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.
A 26-year-old female with Burkholderia cenocepacia presented with a two-month history of worsening fixed purpuric rash on the lower legs (). Skin biopsy confirmed leucocytoclastic vasculitis. She was treated with dapsone initially without improvement. On commencement of oral prednisolone, there was minimal improvement, which remained stable. Following this, she was managed with topical protopic 0.1%.