Real resilience starts with understanding what matters most to you, explain Aaron Shaw, OTR/L, CHT, CSCS, and Jennifer Edwards, DVM, ACC, CPC, ELI-MP.

From ‘I should’ to ‘Why’?: A different approach to burnout 

“We all know that burnout in [veterinary] medicine is really kind of an epidemic,” cohost Aaron Shaw, OTR/L, CHT, CSCS, begins in this episode of 

The Resilient Vet: Mind and Body Strategies for Success

. In this installment, Shaw and Jennifer Edwards, DVM, ACC, CPC, ELI-MP, dig into why veterinary professionals continue to struggle with burnout despite the abundance of wellness information available.

They suggest that the issue is not a lack of knowledge, but cultural norms and personal barriers that make it difficult to implement meaningful change. According to Shaw and Edwards, addressing burnout starts with identifying an individual’s true “why,” recognizing what gets in the way, and shifting from gathering information to taking action in meaningful, personalized ways.

 it becomes kind of like a drill down process—[we] go a layer deeper, then a layer deeper, then a layer deeper, then a layer deeper, and then a layer deeper.... A lot of people want things like health and fitness and eating well. The “should” comes from sometimes superficial reasons. Like, “I should be skinny or I should look a certain way for society” and all of these things. But what if I don't care? [What if the person says,] “I've got my partner and she loves me just the way I am and I don't care that I'm 20 pounds overweight.” Not everybody is motivated by those “should” factors.

When we really pare it down into what they want for 

—their lives—when they think about their children, when they think about [how] they love nature, when they think about the idea of their children someday having their own children and being a grandparent, hiking a mountain, being able to walk down a beach, being able to get in and out of a fun little car easily, being able to get down on the floor with the neighbor's puppy and play with it...I might not be motivated to go to the gym because I want to be skinny and sexy in a bikini on the beach. That ship has sailed for me. I don't care, honestly. That's not motivating for me. But when I think about my daughter, like, that's my ‘why.’

So, for each person, I would start to really consider what's important to you in your life. For example, if there is a grandchild or a niece or a nephew or a puppy or a beach, that can be your motivation...

Transcript has been lightly edited for clarity and cohesion.

Videos

From ‘I should’ to ‘Why?': A different approach to burnout 

The Veterinary Oral Health Council (VOHC) has granted the VOHC Seal of Acceptance to Tartar Shield Pro Care Natural Pet Toothpaste for tartar control in dogs.

 According to VOHC, regular use of products that have the VOHC Seal of Acceptance will lower the severity of periodontal disease in pets.

According to the American Veterinary Dental College, from whom VOHC is an affiliated entity, the seal is awarded to products that meet the criteria for effectiveness in controlling plaque and/or calculus in dogs and cats.

Currently, 9 veterinary dentists and dental scientists sit on the VOHC Council, along with a nonvoting director.

According to Tartar Shield Pet Products, the developer of Tartar Shield Pro Care, clinical studies following VOHC protocols found that topical application of the toothpaste was associated with reductions in tartar, plaque, and halitosis in dogs.

 The reduction was observed without use of any brushing device.

Tartar Shield Pro Care is an enzymatic toothpaste and is the only chemically-active pet toothpaste that has received the VOHC Seal of Acceptance, according to Tartar Shield Pet Products.

 The toothpaste’s base consists of coconut oil and contains natural and nature-derived ingredients,

 including miswak, malic acid, zinc citrate, and kaolin clay. In its product site, Tartar Shield Pet Products states that the toothpaste is human grade.

“Our unique blend of organic antimicrobials targets the root causes of plaque and tartar, resulting in fresher breath and healthier gums,” states Tartar Shield Pet Products on its product website.

According to the company, the malic acid in the toothpaste is a type of carboxylic acid that is naturally found in a variety of common fruits. Meanwhile, the zinc citrate in the toothpaste is used for its antimicrobial and anti-inflammatory properties, while the coconut oil helps protect dogs’ teeth and gums from microbes and plaque.

“Tartar Shield has demonstrated a strong commitment to scientific rigor and to supporting the VOHC’s mission to provide assurance of clinical efficacy for pet oral care,” Ellen Lowery, DVM, PhD, director of the VOHC, said in a news release.

Other canine toothpastes that have received the VOHC Seal of Acceptance include Petsmile Professional Pet Toothpaste by Supersmile and HealthyMouth Toothpaste/Brush Kit Combination by HealthySmile. The Petsmile Professional Pet Toothpaste received the seal in 2011 for its plaque-controlling properties, and the HealthyMouth Toothpaste/Brush Kit Combination, was recognized shortly after in 2015, also for plaque reduction.

Tartar Shield Natural Pet Toothpaste granted VOHC Seal of Acceptance. News release. Tartar Shield Pet Products. November 17, 2025. Accessed November 19, 2025. https://www.businesswire.com/news/home/20251117759410/en/Tartar-Shield-Natural-Pet-Toothpaste-Granted-VOHC-Seal-of-Acceptance

Veterinary Oral Health Council. Veterinary Oral Health Council. Accessed November 19, 2025. https://vohc.org/

Veterinary Oral Health Council. American Veterinary Dental College. Accessed November 19, 2025. https://avdc.org/veterinary-oral-health-council/

Tartar Shield PRO CARE Toothpaste for Dogs & Cats. Tartar Shield Pet Products. Accessed November 19, 2025. https://www.tartarshield.com/products/pro-care-natural-pet-toothpaste

VOHC accepted products. Veterinary Oral Health Council. Accessed November 19, 2025. https://vohc.org/accepted-products/

Articles

The seal is awarded to products that meet the criteria for effectiveness in controlling plaque and/or calculus in dogs and cats.

VOHC grants Seal of Acceptance to canine toothpaste for tartar control

Hypoadrenocorticism, also known as Addison’s Disease, is an uncommon condition, with an estimated prevalence between 0.06% and 0.28%. Known as “the great pretender,” its vague, nonspecific clinical signs often mimic other illnesses, as do diagnostic findings. Early recognition, diagnosis, and treatment can prevent significant mortality secondary to hyperkalemia, hyponatremia, dehydration, and hypovolemic shock.

The adrenal gland comprises an inner medulla and an outer cortex. Three layers make up the cortex, and each is responsible for hormone production. The outermost layer, the zona glomerulosa, is responsible for mineralocorticoid (aldosterone) production, while glucocorticoids and androgens are produced by the zona fasiculata (middle layer) and reticularis (innermost layer).

Primary hypoadrenocorticism is most common and is most often caused by autoimmune destruction of the medullary layers. Thus, destruction of the zona glomerulosa results in mineralocorticoid deficiency, while cortisol (glucocorticoid) deficiency occurs secondary to destruction of the zona fasiculata and reticularis.

Secondary hypoadrenocorticism is rare. It is caused by lack of secretion of adrenocorticotropic hormone (ACTH) from the pituitary gland or lack of secretion of corticotropin-releasing hormone (CRH) from the hypothalamus. This, in turn, results in atrophy of the zona fasiculata and reticularis, and therefore lack of cortisol production; mineralocorticoid production from the zona glomerulosa is not affected. Secondary hypoadrenocorticism most commonly occurs secondary to neoplasia or intracranial trauma.

Most dogs with primary hypoadrenocorticism are deficient in both glucocorticoids and mineralocorticoids; however, glucocorticoid deficiency can occur without mineralocorticoid deficiency. The latter population lacks electrolyte abnormalities; this is referred to as ‘atypical.’

These dogs can progress to develop mineralocorticoid deficiency, so sodium and potassium should still be monitored in these patients.

Hypoadrenocorticism is thought to have a genetic basis in dogs, but mode of inheritance has not been established. Breeds with a known genetic predisposition include the Nova Scotia duck tolling retriever, standard poodle, bearded collie, and Portuguese water dog.

 Other commonly affected breeds include great dane, West Highland white terrier, Saint Bernard, Wheaten terrier, leonberger, and rottweiler.

 Young to middle-aged female dogs are predisposed.

Hypoadrenocorticism has also been reported in cats, but is rare.

Hypoadrenocorticism can present as an acute crisis or with waxing and waning clinical signs. The most common presentation is with a history of vague symptoms, such as lethargy, inappetence, weight loss, and/or waxing and waning gastrointestinal signs that have not fully responded to traditional supportive therapies. There may be a history of illness developing in association with a stressful event.

The array of clinical signs includes, but is not limited to, vomiting, diarrhea, inappetence, weight loss, lethargy, weakness, collapse, polyuria, polydipsia, shaking, abdominal pain, melena or hematochezia, and hematemesis. Patients in crisis can present with signs of hypovolemic shock, including bradycardia, tachycardia, collapse, hypothermia, weak pulses, and poor capillary refill time. Otherwise, physical examination findings are nonspecific and can include thin body habitus and dehydration.

Diagnostic testing should begin with a minimum database, including complete blood count (CBC) and chemistry panel (including electrolytes). Pertinent CBC findings may include anemia (most often non-regenerative), lymphocytosis (or lack of the lymphopenia expected secondary to a normal stress response), eosinophilia, and neutrophilia. The most common biochemical abnormalities are hyperkalemia, hyponatremia, and hypochloremia. Other common findings include hypercalcemia, azotemia, hyperphosphatemia, hypoglycemia, hypocholesterolemia, and hypoalbuminemia. 

 Abdominal ultrasound often reveals adrenal glands that are much smaller than normal or cannot be identified.

 In patients with severe hyperkalemia, an EKG can reveal bradycardia, lack of P waves, wide QRS complexes, and tall T waves.

Because of the variety of vague presenting symptoms, veterinarians should be testing a large number of dogs for hypoadrenocorticism compared to the small number that are definitively diagnosed with the disease.

 Several studies have documented that measurement of basal (resting) serum or plasma cortisol is a reliable screening test for dogs with a clinical history consistent with hypoadrenocorticism, with a 100% sensitivity for a cutoff of ≤2 µg/dL. This diagnosis is less likely if the cortisol is >2 µg/dL

Because a basal cortisol of ≤2 µg/dL has a low specificity and a low positive predictive value, an ACTH stimulation test must be performed in these patients to obtain a definitive diagnosis.

 Although cosyntropin doses of 5 µg/kg IV are most commonly employed, one study showed that doses of 1 µg/kg IV may be sufficient.

Treatment of hypoadrenocorticism can be divided into management of the acute crisis and chronic management. Treatment of a hypoadrenocortical crisis is focused on restoration of tissue perfusion and correction of hypovolemia with IV fluid therapy, correction of electrolyte abnormalities, correction of hypoglycemia (if applicable), restoration of acid-base balance, and providing glucocorticoid support.

 ECG should be monitored, and immediate treatment initiated for hyperkalemia if it is severe enough to cause ECG changes.

Intravenous regular insulin and dextrose should be utilized to shift potassium into cells along with glucose; blood glucose should be monitored for 6 hours concurrent with weaning of dextrose supplementation.

 Calcium gluconate 10% is cardioprotective and can be administered to antagonize the cardiac effects of hyperkalemia.

 A rapidly acting corticosteroid such as dexamethasone sodium phosphate should be administered to provide glucocorticoid support. A reasonable starting dose is 0.1-0.2mg/kg IV every 24 hours until an oral glucocorticoid, usually prednisone or prednisolone, can be tolerated. Mineralocorticoid supplementation should be delayed until the patient has recovered, and electrolytes are normal or nearly normal, and the patient’s perfusion has been restored.

Chronic therapy for typical hypoadrenocorticism entails both mineralocorticoid and glucocorticoid supplementation; only glucocorticoid supplementation is required for an atypical Addisonian. Prednisone/prednisolone is used most with a starting dose of 0.2-0.25 mg/kg/day.

 Once a diagnosis of hypoadrenocorticism has been established, the ACTH stimulation test is no longer useful; dose adjustments are made based on subjective information provided by the owner, making good client communication imperative for management.

The glucocorticoid dose can be tapered to the minimum amount necessary, usually 0.1-0.2 mg/kg/day, to prevent symptoms of hypoadrenocorticism while avoiding side effects of corticosteroids.

 For some large breed dogs, a dose of slightly less than 0.1 mg/kg/day may be required to accomplish these goals. During periods of stress, increased doses of glucocorticoids should be recommended; the author typically doubles the prednisone/prednisolone dose during the event and for 2-3 days before and after.

Either desoxycorticosterone pivalate (DOCP) or fludrocortisone acetate can be used for mineralocorticoid supplementation. The starting dose of fludrocortisone is 0.02 mg/kg/day orally, divided into 2 doses.

 Electrolytes should be monitored weekly until stable within normal range, and the dose can be adjusted by 0.05-0.1 mg/kg/day as needed.

 Fludrocortisone has glucocorticoid properties, therefore only about 50% of dogs treated with this medication will also require prednisone, though both should be started as initial management.

 The prednisone dose can then be tapered to the minimum dose necessary to prevent symptoms while controlling side effects.

DOCP is a long-acting mineralocorticoid supplement with no glucocorticoid activity. Traditionally, the starting dose has been 2.2 mg/kg subcutaneously or intramuscularly every 25-30 days (most commonly), but more recent studies have demonstrated that low-dose DOCP (1.1-1.5 mg/kg every 28-30 days) is safe and effective for most dogs.

After initiation of treatment with DOCP, electrolyte levels should ideally be rechecked at weeks 2, 3, and 4 to determine the duration of action, dose, and dosing interval.

 For both therapies, once an appropriate dose (and dosing interval for DOCP) has been established, electrolytes should be checked every 3-6 months indefinitely. 

Prognosis for hypoadrenocorticism is excellent with prompt treatment of the initial crisis and early diagnosis.

 Addisonian patients can have a normal quality of life and life expectancy, and most die of unrelated causes.

Guzmán Ramos PJ, Bennaim M, Shiel RE, Mooney CT. Diagnosis of canine spontaneous hypoadrenocorticism. 

. 2022;9(1):6. Published 2022 May 3. doi:10.1186/s40575-022-00119-4

Van Lanen K, Sande A. Canine hypoadrenocorticism: pathogenesis, diagnosis, and treatment. 

. 2014;29(4):88-95. doi:10.1053/j.tcam.2014.10.001

Keich WLR, Smith C, New J. Canine hypoadrenocorticism (Addison´s disease). 

Hess RS. Hypoadrenocorticism. In: Cote E, Ettinger SJ, Feldman EC, eds. 

Ettinger’s Textbook of Veterinary Internal Medicine

. Ninth ed. Philadelphia: Elsevier; 2024: 2036-2045.

Scott-Moncrieff JC. Hypoadrenocorticism. In: Feldman EC, Nelson, RW, Reusch CE, Scott-Moncrieff JC, Behrend, EN, eds. 

Canine and Feline Endocrinology and Reproduction.

 4th ed. St. Louis: Elsevier: 2015: 485-520.

Peterson ME, Kintzer PP. Hypoadrenocorticism. In: Bonagura JD, Twedt DC, eds. 

. XIV ed. St. Louis: Elsevier; 2009: 231–235.

Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993). 

Oberbauer AM, Benemann KS, Belanger JM, Wagner DR, Ward JH, Famula TR. Inheritance of hypoadrenocorticism in bearded collies. 

. 2002;63(5):643-647. doi:10.2460/ajvr.2002.63.643

Famula TR, Belanger JM, Oberbauer AM. Heritability and complex segregation analysis of hypoadrenocorticism in the standard poodle. 

. 2003;44(1):8-12. doi:10.1111/j.1748-5827.2003.tb00096.x

Hughes AM, Nelson RW, Famula TR, Bannasch DL. Clinical features and heritability of hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers: 25 cases (1994-2006). 

. 2007;231(3):407-412. doi:10.2460/javma.231.3.407

Glebocka MJ, Boag A. Hypoadrenocorticism in cats: a 40-year update. 

. 2024;26(9):1098612X241248381. doi:10.1177/1098612X241248381

Lennon EM, Boyle TE, Hutchins RG, et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). 

. 2007;231(3):413-416. doi:10.2460/javma.231.3.413

Bovens C, Tennant K, Reeve J, Murphy KF. Basal serum cortisol concentration as a screening test for hypoadrenocorticism in dogs. 

. 2014;28(5):1541-1545. doi:10.1111/jvim.12415

Gold AJ, Langlois DK, Refsal KR. Evaluation of Basal Serum or Plasma Cortisol Concentrations for the Diagnosis of Hypoadrenocorticism in Dogs. 

. 2016;30(6):1798-1805. doi:10.1111/jvim.14589

Botsford A, Behrend EN, Kemppainen RJ, Gaillard PR, Oprandy F, Lee HP. Low-dose ACTH stimulation testing in dogs suspected of hypoadrenocorticism. 

. 2018;32(6):1886-1890. doi:10.1111/jvim.15256

Vincent AM, Okonkowski LK, Brudvig JM, et al. Low-dose desoxycorticosterone pivalate treatment of hypoadrenocorticism in dogs: A randomized controlled clinical trial. 

. 2021;35(4):1720-1728. doi:10.1111/jvim.16195

Sieber-Ruckstuhl NS, Reusch CE, Hofer-Inteeworn N, et al. Evaluation of a low-dose desoxycorticosterone pivalate treatment protocol for long-term management of dogs with primary hypoadrenocorticism. 

. 2019;33(3):1266-1271. doi:10.1111/jvim.15475

Discover the complexities of Addison's disease in dogs, including diagnosis, treatment options, and management strategies for hypoadrenocorticism.

Hypoadrenocorticism: The great pretender

Lindsay Hallman, CVT, CCMT, VTS (Oncology) and Katelyn McDonald, CVT, VTS (Oncology), discuss methods for a calm administration.

Considering patient behavior with chemotherapy

Administering chemotherapy can pose challenges for the veterinary team. In a 

 interview, Lindsay Hallman, CVT, CCMT, VTS (Oncology) and Katelyn McDonald, CVT, VTS (Oncology), veterinary technician specialists at Mount Laurel Animal Hospital in New Jersey, discussed how a patient’s behavior can affect the treatment process. In this video showing part of the interview, they address methods that can help ensure a calm chemotherapy administration as well as a positive patient experience.

The following is a transcript of the video, lightly edited for clarity:

: What patient behaviors should be considered when administering chemotherapy?

Lindsay Hallman, CVT, CCMT, VTS (Oncology): 

We work really closely with our behavior department [at Mount Laurel Animal Hospital]. We are touching base with our behavior nurses and our board-certified behaviorists on a pretty regular basis. I would say probably 75%, if not higher, of our patients do come in on some form of anti-anxiety medication. Not that all of them are not good or super wiggly— some of them are absolutely perfect angels. It's just that if they have to come in and see us every single week, we don't want them to be stressed at all.

The goal of chemotherapy and oncology in general is for quality, not quantity. That's really what our main focus is. And if they have to come in every week and they're anxious or nervous or shaking, that's not a quality experience for them. So we want everything to be really as calm and relaxed as possible.

We tend to play calming music in our room. We keep trying to [have] things a little bit on the quiet side. We're at the very end of the building, at the end of a hallway, so it generally ends up being a pretty quiet space for them.

But, behavior is something that we work really closely with [the veterinary team] to make sure that our patients are all really comfortable. We have a very large arsenal of behavior medications to use, thanks to our boarded behaviorist. So if something's not working, we're always shifting things around and playing with different medications, but we try and keep them as calm and as happy as possible.

Sometimes it can be challenging for owners to hear that they can't be with their pets during chemotherapy. Very often, owners have the conception that the pets are going to behave better with them. They're going to be calmer with them, which may in fact, be true, but from a safety standpoint, we cannot have owners with us while we're administering chemotherapy to their pets.

In addition to having the behavior medications and consulting with our behavior team, like Lindsay said, we have an arsenal of different goodies and treats and things to promote a positive experience when they come in. So we are the cookie monsters.

When they come in, we very often have patients that are very apprehensive, nervous at the beginning of their treatment. But as time goes on, we establish relationships with these patients. They get to know us. They get excited to see us walk out into the waiting room and come back. We're able to be there with things like lick mats slathered in peanut butter that they will actually consume while they are receiving their treatment. So they get to go to their happy place simultaneously while we are administering chemotherapy. It's honestly a very different experience than I think what a lot of people have in their heads.

Lindsay Hallman, CVT, CCMT, VTS (Oncology) and Katelyn McDonald, CVT, VTS (Oncology), discuss methods for a calm administration and positive pet experience.

In recent years, notable strides have been made in treating feline infectious peritonitis (FIP), particularly in 2024, with GS-441524 becoming available in the US and Wedgewood becoming the first US veterinary compounding pharmacy to offer molnupiravir.

, our host Adam Christman, DVM, MBA, and guest Kelly Chappell, DVM, DACVIM (Small Animal), talk more about the current state of treating FIP in veterinary medicine. They also dive into the struggles of definitively diagnosing this disease in clinical practice, as well as available treatments and alternatives. 

Below is a partial transcript, edited lightly for clarity.

[Because] we can very rarely obtain a definitive diagnosis of [FIP] in clinical practice, what testing and tools can we use for a more presumptive FIP diagnosis?

Kelly Chappell, DVM, DACVIM (Small Animal): 

It's such a good question, and I will say the diagnosis of FIP is still the bane of my existence. As happy as I am that we can treat it, diagnosis is still super frustrating. As most people know, definitive diagnosis is really going to be with that histopathology and immunohistochemistry, which requires us to get surgical samples, [requiring] surgery and anesthesia. [And] most of the time, we're not going to put these sick cats through [that], so [we're often] relying on a more presumptive diagnosis. 

I often think about it as a building block system, as I'm often trying to check a certain number of boxes to make myself feel like I'm fitting into that presumptive diagnosis. One of the first building blocks that I'll look at is the signalment and vitals. FIP can occur [at] any age [for cats], but we definitely see it in cats [younger] than 2 years—most commonly pure-breed cats. Male cats are also slightly overrepresented in some studies.

Fever is really common in cats with FIP, [occurring in] about 70% of cats with FIP. In a 2017 study that looked at cats with fevers, FIP was the most common condition diagnosed in cats referred for fever. So whenever I see a young cat with a fever, it always picks [up] my little FIP flags. 

One of the next building blocks I'll commonly look at is a chemistry panel, looking at the globulins, albumin-globulin ratio, and bilirubin. The globulin number itself could be [within] a normal range but still have an abnormal albumin-globulin ratio. So if my [chemistry] panel doesn't automatically calculate my albumin-globulin ratio, I'm always calculating that. [An] albumin-globulin ratio greater than 0.8 has a really high negative predictive value, meaning it's really helpful in ruling out FIP. So if I have a cat where maybe I have FIP on my differential list, and it's greater than 0.8, I feel pretty good to bring it lower down on my differential list. An albumin-globulin ratio less than 0.6—and especially less than 0.4—again, is another thing that piques my flags up for FIP in those cats.

McCafferty C. Compounded oral FIP treatment is now available. 

. June 14, 2024. Accessed November 18, 2025. https://www.dvm360.com/view/compounded-oral-fip-treatment-is-now-available

McCafferty C. Wedgewood announces FIP treatment. 

. September 19, 2024. Accessed November 18, 2025. https://www.dvm360.com/view/wedgewood-announces-fip-treatment

Podcasts

Discover the latest advancements in feline infectious peritonitis (FIP) treatment and diagnosis in veterinary medicine, featuring expert insights on effective strategies and alternatives.

Demystifying FIP: Testing, treatment advances, and practical takeaways

A study by researchers at the University of Surrey in Guildford, England, and the University of Bristol found that “high-risk” strains of avian pathogenic 

 (APEC) are more diverse and behave more differently than previously assumed.

 The findings suggest a reason for why colibacillosis—an infection caused by strains of APEC—remains challenging to control in livestock and poultry, and highlights a need for broader vaccine and disease management strategies that cover a larger range of pathogenic strains.

Colibacillosis is one of the most common and costly bacterial diseases in the world.

 Every year, the disease causes the loss of millions of dollars, greatly affecting poultry production.

Among other complications, colibacillosis can lead to acute fatal septicemia, airsacculitis, pericarditis, perihepatitis, peritonitis, and lymphocytic depletion of the bursa and thymus.

“Our research shows that a one-size-fits-all approach to controlling avian pathogenic 

 infections is not effective. Current vaccination strategies often target specific strains, but they may not protect against emerging APEC threats. Therefore, we need to develop new vaccines that can target a variety of APEC strains,” Jai Mehat, BSc, PGCert, PhD, FHEA, senior author of the UK-based study and lecturer in molecular bacteriology at the University of Surrey, said in a news report.

, looked at a colibacillosis outbreak in turkeys in the UK and identified a strain called ST101 that was the main cause of the break, responsible for nearly 60% of the infections. According to 

, this strain had not been reported previously as the primary cause of the APEC outbreak in turkeys in the UK.

Researchers at the University of Surrey compared ST101 with other high-risk APEC strains and found that the ST101, along with ST95 and ST140 strains, were especially effective at invading and surviving inside chicken gut cells and immune cells compared with ST23 and ST117 strains. The ST117 strain, however, proved the most lethal in an insect infection model, despite being less effective at cellular invasion. This finding suggests different strains cause disease in different ways.

Shahriar Behboudi, DVM, PhD, coauthor of the study and a professor in correlates of immune protection at the University of Bristol, said that existing vaccines target only certain strains, and broad-spectrum control measures are needed. “We extrapolate that broad-spectrum control measures, including the induction of trained immunity in chickens to control diverse strains, offer more effective protection, as current vaccines typically target specific strains and may fail against emerging APEC threats,” he said.

“Infections caused by APEC are a foremost threat to farmed poultry. Increasing our surveillance of poultry flocks to better understand the presence and evolution of APEC strains will ensure our animals’ welfare, and, as a result, the safety of our food,” concluded Sara Perez, DVM, MSc, CertPMP, MRCVS, study coauthor and veterinary director at Poultry Health Services.

Adams JRG, Long H, Birdsall CA, et al. High‑risk clonal groups of avian pathogenic 

 (APEC) demonstrate heterogeneous phenotypic characteristics in vitro and in vivo. 

 2025;16(1):2546682. doi:10.1080/21505594.2025.2546682

Colibacillosis in poultry. Merck Veterinary Manual. Updated October 2025. Accessed November 18, 2025. https://www.merckvetmanual.com/poultry/colibacillosis/colibacillosis-in-poultry

New research reveals diverse APEC threats for poultry. 

. October 26, 2025. Accessed November 18, 2025. https://www.feedandadditive.com/new-research-reveals-diverse-apec-threats-for-poultry/

"Our research shows that a one-size-fits-all approach to controlling avian pathogenic E coli infections is not effective," said Jai Mehat, BSc, PGCert, PhD, FHEA, coauthor of the study.