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Legionella pneumophila is associated with outbreaks of either Pontiac fever, a self-limited influenzalike condition without pneumonia, or Legionnaires' disease, a severe pneumonic disease affecting elderly or immunocompromised individuals. An outbreak of both Legionnaires' disease and Pontiac fever after a point-source exposure to L pneumophila was studied. Our observations demonstrated the spectrum of illness that L pneumophila may cause and emphasized the importance of host factors in affecting the expression of infection.

A multistate outbreak of Legionnaires' disease occurred among nine tour groups of senior citizens returning from stays at one of two lodges in a Vermont resort in October 1987. Interviews and serologic studies of 383 (85%) of the tour members revealed 17 individuals (attack rate, 4.4%) with radiologically documented pneumonia and laboratory evidence of legionellosis. A survey of tour groups staying at four nearby lodges and of Vermont-area medical facilities revealed no additional cases. Environmental investigation of common tour stops revealed no likely aerosol source of Legionella infection outside the lodges. Legionella pneumophila serogroup 1 was isolated from water sources at both implicated lodges, and the monoclonal antibody subtype matched those of the isolates from six patients from whom clinical isolates were obtained. The cultures reacted with monoclonal antibodies MAB1, MAB2, 33G2, and 144C2 to yield a 1,2,5,7 or a Benidorm 030E pattern. The strains were also identical by alloenzyme electrophoresis and DNA ribotyping techniques. The epidemiologic and laboratory data suggest that concurrent outbreaks occurred following exposures to the same L. pneumophila serogroup 1 strain at two separate lodges. Multiple molecular subtyping techniques can provide essential information for epidemiologic investigations of Legionnaires' disease.

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.

Legionnaires' disease is a relatively common cause of community-acquired pneumonia and of some outbreaks of hospital-acquired pneumonia. Moreover, Legionella pneumophila is frequently involved in the aetiology of the subset of pneumonias that is characterised by severe clinical course and high mortality. No sure clinical, radiographical or analytical features are useful in differentiating Legionella infection from other aetiologies of pneumonia. On the basis of these data, a rational initial therapeutic approach to community-acquired pneumonia, as well as to nosocomial pneumonia in certain circumstances, has to include an antimicrobial agent that is clinically effective against Legionella spp. Clinical studies have provided evidence that erythromycin is the first-line treatment. An intravenous dosage of 1g every 6 hours as initial therapy will be effective in most cases. Parenteral treatment may be switched to oral administration only after clinical response is observed. In vitro susceptibilities and preliminary experimental and clinical results suggest that clarithromycin will most likely become the preferred treatment once an intravenous preparation is available worldwide. However, orally administered clarithromycin at the dosage of 500 mg every 12 hours may be recommended in those developing countries in which health systems cannot afford the costs of intravenous therapy. In the case of clinically severe illness or in seriously immunosuppressed hosts with confirmed legionellosis, a combined therapeutic approach is warranted. Rifampicin 600 mg every 12 hours intravenously or orally has to be added to the usual dosage of erythromycin. Other alternative therapies, but with less distinct clinical efficacy, that can be combined with erythromycin are doxycycline 100 mg every 12 hours intravenously or orally, and intravenous ciprofloxacin 200 mg every 6 hours.

Ten patients from a rehabilitation center were admitted to hospital with serious respiratory infections within ten weeks. An outbreak of Legionnaire's disease was suspected based on the epidemic and atypical manifestation of pneumonia and could be proven microbiologically. Pulmonary and extrapulmonary complications included respiratory failure, lung abscess, transitory renal impairment in five patients and acute renal failure requiring dialysis in one, tetraparesis caused by peripheral neuropathy and acute psychosis. Three patients died despite immediate institution of therapy with erythromycin. Legionella pneumophila serogroup 1 subtype Pontiac was isolated from a bronchial lavage sample of one patient and from the water supply of the rehabilitation center. Monoclonal antibody subtyping and restriction endonuclease analysis were performed on both environmental and patient isolates. Potable water was identified as the source of the outbreak based on identical patterns on restriction endonuclease analysis. Despite thermic and chemical disinfection with chlorination (up to 15 ppm) in the rehabilitation clinic, an eleventh case of Legionnaire's disease was detected 11 months later.

Pulmonary artery sling with concomitant funnel-shaped tracheal stenosis is a rare but potentially lethal congenital condition. Conventional surgical division and reanastomosis of the aberrant left pulmonary artery to the main pulmonary artery carries a high risk of postoperative ventilatory difficulty from an uncorrected tracheal stenosis. A primary tracheal approach via a right thoracotomy without pulmonary bypass is described.

Legionella pneumophila, the causative agent of Legionnaires' disease is a facultative intracellular bacterium, which in the course of human infection multiplies in lung macrophages predominantly manifesting as pneumonia. The natural habitat of Legionella is found in sweet water reservoirs and man-made water systems. Virulent L. pneumophila spontaneously convert to an avirulent status at a high frequency. Genetic approaches have led to the identification of various L. pneumophila genes. The mip (macrophage infectivity potentiator) determinant remains at present the sole established virulence factor. The Mip protein exhibits activity of a peptidyl prolyl cis trans isomerase (PPIase), an enzyme which is able to bind the immunosuppressant FK506 and is involved in protein folding. The recently cloned major outer membrane protein (MOMP) could play a role in the uptake of legionellae by macrophages. Cellular models are useful in studying the intracellular replication of legionellae in eukaryotic cells. Human cell lines and protozoan models are appropriate for this purpose. By using U 937 macrophage-like cells and Acanthamoeba castellanii as hosts, we could discriminate virulent and avirulent L. pneumophila variants since only the virulent strain was capable of intracellular growth at 37 degrees C. By using these systems we further demonstrated that a hemolytic factor cloned and characterized in our laboratory, legiolysin (lly), had no influence on the intracellular growth of L. pneumophila.

Legionella pneumonia was diagnosed in two patients receiving triple immunosuppressive drug therapy after renal transplantation. High fever was the predominant symptom of these patients. Hyponatremia, leucopenia and anemia were also observed. The disease was diagnosed by immunofluorescence antigen technique and easily controlled with erythromycin therapy.

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.

It has been difficult to confirm that a given building is responsible for allergic symptomatology, exacerbation of asthma, or immunological dysfunction. In fact, in most studies, few objective immunological parameters have been studied and only rarely has there been any quantitation of IgE or secondary mediators. Furthermore, although many studies deal with rhinitis or respiratory tract irritation, there is a misconception that all such symptoms are allergic in nature, and studies attempting to prove that allergies are caused by buildings frequently neglect to prove that these are indeed true allergic responses. In addition, many of the symptoms that people attribute to sick building syndrome (SBS) or building-related illness, such as headaches, dizziness, fatigue, nausea, cough, and eye irritation, are subjective, and studies often fail to take into account other possible causes that may be inherent in the subjects, such as sinusitis, hyperventilation syndrome, or psychosomatic illness. Unfortunately, most clinical studies on SBS pay little attention to the preexisting conditions that a subject may have and discount the possibility that the inciting agent does not cause symptoms, but merely exacerbates a preexisting condition. Moreover, they offer no information about the nature of the mechanisms of action or pathophysiological relationships. Clearly, further studies are necessary to further explain the complexity of complaints that currently exist. Indeed, SBS might properly be paraphrased as "what is it?--if it is!"

One hundred and eleven cases of legionnaires' disease were reported in England and Wales in 1991, a smaller total than in any year since reporting began in the late 1970s. Four cases were hospital acquired and a further nine may have been associated with a hospital stay. Nosocomial legionellosis remains a cause for concern. Fifty-two cases were associated with travel abroad.

A series of nosocomial Legionella infections in a rehabilitation center is reported. In a three months period a total of 10 pneumonias with 3 deaths occurred (8 patients, 1 companion, 1 staff member). Serologic analysis proved additional Legionella infections within the nursing staff. The warm-water system was proved to be the source of infection by isolating Legionella pneumophila serogroup 1 subtype Pontiac both in warm-water and patients samples. The air conditioning system could not be ruled out as another (secondary) route of exposure because of shortcomings in construction. Conclusions about prevention and the course of the disease are discussed and standards for warm-water and air conditioning systems are proposed.

This article summarizes the health effects of indoor air pollutants and the modalities available to control them. The pollutants discussed include active and passive exposure to tobacco smoke; combustion products of carbon monoxide; nitrogen dioxide; products of biofuels, including wood and coal; biologic agents leading to immune responses, such as house dust mites, cockroaches, fungi, animal dander, and urine; biologic agents associated with infection such as Legionella and tuberculosis; formaldehyde; and volatile organic compounds. An approach to assessing building-related illness and "tight building" syndrome is presented. Finally, the article reviews recent data on hospital-related asthma and exposures to potential respiratory hazards such as antineoplastic agents, anesthetic gases, and ethylene oxide.

We determined the natural history of the colonization of our hospital's potable water by culturing water approximately biweekly from 20 sites throughout the hospital for 4 years. Overall, 545 (24.7%) of the 2200 samples grew Legionella pneumophila. During hyperchlorination, 11.7% of the samples were positive while 41.6% were positive in the absence of chlorination. There was no seasonal trend towards positivity, but there was marked inter-site variation in the semi-quantitative culture results. However, a single strain of legionella (as defined by plasmid profiling) tended to persist at a site. Such a site was a unique ecological niche in that different sites in the same wing were populated by distinct strains. The two wings of our hospital had a significantly different distribution of strains of legionella-plasmid profile type III predominated in the Victoria Wing while types II and VI predominated in Centennial Wing. Twenty-four of our 28 cases of nosocomial Legionnaires' disease occurred in the Centennial Wing. Three of the four cases in the Victoria Wing were caused by plasmid profile type III while 18 of the 24 isolates from patients who acquired their infection in the Centennial Wing were type II. We conclude that each water outlet serves as its own ecological niche of L. pneumophila.

From 10 October through 13 November 1989, 33 patients were hospitalized with legionnaires' disease in Bogalusa, Louisiana. A case-control study revealed case-patients were more likely than controls to have shopped at grocery store A (93% vs. 52%; odds ratio [OR], 11.6; 95% confidence interval [CI], 2.3-78.7) in the 10 days before illness. Among those who shopped at grocery store A, case-patients were more likely to shop for greater than 30 min (OR, 18.0; CI, 2.0-407.8) and to buy produce items located close to an ultrasonic mist machine (OR, 7.4; CI, 1.3-56.2). Employees of grocery store A were more likely than employees of other grocery stores in Bogalusa to have antibody titers of greater than or equal to 1:128 to Legionella pneumophila serogroup 1 (Lp-1; relative risk, 2.9; CI, 1.3-6.8). Lp-1 was isolated from water in the reservoir of the mist machine. The monoclonal antibody subtype of the isolate was identical to organisms identified in two patients. Viable Lp-1 was isolated from mist produced by the machine. Aerosols from a grocery store mist machine were the source of this outbreak.

Ten days after starting military service in a police barracks a 25-year-old man developed left middle and lower lobe pneumonia which did not respond to ampicillin (8 g daily) and gentamycin (120 mg daily). Parenteral administration of doxycycline (100 mg daily) was equally ineffective. However, the fever fell on administration of cefotiam (4 g daily). Antibody tests demonstrated Legionella pneumophila serogroup 1 as the causative organism. Because of the confined accommodation of the conscripts the source of the infection was thought to be the hot water system in the barracks. In two other policemen the demonstration of antibodies and of urine antigens confirmed Legionella infection as cause of an acute respiratory illness (Pontiac disease). Legionella pneumophila serogroup 1 subtype Philadelphia, 1-8 colony-forming units per ml, was isolated from six of 14 hot water samples in the barracks. This subtype possesses a virulence-associated antigen which is found in the majority of patient isolates of Legionella pneumophila serogroup 1.

We cultured potable water from seven institutions (six hospitals and one medical school) every 2 weeks for 6 months for Legionella pneumophila. All of the institutions were located close to each other and received water from the same freshwater source. Two institutions (the medical school and hospital F, a maternity hospital) never had L. pneumophila isolated from their potable water. The remaining five had 17 to 72% of their water samples positive for L. pneumophila. Most of the isolates were serogroup 1; however, in hospital B serogroup 5 accounted for 56% of the isolates. Oxford and OLDA monoclonal antibody subtypes of L. pneumophila serogroup 1 coexisted in four of the five institutions, while subtype France only was found in one institution. All 10 isolates from this institution lacked plasmids. The other four institutions had Legionella populations with plasmid profiles II, III, and VI. Two of these institutions also had isolates with no plasmids. The distribution of the plasmid types was significantly different for all institutions except C and D. The distribution of monoclonal antibody subtypes was significantly different for L. pneumophila isolates recovered from institutions C and D. There were no characteristics that distinguished the culture-positive institutions from the culture-negative areas. We conclude that diverse populations of L. pneumophila exist within these institutions despite their geographic proximity and identical potable water source.

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.

From June 1989 to March 1990 there were eight cases of Legionnaires' disease caused by Legionella pneumophila serogroup 1 in a renal transplant unit. There were seven cases of pneumonia and one case of pleural effusion. A study was conducted to identify the source of the outbreak. Legionella anisa was cultured from tap water. Twenty-seven staff members of the unit were serologically tested and antibody titres were positive in two. The probable source of infection was the potable water system. Control measures were hyperchlorination and heating of the water, after which there were no further cases during 5 months' follow up. We believe this is the first reported Legionnaires' disease outbreak in Latin America.

Medical science has made tremendous strides in overcoming infectious diseases in the 20th century. Despite this, several epidemics of previously unrecognized diseases have occurred during the last 15 years. These diseases include Lyme disease, Legionnaires' disease, toxic shock syndrome, and AIDS. Examination of past epidemics, including the plague of Athens, the black death, syphilis, and influenza, suggests that the sudden occurrence of diseases that were previously unrecognized is not unusual. Analysis of the new infectious disease indicates that while all four appeared suddenly, isolated cases of the disease occurred before the actual epidemic. Further, all four new diseases were found to be due to agents or toxins that were not previously recognized. Epidemics due to new infectious diseases may arise by several mechanisms, including mutation of the pathogen to a virulent form and introduction of an infectious agent into a nonimmune population. Environmental and behavioral factors may play an important role, as illustrated by toxic shock syndrome, Legionnaires' disease, and AIDS. On the other hand, epidemic diseases tend to abate over time because of changes in the infecting pathogen and in the host. Hence, epidemics can be seen as cycles; new diseases will arise periodically, occasionally with a devastating outcome. With time the effects of these diseases on the population will ameliorate. The cycle will begin again when a new disease emerges.

Legionella pneumonia is an increasingly frequently reported complication in immunocompromised patients, particularly patients with hairy cell leukemia (HCL) in active phase. The most important predisposing factor seems to be the quantitative and qualitative defect of the monocytic-macrophagic system characteristic of HCL. We report a case of severe Legionella pneumophila infection with multisystem involvement in a patient with HCL in stable partial remission obtained after therapy with interferon. In our patient recovery of a normal monocyte count did not protect against a legionella infection, indicating that this pathogen should always be sought in HCL patients even those in clinical and hematologic remission. Early diagnosis and appropriate treatment may reduce the mortality of this serious complication.

We studied all cases of nosocomial pneumonia at our 800-bed tertiary care hospital from September 1983 to September 1987. Of the 813 cases of nosocomial pneumonia, 31 (3.8%) were definite (isolation of organism or fourfold rise in titer) and 21 (2.5%) were possible cases (single or stable antibody titer of greater than or equal to 1:256) of legionnaires' disease. The definite cases involved a more severe form of pneumonia and a significantly higher mortality rate--64% versus 14% (p less than 0.0009) compared with the possible cases. Despite attempted comprehensive surveillance, only four (13%) of the definite cases of legionnaires' disease were found that would not have been diagnosed if the study were not ongoing. The yield from adequate (4- to 6-week convalescent serum samples) serologic testing was 5%, whereas the yield from sputum culture was 11%. We conclude that targeted surveillance of immunosuppressed patients with nosocomial pneumonia by culture of respiratory tract secretions for Legionella pneumophila is adequate for monitoring for the presence of legionnaires' disease in a hospital.

Guidelines for the prevention of nosocomial pneumonia specify that only sterile fluids should be used for aerosol therapy; however, this recommendation may not be uniformly followed. Thirteen patients with nosocomial pneumonia due to Legionella pneumophila serogroup 3 (Lp3) were identified at a community hospital in the period from 1984 through 1988; 12 patients (92%) had chronic obstructive pulmonary disease; and 9 patients (69%) died. An epidemiologic investigation suggested that the use of nebulizers to deliver medication was associated with acquiring legionnaires' disease. The hospital potable water system was contaminated with Lp3, and a survey indicated that tap water was commonly used to wash medication nebulizers. Lp3 in respirable-size droplets was isolated from aerosols generated by a nebulizer containing Lp3 at one-tenth the concentration found in the hospital potable water. These findings support the recommendation that only sterile fluids be used for filling or cleaning respiratory care equipment and suggest that this guideline is not universally followed.

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.

A patient with chronic lymphocytic leukaemia (CLL) and severe persisting neutropenia due to marrow infiltration of his leukaemia, developed bilateral Legionella pneumophila pneumonia for which he was treated with erythromycin, rifampin and ciprofloxacin. To increase the number of circulating polymorphonuclear neutrophils, the patient was treated with recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) at a dose of 2 micrograms protein/kg bodyweight s.c./12 h. GM-CSF therapy resulted in a sustained rise of the neutrophil count from the fifth day of treatment onwards, without showing an effect on the number of circulating leukemic cells. The patient completely recovered from his pneumonia. It is suggested that the rise of the neutrophil count, due to GM-CSF, contributed to the improvement of the infection of this patient. Our observation illustrates that GM-CSF can be given safely to CLL-patients and that it can be used effectively in CLL patients with severe bacterial infections to restore neutropenia.

We report the outcome of nosocomial legionnaires' disease in three patients who were isolated in the same sterile unit after allogeneic bone marrow transplantation. In all three cases the disease presented with dramatic pulmonary symptoms, and diagnosis was ascertained by direct immunofluorescence on bronchoalveolar fluids. None of the patients underwent seroconversion. This report draws attention to: (1) the fact that bacteriological filters do not ensure absolute security; (2) the need for frequent monitoring of the two factors governing legionella growth, water temperature and chlorination; and (3) the effectiveness of quinolones as a curative and prophylactic treatment of legionnaires' disease in transplanted patients avoiding pharmacological cyclosporin interaction.

The study of the biological properties of monoclonal antibodies (McAb) to L. pneumophila cytolysin has been carried out. These McAb have been shown to possess no capacity for the in vitro neutralization of cytolysin and the protection of guinea pigs from aerosol infection with L. pneumophila. Still the protective effect of the McAb under study has been observed in experiments with the intraperitoneal infection of guinea pigs, which is indicative of the possibility, in principle, of involving humoral immunity into the protection of the body from Legionella infection.

We report on 20 cases of Legionnaires' Disease (LD) in heart transplant recipients during a two-year study. The overall frequency in this setting amounts thus to 17% (20/115). In contrast, the frequency of legionellosis in postoperative cardiac patients without immunosuppression was only 4.7% (4/84). Legionellosis was diagnosed by culture and/or antibody detection in ten (20) as well as by the detection of urinary antigens in all 20 patients. Only nine (20) patients developed pneumonia, whereas five patients presented with nodular infiltrates. The remaining six patients had moderate fever with no signs of lung infection. In contrast to the majority of patients with other underlying diseases, antigen shedding lasted for long periods in most transplant patients. In high risk patients the application of conventional diagnostic methods together with regular urinary antigen testings (i.e. twice a week) may be advantageous for the early diagnosis of Legionella infection.

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.

Legionella pneumophila has frequently been recognised as a cause of infection in tourists. From 1973 to 1987, 117 cases of legionellosis were reported in tourists who spent one or more weeks in Italian summer resorts. 6 (5.1%) patients died. 42 (35.9%) were sporadic cases, and 75 (64.1%) were related to clusters or outbreaks. Among the 117 cases, 63 were reported to the Istituto Superiore di Sanità by the health authorities of other countries. Some travellers became ill while in Italy, others soon after they returned home. All tourists but two had stayed in hotels. L. pneumophila was isolated from the water system of 10 hotels, and in another hotel the same Legionella species was detected by direct immunofluorescence. Persistent and/or recurrent sources of infection seem to be present in some summer resorts on the Adriatic Coast and in the Lake Garda area in northern Italy. Some groups of cases were associated with particular hotels over a period of several months and sometimes years. Investigations have implicated potable water as the likely vehicle and the source of infection for tourists. The need of a greater awareness amongst clinicians that travel is a risk factor for legionellosis, and for better international surveillance and cooperation, is stressed.

Four cases of hospital acquired pneumonia are reported in children aged from 10 days to 7 years, in whom L. pneumophila serogroup 6 was isolated. All patients were sporadic cases occurring during a two year period (1987-1988) in the Pediatric Hospital of our institution. L. pneumophila was isolated in samples of pleural fluid, lung biopsy, tracheal aspirate, bronchial brushing and bronchoalveolar lavage. All our patients were immunologically depressed and three died. Only in two cases of erythromycin therapy was administered, as the etiology of their pneumonia was not suspected. The literature on other reported cases of infantile legionellosis is discussed.

An 11 year-old girl was diagnosed as acute lymphoblastic leukemia (ALL) on November 26th 1979 and was induced into complete remission with vincristine and prednisolon. After consolidation therapy with daunomycin, vincristine and prednisolone, she developed pneumonia on January 21st 1980. No cause of pneumonia was found by sputum culture or serologic tests. Treatment with cefmetazol (CMZ), sulbenicillin (SBPC) and minocycline (MINO) was not effective but 9 g/day of LCM made a remarkable effect. Indirect immunofluorescence assay of antibody showed x 512 titers on January 22nd and in her recovery period, the titers showed eight times increased up to x 4,000. The diagnosis of Legionellosis was made on CDC's criteria. She recovered completely with sequential lincomycin (LCM) and erythromycin (EM) therapy. On October 1989, she is still in the first complete remission of ALL for more than 8 years.

This survey assessed the maintenance of evaporative cooling towers in Glasgow, following two Legionnaires' disease outbreaks. Information was obtained from 76 of 81 premises and a maintenance score was calculated for each of 174 towers. The quality of maintenance was extremely varied (range of maintenance scores, 8-30; mean, 22 (S.D., 5.0); median, 23; maximum possible, 33) and some towers were neglected. Breaches of maintenance principles were mainly structural and organizational, e.g. inadequate drift control, rather than failure to use chemicals. Low maintenance scores were associated with no log book, no guidelines, no change in procedures in last 5 years, solitary cooling towers, and towers on industrial premises. Despite intense publicity the standard of cooling tower maintenance in Glasgow remained a concern. Information campaigns directed at those responsible for cooling-tower maintenance are necessary.

Hospital-acquired legionella pneumonia is emerging as a major problem; potable water distribution systems have been shown to be the primary reservoirs for the legionella organisms. As a result, disinfection measures have been developed to eradicate the organism from the hospital water supply. Each disinfection modality differs in its design and application such that choosing an appropriate cost-effective control measure requires careful analysis and planning. We assess in comparative fashion the disinfection modalities of thermal eradication ("heat-and-flush"), instantaneous steam-heating system, chlorination, ultraviolet light irradiation, ozonation and metal ionization. The theoretical bases, the actual procedure or system, the logistics of implementation, the costs and personnel requirements and the advantages and disadvantages are presented for each modality. Criteria for selection of a method, the use of combinations of methods, parameters for installation, pitfalls in implementation and a plan for subsequent environmental surveillance are discussed in detail.

A case of pneumonia related to 2 serogroups (1 and 8) of Legionella pneumophila (Lp) in a 10-day-old boy is described together with the epidemiological survey in the maternity ward which made it possible to establish its nosocomial origin. Rodshaped bacteria reacting with an Lp genus-specific monoclonal antibody and serogroup 1 and 8 polyclonal sera were detected in bronchoalveolar lavages (BAL) collected on day 13. Serogroups 1 and 8 were recovered from cultures of BAL collected on days 12 and 13. Fourfold or more antibody rises to serogroups 1, 5, 8 and 10 of Lp were observed in sequential serum specimens. Water samples collected from the tank and mixer of the maternity ward grew serogroups 1 and 8 of Lp. Serogroup 1 was detected in large amounts in water samples taken at several points of the hot water supply system and from the oxygen nebulizers and the feeding-bottle heater. Analysis of the Lp serogroup 1 strains isolated from the water by subgroup-specific monoclonal antibodies revealed the presence of 4 different subgroups, one of which was identical to the Lp 1 subgroup isolated from the neonate's BAL. This latter subgroup, reactive with McKinney monoclonal antibody Mab 2, has been described as highly virulent. No other case of legionellosis was recorded in the maternity ward.

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.