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J P Bédos

Publications and source records attributed to J P Bédos.

At least 19 recordsLinked to original sources
PubMed2006

Efficacy of cethromycin, a new ketolide, against Streptococcus pneumoniae susceptible or resistant to erythromycin in a murine pneumonia model.

Cethromycin is a ketolide with in vitro activity against macrolide-sensitive and -resistant strains of Streptococcus pneumoniae. We compared its in vivo efficacy to erythromycin in a mouse model of acute pneumonia induced by two virulent clinical strains: a serotype 3 susceptible strain (P-4241) (MICs: erythromycin, 0.03 microg/ml; cethromycin, 0.015 microg/ml) and a serotype 1 strain resistant to erythromycin (P-6254; phenotypically MLSB constitutive) (MICs: erythromycin, 1,024 microg/ml; cethromycin, 0.03 microg/ml). Immunocompetent mice were infected with 10(5) CFU of each strain. Six treatments given either subcutaneously (s.c.) or per os (p.o.) at 12-h intervals were initiated at 6 or 12 h after infection. Against P-4241, cethromycin given s.c. at 25 or 12.5 mg/kg protected 100% of the animals, with lungs and blood completely cleared of bacteria. Given p.o., cethromycin maintained its efficacy with 100 and 86% survival at 25 and 12.5 mg/kg, respectively. Erythromycin, given s.c. at 50 or 37.5 mg/kg, provided 50 and 38% survival rates, respectively. Against P-6254, cethromycin was effective at 25 mg/kg (100% survival) regardless of the administration route, whereas only 25 and 8% of animals survived after a 75-mg/kg erythromycin treatment given s.c. and p.o., respectively. The serum protein binding levels of cethromycin were 94.8 and 88.5% after doses of 12.5 and 25 mg/kg, respectively. The higher in vivo activity of cethromycin compared to erythromycin could be explained by favorable pharmacokinetic/pharmacodynamic indexes against P-6254 but not against P-4241.

Animals↗
PubMed2005

Activity of gemifloxacin against quinolone-resistant Streptococcus pneumoniae strains in vitro and in a mouse pneumonia model.

Gemifloxacin is a novel fluoronaphthyridone quinolone with enhanced in vitro activity against Streptococcus pneumoniae. We investigated the activities of gemifloxacin and trovafloxacin, their abilities to select for resistance in vitro and in vivo, and their efficacies in a mouse model of acute pneumonia. Immunocompetent Swiss mice were infected with 10(5) CFU of a virulent, encapsulated S. pneumoniae strain, P-4241, or its isogenic parC, gyrA, parC gyrA, and efflux mutant derivatives (serotype 3); and leukopenic mice were infected with 10(7) CFU of two poorly virulent clinical strains (serotype 11A) carrying either a parE mutation or a parC, gyrA, and parE triple mutation. The drugs were administered six times every 12 h, starting at either 3 or 18 h postinfection. In vitro, gemifloxacin was the most potent agent against strains with and without acquired resistance to fluoroquinolones. While control mice died within 6 days, gemifloxacin at doses of 25 and 50 mg/kg of body weight was highly effective (survival rates, 90 to 100%) against the wild-type strain and against mutants harboring a single mutation, corresponding to area under the time-versus-serum concentration curve at 24 h (AUC(24))/MIC ratios of 56.5 to 113, and provided a 40% survival rate against a mutant with a double mutation (parC and gyrA). A total AUC(24)/MIC ratio of 28.5 was associated with poor efficacy and the emergence of resistant mutants. Trovafloxacin was as effective as gemifloxacin against mutants with single mutations but did not provide any protection against the mutant with double mutations, despite treatment with a high dose of 200 mg/kg. Gemifloxacin preferentially selected for parC mutants both in vitro and in vivo.

Animals↗
PubMed2004

Efficacy of BB-83698, a novel peptide deformylase inhibitor, in a mouse model of pneumococcal pneumonia.

The efficacy of BB-83698, a novel potent peptide deformylase inhibitor, was evaluated in a mouse model of acute pneumonia. The Streptococcus pneumoniae isolates tested included four virulent strains (one penicillin-susceptible wild-type strain, one macrolide-resistant strain, and two quinolone-resistant mutants [a mutant carrying mutations in ParC and GyrA and an efflux mutant] isogenic to the wild type) and two poorly virulent penicillin-resistant strains. Pneumonia was induced by intratracheal inoculation of 10(5) CFU (virulent strains) into immunocompetent mice or 10(7) CFU (less virulent strains) into leukopenic mice. Animals received three or six subcutaneous injections of antibiotics at 12- or 24-h intervals, with antibiotic treatment initiated at 3, 6, 12, or 18 h postinfection (p.i.). BB-83698 showed potent in vitro activity against all strains (MICs, 0.06 to 0.25 micro g/ml). In the in vivo model, all control animals died within 2 to 5 days of infection. BB-83698 (80 mg/kg of body weight twice daily or 160 mg/kg once daily) protected 70 to 100% of the animals, as measured 10 days p.i., regardless of the preexisting resistance mechanisms. In contrast, the survival rates for animals treated with the comparator antibiotics were 30% for animals treated with erythromycin (100 mg/kg) and infected with the macrolide-resistant strain, 34% for animals treated with amoxicillin (200 mg/kg every 8 h) and infected with the penicillin-resistant strain, and 0 and 78% for animals treated with ciprofloxacin (250 mg/kg) and infected with the ParC and GyrA mutant and the efflux mutant, respectively. At 80 mg/kg, BB-83698 generated a peak concentration in lung tissue of 61.9 micro g/ml within 1 h and areas under the concentration-times curves of 57.4 and 229.4 micro g. h/ml for plasma and lung tissue, respectively. The emergence of S. pneumoniae isolates with reduced susceptibilities to BB-83698 was not observed following treatment with a suboptimal dosing regimen. In conclusion, the potent in vitro activity of BB-83698 against S. pneumoniae, including resistant strains, translates into good in vivo efficacy in a mouse pneumonia model.

Amidohydrolases↗
PubMed2004

Activities of garenoxacin against quinolone-resistant Streptococcus pneumoniae strains in vitro and in a mouse pneumonia model.

Garenoxacin is a novel des-F(6) quinolone with enhanced in vitro activities against both gram-positive and gram-negative bacteria. We compared the activity of garenoxacin with that of trovafloxacin (TVA) against Streptococcus pneumoniae, together with their efficacies and their capacities to select for resistant mutants, in a mouse model of acute pneumonia. In vitro, garenoxacin was more potent than TVA against wild-type S. pneumoniae and against a mutant with a single mutation (parC), a mutant with double mutations (gyrA and parC), and a mutant with triple mutations (gyrA, parC, and parE). Swiss mice were infected with 10(5) CFU of virulent, encapsulated S. pneumoniae strain P-4241 or its derived isogenic parC, gyrA, gyrA parC, and efflux mutants and 10(7) CFU of poorly virulent clinical strains carrying a parE mutation or gyrA, parC, and parE mutations. The drugs were administered six times, every 12 h, beginning at either 3 or 18 h postinfection. The pulmonary pharmacokinetic parameters in mice infected with strain P-4241 and treated with garenoxacin or TVA (25 mg/kg of body weight) were as follows: maximum concentration of drug in serum (C(max); 17.3 and 21.2 micro g/ml, respectively), C(max)/MIC ratio (288 and 170, respectively), area under the concentration-time curve (AUC; 48.5 and 250 microg. h/ml, respectively), and AUC/MIC ratio (808 and 2000, respectively). Garenoxacin at 25 and 50 mg/kg was highly effective (survival rates, 85 to 100%) against the wild-type strain and mutants harboring a single mutation. TVA was as effective as garenoxacin against these strains. TVA at 200 mg/kg and garenoxacin at 50 mg/kg were ineffective against the mutant with the parC and gyrA double mutations and the mutant with the gyrA, parC, and parE triple mutations. The efficacy of garenoxacin was reduced only when strains bore several mutations for quinolone resistance.

Animals↗
PubMed2004

Efficacy of BAL5788, a prodrug of cephalosporin BAL9141, in a mouse model of acute pneumococcal pneumonia.

BAL5788 is a water-soluble prodrug of BAL9141, a new broad-spectrum cephalosporin with high levels of in vitro activity against methicillin- and vancomycin-resistant staphylococci and penicillin-resistant streptococci. In plasma BAL5788 is rapidly converted to BAL9141. We studied the activity of BAL5788 in a mouse model of acute pneumococcal pneumonia. Leukopenic female Swiss albino mice were challenged intratracheally with 10(7) CFU of clinical Streptococcus pneumoniae strains P-52181 (Pen(s) Cro(s) Ctx(s)), P-15986 (Pen(r) Cro(s) Ctx(s)), P-40422 (Pen(r) Cro(r) Ctx(r)), and P-40984 (Pen(r) Cro(r) Ctx(r)). Infected mice received subcutaneous (s.c.) injections of BAL5788 or ceftriaxone starting 3 h after pneumococcal challenge. Uninfected nonleukopenic mice received single s.c. doses of BAL5788 to determine the BAL9141 concentration-time profiles in serum and lungs. Untreated control mice died within 5 days postinfection. Ten-day cumulative survival rates for infected mice receiving BAL5788 (total daily doses of BAL9141 equivalents, 2.1 to 75 mg/kg of body weight) ranged from 57 to 100%, whereas with ceftriaxone (total daily doses, 10 to 400 mg/kg), the survival rates varied between 13 and 100%. In mice infected with P-15986, the survival rates achieved with BAL5788 (BAL9141 equivalent, 8.4 mg/kg) and those achieved with ceftriaxone (50 mg/kg) were significantly different (93 versus 13%; P < 0.0001) in favor of BAL5788; the outcomes of the trials with all other strains were not significantly different between the two antibiotics, but markedly lower doses of BAL5788 than ceftriaxone were required to obtain similar survival rates. Pharmacokinetic data showed that BAL9141 was effective against the four pneumococcal strains tested at very low values of the time above the MIC (T > MIC), which ranged from 9 to 18% of the dosing interval, whereas the values of T > MICs for ceftriaxone ranged from 30 to 50% of the dosing interval.

Animals↗
PubMed2000

Nuclear factor-kappaB activation in mouse lung lavage cells in response to Streptococcus pneumoniae pulmonary infection.

OBJECTIVES: To assess the state and activation kinetics of the nuclear transcription regulatory protein nuclear factor-kappB (NF-kappaB) in lung lavage cells in a murine pneumococcal pneumonia model and to determine how the virulence of the infecting organisms altered the activation state of NF-kappaB. DESIGN: Experimental, comparative study of three Streptococcus pneumoniae strains that induced three distinct pulmonary diseases. SETTING: Experimental laboratory in a university-based medical center. SUBJECTS: Female BALB/cby mice, 8-10 wks of age. INTERVENTIONS: We randomly divided the mice into the following five groups: a) the control group; b) animals infected by virulent encapsulated S. pneumoniae P4241 strain; c) animals infected by avirulent encapsulated S. pneumoniae P15986 strain; d) animals infected by avirulent unencapsulated S. pneumoniae R6 strain; e) animals infected by virulent lysed S. pneumoniae P4241 strain. Animals were anesthetized and infected by intratracheal delivery of 4 x 10(5) colony-forming units (CFU) of S. pneumoniae per mouse or bacterial components equivalent to 4 x 10(5) CFU for lysed S. pneumoniae challenge. After intratracheal challenge with virulent encapsulated strain P4241, mice developed acute pneumonia, became bacteremic, and died within 3 to 5 days. None of the mice infected with the avirulent encapsulated strain P15986 or the avirulent unencapsulated strain R6 died. After collection of lung lavage cells and nuclear extraction, NF-kappaB activation was determined 1 hr, 4 hrs, 6 hrs and 24 hrs after pneumococcal infection. At the same time, pulmonary and blood clearance, bronchoalveolar lavage cells population, and tumor necrosis factor-alpha production were assessed (six mice per time point). MEASUREMENTS AND MAIN RESULTS: NF-kappaB was constitutively expressed within nuclear extracts of lung lavage cells from uninfected control mice. A significant increase in NF-kappaB activation was detected within 1 hr after injection of virulent lysed S. pneumoniae P4241 strain (bacterial components equivalent to 4 x 10(5) CFU), and was still present 24 hrs after the injection. After live pneumococcal challenge, significant NF-kappaB activation was detected within 4 hrs with a peak at 24 hrs. Responses to all three strains (P4241, P15986 and R6) were time-dependent (p < .0001), as NF-kappaB activation gradually increased during the first 24 hrs. Moreover, compared with the control uninfected mice, the intensity of the retarded KB oligonucleotide, as determined by densitometry, was increased approximately four- to five-fold and seven-fold in reactions containing nuclear extracts isolated 24 hrs after infection with the avirulent strains P15986 or R6 and the virulent strain P4241, respectively. With the virulent strain P4241, responses were significantly stronger than with the avirulent strains P15986 and R6 (p < .01). Responses were of similar order with avirulent strains P15986 and R6 (p > .05). CONCLUSION: Pulmonary infection by S. pneumoniae induced delayed and time-dependent activation of NF-kappaB in mouse lung lavage cells. The degree of NF-kappaB activation in lung lavage cells correlated with the virulence of the infecting organisms. Our results suggest that the more severe the infection, the higher the rise in NF-kappaB.

Animals↗
PubMed2000

Relationship between capsular type, penicillin susceptibility, and virulence of human Streptococcus pneumoniae isolates in mice.

We examined the relationship between penicillin susceptibility, peritoneal virulence in Swiss mice, and capsular type in a selection of 122 clinical Streptococcus pneumoniae isolates belonging to 24 serotypes. Regardless of the serotype, all 32 virulent strains were susceptible to penicillin, and all 41 strains with diminished susceptibility or resistance to penicillin were avirulent. The remaining 49 strains were both susceptible to penicillin and avirulent, irrespective of the serotype. On the basis of their capsular type and pathogenic behavior, strains fell into one of four groups. In the group consisting of serotypes 1, 3, and 4 (n = 16), strains were predominantly virulent (81.3%), and all were penicillin susceptible. In the serotype 6 group (n = 32), the frequency of virulence was significantly lower (34.4 versus 81.3%, P = 0.002), and strains were predominantly penicillin susceptible (71.9%). In the group composed of serotypes 9, 14, 19, and 23 (n = 50), all strains were avirulent, and 56% had decreased susceptibility (n = 12) or resistance to (n = 16) penicillin. The fourth group was heterogenous, as it pooled 24 strains of 15 different serotypes; in this group the frequency of virulence was 33.3%, and strains were predominantly penicillin susceptible (83.3%). These data point to a complex relationship between penicillin susceptibility and virulence in mice but do not entirely separate these characteristics from the role of the capsular type. The possibility that the mechanisms conferring penicillin resistance are related to those leading to a loss of virulence is supported by these findings.

Animals↗
PubMed1999

[Current microbiologic problems. Pulmonary infection by Streptococcus pneumoniae. Current physiopathological aspects].

STILL A SERIOUS DISEASE: Despite advances in antibiotic therapy, and despite the emergence of beta-lactam-resistant strains, mortality of pneumococcal pneumonia has remained relatively unchanged. The pathogenicity of a pneumococcal strain results from an interaction between a specific host with its own capacity to "resist or yield" to the multiple virulence factors intrinsic to each S. pneumoniae strain. ROLE OF THE CAPSULE: The capsule is the pneumococci's principal arm of resistance against the host's defense systems. There is a wide variability depending on the capsule serotype. Inversely, the capsule plays no role in triggering the inflammatory reaction which is secondary to substances released from the bacterial wall such as teichoic acid and peptidoglycan. HOST RESPONSE: The molecular mechanisms of cellular activation and induction of proinflammatory cytokines triggered by S. pneumoniae follow similar pathways which are different from those for endotoxin triggered by Gram negative bacteria. PERSPECTIVES: A better understanding of the clinical expression, distinguishing simple nasopharyngeal carriage from bacterial pneumonia should lead to the design of new therapeutic agents which will reduce the capacity of certain S. pneumoniae strains to invade the host and trigger deleterious inflammatory reactions.

Humans↗
PubMed1999

Pneumocystis carinii pneumonia requiring intensive care management: survival and prognostic study in 110 patients with human immunodeficiency virus.

OBJECTIVE: To perform a descriptive study of patients with acute respiratory failure secondary to acquired immunodeficiency syndrome-related Pneumocystis carinii pneumonia and to identify variables that are predictive of death within 3 months. DESIGN: Case series study. SETTING: Infectious disease intensive care unit (ICU) in a university hospital. PATIENTS: Detailed clinical, laboratory, and ventilatory data were collected prospectively within 48 hrs of admission and during the ICU stay in 110 consecutive human immunodeficiency virus-infected patients requiring ICU management with or without mechanical ventilation for P. carinii pneumonia-related acute respiratory failure. MEASUREMENTS AND MAIN RESULTS: Continuous positive airway pressure was used initially in 66 (60%) patients. Among the 34 patients (31%) who required mechanical ventilation, including 12 at admission and 22 after failure of continuous positive airway pressure, 76% died. The 3-month mortality rate after ICU admission was estimated at 34.6% (95% confidence interval [CI], 25%-44%). The 1-yr survival rate was estimated at 47% (95% CI, 36%-58%). With successive multiple logistic regression models analyzing the relative prognostic importance of baseline clinical and laboratory tests variables, ventilation variables, and events in the ICU, only delayed mechanical ventilation after 3 days (odd ratio [OR], 6.7; 95% CI, 1.9-23.9), duration of mechanical ventilation of > or = 5 days (OR, 2.8; 95% CI, 1.1-6.9), nosocomial infection (OR, 5.2; 95% CI, 2.1-12.9), and pneumothorax (OR, 5; 95% CI, 1.7-14.7) were predictive of death within 3 months of ICU admission. Among patients with delayed mechanical ventilation on day 3 or later and with a pneumothorax associated or not associated with a nosocomial infection, the predicted probability of 3-month death was close to 100%. CONCLUSIONS: Our data suggest that the most significant predictive factors of death were identifiable during the course of P. carinii pneumonia-related acute respiratory failure rather than at admission and can help in bedside decisions to withdraw intensive care support in such patients.

AIDS-Related Opportunistic Infections↗
PubMed1998

[Would ampicillin alone again be enough for treating community-acquired pneumonias?].

MORE THAN SEMANTICS: The complexity of the problem raised by this apparently simple question becomes apparent if one examines the meanings behind the words. STILL SUFFICIENT: Globally, the frequency of pathogens known to cause community-acquired pneumonia has changed little over time: Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumoniae. The real question is the emergence of S. Pneumoniae resistant strains. Currently, the frequency of penicillin or ampicillin resistant strains (less then 10%) is not associated with an increased rate of treatment failure or mortality. "High" doses (150-200 MU/kg/d for penicillin or 2 g t.i.d. for ampicillin) can still be expected to control suspected or certain resistant pneumococcal pneumonia. STILL SUFFICIENT: Would other antimicrobials be more effective? In France, "consensual" use of amoxicillin (1 g t.i.d.) "covers" 98% of the situations as resistant strains are found in only 2% of the adult cases. Thus, the lower frequency of pneumococcal resistance to cefotaxime or ceftriaxone (less than 0.5%) would not warrant their use in most cases of community-acquired pneumococcal pneumonia. Inversely, combination regimens with ampicillin or amoxicillin and cefotaxime or ceftriaxone or the amoxicillin-clavulanic acid association at standard doses provide good therapeutic alternatives for empirical prescriptions in cases with a high risk of infection other than pneumococcal infection (H.influenzae, methicillin-sensitive Staphylococcus aureus). The remarkable anti-pneumococcal activity of imipenem, vancomycin and teicoplanin should, for the time being, be reserved for selected patients with cross allergic reactions to penicillins and cephalosporins. EMPIRICAL REGIMENS: In case of severe community-acquired pneumonia, a combination regimen should be the rule in order to "cover" as many bacteria as possible. In the "healthy" adult under 60 years of age, amoxicillin combined with a macrolide or a fluoroquinolone can be recommended. OUTLOOK: Bacteriological efficacy is not synonymous with cure. Secondary inflammatory processes and subsequent septic shock remain a major challenge.

Adult↗
PubMed1998

Isolated right-sided Bartonella quintana endocarditis in an immunocompetent adult.

Bartonella quintana is a recently recognized cause of culture-negative left-sided endocarditis. We report a case of isolated tricuspid endocarditis caused by B. quintana in a 65-year-old alcoholic man, who also had immune-complex glomerulonephritis. B. quintana was established as the cause of the endocarditis based on serological tests and on failure of extensive efforts to isolate an alternative organism. The patient improved gradually on antibiotic therapy and did not require surgery. To our knowledge, this is the first report of isolated right-sided endocarditis caused by B. quintana. Although uncommon, Bartonella should be considered in patients with isolated right-sided culture-negative endocarditis.

Aged↗
PubMed1998

Efficacy of trovafloxacin against penicillin-susceptible and multiresistant strains of Streptococcus pneumoniae in a mouse pneumonia model.

The increasing emergence of penicillin-resistant and multidrug-resistant strains of Streptococcus pneumoniae will create a serious therapeutic problem in coming years. Trovafloxacin is a novel naphthyridone quinolone with promising activity against S. pneumoniae, including penicillin-resistant strains (MIC for 90% of the isolates tested, 0.25 microg/ml). We compared its in vivo efficacy with that of other fluoroquinolones (ciprofloxacin, temafloxacin, and sparfloxacin) and a reference beta-lactam (amoxicillin) in a model of acute experimental pneumonia. Immunocompetent Swiss mice were infected by peroral tracheal delivery of a virulent, penicillin-susceptible strain (MIC, 0.03 microg/ml); leukopenic Swiss mice were infected with three poorly virulent, penicillin-resistant strains (MICs, 4 to 8 microg/ml) and a ciprofloxacin-resistant strain (MIC, 32 microg/ml). Treatments were started 6 h (immunocompetent mice) or 3 h (leukopenic mice) after infection. Doses ranging from 12.5 to 300 mg/kg were given at 12- or 8-h intervals for 3 days. Trovafloxacin (25 mg/kg) was the most effective agent in vivo against penicillin-susceptible and -resistant strains. Corresponding survival rates were 2- to 4-fold higher than with 50-mg/kg sparfloxacin or temafloxacin and 8- to 16-fold higher than with 100-mg/kg ciprofloxacin. The ratios of the area under the concentration-time curve to the MIC in serum and lung tissue were more favorable with trovafloxacin than with the other quinolones. Efficacy in vivo correlated with pharmacokinetic parameters. Trovafloxacin shows potential for the treatment of infections due to penicillin-susceptible and -resistant S. pneumoniae but appears to be ineffective against a ciprofloxacin-resistant strain.

Animals↗
PubMed1998

Predictors of short- and long-term survival in HIV-infected patients admitted to the ICU.

STUDY OBJECTIVES: To evaluate the prognosis of HIV-infected patients admitted to ICUs and to identify factors predictive of short- and long-term survival. DESIGN: A prospective study from January 1, 1990, to December 31, 1992, including all consecutive HIV-infected patients admitted to our ICU for the first time. ICU survivors were followed up until January 1, 1994. SETTING: An 18-bed infectious diseases ICU in a 1,300-bed university hospital in Paris. PATIENTS: Four hundred twenty-one HIV-related admissions were recorded during the study period (33.5% of 1,258 admissions to ICU); 354 HIV-infected patients were first ICU admissions and were analyzed. MEASUREMENTS AND RESULTS: Predictive factors on univariate and multivariate analyses (logistic regression and Cox model) for short- and long-term mortality were performed. Respiratory failure was the main cause of admission (49.2%), followed by neurologic disorders (26.8%), sepsis (10.2%), heart failure (4.5%), and miscellaneous disorders (9.3%). For these groups, in-ICU and in-hospital mortality rates were as follows: 16.7% and 33.9%; 23.2% and 41.1%; 38.9% and 58.3%; 25% and 68.8%; and 12.1% and 24.2%, respectively. In-ICU and in-hospital mortality rates were significantly different across the groups (p=0.026 and 0.002, respectively). Multivariate analysis showed that the in-hospital outcome was significantly associated with functional status (p=0.05), time since AIDS diagnosis (p=0.04), HIV disease stage (0.016), simplified acute physiology score (SAPS I) (p=0.06), need for mechanical ventilation (p<0.000001), and its duration (p=0.0001). In the 281 patients who were discharged alive from the ICU, cumulative survival rates were 51%+/-38% at 6 months, 28%+/-38% at 12 months, and 18%+/-30% at 24 months. Median and crude mean+/-SD survival times were 199 days and 316+/-343 days. Multivariate analysis showed that the long-term outcome was significantly associated with functional status (p=0.000001), weight loss (p=0.00001), the CD4 count (p=0.00001), the HIV disease stage (p=0.01), the duration of AIDS (p=0.001), the admission cause group (p=0.03), and the SAPS I at admission (p=0.00001). CONCLUSIONS: The short-term (in-ICU and in-hospital) outcome of HIV-infected patients was mainly related to the severity of the acute illness (SAPS I, cause of admission, need for and duration of mechanical ventilation), and to the preadmission health status, based on functional status and weight loss. Some of these parameters, in particular the SAPS I and preadmission health status, also influenced the long-term outcome. Whereas HIV-related variables had little impact on the in-ICU outcome, they were closely related with the in-hospital outcome and even more strikingly with the long-term outcome. Thus, the life expectancy of HIV-infected patients, which depends primarily on the natural history of the HIV infection, is the most powerful determinant of the long-term prognosis. Our results confirm that ICU support for HIV-infected patients should not be considered futile.

APACHE↗