Disclaimer: ScottiePhile provides resources for informational purposes. The materials contained here are not intended to be used for the diagnosis or treatment of health problems or as a substitute for consulting a veterinarian.
A better way to prepare dogs for colonoscopy
By Unknown Author
Source: Animal Health Newsletter, Cornell University, July 1990, Editor: Katherine Houpt, VMD, PhD, 53 Park Place, New York, NY 10007. Customer Service 1-800-525-0643.
If you are one of hundreds of thousands of people who have had a colonoscopic examination for an intestinal problem, you probably remember the preparation, including the inevitable enemas. Dogs with suspected disease of the large intestine-and there are many such patients-have had to go through a similar preparation before colonoscopy and then again if surgery is required. The difficulty with these multiple enemas in dogs is that they are often inefficient. In many cases, fecal matter is retained in the colon, blocking adequate visualization with the colonoscope.
A new approach to the problem has now been described by Keith Richter, DVM, and Mark Cleveland, PhD, after working with a large number of dogs at Boston's Angell Memorial Animal Hospital. In place of the standard preexamination enemas, the dogs were given a specially prepared gastrointestinal lavage solution by mouth. The solution, given by stomach tube, flushed fecal material from the colon more efficiently than enemas, resulting in superior colon cleaning and, therefore, better direct visual inspection of the colon.
Original Doc: colon.doc
A Congenital Disorder of Myelination in Two Related Scottish Terrier Puppies
VanHam, L., M. Desmidt*
Dept. of Small Animal Medicine and Dept. of Pathology(*)
State University of Ghent,
Casinoplein 24,B - 9000 Ghent, Belgium
A congenital disorder of myelination is reported in two related Scottish Terrier puppies. The condition was manifested clinically as whole body tremors which became progressively worse with activity and excitement and which diminished during rest or sleep. Case two, in addition had a mild bilateral hind limb paresis. No improvement of the tremor was seen with time and both dogs were finally euthanized. Examination of paraffin-embedded sections of the central nervous system, revealed severe white substance pathology suggestive of dysmyelinogenesis. Myelin-specific stains stained less intensely in comparision with a normal four month old dog. Due to suboptimal fixation techniques however, it was not possible to differentiate between dysmyelination or hypomyelination on plastic-embedded semi-thin sections.
Demyelination, dysmyelination and hypomyelination are all disorders of myelination of the central nervous sytem (Duncan 1987). Demyelination refers to a situation in which previously formed myelin sheaths are lost, with sparing of axons. Demyelination is associated with an acquired tremor. Hypomyelination and dysmyelination are developmental disorders, resulting from an insult prior to or during myelination. They are associated with a congenital tremor. In hypomyelination, axons are usually thinly myelinated, with predominantly normal myelin. They are occasionally nonmyelinated. Dysmyelination is characterized by predominantly nonmyelinated axons and occasionally thinly myelinated axons, usually with abnormal myelin (Jackson and Duncan 1989). The peripheral nervous system is always normally myelinated. Abnormal myelination has been reported in a variety of animal species (Braund 1986; Oliver and others 1987), including dogs. This article reports cases in two related Scottish terrier puppies and briefly reviews the canine disorders of myelination reported in the literature.
...TEXT MISSING... body tremors were noticed for the first time at the age of ten weeks. They were said to be accompanied by high fever. The litter (seven puppies) had been delivered through cesarean section. There had been one dead puppy at birth and one other, that was very small, had died after a few days. The other puppies in the litter were normal. The puppy had been treated by the referring veterinarian with steroids and antibiotics, without any result. On presentation it was alert and responsive and showed generalized body tremors which became progressively worse on excitement and activity and diminished during rest or sleep. Neurological examination revealed no abnormalities except for the tremors. A differential diagnosis of cerebellar disease, abnormal myelination, and tremor of idiopathic, metabolic or toxic origin was proposed. Blood and urine samples were taken, the dog was anaesthetized and a CSF tap was done. None of these revealed any abnormalities. Since the dog's condition remained static, the owner finally requested euthanasia. Macroscopic examination of the central nervous system revealed no abnormalities.
The second case was presented to us three months later. This puppy belonged to the same owner. It was a different litter from the first one, however, both litters had the same father. According to the breeder, this father had given one other puppy with similar symptoms in still another litter. The second puppy was a male puppy of four and a halve months. According to the referring veterinarian symptoms had started at two to three months of age. The dog initially showed paresis in both hind limbs. Gradually whole body tremors appeared. The other puppies in the litter were all said to be normal. On presentation, neurological examination revealed generalized body tremors and bilateral hind limb paresis. Conscious proprioception, hopping and tactile placing reflexes were delayed in both hind legs. In this dog too, blood and urine samples were taken, the dog was anaesthetized and a CSF tap was done. None of these revealed significant abnormalities. Once again the owner requested euthanasia. Macroscopic examination of the central nervous system of this puppy too revealed no abnormalities.
Histopathological examination of haematoxyline-eosine stained paraffin-embedded sections in both cases revealed a severe, diffuse pathology of the white substance with vacuolization, which was also visible in different nuclei, and pronounced gliosis with many microglia cells and atypical astrocytes. The axons seemed to be normal. These changes suggested primary metabolic disease of the white substance, probably dysmyelinogenesis. Myelin-specific stains (luxol fast blue) on paraffin-embedded sections stained less intensely in comparison with a normal four month old dog. Unfortunately, due to suboptimal fixation techniques, it was not possible to differentiate between dysmyelination and hypomelination on toluidine blue stained plastic-embedded semi-thin sections.
In dogs there have been case descriptions of dysmyelination or hypomyelination in chow chows (Vandervelde and others 1978; Vandevelde and others 1981), Springer spaniels (Griffiths and others...TEXT MISSING...weimaraners (Kornegay and others 1987), and Bernese mountain dogs (Palmer and others 1987). Of these, hypomyelination in the Springer spaniel has been studied in detail (Duncan 1987). Furthermore there have been single case studies in a Dalmation puppy (Green and others 1977) and in a male spaniel pupy (van den/Akker 1958). Recently, a hypomyelination of the peripheral nervous system was described in two golden retriever littermates (Braund and others 1989; Matz and others 1990). The central nervous system, however, was normally myelinated. In the Scottish terrier dog, the only congenital nervous system disease described is a myeloencephalopathy resembling Alexander's disease (Cox and others 1986). Disorders of myelination have not been reported yet in this breed.
Disorders of melination always affect pups. In the Springer spaniel, only male pups are clinically affected (Griffiths and others 1981). Some female offspring of carrier dogs also develop a tremor, but this resolves with age (Duncan 1987; Jackson and Duncan 1989). In the chow chow and the Bernese mountain dog both male and female pups are affected (Vandervelde and others 1978; Palmer and others 1987). In the samoyed many of the dead or trembling puppies are male. (Cummings and others 1986), in the weimaraner all except one (Kornegay and others 1987). Both Scotties were male too.
A genetic basis has been shown in the Springer spaniel pup (X- linked recessive inheritance) (Griffiths and others 1981). In some other breeds the disease is believed to be hereditary (chow chow) (Vandevelde and others 1978; Vandervelde and others 1981); samoyed (Cummings and others 1986); weimaraner (Kornegay and others 1987); Bernese mountain dog (Palmer and others 1987). However, conclusive evidence for these breeds is still lacking. Other potential causes include in utero viral infection, intoxication and, less likely, physical agents (e.g. irradiation) (Mayhew and others 1984; Cummings and others 1986; Kornegay and others 1987; Jackson and Duncan 1989). In the Scottish terrier, since both puppies had the same father, a hereditary basis is likely.
All affected pups, including these two Scottish terrier pups, show whole body tremors during activity or excitement and they are normal at rest and during sleep. The severity of the tremor, however, is very different. It is most severe in the shaking pup (Springer spaniel) and samoyed and less severe in the other, where it appears that recovery occurs in time (Braund 1986; Duncan 1987). Severity of the tremor is clearly correlated with the myelin deficit. In dogs with severe tremor, gross examination of the central nervous system reveals a pallor of the white matter with a poor contrast between it and adjacent gray matter (Duncan 1987). Affected pups are reduced in weight and size. Neurological testing is difficult in these pups, but usually they appear to be normal (Jackson and Duncan 1989). Absent or very slow dysmetric postural reactions are reported in the Dalmation puppy (Green and others 1977) and in Samoyed (Cummings and others 1986). Paresis in the hind limbs and absent postural reactions were present in the second Scottish terrier puppy.
...TEXT MISSING...progressive, cerebellar hypoplasia, in which signs are static and accompanied by severe ataxia, dysmetria and intention tremor (Palmer and others 1987), and systemic disease of a variable cause (Kornegay 1986; Duncan 1987). The tremor is more severe with involvement of the entire body in myelin-deficient conditions. Differentiating should be possible on neurological examinations. However, neurological evaluation of severely affected dogs in the latter case is often difficult (Duncan 1987). Other conditions producing generalized tremors occur in adult or older dogs, are often accompanied by other systemic or neurologic signs and can be related to a number of metabolic or toxic conditions (de Lahunta 1983; Chrisman 1982; Mayhew and others 1984; Jackson and Duncan 1989). These include hypocalcaemia, hypoglycaemia, azotaemia, hyperammonaemia, and poisoning with metaldehye, organophosphahte, chlorinated hydrocarbon, fluoracetate, strychnine and lead (Mayhew and others 1984; Farrow 1986). Occasionally diffuse non-suppurative encephalomyelitis may cause whole body tremor (Palmer 1976; de Lahunta 1983). In addition, an acute onset of head and whole body tremor is seen occasionally in adult dogs, especially in small breeds of white dogs (de Lahunta 1983; Chrisman 1982; Mayhew and others 1984; Farrow 1986). Furthermore, many idiopathic tremor syndromes occur in which no structural abnormalities can be detected in either nervous or other tissues (Farrow 1986). If a congenital hypomyelinating disorder is suspected, the breeding history and potential prenatal exposure to viruses or chemical or physcial myelinotoxic agents should be investigated. Confirmation of the diagnosis is only possible on necropsy. Light microscopic examination of toluidine blue-stained plastic-embedded sections, as oppposed to paraffin-embedded material, and electron microscopic examination allow a more accurate assessment of the state of myelination of the central nervous system (Palmer and others 1987; Jackson and Duncan 1989). In our cases haematoxyline- eosine and luxol fast blue stains of plastic-embedded sections indicated a myelin I myelination disorder. Unfortunately, due to suboptimal fixation techniques, the morphological preservation of the myelin in the plastic embedded material was insuffient to allow any further examination. Therefore we are looking forward to other cases in the Scottish terrier to preform a more thorough neuropathological examination.
Springer spaniel affected puppies die by the age of two to three months, as they are unable to feed themselves (Duncan 1987; Jackson and Duncan 1989). Samoyeds too, do not improve (Cummings and others 1986). Chow chows, weimaraners and Bernese mountain dogs do sometimes spontaneously improve at the age of six to twelve months (Vandervelde and others 1978; Vandeveld and others 1981; Kornegay and others 1987; Palmer and others 1987; Vandevelde and Fankhauser 1987), and one of two affected mongrels improved as well (Mayhew and others 1984).
In the chow chow improvement is accompanied by progressive myelination (Vandevelde and others 1981). the clinical improvement noted in all but the Samoyed and Springer spaniels suggest that the lesions were reversible and therefore perhaps more likely to be acquired (Jackson and Duncan 1989). In the Scottish terrier puppies, the condition appeared to be static.
There is no effective treatment. If a genetic disorder is suspected, breeders should be informed and eradication attempted. Many of the animals recover and become essentially normal pets; therefore, if possible, affected puppies should be maintained for 3 to 4 months and observed for any clinical improvement (Jackson and Duncan 1989).
Thanks are due to Prof. M. Vandevelde for interpretation of the neuropathological results. Thanks are due to Dr. Sinjan K. and Dr. Meulemans J. for referring cases one and two respectively.
Braund, K.G. (1986) Hypomyelinogenesis, in Clinical syndromes in veterinary neurology. Williams & Wilkins. Baltimore. pp. 118-119.
Braund, K.G., Mehta, J.R., Toivo-Kinnucan, M., Amling, K.A., Shell, L.G. & Matz, M.E. (1989) Congenital hypomyelinating polyneuropathy in two Golden retriever littemates. Veterinary Pathology 26, pp. 202-208.
Chrisman, C.L. (1982) Ophistotonos, tetanus, tetany, tremors, myoclonus and other muscle spasms, in Problems in small animal neurology. Lea & Febiger. Philadelphia. pp. 285-297.
Cummings, J.F., Summers, B.A., de Lahunta, A. & Lawson, C. (1986) Tremors in Samoyed pups with oligodendrocyte deficiencies and hypomyelination. Acta Neuropatholigica (Berlin) 71, 267-277.
de Lahunta, A. (1983) in Veterinary neuroanatomy and clinical neurology 2nd edn. W.B. Saunders. Philadelphia pp. 150.
Duncan, I.D., Griffiths, I.R. & Munz, M. (1983) Shaking pups: a disorder of central myelination...TEXT MISSING...
Duncan, I.D. (1987) Abnormalities of myelination of the central nervous system associated with congenital tremor. Journal of Veterinary Internal Medicine 1, 10-23.
Farrow, B.R.H. (1986) Generalized tremor syndrome, in Current Veterinary Theraphy IX. Small Animal Practice. W.B. Saunders. Philadelphia, pp. 800-801.
Green, C.E., Vandervelde, M. & Hoff, E.J. (1977) Congenital cerebrospinal hypmyelinogenesis in a pup. Journal of the American Veterinary Medical Association 171, 534-536.
Griffiths, I.R., Duncan, I.D., McCulloch, M. & Harvey, M.J.A. (1981) Shaking pups: a disorder of cnetral myelination in the spaniel dog. I. Clinical, genetic and light - microscopical observations. Journal of the Neurological Sciences 50, 423-433.
Jackson, K.F. & Duncan, I.D. (1989) Hypomyelination in dogs in Current Veterinary Therapy X. Small Animal Practice. W.B. Saunders. Philadelphia, pp. 834-838.
Kornegay, J.N. (1986) Congenital and degenerative diseases of the central nervous system, in Neurologic Disorders. Churchill Livingstone. New York. pp. 109-129.
Kornegay, J.N., Goodwin, M.A. & Spyridakins, L.K. (1987) Hypomyelination in Weimaraner dogs. Acta Neuropathologica (Berlin) 72, 394-401.
Matz, M.E., Shell, L. & Braund, K.G. (1990) Peripheral hypomyelinztion in two Golden Retriever littermates. Journal of the American Veterinary Medical Association 197, 228-230.
Mayhew, I.G., Blakemore, W.F., Palmer, A.C. & Clarke, C.J. (1984) Tremor syndrome and hypomyelination in lurcher pups. Journal of Small Animal Practice 25, 551-559.
Nadon, N., Duncan, I.D. & Hudson, L. (1988) Molecular analysis of the shaking pup mutation. Soc. Neuroscience 14, 829.
Oliver, J.E., Hoerlein, B.F. & Mayhew, I.G. (1987) Cerebrospinal dysmyelinogenesis, in Veterinary neurology. W.B. Saunders. Philadelphia pp. 190-192.
Palmer, A.C., Blakemore, W.F., Wallace, M.E., Wilkes, M.K., Herrtage, M.E. & Matic, S.E. (1987) Recognition of 'trembler', a hypomyelination condition in the Bernese Mountain Dog. Veterinary Record 120, 609-612.
Vandevelds, M., Braund, K.G., Walker, T.L. & Kornegay, J.N. (1987) dysmyelination of the central nervous system in the chow chow dog. Acta Neuropathol. (Berlin) 42, 211-215.
Vandervelde, M., Braund, K.G., Luttgen, P.J. & Higgins, R.J. (1981) Dysmyelination in chow chow dogs: further studies in older dogs. Acta Neuropathol. (Berlin) 55, 81-87.
Vandervelde, M. & Fankhauser, R. (1987) Hypomyelinogenese, in Einfuhrung in die veterinarmedizinische neurologie. Paul Parey. Berlin and Hungary. p. 249.
Original Doc: tremor.doc
News from the Canine Gastric
By Larry Glickman
Dilatation‑Volvulus Research Program
School of Veterinary Medicine,
Purdue University, W. Lafayette IN 47907‑1243
Phone: (317) 494‑7543 FAX: (317)494‑9830
Confidentially -- The names of dogs and owners in our studies are kept confidential unless the owners grant permission to use them in the newsletter.
Material in BLOAT NOTEs is not copyrighted and may be freely reproduced.
Source: BLOAT NOTEs, Newsletter, Issue 93-2, December 1993.
Dr. Larry Glickman (Principal Investigator) was notified that the Morris Animal Foundation approved the new grant for bloat research at Purdue through August 1995.
Objectives and status of the studies:
1. Radiographic Morphometry Study ‑-Objective: Use radiographs to assess chest conformation as a risk factor for bloat (see col. 2).
2. Inheritance Patterns of Bloat Risk ‑-Objective: Characterize the role of inheritance in the risk of developing bloat. Breeders will be asked to supply pedigrees and other information.
3. Practitioner/Owner Case‑Control Study ‑-Objective: Expand the ongoing study of risk factors ‑‑ those that predispose a dog to bloat and those that precipitate an episode. More veterinarians are being recruited to provide data from dogs with bloat (cases) and those without bloat (controls).
4. Practitioner/Owner Prospective Survival Study ‑‑ Objective: Expand and extend the ongoing follow‑up study of dogs with bloat to identify prognostic factors for survival and recurrence.
Are Deep‑Chested Dogs More Susceptible to Bloat?
In a previous study funded by the Morris Animal Foundation (BLOAT NOTEs May 1993), we examined the pattern of occurrence of bloat for 5802 dogs. Pure‑breed dogs were 3 times as likely to develop bloat as mixed‑breed dogs, and in general, the larger the breed, the greater the risk. However, even among breeds of similar body size, there were marked differences in risk. For example, the "Setter" breeds (Irish and English) were at relatively high risk, while the "Retrievers' breeds (Chesapeake, Labrador, Golden) were much less likely to bloat. Also, the Basset Hound had the 6th highest risk of bloat among all pure breeds despite the fact that it usually weighs <50 lb.
This pattern of breed risk led us to suspect that conformation of the chest (and probably abdomen) is an important factor in predisposition to bloat. We hypothesized that breeds typically having a greater chest depth/width ratio would be more likely to bloat because the deeper chest and abdomen would allow the stomach and its ligaments to stretch in the ventral direction, especially when weighted down by water and ingesta. Chronic stretching would then increase the probability of twisting (volvulus, torsion), especially when the stomach is full and a rotational force is exerted, as when the dog rolls over or exercises.
This hypothesis is being tested in a second 2‑year study funded by the Morris Animal Foundation and by donations from several breed clubs and individual donors. Since the risk of bloat for many pure breeds has been determined, we now need to characterize chest size for the same breeds and compare the two measures.
Chest size is currently being assessed by utilizing thousands of chest radiographs that were taken on dogs that at the Purdue Veterinary Teaching Hospital since 1980. The goal is to determine the average adult chest size, namely depth, width, length, for each pure breed for which we have information concerning bloat risk and then to relate the measures of chest size with breed risk. While the study will not be completed for another 6‑12 months, the
preliminary findings are so interesting that we felt you should be aware of them.
When the risk of bloat for each of 7 pure breeds is plotted on the horizontal axis and the chest depth/width ratio on the vertical axis, the two measures appear to be highly correlated. There is an almost linear increase in bloat risk by breed with an increase in the chest depth/width ratio for those 7 breeds. In this example, 63% of the variation in bloat risk can be explained by a change in the chest depth/width ratio alone!
A word of caution: these are only preliminary results which need to be confirmed in a much larger number of dogs and dog breeds. Also, in the practitioner/owner case control study of risk factors, we are measuring chest size (and abdominal size) in dogs that had bloat and comparing these with the same measures in dogs of the same breed and age that did not have bloat.
Studies such as those described above will enable us to better understand the genetic and environmental determinants of bloat. This knowledge is critical in order to develop meaningful recommendations to breeders to prevent bloat. As for diseases like heart disease, cancer, and diabetes, which are multifactorial in their origin, a variety of research studies in dogs will be needed to shed light on the causes of bloat. This will take time, collaboration, and a continuing commitment by breeders and veterinary researchers.
Gary C. Lantz, DVM
(Dr. Lantz, Professor of Small Animal Surgery, Purdue University School of Veterinary Medicine, launches a new feature in the newsletter with his comments about bloat. He has had years of experience treating dogs with bloat and conducting clinical research, and is a co-investigator in the current epidemiologic studies at Purdue.)
Bloat is a life‑threatening disease in dogs. In order to provide a greater understanding of this problem and to emphasize the urgency of seeking medical treatment when bloat occurs, we have answered some questions that are commonly asked.
1. What is bloat?
Bloat is a gastrointestinal disease affecting primarily large and giant dog breeds and has an approximately 30% mortality rate. It is a rapidly progressing disease that can occur at any time. It requires immediate medical attention. In brief, the stomach distends and rotates for reasons as yet unknown. The distended, rotated stomach compresses two large veins located in the abdominal cavity that return large volumes of blood to the heart for recirculation through the body. When this venous return to the heart is reduced in bloat, the heart does not pump a normal volume of blood to the body tissues. Therefore, body cells are deprived of normal amounts of oxygen and nutrients. Body functions begin to fail. The patient goes into shock and this requires immediate treatment.
2. What are other names for bloat?
Bloat is also known as canine gastric dilatation‑volvulus (CGDV), gastric rotation, gastric torsion, or gastric distention. Actually the term "bloat" has been applied to two different clinical findings that are probably part of the same disease process.
Bloat with a distended and rotated stomach requires surgery as part of the treatment. Bloat with a distended stomach that is not rotated may not require immediate surgery. The clinical signs of each type of bloat are identical, and each can cause rapid death. The distinction between the bloat types is made on x‑ray evaluation of the stomach and not by clinical examination alone.
3. What causes bloat?
The specific cause(s) for bloat have not yet been determined. Theories include: various factors contributing to the abnormal anatomy and/or function of the stomach; various types of dog foods; eating and drinking large volumes of food and water before or after periods of exercise; and body conformation. Genetics may play an important role. A combination of factors may be involved.
4. What are the clinical signs of bloat?
Progressing from early to late signs:
a. Pacing and restlessness b. Head turning to look at abdomen c. Distention of the abdomen d. Rapid, shallow breathing e. Nonproductive vomiting f. Salivation 9. Recumbent: semi‑comatose or comatose.
The clinical signs can begin suddenly, at any time, and may progress rapidly to coma and death. If bloat is suspected, it is imperative that the dog be examined by a veterinarian immediately.
5. Can it wait until later? My schedule is full.
ABSOLUTELY NOT! The progression of shock in a bloated dog can be very rapid. A perfectly normal dog may be dead from this disease as soon as 2 to 3 hours after onset of clinical signs. If this disease is suspected, the patient must be examined by a veterinarian immediately. The earlier a patient is diagnosed and treated, the better are the chances for survival.
6. How is bloat treated?
The first step is the treatment of shock. This is accomplished by decompression of the distended stomach (by inserting a needle through the abdominal wall and/or passing a tube into the stomach via the oral cavity) and by the administration of intravenous fluids and other drugs to improve blood circulation throughout the body. Vital signs and other body functions must be monitored carefully.
Surgical correction of the rotated stomach follows and can usually be performed within 2 hours of presentation of the patient to the veterinarian. (Some patients in the earlier stage of bloat may be ready for immediate surgery. Other patients in the later stage of bloat may require a little longer period of medical stabilization before surgery is performed.) As part of the surgical procedure, a gastropexy is performed, i.e., the right side of the stomach is attached to the body wall. This attachment will heal and become permanent so that the stomach rotation will not recur. Several effective gastropexy techniques are available. Gastropexy has a 3% to 5% failure rate, that is, a permanent adhesion does not form. If gastropexy is not performed, the recurrence rate of bloat is about 68% to 80%.
7. I can take my dog home right after surgery and it will be OK, right?
Intensive postoperative care in the hospital is needed for several days. The bloat patient has been through a very traumatic disease process and a major surgery. Also, many complications can arise in the first 3 to 4 postoperative days. Most patient deaths occur during this time period.
8. How can I prevent bloat from happening?
Since the cause of bloat is unknown, specific recommendations to prevent it cannot be made at this time. Current recommendations include pre‑moistening dry food to reduce stomach distention after eating, dividing the daily ration into 2 or 3 smaller meals, and limiting activity for at least 1 hour before and after eating.
9. What should I do to prepare for a possible episode of this disease?
You should know the clinical signs of bloat that are listed above. You should know where the nearest emergency veterinary medical facility is. Remember that a gastropexy will probably prevent rotation of the stomach in the future, but stomach distention can still occur. Severe distention without stomach rotation has identical clinical signs and may be just as fatal as stomach distention with rotation.
10. What can I do to help promote bloatresearch?
Donations designated for bloat research may be sent to the Morris Animal Foundation, 45 Inverness Drive East, Englewood CO, 80112‑5480, or to CGDV Research Program, School of Veterinary Medicine, Purdue University, W. Lafayette IN 47907‑1243.
An Insight into Bloat Research at Purdue: Epidemiology vs Clinical Medicine
Dr. Glickman thinks of diseases from several viewpoints. He has been a clinical veterinarian and is now an epidemiologist on the Purdue faculty‑‑ and a dog owner. His comments follow.
Practicing clinical veterinarians are, for the most part, concerned with individual patients. They see each patient, take a history from the owner, and do a physical examination. They often develop a close personal relationship with the owner and come to understand the pet's role in the family. Each patient is special to a clinical veterinarian and he or she bears a personal responsibility to each one. However, clinical veterinarians are typically not interested in someone else's patients, even if they have the same diseases as do their own patients. Clinical veterinarians are generally oriented toward diagnosis and treatment, which requires an understanding of the mechanisms of disease.
Epidemiology is the discipline that deals with the distribution and determinants of disease in populations. Epidemiologist are primarily concerned with all individuals in a particular population who have the same disease, and they do not normally come into contact with the animals that they study. Once a diagnosis has been established, epidemiologist are more interested in trying to determine why some animals developed a disease and others did not, rather than in treating individual patients. The goal of epidemiology is to identify the risk factors for a disease; that is, characteristics, behaviors, and exposures of animals that increase their likelihood of subsequently developing a disease. However, when questions arise as to what is the best treatment for a given disease, epidemiologist work with clinicians to design experiments (clinical trials) using patients to best answer these questions. Computers and biostatistics are the main tools of epidemiologists, but like clinicians they must also understand the mechanisms by which diseases occur.
In recent years clinicians and epidemiologists have become aware that their fields interrelate. The Bloat Research Project at Purdue University is an example of how veterinarians with advanced training in different disciplines work together to not only address the problem of how to better treat dogs with bloat, but also to understand the genetic and environmental factors that resulted in their bloating. If we can gain insights into the mechanisms of bloat, it should be possible to identify those dogs that are at high risk of bloat and make meaningful recommendations to reduce the likelihood of an episode occurring in the future. This is an example of why epidemiology is regarded as the basic science of disease prevention and control. ‑Larry Glickman
Breeder and Veterinarian Help With Pilot Study
Often one or more small feasibility or pilot studies are needed before designing a full scale research study. As we plan the study of inheritance patterns of bloat risk, two volunteers are providing data for a study in Great Danes. Barbara Renkosiewicz, LINBAR Kennels, West Chicago IL, has been obtaining pedigree information and Dr. Steve Borowiak, Animal Medical Clinic, Wheaton IL, has been measuring dogs. This will help answer some questions about how feasible it will be to get complete pedigree information and whether it will be possible to obtain measurements from a number of dogs listed on a pedigree.
An important aspect of the case‑control study of risk factors for bloat involves measuring dogs which have had a bloat episode (cases) and dogs of the same breed or size which have not had bloat (controls). A wooden device ("Canine Caliper") was designed and manufactured especially for this study by a woodworker at Purdue, Norman (Shorty) Henry. The caliper is used to measure the depth and width of the chest and abdomen of dogs of any size and is used by the veterinary clinics participating in the study.
Dogs are enrolled in the Purdue study by referral from their veterinarian. Usually the veterinarian or veterinary technician measures the dog at the clinic as part of the process of recording medical information. One group of dogs, however, was enrolled in the study after the dogs had been treated for bloat and left the clinic. The medical information was available, but measurements were still needed. Tim Emerick, a Research Technician in the Department of Veterinary Pathobiology at Purdue, obtained these measurements by visiting the owners of the dogs in their homes. His comments follow.
I found measuring dogs with CGDV enjoyable, and certainly this can be attributed to the very caring owners of these animals who have experienced this life threatening disease. Having taken these measurements of dogs of different breeds and ages, I can say that it has been an interesting learning experience for both the owners and myself.
There are 7 measurements that we need for each dog: 1) overall length of the dog; 2) height of the dog; 3) length of the chest; 4) depth of the chest; 5) width of the chest; 6) depth of the abdomen; and 7) width of the abdomen. The first 3 measurements are made with an ordinary seamstress tape, while the last 4 measurements are made with the Canine Caliper. This wooden device is really very simple to use. It is placed on the animal and the sliding caliper arm is moved along the frame until it touches the animal. A knob locks the arm in place, and then the measurement can be read and recorded. The whole procedure takes no more than 5 minutes to perform.
Most of the dogs I measured did not mind the process at all, and in fact seemed to enjoy all the added attention. I made the measurements while the owner held the dog, except in a couple of instances where the owners felt that their dog might not cooperate or possibly try to nip at me. In those instances I simply stood back from the dog and explained to the owner which specific areas to measure. This worked well, and allowed our research group to gather information that we could not have gotten any other way.
Measuring breeds from Basset Hounds to Great Danes allowed me to see a diverse array of dogs that have survived the terrible affliction of bloat and seem to be functioning normally. On my measurement expeditions, I was always deluged with questions about the disease. Unfortunately, there has been a lack of research on this disease and I was not able to offer much in the way of answers. It is evident from the painful stories these CGDV dog owners shared that they are very interested in preventing this disease from occurring again. We are really grateful to these owners for their willingness to help us in our research and for their hospitality during these visits. ‑‑ Tim Emerick
Original Doc: bloat1.doc
Aspects of Food and Food Suppliments in Skin Disease
By Alexander Werner, VMD, Diplomate ACVD
Animal Dermatology Centers, Los Angeles, California
Source: Breeder Forum, Pedigree food for dogs, 3250 East 44th Street, PO Box 58853, Vernon, CA 90048-0853. Volume 2, Number 1, pp. 3-9.
The skin is the largest organ of the body, representing between 12% and 24% of body weight. The skin performs a myriad of functions, most important of which is protecting the internal organs. It also regulates body temperature, stores and synthesizes nutrients, receives sensory input, regulates immune functions, and provides pigmentation. Because of its size and very active metabolism, the skin uses a large proportion of the body's energy and nutrients (up to 30% of the animal's daily protein intake.) Therefore, the quality and quantity of food has a direct effect on the skin; malnutrition, food allergy, or intestinal problems can result in skin disease.
In general, the nutritional requirements of the skin are similar to those of the rest of the body. During the past two decades, the scientific and medical community have focused their attention on animal nutrition. Guidlines for nutrient requirements have been established for livestock and companion animals. Requirements for specific nutrients are constantly updated as medical knowledge increases. Because many superbly formulated commercial diets are readily available for companion animals, nutritional deficiencies and imbalances are uncommon. In general, it can be difficult to determine if a dermatosis has a nutritional basis because skin diseases can look similar despite widely varied causes. Scaling, hair loss, and a dull haircoat are commonly associated with nutritional disease; however, these signs are frequently seen in other dermatoses as well. Confirming a nutritional dermatosis requires diagnostic testing as well as clinical improvement of the skin in response to specific diet manipulations.
This article focuses on three nutrition-related topics affecting the health of the skin. The first, cutaneous food hypersensitivity, is an often suspected, but infrequently diagnosed, cause of dermatitis. Food hypersensitivity is the least common allergic cause of skin disease in the dog, yet food is often incriminated when itching and scaling are present. Food allergy may represent less than 1% of the cases of skin disease seen in general practice and less than 10% seen in the dermatology practice. Ingested materials provide a constant barrage of potential allergens to the intestine. Major food ingredients of commercial diets are similar to the "table scrap" diets of yesterday, so it is unlikely that many dogs are allergic to their diets. The plenthora of special "hypoallergenic" diets on the market has caused great confusion and has made it difficult to diagnose food allergy. Thus, other causes of skin disease must be investigated before blaming the problem on food allergy.
The body obtains the nutrients it needs by abosrbing substances via the intestinal tract. Dramatic changes occur from the time food is chewed until unused waste products are excreted. Digestive enzymes from the salivary glands and stomach reduce proteins and carbohydrates to basic compounds, normal gut bacteria degrade less digestible nutrients, and gastrointestinal cells alter and absorb molecules, bringing food particles into the body. These nutrient components may then join other molecules for transportation, and are finally altered by individual body cells for their use. At any point along this route, nutrient molecules can either lose or gain their allergenic potential. Proteins are expecially good allergens. Therefore, when considering food as a possible cause for allergic skin disease, three concepts are important to remember: (1) allergic skin reactions caused by food are uncommon; (2) the specific nutrient that becomes allergenic may not be in the same form as it was when ingested; and (3) proteins are more likely to cause reactions than are other nutrients.
With cutaneous food allergy, the allergenic nutrient is usually a major component of the food or food additive. Unless drastic changes occur in the diet formulation, most dogs will receive the allergen daily. The ingredients commonly associated with allergy include beef, milk products, and grains. Sensitization can be very gradual, and most dogs that develop cutaneous food allergy have eaten the offending diet for months or years. Breeds that may be predisposed to food allergy include the miniature schnauzer, golden retriever, West Highland white terrier, Scottish terrier, and Shar pei. Food allergy has been reported most often in dogs under six months of age and in dogs over six years of age.
The immune response to a food allergy is believed to be an immediate-type hypersensitivity. The body produces a specific antibody against the food allergen. When the allergen is ingested, it combines with its antibody and causes specialized immune cells (mast cells) to release histamine and other potent inflammatory chemicals. Other types of immunologic responses have been proposed for food hypersensitivity and the precise mechanism responsible for food allergy is probably quite complex.
Cutaneous food allergy reactions can look like many itchy or non-itchy dermatoses. Severe itchiness is usually present with this condition and can result in self-mutilation. The itch associated with food allergy does not vary with the season of the year. Nonetheless, if the animal has concurrent seasonal allergies, the signs of disease may worsen when these other allergies flare-up. Clinical signs of disease vary, but tend to localize around the face and neck. Severe and recurrent ear infections, face-rubbing, licking between the toes, and scratching of the neck and armpit regions are signs suggestive of food allergy. In a few cases, only ear disease may be present. Unfortunately, food allergy can also present in many unusual ways, making diagnosis difficult. Compared with inhaled allergic dermatitis (i.e., pollen allergy, hay fever, or atopy), food allergy does not usually improve very much with the administration of steroids or antihistamines.
Gastrointestinal food intolerance (i.e., vomiting, diarrhea) is seen in less than 20% of dogs with food allergy; conversely, dogs with gastrointestinal signs of food allergy are rarely itchy. Animals previously diagnosed with other cutaneous allergies (e.g., flea-bite hypersensitivity, inhaled allergic dermatitis) are at a higher risk for developing food allergy; the predisposition to allergy appears to be inherited.
Diseases other than cutaneous food allergy that should be considered for dogs with severe head and ear itchiness include flea-bite hypersensitivity, inhaled allergic dermatitis, scabies, primary ear infection, and bacterial skin infection. Because other, but less frequent, types of dermatoses can be similar in appearance, a qualified veterinarian with dermatology experience should examine animals with skin disease before changes in diet are made.
The diagnosis of food allergy relies primarily on a food elimination trial and subsequent challenge. Other diagnostic tools include skin biopsy and serum allergy testing. Suspicion of food allergy can increase with compatible findings in biopsied skin samples. Although similar biopsy results may be found with all skin allergies, a pathologist trained specifically in skin diseases (dermatopathologist) may be able to determine if a food allergy is a possible cause of the disease. Serum allergy testing, which measures allergen-specific antibody in the blood of animals, is now used frequently for diagnosing inhaled allergic dermatitis. This test is less accurate for food allergy, however. Serum allergy testing is not consistently diagnostic for either food allergy or inhaled allergic dermatitis. Nonetheless, this test may help to determine which specific allergen(s) is producing the disease. Intradermal skin testing is considered the most precise method for diagnosing inhaled allergic dermatitis. With this test, small amounts of suspected allergens, including food components, are injected into the skin. The skin is then observed for reactions. Others and myself have noted a poor correlation between results of serum testing, intradermal testing for food allergens, and clinical results of feeding trials. Therefore, these indirect forms of testing cannot be recommended for diagnosis of cutaneous food allergies.
A recent controversial test for food allergy involves applying food allergens directly onto the stomach wall. Using an endoscope, the stomach wall is sprayed with food proteins and then observed for allergic reactions. This test is usually impractical because it requires the animal to be anesthetized and can only be used to test a limited number of foods. With modifications, the test may become beneficial.
The food elimination trial remains the most reliable means of diagnosing food allergy. Food trials are not easy to perform, however. Owners must be prepared to feed their pets certain restrictive diets for a long period of time. Ideally, the pet should be fed one protein source and one carbohydrate source that it has never eaten before. With the current trend toward unusual diet formulations, finding an appropriate trial food can be challenging. Examples of useful proteins include pinto beans, tofu, fish (for dogs only; commercial cat diets frequently contain fish products), pork, venison, or rabbit. Carbohydrate sources are more limited and include potatoes and whole-grain rice. The availability and palatability of the food and the pet's feeding history must be taken into account when choosing the protein and carbohydrate sources. It is imperative that all other foods and treats, including rawhide chews, flavored biscuits, pet vitamins, and flavored chewable medications (including meat-based heartworm preventatives) are removed from the pet's diet. Food elimination trials may frequently fail because of inadvertent feeding of an inappropriate treat.
Simply substituting one commercial diet for another is not an appropriate food elimination trial. Most commercial diets are nutritionally balanced and contain very similar ingredients. Even diets advertised as "hypoallergenic" contain more ingredients than one protein source and one carbohydrate source. One recent study demonstrated that more than 15% of dogs diagnosed with food allergy could not tolerate a commercial diet formulated specifically for this disease. In the near future, several food companies are expected to release limited-antigen diets that contain a minimal number of ingredients. These diets will be available only by prescription. Hopefully, they will make diagnosing and managing food allergy more tolerable.
A food elimination trial must continue until improvement is noted. In some instances, a response may be seen in as few as 3 weeks or in as long as 10 weeks. Once improvement is seen, the pet is then "challenged" with the original diet. If symptoms return within seven days, the animal has a cutaneous food allergy. The elimination diet is fed until signs resolve again; single food items may then be introduced to find an acceptable commercial diet. It must be remembered that food elimination diets are intentionally incomplete and unbalanced. Therefore, they cannot be used for longer than 12 weeks without risking malnutrition. The evenutal goal is to find a tolerable commercial food or a balanced home-cooked diet for long-term maintenance.
To summarize, food allergy is an uncommon cause of skin disease in pets. Signs most often involve itchiness of the face, feet, and ears. Food allergy should be suspected in animals for which other causes of nonseasonal itch cannot be determined or in which previously controlled itch has become nonresponsive to treatment. Diagnosis relies on the feeding of a restrictive elimination diet and the recurrence of signs when the original diet is reinstituted. Lifelong control of the problem requires finding an acceptable balanced diet for the pet.
As mentioned above, malnutrition in companion animals is rare in the United States because of the large variety of balanced and palatable commercial diets available. In other countries, where dogs must rely on scraps, garbage, or poor-quality commercial diets, dermatoses caused by malnutrition are more frequent. For example, dogs with demodectic mange responded dramatically to vitamin E supplementation in a study from South America. Similar results were not noted in dogs treated in the United. States, perhaps because the South American dogs lacked adequate dietary vitamin E.
Some commercial diets may fail to provide adequate nutrition for all stages of an animal's life. The growing, working, pregnant, or nursing pet requires a diet that is of higher quality and has more calories than does the sedentary, older animal. Also, the published minimal nutritional requirements represent the lowest acceptable level for individual nutrients only. Nutrient types, such as protein and fat, are not indicated, as well as the specific availability of these nutrients from the diet. For instance, a diet with a high protein content may actually provide a protein source that the animal cannot utilize. Even the moderately active dog may require a diet that supercedes published guidelines. In general, most dogs will ingest an adequate amount of nutrients if fed a sufficient quantity of a balanced commercial diet.
Any animal that loses a great deal of weight must be examined for metabolic disease. If a physiologic reason for the weight loss is ruled out, a comprehensive evaluation of the circumstances involving the feeding of the animal should be made. Physiologic reasons for weight loss include primary gastrointestinal disease (i.e., the inability to absorb or metabolize nutrients) and general systemic illness. Nonphysiologic malnutrition in the adult animal is most often associated with either:
*Poor-quality (generic) commercial food;
* Outdated food in which the nutrient potency has declined
* Excessive supplementation of a specific nutrient;
* Insufficient amount of food (or excessive competition for food);
* A diet consisting primarily of table scraps; or
* The extended use of a nutrient-restricted, unbalanced diet (food elimination trials).
For example, nonphysiologic malnutrition can occur from feeding improperly stored food that allows fats to leach out or become rancid. Malnutrition resulting from the above causes can be easily corrected by feeding animals separately, by feeding fresh, properly stored food, and by using only high-quality diets.
Malnutrition resulting from the feeding of elimination diets for longer than 12 weeks may be more common than currently thought. When an animal improves after being fed one of these diets, some owners may not be willing to risk a relapse by weaning the dog onto a balanced diet. After a period of time, essential nutrients and body stores of basic dietary components are exhausted.
Signs of malnutrition can be obvious or inapparent. For example, a recent association between fatal heart disease in cats and the lack of taurine (an amino acid) in commercial cat diets resulted in the reformulation of most of these diets. More classic signs of malnutrition include excessive scaling; a dry, greasy, or brittle haircoat; abnormal shedding or hair loss; and weight loss.
The skin has high requirements for fat, protein, and essential nutrients. Changes in the appearance of the skin and coat caused by malnutrition reflect alterations in the skin's production of hair, cells, and natural oils. These changes reduce the skin's ability to fight disease and to stop the growth of abnormal bacteria, predisposing the skin to secondary infections.
Currently, concentrations of individual nutrients in the skin cannot be easily measured. Therefore, the diagnosis of malnutrition is usually confirmed by correcting the cause of the dietary insufficiency. After instituting a nutritionally balanced diet, good health should return within 12 weeks. Failure to respond to a balanced diet requires reassessment of the diagnosis.
ESSENTIAL FATTY ACIDS
Deficiency of essential fatty acids in companion animals is uncommon for the reasons mentioned above. There has been great interest in the response of various skin diseases to high-level supplementation of fatty acids, however. Dietary fats (also referred to as oils or lipids) are a source of essential fatty acids. All essential fatty acids are polyunsaturated (i.e., the long carbon chains of these nutrients contain double bonds; the position of the double bond also determines the fatty acid name). The term essential indicates that these nutrients are required for normal body function and cannot be manufactured by the body ( i.e., they must be supplied by the diet). Essential fatty acids are important to the skin as major cell membrane components and as inflammatory chemical precursors. The most important essential fatty acid is linoleic acid, which is derived from vegetable oils, especially safflower oil. Other essential fatty acids include x- linolenic acid, which is derived from leafy vegetables; y-linolenic acid, which is derived from the oil of the evening primrose; and eicosapentaenoic acid, which is derived from fish oil. Normal levels of these nutrients, as supplied in balanced diets, are important for healthy skin and hair.
Certain inflammatory skin diseases are partially caused by abnormal fatty-acid metabolism or increased levels of inflammatory chemicals, specifically eicosanoids. Both proinflammatory and anti-inflammatory mediators can be produced. The eicosanoid mediators, which are known as prostaglandins and leukotrienes, are chemicals produced from arachidonic acid in cell walls. These two classes of molecules are exceptionally potent and cause severe reactions when released. Depending upon the specific prostaglandin or leukotriene synthesized, proinflammatory or anti-inflammatory reactions can predominate.
The pathways that produce proinflammatory and anti-inflammatory prostaglandins and leukotrienes are as complex as their names. By supplementing specific types of fatty acids, pathways that produce anti-inflammatory chemicals are favored. This results in an overall decrease in inflammation as the skin's chemical components change.
Unlike other drugs that can produce serious side effects, essential fatty acids use the body's natural biochemistry to reduce inflammation. Therefore, if side effects, such as pancreatitis, vomiting, and diarrhea, occur at all, they are generally mild. These effects can often be eliminated by reducing the amount of fats or other fatty acids in the diet.
Essential fatty acid supplementation is not a cure-all. Other causes of inflammation, such as fleas, infections, or allergies, must be controlled first. Essential fatty acids can make an itchy dog less itchy. Nonetheless, it is unrealistic to expect clinical signs to resolve by only using fatty acids. In recent investigations, an adequate response to essential fatty acid supplementation was reported in up to 20% of cases with inhaled allergic dermatitis. In the majority of dogs studied,essential fatty acids decreased the level of itch and, most importantly, decreased the dosages of other medications.
A minimum of three to six weeks of supplementation is required to attain sufficient levels of essential fatty acids in the skin. The dosage of essential fatty acids necessary to achieve these results is currently unknown. Several reports have suggested that supplementation at two to five times the dosage currently recommended by manufacturers may increase the response to therapy. Excessive amounts of essential fatty acids, however, may decrease their efficacy. Therefore, until effective dosages have been established, supplementation at the manufacturer's recommended level should be administered initially. If a response is not noted within eight weeks, the animal's condition should be reassessed and an increase in the dosage should be considered.
The skin is a dynamic organ that requires a significant level of nutrition for healthy development. Diets that fail to supply sufficient levels of nutrients to the skin are rare in the United States. Nonetheless, some skin diseases are produced by (or respond to) a change in feeding habits, foods, or adding supplements to the diet.
Cutaneous food allergy is the least common of the skin-related allergies. It is best diagnosed by feeding a strict elimination diet and then challenging the animal with the original diet. The availability of limited-antigen diets, available only by prescription, will make it more convenient to diagnose this ailment. Malnutrition is also uncommon and is easily corrected with a quality balanced diet that is properly fed and stored. Supplementing the diet with essential fatty acids has been shown to be effective in assisting in the control of itchy skin diseases. When used in conjunction with a proper diagnosis and the control of concurrent problems, essential fatty acids are safe for augmenting the body's natural responses toward disease.
1. Jeffers JG, Shanley KJ, Meyer EK: Diagnostic testing of dogs for food hypersensitivity. JAVMA 198(2):245-250, 1991.
Codner EC, Tharcher CD: Nutritional management of skin disease. Compend Contin Educ Pract Vet 15(3):411-419. 1003/
Muller GH, Kirk RW, Scott DW (eds): Small Animal Dermatology, ed 4. Philadelphia, WB Saunders Co., 1989, pp. 470-474, 796-798.
White PD: Essential fatty acids: Use in management of canine atopy. Compend Contin Educ Pract Vet 15(3): 451-457, 1993.
dermatosis--a disease of the skin
dermatitis--inflammation of the skin
sensitization--exposure to allergen that results in the development of hypersensitivity
scabies--a contagious skin disease caused by Sarcoptes scabiei
biopsy--the removal and examination of tissue from the body
endoscope--an instrument for examining the interior of a hollow organ
demodectic mange--a noncontagious skin disease caused by a species of Demodex
pancreatis--inflammation of the pancreas
Original Doc: SKINDI.
Dog Heatstroke Survival Guide
Know how to treat and prevent this dangerous condition.
What is heatstroke?
In simple terms, heatstroke occurs when a dog loses its natural ability to regulate its body temperature. Dogs don't sweat all over their bodies the way humans do. Canine body temperature is primarily regulated through respiration (i.e., panting). If a dog's respiratory tract cannot evacuate heat quickly enough, heatstroke can occur.
To know whether or not your dog is suffering from heatstroke (as opposed to merely heat exposure), it's important to know the signs of heatstroke.
A dog's normal resting temperature is about 100.5 to 102.5 degrees Fahrenheit. Once a dog's temper ature rises above 105 degrees, physiological changes start to take place, and the dog begins to experience the effects of heatstroke. At 106 to 108 degrees, the dog begins to suffer irreversible damage to the kidneys, liver, gastrointestinal tract, heart and brain.
If a dog is experiencing heatstroke, you may observe excessive panting; hyperventilation; increased salivation; dry gums that become pale, grayish and tacky; rapid or erratic pulse; weakness; confusion; inattention; vomiting; diarrhea; and possible rectal bleeding. If the dog continues to overheat, breathing efforts become slowed or absent, and finally, seizures or coma can occur.