|Year : 2015 | Volume
| Issue : 4 | Page : 117-122
Community-acquired pneumonia due to gram-negative bacteria
Alejandra Grosso1, Angela Famiglietti2, Carlos M Luna1
1 Department of Medicine, Pulmonary Diseases Division, Hospital de Clínicas, Universidad de Buenos Aires, Buenos Aires, Argentina
2 Department of Clinical Biochemistry, Hospital de Clínicas, Universidad de Buenos Aires, Buenos Aires, Argentina
|Date of Web Publication||24-Dec-2015|
Carlos M Luna
Arenales 2557, Piso 1, dto A CP 1425, Ciudad Autónoma de Buenos Aires, Buenos Aires
Source of Support: None, Conflict of Interest: None
Community-acquired pneumonia (CAP) is a frequent infectious disease that can be usually treated in an ambulatory setting. A small percentage of these cases require hospitalization and yet it is the leading infectious cause of hospitalization and death in some countries. A number of these infections is caused by gram-negative bacteria (GNB), which have repeatedly been found to bear an adverse prognostic potential. Its incidence is variable (0-9%) and some species carry a special pathogenicity. Enterobacteriaceae in these studies were more commonly isolated than P. aeruginosa while Acinetobacter spp. and B. cepacia were only occasionally described. The present review has the aim to update the current knowledge about the etiology, classifi cation, antimicrobial resistance, diagnosis, and therapy in CAP due to GNB.
Keywords: Community-acquired pneumonia (CAP), gram-negative bacteria (GNB), pneumonia
|How to cite this article:|
Grosso A, Famiglietti A, Luna CM. Community-acquired pneumonia due to gram-negative bacteria. Community Acquir Infect 2015;2:117-22
| Introduction|| |
Community-acquired pneumonia (CAP) is a frequent infectious disease, ranking as the fifth leading cause of death globally. Key early decisions in CAP management are based on severity scores and presumed pathogens guided according to the clinical presentation, age, presence of comorbidities, and other significant antecedents and site of care.
The vast majority of the patients with CAP are treated in an ambulatory setting  while a small percentage requires hospitalization; however, CAP is the leading infectious cause of hospitalization and death among US adults., The 2007 Infectious Diseases Society of America (IDSA)/American Thoracic Society (ATS) guidelines listed gram-negative bacteria (GNB) among the most common etiologies of CAP in those patients who need to be admitted in the intensive care unit (ICU) for pneumonia but it warns that it that the presence of risk factors for certain specific etiologies must also be taken into account including alcoholism and aspiration for aerobic gram-negative bacilli (AGNB), and chronic obstructive pulmonary disease (COPD), late human immunodeficiency virus (HIV) infection, and lung structural disease (i.e., bronchiectasis) for P. aeruginosa.,
GNB have repeatedly been found to bear an adverse prognostic potential. On the other hand, the reported incidences of GNB CAP in the general population have been quite variable, ranging 0% to 9% for aerobic GNB overall and from 0% to 3% for P. aeruginosa.
The present review has the aim to update the current knowledge about the etiology, classification, antimicrobial resistance, diagnosis, and therapy in CAP due to GNB.
| Role of Gram Negatives in the Etiology|| |
The recognition of the role of GNBs in the etiology of CAP has become more frequent during the last decades due to several reasons including a more efficient microbiological research, a trend to a worsening of the severity of illness of the patients admitted in the ICU and the increase of the life expectancy of the population as old patients have CAP more frequently and they are more usually colonized by GNB., Most of the studies that performed a carefully systematic and comprehensive evaluation of the etiology of CAP found a frequency of these microorganisms in percentages that varied, considering 10 studies performed during the last 15 years, from 0% to 6.7% of cases (mean 2.3%) and 0% to 16% considering those with etiology defined (mean 4.5%) [Table 1].,,,,,,,,, Members of the family Enterobacteriaceae were more commonly isolated in these studies than P. aeruginosa, while Acinetobacter spp. and B. cepacia were only occasionally described. Most of the reports of CAP due to Acinetobacter species were described in specific areas in patients with underlying conditions, leading to an increased risk for the acquisition of CAP due to this bacterium. Cystic fibrosis (CF) patients and those with chronic granulomatous disease are predisposed to B. cepacia pneumonia.
|Table 1: Number and percentage of gram-negative bacteria (GNB), aerobic gram-negative bacilli and P. aeruginosa in the etiology of CAP|
Click here to view
| The Pathogens|| |
There are a number of GNB that could be the potential causative organism of CAP; this review will be focused on a number of these bacteria including some from the family Enterobacteriaceae, P. aeruginosa, B. cepacia, and Acinetobacter spp.
Members of the family Enterobacteriaceae are referred to as “enterics” because the principal habitat of many (but not of all) of these organisms is the lower gastrointestinal tract of several animal species. However, these terms are not synonymous because several species do not typically inhabit the human gastrointestinal tract, and other intestinal pathogens that do not fall within the family are also recognized as enteric bacteria. Alcoholism and diabetes mellitus predispose highly to oropharyngeal colonization with members of this family.Klebsiella pneumoniae, Escherichia coli, Enterobacter cloacae, Proteus mirabilis, and Serratia marcescens are among the commonest representatives of this family that were occasionally found to be the pathogenic organisms in CAP.
P. aeruginosa is the major pathogenic species in the family Pseudomonadaceae and is readily identified as a gram-negative straight or slightly curved rod with a length of range 1-3 μm and a width of 0.5-1.0 μm [Figure 1]. This bacterium emerged as a major human pathogen in the 1960s because of its ability to cause infections in immunocompromised and burned hosts as well as CF patients. The establishment of P. aeruginosa infection in the lung can have serious consequences, particularly for patients with underlying comorbidities or a genetic predisposition such as in CF. Older reports of P. aeruginosa pneumonia describe patients with an acute clinical syndrome and a necrotizing pneumonia. The pathogenesis of this disease is believed to be a direct inoculation of large numbers of the organism into the lungs by aspiration or inhalation.
|Figure 1: Chest x-ray showing homogeneous parenchymal consolidation due to the presence of a voluminous inflammatory exudate that produces the bulging of an interlobar fissure. This radiographic presentation was considered to be typical of Klebsiella infection|
Click here to view
B. cepacia is usually resistant to almost all the available antimicrobials. Uncommonly it causes CAP in previously normal patients. CF patients are particularly prone to acquire pneumonia due to this microorganism.
The genus Acinetobacter has a complex taxonomic history and is a common pathogen of hospital-acquired pneumonia. This pathogen occasionally produces CAP., Risk factors associated with community-acquired Acinetobacter infection include alcoholism, cigarette smoking, chronic lung disease, diabetes mellitus, and residence in a tropical developing community. Acinetobacter Gram-stained sputum examination could be misinterpreted to be other gram-negative or even gram-positive organisms [Figure 2].
|Figure 2: Microphotograph from a Gram-stained smear obtained from a bronchoalveolar lavage showing intracellular gram-positive diplococci. Culture from the bronchoalveolar fluid yielded Acinetobacter spp. at concentration >104 colony-forming units per mL. Acinetobacter-like Moraxella can be pleomorphic, and sometimes appear as gram-positive cocci. These organisms tend to retain the crystal violet stain and appear to be gram-positive|
Click here to view
The presence of gram-negatives as a pathogen of CAP has been found to a factor associated with higher risk of failure among those patients hospitalized because of the presence of CAP.
Community-acquired Acinetobacter has been reported to be the causative microorganism of community-acquired bronchiolitis and tracheobronchitis in healthy children  and can also occur in immunocompromised adults. Adult community-acquired Acinetobacter pneumonia generally occurs in patients with diminished host defenses (e.g., alcoholism, tobacco use, diabetes mellitus, renal failure, underlying pulmonary disease).,, Reports from developing tropical regions document a higher local prevalence of community-acquired Acinetobacter pneumonia compared with temperate climates., One series from tropical northern Australia found community-acquired Acinetobacter pneumonia to account for 10% of all community-acquired bacteremic pneumonias and 21% of gram-negative pneumonias. Mortality in various published series has been 40-64%. The prevalence of community-acquired Acinetobacter pneumonia was speculated to be a consequence of the generally poor health of persons in the communities under study, frequent use of penicillins, and/or genetic predisposition.
Acinetobacter spp. (A. baumannii is the prevalent genomic species but others may cause infection) became an increasingly important cause of nosocomial pneumonia, particularly in ventilator-associated pneumonia (VAP). This organism has intrinsic resistance to some antimicrobials but acquires easily resistance to many others, and survives for a long time in the environment. Acinetobacter is a short, plump, gram-negative (but sometimes difficult to destain) rod, typically 1.0-1.5 mm by 1.5-2.5 mm in the logarithmic phase of growth but often becoming more coccoid in the stationary phase. Pairing or clustering of cells often occurs. Gram stain variability as well as variations in cell size and arrangement can often be observed within a single pure culture. Some rare cases of CAP caused by Acinetobacter spp. happen.
| Diagnosis|| |
Apart from the severity of illness and a more frequent association with older age, there are few data that could help to anticipate the possible role of GNBs in the etiology of CAP in any patient. From the radiologic standpoint, it is worth mentioning that the bulging fissure sign that has been described is characteristic of K. pneumoniae pneumonia [Figure 1] although it could be present in pneumonia due to S. pneumoniae, P. aeruginosa, and S. aureus. Bulging fissures, sharp margins of the advancing border of the pneumonic infiltrate, and early abscess formation are radiologic signs said to be distinctive for Klebsiella pneumonia but are only occasionally observed today.
The most frequent methods for discovering the microbial agent of gram-negative CAP are blood and sputum cultures. In patients with severe pneumonia invasively mechanically ventilated, it is easy to obtain lower respiratory tract secretions either by tracheal aspiration or by more representative specimens present in a significant concentration obtained by invasive or noninvasive bronchoalveolar lavage (≥104 colony forming units per mL) or protected specimen brush (≥103 colony forming units per mL). Multiplex real-time polymerase chain reaction (PCR) methods could be useful for the rapid and simultaneous detection of some gram-negative pathogens and the presence of specific mechanisms of resistance in a clinical specimen. By multiplex real-time PCR assay, it is possible to simultaneously detect and differentiate numerous causative agents of CAP rapidly with high sensitivity and specificity and without being affected by antecedent antibiotics administration. A set of real-time PCR for the detection of eight bacterial species from positive blood culture bottles including E. coli, P. aeruginosa, A. baumannii, E. faecalis, and E. faecium among the GNBs was described.,
| Treatment|| |
According with the recommendations of the 2007 IDSA/ATS guidelines, patients with CAP should be treated for a minimum of 5 days, should be afebrile for 48-72 h, and should have ≤1 CAP-associated sign of clinical instability (temperature <37.8, heart rate <100 beats/min, respiratory rate <24 breaths/min, systolic blood pressure >90 mmHg, arterial oxygen saturation >90% or PaO2 >60 mmHg on room air, ability to maintain oral intake, and normal mental status) before discontinuation of therapy. A longer duration of therapy may be needed if initial therapy was not active against the identified pathogen or if it was complicated by extrapulmonary infection such as meningitis or endocarditis. According with such guidelines when P. aeruginosa infection is a concern, an antipneumococcal, antipseudomonal b-lactam antimicrobial (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus either ciprofloxacin or levofloxacin (750-mg dose) or the above b-lactam plus an aminoglycoside and azithromycin or the above b-lactam plus an aminoglycoside and an antipneumococcal fluoroquinolone should be used [Table 2]. For penicillin-allergic patients, the indication is to substitute aztreonam for the above b-lactam. Pseudomonal CAP requires combination treatment to prevent inappropriate initial therapy, just as Pseudomonas nosocomial pneumonia does. For Enterobacteriaceae, third-generation cephalosporins provide enough coverage; however, a carbapenem should be the drug of choice if an extended-spectrum b-lactamase producer enteric bacteria is to be covered , [Table 2]. Alternatives for such pathogens could be b-lactam/b-lactamase inhibitor (piperacillin-tazobactam for gram-negative bacilli, ticarcillin-clavulanate, ampicillin-sulbactam, or amoxicillin-clavulanate), or a fluoroquinolone. For Acinetobacter spp., third-generation cephalosporin + aminoglycoside or ampicillin-sulbactam were recommended; however, Acinetobacter spp. could be multidrug resistant and could need to adapt the regime. Considering the known susceptibility of such an agent, occasionally intravenous and/or inhaled colistin could be considered as an option , [Table 2]. B. cepacia is a concern limited to CF or chronic granulomatosis disease patients with pneumonia; the isolation of B. cepacia antimicrobial-resistant variants has been found to be associated with CF patients with chronic lung infection exhibiting a severely compromised lung function, subjected to aggressive and longstanding antibiotic therapy. During periods of pulmonary exacerbation the use of combinations, rotating strategies, high doses, and inhaled antimicrobials are used. The role of inhaled antimicrobials for GNB pneumonia is under clinical research, particularly for VAP. Ceftazidime, the more extensively used b-lactam for the prevention and treatment of VAP, had improved clinical outcomes in chronic P. aeruginosa lower respiratory tract infections in patients with CF or bronchiectasis. Inhaled fluoroquinolones (levofloxacin and ciprofloxacin) and a combination of fosfomycin and tobramycin was associated with improved microbiological or clinical outcomes in chronic lower respiratory tract infection (LRTI) in patients with CF or bronchiectasis. For multiple drug-resistant GNBs, it could be possible that inhaled antimicrobials could have some role in the therapy of selected cases of GNB CAP.
|Table 2: Recommended antimicrobial therapy for specifi c pathogens, from ATS and ERS guidelines,,, modified|
Click here to view
Newer antibiotics: Ceftaroline, an advanced-generation, parenteral cephalosporin has been described as a “fifth generation” cephalosporin in the literature. GNB spectrum activity includes non- Extended-spectrum b-lactamase (ESBL)-producing strains of E. coli and K. pneumoniae but not P. aeruginosa. The in vitro activity of ceftaroline against Enterobacteriaceae is similar to that of other expanded spectrum cephalosporins, including ceftriaxone and another third generation agent, as ceftazidime. Ceftaroline fosamil demonstrated noninferiority to intravenous ceftriaxone in patients hospitalized with CAP [Pneumonia Outcomes Research Team (PORT) risk class III or IV]; patients with CAP admitted to the ICU were not evaluated. Diarrhea was a common reported adverse event but the risk of Clostridium difficile-associated diarrhea with ceftaroline fosamil was low. One limitation of the drug is the lack of an oral formulation and the requirement for twice daily administration.
| Outcome|| |
Luna et al. looking at the risk factors for mortality in a study looking at the etiology, epidemiology, and outcome in the general population with CAP observed that aerobic GNB as the pathogen of CAP was one of the prognostic factors associated with mortality in multivariate analysis.
Similarly, Arancibia et al. found that the mortality of patients with GNB pneumonia in their cohort was 32% (19/60), significantly higher than the mortality observed in those in the non-GNB group, which was 9%, (44/499). They found that in the multivariate analysis in their cohort, GNB pneumonia was one of the few conditions that were independently predictors of death.
| Risk Factors|| |
Arancibia et al. reported their experience in a cohort of 559 patients admitted with CAP. They found that the incidence of GNB CAP (including P. aeruginosa) was 11% (60/559). Although the age tended to be higher in those patients with CAP due to GNBs (69/72-year-old), this difference was not significant. These authors defined the following risk factors as independent predictors of GNB pneumonia: Probable aspiration, odds ratio (OR), 2.3; 95% confidence interval (CI): 1.02-5,2; P = 0.04; previous hospital admission, OR, 3.5; 95% CI, 1.7-7.1; P< 0.001; previous antimicrobial treatment, OR, 1.9; 95% CI, 1.01-3.7; 9 = 0.049 and the presence of pulmonary comorbidity, OR, 2.8; 95% CI, 1.5-5.5; P = 0.02. In a subgroup analysis of P. aeruginosa pneumonia, pulmonary comorbidity OR 5.8, 95% CI, 2.2-15.3, P< 0.001 and previous hospital admission OR 3.4, 95% CI, 1.6-7.4, P = 0.002 were predictive. A number of these cases of GNB CAP are related to the presence of an underlying risk of aspiration.
Aspiration pneumonia, in most of the cases, is due to microorganisms that colonize the oropharynx, an essential step in its pathogenesis. The elderly have increased oropharyngeal colonization and aerobic GNB as K. pneumoniae and E. coli are among those colonizers.,, Although this increased colonization may be transient, it underlies the increased risk in the elderly of pneumonia due to these pathogens.
| Prevention|| |
There are no specific prevention measures for GNB CAP, as in most of the cases of GNB CAP, airway colonization apparently appears to precede the development of pneumonia; rational use of antimicrobials to avoid the colonization due to the unnecessary administration of antibiotics, prevention of aspiration and general measures of treatment for chronic respiratory conditions in COPD, bronchiectasis, and CF patients, and the control of other underlying conditions (smoking, diabetes mellitus, congestive cardiac failure, etc.) should be among the preventive measures. Vaccination for influenza and S. pneumoniae should be offered to all the patients by the time of discharge or during outpatient treatment. Smoking cessation should be attempted while smokers are hospitalized; this is something particularly important in those patients who are admitted for pneumonia.
| Conclusion|| |
GNB is the etiological agent of CAP in a relatively low number pneumonia of patients. These pathogens produce lung infection, especially in older patients harboring chronic respiratory diseases. The commonest agents producing GNB CAP are Enterobacteriaceae and P. aeruginosa although Burkholderia cepacia and Acinetobacter spp. could be present under some epidemiological and personal conditions.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
The Global Burden of Disease, update 2008. 2008. Available from: www.who.int/healthinfo/...burden_disease/GBD_report_2004update_full.pdf. [Last accessed on 2015 Jul 25].
Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, et al
.; Infectious Diseases Society of America; American Thoracic Society. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44(Suppl 2):S27-72.
Niederman MS, Mandell LA, Anzueto A, Bass JB, Broughton WA, Campbell GD, et al
.; American Thoracic Society. Guidelines for the management of adults with community-acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention. Am J Respir Crit Care Med 2001;163: 1730-54.
Jain S, Self WH, Wunderink RG, Fakhran S, Balk R, Bramley AM, et al
.; CDC EPIC Study Team. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N
Engl J Med 2015;373:415-27.
Marrie TJ, Poulin-Costello M, Beecroft MD, Herman-Gnjidic Z. Etiology of community-acquired pneumonia treated in an ambulatory setting. Respir Med 2005;99:60-5.
Paganin F, Lilienthal F, Bourdin A, Lugagne N, Tixier F, Génin R, et al
. Severe community-acquired pneumonia: Assessment of microbial aetiology as mortality factor. Eur Respir J 2004;24:779-85.
Arancibia F, Bauer TT, Ewig S, Mensa J, Gonzalez J, Niederman MS, et al
. Community-acquired pneumonia due to gram-negative bacteria and pseudomonas aeruginosa: Incidence, risk, and prognosis. Arch Intern Med 2002;162:1849-58.
Luna CM, Calmaggi A, Caberloto O, Gentile J, Valentini R, Ciruzzi J, et al
.; Grupo Argentino de Estudio de la NAC. Pneumonia acquired in the community. Practical guide elaborated by a committee intersocieties. Medicina (Buenos Aires) 2003;63:319-43.
Ewig S, Birkner N, Strauss R, Schaefer E, Pauletzki J, Bischoff H, et al
. New perspectives on community-acquired pneumonia in 388 406 patients. Results from a nationwide mandatory performance measurement programme in healthcare quality. Thorax 2009;64:1062-9.
El-Solh A, Sikka P, Ramadan F, Davies J. Etiology of severe pneumonia in the very elderly. Am J Respir Crit Care Med 2001;163:645-51.
Luna CM, Famiglietti A, Absi R, Videla AJ, Nogueira FJ, Fuenzalida AD, et al
. Community-acquired pneumonia: Etiology, epidemiology, and outcome at a teaching hospital in Argentina. Chest 2000;118:1344-54.
Almirall J, Bolíbar I, Vidal J, Sauca G, Coll P, Niklasson B, et al
. Epidemiology of community-acquired pneumonia in adults: A population-based study. Eur Respir J 2000;15:757-63.
Laing R, Slater W, Coles C, Chambers S, Frampton C, Jackson R, et al
. Community-acquired pneumonia in Christchurch and Waikato 1999-2000: Microbiology and epidemiology. N
Z Med J 2001;114:488-92.
Jokinen C, Heiskanen L, Juvonen H, Kallinen S, Kleemola M, Koskela M, et al
. Microbial etiology of community-acquired pneumonia in the adult population of 4 municipalities in eastern Finland. Clin Infect Dis 2001;32:1141-54.
Garbino J, Sommer R, Gerber A, Regamey C, Vernazza P, Gennè D, et al
. Prospective epidemiologic survey of patients with community-acquired pneumonia requiring hospitalization in Switzerland. Int J Infect Dis 2002;6:288-93.
Díaz A, Barria P, Niederman M, Restrepo MI, Dreyse J, Fuentes G, et al
. Etiology of community-acquired pneumonia in hospitalized patients in chile: The increasing prevalence of respiratory viruses among classic pathogens. Chest 2007;131:779-87.
Charles PG, Whitby M, Fuller AJ, Stirling R, Wright AA, Korman TM, et al
.; Australian CAP Study Collaboration. The etiology of community-acquired pneumonia in Australia: Why penicillin plus doxycycline or a macrolide is the most appropriate therapy. Clin Infect Dis 2008;46:1513-21.
Mermond S, Berlioz-Arthaud A, Estivals M, Baumann F, Levenes H, Martin PM. Aetiology of community-acquired pneumonia in hospitalized adult patients in New Caledonia. Trop Med Int Health 2010;15:1517-24.
Capelastegui A, España PP, Bilbao A, Gamazo J, Medel F, Salgado J, et al
.; Poblational Study of Pneumonia (PSoP) Group. Etiology of community-acquired pneumonia in a population-based study: Link between etiology and patients characteristics, process-of-care, clinical evolution and outcomes. BMC Infect Dis 2012;12:134.
Tao LL, Hu BJ, He LX, Wei L, Xie HM, Wang BQ, et al
. Etiology and antimicrobial resistance of community-acquired pneumonia in adult patients in China. Chin Med J (Engl) 2012;125:2967-72.
Mackowiak PA, Martin RM, Jones SR, Smith JW. Pharyngeal colonization by gram-negative acilli in aspiration-prone persons. Arch Intern Med 1978;138:1224-7.
Tillotson JR, Lerner AM. Characteristics of nonbacteremic Pseudomonas pneumonia. Ann Intern Med 1968;68:295-307.
Davis JS, McMillan M, Swaminathan A, Kelly JA, Piera KE, Baird RW, et al
. A 16-year prospective study of community-onset bacteremic Acinetobacter pneumonia: Low mortality with appropriate initial empirical antibiotic protocols. Chest 2014;146:1038-45.
Leung WS, Chu CM, Tsang KY, Lo FH, Lo KF, Ho PI. Fulminant community-acquired Acinetobacter baumannii pneumonia as a distinct clinical syndrome. Chest 2006;129:102-9.
Dexter C, Murray GL, Paulsen IT, Peleg AY. Community-acquired Acinetobacter baumannii: Clinical characteristics, epidemiology and pathogenesis. Expert Rev Anti Infect Ther 2015;13:567-73.
O'Connell CJ, Hamilton R. Gram-negative rod infections; II. Acinetobacter infections in general hospital. NY State J Med 1981;81:750-3.
Goodhart GL, Abrutyn E, Watson R, Root RK, Egert J. Community-acquired Acinetobacter calcoaceticus var anitratus pneumonia. JAMA 1977;238:1516-8.
Anstey NM, Currie BJ, Hassell M, Palmer D, Dwyer B, Seifert H. Community-acquired bacteremic Acinetobacter pneumonia in tropical Australia is caused by diverse strains of Acinetobacter baumannii, with carriage in the throat of at-risk groups. J Clin Microbiol 2002;40:685-6.
Chen MZ, Hsueh PR, Lee LN, Yu CJ, Yang PC, Luh KT. Severe community-acquired pneumonia due to Acinetobacter baumannii. Chest 2001;120:1072-7.
Barnes DJ, Naraqi S, Igo JD. Community-acquired Acinetobacter pneumonia in adults in Papua New Guinea. Rev Infect Dis 1988;10:636-9.
Baumann P, Doudoroff M, Stanier RY. A study of the Moraxella group. II. Oxidase-negative species (genus Acinetobacter). J Bacteriol 1968;95:1520-41.
Cillóniz C, Ewig S, Polverino E, Marcos MA, Prina E, Sellares J, et al
. Community-acquired pneumonia in outpatients: Aetiology and outcomes. Eur Respir J 2012;40:931-8.
Zhu L, Shen DX, Zhou Q, Liu CJ, Li Z, Fang X, et al
. Universal Probe Library based real-time PCR for rapid detection of bacterial pathogens from positive blood culture bottles. World J Microbiol Biotechnol 2014;30:967-75.
Geyer CN, Hanson ND. Rapid PCR amplification protocols decrease the turn-around time for detection of antibiotic resistance genes in Gram-negative pathogens. Diagn Microbiol Infect Dis 2013;77: 113-7.
Woodhead M, Blasi F, Ewig S, Garau J, Huchon G, Ieven M, et al
.; Joint Taskforce of the European Respiratory Society and European Society for Clinical Microbiology and Infectious Diseases. Guidelines for the management of adult lower respiratory tract infections--full version. Clin Microbiol Infect 2011;17(Suppl 6):E1-59.
Leitão JH, Sousa SA, Cunha MV, Salgado MJ, Melo-Cristino J, Barreto MC, et al
. Variation of the antimicrobial susceptibility profiles of Burkholderia cepacia
complex clonal isolates obtained from chronically infected cystic fibrosis patients: A five-year survey in the major Portuguese treatment center. Eur J Clin Microbiol Infect Dis 2008;27:1101-11.
Falagas ME, Trigkidis KK, Vardakas KZ. Inhaled antibiotics beyond aminoglycosides, polymyxins and aztreonam: A systematic review. Int J Antimicrob Agents 2015;45:221-33.
Frampton JE. Ceftaroline fosamil: A review of its use in the treatment of complicated skin and soft tissue infections and community-acquired pneumonia. Drugs 2013;73:1067-94.
Palmer LB, Albulak K, Fields S, Filkin AM, Simon S, Smaldone GC. Oral clearance and pathogenic oropharyngeal colonization in the elderly. Am J Respir Crit Care Med 2001;164:464-8.
Michielsen W, Vandevondele D, Verschraegen G, Claeys G, Afschrift M. Bacterial surveillance cultures in a geriatric ward. Age Ageing 1993;22:221-6.
Sveinbjörnsdóttir S, Gudmundsson S, Briem H. Oropharyngeal colonization in the elderly. Eur J Clin Microbiol Infect Dis 1991;10:959-63.
[Figure 1], [Figure 2]
[Table 1], [Table 2]
|This article has been cited by|
||Classification of features shape of Gram-negative bacterial using an extreme learning machine
| ||B D Satoto,M I Utoyo,R Rulaningtyas,E B Koendhori |
| ||IOP Conference Series: Earth and Environmental Science. 2020; 524: 012005 |
|[Pubmed] | [DOI]|
||Factors Associated with Multidrug-Resistant Pathogens in Community-Acquired Pneumonia Patients Hospitalized in a Provincial Teaching Hospital in Indonesia
| ||Arto Yuwono Soeroto,Ining Kartika Tarmidi,Guntur Darmawan,Geraldo Laurus,Prayudi Santoso |
| ||Shiraz E-Medical Journal. 2020; In Press(In Press) |
|[Pubmed] | [DOI]|
||A Malaysian ex-smoker with cough, breathlessness and nonresolving bronchospasm
| ||Jo Anne Lim,Natrajan Caruppaiya,Noriza Zainol Abidin,Boon Tat Khor,Tharmalingam Palanivelu,Sunita Devi Hukam Gopal Chand,Aznita Ibrahim |
| ||Breathe. 2019; 15(4): 324 |
|[Pubmed] | [DOI]|
||Characterization of the population structure, drug resistance mechanisms and plasmids of the community-associated Enterobacter cloacae complex in China
| ||Kai Zhou,Wei Yu,Xiaoli Cao,Ping Shen,Haifeng Lu,Qixia Luo,John W A Rossen,Yonghong Xiao |
| ||Journal of Antimicrobial Chemotherapy. 2017; |
|[Pubmed] | [DOI]|