In early February 2012, a beef producer contacted the Lismore District Veterinarian of the North Coast Livestock Health and Pest Authority (LHPA) about a severely pale calf.
The producer was concerned that the calf had contracted a congenital disease from a bull purchased 18 months earlier. This bull had been diagnosed with pneumonia 14 months earlier. The pneumonia was refractory to treatment with antibiotic therapy. The bull had sired 4 calves that were also pale in the gums whilst being kept as a breeder on the property and had since died.
The property runs about 120 head of cattle, which are all drenched regularly (every 3 months) with a pour on drench containing moxidectin. Even young calves still suckling on their mothers are drenched, some only several weeks of age.
The paddocks were excessively wet when visited due to heavy rainfall in the weeks prior to the case.
The most severely affected calf had severe pallor of its gums, jaundice, pyrexia (40.6), dyspnoea, normal lung sounds, normal heart and respiratory rates, lethargy, and was in poor body condition.
No urine or faeces were obtained from the calf. The calf died approximately one week after this examination and the District Veterinarian was only advised 72 hours later, at which point a necropsy was not possible.
At the time that the calf died, 12 other calves presented with similar problems. They had a history of variable amounts of scours and poor growth. The calves’ ages ranged from 6 weeks to 4 months. Faeces were collected from 8 of the calves and blood from 3.
Blood (EDTA, Lithium Heparin), blood smears and hair were submitted for haematology, serology/ELISA, blood parasite examination and pestivirus virology respectively.
Haematology showed anisocytosis, microcytosis, macrocytosis, basophilic stippling, Howell-Jolly Bodies and white blood cell (WBC) autolysis. The haematocrit was 10%, which confirmed the suspicion of severe anaemia. The blood smear was negative for any blood parasites, which was interesting as the veterinary pathologist suggested the red blood cell changes may be consistent with Theileriosis.
Serological testing for Leptospira spp. performed was negative. Antigen testing for pestivirus was also negative.
A liver Fluke ELISA was later undertaken and had an S/P Ratio value of 107, which was considered positive.
The results for the later group of calves were then obtained and the faecal worm counts were positive for heavy strongyle burdens in each of the calves.
Disease on this farm was diagnosed as helminthiasis and immature liver fluke infestation. Disease from liver fluke is not commonly reported in calves less than 4 months of age but is conceivable under the right conditions. There is a possibility that Theileria parasites also contributed to the clinical signs of the most severely affected calf that ultimately died.
The pathogeneses of both Fascioliasis and gastrointestinal worm burden on this farm are an interesting example of the Host-Pathogen-Environment (HPE) triad.
HPE is a pathological concept that acknowledges the relationship between the host, environment and pathogen in disease progression (Figure 1).
Essentially, the stronglye larvae and Fasciola metacercariae are heavily influenced by the environment, which in turn, increases their pathogenicity.
The specific factors that may have contributed to this case are as follows:
These factors all combined to form a serious problem for this producer. The producer should be advised to change the drenching regime based on worm egg count reduction testing, feed supplements that are high in energy and ideally move the cattle to higher ungrazed pastures immediately after drenching with an anthelmintic effective against both strongyle worms and fasciola.