CASE NOTES
'Dummy' Calves - a BVDV Syndrome
Matt Ball- District Veterinarian Lismore and Adrian Philbey - Laboratory Leader, State Veterinary Diagnostic Laboratory
Posted Flock & Herd September 2011
Introduction
The North Coast LHPA has a local ‘Pestivirus project’. This project is attempting to increase the regional detection rate of bovine viral diarrhoea virus (BVDV) persistently infected (PI) cattle, encourage their removal from herds and educate producers to implement appropriate biosecurity measures. The project funds the laboratory testing of ‘suspect’ PI animals. The introduction of ‘in calf’ cattle is a risk for the entry of BVDV to a herd. There is no laboratory test that can identify if the calf could be carrying pestivirus until it is born.
The North Coast of NSW can be prone to arboviral disease in calves that are born from dams that originated from out of the region. This risk can be managed by ensuring that non-pregnant introduced females are exposed to a full season of biting insects before being mated. This usually allows them to develop immunity to arboviruses such as Akabane virus.
This case study outlines a disease investigation in a herd that was already vaccinating against BVDV and introduced some out-of-area ‘in calf’ cattle. Signs of disease in calves born from the introduced cattle led the North Coast LHPA to fund testing for BVDV. The case involved collaboration between: the North Coast LHPA, NSW State Veterinary Diagnostic Laboratory, the Virology Laboratory at the Elizabeth Macarthur Agricultural Institute, a private veterinarian (Neil Farquhar) and a veterinarian employed by Pfizer Animal Health (Lee Taylor).
History
A farmer at Cudgera Creek reported neurological signs in recently born calves and a recent stillbirth. The stillbirth was in a homebred cow. The calves with neurological signs were all born from a group of 15 recently introduced Angus heifers.
The Angus heifers were born in Narrabri and were introduced to another property on the North Coast as weaners. After being on the property for over 12 months, the heifers were joined to an Angus bull and then retained on the same property for most of the pregnancy before being sold to the Cudgera Creek farmer. This history is important because it indicates that, before becoming pregnant, the heifers had a full season of exposure to biting insects, thus minimising the chance of arboviral disease, such as Akabane disease.
The heifers were sold to the Cudgera Creek farmer, when they were in late pregnancy, in mid-May 2011. Shortly after arrival, the heifers were vaccinated with BVDV vaccine (Pestigard - Pfizer Animal Health). All breeding cattle are vaccinated against BVDV on this farm. Calving commenced on 28th June 2011 and five calves were born in a short period. There was a delay before a further five calves were born from 23rd July 2011 onwards. As of late August, the remaining 7 heifers had not calved.
The 15 heifers bought by the Cudgera Creek farmer were part of a mob of about 80 from the other North Coast property sold at the Casino saleyards. Another purchaser of 43 of these heifers was contacted. He had not observed signs of disease in newborn calves but did report a split protracted calving pattern.
CLINICAL SIGNS AND EXAMINATION
One of the first five calves born at Cudgera Creek was described by the farmer as ‘silly’ and poor to suck. Of the latter five calves born, one was 3-4 weeks premature and stillborn and another three were slow to suckle with slight ataxia.
One of the live calves was observed suckling and examined by both a district veterinarian from the North Coast LHPA and a private veterinarian. The calf was not able to find a teat but, when guided by the farmer, could suckle well. After feeding, the calf would occasionally appear weak and wobbly. On examination, the calf appeared partially blind, with a reduced menace response. The calf performed adequately with ‘wheelbarrowing’ and ‘hemi-walking’. Other aspects of a basic neurological examination were normal. There was no cleft palate or other oral abnormalities. Normal suckling was induced when a finger was placed in the mouth. Sometimes the calf would have its tongue protruding. When this and other calves were exercised, they appeared to be in slight respiratory distress, with their tongues hanging out. Drooling was not observed.
The group of introduced heifers were in excellent body condition.
Post-mortem examination
The calf that was previously examined progressively deteriorated and required euthanasia by the farmer. The post-mortem examination could not occur till the following day and was limited by autolysis in major abdominal organs and by damage that occurred in the brain from the firearm euthanasia. No obvious abnormalities were detected on gross examination but it was not possible to determine the presence of mild hydrocephalus or if one or both sides of the cerebellum were abnormal in size because of the damage by the firearm.
LABORATORY TESTING AND RESULTS
Testing was done to consider infectious and genetic causes of the observed signs:
- The homebred stillborn calf was negative for BVDV antigen. Histopathology of the brain of this calf revealed occasional perivascular haemorrhages in the cerebellar white matter without any inflammatory reaction. There was no evidence of Neospora infection. The haemorrhages were assumed to be due to terminal trauma.
- Two of the calves from the introduced heifers (including the examined calf) were also negative for BVDV antigen.
- Hair from two calves was tested for alpha-mannosidosis and results were negative.
- No significant lesions were found by histopathological examination of the brain from the calf that was euthanased. This included an examination of a portion of the cerebellum.
- The mother of the calf that was euthanased had a Pestivirus Antibody AGID of 2. This was interpreted by the pathologist as not being from vaccination but from natural exposure at some time in the past.
Discussion
A definitive diagnosis was not possible in this case. The case included a number of different syndromes that each may have had a different diagnosis. The homebred stillbirth was unlikely to be related to the neurological signs in the calves from the introduced cattle and may have been from a traumatic birth. The prolonged calving pattern may simply be from management factors or could have been from infectious causes, such as vibriosis or pestivirus. The cause of the difficulty in suckling, blindness, respiratory distress, ataxia and neurological signs in the calves can only be hypothesised. Arboviral disease seems unlikely but is possible. Common causes of bovine apparent blindness, such as lead and polioencephalomalacia, were also considered to be unlikely.
Cerebellar hypoplasia and other congenital defects from BVDV exposure would explain the apparent blindness and many of the other clinical signs in the calves. If BVDV was responsible for the signs of disease in these calves it must have occurred from exposure to the virus during the second trimester. Calves exposed during the second trimester to BVDV may be able to clear the virus from their body, test as antigen negative but still have sustained damage to their bodies. Such calves often will have seroconverted in utero and will be BVDV antibody positive, although it can be difficult to distinguish such antibodies from maternally derived antibodies that have been acquired from a seropositive dam through ingestion of colostrum. If the producer is willing, other testing could be done in an attempt to determine if pestivirus was involved and if there was any breach of farm biosecurity for BVDV. This could include pestivirus serology on the other heifers, pestivirus antigen testing on all heifer calves born and, if possible, pestivirus serology on affected calves before they ingest colostrum.
Although the cause of disease in calves on this property was not determined, this case study is a reminder that the introduction of ‘in calf’ females and cattle introduced from outside our region can pose disease risks to North Coast herds.