A local beef cattle enterprise had incurred significant losses due to pestivirus over the preceding 12 months. A 3 year old cow with sudden onset of weight loss was presented for examination. Testing indicated that pestivirus was not the likely cause. This cow subsequently died and was post mortemed. On PM a large abscess was found in the wall of the left ventricle of the heart.
Seasonal conditions and pasture quality were excellent and would not account for the condition of this cow.
The cow had recently been treated with a macrocyclic lactone injectable anthelmintic and flukicide.
The property has a history of pestivirus testing for over 30 years. During this time persistently infected animals were identified and vaccine manufactured from the serum of these animals. The owners are well aware of the clinical presentation of pestivirus and routinely identify clinical cases and have them sampled.
The cow was examined on the 5th December.
She presented having lost weight rapidly with a stilted gait and was reluctant to move. Once moving she appeared lame but not repeatedly in the same limb. On examination no joint swelling or obvious cause of lameness was seem.
The cow had clear saliva drooling from the mouth. On closer examination no oral lesions were found but submandibular oedema was noted.
The cow had a normal temperature. On the 22nd of December the cow was found dead and was post mortemed on the 23rd. The cow had been dragged out of a patch of thistles for operator comfort but no signs of struggling before death were evident.
Subcutaneous fat and abdominal fat was yellowish in colour. The serosal surface of the stomachs was hyperaemic (Figure 1).
There were adhesions between the reticulum, abomasum, liver and diaphragm.
The cardiac and caudal lung lobes were reddened, blotchy and rubbery. The dorsal lung lobe was normal.
Between the apex of the heart, the mediastinum and the diaphragm there appeared to be adhesions or gelatinous connective tissue (autolysis).
The heart was enlarged. There was no excess fluid in the pericardial sac and the surface of the heart was reddened. On incising the heart 250 mls of thick creamy fluid was released from a lesion in the cardiac muscle (Figure 2).
In 2011 an unusually high number of these PIs were detected with 25% found in one mob of replacement heifers (testing by Pfizer Australia, results not available to publish).
Laboratory testing was carried out on blood samples collected on the 5th December 2011. Tests were undertaken to determine the likely involvement of Pestivirus or Chlamydia, both of which returned negative results.
Initial investigation of this case was prompted by the long history of pestivirus and its clinical manifestations in the herd, along with the presentation as a depressed slobbering animal. As mentioned in the clinical findings no lesions consistent with Foot and Mouth Disease were seen.
During spring and early summer 2011 a number of animals in the New England LHPA area returned titres to Chlamydia and with the lameness, depression and respiratory signs, made this a reasonable differential diagnosis.
No samples were taken at post mortem as the carcass was only just fresh enough to PM but well past sampling. The question arises how did the infectious agent get into the heart. Pericardial reaction is usually copious, fibropurulent and putrid (Jubb et al., 1985a). I have previously post-mortemed a number of animals with Hardware Disease and found abscesses or tracts between the reticulum and the heart and on one occasion found the piece of wire. In this case there were adhesions but not to the extent I would have expected and no other pockets of infection.
As soon as a foreign body penetrates the serosa, a local fibrinous peritonitis develops, leading to dense adhesion of variable extent between the reticulum and adjacent structures. Further progression is ordinarily slow and produces a canal surrounded by chronic granulation tissue and containing besides the foreign body, ingesta, purulent exudates and detritus (Jubb et al., 1985a; Radostits et al., 1994). I certainly did not see any pathology as graphic as this.
The infectious agent may have been spread haematologically, such as Listeria spp or Actinobacillus spp from a suppurative focus and produced a focus of acute inflammation that may have developed into an abscess with destruction of underlying tissues (Jubb et al., 1985b).
I favour the second pathogenesis as the chronic inflammatory lesions described in the literature did not occur.
It was good to be able to give the farmer a diagnosis that did not involve pestivirus. It also explained the depression, reluctance to move, submandibular oedema and rapid shallow breathing.