Abstract

Melioidosis is an endemic to several South Asian countries. Now it is a treatable emerging infection in India. In our case a 51 year old man was presented with intermittent fever and left sided chest pain for 3months. He was a pet lover, had 10 cats and 8 dogs at home. He is an ex-smoker and alcoholic. He has been a diabetic for past 7 years. From the radiological and clinical findings he was diagnosed to have melioidosis of left lung. In progressive years he had relapse of the disease with liver and spleen abscess.

Key words:

burkholderia pseudomallei , melioidosis, liver abscess, spleen abscess.

Authors:

1. Dr. Dinulal P.P, Junior resident, Department of general surgery, Government medical college, Calicut
2. Aleen Catharine, 5th year Pharm D, National college of pharmacy, Calicut
3. Manas Joshi, 5th year Pharm D, National college of pharmacy, Calicut
4. Thenu Jacob, 5th year Pharm D, National college of pharmacy, Calicut

Introduction :

Melioidosis is a disease caused by gram negative organism, burkholderia pseudomallei. It was considered as a glanders like disease. The etiological agent was first described by Whitmore and Krishnaswami. Later on Stanton and Flecther named the disease as melioidosis. The organism is found in contaminated soil and water. It can resist nutrient deficiency, acid and alkali pH, disinfectant, antiseptic solution, extreme temperatures and can adapt to host defensive enzymes. This disease is seen in both humans and animals. Diabetes mellitus, alcoholism, male gender are the predisposing factors of the infection. The disease can affect any organs, and can mimic many diseases. The classical symptoms of the disease are fever, chest pain and osteomyelitis. This disease is categorized as acute localized, acute pulmonary, disseminated and chronic suppurative infection. They are treated by ceftazidime, carbepenems, amoxicillin + clavulonic acid.

Case report:

A 50 year old male living in Tirur, Kerala, India was presented with intermittent high grade fever with chills and left sided chest pain for 3 months. He is an ex-smoker and chronic alcoholic having diabetes for 7 years. He had 10 cats and 8 dogs at home and had close contact with his pets. He doesn’t remember any experiences of outdoor injury. He had no relevant history of travel.

On 1 May 2013, patient experienced high grade fever with chills, generalized weakness, fatigue and weight loss. The erythrocyte sedimentation rate was 70 mm in 1st hour. White blood cell count was 8000/mm3 with 51% neutrophil,45% lymphocytes and 4% eosinophil. C-reactive protein level was elevated as 26.6µg/Dl. On 3may 2013 computed tomography of thorax revealed loculated left pleural effusion with passive collapse of underlying lung fields and necrotic posterior mediastinal lymph nodes. The above features was likely of infective etiology possibly koch’s. The multiple peripherally enhancing hypodense lesions in spleen likely represented microabscess or granulomas. On 5 may, pleural fluid analysis showed adenosisne deaminase10 IU/L, protein 6g/dL, sugar 232 mg%, neutrophil 06 %, lymphocyte 95 %,white blood cell count 62/µL. From discrepancies of spiked fever and other clinical, radiological findings the patient was suspected to have pleural effusion and pulmonary tuberculosis. He was started with empirical anti tubercular therapy and discharged on 6 may 2013.

On 12 July 2013, he developed swelling on left chest wall and pleuritic chest pain. Computed tomography guide aspiration of pus from chest wall showed heavy growth of burkholderia species sensitive to chloramphenicol, imepenem, tetracycline, clotrimoxazole, ceftazidime. On 18 July, computed tomography guided aspiration of pus from liver abscess had moderate growth of burkholderia pseudomallei. The chest X ray showed decreased rib space on left lower ribs and diaphragm pulled up in left side. On 19 July, bronchial wash with cytology isolated pseudomonas aeriginosa resistant to co- trimoxazole, sensitive to amikacin, cefepime, ceftazidime, ciprofloxacin, gentamycin, imepenem, meropenam, ofloxacin, piperacillin. On 20 July, computed tomography revealed multiple areas of left subsegmental atelectasis in basal segments of left lower lobe. Minimally displaced fracture in lateral aspect of 8th rib with adjacent collection osteomyelitis to be excluded. Multiple non enhancing hypodense areas with features of splenic cyst were present. On comparing with previous CT, pleural effusion was resolved completely. From the clinical evidence final diagnosis of pleuropulmonary melioidosis with osteomyelitis 8th left rib was made. Patient was responsive to imipenem and cilastatin combination. He was on his ATT combination phase. Fever was subsided and patient was discharged on 23 July 2013.

On 24 November 2014, patient was again admitted with spiked fever and generalized tiredness. The previous history of melioidosis went unnoticed. The clinical condition was suspected of malaria and treated with antimalarials.

On 11 February 2015 patient was admitted with high grade fever with chills, generalized weakness and fatigue. Routine laboratory investigations revealed erythrocyte sedimentation rate of 110 mm in 1st hour, white blood cell count was 6600 cells/mm3, high blood sugar of (randomized blood sugar) 160 mg%, serum alkaline phosphate of 169 IU/dL, total protein to albumin ratio of 7.6/3.1. Peripheral smear showed microcytic hypochromic RBC, preterm neutrophils with toxic granules and mild thrombocytopenia.

On 12 February, ultra sonogram showed liver mildly enlarged on right lobe (15.3 × 6.3 × 5.8 × 5.6 mm) with solid cystic irregular and ill-defined mass in left lobe. Spleen was irregular in size with multiple small cystic linear avascular structure scattered in parenchyma. On 13 February, high dose contrast enhanced computed tomography( CECT ) of abdomen showed multiple non enhancing hypodense areas in left lobe of liver, the largest measures of 6 × 4.3 × 7 mm extending to supcapsular location and spleen with multiple non enhancing lesions. On 15 February, pus drained from liver abscess was positive to burkholderia pseudomallei by culture. Blood sugar was not controlled with plain insulin, but inj. Human mixtard and metformin combination could control it. Patient was started with ciprofloxacin and metronidazole, but when fever spiked despite the treatment piperacillin tazobactam combination was tried. After isolation of Burkholderia species, patient was given inj.ceftazidime. The 28 days treatment could reduce fever and have good diabetic control. Patient was discharged on 11 march 2015 with better health status.

Discussion:

Melioidosis is a rare endemic caused by brukolderia pseudomallei found in soil and water. They mimic many diseases and cause multiple organ dysfunctions. Animals and humans usually acquire this disease from contaminated environment. Transmission of the disease is by ingestion, inhalation or by wounds and abrasions. Infected animals shed the organism through wound exudates, nasal secretions, milk, feces and urine which can survive the divesting temperature and pH of soil for several months. A human with exposed wound with this soil gets infected. Unless the predisposing factors like diabetes mellitus, liver dysfunction, alcoholism and general physical wellbeing are controlled the patient will have relapses of the disease. Early detection and prevention of the disease can reduce the significant mortality and morbidity of the disease.

Reference :

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