Research indicates reptiles have a recognition pattern for their owners, says Jb Minter, DVM, MS, DACZMResearch indicates reptiles have a recognition pattern for their owners, says Jb Minter, DVM, MS, DACZM

Reptile medicine and the human-animal bond

In this interview, Jb Minter, DVM, MS, DACZM, talks about the emotional bond between reptiles and their owners, emphasizing that this bond is as real as the bond between a dog or cat and their caretaker. According to Minter, research indicates that reptiles may be capable of developing a bond with their owner. He also highlights the growing field of reptile medicine, encouraging veterinarians to develop a foundational understanding of reptile care to help them feel more confident when presented with these animals.

Below is the interview transcript, lightly edited for clarity:

The big thing for me is to make sure that small animal veterinarians understand that there is an emotional bond between the humans and the reptiles and what people are now expecting. It's an important aspect. We don't really delve into the emotional bond that people have with their pets, and obviously most people understand this with dogs and cats. But reptile owners, a lot of reptile owners feel the same way about their lizard or their snake that someone may feel about their Yorkie or their Pomeranian.

There's a lot of research out there that indicates that even reptiles have a recognition pattern for their owners and they may be developing a bond for a particular owner. So, understanding that bond is pretty critical. So, while diagnosing and treating some of these diseases may be challenging...a lot more people are up for the challenge than they may initially want to think about. So giving them some, just some basic understanding so they feel comfortable when somebody walks in with that pet lizard, they don't have an anxiety attack and start freaking out. It's like you can deal with this. It's not that complicated. And again, if you don't know, there's books out there, there's continuing education, there's people that likely do know that are willing to help them. The future of reptile medicine is growing. It's growing exponentially, almost logarithmic of how much information is coming in and out there about reptiles. So it's this ongoing research in reptile anesthesia, pain management, and surgery is going to be vital. It's making sure that people understand that by staying current with these they can see a lot more patients, they can provide optimal care for the people that want their reptile pets to be seen.

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Reptiles have a recognition pattern for their owners, says Jb Minter, DVM, MS, DACZM

Joya Griffin, DVM, DACVD, explains what this disease is, signs, diagnosis, and treatment

Paraneoplastic alopecia in cats

In this interview discussing her Fetch dvm360 conference session 

Kitty Conundrums: Dermatologic CATastrophies

, Joya Griffin, DVM, DACVD, talks about paraneoplastic alopecia—a unique disease to cats. Griffin discusses signs of the disease, as well as diagnostics and treatment for underlying diseases, as paraneoplastic alopecia is often an indicator of an internal disease.

Below is a partial transcript, lightly edited for clarity

 So one of the kind of coolest disease processes—maybe not the coolest for the cat—is paraneoplastic alopecia. And this is really a disease that is very specific to the cat, there really aren't any human or dog corollaries to this disease, and when you see it, once you see it, you will recognize it again. But these cats have almost completely bald areas on their skin. That alopecia is pretty striking. It goes from fairly normal hair to completely smooth, almost shiny alopecia.

And in some of the cases, the hair at the edges will just sort of pull out, like it toughs out and peels away. And these cases sometimes can have thin skin as well and really cats cannot create that extreme level of alopecia. And in general, cats don't really have alopecic diseases. They're fairly rare in cats, unless it's traumatic alopecia. So, whenever I see this, I know right away that I need to look for internal disease, either with CBC chemistry panel, abdominal ultrasounds, x-rays to try to determine the cause of it, and then we are also doing biopsies to confirm the diagnosis as well.

Unfortunately, treatment for paraneoplastic alopecia is really aimed at trying to control the internal disease, which often is something that's devastating, so we don't always have great options for those cases but I think diagnosing them quickly will help to provide some level of relief, and, you know, symptomatic treatment for those patients, if we can recognize that the skin is related to something going on internally.

Joya Griffin, DVM, DACVD, explains what how to recognize, diagnosis, and treat feline paraneoplastic alopecia 

The abnormal accumulation of extravascular fluid, pulmonary edema, settles in the lung interstitium and alveoli. There, it causes chaos, said cardiologist Gordon Peddle, VMD, DACVIM, who spoke at the 2025 Unique Seminar Destinations Annual Winter Seminar.

Affected animals can experience ventilation-perfusion mismatch, hypoxemia, impaired lung tissue compliance, respiratory fatigue, and even death. Clinical signs include coughing, dyspnea, cyanosis, frothy oronasal exudate, and collapse.

Ground zero for pulmonary edema, Peddle said, is the alveolar-capillary membrane. This vital partition allows gas exchange between the capillaries and alveoli while shielding these vulnerable air sacs from fluid incursion. Pulmonary edema occurs when fluid leaks through the capillary endothelium and enters the interstitial space, ultimately breaching adjacent alveoli.

The alveolar-capillary wall holding back the waters can be directly defaced by pneumonia, contusions, emboli, toxins, and drowning,

 but indirect inflammatory forces such as sepsis and ischemia may also harm it. All these low-pressure mechanisms alter membrane permeability.

Fluid movement across the semipermeable vessel walls is regulated by Starling forces that result from the interplay between hydrostatic and colloid osmotic pressures.

 “There’s a pretty decent balance at all times,” Peddle said.

Elevated pulmonary arterial load or passive rises in pulmonary venous pressures associated with congestive heart failure (CHF) can disrupt this delicate balance, as can dropping plasma oncotic pressure or increased negativity of pulmonary interstitial pressure.

The lymphatic system plays a crucial role in fluid balance by utilizing oncotic pressures to draw excess fluid from the interstitium. In this way, the lymphatics help prevent alveolar flooding.

There are several types of pulmonary edema with mechanisms that are poorly understood, including neurogenic, postanesthesia, and high-altitude pulmonary edema.

Pathophysiology of fluid exchange and pulmonary edema

Whatever the inciting cause, pulmonary edema results from disruptions in complex forces that govern fluid exchange in the lungs.

 When the difference between capillary and interstitial hydrostatic pressure on the arterial side (flow) exceeds the difference between capillary and interstitial colloid osmotic pressure (protective clearance), fluid flows into the interstitium and then breaches the alveoli.

Pressure chambers typically come with safety valves, and lungs are no different. When left atrial pressure mounts, ensuing pulmonary hypertension is met with compensatory blood redistribution via capillary distension and recruitment.

However, pulmonary capillary pressure gauges are set to 8 to 12 mm Hg. Once left atrial pressure rises above the threshold of 23 to 28 mm Hg, Peddle explained, cardiogenic pulmonary edema starts to build in 3 phases.

 In the first, edema formation prompts recruitment and hypertrophy of lymphatic vessels, which pull out fluid and thereby maintain normal interstitial volume.

In the second—acute—stage, which lasts about 4 hours, left atrial pressures continue to climb, and the interstitial filtration level peaks. Lymphatic drainage rises slowly, and glycosaminoglycans present in the extracellular matrix of the lungs allow the interstitium to soak up some expansion in fluid without alveolar flooding.

The third stage occurs once the volume capacity of the interstitial space is exceeded. The alveolar epithelial junction separates at the cellular level, and fluid washes into the alveoli in an all-or-none fashion within each unit. (Neighboring alveolar chambers that have not been ruptured show minimal reduction in respiratory gas exchange.)

“The dog is like a glass of water, and it’s filling up and then spilling onto the table,” Peddle said. “That’s pulmonary edema.”

Additionally, chronic surges in pulmonary capillary pressure lead to structural changes in lung parenchyma and vasculature.

 This remolding consists of alveolar and vascular fibrosis, causing irreversible lung and pulmonary artery disease. The pulmonary vein thickens, and lymphatic dilatation occurs. All these changes contribute to the development of pulmonary hypertension and, eventually, right-sided CHF (cor pulmonale).

Pneumocyte channels are like built-in "wet vacs" that are located within the alveoli and upregulate to clear pulmonary edema.

 Once siphoned from the air sacs, fluid must be drained from the interstitium. This is accomplished by small, contractile lymphatic vessels that utilize intraluminal valves to move fluid out of the interstitial space and toward the lymph nodes. Lymphatic flow can escalate several-fold before getting overwhelmed.

Cardiogenic pulmonary edema is diagnosed by history, physical exam, and radiographic evidence of pulmonary edema affecting mainly the perihilar fields or the lung fields diffusely.

Treatment aims to improve cardiac performance, expand vascular capacity, and lower intravascular volume. Beta agonists can be employed to directly clear alveolar fluid. Diuretics such as furosemide boost urine output to lower intravascular volume and sometimes trigger rapid pulmonary vasodilatation.

While reducing further alveolar flooding, diuretics do not directly

siphon alveolar fluid; for this reason, rapid administration of high doses of diuretics alone—compared with standard dosing—does not significantly clear edema and relieve dyspnea in dogs and cats with CHF. Ancillary therapies must usually be added to the mix.

Low-pressure NCPE, or permeability edema, results from lung injury that disrupts endothelial integrity.

 One potential cause is airway obstruction, which can arise through brachycephalic disease, strangulation, laryngeal pathology, respiratory collapse, or an airway mass or foreign body.

“Picture the golden retriever that plugs his airway with a tennis ball while playing outside,” Peddle said.

Whatever the airway jam, the result is falling negative intrathoracic pressure, hypoxia-induced microlesions in the alveolar-capillary unit, increased sympathetic tone, and hikes in hydrostatic pressure.

Another brand of NCPE is neurogenic edema, likely linked to vasoconstrictive and hypertensive changes wrought by central nervous system insults. These include head trauma, hemorrhage, seizures, and electrocution.

Lastly, NCPE can be the indirect fallout of damage by systemic disease or direct lung injury from smoke, toxins, or excessive heat—all of which produce inflammation. Water aspiration that occurs in near-drowning traumatizes the alveolar-capillary border directly and produces barotrauma from forceful ventilation.

Unlike cardiogenic pulmonary edema, which happens in stages, NCPE rushes in. The acute nature of most types of lung injury and the wide-reaching damage they incur lead to rapid alveolar flooding that can manifest as acute respiratory distress syndrome.

Dogs and cats with NCPE typically present with hypoxemia and hyperglycemia.

According to published data, imaging shows interstitial/mixed interstitial-alveolar pulmonary pattern, favoring symmetric (77%), peripheral (92%), and dorsal (58%) distribution; asymmetric pattern is typically post obstructive.

There exists no therapy to lessen pulmonary capillary hyperpermeability. Clinical management focuses on addressing the underlying etiology, providing respiratory support, and allowing time to heal. Conservative administration of fluids and diuretics may be used effectively.

 Overall, NCPE survival rates have been reported at 65% to 68%.

Peddle G. Taking on water: the pathophysiology of pulmonary edema. Presented at: Unique Seminar Destinations; February 8-15, 2025; Cancun, Mexico. 

Murray JF. Pulmonary edema: pathophysiology and diagnosis.

Joost JL, Bierens M, Lunetta P, et al. Physiology of drowning: a review. 

. 2016;31:147-166. doi:10.1152/physiol.00002.2015

Ingbar DH. Cardiogenic pulmonary edema: mechanisms and treatment–an intensivist’s view. 

. 2019;25:371-378. doi:10.1097/MCC.0000000000000626

Drobatz KJ, Saunders M, Pugh CR, et al. Noncardiogenic pulmonary edema in dogs and cats: 26 cases (1987-1993). 

Bouyssou S, Specchi S, Desquilbet L, et al. Radiographic appearance of presumed noncardiogenic pulmonary edema and correlation with the underlying cause in dogs and cats. 

. 2017;58(3):259-265. doi:10.1111/vru.12468

Ali J, Chernicki W, Wood LD. Effect of furosemide in canine low-pressure pulmonary edema. 

. 1979;64(5):1494-1504. doi:10.1172/JCI109608

Articles

Fluid in the lungs can lead to serious consequences for patients with the condition.  

The buildup of pulmonary edema

Patients coming into the clinic with chronic enteropathy (CE) are characterized by persistent gastrointestinal (GI) symptoms, including diarrhea, inappetence, vomiting, and weight loss, that last for over 2 to 3 weeks. Traditionally, CE is classified as food-responsive, antimicrobial-responsive enteropathy, and immunosuppressant-responsive enteropathy, with other classifications like fiber-responsive and nonresponsive enteropathy. According to Laura Gaylord, DVM, DACVIM (Nutrition), because these classifications may overlap or represent a continuum of the state of the disease, nutritional management remains the cornerstone of CE treatments.

During her lecture at the 2025 Fetch Charlotte Conference, Gaylord shared with attendees how they can manage CE in their patients with a multimodal approach to nutrition and how recent advancements in research have the role of gut dysbiosis in CE.

Patient history, dietary review, diagnostic workup, and physical examination are required when it comes to creating an appropriate treatment plan for CE and veterinary teams should assess clinical signs.

“The first sign, I think, is often inappetence, picky eaters, or variable appetites. So if you get these younger dogs that...your owners are saying, 'well, he's picky and he won't eat,' and it's a puppy that makes no sense, right? Their body is growing and should have a higher, longer drive so they're not eating. I always say, I give the dogs credit. I assume it's a medical reason, not a behavioral one until I ruled everything else out,” explained Gaylord.

“Yes, you do have those special owners that say behavior problems, but don't jump to that. Give the owner credit. Give the pet credit. Make sure you're doing your work like you would any other sick pet, even if it is just picky eating,” she continued.

Along with eating clinical signs, patients with CE can present to the clinic with vomiting, diarrhea, weight loss, with the possibility of additional systems such as regurgitation, flatulence, hematemesis, hematochezia, melena, and constipation, which can help professionals with disease localization within the GI tract.

The diagnostics could include complete blood count, urinalysis, blood chemistry, thyroid testing, imaging, pancreatic enzyme testing, vitamin B status, and ACTH stimulation testing. In cases where there is inflammatory bowel disease or neoplastic conditions such as lymphoma are suspected, an endoscopic or surgical biopsy may be necessary.

Diagnosing and managing all lies within diet trials. When conducting a diet trial with patients, the chosen diet needs to be strictly fed and all noncompliant foods eliminated. A clinical response to the trials can be assessed within 2-3 weeks, and some cases could require multiple trials before finding the right diet for the patient. Gaylord said that hydrolyzed protein and novel protein diets are common, but upcoming evidence is suggesting individualized diet formulated based on microbiome profiling could enhance diet trial outcomes.

“Diet trials can be both diagnostic and therapeutic, so we're going to choose foods, and we're testing to see that they're better, but it also, in hindsight, kind of gives you information. We want to make logical diet changes. So we're looking at the diets that were already fed, already tried. We could gather information from that, or the diets you are trying each step of the way, that's going to help you make the next diet selection. More than one diet trial is needed often,” said Gaylord.

“So second best tip I have for you, tell your clients from the start, you need to be prepared, we're going to have to do a few diet trials. We may not pick the best diet on the first trial. So 2 trial, 3 trials, have their mindset already ready for the fact that we might have to do more than one diet trial,” she concluded.

Gaylord also explained that these trials could take up to 12 weeks, but usually last for 8, it just depends on how spread out the patient’s symptoms are. When it comes to selecting the nutrient profile for the trial, previous diets can be used as a guide to pick the appropriate therapeutic diet. Veterinary professionals should consider highly digestible/gastroenteric diets, novel/hydrolyzed protein, or high-fiber diets, but some cases call for a combination of these if needed. Diet trials for patients must also consider the individual patient’s needs, disease localization, and clinical history. 

Gaylord also explained the impact of dietary fiber on gut microbiota and the potential benefits of prebiotic and probiotic supplementations for stabilizing or supporting gut balance—an area that is currently in active research.

Owners should be informed that CE is not primarily caused by pathogenic bacteria, and antibiotics are rarely indicated. Adherence to diet trials is crucial, and multiple may be needed to determine an effective nutritional plan. A complete resolution is uncommon, so diet trials will remain a key diagnostic and therapeutic tool to help manage CE.

Gaylord L. Gut check: A fresh look at managing chronic enteropathy in dogs. Presented at: Fetch Charlotte; Charlotte, North Carolina. March 14-16, 2025.

Laura Gaylord, DVM, DACVIM (Nutrition) shares the role of diet trials in chronic enteropathy patients during her lecture at Fetch Charlotte

Rethinking chronic enteropathy management in canine patients 

Oral health conditions often lead to pain and discomfort, and may also link to other health issues. Disease prevention and early-stage treatment can keep patients’ healthy.

World Oral Health Day—March 20, 2025—encourages the healthcare community to educate the patients and clients they serve.

 In recognition of this awareness holiday, here are several recent articles that highlight dentistry care, authored by expert contributors:

Industry leader Jan Bellows, DVM, DAVDC, DABVP, FAVD, shares some of the slipups and solutions he learned from throughout his career. These include extraction errors, postprocedural complications, and procedural oversights, among others.

Offering and promoting oral health services can help boost the bottom line. Written by Kathryn Primm, DVM, CVPM, this article outlines how a good dental program can enhance 3 pillars of health for a practice: the average dollar amount of per-client transactions, the number of patients visiting a clinic or hospital, and interest from new clients.

Wendy S. Myers, CVJ, provides 8 tips for confident discussions with clients about their pets’ dental diagnoses, and follow-up care. Myers, the “Queen of Scripts,” also offers terminology and specific phrasing that can help make the most of the conversation.

About World Oral Health Day. World Dental Federation. Accessed March 20, 2025. https://www.worldoralhealthday.org/about

Several recent articles about dentistry care, authored by expert contributors, are highlighted.

3 must-reads for World Oral Health Day

A highly pathogenic avian influenza (HPAI) outbreak has recently been reported in a broiler farm in Mississippi. The outbreak involves the H7N9 strain of the virus, a subtype that had not been detected in poultry in the United States since 2017.

The virus was found in a commercial poultry flock in Noxubee County, located in the eastern part of the state along the Alabama border

Clinical signs of the H7N9 outbreak, including an increase in deaths, were noticed on March 8, 2025. By March 13, 47,654 birds at the affected facility had been depopulated.

Birds infected with HPAI may exhibit the following signs

Swelling or purple discoloration of the head, eyelids, comb, or hocks

According to the Mississippi Board of Animal Health (MBAH), the Mississippi Veterinary Research and Diagnostic Laboratory, part of the National Animal Health Laboratory Network, conducted tests on samples from the poultry. The samples were later confirmed positive for HPAI by the Animal and Plant Health Inspection Service (APHIS) National Veterinary Services Laboratories in Ames, Iowa.

As per the MBAH, the birds on the property were depopulated and did not enter the food supply. Moreover, the affected premises were quarantined by the state veterinarian. Currently, the MBAH and Mississippi’s federal animal health officials are working on a joint incident response.

“The MBAH is actively working with the poultry industry to increase monitoring of flocks statewide,” wrote the MBAH in its announcement.

 This most recent outbreak of HPAI in commercial poultry is Mississippi’s third case of the virus in these animals since the spring of 2023.

Since November 2024, HPAI has been identified in migratory waterfowl across various regions of Mississippi, according to the agency. “The poultry industry was notified and put on high alert to increase biosecurity and surveillance for HPAI,” they continued.

In its announcement, the MBAH emphasized the importance of hobby poultry owners being aware of the signs of HPAI. The agency also encouraged these persons to follow good 

. Illness and/or deaths in birds should be reported through the 

, where information will be sent to a state or federal veterinarian in the state for evaluation.

“Dead birds should be double-bagged and refrigerated for possible testing,” wrote the MBAH.

 “Precautions should be taken when handling sick or dead birds including proper handwashing, using gloves, wearing masks, and sanitation of surfaces that come into contact with sick or dead birds to prevent the spread of avian influenza to people.”

According to the World Organization for Animal Health (WOAH), the H7N9 subtype of HPAI comes from a North American wild bird lineage.

 Prior to the most recent outbreak, the last instance of highly pathogenic H7N9 in US poultry was confirmed in March 2017 with outbreaks in 2 commercial poultry farms in Tennessee.

Although the H5N1 strain is the most prevalent strain of HPAI, H7N9 has shown to have a higher mortality rate. The H7N9 strain, according to the World Health Organization, has resulted in the death of 39% of reported humans infections since early 2013.

Schnirring L. H7N9 avian flu strikes Mississippi broiler farm. University of Minnesota. March 17, 2025. Accessed March 19, 2025. 

https://www.cidrap.umn.edu/avian-influenza-bird-flu/h7n9-avian-flu-strikes-mississippi-broiler-farm

Highly pathogenic avian influenza diagnosed in Mississippi poultry flock. News release. State of Mississippi Board of Animal Health. March 12, 2025. Acccessed March 19, 2025. 

https://www.mbah.ms.gov/wp-content/uploads/Press-Release-Noxubee-County-Highly-Pathogenic-Avian-Influenza-Diagnosed-in-Mississippi-Poultry-Flock.pdf

Avian influenza weekly update number 983. World Health Organization. January 31, 2025. Accessed March 19, 2025. 

https://cdn.who.int/media/docs/default-source/wpro---documents/emergency/surveillance/avian-influenza/ai_20250131.pdf?sfvrsn=5f006f99_149

The outbreak resulted in the depopulation of 47,654 birds