History

A 7-year-old Aberdeen-Angus cow in its fourth month of pregnancy was evaluated at the University of Georgia Veterinary Teaching Hospital because of inappetence and bilateral abdominal distension of 3 days' duration. The cow had developed a vaginal discharge 6 days prior to the evaluation and was treated with penicillin (20,000 U/kg [9,091 U/lb], IM, q 12 h) and flunixin meglumine (1.1 mg/kg [0.5 mg/lb], IM, q 24 h).

Clinical and Gross Findings

At admission to the hospital, the cow was in good body condition (body condition score, 6/9), had signs of depression, and was markedly tachypneic (100 breaths/min). The left side of the abdomen was severely distended, and the right ventral portion of the abdomen was moderately distended. Further examination revealed tachycardia (100 beats/min). Auscultation over the left paralumbar fossa revealed no rumen contractions; a gas cap was present in the rumen. Auscultation of the right flank revealed decreased gastrointestinal sounds; however, simultaneous auscultation and percussion did not elicit a definitive ping consistent with gas distension of the abomasum. Palpation of the superficial lymph nodes revealed no abnormalities, and no signs of pain were elicited upon application of firm pressure to the cranioventral portion of the abdomen (grunt test). A sample of rumen fluid was collected via nasoruminal intubation; the fluid appeared grossly normal and had a normal odor (pH, approx 7). Findings of an ultrasonographic examination of the abdomen were consistent with gas distention of the rumen and ileus. No free fluid was evident within the peritoneal cavity

A CBC revealed mild leukocytosis (12,100 cells/μL; reference interval, 4,000 to 12,000 cells/μL) that was characterized by moderate lymphocytosis (9,075 cells/μL; reference interval, 2,500 to 7,500 cells/L). Serum biochemical abnormalities included high creatinine concentration (3.8 mg/dL; reference interval, 1.0 to 2.0 mg/dL), high-normal albumin concentration (3.5 mg/dL; reference interval, 3.0 to 3.6 mg/dL), hyponatremia (136 mmol/L; reference interval, 139 to 146 mmol/L), hypokalemia (3.2 mmol/L; reference interval, 3.6 to 4.7 mmol/L), and hypochloremia (77 mmol/L; reference interval, 98 to 109 mmol/L). Venous blood gas analysis revealed alkalemia (pH, 7.70; reference interval, 7.35 to 7.50), high bicarbonate concentration (43 mmol/L; reference interval, 22 to 31 mmol/L), and hyperlactatemia (2.6 mmol/L; reference interval, < 1.5 mmol/L). The cow received fluids with supplemental electrolytes and dextrose IV, and the rumen was trocarized. Despite treatment, the cow's clinical condition deteriorated and the animal died. A complete necropsy was performed.

On gross examination, the rumen and abomasum were moderately distended with apparently normal ingesta. In the pyloric region, the abomasal wall was markedly thickened with multifocal to coalescing masses that were tan and soft and bulged on the cut surface and that ranged in size from 3 × 2 × 2 cm to 18 × 10 × 10 cm (Figure 1). Multiple areas of the wall of the reticulum were also thickened, and the cut surfaces of these thickened areas were similar in appearance to the masses in the abomasum. The abomasal mucosa contained multifocal ulcers that ranged from 1 to 6 cm in diameter. Examination of the heart revealed several white 1-cm-diameter nodules in the auricles.

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Photographs of the pyloric region of the abomasum (A) and a cross section of the abomasum wall (B) in a 7-year-old cow that was evaluated because of inappetence, bilateral abdominal distension, and evidence of abomasal outflow obstruction. Notice the multifocal to coalescing masses in the pyloric region; the masses were tan and soft and caused marked thickening of the abomasal wall. Multifocal ulcers were associated with the masses. Similar masses were present in the reticulum.

Citation: Journal of the American Veterinary Medical Association 238, 1; 10.2460/javma.238.1.47

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Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →

Histopathologic Findings

At necropsy, major organs were removed and subsequently fixed in neutral-buffered 10% formalin and processed for histologic examination. Histologically, the abomasal masses were composed of sheets of neoplastic lymphocytes that formed large nodules and markedly expanded and replaced the submucosa and tunica muscularis. Neoplastic lymphocytes also infiltrated the muscularis mucosa. Additionally, there was focally extensive ulceration of the abomasal mucosa, with associated purulent inflammation and granulation tissue, adjacent to the neoplasm (Figure 2). Neoplastic lymphocytes were large (immature), and the mean number of mitotic figures observed per hpf (100× [oil]) was 1.6 (Figure 3). The thickened areas in the reticulum and the nodules in the auricles of the heart were composed of similar neoplastic lymphocytes.

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Photomicrograph of a section of tissue obtained from an affected area of the cow's abomasum in Figure 1. In this location, the submucosa is expanded by a neoplasm, which has infiltrated the muscularis mucosa (asterisk). A focally extensive area of ulceration of the mucosa (arrow) is visible. H&E stain; bar = 2 mm.

Citation: Journal of the American Veterinary Medical Association 238, 1; 10.2460/javma.238.1.47

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Photomicrograph of a section of the abomasal neoplasm in Figure 1. The neoplasm is composed of sheets of immature lymphocytes. Several mitotic figures are present in the image (arrows). H&E stain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 238, 1; 10.2460/javma.238.1.47

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Morphologic Diagnosis

Lymphoma involving the abomasum (with abomasal ulceration), reticulum, and heart.

Comments

The cow of this report had classic signs of an abomasal outflow obstruction, including abdominal distention and hypochloremic metabolic alkalosis. Traditionally, hypochloremic metabolic alkalosis was considered a consequence of sequestration of hydrogen and chloride ions within the rumen.¹ Proponents of the strong ion theory suggest that it is the loss of chloride ions from the plasma into the abomasum that causes alkalosis subsequent to an increase in the strong ion difference.² Hypokalemia develops as a result of inappetence and alkalosis. Mechanical causes of an outflow obstruction include foreign bodies, pyloric masses, impaction as a result of excessive intake of poor-quality roughage, or abomasal displacement. Functional causes of pyloric outflow obstruction could include vagal indigestion secondary to traumatic reticuloperitonitis.¹ Surgical intervention is often needed to diagnose and treat bovids with abomasal outflow obstructions.¹

Bovine lymphoma can be subdivided into sporadic and enzootic forms. There are 3 types of sporadic disease: juvenile multicentric, thymic, and cutaneous lymphomas. Juvenile lymphoma develops in cattle < 2 years of age and causes signs of depression, progressive weight loss, and lymphadenopathy.³ Thymic lymphoma develops in cattle that are 6 to 24 months old; the lymphoma develops in the cervical or thoracic part of the thymus, which results in presternal swelling, jugular distension, and local edema. Cutaneous lymphoma develops in cattle that are 1 to 4 years old; this type of lymphoma is characterized by the development of multiple skin nodules, and most affected animals develop internal metastatic tumors.³ All 3 forms of sporadic lymphoma ultimately result in death of the affected animal. No infectious agent has ever been associated with the sporadic form of lymphoma. In contrast, enzootic lymphoma develops in approximately 1.7% of cattle infected with bovine leukemia virus (BLV), a C-type oncovirus in the Retroviridae family. Infection most often occurs in dairy cattle that are 4 to 8 years old. Peripheral and visceral lymphadenopathies are common early findings, although such changes were not present in the cow of this report. Many bovids with the enzootic form of lymphoma develop internal masses, and the abomasum is a common site for tumor development.³ The heart, kidneys, uterus, and vertebral canal are also frequently affected. Clinical signs vary considerably depending on the location of tumor masses. In the cow of this report, lymphoma was also detected in the reticulum and the heart. Approximately 30% of affected animals develop persistent lymphocytosis, and circulating atypical or immature lymphocytes are evident in some cases.^1,3 The cow of this report had only mild lymphocytosis, and lymphocyte morphology was suggestive of a reactive population; however, serologic evaluation for anti-BLV antibodies was not performed.

Bovine leukemia virus is widely distributed in the cattle population and endemic in many herds in the United States.^4,5 Infections generally result from transfer of infected lymphocytes, which occurs, for example, when surgical equipment (used for procedures such as dehorning) is not adequately cleaned of residual blood between uses on multiple animals; infected lymphocytes can also be transferred via colostrum.³ The virus does not persist outside the host, so contact or environmental contamination is not a source of infection.⁶ Although clinical disease develops in only a small percentage of infected animals, infections with BLV are important to the cattle industry because of decreased production, condemnation of carcasses, and export requirements.^5,7,8 Although infection is more common in dairy herds, results of a survey of US beef cattle operations indicated that 38.7% of 403 tested cow-calf operations had at least 1 BLV-infected animal.⁵ In almost half of those 403 premises, ≥ 25% of cows were infected; in 12.2% of the herds, ≥ 75% of cows were infected.⁵ In the dairy industry, seropositivity for BLV was associated with losses to producers and consumers of $285 million and $240 million, respectively, in 1996.⁹ Because there is no effective vaccination or treatment for BLV, control relies on management practices that reduce transmission and on testing and culling programs.⁷ Testing of serum samples obtained from calves > 6 months old with an agar gel immunodiffusion assay is the most frequently used means of surveillance. Almost all infected animals will develop detectable serum antiviral antibodies; seroconversion occurs approximately 5 weeks after exposure, although it may be delayed in some cases.¹⁰