INDIVIDUAL TASK

Learning Unit 2
Anjing Diare Berdarah
BLOK 19 HEWAN KESAYANGAN 2

Created by :
Name
NIM
Group:

: Annisa Wening M. Putri

: 12/333996/KH/7453
:6

FACULTY OF VETERINARY MEDICINE

UNIVERSITY OF GADJAH MADA
YOGYAKARTA
2015
I.

LEARNING OBJECTIVE
1. 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.

DISCUSSION
1. The Pathogenesis and the Cinical Sign of Parvovirus
1.1.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
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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).

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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 Sign
a. Enteritis Form
There 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 Syndrome
The 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
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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 Parvovirus
2.1. Methods to Diagnose
a. 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. ELISA
Fortunately, 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-

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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 Diagnose
A differential diagnosis would include anticoagulant rodenticides, canine
bocavirus, intestinal parasites (particularly Blastocystis spp, Giardia

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intestinalis, Toxocara canis, Isospora spp, Trichuris vulpis) and hemorrhagic

gastroenteritis due to Clostridium spp.
a. Coronavirus
Coronavirus 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 Virus
Distemper 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. Rotavirus
The 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.

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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 Parvovirus
3.1.Treatment
There 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 Therapy
A 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),
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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-emetic
Anti-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 2adrenergic antagonists (e.g. chlorpromazine, prochlorperazine), D2dopaminergic 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).

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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 Plasma
Fresh 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
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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 Therapy
The 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. Potassium
If 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).

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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 Therapy
Antimicrobial 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 (AmikacinFresenius, 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 administered
to 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 therapy
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Patients 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. Nutrition
Early 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
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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 re3.2.

introduced after appetite and stool have returned to normal (Karen, 2014).
Prevention
a. 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

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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. 1 st 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
Jersey
Greene, C.E. 2012. Infectious Diseases of Dog and Cat. 4th ed. Saunders Elsevier, USA
Karen, M.2014. Successful Management Strategies for Canine Parvovirus. Ohio : The Ohio
State University
Lane, 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. Paris
Masson, G.1999.Pathogenesis of Canine Parvovirus.___: DVM News
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Nandi, 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) :
1366-1376
Quinn, 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, Iowa
Tilley, L.P., dan Smith, F.W.K., 2004. The 5-Minute Veterinary Consult Canine and Feline
Third Edition. Lippincott Williams & Wilkins: Philadelphia.

MEtoclopramid
The 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

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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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