Information from GoatConnection.com|
Young Ruminant Diarrhea
By Dr. Lisa Williamson
Oct 27, 2002, 11:17pm
AMS 5350 Large Animal Digestive System
Young Ruminant Diarrhea
Dr. Lisa Williamson
Table of Contents
Clostridium perfringens - related diseases
Young Ruminant Diarrhea AQS Session
Diarrhea is a common complaint in calves and other young ruminants, particularly in the first few months of life. Many of the pathogens and management practices that cause diarrhea in calves also affect lambs, goats and modified ruminants such as llamas. Most herds have been exposed to diarrhea-causing pathogens, and management practices will largely determine the health impact that those pathogens will have on the youngstock. In "real life", most young ruminant diarrheas are caused by more than one factor or pathologic agent. It is important to be able to correctly diagnose and appropriately treat diarrhea in livestock, and to be able to suggest management strategies that will prevent further outbreaks of disease. Several pathogens are zoonotic agents (Salmonella spp., Cryptosporidium spp., Giardia spp., and certain types of enteropathogenic E. coli) so great care must be taken when handling diarrheic animals, contaminated bedding, and fecal samples to avoid contaminating yourself and others.
1. septicemic colibacillosis
2. enteric colibacillosis
Clinical signs. Disease most commonly occurs in the first 2 weeks of life. Neonates show sign of progressive depression and inappetence, followed by watery diarrhea. Signs of sepsis such as fever (more protracted cases), hypothermia (peracute and terminal cases), scleral injection, mucous membrane abnormalities, and tachycardia occur commonly. Disease progression depends on the virulence of the E. coli serotype and the vulnerability of the patient. For example, calves with complete failure of passive transfer can develop coma and death within 6 hours of the onset of clinical signs. In more slowly progressing cases, bacteremia can result in signs of meningitis, physitis and synovitis. Prognosis is guarded to poor for survival.
Pathogenesis. Opportunistic E. coli organisms invade through umbilical (most common), nasal, or oropharyngeal routes. Clinical signs develop approximately 24 hour after inoculation. Risk factors: (1) complete or partial failure of passive transfer, and (2) exposure to a serotype of E. coli that is able to invade into the bloodstream and rapidly multiply.
Diagnosis. Suspect this disease whenever a neonate presents with prominent signs of sepsis, particularly if these signs precede the onset of diarrhea. The organism can often be cultured from blood, and from affected synovial and cerebrospinal fluid.
Postmortem signs include petechial and ecchymotic hemorrhages on serosal surfaces. The E. coli often can be isolated from various organs. Fecal culture/analysis is of limited value because coliforms are normal inhabitants of the intestinal tract and the causative E. coli lack distinguishing antigenic features (in contrast to enterotoxigenic E. coli).
Treatment. Therapy is costly and time-consuming, and prognosis for survival is guarded. These factors, and the chance of joint and physeal complications, should be discussed with owner prior to embarking on therapy. Results are best when aggressive treatment is started early in the course of the disease. The patient's serum IgG status and blood glucose can be assessed on the farm. Samples should be taken prior to antibiotic therapy for microbiological analysis (blood, synovial fluid), and ideally, blood should be obtained for complete blood count and select chemistries (e.g. total protein, creatinine and electrolyte concentrations).
A. Hypoglycemic patients need immediate intravenous (IV) glucose administration. (Note: a neonatal calf is essentially a monogastric, and blood glucose concentration is normally 95-110 mg/dl.) If the blood glucose (BG) is equal to or below 50 mg/dl, give 10% glucose IV (5-10 ml/kg) and then reassess the blood glucose. If BG is between 80 and 50 mg/dl, 5% glucose or 2.5% glucose in half-strength acetated Ringer's solution are good initial choices. If hypoglycemia is the main cause of the depression, the patient's attitude will rapidly improve within 1-2 hours.
B. Continued fluid therapy (2.5 - 5 ml/kg/hr) is recommended for critically ill neonates until rehydrated and stabilized. Oral rehydration can then be used.
C. Neonatal calves with failure of passive transfer: IV administration of normal bovine plasma (20-80 ml per kg).
D. Systemic broad-spectrum antibiotic therapy is essential. Although the Gram negative spectrum is the most important consideration when treating a suspected coliform infection, there is no guarantee that the bacteremia is caused exclusively by a coliform until culture results are back; by then, it is too late for the patient! Intravenous antibiotic administration is preferred over other routes because it rapidly achieves high blood levels. Good initial choices: ceftiofur (Naxcel at 1-4 mg/kg every 12 hours) and penicillin (22,000 I.U. per kg IV every 6 hrs, or I.M. every 12 hrs). Approved sulfonamides such as sulfadimethoxine (Albon) , and sulfachlorpyridazine (Vetisulid) have a good Gram negative spectrum, but are bacteriostatic. Aminoglycoside use should be reserved for valuable animals not intended for food, and for situations where culture and sensitivity indicates that the organism is resistant to approved drugs but sensitive to the aminoglycoside. Aminoglycoside treatment can result in prolonged tissue residues (18 months)! Conventional chloramphenicol preparations should not be used food animals. However, florfenicol (nuflorTM) is labeled for food animal use.
E. Other supportive therapy: minimize environmental stress; keep patient warm and dry. Insure adequate nutrition.
Clinical signs. Diarrhea typically occurs in the first 7 days of life. The feces are fluid or pasty in consistency, and are typically white-to-pale yellow in color. Hence the layperson description, "white scours". The tail and hindquarters are heavily soiled with feces. Affected calves become weak, depressed, and anorectic as their fluid deficits and electrolyte/ acid-base disturbances worsen. Affected animals either recover or die within 5 days.
Pathogenesis. Calves and lambs that fail to ingest adequate amounts of colostrum are most at risk. Chilling, crowding, and dirty, pathogen-rich environments increase susceptibility to disease. Enteric colibacillosis is caused by strains of E. coli that are enterotoxigenic. Enterotoxigenic E. coli (ETEC) have 2 pathogenic weapons: (1) attachment factors (pili) that allow them to attach to the small intestinal brush border, and (2): an enterotoxin that causes crypt cells to hypersecrete fluids and electrolytes.
Historically, the main pilar antigen found in calf and lamb ETEC infections was designated as K99. Because the K designation is also used to name capsular antigens, the K99 antigens are now called F5 in some diagnostic centers. An F41 pilar antigen is also detected in some calf and lamb ETEC diarrheas.
Clin path findings. Calves with diarrhea (regardless of the etiologic agent) lose large quantities of water, potassium, sodium, chloride, and bicarbonate, and develop a metabolic acidosis. The loss of bicarbonate coupled with lactic acid production and decreased renal perfusion cause the metabolic acidosis. Although total body potassium levels are decreased, hyperkalemia is often noted in diarrheic calves (secondary to the acidosis). Hyperkalemia is cardiotoxic, particularly if in combination with hyponatremia, acidosis, and hypocalcemia. Bradycardia, decreased p wave amplitude and increased t wave amplitude on ECG, and cardiac standstill are signs associated with serum potassium concentrations of over 7 meq/l. Hypoglycemia is also a common finding because neonates lack adequate energy reserves to sustain them during periods of inappetence.
Diagnosis. Observe clinical signs consistent with the disease in the appropriate age group. Postmortem exam reveals fluid-filled loops of small intestines. Since the bacteria does not invade into the mucosa, there are no gross or histopathologic lesions. Feces can be submitted to a diagnostic center for an ELISA test to detect the pilar antigens (K99, F41). In a pure ETEC infection, fecal pH is alkaline secondary to loss of bicarbonate. However, it is not unusual for several pathogens to team up to make calves sick (mixed infections with ETEC and viral agents), so the fecal pH test might not be very revealing in all cases.
A. Fluid therapy is the most important treatment! Severe dehydration: treat with IV fluids. In calves that are mildly to moderately dehydrated (8% or less), oral fluid therapy is an effective route. Alternate oral electrolyte solutions every 6 hours with whole cow's milk (or high quality milk replacer) via a nurse bottle or esophageal feeder. Do not mix the electrolyte solutions with the milk because it will interfere with development of the casein clot, thereby causing a nutritional diarrhea. Continued feeding of milk sustains the growth of diarrheic calves and promotes regeneration of damaged mucosa (Can J Vet Res 1989;53:477).
Typical Feeding Schedule for 50 kg Diarrheic Calf
(1 liter = 2 pints)
6 AM and 6 PM: 1-2 liters oral electrolytes
12 noon and 12 AM: 2 liters milk or milk replacer
Oral electrolyte solutions are formulated to rehydrate, replace electrolytes (potassium, sodium, chloride, bicarbonate), and to alkalinize the recipient. Bicarbonate is the best alkalinizing agent; others alkalinizing agents include acetate and citrate. An energy source (glucose, glycine) is added primarily to facilitate small intestinal uptake of electrolytes. The energy level in all these formulations is insufficient to meet all the calf's caloric demands. In fact, they can starve to death if food is withheld for over 48 hours! The ideal oral electrolyte solutions are hyperosmotic (relative to plasma), have an electrolyte composition similar to plasma, contain an alkalinizing agent (preferably bicarb) and supply an energy source (primarily as glucose). Commercial products vary greatly in cost and in quality.
B. Flunixin meglumine (1 mg/kg IV or IM Q 12-24 hrs) for anti-prostaglandin (anti-secretory) effect. Make sure patient is being hydrated, and do not treat with NSAI abents for more than 1-3 days (risk of abomasal ulceration)
C. Bismuth subsalicylate (peptobismol or corrective mixture): 2-4 ml/kg orally every 6 hours for local anti-prostaglandin effect. Feces will become black!
D. Plasma therapy indicated if failure of passive transfer detected.
E. Parenteral antibiotics as described in previous section (if concurrent sepsis suspected).
Prevention. Insure that calf receives colostral immunity. In problem herds, cows can be vaccinated with a K99 bacterin in the prepartum period. The calf ingests protective antibody in the colostrum. Alternatively, calves can be inoculated orally right after birth with a K99 monoclonal antibody preparation. The antibody prevents binding of the K99-associated ETEC to the small intestinal epithelium. A vaccine for the F41 ETEC is not available.
Other types of E. coli infections in calves
Enterohemorrhagic E. coli (EHEC) is an emerging contributor to the calf diarrhea complex. It produces a hemorrhagic enterocolitis in calves 2 weeks to 2 months of age. The bacterium primarily colonizes the colon and produces a lesion in the mucosa referred to as an attaching and effacing lesion. Verotoxins produced by the EHEC cause vascular injury, thereby producing symptoms of bloody diarrhea. If EHEC infection is suspected, submit feces (or chilled colon sample) to a diagnostic center and request a verotoxin assay.
Note: in contrast to ETEC, the EHEC bacteria do not cause hypersecretion and have no pilar antigens (JAVMA 1990; 196:897). Recent evidence shows some EHEC E. coli that cause asymptomatic infections in calves can cause severe illness in people (the infamous 0157:H7 "Jack-in-the-Box" pathogen).
Rotaviruses and coronaviruses are the most common causes of viral diarrhea in calves. Rotavirus infections occur earlier in life and produce milder lesions than do coronaviral infections. Both viruses cause varying degrees of dehydration, acidosis, and electrolyte derangements (hyponatremia, hypochloremia, hyperkalemia).
Clinical signs. Rapid onset of diarrhea in calves from 1 day of age up to about 3 weeks of age; most cases occur in the first week of life. The clinical signs mimic enteric colibacillosis: yellow watery diarrhea, mild depression (worsens as fluid, acid-base and electrolyte disturbances worsen), inappetence, and reluctance to stand. Uncomplicated cases are self-limiting and symptomatic for only 1-2 days. However, secondary infections occur commonly, and will influence the ultimate clinical course of the illness.
Pathogenesis. Calves are mainly infected through an orofecal route. The organism is very hardy in the environment, and is resistant to inactivation by most disinfectants. The presence of colostral antibodies in the bowel lumen is protective initially, but once the antibody level in the milk declines in a few days, the calf is susceptible to infection.
Rotaviruses invade the tall columnar cells at the tips of the small intestinal villi. The infected cells are desquamated, and the villar tip atrophies. The absorptive and digestive functions (lactase secretion, etc.) of the villar tips are impaired, yet secretion by the crypt cells continues in an uninterrupted fashion. Bacterial fermentation renders undigested, unabsorbed nutrients into osmotically active small acids that draw more fluid into the digestive tract. As a result, the feces from animals with pure rotaviral infections will be acidic.
Diagnosis. Antemortem tests: a rotazyme ELISA test or a radioimmunoassay can be performed on a fresh fecal sample to detect rotavirus antigen. For best results, collect samples within the first 24 to 48 hours of the onset of the disease. Perform electron microscopy on feces to visualize organisms.
Postmortem: note lesions on histopathologic exam; do specific fluorescent antibody staining of frozen sections.
Treatment. Fluid therapy (as described under enteric colibacillosis section) is the most important aspect of treatment. Commercial lactase supplementation (LactaidTM) in milk is beneficial with rotaviral/coronaviral infections because it aids in digestion of lactose. Provide good nursing care. Antibiotic therapy is reserved for cases of diarrhea where a bacterial component is suspected.
1. Vaccines are available to give to prepartum cows to boost colostral immunity, and to give to neonatal calves orally. These products have historically yielded poor results.
2. Follow recommendations under management considerations section.
Clinical signs. Coronarius infections occur most commonly in calves that are 7-10 days old, but can occur up to 3 weeks of age. Clinical sign are similar to but more severe than a pure rotaviral infection because both small and large bowel is affected.
Pathogenesis. The virus (Coronaviridae family) gains entrance through an orofecal route of exposure. Both colonic and small intestinal columnar epithelium cells on the villi are infected. As a result, more severe fluid and electrolyte losses occur and recovery from a pure coronavirus infection takes longer than recovery from a pure rotavirus infection. The mechanism for the diarrhea is similar for coronaviral and rotaviral infections: loss of the villar digestive and absorptive function leads to an osmotic diarrhea. As in the case of rotaviral infections, pure coronaviral infections result in acidic feces.
Diagnosis. The distinct halo (corona) that surrounds the organism is visualized by electron microscopy using a negative staining procedure. ELISA tests are NOT available to detect coronavirus. Histopathology of the intestine allows visualization of the villar damage. Fluorescent antibody staining of frozen sections of intestine will demonstrate presence of the virus.
Treatment and control. Same as for rotaviral infections. Vaccines available are of limited efficacy.
Bovine Viral Diarrhea (BVD)
Bovine viral diarrhea virus is a potent immunosuppressive agent. Exposure of an otherwise immunocompetent calf to the virus can cause transient diarrhea and shallow erosions in the digestive tract. Erosions are visible in the oral mucosa and on the hard palate. Thrombocytopenia has been recognized in association with some cases of acute BVD infections in calves and adults. The immunosuppressive properties of the BVD virus make calves much more susceptible to infections with other infectious agents.
Calves that are born with a persistent BVD infection as a result of exposure to the virus in the first 4 months of gestation are particularly vulnerable to other infections. These persistently infected calves often present with a complaint of chronic unthriftiness, intermittent diarrhea, and failure to grow normally. The vast majority of these calves die in the first year of life as a result of a disease from which an immunocompetent calf would have easily recovered.
Clostridium perfringens - related diseases
Clostridium perfringens is a Gram-positive, anaerobic spore-forming rod that can exist for several months in the soil after being discharged in the feces. These organisms are also present in small numbers in the digestive tract of healthy animals. There are 5 types of C. perfringens that are known to produce enteric disease in people and domestic animals: types A, B, C, D, and E. They are categorized based on the toxins they produce. Each toxin produces a different type of lesion. The most important types of C. perfringens in North America are C. perfringens types C and D. Clostridium perfringens type C primarily affects neonatal animals. Clostridium perfringens type D typically affects older youngsters that are nursing high-producing dams, and recently weaned animals that are placed on diets that contain an excess of carbohydrates (grain, bread), such as a feedlot situation. In rare situations, C. perfringens type D can cause hemorrhagic diarrhea in ruminants.
C. perfringens type C
Synonyms: necrotic enteritis, hemorrhagic enterotoxemia.
Clinical signs. Peracute onset of bloating, abdominal pain, convulsions, and diarrhea in neonatal (1-10 day old) calves, kids, llamas, and lambs. Affected animals can die of hemorrhagic enteritis before diarrhea even develops. The diarrhea, when noted, is explosive and yellow to dark brown (digested blood) in color. Red-streaked strips of necrotic mucosa is noted in the feces of some affected animals. Neurologic signs are prominent in animals with more prolonged survival. The mortality rate is high despite therapeutic intervention.
Pathogenesis. C. perfringens type C produces beta toxin, a potent cytotoxic agent. The beta toxin causes mucosal cell inflammation and destruction in the small intestines. Normally the beta toxin is destroyed by proteolytic enzymes (trypsin) in the digestive tract. Neonates are more susceptible to disease than adult animals because they have less proteolytic enzymes in their digestive tract than adults. Furthermore, a factor in colostrum inhibits trypin's proteolytic activity, so colostrum ingestion might actually increase the animal's vulnerability to the beta toxin.
Diagnosis. Disease is rapidly fatal once clinical signs are noted so diagnosis is often made postmortem. Necropsy findings: extensive hemorrhage in the distal small intestinal tract and mesenteric lymph nodes. Isolation of C. perfringens from intestinal contents is not conclusive because some types are commensal (normally found in the G.I. track). Observation of large numbers of Gram positive rods on a fecal smear supports a diagnosis, but definitive diagnosis is made with an ELISA test that detects the beta toxin.
Treatment and prevention. Given the fulminant, fatal nature of the disease, treatment is rarely successful. Aggressive intravenous fluid therapy, penicillin therapy, and nonsteroidal anti-inflammatory therapy should be initiated in valuable animals. Administer C and D antitoxin subcutaneously to all neonates at risk. Prevent the disease through vaccination of pregnant animals in the final 4-6 weeks of pregnancy.
Clostridium perfringens type D
Synonyms: enterotoxemia, overeating disease, pulpy kidney disease
Clinical signs. Diarrhea, convulsions and sudden death in a rapidly growing, well-fed animal is a common presentation. The disease is seen most frequently in lambs (particularly in single lambs less than 12 weeks old nursing a high producing ewe), and to a lesser extent in kids, 1-3 month old calves, and feedlot cattle. Hyperglycemia and glucosuria are common clinical features in sheep. Death can occur within 30 to 60 minutes after showing signs. Neurologic signs such as ataxia, trembling, opisthotonis, head-pressing, vocalization, convulsions, and coma are prominent in calves and lambs. Animals that recover can have residual neurologic deficits (focal symmetric encephalomalacia). Diarrhea characterized by dark, loose feces is noted if the animal survives for more than a day.
Goats can also present with peracute bloody diarrhea and CNS malacia. However, chronic sublethal diarrhea has been reported in a few adult goats as the only presenting sign (JAVMA 1992;200:2,p214). In our practice area, we have seen adult goats die from enterotoxemia within 48 hours of showing signs of depression and diarrhea. The affected goats were on a high concentrate diet.
Pathogenesis. Clostridium perfringens type D is a commensal organism in the intestinal tract of sheep, goats and cattle. The acid environment of the abomasum, normal peristalsis, and limited quantities of fermentable substrate in the intestinal tract prevent overgrowth of the of the organisms under normal circumstances.
Several conditions favor overgrowth of C. perfringens in the digestive tract: 1) a diet excessive in protein and carbohydrates, 2) abrupt feeding changes that disturb the normal intestinal flora, and 3) a pre-existing insult to the small intestinal mucosa.
C. perfringens elaborates an epsilon toxin that causes increases intestinal permeability, thereby facilitating its own absorption into general circulation. The epsilon toxin subsequently increases vascular permeability in many organs, most notably in the central nervous system, kidneys, and liver. Hepatic metabolism of glycogen is altered, resulting in hyperglycemia/glucosuria.
Diagnosis. Postmortem findings of hyperemic small intestine, petechial hemorrhages on serosal surfaces, focal necrosis and edema in the brain, glucosuria, and rapid autolysis of the kidney (pulpy kidney disease; most pronounced in sheep) are strongly supportive findings. Observation of large numbers of Gram positive rods on a fecal smear also supports the diagnosis. Definitive diagnosis is made using the epsilon toxin ELISA test.
Treatment. Treatment of severe, rapidly progressing cases of enterotoxemia are not very rewarding because the effects of the epsilon toxin are not reversible. Treatment of the chronic form seen in adult goats is more amenable to therapy.
Treatment consists of the administration of antitoxin, parenteral penicillin, and intravenous fluid therapy. Central nervous system anti-edema drugs (nonsteroidals, DMSO IV at 1 g/kg) are indicated if severe neurologic signs are noted. Parenteral thiamine supplementation is recommended whenever a ruminant shows signs of cerebral and digestive disorders; polioencephalomalacia (PEM) also can develop secondary to a carbohydrate overload. Enterotoxemia and PEM can occur concomitantly.
These comments pertain to C. perfringens type C and D:
Passive protection: Clostridium perfringens C and D antitoxin is commercially available, and should be immediately administered subcutaneously to symptomatic animals. The dose can be repeated every 8-12 hours in sick animals until clinical signs resolve. All susceptible animals on the farm should be given a dose of C and D antitoxin for prophylaxis.
Vaccination: A vaccination program for ruminants should include C and D toxoid. The initial vaccination protocol consists of 2 injections subcutaneously one month apart. Calves, lambs kids, and young llamas are vaccinated at least 2 times (30 days apart) between 1 and 4 months of age. Use C/DT (C.perfringens type C and D, tetanus toxoid) in small ruminants. When vaccinating goats, be sure to use a C/DT product specifically labeled for goats. After the initial vaccination series, annual boosters are recommended. The vaccines are very irritating at the site of injection, and can incite a granuloma that will persist for a month or more. Warn clients of this effect, particularly in show animals! Vaccinate show animals in the axilla or any location where the lump would not be visible. Do not give IM in food animals even though label says this is an acceptable route; the resultant muscle damage significantly decreases carcass value.
Clinical signs. The causative organism, Cryptosporidium parvum, causes diarrhea in 1-4 week old calves, lambs, and kids. They are susceptible until they become functional ruminants. The diarrhea is diffuse, watery and yellowish in color. The feces can contain undigested milk, blood, fibrin, and mucus. Moderate dehydration, mild-to-moderate depression, tenesmus, and low-grade fever are common signs. Chronically affected animals become emaciated. The disease typically causes high morbidity and low mortality. Most uncomplicated cases will recover in 6 to 10 days Relapses are fairly common, and can occur from auto-reexposure.
Note: This organism is a potent zoonotic agent: it readily affects people (especially fourth year veterinary students) and produces painful diarrhea and influenza-like symptoms. It causes a persistent and often fatal diarrhea in immunosuppressed animals and people.
Pathogenesis. The protozoan organism infects the brush border (microvilli) of the intestinal cells; it does not invade into the cytoplasm. A membrane developed by the host surrounds the organism, thereby protecting it from antimicrobial agents. Unlike coccidial oocysts, C. parvum oocysts are already sporulated as soon as they pass in the feces, and therefore are immediately infectious.
Transmission occurs when an animal ingests the sporulated oocysts. The infection leads to villus atrophy and to crypt cell hyperplasia. Diarrhea results from malabsorption and maldigestion, and increased secretory activity.
Diagnosis. Fecal flotation in Sheather's solution (a sucrose solution with a specific gravity of 1.27) is a sensitive and practical diagnostic procedure that can be performed at most veterinary clinics. The oocysts are transparent and much smaller than coccidia and helminth eggs.
Samples submitted to a diagnostic lab: request specific tests for cryptosporidia; special stains are needed so that the protozoa can be distinguished from yeasts.
Treatment and control. Currently there are no effective drugs labeled for elimination of the parasite. However, decoquinate (deccox) administered orally at 4.5x the label dosage for 1-3 weeks is showing promising results in affected calves. Fluid therapy, nonsteroidal anti-inflammatory drugs (flunixin meglumine), lactase treatment of the milk, and good nursing care are important mainstays of therapy. Good hygiene decreases the likelihood of disease and helps prevent reinfection. The oocysts are resistant to most disinfectants. They are most effectively destroyed by fumigation of contaminated areas and utensils with 5% ammonia solution, or 10% formalin solution.
Clinical signs. Most ruminants are exposed to low levels of coccidial organisms early in their life, resulting in subclinical infections and development of immunity. Interestingly, the immunity is not sterile, and many clinically normal ruminants shed low levels of oocysts in their feces. Clinical coccidiosis is a manmade problem that occurs primarily in nonimmune, stressed animals that are crowded together in lots or stables that are heavily contaminated by oocysts. Clinical signs are noted in animals over 3 weeks of age. The most common sign of coccidiosis (and the main economic impact of the disease) is failure of youngstock to grow and gain weight to their full potential. Severely affected animals will pass watery feces that might contain fresh blood. Tenesmus, when present, can lead to rectal prolapse. In some cases, the feces can look like pure unclotted blood, and can contain mucus, fibrin casts, and mucosal strands. Anemia, hypoproteinemia and dehydration can develop as a result of massive destruction and loss of the intestinal epithelium. Although most animals recover after a mild bout of coccidiosis, gut function and appetite do not return to normal for many weeks. Recovering animal remain unthrifty and fail to gain weight compared to unaffected contemporaries; the difference in body weights are still appreciable 10 months after the disease outbreak. Nervous signs that resemble hypomagnesemia are occasionally noted in young cattle with coccidiosis.
Pathogenesis. Coccidiosis is caused by an intracellular protozoan parasite. Eimeria species cause all the known coccidial infections in domestic ruminants. Unsporulated single cell oocysts are passed in the feces. It takes at least 48 hours for them to sporulate in the environment into an infective stage. After ingestion, released sporozoites invade into the intestinal epithelial cells and begin reproductive stages. Clinical signs develop approximately 2 weeks after the infective oocysts are ingested. The developing parasites rupture intestinal epithelial cells and invade new cells several times before the infection becomes patent (oocysts in the feces). Widespread loss of intestinal mucosa allows loss of fluid, plasma proteins (albumin), and blood into the bowel lumen. Surviving animals have severe villous atrophy that results in signs of maldigestion and malabsorption.
Diagnosis. Observation of massive numbers of oocytes on a fecal smear or routine fecal flotation reflects a severe infection. This finding in the presence of clinical signs supports a diagnosis of coccidiosis. It is important to remember that acute cases might not yet have a patent infection; a negative fecal does not rule out coccidiosis! It is also important to realize that the presence of small numbers of oocytes in the feces is a normal finding in ruminants; many immune animals shed them fairly constantly. Also, not all species of coccidia are pathologic.
Postmortem (gross and microscopic) findings are diagnostic.
Treatment. Supportive therapy consists of fluids, nutritional support, blood transfusion (if PCV 1500 mg/dl+++
7. Calves that are being raised on commercial milk replacers need high quality milk replacers that use real milk proteins (more digestible than vegetable proteins). When available, real milk is the best food! Feed calves, lambs etc at least every 12 hours and preferably at the same time every day. To maintain optimal growth, calves need to be fed replacer (or milk) at the rate of 12-15 % of their body weight per 24 hours (divided into at least 2 feedings).
8. Get a diagnosis: in herds with an outbreak of diarrhea that is causing significant morbidity and mortality, postmortem examination of a freshly dead animal is the most expedient and cost-efficient way to get a diagnosis. Your Georgia State Diagnostic Lab provides an invaluable and incredibly inexpensive service. If harvesting diagnostic samples from a dead animal on the farm, submit chilled (not frozen) segments of small intestine for microbiology, and segments in formalin for histopathological studies. Fecal samples should be collected and submitted to a diagnostic facility as soon as possible after signs of diarrhea develop.
9. Transfaunation of rumen contents from a healthy donor to ruminant with gastrointestinal problems is a valuable aid to re-establishing normal gut flora and appetite.
Young Ruminant Diarrhea AQS Session
The owners of a 5 day old Angus heifer calf telephone your office secretary. They noted that the calf was depressed and unwilling to stand and nurse her dam this morning. Fresh blood was seen on the calf's perineal area. The owners said the calf appeared normal the previous evening. As you drive up the drive, you see an elderly couple hovering anxiously over the recumbent calf. Physical examination reveals moderate depression. She is too weak to stand for more than a few seconds. Her temperature is 103.8 degrees F, pulse is 120 BPM, and respiratory rate is 44 BPM. The nasal mucosa is dark pink, and the plantum is completely dry. The capillary refill time is 2.5-3 seconds. The eyes are sunken and skin turgor reduced. The calf's ears and limbs are cool to the touch. The sclera are 3+ injected. No crackles or wheezes are ausculted in the thorax. The abdomen is tucked up and the calf appears gaunt. Her estimated body weight is 45 pounds (20 kg). Dried feces with blood in them are present on the calf's tail and buttocks. The umbilicus is slightly swollen. A visual blood glucose test indicates the calf's blood glucose is approximately 40%.
1. Summarize your abnormal physical findings.
2. List your etiologic considerations.
3. What other tests would you like to perform?
4. How would you treat this calf? Outline an immediate plan of action.
5. The owners want a prognosis and an estimate for treatment of the calf.
6. The owners are also asking about whether or not their other calves are at risk. What would you tell them at this point?
This article is brought to you as a service of
GoatConnection.com - Khimaira Inc. Authors retain all
copyrights, responsibilities and privileges thereof. This is a
'community-built' project, and we try to compile helpful information,
but can offer no warranties for accuracy of information.
veterinary assistance, please seek the advice of a licensed veterinarian.