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 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 15  |  Issue : 2  |  Page : 90-94

Scrub typhus in children


Pediatric Infectious Diseases, Department of Paediatrics, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication18-May-2017

Correspondence Address:
Winsley Rose
Department of Child Health, Christian Medical College, Vellore - 632 004, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_26_17

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  Abstract 


Scrub typhus is a mite-borne acute febrile illness caused by Orientia tsutsugamushi, and is transmitted by the bite of the trombiculid mite. It presents with high-grade fever which may be associated with nonspecific signs and symptoms such as rash, muscle and abdominal pain, headache, and lymph node enlargement. Scrub typhus is, therefore, one of the differential diagnoses to be considered in a child with acute undifferentiated febrile illness, especially if the disease is endemic to the region. The presence of a painless eschar at the site of the bite is an important pointer to the diagnosis. The illness responds well to antibiotics, usually within 48 h.

Keywords: Eschar, rickettsial disease, scrub typhus, scrub typhus treatment


How to cite this article:
Rose W. Scrub typhus in children. Curr Med Issues 2017;15:90-4

How to cite this URL:
Rose W. Scrub typhus in children. Curr Med Issues [serial online] 2017 [cited 2019 Nov 13];15:90-4. Available from: http://www.cmijournal.org/text.asp?2017/15/2/90/206516




  Introduction Top


Scrub typhus, caused by the Gram-negative bacterium of family Rickettsiaceae, is the most common rickettsial infection in India. The organism is classified under the “typhus group” of rickettsial diseases [Table 1]. It presents as an acute febrile illness which may be associated with nonspecific signs and symptoms. Scrub typhus is, therefore, one of the differential diagnoses to be considered in a child with acute undifferentiated febrile illness (fever with no specific differentiating features). Diagnostic laboratory investigations like the Weil–Felix test are inexpensive and widely available but have limited sensitivity. The diagnosis is based on a combination of clinical suspicion, endemicity of scrub typhus to the region, season of the year and is confirmed by laboratory investigations.
Table 1: Classification of rickettsial diseases

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Scrub typhus - Key points

  • Acute febrile illness caused by Orientia tsutsugamushi and spread by the bite of the larval form of the trombiculid mite.
  • It is one of the differential diagnoses to be considered in a child presenting with acute undifferentiated fever.
  • A painless eschar, enlarged liver or spleen, and thrombocytopenia are pointers towards the possibility of scrub typhus.
  • If scrub typhus is endemic to the locality, it is important to search for an eschar, especially in the folds of the axilla, neck, and groin.
  • Weil–Felix test has poor sensitivity. Scrub typhus IgM by ELISA is useful for confirmatory diagnosis, but is useful only after 5–7 days following onset of illness.
  • Treatment: Doxycycline (4.5 mg/kg/day in two divided doses up to a maximum of 100 mg twice daily for 7–14 days). Alternatives are azithromycin or chloramphenicol.



  Epidemiology Top


An estimated 1 billion people are at risk of scrub typhus and about 1 million cases are estimated to occur annually.[1] Scrub typhus is endemic in the so-called tsutsugamushi triangle [Figure 1].[2] It is a zoonotic disease, with humans being accidental hosts. Scrub typhus is becoming widespread in India with distinct seasonality.[3],[4],[5] The illness often has a seasonal increase in incidence. The season for scrub typhus around Vellore, South India is between August and January with the peak being in October and November. The trombiculid mite acts as the vector and reservoir of the infection, and the disease is endemic in certain regions or ecological patches which are conducive to mite populations. These regions are called “mite islands” and are usually associated with specific habitats such as abandoned plantations, shrubby areas at the borders of forests and fields, gardens or rice fields, forest clearings overgrown with shrubs, river banks, and grassy fields.[6],[7]
Figure 1: “Tsutsugamushi” triangle[2].

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  Causative Organism Top


Scrub typhus is caused by Orientia tsutsugamushi, a Gram-negative bacterium of family Rickettsiaceae. It is an intracellular pathogen, and many antigenic strains have been identified over the years from the original three strains (Karp, Kato, and Gilliam). Infection with one strain of the pathogen does not provide immunity to the other strains.


  Transmission Top


The organism is transmitted by the chigger (larval form) [Figure 2] of the trombiculid mite (genus Leptotrombidium).
Figure 2: (a and b) Chigger of trombiculid mite.

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The mites are small (0.2–0.4 mm size) and have a four-stage life cycle: egg, larva (chigger), nymph and adult [Figure 3]. Only the bite of an infected chigger transmits disease. The chiggers are usually found in dense scrub vegetation; the other stages are free-living in the soil. At the site of the mite bite, there is a characteristic painless black eschar that is useful for diagnosis, when discovered. Scrub typhus is transmitted only by vectors and not from person-to-person. The incubation period of scrub typhus is about 5–20 days (mean 10–12 days) after the initial chigger bite.[8]
Figure 3: Adult trombiculid mite.

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The mites act as the primary reservoirs for O. tsutsugamushi and once infected by feeding on the body fluid of mammals, they maintain their infectivity throughout their life stages by transovarial transmission and transstadial transmission.[9] Chigger mite populations can autonomously maintain their infectivity over a long period of time. In this way, mites are both the vector and the reservoir for scrub typhus.


  Clinical Features Top


Scrub typhus often presents as a febrile illness and should be considered as one of the differential diagnoses in a child with acute undifferentiated febrile illness (fever with no specific differentiating features), especially if the disease is endemic to the region [Table 2].
Table 2: Differential diagnoses for acute undifferentiated fever in children#,*

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The chigger seeks out moist areas of the body to bite, and after the bite often remains for 1–3 days. The bite is painless, and there may be a transient localized itch. A painless eschar [Figure 4], may be found at the site of the bite which is often found in the groin, axillae, genitalia, or neck (the features and distribution of eschars are discussed in greater detail below).
Figure 4: Painless eschar - a hallmark of scrub typhus diagnosis.

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There is an incubation period of 7–10 days before symptoms manifest. The illness begins with fever, headache, and generalized bodyache. Fever, vomiting, and abdominal pain are the most common symptoms; cough and difficulty in breathing may be seen in some individuals [Table 3]. A spotted rash on the trunk may be present. The examination may show liver and spleen enlargement in a significant proportion of those infected.[9] More virulent strains of O. tsutsugamushi can cause hemorrhaging and intravascular coagulation.
Table 3: Clinical features of scrub typhus in children

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  Complications Top


Complications may include atypical pneumonia, overwhelming pneumonia with acute respiratory distress syndrome (ARDS)-like presentation, meningitis, meningoencephalitis, myocarditis, hepatitis, acute renal failure, and disseminated intravascular coagulation. Sometimes palpable purpura (typical of vasculitis) may be seen. Occasionally, petechiae enlarge to form ecchymosis or gangrenous patches may occur. Rarely gangrene of digits, earlobes, scrotum, nose, or limbs may occur secondary to vasculitis and thrombosis.

[Figure 4] shows eschar at the site of chigger bite.


  Diagnosis Top


Infected individuals usually present with nonspecific symptoms and laboratory tests are nonspecific, especially in the early stages of the illness. The nonspecificity of presentation, the low index of suspicion and the poor availability of diagnostic tests often lead to delayed diagnosis and significant morbidity and mortality. Diagnosis of the illness, therefore, depends on clinical suspicion, presence of an eschar, epidemiological clues, and laboratory features (in the latter part of the illness).

Eschar

Finding an eschar is a very important clue to diagnosis and may be considered as a diagnostic hallmark. It is seen in about 20%–87% of cases.[9],[10] The eschar, similar to a scab that results from a minor trauma, is often small and painless.

The chiggers are more likely to bite the moist areas of the body. Hence a search for an eschar must be made, especially in the folds of the axilla, neck and groin, behind the ear, neck, and covered areas. It is preferable to remove clothes and undergarments/diaper of children for a thorough examination. The distribution of eschars in children and adults is given in [Table 4] and [Figure 5]. Children tend to have more eschars on the head, face, and neck when compared to adults.[9],[10]
Table 4: Distribution of eschar in children and adults

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Figure 5: Distribution of eschar.

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Epidemiological clues

Consider scrub typhus as a diagnosis, especially in regions where the disease is endemic.

Laboratory investigations

Thrombocytopenia (usually <100,000/mm [3]), low or normal leukocyte count and hyponatremia are clues to the early diagnosis. Liver enzymes (Aspartate Aminotransferase and Alanine Aminotransferase) are usually elevated and serum creatinine may also be elevated. Hypoalbuminemia is common.

Diagnostic investigations

Weil–Felix test, a heterophile antibody test based on the sharing of antigens between Rickettsia and Proteus can be done after 5–7 days from the onset of fever. An OX K titer of 1:80 or more is to be considered positive [Table 5]. The test has poor sensitivity (43%–59%) at a titer breakpoint of 1:80, but has very high specificity (94%–98%).
Table 5: Weil-Felix test - antibody response to antigens

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Scrub typhus IgM by ELISA can be done after 5–7 days of onset of fever with good sensitivity (93%) and specificity (91%).[11] Polymerase chain reaction for scrub typhus can be done from the eschar.[12]


  Treatment Top


The preferred drug for treatment of scrub typhus irrespective of age is doxycycline (4.5 mg/kg/day in two divided doses up to a maximum of 100 mg twice daily for 7–14 days). Alternative drugs that can be used are azithromycin (10 mg/kg/day for 5 days) or chloramphenicol (50–100 mg/kg/day in four divided doses for 7–14 days).

In India, it is recommended that if a child presents with undifferentiated fever of 5 days duration and malaria, dengue, and typhoid have been ruled out; the child should be administered doxycycline or azithromyicin. If the rickettsial infection is considered a possibility, it is recommended that antibiotics be started, without waiting for laboratory confirmation.[6]

Oral preparations are often adequate, though parenteral preparations of doxycycline and azithromycin may be useful in very sick children. With appropriate antibiotics, the patients typically become afebrile within 48 h of starting treatment.[13]


  Prognosis Top


If diagnosed and treated early, prognosis is good with very little mortality (about 3%) and almost no term morbidity. Mortality is often due to complications such as ARDS and multi-organ dysfunction.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Watt G, Parola P. Scrub typhus and tropical rickettsioses. Curr Opin Infect Dis 2003;16:429-36.  Back to cited text no. 1
[PUBMED]    
2.
Seong SY, Choi MS, Kim IS. Orientia tsutsugamushi infection: Overview and immune responses. Microbes Infect 2001;3:11-21.  Back to cited text no. 2
    
3.
Ahmad S, Srivastava S, Verma SK, Puri P, Shirazi N. Scrub typhus in Uttarakhand, India: A common rickettsial disease in an uncommon geographical region. Trop Doct 2010;40:188-90.  Back to cited text no. 3
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4.
Isaac R, Varghese GM, Mathai E, Manjula J, Joseph I. Scrub typhus: Prevalence and diagnostic issues in rural Southern India. Clin Infect Dis 2004;39:1395-6.  Back to cited text no. 4
    
5.
Mathai E, Rolain JM, Verghese GM, Abraham OC, Mathai D, Mathai M, et al. Outbreak of scrub typhus in Southern India during the cooler months. Ann N Y Acad Sci 2003;990:359-64.  Back to cited text no. 5
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6.
Rahi M, Gupte MD, Bhargava A, Varghese GM, Arora R. DHR-ICMR Guidelines for diagnosis and management of rickettsial diseases in India. Indian J Med Res 2015;141:417-22.  Back to cited text no. 6
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7.
Sharma P, Kakkar R, Kaore SN, Yadav VK, Sharma R. Geographical distribution, effect of season and life cycle of scrub typhus. JK Sci 2010;12:63-4.  Back to cited text no. 7
    
8.
Available from: http://www.searo.who.int/entity/emerging_diseases/ CDS_faq_Scrub_Typhus.pdf. [Last accessed on 2017 Mar 20].  Back to cited text no. 8
    
9.
Rose W, Rajan RJ, Punnen A, Ghosh U. Distribution of eschar in pediatric scrub typhus. J Trop Pediatr 2016;62:415-20.  Back to cited text no. 9
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10.
Kundavaram AP, Jonathan AJ, Nathaniel SD, Varghese GM. Eschar in scrub typhus: A valuable clue to the diagnosis. J Postgrad Med 2013;59:177-8.  Back to cited text no. 10
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11.
Blacksell SD, Tanganuchitcharnchai A, Nawtaisong P, Kantipong P, Laongnualpanich A, Day NP, et al. Diagnostic accuracy of the InBios scrub typhus detect enzyme-linked immunoassay for the detection of IgM antibodies in Northern Thailand. Clin Vaccine Immunol 2015;23:148-54.  Back to cited text no. 11
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12.
Kim DM, Kim HL, Park CY, Yang TY, Lee JH, Yang JT, et al. Clinical usefulness of eschar polymerase chain reaction for the diagnosis of scrub typhus: A prospective study. Clin Infect Dis 2006;43:1296-300.  Back to cited text no. 12
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13.
Sheehy TW, Hazlett D, Turk RE. Scrub typhus. A comparison of chloramphenicol and tetracycline in its treatment. Arch Intern Med 1973;132:77-80.  Back to cited text no. 13
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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  In this article
Abstract
Introduction
Epidemiology
Causative Organism
Transmission
Clinical Features
Complications
Diagnosis
Treatment
Prognosis
References
Article Figures
Article Tables

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