Late-onset Nosocomial Pneumonia Research Articles

Etiology of Hospital-Acquired Pneumonia (HAP) and Ventilator-Associated Pneumonia (VAP) in Tertiary-Care Hospitals in Thailand: A Multicenter, Retrospective Cohort Study.

To describe the top three causative organisms of hospital acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) in Thailand. This multi-center retrospective cohort study included HAP/VAP patients hospitalized in 2019 in three university-affiliated hospitals and a private hospital in Bangkok, Thailand. Medical records of patients with a documented diagnosis of nosocomial pneumonia (NP) were systematically reviewed to collect data on demographic, clinical, microbiological, and 30-day readmission due to NP. A total of 240 patients were included in the study, comprises patients with VAP (62.9%), HAP (36.7%), and ventilated HAP (vHAP) (0.4%). All of the patients had late-onset NP, occurring after five days of hospitalization with median time to NP of 13 days (interquartile range [IQR] 6-25 days) from admission. The top three causative pathogens of NP were Acinetobacter baumannii (44.2%), Pseudomonas aeruginosa (34.6%), and Klebsiella pneumoniae (28.3%). A high rate of carbapenem resistance (CR) in A. baumannii (92.5%) was observed. Lower rates of CR were observed in K. pneumoniae (20.6%) and P. aeruginosa isolates (16.9%). Readmission rate due to NP within 30 days after discharge was less than 2% with median time of 4 days (IQR 3-20 days) after discharge. After diagnosis of NP, 19 patients were transferred to intensive care units with median length of stays of 11 days (IQR 3-24 days). Fifty-one percent of HAP patients received mechanical ventilation support after the diagnosis of NP with median length of mechanical ventilation use of 12 days (IQR 6-22 days). A. baumannii, with its significant carbapenem resistance, presents a major HAP/VAP pathogens and imposes a substantial burden on healthcare resources in this study. Implementation of regular surveillance for causative organisms of NP and their susceptibility profiles are critical for the success of HAP/VAP management, and reducing the related burden of healthcare resources.

Role of clinical pulmonary infection score and serum C-reactive protein in detecting the efficacy of therapeutic choices in the management of Enterobacter aerogenes nosocomial pneumonia

Introduction and background Nosocomial pneumonia is the second most common nosocomial infection. It is usually bacterial in origin. Nosocomial pneumonia is responsible for 25% of infections in the ICU. Early-onset nosocomial pneumonia tends to carry a better prognosis than does late-onset nosocomial pneumonia. Patients and methods This study was planned to evaluate the role of the clinical pulmonary infection score (CPIS) and C-reactive protein (CRP) in detecting the efficacy of antibiotic therapy chosen for treatment of nosocomial Enterobacter pneumonia. In all, 200 patients admitted to the ICU who had evidence of pneumonia were included in the study. Patients were followed up by evaluating their serum CRP levels and CPIS during the first 8 days of admission. Results Enterobacter aerogenes represented 24% of nosocomial pneumonia cases in the study. An overall 70.8% of patients with E. aerogenes detected in culture and sensitivity were sensitive to both amikacin and levofloxacin. Those patients received only amikacin. Sixteen patients provided good response to amikacin. The remaining 18 patients showed poor response to amikacin therapy (proved by insignificant differences between CPIS and CRP on the first and fourth day of admission). In the case of these patients levofloxacin was added to antibiotic therapy and they were followed up for a further 4 days. The results demonstrated that 16 patients provided good response to amikacin and levofloxacin on the fifth and eighth days. Conclusion This study demonstrated that CPIS and serum CRP can be used as indicators of the efficacy of antibiotics in nosocomial pneumonia.

Emergence of methicillin-resistant Staphylococcus aureus USA300 genotype as a major cause of late-onset nosocomial pneumonia in intensive care patients in the USA

To compare demographic and clinical characteristics, and methicillin-resistant Staphylococcus aureus (MRSA) strain characteristics, in patients with early-onset (EO) and late-onset (LO) MRSA nosocomial pneumonia. This was a retrospective analysis of data from a multicenter observational study of nosocomial pneumonia patients admitted between November 2008 and July 2010. Laboratory analyses performed on MRSA isolates included confirmation of antimicrobial susceptibility and heteroresistance to vancomycin, USA typing, staphylococcal cassette chromosome (SCC) mec typing, and detection of Panton-Valentine leukocidin (PVL) genes. We identified 134 patients; 42 (31%) had EO MRSA pneumonia and 92 (69%) had LO MRSA pneumonia. The patients in the LO group were more likely to have risk factors for multidrug-resistant pathogens (98% vs. 76%, p<0.001). The MRSA USA300 strain was found with equal frequency in the EO and LO groups. Likewise, both groups had similar frequencies of isolates exhibiting PVL and SCCmec type IV. Our findings provide further evidence of the continued migration of community-associated MRSA into the healthcare setting in the USA. MRSA USA300 genotype has emerged as a significant cause of LO nosocomial pneumonia in intensive care units. Appropriate anti-MRSA antimicrobial therapy should be considered for both EO and LO hospital-acquired pneumonia and ventilator-associated pneumonia.

The risk of late-onset nosocomial pneumonia is increased in patients receiving ranitidine and omeprazole

The risk of late-onset nosocomial pneumonia is increased in patients receiving ranitidine and omeprazole

Empiric broad-spectrum antibiotic therapy of nosocomial pneumonia in the intensive care unit: a prospective observational study

IntroductionAntibiotic de-escalation, which consists of the initial institution of empiric broad-spectrum antibiotics followed by antibiotic streamlining driven by microbiological documentation, is thought to provide maximum benefit for the individual patient, while reducing the selection pressure for resistance.MethodsTo assess a carbapenem-based de-escalating strategy in nosocomial pneumonia (NP), a prospective observational study was conducted in critically ill patients with NP treated empirically with imipenem ± aminoglycoside/glycopeptide in 24 intensive care units of Spanish general hospitals. Overall, 244 patients were assessable (91% with late-onset NP). The primary outcome was therapeutic success 7–9 days post therapy.ResultsMicrobial identification – based on cultures of tracheal aspirates in 82% of patients, cultures of protected specimen brush in 33%, and cultures of bronchoalveolar lavage in 4% – was only available for 131 (54%) patients. Initial antibiotics were inadequate for 23 (9%) patients. Of the remaining patients, antibiotics were streamlined in 56 (23%) patients and remained unchanged in 14 (6%) patients based on microbiology data, in 38 (16%) patients despite microbiology data favouring de-escalation, and in 113 (46%) patients due to unknown aetiology. Overall, de-escalation was implemented in only 23% of patients with potentially multiresistant pathogens, compared with 68% of patients with the remaining pathogens (P < 0.001). Response rates were 53% for patients continuously treated with imipenem-based regimens and 50% for the de-escalated patients. Higher Acute Physiology, Age, and Chronic Health Evaluation II scores were associated with greater mortality, whereas adequate empiric antibiotic therapy protected against fatal outcomes. No increase of superinfection rates caused by emerging pathogens was observed. The costs associated with de-escalation were mainly dependent on the duration of hospitalization.ConclusionThis study mainly highlights the current practice of a specific algorithm of de-escalation solely based on the available microbiological data, and highlights the barriers to using it more widely. In this setting, de-escalation was less likely to occur in the presence of potentially multiresistant pathogens. Prior antibiotic administration and the low use of bronchoscopic techniques may have influenced negatively the implementation of de-escalation. Optimization of de-escalation strategies for NP should rely on a correct choice of empiric antibiotics, on appropriate microbiological investigations, and on a balanced interpretation of microbiological and clinical data.

Nosocomial pneumonia.

Nosocomial pneumonia (NP) is defined as pneumonia that develops within 48 hours or more of hospital admission and which was not developing at the time of admission. Nosocomial pneumonia, also known as hospital-acquired pneumonia (HAP), is the second most common hospital infection, while ventilator-associated pneumonia represents the most common intensive care unit (ICU) infection. Nosocomial pneumonia significantly contributes to morbidity, mortality, and escalating healthcare costs because of increases in antibiotic prescription and administration, length of ICU stay, and length of hospital stay. Aspiration and colonization of the upper respiratory tract seem to be the major pathogenetic mechanisms for the development of NP, either in intubated or spontaneously breathing patients. The microbiology of NP depends on the timing of onset. In early-onset NP, the responsible pathogens are generally endogenous community-acquired pathogens. In late-onset NP, the responsible microbes include potentially multi-drug-resistant nosocomial organisms residing in oropharyngeal or gastric contents. Important risk factors for development of NP include coma, intubation, prolonged mechanical ventilation, repeated intubations, supine positioning, and long-term antibiotic use. The most significant preventive measures include routine hand washing and avoidance of (1) the supine position, (2) inappropriate antibiotics, and (3) overuse of H2-antagonists for stress ulcer prophylaxis. Accurate diagnosis of NP is difficult and controversial, warranting consideration for the application of invasive quantitative culture techniques over tracheal aspirates. Empiric antibiotic treatment should be prompt, starting on clinical suspicion, and based on local ICU pathogen epidemiology and antibiotic resistance patterns and on a deescalating antibiotic strategy. Innovative antibiotic strategies, such as antibiotic rotation, to help prevent the emergence of multi-drug-resistant pathogens and improve survival should be considered.

Epidemiology of Nosocomial Pneumonia in Infants After Cardiac Surgery

The pattern of nosocomial pneumonia (NP) in infants in a pediatric surgical ICU after cardiac surgery may differ from that seen in adult ICUs. The primary aim of this study was to describe the epidemiology of NP in infants after cardiac surgery and, secondarily, to describe the changes of the distribution and antibiotic resistance of the pathogen during the last 3 years. Data were collected between June 1999 and June 2002 from 311 consecutive infants who underwent open-heart surgery in our hospital. We retrospectively analyzed the distribution and antibiotic resistance pattern of all the pathogenic microbial isolates cultured from lower respiratory tract aspirations. Of 311 infants, 67 patients (21.5%) acquired NP after cardiac surgery. The incidence of NP was more frequently associated with complex congenital heart defect (CHD) compared to simple CHD (43% vs 15.9%, chi(2) = 22.47, p < 0.0001). The proportion of late-onset NP was higher in patients with complex CHD (chi(2) = 6.02, p = 0.014). A total of 79 pathogenic microbial strains were isolated. Gram-negative bacilli (GNB) were the most frequent isolates (68 isolates, 86.1%), followed by fungi (6 isolates, 7.6%) and Gram-positive cocci (5 isolates, 6.3%). The main GNB were Acinetobacter baumanii (11 isolates, 13.9%), Pseudomonas aeruginosa (10 isolates, 12.7%); other commonly seen GNB were Flavobacterium meningosepticum (7 isolates, 8.9%), Klebsiella pneumoniae (7 isolates, 8.9%), Escherichia coli (6 isolates, 7.6%), and Xanthomonas maltophilia (5 isolates, 6.2%). The most commonly seen Gram-positive cocci were Staphylococcus aureus (2 isolates, 2.5%) and Staphylococcus epidermidis (2 isolates, 2.5%). The frequent fungi were Candida albicans (5 isolates, 6.3%). Most GNB were sensitive to cefoperazone-sulbactum, piperacillin-tazobactam, imipenem, ciprofloxacin, amikacin. The bacteria producing extended spectrum beta-lactamases were mainly from K pneumoniae and E coli; the susceptibility of ESBL-producing strains to imipenem was 100%. There were one case of methicillin-resistant S aureus (MRSA) and 1 case of methicillin-resistant S epidermidis; their susceptibility to vancomycin, gentamycin, and ciprofloxacin were 100%. From 1999 to 2002 in infants with NP after open-heart surgery, there was a trend of increasing frequency of multiresistant GNB such as A baumanii, P aeruginosa, and K pneumoniae. However, no remarkable changes of distribution were found in Gram-positive cocci and fungi in the 3-year period. Early onset episodes of NP were frequently caused by Haemophilus influenzae, methicillin-sensitive S aureus, and other susceptible Enterobacteriaceae. Conversely, in patients who acquired late-onset NP, P aeruginosa, A baumannii, other multiresistant GNB, MRSA, and fungi were the predominant organisms. The pattern of pathogens and their antibiotic-resistance patterns in NP in infants after cardiac surgery had not shown an increasing prevalence of Gram-positive pathogens as reported by several adult ICUs. GNB still remained the most common pathogens during the last 3 years in our hospital. There was a trend of increasing antibiotic resistance in these isolates.

Nosocomial pneumonia.

Despite abundant literature on the management of nosocomial pneumonia, a number of aspects, from diagnosis to the therapy of nosocomial pneumonia, are still controversial. This review focuses on recent advances that can aid in the day-to-day care of these critically ill patients. The risk factors for nosocomial pneumonia in specific subsets of trauma, postoperative and burn injury patients have been identified, with emphasis on the type of pneumonia developing in these populations - early or late onset nosocomial pneumonia. Resolution of nosocomial pneumonia, in terms of improvement of clinical parameters such as oxygenation, fever, leukocytosis and bacterial eradication, has been reported, and these data can lead to a better understanding of the natural course of the disease. The importance of initial, accurate empiric therapy in improving mortality in nosocomial pneumonia has been reinforced by multiple studies. Newer techniques to study colonization and the routes of spread of pathogenic organisms in the intensive care unit are adding to our understanding of how pneumonia develops, the role of infection control measures and the types of strategies that are needed for prevention. Oral decontamination is showing promise as a technique to prevent ventilator-associated pneumonia, and noninvasive ventilation has been shown to be useful in various etiologies of respiratory failure, with the beneficial effect of reducing the incidence of ventilator-associated pneumonia and its associated mortality. The implementation of protocolized treatment guidelines and antibiotic rotation policies are emerging as useful tools for reducing the frequency of antibiotic resistance and the impact of nosocomial pneumonia. There is a better understanding of nosocomial pneumonia risk factors, mechanisms of bacterial colonization, and resolution of illness, with exciting developments in prevention and treatment emerging, and these data can help us achieve more effective management of this complex illness.

Risk factors for late-onset nosocomial pneumonia caused by Stenotrophomonas maltophilia in critically ill trauma patients.

Patients with nosocomial pneumonia caused by Stenotrophomonas maltophilia often receive inadequate empiric antibiotic therapy, potentially increasing mortality. Knowledge of the risk factors associated with S. maltophilia pneumonia may better guide the selection of empiric antibiotic therapy. Potential risk factors for S. maltophilia pneumonia were retrospectively analyzed for critically ill trauma patients with late-onset gram-negative pneumonia. The effects of S. maltophilia infection and inadequate empiric antibiotic therapy on patient outcomes were also assessed. By multivariate analysis, S. maltophilia pneumonia was found to be associated with cefepime exposure and tracheostomy in patients with a single pneumonia episode and with higher Injury Severity Score and pulmonary contusion in patients with multiple pneumonia episodes. S. maltophilia pneumonia was associated with increased patient morbidity; only inadequate empiric antibiotic therapy was associated with a higher mortality rate. In critically ill trauma patients with late-onset ventilator-associated pneumonia and these risk factors, empiric antibiotic therapy should include agents active against S. maltophilia.

Mortality associated with late-onset pneumonia in the intensive care unit: results of a multi-center cohort study.

To evaluate the attributable mortality associated with late-onset nosocomial pneumonia (LOP) while taking into account the severity at admission, the evolution of the patients during the first 4 days after admission to the ICU and the appropriateness of initial empiric antibiotic treatment. Multicenter cohort study with prospective standardization of diagnostic interventions when nosocomial pneumonia develops. Medical and surgical ICUs of four university-affiliated teaching hospitals. Seven hundred sixty-four consecutive patients requiring ICU hospitalization for at least 4 days. The clinical and biological data as well as the therapeutic data and the outcome were prospectively recorded from the day of admission to ICU discharge. Simplified Acute Physiologic Score (SAPS II) and Logistic Organ Dysfunction (LOD) score were collected and computed within the first 4 calendar days of ICU admission. Variables associated with the outcome were selected using a stepwise Cox model. The time to acquisition of the first LOP was then introduced in the final model as a time-dependent covariate. The analysis was stratified by ICU center. Finally, as initial antibiotic therapy could have an impact on the increased risk of death induced by LOP, the Cox model was applied again introducing LOP immediately adequately treated and LOP not immediately adequately treated as two different time-dependent covariates. Late-onset pneumonia developed in 89 patients (12%). A McCabe score of more than 1, SAPS II score and increases in SAPS between days 1 and 2, days 2 and 3, and days 3 and 4 were significantly associated with an increased risk of death. When the time to acquisition of the first episode of LOP was introduced into the Cox model, the LOP occurrence was associated with increased mortality, even adjusted over the selected prognostic parameters and after stratification by center (hazard ratio (HR)=1.53, 95% CI 1.02-2.3, p=0.04). When LOP immediately adequately treated and LOP not immediately adequately treated were separately introduced into the Cox model, inappropriately treated LOP remained significantly associated with an increased risk of mortality (HR=1.69, 95% CI 1.08-2.65, p=0.022), whereas appropriately treated LOP did not (HR=1.44, 95% CI 0.75-2.76, p=0.27). These data suggest that, in addition to severity scores, the underlying medical conditions and the evolution of severity within the first 4 days in ICU, late-onset pneumonia independently contribute to ICU patient mortality when empirical antibiotic treatment is not immediately appropriate.

Early-Onset Versus Late-Onset Nosocomial Pneumonia in ICU

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A Comparative Analysis of Patients With Early-Onset vs Late-Onset Nosocomial Pneumonia in the ICU Setting

To compare the clinical outcomes of critically ill patients developing early-onset nosocomial pneumonia (NP; ie, within 96 h of ICU admission) and late-onset NP (ie, occurring after 96 h of ICU admission). Prospective cohort study. A medical ICU and a surgical ICU from a university-affiliated urban teaching hospital. Between July 1997 and November 1998, 3, 668 patients were prospectively evaluated. Prospective patient surveillance and data collection. Four hundred twenty patients (11.5%) developed NP. Early-onset NP was observed in 235 patients (56.0%), whereas 185 patients (44.0%) developed late-onset NP. Among patients with early onset NP, 114 patients (48. 5%) spent at least 24 h in the hospital prior to ICU admission, compared to 57 patients (30.8%) with late-onset NP (p = 0.001). One hundred eighty-three patients (77.9%) with early-onset NP received antibiotics prior to the development of NP, as compared to 162 patients (87.6%) with late-onset NP (p = 0.010). The most common pathogens associated with early-onset NP were Pseudomonas aeruginosa (25.1%), oxacillin-sensitive Staphylococcus aureus (OSSA; 17.9%), oxacillin-resistant S aureus (ORSA; 17.9%), and Enterobacter species (10.2%). P aeruginosa (38.4%), ORSA (21.1%), Stenotrophomonas maltophilia (11.4%), OSSA (10.8%), and Enterobacter species (10.3%) were the most common pathogens associated with late-onset NP. The ICU length of stay was significantly longer for patients with early-onset NP (10.3 +/- 8.3 days; p < 0.001) and late-onset NP (21. 0 +/- 13.7 days; p < 0.001), as compared to patients without NP (3.5 +/- 3.2 days). Hospital mortality was significantly greater for patients with early-onset NP (37.9%; p = 0.001) and late-onset NP (41.1%; p = 0.001) compared to patients without NP (13.1%). Both early-onset and late-onset NP are associated with increased hospital mortality rates and prolonged lengths of stay. The pathogens associated with NP were similar for both groups. This may be due, in part, to the prior hospitalization and use of antibiotics in many patients developing early-onset NP. These data suggest that P aeruginosa and ORSA can be important pathogens associated with early-onset NP in the ICU setting. Additionally, clinicians should be aware of the common microorganisms associated with both early-onset NP and late-onset NP in their hospitals in order to avoid the administration of inadequate antimicrobial treatment.

Nosocomial Pneumonia in Mechanically Ventilated Patients Receiving Antacid, Ranitidine, or Sucralfate as Prophylaxis for Stress Ulcer

To assess three anti-stress ulcer prophylaxis regimens in mechanically ventilated patients for bacterial colonization, early- and late-onset nosocomial pneumonia, and gastrointestinal bleeding. Randomized controlled trial. Consecutive eligible patients with mechanical ventilation and a nasogastric tube. Of 258 eligible patients, 244 were assessable. Medical and surgical intensive care units. At intubation, patients were randomly assigned to receive one of the following: antacid (a suspension of aluminum hydroxide and magnesium hydroxide), 20 mL every 2 hours; ranitidine, 150 mg as a continuous intravenous infusion; or sucralfate, 1 g every 4 hours. Using predetermined criteria, the incidence of gastric bleeding, gastric colonization, early-onset pneumonia, and late-onset pneumonia was assessed in patients intubated for more than 24 hours. Of 244 assessable patients, macroscopic gastric bleeding was observed in 10%, 4%, and 6% of patients assigned to receive sucralfate, antacid, and ranitidine, respectively (P > 0.2). The incidence of early-onset pneumonia was not statistically different among the three treatment groups (P > 0.2). Among the 213 patients observed for more than 4 days, late-onset pneumonia was observed in 5% of the patients who received sucralfate compared with 16% and 21% of the patients who received antacid or ranitidine, respectively (P = 0.022). Mortality was not statistically different among the three treatment groups. Patients who received sucralfate had a lower median gastric pH (P < 0.001) and less frequent gastric colonization compared with the other groups (P = 0.015). Using molecular typing, 84% of the patients with late-onset gram-negative bacillary pneumonia were found to have gastric colonization with the same bacteria before pneumonia developed. Stress ulcer prophylaxis with sucralfate reduces the risk for late-onset pneumonia in ventilated patients compared with antacid or ranitidine.