11 - winter dysentery, salmonella, peritonitis, fat necrosis

winter dystentery

bovine coronavirus

occurs in colder months

outbreak lasts < 2 weeks

1-2% mortality (rare)

fecal-oral route transmission

viral damage to colon/SI

clinical findings

sudden-onset explosive diarrhea, bubbly in puddles, thick mucus, melena

anorexia, depression

decreased milk production

decreased BCS

dehydration after 2 days

decreased rumen motility

PU/PD

afebrile

diagnosis

PCR

paired serology

treatment

spontaneous recovery

supportive care

control

biosecurity

no vaccine

salmonella

GNR

zoonotic

enteritis

GI infection → diarrhea, inflammation

typically occurs following exposure to large dose of virulent strain

significant reduction in milk production

common to shed w/o symptoms after infection

uncommon to persistently shed thorughout life

fecal-oral transmission

most common during cold months

mostly in lower ileum, cecum, spiral colon

watery to mucoid diarrhea, ± fibrin/blood

abortion may occur

diagnosis

culture

gold standard

repeated culture isolation of pathogen

single isolation may confirm acute infection

limitations: low sensitivity in chronically infected animals, may fail to detect subclinical carriers → intermittent shedding

PCR

highly sensitive

postive result not definitive for clinical disease

can use to serotype

serology

herd-level surveillance/monitoring

less reliable for dx individual clinical cases

treatment

abx, supportive care

fluid therapy

abx may cause endotoxin release

control

source animals from Salmonella-free herds

identify and cull chronically infected animals

good husbandry practices

biosecurity

Peritonitis

inflammation of serous membranes lining peritoneal cavity

infectious or noninfectious causes

generally non-contagious

may cause adhesions/impair organ function

peritoneum and omentum attempt to wall off areas of contamination

    cr abdomen adhesions → no problem

    cd abdomen adhesions → intestinal obstruction

etiology

primary

less common

infection spread hematogenously

immunocompromised animals

secondary peritonitis

more common

infectious or non-infectious, idiopathic

leakage or perforation of gastrointestinal organs

diagnosis

clincal signs

rectal palpation

abdominoparacentesis

peritoneal fluid analysis

cytology: inflammatory cells, bacteria

culture: infectious agents

management/treatment

generally poor prognosis

peritoneal lavage

fluid therapy/supportive care

aggressive systemic abx

surigcal intervention → repairs, necrotic tissue removal

fat necrosis

hard, necrotic fat masses within peritoneal cavity

cannel island breeds, japanese black cattle

beef cattle >2yo

can be mistake for fetus

etiology

associated with high-concentraiton diets, rich in long-chain saturated FAs

grazing tall fescue w/ enotyphodium coenophialum endyphyte

overconditioning, genetic predisposition, lack of exercise

diagnosis

firm, irregular masses on rectal palpation

hyperechoic masses, typically in omentum

r-flank exploartory may be necessary

rarely free-floating in abdomen

treatment/control

masses slowly increase in size

may have spontaneous resolution

remove animals from tall fescue pasture

legume-rich diet