Acute equine colitis is a frequent cause of rapid, severe debilitation and

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1 Vol. 25, No. 8 August CE Article #5 (1.5 contact hours) Refereed Peer Review Comments? Questions? compendium@medimedia.com Web: VetLearn.com Fax: KEY FACTS More than 90% of untreated horses with acute equine colitis die or require euthanasia, but appropriate treatment improves the prognosis in most cases. In contrast to other domestic animals and humans, horses with acute diffuse colitis exhibit sudden, massive cecal and colonic fluid loss and severe electrolyte imbalances that can result in death in a matter of hours. A definitive diagnosis is made in only about 20% to 30% of cases of acute equine colitis. Because there is no cure for acute diarrhea in horses, treatment regimens are directed at rehydration, electrolyte and plasma protein replacement, antiendotoxin therapy, and antimicrobial therapy, when indicated. Acute Equine Colitis Louisiana State University Rebecca Mc Connico, DVM, PhD, DACVIM ABSTRACT: Acute equine colitis can cause rapid, severe debilitation and death in horses. Horses that are treated appropriately may respond and gradually recover over 7 to 14 days. Acute equine colitis-associated diarrhea is sporadic and characterized by intraluminal sequestration of fluid, moderate to severe colic, and profuse watery diarrhea, resulting in endotoxemia, leukopenia, and hypovolemia. The condition usually occurs in horses 2 to 10 years of age. The disease has a sudden onset and rapid progression and is often preceded by a stressful event. A definitive diagnosis is made in only about 20% to 30% of cases. Treatment in horses is extremely costly because of the massive fluid therapy requirement. There is no cure for acute diarrhea in horses; treatment regimens are directed at rehydration, electrolyte and plasma protein replacement, antiendotoxin therapy, and antimicrobial therapy, when indicated. Acute equine colitis is a frequent cause of rapid, severe debilitation and death in horses. Over 90% of untreated horses die or require euthanasia, but horses that are treated appropriately usually respond and gradually recover in 7 to 14 days. 1 Since the early 1900s, numerous reports have described a number of different acute diarrheal conditions in horses, which all appear to share a common characteristic clinical presentation. Acute equine colitis-associated diarrhea is sporadic in occurrence and is characterized by intraluminal sequestration of fluid, moderate to severe colic, and profuse watery diarrhea, with resultant endotoxemia, leukopenia, and hypovolemia. The condition can affect adult horses of all ages but usually occurs in horses between the ages of 2 and 10 years. Disease onset is sudden with a rapid progression and is often preceded by a stressful event. A definitive diagnosis is made in only about 20% to 30% of cases. 2 The majority of ante- and postmortem diagnostic tests to determine etiology remain speculative. Treatment of the condition in horses is extremely costly because of the massive fluid therapy requirement. Currently, there is no curative treatment for acute diarrhea in horses, and treatment strategies are directed at rehydration, electrolyte and plasma protein replacement, antiendotoxemia therapy, and antimicrobial therapy, when indicated. PATHOPHYSIOLOGY AND CLINICAL SIGNS Acute colitis-associated diarrhea is a result of abnormal fluid and ion transport by cecal and colonic mucosa. Loss of fluid by the large intestine can result from malabsorptive or hypersecretory processes and is often a combination of the two. 3 Colonic secretory processes are a function of the crypt epithelium, whereas absorptive processes are limited to surface epithelial cells. Under normal baseline conditions, there is an underlying secretion by crypt epithelium, which is

2 624 Equine Compendium August 2003 Table 1. Differentiating Characteristics of Specific Causes of Acute Equine Colitis Salmonella spp Etiology Clostridium spp (Clostridium cadaveris, Clostridium difficile) Neorickettsia risticii (formerly known as Ehrlichia risticii) Cyathostomes and strongyles NSAIDs Antibiotic associated (e.g., tetracyclines, macrolides, cephalosporins, clindamycin, lincomycin, florfenicol, potentiated sulfas) Arsenic poisoning Cantharidin toxicosis Colitis-X/necrotizing enterocolitis Sand ingestion PCR = polymerase chain reaction. Differentiating Characteristic(s) Positive bacterial culture or positive PCR analysis >10 3 colony forming units/gram (feces or intestinal contents), demonstration of enterotoxin or cytotoxin A or B (C. difficile) Seasonal incidence (July October), more common near freshwater rivers/ponds (United States [e.g., California, Minnesota, mid- Atlantic states, New York, Ohio], Canada, and Europe), presence of biphasic fever and/or laminitis, significant rise or fall in serum antibody titer, positive PCR for organism (feces or blood) Seasonal incidence (late winter early spring); associated with anthelmintic therapy, inadequate deworming programs, and parasite resistance Slower onset; oral, gastric, and intestinal ulcerations; early ventral edema associated with protein-losing enteropathy History of antibiotic use Marked tenesmus, muscle tremors, extreme toxemia, hemorrhagic diarrhea; extremely short clinical course Blister beetles in hay (usually alfalfa), skin acantholysis, oral erosions, painful urination, blood in urine, synchronous diaphragmatic flutter, hypocalcemia, hypomagnesemia, cantharidin in urine or stomach contents Necropsy findings include massive hemorrhage and necrosis of cecum and large colon History of the presence of sand in the horse s housing/pasture/stable area, presence of sand in feces, abdominal borborygmal sounds compatible with sand ingestion masked by a greater rate of absorption by surface epithelial cells. 3 Abnormal forces influencing the rates of secretion and/or absorption can result in massive, uncontrolled secretion and malabsorption by large intestinal mucosal epithelial cells, leading to rapid dehydration and death. Acute equine colitis is a general term referring to inflammation of the cecum (typhlitis) and/or colon (colitis) with subsequent rapid onset of diarrhea in adult horses. In contrast to other domestic animals and humans, the horse exhibits sudden, massive fluid loss and severe electrolyte imbalances that can result in death in a matter of hours. The reasons for this unfortunate but distinctive clinical presentation in horses may be due to several physiologic processes that appear to be unique to Equidae. One possibility may be due to the massive population of gram-negative endotoxinbearing bacteria, which reside in the large intestine, particularly the cecum. 4,5 Secondly, equine large intestinal tissue manifests a marked increase in mucosal prostaglandin levels exhibited by an increased chloride secretory response compared with other domestic species. 4 A third possibility is that stimulation of the large population of resident intestinal mucosal/submucosal phagocytic granulocytes (i.e., eosinophils) following mucosal barrier disruption causes an intense diffuse inflammatory response in the gut. 6 Preformed inflammatory mediators (e.g., histamine, serotonin, adenosine) and newly synthesized mediators (e.g., prostaglandins, leukotrienes, platelet-activating factor, various cytokines, the inducible form of nitric oxide, reactive oxygen metabolites) can initiate intestinal secretion both by directly stimulating the enterocyte and/or indirectly by acting on enteric nerves to

3 Compendium August 2003 Acute Equine Colitis 625 Figure 1 The blanched region above the 4 th incisor from the right indicates prolonged capillary refill time in a horse with acute colitis. Figure 2 Feces from horses with colitis have a significant liquid component that contributes to the profound hypovolemia and electrolyte imbalances. induce neurotransmitter-mediator intestinal secretion. 7 Several authors have suggested speculative or definitive causes of acute equine colitis. There is some agreement amongst equine clinicians that certain distinctive clinical, pathologic, or diagnostic characteristics help to differentiate between specific acute colitis-associated conditions (Table 1). Irrespective of the initiating cause, common clinical and pathologic features implicate a common pathophysiologic pathway. Typical hematologic findings include hypovolemia, dehydration, metabolic acidemia, electrolyte derangements (i.e., hyponatremia, hypochloremia, hypocapnia, hypokalemia, hypocalcemia), leukopenia with a left shift, toxic neutrophils, lymphopenia, and azotemia. Clinically, the patient presents with depression, anorexia, fever, tachycardia, dry/sticky mucous membranes, increased skin tent, prolonged capillary refill time (Figure 1), colic, and watery, often fetid diarrhea (Figure 2). Gross necropsy findings usually reveal edema, with or without hemorrhagic typhlitis/colitis (Figure 3), with massive intraluminal sequestration of fluid ingesta (Figure 4). Common microscopic abnormalities include superficial mucosal injury affecting the distal ileum, cecum, and large colon characterized by mucosal epithelial ulceration and erosion, mucosal and submucosal edema, and varying degrees of mucosal inflammation. 8,9 These lesions may enhance net fluid movement into the intestinal lumen by decreasing net solute absorption, increasing mucosal permeability, and stimulating prostaglandin-mediated ion secretion. Disrupted epithelium allows transmural migration of endotoxin. CLINICAL EVALUATION Frequently, horses with impending colitis will begin showing signs of lethargy, inappetence, and colic several hours before passing liquid feces. Physical examination during this early period may reveal increased respiratory rate and/or heart rate due to abdominal discomfort (intraluminal sequestration of fluid or gas or inflammatory mediator activity) as well as increased rectal temperature due to toxin absorption through a disrupted cecal or colonic mucosal barrier. Signs of abdominal discomfort can range from very mild (e.g., recumbency, inappetence) to severe (e.g., rolling, thrashing). There is

4 626 Equine Compendium August 2003 Figure 3 Gross necropsy specimen of a horse with a 6-hour duration of colic and 2-hour duration of watery diarrhea. Note black discoloration of the cecum, indicating severe inflammation and necrosis. Figure 4 Colonic contents of a horse that died of acute colitis. Note copious volume of colonic fluid ingesta. often gross abdominal distension. These cases may be confused with other large bowel disorders, including large colon torsion or volvulus. Acute equine colitis should be considered an emergency, and early evaluation and treatment by a veterinarian is critical if the patient is to survive. Horses with sudden onset of colitis will sequester a large volume of fluid intraluminally, and then within a few hours, these horses usually begin to pass the liquid ingesta in the form of profuse watery diarrhea. The volume of fluid lost from the intestinal tract in this way can equal the entire amount of the animal s extracellular fluid volume; therefore, signs of dehydration and hypovolemia may be severe. 3 Varying degrees of abdominal discomfort are evident and range from marked lethargy to severe signs of colic. Mucous membranes may be tacky with a delayed capillary refill time, and skin turgor will be reduced. Systemic absorption of endotoxin can result in peripheral arteriovenous shunting and classic brick red mucous membranes. Hypovolemia and subsequent circulatory shock will cause purple mucous membranes and weak peripheral pulses. Horses with acute colitis are prone to laminitis and may exhibit signs, such as lameness, bounding digital pulses, or elevated hoof temperature, at any time during the course of the disease. LABORATORY TESTS Assessment of a patient s hemogram and serum chemistry profile is important for determining the degree of systemic illness as well as plasma volume replacement needs. Packed cell volume (PCV) and total plasma protein values are usually elevated, indicating the degree of dehydration. Total plasma protein values that are in the normal or below normal range in a clinically dehydrated horse with an elevated PCV suggest overall protein loss. Daily PCV and total plasma protein assessment are useful for monitoring a patient s daily fluid and protein needs. Total and differential white blood cell (WBC) counts usually reveal neutropenic leukopenia. Often, there are banded neutrophils (left shift), and granulocytes will have toxic morphology, including cytoplasmic foaminess, vacuolation, basophilia, toxic granule formation, and the presence of Döhle bodies. 10 Signs of overall improvement usually correlate with a decrease in the presence of abnormal WBC parameters, including morphology. Horses in the later stages of acute colitis may have increased fibrinogen and neutrophilic leukocytosis, indicating an overall inflammatory response. Serum chemistry analysis should include the following: sodium, chloride, potassium, calcium, blood urea nitrogen, creatinine, and acid base status. Horses with acute colitis usually have metabolic acidemia, electrolyte derangements (i.e., hyponatremia, hypochloremia, hypocapnia, hypokalemia, hypocalcemia), and azotemia. DETERMINATION OF AN ETIOLOGY Historical patient information is extremely useful for determining what may have triggered the colitis, especially if the history includes treatment with specific pharmacologic agents (e.g., NSAIDs, antibiotics, anthelmintic agents), changes in diet, inadequate deworming history, or a stressful event. Ruling out specific infectious agents in patients with colitis is of paramount importance. Of particular concern is Salmonella spp associated colitis because these organisms pose an

5 Compendium August 2003 Acute Equine Colitis 627 increased risk of infection to other contact animals as well as pose an increased zoonotic potential. Because Salmonella organisms are often intermittently shed, five consecutive fecal samples for culture and sensitivity or three consecutive fecal samples for polymerase chain reaction (PCR) taken 24 hours apart should be submitted. Three fecal samples analyzed by PCR technique (Salmonella PCR; Texas Veterinary Medical Diagnostic Laboratory, College Station) 11 for the presence of Salmonella spp gives a level of confidence similar to that obtained by testing five samples by culture. Because watery feces are more difficult to culture for Salmonella spp due to a dilutional effect, samples for culture or PCR should contain at least 5 to 10 grams of feces. Neorickettsia risticii (formerly known as Ehrlichia risticii), the causative agent of Potomac horse fever, causes a biphasic fever, laminitis, and colitis of variable severity. 12 The disease is widespread in the United States (e.g., California, Minnesota, Mid-Atlantic states, New York, Ohio), Canada, and Europe, with the highest incidence of disease occurring near freshwater ponds and streams. 13 There is a seasonal occurrence during late spring through early fall in temperate climates. N. risticii associated colitis has a specific and effective treatment. The diagnosis of N. risticii infection may be supported by paired serum titers using immunofluorescent antibody testing techniques, but confirmatory diagnosis is made via antigen detection by either 1) identification of N. risticii morula within WBCs during the acute phase of the disease, 2) isolation of the organism from WBCs, or 3) PCR of WBCs or feces. 13 Clostridium difficile has been implicated as a cause of colitis in horses treated with antibiotics, in mares when their foals are being treated with erythromycin and rifampin for Rhodococcus equi pneumonia, as well as in untreated horses with diarrhea. 14 Since Clostridium spp (in particular Clostridium tetani ) are a common inhabitant of the equine gastrointestinal tract, standard fecal culture techniques are not very useful for diagnosis unless quantitative analyses are performed. Culture techniques are available for differentiating C. difficile from other clostridial organisms but are more expensive and require specific culture requirements. When sending samples to an outside laboratory for testing, several grams of feces should be submitted immediately or transported frozen or on-ice in airtight containers. Commercially available cytotoxin assays for determination of C. difficile toxin (A and B) are available and more suggestive of C. difficile associated diarrhea. These tests use ELISA- or PCR-based technology. Intestinal parasites (i.e., encysted cyathostomes, large strongyles) may play a role in causing acute adult equine colitis, although advances in developing more effective deworming products and practices have made this less of a concern. However, development of resistance to available anthelmintic products by some intestinal parasites prohibits the clinician from totally ruling out this etiology. Fecal egg counts are useful in determining a role for parasites. Horses with no or minimal fecal egg counts may still have immature encysted larvae, causing intestinal inflammation. There is no clear evidence that Clostridium perfringens, 14 Cryptosporidium spp, or Giardia spp should be implicated as a cause of the adult form of acute colitis. These organisms are more commonly associated with neonatal enterocolitis. TREATMENT Although each case of acute equine colitis is unique with regard to etiologic agent and events leading up to the disease, most cases appear to share a common characteristic clinical presentation, and the mechanisms leading to electrolyte imbalances, fluid loss, and endotoxemia/septicemia are similar. There is usually no curative treatment; therefore, treatment regimens are supportive and aimed at plasma volume replacement (colloid and crystalloid fluid replacement), analgesia and antiinflammatory therapy, antiendotoxin therapy, antimicrobial therapy, if indicated, and nutritional support. Fluid Therapy Aggressive IV polyionic fluid therapy should be instituted immediately in a horse with acute colitis. The total fluid deficit should be calculated based on clinical assessment of dehydration (e.g., for patients with 8% or moderate dehydration, total fluid deficit would be calculated as follows: kg body weight = 36 L), and replacement fluids should be administered rapidly (up to 6 to 10 L/hr per 450-kg adult horse). After replacement fluids have been administered and the horse is well hydrated, fluid amounts should be adjusted and may still be as high as 120 ml/kg/day in horses. This large volume is necessary to meet maintenance requirements as well as ongoing losses. Small volume hypertonic saline therapy has the ability to expand blood volume and elevate systemic blood pressure and cardiac output. Fluid moves from the extracellular fluid space into the vascular compartment in response to the hypertonic solution in the vascular space. This treatment has been shown to rapidly normalize compromised microcirculation and thus prevent complications, such as sepsis and multisystem organ failure. The use of 1 to 2 L of hypertonic saline (7% sodium chloride [NaCl]) improved systemic blood pressure and cardiac output in horses with hemorrhagic shock and in a model of equine endotox-

6 628 Equine Compendium August 2003 emia. 15,16 To maximize the effectiveness of hypertonic saline, immediately after its administration a large volume of balanced polyionic fluid solution should be administered IV (at least 2 L/hour) until the hydration deficit has been corrected. Many horses with colitis-associated dehydration and electrolyte imbalances will voluntarily consume various types of electrolyte mixture. In addition to offering a fresh clean water source, offering mixtures of electrolytes in water may be beneficial to some patients. Mixtures that can be considered include 1) water with baking soda (10 g/l), 2) water with NaCl/potassium chloride (Lite Salt; 6 to 10 g/l), and 3) water with a commercial electrolyte solution. Hypoproteinemia Horses with acute colitis that continue to pass large volumes of diarrhea frequently (for over 36 to 48 hours) will most likely experience protein loss from the inflamed and disrupted intestinal mucosal barrier and from systemic protein catabolism. Decreased colloid oncotic pressure leads to decreased effective circulating fluid volume and edema. Total plasma protein may decline to 2 to 3 g/dl, and albumin may decrease to less than 2.0 g/dl. Fresh or fresh-frozen plasma is ideal for the replacement of functional proteins. Treatment with IV plasma therapy or a combination of plasma and synthetic colloid (e.g., hydroxyethyl starch, such as 6% Hetastarch; Abbott Laboratories) should be considered as soon as there is evidence of a consistent decline in total plasma protein or albumin (<2.0 g/dl), or if the horse is developing dependent edema. Fresh plasma (preferred) or fresh-frozen plasma is the treatment of choice if protein loss is accompanied by coagulation disorders. An average-size horse (450 kg) requires approximately 6 to 10 L of plasma (albumin 3.0 g/dl) or synthetic colloid to improve plasma oncotic pressure. Administration of additional aliquots of 2 to 10 L of a colloidal solution may be necessary if the colitis crisis continues. In addition to albumin (the major colloid component), plasma contains other components that provide overall systemic support (e.g., fibronectins, complement inhibitors, elastase and proteinase inhibitors, antithrombin III). Hetastarch (6%) may be administered at 5 to 10 ml/kg. Because of the large size of the starch molecules, this solution is an effective plasma volume expander, resulting in sustained dose-dependent decreases in PCV and plasma protein concentration with increased oncotic pressure. The cost of an appropriate amount of commercial plasma or synthetic colloid solution for treatment of adult horses with acute colitis may be cost prohibitive, but the treatment is often lifesaving. Antiendotoxin Therapy Horses with acute colitis absorb large amounts of endotoxin (from the disrupted intestinal mucosal barrier), thereby putting these horses at a very high risk for developing laminitis, thrombophlebitis, and disseminated intravascular coagulation. Digital pulses should be monitored every 4 to 6 hours until systemic signs of acute colitis have abated (i.e., fever, leukopenia, brickred oral mucous membrane color). Along with fluid therapy and general supportive care, specific treatment to combat endotoxemia is crucial for patient survival. Choice of treatment options is based on severity of disease, renal function, hydration status, and economics. The primary target areas for managing and treating endotoxemia in horses with acute colitis include: 1) endotoxin-neutralization prior to interaction with inflammatory cells; 2) prevention of the synthesis, release, or action of mediator activity; and 3) general supportive care (discussed earlier). 17 Endotoxin Neutralization Endoserum (Immvac, Inc., Columbia, MO) is hyperimmune serum taken from horses vaccinated with Salmonella typhimurium Re mutant. The recommended dosage is 1.5 ml/kg body weight IV diluted 1:10 or 1:20 in sterile isotonic saline or lactated Ringer s solution. Dilution at this ratio is recommended to minimize the risk of immune-mediated hypersensitivity reactions. Polymyxin B binds and neutralizes endotoxin via the lipid A region of the endotoxin molecule. The recommended dosage in horses is 1,000 to 6,000 IU/kg body weight IV q8 12h for up to 3 days. Due to the possibility of causing nephrotoxic side effects, polymyxin B should be used judiciously; its use in azotemic patients is not recommended. Prevention of Endotoxin Endogenous Mediator Activity Flunixin meglumine (1.1 mg/kg IV) is the most effective NSAID in preventing endotoxin-induced prostanoid synthesis in horses to date. Low-dose flunixin meglumine (0.25 mg/kg tid or qid) is recommended and has a reduced risk of potential side effects (reduced risk of gastrointestinal ulceration, ileus, and renal papillary necrosis) compared with other NSAID regimens. Corticosteroid therapy has been shown to inhibit the arachidonic acid pathway mediator activity in vitro, but the clinical use may be associated with potentiating laminitis. A single dose of a short-acting corticosteroid (prednisolone sodium succinate [1 mg/kg IV]) may be effective during acute endotoxemia without increasing the risk of laminitis. Dimethyl sulfoxide may be useful in blocking lipid peroxidation at a dose of 0.1 g/kg IV

7 Compendium August 2003 Acute Equine Colitis 629 (higher doses have been associated with exacerbating intestinal reperfusion injury in horses). Allopurinol has been used at a dose of 5 mg/kg IV for blockade of lipid peroxidation. Pentoxifylline (a phosphodiesterase inhibitor; 8 mg/kg PO tid) may be useful in horses with a high risk of developing laminitis because this drug has been shown to block endotoxin-induced cytokine, thromboxane, and thromboplastin production. Antiinflammatories and Analgesia NSAIDs (flunixin meglumine [1.1 mg/kg IV q12h] or phenylbutazone [2.2 mg/kg PO or IV q12h]) are the most frequently used group of drugs for treating abdominal pain in horses. Clinicians must weigh the benefit of the analgesic effect of NSAIDs with the possibility of further damaging the bowel by potentially blocking the protective effects of intestinal mucosal prostaglandins. Endogenous prostaglandins have been repeatedly shown to be important inhibitors of the development of intestinal inflammation, and blocking these with NSAIDs may slow the recovery and healing of inflamed cecal or colonic mucosa. 18 Alternative choices for analgesia need to be considered. Butorphanol (an opioid analgesic; 0.02 to 0.08 mg/kg IM or IV) combined with detomidine (an α-agonist; 0.01 to 0.02 mg/kg IM) given q6 8h is a useful combination that has minimal effects on gastrointestinal motility. Constant butorphanol infusion at a dose rate of 13 µg/kg body weight/hr IV (15 mg/5 L lactated Ringer s solution at 2 L/hr for a 1,000-lb horse) diluted in lactated Ringer s solution has been shown to be useful in colic situations as an alternative to NSAID therapy. 19 Antimicrobial Therapy In horses that are highly suspected of having equine N. risticii associated colitis (geographic risk, clinical and clinicopathologic data support, with or without organism identification), tetracycline therapy (6 to 10 mg/kg IV q12h) has been shown to be effective under both clinical and experimental conditions. 20 The use of broadspectrum IV antibiotics in patients with acute colitis with unknown etiology should be judicious and is not always indicated. Mild and transient neutropenia or fever may not justify the use of broad-spectrum antimicrobials but should be considered when the patient has profound or persistent neutropenia and may be at an increased risk for complications associated with sepsis, such as peritonitis, pneumonia, cellulitis, thrombophlebitis, and disseminated intravascular coagulation. Potassium penicillin (22,000 IU/kg q6h) in combination with gentamicin (4.4 to 6.6 mg/kg q24h) is a commonly used therapeutic regimen in patients with ongoing systemic disease. Oral broad-spectrum antimicrobial medications are not recommended because they may further disrupt the intestinal microbial population. Oral metronidazole (10 to 15 mg/kg q8h) may be indicated in cases in which Clostridium spp (i.e., C. difficile) are suspected as playing a role in the pathogenesis of the disease. In addition, metronidazole may have local antiinflammatory effects (exact mechanism is not completely understood) and may be effective in treating acute equine colitis of unknown etiology. 21 Treatment with metronidazole has been associated with causing anorexia in some horses. Antisecretory Therapy Effective antisecretory medications targeting the equine large colon have not been identified. It is unlikely that bismuth subsalicylate or similar protectant agents are effective for treating large bowel diarrhea in adult horses because of the high volume of large intestinal contents. Management of Nutrition The nutritional needs of horses with acute colitis should be considered. Most horses are partially or completely anorectic along with having total body protein loss from cachexia and protein-losing enteropathy. Partial or total parenteral nutrition may be indicated in horses that remain anorectic for more than 3 to 4 days. Nutritional management of anorectic equine patients is covered in detail elsewhere. 22 Horses with colitis will often have some appetite and should be encouraged to continue eating good-quality hay, fresh green grass, and highly digestible 12% to 14% protein concentrate feeds. Horses that continue to eat usually have a better chance of recovery. PROGNOSIS AND RECOVERY Rapid institution of appropriate therapy improves the prognosis for horses with acute colitis. However, these patients can rapidly deteriorate in the face of the most aggressive medical treatment. Horses that continue to have frequent episodes of profuse watery diarrhea and systemic signs of ongoing endotoxemia and septicemia have a poorer prognosis for recovery. In addition, diarrheic horses that are azotemic and have clinicopathologic findings consistent with ongoing hemoconcentration and hypoproteinemia have a poor prognosis for survival. Antimicrobial administration may induce diarrhea, and antimicrobial-associated diarrhea may have a worse prognosis than other types of acute diarrhea. 23 Frequent complications of acute equine colitis include laminitis, thrombophlebitis, debilitation, and marked weight loss. REFERENCES 1. White NA: Epidemiology and etiology of colic, in White NA (ed): The Equine Acute Abdomen. Philadelphia, Lea & Febiger, 1990, pp

8 630 Equine Compendium August Merritt AM, Bolton JR, Cimrich R: Differential diagnosis of diarrhoea in horses over six months of age. Proc 1st Intl Equine Vet Conf : Argenzio RA: Pathophysiology of diarrhea, in Anderson NV (ed): Veterinary Gastroenterology, ed 2. Philadelphia, Lea & Febiger, 1992, pp Clarke LL, Argenzio RA: NaCl transport across equine proximal colon and the effect of endogenous prostanoids. Am J Physiol 259:G62 G69, Moore JN, Morris DD: Endotoxemia and septicemia in horses. JAVMA 200: , McConnico RS, Weinstock D, Poston MB, Roberts MC: Myeloperoxidase activity of the large intestine in an equine model of acute colitis. Am J Vet Res 60: , Powell DW: Immunophysiology of intestinal electrolyte transport, in Handbook of Physiology: The Gastrointestinal System. Rockville, MD, American Physiological Society, 1991, pp Rooney JR, Bryans JT, Prickett ME, Zent WW: Exhaustion shock in the horse. Cornell Vet 56: , Meschter CL, Tyler DE, White NA, Moore J: Histologic findings in the gastrointestinal tract of horses with colic. Am J Vet Res 47: , Whitlock RH: Colitis: Differential diagnosis and treatment. Equine Vet J 18: , Cohen ND, Martin LJ, Simpson RB, et al: Comparison of polymerase chain reaction and microbiological culture for detection of salmonellae in equine feces and environmental samples. Am J Vet Res 57(6): , Rikihisa Y, Perry BD, Cordes DO: Rickettsial link with acute equine diarrhea. Vet Rec 115:390, Pusterla N, Madigan JE, Chae J-S, et al: Helminthic transmission and isolation of Ehrlichia risticii, the causative agent of Potomac horse fever, by using trematode stages from freshwater stream snails. J Clin Microbiol 38: , Weese JS, Staempfli HR, Prescott JF: A prospective study of the roles of Clostridium difficile and enterotoxigenic Clostridium perfringens in equine diarrhoea. Equine Vet J 33(4): , Bertone JJ, Gossett KA, Shoemaker KE, et al: Effect of hypertonic vs isotonic saline solution on responses to sublethal Escherichia coli endotoxemia in horses. Am J Vet Res 51(7): , Schmall LM, Muir WW, Robertson JT: Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock. Equine Vet J 22(4): , Barton MH: Endotoxemia, in Robinson NE (ed): Current Therapy in Equine Medicine V. Philadelphia, WB Saunders, 2003, pp Tomlinson J, Blikslager A: Role of nonsteroidal antiinflammatory drugs in gastrointestinal tract injury and repair. JAVMA 222(7): , Sellon DC, Roberts MC, Blikslager A, Papich MG: Effects of continuous intravenous infusion of butorphanol in horses after exploratory celiotomy. Proc 7 th Intl Equine Colic Res Symp:21, Palmer JE, Benson SE, Whitlock RH: Effect of treatment with oxytetracycline during the acute stages of experimentallyinduced equine ehrlichial colitis in ponies. Am J Vet Res 53: , McGorum BC, Dixon PM, Smith DG: Use of metronidazole in equine acute idiopathic toxaemic colitis. Vet Rec 142(23): , Lopes MA, White NA: Parenteral nutrition for horses with gastrointestinal disease: A retrospective study of 79 cases. Equine Vet J 34(3): , Cohen ND, Woods AM: Characteristics and risk factors for failure of horses with acute diarrhea to survive: 122 cases ( ). JAVMA 214(3): , ARTICLE #5 CE TEST The article you have read qualifies for 1.5 contact hours of Continuing Education Credit from the Auburn University College of Veterinary Medicine. Choose the best answer to each of the following questions; then mark your answers on the postage-paid envelope inserted in Compendium. 1. Which statement regarding the management of adult horses with acute equine colitis is true? a. It usually resolves on its own and rarely requires veterinary intervention. b. It is often a life-threatening condition and should be treated as an emergency. c. Horses with acute equine colitis and hypovolemia can safely be treated with oral broad-spectrum antimicrobials and phenylbutazone as long as fresh water is available. d. Horses with acute colitis rarely survive despite aggressive medical treatment. 2. Horses with acute colitis exhibit sudden, massive fluid loss and severe electrolyte imbalances as a result of all of the following factors except a. the presence of a massive population of gram-negative endotoxin-bearing bacteria, which reside in the large intestine. b. the presence of a massive population of endotoxinbearing protozoal organisms, which reside in the large intestine. c. a marked increase in equine large intestinal prostaglandin levels with a subsequent increase in chloride secretory response compared with other domestic species. d. stimulation of a large population of resident intestinal mucosal/submucosal phagocytic granulocytes following mucosal barrier disruption and subsequent intense diffuse intestinal inflammatory response. 3. What percentage of acute equine colitis cases have a definitive cause identified? a. 20% to 30% c. 60% to 70% b. 40% to 50% d. 80% to 90% 4. Adult horses with acute colitis usually have abnormal blood work values including a. mature neutrophilia with a left shift, hemoconcentration, hyponatremia, hyperkalemia, metabolic acidemia, and azotemia. b. neutropenia with a left shift, lymphocytosis, hypercalcemia, hyperproteinemia, and a normal PCV.

9 Compendium August 2003 Acute Equine Colitis 631 c. neutropenia with a left shift, hemoconcentration, azotemia, hyponatremia, hypochloremia, and metabolic alkalemia. d. neutropenia with a left shift, azotemia, hemoconcentration, hyponatremia, hypokalemia, and metabolic acidemia. 5. It is important to rule out some major etiologies of acute equine colitis due to the zoonotic potential of which of the following organisms? a. Salmonella spp c. large strongyles b. N. risticii d. cyathostomes 6. IV fluid replacement for a 450-kg (about 1,000-lb) adult horse with acute colitis with prolonged capillary refill time of greater than 3 seconds, minimal skin elasticity, and PCV equal to 65% should be approximately L. a. 15 to 20 c. 35 to 40 b. 25 to 30 d. 45 to When providing colloid replacement therapy to a hypoproteinemic adult equine patient with colitis and thrombophlebitis, the preferred product is a. fresh-frozen equine plasma. b. fresh equine plasma. c. 6% hydroxy ethyl starch solution (Hetastarch). d. 7% hypertonic saline. 8. Which of the following antimicrobial therapies have been shown to be effective in treating horses with acute toxemic colitis of unknown etiology? a. potentiated sulfas c. florfenicol b. neomycin d. metronidazole 9. Which of the following antimicrobial therapies have been shown to be effective in treating horses with suspected N. risticii associated colitis? a. penicillin c. tetracycline b. enrofloxacin d. erythromycin 10. Which statement regarding the treatment of endotoxemia in horses with acute colitis is true? a. Phenylbutazone is the most effective available NSAID for treating endotoxemia in horses. b. Polymyxin B binds and neutralizes endotoxin; however, it should not be used in horses because of the possibility of nephrotoxic side effects. c. Endoserum is hyperimmune serum used to neutralize endotoxin in horses with colitis and should be diluted 1:10 or 1:20 in sterile isotonic saline or lactated Ringer s solution to minimize the risk of immune-mediated hypersensitivity reactions. d. Allopurinol, dimethyl sulfoxide, and pentoxifylline neutralize endotoxin and are, therefore, effective for use in horses with colitis.