Saturday, May 6, 2017

Hantavirus Fatality in Tri-Cities Area

A young woman, Shannon Davis, 24 years old and a mother of three, has died from hantavirus in the Tri-Cities area of Eastern Washington. This was the fourth case of hantavirus in a five month span in Washington state and it brings the fatality rate back to 50%.

Details are not yet available, but this reinforces the evidence for an increased risk for hantavirus exposure this year. Year-by-year spikes in numbers of cases are common, even on a national basis, for reasons both known, and unknown.

More can be learned in this piece in Outbreak News.
This post will be updated as information about the local ecosystem in that area of Franklin county are obtained.

My deepest condolences to Shannon Davis' family and loved ones.


Monday, May 1, 2017

No One Asks if You Rode in a Car

What have I got to do with this?
When patients present at ER and Urgent Care rooms with respiratory symptoms that resemble the flu – or hantavirus – they are supposed to be asked by healthcare providers if they have had contact with rodents in the previous month or so. If so, hantavirus is to be suspected, even if still highly improbable. If not, the small probability attributed to hantavirus becomes even smaller, and the quest for a diagnosis and treatment plan goes on.

But no one asks if you rode in a car, a truck, or a tractor cab. Virtually everyone does so, frequently, so what would be the point? 

If people are, as I've theorized in previous posts, contracting hantavirus by exposure in vehicle cabin air systems, this first line of hantavirus detection simply misses it. Even after diagnosis, many patients who have hantavirus report that they cannot recall having had any kind of contact with rodents.

Detection of hantavirus does not get much better from there.  

Hantavirus Pulmonary Syndrome is a Zebra

Sin Nombre hantavirus infection is thought to be extremely rare in humans. Only about 700 cases have been documented. That makes hantavirus a zebra disease.

Zebras are also rare compared to horses. Unless you happen to be on the Serengeti plains.

When doctors are diagnosing a difficult illness, they are trained to have a rule-of-thumb in the back of their minds. "When you hear hoof beats, don't look for zebras." The odds that your particular patient will turn out to have an extremely rare, "zebra" of an illness, are very low. So don't even look for them, keep your eyes peeled for horses or you will waste valuable time and delay the patient's diagnosis.

But there can be a problem with that. If you don't look for something, you have a reduced chance of finding it. When a disease is a zebra disease, it tends to be misdiagnosed, or missed entirely.

Dr. Hudzik, Dr. SzkodzinskiProf. Polonski: "During medical training, students and residents are being taught a quintessential maxim of clinical medicine—“When you hear hoofbeats, think of horses, not zebras”. Common diseases are what physicians should expect to encounter. Unfortunately, in a world of horses, the hoofbeats of zebras too often go unrecognized or misdiagnosed."

Could hantavirus pulmonary syndrome (HPS) be being misdiagnosed, because it is a rare, zebra of a disease that few practitioners have ever encountered? What measures are in place to capture HPS cases?

Reportable Disease

Because of its severity and high morbidity, about 40%, hantavirus is classified as a reportable disease, the Centers for Disease Control (CDC) is to be notified when cases are diagnosed by local healthcare practitioners. I have been assured by a CDC scientist that this system catches all of the HPS cases, at least in Western Washington. But what if cases of hantavirus infection are simply missed in the first place? 

The number of cases of hantavirus pulmonary syndrome (HPS) that are reported in the CDC's final statistics comprise only those that made it through the gauntlet of being suspected or spotted in blood work, then tested for, and finally forced through the resistance that some care providers show to diagnosing this rare illness. 

This is not the same as the number of actual HPS cases. 

As I studied hantavirus I grew concerned that that exposure difference, automobile cabin air systems, may be causing HPS cases and also causing them to be misdiagnosed. It even seemed possible that there could be a significant number of them. Of course, if you die, or nearly die, a significant number is 1.

Urgent Care Presentation

From the Centers for Disease Control's page on hantavirus pulmonary syndrome, the primary source of guidance on HPS for Emergency and Urgent Care rooms around the country:

"The earlier the patient is brought in to intensive care, the better. If a patient is experiencing full distress, it is less likely the treatment will be effective.

Therefore, if you have been around rodents and have symptoms of fever, deep muscle aches, and severe shortness of breath, see your doctor immediately. Be sure to tell your doctor that you have been around rodents—this will alert your physician to look closely for any rodent-carried disease, such as HPS."

According to this guidance, it is incumbent on the patient, the seriously ill person that may be collapsing into hantavirus pulmonary syndrome, to inform the physician that they have had contact with rodents, probably, some time between seven days and seven weeks previously. 

For this measure to work, there has to be extensive public outreach to inform potential patients, which could include almost anyone. Those people have to recall that outreach warning while they are seriously ill (or be fortunate enough to have a friend or family member know that you swept the garage) and you have to think to tell the doctor about it.  

Hantavirus infection should also be suspected if a particular combination of blood test results is obtained. The combination is called a tetrad of symptoms because there are four changes that, together, suggest hantavirus infection. If that tetrad is spotted in the blood count test tests by someone knowledgeable enough to look for it, hantavirus should be suspected. The patient would then likely be tested for antibodies.

Even in the modern, excellent medical facility where my wife recovered, none of our doctors, nurses, or techs had ever encountered hantavirus before as is likely the case with most Hanta patients. It was almost literally the last thing anyone thought of or discussed during a week of brain-wracking over what was going wrong. They did not know what was wrong, so, they treated for everything they could, and provided supportive care. That was the right treatment, (fortunately!) but it does not hinge on, nor support, the diagnosis of hantavirus.

Diagnosis of hantavirus requires testing for antibodies to it, and that is not a trivial thing.

Hantavirus Antibody Testing

Testing requires that the doctors apply for permission from the CDC, almost the only place in the country that performs such testing. They must apply by going through their county or state health departments. The Protocol for Specimen Submission can be found in the CDC website, here:

It includes information on how to obtain the specimen, and ship it in a refrigerated package, along with links to the two forms that are to be completed, and the phone number to call to notify them when you are ready to transmit the specimens after you've received permission, and the International Air Transit Authority regulations to meet for how you package the specimen, and so forth. 

All very helpful. And a lot of time-consuming paperwork. 

Of course, when the physician receives the test results it will be too late to make any changes to patient care. The HPS patient will be dead or recovering by then. Even if results were quicker, there is no specific treatment for hantavirus, aside from caution in administering fluids, which can trigger refractory pulmonary edema. Those fluids were probably already administered during a life-saving effort to stabilize plunging blood pressure a couple days previously.  

By the time that it is received, a positive detection of hantavirus antibodies does not really change patient care. It is also not practical to test every patient for hantavirus, with its extreme rarity the number of false positives might outnumber the true positives.

Signal to Noise Ratio

Even if you aren't expecting a zebra, if one walks up and presents itself, it would be hard to miss. Right?

What if that zebra was engulfed in teaming throngs of horses, gazelles, and zebu? What if HPS resembled other diseases that were far more common? When something could be lost in a cloud of similar things, you have to think about something called signal to noise ratio, (S/N).
Just one of the gang.

HPS patients present with symptoms that resemble a variety of other diseases, syndromes and categories of illness. Influenza, or flu-like illness, is a common early diagnosis. Community acquired pneumonia (CAP), a category, is the catch-all term for respiratory problems that the hospital didn't transmit. CAP can be caused by numerous pathogens, viral and bacterial. Identification of the particular pathogen in a patient is unusual. 

Community acquired pneumonia becomes a catch-all term that is applied when a patient presents with impaired breathing from what is often an undetermined agent or insult to their system. Community acquired pneumonia strikes somewhere between four and five million people in the U.S. per year. 

HPS is one of many "insults" to the system that can cause what is called Acute Respiratory Distress Syndrome, (ARDS), a relatively new and still controversial classification of sudden respiratory collapse that may result from any of a variety of "insults" to the patient. These collapses follow a general pattern, and have a mortality rate of about 40%, about the same as HPS. Somewhere between 50,000 and 100,000 people per year are struck by ARDS in the U.S.

The huge range in these numbers reflects widely varying estimates of the number of severe illnesses and deaths that fall into this syndrome. A study of post mortem victims of respiratory collapse found that about half of all patients that met the criteria for ARDS were not diagnosed as having had ARDS while they were alive. That's a matter of multiple, somewhat different definitions and criteria.
Zebra herd on the Serengeti plain.
From National Geographic

Differentiating ARDS caused by hantavirus from ARDS caused by requires some means of differentiation. Unfortunately, there are only general reasons for guidance. Hantavirus can be ruled out for cases of ARDS that have a clear source, such as a recent surgery or other illness. But hantavirus is only suggested as a faint possibility in cases with known exposure to rodents, and patients often have no way of knowing that they had that exposure, some weeks previously.

Misdiagnosis of hantavirus was recently reported in a case in Brazil, where the HPS syndrome is a newly identified condition. Hantavirus misdiagnosed as Dengue In places where the medical community is not trained to look for hanta, it tends to get missed. A kind of "latching" effect may appear in the statistics for this reason, with states reporting hantavirus enough to get press coverage tending to find more of it afterward.


I can't be certain that people have been contracting hantavirus through infestations of their cabin air systems, but neither can anyone be assured that they are not.

There are reasons to believe that significant numbers of cases of hantavirus go undiagnosed in both Mexico and the United States.

Effort should be undertaken to better determine the scope of undiagnosed hantavirus from any source, and the particular question of whether vehicle cabin air systems are a mode of infection that has slipped "under the radar" of hantavirus detection.

Some comments on related webpages and excerpts from related references

The CDC webpage on hantavirus transmission makes no mention of vehicles, let alone of vehicle cabin air system infestations. 

The King County Public Health site now has a pretty good update on hantavirus posted here: 

This advisory is mainly directed at health care providers. It now specifically calls out vehicle cabin air systems as suspected transmission mechanisms. These changes probably would have never happened if it were not for this website calling attention to these issues. 

Unfortunately, the general hantavirus information page and the Health Insider article make no mention of checking cabin air filters for deer mouse infestation. It does not mention that this common site of Deer mouse infestation even exists. 

This needs to be changed, and the information for health care providers needs to be disseminated on a national basis. It would also be reasonable to develop some form of instruction that for patients presenting with symptoms resembling hantavirus, someone with proper ventilator mask and gloves should check the cabin air filters of vehicles they have used for signs of rodent infestation.

 “Nucleotide sequence data from 5 antibody-positive rodents indicated that Sin Nombre virus (the major cause of hantavirus pulmonary syndrome [HPS] in the United States) is enzootic in the Mexican states of Nuevo León, San Luis Potosí, Tamaulipas, and Veracruz. However, HPS has not been reported from these states, which suggests that in northeastern Mexico, HPS has been confused with other rapidly progressive, life-threatening respiratory diseases."

"The results of this study indicate that SNV is widely distributed in northeastern Mexico. The geographic distribution of Deer mice (P. maniculatus) in Mexico includes 23 states (28), and ≈20 million persons lived in rural areas in this 23-state region in 2010 (32). Yet, to our knowledge, no cases of HPS have been reported from northeastern Mexico or elsewhere in Mexico."

We hypothesize that HPS caused by SNV in Mexico has been confused with other rapidly progressive, life- threatening respiratory diseases (e.g., plague, tularemia, pneumococcal pneumonia, influenza).”
Hantavirus cases by state of reporting from CDC. Note that many states
have never reported hantavirus, even though they have plenty of mice.
Same with three northernmost states of Mexico, as described above.
"Taken together, our preliminary results suggest that ARDS/ALI are likely under recognized conditions, particularly in critically ill patients requiring prolonged mechanical ventilation. Earlier studies have estimated the mortality due to ARDS/ALI at around 133,500 deaths per year in the United States6. Given the possible under recognition however, ARDS/ALI are conditions likely responsible for even more deaths in the population. Besides mortality, ARDS/ ALI also leads to large amounts of costly and often debilitating morbidity in surviving patients and their caregivers1,3,6. Outcomes studies have consistently found significant functional and neuropsychological derangements at both 1 year and 5 years post illness1,2,3. Perhaps better identification of ARDS/ALI in the first place may help to more efficiently allocate health care resources – in turn potentially preventing some of the typical long-term sequelae currently experienced by survivors and their caregivers.
Before making any firm conclusions however, it should be noted that although the results of our preliminary study are suggestive of under recognition of ARDS/ALI, they are subject to a number of important limitations."
The incidence of ARDS in Maryland is in the range of 10-14 cases per 100,000 people. The ARDS mortality rate is 36% to 52%, similar to that calculated in previous studies.

The aetiology of community-acquired pneumonia (CAP) has been studied in various regions and settings. While these studies differ considerably in patient populations, diagnostic methodology, and presence of confounders, one intriguing constant finding is the failure to detect a pathogen in ∼30–60% of cases 19. Among the factors which may explain this observation, ambulatory antimicrobial pretreatment is the most attractive. Accordingly, there is evidence from the literature that the majority of cases of unknown aetiology may be caused by Streptococcus pneumoniae, a pathogen which is easily missed after one single dose of antimicrobial treatment 1, 10. Conversely, the recognition of Legionella pneumophila and Chlamydia pneumoniae has taught that unrecognised pathogens may represent important causes of CAP.
My interview with Outbreak News and coverage of the cabin air system question.

* Note  These posts will use Hanta to specifically indicate the Sin Nombre strain of hantavirus. 

Wednesday, April 5, 2017

Elevated Threat from Hantavirus in Parts of Western Washington

Juvenile deer mouse. He must have been fearless or ill.
I took this with an iPhone at close range. 
Update to elevated hantavirus risk warning issued April, 5.  As of April 26, 2017, the invasion of Deer mice appears to be continuing. With the spring weather they are in their breeding season and are at least as much of a threat as they were during the period in which the three recent confirmed cases occurred. For this reason, The warning I'm extending the warning issued below until further updates. The risk will likely decline with dry, warm, summer weather, if we get that. 

A cluster of sin nombre hantavirus cases comprising at least three people has occurred in Western Washington. This, combined with observations of the local environments of these patients, makes it possible and appropriate to warn of an elevated risk of contracting hantavirus in similar areas for the near future. This warning is intended to have greater specificity than those issued by local health authorities.

Observations have confirmed that all three of these recent hantavirus patients, along with an earlier (1999) case near Monroe, lived in areas with significant populations of big leaf maple trees. These trees have recently produced very large crops of maple seeds that are a favored food for deer mice, the local reservoir species for hantavirus. This has resulted in what appears to be greater abundance of deer mice in the area.

In general, a higher population of deer mice leads to a higher portion of the deer mice contracting hantavirus, and to more of them shedding hantavirus particles in their urine and feces.

This means that it is likely that there are both a greater number of deer mice, and that they shedding a greater amount of hantavirus than is usually the case.

In addition, heavy rainfall in Western Washington has placed these deer mice under environmental stress, their food sources are now depleted and rotting and their underground burrows are often flooded. As a result, there exists an increase in the number of deer mouse intrusions into human homes, vehicles, outbuildings, garages, and vehicle cabin air handling systems.

It is probable that: In areas where big leaf maple trees grow, which includes much of the Western Washington lowland forest region, from the foothills of the Cascades to near coastal areas,
Big leaf maples trees with massive seed clusters.
 Fall, 2016.  The leaves are 10" to 12" across.
a higher abundance of deer mice shedding hantavirus particles at a greater than usual rate, combined with an increased rate of incursion into human environments, has produced an elevated risk of humans contracting hantavirus. 

If your property has big leaf maple trees, or adjoins areas that do, you should take particular care to avoid breathing in dust from mouse debris. This includes extra caution cleaning garages, outbuildings, vehicles, and other areas where these extremely common mice have intruded.

Areas without these trees may also see an increased risk because of ground water saturation driving mice from burrows and rodent spillover from adjacent areas.

The cabin air handling system in a vehicle is suspected in one of these local cases. The filters in these systems in automobiles, trucks, and tractors that have been parked in areas with big leaf maple trees should be inspected for rodent infestation and replaced as needed. Inspection should take place while wearing respirator mask and gloves.

I posted a more detailed analysis of this threat weeks ago, before the third recent local case was reported. Some of the qualifying words could be adjusted, but most of this discussion from March 17 is still correct.

For detailed directions for cleaning up deer mouse debris, look here for a CDC brochure.

The following segment from KIRO–7 news in Seattle gives an excellent summary of current developments. KIRO–7 3rd Hantavirus Case

Tuesday, April 4, 2017

Another Local Hantavirus Case?

Unfortunately, there are now reports of another probable case of hantavirus in the the Cascade foothills of the Puget Sound area. A woman from Issaquah, living near the Squak Mountain area, where the recent fatality lived has been hospitalized with what is believed to be the disease.

My deepest hopes for recovery go out to her and her family and loved ones.

Also unfortunately, it appears that the local health authorities continue to believe it there duty to minimize, allay concerns, and generally downplay the very real and current threat of hantavirus.

I spoke with Jeff Duchin, the King County Health Commissioner a week or so ago about this elevated threat. I described, in detail, the increase in deer mouse population that was being seen in the area.

His response was, "We'll just have to wait and see," about whether the the two known hantavirus cases raised concerns. Now we have a third case, and, quoted in the King5 article, "Health officials do not believe the two cases are connected but say there are reports of more deer mice in the area."

Three cases, at least, in rapid sequence after 13 years without a single case is a hantavirus cluster.
On at least a small scale, it is a hantavirus outbreak.

People in areas with big leaf maples trees that are experiencing an increase in deer mouse populations should take particular precautions to protect themselves from airborne mouse debris. 

People should check their cabin air filters in cars, trucks, and tractors. Wear a particle mask and gloves!

People should work to exclude all mice and trap others. Spray with disinfectant and dispose along with the trap. 


Thursday, March 30, 2017

Cabin Air Systems as a Mode of Hantavirus Infection

Image of typical cabin air infestation, found online, including
mouse, built directly atop a vehicle's cabin air filter.
Notice how dry the corpse looks. 
Both the wi-fi and the coffee were good and free in the ICU where my wife had collapsed into hantavirus pulmonary syndrome (HPS), so when my reeling subsided a bit I began to do some research. First, since she was still intubated, I found a keen interest in the extubation process. I wanted to understand as much as possible to be able to communicate with the doctors and nurses (who were excellent). More on that in a future post on "ICU-itis."

Then I learned that they had tested her for hantavirus, and I took an interest in that, began to research it, and thought more carefully through our potential exposures. How could she have contracted it? Could it really be her car, which we had worried about? I removed her van's filter and checked for mouse activity. I found it – chewed fiberglass insulation, maple seed shells, and other mouse debris.

When she was first admitted we had answered "yes" to possible rodent exposure. We had previously spotted mouse nest material and other debris atop the cabin air filter in her minivan, a Toyota, Sienna, a couple years before. At that time I cleaned it out, googled it, and found rodents to be a common problem that no one seemed to have a solution for, especially for this common model vehicle.

I thought I had to screened off the entrance, and, given the extreme rarity of hantavirus, and many other things to do, I left it at that, with occasional inspections and clean outs. In retrospect, I didn't take the threat of hantavirus seriously enough.

I had been driving that same car to and from the hospital. Fortunately, I drove with the windows down and the fan at the lowest setting. Still, perhaps it was time to switch to my Honda, Accord. When I checked it for mouse debris atop the filter, it was there as well. Both our vehicles, two of the most common cars on the road, had been invaded by deer mice.

The first pair of positive hantavirus antibody test results came back from the CDC about twelve days after admission. She had been extubated a few days before, only becoming responsive a few days after that, and was slowly regaining the ability to stand up, and to speak, her mind slowly reconnecting with her body after ten days of acute disease and sedation.

She missed our dogs, two miniature Australian shepherds, stating as much in one of her first complete sentences. I found out later that she couldn't remember what they looked like. She wanted to go home, and was very clear about that as well.
Dori and Mick, our dogs from MARS,
the Miniature Australian Rescue Society.

While working on that goal, I studied contraction and incubation time of hantavirus and reviewed our relative, possible exposures in our home, two outbuildings, and vehicles. That discussion will appear in another post, but the similarities and differences in our relative exposures gave me something of a controlled experiment. The largest difference was her much greater exposure to the air and dust from her car's cabin air system.

That led me to wonder about a larger problem. Was it possible that others were contracting sin nombre hantavirus from their cabin air systems?

Although I saw ample speculation in car talk type forums, there appeared to be little to nothing about this exposure mode in the technical literature. The CDC website does not mention it. Neither does the Canadian health agencies' hantavirus information site. I have not found a single mention of mouse infestation of vehicle cabin air systems, from any governmental hantavirus site. Vehicles are mentioned, meaning places like seats an trunks, but the inner passages of the air circulation system are not.

Could my wife's case be unique, even though the mechanism seemed so obvious? Why is there no awareness of other cases of HPS caused in this way.

Which brought me to the question: Is it possible that sin nombre hantavirus infections from vehicle cabin air systems were occurring without being detected and reported?

These questions have several moving parts. Let's break them down to four related questions that should inform them.

1) Is it not only possible  to contract hantavirus through vehicle's cabin air system, but are these systems actually efficient, practical, reasonable mechanisms for conveying biologically active hantavirus virions to human lungs?

2) Are there significant numbers of cabin air infestations by hantavirus carrying deer mice?

3) Could there be a reason that hantavirus infections through cabin air systems are being misdiagnosed, and so be falling through the cracks?

4) Is there some reason that these events could have been statistically camouflaged and so gone unnoticed over the years?  (more on this in upcoming post)

In this post I will show that the answers to all four questions are either certainly or probably yes. In another post I will show that a cabin air system was the probable cause of hantavirus infection in at least one person, my wife. This is not a hypothetical thing. I believe it is probably what nearly killed my wife and I think there is a significant chance that other people may be dying this way.
When I opened the Sienna's filter to photograph for this piece, yesterday,
I found this fresh mouse debris and possible urine stain on the filter.
Sharp metal grating atop filter is a try at a mouse deterrent.

Hantavirus Infection Process

First, let's review what steps have to take place for sin nombre hantavirus to infect a human.

The Sienna filter removed. This is just a tiny amount of material.
Most infestations involve far more (see those posts). That may
be because the expanded steel grating we placed atop the filter
(see first pic) succeeded in discouraging nesting, at least. 
Specifically, what has to happen in the process of human infection from mouse-carried hantavirus through inhalation of the virus, which is widely believed to be the most common mode of infection. This process has to involve the delivery of hantavirus virions from an infected mouse to human lungs in sufficient numbers, and in good enough condition, to cause infection.

To become infected with hantavirus it is apparently necessary to inhale a significant number of the virus virions, the portable, particle-like form of the virus. One, or just a few virions will perish or be destroyed by the bodies' defenses. If the disease were that contagious it would be vastly more common.

A virus that has evolved while living in humans for many generations is likely to be well-adapted to working with human anatomy. In that case, the virus probably has a good chance of achieving a new infection in another human with only a small number of virions. Some diseases are believed to be transmitted by as few as, literally, a few virions. Even though the amount of virus discharged into a human by a mosquito is likely small, it can transmit diseases that are well adapted to their new human host.

Hantavirus, however, is transmitted to humans from rodents, its host species, the species that the virus has evolved with. Differences and similarities in hantavirus genes closely match the differences and similarities in their host species. A hantavirus that is endemic to deer mice is likely to be very similar to a hanta that is endemic to the closely-related white footed mouse, another New World mouse. Both of those hantaviruses are likely to be dissimilar to those that have evolved alongside an Old World rodent species.

Both viruses are adapted to living in rodents, not people. When they infect people they have crossed species and will be performing their genetic surgery on cells they are not as familiar with, in an evolutionary sense. People and rodents are very similar, about 99% of our genes are identical with mice. This explains a lot of things, but those things are outside the scope of this post.

The 99% similarity gives a hantavirus a good head start at coopting the genetic mechanisms of our cells, but the 1% difference means that zoonotic viruses tend to do damage and cause severe illness. It also may mean that it is more difficult for hantavirus to infect a human than yet another mouse, after thousands of years of practice. Although I'm not aware of any actual experimental data, it appears that some significant number of hantavirus virions must be inhaled for an infection to occur.

Although it is possible to become infected by a mouse bite, these cases are extremely rare. Deer mice are shy, reclusive folk. It is also possible to become infected by touching something contaminated with mouse urine or feces while cleaning, and then rubbing your eyes or touching your mouth.

But the most probable, or at least the most common mechanism of infection is believed to be inhalation of the hantavirus virions. The lungs are the primary target of the sin nombre genus of hantavirus that causes hantavirus pulmonary syndrome, HPS.

So we have a human exposure requirement that involves inhalation (for this case) of some number of active hantavirus virions.

To be inhaled, those virions have to somehow become airborne. To do that, they must be finely divided into an aerosol, a cloud of material in droplets or particles so fine that that it moves along with the air and circulates freely with it. If the particles are fine enough, they will flow with the air all the way down into the finest passages of the lungs. Smoke, clouds, mist from aerosol spray cans are all example of aerosols.

Viruses and Virions

"Virion" ought to be a common term, but it isn't. Hantavirus virions, the “portable” form of the virus, are roughly the shape of round balls that are about 160 nanometers in diameter. That’s about 6 millionths of an inch or 1/500th the diameter of a typical human hair – far too small to see with light. A typical polyethylene sandwich bag is about 25 µ in thickness, also called “one mil” meaning 1/1000th of an inch. It would take about 150 hantavirus virions to span across that 1 mil of thickness. 

Hantavirus is a single stranded, negative sense, RNA virus, designated –ssRNA in a system called the Baltimore Classification. That means that it is coded by a single strand of RNA, ribonucleic acid, that is twisted in a negative spiral direction in relation to functional groups at its ends. The RNA is coiled up tightly inside an enclosure that surrounds and protects it, and performs other functions, and that is made from proteins that are coded by the RNA. That protein coat is, in turn, surrounded by a membrane comprised of lipids, fatty molecules. 

Finally, the surface of the hantavirus virion is studded with two kinds of viral surface glycoproteins, designated Gn and Gc. These are molecular lock-picking systems, in a way, that begin the cell infection process by penetrating cell walls in the species under attack. Working as a team, the two glycoproteins deliver the virion to the cell interior, where its RNA and other parts begin a hostile take-over of the cellular processes. 

These components are manufactured inside the cells of host species after they have been conquered and repurposed by the virus. It is only when the hantavirus virion is at home inside a host cell that it really “comes alive.” While a virion is a purposeful clump of RNA and proteins that cannot reproduce itself and that has no metabolism, a cell that has been coopted by that virion is humming factory of metabolism and of reproduction – of virus components.

These components are ultimately assembled in some fashion by the same cells molecular scaffolding and equipment and at the point when the cells resources have been completely consumed it is them opened up in the end game of the virus and the new family of virions are released. When and where the virions are released and conveyed into the excreta or other shed products from the host species is of significant importance because that is part of the pathway all the virus from a whole species to the human being.

Hantavirus virions continue their journey by being expelled with the urine and feces of the mice. Mouse urine contains the salt, urea, and a surprisingly high concentration of proteins. If a human had such a high concentration they would have proteinuria, and would be very ill. The virions, less than 1/5 of a micron in diameter (160 nm) are suspended in this soup of water, urea, and proteins, and flow along with that fluid.

Electron microscope image of hantavirus virions.
An electron micrograph of hantavirus virions appears at right. The RNA that codes for the virus is coiled and coiled again into a tight mass inside the virion. This is coated with a protein shell, which is coated with a second, protective shell, and studded with 

These particles are so small that it is fairly unlikely that they will become completely separated out from other materials, that is, aerosolized down to individual virion particles. Such a fine division of material is not energetically favorable. The finer the division in a fluid, or any material, the more energy must be added from the bulk form to overcome the surface energy of that material. This is the energy that makes water draw itself into rounded drops, and that sucks liquids up into capillary tubes. 

A molecule of water is more stable, at lower energy, when it is able to stick to other water molecules all around it, on all six sides of the single molecule. This is the state of most molecules in a fluid. The ones that are on the outside surface, however, are only stuck to other molecules on five sides, with the side facing the air only very weakly linked to the gaseous air above it. When you divide bulk water down into finer and finer drops, you have relatively more and more molecules on the surface of the drop compared to those inside of it. 

If you divide the water down into individual, separated molecules, they are no longer stuck to any other molecules, and you have water in gaseous form, steam. The difference in energy between liquid water close to 100ºC (212 ºF) and gaseous water, still at 100 ºC, is enormous. It is called the heat of vaporization of water.  

Nano-divided water droplets are very unstable – they want to stick to anything, anything at all that approaches them. They will stick to oil, metal, Teflon, anything they can approach will lower their energy, so they stick to it, and tight. Even so, at elevated temperatures other molecules blast them or shake them off the surface and they return to a gas form as rapidly as they condensed out.

Something similar has to happen for virus virions to be finely separated. For a water nozzle to make finely divided mist, it has to have a large pressure difference to provide the surface energy. For a soup of virions in mouse urine (water, urea and protein) energy has to come from somewhere. For urine and feces lying in a corner of a garage, this energy simply isn’t there, and the material remains safely undisturbed until it denatures.

If that garage corner is swept with a dry broom, however, very substantial amounts of energy are released in a very localized way where the tips of the broom bristles scrape against the floor surface. This kind of scraping relates to “dry friction” and is a complex phenomenon. It is often characterized by something called “stick slip behavior,” wherein the interface between the bristle and the floor surface and debris alternately sticks, staying locked in place, then breaks free and slips, displacing some distance before enough elastic strain is released so it can stick again. Every slip means that something has broken loose somewhere, and perhaps become floating dust. 

Time is of the Essence

The virions must make the journey from the mouse to human lungs in a limited amount of time. They must still be viable virions when they complete the trip so that they can penetrate a cell wall and take over the cell's machinery to replicate themselves. The lifetimes of the virions vary with the environment they are in. Exposed to the dry air, they decay to 1/10 their number in only two hours. At that rate, 18 hours later they would be reduced to one billionth the original number, and would be unlikely to infect.

Under moist conditions, however, the virions are more durable, lasting about two days for every reduction to one tenth their former numbers. At that rate it may take weeks for them to be completely neutralized.

Most hantavirus infections have occurred under desert-like conditions, such as near the Four Corners region of Arizona, Utah, Colorado, and New Mexico. The dry, low humidity conditions in these places make it relatively easy for the virus particles to separate from the fluid that otherwise binds them into liquid material. Liquids are much more stable, in general, than gases. To make a gas out of the liquid takes a lot of energy. To make a finely divided aerosol out of liquid also takes energy.

That energy goes into creating new surface area material from material that was in the interior of the liquid. The relative amount of surface to interior increases with the fineness of the droplets. The amount of energy depends on what is called surface free energy, or surface tension.

Water has a very high surface free energy, so it is fairly difficult to make into a mist. If you add a surfactant, a detergent to that water, it lowers the surface energy and makes it easier to, say, blow bubbles or form a fine mist. The bile salts in urine act as surfactants, reducing it below that of water alone. There is still a substantial energy barrier to mouse urine aerosol formation. When expelled from the mouse, small amounts may pass into the air, a known hazard in research facilities, but most of it strikes some surface, is adsorbed onto that surface, again, by surface free energy, and then it goes nowhere.

Over time, hours, days, or at most weeks, it will degrade and be fairly harmless, as far as hantavirus is concerned, but it will still be disgusting. When an infected mouse pees in the corner of your garage, you hardly ever come down with HPS because the virus simply degrades in place.

Unless, of course, you sweep it with a broom while it is still "fresh," generating very strong forces at the tips of the bristles and bringing up dust. Dust is often difficult to see. If a bright light like a pen laser is used in a darkened room, it is surprising what little particles it will illuminate.

Or unless vacuum it.  Vacuum cleaners draw in dust and dirt, and filter out most of it, but not all. Virions are far smaller than the pores in any vacuum, even those with HEPPA filters and cyclones. The virus particles are drawn against the filter surface by the very high velocity airflow that exists within these cleaners. Most of the surface of the filter is closed, remember, so the small amount of its surface that is drawing through air is rushing at very high speed.

Both brooms and vacuum cleaners are known mechanisms for causing HPS. The physical mechanism of aerosolizing the material and bringing it to the lungs is clear. Infections caused this way, while believed to be the most common means, remain relatively rare, probably because most virus particles that are vacuumed or swept have been out of the mouse for days or weeks, and are no longer biologically active. If the urine is still moist, the virions are much less likely to be separated into airborne particles. It will simply wet the tips of the broom and smear on the floor a bit.

When most of the water in urine has evaporated, a residue of bile salts, protein bits, and hantavirus virions will be left behind. The salts are likely to make this residue hygroscopic, tending to attract and hold water to some extent.The hygroscopic mix of mostly dried urine will retain some coating of water that is likely to promote longer active life in the virions.

Moist virions are fairly durable, dry virions are more vulnerable. Most known HPS cases have been in dry climates. The Seattle cases stand out as exceptions, having happened in a very wet season in the Puget Sound region. This basic difference in vision environment outside its host suggests that a different mechanism may be favored for transmission in wet-climate hantavirus cases.

But if the air is dry enough, the attractive forces between water and mouse urine residue are overcome and the evaporating water leaves behind relatively dried material. The surfaces of the virions will now be more weakly bonded to other material than they were to the aqueous urine because of the lower surface free energy of the less polar species present. As distinct, spherical, structurally sound units, the virions could separate from the dried urine under the abrasive action of a broom bristle or a strong breeze, becoming airborne and finding their way into lungs.

But the dryness that is required means that time is on your side. The time delay between ejection from the mouse and ingestion to the lungs provides what may be the tightest bottleneck in the infection process. The vast majority of all hantavirus shed by mice is oxidized, destroyed by UV light, or otherwise degraded. Only the tiniest of fractions makes the trip to human lungs in time to do great harm.

A dry environment tends to favor both aerosolization and dust formation that can transport the virus, but, the delivery must be prompt once the material has become exposed to air and dried, or the virions will have degraded.

Cabin Air Systems

Vacuum cleaners, which can draw mouse excreta against a filter, are known mechanisms of hantavirus infection both from specific cases and because of clear, physically realistic reasons. Keep that in mind as we finally look at cabin air systems. Cabin air systems are comprised of the fan, filter, valves, outlets, controls and inlet that provide the air you breath in a vehicle such as an automobile, truck, or tractor.

These systems are distinct from the engine air filter and intake. Cabin air is drawn in through a passage that keeps it separated from the vapors in the engine compartment. Cabin air filters are typically located behind the glove compartment, and are accessed by emptying it, releasing a retaining band, squeezing in the sides and pulling it forward. The filter is removed by squeezing the clips on its sides and sliding it forward. Only do so wearing gloves and a respirator mask. 

People in "car talk" type online forums have speculated for years about the possibility of cabin air hantavirus infection as a possibility and a cause for concern. Many of them have posted images of their own invaded and inhabited cabin air systems, the filter elements having been made the living, eating, and excreting quarters of deer mice and other rodents.

Links to three posts with images of cabin air system rodent infestations are below. These are a small fraction of the online images put up by the fraction people that went through the trouble to photograph their mouse nest covered cabin air filters and post them online in discussion forums. These invasions are somewhere between common, and ubiquitous.

Cabin Air Infestations 1  Cabin Air Infestations 2       Cabin Air Infestations 3

So the answer to "2) Are there significant numbers of cabin air infestations by hantavirus carrying deer mice?" is yes. There must be thousands, at the very least, and possibly tens, or hundreds of thousands of cases of mouse infestations of vehicle cabin air systems. Compiling data to quantitate this is a project for someone out there.

Now consider what happens when an infected mouse builds a nest atop a cabin air filter, and the vehicle's driver enters the vehicle and starts the engine. The mice living within will be startled by the sounds of the vehicle being entered, and terrified when the car is started and the heater fan is actuated. They will be in a virtual tornado of air motion. The natural reaction is a defensive move to make themselves less attractive to predators. They will expel urine and feces. Fresh, hantavirus laced urine and feces.

As the air system operates this urine will be rapidly dried, because the heater will lower the humidity rapidly, or the AC will dehumidify it even more rapidly, and the Defrost setting will dry it fastest of all, dehumidifying the air by operating the AC compressor, and simultaneously operating the heating elements, drawing warm, desiccated air directly through the excrement and filter element.

At some point, potentially aided by holes chewed in the filter element, (see above image) the hantavirus virions will become dried and somewhat separable from the matrix of bile solids left behind by the dried urine, and similarly for virions within the feces. T

There is a clear mechanism for cabin air systems rapidly drying, and rapidly aerosolizing fresh, active, virion material and directly passing it to the vehicle's interior and passenger lungs.

The answer to question (1) above is yes. "1) Is it not only possible  to contract hantavirus through vehicle's cabin air system, but are these systems actually efficient, practical, reasonable mechanisms for conveying biologically active hantavirus virions to human lungs?"

I will get to (3) and (4) in an upcoming post.

Hantavirus infection via cabin air systems is a problem that should be much more seriously investigated and responded to.

The above analysis might be regarded as speculative, or of theoretical nature, a theory constructed to explain something that has not been observed. But we also have a specific case.

The reasons why my wife and I both suspect that my wife contracted hantavirus through exposure from her vehicle's cabin air system will be explained in more detail in a future post on cabin air systems. 


* Throughout this post I may use "hanta" as a shorthand that specifically means the sin nombre strain of hantavirus.

This is one of the strings of comments that is coming to me regarding cabin air infestations. This one was through Facebook. Other cases of this  clearly show that this is a widespread problem in rural King County.

Kathleen   "Mark, thank you for sharing your experience and research. We live in in the woods north of Issaquah and have been battling a deer mouse invasion in our vehicles. After viewing this video and your site, we found contaminated cabin air filters in both our Toyotas which is terribly unnerving. Thanks for trying to sound the alarm."

Mark   "Thank you, Kathleen. I would like to share your comment with the King Co. health folks...."

Kathleen       "Yes, you can share it. We have our vehicles serviced regularly. We thought we had done a good job of cleaning up by having the interior steam cleaned, wiping surfaces with 10% bleach and placing rodent repellent packs in strategic places. We never thought to check the cabin air filters. We took our cars to the dealership today. They offered us an ozone treatment and sprayed a scent deterrent in vents, but told us there was no way of blocking rodent entrance to the ventilation. They suggested we stay vigilant with trapping and to replace scent repellent regularly. We farmers in the Snoqualmie Valley have noticed a big increase in mice. Despite the fact that we keep all poultry feed in metal cans, have barn cats on duty, and trap regularly, we can't keep up the this years population explosion. I wish there was something I could do to know that the virus is not incubating in my kids right now. I sent a comment already to King County Public Health about our cabin air filter being heavily contaminated."