[Lung abscess caused by Rhodococcus equi in HIV infection: two cases].
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Biomedical subjects
Publications and source records attributed to G Pialoux.
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Rhodococcus (Corynebacterium) equi is a well-known Gram positive bacillus which is usually pathogenic in farm animals but rarely causes diseases in humans. Only 30 cases of human infection have been reported in the literature. R. equi has recently been added to the list of opportunistic agents in severe HIV infection. Its most common manifestation in immunocompromised is a slowly progressive pneumonia which may cavitate. R. equi pulmonary infections are difficult to treat: they usually require prolonged parenteral antibiotic therapy and often need surgical treatment. Two cases of cavitary pneumonia in patients with severe HIV infection are reported here. In one case the disease was associated with pulmonary Kaposi sarcoma and pneumocystis pneumonia; the other case was the first opportunistic infection in the course of HIV infection.
Acalculous cholecystitis and sclerosing cholangitis due to Cryptosporidium sp, and cytomegalovirus have been described in patients with the acquired immunodeficiency syndrome (AIDS). However, in about 40% of cases of AIDS-related biliary disease, no opportunistic pathogen is identified. The current case report describes the first case, to the best of the authors' knowledge, of AIDS-related sclerosing cholangitis associated with microsporidiosis. Enterocytozoon bieneusi was detected in the duodenum and bile by means of light microscopy and confirmed by electron microscopy. Microsporidian infection should be suspected in patients with AIDS-related sclerosing cholangitis as well as in cases of diarrhea in which none of the usual pathogens are found.
In progressive systemic scleroderma, a disease of protean manifestations, involvement of the gastrointestinal tract is noted infrequently in patients who are asymptomatic, and is rarely fatal. We report the case of a 65-year-old woman who was admitted for ascitis related to a non A, non B cirrhosis. The patient presented with bacterial peritonitis due to colonic perforation by fecal impaction associated with sclerodermic involvement. Pathologic study of the resected colon showed that the true muscularis was very atrophic and fibrotic, characteristic of scleroderma. To our knowledge, this cause of ascitic fluid infection has not been previously reported.
Various polymerase chain reaction (PCR) assays have been devised for the rapid identification of mycobacteria in clinical specimens. To assess the value of such assays in routine laboratory work the results obtained by PCR were compared with those obtained by standard microbiological methods for 514 specimens collected for investigation of mycobacterial infection. Specimens were tested for the presence of Mycobacterium tuberculosis complex and atypical mycobacteria in two assays, one based on amplification of the 65 kDa gene and the other on the IS6110 insertion sequence. For the 489 samples that did not contain inhibitors of the amplification reaction PCR findings correlated well with bacteriological and/or clinical data in 476 (97.4%). 6 PCR results turned out to be false negatives, 3 to be false positives and 4 to be mis-identification of strains. Pre-treatment of samples with guanidium thiocyanate reduced the proportion of false-negative results and of samples that contained inhibitors. This study confirms the potential of DNA amplification for early diagnosis of mycobacterial infections.
R 82913, a tetrahydroimidazobenzodiazepinthione (TIBO) derivative with potent activity against human immunodeficiency virus 1 (HIV-1) in vitro, was given to 22 patients with AIDS or AIDS-related complex in a dose-escalating pilot study. Doses of 10 to 300 mg administered daily by intravenous infusion were well tolerated for up to 50 weeks, with no haematological or biochemical evidence of toxicity. Mean OKT4 cell count rose slightly during the second month of treatment when higher steady-state plasma concentrations of the drug were achieved. Median p24 antigen concentration fell by 41% during the first month of therapy. When the rise in p24 antigen before therapy was compared to the fall during treatment, end-point analysis showed a significant difference (p less than 0.03). The combination of potent antiretroviral activity in vitro and the observed effect on HIV p24 antigen and absence of toxicity in vivo indicate that R 82913 and related TIBO derivatives merit further study in the treatment of retroviral infections.
A case of neoplastic transformation of lesions of chromoblastomycosis is reported in a 67-year-old farmer from French Guyana. An interesting aspect of this case was the appearance of new cutaneous lesions of chromoblastomycosis, in a different site from the original lesion, and the presence of an infected synovial cyst. The potential therapeutic role of itraconazole is discussed.
B cell subpopulations, as defined by double-labelling techniques with CD5 and CD19 monoclonal antibodies (MoAbs), were serially studied in 335 HIV-1 seropositive patients. At the time of the first consultation, no important modifications in either CD5+ or CD5- subpopulations were observed, whatever the stage of the disease. However, in 18 out of the 335 patients (5.37%), a sharp increase in B cells exceeding 20% and 300/mm3 was observed. This increase in B cells was mainly accounted for CD5-CD19+ B cell subpopulations and was associated with: (i) evolution of the disease, since only four patients presented it at their first consultation (one lymphadenopathy-associated syndrome (LAS) and three AIDS); (ii) advanced stages of disease since, at the time of B cell augmentation, two patients were staged as LAS, four as ARC and 12 as AIDS; (iii) a high incidence of non-Hodgkin's lymphomas (NHL) since three out of the 18 patients presented a histologically confirmed NHL and three others a clinical pattern compatible with this diagnosis. However, in three patients with B hyperlymphocytosis, polymerase chain reaction (PCR) studies of immunoglobulin gene rearrangement revealed the existence of a polyclonal expansion of B cells. These results justify inclusion of a pan-B cell marker in routine phenotypic studies of HIV-infected individuals, as well as the search for NHL among patients presenting this abnormality.
Carbapenem resistance was studied in a clinical isolate of Enterobacter cloacae, strain 201 (MIC of imipenem and meropenem, 16 micrograms/ml). This strain was analyzed comparatively with the carbapenem-susceptible parent strain 200, an equally susceptible revertant, 201-Rev, and in vitro-selected mutants with different levels of carbapenem resistance. All strains produced similarly high amounts of the same cephalosporinase (pIapp = 8.8). Strain 201 apparently lacked two major outer membrane proteins of ca. 37 and 38 kDa, while 201-Rev produced only the 37-kDa protein. The permeability coefficient, determined with cephaloridine, was reduced up to ninefold in the resistant strains which also showed a substantial reduction in the uptake of [14C]meropenem. The introduction of the plasmid-borne ampD gene (whose product decreases the expression of ampC) resulted in almost complete cessation of cephalosporinase production in all strains and a substantial decrease in the MICs of the carbapenems which remained, however, 8- to 16-fold higher than those determined for the susceptible strains containing the ampD gene. This "residual" resistance was attributed to reduced outer membrane permeability. The contribution of cephalosporinase production was verified in a reverse experiment, in which the introduction of ampC into a low-level cephalosporinase producer resulted in a fourfold increase in the carbapenem MICs. From these results, we infer that reduced outer membrane permeability and high-level cephalosporinase production can operate in conjunction in clinical isolates of E. cloacae to confer imipenem resistance.
A case of strongyloidiasis hyperinfection is reported in a 59 year-old man who presented cortico-dependent bronchial asthma. Several points of this case are uncommon: the long latency period (40 years), simultaneous aggravation of asthma requiring increasing doses of corticosteroids, and above all, liver and biliary tract involvement. Disseminated strongyloidiasis is widely believed to be precipitated by impairment of cell-mediated immunity. It is therefore unlikely that infestation of the liver and the biliary tract can interfere with hepatic function.
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Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease which occurs in immunodepressed subjects and is particularly frequent in AIDS. Some authors having drawn attention to the protean aspect of the disease and claimed that AIDS may lose its basic characteristics and affect the grey matter as well as the white matter, we reviewed a series of 8 patients who had been biopsied and/or autopsied and had been examined at least once by MRI. In this series, contrary to what is regularly observed in toxoplasmic abscesses we did not find any lesion of the grey matter or any mass effect. On the other hand, we confirmed that PLM is not multifocal in all cases and that it course may be interrupted by prolonged remissions. The MRI criteria for PML therefore are reliable, provided multiple T2-weighted slices in coronal plane are performed, clearly showing the anatomy of the white fibres affected. However, it must be borne in mind that HIV-infected patients often have other associated brain pathologies, especially when the immune deficiency increases.
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Intrathecal (IT) immunity was assessed by simultaneous analysis of paired cerebrospinal fluid (CSF) and sera of 37 patients infected by human immunodeficiency virus-1 (HIV-1). Only 8 of these 37 patients had no neurological or neuropsychiatric symptoms. There were 3 prominent abnormalities observed: (1) IT IgA production occurred in 15 patients, IT IgM production in 14 patients, and IT IgG production in 34 patients. (2) IT Anti-HIV-1 antibody specific activity (ASA) was higher than in serum in 33 of the 37 patients indicating that IT synthesis of antibody specific for HIV-1 occurs even in asymptomatic patients; IT anti-HIV-1 antibody synthesis was not correlated with clinical severity or neurological involvement. IT anti-herpes simplex ASA was also higher than serum ASA in 6 patients indicating a possible associated herpes simplex virus infection. (3) IT production of the complement component C4 was found frequently and was highly correlated with increased serum C4. IT C3 levels were decreased in 21 of 37 patients indicating that complement activation is a frequent accompaniment of the IT immune response in HIV-1-positive patients. These results indicate a unique and localized IT immune response which is different from the pattern observed in the systemic immune compartment in HIV-1-seropositive individuals and from the pattern common to the other CNS infectious diseases.
Blood samples were studied, prior to medical terminations of pregnancy, in two second trimester fetuses with HIV-positive mothers. Fetal blood was obtained from the umbilical vein under ultrasound guidance. No evidence of infection was found in either fetus. In particular, lymphocyte subpopulations were at normal levels and cultures yielded no reverse transcriptase activity. Postmortem findings were normal. Reliable means for prenatal diagnosis of HIV infection, with a minimal risk of false-negative results, have yet to be developed. However, further studies using fetal blood sampling should be useful for the management of HIV-positive pregnancies.
CD1 monoclonal antibodies were assayed on peripheral blood mononuclear leukocytes (PBML) of type 1 human immunodeficiency virus (HIV1)-infected patients using immunogold technique. Using IOT6 monoclonal antibody, a significant increase of the CD1 positive cells per microliter of blood was found in acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) patients (265 +/- 34/microliters, n = 44 and 491 +/- 64/microliters, n = 36, respectively) as compared to controls (108 +/- 11/microliters, n = 43, P less than 0.001). These findings were confirmed with four other CD1 monoclonal antibodies in six patients. Characterisation of these CD1 positive cells showed that they were double stained with either CD4 or CD8 monoclonal antibodies. Moreover, cytochemical analysis of these cells showed the absence of myeloperoxidase activity and ultrastructural examination did not reveal Birbeck granules, well known to characterise the Langerhans cells. Further investigations are warranted to assess the biological and clinical relevance of these findings.