Antibiotic Treatment for Yaws – A Plan to Eradicate the Disease

Yaws is an infectious disease that is prevalent among human populations in the tropical regions.  It is a disfiguring ailment that impacts hundreds of thousands of individuals.   There are not many fatalities associated with yaws; however, it produces considerable suffering among those afflicted, especially children.  The primary symptoms include serious skin ulcers especially on the face, back, buttocks and legs.  It has been reported that approximately 100,000 new cases show up every year, of which 75% are children.  Although most suffers heal over time with no chronic side effects, about 10% suffer from erosion of connective tissues including cartilage and bone.

The pathogen responsible for yaws is Treponema pallidum - an organism closely related to the infectious agent that causes syphilis.  However, unlike syphilis, yaws is not sexually transmitted.  Yaws is readily treated by the use of antibiotics.  An attempt was made in 1952 to completely eradicate this disease using benzathine penicillin in over 46 countries.  As a result of this intensive effort, disease incidence had dropped by 95 percent, but by the 1970s, the disease began to return and ultimately reached current levels.

In 2012, a new plan has emerged, sponsored by the World Health Organization (WHO), to eradicate the disease – referred to as the Morges Plan.  The ambitious strategy involved is to use the relatively inexpensive antibiotic azithromycin requiring only one oral dose.  In addition to administering this drug to those individuals infected, the plan is to include at least 90% of the population in the infected areas.  This strategy is designed to treat not only those individuals who are clearly ill but also those with latent infection and who are asymptomatic.

Epidemiologists are hopeful that this scheme might prove successful, but are also aware of the many obstacles that have to be overcome including the magnitude of the administrative task involved, the scope of the project and its cost. 

The Role of Dopamine Deficiency in Obesity

Dopamine, a potent neural transmitter found in the human brain, has been implicated in a variety of reward circuits including eating.  It has been well established that the production of dopamine in the dorsal striatum of the brain markedly increases during feeding in both rodents and humans.  Controlled levels of dopamine production are also required for normal eating behavior.  These finding are consistent with the known role that dopamine plays in the reward circuitry of the brain. 

Given this critical role played by dopamine in relation to eating behavior, it has been suggested that overeating may be a compensation for a diminished function in regard to the reward circuitry dependent upon dopamine levels.  In fact, dopamine receptor deficiency has been reported in studies involving obese patients.  This is certainly consistent with significantly reduced response to food stimuli in individuals suffering from obesity.  Additionally, rats that were purposefully depleted of dopamine receptors demonstrated obsessive feeding behavior.

The physiological mechanism linking incessant high-fat intake to dopamine deficiency has been unclear.   Dr. Luis A. Tellez and his colleagues at the John B Pierce Laboratory in New Haven, CT focused their research in an attempt to elucidate the physiological mechanism linking obesity and dopamine levels in the brain.  In their experimental approach, they administered oleoylethanolamine to mice fed a diet rich in fat.  Oleoylethanolamine is, in fact, a lipid messenger whose production is suppressed in individuals subjected to high-fat dietary intake.  Upon administration of this lipid messenger, the experimental mice demonstrated increased levels of dopamine release.   Exposure of these mice to oleoylethanolamine also reinstated normal eating habits.

From these data, the authors of this report concluded that high-fat dietary intake as evidence of gastrointestinal malfunction seems to play a pivotal role in dopamine deficiency and, most importantly, restoring gut-related lipid messenger may  increase the reward feedback mechanism in regard to the intake of healthier lower-fat food.