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118 Cards in this Set
- Front
- Back
Tuberculosis is caused by what organism? |
Mycobacterium bovis |
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Clinical signs of tuberculosis? |
Early: often asymptomatic Fluctuating fever, weakness, inappetence, moist cough, dyspnea or tachypnea, LN enlargement |
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What kind of virus is BVDV? |
pestivirus: + sense RNA, enveloped |
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BVDV effects what? |
oral cavity to GI tract --> mechanism is dysfunction and death of mucosal epithelial cells preceded by dysfunction and death of lymphocytes in MALT |
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BVDV reservoir? |
Persistently infected animals (they won't clear the infection because the immune system recognizes it as self 45-125 days gestation) |
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What kind of BVDV vaccine is important not to give to a pregnant cow? |
MLV --> can infect fetus |
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BVDV presentation: reproductive losses? |
congenital defects (cerebellar hypoplasia), performance losses |
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BVDV signs |
panleukopenia, respiratory issues, ataxia, stumbling, failure to nurse fever, lethargy, loss of appetite, ocular discharge, oral lesions, diarrhea and decreasing milk production |
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Q fever is what etiology? |
Coxiella burnetti
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Q fever presents how: |
abortion in sheep |
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Coxiella burnetti is what kind of pathogen? |
gram -, obligate intracellular bacterial pathogen, highly resistant to environmental stressors such as temp, osmotic pressure and UV light |
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What is the lifecycle of Q fever? |
Coxiella burnetti cycles in cattle, sheep and goats. Transmission is by directed contact or inhalation. --> remains latent until pregnancy when there is activation and infection of the intestine, uterus, placenta and fetal fluids --> abortion and stillbirths |
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What species is a possible long time shedder of Q fever? |
cattle |
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Is there a vaccine for Q fever? |
yes, a killed vaccine
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Anthrax is what agent? |
Bacillus anthracis |
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Pathogenesis of anthrax? |
infection gains entrance to the body by ingestion, inhalation, or through the skin --> resistance to phagocytosis allows them to proliferate in lymph nodes --> septicemia with massive organ invasion eventually occurs
lethal toxin production causes edema and tissue damage, death resulting from shock and ARF |
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An interesting fact with anthrax infection post mortem? |
no rigor mortis |
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Treatment/prevention for anthrax? |
severely affected are unlikely to recover. Streptomycin or oxytet can be used in Tx of clinical cases vaccination in cattle and sheep antiserum within 5 days, expensive |
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Etiology behind blackleg? What is it? |
Clostridium charuvei : gram + sport forming, rod shaped bacteria |
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Clostridium chaurvoei or _______________ lives where?
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Black leg lives in the soil |
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True blackleg is common to what species and via what route of infection? |
Cattle where infected wounds are entries of infection |
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Pathogenesis behind blackleg or ______________? |
Clostridium chavouei produces a toxin that causes severe necrotizing myositis locally in skeletal muscles and a systemic toxemia that is fatal |
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Treatment/prevention for Clostridium chavoei or _________________? |
Blackleg treatment includes: penicillin and surgical debridement of the lesion. Vaccinate Recovery is low |
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Bovine leukosis is also called what? What is the etiologic agent? Then tell me more about the agent? |
Bovine Lymphosarcoma caused by Bovine leukemia virus: C type oncovirus in the Retroviridae family |
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What is most common with Bovine leukosis infection. Etiology again please. |
Bovine leukemia virus commonly presents with persistent infection followed by persistent lymphocytosis with a small % developing lymphosarcoma |
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How is Bovine leukosis transmitted? |
horizontally: infected lymphocytes in blood from parturition, rectal palpation, blood sucking insects |
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What other condition is bovine leukosis or ______________ caused by _______________ associated with? |
Bovine lymphosarcoma Bovine leukemia virus immune compromised animals beause of concurrent trichophyton verrucosum infection |
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What are clinical signs associated with bovine leukosis? |
no clinical signs during stage of infection and persistent lymphocytosis lymphosarcoma: loss of condition, inappetence, weakness, pallor and loss in milk production may also be associated with CHF, abomasal ulceration and lymph node enlargement |
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Pathogenesis of bovine leukosis? |
virus establishes a persistent infection in B lympocytes 80% of animals have a depressed IgM globulin production |
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Treatment for bovine leukosis or _______________ caused by _______________? |
No treatment. bovine lymphosarcoma bovine leukemia virus |
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Anaplasma in cattle is caused by what pathogen? |
Anaplasma marginale |
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What is the pathogen that causes anaplasma in cattle? |
Anaplasma marginale is an obligate intra-erythrocyte parasite of the rickettsiales family. |
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Anaplasma in cattle is transmitted how? |
ticks, particularly Dermacenter spp and Boophilus spp. |
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Does the pathogen behind cattle anaplasmosis or ______________ require the tick? |
Yes, Anaplasma marginale, matures and used the tick for maturative lifecycle stages |
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Presentation for cattle anaplasmosis? |
fever, anemia, reproductive losses, performance losses and mortality |
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What is the pathogenesis behind cattle anaplasmosis? |
infect mature RBC and cause anemia |
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Diagnose anaplasma? |
blood smear, PCR, ELISA |
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Treatment for cattle anaplasma? |
abx, blood transfusion |
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Anaplasma species in other species?
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Anaplasma ovis for sheep and goats |
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Babesiosis is also called what? |
Texas fever or cattle tick fever |
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Babesiosis occurs in what species? |
cattle, sheep, goats, horses, cervids, and pigs |
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Transmission of babesiosis? |
by ticks: Rhipicephalus, Dermaceter
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Babesiosis in different species? Cattle? |
Babesia bovis, B bigemina, divergens and major
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Babesiosis species in horses? |
B. equi, caballi |
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Clinical signs of babesiosis? |
anemia, hemoglobinuria, jaundice, high case fatality, +/- fever, depression, weakness, emaciation... |
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Pathogenesis of babesiosis? |
protozoa are present in the bloodstream --> engulfed via endocytosis into RBC --> maturity producing merozoites --> lysis of RBC = hemolytic anemia this causes release of inflammatory mediators --> vasodilation and hypotension --> increasing vascular permeability --> shock and DIC |
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Do all animals die from babesiosis infection? |
no. The ones that survive the initial insult may become carriers. Subclinical infections can be reactivated. |
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Treatment of babesiosis? |
diminazen aceturate, imidocarb dipropionate or anicarbolide disethionate |
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When you think rinderpest what do you think?
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Reportable! And not in the US. (lol) |
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Rinderpest is caused by what?
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Morbilivirus (paramyxoviridae) |
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Who does rinderpest affect? |
Ruminants and rarely swine |
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What is the pathogenesis of rinderpest? |
inhalation or ingestion --> infects URT --> replicates in tonsils and regional lymph nodes --> replicates in monocytes, lymphocytes, and epithelial cells (leukopenia results) |
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Rinderpest clinical signs? |
fever, oculonasal discharge, salivation, ulcerative stomatitis, diarrhea, dehydration, death (case fatality 100%) |
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Treatment for Rinderpest? |
none |
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Malignant catarrhal fever is characterized by what? |
Rhinitis, keratoconjunctivitis, and GI lesions |
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Malignant catarrhal fever is caused by what? |
Two infectious agents: herpes viruses |
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Malignant catarrhal fever affects what species? |
cattle, deer and buffalo |
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There are 3 forms of Malignant Catarrhal fever, what are they? |
Peracute
alimentary tract "head and eye" form |
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Diagnosis and treatment for Malignant Catarrhal fever? |
Diagnosis: necropsy, isolation difficult Treatment: none. Important to distinguish from other diseases |
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White muscle disease is caused by what? |
Vitamin E or Selenium deficiency.
|
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What occurs in White Muscle disease? |
accumulation of free radicals leading to muscle degeneration and a calcium deposit necrosis |
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What are some signs fo White Muscle Disease? |
lameness, locomotor impairment, dyspnea is diaphragm is affected |
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What is the etiologic agent that causes Botulism? |
Clostriudium botulinum |
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What is Clostridium botulinum? |
Gram +, spore-forming anaerobe commonly found in the soil |
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How many types of Clostridium botulinum ? |
There are 4 types: A, B, C (N America) and D |
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MOA of botulism? |
blood stream --> enters axons and presynaptic terminals --> disables the SNARE protein --> prevents the fusion of vesicles and thus exocytosis and neurotransmitter release --> NO ACh release into the synaptic space --> flaccid paralysis |
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Clinical signs of botulism? |
Ascending flaccid paralysis leading eventually to death due to diaphragm paralysis and respiratory failure |
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Etiologic agent behind Tetanus. |
Clostridium tetani |
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What is Clostridium tetani? |
gram +, anaerobic bacillus, spore forming |
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Pathogenesis of tetanus? |
Tetanus toxin is taken up into the nerve terminals of the lower motor neurons (nerves that activate voluntary muscle) --> retrograde transport in axons --> toxin taken up by nerve endings of inhibitory GABA-nergic --> cleaves VAMP --> inhibits the release of GABA and glycine = partial, functional denervation of the LMN --> LMN hyperactivity and increased muscle activity in the form of rigidity and spasms |
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Treatment/prevention of tetanus? |
tetanus toxoid vx. Tetanus vx |
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What is the etiology behind Infectious Bovine Keratoconjunctivits? |
Moraxella bovis or M bovoculi Can be Mycoplasma or BHV-1 |
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IBK infects young or old? |
more often young |
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IBK looks like what? |
tearing --> indicates ACTIVE infection corneal opacity conjunctivitis corneal ulcer --> can lead to ruptured cornea |
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Diagnosis of IBK? |
conjunctival swab staining |
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Treatment for IBK? |
parenteral abx (broad spectrum --> oxytet, ceftiofur) topical or subconj abx NSAIDs Patch surgery |
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Bluetongue is caused by what? |
bluetongue virus |
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Bluetongue occurs in what species? |
domestic and wild ruminants Bigger problem in sheep |
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Bluetongue virus is what? |
dsRNA, non-enveloped |
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Clinical signs of Bluetongue: what are the general forms of the disease? |
Manifested in two ways: Reproductive syndrome Vasculitis disease |
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Clinical signs of Bluetongue more specifically? |
Transient fever, edema of the face, lips, muzzle and ears. Extensive salivation and hyperemia of the oral mucosa. Oral petechial hemorrhages, erosions and ulcers Profuse serous nasal discharge may also occur --> mucopurulent too |
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What is one sign not typically seen with Bluetongue infections? |
a blue tongue. HA |
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What is a common clinical finding complicates Bluetongue infection? |
Secondary bacterial bronchopneumonia |
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Treatment for Bluetongue? |
Supportive mainly. Abx for secondary infections and NSAIDs to battle coronitis |
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What are some toxins that cause bovine abortion? |
Ponderosa pine needles. Locoweed Broon snakewood Moldy sweet clover Mycotoxins Nitrates |
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What is the biggest concern with ponderosa pine needle toxicity? |
3rd trimester abortion |
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Locoweed causes what mainly? |
repro problems: from altered sexual behavior to increased embryonic loss to abortion and abnormal mother instincts |
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Broom snakeweed commonly looks like what in patients? |
Lots: from abortion storms, to listlessness, to gastroenteritis, to crusty mucopurulent nasal discharge |
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Does Broom Snakeweed taste good? |
No, it really will only be consumed if there is nothing else |
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Moldy Sweet Clover work in the liver doing what? |
Interferes with synthesis of Vitamin K dep factors |
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Moldy Sweet Clover causes what ultimately? |
hemorrhage |
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How long does it take signs to appear for Moldy Sweet Clover?
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3-6 weeks |
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How are nitrates useful to ruminants?
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nitrates consumed are turned into ammonia int he rumen by microbes, then into protein that can be digested |
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What is the rate limiting step in the nitrate pathway? |
Nitrate is converted to nitrite faster than nitrite is converted to ammonia |
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What does it mean to have high levels of nitrite in the rumen? |
Nitrite is absorbed into the bloodstream and will convert hemoglobin to methemoglobin which is unable to transport oxygen |
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How often does nitrate toxicity occur? |
Hard to tell because some plants may or may not have enough to too much in terms of recommended levels |
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Dictyyocaulus viviparous is what? |
lungworm |
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Dictyocaulus viviparous infects what site? |
infects: trachea and larger bronchi |
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Lungworms or _________________ has what kind of lifecycle in short? |
Dictycaulus viviparous adult worms found in the trachea --> females lay eggs --> coughed up and swallowed --> L2-L3 in feces --> new host ingest eggs --> Larvae migrate via blood to respiratory tree |
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Clinical signs of lungworm or ____________________ infection? |
CS: coughing and tachypnea, parasitic pneumonia, interstitial emphysema, pulmonary edema Dictyocaulus viviparous |
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Who is commonly affected by Dictyocaulus viviparous? |
first season calves |
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Treatment for lungworms? |
ivermectin, vaccine |
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For fun, what is the lungworm species of horses? |
Dictyocaulus arnfeldi |
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Trichostrongylus axei or _________________________ infects where? |
Stromach hairworm infects the abomasum and small intestine |
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Stomach worm or __________________ lifecycle in short? |
Trichostrongylus axei direct lifecycle: larvae are ingested --> insheath --> penetrate intestine |
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Treatment for stomcch hairworm or _____________________. |
pyrantel, albendazole, fendendazole, ivermectin Trichostrongylus axei |
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Signs of stomach hairworm infection? |
seldom pathogenic: weight loss, anorexia |
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Barberpole worm is also known as.....____________. (scientific name) |
Haemonchus sp. |
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Haemonchus sp or _______________________ infects what part of the GI? |
abomasum |
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What is the lifecycle in short of the Barberpole worm, or ______________________. |
L1 hatch in the pasture --> develop into L3 in 5 days --> L3 is ingested --> moults to L4 --> L4 penetrates the lining of the abomasum Haemonchus sp. |
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Clinical signs of barberpole worm infection? |
anemia, hypoproteinemia, edema (bottle jaw), weight loss, weakness, rough coat, anorexia |
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Treatment for _________________ or barberpole infection? |
Hawmonchus spp albendazole, ivermectin |
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Cooperia infects what site? |
small intestine |
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Life cycle of cooperia? |
worms do no suck blood! Persist with ostertagia and haemonchus |
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Clinical signs for Cooperia infection? |
anorexia, villous atrophy and diarrhea, decreased weight gain |
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Treatment for Cooperia? |
albendazole, fenbendazole, levamisole, ivermectin |
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Brown stomach worm or _____________________ infects what GI site? |
Ostertagia ostertagi abomasum, specifically the gastric fundus and pylorus |
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Lifecycle in short of Ostertagia ostertagi or _________________________. |
17-21 days post ingestion parasite emerges from gastric glands --> releases eggs --> transmission continues by another animal consuming Brown stomach worm |