Jejunal hemorrhage syndrome in 2 Canadian beef cows

Abstract

Two beef cows were presented with a history of anorexia and abdominal pain. Both cows were euthanized. Necropsy revealed the presence of a segmental area of ulceration, necrosis, and intraluminal blood clots in the jejunum. Jejunal hemorrhage syndrome is an emerging disease and has not been reported previously in beef cattle.

Case 1. A 3-year-old Simmental cow was presented, from a closed 120-cow/calf herd, with a 2-day history of restlessness, discomfort, anorexia, and exhibiting signs of abdominal pain. The cows were fed free-choice legume hay and 1.4 to 1.8 kg of oats per head per day. The cattle were administered 7-way Clostridium spp. and Haemophilus somnus (Ultrabac 7/ Somubac; Pfizer Canada, London, Ontario), and bovine respiratory syncytial virus, parainfluenza III virus and infectious bovine rhinotracheitis virus (Bovi-Shield 4; Pfizer Canada) vaccines.

On clinical examination, the temperature and respiration rate were normal, and the heart rate was 126/min. Hydration was normal, as judged by skin elasticity, eye-ball position, and normal capillary refill time. Rumen contractions were weak and no “pings” or fluid-splashing sounds were detectable over the left flank. Fluid-splashing sounds were audible on succussion of the right abdomen and a “ping” was audible on simultaneous auscultation and percussion. On transrectal examination, a small amount of dark feces resembling melena was present, and distended firm loops of small intestine, a large distended viscus, and the mesenteric artery were palpable in the right dorsal abdomen. A fecal occult blood test was not performed. Blood gas analysis of a venous blood sample revealed a hypochloremic, hypokalemic metabolic alkalosis with a compensatory respiratory acidosis (Table 1). The serum sodium concentration was slightly low. Obstruction of the proximal part of the small intestine was suspected, and a right flank exploratory laparotomy was done.

Table 1.

Blood gas analysis values (venous sample) of 2 beef cows with jejunal hemorrhage syndrome

	Case 1	Case 2	Reference range (1)
pH	7.521	7.48	7.35–7.50
PCO2 (mm of Hg)	66.1	68.2	34–45
HCO3 (mmol/L)	53.6	50.1	20–30
TCO2 (mmol/L)	55.6	52.1	20–30
Na (mmol/L)	129.7	140.3	132–152
K (mmol/L)	1.59	2.03	3.9–5.8
Cl (mmol/L)	73	77	95–110

PCO₂ — partial pressure of carbon dioxide; HCO₃ — bicarbonate; TCO₂ — total carbon dioxide; Na — sodium; K — potassium; Cl — chloride

A distended abomasum was immediately apparent upon entry into the abdomen; it was decompressed by using closed suction. Approximately 60 cm of distended small intestine, firm to the touch, was detected and exteriorized. The serosal surface was markedly hemorrhagic and had fibrin tags. A tight mesenteric band prevented adequate exteriorization; during manipulation the intestine ruptured orad and aborad to the lesion. The aboral segment retracted into the abdomen discharging intestinal contents into the peritoneal cavity. The cow was euthanized.

The 1-meter portion of dark red small intestine was removed from the abdomen during surgery and submitted along with the carcass for postmortem examination. This segment of intestine contained a firm blood clot and the mucosa was red. Samples from this segment were fixed in 10% formalin about 1 h after death. On gross examination, the first 2.2 m of small intestine appeared normal. At this point, there was an area of ulceration, about 2 cm in diameter, with a blood clot attached and separation of the surrounding mucosa, apparently due to the hemorrhage. There was also hemorrhage in the adjacent mesentery. The continuity of the intestine was interrupted by the segment that had been removed. The only abnormalities detected in the remainder of the small intestine were a few free blood clots in the lumen. The large intestine contained scant fluid contents. No feces were present in the rectum. Blood clots, some intestinal contents, and fibrin were present in the abdominal cavity, especially on the right side of the rumen. There was moderate congestion of the lungs. There was locally extensive necrosis in an area, about 10 cm², beneath the skin and within the thigh muscles of the left hind leg. No other abnormalities were present.

Histological sections of tissues were cut at 5μm, and stained with hematoxylin and eosin (HE) in a routine manner. In sections of the jejunum removed at surgery, there was locally extensive ulceration with severe neutrophil infiltration at the ulcerated surface. There was congestion and hemorrhage in the remaining wall and prominent fibroblast proliferation near the surface in some areas. In other sections, there was blood in the lumen and moderate enteritis, with edema, lymphocyte, plasma cell, and eosinophil infiltration in the lamina propria. This inflammatory cell infiltration was mildly increased over the normal population.

In sections of jejunum collected at necropsy from the site of ulceration and hemorrhage, there was chronic ulceration with fibrosis in one section, as described above. In the mucosa adjacent to the ulcer, there was moderate focal crypt necrosis and a single dilated crypt containing numerous degenerating eosinophils. There were numerous long bacilli and traces of plant material in the blood clot in the lumen. In another section, there was severe autolysis and edema was evident in the submucosa.

In the ileum, there was loss of mucosa, possibly due to autolysis, and severe hemorrhage overlying the Peyer's patches. There was also evidence of moderate autolysis in the colon. In the liver, there was mild acute periacinar necrosis, consistent with terminal anoxia. In the spleen, there was mild lymphoid necrosis in follicles and several macrophages containing hemosiderin in the sinuses.

Incidental findings included moderate congestion and edema in the lung and numerous Sarcocystis spp. in the heart muscle. No abnormalities were detected in the kidney or mesenteric lymph node.

A diagnosis of jejunal hemorrhage syndrome (JHS) was made, based on the gross and microscopic findings. Toxigenic strains of Clostridium perfringens type A were cultured from the intestine and identified by polymerase chain reaction (PCR), according to previously published procedures (2). No Salmonella spp. were cultured, and the intestine was not tested for bovine viral diarrhea virus (BVDV).

Case 2. A 5-year-old Simmental cow was presented with a history of anorexia and scant tarry feces and a slightly distended abdomen. The animal was from a closed 81-cow herd, 2 of which had died previously exhibiting similar clinical signs. The cattle were administered 8-way clostridial (Ultrabac 8; Pfizer Canada), BVDV (type 1 and 2) (Triangle 1 + Type II BVD; Ayerst Canada, Guelph, Ontario), and Campylobacter fetus (Vibrin; Pfizer Canada) vaccines. A necropsy performed by a veterinarian revealed that the 1st cow that died had peritonitis associated with a perforating abomasal ulcer; the 2nd cow was not necropsied. Cattle were fed oat hay from round bales with no grain supplement.

On physical examination, the rectal temperature and respiratory and heart rates were normal. The cow was depressed and mildly dehydrated. Rumen contractions were weak and no “pings” or fluid-splashing sounds were detectable over the left abdomen. Fluid-splashing sounds over the right flank were audible on succession and a “ping” was audible on percussion caudal and dorsal to the last rib. On transrectal examination, a small amount of dark feces resembling melena was present, distended loops of intestine were not palpable, and the rumen was slightly distended. A fecal occult blood test was not performed. The packed cell volume and total protein were within normal range. Blood gas analysis of a venous blood sample revealed a hypochloremic, hypokalemic metabolic alkalosis with a compensatory respiratory acidosis (Table 1). The cow was given isotonic sodium chloride containing 20 mEq potassium chloride/L, IV. The cow did not improve following 2 d of supportive treatment. She remained anorexic and passed small amounts of dark red watery feces. The cow was euthanized.

At necropsy, the abdomen was moderately distended due to marked dilatation of the small intestine. A 60-cm segment of proximal jejunum was dark red to black and filled with a large blood clot. There was extensive fibrinous exudate on the serosa and the intestinal wall appeared necrotic. Thrombosis was not evident. There were also large, intraluminal blood clots in the remainder of the small intestine. No other abnormalities were detected in the carcass.

Histological sections of tissues were cut at 5 μm, and stained with HE in a routine manner. Examination was limited because of autolysis. In the jejunum, there were extensive areas of mucosal necrosis and hemorrhage with numerous bacteria present. There were extensive hemorrhages, and fibroblast and vascular endothelial cell proliferation throughout the muscular portions of the bowel. There was extensive fibrin and neutrophil infiltration on the serosal surface. The ileum was too autolyzed to evaluate. There was subacute, multifocal, myocardial necrosis, with Purkinje cell inflammation and necrosis in one section, and numerous Sarcocystis spp. present throughout. Other tissues were not examined. No BVDV antigens were detected when the avidin biotin complex peroxidase method was used, and Salmonella spp. culture was negative. Clostridium perfringens were cultured from the intestine but were not typed. A diagnosis of JHS was made, based on the gross and microscopic findings.

Jejunal hemorrhage syndrome is a newly recognized syndrome (3); it is also called “acute hemorrhagic enteritis of the small intestine,” “intraluminal-intramural hemorrhage of the small intestine,” and “hemorrhagic bowel syndrome”(4,5). It causes obstruction of the jejunum with sloughed mucosa and clotted blood (3). The etiology is unknown, but C. perfringens type A has been incriminated (6). The organism has been isolated from the lesions of clinical cases and feed samples (6). In previous cases, the C. perfringens type A isolate was beta toxin positive (3,5). Clostridium perfringens was isolated from both of our cases; in case 1, it was typed as toxinogenic type A by PCR, but not beta toxin positive. Experimental inoculation of a pure culture of C. perfringens type A, isolated from clinical cases, into the proximal jejunum failed to produce the syndrome in 12 adult nonlactating dairy cows (3). The syndrome has been reported in dairy cows (5,6), but has not yet been well described in beef cows, with the exception of a single Angus cow (Santaschi EM, personal communication). The morbidity in JHS is very low, but the mortality of affected animals approaches 85% to 100% (6). In our cases, the history and clinical findings suggested the presence of an acute intestinal obstruction and were similar in certain aspects to what has been described before for JHS in dairy cattle (1,5,6). The findings on transrectal palpation in case 1 and the laboratory results in both cases support the presence of a functional or physical obstruction of the proximal part of the small intestine. Jejunal hemorrhage syndrome is difficult to differentiate clinically from other causes of acute intestinal obstruction, such as intestinal intussusception and volvulus. A definitive diagnosis is made by microscopic examination of the intestine collected at laparotomy or necropsy. The high fatality rate of this syndrome makes it important to make an early diagnosis, if surgical intervention is to be effective. In our cases, medical and surgical treatment together in case 1 and medical alone in case 2 were not rewarding. In a previous report, 7/8 cows died despite medical treatment, and 9/13 cows that underwent surgery subsequently died or were euthanized (5). The severity and duration of the syndrome makes it difficult to treat medically. Since surgical correction of the lesion doesn’t seem to be plausible, searching for a method of prevention could be more rewarding. CVJ