Review of Companion Animal Vaccine and Immunoprophylaxis

Vaccine 27 (2009) 491–504
Contents lists available at ScienceDirect
Vaccine
journal homepage: www.elsevier.com/locate/vaccine
Review
Review of companion animal viral diseases and immunoprophylaxis

J.R. Patel a,∗ , J.G.M. Heldens b
a
JAS Biologicals Limited, The Centre for Veterinary Science, Madingley Road, Cambridge CB3OES, UK
b
Intervet Schering-Plough Animal Health, W. de Köverstraat 35, 5830 AH Boxmeer, The Netherlands
a r t i c l e i n f o a b s t r a c t
Article history: In this article we review important established, newly emergent and potential viral diseases of cats, dogs
Received 11 August 2008 and rabbits. Topics covered include virus epidemiology, disease pathogenesis, existing and prospective
Accepted 5 November 2008 immunoprophylaxis against the viruses. For some feline viruses, notably the immunodeficiency virus,
Available online 27 November 2008
leukaemia virus and peritonitis virus, available vaccines are poorly efficacious but there are good prospects
for this. A further challenge for the industry is likely to be due to viruses jumping species and the emergence
Keywords:
of more virulent variants of established viruses resulting from mutations as has been the case for the canine
Veterinary viruses
parvovirus, coronaviruses and feline calicivirus.
Viral vaccines
Viral diseases © 2008 Elsevier Ltd. All rights reserved.
Epidemiology
Pathogenesis
Companion animals
Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 491
2. DNA viruses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492
2.1. Herpesviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492
2.2. Adenoviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492
2.3. Poxviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492
2.4. Parvoviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
3. RNA viruses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
3.1. Caliciviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
3.2. Coronaviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 494
3.3. Paramyxoviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495
3.4. Rhabdoviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495
3.5. Retroviridae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495
4. Emergent and potential virus diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 496
5. Immunoprophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 496
6. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 500
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 501
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 501
1. Introduction understanding disease pathogenesis, virus transmission in the field

and prophylactic control of diseases. Companion animal viral vac-
Viruses of many families cause disease in small companion cines represent a significant share of the global veterinary vaccines
animals and there is much academic and industrial interest in market to which several manufacturers offer products. Most prod-
ucts, however, are formulated using old vaccine viral strains which
in some instances, are in need of updating in view of emergence of
∗ Corresponding author. more virulent strains in the field. Pathogenic mutants with altered
E-mail address: [email protected] (J.R. Patel). organ tropism have for instance emerged in case of carnivore par-
0264-410X/$ – see front matter © 2008 Elsevier Ltd. All rights reserved.
doi:10.1016/j.vaccine.2008.11.027
492 J.R. Patel, J.G.M. Heldens / Vaccine 27 (2009) 491–504
vovirus, calicivirus and coronavirus. Hence there is, in our view, 2.2. Adenoviridae
the need for an appraisal of the current status of the new viral
mutants and associated diseases and current and prospective vac- Adenoviruses were first named in 1956 to cluster a new group of
cines. Important areas considered in viral family are epidemiology cytopathic viruses recovered from explanted human adenoid and
of infections particularly mode of virus transmission, associated tonsillar tissue. The family has two genera, the mastaadenoviruses
diseases and key determinants in disease pathogenesis. Current from mammals and aviadenoviruses from birds. Genera are further
immunoprophylaxis in relation to prospects of improved and safer classified into subgenus, species and strains. Adenoviruses cause
vaccines and some difficulties in achieving these objectives for par- disease in dogs and pigeons. Two antigenically related adenoviruses
ticular viral diseases are reviewed as well. Newly emerging and species can cause significant disease in domestic dogs and other
potential diseases are discussed in the last section. The companion canids. The two viruses involved are commonly known as canine
animals presently considered are cats, dogs and rabbits. Unusual adenovirus-1 (CAV-1) and 2 (CAV-2) and also as infectious canine
pets such as ferrets, mice, hamsters and snakes in view of the enor- hepatitis virus and infectious canine laryngotracheitis virus respec-
mity of the task were considered out of scope. Horses [1–3] and tively. The close antigenic cross-reactivity is seen at the level of
pigeons [4] have already been covered recently. significant reciprocal but unequal cross-neutralisation. The viruses
are however unequivocally distinguished by DNA fingerprinting of
2. DNA viruses endonuclease digests of viral DNA. CAV-1 occurs worldwide and
infects and replicates in oropharynx after the ingestion of infectious
2.1. Herpesviridae material from respiratory secretions, urine or faeces. The primary
replication in tonsils, Peyers patches and epithelia of oropharynx
Herpesviruses are enveloped, icosahedral viruses with a lin- and bowel results in lymphoid cell viraemia which initiates sec-
ear double stranded DNA. Taxonomically, members have been ondary infection of parenchyma of liver, kidney and lining of blood
placed in three subfamilies, alpha, beta and gammaherpesvirinae vessel and sinusoids in these organs and other sites. Infected cells
based on their biology [5]. An important characteristic of inves- die and lyse leading to mainly pinpoint bleeds and haemorrhages
tigated mammalian and avian herpesviruses is their ability to and some times a large bleed if a major vessel is involved. CAV-
establish latency and remain latent in their primary host for life 1 causes fatal hepatitis in newly weaned puppies and susceptible
and recrudesce from latency in response to certain stimuli and be young dogs. Other lesions due to CAV-1 infection comprise subcuta-
shed. In latent state, multiple copies of viral DNA are demonstrate- neous oedema, ascites and oedema of the gall bladder wall, immune
able as episomes without active synthesis of viral proteins and complex keratitis and nephritis. Older dogs may be susceptible but
precursors. Alphaherpesviruses tend to frequently but not exclu- signs are milder with enlargement of tonsils, sub-maxillary lymph
sively, become latent in neural cells of cranial or sacral ganglia, nodes and sometimes immune complex keratitis. Isolates of CAV-
the beta and the gammaviruses in lymphoid cells. Distinct her- 1 vary in virulence for the domestic dog, some cause sub-clinical
pesviruses cause disease in cats and dogs while rabbits may not diseases while others acute disease with severe abdominal pain
be the natural host to significant herpesvirus disease. However, followed by death. Wild and farmed dogs are highly susceptible to
rabbits have been used as models to study disease pathogene- some strains of CAV-1 encephalitis. CAV-1 can often cause immune
sis of some alphaherpesviruses [6] and also gammaherpesvirus complex vasculitis, commonly known as blue eye.
[7,8]. CAV-2 transmission among dogs is mainly by inhalation and
Canine alphaherpesvirus-1 (CHV-1) was first identified in USA virus is widely prevalent. CAV-2 is a major cause of kennel cough
in 1965 as the cause of a highly fatal, generalised hemorrhagic dis- syndrome. CAV-2 causes extensive lesions in the upper and the
ease in pups less than 4 weeks of age (fading puppy disease) and lower respiratory tract resulting in interstitial pneumonia often
has subsequently been detected in most countries where diagnosis with necrotising bronchitis and bronchiolitis, focal necrosis of the
was undertaken. However, CHV-1 prevalence in the dog popula- turbinate and tonsillar epithelium. The disease is more severe when
tion as a whole is low [9], although it may be highly prevalent in associated with concurrent bacterial infection. Often the bronchial
kennels. CHV-1 spreads by aerosol and initiates infection in the nodes are congested and haemorrhagic but gross liver and gall blad-
oropharyngeal mucosa and the local lymph nodes and results in der lesions are usually absent. CAV-2 infection in dogs has not been
reticuloendothelial cell viraemia. In puppies less than 3 weeks of associated with hepatitis. Other signs of CAV-2 infection may be
age, viraemia disseminates the virus systemically and after replica- fever, mild depression and nasal and/or ocular discharge; corneal
tion in organs, causes widespread petechiation in the liver, kidneys, opacity is sometimes seen.
lungs and lymph nodes. Severely affected puppies may die. In adult
dogs, CHV-1 infection is less severe and may cause cough and dysp- 2.3. Poxviridae
noea in individuals with generalised infection of the bronchial tree
and may be part of the kennel cough syndrome and/or reproductive Members are large, enveloped, highly resistant viruses with a
failure. double-stranded linear DNA genome which replicates in cytoplasm
The cat alphaherpesvirus-1 (FHV-1) is also transmitted by of infected cells. The subfamily Chordopoxvirinae has members
aerosol followed by viral replication in nasal and conjuncti- affecting vertebrates classified into six genera [10]. The verte-
val epithelium and subsequent dissemination of progeny virus brate poxviruses usually produce proliferative focal lesions and
throughout the bronchial tree. Typical clinical signs of FHV-1 are occasionally fatal when they generalise. Members are very sta-
infection are rhinitis, bronchitis, conjunctivitis, nasal discharge, ble and virus shed in scabs survives for months or years in dust
dyspnoea, fever, coughing and inappetance. The FHV-1 disease particularly in dry conditions. Companion animal species affected
has some clinical similarities to FCV respiratory disease and is by poxviruses are rabbits, pigeons and mild disease due to cow-
commonly referred to as feline viral rhinotracheitis (FVR). Sec- poxvirus has been reported in cats. Myxomavirus (MV) in genus
ondary bacterial bronchopneumonia, commonly in kittens but leporipoxvirus causes myxomatosis, a systemic and usually a fatal
rarely in older cats, may result in death. Experimentally, both disease in European rabbits (Oryctolagus cuniculus) but a benign dis-
FHV-1 and CHV-1 were found to cause vaginitis. The incuba- ease in its natural host, Sylvilagus rabbits in the Americas [11,12].
tion period for the common disease signs for both viruses is 1–2 MV spreads mechanically by blood-feeding arthropod vectors such
days. as mosquitoes and fleas and to a lesser degree by direct contact
J.R. Patel, J.G.M. Heldens / Vaccine 27 (2009) 491–504 493
or aerosol [9]. Virus remains infectious for several months in vec- in the mucosa and lymphoid tissue of the buccal cavity and result
tors. In rabbit MV replicates subcutaneously locally followed by in leukocyte-associated viraemia followed by progeny virus spread
viraemia and generalised dissemination to connective tissue cells to internal organs. In puppies ingested virus replicates in crypts
initiating a proliferative response and exudative erythematous der- of small intestine resulting in leukocyte viraemia, viral dissemina-
matitis around the face, eyes and skin surfaces generally. The lesions tion and secondary infection of the liver and of cardiac myocytes
become ulcerated and covered with weeping crusts [11,12]. Field although the latter is rarely seen today due to effective vaccina-
epizootics have resulted in mortality rates approaching 100%. tion. Infection of these vital organs may cause eventual heart failure
Cats occasionally become infected with a poxvirus which is associated with pulmonary oedema, hepatomegaly and ascites.
indistinguishable from cow poxvirus in genus orthopoxvirus. Infec- Mortality is high. In older dogs ingested virus replicates in intesti-
tion in cats is acquired from rodent bites and develops as small red nal crypts which more commonly results in vomiting, diarrhoea
macular eruptions which develop into papules or ulcers which scab and leucopoenia with high morbidity but low mortality.
over several days on the legs and/or head which in some infected Pathogenesis of FPLV infection in cats is similar to CPV disease
cats become more widespread and may spread to lungs. in dogs. Viraemia following the respiratory and the enteric phases
of viral replication leads to secondary infection of bone marrow,
2.4. Parvoviridae spleen and lymph nodes. This results in transient leukocytosis fol-
lowed by a marked leucopoenia and anaemia. Virus is shed by most
Members are the smallest, along with circoviruses, of DNA routes 2–6 days after infection.
viruses and include important pathogens of cats and dogs. Par-
voviruses and circoviruses have a predilection for replication in 3. RNA viruses
rapidly dividing cells of bone marrow, enteric epithelium and the
foetus. A parvovirus with predilection for rabbit small intestine and 3.1. Caliciviridae
lymphoid tissues and liver has been known for sometime but the
virus does not appear to be a significant rabbit pathogen and only Members are non-enveloped icosahedral very small (27–40 nm)
causes mild catarrhal enteritis [13]. Members have an icosahedral viruses with a linear, positive sense single stranded RNA genome
capsid with an over all diameter of 18–25 nm and contain linear, and replicate in cell cytoplasm. Three viral species in family Cali-
single-stranded DNA. civiridae cause significant diseases in cats, rabbits and brown hares.
The known carnivore parvoviruses named feline panleukope- Feline calicivirus (FCV) belongs to the distinct phylogenetic clade
nia virus (FPLV), canine parvovirus (CPV-types 1, 2, 2a, 2b and in genus vesivirus. Rabbit haemorrhagic disease virus (RHDV) and
2c), mink enteritis virus (MEV-types 1, 2 and 3) and those iso- European brown hare syndrome virus (EBHSV) belong to the dis-
lated from wild felids and canids such as raccoons, foxes (red and tinct phylogenetic clade in genus lagovirus. RHDV and EBHSV share
blue species), leopards and cheetahs are genetically related and antigenic epitopes which elicit cross-protective antibodies. Cali-
interspecies transmissions among carnivores occur readily [14,15]. civiruses are not considered significant pathogens of domestic dogs
CPV-2 was first recognised in 1978 as the cause of new disease in nor are they isolated frequently. However both FCV related and
dogs which rapidly spread worldwide [16–19]. Evidence suggests unrelated caliciviruses have been isolated from faeces of puppies
that the CPV arose from the long recognised FPLV or related virus and dogs with diarrhoea [31–33]. Canine caliciviruses (CCoV) at
infecting another carnivore such as mink, raccoon, artic fox or other. present remain unclassified [34]. However, it is possible that one
The new virus differed from FPLV like viruses in less than 1% in or more of these dog isolates of caliciviruses have the potential to
genomic sequence [20–23]. However, the life of firstly identified adapt, spread and establish in dog populations to cause clinically
CPV variant in nature was brief [24]. By 1981 CPV-2 was replaced important disease. Caliciviruses do mutate readily in nature as is
by CPV-2a which in turn was replaced between 1984 and 1990 indicated by the emergence of a highly virulent haemorrhagic vari-
by CPV-2b. In each case the replacement was global. Interestingly, ant of FCV [35–37] which has spread rapidly [38,39]. The newly
CPV-2 and its 2a and 2b variants differed by less than 0.2% in their emergent FCV variants have been named virulent systemic FCV
genome sequence and involved substitution of 3–4 amino acids in (VS-FCV) to distinguish them from the common FCV strains. FCV
virus capsid protein VP2 [20–23,25]. This change was ongoing with has a worldwide distribution while VS-FCV is, at present, limited
the identification of CPV-2c in late 1990s [26]. The latter variant has to USA and the UK [36] but very likely to become more prevalent.
also spread widely [27]. CPV-2c has one amino acid substitution VS-FCV strains appear to have arisen independently of one another
in VP2 [26]. Whilst this change in VP2 is minor it was nonetheless and have not spread from a single case [37]. Both virus types are
significant in conferring a broader host range phenotype to the vari- excreted in urine, saliva, ocular and respiratory secretions and are
ants. Thus experimentally cats were refractory to infection by CPV-2 transmitted via aerosol, orally and on fomites. Usually, virus shed-
but readily susceptible to infection by CPV-2a and 2b viruses [23]. ding is for up to 2 weeks but some recovered cats shed the virus
These viruses occur worldwide and are evolving rapidly [28,15,29]. intermittently [40]. Primary infection by both virus types is often in
However, their evolutionary history is complex and possibly not the upper respiratory tract and/or oral mucosa with an incubation
fully unravelled and it has been suggested that their current clas- period of 2–3 days resulting in epithelial cell necrosis with vesicle
sification and naming of new isolates needs revision [15]. or ulceration of the external nares and oral mucosa. Virulent FCV
A key factor in the epidemiology and evolution of carnivore strains may also cause interstitial pneumonia. Infected cats may
parvoviruses has been the virus tropism for the gut and the sur- also manifest fever, anorexia, conjunctivitis, lethargy and stiffness,
vival of virus shed in faeces for long periods (several months to nasal and ocular discharge, sneezing and rales. Some FCV but most
2 years). Faecal-oral route is the main mode of virus transmis- VS-FCV strains are fatal [35,36].
sion of these important carnivore viruses. However, in vivo tissue RHDV and EBHSV infections are highly contagious and acute
tropism of FPLV and CPV vary with respect to ability to replicate fatal diseases caused by distinct but antigenically related cali-
in enteric epithelium and produce faecal virus in quantity. In cats civiruses. RHD was first reported in the People’s Republic of China
FPLV replicates in lymph nodes, thymus, spleen and intestine and in imported Angora rabbits imported from German Democratic
large quantities are shed in faeces while in dogs FPLV replication Republic [41] while EBHS was described in brown hares (Lepus
occurs in the thymus and bone marrow but not in the gut and europeus) and mountain hares (Lepus timidus) in 1981 in Sweden
mesenteric lymph node [30]. CPV and FPLV also initiate infection [42]. However, epidemiological investigations indicated presence
of these viruses in Europe much before the above published reports. (CCoV), cat (FCoV), human (HCoV-229E), pig epidemic diarrhoea
One line of data supporting this conclusion was the detection of (PEDV), pig respiratory (PRCoV), pig transmissible gastroenteritis
RHDV antibodies in rabbit sera collected in early 1970s [43]. RHDV (TGEV) CoVs. Group 2 species are bovine (BCoV), human (HCoV-
is endemic in most parts of Europe, Asia and parts of Africa, Australia OC43), mouse (MHV), pig haemagglutinating encephalomyelitis
and New Zealand. RHDV was imported into Australia in 1991 for bio- (HEV), SARS (SARS-CoV), canine respiratory coronavirus (CRCoV)
logical control of wild rabbits but the virus escaped from Wardang and other CoVs. Group 3 consists exclusively of avian CoVs. Most
island quarantine facility in 1995 and became established across members usually cause mild enteric and/or respiratory disease and
Southern Australia [44]. Insect vectors were suspected as to have hence are generally considered of minor clinical importance. There
spread the virus from Wardang Island [45]. EBHSV is widespread are however exceptions (see below). The large genome is prone to
wherever hares (L. europeus and sub species) are endemic as is the high frequency mutations [58–60]. CoVs have the potential to jump
case in Europe [46]. Rabbit species vary in their susceptibility to the species barrier and cause severe disease as was the case for
RHDV infection. American cottontail rabbits (Sylvilagus floridanus) severe acute respiratory syndrome (SARS) in Southern China [61].
appear to be refractory to infection by RHDV [47,48]. RHDV trans- Studies by different groups demonstrated that SARS-CoV succeeded
mission is by direct contact and via fomites [45]. Thus primary in spillover from a wildlife reservoir (probably bats) to human pop-
infection is at an oral and/or conjunctival mucosa. EBHSV is likely ulation via an intermediate host(s) and that rapid viral evolution
to be similarly transmitted among hares. Flies of the genus Phormia played a key role in the adaptation of SARS-CoVs in at least two non-
in Europe transmit RHDV via the conjunctiva while in Australia reservoir species within a short period [62]. It has been shown that
bush flies (Musa vestustissima) and blow flies (Caliphora dubia) cats and ferrets can be infected with this virus as well [63]. Virus
were identified as potential vectors [49,50,45]. Rabbit fleas (Siplop- transmission is by inhalation and/or ingestion of virus in faeces,
syllus cuniculi and Xenopsylla cunicularis) and mosquitoes (Culex saliva and aerosol. This results in limited virus replication in upper
annulirostris) were shown to transmit RHDV to rabbits under labo- respiratory tract (URT) and/or intestinal mucosa and associated
ratory conditions [51,45]. Molecular epidemiological studies, thus lymphoid tissues and progeny virus does not normally or only limit-
far, have shown a low (less than 10% nucleotide) genomic varia- edly generalises to internal organs with some exceptions. However
tion among RHDV isolates collected over a period of several years combined secondary bacterial infection often exacerbates the clin-
from different geographical areas [52,53]. However, natural muta- ical disease. Dogs are susceptible to two CoVs, the enteric (CCoV)
tional changes in the field have been recorded [54]. A question [64] and the newly recognised respiratory CoV (CRCoV) [65,66]; the
that remains unresolved is that of how virus persists in nature latter virus has been placed in antigenic group 2 along with BCoV
from year to year. Typically in the field RHDV infected rabbits die and others. The group 1 CCoVs have been placed into two serotypes
within 24–48 h with few outward signs excepting bloody mucous (I and II). CCoVs primarily cause mild enteric disease in puppies
discharge from the nose. manifest as fever, depression, anorexia and diarrhoea. Severe dis-
Following the primary replication in oronasal and/or ocular ease due to CCoV is infrequent [60]. However, a pantropic virulent
mucosa RHDV infects macrophages and other mononuclear cells variant of serotype II CCoV with much broader viscerotropic pheno-
(circulatory and alveolar macrophages) and these infected cells dis- type was recognised recently [67]. This variant (designated CB/05),
seminate the virus to the internal organs particularly the liver and in addition to the usual enteric replication, also spreads to and repli-
kidneys where virus undergoes secondary replication [55]. Cells of cates in internal organs (lungs, spleen, liver, kidney and brain) and
the mononuclear phagocyte lineage are also likely to be involved was the cause of deaths of some dogs [67–69].
in transmission of EBHSV to the internal organs of infected hares. FCoVs occur as two serotypes with different serological and bio-
In both RHD and EBHS, a consistent finding is severe necrotising logical characteristics, particularly in sequence homology of the
hepatitis, characteristic lesion being coagulation liver necrosis in viral surface S glycoprotein [59]. Like CCoVs, most FCoVs cause mild
RHD and lytic necrosis in EBHS [56]. However, the two diseases enteric disease but could give rise to highly pathogenic variants
also have characteristic pathological differences. In RHD, dissemi- in individual infections causing peritonitis (FIP). Both serotypes of
nated intravascular coagulation (DIC) and thrombi in kidneys and FCoV mutate to virulent FIPV variants. Their relative prevalence
lungs are common lesions while DIC has not been observed in in nature varies but type I FIPV/FCoV strains are generally domi-
hares with EBHS and haemorrhages are also infrequent [56]. Deple- nant in the field [70]. FIPV variants of FCoV have been the cause
tion of splenic lymphocytes is observed in both diseases. Apoptosis of fatal peritonitis in some cases [71,72]. FCoVs are transmitted
of hepatocytes, macrophages and endothelial cells along with DIC via the faecal-oral route and primarily replicate in enterocytes [73]
and progressive jaundice are common features in RHD of rabbits from where the progeny virus disseminates to internal organs via
[57]. An interesting hypothesis put forward to explain the differ- monocyte-associated viraemia. Although FCoV is highly prevalent,
ences in types of lesions between RHD and EBHS was suggested FIP morbidity is relatively low, rarely exceeding 5% [73]. Feline
as due to the genetic difference between the two affected lago- infectious peritonitis (FIP) is a progressive debilitating disease.
morphs species. Evidence supporting this hypothesis has been the A pathognomic feature of FIP is widespread occurrence of pyo-
observation of liver lesions in RHDV infected hares that were indis- granulomatous lesions in majority of organs (lungs, liver, spleen,
tinguishable from those seen following EBHSV disease of hares [56]. omentum and brain) and other tissues [74,75]. Other features of
Thus the type of lesions is apparently not determined by the virus FIP involve a marked T-cell depletion, particularly in end-stage FIP
species. As in FCV infection of cats, protection against RHDV disease [76] and hypergammaglobulinemia [77]; B-cell leucopoenia is also
is conferred by virus neutralising antibody to the major viral capsid a feature in FIP disease [78]. The T-cell depletion is apparently not
protein namely VP60 in RHDV. the result of virus infection since T-cells appear not to support virus
replication [76]. Other important determinants in FIP pathogenesis
3.2. Coronaviridae appear to be (i) dissemination of mutant progeny FIPV by acti-
vated macrophages and monocytes and their availability [79] and
Coronaviruses (CoVs) (family Coronaviridae, order Nidovirales) (ii) types of viral S protein neutralising antibodies at suboptimal
are a group of enveloped positive-strand large RNA viruses of concentration which opsonise the virus and enhance its infectivity
mammals and birds and are found worldwide. The coronavirus for target cells via Fc receptor mediated attachment [80–82]. There
genus has been classified into three clusters or groups based is also complement activation with resultant platelet aggregation,
on antigenic cross reactivity and other criteria. Group 1 has dog intravascular coagulation necrotising lesions and exudation of fluid
into the abdomen and thoracic cavity in the so-called wet form of aerosols as well. The control of rabies in different regions of the
FIP. Wet FIP is most common in kittens under one year of age and world poses very different problems, depending on which reservoir
the incidence declines by 5 years of age when the dry form of FIP hosts are present and the level of infection therein [9].
is more common [82]. Whilst there is no protective immunity in
wet FIP, the dry form is a result of partial immunological protection 3.5. Retroviridae
[82–83]. Some of these pathogenetic features of FIP notably the T-
cell lymphopenia, multiphasic disease course and viral persistence The family name derives from members possessing reverse tran-
have been seen in SARS. Both these diseases are an enigma possibly scriptase enzyme (RT). The family is sub divided into 3 subfamilies:
stemming from virus-induced immune dysregulation. Oncovirinae, Lentivirinae and Spumavirinae. Members in the sub-
family are further classified as genera, subgenera and species. Virus
3.3. Paramyxoviridae particles are enveloped covering an icosahedral capsid containing
helical nucleocapsid. The genome comprises two copies of linear
Members in the family are enveloped viruses with sin- positive-sense, single-stranded RNA (+ssRNA) which is not infec-
gle stranded negative-sense RNA genome.Currently the family tious per se. The viral genome occurs as an inverted dimer held
Paramyxoviridae has two subfamilies named Paramyxovirinae and together at the 5 end by hydrogen bonds possibly through base par-
Pneumovirinae.The former has five genera: respirovirus, morbil- ing. Retrovirus replication is unique among +ssRNA viruses because
livirus, rubulavirus, henipavirus and avulavirus. The latter has two they first convert +ssRNA to −DNA copy using the virion RT (RNA
genera: pneumovirus and metapneumovirus. The members sur- dependent DNA polymerase) and then a circular double-stranded
vive moderately well in the environment; all replicate in the upper (DS) DNA copy which is integrated into host cell chromosome by
respiratory tract epithelium and have a broad host range affecting a second viral enzyme, a DNA ligase. The integrated DS DNA then
farm and companion animals, birds and man. Some members also codes for new +ssRNAs which then serve as new genomes or mes-
have cell tropism for reticuloendothelial, enteric and neural cells senger RNAs. The later stage of viral replication is catalysed using
causing significant pathology and disease of the bowel and/or CNS. cellular enzymes and organelles.
In dogs two members are significant pathogens. The viruses con- In companion animals Feline leukaemia virus (FeLV) in sub-
cerned are canine distemper virus (CDV) in genus morbillivirus and family Oncovirinae and feline immunodeficiency virus (FIV) in
parainfluenzavirus-2 (PIV-2) in genus respirovirus. Both viruses are subfamily Lentivirinae cause significant diseases in cats. However
transmitted by aerosol which initiates primary infection in respira- in dogs and rabbits retroviruses are not significant pathogens. FeLV
tory tract and/or tonsilar epithelium and dissemination throughout is a leading killer of cats causing lymphosarcoma and leukaemia
the bronchial tree. Two-5 days later respiratory disease may follow which are the most important and common tumours of cats. Cats
with signs of primary fever, dyspnoea, nasal discharge, inappetance. become infected through close contact with other infected cats
Progeny virus from primary CDV replication also initiates infection and ingestion of or contamination from licking of wounds by infec-
of macrophages and then of lymphocytes both of which dissem- tious saliva during mutual grooming. Virus replicates in oropharynx
inate the progeny virus to the epithelium and lymphoid tissue and/or leukocytes followed by viraemia due to infected leuko-
of small intestine giving rise to vomiting and diarrhoea and then cytes (B cells, monocytes and macrophages) which disseminate the
anorexia. Other organs infected following macrophage-lymphocyte virus to bone marrow, thymus, salivary glands and reproductive
viraemia are neurones and brain macrophages and epithelia of organs. In the majority of cats FeLV causes a self limiting infection.
endometrium. Significant infection at these sites may result in CNS But in some 30% of infected cats a persistent infection remains
disease and/or transplacental invasion of the foetus which may depending on age. They remain non-viraemic with neutralising
die. The CNS disease signs observed are ataxia, muscle tremors and Feline Oncovirus Membrane Associated (FOCMA) antibodies.
and paralysis and coma. PIV-2 has been associated with kennel They do not shed virus and do not develop leukaemia. However, in
cough. Severe disease results during combined infection with CDV some cats, a persistent viremia is accompanied with high FOCMA
or Bordetella bronchiseptica. specific antibodies. These cats develop neutralising antibodies and
become healthy or the FOCMA antibodies decline and the cats
3.4. Rhabdoviridae develop leukaemia. Persistently infected cats are the source of dis-
ease spread. The virus is immune suppressive in those cats upon
Rabies virus (RV) in genus lyssavirus of family Rhabdoviridae has infection of T and B lymphocytes and myeloid cells. This is mani-
long been the most feared zoonosis. All mammals are susceptible to fest as lymphoid or myeloid leukaemia with increased blood count
RV. Viral particles are bacilliform and/or bullet-shaped, enveloped of lymphoblasts or myeloblasts, respectively, and lymphosarcoma.
and contain one molecule of non-infectious, linear, negative-sense, On the other hand infection may also lead to severe immunode-
single-stranded RNA. Common reservoir hosts are members of ficiency without lymphosarcoma development. Although the viral
canids (fox, dog, wolf and jackal), mustelidae (skunk, polecat and genome has been demonstrated in the tumours, the virus itself can
some other species) and chiropetra (bats). RV transmission is usu- be rarely isolated from such tumours. Generalised B cell tumours of
ally by bite of infected animals shedding virus produced in salivary lymph nodes (known as multicentric lymphosarcoma), thymic and
gland. Primary virus replication occurs in muscle fibres at the site of alimentary lymphosarcomas have been observed in FeLV infected
bite from where the progeny virus gains access into the nerve fibres cats. In the thymic form there is marked T cell hyperplasia enlarging
and migrates along the axoplasm centripetally. Once in the neurone thymus which eventually fills most of the thoracic cavity caus-
cell body virus replicates followed by centrifugal migration down ing dyspnoea. In the alimentary form B cell tumours develop in
the cranial nerves to the salivary gland where the virus replicates the wall of the intestine. These FeLV induced neoplasms may also
and is shed in saliva. RV occurs worldwide with the exception of result in haemolytic or hypoplastic anaemia, immunosuppression
countries which practice strict quarantine regulations. Rabies is an and reproductive failure. Infection of placenta followed by transpla-
increasing threat to cats and dogs in endemic areas and the infec- cental infection of foetus may result in foetal death.
tion is almost always fatal after a paralytic and respiratory distress FIV is found worldwide in domestic cats and wild felids namely
disease. In usual circumstances the only risk of rabies virus trans- snow leopards, lions, tigers, jaguars and bobcats. FIV infection in
mission is by the bite or scratch of a rabid animal, highly humid cats has three stages, just like HIV infection in humans. The initial
environment such as in bat caves the virus may be transmitted via acute stage is characterised by fever, swollen lymph nodes, oral,
respiratory, eye and intestinal symptoms which may be recurrent to these new important pathogens. Transmission of both heni-
or chronic in occurrence. Affected cats may have nasal and eye dis- paviruses to cats is possible since infected horses and pigs shed
charge, cloudy cornea and diarrhoea. In the second latent stage, virus oronasally [97,98]. Experimentally cats were susceptible to
often lasting many years the immune system is slowly destroyed Hendravirus by subcutaneous, intranasal, oral inoculation and also
leading to immunodeficiency followed by the third AIDS-like stage. to in contact transmission resulting in severe interstitial pneumo-
Feline immunodeficiency virus is shed mainly in the saliva and the nia, generalised thrombosis and necrosis of small blood vessels and
principal mode of transmission is through bites. In this perspec- necrotic lesions in lungs, intestine, liver and kidneys; infected cats
tive free-roaming animals are at the greatest risk of infection and shed virus in secretions of oropharynx and urine [99]. Oronasal
hence FIV is uncommon in closed catteries. Sexual contact does not inoculation of cats with a human isolate of Nipahvirus resulted
appear to be a significant mode of transmission although the virus in febrile respiratory and neurological disease in cats which also
may be shed in semen. The virus is transmitted to kittens from incurred vasculatis and haemorrhages in lymph nodes, trachea,
acutely infected queens through colostrum and milk [9]. lung and pulmonary infarcts.
Another potential cat pathogen is West Nile virus (WNV).
WNV is mosquito-transmitted flavivirus belonging to the Japanese
4. Emergent and potential virus diseases encephalitis (JE) serocomplex of the family Flaviviridae [100]. All
members of the JE complex are transmitted by mosquitoes. Bird-
An important event in companion animal viral disease ecology feeding mosquitoes are the principal vectors of WNV. WNV has
has been the jump by contemporary strains of equine influenza been isolated from 43 mosquitoe species mainly of the genus
H3N8 virus (Orthomyxovirus) to racing dogs first recognised during Culex [101]. High long-term viraemia, sufficient to infect vector
an outbreak of respiratory disease in racing greyhounds at a kennel mosquitoes is required for field transmission of WNV. The latter
in Florida in January 2004 [84]. In this outbreak 8 greyhounds died occurs in infected birds which are the principal reservoir hosts
of haemorrhagic pneumonia while 14 remaining dogs had a milder of WNV whereas mammals are less important. Bird-mosquitoe
illness manifest initially as fever and then coughing for 10–14 days. cycle in wetlands is the common mode of WNV transmission but
A variety of tests including genetic sequence analysis and phylo- bird-tick cycle in certain dry and warm habitats also occurs [101].
genetic comparisons led to the conclusion that all three canine Importantly for this paper WNV naturally infects dogs [102–105],
flu virus isolates from January 2004 outbreak had evolved from cats [104]. Susceptibility of dogs and cats to WNV has also been
equine influenza H3N8 virus and formed a single phylogenetic clus- investigated experimentally [106]. Strains of WNV vary signifi-
ter. The prototype strain was then named A/canine/Florida/43/2004 cantly in virulence for mammalian and avian species [107–109].
(canine/FL/04).These authors also concluded that the entire (all The insect bite results in viraemia and visceral viral replication
eight RNA segments) of the horse virus had been transmitted to the which produces secondary viraemia which could lead to CNS infec-
dog. This may have been neither the first nor the last episode of the tion. The visceral viral replication may cause fever, depression
disease. Tests on archival dog sera and lung tissue and dog sera col- anorexia and some mortality while CNS replication may result in
lected in early 2005 from various states of USA indicate occurrence encephalitis and neurological signs such as tremors, ataxia and
of canine H3N8 influenza virus prior to and after the 2004 outbreak death [110,108,111]. Infected dogs and cats may undergo this pat-
[84]. These authors also provide evidence of the virus’s transmissi- tern of disease pathogenesis although it is very rare for cats and
bility to pet dogs and the data suggest virus transmission by virus dogs to be infected in the wild.
aerosol. Occurrence of an isolated case of canine H3N8 flu virus
in the UK was identified by serology [85]. One important factor in 5. Immunoprophylaxis
interspecies transmission of any virus including influenza viruses is
the presence of appropriate viral receptors in the respiratory tract As described earlier, vaccines are available for many years
epithelial cells of the novel host. The equine influenza haemag- against the common well known diseases. For dog viral (and bacte-
glutinin recognises ␣2,3 sialic acid linkages. Of concern would be rial) diseases, vaccines offered by the major companies are against
if the new H3N8 dog flu virus became more widespread in dog CDV, CAV-1 and 2, CPV, CPI-2 and rabies and some companies also
populations and if it jumped to cats. The dog is also susceptible for CCoV and one for CHV-1 in various combinations. For the cat
to highly pathogenic avian influenza (HPAI) virus of H5N1 subtype vaccines are available against diseases caused by FPLV, FCV, FHV-1,
[86,87] and the virus was the cause of fatal dog infection in Thai- FeLV, FCoV, FIPV, FIV and rabies virus. Vaccines from the companies
land [88,86]. Suceptibility of dogs to HPAI H5N1 disease has been are broadly similar in formulation and presentations (Tables 1 and 2
reproduced experimentally [87]. ) but vary with respect to the number of components. Furthermore,
HPAI H5N1 virus has also jumped to domestic cats and wild it is important to point out that some vaccine components consist
felids and natural HPAI H5N1 virus infection was the cause of fatal of live antigens whereas others of killed. The choice between live
disease in domestic cats and other large felids such as tigers and and killed depends largely on the immunological response which
leopards in Thailand [89,90,86]. The susceptibility of domestic cats is to be induced and the immunological background of the tar-
to HPAI H5N1 virus was also proven experimentally [91–93,87]. The get animal (presence of maternal derived antibodies, age at which
availability of appropriate receptor(s) in the lower respiratory tract the animal is supposed to be immune, etc.) Tables 1 and 2 rep-
(LTR) of the novel host is an important prerequisite for the novel resent the licensures in the UK, but it should be noted here that
virus to initiate infection in the new host and cause viral pneumo- in other countries, not all or other formulations may be licensed
nia. Like the dog, cat LTR (and also human’s) has terminal ␣2,3-Gal due to national or economic reasons. Viral vaccines are sometimes
linkages in the LTR [94] which are the preferred ligands for H5N1 dissolved in solvents containing bacterial components such as the
virus and apparently also for H3N8 influenza virus. Leptospira spp. and Bordetella brochispetica antigens. In the UK, for
In view of the fact that two newly emergent paramyxoviruses the dog viruses the number of products ranges from 3 (Pfizer) to
in the new genus henipavirus namely Hendravirus and Nipahvirus as many as 8 (Schering-Plough, S-P). Most companies have 5–6
have jumped species from reservoir petropid fruit bats to man, products, mostly as polyvalent (multi-disease) vaccines. For the
horses and pigs in Australia and the Far East causing fatalities cat, the products range is 2 (S-P, Virbac), 4 (Intervet), to 6 (F-D,
in all three unnatural hosts [95,96] it is important to be aware Merial). The reason for the multiple product range is likely to be
of experimental studies showing susceptibility of domestic cats the vaccine duration of immunity (DOI) varying from 1 year or
Table 1
Canine viral disease vaccines.
Company and trade name Vaccine Presentation Handling and claims
FORT DODGE 1. PPI + L V. LFD CPV (SAH) + CPI-5 V. K-L. Reconstitute V. LFD with K-L and apply S/C from 6 to 10 weeks
Duramune Range and again 3–4 weeks later. OI: from 2 weeks DOI: 1 year; CPI-5
unknown. Contra-indicated for pregnant bitches.
2. PPI + LC V. LFD: CPV (SAH) + CPI-5 (FDL) and V. As with PPI + L. OI: From 2 weeks. DOI: 1 year; CPI-5 unknown.
K-L + K-CCoV (TN449). Contra-indicated for pregnant bitches.
3. DAPPI + L V. LFD: CDV (Onderstepoort) +CAV-2 As with PPI + L. OI: From 2 weeks. DOI: 3 years for CDV, CAV and
(V197) + CPV (SAH) + CPI-5 (FDL) and V. K-L. CPV but CPI-5 unknown. Contra-indicated for pregnant bitches.
4. DAPPI + LC Same live viruses as 3 and V.-K + K-CCoV As with PPI + L. OI: From 2 weeks. DOI: 1 year for all antigens
(TN449). except CPI-5. Contra-indicated for pregnant and lactating
bitches.
5. PPI + LC Same live viruses as 1 and V. K-L + K-CCoV As with PPI + L. OI: From 2 weeks. DOI: 1 year for all antigens
(TN449). but CPI-5 unknown.
6. Puppy DP + C V. LFD: CDV (Onderstepoort) + CPV (SAH) and Reconstitute V. LFD with solvent and apply S/C from 6 to 10
V. K-CCoV (TN449) and solvent. weeks and again 2–4 weeks later. OI: from 2 weeks. DOI: 1
year. Contra-indicated for pregnant and lactating bitches.
INTERVET Nobivac 1.DHP V. LFD: CDV (Onderstepoort) + CAV-2 Reconstitute V. LFD with solvent or Nobivac Lepto2 or Nobivac
Range (Manhattan LPV3) + CPV (1543 ) and solvent. Rabies and apply S/C from 6 weeks and again at 10 weeks. OI: 1
week (CDV and CPV) 2 weeks (CAV). DOI: 3 years.
2. DHPPI Same as DHP + live CPI-5 and solvent. As with DHP vaccine. OI: 1 week (CDV, CPV and CAV) and 4
weeks (CPI-5). DOI: 3 years (CDV, CPV and CAV); CPI-5
unknown.
3. Parvo-C V. LFD CPV and solvent. Reconstitute as per DHP vaccine and apply S/C from 4 weeks
and booster at 10 weeks but a single dose for puppies 10 weeks
and older. OI: 1 week. DOI: 3 years.
4. PI V. LFD CPI-5 (Cornell) and solvent. Reconstitute as per DHP Vaccine and apply S/C from 8 weeks
and booster 2–4 weeks later. OI: 4 weeks. DOI: unknown.
5. Rabies V. K-Rabies (pasteur RIV) + Al (OH) adjuvant. Apply S/C to dogs and cats from 4 weeks when puppies should
be boosted at 3 months. OI: 2–3 weeks. DOI: 3 years.
MERIAL Eurican 1. Herpes 205 V. K-CHV-1 (F205) gB glycoprotein Apply S/C near or soon after mating and again 1–2 weeks
Range (0.3–1.75 ␮g) in oil adjuvant. before whelping and similarly at or during each pregnancy.
2. DHPPI V.LFD: CDV + CAV + CPV + CPI-2. Reconstitute with Eurican L vaccine and apply S/C from 8
weeks and boost 3–5 weeks later and then annually.
3. L V. K-L As with DHPPI. OI: 2 weeks. DOI: 1 year.
4. P V. LFD: CPV. As with DHPPI but single injection for dogs 12 weeks and older.
OI: 1 week. DOI: 1 year.
5. Rabisin V. K-Rabies with Al (OH) adjuvant. Apply S/C to dogs and cats from 3 months and boost every 2
years.
PFIZER Vangard 1. 7 V. LFD: CDV (Synder Hill) + CAV-2 Reconstitute V. LFD with V. LS + K-L and apply S/C twice 2
Range (Manhattan) + CPI-5 (NL) V. LS: CPV weeks apart to puppies 10 weeks and younger but single dose
(NL-35-D) + K-L. for older dogs OI: 2 weeks. DOI: 1 year (also for CAV-1) but
unknown for CPI-5. Contra-indicated for pregnant bitches.
CPV V. LS CPV (NL35-D). As per Vangard 7. OI: 2 weeks. DOI: 1 year. Contra-indicated for
pregnant bitches.
CPV-L V. LS CPV (NL35-D) + K-L As per Vangard 7. Same claims as CPV vaccine.
Contra-indicated for pregnant bitches.
SCHERING–PLOUGH 1.Dog DA2 PPI/CVL V. LFD: CDV (Distemperoid) + CAV-2 Reconstitute V. LFD with V. K-CC+ K-L and apply S/C or I/M
Procyon & (Ditchfield) + CPV (SAH 2b) + CPI (Philips from 6 weeks and boost 3–4 weeks later. OI: 3–4 weeks. DOI: 3
Quantum Range Roxane) V. K-CCoV (FEC-SAH) + K-L. years for CDV, CAV (1 and 2) and CPV; 1 year for CPI, CCoV and
Lepto serovars.
2. Dog DA2 PPI/L Same as DA2 PPI/CVL but without CCoV. Same as DA2 PPI/CVL vaccine for the components present
including claims.
3. Dog PI/CVL V. LFD: CPI (Philips Roxane) V. K-CCoV (FEC Reconstitute as vaccines 1 and 2. Same claims for the active
SAH) + K-L (115 and 117). components present in DA2 PPI/CVL.
4. Dog PI/L Same as vaccine 3 but without CCoV antigen. Reconstitute and apply as vaccine 1. Same claims for the
components present in vaccine 1.
5. Dog 7 V. LFD: CDV + CAV-2 + CPI-2 V. LS CPV + K-L. Reconstitute V. LFD with V. LS CPV + K-L + and apply S/C twice
from 10 weeks and again at 12 weeks but a single dose to older
puppies and then annually.
6. Dog CPV V. LS CPV. Apply S/C from 6 weeks and again at 12 weeks and then
annually. There are other options.
7. Dog CPV-L V. LS CPV + K-L. Apply as per Quantum CPV.
8. Rabies V. K-Rabies (Flury) suspension with Al (OH) Apply S/C to dogs and cats from 3 months and then every 3
Adjuvant. years.
VIRBAC Canigen 1. DHP V. LFD CDV (Onderstepoort) + CAV-2 Reconstitute V. LFD with solvent or Canigen Lepto 2 or Canigen
Range (Manhatan) + CPV (1543 ) and solvent. Rabies and apply S/C from 6 weeks and again at 12 weeks. OI: 1
week for CDV and CPV and 2 weeks. DOI: 3 years when booster
recommended.
Table 1 (Continued)
2. DHPPI V. LFD: CDV + CAV-2 + CPV + CPI and solvent. Reconstitute V. LFD with Canigen
Lepto 2 or solvent and apply S/C
from 6 weeks and again 4 weeks
later. Additional dose of Canigen PI
recommended at 8 weeks. DOI: 3
years for CDV, CPV and CAV and 1
year for CPI when booster
recommended. Not recommended
for ferret and mink.
3. PI V. LFD: CPI and solvent. Reconstitute V. LFD with solvent or
Canigen Lepto 2 or Canigen Rabies
and apply S/C from 8 weeks and
again 2–4 weeks later but a single
dose 12 weeks onwards and then
annual booster. OI: 4 weeks. DOI: 1
year.
4. Rabies V. K-Rabies (Pasteur Apply S/C or I/M to dogs and cats
RIV) + aluminium phosphate from 3 months and then every 3
adjuvant. years. OI: 2–3 weeks. DOI: 3 years.
Vaccines are sold in the UK. It is therefore possible, dependent on licensing authorisation sought by the companies, that there is variation in products and product composition
available in other countries. Tables are merely a guide to actual formulations that are possible.
Abbreviations: V. = vial of; LFD = live freeze dried pellet of viruses; LS = live suspension of; K = inactivated, as liquid suspension or emulsion of; S = suspension; L = mixture
of Leptospira serovars canicola and icterohaemorrhagiae; + = combined with; OI = onset of immunity in weeks after the primary course of vaccination; DOI = duration of
immunity in years; MDA = maternally derived antibody to antigen(s); S/C = subcutaneous; I/M = intramuscular. See text for abbreviated virus names.
less (CPI-2, FeLV) to 3 years (CDV, CAV-2, CPV and rabies virus); vaccine based on the Onsterstepoort strain is safe and efficacious
for most diseases one vaccine formulation would protect against in Lions by eliciting a protective neutralising antibody response
diseases ranges from 5 to 8 and 2 to 5 for the dog and cat viral [119]. The same vaccine has been used effectively in otters and
and bacterial diseases, respectively. It should be noted that not seals (showing vaccine efficacy in the face of Phocine distemper
all companies claim DOI of 3 years for CPV disease. Also notewor- outbreak (Intervet/Schering-Plough, unpublished). The live vaccine
thy is the fact that most, with an odd exception, of these vaccines safety concern and the global CDV distribution involving a wide
were derived by conventional attenuation and/or inactivation pro- variety of susceptible species, require new safe vaccines for the pro-
cesses in tissue culture some 10–20 years ago. The tissue culture tection of wild species as well as eradication or reduction of CDV
technologies have been much refined to aid the production, qual- from wildlife [115]. A further requirement is strategies for wildlife
ity (purity and control) and improved yield of active components. vaccination as has been used for rabies and anticipated for RHDV
Another important point to mention is that these various vaccines and MV diseases of wild rabbits (see below).
contain different viral strains and their efficacy was assessed using Although canine H3N8 flu virus disease is quite new, plans for
different challenges (virus strains, inocula, animals) and sample vaccine against it were afoot soon after the outbreak of the fatal
analysis was using different tests. This clearly does not allow an respiratory disease [84]. These authors were working towards a
objective analysis of their relative efficacy. Because of the age of vaccine for this new dog disease (personal communication by Dr.
these vaccines and the recent emergence of virulent variants of Cyanda Crawford to Allison Clark [120]. That there is commer-
some viruses notably CPV (the 2a, 2b and 2c variants) and FCV (VS- cial interest in canine H3N8 flu virus vaccine is indicated by a
FCV) [22,23,112] and the new respiratory coronavirus (see above recent controlled efficacy study in dogs with two experimental
for references) the need for assessment of efficacy of these now canarypoxvirus-H3 subtypes (from two strains) live recombinant
old vaccines against the newly emergent viruses is clearly nec- vaccine [121]. This study was a joint effort by Merial, Sanofi Pasteur
essary but would be costly. There are only limited investigations and Cornell University.
on this subject. An exception, to our knowledge, is the recent con- For the cat there are FCV vaccines from several companies
trolled study in susceptible dogs for CPV 2 component in Nobivac (Table 2) but their efficacy against the newly emergent VS-FCV
DHPPi (Table 1) against CPV 2c oral challenge which showed that [35,112] remains unknown. The development of vaccines against
the vaccine was fully cross protective [113]. Published informa- FIP coronavirus (FIPV) has proved cumbersome and consequently
tion on the prevalence and the incidence of disease due to the there is only one (Pfizer’s, not in Table 2) live intranasal temperature
recently recognised group 2 respiratory coronavirus [65] is limited sensitive (TS) vaccine licensed in some countries [122,123]. How-
but this could be another pathogen for which immunoprophylaxis ever efficacy of this TS FIPV vaccine is a matter of debate [124,125].
may be needed. Domestic and scavenging dogs are a significant A promising experimental oronasal live FIPV vaccine lacking group-
source of human rabies worldwide and vaccination of dogs has been specific gene cluster 3abc, derived by site directed mutagenesis of
highly beneficial in this respect [114]. CDV is a cause of fatal dis- a virulent lethal FIPV strain was an innocuous efficacious vaccine
ease in many species of carnivores. CDV related viruses have been [126]. Clearly there is a way to derive an effective FIPV vaccine.
identified in seals (phocid distemper virus), dolphins, whales and The observation that cats can recover naturally from FeLV infec-
porpoises [115,116], and vaccination strategies have shown some tion led to development of vaccines (see Table 2). These however
success [117]. CDV transmitted by domestic dogs was associated are not fully protective [127–129]. Thus there is an ongoing effort to
with fatal neurological disease in lions in Serengeti National Park develop improved effective FeLV vaccines. The target is for a vaccine
in Tanzania and dog vaccination against CDV in affected areas was that would prevent establishment of both viraemia and latent bone
beneficial [118]. Although currently available live CDV vaccines are marrow infection. The approaches investigated have been vaccinia-
suitable for immunising domestic dogs and farmed mink. A CDV FeLV [130], canarypox-FeLV [131] and FHV-1-FeLV [132] live vector
Table 2
Feline viral disease vaccines.
FORT DODGE 1. FELV V. K-FELV (A7B) + adjuvant. Apply twice S/C 3–4 weeks apart from 9 weeks
Fevaxyn & Katavac and boost annually. Can be used to reconstitute
Range Katavac CHP.
2. ICHP V. K-FPLV + FHV-1 + FCV + mineral oil adjuvant. Apply twice S/C 3–4 weeks apart from 8 weeks
and then annually.
3. ICHPCHLAM V. K-FPLV + FHV-1 + FCV + Chlamydophila As ICHP from 8 weeks.
psittaci + mineral oil adjuvant.
4. PENTOFEL V. K-FPLV + FHV-1 + FCV + Chlamydophila As ICHP from 9 weeks.
psittaci + FeLV + adjuvant (Ethylene/maleic
anhydride + neocryl XK-62 + emulsigen SA).
5. KATAVAC CHP V. LFD: FCV + FHV-1 + FPLV and solvent. Reconstitute V. LFD in solvent or Fevaxyn FELV
and apply S/C to kittens from 9 weeks but once
to cats 12 weeks and older.
6. KATAVAC ECLIPSE V. LFD: FCV + FHV-1 + FPLV V. Fevaxyn FeLV. Reconstitute V. LFD with V.K-FeLV and apply
twice S/C 3–4 weeks apart from 9 weeks and
boost annually.
INTERVET 1. DUCAT‘ V.LFD: FHV-1 (G2620A) + FCV (F9) and solvent. Reconstitute V. LFD with solvent or Nobivac
Nobi- Rabies (Table 1) and apply S/C to cats from 8
vac weeks onwards and again 3–4 weeks later and
Range boost annually.
2. FELV V. Subunit p45 FeLV envelope + Al (OH) and Apply S/C or I/M twice from 9 weeks onwards 3
Quil A. weeks apart and boost annually. OI: 3–4 weeks.
3. FORCAT V. LFD: FHV-1 (G2620A) + FCV (F9) + FPLV Reconstitute V. LFD with Nobivac FELV or
(MW-1) + Chlamydophila felis (Baker). Rabies or solvent and apply S/C twice 3–4
weeks apart 9 weeks onwards and boost
annually. OI: 3–4 weeks. DOI: 1 year (FHV-1,
FCV and C. Felis) and 3 years (FPLV).
4. TRICAT V. LFD: FHV-1 + FCV + FPLV and solvent. As with FORCAT. O I: 1 week (all antigens).
MERIAL Purevax 1. FELV V. Suspension of live Canarypox (vCP97)-FeLV Apply S/C twice 3–5 weeks apart from 8 weeks
Range recombinant and solvent. and boost annually. Contra-indicated for
pregnant animals but indicated for lactating
cats.
2. RC V. LFD: FHV-1 (F2) + K-FCV (431 and G1) and As with FELV. For high levels of MDA delay
solvent. vaccination to 12 weeks and primary course
booster 3–4 weeks later.
3. RCP V. LFD: FHV-1 (F2) + FPLV (PLIIV) + K-FCV (431 As with RC.
and G1) and solvent.
4. RCPCH V. LFD: FHV-1 (F2) + FPLV (PLIIV) + C. felis (905) As with RCP from 8 weeks.
and solvent.
5. RCPCHFELV V.LFD: FHV-1 (F2) + FPLV + C. felis As with RC or RCP.
(905) + Canarypox-FeLV + K-FCV (431 and G1)
solvent.
6. RCPFELV V. LFD FHV-1 (F2) + FPLV (PLIIV) + Canarypox As with RC or RCP.
(vCP97)-FeLV recombinant + K-FCV (431 and
G1) and solvent.
Pfizer Felocell 1. CVR V. LFD: FPLV (snow leopard strain) + FHV-1 Reconstitute V. LFD with solvent and apply S/C
(FVRm) + FCV (F9) and solvent. twice 3–4 weeks apart from 9 weeks and boost
annually. Contra-indicated for pregnant
queens.
SCHERING-PLOUGH Cat CVRP V. LFD FCV + FHV-1 + FPLV and solvent. Reconstitute V. LFD with solvent or Quantum
Quantum Range cat FELV and apply S/C twice 3–4 weeks apart
from 9 weeks and boost annually.
Contra-indicated for pregnant cats. OI: 3
weeks. DOI: 1 year.
Cat FELV Suspension of subunit FeLV glycoprotein 70 As with Quantum CVRP but safe for pregnant
and FOCMA antigens + adjuvant. cats. OI: 3 weeks. DOI: 1 year.
VIRBAC 1. Feligen RCP V. LFD: FPLV (DSV LR 72) + FHV-1 (F2) + FCV Reconstitute V. LFD with solvent or Leucogen
(F9) and solvent. and apply twice S/C from 9 weeks and again 2
weeks later and then annually.
Contra-indicated in pregnancy.
2. Leucogen V. p45 FeLV envelope antigen expressed in E. Apply S/C or I/M twice from 9 weeks and again
coli + Al (OH) and Quil A as adjuvants. 2–3 weeks later and then annually.
Recommended for queens prior to mating.
See Table 1 text for rabies virus vaccine for immunising cats. See legend of Table 1.
vaccines. The vaccinia-FeLV vaccine was ineffective while the other FIV is a cause of significant disease in domestic cats world-
two live vector vaccines were not better than existing vaccines. wide. Immunoprophylaxis for FIV disease is limited and only one
However, experimental vaccines that showed excellent protection company (F-D) offers a vaccine, approved in spring 2002. Cur-
were the FeLV iscoms [133] and FeLV DNA co-administered with rently the use of the vaccine is not recommended by The American
interleukin 12 (IL-12) and IL-18 cytokine genes [134]. Association of Feline Practitioners. Like its human counterpart, the
Table 3
Rabbit and Pigeon viral disease vaccines.
Vaccines for rabbits

CEVA Lapinject VHD V. K-RDDV (P174) + oil adjuvant. Apply S/C from 5 weeks and boost
annually. OI: 6 days. DOI: 1 year. Safe
for pregnant rabbits.
FORT DODGE Cylap V. K-RHDV + oil adjuvant. Apply twice S/C from 2.5 to 3 months
and 4 weeks later and then annually.
Safe for pregnant rabbits.
INTERVET Nobivac Myxo V. LFD: Shope fibroma virus and solvent. Reconstitute V. LFD with solvent and
virus and solvent and apply intra
dermally or S/C from 6 weeks and older
rabbits. OI: 2 weeks and DOI: 6
months. Contra-indicated for breeding
and pregnant rabbits.
Vaccines for pigeons

FORT DODGE 1. PMV V. K-PMV-1 + adjuvant. Apply S/C to racing and show pigeons
Colombovac Range from 3 weeks and then annually. Adult
birds can be similarly vaccinated.
2. PMV/POX V. LFD PPV V. K-PMV-1 + adjuvant. Reconstitute V.LFD PPV with V.
K-PMV-1 and apply S/C to racing and
show pigeons from 6 weeks and then
annually. Adult birds can be similarly
vaccinated.
INTERVET NOBILIS PARAMYXO V. K-PMV-1 + mineral oil adjuvant. Apply S/C from 6 weeks before race or
exhibition and then annually. OI: 4
weeks. DOI: 1 year.
See legend of Table 1.
immunodeficiency virus of human AIDS, FIV presents a formidable RHDV has failed to grow in tissue culture, various expression vec-
challenge for vaccine development despite a vigorous host immune tors have been developed for the production of RHDV capsid VP60
response to the virus. Various approaches for a vaccine have been protein. These vectors comprise E. Coli [142], Saccharomyces cere-
investigated [135] with some success. It has been shown that visae [143], poxviruses: myxoma [144], vaccinia [145], canarypox
a multi-epitopic vaccine for instance does induce an immune [146]. VP60 was also produced in rabbit kidney cell line RK-13
response which is not protective [136]. An important difficulty has [147] and potato [148] and baculovirus [149]. Many of the vector
been the strain specificity of vaccines in that experimental vaccines expressed VP60 antigens incorporated into experimental vaccines
were not protective for heterologous strains [137]. The newly emer- were immunogenic and protective for rabbits against fatal RHDV
gent HPAI H5N1 induced viral disease in dogs and cats is clearly challenge [150]. Commercially only one MV disease for domestic
a new challenge for the institutional and industrial virologists to rabbits is marketed by Intervet (Table 3). The latter is a live het-
develop yet another vaccine. In this regard a conventional killed erotypic vaccine based on less pathogenic leporipox Shope fibroma
adjuvanted H5N6 flu virus vaccine was protective against lethal virus. For both RHDV and MV diseases a key requirement is vac-
HPAI H5N1 experimental challenge in a controlled efficacy study in cines which could be used for both domestic and wild rabbits.
cats [93]. The latter play an important ecological role in Mediterranean and
Booster vaccination after the primary course and DOI is an other ecosystems. This entails a strategy for wildlife immunisation
important issue in the recent vaccination debate particularly for which is feasible as has been achieved for sylvatic rabies control
the dog and cat vaccines. However, the time for the booster vacci- in Europe and North America by oral vaccines delivered by baiting
nation is difficult to assess since (i) response of individual animals [151–153]. Other methods are delivery by biting insects and/or by
to routine vaccination is highly variable which is also influenced direct horizontal animal to animal vaccine spread. All these three
by the level of MDA at primary vaccination, (ii) the frequency of modes of vaccination against RHDV and MV diseases were ele-
field exposure is often unknown and (iii) products vary with respect gantly demonstrated by controlled experimental challenge studies
to potency and formulation. Antibody test may be appropriate for [150]. However we do wonder if such a vaccine would indeed be
establishing residual immunity for some antigens but not all and commercialised.
the cost is likely to exceed that of booster vaccination [138]. How-
ever, in general, for the so-called core dog vaccines for CAV-2, CDV, 6. Conclusions
CPV and rabies and cat vaccines for FPLV, FCV, FHV-1 and rabies
published data suggest a minimum DOI of 3 years [139]. Therefore The main conclusions we draw from the above account of impor-
for these core vaccines a general vaccination guideline should be tant viral diseases of cats, dogs and rabbits are:
first vaccination at as early as 6 weeks of age or older (>12 weeks)
depending on disease and available vaccine type (live versus killed), 1. Viruses from several different families naturally infect these
then again at 1 year and then every 3 years. For the non-core vac- companion animals and cause significant disease. Most of the
cines yearly boosters are recommended. Animals with high MDA viruses are transmitted via the oropharyngeal route by virus shed
may require two vaccinations in the primary vaccination regimes. in secretions of saliva, nasal mucus, aerosol and/or faeces. Virus
For rabbits, diseases covered by vaccine companies are those in secretions is inhaled and/or ingested and initiates primary
due to RHDV and MV but the choice of vaccines is rather lim- replication in mucosa of the respiratory and/or intestinal tracts;
ited (Table 3). For RHDV CEVA and F-D have a similar formulation rabies virus shed in saliva, is however delivered to myocytes, the
of rabbit grown liver antigen [140,141] plus oil adjuvant. Since site of primary replication, via bite while myxomavirus is trans-
mitted by blood feeding arthropod vectors such as mosquitoes, [7] Patel JR, Didlick SD. Epidemiology, disease and control of infections in rumi-
fleas and others in addition to inhalation of virus. nants by herpesviruses—an overview. Journal of South African Veterinary
Association 2008;79(1):8–14.
2. In disease pathogenesis an important determinant for signifi- [8] Schock A, Reid HW. Characterisation of the lymphoproliferation in rabbits
cant disease is if the virus is able to infect leukocytes and then experimentally affected with malignant catarrhal fever. Veterinary Microbi-
be disseminated to internal organs for secondary replication ology 1996;53(1–2):111–9.
[9] Murphy FA, Gibbs EPJ, Horzinek MC, Studdert MJ. Veterinary virology. 3rd ed.
and cause pathology. However most cat and dog coronaviruses London: Academic Press; 1999.
are generally restricted to the primary site of infection and [10] Virustaxonomy: classification and nomenclature of viruses.Murphy FA, Fau-
cause acute, self-limiting mild enteric or respiratory and disease. quet CM, Bishop DHL, Ghabrial SA, Tarvis AW, Martelli GP, Mayo MA, Summers
MD, editors. Sixth report of the international committee for the taxonomy of
Vicerotopic virulent strains also occur naturally with variable viruses. Archives of virology. Vienna, Austria: Springer–Verlag; 1995 [supple-
frequency following mutational changes. Examples are FCoVs ment 1E].
causing infectious peritonitis and the recent cases of genotype [11] Fenner F, Ross J. Myxomatosis. In: Tompson HV, King CM, editors. The Euro-
pean rabbit. The history and biology of a successful colonizer. Oxford, England:
2 CCoV strain CB/05 disease in dogs. Like the coronaviruses,
Oxford University Press; 1994. p. 205–40.
most calicivirus infections of cats are limited to the respiratory [12] Kerr PJ, Best SM. Myxoma virus in rabbits. Reviews of Scientific and Technical
tract resulting in self-limiting disease but recent emergence of Office of OIE 1998;17:256–68.
vicerotropic VS-FCV variants cause severe disease in cats and the [13] Matsunaga Y, Chino F. Experimental infection of young rabbits with rabbit
parvovirus. Archives of Virology 1981;68(3–4):257–64.
disease pathogenesis has similarities to the usually fatal disease [14] Parrish CR, Carmichael LE. Antigenic structure and variation of canine par-
of rabbits due to RHDV. Leukocyte-associated viraemia is also vovirus type-2, feline panleukopenia virus, and mink enteritis virus. Virology
important in parvovirus disease of cats and dogs and related wild 1983;129(2):401–14.
[15] Ikeda Y, Nakamura K, Miyazawa T, Takahashi E, Mochizuki M. Feline host
felids and canids. range of canine parvovirus: recent emergence of new antigenic types in cats.
3. The tropism for enteric epithelium and virus survival in faces has Emerging Infectious Diseases 2002;8(4):341–6.
been important in evolution of the carnivore parvoviruses. CPV [16] Kelly WR. An enteric disease of dogs resembling feline panleucopaenia. Aus-
tralian Veterinary Journal 1978;54(12):593.
has naturally evolved relatively rapidly and the small evolution- [17] Appel MJ, Cooper BJ, Greisen H, Scott F, Carmichael LE. Canine viral enteritis. I.
ary changes have been in virus capsid VP2 gene and interestingly Status report on corona- and parvo-like viral enteritis. Cornell Veterianarian
were associated with the loss and then renovation of the feline 1979;69:123–33.
[18] Kelly WR, Atwell RB. Diffuse subacute myocarditis of possible viral aetiology: a
host range. cause of sudden death in pups. Australian Veterinary Journal 1979;55(1):36–7.
4. For the established viruses of the cats and dogs there is a good [19] Gumbrell RC. Parvovirus infection in dogs. New Zealand Veterinary Journal
choice of vaccines developed 10–20 years ago. Hence, they are 1979;27(6):113.
[20] Parrish CR, Aquadro CF, Strassheim LM, Evermann JF, Sgro J-Y, Mohammed
due for re-assessment for their efficacy for some components
HO. Rapid antigenic-type replacement and DNA sequence evolution of canine
notably the newly emergent CPVs and VS-FCV. There is however parvovirus. Journal of Virology 1991;65:6544–52.
the need for improved vaccines for FIPV, FeLV and FIV. This is [21] Parrish CR. The emergence and evaluation of canine parvovirus—an example
also the case for MV and RHDV vaccines for rabbits. Also needed of recent range mutation. Seminars in Virology 1994;5:121–32.
[22] Truyen U, Gruenberg A, Chang SF, Obermaier B, Veijalainen P, Parrish CR. Evo-
is RHDV vaccine for wild rabbits. lution of the feline-subgroup parvoviruses and the control of canine host
5. The recent emergence of HPAI H5N1 disease in cats and other range in vivo. Journal of Virology 1995;69(8):4702–10.
large felids and that of H3N8 equine influenza virus in dogs are [23] Truyen U, Platzer G, Parrish CR. Antigenic type distribution among canine
parvoviruses in dogs and cats in Germany. Veterinary record 1996;138:365–6.
significant developments and may require vaccines should the [24] Parrish CR, O’Connell PH, Evermann JF, Carmichael LE. Natural variation of
viruses get established in these novel hosts and spread more canine parvovirus. Science 1985;230(4729):1046–8.
widely. Also we should be aware that cats and dogs have the [25] Steinel A, Munson L, van Vuuren M, Truyen U. Genetic characterization of
feline parvovirus sequences from various carnivores. Journal General Virology
potential to acquire new viral diseases for example those due 2000;81:345–50.
henipa paramyxoviruses. [26] Buonavoglia C, Martella V, Pratelli A, Tempesta M, Cavalli A, Buonavoglia D,
et al. Evidence for evolution of canine parvovirus type-2 in Italy. Journal of
Acknowledgements General Virology 2001;82:3021–5.
[27] Nakamura M, Tohya Y, Miyazawa T, Mochizuki M, Phung HTT, Nguyen NH,
et al. A novel antigenic variant of canine parvovirus from a Vietnamese dog.
We are grateful to Miss Hanny van Lare for typing the refer- Archives of Virology 2004;149:2261–9.
ence list. JP’s thanks to Miss Susan Didlick for help with tricky [28] Ikeda Y, Mochizuki M, Naito R, Nakmura K, Mikami T, Takahashi E. Pre-
computer manoevers. We grately thank Professor Dr. Peter Rottier dominance of canaine parvovirus (CPV) in unvaccinated cat populations and
emergence of new antigenic types of CPV in cats. Virology 2000;278(1):13–9.
and Dr. Herman Egberink (University of Utrecht, Faculty of Vet- [29] Gamoh K, Shimazaki Y, Makie H, Senda M, Itoh O, Inoue Y. The pathogenicity
erinary Medicine, NL) and Drs. Jac Bergman and Stuart Chalmers of canine parvovirus type 2b, FP84 strain isolated from a domestic cat, in
(Intervet Schering Plough Animal Health) for their time and critical domestic cats. Journal of Veterinary Medicinal Science 2003;65:1027–9.
[30] Pollock RV, Carmichael LE. Canine viral enteritis. Veterinary Clinic North
comments on the subject of this article. American Small Animal Practice 1983;13(3):551–66.
[31] Evermann JF, McKeirnan AJ, Smith AW, Skilling DE, Ott RL. Isolation and iden-
References tification of caliciviruses from dogs with enteric infections. American Journal
Veterinary Research 1985;46(1):218–20.
[1] Patel JR, Heldens J. Equine herpesvirus 1 (EHV-1) and 4 (EHV-4)-epidemiology, [32] Schaffer FL, Soergel ME, Black JW, Skilling DE, Smith AW, Cubitt WD. Charac-
disease and immunoprophylaxis: A brief review. The veterinary Journal terization of a new calicivirus isolated from feces of a dog. Archives of Virology
2005;170:14–23. 1985;84(3–4):181–95.
[2] Heldens JG, Patel JR, Chanter N, Ten Thij GJ, Gravendijck M, Schijns VE, et al. [33] Mochizuki M, Kawanishi A, Sakamoto H, Tashiro S, Fujimoto R, Ohwaki M.
Veterinary vaccine development from an industrial perspective. Veterinary A calicivirus isolated from a dog with fatal diarrhoea. Veterinary Record
Journal 2008;178:7–20 [Epub ahead of print]. 1993;132(9):221–2.
[3] Patel JR, Heldens JG. Immunoprophylaxis against important virus diseases of [34] Pratelli A, Greco G, Camero M, Corrente M, Normanno G, Buonavoglia C.
horses, farm animals and birds. Vaccine, submitted for publication. Isolation and identification of a calicivirus from a dog with diarrhoea. New
[4] Marlier D, Vindevogel H. Viral infections in pigeons. Veterinary Journal Microbiology 2000;23(3):257–60.
2006;172(1):40–51. [35] Pedersen NC, Elliot JB, Glasgow A, Poland A, Keel K. An isolated epizootic
[5] Roizman B, Desrosier RC, Fleckenstein B, Lopez C, Minson AC, Studdert MJ. hemorrhagic-like fever in cats caused by a novel and highly virulent strain of
Family herpesviridae. In: Murphy FA, Fauquet CM, Bishop DHL, Ghabrial SA, feline calicivirus. Veterinary Microbiology 2000;73:281–300.
Jarvis AW, Martelli GP, Mayo MA, Summers MD, editors. Virus Taxonomy, 6th [36] Radford A, Coyne K, Dawson S, Porter C, Gaskell R. Feline calicivirus. Veterinary
report of the International Committee on Taxonomy of Viruses. Archives of Research 2007;38:319–35.
Virology. Wien, New York: Springer–Verlag; 1995, p. 114–27 [Supplement 10]. [37] Ossiboff R, Sheh A, Shotton J, Pesavento P, Parker J. Feline caliciviruses (FCVs)
[6] Meyer G, Lemaire, Lyaku J, Pastoret PP, Thiry E. Establishment of a rabbit isolated from cats with virulent systemic disease possess in vitro pheno-
model for bovine herpesvirus type 5 neurological acute infection. Veterinary types distinct from those of other FCV isolates. Journal of General Virology
Microbiology 1996;51:27–40. 2007;88:506–17.
[38] Kate F, Pasavento PA, Pederson NC, Poland AM, Wilson E, Foley JE. An out- RB, editors. Virus taxonomy, classification and nomenclature of viruses. New
break of virulent systemic feline calicivirus disease. Journal of the American York: Academic Press; 2000. p. 835–49.
Veterinary Medical Association 2004;224:241–9. [65] Erles K, Toomey C, Brooks HW, Brownlie J. Detection of a group 2
[39] Pasavento PA, MacLachlan NJ, Dillard-Telm L, Grant CK, Hurley KF, et al. Patho- coronavirus in dogs with canine infectious respiratory disease. Virology
logic, immunohistochemical and electron microscopic findings in naturally 2003;310(2):216–23.
occurring virulent systemic feline calicivirus infection in cats. Veterinary [66] Decaro N, Desario C, Elia G, Mari V, Lucente MS, Cordioli P, et al. Serological
Pathology 2004;41:257–326. and molecular evidence that canine respiratory coronavirus is circulating in
[40] Coyne K, Dawson S, Radvord A, Cripps P, Portes C, McCraken C, et al. Long- Italy. Veterinary Microbiology 2007;121:225–30.
term analysis of feline calicivirus prevalence and viral shedding patterns [67] Buonavoglia C, Decaro N, Martella V, Elia G, Campolo M, Desario C, et al.
in naturally infected colonies of domestic cats. Veterinary Microbiotogy Canine coronavirus highly pathogenic for dog. Emerging infectious diseases
2006;118:12–25. 2006;12:492–4.
[41] Liu SJ, Xue HP, Pu BQ, Qian SH. A new viral disease in rabbits. Animal Hus- [68] Decaro N, Martella V, Elia G, Campolo M, Desario C, Cuirone F, et al. Molec-
bandry and Veterinary Medicine 1984;16:253–5. ular characterization of the virulent canine coronavirus CB/05 strain. Virus
[42] Gustafson K, Svensson T, Uggla A. Studies ora idiopathic syndrome in the Research 2007;125:54–60.
brown hare (Lepus europeus P.) and mountain hare (Lepus timidus L.) in Swe- [69] Decaro N, Campolo M, Lorusso A, Desario C, Mari V, Colaianni ML, et
den, with special reference to hepatic lesions. Journal of Veterinary Medicine al. Experimental infection of dogs with a novel strain of caine coron-
A 1989;36:631–7. avirus causing systemic disease and lymphopenia. Veterinary Microbiology
[43] Moussa A, Chasey D, Lavazza A, Cappucci L, Smid B, Meyers G, et al. 2008;128:253–60.
Haemorrhagic disease of lagomorphs: evidence for a calicivirus. Veterinary [70] Hohdatsu T, Okada S, Ishizuka Y, Yamada H, Koyama H. The prevalence of types
Microbiology 1992;33:375–81. I and II feline coronavirus infections in cats. Journal of Veterinary Medical
[44] Fenner F, Fantini B. Biological control of vertebrate pets. The history of Science 1992;54:557–62.
myxomatosis—an experiment in evolution. Wallingford, Oxford: CABI Pub- [71] Poland AM, Vennema H, Foley JH, Pedersen NC. Two related strains of feline
lishing; 1999. pp. 237–272 [chapter 11]. infectious peritonitis virus isolated from immunocompromised cats with
[45] Cooke BD. Rabbit haemorrhagic disease: field epidemiology and the feline enteric coronavirus. Journal of Clinical Microbiology 1996;34:3180–4.
management of wild rabbit populations. Scientific and Technical Review [72] Vennema H, Poland A, Foley J, Pedersen NC. Feline infectious peritonitis
(International Office of epizootics) 2002;21:347–58. viruses arise by mutation from endemic feline enteric coronaviruses. Virology
[46] Guberti V, De Marro MA, Riga F, Lavazza A, Trocchi V, Capucci L. Virol- 1998;243(1):150–7.
ogy and species conservation: the case of EBHSV and the Italian hare [73] Pedersen NC. An overview of feline enteric coronavirus and infectious peri-
(Lepus corcicanus). In: Proceedings of the Bresica conference. 2000. p. 198– tonitis virus infections. Feline Practice 1995;23:7–20.
9. [74] de Groot RJH, Horzineck MC. Feline infectious peritonitis. In: Siddell SG, editor.
[47] Gregg DA, House C, Meyer R, Beringer M. Viral haemorrhagic disease of rabbits The coronaviridae. New York, NY: Plenum Press; 1995. p. 293–309.
in Mexico: epidemiology and viral characterization. Reviews of Scientific and [75] Groot-Mijnes JDF, van dun JM, van der Most RJ, de Groot RJ. Natural history of
Technical Office of OIE 1991;10:435–51. a recurrent feline coronavirus infection and the role of cellular immunity in
[48] Meneguz PG, Capucci L, Nieddu D, Lavazza A. Role of Sylvilagus floridanus in survival and disease. Journal of Virology 2005;79:1036–44.
the epidemiology of rabbit haemorrhagic disease and European brown hare [76] Haagman BL, Egberink HF, Horzinek MC. Apoptosis and T-cell depletion during
syndrome. In: Proceedings of the Brescia conference. 2000. p. 207–8. feline infectious peritonitis. Journal of Virology 1996;70:8977–83.
[49] Heath ACG, Heyward R, Norbury G. Blowflies (Calliphoridee) as potential vec- [77] Ward JM, Gribble DH, Dungworth DL. Feline infectious peritonitis: experi-
tors of rabbit haemorrhagic disease in New Zealand. Royal Society of New mental evidence for its multiphasic nature. American Journal of Veterinary
Zealand. Miscellaneous Series 1998;55:85–8. Research 1974;35:1271–5.
[50] Asgari S, Hardy JRE, Sinclair RG, Cooke BD. Field evidence of mechani- [78] Kipar A, Köhler K, Leukert W, Reinacher M. Evaluation of lymphatic tissue
cal transmission of rabbit haemorrhagic disease (HDV) by flies (Diptera: activity in cats with spontaneous feline infectious peritonitis. Journal of Com-
Calliphoridae) among wild rabbits in Australia. Virus Research 1998;54: parative Pathology 2001;125:182–91.
123–32. [79] Stoddart CA, Scott FW. Isolation and identification of feline peritoneal
[51] Lenghaus C, Westbury H, Collins B, Ratnamohran M, Morrissy C. Overview macrophages for in vitro studies of coronavirus-macrophage interactions.
of the RHD project in Australia. In: Munro RK, Williams RT, editors. Rabbit Journal of Leukocyte Biology 1988;44(5):319–28.
haemorrhagic disease: issues for assessment for biological control. Canberra: [80] Corapi WV, Olsen CW, Scott FW. Monoclonal antibody analysis of neutrali-
Australian Government Printing Service; 1994. p. 104–29. sation and antibody dependent enhancement of feline infectious peritonitis
[52] Le Gall G, Arnauld C, Boilletot E, Morisse JP, Rasschaest D. Molecular epi- virus. Journal of Virology 1992;66:6695–705.
demiology rabbit haemorrhagic virus outbreaks in France during 1988–1995. [81] Weiss RC, Scott FW. Antibody-mediated enhancement of disease in feline
Journal of General Virology 1998;79:11–6. infectious peritonitis: comparisons with dengue hemorrhagic fever. Compar-
[53] Nowotny N, Ros-Bascunana C, Ballagi-Pordany A, Gavier-Widen D, Uhlen H, ative Immunology, Microbiology of Infectious Diseases 1981;4(2):175–89.
Belak S. Phylogenetic analysis of rabbit haemorrhagic disease and European [82] Pedersen NC. Virologic and immunologic aspects of feline infectious peri-
brown hear syndrome viruses by comparision of sequences foom the capsid tonitis virus infection. Advances in Experimental Medicine and Biology
protein gene. Archives of Virology 1997;142:657–73. 1987;218:529–50.
[54] Grazolli S, Agnoletti F, Scicluna MT, Masoero N, Guercio A, Fallacara F, et al. [83] Ingersoll JD, Wylie DE. Identification of viral antigens that induce antibody
Rabbit haemorrhagic disease virus (RHDV) subtype A (RHDVa) is replacing responses on exposure to coronaviruses. American Journal of Veterinary
the original strain in some Italian regions. In: Proceedings of the Brescia Research 1988;49:1467–71.
Conference. 2000. p. 202–3. [84] Crawford PC, Dubovi EJ, Castleman WL, Stephenson I, Gibbes EPJ, Chen L, et
[55] Ramiro-Ibanez F, Martin-Alonso JM, Palencia PG, Parra F, Alonso C. al. Transmission of equine influenza virus to dogs. Science 2005;310:482–
Macrophage tropsim of rabbit hemmorrhagic disease virus associated with 5.
vascular pathology. Virus Research 1999;60:21–8. [85] Smith KC, Daly JM, Blunden AS, Laurence CJ. Canine influenza virus. Veterinary
[56] Fuchs A, Weissenböck H. Comparative histopathological study of rabbit haem- Record 2005;157(19):599.
orrhagic disease (RHD) and European brown hare syndrome (EBHS). Journal [86] Thiry E, Zicola A, Addie D, Egberink H, Hartmann K, Lutz H, et al. Highly
of Comparative Pathology 1992;107:103–13. pathogenic avian influenza H5N1 virus in cats and other carnivores. Veteri-
[57] Alonso C, Ovideo JM, Martin-Alonso JM, Diaz E, Boga JA, Para F. Programmed nary Microbiology 2007;122:25–31.
cell death in the pathogenisis of rabbit hemorrhagic disease. Archives of Virol- [87] Giese M, Harder TC, Teifke JP, Klopfleisch R, Briethaupt A, Mettenleiter TC, et
ogy 1998;143:321–32. al. Experimental and natural contact exposure of dogs with avian influenza
[58] Lai MM, Cavanagh D. The molecular biology coronaviruses. Advances in Virus virus (H5N1). Emerging Infectious Diseases 2008;14:308–10.
Research 1997;48:1–100. [88] Songserm T, Amonsin A, Jam-On R, Sae-Heng N, Pariyothorn N, Payungporn
[59] Herrewegh AA, Smeenk I, Horzinek MC, Rottier PJ, de Groot RJ. Feline S, et al. Fatal avian influenza A H5N1 in a dog. Emerging Infectious diseases
coronavirus type II strains 79-1683 and 79-1146 originate from a double 2006;12:1744–7.
recombination between feline coronavirus type I and canine coronavirus. [89] Kuiken T, Fouchier R, Rimmelzwaan G, Osterhaus A, Roeder P. Feline friend or
Journal of Virology 1998;72(5):4508–14. potential foe? Nature 2006;440:741–2.
[60] Pratelli A. Genetic evolution of canine coronavirus and recent advances in [90] Songserm T, Amonsin A, Jam-On R, Sae-Heng N, Meemak N, Pariyothorn N, et
prophylax is. Veterinary Research 2006;37:191–200. al. Avian influenza H5N1 in naturally infected domestic cat. Emerging Infec-
[61] Groneberg DA, Hilgenfeld R, Zabel P. Molecular mechanisms of severe acute tious Diseases 2006;12:681–3.
respiratory syndrome (SARS). Respiratory Research 2005;6:8. [91] Kuiken T, Rimmelzwaan G, van Riel D, van Amerongen G, Baars M, Fouchier
[62] Wang LF, Eaton BT. Bats, civets and the emergence of SARS. Current Topics in R, et al. Avian H5N1 influenza in cats. Science 2004;306:241.
Microbiology and Immunology 2007;315:325–44. [92] Rimmelzwaan GF, van Riel D, Baars M, Bestebroer TM, Fouchier RA, Osterhaus
[63] Martina BE, Haagmans BL, Fouchier RA, Rimmelzwaan GF, Van Amerongen ADME, et al. Influenza A virus (H5N1) infection in cats causes systemic dis-
G, Peris JS, et al. Virology: SARS virus infection of cats and ferrets. Nature ease with potential novel routes of virus spread within and between hosts.
2003;425:915. American Journal of Pathology 2006;168:176–83.
[64] Enjuanes L, Brian D, Cavanagh D, Holmes K, Lai MHC, Laude H, et al. Family [93] Vahlenkamp TW, Harder TC, Giese M, Lin F, Tiefke JP, Klopfleisch R, et al. Pro-
coronaviridae. In: van Regenmortel MHV, Fauquet CM, Bishop DHL, Carstens tection of cats against lethal influenza H5N1 challenge infection. Journal of
EB, Estes MK, Lemon SM, Maniloff J, Mayo MA, McGeoch DJ, Pringle CR, Wicher General Virology 2008;89:968–74.
[94] Van Riel D, Munster VJ, de Wit E, Rimmelzwaan GF, Fouchier RAM, oster- [123] Gerber JD. Overview of the development of a modified live temperature sen-
haus ADME, et al. H5N1 virus attachment to lower respiratory tract. Science sitive FIP virus vaccine. Feline Practice 1995;23:62–6.
2006;312:399. [124] Fehr D, Holznagel E, Bolla S, Hauser B, Herrewegh AA, Horzinek MC, et al.
[95] Halpin K, Young PL, Field HE, Mackenzie JS. Isolation of Hendra virus from Placebo-controlled evaluation of a modified live virus vaccine against feline
pteropid bats, a natural reservoir of Hendra virus. Journal of General Virology infectious peritonitis: safety and efficacy under field conditions. Vaccine
2000;81:1927–32. 1997;15:1101–9.
[96] Chua KB, Koh CL, Hooi PS, Wee KF, Chua BH, Chan YP, et al. Isola- [125] McArdle FB, Tennat B, Bennett M, Kelly DF, Gaskell CJ, Gaskell RM. Indepen-
tion of Nipah virus from Malaysian Island flying foxes. Microbes Infection dent evaluation of a modified live FIPV vaccine under experimental conditions
2002;4(2):145–51. (University of Liverpool experience). Feline Practice 1995;23:67–71.
[97] Middleton DJ, Westbury HA, Morrissy CJ, van der Heide BM, Russell GM, Braun [126] Haijema BJ, Volders H, Rottier PJM. Live, attenuated coronavirus vac-
MA, et al. Experimental Nipah virus infection in pigs and cats. Journal of cines through the directed deletion of group specific genes provide
Comparative Pathology 2002;126(2–3):124–36. protection against feline infectious peritonitis. Journal of General Virology
[98] Hsu VP, Hossain MJ, Parashar UD, Ali MM, Ksiazek TG, Kuzmin I, et al. Nipah 2004;78:3863–71.
virus encephalitis re-emergence, Bangladesh. Emerging Infectious Diseases [127] Jarrett O, Ganiere JP. Comparative studies of the efficacy of a recombinant
2004;10(12):2082–7. feline leukemia virus vaccine. Veterinary Record 1996;138:7–11.
[99] Hooper CD, Sparkes AH, Harbour DA. Feline immunodeficiency virus. In: Chan- [128] Legendre AM, Hawks DM, Sebring R, Rohrbach L, Chavez L, Chu HJ, et al. Com-
dler EA, Gaskell CJ, Gaskell RM, editors. Feline medicine and therapeutics. parison of the efficacy of three commercial feline leukemia virus vaccines
Cambridge, MA: Blackwell Scientific Publications; 1994. p. 506–14. in a natural exposure challenge. Journal of the American Veterinary Medical
[100] Calisher CH, Karabatsos N, Dalrymple JM, Shope RE, Porterfield JS, West- Association 1991;199:1456–62.
away EG, et al. Antigenic relationships between flaviviruses as determined by [129] Pollock RV, Scarlett JM. Randomised blind trial of a commercial FeLV vaccine.
cross-neutralization tests with polyclonal antisera. Journal of General Virol- Journal of the American Veterinary Medical Association 1990;196:611–6.
ogy 1989;70:37–43. [130] Gilbert JH, Pedersen NC, Nunberg JH. Feline leukemia virus envelope pro-
[101] Hubálek Z, Halouzka J. West Nile fever—a reemerging mosquito-borne viral tein expression encoded by a recombinant vaccinia virus: apparent lack of
disease in Europe. Emerging Infectious Diseases 1999;5(5):643–50. immunogenicity in vaccinated animals. Virus Research 1987;7:49–67.
[102] Simpson VR, Kuebart G, Barnard B. A fatal case of Wesselsbron disease in a [131] Tartaglia J, Jarrett O, Niel JC, Desmettre P, Paoletti E. Protection of cats against
dog. Veterinary Record 1979;105(14):329. feline leukemia virus by vaccination with a canarypox virus recombinant
[103] Blackburn NK, Reyers F, Berry WL, Shepherd AJ. Susceptibility of dogs to West ALVAC-FL. Journal of Virology 1993;67:2370–5.
Nile virus: a survey and pathogenicity trial. Journal of Comparative Pathology [132] Wardley RC, Berlinski PJ, Thomsen DR, Meyer AL, Post LE. The use of feline
1989;100(1):59–66. herpesvirus and baculovirus vaccine vectors for the gag and env genes of
[104] Komar N. West Nile viral encephalitis. Revue Scientifique et Technique feline leukemia virus. Journal of General Virology 1992;73:1811–8.
2000;19(1):166–76. [133] Osterhaus A, Weijer K, Uytdehaag F, Jarrett O, Sundquist B, Morein B. Induction
[105] Lichtensteiger CA, Heinz-Taheny K, Osborne TS, Novak RJ, Lewis BA, Firth of protective immune response in cats by vaccination with feline leukemia
ML. West Nile virus encephalitis and myocarditis in wolf and dog. Emerging virus in Iscom. Journal of Immunology 1985;135:591–6.
Infectious Diseases 2003;9(10):1303–6. [134] Hanlon L, Argyle D, Bain D, Nicolson L, Dunham S, Golder MC, et al. Feline
[106] Austgen LE, Bowen RA, Bunning ML, Davis BS, Mitchell CJ, Chang GJ. Experi- leukemia virus DNA vaccine efficacy is enhanced by co-administration with
mental infection of cats and dogs with West Nile virus. Emerging Infectious interleukin-12 (IL-12) and IL-18 expression vectors. Journal of Virology
Diseases 2004;10(1):82–6. 2001;75:8424–33.
[107] McMinn PC. The molecular basis of virulence of the encephalitogenic fla- [135] Hosie MJ, Flynn JN, Rigby MA, Cannon C, Dunsford T, Mackay NA, et al. DNA vac-
viviruses. Journal of General Virology 1997;78:2711–22. cination affords significant protection against feline immunodeficiency virus
[108] Cantile C, Del Piero F, Di Guardo G, Arispici M. Pathologic and immunohisto- infection without inducing detectable antiviral antibodies. Journal of Virology
chemical findings in naturally occuring West Nile virus infection in horses. 1998;72(9):7310–9 [erratum in: J Virol 1998;72(10):8460].
Veterinary Pathology 2001;38(4):414–21. [136] Flynn JN, Cannon CA, Neil JC, Jarrett O. Vaccination with a feline immun-
[109] Beasley DW, Li L, Suderman MT, Barrett AD. Mouse neuroinvasive phenotype odeficiency virus multiepitopic peptide induces cell-mediated and humoral
of West Nile virus strains varies depending upon virus genotype. Virology immune responses in cats, but not confer protection. Journal of Virology
2002;296(1):17–23. 1997;71:7586–92.
[110] Steele KE, Linn MJ, Schoepp RJ, Komar N, Geisbert TW, Manduca RM, et al. [137] Hosie M, Osborne R, Yamamoto JK, Neil JC, Jarrett O. Protection against
Pathology of fatal West Nile virus infections in native and exotic birds dur- homologous but not heterologous challenge induced by inactivated feline
ing the 1999 outbreak in New York City, New York. Veterinary Pathology immunodeficiency virus vaccines. Journal of Virology 1995;69:1253–5.
2000;37(3):208–24. [138] Burr P. Serological testing—an alternative to boosters? Veterinary Microbiol-
[111] Read RW, Rodriguez DB, Summers BA. West Nile virus encephalitis in a dog. ogy 2006;117:39–42.
Veterinary Pathology 2005;42:219–22. [139] Schultz RD. Duration of immunity for canine and feline vaccines: a review.
[112] Radford AD, Dawson S, Coyne KP, Porter CJ, Gaskell RM. The challenge for Veterinary Microbiology 2006;117:75–9.
the next generation of feline calicivirus vaccines. Veterinary Microbiology [140] Arguello JL. Viral haemorrhagic disease of rabbits: vaccination and immune
2006;117:14–8. response. Review of Scientific and Technical Office of OIE 1991;10:471–80.
[113] Spibey N, Greenwood NM, Sutton D, Chalmers WSK, Tarpey I. Canine par- [141] Ohlinger VF, Thiel HJ. Rabbit hemorrhagic disease (RHD): characterization of
vovirus type 2 vaccine protects against virulent challenge with type 2c virus. the causative calicivirus. Veterinary Research 1993;24:103–16.
Veterinary Microbiology 2008;128:48–55. [142] Boga JA, Casais R, Martin MS, Martin-Alonse JM, Cármenes RS, Prieto M, et al.
[114] Cleaveland S, Kaase M, Knobel D, Laurenson MK. Canine vaccination- Molecular cloning, sequencing and expression in Escherichia coli of the capsid
providing broader benefits for disease control. Veterinary Microbiology protein gene from rabbit haemorrhagic disease virus (Spanish isolate AST/89).
2006;117:43–50. Journal of General Virology 1994;75:2409–13.
[115] Barrett T. Morbilli virus infections, with special emphasis on morbilli viruses [143] Boga JA, Martin-Alonso JM, Casais R, Parra F. A single dose immunization
of carnivores. Veterinary Microbiology 1999;69:3–13. with rabbit haemorrhagic disease virus major capsid protein produced in
[116] Osterhaus AD, Vedder EJ. Identification of virus causing recent seal deaths. saccharomyces cerevisiqe induces protection. Journal of General Virology
Nature 1988;335(6185):20. 1997;78:2315–8.
[117] Visser IK, vd Bildt MW, Brugge HN, Reijnders PJ, Vedder EJ, Kuiper J, et al. [144] Bertagnoli S, Gelfi J, Gall G, Boilletot E, Vautherot JF, Rasschaert D, et al.
Vaccination of harbour seals (Phoca vitulina) against phocid distemper with Protection against myxomatosis and rabbit viral hemorrhagic disease with
two different inactivated canine distemper virus (CDV) vaccines. Vaccine recombinant myxoma viruses expressing rabbit hemorrhagic disease virus
1989;7(6):521–6. capsid protein. Journal of Virology 1996;70:5061–6.
[118] Cleaveland S, Appel MGK, Chalmers WSK, Chillingworth C, Kaase M, Dye [145] Bertagnoli S, Gelfi J, Petit F, Vautherot JF, Rasschaert D, Laurent S, et al. Protec-
C. Serological and demographic evidence for domestic dogs as a source tion of rabbits against rabbit viral haemorrhagic disease with a vaccine–RHDV
of canine distemper virus for Serengeti wildlife. Veterinary Microbiology recombinant virus. Vaccine 1996:506–10.
2000;72:217–27. [146] Fischer L, Le Gras X, Mason PW, Paoletti E. A recombinant canasypox virus
[119] Kock R, Chalmers WS, Mwanzia J, Chillingworth C, Wambua J, Coleman PG, et protects rabbits against a lethal rabbit hemorrhagic disease virus (RHDV)
al. Canine distemper antibodies in lions of the Masai Mara. Veterinary Record challenge. Vaccine 1997;15:90–6.
1998;142(24):662–5 [erratum in: Veterinary Record 1998;142(26):721]. [147] Schirrmeier H, Reimann I, Riebe R, Kilian A, Keij G. Novel approaches in vac-
[120] Clark A. Canine influenza virus surfaces. Journal of the American Veterinary cination against rabbit haemorrhagic disease. In: Proceedings of the Brescia
Medical Association 2005;227:1377–8. Conference. 2000. p. 206.
[121] Karaca K, Dubovi EJ, Siger L, Robles A, Audonnet J-C, Jiansheng Y, et al. Evalu- [148] Castanon S, Marin MS, Martin-Alonso JM, Boga JA, Casais R, Mumara JM, et al.
ation of the ability of canarypox-vectored equine influenza virus vaccines to Immunization with potato plants expressing. Vp68 protein protects against
induce humoral immune responses against canine influenza viruses in dogs. rabbit hemorrhagic disease virus. Journal of virology 1999;73:4452–5.
American Journal of Veterinary Research 2007;68:208–12. [149] Laurent S, Vautherot JF, Madelaine MF, Le Gall G, Rasschaert D. Recombinant
[122] Gerber JD, Ingersoll JD, Gast AM, Christanson KK, Selzer NL, Landon RM, et al. rabbit hemorrhagic disease virus capsid protein expressed in baculovirus self-
Pprotection against feline infectious peritonitis by intranasal inoculation of a assembles into virus like partictes and induces protection. Jounal of Virology
temperature-sensitive FIPV vaccine. Vaccine 1990;8:536–42. 1994;68:6794–8.
[150] Barcena J, Morales M, Vazquez B, Boga JA, Parra F, Lucientes J, et al. [152] Pastoret PP, Brochier B. The development and use of a vaccinia-rabies recom-
Horizontal transmissible protection against myxomatosis and rabbit hem- binant oral vaccine for the control of wildlife rabies: a link between Jenner
orrhagic disease by using a recombinant myxoma virus. Journal of Virology and Pasteur. Epidemiology and Infection 1998;116:235–40.
2000;74:1114–23. [153] Niin E, Laine M, Guiot AL, Demerson JM, Cliquet F. Rabies in Estonia: situation
[151] Brochier B, Aubert MF, Pastoret PP, Masson E, Schon J, Lombard M, et al. before and after the first campaigns of oral vaccination of wildlife with SAG2
Field use of a vaccinia-rabies recombinant vaccine for the control of sylvatic vaccine bait. Vaccine 2008;26:3556–65.
rabies in Europe and North-America. Scientific and Technical Review (OIE)
1996;15:947–70.

Review of Companion Animal Vaccine and Immunoprophylaxis

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Vaccine 27 (2009) 491–504

Contents lists available at ScienceDirect

Review of companion animal viral diseases and immunoprophylaxis

1. Introduction understanding disease pathogenesis, virus transmission in the ﬁeld

Company and trade name Vaccine Presentation Handling and claims

Company and trade name Vaccine Presentation Handling and claims

Company and trade name Vaccine Presentation Handling and claims

Company and trade name Vaccine Presentation Handling and claims

Vaccines for rabbits

Vaccines for pigeons

See legend of Table 1.

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