[Questions and answers regarding infectious endocarditis].
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Biomedical subjects
Publications and source records attributed to A Pahissa.
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BACKGROUND: Immunosuppression caused by human immunodeficiency virus 1 (HIV) infection appears to modify the clinical characteristics and to increase the severity of several bacterial infections. The impact of HIV infection and the degree of immunosuppression on the clinical characteristics and outcome of infective endocarditis (IE) in intravenous (IV) drug users has not been well characterized. METHODS: Prospective cohort study among 292 consecutive IV drug users with IE diagnosed in 2 academic institutional hospitals in Barcelona, Spain, from January 1, 1984, to October 31, 1995. Serostatus of HIV infection was documented in 283 patients. We measured demographics, clinical and biological data, cause, echocardiographic findings, HIV serostatus and classification, CD4 cell count, complications, and mortality. RESULTS: Among the 283 episodes of IE, 216 (76.3%) were in HIV-infected patients and 67 (23.7%) in non-HIV-infected patients. Rate of IE per 1000 admissions ranged from 0.17 to 0.82 per year, peaking in 1989. Characteristics of IE independently associated with HIV infection were right-side involvement (odds ratio [OR], 7.6; 95% confidence interval [CI], 3.5-16.7), a micro-organism different from viridans streptococci (OR, 2.5; 95% CI, 1.1-5.9), duration of drug abuse longer than 5 years (OR, 5.0; 95% CI, 2.4-10.3), and white blood cell count of no more than 10 X 10(9)/L (OR, 2.2; 95% CI, 1.1-4.2). There were no significant differences in mortality due to IE according to HIV serostatus. Among the 216 patients with HIV infection, the variables independently associated with worse outcome were CD4 cell count lower than 0.200 x 10(9)/L and left-sided or mixed IE. CONCLUSIONS: Although there is a difference in clinical presentation in IE in IV drug users, outcome was similar according to their HIV status. However, among HIV-infected patients, severe immunosuppression and mixed or left-side valvular involvement were strong risk factors for mortality.
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Herpes zoster leukoencephalitis is a rare complication of varicella-zoster virus infection. Associated with high mortality, the majority of cases have been discovered postmortem; today, however, magnetic resonance imaging is being used successfully as an aid in the diagnosis of this disease. The first two reported cases of HIV-infected patients with herpes zoster leukoencephalitis who recovered clinically and showed complete resolution of the magnetic resonance demyelination images after acyclovir treatment are described. In addition, the cases of herpes zoster leukoencephalitis reported in the literature to date are reviewed.
To determine whether cytomegalovirus (CMV) disease is an independent risk factor for graft loss and death after orthotopic liver transplantation, we performed a 3-year follow-up study of 143 consecutive liver transplant recipients and six patients who underwent retransplantation. Thirty-seven patients (25%) had had CMV disease and were alive after treatment. Fifty-two deaths and eight graft losses occurred. The cumulative incidence of graft failure at 1 and 3 years of follow-up were 40% and 63%, respectively, for patients with CMV disease, compared with 22% and 33%, respectively, for those without CMV disease (P < .05, logrank test). Cumulative probabilities of survival for patients with and without CMV disease were 64% and 82%, respectively, at 1 year and 46% and 69%, respectively, after 3 years (P < .05, logrank test). Multivariate analysis with use of a time-dependent Cox model showed that previous CMV disease was an independent risk factor for graft loss at 1 and 3 years of follow-up (P = .04 and P = .007) and for patient survival (P = .04 and P = .01). Our results indicate that CMV disease is a significant independent risk factor for graft loss and patient survival after liver transplantation.
We prospectively reviewed all cases of purulent meningitis among human immunodeficiency virus (HIV) type 1-infected patients > 14 years old that occurred at the Hospital General Vall d'Hebron (Barcelona) during the period 1 January 1985 through 31 March 1997. There were 12 episodes of purulent meningitis in nine of 2,150 HIV-1-infected patients. The annual rate of purulent meningitis was 0.465 cases per 1,000 patients, a rate that is 150 times higher than that for the general population. During 10 episodes, CD4+ lymphocyte counts were < 200/mm3. The etiologic organism was Streptococcus pneumoniae in nine episodes (seven episodes occurred in four splenectomized patients), and Escherichia coli, Streptococcus agalactiae, and Enterococcus faecium each caused one episode. Clinical features and cerebrospinal fluid abnormalities were similar to those observed among patients without HIV-1 infection. All patients had bacteremia. The overall mortality was 8.3%. We conclude that purulent meningitis, particularly pneumococcal meningitis, is more frequent among HIV-1-infected patients than in the general population. The prognosis for HIV-1-infected patients is better than for HIV-1-negative patients.
Our objective in this study was to determine the efficacy of 2 grams a day of oral acyclovir administered for 16 weeks after transplantation for the prevention of cytomegalovirus (CMV) infection and disease in CMV-seropositive liver transplant recipients. Seventy-three adult liver transplant recipients, seropositive for CMV, were randomized to receive either 2 grams a day of oral acyclovir for 16 weeks after transplantation or no prophylaxis. The incidence of CMV disease was significantly lower in the acyclovir group (5%) than in the control group (27%; P < 0.05). By log-rank analysis, the differences in the probability of presenting CMV disease over the first 16 weeks and over the 1st year were also significant (P < 0.05). We conclude that 2 grams a day of oral acyclovir provides effective prophylaxis against CMV disease in CMV-seropositive liver transplant recipients.
From 1979 to 1996, 58 patients (mean age, 39.4 years) were treated for bacteremia due to Campylobacter species at the Hospitals Vall d'Hebron in Barcelona, Spain. Bacteremia was considered to be hospital acquired in 30% of these patients. Almost all the patients (93%) had underlying conditions; liver cirrhosis was the most frequent (34% of patients), and neoplasia, immunosuppressive therapy, and human immunodeficiency virus disease were also common. Of the 58 Campylobacter strains isolated, 81% were C. jejuni, 10% were Campylobacter species, 7% were C. fetus, and one (2%) was C. coli. Resistance rates were: cephalothin, 82%; co-trimoxazole, 79%; quinolones, 54%; ampicillin, 20%; amoxicillin/clavulanate, 4%; erythromycin, 7%; gentamicin, 0; and tetracyclines, 0. Even though the majority of patients were immunocompromised, mortality was low (10.5%), and only one patient relapsed. Because of the high level of resistance to the quinolones in Campylobacter species, these drugs should not be used as empirical treatment, at least in Spain. Although the macrolides remain the antibiotics of choice, amoxicillin/clavulanate may be an effective alternative therapy.
A prospective study of the clinical characteristics and evolutionary patterns of 59 cases of late prosthetic valve endocarditis (LPVE) that occurred between January 1975 and December 1994 was performed. Of these 59 cases of LPVE, 48 involved mechanical valves and 11 involved biological valves. Etiologies were as follows: streptococci, 41% of cases; staphylococci, 25%; enterococci, 13%; and miscellaneous, 21%. Echocardiography documented vegetations in 21 patients, paravalvular abscesses in 10, and prosthetic leaks in 34. Emboli occurred in 22 patients, and heart failure in 19 patients. Forty-two patients received medical treatment alone, and 17 received medical treatment and underwent valve replacement surgery. The in-hospital mortality rate was 25%; staphylococcal infection caused 67% of deaths, streptococcal infection caused 5%, and other etiologies caused 23% (P = .0004). After adjustment for age and type of prosthesis, multiple logistic regression revealed an odds ratio for death due to nonstreptococcal infections of 9.67. The overall survival rate was 59% at 5 years and 52% at 10 years. During follow-up, 17 patients needed new valves. At the end of follow-up, only 13 patients remained alive and had the same prosthesis that they had at the time of the diagnosis of LPVE.
A model of pneumonia due to Streptococcus pneumoniae resistant to penicillin was developed in immunocompetent Wistar rats and was used to evaluate the efficacies of different doses of penicillin, cefotaxime, cefpirome, and vancomycin. Adult Wistar rats were challenged by intratracheal inoculation with 3 x 10(9) CFU of one strain of S. pneumoniae resistant to penicillin (MICs of penicillin, cefotaxime, cefpirome, and vancomycin, 2, 1, 0.5, and 0.5 microg/ml, respectively) suspended in brain heart broth supplemented with 0.7% agar. The rats experienced a fatal pneumonia, dying within 5 days and with peak mortality (70 to 80%) occurring 48 to 72 h after infection, and the bacterial counts in the lungs persisted from 8.87 +/- 0.3 log10 CFU/g of lung at 24 h of the infection to 9.1 +/- 0.3 log10 CFU/g at 72 h. Four hours after infection the animals were randomized into the following treatment groups: (i) control without treatment, (ii) penicillin G at 100,000 IU/kg of body weight every 2 h, (iii) penicillin G at 250,000 IU/kg every 2 h, (iv) cefotaxime at 100 mg/kg every 2 h, (v) cefpirome at 200 mg/kg every 2 h, and (vi) vancomycin at 50 mg/kg every 8 h. Two different protocols were used for the therapeutic efficacy studies: four doses of beta-lactams and one dose of vancomycin or eight doses of beta-lactams and two doses of vancomycin. Results of the therapy for experimental pneumonia caused by penicillin-resistant S. pneumoniae showed that initially, all the antimicrobial agents tested had similar efficacies, but when we prolonged the treatment, higher doses of penicillin, cefotaxime, and cefpirome were more effective than penicillin at lower doses in decreasing the residual bacterial titers in the lungs. Also, when we extended the treatment, vancomycin was more efficacious than penicillin at lower doses but was less efficacious than higher doses of penicillin or cefpirome. The model that we have developed is simple and amenable for inducing pneumonia in immunocompetent rats and could be used to explore the pathophysiology and to evaluate optimal therapy of this infection in the immunocompetent host.
Rhodococcus equi is a cause of lung infection in immunosuppressed hosts. Since the start of the HIV epidemic, 76 cases of R. equi lung infection (MEDLINE 1985-96) affecting this population have been described. We report 2 additional cases and review the clinical data, radiological findings, treatment and outcome of these 78 patients. The mean age of these patients was 33 y; 69 were male. 71 met the criteria for AIDS (CDC 1993). Fever and cough were the presenting complaints in the majority of patients (84.3%). A single cavitary lung lesion in the upper lobes was the most common radiological finding (57.7%), although multiple cavitations, alveolar infiltrates and pleural effusion were also found. Treatment usually was based on synergistic antibiotic combinations for a long period of time determined on an individual basis. Surgery was performed only in 11 patients. Death attributable directly to R. equi infection is low (15.4%), however only half of the patients (53.8%) were completely cured. We conclude that R. equi infection should be strongly considered in any HIV patient who presents with cavitary lesions in the lung, especially if mycobacteria are not identified. Treatment must be based on synergistic antibiotic combinations, and surgery relegated to cases of chronic single cavitary lesions not responding to antibiotics.
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BACKGROUND: It is often difficult to administer extended antibiotic therapy in the hospital for right-sided Staphylococcus aureus endocarditis. Although the effectiveness of single-drug therapy given for 4 to 6 weeks and that of two-drug therapy given for 2 weeks have been shown, no data are available on the effectiveness of short-course single-drug therapy. OBJECTIVE: To compare the efficacy of cloxacillin alone with that of cloxacillin plus gentamicin for the 2-week treatment of right-sided S. aureus endocarditis in intravenous drug users. DESIGN: Open, randomized study. SETTING: An academic tertiary care hospital in Barcelona, Spain. PATIENTS: 90 consecutive intravenous drug users who had isolated tricuspid valve endocarditis caused by methicillin-susceptible S. aureus, had no allergy to study medications, and had no systemic infectious complications that required prolonged therapy. An efficacy subset consisted of 74 of these patients who did not meet an exclusion criterion. INTERVENTION: Cloxacillin (2 g intravenously every 4 hours for 14 days) alone or combined with gentamicin (1 mg/kg of body weight intravenously every 8 hours for 7 days). MEASUREMENTS: Clinical or microbiological evidence of active infection after 2 weeks of therapy, relapse of staphylococcal infection, or death. RESULTS: In an analysis of the efficacy subset, treatment was successful in 34 of the 38 patients who received cloxacillin alone (89% [95% CI, 75% to 97%]) and 31 of the 36 patients who received cloxacillin plus gentamicin (86% [CI, 71% to 95%]). Three patients died: one in the cloxacillin group and two in the combination therapy group. Of the 37 patients who completed 2-week treatment with cloxacillin, 34 (92%) were cured, and 3 (8%) needed prolonged treatment to cure the infection. Of the 34 patients who completed 2-week treatment with cloxacillin plus gentamicin, 32 (94%) were cured and 2 (6%) required treatment for 4 weeks. One patient in the combination group had relapse. CONCLUSIONS: A penicillinase-resistant penicillin used as single-agent therapy for 2 weeks was effective for most patients with isolated tricuspid endocarditis caused by methicillin-susceptible S. aureus. Adding gentamicin did not appear to provide any therapeutic advantages. Additional studies to confirm the therapeutic equivalence of short-course therapy with penicillinase-resistant penicillin alone and therapy with combined regimens are warranted.
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Four cases of pleural cryptococcosis as the form of onset of cryptococcosis in patients with human immunodeficiency virus (HIV) infection are reported. In two out of the four cases cryptococci were simultaneously isolated in other localizations (blood and meninges). In the two remaining patients the pleura was the only site of the disease, with serum determination of the cryptococci antigen being negative in one. The four patients evolved favourably, with three being exclusively treated with fluconazol. Pleuritis is an infrequent manifestation in cryptococcosis although it may be the form of onset and the only localization of the disease. Only 10 cases have been reported in patients with HIV infection. The present four cases represent 11% of the authors' series of cryptococcosis in AIDS patients. The diagnostic possibility of cryptococcosis should be considered in patients with human immunodeficiency virus infection presenting pleural effusion.