COMMUNITY ACQUIRED PNEUMONIA - TYPICAL OR ATYPICAL ?

Pneumonia continues to play an important role in medicine. It denotes inflammation of the lung parenchyma caused by a microbial agent. Community acquired pneumonia (CAP) is the most important infection in clinical medicine world wide.

Clinically, CAP is often classified as “typical” or “atypical.” In typical pneumonia. There is sudden onset of fever, chills, pleuritic chest pain and productive cough. Typical pneumonia is usually caused by bacterial pathogens like Streptococcus pneumoniae, Staphylococcus aureus. Klebsiella pneumoniae, Haemophilus influenzae etc. In contrast, atypical CAP is characterized by preceeding upper airway symptoms, myalgias, fever without chills, headache and unproductive cough. The causative organisms responsible for atypical pneumonia include Viruses, Mycoplasma pneumoniae, Legionella pneumophilia, Chlamydia psittaci and Coxiella burnetli etc.

In typical pneumonia total leucocyte counts, ESR and CRP are mostly raised; in contrast to atypical pneumonia, where these parameters are usually normal or only slightly raised. Radiologically, chest radiograph will show lobar or segmental homogeneous opacity in over 80% of typical bacterial pneumonias. But this finding can also be seen in nearly half the cases of atypical infection. In atypical pneumonias, diffuse patchy or ground glass shadows are more commonly observed.

In Western countries, nearly 60 - 80% of CAP are caused by bacteria, 10 - 20-% by atypical organisms and a similar proportion by viruses. Over the past few years, several studies have shown that atypical organisms are common, being present in upto 40% of all CAP patients, often as copathogens along with bacterial organisms¹. From India, atypical organisms have rarely been isolated from patients with CAP, mainly due to lack of facilities for culture/serology of these organisms.

A number of studies have concluded that there is little use of classifying CAP into atypical or typical one, on the basis of clinical features of radiology, as this classification often cannot predict microbial aetiology and thus help in planning the management. In one study, clinical features were only 40 percent accurate in telling the difference between pneumococcal, mycoplasma and other pneumonic infections². Similarly, in a study of 196 patients with CAP, multilobar disease, pleural effusion, lobar collapse and cavitations were sufficient common in patients with pneumococcal pneumonia, Legionnaires disease, mycoplasma and psittacosis so that the radiology could not be used to determine bacterial aetiology³.

There are two main reasons why clinical features correlate poorly with the microbial aetiology. Certain pathogens such as legionella and C psittacci often produce clinical picture that mimics both typical and atypical syndromes. Secondly, if the host′s immune response is impaired because of comorbid illness or advanced age, even then the clinical features may be changed. Here even bacterial pathogens can produce atypical clinical or radiological features.

For guiding therapy for CAP, knowledge of the potential pathogen is very important. As discussed above, in clinical practice it is often difficult to predict the microbial aetiology on the basis of clinico-radiological picture. The typical pneumonias often respond well to (3 lactam antibiotics where as atypical pathogens, being intracellular, do not respond to (3 lactams but respond to antibiotic such as macrolides, tetracyclines and some quinolones.

In view of these observations, it seems that classifying CAP into typical and atypical may not be very helpful in planning the effective management of CAP. A judicious use of epidemiology, laboratory data and clinical findings is needed to achieve this target.