Mycoplasma-like organisms in Hodgkin's disease

Mycoplasma-like organisms in Hodgkin's disease

centre treats approximately 50 new patients per year with Similar specialist units in the largest hospitals in this disease. central and eastern Slo...

573KB Sizes 0 Downloads 58 Views

centre treats

approximately 50 new patients per year with Similar specialist units in the largest hospitals in

this disease. central and eastern Slovakia have been established. It has been clearly shown that centralisation of treatment of nonseminomatous cancers improves outcome in addition to any benefit from being enrolled into clinical protocols.I Ivan Plesko, Dalibor Ondrus, *Peter

Boyle

Cancer Research Institute, Slovak Academy of Sciences, 812 32 Bratislava, Slovakia; Department of Urology, Comenius University Medical School, Bratislava, Slovakia; and *Division of Epidemiology and Biostatistics, European Institute of Oncology, 20141 Milan, Italy

1 Boyle P, Kaye SB, Robertson AG Changes in testicular cancer in Scotland. Eur J Cancer Clin Oncol 1987; 23: 827 30 2 Boyle P, Maisonneuve P, Kaye SB. Testicular cancer in Central Europe. Lancet 1990; 335: 1033 3 Ondrus D, Hornal M, Matoska J, Kausitz J, Belan V, Carsky S. Chemotherapy of testicular cancer: 10-year experience. Neoplasma 4

1993; 40: 247-53. Harding M, Paul J, Gillis CR, Kaye SB. Management of malignant teratoma: does referral to a specialist unit matter? Lancet 1993, 341:

depigmentation 31% (figure, top). 75% of patients’ children had hair alterations: torsions 58% and swelling 25%. Electronmicroscopy confirmed these findings (figure, bottom). No control subject showed morphological alterations. This is the first report of hair abnormalities in Alzheimer’s disease. Some people with neurogenetic or metabolic diseases (such as Steinert disease and Lesch-Nyhan disease) have similar abnormalities. We are studying hair from people with familial Alzheimer’s disease (in which a specific genetic defect can be detected on chromosome 1, 14, or 21) and other types of dementias to define better the use of this abnormality in the diagnosis of Alzheimer’s disease. *G Bruno, L Brusa, A Rossi, S Calvieri *Department of Neurological Sciences and Institute of Dermatology, University of Rome "La Sapienza", 00185 Roma, Italia

1

McKann G, Drachman B, Folstein M. Clinical diagnosis of Alzheimer disease: report of the NINCDS-ADRDA. Neurology 1984; 34: 939-44.

999-1002.

Hair abnormalities in Alzheimer’s disease SiR-Most reports on the involvement of skin in Alzheimer’s disease have focused on biopsies (amyloid deposits) and culture of fibroblasts (alterations of enzymic activities and cell metabolism). We examined hair samples from 13 patients (nine M, four F) (mean age 66 [SD 3]) with mild to severe Alzheimer’s disease (MMSE score from 8 to 21), 12 unaffected children (five M, seven F) (mean age 36 [2]); and 15 normal controls (mean age 65-3 [5]) (seven M, eight F). Diagnosis of Alzheimer’s disease was based on NINCDSADRDA criteria.’ Hair samples were cut in the first cm from the parietal areas of the scalp and kept in sterile glass tubes. Samples were studied under direct and polarised light with a Leitz Laborlux 12POL microscope; then under a scanning electron microscope (Philips 515/s). The examiner was blind to the origin of the samples. The analysis of the hair shaft under direct and polarised light showed changes in 85% of patients with Alzheimer’s disease: torsions 54%, cuticular alterations 38%, and

Mycoplasma-like organisms in Hodgkin’s disease SiR-Sauter presents a case for the possible role of bacteria in the aetiology of Hodgkin’s disease.’ He offers crown gall

model;

suggest mycoplasma-like organisms (MLO). proliferative disease in plants and have the potential to cause proliferative disease in human beings. Furthermore, Hodgkin’s disease has many features seen in as a

MLO

we

cause

MLO disease.2 MLO are non-cultivable cell-wall-deficient intracellular bacteria. They replace the cytoplasm and destroy the nucleus of parasitised cells to cause cellular proliferation, dysfunction, and death. They are well-known plant pathogens and respond to antibiotics.’ They have been identified within intraocular leucocytes2,3 and retinal-pigment epithelial cells4 of patients with chronic idiopathic intraocular inflammation. Human MLO inoculated into murine eyelids produce lymphocytic inflammatory orbital pseudotumours and intraocular inflammations. The organism disseminates to the major organs to produce morbidity and accelerated mortality. A lymphocytic response with histopathological features of collagen vascular disease is seen.2 Human-MLO and mouse-MLO diseases respond to

rifampicin. 2,4 MLO produce granulomatous inflammation in human beings and in mice. We suggest this could be a reaction to MLO hopanoids. Hopanoids are inert lipids found only in bacteria and a few species of ferns. They are structurally and functionally similar to cholesterol in mammalian cells.s We have detected hopanoids within MLO-parasitised ocular leucocytes, but technical difficulties have prevented characterisation of the lipid-side chain (unpublished observations). Extracellular mycoplasmas possess potent lymphocytic mitogens, mutagens, and toxins and it is reasonable to assume MLO have similar properties. MLO-parasitised cells display distinctive ultrastructural nuclear changes including perinuclear halos, nuclear lysis, clumping of nuclear

Figure: Top:

patient with

cuticular alterations in hairs of a Alzheimer’s; polarised light microscopy. Bottom: torsion in hair; electron microscopy

chromatin, destruction of nuclear membranes, and eventual loss of the nucleus.2 We believe these changes are signs of MLO parasitisation and are responsible for proliferative disease. We have observed systemic lymphoproliferative disease in MLO-inoculated mice which was not seen in controls. Despite decades of effort, no culture system exists for MLO. They can, however, be readily detected by common laboratory techniques. Transmission electronmicroscopy 901

identities their unique ultrastructure within involved cells. Their distinct 16s bacterial ribosomal subunit DNA allows identification and speciation. The identification of MLO in Hodgkin’s disease could be an interesting development. Lewis Johnson, *Emil Wirostko, William Wirostko, Barbara Wirostko Department of Pathology and *Edward S Harkness Eye Institute, ColumbiaPresbyterian Medical Center, New York, NY 10032, USA; Eye Institute, Medical College of Wisconsin, Milwaukee, Wisconsin; and Department of Ophthalmology, Cornell University Medical Center, New York

1 2

3

4 5

Sauter S. Is Hodgkin’s disease a human counterpart of bacterially induced crown-gall tumours? Lancet 1995; 346: 1433. Wirostko E, Johnson LA, Wirostko BM, Farris RL. Mycoplasma-like organisms and ophthalmic disease. Trans Am Ophthal Soc 1993; 91: 85-98. Steel DH, Richardson J, Aitken DA. Acute bilateral optic disc neovascularization. Retina 1994; 14: 362-69. Fould WS. The uses and limitations of intracular biopsy. Eye 1992; 6: 11-27. Ourisson G, Rohmer M, Poralla K. Prokaryotic hopanoids and other polyterpenoid sterol surrogates. Ann Rev Microbiol 1987; 41: 301-33.

Strong preference "to donate" among HIV-

positive

blood donors in Zimbabwe

SiR-Post-donation interviews with blood donors testing in the USA found that obtaining HIV test results was a motivating factor in the decision to donate blood.1.2 Counselling of HIV-positive donors at the Zimbabwe National Blood Transfusion Service (NBTS) appears to corroborate these findings. Because there are no voluntary free HIV testing sites in Zimbabwe, voluntary blood donation may provide an opportunity for persons to determine their serostatus. The clear implication is that persons at risk for HIV infection who are seeking to know their serostatus might be a substantial source of laboratory false-negative and "window period" blood donations. In an attempt to distinguish between persons seeking HIV testing and those wishing to become regular blood donors, we offered confidential HIV counselling and testing to a consecutive sample of 1239 voluntary, first-time, adult blood donors in Harare, Zimbabwe. After explaining the importance of not donating blood if at risk for transfusiontransmissible infections, donors were given the option of giving a sample of blood that would be tested for HIV, syphilis, hepatitis B, and hepatitis C in lieu of donating a full unit of blood. While persons choosing either option may obtain their test results, no additional incentives were offered to donate a full unit of blood. All persons screening negative for the four infections were invited to become regular donors. Despite a high overall prevalence of HIV infection (14-8%), only 23 of the 1239 blood donors (1 -9%) chose confidential HIV counselling and testing over donating a full unit of blood. Furthermore, only 8-7% of persons choosing "to test" (two of 23) were HIV positive compared with 14-9% of persons choosing "to donate" (181 of 1216), a non-significant trend towards decreased HIV prevalence among those choosing "to test" (p=041). The vast majority of HIV-positive donors (98-9%) chose "to donate". Offering confidential HIV counselling and testing at the time of blood donor recruitment did not identify a substantial number of persons seeking HIV testing, nor did it identify donors likely to be HIV positive. The stigma of being identified as "at risk", coupled with availability of test results when choosing "to donate", may have created a strong bias against choosing "to test". Other mechanisms are required to encourage self-deferral among high-risk persons volunteering for blood donation in order to be

HIV-positive

902

identify donors likely to be HIV While free HIV counselling and testing may serve a positive. vital role in slowing the wider HIV epidemic, our findings suggest that offering free testing at the time of blood donation in Zimbabwe is not likely to reduce HIV contamination in the blood supply. tested for HIV and to

David Mvere, Rodwell Shamu, Regis Makoni, Shán Elizabeth Nhau, *William McFarland

Lloyd,

*Center for AIDS Prevention Studies, University of California, San Francisco, California, 94105, USA; and the Zimbabwe National Blood Transfusion Service Box A 101, Avondale, Harare, Zimbabwe

1 2

Kleinman SH. Interview studies of HIV seropositive donors. Vox Sang 1994; 67 (suppl): 265-66. Doll LS, Petersen LR, White CR, Ward JW. Human immunodeficiency virus type 1-infected blood donors: behavioural characteristics and reasons for donation. Transfusion 1991; 31: 704-09.

HIV-1 group O and group M dual infection in Bénin SIR-HIV-1 is subdivided into group M (Major) viruses, which are worldwide, and group 0 (Outlier) viruses, which have been reported mainly in Cameroon and among Cameroon people living in France, Germany, and Belgium.’ Between 1993 and 1994, sera from 142 HIV-1-

seropositive people (128 prostitutes, eight pregnant women, six people consulting for STD symptoms) were collected in Benin. Antibody reactivity to synthetic group 0 V3-loop peptides, ANT70, CA9,’ and VI6862 was monitored with ELISA. 1,3 Reactive samples were confirmed by line immunoassay (LIA) (Innogenetics, Belgium, for research purposes only)’ and specific "in house" group 0 ANT70, CA9, and VI686 western blots.I,3 Antibody reaction with group 0 ANT70 V3-loop peptide in LIA and/or with gpl20 envelope proteins on a specific ANT70 western blot is considered indicative of group 0 infection.I,3 20 out of 142 HIV-1-seropositive people had antibody reactivity to one or more group 0 V3-loop peptides in ELISA. One out of 20 reactive samples reacted with the group 0ANT70 V3-loop peptide in LIA, and had antibodies to p66, gp41, p33, p24 on group 0 ANT70, CA9, and VI686 western blot, suggesting group 0 infection. To confirm this result, RNA was extracted from the serum of this individual and RT-PCR was carried out with specific primers to distinguish group 0 and M infection. For both group 0specific and M-specific primers, we previously reported 100% sensitivity and specificity.4 PCR was positive with both group 0-specific and M-specific primers, which suggested a mixed group O/M infection. Sequencing and phylogenetic analysis of the amplified pol fragments (267 bp)2 confirmed this observation. The HIV-1 group O/M dually infected individual was a woman, 19 years old when the sample was collected in 1993. She was married and pregnant with her third child. She was of a Benin origin (a Fon) but was born in Côte d’Ivoire. Double infection with genetically very diverse HIV-1 group M and 0 viruses may occur. Benin is the fifth African country where group 0 infection is reported (others are Cameroon, Gabon, Equatorial Guinea, and Nigeria). Laboratory work Nationaal Fonds

supported by grant number 3-3025-91 of the Wetenschappelijk Onderzoek, Brussels. Field work was supported by grants from the WHO Global Program on AIDS (STDlSI6/181/27) and the Reseau Sida of the Association des universites partiellement ou entierement de langue franaise (X/1.20.02/0l/93.10.4) was

voor

L Heyndrickx, M Alary, *W Janssens, N Davo, G van der Groen *Department of Microbiology, Institute of Tropical Medicine, Antwerpen, Belgium; Centre de Recherche, Hôpital du St-Sacrement, Québec, Canada; Programme national de lutte contre le sida, Cotonou, Bénin; CREDESA, Pahou, Bénin