In the late 17th century, the Dutch scientist Antonie van Leeuwenhoek created a new type of microscope lens and brought an entire world of tiny organisms into focus. Looking at his own dental plaque, he wrote: "I then most always saw with great wonder, that in the said matter there were many very little living animalcules', very prettily a-moving." These little creatures were intriguing but seemingly unimportant, and few others picked up the baton from van Leeuwenhoek. That changed in the19th century, when Louis Pasteur and Robert Koch proved that some of these microbes were behind important diseases.
17世纪末，荷兰科学家安东尼·范·列文虎克（Antonie van Leeuwenhoek）发明了一种新型的显微镜镜头，并将整个微小生物世界聚焦于焦点。看着自己的牙菌斑，他写道：“当时我总是惊奇地看到，在上面提到的东西中，有很多非常小的活的微生物，非常美丽动人。”这些小动物很有趣，但似乎并不重要，很少有人从范·列文虎克手中接过接力棒。这种情况在19世纪发生了变化，路易斯·巴斯德和罗伯特·科赫证明其中一些微生物是重要疾病的幕后黑手。
That framing has stuck. Microbes are everywhere, but we take their presence on phones, keyboards, and toilet seats as a sign of filth and squalor. They fill our bodies, helping us to digest our food and safeguard our health, but we view them as adversaries to be drugged and conquered.
这种（认知）框架是停滞不前的。微生物无处不在，但我们把手机、键盘和马桶座上的微生物视为肮脏和肮脏的标志。它们充满了我们的身体，帮助我们消化食物，保护我们的健康，而我们把它们视为需要开药和征服的对手。
This antagonism is understandable. Aside from those of us with access to microscopes, most people will never see microbes with their own eyes. And so we tend to identify microbes with the disease causing minority among them, the little buggers that trigger the tickling mist of a sneeze or the pustule' on otherwise smooth skin. We become aware of their existence when they threaten our lives, and for much of our history, that threat was substantial. Epidemics of smallpox, cholera, tuberculosis, and plague have traumatised humanity, and the fear of these diseases has contaminated our entire culture, from our religious rites to Hollywood films such as Contagion (2012) or Outbreak (1995).
这种对立是可以理解的。除了我们这些有显微镜的人，大多数人都不会用自己的眼睛看到微生物。我们倾向于将微生物等同于它们中少数致病微生物，这些讨厌的小东西会诱发令人发痒的喷嚏或者让光滑的皮肤起脓疱。当它们威胁我们的生命时，我们意识到它们的存在，在我们的历史上，这种威胁是巨大的。天花、、结核病和瘟疫的流行给人类带来了创伤，对这些疾病的恐惧已经
污染了我们的整个文化，从我们的宗教仪式到好莱坞电影，如《传染病》（2012）或《爆发》（1995）。
When microbes are n't killing us, we are largely oblivious to them. So, we construct narratives of hosts and pathogens, heroes and villains, us and them. Those that cause disease exist to reproduce at our expense, and we need new ways of resisting them. And so we study how they evolve to outfox our immune system or to spread more easily from one person to another. We identify genes that allow them to cause disease and we label those genes as "virulence factors". We place ourselves at the centre of their world. We make it all about us.
当微生物没有杀死我们时，我们基本上对它们视而不见。因此，我们构建了宿主和病原体、英雄和恶棍、我们和他们的故事。那些导致疾病的生物以我们为寄主繁殖，我们需要新的方法来抵抗它们。因此，我们研究它们是如何进化来战胜我们的免疫系统，或者更容易从一个人传播到另一个人。我们识别了使它们致病的基因，并将这些基因标记为毒力因子。我们把自己置于世界的中心。所有的一切都是为了我们自己。
But a growing number of studies show that our anthropocentric' view is sometimes unjustified. The adaptations that allow bacteria, fungi and other pathogens to cause us harm can easily evolve outsid
e the context of human disease. They are part of a microbial narrative that affects us, and can even kill us, but that isn't about us. This concept is known as the coincidental evolution hypothesis or, as the Emory University microbiologist Bruce Levin described it in 2008, the "shit happens" hypothesis.
但越来越多的研究表明，我们以人类为中心的观点有时是不合理的。允许细菌、真菌和其他病原体对我们造成伤害的适应很容易在人类疾病的背景之外演变。它们是影响我们的微生物叙事的一部分，甚至可以杀死我们，但这与我们无关。这一概念被称为巧合进化假说，或者正如埃默里大学微生物学家布鲁斯·莱文（Bruce Levin）在2008年所描述的，“扯淡的假说”。
This hypothesis does not apply to all infections, and is almost certainly irrelevant viruses, which always need to reproduce in a host. Nor does it apply to the many bacteria and fungi, such as Staphylococcus aureus or Candida albicans, that are long-standing human pathogens and well-adapted to us. But it does explain some weird aspects of many diseases.
这一假设并不适用于所有类型的感染，几乎可以确定的是，该假设与病毒没有任何关系；病毒必须在寄生体内繁殖。它也不适用于许多细菌和真菌，如金黄葡萄球菌或白念珠菌，这些细菌和真菌是长期存在的人类病原体，对我们非常适应。但它确实解释了许多疾病的一些奇怪方面。
Why, for example, would bacteria harm
the hosts that they depend on for survival? In some cases, the answer is obvious: They cause symptoms such as sneezing or coughing, that help them to spread. But what about S.pneumoniae? Strains that sit harmlessly in a host's airways are already capable of spreading to another individual The virulent forms, which descend deeper into the respiratory tract, are actually less contagious. The same goes for bugs such as Hemophilus influenzae and Neisseria meningitidis, which can inflame the protective membranes around the brain and lead to life-threatening cases of bacterial meningitis. In doing so, they risk capsizing their own ship without any hope of boarding a new one.
例如，为什么细菌会伤害它们赖以生存的宿主？在某些情况下，答案很明显：它们会导致打喷嚏或咳嗽等症状，从而帮助它们传播。但是肺炎链球菌呢？那些存在在呼吸道的菌株能够不损伤的传播到另外的个体上去，这种致命的形式。毒株深入呼吸道，实际上传染性较低。流感嗜血杆菌和脑膜炎奈瑟菌等细菌也是如此，它们会使大脑周围的保护膜发炎，导致危及生命的细菌性脑膜炎病例。在这样做的过程中，他们会冒着翻船的风险，没有任何登上新船的希望。
understandable
The coincidental evolution hypothesis helps to resolve these paradoxes. It tells us that at least some human diseases have nothing to do with us at all.
巧合进化假说有助于解决这些悖论。它告诉我们，至少有些人类疾病与微生物毫无关系。
The coincidental evolution hypothesis explains a number of other recent discoveries about microbes. Scientists have found antibiotic resistance genes in bacteria that have been frozen for 30,000 years, or isolated in million-year-old caves. We might think of antibiotics as modern inventions, but they're actually weapons that bacteria have been using against each other for eons, or at least well before Alexander Fleming noticed a funky mould in a Petri dish in 1928. Antibiotic resistance genes evolved as part of this ancient war, but they also help today's microbes to deal with the medicines that we mass-produce.
巧合进化假说解释了最近关于微生物的一些发现。科学家们已经在细菌中发现了抗生素耐药基因，这些细菌已经被冷冻了30000年，或者在有百万年历史的洞穴中被分离出来。我们可能会认为抗生素是现代发明，但在极漫长的时间里它们实际上是细菌用来对付其他细菌的武器——早在1928年亚历山大·弗莱明（Alexander Fleming）注意到培养皿中有一种奇怪的臭霉菌细菌之前。抗生素耐药基因是这场古老战争的一部分，但它们也有助于今天的微生物处理我们大量生产的药物。
Likewise, many of the "virulence genes" that help pathogens to cause disease have counterparts in marine microbes with no track record of infecting humans. And some supposedly pathogenic
bacteria were often common parts of the environment. "These organisms become accidental pathog
ens," says the microbiologist Arturo Casadevall from Yeshiva University in New York "They'll still be there even if you remove all the animals from the planet. And yet, evolution selected for just the right combination of traits to cause disease in humans."
同样，许多帮助病原体致病的“毒力基因”在海洋微生物中也有对应的基因，但没有感染人类的记录。一些被认为是致病细菌的细菌通常是环境中常见的部分。纽约Yeshiva大学的微生物学家阿图罗·卡萨德瓦尔（Arturo Casadevall）表示：“这些生物会成为偶然的病原体，即使你将所有动物从地球上移除，它们仍会存在。然而，那些带有某些特征的正确组合后的自然选择仍会使人类患上疾病。”
Vibrio cholerae, the bacterium that causes cholera, is a good example. Scientists used to regard it as a human pathogen that spreads when the faces" of infected people seep into water supplies. We now know that it's mainly a marine species that attaches itself to the shells of small crustaceans", and occasionally makes its way into our water supply. "In the last decade, people have begun to accept that a lot of these opportunistic pathogens that people assumed were only in the environment transiently between human hosts are actually environmental bacteria that occasionally end up in humans," says Diane McDougald from the University of New South Wales, who studies V.cholerae.
引起的细菌就是一个很好的例子。科学家们曾将其视为一种人类病原体，当感染者的粪便渗
入水源时会传播。我们现在知道，它主要是一种附着在小型甲壳类动物外壳上的海洋物种，偶尔会进入我们的水源。在过去十年里，人们的看法开始发生转变，不再想当然的认为形形的条件致病菌只是穿梭于人类寄主间时在环境中短暂停留，而是认为他们实际上存在于环境当中，侵入人体只是一个偶然的结果。来自新南威尔士大学的Diane McDougald说。
Many of the pathogens we fear most are mere tourists on the human body. Their real homes are oceans, caves, or soils. To understand them, we need to understand them within their natural ecology. Soil, for example, is an extreme habitat for a microbe: harsh and constantly changing. It can quickly oscillate from flood to drought, from scalding heat to freezing cold, and total darkness to intense solar radiation. It's rife with other competing microbes, and crawling with hungry predators. We fear lions and tigers and bears; bacteria have to contend with phage viruses, nematode worms, and predatory amoebas(变形虫).
我们最担心的许多病原体仅仅是人体上的游客。他们真正的家是海洋、洞穴或土壤。要了解它们，我们需要在它们的自然生态中了解它们。例如，土壤是微生物的
极端栖息地：严酷且不断变化。从洪水到干旱，从酷热到严寒，从完全的黑暗到强烈的太阳辐射，它都能迅速地振荡。它充斥着其他相互竞争的微生物，到处都是饥饿的食肉动物。我们害怕狮子、老虎和熊；细菌必须与噬菌体病毒、线虫和捕食性变形虫做斗争。
All of these conditions can lead to adaptations that make microbes accidentally suited for life in a human host. We are, after all, just another environment. A thick capsule that shields a microbe from dehydration could also shield it from our immune system. A spore that is adapted for travelling through the air can be easily inhaled into a respiratory tract.
所有这些条件都可能导致适应，并使微生物意外地适合人类宿主的生活。毕竟，我们只是另一个环境。保护微生物不脱水的厚胶囊也可以保护微生物不受我们免疫系统的影响。适合在空气中传播的“孢子”很容易被吸入呼吸道。
Scientists have demonstrated many of these coincidental adaptations by exposing bacteria to a natural threat and showing that they then become better at infecting humans and other mammals. Escherichia coli, for example, is a common gut bacterium, and a darling of laboratory scientists. In its natural environments, whether the soil or the gut of a mammal, it is menaced by predatory amoebas, which threaten to engulf and digest it In 2010, the French scientist Frantz Depaulis and colleagues found li strain called 536 that resists these predators, with genes that protect it from the amoebas' digestive enzymes and allow it to scavenge nutrients such as iron. Rather than being disintegrated, it actually grows inside its would-be predator and eventually kills it from within.
科学家们通过将细菌暴露在自然威胁下，并证明它们随后更善于感染人类和其他哺乳动物，证明了许多这种巧合的适应。例如，大肠杆菌是一种常见的肠道细菌，也是实验室科学家的宠儿。在自然环境中，无论是土壤还是哺乳动物的肠道，它都受到捕食变形虫的威胁，这些变形虫可能会吞噬并消化它。2010年，法国科学家弗朗茨·德保利斯(Frantz Depaulis)和同事们发现了一种名为536的大肠杆菌菌株，它能抵抗这些捕食者，其基因可以保护它不受变形虫消化酶的伤害，并允许它吞噬铁等营养物质。它并没有被分解，而是在捕食者的体内生长，并最终从内部将其杀死。
Many of these protective genes also allow strains of the mostly li to cause severe illness in humans, mice and other mammals. This makes perfect sense. Many of our immune cells, like macrophages, engulf and digest microbes just as amoebas do, so an amoeba-proof bacterium is also a macrophage-proof one. By adapting to their natural predators, strains li are coincidentally pre adapted to foil our immune system.
许多这些
保护基因也使得大部分无害的大肠杆菌菌株在人类、老鼠和其他哺乳动物中引发严重疾病。这很有道理，我们的许多免疫细胞，比如巨噬细胞，就像变形虫一样吞噬和消化微生物，所以一种能抵抗变形虫的细菌也能抵抗巨噬细胞。通过适应它们的天敌，大肠杆菌菌株碰巧预先适应了我们的免疫系统。
The coincidental evolution hypothesis might be irksome to some. What are the odds that an adaptation to one challenge would perfectly predispose an organism to another? The answer, it seems, is: pretty high. Evolution, however, is all about small probabilities manifesting through long timescales and large numbers - and microbes have both. They have been living on the planet for billions of years, and there are countless legions of them.
这种巧合的进化假说可能会让一些人感到厌烦。一个有机体对一种挑战的适应会使它完全倾向于另一种挑战的几率有多大?答案似乎是：相当高。然而，所谓进化，就是通过漫长的时间尺度和巨大的数量而得以显现的种种细小可能性——而微生物两者兼而有之。它们已经在地球上生活了数十亿年，有无数的对此适应的军队。
Casadevall likes to say that each microbe holds a different hand of cards -adaptations that allow it to cope with its environment. Most of these combinations are meaningless to us. A bacterium might be able to resist being digested by other cells, but it might not be able to grow at 37 degrees Celsius. It might grow at the right temperature, but it might not be able to tolerate our slightly alkaline pH levels. But that doesn't matter. There are so many microbes out there that some of them will end up with a hand that lets them muscle their way into our game. "If you take all the microbial species in the world and imagine that they have these traits randomly, you can find pathogenic microbes for practically an
ything," says Casadevall.
Casadevall喜欢说，每一种微生物都有不同的适应能力，用以适应环境。这些组合中的大多数对我们来说是毫无意义的。细菌可能能够抵抗被其他细胞消化，但它可能无法在37摄氏度的温度下生长。它可能在合适的温度下生长，但它可能无法忍受我们的微碱性pH值水平。但这并不重要。世界上有那么多种微生物，最终总有一些会凭借某种特性侵入人体。“如果你把世界上所有的微生物物种，想象它们随机地具有这些特征，你几乎可以到任何东西的致病微生物”卡萨德沃尔说。

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