Why I vaccinate my kids

Being a new parent is exhausting. All of a sudden, you’re out of the hospital and on your own with this amazing, tiny human, and you alone are responsible for her care. You’re given reams of paperwork about feeding and sleeping, developmental milestones, red flags to look out for. You’re inundated with information you barely have time to look at. Mom is trying to heal from childbirth while barely sleeping, while her partner is trying to pick up the slack and pitch in as much as possible. You both fumble with the car seat, thinking that NASA must have equipment that’s easier to figure out. You obsessively check your sleeping baby to make sure she’s still breathing. You worry about every sneeze and try to decipher her cries. Is the diaper too tight? Is this acne normal? What do I do about her poor dandruffy head?

Do I vaccinate?

vaccineWilliam receiving the first of  his 2-month vaccinations

I know it can be scary. You might have heard from friends or relatives, or read on the internet, that vaccines can harm your baby. You may be concerned about autism, or think that “natural immunity” is better than that which develops from injections. You may think that the diseases she’s being vaccinated against “aren’t all that bad,” or that kids today receive too many vaccines. You might feel that your physician is “bought out” by “big Pharma” and that your health care providers are writing off your concerns.

I know you just want to do what’s best for your child. I feel you. I’m the parent of a teenager, a tween, and a 2-month old. Here is why I vaccinate my children.

William vax 2William receiving his vaccinations

I’ve spent almost 20 years of my life studying infectious diseases up-close and personal, not from random websites on Google. I’ve worked with viruses and bacteria in the lab. I respect what germs are capable of. I worry about vaccine-preventable diseases coming back because of low levels of herd immunity. I cry over stories of babies lost to pertussis and other vaccine-preventable diseases. As I’ve noted before, chicken pox has played a role in the deaths of two family members, so I don’t view that as just a “harmless childhood disease.” Vaccines have eradicated or severely reduced many of the deadliest diseases from the past: smallpox, polio, measles, diptheria.

But that’s not the only reason I vaccinate. I vaccinate because I’m all too aware of the nasty diseases out there that still don’t have an effective vaccine. My current work focuses on a germ called methicillin-resistant Staphylococcus aureus (“MRSA”), a “superbug” which kills about 11,000 people every year in the United States. We have no vaccine. I previously worked on two different types of Streptococcus: group A and group B. Group B is mainly a problem for babies, and kills about 2,000 of them every year. It leaves many others with permanent brain damage after infection. We have no vaccine. Group A kills about 1,500 people each year in the U.S. and can cause nasty (and deadly) infections like necrotizing fasciitis (the “flesh-eating disease”). We  have no vaccine. These are all despite the fact that we still have antibiotics to treat most of these infections (though untreatable infections are increasing). Infectious diseases still injure and kill, despite our nutritional status, despite appropriate vitamin D levels, despite sanitation improvements, despite breastfeeding, despite handwashing, despite everything we do to keep our kids healthy. This is why protection via vaccination is so important for the diseases where it’s available. If vaccines were available for the diseases I listed above, I’d have my kids get them in a heartbeat.

w after vax 1William with daddy, right after finishing his vaccinations

I’ve done my best to keep my kids healthy and safe. I nag about bicycle helmets and make sure they’re getting exercise. I make them eat vegetables. I don’t move the car until everyone is buckled up. My older kids were in booster seats for what felt like forever, as both were on the small size for their age. Vaccinations are just one more part of this arsenal. I’m well versed in the safety data and know that most vaccine side effects are minimal (fever, soreness at injection site). They don’t cause autism, or SIDS, or any of the other claims made by dubious sites such as Natural News or Mercola. They do save lives and prevent disease by training the body to recognize and fight germs.

My youngest recently went in for his 2-month shots. He cried a bit when he received them, but not any worse than he does when he needs to be burped, changed, or held. He slept a little extra that evening, but was back on his normal schedule the next day. At his visit, he received the oral rotavirus vaccine; his second Hepatitis B shot; his pneumococcal vaccination; and the combination shot including diptheria, pertussis, tetanus, polio, and Haemophilus influenzae (DTaP/polio/Hib). Each one I see as a small measure to support his health and safety, as well as my own peace of mind, knowing that I did what I could to protect him from infections that used to kill thousands of children every year. Some still do when vaccination isn’t available or accepted–measles killed over 120,000 people in 2012, most of them young children who hadn’t been vaccinated.

W after vax 3William at home after his vaccinations

We all try to do the best by our children. As a scientist who’s studied infectious diseases, vaccination is a no-brainer for me, and I worry for the children out there who are left undefended against these infections because of misinformation and wrongly-placed fears. I know these parents are trying to do right by their kids, but infectious diseases don’t recognize good intentions. As I sit here with my baby breathing softly beside me, I am thankful for those who came before me and dedicated their lives to protecting children like him, and grateful that he will never have to suffer from infections that were the scourge of earlier generations.

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Guest post: Will new FDA guidelines reduce threat from superbugs?

Guest post by Tim Fothergill, Ph.D.

In January of this year the British Chief Medical Officer urged her government to add  threat posed by superbugs to the official list of “Apocalypses to Worry About” along with catastrophic terrorist attacks and massive flooding. With typical British understatement, its actual name is the National Risk Register of Civil Emergencies but a very stark picture was painted of a post-antibiotic world in which routine operations, such as hip replacements, could prove fatal. In September, The Centers for Disease Control in the US issued a similar statement which estimated that 23,000 people die every year in the US from antibiotic resistant infections. So what is it that has Dame Sally Davies and so many others so worried?

“Superbug” is a term used to describe bacteria which are resistant to many common antibiotics which are used to treat infection. Resistance to these drugs makes treatment more difficult and has increased mortality rates. As resistance to individual antibiotics becomes more prevalent the number of deaths is only set to increase, especially because there is a dearth of research into new antibiotics. Antibiotics are used medically in the short term, so don’t offer the same kind of return on investment for the pharmaceutical companies as drugs for chronic diseases or long-term treatments, such as anti-depressants or hypertension medications. Even more worryingly of all is that strains of potentially deadly infectious bacteria, such tuberculosis have already been identified that are resistant to every potential drug.

Against this background the FDA’s announcement of a plan to phase out the agricultural use of antibiotics is very welcome. Many animals raised for human production are fed antibiotics as a matter of course to boost growth rates. The animals are not suffering from infection, but the drugs can help them grow faster, resulting in a more efficient production of meat for the market. For most drugs, there is a mandatory withdrawal period during which the animals are fed no antibiotics so that they will clear out of the meat prior to slaughter. However, the antibiotics can impact the food supply and human health in other ways. Not only is there concern about meat contaminated with resistant bacteria but the standard agricultural practice of using animal waste as fertilizer only increases the risk of releasing resistant bacteria into the environment contributes to the spread of resistance. This is of particular concern if the land fertilized in this manner is subsequently used to grow food crops that are typically consumed raw. Previous recalls due to bacterial contamination have included spinach and cantaloupe melons. The potential for harm would only have been greater if these cases had involved superbugs, but this possibility is becoming more and more likely. Resistant bacteria that are spread onto crops via animal manure fertilizer have been demonstrated to not only persist in the soil but to also pass the genes for antibiotic resistance onto other species. As we have no control over this genetic transfer it is quite possible that they spread to even more pathogenic species.

The FDA’s proposal to limit antibiotics in cattle feed would seem like good news then. However, the most significant caveat with this plan is that it is voluntary and as such is dependent on the cooperation of the drug producers and farmers. Two of the largest antibiotic producers, Zoetis and Elanco, have indicated that they will no longer labelling their products as suitable for growth promotion. Any subsequent use of these antibiotics for growth promotion would be “off-label” and something that the FDA can and does regulate. However, as with all regulation the devil will be in the details. We do not know yet what the change in labelling will actually say. If their new label can be interpreted in such a way that cattle are still regularly fed antibiotics then nothing will have been achieved.

For example, in Denmark they found that after introducing a ban on antibiotic use for growth promotion in cattle that the quantities of antibiotics actually increased. Animals no longer fed a sub-therapeutic level of antibiotic became more susceptible to infection and thus need therapeutic treatment more often. At first glance this might seem as if little has changed but antibiotics taken at therapeutic levels for the prescribed duration will result in fewer occurrences of resistance to the antibiotic in question. Anybody who has been told by their doctor to ensure that they take the full course for an infection will know this. By reserving antibiotic use for therapeutic use only, where it is needed in greater quantities to fight infections, not only will there be fewer superbugs released into the environment, but the drug companies will stand to increase their sales. This might explain their willingness to cooperate with these proposals. Their other option would be to switch production to antibiotics which are not regarded as being important for human health (such as the ionophores) as these are not covered by these new proposals. However, this is something that would presumably involve some cost to them.

It is also worth comparing the timescale for voluntary phase-out (three years) with the length of time it would take the FDA (presumably in collaboration with the USDA) to implement a strategy for an obligatory regulatory framework, which might have more teeth in terms of enforcement, but which is not yet on the table. The FDA has many admirable qualities but turning on a dime is not one of them. This process would take at least that long if not longer. What we do not know at this point is whether there are plans for the FDA to pursue such mandatory regulation if this voluntary arrangement is found not to be working. Such efforts would presumably require specific budgeting and it seems unlikely that this will happen any time soon given the current state of Congressional deliberations on budget matters. Another possible mandatory option would be Louise Slaughter’s PAMTA bill which is currently with the Health Subcommittee.

If our goal is to reduce the spread of antibiotic resistant bacteria from agriculture then the FDA plan may in fact be the best option, and it is certainly better than doing nothing. Mandatory regulation seems unlikely at this point. However, accountability is still vital to the success of this voluntary agreement. What form could this accountability take? The FDA must be prepared to state publicly if insufficient progress is being made. Also, it is to be hoped that increased demand from major chains like Chipotle, McDonalds and KFC will help. If they were to make this demand then cattle production would change at a much faster pace than that proposed currently. This means that consumers are in a position to contribute by choosing to support suppliers of meat produced in a way consistent with these new guidelines.

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Tim Fothergill, Ph.D. is a microbiologist with over a decade of experience in researching the mechanisms for the spread of antibiotic resistance. This interest has led him to the intersection of antibiotic resistance in bacteria and policy, where his is now looking at the implications and consequences of legislation and regulation around antibiotic use. As a result, he has become concerned that the threat posed by overuse of antibiotics needs to be taken more seriously. But it’s not all doom and gloom: his interest in instrumentation and general microbiology extends to brewing his own beer.

 

The microbiology of zombies, part V: beware the bite?

Now that seemingly the flu outbreak storyline has been wrapped up on The Walking Dead (unsurprisingly, but disappointingly, with their ineffective treatments proving to be miracle cures), there’s still one more zombie microbiology topic I’d like to cover: what’s up with the bite, and is it the cause of death? I said previously:

“We know the pathogen can certainly be spread by bites and then cause zombification that way…”

but one commenter disagreed, noting:

“I don’t think we have evidence for that from the show. I think it clearer that zombie bites cause death, and there doesn’t seem to be evidence that the agent that causes death also causes zombieism (or vice versa). In Walking dead, any death is a sufficient condition for becoming a zombie. I would guess that zombies cause death because of a massive polymicrobial infection/sepsis.”

So, could death be due to massive sepsis (an overwhelming immune response to infection, which can lead to organ failure and death) via the bite, rather than the introduction of a specific zombie pathogen? It’s certainly not the first time I’ve seen that argument. Even the Zombie Research Society has put that forth as a hypothesis (and Matt Mogk has written of it in his book as well). However, I don’t buy it for a few reasons.

First and foremost, human bites simply aren’t that deadly. Even in a study of patients presenting to emergency rooms (which are probably the most serious of bites), none were found to have sepsis. Well, you might say, maybe more would have had this if antibiotics weren’t available, which would be the case with TWD (well, except now they have them, but I digress…) A Medscape article addresses this, noting that prior to the antibiotic era, up to 20% of bites caused amputation of a finger–but still, a local nasty infection, not necessarily sepsis. Even in a 1936 NEJM paper studying bites, only 2 deaths are noted, and both are in “delayed cases”–individuals who waited 5 days post-bite to present to the hospital. In these cases, the cause of death is indeed listed as “extensive sepsis.”

However, it should be noted that hand bites in particular—the subjects of those papers and articles above– seem to be rather nasty. Per Medscape again, “… most human bite injuries occur on the hands, and hand wounds from any cause have higher infection rates than do similar wounds in other anatomic locations.” So, these papers focus on the worst types of bites (hand injuries) at the most severe locations (presenting to emergency rooms), and thus should be considered likely a worst-case scenario for our potential infectees: that, even if bitten, a minority of them would have serious complications, and a minority of those might perish of sepsis. This doesn’t match up with what we see in the show.

You might argue that the process of zombification would modify/increase the nasty bugs living in the mouth. I agree–rotting in this manner certainly could alter the presence and types of organisms that would be present in the mouth, and therefore possibly make them more deadly and more likely to result in a sepsis death of the bitten. However, even accounting for rapid reproduction rates for microbes (mostly bacterial when you’re talking about sepsis and oral germs), this doesn’t seem to be a satisfactory answer, as one can quickly die and be reanimated and immediately have the potential for a deadly bite. It could also be argued then that therefore *everyone*, living or dead, would also possess this quality in that case–it shouldn’t matter if the bite is from a zombie or from a living person; the result should be the same (sepsis and zombification).

Further, in the human bite literature, there are two types of bites typically described: occlusive bites and clenched-fist injuries. The former is probably what you think of when you think zombie bites: mouth open, teeth coming together on the skin, chomp, chomp, chomp. Clenched-fist injuries are what happens when someone strikes another person’s teeth with, as the name suggests, their clenched fist, often scraping the knuckles: basically, a punch that strikes the teeth/mouth. While on the Walking Dead the former universally mean death (except in the case of really quick amputation of the bitten part, like we saw with Hershel’s leg), we’ve seen many examples of the latter—how many fistfights has Rick alone gotten into now? Not to mention, scenes like this:

 So if one is going to support the “polymicrobial infection as a result of bites” scenario for zombification, the issues of living biters need to be explained away as well.

Others have argued along similar lines regarding bites and sepsis, suggesting that the zombie bite is analogous to what happens to the prey of the Komodo dragon:

“Animals that escape the jaws of a Komodo will only feel lucky briefly. Dragon saliva teems with over 50 strains of bacteria, and within 24 hours, the stricken creature usually dies of blood poisoning. Dragons calmly follow an escapee for miles as the bacteria takes effect, using their keen sense of smell to hone in on the corpse.”

The problem with that analogy is that it’s based on a myth. That’s not what really happens: the dragon actually has venom, as I noted way back in 2005 (and Ed Yong updated recently, both based on the work of Bryan Greig Fry). It’s not their bacteria that kill their prey, but their venom. Do zombies suddenly become venomous? Doubtful. So, another idea shot down.

To me, the most convincing scenario, and the one that seems to jibe with both the idea that everyone is infected and with the little we know about the epidemiology of the outbreak, is that the immune system keeps the “zombie virus” under control while one is still alive and healthy. When one dies, the virus is allowed to replicate unchecked, resulting in both zombification/reanimation as the infection proceeds unabated throughout the body. The virus would also replicate (probably within the salivary glands) in order to enable transmission to the next bite victim. A zombie bite then introduces a large amount of this virus right into the bloodstream of the target, which overwhelms the body’s defenses and is responsible for both death and subsequent zombification—like rabies virus on steroids—and the cycle perpetuates itself.

Bottom line is that with the sepsis model, you have to explain more anomalies than with a virus-death model. You’d need to postulate immediate changes in the oral microbiome that aren’t readily accounted-for, but would be responsible for the 100% fatality rates upon receiving a bite (but ONLY a zombie bite, and not a live-human bite), while with the novel zombie virus model you get a bit more carte blanche to account for the transmission and certain death. That seems a much better explanation to me.

 Works Cited:

Welch CE. Human bite infections of the hand. NEJM, 215:901. 1936.

Talan DE et al. Clinical Presentation and Bacteriological Analysis of Infected Human Bites in Patients Presenting to Emergency Departments. CID, 37:1481. 2003.

See also:

Part I: the microbiology of zombies

Part II: ineffective treatments and how not to survive the apocalypse

Part III: “We’re all infected”

Part IV: hidden infections

The microbiology of zombies, part IV: hidden infections

(As previously, spoilers abound)

So on this week’s Walking Dead soap opera, we find that Daryl/Michonne’s group is still out and about searching for medical supplies. Back at the prison, the food situation is dire (apparently all the food stores were in the cell block where the infection broke out), so Rick and Carol head out to look for both medicines and food from the local ‘burbs. During their outing, discussion ensues of Carol’s attempt to stop the prison’s apparent influenza outbreak by killing two people who, at that point, were the only ones showing symptoms of disease. Rick decides he can’t trust her, and ends up banishing her from the group.

Carol said multiple times that she was trying to do the right thing, to protect the rest of the group from those who were sick and was only trying to end the outbreak. However, here’s where some knowledge of infectious disease would have helped her. Every disease has an incubation period: the time when the microbe is multiplying in your body, but you’re not showing any physical disease symptoms yet. This can be short–as little as perhaps a few hours for something like Salmonella food poisoning. It can be extremely extended, as I mentioned with rabies virus in my previous post, where the incubation period can be months to years. With influenza, the typical incubation period is 2 days, but it can be as short as 1 or as long as 4-5. The kicker is that a person who’s incubating flu can still spread it even before they show symptoms of the illness. So just because Karen and David were the only ones actively coughing and looking miserable, Carol was mistaken in her assumption that they were the only ones infected, and that she could stop the outbreak by snuffing them.

This is the difference between two similar concepts, quarantine and isolation. People who have been *exposed* to an infectious agent, but are not yet showing any signs of illness, can be quarantined to keep them away from others due to their *potential* to spread a disease. Those who are already showing signs and symptoms are placed into *isolation* to keep them from spreading it–they’re a known quantity. The prison group has used primarily isolation to keep the infection from spreading: they’re putting the ill in the Death Row cell blocks as an isolation area, and those who are well can roam around as they choose. (Maggie, for instance, hasn’t been sent to quarantine even though she clearly was exposed to the illness by being in such close contact with Glenn).

However, one thing that the group hasn’t yet determined (probably because no one has recovered as of yet) is how long they’re going to keep anyone who gets better in the isolation area. Though adults usually stop releasing influenza virus even before their symptoms are completely gone, kids can shed the virus for a long time: up to two weeks after their symptoms started according to one study (and others have found similar results). So while right now they have the healthy young children segregated from everyone else for their own protection, in theory, if Lizzie (the flu-infected child currently in held in isolation) gets well and is released back to the healthy kid’s room, she could simply re-start the outbreak there, among the most susceptible. 

This is why disease eradication is so difficult, and why it’s been accomplished for so few pathogens to date: many pathogens can spread on the sly, even when people don’t know they’re sick. For influenza, even if it’s knocked down in this group (and of course, it soon will be one way or another–at some point, the susceptible hosts in the prison will be exhausted, either by infection & recovery or by death), there is always another reservoir of disease out there. It may be other humans. Darryl/Michonne’s group finally made it to the veterinary school mentioned two episodes ago, and the zombies they ended up fighting there had clinical signs that looked an awful lot like the survivors had seen at the prison: blood that had come from the eyes and nose. Had flu been circulating there as well? It’s a vet school, pigs could certainly be housed (there were a number of animal cages, and could easily be an outdoor space for livestock somewhere). So pigs could be serving as a reservoir. Flu can also come from a number of other animals–most notably, birds, who don’t even have to appear sick to transmit the infection to people.

Infections can be sneaky and unseen, as this group should well know.

See also:

Part I: the microbiology of zombies

Part II: ineffective treatments and how not to survive the apocalypse

Part III: “We’re all infected”

The microbiology of zombies, part III: “We’re all infected”

Warning: here be spoilers

In many latter-day zombie movies, books, and TV shows, zombie-ism has a biological cause. In 28 Days Later, the infection is caused by the “Rage” virus, which escaped from a lab when animal rights activists break in and release a group of infected chimpanzees. Of course, one of the animals promptly bites one of its “liberators,” and the infection spreads rapidly throughout Great Britain. In Zombieland, it’s a mutated form of “mad cow” disease. The Crazies, it’s the Trixie virus; World War Z, the Solanum virus; Resident Evil, the T virus. I could go on and on. Zombie causation has clearly evolved from the early days of radiation or curses, and has become a biological phenomenon in most modern zombie tales.

The Walking Dead is no exception. Though the claim is made in season 1, episode 6 (“TS-19”) that the outbreak could be caused by just about anything–bacteria, virus, parasite, act of God–I call shenanigans. In the previous episode (“Wildfire”), Jenner, the CDC scientist, is processing tissue taken from Test Subject 19, and the visualization under his microscope looks very viral. Of course, take this with a few pounds of salt, since he’s using a light microscope and can also see the nice alpha-helical DNA strains within the pathogen (in real life, things just don’t look like this) and unless you’re one of the giant viruses, you can’t see viruses, much less DNA, under the microscope Jenner uses anyway. But still, it looks pretty viral-y to me, which is why I typically refer to it that way:

screenshot wildfire virus

Microbial zombification makes sense in today’s culture. My colleague Brooks Landon notes: “…zombies represent a better monster for the modern, post-9/11 world. They provide a release for feelings of being overwhelmed by abstract and intractable events like global economic crises, terrorism, and pandemics.” In the past decade or so, we’ve seen the emergence of SARS, multiple outbreaks of influenza including a new pandemic strain, the continuing HIV crisis, Nipah, Hendra, more Ebola, just to name a handful. Infectious diseases are commonly in the news, and many times are unfortunately over-hyped, leading to a collective nervousness of all things microbial.

The infected zombie is further boosted by a number of recent studies, largely in insects, that demonstrate a type of pathogen-directed “mind control:” zombie ants, zombie grasshoppers, and zombie cockroaches, just to name a few. A recent video game has exploited the ant fungus idea, mutating it into a form that infects humans. Even rodents (and possibly humans) can have their behavior apparently influenced by a parasite called Toxoplasma gondii, which makes rodents lose their fear of cat scents and may influence the development of schizophrenia in humans, or more controversially, even affect sexual inhibitions. If germs are already controlling our minds–why couldn’t they turn us into zombies?

And certainly, there are some candidate microbes which could, in theory, cause at least the “living” form of zombie-ism, even if they couldn’t necessarily raise you from the dead. The Trixie virus, for example, is supposed to be a weaponized rhabdovirus–the family of viruses that includes rabies. Rabies virus infection certainly causes aggression and biting. The virus is spread via saliva, so biting is the main way it is transmitted between animals. In a recent book, Rabid, the authors trace rabies through history, and note that it may be at the root of many zombie (and vampire) tales. Rabies can also hide out in the body for awhile before showing symptoms, as the virus travels up the nerves toward the brain. This is why a bite near the head progresses to symptoms much faster than, say, one to the foot. Typical time from bite to symptoms is in the neighborhood of 6 weeks, depending on the location of the bite and dose of virus one receives, but extreme cases have been documented, with symptoms not showing up for as long as 8 years. And, like has been done on The Walking Dead, one of the ways that bitten victims would try to avoid symptoms would be to cut off the affected limb before the infection spread. (Ouch).

Could something like the “we’re all infected” scenario used in the Walking Dead occur in real life? Maybe. With rabies, victims could appear physically fine for months to years. Even more extreme, there are a number of germs which can remain with people throughout their entire life. The virus that causes chicken pox, for example, doesn’t ever really go away. Your body fights it off enough to keep it in check after the initial rash, but it hides out  in your nerves and can come back in later years as shingles. Other herpes family viruses have a similar lifestyle: symptoms can come and go, but the virus never really leaves. The human papilloma virus (HPV) can also persist for years in some people (most infected people appear to clear this one, though). A bacterium called Helicobacter pylori can live very happily in a person’s stomach–sometimes causing ulcers, but going completely undetected and causing no symptoms in most people. And of course, HIV, which does not go away except in a few notable and high-profile cases. So the concept is, as they say, biologically plausible.

The problem isn’t necessarily with the microbiology, then, but with the epidemiology. How did everyone get infected so quickly? We know that the plague took an incredibly short time to spread (Jenner says less than 200 days in the first season, and “less than 63 days” since it went pandemic)–but how? That’s a missing link in this scenario. We know the pathogen can certainly be spread by bites and then cause zombification that way, but other forms of inoculation (such as getting sprayed in the eyes or nose with zombie blood) don’t seem to have that effect. Is it in the water? If so, that would be some damn rapid spread, since early on Jenner noted that this appeared to be a true pandemic–present around the world. How would that happen?

In the air? Possibly, but even most airborne microbes don’t hang out indefinitely; they’re dispersed by wind to levels below those able to cause infection, or killed by sunlight or other environmental conditions. So even if you had a herpes- or HIV-like virus that could hide out in the body for an extended period of time without causing symptoms, how did *everyone* get it in such a short timeframe? Some scenarios in other books and movies put the blame on bioterrorism. The above-mentioned Trixie virus, for example, was a bioweapon which was only accidentally released when the plane carrying it crashed. Spread of Trixie in the movie ended up being only local, but transmission beyond that is hinted at the end. A true bioterrorist attack could, theoretically, account for simultaneous outbreaks all over the world.

Finally, though the “infected zombie” is now the most common type, it should be noted that this isn’t really new. George Romero, widely recognized as the grandfather of the modern zombie, acknowledges that he “ripped off” his idea for Night of the Living Dead from Richard Matheson’s I am Legend–a vampire story from 1954. The cause of that vampirism?

Bacillus vampiris–a bacterium.

 

See also:

Part I: the microbiology of zombies

Part II: ineffective treatments and how not to survive the apocalypse

Part IV: hidden infections

The microbiology of zombies, part II: ineffective treatments and how not to survive the apocalypse

(Spoilers. And things.)

After the start of season 4 of the Walking Dead and the introduction of a new nemesis: a fast-spreading, deadly infectious disease that seems to be a strain of influenza, I was looking forward to the plot arc of this season.

And then episode 3, “Isolation”, happened. From an infectious disease standpoint, I say, bah.

At the end of the previous episode, “Infected”, the group had decided to lock up anyone who was showing signs of the infectious disease within the death row cellblock, so that they would not further spread the disease, and to put the children and elderly (as the most vulnerable population) in another area to keep them safe from the infection. Quickly it was seen that this wasn’t working well, as people were becoming sick all over and more and more were moving into the isolation cellblock.

So, a council meeting was called of the leaders of the group. One of the decisions which was made, on the advice of Hershel the veterinarian, was to try to scavenge supplies from a college of veterinary medicine approximately 50 miles away from their location at the prison. What supplies?

ANTIBIOTICS.

For the micro people reading, you’ll see why my rage started boiling a bit at this point. Hershel was the one who’d suggested this was an influenza outbreak (and therefore, caused by a virus) in the prior episode. He is familiar with the disease (and there is another physician, Dr. Subramanian, who has been treating the ill and has seen the rapid course of the disease–of course, he is now sick himself). It is true that influenza can be complicated by a secondary bacterial infection: that those sick with the flu could develop pneumonia due to Staphylococcus aureus or other bacteria, and that these bacterial infections would respond to antibiotic treatment. But, when the course of disease is as rapid as it appears to be during this outbreak, it’s more likely that people are dying from primary influenza infections, which are most certainly NOT treatable with antibiotics. There are antiviral drugs that can treat influenza infections if given early in the disease course (such as oseltamivir or zanamivir ), but I think the odds of those being stocked at a veterinary school would be pretty slim.

So, rather than at least try for some kind of medically plausible scenario (is that really too much to ask?), Daryl, Michonne, Tyreese and Bob the medic take off in search of completely ineffective antibiotics,and run into an enormous zombie horde on the way. Hershel, in the interim, leaves the relative safety of the prison (he was ensconced with the children as a “high risk” individual) and wanders out into the woods to pick berries and leaves to brew elderberry tea. A folk remedy, there are a few peer-reviewed publications which suggest that elderberries or elder flower might have some properties that do work to treat influenza, so at least here Hershel is, well, sucking somewhat less here when it comes to proposing medical interventions to help those suffering than he did with his terrible antibiotics idea.

Hershel does end up with his tea, taking it into the isolation cell block and distributing it to the infected. This includes Dr. Subramanian, who repays the favor by coughing bloody sputum all over Hershel’s face. (Seriously, he doesn’t even know how to cough into his elbow? Even the little girl talking to Carol did that correctly).

From the previews of next week’s episode, “Indifference”, it appears there will be more searches for drugs, while presumably the horde advances toward the prison. I anticipate a miracle cure of some kind for Glenn at the least, but remain annoyed that the writers are touting antibiotics for a viral infection when flu season is upon us.

See also:

Part I: the microbiology of zombies

Part III: “We’re all infected”

Part IV: hidden infections

Student guest post: Cancer isn’t contagious…or is it??

Student guest post by McKenzie Steger

Off the southeastern coast of Australia lies a small island that in the 1700 and 1800’s was inhabited by the very worst of Europe’s criminals and is now the only natural home in the world to a species named after the devil himself. Decades later beginning in 1996 Tasmanian devils were going about their nocturnal lifestyle in normal devilish fashion feasting on small mammals and birds, finding mates and reproducing, occasionally fighting with one another and so on. (1) Just as criminals divvied up their booty hundreds of years before, the devils were sharing something of their own—only something of much less value. It turns out they were transmitting to one another a rare and contagious form of cancer known as Devil Facial Tumor Disease or DFTD. Once infected, facial tumors developed and the devil faced 100% mortality most often due to inability to eat or airway obstruction. Over the last 17 years the result of this highly contagious and fatal cancer has been the elimination of over half of the devil population throughout Tasmania. (2)

mckenzie picture

Source: http://www.discoverworld.ru/park-tasmanijskogo-dyavola-17528/

DFTD is not alone when it comes to transmissible forms of cancer. For over six thousand years dogs, jackals, wolves, and coyotes across the globe have experienced their own “contagious” cancer in the form of canine transmissible venereal tumor—C TVT and also called Sticker’s sarcoma. (2) CTVT is generally considered the first known cell line to be malignant having been described in the mid 1800’s. These unique growths like DFTD can spread from one individual to the next, but in the case of CTVT this most commonly occurs during coitus, licking, and biting infected areas. CTVT lesions usually establish in the genitals or in close proximity as a result. CTVT is unique in that only an estimated 7% of cases metastasize unlike in DFTD cases where 65% of them result in metastasis. CTVT rarely results in severe clinical illness but instead nearly always regresses on its own. (3)

So what is it that makes DFTD and CTVT so “contagious”? Essentially it boils down to host immunity. In the case of DFTD, devils pass on tumor cells when they are in close physical contact with others during mating or fighting. The Tasmanian devil population simply lacks the genetic diversity to be able to immunologically recognize and ward off the tumor and thus, these highly virulent and metastatic cells set up camp in the new host tissue and invade in no time. Interestingly, studies have shown that the DFTD cells are unique, containing only 13 pairs of chromosomes instead of 14 like most cells. Technology has also shown the very same cell line that began the DFTD devastation—thought to be of Schwann cell origin—is the very same one being transmitted throughout devil populations today. (2)

In contrast, CTVT, a histiocytic tumor (4), affects mammals rather than marsupials which have much greater diversity within the population and a more advanced capability to detect foreign and potentially invasive cells. This is due to the MHC-1 molecules or multiple histocompatibility complexes that help the body’s immune system to recognize foreign substances. CTVT is so effective in transmission because it down regulates these MHC-1 molecules effectively “hiding” the invasive cells from the body’s immune system. At some point however, this mechanism is overcome and the CTVT is recognized and killed by the body in animals that are immunologically sound. (2)

What about transmissible cancer in humans? The good news is that no comparable strain of such a killer contagious cancer has been recognized in humans compared to what devils in the “land down under” are experiencing. The bad news is that there are technically forms of cancer affecting man that result from contagious agents. Estimations attribute 15% of tumors world-wide to contagious pathogens including mainly viruses but also bacteria and parasites as well. Most documentation of cancer transmission cases in humans are reported in individual case reports, however, highlighting the rarity and unlikelihood of this occurrence. (2) Nonetheless, it still occurs. Hepatitis B and C viruses, herpes viruses, human immunodeficiency virus (HIV), and papilloma viruses are just a few examples of viruses that can develop into cancer in patients or predispose them to tumor formation. Bacterial etiologies include members of the Chlamydia, Helicobacter, Borellia, and Campylobacter families. There are also a few select parasites classified as Group I and Group II carcinogens including members of the Schistosoma, Opisthorchis, and Clonorchis families. So really, “contagious cancer” in humans is due to contagious or infectious etiologies and not necessarily direct contact transmission. Although there are documented and potential exceptions including cancer spread through tissue grafts, organ transplants, papillomavirus transmission during sexual intercourse and other isolated events. (1)

At the end of the day, the presence, history, transmission, and pathogenesis of transmissible cancers in Tasmanian devils, dogs, and the few cases documented in humans provides insight regarding the immune mechanisms that do and those that do not allow cancer to develop. The key difference here is mammals verses marsupials and the reality that mammals have a more advanced immune system allowing them to better overcome cancer and other foreign invasions. A better understanding of both CTVT and DFTD has and will likely continue to allow researchers better insight into mechanisms of immune system invasion of various types of cancer. (1)

Sources:

(1)   http://www.dpiw.tas.gov.au/inter.nsf/WebPages/BHAN-5358KH

(2)   Welsh JS. Contagious Cancer. Oncologist. 2011 January; 16(1): 1–4. Published online 2011 January 6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228048/

(3)   Belov K. Contagious cancer: Lessons from the devil and the dog. BioEssays: Volume 34 (4), pages 285–292, April 2012. http://onlinelibrary.wiley.com/doi/10.1002/bies.201100161/full

Picture: http://www.discoverworld.ru/park-tasmanijskogo-dyavola-17528/

 

Student guest post: New Study Finds that the Flu has Multiple Ways of Spreading

Student guest post by Sean McCaul

Sean pic 1

Image Source:  http://www.cejournal.net/?p=1934

The next time somebody in your office or household has the flu, you might want to consider keeping your distance.  A new study published this month in Nature Communications suggests that about half of the transmission of influenza A results from inhalation of microscopic infectious droplets created by the coughing and sneezing of people infected with the flu.  The flu virus hitches a ride in these droplets, and may infect nearby susceptible people who breathe them in.1

The influenza A virus generally causes fever, coughing, body aches, runny nose, sore throat, headache, and fatigue.  Vomiting and diarrhea may occur, but are more common in children.3 Fever and most other clinical signs usually resolve within 5 to 7 days, but coughing may last two weeks or more.2 Children under 2 years old and the elderly are at greatest risk for complications such as pneumonia, and over 90% of influenza deaths are in people over age 65.2

Seasonal outbreaks of influenza are common in the United States, and typically occur during winter months.  During and average outbreak, 5% to 20% of the people in a community may become ill with the flu, and up to half of the people in environments like schools and nursing homes may get sick.2

In adults with healthy immune systems, the flu virus is shed in highest numbers during the first 3 to 5 days of illness, making spread of the flu most likely during this time.  Children may shed the virus for up to 10 days, and people with weakened immune systems may shed the virus even longer.2 In a typical outbreak, a person sick with the flu passes the illness on to an average of 1 to 2 other people.1,2

Previously, influenza A viruses were thought to be transmitted primarily by direct contact and by larger (but still very tiny) droplets generated by coughing, sneezing, and talking.1,2,3  These droplets are capable of travelling 1 to 2 meters, where they may come to rest in the eyes, nose, or mouth of a susceptible person and cause them to become sick with the flu.  These droplets may also fall upon nearby surfaces and objects, where the flu virus can survive for hours.  A person touching these surfaces or objects may get the flu virus on their hands, and then transfer the virus to their eyes, nose or mouth and become ill.1,2

The recent study, published on June 4, 2013, used a mathematical model of influenza virus transmission to evaluate the data from two previously published studies of the effectiveness of hand hygiene and facemasks for the reduction of transmission of influenza A viruses.   It suggests that the flu virus may survive in very tiny droplets created by coughing and sneezing that can remain suspended in the air as an aerosol long enough to be inhaled by nearby susceptible people.   The study shows that aerosols are an important route of transmission of the virus, and may account for as much as 50% of the spread of the flu.1

Sean pic 2

Image Source:  http://www.livescience.com/32307-why-do-bright-lights-make-me-sneeze.html

How you get the flu may determine, in part, how ill you get.  Influenza researchers have long suspected that inhalation of aerosols containing the flu virus can lead to more severe illness than exposure to the flu virus by direct contact or by the settling of larger droplets in the eyes, mouth or nose of susceptible people.  This is thought to be because larger droplets are trapped by the defense mechanisms of the upper respiratory tract, such as the large surface area of the nasal turbinates and the mucus lining the nose, pharynx, and trachea.  Smaller droplets, meanwhile, are capable of being inhaled deep into the lungs, resulting in infection in the lower respiratory tract which can cause more severe disease.  The current study found that there was an increased risk for fever plus cough in people suspected to have contracted the flu by inhalation of infective aerosols, which is consistent with current ideas regarding the importance of the route of infection.1

Understanding the routes of transmission of influenza is also important for designing control measures to reduce the spread of this disease.    Interventions such as increased hand hygiene and facemasks help to limit transmission of influenza by larger droplets produced by coughing and sneezing, but may offer little protection from inhaled aerosols.1 Additional methods for controlling the spread of influenza through aerosols, such as improved ventilation of enclosed spaces, ultraviolet lights (which are capable of killing the flu virus), and minimizing exposure to those infected with the flu could reduce the risk of becoming sick.1

So, what can you do avoid getting the flu?  The most effective way is to get vaccinated before flu season.  In the United States, flu season can start as early as October, though the peak months for flu are January and February, and sometimes even later.3 Because the flu strains circulating through the population change from year to year, you should be vaccinated each year.  The vaccine is developed to prevent illness caused by the flu strains likely to cause outbreaks during the flu season, but may not prevent illness from novel or unanticipated strains causing outbreaks.  Some people, such as babies less than 6 months old and those with allergies to eggs should not receive the flu vaccine.3  So the CDC recommends that you take additional preventive measures, such as good hand hygiene, avoid close contact with people who are sick with the flu, avoid touching your eyes, nose, and mouth, and practice good health habits such as remaining well hydrated, eating a healthy diet, exercising, and getting plenty of rest.5

If you do get the flu, what can you do to avoid infecting your family, friends, and colleagues?  First, avoid close contact with others.  Stay home from school or work if at all possible, and don’t run errands while you are sick.  In this way, you can avoid exposing others to your illness.  Second, cover your nose and mouth when you cough or sneeze.  Experts recommend that you cough and sneeze into a cloth or into your elbow, so that you don’t contaminate your hands, which are commonly implicated in the spread of the flu.  This simple practice can reduce the amount of infectious material you spread into your environment.  Practice good hand hygiene, particularly before touching doorknobs and other items that may leave the virus where others are likely to become exposed.5

References

  1. Cowling, B.J., Dennis, K.M., Fang, V.J., Suntarattiwong, P., Olsen, S.J., Levy, J., Uyeki, T.M., Leung, G.M., Malik Peiris, J.S., Chotpitayasunondh, T., Nishiura, H., & Simmerman, J.M. (2013).  Aerosol Transmission is an Important Mode of Influenza A Virus Spread.  Nature Communications, DOI: 10.1038/ncomms2922  LINK
  2. Bridges, C.B., Fry, A., Fukuda, Shindo, N., & Stohr, K. (2010).  Influenza (Seasonal).  In Heymann, D.L. (Ed.).  Control of Communicable Diseases Manual.  American Public Health Association, Unbound™ Mobile Platform
  3. Centers for Disease Control (February 13, 2013), Key Facts About Influenza (Flu) and Flu Vaccine, accessed at http://www.cdc.gov/flu/keyfacts.htm , June 8, 2013
  4. Centers for Disease Control (May 6, 2013), What You Should Know for the 2013-2014 Flu Season, accessed at http://www.cdc.gov/flu/about/season/flu-season-2013-2014.htm, June 8, 2013
  5. Centers for Disease Control (January 11, 2013) Preventing the Flu: Good Health Habits Can Help Stop Germs, accessed at http://www.cdc.gov/flu/protect/habits.htm, June 8, 2013
  6. Flu Virus Image:  Tom Yulsman (May 26, 2009), U.S. and Other Countries Fail to Adequately Monitor Pigs for Flu, accessed at http://www.cejournal.net/?p=1934, June 8, 2013
  7. Sneeze Image:  Ben Mauk, photo credit Andrew Davidhazy/RIT (November 28, 2012), Why Do Bright Lights Make Me Sneeze?, accessed at http://www.livescience.com/32307-why-do-bright-lights-make-me-sneeze.html, June 8, 2013