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Recent studies have left absolutely no doubt that tobacco increases susceptibility to bacterial lung infection, even in passive smokers. This relationship also shows a dose-response effect, since the risk reduces spectacularly 10 years after giving up smoking, returning to the level of non-smokers. Streptococcus pneumoniae is the causative microorganism responsible for community-acquired pneumonia (CAP) most frequently associated with smoking, particularly in invasive pneumococcal disease and septic shock. It is not clear how it acts on the progress of pneumonia, but there is evidence to suggest that the prognosis for pneumococcal pneumonia is worse. In CAP caused by Legionella pneumophila, it has also been observed that smoking is the most important risk factor, with the risk rising 121% for each pack of cigarettes smoked a day. Tobacco use may also favor diseases that are also known risk factors for CAP, such as periodontal disease and upper respiratory viral infections. By way of prevention, while giving up smoking should always be proposed, the use of the pneumococcal vaccine is also recommended, regardless of the presence of other comorbidities., (Copyright © 2013 SEPAR. Published by Elsevier Espana. All rights reserved.)

Objective: Community-acquired pneumonia (CAP) remains a major cause of death. No studies have reported the use of rapid influenza diagnostic tests (RIDT) for the etiological diagnosis, and the factors contributing to severity and mortality have not yet been fully investigated. The aim of this study was to review the etiologies of CAP using RIDT and to identify risk factors related to the severity and mortality of the disease., Methods: This retrospective study assessed these factors in hospitalized patients, with special emphasis on microbial etiology., Results: A total of 1,032 patients aged 63.9±18.3 years were studied, 66.2% of whom were men. Microbial identification was obtained in 57.0% of the cases. The most frequent causative microbial agents were Streptococcus pneumoniae, Mycoplasma pneumoniae and the influenza virus, and the second most frequent pathogens in the patients with severe CAP and the non-survivors were S. pneumoniae and the influenza virus. Age (≥65 years), chronic obstructive pulmonary disease, congestive heart failure, diabetes mellitus, dementia and Legionella spp. infection and polymicrobial infection were each found to be independent factors related to severity in the multivariate analysis, whereas "unidentified pathogen" was found to be an independent factor for non-severe CAP. Age (≥65 years), chronic pulmonary aspergillosis, post-lung cancer surgery and severe CAP were found to be independent factors for non-survival according to a multivariate analysis., Conclusion: In addition to S. pneumoniae, the influenza virus was a frequent cause of CAP overall and a frequent causative pathogen in both severe cases of CAP and non-survivors. Legionella spp. infection and polymicrobial infection were found to be an independent factor for the severity of CAP along with advanced age and certain comorbidities. An advanced age, certain respiratory comorbidities and severe CAP were found to be important independent factors for the mortality of CAP.

The Legionellae are Gram-negative bacteria able to survive and replicate in a wide range of protozoan hosts in natural environments, but they also occur in man-made aquatic systems, which are the major source of infection. After transmission to humans via aerosols, Legionella spp. can cause pneumonia (Legionnaires' disease) or influenza-like respiratory infections (Pontiac fever). In children, Legionnaires' disease is uncommon and is mainly diagnosed in children with immunosuppression. The clinical picture of Legionella pneumonia does not allow differentiation from pneumonia caused by others pathogens. The key to diagnosis is performing appropriate microbiological testing. The clinical presentation and the natural course of Legionnaires' disease in children are not clear due to an insufficient number of samples, but morbidity and mortality caused by this infection are extremely high. The mortality rate for legionellosis depends on the promptness of an appropriate antibiotic therapy. Fluoroquinolones are the most efficacious drugs against Legionella. A combination of these drugs with macrolides seems to be promising in the treatment of immunosuppressed patients and individuals with severe legionellosis. Although all Legionella species are considered potentially pathogenic for humans, Legionella pneumophila is the etiological agent responsible for most reported cases of community-acquired and nosocomial legionellosis.

Pulmonary infections are a significant cause of morbidity after liver transplantation; Gram-negative bacilli, cytomegalovirus, and Pneumocystis carinii were the usual pulmonary pathogens in the earlier studies in liver transplant recipients receiving cyclosporine. We prospectively assessed the impact of pulmonary infection in 101 consecutive liver transplant recipients receiving the new immunosuppressive agent tacrolimus (FK506). Fifteen percent (15/101) of the patients had 19 episodes of pneumonia; 58% (11/19) of the pneumonias were bacterial, 37% (7/19) were fungal, and 5% (1/19) were protozoal (Toxoplasma gondii). Twenty-seven percent of the bacterial pneumonias were due to Legionella. None of the patients had cytomegalovirus or P carinii pneumonia. Seven percent (7/10) of the study patients had fungal pneumonitis; 4% had invasive aspergillosis and 3% had cryptococcosis. Mortality was significantly higher (53%, 8/15) for patients with pneumonia than for patients without pneumonia (10%, 9/86, P = 0.0004). Only fungal pneumonias were the direct cause of death; 63% (5/8) of the deaths were in patients with fungal pneumonitis. Our data suggest a changing pattern of microbial etiologies of pneumonitis in the era of modern immunosuppressive agents. We show that P carinii pneumonia and cytomegalovirus can be effectively curtailed with appropriate prophylaxis. Fungal infections, on the contrary, not only constituted a major proportion of the pneumonia, but also carried the highest pneumonia-associated mortality. Legionella infections can be overlooked unless specialized laboratory methodology (cultured on selective media, urinary antigen) are applied routinely on all cases of pneumonia. We recommend routine culture on the water supply for Legionella in all transplant centers.

In lung or heart-lung transplant recipients, complications as a result of pulmonary infections continue to be the most frequent causes of morbidity and mortality. This study was undertaken to identify the contributions of (1) thoracotomy, (2) interruption of lymphatic vessels and bronchial arteries, (3) transplant procedure, (4) drug-induced immunosuppression, and (5) graft allogenicity to the increased risk of pneumonia in lung transplantation. Lewis rats were inoculated with 10(5) colony-forming units of Legionella pneumophila serogroup 1 by direct instillation into the trachea after one of the following: a general anesthetic with no operation; a left thoracotomy; a left thoracotomy with pulmonary hilar stripping; an isogeneic orthotopic left lung transplant with or without immunosuppression; or an allogeneic transplant with immunosuppression with Brown-Norway rats as donors. Immunosuppression was induced with an intramuscular injection of cyclosporine (25 mg/kg of body weight) from the inoculation day to day 3. All rats were killed on day 6, and severity of infection was determined by quantitative culture of Legionella organisms in the lungs and spleen, titer of Legionella urinary antigen, differential cell count in bronchoalveolar lavage fluid, body weight loss, and gross inspection of the lung. Significant increases in lung Legionella concentration occurred as a result of the addition of pulmonary hilar stripping (from 10(5.13 +/- 0.34) in the thoracotomy group to 10(5.66 +/- 0.25) in the thoracotomy with hilar stripping group, p = 0.013) and the addition of immunosuppression (from 10(5.47 +/- 0.47) in the isogeneic transplant group to 10(6.94 +/- 0.52) in the isogeneic transplant with immunosuppression group, p = 0.00016). Thoracotomy, transplant procedures, and allogenicity itself resulted in no significant increases. The results for all other indicators paralleled those for lung culture. We conclude that the combination of drug-induced immunosuppression with lung denervation and interruption of lymphatic vessels and bronchial arteries results in the early development and increased severity of pneumonia in lung transplantation.

Legionella sp has been emerging over the last decade as an important cause of pneumonia both hospital and community-acquired. Following an outbreak in a Renal-Transplant Unit stocked serum was tested for antibodies against Legionella pneumophila serogroup 1, and 5 cases of Legionnaires' Disease were reviewed. Two of the cases were nosocomial and three cases were community-acquired. Clinical and laboratorial aspects were similar to those expected for other causes of pneumonia, however jaundice was encountered in two cases. This study suggests that the real incidence of pneumonia caused by Legionella sp is being underestimated and the authors emphasize the importance of considering Legionnaires' Disease when empirically treating community-acquired pneumonia.

Legionella is a common cause of community- and hospital-acquired pneumonia. New information on the pathogenesis of infection and the host immune response is reviewed. Specialized laboratory tests, especially culture, are necessary for diagnosis since the clinical presentation is nonspecific. New antimicrobial agents and innovative approaches to disinfection of water distribution systems are presented.

We studied, in a prospective way, the characteristics of definitively diagnosed nosocomially acquired pneumonias in our hospital over 36 months. Out of 55 cases, 27 were due to Legionella pneumophila and 28 to other, non-Legionella bacteria. The cases of legionellosis concentrated in July, August, and December. The only risk factors that showed significant differences (p less than 0.05) were general anesthesia and surgery and immunosuppressive disease, which were more frequent in the non-Legionella group, as were chronic liver disease and lowering of consciousness level. The absence of severe underlying disease, chronic or not, was uncommon in both groups, but more frequent in the Legionella group. We observed no differences in the clinical features of the two groups. Mean values of gamma-glutamyltranspeptidase and total bilirubin were higher (p less than 0.05) in the non-Legionella group. The only x-ray data that showed significant difference were pleural effusion, more frequent in the non-Legionella group (p less than 0.02). The mortality rate of legionellosis was 14.6 percent compared to 35.7 percent for the non-Legionella group (p less than 0.05). We conclude that a sure differential diagnosis based on clinical, roentgenographic and analytical features of both groups is not possible. The relatively low mortality rate of the Legionella group, when compared to other series of nosocomial legionellosis, could be due to the standard use of erythromycin in the therapeutic approach to nosocomial-acquired pneumonia in our hospital.

This is a case of postoperative Legionella pneumonia in a full-term infant with hypoplastic left heart syndrome. The infant had an uncomplicated prenatal history, normal vaginal delivery, Apgars of 8 at 1 and 5 minutes, but was cyanotic at birth. At 3 days of age she had a stage 1 Norwood surgical procedure to palliate her congenital heart disease. A synthetic patch was placed over the thoracic midline because of difficulty in reapposing the sternum. Peritoneal dialysis was used to manage renal failure. At 20 days of age she had disseminated intravascular coagulopathy and pneumonia associated with sepsis. Four days later she died. Legionella pneumophila serogroup 1 was isolated from a lung culture taken at autopsy.

Acute pneumonias comprise a group of infectious diseases of different etiology which determines many features of clinico-anatomic manifestations of some of their forms including the extension of inflammatory lesions in the lungs. Usually developing due to disorders in the draining function of the bronchi, disorders of the phagocytic activity of leukocytes and alveolar macrophages as well as the presence of immunodeficient conditions, acute pneumonias emerge as complications of other diseases. From 1962 to the present time the rate of their detection in fatal cases increased from 11.6% to 42.8%. Their most frequent causative agents are staphylococci resistant to most antibiotics used for treatment, less frequently Pseudomonas aeruginosa and pathogenic fungi. Also, an increased role in the etiology of pneumonias of conditionally-pathogenic flora (Proteus, Acinetobacter, Enterobacter, Serratia) and frequent pneumonias caused by mixed microflora are observed. Pneumonias were the immediate cause of death in 19.2% of the fatal cases.

Legionella pneumophila postoperative pneumonia may be an important cause of morbidity and mortality in selected surgical patients. This report presents five postoperative neurosurgical patients in whom the diagnosis of Legionnaires' disease was made. Their clinical course and treatment are presented. Clinical manifestations, methods of diagnosis, and treatment of L. pneumophila pneumonia are discussed. It is pointed out that neurosurgical patients who have received high doses of corticosteroids and who develop nosocomial postoperative pneumonias should be suspected of having Legionnaires' disease.

An epidemiological link was found between contamination of a hospital water-supply by Legionella pneumophila and by Pittsburgh pneumonia agent (PPA) and subsequent cases of nosocomial legionnaires' disease and Pittsburgh pneumonia. The extent of L pneumophila isolation from the water-supply paralleled the occurrence of disease. Whenever L pneumophila was isolated from more than 30% of ten selected water sites, nosocomial legionellosis occurred. The temperature of the hot water tanks was raised to 60-77 degrees C for 72 h, and water outlets were flushed for 30 min with hot water. A decline in numbers of L pneumophila and PPA in the water-supply was followed by a fall in the incidence of legionnaires' disease and Pittsburgh pneumonia. In addition, intermittent raising of the temperature in the hot water system decreased both the number of months in which disease occurred and the proportion of nosocomial pneumonias caused by these organisms.

Sporadic cases and outbreaks of Legionella pneumonia are more commonly recognized; especially among hospitalized patients. Factors predisposing to L. pneumophila pneumonia and the clinical features of this type of pneumonia are similar for epidemic and sporadic cases. It is difficult to compare overall mortality figures of various epidemics and series of sporadic community-acquired cases of Legionella pneumonia, because the factors that determine the severity and outcome of Legionella pneumonia are poorly defined in most series.

We describe the first reported case of pneumonia due to Legionella pneumophila serogroup 12 in the UK. This hospital-associated infection occurred in an immuno-incompetent patient and coincided with a change in character of the local environmental strains of legionellas. The patient produced a serological response both to her own isolate and to L. pneumophila serogroups 1-6. Thus serodiagnosis was attainable using the usual screening antigens.

Between January 1972 and December 1981, 50 patients with severe community-acquired pneumonia were admitted to the intensive care unit of a district general hospital. A causal pathogen was identified in 41 cases (82%). Streptococcus pneumoniae (16 cases), Legionella pneumophila (15 cases) and Staphylococcus aureus (5 cases) were the commonest. Assisted ventilation was required in 44 patients, of whom 25 died (57%). All 5 patients with staphylococcal pneumonia and 12(75%) with pneumococcal pneumonia died. Only 5 (33%) with Legionnaires' disease died. Mortality was significantly associated with age. Recommendations for the management of severe pneumonia are made.