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Swimmers Can Be Prevented
By Dr. P. L. Cunningham, BVSC, MRCVS
From English Dog World 1-17-75.
The following, contributed by Barbara Kingsbury, is an interesting excerpt from a January 17, 1975 Dog World article and is worthy of consideration.
A reader asked for advice on "swimmers" in "Ask Me Another (DW Nov. 8). While I agree with some comments in the reply, my own experience over 38 years of dog breeding has been that with a few simple changes in management, the condition can be entirely prevented.
In particular, the suggestion in the reply "probably inherited" particularly worries me because already I have some misgivings about some of the statements regarding Hip Dysplasia. Toward the end of my comments, you will see why I mention HD.
My comments are based on my own personal experience, here in Australia or results obtained by clients where they have, or have not, taken my advice. I'm writing firstly as a dog breeder of quite a few years experience, and only secondly, as a veterinary surgeon.
Two Scottie bitches were particularly bad whelpers - big puppies, long protracted labor. Their puppies always put on weight quickly after birth, and always, in their litters, we finished up with a couple of swimmers.
On one occasion, they both managed to get under the house and dig holes, in which to whelp. By the time we managed to break down part of a foundation wall, to get to them, they had both whelped five puppies each in a matter of three hours!
The two bitches were completely uncooperative when I tried to settle them down with the babes, in their normal whelping boxes. After a few days of arguing with the mums, I gave up and let them take the pups back under the house, to be nursed in the holes.
Three points about the above story later proved to be very important - 1. Two bad whelpers were able to deliver quickly and easily in holes in the ground; 2. None of the puppies were swimmers in spite of being particularly fat and heavy as young babes; and 3. both bitches were bad whelpers and produced swimmers when on their next mating (fool me!) I made them whelp and nurse in normal whelping boxes.
The next time a Scottie bitch wanted to whelp in a hole in the ground, I let her. She whelped very quickly and easily and I learnt a lot by staying with her constantly and observing what happened.
I noticed that the top diameter of the hole was comparatively narrow for the size of the bitch. The hole was quite deep, with steep sloping sides, such that she could not lie flat out on her side or belly, as she would have to in a normal whelping box. She sat almost upright in the hole, pelvis right down at the bottom with elbows, forelegs and brisket resting at the top edge of the hole. She stayed like this, quietly laboring with no fuss until a puppy's head was through the pelvis and in the vulval region. At this point, the bitch just stood up on her hind legs, with her front legs now standing at the edge of the hole, so that she was almost standing vertically. In this position, the puppy almost fell out of the vulva.
I concluded theoretically, and with reservation, that sitting upright relieved the bitch of any necessity to waste energy using her abdominal muscle to lift the puppies up to the pelvis, and that it almost eliminated the complications that can arise when they are trying to get the puppy's head or hindquarters, in the right position at the pelvic rim.
When the bitch stands upright, with the pup well in the pelvis, the puppy's own weight with a little more labor from mum, makes the last bit easy. At this stage, I couldn't work out how to simulate "hole in the ground conditions," with a man made whelping structure. Also, I could not see how a hole in the ground prevented swimmers, and considered that side of the story probably to be just coincidence.
I promised a (bloodline wise) aging English Ch. Scottie bitch that her next littler would be the last I would expect of her.
She had only one puppy and, being a single, he grew fast and fat. Tragedy struck, for at two weeks old he was an early swimmer - both front and hind legs were out in the frog-like attitude and the sternum was starting to flatten. The more I looked at him, the more I was convinced I had to do something to stop his weight from flattening him any further, and must, in fact, reverse the process. I wondered how I could get the legs in under the body, while the pup was growing rapidly every day and tending to flatten himself more than ever.
In desperation I devised a sling. It was just a wooden butter box about one foot square at the open top. I nailed a piece of loose blanket over the top, such that when the puppy was in it he was lying in a type of square deep hammock. A handful of paper tissue in the bottom (frequently changed) solved the problem of urine, etc. He was only taken off the hammock to feed from mum and even then I held him cupped in my hands so that he could not flatten while he was feeding.
While in sling, no matter where or how he tried to move, the steep sides kept his legs and feet tucked in under his body and, in spite of his weight. It simply was not possible for him to lay with his feet flat out to the sides. This automatically took away most of the strain on his rib cage. Within ten days the pup appeared to be quite normal, with no calcium injections and no vitamin supplements.
Trouble struck again, when he was removed from the sling. At the time I was a great one for newspaper in the baby puppy pens - nice and hygienic as it could be changed frequently and burnt. Within days of walking on slippery newspaper, he was showing signs of spreading again. To create friction, so that he could not slip or slide, I then allowed him to run only on loosely woven corn sacks, which created a lot more work than newspaper, with frequent changing, scrubbing, etc. But it did the trick and he was soon back to normal.
For quite some time this was the method used to "cure" swimmers and it always worked, which at the time led me to the following conclusions:
1. The condition is not due to any basic bone weakness and that calcium or vitamin supplements are not necessary in any therapy.
2. The condition, in itself, is neither congenital nor inherited. It seemed to be simply a "mechanical problem" which only commences at some point following birth and which can be corrected by mechanical means.
Any congenital, or inherited tie up would simply be one "breed of dog."
One day, watching a very hungry litter feed from mum, in a flat floored whelping box, I noticed they were obviously trying to "grip" the floor with their hind feet, in order to suckle comfortably without stretching out.
They were obviously frustrated by the fact that their hind feet sliding out behind them, or frog-like, to the sides. I theorized that this could be the making of a swimmer. Baby puppy bone is very cartilaginous. Could this spread-eagling and frogging at such a tender age create such stress on cartilaginous bones and joints that weaknesses have been created before the puppies start taking weight on their feet? If this were so, the fat overweight puppy, in particular, would be in a pretty precarious predicament mechanically when he started to try to support his own weight.
This made me think about the slings I used to correct swimmers. If a sling-like structure could correct the condition, surely something similar would almost certainly prevent the condition from occurring in the first place, but how to go about it?
I devised slings large enough for bitches to whelp and nurse their puppies in. With Scotties, Westies, Shih Tzus, etc., for convenience, I used wooden frames of the dimension of corn sacks, either on four short legs or, if broad timber planks were used, without legs.
The corn sacks were nailed on reasonably taut, and the bitch encouraged to sleep in it for at least a couple of weeks before whelping (most bitches don't need much encouragement, they seemed to like it and find it comfortable). By the time the bitch was ready to whelp, her weight had stretched it into a nice deep hammock. Because of fetal fluid staining, etc. I changed her over to a spare sling after she finished whelping. So long as the sling is deep enough then, from birth onwards, it is almost impossible for them to get frog-like or flattened, no matter how rapidly they put on weight. The very nature of the structure largely keeps the legs and feet tucked in under the body and they develop lovely rounded rumps and strong fronts, at a very early age. Some clients ask me about the dangers of bitches laying on puppies in a sling. When mum is with them, the puppies always seem to be one side of her or the other. Also of importance, the sling does not have any solid upright sides, so that the puppies cannot be jammed between the side and mum.
Soon after I brought whelping slings into regular use, I noticed that the Scottie bitches, in particular, seemed to whelping more rapidly and easily and were far less exhausted. It then hit me that many of the features of whelping in a sling roughly simulated the conditions of whelping in a hole in the ground. The bitch can, and does, labor with pelvis in a much lower position than the rest of her body. She can, and often does rest forehand and chest on the higher edge of the sling.
The surface on which the puppies run in the early days does seem to be of some importance in preventing late swimmers. For me, newspapers are out, and sacks can be messy and smelly. I overcame this problem by using factory safety matting laid on top of a base of newspaper. This provides a good grip for baby puppy feet. The matting is of mesh type. One extremely important reason for observant breeders to try to ascertain is whether swimmers are simply the post birth result of incorrect management or whether it is congenital or more importantly "inherited" is this - where misguided but well meaning clients have persevered with a swimmer and it has come to me too late to be helped by my ideas on management, I have noticed that such swimmers, apart from general conformation weaknesses, including the "shoulder dysplasia" which the DW mentioned, later frequently also have HD (hip dysplasia), even in breeds where HD is usually not a problem.
If certain systems of management can prevent puppies from being swimmers, and prevent HD often associated with that condition, is it possible that the same management may in some cases, prevent HD in those breeds where HD occurs, unassociated with the condition known as "swimmers?"
With respect, I suggest that many geneticists, and others, working on what I call "PURE HD" may not have had the opportunity to become much involved with cases of swimmers-associated HD. The majority of swimmers are destroyed at a few weeks of age.
The ones that do survive are structurally wrong and often semi-cripples, so no-one concerns themselves with the possibility of HD.
Swimmers-associated HD cases, which survive to adulthood never see a show ring and, I imagine are never used for breeding, so it is unlikely that they are ever brought to the attention of an HD certifying panel.
I can't help but ask--
1. Who has ever proved, by an extensive, properly controlled breeding programme, that HD is always inherited.
2. If such a critical, foolproof and conclusive programme has ever been carried out, just what steps were taken, to eliminate any possibility, that a system of management many have influenced the results obtained?
3. If there is any inherited basis for HD in some breeds, is it also possible that management of baby puppies may sometimes produce an identical picture, such that it is not possible to differentiate between inherited and management produced HD?
4. Is it possible, that some people have unnecessarily bred away from a valuable bloodline, because no-one is sure of the answer to question 3?
If it is possible that some cases of HD are simply the result of faulty management of puppies from birth to five weeks, (and I feel this is the crucial period), it may well explain why geneticists are still not in complete agreement as to the mode of inheritance.
I realize that, over the years, I have been carried away, by sling-rearing. It may not be nearly as important as I think it is, but I imagine that all the breeds I have reared have been better in legs and feet.
If anyone in a large breed cares to try the method, the easiest way is to get an old single bed, remove the wire mattress and replace same with strong canvas. This must be fixed on very taut, initially, as the big mums, and then the weight of the babes, very quickly stretches even canvas.
Because the frame edge of a big breed sling must be a couple of feet off the ground it is important to prevent babies tumbling off and injuring themselves. A narrow strip of fence, perhaps about six inches high tacked around the edge, does the trick (I use strips of plastic-coated mesh).
For the 'little' breed slings this is not necessary, as they are not high enough for the pups to be injured, if they do venture over the side.
Original Doc: swim_3.doc
The Fading Puppy Syndrome
by Richard S. Marcus
This article is reprinted from The Corgi Cryer where it appeared in January of 1988.
Most breeders have had the experience of losing one or more puppies without a readily identifiable cause. This perplexing and heart-breaking problem can lead to a sense of guilt, failure and even incompetence. It can also cause concern over the "breedability" of the dog or bitch involved in the breeding. Many causes of neonatal mortality can be explained by such causes as crushing by the mother, infection, congenital anomalities, premature birth and parasites to name a few. Blunden found surveys of mortality in neonates ranging from 20-30% throughout the world. Johnson found that of puppies born alive, 28% died within the first week of life and another 10% died within the second week. In a study of 518 puppies by Blunden, 8.3% were stillborn while 32% died within the first three weeks of life. Of those that died, 45% died due to causes that were readily identifiable. The other 55% (which amounted to 83 puppies) died of unknown causes. After careful autopsy, these deaths were attributed to the fading puppy syndrome. The syndrome can be described as a complex of disorders that strike puppies that were apparently normal at birth. The syndrome usually presents as a triad of hypothermia, dehydration and hypoglycemia. Puppies are affected shortly after birth and usually will die within 4 - 5 days of first showing symptoms. In this article, I hope to review the symptoms, causes, treatment and prevention in such a way as to help the breeder dramatically reduce its incidence in their puppy population. I urge breeders to work in concert with their veterinarians who are skilled in the early recognition and treatment of some of the processes described below.
Symptoms include lethargy and a weak sucking response in the first two days. This progresses to restlessness, crying , lying on one's side with limb paddling and, occasionally shivering. Holst points out that if crying persists for fifteen minutes or longer, a cause should be sought. A healthy pup who is hungry will cry itself to sleep in less than fifteen minutes whereas one who cries for a longer period of time is in trouble. One of the first things a breeder can check for is hypothermia. Hypothermia is a cooling of the core body temperature below normal. Normal body temperature for the first two weeks of life is from 94-97 degrees F. Hypothermia's causes can be due to something as simple as separation from the mother to the complexity of an overwhelming infection. A core temperature in the range of 78-85 degrees F will cause severe metabolic depression accompanied by cessation of digestive activity. Holst advised against giving food to a puppy whose rectal temperature is below 94 degrees F because of digestive inactivity. She also cautions against rapid warming. Rapid warming will cause the skin and extremities to warm, but the heart and lungs, due to metabolic depression, will not be able to supply the oxygen needed to keep up with the greater metabolic demands of the warm extremities. The puppy should be warmed slowly in an environment with a relative humidity of approximately 60% to prevent dehydration. An ideal means of accomplishing this is by simply holding the puppy next to your own body until a normal temperature is reached, then transfer the puppy onto a heating pad or into an incubator. Lewis, et. al, recommends that warming take place over a period of three hours. He has observed that mothers usually reject hypothermic pups but readily accept them back after rewarming. It is at this point that the puppy can be safely hydrated and evaluated for other problems.
The problem of dehydration must be addressed. This is usually accompanied, at this point in the syndrome, by hypoglycemia (low blood sugar). Both of these problems can be dealt with by feeding the puppy a solution of sugar water (four teaspoons of sugar per 4 ounces of water). The solution should be warmed to approximately 95 degrees F so as not to offset the efforts achieved by rewarming the puppy. This is then fed at the rate of two cc's every 30 minutes per eight ounces of puppy body weight. This can easily be measured and administered by mouth using a disposable plastic syringe with the needle removed.
Infectious causes of fading puppy syndrome include peritonitis, septicemia, herpes virus, canine brucellosis, toxoplasmosis, infectious canine hepatitis, Clostridium perfringens and toxins from bacterial infections. Poor prenatal nutritional status in the bitch can also lead to a litter plagued with this syndrome. Peritonitis is a bacterial infection of the abdominal cavity that usually comes from contamination of the umbilical cord due to poor birthing technique. Symptoms include crying, bloating and an abdomen that is somewhat rigid and tender to palpation. Septicemia is an infection that spreads through the blood stream and is also bacterial in origin. It is often caused by Strep or Staph which are bacteria that are usually found on the skin. Therefore it is postulated that the source of this infection is usually from poor sterile technique in docking tails, clipping dew claws, or cutting the umbilical cord. E. Coli is another common pathogen, but this is usually found residing in the gut and may be indicative of a congenital anomaly of the gut or urinary tract. Symptoms can be similar to those of peritonitis except careful inspection of the puppy will usually reveal an area of local infection such as at the site of a newly clipped dew claw, umbilicus or tail. Herpes is contracted during whelping and is known to be a cause of abortion, stillborn or low-birth weight pups. It generally affects pups during the first three weeks of life because of their low body temperatures. Once body temperatures go above 100 degrees F, it usually ceases to be a problem. Symptoms according to Holst include soft, odorless, yellow-green stool, depression, anorexia, uneasiness and continuous painful crying. Once herpes related crying has begun, viability is seriously compromised. Survivors at this stage usually have significant renal or hepatic impairment.
There are two modes of treatment available. The first is to raise the environmental temperature to 100 degrees F for a minimum of three hours, then reduce it to 95 degrees F for the next 21 hours. Since the virus replicates at temperatures between 95 and 96 degrees F, this should interfere with the virus's survival.
One must remember that maintaining the puppy at these temperatures will increase its fluid and nutritional needs. The second form of treatment which is that used for humans is with a drug called acyclovir, which is available in both an IV and oral form. (At the time of writing this article, I was unable to find literature pertaining to its use in the canine.)
Clostridium perfringens Type A has been recovered with some frequency from the genital tract of both bitches and stud dogs with a history of neonatal loss according to Blunden. The organism can then be cultured from fecal samples of puppies as soon as 24 hours after birth. The organism effects the gut much as a stomach virus effects us. Canine Brucellosis is caused by the Brucella canis bacterium and is transmitted by vaginal and mammary secretions in an infected bitch and via semen in the dog. Recovery may take in excess of two years. Screening is relatively simple.
Hyaline membrane disease is a disease that affects the lungs of premature infants due to immature lungs that don't have sufficient quantities of surfactant, a substance that helps the alveoli (the smallest air sacs) remain open. Surprisingly, research by Blunden, et. al., has not shown this to be a component of the fading puppy complex.
Methods of prevention are obviously what any breeder should turn their attention towards. The breeding pair should be tested for the above mentioned infectious organisms prior to breeding. The utmost of care should be used and sterile techniques employed for tail docking, dew-claw clipping and the securing of the umbilical cord. Fisher feels that perigestational malnourishment of the bitch contributes significantly to the mortality of neonatal puppies. He observes that the clinical signs of malnutrition include an "out of condition" appearance often unnoticed until just after birth, uncontrollable diarrhea during lactation, the fading puppy syndrome, lactation problems and anemia.
Lewis, et. al., recommends that the bitch be examined, checked for parasites, vaccinated if necessary and weighed. It has been found that markedly under or overweight bitches tend toward dystocia, premature birth and the inability to make adequate amounts of colostrum or milk.The hematocrit (percentage of red blood cells in the plasma) should be greater than 37%; the hemoglobin ( the oxygen carrying component of red blood cells) should be greater than 10 g/dl. The total serum protein should be greater than 5 g/dl. A growth/lactation diet should be fed during pregnancy. This consists of a diet containing greater than 29% protein, at least 17% fat and less than 5% fiber. Calcium should be between 1 - 1.85%, phosphorus between 0.8 - 1.6 % and sodium 0.3 - 0.7. The ratio of calcium to phosphorus should be greater in the direction of calcium. Over supplementation of calcium and vitamin D can lead to soft-tissue calcification and physical anomalies in the puppies. It does not help prevent eclampsia. Carbohydrate free diets (such as meat only diets) causes hypoglycemia (low blood sugar) late in the gestational period. One should look for a 15-25% increase in the bitches body weight by the time of whelping due to the rapid increase in fetal size during the last 3-4 weeks of gestation. This may represent as much as a six pound weight gain in the Corgi. The increased size of the uterus may encroach on the filling capacity of the stomach and subsequently multiple feedings may be necessary in the latter period of gestation in order to allow the bitch to have an adequate nutritional intake.
During lactation, the bitches nutritional demands markedly increase. Assuming that the bitch was at optimal weight at the time of whelping. Lewis recommends increasing the amount of food by 1 1/2 that of maintenance for the first week of lactation, by 2 times for the second week and by a factor of three for the third week through weaning. Of course this varies with litter size. If the bitch is in her optimal nutritional state, this should assure adequate amounts of colostrum for all of her puppies.
In conclusion, mysterious neonatal mortality in puppies is hopefully now less mysterious. A concerted effort should be made to identify a puppy in trouble early on. If that puppy is hypothermic, slow rewarming should be instituted immediately then rehydration after a core temperature of 95 degrees F is reached. Next, a careful veterinary examination should be done to rule out an infectious or congenital cause. More importantly, screening of the breeding pair for Brucellosis and Clostridium perfringens should be performed in the name of prophylaxis. Lastly and perhaps most important is assuring the optimal nutritional status of the bitch.
Blunden, AS, Hill, CM, Brown, BD, Morley, CJ. Lung surfactant composition in puppies dying of fading puppy complex. Research in Veterinary Science 1987; 42:113-118.
Blunden, AS. Isolation of Clostridium perfingens from the canine genital tract. The Veterinary Record 1983; 113.133.
Blunden, AS. A review of the fading puppy syndrome (also known as the fading puppy complex). Veterinary Annual
Fisher, EW. Neonatal diseases of dogs and cats. British Veterinary Journal 1982; 136:277-284.
Holst, PA. Newborn puppies in trouble. Canine Reproduction: A BreederÌ Guide. 1985: 175-179.
Johnson, EA. Pediatrics. Auburn Vet 31. 1975; no. 3.
Lewis, LD, Morris, ML, Hand, MS. Small Animal Clinical Nutrition 3rd Edition. 1987, Mark Morris Assn. pp 3-6-3-31.
About the author...
The author is a Physician Associate specializing in Cardiology. He is on staff at St. Francis Hospital and Medical Center in Hartford, Yale - New Haven Hospital, St. Rapheal's Hospital and Danbury Hospital. He has won four first place awards from the Dog Writers Association of America for his writing and editing.
He is the former editor and publisher of The Corgi Cryer, a member of the Dog Writer's Association of America and a past member of the Board of Directors of the Mayflower Pembroke Welsh Corgi Club. He and his wife breed and show Pembroke Welsh Corgis.
Original Doc: neo9.doc
The Pros And Cons Of Early Spaying Or Neutering
By Giselle Hosgood, BVSc, MS, FACVSc, Diplomate ACVS
Source: BREEDER FORUM, (eds) Sokolowski, J.H., Campfield, W., (publisher) Pedigree food for dogs, Vol. 2, No. 1, 1993, pp. 10-15.
neoplasia - the formation of tumors
pyometra - accumulation of pus within the uterus
hypertrophy - the excessive development of an organ
prostatitis - inflammation of the prostate
brucellosis - a generalized infection caused by Brucella species
vaginitis - inflammation of the vagina
incontinence - the inability to control excretory functions
atrophy - a wasting away of a body part or tissue
There is considerable controversy over the indications for and consequences of spaying or neutering very young, prepubescent puppies and kittens. Early spaying or neutering typically refers to performing ovariohysterectomy or castration in puppies and kittens younger than 4 months of age1 (generally from 6 to 12 weeks of age2,3).Traditionally, it had been recommended that spaying or neutering be performed between five to seven months of age.2,4 The need to control the pet population has resulted in investigations concerning early spaying or neutering.5,6 Only 40% to 60% of owners who adopt very young animals from shelters have these pets spayed or neutered (Table 1).5,6 From the breeder's perspective, early spaying or neutering may be beneficial in controlling the indiscriminate breeding of animal. Purchasing young animals that have been spayed or neutered may be especially attractive to the general public.
Facts Concerning the Dog and Cat Population
Approximately 20 to 30 million dogs and cats are handled by animal control centers each year.
Ten percent of these animals are placed in homes; 90% are euthanatized
Animal control costs exceed $500 million annually
For every $1.00 invested in sterilization programs, $6.50 to $9.79 is saved in future animal control costs
Veterinarians have relied on surgical sterilization to control the dog and cat population
BENEFITS OF SPAYING/NEUTERING
In addition to sterilization, spaying or neutering at five to seven months of age has several medical benefits. Mammary neoplasia is the most common tumor seen in intact female dogs7 (approximately 50% of these tumors are malignant). The risk of mammary neoplasia in dogs ovariohysterectomized before their first heat is very low.8 This protective benefit is, however, considerably reduced when ovariohysterectomy is delayed. Dogs ovariohysterectomized before their first head have a 0.5% risk for developing mammary cancer, an 8% risk after their first heat, a 26% risk after two to three heats, and the same risk as intact dogs if they are ovariohysterctomized after four or more heats or after 2.5 years of age.8 Overall, an intact female dog has three to seven times the risk of developing mammary cancer than an ovariohysterectomized dog.9 Ovariohysterectomized females also have no risk of developing ovarian or uterine diseases, such as neoplasia or pyometra.
Mammary tumors are the third most common tumor seen in female cats (nearly 90% of these tumors are malignant). At the time of presentation, many of these tumors have spread to other body organs.9 Although the benefits of ovariohysterectomy against mammary neoplasia are not as clearly defined in cats as they are in dogs, the risk of developing mammary cancer in intact female cats is seven times higher than that of ovariohysterectomized cats.10
In male dogs, the risk of developing prostatic disease - such as benign hypertrophy, prostatitis, and cystic disease - is reduced if castration is performed early in the animal's life. Treatment of prostatic disease is difficult and often associated with complications. Testicular tumors are the second most common tumor in male dogs. After castration, male dogs will not develop testicular disease, such as inflammation and neoplasia. In dogs that have been spayed or neutered, the risk of transmitted venereal diseases, such as transmissible venereal tumor and brucellosis (which affects other body systems besides the reproductive system), is reduced because sexual behavior is diminished.2, 9, 11
AT WHAT AGE SHOULD A DOG OR CAT BE SPAYED/NEUTERED?
The current recommendation for spaying or neutering animals at five to seven months of age is arbitrary ,3,12 and the reasons cited against spaying or neutering dogs younger than four months of age are largely unfounded.1,4,12,13 Early spaying or neutering has been purported to cause stunted growth, obesity, perivulval dermatitis, vaginitis, and behavioral changes.12
The age at which to spay or neuter an animal requires several considerations. The pediatric animal is physiologically immature and will tolerate and respond to anesthesia and surgery differently than an adult animal.14 These factors must be taken into account before an anesthetic is selected. The animal's physiologic state must be closely watched during and after the surgery so that hypothermia, hypoglycemia, or other life‑threatening conditions do notdevelop. With these precautions, the surgery can be performed with relatively little risk.2,4,14-16
The impact of early spaying or neutering on skeletal growth has been investigated. Testosterone and estrogen, although not required, influence growth, maintenance, and aging of the skeleton.2 In one study, spaying/neutering at seven weeks or seven months of age did not affect the rate of bone growth in male or female dogs when compared with intact dogs.2 Nonetheless, early spaying or neutering in dogs will result in a delay in the closure of the growth plate by an average of nine weeks. This delay will cause increased bone length in both male and female dogs, however. If the operation is done at seven months of age, the delay will be seen in male dogs only. Therefore, the belief that prepubertal spaying or neutering stunts growth is not true.2
A predisposition to obesity is often associated with early spaying or neutering. Many factors, however, influence obesity, including how the owner feeds the animal, breed, age, diet, amount of activity, and, possibly, sexual status.2 In a study of 8,268 dogs, 24.3% of these animals were overweight. 17 In this study, obesity was noted in twice as many ovariohysterectomized females than in sexually intact females and castrated males tended to be more overweight than intact males. Experimental studies have failed to confirm this predisposition, however. One study reported that weight gain and daily food consumption were not different between dogs spayed or neutered early, dogs spayed or neutered at seven months of age, and intact dogs.2
In a study of female dogs fed free‑choice, ovariectomized dogs ate and weighed significantly more than intact dogs.18 When ovariohysterectomized and intact female dogs were fed a set amount of the same diet, however, no difference in food consumption or weight gain was noted between the two groups.19 Another study also has noted a significant incidence of indiscriminate appetite in ovariohysterectomized dogs.20 Thus, if diet is controlled, weight gain should not be a problem in ovariohysterectomized dogs.
Ovariectomy in sexually immature rats has been shown to affect body composition differently than in sexually mature rats. Whereas rats that are ovariectomized as adults show some weight gain for a short period following surgery, rats that are ovariectomized when very young show no change in total body fat.21,22 Therefore, the timing of spaying or neutering will affect obesity, and animals that are spayed or neutered after sexual maturity are more likely to gain weight. Castration of male cats has not been associated with weight gain.23
A decrease in activity, which leads to obesity, has also been purported to be associated with spaying or neutering. Contrary to popular belief, dogs spayed or neutered at seven weeks or seven months of age are as active or more active than intact dogs.2 Some investigators have commented that spayed or neutered animals retain immature puppy‑or kitten‑like behavior.21
In one study, the effects of spaying on police dogs were noted. Compared with intact female dogs, ovariohysterectomized dogs had a decrease in aggressiveness and boldness. Nonetheless, the obedience and learning skills seen in both groups were similar.25 Other studies have noted an increase in aggressive behavior in ovariohysterectomized dogs.20 Thus, the effect of spaying or neutering on behavior is not clear and may be influenced by a multitude of factors, especially environmental factors.
In animals that have undergone prepubertal spaying/neutering, changes in secondary sex characteristics of the vulva, prepuce, and penis have been noted. In one study, female dogs that were neutered at seven weeks or seven months of age had a small, infantile vulva compared with that of intact female dogs.2 A reduction in mammary gland development also was noted in the dogs that were ovariohysterectomized before puberty, which caused an infantile appearance of the mammary glands and nipples. Ovariohysterectomy in cats causes similar changes but no clinical consequence has been associated with an infantile vulva or mammary glands.
In male dogs, the effect of early castration on the development of the prepuce, penis, and os penis is more striking. In one study, the prepuce, penis, and os penis of dogs neutered at seven weeks of age were much smaller than those of intact males of similar age. The prepuce, penis, and os penis of male dogs castrated at seven months of age were not as small as those castrated at seven weeks of age but smaller than those of the intact males.9 In all of the neutered dogs, no clinical consequences were apparent. The penis could be easily extruded in all of these dogs.2
A similar infantile appearance of the prepuce and penis has been noted in male cats castrated before five months of age. In these cats, however, complete extrusion of the penis may not be possible because of incomplete separation of the prepucial lining and the penis.26 It has been suggested that irritation and collection of tissue debris in the prepuce possibly predisposes castrated male cats to urinary tract infections.27 Castration has not been shown, however, to increase the risk of urinary tract infection in castrated male cats.23,26 One study noted that the size of the penile urethra in prepubescent male cats that had been castrated was not different from that of intact male cats.26 Based on this information, the study concluded that castrated male cats are not predisposed to urethral obstruction. In another study, castrated and intact male cats fed a calculi‑inducing diet showed no difference in the development or severity of urethral obstruction.23
Urinary incontinence is another purported consequence of early spaying or neutering. Hormone‑responsive or stress‑induced urinary incontinence has been seen in dogs weeks to years after spaying or neutering.28,29 These animals are usually healthy but will leak urine when asleep. Although these dogs may respond to supplementation with estrogen or testosterone, it has not been proven that a lack of estrogen or testosterone is the cause of the problem. Other factors, such as the length of the urethra, position of the urinary bladder, the breed (e.g., Doberman pinchers), and age‑associated muscular atrophy, may cause urinary incontinence.12 If spaying or neutering is associated with the development of hormone‑responsive incontinence, there is no evidence that prepubertal spaying or neutering potentiates the problem. 12
In male dogs, prepubertal castration usually eliminates mounting and copulatory behavior.2,9,30,31 If castration is performed after puberty, sexual behavior will be reduced but mounting and urine marking may still occur.2,30,31
Prepubertal castration of male, cats reduces spraying behavior. Nonetheless, approximately 10% of these cats may still spray, especially if housed with female cats.32 Castration of adult cats has resulted in similar behavior.32 Approximately 5% of ovariohysterectomized cats will spray, especially if housed with other cats. The age of the cat at ovariohysterectomy does not appear to be a factor.32
The stress associated with the surgery for early spaying or neutering has been suggested to affect an animal's immunologic response to disease. Although there is no prospective study on this aspect, the anesthesia and surgery required for spaying or neutering will not affect an animal's ability to mount a good response to vaccination.33 Spaying or neutering is an elective procedure and can be delayed if the animal may have been exposed to an infectious agent.
The effects of early spaying or neutering continue to be studied. New information suggests that the consequences associated with early spaying or neutering are not nearly as detrimental as previously thought and that many reasons against early spaying or neutering are not based on sound scientific information. Changes in secondary sex characteristics appear to be the most profound side effects of early spaying or neutering. Recent studies suggest that early spaying or neutering has very little impact on an animal's health. Currently, it appears that early spaying or neutering has significant merit in preventing disease of the reproductive organs and in controlling the pet population.
1. Chalifoux A, Fanjoy P, Niemi G, et al: Early spay‑neutering of dogs and cats (letter). Can Vet J22:381, 1981.
2. Salmeri KR, Bloomberg MS, Scruggs SL, et al: Gonadectomy in immature dogs: Effects on skeletal, physical and behavioral development. JAVMA 198:1193‑1203, 1991 .
3. Arohnson MG, Fagella AM: Surgical techniques for neutering 6‑ to 14‑week‑old kittens. JAVMA 202: 53‑55, 1993.
4. Olson PN, Nett TM, Bowen RA, et al: A need for sterilization, contraceptives, and abortifacients: Abandoned and unwanted pets. Part 1. Current methods for sterilizing pets. Compend Contin Educ Pract Vet 8:87‑92, 1986.
5. Moulton C: Early spay/neuter: Risks and benefits for shelters. Am Humane Shoptalk 7:1‑6, 1990.
6. Alexander SA, Shane SM: A descriptive study of animals adopted from an animal control center and spay‑neuter compliance. JAVMA, in press.
7. Brodey RS: Canine and feline neoplasia. Adv Vet Sci Comp Med 14:309‑354, 1970.
8. Schneider R, Dorn CR, Taylor DON: Factors influencing canine mammary cancer developments and postsurgical survival. J Natl Cancer Inst 43:1249‑1253, 1969.
9. Johnston SD: Questions and answers on the effects of surgically neutering dogs and cats. JAVMA 198:1206-1214, 1991.
10. Dorn CR, Taylor DON, Schneider R, et al: Survey of animal neoplasms in Alameda and Contra Costa counties, California, II. Cancer morbidity in dogs and cats from Alameda county. J Natl Cancer Inst 40:307‑315, 1968.
11. Hart BL: Problems with objectionable behavior of dogs and cats: Therapeutic use of castration and progestins. Compend Contin Educ Pract Vet 1:461‑465, 1979.
12. Salmeri KR, Olson PN, Bloomberg MS: Elective gonadectomy in dogs: A review. JAVMA 198:11831192, 1991.
13. Jagoe JA, Serpell JA: Optimum time for neutering. Vet Rec 122:447, 1988.
14. Hosgood G: Anesthesia and surgical considerations of puppies and kittens. Compend Contin Educ Pracl Vet 14:345‑359, 1992.
15. Grandy JL, Dunclop Cl: Anesthesia of pups and kittens. JAVA1A 198: 1244‑1249, 1991.
17. Ednay ATB, Smith PM: Study of obesity in dogs visiting veterinary practice in the United Kingdom. Vet Rec118:391‑396, 1986.
18. Houpt KA, Coren B, Hinlz HF, et al: Effect of sex and reproductive status on sucrose preference, food intake, and body weight of dogs. JAVMA 174:1083‑1085, 1979.
19. Le Roux PH: Thyroid status, oestradiol level, work performance, and body mass of ovariectomized bitches and bitches bearing ovarian transplants in the stomach wall. J S Afr Vet Assoc 54:115‑117, 1983.
20. O'Farrell V, Peachey E: Behavioral effects of ovariohysterectomy on bitches. J Sm Anim Pracl 31:595598, 1990.
21. Clark RG, Tarttelin MF: Some effects of ovariectomy and estrogen replacement on body composition in the rat. Physiol Behav 28:963969, 1982.
22. Mook DG, Kenney NJ, Roberts S, et al: Ovarian‑adrenal interactions in regulation of body weight by female rats. J Comp Physiol Psychol 81:198‑211, 1972.
23. Duch DS, Chow FC, Hamar DW, et al: The effects of castration and body weight on the occurrence of the feline urologic syndrome. Feline Pract 8:35‑40, 1978.
24. Lieberman LL: A case for neutering pups and kittens at two months of age. JAVMA 191:518‑521, 1987.
25. Le Roux PH, van der Wall LA: Ovarian autograft as an alternative to ovariectomy in bitches. J S Afr Vet Assoc 48:117‑123, 1977.
26. Herron MA: The effect of prepubertal castration on the penile urethra of the cat. JAVMA 160: 208-211, 1972.
27. Herron MA: A potential consequence of prepubertal feline castration. Feline Pract 1:17‑19, 1971.
28. Krawiec DR: Diagnosis and treatment of acquired canine urinary incontinence. Compan Anim Pract 1:17-19, 1971.
29. Thrusfield MV: Association between urinary incontinence and spaying in bitches. Vef Rec 116:695, 1985.
30. Beach FA, Kuehn RE: Coital behavior in dogs: X. Effects on androgenic stimulation during development on feminine mating responses in females and males. Horm Behav 1:347‑367, 1970.
31. Beach FA: Effects of gonadal hormones on urinary behavior in dogs. Physiol Behav 12:1005-1013, 1974.
32. Hart BL, Cooper L: Factors relating to urine spraying and fighting in prepubertally gonadectomize cats. JAVMA 184:1255‑1258, 1984.
33. Kelly GE: The effect of surgery of dogs on the response to concomitant distemper vaccination. Aug. Vet J 56:556‑557, 1980.
Giselle Hosgood BVSc, MS, FACVs, Diplomate ACVS, Assistant Professor, Surgery, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA.
Dr. Hosgood received the BVSc degree from the University of Queensland, Australia, in 1982. Currently, she is an assistant professor in small animal surgery at Louisiana State University. Dr. Hosgood has a special interest in soft tissue surgery, particularly wound healing and reconstructive surgery, and pediatric surgery. She has given lectures and published articles on these and other aspects of soft tissue surgery.
Original Doc: spay1.doc
The Network: Caring dog people connect for the sake of a litter in trouble.
BY SALLY S. LEAHY
Source: The Network is from the AKC GAZETTE, March, 1988, pp.74-80.
It was the evening of February 13, and my "Valentine litter" was imminent. Missy had been laboring most of the day, and I knew she would be delivering at any time. Missy was a large bitch even for a Great Dane, and though this was her first litter, I was not particularly worried. I live in Azalea, tucked into the Southern Cascade Mountains of Oregon, and our veterinarian was 45 minutes away by car in Roseburg. I had successfully delivered many other Dane pups in this same home. Birthing is, after all, a natural process.
For the last few hours, my husband, Jim, and I had been taking turns sitting in or near the brood box while we waited out the process of delivering the first pup. Each time we traded places, Missy would welcome us with a touch of her wet nose or a head rested briefly on a knee. She was a lovely, gentle bitch with a sweet expression.
It was 8:00 p.m., and once again my turn. When I checked her, I knew that it was now only a matter of minutes, so I invited her into the yard for a short walk and a last chance to relieve herself. She came willingly enough, took a short drink and then followed me back to the brood box.
Following the command of my gesture, she had just stepped with her front feet over the edge of the brood box to enter it, when she suddenly sat down. I thought she was just being clumsy due to the labor and the weight of the litter. I remember teasing her about it as I bent to help her. But even as I did so, her front end collapsed across the brood box edge. She looked up at me with a wild, bewildered expression, and I knew with a sudden terror that something was radically wrong. Before I could lift her body free of the brood box edge and ease her onto the concrete floor outside the box, she was beginning to go rigid in some kind of spasm.
Vaguely I understood that she was going away from me, and I called her name, but she didn't hear me. Her front legs had stiffened straight out from her body, her mouth was curved into a tight grin with her chin pulling in toward her chest, and her eyes saw nothing. Still calling helplessly to her, I laid my hand over her chest and could feel the normal beating of her heart, yet I knew without any doubt that she was dying. And I could think of absolutely nothing to do!
Cry For Help
I flung open the kennel door, raced across the yard and into the house, screaming to Jim to "Get the vet on the phone. I'm losing her! She's dying."
Without a pause I ran back.
Missy was as I had left her, her front legs stiffened, her face in the death grin, her eyes nearly closed. She did not seem to be breathing.
Cupping my hands around that beloved nose and mouth, I tried artificial respiration and at regular intervals checked her heart beat. But slowly that began to weaken and grow irregular. When it stopped, I switched to the CPR technique I had seen but never really learned, all the while still stupidly trying to call her back to me.
In the meantime, my husband had reached Dr. Ross's answering service and had been told to stand by; the operator would try to reach him. His return call came within a minute. Jim had brought the phone out into the yard where he could shout instructions to me. But even as they conferred, I knew I had lost her.
Only those who have experienced a sudden death can ever fully understand the shock it is to those nearest and dearest. One thing is absolutely clear: one cannot accept it.
For ages I had been preparing for a litter of blue Dane puppies. One spring and summer were going to be enlivened with big‑footed, soft‑eared blue bundles of promise, loved and spoiled by two moms--their big four‑legged real one and their big two‑legged foster one. There would be hours of worrying and cuddling and laughing--and the endless pleasure of watching them grow under the watchful eye of their beautiful mother.
And suddenly their mother was gone, and there would be no pups.
I could not accept it.
I ran to the phone. "It's too late, Doctor. I've lost her. Can I save the pups? Can I take them?"
I heard a funny noise from him-- shock, I think--and then he asked quite calmly, "How near to delivery were they?"
"Minutes. She died in delivery."
"Then, yes, you can try, but you have to hurry."
"What do I do? I mean, where and how do I cut? What should I worry about?"
"Cut directly into the abdomen. Get the pups out and get them breathing. Hurry." He gave me his home number. I wrote it down. Then I walked Into the kitchen and lifted out my favorite long bladed paring knife. I went out to the kennel where my husband wafted. He saw the knife I carried. We both looked down at the still form of our beloved Missy.
"Should I do this?" I asked.
"How will we take care of them?" We both worked and were not normally at home during the day. Orphaned pups just weren't on the agenda.
"I don't know." I put my hand on her stomach and felt the churning movements. "Jim, they're still alive in there."
"Do it." This from a man who assured me regularly that he cared not one whit for all this doggy nonsense in which he indulged me.
I Did It
Living on a farm, I had many times dressed out my own chickens or the game my husband occasionally hunted. I told myself this was no different. This was not my darling Missy; this was just a carcass--but with precious living babies inside, dependent on me for a chance at survival.
Using the point of the knife, I penetrated Mlssy's abdomen. Then with the cutting edge facing upward, I sliced an opening directly into the womb.
Instantly we were deluged with an amazing amount of water. I reached into the opening, searched and found a hard form. Cupping my hands around as much of it as possible, I lifted it out, cleared the mucous from the tiny mouth, and handed it to Jim, placenta and all.
"Rub it, shake it, make it breathe."
Wordlessly, he went to work while I dug for another one. I tried in each case to get the nose and mouth cleared before the umbilical was broken, though it was only a vague notion in the back of my mind that this might matter.
In seconds we had a number of pups out and were working on them. The instant a pup would make a noise, we would move to the next and soon had six of them breathing. And that's where we stopped. We made no effort to save the remainder. Too much time was passing, and there were six live squealers demanding further attention.
Later--I have no idea how much later--we had the six pups contentedly stuffed with a goat's milk formula I keep handy when a litter is due, snug in a box in our living room. They seemed perfectly normal and healthy with no screamers and a respectable interest in eating and wiggling.
Emotionally and mentally exhausted, I sat down to call the vet and report on our success. Now, finally, my brain was beginning to work, and I was slowly coming to realize what we had done and what the consequences might be. Even the realization that the pups would have to be fed again, and then again throughout the night seemed an impossible burden. Added to that was my awareness that I had to make some kind of arrangements for their daytime feedings. There was no way I could take off three weeks of work to play foster mother. What had we done?
My conversation with Dr. Ross did little to reassure me. After he congratulated us on a job well done, he reminded me that these were highly at‑risk pups because of the lack of colostrum from the mother. They had no immunity. They had received none of the precious antibodies that would protect them from all the diseases that we didn't even know were around us, not to mention the terrible ones we knew about. I slowly began to realize that now that we had brought these blue velvet bundles into the world, our chances of saving them were not very good. I started to cry.
Here I was trying to cope with the fact that Missy had just died, and I was suddenly having nightmare visions of these pups dying slowly, one by one, over the period of a week while I struggled helplessly, fruitlessly, to keep them alive.
I simply couldn't face that possibility.
Jim, who was in almost the same shape as I, had called our daughter in veterinary school at Oregon State University. We wanted her to know what had happened, of course; but we also were hoping she might be able to help us through some university resource. She was ln Pullman, Washington at this time doing her small animal study.
Since Suz wasn't at home, Jim left a message to have her call when she arrived. Then exhausted and emotionally drained, we sat staring miserably at one another, me with tears dripping and Jim with his face reflecting what I was feeling. Finally, when I could do it, I said what I thought I must, "Jim, I can't handle it. If they're just going to die on us, I'd rather it be now. I couldn't stand it if I had to watch them go one at a time.
He just looked at me for a long time. I could tell from the expression on his face that he understood what I was asking. Finally, he nodded and stood up, "Ill take care of it. You stay here. You don't have to come outside at all. I'll come get them when everything's ready."
He left and I sat there feeling sorry for myself, for Missy, for the little bundles we had so foolishly saved.
The Phone Rang
It was Suzy. I told her the whole story and didn't even choke up until I reached the point at which I tried to tell her what we were about to do.
Thank the good Lord for intelligent, caring offspring.
"You certainly are not!" she informed me in a strong, determined voice. "You will do nothing of the kind. Do you hear me, Mother? You are tired, and you're not thinking now. Go to bed. The morning is time enough to decide what to do--after you've had a little rest. Besides, we don't know enough yet. There may be all kinds of things we can do. Don't you dare destroy those pups.
"Then she hung up and promptly woke up one of her instructors (it was now after midnight) to get some of that advice we needed. She got the advice offered most cheerfully, under the circumstances--and called me back to reinforce her commands.
And, of course, 1 obeyed her, much to my husband's relief.
I can't honestly say I got all that much rest because those pups had to have a feeding every two hours, but, somehow, in the morning things didn't seem so impossible even though 1 still didn't know what I was going to do.
That was Friday. Jim went to work, and I stayed home to feed puppies and try to solve our problem.
As an active member of the Rogue Valley Kennel Club, I was also the show chairman for the club's upcoming participation in the Oregon Cascade Cluster. There was to be a committees' cluster meeting at my home the next day from the five different clubs involved. I was hoping that one of them might know of a newly delivered bitch with colostrum.
Before I could solidify any plans, my son who knew the pups were imminent, called from Eugene, where he was attending the University of Oregon. When he asked how things had gone, he got the whole mess dropped on him. He offered to do some calling for me, so I gave him several names and briefly told him what I hoped for. He did the rest. His calls started a chain of calls--dozens that covered the hundreds of miles between Eugene and Medford. In a matter of a few hours most of southern Oregon's dog people were alerted to my problem and were working to provide me with whatever help they could.
I spent the day answering phone calls, and my mom, who lives nearby (and who, incidentally, thinks dogs are more pesky than pleasant) fed, cuddled and cooed to the little ones. Everyone was hunting for a newly delivered bitch who might spare some colostrum. No luck.
Then a conversation I had with another veterinarian, whose office I had called in the hope of finding a bitch, changed some of my thinking. He advised me that my grace period for the pups getting the colostrum was nearly up anyway. (It's supposed to be the first food they get and must be received within 24 hours.) He reassured me that what Suzy's instructor had said the night before was true: though the pups were high risk, their plight was not impossible. They had a fair chance if I could keep them isolated.
By Saturday when the cluster committees had gathered, I was beginning to believe that perhaps all was not gloom and dismay. And the many gifts that arrived with these people did much to add to my cheer. Several brought various types of livestock colostrum--"just in case." (It is not useful because the antibodies provided are not for dog disease. ) One woman brought sheep's colostrum frozen into neat little two‑ounce ice cubes. Others provided a variety of nipples, a six‑pack of baby formula, a six‑pack of glucose, and offers of homes that would gladly help me carry the feeding burden. In the meantime, Mom had informed me that she, "and no one else," was going to feed the pups during the hours that we were at work. With everyone so eager to keep them alive, I just had to believe we couldn't fail.
The following morning one of the men who had been at the meeting, whom I never met before that evening, called to tell us about an article in the breed columns in the latest GAZETTE. and asked if we had read it. Like everyone else, he wanted to help.
The Call that Saved the Pups
The magazine had arrived only the day before, and puppy feeding was keeping us all busy. We had not read it, and under the circumstances probably would not have during that time. The article by Sarah Meizlik in the Siberian column told of a new version of an old‑fashioned way to give immunity to orphaned pups, pups in the exact position mine were in. (See the reprinted column, "Orphan Puppies.")
We read this excellent article, and I called Dr. Ross and read it to him, then asked "Could we do this?"
His immediate response was an interested, "Sure. Do you want to do it right away?"
"No, let's wait. If they stay healthy and nothing goes wrong, why subject them to so much?" At that time I didn't realize how quickly they could go.
Two wonderful days followed in which our babies thrived. Each was a special delight, and, of course, each had a special identification. Blue Dane puppies all look pretty much alike when they're first born, and my line in particular, which rarely has any white, allows little means of separate identification, Accordingly, we always paint toenails with nail polish for identification. Our tiniest female had a dewclaw painted, so we called her Thumbelina; the other females were First Toe; Index; Third Toe; Baby Toe. The boy--yes, only one male--we called Hulk because he was so much bigger than his sisters. It didn't take us long before we could tell who was whom, even without the nail polish. And now the fun was replacing the fear. Hungry pups would squeal their delight the moment they felt a hand. Every inch would wiggle, and their efforts to grab the nipple made getting started an exercise in excitement. But once they had hold and were sucking happily, ah, the delightful grunts of perfect content. Every nursing, regardless of the hour, made me glad I had not destroyed them.
Three days later, Wednesday morning, I was beginning to worry. During the previous evening's feedings, the puppies' intake of formula had gone steadily downward. (We were keeping careful records of food intake, elimination, weight. ) They had become lethargic and were hard to awaken. When I called home at noon. Mom told me she could not get Thumbelina to eat. By the time we had returned home from work, she was so far gone that she would not respond at all; the others were no longer interested in food.
The Serum Was Ready
At 5:00, I called Dr. Ross and told him we would have to try the immunity plan at once. He agreed, adding, "Give me an hour to find some donor dogs." By 5:30, he called back. "Bring them on in; I've got two donors which ought to provide us with enough blood. "As quick and wonderful as that response was, it hadn't been fast enough for tiny Thumbelina. She had died while we waited.
By the time we arrived at his office an hour later, Dr. Ross had the serum ready. Someone had cared enough to drop whatever they were doing to bring their animals in to help us and I didn't even know these people.
We carried the remaining pups in a covered box into the office. Everyone else was gone, the office closed. There we donned special shirts we had brought with us from home. Dr. Ross met us and led us into one of the examination rooms, and then he, too, went off to change shirts before touching the pups.
The process we were using required blood from dogs living in the same general locale as ours. The plasma would contain the same antibodies that the colostrum would have and could protect the pups from the same diseases. This plasma had to be injected intraperitoneally--right into their tiny tummies.
I held each pup by its shoulders and rear legs--belly up--while he injected them. They didn't like it one bit and squealed loudly in protest. But once we were done with them, I handed them to Jim who immediately offered them a bottle of formula and some sympathy, and the complaints were soon replaced by those contented grunts.
When all was completed, we packed them up and returned home, wondering whether any of it had been worth it. That night they all got a few extra minutes of holding and hugging as we tried to convince each other that the treatment would work. By morning we knew that it had. The pups were back to their normal, healthy, demanding selves. Their appetites were enormous, and they seemed to be doing everything within their limited powers to make up for their one bad day.
The necropsy on Missy revealed no recognizable cause of death. The brain, however, was not checked; and we have since heard several educated guesses that the cause was probably a clot on the brain. We will never really know.
Ten days after the initial injections on the pups, we repeated the process without even considering the wait that had cost us Thumbelina. We again had no trouble at all finding willing donors. This time the donors were Malamutes owned by a breeder friend who warned me she was not to be blamed if my pups developed fuzzy tails with white tips.
They didn't. Instead they grew up to be strong, healthy animals with slightly spoiled personalities. How could they not be spoiled with all the love, concern, and interest lavished on them by so many people?
Friends refer to these pups as the "miracle" litter, and I suppose, in a way that's a good word; but the thing that I will always remember and be eternally grateful for was the generous, caring response that brought us through those terrible days. Such love and interest is not and should not be a miracle. But it is truly the greatest gift anyone can receive.
Many thanks, dog people.
(Update: As of November 30, three of the Danes in the litter had received their championships!)
By Sarah E. Meizlik.
May 10--bitch goes into veterinary hospital--overdue--must have C-section--after surgery goes into shock...dies. Result: Seven puppies--no mother--no colostrum--no immunity.
May 11--puppies placed with surrogate mother whose own puppies are three weeks old; therefore, no colostrum available from bitch. Result: Puppies develop mucous around eyes, very weak even though being tube fed and nursing on bitch.
At this point I was resigned to losing some, if not all, of the litter. Then I remembered attending a symposium which featured Dr. Jean Dodds. Her topic concerned Immune-Mediated Blood Diseases. At the time, I was taking a course in genetics and studying the principles of immunology. Putting two and two together, I called Dr. Dodds and told her of my orphan pups' condition. Diagnosis: lack of immunity. Solution: administration of plasma from dogs living in the same area as the orphan pups who had built up the antibodies to combat those diseases (antigens) found in that environment. Result: Within 24 hours after receiving the plasma, mucous had disappeared, pups nursing actively, crying stopped, stools normal. Sounds like witchcraft--absolutely not!
Here is a layman's interpretation of the immune system's reaction and the dramatic changes just described. But first, a few definitions:
Immunity: resistance to infection either by means of antibodies produced by the mother (active immunity) or by another source and subsequently introduced into the body (passive immunity) by injection.
Antibody: substance produced by the body to counter-act infection and in response to specific antigens.
Antigens: any of several substances, including poisons, enzymes, and proteins, that cause the antibodies to be introduced into the blood stream.
Plasma: the clear fluid portion of the blood containing antibodies.
Colostrum: the creamy, milk-like substance rich in proteins, that is produced by the bitch the first few days after giving birth, which contains the antibodies necessary to combat disease.
Studies suggest that pups in utero develop some progressive immunity to defend themselves against different antigens (diseases). However, increased competence is achieved when they receive the bitch's colostrum in concert with antibodies transferred through the blood from the bitch while they are in utero. It is the colostrum/blood combination which contains the antibodies to combat the threat of disease. In the case of orphan pups, passive immunity, i.e., that acquired from an indirect source, is the only alternative. (Exception: those pups with incompatible blood type of A-positive sire bred to sensitized A-negative bitch.) An injection prepared from sterile blood plasma of healthy adult dogs living in the same locality as the pups can provide the critically important antibodies to commonly encountered environmental pathogens (antigens), normally passively transferred from the mother to the pups in the colostrum. Otherwise, the pups have no protection whatsoever against disease in their surroundings--thus, the mucous, weakness, and crying of my orphan pups. The plasma from healthy dogs in the same surroundings presumably contains the needed antibodies which are given to the new born pups by intraperitoneal (abdominal) injection. Two doses of plasma are needed, given at about 3-7cc per pup, depending upon their size, and at 10-day intervals. This plasma is rapidly absorbed into the blood stream to provide protection like that normally afforded by colostrum.
The immunity provided in this manner may not be as much as or last as long as that from the mother's colostrum, and hence vaccinations should begin a week or two earlier to be on the safe side and in the beginning only killed vaccines should be administered.
Without Dr. Dodd's help with my litter, I doubt they would have survived. I'm happy to report they are all happy, healthy adults. This was indeed a terrible experience, but once again scientific therapy proves successful over the "old wives' tale, hit or miss" approach.
(This article originally appeared in the GAZETTE's Siberian Huskies breed column, February, 1986).
A Bottle-Feeding Aid
German Shepherd Dog breeder Karen S. McCall had written to the GAZETTE recently about the method her breeder friend, Barbara, used to bottle-feed a litter of pups whose dam wasn't producing enough milk.
On the 60th day of her pregnancy, the dam simply stopped eating. Luckily, she had an easy labor and produced nine healthy, normal-sized pups. However, because she continued to eat very little, the pups began to suffer, and one died. The dam, at that point, was diagnosed as having metritis.
The breeder bottle-fed the pups every two hours, and it was a struggle; the pups would become fussy as they nursed from the bottles. After taking less than an ounce, each would jerk its head away from the nipple, squirm and whimper. Despite several variations on the theme--cross-cut nipples, formula nipples, large-hole nipples, multi-hole nipples--nothing worked for long.
Karen and Barbara then discussed the seemingly unnatural position of being held at a 45 degree angle to be fed, so gravity would help the milk go down. She began spoon-feeding the litter.
Soon after that Karen noticed "Sit'n'Sup" in the children's department of a store. It's designed to fit into a nipple, is attached to a plastic straw, and will enable a baby to drink from a bottle while sitting up. Delivering the new nipples and the Sit'n'Sup to Barbara, Karen enthusiastically suggested they try it out.
The change in the pups' attitude was amazing. They were able to nurse horizontally, as they would next to the dam, and they settled right down, kneading their paws and making contented sounds Barbara hadn't heard since the litter was three days old.
The only drawback was that the Sit'n'Sups did not work well after a few days of steady use, so they always kept a new one on hand, just in case.
One more instance of breeder helping breeder, for the sake of the puppies they love.
Sally S. Leahy is a breeder of Great Danes for 12 years, the author bred the first natural-eared blue male to have earned a championship.
The Use and Misuse of Vaginal Cultures in Diagnosing Reproductive Diseases in the Bitch
By Patricia N. Olson, D.V.M.,Ph.D.
Colorado State University, Fort Collins, Colorado
R. L. Jones, D.V.M.,Ph.D.
Michigan State University, East Lansing, Michigan
Whenever inflammatory disease of the reproductive tract of the bitch is diagnosed, the veterinarian must attempt to identify the causative agent before appropriate therapy can be instituted. Frequently, vaginal cultures are obtained in an attempt to correlate various reproductive diseases (e.g., inflammation of the clitoral fossa, vestibule, vagina, cervix or uterus; infertility; abortion; neonatal deaths) with specific infectious agents. Since a variety of microorganisms are present in the vaginas of bitches with and without reproductive diseases, it is often difficult to associate disease with a specific microbial isolate. Approximately 60 per cent of normal bitches harbor aerobic bacteria in the cranial vagina and approximately 90 percent of normal bitches harbor similar organisms in the caudal vagina. Therefore, merely isolating bacteria from the vagina does not constitute a basis for diagnosis of reproductive disease. Conversely, organisms known to cause infertility, abortion, stillbirths or neonatal deaths (e.g. herpesvirus, Brucella canis) are often difficult to isolate. Hence, a negative vaginal culture does not ensure that a bitch is free of infectious disease involving the reproductive system.
Although the owners of stud dogs may require a "negative" vaginal culture before accepting a bitch for a mating, most male dogs also harbor microorganisms in the prepuce and penile urethra that are similar to those present in the vagina of healthy females. Therefore, it is unreasonable to refuse to breed a bitch to a stud dog merely because aerobic bacteria have been isolated from the vagina.
Vaginal cultures are useful in diagnosing and treating certain diseases of the reproductive tract as long as they are carefully interpreted and they correlate with other clinical findings. Although isolating bacteria from the vagina of a healthy bitch does not constitute a diagnosis of reproductive disease, "normal" bacteria may become pathogenic if uterine or vaginal defense mechanisms are altered. For example, diestrous uteri appear more susceptible to bacterial infection, since Escherichia coli can be isolated from nearly 65 per cent of the uteri removed from bitches with pyometra. It has been postulated that E. coli may adhere via the K-antigen to the progesterone-stimulated endometrium and myometrium. Similarly, bacteria are frequently associated with postwhelping metritis. Bacterial overgrowth inthe uterus can follow a prolonged labor, retained puppies or retained membranes, which predisposes the uterus to developing metritis.
Anomalies of the reproductive tract can also predispose the bitch to infection and inflammation when urine or vaginal secretions pool in aberrant locations. Likewise, mechanical irritation or ulceration from clitoral hypertrophy or foreign bodies may render the vagina more susceptible to secondary bacterial infections. Therefore, utilizing vaginal cultures as an aid for diagnosing and treating reproductive diseases can be very useful as long as the veterinarian is aware of the limitation of the test.
Aerobic Bacteria. In a study of 81 postpuberal healthy bitches, aerobic bacteria were isolated from 51 (63 per cent) of the cranial vaginas and from 74 (91 per cent) of the caudal vaginas. Therefore, most normal bitches have and established bacterial flora that can be isolated from vaginal swabs. The types of organisms isolated may vary with the age of the bitch. A higher percentage of prepuberal bitches have coagulase-positive staphylococci present in the vagina than postpuberal animals (Tables 1 to 3). The types of bacteria do not appear to vary with different stages of the estrous cycle (Tables 4 to 6), but an increased number of organisms appear to be present during proestrus and estrus.
Frequently, many bacteria can be observed on vaginal smears obtained from estrous bitches. This is not an abnormal finding unless the bitch has overt signs of vaginitis (inflamed vaginal mucosa, purulent-appearing or foul-smelling vaginal discharge, poliakuria, licking of the vagina), and the vaginal smear contains many toxic-appearing neutrophils. Although many bacteria are frequently present in vaginal smears obtained from normal estrous bitches, neutrophils should be absent or few in number until the bitch enters diestrus.
Anaerobic Bacteria. Vaginal microflora from healthy and infertile bitches were cultured by Osbaldiston and colleagues. The aerobic bacteria isolated were similar to those reported later by other investigators. Anaerobic organisms isolated included Bacteroides melaninogenicus. Corynebacterium spp., Haemophilus aphrophilus, Bacteroides spp., anaerobic enterococci, Peptostreptococcus spp. (hemolytic and nonhemolytic). No correlation could be made by the authors between bacterial flora and infertility. This suggests that canine infertility is not necessarily associated with bacterial infection of the vagina.
Mycoplasma and Ureaplasma. Doig and colleagues attempted the isolation of genital mycoplasmas and ureaplasmas from 136 dogs with varied reproductive histories. Mycoplasma spp. were recovered from 88 per cent of vulvovaginal swabs, 85 per cent of preputial swabs and 72 per cent of semen samples. There was not significant difference in isolation rates among infertile dogs, dogs with evidence of genital disease and fertile animals.
Ureaplasmas were recovered from half of the bitches sampled. Higher, but not statistically significant, isolation rates (75 per cent) were obtained from infertile females with purulent vulvar discharge than for those that were clinically normal and fertile (40 per cent).
In the male dog a significantly higher number of ureaplasmal isolates were obtained from swabs of the prepuce of infertile animals (69 per cent) than fertile dogs (0 per cent), but isolations from semen samples were similar for the two groups. The role of Ureaplasma in infertility in the bitch and stud dog needs further evaluation.
Brucella canis can infect bitches and cause infertility, fetal or neonatal deaths and persistent uterine or vaginal discharges. Since the infection can also exist without overt manifestations, inapparently infected animals are an important source of transmission. The isolation of Brucella canis from blood, vaginal discharges, lymph nodes, placental or fetal tissues is the definitive method of diagnosis. Although bacteremia can persist for long periods of time, nonbacteremic intervals of variable lengths can follow bacteremic phases. Therefore, a negative blood culture cannot rule out a diagnosis of canine brucellosis. Similarly, a negative vaginal culture does not eliminate the possibility of canine brucellosis.
Table 1. Classification of Vaginal Isolates from 20 Pups, 1 to 11 Weeks Old
Type of Isolate
No of Isolates
% of Total Isolates
Pups with Isolate(%)
Coagulase + staphylococci
Coagulase - staphylococci
Total 50 (2.5 isolates/pup)
(From JAVMA 172:708, 1978.)
Table 2. Classification of Vaginal Isolates from 21 Pups, 12 Weeks to 6 Months Old
No. of % of Total Pups with
Type of Isolate Isolates Isolates Isolate (%)
E. coli 8 17.0 38.1
Coagulase + staphylococci 14 29.8 66.7
Coagulase - staphylococci 5 10.6 23.8
Alpha-hemolytic streptococci 4 8.5 19.0
Beta-hemolytic streptococci 3 6.4 14.3
Nonehemolytic streptococci 2 4.3 9.5
Proteus 1 2.1 4.8
Bacillus 3 6.4 14.3
Corynebacterium 2 4.3 9.5
Micrococcus 3 6.4 14.3
Neisseria 1 2.1 4.8
Klebsiella 1 2.1 4.8
Total 47 (2.2 isolates/pup)
(From JAVMA 172:708, 1978).
Table 3. Classification of Vaginal Isolate from 81 Postpuberal Bitches
Cranial Vaginal Swabbings
Number Per Cent Bitches
0f of Total with
Type of Isolate Isolates Isolates Isolate (%)
E. coli 15 19.0 18.5
Coagulase + staphylococci 5 6.3 6.2
Coagulase - staphylococci 5 6.3 6.2
Alpha-hemolytic streptococci 8 10.1 9.9
Beta-hemolytic streptococci 12 15.2 14.8
Nonehemolytic streptococci 3 3.8 3.7
Pasteurella 8 10.1 9.9
Proteus 4 5.1 4.9
Bacillus 3 3.8 3.7
Haemophilus 1 1.3 1.2
Corynebacterium 2 2.5 2.5
Pseudomonas 0 0 0
Moraxella 1 1.3 1.2
Acinetobacte 0 0 0
Flavobacterium 1 1.3 1.2
Lactobacillus 0 0 0
Micrococcus 1 1.3 1.2
Neisseria 2 2.5 2.5
Enterobacter 1 1.3 1.2
Klebsiella 0 0 0
Nonclassified spp. 7 8.9 8.6
Total 79 (0.975 Isolate/bitch)
No growth 30 (37% of total dogs)
Caudal Vaginal Swabbings Number Per Cent Bitches
Of of Total with
Isolates Isolates Isolate (%)
E. coli 25 13.2 30.9
Coagulase + staphylococci 15 7.9 18.5
Coagulase - staphylococci 16 8.4 19.8
Alpha-hemolytic streptococci 18 9.5 22.2
Beta-hemolytic streptococci 15 7.9 18.5
Nonehemolytic streptococci 10 5.3 12.3
Pasteurella 26 13.7 32.1
Proteus 5 2.6 6.2
Bacillus 13 6.8 16.0
Haemophilus 0 0 0
Corynebacterium 12 6.3 14.3
Pseudomonas 2 1.1 2.5
Moraxella 7 3.7 8.6
Acinetobacter 3 1.6 3.7
Flavobacterium 4 2.1 4.9
Lactobacillus 1 0.5 1.2
Micrococcus 3 1.6 3.7
Neisseria 7 3.7 8.6
Enterobacter 1 0.5 1.2
Klebsiella 0 0 0
Nonclassified spp. 7 3.7 8.6
Total 190 (2.35 Isolates/bitch)
No growth 7 (9% of total dogs)
(From JAVMA 172:708, 1978.)
Table 4. Classification of Vaginal Isolates from 34 Anestrous Bitches
Cranial Vaginal Swabbings
Per Cent Dogs
Number of Total with
Type of Isolate of Isolates Isolates Isolate (%)
E. coli 6 26.1 17.6
Coagulase + staphylococci 2 8.7 5.9
Coagulase - staphylococci 1 4.3 2.9
Alpha-hemolytic streptococci 3 13.0 8.8
Beta-hemolytic streptococci 5 21.7 14.7
Nonehemolytic streptococci 0 0 0
Pasteurella 1 4.3 2.9
Proteus 1 4.3 2.9
Bacillus 1 4.3 2.9
Haemophilus 1 4.3 2.9
Corynebacterium 1 4.3 2.9
Pseudomonas 0 0 0
Moraxella 0 0 0
Acinetobacte 0 0 0
Flavobacterium 0 0 0
Lactobacillus 0 0 0
Nonclassified spp. 1 4.3 2.9
Total 23 (0.7 isolate/dog)
No growth 18 (52.9% of total dogs)
Caudal Vaginal Swabbings
Per Cent Dogs
Number of Total with
of Isolates Isolates Isolate (%)
E. coli 8 10.5 23.5
Coagulase + staphylococci 8 10.5 23.5
Coagulase - staphylococci 9 11.8 26.5
Alpha-hemolytic streptococci 8 10.5 23.5
Beta-hemolytic streptococci 9 11.8 26.5
Nonehemolytic streptococci 3 3.9 8.8
Pasteurella 8 10.5 23.5
Proteus 1 1.3 2.9
Bacillus 6 7.9 17.6
Haemophilus 0 0 0
Corynebacterium 6 7.9 17.6
Pseudomonas 1 1.3 2.9
Moraxella 4 5.3 11.8
Acinetobacter 1 1.3 2.9
Flavobacterium 1 1.3 2.9
Lactobacillus 1 1.3 2.9
Nonclassified spp. 2 2.6 5.9
Total 76 (2.2 isolates/dog)
No growth 3 (8.8% of total dogs)
(From Olson PNS: M.S. Thesis, University of Minnesota, 1976.)
Table 5. Classification of Vaginal Isolates From 25 Proestrous-estrous Bitches
Cranial Vaginal Swabbings*
Per Cent Dogs
Number of Total with
Type of Isolate of Isolates Isoates Isolate (%)
E. coli 4 18.2 18.2
Coagulase + staphylococci 1 4.5 4.5
Coagulase - staphylococci 1 4.5 4.5
Alpha-hemolytic streptococci 3 13.6 13.6
Beta-hemolytic streptococci 2 9.1 9.1
Nonehemolytic streptococci 0 0 0
Pasteurella 4 18.2 18.2
Bacillus 0 0 0
Corynebacterium 0 0 0
Moraxella 0 0 0
Acinetobacte 0 0 0
Flavobacterium 1 4.5 4.5
Micrococcus 0 0 0
Neisseria 2 9.1 9.1
Enterobacter 1 4.5 4.5
Nonclassified spp. 3 13.6 13.6
Total 22 (1.0 isolate/dog)
No growth 6 (27.3% of total dogs)
Caudal Vaginal Cultures
Per Cent Dogs
Number of Total with
of Isolates Isolates Isolate (%)
E. coli 10 17.2 40.0
Coagulase + staphylococci 6 10.3 24.0
Coagulase - staphylococci 3 5.2 12.0
Alpha-hemolytic streptococci 6 10.3 24.0
Beta-hemolytic streptococci 3 5.2 12.0
Nonehemolytic streptococci 3 5.2 12.0
Pasteurella 7 12.1 28.0
Bacillus 4 6.9 16.0
Corynebacterium 2 3.4 8.0
Moraxella 1 1.7 4.0
Acinetobacte 1 1.7 4.0
Flavobacterium 3 5.2 12.0
Micrococcus 2 3.4 8.0
Neisseria 4 6.9 16.0
Enterobacter 1 1.7 4.0
Nonclassified spp. 2 3.4 8.0
Total 58 (2.3 isolates/dog)
No growth 1 (4.0% of total dogs)
*Cranial vaginal cultures were obtained on 22 of 25 dogs in this group.
(From Olson PNS: M.S. Thesis. University of Minnesota, 1976.)
Table 6.Classification of Vaginal Isolates From 19 Diestrous or Pregnant Bitches
Cranial Vaginal Swabbings
Per Cent Dogs
Number of Total with
Type of Isolate of Isolates Isolates Isolate (%)
E. coli 3 13.6 15.8
Coagulase + staphylococci 2 9.1 10.5
Coagulase - staphylococci 3 13.6 15.8
Alpha-hemolytic streptococci 1 4.5 5.3
Beta-hemolytic streptococci 2 9.1 10.5
Nonehemolytic streptococci 2 9.1 10.5
Pasteurella 2 9.1 10.5
Proteus 2 9.1 10.5
Bacillus 1 4.5 5.3
Corynebacterium 1 4.5 5.3
Pseudomonas 0 0 0
Moraxella 1 4.5 5.3
Acinetobacte 0 0 0
Micrococcus 0 0 0
Neisseria 0 0 0
Nonclassified spp. 2 9.1 10.5
Total 22 (1.2 isolates/dog)
No growth 6 (31.6% of total dogs)
Caudal Vaginal Cultures
Type of Isolates
Number of isolates
Percert of Total isolates
Dogs with Isolate(%)
Coagulase + staphylococci
Coagulase - staphylococci
Total 46 (2.4 isolates/dog)
No growth 5 (26.3% of total dogs)
(From Olson PNS: M.S. Thesis. University of Minnesota, 1976.)