In February 2006, a previously healthy 58-year-old Sinhalese woman presented to our hospital with a history of intermittent fever, headache, loss of appetite, loss of weight, dry cough, and arthralgia of 5 weeks’ duration. She had no known past medical conditions or any family history of chronic disorders or similar illnesses. She was a housewife who frequently engaged in gardening and had no history of visits to forest areas or working in paddy fields. She was not alcoholic and was a nonsmoker.\nAt the beginning, she had been hospitalized, had undergone investigations, and had received broad-spectrum antibiotics. Due to the nature of the protracted illness with fever, and because she had an erythrocyte sedimentation rate (ESR) above 100 mm/h and increased C-reactive protein (CRP), a course of antituberculous antibiotics had been given over 2 weeks without definitive confirmation of the diagnosis of tuberculosis. While on antituberculous medications, instead of clinical improvement, she showed further deterioration of her illness and developed new problems, including appearance of a tender lump over the right temporal area over the course of 1 week and another similar lump over the anterior aspect of the left thigh of 5 days’ duration. At this juncture, she left the first hospital at her own wish and secured admission to Teaching Hospital Peradeniya (THP).\nOn admission to THP, she looked very ill and feeble and was febrile and tachypneic. She had a tender lump resembling an abscess over the right temporal area. Furthermore, she had similar lumps over the anterior aspect of the left thigh. She had an inflamed, swollen knee and wrist joints with a tender erythematous rash over both shins that resembled erythema nodosum. Her pulse rate was 110 beats/min with blood pressure of 100/65 mmHg. The results of her respiratory system and abdominal examinations were clinically normal. She was conscious, rational, and had no neck stiffness, with a clinically normal neurological examination result.\nBlood samples were taken for basic investigations and culture at this juncture. Diagnostic needle aspirates from the cystic lumps and knee joint effusions were purulent and were sent for bacteriological investigations. Blood samples for cultures were taken under aseptic conditions. Three separate blood cultures were taken in 30-minutes intervals and drawn into standard blood culture bottles. Knee joint and skin lump aspirates also were drawn into separate culture bottles under aseptic conditions. All the samples were transported to the microbiology laboratory, which is located within the hospital premises, and the cultures were done by a consultant microbiologist. Pending investigations, the patient was treated with intravenous (IV) co-amoxiclav (amoxicillin mixed with clavulanic acid).\nOn the fifth day of the patient’s admission, she became drowsy and developed focal seizures involving the right upper and lower limbs and lasting for around 2 minutes. She became drowsy with a Glasgow Coma Scale (GCS) score of 12/15. She moved all her limbs, and her deep tendon reflexes were normal, but she had an upgoing plantar response. She had no neck stiffness, positive Kernig sign, or focal neurological signs. She had persistent tachycardia with low blood pressure of 90/50 mmHg. Her respiratory rate was 30 breaths/min, and she had bibasal crepitations. She had bilateral knee joint effusions, and her knee joints were swollen, warm, erythematous, and tender. A tentative diagnosis of cerebral abscesses was made, and the patient was transferred to the intensive care unit.\nUrgent contrast-enhanced computed tomography of the brain showed a well-defined cystic mass in the right temporal region outside the skull vault and contrast-enhanced changes in the adjacent brain matter. Furthermore, a 12-lead electroencephalogram (EEG) showed a theta-wave focus over the right temporal area with intermittent epileptiform discharges compatible with structural brain damage. The results of her ultrasound examination of the abdomen and an echocardiogram were normal. Her white blood cell count was 3.3 × 109/L with neutrophils of 83% and lymphocytes of 12%. Her ESR was 120 mm/first hour, and her CRP level was 192 mg/L. Her chest x-ray showed multiple peripherally located, ill-defined cystic areas in both lung fields, more in the lung bases, suggestive of multiple lung abscesses. By that time, the blood culture, knee joint aspirate, and skin lump aspirates grew B. pseudomallei, which was confirmed by the local microbiologists with the help of international reference laboratories []. Thus, a diagnosis of melioidosis was confirmed, and treatment commenced.\nFollowing the confirmed diagnosis her antibiotic regimen was changed and started on IV meropenem 1 g 8-hourly for 8 days and later changed to IV imipenem 500 mg 6-hourly, based on the antibiotic sensitivity pattern of the bacterial isolate. Two more antibiotics were added to the regimen at the same time: IV ciprofloxacin 400 mg 12-hourly and IV ceftazidime 2 g 6-hourly. The patient showed gradual improvement of her general condition, and her fever subsided in a few days. However, all three antibiotics were continued for 30 days and changed to an oral antibiotic course comprising cotrimoxazole 1920 mg twice daily plus doxycycline 100 mg twice daily for 20 more weeks. Her seizures were controlled with sodium valproate 200 mg thrice daily. In follow-up, the patient’s chest x-ray, ESR (50 mm/h), CRP (0.7 mg/dl), and liver and renal profiles showed gradual improvement, and the results of her retroviral screening were negative. Her blood sugar and hemoglobin A1c levels were within normal limits. The result of repeat EEG in 3 months’ time was normal, and the patient’s sodium valproate was gradually tapered. After 6 months of antibiotic treatment, her ESR was 12 mm/first hour; her CRP was < 6 mg/L; and all of her other biochemical parameters were normal. Then, she was advised to come back to our hospital for annual screening to check for recurrence of the disease, including ESR and CRP measurement. She has had no recurrence of her illness during the last 13 years and remains well.\nSubsequently, how she contracted the infection was inquired about. She was able to recall contact with soil a few days prior to developing her illness. The footpath leading to her home had a side drain that was filled with mud and soil. She found that a worker had dug up the drain and piled mud and soil on the footpath. The patient, dismantled the piled-up soil with her bare feet and made the footpath accessible.
A 42 year old diabetic woman from North Western Province of Sri Lanka presented with abdominal pain, vomiting and intermittent fever for one month. She had recurrent skin abscesses 6 months before presentation which was treated with incision and drainage and a short course of antibiotics for which there was only partial improvement. Three months before presentation to us she was found to have multiple liver abscesses which were aspirated in a local hospital. The aspirate grew “coliforms” resistant to gentamicin and sensitive to ceftazidime. She was treated with cefuroxime, meropenem, co-amoxyclav and metronidazole; further identification of the organism was not done at the local hospital.\nOn presentation to us she had high fever and tender hepatomegaly. Her body weight was 40 kg. Rest of the examination including nervous system was normal.\nHer full blood count showed leukocytosis [15.7×109/L] and granulocytosis [11.3 × 109/L], ESR was 100 mm in the 1st hour and C-reactive protein was 98.4 mg/L. Ultra sound scan of abdomen showed multiple liver and splenic abscesses.\nPresence of recurrent multiple liver and splenic abscesses in a diabetic patient who had recurrent skin abscess in the past made us consider melioidosis in the differential diagnosis. Intravenous meropenem 2g eight hourly was started empirically and aspirate was sent with a sample of serum to Faculty of Medicine, University of Colombo which serves as the National Reference Laboratory, to confirm the diagnosis. There the aspirate yielded pinpoint colonies on blood, chocolate and Macconkey agar after overnight incubation. Since biochemical panels are not very accurate in diagnosis of Burkholderia pseudomallei, isolate was subjected to PCR which confirmed the diagnosis.\nSerum antibodies to melioidin antigen using an in-house indirect haemagglutination (IHA) test based on that described by Alexander et al. with antigen prepared from local strains of B.pseudomallei [] were positive at a titre of 1:10240.\nAfter confirmation of melioidosis intravenous meropenem was continued. However after a week of treatment the disease course was complicated by bilateral lower limb weakness which progressed over the next 4 days. Her lower limbs were flaccid and deep tendon reflexes were absent. There was no sensory sign or bladder/bowel involvement. Cerebro-spinal fluid analysis showed protein of 114.5 mg/dl, glucose 62 mg/dl, white cells <10 mm9/L and red cells < 10 mm9/L. MRI scan of the brain was normal. The nerve conduction study showed evidence of severe peripheral neuropathy with axonal degeneration; compatible with a primary axonal type inflammatory neuropathy such as acute motor axonal neuropathy or acute sensory motor axonal neuropathy.\nA diagnosis of Guillan-Barre syndrome was made based on Brighton case definition (Table ) () and she was treated with 4 cycles of plasmapharesis on alternate days for which there was marked improvement of neurological deficit.\nWith intravenous meropenem patient further improved and her ESR and CRP became normal. Repeat ultrasound scan of abdomen showed reduction of the size of liver and splenic abscesses.\nEradication therapy with cotrimoxazole 1920 mg 12 hourly and co-amoxyclav 625 mg 8 hourly was started on the seventh week and overlapped with intravenous antibiotic for further two weeks. Patient was discharged to outpatient clinic after two weeks of oral antibiotics with a plan to continue them for12 weeks. At the end of 12 weeks she had no residual neurological weakness and there was no sign of a relapse.