Upon Googling "common cold", you're likely to get the standard laundry list of symptoms: sneezing, coughing, mucus production, headache, fatigue, possibly aches and shivering. Nothing serious. The advice is very general: rest and plenty of warm fluids, avoid chills, take pills, see your doctor if it takes a turn. We're so used to common colds - hence the "common", vulgaris, meaning "low" or "plain" or "ordinary" - that we generally don't give them a second thought. We go to work and school with them, spread them around willy-nilly, shrug them off as little more than a seasonal occurrence. Colds are so mild in most cases that we simply forget we were ever sick.
And because of their seemingly run-of-the-mill nature, very rarely do we see an instance of the cold - that is, a very particular one in an individual patient - described in any meaningful way. Part of this, of course, is the grab-bag nature of cold symptoms, anything from mild intestinal distress to conjunctivitis - nothing to pique our ghoulish interest (see Ebola, Marburg, etc.). Then there's the dependably survivable nature of the affliction. Describing the specific nature of your suffering to a disinterested medical attendant, especially in the era of COVID, will bring you nothing more than a rude awakening about the collapse of personalized medicine: you'll get a proverbial pat on the head, a prescription that does nothing to the cold virus (Z-Pak antibiotics), and a bill for wasting their time. Essentially, Nobody cares. Go home and sweat it out.
Well, I'm here to stand in solidarity with cold sufferers. Comrades, it is time to rise up against injustice. No longer will I stand for Cold Erasure! In this post I'm going to describe every horrific detail of Rick's Great Cold of 2024, and how it Ruined Christmas. I'm doing this for my people; I'm doing this for science; and I'm doing it because my wife put me under strict orders not to leave the house for the rest of the week, so I needed something to keep me occupied.
0. What is a Cold?
Common colds are typified by a viral attack on the epithelial (outer-tissue) cells of the nasopharyngeal region, or upper respiratory tract. The most common of these common cold viruses is the "rhinovirus" - literally "nose-virus" - which is any of the three viruses in the genus Enterovirus ("intestinal-virus" - although members of the genus have many different vectors and symptoms; poliovirus, the cause of Polio, is a member). Infection is caused by contact with droplets of mucus, often carried on the breath or ejected by a sneeze, or by touching surfaces previously infected, and then touching the face or eating. Symptoms can last from a few days to months in severe cases, and can spread to the sinuses (sinusitis), ears (otitis media), and eyes (conjunctivitis). More severe complications can occur if bacteria breeds in hot, backed-up mucus, resulting in secondary bacterial infection. Post-nasal drip can result in pneumonia if mucus gets into the lungs; this is especially worrisome in the sedentary, infirm, and very young, as movement is necessary to help the lungs clear. Rhinoviruses are also implicated as complicators in asthma and other chronic breathing conditions. Rhinoviruses A and C cause more severe symptoms, while Rhinovirus B causes milder or asymptomatic forms.
According to the National Institute of Health, common colds cost the U.S. economy over $40 billion a year. There is no "cure for the common cold", as it is useless to develop a vaccine for a virus that changes even more rapidly and unpredictably than the flu.
This brings up a very important question: what separates colds from flus? Obviously they are caused by different viruses (influenza is divided into A, B, C, and D, which cover several genera of viruses); but the two diseases have a similar range of symptoms and are often mistaken for each other. The difference is in the severity of symptom clusters: colds have more severe nasal symptoms, with sneezing and mucus; while flus produce more fever and joint pain. Flus, rather famously, have the potential to be deadly and pandemic - hence the constant monitoring of avian and swine influenza.
And since we're on the subject of pandemics, COVID-19 differs from both colds and flus both in the type of virus doing the infecting (a coronavirus), and the "dry" nature of its respiratory symptoms: COVID infection is typically marked by an unproductive, hacking cough, along with a bewildering array of symptoms like red eyes, loss of taste and smell, and the brain fog and body pain of "Long COVID", the ramifications of which are still being experienced, and may not be fully understood for years to come.
With that background in mind, we can now examine the events of this year's cold:
1. Outbreak
If this was one continuous cold, which I am tempted to think it was, then the symptoms started back before Thanksgiving. My colds tend to start with depression and negative thinking; I was getting really cranky at work, to the point of comment. This was accompanied by intestinal distress and watery stools on an hourly basis. This tracks because of the strong gut-brain connection; studies have shown that depression can be linked to the gut flora being out of whack. I know it was not the Thanksgiving feast because I was experiencing this distress three days prior to Thanksgiving; previous experience also told me to expect a cold approaching, although the severity of the depression/diarrhea is pretty consistent no matter what and doesn't seem to correspond to the severity of the succeeding cold symptoms.
Now, as for why this occurs: I don't know. I wonder if it has something to do with my particular immune response. Perhaps the invading viruses are killed quickly and cleanly in the nasotracheal region, only for their corpses to be ingested and cause a more severe response down the intestinal tract. Or perhaps it's more of a systemic inflammatory response than I realize. I do have a mild form of dyshidrotic eczema, which are clusters of whitish blisters that appear on the fingers and toes; these are often effected by illness, stress, or any other state that impacts the immune system. Whatever the case, these precursor symptoms act as the heralds of a coming cold; whether the cold actually manifests, or how bad it will be, is undeterminable.
2. First Symptoms
It was about the fist of December when the symptoms really started to kick it. The beginning of December this year was mostly very cold and dry, and I didn't feel horrible to begin with; just the general sore throat, achy head, and night sweats. I don't usually get the typical nasotracheal symptoms to start out with. The intestinal distress slackened somewhat, while a general feeling of malaise set in. I cancelled a couple of plans, but still went to see my folks for Christmas, and set up some pre-Christmas get-togethers for when I was sure the worst of it would have past.
3. Symptoms Worsen
This produced a very particular effect for this particular cold: my middle ears filled with mucus and stayed that way for a good long time. My worst colds all have unique traits that I can remember them by. About ten years ago, I had a cold that made me cough so hard I strained something in my throat, and could only swallow with a weird sideways motion. Three years ago, right in the middle of COVID, I had a banger of a virus that pounded an iron spike from my left nostril into the back of my skull (but apparently wasn't COVID, according to the rapid test - go figure). This year, my cold was a big fan of Ear Stuff, apparently.
The human ear is generally separated into three parts: outer, middle, and inner. The outer ear is the sound capturing organ, including the ear lobe and ear canal; the middle ear is capped by the ear drum and includes the famously tiny bones - the hammer, stirrup, and anvil - that amplfy external vibrations and send them to the inner ear, where microscopic hairs translate vibrations into electrical signals in the auditory nerve.
The middle ear is the important part here: cut off from the outside and the rest of the skull, it has a very precise internal pressure that is maintained through the Eustachian tube, a literal tube that runs from the bottom of the middle ear and opens at the back of the throat, just above the end of the soft palate. Simple actions like swallowing equalize the pressure inside the middle ear by forcing air in or out of the Eustachian tube; if water or other fluid gets into the middle ear, theoretically the Eustachian tube will drain it.
This was my problem: I couldn't get the damn things to drain.
Now, mucus can be forced into the middle ear for a variety of reasons; one of the most common is blowing your nose. In my youth I was told (by well-meaning parties) "Don't blow your nose, just wipe", as otherwise I would force all the mucus into my ears and presumably die of the Worst Ear-Infection Ever. While I don't dispute the first part, generally you can drain the mucus back out of your ears by swallowing, which creates a min-vacuum that equalizes the pressure, or using the same technique to pop your ears on an airplane flight: hold your nose, close your mouth, and blow gently like you're blowing up a balloon. Gentle pressure won't tear your eardrum, and should force the mucus back down your Eustachian tubes.
However, in cases of sickness and immune response with a lot of inflamed tissue and clotted snot, the Eustachian tubes can become blocked. Mucus forces itself up into the inner ear on its own, and then gets stuck. This produces a terrible ache, the feeling of being underwater, and as the fluid becomes denser stops your ears from functioning normally. I kept reaching up to take my earplugs out, only to remember that I wasn't wearing any.
The pressure in my ears, as well as my sinuses, was constant and excruciating. Functioning became difficult. My brain was in a fog. The slow postnasal drip inflamed my throat and caused intense bouts of coughing. I'd experience what I call "fade-outs", where my head would tilt to the side and I'd drift out of consciousness, on and off for about an hour. Sleeping was reduced to maybe two or three hours a night, punctuated by waking up soaking wet, hacking up my lungs while my head felt like it was going to explode.
4. Sinus Infection
I was in the throes of what is rather boringly called a "sinus infection" (Sinusitis), but I think should be called, "Internal hot slimy exploding-head torture". No High Inquisitor could have imagined the simple efficacy of blocking all the exits to the cranial cavities and slowly filling them with warm goo; I would've denounced all my close relatives and admitted to any number of Pagan defilements for a moment of respite. The placement of the sinuses, especially those next to the ear and behind the eye, were actually affecting my senses; it felt like my left eye was being pushed out sideways, and I had the strangest feeling of a blind spot in my vision, though I couldn't pinpoint its location.
4a. On the Wonders of Mucus
To fully understand the implications of sinusitis, we have to understand what mucus is, how it's produced, and how its production changes during an infection. Mucus is mostly water and salts, with a dash of slippery agents and antibiotic chemicals. Our airways, digestive tract, and to some extent reproductive organs are lined with mucus cells that help to clean, hydrate, and lubricate our various tubes. Normal mucus is clear and only slightly viscous, allowing for it to flow quickly, flush out any dust or microbes, and then be reabsorbed by the body.
Things change drastically when an infection occurs. To criminally simplify a very complex process, immune cells detect live microbes and start pumping out inflammatory control chemicals like histamine and cytokines; these causes tissues to swell with water and heat up, while dilating blood vessels and making their membranes "leaky" so that immune cells can squeeze in and out quickly. Another effect of histamine is to signal the mucus cells to go into overdrive, pumping out enormous amounts of fluid. Most of your noticeable immune response, especially in allergic reactions, is due to histamine. Since rhinovirus attacks epithelial cells, which sit right next to the mucus cells, the response is immediate and intense to try and smother the viral attack in waves of goop. The consistency and color of mucus changes during an infection, as the body produces chemicals to change its viscosity, and the fluid becomes jammed with viral particles, exploded epithelial cells, dead white blood cells, and colonizing bacteria.
4b. On the Terrors of Viral Infection
Viruses are pretty astounding: imagine tiny little protein robots that squeeze into cells and re-program their DNA to manufacture more viruses. It would be like a saboteur sneaking into a factory and re-tooling all the equipment to do nothing but make more saboteurs. The genetic machinery has no off-switch, so the viruses squeeze into every available corner of the cell until their membranes literally rupture from the pressure.
And that "pressure" represents millions of viruses. Per cell. Rhinoviruses are especially aggressive in their overwhelming numbers. Before the immune system can get its boots on, the body is already flooded with viruses, each of them fully capable of hijacking a cell and turning out hordes of clones. While we often curse the miserable effects of immune reaction, the alternative is even more horrific: the viruses would literally destroy the epithelium of the nasopharyngeal region, leaving nothing but a necrotic sack of tissue that would render breathing impossible and causing sepsis as bacterial infection sets in. Even a "minor" viral infection like a cold, which flares up and passes multiple times a season, represents an existential threat to the organism. We owe our lives to a hair-trigger immune system willing to pounce on rhinovirus with extreme prejudice.
Immune response to viruses is somewhat strange, in that it doesn't attack the viruses directly. The reason appears to be the overwhelming scale of the invasion, combined with the teeny-tininess of viruses themselves, often thousands of times smaller than immune cells. This is also the reason that antibiotics don't work at all on viral infections (despite the way our medical system throws antibiotics at colds and flus*). Bacteria, fungi, and parasites, as cellular organisms, all maintain a surface integrity that can be punctured and ruptured with chemical attacks. But attacking viruses with the same chemicals is a bit like trying to kill a vast swarm of mosquitoes with full-size surface-to-air missiles: expensive and ultimately futile.
Instead, the immune system launches a three-pronged attack: first, inflammatory proteins disrupt the environment by increasing the temperature and flooding the area with mucus. Most attacking microbes require a slightly cooler environment to maintain homeostasis, which helps explain why infections occur more readily in cooler weather. The increased temperature (and sometimes fever) caused by our immune response effectively stresses the microbes and decreases their ability to multiply and infect. Next, immune cells blast the area with antibodies. Antibodies are special proteins that bind to the surface of viruses and serve a twofold purpose: first, they prevent the virus from binding to their preferred cells and entering their membranes; second, they serve as homing beacons for macrophages, giant immune cells that capture and eat foreign particles. Last, white blood cells identify infected cells - those that are in the midst of serving as viral clone factories - and force them to self-destruct with chemical signals. By identifying and destroying these infected cells, they reduce the viral output from billions to mere thousands. As the viral attack is contained, the immune system switches into mop-up operations, cataloguing the particular strain of invader and storing their characteristic in Memory B cells, which makes the immune system that much faster at identifying and quelling that strain if it attacks again.
This is usually enough for one infection - you get infected, you're sick, you get better. The problem is, you're likely to get sick over and over again over a season. This is because viruses evolve in real time.
4c. Rhinovirus Triumphant
Viruses, especially rhinovirus, evolve fast. Scary fast. Consider the speed at which viruses are pumped out by infected cells: if you want something done fast and cheap, you're going to sacrifice consistency. Each time the cell replicates the viral genetic blueprint, tiny mistakes are made; most of these mistakes have no effect, and some are detrimental; but with billions of the suckers pumping out by the hour, it's only a numbers game until a new functional sub-strain appears that is able to evade the immune system by appearing different than its brethren. This new sub-strain then infects more cells and recreates its evasive ability. The immune system requires time to process the new permutation and produce antibodies to combat it specifically. Some of this new sub-strain will always escape and find a way to pass on to a new host and survive. Sub-strains keep evolving until they have mutated into an entirely new strain of the virus, able to fully evade and infect the same immune system that had previously conquered its ancestors.
There's another wrinkle to the evolutionary equation: horizontal gene transfer. This occurs when snippets of genetic material are swapped between cells, or between cells and viruses. Single-celled organisms like bacteria and archaea are known to swap genes - in fact, this is as much of an engine of evolution as reproductive gene transfer. But with all their genetic messing around, viruses can donate genes to their host cells, pick up genes from their host cells, and even transfer genes between cells. This gives them an even greater probability of developing into a new strain. You may have heard of the "mixing-vat" effect of influenza infecting and circulating between pigs and waterfowl, especially in large open-air markets where livestock are kept in, shall we say, "moist" conditions; essentially, swine and avian influenza swap genes with their hosts and cross the species barrier to create new, more powerful strains. When large numbers of humans are also present, the resulting strains have a new testing lab in which to tinker.
In this environment, it's only a matter of time before a pandemic-level virus is formed. This is probably the origin of the so-called Spanish Flu of 1918, when thousands of soldiers were sequestered in muddy camps with millions of livestock, en route to the European front. Such preparatory camps had been set up in Kansas and France; any one of them could have been the jumping-off point for Spanish Flu, especially if U.S. soldiers were transferred between them.
From my research, the consensus seems to be that COVID-19 emerged in a livestock operation of some kind in the Wuhan province of China.** Most opinion points to "wet markets" where live pigs and fowl are sold; but some evidence indicates industrial farming as an origin point. Bats and even pangolins were even implicated, which seems farfetched until you consider the black market in wildlife medicine - Wing of Bat and Scale of Pangolin will fetch a pretty penny if you have no qualms about international law and destruction of threatened species. Even dead animal parts, including fresh meat, can harbor viruses. It's the mixing of viruses and different host species that supercharges viral evolution and produces the really nasty bugs.
Thankfully, the common cold isn't that nasty - a healthy adult has little to fear, at least in terms of permanent injury and death. I just find it mind-boggling how many cold infections we shrug off every year without even noticing. We only notice particularly long or intense symptoms, and then usually attribute the illness to influenza - even though it was "just" a rhinovirus that caused our suffering.
But why does one particular infection hit us harder than another? How could I have one severe cold that lasted over a month, when all my other colds exhibited precursors (depression, bubble guts) without the actual symptoms? Obviously viral strain and external factors like stress, bodily fitness, and seasonal climate are factors; but there may be another factor: nasal microbiome. Specifically, the presence and ratio of Staphylococcus aureus bacteria in the nose has been implicated in worsening cold symptoms. Staph is a particularly troublesome bug for human beings; it resides on all our surfaces, and while it's normally kept in check by our microbiome, any slight disturbance can allow it to gain a foothold and multiply like mad. Even when not a superbug like Multiple-Resistant Staphylococcus Aureus (MRSA), Staph is a tough bug to get rid of. It can cause a laundry list of ailments in all body systems, from pneumonia to food poisoning, and thrives in hospitals and other "antiseptic" areas.
So what does this have to do with severe colds? Part of the reason Staph is so hard to treat is their ability to evade the immune system. This article from the University of Chicago explains how Staph takes the very weapons of white blood cells and turns them into a toxin that kills macrophages.*** Macrophages, or "big eaters", are the patrols of the body, sniffing out and "tasting" foreign particles and microbes and alerting the immune system of potential infections. When Staph creates a macrophage dead zone, this gives the rhinovirus the opportunity to establish a three-alarm infection before the immune system is even aware of its presence. The more lead-time an infection has to establish itself, the more massive the immune response.
Now the $64,000 question: what causes the higher ratio of Staph in the nasal microbiome that leads to a more severe cold? Microbiomes are touchy, and can be affected by just about anything from shifting weather to a change in diet. In my case, the weather before Thanksgiving had been bouncing between cold and dry to wet and mild, a situation that stresses the body - perhaps just enough to induce a slightly larger presence of Staph in the nasal passages, which was just enough to create a macrophage-free zone that allowed that particularly aggressive strain of rhinovirus to take hold and colonize the sinuses before my immune system could address it. This is all just speculation of course (who doesn't love a good story?) but it does make sense.
5. Resolution
All colds must end, even this nightmare of a cold. Thankfully the majority of the severe symptoms ran their course between Christmas and New Year's Day, when I was off of work. The sleepless nights, the woozy days, the feeling like my head was underwater, the endless rounds of cough syrup (I hate the stuff, it makes me feel weird)...it was finally starting to break up by the time I got back to work. Work seems to help with my cold symptoms: part of it's the adrenaline, which has a dampening effect on the immune system; but physical activity also seems to have a salutory effect on illness, something to do with regulating inflammation and helping the immune system to focus on its target rather than attacking the body. There were thankfully few lasting effects, with only an annoying cough and post-nasal drip to remind me of my ailment.
This cold (or flu?) season has been one of the worst in 20 years; I've known several people who've been clobbered by the same strain or something similar. So please be careful - wash your hands and wear your mask when you can. Here's wishing everybody good health and swift recoveries.
*So if you've ever been to your friendly neighborhood Urgent Care with a cold or flu, you'll be aware of something called a "Z-Pak": a progressive 5-day course of Zithromax (azithromycin). The reasoning is that a loading dose of antibiotics will cure and/or help prevent secondary bacterial infections such as bacterial sinusitis, pneumonia, conjunctivitis, and other problems. If you've been following any medical headlines from the past, oh, twenty years, you'll know that overuse of antibiotics has contributed to the rise of antibiotic-resistant bacteria ("superbugs")...and guess which antibiotic is highly implicated in the rise of antibiotic resistance? I see one of two scenarios at play here: either we're witness to a vast and happy display of medical indifference being perpetrated especially upon poorer Americans in the name of "looking like you're doing something"...or Z-Paks are really just placebos. I really wish my conspiracy theory were true, and Z-Paks were nothing more than sugar pills, because the implications for rampant antibiotic-resistance is frightening.
**...Unless, of course, you believe that it was created in a Chinese bioweapons lab. Which is stupid. And xenophobic. And also, please don't talk to me anymore. Please. I'm so tired.
*** A word of caution: this article explains that a clinical trial showed no effect on cold severity when Staph a. was introduced to an infected host, so take this with a grain of salt. But taken with the University of Chicago article I cite later, I think a compelling case can be built for Staphylococcus aureus affecting cold severity by screwing with immune response.
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