Can We Summarize One Health?

https://veterinaryrecord.bmj.com/content/vetrec/174/4/85/F2.large.jpg

Not likely, but I’ll do my best.

In case you weren’t aware, this blog was the result of a class assignment, encouraging me to research and study different One Health topics and present them in a blog. Needless to say, I learned quite a bit that I was previously unaware of, or had never thought of; not only in the topics that I presented in my blogs, but also in the class discussions.

One Health is a very broad and encompassing subject. All over the world, organizations like the Center for Disease Control and World Health Organization monitor serious diseases and mobilize efforts to control them. They are constantly preparing for serious outbreaks like Ebola and Zika, but those aren’t the only problems plaguing the world. Neglected Tropical Diseases, which are rarely seen in the United States and are easily treated here, ravage less well-developed areas where there is limited access to basic treatment and preventive care. These maladies are no less important in our efforts to make the world healthier.

However, we also covered other topics, such as the emergence of increasingly resistant microbes to antibiotics. Much blame is placed on where we believe the problem originally arose, but in actuality there has been and continues to be irresponsible use everywhere. Prescribing antibiotics for a problem that doesn’t need them, or when they wouldn’t be necessary; failing to finish out the entire antibiotic prescription, and even saving them to use again later; using subtherapeutic levels for growth promotion; both human and animal medicine have failed to use these powerful drugs judiciously. And now, as developing countries increase their use of antibiotics and do not take into account this very serious result of misuse, the danger only increases. And it’s not just microbes that are developing resistance. Insects that carry serious diseases are becoming resistant to insecticides, the most notable example being malaria-carrying mosquitoes. We discussed that control is the best strategy for these problems, as there are currently no new drugs or compounds being developed.

We also learned about what happens when control measures have failed and an outbreak occurs. There is an organized stepwise process that takes place, starting with determining the list of problems and hazards, then moving on to assessing and communicating the risks. Treating the disease is actually one of the last steps. First, it is necessary to quarantine and control movement of the disease to prevent further spread, and then determine what it is that needs to be treated. It is a multifactorial problem that requires cooperation from multiple disciplines in order to effectively eliminate it.

Of course, human, animal and environmental health aren’t just impacted by diseases. Pollution is a serious problem affecting people all over the world, especially in heavily populated areas and in developing countries. Illnesses caused by breathing polluted air and drinking polluted water are serious problems where industrial waste is not well controlled—as seen in China—and poor areas where there are no water sanitization facilities. On a more detailed note, I learned about how many facilities and environments can be carefully designed to control and prevent disease, or improve the experience within. For example, I never knew how much detail went into water fountains to make sure that the opening where the water came out wasn’t contaminated.

One Health is more prevalent than most people know. Hardly any problems affect only humans, or only animals, or only the environment. And it doesn’t just encompass diseases, either. The concept of One Health is that all three groups are interconnected when it comes to health and wellbeing. Obviously, this is very true for most every situation. One Health should be more widely spread and discussed. Through education efforts, we can make people aware of the impact we have on animals and the environment, as well as the impact that animals and the environment have on us.

Origin of the Viruses

This week I was asked to write a blog about viruses and virus-like particles. My professor decided to go easy on me and only wants me to discuss the evolutionary origin theories of viruses and which I think is most likely.

Welp.

Let’s start with a description of what viruses are, and how they are different from other organisms. If you read my last blog,[1] I mentioned that viruses aren’t considered ‘living’ by certain standards because they can’t replicate or produce energy without a cell’s assistance. They are basically a string of RNA or DNA with a protein coat that go around parasitizing cells (animal, plant, bacteria, protozoa, etc.) and reproducing. While some have more “accessories” like proteins that can help them replicate their genome, most lack the complex machinery that even simple cells have for energy production, metabolism, and other life processes. Nothing else on earth seems to look like viruses, so of course in our classification system that likes to group and link things together based on their similarities, viruses are just out there on their own.

https://upload.wikimedia.org/wikipedia/commons/f/f2/Icosahedral_Adenoviruses.jpg

There are three prevalent ideas that have been the main theories for where viruses come from. They are the reduction hypothesis, the escape hypothesis, and the virus-first hypothesis.

The Reduction Hypothesis starts with the presumption that everything started out as primitive cells. During the course of evolution, these cells somehow lost most of their machinery that made them cells, until all that was left was the genome (be it RNA or DNA), a protein coat to protect it, and some elements to help them reproduce that genome once they entered another cell. The fact that there aren’t any organisms that seem to be ‘intermediates’ between cells and viruses seemed to defeat this theory, as it is expected that there would have to be some sort of middle step that the cells went through on their degeneration to viruses. There’s also the question of how cells went from a lipid membrane (the outside-most layer of the cell made up of fatty molecules called lipids) to a protein coat in viruses (the protein capsid that protects the genome). But there is support for this theory in the recently discovered mimivirus and megavirus, both of which are larger than some small bacteria (a very unusual trait, as every other virus discovered up till now was too small to be seen even on a microscope). These viruses also have a very complex genome, and mimivirus in particular has enzymes and proteins that were only expected to be found in true, living cells.[2] Thus, these two viruses can be seen as the necessary intermediate for the reduction hypothesis.

The Escape Hypothesis also starts with cells. The idea is that pieces of cell genome—again, either RNA or DNA—‘escaped’ the primordial cell and decided they wanted to live on their own (figuratively speaking, of course). This theory came from similar genome pieces that we actually see in biology. Plasmids, for example, are small pieces of bacterial DNA that are separate from the cell’s genome. They code for special goodies (like antibiotic resistance) that are not necessary for life, and use their own machinery to replicate those genes. Plasmids are incredibly mobile, and easily passed between bacteria, even bacteria that aren’t related. Thus the idea that something like these could have escaped a bacteria and decided to parasitize the host’s machinery for replication isn’t so far-fetched.[3]

The Virus-first Hypothesis assumes that viruses were the original form, and as cells started to arise, they began to parasitize them and evolve along with them. There are some questions for this theory. If current viruses require cells in order to replicate and survive, what did these ancestral viruses use? If they started out as more primitive than the current viruses, where did they get all the complex components that they have today? If the natural evolutionary process leads to something large and complex like mimiviruses, why are there still small and simple viruses around that didn’t get the memo? There are also supports, however. Early viruses may have found some sort of ‘soup’ of nutrients to grow in, then transitioned to cells once they arose, losing their methods of autonomous replication in the process.[4] There are also, for lack of a better term, biologic components—virus-like particles—that seem to be examples of what these pre-viruses were like. Viroids are the smallest infectious agent known. They are nothing more than a short, circular strand of RNA; no protein coat, no particular complexity, just a little piece of genome floating around infecting cells, like a rogue plasmid. The idea is that these viroids are very similar to what the primordial viruses were like.[5] That still begs the question why so many viroids were completely left behind in the evolutionary journey, but it is unlikely to receive an answer any time soon.

Now on to the second part of the assignment: which theory do I find most likely. It may sound cliché, but I see no reason to choose one to the exclusion of the others. Perhaps there were primitive viroid-like organisms that existed before proper cells developed, then evolved with them to become the viruses we know today. But that explanation doesn’t seem to fit every known virus, such as the mimiviruses which look like intermediates between cells and viruses. Maybe they once were cells, then started to regress until they are now something akin to a virus, but larger and more complex than most any other known. Still other viruses may have arisen from “gene escape events,”[6] like the human hepatitis delta virus which contains coding genes very close to the ones found in human cells.[7]

Science is very limited when it comes to testing things for which we have no current comparison. Using the laws of the present to try and discover the laws of the past can only reveal so much. Thus, the question of the origin of viruses cannot be clearly discovered by what we know now; obviously what happened back then is no longer happening, or at least not in the same way. However, it is still interesting to see the incredible variation among these absurdly simple components, and marvel at how something not even considered to be alive has such a great impact on the world and its inhabitants.

[1] https://vetmedone.health.blog/2019/04/07/how-to-stop-a-virus/

[2] https://www.sciencedirect.com/science/article/pii/S0168170205002376?via%3Dihub

[3] https://mmbr.asm.org/content/74/3/434.long

[4] https://www.sciencedirect.com/science/article/pii/S1879625713001028?via%3Dihub

[5] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609113/

[6] Ibid.

[7] Ibid.

How to Stop a Virus?

Viruses are similar to bacteria in that they are microscopic, disease causing organisms. Unlike bacteria, however, there is a constant debate about whether or not viruses are actually alive. By certain standards, viruses are not living organisms because they depend on a cell to replicate and survive, be it an animal, plant, or bacteria. Nonetheless, viruses are every bit as widespread as bacteria, and some can cause deadly diseases.

For example, Epizootic Hemorrhagic Disease Virus—or EHDV—is a virus that causes severe illness and death in wild ruminant populations, especially white-tailed deer. Within a week of infection, deer will exhibit weakness, drooling and bloody diarrhea. They have a high fever which they try to cool by laying in water, before they suddenly fall unconscious and die.[1] Up to 40% of the deer population can die of this disease.[2]

https://www.realtree.com/sites/default/files/styles/site_large/public/content/inserts/realtree-ehd-deer-misourrideptofconservation.jpg?itok=OASwuiFQ

A type of gnat called Culicoides variipennis carries the virus from one host to another.[3] Luckily, this disease isn’t contagious, meaning that a sick deer isn’t going to give it directly to other deer just from being around them. The virus requires a gnat to take it up from the blood for it to be transmitted to a new host.[4] Thus, most control measures to prevent the disease focus on the intermediate, the culicoides gnat. Removing standing water and spraying insecticides where the gnats tend to mate and live are currently the most effective methods of reducing the fly population and preventing infection with the EHD virus.

Theoretically, a vaccine that could be either injected or given in the feed would be very useful for protecting susceptible animals from the virus. But there are a few problems with developing one.

Firstly, the EHD virus is an RNA virus. This means that rather than its genome being made up of DNA like in animals, it is made up of RNA. There are a few structural and component differences between DNA and RNA, but the important part is the different effect that each one has. RNA is more susceptible to mutations during replication. This, combined with the incredible numbers of virus that are produced, means that the virus changes and adapts incredibly quickly. Any vaccine produced that targets specific pieces of the virus genome would rapidly be worked around.

Secondly, our vaccines to control and prevent viral infections are already limited. Due to the fact that viruses use the host’s cells to replicate, it is difficult to develop safe and effective drugs. Studying the genetic sequence of viruses helps determine what compounds would prevent their replication, but as I said, viruses (especially RNA viruses) mutate rapidly. This is the main problem with flu vaccines; new ones must be manufactured each year, as the previous year’s vaccines are ineffective due to viral mutation.[5]

There may be some steps in the EHD virus cycle that can be targeted. Host cells are very good at recognizing and eliminating viral genome, so the virus wraps its RNA in a protective coat called a capsid, so that the immune system can’t see it. Perhaps a vaccine to the capsid could be developed. This way, the body could catch the virus before it even had a chance to enter the cells, increasing safety and efficacy. Unlike other vaccines that target cell receptors, which are very specific and highly mutable, perhaps the capsid would be less changeable.

Controlling and treating viruses has been a difficult subject for decades. At the moment, the easiest way to prevent Epizootic Hemorrhagic Disease is to prevent the gnat that spreads it.

[1] https://www.michigan.gov/emergingdiseases/0,4579,7-186–26647–,00.html

[2] Given, M. D. (2018) VMED 9250 Section 9-10 Orbi Birna & Paramyxoviridae 181106 [PowerPoint slides].

[3] https://animaldiversity.org/accounts/Culicoides_variipennis/

[4] https://www.michigan.gov/emergingdiseases/0,4579,7-186–26647–,00.html

[5] https://www.medicinenet.com/flu_vaccination/article.htm#what_is_influenza_flu

Sampling Bias

We’ve all experienced research studies in one way or another. Everything from commercials claiming positive customer feedback, to medications prescribed for different conditions underwent some sort of research. Perhaps you’ve even taken part in a research study. But not all studies are equal in terms of accuracy and completeness of information. Nor are all the methods of gathering information for the study equally accurate.

When a scientist wants to study something, first he sets up a test. Then, he needs to look at the group of animals or people that he wants to study. This group—called a population—is made up of individuals who are affected by that something, or likely to be involved in it somehow. Since most populations are far too large to test each individual, most studies try to pick a random number from among the population. The idea is that the smaller sample will more or less represent the larger whole. However, problems arise when the investigators get into sampling bias.

Sampling bias is described as “a sample of a group that does not equally represent the members of that group.”[1] That basically means that some individuals were sampled more than other individuals, resulting in misleading information that doesn’t accurately represent the whole population. For example, if researchers wanted to study the effect of a certain food item on the development of heart disease, but mostly sampled people with unhealthy lifestyles, then the results would be skewed. This could be a random effect that cannot be predicted or prevented, or it could be the result of faulty study planning. Either way, it gives us the wrong answer, and a great deal of planning for population studies involves minimizing this bias.

Now let’s look at this in a real-life setting. Most of us have heard about rabies, and know that raccoons, bats, skunks, and foxes might give it to us if they bite us. Beyond that, only a few who aren’t wildlife or medical specialists learn about the details of this disease. For one thing, more than 90% of the rabies cases reported in the United States since 1980 have been in wildlife, not humans or pets.[2] It actually accounts for very few human deaths, and is the 2^nd rarest disease after polio.[3]

https://www.cdc.gov/rabies/exposure/animals/wildlife_reservoirs.html

This isn’t to say that rabies shouldn’t be taken seriously. It is a deadly disease, and we need to be cautious if we come into contact with wild animals in order to avoid ourselves or our pets becoming infected. There are ongoing projects attempting to eradicate rabies from wildlife so that it’s no longer a threat. To aid in such an endeavor researchers have studied the percent of the wild animal population that is infected with the disease. However, the only test that tells us absolutely whether an animal has rabies or not can only be performed after death.[4] As you may imagine, this can result in a fair amount of sample bias.

If we get our data primarily from the cases that were presented for having rabies, it will seem as though a huge percent of the population is infected. The Center for Disease Control monitors the number of rabies cases reported, and stated: “For the present report, percentages of rabid animals were calculated on the basis of total numbers of animals tested. These percentages are likely not reliable indicators of the true incidence of rabies within animal populations because most animals submitted for testing were selected on the basis of abnormal behavior or visible illness or were involved in a potential exposure incident, biasing the sample submitted for testing.”[5] This means that, since most of the animals caught were abnormal in some way, we only know how many of the abnormal animals have rabies, not how many in the entire population have rabies.

The best way to reduce biased sampling would be to proactively catch and test animals in their natural habitat. This would increase the chances of getting a sample as close to the actual population as possible. This would still pose risks of bias, however. If traps were set out, it could be more likely for weak, sick, very young, or very old animals to be caught, which would affect the results. There would have to be a method of catching representatives from every group of the population: young, old, healthy, sick, weak, strong; and to catch them in the proportion that they exist in the population.

There are certain biases that can never be completely removed. Take this test for an example. What percentage of the wild raccoon population is sick? How many are weak, how many are strong? We can’t know this for sure without sampling the entire population, which is impossible. No matter what we do, there will always be some unknowns, and thus our results will always be a little off from the true number. However, the larger the sample size and the more meticulous the study parameters, the closer our results will be to the actual number.

[1] Sample bias. (n.d.) Medical Dictionary. (2009). Retrieved March 17 2019 from https://medical-dictionary.thefreedictionary.com/Sample+bias

[2] https://avmajournals.avma.org/doi/pdfplus/10.2460/javma.248.7.777

[3] https://cpw.state.co.us/learn/Pages/LivingwithWildlifeBatsRabies.aspx

[4] https://www.cdc.gov/rabies/diagnosis/animals-humans.html

[5] https://avmajournals.avma.org/doi/pdfplus/10.2460/javma.248.7.777

Flea Prevention for People?

This week I was given a rather interesting thought experiment: to take something that we spend most of our day in or around, and design it in some way that addresses a specific one health problem. So I chose clothing; we think about it all the time, but also don’t think about it. Obviously, we wear it all the time, so we could use it to help in multiple ways. Since several of my previous blogs discussed diseases caused or spread by ticks, fleas or mites, I will specifically focus on that.

Many dog owners use topical flea and tick preventative. It’s very convenient: just put a few drops of a liquid on the pet’s back, comb it through, and for 30 days you don’t have to worry about a flea infestation or any nasty diseases from a tick. Has anyone ever considered applying it to people, especially people in areas where neglected tropical diseases run rampant? If clothing could be laced with products to repel or kill pests, many infestations could be prevented or reduced in severity.

https://columbiamosquitosquad.files.wordpress.com/2013/04/dog-getting-application-of-dermal-flea-and-tick-control.jpg

The main ingredient for the topical flea and tick preventative Frontline is methoprene, a chemical that mimics the juvenile insect hormone. This hormone is present before insects molt to the adult stage, and they cannot finish their development so long as it is around. With Frontline, it is used to prevent fleas from being able to complete their life cycle and establish an infestation on a dog. Humans and dogs have no receptors for the compound, so it has little to no effects on us even if we drink or inhale it.[1] It has a faint, fruity smell and no taste, and so is not repulsive to people. As such, this chemical has been added to drinking water to control mosquitos that carry malaria, and used in the production of many food products to prevent spoilage due to insects.[2]

An ingredient for another popular preventative—Advantage Multi—is moxidectin, a drug that kills parasites by disrupting nerve transmission and causing paralysis. It was found safe enough to be used en masse in Africa to prevent infection by a parasitic worm that causes blindness in people.[3] Combined on clothing with a similar chemical called imidacloprid, it could also control mite infestations.

There are, of course several obstacles to utilizing such a method of control. The first and biggest is the long-term development of resistance, a subject I have previously spoken of.[4] Allowing parasites to constantly come into contact with these chemicals will naturally select for some few who can survive, and allow them to rapidly spread their resistance among the population.

Next is the practical problem of manufacturing clothing with these compounds mixed in. Everyone who uses topical flea and tick preventative on their pet knows it must be reapplied regularly. And if the pet gets bathed too often, or takes too many trips into the swimming pool or pond, there is a risk of washing the protection off. Having to reapply the compound to clothing every month or two defeats the purpose of such a measure.

But even allowing for solutions to these difficulties, clothing is not incredibly cheap to manufacture even on its own, and adding insecticide compounds would likely increase the cost. It would be difficult to develop a cost-effective method to be able to produce and distribute clothing to areas of need, and then would require help from anthropologists to make sure the people knew why they had to wear the clothes.

Perhaps an easier medium would be an ankle bracelet similar to the Seresto flea collars used for dogs and cats. If a bracelet would slowly release the insecticide and last for 8 months like the pet product does, it could be a more viable option for distribution. However, it could pose a risk for waste build-up and environmental effects if the bracelets were simply discarded in a trash heap once they no longer provided enough protection for the wearer.

More study and development would have to go into this idea to be able to solve its other problems, most notably the risk of resistance. But if used as part of a multimodal one health approach, it could be one useful piece of the control plan.

[1] https://nepis.epa.gov/Exe/ZyNET.exe/P100MT2M.txt?ZyActionD=ZyDocument&Client=EPA&Index=1991%20Thru%201994&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&UseQField=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5CZYFILES%5CINDEX%20DATA%5C91THRU94%5CTXT%5C00000031%5CP100MT2M.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=hpfr&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=1&ZyEntry=2

[2] https://nepis.epa.gov/Exe/ZyNET.exe/P100MT2M.TXT?ZyActionD=ZyDocument&Client=EPA&Index=1991+Thru+1994&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5Czyfiles%5CIndex%20Data%5C91thru94%5CTxt%5C00000031%5CP100MT2M.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=hpfr&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=1&ZyEntry=1&SeekPage=x&ZyPURL

[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4072596/

[4] https://vetmedone.health.blog/2019/02/11/its-the-resistance/

Pollution Effect

https://www.who.int/airpollution/ambient/health-impacts/en/

Environmental pollution can have devastating health consequences for the people and animals living in the area. Remember the epidemiological triad? The environment corner plays no smaller part in the effect on hosts and agents in the manifestation of disease.

Particulate matter (PM), small solid particles floating in the air, can get into the nose and mouth and cause coughing and irritation. Really small particles can even get down into the lungs and diffuse into the blood stream.[1] These PMs are believed to be the indirect cause of 4.2 million death around the world every year, by causing cancer, heart disease, stroke and difficulty breathing.[2] As many as 29% of deaths from lung cancer, 24% of deaths from stroke, and 43% of deaths from COPD are caused by air pollution.[3]

When we think of air pollution, we usually assume it comes from cars and factories. But one of the largest sources in developing countries of air pollution comes from household pollutants. Cooking or heating fires using wood, dung or coal, without adequate ventilation to get rid of the smoke, are believed to cause 3.8 million premature deaths every year.[4] Of course, mold, hazardous building materials and volatile organic compounds can also cause serious health problems.[5]

Besides causing illness and death in and of themselves, air pollutants can also weaken a person and make them more susceptible to other diseases. Exposure to such pollutants can decrease lung function and cause respiratory infections or aggravated asthma.[6]

So what to do to solve these health problems?

Reduction in harmful emissions in both cities and households require a multipronged approach including education and switching to cleaner sources. In the home, the World Health Organization recommends low-emission stoves to reduce the amount of pollutants that escape into the room. They also suggest ethanol and liquid petroleum for combustion, rather than kerosene and unprocessed coal, which tend to produce dangerous compounds such as carbon monoxide, mercury and arsenic.[7] Simple behavior changes such as drying wood before burning it will improve efficiency and reduce harmful byproducts.[8]

As for air pollution in large cities, many different areas and avenues must be discussed. Encouraging walking, bicycling, or efficient public transport; keeping green spaces within cities; and improving waste reduction, recycling and management can all reduce harmful emissions.[9] When factories began using air scrubbers, it greatly reduced pollution. Air scrubbers are efficient enough to control around 98% of emissions.[10]

This is a difficult and far-reaching problem. City emissions naturally come with industrialization, but home emissions are present even in the poorest areas. Multiple control points must be set up and acted on, and no one method is correct for every area. Each individual environment, health risk and culture must be analyzed individually for a meaningful resolution.

[1] https://www.cdc.gov/air/particulate_matter.html

[2] https://www.who.int/airpollution/ambient/en/

[3] https://www.who.int/airpollution/ambient/health-impacts/en/

[4] https://www.who.int/airpollution/household/health-impacts/en/

[5] https://www.who.int/airpollution/household/pollutants/en/

[6] https://www.who.int/airpollution/ambient/health-impacts/en/

[7] https://www.who.int/airpollution/household/interventions/technology/en/

[8] https://www.who.int/airpollution/household/interventions/behaviour/en/

[9] https://www.who.int/airpollution/ambient/interventions/en/

[10] https://www3.epa.gov/ttn/catc/dir1/ffdg.pdf

Barely Scabing By

https://en.wikipedia.org/wiki/Sarcoptes_scabiei#/media/File:Sarcoptes_scabei_2.jpg

A couple weeks ago I blogged about scabies as a neglected tropical disease that plagues the underprivileged in tropical and sub-tropical climates.

Remember the epidemiological triad?[1] Well, today I’m going to focus on one corner of it: the agent.

I discussed already how many factors influence the incidence of scabies infections in different areas, and how a multifactorial approach would be best to control the mites. The current best strategy to rein in infestations is the mass administration of scabicidal drugs. However, if you will remember my blog from last week,[2] resistance to drugs is a natural process of evolution and develops rapidly. We’ll need another strategy if we want long-term control of this parasite. But what can we do against a disease that thrives among poverty and overcrowding, two problems that are not easily solved? Perhaps knowing more about the parasite itself will help us better control it.

A female scabies mite, once she’s ready to lay her eggs, will slowly make a long burrow underneath the skin, laying her eggs all the while. Once she’s finished, she dies within her burrow.

Her eggs take less than a week to hatch, and usually only around 10% will grow to adulthood. They hatch as larvae, which make shallow burrows to hide in while they molt into mature adults. A fully grown male will then find a female and mate. Since the female will only live a couple months after that, just long enough to lay all her eggs, mating only occurs once.[3] If a person is going to be infested with scabies, it will be by these fertilized females crawling on them from the previous host.

Upon reading about the scabies life cycle, I was interested to find that they only mate once. This reminded me of another parasite which similarly mates only once, and how researchers used that to their advantage.

Cochliomyia hominivorax, otherwise known as the screwworm (named for the spiral, screw-like pattern on the larvae), used to be a dangerous pest that greatly threatened an endangered species of Florida Key deer. Unlike most flies, which only feed on dead flesh, screwworm larvae will actually burrow into and consume healthy tissue in their unfortunate host, and eventually kill them if left untreated. They can lay their eggs in any open wound—even tiny ones made by ticks—as well as the navel of infants, and are attracted to any warm-blooded animal; that includes humans.[4]

Screwworms were first successfully eradicated from the United States in 1984[5] using a rather unique aspect of their physiology: they only breed once. When this was discovered, researchers grew hundreds of male screwworms and sterilized them, then released them into the wild. Many female screwworms laid unfertilized eggs because they mated with a sterile male, and within a few generations the flies were eradicated from U.S. soil.[6]

Perhaps a similar method could be used to control scabies mites in humans. This would be an interesting area of study, however there are certain ethical questions that would need to be addressed: with the screwworms, the males were just released into the environment where the females were; with scabies, which spend their entire life on a host, this would require purposely infesting a human being with more scabies. Sterile or not, this isn’t exactly an acceptable practice. One may argue that the benefit would outweigh the ethical cost, but that is straying into dangerous territory. It may be a viable option for the infested dogs and cats that spread the mites, however.

A less compromising option for human beings would be to find a way to sterilize the scabies population already infesting a person, without bringing harm to the host. This would not be easy, and maybe impossible; radiation was used to sterilize the screwworms, but that obviously cannot be used on a person. If one thing could be said for researchers, however, it’s that they find new, creative solutions to pretty much any problem.

[1] https://vetmedone.health.blog/2019/01/21/hows-about-the-epidemiological-triad/

[2] https://vetmedone.health.blog/2019/02/11/its-the-resistance/

[3] https://www.cdc.gov/dpdx/scabies/index.html

[4] https://www.cdfa.ca.gov/ahfss/Animal_Health/pdfs/Screwworm_Fact_Sheet.pdf

[5] https://www.ars.usda.gov/news-events/news/research-news/2002/usda-celebrates-research-that-eradicated-the-screwworm/

[6] Ibid.

It’s the Resistance

Antimicrobial resistance is a hot topic today. Studies have shown that it is spreading and starting to involve more microorganisms and antibiotics. But what is it, exactly?

Antimicrobials are any medicine designed and used to kill microscopic organisms that cause disease. The term is usually used to refer to bacteria, but it also technically includes fungi, protozoa, viruses, and parasites. However, when a microorganism survives the treatment designed to kill it, it continues to grow and pass on its resistance to its progeny. This is exacerbated by the fact that the other microorganisms that are susceptible to the drug, and die off, used to limit the growth of the resistant organisms by competition for resources. With them gone, the resistant microbe is free to spread throughout the host, unable to be controlled by modern medicines.[1]

https://www.cdc.gov/drugresistance/pdf/5-2013-508.pdf

How widespread is this problem? A Review on Antimicrobial Resistance, completed in May 2016, estimated that 700,000 people die each year from diseases that were resistant to available antibiotics. They also postulate that, by 2050, the number of deaths will increase to 10 million annually.[2]

A commonly held belief is that antibiotic use in animals is the main cause of most antimicrobial resistance. While it is true that antibiotics used to be used as growth promotants—thus exposing bacteria to low levels of antimicrobials, which they could survive and then develop resistance to—the FDA recently instituted the Veterinary Feed Directive (VFD), a program that regulates and limits the use of medically important antimicrobials.[3] What do we mean by “medically important”? Only some of the antibiotics used in food animals are the same as those used in human medicine. Because of the risk of resistance cross-over into humans, producers must consult with a veterinarian and obtain a specific prescription before they are able to use them in their herds.[4] This helps to reduce the development of resistance to antimicrobials used in humans.

Unfortunately, resistance to antimicrobials is a natural result of mutation, rapid growth and gene transfer. The same thing happens even in insecticides, and the consequences can be severe. For example, insecticides are important in the control of mosquitoes that spread malaria. However, 61 countries have reported resistance to at least one of the four classes of insecticide. Resistance is probably more widespread than this, because many countries do not perform adequate monitoring for insecticide resistance.[5]

Resistance to antimicrobials and insecticides are difficult to control, and impossible to prevent. All that can be done is to monitor for resistance, accurately gather data, learn more about the mechanisms of resistance, and develop new methods of control and prevention.[6] It’s a steadily regressing battle, as few breakthroughs have been made in antimicrobials in the past 20 years.[7]

It’s a very difficult subject to talk about considering the likelihood of such a grim outcome. But if awareness of this problem is increased, some solutions may be researched and brought to light.

[1] https://amr-review.org/sites/default/files/160525_Final%20paper_with%20cover.pdf

[2] Ibid.

[3] https://www.fda.gov/AnimalVeterinary/DevelopmentApprovalProcess/ucm449019.htm

[4]https://www.fda.gov/downloads/AnimalVeterinary/GuidanceComplianceEnforcement/GuidanceforIndustry/UCM299624.pdf

[5] https://www.who.int/malaria/areas/vector_control/insecticide_resistance/en/

[6] Ibid.

[7] https://amr-review.org/sites/default/files/160525_Final%20paper_with%20cover.pdf

The First Non-infectious NTD

The World Health Organization has a list of diseases, called neglected tropical diseases (NTDs), that they are working to control through widespread public health policies. These are diseases that are prevalent in tropical and sub-tropical climates in which “Populations living in poverty, without adequate sanitation and in close contact with infectious vectors and domestic animals and livestock are those worst affected.”[1] One of the more recent diseases, as well as the first non-infectious disease to be added to the list, is snake envenomation.

Why was “snake-bite” added to the NTD list? Most people don’t often think of it when someone mentions ‘disease’. There are four criteria that must be fulfilled to be placed on the World Health Organization’s neglected tropical disease list.[2]

Significant burden of the disease; many people are affected, and many die.
Majority of cases occur in tropical or sub-tropical geographical areas, and impacts the poor in particular.
The impact of the disease can be mitigated through treatment and prevention.
The cost of researching and implementing prevention strategies is ultimately cheaper than the disease’s impact.

Snakebites meet all four criterion. 250 species of dangerously venomous snakes are present in 160 countries around the world,[3] and snake-bite encounters occur around 5.5 million times every year. Of these, WHO estimates that 400,000 victims suffer permanent disabilities, and up to 138,000 do not survive.[4] The majority of these bites take place in sub-Saharan Africa, South Asia and South-East Asia where the majority of the world’s population is concentrated. The groups at the highest risk of potentially-fatal bites include poor rural dwellers, agricultural workers (including farmers, herders, fishermen, and hunters), children, pregnant women, and any with restricted or no access to healthcare.[5]

WHO believes that their estimates for the number of snakebites that occur is drastically lower than the actual number of cases, because around half the victims in poor areas will make use of traditional medicines rather than seeking more advanced medical attention. Though this could be due to cultural reasons in some cases, in many others it is because the victims do not have access to proper care.[6]

Antivenom is one of the most common and effective methods of dealing with snake envenomation, and it can be relatively cheap to produce. However, the quality and availability of antivenom can be very limited, especially in poor areas. Inadequate product safety and efficacy, lack of properly trained health personnel, absence of neutralization specifications, and local superstition surrounding snakebites, all contribute to inaccessibility of medical care. Many companies attempting to produce good quality antivenom are driven out by lower quality products sold at cheaper prices.[7]

https://www.who.int/snakebites/antivenoms/Cycle_of_antivenom_market_decline.pdf?ua=1

To effectively be able to provide medical care access around the world, it is not enough to produce vials of antivenom. Like with the other NTDs, a multi-pronged One Health approach will be the most effective strategy. The antivenom must be of tested and guaranteed quality, ensuring effectiveness. Public education programs must also be implemented, to encourage locals to seek proper medical attention after a snakebite, as well as direct them to trusted sources for their antivenom. Protective footwear to protect from bites, netting or other barriers to keep snakes out of homes, keeping paths and other areas clear of refuse piles to reduce hiding places, and cutting grass short to make snakes more visible, are all effective environmental strategies to prevent snakebites.[8]

[1] https://www.who.int/neglected_diseases/diseases/en/

[2] https://www.who.int/snakebites/snakebites_FAQ/en/index1.html

[3] https://www.who.int/snakebites/disease/en/

[4] https://www.who.int/neglected_diseases/news/Snakebite-envenoming-mandate-global-action/en/

[5] https://www.who.int/snakebites/epidemiology/en/

[6] Ibid.

[7] https://www.who.int/snakebites/antivenoms/en/

[8] https://www.who.int/snakebites/snakebites_FAQ/en/index6.html

Featured

How’s About the Epidemiological Triad?

An epidemiological triad is a tool used by One Health professionals to not only identify and categorize a health issue, but to also develop a control plan.

This is a general example of an epidemiological triad.

https://qph.fs.quoracdn.net/main-qimg-6622d9b9a55f6372dbd3e0f293d06676

It has three corners: host, agent and environment.

The ‘agent’ stands for whatever it is that causes the disease. This can be a virus, a bacterium, a toxin, etc. We need to make a distinction between the disease itself and the agent that causes it. The flu disease consists of the common flu symptoms, but the agent that causes the disease is the Influenza virus. Just because someone is infected by the Influenza virus, doesn’t necessarily mean that they will get the flu disease; for example, if they are healthy and have gotten a flu shot, they will be less likely to get sick. In the ‘agent’ section of the triangle they list all the features of the agent that may cause disease.

The ‘host’ is whatever the agent can cause disease in. Some species are resistant or immune to certain agents, and will not come down with the disease even if they are infected. Some animals are naturally resistant to disease by the agent unless certain conditions are fulfilled; for example, if the animal is young, old, stressed, starved, or otherwise weakened. In this section of the triangle they list all the conditions that could predispose a possible host to contracting the disease when infected by the agent.

The ‘environment’ section stands for the environmental conditions that could increase chances of a host coming into contact with the agent, and make the host more susceptible to contracting the disease. In this instance, if the geographical area is favorable to the agent’s survival, if the host is constantly in close contact with infected individuals, has limited access to medicine or sanitation, or other conditions that may make disease more likely.

Here’s an example of an epidemiological triad for an actual disease, Scabies:

This disease is caused by the agent Sarcoptes scabei, a microscopic mite. The unique thing about this agent is that cases of disease are very uncommon in developed countries where most inhabitants have access to healthcare, and are not overcrowded. In developing countries, however, it is one of the most common causes of skin diseases, and is most prevalent in tropical areas where the mites survive best.[1] For this reason, scabies is considered a neglected tropical disease: a disease which disproportionately affects “populations living in poverty, without adequate sanitation, and in close contact with infectious vectors.” [2] Young children and the elderly are particularly susceptible to contracting scabies, as well as secondary complications.

A triad like this is used to find possible control points in the disease cycle. The agent could be controlled by administering scabicide, a medicine that kills the mite. Prevalence of the disease could be lessened by controlling the disease in the stray dogs that can transmit the mite to people.

The triad could also be used to identify areas and situations at high risk for scabies outbreaks, and allow surveillance and preparations to react in case one actually takes place. Right now the World Health Organization recommends mass administration of scabicidal drugs as the most feasible and effective method of controlling the scabies disease.

The epidemiological triad is a good example of what One Health is about: taking into account the whole picture of what leads to disease, by listing and investigating all the factors. Looking at ways to intercept and stop the disease cycle, and not just focusing on treating those who are already infected. Working for the improved health of all people, as well as animals and the environments they live in.

[1] https://www.who.int/neglected_diseases/diseases/scabies/en/

[2] https://www.who.int/neglected_diseases/diseases/en/