Herpes and calici vaccination does not prevent infection

[malernee]

Key points
1. the major cause of feline upper respiratory infection are feline calicivirus(FCV)and feline herpesvirus(FHV).
2. The vaccines available for Feline upper respiratory infections do not prevent infection. They tend to reduce the severity of the symptoms. So one could suspect to see FURI symptoms with any vaccination program.
3. Feline URIs are usually transmitted via direct transfer of infectious materials rather than aerosol in spite of the fact that sneezing may occur . Like our colds, they usually get it from contact with infectious secretions and excretions. Therefore, attention to detail when kennel cleaning to avoid cross contamination and thorough disinfection is critical to getting control of these situations.
Kittens should not be housed with adults and obviously all sick cats should be segregated and the healthy ones handled and cleaned first. Entering kennel animals may benefit from intranasal URI vaccine because of more rapid onset of action compared to parenteral vaccines. Kennels where cats are removed from cages and alowed to come in direct contact with other cats should be avoided at all cost if you plan to board.

FHV was first isolated in 1957 and initially named feline rhinotracheitis virus. Incubation period is about two to six days. Cats become depressed inappetant pyrexic and often develop marked sneezing. Salivation may occur. Ocular and nasal discharge may be serious followed by mucopurulent conjunctivitis. A cough and dyspnea may occur. FHV may be an important cause of morbidity in young animals in breeding colonies. Less often FHV can cause pneumonia or keratitis with desmcemetocele formation. Rarely skin ulceration and neurological signs have also been seen in FHV infected cats. FHV may like FCV produce tongue ulcers but not as frequently as FCV. Abortion most likely is secondary to debilitation and pyrexia has been reported. Damage to nasal turbinates by FHV in acute disease may predispose to chronic rhinosinusitis later in life.
When vaccinating the ability to cause disease must be weighted against ability to produce disease.
Attenuated live calici and herpes vaccinations sold to veterinarians badly need reevaluation. Chronic infections with both FHV and FCV agents are still very common, even in the face of continuous vaccination. acute disease is also seen at times in environments that are being heavily vaccinated, and at least a portion of both acute and chronic disease may be vaccine virus associated. In the case of FCV this high rate of vaccine failure has been blamed on the emergence of vaccine resistant strains in the field. A more likely explanation is the vaccine does not protect against the chronic state and in some cases may be a significant source of both acute and chronic infections. Both FCV and FHV vaccines contain virulence attenuated stains of living virus. However attenuation is marginal and their safety depends largely on their being administered parenterally. If they are given mucosally they cause infection disease. This can occur when <animal> licks the vaccine site and get vaccine virus orally off the skin if 100% is not deposited under the skin. Although immunization with live FHV and FCV vaccine may decrease the frequency and severity of acute disease there is no evidence that they significantly decrease the chronic carrier state. In fact the incidence of FCV carriers is higher today than it was prior to vaccination. We need to reevaluate the use of live FHV and FCV and to consider using killed FHV and FCV vaccinations instead. By using killed FHV and FCV one major source for virus reintroduction and chronic infection can be removed from the environment. However one must weigh the decreased incidence vaccine induced infection against the potential increase in vaccine induced tumors.

>>>Problems with Respiratory Virus Vaccination in Cats

<<<Comp on Cont Ed 15[10]:1347-1354 Oct'93 Review Article 47 Refs
S. Dawson, BVMS, PhD, MRCVS and R. M. Gaskell, BVSc, PhD, MRCVS
Depts. of Veterinary Pathology and Veterinary Clinical Science; University of Liverpool; Veterinary Field Station; Leahurst; Neston, Wirral, UK

-The two main causes of respiratory disease in cats, feline herpesvirus and feline calicivirus, are prevalent despite the availability of vaccines. Both viruses survive interepidemic phases through carriers. With feline herpesvirus, the carrier state is characterized by periods of latency interspersed with episodes of infectious virus shedding, particularly after stress. Shedding is more or less continuous in the feline calicivirus carrier state. In environments where the cat population is dense, infection of kittens is common because of the high incidence of carriers and a possible immunity gap occurring between the time maternally derived antibody loses its effectiveness and vaccinations are commonly given. Vaccine reactions are most likely attributable to field virus, with the kitten incubating the disease at the time of vaccination. Apparent vaccine breakdowns occur because even under ideal conditions, protection is not necessarily complete in all cats. Intercurrent disease can reduce protection afforded by vaccination, and in some cases, levels of virus within a population are so high that clinical disease occurs even in vaccinated cats. (Author Abstract)<<<

>>>Mechanisms for persistence of acute and chronic feline calicivirus infections in the face of vaccination.

<<<Vet Microbiol 1995 Nov;47(1-2):141-56
Pedersen NC ; Hawkins KF
Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis 95616, USA.

-The study was concerned with possible reasons for the persistence of both acute and chronic feline calicivirus (FCV)-induced disease and sustained oral carriage in the field in the face of routine FCV immunization. It was concluded from this study that: 1) the original FCV-F9 strain, which is the basis of most live vaccines, still generates cross-reactive antibodies against almost all field strains in California, 2) vaccine strains derived from
FCV-F9 may not be as broadly cross-protective as the parent strain, 3) whole inactivated FCV-2280 vaccine evokes high virus neutralizing antibody titers with an equally broad spectrum of cross-reactivity as FCV-F9, 4) all vaccine strains of FCV cause acute disease signs and protracted oral shedding when administered orally, 5) strains isolated from the mouth five to ten weeks following oral inoculation can differ from parental virus, usually
appearing more vaccine resistant, 6) cats previously infected with field or vaccine strains develop much less severe acute illness when subsequently infected with heterologous FCV strains but are not protected against the chronic carrier state. Therefore, the persistence of FCV in the field cannot be explained solely by the emergence of vaccine resistant strains and vaccine virus itself may contribute to both acute and chronic infection and
disease. (Author Abstract)<<<

If cats would have a upper respiratory infection with corneal ulcers, it's pretty much got to be herpes. Calici and the others don't do that. Herpes may be complicated by some of the others but if eye ulcers occur it's the main offender.
Trying to find the carrier cats is pretty difficult with herpes as the virus is only shed intermittently and so not all carrier cats will be shedding at any one time.
It may be helpful especially if a nested set PCR is run on the samples. See reference below. However, Herpes can still hide out and may be difficult to pick up carriers if they aren't in an actively shedding state unless you test neural tissues or cornea where latent virus can hang out.



Detection Of Feline Herpesvirus 1 DNA By The Nested Polymerase Chain Reaction.
<<Vet Microbiol 1996 Feb;48(3-4):345-52
Hara M ; Fukuyama M ; Suzuki Y ; Kisikawa S ; Ikeda T ; Kiuchi A ; Tabuchi K

-The thymidine kinase region of feline herpesvirus 1 (FHV 1) genome in ocular/nasal swabs from cats with clinical manifestations of upper respiratory disease was amplified by nested polymerase chain reaction (nested PCR). Two primer pairs were prepared for nested PCR. FHV 1 DNA in ocular/nasal swabs was extracted using instaGene-DNA purification matrix. Nested PCR for the FHV 1 culture supernatants was ten times as sensitive as single PCR. On comparing viral isolation with single PCR and nested PCR for the detection of FHV 1 in ocular/nasal secretions, of 5 samples that yielded infectious virus in cell culture, 3 (60%) were positive in single PCR and 5 (100%) were positive in nested PCR. When 22 ocular/nasal swabs that did not yield FHV 1 were assayed, 3 were negative in both single PCR and nested PCR, 2 were positive in both single and nested PCR and 17 were positive in only nested PCR. Thus, FHV 1 was detected in 19/22 (86.4%) by the nested PCR and in 2/22 (9%) by single PCR. These results show that nested PCR is 4.8 (24 positive samples/5 positive samples) times as sensitive as single PCR. (Author Abstract)

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Feline Upper Respiratory Tract Pathogens: Herpesvirus-1 and Calicivirus
Compend Contin Educ Pract Vet 23[2]:166-175 Feb'01 Review Article 44 Refs

Jane E. Sykes, BVSc (Hons), PhD
University of Minnesota
ABSTRACT: Feline herpesvirus-1 and feline calicivirus are common causes of feline upper respiratory tract disease and can cause clinically indistinguishable syndromes. However, they differ in their physical properties, epidemiology, and spectrum of clinical signs; and the differences can affect the diagnosis, prognosis, and management of these infections. The availability and sensitivity of diagnostic tests also differ for each virus. Diagnosis of both infections can be difficult and is best achieved by combining patient history, physical examination, and microbiologic assay results. Treatment is primarily symptomatic. Vaccination does not prevent infection but can help minimize the severity of clinical signs and duration of shedding.

[guest]

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Calicivirus research


Feline calicivirus (FCV) disease: FCV infection can be inapparent or associated with various acute and chronic disease syndromes in cats. Infection of immunologically naïve animals leads to upper respiratory tract disease accompanied by glossopharyngeal and/or nasal ulceration (12, 13). Infection with more virulent FCV strains can cause pyrexia, depression, dyspnoea, and pneumonia (12). Less commonly, a shifting lameness is seen following acute infection (2, 6). Acute FCV infection has also been reported to cause abortion in pregnant queens (33). After FCV infection, many cats will secrete virus for up to 3 weeks after resolution of clinical signs. Some cats will become asymptomatic carriers, shedding virus for prolonged periods (34). FCV persistently infects the tonsillar epithelium (7, 35), however, the factors that lead to long term persistence are unknown. An uncommon sequela of persistent FCV infection is chronic gingivostomatitis, which may be causally associated with coexisting feline immunodeficiency virus or feline herpesvirus-1 infection (14, 15, 25, 31, 36).

Recently, hypervirulent FCV strains have been associated with a hemorrhagic fever-like syndrome that causes high morbidity and mortality in cats (21, 26). These epizootics of severe disease have occurred in animal shelters or environments where cats are housed in relatively close confinement. In the reported outbreaks infection was spread inadvertently by animal handlers (21, 26). Because FCV is highly contagious and easily spread by fomites and animal handlers, these outbreaks can cause havoc in larger veterinary hospitals and clinics and are, thus, of major concern to veterinarians. These outbreaks are similar to the dramatic outbreaks of Norwalk virus gastroenteritis, a human calicivirus, that have occurred in nursing homes and cruise ships where fomites were also an important factor in spread (1, 5, 18).

FCV vaccines: Although modified-live and inactivated vaccines are available against FCV, there is a significant rate of vaccine failure. Vaccinated animals are largely protected from acute disease symptoms, but are not protected against infection. Upon challenge, most vaccinates become infected and will secrete the challenge virus post-exposure, thus acting as transient virus reservoirs (9). In addition, vaccinated animals can become chronically infected. Although some vaccine failures can be explained by emergence of vaccine-resistant strains, it appears that the vaccine does not protect against development of the chronic carrier state. In addition, the modified live vaccines will occasionally cause mild disease symptoms in vaccinated animals. In the most recent outbreak of highly virulent FCV disease, prior vaccination did not protect against severe disease (26). There is an urgent need for better vaccines and a clearer understanding of the factors involved in virus immunity and persistence.

FCV antigenicity: There is significant antigenic variation in the capsid protein amongst FCV field isolates, which in part explains the poor efficacy of available vaccines. Several studies have attempted to correlate FCV capsid antigenic variation with disease presentation, but have failed thus far to identify any pattern that correlates with disease (10). However, these studies have not included analyses of the newer hypervirulent strains of FCV. Sequence analyses of the capsid protein gene have identified two hypervariable regions designated regions C and E (27). These hypervariable regions appear to contain most of the identified neutralizing epitopes (11, 20, 28, 32). However, other non-neutralizing epitopes lie outside of these regions in more conserved regions of the capsid protein.

FCV molecular biology: Feline caliciviruses are small non-enveloped viruses (~35 nm diameter) that contain a polyadenylated linear ~7.7 kb (+) stranded RNA genome. The genomic RNA contains 3 open reading frames (ORFs). Only ORF1 is translated from the incoming full-length genome, as translation of ORFs 2 and 3 occurs from a subgenomic 2.4 kb mRNA. ORF1 is co-translationally cleaved by a virally-encoded protease to yield at least 5 viral nonstructural proteins. These include the 76 kDa viral proteinase-polymerase, a putative 39 kDa NTPase, 2 potential membrane-associated proteins (p32 and p30) of unknown function, and the 13 kDa Vpg protein which is covalently linked to the 5'-end of the full-length genome and the subgenomic RNA. The Vpg protein likely acts as a eukaryotic cap ortholog. The viral genome is encapsidated by 180 copies of a single mature viral capsid protein (VP1) that is synthesized as a 76 kDa precursor protein (29, 30).

Calicivirus capsid structure: Calicivirus capsids are composed of 180 copies of a single mature capsid protein. The capsid structures of the human Norwalk virus (23) and the San Miguel sea lion virus (unpublished) have been determined to atomic resolution. These structures reveal that the capsid protein has two domains, one that forms the T=3 icosahedral capsid shell, and a second that lies on the surface of the shell and contains the variable regions of the capsid protein, the antigenic sites, and the likely receptor interaction site(s) (22).

Tropism and host range: Caliciviruses have narrow host ranges and FCV infection is believed to be restricted to cats. Recently, however, FCV-like viruses that are antigenically and genetically similar to FCV have been isolated from dogs with mild enteritis (8, 19, 24). A large epidemiologic study of risk factors associated with FCV infection in cats found that contact with dogs was a risk factor (4), raising the possibility of cross-species infections. The San Miguel sea lion calicvirus, in addition to infecting sea lions, can infect other marine mammals and pigs (3). Studies of FCV and canine calicivirus have shown that host range restriction is determined early during the infectious cycle as virus can be recovered from non-permissive cells when they are transfected with viral genomic RNA (20, 21).

Binding and uptake of FCV: Little is known about the binding and uptake of FCV into susceptible cells. A previous study examined the binding of FCV strain CFI/68 to Crandell-Reese feline kidney cells (CRFK) and found that binding occurred between pH 6 to 8, required divalent cations, and was rapid and saturable with a maximum of 1.5 to 3 × 103 viruses bound per cell. FCV binding was reduced by pretreatment of the cells with neuraminidase plus O-glycanase suggesting that the presence of an O-linked sugar molecule on the cell surface might be important (17). However, the cell receptor for FCV has not been further defined.
FCV likely enters host cells by endocytosis as neutralization of the low pH of endosomes by pretreatment of cells with the lysosomatropic drug chloroquine inhibits FCV infection (16). Viruses commonly enter cells by endocytosis prior to penetrating the cellular membrane barrier. In our ongoing studies we are investigating the endocytic route of entry used by FCV.

FCV – a model for human calicivirus disease: Feline caliciviruses are related to similar caliciviruses that infect dogs, mink, sea lions, rabbits, and humans. The human caliciviruses, Norwalk disease virus and the Sapporo-like viruses, are the most common cause of acute adult-onset viral gastroenteritis. Human caliciviruses are highly contagious, persist in the environment, are antigenically variable, and are difficult to manage. For these reasons they have been identified by the NIH as potential bioterrorism agents. The study of human caliciviruses is hindered by the inability to propagate these viruses in tissue culture cells. As FCV is easily grown in tissue culture and shares many of the biological properties of human caliciviruses it has emerged as a model agent for studying the caliciviruses generally.

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[cornelgingarasu]

This is a very interesting article, but it can be considered an accumulation of random data, an attempt to demonstrate the inefficiency of herpes and calici vaccination showing the ubiquity of the virus is related to a feline population, without owner, home, or medical monitoring the only precise data are related to immunological variability, the lesional variability and anarchic contagion ways
If we refer to serious catteries, most of then are colici and herpes free due to obeying the vaccination schedules and sanitary solutions. Where there is a viral infection ,separation according to age can be done, also treatments can be applied and animals can be cured even if the viral carriers are still present.
Street cats have random immunity, can develop different forms of this disease according to their capacity to fight infection – from wild fever and sneezing rhinosinusitis, complete lack of appetite to death caused by pulmonary insufficiency.
These street cats sometimes show an excellent immunity beyond any logic: cats 5-6 months old more resistant than the 3-4 years old; 1-2 cats in a cattery which do not take the disease versus 10 others.
That is why I would consider that the title of the article refers to cats of unknown origin than to cats coming from a well organized and clean cattery.
As an example I would refer to the cats from an exotic short hair cattery which have always been fed (or overfed) during the first hours after birth with maternal milk and the first immunization was administrated at 2-3 months. Some of these cats were sold and even if the owners have not given them any further immunization (after 1 year, 2 years, etc) they have never shown any signs of URI.
It is also possible that within the areas where many cats are present the chronic evolution (very frequent) of URI to be related to panleucopeny as well. The problem of calicinosis has not been studied as thoroughly as those of panleucopeny, herpes virus, chlamidyosis,etc.
.