Abstract
Scrub typhus and its etiological agents, Orientia species, have been around for a very long time. Historical reference to the rickettsial disease scrub typhus was first described in China (313 AD) by Hong Ge in a clinical manual (Zhouhofang) and in Japan (1810 AD) when Hakuju Hashimoto described tsutsuga, a noxious harmful disease in the Niigata prefecture. Other clinicians and scientists in Indonesia, Philippines, Taiwan, Australia, Vietnam, Malaysia, and India reported on diseases most likely to have been scrub typhus in the early 1900s. All of these initial reports about scrub typhus were from an area later designated as the Tsutsugamushi Triangle—an area encompassing Pakistan to the northwest, Japan to the northeast and northern Australia to the south. It was not until the 21st century that endemic scrub typhus occurring outside of the Tsutsugamushi Triangle was considered acceptable. This report describes the early history of scrub typhus, its distribution in and outside the Tsutsugamushi Triangle, and current knowledge of the causative agents, Orientia species.
Highlights
Scrub typhus, a febrile disease with mild to life-threatening manifestations, is characterized by rapid onset of fever, headache, chills, arthralgias and myalgias and often the presentation of eschar prior to and a macularpapular rash following initiation of disease [1,2,3,4,5,6]
In 1915, a fever of unknown etiology among two individuals was reported in Saigon, Vietnam [50] to be a disease similar to that described in Deli, Sumatra, that was later determined to be scrub typhus [24]
These results suggested the presence of scrub typhus in eastern Africa
Summary
A febrile disease with mild to life-threatening manifestations, is characterized by rapid onset of fever, headache, chills, arthralgias and myalgias and often the presentation of eschar prior to and a macularpapular rash following initiation of disease [1,2,3,4,5,6]. Laboratory diagnosis at the time of illness is very difficult, as antibodies do not reach detectable levels for 5–10 days after disease presentation, and the level of orientiae in the blood stream demonstrable by molecular methods only reaches detectable levels sporadically during acute illness and is unapparent after initial treatment with appropriate antibiotic treatment [7]. The specimen of choice, biopsy of eschar and/or rash, is rarely obtained, though the level of Orientia DNA is in abundance, unaffected by prior antibiotic treatment, and maintained in the lesion for the life of the lesion [7]
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