History of Canine Parvovirus

History of Parvo

(CPV2) (more common form)

History of Canine Parvovirus

Canine Parvovirus is one of the most contagious and swift killing disease of dogs. Discovered in the late 1970s, but was not recognized until sometime in 1978 and spread worldwide sometime within a year or two. Dog parvo is very similar to feline panleukopennia (also a parvovius). They are 98% identical, differing only in two amino acids in the viral capsid protein VP2.The early belief was that the feline panleukopenia mutated into CPV2. It is possible that CPV2 is a mutant of an unidentified parvovirus (similar to feline parvovirus (FPV)) of some wild carnivore. A strain of CPV2b (strain FP84) has been shown to cause disease in a small percentage of domestic cats, although vaccination for FPV seems to be protective. CPV2, however, does not cause disease in cats and does so only mildly in mink and raccoons, and is a virus almost exclusively affecting canines.The origin of the canine parvovirus has not been established (http://en.wikipedia.org/wiki/Canine_parvovi

1st Case of Parvo Virus

Sharraqh Afghaans - First Confirmed Case of Parvo in the Midwest - 1979

After 8 years in the Breed (1979), Sharrah’s first litter experienced tragedy and became the first confirmed case of Canine Parvo virus (CPV) in the Midwest. Parvo emerged as an epidemic and tens of thousands of dogs died world wide. 

Read about what canine parvovirus is

What is Canine Parvovirus CPV

Canine parvovirus type 2 (CPV2, colloquially parvo) is a contagious virus mainly affecting dogs. The disease is highly contagious and is spread from dog to dog by direct or indirect contact with their feces. It can be especially severe in puppies that are not protected by maternal antibodies or vaccination. It has two distinct presentations, a cardiac and intestinal form. The common signs of the intestinal form are severe vomiting and dysentery. The cardiac form causes respiratory or cardiovascular failure in young puppies. Treatment often involves veterinary hospitalization. Vaccines can prevent this infection, but mortality can reach 91% in untreated cases. Canine parvovirus will not infect. It is also highly similar to mink enteritis, and the parvoviruses of raccoons and foxes. The early belief was that the feline panleukopenia mutated into CPV2. It is possible that CPV2 is a mutant of an unidentified parvovirus (similar to feline parvovirus (FPV)) of some wild carnivore. A strain of CPV2b (strain FP84) has been shown to cause disease in a small percentage of domestic cats, although vaccination for FPV seems to be protective. CPV2, however, does not cause disease in cats and does so only mildly in mink and raccoons, and is a virus almost exclusively affecting canines.

Two more strains of canine parvovirus CPV2a and CPV2b were identified in 1979 and 1984 respectively. Most cases of canine parvovirus infection are believed to be caused by these two strains, which have replaced the original strain, and the present day virus is different from the one originally discovered although they are indistinguishable by most routine tests. A third type, CPV2c (a Glu-426 mutant), has been discovered in Italy, Vietnam, and Spain

Read about Intestinal Form of Parvo

Intestinal form

Dogs become infected through oral contact with CPV2 in feces, infected soil, or fomites that carry the virus. Following ingestion, the virus replicates in the lymphoid tissue in the throat, and then spreads to the bloodstream. From there, the virus attacks rapidly dividing cells, notably those in the lymph nodes, intestinal crypts, and the bone marrow. There is depletion of lymphocytes in lymph nodes and necrosis and destruction of the intestinal crypts. Anaerobic bacteria that normally reside in the intestines can then cross into the bloodstream, a process known as translocation, and cause sepsis. The most common bacteria involved in severe cases are Clostridia, Campylobacter and salmonella species. This can lead to a syndrome known as Systemic inflammatory response syndrome(SIRS). SIRS leads to a range of complications such as hypercoagulability of the blood, endotoxaemia and acute respiratory distress syndrome(ARDS). Bacterial Myocarditis has also been reported secondarily to sepsis. Dogs with CPV are at risk of intussusception, a condition where part of the intestine prolapses into another part. Three to four days following infection, the virus is shed in the feces for up to three weeks, and the dog may remain an asymptomatic carrier and shed the virus periodically. The virus is usually more deadly if the host is concurrently infested with worms or other intestinal parasites

Read about the Cardiac Form

Cardiac form

This form is less common and affects puppies infected in the uterus or shortly after birth until about 8 weeks of age.The virus attacks the heart muscle and the puppy often dies suddenly or after a brief period of breathing difficulty. On the microscopic level, there are many points of necrosis of the heart muscle that are associated with mononuclear cellular infiltration. The formation of excess fibrous tissue (fibrosis) is often evident in surviving dogs. Myofibers are the site of viral replication within cells.The disease may or may not be accompanied with the signs and symptoms of the intestinal form. However, this form is now rarely seen due to widespread vaccination of breeding dogs.

Even less frequently, the disease may also lead to a generalized infection in neonates and cause lesions and viral replication and attack in other tissues other than the gastrointestinal tissues and heart, but also brain, liver, lungs, kidneys, and adrenal cortex. The lining of the blood vessels are also severely affected, which lead the lesions in this region to hemorrhage.

Read about Treatment

Treatment

Since the disease is a viral infection, there is no real cure for it. Treatment is focused on curing the symptoms and preventing secondary bacterial infections, preferably in a hospital environment. Intensive therapy and system support are the key to recovery. Intravenous fluid and nutrition therapy is crucial in maintaining a dog’s normal body fluid after severe diarrhea and dehydration, and protein and electrolyte levels will be monitored and regulated as necessary. Medications that may be used in the treatment include drugs to curb vomiting (antiemetics), H2 Blockers to reduce nausea, antibiotics, and anthelmintics to fight parasites. The survival rate in dogs is about 70 percent, but death may sometimes result from severe dehydration, a severe secondary bacterial infection, bacterial toxins in the blood, or a severe intestinal hemorrhage. Prognosis is lower for puppies, since they have a less developed immune system. It is common for a puppy that is infected with CPV to suffer shock, and sudden death.

Signs & Symptoms

Signs and symptoms

Dogs that develop the disease show symptoms of the illness within 5 to 10 days. The symptoms include lethargy, vomiting, fever, and diarrhea (usually bloody). Diarrhea and vomiting result in dehydration and secondary infections can set in. Due to dehydration, the dog's electrolyte balance can become critically affected. Because the normal intestinal lining is also compromised, blood and protein leak into the intestines leading to anemia and loss of protein, and endotoxins escaping into the bloodstream, causing endotoxemia. Dogs have a distinctive odor in the later stages of the infection. The white blood cell level falls, further weakening the dog. Any or all of these factors can lead to shock and death. The first sign of CPV is lethargy. Usually the second symptoms would be loss of appetite or diarrhea followed by vomiting.

The Diagnosis

Diagnosis

Diagnosis is made through detection of CPV2 in the feces by either an EIA or a hemagglutination test, or by electron microscopy. PCR has become available to diagnose CPV2, and can be used later in the disease when potentially less virus is being shed in the feces that may not be detectable by EIA. Clinically, the intestinal form of the infection can sometimes be confused with coronavirus or other forms of enteritis. Parvovirus, however, is more serious and the presence of bloody diarrhea, a low white blood cell count, and necrosis of the intestinal lining also point more towards parvovirus, especially in an unvaccinated dog. The cardiac form is typically easier to diagnose because the symptoms are distinct.

Treatment

Treatment

Survival rate depends on how quickly CPV is diagnosed, the age of the animal and how aggressive the treatment is. Treatment usually involves extensive hospitalization, due to the severe dehydration and damage to the intestines and bone marrow. A CPV test should be given as early as possible if CPV is suspected in order to begin early treatment and increase survival rate if the disease is found.

Treatment ideally also consists of crystalloid IV fluids and/or colloids, antinausea injections (antiemetics) such as metoclopramide, dolasetron, ondansetron and prochlorperazine, and antibiotic injections such as cefoxitin, metronidazole, timentin, or enrofloxacin. IV fluids are administered and antinausea and antibiotic injections are given subcutaneously, intramuscularly, or intravenously. The fluids are typically a mix of a sterile, balanced electrolyte solution, with an appropriate amount of B-complex vitamins, dextrose and potassium chloride. Analgesic medications such as buprenorphine are also used to counteract the intestinal discomfort caused by frequent bouts of diarrhea.

In addition to fluids given to achieve adequate rehydration, each time the puppy vomits or has diarrhea in a significant quantity, an equal amount of fluid is administered intravenously. The fluid requirements of a patient are determined by the animal's body weight, weight changes over time, degree of dehydration at presentation and surface area.

A blood plasma transfusion from a donor dog that has already survived CPV is sometimes used to provide passive immunity to the sick dog. Some veterinarians keep these dogs on site, or have frozen serum available. There have been no controlled studies regarding this treatment. Additionally, fresh frozen plasma and human albumin transfusions can help replace the extreme protein losses seen in severe cases and help assure adequate tissue healing.

Once the dog can keep fluids down, the IV fluids are gradually discontinued, and very bland food slowly introduced. Oral antibiotics are administered for a number of days depending on the white blood cell count and the patient's ability to fight off secondary infection. A puppy with minimal symptoms can recover in 2 or 3 days if the IV fluids are begun as soon as symptoms are noticed and the CPV test confirms the diagnosis. If more severe, depending on treatment, puppies can remain ill from 5 days up to 2 weeks. However, even with hospitalization, there is no guarantee that the dog will be cured and survive.

Prognosis

Prognosis

Untreated cases of CPV2 have a mortality rate approaching 91%. With aggressive therapy, survival rates may approach 80-95%. (a 20% to 5% mortality rate).

Prevention

Prevention

The best prevention you can take against CPV infection is to follow the correct protocol for vaccination. Young puppies should be vaccinated at six, nine, and twelve weeks, and should not be socialized with outside dogs until at least two weeks after their last vaccinations. High-risk breeds may require a longer initial vaccination period of up to 22 weeks.

Unconventional Treatments

 Unconventional treatments

There have been anecdotal reports of oseltamivir (Tamiflu) reducing disease severity and hospitalization time in canine parvovirus infection. The drug may limit the ability of the virus to invade the crypt cells of the small intestine and decrease gastrointestinal bacteria colonization and toxin production. Lastly, recombinant feline interferon omega (rFeIFN-ω), produced in silkworm larvae using a baculovirus vector, has been demonstrated by multiple studies to be an effective treatment.