Management Of The Patient With Canine Parvovirus Enteritis
PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 20155Management of the Patientwith Canine Parvovirus EnteritisPhilip R Judge BVSc MVS PG Cert Vet Stud MACVSc (Veterinary Emergency and Critical Care; Medicine of Dogs)Senior Lecturer: Veterinary Emergency and Critical Care, James Cook University, AustraliaDirector: Vet Education Pty Ltd (www.veteducation.net)All documents are copyright to Vet Education Pty Ltd. Permission has been granted for inclusion in the NZVNA conference proceedings.Canine Parvovirus is a highly contagious virus that affectsdogs, resulting in severe gastrointestinal disease andoccasionally cardiac disease. The virus itself is what is termed“non-enveloped”, and is made up of viral DNA. Canineparvovirus infection is a serious viral infection in dogs,and as mentioned above, is highly contagious, being readilytransmitted from one dog to another through contact withinfected faeces.There are some important facts about the virus itself thatunderpin some important aspects of patient management Canine parvovirus is a stable virus that can survive for upto five to seven months in the environment. This means,susceptible dogs can contract the virus simply by contactingand ingesting virus in a contaminated environment. One gram of faeces from an infected, virus-shedding dogis thought to contain enough viral material to infect over10 million susceptible dogs by oral exposure! Canine parvovirus vaccination is very effective inpreventing disease. However, young animals may stillbe at risk of contracting the disease despite vaccination,because antibodies in circulation from maternal colostruminactivate early puppy vaccinations in a number of puppies.In fact, a 12 week vaccination with a modified live canineparvovirus vaccination will be inactivated by colostrumderived antibody in the puppy in approximately 8% ofpuppies. Vaccination protocols that stop at 12 weeks ofage can result in susceptible puppies. The virus initially infects the lymphoid tissue in the pharynxbefore it enters the bloodstream, where it contaminatescells around the body, including the intestines, bonemarrow and dividing cardiac cells in the very young. Canine parvovirus replicates in dividing cells, and thusPhotographs of canine parvovirus. Being non-envelopedrenders the virus extremely resistant to desiccationtypically causes symptoms of disease in tissue with rapidlydividing cells such as the gastrointestinal tract and bonemarrow:- Cells of the intestines replicate rapidly on an ongoingbasis, and are therefore affected by (and destroyed by)parvovirus infection, which results in diarrhoea andvomiting.- Cells of the bone marrow of young dogs are replicating,producing red and white blood cells. Infection withparvovirus affects production of white blood cells, andcan result in profound leukopaenia in infected patients.- In young dogs that are born to unvaccinated parents,and that are infected within the first two weeks of life,the muscles of the heart may be affected as they replicatein the first two weeks of life, causing myocarditis. Asmost dogs have some history of vaccination, cardiacmanifestation of parvovirus has become much lesscommon – because maternal antibody usually providesprotection against parvovirus infection in neonatesduring the first two weeks of life, during myocardialdevelopment. Symptoms appear when the virus infects cells withinthe body. Intestinal cells become infected by day fourof infection – and gastrointestinal symptoms of diseaseusually appear over the subsequent two to three days.Clinical SignsThe clinical signs of canine parvovirus are usually the resultof intestinal and bone marrow cell destruction by the virus,and therefore include the following: Anorexia Depression Vomiting Profuse haemorrhagic diarrhoeaHistopathology slides from a normal myocardium (left) andmyocardium infected with canine parvovirus (right). Note thepresence of large numbers of inflammatory cells and the lossof pink muscle tissue in the infected section.
6PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015 Abdominal discomfortCardiovascular shockDehydrationPyrexiaInfection – resulting from leukopaenia – or decreasedwhite blood cell count, and disruption to the intestinalmucosal barrier, which allows intestinal bacteria to gainaccess to systemic circulation Sudden death and congestive heart failure – may result ifmyocardial damage occurs in very young patientsDiagnosisThe diagnosis of canine parvovirus is made on the basis ofclinical signs and a history of poor vaccination protocol, orlack of vaccination history, along with confirmation usinga faecal antigen test (parvovirus “snap” tests). In addition,because there are many other diseases that may also resultin similar clinical signs, a thorough evaluation of the patientmust be performed as outlined below The diagnostic evaluation of the patient with acutegastroenteritis is critical to ensure that specific therapeuticmodalities are not overlooked, and to ensure that inappropriatetreatment is not administered to the patient. The diagnosticevaluation usually follows the following format:1. History – obtaining a complete and thorough history canaid in directing an appropriate diagnostic approach to thepatient. Pertinent questions to raise during history-takinginclude:a. Diet – current diet, any recent change, previously notedintolerancesb. Behaviour of the patient - scavenging behaviourc. Duration and progression of presenting signsd. Environment – does the patient have access off theowners’ property etc?e. Parasite controlf. Toxin exposure – are there herbicides, pesticides,household products, human medications that thepatient has access to etc.g. Is the patient de-sexed?h. Concurrent medical conditionsi. Previous medical history2. Physical examination – physical examination shouldreveal the presence of the following:a. Fluid deficit – hydration status, evidence of bloodvolume depletionb. Mentationc. Abdominal evaluationi. Conformationii. Auscultationd. Palpation – palpate the abdomen several times duringthe course of initial evaluation. Evaluate for the presenceof pain; abnormal organ shape, size, or position;evidence of obstruction; palpation of unusual structurese.g. tube-like thickening of intestines in intussusceptionetc.e. Pain (nature, severity, location)f. Rectal evaluation – palpate prostate or uterus ifpossible; evaluate stool characteristics. Collect faecesfor evaluationg. Complete full physical examination3. Collect a Patient Data Base – for patients with diarrhoeaas a presenting sign, the following samples should becollected at admission, or shortly following admission, tofacilitate diagnostic evaluation of the patient:a. PCV/TPb. Glucosec. Electrolyte evaluationd. Blood gas analysise. Serum biochemistry and complete blood countf. Urinalysisg. Faecal evaluation – smear, faecal flotation, immunologicassessment e.g. parvovirus, giardia, clostridiumperfringens; culture if required e.g. campylobacter spp.,salmonella spp.h. Abdominal radiography – preferably three views – rightand left lateral and ventro-dorsal recumbency views.Radiographic contrast studies may be carried out basedon results of physical examination, blood tests, andsurvey radiography.i. Abdominal ultrasoundA Note on Faecal AnalysisThe diagnosis of acute infectious gastroenteritis is madeon the basis of history (including the health of in-contactanimals and people); clinical examination, results of serumbiochemistry, CBC and urinalysis, and faecal evaluation.Faecal analysis should begin with faecal flotation – which willenable detection of organisms such as giardia, toxoplasma,and the whipworm Trichuris vulpis etc. Direct faecal smearsare useful for detection of intestinal parasites. A stainedsmear of faeces and immunological techniques can allowdetection of clostridium enterotoxin etc., and faecal culturecan be useful in other infections.Staining of a faecal smear may allow detection of manyorganisms associated with infectious enteritis in dogs andcats, as outlined below:1. Wright’s Giemsa or Diff Quick stain – allows detection ofa. White blood cells – the presence of neutrophils suggestsinflammation, commonly seen in Salmonella spp.,campylobacter spp., or clostridium spp., and shouldprompt faecal culture to be performedb. Bacterial morphology consistent with campylobacterspp., clostridium perfringensc. Mononuclear cell examination – may reveal presence ofHistoplasma spp.2. Methylene Blue staining allows detection ofa. Trophozoites of enteric protozoaA Note on Faecal Elisa Tests for ParvovirusEnteritisThe faecal ELISA tests are very accurate, but can giveerroneous results on occasion – for example: False positive results – where a dog does not haveparvovirus, but tests positive for it – can occur between
PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 20157Faecal analysis may reveal Whipworm (Trichuris) egg (left), Giardia cyst (centre) or hookworm (ancylostoma) egg (right)five and fifteen days following a vaccination False negative results – where a dog has parvovirus, butdoes not test positive for it – can occur if a faecal sampleis taken very early in the disease (within one to four daysof becoming infected). False negative tests should berepeated one to days days later in individuals suspected ofhaving parvovirus based on history and clinical signs.A Note on Blood Test Results for ParvovirusEnteritisBlood test results in parvovirus-infected patients usually shownon-specific changes, with the exception of the following Leukopenia – low white blood cell counts are commonin parvovirus infection due to viral infection of rapidlydividing white blood cell precursors in the bone marrow.- Lymphopaenia – results from damage to lymphocytesduring the initial infection period- Neutropaenia and monocytopenia – result from damageto precursor cells in the bone marrow Biochemistry changes – usually reflect loss of proteinand electrolytes into the gastrointestinal tract, as well aschanges due to dehydration, and tissue hypoxia.- Albumin /- globulin concentrations may be low- Liver enzymes may be slightly elevated- Hypochloraemia may be present, along withhypokalaemia /- hyponatraemia- Urea and creatinine /- phosphorus may be elevatedalso Platelets - numbers may be decreased in severe diseasedue to DIC, and reduced platelet production in the bonemarrow Coagulation profile – the ACT may be prolonged ornormal depending on the degree of illness, with severeillness commonly producing clotting abnormalitiessecondary to extensive tissue damage and DICOther Tests for the Parvovirus PatientDiagnostic imaging – such as radiography and ultrasoundcan be useful in eliminating other causes of vomitingand diarrhoea, and to determine if intestinal obstructionor intussusception is present or not. This is particularlyimportant when evaluating patients with persistent orrecurrent vomiting and/or diarrhoea despite provision ofintensive care over several days in hospital.TreatmentThe treatment for parvovirus enteritis revolves around goodsupportive care of the patient with fluid therapy, analgesia,transfusion therapy, colloid fluid therapy, anti-emetics,Photograph showing intussusception (left) and ultrasound image of intussusception (right) – a common cause of patientdeterioration despite therapy for parvovirus enteritis. Surgery is required to remedy this condition.
8PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015nasogastric suctioning and early nutritional support. Inaddition, supportive care of the intestinal tract is required.In order to be able to effectively care for the intestinal tract insuch a severe illness, we must understand a little about whatthe intestine does in health. By knowing this, we will be able tomore accurately assess, monitor and intervene appropriatelyfor our patients when their intestines are infected or diseased.The Physiology of Intestinal FunctionsThe normal physiological functions of the intestine include: Intestinal motility – the intestine broadly moves in two ways- segmental or ‘mixing’ contractions that facilitate exposureof ingesta with the intestinal mucosa, and propulsivecontractions that facilitate movement of intestinal luminalcontents distally within the gastrointestinal tract. Secretion – Normal intestinal secretion involves thesecretion of an isotonic solution of water and electrolytesinto the intestinal lumen. Secretion may be stimulated bybacteria, bacterial toxins, osmotically active non-absorbedsolutes, drugs, and products of bacterial fermentation. Absorption – absorption of nutrients from the smallintestine occurs through the cells of the villi. Most specificnutrients are absorbed by active means, using specificmembrane-bound transport mechanisms in the cells ofthe intestinal villi. The movement or absorption of wateroccurs either by passive transport along trans-mucosalionic or electrical gradients, by movement of water (solventdrag) or by active, cell-membrane mediated transportprocesses (ATPase pumps). Digestion – digestion of food is facilitated by motility, butprimarily involves action of specific chemical reactionsthat facilitate degradation of food substances into smallmolecules that are able to be absorbed into the systemiccirculation. Digestion begins in the oral cavity with secretionof the enzyme amylase, and continues in the stomach, withsecretion of hydrochloric acid. Chemical reactions in thesmall bowel usually involve the action of cell membraneassociated enzymes such as enterokinase; the action ofpancreatic enzymes, and the action of bile acids.The structure of the intestine facilitates these key physiologicalfunctions. For example, very large quantities of water andelectrolytes are cycled through the intestine each day. Infact, a volume equivalent to approximately half of the body’sextracellular water is secreted and absorbed by the intestinein each 24-hour period; yet the intestine loses only 0.1% ofthis volume in faecal water. However, when normal intestinalsecretory or absorptive capacity or function is disrupted,massive fluid and electrolyte losses may occur – as it does indiarrhoea or vomiting.Treatment of Parvovirus Enteritis in DogsThere is very little specific therapy that can be directedagainst the parvovirus virus itself by the time clinical signs ofillness are evident. Treatment therefore remains supportivefor the vast majority of patients clinically affected withsigns of parvovirus gastroenteritis. In general, fluid therapy,analgesia, intestinal support and nutrition form the basisfor successful patient management. A suggested treatmentrationale follows 1. Intravenous Fluid Therapy – in most patients presentingto the veterinary clinic with vomiting and diarrhoea, thepresumption is that the patient will have lost sufficientfluids to have become dehydrated, even if this is notclinically apparent. Restoration of this fluid deficit isrequired to prevent further gastrointestinal injury, andpatient hemodynamic compromise and renal injury. Fluidtherapy is administered in the following manner:a. Correction of intravascular volume deficits –for patients displaying symptoms of shock orhaemodynamic compromise, such as those with weakpulses, tachycardia, bradycardia, collapse, tacky mucousmembranes etc., initial fluid resuscitation should beginwith rapid intravenous administration of a balancedisotonic crystalloid solution such as Lactated RingersSolution, or normosol-R. Initial fluid rates shouldbe sufficient to correct intravascular volume deficitswithin one hour of patient presentation. The authors’preference is to administer an isotonic crystalloid inboluses of 7-12 ml/kg IV over 10 minutes, followedby patient reassessment, and for this procedure to berepeated until signs of haemodynamic compromise areno longer present – as evidenced by a return of normalpulse quality, improvement in capillary refill time,improved mentation, normal heart rate etc. If significanthaemodynamic improvement is not noted within 30minutes of fluid therapy, a bolus of synthetic colloidsuch as hydroxy-ethyl starch (Voluven) or Pentaspan isadministered at a dose of 3-5 ml/kg, given intravenouslyover 10 minutes to prolong the effectiveness of isotoniccrystalloid therapy within the intravascular space.b. Following correction of intravascular volume deficits,the patients hydration deficit is calculated (hydrationdeficit volume (ml) % dehydration (e.g. 5% 0.05)x bodyweight(kg) x 1000), and this volume of fluid isadministered to the patient over 8-24 hours, in additionto the patients’ normal daily fluid requirement (60 ml/kg/24hrs). Typically, fluid required to replace hydrationdeficits is similar in composition to extracellular fluid,but should be supplemented with potassium, to replacerenal and gastrointestinal loss of potassium. An idealfluid for replacement of hydration deficits is LactatedRingers Solution, supplemented with 20-30 mEq/Lpotassium chloride.c. Following correction of hydration deficits, the patientPhotograph showing intussusception (left) and ultrasoundimage of intussusception (right) – a common cause of patientdeterioration despite therapy for parvovirus enteritis. Surgeryis required to remedy this condition.
PROCEEDINGS OF THE NEW ZEALAND VETERINARY NURSING ASSOCIATION ANNUAL CONFERENCE 2015requires fluid therapy for maintenance of normal bodyfunctions, PLUS replacement of ongoing fluid lossesthrough the gastrointestinal tract, in patients thatcontinue to have diarrhoea and/or vomiting. In mostcases, a fluid type such as Lactated Ringers Solution,with 5% glucose, and 20-30 mEq/L potassium chloride isrequired. In patients without significant gastrointestinalfluid loss, 0.45% sodium chloride solution, 2.5%glucose, and 20-30 mEq/L potassium chloride is usuallysufficient to meet ongoing fluid requirements. In patientswith significant loss of gastrointestinal fluid, bloodor protein, a combination of isotonic crystalloid andcolloid therapy, using hydroxy-ethyl starch, Pentaspan,or blood or fresh frozen plasma transfusion is required,in order to maintain blood volume, hydration status,and colloid oncotic pressure necessary for tissue oxygendelivery to body tissues.d. Plasma and synthetic colloid use: Patients withparvovirus enteritis are high risk, critically ill patientsthat frequently suffer from significant losses ofplasma proteins into the intestinal lumen. This canlead to hypoproteinaemia, hypoalbuminaemia, and,occasionally, coagulation abnormalities. The use offresh frozen plasma and/or synthetic colloids in thesepatients is controversial, but it also has sound rationale.Hypoproteinaemia and hypoalbuminaemia arenegative prognostic indicators in patients with severeillness. They are associated with decreased effectivecirculating blood volume, poor tissue perfusion, andworse outcome. Administration of fresh frozen plasmacan reasonably be considered in any patient withparvovirus enteritis that is critically unwell. Optimumbenefit from transfusion is obtained when transfusion isadministered early in the course of disease, at dose ratesof 10-30 ml/kg intravenously over four to six hours.Following plasma transfusion, synthetic colloids such ashydroxy-ethyl starch or Pentaspan may be administeredat a rate of 10 ml/kg/day in addition to fluid therapy toprovide for maintenance and ongoing losses.2. Dietary management – Nil per Os (NPO) for an initialsix to twelvehour period following admission to hospitalmay be beneficial in most cases of diarrhoea in dogs andcats. NPO decreases the number of osmotic particlesavailable in the intestinal lumen contributing to osmoticdiarrhoea, and allows more rapid re-growth of intestinalvilli, and resumption of intestinal function. Following aninitial short period of bowel rest, micro-enteral nutritionshould commence. Micro-enteral nutrition, using glucose,hydrolyzed proteins and isotonic
Canine Parvovirus is a highly contagious virus that a ects dogs, resulting in severe gastrointestinal disease and occasionally cardiac disease. e virus itself is what is termed “non-enveloped”, and is made up of viral DNA. Canine parvovirus
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