Canine Parvovirus.
Effective understanding of diseases, their causes, possible prevention and treatment are key elements towards maintain a healthy community. Notably, the changing consumerism and lifestyle patterns have created a critical impetus towards intensified evaluation of extended effects of diseases causing pathogens. As Kahn (2005) explains, there is needed greater emphasis on viruses due to their expounded impacts. It is from this consideration that this paper evaluates Canine Parvovirus (CPV-2) to establish its historical orientation, its morphology, the resulting diseases and mechanisms employed to address it.
History and statistics of the Virus
Canine Parvovirus (CPV-2) is a virus that mostly infects dogs and other animals in the Canidae family. Though majority of biologists indicate that CPV-2 mutated from the CPV-1 which had been discovered previously in 1967, a second school of thought argue that it could have mutated from an unidentified carnivore (Truyen, 2006). Unlike the CPV-1 which was not seen to pose a great danger, CPV-2 strain was more aggressive with severe impacts. Following its discovery in 1968 in the United States, efforts to shield puppies turned out to be highly futile. As a result, the virus fast spread to other parts of the globe such as Vietnam, Italy, and the larger Asia. As Kahn (2005) explains, the exposure to different environments culminated to development of a second mutant, CPV-2a which turned out to be even more aggressive and resistant. Presently, CPV-2a and CPV-2b are the most recurrent strains and depict themselves in cardiac and intestinal infections where the affected animal shows signs of vomiting and diarrhea with stains of blood. Due to its fast spread, Truyen (2006) explains that the virus has been referred as one of the greatest threats to the canidae family especially the domesticated pets.
It is worth noting that there is an acute lack of recent statistics on the trends of CPV-2 in the globe. However, Miller and Kate (2009) explain that in the domestic setting, it mostly affects puppies within the age of six weeks to six months. Besides, the virus is very severe and causes death of approximately 80 of affected puppies if untreated. With effective and timely vaccination, Jim and Mark (2009) report that over 85 of the affected puppies could easily move out of danger. After the initial infection, the diseases incubation period is between 4-14 days with major symptoms being vomiting and diarrhea.
Morphology
CPV-2 as Nancy and Pat (2007) explain has a non-enveloped DNA virus with only a single strand and a diameter of between eighteen to twenty six nm (see diagram 1). Besides, it assumes an icosahedrol shape that has been engrossed with key caspids (a coating of protein surrounding the DNA). As Kahn (2005) explains, the casspids form a protective overlapping layer of proteins VP3, VP2 and VP3. Virologists indicate that this protective layer has been very crucial in the different strands development and mutation by providing a unique reactionary environment for new strands. Truyen (2006) explains that CPV-2 virus has continued to evolve with latter strains increasingly being dependent on the host and most importantly on the CPV-2 improved ability to bind with its tranferrin receptor. One peculiar notion of CPV-2 is that it has a high evolution rate which has been correlated to the high nucleotide rate of substitution. While prior studies indicated that CPV2 was common to all canids, the mutant CPV-2a and CPV-2b as Jim and Mark (2009) report have recently been eliminated from feline panleukopemia especially in big cats. Besides, Jim and Mark (2009) continue to report that recent studies in Vietnam indicate CPV-2 have the ability to undergo small antigenic model shifts to even infect felids. In cats, CPV-2 has been reported to mutate faster compared to dogs.
Diagram 1 Canine parvovirus crystallography (Truyen, 2006)
Infections caused by CPV-2
Intestinal CPV-2
CPV-2 causes two major infections to the affected animal. To begin with, the intestinal CPV-2 is reported when the animal is infected via mouth contact either with formites, feces or soil that is infected with CPV-2 viruses (Miller and Kate, 2009). Miller and Kate (2009) continue to say that the ingested virus moves to the lymphatic tissues of the thorax where it replicates before spreading to the main blood stream. The fast spreading virus further continues to multiply in the bone marrow, crypts of the intestine and lymph nodes. The immediate resultant of this multiplication is inherent lymphocytes weakening and crypts destruction in the intestine (Nancy and Pat, 200). At this stage, most of the bacteria that reside in the intestine get into the blood stream when SIRS (Systemic Inflammation Response Syndrome is reported) is reached. At advanced stage, SIRS results to other complications like endotaxemia and section of the infected animals intestine may prolapse and the virus appears in the feces when the animal either dies or remains a carrier.
Cardiac CPV-2
As indicated earlier, after CPV-2 has infected an animal, the subsequent replication leads to the virus spreading through out the body including the reproductive system. Cardiac CPV-2 therefore is a disease where puppies get the infection mainly in the uterus or about eight weeks after birth (Kahn, 2005). Unlike the Intestinal CPV-2, cardiac VPV-2 attacks the infected puppies heart muscles before experiencing breathing difficulty that result to death within a short period of time. In cardiac CPV-2, the virus forms myofibrils where it replicates and spreads to other parts of the body. As - Kahn (2005) continues to say, cardiac CPV-2 is uncommon mainly because the fact that affected animals often die reducing the possibility of passing the infection to the unborn.
Infection in the Uterus has at times been considered a separate form of CPV-2 and takes place when an animal is infected by the virus during pregnancy. Though most animals develop immunity, the virus could have passed and reached the fetus. In such cases the puppies are born with key neurological abnormalities (Kahn, 2005).
Treatment of the disease
Hospitalization and use of drugs
According to Jim and Mark (2009), the treatment of the disease is largely dependent on the ability to detect it early and the actual thoroughness of employed treatment. Notably, hospitalization is often required for animals whose infection is noted at progressive stages. Therefore, as Miller and Kate (2009) explain, CPV-2 treatment involves administration of colloids antiemetics such as dolasetron and injections with antibiotics such as enrofloxacin. While the antibiotics are used to suppress the virus replication in the body, analgesic treatment greatly helps to reduce the intestinal discomfort resulting from increased diarrhea.
Maintaining the body fluids
In addition to that, Truyen (2006) explains that fluids to counteract dehydration must further be balanced with their overall body mass lost during the infection. At this point, veterinary specialists explain that in severe cases, the fluids should be provided using a drip to facilitate direct absorption into the animal circulatory system. In addition, Jim and Mark (2009) argue that stress imposed by resulting disease stress often lowers the puppies blood sugar and should be counteracted by adding dextrose to the drip.
Blood plasma transfer
According to Truyen (2006), the suffering animal could also receive blood plasma transfusion taken from another animal that had successfully survived CPV-2 to boost their immunity against the virus. This is perhaps one of the best methods that are developing for treatment of the disease. However, it is very costly and many people have often preferred the less costly methods for their animals.
Conventional treatment
Currently, use of unconventional treatment like oseltamivir as Jim and Mark (2009) explain, is fast becoming popular among many vets in that it greatly reduces the overall severity of the disease and period required for hospitalization. While the method is indicated to be in its advanced research stages, analysts indicate that this drug has the ability to limit CPV-2 from invading the intestinal crypt cells and further inhibiting toxin production and colonization of intestinal bacteria.
While veterinary authorities have remained skeptical about use of colloidal silver in addressing the virus related infections due for lack of clear documented efficiency , Kahn (2005) claims that that using this drug has the ability to raise the current survival rate of 80 for all the treated cases to 90. It is critical that feeding is restarted gradually as the intestine regains its normal functioning after suppressing the virus to facilitate greater development of the body immunity (Miller and Kate, 2009)
Prevention
Vaccination
Prevention has been considered as one of the most effective method of controlling the occurrence of CPV-2 and its resilience in any region. Immediately after the first strain of the disease was discovered, veterinaries managed to contain it through vaccination. Vaccination as Yuyuan (2008) explains facilitates the ability of the risk animals to develop resistant immunity towards the causative virus. Puppies should be vaccinated at the earliest possible instance to boost their mothers derived immunity. In the United States, animals at risk are vaccinated every year to prevent the resilience of this highly contagious disease. However, veterinaries further advice that it is indeed very critical that effective observation is also maintained to cite possible symptoms of the disease and therefore inform a medical specialist for assessment of possible resistance by the virus (Nancy and Pat, 2007).
Decontamination
Earlier on, it became evident that the immediate surrounding of at risk animals is the main source of the virus for infection to occur. As a result, all equipments used by the animal and its area of the residence should be kept clean and regularly decontaminated to reduce the chances of coming into contact with the virus (Jim and Mark, 2009).
Isolation.
After an animal is noted to have the symptoms of the disease, it is crucial to isolate it and therefore reduce the chances of infecting others. Particularly, Miller and Kate (2009) indicate that special observation should always be provided and infected animals treated before returning them to live together with others.
It is from the above discussion that this paper concludes by supporting the thesis statement effective understanding of diseases, their causes, possible prevention and treatment are key elements towards maintain a healthy community. CPV-2came out as a highly dangerous disease and that is fast undergoing key mutation to develop new strains. It is therefore critical that people emphasize on preventing the disease while seeking early treatment for the affected animals.
History and statistics of the Virus
Canine Parvovirus (CPV-2) is a virus that mostly infects dogs and other animals in the Canidae family. Though majority of biologists indicate that CPV-2 mutated from the CPV-1 which had been discovered previously in 1967, a second school of thought argue that it could have mutated from an unidentified carnivore (Truyen, 2006). Unlike the CPV-1 which was not seen to pose a great danger, CPV-2 strain was more aggressive with severe impacts. Following its discovery in 1968 in the United States, efforts to shield puppies turned out to be highly futile. As a result, the virus fast spread to other parts of the globe such as Vietnam, Italy, and the larger Asia. As Kahn (2005) explains, the exposure to different environments culminated to development of a second mutant, CPV-2a which turned out to be even more aggressive and resistant. Presently, CPV-2a and CPV-2b are the most recurrent strains and depict themselves in cardiac and intestinal infections where the affected animal shows signs of vomiting and diarrhea with stains of blood. Due to its fast spread, Truyen (2006) explains that the virus has been referred as one of the greatest threats to the canidae family especially the domesticated pets.
It is worth noting that there is an acute lack of recent statistics on the trends of CPV-2 in the globe. However, Miller and Kate (2009) explain that in the domestic setting, it mostly affects puppies within the age of six weeks to six months. Besides, the virus is very severe and causes death of approximately 80 of affected puppies if untreated. With effective and timely vaccination, Jim and Mark (2009) report that over 85 of the affected puppies could easily move out of danger. After the initial infection, the diseases incubation period is between 4-14 days with major symptoms being vomiting and diarrhea.
Morphology
CPV-2 as Nancy and Pat (2007) explain has a non-enveloped DNA virus with only a single strand and a diameter of between eighteen to twenty six nm (see diagram 1). Besides, it assumes an icosahedrol shape that has been engrossed with key caspids (a coating of protein surrounding the DNA). As Kahn (2005) explains, the casspids form a protective overlapping layer of proteins VP3, VP2 and VP3. Virologists indicate that this protective layer has been very crucial in the different strands development and mutation by providing a unique reactionary environment for new strands. Truyen (2006) explains that CPV-2 virus has continued to evolve with latter strains increasingly being dependent on the host and most importantly on the CPV-2 improved ability to bind with its tranferrin receptor. One peculiar notion of CPV-2 is that it has a high evolution rate which has been correlated to the high nucleotide rate of substitution. While prior studies indicated that CPV2 was common to all canids, the mutant CPV-2a and CPV-2b as Jim and Mark (2009) report have recently been eliminated from feline panleukopemia especially in big cats. Besides, Jim and Mark (2009) continue to report that recent studies in Vietnam indicate CPV-2 have the ability to undergo small antigenic model shifts to even infect felids. In cats, CPV-2 has been reported to mutate faster compared to dogs.
Diagram 1 Canine parvovirus crystallography (Truyen, 2006)
Infections caused by CPV-2
Intestinal CPV-2
CPV-2 causes two major infections to the affected animal. To begin with, the intestinal CPV-2 is reported when the animal is infected via mouth contact either with formites, feces or soil that is infected with CPV-2 viruses (Miller and Kate, 2009). Miller and Kate (2009) continue to say that the ingested virus moves to the lymphatic tissues of the thorax where it replicates before spreading to the main blood stream. The fast spreading virus further continues to multiply in the bone marrow, crypts of the intestine and lymph nodes. The immediate resultant of this multiplication is inherent lymphocytes weakening and crypts destruction in the intestine (Nancy and Pat, 200). At this stage, most of the bacteria that reside in the intestine get into the blood stream when SIRS (Systemic Inflammation Response Syndrome is reported) is reached. At advanced stage, SIRS results to other complications like endotaxemia and section of the infected animals intestine may prolapse and the virus appears in the feces when the animal either dies or remains a carrier.
Cardiac CPV-2
As indicated earlier, after CPV-2 has infected an animal, the subsequent replication leads to the virus spreading through out the body including the reproductive system. Cardiac CPV-2 therefore is a disease where puppies get the infection mainly in the uterus or about eight weeks after birth (Kahn, 2005). Unlike the Intestinal CPV-2, cardiac VPV-2 attacks the infected puppies heart muscles before experiencing breathing difficulty that result to death within a short period of time. In cardiac CPV-2, the virus forms myofibrils where it replicates and spreads to other parts of the body. As - Kahn (2005) continues to say, cardiac CPV-2 is uncommon mainly because the fact that affected animals often die reducing the possibility of passing the infection to the unborn.
Infection in the Uterus has at times been considered a separate form of CPV-2 and takes place when an animal is infected by the virus during pregnancy. Though most animals develop immunity, the virus could have passed and reached the fetus. In such cases the puppies are born with key neurological abnormalities (Kahn, 2005).
Treatment of the disease
Hospitalization and use of drugs
According to Jim and Mark (2009), the treatment of the disease is largely dependent on the ability to detect it early and the actual thoroughness of employed treatment. Notably, hospitalization is often required for animals whose infection is noted at progressive stages. Therefore, as Miller and Kate (2009) explain, CPV-2 treatment involves administration of colloids antiemetics such as dolasetron and injections with antibiotics such as enrofloxacin. While the antibiotics are used to suppress the virus replication in the body, analgesic treatment greatly helps to reduce the intestinal discomfort resulting from increased diarrhea.
Maintaining the body fluids
In addition to that, Truyen (2006) explains that fluids to counteract dehydration must further be balanced with their overall body mass lost during the infection. At this point, veterinary specialists explain that in severe cases, the fluids should be provided using a drip to facilitate direct absorption into the animal circulatory system. In addition, Jim and Mark (2009) argue that stress imposed by resulting disease stress often lowers the puppies blood sugar and should be counteracted by adding dextrose to the drip.
Blood plasma transfer
According to Truyen (2006), the suffering animal could also receive blood plasma transfusion taken from another animal that had successfully survived CPV-2 to boost their immunity against the virus. This is perhaps one of the best methods that are developing for treatment of the disease. However, it is very costly and many people have often preferred the less costly methods for their animals.
Conventional treatment
Currently, use of unconventional treatment like oseltamivir as Jim and Mark (2009) explain, is fast becoming popular among many vets in that it greatly reduces the overall severity of the disease and period required for hospitalization. While the method is indicated to be in its advanced research stages, analysts indicate that this drug has the ability to limit CPV-2 from invading the intestinal crypt cells and further inhibiting toxin production and colonization of intestinal bacteria.
While veterinary authorities have remained skeptical about use of colloidal silver in addressing the virus related infections due for lack of clear documented efficiency , Kahn (2005) claims that that using this drug has the ability to raise the current survival rate of 80 for all the treated cases to 90. It is critical that feeding is restarted gradually as the intestine regains its normal functioning after suppressing the virus to facilitate greater development of the body immunity (Miller and Kate, 2009)
Prevention
Vaccination
Prevention has been considered as one of the most effective method of controlling the occurrence of CPV-2 and its resilience in any region. Immediately after the first strain of the disease was discovered, veterinaries managed to contain it through vaccination. Vaccination as Yuyuan (2008) explains facilitates the ability of the risk animals to develop resistant immunity towards the causative virus. Puppies should be vaccinated at the earliest possible instance to boost their mothers derived immunity. In the United States, animals at risk are vaccinated every year to prevent the resilience of this highly contagious disease. However, veterinaries further advice that it is indeed very critical that effective observation is also maintained to cite possible symptoms of the disease and therefore inform a medical specialist for assessment of possible resistance by the virus (Nancy and Pat, 2007).
Decontamination
Earlier on, it became evident that the immediate surrounding of at risk animals is the main source of the virus for infection to occur. As a result, all equipments used by the animal and its area of the residence should be kept clean and regularly decontaminated to reduce the chances of coming into contact with the virus (Jim and Mark, 2009).
Isolation.
After an animal is noted to have the symptoms of the disease, it is crucial to isolate it and therefore reduce the chances of infecting others. Particularly, Miller and Kate (2009) indicate that special observation should always be provided and infected animals treated before returning them to live together with others.
It is from the above discussion that this paper concludes by supporting the thesis statement effective understanding of diseases, their causes, possible prevention and treatment are key elements towards maintain a healthy community. CPV-2came out as a highly dangerous disease and that is fast undergoing key mutation to develop new strains. It is therefore critical that people emphasize on preventing the disease while seeking early treatment for the affected animals.
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