Sunday, February 19, 2017
No, they’re not gadgets you can buy via an infomercial. A tad more serious than that. Today, we’re talking about diseases and how they spread. Medical researchers have been using sophisticated computer programs to better understand how major epidemics begin and grow throughout society. We’ve seen how various strains of flu, SARS and the Ebola virus have started small and spread so far and wide to decimate communities with death and destruction with seemingly unfathomable speed. This work has led to a better understanding that such infectious diseases have accelerated through the relevant vulnerable community primarily and significantly by carriers we now call “super-spreaders.”
Wikipedia offers the simplest definition of the term: “A super-spreader is a host—an organism infected with a disease—that infects disproportionally more secondary contacts than other hosts also infected with the same disease. A sick human can be a super-spreader; they would be more likely to infect others than most people with the disease. Super-spreaders are thus of high concern in epidemiology, the study of the spread of diseases.
“Some cases of super-spreading conform to the 20/80 rule, where approximately 20% of infected individuals are responsible for 80% of transmissions, although super-spreading can still be said to occur when super-spreaders account for a higher or lower percentage of transmissions. In epidemics with super-spreading, the majority of individuals infect relatively few secondary contacts.” Simple explanation. Complex analysis and understanding.
The recent (2014-15) devastating Ebola outbreak in West Africa has provided the medical community with a much deeper understanding of this path of causation. On January 5th, PNAS, the journal of the Proceedings of the National Academy of Sciences of the United States of America, released its findings on this epidemic. Here some of the headlines of their report.
From their abstract: “Our results show that superspreaders play a key role in sustaining onward transmission of the epidemic, and they are responsible for a significant proportion (61%) of the infections. Our results also suggest age as a key demographic predictor for superspreading. We also show that community-based cases may have progressed more rapidly than those notified within clinical-care systems, and most transmission events occurred in a relatively short distance (with median value of 2.51 km [1.6 miles]). Our results stress the importance of characterizing superspreading of Ebola, enhance our current understanding of its spatiotemporal dynamics, and highlight the potential importance of targeted control measures.”
The report tells us that a mere 3% of the infected cohort is otherwise responsible for that 61% of the total infected population, all within a tiny radius of contact. This pattern began to be increasingly clear in an August 2011 report from the International Journal of Infectious Diseases as it analyzed the then-recent SARS epidemic: “Studies conducted in the wake of the severe acute respiratory syndrome (SARS) pandemic revealed that, in the absence of super-spreading events, most individuals infect few, if any, secondary contacts. The analysis of SARS transmission, and reports from other outbreaks, unveil a complex scenario in which super-spreading events are shaped by multiple factors, including co-infection with another pathogen, immune suppression, changes in airflow dynamics, delayed hospital admission, misdiagnosis, and inter-hospital transfers. Predicting and identifying super-spreaders open significant medical and public health challenges, and represent important facets of infectious disease management and pandemic preparedness plans.”
Strangely enough, much of the transmission may have been generated by people who were ostensibly seen as care-givers within the local community. Researchers are delving further to identify individuals in any given community like to have serial interface early in the outbreak of any given potential epidemic. “Prof Jonathan Ball, a virologist at the University of Nottingham [noted of the PNAS report:] ‘The recent West African outbreak was on an unprecedented scale and many cases, especially those occurring out in the community, appear to have arisen from a surprisingly small number of infected individuals.
“‘Knowing who is most likely to transmit the virus can help in focusing interventions designed to prevent virus spread, and the current study suggests that infected children and the elderly were more likely to pass their virus on.
“‘Whether this was this due to biological or social factors is unclear, and these will be important questions to address if we are to understand how Ebola virus super-spread occurs.’” BBC.com, February 14th. The dynamics of widening epidemics provides deep insights in to future efforts to control similar outbreaks.
“The researchers concluded that Ebola superspreaders often fit into certain age groups and were based more in the community than in health care facilities. They also continued to spread the disease after many of the people first infected had been placed in care facilities, where transmission was much better controlled.
“If superspreading had been completely controlled, almost two thirds of the infections might have been prevented, scientists said in the study. The researchers also noted that their findings were conservative, since they only focused on people who had been buried safely… This suggests that the role of superspreaders may have been even more profound than this research indicates.” OutbreakNewsToday.com, February 14th.
As we know in this country, scientific research – even in critical medical fields – has been deprioritized and reduced during our recent trends toward fiscal austerity. Had Congress approved earlier continued research into potential immunization approaches, experts tell us that developing a vaccine to have prevented Ebola would have occurred long before the epidemic claimed an estimated 12 thousand lives. It could have reached and decimated us as well. In a time where international travel is so commonplace, the risk of such diseases invading the United States and attacking us is exceptionally obvious.
It seems pennywise and pound foolish to wait until a catastrophe occurs – when fixing the damage or facing the consequences will always be vastly more costly (in lives and monetary damage) than having prevented the problem in the first place. We’ve seen this phenomenon before in failing infrastructure – from the damage from decrepit and underbuilt levees in New Orleans that failed under Hurricane Katrina to the recent failure of a major spillway at California’s Oroville Dam – and we may witness parallel destruction from our failure to invest in medical research. While some infrastructure may get a reprieve in the world of Donald Trump, science – medical or other – is on the chopping block.
“Scientists at federal agencies have been hit with gag orders preventing them from communicating their findings, or in some cases, attending scientific conferences. Social media accounts and websites have been censored, and at least one agency was asked to identify personnel who worked on climate policies. Now there are proposals for slashing research budgets and gutting funding that could affect the training of the next generation of scientists. To top it all off, President Trump’s cabinet nominees and senior advisers include many who are climate deniers or doubters.” Wendy Palen, associate professor of biology at Simon Fraser University and the board chairwoman of the nonprofit Evidence for Democracy, in the February 14th New York Times. While politicians cannot repeal science, they certainly can destroy how we use science for the betterment of us all.
I’m Peter Dekom, and if our own lives are insufficiently import to merit investment to protect us, you really do have to question the role of government.