Parvo virus in dog | Prevention | Treatment
Canine parvovirus-2 (CPV) is pathogenic virus that
causes myocarditis and acute hemorrhagic enteritis in dogs. It is fatal and
contagious disease. It was first discovered in 1997. Its frequent mortality up
to 10%. CPV has originated from mutation of feline panleukopenia virus (FPV)
and then adapt to mink and foxes from dogs.
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| Parvo Virus in dogs: Transmission, prevention and Control |
Incidence
Canine parvovirus infection occurs in members of the
dog family worldwide. It is greater in animal shelters, pet stores, and
breeding kennels. CPV can affect dogs at any age. The crossbreds are less vulnerable
in comparison to pure breeds like Rottweilers, Doberman Pinchers, English
Springer Spaniels and German Shepherd. CPV affects only dogs, and cannot be
transmitted to humans or other species. Most puppies die without medical
treatment. The CPV infection is more dangerous in young puppies. All infected
dogs may not exhibit clinical manifestations.
The different antigenic variants of CPV-2 are prevalent
in different countries.
Transmission/Spread
Canine parvovirus spreads through oral contact with infected feces or contaminated surfaces (e.g., soil, shoes, dog toys etc.). The source of CPV infection is fecal waste from infected dogs. It has been diagnosed wherever in dog shows, obedience trials, breeding and boarding kennels, pet shops, animal shelters, parks and playgrounds. Dogs that are confined to a house or yard and are not in contact with other dogs have much less chance of exposure to CPV. It’s easily transmitted via the hair or feet of infected dogs and also by contaminated objects such as cages or shoes. CPV is hardy and can remain in feces-contaminated ground. The feces of infected dogs contaminate the places such as Veterinary hospitals, pet shops, boarding kennels and commercial breeding establishments. These contaminated premises serve as source of secondary infection to the susceptible canine population.
Pathogenesis
The virus enters the body by the mouth as the puppy
cleans itself or eats food off the ground or floor. There is a 3–7 day
incubation period before the puppy seems obviously ill. Upon entering into the
body, it replicates to large numbers in the lymph nodes. After a couple of
days, significant amounts of virus have been released free into the bloodstream.
Over the next 3–4 days, the viruses go to new organs containing the
rapidly dividing cells like the bone marrow and the delicate intestinal cells
and form large eosinophilic intranuclear inclusion bodies. Within the bone
marrow, the virus is responsible for destruction of young cells of the immune
system and then knocking out the body’s best defense mechanism. The virus
causes most devastating effects in the gastro-intestinal tract. Canine
parvoviral infections are characterized by a drop in white blood cell count due
to the bone marrow infection.
It is in the GI tract where the heaviest damage occurs. The normal intestine possesses little finger-like protrusions called “villi.” Having these tiny fingers greatly increases the surface area available for the absorption of fluid and nutrients. To make the surface area available for absorption, the villi possess “microvilli” which are microscopic protrusions. The cells of the villi are relatively short-lived and are hurriedly replaced by new cells. The source of the new cells is the rapidly dividing area at the foot of the villi called the Crypts of Lieberkuhn. It is right at the crypt where the parvovirus strikes. Without new cells coming from the crypt, the villus becomes blunted and unable to absorb nutrients and diarrhea results. The barrier separating the digestive bacteria from the blood stream breaks down. The diarrhea becomes bloody and bacteria can enter the body causing widespread infection. The virus kills one of two ways, diarrhea and vomiting lead to extreme fluid loss and dehydration until shock and death result. Loss of the intestinal barrier allows bacterial invasion of potentially the entire body.
Symptoms
of Canine Parvovirus
Diarrhea occurs in dogs of any age. Early symptoms
are depression, loss of appetite, vomiting, 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 vomiting 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 3 days after
onset of symptoms. The course of illness is also highly variable depending on
the infectious dose of the virus and clinical signs usually develop from 3 to
5 days following infection and typically persist for 5–7 days. The
morbidity and mortality vary according to the age of the animals, the severity
of challenge and the presence of intercurrent disease problems. Puppies can die
suddenly of shock as early as 2 days into the illness.
The second form of CPV is cardiac syndrome, or
myocarditis, which can affect puppies under 3 months old. Within an
infected litter, 70% pups will die in heart failure by 8 weeks of age and
the remaining 30% will have pathological changes which may result in death many
months or even years later. The most dramatic manifestation of CPV-2
myocarditis is the sudden death in young pups usually about 4 weeks of age.
The collapsed dying pup may have cold, pale mucosae and show gasping
respiration or terminal convulsions. Acute heart failure with respiratory
distress occurs in pups between 4 and 8 weeks of age. Subacute heart
failure occurs in older pups usually 8 weeks or more. They are tachypneic
or dyspneic especially on exercise. The abdomen is swollen with hepatomegaly
and ascitic fluid is blood tinged. There is tachycardia, sometimes with
arrhythmias and a weak pulse. Most animals die by cardiogenic shock. However,
if the animal survives it will suffer from chronic myocardial and circulatory
complications. There is no diarrhea because the virus multiplies rapidly in
muscle cells of the immature heart.
Pathological
Changes
The pathological changes produced by CPV reflect the
requirement of the virus for dividing cells. The macroscopic lesions of CPV
infection are highly variable and relatively non-specific. In the enteric
disease, lesions may be distributed segmentally in the gastrointestinal tract.
The lesions usually affect the jejunum and ileum but not the duodenum and
colon. Affected segments may be somewhat flaccid with sub serosal hemorrhage or
congestion. The mucosal surface is often congested but devoid of exudates.
Mesenteric lymph nodes are frequently enlarged and edematous. Multifocal
petechial hemorrhages are often seen within the cortex of a cut section of
affected lymph nodes during acute stage of the disease and leucopenia is also
common. Thymic cortical necrosis and atrophy are common findings in young dogs.
In cases of parvoviral myocarditis, gross lesions
include cardiac enlargement with prominent dilatation of the left atrium and
ventricle. The lungs often do not collapse when cut although white frothy fluid
may be present in the trachea and bronchi. Evidence of pulmonary edema and
passive congestion of the liver is often present, with the variable degree of
ascites and pleural effusion. The ventricular myocardium frequently contains
visible white streaks associated with the presence of a cellular infiltrate.
Some pups may die from chronic decompensating left sided heart failure weeks or
months after some of their littermates died suddenly with acute myocarditis.
Pulmonary hypertension and myocardial dilation with scarring is often regarded
as the cause of delayed death.
Histopathology
Microscopic lesions relate with CPV infection are
initially confined to areas of proliferating cell population. In the enteric
form of the disease, the early lesions consist of necrosis of the crypt
epithelial cells. Crypt lumenae are often dilated, lined by attenuated
epithelium and filled with necrotic debris. There are intranuclear eosinophilic
inclusion bodies in intact crypt epithelial cells. The villi and lamina propria
may merge as a result of the loss of crypt epithelium and the failure to
replace sloughed villous epithelial cells. These lesions are extensive. Loss of
digestive epithelium and absorptive surface area presumably results in
diarrhea cause by combined effect of maldigestion and malabsorption. Death may
consider as a result of dehydration, electrolyte imbalance, endotoxic shock or
secondary septicemia.
The regeneration of intestinal epithelial cells has
been observed. The remaining intestinal crypts are lined by hyperplastic epithelium.
The shortened villi are layred by new epithelial cells and adjacent villi are
often fused. Necrosis and depletion of small lymphocytes is observed in Peyer’s
patches, the germinal centers of mesenteric lymph nodes, and in splenic nodules
first in infection. Diffuse cortical necrosis of neck occurs in young dogs,
with a related loss in thymic mass. There is regenerative lymphoid hyperplasia
later in this disease.
Canine
Parvovirus Variants in Wild Animals
CPV-2 is related to FPV more than 98% genome homology.
The biological effects of these few genomic changes were enormous, in that
CPV-2 acquired the canine host range, but lost the ability to replicate in cats.
The host ranges of CPV-2 and FPV are complex and differ in vitro and in vivo.
FPV replicates in feline cells in vitro and in cats in vivo, but does not
infect canine cells in vitro and shows only a restricted tissue spectrum in
vivo. CPV-2 does make its copy in canine and feline cells in vitro, but the in
vivo replication is restricted to canides. No feline host has ever been
described to be susceptible to CPV-2, although it replicates to low titers in
mink which is a mustelid, after experimental inoculation. CPV spread to most
populations of domestic and wild carnivores. In 1976, reports from Belgium and
the Netherlands observed that the virus had dispersed throughout the world
infecting wild and domestic canids. Clinical signs of parvovirus disease were
observed in captive and free-ranging coyotes and DNA sequence analysis of the
VP2 gene showed the virus to be CPV-2. Raccoons, in contrast, were shown to be
resistant to CPV-2 infection.
Serologic prevalence, infection or clinical signs of
disease due to CPV viruses were found in jackals (Canis aureus, Canis
adustus, Canis mesomelas), grey foxes (Urocyon littoralis), the San
Joaquin kit fox, Asiatic raccoon dogs (Nyctereutes procyonoides) and the crab
eating fox (Cerdocyon thous) in the Kenya. Canine parvovirus infections were
reported in farmed raccoon dogs and confirmed to be CPV-2 by DNA sequence analysis
of the VP2 gene. CPV-2a and CPV-2b DNA sequences were recovered from six of
nine cheetahs, as well as from one Siberian tiger, all showing clinical symptoms
of parvovirus disease. The very high prevalence of CPV-2a/2b infections in
large cats compared to domestic cats may suggest a higher susceptibility of the
species for these virus types. Since vaccination of domestic cats and dogs is
very effective in preventing disease, parvovirus vaccination of all domestic
and non-domestic carnivores at risk of infection is highly recommended. CPV-2c
type viruses have been isolated from leopard cats but not from domestic cats in
the same area. Phylogenetic analysis indicated that CPV-2c(a) and CPV-2c(b)
have been evolved from CPV-2a and CPV-2b to adapt to leopard cats and lost
neutralizing epitopes compared to former serotypes CPV-2a and CPV-2b.
Diagnosis
The diagnostic tests of this disease are HA
(Haemagglutination), Electron Microscopy (EM), virus isolation using in MDCK,
CRFK or A 72 cell line , Enzyme Linked Immunosorbent Assay (ELISA), Latex
Agglutination Test (LAT), Fluorescent Antibody Test (FAT), CIE test, Virus
neutralization test, PCR and RE digestion , real time PCR, loop-mediated isothermal
amplification (LAMP), nucleic acid hybridization or dot blot, in situ
hybridization, nucleic acid sequencing etc, but they have different stage of
sensitivity and specificity and sometimes yielding false positive cases.
Prevention
and Control
This virus is hardy in the environment. It is able to overcome winter freezing temperatures in the ground outdoors and many household disinfectants are not capable of killing it indoors. Infected dogs shed virus in their stool during the 2 weeks. A typical/average infectious dose for an unvaccinated dog is 1000 viral particles. An infected dog sheds 35 million viral particles per ounce of stool. Shaded areas should be considered contaminated for 7 months. Areas with sunlight should be considered contaminated for 5 months. Most disinfectants cannot kill it, chlorine bleach is quite effective.
There is no way to completely disinfect contaminated
dirt and grass, commonly sunlight and drying has some effect. Mechanical
decontamination by irrigation may be helpful, but the area must be allowed to
dry. Potassium peroxymonosulfate has good activity in the face of organic
matter, and can be sprayed on contaminated areas using a pesticide sprayer.
According to the American Veterinary Medical Association, 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.