Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapeutic efficacy and the treatment days for cure of imipenem/cilastatin sodium (IPM/CS) in treatment of pulmonary infections were prospectively determined in comparison with those of beta-lactams other than carbapenems mainly ceftazidime (CAZ) or sulbactam/cefoperazone (SBT/CPZ). The overall response rate was 84.9% (62/73) in the IPM/CS group and 74.7% (56/75) in the beta-lactam group, the difference not being significant. In the subjects having underlying respiratory diseases, the response rate was 91.1% (41/45) and 73.9% (34/46) in the IPM/CS and beta-lactam groups, respectively. In patients with infections secondary to chronic respiratory disease, the rate was 91.2% (31/34) in the former group and 66.7% (24/36) in the latter group, respectively. The differences were significant for both stratified analyses. The treatment days for cure judged by the attending physician were 12.9 +/- 0.6 days in the IPM/CS group, and 14.5 +/- 0.7 days in the beta-lactam group. The difference was not, however, significant. In patients with mild to moderate infections, the treatment days for cure was 12.0 +/- 0.6 days (n = 64) in the IPM/CS group and 14.3 +/- 0.7 days (n = 70) in the beta-lactam group. In patients with underlying respiratory disease, the treatment days for cure were 11.8 +/- 0.7 days (n = 45) and 14.7 +/- 0.9 days (n = 46) in the IPM/CS and beta-lactam groups, respectively. In patients with infections secondary to chronic respiratory disease, the days were 11.1 +/- 0.7 days (n = 34) and 14.7 +/- 1.1 days (n = 36), respectively. Thus, IPM/CS therapy significantly reduced the number of treatment days until cure. There was, however, no significant difference between the two therapy groups in treatment of the patients with severe infections, those without underlying respiratory disease, or those with pneumonia and/or lung abscess. The treatment days for cure were also assessed by the members of review committee taking into consideration of body temperature, leukocyte count, and C-reactive protein. As the result, it was 6.9 +/- 0.5 days in the IPM/ CS and 10.3 +/- 0.7 days in the beta-lactam groups; respectively, and the difference was significant. Time (days) until cure was also compared between the two groups using survival time analysis, confirming a more rapid response in the IPM/CS group. Although IPM/CS therapy was associated with a shorter response time as assessed by both the attending physicians and the review committee, there were considerable differences between the results of these judgements. Thus, the duration of treatment with injectable antibiotics requires reevaluation in the future. No significant differences were observed between the groups with respect to parameters indicating side effects and laboratory abnormalities. There were no severe symptoms or laboratory findings, and symptoms and changes in laboratory values, if any resolved during the course of therapy or after the withdrawal of treatment. In conclusion, IPM/CS seems to be very useful as first-line therapy for respiratory tract infections and for shortening the duration of treatment.
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PMID:[Imipenem/cilastatin sodium and other beta-lactams for respiratory tract infections: clinical benefit and treatment days for cure]. 1020 83

The number of nosocomial infections caused by Acinetobacter baumannii has increased in recent years. The purposes of this study are to discover the risk factors of transmission to prevent the nosocomial infection of A. baumannii. We retrospectively studied 36 patients with A. baumannii bacteremia at China Medical College Hospital from January 1996 to December 1997. There were 23 males and 13 females. All bacteremia were acquired nosocomially. Malignancy (n = 8) and intracranial hemorrhage (n = 6) were the most common underlying diseases. Only one patient on arterial line disclosed intraarterial catheter-related A. baumannii bacteremia and 3 patients had evidence of A. baumannii pneumonia. Twenty-one patients (58%) had central venous catheters in place at the onset of bacteremia, but none was proven to be catheter-related infection. There were 32 patients (89%) with unknown portal of entry. Multivariate logistic regression analysis revealed that potential risk factors related to A. baumannii bacteremia were prior antimicrobial therapy (P < 0.05). The most common clinical features of A. baumannii bacteremia were, in descending order, fever, leukocytosis, thrombocytopenia and hypotension. Eleven patients (30.6%) died directly from A. baumannii bacteremia. All isolates were resistant to ampicillin, cephalothin, cefonicid and moxalactam. The most alarming evidence was that 19% of isolates showed resistance to imipenem. Our findings emphasized that A. baumannii bacteremia had the following characteristics: usually acquired nosocomially, unknown portal of entry, and high multiresistance, especially the increasing resistance rate to imipenem. Imipenem must be reserved as a last-line agent to treat A. baumannii infections, so we want to suggest that the treatment of choice for A. baumannii is gentamicin, amikacin or ceftazidime.
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PMID:Acinetobacter baumannii bloodstream infection: clinical features and antimicrobial susceptibilities of isolates. 1046 22

Pneumatoceles are cystic lesions of the lungs often seen in children with staphylococcal pneumonia and positive-pressure ventilation. Acinetobacter calcoaceticus is an aerobic, short immobile gram-negative rod, or coccobacillus, which is an omnipresent saprophyte. The variant anitratus is the most clinically significant pathogen in this family, usually presenting as a lower respiratory tract infection. Acinetobacter has been demonstrated to be one of the most common organisms found in the ICU. We present three critically ill surgery patients with Acinetobacter pneumonia, high inspiratory pressures, and the subsequent development of pneumatoceles. One of these patients died from a ruptured pneumatocele, resulting in tension pneumothorax. Treatment of pneumatoceles should center on appropriate intravenous antimicrobial therapy. This should be culture directed but is most often accomplished with Imipenem. Percutaneous, computed tomographic-guided catheter placement or direct tube thoracostomy decompression of the pneumatocele may prevent subsequent rupture and potentially lethal tension pneumothorax.
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PMID:Acinetobacter calcoaceticus pneumonia and the formation of pneumatoceles. 1082 47

Efficacy of panipenem/betamipron (PAPM/BP) against experimental pneumonia caused by penicillin-resistant Streptococcus pneumoniae (PRSP: MIC of benzylpenicillin, > or = 1.56 micrograms/ml) in mice was compared with those of imipenem/cilastatin (IPM/CS), meropenem (MEPM), cefozopran (CZOP), ceftriaxone (CTRX), ampicillin (ABPC), and vancomycin (VCM). The infection was induced by inoculating a PRSP clinical isolate, 9601 (serotype 6) or 10,693 (serotype 19), into ddY male mice intranasally. Drugs were administered subcutaneously at doses of 0.4, 2, and 10 mg/kg, 18, 26, 42, and 50 hours post-infection. Viable cell counts in the lungs were determined 66 hours post-infection. PAPM/BP showed the greatest efficacy against the infections among tested drugs. MICs of PAPM against PRSP 9601 and 10,693 were both 0.125 microgram/ml, which were superior to those of IPM (0.25 and 0.5 microgram/ml, respectively), MEPM (0.5 and 1 microgram/ml, respectively), CZOP (2 and 1 microgram/ml, respectively), CTRX (both 1 microgram/ml), ABPC (both 4 micrograms/ml), and VCM (0.5 and 0.25 microgram/ml, respectively). These results suggest that the potent in vivo activity of PAPM/BP reflects the potent in vitro activity of PAPM. MICs of PAPM, IPM, MEPM, and CZOP against clinical isolates, penicillin-susceptible S. pneumoniae (PSSP: MIC of benzylpenicillin, < or = 0.05 microgram/ml), penicillin-intermediate S. pneumoniae (PISP: MIC of benzylpenicillin, 0.1-0.78 microgram/ml), and PRSP, were tested by an agar dilution method. MIC90s of the drugs against the PSSP, PISP, and PRSP were as follows: PAPM, 0.012, 0.05, and 0.39 microgram/ml; IPM, < or = 0.006, 0.1, and 0.78 microgram/ml; MEPM, 0.05, 0.39, and 1.56 micrograms/ml; and CZOP, 0.2, 0.78, and 6.25 micrograms/ml, respectively. Thus, PAPM showed the most potent activity among tested drugs against clinical isolates of PISP and PRSP.
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PMID:[In vitro and in vivo activities of panipenem against penicillin-resistant Streptococcus pneumoniae]. 1156 55

The treatment of life-threatening infections due to carbapenem-resistant Acinetobacter baumannii has become a serious challenge for physicians worldwide. Often, only colistin shows in general good in vitro activity against these carbapenem-resistant strains, but its antibacterial efficacy in comparison with the antibiotics most used in clinical practice is not well known. We studied the efficacy of colistin versus those of imipenem, sulbactam, tobramycin, and rifampin in an experimental pneumonia model with immunocompetent mice. We used three strains of A. baumannii corresponding to the main clones (A, D, and E) involved in the outbreaks of our hospital, with different grades of resistance to imipenem (imipenem MICs of 1, 8, and 512 microg/ml, respectively) and to the other antibiotics. The MIC of colistin was 0.5 microg/ml for the three strains. Reduction of log(10) CFU/g in lung bacterial counts, clearance of bacteremia, and survival versus results with controls were used as parameters of efficacy. Imipenem and sulbactam (Deltalung counts: -5.38 and -4.64 log(10) CFU/ml) showed the highest level of bactericidal efficacy in infections by susceptible and even intermediate strains. Tobramycin and rifampin (-4.16 and -5.15 log(10) CFU/ml) provided good results against intermediate or moderately resistant strains, in agreement with killing curves and pharmacodynamics. On the contrary, colistin showed the weakest antibacterial effect among the antibiotics tested, both in killing curves and in the in vivo model (-2.39 log(10) CFU/ml; P < 0.05). We conclude that colistin did not appear as a good option for treatment of patients with pneumonia due to carbapenem-resistant A. baumannii strains. Other alternatives, including combinations with rifampin, may offer better therapeutic profiles and thus should be studied.
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PMID:Efficacy of colistin versus beta-lactams, aminoglycosides, and rifampin as monotherapy in a mouse model of pneumonia caused by multiresistant Acinetobacter baumannii. 1201 13

Infection with Burkholderia mallei (formerly Pseudomonas mallei) can cause a subcutaneous infection known as "farcy" or can disseminate to condition known as Glanders. It is primarily a disease affecting horses, donkeys and mules. In humans, Glanders can produce four types of disease: localized form, pulmonary form, septicemia, and chronic form. Necrosis of the tracheobronchial tree and pustular skin lesions characterize acute infection with B. mallei. Other symptoms include febrile pneumonia, if the organism was inhaled, or signs of sepsis and multiple abscesses, if the skin was the port of entry. Glanders is endemic in Africa, Asia, the Middle East, and Central and South America. Glanders has low contiguous potential, but because of the efficacy of aerosolized dissemination and the lethal nature of the disease, B. mallei was considered a candidate for biological warfare. During World War I, Glanders was believed to have been spread to infect large numbers of Russian horses and mules on the Eastern front. The Japanese infected horses, civilians and prisoners of war during World War II. The USA and the Soviet Union have shown interest in B. mallei in their biological warfare program. The treatment is empiric and includes mono or poly-therapy with Ceftazidime, Sulfadiazine, Trimethoprim + Sulfamethoxazol, Gentamicin, Imipenem etc. Aggressive control measures essentially eliminated Glanders from the west. However, with the resurgent concern about biological warfare, B. mallei is now being studied in a few laboratories worldwide. This review provides an overview of the disease and presents the only case reported in the western world since 1949.
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PMID:[Glanders--a potential disease for biological warfare in humans and animals]. 1217 May 62

In spite of the recent medical advances, lower respiratory tract infections are still the most frequent infectious causes of mortality worldwide. The objective of this study was to determine the frequency of occurrence and antimicrobial susceptibility of bacterial isolates collected from hospitalized patients with pneumonia in Latin American medical centers during the first four years of the SENTRY Program. The five most frequently isolated species were (n/%): Pseudomonas aeruginosa (659/26.3%), Staphylococcus aureus (582/23.3%), Klebsiella pneumoniae (255/10.2%), Acinetobacter spp. (239/9.6%), and Enterobacter spp. (134/5.4%). P. aeruginosa demonstrated high rates of resistance to most of the antimicrobials tested. Against P. aeruginosa, the most active agents were meropenem (MIC(50), 1 microg/ml; 71.6% susceptible), amikacin (MIC(50), 4 microg/ml; 71.0% susceptible), and piperacillin/tazobactam (MIC(50), 16 microg/ml; 70.4% susceptible). Imipenem (MIC(50), 1 microg/ml; 84.1% susceptible) and meropenem (MIC(50), 2 microg/ml; 84.9% susceptible) were the most active agents against Acinetobacter spp. followed by tetracycline (MIC(50), </=4 microg/ml; 52.3% susceptible). Although the broad-spectrum cephalosporins had demonstrated excellent in vitro activity against Klebsiella pneumoniae isolates (MIC(50)s range, </= 0.12 to 0.25 microg/ml), elevated rates of resistance (46.3%-58.5%) were observed. Approximately 44.0% and 29.0% of K. pneumoniae and E. coli isolates were considered ESBL producers based on NCCLS criteria, respectively. Overall, the prevalence of methicillin-resistant S. aureus was 46.2%. The most active drugs against this pathogen were vancomycin, teicoplanin, linezolid and quinupristin/dalfopristin. In summary, the SENTRY Antimicrobial Surveillance Program has detected a high prevalence of methicillin-resistant S. aureus and multidrug resistant non-fermentative Gram-negative bacilli isolated from respiratory tract specimens of hospitalized patients with pneumonia in Latin America. Our results emphasize the importance of local surveillance programs in correctly guiding empiric therapy and local intervention programs in attempt to reduce antimicrobial resistance.
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PMID:Respiratory tract pathogens isolated from patients hospitalized with suspected pneumonia in Latin America: frequency of occurrence and antimicrobial susceptibility profile: results from the SENTRY Antimicrobial Surveillance Program (1997-2000). 1249 78

Acinetobacter spp. are predominantly nosocomial pathogens of growing importance. One of their important features is antimicrobial resistance that includes beta-lactams, aminoglycosides and quinolones. Imipenem, considered the most effective drug against Acinetobacter spp., is not universally active against clinical isolates and therapeutic options are necessary. In vitro studies demonstrate the activity of beta-lactamase inhibitors with direct antimicrobial activity, polymyxins, doxycycline and rifampin. Synergy of various combinations has been demonstrated in vitro. Experimental models of infection in mice and rabbits show the efficacy of rifampin and doxycycline. Colistin did not lead to good results in a mouse pneumonia model. There are no randomised, controlled studies on the treatment of Acinetobacter spp. infections. Retrospective comparative studies suggest that ampicillin-sulbactam may be comparable to imipenem in the treatment of pneumonia and bacteraemia. There are a few uncontrolled studies using ampicillin-sulbactam and one study with colistin with results that suggest that they may be acceptable options to treat multi-resistant infections.
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PMID:Treatment of Acinetobacter spp infections. 1287 37

Abstract Sub-inhibitory concentrations of imipenem and meropenem were evaluated for their ability to induce morphological changes with six strains of Acinetobacter baumannii isolated from patients with nosocomial pneumonia. Three strains were susceptible and three were resistant to carbapenems. The strains were grown in the presence of 0 (controls), 0.25x, 0.5x and 1x the MIC of both carbapenems for 4 h, and then examined after Gram's stain. Cells > or = 3 microm in size (spheroplasts) were considered to be altered. Both carbapenems induced significant numbers of spheroplasts compared to controls. Imipenem had more effect against susceptible strains, while meropenem had a greater effect against resistant strains.
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PMID:Morphological changes induced by imipenem and meropenem at sub-inhibitory concentrations in Acinetobacter baumannii. 1537 91

Previous studies have shown decreased in vitro activity of zwitterionic cephalosporins and carbapenems against porin-deficient Klebsiella pneumoniae expressing a plasmid-mediated AmpC-type beta-lactamase (PACBL). The in vitro and in vivo activities of cefepime and imipenem were evaluated against the porin-deficient strain K. pneumoniae C2 and its CMY-2-producing derivative [K. pneumoniae C2(pMG248)]. The MICs (in micrograms/milliliter) of cefepime and imipenem against K. pneumoniae C2 were 0.125 and 0.25, respectively, while the corresponding values against K. pneumoniae C2(pMG248) were 8 and 16. Cefepime showed a greater inoculum effect than imipenem against both strains. Imipenem showed a significant postantibiotic effect (>2 h) against K. pneumoniae C2(pMG248) at 1x, 2x, 4x, 6x, and 8x MIC. The maximum concentrations of drug in serum of cefepime and imipenem in a pneumonia model using mice were 124.1 and 16.9 mug/ml, respectively. DeltaT/MIC for K. pneumoniae C2 and C2(pMG248) were 1.29 h and 0.34 h for imipenem and 2.96 h and 1.27 h for cefepime. Both imipenem (30 mg/kg of body weight every 3 h) and cefepime (60 mg/kg every 4 h), administered for 72 h, increased the survival rate (86.6% and 100%) compared with untreated control animals (26.6%, P < 0.003) infected with K. pneumoniae C2. For the CMY-2-producing strain, imipenem, but not cefepime, increased the survival rate compared to the controls (86.6% and 40% versus 40%, P < 0.01). Bacterial concentration of the lungs was significantly decreased by both antimicrobials. In conclusion, imipenem was more active in terms of survival than cefepime for the treatment of murine pneumonia caused by a porin-deficient K. pneumoniae expressing PACBL CMY-2.
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PMID:Efficacy of cefepime and imipenem in experimental murine pneumonia caused by porin-deficient Klebsiella pneumoniae producing CMY-2 beta-Lactamase. 1604 41


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