Why do you get a fever when youre sick Christian Moro

In 1917, doctors proposed
an outlandish treatment for syphilis,

the incurable bacterial infection
that had ravaged Europe for centuries.

Step 1: Infect patients suffering
from the later stages of syphilis

with the parasite that causes malaria,

the deadly but curable
mosquito-borne disease.

Step 2: Hope that malarial fevers
clear the syphilis.

And step 3: Administer quinine
to curb the malaria.

If all went according to plan,

their patient would be left alive
and free of both diseases.

This killed some 15% of patients,
but for those who survived,

it seemed to work.

It actually became the standard treatment
for syphilis

until penicillin
was widely used decades later.

And its driving force was fever.

There are many mysteries around fever,

but what we do know is that all mammals,

some birds and even a few invertebrate
and plant species feel fever’s heat.

It has persisted
for over 600 million years of evolution.

But it has a significant cost.

For every 1 degree Celsius of temperature
increase in the human body,

there’s a 12.5 percent increase
in energy required,

the equivalent of about 20 minutes
of jogging for some.

So, why and how does your body
produce a fever?

Your core temperature is maintained
via thermoregulation,

a set of processes that usually keep
you around 37 degrees Celsius.

These mechanisms are controlled
by the brain’s hypothalamus,

which detects minute temperature shifts

and sends signals
throughout the body accordingly.

If you’re too hot, the hypothalamus
produces signals

that activate your sweat glands
or make your blood vessels dilate,

moving blood closer
to the skin’s surface—

all of which releases heat
and cools you off.

And if you’re too cold,

your blood vessels will constrict
and you may start to shiver,

which generates heat.

Your body will disrupt its usual
temperature equilibrium to induce a fever,

which sets in above 38 degrees Celsius.

Meanwhile, it has mechanisms
in place to prevent it

from exceeding 41 degrees Celsius,
when organ damage could occur.

Immune cells that are fighting
an infection can induce a fever

by triggering a biochemical cascade
that ultimately instructs

your hypothalamus to increase
your baseline temperature.

Your body then gets to work to meet
its new “set point” using the mechanisms

it would to generate heat when cold.

Until it reaches this new temperature,
you’ll feel comparatively cool,

which is why you might experience chills.

But why does your body do this?

While the jury’s still out on how higher
temperatures directly affect pathogens,

it seems that fever’s main effect

is in rapidly inducing a whole-body
immune response.

Upon exposure to raised
internal temperatures,

some of your cells release
heat shock proteins, or HSPs,

a family of molecules produced
in response to stressful conditions.

These proteins aid lymphocytes,
one of several kinds of white blood cells

that fight pathogens, to travel
more rapidly to infection sites.

HSPs do this by enhancing
the “stickiness” of lymphocytes,

enabling them to adhere to and squeeze
through blood vessel walls

so they can reach the areas
where infection is raging.

In the case of viral infections,

HSPs help tell nearby cells to dampen
their protein production,

which limits their ability to replicate.

This stunts the virus’s spread
because they depend on

their host’s replicative machinery
to reproduce.

It also protects surrounding cells
from damage since some viruses spread

by rupturing their host cells, which can
lead to large-scale destruction,

the build-up of detritus,
and potentially even organ damage.

The ability of HSPs to protect host cells
and enhance immune activity

can limit the pathogen’s
path of destruction inside of the body.

But for all we know about fever’s role
in immune activation,

some clinical trials have shown
that fever suppressor drugs

don’t worsen symptoms or recovery rates.

This is why there’s no definitive rule
on whether to suppress a fever

or let it ride.

Doctors decide on a case-by-case basis.

The fever’s duration and intensity,
as well as their patient’s immune status,

comfort level, and age will all play
a role in their choice of treatments.

And if they do let a fever ride,

they’ll likely prescribe rest and plenty
of fluids to prevent dehydration

while the body wages its heated battle.

1917 年,医生
为梅毒提出了一种奇特的治疗方法,梅毒


一种在欧洲肆虐数百年的无法治愈的细菌感染。

第 1 步:

用导致疟疾的寄生虫感染晚期梅毒患者,疟疾

是一种致命但可治愈的
蚊媒疾病。

第 2 步:希望疟疾热能
清除梅毒。

第三步:服用奎宁
来控制疟疾。

如果一切按计划进行,

他们的病人就可以活着,而且不会患上
这两种疾病。

这杀死了大约 15% 的患者,
但对于那些幸存下来的患者来说,

它似乎奏效了。

它实际上成为梅毒的标准治疗方法

直到
几十年后青霉素被广泛使用。

它的驱动力是发烧。

发烧有很多谜团,

但我们所知道的是,所有哺乳动物、

一些鸟类,甚至一些无脊椎动物
和植物物种都会感受到发烧的热量。

它已经持续
了超过 6 亿年的进化。

但它的成本很高。

人体温度每升高 1 摄氏度
,所需的能量

就会增加 12.5%

,相当于
一些人慢跑约 20 分钟。

那么,您的身体为什么以及如何
产生发烧?

您的核心温度是
通过体温调节来维持的,这

是一组通常使
您保持在 37 摄氏度左右的过程。

这些机制
由大脑的下丘脑控制,

它检测微小的温度变化

并相应地向全身发送信号

如果你太热,下丘脑
会产生信号

,激活你的汗腺
或使你的血管扩张,

使血液更
接近皮肤表面——

所有这些都会释放热量
并让你凉爽。

如果你太冷,

你的血管会收缩
,你可能会开始发抖,

从而产生热量。

您的身体会破坏其通常的
温度平衡,从而引发发烧,发烧温度会

超过 38 摄氏度。

同时,它具有

防止器官损伤超过 41 摄氏度
的机制。

与感染作斗争的免疫细胞可以

通过触发生化级联反应来引发发烧
,最终

指示下丘脑
提高基线温度。

然后,您的身体开始
使用在寒冷时产生热量的机制来满足其新的“设定点”

在它达到这个新温度之前,
你会感觉比较凉爽,

这就是为什么你可能会感到发冷。

但是你的身体为什么会这样呢?

虽然对于
高温如何直接影响病原体尚无定论,

但发烧的主要影响似乎

是迅速引发全身
免疫反应。

在暴露于升高的
内部温度时,

您的一些细胞会释放
热休克蛋白或 HSP,这

是一种
在压力条件下产生的分子家族。

这些蛋白质帮助淋巴细胞
(几种对抗病原体的白细胞之一)

更快地到达感染部位。

HSP 通过增强
淋巴细胞的“粘性”来做到这一点,

使它们能够粘附并
挤压血管壁,

从而
到达感染肆虐的区域。

在病毒感染的情况下,

HSP 有助于告诉附近的细胞抑制
它们的蛋白质产生,

从而限制它们的复制能力。

这阻碍了病毒的传播,
因为它们依赖

宿主的复制机制
进行繁殖。

它还可以保护周围细胞
免受损害,因为一些病毒

通过破坏宿主细胞进行传播,这可能
导致大规模破坏

、碎屑堆积,
甚至可能导致器官损伤。

HSP 保护宿主细胞
和增强免疫活性的能力

可以限制病原体
在体内的破坏路径。

但就我们所知,发烧
在免疫激活中的作用,

一些临床试验表明
,发烧抑制药物

不会恶化症状或恢复率。

这就是为什么对于是
抑制发烧

还是让它继续发烧没有明确的规则。

医生根据具体情况决定。

发烧的持续时间和强度,
以及患者的免疫状态、

舒适度和年龄都将
在他们选择治疗方法中发挥作用。

如果他们真的发烧了,

他们可能会在身体进行激烈的战斗时开出休息和
大量液体以防止脱水的处方