Apurba Ghosh

Epidemic of hand, foot and mouth disease in West Bengal, India in August, 2007: A multicentric study

Background: Hand, foot, and mouth disease (HFMD) is caused mostly by Coxsackievirus A16 (CA16) and enterovirus 71 (EV71). Epidemic of HFMD has occurred in India only once in Kerala in 2003. We report here a recent outbreak of HFMD in three districts of West Bengal, India. Materials and Methods: A case detection system developed with 1) three private clinics in three districts; two at Howrah and one at Hooghly, 2) Pediatrics Department of two medical colleges in Kolkata, 3) 12 practioners of these three districts with 4) a central referral center at Department of Dermatology, NRS Medical College, Kolkata where all cases from this system were confirmed by a single observer. Pediatric Dermatology unit of the Institute of Child Health, Kolkata was another independent unit. Results: A total of 38 cases of HFMD were reported till 08.10.07. Age group ranged from 12 months to 12 years (mean 40.76 months, SD 29.49). Males were slightly higher than females (M:F - 21:17). Disease was distributed mostly over buttocks, knees, hands, feet - both dorsum and palmar or the plantar surface and the oral mucosa. Highest severity noted over the buttocks and the knee. Healing time for skin lesions was 6-13 days (mean 9.13 days, SD 1.93). Oral lesions were found in 33 (86.8%) cases. Conclusion: This outbreak far away from the initial one confirmed regular outsourcing of the virus with possibilities of future epidemics. Also the fact that EV71 induced epidemic is on rise in this part of globe is alarming for India. We hope this early report will be of help for strategic planning for a better management of the disease and prevention of dreaded neurological complications in India.

Childhood hepatitis E infection complicated by acute immune thrombocytopenia.

An 8-year 7-month-old girl, born to nonconsanguineous parents, was initially seen for an episode of gum bleed and painless hematuria. She provided a history of new-onset fatigue, low-grade fever, generalized body ache, and anorexia for 2 weeks before admission. The past history was negative for significant illnesses, allergies, or drug intake. She had her last immunization at the age of 5 years (oral polio vaccine). On examination, she was normotensive, alert, icteric, and mildly anemic. Occasional nonpalpable purpuric spots were noted in both the lower extremities. Oral examination revealed an isolated site of bleeding gum over the left upper second incisor. Abdominal examination revealed tender hepatomegaly (liver span 12 cm) and a nontender spleen that was 2 cm palpable. The chest auscultation was normal. The abdominal ultrasound showed an enlarged liver with increased echotexture. Laboratory investigations revealed isolated thrombocytopenia (21,000/mm), mild conjugated hyperbilirubinemia with elevated liver enzymes (aspartate aminotransferase 1080U/L, alanine aminotransferase 878U/L), and normal alkaline phosphatase, serum albumin, g-glutamyl transferase, prothrombin time, activated partial thromboplastin time, fibrinogen, and D-dimer levels. Urinalysis was significant for plenty of nondysmorphic erythrocytes per highpower field without casts or proteins. She was transfused with platelet concentrates. A bone-marrow aspirate revealed normocellular marrow with normal granulocytic and erythrocytic series and increased number of large, immature megakaryocytes. The serum IgM and IgG anti-Hepatitis E virus (HEV) antibodies were positive using the enzyme-linked immunosorbent assay kits (Genelabs Diagnostics). The optical density ratio for IgM anti-HEV was 3.4 (positive >2) and that for IgG anti-HEV was 3.70 (positive >3). The serologic tests were negative for Hepatitis A, B, and C viruses, Epstein-Barr virus, Cytomegalovirus, Toxoplasma gondii, Dengue virus, Leptospira, Rubella virus, Parvovirus B19, and HIV. The blood and urine cultures remained sterile. The enzyme-linked immunosorbent assay for direct antiplatelet antibodies was positive. Coombs’ test (both direct and indirect), antinuclear antibody, antidouble stranded DNA, antiphospholipid antibodies, anticardiolipin, and cryoglobulins were negative. Intravenous immunoglobulin at 1.0 g/kg/d was administered for 2 days. The platelet count at the end of 1 week was 94,000/mm. There were no further complications during her hospital stay. Clinical evaluation and platelet count at 4 weeks was normal. HEV is a major cause of sporadic and epidemic hepatitis with a worldwide distribution. Mostly asymptomatic, HEV infection is most common in young adults of age 15 to 40 years and commonly presents with a self-limited syndrome of fever, jaundice, anorexia, abdominal pain, and an enlarged tender liver. A variety of hepatotropic viruses are known to cause immune thrombocytopenic purpura, but it is extremely rare in HEV infection. A thorough Medline search revealed only 3 previously reported cases of acute Hepatitis E in adults complicated by autoimmune thrombocytopenia. To our knowledge, this is the first pediatric report on autoimmune thrombocytopenia complicating the course of HEV infection. In view of various corroborating features like isolated thrombocytopenia and otherwise normal peripheral blood smear, normocellular marrow, presence of antiplatelet antibodies, response to intravenous immunoglobulin, and apparent absence of other causes of thrombocytopenia, the present case fits the accepted diagnostic criteria of immune thrombocytopenic purpura. A study from an endemic North Indian region determined the incidence of acute HEV infection at 38.6% of all cases (majority between 11 and 30 y of age) of acute viral hepatitis. Children with acute HEV infection are prone to develop acute liver failure associated with heightened mortality. Given the high incidence of acute HEV infection in endemic areas and the potential for development of acute liver failure, HEV infection should be promptly recognized and treated. In conclusion, although rare, acute HEV infection may be considered one of the etiologies of autoimmune thrombocytopenia in children.

Efficacy and safety of vi-tetanus toxoid conjugated typhoid vaccine (PedaTyph™) in Indian children: School based cluster randomized study

ABSTRACT Vi polysaccharide typhoid vaccines cannot be used in children <2 years owing to poor immunogenic and T cell independent properties. Conjugate vaccine prepared by binding Vi to tetanus toxoids (Vi-TT) induces protective levels even in children <2 years. We evaluated efficacy and safety following vaccination with a Vi-TT vaccine in children 6 months to 12 years of age. Overall, 1765 subjects were recruited from two registered municipal urban slums of southern Kolkata. Most of the children of the slum dwellers attended the schools in the locality which was selected with permission from the school authority. Schools were randomly divided into vaccinated (Test group) and unvaccinated group (Control group). Children and their siblings of test group received 2-doses of PedaTyph™ vaccine at 6 weeks interval. Control group received vaccines as per national guidelines. Adverse events (AEs) were examined after 30 minutes, 1 month and clinical events were observed till 12 months post-vaccination. Incidence of culture positive typhoid fever in the control group was 1.27% vis-a-vis none in vaccine group during 12 months. In subgroup evaluated for immunogenicity, an antibody titer value of 1.8 EU/ml (95% CI: 1.5 EU/ml, 2.2 EU/ml), 32 EU/ml (95% CI: 27.0 EU/ml, 39.0 EU/ml) and 14 EU/ml (95% CI: 12.0 EU/ml, 17.0 EU/ml) at baseline, 6 weeks and 12 months, respectively was observed. Sero-conversion among the sub-group was 100% after 6 weeks of post-vaccination and 83% after 12 months considering 4-fold rise from baseline. The efficacy of vaccine was 100 % (95% CI: 97.6%, 100%) in the first year of follow-up with minimal AEs post vaccination. Vi conjugate typhoid vaccine conferred 100% protection against typhoid fever in 1765 children 6 months to 12 years of age with high immunogenicity in a subgroup from the vaccine arm.

Childhood Hepatitis A Virus Infection Complicated by Pseudotumor Cerebri

A 4-year-old male child with hepatitis A virus (HAV) infection is presented. His disease course was complicated by the development of pseudotumor cerebri (PC), as evidenced by symptoms and signs of increased intracranial pressure in the presence of normal cerebrospinal fluid examination and cranial magnetic resonance scan. The neurological examination was normal with the exception of the right-sided sixth cranial nerve paresis. His neurological course was uncomplicated with spontaneous recovery within three days. To our knowledge, this is the first report in the English literature of PC complicating the course of HAV in a child.

Unilateral Palatal and Abducens Palsy in Childhood Hepatitis A Virus Infection

Isolated cranial nerve paresis in childhood hepatitis A virus infection is rare. The authors report an instance of concomitant right-hand side palatal and abducens palsy, developing in the course of an otherwise uncomplicated hepatitis A virus infection in a 5-year-old girl. The neurological complications were transient, and she recovered completely with supportive therapy.

Congenital Tuberculosis : Late Manifestation of the Maternal Infection

Tuberculosis in pregnancy though not uncommon, congenital tuberculosis continues to be a rare entity. A case of congenital tuberculosis where the mother manifested the disease 3 months after it was diagnosed in the newborn is reported considering its rarity.

Childhood Hepatitis A Virus Infection Complicated by Bell's Palsy

The full blood count was normal. The liver function tests (LFT) showed the following values: total serum bilirubin 4.6 mg/dL (conjugated fraction 3.0), alanine aminotransferase (ALT) 436 IU/L, aspartate aminotransferase (AST) 348 IU/L, prothrombin time (PT) 15 seconds (normal, <12 seconds). Because of the clinical presentation and the deranged LFT, hepatitis screen was undertaken. IgM and IgG antibodies to HAV were detected in the serum of the patient. The serologies for other hepatotrophic viruses (hepatitis B virus [HBV], hepatitis C virus, hepatitis E virus, Epstein-Barr virus, herpes simplex virus, and cytomegalovirus) were negative. Blood and urine cultures remained sterile. Serum ammonia, lactate, and ceruloplasmin values were within the reference range. Abdominal ultrasonography revealed an increase in echogenicity of the liver parenchyma. Cranial computed tomography scans of both the mastoids and fundoscopy were noncontributory. The patient was managed with supportive therapy for both her conditions. Corticosteroids were not used to treat the facial palsy because of the concomitant HAV infection. There was gradual improvement in her condition, with serum bilirubin and liver enzymes returning to normal in 12 days and facial weakness recovering in 1 month.

Infection-associated haemophagocytic lymphohistiocytosis: a case series using steroids only protocol for management.

Haemophagocytic lymphohistiocytosis (HLH) is a heterogeneous group of clinical syndromes characterised by activation and subsequent uncontrolled non-malignant proliferation of T lymphocytes and macrophages, leading to a cytokine storm that accounts for most of its clinical features such as acute febrile illness, hepatosplenomegaly, multi-organ dysfunction and fulminant pancytopenia-resembling severe sepsis. Here, we present a series of 23 cases of infection-associated HLH diagnosed in our hospital within a time period of last three and half years. Though the presentation and progression of disease was variable, the patients shared some common features like prolonged fever unresponsive to broad spectrum antibiotics, organomegaly and cytopenias. In most of the cases, however, the triggering infectious agent could not be identified. They were treated using a steroid only protocol along with supportive measures and showed an excellent response.

‘Face of the giant panda’ sign in Wilson disease

A 16-year-old boy presented with truncal dystonia and arm tremor of 3 years’ duration. He had suffered from fulminant hepatitis at 12 years of age. Icterus with hepatomegaly was noted. Neurological examination revealed dystonia, scanning dysarthria, emotional lability, ‘wing-beating tremor’ of the arms and bilateral Kayser-Fleischer rings. Laboratory investigation confirmed Wilson disease. MR imaging showed hyperintensity of the mid-brain with relative sparing of the red nucleus, superior colliculus and part of the pars reticulate of the substantia nigra with hypointensity of the aqueduct (face of the giant panda appearance; Fig. 1). He was treated with penicillamine and zinc. At 6 months, there was moderate improvement. This classic MR sign was first reported by Hitoshi et al. [1] and occurs due to hyperintense tegmenti seen on T2-W MR images. Concomitant hypointensity of the corpus striatum and superior colliculus is seen, most likely the result of the paramagnetic effects of the deposition of heavy metals, such as iron and copper [2].

Changing epidemiology of hepatitis A virus in Indian children

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