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Vol. 19, No.

3 March 1997 Small Animal Gastroenterology

Continuing Education Article


Refereed Peer Review

Canine Parvovirus.
FOCAL POINT
Part II.Clinical
★Aggressive treatment can
dramatically increase survival of
Signs, Diagnosis,
patients with canine parvovirus
enteritis. and Treatment*
KEY FACTS
■ In-house ELISAs allow for rapid
diagnosis, but false-positives Auburn University
can result when dogs have Douglass K. Macintire, DVM, MS
been recently vaccinated with Saralyn Smith-Carr, DVM, PhD
attenuated virus vaccine, and
false-negatives can result when
antibodies from blood in the
feces bind to antigen.

■ If serum albumin drops below 1.5


g/dl or total protein decreases
below 3.5 g/dl, an intravenous
T wo clinical syndromes occur in dogs infected with canine parvovirus
(CPV): enteritis and myocardial failure. Myocardial failure can occur in
neonatal puppies infected in utero or shortly after birth as a result of
failure of passive transfer of colostral antibodies. In these puppies, CPV infects
rapidly dividing cells of the myocardium, thus resulting in delayed signs of car-
colloid should be given.
diac failure, syncope, arrhythmia, or sudden death. Sometimes, the only evi-
■ Intravenous bactericidal dence of myocardial disease is found at necropsy.
antibiotics are indicated for The myocardial form of CPV infection was seen primarily in the early 1980s.
puppies with neutropenia and It is rare today because of the effectiveness of current vaccination protocols in
hemorrhagic diarrhea. promoting maternal antibody protection in young puppies. This article focuses
on the enteric form of CPV infection.
■ Antiendotoxin should be given
before antibiotics because DIAGNOSIS
endotoxins are released as Clinical Findings
bacteria are killed. The initial clinical signs of enteric CPV infection are nonspecific and include
anorexia, depression, lethargy, and fever. Within 24 to 48 hours, most affected
puppies begin vomiting. Intestinal disease is more severe in puppies with enter-
ic parasites, environmental stresses, low maternal antibody titers, and delayed
or impaired humoral immune response.1,2 With severe dehydration, protein
loss, concomitant infection, and inability to produce a rapid immune response,
this syndrome can rapidly progress to systemic shock and death.
*Part I of this two-part presentation appeared in the February 1997 (Vol. 19, No. 2)
issue of Compendium.
Small Animal The Compendium March 1997

Necrosis of mucosal and Pathologic Findings


lymphoid tissue of the small The gross intestinal lesions
intestine disrupts the gastro- of parvovirus are nonspecific
intestinal mucosal barrier, and variable.1,8 The lesions, if
thus permitting bacterial present, are usually segmen-
translocation. Gram-negative tally distributed, with the
and anaerobic bacteria can ileum and jejunum most of-
enter the general circulation, ten affected. These affected
producing septic shock and sections may be flaccid and
the systemic inflammatory may exhibit serosal hemor-
response syndrome (SIRS). rhage or congestion. The
The outer cell wall of gram- bowel lumen is usually empty
negative bacteria contains but may contain watery hem-
endotoxins (lipopolysaccha- Figure 1—Photomicrograph of the duodenal mucosa from a orrhagic contents. The mesen-
rides [LPS]) that are also po- dog with parvovirus enteritis. There is severe villus collapse teric lymph nodes are usually
tent mediators of systemic and dilatation of the crypt glands secondary to viral-induced enlarged and swollen, with
inflammation.3 necrosis of crypt epithelium. (Courtesy of Dr. J. Newton, petechial hemorrhages in the
In humans, bacterial Department of Pathobiology, Auburn University, Auburn, AL) cortex. Cortical necrosis and
translocation and gut-origin atrophy of the thymus can be
sepsis are believed to be pre- observed in puppies.
disposing factors for adult respiratory distress syndrome The microscopic lesions of CPV are seen in the prolif-
(ARDS) and multiple-organ failure.4 In one study of 88 erating population of cells in the intestinal tract, bone
dogs that died of severe CPV infection, E. coli was isolat- marrow, and lymphoid tissue. In the intestinal tract, the
ed from the lung and/or liver of 90% of the dogs, and early lesions are necrosis of the crypt epithelium, result-
pulmonary lesions similar to those found in humans with ing in dilated crypts that are filled with necrotic debris
ARDS were detected in 69% of the dogs.5 Secondary bac- and/or intranuclear inclusions within crypt epithelial
terial infection with clostridia, Campylobacter species, and cells. With the progression of disease, the villi become
salmonellae has also been reported to occur with par- blunted and malabsorption/maldigestion results (Figure
vovirus infection.6,7 Septicemia and/or endotoxemia may 1). Complete collapse and destruction of the villi occurs
occur as a direct result of these bacterial pathogens. in severe cases. These lesions may be focal or may occur
Transient lymphopenia is the most consistent hema- segmentally throughout the small intestine (and infre-
tologic finding associated with parvovirus infection.2,8 quently in the large intestine). There is usually evidence
Panleukopenia, particularly neutropenia, occurs with of intestinal regeneration, even in severe cases.
severe disease. Blood-loss anemia, often associated with The germinal centers of mesenteric and gut-associated
concurrent internal parasite infection, may be manifest- lymph nodes and the cortical area of the thymus are de-
ed as anemia with panhypoproteinemia. Serum chem- pleted of lymphoid cells. Myeloid and erythroid hy-
istry analyses are nonspecific. Severe potassium loss sec- poplasia occur in the bone marrow during acute dis-
ondary to anorexia, vomiting, and diarrhea may ease. During recovery, there is hyperplasia of lymphoid,
contribute to the depression and weakness. Elevated erythroid, and myeloid cells.
blood urea nitrogen (BUN) and creatinine may occur
as a result of dehydration. Elevation in serum alkaline Diagnostic Testing
phosphatase and alanine transaminase activities may Many tests are available to practicing veterinarians
also occur as a result of hepatic hypoxia caused by seri- for detecting CPV in the feces of infected animals. Solid-
ous hypovolemia. Other electrolyte abnormalities may phase enzyme-linked immunosorbent assays (ELISAs)
occur secondary to vomiting and severe diarrhea and have enabled in-house testing, which allows for rapid
should be monitored. identification, isolation, and treatment of animals with
No specific radiographic findings are associated with CPV infection while clinical signs are still vague. False-
parvovirus infection. Radiographic signs of gastroen- negative results may occur because of binding of test
teritis are fluid- and gas-filled bowel loops. Radiogra- antigen with serum-neutralizing antibodies in bloody
phy or abdominal ultrasonography may be used to in- diarrhea. False-positive results may occur shortly after
vestigate the possibility that a foreign body is causing vaccination with attenuated virus vaccines because of
the clinical signs or to identify intussusception as a fecal shedding of vaccine virus. Samples may also be
complication of severe parvovirus disease. submitted to commercial laboratories for diagnosis, al-

CLINICAL FINDINGS ■ DESCRIPTION OF LESIONS ■ IN-HOUSE ELISAs


The Compendium March 1997 Small Animal

though submission may de- TREATMENT


lay definitive diagnosis by 1 Canine parvovirus infec-
or 2 days. tion can produce severe dehy-
Other tests that are avail- dration, endotoxic or septic
able through university and shock, and multiple-organ
state diagnostic laboratories failure. Without treatment, it
include electron microscopy, is often fatal. However, ag-
hemagglutination (HA), gressive therapy and support-
virus isolation, latex aggluti- ive care (Figure 2) have
nation, and ELISA. These achieved an 85% to 95% sur-
tests are performed on feces vival rate at our hospital (see
from animals in the acute Treatment of Canine Par-
phase of the disease. Com- vovirus Enteritis). The follow-
mercial laboratories can also Figure 2—Canine parvovirus enteritis can be a debilitating ing recommendations should
diagnose parvovirus infec- disease, but most puppies can survive with intensive, aggres- be considered in the treat-
tion in fresh-frozen and for- sive supportive care. ment of all dogs infected with
malin-fixed tissue samples CPV.
by immunocytochemistry,
immunofluorescence assay (IFA), radioimmunoassay Initial Assessment
(RIA), or immunoperoxidase staining procedures. Spe- When an animal is presented to the hospital with a
cialized ELISAs (e.g., indirect ELISA, competitive history suggestive of CPV enteritis, a fecal antigen test
ELISA, and double-antibody sandwich ELISA [DAS- should be performed to confirm the diagnosis if possi-
ELISA]) that are currently being developed for detect- ble. If the test is positive, the animal should be isolated
ing CPV-specific antibodies in serum are reportedly from other hospitalized patients, and all contaminated
more sensitive than hemagglutination inhibition (HI). surfaces should be cleaned with a 1:30 dilution of house-
Various assays that use a polymerase chain reaction hold bleach. Strict cleanliness should be observed to
(PCR) for the detection of parvovirus in feces have avoid spread of the disease to other animals. If the test is
been developed. The PCR test can detect fewer parti- negative, other causes of gastroenteritis (e.g., foreign
cles of CPV than can conventional methods.9–11 This body, pancreatitis, intestinal parasitism, toxicity, or di-
sensitivity may reduce the number of false-negative re- etary indiscretion) should be ruled out. Because of the
sults that occur with fecal ELISAs. The PCR assays are possibility of false-negative results with the fecal antigen
also highly specific and can differentiate wild-type virus test, animals with a compatible history should receive ap-
from vaccine virus, thus eliminating false-positive re- propriate supportive care and be retested 48 hours later.
sults due to recent vaccination.12 Disease severity should be assessed through evalua-
Serum IgM and IgG titers were used to detect par- tion of physical examination findings and blood drawn
vovirus infection when the disease first emerged. A high for an initial minimum data base. Rapid screening tests
IgM titer with a low-to-negative IgG titer was used to that aid in patient assessment and fluid choice include
determine acute CPV infection in dogs with hemor- hematocrit, total solids, serum electrolytes, blood gases,
rhagic diarrhea. Serologic testing was established before and reagent sticks for blood glucose and BUN. A com-
antigen tests were developed and could not be used to plete blood count or blood smear also aids in patient
differentiate between previous subclinical infection, ac- assessment because leukopenia is generally associated
tive infection, or vaccination. with more severe disease and a more guarded prognosis.
Currently, serum antibody testing for parvovirus is Dehydration should be estimated through physical ex-
used to determine whether a dog has been immunized amination findings. Animals with mild dehydration
by vaccination or whether susceptible dogs have been (5% to 7%) have dry, tacky mucous membranes; ani-
exposed to parvovirus. Diagnostic laboratories use HI, mals with moderate dehydration (7% to 10%) have
radial hemolysis, virus or serum neutralization (VN or slow capillary refill time (>1.5 seconds), skin tenting,
SN), IFA, and RIA to detect CPV antibodies. The stan- and sunken eyeballs; and animals with severe dehydra-
dard for demonstration of protective antibody titer has tion (10% to 12%) are usually moribund and in a state
long been the HI test, which measures both IgM and of circulatory collapse.
IgG antibodies in serum. More recently, many laborato-
ries have used the IFA and SN titers to determine the Initial Fluid Therapy
level of protective immunity. Fluid replacement for losses incurred through vomit-

OUTSIDE TESTING ■ FECAL ANTIGEN TEST ■ RAPID SCREENING TESTS


Small Animal The Compendium March 1997

Treatment of Canine Parvovirus Enteritis


Intravenous Fluids Glucose Replacement
■ Begin with balanced electrolyte solution ■ If patient is hypoglycemic, give 0.5 g/kg 10% dextrose
■ Replace deficit (dehydration [%] × body weight [kg]) slowly intravenously
■ Immediately if the patient is in shock (90 ml/kg/hr) ■ After rehydration, add 50–100 ml of 50% dextrose/L of
■ Over 2 to 6 hours if the patient is only dehydrated replacement fluids to make 2.5% to 5% solution
■ Add to replacement volume ■ Consider partial parenteral nutrition for puppies that
■ Maintenance needs (44–66 ml/kg/day) have been anorectic for more than 3 days
■ Continuing losses (estimate amount lost through
vomiting and diarrhea) Consider Anthelmintic
■ Check stool for Giardia organisms, coccidia, or
Antibiotics (parenteral, bactericidal) nematodes
■ For severe cases (leukopenia, hemorrhagic diarrhea), ■ Consider injectable ivermectin (250 µg/kg) for
choose one of the following: nonvomiting dogs—except for collies and related breeds
■ Enrofloxacin (5 mg/kg every 12 hours intravenously)
and ampicillin (22 mg/kg every 8 hours Control Vomiting
intravenously) ■ No oral intake until 24 hours after vomiting has ceased
■ Gentamicina (2.2 mg/kg every 8 hours or 6.6 mg/kg ■ Choose one or more antiemetics:
every 24 hours intravenously) or amikacina (10 mg/kg ■ Metoclopramide (1–2 mg/kg over 24 hours in fluids)
every 12 hours or 20 mg/kg every 24 hours ■ Chlorpromazine (0.1 mg/kg every 4 to 6 hours
intravenously) and amoxicillin (15 mg/kg every 12 intravenously)
hours intravenously) ■ Ondansetron (0.1–0.15 mg/kg every 6 to 12 hours
■ Cefoxitin (25 mg/kg every 6 hours intravenously) intravenously )
■ For milder cases, choose one of the following:
■ Ampicillin (22 mg/kg every 8 hours intravenously) Immunotherapy
■ Cefazolin (20 mg/kg every 8 hours intravenously) ■ Antiendotoxin (4.4 mg/kg diluted 1:1 with fluids,
■ Trimethoprim-sulfadiazine (30 mg/kg every 12 hours administered over 30 to 60 minutes)
subcutaneously) ■ Hyperimmune serum (1.1–2.2 ml/kg intravenously or
subcutaneously)
Electrolyte Replacement
■ Recombinant granulocyte colony-stimulating factor
■ Monitor serum sodium and potassium
(5–10 µg/kg/day subcutaneously)
■ Expect hypokalemia after initial fluid replacement
■ Supplement fluids with potassium (14–20 mEq/L)
Nutrition
Increase Oncotic Pressure ■ Partial parenteral nutrition (3% amino acids, 5%
■ Give plasma if total solids <3.5 g/dl (10–20 ml/kg) dextrose in balanced electrolyte solution)
■ Give whole blood if patient is anemic ■ Early enteral diet
■ Give synthetic colloids (hetastarch) if patient is septic ■ Liquid diet (small amounts frequently)
and edematous (10–20 ml/kg over 24 hours) ■ Glutamine (0.5 g/kg/day in two divided doses in
drinking water)
a Should not be used in dehydrated animals. ■ Easily digestible recovery diet

ing and diarrhea is the cornerstone of treatment for ml/kg/hr may be necessary to restore perfusion. Animals
dogs with CPV enteritis and should be continued until in shock will have pale or muddy mucous membranes
oral intake is resumed. The initial fluid of choice is a and a slow capillary refill time. Fluid therapy should be
balanced electrolyte solution (e.g., lactated Ringer’s so- administered at a fairly rapid rate until mucous mem-
lution). These solutions mimic plasma electrolyte con- brane color becomes pinker and capillary refill time is re-
centrations, are isotonic, and can be given rapidly, if stored to 1 to 1.5 seconds. If circulatory collapse prevents
necessary, to replace acute fluid losses. venous access, fluids can be administered initially via a
The route and rate of initial fluid therapy varies with 20-gauge, 3.8-cm (1.5-inch) spinal needle placed into the
the patient. If CPV infection has resulted in hypovolemic intraosseous space in the shaft of the femur. Once circula-
shock, a rapid intravenous fluid bolus of up to 90 tion has improved with intraosseous fluids, an intra-

FLUID REPLACEMENT ■ SHOCK ■ CIRCULATORY COLLAPSE


The Compendium March 1997 Small Animal

venous catheter can be placed aise. 13 Serum potassium


for continued fluid therapy. should be monitored daily
Animals that are severely de- in these patients. If it is low,
hydrated or in a state of cir- potassium chloride should
culatory collapse cannot ab- be added to the fluids
sorb subcutaneous fluid (Table I). If potassium is in
because of peripheral vaso- the normal range, potassi-
constriction. Also, hypertonic um chloride (14 to 20
solutions should be avoided mEq/L) should be added to
in dehydrated patients. prevent the levels from
Animals that are dehy- dropping.
drated but not in shock Puppies with CPV enteri-
should be rehydrated over 4 tis often experience severe
hours. The amount of fluid Figure 3— Toy-breed puppies, such as this 9-week-old protein-losing enteropathy
given is estimated by the fol- pomeranian, are prone to hypoglycemia secondary to gas- because of destruction of
lowing formula: trointestinal disease and often require intravenous glucose the intestinal villi. If the al-
supplementation. bumin decreases below 1.5
Dehydration (%) × Body g/dl, the total protein de-
weight (kg) = Deficit (L) creases below 3.5 g/dl, or
the animal develops evidence of pitting edema, admin-
Maintenance requirements (2 to 3 ml/kg/hr) as well as istration of a colloidal fluid is indicated to maintain in-
continuing losses from vomiting and diarrhea must also travascular oncotic pressure.14
be taken into consideration during initial fluid therapy. If the puppy is anemic because of parasitism or gas-
trointestinal blood loss, a transfusion of whole blood
Maintenance Fluid Therapy (preferably from a recovered animal with a high CPV
Once perfusion has been restored, the fluid rate can antibody titer) is indicated. A dose of 10 to 20 ml/kg
be decreased to 4 to 6 ml/kg/hr for most patients. Hy- can safely be administered to most puppies over a 4-
dration should be monitored by evaluating mucous hour period. If the puppy is not anemic but is hy-
membrane color, capillary refill time, pulse quality, poproteinemic, a plasma transfusion (10 to 20 ml/kg
packed cell volume and total solids, urine output intravenously) should be administered through an in-
(which should be approximately 1 to 2 ml/kg/hr), and line filter over 2 to 4 hours. In addition to providing
urine specific gravity (which should range from 1.015 oncotic components, whole blood and plasma contain
to 1.020). Fluid therapy must be adjusted to replace antibodies and serum protease inhibitors that may help
continuing losses through vomiting and diarrhea. As neutralize circulating virus and control the systemic in-
fluid losses subside, the fluid rate is gradually tapered. flammatory response associated with the disease. Plas-
Many puppies, particular- ma and blood products are
ly toy breeds or those with TABLE I available though commer-
sepsis, are prone to hypo- Potassium Replacement cial blood banks.
glycemia as a result of CPV If natural colloids are un-
Potassium available, puppies with de-
enteritis (Figure 3). After re-
Chloride
hydration, 2.5% to 5% dex- Serum Added
creased total protein and
trose can be added to the Potassium to Fluid Maximum Infusion Rate a edema should receive a syn-
balanced electrolyte solution (mEq/L) (mEq/L) ml/lb/hr ml/kg/hr thetic colloid, such as heta-
(100 ml of 50% dextrose starch or dextran 70. To
added to 1 L will make a avoid potential volume
5% solution). 3.6–5.0 20 11 25 overload, the dosage of 20
Puppies with anorexia, 3.1–3.5 30 8 17 ml/kg/day should not be ex-
vomiting, and diarrhea are 2.6–3.0 40 5.5 12 ceeded; however, colloid in-
also prone to hypokalemia, 2.1–2.5 60 4 8 fusions can be repeated after
which can result in muscle <2.0 80 3 6 24 hours if needed.15 Col-
weakness, gastrointestinal loids can be given rapidly to
ileus, polyuria, cardiac ar- aSo as not to exceed 0.5 mEq/kg/hr. patients in shock or as a
rhythmia, and general mal- continuous infusion over 24

HYDRATION MAINTENANCE ■ COLLOIDS ■ TRANSFUSIONS


The Compendium March 1997 Small Animal

hours to more stable patients. General guidelines are to that can reduce vomiting by stimulating gastric empty-
supply one third of fluid needs as a colloid and two ing and inhibiting the chemoreceptor trigger zone.21
thirds as a crystalloid solution. The promotility effect may prevent gastric atony and
ileus from occurring in dogs with CPV infection.
Systemic Antibiotics Metoclopramide can be added to the intravenous fluids
Hemorrhagic diarrhea and mucosal sloughing are or administered as a constant-rate infusion of 1.0 to 2.0
commonly seen in dogs with CPV enteritis and indi- mg/kg over 24 hours.
cate breakdown of the gastrointestinal mucosal barrier, If metoclopramide is ineffective in controlling vomit-
which can lead to bacterial translocation, endotoxemia, ing, a more effective antiemetic is chlorpromazine.22
and sepsis.5,16 Severe neutropenia often coincides with This drug is a phenothiazine derivative and acts on the
the severe enteritis and contributes to the risk of sys- emetic center, the chemoreceptor trigger zone, and pe-
temic sepsis. For these reasons, intravenous broad-spec- ripheral receptors to reduce the vomiting reflex. The
trum, bactericidal antibiotics are indicated for severely recommended dosage is 0.1 mg/kg intravenously every
affected puppies.1 A combination of an aminoglycoside 4 to 6 hours or 0.2 to 0.5 mg/kg intramuscularly every
(gentamicin [2.2 mg/kg] or amikacin [10 mg/kg] every 6 to 8 hours, as needed. Phenothiazine derivatives can
8 hours) with a β-lactam antibiotic (ampicillin [2 cause hypotension and systemic vasodilatation through
mg/kg] or cefazolin [22 mg/kg] every 8 hours) provides their α-adrenergic blocking effect and should only be
excellent coverage against gram-negative and anaerobic given after the patient is well hydrated.22
bacteria that may originate from the gut.17 In dogs with intractable vomiting, metoclopramide
Aminoglycosides can cause acute renal failure and and chlorpromazine may be used together, but only
should only be administered after rehydration has been with caution because the potential for side effects may
accomplished.18 Once-a-day dosing of aminoglycosides increase. Dogs should be monitored for restlessness, hy-
may minimize renal damage while maximizing bacterial peractivity, bizarre behavior, or extreme drowsiness. If
kill because of high peak and low trough antibiotic con- any of these signs occur, antiemetic therapy should be
centrations.19 The high dose, however, should never be discontinued.
given to dehydrated patients. Urine sediment should be Intractable vomiting may respond to treatment with
monitored for proteinuria or renal tubule casts, which the new serotonin antagonist ondansetron HCl
would warrant discontinuation of aminoglycoside thera- (Zofran®, Glaxo Wellcome Inc) at dose of 0.1 to 0.15
py. mg/kg intravenously every 6 to 12 hours.23 Although
Enrofloxacin (5 mg/kg every 12 hours) is an alterna- the drug is highly effective and safe, it is also very ex-
tive to the aminoglycosides. It has an excellent gram- pensive.
negative spectrum but is not approved for intravenous Anticholinergic drugs should not be given to dogs
use and may cause cartilage abnormalities in young, with CPV enteritis because these drugs increase the po-
growing animals.20 We have not encountered any prob- tential for gastric atony, ileus, and intussusception of an
lems with enrofloxacin when it is diluted 1:1 with irritated bowel segment.22 Dogs with intractable vomit-
saline and administered slowly (intravenously) for a rel- ing should always be evaluated for foreign body ob-
atively short term (usually 3 to 5 days) in puppies with struction or intussusception. Other causes of continued
CPV enteritis. Rapid administration may cause vomit- vomiting include reflux esophagitis and acute pancre-
ing. atitis. Reflux esophagitis may be manifested by signs of
Mildly affected dogs with adequate white blood cell drooling, nausea, and exaggerated swallowing motions.
counts generally do not require combination antibiotic Treatment involves administration of a systemic antacid
therapy. Appropriate antibiotic choices include ampi- (famotidine [0.5 mg/kg] or ranitidine [5 mg/kg] intra-
cillin, first-generation cephalosporins, or trimetho- venously every 12 hours) and an oral suspension of su-
prim–sulfonamide in these patients. cralfate (1 g dissolved in 10 ml warm water, every 8
hours). Ideally, the antacid should be administered 1 to
Antiemetics 2 hours after the sucralfate.
Vomiting often decreases when oral intake of food
and fluid is discontinued; but in some patients, the Immunotherapy
problem persists and must be treated to reduce fluid Bacterial endotoxemia is believed to be an impor-
losses and increase patient comfort. tant factor in the terminal acute shock that occurs in
The two antiemetics most commonly used in dogs dogs with severe CPV enteritis. A polyvalent equine-
with CPV enteritis are metoclopramide and chlorpro- origin antiserum against LPS endotoxin is available
mazine. Metoclopramide is a gastric promotility drug for use in small animals (SEPTI-serum®—IMMVAC

BACTERICIDAL ANTIBIOTICS ■ ANTIEMETICS ■ ONDANSETRON


Small Animal The Compendium March 1997

Inc). In one study, the mortality rate for dogs with Recombinant Granulocyte
CPV enteritis treated conventionally was 48% (10 of Colony-Stimulating Factor
21 dogs) compared with 17% (5 of 30 dogs) for dogs Recently, the use of recombinant granulocyte colony-
that received antiendotoxin plus conventional treat- stimulating factor (rG-CSF) in dogs with leukopenia
ment.24 It is recommended that the product be ad- secondary to CPV enteritis has been described.31 The
ministered over 30 to 60 minutes at the dosage of 4.4 recommended dose is 5 to 10 µg/kg per day subcuta-
ml/kg and diluted 1:1 with intravenous crystalloid neously. Animals that respond generally show an in-
fluids.25 crease in white blood cell count within 24 hours. Un-
Antiendotoxin should be most effective if it is ad- fortunately, preliminary findings do not show an
ministered before antibiotic therapy because circulat- increased survivability associated with use of this prod-
ing plasma LPS concentrations can increase dramati- uct,32 and it is very expensive (approximately $130 to
cally after an antibiotic kills off gram-negative $150 to treat a puppy).
bacteria.26 Patients receiving equine-origin antiserum
must be observed closely during administration for Eradication of Intestinal Parasites
signs of anaphylaxis. If a second administration of an- Intestinal parasites can exacerbate CPV enteritis by
tiserum is deemed necessary, it should be given within enhancing intestinal cell turnover and subsequent viral
5 to 7 days after the initial treatment. After that time, replication.2 Fecal samples should be evaluated to iden-
a severe immunologic reaction is more likely to oc- tify coccidia, Giardia species, hookworms, round-
cur.27 worms, or whipworms. Appropriate oral therapy can be
Anecdotal reports describe the use of convalescent initiated as soon as vomiting ceases, or ivermectin (250
serum (1.1 to 2.2 ml/kg intravenously or subcuta- µg/kg subcutaneously) can be given–except to collies
neously) collected from dogs that have recovered and related breeds.
from CPV infection in an effort to provide passive
immunity to exposed or infected dogs.2,28 Research is Nutrition
needed to determine the efficacy and safety of this Dogs with severe CPV enteritis may have a pro-
practice. longed course of hospitalization and may require nutri-
tional support to prevent catabolism and immune dys-
Aggressive Adjunctive Treatments function associated with negative nitrogen balance.
Steroids and Flunixin Meglumine Partial parenteral nutrition (PPN) does not supply all
Corticosteroids and flunixin meglumine have shown of the patient’s nutrient needs but can provide short-
beneficial effects in animal models of septic and endo- term support for animals that are expected to recover
toxic shock if administered early in the shock state.29 soon. PPN solutions can be delivered through a periph-
Potential beneficial effects of corticosteroids include eral vein rather than through a large central vein.33
improved tissue perfusion, decreased leukocyte mar- These solutions are usually given at a maintenance dose
gination, enhanced membrane stabilization, and re- (60 ml/kg/day); additional fluid needs are met with
duced absorption of endotoxins. Flunixin meglumine is crystalloid solutions. A commercial product that con-
a potent nonsteroidal antiinflammatory analgesic that tains 3% amino acids, 3% glycerol, and electrolytes can
has antidiarrheal and antipyretic effects and that may be used. A PPN solution can be made by adding 300
reduce the severity of the intestinal inflammation asso- ml of 8.5% amino acid solution to 700 ml of lactated
ciated with CPV infection. Ringer’s solution with 5% dextrose. The addition of
Corticosteroids and flunixin meglumine can cause se- lipid emulsions is controversial. Although lipids are rich
vere gastrointestinal ulceration.30 Because of this possi- in calories, they have been associated with immunosup-
bility, we reserve use of these agents for animals exhibit- pression through impairment of reticuloendothelial
ing early signs of sepsis or endotoxemia: fever, function and white blood cell phagocytosis.34
tachycardia, injected or muddy mucous membranes, Partial parenteral nutrition solutions are hypertonic
and evidence of breakdown of the gastrointestinal mu- and therefore often cause phlebitis near the catheter
cosal barrier. These agents should not be administered site. Catheters must be placed aseptically and the site
until after the initial fluid bolus has been given. In se- monitored carefully for redness, swelling, or pain.35
lect cases, we use either dexamethasone sodium phos- Dextrose solutions should be tapered off gradually to
phate (2 to 4 mg/kg intravenously) or flunixin meglu- prevent rebound hypoglycemia.
mine (1 mg/kg intravenously). Repeated doses are not Most practitioners offer water after vomiting has
recommended because they increase the likelihood of ceased for 12 to 24 hours. Early enteral nutrition is im-
side effects. portant to promote intestinal regeneration. A liquid

ANTIENDOTOXIN ■ STEROIDS ■ FLUNIXIN MEGLUMINE ■ PPN


Small Animal The Compendium March 1997

diet can be offered initially, or a gruel can be made with of canine parvovirus DNA by the nested polymerase chain
an easily digestible, high-carbohydrate, low-fat diet. reaction. Vet Microbiol 41:135–145, 1994.
11. Schunk B, Kraft W, Truyen U: A simple touch-down poly-
The addition of glutamine powder (0.5 g/kg/day in merase chain reaction for the detection of canine parvovirus
two divided doses) to drinking water has been recom- and feline panleukopenia in feces. J Virol Methods 55:427–
mended to promote gastrointestinal healing in dogs re- 433, 1995.
covering from CPV enteritis.36 12. Senda M, Parrish CR, Harasawa R, Gamoh K: Detection by
Various commercial diets are formulated for animals PCR of wild type canine parvovirus which contaminates dog
vaccines. J Clin Microbiol 33:110–113, 1995.
that are recovering from gastrointestinal illness. Intesti- 13. DiBartola SP, Autran de Morais HS: Disorders of potassi-
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