INDIVIDUAL TASKLearning Unit 2Anjing Diare BerdarahBLOK 19 HEWAN KESAYANGAN 2

Created by :Name : Annisa Wening M. Putri

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FACULTY OF VETERINARY MEDICINEUNIVERSITY OF GADJAH MADAYOGYAKARTA2015I. LEARNING OBJECTIVE1. Explain the Pathogenesis and the clinical sign of Parvovirus in small animals.2. Explain the Methods and the Differential Diagnose of Parvovirus.3. Explain the Treatment and Prevention of Parvovirus.

II. DISCUSSION1. The Pathogenesis and the Cinical Sign of Parvovirus1.1. Pathogenesis

Figure 1. Pathogenesis of the Parvovirus (Mason, 1999)The virus spread through direct contact with dogs that infected. Not direct transmission , for example from the faeces contaminated by vomited , also a source of infection (Anonim, 2011). After ingestion, virus can replicate in oropharynx limpoid tissues, then the virus spread using the lymphocyte via blood circulation land lymph. The virus will attacking the cells that actively dividing, like bone marrow, limphoid tissues (Nodus lymphatic, GALT, peyer patches, thymus) and Kripte Lieberkuhn cells in jejunum and ileum distale. Early lymphatic infection, along with the lymphopenia, it is happen before the intestinal infection and gastrointestinal sign.mitosis activity in bone marrow, or myeloid cells dan lymphopoietic tissue causing neutropenia and limphopenia for about 3 days after infection. (Boothe, 2001).

Figure 2. Canine parvovirus structure (source : www.virology.wisc.edu)After the virus reach the intestinal mucose, CPV-2 infect germinal cells intestinum, cells damaged and the villi shorter. Viruses releases in faces start from 3-4 day after infection and the peak when the sign occur. The viruses release decreasing fast and may not be detected after day 10-14 after the beginning infection. Virus replicate inside the intestinal epithelium causing villi to erose, necrosis epithelium, and haemmorhagik diarrhea. Some opportunistic bacteria such as E.coli and even Clostridium spp.,can infect the denudated mucose, causing the second infection. The second infection can cause the higher severity like hypercoagulability, multiorgan failure, even the deathness in puppies (the neonatus that already infected in utero) (Tilley, 2004).CPV can replicate inside miocardium cells that ectively dividing, so this can causing myocarditis can lead to death. Immunosuppresion happen when limphoid tissues and cells developed fast, bone marrow already infected. In puppies age more than 7 weeks, which myocardium development is unfinished, CPV will change the target to gastrointestinal tract, so that clinical sign will occur associated with digestive tract, consistent with the presence of immunosupression caused by infection in limphoid system (Lane and Cooper, 2003).

Figure 3. Small intestine, dog. Cytoplasmic staining in epithelial cells of glandular crypts. Immunoperoxidase-DAB for canine parvovirus. (source : web.ics.purdue.edu)1.2. Clinical Signa. Enteritis FormThere is a broad range in the severity of symptoms shown by dogs infected with parvovirus. Many adult dogs exposed to the virus remain apparently healthy but act as a carrier to transmit the virus to the susceptible animals. The disease in majority of the cases is seen in dogs less than 6 months of age with severe symptoms in puppies younger than 3 months of age. The most common form of the disease is enteritis. It is characterized by vomition, diarrhea, dehydration, dark or bloody faeces and in severe cases fever and lowered WBC counts. Early symptoms are depression, loss of appetite, vomition, high fever and severe diarrhea. There is slight rise of temperature in the initial stage of the disease but gradually turn to subnormal level with advancement of vomition and diarrhea There is no consistent character of the stool, it may be watery, yellow in color or tinged with frank blood in severe cases. Rapid dehydration is a danger and dogs may continue to vomit and have diarrhea until they die, usually three days after onset of symptoms (Nandi et al., 2013).b. Cardiac SyndromeThe second form of CPV is cardiac syndrome, or myocarditis, which can affect puppies under three months of age. Within an infected litter, 70% pups will die in heart failure by 8 weeks of age and the remaining 30% will have pathological changes which may result in death many months or even years later. The most dramatic manifestation of CPV-2 myocarditis is the sudden death in young pups usually about 4 weeks of age (Nandi et al., 2013).

Figure 4. Patho-anatomy change cardial form of infection caused b Parvovirus (Greene, 2012).2. The Methods and the Differential Diagnose of Parvovirus2.1. Methods to Diagnosea. Anamnese (bloody diarrhea, fever, these sign is not spesific) Sudden onset of hemorrhagic diarrhea, fever, and leukopenia in a young, unvaccinated dog is often considered indicative of CPV infection. However, not all dogs with CPV have bloody diarrhea or leukopenia, and other diseases such as parasitic or enteropathogenic bacterial infection can also cause these symptoms. Therefore, definitive diagnosis should be pursued (Karen, 2014).b. ELISAFortunately, practitioners have at their disposal a readily available, easy to use, in-office ELISA test to detect CPV in the feces of infected dogs. These tests are specific, but poorly sensitive for detecting CPV. Viral particles are readily detectable at the peak of shedding (4-7 days post-infection). False negative results may occur if tested early in the disease course, secondary to binding of serum-neutralizing antibodies with antigen in diarrhea or with decline of fecal viral shed (10-12 days post-infection). False positive results may occur after vaccination (3-10 days post-vaccination) with a modified live CPV vaccine (Karen, 2014).While the ELISA test is sufficient for the majority of patients, fecal PCR for viral DNA may be performed in a dog with clinical signs and a negative ELISA test. The CPV PCR has a higher sensitivity and specificity than other methods of viral antigen determination in feces. Quantitative assays (real-time PCR) using blood can also provide an estimation of viral load, which can help distinguish vaccination from natural infection (Karen, 2014)CPV-2b and 2c pose similar health risks for dogs; therefore, genetic sequencing of CPV to determine strain is not necessary for the clinical management of patients (Karen, 2014)c. CPV snap Test A quick and easy diagnostic test is the CPV snap test (available from various manufacturers), which can be used as a patient-side test. The snap test is an immunochromographic test for the quantitative detection of CPV antigen in canine faeces. It has been reported that CPV snap tests have a good specificity compared to alternative tests such as polymerase chain reaction (PCR) and faecal electron microscopy (IEM), but a poorer sensitivity. Both false negative and false positive results can occur. Although rare, false negative results occur because virus shredding is relatively brief (peak shedding between 4 and 7 days post infection) and virus antigen is rarely detectable 12 days after natural infection, which corresponds with clinical illness. Furthermore, if the majority of the intestinal villi have already been sloughed and there are no longer enough villus cells to accommodate CPV, there will not be enough viral antigens shed in the faeces to be identified via the snap test. False positive results will occur if the patient has been vaccinated with a modifiedlive virus (MLV) vaccine within the past 14 days, due to faecal shedding of vaccine-derived virus (Arnota, et al., 2013).d. Electron Microscopy Electroscopic microscopy (EM) of a faecal sample is another highly accurate method of confirming a diagnosis of CPV infection12. A very small volume (0.1 ml) of faeces is required and the test is positive if CPV particles are identified on EM. In cases were the snap test is negative, yet clinically the patient is highly suspicious of having CPV, EM can be done. False positive results can also be obtained within a few days post-vaccination with a modified live virus (MLV)vaccine. 2.2. Differential DiagnoseA differential diagnosis would include anticoagulant rodenticides, canine bocavirus, intestinal parasites (particularly Blastocystis spp, Giardia intestinalis, Toxocara canis, Isospora spp, Trichuris vulpis) and hemorrhagic gastroenteritis due to Clostridium spp.a. CoronavirusCoronavirus is spread through virus-contaminated material orally and feces. Clinical symptoms appear is acute diarrhea and dehydration which follows the incidence of diarrhea. The initial symptoms usually appear are depression followed by weight loss, vomiting fetid, diarrhea, yellow-orange with a soft consistency to dilute. Diarrhea, sometimes with blood. Unlike parvovirus, the virus does not cause fever (Eldredge, 2007). The incubation period is about 1-4 days on the ground, can be found in feces. This virus enters the body through ingestion and then toward the epithelial cells that exist in the intestinal brush border to replicate and form cytoplasmic vacuoles, virions out of the vacuole through cell lysis thereby causing damage to the microvilli of the intestine, but was soon replaced by an increase in the replication of cells immature at crypt intestine, Crypt hyperplasia was not destroyed but get a new form so villi covered by a layer of cuboidal epithelium. Unlike CPV, the coronavirus infection does not cause villous necrosis and hemorrhage (Greene, 2012).b. Distemper VirusDistemper is caused by an RNA virus of 150-300 nm sized paramyxovirus.The virus causes the formation fusion of objects within cells, and cause the formation of inclusion bodies in the cytoplasm is eosinophilic. Distemper is highly contagious, is characterized by increasing body temperature, leukopenia, inflammation of the digestive tract and respiratory, and is often followed by the complications of central nervous disorders (Quinn, et al., 2002)c. RotavirusThe virus is not enveloped, segmented double-stranded RNA, replicates in the cytoplasm, not enveloped, icosahedral structure. The virus causes enteritis in young dogs. The incubation is short, usually less than 24 hours. Clinical symptoms are anorexia, depressed, and stool-shaped pasta and bright colors.d. Salmonella Bacteria Gram negative, rod-shaped, is oxidase negative, facultative. Anaerobic, catalase positive, motile and do not ferment lactose. This is a bacterium that causes bacterial enteritis and usually attacks the mucous ileum, cecum and colon (Quinn, et al., 2002).e. Clostridium Rod-shaped Gram-positive bacteria, produce endospores, anaerobic, catalase-negative, oxidase negative, motile. The bacterium is found in soil, animal digestive tract and feces. These bacteria are normally found in the digestive tract, but if the population is much, can cause enteritis disease, and its toxin capable of causing tetanus (Quinn, et al., 2002).3. The Treatment and The Prevention of Parvovirus3.1. TreatmentThere is no antiviral treatment specific for CPV, therefore the mainstay of treatment is supportive care. The primary goals of supportive care are to restore of fluid and electrolyte balance, prevent secondary bacterial infections, and palliate the symptoms of infection (Karen, 2014). Certain fundamental aspects are the mainstay in treating CPV, namely fluid therapy, anti-emetics, antimicrobials, and nutrition (Arnota et al., 2013).a. Fluid TherapyA cephalic or jugular catheter is aseptically placed at admission and ideally replaced every 72 hours to prevent bacterial colonisation around the catheter site. The initial fluid of choice is a balanced electrolyte solution such as Intramed Ringer-Lactate12 (Fresenius Kabi, Halfway House, RSA), which can be spiked with potassium and 50% dextrose (one litre Ringers lactate drip bag with one vial 15% potassium chloride and 20 ml 50% dextrose). The vast majority of CPV patients will be moderately to severely dehydrated at presentation. Initial fluid administration rate depends on the condition of the patient, but generally can be at high rates of twice maintenance (see table 1) from time of admission, until perfusion is fully restored. Once perfusion is restored, the fluid rate is adjusted according to hydration status of the patient, taking into account ongoing losses from vomiting and diarrhoea. Another approach is to administer fluid in order to replenish the fluid deficit (dehydration % x body mass), then revert to maintenance at 23 ml/kg/hour once the patient is fully hydrated and adjusted accordingly to continuing losses resulting from vomiting and diarrhoea. An anecdotal observation from patients at the hospital is that early aggressive fluid therapy is essential to improve the prognosis; once there is severe dehydration, the prognosis decreases significantly (Arnota et al., 2013)Table 1. Recommended drug based on Arnota et al., (2013).

b. Anti-emeticAnti-emetic treatment is essential to stop the severe emesis associate with CPV infection and if not controlled, life-threatening dehydratio can result. An additional benefit is that by curbing the associated nausea, the patient will resume eating at an earlier stage (Arnota et al., 2014).Persistent vomiting leads to fluid and electrolyte loss, interferes with nutritional support, precludes oral administration of medications, and puts the patient at risk for the development of pneumonia and esophagitis. The most commonly used classes of antiemetics for CPV infection are 2-adrenergic antagonists (e.g. chlorpromazine, prochlorperazine), D2-dopaminergic antagonist (e.g. metoclopramide), 5-HT3-serotonergic antagonists (dolasetron, ondansetron) and NK1 receptor antagonist (e.g. maropitant). It is not uncommon for multimodal antiemetic therapy to be required for severe cases of CPV enteritis (Karen, 2014).The 2-adrenergic antagonists (Chlorpromazine: 0.20.4 mg/kg SQ, IM q 6-8 hr; Prochlorperazine: 0.10.5 mg/kg SQ, IM q 6-8 hr) are phenothiazine derivatives. They limit stimulation of the chemoreceptor trigger zone and emetic center. Their antiemetic effect is potent, however they also can cause sedation and hypotension. They should not be used in dehydrated patients (Karen, 2014).Metoclopramide (0.2-0.4 kg/kg SQ, IM q 6-8 hr; 12 mg/kg/day IV CRI) blocks the chemoreceptor trigger zone, stimulates and coordinates motility of the upper intestinal tract, and increases pressure in the lower esophageal sphincter (Karen, 2014). Metoclopramide (Clopamon, Pharmacare, Woodmead, RSA) is administered as the first-line anti-emetic. On admission a loading dose is given, followed by a constant rate infusion (CRI). If vomiting is still present after 12 hours on a metoclopramide CRI, ondansetron (Mylan-Ondansetron, Mylan, Modderfontein, RSA) is added to the treatment regimen, administered to effect. Ondansetron is a serotonin antagonist and a well-known potent anti-emetic. The majority of patients with CPV will require ondansetron in addition to the metoclopramide CRI, as metoclopramide alone appears to be ineffective in many cases of severe vomiting caused by CPV (Arnota et al., 2013).c. Fresh Frozen PlasmaFresh frozen plasma (FFP) transfusion has been recommended in the treatment of CPV for its ability to provide albumin, immunoglobulins, and serum protease inhibitors, which may help to neutralize circulating virus and control the systemic inflammatory response. However, FFP alone is a poor means of supporting patient albumin concentrations; very large volumes of plasma are required to achieve a small increase in plasma albumin (Karen, 2014). Fresh frozen canine plasma (FFP) is occasionally administered to individual patients that remain clinically critical after 23 days of intensive treatment. FFP is not recommended as a treatment to increase either colloid oncotic pressure or serum albumin levels. FFP has very little effect on oncotic pull, as a large volume of FFP is required to raise the plasma albumin level22.5 ml/kg FFP will raise albumin by a mere 5 g/L20. There is good empirical evidence that FFP supplies antibodies against CPV to benefit affected puppies, which seems to improve survival rates in critical cases. Early use of FFP has a positive effect on the outcome6. FFP may also help by neutralising circulating bacteria and in controlling the systemic inflammatory response often associated with CPV infection. FFP can be administered slowly IV or as a CRI to patients at 20 ml/kg OID when deemed necessary (Arnota et al., 2013).d. Anthelmenthic TherapyThe presence of intestinal parasites can worsen the disease process by enhancing intestinal cell turnover.18 Therefore once the patient can tolerate oral medications, deworming (e.g. fenbendazole: 50 mg/kg PO q24hr for 3 doses) is recommended (Karen, 2014).e. Synthetic Colloids CPV often leads to a decrease in plasma protein levels due to a combination of intestinal haemorrhage and rehydration7. At the OVAH the synthetic colloid hydroxyethyl starch (Voluven 6%, Fresenius Kabi, Halfway House, RSA) is administered to individual patients when the total serum protein (TSP) is below 35 g/L. Voluven is administered slowly intravenously at 20 mg/kg OID. Voluven is effective in increasing oncotic pull within the vasculature when the serum albumin levels are low, thus increasing blood pressure and reducing oedema (Arnota et al., 2013).Puppies suffering from CPV often develop a severe protein-losing enteropathy due to the destruction of intestinal villi. Colloidal support (e.g. Hetastarch, Dextrans) should be considered when total protein drops below 35 g/L or if the patient shows evidence of third space loss of fluid (e.g. ascites, edema). Overzealous colloidal therapy should be avoided to prevent blunting of endogenous hepatic albumin production. Dosage of colloidal fluids is 10-20 mL/kg/day. Boluses of 5 mL/kg may be used to treat shock refractory to crystalloid boluses. When administering colloids, the rate of crystalloids administered should be decreased by 30-40% (Karen, 2014).f. PotassiumIf the patient is anorexic or if hypokalemia is present, potassium chloride should be added to the balanced electrolyte solution after the initial dehydration has been corrected (Karen, 2014).Puppies suffering from severe vomiting and/or anorexia are predisposed to hypokalaemia, which can result in weakness, ileus, and cardiac arrhythmias. Serum potassium levels should be monitored at least daily and potassium supplementation adjusted accordingly. Normal serum potassium levels are between 3.5 and 5.5 mEq/L. Potassium should never be administered at a rate exceeding 0.5 mEq/kg/hour; life-threatening arrhythmias can be the result (Arnota et al., 2013).The following chart (Table.2) gives suggested potassium chloride supplementation rates based on the degree of hypokalemia:

Since fluid rates can be quite high in these patients, ensure that the rate of potassium supplementation does not exceed 0.5 mEq/kg/hr, as rates in excess of this may negatively affect cardiac function (Karen, 2014).g. Antimicrobial TherapyAntimicrobial therapy could prevent sepsis as a result of the transintestinal translocation of bacteria. Combination therapy of a betalactam antibiotic and an aminoglycoside to widen the antibacterial spectrum, especially against Gram-negative rods commonly implicated for causing septicaemia is generally recommended1. Aminoglycosides are also synergistic with the beta-lactam antibiotics17, leading to a very effective combination. IV ampicillin sodium (Ranamp, Ranbaxy, Centurion, RSA), an extended-spectrum penicillin, is used as a first choice.Alternatively, amoxicillin or cephalexin can be used, the former having a better anaerobic spectrum. An aminoglycoside, like amikacin (Amikacin-Fresenius, Bodene, Port Elizabeth, RSA), is added to the treatment regimen only once the patient is fully rehydrated. An important side effect of the aminoglycosides is renal tubular damage, especially if administeredto patients with poor renal perfusion (shock or dehydrated); the duration of treatment should be limited to a maximum of 5 days. Amikacin is considered less nephrotoxic than the other aminoglycosides. Fluorinated quinolones (e.g., enrofloxacin) should be avoided in young, growing dogs, due to the risk of causing damage to the joint cartilage (Karen, 2014).h. Analgesic therapyPatients infected by CPV often exhibit extreme abdominal pain,with intussusception being an important differential diagnosis. Abdominal palpation should be performed every 4 hours to evaluate the abdominal pain and to exclude intussusception. To control the abdominal pain of CPV-infected puppies, buprenorphine (Temgesic, Schering-Plough, Woodmead, RSA) is administered. Buprenorphine is preferred above other opiates due to its longer duration of action (providing analgesia for at least 6 hours), higher safety profile and potential potency of 25 times that of morphine1,22. With severe abdominal pain fentanyl (Fentanyl- Fresenius, Bodene, Port Elizabeth, RSA) used as a CRI could be used instead. Due to the fluid depletion and hypotension in CPV-infected puppies, non-steroidal anti-inflammatory drugs (NSAIDs) should not be used as they may further aggravate the already compromised GIT and kidneys (Karen, 2014).i. NutritionEarly enteral feeding has been shown to help maintain mucosal integrity, which decreases the risk of bacterial translocation.19 In turn, this leads to faster clinical improvement in patients, significant weight gain, and decreased hospitalization times. Therefore, the old recommendations to keep a CPV patient NPO for 24-48 hours beyond the last instance of vomiting are no longer recommended. Administration of dextrose supplementation in intravenous fluids does not constitute nutritional support. Total or partial parenteral nutrition may be used if a patient absolutely does not tolerate enteral feeding, but meticulous catheter care and monitoring should be performed because of the high risk of sepsis in CPV patients (Karen, 2014).To perform enteral nutrition, a nasoesophageal (NE) and nasogastric (NG) tube can be placed with minimal sedation. The benefit of NE tubes is that they do not cross the lower esophageal sphincter, so may cause less gastroesophageal reflux. The benefit of NG tubes is that they allow the practitioner to intermittently measure gastric residual volume. If large residual gastric volumes are consistently measured, a promotility agent (e.g. metoclopramide) should be started. Large residual volumes are defined as greater than 50% of the last volume fed if intermittent bolus feeding or volumes greater than twice what is fed in an hour of CRI feeding. The removal of large residual gastric volumes will also improve patient comfort and nausea (Karen, 2014).As the patient recovers, there may be temporary intestinal malabsorption and protein-losing enteropathy until intestinal villi are repaired. Initial feeding should consist of small amounts of an easily digestible low fat diet fed frequently. The normal diet is gradually re-introduced after appetite and stool have returned to normal (Karen, 2014).3.2. Preventiona. Always keep everything that is closely related to a dog for example clothes, floors, cages. b. Clean and disinfect all surfaces with known exposure to feces from infected canine. Before cleaning the area where infected canine are/were located, first spray a fine mist of water all over surfaces to decrease aerosolizing fecal matter. It should then be thoroughly cleaned with a detergent to remove all fecal material, rinsed, disinfected with an appropriate agent with 10 minutes of contact time, and then rerinsed to remove the disinfectant. Allowing the disinfectant to dry on the surface is preferred. Bleach at a 1:30 dilution is an effective disinfectant on surfaces that have been cleaned of organic matter. Quaternary ammonium compounds are not effective against Canine Parvovirus. Footbaths, hand washing, and cleaning of all instruments and cages exposed to infected canine are necessary.c. Puppies should be isolated from other canine especially those that have been exposed to other dogs at shows or field trails. Puppies should not be exposed to areas where other dogs may have defecated such as yards, pet stores, and parks.a. The most effective way to control the source of infection is by vaccination thoroughly and regularly. 3-month-old puppy should have gotten 2 times parvodog vaccine, the first between the age of 6-8 weeks and at 12 weeks for the second injection. At the age of 8-10 weeks puppies should be vaccinated first Distemper, Hepatitis I, Leptospirosis Parvovirus I and I (usually given together). At the age of 8-10 weeks puppies should be vaccinated first Distemper, Hepatitis I, Leptospirosis Parvovirus I and I (usually given together). Vaccination is important to stimulate the formation of immunity. The vaccine can be given live vaccines or vaccine died. However, it should be noted that this vaccine is not always successful because of the influence of maternal antibodies. (Carter, 2003).

DAFTAR PUSTAKA

Anonim. 2011. Canine Parvovirus,.https//:www.merckvetmanual.com/mvm/index.jsp ?cfile=htm /bc/...htm -. [2 August 2015]Arnota, L; Lobettib, R; Le Roux-Pullenc, L.2013.A Clinical Approach to Treating Canine Parvovirus Infection. Bryanstone : University of Pretoria Boothe, D.M., 2001. Small Animal Clinical Pharmacology and Therapeutics. 1st Edition. Philadelphia :W.B. Saunders Co.Carter, G.R. 2003. A Concise Guide to Infectious and Parasitic Diseases of Dogs and Cats. New York : International Veterinary Information Service (www.ivis.org)Eldrege, D.M. 2007. Dog Owners Home Veterinary Handbook. Wiley Publishing Inc., New JerseyGreene, C.E. 2012. Infectious Diseases of Dog and Cat. 4th ed. Saunders Elsevier, USAKaren, M.2014. Successful Management Strategies for Canine Parvovirus. Ohio : The Ohio State UniversityLane, D.R., Cooper, B.C., 2003, Veterinary Nursing, 3rd.ed, Butterworth Heinemann, UK.Masson. 1997. Parvovirose du chien, In Dictionnaire Pratique de Therapeutique Canine et Feline, fourth-edition. ParisMasson, G.1999.Pathogenesis of Canine Parvovirus.___: DVM NewsNandi, S; Kumar, M; Mohapatra, T.P; Ravishankar.2013. Emergence of Canine Parvovirus - 2 Variants and its Impact on Vaccination.World Applied Sciences Journal Vol 23 (10) :1366-1376Quinn, P.J., Markey, B.K., Carter, M.E., Donelly, W.J.C., Leonard, F.C., Maghire, D. 2002. Veterinary Microbiology and Microbial Disease. Blackwell Science, IowaTilley, L.P., dan Smith, F.W.K., 2004. The 5-Minute Veterinary Consult Canine and Feline Third Edition. Lippincott Williams & Wilkins: Philadelphia.

MEtoclopramidThe motility effects of metoclopramide are beneficial to counteract the gastroparesis frequently found in CPV infection; however, it does increase the risk of intussusception. It can also cause extrapyramidal signs (e.g. involuntary muscle spasms, restlessness, aggression). The antiemetic effect of metoclopramide is relatively weak compared to other antiemetics although it appears to perform better as a CRI rather than intermittent injections. The 5-HT3-serotonergic antagonists (dolasetron: 0.5-0.6 mg/kg IV q 24 hr; ondansetron: 0.10.3 mg/kg IV q 8-12 hr) limit stimulation of the chemoreceptor trigger zone and vagal afferents. Their antiemetic effect is potent. They appear to be fairly well tolerated by dogs, however they are more expensive than the 2-adrenergic antagonists and metoclopramide. Maropitant (1 mg/kg SQ, IV q 24 hr) limits stimulation of the chemoreceptor trigger zone and emetic center. In addition, it may have some visceral analgesic effects. Its antiemetic effect is potent. It is labeled for dogs older than 8 weeks of age. Other than stinging on SQ injection (which can be decreased by keeping the drug refrigerated), it appears to be fairly well tolerated by dogs. While off label, it can be diluted and given slowly IV. In a study comparing maropitant to ondansteron in dogs infected with CPV, maropitant appeared to be equally as effective in controlling vomiting as compared to ondansetron. In addition, dogs treated with maropitant demonstrated improved ability to maintain body weight

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