Globally, Plasmodium vivax and P. falciparum malaria are the most important causes of malaria. Falciparum malaria is generally the most severe form of disease which causes the majority of malaria deaths. Nevertheless, vivax and knowlesi malaria can also result in severe disease and even mortality. In most case series from Europe and North America, malaria frequently comes up as the commonest cause of fever in the returned travellers. Although malaria is not the commonest cause of fever in the returned travellers in Hong Kong, it is a diagnosis that must not be missed because fatalities due to falciparum malaria do occur regularly, and some of these cases in the past had been related to delays in diagnosis or initiating treatment. Malaria must be considered in any sick returned traveller who had stayed in an endemic area. The shortest incubation period for falciparum malaria is 7 to 8 days. There are no pathognomonic symptoms and signs of malaria. Malaria is often mis-diagnosed as other diseases such as respiratory tract infection, gastroenteritis, or bacterial sepsis. The classical periodic fever is present in only a minority of patients at the time of presentation. One should be aware of common pitfalls in the diagnosis and treatment of malaria. Patients with severe malaria should be treated and monitored in intensive care settings. For severe malaria, intravenous artemisinin is the drug of choice because of its rapid clearance of parasitaemia. Radical cure with primaquine should be offered to patients with vivax and ovale malaria after checking the glucose-6-phosphate dehydrogenase status.
 

Influenza infection can lead to a variety of neurologic complications including influenza‐associated encephalitis/encephalopathy, acute necrotizing encephalitis, febrile convulsion, acute encephalopathy with biphasic seizures and late reduced diffusion, acute disseminated encephalomyelitisas, Guillain–Barré syndrome, Reye's syndrome, and encephalitis lethargica. 
The neurological complication of 1918 Spanish Influenza A pandemic is dominated by encephalitis lethargica. Juvenile form of encephalitis lethargica is characterized by a change in personality and rapid transformation of the victim from normal behavior to delinquency, often leading to institutionalization. The non-structural NS1 protein and PB1-F2 protein through inhibiting the interferon response and induction of apoptosis via opening of the mitochondrial transmembrane transition pore contribute to the virulence of the virus. 
With the emergency of human H2H2 and H3N2 influenza A virus the neurological complication is initially dominated by the development of Reye’s syndrome due to the use of aspirin. Influenza-associated neurological complication is uncommon in Caucasians children after the withdrawal of aspirin in the management of influenza A virus infection. After the withdrawal of influenza vaccination program in children in Japan, Japan has experienced an upsurge of influenza-associated encephalopathy that may rapidly progress to necrotizing encephalitis during acute influenza infection due to the prevalence of mitochondrial beta-oxidation disorder among the Japanese population. Cytokine dysregulation, microglial activation and apoptosis are pivotal in the pathogenesis of influenza-associated encephalopathy. 
The 2009 H1N1 influenza virus contain a non-structural gene segment that can produce potent cytokine dysregulation. Most of the severe cases and death of 2009 H1N1 influenza A infection in children in the western world presented with respiratory complications with influenza-associated neurologic complications observed in only around 4% of patients. In contrast, the leading causes of death among children with 2009PV in Japan were encephalopathy and unexpected cardiopulmonary arrest. Deaths associated with respiratory failure were infrequent and occurred primarily among children with preexisting conditions.