Swine dysentery

Swine dysentery

D J TAYLOR

Introduction

Swine dysentery (SD) is caused by the anaerobic spirochaete, Brachyspira hyodysenteriae, and in the typical acute disease is characterized by dysentery and the development of an acute diphtheritic to necrotic enteritis with haemorrhage of the caecum and colon in weaned, growing, finishing and adult pigs. It results in temporary loss of condition, chronic wasting, or death. It is an important enteric disease which, in many countries, is second in importance only to Escherichia coli enteritis.

The disease was first described in 1921 by Whiting and his co-workers in the USA who were able to reproduce it in transmission experiments using the gut contents of affected animals, thus proving that it was transmissible.34 It was recorded in many countries of the world but the aetiological agent was unknown until 1971 when Taylor and Alexander described the isolation of a spirochaete and the reproduction of the disease by feeding pure cultures of it to pigs.30 Shortly after that, Harris and his co-workers in the USA con- firmed their findings and named the organism Treponema hyodysenteriae. 10, 14 Both the organism and the disease have been extensively studied since then. This knowledge has been applied to methods used to diagnose, treat and control the disease, but has not yet resulted in a universally applicable vaccine.

Aetiology

The aetiological agent of SD is now named Brachyspira hyodysenteriae (formerly Serpulina or Treponema hyodysenteriae) 23 and forms one of a group of large oxygen-tolerant anaerobic spirochaetes found primarily in the large intestines of pigs and other mammals and birds. Brachyspira hyodysenteriae is 6 to l0 µm in length, flexible and active when viewed by phase contrast microscopy, and stains readily with aniline dyes such as carbol fuchsin. The cell contains a protoplasmic cylinder 350 nm in diameter with pointed ends and 7 to 14 fibrils inserting at each end and is surrounded by an envelope.

The organism can be grown on horseblood agar in atmospheres containing 5 per cent carbon dioxide and 95 per cent hydrogen. It forms colonies 1 mm in diameter surrounded by β-haemolysis after 48 hours’ incubation. β-haemolysis results from the secretion of a powerful haemolysin,21 tlyA,15 stimulated by the presence of ribonucleic acid and two weaker haemolysins, tlyB and tlyC.

Brachyspira hyodysenteriae is strongly β-haemolytic, indole positive, β-galactosidase negative, hippurate negative, and is antigenically distinct from other Brachyspira spp. Its specific antigens include a 36 kDa protein, 10 kDa envelope protein and a 46 kDa periplasmic flagellar protein.17 Multilocus enzyme electrophoresis, 16S rRNA sequences, DNA:DNA hybridization, whole cell DNA probes and restriction enzyme analysis (REA) can all be used to identify B. hyodysenteriae. The species can be subdivided into 11 serogroups based on lipopolysaccharide antigens and these can be further subdivided into serovars and REA or electrophoretic types (ET).12 It is sensitive to drying4 and acid conditions (pH <6,0), and is readily destroyed by heat but can survive in organic matter for days or weeks.

Epidemiology

Swine dysentery occurs worldwide. Recent figures vary from country to country but in 1993, 11 per cent of herds in the USA were considered to be infected. Figures for the UK in 1994 suggested that 4,7 per cent of herds were infected (10,5 per cent breeding herds). Increasing numbers of herds are being founded using SD-free breeding stock housed in isolation. Dysentery-free pigs are being used in feeding enterprises, and separate site weaning and rearing operations are all reducing the prevalence of the disease in many countries below the historic levels of 30 to 40 per cent of herds.

Whole sectors of a country’s pig industry such as breeding companies and their multiplying herds may be free from the disease.

Swine dysentery is transmitted to healthy, susceptible pigs by the ingestion of the faeces of affected or carrier animals or of material contaminated with their faeces.

Faecal shedding of the organism occurs during the incubation period of the disease (in the field this varies between 7 and 60 days but is usually 4 to 14 days in experimentally infected animals), its clinical course, and for up to 90 days following clinical recovery. Farms on which an outbreak of the disease has occurred remain infected unless depopulation and disinfection or a whole herd treatment have been carried out.33 At least two electrophoretic or REA types have been identi- fied on individual farms, and B. hyodysenteriae appears to be a recombinant species with an epidemic population structure in which a few ETs have spread widely. 32

Pigs of all ages are affected although the peak prevalence is in weaned pigs of 6 to 12 weeks of age. The disease can be particularly severe in sows at farrowing or mid-lactation. It is usually introduced onto farms by the purchase of infected pigs, and spreads slowly from pen to pen by means of drainage channels or movement of infected pigs, by pig-to-pig contact, or by infected boots and implements.

The morbidity rate may reach 75 per cent of all pigs on the farm and mortality rates vary from between 5 and 25 per cent. Some immunity results following recovery from infection with SD and recovered pigs rarely suffer relapses upon re-infection. Antibodies to the causal spirochaete have been...

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