Though I’ve kept a careful watch, I haven’t seen many black widows in the last few years. In fact, I’ve congratulated myself for eliminating the kind of places they prefer. Which should have raised alarms. I rarely congratulate myself without stumbling, almost immediately, into awkwardness.
Last fall, as we checked off our list of winter preparations for the yard, I found a cluster of delicately spiky spider eggs. They looked like burrs, and I made a distracted mental note to see if the internet could tell me what kind of spiders make burr-shaped egg sacs.
Of course, my distracted mental note slipped into foggy forgetfulness. Then, while doing something completely non-spider related about two weeks ago, I found two more burr-shaped egg sacs in a messy web woven between the spokes of a bicycle I never ride. (The bicycle is stored in our Garage of Entropy, which we try to keep tidy despite the garage’s preference for chaos.)
This time I made a firmer mental note, and later that day an internet search told me exactly what kind of spider had made the fascinating eggs in my garage. A brown widow. (Arachnophobes, look away!)
I think this is a good place for another butterfly…
According to bugguide.net (one of my favorite research resources), brown widows are an introduced species in the US: “It was introduced in Florida and has since been observed moving north through Georgia, and into South Carolina; it has also been officially recorded in California, Alabama, Mississippi, and Texas.” Obviously, this information is a bit dated. Our brown widows are two states north of South Carolina.
I use the plural “our brown widows” with a shiver.
Now that I know what to look for, the garage and yard are positively infested.
Bugguide.net says that brown widow spiders are one of the “most human-adapted” introduced species. What’s more, “It reproduces frequently and disperses rapidly, making it nearly impossible to control.” Each female spider, the information page notes, can produce up to 5000 young per season, and females can live as long as three years.
Despite a years-long effort to subdue my arachnophobia, these brown widow photos make me sweaty and anxious. How about a tufted titmouse, to break the tension?
“The bite of a brown widow spider is minor in comparison to that of a black widow. Although one frequently cited study demonstrates that, drop per drop, brown widow spider venom is as toxic as other widow species, venom toxicity is only one aspect when considering a spider’s bite potential. An African study with 15 verified bites demonstrated that the brown widow spider bite victims showed none of the classic symptoms of latrodectism, a response induced by neurotoxins in the venom of spiders in the genus Latrodectus (e.g., brown widows, black widows [L. mactans], Australian redbacks [L. hasselti], European black widow [L. tredecimguttatus], and New Zealand’s katipo spider [L. katipo]). The reason for the weaker effect of brown widow bites on humans is possibly because the brown widow does not have or cannot inject as much venom as its larger relatives. The two major symptoms of a brown widow bite were that the bite hurt when it was inflicted and it left a red mark. These two symptoms are not much different from the bite of normal household spiders. However, there is one recent report of a verified brown widow bite manifesting in more severe symptoms that required hospitalization of the bite victim.”
“Currently, the brown widow spider does not pose the same medical concerns as the black widow spider. Bites from the brown widow do not cause the same symptoms as the black widow. Brown widow spider venom is twice as potent as black widow venom, it is believed the brown widow does not inject the same amount of neurotoxin. This, results in the decreased severity of symptoms in the form of cramping or nausea. This species is timid avoids human interaction. In fact, males and immature brown widow spiders do not bite at all. This species will fall to the ground in a ball as if it were dead as a defense mechanism, but should not be handled. Brown widow spiders bite out of defense, and it will only occur by mature females.”
“Symptoms: Black widow bites to humans may result in a variety of systemic symptoms (Sampayo 1943 and 1944). Typically, brown widow bites are not as serious as those of the black widow, and pain is usually restricted to the area immediately adjacent to the bite wound (Almeida et al. 2009, Foelix 2011, Suchard 2009). Also, approximately 15% of bites may be “dry” with no venom injected (Reyes-Lugo et al. 2009). However, some bites do cause the more severe, systemic symptoms characteristic of black widows (Arnold and Ryan 2009, Goddard et al. 2008, Müller 1993a).
“Müller (1993a) reported the incidence of the following systemic symptoms from 15 cases of brown widow bites in South Africa: generalized muscle pain and cramps (2), abdominal pain and cramps (4), weakness in legs and difficulty in walking (2), pain in regional lymph nodes (2), and raised temperature (2).”
While some pest control sites list brown widow spiders as living in central and eastern Virginia, the Virginia Cooperative Extension information page about widow spiders lists brown widows as mostly occurring in Florida and Texas, noting that black widows are the primary widow species found in Virginia. So I’m considering this post as a sort of public service message for readers living in Virginia. Brown widows are here (and likely have been here for a while).
And now, after all of these photos of brown widow spiders and their spiky eggs, I think it’s best to close with a few images that don’t make me feel shivery and icky inside…
Here are some links to articles that are more interesting and more important than what has been happening in my yard:
Note: I am implementing two practices in this blog post, practices I plan to continue. The first is evident in my photo captions, which are image descriptions for the visually impaired. The second practice will provide content warnings for my lists of links. I’m ashamed that I didn’t implement both of these practices earlier.
I would appreciate feedback regarding my image descriptions and content warnings. I’m happy to add more information and/or edit as requested, so please comment with suggestions.
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.
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.
Actually, they’re not very good listeners at all.
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.
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?
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.
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.)
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.
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 manul, Otocolobus 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.
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.)
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.
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.)
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.
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.
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.
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.
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.
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.)
Between 60% and 90% of the cats in shelters or in multi-cat environments will, at some point, become infected with FCoV.
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.
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.
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
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
It’s been two years since my last post. Two entire years of an ongoing search for balance. Any and all versions of balance.
In this search, as with everything else, I fail more often than succeed. But failure is, of itself, productive.
Except, the word “productive” is problematic, isn’t it? What, exactly, constitutes productivity? If the results of my labors are largely invisible, even intangible, have I truly been productive?
“What Heisenberg discovered was that the limit to our ability to observe the universe determines the boundaries of reality. Physical reality and observability are tied together. If you and I cannot observe it, it does not exist… or is it perhaps, if it exists, it is because you and I observe it?” Evan Harris Walker in The Physics of Consciousness: The Quantum Mind and the Meaning of Life (1)
Maybe some adage applies, based on the laws of thermodynamics. Maybe I create and destroy in equal measures, so the sum of my productivity is zero. A cancellation of balances. Any and all versions of balance.
Or maybe words matter less than I imagine, and imagination matters more, when shaped into words.
“…nature is a chaos of forms and colors and shapes and forces, and the various ways in which that chaos has been untangled and made legible should never be taken as nature’s truth but rather as nature’s possibility within a human imaginary.” Rachel Poliquin in The Breathless Zoo: Taxidermy and the Cultures of Longing (2)
Independent of my blog activity, independent of words and definitions, the yard’s wheel bugs flourish and die and flourish and die with seasonal regularity.
The first generation I followed, in the summer of 2017, never knew life without my looming camera-presence. I found their egg clusters in the winter of 2016 and photographed them through their own egg-laying.
But I largely abandoned my camera the next year, so the next generation escaped my looming camera-presence. Can I prove that they flourished, without photos? That they were overtly and conspicuously productive? Populating the live oak and pear tree, the wax myrtles and pollinator beds. Always hunting and molting, destroying and creating.
Always, in my imagination, a chitin metaphor to be used in a future poem or blog post.
When I began planning this post, my long-awaited wheel bug post, I discovered what I should have expected all along. The yard’s current wheel bugs, unaccustomed to a looming camera-presence, are difficult to photograph.
These last photos, all taken yesterday, are the result of two weeks’ searching and stalking and standing quietly under the live oak. Two weeks for a set of blog photos.
Two weeks of productive creativity. Because I did other things, during those two weeks, but I approached each task with a bit more creativity than usual.
And now, a blog post! At last!
A brief moment of imperfect balance, two years in the making. Word-shaped and shared.
When we lost Scamper last spring, we were already in the process of losing Vanna, too. Vanna had been diagnosed with intestinal lymphoma two years earlier, and, after thriving for longer than expected under the excellent care of her veterinarian, she was beginning to lose ground.
Vanna had been my mother’s cat, which undoubtedly contributed to the depth of my attachment. She was a living link to an unrecoverable past.
What’s more, she flourished in Virginia. In Tennessee, among Mother’s four cats, Vanna had been the neurotic one. The reclusive, skittish one, rarely glimpsed by visitors.
When the cancer finally overwhelmed her, almost exactly a month after we said goodbye to Scamper, I stumbled into another depression.
Our lively household of three cats had been reduced, in a month’s time, to a quiet household of one. I couldn’t write about Vanna’s death. Could barely talk about it.
Within a year we were losing Sabrina, too.
Sabrina was the sweetest, gentlest cat I’ve ever owned. Perhaps the sweetest and gentlest cat I’ve ever met.
She and Scamper had been rescued, at only a few weeks of age, from a construction site.
She suffered a serious injury at about twelve weeks old, losing one of her eyes and undergoing multiple surgeries to salvage the vision in her other eye. She lived the rest of her life with a slowly advancing cataract, but didn’t seem bothered by her limited vision.
She played and romped through adolescence, survived an episode of liver failure in early middle-age, and settled into her senior years with the same calm serenity she had shown from kittenhood.
I had hoped, of course, that we might have a few more years with her, after losing Scamper and Vanna in such close succession. But in November Sabrina began showing signs of discomfort while defecating, our first hint of the rectal tumor that, while repeatedly testing benign on biopsy, was likely malignant at its core.
By March she was too uncomfortable to continue. So I made yet another last trip to our wonderful vet and said yet another goodbye.
How many goodbyes, now? Four, since starting this blog. Indigo. Scamper. Vanna and Sabrina. Before them, Spice.
Spice’s years as a feral cat ended in 1994, the moment I saw her huddled in the back of a cage with a vast, scabbed wound covering her neck and shoulders. She nosed forward to sniff my hand, speaking in unmistakable cat-language. My name is Spice, and I’ve been waiting for you.
Spice was my constant companion for fifteen years. We shared a dorm, an apartment, a duplex (with my future husband), and, in her final years, a house in the suburbs.
She taught Sabrina and Scamper how to be cats, and they kept her young longer than time should have allowed.
Losing her closed a door on my twenties and thirties. I would never be twenty or thirty again, and I would never have another cat like Spice.
All those that came before
Before Spice? The list is long, stretching through memory into the hazy nostalgia of childhood. Mischief and Jackson. Diana. Gizmo and Annie. Morgan and Shere Khan. Sadie and Daisy. Sheena and Poppy. (This list is far from complete, and includes none of the dogs. I’ll save dogs for a later post.)
Many of our cats were named for characters in books and movies. Some came to us already named, relinquished by owners who could no longer keep them, owners who were happy to let an eager young vet assistant adopt the cats they were losing to eviction, a family illness, or one of life’s other jarring turns.
Some of the cats materialized out of thin air, simply showing up in the yard. Others were dumped on the driveway, plucked from parking lots, and chased down in ditches by a trio of sisters who found it biologically impossible to just keep driving. Mother simply sighed and made room for them all, a tide of cats drifting in and out of our lives, in and out of the house each morning and night.
They were never all in the house at the same time, thankfully. Most preferred the yard, sheds, and pasture, most of the time.
Cats have been one of the few constants in my life. They’ve shared all of my memories, every place I’ve ever called home, and almost every job I’ve ever had. I don’t know how to be without cats. In the end, loving cats is part of how I love myself. So…
Duchess and Marie (two of a group named for the Aristocats) were trapped in a warehouse in early June, along with two male kittens about the same age. I saw their photo on social media, contacted Cat Team 7, and the rest is happy history.
They were quite shy, in their first weeks here.
Duchess (or Dutch, because sometimes she’s more Killjoy than Aristocat)
Marie (just Marie, because it fits)
It didn’t take them long to settle in. They have plenty of windows, soft beds, toys, and treats.
They are closely bonded, more dependent on each other than Sabrina and Scamper were. They’re rarely apart.
(Except when Marie plays fetch. Dutch, who has no interest in fetching, stalks the action until she can tempt Marie into a thunderous, romping game of chase.)
And me? I’m sharing my life with cats again. That’s enough for now.
Recommended reading about topics that are more urgent and more important than my cat memories: