Legionellosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Legionellosis is an infectious disease caused by Legionella species, a pleomorphic, aerobic, catalase-positive, oxidase-positive, non-spore-forming, non-capsulated, motile, Gram-negative bacteria. The majority of cases of legionellosis are reported between the Summer and early Fall (between June and October). Approximately 8,000-18,000 individuals are hospitalized annually in the USA for Legionnaires’ disease with a case fatality rate ranging between 10% to 35%. Legionellosis may be classified into three types based upon the affected organ systems and the clinical presentation: pulmonary infection (Legionnaires’ disease), extrapulmonary infection, and Pontiac fever. Legionella is usually transmitted by aerosol droplets when individuals breathe in contaminated mist or vapor (e.g. whirlpool spa, river, cruise ships, cooling towers, air conditioners, water supply systems). L. pneumophila usually invades host cells and replicates intracellularly. In Legionnaires’ disease, the majority of exposed patients do not develop any symptoms. Patients who develop clinical manifestations usually report pneumonia-like symptoms that worsen at 4 to 6 days following onset of symptoms and eventually resolve by day 5 to 10 of symptom-onset. Approximately 1% to 35% of individuals progress to develop Legionnaires’-related complications and death. Complications of Legionnaires’ disease include empyema, lung failure, acute kidney injury, endocarditis, neurological disease, septic shock, and multi-organ failure. The prognosis is generally good for healthy patients, but patients with co-morbidities are at higher risk of developing complications and death. In contrast, Pontiac fever has a high attack rate but is associated with mild flu-like symptoms that resolve within 1 to 2 days and is almost always self-limited without any complications. The most important risk factor in the development of legionellosis is recent exposure to either aerosolized water or contaminated water. Other risk factors include old age, concomitant lung disease, active smoking status, and immunosuppression. Urine antigen testing in the first-line diagnostic method. Culture of the lower respiratory secretion is the gold standard for the detection of Legionella and diagnosis of Legionnaires’ disease. Imaging may also be indicated among patients with Legionnaires’ disease. Pharmacologic medical therapy is indicated in Legionnaires’ disease, but not in Pontiac fever. The preferred regimens for both mild and moderate-to-severe Legionnaires’ disease include either azithromycin or a fluoroquinolone. Patients who develop legionellosis-related complications may require other or additional pharmacologic agents. There is no vaccine against legionellosis, and antibiotic prophylaxis is not effective.

Legionnaires’ disease acquired its name in 1976 when an outbreak of pneumonia occurred among people attending a convention of the American Legion in Philadelphia. On January 18, 1977 the causative agent was identified as a previously unknown bacterium, subsequently named Legionella.

Legionellosis may be classified into three types based upon the affected organ systems and the clinical presentation: pulmonary infection (Legionnaires’ disease), extrapulmonary infection, and Pontiac fever. Legionellosis may also be classified based on the infectious species responsible for the disease.

Legionella is usually transmitted by aerosol droplets when individuals breathe in contaminated mist or vapor (e.g. whirlpool spa, river, cruise ships, cooling towers, air conditioners, water supply systems). L. pneumophila usually invades the host cells and replicates intracellularly. Legionella is internalized using pseudopods and protects itself in a membrane-bound vacuole that does not fuse with lysosomes.

L.pneumophila is a ubiquitous aquatic organism that thrives in warm environments (32°- 45°C). L. pneumophila is a pleomorphic, aerobic, catalase-positive, oxidase-positive, non-spore-forming, non-capsulated, motile, Gram-negative bacteria. Although Legionella is categorized as a Gram-negative bacterium, it stains poorly to Gram stain due to its unique lipopolysaccharide-content in the outer psuedospamodulating leaflet of the outer cell membrane.

Legionellosis must be differentiated from other causes of fever, dyspnea, cough, and sputum production, such as bacterial pneumonia, viral pneumonia, and other causes of atypical pneumonia.

The majority of cases of legionellosis are reported between the Summer and early Fall (between June and October). Approximately 8,000-18,000 individuals are hospitalized annually in the USA for Legionnaires’ disease with a case fatality rate ranging between 10% to 35%. The median case-patient age is 61 years, and the male to female ratio is 1.8 to 1.

The most important risk factor in the development of legionellosis is recent exposure to either aerosolized water or contaminated water. Other risk factors include old age, concomitant lung disease, active smoking status, and immunosuppression.

In Legionnaires’ disease, the majority of exposed patients do not develop any symptoms. Patients who develop clinical manifestations usually report pneumonia-like symptoms that worsen at 4 to 6 days following onset of symptoms and eventually resolve by day 5 to 10 of symptom-onset. Approximately 1% to 35% of individuals progress to develop Legionnaires’-related complications and death. Complications of Legionnaires’ disease include empyema, lung failure, acute kidney injury, endocarditis, neurological disease, septic shock, and multi-organ failure. The prognosis is generally good for healthy patients, but patients with co-morbidities are at higher risk of developing complications and death. In contrast, Pontiac fever has a high attack rate but is associated with mild flu-like symptoms that resolve within 1 to 2 days and is almost always self-limited without any complications.

Legionellosis may manifest with either Legionnaires’ disease or Pontiac Fever. Legionnaires’ disease is more severe and typically manifests with fatigue, malaise, symptoms of pneumonia (fever, dyspnea, chest pain, and cough) and occasionally diarrhea and nausea. In contrast, Pontiac fever is a milder form of respiratory flu-like disease (fever and cough) but does not result in pneumonia. Patients with legionellosis often report a recent history of travel, hospitalization, exposure to contaminated water, or exposure to healthcare settings.

Physical examination may be remarkable for fever, as well as consolidation and crackles on pulmonary auscultation. Patients with advanced disease may develop neurological signs, including altered mental status, weakness, and ataxia.

Laboratory abnormalities in Legionnaires’ disease include leukocytosis with relative lymphopenia, hyponatremia, hypophosphatemia, and elevated levels of AST/ALT, CPK, ESR, CRP, LDH, and ferritin. Urine antigen testing in the first-line diagnostic method. Culture of the lower respiratory secretion is the gold standard for the detection of Legionella and diagnosis of Legionnaires’ disease.

Common chest x-ray findings in Legionnaires’ disease include consolidation and pleural effusion. There are usually no chest x-ray findings in Pontiac fever.

In Legionnaires’ disease, chest CT findings may include bilateral, multiple affected segments and peripheral lung consolidation with ground glass opacity. There are usually no chest CT findings in Pontiac fever.

Additional studies are not required for the diagnosis of legionellosis.

Pharmacologic medical therapy is indicated in Legionnaires’ disease. The preferred regimens for both mild and moderate-to-severe pneumonia include either azithromycin or a fluoroquinolone. Patients who develop legionellosis-related complications may require other or additional pharmacologic agents. Pontiac fever is self-limited and may be treated with symptomatic therapy only.

There is no vaccine against legionellosis, and antibiotic prophylaxis is not effective. Travelers at increased risk for infection, such as the elderly or those with immunocompromising conditions such as cancer or diabetes, may choose to avoid high-risk areas, such as whirlpool spas.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ogechukwu Hannah Nnabude, MD Tarek Nafee, M.D. [2]

Legionnaires’ disease acquired its name in 1976 when an outbreak of pneumonia occurred among people attending a convention of the American Legion in Philadelphia. On January 18, 1977 the causative agent was identified as a previously unknown bacterium, subsequently named Legionella. There have been numerous outbreaks of Legionnaires since it was first discovered. Some of the outbreaks of Legionella are listed below in chronological order.

The first recognized Legionella outbreak occurred in 1976 during a meeting of the American Legion in Philadelphia, Pennsylvania. About 29 of the 182 people that contracted the infection died ^[1]. It was after the bacterium had been successfully isolated that previous cases of Legionella were identified.

In 1985, Stafford District General Hospital experienced a Legionella outbreak. A total of 68 confirmed cases were treated in hospital and 22 of these patients died. A further 35 patients were suspected cases of Legionnaires’ disease, 14 of whom only required treatment at home. Legionella was found in the water within the cooling tower and a chiller unit which cooled the air entering the outpatient department. The chiller unit is believed to be the major source of the outbreak ^[2].

During a flower exhibition in Bovenkarspel, Netherlands, an outbreak of Legionella occurred. It is believed to have been caused by a contamination of the whirlpools in halls 3 and 4, and the sprinkler in hall 8, all of which tested culture positive for Legionella. There were 133 confirmed cases and 55 possible cases out of the 77061 visitors to the exhibition ^[3].

In Murcia, Spain, over 800 suspected cases of Legionnaires’ disease were recorded. Of these cases, 449 were confirmed to be caused by Legionella. This is currently the largest outbreak of Legionella ever recorded. About 1% of affected patients died from the disease ^[4].

The first recognized outbreak of Legionella in Norway was in 2001 when 28 people were infected in the city of Stavanger, and seven died. Of the 28 patients, 21 were within the city of Stavanger, five were in other areas in Norway, and two were from other countries, with one being in England and the other in Germany. This was initially a mystery to the investigators. However, it was discovered that a cooling unit from a nearby hotel was the source of the infection. The air outlet was found to be just over 16 feet above the ground and located close to a bus station. This was determined source of contact for the patient in Germany and the patient in England ^[5]

In 2002, six women and one man in Barrow-In-Furness died as a result of the illness, another 172 people also contracted the disease. The outbreak was traced to a contaminated cooling tower at the town’s Forum 28 arts center.

Between November 2003 and January 2004, an outbreak of Legionnaires’ disease occurred in Pas-de-Calais, France. There were 18 fatalities out of the 86 laboratory-confirmed cases, giving the outbreak a mortality rate of about 21%. A Legionella pneumophila strain named Lens was isolated from samples of air, wastewater, and cooling towers from plant A. Researchers determined that the dispersion extended over a distance of at least 6 km (3.75 miles) from the plant. ^[6]

In May 2005 there was another outbreak of Legionnaires’ disease in Norway, in the town of Fredrikstad. Initially, 56 patients were confirmed infected and ten people were dead. However, on serological testing of other patients with community acquired pneumonia, another 47 patients were discovered to have the disease, bringing the total for the oubreak to at least 103, 16 of whom are probable cases. The source of the outbreak unexpectedly came from an air scrubber that disseminated that bacterium over a distance of about 10 km (6.25 miles). ^{[7] [8]}

In mid-2005, Christchurch, New Zealand experienced an outbreak of Legionnaires’ disease. There were 3 deaths out of the 19 confirmed cases. Legionella pneumophila serogroup 1 (Lpsg1) was identified as the causative agent for all cases. A water cooling tower located in the center of the clusters is believed to be the source of the outbreak^[9].

An outbreak of Legionnaires’ disease at the Seven Oaks Home for the Aged, a nursing home in Toronto, in the province of Ontario, Canada from September to October 2005 resulted in illness in 135 people, 23 (17%) of whom died. Researchers confirmed that a contaminated air conditioning cooling tower was the source of the outbreak. ^[10]

An outbreak linked to contaminated water in an industrial cooling tower caused 181 confirmed cases, 14 of which resulted in death ^[11].

In 2012, 50 confirmed cases and 49 suspected cases of Legionella occurred in Edinburg, Scotland. It led to the death of 4 people. Cooling towers in the affected area are suspected to be the cause of the outbreak. ^[12]

A widespread outbreak in the Vila Franca de Xira district infected 377 people, and caused the death of 14. A combination of factors led to the outbreak becoming widespread including temperatures that were unusually high for that time of the year, leading to increased proliferation of Legionella in the cooling tower to which the outbreak was traced, and the high humidity that is believed to increase the spread of Legionella ^{[13] [14]}.

Whirlpool spas at a state fair were linked to a Legionella outbreak in Fletcher, North Carolina, United States that claimed the lives of 4 out of the 136 confirmed cases people infected. ^[15]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] {{AE}]Tarek Nafee, M.D. [2] Ogechukwu Hannah Nnabude, MD

Legionellosis may be classified into three clinically different diseases, all of which vary in disease presentation, organ system affected, and severity: pulmonary infection (Legionnaires’ disease), extrapulmonary infection, and Pontiac fever, which has causes only mild disease. Legionellosis may also be classified based on the causative species.

Legionellosis may be classified into three types based upon affected organ systems and clinical presentation:

Legionnaires’ disease may further be classified into:

• Community-acquired Legionnaires’ disease, which is most commonly caused by L. pneumophila ^[1]
• Healthcare associated Legionnaires’ disease which is also most commonly caused by L. pneumophila ^[2]
• Pittsburgh pneumonia which is caused by L. micdadei ^[3]

Legionella can skin infection soft tissue infection, endocarditis, wound infection, joint infection, and graft infection.

• Pontiac fever produces a mild, self-limiting, non-fatal illness without symptoms or radiologic findings of pneumonia. A comparison of Pontiac fever and Legionnaires’ disease is as follows:

Legionellosis may also be classified based on the infectious species responsible for the disease. Species of Legionella include:

• L. pneumophila
• L. feeleii
• L. sainthelensi
• L. micdadei

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

Legionella is often transmitted by aerosolized droplets produced from contaminated whirlpool spa, river, cruise ships, cooling towers, air conditioners, water supply systems . L. pneumophila usually invades the host cells and replicates intracellularly. Legionella is internalized using pseudopods and protects itself in a membrane-bound vacuole that does not fuse with lysosomes.

• Legionella is acquired by inhaling droplets from contaminated water sources such as faucets, showers, humidifiers, whirlpool spa, river, cruise ships, cooling towers, air conditioners, water supply systems ^[1]. L. longbeachae is thought to be transmitted by compost during gardening activity^[2]. However, it has also been seen in industrial coolers ^[3].
• Although is is believed that Legionella is not transmitted from one person to another person ^[4], there have been reports of person to person transmission ^[5].
• Healthcare-associated transmission of Legionella is common and has a higher mortality rate.

• Legionella are able to live within amoebic cells. Free-living amoebae may be responsible for enabling Legionella to better survive environmental hazards, adapt to living within macrophages, and may be a significant reservoir of Legionella. These amoebae may assist Legionella to remain undetected within the human environments ^[6].
• Legionella invades the host cells and replicates intracellularly.
• The internalisation of the bacteria can be enhanced by the presence of antibody and complement but is not absolutely required.
• A pseudopod coils around the bacterium in this unique form of phagocytosis.
• Once internalised, the bacteria surround themselves in a membrane-bound vacuole that does not fuse with lysosomes that would otherwise degrade the bacteria. In this protected compartment the bacteria multiply.
• The bacteria use a Type IVB secretion system known as Icm/Dot to inject effector proteins into the host.
• These effectors are involved in increasing the bacteria’s ability to survive inside the host cell. They also secrete a 39kDa metalloprotease into culture fluids, which is cytotoxic for some cultured tissue culture cells.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

L.pneumophila is a ubiquitous aquatic organism that thrives in warm environments (32°- 45°C). L. pneumophila is a pleomorphic, aerobic, catalase-positive, oxidase-positive, non-spore-forming, non-capsulated, motile, Gram-negative bacteria. Although Legionella is categorized as a Gram-negative bacterium, it stains poorly to Gram stain due to its unique lipopolysaccharide-content in the outer psuedospamodulating leaflet of the outer cell membrane.

• Bacteria; Proteobacteria; Gammaproteobacteria; Legionellales; Legionellaceae

• L.pneumophila is a ubiquitous aquatic organism that thrives in warm environments (32°- 45°C).
• L. pneumophila is a pleomorphic, aerobic, catalase-positive, oxidase-positive, non-spore-forming, non-capsulated, motile, Gram-negative bacteria.
• Although Legionella is categorized as a Gram-negative bacterium, it stains poorly to Gram stain due to its unique lipopolysaccharide-content in the outer psuedospamodulating leaflet of the outer cell membrane.^[1]
• Legionella is non-fermentative and is unable to hydrolyse gelatin or produce urease.
• At least 46 species and 70 serogroups of Legionella have been identified.

Legionella grow on buffered charcoal yeast enriched with L-cysteine ^[2]

• The natural habitat of Legionella is freshwater, where they often live within protozoa such as Vermamoeba vermiformis, Acanthamoeba spp., Tetrahymena pyriformis, and Naegleria spp ^[3]. It utilizes a similar method to enter and infect phagocytes ^[3].

• One of the unique characteristics of Legionella pneumophila is that is has the ability to thrive within a large variety of hosts ^[4].
• There are two major phases to the life cycle.

• The first is called the replicative phase. During this period, the bacteria are nonmotile and have a low infectivity.
• In the second phase, called the infectious phase, the bacteria are shorter and thicker.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ogechukwu Hannah Nnabude, MD

Legionnaires’ disease must be differentiated from other causes of fever, dyspnea, cough, and sputum production, such as bacterial pneumonia, viral pneumonia, and other causes of atypical pneumonia.

Legionnaires’ disease must be differentiated from other causes of fever, dyspnea, cough, and sputum production, such as bacterial pneumonia, viral pneumonia, and other causes of atypical pneumonia.^[1]

Disease	Clinical manifestation	Lab findings	Imaging findings	Chest X-ray
Legionnaires’ disease [2] [3] [4]	Dry cough High grade fever Bronchial breath sounds Asthenia Progressive dyspnea diarrhea Seizures and other neurological findings nausea, and vomiting Adult respiratory distress syndrome	Legionella urinary antigen positive Leukocytosis with relative lymphopenia Hyponatremia Hypophosphatemia	Alveolar consolidation on chest radiograph Lobar consolidation on chest radiograph
Q fever [5] [6]	Fever Dry cough Dyspnea Pleuritic chest pain myalgia headache	Antibody detection using indirect immunofluorescence (IIF) PCR C. burnetii cultivated on special media such as embryonated eggs or cell culture A two-to-three fold increase in AST and ALT	Multiple soft infiltrative shadows on CXR
Mycoplasma pneumonia [7] [8]	Dry cough Fever Pharyngitis Nausea and vomiting Sinus congestion Pleuritic chest pain Inflamed, opaque, hypomobile tympanic membrane	Lymphocytosis Cold agglutinins positive Positive CoNombs test Leukocytosis Thrombocytosis	Alveolar consolidation on chest radiograph Interstitial infiltrate on chest radiograph Lobar consolidation on chest radiograph
Chlamydia pneumonia	Associated with upper respiratory tract symptoms Associated with extrapulmonary maifestations such as: Meningitis Guillain-Barre syndrome	Normal WBC count Positive antichlamydial antibody
Acute interstitial pneumonia	Dry cough Progressive dyspnea	Nonspecific	Disseminated consolidation on chest radiograph Interstitial infiltrate on chest radiograph Increased uptake on gallium scan
Pneumococcal pneumonia	High grade fever Hemoptysis Fine rales Pleuritic chest pain Increased breath sounds Bronchial breath sounds Dullness on chest percussion Purulent sputum Shallow respiration Pectoriloquy Increased tactile fremitus Productive cough Egophony	Gram positive diplococci on sputum Gram stain Pleural effusion (exudative) Respiratory alkalosis	Parenchymal hyperlucency on chest radiograph Increased uptake on gallium scan Unilateral diaphragm elevation on chest radiograph Alveolar consolidation on chest radiograph Lobar consolidation on chest radiograph
Pneumocystis carinii pneumonia	Immunosuppressive state Subcutaneous emphysema Hacking cough Progressive dyspnea	Respiratory alkalosis Serum beta-D-glucan elevation	Alveolar consolidation on chest radiograph Lobar consolidation on chest radiograph Interstitial infiltrate on chest radiograph Pneumomediastinum on chest radiograph
Pulmonary embolism	Calf pain or swelling Decreased pulse pressure Dyspnea Hemoptysis Hyperventilation Immobility Increased pulmonic component of heart sound Pleuritic chest pain Prior DVT Pulmonary hypertension Right ventricular heave Right-to-left shunt Substernal chest pain Tachypnea Thrombophlebitis Venous stasis Bone fracture	D-dimer elevation Hypocapnia Hypoxia Pleural effusion (exudative or bloody) Atrial fibrillation on ECG Right axis deviation on ECG Right ventricular overload on ECG	Normal chest radiograph Atelectasis on chest radiograph Lobar consolidation on chest radiograph Prominent pulmonary artery on chest radiograph Hampton’s hump on chest radiograph Right ventricular enlargement on echocardiography Thrombus on echocardiography Segmental perfusion defect on lung scan V/Q mismatch on lung scan
Viral pneumonia	Pleuritic chest pain Bronchial breath sounds Recent influenza Fine rales Bronchovesicular breath sounds	Lymphocytosis Respiratory alkalosis	Lobar consolidation on chest radiograph Interstitial infiltrate on chest radiograph

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

The majority of cases of legionellosis are reported between the Summer and early Fall (between June and October). Approximately 8,000-18,000 individuals are hospitalized annually in the USA for Legionnaires’ disease with a case fatality rate ranging between 10% to 35%. The median case-patient age is 61 years, and the male to female ratio is 1.8 to 1.

• In USA, the incidence of legionellosis ranges between 1-3 cases per 100,000 individuals.
• Approximately 8,000-18,000 individuals are hospitalized annually in the USA for legionellosis.
• The incidence of legionellosis is believed to be increasing over the last 10-15 years.

• The case fatality rate of legionellosis ranges between 10% to 35%.
• Hospital-acquired legionellosis is associated with a higher case fatality rate compared with community-acquired legionellosis.

• The median case-patient age is 61 years.
• Patients of all ages may acquire legionellosis, but elderly patients older than 65 years of age are at higher risk.

• Males are slightly more likely to develop legionellosis.
• The male to female ratio is 1.8 to 1.

• There is no racial predilection to the development of legionellosis.

• The majority of cases of legionellosis are reported between the Summer and early Fall (between June and October).

• Although approximately 8,000 – 18,000 individuals are hospitalized with legionellosis in the U.S. each year, the disease is thought to be significantly under-reported with estimated of 2%-10% of cases being reported.
• In USA, legionellosis is a reportable condition in most states

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D., Serge Korjian M.D.

The most important risk factor in the development of legionellosis is recent exposure to either aerosolized water or contaminated water. Other risk factors include old age, concomitant lung disease, active smoking status, and immunosuppression.

Risk factors of legionellosis include:^[1]

• Exposure to aquatic enviroments: aerosolized water, contaminated drinking water, whirlpool spas, water supply systems, or cooling towers (most important risk factors)
• Old Age (> 50 years)
• Recent travel with an overnight stay outside of the home
• Current or former smokers
• Recent exposure to repairs or maintenance work on domestic plumbing
• Chronic lung disease (namely COPD)
• Diabetes mellitus
• Hepatic insufficiency
• Renal insufficiency
• Immunosuppression
• Malignancy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Legionnaires’ disease can be very serious and can cause death in up to 5% to 30% of cases. Most cases can be treated successfully with antibiotics [drugs that kill bacteria in the body], and healthy people usually recover from infection.

Current treatments of choice are the respiratory tract quinolones (levofloxacin, moxifloxacin, gemifloxacin) or newer macrolides (azithromycin, clarithromycin, roxithromycin). The antibiotics used most frequently have been levofloxacin and azithromycin. Macrolides are used in all age groups while tetracyclines are prescribed for children above the age of 12 and quinolones above the age of 18.
Rifampin can be used in combination with a quinolone or macrolide. Tetracyclines and erythromycin led to improved outcome compared to other antibiotics in the original American Legion outbreak. These antibiotics are effective because they have excellent intracellular penetration and Legionella infects cells. The mortality at the original American Legion convention in 1976 was high (34 deaths in 180 infected individuals) because the antibiotics used (including penicillins, cephalosporins, and aminoglycosides) had poor intracellular penetration. Mortality has plunged to less than 5% if therapy is started quickly. Delay in giving the appropriate antibiotic leads to higher mortality.

Pontiac fever requires no specific antibiotic treatment.

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