Posted in Psychology & Medicine

Sleeping Sickness

A woman travelling in Africa is bitten by what appears to be a mosquito. She swats the insect and keeps on going about her journey. The next week, she finds that she has a small nodule where she was bit. She is also feeling slightly unwell, with fever and fatigue. Over the following two weeks, her fever worsens (coming and going intermittently) and she notices large lumps along the back of her neck. By this stage, she is experiencing muscle and joint pain as well. After returning home from her trip, she finds that her symptoms have not resolved. On top of her fever and pains, she begins experiencing headaches, mood swings, lethargy, confusion, clumsiness, delayed response to pain, sleepiness during the day and insomnia at night. She begins to worry that something is wrong, but she believes that it is a bad flu and does not see a doctor. Her symptoms worsen with time (sleeping up to 15 hours a day), until one day, she falls asleep and does not wake up. She is taken to a hospital, where it is discovered she is in a coma. She dies within a week.

This is the typical presentation of sleeping sickness, also known as human African trypanosomiasis. It is an infectious disease caused by a protozoan parasite called Trypanosoma brucei (comes in two types: T. brucei rhodesiense (East African type) and T. brucei gambiense (West African type)), which is transmitted by tsetse flies – a bloodsucking fly endemic to sub-Saharan Africa (there are also case reports of sexual transmission between people). When infected, the parasite rapidly proliferates in the patient’s bloodstream. It is not detected by the host immune system, thanks to a surface protein called VSG. This allows it to spread through the patient swiftly and silently via the circulatory and lymphatic systems. The early symptoms (intermittent fever, rash, lymph node enlargement), typically presenting about a week or two after infection, are due to the parasite spreading through the blood and lymph. As the infection spreads, the parasites begin to invade the central nervous system (although in the West African type of the disease, patients often die from the toxic effects of the parasite replicating in the blood before they reach this stage).

As the infection spreads through the CNS, it causes the neurological symptoms described in the case. The sleepiness (from where the disease gets its name from) worsens as the disease progresses, with patients finding it difficult to wake up in the morning, even sleeping for over 20 hours. The sleepiness is caused by a chemical called tryptophol, which is produced by the parasite. Essentially, the neurological symptoms appear as if the person’s brain is slowing down, until they fall into a coma, resulting in death without treatment (usually within 2~3 years since the infection).

Sleeping sickness is invariably fatal unless treated early. Once the patient reaches the second stage (neurological phase), treatment becomes very difficult. The current first line treatment is a drug called melarsoprol, which is a form of arsenic. Because of its toxic nature, it is extremely dangerous and there is around an 8% chance of the patient dying from side effects. Fortunately, there are less dangerous and more effective treatments such as eflornithine (which only works for the West African type) being developed.

Posted in Psychology & Medicine

Laughter Epidemic

It is said that laughter is infectious. In 1962, an extreme case of “laughter infection” happened in village in Tanzania. The phenomenon originated in a boarding school for girls. On January 30, three girls spontaneously burst out in laughter and could not stop themselves from laughing. Soon after, the whole class was suffering from fits of uncontrollable laughter. The “infection” then spread throughout the school, claiming 95 of the 159 students over a stretch of two months. This strange symptom of uncontrollable laughter lasted anywhere from a few hours to 16 days. Interestingly, teachers were not affected and only girls between the ages of 12 to 18 were affected. By March 18, the school was forced to close down due to students not being able to focus during class.

The laughter epidemic was not localised to the school. After the school shut down and the girls returned home, fellow villagers were afflicted by the laughing disease, resulting in 217 villagers being “infected” by May (mostly children and teenagers). By June, the laughing epidemic spread to another nearby school, affecting 48 girls. The epidemic then went on to claim two more schools, forcing them to close down. By the time the epidemic died down (6 to 18 months after “patient zero”), it had affected over a 1000 people and shut down 14 schools.

So what was this strange disease? Was it some new viral infection causing neurological symptoms? Was it a toxin in the water supply? The answer was even simpler: mass psychogenic illness, also known as mass hysteria. Mass hysteria is a psychological phenomenon that occurs in groups placed in high-tension situations, such as within an airplane. This setting is perfect for triggering a mass delusion, causing the person to believe they are suffering from a physical disease. The trigger is usually another “patient” and the hysteria spreads like wildfire, usually by people seeing affected victims. Although the above case makes mass hysteria look like a harmless, amusing phenomenon, psychosomatism (when the mind tricks the body into thinking it is sick) can cause symptoms such rashes, fevers, vomiting and even paralysis. In fact, all of these symptoms were also reported during the Tanganyika laughter epidemic.

Posted in Science & Nature

Northern White-Faced Owl

The northern white-faced owl, found in the Sahara Desert of Africa, is a small, cute bird of about 22~24cm length. It is famous for a very unique defence mechanism. As shown in the photo, it normally has a round, puffy appearance, but when faced with a fearsome predator like a hawk, it undergoes a drastic transformation. The owl shrinks itself as much as possible to avoid the enemy’s attention, while looking like a sick bird that has lost a lot of weight. This appearance gives the predator the impression that the owl is not worth the effort of hunting and lowers the chance of it attacking. The ability to shrink to half its original width is achieved through elongating its body and pulling in its feathers as much as possible. Also, when assuming this shape, the owl always faces the predator and poses at an angle to minimise its exposure.

This transformation is only seen when the owl is placed in front of a large predator like a hawk or a much larger owl. When in front of a similarly-sized owl, it exhibits a different transformation where it flares up its wings to make itself look much larger, intimidating the opposition. But this behaviour is common in many other species of owls, whereas the shrinking performance is a rare behaviour only seen in the northern white-faced owl.

(Video showing transformation: http://www.youtube.com/watch?v=gFwgblszf6s)

Posted in Science & Nature

Mitochondrial Eve

We were all born from our parents. Our parents were all born from our grandparents. Everyone has a family tree and a root. If so, is it possible to find the beginning of mankind – our true “root”?

Our cells have an organelle (a part of the cell) called mitochondria. Mitochondria act as the cell’s engine and allow the cell to generate energy through respiration. An interesting fact about them is that they are not originally “ours”. About 1.5 billion years ago, there was an event where a prokaryote (cells without a nucleus, like a bacteria) invaded (or was eaten by) a eukaryote (cells with nuclei, like our cells). The prokaryote and the cell began a symbiosis and the prokaryote became a part of the cell.

Due to the external origin of mitochondria, they have a different genome to us. This is called mitochondrial DNA, shortened to mtDNA, which allows mitochondria to divide and synthesise proteins without the help of the host cell. It used to be a completely independent organism, but it has lost some of its functions to the cell.

mtDNA is inherited in a different way to normal DNA. Normally we receive half of our mother’s and half of our father’s genes, but we only inherit our mother’s mtDNA. This is because sperm keeps mitochondria in the tail which is lost during fertilisation, meaning our father’s mitochondria cannot be inherited. The only way to gain mitochondria is from those in the cytoplasm (the material that fills cells) of our mother’s egg. This is known as maternal inheritance.

Using this information, scientists compared a large sample of people’s mtDNA to turn back the clock. Knowing that a child and its mother share the same mtDNA and the mother and grandmother share the same mtDNA, we can analyse mtDNA to find the origin of mankind, or our first common female ancestor – also called Mitochondrial Eve.

Mitochondrial Eve is estimated to have lived 200,000 years ago in Africa, thus she is also known as African Eve. Her mtDNA is an ancient heirloom passed along generation after generation to us, as evidence of evolution. Every living person on the face of the Earth is a descendant of her. So in some ways, it could be said that we truly are one big family.

Posted in History & Literature

Black And White

The following poem was written by an African child. It was nominated by the UN as the Best Poem of 2006.

When I born, I black
When I grow up, I black
When I go in sun, I black
When I scared, I black
When I sick, I black
And when I die, I still black

And you white fellow

When you born, you pink
When you grow up, you white
When you go in sun, you red
When you cold, you blue
When you scared, you yellow
When you sick, you green
And when you die, you gray

And you calling me coloured?