Prevalence and geographic origin of pigs with serological evidence of infection with Leptospira interrogans serovar pomona slaughtered in abattoirs in Victoria, Australia.

A set of 10,440 sera was collected from pigs slaughtered at Victorian abattoirs. These sera were subjected to the microscopic agglutination test for antibodies to Leptospira interrogans serovar pomona. Identification of the herd of origin was possible for 6511 pigs, and these were derived from 167 herds in Victoria (84% of sera), from 32 herds in New South Wales (8% of sera) and 29 herds in South Australia (8% of sera). The overall prevalence of titres of 512 and above was 3.7%. This was higher (5.3%) among pigs for which the property of origin was unknown than among pigs with identified properties of origin. Among the latter the prevalence was 2.7% (Victoria 0.6%, New South Wales 1.3%, South Australia 25.2%.) Most of the pigs with unknown properties of origin were derived from market groups and were probably typically from smaller herds. Within Victoria a comparison of results with the known pig populations of the 12 statistical divisions indicated that infection was spread throughout the State. Of the 228 identified herds of origin sampled, 32 (14%) had at least one pig with a high titre. However, this may underestimate the proportion of infected herds, as in many cases only a few serum samples were obtained. Of 73 herds from which 25 or more serum samples were obtained, serological evidence of infection was obtained in 18 herds (25%).

Simulation of the economic impact of proliferative enteritis on pig production in Australia.

The economic impact of proliferative enteritis (PE) on an 'average' pig farm was calculated using the AUSPIG decision support system. Inputs were modelled on actual cases of PE, in which affected herds suffered from depressed growth rate, decreased feed efficiency and stock losses. The costs associated with non-haemorrhagic PE and proliferative haemorrhagic enteropathy ranged from $15/sow/yr to $141/sow/yr, respectively, depending on the clinical severity of the disease, incidence of infection and the type of medication strategy used to treat and control the disease.

Outbreaks of proliferative haemorrhagic enteropathy on two pig farms.

Clinical signs of proliferative haemorrhagic enteropathy (PHE) including anaemia, dysentery and sudden death were observed in finisher pigs and young breeding stock on 2 farms. On farm A, PHE occurred 12 months after repopulation of the farm. Other outbreaks of PHE occurred after the withdrawal of therapeutic concentrations of in-feed antibacterial agents (farm A), or after monensin sodium (100 g/t) replaced olaquindox (100 g/t) in feed (farm B). The outbreaks, the possible sources of contamination and the role of antibacterial feed additives in the treatment and control of PHE are described.

Prevalence of proliferative enteritis on pig farms in Australia.

Three surveys, undertaken to assess the prevalence of proliferative enteritis (PE) on pig farms in Australia and to investigate risk factors associated with clinical disease, indicated that PE was a common disease in pig farms. Forty of the 71 (56%) randomly-selected producers had either observed PE or had a veterinarian diagnose the disease in their herd during 1988 to 1990. A relatively low prevalence of the disease was recorded at veterinary diagnostic laboratories, and this suggested that diagnoses of PE were often not confirmed by histopathological examination of the intestines of affected pigs. Non-haemorrhagic PE occurred most often in six- to 24-week-old pigs, but was also reported in 52-week-old pigs. Proliferative haemorrhagic enteropathy usually affected pigs over 16 weeks of age, but was also reported in pigs as young as six weeks and as old as four years of age. A survey of pig-specialist veterinarians indicated that most veterinarians diagnosed PE based on clinical and gross pathological examination of affected pigs, without laboratory confirmation. There were difficulties associated with measuring the prevalence of PE among herds, including the effectiveness of antibacterials for its prevention and control, its subclinical nature and probable mis-diagnoses. This study highlighted the need for an ante-mortem diagnostic test to measure the prevalence of PE more accurately.

Enzyme-linked immunosorbent assay for measuring ileal symbiont intracellularis-specific immunoglobulin G response in sera of pigs.

Proliferative enteritis (PE) is a common intestinal disease on pig farms. The disease is caused by ileal symbiont (IS) intracellularis (Campylobacter-like organisms) bacteria. An enzyme-linked immunosorbent assay (ELISA) was developed to measure IS intracellularis-specific immunoglobulin G (IgG) response in the sera of pigs. The antigen used in the ELISA was filtered, percoll gradient-purified IS intracellularis extracted from the intestines of pigs affected with proliferative hemorrhagic enteropathy. The antibody responses of pigs challenged with intestinal homogenates from pigs affected with proliferative hemorrhagic enteropathy containing IS intracellularis or percoll-gradient purified IS intracellularis were low and variable. The low IgG titers measured in challenged pigs support previous findings that IgG plays a minor role in the immune response of pigs to IS intracellularis. On a farm in which infection was endemic, pigs seroconverted at between 7 and 24 weeks of age. High IgG titers, indicative of maternally acquired antibody, were present in 3-week-old pigs. The IgG titers in piglets were lowest at 6 weeks of age, which approximates the age of onset of clinical disease. These results suggest that IgG plays a role in determining the susceptibilities of pigs to natural infection. Measurements of seroconversion by the ELISA might aid in epidemiological investigations of PE in naturally infected herds. However, the variable antibody responses in experimentally challenged pigs would seem to limit its usefulness as an antemortem diagnostic test for PE.

Simulation of the economic impact of transmissible gastroenteritis on commercial pig production in Australia.

A simulation model (AUSPIG) was used to predict the effect of an increase in piglet deaths, and a reduction in growth rate and an increase in feed conversion ratio of grower pigs on the profitability of two herds representative of the Australian pig industry caused by the introduction of transmissible gastroenteritis virus (TGE) into those herds. For each herd, mortality rates for piglets under 1 week of age of 50% and 95% were assumed to represent a 'moderate' and a 'severe' outbreak, respectively. A reduction in net revenue of 70% was predicted to occur in the 6 months after a 'moderate' outbreak of TGE (100% for a 'severe' outbreak). This represents a total loss of between $260 and $330 per breeding sow in the 12 months after infection with the TGE virus. The likely financial impact of an outbreak of TGE on an Australian piggery is substantial and should be considered when addressing quarantine issues.

Causes of preweaning mortality on a large intensive piggery.

Causes of preweaning mortality were examined on a large intensive piggery. Diagnosis was made using comprehensive clinical histories combined with post-mortem data. Two thousand four hundred and twenty-six piglets were born in 238 litters. Pre-parturient and parturient losses were 2.9% and 5.4% of the total numbers of piglets born. Birth to weaning mortality was 11.3%. Among piglets born alive, overlaying was the most frequent cause of death (2.1%), followed by deaths due to diarrhoea (1.7%), anaemia (1.2%), savaging (1.1%) and losses of small weak piglets (0.9%). Most deaths, including stillbirths, were associated with below average birth weight, and two-thirds of all deaths of liveborn pigs occurred within 4 days of birth. Increased litter size resulted in decreased birth weights, an increased percentage of stillborn piglets and mummified foetuses, but duration of parturition was not affected. Stillborn piglets were born late in the litter and after a longer interval between pigs born (interpig interval). Over 70% of deaths due to overlay were in previously healthy piglets, but some were associated with illness of the sow (18%) or both sow and piglet (3%). Savaging was confined mainly to first parity sows and was responsible for 20% of all deaths in these litters. Sixty-two per cent of all piglets with a birth weight of less than 800g were stillborn or died before weaning compared with 18.7% mortality for all piglets. Anaemia in piglets was considered to be due to umbilical haemorrhage. Anaemic piglets had a 36% mortality to weaning compared with 10% for non-anaemic piglets.(ABSTRACT TRUNCATED AT 250 WORDS)

Farm studies of porcine parvovirus infection.

Epizootics of reproductive failure associated with porcine parvovirus infection were investigated on 38 farms. Mummification was common to all epizootics. The mean number of mummified fetuses per affected litter was 3.1. Mean number of pigs born alive for gilts and sows farrowing litters with mummified fetuses was 5.0, but for sows without mummified litters on the same farms it was 9.0. Mummified fetuses were observed in aborted litters on 8 (21.1%) farms. Gilts and sows that appeared pregnant but "lost" their swollen abdomens and failed to farrow were observed on 12 (39.5%) farms. Delayed return to estrus was evident on only 3 (7.9%) farms with a continuous farrowing program. On 21 farms with a batch farrowing program, only 2 (10%) epizootics involved more than 1 batch. Up to 100% of the pregnant swine in the group farrowing together produced mummified pigs, but less than 20% of the breeding herd was affected in 26 (68.4%) cases. The prevalence of disease was not related to herd size, housing, or farrowing management.

Effect of porcine parvovirus serostatus on the reproductive performance of mated gilts in an infected herd.

Gifts from 2 commercial swine operations (farm A and farm B) that were bred each week were tested for porcine parvovirus antibody. On farm A, 21.9% (weekly, 2% to 35%) of the 657 gilts tested over a 16-week period were seronegative within 1 week of mating. On farm B, 17.7% (weekly, o to 40%) of the 164 gilts tested over a 10 week period were seronegative within 1 week of mating. Eighty-one gilts from farm A which were seronegative at time of mating were retested at the end of the gestation. Of the 81 gilts, 4 1 had developed antibody titers. The litter size decreased by 1.3 live pigs/litter. The percentage of small litters (less than or equal to 6 born alive) in the group that seroconverted was 36.6% compared with 10% in the gilts that remained seronegative throughout gestation.

Atypical porcine enterovirus encephalomyelitis: possible interraction between enteroviruses and arsenicals.

Porcine enteroviruses were isolated from weaner pigs that had nervous signs and mild non-suppurative meningoencephalomyelitis and ganglioneuritis. The clinical signs and lesions were not typical of enterovirus infection and it is believed that an organic arsenical present in feed enhanced pathogenicity of enteroviruses. Severe non-suppurative polioencephalomyelitis and ganglioneuritis were produced in gnotobiotic pigs by oral inoculation of the viruses.