|Year : 2015 | Volume
| Issue : 3 | Page : 286-288
Pediatric melioidosis: Call for better awareness and early diagnosis!
Tina Damodar, Meena Dias, Neethu Kishor, Hilda Pinto
Department of Microbiology, Fr. Muller Medical College, Mangalore, Karnataka, India
|Date of Web Publication||12-Jun-2015|
Dr. Meena Dias
S-3, Casa Leila, S.L Mathias Road, Falnir, Mangalore, Karnataka - 575 002
Source of Support: None, Conflict of Interest: None
Pediatric melioidosis is an under-diagnosed entity and rarely reported from India. This condition, if not treated early and appropriately, can have a fatal outcome. A 17-month-old female child presented with fever and ulcer on the right leg; she eventually succumbed to the infection. Culture from blood and wound swab from ulcer site grew Burkholderia pseudomallei.
Keywords: Burkholderia pseudomallei, pediatric sepsis, paediatric meliodiosis
|How to cite this article:|
Damodar T, Dias M, Kishor N, Pinto H. Pediatric melioidosis: Call for better awareness and early diagnosis!. CHRISMED J Health Res 2015;2:286-8
|How to cite this URL:|
Damodar T, Dias M, Kishor N, Pinto H. Pediatric melioidosis: Call for better awareness and early diagnosis!. CHRISMED J Health Res [serial online] 2015 [cited 2021 Sep 20];2:286-8. Available from: https://www.cjhr.org/text.asp?2015/2/3/286/158718
| Introduction|| |
Melioidosis, caused by the soil saprophyte Burkholderia pseudomallei, is endemic in South-East Asia and Northern Australia. , It has been increasingly reported in India in recent years especially in the southern coastal part of the country, majorly in the adult age group with underlying chronic illness, such as diabetes mellitus.  Melioidosis in children is rarely reported and calls for increased awareness and early diagnosis pertaining to its varied manifestations and high morbidity and mortality if not treated appropriately.
| Case report|| |
A 17-month-old female child of farmer parents, resident of Ankola in coastal Karnataka, a small town with agriculture as main occupation was admitted to the hospital with ulcer on right leg since 20 days, fever since 10 days and cough since 5 days. The ulcer was 1 × 1 × 2 cm, present on the lateral aspect of the right leg with swelling and erythema of the surrounding skin. The ulcer started as a pustule initially which gradually increased in size and burst open to form an ulcer. A similar pustule was present on the right sole. Fever was high grade, intermittent type and reduced on medication. Child was born to non-consanguineous parents, with insignificant family and antenatal history. Her developmental milestones were normal, and she was fully vaccinated. On general physical examination, the child was conscious, febrile and irritable with toxic look, had tachypnea and tachycardia, weighed 8 kg, and anthropometrical measures revealed Grade II malnutrition for age. There was no past medical or family history to suggest that the child could have an inherited or acquired immunodeficiency. Her pulse was 152/min and BP 82/50 mm Hg, temperature 104°F, respiratory rate 52/min. On auscultation, there was reduced air entry in the right side of the chest in the region around the axilla. Other systems were within normal limits.
Routine blood examinations revealed raised leukocyte count (15,600/mm 3 ), neutrophilia (79%), C-reactive protein 243 mg/l, serum sodium-121 mEq/L, serum potassium-5.36 mEq/L, serum bicarbonate 165 mEq/L, prolonged coagulation studies and microcytic hypochromic anemia with hemoglobin 8 g%. ELISA test for the qualitative determination of antibodies to human immunodeficiency virus type 1 and 2 viruses was nonreactive. ELISA test for hepatitis B surface antigen was nonreactive. Chest X-ray showed a patchy opacity in right middle zone. BACTEC Blood culture and wound swab from the site of the ulcer were sent on day of admission that grew B. pseudomallei on the 2 rd day. Salient features of identification of the isolate included, oxidase positive, Gram-negative bacilli with safety pin appearance (bipolar staining) on Gram's staining [Figure 1]; rough, wrinkled colonies with metallic sheen on MacConkey's agar [Figure 2] and blood agar and resistance to polymyxin B (300 μg/disc). Further biochemical reactions on the isolated colonies showed oxidative utilization of glucose, lactose and maltose. Lysine was not decarboxylated, arginine was dihydrolyzed and nitrates were reduced to nitrites. The colonies grew at 42°C.  Antibiotic susceptibility testing was performed by disk diffusion test according to the Clinical Laboratory Standards Institute guidelines. The isolate was susceptible to Amoxicillin-clavulanic acid, ceftazidime, cotrimoxazole, imepenem and meropenem, but resistant to gentamicin, amikacin, ciprofloxacin. This unusual antibiotic susceptibility pattern was also suggestive of B. pseudomallei.
|Figure 2: MacConkey's agar showing wrinkled colonies with metallic sheen|
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There was a previous history of high-grade fever with cough for which she was hospitalized 15 days back and diagnosed with right lobar pneumonia. Such episodes were there since a month. She was treated with ceftriaxone and amikacin and discharged on the 5 th day. No microbiological investigations were done that time.
During the present hospitalization, initial empirical antibiotic therapy was started with Injection Vancomycin Q8 hourly and Injection Amikacin 125 mg I.V OD. On day 2 of admission, her condition worsened, she developed hypotension and drowsiness. She was shifted to the pediatric ICU, given I.V fluid bolus and started on Dopamine. Child had sudden cardiorespiratory arrest and succumbed to the infection on Day 2.
| Discussion|| |
Pediatric melioidosis is recognized as a leading cause of bacterial sepsis in children residing in Thailand,  Malaysia  and Australia.  In India, it was first reported in a child from Maharashtra in 1990,  thereafter, only fewer cases have been reported in children. , This to a certain extent ascertains the fact that melioidosis is probably underdiagnosed or under reported due to lack of awareness amongst pediatricians and microbiologist and its ability to mimic any community acquired bacterial sepsis, pneumonia, abscess especially that produced by Staphylococcus or tuberculosis. 
Melioidosis can present as an acute illness with pneumonia, septicemia, coagulopathy and shock or patients can also develop chronic infection involving the lungs, bones, joints, liver, spleen, lymph nodes, myocardium, brain and skin usually simulating a variety of diseases including tuberculosis. The condition is mainly reported among patients with underlying chronic illness, such as diabetes mellitus (most common), alcohol intake, chronic renal or lung disease or immunosuppression. , Presence of malnutrition in developing countries is also known to contribute to a higher mortality rate in melioidosis,  which could also be a contributing factor in this case.
The western coastal region of India seems to be an ideal setting for endemicity of this disease, with an annual rainfall of about 300 cm.  Being a resident of the coastal area, the child must have acquired the infection by inhalation or by direct contact of minor skin lesions with the infective source, most likely the soil.
Pulmonary involvement is the commonest finding in patients with melioidosis.  The presentation varies from mild tracheobronchitis to overwhelming cavitary pneumonia, long-standing suppurative focal abscesses, fulminant septicemia, shock and coma, with death being the occasional culminating event. The mortality is over 90% in untreated septicemia, and about 20-75% when treated. Once septic shock develops, the case fatality rate is approximately 95%. , How et al. looked at a group of 14 children with melioidosis from the central Malaysian state of Pahang. In this series, eight patients had septicemia on admission and six had localized infection. Five out of the eight patients with septicemia had shock, with a case fatality of 80%.  Our patient succumbed to the illness after developing septic shock.
The radiological findings in the acute form include focal consolidation or multiple small pulmonary nodules that start at the upper lobes and may progress to cavity or abscess formation.  There is a possibility that a diagnosis of acute pulmonary melioidosis was missed in the previous hospitalization of the child. However, since there was no microbiological confirmation, it remains unknown whether the present condition was a recurrence of previous melioidosis, ongoing infection or acute infection in the present hospitalization.
Children with melioidosis do not respond to ceftriaxone and gentamicin (the empirical regimen for sepsis), which underscores the need for a high index of suspicion of this condition. The treatment objectives are to reduce mortality and morbidity and to prevent recurrent infection in melioidosis. In children with severe infections, initial parenteral eradication therapy with ceftazidime (40 mg/kg/dose) or IV meropenem (25 mg/kg/dose) eight hourly should be administered for at least 2 weeks. Then a 20 weeks oral maintenance therapy with co-trimoxazole (trimethoprim 8 mg/kg/day) and doxycycline (4 mg/kg/day) in two divided doses are recommended. In children below 8 years and pregnant women, amoxycillin/clavulanate (15 mg amoxy-cillin/kg/dose for three divided dose) is advised instead of doxycycline. Because relapse is common with melioidosis, treatment with an oral antibiotic such as amoxicillin-clavulanate should be continued for a couple of weeks and the child should be followed-up to ensure remission. 
| Conclusion|| |
The present case focuses the need to record the presence of pediatric melioidosis in India. It also emphasizes the importance of diagnostic confirmation of the condition through culture of B. pseudomallei along with the antibiotic susceptibility testing before initiating antibiotics. The case was probably missed due to lack of clinical awareness and early diagnosis leading to the development of septic shock and mortality of the child. A high index of suspicion among pediatricians and microbiologists of the infection is the need of the hour especially in the coastal regions of the country.
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[Figure 1], [Figure 2]