The sudden death of Dr Sheik Umar Khan while treating patients infected with the Ebola virus in Sierra Leone is a tragic reminder of the risks that infectious disease specialists run when confronting deadly new animal pathogens. Since Ebola ‘re-emerged’ in Guinea in March more than 1200 people have been infected with the hemorrhagic fever and fully half have died. Now with reports that a Liberian man who recently boarded a flight from Tome to Lagos has also died there are understandable fears that the virus could escape Africa.
Ebola is scary not only because of its Hammer horror symptoms – violent stomach pains, vomiting and internal bleeding – but because there is no vaccine and no one is sure where the virus resides between outbreaks (though fruit bats and chimps are suspected of being important vectors). These unknowns, plus the fact that some strains of the virus have a 90 percent case fatality rate, are sufficient to persuade most people to keep their distance.
But for medical microbiologists, whose job it is to understand new rain forest pathogens and find a cure, they are part of the fascination. Indeed, the history of medical microbiology is littered with individuals who were prepared to run extraordinary risks in search of the causative agents of epidemics or simply to prove a scientific point.
Perhaps the most foolhardy example is the Bavarian doctor Max von Pettenkofer’s attempt in 1900 to disprove that a bacillus was the cause of cholera by drinking a cup of tea laced with cholera vibrio cultured from a patient’s stools. Pettenkofer, who thought the composition of the soil and the bacillus’s interaction with groundwater was necessary to contract the disease, fell violently ill but somehow survived the experiment.
Less fortunate was the Rockefeller bacteriologist Paul Lewis. In 1929 Lewis volunteered to go to Brazil to set up a laboratory to study yellow fever. A month before another Rockefeller researcher, Hideyo Noguchi, had died of the deadly ‘yellow jack’ in Ghana while trying to prove that a spiral-shaped bacterium was the cause of the disease (in fact, yellow fever is due to a flavivirus spread by mosquitoes). In other words, Lewis could have no doubt the assignment was dangerous. Nevertheless, it was his hope that he would be able to establish the cause once and for all and, perhaps, win the Nobel prize in the process. It wasn’t to be. Within months of arriving in Belen, Lewis also contracted yellow fever and died. According to John Barry, who records the episode in his book, The Great Influenza, Lewis’s illness took a particularly severe course:
“…the virus attacked the mucosa in his stomach, which bled, giving the vomit the dark color; it attacked the bone marrow, causing violent aching. An intense, searing headache gave him no rest, except perhaps when he was delirious. He had seizures. His colleagues packed him in ice and tried to keep him hydrated but there was little else they could do.”
In the case of the French bacteriologist Charles Nicolle it was the louse that persuaded him to run similar risks. For years people had observed that typhus was associated with poverty, dirt and poor hygiene but it wasn’t until 1909 that Nicolle put two-and-two together and realised that it wasn’t dirt that that caused typhus but lice hidden in dirty clothing. Nicolle’s epiphany came at the doors to the Sadiki Hospital in Tunis when he noticed that patients deprived of their clothes at the entrance ceased to be infectious on the wards. But not content with winning the 1928 Nobel prize for his explication of the louse-man transmission cycle of typhus, in 1934 Nicolle decided to also investigate the rat-man version of the disease. For his pains he contracted murine typhus accompanied by a nasty case of tachycardia, dying two years later at the age of 69.
Despite the alarming reports coming out of west Africa, it is unlikely that Ebola will ever threaten Europe or the United States to the same degree that typhus once did – global pathogen surveillance systems are now so sophisticated, we are told, that biosecurity experts will halt the bug at the border or, if not there, then in secure hospitals. But in the 1930s, when most viruses could not be visualised through a microscope and few researchers realised the extent to which people could harbor microbial pathogens in their stools, blood and sputum, new animal diseases were not so easy to detect and death often came in the unlikeliest of forms
One of the unlikeliest and deadliest of all was psittacosis, a bacterial disease spread by parrots and parakeets. A tiny intracellular parasite, psittacosis causes occasional die-offs in wild birds but generally results in a low-level immunising infection. When parakeets (budgerigars) are confined in cages or closed breeding pens, however, this immunity can wane and many birds become visibly diseased, shedding the parasite in their droppings. In warm dry climates, the droppings rapidly desiccate in air, turning them into deadly aerosols.
Before the discovery of tetracyclines, this made the budgerigar an emissary of death, particularly in California where the Depression had sparked a huge industry in backyard aviaries and it was common to give parakeets and parrots as ‘love birds’ . The result was that by 1930 the nation was in the grip of a pandemic of ‘parrot fever’.
Though not as gruesome as Ebola, parrot fever proved just as deadly, with a case fatality rate of between 40 to 60 percent. Unlike Ebola, psittacosis was also highly contagious. All you had to do in order to contract the infection was linger too long in the same room as an infectious budgerigar or, if you were a laboratory technician, make an elementary error while handling contaminated material from birds.
Indeed, in the winter of 1930 two technicians at the Hygienic Laboratory in Baltimore died while preparing live serum vaccines for stricken patients in other parts of America. Five years later in San Francisco, Karl Friedrich Meyer, who had done more than anyone to elucidate the etiology and ecology of the disease, also fell victim. For more than two weeks, Meyer lay mortally ill, his body racked by fever, chills, abdominal pains and a hacking cough. Meyer survived but Anne Pabst, a bacteriologist at the National Institute of Health, was not so lucky, dying of ‘meningitis’ after contracting a similar laboratory infection. The following day, her obituary notice appeared in the San Francisco News under the headline ‘Soldier of Medicine’.
But perhaps the greatest tribute paid to one of these medical soldiers was the obituary notice that appeared in 1911 for Howard Taylor Ricketts. After serving as a medical intern in Chicago, Ricketts became fascinated with Rocky Mountain Spotted Fever, which is caused by a bacterium-like organism in the same family as typhus but spread by ticks rather than the louse. In 1906, Ricketts became the first person to transmit the disease to guinea pigs, leading to the genus being named Rickettsia in his honour. Not content with this achievement, however, in 1909 he travelled to Mexico City to study tabardillo, another typhus-like disease. In April 1910 he reported that, like typhus in Tunis, tabardillo was very probably due to the louse. But the knowledge came to late to save him. While making the rounds of a local hospital Ricketts contracted the disease, most likely from a louse-infested patient, dying soon afterwards.
Though separated by more than a century, Ricketts death and the notice that accompanied serves as an equally fitting tribute to Dr Khan:
“Those near to him know that he fully understood the dangers to which he would be exposed and the risks that he would run. He decided he would take those risks, meet the dangers with all possible means of prevention, and do the work that would come to his hands. And so he made the great sacrifice and gave all that a man can give for his fellow men.”