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(Chest. 2006;129:102-109.)
© 2006 American College of Chest Physicians

Fulminant Community-Acquired Acinetobacter baumannii Pneumonia as a Distinct Clinical Syndrome*

Wah-Shing Leung, MRCP; Chung-Ming Chu, FCCP; Kay-Yang Tsang, MRCP; Fu-Hang Lo, MRCP; King-Fan Lo, MRCP and Pak-Leung Ho, MRCPath

* From the Department of Medicine and Geriatrics (Drs. Leung, Chu, Tsang, F.-H. Lo, and K.-F. Lo), United Christian Hospital, Hong Kong SAR, Peoples Republic of China; and the Department of Microbiology (Dr. Ho), Division of Infectious Disease, Queen Mary Hospital, University of Hong Kong, Hong Kong SAR, Peoples Republic of China.

Correspondence to: Pak-Leung Ho, Division of Infectious Disease, Department of Microbiology and Centre of Infection, Queen Mary Hospital, University of Hong Kong, Pokfulam Rd, Pokfulam, Hong Kong SAR, Peoples Republic of China; e-mail: plho{at}hkucc.hku.hk

Abstract

Study objectives: Acinetobacter baumannii (AB) is an important cause of hospital-acquired pneumonia (HAP), and an uncommon but important cause of community-acquired pneumonia (CAP) with high mortality. To better characterize CAP-AB, we compared its clinical features and outcomes with a control group of HAP-AB patients.

Methods: This is a retrospective case-control study comparing CAP-AB and HAP-AB patients, which was performed at United Christian Hospital between July 2000 and December 2003.

Results: There were 19 cases of CAP-AB and 74 cases of HAP-AB. When compared with the HAP-AB group, the CAP-AB group had more ever-smokers (84.3% vs 55.4%, respectively; p = 0.031), more COPD patients (63.2% vs 29.7%, respectively; p = 0.014), and fewer median days of hospitalization (HAP-AB group, median, 0 days; CAP-AB group, 0 days [range, 0 to 30 days]; p = 0.049) in the previous year. The CAP-AB group had more patients with positive blood culture findings (31.6% vs 0%, respectively; p < 0.001), a higher frequency of ARDS (84.2% vs 17.6%, respectively; p < 0.001), and disseminated intravascular coagulation (DIC) (57.9% vs 8.1%, respectively; p < 0.001). The median survival time was only 8 days in the CAP-AB group, vs 103 days in the HAP-AB group (p = 0.003). Factors associated with the higher mortality in the CAP-AB group included the presence of AB bacteremia (p = 0.040), platelet count of < 120 x 109 cells/L (p = 0.026), pH < 7.35 on presentation (p = 0.047), and the presence of DIC (p = 0.004).

Conclusions: CAP-AB appears to be a unique clinical entity with a high incidence of bacteremia, ARDS, DIC, and death, when compared to HAP-AB. Further studies are needed to investigate the mechanism of the fulminant nature of CAP-AB.

Key Words: Acinetobacter baumannii • community-acquired pneumonia • hospital-acquired pneumonia

Acinetobacter baumannii (AB) is a Gram-negative coccobacillus that is ubiquitous in fresh water and soil, and is also found frequently as a skin and throat commensal in humans.1 It is well-known because of the development of multiple drug resistance23 and as an important cause of hospital-acquired pneumonia (HAP).4567

It is also increasingly recognized as an uncommon but important cause of community-acquired pneumonia (CAP).89101112131415 CAP-AB appears to be characterized by a fulminant course, with an acute onset of dyspnea, cough, and fever that rapidly progresses to respiratory failure and shock. The mortality rate from CAP-AB is high (40 to 64%),89101112131415 and it appears to be higher than the overall mortality rate (24%) resulting from severe CAP.16 However, these case series did not have any control group to which the clinical features and outcomes of CAP-AB could be compared. In order to better characterize CAP-AB, we performed a retrospective study of CAP-AB, and compared its clinical features and outcomes with a control group comprising patients with HAP-AB.

Methods and Materials

Patients and Study Design
This is a retrospective case-control study comparing CAP-AB patients with a control group of HAP-AB patients at United Christian Hospital, which is a regional hospital with 1,200 acute care beds and serving a population of approximately 500,000 persons in Hong Kong. We systematically searched the computer database of our microbiology laboratory for patients with positive culture findings for AB between July 2000 and December 2003. We determined whether they were eligible for the study using the criteria listed below. We then abstracted the hospital records of these patients using a standardized database. Only cases of CAP-AB and HAP-AB were included. This study was approved by the Institutional Review Board at the United Christian Hospital.

Pneumonia was defined by clinical and radiographic criteria, as described by the Centers for Disease Control and Prevention.17 Pneumonia was considered to be CAP if it was acquired outside a hospital or nursing home and the patient had not been hospitalized in the month before the development of pneumonia. Pneumonia was considered to be HAP if the onset had occurred ≥ 48 h after hospital admission and was judged not to have been incubating before hospital admission. Some of the HAP patients had ventilator-associated pneumonia (VAP), which was diagnosed if the onset had occurred ≥ 48 h after the initiation of mechanical ventilation and was judged not to have been incubating before the initiation of mechanical ventilation.

All microbiological specimens were taken before the initiation of therapy with antibiotics. AB was considered as a "definite pathogen" if it was cultured from blood or pleural fluid.18 AB was considered as a "probable pathogen" if it was cultured in the sputum culture or tracheal aspirate before the initiation of antibiotic therapy.19 A valid specimen needed to have ≥ 25 neutrophils present on a Gram stain and ≤ 10 epithelial cells per high-power field.20

Clinical, laboratory, radiologic, and microbiological data were collected. Clinical data included age, sex, underlying disease, Charlson comorbidity score,21 prior treatment (including hospitalization, surgery, and steroid and antibiotic use for > 1 day within 1 year of pneumonia), clinical presentation, pneumonia severity index,22 acute physiology and chronic health evaluation (APACHE) II score,23 complications, and mortality. Laboratory data included hematologic tests, biochemical tests, arterial blood gas analysis findings, and culture and sensitivity results from appropriate clinical specimens. Radiologic data included the presence of consolidation and/or pleural effusion on chest radiograph (CXR). The CXR was reviewed for the presence of lobar consolidation or bronchopneumonic changes. Microbiological data included antimicrobial susceptibility and the presence of other pathogens cultured in the same specimen. Growth was categorized semi-quantitatively as "scanty," "moderate," or "heavy" according to standardized criteria.24 Antimicrobial susceptibility testing was performed using disk diffusion according to the National Committee for Clinical Laboratory standards.25 The antimicrobial agents tested were as follows: ciprofloxacin; cotrimoxazole; gentamicin; tobramycin; amikacin; piperacillin; ticarcillin-clavulanate; ampicillin-sulbactam; cefoperazone-sulbactam; and imipenem. Empirical antibiotics were given according to prevailing guidelines.172627

Definition of Terms
AB bacteremia was defined as the isolation of AB in one or more cultures of blood specimens in association with clinical features of sepsis. COPD was diagnosed using the standard criteria recommended by the American Thoracic Society.28 An ever-smoker was defined as a current or former smoker. Other lung diseases included bronchiectasis, asthma, lung fibrosis, and old pulmonary tuberculosis. Standard definitions of ARDS,29 disseminated intravascular coagulopathy (DIC),30 septic shock31 were employed throughout this study. Hyperglycemia was defined as a spot glucose concentration of > 11 mmol/L. The initial antibiotic therapy for the episode of AB pneumonia comprised agents that were administered in the first 12 h. The therapy was considered to be appropriate if in vitro susceptibility was confirmed (or inferred) by laboratory testing results. Resistance to macrolides was assumed for all of the AB isolates. Therapy was considered to be inappropriate if the isolate was susceptible only to the aminoglycoside component. All microbiological specimens were obtained before the initiation of antibiotic therapy.

Statistical Analysis
Data were expressed as the mean (SD) or the median (range) as appropriate unless otherwise specified. The {chi}2 test or Fisher exact test was used to compare categoric variables between CAP-AB and HAP-AB groups where appropriate. The Student t test or the Mann-Whitney U test was used to compare continuous variables between the two groups, depending on the nature of the data. Life table analysis was performed to analyze the survival of CAP-AB patients. Potential risk factors for worse prognosis in the CAP-AB group were tested by log-rank test (categoric variables) or Cox regression (continuous variables). A two-tailed p value of < 0.05 was considered to be statistically significant. All statistical analyses were performed using statistical software (SPSS, version 11.0; SPSS Inc; Chicago, IL).

Results

There were 19 cases of CAP-AB and 74 cases of HAP-AB, of which 51 cases were VAP, during the 42-month study period.

Baseline Characteristics
In the 19 CAP-AB cases, 16 patients were male (84%) and 3 patients were female (16%). The mean age was 72.6 years (SD, 9.6 years). Almost all of the patients (18 of 19 patients; 95%) had some underlying chronic illness, including COPD, diabetes mellitus, hypertension, heart disease, and carcinoma.

Compared to the HAP-AB group, the CAP-AB group had more ever-smokers, more COPD patients, fewer patients with other non-COPD chronic lung diseases, and a lower number of hospitalization in the previous year. There was no significant difference in the number of other nonpulmonary comorbidities in both groups (Table 1 ).


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  		Table 1.. Comparison of Baseline Characteristics of CAP-AB and HAP-AB*

 
Clinical Presentation
The majority of CAP-AB patients presented with acute onset of fever, shortness of breath, and cough. The initial presentation was characterized by severe respiratory distress. When compared with patients in the HAP-AB group, more CAP-AB patients had shortness of breath, cough, and pleuritic chest pain on presentation, while sputum production was less common. In a subgroup analysis excluding patients who were intubated and mechanically ventilated, shortness of breath was more common in CAP-AB patients (p = 0.036), while sputum production was less common (p = 0.005; data not shown). The APACHE II score was not significantly different in both groups. In terms of hematologic parameters, the CAP-AB group had higher mean hemoglobin levels, lower total WBC count, absolute neutrophil count, platelet count, and more prolonged activated partial thromboplastin time than the HAP-AB group. For radiographic features, lobar consolidation was more common in the CAP-AB group, while pleural effusion and cavitatory changes were not present in this group (Table 2 ). Pleural effusions developed in nine patients in the HAP-AB group (12.1%); however, the amounts of fluid were considered too small to warrant thoracocentesis.


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  		Table 2.. Comparison of Clinical Presentation of CAP-AB and HAP-AB*

 
Treatment and Antimicrobial Sensitivity
A significant proportion (32%) of CAP-AB patients had bacteremia on presentation. Four patients in the CAP-AB group had other organisms cultured in the sputum sample (Streptococcus pneumoniae, 2 patients; Pseudomonas aeruginosa, 2 patients). However, AB was considered as the pathogen as it was also cultured in the blood culture of these four patients. Moderate and heavy growths of AB were reported in the respiratory specimens of CAP-AB patients in 21.1% and 78.9% of patients, respectively; the AB growth in HAP-AB patients was 24.3% and 75.7%, respectively. No patient underwent diagnostic BAL or protected specimen brush procedures in this study. Empirical antibiotics received by CAP-AB patients before culture and sensitivity usually comprised a combination of a ß-lactam and a macrolide. All of the AB isolates in the CAP-AB group were sensitive to amikacin, ticarcillin/clavulanate, cefoperazone/sulbactam, and ampicillin/sulbactam, while they were less sensitive to gentamicin (14 of 19 patients; 73.7%), tobramycin (14 of 19 patients; 73.7%), ciprofloxacin (9 of 19 patients; 47.4%), cotrimoxazole (9 of 19 patients; 47.4%), and piperacillin (6 of 19 patients; 31.6%).

When compared to the HAP-AB group, the CAP-AB group had a higher percentage of patients with positive blood culture findings, while positive findings in sputum or tracheal aspirates was not significantly different (Table 2). Bacteria other than AB cultured in the respiratory specimen was more commonly observed in the HAP-AB group than in the CAP-AB group (66.2% vs 21.1%, respectively; p = 0.001). However, AB was considered to be the predominant organism on direct Gram smear, and so it was considered as a probable pathogen. The antibiotics that were initially used are listed in Table 3 . Thirty-two percent of CAP-AB patients received adequate antibiotic coverage for the strains of AB isolated vs 20.3% of HAP-AB patients, and this was not statistically significant. This indicated that most patients were not receiving adequate bacterial coverage before the sensitivity result. The antibiotic was changed in 52.6% of CAP-AB patients and in 67.6% of HAP-AB patients, and again this was not statistically significant. There were significant differences in the antibiotic sensitivity pattern between the two groups. Strains found in the CAP-AB group had lower sensitivity rate to ciprofloxacin (47.4% vs 78.4%, respectively; p = 0.011), cotrimoxazole (47.4% vs 81.1%, respectively; p = 0.006), and tobramycin (73.7% vs 97.3%, respectively; p = 0.004), but higher sensitivity rates to ticarcillin/clavulanate (100% vs 73.0%, respectively; p = 0.010) than those found in the HAP-AB group.


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  		Table 3.. Comparison of the Initial Antimicrobial Treatment for CAP-AB and HAP-AB*

 
Complications and Outcomes
There was a higher frequency of ARDS (84.2% vs 17.6%, respectively; p < 0.001) and DIC (57.9% vs 8.1%, respectively; p < 0.001) in the CAP-AB group than in the HAP-AB group. The frequency of shock requiring inotropic support (CAP-AB group, 57.9%; HAP-AB group, 43.2%; p = 0.307), the requirement of mechanical ventilation (CAP-AB group, 63.2%; HAP-AB group, 66.2%; p = 0.79), and acute renal failure requiring dialysis (CAP-AB group, 15.8%; HAP-AB group, 6.8%; p = 0.35) was not significantly different. The CAP-AB group had a significantly worse prognosis compared to the HAP-AB group, with a higher 30-day mortality rate in the CAP-AB group (57.8% vs 35.4%, respectively; p < 0.001) [Fig 1 ].


Figure 1
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  		Figure 1.. Figure 1. Survival curve for CAP-AB and HAP-AB patients.

 
The following parameters were found to be associated with higher mortality in the CAP-AB group: presence of AB bacteremia (p = 0.040); platelet count of < 120 x 109 cells/L (p = 0.026); pH < 7.35 on presentation (p = 0.047); and the presence of DIC (p = 0.004). Unexpectedly, adequate empirical antibiotic therapy within first 12 h of diagnosis was not associated with improved survival in the CAP-AB group (3 of 6 patients died [50%]) when compared to patients who received inadequate coverage (7 of 13 patients died [54%]; p = 0.879 [log-rank test]). A subgroup analysis was performed including only CAP-AB patients who survived the initial 48 h (13 patients), so that the antibiotics administered initially would have adequate time to act. Again, patients treated with adequate initial antibiotics had no significant difference in mortality (one of four patients died [25%]) from patients treated with inadequate initial antibiotics (three of nine patients died [33.3%]; p = 0.598 [log-rank test]). Five of eight CAP-AB patients (62.5%) who received a combination of third-generation cephalosporins and aminoglycosides survived, vs 4 of 11 patients (36.4%) who did not receive this combination and survived (p = 0.337 [log-rank test]). In four patients, the antibiotics used were changed based on susceptibility results, and three of those patients survived. Other factors, including age, APACHE II score, and Charlson comorbidity score, were not associated with poor survival in the CAP-AB group. Multivariate analysis was not performed due to the small number of patients.

Discussion

To the best of our knowledge, the current study is the largest series89101112131415 of CAP-AB patients reported in the literature so far, and it is also unique in having a group of HAP-AB patients for comparison. CAP-AB was shown to be significantly different from HAP-AB in several aspects. First, CAP-AB patients were more likely to be ever-smokers and to have COPD, while other lung diseases or comorbid conditions, such as liver cirrhosis, diabetes mellitus, malignancy, and hematologic malignancy, were not predisposing factors. Second, the clinical presentation was more acute and fulminant with the conditions of more patients complicated by ARDS, and DIC. Third, CAP-AB patients were likely to have AB bacteremia on presentation and were less likely to have other concomitant organisms grown in culture from the same respiratory specimen. Fourth, antibiotic sensitivity was significantly different in the two groups, with HAP-AB isolates being more resistant than the CAP-AB isolates. Nevertheless, the appropriate empirical coverage of CAP-AB did not seem to alter the dismal prognosis. Finally, patients in the CAP-AB group had significantly higher mortality than patients in the HAP-AB group. Therefore, we propose that CAP-AB is a unique clinical entity, characterized by a high incidence of bacteremia, ARDS, DIC, and early deaths.

Our study showed that CAP-AB usually occurs in elderly people with underlying COPD, and has a very acute and fulminant clinical course with very high mortality. Our findings confirm the observations made in previous uncontrolled case series.89101112131415 Anstey et al9 reported a series of 11 cases of blood culture-positive CAP-AB in Darwin in the Northern Territory of Australia during the 10-year period from March 1981 through February 1991. They found that the demographic risk factors included male gender, age > 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. A high mortality rate (64%) was observed in this cohort. A fatal outcome was strongly associated with inappropriate initial antibiotic therapy and shock at presentation. Chen et al15 did a retrospective review of 13 (9 men and 4 women; age range, 37 to 85 years) patients with CAP-AB. They found that conditions associated with CAP-AB included male gender, old age, alcoholism, malignancy, cerebrovascular disease, diabetes mellitus, renal disease, and liver cirrhosis. Twelve patients (92%) had a fulminant course presenting with septic shock and respiratory failure, and 11 patients (85%) needed ventilator support and were treated in an ICU. All patients had positive blood culture results. A high mortality rate (62%) was again observed. The mortality rate reported in our study (57.8%) and previous studies89101112131415 among patients with CAP-AB was comparable to those reported for patients with severe CAP due to S pneumoniae (40 to 75%), Legionella pneumophila (33 to 56%), or Staphylococcus aureus (72 to 100%) in the Nottingham series.32 Some findings that are not present in our series are the absence of pleural effusion15 and cavitation seen on the CXR.15

Our study found that the following factors were associated with higher mortality in the CAP-AB group: AB bacteremia; platelet count of < 120 x 109 cells/L; pH < 7.35 on presentation; and the presence of DIC. In contrast to the study by Anstey et al,9 our study showed that survival among CAP-AB patients was not improved with appropriate empirical antibiotics treatment. It appears that AB triggers severe systemic inflammatory response syndrome very early on in the course of CAP-AB, together with septic shock, DIC, and ARDS. Antibiotic therapy and supportive treatment are therefore often unable to salvage the patients with CAP-AB. In the study by Chen et al,15 four of the five patients who survived the infection were treated with a combination of a third-generation cephalosporin and an aminoglycoside. In our study, although a trend to better survival was noted in patients treated with this combination vs treatment with other antibiotics, no statistical significance was detected.

AB was recognized as a hospital-acquired pathogen, especially in patients with VAP. HAP-AB is regarded as a heterogeneous disorder, and the prognosis usually depends on the underlying condition but not on the acquisition of AB infection itself.53334 On the contrary, CAP-AB seems to be a distinct clinical syndrome. The question of why CAP-AB is more fulminant than HAP-AB, when they are both caused by the same organism, is intriguing. A few postulates are possible.

The pathogenetic mechanism of AB is poorly understood. A limited number of virulence factors reduce this bacterium to the role of an opportunist. Although growth in an environment with an acidic pH at lower temperatures may enhance its ability to invade devitalized tissue, no known cytotoxins are produced. Lipopolysaccharide is present in the cell wall, but little is known of its endotoxigenic potential in humans. Most experts think that it is an opportunistic organism.35 On the other hand, AB and Neisseria meningitidis belong to the same family of Neisseriaceae, and they both have lipopolysaccharides in the outer membrane.35 Excellent reviews are available that have addressed the general and immunologic aspects of meningococcal disease, the role of cytokines, and the role of N meningitidis lipopolysaccharides in the pathophysiology.3637 Clinically, there are a number of features that are similar between CAP-AB infection and infection caused by N meningitidis, including septic shock and DIC. Lipopolysaccharides may play an important role in the pathogenesis of CAP-AB, which may explain its fulminant nature. However, this does not explain why CAP-AB is more fulminant than HAP-AB, since both are caused by the same organism.

It is also possible that the fulminant course of disease in CAP-AB patients is due to a selection bias, in which only the most severely affected patients with CAP-AB are admitted to hospital, while patients with milder cases are treated in the community. Acinetobacter sp is ubiquitous, and the source of infection is likely environmental.1 CAP-AB generally occurs in patients with diminished host defenses (eg, due to alcoholism, tobacco use, diabetes mellitus, renal failure, or underlying pulmonary disease).89101112131415 It is possible that subclinical infection may occur in people exposed to an environmental source of AB, but invasive diseases occur only in hosts with diminished local defense or general immunity, similar to infections caused by L pneumophila. L pneumophila infection can manifest in the following two different forms: Pontiac fever, which is a mild, self-limiting febrile illness without pneumonia; and Legionnaires disease, which is a highly lethal form of pneumonia. It is not known why these two different forms occur, but the size of the inoculum and the host factors are probably important determinants.38 However, this postulate does not explain why CAP-AB is more fulminant than HAP-AB. Patients with HAP-AB (especially those with VAP) are also immunocompromised in many ways, but AB seems to have caused a milder disease in HAP-AB patients.

Alternatively, the possibility of a specific immunologic predisposition to AB infection has also been postulated.39 Anstey et al9 proposed that complement deficiency might predispose an individual to AB infection and that this might have contributed to the higher prevalence of the disease in the Aborigines in Northern Australia. However, the occurrence of a complement deficiency as a cause of fulminant CAP-AB has not yet been documented. Moreover, complement deficiency cannot explain why CAP-AB occurs in older age and why these patients had not experienced severe infections caused by other encapsulated organisms in the past.

Perhaps a more promising hypothesis is that the strains causing CAP-AB and HAP-AB are different. Using pulsed-field electrophoresis to analyze the restriction fragments, Zeana and colleagues40 showed that AB isolates from the community were characterized by a large variety of unrelated strains (83.3%), and that they were distinct from hospital isolates of which 58.3% were closely related. Furthermore, the AB strains from the hospital had a higher rate of multiple drug resistance (hospital isolates, 36.6%; community isolates, 0%; p < 0.005). But this study was limited by the fact that the community strains were from healthy individuals instead of from patients with infection. In future studies, it would be imperative to examine whether there are important differences between the CAP-AB strains (especially in bacteremic patients) and the HAP-AB strains on proteomic and genomic levels.

As AB is an uncommon pathogen in CAP, current antibiotic guidelines are not targeted toward treating AB.1726 This accounts for the inadequate empirical coverage for our group of CAP-AB patients (68.4%), especially if therapeutic combinations of salbactam-containing antibiotics are not used. Therefore, it is very important that we have increased awareness of AB as a cause of severe CAP; then we will be able to choose the appropriate antibiotics for treatment. For the treatment of patients with HAP-AB, inadequate empirical coverage (79.7%), despite adherence to the prevailing guidelines,27 was due to the presence of resistance to multiple antibiotics.

Our study has several limitations that merit consideration. First, it was a retrospective study and is prone to missing data. A prospective study is difficult to perform for CAP-AB, given its rarity, but fortunately we were able to collect the majority of the data that were required for analysis. Second, patients with VAP-AB may not be able to experience or report symptoms such as cough, shortness of breath, or pleuritic chest pain, causing a spuriously low prevalence of these symptoms in the HAP-AB group. Third, establishing a definite diagnosis of pneumonia due to AB based on respiratory specimens, especially for nosocomial pneumonia, is difficult, given that this bacterium frequently colonizes mucosal surfaces in hospitalized patients, and that there is no specific microbiological marker for nosocomial pneumonia, even with quantitative bacterial cultures.41 However, in our series, we only selected patients with overt clinical symptoms and signs of pneumonia to minimize the diagnostic uncertainties. Furthermore, for all HAP-AB patients, AB was shown to be the predominant organism on direct Gram smear, and so it was a probable pathogen.

Conclusion

In conclusion, CAP-AB is a clinically unique entity, with a high incidence of bacteremia, ARDS, septic shock, DIC, and early death. Although it is an uncommon cause of CAP, it merits special attention as the mortality rate is very high. Further studies should be performed to explore the pathogenetic mechanisms and optimal treatment of CAP-AB.

Footnotes

Abbreviations: AB = Acinetobacter baumannii; APACHE = acute physiology and chronic health evaluation score; CAP = community-acquired pneumonia; CXR = chest radiograph; DIC = disseminated intravascular coagulopathy; HAP = hospital-acquired pneumonia; VAP = ventilator-associated pneumonia

This work was submitted by Dr Wah-Shing Leung to the University of Hong Kong in partial fulfillment of the requirement for the Postgraduate Diploma in Infectious Diseases. Part of the data in this study was submitted to the Chest 2005 conference in abstract form.

Received for publication April 27, 2005. Accepted for publication June 24, 2005.

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