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Table of Contents    
EDITORIAL
Year : 2015  |  Volume : 63  |  Issue : 2  |  Page : 130-132

Scrub typhus


Department of Neurology, Burdwan Medical College, Burdwan, West Bengal, India

Date of Web Publication5-May-2015

Correspondence Address:
Shyamal Kumar Das
Department of Neurology, Burdwan Medical College, Burdwan, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.156270

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How to cite this article:
Das SK, Dubey S. Scrub typhus. Neurol India 2015;63:130-2

How to cite this URL:
Das SK, Dubey S. Scrub typhus. Neurol India [serial online] 2015 [cited 2019 Oct 18];63:130-2. Available from: http://www.neurologyindia.com/text.asp?2015/63/2/130/156270


Scrub typhus, caused by Orientia (Ricketssia) tsutsugamushi ('tsutsuga' means 'small and dangerous' and 'Mushi' means insect or mite), is a zoonotic infectious disease that is transmitted to humans by an arthropod vector (mite) of the trombiculide family. The term 'scrub' is used because of the type of vegetation (the terrain between woods and clearings) that harbors the vectors. The endemic areas can also be sandy and semiarid lands and mountainous deserts. 'Typhus' comes from the Greek word meaning 'fever with stupor' or 'smoke.' [1]

Orientia tsutsugamushi
is an obligate intracellular, gram-negative organism that grows freely in the cytoplasm of the infected cells. Its life cycle is maintained by the transovarian transmission in trombiculide mites. After hatching, the infected larval mites (chiggers, the only stage that feeds on the host) inoculate the skin of organisms. Infected chiggers are particularly found in dense areas of scrub vegetation during the wet season, which is when the mites lay their eggs. [2]

Scrub typhus was first described in Japan in 1899. Scrub typhus is endemic in the 'Tsutsugamushi triangle' that extends from northern Japan and far-eastern Russia in the north, to northern Australia in the south, and to Pakistan in the west. It is a re-emerging disease in India. Scrub typhus is prevalent throughout India. Epidemic outbreaks of scrub typhus occurred in Assam and West Bengal during the Second World War. Outbreaks were also reported from the sub-Himalayan belt from Jammu to Nagaland and from Himachal Pradesh, Pondicherry, Tamil Nadu, Sikkim and Darjeeling. Outbreaks are usually in the rainy season; however, some outbreaks from South India were also reported during the winter months. [3],[4],[5]

Scrub typhus may present with myriad manifestations but most of the clinical signs and symptoms are non-specific and make the diagnosis difficult. The incubation period of scrub typhus ranges from 7-21 days. The classical clinical finding of the primary infection (present only in 30% patients) is a vesicular lesion at the site of the bite by the mite, that later converts into an eschar or an ulcer with an associated regional lymphadenopathy (the classical sites are the groin, axilla, genitalia and neck). However, secondary infection lacks the classical signs and symptoms. This fact, along with poor availability of diagnostic facilities, renders the clinical diagnosis difficult most of the times. The clinical spectrum is varied with most infections being of mild to moderate severity that include headache, cough, myalgia, bilateral hyperemic conjunctivae, lymphadenopathy and hepato-splenomegaly. The disease may get exacerbated with precipitation of an acute respiratory distress syndrome (ARDS). A low hematocrit, a high white blood cell count, a raised bilirubin and the delayed institution of antibiotic therapy are the risk factors for the development of ARDS. Apart from ARDS, its other complications include disseminated intravascular coagulation, meningitis and myocarditis. [6],[7],[8],[9],[10]

Central nervous system (CNS) involvement is often a prominent aspect of the clinical manifestations in scrub typhus infection presenting as meningitis or as meningo-encephalitis. CNS involvement occurs in 12.5-26% of the affected patients. [11],[12] The causative agent appears to enter the CNS by infecting the circulating monocytes during a meningeal inflammation or by directly invading the endothelium through the luminal membrane and then being released, through the basal cell membrane, into the perivascular space. [13] However, in the absence of a pathognomonic eschar, scrub typhus meningitis/meningo-encephalitis remains undetected and is often wrongly treated as pyogenic, viral or tuberculous meningitis. Other CNS complications of scrub typhus include seizures, opso-myoclonus, acute disseminated encephalomyelitis, transient  Parkinsonism More Details, acute transverse myelitis and coma. [14],[15],[16],[17] Cranial nerve deficits have been reported in up to 25% of patients, with the adbucens nerve being the most commonly involved nerve. [18] Trigeminal neuralgia, acute sensorineural hearing loss and facial nerve palsy have also been reported. [19],[20],[21] The reported peripheral nervous system complications include mononeuritis multiplex, brachial plexus neuropathy, polyneuropathy and Guillain-Barre syndrome. [22],[23],[24]

The diagnosis of scrub typhus is confirmed by immunoglobulin M (IgM) and enzyme-linked immunosorbent assay (ELISA) positivity and/or the presence of a pathognomonic eschar. Polymerase chain reaction (PCR) confirmation should be obtained, whenever feasible, including a PCR conducted on the cerebrospinal fluid (CSF) in patients with suspected meningitis/meningoencephalitis. The gold standard for its diagnosis is the indirect immuno-fluorescence antibody (IFA) test. The organism may be grown by inoculation of the patient's blood into tissue cultures or in mice but requires a minimum of 27 days for exhibiting significant growth. Other supportive blood tests such as the complete hemogram, liver function tests, renal function tests as well as chest radiographs and ultrasound of the abdomen should be done to exclude a multi-system involvement. [25],[26]

Doxycycline is the drug of choice. Azithromycin and cholamphenicol are effective alternatives. Azithromycin is also the drug of choice in children and in pregnant women. In resistant serotypes, rifampicin added as a supplemental therapy to azithromycin or doxycycline is effective. Weekly doxycycline is effective for chemoprophylaxis. No effective vaccine is available. In untreated cases, the mortality ranges from 0 - 30% and is significantly higher in patients with ARDS. [27],[28]

Abhilas et al in this issue, [29] reported that the mean duration of fever before presentation was of 9.3 ± 4.8 days. The presence of an eschar was documented in 27.3% of the patients with the common sites being the groin, genitalia, axilla, neck and infra-mammary folds. The most common presenting complaints were headache (64.2%), nausea/vomiting (60%), altered sensorium (53.7%) and seizures (22.1%). Although they also found a high C.S.F white blood cell count, high protein and low sugar in scrub typhus meningitis/meningo-encephalitis, only a high CSF protein level was found to be a predictor of mortality. They also observed that a multi-system involvement, especially the hepatic and pulmonary affliction, was associated with a graver prognosis. This is a comprehensive study and the results are consistent with the existing literature. This study is invaluable, as it has focused on the Indian scenario of scrub typhus that has been under-reported till date.

 
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