Sleeping sickness and tsetse flies

The protozoan pathogens, the unicellular organisms that are not bacterial, but are responsible for some of the deadliest diseases in the world  including malaria, sleeping sickness and toxoplasmosis.
Although some of these protozoa can be taken up directly through contact with fecal matter or infected water, many of them rely on animal vectors for part of their life-cycle. As a result, the study and control of these vectors plays a major part in the fight against the disease. Recently, PLoS Neglected Tropical Diseases put together a whole collection of articles and editorials about the Tsetse fly: the vector for the protozoa that causes sleeping sickness.
The tsetse fly! From the PLoS collection. Image Credit: Geoffrey M. Attardo, Research Scientist at the Yale School of Public Health.
Sleeping sickness is caused by a parasite called Trypanosoma brucei. T. brucei is made up of a single eukaryotic cell, and therefore contains all the internal features of such a cell: nucleus, mitochondria, Golgi apparatus and internal membrane systems. It also has a tail, or flagellum, for most of its life-cycle. The life-cycle is complex and involves several changes in form for the protozoa. After being injected into the human blood stream by the tsetse fly, the parasite can swim to various sites in the body and multiply in bodily fluids including lymph and spinal fluid. Parasites in the blood are then picked up by another tsetse fly taking a meal. They are taken into the fly gut and then make their way to the salivary glands ready to be injected into another human.
The T. brucei lifecycle, including morphology changes and reproduction. From the Center for Disease Control.
The symptoms of sleeping sickness include joint pain, headaches and fever along with a drowsiness that gives the disease its name. Unfortunately T. brucei is able to cross the blood-brain barrier and once inside the central nervous system is causes the patient to become lethargic or insane followed by a coma and death. There are two main varieties of sleeping sickness caused by two different subspecies of T. brucei. One is a longer term chronic disease which can persist for several years with only mild symptoms before it gets into the central nervous system. The other is far more severe and acute – causing death within 3-12 months of infection. There is also a related disease which causes sleeping sickness in cattle and livestock.
One of the difficulties in eradicating sleeping sickness is that because T. brucei can change its outer protein coat there are no effective vaccines against it. There are also no existing natural cures, such as quinine for treating malaria. The most successful approaches to the disease are therefore those that rely on controlling the vector: the tsetse fly. The use of traps and insecticides to remove the insect vector leads to a decrease in the incidence of the disease. Very recently the complete genome sequence of the fly has been released which, along with research into its immune, digestive and reproductive systems should improve efforts to effectively remove it from areas where sleeping sickness is endemic.

Comments

Post a Comment

Popular posts from this blog

Extreme stress in childhood is toxic to your DNA

Image
The real danger of separating children from parents is not the psychological stress – it’s the biological time bomb. The screaming and crying, the anguish and desolation is gut-wrenching. But the fallout pales in comparison to the less visible long-term effects that are more sinister and dangerous. Separating children from their parents, in a strange land, among strangers, causes the most extreme life stress a child can experience. And it causes profound and irreversible changes in how their DNA is packaged and which genes are turned on and off in the cells of the body, in organs like the pancreas, the lungs, heart and brain – leading to lifelong changes in its structure and function. I am the director of the Lieber Institute for Brain Development and the Maltz Research Laboratories at the Johns Hopkins University School of Medicine, where scientists study how genes and the environment shape the development of the human brain. Our studies and those of many other resea
Read more

HIV lies dormant in brain?

Image
The HIV virus, which causes AIDS, has long been known to target and disable cells of the immune system, which are responsible for fighting off invading microorganisms and for suppressing malignant cancers. More recently, researchers also learned HIV not only targets immune cells in the bloodstream but also in the brain and spinal cord and that HIV can lie dormant in a person’s body for many years. My mentor, Dr. Habibeh Khoshbouei , has been working on this problem and learned that one consequence of HIV in the brain is that age-related diseases develop much earlier . This includes neurological conditions such as Alzheimer’s and Parkinson’s disease , as well as an increased susceptibility to drug addiction . Our lab wanted to learn why. HIV effects persist despite treatment HIV, the virus that causes AIDS, is shown budding out of an immune cell, which the virus infects and uses to replicate. NIH, via Wi
Read more

How Bacteria Break Through The Blood-Brain Barrier

The bacteria that sneak past the brain's defenses to cause deadly bacterial meningitis are clever adversaries - they convince their host that they are harmless yet then have freedom to cause disease by taking advantage of a molecular warning signal and inducing the brain's cellular armor to temporarily break down, letting in the bacterial horde. The blood-brain barrier is a thin network of blood vessels whose cells abut each other very closely, forming protein junctions too tight for bacteria and viruses to fit through. The barrier's purpose is to prevent unwanted material from crossing over from the surrounding bloodstream into brain tissue. "You can think of the blood-brain barrier as a brick wall," explains Brandon Kim, a biology graduate student at San Diego State University. "Each cell of the blood-brain barrier is a brick and these tight junctions are the mortar." Like castle guards, the cells that form this barrier can selectiv
Read more