IMA Guidelines for Scrub Typhus Encephalitis

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Prof Dr Binay Karak, Prof Dr Bhupendra Chaudhary & Dr KK Aggarwal

Scrub typhus encephalitis is a mite- borne infectious disease caused by Orientia tsutsugamushi bacteria and transmitted by bite of larval mites (chiggers) is a re-emerging infection with significant morbidity and mortality, limited to region known as ‘tsutsugamushi triangle’ of south and south-east Asia.

Clinical features: Non-specific and includes high grade fever, severe headache, diffuse myalgia, gastrointestinal (vomiting and loose motions) and respiratory tract symptoms (cough and breathlessness), maculopapular rash and lymphadenopathy – all mimicking viral infectious disease. Later altered sensorium, delirium, confusion and seizure develop leading to aseptic meningitis to frank meningoencephalitis. It can cause multiorgan failure.

Scrub typhus lasts for 14 to 21 days without treatment. Death may occur as a result of these complications, usually late in the second week of the illness.

Rash: Approximately one-half of all patients develop a characteristically nonpruritic, macular or maculopapular rash. The rash typically begins on the abdomen and spreads to the extremities. The face is also often involved.

Eschar (pathognomonic or diagnostic clue): Seen in early phase of disease, at the site of chigger bite. It is a painless ulcer up to 1 cm with a black necrotic center (resembling the mark of cigarette burn) with surrounding hyperemia, mostly on exposed body parts like legs, neck, axilla, chest, abdomen and groin. Localized, and subsequent generalized lymphadenopathy, occurs in the majority of patients, and may be accompanied by inflammation of the lymphatic sinuses, splenomegaly, and portal triaditis.

In later stages atypical pneumonia, respiratory failure, ARDS and acute renal failure along with myocarditis complicates the disease.

Incubation period: Infection commonly presents as an acute febrile illness 7 to 10 days after the bite of an infected larval trombiculid mite (chigger).

Lab diagnosis
• IgM Elisa / Weil Felix reaction / PCR from eschar and blood.
• CSF findings are non-specific.
• Eschar biopsy if diagnostic in presence of lymphohistiocytic vasculitis.

Differential diagnosis: Malaria, dengue, leptospirosis and other rickettsial diseases

Treatment: Doxycycline is DOC (orally or IV)

Adults

• Doxycycline 200 mg / day in two divided doses for individuals above 45 kg for 7 days (orally or intravenously) or,
• Azithromycin 500 mg in a single dose for 5 days (orally or IV), or
• Chloramphenicol or Tetracycline 500 mg in 4 divided doses for 7 days (orally or IV)

Regimens as short as one day of doxycycline (400 mg given in two divided doses) have been effective in scrub typhus but are associated with an increased risk of relapse.

Doxycycline is contraindicated in pregnant women. The preferred agent is azithromycin (DOC) 500 mg in a single dose for 5 days

Children

• Doxycycline 4.5 mg/kg/day in two divided doses for children below 45 kg, or
• Azithromycin in single dose of 10 mg / kg for 5 days, or
• Chloramphenicol or Tetracycline 150 mg / kg / day for 5 days

If not treated early in the course, case fatality rate is as high as up to 60%.

Therapeutic diagnosis

Patients treated with appropriate antibiotics typically become afebrile within 48 hours of starting therapy. This response to treatment is useful diagnostically; failure of defervescence within 48 hours is often considered evidence that scrub typhus is not present. Delayed defervescence if present is associated with jaundice and relative bradycardia.

Prevention

There is no vaccine. Hence, prevention consists of chemoprophylaxis and mite control.

• Chemoprophylaxis: In endemic areas, a single dose of doxycycline (200 mg) weekly: started before exposure to 6 weeks after exposure

• Mite control: Application of insect repellants and miticide to both skin and clothing such as N, N, Diethyl-3-methyl benzamide (DEET), permethrin or benzyl benzoate, etc. Intensive efforts at rodent control may paradoxically increase the risk of human disease. In this setting, chiggers lose their preferred and normal hosts, thereby becoming more likely to bite humans.

• Early case detection, public education, rodent control and habit modification are other important preventive measures.