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1.0: Introduction (not done) Canine Parvovirus (CPV), despite being thoroughly researched since its emergence in the late 1970s, is still one of the main causes of death in juvenile dogs. Vaccination is the best preventative measure, which is why it is essential(Summers, 2020). The virus mainly presents itself as clinical signs of gastroenteritis, hematochezia and emesis. (Altman et al., 2017) The high mortality rate is due to the high rate of vaccination failures. The main cause for these vaccine failures is the interference of materially derived antibodies in juvenile dogs. These antibodies inhibit immunity from the disease by neutralising antibodies produced by the vaccine, making juvenile dogs vulnerable (Decaro et al., 2020). The secondary cause for immunity failure is non-respondents to the vaccination. The immune systems of non-respondents do not generate antibodies after being introduced to the vaccine (How do Vaccines Work? 2018). There are different methods that are effective in overcoming the interference of maternally derived antibodies. However, they are not suitable for every case and are not always effective which makes full immunity and eradication of the virus unlikely. The scope of the report is to emphasise the importance of vaccination against CPV to specifically highlight the concern of immunisation failures. 2.0: Canine Parvovirus CPV is a disease that infects and inflames the intestine. It is one of the most resistant viruses known, and it can survive for years in contaminated environments. There are three prominent strains that circulate worldwide, and dogs can be coinfected with multiple strains at once. These three strains are termed CPV-2a, CPV-2b and CPV-2c (Altman et al., 2017). The best preventative measure is vaccination, which is crucial, as CPV can be fatal in most cases (Summers, 2020). Goddard and Leisewitz (2010); cited by Altman et al(2017), reports that prognosis when infected without treatment is only 9%. The most typical clinical signs are vomiting and hematochezia. CPV is most commonly spread through a faecal-oral route, so dogs with CPV should be strictly isolated, especially in kennels, veterinary practices or anywhere with other dogs. Isolation is critical, because even if the dogs associating with the infected dog have been vaccinated, this does not mean that it has been an effective course of vaccination. (Mokhtari et al., 2017) 3.0: Vaccinations The “aim of vaccination is to create a level of protective immunity to infection in an animal” (Day, 2012) from specific, possibly fatal diseases. All dogs should be vaccinated, especially if there are multiple dogs living together that can pass diseases from one another. Puppies need to be kept up to date with their vaccinations, as they have weaker, immature immune systems. All dogs should receive, no matter the circumstances or location, all core vaccines. Decaro et al., (2020) states that core vaccines protect dogs from globally distributed diseases that are fatal. The CPV vaccination is one of five core vaccines. For puppies, vaccinations should be started between six to eight weeks of age. The CPV vaccination, of the Nobivac range, requires a booster every 3 years (Hill,2006). 3.1: What Are Vaccinations? Vaccinations introduce the immune system to the antigen of specific viruses, meaning that when the real antigens enter the body, the immune system already knows how to fight them and already has antigens suited to attack the virus (How do Vaccines Work? 2018). The antigenic material introduced is in an inactivated, or harmless form, however it still initiates an immune response ( Aspinall and Cappello, 2020). The body's immune system will retain memory of how to fight off the disease the body is vaccinated against, which means that when the real pathogen enters the immune system it is recognised and The introduction of these antibodies “should mimic the natural response of the immune system” by initiating a humoral response (Day, 2012). Antigens are naturally produced by B lymphocytes when stimulated by a foreign or invading substance entering the body. The antibody combines with the antigen and neutralises it. (Aspinall and Cappello, 2020). 4.1: Vaccination Failures Although vaccination distribution is thorough and consistent, CPV still has one of the highest canine mortality rates, especially in juvenile dogs. As shown in Figure 1, this is mainly due to the development of non-respondents and maternally derived antibodies (MDA).Figure 1 highlights the main factors that contribute to vaccination failures. The thickness of the border is proportionate to the impact of the specific factor. This shows that maternal Immunity and non-responders are the two leading factors, with maternal immunity having the largest impact on the success of the vaccination. (Decaro et al., 2020) In Australia, they studied 1,451 dogs infected with CPV, 3.3% of these dogs that were infected had completed the full recommended vaccination course (Ling et al., 2012), meaning their immune systems did not respond typically to the vaccination. Non-respondents to the vaccination fail to retain the antigens in their blood, meaning their immune systems react to the disease the same way an unvaccinated dog would. (How do Vaccines Work? 2018) Figure 1- The causes of immunisation failures after the CPV vaccination (Decaro et al., 2020, pp.4) 4.2: Maternally Derived Antibodies Antibodies in puppies are mostly passed down from mother to neonate through colostrum, within the first 24 hours of birth, although some are also transferred through the placenta. Antibodies enter the bloodstream and defend the neonatal immune system until their immune systems are mature and can actively produce their own antibodies (Niewiesk, S, 2014). The amount of MDA present decreases overtime. After the administration of the CPV vaccination, the MDA can block active immunisation and interfere with the effectiveness of the vaccine by neutralising antibodies. This causes an immunity gap, which is the period of time in which the amount of MDA is too low to offer enough protection against CPV, whilst also blocking the vaccination from being effective by neutralising the antibodies created. This gap usually lasts 2-3 weeks, in which time the infants are vulnerable and can be infected with CPV. (Decaro et al., 2020) 4.3: Overcoming Maternal Antibody Interference There have been a few experiments done to test how different types of administration and vaccines can overcome the interference of MDA. Administering the vaccination intranasally and orally to the parental canine have been proven effective in reducing MDA interference in the neonates, however no CPV vaccine has been registered for approval to be administered this way. Additionally, administering the vaccines in this way is also less effective than the registered way of administration for the parent. Another method explored was the use of high-titre vaccines. High-titre vaccines are commercially available and are beneficial in overcoming MDA interference because they contain viral titres 2-3 logs higher than the traditional vaccine. This means that it contains more antigens of the disease than normal vaccinations. Therefore the quantity of MDA in the infant can not neutralise all of the antibodies in the vaccination, making the vaccination still effective and inducing an active immune response, meaning the infant should not be exposed to an immunity gap, resulting in supposedly effective vaccination. However, this requires serum collection, which gets delivered to specialised laboratory to await results that determine the levels of MDA in the blood. (Decaro et al., 2020) This is a long, costly process which is not yet refined or common practice