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Prior to the intensification of pig production in the 1970’s, case reports of proliferative entero-pathy (Ileitis) due to Lawsonia intracellularis were noted worldwide, but were confined to occasional cases of acute or chronic lesions. At that time, epidemic and parasitic diseases with similar manifestations were common.

This complicated the diagnosis of chronic proliferative enteropathy. Furthermore, no definitive diagnostic laboratory confirmation was available.

From 1970 onwards, many pig farming areas worldwide had switched to intensive production and severe outbreaks of proliferative entero-pathy were reported in USA, Australia, Great Britain and Denmark. It is possible however that there was no true increase in incidence, merely a switch from the common chronic form to the more visible acute form. Prior to intensification, it was perceived there were numerous other enteric diseases, such as swine dysentery, salmonellosis or intestinal parasitism which took diagnostic priority over a diagnosis of proliferative enteropathy.

The true nature of proliferative enteropathy was only discovered in 1973 when Alan Rowland and Gordon Lawson, in Edinburgh, Scotland, first saw the curved intracellular bacteria that cause the disease (Rowland and Lawson 1974). Unfortunately, it would take another 20 years before this organism was cultured and identified, and Koch’s postulates determining the cause of the disease were fulfilled. During those 20 years, considerable confusion arose as to the real nature of the intracellular bacteria and many types of Campylobacter bacteria thought to be involved were examined unsuccessfully. In fact, the primary agent of disease is Lawsonia intracellularis, which is part of the Desulfovibrio family and has a typical “vibrio” bacteria shape.