Community-acquired Acinetobacter Pneumonia Research Articles

Community-Acquired, Bacteraemic Acinetobacter Baumannii Pneumonia: A Retrospective Review of Cases in Tropical Queensland, Australia.

Community-acquired Acinetobacter pneumonia (CAAP) typically presents with rapid progression to fulminant disease and is complicated by high mortality. Australian epidemiological studies are few. We conducted a retrospective study on bacteraemic cases of CAAP over twenty years (2000-2019) in North Queensland. Cases were selected on microbiologic, clinical, and radiographic parameters. Data on patient demographics were obtained, along with microbial, antibiotic, mortality and climatic data. 28 cases of CAAP were included. Nineteen (67.9%) were male, twenty-three (82.1%) were Indigenous Australians, and the mean age was 45.9 years. Most presentations were of moderate to severe pneumonia (25/28 (89.3%)). Furthermore, 90% of cases had two or more risk factors. The strongest risk factors for CAAP were alcohol excess and tobacco use. No statistically significant difference in presenting severity, ICU admission or mortality was seen between dry- and wet-season disease. Dry-season disease accounted for 35.7% of cases. Overall mortality was 28.6%. Early use of meropenem or gentamicin reduced mortality irrespective of presenting severity (mortality 17.6%) Non-targeted antibiotic therapy was associated with a non-significant difference in mortality of 44.4%. Early administration of targeted antibiotics can mitigate a high mortality rate. The choice of antibiotic therapy for community-acquired pneumonia should be based on severity, risk factors and clinical suspicion of CAAP rather than seasonality.

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

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%. 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. 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%. 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.

COMMUNITY-ACQUIRED ACINETOBACTER BAUMANII PNEUMONIA IN A 75-YEAR-OLD VETERAN.

Acinetobacter baumanii is a well-known causative agent of nosocomial infections. However, community-acquired A. baumanii pneumonia is rare in the United States; thus, we present this case of community-acquired pneumonia with a fulminant course. A 75-year-old Caucasian male with hypertension, moderate chronic obstructive lung disease, alcoholism, and diabetes mellitus presented with dyspnea, changes in behavior, hypotension, and hypoxemia with diffuse wheezes and crackles. Chest radiography showed dense right base infiltrate. He had profound respiratory distress started on BiPAP support and was treated with azithromycin and ceftriaxone. Blood Gram stain showed gram-negative diplococci, suggesting Neisseria meningitidis infection. CSF fluid was negative for infection. Final blood culture grew A. baumanii. Antibiotics were changed to imipenem and vancomycin. His condition continued to deteriorate, and the patient9s family decided to withdraw care, leading to the patient9s demise. Risk factors associated with community-acquired Acinetobacter pneumonia are smoking, significant alcohol use, and/or concomitant comorbid conditions (COPD, HTN, DM). Patients present with fever, cough, and dyspnea and progresses to shock with a very fulminant course. A HIGH index of suspicion is warranted during the initial course. The organism has been described as a gram-negative coccibacilli. Rarely, as in our case, it may initially be described as a gram-negative diplococcus, leading to the delay in appropriate therapy. With the increasing prevalence of hospital-acquired Acinetobacter infection, we need to maintain high vigilance in the bacterial flora responsible for community-acquired pneumonia.

Chronic community-acquired Acinetobacter pneumonia that responded slowly to rifampicin in the anti-tuberculous regime

Acinetobacter baumannii is a well-known cause of hospital-acquired pneumonia. Occasionally, it can present as an acute community-acquired pneumonia with a fulminant course. However, the occurrence of the chronic form of community-acquired Acinetobacter pneumonia is yet to be highlighted. We describe a 62-year-old, HIV negative, non-diabetic male, who was referred for evaluation of consolidation and cavitation in the apicoposterior segment of the left upper lobe for 4 months. For this, he had received anti-tuberculous therapy, which included rifampicin. On investigation, a diagnosis of chronic community-acquired pneumonia due to Acinetobacter baumannii was made. The steady clinico–radiologic improvement observed was attributed to rifampicin in the anti-tuberculous regime. Subsequently, an aspergilloma formed in the cavity.

Community-acquired bacteremic Acinetobacter pneumonia in tropical Australia is caused by diverse strains of Acinetobacter baumannii, with carriage in the throat in at-risk groups.

Acinetobacter isolates from eight subjects with community-acquired Acinetobacter pneumonia (CAAP), a major cause of fatal community-acquired pneumonia in tropical Australia, were phenotypically and genotypically confirmed by pulsed-field gel electrophoresis analysis to be broadly diverse Acinetobacter baumannii strains. Wet-season throat carriage of A. baumannii was found in 10% of community residents with excess levels of alcohol consumption, the major at-risk group for CAAP.

Community-acquired Acinetobacter pneumonia: A case report

A 35-year-old male with glucose-6-phosphate dehydrogenase (G6PD) deficiency was admitted because of right chest (pleuritic) pain, fever, cough with scarce production of blood-tinged sputum, and generalized yellowish discolouration of skin for 2 days. Radiographic examination revealed right lower lobe necrotizing pneumonia. Hypotension, dyspnoea and severe haemolysis was noted the next day. Echo-guided lung aspiration and sputum cultures both grew Acinetobacter baumannii. Antibiotic therapy was started immediately, but fever persisted and abscess formation was noted 1 week later. After aggressive supportive and antibiotic therapy, he made a slow but complete recovery from the pneumonia, and was then discharged in a stable condition. Acinetobacter baumannii is a well-known causative agent of nosocomial infections, particularly in intensive units. Community-acquired pneumonia, however, is quite rare, and usually has a fulminant course and high case fatality rate.

Community-acquired Acinetobacter pneumonia in the Northern Territory of Australia.

Eleven cases of blood culture-positive, community-acquired pneumonia due to the human commensal Acinetobacter baumannii were studied in Darwin in the Northern Territory of Australia during the 10-year period from March 1981 through February 1991. Demographic risk factors included male gender, age of greater than 45 years, and Aboriginal ethnic background. Multiple clinical risk factors, including cigarette smoking, alcoholism, chronic obstructive airway disease, and diabetes mellitus, were noted in all cases and contributed to the high mortality (64%). In all cases pneumonia was clinically fulminant. A fatal outcome was strongly associated with inappropriate initial antibiotic therapy. All tested isolates of Acinetobacter were sensitive to gentamicin and resistant to cefotaxime. The 34 previously reported cases of community-acquired acinetobacter pneumonia are reviewed, and appropriate therapeutic regimens are identified.

Frequent hospital admissions for bacterial infections among Aboriginal people with diabetes in central Australia

To determine hospital-based morbidity and mortality from bacterial infections among Aboriginal people with diabetes in central Australia. Examination of medical records on diabetic inpatients between January 1984 and December 1986. Alice Springs Hospital in central Australia, covering an Aboriginal population of about 12,500 people. Subjects admitted with a bacterial infection (n = 165) were selected from the database of all Aboriginal people known to have diabetes in the region (n = 374; all had non-insulin dependent diabetes). Number of admissions, type and site of infections, causative organisms, duration of hospital stay and cause of death. The 281 admissions for infections accounted for 4.6% of adult Aboriginal admissions to hospital. Thirteen patients died. Eleven patients required amputation of a digit or limb. In 1986, 13/200 patients admitted with diabetes had bacteraemia compared with 14/1885 patients who did not have diabetes. One patient had Fournier's gangrene, one had malignant otitis externa, one community acquired Acinetobacter pneumonia, one pneumonia with Succinivibrio spp. found in blood cultures, and one meningitis and transverse myelopathy with Streptococcus milleri found in blood cultures. The frequency, type and severity of infections in the relatively young patients result in high personal costs to the community and financial costs to the health care system. Standard preventive measures must be implemented to control severe bacterial infections among subjects with diabetes in this socially and economically marginalised population group.

A case of community-acquired acinetobacter calcoaceticus pneumonia.

Acinetobacter calcoaceticus var anitratus, a non-fermentative gram negative bacillus, has been infrequently reported as a cause of community-acquired pneumonia. Bacteremic community-acquired pneumonia caused by Acinetobacter is a fulminant disease with a high mortality (above 40 per cent in the reported case). The onset of the illness is rapid but nonspecific with fever, productive cough, pleuritic pain and rapid prostration. And the patients frequently present with respiratory distress, severe hypoxemia, leukopenia and septic shock. We experienced a case of community-acquired Acinetobacter pneumonia who underwent respiratory support with mechanical ventilator for about 4 weeks and survived. We report the case with review of literature.

Community-acquired acinetobacter pneumonia in adults in Papua New Guinea.

Acinetobacter calcoaceticus, an aerobic gram-negative coccobacillus, is a rare cause of community-acquired pneumonia. It most commonly causes nosocomial infections, particularly in elderly debilitated patients who have undergone surgery, instrumentation, and antibiotic therapy. In a study of acute pneumonia in adults, five cases of community-acquired acinetobacter pneumonia were observed over an 11-month period. Other than chronic pulmonary disease (two patients), no serious underlying diseases existed in these patients. Lobar consolidation was the predominant radiologic pattern. The mortality rate was 40%, and mortality was directly related to therapy with inappropriate antibiotics. The reason for this relatively high prevalence of community-acquired acinetobacter pneumonia in the population studied is not known. Possible explanations include the high prevalence of chronic pulmonary disease, indiscriminate use of penicillin, and an unknown immunodeficiency state.

Community-acquired Acinetobacter pneumonia in a cardiac transplant recipient

Community-acquired Acinetobacter pneumonia in a cardiac transplant recipient

Community-acquired acinetobacter pneumonia

Acinetobacter calcoaceticus var anitratus, a nonfermentative gram-negative bacillus, has been infrequently reported as a cause of community-acquired pneumonia. In this paper we describe the course of six recent patients with community-acquired, bacteremic pneumonia due to this organism and review the six previously reported cases. Our experience suggests this organism is a more common cause of community-acquired pneumonia than previously thought. Acinetobacter pneumonia occurs in older persons with chronic disease, especially alcoholism. It is a fulminant illness with respiratory distress, hypoxemia, leukopenia and shock. Chest roentgenograms reveal a lobar or bronchopneumonic infiltrate which often becomes bilateral within 24 hours of admission to the hospital. Pleural effusions are common. The mortality rate is 43 per cent. Factors that predict a fatal outcome are granulocytopenia, empyema and therapy with inappropriate antibiotics. Therapy with appropriate antibiotics, especially carbenicillin and an aminoglycoside, increases survival.