THERAPEUTIC MANAGEMENT OF DOGS AFFECTED WITH CANINE PARVO VIRUS (CPV) INFECTION  

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CONTROL & MANAGEMENT OF PARVOVIRUS INFECTION IN DOGS
CONTROL & MANAGEMENT OF PARVOVIRUS INFECTION IN DOGS

THERAPEUTIC MANAGEMENT OF DOGS AFFECTED WITH CANINE PARVO VIRUS (CPV) INFECTION  

Dr.RAJESH KUMAR SINGH,JAMSHEDPUR 

Dogs most at risk from canine parvovirus

Puppies aged between six weeks and six months old, along with unvaccinated or incompletely vaccinated dogs, are most likely to catch canine parvovirus. Meanwhile, certain breeds, including American Pit Bull Terriers, Doberman Pinschers, English Springer Spaniels, German Shepherds and Rottweilers, are at increased risk. Among dogs older than six months, intact males are more likely than intact females to develop parvo. In very rare cases, dogs who are up to date with their vaccinations may develop canine parvovirus.

Canine parvovirus (CPV) is a virulent infection that is characterized by vomiting, bloody diarrhea, and leukopenia. Most commonly seen in dogs less than one year of age, without treatment most victims of the virus will die. Parvovirus stricken dogs frequently present with dull mentation, dehydration, abnormal body temperature, tachycardia, and tachypnea. Severe cases of parvovirus can also result in sepsis and multiple organ failure. Treatment protocols typically consist of aggressive fluid therapy to combat dehydration and ongoing losses, antibiotic therapy to combat secondary bacterial infections, and the reintroduction of enteral nutrition. Adjunctive treatments showing future promise against the devastation of canine parvovirus include antiendotoxins, canine IgG, and more recently, the neuraminidase inhibitor Tamiflu. Nursing care protocols are vital in order to improve patient outcome; emphasis on the physical exam, practicing sterile technique, strong observational skills, and specialty equipment utilization and interpretation are important.

Treatment for canine parvovirus

CPV is most common in dogs between the ages of 6 weeks and 6 months. Early clinical signs are lethargy, anorexia, vomiting, and fever. Further progression of the disease will produce generalized weakness, dehydration, and severe vomiting and diarrhea. Without immediate treatment, patients can become hypotensive, septic, and in multi-organ failure. Other clinical signs to monitor include weakness or seizures associated with hypoglycemia, particularly in puppies or toy breeds. Following rehydration, 2.5% to 5%dextrose can be added to a balanced electrolyte solution. Other clinical signs include muscle weakness associated with hypokalemia, particularly in puppies with anorexia, vomiting, and diarrhea. Severe hypokalemia can also result in gastrointestinal ileus, polyuria,cardiac arrhythmias, and general malaise. Serum potassium should be monitored daily in these patients, and supplemented accordingly.

Fluid therapy to correct dehydration and perfusion abnormalities is essential in the patient with CPV, and is considered the cornerstone of treatment. Fluid volume replacement is calculated by first evaluating existing deficits (rehydration), adding maintenance needs, and then calculating continuing losses (e.g., vomiting, diarrhea). Dehydration is typically corrected over 4 to 6 hours; the remaining deficit and maintenance volumes over a 24-hour period of time. Slow replacement is necessary to allow equilibration between intracellular and extracellular compartments. More rapid administration rates results in hypervolemia with subsequent loss of fluids in the urine. Route of administration of fluids is typically intravenous; subcutaneous fluids will not be absorbed by animals with severe dehydration or circulatory collapse because of peripheral vasoconstriction.

It is important to note that the clinical response of the animal to the fluid therapy. Signs of excessive rates of fluid administration include restlessness, serous nasal discharge, moist lung sounds, coughing, and protrusion of the eye from the orbit, and vomiting and diarrhea. Signs of an under perfused or dehydrated animal include tacky, pale and dry mucus membranes, prolonged capillary refill time, tachycardia, and poor mentation. Monitoring central venous pressure, obtaining serial body weights, monitoring urine production can also be useful tools in assessing a patient’s response to fluid therapy. Urine output should approximate 1 to 2 mL/kg/hr, and urine specific gravity should range from 1.015 to 1.020.

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The initial fluid of choice is typically a balanced electrolyte crystalloid solution, such as Lactated Ringers or Normosol; electrolyte abnormalities are commonly seen in CPV due to excessive fluid loss (vomiting and diarrhea). If CPV infection has resulted in hypovolemic shock, a rapid intravenous crystalloid fluid bolus of up to 90 mL/kg/hr may be necessary to restore perfusion. Hypertonic solutions are contraindicated to correct malperfusion (shock) in the dehydrated patient; colloid solutions can be useful in resuscitation from shock, particularly when albumin in plasma is less than 2.0 g/dL. Colloids are also useful in the CPV patient in septic shock, which can result in a massive extravasation of fluid through leaky, vasodilated capillaries. In addition, the use of colloid solutions can help prevent peripheral constriction by retaining intravascular volume and can prevent pulmonary edema. Colloid therapy can also be used to correct oncotic pressure. Clinical signs to monitor for low colloid oncotic pressure or low albumin include pitting edema.

There’s no specific drug to treat parvovirus in dogs but those affected by the disease have a far greater chance of survival if they receive early, aggressive treatment and intensive nursing care.

Treatment may include:

  • Intravenous fluids (a drip) to treat shock and correct dehydration and electrolyte abnormalities
  • Anti-sickness medication
  • Painkillers
  • Plasma transfusions and/or blood transfusions to replace proteins and cells
  • Antibiotics to treat or prevent secondary infections as a result of the effects of parvovirus infection
  • Tube feeding

 

STANDARD LINE OF TREATMENT WHICH I FOLLOW IN SOME TYPICAL CASES

The patients are treated with the following drug regimen:

ceftriaxone with tazobactam @ 20 mg/kg b.wt., intravenously twice a day, ondansetron @ 0.2 mg/kg b.wt., intravenously twice a day upto the remission of emesis, ethamsylate @ 10 mg/kg b.wt., is given intravenously in cases with severe haemorrhagic enteritis, fluid therapy is initiated with isotonic Ringer’s lactate (RL) as the initial choice for replacement along with which 5 % dextrose normal saline (DNS), potassium chloride and hetastarch are supplemented in some cases. Apart from them, dietary recommendations are advised for the patients. The patients are monitored regularly for 5 days.

NB-Always consult your vet for proper Diagnosis and Treatment of your pet.This write-up is just for awareness purpose.Plz dnt happy this without taking consent of your vet.

Hemorrhagic diarrhea

and mucosal sloughing are also commonly seen in dogs with CPV enteritis. The technician should monitor packed cell volume and total protein with regularity. Blood products, such as fresh whole blood, whole blood, fresh-frozen plasma and plasma transfusions can be given to correct anemia, correct hypoproteinemia, and treat disseminated intravascular coagulation (DIC) if present. (There are also speculations that blood products can also provide passive immunity; serum from dogs recovering from parvovirus has been used anecdotally with presumed benefits). CPV patients can also experience a severe protein losing enteropathy because of destruction of the intestinal villi; administration of a colloid fluid is indicated if the albumin decreases below 1.5 g/dL and the total protein decreases below 4.0 g/dL. If natural colloids are not available, puppies with decreased total protein and edema should receive a synthetic colloid, such as Hetastarch or dextran 70. To avoid potential volume overload, the dosage of 20 mL/kg/day should not be exceeded. Other standard therapies for CPV include antibiotics, antiemetics, reintroduction of enteral nutrition, and alternative therapies such as antiendotoxins, biological response modifiers, and neuraminidase inhibitor Tamiflu.

Systemic antibiotics are important in the CPV patient, as the hemorrhagic diarrhea and mucosal sloughing indicate breakdown of the GI mucosal barrier which can lead to bacterial translocation, endotoxemia, and sepsis. Severe neutropenia is common with severe enteritis, which contributes to the risk of systemic sepsis. Consequently, treatment with intravenous broad-spectrum, bactericidal antibiotics is indicated in severe cases of CPV. Mildly affected dogs with an adequate white blood cell count generally do not require combination antibiotic therapy. Neutropenic patients should be handled with sterile technique by all personnel. Sterile technique protocols should include wearing examination gloves when handling the patient, sterile placement of any intravenous catheter, intravenous injections completed with sterility, and keeping IV lines connected at all times (including walks).

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Antiemetic therapy is also important in the CPV patient, as persistent vomiting increases fluid losses, prevents oral intake of food, and can cause aspiration pneumonia in the weak patient. Commonly used antiemetics are metoclopromide and chlorpromazine; metoclopramide is a gastric promotility drug which can reduce vomiting by stimulating gastric emptying and inhibiting the chemoreceptor trigger zone. Metaclopramide may also prevent gastric atony and ileus from occurring by promoting gastric motility. Metoclopramide can be added to the intravenous fluids or administered in a separate drip at a dosage of 1.0 to 2.0 mg/kg/24 hours and given as a constant rate infusion. Antiemetic agent chlorpromazine can also be utilized if the metoclopramide is ineffective in controlling vomiting. Chlorpromazine is a phenothiazine derivative and acts on the emetic center, the chemoreceptor trigger zone, and peripheral receptors to reduce the vomiting reflex. Phenothiazine derivatives can cause hypotension and systemic vasodilation via their alpha adrenergic blocking effect and should only be given after the patient is well hydrated; the technician should watch patient mentation and monitor for restlessness, hyperactivity, bizarre behavior, or extreme drowsiness. Any abnormal clinical sign noted in associated with antiemetic therapy should warrant discontinuation of the pharmaceutical. Ondansetron (Zofran, Cerenex Pharmaceuticals), a serotonin antagonist, is highly effective and safe antiemetic for persistent vomiting. Maropitant (Cerenia, Pfizer Animal Health) is also a very effective antiemetic and can be given intravenously for visceral pain. Cerenia can be given in combination with raglan if vomiting is refractory and/or severe.

 

Other standard treatment of CPV includes the eradication of intestinal parasites; the presence of intestinal parasites has been identified as a factor, which can exacerbate CPV infection by enhancing intestinal cell turnover and subsequent viral replication. Fecal samples should be evaluated to identify coccidia, Giardia sp, hookworms, roundworms, or whipworms. Appropriate oral therapy can be initiated as soon as vomiting ceases. Nutritional support should also be instituted to prevent catabolism and immune dysfunction; dextrose supplemented to intravenous fluids should not be considered as adequate nutritional support. Options for the CPV patient with persistent vomiting include partial parenteral nutrition (PPN), although PPN does not supply all of the patient’s nutrient needs. PPN can provide short-term support for animals that are expected to recover soon, and can be delivered through a peripheral venous catheter as opposed to a large central venous catheter. PPN solutions are usually given at a maintenance dose (60 mL/kg/day). Common PPN complications are typically catheter related, such as phlebitis, infection, pain, or limb edema. Sterile technique should be practiced in order to avoid infection, and insertion site inspected daily followed by a sterile dressing. PPN solutions containing dextrose should be tapered off gradually to prevent rebound hypoglycemia. Enteral support should be addressed after vomiting has ceased for 12 to 24 hours; water is offered first, followed by an easily digestible (high carbohydrate, low fat) liquid diet or gruel. Glutamine powder (0.5 g/kg divided every 12 hours) can be added to drinking water to promote gastrointestinal healing. A normal diet is gradually re-introduced after appetite and stool have returned to normal.

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Alternative treatments include antiendotoxins, of theoretical benefit because of the presumed role of bacterial endotoxemia. Bacterial endotoxemia is believed to be an important factor in the terminal acute shock phase which occurs in severe cases of CPV. A polyvalent equine origin antiserum against lipopolysaccharide (LPS) endotoxin is available for use in small animals (SEPTI-serum, Immvac). It is recommended that the product be administered over 30 to 60 minutes (4.4 mL/kg and diluted 1:1 with intravenous crystalloid fluids) and before antibiotic therapy, as circulating plasma LPS concentrations can increase dramatically following antibiotic kill-off of gram-negative bacteria. Patients receiving equine origin antiserum must be observed closely during administration for signs of anaphylaxis. If a second administration of antiserum is deemed necessary, it should be given within 5 to 7 days following the initial treatment. After that time, a severe immunologic reaction is more likely to occur.

A promising alternative treatment for CPV includes neuraminidase inhibitor Tamiflu. Bacterial neuramini-dases dissolve the GI mucus layer, remove IgA that protect epithelial cells, allow bacteria to colonize and attach on to the GI epithelial cell surface, supply sialic acid molecules in order to produce toxins, and dissolve neuramic acid to create portals for bacteria to enter the submucosal tissue. It is theorized that Tamiflu suppresses the amount of sialic acid available for bacteria to use to proliferate/colonize/produce endotoxins: keep in mind that Tamiflu does not inhibit the CPV from replicating. Tamiflu at the appropriate dose and administration route will stop neuraminidase processes, and has shown promising results in improving patient outcome from the devastating effects of CPV.

How to prevent parvo in dogs?

Vaccination is the most effective way to prevent your dog contracting parvovirus. Your dog’s annual vaccination will include a component against canine parvovirus and it’s important to maintain up-to-date vaccinations as your dog gets older. Puppies can be vaccinated from six weeks.

Good hygiene is also vital to preventing parvovirus from spreading. If you suspect you have come into contact with faeces infected by parvovirus, you should wash the affected area with household bleach. Soiled bedding should be discarded and all kennels, collars, bowls and leads appropriately cleaned and sterilised.

Infected dogs should be kept away from other dogs until they have recovered fully.

The best way to prevent parvovirus is through good hygiene and vaccination. Make sure to get your puppies vaccinated, and be sure your adult dogs are kept up-to-date on their parvovirus vaccination.
Puppies have immunity from their mothers early in life, but should receive their first vaccine between 6 and 8 weeks of age (after weaning), and then two boosters at three-week intervals.

Until a puppy has received its complete series of vaccinations, pet owners should use caution when bringing their pet to places where young puppies or dogs with unknown vaccination histories congregate. This includes pet-friendly restaurants, popular hiking trails, boarding facilities, and especially dog parks.

Puppies should be sequestered until three to four weeks after their third vaccine—this is when full immunity is achieved. It is also important to note that fully-vaccinated dogs have become sick with Parvo, so always be aware of possible symptoms.

Reference-On Request

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