A 42-year-old Sri Lankan man presented to the Colombo North Teaching Hospital, Ragama, Sri Lanka (CNTH) with a febrile illness of 6 days, accompanied by headache and constitutional symptoms. He was a grocer from Minuwangoda, a suburban area in the Western Province situated 44 km from Colombo. He was initially investigated and treated at a regional hospital for 4 days, and was transferred to the CNTH for specialized care. He gave a history of type 2 diabetes mellitus for 5 years without microvascular or macrovascular complications, and was a nonsmoker and a teetotaler. There were no specific symptoms suggesting a source of infection such as cough, abdominal pain, urinary symptoms, etc. He was febrile with a temperature of 39.10 C, and examination of the heart, lungs and abdomen was unremarkable. There was no papilloedema, focal neurological signs, pyramidal signs or neck stiffness. Initial laboratory work up revealed features of a bacterial infection, with neutrophil leukocytosis and elevated inflammatory markers (erythrocyte sedimentation rate – 101 mm/1st hour, C-reactive protein - 220 mg/dl). Initial blood cultures done at the regional hospital had yielded an isolate, which was reported as a Pseudomonas species; this was sensitive to ceftazidime, imipenem and meropenem and resistant to gentamicin and ceftriaxone. Other basic laboratory investigations including renal and liver function tests, electrolyte panel and urinalysis were normal. Chest x-ray and ultrasound scan of the abdomen were normal, and the trans-thoracic 2-D echo did not show any vegetations. As the unusual antibiotic sensitivity pattern suggested the possibility of melioidosis, blood was sent for serological testing to a specialized Melioidosis Research Laboratory at the Faculty of Medicine, University of Colombo.\nHe had been initially treated with intravenous ceftriaxone, and later with ceftazidime according to the antibiotic sensitivity pattern. Although the frequency and intensity of fever spikes reduced with treatment, he continued to have low grade fever and complain of anorexia, malaise and lethargy. On the 4th day after admission to the CNTH (day 10 of the illness), he developed simple partial seizures involving the left lower limb, progressing to persistent numbness of the left side of the body. An urgent CT scan of the head revealed a subdural collection over the right fronto-parietal region with gas locules and obliteration of sulci and gyri, without definite evidence of abscess formation (Fig. ). Contrast enhanced MRI scan of the brain demonstrated a subdural collection in the right fronto-temporo-parietal region with possible abscess formation in the right parietal region (Fig. ). Seizures were treated with oral sodium valproate and phenytoin sodium. He was referred for neurosurgical opinion, and the subdural collection was managed conservatively. Results of the indirect hemagglutination assay (IHA) for melioidosis antibodies were received on the following day; an antibody titre of more than 1/10,240 was strongly suggestive of an acute infection with Burkhoderia pseudomallei and a diagnosis of cerebral melioidosis was made.\nAntibiotics were changed to intravenous meropenem and oral trimethoprim/sulfamethoxazole (Co-trimoxazole/TMP-SMX). Initial intensive therapy with these antibiotics was continued for 8 weeks, until clinical improvement was evident with resolution of inflammatory markers and radiological improvement confirmed by repeat MRI scan of the brain. (Fig. ) Repeat blood cultures were sterile after 2 weeks of treatment with antibiotics. There were no further seizures, and the fever and the neurological symptoms resolved completely. He was discharged home with oral TMP-SMX and doxycycline, which were continued for 6 months, and the antiepileptics were gradually tailed off. At 6 months follow up he was asymptomatic. (Fig. ).
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.