AAEP FOCUS ON THE FIRST YEAR OF LIFE PROCEEDINGS / 2014

Farm Management of Diarrhea Peter R. Morresey, BVSc, MACVSc, DACT, DACVIM  Author’s address—Rood and Riddle Equine Hospital, PO Box 12070, Lexington, KY 40580-2070; e-mail: [email protected].

differential diagnoses should be considered and presumptively managed if signs are suggestive. In the absence of a definitive diagnosis, appropriate fluid therapy and general supportive care are indicated. Infectious Agents: Bacterial

I. INTRODUCTION

Salmonella

D

In highly concentrated populations of horses, Salmonella infection is of particular concern. Outbreaks in adult populations are reported at veterinary referral hospitals, on breeding farms, and at racetracks. Stressors such as dietary changes, surgery, transport, heat exposure and concurrent illness increase the likelihood of infection.2-9 Once Salmonella has overcome the host defense mechanisms, the bacteria migrate through the enterocytes and reach the lamina propria where they stimulate an inflammatory response. Lymphatic spread to regional lymph nodes occurs promoting further inflammation. Distribution of Salmonella organisms to the systemic circulation may occur via efferent lymphatics.

iarrhea is a very common occurrence in the neonatal and juvenile foal. Not all cases involve an infectious etiology, with sometimes apparent pathogens recovered during a diagnostic work-up that are not clinically significant in the case of interest. During the investigation and management of onfarm cases of diarrhea, it is important to establish a diagnosis (if possible), treat the affected individual(s) efficaciously, and minimize potential for dissemination of any infectious organism to avoid an outbreak and the establishment of an environmental reservoir.

II. PATHOPHYSIOLOGY OF DIARRHEA

Clinical signs of salmonellosis are variable, ranging from mild enteritis to sepsis and shock. Intestinal fluid loss occurs due to active fluid loss through hypersecretion, and passive fluid loss by malabsorption due to profound inflammation. Diagnosis of Salmonella is confirmed by positive fecal or blood cultures and/or polymerase chain reaction (PCR).

Diarrhea may be categorized according to the etiology (infectious, non-infectious) or the pathophysiology, which can include hypersecretion, increased mucosal permeability (exudation), malabsorption, osmotic draw and abnormal intestinal motility, acting either singly or in varying combinations.1

Treatment for Salmonella infection is aimed at maintaining hydration and electrolyte balance. As neonates and younger foals are at high risk for translocation and bacteremia, systemic antimicrobials are indicated to counter the potential for infection of physeal and synovial structures.

Regardless of the cause, patients with severe acute diarrhea may show signs of systemic inflammation. Disturbances of the cecocolic flora can cause increased production of bacterial toxins (lipopolysaccharide, LPS) which promote release of cytokines and other inflammatory mediators. Mucosal permeability may increase, resulting in a net fluid loss into the intestinal lumen, as well as edema, exudation, and toxin absorption into the bloodstream. Fluid, electrolyte, protein, anticoagulant, and procoagulant substances are lost to the gut lumen. In more severe cases hypovolemia, hypoalbuminemia, coagulopathy, acidemia, and shock (distributive and endotoxic) ensue.

Intestinal Clostridiosis These gram-positive organisms are found in the intestinal tracts of domestic animals and are widely distributed throughout the environment, including the soil. Endospore production enables survival under adverse environmental condition. Potent exotoxins are responsible for a variety of intestinal diseases in domestic animals. Clinical disease results from Clostridium perfringens biotypes A and C and Clostridium difficile. While most studies suggest that biotypes A and then C are the most important in adult horses, there are reports of biotypes A through E being associated with enteric disease of foals.10 The

III. COMMON CONDITIONS In many cases an etiological agent is not found; however, during a clinical examination of an affected foal the following

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organism is more frequently isolated from studfarm soil samples than farms with only mature horses.11 Several antimicrobials have been implicated in the development of Cl. difficile-associated diarrhea, including -lactam antibiotics,12 gentamicin,13 potentiated sulfonamides12,13 and erythromycin.14,15 Clostridium difficile is also found in the feces of healthy horses and foals, implying healthy equids may function as a potential reservoir.11

Lawsonia intracellularis Equine proliferative enteropathy (EPE) is a fecal-oral transmissible enteric disease caused by Lawsonia intracellularis. Although the condition is considered to have a sporadic case distribution, apparent outbreaks are reported. Equine proliferative enteropathy affects weanling foals chiefly between the ages of three and six months although yearling (and rarely adult) cases occur.

At least five toxins have been identified. Toxin A is an enterotoxin which causes intestinal fluid accumulation and is pro-inflammatory. Toxin B is a potent cytotoxin. These toxins act synergistically to cause intestinal disruption. Both toxin genes are present in the majority of Cl. difficile isolates from horses with acute enteric disease; however, variations have been discovered.16

Presenting signs include depression, fever, weight loss, colic, diarrhea, and ventral edema. Clinical pathology findings include leukocytosis, anemia, mild to severe hypoalbuminemia and variably hyperfibrinogenemia. Hyponatremia, hypokalemia, hypocalcemia, and metabolic acidosis are present. Abdominal ultrasonography reveals loops of thickened small intestinal wall, and in severe cases the entire small intestine is affected with apparent large colon involvement in some cases.

Diarrhea induced by Clostridium sp. is more common during the early neonatal period. Disease induced by Cl. perfringens biotype C is associated with abdominal distention, colic, shock, hemorrhagic diarrhea and high mortality. The syndrome is commonly seen within the first 48 hours of life, usually in vigorous foals with high milk intake. Diagnosis is confirmed by identifying toxin within the feces or intestinal luminal content, and recovery of the organism and biotyping by PCR for toxin gene identification.

Antemortem diagnosis of EPE depends on a combination of characteristic clinical findings, serological testing for specific L. intracellularis antibodies, and detection by PCR in feces. Gross pathologic lesions in EPE are characteristic with mucosal hypertrophy of the ileum and terminal jejunum, sometimes involving the entire small intestine.18 Histologic examination with Warthin-Starry silver staining, immunohistochemistry, and small intestinal hyperplasia with curved intracellular bacteria in the apical cytoplasm of crypt cells is confirmatory.19

Treatment is often unrewarding in established cases. Antimicrobial agents (penicillin and metronidazole), NSAID, plasma, correction of fluid and electrolyte derangements, use of probiotics to provide a more favorable enteric flora, and C. perfringens biotype C antitoxin are indicated. Enteric disease associated with C. perfringens biotype A has been seen in newborn foals, with transient and variable clinical presentation. This biotype is, however, present in the feces of healthy young foals.10 Likewise, the role of C. difficile in juvenile diarrhea is not clear. Prevalence varies with geographic location but C. difficile appears to be a rare isolate in older suckling foals. Treatment is as above for C. perfringens without specific antitoxin.

Treatment entails correction of fluid and electrolyte deficits. A combination of crystalloid and colloid therapy will be required. Early administration of plasma or hetastarch is beneficial as foals usually become profoundly hypoalbuminemic before diagnosis and during the period of early treatment. Antiinflammatory, antidiarrheal, antiulcer therapy and pain management will be necessary. A number of antimicrobials have proven effective in this condition including macrolides, chloramphenicol, oxytetracycline and doxycycline.20-22 Rhodococcus equi

Samples should be collected and shipped in an appropriate container. The isolation of C. difficile is usually considered significant in foals of all ages but it is not uncommon to identify foals that are culture positive but toxin-negative. Recovery of C. perfringens from diarrheic foals is also of questionable significance because the organism, particularly C. perfringens biotype A, is commonly present in the feces of healthy foals.

Sporadic cases of diarrhea may result from extrapulmonary R. equi infection.23,24 Inflammation secondary to infection of the mesenteric lymph nodes or the presence of a mesenteric or peritoneal abscess may be responsible. In some cases, severe erosive mucosal inflammation (enterotyphlocolitis) is present. Infectious Agents: Viral

Enterococcus durans Rotavirus Enterococcus durans has been isolated from diarrhea cases in many species.17 It is commonly isolated from the feces of young foals with diarrhea in association with other potential diarrhea pathogens. The organism is found to colonize the small intestinal mucosa and it was associated with moderate pathology.17 Diarrhea is likely to be age dependent in its severity.

Rotavirus invades the intestinal epithelium affecting the brush border of the villi which are responsible for small intestinal degradation of disaccharides to monosaccharides to enable absorption. Loss of the brush border decreases lactase production resulting in lactose maldigestion. Lactose remaining in the intestine is highly osmotically active, thus drawing fluid intraluminally. A further increase in osmotic draw occurs from 61

AAEP FOCUS ON THE FIRST YEAR OF LIFE PROCEEDINGS / 2014 bacteria in the large intestine fermenting the retained lactose to volatile fatty acids. Clinical signs of disease occur most often in young foals, usually 3 months of age or less. Diarrhea, abdominal distension, colic, depression and anorexia occur. Rotavirus is reported as the most common cause of diarrhea in foals in a Kentucky study.25 Infected foals may shed rotavirus for up to 10 days. This may continue asymptomatically up to 8 months following infection. The virus is environmentally persistent for 9 months.

strongyles, threadworms and tapeworms may also be problematic. Non-Infectious: Management, Nutritional, Iatrogenic Lactose Intolerance Lactose intolerance is a secondary problem most commonly associated with rotavirus infection, but it can be caused by any condition affecting the small intestine.30 Continued ingestion of lactose in severely diarrheic foals is therefore detrimental, exacerbating fluid and electrolyte losses by osmotic draw. 31

Diagnosis requires detection of the virus in feces by ELISA, latex agglutination or electron microscopy. As there is no specific treatment for rotavirus infection, therapies are empirical and symptomatic, consisting of fluid therapy and supportive care. Vaccination of pregnant mares may be of use in control on infected farms.

Dietary Alterations Commensal flora can be easily disrupted, compromising its role in suppressing pathogen overgrowth. Dietary alteration has been identified in one study as an important risk factor for Salmonella sp. in hospitalized horses.32 Changes in the intestinal microflora and alterations in villus structure increasing the potential for diarrhea can occur with prolonged fasting, emphasizing the importance of a consistent feeding program especially in the compromised neonate.

Coronavirus Coronavirus has been isolated from the feces of diarrheic foals; however, the significance and true incidence or infection is not known.26,27 Infectious Agents: Protozoal

Disturbances of Colonic Flora – Antimicrobial Associated Diarrhea

Cryptosporidia Infection appears widespread therefore the role of cryptosporidium in foal diarrhea remains controversial. In one study the number of foals with diarrhea or soft feces was not significantly different between positive and negative foals,28 although cryptosporidium has been implicated in the death of foals.

The relationship between antimicrobials and diarrhea is complex and inconsistent. It is difficult to establish a linkage between pathogen and antimicrobial in the genesis of disease. Any broad-spectrum antibiotic has the potential to disrupt local protective flora and to allow intestinal overgrowth of potential pathogens. Loss of colonization resistance through alterations in the gastrointestinal microflora, altered colonic fermentation, and increased toxin production by overgrowing pathogenic organisms are major causative factors in human cases.33 Most classes of antibiotics have been implicated in human antimicrobial associated diarrhea, with cephalosporins, penicillins, and clindamycin overrepresented.33 A recent equine study confirmed the association of antimicrobial usage with diarrhea but did not implicate any particular class of antimicrobials.34

Detection of oocysts in fecal samples requires acid-fast staining, immunofluorescence assays, or flow cytometry. Detection of the small oocysts in fecal samples requires considerable laboratory expertise, therefore the clinician should specifically state that detection of cryptosporidium is indicated. Treatment is generally supportive and centers on fluid and electrolyte replacement. Prevention includes environmental disinfection and isolation of infected foals. Giardia

IV. DIAGNOSTIC PROCEDURES

Prevalence is considered to be as high as 35% but data associating shedding with disease are lacking. Suckling foals with diarrhea and high Giardia counts have been reported to respond to metronidazole administration.29

Physical Examination Fever or hypothermia may be present. Depression, dehydration and abdominal pain are commonplace. Tachycardia is variable due to individual tolerance to pain and varying response to hypovolemia. Poor pulse pressure is suggestive of hypovolemic or distributive shock. A bounding pulse may indicate the early hyperdynamic phase of endotoxemia. Respiratory rate and depth may increase in compensation for developing metabolic acidosis secondary to hypovolemia. Abdominal distension sometimes occurs due to severe fluid accumulation in the colon. With more serious infectious causes such as Salmonella in foals less than 2 months of age extra-intestinal disease is common

Infectious Agents: Helminth Parasites Foals and weanlings are susceptible to a wide range of gastrointestinal parasites as, unlike adults, they have not developed any degree of resistance to infestation. The most likely to cause disease is the ascarid Parascaris equorum. Following the tissue migratory phase through the lungs and liver, the parasite comes to reside in the small intestine where enteritis, diarrhea and impaction can result. Cyathostomes, 62

AAEP FOCUS ON THE FIRST YEAR OF LIFE PROCEEDINGS / 2014 and includes uveitis, infective synovitis, osteomyelitis, pneumonia, and meningitis.35

is required for detection. Fecal samples for parasite egg presence is advisable in older foals.

Ultrasonography

The reader is referred to the excellent summary table in Mallicote et al, 2012.36

Rapid assessment can be made of gastrointestinal wall thickness, small and large intestinal diameter, content and motility, stomach size, quantity and nature of peritoneal fluid, and position of the viscera and intestinal tract. The presence of a mesenteric lymphadenopathy or abscess suggesting extrapulmonary R. equi infection could be detected which may be then confirmed, in some cases, by tracheal aspiration or abdominocentesis.

V. INDIVIDUAL CASE MANAGEMENT Diarrhea treatment may be extensive depending on severity and chronicity, requiring fluid and electrolyte replacement, correction of acid-base disturbances, control of hypoproteinemia, diminishment of inflammation, countering of endotoxin effects if present, analgesia if required, topical mucosal treatments aimed at protection and repair, and the judicious use of antimicrobials when indicated by signalment or clinical suspicion of a specific causative infectious agent.

Clinical Pathology With more serious infectious causes of diarrhea, a complete blood count may find neutropenia with a toxic left shift in the initial stages, progressing to a rebound neutrophilia as the disease becomes of longer duration. Anemia may be present in chronic cases. Fibrinogen will be variably elevated depending on severity of colonic inflammation and the presence of secondary inflammatory foci (pneumonia, synovitis). Hypoproteinemia (chiefly albumin although globulin will decrease in chronic or severe cases) results from depressed feed intake and gastrointestinal losses. Electrolyte derangements also occur, with hyponatremia being the most clinically significant. Sodium is lost with the electrolyte rich fluids of the gastrointestinal content. Also, as Na is bound to albumin, levels are further depressed with protein loss. Hyponatremia may be worsened by overconsumption of fresh water causing a dilutional effect. Other findings include hypochloremia, decreased bicarbonate, and elevated lactate. Azotemia may occur with hypovolemia and dehydration. Non-specific elevations of hepatic enzymes secondary to hypoxia (from hypovolemia) and inflammatory changes may occur.

Fluids The reader is referred to the excellent reviews by Seahorn et al,37 Cook et al,38 Magdesian,39 and Hart (pages 93 to 97 in these proceedings). Calculation of required resuscitative and maintenance volumes is essential as the underestimation of fluid volumes required in the diarrheic foal is commonplace. Three fluid volumes must be considered: maintenance, deficit and ongoing losses.   

Maintenance: can be assumed to be 10% of foal bodyweight. Deficit: mild (5%), moderate (8%), severe (10%) of bodyweight. Ongoing losses: estimate volume of diarrhea or reflux.

Bolus crystalloid fluids can be given in the initial stages of resuscitation (20 ml/kg incremental loads over 15 - 30 minutes). Colloids are also useful to administer in a bolus fashion during initial treatment of hypovolemia, with incremental doses of 3 – 10 ml/kg. Following each dose reassessment of volemic status to determine further need for fluids is required. Once stable, the foal can be transitioned to a maintenance rate of fluids (5 – 10% of bodyweight over 24 hours) with further consideration of ongoing losses.

In neonatal cases, an assessment of colostral immunoglobulin transfer and blood culture are important to perform. Pathogen Testing Diarrhea associated with the most serious infectious neonatal differentials (Salmonella, rotavirus, Clostridia) is most often clinically indistinguishable, making establishment of a specific etiology vitally important where targeted treatment is possible. Fecal culture (serial, up to five in the presence of suspected Salmonella) and PCR is advisable in all cases. While PCR is more rapid, it is unable to differentiate between viable and inactivated pathogens, and does not provide the sensitivity information successful culture does. In the case of clostridial diarrhea, toxin production is thought more important as nontoxigenic strains of both C. difficile and C. perfringens are found in normal feces, and the organism is difficult to grow in culture. Toxins A and B for C. difficile are detectable by PCR or ELISA. Rotavirus may be diagnosed by latex agglutination or ELISA testing. Electron microscopy can be used as a nonspecific screen for viral particles; however, the clinical significance of all recovered cannot be certain. Cryptosporidia may be seen with acid fast stain although considerable expertise

Concurrent or sequential administration of both crystalloids and colloids is advantageous. Crystalloids distribute to the extracellular fluid space, with approximately 75% distributing to the interstitial fluid space, allowing interstitial rehydration. Although desirable in most cases, this event is deleterious when edema formation results. Also, expanding intravascular fluid volume with crystalloids in hypovolemic patients results in a decrease in plasma protein concentrations which decreases colloid oncotic pressure. Colloids, however, are restricted to the intravascular space making them useful in hypovolemic shock as they allow rapid intravascular fluid expansion. The increase in colloid oncotic pressure by the administration of colloids causes increased retention of crystalloid fluids within the intravascular fluid compartment. Plasma supplies albumin 63

AAEP FOCUS ON THE FIRST YEAR OF LIFE PROCEEDINGS / 2014 for oncotic pressure and drug carriage, along with antithrombin and immunoglobulins. Hetastarch is less expensive, has only oncotic properties, and cannot be measured by a refractometer. The author prefers to give both products in tandem.

Electrolyte Supplementation Hypokalemia can be managed by addition of KCl to intravenous replacement fluids (20-40 mEq/L) and can be administrated safely if the rate of administration does not exceed 0.5 mEq/kg/h. KCl can also be administered orally for several days. Sodium bicarbonate may be used in severe metabolic acidosis not corrected with volume expansion and once hypokalemia has been addressed. Half the calculated dose is given slowly intravenously over 20 minutes, and the rest of the dose in crystalloid fluids over 4 hours. Oral supplementation is also possible.

Antidiarrheals/Absorbents A number of absorbent materials are in common usage. Bentonite clay and dioctahedral smectite act as absorbents. Bismuth subsalicylate has both toxin absorbent and local antiinflammatory effects. Activated charcoal is very effective for adsorbing bacterial enterotoxins and endotoxins. Kaolin and pectin are often used in combination to absorb toxins; however, clinical studies have not demonstrated unequivocal benefits from administration.40,41

Nutritional Requirements Loss of body condition and protein-energy requirements during convalescence must be addressed. Intravenous glucose containing solutions are incomplete and appropriate for only short-term (24 hour) usage. Solutions containing 5% dextrose are easily made and readily available. They should not be used for large volume resuscitation as excessive amounts of glucose are administered causing hyperglycemia, and 5% dextrose in water should be avoided due to lack of electrolyte content. Caloric content of a 5% dextrose solution is 0.17 kcal/mL, so to provide approximately 40 kcal/kg/d an infusion of 10 mL/kg/h must be used. For an average foal (50 kg bodyweight) a daily volume of 10 mL/kg/h x 50 kg x 24 hours = 12 L must be given. This volume will likely not be well tolerated by the foal. Therefore the established maintenance rate of fluids (4-5 mL/kg/h) will only provide less than half the required caloric intake.

Gastric Ulcer Prophylaxis Some cases of ulceration are clinically silent until serious sequelae have occurred. Compatible clinical signs include any or all of decreased suckling, poor body condition, diarrhoea, bruxism, ptyalism and intermittent colic of varying severity. The use of H2 receptor blockers (cimetidine, ranitidine) or proton pump inhibitors (omeprazole) is recommended in diarrheic foals. Mucosal protectants (sucralfate) are also of use. However, appropriate acid production does provide significant protection against overgrowth of introduced enteric pathogens.42 The use of these medications in foals should be considered on an individual basis as ulcer prophylaxis in a hospital setting has been associated with higher rates of diarrhea.43 Analgesics and Anti-Inflammatories

Higher concentrations of dextrose are therefore indicated. A 50% solution of dextrose provides 1.7 kcal/mL with an infusion of 1 mL/kg/h therefore providing approximately 40 kcal/kg/d. This should not be administered without a pump or concurrent isotonic fluids as the hypertonic nature of the dextrose solution may cause severe endothelial injury predisposing to thrombosis. Alternatively a 10% dextrose solution made in isotonic fluids can be administered. None of these solutions are suitable for bolus administration and therefore in many situations attempting complete caloric support by these means is impractical.

Non-steroidal anti-inflammatory drug (NSAID) usage is widely practiced in diarrhea cases for the control of fever, mucosal inflammation, and analgesia. Care in their usage must be practiced as in compromised patients exacerbation of renal pathology is possible. Therefore correction of fluid and protein deficits must be prior to or concurrent with NSAID administration. Antimicrobials As a large number of diarrhea and colitis cases do not have a specific infectious agent recovered the indiscriminant use of antimicrobials is to be discouraged. However, protection of the severely neutropenic or neonatal foal from secondary infections (pneumonia, catheter site sepsis) by the use of parenteral antimicrobials is rational. Neonates and younger foals are at considerably higher risk from bacteremia during colitis, with infection of synovial and physeal tissues having potentially devastating consequences. In one study, half of foals less than 30 days of age admitted to a referral hospital for diarrhea were bacteremic.44 Metronidazole is indicated in confirmed C. difficile cases. Foals with salmonellosis are routinely treated with antimicrobial drugs to attempt removal of Salmonella sp. and prevention of dissemination to other tissues, however some Salmonella sp. are highly resistant, endotoxin may be released, and further derangement of the colonic flora may occur.

Parenteral nutrition enables nutritional support without worsening diarrhea; however, considerable attention must be paid to sterile technique and monitoring of these foals (blood glucose), rendering this difficult to perform in farm situation. Probiotic Usage Although in widespread usage, some studies have shown no benefit in the use of probiotic preparations with regards to disturbances of fecal flora (Salmonella sp. shedding), duration of hospitalization or prevalence of clinical signs.4,45 Anecdotally, probiotics may be useful as both treatment for the affected foal and as a preventative for other newborn foals on the property. The use of Saccharomyces boulardii has been 64

AAEP FOCUS ON THE FIRST YEAR OF LIFE PROCEEDINGS / 2014 reviewed favorably.46 However, in one survey many products did not contain the appropriate or specified organisms.47

of infection are only effective if repeatedly and consistently used. Unwitting contamination of grossly clean utensils and stall surroundings may allow fomite spread to previously uninfected surfaces and areas. Farm personnel should also be made aware that some infectious agents, chiefly Salmonella and Cryptosporidia, may cause human illness.

Acute Diarrhea Acute diarrhea tends to be rapid in onset and self-limiting in uncomplicated cases. The main goal of any treatment plan is to re-establish homeostasis, as fluid, electrolyte and protein losses can be substantial. Hypovolemia, circulatory shock and endotoxin absorption are possible.

Isolation Protocol While experiencing clinical disease, foals should be physically isolated from the remainder of the herd. However, foals that have apparently recovered clinically may continue to pass unformed feces and shed infectious organisms, therefore they should continue to be handled with protocols to avoid spread of infected feces from the isolation area to the general farm area. The duration of isolation and release protocol is governed by the identity of the infectious agent if known. In the case of Salmonella, horses may shed the bacteria for unknown periods of time. From 30 up to 90 days may be required, with a series of five negative fecal cultures advisable prior to release. Nonspecific recommendations for other organisms could include a period of 14 days following normalization of fecal consistency. Fecal shedding of the infectious organism or recurrence of diarrhea may occur if the recovered foal is placed in a stressful situation (weaning, veterinary procedures, transport).

Fluid replacement, depending on the status of the patient, can be administered relatively rapidly. Hypertonic saline 7.5% can be given (5–10 mL/kg over 20 minutes) for initial resuscitation during hypovolemia, but care should be exercised in hyponatremia. This should be followed as soon as practical with the administration of isotonic solutions with electrolyte derangements managed as previously detailed. Colloids can be used to maintain the fluid in the vascular space. Hyperimmune antisera or plasma is useful in endotoxemia although reports of efficacy are inconsistent. Flunixin meglumine, ketoprofen, or firocoxib are appropriate choices for analgesia and to aid in countering the effects of endotoxin. Care must be exercised with usage of NSAID in dehydrated foals due to potential for renal damage.48

Cleaning and Disinfection The use of broad-spectrum antimicrobials in the treatment of acute enterocolitis in the neonate or severely neutropenic juvenile foal can be considered rational.

Decontamination of the infected environment is a multi-stage process, involving the removal of organic matter, physical cleaning and degreasing of the area, and finally disinfection to render infectious agents inert.

Chronic Diarrhea Chronic diarrhea may be progressive in onset, accompany a concurrent debilitating disease, or be an extension of acute intestinal inflammation and scarring resulting in a disease process of extended duration. Colonic dysfunction is always present as the colon is the major organ responsible for water reabsorption.49 Only anecdotal evidence exists for treatments including colonic and fecal transfaunation, and conflicting information exists regarding probiotics. Although transfaunation is practiced in the management of chronic diarrheas, recommendations as to transfaunate source and volume, and preparatory treatment of the recipient are vague and anecdotal. Concern is raised as to whether the bacteria and protozoa will survive passage through the low pH of the stomach. Therefore transfaunation following acid suppression of the recipient is rational.

Removal of bedding, fecal material and contaminated feed is the first step to decontamination of the environment. During this phase it is important not to spread infected material, therefore care should be taken by handling it separately and with appropriate barrier precautions. Cleaning begins after organic matter has been removed. Scraping and scrubbing of the walls and floor with a detergent solution and then rinsing with water is required. Care should be taken not to disseminate by droplets infectious agents at this stage by the overuse of pressure washing. The area should be allowed to dry. Following cleaning, disinfection is performed with one of the various categories of disinfectants: phenolics, chlorine, iodophors, and quaternary ammonium compounds.50 Phenolic disinfectants are effective in the presence of organic debris and will kill bacteria and viruses (including rotavirus). Chlorinecontaining compounds are inactivated by organic material necessitating a thorough cleaning prior to usage, are corrosive, will cause discoloration, and are ineffective against rotavirus. Iodophors are also corrosive and rendered inactive by organic material. Quaternary ammonium compounds are also inactivated by organic material, are incompatible with soaps and detergents, and may not be as effective against infectious agents as other classes of compounds.

VI. OUTBREAK SITUATION Handling Affected Foals Barrier precautions (gloves, disposable/protective clothing, foot dips, hand washing with soap and hand sanitizers) should be used when contacting diarrheic foals or their feces to avoid cross-contamination. It is imperative that farm personnel are impressed upon that any precautions taken to prevent the spread 65

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VII. SUMMARY Diarrhea in the foal can be self-limiting or life-threatening depending on the causative agent, the immune status of the foal, and the therapeutic response to infection by the owner and veterinarian. Many infectious agents are widespread in the equine population, and cause problems when resistance to infection is overcome or sufficient numbers of infectious organisms accumulate in the environment. The cornerstone of treatment is restoration of appropriate fluid and acid-base balance while a diagnosis is reached allowing more specific treatment, if this exists.

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