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Northern Territory Department of Health Library Services Historical Collection
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NORTHERN TERRITORY OF AUSTRALIA
Your 'Ref:
Our Ref:
18 October 1990
Dr I Humphrey
Consultant Paediatrician ROYAL DARWIN HOSPITAL
Dear Dr Humphrey
3 0820 00012776 6
DEPARTMENT OF HEAL1H AND COMMUNITY SERVICES
ROYAL DARWIN HOSPITAL
Please find enclosed 4 copies of my study "Community-Acquired Acinetobacter pneumonia in the Northern Territory of Australia".
This retrospective study was undertaken following a fatal case of community-acquired Acinetobacter pneumonia earlier this year.
The study was done in conjunction with Dr B Currie and Ms K Withnall. My contribution included case finding from blood cu 1 t u.r e r e c o r d s 1 9 8 1 - 1 9 9 0 , r e v i e w o f h o s p i t a 1 r e c o r d s o f a 11 patients with Acinetobacter bacteremia, a literature search, and the composition of the introduction, methods, results and much of the discussion.
Because sufficient results are not yet available for the SLE Study, I will not be submitting this for presentation.
Yours sincerely
DR NICK ANSTEY
DL HIST 616.241 ANS 1990
: (089) 22 8888 089) 22 8286
All correspondence to: Medical Superintendent Royal Darwin Hospital PO Box 41326 CASUARINA NT 0811
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COMMUNITY-ACQUIRED ACINETOBACTER TERRITORY OF AUSTRALIA
AUTHORS:
NM Anstey*, Department of Medicine Royal Darwin Hospital
CASUARINA
0810NORTHERN TERRITORY, AUSTRALIA
PNEUMONIA
BJ Currie, Menzies School of Health Research CASUARINA
0810NORTHERN TERRITORY, AUSTRALIA
KM Withnall, Pathology Department Royal Darwin Hospital
CASUARINA
0810NORTHERN TERRITORY, AUSTRALIA
ACKNOWLEDGEMENTS:
IN THE
We thank Mrs J Albion for secretarial assistance preparation of the manuscript.
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ABSTRACT
Ten cases of blood culture-positive community-acquired pneumonia due to the human commensal Acinetobacter baumannii are described from Darwin in the Northern Territory of Australia in the ten year period 1981-1990. Demographic risk factors included male sex, age greater than 45 years and Aboriginal race. Multiple clinical risk factors, including cigarette smoking, alcoholism, chronic obstructive airways disease and diabetes mellitus, were present in all cases, contributing to the 70% mortality rate. The pneumonias were clinically fulminant. Mortality was strongly associated with inappropriate initial antibiotic therapy. The Acinetobacter were all sensitive to gentamicin and resistant to cefotaxime.
Appropriate treatment regimens are discussed.
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INTRODUCTION
Acinetobacter _baumannii, previously known as Acinetobacter var.
ca
~_?_a~~J.~~~-~~!...!:..!:.~!:..~ (
1- 3 ) , i s a gram neg at i v e co cc ob a c i 11 u s which is ubiquitous in fresh water and soil, and which occurs frequently as a skin and throat commensal in humans ( 4). It has also been well documented as a pathogen in nosocomial infections, particularlyendotracheal
pneumonia intubation,
following tracheostomy
antibiotic treatment, or residence in an intensive care unit (5,6). Community-acquired Acinetobacter pneumonia is much less common, with only 33 blood-culture positive cases having been described (7-23). However, while generally considered rare, it has been recognized for some time to have been a not infrequent cause of severe gram negative community-acquired pneumonia in the Northern Territory of Australia. We describe here the largest series of community-acquired Acinetobacter pneumonia yet reported.
METHODS
All Acinetobacter isolates from blood cultures taken at Royal Darwin Hospital in the Northern Territory of Australia in the 10 year period March 1981 to February 1990, were studied. Blood culture records were not available for May-December 1981 or for July-December 1982.
Species identification had been made biochemically using the API 20E system (API system SA. La Balme Les Grottes, 38390 Montalieu Vercieu, France). Antibiotic sensitivities were performed using the calibrated dichotomous sensitivity (CDS) method (24).
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The hospital records for all patients whose blood cultures grew Acinetobacter calcoaceticus var. anitratus were reviewed.
A diagnosis of acute pneumonia was made if there was adequate documentation of recent onset of symptoms, clinical signs of pneumonia on presentation and a chest x-ray infiltrate. Patients were excluded if they had been admitted to hospital in the month prior to presentation or if the pneumonia developed whilst an inpatient.
RESULTS:
Ten blood culture positive cases of community-acquired Acinetobacter pneumonia were found over the ten year period.
During the same period there were five blood-culture positive cases of nosocomial Acinetobacter pneumonia and 2 cases of nosocomial Acinetobacter septicaemia (with unknown primary focus).
All ten cases of community-acquired pneumonia were due to Acinetobacter calcoaceticus var. an i t r a t u s ( ~.:_!:~um ~~~UJ
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and ineach case Acinetobacter grew from at least two bottles.
The mean age of patients was 57 (range 44-70). Nine out of the ten cases were male. Half of the patients were Aboriginal. The other half were Caucasian.
season (November-March).
80% of cases occurred in the wet All cases had at least two (mean 3) clinical risk factors (see Table 1 ) ' the most common being cigarette smoking and alcoholism. Mean duration of symptoms was 2
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days (range 1-4). Two were afebrile on presentation. Only five had a raised white cell count (>ll.Oxl09
/l) on admission; one case was leucopenic with total WCC of 3.6xl0 /1. 9 Nine out of the ten cases were lymphopenic (lymphocytes
<l.
5xl0 g/1). 9 Three out ofeight cases had low serum albumin (range 30-33 g/1) and total protein (range 56-60 g/1). There was no propensity for site of consolidation (right upper lobe 30%, right lower lobe 20%, left upper lobe 20%, left lower lobe 30%). In the eight cases in which sputum was obtained on presentation, gram negative bacilli were the predominant population seen in four.
grew Acinetobacter.
Five sputa subsequently
Antibiotic sensitivities are given in Table 2. Of note is the resistance of isolates to cefotaxime (six out of six resistant) and ampicillin (nine out of ten resistant) and the universal sensitivity to gentamicin.
Initial treatment was with ampicillin alone (4 cases), benzyl penicillin alone ( 1 case), ampicillin plus benzyl pencillin ( 1 case), ampicillin plus gentamicin ( 1 case), ceftriaxone ( 1 case), cefotaxime and piperacillin ( 1 case) and kanamycin, chloramphenicol and benzyl penicillin (1 case).
The mortality rate was 70%. Of the seven deaths, four were Aboriginals and three Caucasians. The clinical course was fulminant, four out of the seven deaths occurring within 24 hours of admission. The Acinetobacter were resistant to the initial
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antibiotic therapy in six of the seven cases that died. Amongst the three survivors, appropriate antibiotic coverage was provided from the start in two cases and on the following day in the third.
Two of the three survivors were successfully treated with piperacillin without an aminoglycoside; the other with gentamicin and the ineffective ampicillin.
Necropsy was performed in only one of the seven deaths. This showed widespread bronchopneumonia, evidence of chronic bronchitis, moderate hepatic fatty change, and an old quiescent abscess cavity in one lung.
DISCUSSION:
Since the first reported cases of community-acquired Acinetobacter pneumonia in the USA and the UK (7, 8) this entity has been increasingly documented in tropical developing countries, the most recent series ( 19, 20) being from Thailand and Papua New Guinea.
Only two cases, both fatal, have been previously reported in Australia, one from subtropical Brisbane, (9), the other from temperate New South Wales ( 2 2). A fatal case has occurred recently in Alice Springs in the arid centre of Australia (M
Patel, personal communication).
This series shows that it is a significant cause of community- acquired
Australia,
gram negative being twice
pneumonia in the tropical north of as common as nosocomial Acinetobacter
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pneumonia at Royal Darwin Hospital. In the 28 month period January 1988 April 1990, Acinetobacter calcoaceticus var.
anitratus accounted for 11% of blood culture positive community acquired pneumonia at Royal Darwin Hospital, and 21% of gram negative community-acquired pneumonia. Because only blood culture positive cases of pneumonia have been included in this series, the data represent an underestimate of true incidence.
The male predominance seen in this study has been previously noted (14,19,20). Alcoholism, cigarette smoking, chronic obstructive airways disease and diabetes mellitus are confirmed as major risk factors for Acinetobacter pneumonia, a combination of at least two occurring in all patients in our series. The mortality rate of 70% is the highest yet reported for community-acquired Acinetobacter pneumonia [case fatality rate in all previously reported cases was 55%]. This may well reflect the greater number of risk factors present in the patients in our series.
Aboriginal patients were over-represented in this series. This may well reflect the higher prevalence of alcoholism, cigarette smoking and type II diabetes in the Aboriginal population (25,26), as well as generally poor living conditions. The possibility of an immunologically based predisposition to Acinetobacter infection has also been raised (20). Altered immune function in adult Papua New Guinea highlanders with pneumonia has recently been described
( 27). Also recently documented ( 28) is the greater frequency of
complement component C4A and C4B deficiency and of C4A*QO and
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C4B*QO null alleles in Darwin Aborigines than in Caucasian Canberra blood donors. C4B deficiency is a risk factor for bacteremia with encapsulated organisms (29). Studies assessing the importance of immune function and complement phenotype in severe pneumonia are currently in progress in Northern Australia.
Appropriate antibiotic therapy for community acquired Acinetobacter includes gentamicin (or another aminoglycoside) (14, 19, 20) and imipenem. This is supported by our sensitivites.
Only one case Acinetobacter has
of been
gentamicin described
resistant (23). In
community-acquired contrast, gentamicin resistance occurs in up to 91% of hospital acquired infections (30). Although in vitro sensitivity to a proportion of hospital- acquired strains has been documented with ceftazidime (31,32), the presence of inducible beta lactamases in Acinetobacter (33) means that these results may not correlate with in vivo sensitivities.
All six isolates tested in our series were resistant to cefotaxime. Therefore there seems to be no role for the use of third generation cephalosporins in Acinetobacter pneumonia,
recommendation recently (22). Community-acquired are sensitive to carbenicillin in vitro despite such a
Acinetobacter
(14,16,17,19). In vitro synergism with the combination of an aminoglycoside and carbenicillin has also been documented ( 5).
However, whilst two of the survivors responded to piperacillin alone, extended spectrum (antipseudomonal) penicillins induce beta lactamases in vivo (34) and may result in the emergence of resistance during therapy (33).
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Our data suggests that early treatment with an antibiotic to which Acinetobacter is sensitive has a crucial bearing on survival.
This has also been noted in Papua New Guinea (20). Because of the fulminant course of Acinetobacter pneumonia it is inappropriate to await blood culture results or clinical response to initial treatment
in those
before instituting with risk factors
specific anti-Acinetobacter coverage for gram negative pneumonia. In tropical northern Australia, antibiotic choice is complicated by the occurrence of Pseudomonas pseudomallei in the same at-risk groups (35). In the 28 month period January 1988 - April 1990, there were seven cases of P seudomonas pseudomallei pneumonia in addition to the three cases of community-acquired Acinetobacter pneumonia. The antibiotic of choice for Pseudomonas pseudomallei is ceftazidime
(36).
Our current management policy in patients with severe pneumonia and risk factors is to begin empirical therapy with ceftazidime and gentamicin. Imipenem may be a good alternative in this situation. Isolates of Pseudomonas pseudomallei in our laboratory are very sensitive to imipenem, as was the one community-acquired Acinetobacter strain tested so far.Hercouet, et al (37) found all of 142 hospital-acquired isolates of Acinetobacter sensitive to imipenem.
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Jimenez P, Torres A, Rodrigues-Roisin R, de la Bellacasa JP, Aznar R, Gatell JM, Agusti Vidal A. Incidence and aetiology of pneumonia acquired during mechanical ventilation. Crit Care Med 1989; 17:882-885
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White NJ' Dance D A B, Chaowagul W, Wattanagoon Y, Wuthiekanun V, P itakwatchara N.
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TABLE 1
RISK FACTORS PRESENT IN 10 CASES OF COMMUNITY-ACQUIRED ACINETOBACTER PNEUMONIA
DEMOGRAPHIC:
KALK
AGE) 45 YEARS ABORIGINAL
CLINICAL:
SMOKER ALCOHOLISM
PAST HISTORY PNEUMONIA CHRONIC OBSTRUCTIVE AIRWAYS DISEASE
TYPE II DIABETES CONGESTIVE CARDIAC FAILURE
SILICOSIS
STEROID THERAPY
No.
9 9 5
8*
8*
5*
5
3 2
1 1
%
90 90 50
89 89 62 50
30 20
10 10
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Information not documented in all ten cases, ,
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TABLE 2
COMMUNITY ACQUIRED
ACINETOBACTKR ANTIBIOTIC SENSITIVITIES
No. TESTED No. SENSITIVE% SENSITIVE
CEFOTAXIME 6 0 0
TRIMETHOPRIM 10 0 0
CHLORAMPHENICOL 4 0 0
AMPICILLIN 10 1 10
SULPHONAMIDE 10 8 80
TETRACYCLINE 10 9 90
GKNTAMICIN 10 10 100
TOBRAMYCIN 2 2 100
TICARCILLIN 1 1 100
IMIPENEM 1 1 100
CIPROFLOXACIN 1 1 100
