13 June, New Straits Times (Focus), pg. 11
COXSACKIE B has killed more than 20 children. Their deaths have struck at the heart of the nation. We are concerned and sympathise with the families hurt by the loss of a child. And we know there are important lessons to be learned.
To understand what happened in Sarawak, we must understand Coxsackie itself. It belongs to a family known as enteroviruses. It was first isolated in Coxsackie, New York, in 1948. Coxsackie grows in the stomach and can spread in many ways. Recently, the Institute for Medical Research identified Coxsackie B as the "culprit agent" of the epidemic in Sarawak.
Enteroviruses cause paralysis, inflammation of the brain and the linings of the lungs and heart. They also cause fever with rashes. The members of the enterovirus group include Coxsackie types A and B, poliovirus and echovirus. They are resistant to common disinfectants.
Coxsackie mutates genetically over long periods of time. Sometimes it alters its known patterns of behaviour, including its preferred targets. Coxsackie B, by reputation, is like an intercontinental ballistic missile. It can change targets, and raise its destructive capability more easily than Coxsackie A.
The capacity to mutate is in-built, and co-relates with disease outbreaks. Every two to five years, Coxsackie B produces a new "model" which attacks very young children, who by virtue of their age have never been exposed to this virus. That lack of specific immunity makes them ultra-vulnerable. The vast majority of children do recover. Some, sadly, suffer vital organ damage and may die.
Scientists call this mutating pattern a "genetic drift" as this phenomenon is relatively slow. In contrast, the HIV can mutate rapidly.
Coxsackie B, the 'culprit agent' of the outbreak in Sarawak, has the capacity to mutate, and every two to five years, it produces a new model which attacks the very young, writes DR W.M. CHONG SPOTTED ON THE HAND
... These "rashes" look so mild that we cannot imagine them as being part of a serious condition. This picture shows one symtom of Coxsackie Hand, Foot and Mouth disease.The current Sarawak outbreak suggests very strongly that this particular strain of Coxsackie B has a tendency to seek and destroy heart muscle tissue, causing a condition called myocarditis. This is a Latin word meaning inflammation of the heart muscle. This can trigger a variety of disruptions to the heart's operations. Myocarditis may progress to heart failure over months or years.
The outbreak in Sarawak has presented an unusual scenario - this strain seems to be highly aggressive. Instead of taking months or years to cause heart failure, this one is taking just a few days.
Doctors also watch for disturbance of the rhythm of the heartbeat. The heart has its own electrical circuit to synchronise its pumps. Myocarditis can bring about circuit failure. This can cause a variety of problems including palpitations, slow heartbeat and, even cardiac arrest. This electrical disturbance can be temporary or permanent and worsen over time.
How is the damage done? Basically, the virus confuses the body's defence system. First, the body detects the presence of an enemy using its antigen recognition system. The virus, meanwhile, may mimic the protein structure of the heart muscle, and sometimes, may even interact and alter the antigenic configuration there.
When this happens, the body's defence system reads the signals wrongly. It deploys killer white cells to attack the enemy. The white cells do two things. One, it fires virus-seeking missiles called antibodies to neutralise Coxsackie B and removes it from the battlefield. Two, the white cells also attack the wrong target: the heart. Like in the movie Courage Under Fire, the white cells attack one of its own life support systems. The second scenario transpires over months, sometimes years.
This, basically, is the classical theory. The situation in Sarawak suggests something different. In this outbreak, it seems the virus itself - not the white cells is attacking the heart muscle. This is suggested by the extremely short time phase between infection and heart failure.
Why the heart? Scientists know that some viruses have tissue affinity, meaning they home in on one or two particular types of body tissue. Coxsackie B goes for the muscles of the heart, where the virus locks on to receptor sites.
Coxsackie outbreaks are not unique events in history. The largest epidemic in Britain happened in 1994. It was Type A, and involved "hand, foot and mouth" disease. Most of the 952 cases were children aged one to four. Previous epidemics occurred in 1988 and 1990. Most strains of Coxsackie A don't attack the heart. However, one strain called Coxsackie A16 does attack the heart but this is rare. Coxsackie A is associated with "hand, foot and mouth" disease and was first documented in 1957, nearly a decade after the virus was first identified.
Last year, one medical journal reported surprising success in treating patients with Coxsackie A16. They used a drug called acyclovir, an anti-viral chemical normally used to treat herpes simplex. The study was not conclusive. It speculated that in these patients, something else was at work: these are the interferons, which are chemical messages sent from cell to cell like warnings to uninfected cells to defend themselves.
To identify a virus in the midst of an epidemic, scientists examine the genetic structure of the suspect. Right now, the state-of-the-art technique is the polymerase chain reaction (PCR) test. It requires only minute fragments of the virus. In the case of Coxsackie, the PCR technique is modified to accommodate its peculiar genetic configuration. This is called the Reverse Transcription PCR. In the hospital, diagnosis will be supported by an antibody count. The virus may cause liver inflammation, manifested by an increase in liver enzymes, which can aid diagnosis in adults.
Enteroviruses are everywhere. Infection without symptoms is common. In most cases, the symptoms are so mild, so minor, that the disease is brushed off as a non-specific runny nose. In an outbreak, the chances of infection with illness rise mainly because the organism is especially potent.
In Sarawak, doctors have treated some 4,000 people suspected of having the virus, in the form of hand, foot and mouth disease. This may be just the tip of the iceberg. More people may be infected but are not showing any symptoms. This group of people is capable of transporting the virus over long distances not realising that they ar e infecting others along the way.
Enteroviral myocarditis is a relatively benign condition in adults. In some adults, this may have no long-term effect. In others, it can bring about serious heart problems such as abnormal heartbeat or even heart failure later in life.
The "Achilles heel" of the Coxsackie B virus is that it is readily inactivated by certain a gents: ultraviolet light, chlorine, formalin and heating to 560C. These can be weapons in an outbreak.
In the larger scheme of things, sanitation, sewage control (with the chemicals described above) and eliminating insect carriers (like flies and cockroaches) will be helpful. Also, reducing person-to-person spread by regular hand-washing, and using a hankerchief while sneezing.
Closing daycare centres and nursery schools was the right move. Young children should be taught hand-washing and toilet hygiene. Pregnant women produce antibodies to protect their foetuses. Even so, a pregnant woman suspected of having an enteroviral infection should be closely managed by her doctor. Like all children, new-borns are vulnerable.
Humanity has survived many epidemics of all kinds of illnesses. Each outbreak teaches us something new about ourselves and our environment. The experience in Sarawak will lead us to more refined medical technology, sanitation, basic hygiene, public health and prepare us for the next battle. Diseases may demonstrate the frailty.
