Livestock Ii General Iii

Front 1

Tuberculosis is caused by what organism?

Back 1

Mycobacterium bovis

Front 2

Clinical signs of tuberculosis?

Back 2

Early: often asymptomatic

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

Front 3

What kind of virus is BVDV?

Back 3

pestivirus: + sense RNA, enveloped

Front 4

BVDV effects what?

Back 4

oral cavity to GI tract --> mechanism is dysfunction and death of mucosal epithelial cells preceded by dysfunction and death of lymphocytes in MALT

Front 5

BVDV reservoir?

Back 5

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

Front 6

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

Back 6

MLV --> can infect fetus

Front 7

BVDV presentation: reproductive losses?

Back 7

congenital defects (cerebellar hypoplasia), performance losses

Front 8

BVDV signs

Back 8

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

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

Front 9

Q fever is what etiology?

Back 9

Coxiella burnetti

Front 10

Q fever presents how:

Back 10

abortion in sheep

Front 11

Coxiella burnetti is what kind of pathogen?

Back 11

gram -, obligate intracellular bacterial pathogen, highly resistant to environmental stressors such as temp, osmotic pressure and UV light

Front 12

What is the lifecycle of Q fever?

Back 12

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

Front 13

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

Back 13

cattle

Front 14

Is there a vaccine for Q fever?

Back 14

yes, a killed vaccine

Front 15

Anthrax is what agent?

Back 15

Bacillus anthracis

Front 16

Pathogenesis of anthrax?

Back 16

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

Front 17

An interesting fact with anthrax infection post mortem?

Back 17

no rigor mortis

Front 18

Treatment/prevention for anthrax?

Back 18

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

Front 19

Etiology behind blackleg? What is it?

Back 19

Clostridium charuvei : gram + sport forming, rod shaped bacteria

Front 20

Clostridium chaurvoei or _______________ lives where?

Back 20

Black leg lives in the soil

Front 21

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

Back 21

Cattle where infected wounds are entries of infection

Front 22

Pathogenesis behind blackleg or ______________?

Back 22

Clostridium chavouei produces a toxin that causes severe necrotizing myositis locally in skeletal muscles and a systemic toxemia that is fatal

Front 23

Treatment/prevention for Clostridium chavoei or _________________?

Back 23

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

Vaccinate

Recovery is low

Front 24

Bovine leukosis is also called what? What is the etiologic agent? Then tell me more about the agent?

Back 24

Bovine Lymphosarcoma caused by Bovine leukemia virus: C type oncovirus in the Retroviridae family

Front 25

What is most common with Bovine leukosis infection. Etiology again please.

Back 25

Bovine leukemia virus commonly presents with persistent infection followed by persistent lymphocytosis with a small % developing lymphosarcoma

Front 26

How is Bovine leukosis transmitted?

Back 26

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

Front 27

What other condition is bovine leukosis or ______________ caused by _______________ associated with?

Back 27

Bovine lymphosarcoma

Bovine leukemia virus

immune compromised animals beause of concurrent trichophyton verrucosum infection

Front 28

What are clinical signs associated with bovine leukosis?

Back 28

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

Front 29

Pathogenesis of bovine leukosis?

Back 29

virus establishes a persistent infection in B lympocytes

80% of animals have a depressed IgM globulin production

Front 30

Treatment for bovine leukosis or _______________ caused by _______________?

Back 30

No treatment.

bovine lymphosarcoma

bovine leukemia virus

Front 31

Anaplasma in cattle is caused by what pathogen?

Back 31

Anaplasma marginale

Front 32

What is the pathogen that causes anaplasma in cattle?

Back 32

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

Front 33

Anaplasma in cattle is transmitted how?

Back 33

ticks, particularly Dermacenter spp and Boophilus spp.

Front 34

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

Back 34

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

Front 35

Presentation for cattle anaplasmosis?

Back 35

fever, anemia, reproductive losses, performance losses and mortality

Front 36

What is the pathogenesis behind cattle anaplasmosis?

Back 36

infect mature RBC and cause anemia

Front 37

Diagnose anaplasma?

Back 37

blood smear, PCR, ELISA

Front 38

Treatment for cattle anaplasma?

Back 38

abx, blood transfusion

Front 39

Anaplasma species in other species?

Back 39

Anaplasma ovis for sheep and goats

Front 40

Babesiosis is also called what?

Back 40

Texas fever or cattle tick fever

Front 41

Babesiosis occurs in what species?

Back 41

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

Front 42

Transmission of babesiosis?

Back 42

by ticks: Rhipicephalus, Dermaceter

Front 43

Babesiosis in different species? Cattle?

Back 43

Babesia bovis, B bigemina, divergens and major

Front 44

Babesiosis species in horses?

Back 44

B. equi, caballi

Front 45

Clinical signs of babesiosis?

Back 45

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

Front 46

Pathogenesis of babesiosis?

Back 46

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

Front 47

Do all animals die from babesiosis infection?

Back 47

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

Subclinical infections can be reactivated.

Front 48

Treatment of babesiosis?

Back 48

diminazen aceturate, imidocarb dipropionate or anicarbolide disethionate

Front 49

When you think rinderpest what do you think?

Back 49

Reportable! And not in the US. (lol)

Front 50

Rinderpest is caused by what?

Back 50

Morbilivirus (paramyxoviridae)

Front 51

Who does rinderpest affect?

Back 51

Ruminants and rarely swine

Front 52

What is the pathogenesis of rinderpest?

Back 52

inhalation or ingestion --> infects URT --> replicates in tonsils and regional lymph nodes --> replicates in monocytes, lymphocytes, and epithelial cells (leukopenia results)

Front 53

Rinderpest clinical signs?

Back 53

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

Front 54

Treatment for Rinderpest?

Back 54

none

Front 55

Malignant catarrhal fever is characterized by what?

Back 55

Rhinitis, keratoconjunctivitis, and GI lesions

Front 56

Malignant catarrhal fever is caused by what?

Back 56

Two infectious agents: herpes viruses

Front 57

Malignant catarrhal fever affects what species?

Back 57

cattle, deer and buffalo

Front 58

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

Back 58

Peracute

alimentary tract

"head and eye" form

Front 59

Diagnosis and treatment for Malignant Catarrhal fever?

Back 59

Diagnosis: necropsy, isolation difficult

Treatment: none. Important to distinguish from other diseases

Front 60

White muscle disease is caused by what?

Back 60

Vitamin E or Selenium deficiency.

Front 61

What occurs in White Muscle disease?

Back 61

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

Front 62

What are some signs fo White Muscle Disease?

Back 62

lameness, locomotor impairment, dyspnea is diaphragm is affected

Front 63

What is the etiologic agent that causes Botulism?

Back 63

Clostriudium botulinum

Front 64

What is Clostridium botulinum?

Back 64

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

Front 65

How many types of Clostridium botulinum ?

Back 65

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

Front 66

MOA of botulism?

Back 66

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

Front 67

Clinical signs of botulism?

Back 67

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

Front 68

Etiologic agent behind Tetanus.

Back 68

Clostridium tetani

Front 69

What is Clostridium tetani?

Back 69

gram +, anaerobic bacillus, spore forming

Front 70

Pathogenesis of tetanus?

Back 70

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

Front 71

Treatment/prevention of tetanus?

Back 71

tetanus toxoid vx.

Tetanus vx

Front 72

What is the etiology behind Infectious Bovine Keratoconjunctivits?

Back 72

Moraxella bovis or M bovoculi

Can be Mycoplasma or BHV-1

Front 73

IBK infects young or old?

Back 73

more often young

Front 74

IBK looks like what?

Back 74

tearing --> indicates ACTIVE infection

corneal opacity

conjunctivitis

corneal ulcer --> can lead to ruptured cornea

Front 75

Diagnosis of IBK?

Back 75

conjunctival swab

staining

Front 76

Treatment for IBK?

Back 76

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

topical or subconj abx

NSAIDs

Patch

surgery

Front 77

Bluetongue is caused by what?

Back 77

bluetongue virus

Front 78

Bluetongue occurs in what species?

Back 78

domestic and wild ruminants

Bigger problem in sheep

Front 79

Bluetongue virus is what?

Back 79

dsRNA, non-enveloped

Front 80

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

Back 80

Manifested in two ways:

Reproductive syndrome

Vasculitis disease

Front 81

Clinical signs of Bluetongue more specifically?

Back 81

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

Front 82

What is one sign not typically seen with Bluetongue infections?

Back 82

a blue tongue. HA

Front 83

What is a common clinical finding complicates Bluetongue infection?

Back 83

Secondary bacterial bronchopneumonia

Front 84

Treatment for Bluetongue?

Back 84

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

Front 85

What are some toxins that cause bovine abortion?

Back 85

Ponderosa pine needles.

Locoweed

Broon snakewood

Moldy sweet clover

Mycotoxins

Nitrates

Front 86

What is the biggest concern with ponderosa pine needle toxicity?

Back 86

3rd trimester abortion

Front 87

Locoweed causes what mainly?

Back 87

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

Front 88

Broom snakeweed commonly looks like what in patients?

Back 88

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

Front 89

Does Broom Snakeweed taste good?

Back 89

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

Front 90

Moldy Sweet Clover work in the liver doing what?

Back 90

Interferes with synthesis of Vitamin K dep factors

Front 91

Moldy Sweet Clover causes what ultimately?

Back 91

hemorrhage

Front 92

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

Back 92

3-6 weeks

Front 93

How are nitrates useful to ruminants?

Back 93

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

Front 94

What is the rate limiting step in the nitrate pathway?

Back 94

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

Front 95

What does it mean to have high levels of nitrite in the rumen?

Back 95

Nitrite is absorbed into the bloodstream and will convert hemoglobin to methemoglobin which is unable to transport oxygen

Front 96

How often does nitrate toxicity occur?

Back 96

Hard to tell because some plants may or may not have enough to too much in terms of recommended levels

Front 97

Dictyyocaulus viviparous is what?

Back 97

lungworm

Front 98

Dictyocaulus viviparous infects what site?

Back 98

infects: trachea and larger bronchi

Front 99

Lungworms or _________________ has what kind of lifecycle in short?

Back 99

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

Front 100

Clinical signs of lungworm or ____________________ infection?

Back 100

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

Dictyocaulus viviparous

Front 101

Who is commonly affected by Dictyocaulus viviparous?

Back 101

first season calves

Front 102

Treatment for lungworms?

Back 102

ivermectin, vaccine

Front 103

For fun, what is the lungworm species of horses?

Back 103

Dictyocaulus arnfeldi

Front 104

Trichostrongylus axei or _________________________ infects where?

Back 104

Stromach hairworm

infects the abomasum and small intestine

Front 105

Stomach worm or __________________ lifecycle in short?

Back 105

Trichostrongylus axei

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

Front 106

Treatment for stomcch hairworm or _____________________.

Back 106

pyrantel, albendazole, fendendazole, ivermectin

Trichostrongylus axei

Front 107

Signs of stomach hairworm infection?

Back 107

seldom pathogenic: weight loss, anorexia

Front 108

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

Back 108

Haemonchus sp.

Front 109

Haemonchus sp or _______________________ infects what part of the GI?

Back 109

abomasum

Front 110

What is the lifecycle in short of the Barberpole worm, or ______________________.

Back 110

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.

Front 111

Clinical signs of barberpole worm infection?

Back 111

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

Front 112

Treatment for _________________ or barberpole infection?

Back 112

Hawmonchus spp

albendazole, ivermectin

Front 113

Cooperia infects what site?

Back 113

small intestine

Front 114

Life cycle of cooperia?

Back 114

worms do no suck blood! Persist with ostertagia and haemonchus

Front 115

Clinical signs for Cooperia infection?

Back 115

anorexia, villous atrophy and diarrhea, decreased weight gain

Front 116

Treatment for Cooperia?

Back 116

albendazole, fenbendazole, levamisole, ivermectin

Front 117

Brown stomach worm or _____________________ infects what GI site?

Back 117

Ostertagia ostertagi

abomasum, specifically the gastric fundus and pylorus

Front 118

Lifecycle in short of Ostertagia ostertagi or _________________________.

Back 118

17-21 days post ingestion parasite emerges from gastric glands --> releases eggs --> transmission continues by another animal consuming

Brown stomach worm