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!Food And Fiber Medicine (Large Animal) > GI Diseases Of Food Animals > Flashcards

GI Diseases Of Food Animals Flashcards

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1
Q

Neonatal Calf Diarrhea Complex

A

Calves 1-60 d
Causes economic losses due to death, ↓ weight gain and tx cost
In cattle, sheep and goats

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2
Q

CS of NCD

A

Diarrhea
Fluid and weight loss
Metabolic acidosis
Recumbency and depression
Death if untreated

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3
Q

Causative agents of NCD

A

Enterogenic E. Coli (ETEC), Rotavirus, coronavirus and cryptosporidia in beef cattle

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4
Q

For NCD _________ is more frequent in intensively reared calves (_________)

A

Salmonella
Dairy

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5
Q

ETEC in NCD

A

2 virulence factors include fimbriae/ pili F5 (K99) and enterotoxins

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6
Q

Rotavirus in NCD

A

Most common causes of diarrhea in calves
7 serogroups with A*, B and C in cattle

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7
Q

Coronavirus in NCD

A

> 70% of cows shed coronavirus in feces (other in nasal secretions)
Infects calves by oral and resp. routes

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8
Q

Cryptosporidia in NCD

A

C. Parvum, bovis, andersoni and ryanae in cattle
Parvum is the main cause in dairy calves: genotype 1 (hominis in humans), genotype 2 (ruminants and some humans)

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9
Q

Salmonella in NCD

A

2200 serotypes
< 40 cause 80% of dz in livestock (serotypes B,C,D,E)
Release endotoxins and GI inflammation (typhimurium)

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10
Q

Mode of transmission for NCD

A

Ingestion and inhalation

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11
Q

Age distribution for NCD

A

1-6d : ETEC, rota, corona
7-9: rota, cryptosporidia, corona, ETEC
13-15: cryptosporidia, rota, corona
19-24: cryptosporidia
25-30: corona, ETEC
31-60: rota, ETEC

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12
Q

Which causative agents of NCD causes increased intestinal secretions?

A

ETEC, Salmonella, rotavirus, coronavirus, and clostridia

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13
Q

Increased intestinal secretion in NCD with ETEC and salmonella

A

ETEC and salmonella: secrete enterotoxins and endotoxins —> stimulate ↑ secretion by enterocytes —> lose Na, Cl, K and HC03 —> metabolic acidosis

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14
Q

Increased intestinal secretion in NCD with rota and coronavirus

A

Compensatory hyperplasia of intestinal crypt cells

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15
Q

Increased intestinal secretion in NCD with salmonella and clostridia

A

Severe inflammation —> ↑ mucosal pore size in enterocytes and ↑ prostaglandin production

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16
Q

Decreased intestinal absorption in NCD

A

Rota, corona, cryptosporidia: destroy absorptive epithelial cells —> ↓ absorption —> ↑ fermentation of food —> bacterial overgrowth —> endotoxin release —> fever and depression —> osmotic diarrhea

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17
Q

Dx of NCD

A

CS and age distribution
Fecal culture (ETEC and salmonella)
Immunoassays
FA, ELISA, slide agglutination, PCR, electron microscopy (rota, corona, crypto)

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18
Q

Prognosis of NCD

A

Guarded

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19
Q

Fluid tx for NCD

A

Corrects dehydration and acidosis
Rehydration: % dehydration x wgt
Maintenance: 50-100 ml/kg/dy
0.9% NaCl balanced electrolyte (normosol, plasmalyte)

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20
Q

Prevention and control for NCD

A

Vx for salmonella, ETEC, rota and corona

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21
Q

Winter dysentery/ Calf Diarrhea/ Bovine coronavirus

A

Winter dysentery (adults) and calf diarrhea (calves)
Acute contagious viral dz of dairy cattle, colder winter months

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22
Q

Etiology of Winter Dysentery

A

RNA virus, family coronaviridae

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23
Q

Bluetongue

A

Anthropod-borne viral dz of ruminants
Import restrictions in endemic countries
Family reoviridae , genus orbivirus

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24
Q

Features of bluetongue

A

RNA virus
5/24 serotypes in the US (2, 10, 11, 13, 17)
Related to African Horse Sickness and Epizootic Hemorrhagic Dz

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25
Q

Mode of transmission of Bluetongue

A

Main vector: Culicoides gnats (C. Sonorensis)
Transmitted via semen and transplacentally

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26
Q

Susceptible hosts of Bluetongue

A

Sheep
Cattle (CS rare in cattle)
Worldwide (mainly Africa)

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27
Q

Pathogenicity of Bluetongue

A

Low pathogenicity of virus in endemic animals
Outbreaks with new animals or new vectors introduced
Midsummer- early fall

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28
Q

When is Bluetongue more severe?

A

When previous exposure (sensitization) has occurred

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29
Q

Classical Bluetongue dz

A

Facial edema, excessive salivation, nasal discharge, hyperemia of oral mucosa, erosion and ulceration of oral mucosa
Bluetongue, secondary bacterial pneumonia, diarrhea, lameness and broken wool

30
Q

Reproductive syndromes of Bluetongue

A

Late term abortions
Stillbirths
Weak “dumb” lambs

31
Q

Pathology of Bluetongue

A

Infects vascular endothelial cells
Teratogencity
Elevate fetal cortisol —> late term abortion

32
Q

Lesions of Bluetongue

A

Unusual hemorrhage in an organ, especially in the heart

33
Q

Dx of Bluetongue

A

CS
Most definitive: virus isolation

34
Q

Prevention of Bluetongue

A

Control muddy conditions
Gnats that feed on sheep dewormed with ivermectin will die (not b4 exchanging virus)
Modified live Vx

35
Q

T/F: Bluetongue is a reportable dz?

A

TRUE

36
Q

Johns’s Disease (Paratuberculosis)

A

Insidious chr. Infection of ruminants.
Economic losses due to ↓ milk production, wgt. @ slaughter, premature culling, etc.

37
Q

What is the causative agent of Johne’s Disease

A

Mycobacterium paratuberculosis (M. johnei)
Acid-fast bacillus, remain below the BM

38
Q

Johne’s Disease distribution

A

25-35% dairy herds infected, lower rates in beef
All ruminants can be infected
Angus, Shorthorn, Jersey and Guernsey

39
Q

Mode of transmission of Johne’s Disease

A

Ingestion of feed contaminated with feces and colostrum
25% infected in utero with CS, 18% without

40
Q

CS in cattle with Johne’s Disease?

A

Gradual WL despite a good appetite → pipestream diarrhea without tenesmus
Emaciated, bottle jaw, lethargy, then death

41
Q

Stage 1 of Johne’s Disease

A

Silent infection in young cattle up to 2y
No CS, hard to detect

42
Q

Stage 2 of Johne’s Disease

A

Inapparent carrier adults
No CS, shedding organism to environment

43
Q

Stage 3 of Johne’s Disease

A

Clinica dz
WL and diarrhea, milk production ↓, appetite normal
+ lab results

44
Q

Stage 4 of Johne’s Disease

A

Advanced clinical dz
Weak, emaciated, pipestream diarrhea, bottle jaw and death (few week progression)

45
Q

Pathogenesis of Johne’s Disease

A

M. paratuberculosis ingested → multiply in ileum → gradual thickening → ↓ absorption and gradual protein leakage → CS

46
Q

Dx of Johne’s Disease

A

Bx terminal ileum
Fecal cx and isolation**

47
Q

Johne’s Disease prognosis

A

Poor, dz is progressive

48
Q

Johne’s Disease prevention and control

A

Eliminate infected animals
Annual fecal cx testing and culling of + animals
Killed vx

49
Q

Johne’s Disease public health implications

A

Reportable
M. paratuberculosis causes Crohn’s dz in humans via pasteurized milk and drinking water

50
Q

Bovine Viral Diarrhea/ Mucosal Dz

A

Single stranded RNA virus
Constant mutations= antigenic diversity
Cattle mainly, goats, sheep, wild rums

51
Q

Biotype v strains

A

Biotype: same surface Ags, difference is what the virus does
Strain: Different surface Ags

52
Q

Noncytopathic/ NCP BVDV

A

90% of BVDV infections
Transplacental infections → abortions, congential anomalies, persistently infected offspring

53
Q

Cytopathic/ CP BVDV

A

Rare, causes dz in cattle with MD
Acute, fatal dz of PI cattle infected with NCP + CP BVDV (mutation)
Abortions and congenital anomalies

54
Q

BVD strains

A

T1: most prevalent
T2: isolated from cases of peracute BVD and hemorrhagic syndrome and PI calves from dams vx against BVD

55
Q

Mode of transmission of BVDV

A

Direct: ingestion or inhalation
Indirect: insect vectors, feed, equipment
Transplacental trans from immunocompetent or PI dam to fetus

56
Q

How is BVDV shed?

A

In saliva, nasal secretions, blood, feces, urine
Uterine fluids, place gas and sperm

57
Q

Acute BVD

A

6-24m
Ocularnasal discharge, oral erosions, leukopenia and opportunistic infections

58
Q

How does acute BVD affect the immune system?

A

Neutropenia
↓ macro migration
Inhibits lymphocyte blastogenesis —> ↓ B and T cell response

59
Q

Peracute BVD

A

Type 2 can cause in calves less than 6m old
Or hemorrhagic syndrome in cows over 24m old (thrombocytopenia, Petechial hemorrhage and blood feces)

60
Q

What are the differentials for acute BVD

A

Diarrhea in young: rota, crypto, E. Coli
Calf pneumonia: salmonella, Johnes, parasites, copper deficiency
Erosions: MCF, Bluetongue

61
Q

In utero infection of BVD

A

In semen if PI bulls
Transplacental from dam to fetus
Embryonic death —> repeat breeder problem

62
Q

In utero infection of BVD @ 50- 100d

A

Fetal death —> first trimester abortion

63
Q

In utero infection of BVD @ 100-150d

A

Congenital anomalies: hydrocephalus, cerebellar hypoplasia, pulmonary hypoplasia

64
Q

In utero infection of BVD <125d gestation

A

Immunotolerant
PI clad may die in utero
Weak @ birth
Or born normal

65
Q

In utero infection of BVD in immunocompetent fetus @ 150-200d

A

Fetus had serum neutralizing Abs
May still die and be aborted (organ damage)

66
Q

BVD in PI animals

A

Shed NCP while appearing norm
Claves have death rate of 50% in first 12m,
If with CP + NCP they get mucosal dz

67
Q

Mucosal dz

A

Fever, anorexia, tachypnea, polypnea, ↓ milk production, watery bloody diarrhea, death within 3-10d
Non-healing skin erosions

68
Q

Pathology of BVD

A

Infects resp. Tract and tonsils
Damages epithelial tissues of GI. resp, and integumentary systems

69
Q

Dx of BVD

A

CS + leukopenia
Necropsy: GI erosions, swollen and necrotic Peyer’s patches, watery and foul-smelling bowel, secondary pneumonia or mastitis

70
Q

Modified live Vx

A

Humoral and cell-mediated immunity
Vaccine breaks (ineffective)
Vx- induced immunosuppression, abortion or congenital anomalies

71
Q

Modified live Vx (BVD)

A

Humoral and cell-mediated immunity
Vaccine breaks (ineffective)
Vx- induced immunosuppression, abortion or congenital anomalies

72
Q

Killed BVD vx

A

BEST METHODS
Safe for preggo cows
Induce cell-mediated immunity
Need booster 3-4w

!Food And Fiber Medicine (Large Animal) (10 decks)

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