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This chapter examines the life cycle of Onchocerca volvulus. Onchocerca volvulus is a nematode that causes onchocerciasis or “river blindness.” The life cycle of this parasite begins when an infected female black fly of the genus Simulium bites its host. The worms then mature inside the subcutaneous tissues, just underneath the skin. They induce the host to produce a nodule of tissue, often reaching the size of a walnut, where the worms will dwell and lay eggs. The adult parasites also coax the host to supply extension of their body blood circulation to obtain nutrients. The larvae of the worm, called microfilariae, would then irritate the subcutaneous tissues, causing the corneal stroma to thicken, until the host becomes blind.

Onchocerciasis is a skin disease characterized by intense itching and the presence of filaria in the skin of those infected, and which is also associated with blindness. This chapter discusses the evolution of the onchocerciasis program and the lessons learned along the way. It describes the two major onchocerciasis programs—the Onchocerciasis Elimination Program for the Americas (OEPA) and the African Program for Onchocerciasis Control (APOC), and the strategies developed by these initiatives. The emphasis for onchocerciasis eradication has been the “elimination of transmission.” There is also a need to develop surveillance, monitoring, and diagnostic tools to certify that the disease has been eradicated.

A 22-year-old woman returned two months ago from a four-week trip to Kenya. She took mefloquine as antimalarial prophylaxis, which she stopped on return to the UK, and was up to date with vaccinations against yellow fever, typhoid, rabies, and hepatitis A and B. She had developed fever three days earlier, which was associated with headaches, rigors, and myalgia. On the day of admission she was confused and had profuse watery diarrhoea. She had vomited bile twice in the acute medical unit.

On examination, she had a temperature of 40°C, pulse 120 beats per minute and regular, and blood pressure 90/50 mmHg. Fundoscopy revealed a small retinal haemorrhage on the left. She had reduced tissue turgor but there was no lymphadenopathy. There was no meningism. Respiratory and abdominal examinations were normal. She weighed 60 kg.

This paper uses historical census data from Burkina Faso to characterize local demographic pressures, including population shocks associated with internal migration after disease eradication in river valleys, and forced repatriation of migrants from Cote d’Ivoire. We combine those data with a new survey of village elders that was designed to document change over time and differences across villages in local public goods provision, market infrastructure, and property rights. We hypothesize that higher local population densities are associated with more collective services and a transition from open-access to regulated land use, offering a village-level test of fundamental hypotheses about social and political change in Africa. Controlling for year and province fixed effects, we find that villages’ variance in population associated with proximity to river valleys and to Cote d’Ivoire is closely correlated with higher levels of public services, infrastructure, religious facilities, and markets; in addition, villagers’ land is more often governed through individual as opposed to familial rights, with more land-market transactions and stronger regulation of villagers’ forest use. Responding to population growth with improved public services and more private property rights is consistent with both scale effects in public good provision, and changes in the scarcity of land.

The Perils of Pauline is a 1914 film serial in 20 episodes. In each episode, a villain, perhaps a pirate, menaces Pauline, played by Pearl White. In each episode, Pauline seems certain to meet her demise, only to escape or be rescued at the last possible moment. Outdoing the proverbial cat of nine lives, Pauline had 20. The Perils of Pauline bears more than a passing resemblance to drug discovery and development in which some villain, perhaps an issue of safety or efficacy, threatens the life of a project. I know of no better example of this than the course of getting the antibiotic Primaxin from the laboratory to the bedside. The perils of Primaxin plays out in a scientific serial of five episodes in which the project is rescued from impending disaster in each episode. The Primaxin story is one of the great tales of drug discovery in the world of antibiotics—the molecules that have power to prevent or cure bacterial infections. Primaxin is a triumph of the pharmaceutical industry in general and of Merck specifically. Victory did not come easily. The road from a drug discovery start to a marketable human health product is often rough, occasionally very rough, and sometimes impassable. The Primaxin story stands out for the number and nature of bumps and ruts that impeded passage. That Primaxin made it to the market for the benefit of countless patients with infectious diseases is a tribute to the wit and determination of the many scientists who saw it through. That story comes later. Let’s get started with some general background on the field of antibiotics. The next time you have the occasion to explore a cemetery, have a look at the tombstones for people born around 1900. A significant fraction of those tombstones will reveal that the date of death is within 10 years of the date of birth. Simply put, many people born around 1900 or earlier did not live to be 10 years old.

These are the words of Dr. William C. Campbell, hereinafter known as Bill. Bill was Merck’s leading authority on parasitic diseases. He played the leading role in the discovery of the greatest antiparasitic drugs in history—ivermectin and abamectin. Having said this, and as Bill has pointed out, this drug discovery story, like all of them, was the result of a team effort involving hundreds of people. When you start giving credit by naming scientists who contributed, it is tough to know when to stop. If you try to name them all, you get a telephone book for a small village and you will still miss somebody. The other extreme is to name nobody, but I have already violated that alternative. So I will mention four scientists at Merck who, in addition to Bill, were the authors of the publication in the prestigious journal Science of the article announcing the discovery of ivermectin. They are Mike Fisher, the chemist who led the chemistry effort at Merck focused on the avermectins; Ed Stapley, who led Merck’s natural product screening effort; Georg Albers-Schönberg, who headed the group that elucidated the structure of the avermectins; and Ted Jacob, Merck’s leader of animal drug metabolism. Before getting into the story, a word about names—this time about molecules, not scientists. As I relate in this chapter, avermectins are a small family of related molecules. Ivermectin is a chemically modified derivative of one of the avermectins, and abamectin is one of the avermectins. Bill Campbell is an Irishman and native of Donegal. He took himself to Trinity College in Dublin for his undergraduate work where he did research under the direction of J. Desmond Smyth, a noted parasitologist. Near the end of Bill’s undergraduate days at Trinity College, Dr. Arlie Todd of the University of Wisconsin wrote Smyth to ask whether he had any promising students to recommend for graduate study. Smyth recommended Bill to Todd, along with two others.