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April 28 - May 26, 2024
that humanity is a kind of animal, inextricably connected with other animals: in origin and in descent, in sickness and in health.
The matching subgroup was the morbilliviruses, which include rinderpest virus and canine distemper virus (infecting nonhuman animals) and measles (in humans).
Infectious disease is a kind of natural mortar binding one creature to another, one species to another, within the elaborate biophysical edifices we call ecosystems.
Pathogens (disease-causing agents, such as viruses) are relatively small beasts that eat their prey from within.
When a pathogen leaps from some nonhuman animal into a person, and succeeds there in establishing itself as an infectious presence, sometimes causing illness or death, the result is a zoonosis.
In the United States, the polio problem peaked in 1952 with an outbreak that killed more than three thousand victims, many of them children, and left twenty-one thousand at least partially paralyzed.
Zoonotic pathogens can hide. That’s what makes them so interesting, so complicated, and so problematic.
By the cold Darwinian logic of natural selection, evolution codifies happenstance into strategy.
Nearly all zoonotic diseases result from infection by one of six kinds of pathogen: viruses, bacteria, fungi, protists (a group of small, complex creatures such as amoebae, formerly but misleadingly known as protozoans), prions, and worms.
Viruses are the most problematic. They evolve quickly, they are unaffected by antibiotics, they can be elusive, they can be versatile, they can inflict extremely high rates of fatality, and they are fiendishly simple,
Laboratory virologists are not generally knockabout people. You don’t meet them in bars, waving their arms and bragging lustily about the perils of their métier. They tend to be focused, neat, and still, like nuclear engineers.
Evidently it had attacked once, subsided, lingered in latent form for a year, and then reared up and killed him. That was scary in a whole new way.
Lethality from FMD is relatively low but the morbidity (incidence of the disease within a population) tends to be high, meaning that the disease is very contagious, making livestock ill, putting them off their feed, and causing losses of productivity that, in big-volume operations with narrow profit margins, are considered disastrous.
An amplifier host is a creature in which a virus or other pathogen replicates—and from which it spews—with extraordinary abundance.
the longer saga of emerging pathogens. If you assembled a short list of the highlights and high anxieties of that saga within recent decades, it could include not just Machupo but also Marburg (1967), Lassa (1969), Ebola (1976, with Karl Johnson again prominently involved), HIV-1 (inferred in 1981, first isolated in 1983), HIV-2 (1986), Sin Nombre (1993), Hendra (1994), avian flu (1997), Nipah (1998), West Nile (1999), SARS (2003), and the much feared but anticlimactic swine flu of 2009.
these disease outbreaks coming one after another. And they are not simply happening to us; they represent the unintended results of things we are doing. They reflect the convergence of two forms of crisis on our planet. The first crisis is ecological, the second is medical.
Human-caused ecological pressures and disruptions are bringing animal pathogens ever more into contact with human populations, while human technology and behavior are spreading those pathogens ever more widely and quickly.
Mankind’s activities are causing the disintegration (a word chosen carefully) of natural ecosystems at a cataclysmic rate.
Those millions of unknown creatures include viruses, bacteria, fungi, protists, and other organisms, many of which are parasitic. Students of virology now speak of the “virosphere,” a vast realm of organisms that probably dwarfs every other group.
But now the disruption of natural ecosystems seems more and more to be unloosing such microbes into a wider world.
parasitic microbe, thus jostled, evicted, deprived of its habitual host, has two options—to find a new host, a new kind of host . . . or to go extinct. It’s not that they target us especially. It’s that we are so obtrusively, abundantly available.
In some 25 or 27 years, we have doubled in number. A marvelous target for any organism that can adapt itself to invading us.”
Viruses, especially those of a certain sort—those whose genomes consist of RNA rather than DNA, leaving them more prone to mutation—are highly and rapidly adaptive.
The one I prefer simply says that an emerging disease is “an infectious disease whose incidence is increasing following its first introduction into a new host population.” The key words, of course, are “infectious,” “increasing,” and “new host.” A re-emerging disease is one “whose incidence is increasing in an existing host population as a result of long-term changes in its underlying epidemiology.”
Yellow fever re-emerges among humans wherever Aedes aegypti mosquitoes are allowed to resume carrying the virus between infected monkeys and uninfected people.
“Spillover” is the term used by disease ecologists (it has a different use for economists) to denote the moment when a pathogen passes from members of one species, as host, into members of another.
a high case fatality rate, ranging from 60 to 75 percent. Sixty percent is extremely high for any infectious disease (except rabies); it’s probably higher, for instance, than mortalities from bubonic plague in medieval France at the worst moments of the Black Death.
Karesh stood ready with his air rifle, the darts loaded full of tilletamine and zolazepam, drugs of choice for tranquilizing a gorilla.
His working costume was a hazmat suit with a vented hood, rubber boots, a splash apron, and three pairs of gloves, duct taped at the wrists.
Because it allows me to apply what I’ve learned, and to keep learning, and it might save some lives.
Any such spillover in the reverse direction—from humans to a nonhuman species—is known as an anthroponosis.
Their leader was Karl Johnson, the same American physician and virologist who had worked on Machupo virus in Bolivia back in 1963, barely surviving his own infection with that disease.
They knew that this virus was similar to Marburg virus, another lethal agent, identified nine years before; the electron micrographs showed that it was equally filamentous and twisty, like an anguished tapeworm.
Ebola and Marburg, would be classified within a new family, Filoviridae: the filoviruses.
for rabies (almost 100 percent among patients not treated before they show symptoms).
It disappears entirely for years at a time. This is a mercy for public health but a constraint for science.
The spleens were transferred to a biosafety level 4 (BSL-4) laboratory, a new sort of facility since Karl Johnson’s early work (and of which he was one of the pioneering designers), with multiple seals, negative air pressure, elaborate filters, and lab personnel working in space suits—a containment zone
Remember, the human body isn’t the primary habitat of ebolaviruses. The reservoir host is.
Ebolaviruses, judged by experience so far, fit that pattern. Careful medical procedures (such as barrier nursing by way of isolation wards, latex gloves, gowns, masks, and disposable needles and syringes) usually stop them. Sometimes simpler methods can bring a local spillover to a dead end too. This has probably happened more times than we’ll ever know. Advisory: If your husband catches an ebolavirus, give him food and water and love and maybe prayers but keep your distance, wait patiently, hope for the best—and, if he dies, don’t clean out his bowels by hand. Better to step back, blow a
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The current scientific understanding of ebolaviruses constitutes pinpricks of light against a dark background.
because the forest is a hungry place, most of those carcasses could never be inspected and sampled by scientific researchers.
A few patients do bleed to death, Rollin said, but “they don’t explode, and they don’t melt.” In fact, he said, the often-used term “Ebola hemorrhagic fever” is itself a misnomer for Ebola virus disease, because more than half the patients don’t bleed at all. They die of other causes, such as respiratory distress and shutdown (but not dissolution) of internal organs.
Karl said: “Bloody tears is bullshit. Nobody has ever had bloody tears.” Furthermore, Karl noted, “People who die are not formless bags of slime.” Johnson also concurred with Pierre Rollin that the bloodiness angle has been oversold. If you want a really bloody disease, he said, look at Crimean-Congo hemorrhagic fever. Ebola is bad and lethal, sure, but not bad and lethal precisely that way.
Ebola virus disease goes like this: abdominal pain, fever, headache, sore throat, nausea and vomiting, loss of appetite, arthralgia (joint pain), myalgia (muscle pain), asthenia (weakness), tachypnea (rapid breathing), conjunctival injection, and diarrhea.
Additional symptoms including chest pain, hematemesis (vomiting of blood), bleeding from the gums, bloody stools, bleeding from needle-puncture sites, anuria (inability to pee), rash, hiccups, and ringing in the ears have appeared in a smaller fraction of cases.
Still another aspect of the pathology of Ebola virus disease is a phenomenon called disseminated intravascular coagulation, familiar to the medical community as DIC. It’s also known as consumptive coagulopathy (if that helps you), because it involves consumption of too much of the blood’s coagulating capacity in a misdirected way.
Ebolaviruses have force but not reach. You can’t catch one by breathing shared air, but if a smidgen of the virus gets through a break in your skin (and there are always tiny breaks), God help you. In the terms used by the scientists: It’s not very contagious but it’s highly infectious.
Why do you love this work so much? “I don’t know,” she said, and began to ruminate. “I mean, why Ebola?
Ebola virus is not in your habitat. You are in its.