An immunodominant T-cell-stimulatory epitope located near the carboxy terminus of the 38-kDa antigen from M. tuberculosis (38.G, residues 350-369) was found to be M. tuberculosis-complex specific. This was demonstrated by the presence of proliferative and delayed type hypersensitivity (DTH) responses in mice immunized with Mycobacterium tuberculosis and Mycobacterium bovis BCG, whereas mice immunized with M. avium or other non-tuberculous species of mycobacteria showed no such responses. Peptide 38.G stimulated the proliferation of peripheral blood lymphocytes from healthy purified protein derivative (PPD)-positive individuals but not from PPD-negative individuals. It also elicited DTH responses in M. tuberculosis sensitized mice and in PPD-positive healthy human volunteers. Peptide 38.G could therefore prove to be an important component in any new molecularly defined reagent used in the immunodiagnosis of tuberculous infection.

Infection with MRSA is a growing problem in the neurosurgical population, and most cases are hospital-acquired and are associated with longer hospital stays. Asymptomatic colonization by this organism is far more common than infection of the surgical wound, although there is still morbidity due to MRSA sepsis. Most patients with MRSA are discharged before eradication of infection is achieved, thus increasing the risk that the infection will spread in the community. Strict adherence to the basic principles of infection control is the key to eradication of MRSA.

SUMMARYStructural homology between microblal and human stress proteins has been postulated to be a basis forauloimmunizalion in chronic inflammatory diseases. Therefore, we estimated by ELISA titration the antibody levels to mycobaeterial (M) and human (H) recombinant hsp70 and M-hsp65 heatshock proteins in sera of patients with Crohn's disease (n = 29), ulcerative colitis {n = 20) and nontuberculous mycobacteria! disease of the lungs (/i = 20). Antibodies lo H-hsp60. separated by twodimensional gel electrophoresis. were tested in six sera of each group ofpatients. In Crohn's disease, antibody titre.s to the M-hsp65 antigen without detectable H-hsp60 binding were significantly elevated in 52"/i. ofthe patients. In contrast titres to both M-hsp7t)and H-hsp70 were demonstrable and correlated, but increased over control values only in lour (14";,} patients. The anlibody pattern in ulcerative colitis was found to be quite dilTerent: anti-H-hsp60 binding was demonstrable in most patients, although anti-M-hsp65 titres were nol elevated. Furthermore. 25"' i> of patients had significantly elevated titres lo M-hsp70. but not to H-hsp70. In non-tuberculous mycobacterial pulmonary disease, about 5{)"A. ofpatients had elevated titres to both hsp65 and hsp7l mycobacterial antigens bul not to the corresponding human proteins; patients with .'V/r('()/)t;(7(T(»/?(.\(V((j/j/inlection had ihe highest litres in this group. These results demonstrate the e.tistcnce of distinct diseaseassociated patterns in the human antibody response to stress protein antigens. However, these data are not sufficient to imply sensitization with mycobacleria in patients with inflammatory bowel diseases, since certain epilopes of heat-shoek proteins are shared by several bacterial genera.

129/Ola mice resemble WEHI 129J mice in that around 70% of the individuals in any given population resist a primary infection with Schistosoma mansoni. Squashed-organ autoradiographic tracking of [75Se]selenomethionine-labelled parasites has shown that the kinetics of worm migration in 129/Ola mice follows the expected pattern, and that all rodents harbour essentially similar numbers of worms on day 14 post-infection. Combined lung and liver worm recovery techniques have revealed, however, that segregation of mice into 'permissive' and 'non-permissive' individuals can first be detected on day 20. 'Non-permissive' mice are characterized by the absence of schistosome eggs at all times in the liver parenchyma and, in consequence, lack the attendant manifestations of pathology; they do, however, harbour a few stunted worms in the liver and significant numbers of adult schistosomes in the pulmonary vasculature. Histological analysis of sectioned lung tissue from such animals indicates that some lung-located schistosomes feed, pair and lay eggs. Nevertheless, eosinophil-enriched inflammatory reactions develop around such worms and the parasites themselves exhibit various manifestations of trauma, ranging from minor vacuolation to gut herniation and extrusion. The phenomenon of 'non-permissiveness' thus involves retardation of worm development in the liver and, in consequence, relocation of the parasites to the lungs, where they become subject to host effector responses.

SUMMARYThe possible role of infection with Mycobacterimn parattiherculo,sis (MAP) for the etiopathogenesis of Crohn's disease (CD) has been a matter of long-term controversy. In addition to similarities with the pathology of ruminant paratubereulosis, DNA tingerprinting eonfirmed the organism isolated from gut tissue, but thespecificity of the immune repertoire has not as yet been evaluated. We report here on a serologieal study of 29 patients with CD, 20 patients with ulcerative colitis and 18 healthy control subjects, using three antigens attributed with species-specificity and selective immunogenicity following MAP infection. Antibodies binding to the 38-kD band of MAP extract were demonstrable by the Western blot technique in 57% of CD patients. Antibody levels to the 24-kD (p24BCD) eathodic bands, determined by competition ELiSA using a monospecitic niuHne antiserum, and to the 18-kD protease-resistant purified baeterioferritin. delected by standard ELISA. were significantly elevated in 53'yu of CD patients. However, these three antibody specificities tested in individual CD patients did not show any correlation with eaeh other. Thus. 18''^ ofpatients were positive for all three specificities, whilst 84% had antibodies to at least one of the specifie antigens. Although the exact proportion of affected patients is yet to be defined, the serologieal results obtained support the view that MAP infeetion may play an etiological role in Crohn's disease.