Causes of Juvenile and Adult Ruminant Diarrhea

Flashcards covering key terms and definitions related to juvenile and adult ruminant diarrhea, including Coccidiosis, Parasitic Gastroenteritis, Copper Deficiency, Salmonellosis, Johne's Disease, and Winter Dysentery.

Coccidiosis

A disease causing diarrhea in juvenile ruminants, primarily influenced by management practices. It is caused by Eimeria spp. in cattle, sheep, goats, and camelids.

Eimeria spp.

The etiological agent for Coccidiosis in ruminants. Some species cause clinical issues depending on their location in the GI tract.

Oocyst

The infective stage of Eimeria spp. that is ingested by a host, leading to Coccidiosis.

Nervous Coccidiosis

A severe form of Coccidiosis characterized by tremors, muscle fasciculations, convulsions, blindness, and a high mortality rate (>80%).

Coccidiosis Prevention

Primarily management-focused, including removal of feces, decreasing stocking densities, using above feeders, rotating animals and good drainage.

Add amprolium, lasalocid, monensin, decoquinate to feed - Not FDA regulated - questionable effecacy

What are the clinical signs of coccidosis?

1. mostly asymptomatic

2. Acute: profuse diarrhea - mucous and blood, fibrin casts, anemia, anorexia. May die before signs

3. chronic (esp small ag): diarrhea without blood, wasting, stunted, weight loss.

4. Immunity after infection

what is the pathogenesis of coccidosis?

1. invade and cause damage to host intestinal cells -. loss of blood, fluid, albumin, electrolytes

2. Amount of damage:amount of oocysts:environmental contamination:mangament

how do you diagnose coccidiosis?

1. fecal float

2. post mortum: hemorrhagic enteritis, villous blunting, organsims on H and E sections

How do you treat coccidosis?

1. Sulfadimethoxine (→ crytalurua, CNS tox, decreased BM)

2. Amprolium (compete with thiamine → polioencephalomalacia)

3. ionophores - rumensin and monensin (prevent coccidia development)

Parasitic Gastroenteritis (PGE)

The most common cause of chronic diarrhea in the US, leading to decreased feed efficiency, unthriftiness, weight loss, anemia, diarrhea, and edema.

What are some predisposing factors that leave animals at risk for PGE

1. over corwding

2. dry/stressful environment

3. poor deworming hx

Gastrointestinal Nematodes

Several species of nematodes responsible for PGE, often grouped into the HOT/T Complex.

HOT/T Complex

A group of gastrointestinal nematodes including Haemonchus contortus, Ostertagia ostertagi, Trichostrongylus sp., Teladorsagia sp., Cooperia sp., and Oesophagostomum sp.

Type I Ostertagiasis

A form of ostertagiasis primarily affecting calves during their first season on pasture, characterized by anorexia, diarrhea, and poor growth, occurring when L3 larvae directly develop into adults.

fecal oral route

dz peaks in late summer/early fall during the weaning and selling period

Type II Ostertagiasis

A more severe form of ostertagiasis affecting older cattle (circa 1 year old) where encysted L3 larvae emerge from the abomasal mucosa, causing intermittent profuse diarrhea, anorexia, ill thrift, and hypoproteinemia.

emerge in spring after encysting over the winter

Ostertagiasis Pathophysiology

Larval disruption of glandular function in the abomasum, causing cellular hyperplasia ('Moroccan leather' appearance), decreased acid production, increased abomasal pH, decreased appetite, and reduced protein absorption.

Anthelmintics used to treat PGE

Medications such as Macrocyclic lactones and Fenbendazole.

prevention and management of PGE

1. prophylactic anthelmentics - between pasture turn out and midsummer

2. target specific sickly individuals

3. pasture rotation

Copper Deficiency

A condition that can be primary (insufficient dietary copper) or secondary (excess molybdenum, sulfur, iron, or zinc preventing copper absorption/metabolism). Young animals and fetuses are more susceptible.

Secondary Copper Deficiency

A type of copper deficiency caused by antagonistic elements like molybdenum, sulfur, iron, or zinc, which interfere with copper absorption and metabolism.

Clinical Signs of Copper Deficiency

Diarrhea, poor weight gain, weight loss, enzootic neonatal ataxia, achromotrichia, infertility, and lowered immunity.

Liver Biopsy (Copper Deficiency)

Considered the best diagnostic indicator of an animal's copper status, measuring hepatic copper levels.

Copper Supplementation

Treatment for copper deficiency, often given as injectable copper glycinate or oral copper oxide wire particle boluses.

Caution in sheeps

Salmonellosis

A bacterial disease in ruminants caused by Gram-negative Salmonella species, affecting animals of all ages and presenting with variable clinical signs.

Salmonella Dublin

A host-adapted serotype of Salmonella commonly found in cattle, often associated with carrier status and endemic farm problems.

Pathophysiology of salmonellosis

bacti penetrates mucosal membrane → peyer’s patch → penetrate microvilli → laminapropria → macrophages and neuts → mesenteric LN → septicemia

Lipopolysaccharide (LPS)

A biologically active component of Salmonella's cell wall (endotoxin) that causes severe systemic effects like leukopenia, fever, anorexia, shock, and death.

What are the 3 presentation types of salmonellosis?

1. paracute septicemis

2. acute septicemia (predominant form)

3. chronic enteritis (older calves 6-8wks with loose stool)

Peracute Septicemia (Salmonella)

A severe and rapid form of Salmonellosis, typically in calves and lambs (10d - 3 m FPT), characterized by signs of endotoxemia (e.g., scleral injection, petechiation, toxic line) and often leading to death within hours to days.

Acute Enteritis (Salmonella)

The predominant form of Salmonellosis, initially causing fever, anorexia, depression, and dehydration, followed by watery diarrhea that may contain mucosal shreds, casts, blood, and have a foul odor.

may see meningitis, osteomylitis, pneumonia, polyarthritis

Salmonella-Induced Abortion

Can occur via:

1. bacteremia infecting the placenta or fetus

2. endotoxemia and fever causing lysis of the corpus luteum.

how can you df between the two types of salmonella induced abortions?

1. septicemia in fetus → culture positive fetus

2. endotoxemis → PGF2 alpha → lysis of corpus luteum→ culture negative fetus

Chronic Enteritis (Salmonella)

A form of Salmonellosis seen in older calves (6-8 weeks) presenting as 'failure to thrive' with loose stool (not overtly diarrheic) and postmortem findings of localized necrosis and 'button ulcers' in the cecum/colon.

Salmonellosis Control (Biosecurity)

Involves environmental hygiene, strict calving pen management, effective colostrum delivery, good nutrition, identifying carriers, and culling positive animals. ELISA sampling. Rodent control. Vx. Test animals >6mo 

Antimicrobials (Salmonella Treatment)

Used for systemic Salmonella infections to mitigate bacteremia, but generally do not improve diarrhea and may sometimes worsen it by depressing normal flora.

1. TMS - oral form milk fed calves or IV for older

2. cephalosporin

3. aminoglycosides

4. fluoroquinolines - resp only

5. ampicillin

Also fluids, NSAIDS, and plasma transfusion (caution)

What are the clinipath findings in salmonella 

1. severe leukopenia → leukocytosis

2. hyperfibrinogenemia

3. metabolic acidosis

4. hyponaturemia

5. hypokalemia

6. hypoproteinemia

Mycobacterium avium subsp. paratuberculosis (MAP)

The slow-growing, acid-fast bacterium responsible for Johne's Disease, resistant to environmental factors (>1yr) and primarily transmitted via the fecal-oral route.

MAP Pathophysiology

Infection primarily occurs in calves (M cells and peyers patches), with the organism proliferating in the ileal mucosa and regional lymph nodes, leading to a thickened and corrugated intestine after a prolonged incubation period (2-10 yrs).

Clinical Signs of Johne's Disease

Include 'pipestream' diarrhea, weight loss despite a normal appetite, and 'bottle jaw' (submandibular edema) due to hypoproteinemia, typically appearing in animals 2-6 years of age.

Johne’s dz dx

1. Ag:

   1. Fecal culture 

   2. PCR

2. Ab

   1. ELISA

3. Cell mediated immunity - gamma interferon

4. Interdermal of IV johnin test

5. Biopsy ileocecal jx and LN

Fecal Culture (Johne's Disease)

Considered the 'gold standard' for detecting MAP, it can identify infected animals years before clinical signs but is time-consuming and labor-intensive.

Can detect infection 1-4 yrs before infection. but takes 6 mo to grow and culture

ELISA (Johne's Disease)

An antibody-based test useful for herd screening to identify infected asymptomatic cattle and for confirming advanced clinical disease, though less sensitive for individual early infections.

Not as useful in sheep

Johne's Disease 'Tip of the Iceberg' Concept

Describes that for every clinical case of Johne's Disease observed, 15-25% of the herd is likely infected, often subclinically.

Stages of Johne's Disease

1. silent infection

   1. no diarrhea and unlikely to dx dz. Organism is proliferating 

2. Inapparent carriers

   1. no CS, but may see positive tests, contaminate environment

3. clinical Dz

   1. tests positive, minor CS

4. Advanced clinical dz

   1. diarrhea, and all the big signs

Johne's Disease Transmission Routes

Primarily fecal-oral, but also through colostrum, milk, transplacental transmission, and sexually (semen, embryos).

Mycopar (Johne's Disease Vaccine)

A killed oil suspension vaccine for MAP, which reduces the incidence of clinical disease but does not necessarily prevent fecal shedding and interferes with serologic testing.

Requires state vet approval

How do you tx Johne’s

1. No cure, tx symptoms and supportive cate

2. plasma and electrolyte transfussion - watch for transfusion reactions signs (muscle fasciculations, etc). Stop or give NSAID

3. cull :/

Clinical Signs of Winter Dysentery

Include 'explosive' diarrhea (sometimes hemorrhagic), anorexia, depression, decreased milk production, and decreased rumen contractions; usually brief (2-4 days) with spontaneous recovery. No mucosal lesions.

Nov-April

Bovine Coronavirus

Winter Dysentery Diagnosis

Primarily made via PCR to detect Bovine Coronavirus.

Winter Dysentery Treatment

Supportive care focused on fluid therapy, keeping animals eating, and potentially antibiotics, with spontaneous recovery being common.