In order to elucidate the mechanisms for the elimination of Leishmania, the histological evolution of the lesions of cutaneous leishmaniasis was studied in 118 biopsies from four geographical areas known to be associated with different species or sub-species of Leishmania. Basically there were 3 types of response: A, parasites were eliminated within intact macrophages which later evolved as epithelioid cells; B, they were eliminated as a result of the lysis of the macrophages either individually or in small clusters, but the process was incomplete; C, there was necrosis proceeding to completion at the centre of a focalised mass of macrophages. In B and C the release of parasites caused tissue destruction; epithelioid cells were immature and often sparse, though giant cells were seen in C. A more definite tuberculoid response was found in draining lymph nodes. The response (A, B or C) depended partly on the parasite load, partly on geographical factors. The relative proportions of macrophages, plasma cells and lymphocytes in the lesions varied with the parasite index, but the relationship was the same in all 3 types of response. This suggested that the 3 responses might be the outcome of a common immunological mechanism operating at different antigen levels or antigen-antibody ratios.

No abstract

SYNOPSIS An immunofluorescent test, using Giardia lamblia cysts as antigen, gave positive results in 32/36 cases of giardiasis with malabsorption, 0/2 cases of giardiasis without malabsorption, and 0/17 control patients without giardiasis or malabsorption. The test was positive in 10/34 patients with malabsorption in whom G. lamblia could not be detected by stool examination or biopsy; some of these cases were presumed to be cryptic giardiasis. There was a crude correlation between antibody titre and the severity of the histological lesion in thejejunum. The finding of a reliable source of antigen remains a problem.

Summary Skin biopsies of 20 patients with erythema nodosum leprosum were studied histologically, by acid-fast, silver and immunological methods for the demonstration of bacterial antigen, and by immuno-peroxidase for � variety of immunological fa ctors. The results were compared with those in 10 non-reacting lepromatous patients.At the centre of the ENL lesions there was always disintegration of macrophages and release of bacterial antigen, comprising cell walls and particulate or diffuse components of My cobacterium leprae. These products were found to combine first with IgM, later with IgG, which together with complement components of the classical pathway were present at the same sites. These complexes were fo und both extracellularly and in neutrophils and macrophages, and were constant features of acute stage lesions. C-reactive protein and B-lipoprotein were present in varying amounts and were associated partly with connective tissue. It is thought that CRP, and the related SAP, may be factors in the disruption or repair of elastic and collagen, which are conspicuous in some ENL lesions. The results support the view that ENL is an immune complex phenomenon, possibly self-perpetuating, occurring at the site of breakdown of small lepromatous granulomas. The immune complexes are extravascular and in this respect ENL differs from the classical 'serum sickness' described by Arthus.Erythema nodosum leprosum (ENL) is a reactional episode of lepromatous leprosy where large amounts of mycobacterial antigen and of corresponding antibodies provide evidence for an immune complex aetiology. Support for this hypothesis comes from disease manifestations,1 from the binding of C 1 q of sera fr om patients with ENL,2-5 and fr om the deposition of C 3 and immunoglobulins IgG and IgM in glomeruli.6, 7 ENL has been regarded as a clinical manifestation of the Arthus reaction because of the demonstration of granular deposits of C 3 and immunoglobulin in the lesions of some patients.8 The same group of workers in subsequent reports9, 1 0 concluded that the reaction was due to the trapping of 0305-7518/83/054095+ 13 $01 .00

E, EA and EAC rosetting techniques and Ig fluorescence were used in a study of receptor sites in cryostat sections of lesions through the spectrum of leprosy, and for comparison in some other mycobacterial and granulomatous lesions. Anti-C3, and trypsin were used as blocking agents. Lymphocytes in borderline lepromatous leprosy produced EA adherence and IgG fluorescence indicating B type cells. Lymphocytes in tuberculoid leprosy produced neither E or EA adherence and no fluorescence; these cells were presumed to be T cells. EAC and EA adherence was more marked in areas of macrophage infiltration, where there were few lymphocytes, than over the lympocytes themselves. Two distinct patterns emerged: (i) EA binding together with IgG fluorescence was seen in active lepromatous leprosy and could be localised to the surface of individual macrophages, and (ii) EAC binding together with IgM fluorescence was seen in the granuloma of tuberculoid leprosy and sarcoidosis, but could not be definitely related to cell surface; rather it was diffusely spread over the whole granuloma; EAC adherence was diminished by anti-C3 serum. Trypsin removed EA binding completely, but only diminished EAC adherence. It is suggested that the EA pattern indicates immunoglobulin receptors on macrophage and lymphocyte surfaces: and that the EAC binding (which is stronger than EA) involves C3 and IgM receptors at extracellular sites as well as C3 receptor sites on epithelioid cell surfaces. EA and EAC binding were enhanced in borderline tuberculoid leprosy in reaction and erythema nodosum leprosum, suggesting that immunoglobulin and complement receptor sites increase in number with enhanced hypersensitivity.