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Biomedical subjects

A Zumla

Publications and source records attributed to A Zumla.

At least 73 records · Page 4Linked to original sources
PubMed1994

Gut parasites in HIV-seropositive Zambian adults with diarrhoea.

We undertook a nine month study to define the frequency of parasitic infections in adults with diarrhoea presenting at the medical filter clinic and the Dermatovenereology clinic of the University Teaching Hospital in Lusaka, Zambia. A total of 287 patients with diarrhoea were enrolled in the study; 130 from the adult medicine filter clinic recruitment consulting room and 157 patients from the Dermatovenereology clinic. Of 130 patients from the adult filter clinic, 85 (65%) were HIV-seropositive and 45 (35%) were seronegative for HIV. Out of 85 HIV-seropositive patients, 58 (68.2%) had acute diarrhoea and 27 (31.8%) had chronic diarrhoea. Of the 45 HIV-seronegative patients, 35 (77%) had acute diarrhoea and 10 (23%) had chronic diarrhoea. All of the 157 patients recruited from the Dermatovenereology clinic were HIV-seropositive. Of these, 97 (62%) had chronic diarrhoea; 7 (4%) had acute diarrhoea, and 53 (34%) patients had no diarrhoea. The common parasites detected were Ascaris lumbricoides, hookworm, Entamoeba coli, and Cryptosporidium spp. Isospora belli and Cryptosporidium spp were seen only in the HIV-seropositive group. In the Dermatovenereology clinic there was a statistically significant difference between parasite detection rate of Isospora belli and Cryptosporidium spp in HIV-seropositive patients with chronic diarrhoea compared to asymptomatic HIV-seropositive individuals P < 0.01 and p = 0.05, respectively). A significant difference in detection rates of Entamoeba coli was seen between the HIV-seropositive group in the Dermatovenereology clinic [17 (10.8%) out of 157] compared to 1 (1.5%) out of 85 in the adult medicine filter clinic.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Opportunistic Infections↗
PubMed1993

Seroprevalence of human immunodeficiency virus type 1 infection in Zambian children with tuberculosis.

Descriptions in the medical literature of human immunodeficiency virus type 1 (HIV-1) in children with tuberculosis (TB) are scanty. This study determined the seroprevalence of HIV-1 in 237 hospitalized children between the ages of 1 month and 14 years with a clinical diagnosis of TB (125 males and 112 females) and in 242 control children (149 males and 93 females). The overall HIV-1 seroprevalence rate in patients with TB was 37% (88 of 237) compared with 10.7% (26 of 242) among the control group (P < 0.00001: odds ratio 5.37, 95% confidence interval = 3.21 < 5.37 < 9.47). HIV-1 seropositivity in children with TB ranged from 53% (31 of 58) in the 12- to 18-month age group to 14% (9 of 61) in the 10- to 14-year-olds. The risk of TB attributable to HIV infection was 29%. The predominant clinical presentation in both seronegative (84.6%) and seropositive (89.7%) groups was that of pulmonary TB and there were no significant differences in clinical presentation between the two groups of patients. Only 54.8% of the patients attended follow-up clinics regularly whereas 32% were lost to follow-up within 3 months. Bacillus Calmette-Guérin vaccination coverage was 87.3% among TB patients and 90.5% in the controls. No significant differences in B. Calmette-Guérin vaccination rates between the seronegative and seropositive children were seen. Coinfection with HIV and TB in children is now one of the major public health problems in Zambian children.

AIDS-Related Opportunistic Infections↗
PubMed1993

Cutaneous hypersensitivity reactions due to thiacetazone in the treatment of tuberculosis in Zambian children infected with HIV-I.

Tuberculosis is one of the most common infections in Zambian adults and children infected with HIV. In Africa, cutaneous hypersensitivity reactions attributed to thiacetazone during treatment of tuberculosis in adults infected with HIV-I have been well documented. This study monitored adverse drug reactions during treatment for tuberculosis over an 18 month period (1 April 1990 to 31 October 1991) in 237 children with a clinical diagnosis of tuberculosis (125 boys and 112 girls; 88/237 (37%) infected with HIV-I) and 242 control children (149 boys and 93 girls; 26/242 (11%) infected with HIV-I). Twenty two (9%) of the 237 children with tuberculosis developed hypersensitivity skin reactions during the course of treatment. Adverse skin reactions were seen more often in children infected with HIV than in those who were not (odds ratio 11.65, 95% confidence interval 3.07 to 34.88). These represented 19 (21%) of 88 children infected with HIV and three (2%) of 149 children not infected with HIV. These skin reactions occurred after a period of treatment ranging between two and four weeks among 14 children receiving the HST (isoniazid, streptomycin, thiacetazone) regimen and eight children receiving the HSTR (isoniazid, streptomycin, thiacetazone, rifampicin) regimen. Twelve (55%) of the 22 children who reacted adversely to treatment developed the Stevens-Johnson syndrome. All 12 of these children with the Stevens-Johnson syndrome were infected with HIV. The mortality among these children who developed the Stevens-Johnson syndrome was 91% (11 of 12 died within three days of the onset of the reaction). No further reactions were observed in the 11 children who recovered from the cutaneous hypersensitivity reactions after thiacetazone was discontinued over a period of six months of further treatment of tuberculosis. The results of this study were in part responsible for the recommendations put forward by the World Health Organization to avoid the use of thiacetazone in the treatment of tuberculosis in children infected with HIV.

AIDS-Related Opportunistic Infections↗
PubMed1992

Co-expression of human T cell receptor chains with mouse CD3 on the cell surface of a mouse T cell hybridoma.

In this study we demonstrate that human T cell receptor (TcR) chains can be co-expressed with murine CD3 on the cell surface of a murine T cell hybridoma. Human TcR alpha and beta genes from the Jurkat leukaemic cell line were transfected into a TcR-negative mouse T cell hybridoma, TG40. The Jurkat TcR was successfully co-expressed at the cell surface with mouse CD3 components. Brightly staining transfectants were selected by fluorescence-activated cell sorting, and levels of expression comparable to a normal T cell line were achieved suggesting that the human TcR dimer assembled efficiently with the mouse CD3 complex. Northern blot analysis demonstrated similar levels of TcR messenger RNA to those found in the parental Jurkat line. Although we have not formally demonstrated surface expression of the Jurkat TcR alpha chain, the residual alpha gene transcript which is present in murine TG40 line is non-expressible. In order to test the signalling capacity of this human/mouse complex, the transfectants were stimulated with an anti-V beta 8 monoclonal antibody. This stimulus led to interleukin-2 production by the transfectants, demonstrating the delivery of a transmembrane signal. In addition, B10.A mice were immunised with the transfectants, and the antisera from these mice stained the transfectant and the Jurkat cell line, but not the parental T cell hybridoma. This interspecies transfection approach should now permit us to explore the requirements for T cell activation, the constraints on TcR alpha beta chain pairing, and creates ideal reagents for inducing a mouse anti-human TcR-specific response with a view to producing panels of anti-human TcR monoclonal antibodies.

Animals↗
PubMed1992

Use of a murine T-cell hybridoma expressing human T-cell receptor alpha- and beta-gene products as a tool for the production of human T-cell receptor-specific monoclonal antibodies.

We describe the production of mouse monoclonal antibodies specific for the human TcR using as the immunogen transfected murine T-cell hybridoma cells coexpressing mouse CD3 with human Jurkat TcR alpha and beta chains. The shortage of monoclonal antibodies (mAbs) specific for the human TcR-V alpha and V beta families reflects the difficulties in their production by conventional methods using whole human T cells or purified soluble receptors as immunogens. As an alternative strategy to circumvent these difficulties, we have generated a transfected mouse T-cell line expressing a human (Jurkat) TcR alpha beta dimer in a complex with mouse CD3. The parental mouse T-cell line, TG40, is a cell surface TcR-negative, cytoplasmic CD3-positive variant of the mouse T-cell hybridoma 2B4. The human-TcR alpha beta expressing mouse transfectant was used to immunize mice with the same genetic background as the parent mouse T-cell line, and a human TcR-specific response was successfully achieved. MAb-producing hybridomas were generated by fusing spleen cells from the immunized mice with the mouse myeloma cell line NSO. Of 124 hybridoma supernatants screens, 72 showed reactivity to the human T-cell line Jurkat. Twenty-four of the hybridomas producing human (Jurkat) TcR-specific antibodies were cloned and screened for reactivity to Jurkat TcR. Several IgG2b and IgM mAbs specific for the Jurkat T cell line were selected on the basis of their ability to modulate surface CD3 expression on Jurkat cells. Most of the antibodies do not stain other TcR-expressing human T cell leukemia cell lines, implying specificity for the variable domains of the Jurkat TcR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Chemotherapy and immunity in opportunistic parasitic infections in AIDS.

Parasitic diseases are endemic in parts of the tropics, but there is no convincing evidence that their prevalence or incidence is increasing due to the HIV epidemic. Available scientific data on parasitic infections in patients with the Acquired Immunodeficiency Syndrome (AIDS) suggests a predominance of Pneumocystis carinii, Toxoplasma gondii and Cryptosporidium spp. For reasons which are unclear, parasitic infections such as Plasmodium falciparum, Strongyloides stercoralis and Entamoeba histolytica, where cell-mediated immune responses are also thought to be significant, do not appear to be opportunists of importance. It is being increasingly recognized that chemotherapy for parasitic diseases has a host-dependent component, although scientific data on this subject remain scanty. The management of opportunistic parasitic infections in patients infected with HIV is dogged by failures and relapses, aptly illustrating the notion of the relationship between chemotherapy and the immune response. This review discusses the immunity and chemotherapy of opportunistic parasite infections in patients infected with the Human Immunodeficiency Virus (HIV).

AIDS-Related Opportunistic Infections↗
PubMed1992

Superantigens, T cells, and microbes.

It is well recognized that toxins of Staphylococcus aureus and Streptococcus pyogenes are responsible for a wide range of clinical conditions, although their precise mode of action remains unclear. Recently, there has been a resurgence of interest in these toxins, now grouped with superantigens, because they cause profound alterations in the immune system homeostasis. Superantigens are molecules, including endogenous retroviral gene products and microbial toxins, that share a unique set of characteristics. They bind with high affinity to major histocompatibility complex class II at regions distinct from the conventional antigen binding groove and cause prolific activation or anergy of T cells with certain T cell receptor variable-region gene families. Whilst most of the superantigens described to date are products of bacteria or viruses, the presence of superantigens in parasites and their role in disease pathogenesis remain to be defined. It is probable that associations are present between superantigen-induced proliferation or anergy of peripheral blood T cells and clinical manifestations of human infectious diseases. The identification of these may pave the way toward a better understanding of disease pathogenesis and the possible development of newer immunotherapeutic regimes. This review summarizes the current thinking on microbial superantigens, their association with human T cells, and speculations about their significance.

Animals↗
PubMed1991

T cell receptor expression in Sjögren's syndrome.

T lymphocytes expressing the gamma/delta T cell receptor and B lymphocytes expressing CD5 are known to occur in expanded numbers in the peripheral blood of patients with primary Sjögren's syndrome. The cellular infiltrates for the surface phenotypic markers for alpha/beta and gamma/delta T cell receptors, CD4, CD8, CD45, and CD5 were examined in lip biopsy specimens from two patients with primary Sjögren's syndrome, six with secondary Sjögren's syndrome, and seven healthy controls. Most of the Sjögren's lip biopsy cellular infiltrates were T lymphocytes of the CD4 subset expressing the alpha/beta T cell receptor (mean 70%). The low prevalence of gamma/delta T cell receptor bearing cells in lip biopsy specimens is maintained in Sjögren's syndrome (mean 1.5%), and thus it seems unlikely that these lymphocytes bearing the gamma/delta T cell receptor have a major role in the immunopathology of Sjögren's syndrome. Over 70% of cells within the lesional infiltrate of primary and secondary Sjögren's syndrome expressed the CD5 and CD45 cell surface molecules.

Antigens, CD↗
PubMed1991

Expression of a common idiotype PR4 in the sera of patients with leprosy.

The sera of 187 patients from across the leprosy spectrum were screened for the expression of the PR4 idiotype, which was first identified on a human hybridoma-derived monoclonal antibody from a patient with leprosy and found to react with the Mycobacterium leprae phenolic glycolipid and a variety of polynucleotides. Sixty per cent (51 out of 85) of patients with lepromatous leprosy (LL), 66% (33 out of 49) with borderline lepromatous (BL) disease, 47% (14 out of 30) with borderline tuberculoid (BT) leprosy, and 56% (13 out of 23) of tuberculoid (TT) patients were found to have significantly elevated titres of the PR4 idiotype in their sera compared with endemic controls, irrespective of the presence or absence of endemic malaria. Sera from 52 patients with tuberculosis were also screened as a control for mycobacterial infection. The PR4 idiotype was significantly elevated in 37% (19 out of 52) of these patients. No correlation between idiotype and serum immunoglobulins IgG and IgM was found, indicating that the concentrations of idiotype levels in sera were not merely a reflection of changes in serum immunoglobulin levels. It is hypothesized that the expression of the PR4 idiotype is due to certain germline genes preferentially expressed rather than being the result of polyclonal B cell activation.

Animals↗