To the Editor: Rickettsia australis is the causative organism of Queensland tick typhus, also known as Australian spotted fever. It is an obligate, intracellular organism that invades endothelial cells, causing vasculitis.1,2 Its transmission to humans is via Ixodes tick species, which can occur along the east coast of Australia, but predominantly occur in the north-east.3 R. australis was previously thought to have a low complication rate; however, severe sequelae such as multiorgan failure, severe pneumonia and digital necrosis have emerged in recent years.1

A 54-year-old woman with type 1 diabetes presented to a rural hospital in Queensland with a 1-week history of vomiting, diarrhoea, rigors, and fevers to 39.4°C. Her blood sugar level on arrival was 31 mmol/L (reference range [RR], 3.0–7.8 mmol/L) and diabetic ketoacidosis was diagnosed.

Despite initial treatment, her condition continued to decline, and she was transferred to a tertiary referral centre. Her condition deteriorated into multiorgan failure, requiring ventilation and inotropic support. Triple antibiotic therapy comprising ciprofloxacin, meropenem and doxycycline was initiated.

Results of blood cultures for anaerobic and aerobic bacteria and a vasculitic screen were negative. The patient underwent serial chest x-rays, which demonstrated a resolving left lower lobe collapse/consolidation and a right-sided pleural effusion. Paired sera from Day 1 and Day 11 of admission to the tertiary hospital were tested in parallel for antibodies to R. australis. A rise in R. australis antibody titre, from 256 to 1024 (RR, < 32), supported a diagnosis of rickettsial disease. Serum from Day 1 was negative for antibodies to Mycoplasma, Leptospira, and Brucella species. A family conference later suggested that the patient may have been bitten by an insect; however, no suspicious lesion was identified. Her treatment was changed to intravenous doxycycline monotherapy, and slow improvement was noted.

Two days after admission, the patient developed widespread bullae and dermal necrosis with large areas of affected dermis sloughing off (Box), as well as digital and proximal foot ischaemia. A skin biopsy showed changes consistent with septic vasculitis. The patient was reviewed by a dermatologist, who concluded that it was unlikely to be from a drug reaction.

Thirty-six days after admission, she underwent bilateral below-knee amputations. Formalisation of the stumps was delayed to ensure viable tissue for coverage. Necrotic areas of her lower limbs and arms were also debrided and grafted, and seven of her fingers were amputated at the level of the proximal interphalangeal joint. The patient was discharged to a smaller centre for ongoing rehabilitation and support.

This case highlights the possible severity of R. australis infection, which can be complicated by septic shock, coagulopathy, multiorgan failure and digital gangrene. In addition, diabetes and the resultant ketoacidosis contributed to a compromised host and an unusually severe clinical course.

Bullae and dermal necrosis on the legs of a patient with severe rickettsial disease