Adult diarrhea Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Coccidiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Simple indigestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What proportion of BVD isolates are non-cytopathic?

A

> 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Cytopathic cause degenerative lesions, noncytopathic strains do not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Genotype 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

Within first 100 days of gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What congenital defects can be caused by BVD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Before 125 days of gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Day 180

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the disadvantages of MLVs for BVD?

A

Cause transient immunosuppression and viremia, can cause abortion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What conditions are required for mucosal disease to develop from BVD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the progression of mucosal disease from BVD?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is mucosal disease from BVD diagnosed?

A

Clinical signs and necropsy findings, virus can also be isolated from buffy coat or tissues

28
Q

What is the treatment for mucosal disease from BVD?

A

No treatment- euthanize

29
Q

What type of disease does salmonella cause in ruminants?

A

Acute or chronic diarrhea in adults and juveniles

30
Q

How is salmonella transmitted?

A

Fecal oral route, can be from ingestion of infected milk in neonates

31
Q

Is salmonella a bigger issue in beef or dairy herds?

A

Dairy

32
Q

(T/F) The majority of salmonella infections are subclinical

A

True

33
Q

What are the clinical signs of salmonella?

A

Peracute septicemia/endotoxemia followed by diarrhea, abortion, acute or chronic enteritis

34
Q

How is salmonella diagnosed?

A

Repeated fecal or milk cultures or serologic testing with a serovar-specific test

35
Q

How is salmonella treated?

A

Supportive care, NSAIDs, antibiotics, consider culling

36
Q

What are the main control measures for controlling salmonella?

A

Prevent fecal contamination of feed and water, use good biosecurity, minimize stress, test and cull carrier animals, +/- vaccinate

37
Q

What type of virus likely causes winter dystentery?

A

A coronavirus

38
Q

Which animals are susceptible to winter dysentery?

A

Dairy cattle >2 years old, mostly in the Northern US

39
Q

What are the clinical signs of winter dystentery?

A

Acute, profuse, transient diarrhea (bloody or dark), decreased milk production, respiratory signs, NO fever

40
Q

What factors predispose herds for having winter dysentery outbreaks?

A

Crowded housing with tie-stalls and stress

41
Q

How is winter dysentery diagnosed?

A

History and clinical signs, evidence of viral infection can be supportive

42
Q

How is winter dysentery treated?

A

Supportive care, isolate infected animals

43
Q

What is the causative agent of Johne’s disease?

A

Mycobacterium avium subsp. paratuberculosis

44
Q

How does infection with Johne’s disease usually occur?

A

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
Q

What are the lesions/clinical signs of Johne’s disease?

A

Granulomatous enteritis and lymphadenitis, chronic, watery diarrhea, progressive weight loss despite good appetite, protein losing enteropathy, decreased milk production

46
Q

How is Johne’s disease spread?

A

Spread in macrophages in milk, semen, colostrum, and transplacentally

47
Q

What is the incubation period of Johne’s disease?

A

1.5-2 years

48
Q

How is Johne’s disease diagnosed?

A

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
Q

How is Johne’s disease treated?

A

No treatment, progressive and fatal- euthanize

50
Q

Is Johne’s disease reportable in NC? Does it have a herd quarantine time?

A

Yes reportable
No quarantine time

51
Q

Why is Johne’s disease vaccination not used?

A

Regulated by government, results in permanent granuloma, interferes with TB and JD testing, potentially hazardous to humans, doesn’t prevent infection

52
Q

How does excess molybdenum or sulfate effect ruminants?

A

Causes copper deficiency

53
Q

What animals are at the highest risk of molybdenosis?

A

Pastured animals in alkaline soil

54
Q

What are the clinical signs of molybdenum excess?

A

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
Q

How is molybdenosis diagnosed?

A

Copper serum concentrations <0.2ppm, liver copper concentrations <0.4ppm, or Cu:Mo ratio in the diet <6:1

56
Q

How is molybdenosis treated?

A

Treat secondary copper deficiency with copper supplementation (injections/boluses)

57
Q

What is type 1 ostergiasis?

A

Associated with high pasture worm burden- occurs in the summer and fall in the Southeast

58
Q

What is type 2 ostergiasis?

A

Associated with emergence of hypobiotic larvae in the abomasum- primarily occurs in the spring in the Southeast

59
Q

What are the clinical signs of ostertagiasis?

A

Diarrhea, decreased feed intake and efficiency, rough hair coat, ventral edema (bottle jaw)

60
Q

How is ostertagiasis diagnosed?

A

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
Q

How is ostertagiasis treated?

A

Anthelmintics- moxidectin, eprinomectin, ivermectin, doramectin, fenbendazole

62
Q

What are the clinical signs associated with abomasal lymphosarcoma?

A

Weight loss, chronic diarrhea

63
Q

How is abomasal lymphosarcoma diagnosed?

A

Biopsy and histopathologic examination
Negative BLV titer rules out, positive titer does not confirm

64
Q

Which animals are predisposed to abdominal fat necrosis?

A

Jersey and Guernsey cattle, animals on fescue pasture, older animals

65
Q

What are the clinical signs of abdominal fat necrosis?

A

Weight loss, anorexia, diarrhea, constipation, abdominal enlargement, GI tract obstruction

66
Q

How is abdominal fat necrosis diagnosed?

A

Rectal exam, finding necrotic fat during necropsy or exploratory

67
Q

How is abdominal fat necrosis treated?

A

Isoprothiolane (fungicide)- expensive drug not available in US
Usually progressive and fatal