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Original Research: Chest Infections |

A 16-Year Prospective Study of Community-Onset Bacteremic Acinetobacter PneumoniaCommunity-Onset Acinetobacter Pneumonia: Low Mortality With Appropriate Initial Empirical Antibiotic Protocols FREE TO VIEW

Joshua S. Davis, MBBS, PhD; Mark McMillan, BN; Ashwin Swaminathan, MBBS; John A. Kelly, MBBS; Kim E. Piera, BSc; Robert W. Baird, MBBS; Bart J. Currie, MBBS; Nicholas M. Anstey, MBBS, PhD
Author and Funding Information

From the Global and Tropical Health Division (Drs Davis, Currie, and Anstey; Mr McMillan; and Ms Piera), Menzies School of Health Research, Charles Darwin University; and Department of Infectious Diseases (Drs Davis, Swaminathan, Kelly, Baird, Currie, and Anstey) and Department of Microbiology (Drs Swaminathan, Kelly, and Baird), Royal Darwin Hospital, Darwin, NT, Australia.

CORRESPONDENCE TO: Joshua S. Davis, MBBS, PhD, Menzies School of Health Research, PO Box 41096, Casuarina, Darwin, NT 0811, Australia; e-mail: joshua.davis@menzies.edu.au


FUNDING/SUPPORT: This work was supported by the National Health and Medical Research Council of Australia [program grant 1037304, practitioner fellowship to Dr Anstey 1042072, and early career fellowship 1013411 to Dr Davis].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(4):1038-1045. doi:10.1378/chest.13-3065
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BACKGROUND:  The genus Acinetobacter, well known as a nosocomial pathogen, can also cause severe community-onset pneumonia. Previous small case series have suggested fulminant disease and a pooled hospital mortality of > 60%.

METHODS:  We conducted a prospective observational study of all episodes of bacteremic, community-onset, and radiologically confirmed pneumonia due to Acinetobacter species at a tertiary referral hospital in tropical Australia from 1997 to 2012 following the introduction of routine empirical treatment protocols covering Acinetobacter. Demographic, clinical, microbiologic, and outcome data were collected.

RESULTS:  There were 41 episodes of bacteremic community-onset Acinetobacter pneumonia, of which 36 had no indicators suggesting health-care-associated infection. Of these, 38 (93%) were Indigenous Australians, one-half were men, the average age was 44.1 years, and 36 episodes (88%) occurred during the rainy season. All patients had at least one risk factor, with hazardous alcohol intake in 82%. Of the 37 isolates available for molecular speciation, 35 were Acinetobacter baumannii and two were Acinetobacter nosocomialis. All isolates were susceptible in vitro to gentamicin, meropenem, and ciprofloxacin, but only one was fully susceptible to ceftriaxone. ICU admission was required in 80%. All 41 patients received appropriate antibiotics within the first 24 h of admission, and 28- and 90-day mortality were both low at 11%.

CONCLUSIONS:  Community-acquired Acinetobacter pneumonia is a severe disease, with the majority of patients requiring ICU admission. Most patients have risk factors, particularly hazardous alcohol use. Despite this severity, correct initial empirical antibiotic therapy in all patients was associated with low mortality.

Figures in this Article

The genus Acinetobacter is well known as a nosocomial pathogen with a tendency to develop resistance to multiple antibiotics and to infect relatively immunocompromised hosts, particularly patients in the ICU.1 It can also cause community-acquired infections, particularly fulminant pneumonia.2 Although community-acquired Acinetobacter infections are less common than nosocomial infections, they have attracted growing interest in the past decade because of the emerging recognition of their high associated mortality and its importance as a pathogen following trauma in wars and natural disasters.3 Community-acquired Acinetobacter pneumonia (CAAP) is increasingly recognized as an important entity, particularly in tropical and subtropical areas, because usual empirical antimicrobial regimens for pneumonia do not cover this organism, and its reported mortality is approximately 60%.47 Hence, accurate data about the epidemiology, risk factors, and clinical presentation of CAAP to identify patients requiring empirical antibiotic coverage are needed.

Several case series of community-onset Acinetobacter pneumonia (COAP)411 and multiple case reports2,4 have described a high mortality, lack of the antibiotic resistance usual in nosocomial infections from this genus, and the presence of risk factors, including hazardous alcohol use, smoking, chronic lung disease, and chronic renal disease. These case series were small (median, nine patients with COAP; range, five to 23 patients) and retrospective, and most did not use rigorous definitions of true community-acquired infection.4,5,7,8,1012

Important questions remain about COAP, including how to best identify those at risk for targeted empirical therapy and whether adherence to empirical antibiotic protocols covering Acinetobacter can reduce mortality. In the largest series to date to our knowledge, we report our experience with bacteremic COAP over a 16-year period in tropical northern Australia following the introduction of empirical antibiotic protocols, including activity against this bacterium.

Patients and Setting

This study was conducted at Royal Darwin Hospital (RDH), a 350-bed tertiary referral hospital in Darwin in tropical Northern Territory, Australia, 12.5° south of the equator. RDH is the only referral hospital in the region and serves a population of approximately 170,000 people spread over an area of 500,000 km2. Approximately 30% of the population served are Indigenous Australians.

We conducted a prospective cohort study of all patients presenting to RDH with Acinetobacter bacteremia and community-onset pneumonia between January 1, 1997, and December 31, 2012, comprising patients enrolled since a previous RDH series,4,12 with the exception of one patient with health-care-associated COAP who was included in a molecular genetics article.12

Patients were included if they met all of the following criteria:

  1. Community-onset infection (the patient was either not in the hospital or had been in the hospital for < 48 h at the time the positive blood culture was collected)

  2. Blood culture containing Acinetobacter species

  3. Presence of pneumonia within 48 h of the positive blood culture being collected

    • Chest radiograph (CXR) or CT scan showing changes consistent with acute pneumonia AND

    • At least two clinical features of acute pneumonia (including fever, new cough, sputum production, dyspnea, chest pain, and bronchial breath sounds on auscultation)

  4. Blood culture isolate judged to be clinically significant

    • Pure growth of Acinetobacter species in blood OR

    • Mixed growth of Acinetobacter in blood, with Acinetobacter also grown from sputum

Patients were prospectively identified by the microbiology laboratory, which informed a member of the study team. Demographic and clinical data from medical records and hospital databases were collected using a standardized case report form. All CXRs and CT scans were interpreted by either an infectious diseases physician (J. S. D. or N. M. A.) or a radiologist.

Definitions

Indicators of health-care-associated infection (HCAI) were taken from Friedman et al.13 Hazardous alcohol use was defined as an average of > 40 g/d ethanol for men or > 20 g/d for women.14 Binge alcohol drinking was defined as a reported intake of > 100 g ethanol in the past 48 h or a blood alcohol concentration > 0.10% at hospital admission. Immunosuppression was defined as any of the following: (1) HIV infection; (2) corticosteroids > 20 mg/d prednisone or the equivalent for > 14 days within the past 3 months; and (3) other immunosuppressive medications for organ transplant, malignancy, or autoimmune disorders within the past 30 days.

Antibiotic treatment was considered appropriate if the patient received at least one IV antibiotic within the first 24 h of admission to which the isolate was susceptible in vitro. Disease severity was estimated by using the presence of severe sepsis (as defined in the Recombinant Human Protein C Worldwide Evaluation in Severe Sepsis [PROWESS] study)15 and the SMART-COP (systolic BP, multilobar chest radiographic involvement, albumin level, respiratory rate, tachycardia, confusion, oxygenation, and arterial pH) score.16

Ethics

The study was approved by the Human Research Ethics Committee of the Menzies School of Health Research and Northern Territory Department of Health (approval number 04/20), who waived the requirement for individual patient consent.

Microbiology Methods

Isolates were identified to the level of Acinetobacter species using phenotypic biochemical testing and automated susceptibility testing performed with a Microscan (Siemens AG) from 1997 to 2001 and a Vitek 2 (bioMérieux, Inc) from 2001 to 2012.17 A multiplex polymerase chain reaction (PCR) was used to identify isolates to the species level, as described by Higgins et al.18 In brief, clinical isolates were cultured overnight and DNA extracted from a 1-μL loopful of a colony using a QIAamp DNA extraction kit (QIAGEN). The gyrB gene was amplified with Sp2F, Sp4F, Sp4R, D14, D19, D16, and D8 primers to identify Acinetobacter baumannii, Acinetobacter nosocomialis (previously known as genospecies 13TU), Acinetobacter pittii (previously known as genospecies 3), and Acinetobacter calcoaceticus.

Data Management and Statistical Analysis

After a hand check of all case record forms, data were entered into a purpose-built database (EpiData 3.1; EpiData Association) and analyzed using Stata 10 (StataCorp LP) software. Continuous variables were compared by Mann-Whitney U test or Student t test for nonparametric and parametric variables, respectively. Categorical variables were compared by Fisher exact test. Seasonality was assessed by Edward test.19 ORs for risk factors were determined by using a case-control model, where the population of the Northern Territory was treated as the control but only where accurate data on risk factor prevalence in the population could be found. P < .05 was considered significant.

Demographics and Risk Factors

There were 41 episodes of COAP in 36 individuals. Nearly all episodes (38 of 41 [93%]) were in Indigenous Australians; one-half of the episodes occurred in men, and the average age was 44.1 years. All patients were adults, with an age range of 25 to 68 years (Table 1).

Table Graphic Jump Location
TABLE 1 ]  Demographics, Clinical Features, and Outcomes of 41 Episodes of Bacteremic, Community-Onset Acinetobacter Pneumonia

Data are presented as mean ± SD, No. (%), or median (interquartile range). SMART-COP = systolic BP, multilobar chest radiographic involvement, albumin level, respiratory rate, tachycardia, confusion, oxygenation, and arterial pH.

a 

n = 26 because complete data were not available for all patients.

b 

Mortality data only available for residents of the Northern Territory.

In 36 of the 41 episodes, no factors suggested possible HCAI, and these were considered to be definite community-acquired pneumonia. Of the remaining five episodes, three patients had been admitted to a hospital within the past 90 days, and two were receiving regular hemodialysis. There were no significant differences between those with and without indicators of possible HCAI.

All patients had at least one risk factor, with hazardous alcohol use and smoking both present in > 80% (Table 2). It is also notable that 50% of patients had engaged in binge drinking of alcohol with the past 48 h and that no patient met traditional definitions of immunosuppression.

Table Graphic Jump Location
TABLE 2 ]  Putative Risk Factors for Community-Onset Acinetobacter Pneumonia
a 

n = 41 unless otherwise indicated.

b 

Data were only included if a sufficient amount was available to accurately quantify their use.

c 

Defined as a clinically recorded diagnosis of COPD or bronchiectasis.

d 

Defined as the need for hemodialysis, peritoneal dialysis, or estimated glomerular filtration rate < 30 mL/min.

e 

At least one of hazardous alcohol use, chronic lung disease, or diabetes mellitus, with or without smoking.

Clinical Presentation, Pathology, and Radiology

The most common symptoms were cough, dyspnea, and fever in > 90% of episodes (Table 1). Sputum was commonly described as blood stained (41%) or purulent (25%). The illness developed rapidly, with a median time from initial symptom onset to hospital presentation of 3 days, despite > 50% of patients living in remote areas. COAP appears to be a very severe illness, with 83% of patients meeting the criteria for severe sepsis, 80% requiring admission to the ICU, and 88% being coded as severe pneumonia according to SMART-COP criteria. However, mortality was low, with death at 28 and 90 days occurring in only four patients (11%). Blood analysis on day 1 of admission revealed neutrophilia, lymphopenia, thrombocytopenia, and hypoalbuminemia in most patients (Table 3), consistent with severe bacterial sepsis. CXR in the first 48 h revealed no predilection for either the right or left lung (Table 3) or for the upper lobes over the lower lobes. Most patients (73%) presented with lobar consolidation, with 12% having whiteout of an entire lung and 17% having a pleural effusion. Cavitation was not seen in any patient.

Table Graphic Jump Location
TABLE 3 ]  Radiology and Blood Test Abnormalities

Data are presented as median (interquartile range) or No. (%) unless otherwise indicated. n = 41 unless otherwise indicated. ALT = alanine aminotransferase.

Microbiology and Antimicrobial Susceptibility

Acinetobacter species grew from sputum or endotracheal aspirate from 24 patients (58%). Bacterial isolates were available for PCR-based speciation in 37 of 41 patients. Of these, all PCRs amplified the A baumannii complex primers. Thirty-five were identified as A baumannii and two as A nosocomialis. The patients with A nosocomialis infection were both women aged 31 and 33 years with, typically, severe presentations of CAAP and no indicators of HCAI. The cultures of the four patients for whom no isolate was available for PCR were considered to be A baumannii complex not otherwise specified2 (Table 4).

Table Graphic Jump Location
TABLE 4 ]  Antibiotic Susceptibility

Isolates are only included in the table if data are available for at least 15 isolates.

Seasonality

A median of three cases of COAP occurred per year (range, 0-5). The majority of cases (34 of 41 [83%]) occurred in the warmer, wetter months of October to April (the “wet season”). The total number of cases occurring in each calendar month correlated with the mean rainfall for that month (Spearman ρ = 0.76, P < .004), and Edward test was highly significant for seasonality (P < .001) (Fig 1).

Figure Jump LinkFigure 1 –  Total number of cases of community-onset Acinetobacter pneumonia by mo compared with average rainfall. The solid line represents the total number of cases (left y-axis); the dotted line represents the mean monthly rainfall (in millimeters) at Darwin airport for the period of 1981 to 2010 (right y-axis).Grahic Jump Location
Management and Outcomes

Before February 1990, there was no standardized protocol for antibiotic treatment of community-acquired pneumonia at RDH, with antibiotic therapy being at the discretion of the treating clinician. After a death from CAAP in February 1990,4 a protocol was introduced. This protocol has evolved over time, but it has consistently included empirical antibiotic coverage targeting both Acinetobacter and Burkholderia pseudomallei in all patients with severe pneumonia and in anyone with risk factors for infection with these organisms.24 This empirical coverage consists of adding gentamicin for 24 to 48 h to ceftriaxone treatment but not to meropenem treatment (which is used to cover Burkholderia pseudomallei in the wet season). Targeted therapy for those with confirmed COAP is IV meropenem until stable followed by oral ciprofloxacin to complete 14 days.

All patients received appropriate antibiotics within the first 24 h of admission. The initial antibiotic regimen included gentamicin in 30 episodes, ceftriaxione in 23 (all of whom received concurrent gentamicin), meropenem in 18, and concomitant azithromycin in 12. Of the 33 patients who were admitted to the ICU, 24 received invasive positive pressure ventilation, and four were treated with noninvasive ventilation. Of note, the fact that all patients received appropriate initial antimicrobial therapy with only 11% dying differs substantially from all previous case series of COAP (Table 5), underlining the importance of having local antibiotic policies that appropriately target Acinetobacter in tropical regions.

Table Graphic Jump Location
TABLE 5 ]  Relationship Between Hospital Mortality and Appropriate Initial Antimicrobial Therapy in Five Different Cohort Studies of Community-Onset Acinetobacter Pneumonia

All published case series were examined and included in this table if they reported sufficient information.

a 

The current cohort.

In this 16-year prospective cohort study, we describe 41 episodes of COAP of which 36 were strictly defined CAAP. To our knowledge, this is the largest published cohort of this condition to date and shows that although usually caused by A baumannii, CAAP can also occur with A nosocomialis. It extends the findings of earlier smaller retrospective case series and reports2,411 in that CAAP is a severe disease that mostly occurs in patients with a history of hazardous alcohol use, chronic lung disease, and chronic renal disease; typically presents as a rapid onset of pneumonia with bloody or purulent sputum, lobar consolidation on CXR, and acute sepsis-related organ dysfunction; and occurs predominantly in tropical areas during the wet season.

However, the most striking finding from this cohort not previously reported is that adherence to early appropriate antimicrobial treatment protocols is associated with a dramatic decrease in mortality compared with that reported in previous series, including from our own center prior to a change in pneumonia treatment policy.4 There may be, of course, other factors contributing to the low mortality we observed. First, the patients were relatively young (mean age = 44 years), and age is a powerful determinant of outcome in severe sepsis.25 Second, there have been progressive improvements in supportive care for severe sepsis at our own hospital and globally over the past 2 decades, but this should have equally affected other cohorts from resource-rich countries, particularly those studied in the past decade, including Singapore in 2009,6 Hong Kong in 2006,5 and Taiwan in 2002.10 The striking consistency of high mortality rates (62%-64%) and low rates of initial appropriate antimicrobial therapy (13%, 31%, 32%, and 36%) across the four case series included in Table 5 suggest that the 100% rate of appropriate early antimicrobial therapy is at least an important part of the explanation for our low observed mortality rate of 11%. This interpretation is supported by studies in other types of pneumonia26,27 and septic shock,28 which showed that appropriate antibiotic therapy in the first 24 h is a key determinant of outcome.

Because many protocols for the empirical treatment of community-acquired pneumonia do not contain antibiotics that reliably cover community Acinetobacter species,29,30 it is important for hospitals in tropical and subtropical areas to define which patients should receive broader empirical antibiotics to cover the possibility of COAP. In the current study, 95% of patients had at least one of the three main risk factors: hazardous alcohol use, chronic lung disease, and diabetes mellitus. Hence, a lack of all three of these factors makes COAP very unlikely. Furthermore, 83% of cases occurred during the wet season. Because bacteremic COAP is relatively uncommon, one could consider targeting empirical treatment only to those with risk factors during the wet season.

It is difficult to prove with the current study design that the comorbidity data collected are indeed risk factors for COAP rather than simply for bacteremic pneumonia in general. However, a comparison with a 2009 non-Acinetobacter bacteremic severe pneumonia cohort previously published from our center31 suggests a specific association with COAP: Hazardous alcohol use (82% vs 53%, P = .006), chronic lung disease (41% vs 17%, P = .02), and smoking (86% vs 52%, P = .002) are all significantly more common in the bacteremic Acinetobacter cohort, whereas diabetes (27% vs 11%, P = .06) and chronic renal disease (17% vs 6%, P = .10) are nonsignificantly more common.

This study has several limitations. Although prospective, not all data and isolates were gathered. However, the small amount of missing data should not have affected the conclusions because we did not attempt to impute or otherwise include them in the analysis. This is an observational study, and, hence, only associations and not causation can be demonstrated. The fact that the majority of patients were Indigenous Australians may raise concerns about the applicability of the data to other settings. However, that similar COAP descriptions have been published from multiple other tropical countries suggests that geography, environment, and prevalence of acquired clinical risk factors, rather than genetic aspects of the host, are important in determining the occurrence of COAP in a given region. The strengths of this study include its large sample size relative to previous case series, rigorous definitions of CAAP and COAP, that all patients had bacteremia, and documentation of the effect of appropriate initial empirical treatment protocols.

An important outstanding question is explaining the observed differences between nosocomial and community-acquired Acinetobacter infections. These differences are likely to be due to a combination of organism and host factors. Host factors are certainly an important part of this explanation given that all patients in the current cohort and the majority in other published cohorts had risk factors. A recent binge of alcohol drinking was present in at least 50% of the present patients; the mechanism for this may be a combination of the direct tropic-32 and virulence-inducing33,34 effects of ethanol on Acinetobacter species and alcohol-induced impaired neutrophil and macrophage function.35,36 Furthermore, with 10% of at-risk patients in the community having throat colonization of A baumannii in the wet season in tropical Australia,12 alcohol-associated microaspiration of Acinetobacter has been proposed to contribute to both the seasonal predominance of COAP and its association with binge drinking. Whole-genome sequencing of a single isolate from a patient with bacteremic CAAP shows that the absence of antibiotic resistance can be explained by a lack of the A baumannii antibiotic resistance island, but no clear evidence of increased virulence of this isolate compared with reference nosocomial isolates was seen.37 Larger studies are needed to clarify this.

In conclusion, COAP almost exclusively occurs in people with one or more of the putative risk factors of hazardous alcohol use, chronic lung disease, and diabetes mellitus and causes very severe disease. However, early appropriate empirical antimicrobial therapy can lead to excellent outcomes.

Author contributions: J. S. D. had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. J. S. D., B. J. C., and N. M. A. contributed to the study concept and design; J. S. D., M. M., A. S., J. A. K., K. E. P., R. W. B., B. J. C., and N. M. A contributed to the data collection and final manuscript; J. S. D., M. M., and N. M. A. contributed to the data analysis; A. S., J. A. K., K. E. P., and R. W. B. contributed to the laboratory procedures; and J. S. D. and N. M. A. wrote the manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript.

Other contributions: The authors thank Paul Southwell, BSc, for assistance with clinical microbiology laboratory procedures; Phil Giffard, PhD, Steven Tong, MBBS, PhD, and Anton Peleg, MBBS, PhD, for advice about molecular typing of isolates; and all infectious diseases, general medical, ED, intensive care, and microbiology consultants and registrars who worked at RDH during the study period for help with identifying and caring for the patients.

CAAP

community-acquired Acinetobacter pneumonia

COAP

community-onset Acinetobacter pneumonia

CXR

chest radiograph

HCAI

health-care-associated infection

PCR

polymerase chain reaction

RDH

Royal Darwin Hospital

SMART-COP

systolic BP, multilobar chest radiographic involvement, albumin level, respiratory rate, tachycardia, confusion, oxygenation, and arterial pH

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Camarena L, Bruno V, Euskirchen G, Poggio S, Snyder M. Molecular mechanisms of ethanol-induced pathogenesis revealed by RNA-sequencing. PLoS Pathog. 2010;6(4):e1000834. [CrossRef] [PubMed]
 
Patel M, Keshavarzian A, Kottapalli V, Badie B, Winship D, Fields JZ. Human neutrophil functions are inhibited in vitro by clinically relevant ethanol concentrations. Alcohol Clin Exp Res. 1996;20(2):275-283. [CrossRef] [PubMed]
 
Asplund MB, Coelho C, Cordero RJ, Martinez LR. Alcohol impairs J774.16 macrophage-like cell antimicrobial functions inAcinetobacter baumanniiinfection. Virulence. 2013;4(6):467-472. [CrossRef] [PubMed]
 
Farrugia DN, Elbourne LD, Hassan KA, et al. The complete genome and phenome of a community-acquired Acinetobacter baumannii. PLoS One. 2013;8(3):e58628. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  Total number of cases of community-onset Acinetobacter pneumonia by mo compared with average rainfall. The solid line represents the total number of cases (left y-axis); the dotted line represents the mean monthly rainfall (in millimeters) at Darwin airport for the period of 1981 to 2010 (right y-axis).Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Demographics, Clinical Features, and Outcomes of 41 Episodes of Bacteremic, Community-Onset Acinetobacter Pneumonia

Data are presented as mean ± SD, No. (%), or median (interquartile range). SMART-COP = systolic BP, multilobar chest radiographic involvement, albumin level, respiratory rate, tachycardia, confusion, oxygenation, and arterial pH.

a 

n = 26 because complete data were not available for all patients.

b 

Mortality data only available for residents of the Northern Territory.

Table Graphic Jump Location
TABLE 2 ]  Putative Risk Factors for Community-Onset Acinetobacter Pneumonia
a 

n = 41 unless otherwise indicated.

b 

Data were only included if a sufficient amount was available to accurately quantify their use.

c 

Defined as a clinically recorded diagnosis of COPD or bronchiectasis.

d 

Defined as the need for hemodialysis, peritoneal dialysis, or estimated glomerular filtration rate < 30 mL/min.

e 

At least one of hazardous alcohol use, chronic lung disease, or diabetes mellitus, with or without smoking.

Table Graphic Jump Location
TABLE 3 ]  Radiology and Blood Test Abnormalities

Data are presented as median (interquartile range) or No. (%) unless otherwise indicated. n = 41 unless otherwise indicated. ALT = alanine aminotransferase.

Table Graphic Jump Location
TABLE 4 ]  Antibiotic Susceptibility

Isolates are only included in the table if data are available for at least 15 isolates.

Table Graphic Jump Location
TABLE 5 ]  Relationship Between Hospital Mortality and Appropriate Initial Antimicrobial Therapy in Five Different Cohort Studies of Community-Onset Acinetobacter Pneumonia

All published case series were examined and included in this table if they reported sufficient information.

a 

The current cohort.

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Patel M, Keshavarzian A, Kottapalli V, Badie B, Winship D, Fields JZ. Human neutrophil functions are inhibited in vitro by clinically relevant ethanol concentrations. Alcohol Clin Exp Res. 1996;20(2):275-283. [CrossRef] [PubMed]
 
Asplund MB, Coelho C, Cordero RJ, Martinez LR. Alcohol impairs J774.16 macrophage-like cell antimicrobial functions inAcinetobacter baumanniiinfection. Virulence. 2013;4(6):467-472. [CrossRef] [PubMed]
 
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