Adult diarrhea Flashcards
What age group is unlikely to experience diarrhea and why
3 week to 6 month old ruminants- passed neonatal period and now have maternal antibody
What is the most common cause of diarrhea in 3 week to 6 month old ruminants?
Coccidiosis
What is the most common cause of acute diarrhea in adult ruminants?
Simple indigestion
Describe the symptoms of simple indigestion
Decrease in appetite and milk production, rumen hypomotility, mild bloat, abnormal feces, generally signs are mild and multiple animals are affected
How do you diagnose simple indigestion?
Rule out other causes of acute diarrhea, perform rumen fluid analysis (change in color/consistency/pH), look at management
What proportion of BVD isolates are non-cytopathic?
> 90%
How do cytopathic and non-cytopathic strains of BVD differ?
Cytopathic cause degenerative lesions, noncytopathic strains do not
Which genotype of BVD has been associated with recent outbreaks of severe acute disease?
Genotype 2
Describe the pathophysiology of BVD
Spreads mainly through direct contact with secretions of viremic animals; naive animal is exposed -> virus is taken up by reticuloendothelial cells in spleen and lymph nodes -> replicates within lymphocytes and macrophages and viremia occurs -> virus colonizes GI, respiratory, and reproductive tracts -> virus shed for up to 10 days
What are the clinical signs and sequella of BVD infection?
Can be asymptomatic or mild symptoms with diarrhea, fever, decreased feed intake, decreased milk production, oral erosions. Main complications are immunosupprsesion, fetal disease/death, and hemorrhage.
Describe immunosuppression from BVD
Immunosuppression lasts about 3 weeks, due to transient leukopenia and lymphopenia with altered T and B cell, neutrophil, monocyte, and macrophage function
Makes animals particularly susceptible for respiratory disease
Describe hemorrhage from BVD
Some strains of BVD can cause marked thrombocytopenia, may see petechia and ecchymoses, bleeding from injection sites, bloody diarrhea, epistaxis
Platelet production is not decreased so thrombocytopenia is due to destruction/sequestration
When does a cow need to be exposed to BVD to cause reproductive failure?
Within first 100 days of gestation
What might you see in fetuses from cows infected with BVD in the first 100 days of gestation?
Abortion, mummification, or infertility of cow
When does a cow need to be exposed to BVD for it to cause congenital defects in the fetus?
60 to 180 days of gestation
What congenital defects can be caused by BVD?
Cerebellar hypoplasia, ocular abnormalities, musculoskeletal abnormalities, skin/haircoat deformities
When do cows need to be infected with BVD for the calf to become persistently infected?
Before 125 days of gestation
Describe the process of an animal becoming persistently infected
Dam becomes infected in first 125 days of gestation, fetus develops permanent immunologic tolerance to that strain of BVD and sees it as “self”, calves may be “poor doers” but can appear normal, if they reproduce their offspring will be persistently infected
After what day of gestation will infection with BVD cause a normal calf that is seropositive?
Day 180
How is acute BVD diagnosed?
IFA, virus isolation from buffy coat, serology (4 fold rise in AB titer over 4 weeks), necropsy with depletion of lymphocytes in Peyer’s patches and lymph nodes and erosions in oral cavity and/or GI tract
How is chronic BVD diagnosed?
Virus isolation (2 positive tests 3-4w apart), ELISA assays, group screening with pooled PCR of serum or milk, skin biopsies stained for monoclonal antibodies or used for antigen ELISA assay
How is BVD treated?
No specific treatment, supportive care with fluids and antibiotics for secondary infections
PI animals should be culled when identified
How is BVD controlled?
Identification of PI animals, test incoming animals, vaccinate at least one month before breeding with MLV, vaccinate calves at <6 months and booster after 6 months of age
What are the disadvantages of MLVs for BVD?
Cause transient immunosuppression and viremia, can cause abortion
What conditions are required for mucosal disease to develop from BVD?
Fetus is exposed in utero to non-cytopathic strain at <125 days
Calf must then later be exposed to antigenically similar cytopathic strain
Calf cannot mount an immune response against the cytopathic strain, so severe cytopathic lesions develop
Describe the progression of mucosal disease from BVD?
Acute fever, anorexia, depression, mucosal erosions, hypersalivation, profuse diarrhea, coronary band erosions and skin erosions. Progresses quickly and almost always fatal in 5-7 days.
How is mucosal disease from BVD diagnosed?
Clinical signs and necropsy findings, virus can also be isolated from buffy coat or tissues
What is the treatment for mucosal disease from BVD?
No treatment- euthanize
What type of disease does salmonella cause in ruminants?
Acute or chronic diarrhea in adults and juveniles
How is salmonella transmitted?
Fecal oral route, can be from ingestion of infected milk in neonates
Is salmonella a bigger issue in beef or dairy herds?
Dairy
(T/F) The majority of salmonella infections are subclinical
True
What are the clinical signs of salmonella?
Peracute septicemia/endotoxemia followed by diarrhea, abortion, acute or chronic enteritis
How is salmonella diagnosed?
Repeated fecal or milk cultures or serologic testing with a serovar-specific test
How is salmonella treated?
Supportive care, NSAIDs, antibiotics, consider culling
What are the main control measures for controlling salmonella?
Prevent fecal contamination of feed and water, use good biosecurity, minimize stress, test and cull carrier animals, +/- vaccinate
What type of virus likely causes winter dystentery?
A coronavirus
Which animals are susceptible to winter dysentery?
Dairy cattle >2 years old, mostly in the Northern US
What are the clinical signs of winter dystentery?
Acute, profuse, transient diarrhea (bloody or dark), decreased milk production, respiratory signs, NO fever
What factors predispose herds for having winter dysentery outbreaks?
Crowded housing with tie-stalls and stress
How is winter dysentery diagnosed?
History and clinical signs, evidence of viral infection can be supportive
How is winter dysentery treated?
Supportive care, isolate infected animals
What is the causative agent of Johne’s disease?
Mycobacterium avium subsp. paratuberculosis
How does infection with Johne’s disease usually occur?
Calves ingest the bacterium in the first few months of life and it colonizes the ileum, cecum, and ileocecal lymph node, then spreads as they age
What are the lesions/clinical signs of Johne’s disease?
Granulomatous enteritis and lymphadenitis, chronic, watery diarrhea, progressive weight loss despite good appetite, protein losing enteropathy, decreased milk production
How is Johne’s disease spread?
Spread in macrophages in milk, semen, colostrum, and transplacentally
What is the incubation period of Johne’s disease?
1.5-2 years
How is Johne’s disease diagnosed?
Difficult to diagnose, use history and clinical signs, fecal culture (gold standard but takes a long time/difficult to culture), fecal smear with clumps of acid-fast bacilli (not very sensitive), PCR (not very sensitive), serology- ELISA most common (fairly sensitive), laparotomy or necropsy
Johnin test- intradermal test that was used historically
How is Johne’s disease treated?
No treatment, progressive and fatal- euthanize
Is Johne’s disease reportable in NC? Does it have a herd quarantine time?
Yes reportable
No quarantine time
Why is Johne’s disease vaccination not used?
Regulated by government, results in permanent granuloma, interferes with TB and JD testing, potentially hazardous to humans, doesn’t prevent infection
How does excess molybdenum or sulfate effect ruminants?
Causes copper deficiency
What animals are at the highest risk of molybdenosis?
Pastured animals in alkaline soil
What are the clinical signs of molybdenum excess?
Same as copper deficiency signs- weight loss, diarrhea, decreased milk production, hypotrichosis, physeal widening, osteoporosis, decreased fertility, immune dysfunction, swayback/ataxia in lambs and kids
How is molybdenosis diagnosed?
Copper serum concentrations <0.2ppm, liver copper concentrations <0.4ppm, or Cu:Mo ratio in the diet <6:1
How is molybdenosis treated?
Treat secondary copper deficiency with copper supplementation (injections/boluses)
What is type 1 ostergiasis?
Associated with high pasture worm burden- occurs in the summer and fall in the Southeast
What is type 2 ostergiasis?
Associated with emergence of hypobiotic larvae in the abomasum- primarily occurs in the spring in the Southeast
What are the clinical signs of ostertagiasis?
Diarrhea, decreased feed intake and efficiency, rough hair coat, ventral edema (bottle jaw)
How is ostertagiasis diagnosed?
Fecal with >2,000 eggs/g highly suggestive
Plasma pepsinogen concentration >3,000 IU highly suggestive, rarely used
May be diagnosed based on response to treatment
How is ostertagiasis treated?
Anthelmintics- moxidectin, eprinomectin, ivermectin, doramectin, fenbendazole
What are the clinical signs associated with abomasal lymphosarcoma?
Weight loss, chronic diarrhea
How is abomasal lymphosarcoma diagnosed?
Biopsy and histopathologic examination
Negative BLV titer rules out, positive titer does not confirm
Which animals are predisposed to abdominal fat necrosis?
Jersey and Guernsey cattle, animals on fescue pasture, older animals
What are the clinical signs of abdominal fat necrosis?
Weight loss, anorexia, diarrhea, constipation, abdominal enlargement, GI tract obstruction
How is abdominal fat necrosis diagnosed?
Rectal exam, finding necrotic fat during necropsy or exploratory
How is abdominal fat necrosis treated?
Isoprothiolane (fungicide)- expensive drug not available in US
Usually progressive and fatal
