Diarrhea
In the United States, acute diarrhea is the second most commonly reported illness after respiratory infections. Worldwide, diarrhea is the leading cause of death in children under four years of age.
Diarrhea is best defined as an abnormal looseness of the stool, and may include changes in stool frequency, consistency, urgency and continence, often with the related symptoms of cramping and bloating. The symptom of diarrhea, however, is to a large extent subjective; people define it based on their own experience. Diarrhea becomes a problem when the change in bowel habits becomes annoying or distressing to the individual, or when it is associated with or causes a change in the person's well-being.
Acute Diarrhea
Acute diarrhea is defined as the passage of a greater number of stools of looser form than is customary, with a duration lasting no longer than 2 weeks, often with discomfort from associated gas, cramping and bloating. Severity of diarrhea may be defined as mild (no changes in activities required by the patient), moderate (change in activities required but the person is able to function), or severe (patient is disabled, often confined to bed or room). The incidence of acute diarrhea in the United States is approximately one episode per person per year, making it one of the most common medical
disorders seen by primary care practitioners.
Patients with intense diarrhea and large fluid and electrolyte losses may develop dehydration that will need medical evaluation. Dehydrating illness is particularly problematic for the very young or very old. No firm conclusions can be drawn from the symptoms or the severity of the illness as to its likely cause.
Causes of Acute Diarrhea
The volume of the diarrhea may help to localize the disease process within the GI tract. Frequent, small-volume bowel movements typically are associated with diseases of the left colon or rectum, and watery large-volume diarrhea suggest disorders of the small bowel or proximal colon. Urgency and cramping typically indicates inflammation in the rectum.
Nocturnal diarrhea may be seen in infectious colitis or severe inflammatory bowel disease, and is not a feature of irritable bowel syndrome.
It is important to investigate medication use; acute diarrhea is a common side-effect of a "new" medicine or one containing magnesium. Antibiotic-associated diarrhea is frequent, whether as a result of the medication itself or secondary to the production of a toxin by Clostridium difficile. The use of alcohol or illicit drugs (particularly methamphetamine) isanother factor.
The intake of coffee, tea or colas may lead to caffeine- or methylxanthine-induced diarrhea. Dietetic foods, gums or mints
may contain poorly-absorbed sugars such as sorbitol or mannitol which cause osmotic diarrhea.
"Traveler's diarrhea", usually caused by enterotoxigenic Escherichia coli, is very common, particularly in travelers to developing portions of the world, such as Mexico, the Mid-East and India. Some more unusual infections are suggested by the site of the recent travel. For example, camping in the mountains (and drinking untreated water) raises concern for Giardia lamblia infection. With increased international and adventure travel have come more exotic pathogens that need to be considered. Infection with Cyclospora cayetanensis or Cryptosporidium parvum from travel to Nepal or St. Petersburg (Leningrad) respectively, are illustrative.
Living in proximity to farm animals, or visiting petting zoos may lead to exposure to Salmonella, Brucella, or Cryptosporidia. Eating contaminated foods such as ground beef may expose a person to Escherichia coli O157:H7, a cause of bloody diarrhea. Campylobacter infection may result from eating undercooked chicken or turkey. Health care workers are at increased risk for nosocomial infections (e.g. Clostridium difficile). Sexual orientation and practices may
yield clues as to the etiology of diarrhea. Anal intercourse is a risk factor for proctitis, caused by Entamoeba histolytica, Treponema pallidum (syphilis), Neisseria gonorrhoeae, Chlamydia or Herpes simplex in addition to more common bacterial pathogens. With the AIDS pandemic, one needs to be alert for opportunistic infections that may present as acute diarrheal illness.
A distended, rigid or tender abdomen may indicate a potential medical emergency and a requirement for immediate,
aggressive evaluation of its cause. Most episodes of acute diarrhea are managed by the affected person or by a family member with dietary modifications or with the use of available over-the-counter medications -- some can assist in reducing frequency of stools, others address symptoms of gas or bloating and newer combined formulations can do both.
Laboratory Testing for Acute Diarrhea
In patients with mild, acute diarrhea, no immediate laboratory evaluation is needed as the results often will become available only after symptoms have subsided. Laboratory evaluation should be restricted to patients with severe diarrhea or when illness is complicated by the presence of dysentery or fever, or when the duration of illness becomes protracted.
Stool cultures are not routinely indicated. They should be performed in patients with severe diarrhea and fever, dysentery, fecal leukocytes or a prolonged (greater than 14 days) diarrheal illness.
Examination of stool for ova and parasites is indicated in patients with prolonged diarrhea, or who have particular circumstances (e.g., travel, occupation, immunocompromised status) that make them susceptible to parasitic infestation.
When parasites are suspected, obtaining three fresh stool samples for immediate examination will provide optimal yield.
Conventional Treatment of Acute Diarrhea
Fluid repletion through oral replacement solutions is important even for the majority of patients who have mild diarrhea.
The World Health Organization solution as well as commercially-available preparations can be given both for dehydration and maintenance fluid requirements. These solutions are preferable to dilute fruit juices, non-carbonated soft drinks, or tea with sugar. Dietary modifications also may be helpful to the patient with mild, acute diarrhea. Milk and dairy products should be withheld for 24-48 hours, and initial refeeding may begin with cereals, starches, soups and broth.
Therapy with antidiarrheal medications is indicated for relief of the debilitating symptoms that accompany many diarrheal illnesses. Most patients can take antidiarrheal medications safely to improve their symptoms, although care must be taken not to administer antimotility agents to patients in whom toxin-producing or invasive bacteria is suspected.
Attapulgite binds water, as a result of which stools are better formed. Attapulgite and kaolin are believed to work also by adsorbing the causative agent (bacteria or germs) and removing it from the body. It is recognized as one of the safer antidiarrheal therapies because it exerts its effect only within the bowel lumen. Another agent, bismuth subsalicylate exerts its effect both through its antisecretory salicylate moiety and possibly also by its antimicrobial activity; it improves the symptoms of nausea and vomiting that are associated with gastroenteritis. Since bismuth subsalicylate contains
non-aspirin salicylate, care must be taken when it is used in patients taking medication for anticoagulation, diabetes or gout.
Most of the commonly-employed antidiarrheal medications are antimotility agents that act by slowing intestinal motility, thereby increasing intraluminal fluid time and allowing for greater intestinal fluid absorption. One of the most widely-used and easily-tolerated of these medications is loperamide. Caution must be taken when considering administration of an antimotility antidiarrheal agent in a patient with high fever or dysentery as these medications may lead to a worsening of infectious diarrhea due to bowel stasis and increased bowel wall penetration by invasive pathogens (e.g. Shigella). The
use of agents such as loperamide in acute diarrhea, and particularly in traveler's diarrhea, is usually safe in the absence of bloody diarrhea or high fever. Patients with diarrhea often have associated symptoms of nausea and bloating, and combination therapy with loperamide and simethicone is now available. Novel antisecretory compounds, which improve diarrhea through more physiologic mechanisms than do currently-available agents, are in development and may become an important part of therapy in the future.
Patients in whom the use of antibiotics may be useful include those who have criteria of severe illness: high fever, signs of systemic toxicity, dysentery or moderate to severe "traveler's diarrhea". In general, the drug of choice is a fluoroquinolone, given for one to three days. Specific therapy may be directed if stool cultures or other studies reveal a particular pathogen.
When diarrhea is more intense (for example, passage of more than 6 unformed stools per 24 hours, or associated with blood) or lasts longer than 48 hours, medical evaluation and treatment should be sought.
Chronic Diarrhea
Chronic diarrhea, especially if associated with abdominal pain or systemic symptoms, can limit activity, adversely influence quality of life, and pose diagnostic and management challenges to health care providers. Chronic diarrhea is defined as an increased stool frequency and fluidity (looseness) lasting more than two weeks. It should be distinguished from other conditions such as incontinence, which is involuntary defecation. Careful history and physical examination can determine the likely cause of most chronic diarrhea and direct subsequent diagnostic evaluation and treatment. One approach to the problem is to determine whether diarrheal stools are bloody, fatty or watery.
The most likely cause of chronic bloody diarrhea is inflammatory bowel disease (IBD), i.e. ulcerative colitis or Crohn's disease. Symptoms of tenesmus or incomplete evacuation suggest rectal inflammation. A palpable abdominal mass or tenderness, perianal fistulae, oral aphthous ulcers, sacroiliac, spinal or peripheral arthropathy, or skin changes (erythema nodosum or pyoderma gangrenosum) all suggest a diagnosis of inflammatory bowel disease.
Less common causes of chronic bloody diarrhea include ischemia, infections (Campylobacter jejuni, Clostridium difficile, Entamoeba histolytica, Yersinia and Cytomegalovirus), radiation orchemotherapy, and colon cancer or polyps (villous adenoma).
Maldigestion or malabsorption of fat can lead to chronic diarrhea. Fatty stools typically are bulky, greasy, and particularly malodorous. They may float because of excess gas content resulting from bacterial fermentation of unabsorbed dietary material. Individuals with maldigestion often are not systemically ill and can maintain their weight and activity in spite of massive steatorrhea because of a voracious appetite. The most frequent cause of maldigestion is
pancreatic insufficiency caused by chronic pancreatitis. Those with suspected maldigestion should be asked about alcohol abuse, the most common cause of chronic pancreatitis in the United States. Severe or recurrent abdominal pain, profound weight loss, abdominal trauma or a positive family history may suggest less common causes of pancreatic insufficiency such as traumatic or hereditary pancreatitis, cystic fibrosis, congenital structural pancreatic abnormalities (pancreas divisum) or pancreatic cancer. Bile salt deficiency due to biliary tract obstruction, cholestatic liver disease, bacterial overgrowth or excessive stool losses (IBD, terminal ileal resection) also can lead to maldigestion but usually this is not associated with significant steatorrhea.
Small bowel mucosal disease or surgical resection (e.g., for Crohn's disease or bowel infarction) leads to malabsorption of fats as well as carbohydrates, proteins, vitamins and minerals, all of which can result in weight loss and various systemic signs and symptoms. Gluten-sensitive enteropathy (celiac sprue) is the most common mucosal cause of malabsorption in the United States. Individuals with sprue are likely to have a positive family history, history of diabetes or skin lesions (dermatitis herpetiformis) and have manifestations of panmalabsorption dating back to childhood or adolescence. Short stature, weakness due to multifactorial anemia (iron, folate and occasional vitamin B12 deficiency), bone pain and spontaneous fractures from vitamin D and calcium malabsorption, bruising and bleeding related to vitamin K deficiency, gas and bloating due to carbohydrate malabsorption, and edema from albumin and protein loss are typical complaints of those with sprue and other small bowel mucosal diseases. Whipple's disease, tropical sprue, and Zollinger-Ellison syndrome are less common mucosal conditions leading to malabsorption.
Many disorders can cause chronic watery diarrhea including carbohydrate malabsorption (lactose intolerance, sorbitol, fructose), intestinal infections or inflammation, unusual hormone-secreting tumors, and irritable bowel syndrome. Careful medication history is important since such medications as NSAIDs, antacids, elixirs (containing sorbitol and fructose), antihypertensives, cholinergic agents, antibiotics, and antiarrhythmics all can cause diarrhea in some individuals. Most commonly, carbohydrate malabsorption induces an osmotic diarrhea accompanied by abdominal bloating and flatulence that is associated with meals. Such osmotic diarrhea typically abates during periods of fasting. Lactase deficiency, either
ethnically acquired (more common in Asian-Americans, African- Americans) or secondary to acute infectious enteritis can lead to diarrhea following ingestion of milk, cheese, ice cream and other dairy products. Less commonly recognized causes of diarrhea due to carbohydrate malabsorption include ingestion of sorbitol and fructose found in certain soft drinks, juices, dried fruits, and "sugar-free" gum or candy. A history of any relation of diarrhea to foods is important to obtain, particularly in children who seem to be more sensitive to ingested sorbitol and fructose and in older adults who may have chronic mesenteric ischemia.
Giardiasis can produce chronic symptoms, as can some opportunistic infections (e.g., microsporidiosis, cryptosporidiosis, infection with MAI or CMV) in immunosuppressed individuals. Epidemics of chronic diarrhea have occurred following ingestion of unpasteurized milk (Brainerd's diarrhea) but no infectious agent has been isolated in such cases. In some individuals, diarrhea may persist for months following apparent acute infectious enteritis, presumably due to secondary carbohydrate malabsorption or dysmotility from intestinal neuromuscular injury. An unusual condition, microscopic colitis, can cause chronic persistent watery diarrhea in middle-aged or older individuals. While the cause of
microscopic colitis is unknown, it has been linked to gluten-sensitive enteropathy, diabetes, and NSAID use, and can, in some individuals, cause nocturnal stooling and fecal incontinence.
Diabetes presumably causes chronic watery diarrhea as a result of intestinal neuropathy, bacterial overgrowth, or both.
Diabetic diarrhea can occur at night, be interspersed with periods of constipation, and be associated with fecal incontinence. Individuals with diabetic diarrhea usually have severe long-standing glucose intolerance associated with other diabetic complications such as retinopathy, nephropathy and neuropathy.
Several unusual hormone-producing neoplasms can cause watery diarrhea. These include carcinoid tumors and tumors producing vasoactive intestinal polypeptide and glucagon. Large volume and frequent watery stools that persist during fasting and that are associated with severe fluid and electrolyte abnormalities and dehydration characterize these endocrine neoplasms. Family history of multiple endocrine neoplastic syndrome; a history of severe ulcer disease (Zollinger-Ellison syndrome); episodic hypotension, vasomotor flushing, or valvular cardiac disease (carcinoid syndrome); or the presence of a scaling, erythematous dermatitis (necrolytic migratory erythema in a patient with a glucagonoma) may offer clues to the diagnosis.
Irritable bowel syndrome (IBS) is the reason patients most commonly seek attention for chronic watery diarrhea. It is important to distinguish IBS from other conditions that cause chronic diarrhea, since in most persons with IBS, the problem is frequent defecation rather than voluminous diarrhea. Abdominal pain is the key symptom of IBS, and frequent stools often contain mucus and are accompanied by or preceded by abdominal cramps, and abdominal pain is the key symptom of IBS. Periods of loose stools can be interspersed with periods of constipation. IBS symptoms may worsen during times of emotional or physiologic stress. Those with especially severe symptoms and persistent lower abdominal pain may have been physically or sexually abused in the past. While a diagnosis of "non-disease" is often difficult to make, irritable bowel syndrome is thought to be a functional disorder (dysmotility) since no anatomic or organic intestinal problems are found to explain the symptoms.
Laboratory Testing for Chronic Diarrhea The purposes of basic laboratory tests are a) to assess the impact of chronic diarrhea on the patient's overall nutritional and electrolyte status, and b) to form a preliminary judgment about the characteristics of the diarrhea. A complete blood count should be obtained to look for evidence of anemia or an abnormal white blood cell count. Biochemical screening
should include serum electrolytes, tests of renal function (blood urea nitrogen and creatinine) and a basic nutritional assessment, consisting of a lymphocyte count and measurements of serum calcium, phosphorus, total protein and albumin levels.
The type of diarrhea can be defined by evaluation of a random (spot) stool sample. The spot stool sample can be assessed for blood by means of a stool guaiac test (e.g. Hemoccult slide). The presence of blood suggests an inflammatory or neoplastic cause for the diarrhea, but occult blood also can be seen in celiac disease and other spruce-like syndromes. The presence of pus in the stool
indicates an inflammatory cause of diarrhea. This can be assessed by staining a stool smear with Wright's stain and looking for white blood cells. A latex agglutination test for the neutrophil enzyme, lactoferrin, is of proven value for detecting neutrophils in acute infectious diarrheas and in pseudomembranous colitis. Its value in chronic diarrhea has not yet been assessed.
Diarrhea that contains neither blood, pus, nor fat is categorized as being watery diarrhea. This usually indicates a problem with the intestinal absorption of salt and water, and can be due to secretory states or to osmotic diarrheas.
Ultrasound examination and abdominal CT scan have a limited role in the evaluation of chronic diarrhea. Endoscopy usually is more specific than X-ray studies because it allows direct inspection of the mucosa, detection of superficial lesions, and the ability to biopsy the mucosa. Upper endoscopy facilitates small bowel mucosal biopsy, which is essential in establishing the diagnosis of proximal small bowel diseases, most commonly celiac sprue, but also Whipple's disease and Crohn's disease. In immunosuppressed patients, the diagnosis of parasitic infestation, e.g. microsporidia, cryptosporidia, Isospora belli, as well as cytomegalovirus infection can be made by small bowel biopsy. Giardia lamblia can cause chronic diarrhea and usually is detected in stool specimens. Occasionally, however, the organism is identified in a small bowel biopsy or by a string test. The latter examination utilizes a swallowed string to obtain a specimen of mucus from the duodenal lumen, and the mucus is subsequently examined for the presence of the organism. This test is particularly helpful in evaluation of children in whom the risks and discomforts of endoscopy may not be well tolerated.
A stool pH of less than 5.3 suggests carbohydrate malabsorption because colonic bacteria produce short-chain fatty acids from malabsorbed carbohydrate. If stool pH is over 5.6, it is unlikely that carbohydrate malabsorption by itself explains the diarrhea. Generalized malabsorption can produce stool pH over 5.3, however, because of buffering by other substances.
Surreptitious laxative abuse continues to be an important and underappreciated cause of chronic diarrhea. Laxative screening includes tests for magnesium, phosphate and sulfate in stool water or urine.
When a specific diagnosis is made, specific treatment often can afford a cure of chronic diarrhea. Some experts recommend that patients should receive antibiotic therapy with metronidazole or antibiotics directed against enteric pathogens before any evaluation of chronic diarrhea is started. For most patients who have been evaluated to some extent, several other options are recommended. These include use of opiate antidiarrheal drugs, the somatostatin analogue, octreotide, and intraluminal agents, such as clays, charcoal, bile acid binding resins, bismuth compounds and fiber.
Antimotility agents and opiates are the most effective empiric therapy for diarrhea. They not only relieve symptoms of frequency and urgency, but also reduce stool weight. Many patients respond to diphenoxylate or loperamide, but patients who do not respond to these therapies should be not be denied more potent opiates, such as codeine, opium or morphine, for fear of addiction.
Chronic diarrhea can cause the friendly Bifidobacterium bifidum to be expelled from the colon and Candida may then proliferate.
Nutrients Zinc Requirement
Diarrhea causes a loss of zinc and therefore digestive diseases or gastrointestinal surgery that result in diarrhea are often associated with a deficiency.
Potassium Need
Diarrhea causes additional fluid loss and can result in potassium depletion.
Risk factors for Diarrhea:
Digestion, Diverticular Disease
Environment / Toxicity
Mercury Toxicity (Amalgam Illness)
Fluoride Toxicity
Chronic diarrhoea is an early sign of fluorosis.
Nutrients Vitamin A Requirement
Tumors, Malignant
Carcinoid Cancer
Diarrhea can occur along with facial flushing or by itself. Stools are watery
and the diarrhea can be mild to severe. Episodes can occur several times
each day and can interfere with daily life.
Diarrhea suggests the following may be present:
Digestion Diverticular Disease
Tumors, Malignant
Carcinoid Cancer
Diarrhea can occur along with facial flushing or by itself. Stools are watery
and the diarrhea can be mild to severe. Episodes can occur several times each day and can interfere with daily life.
Diarrhea can lead to: Dehydration ;
Diarrhea can rapidly drain your body of water, causing dehydration.
Nutrients
Potassium Need
Diarrhea causes additional fluid loss and can result in potassium depletion.
Zinc Requirement
Diarrhea causes a loss of zinc and therefore digestive diseases or gastrointestinal surgery that result in diarrhea are often associated with a deficiency.
Recommendations and treatments for Diarrhea: Animal-based
Probiotics
A study of hospitalized children showed that a combination of Lactobacillus acidophilus and Bifidobacterium infantis was effective in treating acute diarrhea. One of the more common causes for hospitalization of infants and young children is dehydration related to acute diarrhea, especially from a rotavirus.
Lactobacilli in the intestines play an important role in developing natural defenses against both intestinal bacterial and viral infections. In the study group, the frequency of diarrhea improved on the first and second days of hospitalization and the duration of diarrhea during hospitalization also decreased. The researchers concluded "Oral bacterial therapy is an effective adjuvant therapy in rotavirus positive and negative children with diarrhea and can safely be administered during an episode of acute diarrhea." [Acta Paediatr Taiwan 2001 Sep-Oct; 42(5): pp.301-5]
Activated Charcoal
In an acute bacterial or viral infection of the GI tract, taking activated charcoal orally often stops the diarrhea. It works by adsorbing the organisms causing the infection and, since charcoal itself is not absorbed, it carries the offending organisms safely out of the body. A typical dose is 2 to 4 capsules, 4 or more times per day for up to 2 days.
Charcoal is considered one of the first aid remedies for diarrhea. When "activated charcoal" is not available, less effective regular charcoal will often work. It can be made by burning toast and scraping the charcoal from it's surface. This process is repeated until you have created as much as you need. Although not as convenient as capsules, the powder can be placed in the mouth and rinsed down with liquid. If there are no signs of improvement within the first day, medical help should be sought.
Diet
Juicing
Carrot juice and concentrated carrot oligosaccharides have been used in Europe for bacterial diarrhea for almost a century.
Extract
Nutritional Yeast
A thoroughly researched yeast, Saccharomyces boulardii, has been used in Europe for control of nonspecific diarrhea for several decades. Controlled studies have demonstrated its effectiveness inreventing antibiotic-associated diarrhea and Clostridium difficile colitis.
Brewer’s yeast, Saccharomyces cerevisiae, perhaps by changing the bacterial flora in the large intestine, may be helpful in the treatment of some cases of infectious diarrhea, but to a lesser degree.
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.
Coliform Diseases
1. septicemic colibacillosis
2. enteric colibacillosis
Septicemic 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.
Enteric Colibacillosis
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.
Treatment:
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).
Viral Diarrhea
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).
Rotavirus infection
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.
Control.
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.
Coronavirus infection
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. iagnosis. 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.
Prevention
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.
Cryptosporidiosis
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.
Coccidiosis
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<15%), and antibiotics to manage secondary bacterial invaders. Anticoccidial therapy is needed to halt further epithelial destruction. Many coccidiostats are used for treatment and prevention of the disease. Amprolium is used as a preventative (added to milk) and as a treatment.
Sulfa drugs such as Albon® are also used to treat coccidiosis.
Amprolium (Corid, Amprol)
Treatment:cattle: 10 mg/kg daily for 5 days
sheep: 50 mg/kg daily for 5 days
goats: 100 mg/kg daily for 5 days
Prevention:5-10 mg/kg for 21 days (cattle, goats, sheep)
Prevention. Decoquinate (deccox), and ionophore antibiotics such as monensin (Rumensim®) and lasalocid (Bovatec®) can be fed to youngstock on a daily basis in grain starter rations. However, the use of coccidiostats as a preventative is not a substitute for good management. There are drawbacks to their use: many of the drugs are static rather than cidal, and they affect only late developmental stages of the parasite. Therefore all mucosal damage is not prevented. As a result, the parasite's developmental cycle can resume once drug intake is interrupted. Lastly, the drugs themselves are not benign. Ionophores in
particular have a narrow margin of safety, and are deadly if inadvertently fed to horses. In ruminants, amprolium can cause
neurologic signs secondary to thiamine deficiency (PEM), when fed at high concentrations.
Note: Only deccox and monensin are labeled for use in goats. Albon can be used for treatment extra-label by virtue of the client-veterinary-patient relationship.
Environmental control. Prevent overcrowding, or raise young stock on slatted floors. Coccidia oocysts are susceptible to high temperatures (boiling water, steam), desiccation, and freezing temperatures. They are resistant to most disinfectants except ammonia and formalin.
Salmonellosis
Salmonellosis is a ubiquitous disease that affects practically all species of vertebrates. It can affect all ages, but clinical signs
appear most commonly in young, old, and debilitated animals and people. It is important to realize that Salmonella is a zoonotic that can cause fatality in people. According to the CDC, salmonellosis is the most important animal-borne bacterial infection in people! Veterinarians and their families are at risk, even when handling livestock that appear healthy.
In ruminants, two clinical forms exist: an enteric and a septicemic form. Calves, lambs, and kids are especially vulnerable to septicemia. Failure of passive transfer, crowding, chilling, transport, and poor nutrition make young animals more susceptible to the disease. Adults primarily show the enteric form.
Clinical signs in youngstock. Calves and kids 1-12 weeks of age, and in lambs that have just been shipped to a feedlot are most susceptible. They can present initially with enteral signs, and terminally show signs of septicemia. Alternatively, youngstock can die of acute septicemia before signs of diarrhea even develop. Pneumonia, polyarthritis, and meningitis are potential consequences of septicemia. The diarrhea associated with salmonellosis can manifest itself in many different ways.
The diarrhea is often watery, and can contains shreds of mucosa, mucus, fibrin, and blood. Morbidity and mortality rates are
high.
Classic hematologic changes in animals of all ages are leukopenia (mainly a profound neutropenia), left shift, toxic changes in
neutrophils, and hemoconcentration. After 24-48 hours, rebound neutrophilia occurs. Hyperfibrinogenemia is noted in 2-3
days secondary to inflammatory changes in the bowel mucosa. Hypoproteinemia can result from exudation of plasma and
blood through damaged intestinal mucosa. Morbidity and mortality are high in groups of susceptible, stressed animals that are
exposed to large quantities of virulent Salmonella bacterium.
Clinical signs in adults. Acute salmonellosis is characterized by depression, fever, decreased milk production, and severe
diarrhea. The feces vary in consistency (watery to soft), and can contain fibrin, blood, and mucus. Abortion can occur in pregnant animals. Adults generally develop enteric salmonellosis, and very rarely develop septicemia. The disease occurs sporadically in adult herds, but occasionally occurs as an epidemic. Periparturient cows are most likely to show clinical signs.
The hematologic changes are described above. Chronic salmonellosis can develop in adults, characterized by persistent diarrhea and unthriftiness.
Pathogenesis. Salmonellae are Gram negative aerobic (and facultatively anaerobic) bacterial rods. Salmonellae are grouped
into serogroups A-Z according to their antigenic characteristics. Inoculation generally occurs through ingestion of organisms in
fecal matter. The Salmonellae rapidly invade intestinal epithelium and regional lymph nodes. The infection remains localized in these tissues in the enteric form. In the septicemic form, bacterium invade into general circulation. Systemic and hematologic abnormalities are caused by absorption of endotoxin into circulation. Diarrhea is caused by inflammatory changes produced by invasion into and destruction of intestinal epithelium. Some Salmonella serovars also secrete enterotoxins which stimulate crypt cells to secrete fluid and electrolytes.
Salmonella typhimurium (group B) is the most commonly isolated serovar from domestic animals. It is a nonhost-adapted serovar, and therefore is less likely to establish a "carrier state" in recovered animals. Infection with a nonhost-adapted Salmonella spp. results in transient shedding of organisms (3-16 weeks). The most common sources of infection are contaminated food and water. Approximately 40% of all animal-origin feed additives (bone and fish
meal) are contaminated with Salmonella spp. Human sewage has also been tracked down as a source of infection in some herd outbreaks. Rodents, birds, and other animals spread infection through their feces and their carcasses.
Salmonella dublin (group D) is host-adapted in cattle, and commonly produces a carrier state in recovered animals.
The organisms can survive as intracellular parasites inside cells of the mononuclear phagocytic system in the face of high serum neutralizing antibody titers. Shedding occurs intermittently, and is maximized by stress factors. In outbreaks of salmonellosis caused by Salmonella dublin, an inapparent shedder is the most likely source. These asymptomatic carriers can shed organisms in their feces and milk for the remainder of their life. Calves that are fed raw, contaminated milk from the bulk tank can be infected by this route (JAVMA 1992;201:p864).
Diagnosis. Youngstock: suspect septicemic salmonellosis when you see signs of fever, neutropenia, and diarrhea (especially if it contains mucus, blood, and fibrin) associated with high mortality. Gross lesions include reddened or necrotic intestinal mucosa with a fibrin coating, swollen hemorrhagic regional lymph nodes, and loose, bloody feces in the bowel lumen.
Definitive diagnosis is made by isolating the organism from feces, blood and other tissues. The distal small intestines, cecum,colon, Peyer's patches, regional lymph nodes, liver, gall bladder, and lung are the best tissues to culture.
Adults: clinicals signs as noted, and isolation of the organism from feces, or from a rectal scraping or biopsy. Fecal shedding is
sporadic, so 3-5 fecal cultures are recommended before you can say with any assurance that the animal is Salmonella-negative. Cattle that are carriers of S. dublin can be identified by serologic testing using an ELISA test that detects antibodies against S. dublin in the milk or serum (AJVR: 1993;vol 34:1391). Positive animals should be retested in 60 days. Because persistent seropositivity is consistent with the carrier state, those animals positive on the second ELISA should be culled even if fecal cultures are negative.
Treatment and control.
Youngstock: In summary, it is prudent to assume that youngsters with salmonellosis are septicemic and treat accordingly!
Treatment consists of broad-spectrum parenteral antibiotics, IV and oral fluid therapy, nonsteroidal anti-inflammatory therapy,oral bismuth subsalicylate, and good nursing care. Sick calves must be isolated from well ones, and great care taken to sterilize utensils after they are used on sick calves. Handlers must take special precautions (wash hands, wear different coveralls and boots) to prevent spread between groups. Feed whole cow's milk rather than replacer whenever feasible to calves with enteric disorders (it is more digestible). Initial antibiotic choices can be made based on recent culture/sensitivity results from other bovine Salmonella isolates in your area, then therapy can be continued based on culture/sensitivity results from the animal you are treating.
Sensitivity data compiled from 1993 bovine Salmonella isolates at the UGA Diagnostic Lab indicate that amikacin (100%), ceftiofur (92%), trimethoprim sulfa (92%), and gentacin (88%) are good choices. Apicillin (60%) was an intermediate choice. Resistance is common to drugs such as tetracycline, sulfadimethoxine, penicillin and erythromycin.
Remember that aminoglycoside therapy can result in prolonged tissue residues, so do not use them in food animals unless the owner is willing to withhold animal from market for at least 18 months, and your culture results show these drugs are the only effective choices. In practice, ceftiofur is an excellent initial choice because it is effective, approved and affordable.
Adults: systemic antibiotic therapy is generally discouraged. The antibiotics are ineffective in eliminating the carrier state and might prolong shedding time even in nonhost-adapted infections. Treatment is supportive (IV or oral fluids: bismuth subsalicylate). Keep affected animals strictly isolated until they are no longer shedding organisms or they have been eliminated from the herd. When outbreaks are caused by an unusual isolate, suspect feed or water contamination. As indicated previously, S. dublin infections are spread by inapparent shedders. Efforts to control disease spread should be directed at
detecting the carriers through the use of the ELISA test and fecal cultures, and eliminating them from the herd.
Vaccine. A Salmonella dublin/typhimurium bacterin is commercially available. It has some benefit when used on pregnant cows in the last 4-6 weeks of gestation because it induces a short-lived spike in serum antibodies, thereby concentrating anti-salmonella antibodies in colostrum. Neonates that ingest the colostrum receive passive immunity for 3-6 weeks. The vaccine otherwise performs poorly, and is associated with adverse reactions ranging from fever and inappetence to anaphylaxis and acute death. New genetically engineered modified live vaccines are being developed but are not yet available.
Environmental control. Salmonella organisms are very hardy; they can survive in manure and stagnant water for 10 months or more. They survive freezing, but are destroyed by extreme heat and dessication. Phenylphenolic disinfectants (O-Syl,One-Stroke Environ) and formalin fumigation are effective against Salmonella organisms. Pens should be depopulated,steam-cleaned, and disinfected between groups, especially after a disease outbreak. Inadequate cleaning/disinfecting procedures can perpetuate salmonellosis problems on a farm.
Giardiosis
Giardia are protozoan parasites that infect the small intestine. They are not as host-specific as previously thought, and can spread between people, companion animals and livestock. Giardiosis is a recently recognized cause of calf diarrhea. Because it is a zoonotic, care must be taken when handling diarrheic calves to avoid infecting yourself and other patients. Chronic antibiotic therapy can make the GI tract more vulnerable to infection.
Clinical signs. Giardiosis occurs in young ruminants 2 weeks to 2 months of age. The disease is characterized by pasty diarrhea, weight loss, illthrift, and failure to grow. The diarrhea can be chronic intermittent, or continual in nature. Signs can last for as little as 2 days and as long as 6 weeks. Spread is orofecal, and immunity against the organism develops very slowly.
The infection causes maldigestion and malabsorption. As a result, infected animals shed infective cysts for a prolonged period
of time, and are a source of infection to susceptible young animals.
Diagnosis. Fecal flotation: add fresh feces to 33% zinc sulfate solution. Add a drop of Lugol's iodine to the ZnSO4 in order
to enhance visualization of the giardia cysts. Light to moderate infections are often overlooked because shedding is sporadic.
Three negative fecal flotations are needed before you can call the animal free of giardiosis. ELISA and immunofluorescence also can be used to diagnose giardia infections in formalin-preserved fecal samples.
Treatment and control. No drugs are approved for use in food animals. Extra-label use of fenbendazole (50 mg/kg) for 5
days is effective in calves. Environmental control is very important to prevent re-exposure and spread to other animals. Cysts survive well in water, but are killed by chlorination. Cysts are susceptible to the drying effect of sunlight. Quarternary ammonium salts are also effective disinfectants.
Dietary Causes
Milk replacers, no matter how well formulated, are a source of dietary stress because plant-origin proteins (soy, etc.) are not as digestible as true milk proteins. These products can cause diarrhea secondary to maldigestion. Presently, good-quality milk replacers are about as expensive as feeding cow's milk. Colostrum can be saved through refrigeration or fermentation and fed to calves. Whole milk can be used to raise calves when colostrum supplies are depleted. On a dairy, this approach makes economic sense because the decreased losses from gastrointestinal disease and the improved growth rate in replacement heifers more than offsets lost income from sale of the milk. Whole pasteurized milk can be purchased at a reduced price from grocery stores when it is at or near it's expiration date.
If milk replacers are the only alternative, do not recommend "cheap" products. This rule is particularly important in calves under 4 weeks of age. Feed products formulated with milk proteins, and avoid antibiotic-medicated products whenever possible.
Frequent feedings are more physiologic than 2 large feedings per day because engorgement of the abomasum with milk reduces the normal acidification of the proximal duodenum. This acidification process inhibits coliform proliferation, thereby protecting the neonate against coliform-mediated GI diseases.
Acidified milk replacers are formulated for use in an ad-lib feeding system. The product stays fresh for up to 3 days.
Advantages include reduced labor and a more physiologic feeding regimen. Calves (especially under 3 weeks of age) fed ad-lib gain more weight and have fewer intestinal problems than calves on a twice daily feeding regimen.
General Management Suggestions to Control Diarrheal Diseases on the Farm
1. Calf hutches are highly recommended for situations in which multiple calves are being raised by hand (dairy calves).
Nose-to-nose and oro-fecal contact is prevented between calves, so diseases are not spread as readily. Calves should spend the first 2-3 months of life in hutches prior to being moved into small groups. Calf hutch guidelines: have a sufficient number of hutches and enough space to spread them out (place as far apart as they are wide and long). Clean and move hutches to a clean environment on a weekly basis. Keep 15% more hutches available than you anticipate that you will need.
2. Wash and sanitize feeding utensils (bottles, nipples) between feedings. A 0.25% sodium hypochlorite (bleach) solution works well to kill most pathogens. Rinse thoroughly after disinfection. (Don't use bleach on galvanized buckets-it dissolves the zinc and can lead to zinc toxicity).
3. Keep areas where animals congregate as clean and well-drained as possible. Dirty, wet areas promote amplification of pathogens in the environment. Areas and stalls used for holding mothers and their babies, and for housing bottle-fed calves need to be thoroughly cleaned and disinfected between groups. Avoid over-stocking (crowding) pastured animals. Thumb rule: allow at least 1.5-2 acres of well-maintained grassland per cow.
4. Segregate sick animals from the healthy animals. Use separate equipment, and (if possible) different personnel to handle
these groups of animals to avoid fomite-mediated spread of disease. Wash hands, disinfect (or change) footwear, and change
coveralls after handling sick animals.
5. Insure that all newborn ruminants receive colostrum shortly after birth. Failure of passive transfer (FTP) is one of the most
common predisposing factors to infectious disease especially in the first 2-4 weeks of life! It is particularly a problem in dairy
calves. One strategy used to combat the problem is to force feed colostrum at a dosage of approximately 10% body weight
within the first 12 hours of life (the sooner the better). Absorption of whole immunoglobulins by specialized enterocytes occurs
over the first 24 hours of extrauterine life. This special adaptation rapidly diminishes after the first few hours as the specialized
enterocytes are replaced by enterocytes incapable of absorbing intact immunoglobulins.
6. Check adequacy of passive transfer. Sodium sulfite turbidity, glutaraldehyde precipitation both give semiquantitative, rapid
results. Radioimmunodiffusion is more quantitative, but takes 18-24 hrs for results.
Calves, lambs, goats: serum IgG should be 1500 mg/dl or greater.
Llama babies, foals: greater than or equal to 800 mg/dl IgG.
The serum total protein can be used as a crude indicator of passive transfer in euhydrated young ruminants; it should be
5.0 g/dl or greater in neonates that absorbed adequate colostral antibody concentrations.
Sodium sulfite turbidity test
This test is an easy and quick way to test immunoglobulin status in calves. Prepare 3 concentrations of sodium sulfite:
14%, 16%, and 18% (14 grams of sodium sulfite added to 86 ml of water yields a 14% solution). A pharmacist can
prepare the stock solutions. Keep them sealed in dark air-tight bottles at room temperature.
Procedure: Add 0.1 ml of serum to 1.9 ml of each stock solution in a clear test tube. Wait one hour for precipitation to occur (mostly precipitated within 10 min), shake tube, and observe for turbidity. A positive tube is too turbid to read newsprint through.
Interpretation
Approx IgG conc 18% 16% 14%
< 500 mg/dl+--
500-1500 mg/dl++-
> 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.
LAMS 5350
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?
