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Infectious Diseases in Clinical Practice:
doi: 10.1097/IPC.0b013e318042e19a
Letters to the Editor

Etiology and Evaluation of Pneumonia in Recruit Military Personnel: 1-Year Experience

Papadopoulos, Nikolaos MD*; Karathanasis, Apostolos MD†; Antonakopoulos, Nikolaos*; Liverezas, Anastasios*; Apostolopoulos, Georgios MD*

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*Internal Medicine Department and †Microbiology Department, 411 General Army Hospital, Tripoli, Greece npnck7@yahoo.com

To the Editor:

Community-acquired pneumonia (CAP) is a common and serious illness with considerable morbidity and mortality. There is seasonal variation, with more cases occurring during the winter months. There are more than 100 microbes (bacteria, viruses, fungi, and parasites) that can cause CAP. Most cases of pneumonia are caused by 4 or 5 microorganisms, but the distribution of pathogens varies with the clinical setting. Streptococcus pneumoniae is the most frequently isolated pathogen. Relative to other pathogens, respiratory viruses, Mycoplasma pneumoniae, Legionella species, Chlamydophila (formerly Chlamydia) pneumoniae, and Haemophilus influenzae are also common. Mycoplasma pneumoniae and adenovirus respiratory tract infections have been reported to be more frequent in young military personnel.1,2 A microbiological diagnosis is confirmed in approximately 60% of cases of CAP in research studies and in only approximately 20% of cases in everyday practice.3-5

We studied 38 recruits (mean age, 24 years) with radiographic evidence of pneumonia during a 12-month period to determine the local microbial spectrum and investigate possible correlations between parameters such as leukocytosis, hypoxygenation, hypocapnia, seasons, smoking, systemic inflammatory response syndrome (SIRS), sepsis, microbial etiologies, and prognosis based on CURB-65 model.6

All cases were admitted to our hospital from regional boot camps, and all of them were hospitalized, detached severity. The following data were recorded on admission: age, smoking, antimicrobial treatment before hospital admission, duration of symptoms before the diagnosis of pneumonia, clinical symptoms (body temperature, pleuritic chest pain, purulent sputum, and confusion) clinical presentation (respiratory rate, heart rate, and arterial systolic and diastolic blood pressures), results of blood gas analysis, chest radiographic pattern (alveolar, interstitial or mixed infiltrate, and unilateral versus bilateral involvement), leukocyte count, and serum biochemistry analysis. On admission, all patients were classified in prognostic groups (I, II, and III) based on CURB-65 model.6 Regular microbial investigation included examination of sputum (Gram stain and cultures) and serology. Sampling of pleural fluid and blood cultures were performed on selected patients. Representative sputum originating from the lower respiratory tract was defined as that containing more than 25 granulocytes and less than 10 epithelial cells per low-power field. The etiology of pneumonia was classified as presumptive if a valid sputum sample yielded 1 or more predominant bacterial strains. The etiology was considered definite if one of the following criteria was met: (1) blood cultures yielding a bacterial; (2) pleural fluid cultures yielding a bacterial pathogen; (3) seroconversion (ie, a 4-fold increase in immunoglobulin [Ig] G titers for C. pneumoniae [IgG ≥ 1:512]) and respiratory viruses, (ie, Influenza viruses A and B, parainfluenza viruses 1 to 3, respiratory syncytial virus, and adenovirus); and (4) a single increased IgM titer for C. pneumoniae of 1:32 or greater and M. pneumoniae at any titer. Both, presumptive and definite, diagnoses were equal in statistical analysis.

The microbial etiology was determined (presumptive and definite diagnoses) in 27 (71%) of 38 cases: M. pneumoniae in 11 cases (29%), S. pneumoniae in 9 cases (24%), and adenovirus in 7 cases (7%). Etiology was not clarified in 11 patients (29%). Prognosis classification with CURB-65 model revealed 25 cases (66%) as class I and 13 cases (34%) as class II. No class III cases were found. Smokers were 26 patients (68%). Leukocytosis of 12 × 109/L or greater was in 18 patients (47%), and less than 4000 × 109/L in 1 case. Severe hypoxygenation as Po2 of less than 60 mm Hg was in 12 patients (32%); hypocapnia as Pco2 of less than 32 mm Hg was in 16 cases (42%). Temperature of greater than 38°C was in 19 cases (50%), and heart rate of greater than 90/min was in 19 cases (50%). The SIRS and sepsis criteria were present in 19 patients (50%). One of them was classified as severe sepsis. There was seasonal variation: during winter, 13 cases (34%); during spring, 13 cases (34%); during summer, 5 cases (13%); and during autumn, 7 cases (18%).

Possible correlations between microbial etiologies, seasons, SIRS parameters (temperature; heart rate; Pco2, <32 mm Hg; and white blood cells), severe hypoxygenation (Po2, <60 mm Hg), and CURB-65 classification were evaluated with nonparametric statistical analysis (crosstabs with Pearson correlation coefficients). Significant correlation (significance, <0.05) occurred between the number of white blood cells (>12 × 109/L), severe hypoxygenation (Po2, <60 mm Hg), hypocapnia (Pco2, <32 mm Hg), presence of SIRS/sepsis, seasonal variation (winter and spring), etiology (S. pneumoniae), and the CURB-65 classification.

The main result was that these young men were more likely to have an etiology comprising atypical bacterial or viral pathogen (together, M. pneumoniae and adenovirus were present in 18 cases [36%]). Most cases occurred during winter and spring: total of 26 cases (68%). These findings have been previously reported in literature.1,7 Maybe, the large number of recruits living under "close contact" conditions in camps is responsible for easy transmission of atypical bacterial or viral pathogens among them.

Second result of this pilot study was that the presence of SIRS/sepsis, the seasonal variation, the severe hypoxygenation, and the infection by S. pneumoniae had a significant correlation with CURB-65 model for classification of pneumonia. Several studies of patients with severe pneumonia in intensive care unit have shown parameters such as S. pneumoniae and bacteremia8 to be significant risk factors for death. Our study had a limited number of patients and did not involve patients in intensive care unit or prognostic class III (based on CURB-65 model). However, there was a correlation between factors such as etiology, SIRS/sepsis, and prognosis by CURB-65 classification. Further evaluation in a larger group of patients is needed to establish these findings.

Nikolaos Papadopoulos, MD*

Apostolos Karathanasis, MD†

Nikolaos Antonakopoulos*

Anastasios Liverezas*

Georgios Apostolopoulos, MD*

*Internal Medicine Department

and †Microbiology Department

411 General Army Hospital

Tripoli, Greece

npnck7@yahoo.com

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REFERENCES

1. Gray GC, Hyams KC, Wang SP. Mycoplasma pneumoniae and Chlamydia pneumoniae strain TWAR infections in US Marine Corps recruits. Mil Med. 1994;159:292-294.

2. Top FH Jr. Control of adenovirus acute respiratory disease in US Army trainees. Yale J Biol Med. 1975;48:185-195.

3. Marrie TJ, Poulin-Costello M, Beecroft MD, et al. Etiology of community-acquired pneumonia treated in an ambulatory setting. Respir Med. 2005;99(1):60-65.

4. Michetti G, Pugliese C, Bamberga M, et al. Community-acquired pneumonia: is there difference in etiology between hospitalized and out-patients? Minerva Med. 1995;86(9): 341-351.

5. Bochud PY, Moser F, Erard P. Community-acquired pneumonia. A prospective outpatient study. Medicine (Baltimore). 2001;80(2):75-87.

6. Aujesky D, Auble TE, Yealy DM. Prospective comparison of three validated prediction rules for prognosis in community-acquired pneumonia. Am J Med. 2005;118(4):384-392.

7. Beovic B, Bonac B, Kese D. Aetiology and clinical presentation of mild community-acquired bacterial pneumonia. Eur J Clin Microbiol Infect Dis. 2003;22(10):584-591.

8. Moine P, Vercken JB, Chevret S. Severe community-acquired pneumonia: etiology, epidemiology, and prognosis factors. French Study Group for community-acquired pneumonia in the intensive care unit. Chest. 1994;105: 1487-1495.

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