Outbreak ofPneumocystis carinii pneumonia in a renal transplant unit

The charts for seven renal transplant recipients who developedPneumocystis carinii pneumonia were reviewed. They included six men and one woman transplanted a mean of 150 days before the diagnosis of this infection. Six presented at least one episode of acute graft rejection. Cytomegalovirus pneumonia was diagnosed in six of the patients. All patients were treated with cotrimoxazole. Global mortality was 43 %. In additional to the classic hypothesis of latentPneumocystis carinii reactivation in immunocompromised hosts, this and previous reports of outbreaks strongly suggest either a person-to-person transmission or acquisition from the environment. Molecular typing of isolates could be of value in identifying the source of such outbreaks. Chemoprophylaxis should be more systematically administered to renal transplant patients, co-trimoxazole being the drug of choice.     

Seroprevalence of anti-HIV antibodies in a rural Haitian population

A sero-epidemiological study was conducted from July to August 1988, in a haitian population living in rural area. Out of 116 serum samples searched for H1V1 antibodies and anti-HTLV1, 5.2% and 4.3% were reactive, respectively. Both positivity H1V1/HTLV1 was observed in one case. HBs Ag carriers were 13%. Analysis of seroreactive people in this population enhances the epidemiological trends of AIDS in Caribbean (rural spreading, heterosexual transmission, sex ratio levelling) which relate to african type AIDS.     

Squash Procedure for Protein Immunolocalization in Meiotic Cells

Several techniques have been developed for protein immunolocalization in meiotic cells. However, most of them include treatments that lead to cell disruption and are only suitable for prophase-I cells. We describe a novel squash procedure of cell preparation for protein immunolabelling of different meiotic stages. This procedure is an alternative to both cryosectioning and whole spreading procedures. We present results obtained in mouse spermatocytes with three different antibodies: the MPM-2 mAb against mitotic phosphoepitopes, an anticentromere serum and a polyclonal serum against the SCP3 protein of the axial elements and lateral elements of the synaptonemal complex. The procedure was tested for single and double immunolabelling. With this technique a large number of cells at different meiotic stages can be analysed. Cell stages are easily identified and cell and chromosome structures are preserved. Thus, it allows the study of chromosome behaviour and the relations hips between the different structural elements of the cell throughout meiotic divisions. Our procedure is also suitable for three-dimensional (3D) analyses and proved to be reliable in a wide range of systems including insects and mammals. In addition, the procedure may be interesting to obtain a rapid immunological diagnosis.     

Role of lymphocyte activation products (LAP) in cell-mediated immunity. I. Preparation and partial purification of guinea-pig LAP

Partial purification of soluble products of guinea-pig lymphocyte activation (LAP) was undertaken by fractional precipitation with ammonium sulphate, ion-exchange and Sephadex chromatography, and by immune precipitation of inducing antigen and of contaminating serum protein. During these purification steps the activity of macrophage migration-inhibition factor (MIF) was concentrated up to 1300-fold and separated from inducing antigen and serum protein. An endpoint assay was devised for expressing antigen-induced MIF activity of LAP fractions as weights of material giving 30% inhibition of migration (MI₃₀ doses).

MIF activity precipitated between 50% and 80% saturated ammonium sulphate and eluted from DEAE-cellulose at pH 7·9 at intermediate salt concentrations (0·03–0·2 M phosphate). On Sephadex gel filtration MIF activity was concentrated in fractions of molecular weight range 56,000–82,000 with a smaller amount of activity eluting from 20,000–56,000. After immune precipitation of extraneous protein and elution from DEAE-cellulose, LAP material was found to have an MI₃₀ dose of 0·4 μg.

Materials representative of antigen and serum protein-depleted MIF were selected for intralymphatic injection in order to determine whether MIF-rich LAP fractions were able to induce paracortical distension in guinea-pig lymph nodes (see following paper).

     

Marek's disease virus-induced transient paralysis in chickens. 3. Differentiation of field cases from classical Marek's disease by central nervous system lesions

Vasculitis with intramural pseudocyst formation primarily in the cerebellar white matter, but also in nuclei of the medulla, resulted in leakage of IgG and albumin and vacuolation of the neuropil (vasogenic oedema) in brains from chickens with clinical signs of Marek's disease virus (MDV)-induced transient paralysis (TP). Demyelination was absent. Chickens that had recovered from TP had a restored blood-brain-barrier, indicated by the rarity of vasculitis and vascular intramural pseudocysts in the cerebellum. In addition, the vacuolation and protein leakage were greatly decreased. The minor vacuolation resulted primarily from intramyelinic (cytotoxic) oedema. The small quantity of extravascular protein was being removed by microglial cells and astrocytes. In one chicken which failed to fully recover from TP (TP-prolonged) there was neither vasogenic oedema, cytotoxic oedema, nor vasculitis in the cerebellum. The medulla of the TP-prolonged chicken had a severe lymphocytosis, swollen axons, neuronal degeneration, secondary demyelination and some associated serum protein leakage. All TP-affected and TP-recovered chickens, and the TP-prolonged chicken, had perivascular mononuclear cell cuffs within all brain sections. Chickens with classical Marek's disease (MD) generally lacked CNS vacuolation, perivascular mononuclear cell cuffs, vasculitis and serum protein leakage. However, in a few cases of MD with severe perivascular mononuclear cell cuffs, focal demyelinating plaques were seen. These plaques had associated vacuolation, serum protein leakage, axonal spheroids and neuronal degeneration.