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Legionnaires' disease: A review of 79 community acquired cases in Nottingham
Abstract
Seventy nine cases of sporadic, community acquired legionnaires' disease have been reviewed. Annual and seasonal variation in incidence was noted. The mean age of the patients was 53 years and 50 (63%) were male. Pre-existing chronic diseases were present in only 23 (29%), including two patients receiving immunosuppressive treatment. Common symptoms included unproductive cough, dyspnoea, chest pain, headache, confusion, nausea, vomiting, and diarrhoea. Respiratory symptoms were absent, however, in 17 (22%). Localising chest signs were present in 74 (95%) cases. Frequent laboratory findings included lymphopenia, high erythrocyte sedimentation rate, hyponatraemia, raised urea and creatinine concentrations, abnormal liver function, hypophosphataemia, hypoalbuminaemia, proteinuria, and haematuria. Thirteen patients died (16%), including nine of 20 who received assisted ventilation. The mortality rate in patients treated with erythromycin (11%) was lower than in those who received other antibiotics (23%), but this difference was not statistically significant. Of the features noted on admission, only a high plasma urea concentration was significantly associated with death. Sporadic community acquired legionnaires' disease is a not uncommon disorder, which with appropriate treatment has a prognosis similar to that of other forms of community acquired pneumonia.
... Studies have demonstrated increased risks of mortality and cardiovascular events in CKD, ESRD, and critically ill patients with hyperphosphatemia [11,[13][14][15][16]. Conversely, hypophosphatemia has been reportedly associated with increased mortality especially 55 in patients with sepsis [2,8,[22][23][24][25][26][27][28][29]. However, little is known about the impact of admission phosphate on the risk of in-hospital mortality in the general hospitalized population. ...
... Previous studies have shown conflicting data regarding mortality risk in hospitalized patients with hypophosphatemia 230 [2,8,[22][23][24][25][26][27][28][29]. Severe hypophosphatemia can cause rhabdomyolysis, metabolic encephalopathy, and respiratory failure [1], and a few studies have demonstrated reduced hospital survival in patients with hypophosphatemia [2,8,[22][23][24][25][26][27][28][29], especially in septic patients [22]. ...
... Previous studies have shown conflicting data regarding mortality risk in hospitalized patients with hypophosphatemia 230 [2,8,[22][23][24][25][26][27][28][29]. Severe hypophosphatemia can cause rhabdomyolysis, metabolic encephalopathy, and respiratory failure [1], and a few studies have demonstrated reduced hospital survival in patients with hypophosphatemia [2,8,[22][23][24][25][26][27][28][29], especially in septic patients [22]. Several studies involving cardiac surgical and dia-235 betic ketoacidosis patients, however, did not show an association between hypophosphatemia and increased mortality after adjusting for potential confounders [8,24]. ...
Background: The aim of this study was to assess the relationship between admission serum phosphate levels and in-hospital mortality in all hospitalized patients.
Methods: All adult hospitalized patients who had admission serum phosphate available between years 2009 and 2013 were enrolled. Admission serum phosphate was categorized based on its distribution into six groups (<2.5, 2.5-3.0, 3.1-3.6, 3.7-4.2, 4.3-4.8 and ≥4.9 mg/dL). The odds ratio (OR) of in-hospital mortality by admission serum phosphate, using the phosphate category of 3.1-3.6 mg/dL as the reference group, was obtained by logistic regression analysis.
Results: 42,336 patients were studied. The lowest incidence of in-hospital mortality was associated with a serum phosphate within 3.1-4.2 mg/dL. A U-shaped curve emerged demonstrating higher in-hospital mortality associated with both serum phosphate <3.1 and >4.2 mg/dL. After adjusting for potential confounders, both serum phosphate <2.5 and >4.2 mg/dL were associated with in-hospital mortality with ORs of 1.60 (95%CI 1.25-2.05), 1.60 (95%CI 1.29-1.97) and 3.89 (95%CI 3.20-4.74) when serum phosphate were <2.5, 4.3-4.8 and ≥4.9 mg/dL, respectively. Among subgroups of patients with chronic kidney disease (CKD) and cardiovascular disease (CVD), the highest mortality was associated with a serum phosphate ≥4.9 mg/dL with ORs of 4.11 (95%CI 3.16-5.39) in CKD patients and 5.11 (95%CI 3.33-7.95) in CVD patients.
Conclusion: Hospitalized patients with admission serum phosphate <2.5 and >4.2 mg/dL are associated with an increased risk of in-hospital mortality. The highest mortality risk is associated with CKD and CVD patients with admission hyperphosphatemia.
... However, other patient habits and comorbidities, including diabetes mellitus, smoking, substance abuse, AIDS, and chronic lung diseases, were not uniquely associated with either form of the disease, which is in concordance with findings from prior studies. 12,13 Clinically speaking, the absence of classic respiratory symptoms on initial presentation in more than 50% of cases makes a specific diagnosis challenging to identify. 14 We observed more patients presenting with only respiratory symptoms among the epidemic cases. ...
... Gastrointestinal system involvement, especially diarrhea, was the most common nonpulmonary condition in both groups, as similarly seen in previous reports. 13,15,16 However, gastrointestinal symptoms were only present in 9% of patients in our study. Severe neurological complications may be associated with Legionnaires' disease, 17 but none of our patients had focal neurological symptoms. ...
... The frequencies of other laboratory abnormalities in our patients were similar to those in other published studies. 13,18 For example, hyponatremia and mild transaminitis occurred in more than 50% and 30% of patients, respectively, with no significant difference observed between patients with ELD and SLD. Legionnaires' disease can be diagnosed by antigen detection or culture methods. ...
BACKGROUND
In 2015, New York City experienced the worst outbreak of Legionnaires’ disease in the history of the city. We compare patients seen during the 2015 outbreak with sporadic cases of Legionella during the past 5 years.
METHODS
We conducted a retrospective chart review of 90 patients with Legionnaires’ disease, including sporadic cases of Legionella infection admitted from 2010 to 2015 (n = 55) and cases admitted during the 2015 outbreak (n = 35).
RESULTS
We saw no significant differences between the 2 groups regarding demographics, smoking habits, alcohol intake, underlying medical disease, or residence type. Univariate and multivariate analyses showed that patients with sporadic case of Legionella had a longer stay in the hospital and intensive care unit as well as an increased stay in mechanical ventilation. Short-term mortality, discharge disposition, and most clinical parameters did not differ significantly between the 2 groups.
CONCLUSIONS
We found no specific clinicoradiological characteristics that could differentiate sporadic from epidemic cases of Legionella. Early recognition and high suspicion for Legionnaires’ disease are critical to provide appropriate treatment. Cluster of cases should increase suspicion for an outbreak.
... However, involvement of extrapulmonary organ systems was also mentioned to provide helpful clues and to sometimes support the suspicion of legionellosis on clinical grounds [2]. In our patients extrapulmonary involvement was observed in an even lower range than in other series, whereas respiratory symptoms were seen in similar proportions [34,35]. The spectrum of laboratory value alterations was similar to other studies [13,35]. ...
... In our patients extrapulmonary involvement was observed in an even lower range than in other series, whereas respiratory symptoms were seen in similar proportions [34,35]. The spectrum of laboratory value alterations was similar to other studies [13,35]. Low sodium values which were found to be frequently associated with legionellosis, were found less often than in other studies [13,35]. ...
... The spectrum of laboratory value alterations was similar to other studies [13,35]. Low sodium values which were found to be frequently associated with legionellosis, were found less often than in other studies [13,35]. ...
In a two-year prospective study of patients hospitalized because of community-acquired pneumonia, the incidence of legionellosis was found to be 3.8% (17/442 cases). After S. pneumoniae, M. pneumoniae and influenzae viruses, legionellae were the fourth most frequently identified pneumonia agents. We evaluated the clinical data from 41 cases with legionellosis, 17 diagnosed in this prospective study and 24 prior to the study. The age range of all patients (22 women, 19 men) was 24-78 yrs (median 61.3 yrs), 14 of 41 cases (34.1%) had extrapulmonary organ involvement. Twelve patients (29.3%) died. The fatality rate was 4.5% (1/22 cases) in patients treated with erythromycin, and 57.9% (11/19 cases) in patients treated with other antibiotics. Antibiotics effective in legionellosis should be added to the routine therapy of community-acquired pneumonia when this aetiology can not be excluded.
... Experience accumulated since its first description in 1976 [1] has led to a good understanding of this infection both in the hospital and community environment. Despite the large number of reports of Legionella pneumonia infection23456789, information concerning differences in clinical, radiological, and outcome aspects between nosocomial and community-acquired cases are very scarce. Previous reports have suggested that clinical aspects of nosocomial and community cases are similar [10]. ...
... Whilst in the NALP group, old age and intrinsic and extrinsic risk factors were common in many patients, reflecting the hospital population characteristics, the typical patient in the CALP group was a smoking and drinking middle-aged man, with a low frequency of pre-existing chronic diseases, except for chronic lung disease. These observations are similar to those of WOODHEAD and MACFARLANE [9] , suggesting that pre-existing chronic diseases in CALP are not an essential condition to acquire Legionella pneumonia . Our study suggests that the clinical findings of nosocomial and community-acquired Legionella pneumophila pneumonias are quite similar. ...
... However, either cough, chest pain, dyspnoea or respiratory insufficiency generally develops in most patients after the first 72 h of illness. The extrapulmonary findings in Legionella pneumonia are common [6, 9,151617181920, the pathogenesis of which may be diverse [15, 16, 21, 22] . The incidence of neurological and gastrointestinal manifestations was lower in our series than in other published studies [6, 9, 10, 20, 23] . ...
Previous reports have suggested that nosocomial and community Legionella pneumonia cases are similar. However, community and hospital characteristics, such as aquatic environment, antibiotic pressure (usage) and populations, are quite different, leading to the suspicion that Legionella infection may differ in the two settings. Univariate and multivariate analyses were performed to compare demographic data, risk factors, clinical, radiological and outcome data between 125 nosocomial and 33 community-acquired cases of Legionella pneumophila infection. Patients in the nosocomially acquired Legionella pneumonia (NALP) group were older than those in the community-acquired Legionella pneumonia (CALP) group. Univariate analysis showed that smoking habit, cough, thoracic pain, and extrapulmonary manifestations were more prevalent in the CALP group, whilst chronic lung disease and cancer were more prevalent in the NALP group. Moreover, patients in the NALP group were more likely to have received oxygen and corticosteroid therapy and also to have altered creatinine values than patients in the CALP group, whilst more patients in the latter group had altered alanine amino-transferase values. However, multivariate analysis failed to confirm most of these differences. Smoking habit and blood creatinine levels were the only variables remaining significant. In conclusion, demographic, clinical, laboratory, radiological and outcome data in nosocomial and community-acquired Legionella pneumonia are quite similar.
... Despite the conflicting data on the impacts of hypophosphatemia on patient survival [12,[35][36][37][38][39][40][41][42][43], when compared with patients with normal phosphate levels, studies have demonstrated that hypophosphatemia is also associated with increased hospital mortality [12,16,[35][36][37][38][39][40][41][42][43]. Furthermore, severe hypophosphatemia has been reported to cause rhabdomyolysis, respiratory failure, and metabolic encephalopathy [4,31]. ...
... Despite the conflicting data on the impacts of hypophosphatemia on patient survival [12,[35][36][37][38][39][40][41][42][43], when compared with patients with normal phosphate levels, studies have demonstrated that hypophosphatemia is also associated with increased hospital mortality [12,16,[35][36][37][38][39][40][41][42][43]. Furthermore, severe hypophosphatemia has been reported to cause rhabdomyolysis, respiratory failure, and metabolic encephalopathy [4,31]. ...
Background:
The goal of this study was to categorize patients with abnormal serum phosphate upon hospital admission into distinct clusters utilizing an unsupervised machine learning approach, and to assess the mortality risk associated with these clusters.
Methods:
We utilized the consensus clustering approach on demographic information, comorbidities, principal diagnoses, and laboratory data of hypophosphatemia (serum phosphate ≤ 2.4 mg/dL) and hyperphosphatemia cohorts (serum phosphate ≥ 4.6 mg/dL). The standardized mean difference was applied to determine each cluster's key features. We assessed the association of the clusters with mortality.
Results:
In the hypophosphatemia cohort (n = 3113), the consensus cluster analysis identified two clusters. The key features of patients in Cluster 2, compared with Cluster 1, included: older age; a higher comorbidity burden, particularly hypertension; diabetes mellitus; coronary artery disease; lower eGFR; and more acute kidney injury (AKI) at admission. Cluster 2 had a comparable hospital mortality (3.7% vs. 2.9%; p = 0.17), but a higher one-year mortality (26.8% vs. 14.0%; p < 0.001), and five-year mortality (20.2% vs. 44.3%; p < 0.001), compared to Cluster 1. In the hyperphosphatemia cohort (n = 7252), the analysis identified two clusters. The key features of patients in Cluster 2, compared with Cluster 1, included: older age; more primary admission for kidney disease; more history of hypertension; more end-stage kidney disease; more AKI at admission; and higher admission potassium, magnesium, and phosphate. Cluster 2 had a higher hospital (8.9% vs. 2.4%; p < 0.001) one-year mortality (32.9% vs. 14.8%; p < 0.001), and five-year mortality (24.5% vs. 51.1%; p < 0.001), compared with Cluster 1.
Conclusion:
Our cluster analysis classified clinically distinct phenotypes with different mortality risks among hospitalized patients with serum phosphate derangements. Age, comorbidities, and kidney function were the key features that differentiated the phenotypes.
... Among laboratory findings on hospital admission in patients with LD, absolute lymphocytopenia was observed in the majority of patients [22,23]. Furthermore, LD is characterized by accumulation of activated T-cells in the lungs [24]. ...
... Lymphocytopenia has been observed in patients presenting with community-acquired LD and has recently been identified as a possible key diagnostic marker in this disease [22,23]. Here, we confirm that the acute phase of LD is characterized by absolute lymphocytopenia. ...
Absolute lymphocytopenia is recognised as an important hallmark of the immune response to severe infection and observed in patients with Legionnaires' disease. To explore the immune response, we studied the dynamics of peripheral blood lymphocyte subpopulations in the acute and subacute phase of LD.
EDTA-anticoagulated blood was obtained from eight patients on the day the diagnosis was made through detection of L. pneumophila serogroup 1 antigen in urine. A second blood sample was obtained in the subacute phase. Multiparametric flow cytometry was used to calculate lymphocyte counts and values for B-cells, T-cells, NK cells, CD4(+) and CD8(+) T-cells. Expression of activation markers was analysed. The values obtained in the subacute phase were compared with an age and gender matched control group. Absolute lymphocyte count (×10(9)/l, median and range) significantly increased from 0.8 (0.4-1.6) in the acute phase to 1.4 (0.8-3.4) in the subacute phase. B-cell count showed no significant change, while T-cell count (×10(6)/l, median and range) significantly increased in the subacute phase (495 (182-1024) versus 979 (507-2708), p = 0.012) as a result of significant increases in both CD4(+) and CD8(+) T-cell counts (374 (146-629) versus 763 (400-1507), p = 0.012 and 119 (29-328) versus 224 (107-862), p = 0.012). In the subacute phase of LD, significant increases were observed in absolute counts of activated CD4(+) T-cells, naïve CD4(+) T-cells and memory CD4(+) T-cells. In the CD8(+) T-cell compartment, activated CD8(+) T-cells, naïve CD8(+) T-cell and memory CD8(+) T-cells were significantly increased (p<0.05).
The acute phase of LD is characterized by absolute lymphocytopenia, which recovers in the subacute phase with an increase in absolute T-cells and re-emergence of activated CD4(+) and CD8(+) T cells. These observations are in line with the suggested role for T-cell activation in the immune response to LD.
... 45 Over the 12-year peiod 1972-1984, however, the same researchers found 90 confirmed cases of Legionnaires' disease and concluded that 79 were community-acquired and only seven had returned from abroad. 61 They noted a marked annual fluctuation in number of cases e.g. four in 1982 and 1984, and 14 in 1980. ...
... four in 1982 and 1984, and 14 in 1980. 61 Bhopal et al. also reported such variation. 4 ' 6 Clearly, extrapolations from data based on short-term studies are not valid. ...
This review considers the value of the observation that Legionnaires' disease varies geographically. Estimates of disease
incidence, derived from case registers and from studies measuring the proportion of cases of pneumonia which are Legionnaires'
disease, and of the prevalence of the population with antibody, show that there is geographical variation in disease frequency.
Much, but not all, of this variation is artefact due to differences in definitions, diagnostic methods, surveillance systems
and data presentation. Some of the variation is attributed to publication bias, e.g. in 10 small studies (<100 patients) 13.2%
of pneumonia patients had Legionnaires' disease but in five large studies (≥500 patients) the figure was 3.6%. Research to
explain variations has been neglected but a few studies have provided important insights into disease transmission. Future
studies should: be based on agreed disease definitions and data collection and analysis methods; analyse subgroups separately;
and collect data to develop explanations for geographical variation
... Typical presentations of Legionella pneumonia may include a high fever, chills, cough (which may or may not be productive), shortness of breath, muscle aches, and headaches [2,3]. Interestingly, gastrointestinal symptoms such as nausea, vomiting, and diarrhea commonly occur [4]. Laboratory abnormalities may involve elevated aminotransferases, elevated C-reactive protein, and hyponatremia. ...
... Legionella pneumophila causes a fatal form of pneumonia that presents with a wide variety of clinical symptoms and is often difficult to diagnose. The main symptoms are similar to those of common variants of pneumonia, including cough and fever, while extrapulmonary symptoms such as gastrointestinal symptoms (diarrhea and abdominal pain) and neurological symptoms (headache and disorientation) are also relatively common [1][2][3]. ...
Legionella pneumonia is a potentially fatal form of pneumonia that causes various clinical symptoms and is often difficult to diagnose. For the diagnosis, it is important to inquire about the patient's history of exposure to sewage or soil, although there are rare cases of Legionella pneumonia with no history of exposure. In this study, we present a case of Legionella pneumonia in a 72-year-old man with no history of wastewater exposure from public baths or other sources. The patient presented to our emergency department with fever, chills, and shivering. The antigen test of the urine for Legionella was negative, and chest radiography showed patchy infiltrates in the right lower lung field that was suspicious for pneumonia. The patient was treated with intravenous ceftriaxone (2 g/day) for right-sided pneumonia and was intubated on day 1 due to poor oxygenation and a tendency towards exacerbation to acute respiratory distress syndrome. The fever resolved after day 3 (36.4-36.9°C), and the patient was extubated on day 6. A positive sputum polymerase chain reaction (PCR) test for Legionella deoxyribonucleic acid (DNA) (type 1) was performed on day 6, and levofloxacin and dexamethasone therapy was administered. After completing a 10-day course of levofloxacin, the patient's symptoms were cured. Although it is important to note the patient's background, symptoms, and information on the clinical course, including laboratory values, to include a diagnosis of Legionella pneumonia, it is impractical to suspect Legionella pneumonia in all patients admitted to the hospital with pneumonia and to administer new quinolone antimicrobials. However, it is important to re-evaluate the diagnosis and intervene in treatment when β-lactam antimicrobials are ineffective or when extrapulmonary symptoms are present, as in this case.
... Клинические проявления определяю тся длительно стью и выраженностью ГФ, симптомы появляются при снижении концентрации фосфата в плазме менее 1,0 мг/дл (0,32 ммоль/л) [ М ногочисленные исследования показывают взаимо связь между ГФ и повышенной смертностью [107][108][109][110][111][112][113][114][115][116]. Примечательно, что в одном ретроспективном исследо вании тяж елая ГФ была ассоциирована с четы рехкрат ным увеличением риска смерти от всех причин [117]. ...
Hypophosphatemia (GF) is defined as a decrease in the level of inorganic phosphorus in the blood serum below 2.5 mg/dl (0.81 mmol/L). One of the reasons for the development of GF can be the use of a number of medications: diuretics, some antibacterial drugs, insulin, antacids, glucose solutions for parenteral administration, antitumor drugs. The true prevalence of drug-induced (DI) HB is unknown, because the phosphate level is not evaluated routinely, but only when GF is suspected. The most common mechanism for the development of DI GF is an increase in the excretion of phosphates by the kidneys. In most cases, DI GF is asymptomatic and regresses after discontinuation of the inducer drug. To compensate for the phosphate deficiency, non-drug methods (diet) and pharmacotherapy are used. Prevention of DI GF involves avoiding the use of drugs, the reception of which is associated with the development of DI GF, especially in patients at risk of developing GF.
... In the present study, we found no association between hypophosphatemia and mortality. On the other hand, many other studies have found an association between hypophosphatemia and increased mortality [13,14,[21][22][23][24][25][26][27][28]. Severe hypophosphatemia has been reported to predict an increase of up to 8-fold in mortality in sepsis patients [21]. ...
Background:
Phosphate imbalances or disorders have a high risk of morbidity and mortality in patients with chronic kidney disease. It is unknown if this finding extends to mortality in patients presenting at an emergency room with or without normal kidney function.
Methods and patients:
This cross sectional analysis included all emergency room patients between 2010 and 2011 at the Inselspital Bern, Switzerland. A multivariable cox regression model was applied to assess the association between phosphate levels and in-hospital mortality up to 28 days.
Results:
22,239 subjects were screened for the study. Plasma phosphate concentrations were measured in 2,390 patients on hospital admission and were included in the analysis. 3.5% of the 480 patients with hypophosphatemia and 10.7% of the 215 patients with hyperphosphatemia died. In univariate analysis, phosphate levels were associated with mortality, age, diuretic therapy and kidney function (all p<0.001). In a multivariate Cox regression model, hyperphosphatemia (OR 3.29, p<0.001) was a strong independent risk factor for mortality. Hypophosphatemia was not associated with mortality (p>0.05).
Conclusion:
Hyperphosphatemia is associated with 28-day in-hospital mortality in an unselected cohort of patients presenting in an emergency room.
... We were reliant on obtaining respiratory specimens for testing. As many as half of patients with Legionnaires' disease may not produce sputum [16][17][18][19], so we will have missed cases from patients who could not expectorate. We were also reliant on the recording of clinical information on specimen requisition forms by clinicians. ...
Background. Legionnaires' disease cannot be clinically or radiographically distinguished from other causes of pneumonia, and specific tests are required to make the diagnosis. Currently, testing occurs erratically and, instead, clinicians rely on empiric treatment strategies and ignore public health implications of the diagnosis. We aimed to measure the increase in case detection of Legionnaires' disease following the introduction of routine polymerase chain reaction (PCR) testing of respiratory specimens. PCR is the most sensitive diagnostic tool for Legionnaires' disease.Methods. In a quasi-experimental study in Christchurch, New Zealand, we compared the number of cases of Legionnaires' disease requiring hospitalization diagnosed during a 2-year period before the introduction of a routine PCR testing strategy (November 2008-October 2010) with a similar period after the introduction (November 2010-October 2012). With this testing strategy, all respiratory specimens from hospitalized patients with pneumonia sent to the region's sole tertiary-level laboratory were tested for Legionella by PCR, whether requested or not.Results. During November 2008 to October 2010, there were 22 cases of Legionnaires' disease compared with 92 during November 2010 to October 2012. Of 1834 samples tested since November 2010, 1 in 20 was positive, increasing to 1 in 9 during peak Legionella season (November to January). Increasing bacterial load was associated with increasing disease severity.Conclusions. In our region, the burden of Legionnaires' disease is much greater than was previously recognized. Routine PCR testing provides results within a clinically relevant time frame and enables improved characterization of the regional epidemiology of Legionnaires' disease. © 2013 The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: [email protected]
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... In a 1983 article in The Practitioner, John Macfarlane, wrote that, 'If recovery [from pneumonia] is slow but the patient not seriously ill, an atypical pneumonia [such as Legionnaires' disease] is a possibility and a change to Erythromycin should be considered.' 100 A study from the Nottingham group concluded 'early use [of erythromycin] by general practitioners, especially during the course of an epidemic and in areas where Legionnaires' disease is known to occur, may be of advantage.' 101 As noted above, the experience of this group, and others like it from Glasgow and London, was a key resource for the development and dissemination of knowledge of Legionnaires' disease in Britain, however, it may also have contributed to an inappropriately high profile of Legionnaires' disease as a cause of pneumonia in medical circles, particularly when directed at doctors in localities where it was less prevalent. ...
Legionnaires' disease is now routinely discussed as an 'emerging infectious disease' (EID) and is said to be one of the earliest such diseases to be recognised. It first appeared in 1976 and its cause was identified in 1977, the same year that Ebola fever, Hantaan virus and Campylobacter jejuni arrived. The designation of Legionnaires' disease as an EID was retrospective; it was not and could not be otherwise as the category only gained currency in the early 1990s. In this article we reflect on the changing medical understanding and social profile of Legionnaires' disease in the decade or so from its recognition to the creation of EIDs, especially its ambivalent position between public health and clinical medicine. However, we question any simple opposition, between public health experts who approached Legionnaires' disease as a new and worrying environmental threat that could be prevented, and clinicians who saw it as another cause of pneumonia that could be managed by improved diagnosis and treatment. We argue that in the British context of public spending cuts and the reform of public health, the category of 'new' diseases, in which Legionnaires' disease was central, was mobilised ahead of the EID lobby of the early 1990s, by interested groups in medicine to defend infectious diseases services.
... Little evidence exists as to the effect of comorbidities on either acquisition or severity of LP. British 23 and Spanish 24 studies have demonstrated chronic illness and worsening kidney function to be associated with poorer outcome, as is chronic lung disease. There is little evidence for the severity of LP in immunosuppressed patients, although one study following up patients with systemic lupus erythematosus taking infliximab reported a death secondary to LP. 25 However, only a small number in our series were im-munosuppressed or had chronic kidney disease. ...
As the recent outbreaks in Edinburgh and Camarthen, UK, have shown, Legionella pneumonia (LP) remains a significant public health problem, which is not only confined to those who have travelled abroad. In both outbreaks and sporadic cases, diagnosis can go unrecognised. We reviewed the demographics, comorbidities, diagnosis, treatment and clinical outcome of LP cases over five years in a district general hospital in northwest England. Over half of LP cases were UK acquired and 'classic' clinical features were common. Clinical criteria for diagnosing LP were confirmed, but few sputum samples were sent to reference laboratories, limiting further essential epidemiological mapping of UK cases. Following current UK community-acquired pneumonia guidance would have missed nearly one quarter of LP cases in our series, potentially leading to further morbidity and mortality.
... Multiple studies show an association between hypophosphatemia and increased mortality [10,12,14,35,545556575859. Severe hypophosphatemia has been reported to predict up to eightfold increased mortality rate in sepsis patients [10] . ...
Currently no evidence-based guideline exists for the approach to hypophosphatemia in critically ill patients.
We performed a narrative review of the medical literature to identify the incidence, symptoms, and treatment of hypophosphatemia in critically ill patients. Specifically, we searched for answers to the questions whether correction of hypophosphatemia is associated with improved outcome, and whether a certain treatment strategy is superior.
Incidence: hypophosphatemia is frequently encountered in the intensive care unit; and critically ill patients are at increased risk for developing hypophosphatemia due to the presence of multiple causal factors. Symptoms: hypophosphatemia may lead to a multitude of symptoms, including cardiac and respiratory failure. Treatment: hypophosphatemia is generally corrected when it is symptomatic or severe. However, although multiple studies confirm the efficacy and safety of intravenous phosphate administration, it remains uncertain when and how to correct hypophosphatemia. Outcome: in some studies, hypophosphatemia was associated with higher mortality; a paucity of randomized controlled evidence exists for whether correction of hypophosphatemia improves the outcome in critically ill patients.
Additional studies addressing the current approach to hypophosphatemia in critically ill patients are required. Studies should focus on the association between hypophosphatemia and morbidity and/or mortality, as well as the effect of correction of this electrolyte disorder.
... Legionellae can be isolated from a variety of sample types, although lower respiratory tract secretions (e.g., sputum and bronchoscopy samples) are the samples of choice. The major limitation of sputum culture is that fewer than one-half of patients with legionnaires disease produce sputum [9][10][11][12]. Other factors influence the sensitivity of culture once a sputum sample is obtained. ...
... Legionellae can be isolated from a variety of sample types, although lower respiratory tract secretions (e.g., sputum and bronchoscopy samples) are the samples of choice. The major limitation of sputum culture is that fewer than one-half of patients with legionnaires disease produce sputum9101112. Other factors influence the sensitivity of culture once a sputum sample is obtained. ...
Legionellae, which are important causes of pneumonia in humans, continue to be incorrectly labeled as exotic pathogens. The
ability to diagnose Legionella infection is limited by the nonspecific nature of clinical features and the shortcomings of diagnostic tests. Despite recent
improvements, existing diagnostic tests for Legionella infection either lack sensitivity for detecting all clinically important legionellae or are unable to provide results within
a clinically useful time frame. Understanding local Legionella epidemiology is important for making decisions about whether to test for Legionella infection and which diagnostic tests to use. In most situations, the use of both the urinary antigen test plus sputum culture
is the best diagnostic combination. Polymerase chain reaction (PCR) is a promising tool, but standardized assays are not commercially
available. Further work needs to focus on the development of urinary antigen tests assays that detect a wider range of pathogenic
legionellae and on the development of standardized PCR assays.
Psittakoz Epidemiyolojisi, Tanı ve Tedavisi Gülşah TUNÇER Doku Nematodları Cumhur ÖZMEN Tetanoz Selva ALA SELEK Leptospiroz Epidemiyolojisi, Tanı ve Tedavisi Çağla KESKİN SARITAŞ Kırım Kongo Kanamalı Ateşi Merve YILDIZ ERGİN Şigelloz Ezgi YILMAZ İntegronlar Ahmet ÇALIŞKAN Gözde Gülcan ÜNAL Brucella ve Tanı Testleri Kamuran ŞANLI Legionella Türleri ve Lejyoner Hastalığı Eda ALP GÖKER Hantavirüs Enfeksiyonları Pınar GÜRKAYNAK Tularemi Elif AGÜLOĞLU BALİ
This chapter discusses factors unique to individual patients (host factors) that predispose them to respiratory tract infection. These factors can be divided into three groups: alterations in immunity, anatomic alterations, and alterations in the airways' protective mechanisms. The chapter covers environmental factors that play a role in the pathogenesis of respiratory tract infections and how those factors help determine not only who becomes infected but also which lower respiratory tract infection they get. It provides a sampling of how geographic, institutional, family, home, avocational, and other exposures play epidemiologic and pathophysiologic roles in the types of pneumonia that patients can acquire. Changes in the ageing immune system may account for differences in symptom presentation and clinical detection via immunologic testing. In immunocompromised patients larger infiltrates or larger cavitating nodules may result, and there is a distinct predisposition to dissemination with resultant meningoencephalitis.
Background
Legionellosis in the setting of preexisting endovascular prosthetic graft may represent a Coxiella burnetii infection as antibody cross-reactivity exists.
Methods
We present a 63-year-old man status-post endovascular aneurysm repair (EVAR) with a history of ankylosing spondylitis, chronic obstructive pulmonary disease asthma, coronary artery disease with myocardial infarction, hypertension, and hyperlipidemia who presented with clinical symptoms of legionellosis. This was confirmed with a positive urine antigen test.
Results
He completed a 21-day course of azithromycin for Legionella . His leukocytosis and liver function tests normalized, but he had continued lethargy and a persistently elevated erythrocyte sedimentation rate and C-reactive protein. Imaging showed a radiographically infected EVAR graft (placed 10 months prior). The EVAR was explanted and the operating room cultures grew C. burnetii . Prolonged hydroxychloroquine and doxycycline therapy were required for vascular manifestations of Coxiella as azithromycin provides inappropriate coverage.
Conclusions
Persistent constitutional symptoms in the setting of an EVAR require expanded investigation, especially in the setting of legionellosis.
Introduction
Bacterial culture remains the gold standard for the diagnosis of legionellosis. However, past reports indicate that most physicians use the urinary antigen test (UAT) alone. Combining it with other tests is important, especially in patients with negative UAT results. The aim of this study was to investigate the current situation of legionellosis diagnostics and clarify the issues that need to be addressed.
Methods
Between March 1, 2021 and April 30, 2021, a questionnaire survey was conducted in an anonymous manner among physicians working in Japan. Questionnaires were generated on a website and asked questions in a multiple-choice format.
Results
Valid responses were received from 309 physicians during the study period. Most (92.9%) physicians reported using UAT as the initial test for patients suspected of having legionellosis, and <10% reported using other tests (e.g., culture, nucleic acid amplification test [NAAT], Gimenez staining, and serum antibody titer measurement [ATM]). When the initial test result was negative, 63% of physicians reported not conducting additional tests. Even when they chose to run additional tests, at most 27.8%, 23.6%, 12.3%, and 10.4% of all physicians used NAAT, culture, Gimenez staining, and serum ATM, respectively. The major reasons for not using tests other than UAT were “unavailability in the medical facility,” “long turn-around time,” and “difficult to collect sputum.”
Conclusions
The present survey revealed that most physicians in Japan used UAT alone for diagnosing legionellosis. Eliminating barriers to creating a reasonable environment and edification of physicians are needed to improve the current situation.
Chronic chest pain (CP) can have many origins, including problems with the heart, lungs, and digestive organs. The leading diagnostic consideration in patients with chronic CP is coronary artery disease. Non-cardiac CP is related to the lung diseases and problems with esophagus, stomach, gallbladder, and pancreas. Other causes include bone, muscle, nurve, and mental problems.
Background:
Legionnaires' disease is under-diagnosed because of inconsistent use of diagnostic tests and uncertainty about whom to test. We assessed the increase in case detection following large-scale introduction of routine PCR testing of respiratory specimens in New Zealand.
Methods:
LegiNZ was a national surveillance study done over 1-year in which active case-finding was used to maximise the identification of cases of Legionnaires' disease in hospitals. Respiratory specimens from patients of any age with pneumonia, who could provide an eligible lower respiratory specimen, admitted to one of 20 participating hospitals, covering a catchment area of 96% of New Zealand's population, were routinely tested for legionella by PCR. Additional cases of Legionnaires' disease in hospital were identified through mandatory notification.
Findings:
Between May 21, 2015, and May 20, 2016, 5622 eligible specimens from 4862 patients were tested by PCR. From these, 197 cases of Legionnaires' disease were detected. An additional 41 cases were identified from notification data, giving 238 cases requiring hospitalisation. The overall incidence of Legionnaires' disease cases in hospital in the study area was 5·4 per 100 000 people per year, and Legionella longbeachae was the predominant cause, found in 150 (63%) of 238 cases.
Interpretation:
The rate of notified disease during the study period was three-times the average over the preceding 3 years. Active case-finding through systematic PCR testing better clarified the regional epidemiology of Legionnaires' disease and uncovered an otherwise hidden burden of disease. These data inform local Legionnaires' disease testing strategies, allow targeted antibiotic therapy, and help identify outbreaks and effective prevention strategies. The same approach might have similar benefits if applied elsewhere in the world.
Funding:
Health Research Council of New Zealand.
A male patient in his mid-60s presented with a severe pneumonia following return to the UK after travel to Crete. He was diagnosed with Legionnaire’s disease (caused by an uncommon serogroup of Legionella pneumophila ). He was pancytopenic on admission, and during a long stay on critical care he was diagnosed with a disseminated Aspergillus infection. Bone marrow aspiration revealed an underlying hairy cell leukaemia that undoubtedly contributed to his acute presentation and subsequent invasive fungal infection.
Legionnaire’s disease is a common cause of community-acquired pneumonia (CAP). Although no single clinical feature is diagnostic, if characteristic extrapulmonary findings are present a presumptive clinical syndromic diagnosis is possible. Depending on geographic location, season, and physician awareness, Legionnaire’s disease may be included in the differential diagnosis of CAP. Some antibiotics effective against Legionella sp are also effective in treating the typical bacterial causes of CAP. From an antimicrobial stewardship program (ASP) perspective, monotherapy is preferred to double-drug therapy. From an ASP and pharmacoeconomic standpoint, monotherapy with doxycycline or a respiratory quinolone provides optimal cost effective therapy.
Whenever the cardinal manifestations of a disorder occur in similar disorders, there is potential for a disease mimic. Legionnaire's disease has protean manifestations and has the potential to mimic or be mimicked by other community acquired pneumonias (CAPs). In CAPs caused by other than Legionella species, the more characteristic features in common with legionnaire's disease the more difficult the diagnostic conundrum. In hospitalized adults with CAP, legionnaire's disease may mimic influenza or other viral pneumonias. Of the bacterial causes of CAP, psittacosis and Q fever, but not tularemia, are frequent mimics of legionnaire's disease.
Legionnaire's disease has been recognized as a cause of severe community-acquired pneumonia (CAP). Legionnaire's disease has characteristic extrapulmonary findings that are the basis for a presumptive clinical diagnosis. The widespread use of Legionella culture, sputum DFA, serology, urinary antigen testing, and polymerase chain reaction have allowed earlier diagnosis of Legionnaire's disease. Excluding common source outbreaks, CAP caused by Legionnaire's disease is manifested as sporadic cases. In contrast, nosocomial Legionnaire's disease occurs in clusters or outbreaks from common Legionella species-contaminated water sources. Improved diagnostic tests have permitted accurate diagnosis. Bacterial coinfections with Legionnaire's disease are uncommon, but when present, are most often associated with bacteremia pneumococcal pneumonia.
Legionnaires’ disease is a form of pneumonia, caused by bacteria of the genus Legionella. In contrast, Pontiac fever is a self-limited influenza-like illness, without pneumonia, that is associated with Legionella spp too. The name of this infection is in reference to an outbreak of pneumonia that affected 221 people and caused 34 deaths during the 58th American Legion Convention celebrated in Philadelphia during the summer of 1976 [1]. Epidemiologically, the Philadelphia outbreak was similar in many aspects to two large outbreaks of febrile disease, one in 1965 (District of Columbia) and the other in 1968 (Pontiac, Michigan). The Columbia outbreak involved patients in a large psychiatric hospital in which there were 81 cases and 12 deaths [2]. The Pontiac outbreak was very different, of the 144 documented cases neither death nor pneumonia were demonstrated.
lung diseases;pulmonary diseases;hypoxia;gene expression;trout hepatocytes
2), Neusa Augusta de Oliveira MAZIERI (3), Cid Vieira Franco de GODOY (4) & Antonino dos Santos ROCHA (5) RESUMO Relatam os autores isolamento de Legionella pneumophila sorogrupo 1, acom-panhado de evidências sorológicas de infecção atual, em homem de 40 anos com infecção respiratória grave que evoluiu para insuficiência respiratória aguda. Esta foi caracterizada por hipoxemia severa refratária a altas concentrações de oxigênio e radiograficamente por infiltrados difusos em ambos pulmões. Com introdução de clindamicina, amicacina, ceftriaxone e ventilação à volume com Pressão Expira tória Positiva Final (PEEP) de 14 cm de H20, houve estabilização do quadro e gradual recuperação. Suspeitando-se de legionelose, foi colhido sangue e secreção traqueal para exa-mes específicos. A secreção traqueal foi semeada em meio BCYE com isolamento de bacilo gram-negativo, identificado como Legionella pneumophila sorogrupo 1 por características culturais, bioquímicas e reações de imunofluorescência direta e de aglutinação em lâmina. O estudo sorológico revelou títulos de anticorpos 128, 1024, 4096 e 8192 para amostras coletadas na 1?, 3'?, 4? e 6? semanas após o início do quadro. Os resultados definitivos foram obtidos com o paciente em recuperação. É realçada a comprovação da presença de Legionella sp. como agente patológico em nosso meio; a importância das medidas de suporte na evolução do paciente; a necessidade de se pensar neste agente no diagnóstico diferencial de pneumonias e de se pesquisar mais esta etiologia com metodologia laboratorial específica. UNITERMOS: Legionella pneumophila; Isolamento; Insuficiência respiratória aguda. INTRODUÇÃO As pneumopatias infecciosas representam preciso, mesmo em se tratando de agentes bacte-sempre um desafio ao esclarecimento etiológico rianos clássicos. Formas atípicas podem ser de (1) O caso clínico deste trabalho foi apresentado no XXIV Congresso Brasileiro de Pneumologia e Tisiologia. realizado de 7 a 10 de setembro de 1988 em Curitiba, Paraná, Brasil. (2) Medico Assistente da Divisão de Clínica Médica do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (FMUSP). São Paulo, SP, Brasil. (3) Farmacêutica Bioquímica — Laboratório de Investigação Médica LIM/54 — HC FMUSP. São Paulo, SP, Brasil. (4) Prof. Resp. Disc. Patol. Clínica — Departamento de Patologia da FMUSP — LIM/54 e Instituto de Medicina Tropical de São Paulo. São Paulo, SP, Brasil. (5) Prof. Titular da Disciplina de Clínica Geral e Propedêutica da FMUSP. São Paulo, SP, Brasil.
A cross-sectional study was conducted to establish whether, and to what extent, the most prevalent etiological agents in community-acquired pneumonia (CAP) are associated with obstructive airways disease (OAD). Data concerning 126 patients who had previously been hospitalized for an episode of CAP caused by 1 of the 4 most frequently isolated pathogens (Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia species, and Legionella pneumophila) were obtained from our database. The history of these patients and objective parameters such as pulmonary function tests, bronchial hyperresponsiveness (BHR), and skin tests with common aero-allergens had been recorded after an episode of CAP. Seventy-eight of the 126 patients participated in the study: 33 with S. pneumoniae as proven etiological agent, 22 with M. pneumoniae, 13 with Chlamydia species, and 10 with L. pneumophila pneumonia. OAD was detected by objective parameters in 59% of all patients, with the greatest airflow limitation detected in the pneumococcal pneumonia group. Reversibility and BHR (PC20-histamine) were independent of the etiological agent. Allergy was seen significantly more frequently in the mycoplasmal pneumonia group than in the others. Smoking, with the highest percentage in the L. pneumonia group, was not related to the extent of airflow limitation or BHR. The hypothesis that OAD is a risk factor for acquiring CAP, which may be suggested by our study, should be further examined by objective parameters in a case-controlled study.
The term atypical pneumonia was first used in 1938, and by the 1970s it was widely used to refer to pneumonia due to Mycoplasma pneumoniae, Legionella pneumophila (or other Legionella species), and Chlamydophila pneumoniae. However, in the purest sense all pneumonias other than the classic bacterial pneumonias are atypical. Currently many favor abolition of the term atypical pneumonia.
This review categorizes atypical pneumonia pathogens as conventional ones; viral agents and emerging atypical pneumonia pathogens. We emphasize viral pneumonia because with the increasing availability of multiplex polymerase chain reaction we can identify the agent(s) responsible for viral pneumonia. By using a sensitive assay for procalcitonin one can distinguish between viral and bacterial pneumonia. This allows pneumonia to be categorized as bacterial or viral at the time of admission to hospital or at discharge from the emergency department and soon thereafter further classified as to the etiology, which should be stated as definite or probable.
It has been over two decades since the outbreak of “Legionnaires” disease at the American Legion Convention in Philadelphia,Pennsylvania,and
Legionella pneumophila was found to be the causative pathogen (1,2). Moreover,a retrospective review demonstrated that Legionella pneumophila was responsible for the outbreaks of both Legionnaires’ disease and Pontiac fever as early as 1965 (3). The Legionellaceae family contains more that 30 species and the most common cause of disease in humans is Legionella pneumophila. Other species with a genius Legionella are often referred to as Legionella-like organism,differing from Legionella pneumophila in at least one phenotype and included L micdadei,also know as the Tatlockia micdadei or more commonly the Pittsburgh pneumonia agent and L bozemanii. All three of these organisms cause community acquired pneumonia as well as nosocomial pneumonia. At least 16 other species
have been implicated in human disease of the upper and lower airway (4).
The frequency of community-acquired pneumonia coupled with its mortality rate of 10 to 25% is of growing concern to clinicians. A prospective study of 67 patients with severe community-acquired pneumonia was carried out to determine the causative agents, the impact fore-knowledge of the etiology has on the outcome, the value of clinical and radiologic criteria in predicting the evolution, and the efficacy of empirical therapy. The study group included 45 men and 22 women (mean age: 56.8 +/- 16.6 yr), and 46.2% suffered from a concurrent debilitating disease. The cause of pneumonia was diagnosed in 32 cases, and the most common pathogens were Streptococcus pneumoniae (37.5%), Legionella pneumophila (21.8%), and gram-negative bacilli (25.0%). The fact that fungal infections were present in three patients and Pneumocystis carinii in one are worthy of note. The overall death rate was 20.8%. A fatal outcome was related to the age of the patient (p less than 0.05), the presence of debilitating disease (p = 0.026), and septic shock (p = 0.0009). Diagnosis of the causative agents did not aid in increasing the survival rate, but it did allow for better patient management. Most of the patients (85.1%) initiated on treatment with erythromycin plus tobramycin recovered, but only 68.4% of the subjects commenced on treatment with other therapeutics survived. Furthermore, it was necessary to modify the therapy of a greater percentage of the latter group (p less than 0.025). Gram-negative bacillary pneumonia was a frequent finding among the patients who did not recover, making empirical treatment with erythromycin plus third generation cephalosporins most advisable for severe cases of community-acquired pneumonia.
Isolation of Legionella pneumophila sero-group 1 with serological evidence of present infection is reported from a 40 year-old male with serious respiratory infection which developed into acute respiratory failure. It was characterized by severe hypoxemia resistant to high inspired oxygen concentrations and radiographically by diffuse infiltrates in both lungs suggesting the clinical aspect of ARDS. Following the introduction of clindamycin, amikacin, ceftriaxone, volume-cycled ventilator and positive end expiratory pressure (PEEP) of 14 cm H2O, stabilization of clinical conditions and gradual recovery were achieved. Suspecting of legionellosis, blood and tracheal secretions specimens were collected for specific laboratory research. From tracheal secretion cultivated in BCYE medium, gran-negative bacilli were isolated and identified as Legionella pneumophila serogroup 1 through cultural and biochemical characteristics and direct immunofluorescence and slide agglutination tests. Serology (IFA) with blood samples collecting during the 1st, 3rd, 4th and 6th weeks of illness demonstrated antibody titers to the isolated microorganism of 128, 1024, 4096 and 8192, respectively. Definitive results were obtained during the patient's recovery. The authors emphasize: a) the demonstration of the presence of Legionella sp. as a pathogenic agent in Brazil; b) the importance of supportive care in the clinical outcome; c) the need of remembering this pathogen while making differential diagnosis of pneumonias and of continuing to pursue this etiology with specific laboratory methodology.
Legionnaires' disease is a distinct clinical entity caused by Legionella pneumophila. Following an epidemic of pneumonia in Philadelphia in 1976, it was found that the bacterium had in fact been first isolated in 1947. Other species of Legionella have been identified, many of which are indistinguishable from L. pneumophila infection. Legionella species also cause extrapulmonary infections and a mild nonpneumonic form of disease known in its epidemic form as Pontiac Fever.
The annual number of confirmed cases of Legionnaires' disease in both Nottingham, and England and Wales, reached a peak in 1980 and has since declined. Legionella infection is a rare cause of community-acquired pneumonia managed at home (accounting for less than 1% of cases), more common in those admitted to hospital (5-15%) and more common still in patients with severe pneumonia as seen on an intensive care unit (up to 30% of cases). Antibiotic therapy for any patient with moderate or severe pneumonia of uncertain aetiology should cover legionella infection.
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.
The aim of this study was to compare the clinical, biological, and radiologic features of presentation in the emergency ward of community-acquired pneumonia (CAP) by Legionella pneumophila (LP) and other community-acquired bacterial pneumonias to help in early diagnosis of CAP by LP. Three hundred ninety-two patients with CAP were studied prospectively in the emergency department of a 600-bed university hospital. Univariate and multivariate analyses were performed to compare epidemiologic and demographic data and clinical, analytical, and radiologic features of presentation in 48 patients with CAP by LP and 125 patients with CAP by other bacterial etiology (68 by Streptococcus pneumoniae, 41 by Chlamydia pneumoniae, 5 by Mycoplasma pneumoniae, 4 by Coxiella burnetii, 3 by Pseudomonas aeruginosa, 2 by Haemophilus influenzae, and 2 by Nocardia species. Univariate analysis showed that CAP by LP was more frequent in middle-aged, male healthy (but alcohol drinking) patients than CAP by other etiology. Moreover, the lack of response to previous beta-lactamic drugs, headache, diarrhea, severe hyponatremia, and elevation in serum creatine kinase (CK) levels on presentation were more frequent in CAP by LP, while cough, expectoration, and thoracic pain were more frequent in CAP by other bacterial etiology. However, multivariate analysis only confirmed these differences with respect to lack of underlying disease, diarrhea, and elevation in the CK level. We conclude that detailed analysis of features of presentation of CAP allows suspicion of Legionnaire's disease in the emergency department. The initiation of antibiotic treatment, including a macrolide, and the performance of rapid diagnostic techniques are mandatory in these cases.
Many physicians are unaware of the limitations of the available tests for diagnosing infections with Legionella organisms. Geographic differences in the importance of nonpneumophila Legionella species as pathogens are underrecognized, in part because available diagnostic tests are biased toward the detection of pneumophila serogroup 1. Routine laboratory practices reduce the likelihood of culturing Legionella species from clinical isolates. Failure of seroconversion is common, particularly with nonpneumophila species; even when seroconversion occurs, it may take much longer than 4 weeks. Urinary antigen testing has insufficient sensitivity to affect clinical management in most regions of the United States, as it can reliably detect only L. pneumophila serogroup 1 infections. Polymerase chain reaction-based techniques offer hope of providing highly sensitive, rapid diagnostic tests for all Legionella species, but limitations in the current tests will make validating them difficult.
To measure the ability of a set of clinical parameters, the Winthrop-University Hospital (WUH) criteria, to identify Legionella pneumonia while discriminating against bacteremic pneumococcal pneumonia at the time of hospitalization for community-acquired pneumonia (CAP).
Retrospective case-control study.
An urban county hospital and a tertiary-care Veterans Affairs hospital.
Thirty-seven patients with Legionella pneumonia (diagnosed by a positive result of a urinary Legionella antigen test) and 31 patients with bacteremic pneumococcal pneumonia. A subgroup of patients with all required laboratory criteria were studied further.
The WUH criteria correctly identified 29 of 37 patients with Legionella pneumonia (sensitivity, 78%; 95% confidence interval [CI], 61 to 90%), while successfully excluding legionellosis in 20 of 31 patients with bacteremic pneumococcal pneumonia (specificity, 65%; 95% CI, 45 to 80%). The positive and negative predictive values, adjusted for a relative prevalence of 1:3 between Legionella and Streptococcus pneumoniae bacteremia, were 42% (95% CI, 25 to 61%) and 90% (95% CI, 74 to 97%), respectively. In the subgroup analysis, the WUH criteria were successful in identifying 20 of 23 patients with Legionella pneumonia (sensitivity, 87%; 95% CI, 65 to 97%), while excluding legionellosis in 9 of 18 patients with bacteremic pneumococcal pneumonia (specificity, 50%; 95% CI, 27 to 73%). The adjusted positive and negative predictive values for a 1:3 relative prevalence were 37% (95% CI, 20 to 59%) and 92% (95% CI, 62 to 98%), respectively. The predictive values were changed in the directions expected for an increased relative prevalence of 1:1. The areas under the receiver operating characteristic curves were 0.72 +/- 0.06 for the entire study group and 0.68 +/- 0.09 for the subgroup.
Although the WUH criteria discriminated fairly well between cases (mean +/- SE) and control subjects, the sensitivity is not high enough to exclude legionellosis confidently. These results suggest that empiric therapy for Legionella pneumonia should be included in the initial antibiotic regimen for hospitalized patients with CAP.
The atypical pathogens in community-acquired pneumonia traditionally have included Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella spp. Recent studies documenting their epidemiology and clinical characteristics have shown that these organisms are indistinguishable from the pneumococcus. Furthermore, therapy no longer depends on the specific bacterial cause of community-acquired pneumonia. Etiologic diagnosis is still difficult, although new methods are becoming available. This article focuses on these issues and on why the term atypical is no longer meaningful.
The pathogenesis of the widespread effects of legionella infection is not known. Direct bacterial invasion, circulating toxins, immunologically mediated damage or a combination of these are the most likely mechanisms. There is little current evidence for the involvement of an immunological process. A number of toxins, both exotoxins and a weak endotoxin, have been associated with legionellae[97], but these are unlikely to be sufficiently potent to produce such distant effects. Dissemination of legionella organisms has been demonstrated on a number of occasions. The organisms have been cultured from lung, blood[98,99], brain and liver[68], pleural[17] and pericardial fluids[37], perirectal abscess[87] and an excised prosthetic mitral valve[48]. Routine histological stains have revealed organisms in lung[18,40], pleural[32], kidney[32] and brain[58] and, with immunofluorescent staining, lymph nodes, spleen, bone marrow[18,89], colon[86], myocardium[40] and arteriovenous fistulae[49] have also been shown to contain legionella organisms. Of commonly affected tissues only skeletal muscle, skin, pancreas and cerebrospinal fluid have so far failed to yield either legionella organisms or antigen. Clearly, direct spread of the organisms may occur, but the high frequency of immunosuppressed patients in the studies so far performed and the rarity of blood culture isolation suggests that dissemination may only occur in exceptional circumstances or as an agonal event. Despite the growth in our knowledge of LD in the last nine years there remains to be learnt about this fascinating disease. Analysis of information from the Staffordshire outbreak will certainly be of immense interest.
An explosive, common-source outbreak of pneumonia caused by a previously unrecognized bacterium affected primarily persons attending an American Legion convention in Philadelphia in July, 1976. Twenty-nine of 182 cases were fatal. Spread of the bacterium appeared to be air borne. The source of the bacterium was not found, but epidemiologic analysis suggested that exposure may have occurred in the lobby of the headquarters hotel or in the area immediately surrounding the hotel. Person-to-person spread seemed not to have occurred. Many hotel employees appeared to be immune, suggesting that the agent may have been present in the vicinity, perhaps intermittently, for two or more years.
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Pneumococcal capsular antigens can be detected in lung tissue by counter-current immunoelectrophoresis even when, following antibiotics, post-mortem bacterilogy suggests that Escherichia coli has replaced pneumococci. The results suggest that antipneumococcal therapy would benefit at least 55% of patients critically ill with lung infection and that the potentially toxic drugs directed at coliform bacteria may be unnecessary.
We investigated six men and a woman suspected of suffering from congenital immotility of cilia. All had chronic airway infections, and the men had immotile spermatozoa. The woman and three men had Kartagener's syndrome. The investigations included measurements of the mucociliary transport in the lower airways and ultrastructural studies of the sperm tails or respiratory cilia (or both). Mucociliary transport was significantly delayed. Sperm tails lacked dynein arms in five patients. Respiratory cilia from the women and two men lacked dynein arms and were irregularly oriented. The results support the hypothesis that a congenital defect in the cilia and sperm tails will cause chronic respiratory-tract infections and male sterility--the immotile-cilia syndrome. In about half these patients there will also be a situs inversus--i.e., Kartagener's syndrome.
The results of serologic, cultural, and DNA relatedness studies have shown that the Legionnaires' disease (LD) bacterium and an unclassified agent isolated in 1947 are the same species. Both organisms grew on charcoal-yeast extract agar, enriched Mueller-Hinton agar, and F-G agar, but neither grew on blood agar, trypticase soy agar, or in thioglycollate broth. Both agents reacted with convalescent sera from patients with Legionnaires' disease and convalescent sera from guinea pigs infected experimentally with the LD bacterium. The percentage of guanine plus cytosine in DNA preparations from each organism was ascertained by thermal denaturation to be 39%. In DNA hybridization reactions the 1947 isolate showed the same degree of relatedness to Philadelphia 1 strain of the LD bacterium as did three recent isolates of the bacterium. The LD bacterium was also shown to be antigenically related to another unclassified organism isolated in 1959.
Early diagnosis of Legionnaires' disease is difficult because other pathogens cause a similar clinical picture and microbiologic tests are usually only of retrospective value. Since May 1977, 17 patients with sporadic cases of Legionnaires' disease have been admitted, all previously well, the diagnosis being made with standard serologic or bacteriologic criteria. From the clinical, laboratory, and radiologic findings, we propose criteria that may enable the clinician to make a diagnosis earlier in many cases, differentiating them from other pneumonias. Within 24 hours of admission, any three of the following four features are strongly suggestive of Legionnaires' disease: [1] prodromal "viral" illness, [2] dry cough or confusion or diarrhoea, [3] lymphopenia without marked neutrophilia, [4] hyponatremia. Two thirds of cases had at least three of these features, and no false-positive diagnoses would have been made in other pneumonias that were serologically negative for Legionnaires' disease if these proposed criteria had been applied diagnostically. In the next few days the diagnosis is very likely if microbiologic tests are negative and if there is radiologic extension, abnormal liver function test results, or hypoalbuminemia.
A review of the medical records of 123 persons with Legionnaires' disease hospitalized in the 1976 Philadelphia epidemic showed that the manifestations of infection ranged from mild grippe to a severe pneumonia that also involved other organ systems. Early in the illness, constitutional symptoms predominated. Fever, malaise, myalgia, rigors, confusion, headache, and diarrhea were usually followed by nonproductive cough and dyspnea. Physical examination showed few abnormalities other than rales. Moderate leukocytosis with left shift, elevated erythrocyte sedimentation rate, elevation of serum levels of liver enzymes, and hematuria and proteinuria were characteristic. Chest radiograph showed patchy, often nodular, areas of consolidation. Progression of pneumonia led to respiratory failure and the need for mechanical ventilatory assistance for 19 patients; renal failure, primarily after shock, occurred in 18 persons. Twenty-six patients died. Treatment with erythromycin or tetracycline resulted in the lowest case-fatality ratios, but the associations were not statistically significant.
Legionnaires' disease is increasingly recognised as a cause of community acquired pneumonia. Although there are no controlled trials of antimicrobial chemotherapy in legionnaires' disease, an early bacteriological diagnosis will confirm the need for treatment directed at Legionella or will redirect treatment should another pathogen be isolated. Serological tests provide only a retrospective diagnosis; while rapid antigen detection (for example, by ELISA or latex agglutination with urine samples), although permitting early diagnosis, does not allow isolation of the organism. We report three cases of legionella pneumonia where the organism was isolated from material obtained during life by bronchoscopy.
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.
The cause of primary pneumonia was diagnosed in 124 of 127 consecutive adult patients admitted to hospital with community-acquired illness. Pneumococcal infection was found in 96 (76%) patients and legionnaries' disease was the second commonest infection identified (15%). Other bacterial infections were uncommon. 11 patients had atypical pneumonia, including 7 with psittacosis. There were several mixed infections and most of the 11 patients with viral infections also had bacterial pneumonia. 19 patients died (15%) and mortality was associated with increasing age, the presence of coexisting disease, and the cause of the pneumonia. Recognition of the most likely causes of severe pneumonia allows logical initial antibiotic treatment for such patients admitted to hospital.
A guinea pig model of Legionnaires' disease was produced by intratracheal inoculation of Legionella pneumophila. The bacterial inoculum given reproducibly resulted in a 95% fatality rate in untreated animals. These animals had lung histopathologic and bacteriologic findings almost identical to those found in human Legionnaires' disease. Administration of cefoxitin and gentamicin, which inhibited the infecting strain in low antibiotic concentration in vitro, was no more effective than saline; this occurred despite adequate serum and lung levels of the drugs. Erythromycin, rifampin, doxycycline, and cotrimoxazole significantly reduced fatality rates. The combinations of erythromycin with rifampin and doxycycline with rifampin were not significantly better or worse than use of either drug alone. In animals treated with any regimen containing rifampin, a dramatically higher rate of bacterial killing was observed than that observed in those animals treated with erythromycin or doxycycline alone. Also, animals treated with any regimen containing rifampin had significantly less late lung histologic evidence of pneumonia than did those treated with other agents. No rifampin-induced resistance was found. This animal model reflects prior clinical findings, provides experimental grounds for therapy with drugs other than erythromycin, and suggests that therapy of Legionnaires' disease should probably include rifampin in most cases.
To add information about sporadic Legionnaires' disease, 87 cases of L. pneumophila pneumonia were reviewed. Twenty cases were nosocomial infections and 67 cases were community-acquired. Most cases (64%) occurred between July and October.
The mean age of patients was 51.4 years and males outnumbered females 2.5:1.0. Thirty-one percent of patients were receiving corticosteroid, immunosuppressive, or antineoplastic chemotherapy when illness began. Immunosuppression at onset of illness was more common in nosocomial infections (90%) than in community-acquired infections (14%). Seventy percent of patients had underlying diseases. Malignancies, renal failure, and transplantation were the most common conditions underlying nosocomial infections. Chronic lung disease and malignancies were the most common diseases underlying community-acquired infections. The case-fatality rate in nosocomial infection (70%) was greater than that in community-acquired disease (22%).
Clinical, laboratory, and radiologic features of the cases were examined. Illness ranged from mild to severe. Extra pulmonary findings of encephalopathy and renal failure were more common in fatal than in non-fatal cases. Indirect immunofluorescent and microagglutination antibody responses plateaued by the fourth week of illness.
Twenty-nine patients died. The case-fatality rate of patients receiving erythromycin (6%) was less than that of patients receiving penicillin (36%), ampicillin (28%), cephalosporin (32%), or aminoglycosides (41%). Despite erythromycin therapy, the case fatality rate for nosocomial L. pneumophilia pneumonia was unacceptably high (25%).
Urine and serum specimens from three patients with pneumonia caused by Legionella pneumophila serogroup 1 (Lp1) were tested by enzyme-linked immunosorbent assay (ELISA) for Lp1-soluble antigen. A three-layer direct ELISA with polyclonal antibodies and a four-layer indirect ELISA with both polyclonal and monoclonal antibodies were used. Lp1 antigen was detected in both urine and serum from the three patients. As determined by ELISA, the concentration of antigen was 30- to 100-fold less in serum than in urine collected on the same day. In some instances the indirect ELISA was more sensitive than the direct ELISA, but in others it was less sensitive, depending on the monoclonal antibody used. The subgroup of the infecting Lp1 organism was determined based on antigenic determinants expressed in the urine. This study illustrates the use of serum as well as urine as an antigen reservoir in the laboratory diagnosis of legionellosis by ELISA and the potential for developing more sensitive antigen detection systems by the judicious use of monoclonal antibodies.
The protean manifestations of Legionnaires' disease are described in an analysis of 12 sporadic cases. Two forms of the disease have been delineated. One variant (Group A) consisted of six patients who had a mild form of non-progressive pneumonia with minimum extra-pulmonary involvement. Six patients (Group B) were differentiated by rapidly progressive pulmonary infiltrates, severe hypoxia and respiratory failure, plus a higher frequency of band neutrophils and extra-pulmonary manifestations. Particularly notable were evidence of severe myositis (elevated creatinine phosphokinase and lactate dehydrogenase), anaemia, and neurological findings which included alterations in the sensorium, meningitis, and convulsions. Cerebrospinal fluid (CSF) abnormalities were seen frequently in patients with neurological manifestations, and necropsy findings in one patient suggested that the Legionnaires' bacillus was capable of producing a fatal leucoencephalitis. Renal findings included haematuria, proteinuria and oliguric renal failure. Hepatic transaminases (SGPT, SGOT) were elevated in six patients and serum bilirubin was abnormal in five. Alkaline phosphatase values were normal to minimally elevated. The gastrointestinal symptoms commonly considered to be a frequent initial manifestation of Legionnaires' disease were rare in this series. Recommendations for instituting empirical therapy, based upon recognition of a clinical syndrome which should suggest the diagnosis of Legionnaires' disease, are included.
The efficacy of erythromycin, gentamicin and rifampicin has been compared in the treatment of experimental airborne Legionnaires' disease in guinea-pigs. Evaluation was based on survival of animals after 1LD50 or 10LD50 infection, on numbers of Legionella pneumophila in the lungs and on the extent of histopathological lesions. All three drugs were effective in increasing survival in 1LD50 infections, but only rifampicin gave any protection against 10LD50 infection. Rifampicin was the most effective agent in eliminating viable L. pneumophila from the lungs and also in preventing pulmonary lesions.
The features of the chest radiographs of 49 adults with legionnaires' disease were compared with those of 91 adults with pneumococcal pneumonia (31 of whom had bacteraemia or antigenaemia), 46 with mycoplasma pneumonia, and 10 with psittacosis pneumonia. No distinctive pattern was seen for any group. Homogeneous shadowing was more frequent in legionnaires' disease (40/49 cases) (p less than 0.005), bacteraemic pneumococcal pneumonia (25/31) (p less than 0.01) and non-bacteraemic pneumococcal pneumonia (42/60) (p less than 0.05) than in mycoplasma pneumonia (23/46). Multilobe disease at presentation was commoner in bacteraemic pneumococcal pneumonia (20/31) than in non-bacteraemic pneumococcal pneumonia (15/60) (p less than 0.001) or legionnaires' disease (19/49) (p less than 0.025). In bacteraemic pneumococcal pneumonia multilobe disease at presentation was associated with increased mortality. Pleural effusions and some degree of lung collapse were seen in all groups, although effusions were commoner in bacteraemic pneumococcal pneumonia. Cavitation was unusual. Lymphadenopathy occurred only in mycoplasma pneumonia (10/46). Radiographic deterioration was particularly a feature of legionnaires' disease (30/46) and bacteraemic pneumococcal pneumonia (14/27), and these groups also showed slow radiographic resolution in survivors. Radiographic resolution was fastest with mycoplasma pneumonia; psittacosis and non-bacteraemic pneumococcal pneumonia cleared at an intermediate rate. Residual intrapulmonary streaky opacities remained in over a quarter of survivors from legionnaires' disease (12/42) and bacteraemic pneumococcal pneumonia (5/19).
During a three-year-period, serum samples from 209 patients with acute pneumonia were tested for antibodies to Legionella pneumophila, using an indirect micro-immunofluorescent antibody test performed with heat-killed serogroup specific antigens. Low antibody levels, defined by titres ranging from 32 to 128, were demonstrated in 73 of the patients. Seroconversion indicating current L. pneumophila, Serogroup 1, infection was documented in 3 previously healthy individuals. High IgM antibody titres suggested such an infection in 3 other patients. Thirteen patients showed either static or single antibody titres of 256 or greater. Only 7 of these patients had antibodies detectable with formalin-inactivated L. pneumophila, Serogroup 1, antigen. The high frequency of stationary antibody titres to heat-inactivated L. pneumophila antigen found in the present study suggests that formalin-inactivated organisms may be a superior antigen for the serodiagnosis of current Legionnaires' disease.
From August 27 to September 21, 1979, 58 patients fell ill with Legionnaires' disease (LD) in the town Västerås, Sweden. All patients had been staying in the town some time during 2 weeks preceding their illness, as had 10 LD patients who fell ill from mid-June to mid-August the same year. Clinically, high fever, headache, dizziness and gastrointestinal symptoms were dominating. Respiratory symptoms were moderate, radiologically verified pneumonia was seen in 59 of 64 patients examined. One patient died. The diagnosis was verified by serology, using the IFL method, in all cases. Legionella pneumophila serogroup 1 was isolated from a closed lung biopsy from 3 patients. Isolates of identical strains were made from the cooling tower on the roof of an indoor shopping centre in Västerås, visited by 57 of the patients during the incubation period.
Twenty-three fatal sporadic cases of serogroup 1 Legionella pneumophila pneumonia have been analyzed. Bilateral consolidating fibrinopurulent pneumonia was evident in most cases. In four leukopenic immunosuppressed subjects, and acute fibrinoserous pneumonia with a remarkable lack on inflammation was present. The bacterium was found at extrathoracic sites in 27% of the cases. Involvement of the spleen (25%), bone marrow (13%), and kidneys (4.5%) suggests that hematogenous spread of the infection is not uncommon. Involvement of the hilar lymph nodes in 44% of the cases, and multiple peripheral lymph nodes in one case, suggest that lymphatic vessels may also be an important pathway of dissemination. We concluded that systemic spread of L pneumophila is not uncommon in seriously ill patients and we believe that some of the unusual extrathoracic manifestations of this disease may be related to bacteremia.
Sixty-five cases of nosocomially acquired Legionnaires' disease are reported and the world literature is reviewed. The etiologic agent, Legionnella pneumophila, has been isolated from several environmental sources at outbreak sites. Legionnaires' disease appears to be acquired by inhalation and is primarily manifested by severe, potentially fatal, pneumonia. Characteristic clinical disease consists of high fever with relative bradycardia, dry cough, chills, diarrhea, and pleuritic pain. Although no single feature is pathognomonic, the clinical presentation is usually sufficiently characteristic to suggest the diagnosis. The diagnosis of Legionnaires' disease during acute illness may be established by culture of Legionella pneumophila, or by demonstration of the bacterium using special stains. However, in most instances, the physician must make a presumptive diagnosis based on the clinical presentation in order to institute appropriate antimicrobial therapy. Retrospective confirmation of the diagnosis may be made by serologic studies in most instances. Erythromycin is, at this time, the drug of choice for the treatment of Legionnaires' disease. A prompt salutory response following institution of erythromycin therapy is typical.
Formolised yolk sac antigens of Legionella pneumophila serogroups 1-6 were used to test 1792 serum specimens from 1431 patients with respiratory illness of serological evidence of Legionnaires' disease (LD). Thirty-five patients showed titres against the serogroup 1 antigen diagnostic for LD. Only two further cases were considered to have non-serogroup I infections (both serogroup 4) indicating that such infections are rare. Titres of greater than 1/16 against the serogroup 1 antigen occur in only 3% of subjects without LD and thus the demonstration of such a titre in patients with pneumonia during the early phase of illness can alert the clinician to the likelihood of LD. The supply of serogroup 1 antigen from the Division of Microbiological Reagents and Quality Control to routine diagnostic laboratories will be continued and monovalent serogroup 2-6 antigens will continue to be made available to reference laboratories.
An enzyme-linked immunosorbent assay was developed to detect urinary antigen excreted by patients with Legionnaires' disease. Of 47 patients tested, antigen was detected in 39. Of these 39 specimens, 35 gave clearly positive results by visual analysis; four others required spectrophotometric verification of positive results. Antigen was not detected in any of 178 urine specimens from patients with other pulmonary, bacteremic or urinary tract infections after a quick and simple confirmatory test. The assay required more time to perform than a previously described radioimmunoassay but was of equivalent sensitivity and specificity and did not require expensive equipment or contract with radioactive reagents. We conclude that enzyme-linked immunosorbent assay is a rapid, sensitive and specific means for rapidly diagnosing legionnaires' disease that can be performed in clinical laboratories unwilling or unable to use radioisotopes.
In an attempt to ascertain the incidence of Legionnaires' disease at our hospital, a prospective case-control pneumonia study was conducted for 11 months. Specialized diagnostic tests for Legionella pneumophila, including serologic study, direct immunofluorescent examination, and selective culture, were made routinely available in our hospital. To our surprise, L. pneumophila was the most common cause of pneumonia (22.5 percent) attributable to a single pathogen, followed by Streptococcus pneumoniae (10.6 percent). In 68.8 percent of the cases, Legionnaires' pneumonia was hospital-acquired. In contrast to other investigators, we found that abdominal pain, diarrhea, neurologic signs, abnormal liver function results, hypophosphatemia, and hematuria did not occur significantly more frequently in pneumonia caused by L. pneumophila than in that caused by other microorganisms. However, hyponatremia within five days of onset of pneumonia occurred significantly more frequently in Legionnaires' disease (p less than 0.0001). Since the clinical presentation is nonspecific, specialized laboratory tests are necessary to make the diagnosis. As a result of our experience, we suggest an approach using serologic tests as a screen to determine whether more specialized tests for Legionnaires' disease should be introduced into a hospital without previously recognized cases of Legionnaires' disease.
The incidence of bacterial, viral, mycoplasma, and rickettsial infections has been assessed prospectively in 210 adult patients with pneumonia who presented to a district hospital over a six-year period. One hundred and thirteen infective agents were detected in 103 patients. The agent most frequently detected was Mycoplasma pneumoniae which accounted for 30 infections. A bacterial pathogen was found in 43 patients. Streptococcus pneumoniae was the most common of these (24 patients); Staphylococcus aureus (eight), Haemophilus influenzae (four), Klebsiella spp (three), and Legionella pneumophila (three) were all less common. Chlamydial or rickettsial infections (Psittacosis or Q fever) were detected in nine patients. Viral infections were found in 31 patients (22 influenza A, four influenza B, two parainfluenza, and three respiratory syncytial virus). There were 10 patients in whom more than one pathogen was identified. In 107 patients no pathogens could be identified. Seventy-five per cent of these patients had either received antibiotics before entering hospital, or were unable to produce any sputum for culture. The incidence of bacterial pneumonia has probably therefore been underestimated. Nevertheless this survey does emphasise the importance of M pneumoniae as a pathogen in patients with pneumonia presenting to hospital.
Thirty-three isolates of Legionella pneumophila, all except one of which were clinical isolates, were tested against 20 antimicrobial
agents by using an agar dilution technique. Erythromycin, rifamp]in, and rosaramycin were the most active agents tested. Aminoglycosides,
chloramphenicol, and cefoxitin also inhibited the organisms at low concentrations. Other agents, including moxalactam, cefoperazone,
and cephalosporins, exhibited moderate to little activity. Tetracycline, doxycycline and minocyeline were apparently inactivated
by charcoal-yeast extract medium. There was slight inoculum dependence noted with most of the antimicrobials tested, particularly
the beta-lactam agents. There was no consistent difference in susceptibility between Center for Disease Control-supplied stock
strains and recent clinical isolates, but there were marked differences with some agents. Susceptibility testing needs to
be standardized in view of the influence of inoculum size, strain variation, and the medium used.
As of 30 September 1979, 1005 confirmed cases of sporadic legionellosis caused by Legionella pneumophila serogroups 1 to 4 in U.S. residents had been reported to the Centers for Disease Control; 19% were fatal. All but 2% of the 1005 cases were associated with pneumonia documented by chest radiograph. About 75% of the cases occurred in June through October. The risk of acquiring sporadic legionellosis was increased among males and persons 50 years or older; persons with renal disease necessitating dialysis or transplantation, with chronic bronchitis or emphysema, with diabetes mellitus, and with cancer (10 selected sites or types); persons who smoke; and persons being treated with immunosuppressive drugs. Increasing age and chronic bronchitis or emphysema were associated with increased risk of death. The sensitivity of culturing L. pneumophila from specimens positive by direct immunofluorescence was estimated to be 45%. The distribution of serogroups 1, 2, 3, and 4 of L. pneumophila in 57 fresh, not previously examined direct fluorescent antibody-positive specimens was 84%, 11%, 4%, and 2%, respectively; all 26 strains isolated from these specimens were of one of these four serogroups.
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