COVID-19, Pets and Other Animals
Can Cats and Dogs Get COVID19?
The short answer is that cats are especially susceptible to SARS-CoV-2 infection and are able to transmit it and contract it from humans. Dogs are less susceptible to infection, but they are capable of doing so. More research is needed to determine how likely dogs are to transmit the virus or contract it from humans. Many other animals are also susceptible to infection, some highly so and some less so, and, based on the latter two papers discussed below, all vertebrates should be presumed to be susceptible unless there is solid evidence that they cannot become infected. So, if you are quarantined or self-isolating, your pet should be quarantined and self-isolated (with or seperated from you as your living conditions and isolation conditions allow) as well, so as to prevent spread to others. By that same token, you should observe the same distancing and other precautions for your pet as for yourself to protect your pet. And, by all means, do not pet someone else’s pet or a stray animal, especially a cat!
The long answer is that we know many animal species are susceptible to SARS-CoV-2 infection. Afterall, the virus originated in a species of bat (the horseshoe bat) and most likely made its way to humans via an intermediate animal that lives in proximity to that bat. Recent highly-reliable reports have also confirmed transmission from humans to tigers and dogs. And now, we have studies that also confirm that ferrets, cats and dogs are all susceptible to SARS-CoV-2 (the virus that causes COVID-19) infection and that suggest that a much broader range of animals is also likely to be susceptible. (I note at the outset that none of the papers discussed here have yet been formally peer reviewed, and are available only as pre-prints. However, they each involve multiple authors (a sort of peer review in and of itself) and are generally considered reliable.)
The first study, published March 31, 2020, involved a series of experiments on live animals–ferrets, cats, dogs, pigs, chickens and ducks. For the dogs (beagles, in this case), pigs, chickens and ducks, five of each animal were innoculated nasally with SARS-CoV-2 and housed with two un-innoculated animals. Nasal and rectal swabs were collected every other day for 14 days, and an antibodies (serological) test was run on day 14. Except for the dogs, none of these animals tested positive either for viral RNA or antibodies, indicating that none of those animals became infected despite being innoculated with the virus. This suggests that neither pigs, chickens, nor ducks are particularly susceptible to infection, at least intranasally. (Of course, this is a very small sample size and susceptibility is not an either/or concept but rather is a matter of degree, so caution is warranted.)
As for the dogs, neither of the un-innoculated dogs tested positive either for viral RNA or antibodies, meaning that dog-to-dog transmission did not happen in this small sample. For the innoculated dogs, three positive for viral RNA on their rectal swabs (at day 2 for two of the dogs and day 6 for the third one) and two tested positive for antibodies. One of the viral RNA positive dogs was euthanized on day 4 and several of its organs and tissues tested. None of the tested tissues or organs were positive for viral RNA. These results suggest that dogs (beagles, at least) are susceptible to infection, although perhaps not highly susceptible. Given the small number of dogs used in this experiment and in light of the Hong Kong report linked to above, additional studies would be needed to rule out the possibility of dog-to-dog (or dog-to-human, or vice versa) transmission. So, that remains an open question.
The cat and ferret experiments were more involved and included additional experiments. For the cats, 5 were innoculated with the virus, and an un-innoculated cat was placed in a cage next to each of the innoculated cats. Two of the innoculated cats were euthanized on day 6, and infectious virus was found in several tissues (mainly in the nasal region and just below it). By day 5, all three of the other innoculated cats and one of the un-innoculated cats had viral RNA in their feces. All of the remaining cats with viral RNA were euthanized on day 11, and viral RNA was found in several tissues. The remaining cats were euthanized the next day and viral RNA was found in several of their tissues. Two of the exposed, un-innoculated cats were the only cats not to test positive for viral RNA. One of those two did test positive for antibodies. These results suggest (a) that cats are highly susceptible to SARS-CoV-2 infection, and (b) that they are capable of transmitting it to each other via respiratory droplets (and, by extension, to humans or others).
The ferret experiments differed in several respects from the other experiments. For example, they did not place un-innoculated ferrets next to innoculated ferrets to assess transmissibility. Infectious virus was found in all (innoculated) ferrets, and they all developed antibodies. The researchers also took samples from various tissues and concluded that the virus can replicate in the ferret upper respiratory tract but not in the other organs they sampled. These results suggest that ferrets are highly susceptible to SARS-CoV-2, but no conclusions about transmissibility among ferrets can be drawn from this study.
The second study was published on April 18, 2020. That study was an altogether different sort of study. No animals were harmed in performing it. A large team of researchers that spans the globe and its top universities and research centers reviewed the DNA sequences of 410 vertebrates to assess whether their cells contained the right chemicals to allow infection.
Specifically, an enzyme called Angiotensin I converting enzyme 2 (ACE2) sits on the membrane of various cells located throughout the human body, including in the lungs, GI tract, testes, brain and many other sites. SARS-CoV-2 has, among other structures, “spikes” on its surface. If you’ve seen an illustration or image of the virus (or any coronavirus), these are the 100s of appendages that you see coming out of the spherical structure that give it its crown- (i.e., corona-) like appearance and name. When one of these spikes comes into contact with ACE2 (and only ACE2), they stick to each other. Because ACE2 sits on the cell membrane, the virus can use this as a point of entry into the inside of a cell and can either inject its RNA into the cell or burrow itself into the cell. (And the converse is also true, that without ACE2-spike binding, there can be no infection, which is why most of the vaccines under development are specifically targeting the spike.) Once inside, it can do its normal virus business–re-writing the cell’s software to produce more virus to further its spread and reproduction within the body and to new hosts.
Key amino acids on the spikes bind to greater or lesser degrees with counterpart amino acids on the ACE2. The more of these key acids that make contact with their binding counterparts and the stronger the bond that is formed upon such contact, the more likely infection is to occur. Humans are not the only animals to have ACE2. In fact, many (maybe all?) vertebrates have some version of ACE2 in their bodies. However, as a consequence of their separate evolutionary paths, most ACE2 versions are made up of different amino acids than human ACE2. Some of these differences are immaterial–the substituted amino acid is just as “sticky” as the human version. Other substitutions may actually repel their counterparts in the spike. And many other substitutions will fall somewhere between those two extremes. Yet another consideration is that certain amino acid combinations seem to be more important than others in ensuring a bond between ACE2 and a spike.
In this study, the authors reviewed the DNA of the versions of ACE2 possessed by 410 unique vertebrate species to determine how close the match was, whether substitutions were more likely to bind or repel their counterparts, and whether more critical amino acids were present, in order to estimate how likely a particular animal’s version of ACE2 is to bind with the SARS-CoV-2 spike. They then assigned each species to one of five categories of likelihood of susceptibility ranging from “Very High” to “Very Low”.
The results are shown on page 25 of the pre-print, and they are fascinating. First, you should note there is not much difference in ACE2 within different animals of the same taxonomic family (other than bats, which we will get to in the next paper) or even among closely related families. So, for example, on the critical binding amino acids displayed in the table, human ACE2 is identical to that of nearly all the studied apes, gorillas, bonobos, monkeys and other primates. The three studied camel species had identical ACE2, as do donkeys and horses. (This pattern also shows up in the third study, discussed below.) From this, we should not expect much variation in susceptibility from, say, one dog or cat breed to another.
Here are some of the results for some of the animals humans often interact with (either as farm animals or pets):
–Very High or High Susceptibility categories–I didn’t recognize any pet or farm animals in this category.
–Medium Susceptibility category–cows, goats, cats, and sheep.
–Low Susceptibility category–dogs, donkeys, horses and pigs.
–Very Low Susceptibility category–ferrets and, interestingly, the horseshoe bat, which is believed to be the specific bat species from which SARS-CoV-2 originated.
Since we know, from the first study, that ferrets are, in fact, highly susceptible and, from other research, that horseshoe bats can contract and spread SARS-CoV-2, the fact that these are among the least susceptible animals tells us either that nearly all vertebrates are likely to be susceptible or that ACE2/spike binding is not the entire story. I suspect the answer is both. For example, some animals that are susceptible aren’t as likely to spread it because they don’t shed the virus in the same way. Cats cough, sneeze, lick each other and hiss and dogs bark . . . directly at each other even . . . often at the same time as each other. All of these are probably better means of transmission than a horse’s occasional snorts or “talking”, which are often aimed at nothing and noone in particular. Cows moo, but not necessarily with the same force as a dog bark or cat hiss and not, in any event, aimed at another cow or person. There are undoubtedly other factors at work as well.
The third study, published on April 20, 2020, was similar to the second one in that it was based on the genomes of several species. However, this study was especially focused on the originator of the virus (and the previous SARS-CoV-1)–bats. The thrust of the third paper is that ACE2 in bats has been evolving at a much faster clip than in other animals, suggesting that they are especially susceptible to a range of SARS-CoV viruses and have adapted over time to them. Figure 1 shows this dramatically, as the table on the left (showing other animals) has much more white space (indicating a match or close match) than the one on the right (showing bat species only), even at a first glance. The results show that, while very little inter-species variation exists among evolutinarily close species (humans and bonobos, for example), there is wide diversity in ACE2 across the 90 different bat species examined. Figure 1 (near the end of the paper) reports results of their multi-species study of seven critical ACE2-spike binding amino acid residues and reports variations as compared with human ACE2-spike amino acid residues. (Amino acid “residue” is just the original amino acid, minus the chemicals that it loses when it joins with another amino acid.) In their model, only two fox, wolf, cat or ferret ACE2-spike residues varied from human ACE2 (one of which was not significantly different). (I don’t believe they included dog residues, so I included fox and wolf as approximations.) Cow and pig ACE2-spike residues varied in only one of the residues. Many other species detailed in Figure 1 appear to differ little from their human counterparts and thus may be susceptible to SARS-CoV-2 infection.
Thus, many animals are likely susceptible to COVID-19 and are likely capable of transmitting or contracting the virus that causes it. Although there are many implications from these findings, the most immediate one is to observe all recommended distancing and other applicable precautions that apply to you for your pet as well and avoid contact (both for you and your pet) with animals that are not yours.
I have a 20 lb poodle age 18 with Cushings taking Vetoryl for months but symptoms are not getting much better lots of swollen tumors all over body and panting . Please take me to best vet advice 949-444-9067- I will take my beloved service dog anyplace to help her symptoms . Jerri Beardslee San Clemente CA please text me because I get too much junk email or use firstname.lastname@example.org. Cell 949-444-9067 . Thank you
Trilostane does not require an induction phase as mitotane does. However, small adjustments to the dose of trilostane are often needed early in treatment, and over the life of your dog, other changes may be made based on routine monitoring of blood tests and how well the clinical signs of Cushing’s disease are being controlled. Trilostane may also need to be administered up to twice per day for the rest of your dog’s life.
My Eskimo, 13 this November, has been taking flax lignans 25mg morning and melatonin 5mg at night for 3 wks now and already I see the last hot spot healed. Energy level is still low; he sleeps most of the day. Panting at night has also decreased noticeably. I also giver him Prana Pets Adrenal Support drops, 3-5 daily. I give the lignans with a little yogurt with live cultures for better aborptions. Any other advice would be very welcome.
That’s great to hear you’re having some improvements! What is the weight of your dog? Have you talked to your vet or the company you purchase lignans/melatonin through to see about potentially lowering the dosage of melatonin?
Now taking combo pill 20 flax lignans with 3 mg melatonin since one month. Night panting still unresolved but thirst and hunger normal and energy good. Weight 29 and steady. Any questions or comments I will be glad to answer and to share treatment ideas. I want to talk to others using dietary plans instead of Vetoryl or Trilostane, which I consider too hard on the system. 949.231.7518 Sean
melatonin reduced to 21/2 mg melatonin at night. Added fresh dandelion greens chopped in his food : chicken innards lightly cooked to make broth. He is doing well. Exercising morning and afternoon. Will be 14 in November. Give probiotic several times/wk. No excessive drinking. No panting at night. Hair loss minimal but no skin infections. If dandelion greens not available, use drops available in many liquid formulas. Available to help if you wish to text 949.231.7518 Sean