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

GI Diseases Of Food Animals Flashcards

(72 cards)

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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
Mode of transmission of Bluetongue
Main vector: Culicoides gnats (C. Sonorensis) Transmitted via semen and transplacentally
26
Susceptible hosts of Bluetongue
Sheep Cattle (CS rare in cattle) Worldwide (mainly Africa)
27
Pathogenicity of Bluetongue
Low pathogenicity of virus in endemic animals Outbreaks with new animals or new vectors introduced Midsummer- early fall
28
When is Bluetongue more severe?
When previous exposure (sensitization) has occurred
29
Classical Bluetongue dz
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
Reproductive syndromes of Bluetongue
Late term abortions Stillbirths Weak “dumb” lambs
31
Pathology of Bluetongue
Infects vascular endothelial cells Teratogencity Elevate fetal cortisol —> late term abortion
32
Lesions of Bluetongue
Unusual hemorrhage in an organ, especially in the heart
33
Dx of Bluetongue
CS Most definitive: virus isolation
34
Prevention of Bluetongue
Control muddy conditions Gnats that feed on sheep dewormed with ivermectin will die (not b4 exchanging virus) Modified live Vx
35
T/F: Bluetongue is a reportable dz?
TRUE
36
Johns’s Disease (Paratuberculosis)
Insidious chr. Infection of ruminants. Economic losses due to ↓ milk production, wgt. @ slaughter, premature culling, etc.
37
What is the causative agent of Johne's Disease
Mycobacterium paratuberculosis (M. johnei) Acid-fast bacillus, remain below the BM
38
Johne's Disease distribution
25-35% dairy herds infected, lower rates in beef All ruminants can be infected Angus, Shorthorn, Jersey and Guernsey
39
Mode of transmission of Johne's Disease
Ingestion of feed contaminated with feces and colostrum 25% infected in utero with CS, 18% without
40
CS in cattle with Johne's Disease?
Gradual WL despite a good appetite → pipestream diarrhea without tenesmus Emaciated, bottle jaw, lethargy, then death
41
Stage 1 of Johne's Disease
Silent infection in young cattle up to 2y No CS, hard to detect
42
Stage 2 of Johne's Disease
Inapparent carrier adults No CS, shedding organism to environment
43
Stage 3 of Johne's Disease
Clinica dz WL and diarrhea, milk production ↓, appetite normal + lab results
44
Stage 4 of Johne's Disease
Advanced clinical dz Weak, emaciated, pipestream diarrhea, bottle jaw and death (few week progression)
45
Pathogenesis of Johne's Disease
M. paratuberculosis ingested → multiply in ileum → gradual thickening → ↓ absorption and gradual protein leakage → CS
46
Dx of Johne's Disease
Bx terminal ileum Fecal cx and isolation**
47
Johne's Disease prognosis
Poor, dz is progressive
48
Johne's Disease prevention and control
Eliminate infected animals Annual fecal cx testing and culling of + animals Killed vx
49
Johne's Disease public health implications
Reportable M. paratuberculosis causes Crohn's dz in humans via pasteurized milk and drinking water
50
Bovine Viral Diarrhea/ Mucosal Dz
Single stranded RNA virus Constant mutations= antigenic diversity Cattle mainly, goats, sheep, wild rums
51
Biotype v strains
Biotype: same surface Ags, difference is what the virus does Strain: Different surface Ags
52
Noncytopathic/ NCP BVDV
90% of BVDV infections Transplacental infections → abortions, congential anomalies, persistently infected offspring
53
Cytopathic/ CP BVDV
Rare, causes dz in cattle with MD Acute, fatal dz of PI cattle infected with NCP + CP BVDV (mutation) Abortions and congenital anomalies
54
BVD strains
T1: most prevalent T2: isolated from cases of peracute BVD and hemorrhagic syndrome and PI calves from dams vx against BVD
55
Mode of transmission of BVDV
Direct: ingestion or inhalation Indirect: insect vectors, feed, equipment Transplacental trans from immunocompetent or PI dam to fetus
56
How is BVDV shed?
In saliva, nasal secretions, blood, feces, urine Uterine fluids, place gas and sperm
57
Acute BVD
6-24m Ocularnasal discharge, oral erosions, leukopenia and opportunistic infections
58
How does acute BVD affect the immune system?
Neutropenia ↓ macro migration Inhibits lymphocyte blastogenesis —> ↓ B and T cell response
59
Peracute BVD
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
What are the differentials for acute BVD
Diarrhea in young: rota, crypto, E. Coli Calf pneumonia: salmonella, Johnes, parasites, copper deficiency Erosions: MCF, Bluetongue
61
In utero infection of BVD
In semen if PI bulls Transplacental from dam to fetus Embryonic death —> repeat breeder problem
62
In utero infection of BVD @ 50- 100d
Fetal death —> first trimester abortion
63
In utero infection of BVD @ 100-150d
Congenital anomalies: hydrocephalus, cerebellar hypoplasia, pulmonary hypoplasia
64
In utero infection of BVD <125d gestation
Immunotolerant PI clad may die in utero Weak @ birth Or born normal
65
In utero infection of BVD in immunocompetent fetus @ 150-200d
Fetus had serum neutralizing Abs May still die and be aborted (organ damage)
66
BVD in PI animals
Shed NCP while appearing norm Claves have death rate of 50% in first 12m, If with CP + NCP they get mucosal dz
67
Mucosal dz
Fever, anorexia, tachypnea, polypnea, ↓ milk production, watery bloody diarrhea, death within 3-10d Non-healing skin erosions
68
Pathology of BVD
Infects resp. Tract and tonsils Damages epithelial tissues of GI. resp, and integumentary systems
69
Dx of BVD
CS + leukopenia Necropsy: GI erosions, swollen and necrotic Peyer’s patches, watery and foul-smelling bowel, secondary pneumonia or mastitis
70
Modified live Vx
Humoral and cell-mediated immunity Vaccine breaks (ineffective) Vx- induced immunosuppression, abortion or congenital anomalies
71
Modified live Vx (BVD)
Humoral and cell-mediated immunity Vaccine breaks (ineffective) Vx- induced immunosuppression, abortion or congenital anomalies
72
Killed BVD vx
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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