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Bacillary haemoglobinuria in dairy cows

SIR, – We read with interest the letter from Michael Millar and others (VR, July 8, 2006, vol 159, p 59) regarding outbreaks of postparturient haemoglobinuria in dairy herds. Its timely publication prompted us to remind colleagues of a further differential diagnosis for haemoglobinuria in dairy cows that was not mentioned in this letter, namely bacillary haemoglobinuria, a suspect case of which was presented to us in early July. A single fourth-lactation Holstein Friesian cow at five months’ gestation was affected, one of 15 recently purchased from Somerset and introduced into a large dairy herd in the New Forest in Hampshire. The cow presented with redbrown urine, a haemorrhagic scour, milk drop and lethargy. On clinical examination, pyrexia, increased respiratory and heart rates, an absence of rumen activity and jaundiced mucous membranes were noted, and the cow appeared to be dehydrated. No ticks were seen on the body surface. Blood and urine samples were collected. Haematological examination revealed severe anaemia (haematocrit 12·2 per cent, reference range 22·0 to 40·0 per cent) accompanied by marked leucocytosis (white cell count 25·5 x 109/l, reference range 3·5 x 109 to 7·0 x 109/l) with many toxic neutrophils and reactive lymphocytes. Microscopic examination of a stained blood smear showed no Babesia species. The spun urine sediment was also examined microscopically, but no erythrocytes were seen, suggesting that the urine discoloration described was related to haemo globinuria rather than haematuria. Biochemistry results confirmed severe liver damage, and plasma copper levels were marginally elevated but not considered indicative of copper toxicity. These results are summarised in Table 1. Successful treatment of bacillary haemoglobinuria has been reported with large doses of penicillin (Williams 1964), yet despite a high dose of procaine penicillin and dihydrostreptomycin sulphate (Pen & Strep; Norbrook), the affected cow deteriorated dramatically and died 24 hours later. An on-farm postmortem examination was undertaken, in which the major features included a generalised jaundice, a mahogany-coloured liver containing a 5 cm diameter yellow necrotic infarct, and dark brown urine in the bladder and kidney cortex. No migrating immature flukes or obvious liver damage were noted. These findings in conjunction with the clinical signs described were considered to be typical of bacillary haemoglobinuria. It is possible to confirm the diagnosis by demonstration of the causal organism by fluorescent antibody tests on liver lesions (Harwood and Watson 2004), but this test can only be interpreted accurately in very fresh material, and by the time the postmortem examination was undertaken the cow was already autolysing due to the high ambient temperatures. A liver fluke ELISA was undertaken on stored serum, and this gave a positive result at 34·09 per cent positivity. This validated test did suggest exposure to Fasciola hepatica, but as antibodies can persist for up to 10 months, exposure could have been historical. Although macroscopic evidence of fluke damage was not evident postmortem, it is conceivable that tissue damage could have occurred as a result of migrating flukes, thus acting as a stimulus for clostridial spore proliferation. The development of bacillary haemoglobinuria is associated with the proliferation of Clostridium haemolyticum (Clostridium novyi type D) and presents clinically with pyrexia, jaundice and haemo globinuria. Like other clostridia, the causal organism is a soil-borne anaerobe, whose spores can survive in soil for many weeks, and can also be a gut commensal, thereby potentially spreading infection via faecal excretion between farms as animals (cattle and some wild animals) move between fields. Following ingestion, the organism is transported via the intestinal wall to various organs, including the liver, kidneys and bone marrow (Marshall 1959), where spores become latent. As with infectious necrotic hepatitis (black disease, caused by C novyi type B), the infection is activated by liver damage, most commonly due to migrating immature liver flukes. The course of the disease is rapid and the outcome almost invariably fatal (Harwood and Watson 2004). This is not a common diagnosis in the UK, and is particularly unusual in the Hampshire area. It is usually associated with higher rainfall areas of the UK, particularly in the west and southwest, where both the organism and the Lymnaea species snail host of liver fluke thrive (Andrews and others 2004). As this cow was purchased from Somerset it is likely that it was initially infected there, with the activation of the infection occurring following its introduction to the Hampshire herd. Although rarely diagnosed, bacillary haemoglobinuria should nevertheless be considered as a differential diagnosis for haemoglobinuria, particularly in grazing cattle.