Authors Posts by Michelle Gerhard Jasny V.M.D.

Michelle Gerhard Jasny V.M.D.

Michelle Gerhard Jasny V.M.D.
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Michelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury.

Piglet, a nine-year-old tabby cat, looked me right in the eye. It was midnight. I don’t usually offer nighttime care, but Piglet had arrived on emergency 24 hours earlier for a urinary tract blockage and I’d been checking his bladder repeatedly ever since. Feline Lower Urinary Tract Disease is a common syndrome encountered in veterinary medicine, a catchall name encompassing a multitude of problems that all result in inflammation of the bladder and/or urethra.

We call it FLUTD (pronounced fluted) for short. Although it occurs in both sexes, in tomcats FLUTD can be life-threatening. It’s all about anatomy. In female cats, the urethra (the tube which carries urine from the bladder out of the body) is short, ending in a relatively wide opening inside the vulva. In male cats, the urethra travels farther. The last inch becomes very narrow and makes an “S” shaped curve before reaching the tip of the penis.

In FLUTD, urine from the inflamed bladder may contain mucous, crystals, red and white blood cells, bladder epithelial cells, even tiny bladder stones. This material can get stuck in that narrow male urethra causing an obstruction. With the urethra blocked, urine backs up. The bladder becomes excessively distended and tense. Clinical signs can include non-productive straining to urinate, abdominal pain, licking the genitals, loss of appetite, vomiting, acute kidney failure, severe electrolyte imbalances, possible bladder rupture, and eventually collapse, and death.

When Piglet arrived, the first thing we needed to do was relieve the obstruction by putting in a urinary catheter. Easier said than done. Sedation or even general anesthesia is often needed. My friend, Piglet, was feeling pretty badly, however, leaving him sufficiently apathetic that I was able to start placing the urinary catheter without knocking him out. As expected, within a centimeter from the tip of his penis, the catheter encountered resistance — the obstruction. What we do then is simple. We try to flush the junk out of the way by pulsing blasts of sterile saline through the catheter with a syringe, then advance the catheter farther and farther until it reaches the bladder.

Piglet’s case was tough, requiring multiple flushes but we eventually got the catheter in and were able to empty out the urine. Once the catheter is in place, sometimes we just flush the bladder, then pull out the catheter. Other times we sew it in place for a day or two, allowing time to treat the FLUTD without having to worry about our patient reblocking. Ah, there’s the rub. Cats with urethral obstruction have a high risk of blocking again in the first few days to weeks after the initial episode.

Piglet was one of those cats. In fact, Piglet seemed to have almost every complication possible. The night he first presented, he was in kidney failure due to the length of time he was blocked. Luckily, relieving the obstruction, followed by several days of intravenous fluid, returned his renal function to nearly normal. Then there was the issue that his bladder had been distended so long it had lost its ability to contract well. I knew by keeping his bladder emptied and using medication to stimulate muscle contraction, it would most likely regain contractility.

That’s where things stood that Saturday night. I had pulled the catheter earlier, hoping he could now pee on his own. But he couldn’t. With no one around to hold him for me, I had worked on developing a rapport with him. I petted him. I talked to him. “Let me help you,” I said soothingly, placing one hand on either side of his belly and gently squeezing out the urine. It hadn’t been coming in a good stream, but at least it was coming out, and he was letting me do it every few hours.

Then, at midnight, I squeezed him and nothing came out. His bladder was tense and distended again. Now I pride myself on being good with cats. Piglet and I understood each other, right? Such hubris. Piglet suddenly had enough. He turned without warning and sank his fangs deep into my arm. I think it hurt my feelings almost as much as my arm. So there we were. I had to sedate him and relieved the blockage. Again. Sew the catheter in place. Again. And add an Elizabethan collar to keep him from chewing it all out.Over the next few days Piglet proved to be a Houdini, pulling out every catheter I put in, despite sutures, despite the E-collar. I put on a bigger collar. He managed to get it off overnight. And he kept reblocking. Each time he needed sedation to replace the catheter. Urine culture showed a bacterial infection, resistant to all the usual antibiotics. Radiographs revealed multiple small bladder stones. By the end of a week it was apparent Piglet needed a perineal urethrostomy, often simply referred to by vets as a P.U.

Perineal urethrostomy is surgery intended to prevent the recurrence of obstruction by creating a wider outlet for the urine flow. The surgeon actually removes the penis, which contains that narrow S-shaped portion of the urethra, and makes a new opening, more like a female cat’s. Sounds bad, I know, but without that P.U. surgery, Piglet can’t pee. If he can’t pee, he can’t survive. As many as a third of all cats presented for urethral obstruction are eventually euthanized due to repeated blockage. Cats with P.U.s are still susceptible to FLUTD, but it is no longer life-threatening.

Piglet’s surgery went well. The stones were removed. The specialists were not overly concerned about the bacterial infection. Now we just have to hope he heals well, his bladder contracts normally, and that there is not too much residual kidney dysfunction.

Me? When my arm started to swell up and turn bright red, I saw the doctor and got some antibiotics. But I don’t hold a grudge. I’m one of Piglet’s biggest fans, despite that momentary lapse when he forgot how good I am with cats.

Hunter is a seven-month-old Bernese Mountain Dog. Just a puppy, he already weighs 76 wiggly pounds. If you haven’t had the pleasure of meeting a Bernese, this breed is one of several varieties of Swiss Mountain Dogs with an ancient heritage. Their ancestors are thought to have developed two thousand years ago from crossbreeding between mastiffs brought to the region by Roman invaders and local farm dogs that worked driving cattle, pulling carts to market, and being both watchdogs and companions.

These beautiful animals had many names including Farmer’s Dog, Gelbackler (Yellow Cheeks), Vierauger (Four Eyes, because of the facial markings), and my particular favorite, Cheese Factory Dog. In the early 1900s, dog fanciers pronounced them one breed, dubbing them “Durrbachlers,” after the Durrbach region in the canton of Bern. In 1908, Dr. Albert Heim, a professor, geologist, and canine researcher, introduced the name “Berner Sennenhund,” which means “Bernese Alpine Herder’s Dog.” This has remained the breed’s official name in Switzerland to this day, though they are often referred to affectionately as simply “Berners.”

Berners are sturdy, powerful dogs with long, silky black coats highlighted by dramatic rust and white markings. Bred to work, they need both exercise and interesting activity to stay healthy. They do best when exposed to many people when young. Berners are not for everyone. They’re big. They’re hairy. They like to be an integral part of the family and may not do well if left alone long or cooped up in a kennel or small space.

Our friend, Hunter, had plenty of company and exercise, his owners being well aware of a Berner’s needs, especially since his mom is my longtime assistant, Elise. She also knows that Berners have a notoriously short life expectancy, often only seven to eight years, although some lines may live longer and that purebred dogs have a higher risk of genetic disorders than mutts.

There is an old Swiss saying about Berners and related breeds. “Three years a young dog, three years a good dog, three years an old dog.” But the heart wants what the heart wants, and Elise and her husband, Daniel, wanted a Berner.

Last week Hunter spent the day playing at a relative’s house. He seemed fine that evening but next morning woke up lame on his left front leg. Hunter was so thrilled to visit Elise and me at work that day that it took two helpers just to take his temperature as he danced and squirmed on the table. His temperature was a bit elevated, but this is not uncommon in excited, active dogs. After a quick look at his general demeanor I went right to the gimpy leg, beginning with the foot. Owners frequently bring in limping dogs, saying “Maybe he has a thorn in his paw.” This is what comes from making school children read Aesop’s fable of Androcles and the lion. In 30 years of practice, and thousands of limping dogs, I have only seen an actual thorn (or any other foreign body) in a paw a handful of times. Nonetheless, I always check that first.

Hunter’s paw was fine. Working my way up I palpated each bone, and flexed and extended each joint while Elise tried to hold him still. Metacarpals, check. Carpus, check. Radius, ulna, check. Elbow, check. Humerus, check. Shoulder, ch… YOW. Hunter let out a sharp yelp when I hyperextended his shoulder. I let him relax a minute, then tried again. YOW.

I wasn’t being mean. I needed to confirm the reaction was repeatable, indicative of a real problem, not just a fluke. “It’s his shoulder,” I concluded. “Let’s watch him walk.” Hunter’s gait supported my findings. He placed his foot firmly on the ground, without hesitation. Dogs with paw injuries put the foot down tentatively, if at all. But as Hunter moved to bear more weight on that side, it hurt, so he shifted quickly back to the other leg. Voila. Limping Berner. Maybe he sprained it playing, but there was another more serious possibility.

Osteochondrosis dissecans (OCD) is a developmental problem affecting the cartilage that covers the ends of certain bones inside certain joints. Shoulders are most frequently affected, but OCD may occur in elbows, knees, or hocks. Most common in rapidly growing, large breed male dogs between four and ten months of age, no one knows the exact cause, but factors implicated include genetics, over-nutrition, hormones, excessive calcium intake, and trauma.

Imagine the shoulder joint. The top of the big arm bone, the humerus, is shaped like a ball and is coated with a smooth cartilage surface that allows the joint to rotate unimpeded. Now imagine a small area of that coating is abnormal — hard, thickened, and rough. It is more susceptible to injury and inflammation and eventually creates a small flap. Bits may even break free, creating tiny foreign bodies called “joint mice,” and leaving a divot in the surface of the humeral head. The degree of lameness varies with the severity of the lesion and may fluctuate with activity. Definitive diagnosis requires radiographs.

Treatment for OCD can start with conservative medical approach. Mild cases may do fine with just rest and medication, but, depending on the severity, untreated dogs are at risk for ongoing lameness and crippling. These require surgery, the earlier the better, to remove loose fragments, curette the defect, and try to stimulate healing. If one shoulder is affected, the other may be too. It is important to check both sides. Prognosis post-surgically is good, with 75 percent of patients eventually returning completely to normal. Since Hunter would barely hold still for an exam, properly positioned X-rays were going to require sedation.

“Let’s start with rest and pain medication. It may just be a sprain, “I said, optimistically. “If he doesn’t improve, we’ll anesthetize him for radiographs, check for OCD, and send you to the orthopedic specialist if necessary.” Hunter agreed with enthusiasm, wagging his whole body so hard he almost knocked me over. Three years, a young dog. Yup.

Dog Quixote is an 85-pound, senior Labrador retriever. We’ve known for a while about his hip dysplasia and arthritis, but one morning he took a dramatic turn for the worse. He just couldn’t get up. At all. I get millions of calls about old dogs who “can’t get up.” The majority are jauntily trotting around by the time they arrive at my office.

Many geriatric dogs simply get so stiff and achy they have trouble hoisting themselves up and getting their footing and balance, especially after lying down for a long time, after excessive exercise, or on slippery floors. Often all they need is a rubber-backed carpet for traction, a little assistance getting up, and arthritis medications.

But Quixote could barely lift his head. His owners carried him in on a homemade stretcher. When we tried using a sling to help him stand, he collapsed to the floor. His size and the degree of weakness made it hard to effectively evaluate his reflexes, but he did have feeling in all his limbs, and the ability to move them. He cried out when I touched various places, but it seemed more from anxiety than actual pain. Otherwise Quixote was bright-eyed and alert, eagerly eating the liver treat I offered.

Collapse is defined as the inability to support weight and walk without assistance. There is a long list of possible causes. We immediately ruled out respiratory and cardiac disease, and heat stroke, since he was breathing well, heart and lungs sounded fine, temperature was normal. Blood tests quickly ruled out metabolic disturbances that alter neuromuscular function such as low calcium, blood sugar, or potassium levels. That left us three categories of disease that could cause Quixote’s infirmity — orthopedic, neuromuscular, or neurological.

Orthopedic collapse is simply failure of the skeleton and/or joints to support an animal’s weight. In Quixote’s case there were pre-existing problems in his hips and knees, but we had never seen such severe symptoms, nor had his front legs ever been affected.

“His joint disease could certainly be contributing to his difficulties,” I said, “but it’s unlikely that’s the sole cause.” We needed to look further.

Neuromuscular collapse occurs when there is dysfunction in nerve conduction, in transmission of signals from nerve to muscle, or in the muscles’ ability to respond. This includes odd diseases like tick paralysis, myasthenia gravis, and polyradiculoneuritis, a.k.a. coonhound paralysis. Tick paralysis is caused by a neurotoxin in the saliva of certain ticks. It comes on fast, starting with the hind legs and rapidly progressing forward until the dog is completely paralyzed. Diagnosis is made by finding and removing the tick, and seeing if the patient improves. Without removing the tick, dogs may die from respiratory failure. Just what we need, huh? One more tick disease to worry about.

Polyradiculoneuritis is a similar progressive paralysis and is often linked to exposure to raccoon saliva, hence the alternate name “coonhound paralysis,” although many cases have no known initiating cause. Diagnosis is made on history and clinical signs. Most affected dogs spontaneously improve within three weeks and recover completely in two to four months.

One final neuromuscular disease to consider was acquired myasthenia gravis, an autoimmune disease affecting the receptors at the junctions between nerves and muscles, causing extreme muscle weakness.

But Quixote’s presentation did not fit any of the neuromuscular disorders exactly, so our diagnostic process went on to consider neurological diseases in which nerve impulses in the brain or spinal cord either fail to generate or are not communicated properly to the body. “Probably not in his brain,” I thought, since his mental status and cranial nerve functions were all normal. It was time to consider various spinal cord diseases.

Fibrocartilaginous embolism (FCE) occurs when a bit of gelatinous material from inside an intervertebral disc extrudes into an artery supplying the spinal cord. Exact symptoms depend on the exact location of the embolism, though classic presentation is sudden onset of weakness, without pain, often affecting only one side of the body. Definitive diagnosis requires MRI. FCE is most common in large breeds, like Quixote, although it typically affects younger dogs. Treatment is simply supportive care and most dogs improve with time. FCE is usually painless, and not progressive, but by Day Two, Quixote was a bit worse and clearly painful when I gently flexed his neck side to side. Probably not FCE. We were narrowing things down to intervertebral disc disease ( IVD).

Intervertebral discs are little cushions that sit between the vertebrae acting like shock absorbers. As animals age, these discs become less flexible and can push out into areas they shouldn’t, putting pressure on the spinal cord and/or nerve roots. Radiographs can help support a diagnosis, but MRI is often needed for a definitive answer and helps rule out other things like spinal cord tumor. Again, exact symptoms depend on exact location, as well as the severity of the disc herniation. Our radiographs showed an area in Quixote’s neck consistent with IVD. We also saw spondylosis deformans in his back, a non-inflammatory condition in which new bone forms bridging vertebrae together. This is fairly common in older dogs and is often of minimal clinical significance, although Quixote’s was quite extensive. With a presumptive diagnosis of IVD, we gave Quixote intravenous corticosteroids to reduce spinal cord swelling, emptied his bladder with a catheter since we weren’t sure he could urinate, then sent him home with oral steroids, analgesics, and antibiotics to cover for diskospondylitis, a bacterial infection of the intervertebral discs. His mom and I emailed back and forth constantly. Day Three Quixote heaved himself up, ran outside, urinated and defecated, then collapsed again. Same thing next day. His owner sent me video. His hind end staggered. His left front foot knuckled under. But he walked. Quixote is on his way now to an appointment with the neurologist. We hope an MRI and the specialist’s expertise will confirm a definitive diagnosis and treatment plan in hopes that Dog Quixote will soon get his feet solidly back under him.

Just past dawn Saturday, a call from my answering service rouses me. Coal, the cat, is not moving. His owners are afraid he has been poisoned. I shake myself awake, collecting my thoughts.

Being finicky, cats are less prone to eating strange substances than dogs, so true cases of toxicity are infrequent in felines. There are always worrisome items like antifreeze or lilies, but, more often than not, what a cat owner thinks is poisoning is something more common, like a fever.

Sure enough, when Coal arrived at my office he had a temperature of 104.5, well over the normal 101-102.5. I examined him. No wounds. No abscesses. Heart and lungs sounded fine, though his breathing was rapid and shallow. His tail twitched when I squeezed his abdomen, but he didn’t seem like it hurt. His third eyelids were up. He was slightly dehydrated, but his gums were a healthy pink.

“It’s a UFO,” I said, my standard stupid joke. Actually, it’s an FUO — Fever of Unknown Origin. “We see a lot of these in cats. There are many possible causes.”

Fever in a previously healthy young cat is usually caused by a viral or bacterial infection. If viral, it could be one of the big, bad viruses, like Feline Leukemia or Feline Immunodeficiency virus. Or it could be a milder disease, some nonspecific virus we can’t test for but that will pass on its own with time and TLC. Bacterial infections can also range from mild to something potentially deadly, like tularemia.

“Does he hunt?” I asked. Knowing an outdoor cat’s preferred prey can help steer us in the right diagnostic direction. Cats who prefer bunnies to birds or mice have a greater risk of contracting tularemia. Coal did hunt occasionally, but they had not seen him with any rabbits.As we continued talking, I observed Coal, flat on his side on the table, eyes half closed. Not good.

Even with a fever, most cats stay at least marginally alert in strange surroundings like the vet’s office. Coal was really down and out. What’s going on? I wondered, patting him gently and gazing into his face. Tell me, little guy, what’s wrong? Coal stared back limply, and purred.

“I’m worried,” I said. “He’s so spiritless. We should run some tests.” His owners agreed.

We quickly ruled out Feline Leukemia and Immunodeficiency Viruses, then ran an in-house screen for tick-borne diseases. “This is designed specifically for dogs, ” I explained, “but I do occasionally use it for cats. It’s fast and may help us figure out what’s going on.”

Soon after, two bright blue spots appeared in the results window. Coal was positive for antibodies to the organism called Anaplasma.

Anaplasma phagocytophilum (previously known as Ehrlichia equi) is a bacterium transmitted by deer ticks. Depending on the strain, susceptible species include deer, coyotes, mountain lions, horses, llamas, people, dogs, and — rarely — cats. Clinical signs of illness usually occur one to two weeks after the tick bite. In dogs, typical symptoms are fever, lethargy, depression, anorexia, muscle pain, stiffness, lameness, and reluctance to move. Occasionally dogs may also exhibit vomiting, diarrhea, coughing, labored breathing, swollen lymph nodes, and/or central nervous system signs such as incoordination or seizures. There are few documented cases of anaplasmosis in cats but symptoms reported in kitties are similar — primarily fever, lethargy, depression, and anorexia.

Coal certainly fit that picture, but our positive in-hospital test only meant he had been exposed to the organism and made antibodies. It didn’t necessarily confirm a current infection. Definitive diagnosis of anaplasmosis can be made in two ways. The bacteria infect white blood cells, forming little microcolonies called morulae.

Seeing these morulae on a blood smear under the microscope is one way to confirm diagnosis. I made slides of Coal’s blood, stained them, and searched in vain for morulae, but the fact that I couldn’t find them didn’t rule out anaplasmosis. Even in confirmed cases, morulae are only rarely found in feline blood. The second way to confirm would be to send out blood for a moderately expensive test called polymerase chain reaction (PCR) assay. But Coal was too sick to wait for results. He needed treatment now.

The drug of choice for many tick-borne diseases, including anaplasmosis, is doxycycline. For cats, this presents a dilemma as they can have a quirky reaction to this antibiotic when it is given in tablet or capsule form — inflammation of the esophagus. This may lead to a permanent stricture that can interfere with normal passage of food from mouth to stomach. To avoid this problem, we ordered a liquid doxy preparation from a compounding pharmacy, and to cover our bases for other infections, such as tularemia, prescribed an additional antibiotic called enrofloxacin. I sent him home that first night, hoping I had correctly communed with Coal and interpreted the clues he was giving us.

Returning several days later for a recheck, his mom confided that she had phoned her “animal communicator” about Coal’s case. She knows I am a bit of a skeptic when it comes to things like over-the-phone divining of an animal’s medical condition, but, hey, who am I to say? People didn’t use to believe in bacteria or viruses.

“The animal communicator says Coal has a headache,” she said, then asked “Why would he have a headache?” Well, the CDC page on anaplasmosis in people lists headache as the second symptom, right after fever.

“Your animal communicator’s reading is consistent with my presumptive diagnosis,” I laughed.

Coal’s mom laughed too. “Know what she says cats call you veterinarians?” I couldn’t wait to hear. “The Smelly Humans.” I considered the appellation. I suppose it fit. We veterinarians spend our days among multiple animals, bodily fluids, disinfectants, and other odoriferous items.

Coal looked at me from where he sat on my exam table. He was clearly feeling better, no longer laid out flat as a pancake. “That’s Doctor Smelly Human to you,” I thought.

Coal just looked smug, and purred.

When Maya was young, her owner thought he might let the big Rottweiler have a litter of pups. I gave my spiel about pet overpopulation, and the increased risk of mammary and uterine cancer as well as urogenital infections in unspayed dogs, then launched into my spiel about responsible breeding. So when Maya was four years old, we took radiographs to evaluate her hips for dysplasia. We discovered her conformation wasn’t great, making her a dubious candidate for breeding. It seemed she might be infertile anyway, as her heats were erratic and unusually mild. “You should have her spayed,” I suggested regularly.

But somehow the years slipped by. Maya had a bout of tick-borne disease, an unfortunate encounter with a fishhook, a case of “dry eye,” but she remained unspayed. More time passed. Now she was an old lady, with an old lady’s share of lumps and bumps, not surprisingly including several in her mammary area.

Spaying a dog before their first heat reduces the risk of mammary tumors to less than one percent compared to intact females. After one heat, the odds are eight percent. After two heats, 26 percent. By the third, spaying does not significantly reduce the incidence of mammary cancer. The good news is that as many as half of canine mammary tumors are benign. Due to her age, and the reasonable chance the masses were benign, Maya’s owner opted against surgical removal, and since it seemed silly to make a fuss at this late stage, I lightened up about urging him to spay her.

Then this July, during that awful heat wave, Maya started drinking and urinating excessively. At first, her owner didn’t think much of it. It was so stinking hot, of course she was drinking more. Then her appetite waned. “She’s barely eaten for a day and a half,” he told me. “Though she did eat a biscuit from the bank.”

I examined her. Temperature, weight, heart, lungs, all fine. Abdomen — well, at almost 100 pounds, she was too big for me to palpate much. I advised blood work and a urinalysis. Excessive urination and drinking are technically called polyuria and polydipsia, abbreviated as PU/PD. A chemistry profile would help evaluate for kidney failure, Cushing’s disease, diabetes, and other metabolic conditions that cause PU/PD. A complete blood count (CBC) would determine if she was anemic, or if there was an infection lurking. A urinalysis might reveal a urinary tract infection, and give us other useful information. I sent Maya home on broad-spectrum antibiotics, pending test results.

Back in the lab, I noted that the urine was pale, almost straw color. Using a refractometer, I checked the specific gravity. The urine was unusually dilute, almost like water. After spinning the sample in the centrifuge, I poured off the supernatant, added stain, then examined this sediment on a slide under the microscope. (If you don’t know supernatant from precipitate, go back to high school chemistry class!) Not much exciting. None of the inflammatory cells expected if this was a simple urinary tract infection.

Moving on to blood tests, her kidney, liver, blood sugar, and electrolytes were all normal. She was mildly anemic. Her white blood cell count was moderately elevated. Hmmmm. I put on my thinking cap. She was the right age range for a splenic tumor. That could cause anemia. She might have pyelonephritis — an infection up in the kidneys. She might have… Oh, drat! She might have a pyometra.

Pyometra literally means pus-filled uterus. When a dog goes into heat, the cervix relaxes to allow sperm to enter. Sometimes bacteria can invade instead. In older unspayed females, long-term hormone influences cause a pathological change in the uterine lining called cystic endometrial hyperplasia. This abnormal uterine lining is especially conducive to bacterial growth and massive infection can result.

Pyometra usually occurs one to two months after a heat cycle. If the cervix remains open, pus may drain from the dog’s vulva, but if the cervix closes, purulent material stays sequestered inside. The uterus can become extremely distended with pus. Toxins and bacteria may leak into the bloodstream making the dog extremely sick, the uterus may even rupture, but clinical signs of pyometra can be fairly nonspecific and vague, especially in the early stages. Symptoms may include depression, lethargy, poor appetite, PU/PD, vomiting, abdominal distension, vaginal discharge, and/or occasionally fever.

In some cases, the enlarged uterus can be felt by palpating the belly (taking care not to press too hard and risk a rupture), but radiographs, or even ultrasound, are often required for definitive diagnosis. Laboratory abnormalities may include anemia and elevated white blood cell count, as noted on Maya’s tests, as well as others we didn’t see with our patient, such as kidney dysfunction, low blood sugar, and electrolyte imbalances.

Pyometra is a life-threatening disease, especially if the cervix is closed. Recommended treatment is immediate surgical removal of the infected uterus. Risks of surgery include rupture of the pus-filled uterus into the abdomen, peritonitis, sepsis, kidney failure, disseminated intravascular coagulation, even aspiration pneumonia. The surgery can be difficult, and expensive, usually requiring several days of hospitalization.

Occasionally, if it is a valuable breeding animal, medical management with antibiotics and hormones can be attempted, but this is risky, and the problem tends to recur with each subsequent heat. Reviewing Maya’s previous history, I noted she had experienced similar symptoms last year and had recovered with oral antibiotics. This year seemed worse. Without definitive diagnosis by X-ray or ultrasound, I couldn’t say for sure, but pyometra was certainly a possibility, in which case, her life was in danger. As is often the case in veterinary medicine, age, prognosis, other ailments, and finances all had to be considered when deciding whether to pursue further diagnostics and surgery.

For now, we are hoping it’s not pyometra, and that she will again respond to medical treatment. But her case is a cautionary tale about some of the serious problems that may affect an unspayed female dog.

Retronym. I thought I had made it up but learned that the term was coined by a guy named Frank Mankiewicz in 1980. You know, those words we didn’t need back when all clocks were analog, all phones were land lines, and all documents were hard copy? Now although I love my computerized vaccination reminders and my cell phone, I still cling to a faux-leather, spiral-bound, paper appointment book where we scrawl our schedule in number two pencil. “10:00 Smith, K-9, Tunny, ADR. ” That’s “Ain’t Doin’ Right,” our catchall abbreviation for animals with nonspecific malaise.

This time of year, many ADRs turn out to be tick-borne diseases, so when Tunny, a middle-aged border collie cross, first arrived, that is what I expected. Until I checked his color. Not his coat color. The color of his gums. Unless pigmented black, these mucous membranes should be a healthy pink, but Tunny’s were pale, almost white. I glanced up, catching the eye of my assistant, Elise. She had seen it too and knew Tunny was in trouble.

“I just want to do a little test,” I explained, palpating Tunny’s tummy. Many things can cause pallor — but the most common in middle-aged dogs is a bleeding tumor of the spleen. I didn’t feel any unusual masses but could check quickly for internal bleeding by abdominocentesis, a five-second procedure tapping the belly with a needle and syringe. “No blood,” I reported, relieved, but still mightily concerned. It was time for further diagnostics.

Radiographs revealed an enlarged spleen but no obvious tumors. Blood tests showed severe anemia.When an animal is this anemic, there are three things that could be happening. He could be losing red blood cells through bleeding. Tunny had no visible source of blood loss — no nosebleeds, no bloody vomit or stool, no trauma. The abdominocentesis had not found blood in his abdomen, but I still couldn’t completely rule out a small tumor on the spleen, or even his heart, that didn’t show on x-ray. Referring Tunny for an ultrasound could help determine this.

The second possible cause for anemia is lack of red blood cell production. This happens with things like bone marrow cancer. The third is red blood cell destruction. When the body recognizes an abnormal blood cell, such as one infected with a blood parasite like Babesia, that cell is removed from circulation and broken down by the immune system. But red blood cell destruction can also happen spontaneously (and excessively) in a disease called autoimmune hemolytic anemia (AIHA).

AIHA occurs in dogs of both sexes and all ages, though some studies suggest middle-aged spayed females are at greatest risk. Breeds predisposed to the syndrome include cocker spaniels, springer spaniels, collies, miniature schnauzers, Dobermans, bichon frises, and Old English sheepdogs. Almost half of reported cases occur in the spring, especially May and June. Owners may notice progressive lethargy and weakness, poor appetite, vomiting, and discolored urine.

On physical exam, a veterinarian may find pale mucous membranes, elevated heart and respiratory rates, enlarged spleen or liver, heart murmur, and/or jaundice. Mortality rates can run as high as sixty percent.

Tunny’s family had difficult decisions to make. He needed an ultrasound to definitively rule out bleeding tumors. He needed further diagnostics to determine the precise cause of his anemia. He needed a blood transfusion while these tests were being pursued. Tunny’s situation was precarious. Hospitalization at a facility with ICU, specialists, blood bank, and round-the-clock care would optimize his chance of survival.

It is a particularly tough decision for Islanders, as this level of intervention requires a burdensome trip to the mainland. When I first came to the Vineyard, thirty years ago, few people opted to make that trek, and the standard of care for animals was far different. In those days we might make our best guess and send Tunny home with a handful of pills and a prayer. We might give Tunny a transfusion, using our own pet as a donor, without anything but the most rudimentary cross-matching to check compatibility. Sick animals often spent the night alone in unattended hospital cages. On the other hand, owners rarely ended up with huge veterinary bills.

Tunny’s owners lovingly opted to go to the specialists, but before leaving we had a heart-to-heart about prognosis and cost. “They won’t be able to tell if he is going to make it right away,” I said. ” They’ll probably advise several days of intensive care, maybe longer.” We discussed pragmatic options. The reality was that if Tunny was so sick that he needed more than one transfusion, his odds of recovery dropped dramatically, and the cost of more than a brief stay would be very high.

Over the next twenty-four hours Tunny was definitively diagnosed with AIHA. He was given a special transfusion of several units of packed red blood cells, kept in an oxygen cage, and started on an aggressive medical protocol. As anticipated, the specialists wanted him to remain hospitalized, but his owners were prepared. They had thought it through and made rational choices — emotional, medical, and financial. If Tunny was going to respond to the current protocol, we would know in a few days, whether he stayed hospitalized or not. Constant monitoring might give us more information, but wouldn’t necessarily change the outcome. And if he wasn’t responding well, his owners didn’t want heroic measures, nor did they want him spending his last days in a hospital cage, no matter how fancy.

Together we modified Tunny’s regimen to one we could manage here on Island as an outpatient. It’s a gift to have access to state-of-the-art medical care, but it is also both wise and compassionate to set limits. Maybe we need a retronym for the old-school, common-sense approach to veterinary medicine. Tunny received the initial benefits the specialists could provide, but now he needed to come home. Maybe that’s the retronym. Home care. Home, where he could be with the people who loved him, regardless of what lay ahead.

Like many baby boomers who spent their youth eschewing sunblock while basking on the beach, I now have some pesty spots on my face called actinic keratosis. Also known as solar keratosis, these rough, scaley patches are often considered precancerous, so my dermatologist repeatedly froze the areas with liquid nitrogen. But the spots kept coming back, so we moved on to a topical form of chemotherapy called fluorouracil, also known as Carac, Fluoroplax, Efudex, 5-fluorouracil, or just 5 F-U. I would apply a dab to each spot, then blot off the excess with a tissue, that I then tossed in the bathroom trash. What I didn’t think about was the fact that our bathroom trash has no lid and is full of dog-tempting items like paper products and dental floss.

We all know medications that come as pills and capsules and are dispensed in vials with child-proof caps can be problematic if Flyer, the Foxhound, eats them, but what about when he chews up a tube of antibiotic ointment? Or eats a tissue tossed in the trash after wiping the 5-FU? Let’s talk topical toxicity.

A topical medication is one that is applied to the skin. It may be intended to work locally, like antibiotic ointment on a cut, or to absorb into the blood, like a nicotine patch for quitting smoking. But it is never intended to be eaten, and although most topicals are relatively safe even if ingested, some are not, and a few are truly deadly.

Over-the-counter topicals like antibiotic or steroid ointments, and zinc-containing products such as diaper rash ointment and some sunscreens typically cause only mild self-limiting illness when ingested, but if Flyer eats a tube of something, be sure you know what was in it, and check with your veterinarian. Zinc oxide is a strong gastric irritant, so if Fly downs the Desitin, he may end up with a bad bout of vomiting. Treatment is simple supportive care except in the rare situation where an animal ingests enough to cause actual zinc poisoning, which causes severe anemia and usually requires blood transfusions.

Most veterinary cases of true zinc poisoning are the result of dogs swallowing pennies, which since 1983 have been made of zinc with a thin copper coating, but there is one reported case in which a person was applying a thick coating of diaper cream to a rectal mass on a dog every day. The dog then proceeded to lick it off, ultimately eating about three-quarters of a pound of Desitin over a four-day period, resulting in severe zinc poisoning. The dog survived but only after aggressive treatment.

Then we have “natural” products, like tea tree oil. It’s natural so it must be safe, right? Wrong. Extracted from leaves of the Australian Melaleuca alternafolia tree, this stuff is relatively safe when diluted, but many people buy it as pure oil. Put that high test product on Fly’s skin, and it will rapidly absorb into his blood stream. Even worse if he eats it. Less than two teaspoons can be toxic, whether ingested or applied to the skin, causing weakness, central nervous system depression, incoordination, tremors, hypothermia, even liver damage. Treatment is supportive care, and removing as much of the product as possible by washing Fly with something like Dawn dishwashing soap which is good at removing oily substances.

Oil of wintergreen is another of those things that sounds harmless. It’s in all kinds of ointments, liniment, and sports rubs. BenGay, Heet, Icyhot. Or you can buy pure oil in homey-looking little bottles that make you feel all organic. But despite its plant origins, and the fact that you may think of it as simply a flavor of gum or kind of tea, oil of wintergreen is methyl salicylate, a relative of acetylsalicylic acid, i.e., aspirin. You can find salicylates in many medicated face washes and acne control products from Noxema to Clearasil.

Salicylate overdose can lead to vomiting, gastrointestinal bleeding, elevated body temperature, weakness, depression, and incoordination. In very severe cases you can see stomach perforation, anemia, clotting problems, liver or kidney failure, and coma. There is no antidote, so treatment involves supportive care. Dogs can metabolize and excrete salicylates pretty rapidly, but cats cannot, putting them at much greater risk of salicylate poisoning.

People are not immune either. The death of one teenage athlete was attributed to overuse of a topical oil of wintergreen product. One teaspoon of pure oil of wintergreen is equivalent to about 20 adult-strength aspirin tablets and drinking it has caused quite a number of fatalities in small children. I doubt any of the people involved in these tragic cases had any idea the product could be lethal.

Which brings us back to 5-FU. Even tiny amounts can be toxic to pets. For cats, any exposure at all is dangerous. If you apply some to your face, forget to wash up, then go pat Purrbaby, who then grooms herself, ingesting a dab of 5-FU… It could be fatal. In dogs, it may take a little more, but it is still extraordinarily toxic. If Fly chews that tube, clinical symptoms develop within five hours including persistent vomiting, sloughing of the gastrointestinal tract, multiple organ failure, and severe seizures that do not respond to treatment. Seventy-five percent of affected dogs die within one week. So when I came home one day to find our dog, Flower, had happily tossed the bathroom trash in search of tasty tidbits, I was really worried. From then on I made sure tissues used to dab 5-FU were discarded in a pet-proof bin.

Don’t assume that because you can buy something over the counter, or because it comes in a tube, or because it’s “natural,” that it’s not dangerous. Keep these products stored securely. Remember, dogs and cats will lick off goop you apply topically. Check with your veterinarian before intentionally putting anything on your pet, and also if Fly gets into the ointment or anything else he shouldn’t.

Currer, an older dachshund, had gotten tangled up in a rope and hurt her foot, but that wasn’t her only complaint. There was a big bald patch on her back, the surrounding fur caked with odd, whitish debris. “That started when the cat scratched her,” Currer’s mom said.

I tugged gently on a tuft. The whole wad peeled away, leaving an even larger naked spot. I shook my head. “Doesn’t look like something from an injury,” I said, gazing thoughtfully at my patient. She was swaybacked — a concave arch in her upper back, an upward hunch in the lower. Her belly was plump and round, almost distended, though nothing abnormal noted on palpation. “Let’s treat that foot, plus antibiotics and medicated shampoo for the skin infection,” I suggested. “We’ll see how it goes.” We talked more about dachshunds, their propensity for back problems, and the need to get Currer’s weight down. Then I sent them on their way.

Though the limp improved, Currer soon returned. Not sure which things were significant, her owner provided me with a list of woes. “I think the glands in her neck were bigger, though not anymore,” she said. A mass that had been present in the anal area for many years had recently gotten larger, then drained some fluid, and returned to how it had looked previously. One time Currer cried when she tried to open her mouth. The dog was drinking and urinating more than normally, and having accidents in the house.

“TMI!” my brain protested, reeling with diagnostic possibilities. “We need to run some tests,” I said aloud, preparing to draw blood. A few hours later, lab work in hand, I had a suspicion of which symptoms were relevant and what might be wrong.

Hyperadrenocorticism (HAC), also known as Cushing’s disease, is a disorder caused by the ill effects of long-term excessive cortisol. Why does Currer have too much cortisol in her body? The most common reason is a benign pituitary tumor, which, although usually not malignant, does secrete a hormone called ACTH. That’s adrenocorticotropic hormone.

Don’t be scared by the big words. The concept is pretty simple. The pituitary gland in the brain is supposed to tell the adrenal glands, which sit in the belly alongside the kidneys, how much cortisol to produce. In a normal dog, when cortisol reaches the proper levels, the pituitary is happy and stops producing ACTH. The adrenal glands get the message and stop making cortisol. In HAC, that tiny pituitary tumor just doesn’t have an “off” switch. It keeps pumping out ACTH, pushing the poor adrenal glands to keep pumping out cortisol. This scenario accounts for about 85 percent of HAC cases. The remaining 15 percent are caused by tumors right in the adrenal glands, about half of which are malignant.

Regardless of the source, cortisol overload affects many different systems. The severity and specific signs depend on many factors and can vary greatly, case to case. Most dogs exhibit excessive drinking and urination. They are often inordinately hungry. The cortisol affects muscle tone and fat distribution, leading to a pot-bellied appearance. Other signs can include enlarged liver, hair loss, lethargy, muscle weakness, obesity, muscle atrophy, pimples, panting, incontinence, facial nerve paralysis, and a variety of skin disorders including thin, wrinkled skin, poor healing, and hair loss. HAC is common in dogs. Poodles, dachshunds, Boston terriers, boxers, schnauzers, and beagles are particularly prone. Most affected dogs are middle-aged or older, though it can occasionally be seen in younger animals.

Currer fit the picture. An older dachshund. Drinking and peeing excessively. Pot-bellied appearance. Skin problems. Our initial blood work also gave us a few clues that we were headed in the right direction, specifically a dramatically elevated enzyme called alkaline phosphotase. So we had our diagnosis, right? Not so fast.

Definitive diagnosis of HAC can be both challenging and expensive. First we tested Currer’s urine. It was unusually dilute, supporting the owner’s observation of excessive drinking and urination. A urine cortisol creatinine ratio found cortisol in Currer’s urine, another piece of data consistent with HAC, but still not definitive. There are two main tests veterinarians use for HAC, low dose dexamethasone suppression test or ACTH stimulation test. Sometimes both. I’ll spare you the details but simply say that by measuring how the adrenal glands and/or pituitary respond to administration of certain substances, we can usually confirm our diagnosis. Sometimes these tests also help distinguish whether the cause is pituitary tumor versus adrenal gland tumor, but often imaging techniques like ultrasound or even MRI are indicated to differentiate these two possibilities.

Several kinds of treatment are available for pituitary-dependent HAC. Lysodren and Trilostane are both drugs given orally. Lysodren selectively kills off part of the adrenal glands, thus lowering cortisol production. Trilostane inhibits an enzyme involved in cortisol synthesis. Both drugs must be given under close supervision with frequent monitoring, as they can occasionally create the opposite situation, a disorder called hypoadrenocorticism or Addison’s disease, which can be rapidly fatal. Since neither drug eliminates the pituitary tumor, lifelong therapy is required. Other medications sometimes tried include an antifungal drug called ketaconazole that interferes with cortisol production and an MAO-inhibitor called selegiline, or L-deprenyl, which suppresses ACTH production in the pituitary. Treatment for the adrenal form of HAC may be surgical, or medical, depending on the tumor, whether it is benign or malignant, and if it has spread. The prognosis for the adrenal form is usually much worse than for the pituitary-dependent form.

We sometimes opt not to treat HAC until symptoms are severe enough to cause obvious issues for either dog or owner. We are still deciding how to proceed with Currer. At 13 years old, we have to factor in the cost of all these diagnostics, medications, and monitoring, to think about possible side effects, and consider whether treatment will improve the quality of life for both her and her mom. Her symptoms are clearly progressing, but, at least today, she is still spunky and enjoying life.

Ty is a 17-year-old, 400-pound tiger in the care of Wildlife Rescue and Rehabilitation Inc. of Seminole, a group that helps with animals that have been seized by Florida law enforcement. I don’t know Ty’s whole story, but I assume he was a victim of the exotic pet trade, that bizarre bit of human nature that leads people into thinking it would be a good idea to have a lion, tiger, bear, or alligator for a pet instead of a nice cocker spaniel. But don’t get me started on the stupid things people do with animals.

Thankfully, Ty was in good hands with the nonprofit rescue organization. When he stopped eating for almost two weeks, they brought him to BluePearl Veterinary Partners, a huge specialty and referral center in Tampa that employs around 250 veterinarians and a support staff of more than a thousand. The first veterinarian to see him was an internal medicine specialist, who took radiographs, performed an ultrasound, and finally passed a scope down into Ty’s stomach to actually take a peek right in the tiger’s tummy.

As a veterinarian myself, I can just picture the procedure. Okay, folks, what follows is strictly my imagination and may have nothing to do with what really took place.

Ty lies anesthetized on the table. All the staff members who can find a legitimate excuse to be in the room are gathered around, because when else will they get a chance to be that close to a tiger? The veterinarian advances a flexible fiberoptic endoscope through Ty’s mouth, down his esophagus, into the stomach. “What the heck is that?” he exclaims, catching a glimpse of a large expanse of coarse brown fur. “I think he swallowed a whole racoon!” he exclaims. But the mass has no feet, no face, no form. It is just a great big wad of fur. It’s…OMG…the staff giggles nervously. Ty has a ginormous hairball.

Technically called trichobezoars, hairballs commonly occur in many species, including cats, rabbits, ferrets, even chinchillas. A hairball is exactly what it sounds like, an accumulation of fur ingested via grooming that gets stuck in the stomach and packs together to form what is essentially a gastric foreign body. It’s simply too big to come up easily via vomiting, or to pass uneventfully into the intestines. It just sits there in the stomach, often irritating the gastric lining and taking up space where the kitty chow is supposed to be going.

Let’s let sleeping tigers lie for a minute, and talk about our house cat, Chucky, a normal, healthy guy with a good appetite. He’s feeling fine except he has recently started doing this revolting, heaving, racking hack several times a day. It’s hard to tell if he’s coughing or trying to upchuck. You may want to consult your veterinarian right away to make sure the symptoms don’t indicate something more serious — asthma, an intestinal obstruction, even heart failure.

But if you’ve seen the ol’ hairball hack before, and Chucky seems okay otherwise, you can try starting with over-the-counter hairball medication, which is essentially flavored petroleum jelly. The concept is it will lubricate the hairball, maybe even help loosen and “degrade” it into a less dense mass of fur, thus allowing it to pass up or down. Many cats will lick these medications off a plate or mixed in wet food. It comes in yummy varieties like tuna, or even catnip.

Other cats require a little more encouragement. I like to load the goop into a syringe (no needle), then slowly squirt it, bit by bit, into the back of Chucky’s mouth, so I am sure he gets a good dose. Don’t bother with trying butter or vegetable oil. These just get digested. Don’t try to force mineral oil down Chucky’s throat either. Mineral oil doesn’t elicit a good cough reflex, meaning Chucky could inhale it by mistake resulting in a nasty pneumonia. Stick to commercially-prepared hairball remedies. They can be messy, sticky, gooey, but I believe they are frequently effective if given in adequate amounts as directed on the tube, or by your veterinarian.

Just so you know, many feline specialists would disagree with me. They say that hairballs usually indicate underlying gastric inflammation or a motility disorder warranting diagnostics and that there is no scientific evidence that lubricants help. While it is true I can’t find any scientific studies on the efficacy of these products, I have seen them work time after time in cats. I respectively suggest that the specialists simply don’t see the millions of routine hairball cases that we general practitioners encounter. We fix the easy ones and send the more complex cases on to them.

Consuming hair through grooming and hunting is a natural part of a cat’s life in the wild. Their bodies should be designed to handle a little fur. And they usually do. But a house cat’s life is not precisely the same as living in the wild. The diet is different. Chucky probably gets less exercise. These things may all contribute to reduced gastric motility. One study showed that hairballs are more common in long-haired cats and their frequency increases with age. Studies also show that added dietary fiber can reduce the frequency of vomiting and hairballs. So if Chucky has recurrent trichobezoars, switching to a commercial “hairball” diet makes sense. There are a few instances in which you should be sure to consult your veterinarian: If a fiber-rich diet and over-the-counter lubricant medication don’t solve the problem. If Chucky shows any other signs besides the occasional Hairball Hack. If you are dealing with a rabbit, ferret, chinchilla or some other non-feline friend. If the animal with the hairball is a 400-pound tiger.

Ty’s trichobeozar was way too big to pull out with the scope or for the tiger to pass naturally. It was removed surgically. The mass of fur weighed in at four pounds and was the size of a basketball. Now that’s a hairball.

The owner of each cat has a different theory about the source of the problem. “I think Tom has fleas on his face,”one says, pointing to the black, pepper-like dandruff on his cat’s chin. “Puss must have gotten into something in the garage,” says another, thinking the debris is dried paint, motor oil, or some other such substance. A third hadn’t noticed and is surprised when I point out the redness, pimples, and hair loss on Kitty’s chin.

Feline chin acne is a fairly common skin disease of unknown cause. It can occur in cats of any age, sex, or breed. Acne is by definition a condition in which hair follicles become clogged with oil and dead skin cells but we don’t know for sure why one cat develops it and another doesn’t. So let’s take our hypothetical kitty, Zitty. The first thing Zitty’s owner notices are little black specks of stuff in the fur on her cat’s chin. Yup, it sure looks like flea dirt — our euphemistic term for flea excrement. You can definitively determine if a black speck has come from the back end of a flea by placing it on a wet piece of white paper towel. Because fleas feed on blood, flea poop will “bleed” a rusty-red ring on a damp towel. With chin acne, the black specks are not flea dirt, so where do they come from?

In the early stages of feline chin acne, material accumulating in abnormal hair follicles produces visible comedones, or blackheads, on the chin, at the corners of the mouth and edges of the lower lip. As bits of discolored debris flake off, the darkening of the fur progresses. The area sometimes becomes a little red. Secondary bacterial infection can lead to more intense crusting, swelling, and redness. Itchiness can cause Zitty to scratch or rub resulting in patches of hair loss. In very severe cases, the entire chin may become thickened or scarred.

If you see those specks on Zitty’s chin, it is a great idea to get a good flea comb and then, well, literally go over him with a fine-toothed comb to check for evidence of fleas elsewhere on his body. The strip of fur down the middle of his back to the base of the tail is often the best place to comb for fleas, though in some cats the little critters like to hang out on the belly, or even the head and neck. Comb everywhere. If you find live fleas or black specks on places other than his chin, you know you need start thorough flea control immediately. Occasionally that is all that is needed to clear up a case of feline chin acne, but often Zitty is flea-free, so we can’t blame his problem on that.

There are many theories about the underlying causes of feline chin acne. Some cases are the result of allergies or hypersensitivity. I always recommend making sure all Zitty’s food and water bowls are made from stainless steel, glass, or other non-reactive material. I have seen a few cats improve dramatically when all plastic bowls were removed, but this does cure the acne in the majority of cases. Zitty may simply have an inherent problem with excessive or abnormal production of sebum (the oily stuff made by the sebaceous glands associated with the hair follicles) just like some people have problems with overly oily skin.

Another theory impugns Zitty’s personal hygiene habits, suggesting that cats with chin acne tend to be poor groomers, allowing the oils to build up on their skin. Like with people, stress and other conditions that weaken the immune system seem to increase the risk of acne. On the other hand, hormonal influences that play such a significant role in human adolescent acne do not seem to be a factor for cats.

So what are we to do about Zitty’s zitty chin? After ruling out fleas and eliminating obvious sources of irritation or contact allergy, there are several other diseases on our differential diagnosis list. Specialists generally recommend a number of tests to check for mange mites and fungal infections like ringworm, and to identify specific types of bacteria or yeast. Biopsies of the area can definitively rule out conditions like eosinophilic granuloma (a syndrome that deserves its own article) but frankly, in most cases, if it walks like a duck and quacks like a duck, it’s a duck. Or a zit.

Treatment depends on the severity of the problem. In some cases it is helpful to clip the fur off Zitty’s chin, making the area easier to clean and treat. Occasionally clipping increases local irritation. A warm compress can help soften the debris and the area can be washed gently with benzoyl peroxide shampoo and treated with 2.5 percent benzoyl peroxide gel. This flushes the hair follicles and inhibits blackhead formation. Some cats get more irritated with this gel, so if the problem worsens, talk with your veterinarian about substituting a different cleansing agent like a salicylic acid wipe. If there is secondary bacterial or yeast infection, your veterinarian may prescribe topical antibiotic or antifungal ointment. In more serious cases, oral medication may be warranted. Deep-seated bacterial infections may require oral antibiotics for as long as six weeks. Zitty may also benefit from omega-3 fatty acid supplements like fish oil. Such products often help with a multitude of skin conditions. Occasionally chin acne can be so bad that oral corticosteroids like prednisone are indicated to reduce swelling and inflammation, or even treatment with retinoids for severe refractory cases, but these situations are uncommon.

Although amenable to treatment, feline chin acne does tend to be recurrent, requiring lifelong care to control it. But the prognosis is good. If the acne is mild, it is primarily a cosmetic problem and unless Zitty is going to the prom soon, it probably doesn’t bother him much or affect his quality of life.