A producer in the Mountain Creek area near Holbrook contacted the Authority because he had lost several young calves at foot suddenly a month ago. He moved the cows and calves to a new paddock and was hand feeding them hay. One calf was described as 'not doing well', weak and reluctant to move or having difficulty moving and throwing fits when stressed. It had been down for about 2 days prior to euthanasia and examination.
A male Hereford calf about 12 -16 weeks old presented in lateral recumbancy with nystagmus and bilateral ventral rotation of the eyeballs, mucocatarrhal nasal discharge and carpal joint swelling. It was unable to stand.
On opening the abdomen there was extensive fibrinous to mucofibrinous clots, sheets and tags across the viscera and involving the omentum. There was a fibrin sheet over the liver, which was pale and larger than normal. There was scant clear yellow fluid in the abdomen. There was also a small amount of clear yellow fluid in the thorax and fibrin tags on the costal surface. There was one point of adhesion to the chest wall from the right cranial lobe of the lung and a depressed stellate lesion on the lung extending into the parenchyma about 1 cm.
Thoracic lymph node appeared enlarged. The head was split longitudinally to remove the brain and inflammation in the nasal cavity was apparent. The owner was reluctant to spend a great deal on investigation so a Chlamydia complement fixation test was requested. This returned a strong positive at 32(>8) which suggested recent exposure to Chlamydophilla.
Histopathology was accessed through the University of Sydney veterinary teaching programme and the lesion diagnoses were a moderate diffuse suppurative meningoencephalitis with lymphocytic and neutrophillic thrombotic vasculitis, focal mild fibrinous bronchopneumonia with intralesional fungal hyphae from the stellate lung lesion and multifocal moderate neuronal necrosis and acute malacia.
The histopathology report stated that the lesions were widespread in the CNS, explaining the clinical signs displayed by the calf. The calf had been unwell for approximately a week and been down for 24-48 hours prior to euthanasia. As well as the lesions described from histopathology the calf showed an extensive serofibrinous peritonitis and mild fibrinous pleurisy on gross examination at autopsy.
This gross finding in conjunction with central nervous system clinical signs would be consistent with Sporadic Bovine Encephalomyelitis caused by Chlamydophila psittaci (formerly Chlamydia psittaci). Sporadic Bovine Encephalitis was amongst the differential diagnoses but the histopathology lesions were also consistent with thromboembolic meningoencephalitis caused by Hemophilus somnus.
At around the same time another property near Walla Walla in the Hume LHPA also lost 2 calves at about 4-5 months of age. The deaths occurred a month apart and the owner, when questioned, recalled some lameness in younger calves. The calf autopsied at Walla Walla also had serofibrinous peritonitis, had a temperature of 40C, and returned a positive chlamydial titre. Histopathology (courtesy of the Charles Sturt University veterinary teaching programme) showed typical CNS lesions for a diagnosis of Sporadic Bovine Encephalomyelitis.
It is unclear whether the original sudden deaths observed in younger calves at the Mountain Creek property, and the cause of our involvement in this case, were related to the lesions observed in the calf that was autopsied there. I had expected a straight forward histopathology report supporting my clinical diagnosis of SBE, especially with a positive Chlamydial titre. The length of the calf's illness and time spent recumbent may have created more extensive histopathology and secondary lesions.
I would like to thank both University of Sydney and Charles Sturt University and their pathologists for their assistance with both these cases. Sometimes you don't get back what you expect from Histopathology - which is why it is always worthwhile.