The accident that changed the world Allison Ramsey and Mary Staicu

London, 1928: a group of mold spores
surf a breeze through a lab.

They drift onto a petri dish,
and when they land,

they germinate a medical revolution.

This lab belongs to Alexander Fleming,
a Scottish scientist

investigating the properties
of infectious bacteria.

At this time,
Fleming is away on vacation.

When he returns, he finds
a colony of mold growing on a petri dish

he’d forgotten to place in his incubator.

And around this colony of mold
is a zone

completely and unexpectedly
clear of bacteria.

In studying this mysterious phenomenon,

Fleming came to realize that the mold
was secreting some kind of compound

that was killing the bacteria.

The mold was a species
in the Penicillium genus,

so Fleming dubbed
the antibacterial compound “penicillin.”

What Fleming stumbled upon
was a microbial defense system.

The penicillium mold
constantly produces penicillin

in order to defend itself from threats,

such as nearby bacterial colonies
that might consume its resources.

Penicillin destroys
many types of bacteria

by disrupting synthesis
of their cell walls.

These walls get their strength
from a thick, protective mesh of sugars

and amino acids,

that are constantly being
broken down and rebuilt.

Penicillin binds to one of the compounds
that weaves this mesh together

and prevents the wall from being
reconstructed at a critical phase.

Meanwhile, penicillin stimulates
the release of highly reactive molecules

that cause additional damage.

Eventually, the cell’s structure
breaks down completely.

This two-pronged attack
is lethal to a wide range of bacteria,

whether in petri-dishes,
our bodies, or elsewhere.

It’s not, however,
harmful to our own cells,

because those don’t have cell walls.

For a decade or so
after Fleming’s discovery,

penicillin remained
a laboratory curiosity.

But during World War II,

researchers figured out how to isolate
the active compound

and grow the mold in larger quantities.

They then went on to win
the Nobel Prize for their work.

Teams at Oxford and several American
drug companies continued development,

and within a few years
it was commercially available.

Penicillin and similar compounds quickly
transformed the treatment of infections.

For the time being,

they remain some of the most important,
life-saving antibiotics used in medicine.

However, the more we use any antibiotic,
the more bacteria evolve resistance to it.

In the case of penicillin,

some bacteria produce compounds
that can break down the key structure

that interferes with cell wall synthesis.

As antibiotic use has increased,

more and more bacteria
have evolved this defense,

making these antibiotics ineffective

against a growing number
of bacterial infections.

This means it’s essential that doctors
not overprescribe the drug.

Meanwhile, 5 to 15% of patients
in developed countries

self-identify as allergic to penicillin,

making it the most commonly reported
drug allergy.

However, the vast majority— over 90%—
of people

who think they’re allergic
to penicillin actually are not.

Why the misperception?

Many patients acquire the allergy label
as children,

when a rash appears after they’re treated
for an infection with penicillin

or closely related drugs.

The rash is often blamed on penicillin,

while the more likely culprit
is the original infection,

or a reaction between the infection
and the antibiotic.

However, genuine penicillin allergies,

where our immune systems
mistake penicillin for an attacker,

do occur rarely
and can be very dangerous.

So if you think you’re allergic
but don’t know for sure,

your best bet is to visit an allergist.

They’ll complete an evaluation
that’ll confirm

whether or not you have the allergy.

Even if you do have a penicillin allergy,

your immune cells that react to the drug
may lose their ability to recognize it.

In fact, about 80% of people
who are allergic to penicillin

outgrow their allergy
within ten years.

This is great news for people
who currently identify

as allergic to penicillin;

the drug may one day save their lives,
as it has done for so many others.

伦敦,1928 年:一群霉菌孢子
在实验室中轻风飘扬。

它们漂流到培养皿上
,当它们降落时,

它们会引发一场医学革命。

该实验室属于调查传染性细菌特性的苏格兰科学家亚历山大·弗莱明 (Alexander Fleming)

此时,
弗莱明正在休假。

当他回来时,他发现
在他忘记放入孵化器的培养皿上长了一个霉菌菌落

在这个霉菌群周围
是一个

完全出乎意料
地没有细菌的区域。

在研究这一神秘现象时,

弗莱明意识到霉菌
正在分泌某种

可以杀死细菌的化合物。

这种霉菌是
青霉属的一种,

因此弗莱明将
这种抗菌化合物称为“青霉素”。

弗莱明偶然发现的
是一种微生物防御系统。

青霉菌
不断产生青霉素

以保护自己免受威胁,

例如附近
可能消耗其资源的细菌菌落。

青霉素

通过破坏
细胞壁的合成来破坏多种细菌。

这些墙的强度
来自一层厚厚的糖和氨基酸保护网,

这些网不断被
分解和重建。

青霉素与
将这种网格编织在一起的化合物之一结合,

并防止
在关键阶段重建壁。

同时,青霉素会刺激
高反应性分子的释放,

从而造成额外的伤害。

最终,细胞的结构
完全分解。

这种双管齐下的攻击
对各种细菌都是致命的,

无论是在培养皿、
我们的身体还是其他地方。

然而,它对
我们自己的细胞没有害处,

因为它们没有细胞壁。

在弗莱明发现之后的十年左右,

青霉素一直
是实验室的新奇事物。

但是在第二次世界大战期间,

研究人员想出了如何
分离活性化合物

并大量生长霉菌。

然后他们继续
为他们的工作赢得诺贝尔奖。

牛津大学和几家美国
制药公司的团队继续开发,

并在
几年内上市。

青霉素和类似化合物迅速
改变了感染的治疗方法。

就目前而言,

它们仍然是医学上使用的一些最重要、最能
挽救生命的抗生素。

然而,我们使用任何抗生素
的次数越多,细菌就越会对它产生抗药性。

在青霉素的情况下,

一些细菌产生的
化合物可以分解

干扰细胞壁合成的关键结构。

随着抗生素使用量的增加,

越来越多的
细菌进化出这种防御能力,

使这些抗生素

对越来越多
的细菌感染无效。

这意味着医生不要过度开药,这一点很重要

同时,发达国家有5%~15%的患者

自认对青霉素过敏

,是最常报告的
药物过敏。

然而,绝大多数(超过 90%

)认为自己对青霉素过敏的人
实际上并没有。

为什么会有误解?

许多患者在儿童时期获得过敏标签

当他们
因青霉素

或密切相关的药物感染治疗后出现皮疹时。

皮疹通常归咎于青霉素,

而更可能的罪魁祸首
是原始感染,

或感染与抗生素之间的反应

然而,真正的青霉素过敏,

即我们的免疫系统将
青霉素误认为是攻击者,

这种情况很少发生,
而且可能非常危险。

因此,如果您认为自己过敏
但不确定

,最好的办法是去看过敏专科医生。

他们将完成一项评估
,以确认

您是否有过敏症。

即使您确实对青霉素过敏,

对药物起反应的免疫细胞也
可能会失去识别它的能力。

事实上,大约 80%
对青霉素

过敏的人会
在十年内摆脱过敏。

这对于目前对青霉素过敏的人来说是个好消息

有朝一日,这种药物可能会挽救他们的生命,
就像它为许多其他人所做的那样。