GI Diseases Of Food Animals Flashcards
Neonatal Calf Diarrhea Complex
Calves 1-60 d
Causes economic losses due to death, ↓ weight gain and tx cost
In cattle, sheep and goats
CS of NCD
Diarrhea
Fluid and weight loss
Metabolic acidosis
Recumbency and depression
Death if untreated
Causative agents of NCD
Enterogenic E. Coli (ETEC), Rotavirus, coronavirus and cryptosporidia in beef cattle
For NCD _________ is more frequent in intensively reared calves (_________)
Salmonella
Dairy
ETEC in NCD
2 virulence factors include fimbriae/ pili F5 (K99) and enterotoxins
Rotavirus in NCD
Most common causes of diarrhea in calves
7 serogroups with A*, B and C in cattle
Coronavirus in NCD
> 70% of cows shed coronavirus in feces (other in nasal secretions)
Infects calves by oral and resp. routes
Cryptosporidia in NCD
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)
Salmonella in NCD
2200 serotypes
< 40 cause 80% of dz in livestock (serotypes B,C,D,E)
Release endotoxins and GI inflammation (typhimurium)
Mode of transmission for NCD
Ingestion and inhalation
Age distribution for NCD
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
Which causative agents of NCD causes increased intestinal secretions?
ETEC, Salmonella, rotavirus, coronavirus, and clostridia
Increased intestinal secretion in NCD with ETEC and salmonella
ETEC and salmonella: secrete enterotoxins and endotoxins —> stimulate ↑ secretion by enterocytes —> lose Na, Cl, K and HC03 —> metabolic acidosis
Increased intestinal secretion in NCD with rota and coronavirus
Compensatory hyperplasia of intestinal crypt cells
Increased intestinal secretion in NCD with salmonella and clostridia
Severe inflammation —> ↑ mucosal pore size in enterocytes and ↑ prostaglandin production
Decreased intestinal absorption in NCD
Rota, corona, cryptosporidia: destroy absorptive epithelial cells —> ↓ absorption —> ↑ fermentation of food —> bacterial overgrowth —> endotoxin release —> fever and depression —> osmotic diarrhea
Dx of NCD
CS and age distribution
Fecal culture (ETEC and salmonella)
Immunoassays
FA, ELISA, slide agglutination, PCR, electron microscopy (rota, corona, crypto)
Prognosis of NCD
Guarded
Fluid tx for NCD
Corrects dehydration and acidosis
Rehydration: % dehydration x wgt
Maintenance: 50-100 ml/kg/dy
0.9% NaCl balanced electrolyte (normosol, plasmalyte)
Prevention and control for NCD
Vx for salmonella, ETEC, rota and corona
Winter dysentery/ Calf Diarrhea/ Bovine coronavirus
Winter dysentery (adults) and calf diarrhea (calves)
Acute contagious viral dz of dairy cattle, colder winter months
Etiology of Winter Dysentery
RNA virus, family coronaviridae
Bluetongue
Anthropod-borne viral dz of ruminants
Import restrictions in endemic countries
Family reoviridae , genus orbivirus
Features of bluetongue
RNA virus
5/24 serotypes in the US (2, 10, 11, 13, 17)
Related to African Horse Sickness and Epizootic Hemorrhagic Dz
Mode of transmission of Bluetongue
Main vector: Culicoides gnats (C. Sonorensis)
Transmitted via semen and transplacentally
Susceptible hosts of Bluetongue
Sheep
Cattle (CS rare in cattle)
Worldwide (mainly Africa)
Pathogenicity of Bluetongue
Low pathogenicity of virus in endemic animals
Outbreaks with new animals or new vectors introduced
Midsummer- early fall
When is Bluetongue more severe?
When previous exposure (sensitization) has occurred
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
Reproductive syndromes of Bluetongue
Late term abortions
Stillbirths
Weak “dumb” lambs
Pathology of Bluetongue
Infects vascular endothelial cells
Teratogencity
Elevate fetal cortisol —> late term abortion
Lesions of Bluetongue
Unusual hemorrhage in an organ, especially in the heart
Dx of Bluetongue
CS
Most definitive: virus isolation
Prevention of Bluetongue
Control muddy conditions
Gnats that feed on sheep dewormed with ivermectin will die (not b4 exchanging virus)
Modified live Vx
T/F: Bluetongue is a reportable dz?
TRUE
Johns’s Disease (Paratuberculosis)
Insidious chr. Infection of ruminants.
Economic losses due to ↓ milk production, wgt. @ slaughter, premature culling, etc.
What is the causative agent of Johne’s Disease
Mycobacterium paratuberculosis (M. johnei)
Acid-fast bacillus, remain below the BM
Johne’s Disease distribution
25-35% dairy herds infected, lower rates in beef
All ruminants can be infected
Angus, Shorthorn, Jersey and Guernsey
Mode of transmission of Johne’s Disease
Ingestion of feed contaminated with feces and colostrum
25% infected in utero with CS, 18% without
CS in cattle with Johne’s Disease?
Gradual WL despite a good appetite → pipestream diarrhea without tenesmus
Emaciated, bottle jaw, lethargy, then death
Stage 1 of Johne’s Disease
Silent infection in young cattle up to 2y
No CS, hard to detect
Stage 2 of Johne’s Disease
Inapparent carrier adults
No CS, shedding organism to environment
Stage 3 of Johne’s Disease
Clinica dz
WL and diarrhea, milk production ↓, appetite normal
+ lab results
Stage 4 of Johne’s Disease
Advanced clinical dz
Weak, emaciated, pipestream diarrhea, bottle jaw and death (few week progression)
Pathogenesis of Johne’s Disease
M. paratuberculosis ingested → multiply in ileum → gradual thickening → ↓ absorption and gradual protein leakage → CS
Dx of Johne’s Disease
Bx terminal ileum
Fecal cx and isolation**
Johne’s Disease prognosis
Poor, dz is progressive
Johne’s Disease prevention and control
Eliminate infected animals
Annual fecal cx testing and culling of + animals
Killed vx
Johne’s Disease public health implications
Reportable
M. paratuberculosis causes Crohn’s dz in humans via pasteurized milk and drinking water
Bovine Viral Diarrhea/ Mucosal Dz
Single stranded RNA virus
Constant mutations= antigenic diversity
Cattle mainly, goats, sheep, wild rums
Biotype v strains
Biotype: same surface Ags, difference is what the virus does
Strain: Different surface Ags
Noncytopathic/ NCP BVDV
90% of BVDV infections
Transplacental infections → abortions, congential anomalies, persistently infected offspring
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
BVD strains
T1: most prevalent
T2: isolated from cases of peracute BVD and hemorrhagic syndrome and PI calves from dams vx against BVD
Mode of transmission of BVDV
Direct: ingestion or inhalation
Indirect: insect vectors, feed, equipment
Transplacental trans from immunocompetent or PI dam to fetus
How is BVDV shed?
In saliva, nasal secretions, blood, feces, urine
Uterine fluids, place gas and sperm
Acute BVD
6-24m
Ocularnasal discharge, oral erosions, leukopenia and opportunistic infections
How does acute BVD affect the immune system?
Neutropenia
↓ macro migration
Inhibits lymphocyte blastogenesis —> ↓ B and T cell response
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)
What are the differentials for acute BVD
Diarrhea in young: rota, crypto, E. Coli
Calf pneumonia: salmonella, Johnes, parasites, copper deficiency
Erosions: MCF, Bluetongue
In utero infection of BVD
In semen if PI bulls
Transplacental from dam to fetus
Embryonic death —> repeat breeder problem
In utero infection of BVD @ 50- 100d
Fetal death —> first trimester abortion
In utero infection of BVD @ 100-150d
Congenital anomalies: hydrocephalus, cerebellar hypoplasia, pulmonary hypoplasia
In utero infection of BVD <125d gestation
Immunotolerant
PI clad may die in utero
Weak @ birth
Or born normal
In utero infection of BVD in immunocompetent fetus @ 150-200d
Fetus had serum neutralizing Abs
May still die and be aborted (organ damage)
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
Mucosal dz
Fever, anorexia, tachypnea, polypnea, ↓ milk production, watery bloody diarrhea, death within 3-10d
Non-healing skin erosions
Pathology of BVD
Infects resp. Tract and tonsils
Damages epithelial tissues of GI. resp, and integumentary systems
Dx of BVD
CS + leukopenia
Necropsy: GI erosions, swollen and necrotic Peyer’s patches, watery and foul-smelling bowel, secondary pneumonia or mastitis
Modified live Vx
Humoral and cell-mediated immunity
Vaccine breaks (ineffective)
Vx- induced immunosuppression, abortion or congenital anomalies
Modified live Vx (BVD)
Humoral and cell-mediated immunity
Vaccine breaks (ineffective)
Vx- induced immunosuppression, abortion or congenital anomalies
Killed BVD vx
BEST METHODS
Safe for preggo cows
Induce cell-mediated immunity
Need booster 3-4w
