More than four decades ago, Rickettsia australis was discovered to be the etiologic agent of Queensland tick typhus (QTT), yet many unanswered questions persist about the ecology, epidemiology, and clinical features of this disease. We review 46 previously published cases of QTT along with 16 cases discovered by active surveillance. QTT is usually a mild disease. Patients often have regional lymphadenopathy and eschars. Some have vesicular rashes. Because clinical features overlap, serologic tests are necessary to distinguish QTT from other endemic Australian rickettsial diseases (scrub and murine typhus). Only two tick vectors of R. australis have been identified: Ixodes holocyclus and Ixodes tasmani. Until rickettsiae are isolated from patients in Victoria and Tasmania, it remains unproven that spotted fever group infections in these locations are due to R. australis. However, available serologic, epidemiologic, and clinical data suggest that QTT is not confined to the area in which R. australis was first isolated (Queensland); rather, it occurs along a 3,200-km span of eastern coastal Australia, from tropical to temperate climates.

Adolescent↗

PubMedDate not supplied

Regulation of preglomerular microvascular 20-hydroxyeicosatetraenoic acid levels by salt depletion.

BACKGROUND: 20-hydroxyeicosatetraenoic acid (20-HETE) is the preeminent renal eicosanoid. The protean properties of 20-HETE - vasoactivity, mitogenicity and modulation of transport in key nephron segments - serve as the basis for the essential roles of 20-HETE in the regulation of the renal circulation and electrolyte excretion and as a second messenger for endothelin-1 (ET-1) and a mediator of selective renal effects of angiotensin II (AII). Renal autoregulation and tubular glomerular feedback are mediated by 20-HETE through constriction of preglomerular microvessels, particularly afferent arterioles. METHODS AND RESULTS: We had reported that rat preglomerular microvessels (PGMV; afferent-interlobular-arcuate/interlobular) in response to angiotensin II (AII) generate primarily 20-HETE and lesser quantities of 19-HETE. We have now addressed a possible link between the renin-angiotensin-system (RAS) and induction of cyclooxygenase (COX-2). As Na+ deprivation induces COX-2 expression/activity in the renal cortex and AII stimulates release of 20-HETE from PGMV, we used a stimulus, low dietary salt, to activate the RAS and COX-2 and thereby explore potential interactions involving 20-HETE and COX-2. CONCLUSIONS: The capacity of COX to metabolize 20-HETE to prostaglandin analogs e.g., 20-OH PGF2a and 20-OH PGE2, may be critical to modifying the renal vascular and tubular actions of the eicosanoids.

Animals↗