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Ruminant Final > Adult diarrhea > Flashcards

Adult diarrhea Flashcards

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1
Q

What age group is unlikely to experience diarrhea and why

A

3 week to 6 month old ruminants- passed neonatal period and now have maternal antibody

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2
Q

What is the most common cause of diarrhea in 3 week to 6 month old ruminants?

A

Coccidiosis

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3
Q

What is the most common cause of acute diarrhea in adult ruminants?

A

Simple indigestion

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4
Q

Describe the symptoms of simple indigestion

A

Decrease in appetite and milk production, rumen hypomotility, mild bloat, abnormal feces, generally signs are mild and multiple animals are affected

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5
Q

How do you diagnose simple indigestion?

A

Rule out other causes of acute diarrhea, perform rumen fluid analysis (change in color/consistency/pH), look at management

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6
Q

What proportion of BVD isolates are non-cytopathic?

A

> 90%

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7
Q

How do cytopathic and non-cytopathic strains of BVD differ?

A

Cytopathic cause degenerative lesions, noncytopathic strains do not

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8
Q

Which genotype of BVD has been associated with recent outbreaks of severe acute disease?

A

Genotype 2

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9
Q

Describe the pathophysiology of BVD

A

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

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10
Q

What are the clinical signs and sequella of BVD infection?

A

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.

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11
Q

Describe immunosuppression from BVD

A

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

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12
Q

Describe hemorrhage from BVD

A

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

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13
Q

When does a cow need to be exposed to BVD to cause reproductive failure?

A

Within first 100 days of gestation

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14
Q

What might you see in fetuses from cows infected with BVD in the first 100 days of gestation?

A

Abortion, mummification, or infertility of cow

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15
Q

When does a cow need to be exposed to BVD for it to cause congenital defects in the fetus?

A

60 to 180 days of gestation

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16
Q

What congenital defects can be caused by BVD?

A

Cerebellar hypoplasia, ocular abnormalities, musculoskeletal abnormalities, skin/haircoat deformities

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17
Q

When do cows need to be infected with BVD for the calf to become persistently infected?

A

Before 125 days of gestation

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18
Q

Describe the process of an animal becoming persistently infected

A

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

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19
Q

After what day of gestation will infection with BVD cause a normal calf that is seropositive?

A

Day 180

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20
Q

How is acute BVD diagnosed?

A

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

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21
Q

How is chronic BVD diagnosed?

A

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

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22
Q

How is BVD treated?

A

No specific treatment, supportive care with fluids and antibiotics for secondary infections
PI animals should be culled when identified

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23
Q

How is BVD controlled?

A

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

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24
Q

What are the disadvantages of MLVs for BVD?

A

Cause transient immunosuppression and viremia, can cause abortion

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25
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
26
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.
27
How is mucosal disease from BVD diagnosed?
Clinical signs and necropsy findings, virus can also be isolated from buffy coat or tissues
28
What is the treatment for mucosal disease from BVD?
No treatment- euthanize
29
What type of disease does salmonella cause in ruminants?
Acute or chronic diarrhea in adults and juveniles
30
How is salmonella transmitted?
Fecal oral route, can be from ingestion of infected milk in neonates
31
Is salmonella a bigger issue in beef or dairy herds?
Dairy
32
(T/F) The majority of salmonella infections are subclinical
True
33
What are the clinical signs of salmonella?
Peracute septicemia/endotoxemia followed by diarrhea, abortion, acute or chronic enteritis
34
How is salmonella diagnosed?
Repeated fecal or milk cultures or serologic testing with a serovar-specific test
35
How is salmonella treated?
Supportive care, NSAIDs, antibiotics, consider culling
36
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
37
What type of virus likely causes winter dystentery?
A coronavirus
38
Which animals are susceptible to winter dysentery?
Dairy cattle >2 years old, mostly in the Northern US
39
What are the clinical signs of winter dystentery?
Acute, profuse, transient diarrhea (bloody or dark), decreased milk production, respiratory signs, NO fever
40
What factors predispose herds for having winter dysentery outbreaks?
Crowded housing with tie-stalls and stress
41
How is winter dysentery diagnosed?
History and clinical signs, evidence of viral infection can be supportive
42
How is winter dysentery treated?
Supportive care, isolate infected animals
43
What is the causative agent of Johne's disease?
Mycobacterium avium subsp. paratuberculosis
44
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
45
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
46
How is Johne's disease spread?
Spread in macrophages in milk, semen, colostrum, and transplacentally
47
What is the incubation period of Johne's disease?
1.5-2 years
48
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
49
How is Johne's disease treated?
No treatment, progressive and fatal- euthanize
50
Is Johne's disease reportable in NC? Does it have a herd quarantine time?
Yes reportable No quarantine time
51
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
52
How does excess molybdenum or sulfate effect ruminants?
Causes copper deficiency
53
What animals are at the highest risk of molybdenosis?
Pastured animals in alkaline soil
54
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
55
How is molybdenosis diagnosed?
Copper serum concentrations <0.2ppm, liver copper concentrations <0.4ppm, or Cu:Mo ratio in the diet <6:1
56
How is molybdenosis treated?
Treat secondary copper deficiency with copper supplementation (injections/boluses)
57
What is type 1 ostergiasis?
Associated with high pasture worm burden- occurs in the summer and fall in the Southeast
58
What is type 2 ostergiasis?
Associated with emergence of hypobiotic larvae in the abomasum- primarily occurs in the spring in the Southeast
59
What are the clinical signs of ostertagiasis?
Diarrhea, decreased feed intake and efficiency, rough hair coat, ventral edema (bottle jaw)
60
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
61
How is ostertagiasis treated?
Anthelmintics- moxidectin, eprinomectin, ivermectin, doramectin, fenbendazole
62
What are the clinical signs associated with abomasal lymphosarcoma?
Weight loss, chronic diarrhea
63
How is abomasal lymphosarcoma diagnosed?
Biopsy and histopathologic examination Negative BLV titer rules out, positive titer does not confirm
64
Which animals are predisposed to abdominal fat necrosis?
Jersey and Guernsey cattle, animals on fescue pasture, older animals
65
What are the clinical signs of abdominal fat necrosis?
Weight loss, anorexia, diarrhea, constipation, abdominal enlargement, GI tract obstruction
66
How is abdominal fat necrosis diagnosed?
Rectal exam, finding necrotic fat during necropsy or exploratory
67
How is abdominal fat necrosis treated?
Isoprothiolane (fungicide)- expensive drug not available in US Usually progressive and fatal

Ruminant Final (12 decks)

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