by Marcia Herman

Veterinary diagnostic tools have advanced remarkably in the last 10 or so years, yet they don’t always help veterinarians make accurate diagnoses when the problem is a rare or complicated one. If Tucker had been able to talk, he’d have had quite a story to tell. All his veterinarians tried hard to help him and used countless diagnostics to determine what was wrong with him, but only the last diagnostics told us what was wrong; it was kidney disease.

February 1993. I never wanted a greyhound puppy; I was perfectly happy with my adult greyhounds, a whippet, and our cats. Then it happened.  He wouldn’t leave me or my heart alone. He stretched as far as his little six-and-a-half pound, six-and-a-half-week-old body would stretch; he pawed my knees, play bowed, and smiled at me. We brought home this too-young puppy who smiled at us for 10 years. His name became Tucker. We thought he’d be healthy since he had never seen a race track. We were wrong.

The Wormy Puppy

Tucker’s first visit to the veterinarian the day after bringing him home was traumatic. He was so tiny I put him into a cat carrier. He was claustrophobic. He screamed. He drooled. He bit his tongue. We lived through that, but what was to follow shocked me. The veterinarian said he had the worst case of roundworms he had ever seen. If he hadn’t been dewormed soon, he would have died from them. Shortly after taking his dewormer, he deposited spaghetti-like roundworms in a cat litter box in the kitchen; it was too cold and snowy to take him outside.  At this point, I knew then living with him would be a different can of worms. And it was.

Not only did he have a worm problem, he urinated every 10 minutes. Another veterinarian told me he had something similar to puppy vaginitis. I was never sure how that was related to a urinary problem in a male, but the veterinarian said not to worry; he’ll be over it by the time he’s eight weeks old. Sure enough. On his eight-week birthday, not only did Tucky stop the constant peeing, he was suddenly housebroken.

Tucker played hard, as puppies do, so hard that one running and tumbling episode madehim scream like a banshee. He continued running, and his inexperienced mother (me) thought he was all right. Not so. Unbeknown to us, he might have had a racing injury in the yard. He continued playing the hard play of puppies. He grew up into a handsome, very active young man anyway, strong, but still a bit on the scrawny side.

Young, Sore, Stiff-necked

In 1995, at two, he finally calmed down a bit, but his neck and right scapula were sore to the touch. By then, Lyme disease testing had come of age, and we knew a stiff neck is a symptom of Lyme. During his exam we drew blood and sent it to Protatek Reference Laboratory to check for Lyme disease. His Lyme titer came back negative, so we gave him the first version of the Lyme vaccine; we wanted to protect him from further pain if he ever got this devastating disease. Yet something was not right. He began peeing a lot again. Was this a leftover from his puppy days? The urine was concentrated; no one took it as an indicator of a problem. Was this a result of the Lyme vaccine?

In 1997, Tucker needed a teeth cleaning. While under anesthesia, the veterinarians tried to see if his neck had relaxed enough to straighten. No. Oddly, his neck remained crooked; it still hurt and caused him to limp from time to time. As luck would have it, at that time we found a video tape of him running in the yard when he was about 10 weeks old – with the tumble in the yard and the scream documented. He then came in and drank a lot of water. I heard myself eerily commenting, “There he goes, tanking up again.”  He started wearing a harness to protect his neck and shoulder from further trauma. In the meantime, the efficacy of Lyme shots was in doubt by some veterinarians and some researchers.  I became wary of the Lyme boosters and stopped giving them. In 1998 we continued looking for reasons for his sore neck and shoulder. Tests and radiographs still showed nothing.

A Turn for the Worse

In 1999 Tucker required another tooth cleaning. This time, his pre-anesthetic blood work showed a slightly elevated creatinine level, heralding the beginning of a possible kidney problem. Other than that oddity and his stiff neck, all else seemed fine, according to tests. By then Tucker weighed 80 fat-free pounds. Yet, even though he looked so handsome, he couldn’t run; all he had been able to manage for the last 4 years was an odd rocking horse gallop. He still joyfully ran like a rocking horse, went on walks, and adored riding in the van, seated like a person in the back of the van, rump on the seat, front feet firmly planted on the floor. Strangers stopped and marveled at the round-eyed, human-like dog sitting like a person in our vehicle. He made people smile but the downward spiral had already begun.

In the summer of 1999 we saw his right front foot swelling. There was no bite, no splinter and a foot xray and a biopsy showed nothing. Just to be safe we soaked the foot in a povidine/water solution three times a day. The swelling went down in a week but he had a slight limp from now on.  On the morning of August 14, 1999 at the age of six and a half, Tucker appeared to have had a bad stroke. His neck was twisted grotesquely to the left. He couldn’t get up. He vomited his breakfast and didn’t eat more than a bite of food on a good day for three weeks. Although he was fully aware, he thrashed for a few hours as though he were seizing.

Our regular veterinarian, Dr. Joe Giangarra, quickly gave him stabilizing meds and intravenous (IV) hydration for support. After three hours, Dr. Joe told us he was still too severely ill to be handled in his office; he needed a hospital setting. Tucker was admitted to the Veterinary Emergency Service (VES) in Cheshire, Connecticut and stayed there with his neck in that twisted position for three endless days. The VES performed numerous tests and procedures, which included 12 bags of supportive IV fluids. Tests included one each of CBC, calcium serum tests; two platelet counts (they were a bit low), glucose, electrolytes, and tick serologies; a CT scan showing enlarged lateral ventricles, enhanced meninges; and a spinal tap. Oddly, they did no urinalysis. Despite all the diagnostics and supportive care, the local ER was stumped and Tucker still couldn’t straighten out his body. The veterinarians told us to consider putting him to sleep if he didn’t improve soon. No way, we said; the body may have been twisted but the light was still in his eyes; we knew it was not time to say good bye. His Lyme titer was now low positive.

We immediately arranged to admit him to the Tufts New England Veterinary Medical Center for more advanced care, observation, and their up-to-date technology. The intake sheet stated he “presented with Stroke? Severe vestibular signs, right pupil smaller than left. Eye rolled medially, head turning to right (?) side.” We thought vestibular disease was for old dogs, not dogs in their prime ….

After a day and a half there, his Tufts veterinarian, Dr. Brosnan, asked if we would mind making the pilgrimage — a 90-minute drive — to Tufts and try to feed Tuck. Hallelujah! We came and he ate.  Dr. Brosnan helped him to his feet and he was able to stand, with help.

We went home without Tucker, praying our visit would kick start his recovery. After we left, he reverted to his previous recumbent, fasting state. On the third day, and after having one each of blood, coagulation, and kidney profiles, a CBC, another tick serology, an ultrasound of an unknown organ, a skin punch biopsy to see if he had a disease affecting blood vessels, and radiographs for good measure, we heard the same story; no changes. Tucker still rolled to the floor when the veterinarians stood him up in his private run, and he wouldn’t eat. What do you want to do next, they asked? We took him home after six days in two animal ERs.

With that decision came the long-awaited non-diagnosis. Tufts listed high blood pressure, vestibular disease, superficial and perivascular dermatitis (mild), thrombocytopenia, and hepatopathy and gave us Enalapril for the high blood pressure. Despite the big words, they found nothing definitive that could have caused such a dramatic problem. They didn’t know why he had high blood pressure either, but because his BP was elevated on numerous tries, we were told to give him Enalapril and monitor his blood pressure weekly until it dropped to normal dog levels.  The thrombocytopenia was a red flag, but it didn’t seem to be of importance to the veterinarians at the time. Kidney problems also were not on the short list of possibilities.

As soon as Tucker got out of the Tufts building and was taken from the gurney to stand him near the van, he emerged from his fog. He recognized the van and lurched toward it, smiling. He didn’t fall; he stayed on his feet until we helped him into the van whereupon he fell into the deep sleep of exhaustion and relief. It was a glorious, hope-filled moment when he walked one step towards the van, but he couldn’t get up for another week once we got him home.

Doug and I took turns tending to Tucker day and night on the kitchen floor as he was too ill to be in the carpeted bedroom. We kept plying him with nourishment, most of which he refused, and tried to minimize bedsores. He still wasn’t eating or going outside to eliminate. After a week of this, the swirling in his head must have stopped or slowed down considerably. He got up on his own and staggered around; so did we! He went out, peed, and did a lurch around the yard. Our hearts were in our mouths, but he was acting like an Olympic gold medal winner even though he fell on one of his shoulder bedsores. He came to us after that first romp following the “stroke” and made it clear how much he really loved us and his romp in the yard.

The High Blood Pressure

Over the next two months, Tucker had frequent Doppler blood pressure readings, blood tests, and examinations whenever he experienced off-and-on dizziness, inability to walk, inappetence, vomiting, and the eye-twitching that normally goes with vestibular/neurological problems. Seeing the symptoms first hand and the test results on paper didn’t help the veterinarians make a diagnosis.

Between February 2000 and September 2001, Tucker had more episodes of the same and added a few other problems, including glazed eyes, two grand mal seizures in late spring of 2000, and an odd swiveling gait in his rear legs. The most frightening additions were the newly-erratic heartbeats and extended periods of panting after walks and in the middle of the night. Incredibly, test results were still normal and radiographs showed a touch of hip arthritis. Scattered throughout this time frame were periods of fairly good health. We enjoyed many hikes and rides, but the signs of pain were always there. A low dose of prednisone every other day seemed to be the only way to keep his soreness at bay. Still we were always waiting for the shoe to drop.

Because the tests were normal even though some days he couldn’t get up, we opted for more esoteric diagnostics starting in April 2000. Our quest for answers led us to 55 radiographs (30 of which were dental), an EKG, seven blood chemistries and blood counts, two each of thyroid and Ehrlichiosis tests, and one each of Lyme, Babesia, Rocky Mountain Spotted Fever, Toxoplasmosis, Neospora, Leptospirosis, ANA, Coombs, CPK Isoenzymatic Band, electrolytes, urinalysis, and heartworm tests.  Only the Toxoplasmosis and the CPK Bands test showed anything abnormal and only slightly abnormal at that. We tried (not all at once) Soloxine, Enalapril, Antirobe, Clindamycin, Adaquan shots, Cosequin DS, Neo Poly Dex drops, Cephalexin, and metronadazole. Nothing helped, so we eventually stopped all medications except the prednisone. Big mistake; we should have given him the Enalapril forever.

As time marched on and as Tucker became known as a tick magnet extraordinaire, a tick disease – Lyme Disease in particular – seemed to be a distinct possibility as being at the root of his problems. Could it be that the Lyme disease was back because of the Lyme vaccines series he had had years earlier?

Kidney and Lyme Problems

By May 2002, we found ourselves with Dr. Kristine Matz, a highly-respected and knowledgeable veterinarian.  She had been primarily an emergency-room veterinarian until this point. As an ER veterinarian, she is accustomed to seeing animals in crisis and has developed great expertise in quickly sleuthing out mysterious diseases. As a bonus, she knows how to do ultrasounds and interpret them on the spot. This skill soon proved invaluable.

The now nine-year-old Tucker’s first exam with Dr. Matz was supposed to be an introductory visit. Within one minute Dr. Matz was floored; she told me to listen to his erratic heart beat and noisy lung sounds. Now I was floored; he had not been acting at all ill! A chest x-ray showed a somewhat cloudy appearance in a lung. Dr. Matz was even more floored when I started explaining his long mysterious medical maladies. She took his medical history home; it filled a thick three-ring binder and it couldn’t be read at the office. She studied it thoroughly, practically memorizing it, and made notes on all the exam records. After digesting it all, Dr. Matz decided doing an ultrasound of his major organs was in order as well as standard blood and urine tests. Her choices of diagnostics were correct; she discovered tiny, almost non-functioning kidneys and that the other organs, with the exception of cloudy lungs, appeared normal.

So why were his kidneys so bad even though his blood work and demeanor didn’t indicate a dog with shriveled kidneys? On a hunch and unbeknown to us, Dr. Matz suspected Lyme disease and ran an IDEXX Snap 3Dx Test. This test indicated chronic Lyme disease; at last we had something to work on. He had developed it despite having had Lyme shots in the past. This time, when we sent blood to the renowned Protatek Reference Laboratory for verification, the blood test came back with a Lyme titer of 1:10,240. We treated him with amoxicillin rather than the usual doxycyline which upset his stomach. After for two months he felt much better. He came alive, to be precise. His heartbeat became steadier and he had matching femoral pulses most days. Hurrah!  Yet, the next titer taken in mid-September was much higher; it was 1:81,920. This disappointment took our breath away because he appeared to feel excellent. Why did he feel well? Perhaps because Lyme titers build up even after the infection is gone or perhaps the spirochetes were sequestered in tissue somewhere and just resting before the next onslaught?

Always thinking Tucker would never live to see seven, we quietly breathed sighs of relief as he attained birthdays seven, eight, and nine.  When he turned 10 on January 12, 2003, we threw a birthday party for him. He was in his glory and had the time of his life.  He looked great; he weighed 72 pounds. The Lyme disease seemed to be held at bay despite the high titer. He was feeling so well that we tried to wean him off the prednisone. We couldn’t manage to do it; not having it took the lights out of his eyes.

Spleen Problems Emerge

After feeling the best he’d felt in years between September 2002 into January 2003, Tuck became terribly ill, but in a totally new way. During the worst February weather we had in recent memory, worse than the winter he was born, Tucker developed a diseased spleen. Although Tucker had been quite ill before, it had been child’s play compared to what happened now. His diseased spleen caused him to vomit continually for hours. The pain was excruciating; he couldn’t walk outside without curling his hind end under his middle and crashing into the snow in zero degree weather. He couldn’t walk around inside either.

The spleen is a silent organ. It is a blood cleaner but technically is not necessary for life. But the possessor of a diseased or injured spleen will know it eventually. Either there will be no symptoms and the spleen will rupture, usually causing a quick death or it becomes progressively diseased and a deathly illness ensues. Tucker, for once, was “lucky” and had the latter type of manifestation.

Tucker spent three days in the same local ER where he was in 1999. Amazingly, many of the staff remembered him; they loved and admired his spunk and they gave him the royal treatment, not an easy feat in a hospital filled with dozens of ill and injured patients. Dr. Matz watched him like a hawk. He went through IV (re)hydration again. This revived him enough to come home for us to attempt to build him up before performing a needed splenectomy. An animal communicator simultaneously told me that Tucker “told” her he had two bad spots inside and would like to have them out when he felt better. This was vague and I silently questioned that. Two spots? The spleen and where else? We couldn’t tell.

The Operation

When he seemed stronger we arranged the splenectomy. It was a last ditch effort. We didn’t expect him to make it through surgery as so many splenectomy patients die on the table or don’t live long afterward because of internal bleeding problems. He lived. We attribute that to a full day in the ER having planned IV hydration before surgery and three days of the same afterward as well as being monitored constantly. Oh, and the two bad spots? A portion of a liver lobe had also become diseased; it hadn’t appeared on the latest ultrasound!

Incredibly the splenectomy/liver surgery lowered his Lyme titer from 1:10,240 to 1:1,280. We were ecstatic, thinking the Lyme was now finally out of his body. It had to be; after all, he was joyfully running double suspension style again, something he hadn’t done since he was a wee puppy. Not so. It was still sequestered. Now, two months post splenectomy and his 1:1,280 titer, the titer had increased back to 1:10,240 and he had another “episode” again requiring another round of IV hydration. Back to amoxicillin and we continue monitoring his kidney and cardiac problems and wonder where the Lyme spirochetes are now sequestered.

Lyme Disease Reappears and We Say Goodbye

By now, we knew the Lyme disease had damaged his kidneys and sometimes affected his heartbeat, but the good news (so to speak) is that he didn’t have the usually-fatal-within-six-months Lyme nephrits. Instead he appeared to have Lyme-induced glomerulornephritis, a process that takes longer to become fatal.

August 2003. His back seemed to be getting intermittently sore again. As we were about to go for a second walk of the day, he inexplicably splayed his rear legs on the way to the door. He got up and continued onward with his usual “let’s go!” attitude, but this time he went down again for real. It looked like he had another stroke, to the spine this time. His groin was extremely painful now. When Dr. Matz checked his blood a few minutes later, we were horrified to see that his PCV (packed cell volume) was at 24. The number should have been 60. He was bleeding somewhere and we didn’t know where. The painful groin should have been a clue, but we attributed it to the leg splaying he had been doing lately. Little did we know the splaying was related to a bleeding problem and renal failure, not a back or muscle problem. We went home and we lived a very quiet life.

After one final physical exam the next month showing nothing new and were essentially normal for him, we all prayed we hadn’t missed something fixable. We peacefully ended his life’s journey at the veterinarian’s office at 4 p.m. in the presence of people he loved. He left at the speed of light. At Dr. Matz’s urging, Tucker would have a necropsy. The necropsy – the final diagnostic – would show we couldn’t have done anything more, but it showed we missed what was at the root of it all.

The Necropsy Solves the Mysteries

The report concluded: “chronic glomerulonephritis and interstitial fibrosis; retroperitoneal and renal capsular hemorrhage; myocardial arteriosclerosis, fibrosis and stromal adipose; acute focal pulmonary edema and hemorrhage, and intramural hemorrhage, urinary bladder.”

In plain English, the glomerular tubules going into the kidney weren’t filtering his wastes; this made his kidneys fibrous (scarred). His scarred kidneys were slowly bleeding into the abdominal wall between the kidneys to bladder. His kidney capsule (the material covering the kidneys) had ruptured. There was also bleeding in the walls of the bladder. The retroperitoneal bleeding, which is bleeding in the space behind the peritoneum but in front of the vertebral column and lumbar muscles and where the kidneys and other systems lie, created pain and pressure on the nerves going to the legs. This was the cause of his sore back and groin pain. We know that glomerulonephritis is an immune-mediated condition that may cause a bleeding problem and that the prognosis is poor.

How much effect did the Lyme have?  One thing we do know; we will look to the kidneys the next time we see a hound with similar symptoms that defy diagnosis. Another thing we know is that a disease called idiopathic mesangiocapillary glomerulonephritis in humans presents with the same symptoms as Tucker’s, including normal kidney function results. Tucker may have had a human illness, one not identified in veterinary literature. The fix? A kidney transplant, which is not an option to date. The proper way to treat this disease is to give Enalapril long term. This protects the kidneys. Tufts had prescribed it early on but we were never told it was necessary to give it for life. This regrettable lack of communication caused him to  lose his battle prematurely.

Tucker was not always at the veterinarian’s and he really was the epitome of optimism and joy. On his good days he had a wonderful life and lived and loved like any other dog. Was Tucker really our first and last puppy? No. We did it all again in May, 1998. Cullen is as healthy as the proverbial horse. May he stay that way.  Our retired racer, 11-year-old Sparkle, hopes she is retired from her second career as puppy raiser. We’ll see ….

WAG TALES