Jejunal hemorrhagic syndrome
Jejunal hemorrhagic syndrome (JHS) is a rapidly fatal intestinal infection caused by Clostridium species bacteria. There are several types of disease that are dependent upon the type of toxin that is released by C. perfringens. Type “A,” or alpha toxin, seems to be the most often detected causative agent. C. perfringens is also a normal flora in healthy livestock intestines.
Bacteria proliferate rapidly within the intestinal tract and invade the wall or mucosa of the intestine. This process, along with alpha toxin production, contributes to the putrefaction process after the affected animal dies. The alpha toxin targets animal cell membranes and is a necessary factor for C. perfringens to create tissue damage.
Animals may show an array of signs—ranging from acute illness to death. Clinical signs of infection include sudden decreases in feed consumption, loss of milk production, muscle fasciculations and deteriorating body condition. Animals also will often show distension of the abdomen and pass dark, bloody bowel movements. A “ping” can typically be ausculted over the right intestinal tract, along with ausculting decreased rumen motility. Feed intake and milk production will be significantly reduced, as well.
Changes in fecal matter texture and color can be attributed to the devitalization of affected intestinal segments; the jejunum—part of the small intestine—is most commonly targeted by infective organisms. A significant amount of blood may collect within segments of the intestinal tract, causing obstruction of normal ingesta flow.
Severe cases will suffer necrosis of the intestine, peritonitis and toxic shock due to bacterial spread in the bloodstream.
Incidence of disease has been noted to be higher in the fall and winter months, and often within the first three months of lactation. Animals receiving a high energy feed are also more at risk of infection, as this may perpetuate bacterial overgrowth within the intestinal tract, as well as an associated rumen acidosis.
Ultrasound may be used for diagnostic purposes. Your veterinarian will likely find dilated loops of small intestine, as well as thickening of the intestine wall. Low intensity segments on the ultrasound screen indicate regions of pooled or clotted blood and fluid. Animals are often low in blood calcium levels, which may trigger the onset of muscle spasms. Other blood work findings include increased blood urea nitrogen, glucose, magnesium and phosphorus. Necropsy samples demonstrate dark red to purple discolored intestine; large amounts of blood and clots are within the segments.
A possible link between zinc and increased infection rates may have been detected according to recent research reported in the Journal of the American Veterinary Medical Association (Volume 243, August 1, 2013). When zinc was present in a higher bioavailable amount within small intestines of cattle, alpha toxin was more apt to flourish in dangerous levels. Another association has been suspected in mature cattle fed high protein diets.
The common mold Aspergillus fumigatus has also been described as a potential instigator of infection. It can be found both in the soil and feed products. This mycotoxin is found in hay and corn silage and affects approximately 25 percent of crops worldwide every year. Humans with immunocompromised organ systems have shown a similar hemorrhagic disease to JHS when affected by A. fumigatus. Blood and intestinal samples have also detected DNA of this mold from cattle suffering JHS, but not within healthy samples. This mold is thought to possibly impair the cow’s immune system enough to aid in creating concurrent bacterial disease that the animal cannot overcome.
The prognosis for affected animals is poor, with a fatality rate often exceeding 85 percent in herd outbreak scenarios. Early identification and treatment is vital. Medical management may include intravenous fluids, antibiotics and anti-inflammatory agents. No specific antitoxin is available for the alpha toxin. Some surgical salvage cases have shown success by opening the abdomen and removing affected intestine segments and contaminated contents.
Preventive strategies are variable and include vaccinations, feed additives and nutritional management to decrease incidence of infection.
Unfortunately, vaccines have been more targeted towards types “C” and “D” and may not provide adequate protection. An autogenous toxoid vaccine created from affected herd isolates has been a consideration in the research market. Rumen acidosis may be monitored by adjusting feed so that cattle can achieve the highest production level while maintaining a neutral intake of concentrates. Some feeds may also include a mold inhibitor in situations where Aspergillus is a potential issue.
Please contact your nutritionist and veterinarian with any questions that you may have about preventing this deadly illness on your farm. — Dr. Genevieve Grammer
[Dr. Genevieve Grammer is a mixed-species veterinarian practicing in eastern Colorado. Please direct correspondence to drgigi19@ gmail.com]