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Adult Ruminant Diarrhea

Description
Table of Contents


  • 1. Gastrointestinal Nematode Parasites
  • 2. Johnes Disease (Paratuberculosis)
  • 3. Bovine Viral Diarrhea
  • 4. Arsenic Toxicosis
  • 5. Fescue Toxicosis
  • 6. Bovine Lymphosarcoma
  • 7. Winter Dysentery
  • 8. Copper Deficiency / Molybdenum Excess
  • 9. Malignant Catarrhal Fever
  • 10. Rumen Lactic Acidosis
  • 11. Miscellaneous Nonenteric Causes of Diarrhea




    Many enteric and nonenteric diseases can cause diarrhea in cattle. Herd outbreaks of diarrhea are usually associated with gastrointestinal parasites, food or water-borne illnesses, and introduction of an infectious agent into a naive population. Bovine viral diarrhea can cause a herd outbreak or occur sporadically. Copper deficiency, Johnes disease, lymphosarcoma, and fat necrosis can also present as herd problems or as sporadic problems. Heart failure, peritonitis, liver failure, and thrombosis of the vena cava generally occur as sporadic problems that only affect a single animal in a herd.




    1. Gastrointestinal Nematode Parasites


    Parasitism is the most common cause of chronic diarrhea in cattle, sheep, and goats. Age, housing, climate, and stocking density strongly affect the epidemiology of endoparasitism. Both young animals and adults are susceptible, but generally symptoms are most apparent in cattle under 4 years of age. Cattle have co-evolved with their nematodal parasites, and tend to form strong immunity to them providing their nutritional status is adequate. In contrast, small ruminants (especially goats) develop little-to-no immunity to nematodal parasites and remain vulnerable their entire life. Pastured animals are more likely to accumulate large parasite burdens compared to housed animals. Wet, warm environments favor survival of immature parasites on pasture, especially if the winters are mild. Optimal temperatures: 70-80 degrees F, and 95% humidity. Overgrazing of pastures force animals to graze closer to fecal pads where the parasite infectivity is the highest (larvae are concentrated within a meter of fecal pads). Ideally each cow/calf pair should have at least 2 acres of grazing land. Small ruminants need an acre per five animals. Producers with limited acreage, a high stocking rate, and young animals need to be particularly vigilant by periodically assessing their parasite control program. Quantitation of parasite ova in a composite fecal sample provides useful information concerning the effectiveness of the anthelmintics used in the herd, and the appropriate deworming interval.

    Ostertagia Ostertagi
    This parasite is the most pathogenic and economically important parasite of cattle in the southeastern United States. Symptoms of ostertagiasis include profuse watery green diarrhea, rapid weight loss, mild to moderate anemia, hypoproteinemia, rough haircoat, anorexia, and submandibular edema. Subclinical disease reduces weight gain and productivity. Cattle and to a lesser extent, sheep, goats, and llamas are affected. Several clinical syndromes are associated with this parasite.

    Type I Ostertagiasis
    This syndrome occurs in suckling and weaned ruminants in their first grazing season. Approximately 1-2 weeks after leaving the body, eggs produced by adult parasites become infective L3 larvae. After the ruminant ingests the L3 larvae, the parasites invade abomasal glands, develop to adulthood and emerge from the glands in 3 weeks. During emergence, HCL-producing cells (parietal cells) and cells that secrete pepsinogen (chief cells) are damaged. The resulting elevation in abomasal pH prevents conversion of pepsinogen to pepsin thereby disrupting protein digestion. The parasites also destroy epithelium and intercellular junctions, allowing serum proteins and red blood cells to leak into the abomasal lumen, and pepsinogen into the circulation. Type I ostertagiasis has a good prognosis if treated with effective anthelmintics.
    Pretype II Ostertagiasis
    The L4 larvae in the abomasal glands undergo arrested development (hypobiosis) for up to 4 months in response to harsh climatic conditions (hot dry summer in the southern United States, and cold winter in the northern United States).

    Type II Ostertagiasis
    When weather favorable for survival of encysted larva returns, the dormant larvae in the abomasal glands resume development. The accumulated larvae emerge "en masse" from abomasal glands, causing much more severe pathology than type I ostertagiasis. Anemia, bottlejaw (submandibular edema), diarrhea and weight loss occur in about 10% of cattle that experience massive emergence of larvae. Type II ostertagiasis occurs primarily in young cattle (1-4 years old). Clinical cases occur in autumn in the southern United States and spring in the northern US. Prognosis is more guarded with type II than type I ostertagiasis. Cattle with type II ostertagiasis often have fecal egg counts of >2,000 eggs per gram, and elevated serum pepsinogen concentrations. Postmortem findings include edematous abomasal mucosa and abnormally high abomasal pH (>3).

    Control of ostertagia.
    Pasture rotation, avoidance of overgrazing, and strategic use of anthelmintics are the main defenses against excessive parasitism. A low level of parasitism is desirable because it stimulates natural immunity. The parasite control program's primary goal is to maintain pasture infectivity at below 200 eggs per gram. Fecal egg counts can be checked in the spring, and all beef calves and their dams dewormed if > 200 EPG. Cattle should be moved to a "clean" pasture. All cattle should be dewormed in the early autumn before moving to winter grazing. This strategy reduces the number of larvae on pastures and consequently the number available to become hypobiotic. Midsummer heat >90 degrees F, and sustained winter temperatures below 50 degrees F sterilizes pasture larvae.

    Anthelmentic Cattle & Sheep Dose
    ivermectin 200 ug/kg P.O.
    albendazole 10 ug/kg P.O.
    levamisole 8 mg/kg P.O.

    Anthelmentic Goat Dose
    ivermectin 400 ug/kg P.O.
    albendazole 200 ug/kg P.O.
    levamisole 10-12 mg/kg P.O.
    levamisole 10-12 mg/kg P.O.



    Hemonchus contortus
    Hemonchus contortus is the most life-threatening nematodal parasite known to goats and sheep living in the Southeastern United States. Large burdens accumulate rapidly in the warm months of the year, and can exsanguinate and kill a host in as little time as 2-3 weeks. H. Contortus severely damages the abomasal mucosa, thereby causing maldigestion, anemia, hypoproteinemia, and diarrhea.
    Small ruminants, particularly goats, did not co-evolve with the parasite. As a result, very little immunity develops from exposure to it. Further, the rapid generation time (3 weeks) and frequent exposure to anthelmintics has enabled Hemonchus to develop drug resistance against all major classes of anthelmintics. Benzimidazole resistance is particularly widespread. Parasite control in small ruminants is therefore a major health concern, and could well be the most limiting factor in sustaining a small ruminant industry in this part of the country.

    Control measures
    Sensible us of rotational grazing in conjunction with anthelmintics is the best way to reduce the frequency of treatments and keep the number of parasites accumulated from reaching a health-threatening level. The parasite's life cycle can be used to help break the transmission cycle. Once the larvae hatches out of feces, it passively moves up a grass blade in dew and must be consumed by a host before it uses up it's energy reserves. Three months of hot dry weather will effectively kill the free living stages of Hemonchus on pasture. During cool months, up to 6 months are needed to achieve larval die-off. Since transmission is highest in the warm months, one strategy is to deworm the small ruminant herd/flock with an effective anthelmintic in late winter, keep them in a dry lot for 1-2 days while they are passing infective larvae, and then move them to a "clean" pasture that has been rested an appropriate length of time. Treatment intervals through the summer will depend on how quickly Hemonchus burdens accumulate in the environment. Several composite fecal samples can be submitted for McMaster egg counts to spot check the herd/flock. If it exceeds 500 eggs per gram, dewormed with a good larvicidal anthelmintic (to help eliminate hypobiotic parasites) and moved to a "clean" field. The frequency of deworming should be less during the cool months since pasture transmission is minimal.

    Ways to assess anthelmintic efficacy:
    1. Drench Rite Test: an in vitro assay that involves harvesting larvae from a fecal sample, and then exposing them to various dewormers to determine which ones are effective.
    2. Fecal egg reduction test: take pre-treatment fecal egg counts (FEC's) from 24-32 animals. Divide them into 3-4 groups depending on the number of drugs tested (have 8 animals in each group). Deworm the animals with the chosen compound. Keep 1 group as a control group (not dewormed). Repeat the FEC in 2 weeks. An effective drug should reduce the pre-treatment FEC by at least 95%.

    Important Practice Tips:
    1. Goats metabolize drugs much more quickly than cattle and sheep. Use 1.5 to 2 times the label dosage for the avermectins, benzimidazoles, and morantel anthelmintics. Levamisole has a very small safety margin. Do not overdose it or the animal could have a fatal reaction.
    2. Dose anthelmintics carefully! Underdosing promotes resistance. Whenever possible, weigh animals prior to dosing to insure a therapeutic dosing, and to avoid overdosing less safe drugs (levamisole).
    3. Two classes of anthelmintic can be used simultaneously for synergistic effect. This strategy is particularly important if treating a sheep or goat with a severe parasite burden. It is also a useful way to treat recently acquired goats to try and eliminate any resistant parasites that they might have otherwise added to the herd/flock.




    2. Johnes Disease (Paratuberculosis)


    Clinical Signs.
    Affected cattle, sheep and goats develop progressive emaciation. Typical age of onset of obvious clinical signs: 2-7 yrs. Cattle develop profuse, chronic, nonfetid diarrhea (no blood or fibrin), progressive weight loss, and submandibular and brisket edema. Chronic weight loss is the most common clinical sign in small ruminants; they do not commonly develop diarrhea but pasty unpelleted feces are occasionally noted. Appetite and rectal temperatures are normal in most cases.

    Subclinical disease exists for years before the affected animal shows typical the clinical signs of weight loss ± diarrhea. Subclinically affected dairy animals economically impact the herd by producing less milk than unaffected herdmates. Subclinical animals shed less organisms than clinically apparent cases, but still provide a source of infective organisms to other animals in the herd.
    Typical clin path findings: decreased serum total protein and albumin, elevated CK and ALP, and hyperphosphatemia (reason unclear).
    Pathogenesis. The disease is caused by Mycobacterium paratuberculosis, a Gram positive, acid fast bacterial rod. The organism was isolated in 1826 by Drs. Johne (pronounced "yoney") and Frothingham. Transmission is primarily by the oral-fecal route. The majority of infections occur shortly after birth when the animals are most susceptible. After 6 months of age, cattle become more resistant to infection, and a much higher dose is needed to cause infection. At least 25% of heavily infected cows spread the disease transplacentally to their fetuses, and shed organisms in their milk. Infected bulls shed organisms in their semen, but sexual transmission has not been proven.


    Once ingested, organisms invade the lamina propria of the ileum, cecum and colon, and slowly multiply. The organisms incite a granulomatous reaction (macrophages, lymphocytes) in the bowel, and spread to regional lymph nodes via infected macrophages. The progressive inflammatory response distorts the lamina propria, causing leakage of protein-rich fluid into the intestinal lumen and malabsorption of nutrients. The ileal, cecal, and colonic mucosa becomes grossly thickened and corrugated in appearance as the disease advances in most cattle breeds (not always evident in bos indicus and small ruminants). Subclinically affected animals shed low numbers of organisms (<100/gram of feces) compared to clinically affected animals (100,000 to 6 million/gram of feces).
    Three Disease Stages
    1. Stage 1: preclinical/prepatent
    2. Stage 2: preclinical/patent
    3. Stage 3: clinical and patent

    Diagnosis.
    Currently, there is not a reliable method of detecting subclinical infections in animals, so eradication of this disease is very difficult to accomplish.
    1) fecal culture. 2-5 gms feces needed. Specificity 100%. Sensitivity: 50% in late subclinical and clinically affected animals. Subclinical animals shed intermittently or at levels below detection (more false negatives). It takes 8-16 weeks to obtain results of the fecal culture! Note: the cattle strain will grow on culture but the sheep strain will not grow in medium.

    2) Tissue morphology. Demonstration of acid-fast Gram positive organisms in the ileum, cecum, colon, and regional lymph nodes (taken by laporatomy or at necropsy) is very supportive of the diagnosis. Although rectal scrapings can be used as supportive evidence of infection, occasional false positives can arise because saprophytic (nonpathogenic) mycobacterium are occasionally present in this area. False negatives also can occur if the disease is not advanced enough to involve the rectal mucosa.

    3) Serologic Tests (detects antibodies)
    Agar gel immunodiffusion
    Approx 100% specific but lacks sensitivity in subclinical cases (only 26% detected). In clinically affected cases, sensitivity is improved to 60-80%.
    Complement fixation
    Sensitivity and specificity similar to AGID. This test is used for international import/export testing.
    ELISA (IDEXX Labs)
    Approved in 1992 by USDA. This new ELISA is superior to AGID and CF tests for detecting subclinical cases, and its specificity is excellent (99.7%). Sensitivity for detecting subclinical cases (stages 1 and 2):46%. Sensitivity for detecting clinical (stage 3) cases :88%. This test is currently being recommended for screening herds and replacement heifers and cows prior to purchase (JAVMA 1993; 203:1456).

    The most rapid way to facilitate eradication of Johnes animals from the herd is to use fecal culture and the ELISA in combination on an annual basis. However, use of the ELISA alone is more cost effective, but eradication will take longer.

    Treatment.
    There is no practical and effective treatment, and infected animals should be culled for slaughter purposes. The progeny of infected cows are very likely to be infected. In rare instances, very valuable cows have been treated with clofazimine. Clinical signs regress but treated animals continue to shed organisms. This treatment is cost-prohibitive in most situations.

    Control
    1) Test and cull program. Test cattle 2 years old and older annually with ELISA test and/or fecal culture. Cull positive cows and their offspring.
    2) Only purchase cattle from herds that test routinely for Johnes, and maintain a low herd prevalence (<2% positive). Test cattle prior to purchase. Note: in Wisconsin, there is an implied warranty that cattle sold in the State are Johnes-free.
    3) Use semen only from Johnes-free bulls.
    4) In problem herds, dairy calves can be removed from cows at birth, fed colostrum and milk from Johnes-negative cows, and housed in a separate facility away from the milking herd for at least the first 6 months of life. (This tactic will fail if calves were infected in utero)
    5) Areas that remain wet and swampy must be drained, and feces removed in order to reduce the number of organisms in the environment (organism can survive 9-11 mos in feces and soil).
    6) Vaccine. The vaccine is not a substitute for sanitation and test/removal practices. It's use is severely restricted, and highly regulated by State authorities. A State Veterinarian will authorize it's use only in herds that have already complied with other control measures. Only a few states currently allow its use: Wisconsin and Pennsylvania. Neonates between the age of 1-35 days are vaccinated with the bacterin in the brisket. Granulomas commonly form at the injection site, and vaccinates will have a positive TB test (the main reason for the tight regulation). Vaccinates still shed organisms but are less likely to become clinically ill. People handling the vaccine must avoid accidental self-injection (causes persistent granuloma formation).





    3. Bovine Viral Diarrhea


    Bovine viral diarrhea causes significant losses to the cattle industry through decreased milk production, reproductive problems (failure to conceive, abortions, fetal anomalies) and through the development of weak, unthrifty calves which frequently succumb to other diseases before reaching one year of age. The bovine viral diarrhea virus (BVDV) is a single-strand RNA Togavirus. Random detection of viral neutralizing antibodies to BVDV indicate that 60-90% of cattle in North America are seropositive (exposed). BVDV can cause inapparent infections in sheep, pigs, goats and wild ruminants; these species serve as reservoirs of infection for cattle.

    The BVDV has two biotypes and a diverse range of serotypic identities. Biotypic and antigenic variations occur independently. In cell culture, the cytopathic (CP) biotype induces vacuolization and cell death 2-3 days after inoculation, whereas the noncytopathic (NCP) biotype causes only minimal changes in cell culture. The antigenic diversity noted in field isolates of BVDV are caused by the enormous capacity for mutation at the major envelope glycoprotein gp53. This diversity causes many difficulties in developing suitable vaccines: antibodies developed against one BVDV isolate will not necessarily cross protect against challenge by a sufficiently different BVDV. This problem also impedes our ability to reliably test animals for BVDV. For example, an FA conjugate made with antibodies against one BVDV strain might not cross-react with a sufficiently different virus, thereby resulting in a false negative test result. To further compound the complexity, two genotypes (type 1 and type 2) have been recognized. Type 1 is considered to be much more virulent.

    Horizontal transmission of BVDV occurs through contact with contaminated oculonasal discharge, saliva, urine, uterine secretions, milk, blood, feces and semen. Transmission can occur through BVDV-contaminated feed, equipment, and personnel, and through blood-feeding insects. Vertical transmission is common because the virus readily crosses the placenta.


    Clinical Syndromes
    The disease causes different syndromes depending primarily on the immune status of the animal. "Bovine viral diarrhea "(BVD) refers to an acute infection in susceptible immunocompetent cattle. The infection is subclinical in 70-90% of the cases. However, the immunosuppressive effect of the BVDV increases host susceptibility to a variety of other pathogens (pasteurellosis, etc.). Clinical signs of BVDV infection include fever, oculonasal discharge, depression, inappetence, drop in milk production, and transient diarrhea. Shallow ulcerations are often evident in the oral cavity. On postmortem exam, mild lesions are identified primarily in the alimentary, respiratory and lymphoid tissues. Affected cattle shed virus in their secretions until serum neutralizing antibodies eliminate the viremic stage (14-21 days). Abortion occurs 1-2 months after viremia eliminated.

    A new syndrome characterized by thrombocytopenia and hemorrhage is being noted sporadically in immunocompetent cattle with acute BVDV infections. Clinical signs such as bloody diarrhea, epistaxis, and prolonged bleeding from injection sites and insect bites are associated with platelet counts below 25,000/ul.


    Effects on the fetus
    The fetopathic consequences of a noncytopathic BVDV infection in a pregnant, susceptible cow depends on the calf's gestational age.

    Within the first 120 days: Transplacental infection during the first four months of gestation can result in fetal resorption, abortion, retention and mummification, or in the development of persistently infected (PI) calves. Persistent infection develops because the calf's immune system is too immature to recognize the NC BVDV as "non-self". Consequently, they become immunotolerant of the virus. These persistently affected calves are often poor-doers in extrauterine life, and are generally smaller and less thrifty than their immunocompetent contemporaries. Most of these PI calves succumb to calfhood diseases or mucosal disease after maternal antibody wanes. Maternally derived antibody declines more rapidly in PI calves than in non-PI calves, and viral isolation from the blood is often possible by 2-4 months of age. These persistently affected calves are a natural reservoir of noncytopathic virus. They shed enormous quantities of virus in all their secretions on a continual basis.

    The embryo transfer industry created new opportunities for the development of persistently infected calves. Adventitious noncytopathic BVDV is a frequent contaminant of fetal calf serum, which is routinely used during the transfer of harvested embryos into recipient dams. Because embryo transfer calves are genetically valuable, the risk for spreading the virus by those surviving to reproductive age is magnified accordingly. The use of calf sera free of adventitious BVDV is now a major concern of persons involved in the embryo transfer industry. Recipient cows should be adequately immunized against BVDV, and tested to insure they are not persistently infected individuals.



    100-150 gestational days:
    Exposure of the fetus to noncytopathic BVDV results in the development of congenital abnormalities. This developmental period is critical because the final stages of organogenesis of the nervous system and eye are occurring, and the fetus is developing the ability to mount an immunologic response to the virus. The majority of congenital malformations are caused by antibody-antigen reactions in developing tissue. Consequences of BVDV infection between days 100 and 150 include partial hypotrichosis (alopecia), thymic hypoplasia, arthrogryposis, and brachygnathism. Ocular abnormalities include microphthalmia, cataract formation, retinal dysplasia, and optic neuritis. Central nervous system abnormalities include hydrocephalus, cavitation of the cerebrum (hydranencephaly), cerebellar hypoplasia, and hypomyelinogenesis.



    150 -200 gestational days:
    The fetus is now immunocompetent, so exposure to BVDV results only in the development of fetal neutralizing antibody. The calf will be normal at birth.


    Syndromes in Persistently - Infected Cattle
    An estimated 1.7% of the adult cattle population is persistently infected with BVDV. These animals pose an enormous hazard to the herd because they continually shed large quantities of virus (1x106-1x109 virions/ml) in their secretions and excretions. Calves from persistently infected cows are also persistently infected, so family lines of PI cattle can become established within a herd! Persistently affected animals that become superinfected with a cytopathic BVD virus have three possible outcomes: mucosal disease, chronic BVD, or no clinical effect. The ultimate outcome will depend on how similar the superinfecting BVD virus is to the persistently present noncytopathic BVD virus.

    Mucosal disease is a sporadic form of BVDV infection which has a low morbidity (5%) but high mortality rate (90-100%). This manifestation occurs when cattle persistently infected with noncytopathic BVDV virus become superinfected with an antigenically identical cytopathic virus. Mucosal disease is characterized by severe pyrexia, leukopenia, depression, weakness, profuse bloody diarrhea and rapid dehydration. Severe erosive lesions develop in the lips, gingiva, tongue, and dental pad. Lameness occurs secondary to laminitis and erosive interdigital lesions. Most animals die within 3-10 days after onset of signs. Extensive erosions and ulcers are evident throughout the digestive tract on postmortem examination.

    Chronic BVD develops when the persistently affected bovine becomes superinfected with an antigenically similar (but not identical) cytopathic BVD virus. Clinical signs include severe weight loss, chronic bloat, continual or intermittent diarrhea, lameness, hyperkeratotic skin, patchy alopecia, conjunctivitis, blunted oral papillae and chronic erosions in the mouth, around the vulva, coronary bands, and in the interdigital clefts. Animals with chronic BVD often die from severe debilitation.

    No clinical effect: if the persistently present NC BVD is antigenically dissimilar the superinfecting CP BVD, the only response will be development of antibodies against the superinfecting BVD.


    Diagnosis and Control.
    The most important aspects of control are to (1) identify and eliminate persistently infected cattle and (2) prevent transplacental infections.

    Climate. A microtiter immunoperoxidase assay (Cornell Diagnostic Lab) has been developed to screen entire herds for viral antigen. Cattle positive for presence of virus should be retested in 3-4 weeks. If still positive, they should be considered persistently infected and eliminated from the herd.

    Individual animals can be screened by viral isolation or FA testing on the buffy coat of an anticoagulated blood sample, and on postmortem tissues from the gastrointestinal tract.

    Calves can be reliably tested for persistent infections by 6-8 months of age. Unthrifty, poor-doing calves are always suspect, and can be culled or at least separated from healthy calves until tested to confirm their status. Positive animals (2 positives at 3 week intervals) are culled. The maternal line of positive calves should be checked for persistent infection also.

    Vaccination.
    Immunization against BVD is an important part of a herd health program for cattle. Calves should be vaccinated twice at 4 week intervals at 3-6 months of age. Adult cattle should be boostered 3-4 weeks prior to breeding to maximize protection during the most vulnerable months of gestation (the first 120 days). Controversy exists concerning which type of vaccine to use: killed or modified live. Both types of vaccines induce neutralizing antibodies capable of reacting to a wide antigenic variety of BVDV isolates in vitro by 21 days post-vaccination. Modified live vaccines have several disadvantages: they can induce fetopathy and cause profound immunosuppression in otherwise immunocompetent cattle. Also, use of modified live vaccines can induce outbreaks of mucosal disease in persistently infected animals, providing the vaccinal strain is antigenically similar to the persistently infecting strain. The main advantages of modified live vaccines is that they provide superior cell mediated immunity compared to killed products and are less expensive. Many producers use modified live vaccines in youngstock providing they are isolated from the brood cows. Killed products are the safest choice in herd situations where the vaccinates cannot be completely segregated from pregnant cows. Cattle in problem herds and intensive management situations can be vaccinated every 4 to 6 months with killed products in order to maintain a broad spectrum protection from all BVD strains. Additionally, use of BVD vaccines from different companies can provide broader exposure to different BVDV isolates.





    4. Arsenic Toxicosis


    Clinical signs.
    Herd outbreak of severe depression, abdominal pain, tachycardia, ataxia, weakness, salivation, rumen atony, and watery, bloody diarrhea. Severely affected animals die within hours. Subacute cases can die in 2-3 days from dehydration and renal failure.
    Pathogenesis. Arsenic is a heavy metal. After absorption, it binds to sulfhydral groups in enzymes and cofactors of important pathways such as the Krebs cycle. Binding impairs oxidative functions in highly metabolic tissues such as the gut, kidneys and brain. Cellular edema and destruction cause clinical signs.
    Organic and inorganic arsenic products are used as herbicides, wood preservatives, insecticides (boll weevil poison), snail/slug bait, and rodenticides. Arsenic has been used medicinally in tick dips for dogs and rumenatorics. Cows like the taste of arsenic. Toxicity results from consumption of the raw arsenical, consumption of contaminated grass clippings, and exposure to burned wood preserved with arsenic compounds. Toxicosis can occur in animals grazing in old orchards where arsenicals were used for insect control; the arsenic can persist in topsoil for many years. Calves that nurse arsenic-poisoned cows can be poisoned through the milk.

    Diagnosis.
    Clinical signs of abdominal pain, scleral injection, bloody diarrhea coupled with exposure to an arsenical. Arsenic concentration can be determined in the liver, kidney, urine, and rumen contents. Soil and water can also be tested for arsenicals.

    Treatment.
    Prognosis is poor unless treatment is given promptly. Oral sodium thiosulfate (60g Q 6 hrs) is recommended to bind arsenic in the gastrointestinal tract; it can also be administered intravenously (30-60 g as a 10% solution). Aggressive fluid therapy is needed to combat severe shock and to promote renal blood flow. Kaolin pectolin is useful as a gastrointestinal protectant.
    Note: recovered animals must be withheld from slaughter for at least one year. Milk from exposed cows can be toxic!





    5. Fescue Toxicosis


    Clinical signs.
    Low grade to moderate diarrhea can develop in adult cattle; the feces do not contain blood or fibrin. Affected cattle gradually lose weight. In some cases, hard, gritty masses can often be palpated per rectum in the pelvic inlet. Small bowel and spiral colon involvement might also be palpable on rectal examination.

    Pathogenesis.
    Fescue toxicosis causes diarrhea by interfering with normal motility. Ergot alkaloids produced by the fungal endophyte, Neotyphodium coenophialum (formerly called Acremonium coenophialum) act as dopamine agonists. In the gastrointestinal tract, activation of the dopamine receptors results in less segmental activity, more rapid movement of ingesta through the tract, and decreased nutrient absorption. If fat necrosis is present, the hard irregularly shaped masses can encompass loops of intestine, and cause partial and eventually total obstruction of the bowel. Complete obstruction of the intestine results in abdominal distention, and scant fecal production (rather than diarrhea). If the proximal small bowel is obstructed, hypochloremic metabolic alkalosis can arise.
    Many of the other clinical signs associated with the endophyte alkaloids are also caused by overactivation of dopamine pathways. Cattle develop hyperthermia ("summer slump syndrome"), weight loss, reduced appetite, and occasionally necrosis of distal extremities in cold weather (tail switch and feet; a.k.a. "fescue foot"). Poor reproductive performance also contributes greatly to the economic losses associated with fescue toxicosis. These problems, with the exception of fescue foot, are quite common in the Southeastern United States because the endophyte-contaminated fescue is so prevalent. Infected fescue has almost completely replaced noninfected fescue in many parts of the country because the endophyte-infected grass is hardier than endophyte-free fescue plants.

    Treatment.
    Removal of cattle from the endophyte contaminated forage causes regression of many clinical signs in several days. Remission of masses takes weeks after endophyte-contaminated fescue is removed from the cattle's diet. This tactic is beneficial for cattle that are not completely obstructed. Research is currently underway to determine the best way to protect cattle from the harmful effects of the endophyte. Dopamine antagonists (domperidone, metoclopramide etc.) are showing promise, as are vaccines that stimulate antibodies against ergot alkaloids.

    Pasture management strategies: to reduce the effect of the endophyte, overseed with clover, and keep the pasture mowed closely to prevent seed head formation. Recent break-through: a nontoxic endophyte has been developed that gives the pasture grass all the beneficial effects of the toxic endophate, but has none of the animal ill effects.





    6. Bovine Lymphosarcoma


    Clinical signs.
    Diarrhea is one of many clinical signs associated with adult multicentric lymphosarcoma, and it is not a consistent sign. Invasion of the lamina propria with neoplastic cells can cause malabsorption and diarrhea. Masses associated with the wall of the intestine also can cause diarrhea by interfering with motility, much like fat necrosis. Other common signs of lymphoid neoplasia in cattle include weight loss, decreased milk production, abomasal ulceration, infertility, cardiac tumorization, enlarged lymph nodes(external and internal), exosthalmos, and recumbancy. The disease has a higher prevalence in dairy cattle than beef cattle.

    Pathogenesis.
    The adult enzootic form of bovine lymphosarcoma is caused by a retrovirus called the bovine leukosis virus (BLV). The virus is species-specific for cattle. The virus is highly associated with lymphocytes. As little as 0.1 ml of blood from a BLV-positive animal injected into a seronegative bovine can cause seroconversion. The bovine leukosis virus is spread hematogenously by blood-sucking insects, by blood-contaminated surgical equipment, ear-taggers, needles, dehorners, rectal sleeves, etc., and during blood transfusions. Transmission also can occur (to a lesser degree) through BLV-contaminated colostrum. In utero infection can occur in BLV positive dams; the incidence is probably less than 10%. Transmission through semen is possible through natural cover, providing a reproductive inflammation is present and the bull is BLV positive. Transmission by this route is unlikely however, especially if artificial is insemination is used (semen with high lymphocyte counts is discarded, and the ejaculate is routinely diluted).
    As in the case of most retroviral infections, infected animals are infected for life despite a strong humeral response. Only a small percentage of BLV-infected bovines actually develop tumors (1 to 5%) but some herds have an unusually high incidence of tumor development; genetics might play a role in this phenomenon. Clinical signs (tumors) rarely appear before 2 years of age, and are most commonly noted in 5-8 year old cattle. Tumors most commonly develop in the abomasum, heart, spleen, lumbar spinal cord, uterus, peripheral lymph nodes, and retrobulbar tissues. Economic losses arise from carcass condemnation. Furthermore, BLV positive cows produce less milk. Indirect economic losses occur from loss of sales to foreign countries (BLV positive animals, semen, embryos restricted from import).

    Diagnosis.
    In adult cattle, a positive BLV AGID indicates the animal has anti-BLV antibodies and is therefore infected with the retrovirus. A negative BLV test allows you to take lymphosarcoma off your list of rule outs for chronic diarrhea because the test is sensitive and specific. A positive test only means that this disease remains an etiologic consideration as a contributor to the diarrhea.
    A calf less than 8 months of age might test positive if it ingested colostral antibodies from a BLV positive cow. Retest the calf after it reaches 8 months of age in order to determine if the calf is truly infected.
    Persistent lymphocytosis develops in approximately one third of BLV-positve cattle even in the absence of other clinical signs. However, approximately 75% of the cattle with tumors have peripheral lymphocytosis. Abnormal lymphocytes can occasionally be noted in the peripheral blood. Moderate-to-severe anemia can be present in animals with bleeding abomasal lesions secondary to tumorization.
    Findings of enlarged peripheral lymph nodes on physical (and rectal) exam, and a biopsy (preferred to an aspirate) of an abnormal node make the diagnosis more definitive. Conclusive evidence that the diarrhea is caused by lymphosarcoma comes from gross and microscopic findings of lymphoid tumors involving the digestive tract during laparotomy or on a postmortem examination.

    Control.
    No vaccines are available, so control must be made through management changes. Positive animals can be culled but this is an expensive strategy and not very practical in the United States (at this time). It is most applicable in herds where valuable calves are being raised for sale in foreign markets. A more practical approach is to segregate positive animals from negative animals, and to take measures to decrease transmission. However, segregation is not possible for all producers. The good news is that the incidence of seropositivity can be significantly reduced over time by simply following the guidelines below.

    Guidelines for decreasing transmission of the virus:
    1. Use individual sterile needles
    2. Replace rectal sleeves between animals
    3. Rinse and disinfect tattoo dehorning equipment, and other surgical equipment between animals. Chlorhexidine and dilute sodium hypochlorite are good disinfectants.
    4. Feed calves only pasteurized colostrum
    5. Insect control
    6. Use BLV negative bulls





    7. Winter Dysentery


    Clinical signs.
    This epizootic disease typically occurs in the cool months of the year in herds of housed cattle (usually dairy cows). Adults are most commonly affected. Acute diarrhea, anorexia, mild depression, and dropped milk production affecting multiple animals are the common presenting complaints. The feces are dark-colored, profuse, and can be streaked with blood and mucus. Illness lasts approximately 1-4 days in individual animals. Mortality is less than 1%, and losses are primarily in terms of milk production. The disease runs its course in the herd in 2 weeks (6-8 weeks in larger herds).

    Diagnosis.
    Rule out other infectious and nutritional diseases prior to making this "diagnosis of exclusion".

    Pathogenesis.
    For over 60 years, the cause of winter dysentery has remained an enigma. Recent evidence strongly supports bovine coronavirus as the cause for this syndrome. Colonic mucosa develops necrotizing, hemorrhagic lesions. Diarrhea occurs as a result of inflammation and hypersecretion.

    Treatment.
    Supportive only (provide food, electrolytes, water). Recovery is spontaneous within a few days without specific therapy.





    8. Copper Deficiency / Molybdenum Excess


    Clinical signs.
    Signs include profuse watery diarrhea, poor weight gain/weight loss, poor haircoats, depigmentation, pale mucous membranes, and microcytic hypochromic anemia (iron deficiency). Loss of wool crimp and depigmentation can develop in affected sheep. Epiphyseal enlargement and stiff gait occurs in many young ruminants. Copper deficiency in kids and lambs causes "enzootic neonatal ataxia" (swayback); it is characterized by pelvic limb ataxia that progresses to the forelimbs. Spontaneous fractures are also reported in association with copper deficiency.

    Pathogenesis.
    Copper is an essential cofactor in many mammalian enzymes (iron utilization, prevention of cellular oxidative damage, collagen synthesis, pigment formation, etc.). Dietary copper deficiency as well as impairment of alimentary absorption of copper produces the disease. There is an important dietary relationship between dietary copper, sulfate and molybdenum. If dietary sulfur or molybdenum are fed in excessive amounts, copper absorption in the GI tract is drastically reduced. Excessive dietary calcium also interferes with copper absorption.

    Diagnosis.
    Liver copper levels are the most reliable test for the copper status of the animal, but antemortem sampling (liver biopsy) involves some risk to a living animal. Blood testing is less useful, as these levels are the last to fall in a deficient state. However, they are often employed since testing is noninvasive. Feed analysis (copper, sulfur, molybdenum).

    Treatment and prevention.
    Treatment: SQ copper glycinate, or dietary copper supplementation in a salt-mineral mix. Copper oxide wire boluses are a useful way to supply longterm (4.5 mos) therapy. The boluses lodge in the rumen and slowly release copper.





    9. Malignant Catarrhal Fever


    Clinical signs.
    Sporatic and highly fatal disease of cattle, deer, bison, buffalo, and rabbits. Incubation time: 3-10 weeks. Severe fever (106-108 F), profuse mucopurulent nasal and ocular discharge, severe corneal opacity, bronchopneumonia, lymphadenopathy, oral erosions, salivation, scabby muzzle, cracking skin, and profuse diarrhea (± blood) characterize malignant catarrhal fever (MCF). Scabby horns and coronary bands, lameness, hematuria, and encephalitis are prominent signs in some cases. The disease occurs sporadically in North America. The mortality rate in clinically affected animals is 95-100%. The disease
    Etiologic differentials include BVD, bluetongue, rinderpest (exotic), vesicular stomatitis, and foot and mouth disease (exotic).

    Pathogenesis.
    Herpesvirus attacks vascular epithelium, thereby producing a severe, necrotizing vasculitis. Two forms are recognized: a wildebeest-associated (African) form and a sheep-associated form. The sheep-associated form occurs in Europe, Australia, Asia, and North America. It usually occurs on farms where there is some contact between sheep and cattle. Assymptomatic cattle and deer also can be reservoirs of infection! Cattle are dead end hosts for the virus. The means by which the virus is spread in nature is not understood. The sheep associated form appears to be most transmissible at lambing time.

    Diagnosis.
    1) Clinical signs.
    2) Postmortem exam demonstrates widespread vascular and endothelial lesions. Gastrointestinal ulcerations, urinary bladder ulcers, lymphoid hyperplasia, and ocular and CNS degeneration.
    3) Viral isolation from buffy coat cells
    4) serum neutralization of 1:4 and greater
    5) rabbit inoculation

    Treatment.
    Unsuccessful in animals with severe signs

    Prevention.
    Prevent contact with sheep and African wildlife. Isolate affected animals.
    Modified live and killed vaccines are available but are of limited efficacy (not protective in the face of challenge).





    10. Rumen Lactic Acidosis


    Synonyms:
    grain overload, toxic indigestion

    When ruminants ingest simple, readily fermentable carbohydrates (examples: grains, breads, fruit, beets, potatoes) in excess, especially when they are not accustomed to these feedstuffs, ruminal microorganisms are altered. The severity of the disease is related to the amount of carbohydrate ingested over time, and the degree of rumen microbial adaptation prior to the insult. Acute rumen acidosis varies in severity from a mild disease (anorexia, decreased GI motility, transient diarrhea) to an severe syndrome characterized by severe bloating, hemoconcentration, tachycardia, diarrhea, prostration and death.

    Pathogenesis.
    The sudden presence of excessive amounts of carbohydrates in the rumen favors rapid overgrowth of organisms (Strep. bovis and lactobacilli) that make lactic acid as a metabolic byproduct. These lactic acid producers multiply rapidly, and use substrates less efficiently than slow-growing cellulolytic species. The rumen pH (normally 6.5 - 7) drops as lactic acid accumulates. In mild cases, the rumen acidosis causes inappetence and slight diarrhea; recovery occurs in 1-2 days. In severe cases, rumen pH continues to decline. When the rumen pH reaches 5-5.5, a large percentage of the normal rumen microflora (slow-growing cellulolytic bacteria) die because they cannot tolerate the acid environment and the increasing osmolality. The osmotic action of the lactic acid eventually causes the rumen osmolality to exceed plasma osmolality. Consequently, fluids are pulled from the vascular compartment into the rumen, resulting in hemoconcentration, a splashy, enlarged rumen, and diarrhea. The lactic acid is corrosive to the rumen wall. The mucosal barrier in the rumen is disrupted, so bacteria, fungi and endotoxin can be absorbed into portal circulation, leading to thrombosis and abscessation in the liver and associated vessels. By the time the rumen pH reaches 4.5 or less, prognosis for survival is guarded to extremely poor.
    Diagnosis. History and clinical signs. Check rumen pH. Peripheral (venous) blood gases show varying degree of acidosis.

    Treatment.
    Mild cases respond to oral alkalinizing agents such as magnesium hydroxide (Carmalax). Parenteral B complex vitamins are indicated until the rumen microfora can resume normal function. More severe cases also need intravenous fluid therapy, NSAI agents, and systemic antibiotics (preventative measure against liver abscessation). A rumenotomy and transfaunation are indicated in severely affected valuable animals to increase the likelihood of survival.





    11. Miscellaneous Nonenteric Causes of Diarrhea


    This section briefly reviews nonenteric problems that can result in diarrhea through one or several mechanisms: decreased vascular onchotic pressure, increased vascular hydrostatic pressure, and altered vascular permeability. A careful physical examination and biochemical profiling can place these rule outs in perspective.

    Thrombosis of the caudal vena cava
    This disorder is a potential (yet uncommon) complication of rumen lactic acidosis. Bacteria absorbed into the portal vein during a bout of rumenitis can lead to bacterial abscessation in the liver. Erosion of the abscess into the caudal vena cava results in thrombophlebitis and occlusion of blood flow. Occlusion of the caudal vena cava increases hydrostatic pressure in capillary beds and lymphatics, and favors a net loss of fluids into the intestinal lumen. Signs include abdominal distention and diarrhea. Turgid congestion of the subcutaneous abdominal veins (caudal superficial epigastric vein) and not other large veins (jugular, etc.) is an important diagnostic sign.


    Liver Failure
    Liver failure can contribute to development of diarrhea in 3 ways:
    1) failure to make albumin and other proteins results in lowered plasma osmotic pressure, so fluids tend to move out of the vasculature.
    2) Extensive fibrosis impairs portal blood flow, thereby increasing passive congestion (hydrostatic pressure).
    3) Failure to remove bile salts from the gut leads to their persistence in the bowel lumen; these salts act as irritants, and can disrupt tight junctions between colonic cells.


    Heart Failure
    Right-sided heart failure can result in signs of diarrhea by causing an increase in hydrostatic pressure in capillary beds. The pressure increase forces more fluid out of the vasculature and into the interstitium (generalized edema) and other body spaces (pleura, peritoneal cavity, intestinal lumen). Findings of persistent tachycardia, generalized venous distention, murmurs, arrhythmia, an abnormal echocardiogram, and an elevated central venous pressure support a diagnosis of heart failure.


    Glomerulonephritis
    Damaged glomeruli allow massive quantities of albumin to escape from plasma into the urine. Plasma colloid osmotic pressure is reduced secondary to hypoalbuminemia, so fluid moves out of the vasculature and into the interstitium and "third space" compartments (pleura, peritoneal cavity, intestinal lumen). Amyloidosis secondary to chronic antigenic stimulation leads to deposition of amyloid in the kidneys, liver, adrenal glands, and intestinal wall. The kidneys feel smoothly enlarged and are nonpainful on palpation. Typical clinical pathology findings: massive proteinuria, and reduced serum total protein and albumin concentrations.
    Bacterial glomerulonephritis (Corynebacterium renale, E. coli ) also damages glomeruli. The affected kidney(s) is/are enlarged and painful. Pyuria, bacteria, hematuria, and massive proteiuria are identified on urinalysis. An inflammatory leukogram and reduced serum total protein and albumin concentrations are common findings.


    Peritonitis
    Peritonitis from traumatic reticulitis, ruptured abscess, uterine rupture, surgical contamination, perforated bowel, or a penetrating foreign body causes diarrhea secondary to inflammatory changes in the peritoneal lining, and pain. The gastrointestinal tract becomes hypomotile (less mixing) and transit time increases. In addition, endotoxin absorbed into general circulation contributes to the diarrhea by setting off a "mediator cascade" that ultimately alters capillary permeability in the bowel (and elsewhere).
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