[4] In the midst of the outbreak in Sarawak, Coxsackie B virus (CV-B) was initially thought to be the causative agent based on the clinical presentation of myocarditis, but not detected among the deceased children.
After a few months, Enterovirus-71 was isolated from deceased children in Peninsular Malaysia that died from brainstem encephalomyelitis.
Common symptoms at this stage are fever, sore throat, exanthem (especially maculopapular rash) at palms, feet, and buttocks.
The disease can also affect the oral cavity, causing vesicles (small blisters) and ulcers on the tongue and soft palate.
Stage 2 is characterised by central nervous system involvement, causing meningoencephalitis, and polio-like syndrome such as poliomyelitis-like paralysis, and non-paralytic poliomyelitis (aseptic meningitis).
[4] In Sarawak, the most frequent symptoms of a child with central nervous system involvement are fever more than 38 degree Celsius for more than 3 days and lethargy.
[4] Through autopsies performed on the deceased children, their deaths are caused by several symptoms linked to the disease such as poor peripheral perfusion, tachycardia and cardiac failures with earlier developed symptoms such as shock, pallor, cold extremities, delayed capillary refill and weak peripheral pulses.
Adults usually do not show any symptoms of HFMD, but may shed the virus and infect other children in the process.
Enterovirus may persist in the environment for three days under room temperatures such as in sewage and water systems.
The exact mechanism of immunoglobulin therapy in treating the disease is unknown, but it can reduce the level of inflammatory markers produced against the EV-71 virus in children with pulmonary oedema (accumulation of water within lung tissues and air spaces.
A high level of inflammatory markers causes cytokine storm which is life-threatening instead of helping to fight against the infection.