Using a novel statistical model, a research team led by Columbia University’s Mailman School of Public Health mapped the spread of the 2014-2015 Ebola outbreak in Sierra Leone, providing the most detailed picture to date on how and where the disease spread and identifying two critical opportunities to control the epidemic. The result, published in the Journal of the Royal Society Interface, matches with details known about the early phase of the Ebola outbreak, suggesting the real-time value of the method to health authorities as they plan interventions to contain future outbreaks, and not just of Ebola. Their analysis uses data from the Sierra Leone Ministry of Health and Sanitation to chart the course of the Ebola outbreak, beginning with the arrival of the disease in the border district of Kailahun in late May 2014. By mid-June, Ebola spread west to nearby Kenema—a pathway consistent with a recent field investigation. At its peak, 67 percent of Ebola cases in Kenema were imported from Kailahun; by early July, the epidemic was firmly established in Kenema with most cases infected locally. From Kenema, the outbreak continued west, south, and north. Beginning in early July, a second path emerged in capital city, Freetown, spreading east to Port Loko by late July, then quickly east and south. Because of their many connections to other districts, Kenema and Port Loko were critical junction points for the outbreak. At these points, windows of opportunity may have existed for controlling the spread of Ebola within Sierra Leone, the study suggests. The researchers estimate that the first window, before Ebola reached Kenema, was approximately one month. The second window, before it reached Port Loko, was much shorter. The method described in the paper uses three principal ingredients: the home district of the Ebola-positive patient, the population of that district, and geographic distance between districts—all information that was available during the outbreak. “While this analysis is too late to be used for application to and intervention in the Ebola epidemic, the method we used could be useful for future disease outbreaks, and not just for Ebola,” said Jeffrey Shaman, Ph.D., the study’s senior author and associate professor of Environmental Health Sciences at the Mailman School. “To be able to infer the spatial-temporal course of an outbreak and the rate of its spread between population centers in real time,” Shaman continues, “may greatly aid public health planning, including the level and speed of deployment of intervention measures such as how many doctors and beds are needed and where to put them.” The traditional method to track disease spread is contract tracing, in which health workers interview patients and everyone they came into contact with. “Contact tracing is highly labor intensive,” said lead author Wan Yang, Ph.D., associate research scientist at the Mailman School. “Especially in resource-poor areas, an epidemic like Ebola can easily outrun any such effort to track it. The minimal information needed in our method makes it a particularly valuable tool to aid public health efforts during a novel disease outbreak in these areas.” During the Ebola outbreak, there was a collapse of the healthcare system in Sierra Leone. Observational data were very limited and error-laden. “Having the ability to infer the course of the outbreak gives officials the ability to see what’s happening rather than flying completely blind,” Shaman said. “In a public health emergency, it’s critical that they have as much information as possible so they can make informed decisions. “If you had perfect observation,” Shaman adds, “you wouldn’t need these methods, but you’re never going to get that.” Previous work by Shaman and Yang has used computational methods to predict infectious disease spread. Beginning in the summer of 2014, they generated weekly estimates of countrywide Ebola incidence in Sierra Leone, Guinea, and Liberia. They also developed a prize-winning method to forecast seasonal influenza. Forecasts are available online at Columbia Prediction of Infectious Diseases. Additional authors include co-first author Wenyi Zhang, Ruifu Yang, Yong Chen, Zeliang Chen, and Chao Liu of the China Mobile Laboratory Response Team for Ebola in Sierra Leone; David Kargbo, Abdul Kamara, and Brima Kargbo of the Sierra Leone Ministry of Health and Sanitation; Sasikiran Kandula of the Mailman School; and Alicia Karspeck of the National Center for Atmospheric Research. The study was supported by grants from the National Institutes of Health and the Research and Policy for Infectious Disease Dynamics program of the Department of Homeland Security. Jeffrey Shaman discloses consulting for J. Walter Thompson and Axon Advisors, as well as partial ownership of SK Analytics.
Das K.M.,King Fahad Medical City |
Lee E.Y.,Harvard University |
Enani M.A.,Infectious Disease |
AlJawder S.E.,King Fahad Medical City |
And 6 more authors.
American Journal of Roentgenology | Year: 2015
Objective. The purpose of this article is to retrospectively analyze chest CT findings for 15 patients with Middle East respiratory syndrome coronavirus and to identify features associated with survival. MATERIALS AND METHODS. Patients were assigned to group 1 if they died (n = 9) and to group 2 if they made a full recovery (n = 6). Two reviewers scored chest radiographs and CT examinations for segmental involvement, ground-glass opacities, consolidation, and interstitial thickening. Results. Eight patients had ground-glass opacity (53%), five had ground-glass and consolidation in combination (33%), five had pleural effusion (33%), and four patients had interlobular thickening (27%). Of 281 CT findings, 151 (54%) were peripheral, 68 (24%) were central, and 62 (22%) had a mixed location. The number of involved lung segments was higher in group 1. The lower lobe was more commonly involved (mean, 12.2 segments) than in the upper and middle lobes combined (mean, 6.3 segments). The mean number of lung segments involved was 12.3 segments in group 1 and 3.4 segments in group 2. The CT lung score (mean ± SD, 15.78 ± 7.9 vs 7.3 ± 5.7, p = 0.003), chest radiographic score (20.8 ± 1.7 vs 5.6 ± 5.4; p = 0.001), and mechanical ventilation duration (13.11 ± 8.3 vs 0.5 ± 1.2 days; p = 0.002) were higher in group 1. All nine group 1 patients and three of six group 2 patients had pleural effusion (p = 0.52). Conclusion. CT of patients with Middle East respiratory syndrome coronavirus predominantly showed ground-glass opacities, with peripheral lower lobe preference. Pleural effusion and higher CT lung and chest radiographic scores correlate with poor prognosis and short-term mortality. © American Roentgen Ray Society. Source
Cooper T.W.,Infectious Disease |
Cooper T.W.,University of Texas at Dallas |
Pass S.E.,Texas Tech University Health Sciences Center |
Brouse S.D.,Texas Tech University Health Sciences Center |
Hall II R.G.,Texas Tech University Health Sciences Center
Annals of Pharmacotherapy | Year: 2011
OBJECTIVE: To discuss treatment options that can be used for treatment of Acinetobacterinfections. DATA SOURCES: A MEDLINE search (1966-November 2010) was conducted to identify English-language literature on pharmacotherapy of Acinetobacterand the bibliographies of pertinent articles. Programs and abstracts from infectious diseases meetings were also searched. Search terms included Acinetobacter, multidrug resistance, pharmacokinetics, pharmacodynamics, Monte Carlo simulation, nosocomial pneumonia, carbapenems, polymyxins, sulbactam, aminoglycosides, tetracyclines, tigecycline, rifampin, and fluoroquinolones. DATA SELECTION AND DATA EXTRACTION: All articles were critically evaluated and all pertinent information was included in this review. DATA SYNTHESIS: Multidrug resistant (MDR) Acinetobacter, defined as resistance to 3 or more antimicrobial classes, has increased over the past decade. The incidence of carbapenem-resistant Acinetobacteris also increasing, leading to an increased use of dose optimization techniques and/or alternative antimicrobials, which is driven by local susceptibility patterns. However, Acinetobacterinfections that are resistant to all commercially available antibiotics have been reported. General principles are available to guide dose optimization of aminoglycosides, β-lactams, fluoroquinolones, and tigecycline for infections due to gram-negative pathogens. Unfortunately, data specific to patients with Acinetobacterinfections are limited. Recent pharmacokinetic-pharmacodynamic information has shed light on colistin dosing. The dilemma with colistin is its concentration-dependent killing, which makes once-daily dosing seem like an attractive option, but its short postantibiotic effect limits a clinician's ability to extend the dosing interval. Localized delivery of antimicrobials is also an attractive option due to the ability to increase drug concentration at the infection site while minimizing systemic adverse events, but more data are needed regarding this approach. CONCLUSIONS: Increased reliance on dosage optimization, combination therapy, and localized delivery of antimicrobials are methods to pursue positive clinical outcomes in MDR Acinetobacterinfections since novel antimicrobials will not be available for several years. Well-designed clinical trials with MDR Acinetobacter are needed to define the best treatment options for these patients. Source
The alarming spread of the Zika virus — caused in major part by the infamous Aedes aegypti mosquito, which can also carry dengue, yellow fever and chikungunya virus — is looking more and more like a public health catastrophe. But it’s also, say experts, something else: The latest example of how human alterations to their environments, in the broadest sense, can empower disease-carrying organisms like Aedes and the viruses they bring with them. That mosquito, in particular, thrives in “artificially human-made habitats,” says Durland Fish, a professor of microbial diseases and also forestry and environmental studies at Yale University. “Tires and cans and plastic containers and rain barrels, and things like that.” [Zika virus: WHO declares global public health emergency, says causal link to brain defects ‘strongly suspected’] “It doesn’t live in the ground, or in swamps, or any other kinds of places where you would normally find mosquitoes,” Fish continues. “So humans have created an environment for it to proliferate, by having all of these water containing containers around, and the mosquito has adapted so well…it’s really kind of a human parasite. It’s like the cockroach of the mosquito world.” And unfortunately, what’s true of Aedes aegypti is true of many other disease vectors, and many other diseases — a major problem that Fish says the world still isn’t really grappling with. That’s not to say that other factors — like poverty, globalization, and advanced transportation systems that can carry not only people but also diseases and their vectors — aren’t equally important. But researchers such as Fish suggest that environmental factors have been neglected and, with no vaccine available for Zika, are also a key part of the solution. So let’s examine some of the major ways that human-caused environmental changes have been shown to worsen the spread of diseases — before examining why more isn’t being done about this problem: First, let’s start with the current Zika situation and its cause. You can make the case that the Aedes mosquito has been thriving thanks to “environmental degradation” in key areas in Brazil and other countries, says Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine. “You see not only poverty, but the environmental degradation, uncollected garbage, discarded tires filled with water, areas of un-drained water,” he says. These create habitats for mosquitoes, which then spread deadly viruses. As Hotez’s words suggest, it can be difficult to disentangle urban growth and waste from other factors, like poverty. But Fish argues that while Zika does primarily affect the poor, “even people who are wealthy, and live in different kinds of communities, these mosquitoes still can occur in those areas, in flower pot bases, and ornamental plants. They’re not totally immune, but not as hard hit as people in the poor areas of town.” “There are many other factors that have contributed to the emergence [of Zika], but the principal drivers have been human population growth, unplanned urban growth, globalization and lack of effective vector control,” adds Duane Gubler, the founding director of the Signature Research Program in Emerging Infectious Disease at the Duke-NUS Graduate Medical School in Singapore. This is not, of course, the first time that urbanization and city planning have been connected with disease transmission. That particular story goes at least back to 1854, when John Snow, studying a cholera outbreak in London, found that it was linked to the dumping of sewage into the Thames river and then drawing on Thames water for people to drink. Zika may be primarily a story about how certain kinds of urban environments and urban waste empower mosquitoes, but what’s striking is how many other kinds of environmental changes have also been shown to make disease vectors worse: One of the most consequential things humans can do to the environment is damming a large river so that it can be used for hydropower or to create reservoirs. There have been many complaints about how dams can damage ecosystems, but there is also considerable evidence that the way they change watery environments can foster vector-borne disease. “Dam building is one of the biggest factors in the emergence of schistosomiasis, the dam on the Upper Volta promoted the massive emergence of schistosomiasis in Ghana,” says Hotez. Schistosomiasis is a devastating disease spread by parasite-carrying freshwater snails to humans who swim in tainted water. Dams and other water management projects can make it worse because they can bring people and these snails together. “Water impoundments of all sizes, including man-made lakes and irrigation systems, provide excellent habitats for freshwater snails and encourage close and frequent contact between people and infected water,” says a report on snail-borne diseases by the World Health Organization. Schistosomiasis is a devastating disease, but even worse is malaria — which can also be worsened by major dam projects. Recent research suggests that dams in sub-Saharan Africa are responsible for “at least 1.1 million new malaria cases in Africa every year,” the Post’s Joby Warrick reported last year. That’s because water impounded by dams can create habitats for malaria-transmitting mosquitoes. [Malaria cases in Africa are soaring. Here’s the surprising reason why] Or take yet another example. In the Senegal River basin of West Africa in 1987, a major epidemic of Rift Valley fever occurred. The cause? “A series of ecological modifications to the Senegal River were instituted by the Mauritanian and Senegalese governments in cooperation with internationally sponsored programs,” including two dams, reported Kenneth J. Linthicum of the U.S. Department of Agriculture’s Center for Medical, Agricultural, and Veterinary Entomology and a group of colleagues. One of the dams led to “extensive flooding and vegetation growth” and researchers then observed humans cultivating rice in the same place that large numbers of Culex mosquitoes were spawning. The researchers conclude that it’s a classic case of how “landscape modification can contribute to endemism of diseases.” And just as it goes for dams, so chopping or burning down forests has also been widely implicated in increasing disease transmission to humans. Our own Chelsea Harvey reported recently on how deforestation seems to be another key enabler of malaria transmission in Malaysia, where it has brought humans and macaques into closer proximity, allowing mosquitoes to become a go-between and transfer the disease. And that’s just one example of how chopping down trees can worsen the spread of disease. “Deforestation has been a huge issue in the emergence of disease. It promoted Ebola in West Africa. It promoted Nipah and SARS in South Asia,” says Hotez. In Africa, where malaria is most devastating, deforestation is yet again involved. For instance, deforested areas tend to be hotter, because they lack the cooling influence of trees, and those warmer temperatures can affect key parts of the mosquito life cycle. Thus, report Jonathan Patz and Sarah Olson of the University of Wisconsin, the blood-feeding and egg laying cycle of female Anopheles gambiae mosquitoes (the deadly vector in this case) in Kenya was found to be as much as 52 percent shorter in deforested areas. [By cutting down forests, humans may be giving themselves malaria] “Deforestation and cultivation of natural swamps in the African highlands creates conditions favourable for the survival of An. gambiae larvae, making an analysis of the effects of land-use change on local climate, habitat, and biodiversity key to any malaria-risk assessments,” the authors conclude. And then, well, there’s climate change. This is where we mess with the globe’s average temperatures, and thereby potentially change the comfortable ranges of vast numbers of species — including insect vectors of disease. It stands to reason that diseases of the tropics, like malaria and dengue and yellow fever, will be more able to penetrate out of the tropics if we shift the climate to make temperate latitudes hotter. “Globally, temperature increases of 2-3ºC would increase the number of people who, in climatic terms, are at risk of malaria by around 3- 5%, i.e. several hundred million,” concludes the WHO. “Further, the seasonal duration of malaria would increase in many currently endemic areas.” Aedes aegypti, and all the diseases that it brings, are also expected to thrive in a warmer climate. “Dengue mosquitoes reproduce more quickly and bite more frequently at higher temperatures,” says WHO. And then there’s the Asian tiger mosquito, Aedes albopictus, which is also a threat for transmission of dengue, Zika, and other diseases. Aedes albopictus has already expanded into much of the United States and as a recent study by a group of US mosquito control researchers at several state agencies and Rutgers University found, climate change should worsen that spread: What we can do It’s crucial to emphasize that while environmental factors are clearly implicated in the spread of these diseases, they aren’t the only ones. “The big four are poverty, conflict, human migrations, and environmental factors. And most of those environmental factors are probably man-made,” says Peter Hotez. As Hotez notes, human migrations — especially in aircraft and ships — are also responsible for helping to spread both diseases and also their vectors all around the world. Aedes aegypti originated in Africa. Aedes albopictus was originally from Asia. Now they’re both all over the place. If you count species introductions into new places as another form of human-caused environmental assault (and there are good grounds for doing so) then this may be the most devastating of all from a disease standpoint. So what can we do? Yale’s Durland Fish argues that we have to pay much more attention to how large projects involving forests, dams, wetlands and more change the ecology of diseases by changing the habitats of their vectors. And that we need to think about diseases from a much more ecological standpoint in general. “You should be able to understand how these simple man-made aquatic habitats, how do they produce mosquitoes, what are the biological processes involved, in turning a mosquito egg into an adult mosquito,” he says of Aedes aegypti. “And we don’t understand that process.” Fish says the medical world tends to pursue cures like vaccines, rather than ecological understanding that can lead to better prevention. When it comes to Zika, says Fish, “You have to do something about the mosquitoes, and that’s strictly an environmental problem, there’s no medical applications to that. And focusing on that as an environmental issue is going to have the greatest impact on protecting people.” Why the U.S. East Coast could be a major ‘hotspot’ for rising seas What Ted Cruz’s Iowa victory says about the politics of ethanol and renewable fuels It’s not just Flint: Poor communities across the U.S. live with ‘extreme’ polluters For more, you can sign up for our weekly newsletter here, and follow us on Twitter here.
When MIT moved from Boston to Cambridge in 1916, it built a new campus designed to foster collaboration across disparate disciplines. As the Institute celebrates the centennial of that historic move, more than a dozen faculty from multiple departments across all five schools will gather for a symposium in Kresge Auditorium on Tuesday, April 12, to present short, exciting talks on their groundbreaking research — tied together by an immersive, multimedia campus tour by foot, drone, and skateboard. Come explore! President L. Rafael Reif will open the symposium session at 1:30 p.m., preceded by lunch and a graduate student poster session starting at noon. The faculty talks and multimedia tour run two hours (1:30-3:30 p.m.) and will be followed by a reception in Kresge Lobby from 3:30 to 5 p.m. Registration, including lunch and reception, is free for MIT staff, faculty, and students, and $20 for other attendees. Advance registration is encouraged and will be available until 11:59 p.m. on Thursday, April 7. After the deadline, registration will be available onsite on April 12. Contact MIT Conference Services with questions. Welcome L. Rafael Reif, MIT president "Emerging Markets Drive Global Solutions" Amos Winter, assistant professor in the Department of Mechanical Engineering "Fluid Dynamics of Infectious Disease Transmission" Lydia Bourouiba, Esther and Harold E. Edgerton Career Development Professor in the Department of Civil and Environmental Engineering "Exploring Quantum Behavior in Flatland" Pablo Jarillo-Herrero, Mitsui Career Development Associate Professor of Physics "Uncovering Photosynthesis at the Nanoscale" Gabriela Schlau-Cohen, assistant professor in the Department of Chemistry "What Inventions Are We Missing?" Heidi Williams, Class of 1957 Career Development Assistant Professor, Economics "Mobile Technologies and Financial Inclusion in Africa" Tavneet Suri, Maurice J. Strong Career Development Associate Professor in the MIT Sloan School of Management "Rethinking China’s Growth Model" Yasheng Huang, International Program Professor in Chinese Economy and Business and associate dean of the MIT Sloan School of Management "From Nature-inspired Design to Design-inspired Nature" Neri Oxman, Sony Corporation Career Development Associate Professor in the MIT Media Lab "Using Biology for Chemistry’s Sake" Kristala Prather, Theodore T. Miller Associate Professor in the Department of Chemical Engineering "Wireless Systems that Extend Our Senses" Dina Katabi, Andrew and Erna Viterbi Professor in the Department of Electrical Engineering and Computer Science "Where the Wild Things Will Be (in 100 Years)" Katharina Ribbeck, Eugene Bell Career Development Professor of Tissue Engineering in the Department of Biological Engineering "Is There Music at MIT?" Marcus Thompson, Institute Professor and Robert R. Taylor Professor of Music "Cities of a New Future" John Fernandez, associate professor in the Department of Architecture Closing Remarks Rebecca Saxe, symposium cochair and professor of cognitive neuroscience in the Department of Brain and Cognitive Sciences John Ochsendorf, chair of the MIT2016 Steering Committee, symposium cochair, and Class of 1942 Professor in the departments of Architecture and Civil and Environmental Engineering The symposium is part of MIT2016: Celebrating a Century in Cambridge, a program running Feb. 29 to June 4 as MIT commemorates 100 years at its “new” campus.