The Hippo with Toothache

by Lucy H Spelman

  Like all doctors, zoo vets prefer to base their therapy on a specific diagnosis. But while tests are pending, our patient may be suffering. If we think we can help the animal feel better, without doing harm, we will prescribe nonspecific treatment, or perhaps treat for the most likely problem. The patient’s response to therapy often helps us to confirm or refute our best-guess diagnosis. Sometimes the definitive test result comes in long after the animal has healed.

  But as the stories in this section show, some puzzles elude solution—at least in the beginning. Others are solved in time to save the patient. And some, to our great frustration, remain unsolved. The patients here include a Bengal tiger, a giant Pacific octopus, a white rhino, a group of dung beetles, a red-ruffed lemur, and a Pacific bottlenose dolphin.

  Lucy H. Spelman, DVM

  The Limping Tiger

  by David Taylor, BVMS

  Tiger! Tiger! Burning bright

  In the forests of the night,

  What immortal hand or eye

  Could frame thy fearful symmetry?

  —WILLIAM BLAKE, “THE TIGER”

  ZELDA, THE BENGAL tigress at Windsor Safari Park in the UK, was not displaying much fearful symmetry. She padded unsteadily across the green sward of the reserve where she and twelve of her fellow tigers lived. I stood next to Ginger, the highly experienced ex–circus man in charge of the park’s big-cat collection.

  “It beats me,” he said. “Fit as a fiddle two days ago. Look at her now! I put her in a small cage this morning and checked her legs. Nothing amiss that I could see. No bite wounds, no overgrown claws pricking her foot pads.” He shook his head slowly. Zelda was Ginger’s particular favorite. He had helped me deliver her when her mother had difficulty giving birth six years earlier, in 1982.

  “Let’s get her inside,” I replied. “We’ll have a proper look at her under anesthesia.”

  By gently guiding her with a Land Rover, Ginger and his men persuaded Zelda to go into her night-house. I used my dart pistol to inject her with a light dose of ketamine, a short-acting anesthetic.

  Five minutes after the flying dart hit her rump, she was asleep. We could safely enter her quarters. Ginger unlocked the door and I went in. (I have always made a point of being the first to enter when a potentially dangerous beast has been sedated. Since the vet picks the drug and the dose, he or she should take responsibility for the initial close encounter with the animal—just in case it isn’t drowsing quite as deeply as it might appear.)

  I knelt beside this most magnificent of cats as she lay on her side, resting on a bed of wooden railroad ties covered with a layer of straw. I checked her heart and lungs with my stethoscope and took her pulse by feeling beneath her uppermost hind leg for the femoral artery. All fine. I reckoned I had about ten minutes before she began to rouse significantly. I ran my fingers over her limbs. I could find nothing wrong with her great paws, nor were there any abnormal swellings along the long bones of her legs. One by one, I felt her joints, moving and gently pinching them. Was their movement smooth? Could I feel any loss of fluidity, any “scrunching” sensation of bone rubbing against bone? Were the ones on her right side the same size and shape as those on her left?

  I soon felt something. One—nay, both—of her knee joints were puffier than normal. Then I got the impression that one hock (ankle) joint and both the carpal (wrist) joints of her forelegs were enlarged. I could feel extra fluid under pressure between the adjoining bones.

  “What do you think, Doc?” whispered Ginger, kneeling beside me.

  “Joints for sure,” I replied, “but what exactly I don’t know. Could be arthritis, perhaps caused by a bacterial infection. Never seen anything quite like it in big cats before.”

  On occasion, I had dealt with cases of multiple joint inflammation, or polyarthritis, in other species. We had a case in a giraffe, also at Windsor, that we ended up treating with acupuncture. But I had never heard of it in big cats in zoos or circuses. I decided to give Zelda a course of antibiotics together with anti-inflammatory corticosteroid drugs. We gave this to her by injection and planned to continue dosing her in her food.

  “I’ll come back to see her again in five days.”

  The telephone rang early next morning. It was Ginger reporting that Zelda’s condition had worsened markedly. She could barely walk and was unable to leave the night-house. I set off at once for the safari park. As I drove, I puzzled over the tigress’s condition. She wasn’t old, so age-related osteoarthritis seemed unlikely. Could it be septic arthritis caused by bacteria arriving via the bloodstream? Possible, but I’d never seen or heard of such a condition in big cats. What to do? Radiography perhaps. Draw off a sample of what might well be purulent joint fluid for bacteriological culture? Probably the best course. Treatment? For the moment at least continue antibiotics, switch from corticosteroids to nonsteroidal anti-inflammatory drugs until I had a precise diagnosis. Certainly, I had to relieve Zelda’s pain as a priority.

  Ginger was waiting by the tiger area gate when I arrived. “She’s bad, Doc,” he said as we walked to the night-houses. “An’ on top of her lameness, her appetite’s gone and bless me if her eyes aren’t changing color!”

  “What do you mean?” I asked, eyebrows raised.

  “The shine has gone; they’re dark-colored now.” He muttered an oath under his breath.

  The tigress lay awkwardly on her bedding. The swollen joints were now plain to see and, yes, her eyes did appear to have changed color. I immediately set about preparing a flying dart and filling it with ketamine. The cat managed a growl of protest when the dart hit her.

  As soon as she was drowsing peacefully, I began by inspecting her head with the apparently color-changed eyes. Looking closely, I confirmed what Ginger had described. Her eyes were indeed darker. The effect was caused by an accumulation of dark blood in the anterior chamber, between the front of the iris and the back of the cornea, of each eye. This was something I had never seen before in any species of cat—hyphema, bleeding within the eye.

  Next, I turned to the puffy joints. After shaving and disinfecting a small area of skin over one hock, I passed a sterile hypodermic needle into the enlarged joint cavity and attached a syringe. Pulling back the plunger, I waited for fluid to emerge. Straightaway it did. Within a couple of seconds, I had a syringe full of pure blood. Oh Lord, I thought, blood in the eyes, blood in the joints, blood perhaps leaking elsewhere in the body. I think I know what this might be.

  Ginger saw the worried expression on my face. A small tear glistened on his cheek. This burly, chain-smoking, beer-loving, three-fry-ups-a-day head keeper—who knew more about the ways of big cats than any other animal man I had ever worked with—understood Zelda was in trouble.

  “T’aint serious, is it, Doc?” he murmured. “Arthritis can’t kill, can it?”

  “I’m afraid it is serious, Ginger,” I replied. “If I’m right, Zelda has been poisoned.”

  There was a long pause before my companion spoke again. “Poisoned? By what? How? Who by?”

  “A chemical that stops blood clotting. The most likely culprit is the rodent poison coumarin, better known as warfarin. Kills rats and mice by causing them to hemorrhage internally. Sometimes happens in domestic animals that eat rat poison, though I’ve never seen it in exotic cats. Are you using warfarin to control pests in the reserve?” I knew that the stuff was sometimes used in zoos to get rid of rodents.

  “Warfarin. Yes, it’s used by the pest control firm that the park contracts, but it’s never put down in bait boxes inside the reserves, only outside where our animals couldn’t get at it.”

  “Do you ever see rats in the reserves?”

  “Occasionally. I’ve seen tigers, lions, and cheetahs sometimes chasing one.”

  “And catching and eating it?”

  Ginger thought for a moment and then said, “I have seen it happen.”

  I decided to take a blood sample from Zelda while she still slept and send it to the local laboratory. The key te
st I wanted to run was called a prothrombin time, a measure of blood coagulation time. My problem now was that although I knew what a normal prothrombin time should be for humans and domestic cats (both the same, between eleven and fourteen seconds), I had no idea what it should be for tigers.

  “Let’s drive round the reserve and see if all the other cats seem okay. I’ll also knock out Zeinab, Zelda’s mother, so I can take a blood sample from her for comparison.” As we left Zelda’s night-house I saw her pass a little urine; it was the color of rosé wine.

  All of the other tigers seemed perfectly healthy. Using my telescopic dart rifle, I injected Zeinab’s shoulder and within a few minutes had the necessary blood. While the two samples were sent to the lab, I called the big-cat keepers together and explained what I thought had happened.

  “An animal doesn’t have to eat warfarin itself to be poisoned. It can also happen if it eats an animal that already is suffering or dead from consuming warfarin. Usually for poisoning to happen, the warfarin has to be ingested on several occasions, but some species can be affected after a single dose. We just don’t know how sensitive tigers are. Have any of you guys seen rats inside the tiger reserve?” I asked.

  Several of the men nodded at once.

  One keeper said, “Actually I saw Zelda chasing a rat, killing it, and eating it a few days ago. She didn’t have to make much of an effort. It was walking slowly and staggering a bit across some short grass.”

  Here was a highly plausible explanation for how Zelda became sickened by warfarin. A rat eats the poison bait outside the tiger reserve, falls ill, and, when close to death, goes blindly through the chain-link fence and wobbles its way into the jaws of the tigress.

  Within an hour, the laboratory rang. Zelda’s prothrombin time was fifty-five seconds; her mother’s blood coagulated normally in twelve seconds. I was now certain that the tigress was poisoned by warfarin.

  Warfarin achieves its toxic effect by attacking vitamin K, an essential component of the blood-clotting mechanism. Treatment for Zelda meant big doses of vitamin K for the next few days at least. We put an urgent call to the pharmaceutical wholesalers for a courier to be sent to the park at once, bringing more vitamin K injectable solution than I’d ever used in my whole career.

  By this time, Zelda had come round from the anesthetic, so I gave her the first dose by flying dart from a blowpipe. Later that day I repeated the procedure.

  Within twenty-four hours, there was a noticeable improvement in the tigress. She could rise to her feet and walk with less difficulty. Twice a day for the next week, I gave her more vitamin K by blow dart. By the third day, her eyes were back to their usual appearance of burnished gold. The blood in the anterior chamber gradually reabsorbed. The color of her urine also returned to normal, clear yellow, and so did her appetite.

  Ten days later, the joint swellings had fully resolved and Zelda could walk, run, and spring with her usual elegant fluidity. Another prothrombin test gave us a gratifying reading of fifteen.

  Ginger and I went to the pub in Windsor to celebrate Zelda’s recovery. Warfarin would no longer be used by the rodent controllers at the safari park, he informed me. I announced that I’d be presenting the park with a pair of Lancashire heelers, the best little ratting dogs I’d ever come across.

  Soon the dogs joined the safari park staff and began patrolling the grounds with the security men during the night. Rats were never much of a problem in Windsor Safari Park from then on. Zelda herself went on to have several litters of fine cubs.

  Sadly, the safari park closed several years later. I bumped into Ginger while walking through Windsor. We talked about his tigers, which had been relocated to parks in the English Midlands.

  “Went to see old Zelda a couple of weeks ago,” he told me. “She’s in fine fettle. But I’ll tell you what, Doc, we should all keep away from hospitals. These physicians are a dangerous lot! My pal’s had heart trouble and the quacks wanted to put him on warfarin—same stuff as poisoned Zelda!”

  I reassured my friend that the infamous rat poison was nowadays being used as a lifesaving anticoagulant in the blood of human patients. Ginger looked doubtful. On that note, we adjourned to the pub.

  ABOUT THE AUTHOR

  David Taylor received his veterinary degree from the University of Glasgow Veterinary School in 1956 and was appointed a fellow of the Royal College of Veterinary Surgeons in Diseases of Zoo Primates in 1968. He founded the International Zoo Veterinary Group in 1969 and has worked in countries all over the world. In recent years, Dr. Taylor has specialized in marine mammal medicine. He is also the author of some fifty books on animal matters, including seven autobiographical volumes in the Zoovet series. He is married with two daughters and lives just outside of London.

  Sliced Bananas in Jell-O

  by Michael Stoskopf, DVM, PhD

  “WHEN DID IT start?”

  “I don’t know for sure. Two weeks ago she was a bit slower to come out. Not as aggressive as usual. Now she isn’t eating at all. Is it happening already?”

  “I hope not. It shouldn’t be. She isn’t that big yet, but this is how they say it starts. The whole thing doesn’t make much sense to me.”

  “To me either, Doc, but they sure are delicate. We’ve had Bertha months longer than any of the others, and everyone says they only live three years. When she got to Baltimore last year [1984], I’m sure she had to be at least a year old. They don’t grow very fast when they are here. I’m guessing she is between two and three years old.”

  “I don’t get it either, Doug, the whole thing is strange. Endocrine glands suddenly enlarging beside the optic nerves, and then—instant senility. It doesn’t seem right. I know nature is stranger than fiction, but I’m not sure I can buy into such a large and intelligent animal being essentially disposable. They have to live longer in the wild. Besides, the first ones we had arrived nearly dead, did poorly in our water, or injured themselves escaping. We’ve only seen the large optic glands on one animal, Ollie, and he was a male, and much larger than Bertha. Maybe the glands aren’t the issue at all.”

  “Maybe, Doc. I hope you’re right, but what do we do with Bertha?”

  While we talked, Doug, the senior aquarist in charge of the octopus gallery, didn’t break his steady observations of the giant Pacific octopus, Bertha. Bertha sat holed up in her favorite large broken crock, holding herself in position with her large suckered tentacles. Her expiratory siphons moved rhythmically, bringing oxygenated water past her gills. Her color was a vibrant mottled red with black patterns, a good sign. The earlier animals had become pale a few weeks before their deaths. There also was no evidence that Bertha was picking at herself—yet. We had watched Bertha’s predecessor, Ollie, pull at his own flesh, creating large irregular ulcers on his mantle. A few weeks later he finally died, despite our best efforts to treat the wounds.

  If it weren’t for Doug’s intense familiarity with Bertha’s moods and habits, no one would suspect anything was wrong with her. Maybe it was something simple like indigestion, and not the fatal octopus endocrine senility syndrome. I’d found this strange syndrome described in a fifteen-year-old article in Science magazine. But if Bertha’s problem wasn’t senility, what was it? How could we find out what the problem was?

  The aquarium had struggled to learn how to house these big, intelligent invertebrate animals. First there were the shipment problems. The very large wild-caught specimens didn’t do well on cross-country trips from their northern Pacific range, even when shipped inside specially designed high-tech life-support barrels. If your aquarium wasn’t on the West Coast, then catching and shipping smaller animals was the only answer. Unfortunately, octopi that arrived in good condition then proved capable of escaping from the exhibit with impunity.

  They could maneuver through unbelievably small cracks between the heaviest tank lids and the exhibit walls. Once out of the exhibit, they’d be stranded on the floor behind the exhibit, without access to saltwater. Though the escaped anima
ls would be found alive when the aquarists came in early in the morning, they never fared well afterward. When heavier lids on the exhibit didn’t solve the problem, we lined the top of the exhibit with artificial turf, a plastic material that prevents the eight-tentacled, Houdini-like animals from attaching their powerful suckers to gain purchase to allow them to squeeze under the display lids.

  The escapees taught us something else. Sometimes it was hard to tell if the octopus was alive. One of the first animals to escape was found lying apparently lifeless on the floor in a back room near its tank. The octopus was pronounced dead and delivered in a sealed plastic bag to the pathologists at the university. But when the pathologist took the supposedly dead animal out of the refrigerator and started to prepare for the necropsy examination, the octopus reached up and grabbed the arm of the startled scientist. A police car, sirens blaring, escorted the animal back through the city to the aquarium. Sadly, several days of supportive care, monitoring, and all of our efforts to revive the animal met with no success. But I did learn a great deal about octopi in the process, like how to take a blood sample and how to read an octopus EKG.

  At first glance no one would think of Bertha as delicate. However, like other cephalopods, giant Pacific octopi are very sensitive to tiny amounts of toxic metals and slight imbalances of essential elements in their water. And the water must be cold. Facilities successfully keeping these animals alive for long periods in the past all had natural seawater pumped into their exhibits, an advantage we didn’t enjoy. Keeping giant octopi healthy with artificially made seawater posed many unexplored challenges. Water that is perfectly suitable even for delicate corals, another type of aquatic invertebrate, can prove problematic for an octopus. There’s also the difficulty that when octopi become agitated, they release a dark plume of chemicals popularly known as ink. In the wild, an octopus uses this discharge to befuddle prey or to serve as a distraction while escaping its own predators. The ink contains several neuroactive compounds that cause disorientation and confusion. An octopus in the wild would normally move rapidly away from an area it had inked to avoid being affected. In the exhibit tank, of course, that isn’t possible.