The present article describes a case report of abomasal ulceration in a buffalo. Abomasal ulceration was confirmed on post-mortem examination and was ascribed to meloxicam over dosage. The clinical findings, haemato-biochemical parameters, peritoneal fluid changes and post-mortem findings are described.
Meloxicam is a non-steroidal anti-inflammatory drug (NSAID) with analgesic, anti-inflammatory and antipyretic properties. Despite these beneficial properties, its use can lead to many side-effects, like gastrointestinal ulceration and inhibition of platelet aggregation (Radi and Khan 2006). Several clinical reports and research articles regarding abomasal ulceration (Smith et al., 1983; Costa et al., 2002; Hussain et al., 2011) in cattle are reported in literature however, it is rarely associated with the use of NSAID (Shridar and Narayanan, 2007). There are only a few reports of abomasal ulceration in buffaloes but that are erosions or Type 1 ulcers (Tajik et al., 2013; Hussain et al., 2015). Here a case of abomasal ulceration in a buffalo due to prolonged high dose of meloxicam is described.
A five year old Murrah buffalo was presented to large animal clinic of Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India, in the year 2012, with primary complaint of sudden anorexia from last four days, although water intake was normal. According to the owner the buffalo had history of chronic mastitis and had inappetance from last 10days. Meloxicam (@about 1mg/kg body weight twice daily) had been administered to the buffalo from last 15days as anti-inflammatory for chronic mastitis. Also the owner had administered gentamicin (@3mg/kg body weight twice daily) for about 10days. There had been no response to this treatment rather the buffalo developed melena and general condition of the buffalo deteriorated over the last one week. The buffalo showed signs of abdominal pain from last two days and abdominal distension became visible. The buffalo and other herd mates were routinely fed with green fodder and concentrate as per their milk productions status.
Clinical Observations and Treatment
On physical examination, the buffalo was very dull, eyes were moderately sunken, temperature was 39.6oC and respiratory rate was 40 per minute. The mucous membranes were pale, heart rate was elevated (100 per minute) and faeces were tarry in colour (Fig. 1).
Fig. 1: Tarry colour faeces in buffalo suffering from abomasal ulceration
There were no ruminal contractions and abdomen was bilaterally distended. Udder was hard to touch and was fibrosed. No milk was obtained by teat stripping. On rectal examination the rumen was distended and mushy, loose tarry faeces were present in rectum and intestines were moderately dilated. Faecal sample was tested for occult blood by commercially available HEMOSPOT test card (Crest Biosystems, A Division of Coral Clinical Systems, Goa, India) as per the manufacturers’ guidelines. Positive test result was indicated by appearance of blue colour on the test card (Fig. 2). Abdominocentesis at post xyphoid site, right caudal site (anterior to base of udder) and many other sites, revealed free flowing, slightly turbid, off smelling peritoneal fluid. The total protein content (4.2g/dL) and total cell count (5800/μL) of peritoneal fluid were increased. Differential count revealed 93% neutrophils and 7% lymphocytes. Cytological examination of peritoneal fluid smear revealed large number of polymorphonuclear cells, cocci and macrophages with engulfed bacteria (Fig. 3).
Fig. 2: Positive faecal occult blood test indicated (blue colour on the test card)
Fig.3: Polymorph nuclear cells, cocci, macrophages with engulfed bacteria in peritoneal fluid-Leishman stain (100X)
Foreign body syndrome was ruled out by radiography of reticular area. Haematological analysis revealed anaemia, leukopenia, thrombocytopenia (Table 1), marked left shift and severe toxic changes in neutrophils. Blood smear was negative for any blood protozoa. Blood biochemical analysis showed altered liver and kidney functions, increased glucose and lactate, and decreased levels of albumin, potassium, chloride, calcium and phosphorus (Table 1). The rumen fluid chloride concentration was 40mEq/l.
On the basis of above findings, diagnosis of abomasal ulceration was established. The animal was treated with ceftiofur (@ 2.2 mg/Kg body weight intramuscularly once daily), enrofloxacin (@ 7.5 mg/Kg body weight intramuscularly twice daily) and metronidazole (@ 10 mg/Kg body weight intravenously twice daily) along with antacid (rantidine) fluid therapy and supportive care. The animal did not show any recovery signs and died on next day.
Table1: Haematological and biochemical parameters of blood
|Total Bilirubin (mg/dL)||1.24||0.01-0.5|
|Total protein (g/dL)||7.2||3.74-7.46|
Post-mortem examination revealed diffuse fibrinous peritonitis. A perforated ulcer along with multiple Type 1b ulcers was observed in the abomasum (Fig. 4). The intestines were dilated and mild hyperemia of mucosa was observed. Heart showed epicardial and endocardial haemorrhages. The gall bladder was distended.
Fig. 4: Single perforated ulcer (arrow) and multiple Type 1b abomasal ulcers on post-mortem
The abomasal ulceration in present case was attributed to overdosing and prolonged use of meloxicam. Meloxicam used in present case was almost six times the recommended dose rate (0.2-0.3mg/Kg body weight per day) as the animal was prescribed it twice a day. As reported earlier (Smith et al., 1983), concentrate feeding could have been considered a predisposing factor, but all animals in the herd were exposed to the same conditions (dietary and environmental) and only this buffalo (treated with meloxicam) developed ulceration. Stress of chronic mastitis could have induced glucocorticoid release, resulted in high level of hydrochloric acid in the abomasum and then ulceration.
Anaemia, leukopenia and thrombocytopenia could be attributed to continued loss of blood due to bleeding ulcers of abomasum. The possible cause of higher liver enzymes could be necrosis of liver due to toxaemia from generalized peritonitis (Garry, 2000). Dehydration and blood loss from ulcers could be the causes for hypoperfusion and increased lactate level (Allen and Holm, 2008). Abomasal reflux could be the cause for dehydration, hypochloremia, hypokalemia and azotemia (Hussain et al., 2011). Hypocalcaemia and hypophosphatemia may be due to less assimilation of feed materials. The peritoneal fluid changes were attributed to generalized peritonitis due to leakage of abomasal contents into peritoneal cavity.
it is suggested that prolonged meloxicam over dosage can lead to abomasal ulceration in buffalo.