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118 Cards in this Set

  • Front
  • Back

Tuberculosis is caused by what organism?

Mycobacterium bovis

Clinical signs of tuberculosis?

Early: often asymptomatic

Fluctuating fever, weakness, inappetence, moist cough, dyspnea or tachypnea, LN enlargement

What kind of virus is BVDV?

pestivirus: + sense RNA, enveloped

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

BVDV reservoir?

Persistently infected animals (they won't clear the infection because the immune system recognizes it as self 45-125 days gestation)

What kind of BVDV vaccine is important not to give to a pregnant cow?

MLV --> can infect fetus

BVDV presentation: reproductive losses?

congenital defects (cerebellar hypoplasia), performance losses

BVDV signs

panleukopenia, respiratory issues, ataxia, stumbling, failure to nurse

fever, lethargy, loss of appetite, ocular discharge, oral lesions, diarrhea and decreasing milk production

Q fever is what etiology?

Coxiella burnetti

Q fever presents how:

abortion in sheep

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

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

What species is a possible long time shedder of Q fever?


Is there a vaccine for Q fever?

yes, a killed vaccine

Anthrax is what agent?

Bacillus anthracis

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

An interesting fact with anthrax infection post mortem?

no rigor mortis

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

Etiology behind blackleg? What is it?

Clostridium charuvei : gram + sport forming, rod shaped bacteria

Clostridium chaurvoei or _______________ lives where?

Black leg lives in the soil

True blackleg is common to what species and via what route of infection?

Cattle where infected wounds are entries of infection

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

Treatment/prevention for Clostridium chavoei or _________________?

Blackleg treatment includes: penicillin and surgical debridement of the lesion.


Recovery is low

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

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

How is Bovine leukosis transmitted?

horizontally: infected lymphocytes in blood from parturition, rectal palpation, blood sucking insects

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

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

Pathogenesis of bovine leukosis?

virus establishes a persistent infection in B lympocytes

80% of animals have a depressed IgM globulin production

Treatment for bovine leukosis or _______________ caused by _______________?

No treatment.

bovine lymphosarcoma

bovine leukemia virus

Anaplasma in cattle is caused by what pathogen?

Anaplasma marginale

What is the pathogen that causes anaplasma in cattle?

Anaplasma marginale is an obligate intra-erythrocyte parasite of the rickettsiales family.

Anaplasma in cattle is transmitted how?

ticks, particularly Dermacenter spp and Boophilus spp.

Does the pathogen behind cattle anaplasmosis or ______________ require the tick?

Yes, Anaplasma marginale, matures and used the tick for maturative lifecycle stages

Presentation for cattle anaplasmosis?

fever, anemia, reproductive losses, performance losses and mortality

What is the pathogenesis behind cattle anaplasmosis?

infect mature RBC and cause anemia

Diagnose anaplasma?

blood smear, PCR, ELISA

Treatment for cattle anaplasma?

abx, blood transfusion

Anaplasma species in other species?

Anaplasma ovis for sheep and goats

Babesiosis is also called what?

Texas fever or cattle tick fever

Babesiosis occurs in what species?

cattle, sheep, goats, horses, cervids, and pigs

Transmission of babesiosis?

by ticks: Rhipicephalus, Dermaceter

Babesiosis in different species? Cattle?

Babesia bovis, B bigemina, divergens and major

Babesiosis species in horses?

B. equi, caballi

Clinical signs of babesiosis?

anemia, hemoglobinuria, jaundice, high case fatality, +/- fever, depression, weakness, emaciation...

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

Do all animals die from babesiosis infection?

no. The ones that survive the initial insult may become carriers.

Subclinical infections can be reactivated.

Treatment of babesiosis?

diminazen aceturate, imidocarb dipropionate or anicarbolide disethionate

When you think rinderpest what do you think?

Reportable! And not in the US. (lol)

Rinderpest is caused by what?

Morbilivirus (paramyxoviridae)

Who does rinderpest affect?

Ruminants and rarely swine

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)

Rinderpest clinical signs?

fever, oculonasal discharge, salivation, ulcerative stomatitis, diarrhea, dehydration, death (case fatality 100%)

Treatment for Rinderpest?


Malignant catarrhal fever is characterized by what?

Rhinitis, keratoconjunctivitis, and GI lesions

Malignant catarrhal fever is caused by what?

Two infectious agents: herpes viruses

Malignant catarrhal fever affects what species?

cattle, deer and buffalo

There are 3 forms of Malignant Catarrhal fever, what are they?


alimentary tract

"head and eye" form

Diagnosis and treatment for Malignant Catarrhal fever?

Diagnosis: necropsy, isolation difficult

Treatment: none. Important to distinguish from other diseases

White muscle disease is caused by what?

Vitamin E or Selenium deficiency.

What occurs in White Muscle disease?

accumulation of free radicals leading to muscle degeneration and a calcium deposit necrosis

What are some signs fo White Muscle Disease?

lameness, locomotor impairment, dyspnea is diaphragm is affected

What is the etiologic agent that causes Botulism?

Clostriudium botulinum

What is Clostridium botulinum?

Gram +, spore-forming anaerobe commonly found in the soil

How many types of Clostridium botulinum ?

There are 4 types: A, B, C (N America) and D

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

Clinical signs of botulism?

Ascending flaccid paralysis leading eventually to death due to diaphragm paralysis and respiratory failure

Etiologic agent behind Tetanus.

Clostridium tetani

What is Clostridium tetani?

gram +, anaerobic bacillus, spore forming

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

Treatment/prevention of tetanus?

tetanus toxoid vx.

Tetanus vx

What is the etiology behind Infectious Bovine Keratoconjunctivits?

Moraxella bovis or M bovoculi

Can be Mycoplasma or BHV-1

IBK infects young or old?

more often young

IBK looks like what?

tearing --> indicates ACTIVE infection

corneal opacity


corneal ulcer --> can lead to ruptured cornea

Diagnosis of IBK?

conjunctival swab


Treatment for IBK?

parenteral abx (broad spectrum --> oxytet, ceftiofur)

topical or subconj abx




Bluetongue is caused by what?

bluetongue virus

Bluetongue occurs in what species?

domestic and wild ruminants

Bigger problem in sheep

Bluetongue virus is what?

dsRNA, non-enveloped

Clinical signs of Bluetongue: what are the general forms of the disease?

Manifested in two ways:

Reproductive syndrome

Vasculitis disease

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

What is one sign not typically seen with Bluetongue infections?

a blue tongue. HA

What is a common clinical finding complicates Bluetongue infection?

Secondary bacterial bronchopneumonia

Treatment for Bluetongue?

Supportive mainly. Abx for secondary infections and NSAIDs to battle coronitis

What are some toxins that cause bovine abortion?

Ponderosa pine needles.


Broon snakewood

Moldy sweet clover



What is the biggest concern with ponderosa pine needle toxicity?

3rd trimester abortion

Locoweed causes what mainly?

repro problems: from altered sexual behavior to increased embryonic loss to abortion and abnormal mother instincts

Broom snakeweed commonly looks like what in patients?

Lots: from abortion storms, to listlessness, to gastroenteritis, to crusty mucopurulent nasal discharge

Does Broom Snakeweed taste good?

No, it really will only be consumed if there is nothing else

Moldy Sweet Clover work in the liver doing what?

Interferes with synthesis of Vitamin K dep factors

Moldy Sweet Clover causes what ultimately?


How long does it take signs to appear for Moldy Sweet Clover?

3-6 weeks

How are nitrates useful to ruminants?

nitrates consumed are turned into ammonia int he rumen by microbes, then into protein that can be digested

What is the rate limiting step in the nitrate pathway?

Nitrate is converted to nitrite faster than nitrite is converted to ammonia

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

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

Dictyyocaulus viviparous is what?


Dictyocaulus viviparous infects what site?

infects: trachea and larger bronchi

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

Clinical signs of lungworm or ____________________ infection?

CS: coughing and tachypnea, parasitic pneumonia, interstitial emphysema, pulmonary edema

Dictyocaulus viviparous

Who is commonly affected by Dictyocaulus viviparous?

first season calves

Treatment for lungworms?

ivermectin, vaccine

For fun, what is the lungworm species of horses?

Dictyocaulus arnfeldi

Trichostrongylus axei or _________________________ infects where?

Stromach hairworm

infects the abomasum and small intestine

Stomach worm or __________________ lifecycle in short?

Trichostrongylus axei

direct lifecycle: larvae are ingested --> insheath --> penetrate intestine

Treatment for stomcch hairworm or _____________________.

pyrantel, albendazole, fendendazole, ivermectin

Trichostrongylus axei

Signs of stomach hairworm infection?

seldom pathogenic: weight loss, anorexia

Barberpole worm is also known as.....____________. (scientific name)

Haemonchus sp.

Haemonchus sp or _______________________ infects what part of the GI?


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.

Clinical signs of barberpole worm infection?

anemia, hypoproteinemia, edema (bottle jaw), weight loss, weakness, rough coat, anorexia

Treatment for _________________ or barberpole infection?

Hawmonchus spp

albendazole, ivermectin

Cooperia infects what site?

small intestine

Life cycle of cooperia?

worms do no suck blood! Persist with ostertagia and haemonchus

Clinical signs for Cooperia infection?

anorexia, villous atrophy and diarrhea, decreased weight gain

Treatment for Cooperia?

albendazole, fenbendazole, levamisole, ivermectin

Brown stomach worm or _____________________ infects what GI site?

Ostertagia ostertagi

abomasum, specifically the gastric fundus and pylorus

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