A Post about Coronaviruses

Something has been bothering me for a while, which means this post has been brewing for a while. (It’s also been edited a few times, since posting. Mostly in this introductory section, where I’ve cut and rearranged because the first version had too many words and asides.)

I’m going to talk about coronaviruses.

Marie and Duchess sitting on a carpeted floor, looking up at the camera. Marie is a pale gray watermarked tabby cat. Duchess is a pale gray and orange tortoiseshell cat with a clipped left ear.

This post is a departure for me. In talking/writing about coronaviruses on this blog, I’m breaching the barrier between my two worlds. Between my relaxing world of creativity, where I indulge myself with poetry and photos and blog posts, and my anxious world of responsibilities, where I worry about knowledge and knowledge gaps and the idea that facts about the natural world exist but are seldom fully grasped.

In my anxious world of responsibilities, I’ve been talking about coronaviruses for much of the past year. But only with friends and family. And cats. Marie and Dutch are attentive listeners.


Marie, a pale gray watermarked tabby cat, is looking out of the window from her perch on a flannel blanket at the foot of a bed. Duchess, a pale gray and orange tortoiseshell cat, is sprawled in her back, yawning, in a chair in front of the window.

Actually, they’re not very good listeners at all.

Two cats, Marie and Duchess, are sitting on a carpeted floor, looking into their wire and canvas expandable play tunnels. One tunnel is green, the other is blue. Their heads and shoulders are fully inside the tunnels, so only their backs and tails are visible.

Moving on…

Two cats, Marie and Duchess, are sitting on a red mat, backs to the camera, looking out of a door that has windowpanes extending almost to the floor.

In this post, I’m going to explain some of what I know about feline coronavirus. Then I’m going to explain why I’ve been talking to my friends and family and cats about feline coronavirus during the COVID-19 pandemic.

Part I

The coronavirus family tree

To be clear, feline coronavirus is a distinctly different virus from COVID-19.

Taxonomically, both feline coronavirus and COVID-19 belong to the subfamily orthocoronavirinae (previously called coronavirinae), but they are in different genera. COVID-19 is in the genus betacoronavirus, while feline coronavirus is in the genus alphacoronavirus.

But what do these classifications mean? Obviously, they mean that feline coronavirus and COVID-19 are somewhat related, but does “somewhat related” mean anything useful for bloggers and readers and cats?

Two cats, Marie and Duchess, are looking at the camera while sitting on a gray desk chair that is in front of a white desk. The desk is stacked with papers and a spiral notebook. Marie is a pale gray watermarked tabby cat. Duchess is a pale gray and orange tortoiseshell cat with a clipped left ear.

A linguist might say It depends on what you mean by ‘useful.’ An editor might say The question needs editing before it can be answerable. And a taxonomist would likely say Please stop before you even start, because viral taxonomy follows its own rules and should not be compared to cats.

Two cats, Marie and Duchess, are sitting on a gray blanket with their backs to the camera, looking out of a window. Both have their front feet on the window sill. The tension in their bodies indicates that they are very interested in whatever is off-camera, outside the window.

The history of the taxonomy, classification, and nomenclature of viruses is an interesting study of its own. Efforts to classify viruses began in the 1960s and continue today, with a major expansion of the classification system having been proposed as recently as 2017. Currently, the family tree of coronaviruses looks something like this (Decaro & Lorusso 2020; Kipar & Meli, 2014):

  • Order – Nidovirales
    • Family – coronaviridae
      • Subfamily – coronavirinae (as of 2014) or orthocoronavirinae (as of 2020)
        • Genus – alphacoronavirus, betacoronavirus, deltacoronavirus, and gammacoronavirus

Beyond the genus level of classification, the coronavirus family tree branches into subgenera, species, and subspecies, with some 39 species of coronaviruses distributed across 27 subgenera (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses, 2020).

But again, what do these classifications mean?

In a desperate and thoroughly unscientific attempt to answer this question, I’m borrowing an example from mammalian taxonomy. (Remember the taxonomist’s warning, that viral taxonomy should not be compared to cats? Like I said, the following comparison is thoroughly unscientific. I’ll understand if the taxonomist, or any other reader, snorts in contempt and walks away.)

Two cats, Marie and Duchess, are sleeping together in a cat bed in front of a window. The cat bed is slightly too small for both of them to fit comfortably, so they look slightly uncomfortable. Beside them, there is a second cat bed, which is empty.

In viral taxonomy, feline coronavirus and COVID-19 are in the same subfamily, but in different genera.

In mammalian taxonomy, domestic cats and bobcats are in the same subfamily, but in different genera.

The feline family tree

Dutch and Marie are domestic cats. Spoiled, pampered, much loved house cats.

Two cats, Marie and Duchess, are curled up together on a brightly colored blanket on the floor in front of a glass door. Their backs are to the camera, and they are looking outside.

Taxonomically speaking, Dutch and Marie belong in subfamily Felinae, the genus Felis, and the species catus. Put in the more familiar binomial phrasing of genus-species, Dutch and Marie are Felis catus. By comparison, bobcats also belong to the subfamily Felinae, but are classified in the genus Lynx and species rufus. So, binomially, bobcats are Lynx rufus.

To add a third, and somewhat more complicated, data point (because everything is complicated in taxonomy), Pallas’s cats are also classified in the subfamily Felinae. But some sources place Pallas’s cats in the genus Felis and other sources separate them into the genus Otocolobus. All seem to agree on a species name for Pallas’s cats–manul. So Pallas’s cats are variously listed as Felis manulOtocolobus manul, or Felis (Otocolobus) manul.

Marie and Dutch, being pair-bonded rescue Felis catus, are clearly related to each other. Littermates, maybe. But they are only distantly related to bobcats and Pallas’s cats. Some taxonomists, those who classify Pallas’s cats in the genus Felis, might consider Marie and Dutch more closely related to Pallas’s cats than they are to bobcats. Other taxonomists, those who classify Pallas’s cats in the genus Otocolobus, might consider Marie and Dutch no more closely related to Pallas’s cats than they are to bobcats. For my purposes, it is enough to note that domestic cats, bobcats, and Pallas’s cats are all cats, but they are all distinctly different cats.

A gray cat, Duchess, is mostly hidden in a brown polka-dot cat bed with tall sides. All that can be seen over the sides of the bed are her ears and one hind foot extended over the bed's side, toward the camera. The pads of her foot are visible.

Feline coronavirus and COVID-19 are both coronaviruses, but they are distinctly different coronaviruses.

(Back to the taxonomist’s concerns: Viral taxonomy and mammalian taxonomy are, indeed, different systems. The above comparison is flagrantly unscientific. I offer it as a metaphorical demonstration of the messiness inherent in trying to describe, measure, or quantify relatedness among viruses and/or cats.)

A gray cat, Marie, is mostly hidden under a black sheet and white blanket. All that can be seen is her nose and part of one eye, along with a few toes of one front foot. Her position and tension indicate that she is stalking something from her hiding place under the sheet and blanket.

Part II

As recently as the early 1990s, when I first entered veterinary school, there were many knowledge gaps in the story of feline coronavirus. Now research has illuminated how the virus moves within cat populations and has unraveled some of the complex mechanisms that mediate how the virus affects individual cats.

From here, for the sake of brevity and clarity, I’m going to shorten “feline coronavirus” to FCoV. For one thing, I won’t have to keep typing the whole name. For another, I want to be as clear as possible that coronaviruses are a large and varied group of viruses, while FCoV is a very specific coronavirus that infects cats. Probably even Marie and Dutch, at some point in their lives.

Two cats, Marie and Duchess, are looking at the camera from their positions curled up together in a gray checked cat bed. They were asleep together and just woke up. Their expressions indicate they are interested in the camera.

Yes, even you, my dears. But it’s okay, because the overwhelming majority of cats that become infected with FCoV will have few or no symptoms. Perhaps some diarrhea or other gastrointestinal signs, perhaps some upper respiratory congestion.

(There’s more to the FCoV story, which I’ll come to later. For now, I’ll simply say that I’m grateful Marie and Dutch are among the overwhelming majority of cats who have avoided the “more” part of the FCoV story.)

Two pale gray cats, Marie and Duchess, are sleeping facing each other. Duchess has one front foot wrapped over Marie's neck, and Marie has both front feet propped on Duchess's chest. They are in front of a window, and grass is visible in the background.

Marie and Dutch have likely been infected with FCoV, perhaps on multiple occasions. Because FCoV is “worldwide and ubiquitous among virtually all cat populations”, found in more than 60% of pet cats in multi-cat households and in as many as 90% of kittens in shelters (Pedersen, 2009, p. 227).

FCoV is a single-stranded RNA virus

The particular feature of FCoV that is important to this post, and that has been important in my year-long discussions with friends and family, relates to the way coronaviruses carry their genetic information. Unlike humans and cats (and most other organisms), who carry their genetic information as double strands of DNA, coronaviruses carry their genetic information as single strands of RNA. So FCoV, like all other coronaviruses, employs single-stranded RNA as the primary molecule for carrying genetic information.

Dutch and Marie always go to sleep at this point. It’s okay if you do, too. I’ve fallen asleep several times, myself. But there is a point to this post. I’m getting close to it, and my next tangent about the differences between double-stranded DNA and single-stranded RNA will get even closer.

Two gray cats, Marie and Duchess, are sleeping nose-to-nose curled up together on blanket. The camera is very close to their heads, so their ears are prominently visible.

The double helix packaging of DNA provides a relatively stable structure for passing along genetic information. Each strand of DNA serves as a sort of back-up copy for its partner strand, and the process of DNA copying actually uses this back-up feature to proofread and correct mistakes. Should a strand of DNA break, or should mistakes occur in copying a strand, the back-up copy allows enzymes to repair the breaks and remedy the mistakes. This prevents mutations. Obviously, some mutations slip through, but at a far lower rate than would otherwise occur.

Single strands of RNA are less stable genetic carriers than double-stranded DNA. RNA is a more fragile molecule than DNA, and single-stranded RNA, lacking partner strands, has no back-up copies for enzymatic proofreading. Coronaviruses do have a unique mechanism for proofreading, a complex of enzymes and proteins that proofread key genes (Robson et al., 2020), and this unique mechanism provides some stability. But rapid and frequent mutations still occur.

As a single-stranded RNA virus, FCoV does a poor job of creating exact copies of itself. Every time FCoV copies itself, errors occur. Every time (Kipar & Meli, 2014, p. 507). For that matter, FCoV mutates so often that researchers characterize the array of viruses produced in the course of a single infection as a quasispecies–a group of “related genotypes” (Kipar & Meli, 2014, p. 507). Other researchers use the term “pseudo-strain” (Emmler et al., 2020, p. 792).

In short, within any FCoV infected cat, there are many mutated versions of the FCoV they originally contracted.

Two gray cats are snuggled together in front of a window. The camera is very close. Marie is sleeping with her forehead pressed against Duchess's back. Marie's nose and whiskers are visible. Duchess has her back to the camera and has fallen asleep while looking out of the window.

FCoV and feline infectious peritonitis

The overwhelming majority of cats that become infected with FCoV will have few or no symptoms. Perhaps some diarrhea or other gastrointestinal signs, perhaps some upper respiratory congestion. But there’s more to the story.

For somewhere between about 1% (Pedersen et al., 2012, p. 20) and 12% (Addie et al., 2009, p. 594) of infected cats, their particular FCoV quasispecies mutates into one of a number of forms that are able to cause a devastating and often fatal disease: feline infectious peritonitis (FIP).

I say “able to cause” because the FIP-able quasispecies do not always cause FIP. Some cats can resist FIP, even when their FCoV infection mutates into a form capable of causing FIP. Some cats are resistant at one point in their lives and later become susceptible, others perhaps follow an opposite path. In essence, FIP occurs at intersections between rapidly mutating FCoV quasispecies and the genetics and immune systems of individual cats. When an FCoV quasispecies gains the ability to cause FIP, in a cat that never had or has lost the ability to resist FIP, a deadly cascade of disease may begin.

What I’ve just described is the internal mutation theory of FIP. Put bluntly, this theory says that every case (or cluster of cases) of FIP represents a newly mutated variant of FCoV that is newly capable of causing FIP.

And now, all tangents complete, I come to the point of this post.

Two gray cats, Marie and Duchess, are stretched out together on a blue tie-dyed blanket in front of a window. Marie is asleep with her front feet extended, and Duchess is almost asleep, holding her head up, still, but her eyes are closed.

FIP is not rare.

  • As of 2008, FIP was “one of the leading infectious causes of death among young cats from shelters and catteries” (Pedersen, 2009, p. 225).
  • “In one study, FIP was the most common single cause of disease in cats younger than 2 years of age…. An average of 1-5% of young cattery or shelter cats in the US will die from FIP, with losses in catteries higher than from shelters” (Pedersen, 2009, p. 227).
  • “Up to 12% of FCoV-infected cats may succumb to FIP, with stress predisposing to the development of disease” (Addie et al., 2009, p. 594).

This is the source of my bother. (Remember the bother, all those paragraphs ago, that started this post?)

What does it all mean?

I haven’t found much information about the mutation rates of COVID-19. I feel like the data exists, at least in some rough estimate, but I’ve not found it in a reliable and readily accessible format. And, without ready access to the mutation rates of COVID-19, my frame of reference reverts to my existing knowledge about FCoV.

Two cats are silhouetted in front of a screened window. Both cats have their backs to the camera and are looking with interest at something outside the window. Grass is visible outside.

FCoV and COVID-19 are only distantly related, but all coronaviruses share the genetic instability that comes from having a single-stranded RNA genome. Yes, coronaviruses have a unique mechanism for some stability, but this mechanism can’t completely compensate for the instability that leads to mutations.

A vague measure of the instability of FCoV can be seen in the incidence of FIP in cats around the world. Because each case (or cluster of cases) of FIP represents an FCoV quasispecies that has newly acquired one or more of the mutations that enable FIP.

Remember those word problems in math class?

  1. Think about how many kittens and young cats there are in the world. (While no one counts the number of kittens born each year, the ASPCA estimates that 3.2 million cats enter US animal shelters each year…)
  2. Narrow the number down to all the kittens and young cats in shelters and multi-cat environments, each year. (Hint: That’s still so very many cats.)
  3. Between 60% and 90% of the cats in shelters or in multi-cat environments will, at some point, become infected with FCoV.
  4. Calculate a number that would be between 1% and 12% of FCoV-infected kittens and young cats.

That’s how many cats will develop FIP each year.

According to the internal mutation theory, that’s how many times FCoV mutates, each year, into a form capable of causing FIP in a cat that is incapable of resisting FIP. (To determine the exact number of times FCoV mutates into a form capable of causing FIP, add the times such mutations occur in a resistant cat.)

As a word problem, the math itself is not too complicated. The scope of the problem is obvious, even without exact numbers.

Limiting the emergence of variants is the point

The incidence of FIP represents a direct measure of how often one specific group of FCoV variants emerge in cats. Each case (or cluster of cases) of FIP represents a newly mutated variant of FCoV that is newly capable of causing FIP. And FIP is not rare.

I’ve spent the last year lecturing my family and friends and cats about the mutation rate of FCoV, pleading for everyone to do as much as possible to limit COVID-19’s infection cycles.

Yes, it’s true that FCoV and COVID-19 are only distantly related. (Metaphorically, about as distantly related as domestic cats are to bobcats.) But if the mutation rate of COVID-19 is even a fraction of what is seen with FCoV, the risk of new variants surges with each surge of infections.

While it is scientifically inaccurate and somewhat irresponsible to claim that more dangerous COVID-19 variants are inevitable if infections continue, it is equally inaccurate and irresponsible to claim that more dangerous variants are impossible. This, also, is the point.

A slightly overweight cat (sorry, Duchess, but it's true) is standing on her hind legs with her front feet braced against a closed window. She is silhouetted, and grass, shrubbery, and a wooden fence are visible outside.

P.S. Marie and Duchess (Dutch) would like me to add that they are very good listeners, all the time. It’s just that they prefer listening to things other than my voice.


Addie, D., Belák, S., Boucraut-Baralon, C. Egberink, H., Frymus, T., Gruffydd-Jones, T., Hartmann, K., Hosie, M. J., Lloret, A., Lutz, H., Marsilio, F., Pennisi, M. G., Radford, A. D., Thiry, E., Truyen, U., & Horzinek, M. C. (2009). Feline infectious peritonitis: ABCD guidelines on prevention and management. Journal of Feline Medicine and Surgery 11, 594-604. doi: 10.1016/j.jfms.2009.05.08

Coronaviridae Study Group of the International Committee on Taxonomy of Viruses (2020). The species Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2. Nature Microbiology 5, 536-544. https://doi.org/10.1038/s41564-020-0695-z

Decaro, N. & Lorusso, A. (2020). Novel human coronaviruses (SARS-CoV-2): A lesson from animal coronaviruses. Veterinary Microbiology 244(2020). 1-18. doi: 10.1016/j.vetmic.2020.108693

Emmler, L., Felten, S., Matiasek, K., Balzer, H.-J., Pantchev, N., Leutenegger, C., & Hartmann, K. (2020) Feline coronavirus with and without spike gene mutations detected by real-time RT-PCRs in cats with feline infectious peritonitis. Journal of Feline Medicine and Surgery 22(8). 791-799. doi: 10.1177/1098612X19886671

Kipar, A. & Meli, M. L. (2014). Feline infectious peritonitis: Still an enigma? Veterinary Pathology 51(2). 505-526. doi: 10.1177/0300985814522077

Pedersen, N. C. (2009). A review of feline infectious peritonitis virus infection: 1963-2008. Journal of Feline Medicine and Surgery 11. 225-258. doi: 10.1016/j.jfms.2008.09.008.

Pedersen, N. C., Liu, H., Scarlett, J., Leutenegger, C. M., Golovko, L., Kennedy, H., & Kamal, F. M. (2012). Feline infectious peritonitis: Role of the feline coronavirus 3c gene in intestinal tropism and pathogenicity based upon isolates from resident and adopted shelter cats. Virus Research 165, 17-28. doi: 10.1016/j.virusres.2011.12.020

Robson, F., Khan, K. S., Le, T. K., Paris, C., Demirbag, S., Barfuss, P., Rocchi, P., & Ng, W.-L. (2020). Coronavirus RNA proofreading: Molecular basis and therapeutic targeting. Molecular Cell 79, 710-727. https://doi.org/10.1016/j.molcel.2020.07.027

A Deer in the Suburbs and a Science Major in the Humanities

We live in the suburbs. In the most suburban of suburbs. Our house sits in the end of a cul-de-sac within easy walking distance of two schools, three strip malls, an embarrassment of restaurants, a clamor of gas stations, a smallish city park, and a pair of naval bases.

Suburbia hasn’t overrun all of the fields in our area, nor every wooded lot, but there’s nothing that resembles a wilderness corridor. So the young stag that landed in our yard, in October of 2019, had scrambled across miles of sidewalks and pavement before getting trapped in our cul-de-sac and scraping over our fence.

Only to find more fence, on the other side.I don’t know why the deer decided to stay. Maybe he was exhausted. Maybe he didn’t like how it felt, going over a fence without knowing what was on the other side. Maybe he was relieved to find a yard with no dogs, a pair of small water gardens, some weedy pollinator beds, and a few spots of semi-cover.I was delighted to have a deer guest. Even more delighted to run into an animal control officer who was cruising through the cul-de-sac. She had been alerted to the deer’s mid-morning residential antics and seemed delighted, herself, to find him. She advised me to let him rest for the day, if he would, then open the gate at dusk so he could find his way out. I did, and he did.

In this metaphor, I am neither the deer nor the suburbs. I’m the long-unemployed, middle-aged woman who lives on a cul-de-sac, is trying to give her yard back to the earth, and needs a new skill set.

I have a bachelor’s degree in biology (BS), a doctor of veterinary medicine degree (DVM), and obsessive compulsive disorder (OCD). I’m a BS DVM OCD.

I didn’t know about the OCD until I was in my late twenties, though it started affecting my study and work habits while I was in school. I floundered through an internship, where the pace and stress exacerbated my symptoms and resultant anxieties, then lucked into a great job.

I loved my job and my clients and my patients, and I developed coping mechanisms for the OCD and anxiety. But love and coping mechanisms only got me so far. Eventually I fell apart, changed my work schedule, and fell even more apart. I retired from veterinary practice when I was a young veterinarian, and I’ve been unemployed since.Unemployed, but not idle. I’ve taken care of myself, my family, and my tiny acre of world. And I’ve written many words.

Poetry, fiction, creative non-fiction, nature rambles, random histories of veterinary medicine, random histories of randomness. For more than a decade, I collected thoughts into words and words into files and researched whatever caught my interest. I submitted and published some of my writing, and I was once paid $5 for a poem.

And, while I’ve stopped submitting and publishing in recent years, I’m still writing. Since January of 2020, I’ve been studying professional writing through Old Dominion University’s online Graduate Certificate program.

A science major in the humanities silo. What next?

Hopefully, next will be a yard given back to the earth, a deer surrounded by less fence and more wilderness, and a world without educational silos. (More on these in later posts.)

Mine is a story of immense and unearned privilege, but it is also a story of gratitude and listening. My hope is that, in the end, it will be a story of kindness.

I regret that I do not have a list of links for this post. Much of my reading, over the past two years, has been books instead of internet content. Here are a few of them. If you’ve read these books, I would love to hear your thoughts. Recommendations for further reading are always welcome.

Cultures and Organizations: Software of the Mind by Geert Hofstede, Gert Jan Hofstede, and Michael Minkov

How Forests Think: Toward an Anthropology Beyond the Human by Eduardo Kohn

From Black Codes to Recodification: Removing the Veil from Regulatory Writing by Miriam F. Williams

Silent Spring by Rachel Carson

Historical Capitalism by Immanuel Wallerstein

Trans-Kin: A Guide for Family & Friends of Transgender People edited by Eleanor A. Hubbard and Cameron T. Whitley

The Rhetoric of Risk: Technical Documentation in Hazardous Environments by Beverly Sauer

The Structure of Scientific Revolutions by Thomas S. Kuhn

A Few Butterfly Answers

I ended yesterday’s post about Black Swallowtail Butterflies with a few questions:

I wonder if there is enough summer left for them? Will they emerge and mate this year? Or will they wait until spring, pausing the cycle as they sleep through winter’s dreary interlude?

Chrysalis August 26

This morning, the yard answered with uncharacteristic directness. There is definitely enough summer left — plenty of time for another generation of swallowtails.

Butterfly August 27

Butterfly August 27

Butterfly August 27

Of all the remaining chrysalises, why should the one I photographed yesterday be the one to open today?

Butterfly August 27

Maybe because I had some time available today, for research? Why else would she allow me to photograph the strange fork at the end of her proboscis? I’ve noticed something similar before, but not on all of the butterflies. What’s going on here?

Butterfly August 27

This afternoon I learned that many species of butterflies emerge with their proboscises incompletely fused. After emerging, they mechanically connect the two halves, forming a tube. This has to be done fairly quickly, or the butterfly may end up with a permanently divided (and therefore non-functional) proboscis. In the above photo (taken only minutes after emergence), the process simply wasn’t complete.

The following enlargement, cropped from one of yesterday’s emergence photos, shows the groove that results when the two halves of the proboscis are properly connected. (The tip of this proboscis had a tiny fork remaining, evidence that the butterfly still had a bit of work to do.)

Butterfly 2 August 26

So much complexity, packed into so small a creature. Wonders and miracles in every detail.

Butterfly August 27

Anaxyrus (formerly Bufo)*

Toad May 2

Early in May I found this little toad while I was mowing. After taking a few photos, I helped it into a flower bed and continued mowing, planning out a blog post as I made circuit after circuit around the yard.

I thought it would be a fun exercise to identify my toad. In the past, I’ve had good luck identifying reptiles and amphibians using the information provided on the Virginia Herpetological Society’s website, so I started there.

Have a look at this page from the website, which outlines the anatomy of a toad’s head, particularly the cranial crests, postorbital ridges, and parotid glands. The next page illustrates how these structures help identify three of the six species of toads found in Virginia.

Based on a visible (but not prominent) cranial crest, I narrowed the list of possibilities to either an Eastern American Toad or a Fowler’s Toad. But the pertinent detail for separating these two species, whether or not the postorbital ridge contacts the parotid gland, was not discernible. Falling back on secondary characteristics, I spent some time counting the number of warts in each of the toad’s spots. One or two warts per spot indicates an Eastern American Toad, while Fowler’s Toads have three or more. My toad had one or two in most of its spots, but three in a few. Since the two species are known to hybridize, was this inconsistency enough to identify my toad as a hybrid?

Two of the other listed characteristics aren’t visible in my photos. I can’t say whether my toad had spots on its chest and abdomen, nor if it had any enlarged warts on its tibia. (No enlarged warts are visible in my photos, but the photos do not show the full length of both tibias.)

Having exhausted my vague knowledge of toad anatomy, but still without a definite identification, I was curious as to whether an expert might have better luck. I sent my photos to the Virginia Herpetological Society’s e-mail identification resource, and their prompt response said my toad was likely a Fowler’s Toad. But they added a note: “Toad ID can be a bit tricky…”

Toad May 2

* In the last decade, genetic findings have shaken up the world of toad nomenclature. One of the changes removed some North American toads from the genus Bufo and shifted them into a new group with an old name, Anaxyrus. This article provides a good overview. So, for most of my Virginia toads, Bufo has been reduced to a parenthetical:  Anaxyrus (formerly Bufo). I feel a bit bereft, as Bufo was one of the few genus names I had bothered to memorize, but I suppose Anaxyrus is easy enough to remember. Except, I’m not quite certain why I would ever need to remember the genus names of North American toads…

A Mammal Mystery (and a Dilemma)

This week I spent two afternoons at Back Bay National Wildlife Refuge. The first visit was cold and windy with heavy, low-hanging clouds. My photos from that day are grainy and blurred, including several photos of a rather large mammal crossing one of the many open areas of water.


At first I thought the creature was an otter. It was too big to be a muskrat, and the habitat was wrong for beaver.

But, what about the shape of its head? Doesn’t look like an otter’s head…


Which leaves me with nutria. (Please comment if you can correct or confirm my guess!)


I returned the next day, lured by warmer temperatures, clearing skies, and continuing curiosity. The animal wasn’t there when I arrived, so I walked the other trails for a few hours and circled back at sunset for one more try. By then the light was even worse than the previous day, so I almost missed the familiar form. Forms, because there were two.

Nutria Nov 5

I took a few photos, though I knew it was too dark for my camera’s lens, and I was on the point of leaving (the refuge closes at dusk) when smaller versions of my mystery mammals appeared.

Nutria Nov 5

The waning light defeated my camera, so all I have to share are shadows and silhouettes. My photos don’t show how the young animals played in the water, how they chased each other in widening ripples. How they ventured into open water, then hurried back to the safety of their parents.

I watched, enthralled, until the sun’s light disappeared completely. The scene was charming. Baby animals are always charming.

Except, in the case of nutria, charm quickly fades.

I have mixed feelings about eradication programs aimed at invasive species. Nutria undoubtedly wreak havoc on marsh ecosystems, but what are the chances they can be eradicated permanently? And what is the cost? The bottom line is that all ecosystems change. Coastal ecosystems, in particular, are under immense pressure. Can we hold back the tide? Should we? I’m not proposing that we do nothing, but I suspect eradication is not a sustainable goal.