Rickettsia australis, the causative agent of Queensland tick typhus (QTT), is an obligate intracellular gram-negative bacillus endemic to the east coast of Australia. It is transmitted to humans via the tick vectors, Ixodes holocyclus and Ixodes tasmani. The pathogen displays vascular tropism for endothelial cells of small and medium vessels, leading to vascular necrosis, capillary permeability, and microhaemorrhages. Clinical features are non-specific, making diagnosis challenging. While QTT typically presents with a mild to moderate clinical course, cases of severe systemic vasculitis with life-threatening sequelae appear in the literature. This case underscores the consequences of delayed diagnosis of rickettsial infections and highlights the vascular tropism of R. australis, representing an important infectious aetiology of systemic vasculitis.
We report the case of a 72-year-old previously well female who presented with rapidly progressive systemic illness following a tick bite acquired in a rural endemic area. Her clinical course was initially characterised by a non-specific febrile illness with constitutional upset and an acral maculopapular rash followed by petechiae. Her course was marked by the development of profound endothelial dysfunction manifesting as severe small- and medium-vessel vasculitis, confirmed on CT angiography by the development of multiple visceral artery aneurysms. Catastrophic rupture of one such aneurysm led to a retroperitoneal hematoma. Concomitantly, she developed widespread vascular leakage with third-space fluid transudation into subcutaneous tissues pleural and peritoneal cavities, and progressed to acute respiratory distress syndrome (ARDS) and severe acute kidney injury (AKI). After exclusion of differential diagnoses, including primary idiopathic inflammatory vasculitides, definitive diagnosis was established via convalescent serology, demonstrating a more than fourfold rise in R. australis IgG titres, confirming acute rickettsial infection. Due to a delay in diagnosis, doxycycline was commenced at a late stage, by which time irreversible multiorgan failure had developed, resulting in death.
This case illustrates an uncommon but devastating presentation of R. australis infection, emphasising the organism’s capacity to induce severe vasculitic pathology with high mortality when not promptly recognised. Immunologists must maintain a high index of suspicion for rickettsial disease in patients presenting with systemic inflammatory responses and vasculitic features, with the teaching point that Rickettsial vasculitis can mimic primary idiopathic inflammatory vasculitides. Early empirical doxycycline remains paramount in preventing progression to irreversible organ damage and death.
