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This article was published in 1986
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An Outbreak of Mycotoxicosis in Pigs
Greg Simpson Veterinary Inspector Condobolin P.P. Board Bathurst Street CONDOBOLIN
INTRODUCTION.
Moulds occur on both living plants and stored crops and their effects on animals and man have probably been gravely underestimated (Blood and Henderson 1968). Several types of fungal toxicoses are well known including mouldy corn poisoning, paspalum and ryegrass staggers, ergotism, facial eczema and lupinosis etc. Animals vary widely in their susceptibility to mycotoxicosis. The young tend to be more susceptible than adults but there are considerable species and individual differences in susceptibility as well.
The features which characterise mycotic diseases are that (a) they are not generally transmissible, (b) drug treatment is normally without any effect, (c) outbreaks are seasonal and sporadic and (d) the food consumed by the animal is usually contaminated with a fungus.
This paper details the chronological sequence of events in a local outbreak of mycotoxicosis in pigs following the ingestion of contaminated wheat and resulting in the deaths of approximately 60 pigs of varying ages.
History and clinical findings
The affected piggery runs 30 sows with the total number of pigs on hand at any one time varying between 120 and 150.
Like many piggeries in 'pastoral' zones, management is based on an extensive system with pigs allowed to free range except for growers which are confined to growing pens for market preparation. The Large White is the predominant breed with evidence of some Berkshire infusion. Some nutrition is obtained from foraging with wheat providing the major bulk of the diet. Although the owner is rather keen on pigs as an economic backstop, wheat and sheep are the predominant enterprises on the property.
The problem commenced suddenly when 2 six month old growers became acutely ill. These were examined by a private practitioner and despite treatment with Streptopen® these pigs quickly became recumbent and died soon afterwards. No symptoms were reported at the time but post-mortem of one pig showed mild haemorrhagic enteritis and a tentative diagnosis of Haemorrhagic Bowel Syndrome made. From samples submitted the laboratory reported 'Focal congestion of intestinal mucosa, some oedema and infiltration of mononuclear inflammatory cells. Changes would indicate enteritis but not suggestive of HBE associated with Campylobacter sputorum.
One week later the owner reported that more pigs had developed symptoms and requested a visit to investigate the problem. At that stage a further 5 pigs had died and 8 were sick out of a pen of 16 four to six month old growers. The owner suspected arsenic poisoning as the pen was immediately adjacent to a disused sheep dip sump which had overflowed its contents into the pen following recent heavy rain. Post-mortems were conducted on 2 pigs and samples collected for laboratory testing.
The specimen advice report stated:
Symptoms: acute onset with anorexia, weakness and a characteristic muscle tremor, inco-ordination and some swaying in the hindquarters. Some animals could not rise but lay shuddering. The less affected could rise and move about albeit with a fair amount of inco-ordination and a slight lateral deviation of the head. When forced to move the pigs fall on their knees or side. Later they develop spasms/shudderings and finally tetanic convulsions with death occurring within 24 hours from the onset of symptoms. The odd animal may survive but with residual ataxia and twitching.
Post-mortem: most pigs pass blood from the nose and mouth after death. Slight excess of serofibrinous pericardial exudate, hepatic degeneration varying from slight mottling to total khaki discolouration, some sub-epicardial and endocardial haemorrhages and some haemorrhagic exudation from the gastric and intestinal mucosa
The owner was queried as to the pigs ration but he felt that the feed could not be the problem as he had been using the same (home-grown) supply for the previous six months with no ill effects. Furthermore, a neighbour had purchased a quantity of his wheat and had been using it for pig rations with no problems.
A small amount of unconsumed grain remaining in feed troughs appeared contaminated with mould at the ends of individual grains but this is not uncommon in feed grain retained for home stock feed production which would otherwise incur a dockage when delivered to the Grain Handling Authority. Unfortunately the feed silo was not examined at this visit.
Several diagnostic possibilities were then considered with 'poisoning', mulberry heart disease, salmonellosis, water deprivation/salt poisoning and even Aujeszky's disease. As symptoms somewhat resembled organophosphate poisoning and as contamination via the disused sheep dip sump was possible, atropine mitis® was injected intravenously into one pig as a diagnostic procedure. After a total of 15 mls atropine (9.7 mg) had been slowly injected with no remission of symptoms, organophosphate poisoning was rejected as a possible cause of the problem. Additional post-mortem samples were collected for laboratory examination and as a precautionary measure the owner meshed in an adjacent cattle yard with all pigs being moved to this site. At this stage most of the pigs had become anorectic with only small quantities of feed being consumed.
LABORATORY RESULTS
Laboratory results of submitted samples were as follows: Bacteriology: Cultures of spleen, liver, kidney, lung and mesenteric lymph nodes gave no visible growth. Culture of intestines gave non-significant lactose fermenting coliforms (normal flora). Salmonella culture negative. Smears of blood negative for anthrax.
Toxicology: stomach contents negative.
Histopathology: liver - mild diffuse degenerative changes with swelling and vacuolation of hepatocytes.
kidney - diffuse congestion wiht focal interstitial haemorrhages throughout the cortex. Some degeneration of the
tubular epithelium. No evidence of focal necrosis.
lung - focal areas of consolidation with thickening of alveolar walls. Some suggestion of low grade mycoplasma
infection.
brain - vascular congestion and oedema. No evidence of encephalitis or meningitis of brains or spinal cords.
The laboratory further commented 'a number of possible conditions can be ruled out - in particular a viral encephalitis or salt poisoning and also Mulberry Heart Disease'.
SUBSEQUENT DEVELOPMENTS
After five days had passed from my previous visit with no further news from the property, the owner was contacted for a report on developments. He advised that deaths had continued unabated with a total of 46 pigs having died with no signs of losses ceasing as a number of other pigs were developing symptoms continuously. Deaths had occurred in all ages of pigs including breeding sows, a boar and even young suckling pigs.
A further visit to the property was made and 3 young pigs displaying various stages of nervous symptoms collected for immediate transport to the Regional Veterinary Laboratory at Orange. At this property visit the feed silo was (finally) examined as an acute toxicosis was on reflection still considered the most likely aetiology.
The contents of the silo consisted of approximately 10 bags of wheat. Examination revealed mould contamination ranging from minimal quantities to congealed masses of grey to black mouldy material forming 'plaques' 10 cms in diameter. These 'plaques' had formed on the concrete floor of the silo beneath the grain.
Samples of the contaminated feed were collected for laboratory examination.
Laboratory results for the 3 submitted pigs were as follows:
Pig 1 - arrived dead.
Pig 2 - arrived in terminal stage syndrome and showed virulent continuous muscle fasciculations, trembling and jaw chomping with salivation.
Pig 3 - arrived dull and depressed with hind limb weakness, swaying and collapse. This progressed during the day to being almost like pig 2.
Toxicology - the grain submitted was badly spoiled and was damp. Seeds showed splitting, bacterial contamination and enormous populations of a variety of fungi including Penicillium pascilli and Aspergillus flavus.
Diagnosis - acute toxic insuly [sic] - probably Mycotoxicosis.
DISCUSSION
Penicillium spp. have been implicated in New Zealand as the likely cause of perennial rye grass staggers (di Menna et al. 1978).
This fungus produces fumitremorgins which are contained in the hyphae. In cattle and sheep clinical symptoms of intoxication develop within 7 to 12 days of exposure to the toxin and include tremors, head shaking, inco-ordination, abnormal, staggering gait, stumbling and collapse. The tremors and inco-cordination are stimulated and exacerbated by exercise and excitement (Seawright, 1982).
Aspergillus flavus is a ubiquitous fungus and is found commonly on stored foods (Bryden et al. 1975). Strains of the fungus vary in their capacity to produce toxins.
The toxic effects of aflatoxins are both dose and time dependent. The compounds are readily absorbed from the stomach and metabolised in the liver to a range of toxic and non-toxic metabolites which are then excreted in the urine and milk. The toxins cause hepatic centrilobular necrosis and marked fatty infiltration often accompanied by biliary ductular hyperplasia and cirrhosis. Symptoms of aflatoxacosis include anorexia and depression accompanied by ataxia, dyspnoea and anaemia. There is a high prevalence of toxigenic A. flavus in commercial mixed feed sources and feed ingredients (Bryden et al. 1975). Other species of fungi which can produce similar symptoms of ataxia and tremors include Claviceps spp. and Phomopsis spp.
Factors which make for difficulty in recognising the existence of mycotoxicosis include:
(a) the biological actions of the toxin in the host may be delayed,
(b) diagnosis may depend on recognition of specific clinical signs which may or may not be present,
(c) the toxin may not be uniformly distributed in the environment or the feed and accordingly be difficult to detect,
(d) fungi are often seen contaminating foods which animals appear to eat without detriment.
REFERENCES
- Blood, D.C., and Henderson, T.A., Veterinary Medicine, Bailliere, Tindall and Cassell, London, 1968
- Bryden, W.L., Rajion, M.A., Lloyd, A.B. and Cumming, R.B., (1975), A.V.J. 51, 491-493
- Connole, M.D. and Hill, M.W.N., (1970), A.V.J. 46, 503-505
- di Menna, M.E. and Mantle, P.G., (1978) Res. Vet. Sci., 24, 347-351
- Seawright, A.A., Animal Health in Australia, Chemical and Plant Poisons, Australian Bureau of Animal Health, 1982