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Jejunal Hemorrhage Syndrome
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Session Objectives
To briefly review the literature on the condition covering the last 30 years (1). Provide retrospective information on approximately 100 cases seen at the University of Wisconsin in the last 20 years to help guide clinical decision making (2). To present information regarding risk factors, herd management and prevention (3).
Introduction
Jejunal hemorrhage syndrome (JHS) is now a worldwide disease of predominantly dairy cattle, first documented in the US in 1992. It has since been identified in other parts of North America, Europe, Asia, and the Middle East. It is characterized by rapid, occasionally substantial, obstructive jejunal clot formation that causes affected individuals to become colicky. The condition can clinically mimic other causes of small bowel obstruction. Most affected individuals will pass blood clots in feces over the ensuing 12-24-hour period but significant bowel devitalization, necrosis and peritonitis may accompany intraluminal hemorrhage and obstruction.
Etiology
Much interest regarding etiology has centered on Clostridium perfringens type A, based upon studies identifying the organism in blood clots within the jejunum and feces of affected cattle. Additionally, pathologic investigations have histologically identified large numbers of gram positive rods adjacent to the typical areas of intestinal necrosis. However, attempts to fulfill any of Koch’s postulates with isolates obtained from clinical cases, even in immunocompromised experimental animals, have failed and it is worth remembering that this organism is a commensal. There has also been interest in a possible role for the mold Aspergillus fumigatus, commonly present in livestock environments and feedstuffs. Similarly, no definitive role has been proven for this organism but mold inhibitors are frequently used as feed additives.
Clinical Signs
Affected cattle usually present with peracute colic ranging from moderate to severe. Two retrospective studies have identified that cows tend to be in the 3rd to 5th month of lactation. Rarely, bulls, dry cows and beef animals are affected. Fecal production and character can be informative and helpful in distinguishing JHS from other causes of peracute colic; initially cattle will have scant to absent manure production but over a few hours often develop “tarry” feces with fresher clots mixed-in. Continued, complete absence of fecal production is uncommon but most cattle become visibly distended. Dilated loops of small intestine are visible on ultrasound examination, sometimes with detectable echogenic material consistent with intraluminal clots. Detectable small bowel distension on rectal examination is an inconsistent finding.
Treatment
Although occasional success using purely medical treatment with flunixin, catharctic laxatives or lubricants (usually Epsom salts or mineral oil), Clostridium perfringens type C and D antitoxin and antibiotics (procaine penicillin or ceftiofur) is reported, our approach is to combine medical therapy with surgery. Via a right flank approach, we employ aborad manual massage of the identified clots as the preferred treatment. In over 100 cases we have an approximately 60% discharge rate from the hospital (combining surgery with catharctics, high dose pencillin, flunixin, and fluid therapy). Intraoperatively, if cattle have extensive devitalized intestine, if the clots cannot be broken up and dislodged, or reform almost immediately - these are poor prognostic signs. Most cattle that do well post-operatively produce feces with clots within 1-2 hours (sometimes much less!) of surgery, and importantly continue to do so over the following 12-24 hours. Importantly, there is a lifetime recurrence rate of up to 25% in cattle followed long term.
Prevention
Given the uncertainty over etiology and known risk factors, success with prevention and management continues to be frustrating. Surveys of affected herds in the US reveal that cattle tend to be in the first 5 months post-partum and the median parity is the third lactation. We have observed an increased prevalence in Brown Swiss. Problem farms experience quiet periods interspersed with “outbreaks” when clusters of new cases occur. Energy and protein rich diets that are frequently being adjusted alongside immune and other physiologic stresses associated with early lactation are the predictable scapegoats for these outbreaks. Vaccines against Clostridium perfringens type A, commercial or autologous, and mold inhibitors have been used extensively but no controlled studies exist examining their efficacy. However, transition and early lactation cows undoubtedly benefit from optimizing intestinal health as consistently as possible whether one is referring to JHS or other enteric/metabolic diseases.
References
Available on request
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