The disease under investigation is an infective condition of the bones and soft tissues of the head. Published reports indicate that it is connnon in captive macropods throughout the world, and that it also occurs in wild macropods. The infection has been ascribed to a number of bacterial agents, but in particular to the actinomycetes and to Fusobacterium necrophorum.A survey conducted by post revealed that, of 71 establishments throughout Australia and New Zealand where macropods were kept, the disease was known to have occurred in 27 (38%); the average annual incidence of 'deaths from the disease in these establishments was estimated at 7%. The disease had been recorded in all the commonly held species. There were few differences in management and husbandry between establishments where the disease occurred and those where it did not; however in a greater proportion of the former there were high stocking rates and small enclosures. The use of pelletted feed was more common in establishments where the disease occurred, but there were no other significant differences in the types of feed given, in spite of the fact that injury by sharp feed particles is widely believed to initiate the disease.Because the infection was believed to originate from the oral cavity, a survey was tmdertaken of the oral flora of 59 macropods unaffected by the disease. Organisms isolated, or seen in smears, were classified i.nto broad groups according to their morphology, cultural characteristics, and a limited number of biochemical tests. All the groups of organisms which make up the normal oral flora of humans and domesti.c animals were represented, with the exception of the veillonellae. Actinomycetes were isolated from 63% of samples but F. necrophorum was not detected.Forty animals suffering from jaw disease were examined, together with four heads and 60 skulls from affected animals. The characteristic lesion was a progressive necrotising infection, with liquefaction of soft tissues and erosion and exostosis of bone. In nearly every case the infection appeared to have arisen around a tooth, and in some animals there was generalised peri~dontal disease. Sections of lesions showed foci of coagulation necrosis surrounded by leucocytes; gramnegative filaments were numerous within the necrotic areas. Culture of material from the lesions most commonly yielded a prolific mixed growth, with several anaerobic components; nearly every member of the normal oral flora was represented in at least one lesion. The organisms isolated most frequently were aerobic gram-negative rods, from 89% of lesions, and F. necrophorum, from 86%; the latter was found in larger numbers than any other organism and was isolated in pure culture from five lesions. Actinomycetes were isolated from 31% of lesions and in a pure culture from one lesion. F. necrophorum was also isolated from the mouths of 61% of affected animals. Many affected animals showed loss of condition and moderate anaemia and leucocytosis. Ten were treated with systemic antibiotics, in most cases accompanied by opening and irrigation of the lesion, but in none was permanent resolution achieved.Strains of F. necrophorum isolated from affected macropods produced progressive necrotic lesions when inoculated subcutaneously into mice, guinea pigs, bandicoots and macropods; intraperitoneal inoculation into mice produced abdominal abscesses and death within three days. Inoculation of F. necrophorum in combination with other organisms isolated from affected macropods, produced lesions similar in gross and histological appearance to those produced by F. necrophorum alone. None of the other isolates produced necrotic lesions when inoculated alone or in combinations which lacked F. necrophorum. Superficial inoculation of the gingiva with F. necrophorum, alone or in combination with other organisms, failed to produce macroscopic lesions in rats, guinea pigs, sheep or macropods. Inoculation deep into the gingiva, of F. necrophorum alone or in a mixture of four organisms, was performed in two macropods, and resulted in the development of severe necrotising infections, in one case involving bone, which resembled lesions of jaw disease.These results indicate that F. necrophorum is the infective agent which is responsible for the lesions of jaw disease, but the means by which F. necrophorum gains access to the tissues has not been elucidated. It is suggested that marginal gingivitis and recession of the gums may predispose to the disease, and that the disease is initiated when F. necrophorum, possibly derived from the gastric or intestinal flora, multiplies in periodontal pockets and then invades the deeper tissues.