking for karyomegaly, light basophilic glassy material (this can make the diagnosis alone). Can also test with immunohistochemistry and PCR No treatment Prevention- vaccination |
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Papillomavirus what is the etiology? History? Gross lesions? Diagnosis? Treatment? Prevention? |
Papovaviridae, Papillomavirus in Psittacine birds History- tenesmus if cloacal papilloma Gross lesions- papillomas of beak or cloaca, syndrome of cloacal papilloma and cholangiocarcinoma Diagnose- histopath No treatment, no prevention |
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Psittacine beak and feather dystrophy: Etiology? Occurrence? History? Gross lesions? Diagnosis? |
Circovirus Psittacine birds Abnormally feathering and/or beak and nails Gross lesions- abnromal feathers Diagnosis- histopathwith grape cluster cytoplasmic inclusions, PCR No treatment, no vaccine |
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Amazon Tracheitis Etiology? Occurence? Clinical signs? Gross lesions? Diagnosis? |
Herpesvirus Bourke's or Amazon parrots Respiratory disease and/or death Fibrino to fibrinohemorrhagic rhinitis, conjunctivitis, pharyngitis, laryngitis, tracheitis Histopathology with IN inclusions and syncytia No treatment, no prevention |
