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-JasnyMichelle 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. She can be reached at: drjasny@comcast.net.

“If an orange-faced Oompa Loompa and a grey-faced Oompa Loompa have babies, what percentage of their offspring will have orange faces?” my husband asks. My daughter is studying genetics and her homework is full of chromosomes, genes, dominant and recessive traits.  I smile as my daughter shouts gleefully, “One-fourth orange faces!”

In veterinary medicine, we deal with genetics daily. What’s the difference between Chihuahuas and Great Danes? They’re both dogs, but selective breeding for particular genes makes one huge, the other teensy. Genetics give us the smooshed faces of bulldogs, the wrinkled skin of Shar-Peis. Even behavior and temperament can be driven by genetics — herding behavior, guard dogs, dogs who like water, or retrieve, or track scents. A dog’s breed strongly influences personality and behavior. It also affects predisposition to certain diseases.

“You should review this record before the appointment,” my secretary suggested, the morning after the Oompa Loompas. “Sounds complicated.” The owner had dropped off a list of concerns about his dog, Aberdeen. Difficulty housebreaking. Not responding to commands. Acting like he’s lost. Odd blank stare. Unusual gait. Hypersensitivity to noise. Trouble gaining weight. I then did what every veterinary student is taught to do first. Look at the signalment. That means breed, age, and gender. All these impact the likelihood of various illnesses. Aberdeen was a 15-month-old intact male Llewellin setter. My first thought was that he was so young I should first consider congenital and inherited  problems. My second thought was what the heck is a Llewellin setter? I readily admit I’m kind of lame when it comes to knowing every breed. I have enough trouble remembering where I left my glasses. So I began researching.

The Llewellin setter is a specific “pure” strain of English setter tracing its bloodlines back to a 19th century dog breeder and sportsman named R.L. Purcell Llewellin in South Wales. Ignoring all the doggy politics about whether they are a distinct breed or not, for my purposes the pertinent information was that, medically speaking, they are English setters. Next I researched inherited conditions of English setters. Hip and elbow dysplasia — not relevant. Deafness -— interesting. Hearing-impaired dogs may be hard to train, act lost, not respond to commands. Oh, wait a minute. His owner said Aberdeen was hypersensitive to noise. Scratch deafness.

Then I saw a disease I had never heard of before — neuronal ceroid lipofuscinosis (NCL). An autosomal recessive genetic mutation that causes accumulation of abnormal stuff inside cells in the nervous system, which in turn leads to devastating progressive neurological dysfunction, NCL has been reported in dogs, cats, and humans. (In people it is called Batten disease or Familial Amaurotic Idiocy.) Canine breeds affected include English setters, Tibetan terriers, American Staffordshire terriers and bulldogs, border collies, Australian shepherds, Labrador retriever, Polish Owczarek Nizinnys ( no kidding), and  dachshunds.

Age of onset can span from one year in dachshunds to five years in Tibetan terriers but once NCL begins, it is progressive and typically fatal. Symptoms vary, breed to breed. Most develop vision deficits. Almost all exhibit a change in gait, loss of balance, or incoordination. Dementia with confusion, progressive decline in intelligence, and loss of prior training is common, as is hypersensitivity to sound, touch, and movement. Affected dogs may become withdrawn, fearful, or aggressive. Eventually dogs develop severe seizures and either die or are euthanized by two years of age. There is no cure.

When Aberdeen arrived, I didn’t want to unduly upset his owner. NCL is extremely rare. It was probably something else. Something simple. Something curable. I began my exam. Other than being thin, Aberdeen looked physically healthy. He heard when I made a loud noise. He blinked when I poked my finger at his eyes. His retinas looked fine. He had normal feeling and motion in his legs. Perched on my exam table, he seemed pretty normal, maybe a bit bemused.

“Let me watch him walk,” I said. Aberdeen’s hind legs moved a bit stiffly. His front legs lifted too high with each step as though marching to a drum only he could hear. His dad had mentioned that Aby had recently developed an odd way of cocking his head when offered a treat, so I held out a cookie. Aberdeen slowly extended his neck, tilted his head, then very, very slowly took the treat. I did it again. He did it again. I dropped a treat on the floor. I could tell he had seen and heard it drop, but now couldn’t seem to locate it, searching around an unusually long time before finally finding and eating the tidbit.

“I’d like to record all this and send it to the neurologist,” I said, grabbing my iPad. The owner used treats to entice Aby to walk back and forth as I filmed. Then Aberdeen spontaneously started walking in circles. His owner offered another treat. Aby cocked his head, stretched his neck, and suddenly started spinning in tight circles, like a kid break dancing. He was agitated and growling continually with his head held way up in the air. Dogs with ear infections or balance disorders will frequently have a head tilt and circle, but this was different. There was a weirdness to his behavior that we call “altered mentation,” a kind of dissociation that was clearly neurological. It was time to discuss NCL.

There is a blood test available to screen for the NCL genetic mutation in English setters, so we sent a sample to the researchers in Missouri. The doctors there viewed the video and agreed it might be NCL. If the test comes back negative, Aberdeen still clearly has a problem that should be evaluated by a neurologist who can do further testing and brain imaging. If it turns out to be neuronal ceroid lipofuscinosis, then sadly, there is nothing we can do, other than to alert the breeder that his line of dogs is carrying this rare but fatal genetic condition. If only all genetics were as fun and as easy as orange-faced Oompa Loompas.

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Michelle-JasnyMichelle 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. She can be reached at: drjasny@comcast.net. 

Almost one year old, the playful Bernese mountain dog weighed in at nearly 90 pounds. When he first started behaving as though his back hurt, we weren’t too concerned. “He probably just strained something running around,” we said, prescribing rest and anti-inflammatory pain medication. When that didn’t help, we tried a muscle relaxant, but his symptoms continued. He began to whine and pace at night, sometimes yelping or leaping up suddenly when anyone brushed past him.

Here in the clinic, Bernie walked normally but was anxious, jumping around, and making it hard for us to pinpoint the source of his discomfort. We ruled out Lyme disease with a blood test and added a second pain medication. We discussed radiographs, but since he was so bouncy and would probably need sedation for that, we decided to wait a while longer.

One week later, Bernie slipped and fell on the ice. Immediately after, he developed “posterior paresis,” a weakness in the hind legs resulting in an abnormal gait usually indicative of a spinal cord problem, but we still couldn’t localize any particular place that hurt. “Let’s take those pictures,” I advised.

My main differentials for Bernie at that point included intervertebral disc disease (IVD) or fibrocartilagenous embolism (FCE). In simple English, IVD is a “slipped disc.” FCE is an embolism compromising the blood supply to the spinal cord. It typically affects large breed young dogs. Despite his youth, we also had to consider cancer, as Bernese mountain dogs are very prone to it.  Bernie was now sufficiently subdued to allow us to X-ray without sedation. The films looked normal, but that didn’t rule out anything. It just meant that whatever was causing Bernie’s pain was not visible on plain X-rays.

If it was FCE, there was no rush. FCE is not progressive. There is no specific treatment other than supportive care. The neurological deficits often resolve with time. If it was IVD, that often responds to corticosteroids and rest. As long as he could feel and move his legs, IVD wasn’t urgent, although surgery might ultimately be indicated to relieve pressure on his spinal cord. If it was cancer? Well, that would be a much bigger bridge to cross, should we come to it. We gave Bernie intravenous corticosteroids, prescribed more orally to give at home along with his pain medications, and added tranquilizers to keep him quiet and give his back a chance to heal.

But it was not to be that simple. Bernie’s condition worsened. It was time to consult the specialists.

On initial exam, the neurologist also could not localize Bernie’s pain. That made me feel better. At least I had not missed anything obvious. She and I spoke each day as they gathered information. New radiographs were suspicious for a fracture of Bernie’s third thoracic vertebral body.  No, the fracture wasn’t visible on the films we had taken earlier, and it wasn’t the kind of clean break one would expect from simple trauma. Besides, it would be unlikely for a big healthy puppy to fracture a vertebra just from slipping on the ice — and some of Bernie’s symptoms pre-dated his fall.

The radiologist reported a “moth-eaten” appearance to the bone consistent with either tumor or infection. Either of those might have weakened the bone, resulting in a “pathological fracture” when Bernie slipped. “I’m really concerned it may be a tumor,” the neurologist confided. “Or diskospondylitis, which is almost as difficult to treat.”

Diskospondylitis is a bacterial or fungal infection of the intervertebral disks and adjacent vertebrae. Most often seen in medium to giant breed dogs, especially German shepherds and great Danes, any breed can be affected. It is even occasionally diagnosed in cats. It typically occurs in young to middle-aged individuals, with males being affected twice as often as females. Symptoms vary depending on exact location and severity of the lesion and may develop slowly or suddenly.  Signs may include pain especially when trying to get up, reluctance to jump, a stiff gait, incoordination, weakness, weight loss, poor appetite, lameness, and fever. Radiographs may appear normal for up to a month after the infection starts, but eventually they reveal changes in the intervertebral disk space and adjacent bone. The bacteria are usually spread via the blood, though the primary source of the infection often cannot be determined. It may start as a urinary tract infection, a wound, a foreign body like a grass awn, even dental disease.

Bernie needed more tests — MRI, CT, biopsies, cultures. While waiting for results, the specialists started him on antibiotics. We all held our breath, fingers and toes crossed, that it would not be cancer. The CT confirmed the pathologic fracture and mild spinal cord compression consistent with either diskospondylitis or tumor. The  biopsy showed no cancer.  Urine cultures were negative. Blood cultures, however, were positive for staphylococcus, confirming the diagnosis of bacterial diskospondylitis. The concurrent “sensitivity panel” listed the best antibiotics to combat this specific infection.

Due to the location of his fracture and the presence of infection, surgical stabilization was not advised. We had to depend on Mother Nature to heal the break, and, with our help, to stop the infection. Bernie came home on long-term antibiotics, gradually decreasing corticosteroids, and a cocktail of pain medications. He was outfitted with an elegant vest with handles on the top so his family could easily assist him getting up and walking, though his exercise still needed to be restricted for many weeks as he heals.

This is only the third case of diskospondylitis I have knowingly seen in 30-plus years of practice. We have a saying in medicine — you can’t find something if you don’t look for it. It wasn’t on my initial differential list (that won’t happen again) and it required extensive sophisticated  testing to establish the definitive diagnosis and treatment.

The prognosis for diskospondylitis depends on the degree of spinal cord damage and the organism involved, but Bernie has been improving steadily and we are very hopeful he will make a full recovery.

 

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Sipping my morning tea, I was expecting a mellow Monday. January on the Vineyard, not many appointments scheduled. Then the phone rang. Pip, a 12-pound Cairn terrier mix, had found and consumed part of a block of rat poison.

“Bring Pip. Bring the block. Bring the poison container. Now!” I said.

When a dog eats a potentially toxic substance, it sometimes makes sense to do the math to determine if the amount ingested is truly dangerous before rushing to the vet, but in this case, with rat poison, and such a small dog, it was a case of better safe than sorry. When Pip arrived, we instilled a smidgen of apomorphine under her eyelid where it would be rapidly absorbed and tell her brain that she should vomit.

As she deposited multiple piles of bright green barf on strategically placed newspapers, I examined the rat poison container. Most rodenticides are anticoagulants, i.e., they work by interfering with blood clotting. The nice thing is that there is an easy antidote as long as you begin treatment immediately after ingestion, so I wasn’t initially too worried. Then I read the label.

“Drat,” I swore. “It’s not an anticoagulant. It’s bromethalin.” Bromethalin is a potent neurotoxin that works by disrupting nerve function, leading to central nervous system signs and death by respiratory paralysis…and there is no antidote. “Good thing you got here quickly,” I sighed.

The bait had been in a location that the owner thought the dog couldn’t reach, but somehow Pip had managed. Maybe some big rat had dragged it out. Who knows?

We carefully determined the maximum amount of bait Pip could have eaten. I did the math. LD 50 is shorthand for “Lethal Dose 50%,” the amount of a substance that when ingested will kill 50 percent of the animals. Pip’s exposure was probably about half the LD 50, enough to still be worrisome (though from the mess on my exam room floor, it looked like she had thrown up most of it.).

“We’ll give activated charcoal to help prevent further absorption of any poison left in her gut,” I said. “Take her home and watch her like a hawk. Call if you see anything like hyperexcitability, tremors, or seizures.” If Pip did develop clinical signs, all we would be able to do was give supportive care and hope she would survive.

I went on with my day with a constant nagging worry about Pip in the back of my mind, but as each hour passed, I relaxed a bit more. Then, late afternoon, just when I was feeling confident Pip would be fine, the phone rang. Another dog had just eaten a bottle of ibuprofen.

The dog’s name? Pip. I’m not making this up. This Pip, also a terrier mix, was a bit bigger, at 28 pounds. “Bring Pip. Bring the pill bottle,” I said.

The effect of ibuprofen toxicity in dogs is dose dependent. At lower doses it can cause severe gastrointestinal irritation, even ulceration. Moderate doses can lead to kidney failure, and high doses to central nervous system dysfunction. Fatalities are not uncommon. When Pip arrived we gave him apomorphine while I did the math. His owner thought the bottle had only been half full, maybe less, but couldn’t be sure. It sure was empty now. I read the label. 200 mg tabs. Fifty tabs when the bottle was full. For Pip’s size, 11 tabs would put him at risk for fatal kidney damage.

When Pip hurled, we could only find the remnant of two pills in the vomitus. Did that mean he had only eaten two? Or had he eaten 20 and the rest had just moved down into his intestines. Better safe than sorry. We instituted a treatment protocol of activated charcoal, gastric protectants, antacids, and intravenous fluids. It would be three days before we could be sure he was out of the woods. On Tuesday, we continued his intravenous fluids.

Pip One’s mom reported all was well. I went about my day, no longer worried about Pip One, but concerned about Pip Two. That afternoon another client called. Her dog was drooling and his lips were a bit swollen. Yesterday, on their walk, he had eaten something he found in the woods that was red and crumbly and looked kind of like plastic. She had taken it away from him and still had the remains.

Was his name Pip? I joked. No, it was Booley. “Bring Booley. Bring the red stuff,” I said.

When Booley arrived, I examined the remnant of red, waxy, material. It had a ridged surface pattern and bits of bird seed. All the rat poisons I was familiar with were green, but this sure looked and felt like a rodenticide. A little research determined it was, in fact, the anticoagulant brodifacoum. Since Booley had eaten it the day before, it was too late for vomiting or charcoal. He had already absorbed whatever toxin he had consumed.

Anticoagulant rodenticides are tricky as they take three to five days to cause symptoms. People think that because the dog looks fine at first, they will continue to be fine. Not. Once they start bleeding, the prognosis for survival plummets. I did the math. Worst-case scenario, Booley might have consumed one tenth of the lowest reported LD 50. That is right at the cut-off point where specialists advise treatment. Better safe than sorry. We started Booley on the antidote, vitamin K, advising his owners to keep him quiet and watch carefully for any signs of abnormal bleeding.

By Friday, Pip One was fine, his owner planning how to make the rat poison inaccessible in the future. Pip Two’s mother reported he had rolled on a dead fish and was pretty proud of himself. Booley seems okay, but because brodifacoum is a long-acting poison, he will need 30 days of Vitamin K.

I made myself another cup of tea, hoping for a quiet weekend. After all, it’s January on the Vineyard.

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The three kittens in the carrier peered out curiously. “We weren’t going to get purebreds again,” one of the owners said. The couple had shared their home for years with a beautiful pair of Burmese cats who were now gone. “Then we read about Tonkinese and couldn’t resist.”

Looking at that trio of exquisite faces peeking through the grate, I understood completely, but I didn’t know much about the breed. To me the word Tonkinese conjured up images, not of cats, but of the musical South Pacific. (“How far away, Philadelphia, P.A….from coconut palms and banyan trees and coral sands and Tonkinese.”) I, too, was curious, so I did a little research.

Tonkin is the name given by the French to the northernmost region of Vietnam. In the 1900s, indigenous people from this area emigrated to work on colonial plantations on the island of Vanuatu (formerly called the New Hebrides). Referred to as “Tonkinese” by westerners, James Michener wrote about them in “Tales of the South Pacific,” on which the famous musical was based. So what about Tonkinese cats? Are they from Vietnam, too?

The breed called Tonkinese was developed in North America in the 1960s by crossing Siamese and Burmese cats, so let’s start there. Siamese cats are thought to date back at least to the 1600s. Their introduction to the West began with a pair named Po and Mia given to a departing British Consul-General by the Siamese king in 1884 (Siam, of course, being modern day Thailand). The Siamese Cat Society of America was founded in 1909. Over the decades Siamese breeders altered their appearance to have a thinner body, elongated head, long, skinny legs, and unusually large ears. The Burmese breed began with a single small walnut-brown cat named Wong Mau brought from Asia by a sailor in 1930 and given to Dr. Joseph Thompson in San Francisco. The doctor bred Wong Mau to Siamese cats and, using selective breeding, developed a consistent coat color called sable. Burmese eventually became recognized as a separate breed, with four officially accepted colors — sable, champagne, platinum, and blue.

In the mid-1960s, two breeders in North America began crossing Siamese and Burmese, working to develop a specific “moderate” breed they agreed to call Tonkinese. So, no, Tonkinese don’t actually come from the Tonkin region of Vietnam, but they are descended from cats that originated in southeast Asia. Tonkinese now come in 12 officially recognized colors with varying levels of contrast between body color and “points.” Most have dramatic aqua eyes. Because they started out as hybrids, theoretically Tonkinese are less likely to have inherited medical issues than breeds like Burmese, which have narrower gene pools.

One of the three kittens had an upper respiratory infection, giving his owners a bit of a scare, but this fairly common condition is rarely serious, and Kitten One soon recovered. Then, at five months old, Kitten Two suddenly began pawing his face. We’re not talking gentle rub-the-face-with-the-paw. Two was having repeated intense episodes of frantically clawing at his mouth. His dad even shot a video for me.

“Let’s take a look,” I said calmly, trying to soothe the owner’s anxiety. Two was acting the way a dog does when a bone or stick gets lodged in the mouth. I expected to find something in Two’s mouth, remove it, and be a hero. But I couldn’t see anything unusual. “Let me check under his tongue,” I continued. Occasionally cats playing with string or thread will get it caught around the tongue causing similar behavior. Nope. Nothing under the tongue. The only thing I could see was Two was teething. His adult canines and premolars were erupting and the associated gums were a bit red.

“We read on the Internet about some kind of serious mouth problem in this breed,” the owner volunteered.

“I think he’s just teething,” I stammered, “but I’m not sure.” We decided I would give Two pain medication and keep him for observation while doing further research.

Who knew? It’s called FOPS. Feline Orofacial Pain Syndrome. First recognized in the 1990s, it is characterized by severe oral pain and self-mutilation. It is most common in Burmese cats. Signs can be intermittent or continuous and can be triggered by eating, drinking, grooming, or stress. Current information suggests that there are two different age ranges when FOPS is likely to occur. The first is around six months of age and is associated with teething.

Bingo. There’s our diagnosis for Two.

The second time it occurs is often between 10 and 12 years old. FOPS is defined as “neuropathic pain,” an exaggerated response to a normally painful stimulus. It appears to be a genetic dysfunction of the processing of information from the trigeminal nerve in the brain. Definitive diagnosis is based on clinical signs and by ruling out everything else. This could mean dental X-rays and referral for expensive tests like MRI. The more I read, the more worried I became. Often multiple drugs are needed to control symptoms, sometimes even anticonvulsants. In one study, 10 percent of cases ended up with unremitting, severe self-mutilation leading to euthanasia.

Luckily, Two responded to the first pain medication we tried. He was still pawing, but much less. One article reported that antibiotics can be helpful in cases with underlying dental infections, so we gave an injection of long-acting antibiotic and sent him home with additional doses of pain medication. In case things got worse, we ordered a second recommended drug in kitten-sized tablets from a compounding pharmacy. But we never needed them: within a few days, Two seemed back to normal. I breathed a cautious sigh of relief.

Seventy percent of FOPS cases recur. All we can do right now is hope that Two is in the other 30 percent. Because of the suspected genetic basis, individuals with the syndrome should not be bred. Two’s owners are fine with that. They just want One, Two, and Three to live long, happy, and healthy lives.

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When my daughters were little I read them the Little House On The Prairie series. We loved learning about life on the frontier. The simple pleasures. The ingenuity. The hardships. Sometimes we watched the television show based on the books.

What always struck me was what happened when someone needed a doctor. Pa would hitch up the horse and buggy, then ride as fast as he could into town to find Dr. Hiram Baker, the local physician and veterinarian. When he got to Doc’s office, Pa often found that no one was home. The doctor might be ten miles away, delivering a baby, or tending someone on their deathbed. As far as I remember, there were almost no telephones in Walnut Grove. There were certainly no pagers, no cell phones. Pa couldn’t call, text, or email. If he needed Doc badly enough, he had to physically go track him down. My children couldn’t imagine such a world.

“Well, when I was your age, there were no home computers,” I said while driving them to school. “No wi-fi. No Google. If you wanted to find something out, you had to go to the library, search your subject in a card catalog, find the book in the stacks, look in the index, and see if that book could answer your question.”

They looked aghast. “I love Google,” one sighed. I agreed. It is very cool to have so much information right at our fingertips. Unfortunately, it means we also have a lot of misinformation at our fingertips.

When clients bring me tomes downloaded from “Dr. Google,” I have to wade through all their research, separating the wheat from the chafe. I don’t want to ignore an owner’s efforts. Perhaps there is some new treatment I am not aware of that might be useful. It’s nigh impossible for one lowly veterinarian to keep current with all the advances in medicine these days. But most of the time, I find they are bringing me information about some 21st-century equivalent of snake oil or magic beans.

Then there’s Facebook. I resisted mightily for a long time, but eventually joined in order to find an old friend. Then several old friends found me. That was nice. Then clients started to friend me. Okay. I like my clients. Then people I didn’t know started sending Friend Requests. “Do I know you?” I wanted to ask, but that seemed so rude. Then people started messaging me veterinary questions. All the time.

“It’s bad enough I can’t go to Cronig’s without having to talk about fleas,” I thought grumpily. “Can’t I even waste time on FB reading about everyone else’s perfect lives (children, vacations) without having to play James Herriot!” I longed to move to Walnut Grove where Pa would never hitch up the buggy after dark or on a weekend just to bother Doc about fleas or diarrhea. But in the midst of my Bah Humbugging, I happened to see that one of the animal-focused Facebook folks had shared a link about veterinarians and burnout along with a lovely comment encouraging people to appreciate their veterinarians.

Burnout. Also called compassion fatigue. It is a kind of physical, emotional, and/or mental collapse brought on by overwork, stress, and isolation. Medicine has come a long way since Doc Baker’s day, which is all well and good, but for physicians (and veterinarians) it means a huge amount of ever-burgeoning information to be mastered. This has led to a statistically proven increase in burnout among doctors, often manifested by substance abuse, depression, even suicide.

Doctors on the front lines of health care are at highest risk because they usually work the longest hours for the lowest pay. Primary care docs have a higher rate of burnout than specialists such as dermatologists or pathologists. (Though when you see how busy dermatologists are here on the Vineyard, there’s no doubt they have their share of overwork and stress.). General practice veterinarians are in a similar situation to primary care physicians, facing long hours, hugely diverse demands, and lower pay than their specialist colleagues.

People who are caregivers for the chronically or terminally ill also suffer from the depression associated with burnout. Faced day in, day out with a situation in which a patient doesn’t get better, it is not unusual to succumb to feelings of helplessness and hopelessness.

For veterinarians, because our patients typically have much shorter life spans than human beings, we see an awful lot of death. Probably more than your average primary care physician.

We also play a particularly poignant and personal role, guiding people through decisions about euthanasia, then personally performing the actions that lead to an animal’s passing. Add the loss of control of one’s time that comes with doing emergency work, and technology that now enables us to be available 24/7, and you end up with an emotionally exhausting life. Especially when you consider that most of us went into this business because really, we actually do love animals. Some of us even like the people that own the animals.

And hard as it is for you to lose your beloved pet, it’s hard for your veterinarian too. Hard for us to feel like we couldn’t fix the problem. Hard for us to say good-bye to animals we may have known since they were puppies and kittens. Hard to see you grieve. You, our clients, who often over the years have become our friends.

People in all walks of life suffer from burnout, from depression, from hidden struggles. It’s a good time of year to remember to open our hearts to each other. In the words of Laura Ingalls Wilder, “Christmas Eve was the time when everybody was unselfish. On that one night, Santa Claus was everywhere, because everybody, all together, stopped being selfish and wanted other people to be happy. And in the morning you saw what that had done. ‘If everybody wanted everybody else to be happy, all the time, then would it be Christmas all the time?’ Laura asked, and Ma said, ‘Yes, Laura.’”

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Landon has never been a dog who hides his feelings. Adopted from an off-Island shelter six years ago, no one knew for sure how old this sweet beagle was nor much about his medical history, but when anything hurt, Landon let us know loud and clear with a classic hound dog howl. He suffered periodic neck and back pain, yelping in anticipation if his mom went to lift him. As he got older, he developed a heart murmur, a cough, a benign growth inside his eye called an iridociliary cyst, and a case of separation anxiety. He made himself sick eating chicken bones from the trash and chocolate chips off the counter, but his mom adored him, nursing him tenderly through one thing after another.

As his veterinarian, it was often hard to know when something was really wrong, since Landon would scream any time I touched him. Did his leg hurt, or was he just anxious? What about that tooth? It looked fine, but he shrieked whenever I tried to examine his mouth. I was just thankful his owner knew I was not, in fact, torturing her beloved pet when he carried on this way in the exam room. But when he arrived on emergency late one night there was no doubt Landon’s distress was real. Earlier that evening he had been restless and breathing hard. She had called me, but knowing Landon’s propensity for drama, I hadn’t been overly concerned. “Let’s see if he settles down overnight,” I said, suggesting a little Benadryl to calm him, but several hours later his owner decided he truly needed urgent care.

She was right. Landon walked in my door, his breathing rapid and labored, his stomach heaving in and out as he tried to move air. He held his neck stretched forward in his efforts to breathe and had been coughing badly at home. Putting my stethoscope to his chest, I immediately heard loud crackles. “Sounds like fluid in his lungs,” I said. “And that heart murmur is much louder.”

Landon looked like a classic case of acute congestive heart failure (CHF), a cardiac illness that is usually characterized in dogs by sudden onset of fluid in the lungs. The underlying heart problem may vary. Elderly small dogs often have heart valve disease. Certain large breeds such as Doberman pinschers are prone to a genetic condition affecting the heart muscle called cardiomyopathy. Regardless of the initiating cause, the result is often pulmonary edema — fluid in the lungs. Symptoms may include coughing, rapid, labored respiration, and an elevated heart rate. Landon fit the picture and we made a presumptive diagnosis of CHF.

“I’m giving him a diuretic to draw the fluid out of his lungs, and other medications to support his heart,” I said, then explained how to monitor his sleeping respiratory rate (SRR) at home, i.e., the number of breaths per minute when he was fast asleep. “We’ll repeat doses of the diuretic until his SRR is less than 40. Tomorrow we’ll take radiographs. Maybe consult a cardiologist.”

The next day Landon’s SRR was down to 36 and he was feeling fine, but I still wanted X-rays of his heart and lungs. The films surprised me. There was a little fluid in his lungs, but his heart looked pretty normal. His liver and spleen, however, were enlarged.

“Let’s run a few blood tests,” I suggested, beginning to question my late-night diagnosis. A chemistry profile revealed a few abnormalities including elevated liver enzymes. Moving on to a complete blood count (CBC), my in-house machine kept refusing to register a white blood cell count, lights flashing and error messages telling me to make and examine blood smears under the microscope. That’s what we did, and in no time flat realized that something was desperately wrong. There were way too many of the white blood cells called lymphocytes. Way way too many. A sample sent to the pathology lab the next day confirmed our fears. At more than 10 times normal, Landon’s lymphocyte count was consistent with a diagnosis of lymphoid leukemia.

Lymphoid leukemia is cancer of the bone marrow resulting in a huge proliferation of one specific type of white blood cell, the lymphocyte. It is classified as acute or chronic.

Chronic lymphoid leukemia (CLL) often has an insidious onset with virtually no clinical signs initially. It progresses slowly, leading to weight loss and lethargy. Treatment can be delayed until the dog is feeling poorly. Survival times with chemotherapy range one to three years.

Acute lymphoid leukemia (ALL) has a more dire prognosis with less than half responding to chemotherapy and an average survival time of two to four months. It is more common in younger animals, around four to five years old, but older dogs may be affected. Signs may include lethargy, weight loss, poor appetite, nose bleeds, bruising, increased respiratory rate, labored breathing, lameness, and/or enlarged liver and spleen. Sometimes a pathologist can differentiate ALL from CLL on the CBC, but in Landon’s case we would need additional tests — flow cytometry, ultrasound, possibly liver, spleen, and/or bone marrow aspirates.

Landon’s mom was faced with tough choices. The prognosis for ALL was very poor, no matter what we did. CLL might be treatable, but the medications are extremely expensive. While we were still considering the options, Landon suddenly developed another problem, one more consistent with ALL. He went blind in one eye, the eyeball bulging and red. Despite having been surprisingly stoic so far, he now was obviously in pain and his owner was increasingly concerned about his quality of life.

We started oral corticosteroids in hopes of making him feel better, maybe even getting temporary remission, also eyedrops to lower intraocular pressure, and analgesics for pain. Once again, Landon rallied.

We know his time is short, but we’re taking it one day at a time. Landon is not a dog who hides his feelings, and we trust he will tell us when it’s time to say good-bye.

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Each night of Hanukkah begins with lighting of menorahs. From left: Max Marcus, Jack Crawford, Ali Marcus, Molly Crawford, and Sydney Marcus.

The story of Hanukkah tells the tale of the first documented armed struggle for religious freedom in human history. It begins in the second century B.C.E. when Judea was conquered by the Greco-Persian tyrant Antiochus. Although many urban Jews embraced Hellenistic culture with its emphasis on science, poetry, and athleticism, to rural religious Jews Greek culture smacked of pantheism and idolatry, with its marble statues of gods and deification of the human form. To force them to assimilate, Antiochus outlawed essential Jewish practices. Jews were forbidden to keep their dietary laws, study Torah, or observe the Sabbath. The Temple in Jerusalem was desecrated and the Jews driven out.

A family named Maccabee took refuge in the mountains from where they fought a guerilla war in the face of staggering military odds. The Maccabees became folk heroes, and after three grueling years, recaptured the Temple, and the country. The legend goes that when they reentered the Temple to rekindle the sacred Eternal Light, they found only enough oil for one day. A messenger was sent on the long journey for more holy oil. Miraculously, one tiny cruse of oil burned eight days until he returned. The Hebrew word Hanukkah means “dedication” and refers to the reconsecration of the Temple.

Long considered a “minor” festival, Hanukkah has been celebrated for more than two thousand years. In contemporary times, after the Holocaust decimated the European Jewish population, many Jews found inspiration in the story of the Maccabees. Hanukkah took on even greater emotional significance when the state of Israel was established. In the Diaspora, where Jews live increasingly assimilated lives, the proximity of Hanukkah to Christmas also served to increase the holiday’s prominence. Both observances involve festive lights and gift-giving, but the similarity ends there. This year, due to differences between the solar-based Georgian calendar and the lunar-based Hebrew calendar, Hanukkah will coincide with turkey and football, not Santa Claus and eggnog. Hanukkah actually has far more in common with Thanksgiving, as both commemorate struggles for religious freedom.

The lighting of the candles

Each night of Hanukkah begins with lighting of menorahs, also called chanukiahs. These special candelabras have eight branches, one for each day, and a ninth branch for the shamash, a “servant” candle for lighting the others. Hanukkah candles may not be used for mundane purposes. They are not to be used to light a room, read a book, or accompany dinner. Their sole purpose is to enjoy their beauty and reflect on the miracles of God. Except in times of severest persecution, Hanukkah menorahs are customarily displayed in a window.

After candle-lighting, Jews traditionally eat foods fried in oil, in remembrance of the miracle of the long-burning oil in the Temple. Potato pancakes, called latkes, served with applesauce and sour cream, exemplify the Ashkenazi tradition from Eastern Europe, but there are many other Hanukkah foods. Ljuba Davis of Vineyard Haven keeps alive her family’s Sephardic heritage that reaches back to the expulsion of the Jews from Spain in the 15th century. She makes burmuelos, deep-fried dough drenched in warm honey, and keftes, fried patties made from leeks, onions, eggs, and pine nuts.

West Tisbury resident Geraldine Brooks and her family plan to serve latkes at Thanksgiving dinner. They have a family custom of betting whose candle in the menorah will last the longest. Asked about Hanukkah customs in her native Australia, she says “like all holidays [there], it’s topsy-turvy. It’s early summer, and there’s no snow for the light to flicker on, but we do all the same things.”

Nicole Cabot of West Tisbury agrees. Like many Islanders, her family also observes with latkes, dreidels, and small gifts. Although some parents feel compelled to match the effusive gift-giving associated with the commercialized aspects of Christmas, traditionally Hanukkah presents are small. They might include gelt, or coins, for playing dreidel, a gambling game played with a four-sided top inscribed with four Hebrew letters: nun, gimel, hey, and shin that stand for the Hebrew phrase “A great miracle happened there.” In Israel, dreidels have one letter changed so the phrase becomes “A great miracle happened here.”

On the other side of the world, Dominique Ariel Hendelman, formerly of Edgartown, is observing both Thanksgiving and Hanukkah in Israel. “We are doing a potluck meal that is going to merge the two holidays together,” Dominique reports from Talpiot in eastern Jerusalem, where she is studying Hebrew. “We’ll have a turkey obviously and one of the girls even had cranberries sent from The States because they’re very hard to find here in Israel.” Jelly donuts, called sufganyot, are a traditional Israeli Hanukkah treat. Dominique has a recipe for sweet potato sufganyot to really blend the two celebrations. A freelance writer for the Jerusalem Post, Dominique touches on some deeper political concerns. “We’ll play dreidel and eat stuffing, and try to reconcile the fact that Thanksgiving is not such a nice holiday to celebrate in the first place. Hopefully there will not be any small pox blankets. To me, Thanksgiving is really about over-eating good food and being with family and friends. Hanukkah has a lot of those same elements.”

An act of justice

Acknowledging that humanity still faces many challenges, Judaism teaches that people have a responsibility to participate in tikkun olam — which means “healing the world.” Thus, giving tzedakah is an important part of all Jewish observances including Hanukkah. Loosely translated as “charity,” the word actually is derived from a root meaning righteousness, justice, or fairness. In Judaism, giving charity is not seen as being magnanimous. It is simply an act of justice. Rabbi Caryn Broitman’s family has a tradition of each person choosing a charity to which to donate during Hanukkah and many families encourage their children to place donations in a Tzedakah Box at home or at synagogue. A community Hanukkah celebration is planned at the Martha’s Vineyard Hebrew Center on Wednesday, December 4, at 5 pm. Congregants are asked to bring their menorahs from home. In past years there have been more than 30 menorahs, all lit together. Since this year’s party falls on the eighth night, that could mean 270 candles. All are invited to come and enjoy their light, and reflect on miracles.

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“My daughter has a new cat named Gaia” a client called me the other day with a cautionary tale. “I had loaded the wood stove with newspaper and kindling, then left the door open and turned away to get matches…”

I could see where this was headed. Cats love to explore, to curl up in strange, out-of-the-way places. These are natural instincts with adaptive value. There may be delicious mice under the porch, or tasty birds in the rafters. In the wild, sleeping tucked away in a hiding place keeps slumbering animals safe from predators and retains body heat in cold weather. But sometimes these natural instincts lead kitties astray. Like our caller’s cat.

“I was about to light the fire when I heard rustling inside the stove,” he continued. Sure enough, Gaia had climbed inside the stove and nestled down in the papers. Luckily, the owner realized it before he set anything on fire.

That family’s cats like heating equipment, I thought. Fifteen years ago their cat Ringtail went missing. They searched in vain. The children scoured the neighborhood on bicycles, but he was nowhere to be found. Three weeks after his disappearance, a neighbor called from Philadelphia. An electrician doing repairs in their vacant Vineyard house had heard faint mewing in the walls. Were they missing a cat? Ringtail’s dad immediately went to the house in question and called for the cat. Ringtail meowed. Calling back and forth like a game of Marco Polo, the owner discovered that somehow Ringtail had gotten into the house, then the basement where he crawled into a heating duct. He had traveled deep into the walls, the ducts becoming narrower and narrower, until he found himself lodged in a six-inch-wide pipe, unable to turn around or back out.

Ringtail had dropped from nine pounds down to four. He was skin and bones, weak, dehydrated, hypothermic, and soaked in urine. But he was alert and seemed to know he had been rescued. We started intravenous fluids and warmed him up. Soon he was eating baby food and using his litter box. By the second day, he was able to stand up. By the fourth day he was able to wobble around a bit. After six days hospitalized in my clinic, he had gained two pounds and was ready to go home. He eventually regained all his weight plus some and lived to be almost 18.

I remember another curious cat mishap, involving one of those old gas stoves with the broiler on the bottom near the floor, and a client cooking pork chops. The chef opened the broiler compartment to peek in and see if dinner was ready. Then, turning around to do something else in the kitchen, he realized he hadn’t closed the stove. Without looking, he pushed the broiler door shut with his foot. Seconds later, there was a wild banging inside the stove. He quickly jerked the door open, and his cat came flying out. When the cat arrived at my office soon after, she had a series of parallel grill marks across her back and side, like steak coming off the barbecue. Luckily, her thick fur had protected her well. It was mostly hair that had been burnt, though she had several linear areas of first and second degree burns to the skin, which we treated with topical medication and oral antibiotics. I don’t remember the patient’s name, but we referred to her thereafter as Broiler Kitty.

It’s understandable that cats would be attracted to warm wood stoves, yummy pork chops, and the excitement of exploring duct work, but what about my friend AnneMarie’s curious kitten story. Here’s what she wrote when I asked for details. “When I was living in a big farmhouse in Vermont, I couldn’t find my little black ball of fur (only eight weeks old) one night. After searching everywhere I could think of, and not finding him, I went to bed, figuring he was all curled up somewhere snug. In the morning I asked my roommate to help me pull the refrigerator out from the wall because we had not thought to look behind it. At the same time we saw he was not there, we heard a meow. I looked at her and said, ‘It sounds like he’s in the fridge!’ Sure enough when we opened the door and pulled out the crisper drawer, there he was! I thought he would be in shock and hypothermic, but he came walking out, started purring and wanted to eat. We figured he was in there for about 15 hours! (I remembered the night before I had made a salad and when done just pushed the drawer in and closed the door.) Needless to say, I do think the cold affected his brain cells because even though he was lovable he was not a particularly smart cat!” In honor of his escapade, she named him Crispy Critter, and he also went on to live a long life.

Not every story ends so happily. Don’t leave the clothes dryer door ajar, tempting your pet with that cozy laundry. More than one cat has been badly tumbled, and some killed from being closed inside. In winter, cats who spend time outside are attracted to the warmth and shelter provided by cars and trucks. Some climb inside wheel wells, tucking themselves atop a tire, or crawl under the hood of a recently driven car, where it is nice and toasty. If you turn the car on without warning, a dozing cat inside can be severely injured. Veterinarians call these “Fan Belt Cats,” and the resultant trauma is often life-threatening. So bang on the hood of your vehicle before you get in. Close the dryer door. Check the wood stove. I don’t know how many kittens would actually climb into the vegetable crisper, but at least one did. Never underestimate a feline’s sense of adventure. Don’t let curiosity kill the cat.

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One of the fun parts of writing my column is naming the animals. For hypothetical cases, I might choose something silly. Sweetie Pie, the diabetic cat. Polly Dipsia, the dog who drinks excessive water. When reporting about actual pets, I use pseudonyms to protect the privacy of the owners. Dogs don’t seem to care much. Cats like to read about themselves in the paper, but they know my pseudonym choice is irrelevant as it is never their true “deep and inscrutable singular name.”

Sometimes I go obvious. Tom, the cat, becomes Dick or Harry. The dog Grover becomes Elmo. Sometimes I take a more circuitous route. Leopold becomes Kinshasa. (Know your African history?) Charlotte becomes Currer. (Check out pen names of the Bronte sisters.)

When I write about patients, it is often in the midst of caring for them. Researching the latest helps me keep current medically while simultaneously gathering information for the column. The upshot, however, is that I often don’t know how things are going to turn out when we go to press. A gentleman recently left me a message inquiring about the outcome of one story. “What happened to Thunderbolt? Please call back.”

I was happy to reply, but being a pseudonym, I had no idea who Thunderbolt was or what problem he had. I racked my brain. I checked my old articles about thunderstorms. I thought about dogs named Zeus or Thor. I searched my data base for various terms. I finally gave up. I couldn’t remember. Here at the office we have computerized reminders for follow-up calls. I plug in data when a pet goes home, and later my staff calls owners and gets updates. You don’t have that option, so today here are progress reports about some cases you may have read about in these pages.

Isaac, the overweight golden retriever who went acutely blind soon after starting weight loss medication was diagnosed by MRI with immune-mediated meningitis of unknown cause. The neurologist does not think it was related to the diet medication, though we opted not to use it again with him. He has been on corticosteroids for a year. His vision returned quickly, though when we first tried to lower his cortisone dose he relapsed slightly until we bumped it back up. He’s doing great now, though still plump, and we are very, very slowly weaning down his medication.

Tunny, the border collie cross with autoimmune hemolytic anemia received multiple blood transfusions and other treatment at the specialists but then had to come home a little before the doctors would have liked. He’s doing well on a variety of long-term immunosuppressants as well as medications to protect his gastrointestinal tract from side effects and anticoagulants to lower the risk of blood clots. I was a little concerned about how long it has been taking for

his blood counts to normalize. In my 30 years of practice, all the AIHA cases I have seen either got completely better or passed away by this point, but I check in with the specialists regularly and they reassure me everything is on track.

Don Quixote, the big lab with neck pain who was collapsing and virtually unable to walk, had an MRI that revealed a large lesion in his spine. At first we thought it might be cancer, but it turned out to be a ruptured disc that was removed surgically. Don is dancing around now almost as though nothing ever happened.

Sylvester, the diabetic Maine coon cat, had less definitive results. The special diet did not get his blood sugar under control. Before starting insulin, we decided to send him to the neurologist, who noticed abnormalities in his front legs as well as his hind. She is concerned he may have a primary problem with his muscles or nerves, unrelated to his diabetes, but recommended regulating his blood sugar with insulin first. If he doesn’t improve, the next steps may be MRI, muscle biopsies, or other specialized tests to evaluate his neuromuscular function.

Piglet was the cat with the recurrent urinary tract blockage who needed the penile amputation surgery called a perineal urethrostomy. Surgery went well, after which, on the advice of some specialists, I stopped his antibiotics. Big mistake. Piglet’s kidney failure worsened dramatically soon thereafter. We obtained a urine sample, and cultured a nasty bacteria that turned out to be susceptible to only a very limited number of antibiotics. I prescribed one available at the local human pharmacy. His owners gave it to him faithfully, as well as daily subcutaneous fluids at home. The renal failure turned out to be completely the result of bacterial pyelonephritis, i.e., a kidney infection, which resolved with a month of treatment. He has gained two pounds, his kidney function is normal, and he’s peeing beautifully. It’s funny the things that make me happy.

Maya, the rottie who I was afraid might have the uterine infection called pyometra that is life-threatening without emergency surgery, happily survived to bark another day with just oral antibiotics. But her problem is likely to recur with each heat so her owner is thinking about having her spayed despite her senior age.

Blanche, the cat with feline infectious anemia, and Coal, the kitten with anaplasmosis, both recovered completely with antibiotics, though sadly Coal passed away from other causes. Zev was the cockapoo with the cardiac problem called AV block. The cardiologists suggested a pacemaker, but Zev was not a young dog, so his owner decided to just enjoy whatever time he had left. We had hoped he might live for many months, but he passed away peacefully in his sleep soon after his diagnosis.

I’ve scanned back through years of articles to glean these follow-ups. Still haven’t found Thunderbolt. And now I’ve misplaced the message slip with the caller’s name and number. Perhaps it will come to me, suddenly, like a bolt of lightening. Or maybe you will call and remind me. Please. I promise to report how things turned out.

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You know you’re getting old when women your own age, or even younger, start showing up with Little Dogs. We’re talking dogs that fit in your pocketbook — Yorkshire terriers, teacup poodles, Chihuahuas.

As a teenager, my family had a diminutive cocker spaniel I adored, but by college I youthfully dismissed any canine under 50pounds as Not A Real Dog. I longed for a statuesque Irish wolfhound, but settled for an Irish setter husky cross (who, sadly, ended up having the worst traits of both breeds). As an adult I adopted Heidi, a Labrador with diabetes and cataracts, then Sadie, a Samoyed with glaucoma. Both were blind, but both were big. Then when my kids came along, we got Flower, a mixed breed pup who grew large enough to be a passable substitute for the often requested pony. My younger daughter inherited my penchant for large dogs, yearning for a great dane or Swiss mountain dog, both of which I tell her she can have when she has her own house, hopefully bigger than the one we live in now. But the older I get, the more I understand about owning Little Dogs.

Animals intentionally bred for extreme physical characteristics, like being extra big or extra small, are at greater risk for medical problems. Giant breed dogs have notoriously short life spans, as well as a predisposition for problems like bloat. Pug-faced dogs are known for respiratory difficulties from their smooshed-in snouts. Little Dogs…well, they have their own list.

Take Amigo, the Chihuahua, who came in recently for an introductory examination. At six months old, he weighed less than four pounds. “I can’t let him outside unattended,” his mom said. “A big hawk buzzed him the other day. It just came out of nowhere.” I nodded.

Another Chihuahua owner I know was walking her wee one on a Vineyard beach when a red-tailed hawk swooped down, grabbed her pup by the head, lifting it several feet into the air. Whether it was the weight of the dog, or the effect of an hysterical woman screaming and waving her arms frenetically, the big bird lost its grip and the Chihuahua tumbled to the ground. Miraculously, except for several puncture wounds from the talons, the pup was uninjured. Yup. Better not let Amigo run around outside taunting the local raptors.

Examining young dogs always includes checking for congenital defects, i.e., abnormalities they were born with. Amigo looked fine. Eyes, ok. Teeth, no overbite or underbite. I opened his mouth to look for cleft palate. Nope. I ran my hands over the top of his domed head, gently feeling where the various skull bones join across the crown. Except Amigo’s skull bones didn’t all join in the middle. Instead there was a central area about the size of a nickel that was soft and squooshy.

It’s called a fontanel — a membrane-covered opening between the bones of a young skull. If you’ve raised a baby, you know those “soft spots” on an infant’s head that allow it to squeeze through the birth canal. In people, fontanels close gradually between the age of three months up to two years. In dogs, the fontanel on top of the head should close by 12 weeks of age. But in Chihuahuas, as well as several other toy breeds, the fontanel often doesn’t close. Ever.

Chihuahua fanciers call it a “molera,” saying that it is normal for the breed, and it is not considered a defect by the American Kennel Club Breed Standards. In fact, for many years, the presence of a molera was considered proof of the purity of a dog’s Chihuahua blood line. Here’s where breeders and veterinarians may be at odds. Many veterinarians consider any fontanel that does not close by 12 weeks to be an inherited defect and advise that the dog in question not be used for breeding.

There is also some controversy as to the health implications of persistent fontanels. (A brief aside about grammar. Many people call this condition an “open fontanel.” Technically speaking, that is redundant: by definition, a fontanel is open.) Some veterinarians believe that persistent fontanels are associated with greater risk of hydrocephalus — increased accumulation of cerebral spinal fluid inside the ventricles of the brain. This puts pressure on the brain and can lead to seizures, blindness, pressing of the head into corners, and extreme difficulty in house training. Hydrocephalic dogs may also exhibit the “setting sun sign” in which the eyes point downward and sometimes to the outside. They can be treated temporarily with medications to reduce the pressure, but eventually a shunt should be placed surgically to drain the excess fluid. In their “Molera Statement,” the Chihuahua Club of America cites several studies and veterinarians stating that there is “adequate medical evidence” that a molera does not predispose a Chihuahua to hydrocephalus. But I think the jury is still out on this one.

Amigo was well past the 12-week mark for closure of the fontanel, but some Chihuahua sites claim moleras may continue to get smaller until a dog is up to three years old. I do not know if this is true. I do know that since Amigo appeared neurologically normal there was nothing else we needed to do. If he ever showed signs of hydrocephalus, an ultrasound of the brain could be done via the fontanel, but he has a perfectly good chance of leading a perfectly normal life and never having any problems. I advised his owner to take extra care with his head and to never press the soft spot. If she wanted, there were even places she could purchase a tiny helmet for him. I wondered if Amigo would tolerate such headgear. Then I thought how cute he would look and imagined myself toting around a four-pound dog wearing a mini-bike helmet. That could be as cool as having an Irish wolfhound.

The older I get, the more I understand the charm of Little Dogs.