Food Ani. Med- Small Ruminant Diseases 2

wilsbach's version from 2016-01-20 04:36


Question Answer
Enzootic Nasal Tumor-- what is the common signalment for this dz? (who gets it?)2 - 4 yr. old sheep & goats
how is enzootic nasal tumor transmitted, and how easy is it to elim from the herd?Contagious via nasal fluids. Once in herd hard to eliminate
what is the etiological agent of enzootic nasal tumor? Type D Retrovirus: Enzootic nasal tumor virus
what KIND** of tumor is the enzootic nasal tumor? How common is metastasis?Adenocarcinomas or adenomas. No metastasis has been reported, but it is locally invasive
how are the nasal passages affected in enzootic nasal tumor?retrovirus leads to Neoplastic transformation of epithelial cells of the ethmoid turbinate. Disruption of the nasal septum structure as well as erosion of the cribriform plate has been reported (weird shaped face, trouble breathing) (remember cribriform plate is where cranial nerves pass)
what are clinical signs for enzootic nasal tumor?Uni/bilateral serous, mucoid or mucopurulent discharge, Progressive inspiratory dyspnea (structural changes and space occupying masses), Dullness on percussion over turbinates (open mouth to hear acoustics better if you aren't sure), sneezing, head shaking, loss of condition, Exophthalmos from facial deformity, Subsequent exercise intolerance, open mouth breathing and emaciation
what are some ways to dx Enzootic nasal tumor?PE, rads, enddoscopy, tissue bx and PCR.
tx for enzootic nasal tumor?palliative or slaughter
how can you help prevent enzootic nasal tumor?herd biosecurity.
Oestrus Ovis is aka?nasal bot
what is the signalment of who can get Oestrus Ovis?Sheep and Goats mainly, but can also be humans, dogs and cats. There is NO age predilection and it can occur worldwide
what is the seasonality of Oestrus Ovis like?Fly activity is more common in the warmer months, with peak times in spring and late summer
how is oestrus ovis transmitted? (lifecycle)The adult female fly deposits larvae within a tiny mucous drop in or around the nares, conjunctiva, occasionally lips and mouth. larvae then migrate to the nasal sinus and continue to develop. The larval period lasts about 1-10 months and when mature, they leave the nasal passages, drop to the ground, burrow and pupate (the sheep will sneeze like crazy during this time), The fly emerges, mating occurs and the cycle starts again
what is the pathophysiology of oestrus ovis?Migration of larvae up the nasal cavity induces inflammation. Inflamed tissue may become secondarily infected (eosinophilic inflammation.)
what are 3 major predisposing factors to oestrus ovis?(1) Low altitudes (climate at high altitudes not favorable for development of o. ovis) (2) Medium to large flock size (250), high ovine population density (3) Nose color (dark noses at a higher risk)
which noses do oestrus ovis like?DARKLY COLORED noses
what kinda altitudes does oestrus ovis like?LOW altitudes
what is the nasal discharge caused by oestrus ovis like?Clear, Mucoid, Mucopurulent and Blood tinged
what are the clinical signs of oestrus ovis?Nasal discharge (Clear, Mucoid, Mucopurulent and Blood tinged.), Annoyance (shaking head, sneezing, rubbing nose/face), Weight loss due to decreased feeding, Cx of hypersensitivity. Also see Respiratory distress, pulmonary edema and lung congestion (this is due to the severe and forceful sneezing, not the bot itself)
how can you dx oestrus ovis?Clinical signs, Radiographs of the head, Endoscopy, Serology (mostly used for epidemiological research)
WHEN is the best time to tx oestrus ovis?Treatment is best done after the first freeze* has killed the adult flies, to reduce reinfection rates until the warm weather returns
how do you tx oestrus ovis? (1 tx for in the states, 2 that aren't approved for the states)Ivermectin at 200 μg/ kg PO is effective against the nasal larvae. Also, A 1% Moxidectin injectable dose is effective but not approved for use in the United States. Eprinomectin 0.5 mg/kg topical (post shearing) and doramectin 200 μg/ kg IM are effective but not approved in the United States
what are two things you can do to help prevent oestrus ovis?(1) Prevent with regular anthelmintic treatment after freezes and to prevent long term infections. (Ivermectin) (2) fly control
Ovine Progressive Pneumonia--> signalment of who gets this?SHEEP, and very rarely goats. Adult animals 2-4 years old typically but any age possible
how can OPP be xmitted?Oral (colostrum AND Milk commonly), Aerosolized droplet inhaled, Possible intrauterine transmission
what is the causative agent of OPP?Lentivirus (retrovirus) maedi visna virus (specific type of Lentivirus)
why are there many patterns of dx for OPP?The viruses (lenti/retrovirus) ability to mutate and form new serovars through antigenic drift results in different patterns of the disease
where does the virus which causes ovine progressive pneumonia like to hang out?remember it is a lentivirus (retrovirus, specifically maedi visna virus) so it can enter latent stages. The virus likes to persist in infected monocytes and microphages
explain the pathophysiology of OPPOral or respiratory infection to monocytes to lungs, central nervous system and hemopoeitic tissue may also localize in lymph organs, mammary (hence milk transmission) and kidneys.
When does the OPP virus like to replicate?Virus replicates only on differentiation of monocytes into macrophages
*explain what the OPP virus does to the lungs specifically (pathophysiology)*Within the lungs the virus causes the reticular cells and lymphocytes to proliferate leading to thickening of the intra-alveolar septa and production of adenomatosis (a condition marked by multiple growths consisting of glandular tissue) of the alveolar lining. Chronic, degenerative, slowly progressive pneumonia ensues
clinical signs of OPP?Progressive respiratory failure (duh). Signs open subtle, un-noticed until animal is stressed. Lagging behind flock, coughing and has clear nasal discharge. Exercise intolerance, open mouth breathing. Increased breath sounds on auscultation. No crackles or wheezes on thoracic auscultation (just increased lung sounds), Clinical course may be short 3 – 6 months but may also drag on for years
how are some ways you can dx OPP? (3)(1) Presumptive off clinical signs (2) SEROLOGY (AGID test is test of choice in eradication programs but ELISA are more sensitive.) (3) PCR is more economical than virus isolation on tissues. PCR used to confirm after positive AGID or ELISA serologic testing
how can you dx OPP on necropsy?heavy firm grey blue lungs that do not collapse and have vertical rib impressions. Tracheobronchial and mediastinal lymph nodes are enlarged and bulge on cut surface.
what other dzs must you differentiate OPP from, and how do you do this?Must differentiate from pulmonary adenocarcinoma, pleural abscesses, and pulmonary caseous lymphadenitis. Ultrasound is a good way to do this
how do you tx OPP?NO TX-- abx for 2* infxn
is there a vx for OPP?no
how can you help prevent OPP?Only options are test and cull or isolation
describe the eradication program for OPP. How often should you test for OPP?Use both tests (AGID/ELISA + PCR for confirmation), and repeat tests 2 – 3 times over several months. Two consecutive negative results to confirm clear. Check entire flock 2x a year. Remove all seropositive animals from herd and test new stock
Caprine Arthritis and Encephalitis (CAE)-- what are the 3 disease presentations of this, and WHO is prone to each type?(1) LEM (leukoencephalomalacia) 2 – 6 month old kids and sometimes lambs. (2) Arthritis: 6 months to adult (3) pneumonia: adult
how is CAE transmitted?Oral (colostrum AND Milk commonly) or other infected body fluids. Aerosolized droplet inhaled. Possible intrauterine transmission
what is the causative agent of CAE?Lentivirus from Retroviridae family
explain the pathophysiology of CAEGranulomatous inflammatory reaction caused by immune complexes formed by antibodies against lymphocytes and virus-infected macrophages --> complexes are found in synovium, mammary gland, and CNS
is there a genetic predisposition for CAE or OPP?CAE (genetic predisposition to develop the arthritis)
4 predisposing factors for getting CAE(1) A genetically determined predisposition for development of CAEV arthritis exists and can be identified through the use of DNA fingerprinting (2) Unsanitary management practices (Iatrogenic transmission is possible. Disinfect equipment with quaternary ammonium solutions) (3) Feeding colostrum from infected animals to non-infected animals is a common source of infection. (4) Overcrowding/close contact with infected animals
what are the clinical signs for the LEM (leukoencephalomalacia) part of CAE? (who gets this again?)(lem=2-6mo old kids) Weight loss and failure to grow, Progressive ascending paresis and paralysis (uni/ bilateral posterior paresis and ataxia ), Signs associated with head also seen.
If you have a 5mo old kid suffering from the LEM syndrome of CAE, and you decide to do a CSF tap, what might you see?CSF may have a high protein level and a mononuclear pleocytosis.
which syndrome of CAE is the least latent? Most latent?LEM (leukoencephalomalacia) is least. arthritis is most.
LEM has a faster progression in who?faster in goats than in sheep
which of the 3 syndromes of CAE is the most common?The arthritis (and most common in goats 6mo-adult)
what are the clinical signs of the arthritis syndrome of CAE?Chronic, slow progressive (most latent of all the syndromes) Poly arthritis with associated lameness and pain, Most common of all the syndromes
what are the clinical signs of the pneumonia syndrome of CAE like?Chronic progressive respiratory distress, High latency, usually only found at post mortem. Weight loss and dyspnea are significant findings
Hard bag/ Indurative mastitis is associated with what dz? explain how this happens.This is a problem seen with CAE! Older females clinical but acquired as neonates at nursing (so see signs at first lactation). They will have a Firm and painful udder. Mononuclear infiltration of periductular stroma obliterates normal mammary tissue
what is the best test for herd screening with CAE?AGID (agar gel immunodiffusion) for antibodies
what is the best test for individual testing for CAE?ELISA for detection of whole virus
is PCR a good or a bad test for CAE?you can PCR milk, tissue, and blood for Ag. will be positive near the day of infection as it does not require seroconversion to detect infection. The heterogeneity and low viral load impede this test
can you culture/virus isolate for CAE?you can culture. Isolation is possible but slow (4-8wk) and has poor sensitivity
how helpful are colostral Abs against CAE?useless
what should you know about testing young goat kids for CAE? When is the best time to test?Goat kids may be transiently positive for antibodies during first 8 – 16 weeks of life due to colostrum consumption. Colostral antibodies are not protective but may be present for 90 days of life. Kids may seroconvert to true viral infection due to viral shedding from infected dam. So, you must test kids over 6mo old
what is a big difficulty with the way CAE works and trying to dx them?The profound latency associated with this virus may lead to seropositive animals without clinical disease. Also, Seroconversion in goats is delayed, consequently false negatives are a common feature in the early stages of this disease
how do you tx CAE?supportive tx only
is there a vx for cae?no
how can you help prevent CAE?(NO VX) Test and cull programs and strict biosecurity. Testing should be carried out every 6 months and not on animals less than 90 days old. Strict colostrum management is imperative

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