Murine typhus, also known as endemic typhus, is a flea-borne infectious disease with a worldwide distribution, caused by an obligate intracellular, gram-negative microorganism, Rickettsia typhi [1]. The transmitting agent of R. typhi is the rat flea, Xenopsylla cheopis, although the cat flea, Ctenocephalides felis, has also been implicated [1–4]. Main reservoirs are rats, house mice, opossums, skunks and cats [1–3]. The actual incidence of murine typhus is unclear, as the common clinical manifestations of the disease are non-specific [1,2]. In children, only a small number of studies have focused on the occurrence and on clinical profiles of the disease [3–5]. The aim of this study was to confirm the presence and to assess the clinical and laboratory characteristics of R. typhi infection among children in the area of Chania, Crete, Greece. Forty-one children were hospitalised with acute R. typhi infection in the Pediatric Department of the General Hospital of Chania, from 2001 through to 2006. All other causes included in the differential diagnosis were ruled out. Diagnosis of acute R. typhi infection was considered positive by the combination of compatible clinical features and an indirect immunofluorescence test (Biomerieux, Lyon, France), when specific IgM and ⁄ or IgG titres on admission were >1 ⁄ 400 and >1 ⁄ 960, respectively. All cases were reviewed retrospectively for demographic, clinical and laboratory findings, treatment and outcome. Most admissions (87.8%) occurred between May and October. The mean age was 9.8 years old (range, 1–15 years old). Twenty children (48.8%) were males. History of recent contact with animals was positive in 13 children (31.7%); all 13 children reported contact with cats and 10 ⁄ 13 reported contact with dogs. On admission all patients had fever. Common clinical characteristics were fever, rash, hepatomegaly, splenomegaly and anorexia. Main laboratory features included elevated aspartate aminotransferase and alanine aminotransferase, abnormal chest radiography, thrombocytopenia and leucopenia. CSF analysis in one patient with confusion did not reveal any abnormalities. Clinical and laboratory manifestations found on admission are presented in Table 1. Serologic testing through IFA performed on admission was diagnosed for all 41 children, with a median IgM titre of 1 ⁄ 3200 (range, 1 ⁄ 400 to 1 ⁄ 31200) and a median IgG titre of 1 ⁄ 2880 (range, 1 ⁄ 480 to 1 ⁄ 30720). All children were treated upon admission. Combination therapy was administered to two of them. Antibiotics administered were doxycycline in 19 children (46.3%), chloramphenicol in 12 (29.3%), quinolones in five (12.2%), cephalosporins in three children (7.3%), and a combination of trimethoprim ⁄ sulfamethoxazole and b-lactams in two children (4.9%). The outcome was favourable for all 41 patients; apyrexia was recorded on a mean of 4.9 days after admission (range, 2–12 days). The mean total duration of fever was 9.1 days (range, 3–17 days). No complication or relapse was observed within 1 month of follow-up.