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Table of Contents 
Year : 2017  |  Volume : 62  |  Issue : 5  |  Page : 468-477
Tropical diseases on insurgence: Clinician's perspective

1 Department of Medicine, College of Medicine and Sagar Dutta Medical College, Kolkata, West Bengal, India
2 Department of Dermatology, Dr. B. C. Roy Postgraduate Institute of Paediatric Sciences, Kolkata, West Bengal, India

Date of Web Publication22-Sep-2017

Correspondence Address:
Nilendu Sarma
Associate Professor and Head, Department of Dermatology, Dr. B C Roy Postgraduate Institute of Paediatric Sciences, 111, Narkeldanga Main Road, Phoolbagan, Kolkata - 700 054, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijd.IJD_380_17

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Many known and unknown factors play a synergistic role in the emergence or re-emergence of some infections in a particular area or country. In recent years, India has seen a significant increase in the prevalence of many viral or bacterial diseases. Many are vector borne and are zoonotic disease while others have different source and mode of transmission. These diseases are often associated with high morbidity and mortality. Five important diseases such as leptospirosis, dengue, chikungunya, Japanese encephalitis, and leishmaniasis have been discussed in this article.

Keywords: Chikungunya, Dengue, emerging infections, Japanese Encephalitis, Leptospirosis, Leishmaniasis, Tropical Diseases

How to cite this article:
Chatterjee P, Sarma N, Hansda S. Tropical diseases on insurgence: Clinician's perspective. Indian J Dermatol 2017;62:468-77

How to cite this URL:
Chatterjee P, Sarma N, Hansda S. Tropical diseases on insurgence: Clinician's perspective. Indian J Dermatol [serial online] 2017 [cited 2020 Jul 14];62:468-77. Available from:

What was known?
India is a tropical country and is a major contributor in terms of population and geographical area in the south East Asia, which is considered one of the niche areas for the emerging infectious diseases in the world.

   Introduction Top

An emerging disease is one that has appeared in a population for the first time or that may have existed previously but is rapidly increasing in incidence or geographic range as described by the WHO. Over the past century, with the advent of newer vaccines, antibiotics and improved sanitation have made us able to control many infectious diseases. However, in the last 20 years, there is emergence or increased incidence of certain other infections in defined geographic area and beyond which is becoming a serious matter of concern in the current situation. With the changing climatic condition, the development of drug resistance and various other contributory factors existing organisms are able to infect new host population in a more virulent form. In the recent past, India was hit by many large outbreaks of emerging infections mostly zoonosis. Currently, 22 States and Union Territories of India have reported cases of chikungunya. Although mortality is not common, significant morbidity was caused due to persisting joint disease after 2006 epidemic in India.[1] Acute encephalitic syndrome was another fatal disease with rising incidence in the last 5 years mostly in Uttar Pradesh, Bihar, Assam, and West Bengal, etiology of which remained undetermined in most cases with Japanese encephalitis (JE) attributable in few. Here, we discuss few important infectious diseases that have achieved the designation of emerging infections due to their significant increase in prevalence over the last decade in India and surrounding areas.

   Leptospirosis Top

Leptospirosis is a water-related zoonotic disease contracted through breach in the skin or mucosa by exposure through water contaminated by urine from infected animals, most commonly rodents and rarely other wild and domesticated animals. Human-to-human transmission is rare. Outdoor, agricultural, sewage workers and recreational swimmers are particularly at risk, especially during rainy season. Epidemics may occur during flooding, driving the rodents toward human habitats.

   Etiology Top

Leptospira interrogans is the causative bacteria for leptospirosis, an acute and generalized febrile illness due to vasculitis with varied clinical manifestations ranging from asymptomatic disease to severe multisystem failure due to infections from different serovars (over 200).[2] Clinically, the symptomatic cases have been divided into two groups, namely, anicteric and icteric also called Weil's disease.

Leptospirosis has a variable incubation period of 3–21 days though most of the cases develop within 3–14 days but never after 4 weeks. It is a two-stage disease – first stage called septic phase and lasts for 3–7 days during which the bacteria spreads through blood and different body fluids such as cerebrospinal fluid (CSF).[3],[4] All cases have identical initial symptoms with sudden onset of flu-like disease – intense headache, fever ≥102°F, conjunctival congestion, fatigue, photophobia, acalculous cholecystitis in children, myalgia and soreness (especially back and calf muscles), and a characteristic pinprick/petechiae skin rash mimicking meningitis, developing in the first 2–3 days of illness over any part of the body but most commonly over pressure areas such as the lower extremity.

Clinical features

After a few days of apparent recovery, a few patients with more severe disease enter the second phase (called tissue or immune phase with the clearing of bacteria from blood and intermittent bacterial positivity of CSF and other tissues), with reappearance of initial symptoms and fatigue, psychosis, renal impairment, and meningitic features. One out of ten patients develops very severe infection (depending on the strength of bacterial inoculums, virulent serovar such as icterohemorrhagiae, Batavia, Lai, and poor host immune status) called Weil's disease with hepatic, renal, and multisystem failure occurring rapidly within 10 days and may develop these without any intermittent apparent recovery. Jaundice and renal failure are prominent features. Myocarditis and pulmonary infiltrates are also seen. Hemorrhages from different orifices even internal bleeding are common.[5] These cases can be fatal in up to 40% cases if not properly treated early.

Most patients recover after initial stage within 6–12 weeks. Severe cases may take longer to recover. Immunity after an illness is serovar specific and rarely lasts longer than 10 years.

   Diagnosis Top

Diagnosis in mild cases needs physician's awareness as they mimic flu. During the initial stage, dark-field examination or cultures of blood or CSF may demonstrate the bacteria. During the immune phase, culture is only possible from urine. Serological tests such as IgM ELISA,[6] macroscopic slide agglutination, microscopic agglutination with an initial titer of 1:100, or fourfold rise of titer in paired sera collected 14 days apart are helpful in diagnosis. Blood count reveals anemia with neutrophilic leukocytosis. Severe infections will cause thrombocytopenia. Urinalysis always reveals albuminuria though it may be transient. Proteinuria and hematuria are common. Conjugated hyperbilirubinemia with raised transaminases, raised serum creatinine, and creatinine phosphokinase completes the picture.

   Prevention Top

Protective clothing, wearing protective gloves, and avoidance of potentially infected waters are recommended preventive measures.


Treatment is based on high index of suspicion and should not wait for the confirmation of the diagnosis by laboratory means. Effective antibiotic therapy initiated within 7 days of illness is the cornerstone of therapy. Chloramphenicol, penicillin derivatives, erythromycin, doxycycline, tetracycline, and ceftriaxone [7] have been used effectively. Penicillin may cause Jarisch–Herxheimer reaction in few cases.[8],[9] Postexposure prophylaxis with doxycycline has reduced the incidence of symptomatic disease.[10]

   Dengue Top


Currently, dengue is endemic in more than 125 countries worldwide with about 75% or more disease burden borne by the South-East Asia Region including India and the Western Pacific region [Figure 1]. Since its first reported outbreak in India in 1946, incidence is increasing day by day with outbreaks in almost every corner of the country such as Andhra Pradesh, Delhi, Goa, Haryana, Gujarat, Karnataka, Kerala, Maharashtra, Rajasthan, Uttar Pradesh, Pondicherry, Punjab, Tamil Nadu, West Bengal, and Chandigarh in 2005–2008 [Table 1].
Figure 1: Global dengue outbreaks distribution from 1990–2015. (Reproduced from Guo C, Zhou Z, Wen Z, Liu Y, Zeng C, Xiao D et al. Global Epidemiology of Dengue Outbreaks in 1990-2015: A Systematic Review and Meta-Analysis. Front Cell Infect Microbiol. 2017 Jul 12;7:317)

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Table 1: Yearly prevalence of various dengue serotypes in India

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   Etiology and Vector Top

Dengue is a febrile, Aedes aegtpti mosquito-borne viral illness caused by one of the four antigenically distinct type of dengue flaviviruses (1–4).[11] A patient can be infected with any two or even all four types of dengue virus and can be reinfected once in a lifetime. Apart from mosquito bite, infrequently possible mode of transmission of dengue that has been reported in various literatures is transfusion of blood from an infected donor, injuries by infected sharps to health-care workers, transplantation of organs and tissues from infected donors, and from infected pregnant mother to her fetus by vertical transmission.[12],[13],[14]

Clinical features

Clinical presentation following dengue infection can vary from asymptomatic disease to undifferentiated fever (or viral syndromes), classical dengue fever (DF), dengue hemorrhagic fever (DHF), or dengue shock syndrome, and expanded dengue syndrome.[15],[16] However, with this criterion, some patients with severe dengue manifestation and those with multiorgan failure were missed, so modification in these are being made subsequently such as in 2009 by the WHO [17] and later by the Centers for Disease Control and Prevention [18] in 2015 which includes one extra category – dengue-like illness [Table 2].
Table 2: Dengue case classification - - World Health Organization 2009[16]

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Acute febrile illness with clinical features matching with the case definition of a probable case of dengue as described by the WHO is included in dengue-like illness. Infections such as leptospirosis, malaria, enteric fever, scrub typhus, hantavirus, and chikungunya may have dengue-like presentation, especially during the initial phase of infection. In a study by Suharti et al. ,[19] only about 49% of the total patients tested positive for dengue infection serologically and the rest 51% negative for dengue though all of them had initial features simulating a probable dengue case.

In the febrile phase, symptoms abruptly begin with a high (≥101°F) fever with chills and any two of the four symptoms, namely, severe frontal headache, retro-orbital pain, severe myalgia of back and extremities and arthralgia (termed breakbone) along with nausea, vomiting, abdominal pain, and rarely diarrhea. Sore throat, prostration, and depression are followed by conjunctival congestion and prominent flushing of skin due to cutaneous vasodilation. Initial fever subsides within 4–7 days followed by remission of few hours to few days. Mild hemorrhagic signs such as mucosal bleeding from cheeks and gums and menorrhagia may be seen.[20] Tender hepatomegaly may occur after few days of fever. Progressive leukopenia at this stage should alert the physician to high probability of dengue fever. The tourniquet test, which is positive in ≥50% cases, is a specific test for DF, done by inflating the blood pressure cuff for 5 min over the arm and looking for ≥3 petechia/cm 2 area [Figure 2].
Figure 2: Course of dengue illness. (Reproduced from: Wikipedia, [available online - Accessed on 02.08.2017])

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Four out of five patients develop skin eruptions during the remission of fever. Half of the patients develop a centrifugal macular, maculopapular, scarlatiniform, or petechial eruption [21] typically starting over the dorsum of hands and feet, gradually involving the extremities and torso, and typically sparing the face. The rash may become confluent with small round island-like areas of sparing called white islands in the red sea.[22],[23] The eruption lasts 2 h to several days [Figure 3].
Figure 3: Confluent erythema on the limbs in a child with dengue fever. (Image courtesy Dr. Sandip Sen, Associate Professor, Department of Pediatrics, Dr. B C Roy Post Graduate Institute of Pediatric Science)

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As the fever starts to subside around 3–7 days of illness, there is increased capillary permeability which results in raised hematocrit.[24] Patients without capillary leakage usually improve while those with leakage become worse at this stage. Plasma leakage is variable, and degree of rise of hematocrit above baseline reflects the degree of leakage.

Patients with DHF may have any of the four hemorrhagic manifestations – petechia, purpura, ecchymoses, and epistaxis. Shock, preceded by warning sign of subnormal temperature, is due to significant plasma leakage caused by capillary permeability. Organ hypoperfusion due to prolonged shock result in metabolic acidosis, multiorgan dysfunction (severe hepatitis, encephalitis, and myocarditis ± bleeding), and disseminated intravascular coagulation leading to severe hemorrhage and a fall in hematocrit and rise in leukocyte count may occur.

   Diagnosis Top

Diagnosis of dengue infection can be made both by direct and indirect methods. Direct method includes virus isolation, NS1 antigen detection, and reverse transcriptase-polymerase chain reaction (RT-PCR) for viral genome. Among these, virus isolation and RT-PCR need to be done during the early phase of infection [25] whereas NS1 antigen is positive in the beginning as well as later part of infection.[26],[27] Indirect serological test detects dengue IgM and IgG antibody after around 4–5 days of illness

   Treatment Top

Maintaining intravascular fluid volume by the management of fluid and electrolyte balance and monitoring platelet count and hemodynamics is the cornerstone of therapy. Antipyretics and oral fluids are important. Nonsteroidal anti-inflammatory drugs (NSAIDs) must be avoided lest it may precipitate thrombocytopenia and bleeding. Severe cases may require platelet transfusion. Treatment depends on severity of dengue. More severe cases including unconscious or disoriented patients have to be admitted in high dependency units or intensive therapy units for close observation. These patients may need intravenous fluid therapy, plasma transfusion, or blood transfusion depending on the stage of dengue severity. Renal failure may need support in the form of hemodialysis. Adult respiratory distress syndrome patients may need ventilator support. Liver dysfunction, in most cases, is self-limiting except in severe cases which need appropriate support.

   Chikungunya Top

Chikungunya, first described in 1952–1953 in Makonde plateau of Tanzania,[28] is derived from the Swahili/Makonde word “Kunqunwala,” meaning “to become contorted” or “that which bends up.”

   Etiology and Vector Top

Caused by the bite of Aedes mosquito transmitting the enzootic Togaviridae virus chikungunya, it stands for both the virus (chikungunya virus [CHIKV]) and the disease, characterized by fever, headache, myalgia, rash, and prominent acute and persistent arthralgia. In Africa and Asia, Aedes aegypti and the Aedes albopictus are the predominant vectors of infection.[29],[30]

CHIKV in times of epidemic can circulate between human and mosquito without the need for any animal reservoir. Asymptomatic infection is very rare. The incubation period ranges from 1 to 12 days with the average being 4-5 days. This is followed by chickungunia fever with sudden onset of high fever, severe arthralgia, myalgia,[31],[32] headache, photophobia, and rash,[33] sharing many features with DF.

   Clinical Features Top

The skin rash of chickungunia is present in half of affected patients' torso, limbs, and face, most commonly affecting the limbs with transient maculopapular rashes [34] lasting 2–3 days with occasional pruritus [Figure 4]. Other less common skin lesion includes aphthous-like ulcers, vesiculobullous lesions with desquamation, and vasculitic lesions.
Figure 4: Typical rash of chikungunya on limbs. (Reproduced from: Wikipedia. Available online, accessed on 02.08.2017)

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The polyarthralgia is very prominent, with symmetrical involvement of joints of midtarsal region, foot, ankles, knees, small joints of hands, wrist, and elbow.[35],[36],[37] There is swelling of joints but no other signs of inflammation. Joints already damaged by underlying disorder such as osteoarthritis are particularly prone to become involved. The acute signs and symptoms resolve in 1–2 weeks though the arthralgia can persist for months to years significantly impairing the quality of life.[38] Advanced age more than 45 years, severe pain at onset, and underlying disorders are the most common factors that predict the persistence of arthralgia.

Systemic features such as nausea, vomiting, and abdominal pain are uncommon. Although not neurotropic, rare neurological complications such as encephalopathy, acute flaccid paralysis and Guillain-Barre syndrome, malaise, encephalitis, and meningoencephalitis have been reported. Underlying disorders such as stroke, diabetes, epilepsy, and hypertension may increase the likelihood of neurological complications. Children are most susceptible for neurological sequel. Conjunctivitis, cardiovascular disorders, pneumonia, prerenal failure, and respiratory failure are other rarer systemic features.

Fatality, though rare, is due to heart failure, multiorgan failure, hepatitis, and encephalitis, mostly in neonates and elderly.

   Diagnosis Top

Diagnosis is based on clinical, epidemiological, and laboratory criterion. Acute onset of fever with severe polyarthralgia not explained by other medical disorders is a possible CHIKV infection. If the person comes from an endemic area, the case is classified as probable.[39] Laboratory confirmation is essential as the dengue, other alphaviral infections and endemic malaria are close differentials. Detection of viral nucleic acid by RT-PCR [40] in serum samples 1 day before the onset of symptoms up to the 7th day of illness, isolation of the virus, or detection of the antibody response confirms the diagnosis in acute phase. Later in the illness, diagnosis is confirmed by the detection of an immunological response, either an IgM antibody detectable as early as the 2nd–7th day of illness [36] or a fourfold rise of IgG antibody in paired sera drawn 2 weeks apart. IgG antibody persists for years, but IgM antibody usually becomes undetectable by 3–4 months but may rarely persist for 24 months.

   Treatment Top

NSAIDs are the cornerstones of treatment. Short course of low-dose oral steroids has shown to reduce the severity of pain without affecting the disease outcome in a South Indian cohort. Passive transfer of immunity by CHIKV antibody as a prophylactic measure, chloroquine, and ribavirin is being explored as treatment options. Chloroquine is not recommended as it may interfere with protective antibody response. Ribavirin has shown moderate activity in reducing pain and swelling in chronic arthralgia, however, in small cohorts.[41]

Several vaccines were tried. Live-attenuated and inactivated vaccines, DNA vaccines, alpha-virus chimeras, and virus-like particle vaccines which might offer advantages over inactivated and live-attenuated CHIKV vaccines in terms of efficacy or safety are in several stages of development. Recently, a live recombinant measles-virus-based chickungunia vaccine, which had good immunogenicity, even in the presence of antivector immunity, was found to be safe with a generally acceptable tolerability profile in a double-blind, placebo-controlled, active-comparator, dose-escalation phase I first-in-man trial, placing it as a strong contender for candidate vaccine in man.[42]

   Leishmaniasis Top


The protozoan disease Leishmaniasis, caused by Leishmania donovani , is transmitted to humans by female phlebotomine sandfly (Phlebotomus argentipes ) bite as anthroponotic or zoonotic transmission and has been endemic in the Indian subcontinent since ancient times. Leishmaniasis thrives in poverty,[43] ignorance, lack of health infrastructure, and apathy of pharmaceuticals toward the development of new drugs because of poor prospect of financial gains. Cutaneous leishmaniasis has reached epidemic proportions in Afghanistan and Pakistan and visceral leishmaniasis (Kala-azar in Hindi-black fever, referring to diffuse black pigmentation often seen) in India and Sudan. Bihar (31 districts), West Bengal (6 districts), Jharkhand (4 districts), and Uttar Pradesh (11districts) are highly affected states by this disease. Furthermore, more than 70%–80% Kala-azar cases are reported from Bihar, especially North Bihar; Bihar itself contributes >50% of visceral leishmaniasis load of the world. Darjeeling, Malda, Murshidabad, South 24 Parganas, Nadia, and Hooghly are the affected districts in West Bengal in that order

Etiology and vector

Initiation of infection is by bite of infected female sandflies which inoculates the flagellated promastigote into the skin. These promastigotes are then taken up by immune cells including neutrophils and macrophages where transformation to amastigote occurs which subsequently infects more neighboring cells or distant cells by dissemination. Local and systemic inflammation develops in susceptible patients but is ineffective

   Pathogenesis Top

Both innate and acquired immunities are activated together. Plasma Concentration of specific IgG antibody is highest in chronic nonhealing mucocutaneous and visceral diseases though these antibodies are not protective. Parasitized dendritic cells activate CD4+ and CD8+ cells which take part in cell-mediated immune response producing an inflammatory response and forming granuloma. Th1 response induces macrophage activation and also prevents recrudescence of latent, chronic infection. Th2-associated cytokines such as interleukin-4, -10, -13 and transforming growth factor-beta are also activated and thus limit macrophage activation but foster intracellular infection. The inflammatory response is not polarized in either Th1 or Th2 lines as both coexist. In progressive nonhealing infections such as chronic mucocutaneous and visceral infections, suppressive Th2 predominate over Th1 cell-mediated immunity in either situation is ineffective. The suppressive Th2 response does not extinguish clinically apparent persistent inflammation, the hallmark of leishmaniasis infection.

   Clinical Features Top

The clinical presentation following infection may range from subclinical infection, localized skin lesion, to disseminated infection (cutaneous, mucosal, or visceral) which varies further by endemic region. Diverse parasite (infectivity, pathogenicity, and virulence) and host factors (age, nutritional state,[44] innate, and acquired T-cell-dependent immune responses) and immune-inflammatory response of the host [45] determine the clinical outcome. Tissue macrophages harbor residual parasite lifelong even after treatment.

Expression of visceral infection may be asymptomatic, oligosymptomatic to fully developed Kala-azar. Infection may be either be newly acquired or relapse (usually 6–12 months after successful treatment) or recrudescence from old infection. Relapse may be spontaneous but more often due to some CD4+ T-cell reducing conditions such as antirejection therapy in transplant recipients, steroid therapy, or concurrent HIV infection.

Kala-azar often presents with prolonged fever, pallor, hepatomegaly with remarkable splenomegaly, preserved appetite with significant weight loss, epistaxis, diarrhea, and growth retardation, especially in children. Blackening of skin is characteristic. Anemia, leukopenia, and thrombocytopenia with hypergammaglobulinemia are almost always found. With time, malnutrition and secondary infection sets in preparing the stage for death.

   Diagnosis Top

Gold standard for diagnosis is demonstration of amastigote in clinical specimen from tissue aspirates, sensitivity of which varies according to the tissue selected – splenic (95%), bone marrow (55%–97%) and lymph node (60%).[46],[47],[48],[49] In endemic and epidemic [46],[50],[51] situations, anti-leishmania IgG antibody demonstration by direct agglutination test is also helpful diagnostically. Recently, freeze dried antigen and antibody against K39 antigen detected immunochromatographically [47] in finger prick blood giving excellent rapid results. In symptomatic patients, anti-K39 strip test has high sensitivity (90%–100%)[47],[51],[53] and variable specificity depending on the region.[47],[53],[54],[55] This test obviates the need for invasive tests and can easily be used in Indian visceral leishmaniasis and in Kala-azar dermal leishmaniasis.

   Treatment Top

Till recently, intramuscular antimonial compounds were the benchmark for visceral leishmaniasis treatment. However, widespread development of resistance, particularly in Bihar,[56] has paved the way of intravenous liposomal preparation of amphotericin B for 5 to 10 days,[57] to take the center stage of treatment though prohibitive cost is definitely a factor. Even a single liposomal amphotericin B infusion can provide 90% long-term cure rate. Oral miltefosine [58] is a significant advancement in therapeutic armamentarium as this self-administered drug is also effective in antimony-resistant cases. Paromomycin has completed phase III level testing in India and promises to be a cheap, highly efficacious, minimally toxic 21-day course option. Pentamidine is toxic and much hyped oral. Sitamaquine has failed to demonstrate added benefit when given in conjunction with standard treatment.

   Japanese Encephalitis Top


JE is one of the most important viral encephalitides in Asia. Sporadic cases have been reported in northern Australia and parts of the Western Pacific. This is seen in areas where rice culture and pig farming coexist; thus, it is seen in rural areas mostly [Figure 5].
Figure 5: Countries or areas at risk for Japanese encephalitis. (Reproduced from World Health Organisation 2012, available online Accessed on 07.08.2017)

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First detected in India in 1955 from patients coming from North Tamil Nadu and adjoining Karnataka,[59] and since its first outbreak in 1973 in West Bengal, it has spread to Uttar Pradesh, Assam, Manipur, Karnataka, Bihar, Andhra Pradesh, Goa, Pondicherry, and recently from Kerala and Maharashtra.[60],[61],[62],[63],[64]

Males are affected more than females. In North India, all age groups are affected, but children below 15 years of age [65] are preferentially affected in Southern states. Although 15 different mosquitoes of genera Culex, Aedes, or Anopheles transmit the virus to humans. Culex vishnui and Culex tritaeniorhynchus are the main vectors and Culex seudovishnui and Anopheles subpictus are some secondary vectors in India.[66],[67],[68] The infection is enzootic with pigs as amplifying host and ardeid birds as maintenance host. Human infections are a dead end as no man-to-man transmission is possible because of transient viremia, and most of the vector mosquitoes do not feed on humans by choice. The mosquito thrives in stagnant water, paddy fields, ditches, pools, and puddles; thus, infection is highest in monsoon season in areas where pigs, ardeid birds, and human habitat are in proximity.

   Etiology and Vector Top

JE is a mosquito-borne encephalitic syndrome caused by different mosquito-borne flaviviruses.

   Clinical Features Top

Although the infection is mostly asymptomatic, the true burden is manifold as for every symptomatic case; there are about 500 asymptomatic cases. The incubation period is 5–15 days. The clinical picture can be divided in three stages, a prodromal stage characterized by nonspecific febrile presentation with nausea, vomiting, diarrhea, and cough, an acute aseptic meningitis to encephalitic/meningoencephalitic stage with prominent CNS features such as cerebellar signs, cranial nerve palsies, and cognitive and speech impairments and continuing fever, and a late stage marked either by recovery or persistence of symptoms leading to acute flaccid paralysis [69] or neuron injury causing permanent squealae. A parkinsonian presentation [70] and seizure are typical in severe encephalitic cases. Even after recovery from the primary illness, some patients may develop neuropsychiatric sequelae with cognitive and language impairment which ends up as a cause of an immense social and financial burden, especially for a developing country

   Diagnosis Top

Diagnosis is by (i) virus isolation and propagation by tissue culture, infant mouse inoculation, or mosquito inoculation, or by (ii) antigen detection by antigen capture ELISA or immunofluorescence test, (iii) serological tests by hemagglutination inhibition, ELISA (IgG/IgM), or neutralization, and (iv) genome detection by PCR.[71]

   Prevention Top

Vector control, sanitation, health education, and early diagnosis and treatment are cornerstones of this acute encephalitic syndrome.

   Treatment Top

Treatment is symptomatic with no specific treatment available. Vaccine is available for travelers to endemic region or population at risk in an endemic/epidemic region. Two intramuscular doses of vaccine given 28 days apart are effective with the last dose at least 1 week before travel or expected time of infection. Indian Government has announced 100% immunization of children with JE vaccine as topmost priority.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Krishnamoorthy K, Harichandrakumar KT, Krishna Kumari A, Das LK. Burden of chikungunya in India: Estimates of disability adjusted life years (DALY) lost in 2006 epidemic. J Vector Borne Dis 2009;46:26-35.  Back to cited text no. 1
World Health Organization-International Leptospirosis Society. Human Leptospirosis: Guidance for Diagnosis, Surveillance and Control; 2003. Available from: [Last accessed on 2006 Aug 02].  Back to cited text no. 2
Green-McKenzie J. Leptospirosis in Humans; 2005. Available from: [Last accessed on 2006 Aug 02].  Back to cited text no. 3
Sambasiva RR, Naveen G, P B, Agarwal SK. Leptospirosis in India and the rest of the world. Braz J Infect Dis 2003;7:178-93.  Back to cited text no. 4
Wagenaar JF, Goris MG, Partiningrum DL, Isbandrio B, Hartskeerl RA, Brandjes DP, et al. Coagulation disorders in patients with severe leptospirosis are associated with severe bleeding and mortality. Trop Med Int Health 2010;15:152-9.  Back to cited text no. 5
Goris MG, Kikken V, Straetemans M, Alba S, Goeijenbier M, van Gorp EC, et al. Towards the burden of human leptospirosis: Duration of acute illness and occurrence of post-leptospirosis symptoms of patients in the Netherlands. PLoS One 2013;8:e76549.  Back to cited text no. 6
Panaphut T, Domrongkitchaiporn S, Vibhagool A, Thinkamrop B, Susaengrat W. Ceftriaxone compared with sodium penicillin g for treatment of severe leptospirosis. Clin Infect Dis 2003;36:1507-13.  Back to cited text no. 7
Friedland JS, Warrell DA. The Jarisch-Herxheimer reaction in leptospirosis: Possible pathogenesis and review. Rev Infect Dis 1991;13:207-10.  Back to cited text no. 8
Guerrier G, D'Ortenzio E. The Jarisch-Herxheimer reaction in leptospirosis: A systematic review. PLoS One 2013;8:e59266.  Back to cited text no. 9
Sehgal SC, Sugunan AP, Murhekar MV, Sharma S, Vijayachari P. Randomized controlled trial of doxycycline prophylaxis against leptospirosis in an endemic area. Int J Antimicrob Agents 2000;13:249-55.  Back to cited text no. 10
Gulati S, Maheshwari A. Atypical manifestations of dengue. Trop Med Int Health 2007;12:1087-95.  Back to cited text no. 11
Pozzetto B, Memmi M, Garraud O. Is transfusion-transmitted dengue fever a potential public health threat? World J Virol 2015;4:113-23.  Back to cited text no. 12
Tan FL, Loh DL, Prabhakaran K, Tambyah PA, Yap HK. Dengue haemorrhagic fever after living donor renal transplantation. Nephrol Dial Transplant 2005;20:447-8.  Back to cited text no. 13
Pouliot SH, Xiong X, Harville E, Paz-Soldan V, Tomashek KM, Breart G, et al. Maternal dengue and pregnancy outcomes: A systematic review. Obstet Gynecol Surv 2010;65:107-18.  Back to cited text no. 14
WHO. Comprehensive guidelines for prevention and control of dengue and dengue hemorrhagic fever. World Health Organization, Regional Office for South-East Asia. Available from: docs/B4751.pdf?ua=1. [Last accessed on 2017 Aug 1].  Back to cited text no. 15
Balmaseda A. Assessment of the World Health Organization Scheme for Classification of Dengue severity in Nicaragua. American Journal of Tropical Medicine & Hygiene. 2005;73:1059-1062.  Back to cited text no. 16
World Health Organization. Dengue: Guidelines for Diagnosis, Treatment, Prevention and Control. Geneva, Switzerland: WHO; 2009.  Back to cited text no. 17
Dengue Virus Infections 2015 Case Definition. National Notifiable Diseases Surveillance System (NNDSS). Centres for Disease Control and Prevention (CDC). Available from: [Last accessed on 2017 Aug 07].  Back to cited text no. 18
Suharti C, van Gorp EC, Dolmans WM, Groen J, Hadisaputro S, Djokomoeljanto RJ, et al. Hantavirus infection during dengue virus infection outbreak in Indonesia. Acta Med Indones 2009;41:75–80.  Back to cited text no. 19
Kumar R, Tripathi P, Tripathi S, Kanodia A, Pant S, Venkatesh V, et al. Prevalence and clinical differentiation of dengue fever in children in Northern India. Infection 2008;36:444-9.  Back to cited text no. 20
Dhar S, Malakar R, Ghosh A, Kundu R, Mukhopadhyay M, Banerjee R. The recent epidemic of dengue fever in West Bengal: Clinico-serological pattern. Indian J Dermatol 2006;51:57-9.  Back to cited text no. 21
  [Full text]  
Kautner I, Robinson MJ, Kuhnle U. Dengue virus infection: Epidemiology, pathogenesis, clinical presentation, diagnosis, and prevention. J Pediatr 1997;131:516-24.  Back to cited text no. 22
Ellerin T, Hurtado R, Lockman S, Baden L. Fever in a returned traveler: An “off the cuff” diagnosis. Clin Infect Dis 2003;36:1004-5, 1074-5.  Back to cited text no. 23
Srikiatkhachorn A, Krautrachue A, Ratanaprakarn W, Wongtapradit L, Nithipanya N, Kalayanarooj S, et al. Natural history of plasma leakage in dengue hemorrhagic fever: A serial ultrasonographic study. Pediatr Infect Dis J 2007;26:283-90.  Back to cited text no. 24
Special Programme for Research and Training in Tropical Diseases, World Health Organization. Dengue: Guidelines for Diagnosis, Treatment, Prevention, and Control. New edition. Geneva: TDR, World Health Organization; 2009.  Back to cited text no. 25
Young PR, Hilditch PA, Bletchly C, Halloran W. An antigen capture enzyme-linked immunosorbent assay reveals high levels of the dengue virus protein NS1 in the sera of infected patients. J Clin Microbiol 2000;38:1053-7.  Back to cited text no. 26
Alcon S, Talarmin A, Debruyne M, Falconar A, Deubel V, Flamand M, et al. Enzyme-linked immunosorbent assay specific to Dengue virus type 1 nonstructural protein NS1 reveals circulation of the antigen in the blood during the acute phase of disease in patients experiencing primary or secondary infections. J Clin Microbiol 2002;40:376-81.  Back to cited text no. 27
Zeller H, Van Bortel W, Sudre B. Chikungunya: Its history in Africa and Asia and its spread to new regions in 2013-2014. J Infect Dis 2016;214 Suppl 5:S436-40.  Back to cited text no. 28
Paupy C, Kassa Kassa F, Caron M, Nkoghé D, Leroy EM. A chikungunya outbreak associated with the vector Aedes albopictus in remote villages of Gabon. Vector Borne Zoonotic Dis 2012;12:167-9.  Back to cited text no. 29
Kumar NP, Sabesan S, Krishnamoorthy K, Jambulingam P. Detection of chikungunya virus in wild populations of Aedes albopictus in Kerala State, India. Vector Borne Zoonotic Dis 2012;12:907-11.  Back to cited text no. 30
Thiberville SD, Boisson V, Gaudart J, Simon F, Flahault A, de Lamballerie X, et al. Chikungunya fever: A clinical and virological investigation of outpatients on reunion Island, South-West Indian ocean. PLoS Negl Trop Dis 2013;7:e2004.  Back to cited text no. 31
Mohd Zim MA, Sam IC, Omar SF, Chan YF, AbuBakar S, Kamarulzaman A, et al. Chikungunya infection in Malaysia: Comparison with dengue infection in adults and predictors of persistent arthralgia. J Clin Virol 2013;56:141-5.  Back to cited text no. 32
Schwartz O, Albert ML. Biology and pathogenesis of chikungunya virus. Nat Rev Microbiol 2010;8:491-500.  Back to cited text no. 33
Pakran J, George M, Riyaz N, Arakkal R, George S, Rajan U, et al. Purpuric macules with vesiculobullous lesions: A novel manifestation of chikungunya. Int J Dermatol 2011;50:61-9.  Back to cited text no. 34
Lakshmi V, Neeraja M, Subbalaxmi MV, Parida MM, Dash PK, Santhosh SR, et al. Clinical features and molecular diagnosis of chikungunya fever from South India. Clin Infect Dis 2008;46:1436-42.  Back to cited text no. 35
Pialoux G, Gaüzère BA, Jauréguiberry S, Strobel M. Chikungunya, an epidemic arbovirosis. Lancet Infect Dis 2007;7:319-27.  Back to cited text no. 36
Pialoux G, Gaüzère BA, Strobel M. Chikungunya virus infection: Review through an epidemic. Med Mal Infect 2006;36:253-63.  Back to cited text no. 37
van Aalst M, Nelen CM, Goorhuis A, Stijnis C, Grobusch MP. Long-term sequelae of chikungunya virus disease: A systematic review. Travel Med Infect Dis 2017;15:8-22.  Back to cited text no. 38
World Health Organization. Regional office for South-East Asia. Guidelines for Prevention and Control of Chikungunya Fever. c2009. Available from: Files/Publication_SEA-CD-182.pdf. [Last accessed on 2012 Jul 15].  Back to cited text no. 39
Gaibani P, Landini MP, Sambri V. Diagnostic methods for CHIKV based on serological tools. Methods Mol Biol 2016;1426:63-73.  Back to cited text no. 40
Ravichandran R, Manian M. Ribavirin therapy for chikungunya arthritis. J Infect Dev Ctries 2008;2:140-2.  Back to cited text no. 41
Ramsauer K, Schwameis M, Firbas C, Müllner M, Putnak RJ, Thomas SJ, et al. Immunogenicity, safety, and tolerability of a recombinant measles-virus-based chikungunya vaccine: A randomised, double-blind, placebo-controlled, active-comparator, first-in-man trial. Lancet Infect Dis 2015;15:519-27.  Back to cited text no. 42
World Health Organization. Global Health Observatory Data – Leishmaniasis. 2014. Available from: [Last accessed on 2015 Apr 21].  Back to cited text no. 43
Topno RK, Das VN, Ranjan A, Pandey K, Singh D, Kumar N, et al. Asymptomatic infection with visceral leishmaniasis in a disease-endemic area in Bihar, India. Am J Trop Med Hyg 2010;83:502-6.  Back to cited text no. 44
Singh OP, Hasker E, Sacks D, Boelaert M, Sundar S. Asymptomatic leishmania infection: A new challenge for leishmania control. Clin Infect Dis 2014;58:1424-9.  Back to cited text no. 45
Guerin PJ, Olliaro P, Sundar S, Boelaert M, Croft SL, Desjeux P, et al. Visceral leishmaniasis: Current status of control, diagnosis, and treatment, and a proposed research and development agenda. Lancet Infect Dis 2002;2:494-501.  Back to cited text no. 46
Sundar S, Sahu M, Mehta H, Gupta A, Kohli U, Rai M, et al. Noninvasive management of Indian visceral leishmaniasis: Clinical application of diagnosis by K39 antigen strip testing at a kala-azar referral unit. Clin Infect Dis 2002;35:581-6.  Back to cited text no. 47
Sundar S, Benjamin B. Diagnosis and treatment of Indian visceral leishmaniasis. J Assoc Physicians India 2003;51:195-201.  Back to cited text no. 48
Zijlstra EE, El-Hassan AM. Leishmaniasis in Sudan 3: Visceral leishmaniasis. Trans R Soc Trop Med Hyg 2001;95 Suppl 1:S1-58.  Back to cited text no. 49
Marlet MV, Sang DK, Ritmeijer K, Muga RO, Onsongo J, Davidson RN, et al. Emergence or re-emergence of visceral leishmaniasis in areas of Somalia, North-Eastern Kenya, and South-Eastern Ethiopia in 2000-01. Trans R Soc Trop Med Hyg 2003;97:515-8.  Back to cited text no. 50
Collin S, Davidson R, Ritmeijer K, Keus K, Melaku Y, Kipngetich S, et al. Conflict and kala-azar: Determinants of adverse outcomes of kala-azar among patients in Southern Sudan. Clin Infect Dis 2004;38:612-9.  Back to cited text no. 51
Veeken H, Ritmeijer K, Seaman J, Davidson R. Comparison of an rK39 dipstick rapid test with direct agglutination test and splenic aspiration for the diagnosis of kala-azar in Sudan. Trop Med Int Health 2003;8:164-7.  Back to cited text no. 52
Boelaert M, Rijal S, Regmi S, Singh R, Karki B, Jacquet D, et al. A comparative study of the effectiveness of diagnostic tests for visceral leishmaniasis. Am J Trop Med Hyg 2004;70:72-7.  Back to cited text no. 53
Davies CR, Kaye P, Croft SL, Sundar S. Leishmaniasis: New approaches to disease control. BMJ 2003;326:377-82.  Back to cited text no. 54
Weina PJ, Neafie RC, Wortmann G, Polhemus M, Aronson NE. Old world leishmaniasis: An emerging infection among deployed US military and civilian workers. Clin Infect Dis 2004;39:1674-80.  Back to cited text no. 55
Sundar S, More DK, Singh MK, Singh VP, Sharma S, Makharia A, et al. Failure of pentavalent antimony in visceral leishmaniasis in India: Report from the center of the Indian epidemic. Clin Infect Dis 2000;31:1104-7.  Back to cited text no. 56
Murray HW. Progress in the treatment of a neglected infectious disease: Visceral leishmaniasis. Expert Rev Anti Infect Ther 2004;2:279-92.  Back to cited text no. 57
Sundar S, Jha TK, Thakur CP, Engel J, Sindermann H, Fischer C, et al. Oral miltefosine for Indian visceral leishmaniasis. N Engl J Med 2002;347:1739-46.  Back to cited text no. 58
Smithburn KC, Kerr JA, Gatne PB. Neutralizing antibodies against certain viruses in the sera of residents of India. J Immunol 1954;72:248-57.  Back to cited text no. 59
Chakravarty SK, Sarkar JK, Chakravarty MS, Mukherjee MK, Mukherjee KK, Das BC, et al. The first epidemic of Japanese encephalitis studied in India – Virological studies. Indian J Med Res 1975;63:77-82.  Back to cited text no. 60
Dhanda V, Thenmozhi V, Kumar NP, Hiriyan J, Arunachalam N, Balasubramanian A, et al. Virus isolation from wild-caught mosquitoes during a Japanese encephalitis outbreak in Kerala in 1996. Indian J Med Res 1997;106:4-6.  Back to cited text no. 61
Mohan Rao CV, Prasad SR, Rodrigues JJ, Sharma NG, Shaikh BH, Pavri KM, et al. The first laboratory proven outbreak of Japanese encephalitis in goa. Indian J Med Res 1983;78:745-50.  Back to cited text no. 62
Sharma SN, Panwar BS. An epidemic of Japanese encephalitis in Haryana in the year 1990. J Commun Dis 1991;23:204-5.  Back to cited text no. 63
Prasad SR, Kumar V, Marwaha RK, Batra KL, Rath RK, Pal SR, et al. An epidemic of encephalitis in Haryana: Serological evidence of Japanese encephalitis in a few patients. Indian Pediatr 1993;30:905-10.  Back to cited text no. 64
Tiroumourougane SV, Raghava P, Srinivasan S. Japanese viral encephalitis. Postgrad Med J 2002;78:205-15.  Back to cited text no. 65
Reuben R, Thenmozhi V, Samuel PP, Gajanana A, Mani TR. Mosquito blood feeding patterns as a factor in the epidemiology of Japanese encephalitis in Southern India. Am J Trop Med Hyg 1992;46:654-63.  Back to cited text no. 66
Thenmozhi V, Rajendran R, Ayanar K, Manavalan R, Tyagi BK. Long-term study of Japanese encephalitis virus infection in anopheles subpictus in Cuddalore district, Tamil Nadu, South India. Trop Med Int Health 2006;11:288-93.  Back to cited text no. 67
Mariappan T, Samuel PP, Thenmozhi V, Paramasivan R, Sharma PK, Biswas AK, et al. Entomological investigations into an epidemic of Japanese encephalitis (JE) in Northern districts of West Bengal, India (2011-2012). Indian J Med Res 2014;139:754-61.  Back to cited text no. 68
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Solomon T, Kneen R, Dung NM, Khanh VC, Thuy TT, Ha DQ, et al. Poliomyelitis-like illness due to Japanese encephalitis virus. Lancet 1998;351:1094-7.  Back to cited text no. 69
Solomon T, Dung NM, Kneen R, Gainsborough M, Vaughn DW, Khanh VT, et al. Japanese encephalitis. J Neurol Neurosurg Psychiatry 2000;68:405-15.  Back to cited text no. 70
Shrivastva A, Tripathi NK, Parida M, Dash PK, Jana AM, Lakshmana Rao PV, et al. Comparison of a dipstick enzyme-linked immunosorbent assay with commercial assays for detection of Japanese encephalitis virus-specific IgM antibodies. J Postgrad Med 2008;54:181-5.  Back to cited text no. 71
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What is new? Important emerging infectious diseases in India and surrounding countries have been discussed.


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

  [Table 1], [Table 2]


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