WebCanine.com » Gastro-Intestinal

IBD & Legg-Calve Perthes Disease study

mom — Wed, 27 Jul 2011 20:19:12 +0000

Medical News Today
Research Into IBD, LCPD In Westies May Contribute To Human Disease Research
19 Jul 2011

The Westie Foundation of America (WFA) has announced preliminary findings in two major studies involving the health of West Highland White Terriers also known as Westies. Findings in these and other studies of Westies and other dogs may hold answers for similar human conditions like Inflammatory Bowel Disease (IBD). The studies are jointly funded by the WFA and the AKC Canine Health Foundation (CHF).

In one study, researchers are looking at the role of a mucosal gene driving inflammation Canine IBD, a chronic intestinal disorder that creates a bacterial-driven inflammation in the intestines. In the second, scientists are researching Legg-Calve Perthes Disease (LCPD), a debilitating developmental disease that causes pain, lameness and muscle atrophy of the dogs’ hip joints. Both are considering implications for humans since the diseases share commonalities in disease symptoms and pathology.

In IBD, genetic factors are thought to contribute to the cause of the disease in both dogs and humans and researchers are utilizing unique molecular biology tools to identify key genes which regulate intestinal inflammation, similar to human IBD.

“It is our expectation to identify specific genes which serve as biomarkers for diagnosing canine IBD and for monitoring the effects of therapy. We have now identified a grouping of 17 ‘marker’ genes that may be more critically assessed in future studies,” said Albert E. Jergens, DVM, PhD of Iowa State University, the study’s lead investigator. “We have preliminary evidence that changes in the composition of the intestinal bacteria accompany the abnormal gene patterns…this situation is remarkably similar to the association between people and their intestinal populations causing human IBD (i.e., Crohn’s disease and ulcerative colitis).”

LCPD is an orthopedic disease that may require surgery to relieve the clinical signs. Researchers are using a high-throughput technology to assess nearly 127,000 points in the dog genome. The goal of this project is to identify genes that contribute to the development of LCPD.

Preliminary study findings show LCPD may be inherited in much the opposite way previous studies have shown. Eariler studies suggested LCPD is transmitted in an autosomal recessive pattern. “Our current data suggest the LCPD is inherited in either a dominant or complex fashion,” said Keith E. Murphy, PhD of Clemson University. “Only with more samples will we begin to understand the genetics controlling LCPD.” The investigators currently have samples from 58 Westies, 23 of which have LCPD. One candidate gene identified in humans was investigated in canine LCPD, but was not associated with LCPD in Westies. The results of the candidate gene analysis will be published later this year.

“We are pleased to see such progress in the study of Westies and are even more excited that our work may contribute to human disease research, as well,” said Bebe Pinter, president of WFA. “We anxiously await final results in these studies and in other studies currently being funded by WFA and CHA and look forward to continuing our commitment to research and funding for Westie health.”

Notes:
Full results are expected from both studies after December 31, 2011.

Researchers of LCPF have additional experiments planned for July and are currently recruiting study participants. Interested owners willing to participate in the LCPD study should contact Dr. Alison Starr-Moss at astarr@clemson.edu.

For individuals and organizations interested in supporting future canine research, please contact the Westie Foundation of America .

Source:
Teresa Barnes
Westie Foundation of America

Article URL: http://www.medicalnewstoday.com/releases/231307.php

?

Liver disease & Pancreatitis

mom — Wed, 22 Jun 2011 22:15:53 +0000

Penny Watson [Penny Watson of the Cambridge Veterinary School and a European diplomate in internal medicine] Explores Liver Disease And Canine Pancreatitis, UK
Liver disease is one area where knowledge has advanced at a particularly rapid rate and has overturned many of the old certainties about the diagnosis and management of the condition.
Like all students of her 1980s generation, Dr Watson was told in her undergraduate course that steroids are a frontline treatment in the care of patients with chronic liver disease. But that was based on the assumption that most animals with the disease were just like human patients in suffering from an autoimmune condition. But now the finger of suspicion is pointing towards an infectious agent as the probable cause and in that case giving drugs that will weaken the patient’s immune response is likely to do more harm than good, she says.

Dr Watson will also point out that colleagues will need to buy a new text book if their current volume advises the attending clinician to put any patient with chronic liver problems on a low protein hepatic diet. Patients that are fighting liver disease will often need a higher than normal dietary intake of protein and it is particularly important that it is good quality material, she says. There is also increasing evidence that a diet rich in anti-oxidants can be helpful in managing the condition.

Chronic liver disease in dogs is a particularly frustrating condition to treat because the cause will often appear idiopathic and there is only a limited amount of published evidence to support the different treatment options. But there is anecdotal evidence that some of those options will help recovery and a proper diagnostic work up, including hepatic biopsies will help identify some patients with eminently treatable causes of liver problems.

In a second presentation, Dr Watson will be updating colleagues on another condition that presents difficult clinical challenges for a first opinion practitioner, canine pancreatitis. Again there is little convincing evidence to support any particular treatment option. She will be advising on ways to identify patients with severe disease at the earliest opportunity as the condition is very painful and with a high mortality and so the owners need to be warned of the poor prognosis.

“Dogs don’t drink alcohol, they don’t have gallstones and they don’t suffer from cystic fibrosis, which are the three main causes of acute pancreatitis in people. So we have got to be looking at some of the more unusual causes of this disease if we want to learn anything from our human medical colleagues,” Dr Watson points out.

But there are some strategies used in NHS hospitals that may help recovery in dogs with acute pancreatitis, such as aggressive use of fluid therapy and early attempts at assisted feeding in dogs who may be emetic and have little appetite for food. As in patients with liver disease, the received wisdom 20 years ago was to discourage feeding of patients with such a severely compromised digestive system – so once again the information told to veterinary surgeons-to-be as recently as the 1980s has again been found to be completely inaccurate, she says.

Notes

1. Session titles: Diagnosing and managing acute pancreatitis in the dog, 9am, Saturday 24 September Treatment of chronic liver disease, 10.30am, Saturday 24 September

2. BVA Congress, in association with BSAVA, will be held in London on 22-24 September 2011 under the theme ‘Vets in a Changing World’.

Source:
British Veterinary Association

IBD : inflammatory bowel disease

mom — Wed, 22 Jun 2011 22:04:23 +0000

Canine IBD, UK

When a dog turns up in their consulting room with chronic diarrhoea, vomiting and weight loss, then it is quite likely that the vet will call it a case of inflammatory bowel disease. But that is probably the only thing that they can say with any confidence after identifying one of the most enigmatic and frustrating conditions seen in small animal practice.

The cause of the disease is uncertain, the best treatment is still a mystery and even in those patients that do appear to be getting better, then the owner must appreciate that their pet’s condition is only under temporary control, it is rarely ever cured. However, first opinion practitioners may have a better idea of the task awaiting them and improve the odds of a satisfactory response, after attending the session on the diagnosis and treatment of canine disease by Alex German at this year’s BVA Congress. His talk is part of the excellent clinical programme designed by BSAVA to offer a greater small animal science presence at BVA Congress, 22-24 September, London.

Dr German, holder of a European diploma in internal medicine and a lecturer at the Liverpool veterinary school, will explain that IBD is not a single condition but a group of similar disorders characterised by persistent or recurrent gastrointestinal signs, with histological evidence of intestinal inflammation.

In many respects canine IBD is very like the common human condition, though there are key differences in the underlying pathology, he says. The inflammatory process in the intestinal wall will be found on biopsy to be lymphocytic-plasmacytic in origin whereas the two main forms of human IBD are neutrophilic in ulcerative colitis and granulomatous in Crohn’s disease.

Yet in both species the condition is largely seen to be rooted in a defective immune response triggered by a range of infectious, environmental and genetic factors. The search for specific gene factors has so far proved fruitless but the apparently excessive numbers of cases from particular breeds, notably German shepherd dogs, shar peis and Norwegian lundehunds certainly points in that direction.Another breed which is overrepresented in the list of canine IBD cases in the boxer which has a granulamatous form of disease more closely allied with Crohn’s disease. It is a condition for which US researchers appear to have found a trigger in the form of invasive E coli bacteria infiltrating from the dog’s gut. Dr German says there is increasingly strong evidence to show that an abnormal response to the patient’s normal gut flora is a key feature of the disease in many of its different forms.

Once established there does appear to be mainly an immunological problem and steroid therapy will usually be the mainstay of any successful therapy. But antimicrobial treatment can often be helpful in getting the condition under control, and dietary management particularly with low allergenic hydrolised protein may help to keep it that way. The use of probiotics is favoured by some clinicians but there is no convincing evidence that they can provide significant benefits other than as an adjunct therapy in already well controlled cases.

However, achieving the goal of controlling the symptoms of canine IBD is no easy task and the dog’s owner will have to accept a certain amount of trial and error in the treatment until the specific trigger factors can be identified in that individual animal. But once the particular features of the disease have been found then there is every chance that it can go on to enjoy a good quality of life.

Notes

1. Alex German BVSc(Hons), PhD, CertSAM, DipECVIM-CA, MRCVS is a graduate of Bristol University, and received his PhD from the same institution in 2000. He is currently Royal Canin Senior Lecturer in Small Animal Medicine’ at the University of Liverpool. His research interests include small animal gastroenterology and obesity biology.

2. Session title: Diagnosis and treatment of inflammatory bowel disease in the dog, 9.45am Saturday 24 September

3. BVA Congress, in association with BSAVA, will be held in London on 22-24 September 2011 under the theme ‘Vets in a Changing World’.

Source:
British Veterinary Association

Gastric Dilatation Volvulus (Bloat) update

mom — Mon, 06 Sep 2010 15:55:12 +0000

Gary W. Ellison, DVM, MS, DACVS
University of Florida
Gastric dilatation Volvulus complex also know as bloat is a medical and surgical emergency which is know to primarily affect large and giant breeds of dogs. The disease has also been reported in smaller breeds such as the Pekingese and Dachshund. Mortality has been estimated as high as 30 percent. There are no reliable estimates of how many dogs develop bloat in the United States each year, but in certain breeds such as Irish Setters and Great Danes owners reported an incidence of seven and ten percent respectively. It does appear that purebred dogs are more likely to develop bloat than are mixed breed dogs.

Results of Retrospective Studies
Incidence Several recent reviews by Dr. Larry Glickman at Purdue University utilizing information from the veterinary medical database (VMDB) have discovered some interesting findings:
1) Amongst veterinary institutions the frequency of bloat amongst all dogs ranged from 2.9-6.8 per 1000 dogs
2) Approximately 29 percent of the dogs with gastric dilatation and 33 percent of those with dilatation and volvulus died.
3) Aging of the dog increased risk. Dogs greater than seven years of age are more than twice as likely to have bloat as dogs 2-4 years of age.
4) Purebreds were three times as likely to have bloat as mixed breed dogs.
5) Males are twice as likely to bloat as females yet spaying or neutering has no effect on the risk of bloat.

Studies of Risk Factors
Several risk factors have been identified which may contribute to the establishment of bloat in purebred dogs.

Breed Bloat has been long reported to be more common in large and giant breeds of dogs yet until recently the prevalence of bloat was not compared to the dog population at large. When this data was analyzed statistically, it was found that the Great Dane, St. Bernard, Weimaraner, Irish Setter and Gordon Setter were breeds at greatest risk. An accompanying chart outlines the remainder of the breeds (Table 1).

Chest Conformation Although it is established that large and giant breeds are the breeds at greatest risk it has been shown there are profound differences in the risk of bloat within certain breeds. This possibility seems related to conformation of the animal’s chest. For instance, breeds such as Irish Setters which are at high risk may weigh approximately the same as some of the Retriever breeds yet the Retrievers are at much lower risk than Irish Setters for developing bloat. When looking at this more scientifically it was found that the depth and width of the chest may be the key in predicting which animals within a certain breed may develop bloat. It appears that the chest depth/width ration is highly correlated with risk of bloat, ie. Those animals with deep, narrow chests within a certain breed are much more likely to develop bloat than those dogs with deep wide chests. In using external measurements of chest conformation it was found that within the Great Dane breed the depth/width ration may indeed be useful in identifying animals prone to bloat. Also, Great Danes with moderate and high abdominal height to width ratios were approximately 8 times as likely to develop bloat as those with low abdominal height to width rations. In Irish Setters the chest height to width ration also correlated with those dogs having a higher depth to width ration being much more likely to develop bloat than those animals with a lower depth to width ration. This information is obviously very significant in terms of selective breeding for the reduction of bloat in these breeds.

Diet Exact determinations of types of diet on risk for developing bloat still cannot be made. Although cereal-based diets have incriminated, it is difficult to compare groups since almost all large and giant breeds are fed cereal-based diets. Therefore, further controlled studies will be necessary to determine if cereal-based diets are in fact a risk factor. However, several interesting findings have come to surface with regard to the diet and nutritional management of breeds predisposed to bloat. For instance, it has been shown that dogs who eat one meal a day are almost twice as likely to develop bloat as those fed twice a day. The rate of eating is also very important. Those dogs characterized as slow eaters have the lowest incidence of bloat whereas those dogs characterized as moderately fast eaters have about 2 times the chance of developing bloat and those characterized as fast eaters have almost five times the chance of developing bloat as those being characterized as slow eaters.
Body weight may also be of some significance. Being overweight actually reduced the incidence of bloat compared to dogs that were optimum weight. However, those animals characterized as significantly underweight were about three times as likely to develop bloat as those animals characterized as optimum weight.

Gender It has been shown that males are approximately twice as likely to develop bloat as females. Neutering does not seem to have an effect on the incidence however.

Personality and Environment There does seem to be a direct correlation of the animal’s temperament relating to its tendency to develop bloat. Those animals being characterized as unhappy or fearful were about 2 times as likely to develop bloat as those animals characterized as happy. In addition, the environment may play a role. Stress appears to also significantly increase the chance of the animal developing bloat. Therefore, animals who may undergo significant stress traveling to show, etc. are tow to three times as likely to bloat than those animals who are not significantly affected by the transport. Also activity level may be important with those animals characterized as hyperactive and those animals being categorized as less active were twice as likely to develop bloat than those animals characterized as having a normal activity level.

Summary and Conclusions
With regard to known epidemiologic factors affecting bloat some of the following recommendations can be made. It appears there is a correlation with chest and abdominal height/width ratio with those animals having tall thin chests and abdomens more likely to develop bloat than those with lower, wider chests and abdomens, there selective breeding may possible be recommended to diminish the incidence due to conformation.

With regard to diet and nutrition changes in feeding relating to twice a day feeding versus once a day feeding may be recommended. Also, changing the time of the meal is significant with those animals having constant changes in meal time being approximately 2 times as likely to develop bloat as those being fed at regular intervals. In addition, those animals undergoing a sudden increase in food intake are almost three times as likely to develop bloat as those animals kept on a regular food intake. Therefore, recommendations may be made to keep consistency and times of feeding regulated and to feed the moderate amount of food without sudden increases in the amount fed.

It also appears that reducing the amount of stress on the animal will decrease the chances of bloating. Although no specific recommendations can be made about tranquilization knowing the temperament of your dog may help you in minimizing the amount of stress encountered during travel to and from shows. It also appears that keeping physical activity to a moderate amount that is what the animal is used to, will be more helpful in reducing the chances of bloat than allowing extra activity than normally expected.

Etiology
The exact etiology of GDV is unknown, but it is most likely a multifactorial disease. Ingestion of cereal based diets and water followed by exercise is reported in some but not the majority of cases. Stretching of the hepatogastric or hepatoduodenal ligaments from chronic overeating may allow transposition of the stomach. Gastric outlet obstruction by foreign bodies has been observed in some cases but delayed gastric emptying caused by pyloric hypertrophy is not conclusively proven as a cause of GDV. Splenic torsion or displacement occurs secondarily to GDV rather than initiating it, as was once believed. Gas production secondary to bacterial fermentation by clostridial organisms is a postmortem finding and is not a source of gas in live animals. Aerophagia is a likely cause since gas composition of the gastric lumen resembles atmospheric air and the onset of GDV often follows vigorous exercise, excitement and barking.
Recently there is evidence that gastric motility disorders may induce or follow GDV.

Clinical Signs
Dogs usually demonstrate hypersalivation, retching or unproductive vomiting on presentation. Cranial abdominal distention is apparent and gastric tympany is usually present on blunt percussion of the right anterior quadrant. Hyperpnea or dyspnea accompanied by open mouth breathing indicates hypoxia due to reduced diaphragmatic excursions. Shock is evidenced by pale or injected mucous membranes, prolonged capillary perfusion, tachycardia and weak rapid femoral pulse.

Mechanisms of Rotation
A lack of coordinated gastric contractions due to gastric myoelectric dysrhythmias may slow gastric emptying and contribute to the development of gastric dilatation volvulus (GDV). Food and fluid distension from overeating or gaseous distension from aerophagia causes intra-abdominal angulation of the gastroesophageal junction that prevents belching or vomiting.
Gastric dilatation results. Volvulus occurs when the dilated gastric fundus becomes displaced from a left dorsal to a right ventral position. The pylorus concurrently shifts from its right ventral position to a left, caudal and dorsal position. When viewed from the rear a clockwise rotation occurs in the majority of the animals. The spleen follows the greater curvature to the right. The gastrosplenic ligament and short gastric arteries are often torn during the volvulus.

Initial Management of GDV
Initial patient management involves shock therapy, and gastric decompression followed by management of cardiac arrhythmias. Shock therapy involves fluid loading with 90 ml/kg of lactated Ringers solution of the first hour. The use of hypertonic saline may also be beneficial,
as it has been shown to be beneficial in increasing gastric arterial perfusion. Treatment for acid- base status is controversial with one study indicating normal pH and another indicating the presence of metabolic acidosis in cases of GDV. However, with mild metabolic acidosis Na bicarbonate infusion is not necessary as long as adequate volume replacement with lactated Ringers solution is achieved. Hypokalemia is a common finding associated with GDV and potassium replacement is sometimes warranted. Corticosteroids are administered after initial treatment with intravenous fluids. They cause vasodilation and improved tissue perfusion if fluid volume is adequate. Cardiac dysrhythmias are commonly seen and require careful pre- and postoperative management. Paroxysmal vent4ricular tachycardia, and premature ventricular contractions are most commonly seen. Gastric decompression is accomplished using a pre-measured, well lubricated PVC plastic foal nasogastric tube. Ability to pass the tube into the stomach does not mean that gastric volvulus is not present. If intubation is not possible in the prone position it is attempted in a sitting upright position. Sometimes trocharization is necessary to reduce distension and facilitate tube passage.
The character of the fluid is sometimes important in predicting the status of the gastric lining. Black fetid smelling fluid with flecks of devitalized mucosa indicates that mucosal ischemia is present and often predicts the presence of gastric wall necrosis. After decompression, the stomach is lavaged with 4-5 liters of water using gravity flow, dose syringe or stomach pump.

Radiography
Radiography is always postponed until after patient stabilization. With gastric dilatation the stomach appears as a grossly distended gas and fluid filled structure that occupies the cranial abdomen displacing all remaining viscera posteriorly. The spleen is usually not visible in its normal left ventral location and is often located in a right dorsal position. Gastric volvulus is suspected when the pylorus is located dorsal, cranial and to the left of the midline. After decompression it may take a classic upside down appearance. Left and right lateral views are recommended. On the right lateral view gas can be seen in the pylorus whereas on the left lateral view gas may be seen in the fundus. If stomach position is questionable barium sulfate is administered to identify the pylorus.

Surgical Management
Definitive management of GDV involves 1) repositioning of the stomach with resection of any devitalized gastric wall and 2) a prophylactic gastropexy technique to prevent recurrence. UP to 80 percent recurrence of GDV is reported with gastric decompression or repositioning alone.
We now advocate laparotomy as soon as the patient is a reasonable anesthetic risk. This allows early derotation that increases circulation and allows assessment of gastric wall viability. Areas of necrosis are detected early and resected if possible. With 270o to360o clockwise gastric volvulus the dilated stomach is covered on its ventral aspect by omentum. Reduction is accompanied by passing the had down the left abdominal wall, grasping the pylorus in its left dorsal position and rotating it in a caudal and counter-clockwise manner to its normal right sided location.

Gastrectomy Techniques
Standard methods for gastrectomy involve ligation of branches of the left gastroepileploic arteries and veins allowing areas along the greater curvature of the stomach to be resected. The stomach is resected back to areas of healthy bleeding. Spillage is likely and prevented through the use of Babcock forceps or stay sutures. After resection is complete the stomach is closed in two layers. The mucosa and submucosa are closed with a continuous inverted Cushing pattern of 2-0 or 3-0 PDS or Maxon. The serosa and muscularis are then closed with a similar pattern.
Recently we have relied heavily on the autostapling equipment for rapid gastrectomy procedures with minimum risk of spillage. The TA90 autostapler is used with the green (4.8 mm) or blue (3.5mm) cartridge. Often several end-to-end staple lines have to be placed since each staple line is only 9 cm in length. The surgeon needs to overlap the staple lines by a few mm to prevent leakage between the staples.

Rationale for Gastropexy
By definition gastropexy describes the fixation of the stomach to nearby structures or body wall as a means of preventing recurrence of GDV. Although gastropexy procedures reportedly diminish the recurrency rate of DGV, their reliability in producing permanent adhesions between the stomach and abdominal wall is not well documented.
Most North American surgeons use an antral gastropexy procedure to fix the gastric antrum to the right abdominal wall. The three major categories of permanent antral gastropexies used in North America are the tube gastrostomy described by Parks (1976); the incisional gastropexy described by MacCoy (1982); and the circumcostal gastropexy described by Fallah (1982). In addition, two modifications of muscle flap techniques, one using a muscular flap from the abdominal wall (Shulman, 1986) and another using a belt-loop from the gastric muscularis (Whitney, 1989), have recently been described.

Clinical Results
Potential advantages of the tube gastropexy are that 1) the surgery is rapid and easy, 2) the tube not only creates a permanent adhesion of the gastric antrum to the abdominal wall preventing recurrence of volvulus but also 3) allows for continued gastric decompression in the early postoperative period and 4) slurried food or medications can be offered through the tube. The main disadvantages of the technique are 1) the nursing care and long hospital period required for tube management and 2) the potential for fatal peritonitis secondary to leakage around the tube or early removal by the dog.
Clinical studies of the tube gastrostomy have yielded encouraging results. Flanders (1984) reported recurrence of volvulus in only one of 29 dogs treated with tube gastrostomy for a follow-up time ranging from 14 to 40 months. However there was a mortality rate of 31 percent during the first week after surgery. Johnson (1984) reported on 76 cases where this technique was used with only a five percent recurrence rate. Older studies describe a recurrence rate as high as 29 percent (Walshaw, 2976) as well as a 17 percent complication rate (Fox 1985) including premature dislodging of a tube, peritonitis, subcutaneous cellulites and persistent
stoma drainage.
Advantages of the incisional gastropexy are that 1) the procedure is rapidly done, 2) the stomach lumen is not entered and 3) fibrous connective tissue enters the abdominal rectus muscle and stomach wall to form a strong mature adhesion. The potential disadvantage is that the gaseous decompression is not provided in the postoperative period. The incisional gastropexy is popular among many North American surgeons but unfortunately no good retrospective studies are available to determine its clinical efficacy.
The circumcostal technique has become popular for use in academic medicine because it probably forms a stronger adhesion. It is reported to be more difficult to perform than the other techniques but the author disagrees with this statement. Potential advantages include a 1) viable muscle flap adhesion as well as 2) a more proper anatomic placement of the stomach. Potential disadvantages include a prolonged surgical time, potential for rib fracture and potential for pneumothorax because of the close proximity to the diaphragm. Lieb (1984) reported on 39 dogs with circumcostal gastropexies to have a slightly lower recurrent rate (2.6 percent at 13.7 months) than dogs with tube gastrostomy.
Belt loop gastropexy offers similar advantages to the circumcostal and incisional gastropexies in that the gastric lumen is not entered and the risk of peritonitis is minimal. The technique is easily performed by an unassisted surgeon. Although the belt loop gastropexy has not been evaluated biomechanically one would suspect that breaking strengths would be superior to incisional or tube gastrostomy techniques but not quite as secure as circumcostal techniques since the base of the flap is narrower than the latter technique.

Postoperative Management
Diligent postoperative care is mandatory for successful outcome of the gastric dilatation volvulus patient. Most dogs that die in the postoperative period will do so within the first 3-4 days after surgery. After major gastric resection the animal is kept NPO for a period of 24-48 hours.
Maintenance fluid, electrolyte and acid base status is critical during this period. Maintenance fluid should be given at a rate of 40-60 ml/kg per day. Although many dogs maintain normal serum potassium levels following gastric dilatation volvulus a total body potassium deficit may exist because of the NPO status, vomiting, oral gastric innervation and removal of gastric secretions. Therefore, supplementation of 20 mEq of potassium chloride is usually added to each liter of fluids to help maintain a total body potassium. Hypokalemia can also contribute to the development of cardiac arrhythmias, and gastrointestinal ilius.

The Role of Reperfusion in GDV
Mortality associated with gastric dilatation volvulus is most often due to gastrointestinal ischemia secondary to the large twisted stomach. It has been estimated that mortality can increase to 60 percent in the presence of gastric necrosis. Tissue ischemia to the gastric wall occurs due to reductions in arterial perfusion and venous stasis within the stomach wall. When the stomach is decompressed via the stomach tube and derotated via surgery there is rapid reperfusion of this ischemic tissue. Paradoxically, tissue ischemia followed by reperfusion with oxygenated blood may further increase tissue damage due to a phenomenon known as reperfusion injury.
Reperfusion injury is thought to be mediated through the activity of oxygen-derived free radicals that is based on an iron dependent mechanism. These free radicals result in cellular lipid peroxidation and cell death. Since GDV is associated with high mortality and since most deaths occur within 96 hours of surgical intervention it is plausible that treatment directed toward preventing or moderating reperfusion injury may improve survival following the correction of GDV. Studies in experimental dogs with GDV have shown that xanthene oxidase inhibitors such as allopurinol and iron chelators such as deferoxamine have been helpful in reducing the amount of free radical production consequently minimizing cellular damage due to reperfusion injury and potentially decreasing mortality associated with GDV. Although experimental results are preliminary, it is likely that within five years some of these now experimental drugs will be utilized in emergency centers for the clinical management of GDV.

Bloat Risk Ranking for 24 Purebreeds, Compared with Risk for All Dogs Combined *

Breed

Affected

Not Affected

Risk Rank

Great Daneâ€

St. Bernardâ€

Weimaranerâ€

Irish Setterâ€

Gordon Setterâ€

Standard Poodleâ€

Basset Houndâ€

Doberman Pinscherâ€

Old English Sheepdog

German Shorthaired Pointer

Newfoundland

Airedale Terrier

German Shepherd Dogâ€

Alaskan Malamute

Chesapeake Bay Retriever

Boxer

Collie

Labrador Retriever

English Springer Spaniel

Samoyed

Dachshund

Golden Retrieverâ€¡

American Cocker Spaniel

Miniature Poodleâ€¡

299

180

139

202

130

246

182

158

115

159

*Rank based on unadjusted odds ration (an estimate of relative risk) in purebreeds for which
there were > ten cases and > eight controls. All dogs combined (pure and mixed breeds)
included 1934 cases and 3868 controls.
â€ Risk significantly higher than for all dogs combined.
â€¡Risk significantly lower than for all dogs combined.
From Glickman LT2. Epidemiologic Studies on Bloat in Dogs. Purina Veterinary Previews,1992; 2: 10-15.
References
1) Glickman LT, Glickman NW, Shellenburg DB, et al.: Multiple risk factors for the gastric dilation volvulus syndrome in dogs: A practitioner/owner case control study. J Am Anim Hosp Assoc 33: 197-204, 1997.
2) Glickman LT, Glickman NW, Shellenburg DB, et al.: Epidemiologic studies of bloat in dogs. Purina Veterinary Previews 2: 10-15, 1997.
3) Badylak SF, Lantz GC, Jeffires M: Prevention of reperfusion injury in surgically induced gastric dilatation volvulus in dogs. Am J Vet Res 51:294-299, 1990.
4) Ellison GW: Gastric dilatation volvulus: Surgical prevention. Vet Clinics N Am 27: 513-521, 1993.
5) Glickman LT. Epidemiology of gastric dilatation-volvulus in dogs. Waltham Focus 7:9-11, 1997.

Dog Owners and Breeders Symposium
July 28, 2001
University of Florida
College of Veterinary Medicine

Influence of barometric pressure on GDV (bloat)

mom — Sun, 05 Sep 2010 21:30:19 +0000

Abstract:

Gastric dilatation-volvulus (GDV) is a life-threatening condition in dogs and other species in which the stomach dilates and rotates on itself. The etiology of the disease is multi-factorial, but explicit precipitating causes are unknown. This study sought to determine if there was a significant association between changes in hourly-measured temperature and/or atmospheric pressure and the occurrence of GDV in the population of high-risk working dogs in Texas. The odds of a day being a GDV day, given certain temperature and atmospheric pressure conditions for that day or the day before, was estimated using logistic regression models. There were 57 days in which GDV(s) occurred, representing 2.60% of the days in the 6-year study period. The months of November, December, and January collectively accounted for almost half (47%) of all cases. Disease risk was negatively associated with daily maximum temperature. An increased risk of GDV was weakly associated with the occurrence of large hourly drops in temperature that day and of higher minimum barometric pressure that day and the day before GDV occurrence, but extreme changes were not
predictive of the disease.

pdf

Parvo puppy diarrhea treatment

mom — Mon, 17 Sep 2007 22:25:09 +0000

Canine IGY Plus Gel

A direct fed microbial gel for Dogs and Puppies containing a source of live, naturally occurring microorganisms, pasteurized dried egg product, vitamins and antioxidants

For support of digestive sytem disturbances

PRN Canine IgY Plus Gel is a highly palatable flavored gel intended for use in both dogs and puppies. Manufactured with dried egg product and direct fed microbials, antioxidants and vitamins, Canine IgY Plus supports treatment for digestive system disturbances of known or unknown origin with the highest viral antibody titers in the industry. Developed from cutting-edge technology, Canine IgY Plus also can help puppies bridge over the blank period between natural local immunity and vaccination.

The dried egg product in Canine IgY Plus is characterized by the content of yolk antibodies (IgY immunoglobulin) to microbial agents which can cause disorders in the normal state of the digestive tract, impair physiological digestive functions and affect rearing of pups as well as the general state of health and performance of adult dogs.

The dried egg product is prepared exclusively of eggs laid by hens which have been subjected to specific immunization programs. The egg mass contains antibodies to the most important enteropathogenic agents.

In the canine intestinal tract, these antibodies bind to the surface of canine parvovirus, coronavirus, rotavirus salmonella and E. coli cells creating an antigen-antibody complex in the G.I. tract which prevents the antigen from adhering to the intestinal mucosa and establishing in the intestinal contents. The antibodies enhance the efficacy and/or help bridge the insufficiency of the natural local immunity. Dried egg product, the major component of Canine IgY Plus, contains easily digestible proteins with high nutritional values.

No component of Canine IgY Plus influences the chemical composition or efficacy of drugs used in the treatment of canine intestinal disturbances. PRN Canine IgY Plus does not affect drug activity in the digestive tract, absorption into the blood circulation nor distribution and activity in the organism. This applies to antibiotics as well as other drugs which may be deemed desirable for treatment by the veterinarian.

Guaranteed Analysis: Every 3 cc’s contains a minimum of 2 Billion CFU’s of total Lactic Acid – Producing Bacteria (Enterococcus faecium, Lactobacillus Acidophilus, Bacillus Subtilis, Bacillus Pumilis, Bifidobacterium Bifidum), .3 Billion CFU’s of live yeast (Saccharomyces), .75 gm. of pasteurized sprayed dried egg product. .5 gm. Fructooligosaccharides, 75 mg. Ascorbic Acid, and 45 mg. Vitamin E

Ingredients: Atlantic Salmon Oil containing Omega 3, Liver Flavoring, Dried Enterococcus faecium Fermentation product, Dried Lactobacillus Acidophilus, Bacillus Subtilis, Bacillus Pumilis, Bifidobacterium Bifidum Fermentation product, Sprayed Egg Product, Fructooligosaccharides, Ascorbic Acid and Vitamin E

Canine IgY Plus Gel contains 2 billion CFU’s of LAB, including live cultures of Enterococcus faecium, Lactobacillus acidophilus, Bacillus subtilis, Bacillus pumilus and Bifidobacterium bifidum which propagate rapidly in the canine digestive tract and support growth of other symbiotic intestinal microorganisms. It contains live yeast as well, specifically Saccharomyces cerevisiae (1 Billion cfu’s in 3 cc. Yeast cell walls contain -glucans which are proposed to enhance immune system function.

Bacillus strains are known for optimizing food utilization.
Bifidobacterium bifidum is critical for aiding young animals in the production of LAB and producing enzymes for cell development and cell repair.
Omega 3 fatty acids derived from Atlantic Salmon Oil enhance the immune system and produce anti-inflammatory effects by counterbalancing the pro-inflammatory prostaglandins (PG2) and limiting the secretion of PG2 at the cellular level which reduces pro-inflammatory allergic responses.

Fructo-oligosaccharide (FOS) is a natural source of inulin, a carbohydrate made up of fructose polymers. The FOS cannot be metabolized by monogastics, which lack the enzyme inulinase. The FOS passes to the lower intestine where it is fermented by LAB such as Bifidobacterium. Gram negative bacteria, such as Escherichia coli (E. coli), are unable to grow on FOS; this creates a natural selection process which promotes beneficial bacteria in the lower intestine.

Med-surgical treatment for bloat

mom — Mon, 30 Apr 2007 23:37:44 +0000

Bloat is a life-threatening, acute emergency prepare a bloat kit (google search for bloat kit to choose one), print out this article to keep in a safe place and in your car, to take to the ER vet. Know the symptoms of bloat.

Medical and Surgical Considerations Regarding Bloat Gastric Dilatation Volvulus Syndrome in the Bloodhound

Dr. John Hamil

Of the approximately 1,300,000 dogs registered annually by the AKC only 1500 are bloodhounds. Consequently, most veterinarians will see only a few in their practice lifetime

This brochure is offered by the American Bloodhound Club in an attempt to educate the owners of bloodhounds about the life-threatening nature of this complex syndrome as well as to familiarize veterinarians with some of the peculiarities of our breed and a protocol which has been employed successfully in treating GDV syndrome.

Definition: this is an acute life-threatening condition which initiates complex cardiovascular and metabolic changes that result in high mortality following dilatation and rotation of the stomach on its long axis.

CONCERN: Early recognition of the signs of GDV and immediate veterinary attention will greatly improve survival rate. Only if veterinary care is not accessible should the owner attempt to tube or trocarize the dog, although this may be life saving if you must travel a great distance.

CAUSE: Unkown. Probably multifactorial. No age or sex predilection. The bloodhound’s size, deep chest, frequent ingestion of foreign material, and genetic predisposition make them common victims of this condition. GDV syndrome is seen primarily in large deep chested breeds and, although heritability has not been proven, does seem to be more prevalent in certain lines. This syndrome is often associated with ingestion of large meals and drinking water, post feeding exercise, following general anesthesia, stress (boarding, traveling, showing, breeding, trailing, etc.) ingestion of foreign bodies, and gastroenteritis with vomition.

SIGNS: The observant owner may notice the early vague signs of restlessness, pacing, lethargy, dull, vacant or painful expression, and/or shallow respiration. Repeated measurements around the abdomen at the level of the last rib with a cloth measuring tape will demonstrate early increases in abdominal size if you are in doubt. Every owner should be able to recognize the more sever signs of unresponsiveness, unproductive retching, salivation, arched back, anterior abdominal pain, abdominal distention, abdominal tenseness, pale mucus membranes (eyes and mouth), weak pulse, blue-gray mucus membranes, weakness, inability to stand, moribund appearance, and, with endotoxic shock, red injected mucus membranes and rapid capillary refill time.

RULE OUTS: Small intestinal volvulus, splenic torsion, gastric or intestinal foreign body, intussesception, peritonitis, cardiomyopathy, or pleural effusion. Bloodhounds are predisposed to both dilated and hypertrophic cardiomyopathy. They are very likely to ingest foreign objects and seem to be susceptible to intussusception.

DIAGNOSIS: Signalment, history, clinical signs, xray in right lateral recumbency if not in shock or after decompression, this position may show the pylorus and duodenum dorsal to the cardia.

THERAPY: If in shock, decompress immediately by gastric tube, or if necessary, by trocharization with multiple 16-18 gauge needles at the point of greatest distention or perform temporary gastrostomy in right paracostal area, if necessary. If possible have assistants establish IV and initiate treatment for shock simultaneously. If assistant is not available, decompress first, then follow remainder of protocol.

If not in shock try to pass lubricated stomach tube marked at distance from nose to last rib. If unable to pass stomach tube, stand dog on rear legs and “bounce” up and down. if still unable to pass tube in sitting position, trocarize, if still unsuccessful take to surgery immediately after establishing IV and administering medication.

* start IV LRS (50 cc/lb rapid IV infusion for first hour)

* place IV catheter (multiple if needed for severe shock)

* give corticosteroids (500 mg Soludelta cortef IV) for endotoxic shock

* flunixin meglumine (one time 0.5 mg/lb IV) for endotoxic shock

* gentamycin (1 mg/lb) or cephalothin sodium (10 mg/lb) in initial fluids

* sodium bicarbonate (2 meq/lb in initial fluids) if suspect metabolic acidosis

* metoclopramide (10 mg SQ) improves gastric emptying and antiemetic

* ranitidine (1 mg/lb IV every 8 hours)

* start ECG and cardiac medications (60 mg lidocaine in initial fluids) for expected arrhythmias, give additional lidocaine as needed (1 mg/lb IV bolus)

* pass stomach tube and lavage stomach removing all content, give coative with simethicone. Take to surgery as soon as possible, particularly if digested blood or mucosal shreds are found in stomach content.

Monitor intensively for cardiac complications until surgery, usually within 4-6 hours, some surgeons prefer to wait until the next day. When stable, hopefully with cardiac signs normal, perform permanent abdominal wall gastropexy. Although patient is not as critical at this time, all precautions must be taken:

* Add 60 mg of lidocaine to initial fluids

* Induce anesthesia with Propofol, Numorphan, Ket/Val, etc. (no barbiturates or nitrous oxide)

* Intubate and inflate cuff

* Maintain on isoflurane or halothane 1-2 %

* Lead 2 EKG monitoring

* Careful on incising linea due to presence of distended stomach or spleen

* If markedly distended, decompress stomach with 16-18 gauge needle and suction before trying to derotate

* Remember stomach usually rotates from right to left with pylorus passing ventrally to rest dorsally on left side above the cardia. Always determine position prior to derotation and be gentle, as stomach wall may be friable particularly on greater curvature near cardia. Standing on the right side of the patient in dorsal recumbency, reach across the stomach and elevate the pylorus while pushing the body of the stomach down and away from you, thereby reducing the usual clockwise rotation. If devitalized, excise and close with a 2-layer inverting pattern with 2-0 PDS. Try not to open stomach if it can be avoided.

* have assistant pass stomach tube, empty and lavage stomach

. * Inspect spleen for infraction or thrombosed vessels. Splenectomy if necessary. Always ligate close to spleen.

* Permanent abdominal wall gastropexy (Circumcostal, belt loop, or muscle flap).

* Inspect abdomen. Look for torsed intestinal mesenteries. Resect if necessary.

* Standard abdominal closure.

* Continue cardiac monitoring post operatively until fully recovered from anesthesia. If lidocaine drip fails to control VPC’s:

* Give 3-10 mg/lb quinidine deep IM

* Give 375 mg oral pronestyl every 6 hours

* May need 500 mg oral Procan-S-R every 8 hours If patient experiences tachycardia with rate over 200 bpm

* Give 1/2 mg Inderal IV and monitor return to normal rate. Can repeat as needed up to 3 mg total dose. POST-OP: * NPO for 12 hours

* Tepid water and warm ID gruel tid for 4-5 days, should eat within 24 hours, if not suspect ileus, possibly due to intussesception.

* Canned ID or dry ID soaked in warm water

* 500 mg oral Keflex bid for 7 days

* 10 mg oral cisapride bid for 3 days (same effects as metoclopramide except not antiemetic plus stimulates motility in small and large intestine)

* Antiarrhythmic drugs as needed tapered in 7-10 days

* Recheck, including EKG in 7 days

* Sutures out at 10-14 days

PREVENTION:

* Feed 2-4 times daily

* Soak dry kibble in hot water for 5-10 minutes prior to feeding

* Limit exercise and water consumption for one hour after eating

* Prophylactic gastropexy if relatives have been affected (disadvantage in trying to evaluate breeding potential)

* Add simethicone to food<

Inflammatory bowel disease

mom — Wed, 25 Apr 2007 03:07:54 +0000

IBD has been defined clinically as a spectrum of gastrointestinal disorders associated with chronic i

nflammation of the stomach, intestine and/or colon of unknown pathogenesis and etiology.

Canine I.B.D. Pathogenesis, Diagnosis, and Therapy

Etiology – Inflammatory bowel disease (IBD) has been defined on the basis of clinical, histologic, immunologic, pathophysiologic, and genetic criteria.

Clinical Definition of IBD

IBD has been defined clinically as a spectrum of gastrointestinal disorders associated with chronic inflammation of the stomach, intestine and/or colon of unknown pathogenesis and etiology. A clinical diagnosis of IBD is considered only if affected animals have persistent (>3 weeks in duration) gastrointestinal signs (anorexia, vomiting, weight loss, diarrhea, hematochezia, mucousy feces), failure to respond to dietary (novel protein, hydrolyzed-, anti-oxidant-, or highly digestible diets) or symptomatic therapies (parasiticides, antibiotics, gastrointestinal protectants) alone, failure to document other causes of gastroenterocolitis by thorough diagnostic evaluation, and histologic diagnosis of benign intestinal inflammation (Jergens et al., 2003). Small bowel and large bowel forms of IBD have been reported in both dogs and cats, although large bowel IBD appears to be more prevalent in the dog.

Histologic Definition of IBD

IBD has been defined histologically by the type of inflammatory infiltrate (neutrophilic, eosinophilic, lymphocytic, plasmacytic, granulomatous), associated mucosal pathology (villus atrophy, fusion, crypt collapse), distribution of the lesion (focal or generalized, superficial or deep), severity (mild, moderate, severe), mucosal thickness (mild, moderate, severe), and topography (gastric fundus, gastric antrum, duodenum, jejunum, ileum, cecum, ascending colon, descending colon). As with small intestinal IBD, the histologic assessment of large intestinal IBD lesions has been fraught with subjective interpretations. The lack of objective morphologic criteria has made it difficult to compare tissue findings between pathologists. Subjectivity in histologic assessments have led to the development of IBD grading systems (van der Gaag, 1988; van der Gaag, 1989; Spinato et al., 1990; Roth et al., 1990, Roth et al., 1992; Wilcock, 1992; Leib et al., 1992; Stonehewer et al., 1998). In more recent times, pathologists and internists are increasingly emphasizing architectural changes (villus atrophy, villus fusion, fibrosis) instead of lamina proprial cellularity.

Immunologic Definition of IBD

IBD has been defined immunologically by the innate and adaptive response of the mucosa to gastrointestinal antigens. Although the precise immunologic events of canine IBD remain to be determined, a prevailing hypothesis for the development of IBD is the loss of immunologic tolerance to the normal bacterial flora or food antigens, leading to abnormal T cell immune reactivity in the gut microenvironment. Genetically engineered animal models (e.g., IL-2, IL-10, and T cell receptor knockouts) that develop IBD involve alterations in T cell development and/or function suggesting that T cell populations are responsible for the homeostatic regulation of mucosal immune responses. Immunohistochemical studies of canine IBD have demonstrated an increase in the T cell population of the lamina propria, including CD3+ cells and CD4+ cells, as well as macrophages, neutrophils, and IgA-containing plasma cells. Many of the immunologic features of canine IBD can be explained as an indirect consequence of mucosal T cell activation. Enterocytes are also likely involved in the immunopathogenesis of IBD. Enterocytes are capable of behaving as antigen-presenting cells, and interleukins (e.g., IL-7 and IL-15) produced by enterocytes during acute inflammation activate mucosal lymphocytes. Up-regulation of Toll-like receptor 4 (TLR4) and Toll-like receptor 2 (TLR2) expression contribute to the innate immune response of the colon. Thus, the pathogenesis and pathophysiology of IBD appears to involve the activation of a subset of CD4+ T cells within the intestinal epithelium that overproduce inflammatory cytokines with concomitant loss of a subset of CD4+ T cells, and their associated cytokines, which normally regulate the inflammatory response and protect the gut from injury. Enterocytes, behaving as antigen-presenting cells, contribute to the pathogenesis of this disease (Carding et al.).

Pathophysiologic Definition of IBD

IBD may be defined pathophysiologically in terms of transport, blood flow, and motility abnormalities. The clinical signs of IBD, whether small or large bowel, have long been attributed to the pathophysiology of malabsorption and hypersecretion, but experimental models of canine IBD have instead related clinical signs to the emergence of abnormality motility patterns..

Genetic Definition of IBD

IBD may be defined in genetic terms in several animal species. Crohnâ€™s disease and ulcerative colitis are more common in certain human genotypes, and a mutation in the NOD2 gene (nucleotide-binding oligomerization domain2) has been found in a sub-group of patients with Crohnâ€™s disease (Strober). Genetic influences have not yet been identified in canine or feline IBD, but certain breeds (e.g., German shepherd, Boxers) appear to be at increased risk for the disease.

Pathophysiology

The pathophysiology of colitis-type IBD is explained by at least two interdependent phenomena: the mucosal immune response, and associated changes in motility.

Immune Responses

A generic inflammatory response involving cellular elements (B and T lymphocytes, plasma cells, macrophages, and dendritic cells), secretomotor neurons (e.g., VIP, substance P, and cholinergic neurons), cytokines and interleukins, and inflammatory mediators (e.g., leukotrienes, prostanoids, reactive oxygen metabolites, nitric oxide, 5-HT, IFN-? TNF-? and platelet-activating factor) is typical of canine and feline inflammatory bowel disease. There are many similarities between the inflammatory response of the small and large intestine, but recent immunologic studies suggest that IBD of the canine small intestine is a mixed Th1/Th2 response (German et al. 2001) whereas IBD of the canine colon may be more of a Th1 type response with elaboration of IL-2, IL-12, INF-?, and TNF-a (Ridyard et al. 2001). Other studies of canine colonic IBD have demonstrated increased numbers of mucosal IgA- and IgG-containing cells, CD3+ T cells, nitric oxide (NO), and inducible nitric oxide synthase (iNOS) in the inflamed colonic mucosa. Increases in the CD3+ positive T cell population of the inflamed colon are consistent with increases previously reported in the inflamed canine small intestine. Thus, there are important similarities and differences between small and large bowel IBD.

Motility Changes

Experimental studies of canine IBD have shown that many of the clinical signs (diarrhea, passage of mucus and blood, abdominal pain, tenesmus, and urgency of defecation) are related to motor abnormalities of the colon. Ethanol and acetic acid perfusion of the canine colon induces a colitis-type IBD syndrome indistinguishable from the natural condition (Sethi and Sarna, 1991). Inflammation in this model suppresses the normal phasic contractions of the colon, including the migrating motility complex, and triggers the emergence of giant migrating contractions (GMCs). The appearance of these GMCs in association with inflammation is a major factor in producing diarrhea, abdominal cramping, and urgency of defecation. GMCs are powerful lumen-occluding contractions that rapidly propel pancreatic, biliary, and intestinal secretions in the fasting state, and undigested food in the fed state, to the colon to increase its osmotic load (Sethi and Sarna, 1991). Malabsorption results from direct injury to the epithelial cells and from ultrarapid propulsion of intestinal contents by giant migrating contractions (GMCs) so that sufficient mucosal contact time is not allowed for digestion and absorption to take place.

Inflammation impairs the regulation of the colonic motility patterns at several levels, i.e., enteric neurons, interstitial cells of Cajal, and circular smooth muscle cells. Inflammation-induced changes in the amplitude and duration of the smooth muscle slow wave plateau potentials contribute to the suppression of rhythmic phasic contractions (RPCs). These alterations likely have their origin in structural as well as functional damage to the interstitial cells of Cajal (Lu et al.). At the same time that inflammation suppresses the (RPCs), inflammation sensitizes the colon to the stimulation of GMCs by the neurotransmitter substance P. These findings suggest that SP increases the frequency of GMCs during inflammation, and that selective inhibition of GMCs during inflammation may minimize the symptoms of diarrhea, abdominal discomfort, and urgency of defecation associated with these contractions.

Inflammation suppresses the generation of tone and phasic contractions in the circular smooth muscle cells through multiple molecular mechanisms. Inflammation shifts muscarinic receptor expression in circular smooth muscles from the M3 to the M2 subtype (Jadcherla et al.). This shift has the effect of reducing the overall contractility of the smooth muscle cell. Inflammation also impairs calcium influx and down-regulates the expression of the L-type calcium channel (Liu et al.), which may be important in suppressing phasic contractions and tone while concurrently stimulating GMCs in the inflamed colon. Changes in the open-state probability of the large conductance calcium-activated potassium channels (KCa) partially attenuate this effect (Lu et al.). Inflammation also modifies the signal transduction pathways of circular smooth muscle cells. Phospholipase A2 and protein kinase C (PKC) expression and activation are significantly altered by colonic inflammation and this may partially account for the suppression of tone and phasic contractions (Ali et al.). PKC a, ? and e isoenzyme expression is down-regulated, PKC i and l isoenzyme expression is up-regulated, and the cytosol-to-membrane translocation of PKC is impaired. To worsen matters, the L-type calcium channel (already reduced in its expression) is one of the molecular targets of PKC. Inflammation also activates the transcription factor NF-kB which further suppresses cell contractility (Shi et al.)

Clinical Examination

The clinical signs of colitis-type IBD are those of a large-bowel type diarrhea, i.e., marked increased frequency, reduced fecal volume per defecation, red blood pigments and mucous in feces, and tenesmus. Anorexia, weight loss, and vomiting are occasionally reported in animals with severe IBD of the colon or concurrent IBD of the stomach and/or small intestine. Clinical signs usually wax and wane in their severity. A transient response to symptomatic therapy may occur during the initial stages of IBD. As the condition progresses, diarrhea gradually increases in its frequency and intensity, and may become continuous. In some cases the first bowel movement of the day may be normal or nearly normal, whereas successive bowel movements are reduced in volume and progressively more urgent and painful. During severe episodes, mild fever, depression, and anorexia may occur.

There does not appear to be any sex predilection, but age may be a risk factor with IBD appearing more frequently in middle aged animals (mean age approximately 6 years with a range of 6 months to 20 years). German shepherd and Boxer dogs are at increased risk for IBD, and pure-breed cats appear to be at greater risk. Cats more often present with an upper gastrointestinal form of IBD, whereas dogs are at risk for both small and large bowel IBD.

Physical examination is unremarkable in most cases. Thickened bowel loops may be detected during abdominal palpation if the small bowel is concurrently involved. Digital examination of the anorecturm may evoke pain or reveal irregular mucosa, and blood pigments and mucous may be evident on the exam glove.

Diagnosis

Complete blood counts, serum chemistries, and urinalyses are often normal in mild cases of large bowel IBD. Chronic cases may have one or more subtle abnormalities. One review of canine and feline IBD reported several hematologic abnormalities including mild anemia, leukocytosis, neutrophilia with and without a left shift, eosinophilia, eosinopenia, lymphocytopenia, monocytosis, and basophilia (Jergens). The same study reported several biochemical abnormalities including increased activities of serum alanine aminotransferase and alkaline phosphatase, hypoalbuminemia, hypoproteinemia, hyperamylasemia, hyperglobulinemia, hypokalemia, hypocholesterolemia, and hyperglycemia. No consistent abnormality in the complete blood count or serum chemistry has been identified.

A scoring index for disease activity in canine IBD was recently developed that relates severity of clinical signs to serum acute-phase protein concentrations (C-reactive protein, serum amyloid A â€“ Jergens et al., 2003). The canine IBD activity index (CIBDAI) assigns levels of severity to each of several gastroenterologic signs (e.g., anorexia, vomiting, weight loss, diarrhea), and it appears to be a reliable index of mucosal inflammation in canine IBD. Interestingly, both the CIBDAI and serum concentrations of C-reactive protein (CRP) improve with successful treatment, suggesting that serum CRP is suitable for the laboratory evaluation of therapy in canine IBD. Other acute-phase proteins were less specific than CRP. One important caveat that should be emphasized is that altered CRP is not prima facie evidence of gastrointestinal inflammation. Concurrent infections or other inflammatory conditions could cause an acute-phase response, including CRP, in affected patients.

Treatment The treatment of canine I.B.D. has eight components of therapy: (1) Dietary Management, (2) Exercise, (3) Antibiotics, (4) Probiotics, (5) Anti-Diarrheal Therapy, (6) Restoration of G.I. Motility, (7) Immunosuppressive Therapy, and (8) Behavioral Modification.

Dietary Management

The precise immunologic mechanisms of canine and feline IBD have not yet been determined, but a prevailing hypothesis for the development of IBD is the loss of immunologic tolerance to the normal bacterial flora or food antigens. Accordingly, dietary modification may prove useful in the management of canine and feline IBD. Several nutritional strategies have been proposed including novel proteins, hydrolyzed diets, anti-oxidant diets, medium chain triglyceride supplementation, low fat diets, modifications in the omega-6/omega-3 (w-6/w-3) fatty acid ratio, and fiber supplementation. Of these strategies, some evidence-based medicine has emerged for the use of novel protein, hydrolyzed, and fiber-supplemented diets.

Food sensitivity reactions were suspected or documented in 49% of cats presented because of gastroenterologic problems (with or without concurrent dermatologic problems) in a prospective study of adverse food reactions in cats. Beef, wheat, and corn gluten were the primary ingredients responsible for food sensitivity reactions in that study, and most of the cats responded to the feeding of a chicken- or venison-based selected-protein diet for a minimum of 4 weeks. The authors concluded that adverse reactions to dietary staples are common in cats with chronic gastrointestinal problems and that they can be successfully managed by feeded selected-protein diets. Further support for this concept comes from studies in which gastroenterologic or dermatologic clinical signs were significantly improved by the feeding of novel proteins.

Evidence is accruing that hydrolyzed diets may be useful in the nutritional management of canine IBD. The conceptual basis of the hydrolyzed diet is that oligopeptides are of insufficient size and structure to induce antigen recognition or presentation. In one preliminary study, dogs with inflammatory bowel disease showed significant improvement following the feeding of a hydrolyzed diet although they had failed to respond to the feeding of a novel protein. Clinical improvement could not be solely attributed to the hydrolyzed nature of the protein source because the test diet had other modified features, i.e., high digestibility, cornstarch rather than intact grains, medium chain triglycerides, and an altered ratio of w-6 to w-3 polyunsaturated fatty acids. Additional studies will be required to ascertain the efficacy of this nutritional strategy in the management of IBD.

Fiber-supplemented diets may be useful in the management of irritable bowel syndrome (IBS) in the dog. IBS is a poorly defined syndrome in the dog that may or may not bear resemblance to IBS in humans. Canine IBS has been defined as a chronic large-bowel type diarrhea without known cause and without evidence of colonic inflammation on colonoscopy or biopsy. Dogs fulfilling these criteria were successfully managed with soluble fiber (psyllium hydrophilic mucilloid) supplementation of a highly digestible diet.

Exercise

Experimental IBD in the dog is accompanied by significant abnormalities in the normal colonic motility patterns. Physical exercise has been shown to disrupt the colonic MMCs and to increase the total duration of contractions that are organized as non-migrating motor complexes during the fed state. Exercise also induces GMCs, defecation, and mass movement in both the fasted and fed states. The increased motor activity of the colon and extra GMCs that result from physical exercise may aid in normal colonic motor function.

Antibiotics

Three types of antibiotics (tylosin, metronidazole, oxytetracycline) have been used with some success for the management of small intestinal bacterial overgrowth (SIBO) in dogs. SIBO has not been documented in cats, however, so it’s not clear whether these antibiotics will be as useful in the management of chronic diarrheal states. One study has shown a reduction in the indigenous microflora and an increase in serum cobalamin and albumin concentrations in cats treated with metronidazole.

Probiotics

Probiotics are living organisms with low or no pathogenicity that exert beneficial effects (e.g., stimulation of innate and acquired immunity) on the health of the host. The Gram-positive commensal lactic acid bacteria (e.g., Lactobacilli) have many beneficial health effects, including enhanced lymphocyte proliferation, innate and acquired immunity, and anti-inflammatory cytokine production. Lactobacillus rhamnosus GG, a bacterium used in the production of yogurt, is effective in preventing and treating diarrhea, recurrent Clostridia difficile infection, primary rotavirus infection, and atopic dermatitis in humans. Lactobacillus rhamnosus GG has been safely colonized in the canine gastrointestinal tract, although probiotic effects in the canine intestine have not been firmly established. The probiotic organism, Enterococcus faecium (SF68), has been safely colonized in the canine gastrointestinal tract, and it has been shown to increase fecal IgA content and circulating mature B (CD21+/MHC class II+) cells in young puppies. It has been suggested that this probiotic may be useful in the prevention or treatment of canine gastrointestinal disease. This organism may, however, enhance Campylobacter jejuni adhesion and colonization of the dog intestine, perhaps conferring carrier status on colonized dogs.

Two recent studies have shown that many commercial veterinary probiotic preparations are not accurately represented by label claims. Quality control appears to be deficient for many of these formulations. Until these products are more tightly regulated, veterinarians should probably view product claims with some skepticism.

Anti-Diarrheal Therapy

Four major classes of anti-diarrheal agents are available for use in canine I.B.D. These drugs directly inhibit crypt epithelial secretion or they directly promote villus epithelial absorption.

Prostaglandin Synthetase Inhibitors

1. Sulfasalazine – 10-25 mg/kg TID-QID, PO

2. Olsalazine – 5-10 mg/kg PO, TID-QID (dog)

Opioid Agonists These drugs stimulate absorption, and inhibit secretion of, fluid and electrolytes.

1. Loperamide 0.08 mg/kg TID, PO-preferred drug

2. Diphenoxylate 0.05-0.10 mg/kg TID-QID, PO-available in Lomotil

5-HT3 Serotonin Antagonists – Antagonists of the neuronal 5-HT3 receptor inhibit Cl- and H2O secretion from intestinal epithelial cells.

1. Ondansetron (Zofran, Glaxo) – 0.5-1.0 mg/kg BID, PO

2. Granisetron (Kytril, SmithKline Beecham) – 0.5-1.0 mg/kg BID, PO

Adrenergic Antagonists – These drugs must be used carefully as they can activate -adrenergic receptors in the chemoreceptor trigger zone and cause vomiting.

1. Clonidine 5-10 ?/kg BID-TID, SQ/PO

Restoration of G.I. Motility

The mixed m,d-opioid agonist, loperamide, stimulates colonic fluid and electrolyte absorption while inhibiting colonic propulsive motility. Loperamide (0.08 mg/kg PO TID-QID) may be beneficial in the treatment of difficult or refractory cases of large bowel-type IBD.

Immunosuppressive Therapy

Sulfasalazine Sulfasalazine is a highly effective prostaglandin synthetase inhibitor that has proven efficacy in the therapy of large bowel IBD in the dog. Sulfasalazine is a compound molecule of 5-aminosalicylate (meselamine) and sulfapyridine linked in an azo chemical bond. Following oral dosing, most of the sulfasalazine is transported to the distal gastrointestinal tract where cecal and colonic bacteria metabolize the drug to its component parts. Sulfapyridine is largely absorbed by the colonic mucosa but much of the 5-aminosalicylate remains in the colonic lumen where it inhibits mucosal lipoxygenase and the inflammatory cascade. Sulfasalazine has been recommended for the treatment of canine large bowel IBD at doses of 10-25 mg/kg PO TID for 4-6 weeks. With resolution of clinical signs, sulfasalazine dosages are gradually decreased by 25 per cent at 2-week intervals and eventually discontinued while maintaining dietary management. Salicylates are readily absorbed and induce toxicity in cats, therefore this drug classification should be used with great caution in cats. If used in cats, some authors have recommended using half of the recommended dog dose (i.e., 5-12.5 mg/kg PO TID. Sulfasalazine usage has been associated with the development of keratoconjunctivitis sicca in the dog, so tear production should be assessed subjectively (by the pet owner) and objectively (by the veterinarian) during usage.

Other 5-Aminosalicylates This drug classification was developed to reduce the toxicity of the sulfapyridine portion of the parent molecule (sulfasalazine) and to enhance the efficacy of the 5-aminosalicylate portion. Meselamine (Dipentum, Asachol) and dimeselamine (Olsalazine) are available for use in the treatment of canine large bowel IBD. Olsalazine has been used at a dosage of 5-10 mg/kg PO TID in the dog. Despite the formulation of sulfa-free 5-aminosalicylate preparations, instances of keratoconjunctivitis sicca have still been reported in the dog.

Treatment with Flagyl
Metronidazole

Metronidazole (10-20 mg/kg PO BID-TID) has been used in the treatment of mild to moderate cases of large bowel IBD in both dogs and cats. Metronidazole has been used either as a single agent or in conjunction with 5-aminosalicylates or glucocorticoids. Metronidazole is believed to have several beneficial properties, including anti-bacterial, anti-protozoal, and immunomodulatory effects. Side effects include anorexia, hypersalivation, and vomiting at recommended doses and neurotoxicity (ataxia, nystagmus, head title, and seizures) at higher doses. Side effects usually resolve with discontinuation of therapy but diazepam may accelerate recovery of individual patients.

Glucocorticoids

Anti-inflammatory doses of prednisone or prednisolone (1-2 mg/kg PO SID) may be used to treat IBD in dogs that have failed to respond to dietary management, sulfasalazine, or metronidazole, and as adjunctive therapy to dietary modification in feline IBD. Prednisone or prednisolone is used most frequently, as both have short durations of action, are cost-effective, and are widely available. Equipotent doses of dexamethasone are equally effective but may have more deleterious effects on brush border enzyme activity. Prednisone should be used for 2-4 weeks depending upon the severity of the clinical signs. Higher doses of prednisone (e.g., 2-4 mg/kg PO SID) may be needed to control severe forms of eosinophilic colitis or hypereosinophilic syndrome in cats. Combination therapy with sulfasalazine, metronidazole, or azothioprine may reduce the overall dosage of prednisone needed to achieve remission of clinical signs. As with sulfasalazine, the dose of glucocorticoid may be reduced by 25% at 1-2 week intervals while hopefully maintaining remission with dietary modification.

Because of steroid side effects and suppression of the hypothalamic-pituitary-adrenal axis, several alternative glucocorticoids have been developed that have excellent topical (i.e., mucosal) anti-inflammatory activity but are significantly metabolized during first pass hepatic metabolism. Budesonide has been used for many years as an inhaled medication for asthma, and an enteric-coated form of the drug is now available for treatment of IBD in humans (and animals). There is little evidence-based medicine in support of the use of this medication in canine or feline IBD, but doses of 1 mg/cat or 1 mg/dog per day have been used with some success in anecdotal cases.

Azathioprine Azathioprine is a purine analog that, following DNA incorporation, inhibits lymphocyte activation and proliferation. It is rarely effective as a single agent, and it should instead be used as adjunctive therapy with glucocorticoids. Azathioprine may have a significant steroid-sparing effect in IBD. Doses of 2 mg/kg PO q 24 hours in dogs and 0.3 mg/kg PO q 48 hours in cats have been used with some success in IBD. It may take several weeks or months of therapy for azathioprine to become maximally effective. Cats particularly should be monitored for side effects, including myelosuppression, hepatic disease, and acute pancreatic necrosis.

Cyclosporine

Cyclosporine has been used in the renal transplantation patient for its inhibitory effect on T cell function. In more recent times, cyclosporine has been used in a number of immune-mediated disorders, including keratoconjunctivitis sicca, perianal fistula (anal furunculosis), and IMHA. Anecdotal reports suggest that cyclosporine (3-7 mg/kg PO BID) may be useful in the treatment of some cases of refractory IBD. Evidence-based medicine studies will be needed to establish efficacy, but anecdotal experience would suggest that cyclosporine may be useful in some of the more difficult or refractory cases of IBD.

Chlorambucil

Chlorambucil (2 mg/m2 PO every other day) has been used in place of azathioprine in some difficult or refractory cases of feline IBD.

Behavioral Modification

Inflammatory bowel disease and irritable bowel syndrome very likely have underlying behavioral components. Abnormal personality traits and potential environmental stress factors were identified in 38% of dogs in one study. Multiple factors were present in affected households, including travel, re-location, house construction, separation anxiety, submissive urination, noise sensitivity, and aggression. The role of behavior in the pathogenesis and therapy of canine and feline gastrointestinal disorders remains largely unexplored.

References Available upon request.

Minnesota Veterinary Medical Association Gastroenterology

http://www.mvma.org/Proceedings/Small%20Animal%20Gastro/GastroenterologyTOC.html

http://www.mvma.org/Proceedings/Small%20Animal%20Gastro/Canine%20IBD.html

Robert J. Washabau, VMD, PhD, Dipl. ACVIM
Professor of Medicine and Department Chair
Department of Veterinary Clinical Sciences
College of Veterinary Medicine, University of Minnesota
St. Paul, Minnesota 55108 U.S.A.
(612) 625-5273 Office; (612) 624-0751 FAX
E-Mail:washabau@umn.edu<

Breed related risks for bloat

mom — Wed, 25 Apr 2007 01:31:55 +0000

GRANT

Incidence and Breed Related Risk Factors for Gastric Dilation-Volvulus in Dogs
5-year prospective study by Larry Glickman, VMD, Ph.D., Purdue University

Participating breed clubs Akita, Bloodhound, Collie, Great Dane, Irish Setter, Irish Wolfhound, Newfoundland, Rottweiler, Saint Bernard, Standard Poodle, Weimaraner and the AKC/CHF.
Method

Investigator measured dogs at dog shows and the owners completed a detailed questionnaire concerning the dogs medical history, genetic background, husbandry and eating practices, personality and diet.

Five years later, the investigator called and conducted a follow-up on each the dog.
The incidence of bloat (GDV) was calculated for each breed.
Risk factors were compared to dog measurements and questionnaire responses to determine any correlation.Â Â Results:
STUDY COMPLETED
Results for the Rottweiler
(Data based on 200 dogs)

* Of the 11 breeds tested, the Rottweiler had the lowest incidence of Bloat (1%).
* “Happy/easy going” dogs were found to be less prone to bloat. Rottweiler was listed as the easiest going/confident dog of the 11 breeds surveyed.
* Overweight dogs were less prone to bloat.
* Dogs that are feed 2 – 3 times a day are less prone to bloat.
* Restricting water before or after eating, or elevating the dogs food bowl increased the incidence of bloat.
* Bloat incidence was found to increase with age.
* Giving dogs anti-gas medication on a regular basis, increased the incidence of bloat by 66%.
* Do not breed any animal if there has been a relative that has previously bloated.

http://www.rottweilerhealth.org/grants_funded.html<

Gastropexy

mom — Wed, 25 Apr 2007 01:29:35 +0000

Gastropexy

Finding on use of gastropexy for dog owners:

In a study of 1,920 dogs at risk the following recommendations can be made regarding prophylaxis for bloat:

1 – with prophylactic gastropexy; after an episode of bloat, gastropexy decreased GDV recurrence by 95%. We would consider it to be just as effective as a preventive measure on dogs at risk for GDV (ie; all deep- chested dogs, dogs with first degree relatives with GDV) You should go to a veterinary surgeon to perform the surgery as many vets do this procedure regularly. Also these dogs should be sterilized to prevent passing on bloat risk to their progeny.

2 -Add Simethicone to each feeding (adult human dose)

I believe if the risk of GDV developing in a dog’s lifetime is high, then it is appropriate for owners and veterinarians to consider performing a prophylactic gastropexy (a surgical procedure to prevent the stomach from rotating) in order to prevent a first episode of GDV from occurring. However, I would not recommend that prophylactic gastropexy be done unless the dog were surgically neutered, so as not to increase the pool of dogs in a breed that are prone to develop GDV. Persons considering prophylactic gastropexy for their dog should discuss the procedure with their veterinarian and with owners of dogs that have had this procedure.

To find a veterinarian in your state who performs this surgery I would search for : Board Certified Veterinary Surgeon (your state). Unfortunately, the American College of Veterinary Surgeons does not at this time have a complete listing of Certified surgeons by state.