The present study has some limitations that should be acknowledged. We found marked differences between drinkers and NA control subjects as regards age, gender distribution, COPD and smoking history, and the rate of microbiological diagnosis. Smoking is well-recognized as an independent risk factor for the development of pneumococcal pneumonia.34 Nevertheless, for multivariate analysis the data comparison was adjusted for the presence of COPD as a consequence of smoking. A further confounder might be the differing rate of microbiological diagnosis in ethanol-abusing patients vs nondrinking patients. Nondrinkers were older, were less frequently smokers, and had fewer cases of COPD, therefore having less sputum production, which might impair the diagnosis of S pneumoniae. Nevertheless, the samples that were available for the diagnosis of S pneumoniae (eg, from sputum, blood, BAS, BAL, PSB procedures, and UAG) were similar in ethanol abusers and nondrinking control subjects (A patients, 89%; NA patients, 83%; p = 0.08). Although it was not significant, more nondrinking patients had received treatment with an antibiotic before admission to the hospital (NA patients, 20%; A patients, 13%; p = 0.093), which is a fact that might have further contributed to the lower rate of microbiological diagnosis in the nondrinking group. Further, we did not differentiate between acute and chronic alcohol intoxication. There are known differences between these two entities. Nonetheless, according to the 2000 World Health Organization report45 on alcohol consumption worldwide, heavy drinkers in Spain tend to spread their alcohol consumption over the week, therefore reducing their risk of the acute consequences of drinking (ie, aspiration), but not of the chronic consequences of drinking. This might explain why in the present study the rate of aspiration in A patients did not differ from that of nondrinking control subjects. We think that the aspiration caused by acute alcohol intoxication in A patients in the present study did not play a major role in the pathogenesis of CAP. The design of the present study required two visits of the patient, one shortly after hospital admission and one follow-up visit 2 to 4 weeks later for a final examination and follow-up serology testing. Therefore, aspects of the data, such as the number of days until clinical stability was reached, could not be addressed. Despite this, we think that data, such as ICU admission and length of hospital stay, give a good insight into the evolution of CAP in the studied groups of patients.