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.
The patient, a 55 yr old female with Type 2 diabetes mellitus for the last 14 years, on insulin for 2 years, pre-sented with the complaint of sudden onset weakness of all four limbs for five days. She had a preceding history of severe muscle cramps and paraesthesia for about a month. History revealed that the patient had severe generalised weakness twenty days back, for which she had been admitted in a local hospital and had improved symptomatically (though some amount of muscle pain persisted) with intravenous fluid and injectable medications, the details of which could not be gathered. The onset of quadriparesis was acute, noticed on getting up in the morning, five days prior to admission in our institute. There was no history of unusually high carbohy-drate intake, cold exposure, excessive exertion or alcohol intake the previous night. She denied unexplained sweating, tremors, heat intolerance, prolonged vomiting, or any drug intake over a prolonged period of time. General examination revealed carpopedal spasm, hypertension(160/100 mm Hg) and mild pallor. Neurological examination revealed bilater-ally symmetrical weakness (Gr 1/5) of all four limbs and generalized hyporeflexia. Muscles of the eyes, face, tongue, pharynx, larynx, diaphragm and sphincters were not involved. Higher functions, cranial nerves and sensory system were intact. Plantar was bilaterally flexor. Apart from mild hepatomegaly, systemic examination was normal.\nInvestigations revealed hypokalemia(1.3 mEq/l), hypocalcemia (corrected 5.8 mg/dl) and hypomagnesemia (1.1 mg/dl) with normal sodium and chloride levels. Routine blood examination was normal. Fasting and post prandial plasma glucose was 171mg/dl and 309mg/dl respectively with an HBA1c of 9.5%. Serum osmolality was normal.\nUrinary ketones were negative. Liver function tests were slightly deranged with AST of 71 mg/dl and ALT of 186 mg/dl. Serum protein was 7.09mg/dl, albumin - 3.2 mg/dl, globulin - 3.8mg/dl, serum bilirubin -0.5mg/dl. Serum creatinine was 1.l mg/dl and microalbuminuria was present. CPK and LDH were within normal limits. Thyroid profile was normal. Serum phosphorus was normal and PTH was 50.3 pg/ml(normal–10 to 55 pg/ml). 24 hour urinary calcium was 61mg (normal - 100 to 300mg/24hrs). Urinary potas-sium excretion was 53 mEq/L /day (normal-25-120 mEq/L/day). Blood gas analysis revealed metabolic alkalosis. Electrocardiogram, ultrasound abdomen, plain picture abdomen, X-ray cervical spine and chest X-ray were normal. MRI of brain, spine and abdomen were also normal.\nInitially, the patient was treated with injectable potas-sium, magnesium and calcium preparations. Normalization of serum potassium and calcium was achieved only after total correction of magnesium level. There was gradual improve-ment in muscle power after 24 hours of therapy. Complete recovery was achieved after five days of treatment, following which she was shifted to oral preparations. Glycemic control was achieved using insulin and hypertension was controlled with Amlodepin 5 mg. She was discharged after two weeks on oral calcium(l gm daily) and advised to take diet rich in potassium and magnesium. On subsequent follow up at one and three months, she was asymptomatic with normal electrolyte levels and good glycemic control.