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The FDA has approved India-based Cronus Pharma Specialties’ Carprofen Chewable Tablets (a generic version of Rimadyl—Zoetis PetCare) for dogs.

This nonsteroidal anti-inflammatory drug (NSAID) relieves pain and inflammation associated with osteoarthritis and helps control postoperative pain associated with soft tissue and orthopedic surgeries, according to the Freedom of Information Summary Original Abbreviated New Animal Drug Application.

These tablets can be administered once daily (2 mg/lb of body weight) or twice daily (1 mg/lb). To control postoperative pain, the FDA recommends administering this drug approximately 2 hours before a procedure.

Carprofen Chewable Tablets are scored (except for the unscored 37.5-mg strength), and contain 25, 37.5, 50, 75, or 100 mg of carprofen per tablet. Each tablet size is packaged in bottles containing 60 or 180 tablets.

Carprofen Chewable Tablets should not be used in dogs exhibiting previous hypersensitivity to carprofen and is not intended for use in food-producing animals or in humans.

Adverse reactions to carprofen may include decreased appetite, vomiting, diarrhea, dark or tarry stools, increased water consumption, increased urination, pale gums due to anemia, yellowing of gums, skin or white of the eye due to jaundice, lethargy, incoordination, seizure, or behavioral changes. In rare cases, sudden serious adverse reactions can result in death.

For more information about this new drug, click 

Articles

The new drug has been proven safe and effective in relieving pain and inflammation associated with osteoarthritis.

 FDA approves generic carprofen chewable for dogs

Canine atopic dermatitis is an inflammatory skin condition associated with the production of immunoglobulin E (IgE) specific for a substance that is either ingested or inhaled. Typical signs include pruritus, erythema, lichenification, seborrhea, and lesions from chronic inflammation, licking, chewing, and scratching. House dust mites (HDM) of the 

 genus are the most common allergens recognized by the circulating IgE of atopic dogs. In laboratory experiments, dogs that are sensitized to HDM experience atopic flares when exposed to various species of storage mites. Because storage mites commonly grow on cereals used in commercial pet foods, researchers conducted a literature review to determine whether allergen cross-reactivity could lead to a false-positive diagnosis of food allergy. The results of their study were published in 

The investigators searched two databases for detailed studies using a series of key words. Of 87 identified articles, 10 were selected that were common to both database searches. Five articles reported results from laboratory studies, and five reported on field studies.

HDM was first reported on dry dog food in 1972.

 storage mites were shown to survive and grow on three commercial dry dog foods.

 mites grew on all three dog foods, with the highest numbers of mites found whenever molds had been allowed to grow on the kibble.

In 2015, samples of dog foods stored in nine different sealed plastic bags and in a lidded cup were evaluated to see whether 

 storage mites were discovered in 55% of the bags. Mites had not made holes in the packaging itself but had entered the bags via faulty seals. Lidded cups were not contaminated. The same year, investigators evaluated whether 

 storage mites preferred to grow on protein-, fat- or carbohydrate-rich diets and found they grew best on the dog foods richer in proteins and fat.

Finally, in 2016, several experiments were conducted to evaluate the growth of 

 In the first experiment, mites were found to grow better on green and brown rather than white and red colored kibbles. (Whether the different-colored kibbles had different nutrients was not explained.) The second study found higher mite growth when kibbles were crushed rather than intact, and when the initial mite population density was highest. The third showed that four different strains of 

 mites grew better on crushed dog food than a commercial mite diet. The final experiment confirmed that a high initial mite inoculum leads to a higher final mite count.

In the first field study, 30 purchased and 50 pet owner–obtained commercial dry dog food samples tested with an enzyme-linked immunosorbent assay for HDM were all negative.

In another study, 23 bags of commercial dry dog foods were tested for mite contamination by microscopy.

 Even though the bags were opened and closed twice daily over a 6-week period during this study, storage mites were not discovered.

The influence of different storage conditions on the contamination of dry dog foods with storage mites was first reported in 2008.

 Dry dog food bags were kept for 6 weeks in either laboratory storage with low average temperature and humidity or a ventilated garage with high temperature and humidity. More mites were detected in the bags stored in high temperature and humidity conditions.

In 2011, identical bags of a single commercial dry dog food were stored in 10 different households.

 Each bad was divided equally between the original sack with its reusable seal, a paper bag whose top was rolled for closure, and a plastic box with a sealed lid. These containers were stored next to each other, and the food was sampled every month for storage mite detection. After 3 months, mite numbers were significantly higher in the food samples stored in paper bags (60% of bags had evidence of mites) compared with baseline.

In the last field study, dog owners in eastern Australia provided 20 samples of commercial dry dog foods stored in open bags or storage boxes in home environments.

 The food samples were examined for the presence of storage mites, and a small portion was kept for 2 additional months before their incubation under higher humidity and temperature conditions. Finally, nine new bags of commercial dog foods were purchased and tested as above. Mites were undetectable in any specimens after any of the incubation times. Similarly, storage mites were not observed when opening newly purchased bags or after storing the foods for 6 weeks at room temperature. In contrast, when incubating samples of these foods at high temperature (26 °C [78.8 °F]) and humidity levels (80%), storage mites were present as early as 3 weeks after beginning the experiment and in 78% of foods after 6 weeks of incubation.

Several clear conclusions can be drawn from this literature review. The research shows that storage mites, especially for the most commonly found and studied species 

 can grow in commercial dog kibbles, particularly protein- and fat-rich foods. They proliferate best when the initial contaminating mite density is high, when kibbles are crushed, or when mold overgrowth has occurred due to suboptimal storage. Typically, storage mite contamination is low to undetectable in newly purchased commercial dog food. If bags are stored indoors in temperate conditions, little to no overgrowth occurs. In contrast, when bags are stored in situations with high temperature and humidity, mites can enter through faulty seals and proliferate in the packages.

The allergenic cross-reactivity between the 

 mites have been shown to trigger flares of allergy in laboratory beagles experimentally sensitized with the 

 HDM. Although this cross-reactivity has only been demonstrated in a laboratory setting, atopic dogs with high-levels of 

 HDM–specific IgE are likely to have signs flaring after eating a food contaminated with storage mites. Thus, when performing food trials for the diagnosis of food allergies in dogs (and probably in cats), it makes sense to minimize factors that encourage storage mite proliferation. Using food from newly purchased, sealed bags that have been stored indoors in temperate conditions appears to decrease the risk of mite contamination. A diet trial with home cooked ingredients unlikely to have mite contamination is another option.

1. Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (8): storage mites in commercial pet foods. 

. 2019;15(1):385. doi: 10.1186/s12917-019-2102-7

2. Sinha RN, Paul TC. Survival and multiplication of two stored-product mites on cereals and processed foods. 

 1972;65:1301-1303. doi: 10.1093/jee/65.5.1301.

 mites grown in dog food cultures and the effect mould growth has on mite survival and reproduction. 

 2010;21:58-63. doi: 10.1111/j.1365-3164.2009.00778.x.

4. Hubert J, Nesvorna M, Volek V. Stored product mites (

) infesting food in various types of packaging. 

 2015;65:237-242. doi: 10.1007/s10493-014-9864-1.

5. Erban T, Rybanska D, Hubert J. Population growth of the generalist mite 

) following adaptation to high- or low-fat and high- or low-protein diets and the effect of dietary switch. 

 2015;44:1599-1604. doi: 10.1093/ee/nvv129.

6. Rybanska D, Hubert J, Markovic M, Erban T. Dry dog food integrity and mite strain influence the density-dependent growth of the stored-product mite Tyrophagus putrescentiae (Acari: Acaridida). 

. 2016;109(1):454-460. doi: 10.1093/jee/tov298

7. DeBoer DJ, Schreiner TA. Commercial dry dog food in the north central United States is not contaminated by Dermatophagoides house dust mites. 

. 2001;12(4):183-187. doi: 10.1046/j.0959-4493.2001.00248.x

8. Henneveld K, Beck W, Müller R. Evaluation of storage mites in commercial dry dog food and in the environment as well as their importance in veterinary medicine [in German]. 

 2007;35:325-332. doi: 10.1055/s-0038-1622643

9. Brazis P, Serra M, Sellés A, et al. Evaluation of storage mite contamination of commercial dry dog food. 

. 2008;19(4):209-214. doi: 10.1111/j.1365-3164.2008.00676.x

10. Gill C, McEwan N, McGarry J, et al. House dust and storage mite contamination of dry dog food stored in open bags and sealed boxes in 10 domestic households. 

. 2011;22(2):162-172. doi: 10.1111/j.1365-3164.2010.00931.x

11. Hibberson CE, Vogelnest LJ. Storage mite contamination of commercial dry dog food in south-eastern Australia. 

. 2014;92(6):219-224. doi: 10.1111/avj.12185

Researchers recently reviewed the published literature about growth of storage mites on commercial dry pet foods.

Could storage mites in pet food lead to false-positive food allergy diagnoses?

The first Black man to earn a Doctorate in Veterinary Medicine degree did so 123 years ago, in 1897. Seventy-one years ago, in 1949, the first Black woman followed in his footsteps. It has been 75 years since the establishment of Tuskegee University College of Veterinary Medicine (TUCVM), but African Americans today make up only 2.1% of the veterinarian workforce.

 It’s time for us to address this lack of diversity among American colleges of veterinary medicine.

Despite TUCVM producing roughly 70% of all African-American veterinarians, Black Americans continue to be underrepresented in the profession. In the past 10 years, five new colleges of veterinary medicine were established at Midwestern University, Lincoln Memorial University, Long Island University, University of Arizona, and Texas Tech University. None of these new colleges are at HBCUs.

According to 2019-2020 American Veterinary Medical Association data, 3% of the 13,548 students enrolled in US veterinary schools are Black, with African Americans treading behind all other ethnic-minority groups except for American Indian/Native Alaskans, foreign nationals, and students who choose not to divulge their race/ethnicity.

It is imperative that we address the lack of diversity within the veterinary profession, but to do that we first must address systematic racism and oppression within higher education. The racism, oppression, and bigotry that have been the subject of recent public outcry exist within the confines of classrooms all across America, and lack of representation makes it nearly impossible for Black Americans to pursue a number of careers, including veterinary medicine.

To truly do away with the injustices against African Americans in this country means to provide HBCUs with appropriate funding. Moreover, to increase the number of Black Americans who pursue a Doctorate in Veterinary Medicine degree, there must be more colleges of veterinary medicine at HBCUs. 

It is well past time for another veterinary school at one of our nation’s HBCUs. Take your pick: Delaware State University, Florida A&M University, Lincoln University of Missouri, North Carolina A&T State University, South Carolina State University, Tennessee State University, University of Arkansas Pine Bluff, University of Maryland Eastern Shore, Virginia State University, West Virginia State University, University of the District of Columbia, and many others.

Black lives matter, Black representation matters, and Black veterinarians matter! We are greater than 2.1%.

Jonathan Dumas is a third-semester student at Ross University School of Veterinary Medicine and is the current Student American Veterinary Medical Association/Student Government Association president.

1. Labor force characteristics by race and ethnicity, 2017. U.S. Bureau of Labor Statistics. Published August 2018. Accessed August 11, 2020. 

https://www.bls.gov/opub/reports/race-and-ethnicity/2017/home.htm

2. AAVMC annual data report 2019-2020. American Association of Veterinary Medical Colleges. Accessed August 11, 2020. 

https://www.aavmc.org/assets/site_18/files/data/2019%20aavmc%20annual%20data%20report%20(id%20100175).pdf

One veterinary student explains why establishing veterinary medicine programs at historically black colleges and universities (HBCU) is key to addressing systemic racism within the profession.

Why we need more veterinary colleges at HBCUs

Noted by his peers as one of the 15 most influential veterinarians in North America, Allen Schoen, DVM, MS, walks us through his journey of becoming a pioneer of holistic veterinary medicine. Early on in his career, he tells Dr. Adam Christman DVM, MBA, that he discovered his passion: helping animals that didn’t respond to western medicine.

Recalling this lightbulb moment – Dr. Schoen, who has over 40 years of clinical experience, research and teaching, says he realized he was destined to create a new field in veterinary medicine after attending an acupuncture training course in New York City. Soon after, he followed his heart and embarked on a mission to promote complementary therapies, and eventually helped to set up the first department of veterinary acupuncture outside of China.

Today, Dr. Schoen has the largest holistic integrative veterinary referral practice for both small animals and equine and has written several textbooks and currently hosts his own show, "Awakening With Your Animal Family."

Listen to the full podcast below to learn more about Dr. Schoen’s unique story. If you’d like to be featured on our podcast, 

Podcasts

In this Episode of The Vet Blast Podcast, pioneer of holistic veterinary medicine, Dr. Allen Schoen talks with Dr. Adam Christman about the evolution and continued growth of complementary and alternative veterinary medicine.

Episode 7: Creating a new field in veterinary medicine

All mammals pace their way through similar milestones, from embryogenesis to birth; then infancy, youth, and adolescence; and, finally, maturity, senescence, and death.

 But every species ages at its own clip. Some compress their lives into a couple years, while others, like certain whales, take an entire century to cycle through the life stages.

Because ripening times vary widely among animals, correlating the age of one species with that of another is like comparing apples with oranges. This reality contradicts the age-old credo that we can calculate the human equivalent of a dog’s age simply by multiplying by 7.

Researchers at the University of California San Diego School of Medicine recently created a formula that offers a more accurate comparison of age in humans and dogs. It is based on fluctuations in the way dogs and humans attach methyl groups to the nucleotide bases in their genomes as they advance through the years.

The methylation pattern — or “methylome” — of the cytosine–guanine dinucleotides (CpGs) is an epigenetic mark that modifies gene transcription and thereby regulates the speed at which an organism ages and reaches specific physiologic milestones.

Not only do people and dogs age at mismatched rates, but the two species differ in their racing times between each mile marker. The comparison between them is not linear as the 1:7 years rule of thumb suggests. The data from this study, recently published in 

 illustrates this perfectly. While a 9-year-old dog, for instance, has the approximate genetic wear-and-tear of a 65-year-old human, a canine yearling doesn't equal a 7-year-old child, but instead a 30-year-old human ready to start a family.

Investigators came up with these correlations by collecting blood from 104 Labrador retrievers at different life stages, ranging from 5 weeks to 16 years. The subjects were mostly recruited at canine-centric events, such as dog shows.

Using DNA extracted from whole blood samples, a technique called syntenic bisulfite sequencing was applied to characterize CpG methylomes in regions of the canine genome that mirror those of humans. About 232,000 CpG sites have been found to be conserved between humans and dogs. Of these, 54,469 CpGs were well profiled in both species. Regions included exons, transcription start sites, and CpG chains or “islands.”

The researchers looked at whether the conserved methylation alterations in dogs and humans followed a constant rate of change, and whether this tempo correlated with the lifespan of each species, as is the conventional wisdom.

 For this, they lined up the age of each dog with the average age of its human methylome “twin.” The canine methylomes were also compared with those previously measured in mice.

To resolve whether conserved changes involved particular genetic regions, they coned down their study of CpG methylation sites to 7942 genes for which orthologs were present in all three species. From this, they spotted 394 genes for which methylation values showed conserved age-dependent behavior across species.

These genes occurred within five clusters, primarily developmental in function and concentrated near transcription start sites. Four of these clusters — associated with synapse assembly, neuroepithelial cell differentiation, and anatomic patterning — displayed methylation that amplified with age. The fifth cluster involved leukocyte differentiation and nucleic acid metabolism and demonstrated decreasing methylation with age.

Until now, epigenetic clocks have been used to study methylome data within a species rather than across species. But a review of established methylation values in different species reveals closer epigenetic correlations when using conserved developmental genes (less than 400 in the current study) than when casting a wider genetic net.

Analysis of the data shows that the rate of methylome remodeling is determined not only the lifespan of a species — the shorter-lived the species, the more rapid the remodeling — but also by the timing of key physiologic events.

Tracking changes in how methyl groups attach to DNA strands reveals a conserved, though nonlinear, age-related progression between dogs and people. The study also shows that dogs age more quickly than humans at an early age, then trickle along following sexual maturity.

The highest methylome similarities — and greatest epigenetics-physiology agreement —were observed when pairing young dogs with young humans and senior dogs with aged humans: It’s easier to define a dog in human years at either of these two poles. However, these same genetic comparisons during the intervening adolescent and mature stages are murkier.

One limitation of the study is that it used DNA from whole blood, for which age-dependent drops in leukocyte population occur in both dogs and people. These shifts could influence the findings. Second, the study focused exclusively on Labrador retrievers. Expanding the scope to include other breeds (canine subspecies) could modify the results.

Characterizing epigenetic changes across both breeds and species may help solve more global riddles, such as whether the timing of epigenetic changes early in life influences the overall lifespan of a species, or of a specific individual within a species.

By highlighting conserved patterns of epigenetic changes across species and throughout life, this research suggests that aging is more a continuation of development rather than a distinct process. By matching — or, rather, mismatching — those patterns among dogs and people, we now know that the common question, “How old is my dog in people years?” is not as straightforward as once thought.

Dr. Capuzzi is a small animal veterinarian and journalist based in the Philadelphia area.

Field AE, Robertson NA, Wang T, Havas A, Ideker T, Adams PD. DNA Methylation Clocks in Aging: Categories, Causes, and Consequences. 

. 2018;71(6):882-895. doi: 10.1016/j.molcel.2018.08.008

Wang T,Ma J, Hogan AN, et. al. Quantitative translation of dog-to-human aging by conserved remodeling of the DNA methylene. 

 2020;11:1-10.doi: 10.1016/j.cels.2020.06.006

Alisch RS, Barwick BG, Chopra P, et al. Age-associated DNA methylation in pediatric populations. 

. 2012;22(4):623-632. doi: 10.1101/gr.125187.111

Hannum G, Guinney J, Zhao L, et al. Genome-wide methylation profiles reveal quantitative views of human aging rates. 

. 2013;49(2):359-367. doi: 10.1016/j.molcel.2012.10.016

Maegawa S, Lu Y, Tahara T, et al. Caloric restriction delays age-related methylation drift. 

. 2017;8(1):539. doi: 10.1038/s41467-017-00607-3

Lowe R, Barton C, Jenkins CA, et al. Ageing-associated DNA methylation dynamics are a molecular readout of lifespan variation among mammalian species. 

. 2018;19(1):22. doi: 10.1186/s13059-018-1397-1

Petkovich DA, Podolskiy DI, Lobanov AV, Lee SG, Miller RA, Gladyshev VN. Using DNA methylation profiling to evaluate biological age and longevity interventions. 

. 2017;25(4):954-960.e6. doi: 10.1016/j.cmet.2017.03.016

By tracking age-related progressions in gene methylation patterns of dogs and comparing them with those previously observed in people, researchers have constructed a new “epigenetic clock” for translating dog years to human years.

DNA debunks age-old ratio for dog years to human years 

There are times in practicing veterinary medicine that you just need to stop and think for a bit about the patient you are examining. It is during these moments that a little peace and quiet would be nice.

For me, unlocking the mystery of upper hind end lameness in a horse often requires a tremendous amount of contemplation. I enjoy these cases, but have been known to just sneak off to my office for a few minutes to assimilate the accumulated clues to make a logical decision about what the problem is or what should be done. The more difficult the case, the more quiet I require.

One of my clients is a 5-foot barrel racer who has some world-class horses and is a blast to be around. When Tera shows up with a lame horse, it usually and requires my full concentration. The problem is…Tera is a talker.

When I say she is a talker, I mean this little gal can’t stand a moment of silence. It is almost like she has a pathologic aversion to being in the presence of others with no conversation occurring. She will see to it that something is being said at all times, largely by asking questions. This means that you have to be involved in the process of stamping out quiet with her.

One particular day found me working up a very difficult lameness case for her. I was digging deep into my gray matter trying to piece together the clues to why her 7-year-old gelding was 0.3 seconds off, but the answer was slow in coming. Every time I began to ponder the results of the last portion of the exam, she would sense that things were too quiet and hit me with a volley of questions.

The last thing I wanted to do, of course, was hurt her feelings by asking her to be quiet, so I began looking around for something that would occupy her for a little while as I thought about the problem at hand. She was rambling on about some horse she had ridden 10 years ago that acted a little like this one when it occurred to me that her constantly moving hands were a vital part of her talking arsenal. I began to wonder if the talking would stop if I could somehow still those hands.

As she entered her fifth or sixth paragraph about the horse from 10 years ago, I simply handed her an empty syringe case. She never stopped talking or moving her hands; she simply accepted the case and continued on with the story without so much as a comma. Next, I handed her an empty bottle of carbocaine, which she gladly accepted with her other hand and just rolled right on with the story.

This was actually getting kind of fun. I was beginning to wonder how many things she would hold before she actually looked down to see what they were. So, I handed her a hoof tester, which is used to determine the location of a painful area in the foot of a lame horse. The tester was heavier than the other items and Tera had no readily empty hand to hold it in. This stopped the chatter momentarily, but she simply took the instrument and placed it under her left arm and continued on with the story.

I maintained eye contact with her and made occasional head movements to make her feel as if I was listening intently, all the while handing her more things: an earpiece from an otoscope that was sitting on the counter, then an extension set (still in the package), followed by a digital thermometer and the case it came in. She was still going with the story but her tempo had slowed just a bit. It was now becoming almost impossible to move her hands, which obviously was causing the conversation cortex in her brain to sputter a bit.

I stopped handing her stuff for a second to see if she would notice all the things she was holding for me. Nope. Time to hand over some more. There was little room left to accept things. She had arranged them in various places to make holding them easier, but still had no idea what she was holding. I handed her a package of 2-0 Vicryl suture material, still in the plastic, then a pair of rubber gloves I had just taken off. Not enough? How about a 3-inch stack of 4×4 gauze?

Finally, Tera lost all ability to move her hands. She was now holding enough stuff that she had to mash some of it between her arms and tummy. When this happened, all talking came to a standstill. But she still had not looked to see all I had given her.

A few moments passed with no noise coming from either of us. I just stood there looking at her and finally couldn’t maintain a straight face. She asked what I was giggling about.

“Thanks for holding all that for me,” trickled out the corner of my now laughing mouth. When she looked down to assess what she was holding, Tera started laughing, too. Pretty soon we were both laughing so hard that others in the clinic came over to find out what was going on.

“I guess you figured out that I can’t talk if I don’t move my hands. Well, I was just getting to the good part of that story when you handed me all this stuff,” she said as she started setting it all down on the counter.

“Oh no!” I bellowed before she could get her hands empty. “You have to hold all that until I have had enough quiet time to figure out what is wrong with your horse. Then you can set it all down and start telling me the story again!”

Every time she comes to the clinic now, I greet her with an armful of meaningless stuff and tell her if she can’t be quiet, she is going have to hold it all until I am done.

Bo Brock, DVM, owns Brock Veterinary Clinic in Lamesa, Texas. His latest book is 

Crowded in the Middle of Nowhere: Tales of Humor and Healing From Rural America

When a client won’t stop talking for long enough to allow you complete your diagnostic evaluation, sometimes you have to resort to strange measures.

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