|Year : 2017 | Volume
| Issue : 3 | Page : 426-428
Hantavirus and tuberculosis co-infection in an Indian child
Someshwar Chate1, Ira Shah2, Hiren Doshi1
1 Department of Pediatrics, Pediatric Intensive Care Unit, Balabhai Nanavati Hospital, Mumbai, Maharashtra, India
2 Department of Pediatrics, Pediatric Infectious Diseases Clinic, Balabhai Nanavati Hospital, Mumbai, Maharashtra, India
|Date of Web Publication||12-Oct-2017|
1/B Saguna, 271/B St Francis Road, Vile Parle (W), Mumbai - 400 056, Maharashtra
Source of Support: None, Conflict of Interest: None
Hantaviruses are a group of antigenically distinct viruses carried out in rodents and insectivores. Humans are accidental hosts and get infected by aerosols generated from contaminated urine, faeces and saliva of infected rodents. Hantaviruses are identified as aetiological agents of two human diseases, haemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. Hantavirus causing pulmonary renal disease has rarely been reported in children in India. Hantavirus infection is uncommon under the age of 12 years. We report a 9-year-old girl from Mumbai, India with fever, bilateral pleural effusion, thrombocytopaenia, haemoconcentration and oliguria due to hantavirus infection. She also had associated tuberculosis.
Keywords: Children, hantavirus, India
|How to cite this article:|
Chate S, Shah I, Doshi H. Hantavirus and tuberculosis co-infection in an Indian child. Indian J Med Microbiol 2017;35:426-8
|How to cite this URL:|
Chate S, Shah I, Doshi H. Hantavirus and tuberculosis co-infection in an Indian child. Indian J Med Microbiol [serial online] 2017 [cited 2018 Jan 22];35:426-8. Available from: http://www.ijmm.org/text.asp?2017/35/3/426/216614
| ~ Introduction|| |
Hantaviruses are a genus in the family Bunyaviridae, which are lipid-enveloped viruses with a negative-stranded RNA genome composed of 3 unique segments. The natural reservoirs of hantaviruses are small rodents and transmission to man is believed to occur through the aerosols generated from virus-contaminated rodent faeces, urine or saliva., The worldwide distribution of rodents known to harbour hantaviruses suggests great disease-causing potential. Paediatric infections are uncommon and men are more often infected than women as an occupational risk. About half of cases occur between the month of May and July. Patients are almost exclusively 12–70 years of age; 60% of patients are 20–39 years of age. In 1966, thottapalayam virus, the first indigenous Indian hantavirus species, was isolated from the spleen of a shrew (insectivore), Suncus murinus, captured in Vellore, South India, during field studies of Japanese encephalitis. This is one of the few hantavirus isolates from a non-rodent host. In a study by Chandy et al., 152 serum samples found 23 (14.7%) individuals with febrile illness positive for anti-hantavirus IgM and 5.7% of healthy blood donor samples tested were positive. These findings suggested the presence of hantavirus infections in the Indian population, presenting as symptomatic or asymptomatic infections. Evidence exists for Seoul virus (SEOV)-like infection in 12% and a Puumala virus (PUUV)-like infection in 5% of Indians presenting with a leptospirosis-like clinical picture from Cochin and Chennai area of India. Sero-epidemiological studies have indicated a 4% seropositivity of hantavirus infections in India.
However, hantavirus causing pulmonary renal disease has rarely been reported in children in India. We report a 9-year-old girl with fever, bilateral pleural effusion, thrombocytopaenia, haemoconcentration and oliguria due to hantavirus infection. She also had associated tuberculosis (TB). To the best of our knowledge, co-infection of hantavirus and TB has not been reported earlier.
| ~ Case Report|| |
A 9-year-old girl presented with fever, dry cough mainly during night time with post-tussive vomiting for the past 7–8 days. She also had breathlessness for 3 days. Her younger brother had been treated for tuberculous osteomyelitis and had completed anti-tuberculous therapy (ATT) 1 year ago. There was no recent travel, but there were rats in the house. On admission, the patient was febrile (temperature −102.8°F), had tachycardia (heart rate - 160/min), with cold extremities. Blood pressure was 98/60 mm of hg. Her respiratory rate was 60/min with distress. Oxygen saturation by non-rebreathing mask was 95%, Air entry was reduced on the right side of chest with bronchial breathing on auscultation. Other systems were normal. Her investigations are depicted in [Table 1]. OptiMAL for malaria, dengue IgM, leptospira IgM, Widal test and Weil Felix test were negative. Blood culture did not grow any organism. Chest X-ray showed homogeneous opacity in the right lower lobe with pleural effusion [Figure 1] and ultrasound thorax showed moderate right-sided pleural effusion with internal echoes with underlying consolidation with mild pleural effusion on the left side. Pleural tap was haemorrhagic. CT chest showed right and left lower lobe and medial and lateral segment of right upper lobe consolidation with pleural effusion with bilateral hilar and paratracheal adenopathy [Figure 2]. Quantiferon gold (quantitative) in tube test for TB was positive. Urine for pneumococcal antigen and blood mycoplasma IgM were negative. The child was treated with ATT, intravenous antibiotics and oxygen but had no response. She required inotrope support with invasive ventilation. On day 4 of hospitalisation, she had decreased urine output with haemoconcentration. Hantavirus IgM (Elisa kit of Focus Technologies, Cypress, CA, USA) was positive (3.3, [>1.1 - positive]). Blood transfusion was given 2 times, on the 3rd and 7th day of hospitalisation. She was continued on same management and ionotropes were omitted on the 10th day of hospitalisation, ventilation was omitted on the 10th day. She was discharged on ATT.
|Figure 1: Chest X-ray showed homogeneous opacity in right lower lobe with pleural effusion|
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|Figure 2: Computed tomography chest showed right and left lower lobe and medial and lateral segment of right upper lobe consolidation with pleural effusion with bilateral hilar and paratracheal adenopathy|
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| ~ Discussion|| |
Hantaviruses cause two important disease syndromes; haemorrhagic fever with renal syndrome (HFRS) in Europe and Asia and hantavirus cardiopulmonary syndrome (HCPS) in America. In the Old World, four antigenically related and genetically distinct hantaviruses are known to cause HFRS: hantaan virus, SEOV, PUUV, and Dobrava virus. Several sigmodontine rodent-borne hantaviruses in the New World, including Sin Nombre virus and Andes virus, cause HCPS.
The incubation period of HFRS is 1–5 weeks and the onset of the disease is with fever and influenza-like symptoms., Haemorrhagic manifestations if present are seen as flushing of the face, injection of the conjunctiva and mucous membranes. The disease is conveniently described as having five phases: a febrile phase lasting 3–5 days followed by a hypotensive (shock) phase lasting from a few hours to a few days, a subsequent oliguric phase lasting 3–7 days and finally, a diuretic phase leading to the convalescent phase. Similar clinical presentation was seen in our child with the onset of fever followed by hypotension and shock and then finally oliguria. In patients with severe HFRS, the blood picture shows haemoconcentration, leucocytosis and thrombocytopaenia. Urine analysis shows proteinuria, haematuria and pyuria. Significant elevations of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and creatine kinase enzymes are frequently noticed. Marked polymorphonuclear leucocytosis with a left shift and CD8 + activated cells appear as atypical lymphocytes on a peripheral blood smear. Similar features of thrombocytopaenia, haemoconcentration and elevated liver transaminases were seen in our patient. Although our patient did not have petechiae, she had a haemorrhagic pleural effusion.
HCPS is characterised by sudden and catastrophic pulmonary oedema, resulting in anoxia and acute heart failure. The virus is detected in pulmonary capillaries, suggesting that pulmonary oedema is the consequence of the T-cell attack on virus-infected capillaries. Disease severity is predicted by the level of acute phase viraemia titre. HCPS can be described to occur in two phases, prodromal and cardiopulmonary phase. The prodromal stage is characterised by fever, headache, chills and myalgia. Like HFRS the clinical picture at this phase may be confused with other viral infections. The onset of the cardiopulmonary phase is with pulmonary oedema, dyspnoea and hypoxaemia. Patients with severe illness may progress to cardiac depression, respiratory failure and acidosis leading to fatal arrhythmias.
The clinical diagnosis of hantavirus infections has routinely been confirmed by immunofluorescence antibody assay or enzyme-linked immunosorbent assays. The presence of cross-reacting antibodies makes it difficult to distinguish hantavirus species by serology. Molecular tests based on nested reverse transcriptase polymerase chain reaction have been used for diagnosis.
There are no effective anti-viral drugs for the treatment of all hantavirus infections. Supportive therapy such as adequate oxygenation, inotropic agents such as dobutamine and judicious use of fluid replacement in shock is the best to control progression towards life-threatening symptoms.
Prevention of exposure to rodent excreta is the best way to avoid infection. Simple preventive steps are: decontamination of human dwelling having signs of rodent activity, maintaining rodents as pets should be discouraged and proper storage of food should be practiced. There are a few inactivated vaccines (Hantavax) licenced for use in Korea, but the protective response is short lived. Baculovirus and vaccinia-expressed hantavirus glycoproteins confer protection in animal models. There is ongoing research on nucleic acid vaccines.
| ~ Conclusion|| |
Hantavirus infection should be suspected in children with haemorrhagic fever with renal and pulmonary manifestations in India.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]