Canine parvovirus

Canine parvovirus (type 2) is a contagious virus mainly affecting dogs. The disease is highly infectious 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 vaccination. It has two distinct presentations, a cardiac and intestinal form. The common signs of the intestinal form are severe vomiting and severe haemorrhagic (bloody) diarrhea. 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.

There are two types of canine parvovirus called canine parvovirus type 1 CPV1) and canine parvovirus type 2 (CPV2). CPV2 causes the most serious disease and affects domesticated dogs and wild canids. There are variants of CPV2 called CPV-2a, CPV-2b and CPV-2c. Types 2a and 2b are distinct from the original CPV type 2 in terms of virulence and their ability to infect and cause disease in cats too. CPV-2c is a newly identified variant similar to 2b. The viral protein of 2c contains one amino acid different from CPV-2b but it is believed this could be significant. 2c strains have been identified in parts of Europe, the Americas and in Asia. Emergence of this strain has led to claims of ineffective vaccination of dogs, however studies have shown that the existing CPV vaccines still provide adequate levels of protection against CPV type 2c.

Prevention and decontamination

Prevention is the only way to ensure that a puppy or dog remains healthy since the disease is extremely virulent and contigious. The virus is extremely hardy and has been found to survive in feces and other organic material such as soil for over a year. It survives extremely cold and hot temperatures. The only household disinfectant that kills the virus is bleach.

Weaning puppies can be vaccinated with a modified live virus low passage high titer vaccine at 6 weeks of age, then every 3 to 4 weeks until 15 or 16 weeks. Puppies are initially protected through passive immunity derived from the mother. These maternal antibodies wear off before the puppy's immune system is mature enough to fight off CPV2 infection. Maternal antibodies also interfere with vaccination for CPV2 and can cause vaccine failure. Thus puppies are generally vaccinated in a series of shots, extending from the earliest time that the immunity derived from the mother wears off until after that passive immunity is definitely gone. Older puppies (16 weeks or older) are given 3 vaccinations 3 to 4 weeks apart. The duration of immunity of vaccines for CPV2 has been tested for all major vaccine manufacturers in the United States and has been found to be at least three years after the initial puppy series and a booster 1 year later.

A dog that successfully recovers from CPV2 sheds virus for a few days. Ongoing infection risk is primarily from faecal contamination of the environment due to the virus's ability to survive many months in the environment. Neighbours and family members with dogs should be notified of infected animals so that they can ensure that their dogs are vaccinated or tested for immunity. Vaccine will take up to 2 weeks to reach effective levels of immunity, the contagious individual should remain in quarantine until other animals are protected.

Treatment

Survival rate depends on how quickly CPV is diagnosed, the age of the animal and how aggressive the treatment is. Treatment for severe cases that are not caught early 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 consists of crystalloid IV fluids and/or colloids, antinausea injections (antiemetics) such as metoclopramide, dolasetron, ondansentron, 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 their body weight, weight changes over time, degree of dehydration at presentation and surface area. The hydration status is originally determined by assessment of clinical factors like tacky mucous membranes, concentration of the urine, sunken eyes, poor skin elasticity and bloodtests.

A blood plasmatransfusion 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. However, even with hospitalization, there is no guarantee that the dog will be cured and survive.

Unconventional treatments
There is no specific antiviral treatment for CPV. However, 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. There is also anecdotal evidence suggesting that colloidal silver is effective at treating CPV although currently regulatory authorities are discouraging its use due to potential toxicity issues and lack of demonstrated efficacy. 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.

Canine distemper

Canine distemper is a very serious viral disease affecting animals in the families Canidae, Mustelidae, Mephitidae, Hyaenidae, Airulidae, Procyonidae, Pinnipedae, some Viverridae and Ffelidae (though not domestic catsl; feline distemper or panleukopenia is a different virus exclusive to cats). It is most commonly associated with domestic animals such as dogs, although ferrets are also vaccinated for it. It is a single-stranded RNA virus of the family paramyxovirus, and thus a close relative of measles and rinderpest. Despite extensive vaccination in many regions, it remains a major disease of dogs.

Etymology

The origin of the word distemper is from the Middle Engglish distemperen, meaning to upset the balance of the humors, which is from the Old French destemprer, meaning to disturb, which is from the Vulgar Latin distemperare: Latin dis- and Latin temperare, meaning to not mix properly.

History

Although very similar to the measles virus, CDV seems to have appeared more recently, with the first case described in 1905 by French veterinarian Henri Carré. It was first thought to be related to the Plague and Typhus and resulted from several species of bacteria. It now affects all populations of domestic dog and some populations of wildlife. A vaccine was developed in 1950, yet due to limited use the virus remains prevalent in many populations. The domestic dog has largely been responsible for introducing canine distemper to previously unexposed wildlife and now causes a serious conservation threat to many species of carnivores and some species of marsupials. The virus contributed to the near-extinction of the black-footed ferret. It also may have played a considerable role in the extinction of the Tasmanian tiger and recurrently causes mortality among African Wild dogs. In 1991, the lion population in Serengeti, Tanzania experienced a 20% decline as a result of the disease. The disease has also mutated to form phocid distemper virus, which affects seals.

Infection

Puppies from three to six months old are particularly susceptible. Canine distemper virus (CDV) spreads through the aerosol droplets and through contact with infected bodily fluids including nasal and ocular secretions, feces, and urine 6-22 days after exposure. It can also be spread by food and water contaminated with these fluids. The time between infection and disease is 14 to 18 days, although there can be a fever from three to six days postinfection.

Canine distemper virus tends to orient its infection towards the lymphoid, epithelial, and nervous tissues. The virus initially replicates in the lymphatic tissue of the respiratory tract. The virus then enters the blood stream and infects the lymphatic tissue followed by respiratory, gastrointestinal, urogenital epithelium, the Central Nervous System, and optic nerves. Therefore, the typical pathologic features of canine distemper include lymphoid depletion (causing immunosuppression and leading to secondary infections), interstitial pneumonia, enchepalitis with demyelination, and hyperkeratosis of foot pads.

The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate where complications such as pneumonia and enchepalitis are more common. In older dogs that do develop distemper enchephalomyelitis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV.

Disease progression

The virus first appears in bronchial lymph nodes and tonsils two days after exposure. The virus then enters the blood stream on the second or third day. In older dogs that do develop distemper encephalomyetilis, vestibular disease may present. A first round of acute fever tends to begin around 3 to 8 days after infection which is often accompanied by a low white blood cell count, especially of lymphocytes as well as low platelet count. These signs may or may not be accompanied by anorexia, a runny nose, and discharge from the eye. This first round of fever typically recedes rapidly within 96 hours and then a second round of fever begins around the 11th or 12th day and lasts at least a week. Gastrointestinal and respiratory problems tend to follow which may become complicated with secondary bacterial infections. Inflammation of the brain and spinal cord otherwise known as encephalomyelitis is either associated with this, subsequently follows, or comes completely independent of these problems. A thickening of the footpads sometimes develops and vesicularpustular lesions on the abdomen usually develop. Neurological symptoms typically are found in the animals with thickened footpads from the virus. About half of sufferers experience meningoencephalomyelitis.

Gastrointestinal and respiratory symptoms

Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. When and if the neurological symptoms develop, urination and defecation may become involuntary.

Neurological Symptoms

The symptoms within the central nervous system include a localized involuntary twitching of muscles or groups of muscles, seizures often distinguished by salivation and jaw movements commonly described as “chewing gum fits.” As the condition progresses, the seizures worsen and the dog may fall to its side, exhibiting grand mal convulsions. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly it may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological symptoms may not come until several weeks or months later.Those that survive usually have a small tic or twitch of varying levels of severity. With time this tic will usually diminish.

Diagnosis

The above symptoms, especially fever, respiratory signs, neurological signs, and thickened footpads found in unvaccinated dogs strongly indicate canine distemper. However, several febrile diseases match many of the symptoms of the disease and only recently has differing between canine hepatitis, herpes virus, parainfluenza and leptospirosis been possible. Thus, finding the virus by various methods in the dog's conjunctival cells gives a definitive diagnosis. In older dogs that develop distemper encephalomyetilis, diagnosis may be more difficult since many of these dogs have an adequate vaccination history.

Treatment and prevention

There is no specific treatment for canine distemper. The dog should be treated by a veterinarian, usually with antibiotics for secondary bacterial infections, intravenous fluids, and nutritional supplements. The prognosis is poor. In, vitro, ribavirin, an antiviral effective in treating measles and other viruses, has also shown effective against Canine distemper virus by means of error catastrophe. More research is now needed in vivo.

There exist a number of vaccines against canine distemper for dogs and domestic ferrets, which in many jurisdictions are mandatory for pets. The type of vaccine should be approved for the type of animal being inoculated, or else the animal could actually contract the disease from the vaccine. A dog who has eaten meat infected with Rinderpest can also sometimes receive temporary immunity. Infected animals should be quarantined from other dogs for several months due to the length of time the animal may shed the virus. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20-25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris.

Canine distemper virus and Paget's disease

Paget's disease, a focal destructive disease of bone, has long suspected paramyxoviruses such as CDV, measles, respiratory syncytial virus, simian virus 5, and parainfluenza virus Type 3 as a culprit. Most studies, however, have pointed more directly at CDV and Measles. The virus detection technique in situ RT-PCR has shown CDV in 100% of Pagetic samples whereas other virus detection techniques have been less accurate