In March, 2010, a previously fi t and healthy 67-year-old man presented with an 8-day history of fever with rigors, intermittent confusion, lethargy, and shortness of breath. On admission, he was febrile with a temperature of 39°C and had clinical signs of a left-sided pneumonia, accompanied by general abdominal tenderness. His white blood cell count was 14·8×10/L (number of neutrophils was 11·3×109/L, and lymphocyles 0·2×10/L), and C-reactive protein concentration was raised at 475 mg/L. Renal, and liver function were abnormal: urea concentration was 21·6 mmol/L; creatinine 257 μmol/L; sodium 135 mmol/L; potassium 4 mmol/L; aspartate aminotransferase 115 IU/L; alanine aminotransferase 80 IU/L; and bilirubin 56 μmol/L. A chest radiograph showed complete opacifi cation of his left lung. We suspected an atypical or viral pneumonia; however, urinary legionella and pneumococcal antigens, PCR for infl uenza A and B, and microscopy and culture of endotracheal tube aspirate, were negative. We treated our patient with oxygen, intravenous fl uids, and antibiotics (amoxicillin-clavulanate and clarithromycin), but his respiratory function deteriorated, necessitating transfer to the intensive care unit for intubation. The day after presentation we did a bronchoalveolar lavage to obtain a sputum specimen; we then added levofl oxacin to his treatment. 3 days later, a positive culture result for Legionella longbeachae was confi rmed from growth on legionella-specifi c medium. When we questioned the patient to fi nd out the source of this infection, we discovered that he was a keen gardener and had lacerated his left index fi nger 2 days before the onset of his symptoms, while planting with compost; we presumed that this cut was the site of entry of the organism. Our patient continued to improve and was discharged to a respiratory ward 7 days later. He was discharged home in April, 2010, and was well at followup in May, 2010. Legionnaires’ disease is a common pneumonia that is usually caused by Legionella pneumophila (about 90% of cases); it can be readily diagnosed by urinary antigen testing. Legionnaires’ disease caused by L longbeachae is much less common, and outbreaks in the UK and the USA are sporadic. In the UK, nine cases have been reported since 1984; in the USA the majority of cases reported to the Centers for Disease Control and Prevention between 1990 and 1999 were in immunocompromised patients. L longbeachae has a much higher incidence in Australia, New Zealand, and Japan, where it accounts for about 30% of all cases of Legionnaires’ disease. The clinical presentation and prognosis of disease caused by these Legionella species are similar; however, L longbeachae cannot be detected by urinary antigen testing (which is sensitive only for serogroup 1 species), and disease caused by this organism generally has to be diagnosed by culture of a bronchoalveolar lavage sample. Previous case studies have shown compost to be a source of the infection. The antibiotic choice in the management of Legionnaires’ disease is the same whatever the causative organism. Most cases are resistant to β-lactam antibiotics, but are sensitive to macrolides or new quinolone antibiotics, such as levofl oxacin. Despite the low incidence of Legionnaires’ disease caused by L longbeachae in the UK and the USA, continued treatment with macrolides or quinolones in cases of severe community-acquired pneumonia may be prudent, particularly in those associated with exposure to gardening compost, until full culture results on legionella-specifi c medium are available. The UK Royal Horticultural Society has issued warnings about the risk of contracting Legionnaires’ disease from handling compost and has announced that bags of potting compost will carry cautionary statements.