CHARACTERISTIC FEATURES: Piercing, an act that modifies the body, has progressed considerably in France over the last few years. The population involved has grown and become more diversified. Performed with a solid needle or a catheter, a wide variety of anatomic localizations are concerned, particularly the nose, ears, and navel. The shape of the "rings", generally made of surgical steel, niobium or titanium, varies greatly. Wound healing by epithelialisation can take up to several months. INFECTIOUS RISK: Between 10% and 20% of all piercings lead to a local infection. The most commonly found causal agests are Staphylococcus aureus, group A Streptococcus and Pseudomonas sp. These germs can cause severe life-threatening complications even in common localizations (earlobe). Viral transmission is another risk (hepatitis B, hepatitis C, hepatitis delta, HIV). A few cases of fatal fulminant hepatitis have been described immediately after piercing. SAFETY MEASURES: Generally performed under less than desirable sanitary conditions, safety measures are needed for piercing. Among professional "piercers", a certain number have emphasized the need for providing their clients with safer services. The prevention of infection risk should be a priority for all. Work along this line has been done in the United States and Canada. In light of the impact on public health, it is important to rapidly develop guidelines and regulations for piercing in France. Both professional piercers and health care workers should participate in developing these safety measures in order to assure their implementation.

Intestinal microsporidiosis caused by Enterocytozoon bieneusi is a cause of chronic diarrhoea in patients with HIV infection for which there is no current therapy. This study was designed to assess the safety and efficacy of oral fumagillin in this infection.A dose-escalation trial.Twenty-nine HIV-infected patients with E. bieneusi infection were consecutively enrolled in the trial. Oral doses of fumagillin were given to four groups of patients for 14 days: 10 mg/day (group 1), 20 mg/day (group 2), 40 mg/day (group 3), and 60 mg/day (group 4). Patients were seen at weeks 1, 2, 4 and 6 to assess safety and efficacy. Efficacy was assessed primarily by the clearance of microsporidia from stools and follow-up duodenal biopsies.Thirteen patients complained of abdominal cramps, vomiting or diarrhoea during the study, and three patients had fumagillin withdrawn because of adverse events. Thrombocytopenia, neutropenia and hyperlipasaemia were the most frequent biological adverse events. Twenty-one out of 29 patients transiently cleared microsporidia from their stools during the study. By week 6, however, all patients in groups 1, 2 and 3 had parasitic relapse. Interestingly, eight out of 11 (72%) patients treated with 60 mg/day (group 4) apparently cleared microsporidia from their gastrointestinal tract and gained weight. No parasitic relapse was documented in these eight patients during a mean follow-up of 11.5 months.Treatment with fumagillin at 60 mg/day for 14 days has promise as an effective oral treatment for E. bieneusi infections.

Objective: Intestinal microsporidiosis caused by Enterocytozoon bieneusi is a cause of chronic diarrhoea in patients with HIV infection for which there is no current therapy. This study was designed to assess the safety and efficacy of oral fumagillin in this infection.Design: A dose-escalation trial.Methods: Twenty-nine HIV-infected patients with E. bieneusi infection were consecutively enrolled in the trial. Oral doses of fumagillin were given to four groups of patients for 14 days: 10 mg/day (group 1), 20 mg/day (group 2), 40 mg/day (group 3), and 60 mg/day (group 4). Patients were seen at weeks 1, 2, 4 and 6 to assess safety and efficacy. Efficacy was assessed primarily by the the clearance of microsporidia from stools and follow-up duodenal biopsies.Results: Thirteen patients complained of abdominal cramps, vomiting or diarrhoea during the study, and three patients had fumagillin withdrawn because of adverse events. Thrombocytopenia, neutropenia and hyperlipasaemia were the most frequent biological adverse events. Twenty-one out of 29 patients transiently cleared microsporidia from their stools during the study. By week 6, however, all patients in groups 1, 2 and 3 had parasitic relapse. Interestingly, eight out of 11 (72%) patients treated with 60 mg/day (group 4) apparently cleared microsporidia from their gastrointestinal tract and gained weight. No parasitic relapse was documented in these eight patients during a mean follow-up of 11.5 months.Conclusion: Treatment with fumagillin at 60 mg/day for 14 days has promise as an effective oral treatment for E, bieneusi infections, (C) 2000 Lippincott Williams & Wilkins.

BACKGROUND: Acute renal failure syndromes are frequently encountered in patients with human immunodeficiency virus (HIV) infection. Most reported cases of acute renal failure are related to acute tubular necrosis, but many other causes of renal failure have been described in these patients. METHODS: The present work is a single-institution retrospective study of 92 HIV-infected patients with acute or rapidly progressing renal failure. In 60 cases, a renal biopsy was performed. For each patient we analysed clinical and pathological data, as well as the short-term prognosis. RESULTS: Ten different causes of acute or rapidly progressing renal failure were documented: (i) haemolytic uraemic syndrome (32 patients); (ii) acute tubular necrosis either of ischaemic-toxic origin (18 patients) or due to rhabdomyolysis (six patients); (iii) obstructive renal failure which was either extrinsic (two patients), drug-induced (13 patients) or secondary to paraprotein precipitation (one patient); (iv) HIV-associated nephropathy (14 patients); (v) acute interstitial nephritis (two patients); (vi) various glomerulonephritis (four patients). In most cases, renal failure was severe (the mean creatinine clearance at entry was 12 ml/min). Most patients had a significant improvement in renal function with only symptomatic treatment. Eighteen per cent of the patients died within 2 months of the diagnosis of renal failure. Renal biopsy seems important for the diagnosis but also for the prognosis, at least in the cases of haemolytic-uraemic syndrome, HIV-associated nephropathy and drug-induced micro-obstructive renal failure. CONCLUSION: Vascular and glomerular diseases are frequent causes of acute or rapidly progressing renal failure in HIV-infected patients. Renal biopsy appears to be safe and useful for the diagnosis and the prognosis of the renal failure. High mortality rate is only observed in patients with ischaemic/toxic causes of acute renal failure.

In 26 AIDS patients treated for toxoplasmic encephalitis, the inhibitory effect on Toxoxplasma growth of sequential sera taken before and after initiation of therapy was determined using a culture-based immunoassay and compared with pyrimethamine blood levels. A marked inhibition of Toxoplasma growth was observed 1 day after initiation of therapy with pyrimethamine plus sulfadiazine and was maintained between 67% and 93% throughout the 15-day follow-up period. The degree of inhibition was not correlated to pyrimethamine blood levels and seemed highly potentiated when sulfadiazine rather than macrolides was given in combination with pyrimethamine.

Previous studies have shown that intestinal epithelial cells are capable of acting as APCs selectively activating CD8+ suppressor T cells.This activation appears to be mediated by a novel complex consisting of the class Ib molecule CDld and an associated epithelial cell surface glycoprotein, gplS0.We have postulated that this complex is recognized by the TCR:CD8 co-receptor complex on suppressor T cells and serves to induce their activation.Since gpl80 binds to any CD8 molecule, we wanted to determine whether IECs are targeting a selected subpopulation of "pre-suppressor" cells or whether the CDld:gpl80 complex was transducing a specific signal that promoted suppressor cell generation.To accomplish this, we dissected the signaling pathway activated following IEC:T cell co-cultures.Previous studies had shown that both CD8-associated p561ck and TCR-associated p59fyn were activated in these co-cultures.A two-fold experiment was performed: initially, the ability of IECs to activate both lck and fyn was studied in T cell:IEC co-cultures; then, the ability to recruit the protein tyrosine kinase ZAP70 and the proto-oncogenic substrate vav to both fyn and lck was investigated.Both CD8-associated Ick and TCR-associated fyn were activated by IECs.This activation resulted in the recruitment of zeta chain, ZAP70 and vav to fyn while lck associated with ZAP70 and vav.These experiments were then repeated in the presence or absence of an anti-CDld mAb, D5 or an antigpl80 mAb, B9.Activation of fyn but not lck was blocked by D5 while B9 inhibited IEC-induced activation of lck but not fyn.Furthermore, D5 inhibited the ability of ZAP70, zeta and vav to recruit to fyn but not to lck.Conversely, B9 appeared to inhibit the ability of both ZAP70 and vav to be recruited to lck but not fyn.Lastly, MAP kinase was activated in these co-cultures as well, suggesting that the signaling pathway was similar to that of CTLs.These data suggest that the activation of suppressor T ceils is not accomplished through a unique signaling cascade but rather through a similar cascade to cytolytic T cells.This suggests that T cells are committed at an earlier developmental stage to become either suppressor or cytolytic T cells.

Weight loss is significant in patients with HIV and chronic diarrhea. The aim of our study was to test for the links between weight loss, the level of food intake, and the severity of diarrhea and nutrient malabsorption. One hundred and sixteen patients with HIV and chronic diarrhea underwent a standardized gastrointestinal and nutritional evaluation, which included a questionnaire on diarrhea, a prospective estimation of food intake, a measurement of blood parameters and fecal lipid and nitrogen outputs, a stool examination for bacteria and parasites, and upper and lower digestive tract endoscopy. Diarrhea resulted from an infection by Cryptosporidia, Microsporida, or other pathogens in 22%, 20%, and 13% of the patients, respectively. Diarrhea appeared idiopathic in 45% of the patients. A significant negative correlation existed between the severity of weight loss and the levels of nutrient intake (p < .005), and a significant positive correlation between the severity of weight loss and stool frequency (p < .01). Multiple linear regression identified low caloric intake and high stool frequency as predictive of weight loss. No significant correlation was found between weight loss and the parameters of malabsorption, either by bivariate study or multiple regression. These results suggest that, in patients with HIV and chronic diarrhea, the degree of wasting is significantly related to the levels of dietary intake and the clinical severity of diarrhea, but not to the extent of nutrient malabsorption.

Objective: To study the effect of the protease inhibitor indinavir on body weight and body composition of subjects with HIV-related wasting.Design: Prospective measurement of body weight in patients who had wasting and were treated with indinavir. A subgroup of 16 representative patients also underwent a metabolic study that included measurements of body composition (skinfolds and bioelectrical impedance) and food intake. Seven from this subgroup who did not have chronic diarrhoea also underwent indirect calorimetry for measurement of resting energy expenditure; the nine patients with wasting and chronic diarrhoea had measurements of faecal losses and intestinal permeability using the lactulose-mannitol test.Setting: A tertiary care university hospital.Patients: Two hundred and fourteen HIV-infected patients with wasting (less than 95% of usual body weight) had their body weight measured at day 0; 186 patients had a second body weight measurement within the first 100 days of treatment, and 160 patients were weighed a third time, at a median of 176 days.Results: Body weight increased significantly (P < 0.0001) during treatment, whatever the degree of weight loss at baseline. After a median of 176 days on treatment, body weight had increased in 119 out of the 160 patients followed (74.4%; mean weight gain, 6.3 +/- SD 3.8 kg; range, 1-18 kg), had not changed in 13 (8.1%) and had fallen in 28 (17.5%; mean weight loss, 4.2 +/- 3.0 kg; range, 1-12 kg), relative to baseline. Overall, 119 out of the 214 patients (55.6%) from the initial population gained weight. Fat mass, fat-free mass and body cell mass increased significantly in the 16 patients who underwent metabolic studies, together with energy, protein and lipid intake. In the patients with chronic diarrhoea, intestinal permeability improved but there was no change in intestinal losses. In patients who had wasting but not chronic diarrhoea, resting energy expenditure did not change significantly. Body weight changes correlated with changes in the CD4+ cell count (r = 0.882; P = 0.00001) and, to a lesser extent, with changes in the viral load (r = -0.466; P = 0.047).Conclusion: Indinavir significantly improved the nutritional status of these patients with HIV-related wasting. (C) 1998 Lippincott Williams & Wilkins.

Mycobacterium celatum is a recently described slow-growing species. It was identified on the basis of genomic sequencing that differentiates three types. The present report describes two cases ofMycobacterium celatum type I infection in patients with AIDS. Both patients had CD4+ lymphocyte counts of <10/mm3, were receiving rifabutin prophylaxis, and had attended the same treatment units. The minimum inhibitory concentration of rifabutin for both strains was 8 mg/l, which may account for the failure of prophylaxis. As all type 1 strains have the same pulsedfield gel electrophoresis pattern, nosocomial transmission or acquisition from a common source could not be ruled out.

BACKGROUNDIn children, haemolytic uraemic syndrome (HUS) is associated with high plasma plasminogen activator inhibitor type 1 (PAI-1), which may contribute to the persistence of renal glomerular and arteriolar thrombi. HUS has been described in HIV-infected patients, but the pathophysiology of HUS in these patients is poorly understood. The aim of the study was to investigate plasma fibrinolytic activity in 18 patients with HIV-associated HUS.METHODSWe measured tissue type plasminogen activator (t-PA) and PAI-1 activities in the plasma of 18 HIV-infected patients with biopsy-proven HUS (HIV+/HUS+) and 48 HIV-infected patients without HUS (HIV+/HUS-).RESULTSPatients with HUS had a significantly higher serum creatinine, a lower platelet count and an increased incidence of cytomegalovirus (CMV) infection (72% of patients HIV+/HUS+, vs 25% of patients HIV+/HUS-). Unexpectedly, plasma PAI-1 activity was similar in both groups. However, t-PA activity was significantly higher in HUS cases (11.5 vs 4.5 U/ml, P=0.001). Patients with CMV infection, with or without HUS, had significantly increased t-PA level (P=0.01). Multivariate analysis identified high t-PA (RR=9.21) and CMV infection (RR=3.36) as risk factors for HUS.CONCLUSIONThis study provides evidence that HIV-infected patients with HUS have high plasma t-PA activity. PAI-1 plasma activity is not significantly increased, as opposed to non-HIV-associated HUS. Thus, in the setting of HIV infection, HUS cannot be attributed to decreased fibrinolytic activity.

HIV-infected patients had a body composition study (skinfolds and bioimpedance analysis) and a prospective measurement of oral intakes.Among them, 7 patients without diarrhea had a measurement of resting energy expenditure using indirect calorimetry and 9 patients with diarrhea had a measurement of fecal weight, fecal fat, energy and nitrogen as well as a measurement of intestinal permeability using the lactulose mannitol test.These variables were measured at day 0 and after 144 _+ 105 days of treatment (during this time elapse, 14 patients had gained weight and 2 had lost body weight).Variables were compared using paired Wilcoxon tests and correlations were calculated by the Spearman correlation coeficient.ResultS.Fat mass, fat-free mass and body cell mass increased significantly (9.5 vs 13.3 kg; 45.7 vs 51.7 ; 20.0 vs 23.2 ; p=0.01 for the 3 comparisons).Oral intake in energy, proteins and lipids increased significantly (p=0.05 ; p=0.01 et p=0.05 respectively).In patients with diarrhea, intestinal permeability decreased (p=0.02)but fecal losses did not change.In patients without diarrhea, REE, either expressed in kcal/24h or adjusted to the FFM did not change.Body weight changes were correlated with changes in CD4+ lymphocytes (r = 0.882; p=0.00001) et, to a lesser degree, with changes in viral load (r=--0.466;p=0.047).Conclusion.Under indinavir, body weight gain is due to an increase in both fat mass and fat-free mass.Body weight gain is due to a restoration of cellular immunity and is associated with increased oral intakes.

OBJECTIVE:Intestinal microsporidiosis due to Enterocytozoon bieneusi is a frequent cause of chronic diarrhoea in patients with HIV infection for which there is no available therapy. This study was designed to search for a drug with activity against this organism. DESIGN:Prospective open-labelled Phase II multicentre study. SETTING:University hospitals. PATIENTS:Sixty HIV-infected men with intestinal E. bieneusi infection. INTERVENTIONS:Ten drug regimens were consecutively tested orally for 3 weeks: albendazole plus metronidazole, sulphadiazine plus pyrimethamine, atovaquone, doxycycline plus nifuroxazide, itraconazole, flubendazole, chloroquine, paromomycin, sparfloxacin and fumagillin. Nine evaluable patients per regimen were required, but each patient could be enrolled up to three times in the study. OUTCOME MEASURE:Efficacy was assessed primarily by the clearance of E. bieneusi from stools and intestinal biopsies. The safety of each regimen was also assessed. RESULTS:Only purified fumagillin was able to clear E. bieneusi from stools as well as intestinal biopsies, whereas all other regimens failed to show antiparasitic efficacy. However, only four patients received fumagillin because of drug-induced thrombocytopenia. The four patients who received fumagillin remained free of E. bieneusi infection after a mean follow-up of 10 months. CONCLUSION:Eradication of E. bieneusi from the intestinal tract of patients with HIV infection and persistent immunosuppression is an achievable goal. Our study allowed the identification of oral fumagillin as a potential treatment for intestinal microsporidiosis due to E. bieneusi.

We report the effectiveness of ribavirin in an AIDS patient with multinodular pneumonia due to adenovirus, A 38-year-old AIDS patient who experienced multiple opportunistic infections and whose CD4 lymphocyte count was 5/mm(3) developed bilateral nodular lung opacities. Lung surgical biopsy yielded necrotizing pneumonitis with characteristic nuclear inclusions and positive immunocytology with adenovirus antibodies. Marked clinical and radiological improvement was obtained after intravenous then oral ribavirin. Ribavirin was discontinued after 40 d because of anemia. Relapse of pneumonia with respiratory distress led to death 8 mo later, This observation illustrates a rarely reported pulmonary opportunistic infection in AIDS and the potential value of ribavirin therapy for adenovirus pneumonia.

We conducted a prospective observational study to determine the feasibility and impact of rifabutin prophylaxis (300 mg daily) for human immunodeficiency virus-infected patients whose CD4 cell counts were <100/mm(3). Three hundred seventy-one patients (65.2% of all patients with CD4 cell counts of <100/mm(3) [mean +/- SD, 30 +/- 25/mm(3)]) received rifabutin prophylaxis for a mean duration +/- SD of 35.5 +/- 34.2 weeks; 198 patients (mean CD4 cell count +/- SD, 51.6 +/- 32/mm(3)) did not receive prophylaxis. Rifabutin prophylaxis for 8.4% of patients was interrupted because of adverse events. Mycobacterium avium complex (MAC) bacteremia developed in 17 (4.6%) of 371 patients receiving rifabutin prophylaxis and in 22 (11.1%) of 198 patients not receiving rifabutin prophylaxis. The mean CD4 cell count +/- SD at the diagnosis of MAC bacteremia was lower in patients receiving prophylaxis than in those not receiving prophylaxis (11.5 +/- 6.8/mm(3) vs. 34.7 +/- 36/mm(3), respectively; P <.01). MICs for MAC strains isolated from patients receiving prophylaxis were less than or equal to those for strains isolated from patients not receiving prophylaxis.

Thrombotic microangiopathy (TMA) can occur during the course of human immunodeficiency virus (HIV) infection. Clinical and pathological data for 29 patients with TMA and HIV infection were recorded. In a retrospective case-control study, we analyzed the link between opportunistic infections or drug therapies and TMA. Twenty-five patients (mean CD4+ cell count +/- SD, 71.9 +/- 18.3/mm3) had renal impairment, and four had neurological dysfunction. In one-half the cases, the disease was progressive with isolated fragmentation anemia appearing several months before the clinical symptoms. The diagnosis of TMA was confirmed by histological examination of kidney biopsy specimens (18 cases). Endothelial cytomegalovirus (CMV) inclusions were associated with TMA in nine of 18 cases, whereas histological examination did not detect CMV in any control specimens (P < .001). The case-control study demonstrated a link between TMA and clinical CMV infection (odds ratio, 3.9; 95% confidence interval, 1.1-14). We conclude that TMA is a late complication of HIV infection and can be associated with systemic CMV infection in this setting.

Journal of Eukaryotic MicrobiologyVolume 43, Issue 5 p. 130S-131S Cutaneous Lesions Due to Acanthamoeba sp in a Patient with AIDS ANNE-MARIE DELUOI, ANNE-MARIE DELUOI Parasitology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorMARIE-FRANCOISE TEILHAC, MARIE-FRANCOISE TEILHAC Pathology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorJEAN-LOUIS POIROT, JEAN-LOUIS POIROT Parasitology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorCAROLINE MASLO, CAROLINE MASLO Infect.Dis. Dept. Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorJACQUELINE LUBOINSKI, JACQUELINE LUBOINSKI Pathology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorWILLY ROZENBAUM, WILLY ROZENBAUM Infect.Dis. Dept. Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorFRANCOIS-PATRICE CHATELET, FRANCOIS-PATRICE CHATELET Pathology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this author ANNE-MARIE DELUOI, ANNE-MARIE DELUOI Parasitology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorMARIE-FRANCOISE TEILHAC, MARIE-FRANCOISE TEILHAC Pathology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorJEAN-LOUIS POIROT, JEAN-LOUIS POIROT Parasitology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorCAROLINE MASLO, CAROLINE MASLO Infect.Dis. Dept. Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorJACQUELINE LUBOINSKI, JACQUELINE LUBOINSKI Pathology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorWILLY ROZENBAUM, WILLY ROZENBAUM Infect.Dis. Dept. Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this authorFRANCOIS-PATRICE CHATELET, FRANCOIS-PATRICE CHATELET Pathology Laboratory, Hǒpital Rothschild, 33 Bd de Picpus, 75571, Paris, France.Search for more papers by this author First published: September 1996 https://doi.org/10.1111/j.1550-7408.1996.tb05043.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume43, Issue5September 1996Pages 130S-131S RelatedInformation

The murine leukemia virus LP-BM5 has been used to reproduce the model of murine AIDS in order to evaluate the course of infection with the MO-1 strain of Mycobacterium avium complex (MAC). LP-BM5 was inoculated in C57BL/6 mice by intravenous (i.v.) injection either 8 weeks before an i.v. challenge with 10(3) or 10(6) CFU of MAC (coinfection 1) or 10 days after an i.v. challenge with 10(3) CFU of MAC (coinfection 2). During coinfection 2 experiments, the phenotypic alterations in blood lymphocyte subsets were analyzed. During coinfection 1, LP-BM5 infection tended to decrease the mycobacterial growth, with the difference reaching statistical significance for the lower inoculum (10(3) CFU of MAC) (P<0.001). During coinfection 2, LP-BM5 did not exacerbate MAC infection except in the spleen, at day 90 after LP-BM5 challenge (P<0.001). LP-BM5 infection and the LP-BM5-MAC coinfection increased the numbers of activated CD4+ lymphocytes (CD4+ Ly6AE+) (P<0.001), activated CD8+ lymphocytes (CD8+ Ly6AE+) (P<0.001), and activated B lymphocytes (Ly5+ Ly6AE+) (P<0.001). This activation of T lymphocytes could explain the lack of exacerbation of MAC infection and even the trend to a lower level of MAC infection. Thus, this model of retroviral infection of mice does not seem to be a reliable model of immunodepression for the study of MAC infection and its treatments.