Article forwarded to Promed on 19 October 2000


Since the outbreak of hand, foot and mouth disease in Singapore in September, the State of Johor at the southern tip of peninsular Malaysia, has stepped up its vigilance for the disease. The first fatal case was reported in Johor on 3 October and the number of HFMD cases has increased from 36 in the first week of October to 274 in the past week. Other states which have reported cases are Selangor, Penang, Kedah, Sabah and Terengganu. In a press release today (October 19, 2000, New Straits Times), the HFMD national operations centre stated that up till 18 October, 510 patients have been warded in several states and 393 have sought outpatient treatment.

HFMD is endemic in Malaysia and in 1997, there was a large outbreak which resulted in the death of over 40 children due to brainstem encephalomyelitis. The etiological agent was attributed to enterovirus (EV) 71. Since then, sporadic cases of HFMD caused by Cox A16 and EV71 have been reported in the country.

On 12 October, the first fatal case resulting from HFMD complication was reported in the University Hospital Kuala Lumpur. Below is a description of this case as provided by Assoc. Prof. Dr. Lucy Lum and Dr. Adrian Goh from the Paediatric ICU.

A 3-year-old boy was referred from a private hospital (DSH) to the University Hospital Kuala Lumpur (UHKL) on 11 Oct. He was admitted to DSH on 7 Oct for 1 day of fever and numerous mouth and hand lesions. TWC 12.5, 85% neutrophils. He remained febrile but was neurologically normal. His antibiotics were changed from augmentin to Ceftriaxone on 8th Oct because of persistent fever. Haemodynamically, he was stable with HR 70-80/min. His mouth and hand lesions improved. On 10 Oct, he became lethargic with fluctuating levels of consciousness. He was able to communicate with parents but would drift off into semiconsciousness in mid-sentence. At 7 pm of 10 Oct, he became restless and vomited several times. A CT brain was reported to be normal. At 3 am 11 Oct, his heart rate started to increase and blood pressure 110/60 mmHg. He was cold and pale. An ECHO showed globular LV dyskinesia. He was intubated at 8.30am and pink frothy secretions were noted. At DSH he was given mannitol, lasix, acyclovir and phenobarbitone. He was transferred to UHKL at about 1300 11 Oct. On arrival he was pale, cold, with feeble brachial pulses. BP was unrecordable. His eyes were sunken and liver and spleen were not palpable. An ulcer was noted under the tongue. He has a brief asystole arrest when his ETT was dislodged. Return of spontaneous circulation with 2 doses of adrenalin. A CV line was inserted. CVP was -6 cm H2O. He was started on Dopamine, dobutamine, adrenaline, noradrenalin and milrinone. Pupils 3 mm, reactive and the patient had a flexor response to pain. BP was about 90/60 mmHg. He was too unstable for radiological imaging. Blood lactate improved from 5.9 mmol/L to 1.7 mmol/L. CKMB was 1, suggesting secondary myocardial depression. Ventilation was with pressure control PEEP 4cmH2), FiO2 40%. CXR showed small heart. ECHO LV was dilated and had very poor function. By 8pm 11 Oct, BP has been stable at 90/60 mmHg, but the persistent tachycardia (180-190/min) that could not be explained by the temperature was of concern. At 3 am 12 Oct, he suddenly developed runs of ventricular tachycardia progressing to persistent VT at 230/min, BP 60/40 mmHg. This did not respond to adenosine or lignocaine infusion. At 9am, methylprednisolone 30 mg/kg was given. The tachycardia slowed down to about 180-190/min. At 1220 the heart rate suddenly decreased progressively and he died at 1230.

There is a subtle difference between this case and the cases of 1997. The acute progression of disease in this case was less aggressive than the cases in 1997. However the features also suggest brain stem, esp vasomotor center involvement - tachycardia, transient hypertension, severe vasoconstriction and LV dysfunction.

Virological findings

Since August 2000, the Department of Medical Microbiology, University Malaya Medical Centre, has received over 600 samples from 221 suspected HFMD cases, the majority (206 cases in October) from Johor. The number of hospitals sending samples are Johor (11), Kedah (2), Melaka (1), Negeri Sembilan (1), Sabah (1), Selangor (2) and the Federal Territory (3).

Cox A16 and EV71 viruses have been isolated from several cases of mild HFMD. A different enterovirus was isolated from 2 patients with severe CNS manifestations and 2 fatal cases seen at various hospitals. The isolate stained positive by immunofluorescence using a commercial pan-enterovirus blend but did not react with other enterovirus pools, including for Cox A16 and EV71. Further identification of this enterovirus by neutralization and molecular sequencing is in progress.

Ken Lam
Consultant Virologist
University Hospital Kuala Lumpur
19 October 2000