PARVOVIRIDAE E-mail Web site PETER H. RUSSELL, BVSc, PhD, FRCPath, MRCVS Department of Pathology and Infectious Diseases, The Royal Veterinary College, Royal College Street, London NW1 OTU. E-mail Web site This lecture is the part of THE VIROLOGY COURSE, 2000 (The aim of this foundation course is to link the structure, diagnosis and control of the different families of veterinary viruses in an up-to-date and well-paced manner). This lecture has been updated by Dr Janice Bridger. COURSE OBJECTIVES - hyperlinks to course.htm BOOK LIST - hyperlink to book.htm USEFUL WEBSITES- hyperlink to websites.htm INDEX OF ABBREVIATIONS - hyperlink to index.htm

LEARNING OBJECTIVES Students should be able to: Relate the pathogenesis of feline infectious enteritis virus to its control Explain the origins of canine parvovirus type 2 and its role in canine disease Describe the importance and control of porcine parvovirus as a reproductive pathogen List the species and disease conditions in which papilloma viruses are implicated

FAMILY CHARACTERISTICS - Small, non-enveloped, icosahedral, featureless virions (20nm in diameter) - (-) sense, single-stranded DNA. - Resistant to pH (even gastric acidity), heat, dessication -persist for years in environment - Infect rapidly dividing cells (in the S phase of mitosis) in vivo and in vitro targeting bone marrow, intestinal epithelium and the foetus via a viraemic phase.

DISEASE AND PATHOGENESIS: FELINE PARVOVIRUS DISEASE AND PATHOGENESIS: Disease known as feline infectious enteritis and feline panleucopenia. Often fatal. Most common in kittens but cats of all ages susceptible. Fever, severe enteritis often bloody, dehydration, leucopenia, anaemia. Cerebellar hypoplasia in kittens < 2 weeks. Oral infection followed by initial replication in pharyngeal lymphoid tissue and viraemia, then virus targets rapidly dividing cells in lymph nodes, bone marrow and crypts of small intestine.

FELINE PARVOVIRUS DIAGNOSIS: The lesions of acute cases and post mortem findings are suggestive of feline parvovirus infection. Haematology will show leukopenia. Can be confirmed by haemagglutination (HA) with porcine erythrocytes or virus ELISA using faeces.

FELINE PARVOVIRUS HOST RANGE : All felidae; mustelidae (mink) and some procyonidae (racoons and panda). EPIZOOTIOLOGY: Highly contagious - may be acquired by direct contact with other cats or via fomites (ie.bedding, food dishes). Virus shed at high levels in faeces, vomit, urine, saliva and virus persists in the environment as reisitant. Virus excretion can persist and sub-clinical infections occur, adding to the source of virus. World distribution.

ANTIGENICITY & CONTROL: FELINE PARVOVIRUS ANTIGENICITY & CONTROL: Only one serotype required in vaccine. Effective vaccines are available and are highly recommended; essential for boarding catteries. Either attenuated or killed-adjuvanted vaccines are administered parenterally after maternal immunity has waned - induces systemic immune responses which neutralize the viraemia and prevent virus reaching its target tissues. Most cats will be naturally re-exposed to virus but annual boosters are used as a safeguard.

CANINE PARVOVIRUS TYPE 2 Two canine parvoviruses exist: canine parvovirus type 1 (CPV-1) and canine parvovirus type 2 (CPV-2). CPV-1 has always been present in the canine population (all sera tested have been positive for CPV-1 antibodies) and is avirulent. CPV-2 emerged as a new virus in the late 1970's. It is closer to the feline virus than CPV-1.

CANINE PARVOVIRUS TYPE 2 DISEASE AND PATHOGENESIS: Infection via oropharyngeal route followed by viraemia. Initially, there were two distinct syndromes associated with CPV-2: (1) targeted at rapidly dividing myocardial cells, (2) at the rapidly dividing cells in the crypt epithelium of the small intestine. (1) Sudden death in 3 - 8 week-old puppies. This presented as sudden death or as a "fading puppy syndrome". The virus had a predilection for myocardial cells where intranuclear inclusion bodies developed. Heart failure resulted and this could be sudden in onset and fatal. Partial heart failure resulted in poor exercise tolerance and pulmonary oedema. This disease pattern has largely disappeared because maternal immunity is now common in the dog population. (2) Enteritis in dogs > 8 week-old Serious shortening of the villi occurs because of viral destruction of crypt epithelial cells. Initially, a grey, persistent, foul-smelling diarrhea was associated with infection. More recently, haemorrhagic lesions are found. Morbidity high; mortality around 10%. The former syndrome appears more rarely now, probably due to widespread passive maternal immunity.

CANINE PARVOVIRUS TYPE 2 DIAGNOSIS: For virus use HA or a commercial ELISA, using the supernatant from clarified faeces. CPV-2 will HA porcine erythrocytes (as does the feline parvovirus). Antibody can be detected by HAI or ELISA. Grows in both canine and feline cell lines in the laboratory.

CANINE PARVOVIRUS TYPE 2 HOST RANGE Dogs (but CPV-2a & 2b can cause disease in cats - see below) EPIZOOTIOLOGY. Disease emerged in Australia, United States, UK & Europe and spread rapidly on all 3 continents infecting dogs of all ages. Before this all canine sera were negative for antibodies to CPV-2 but now most are positive. Feline vaccines have been thought of as a possible source of CPV-2 but recent data suggests not and that parvoviruses from wild carnivores could be the source. Variants have emerged (CPV-2a and CPV-2b) with only a few changes in amino acids of the capsid protein gene. Only a few amino acids control the host range. Faecal-oral transmission; resistant in environment.

CANINE PARVOVIRUS TYPE 2 ANTIGENICITY & CONTROL: Antigenic variants occur but only one type is required in vaccine to protect against all strains. Vaccine administered with dog distemper & hepatitis vaccines as a single vaccination at 12/16 weeks of age as passive maternal antibody wanes. Thorough disinfection of the premises where disease has occurred as the virus survives well in the environment.

DISEASE AND PATHOGENESIS PORCINE PARVOVIRUS DISEASE AND PATHOGENESIS The principal viral cause of the SMEDI syndrome in the U.K. (stillbirths, mummification and embryonic deaths). Replicates in the epithelium of the alimentary tract with viraemia without causing clinical signs in fattening and breeding stock. Virus recovered from most excretions. Transplacental infection occurs. In early pregnancy, causes resorption and may maifest as infertility; later in pregnancy, SMEDI syndrome. Congenitally infected pigs may remain as excretors; some piglets in litter escape infection.

PORCINE PARVOVIRUS HOST RANGE: pigs DIAGNOSIS: Immunostaining on foetal tissues; isolation in cell culture; HA on faeces; rising antibody titres in paired serum samples by haemagglutination inhibition.

PORCINE PARVOVIRUS EPIZOOTIOLOGY: Usually contracted from faeces or fomites. About half of pig herds in the UK have evidence of infection (ie are antibody positive). Outbreaks usually resolve because of developing herd immunity but congenitally infected excretors may form a reservoir of infection.

ANTIGENICITY & CONTROL: PORCINE PARVOVIRUS ANTIGENICITY & CONTROL: Single serotype vaccines - inactivated adjuvented vaccines in UK; live attenuated in USA. All progeny should be disposed of as congenitally infected animals (which are persistently infected and intermittently shed virus) may survive from an outbreak.

SUMMARY Cause serious diseases in cats (enteritis/ panleucopenia), dogs (myocarditis/ enteritis) and pigs (SMEDI). Pathogenesis is related to the requirement for rapidly dividing cells for virus replication Vaccines available for each disease which prevent viraemia & hence destruction of rapidly dividing cells.