Ventilator-associated pneumonia (VAP) is the most frequent infection among patients hospitalized in intensive care units, maintaining a high morbidity and mortality. The global incidence of VAP ranges from 8 to 28%. Early-onset VAP is mainly caused by community pathogens with a favorable pattern of antibiotic sensitivity, whereas late-onset VAP is often caused by multidrug-resistant pathogens, mainly methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa and Acinetobacter spp. and enteric Gram-negative bacilli. The diagnosis of VAP remains difficult to confirm, lacking both microbiological analysis and radiological signs of high specificity. The Clinical Infection Pulmonary Score has been proposed to overcome the difficulties related to the diagnosis, but is not applicable to all patient categories. A continuous evaluation of the antimicrobial therapeutic options, along with their pharmacodynamic and pharmacokinetic profiles, is mandatory to create therapeutic protocols and reduce VAP-related mortality.

The most frequent complication from infection after solid organ transplantation is bacterial infection. This complication is more frequent in organ transplantation involving the abdominal cavity, such as liver or pancreas transplantation, and less frequent in heart transplant recipients. The sources, clinical characteristics, antibiotic resistance and clinical outcomes vary according to the time of onset after transplantation. Most bacterial infections during the first month post-transplantation are hospital acquired, and there is usually a high incidence of multidrug-resistant bacterial infections. The higher incidence of complications from bacterial infection in the first month post-transplantation may be associated with high morbidity. Of special interest due to their frequency are infections by S. aureus, enterococci, Gram-negative enteric and non-fermentative bacilli. Opportunistic bacterial infections may occur at any time on the posttransplant timeline, but are more frequent between months two and six, the period in which immunosuppression is higher. The most frequent bacterial species causing opportunistic infections in organ transplant recipients are Listeria monocytogenes and Nocardia spp. After month six, posttransplantation solid organ transplant patients usually develop conventional community-acquired bacterial infections, especially urinary tract infections by E. coli and S. pneumoniae pneumonia. In this article we review the clinical characteristics, epidemiology, diagnosis and prognosis of bacterial infections in solid organ transplant patients.

Implants can be colonized by microorganisms from oral biofilms and may affect peri-implant tissues health. Among these bacteria, pathogens typically associated with periodontitis can be found, such as Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, as well as Gram negative enteric bacilli not typically associated with periodontal diseases.Superinfecting bacteria were characterized from peri-implant lesions in patients with history of periodontitis.Sixty-eight implants were studied in 55 patients; the average patient age was 56 years. Forty-nine implants had peri-implant lesions and 19 were considered stable. Subgingival samples were obtained in affected and stable implants. The samples were streaked on Mac-Conkey agar and incubated at 37°C for 24 hours. The colonies were identified with the kit-BD BBL Crystal E/NF®.Superinfecting organisms were detected in 20 patients--they were seen more frequently at diseased implants (n=15) than at healthy implants (n=5). The prevalence of superinfecting bacteria on the selected implants was 33.8% (n=23/68). These bacteria were more prevalent among affected implants (n=17 or 25%) than those with stable implants n=6 (8.8%). Klebsiella pneumoniae was the most frequent Gram negative rod detected (n=12).One-third of the implants had superinfecting organisms. Implants with a peri-implant lesion had a higher frequency of superinfecting bacteria. Klebsiella pneumoniae was the most common superinfecting organism isolated. A multiple infection caused by superinfecting bacteria was present only at diseased implants. These microbial agents potentially affect implant stability.

This study reports a cluster of septicaemic newborns with imipenem-resistant Escherichia coli in the blood and delineates the possible mechanisms of transmission of imipenem resistance with respect to the New Delhi metallo-β-lactamase (NDM-1) gene.During a point prevalence survey, attempts were made to isolate Gram-negative bacilli (GNB) from the environment of a sick newborn care unit (SNCU) and body sites of neonates. Subsequently, four fresh neonates admitted to the SNCU developed sepsis with E. coli. E. coli isolates from body sites and blood of the newborns were analysed in terms of clonality, carbapenemases, integrons, virulence factors, porins and transmissibility.During the survey, both imipenem-resistant and imipenem-susceptible E. coli were isolated from the body sites of neonates, but none from the environment. None of these neonates developed sepsis. The freshly admitted septicaemic neonates had imipenem-resistant E. coli in their blood, which were similar to the imipenem-susceptible E. coli obtained from the body sites (during the survey) in terms of clonality, phylogroup, virulence and other resistance genes, except possession of bla(NDM-1). Imipenem-resistant E. coli from blood and body sites were not clonal, though both had bla(NDM-1). Besides E. coli, other GNB isolated from the environment and body sites also harboured bla(NDM-1). Imipenem-resistant and imipenem-susceptible E. coli from the blood and body sites respectively, possessed a novel AmpC β-lactamase, bla(CMY-59). The plasmid carrying bla(NDM-1) was transferable.The time frame of isolation and clonal identity indicated a possible transfer of bla(NDM-1) from imipenem-resistant GNB to the imipenem-susceptible E. coli, which subsequently caused septicaemia. This establishes the promiscuous nature of bla(NDM-1) and emphasizes the need for the early recognition of similar isolates.

To review the risk factors, etiologic profile, treatment approaches, and guidelines for the management of nursing home-acquired pneumonia (NHAP).A search of the current literature was conducted using the MEDLINE and Embase databases. This search, limited to studies performed in humans and published in English between January 1, 1990 and October 31, 2009, included the terms 'acquired pneumonia', 'associated pneumonia', 'nursing home', 'long-term care', 'institution', and 'healthcare'.Older age, male gender, swallowing difficulty, and inability to take oral medications are all significant risk factors for pneumonia. Medications such as antipsychotics and anticholinergics, histamine receptor blockers and proton pump inhibitors have also been linked to higher risk of pneumonia. The etiology of NHAP overlaps with that of community-acquired pneumonia (CAP), with Streptococcus pneumoniae and Haemophilus influenzae as predominant pathogens in long-term care facilities. In patients who require hospitalization, Chlamydophila pneumoniae, Staphylococcus aureus, and influenza virus have also been identified. In contrast, the etiology of severe NHAP overlaps with that of hospital-acquired pneumonia (HAP), with S. aureus, including methicillin-resistant S. aureus (MRSA), Pseudomonas aeruginosa, and enteric Gram-negative bacilli as important causative pathogens. Therapy is dependent on disease severity and, on the treatment setting. Respiratory fluoroquinolones or β-lactams plus a macrolide are recommended in patients with NHAP. Patients hospitalized with severe NHAP may require triple combination therapy that covers both MRSA and P. aeruginosa. However, there is little evidence of the clinical superiority of one regimen over another, making it challenging to establish guidelines for the treatment of NHAP in the nursing home setting.There is a pressing need for clinical trials of antibiotic therapy in nursing home patients that would help establish uniform guidelines to standardize therapy in the nursing home setting.

Infections caused by Acinetobacter baumannii are a threat to neonates because of its resistance to antimicrobials, including carbapenems. In 2007, A. baumannii emerged as an important aerobic Gram-negative bacillus (12.5%, 4/32) that caused sepsis in our unit. A. baumannii from the gut of the neonates was analyzed, as this could be indicative of the antibiotic resistance of the organisms. The study attempts to understand the gut colonization with multidrug-resistant A. baumannii among hospitalized neonates with special reference to carbapenem resistance. A. baumannii was found in the gut of 11% of babies. Interestingly, 60.7% (17/28) and 21.4% (6/28) of the isolates from the gut were multidrug-resistant and carbapenem-resistant, respectively. The number of multidrug-resistant and carbapenem-resistant isolates from blood cultures were 3/4 and 1/4, respectively. The study reports for the first time OXA-23 and OXA-58 carbapenemases in A. baumannii from India. Pulsed field gel electrophoresis (PFGE) patterns indicated that the strains were diverse and no epidemic clone existed. Though A. baumannii gut colonization could not be implicated as a risk factor for subsequent sepsis, the high rate of isolation of multidrug-resistant and carbapenem-resistant isolates indicates that these therapeutic options might be drastically reduced among neonates in the future.

Gut microbiota contribute to the health of their hosts, and alterations in the composition of this microbiota can lead to disease. Previously, we demonstrated that indigenous gut bacteria were required for the insecticidal toxin of Bacillus thuringiensis to kill the gypsy moth, Lymantria dispar. B. thuringiensis and its associated insecticidal toxins are commonly used for the control of lepidopteran pests. A variety of factors associated with the insect host, B. thuringiensis strain, and environment affect the wide range of susceptibilities among Lepidoptera, but the interaction of gut bacteria with these factors is not understood. To assess the contribution of gut bacteria to B. thuringiensis susceptibility across a range of Lepidoptera we examined larval mortality of six species in the presence and absence of their indigenous gut bacteria. We then assessed the effect of feeding an enteric bacterium isolated from L. dispar on larval mortality following ingestion of B. thuringiensis toxin.Oral administration of antibiotics reduced larval mortality due to B. thuringiensis in five of six species tested. These included Vanessa cardui (L.), Manduca sexta (L.), Pieris rapae (L.) and Heliothis virescens (F.) treated with a formulation composed of B. thuringiensis cells and toxins (DiPel), and Lymantria dispar (L.) treated with a cell-free formulation of B. thuringiensis toxin (MVPII). Antibiotics eliminated populations of gut bacteria below detectable levels in each of the insects, with the exception of H. virescens, which did not have detectable gut bacteria prior to treatment. Oral administration of the Gram-negative Enterobacter sp. NAB3, an indigenous gut resident of L. dispar, restored larval mortality in all four of the species in which antibiotics both reduced susceptibility to B. thuringiensis and eliminated gut bacteria, but not in H. virescens. In contrast, ingestion of B. thuringiensis toxin (MVPII) following antibiotic treatment significantly increased mortality of Pectinophora gossypiella (Saunders), which was also the only species with detectable gut bacteria that lacked a Gram-negative component. Further, mortality of P. gossypiella larvae reared on diet amended with B. thuringiensis toxin and Enterobacter sp. NAB3 was generally faster than with B. thuringiensis toxin alone.This study demonstrates that in some larval species, indigenous gut bacteria contribute to B. thuringiensis susceptibility. Moreover, the contribution of enteric bacteria to host mortality suggests that perturbations caused by toxin feeding induce otherwise benign gut bacteria to exert pathogenic effects. The interaction between B. thuringiensis and the gut microbiota of Lepidoptera may provide a useful model with which to identify the factors involved in such transitions.

Increasing prevalence of infections caused by multiresistant gram-negative enteric bacilli due to synthesis of extended-spectrum beta-lactamase (ESBL) or to desrepressed chromosomic AmpC beta-lactamase (AmpC) is a major concern in the hospitalized patient population. Renal transplant recipients are especially susceptible to these infections. A cohort observational study in a 3-year period was performed. ESBL-production was determined by phenotypic analysis based on the CLSI recommendations. A multi-variate logistic regression analysis was performed to identify independent variables associated with multi-resistant gram-negative bacilli infection. The study included 417 patients (61 double kidney-pancreas recipients). The incidence of ESBL-producing and desrepressed chromosomic AmpC beta-lactamase resistance was 11.8% (49 patients). The most frequent bacteria isolated was E. coli (35/60 isolations), followed by Klebsiella spp(12/60 isolations). Double kidney-pancreas transplantation(OR 3.5, CI95% 1.6-7.8), previous use of antibiotics(OR 2.1,CI95% 1.1-4.1), posttransplant dialysis requirement (OR 3.1, CI95% 1.5-6.4) and posttransplant urinary obstruction (OR 5.8, CI95% 2.2-14.9) were independent variables associated with these multiresistant gram-negative enteric bacilli infections. The incidence of ESBL-producing and desrepressed AmpC beta-lactamase gram-negative enteric bacilli infection in our population was high. These infections are associated with significant morbidity after renal transplantation.

Bloodstream infections (BSIs) are a major cause of morbidity and mortality in transplant recipients. The aim of this study is to describe the incidence, microbiology and outcomes of BSIs in transplant recipients in Spain. The Spanish Network for Research on Infection in Transplantation (RESITRA) is formed by 16 centers with transplant program in Spain. The incidence and characteristics of BSIs in transplant patients were obtained prospectively from the cohort. We included 3926 transplant recipients (2935 solid organ and 991 hematopoietic stem cell transplants). Overall, 730 episodes of BSIs were recorded with an incidence rate ranging from 3 episodes per 10 000 transplant days in kidney recipients to 44 episodes per 10 000 transplant days in allogeneic hematopoietic stem cell transplantation (HSCT). The most frequent sources were intravascular catheters and the most frequent microorganisms isolated were coagulase-negative staphylococci. Crude mortality of BSIs was 7.8%, being highest in liver recipients (16%). Multidrug resistant nonfermentative gram-negative BSIs had significantly worse prognosis than those caused by their susceptible counterparts (p = 0.015), but no differences were found between resistant and susceptible gram-negative enteric bacilli, S. aureus or Candida spp. BSIs are still a major concern in transplant recipients. The increasing isolations of multiresistant microorganisms represent a challenge for the next years.

Bacteria play a leading role in acute exacerbations of chronic obstructive pulmonary disease (COPD), but we lack predictors of bacterial etiology. We developed a prediction model for infection with gram-negative enteric bacteria (GNEB) and Pseudomonas aeruginosa.Clinical presentation, sputum characteristics, microbial sputum patterns, lung function and previous and concomitant medication were prospectively recorded in patients with moderate to severe exacerbation of COPD. Risk factors for a specific bacterial etiology were calculated and a prediction model developed.A total of 193 patients with acute exacerbation were included. In 121 (62.6%) of them a microbial etiology could be identified, most frequently Haemophilus influenzae (32 strains), Streptococcus pneumoniae (22 strains) and P. aeruginosa (12 strains). Multivariate analysis identified severe airflow obstruction and use of systemic steroids as predictors for exacerbation due to gram-negative enteric bacilli and P. aeruginosa. A prediction model including FEV1 < 35% of predicted value, systemic steroid use and prior antibiotic therapy within preceeding 3 months had a negative predictive of 89%, being a helpful tool in excluding patients at risk of exacerbation due to gram-negative enteric bacilli and P. aeruginosa when all criteria are absent.A simple prediction model based on three factors may identify COPD patients at low risk for exacerbations with gram-negative enteric bacilli and P. aeruginosa. Bacterial Etiology in COPD Exacerbations.