To the Editor: Murine typhus (caused by Rickettsia typhi) has not been previously described in the state of Victoria, although it is well known in Western Australia, Queensland and South Australia.

In 2002, a 49-year-old man presented to Geelong Hospital, Victoria, with a 10-day history of fever, myalgia, rigors, headache, rash, sore throat, dry cough and pleuritic chest pain. On examination, he had a fever (temperature, 39.2°C), hypoxia (oxygen saturation, 91% in room air), tachycardia, a central maculopapular rash and conjunctivitis. Blood tests revealed hyponatraemia, thrombocytopenia, white cell count in the reference range, with left-shifted neutrophil change (toxic granulation and increased immature forms) and a C-reactive protein level of 377 mg/L (reference range, < 10 mg/L).

The patient lived on a hobby farm close to Geelong. Two weeks before becoming unwell, he had cleaned out the contents of a shearing shed, including two rotten sheepskins in which rats had been nesting. He reported generating a lot of dust and debris in the air. He had not noticed any tick, flea or other insect bites.

Serological testing was performed for rickettsia. Baseline serum, taken 10 days after symptom onset, showed antibodies to the typhus group of rickettsiae, R. typhi (murine typhus) and R. prowazekii (epidemic typhus), with a titre of 2000. The titre rose over the following 4 days to 64 000, a fivefold increase, diagnostic of typhus group infection. Antibody titre to the spotted fever group of rickettsiae was significantly lower (peak titre, 8000).

The patient was treated with oral doxycycline and recovered completely.

Murine typhus was first described in Adelaide in 19221 and is now considered endemic in parts of Western Australia and Queensland.2,3 A possible case reported from Melbourne4 was, in retrospect, probably Brill–Zinsser disease (relapsed epidemic typhus). Murine typhus has an incubation period of 8–16 days and is generally self-limiting, although fatalities have occurred.1 The disease typically presents with fevers, prominent myalgia, a central rash, nausea, conjunctivitis, and often significant pulmonary involvement. Unlike the tick-borne spotted fever group of rickettsiae, R. typhi is transmitted by rodent fleas. Transmission occurs either by aerosolisation and inhalation of infected flea faeces, often during demolition or cleaning of rat-infested environments, or, less commonly, by inoculation of faeces into a fleabite.

Murine typhus is usually diagnosed retrospectively by serological testing using microimmunofluorescence. Antibodies are usually detectable 7 to 9 days after disease onset, and IgG may persist for years. Cross-reactivity is seen between R. typhi and R. prowazekii; it is not possible to identify the pathogen by serological testing alone.5 Specific diagnosis is based on known local epidemiology and, as epidemic typhus does not occur in Australia, we believe this was a case of murine typhus, the first described in Victoria.