Listeria monocytogenes occurs widely in the environment and can be isolated from soil, decaying plants and silage. Man and many animal species can also be asymptomatic carriers. L monocytogenes causes visceral (septicaemic) listeriosis in young animals of many species including lambs and calves, neural listeriosis especially in sheep, goats and cattle, abortions in sheep, cattle and goats and iritis (often associated with feeding big bale silage) in cattle (Quin et al 2002). Sheep generally develop neural listeriosis 3-4 weeks after the commencement of silage feeding. Sheep and goats can also abort or become septicaemic after eating L. monocytogenes contaminated silage. Septicaemia usually occurs within 2 days of silage feeding while abortions typically occur 6-13 days later (Radostits et al, 2007). This report deals with two outbreaks of listeriosis in goats caused by the ingestion of silage that originated from a common source.
On 6 July 2006, I was called to Burra creek near Queanbeyan because six of 200 Angora goats had died and 10 were sick with nervous signs. The goats were fed baled silage. The goats had failed to respond to penicillin.
Two goats died with their heads bent under their necks. I was told they stood this way before collapsing. Neurological signs in the surviving goats ranged from head tilting to lateral recumbency with muscle fasciculations (not unlike the symptoms of organophosphate poisoning). Another animal stood with a piece of silage hanging from its mouth. I considered listeriosis, botulism and lead poisoning in the differential diagnosis.
Two goats were post-mortemed. My findings were unremarkable apart from some strands of fibrin between the cerebral hemispheres and the brain stem and the cerebellum and the brain stem.
The brain was culture negative and the liver did not have abnormal quantities of lead. Histopathology revealed severe diffuse perivascular mononuclear cell cuffing, multifocal areas of malacia, demyelination and scattered microabcesses throughout the brain stem. These findings were consistent with a diagnosis of leucoencephalitis caused by Listeria monocytogenes.
I advised the owners to stop feeding the silage.
On 17 August 2006, I was called to a property at Wilton, near Camden because the owner of an Angora stud reported four dead and three sick goats from a herd of approximately 230. The goats were fed silage cut from a crop that had been irrigated with sewerage effluent. The affected goats, the older members of the flock, were in late pregnancy, became sick, and died over 2-3 days. Initially the goats showed interest in feeding but were unable to eat or swallow. Salivation was profuse. They also tended to circle and stagger before becoming prostrate then dying. The affected goats were not treated with antibiotics, but parenteral thiamine failed to elicit a response.
Histopathology revealed a severe diffuse perivascular cuffing, 2-3 cells thick with areas of gliosis and a heavily segmental suppurative submeningeal exudate. A profuse pure growth of Listeria monocytogenes was cultured from the brain confirming the diagnosis of Listeriosis.
L. monocytogenes grows between temperatures of 3-45° C and a pH of 5.6-9.6 (Quin et al 2002). Well made silage is compacted, air free with a pH less than 4.5 so is not conducive to its multiplication. However, silage that is poorly fermented, has pockets of aerobic deterioration or is exposed to the air is prone to L. monocytogenes growth. Baled silage is more difficult to compact and the poorer fermentation, larger surface area and propensity to damage to the plastic covering render it more risky than pit silage.
The producers of this silage incorporated material left from previous cuts. This material would have been subject to aerobic decomposition rendering it more favourable to L. monocytogenes proliferation. The silage was also baled, increasing the risk of listerial growth.