Malignant Catarrhal Fever (MCF) is a generally fatal disease of susceptible cloven-hoofed species, most significantly cattle in Australia. It is usually sporadic, affecting single animals, although can occur in outbreak form. It is caused by infection with a herpesvirus carried by an asymptomatic natural host.
Five different herpesviruses have been recognised as causing MCF. The two most common are alcelaphine herpesvirus 1 (AlCV-1), which causes wildebeest-associated MCF, and ovine herpesvirus-2 (OvHV-2), which causes sheep-associated MCF. Wildebeest associated MCF is exotic to Australia.
This paper describes two unrelated cases of MCF in the Forbes region of the Central West Local Land Services that occurred within 6 weeks of each other.
A single Droughtmaster cow in late pregnancy on a mixed farming property had been unwell for several days. She was part of a mob which had been grazing periodically on the local stock route. A private veterinarian was initially called, and following mild pyrexia and non-specific findings on clinical examination, antibiotic and anti-inflammatory treatments were administered. There was minimal if any response to therapy. The cow would not eat or drink, and developed vision deficits and bloody diarrhoea. After a further three days the owner contacted the local District Veterinarian and a property visit was arranged.
The cow was dull and severely dehydrated with sunken eyes, but aware of her surrounds. She was at least partly blind, moving with a high stepping gait, and was mildly aggressive/distressed when startled. She had bilateral corneal opacity, serous ocular discharge, a slightly purulent nasal discharge and frothy saliva around her lips. Her temperature was 39.9 degrees Celsius, and rectal straining produced a scant amount of bloody diarrhoea. Heart sounds were quiet, and both heart and respiratory rate were mildly increased. Gut sounds were absent. The oral mucosa was dry and there was moderate hyperaemia and significant superficial mucosal erosions within the buccal cavity, particularly on the hard palate and ventral tongue. There were no foot lesions and all other cattle on the property were well.
The owners elected to euthanase the cow by gunshot on humane grounds and requested a necropsy. This revealed a rumen containing a large amount of dry, fibrous content, and poor mucosal papillae development. No material consistent with lead was identified. The omasum was enlarged and impacted with dry ingesta. The abomasum contained a small amount of viscous liquid, and the mucosa was diffusely inflamed with a small number of 1-2mm diameter raised white lesions. The small intestines were congested and thickened, with a rubbery feel, and the serosal surface had a red striped pattern. A live full term bull calf was delivered.
Samples were collected for a low-risk foot and mouth disease (FMD) exclusion, and specific testing for MCF and Salmonella was requested.
Preliminary results received within 24 hours from Elizabeth Macarthur Agricultural Institute (EMAI) laboratory were FMD PCR negative and MCF PCR positive. Salmonella culture was negative. Histopathology identified a marked necrotising ulceration and lymphoproliferation of the intestinal mucosa, with crypt abscessation and necrosis, and intestinal thrombosis, which was strongly consistent with MCF. Follow up testing at Australian Centre Disease Preparedness (ACDP) confirmed samples were both FMD and vesicular stomatitis negative.
A Shorthorn bull on a mixed farming property, purchased three months earlier, was noticed very unwell one morning. The owner described 'milky eyes' and incoordination. He called a private veterinary practitioner (MM), but the bull was dead on arrival.
On examination the veterinarian identified significant bilateral corneal opacity, and oedema of the sclera and congestion of scleral vessels. There was mild crusting of the nares, frothy saliva around the mouth and superficial necrosis of the oral mucosa with significant erosions and sloughing of overlying epithelium. Similar mucosal lesions were also found inside the prepuce with blood-stained preputial discharge, and the testicles were swollen.
The private vet contacted the EAD Hotline to discuss these findings in combination with case history and presentation. Lesions noted on one foot at the coronary band and dew claw appeared to be consistent with trauma rather than the disease process.
Samples were collected for testing at EMAI, including for low-risk FMD exclusion.
Preliminary results from EMAI laboratory were again FMD PCR negative, and MCF PCR positive. Kidney lead levels were not elevated, and follow up testing at ACDP confirmed samples were both FMD and vesicular stomatitis negative.
Transmission of MCF within natural carrier host species occurs in utero, or in early life via direct contact, or aerosol, or potentially ingestion. Infection is lifelong and considered endemic in wildebeest in Africa for AlCV-1, and in sheep worldwide for OvHV-2.
In the field MCF most commonly occurs in cattle, buffalo and deer, but may be seen in other ruminant species and pigs. Clinical disease has also been demonstrated in small laboratory animals, including rabbits.
Within species there is variability in susceptibility to OvHV-2; Bos javanicus domesticus (Bali cattle) are said to be highly susceptible to MCF, as are bison, whereas Bos taurus and Bos indicus cattle are relatively resistant. Deer are also highly susceptible.
Peracute disease is often seen in susceptible species, with few if any clinical signs. Depression with diarrhoea and dysentery may be the only presentation before death. Disease is more likely to be relatively protracted in less susceptible/more resistant species, with a variety of potential clinical signs. Bilateral corneal opacity is characteristic, and the reason MCF was considered a differential in these cases. Other clinical signs often include pyrexia, depression, increased lachrymation, mucopurulent nasal discharge, progressive changes of oral and other mucosa, lymphadenopathy and development of nervous signs.
Close contact between natural carrier host and the susceptible species is usually required for transmission, but disease in a bison herd has been reported across a distance of five kilometres (from a lamb feedlot). Fomites have also been considered a risk for disease. The cow in Case 1 had no obvious recent contact with sheep, although had been grazing on the stock route with the potential for a minor interaction. As an additional consideration the mob had been in a paddock with sheep adjacent on a neighbouring property approximately six months earlier. In Case 2 the bull was in a paddock with sheep which were the likely source of his infection. Sporadic cases of MCF are also reported to occur in susceptible species at Taronga Western Plains Zoo, Dubbo. The exact source of the virus is unknown in these cases – there are no domestic sheep kept within several kilometres of the zoo, and screening of the barbary sheep on one occasion was unable to demonstrate carrier status.
Factors that predispose to shedding from a natural host and transmission to the susceptible species are unknown. Contact with pregnant or recently lambed ewes has been associated with disease.
The exact incubation period has not been defined but has been as long as 9 months in experimentally infected animals, and latency may play a role in this.
Susceptible animals are dead-end hosts and considered not to be a source of disease. Interestingly, and to support this, while sluggish at birth the bull calf delivered in Case 1 is still alive, fit and strong, seven months after delivery.
Due to its sporadic nature in Australian mixed farming properties, biosecurity practices to prevent MCF are not routine, but should be considered for production systems managing highly susceptible species such as bison and deer. Mortalities due to MCF are also a consideration in zoos which often house both potential carriers and susceptible species.