|Year : 2017 | Volume
| Issue : 1 | Page : 11-16
A study of clinical and etiological profile of community-acquired pneumonia with special reference to atypical pneumonia
TC Nagesh Kumar1, Roshna Rafiudeen1, K Rashmi2
1 Department of Medicine, MS Ramaiah Medical College, Bengaluru, Karnataka, India
2 Department of Pathology, MS Ramaiah Medical College, Bengaluru, Karnataka, India
|Date of Web Publication||15-Feb-2018|
Department of Pathology, MS Ramaiah Medical College, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Pneumonia is a leading cause of morbidity and mortality, especially in developing countries. The cause of community-acquired pneumonia (CAP) is often difficult to establish. The most effective methods, especially for the diagnosis of atypical pathogens, are often invasive and may not always be justified. We studied the clinical and etiological profile of CAP, especially with regards to pathogens causing atypical pneumonia.
Aims and Objectives: The aim is to study the clinical profile and etiological agents in patients suffering from CAP in our hospital and to detect proportion of atypical pathogens among these CAP patients.
Methodology: From September 2012 to September 2014, 122 patients were diagnosed as having CAP and were included in this study. After sputum, blood culture, and serological evaluation, they were grouped as having typical and atypical pneumonia. Chi-square test was used as statistical method to compare between these two groups.
Results: Of 122 patients, 40.2% of patients were found to have typical organisms and 20.5% had atypical organisms causing pneumonia. The common etiological agents were Streptococcus pneumoniae (15.6%) and Klebsiella pneumoniae (8.2%) among typical pneumonia and Mycoplasma pneumoniae (7.4%) and Legionella pneumophila (5.7%) among atypical pneumonia cases.
Conclusions: It is difficult to differentiate these causative agents by clinical features alone. Hence, appropriate serological, sputum, and blood culture should be carried out for early diagnosis, prompt treatment and also to reduce complications.
Keywords: Community-acquired pneumonia, etiology, indirect immunofluorescence, typical and atypical pathogens
|How to cite this article:|
Nagesh Kumar T C, Rafiudeen R, Rashmi K. A study of clinical and etiological profile of community-acquired pneumonia with special reference to atypical pneumonia. Ann Nigerian Med 2017;11:11-6
|How to cite this URL:|
Nagesh Kumar T C, Rafiudeen R, Rashmi K. A study of clinical and etiological profile of community-acquired pneumonia with special reference to atypical pneumonia. Ann Nigerian Med [serial online] 2017 [cited 2018 May 24];11:11-6. Available from: http://www.anmjournal.com/text.asp?2017/11/1/11/225611
| Introduction|| |
Community-acquired pneumonia (CAP) is most often defined as a lower respiratory tract infection (LRTI) characterized by cough, fever, chills, fatigue, dyspnea, rigors, and pleuritic chest pain – with or without new infiltrate on chest radiography, acquired outside of a hospital or long-term care setting. CAP is one of the leading causes of morbidity and mortality in the world; the World Health Organization (WHO) global burden of disease study estimated that LRTIs, which include CAP, were 429.2 million episodes of illness worldwide and account for 94.5 million disability-adjusted life years. In adults aged over 59 years, it causes 1.6 million deaths annually still its true incidence which is uncertain as most of the cases go unreported. According to the WHO data, each year three to four million people especially children and elderly died from pneumonia worldwide. Pneumonia is ranked as the sixth leading cause of death in the United States. The problem is much greater in developing countries where pneumonia is the most common cause of hospital visits and admissions in adults.
The CAP is divided into typical and atypical, so as to predict the likely pathogens, and thus facilitate the selection of the appropriate treatment. Typical pneumonia is those caused by organisms such as Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, and Haemophilus influenzae. The history, physical examination, and chest radiography have a modest capacity to detect these cases. A definitive management needs microbiological documentation, but most cases remain undetected by the currently available tests. The importance of the atypical pneumonias is not related to their frequency (approximately 15% of CAPs) but due to their difficulty of diagnosis and their nonresponsiveness to recommended beta-lactam therapy.,,, The rational antibiotic guidelines can be made only if studies are conducted in different parts of the country to know the regional variations in etiology of CAP.
- To study the clinical profiles and etiological agents in patients suffering from CAP
- To detect proportion of atypical pathogens in these cases.
| Methodology|| |
The study was conducted in a tertiary care hospital, from September 2012 to September 2014. This study was prospective study, conducted in department of Medicine. Before taking up this study, it was presented to ethical committee and approval was taken from ethical committee of the hospital. The patients with clinical suspicion of CAP were included in this study after applying inclusion and exclusion criteria. The diagnosis of CAP was considered in according to the Infectious Diseases Society of America/American Thoracic Society consensus guidelines. Those cases fulfilled inclusion criteria, detailed history taken, and examination were done and were subjected to complete blood count, sputum examination, blood culture, renal function tests, liver function tests, and serology if atypical after obtaining informed consent. The chest radiograph was taken for all patients. In addition to these investigations, patients with a probable diagnosis of atypical pneumonia had indirect immunofluorescence (IIF) assay done as per the Japanese Thoracic Society Guidelines. For IIF, 2–4 ml of venous blood was collected from patients of CAP, with atypical features. The samples were centrifuged at 1000 rpm for 10 min at 40°C. The sera were separated and stored at −20°C until assayed with Pneumoslide-M tests. The Pneumoslide-M assay kit is for simultaneous detection of IgM antibodies of multiple atypical pneumonia pathogens. Each slide has 10 wells each containing following antigens: Legionella pneumophila, Mycoplasma pneumoniae, Coxiella brunette, Chlamydophila pneumonia, adenovirus, respiratory syncytial virus, influenza A, influenza B, parainfluenza, and cell control. The serum samples are diluted with 1:1 with phosphate-buffered saline then treated with human IgG sorbent. The sorbent-treated diluted serum was incubated 90 min at 37° with 10 well slide. The slide is washed twice with buffer. A florescent secondary IgM antibody was added to the wells and incubated at 37°C for 30 min. Then, results are interpreted as apple green nuclear fluorescence in 1%–15% cells – adenovirus, RSV, parainfluenza. If entire bacteria shows – Apple green fluorescence – Legionella, Chlamydophila, Coxiella. If only periphery of the cell is stained it is more likely mycoplasma group. For the blood culture, 8–10 ml of aseptically drawn blood sample was incubated in automated blood culture media bottle. These bottles are loaded to BacT/Alert 3Dand incubated overnight at 37°C aerobically. These bottles are removed and subcultured to blood agar and MacConkey agar. If single type of colony is seen, the isolate was identified by standard biochemical test. If multiple types of colonies are seen, they are further cultured on 5% sheep agar and chocolate agar. These are kept in candle jar and incubated at 37°C. The cultures were checked for growth at 24 and 48 h.
Based on the demonstrable agent, patients were categorized as cases of typical, atypical, or undiagnosed (missed) pathogen. The statistical analysis was performed using the Chi-square test. The patients with previous history of hospital admission in the past 1 week, patients suffering from ventilator associated or hospital acquired pneumonia; patients with radiographic evidence of tuberculosis, pulmonary infarction, congestive cardiac failure, or lung cancer were excluded from the study.
| Results|| |
All 122 patients included in this study were divided into two groups, those with typical pneumonia and those with atypical pneumonia; based on sputum and blood culture and IIF assay. The age group of patients varied from 18 to 90 years. Mean age was 56.07 ± 16.52 years. Majority of patients were in the age group 51–60 years of age. Of the 122 patients, 84 (68.9%) were male and 38 (31.1%) were female. The detail of sex distribution is shown in [Figure 1]. Out of the 122 patients studied, 40.2% of patients were found to have typical organisms causing pneumonia and 20.5% had atypical organisms. In 39.3% of the cases, no etiological organism could be demonstrated. The most common etiological agents in our study were S. pneumoniae (15.6%) followed by K. pneumoniae (8.2%) and M. pneumoniae (7.4%). The 45.1% of the 122 patients were smokers while 18.9% were alcoholics. There was no significant difference in these habits between the patients with atypical and typical pneumonia [Figure 2] and [Table 1].
All the 122 patients had presented with complaints of fever and cough, with 95% of patients with typical pneumonia and 56% of atypical pneumonia patients having expectoration. Chi-square test revealed that productive cough was significantly more in typical pneumonia [Table 2]. In our study, the 67.2% of patients were found to have fever at the time of presentation. Dyspnea was significantly more common in patients with typical pneumonia (79.6%) than in atypical pneumonia. Other symptoms included are chest pain (27%), hemoptysis (6.6%), and upper respiratory tract symptoms (6.6%). A symptom of altered sensorium was more common in patients with typical pneumonia (24.5%) than in atypical pneumonia (8%). However, symptoms of headache (48%), myalgia (76%), and gastrointestinal symptoms (40%) were common among the atypical pneumonia cases. Furthermore, it was found that dyspnea was more common in patients with typical pneumonia (79.6%) than in atypical pneumonia. We found that S. pneumoniae was associated with gastrointestinal symptoms in 33% of patients, similar to L. pneumoniae. Patients with K. pneumoniae and H. influenzae also complained of extra pulmonary symptoms. Tachycardia was noted in 40.2% of patients and tachypnea in 50% of patients [Table 2]. In the study, the most common clinical examination finding was presence of crepitation, with 77.6% of patients with typical pneumonia and 76% of patients with atypical pneumonia presenting with it. Bronchial breath sounds were present in 18.4% of cases of typical pneumonia as opposed to only 12% of atypical pneumonia. The other signs included cyanosis in 19 (27%), tachypnea in 17 (24%), and hypotension in nine (13%). We found that anemia was found in 26.5% of the cases with typical pneumonia and 28% of atypical pneumonia. Nearly 30.6% of the cases with typical pneumonia had normal total counts, thus mimicking atypical pneumonia. Deranged renal function tests were found in 8.2% and 8% of cases with typical and atypical pneumonia, respectively. The most common chest radiograph finding was lobar consolidation in 44.2% of all cases, followed by patchy consolidation in 39.3% of the cases. Interstitial pattern was observed in 4.9% of cases and cavitary lesions were seen in one case, which was positive for S. aureus. The most common chest radiograph finding in typical pneumonia was patchy consolidation (57.1%) and lobar consolidation pattern in atypical pneumonia (60%) [Table 3]. In this study, streptococcus pneumonia was isolated by sputum culture in 15.6% of cases; H. influenzae was isolated in 6.6% of the cases, K. pneumonia in 8.2% of the cases, S. aureus in 3.3% of cases, Pseudomonas aeruginosa in 3.3%, and E. coli in 1.6% of the all cases.
The S. pneumoniae was isolated from blood culture in 5.7% of the cases. Hemophilus influenza in 1.6% of the cases, K. pneumonia in 2.5% of the cases, S. aureus in 2.5% of cases, P. aeruginosa in 0.8%, and E. coli in 1.6%, respectively, from blood culture. In 4.9% of cases, the blood culture did not yield any organism; these cases were subjected to IIF assay. The IIF was done in patients with possibility of atypical pneumonia showed M. pneumonia in 7.4% of cases, L. pneumophila in 5.7% of cases, C. burnetii in 3.3% of cases, Chlamydophila psittaci in 2.5% of cases, and influenza virus in 1.6% of total cases.
In the present study, the most common comorbidities seen were chronic obstructive pulmonary disease (COPD) and type II diabetes mellitus (DM). The COPD was found in 20.4% and 24% of typical and atypical pneumonia cases, and DM was seen in 20.4% of typical and 40% of atypical pneumonia cases, respectively.
The most common atypical organism that was detected was M. pneumonia e in 7.4% of cases and L. pneumophila in 5.7% of cases. C. burnetii was diagnosed in 3.3% of cases, C. psittaci in 2.5% of cases, and influenza virus in 1.6% of total cases. The IIF test was negative in 4.9% of cases probably due to improper handling or pathogens other than those detected by Pneumoslide-M.
In this study, 45 (91.8%) patients with typical pneumonia and 100% of patients with atypical pneumonia recovered were discharged. Four (8.2%) patients with typical pneumonia died, two of whom were diagnosed to have S. pneumoniae infection and two with K. pneumoniae.
| Discussion|| |
CAP is a major cause of morbidity and mortality, especially among the elderly and in patients with chronic diseases. The mean age of the patients in our study was 56.07 ± 16.52. Of these, 39.9% of patients were found to be more than 60 years of age. In a study by S Bansal et al., where 42% of 70 patients enrolled in the study belonged to the sixth and seventh decade of life. In a study done by Aroma et al., the mean age group suffering from CAP was 40 years with 20.17% of the cases having age >70 years. A study done in Finland found that the rate of CAP increased for each year of age over 50 years , This increasing age for CAP found in our study could be due to other comorbid condition associated with increasing age. This trend is observed even in other studies quoted above. Pneumonia is a major illness in elderly, with an annual incidence for non-institutionalized patients estimated at between 25 and 44 per 1000 population, which is four times less than that of patients younger than 65 years. An increased incidence of pneumonia in elderly may be due to factors such as impaired mechanical clearance of airways, ineffective mucociliary clearance, decreased effective cough due to weaker respiratory muscles, and loss of elastic recoil of the lungs, defects in humoral, and cell-mediated immunity. They are also more prone for infections as a result of underlying comorbidities.
In the present study, 84 (68.9%) were male and 38 (31.1%) were female. This sex distribution is similar to study by Bilal et al. where 35 (70%) were males. This may be attributed to increased alcoholism and smoking in males and due to resultant comorbid conditions such as COPD. In comparison to our study, 40.2% of patients were found to have typical organisms and 20.5% had atypical organisms causing pneumonia. In a study done by Oberoi et al., atypical pathogens were isolated in 34% of cases. Studies such as that by Jang Wook et al. in Korea and Cunha et al. in USA have showed atypical pathogens in 18.5% and 15% of the cases, respectively.,
In the present study, in 39.3% of the CAP cases, no etiological organism could be demonstrated. In study done by Bansal et al., the etiology could not be ascertained in 35.4% of the patients. Is similar to observed by Oberoi et al., where the etiology remained unknown in 52.3% of cases. There are few studies that have been conducted in ambulatory patients with CAP with an unknown etiology.,, The studies carried out in India showed sputum culture positivity in 10%–33% of patients.,,, Blood cultures were positive in 10%–24% of patients with pneumonia., Thus, stressing the fact that no single test is presently available that can identify pathogen. Other factors such as improper methods of collection of sputum/culture, lack of expertise, and some obligate organisms are difficult to isolate by conventional methods are all contributing factors for negative results.
In the present study, 45.1% were smokers, and in study by Bilal et al., 72% were smokers  In another study by Nuorti et al., 58% of the patients and 24% of the control patients were current smokers. He found that cigarette smoking is the strongest independent risk factor for invasive pneumococcal pneumonia among immunocompetent, nonelderly adults. Smoking leads to alteration in respiratory flora, mechanical clearance, and cellular defenses. It also leads to reduction in ciliary beat frequency and changes in volume and viscoelastic properties of respiratory secretions.,
In study done by Bilal et al. in elderly patients, cough was the most common respiratory symptom noted in 37 (74%) patients, which was productive in only 29 (58%) patients. Other common symptoms included dyspnea (22%), chest pain (20%), altered sensorium (16%), and gastrointestinal symptoms (8%), are similar to our study. There were no significant differences between the symptoms of typical and atypical pneumonia in this study. Similar findings were observed by Oberoi et al. In this study, we found that bronchial breath sounds were found significantly more in no etiological agent which was identified (37.5%), whereas only 18.4% of typical pneumonia cases had this finding. In comparison, in the study by Bansal et al., the most common presenting clinical signs were crepitations in 69 (98%) and bronchial breath sounds in 33 (47%) patients.
Bilal et al. noted anemia in 16 (32%) patients and deranged renal function tests were noted in 20 (40%) patients, which is more than our observation. In same study, patchy infiltration was noted in 9 (18%) and interstitial infiltration in 2 (4%) patients and cavitations in 2 (4%) patients. In the study carried out by Bansal et al., the pattern of lung infiltration was lobar in 56 (80%) and interstitial in 14 (20%) patients.
In the present study, sputum culture was negative in all cases. The S. pneumoniae was most common isolated organism by sputum culture in 15.6%, the rate of isolation around 32% by Bilal et al. and Agarwal et al., respectively., Only by Torres et al. of 403 (80%) cases, sputum culture was positive in 71 (38%). Several other Indian studies have shown sputum culture positivity in only 10%–33% of patients., This low yield in sputum culture could be due to improper method of collection, preservation, and handling of sample.
In the study, 86.9% of patients did not yield any organism on blood culture. The blood culture positivity was very low in all the studies including study by Oberoi et al, which was 22%. Much lower rates were observed in the study carried out by Shah BA et al., were blood culture positivity was only 6%. Such low rates of positive cultures in various studies are either due to early administration of antibiotics or improper methods of collection for culture.
In our study, atypical pneumonia was found in 34% of cases in their study, with Mycoplasma causing 16.5% of infections and Chlamydia in 17.6% of cases. Higher rates of atypical pathogens were seen in a study by Dey et al, with the prevalence of Mycoplasma pneumonia was as high as 35%.,,,, These patients were above 65 years of age. One of the demerits of this study is serological investigation for atypical pneumonia and was performed only in suspected patients.
The implications of our studies are it is very difficult to differentiate of typical and atypical pneumonia based on clinical features alone. To add difficulties, many atypical pneumonia cases mimic typical pneumonia in clinical features and laboratory findings. Thus, all the suspected cases of pneumonia should be screened for both atypical and typical pathogens and more than one test has to done for isolation of organisms for better diagnosis. Hence, appropriate serological investigation and prompt treatment are important to reduce complications and mortality.
| Conclusions|| |
CAP is a common and serious problem encountered in clinical practice. For a rational choice of drugs, the treating physician should make himself/herself aware of the prevalence of various pathogens in the concerned community. Further large-scale studies should be carried out with serological testing for atypical pathogens in all CAP patients, to understand the clinical and etiological profile of CAP in each region.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, et al.
Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44 Suppl 2:S27-72.
Gupta D, Agarwal R, Aggarwal AN, Singh N, Mishra N, Khilnani GC, et al.
Guidelines for diagnosis and management of community- and hospital-acquired pneumonia in adults: Joint ICS/NCCP (I) recommendations. Lung India 2012;29 Suppl 2:S27-62.
Levy ML, Le Jeune I, Woodhead MA, Macfarlaned JT, Lim WS; British Thoracic Society Community Acquired Pneumonia in Adults Guideline Group. Primary care summary of the British Thoracic Society Guidelines for the management of community acquired pneumonia in adults: 2009 update. Endorsed by the Royal College of General Practitioners and the Primary Care Respiratory Society UK. Prim Care Respir J 2010;19:21-7.
Mandell LA, Wunderink R. “Pneumonia”, Harrison's Principles of Internal Medicine. 18th
ed., Vol. 2. New York: McGraw-Hill; 2008. p. 1619-28.
Levy ML, Le Jeune I, Woodhead MA, Macfarlaned JT, Lim WS. Primary care summary of the British Thoracic Society Guidelines for the management of community acquired pneumonia in adults. Prim Care Respir J 2010;20:21-7.
Ishida T, Miyashita N, Nakahama C. Clinical differentiation of atypical pneumonia using Japanese guidelines. Respirology 2007;12:104-10.
Bansal S, Kashyap S, Pal LS, Goel A. Clinical and bacteriological profile of community acquired pneumonia in Shimla, Himachal Pradesh. Indian J Chest Dis Allied Sci 2004;46:17-22.
Bartlett JG, Dowell SF, Mandell LA, File TM Jr., Musher DM, Fine MJ. Practice guidelines for the management of community-acquired pneumonia in adults. Infectious Diseases Society of America. Clin Infect Dis 2000;31:347-82.
Marrie TJ, Peeling RW, Fine MJ, Singer DE, Coley CM, Kapoor WN. Ambulatory patients with community-acquired pneumonia: The frequency of atypical agents and clinical course. Am J Med 1996;101:508-15.
Janssens JP, Krause KH. Pneumonia in the very old. Lancet Infect Dis 2004;4:112-24.
Abdullah BB, Mohammed Z, Ashraf SM, Ali S, Nausheen N. A study of community-acquired pneumonias in elderly individuals in Bijapur, India. Pulmonology 2012;2012:10.
Oberoi A, Agarwal A. Bacteriological profile, serology and antibiotic sensitivity pattern of microorganisms from community acquired pneumonia. JK Sci 2006;8:79-82.
Sohn JW, Park SC, Choi YH, Woo HJ, Cho YK, Lee JS, et al.
Atypical pathogens as etiologic agents in hospitalized patients with community-acquired pneumonia in Korea: A prospective multi-center study. J Korean Med Sci 2006;21:602-7.
Cunha BA, Gingrich D, Rosenbaum GS. Pneumonia syndromes: A clinical approach in the elderly. Geriatrics 1990;45:49-52, 55.
Berntsson E, Lagergård T, Strannegård O, Trollfors B. Etiology of community-acquired pneumonia in out-patients. Eur J Clin Microbiol 1986;5:446-7.
Almirall J, Morato I, Riera F, Verdaguer J, Priu R, Coll P, et al
. Incidence of community-acquired pneumonia and Chlamydia pneumonia
infection: A prospective multicenter study. Eur Respir J 1993;6:14-8.
Steinhoff D, Lode H, Ruckdeschel G, Heidrich B, Rolfs A, Fehrenbach FJ, et al. Chlamydia pneumoniae
as a cause of community-acquired pneumonia in hospitalized patients in Berlin. Clin Infect Dis 1996;22:958-64.
Kulpati DD, Kumar A. Flexible fiberoptic bronchoscopy in lower respiratory tract infection. Indian J Chest Dis Allied Sci 1980;22:39-46.
Kulpati DD, Khastgir T. Reappraisal of pneumonias. J Assoc Physicians India 1988;36:660-4.
Sharma BK, Manjunatha S, Verma S, Singh S, Sagar S. Profile of pneumonias in hospitalized medical patients. Indian J Chest Dis Allied Sci 1988;30:199-204.
Barlett JG. Bacteriological diagnosis of pulmonary infections. In: Sackner MA, editor. Diagnostic Techniques in Pulmonary Disease, Part 1. New York: Marcel Dekker Inc.; 1980. p. 707-45.
Wollschlager C, Khan F. The contribution of blood cultures to the diagnosis and management of community acquired pneumonia. Am Rev Respir Dis 1985;131:80-4.
Nuorti JP, Butler JC, Farley MM, Harrison LH, McGeer A, Kolczak MS, et al.
Cigarette smoking and invasive pneumococcal disease. Active Bacterial Core Surveillance Team. N
Engl J Med 2000;342:681-9.
Almirall J, González CA, Balanzó X, Bolíbar I. Proportion of community-acquired pneumonia cases attributable to tobacco smoking. Chest 1999;116:375-9.
Sherman CB. The health consequences of cigarette smoking. Pulmonary diseases. Med Clin North Am 1992;76:355-75.
Torres A, Dorca J, Zalacaín R, Bello S, El-Ebiary M, Molinos L, et al.
Community-acquired pneumonia in chronic obstructive pulmonary disease: A Spanish multicenter study. Am J Respir Crit Care Med 1996;154:1456-61.
Shah BA, Singh G, Naik MA, Dhobi GN. Bacteriological and clinical profile of community acquired pneumonia in hospitalized patients. Lung India 2010;27:54-7.
] [Full text]
Dey AB, Chaudhary R, Kumar P, Nisar N, Nagarkar KM. Mycoplasma pneumoniae
and community acquired pneumonia. Natl Med J India 2000;13:66-70.
Leroy O, Santré C, Beuscart C, Georges H, Guery B, Jacquier JM, et al.
Afive-year study of severe community-acquired pneumonia with emphasis on prognosis in patients admitted to an Intensive Care Unit. Intensive Care Med 1995;21:24-31.
Porath A, Schlaeffer F, Lieberman D. The epidemiology of community-acquired pneumonia among hospitalized adults. J Infect 1997;34:41-8.
Granton JT, Grossman RF. Community-acquired pneumonia in the elderly patient. Clinical features, epidemiology, and treatment. Clin Chest Med 1993;14:537-53.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3]