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Canine Parvovirus

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Canine Parvovirus 1 CE Credit Canine Parvovirus Brandy Tabor, CVT, VTS (ECC) very sick 4-month-old puppy presents at your veterinary is first vaccinated, the bitch’s antibody titer may still be high clinic. The owner reports acute onset of vomiting and enough to interfere with the immune response but too low for A bloody, foul-smelling diarrhea. When the owner mentions protection.2 This leaves the puppy susceptible for a period of time that the puppy has not been vaccinated, an “alarm sounds” in your because neither the bitch’s antibodies nor the immune response mind. You hope that the puppy is not infected with parvovirus. to the CPV-2 vaccine is enough to prevent infection.2 Canine parvovirus (CPV) is one of the most common infectious CPV-2 is most commonly spread via the fecal–oral route, diseases in unvaccinated dogs younger than 6 months.1 Without although it can also be spread through the fecal–nasal route.1 After treatment of CPV infection, the mortality rate can be as high as the virus is ingested, it replicates in the oropharynx, thymus, and 91%; with aggressive treatment, the mortality rate drops to 4% to mesenteric lymph nodes for 2 days.1,2 The virus then moves into 48%.2 Understanding the pathophysiology of CPV infection is the blood, and marked viremia develops within 1 to 5 days after important for enabling veterinary technicians to provide prompt exposure.1 The virus reaches the intestinal crypts via the blood.1,6 treatment and adequate patient care. Viral shedding begins on day 3 and continues for 7 to 10 days.1 Etiology, Epidemiology, and Transmission Normal Physiology and the Effects of Infection Most viruses create disease by causing degeneration of the cells in Parvovirus attacks rapidly dividing cells such as those in the lym- which they replicate.3 Viruses contain genetic material in the form phoid tissue, thymus, intestinal epithelium, bone marrow, and of RNA or DNA, which produces viral material such as enzymes heart. Reviewing the normal physiology of the systems affected and proteins.3 During viral replication, virions accumulate, causing by CPV-2 infection is helpful for understanding how the infection cells to swell.3 The integrity of the cell membrane is disrupted, affects patients. causing the cell to lyse or become necrotic, both of which result in the release of new virions into the lymph and blood.3 The Thymus, Bone Marrow, death of infected cells, in addition to inflammatory and other Lymph Nodes, Liver, Key Points responses provoked by the virus, causes clinical signs.3 and Spleen Parvoviruses (Parvoviridae) are small, single-stranded, non- The thymus is a central • Canine parvovirus is a significant enveloped, DNA viruses.1,2 It is thought that CPV evolved from lymphoid tissue located be- viral pathogen that can affect dogs feline panleukopenia virus (FPV) or from a form of parvovirus tween the lungs in the pre- of any age but more commonly that affected wildlife and caused hemorrhagic diarrhea.2 There cardial mediastinal space.7 affects puppies. 1,4,5 are two types of CPV: type 1 (CPV-1) and type 2 (CPV-2). In However, in older animals, • To fully understand the effects the 1970s, CPV-1 was more common; currently, CPV-2 is the small fragments of active (pathology and pathophysiology), dominant strain in the United States and causes classic parvoviral thymus can be found in clinical signs, and treatment of 6 8 enteritis. This article focuses on CPV-2 because it is more common bone marrow. The thymus canine parvovirus 2 (CPV-2), and pathogenic. is well developed and very veterinary technicians need to 1,2 CPV-2 primarily affects puppies aged 6 weeks to 6 months. active during late prenatal understand the normal anatomy Parvovirus is less likely to affect older dogs because of their immunity and early postnatal life, and physiology of the body systems 2 through natural infection or immunization. Neonatal puppies making it susceptible to that CPV-2 affects. are likely to be protected by the maternal antibodies for the first CPV-2. Lymphoid stem few weeks of life.2 These antibodies are transferred to puppies cells are produced and pre- • Because of the high morbidity and through colostrum; the antibody titer of a puppy depends on the destined to become B or T mortality associated with CPV-2 serum titer of the bitch at whelping, the size of the litter, and the lymphocytes.9 In young infection and the brief opportunity amount of colostrum absorbed by the puppy.2 The half-life of the animals, predetermined T for treatment, early recognition maternal antibodies is approximately 10 days.2 When a puppy is lymphocytes move via the of infected dogs and immediate, weaned and the antibody titer begins to decrease, immunization blood to the thymus, where aggressive treatment are critical. is essential for continued protection.2 Depending on when a puppy they multiply and become Vetlearn.com | May 2011 | Veterinary Technician E1 ©Copyright 2011 MediMedia Animal Health. This document is for internal purposes only. Reprinting or posting on an external website without written permission from MMAH is a violation of copyright laws. Canine Parvovirus mature T lymphocytes.9 “barrier” function (nonspecific immunity) of the epithelium is Glossary Once mature, T lymphocytes compromised or destroyed, allowing (1) potential pathogens move to other peripheral to enter the blood and (2) massive losses of blood, water, and Antithrombin—inhibits clotting by lymphoid organs, such as the electrolytes. binding to clotting factors and blocking spleen and lymph nodes.9 Fluid that enters the intestinal lumen comes from endogenous their activity T lymphocytes have many secretion within the gastrointestinal (GI) tract and from ingestion 10 Enterocytes—epithelial cells functions that are collectively of food and liquids. Most of the fluid is absorbed from the 10 covering the intestinal villi and crypts referred to as cell-mediated lumen, but a small amount is excreted into the feces. A small immune responses.9 decrease in absorption from the lumen can result in malabsorptive Granulopoiesis—granulocyte When CPV-2 is ingest- diarrhea.10,12 When secretion into the lumen increases, secretory production ed or inhaled, it moves into diarrhea develops.12 Hematopoietic stem cells—bone lymphoid tissues such as CPV-2 infection can cause abdominal pain, which may be elicited marrow cells capable of producing all the mesenteric lymph nodes on palpation. This can be secondary to acute gastroenterocolitis, types of blood cells and the thymus.1,2 CPV-2 enteritis, or intussusception.2 The cause of intussusception is not replicates in these lymphoid completely understood: it is thought that the damaged intestinal Hypovolemic shock—a decrease in tissues for 2 days before wall and the changes in motility are contributing factors.10 As a cardiac output caused by an inadequate dissemination to the crypt wave of peristalsis travels down the intestine, the damaged segment amount of fluid in the vascular system, cells of the small intestine. of intestine does not move and is enveloped by the intestine which leads to insufficient tissue proximal to it.10 Intussusception can cause obstruction, signs of perfusion Small and Large Intestines which include vomiting and diarrhea.2 These may be inappropriately Immunoglobulins—antibodies The small intestine has a disregarded as deteriorating clinical signs due to the infection.2 very large surface area that Interstitial fluid—extracellular fluid Bone Marrow that is outside the vascular system and allows efficient absorption 10 bathes the cells of nutrients. The func- Bone marrow is found in the medullary cavity of long bones and tional unit of the small the interstices of spongy bone.13 In young animals, all bone marrow Intraosseous—within the bone intestine is the crypt–villus is red; as animals age, most red marrow becomes adipose tissue 13 Intussusception—enfolding of one axis, which is composed of called yellow marrow. Red bone marrow contains hematopoietic 14,15 intestinal segment into another the intestinal crypts, a mat- stem cells, which can produce all types of blood cells. He- uration zone, and the villi.10 matopoietic stem cells differentiate into rapidly dividing, commit- Lymphopenia—a decrease in the The intestinal crypts con- ted stem cells called progenitor cells, which differentiate into specific number of lymphocytes in the blood tain epithelial cells that blood cells.15 CPV-2 attacks red bone marrow and progenitor Oncotic pressure—the osmotic rapidly divide and secrete cells, affecting erythrocyte, leukocyte, and platelet counts. pressure due to plasma colloids that most of the intestinal fluid.10 helps control movement across the As cells approach the mat- The Heart capillary wall uration zone, they undergo Heart-wall thickness is mainly determined by the myocardium— final division and become the muscle layer between the endocardium and the epicardium.16 Phlebitis—inflammation of a vein mature enterocytes.10 Once Myocytes—the cells of the myocardium—rapidly divide in utero Thrombocytopenia—a decrease in mature, enterocytes lose the and during the first 2 weeks of life.2 the number of platelets circulating in ability to secrete fluid; in- Myocarditis due to CPV-2 infection affects puppies in utero the blood stead, they develop a plas- or before 8 weeks of age.1,17 Clinical signs of myocarditis due to Thrombosis—formation of a clot ma membrane with a spe- CPV-2 infection can vary. Cardiac signs may be seen without inside a blood vessel cialized region containing previous cardiac disease, or the puppy may
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