THE CANADIAN VETERINARY JOURNAL LA REVUE VETtRINAIRE CANADIENNE Volume 17
FELINE RESPIRATORY INFECTIONS - A CLINICAL REVIEW R. C. Povey The fourth in a series of articles by selected authors, presenting up-to-date informnation on topics of interest to the veterinary profession. This series is sponsored by the CVMA Veterinary Research Trust Fund.
FVRV and FCV between them initiate the majority of infectious respiratory disease problems in the cat. Reoviruses have been isolated and experimentally it is possible to reproduce a mild upper respiratory syndrome with them, but their overall importance appears limited. Myxoviruses such as influenza or parainfluenza have as yet proven of only academic interest and adeno or corona viruses which cause respiratory problems in other species have not been isolated from cats. The feline pneumonitis agent, Chlamydia psittaci, is often mistakenly referred to as a virus. There is considerable controversy over its importance as a significant factor in respiratory disease in the cat, although the term pneumonitis is used indiscriminantly as a blanket term for feline respiratory infections. It is a confusing term and should be avoided. Mycoplasmaceae are claimed to be primary agents in some cat respiratory infections, particularly those involving conjunctivitis but experimentally it has not been possible to regularly produce disease with any isolates. Others consider they may play an important secondary role in intensifying the symptoms of viralinduced disease but in some preliminary observations by the author, even such a secondary role could not be demonstrated. In this same work, Staphylococcus aureus proved a much more potent secondary organism associated with a purulent type of discharge. Some strains of Streptococcus pyogenes, Bordetella bronchiseptica, Pasteurella multocida, and even Escherichia coli, probably can play similar "secondary-invader" roles. They are the organisms most commonly found in association with the fatal bronchopneumonias which cdn follow feline upper respiratory disease. As already stated, the majority of feline respiratory infections are at least induced by
INTRODUCTION THE ADVENT OF NEW VACCINES against viralinduced respiratory disease of the cat, together with significant recent advances in our understanding of the epidemiology of the complex, make the control of this ubiquitous, sometimes fatal, often frustrating, and alwavs troublesome problem nearer becoming a reality. ETIOLOGY Since the description of the feline pneumonitis agent, Miyagawanella felis, now named Chlamydia psittaci, a growing number of infectious organisms have been associated with feline respiratory disease (Table I). Only a few of these are unequivocally capable of producing a primary infection. Feline viral rhinotracheitis virus (FVRV) is one of these and is the most important single factor in infectious respiratory disease of the cat. During the late 1950's and through the 1960's many viral isolates of a type quite distinct from the FVR herpes virus were being made from the respiratory tract and also other tissues of both sick and healthy cats and kittens. These viruses, or at least those which have been sufficiently studied, are closely related. Initially they were referred to as feline picornaviruses, but they have some specific morphological, biophysical and biochemical properties entitling them to be classified as members of the genus Calicivirus although still within the family Picornavirus. Thus it is now usual to refer to this group as feline caliciviruses (FCV) and to feline caliciviral disease (FCD) as the associated syndrome. 'Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2WI. 93
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TABLE I MICRO-ORGANISMS WHICH MAY BE RESPONSIBLE FOR PRIMARY INFECTIOUS RESPIRATORY DISEASE IN CATS
Micro-organisms Feline viral rhinotracheitis virus (feline herpesvirus I) Feline Caliciviruses (formerly feline Picornaviruses) Feline Reovirus Chlamydia psittaci (formerly Miyagawanella felis)
Feline viral rhinotracheitis
Feline caliciviral disease Mild upper respiratory disease Feline pneumonitis (N.B.
? Upper respiratory symptoms, particularly conjunctivitis
5. Mycoplasma spp
TABLE II ISOLATION OF FVRV AND FCV FROM CATS, EITHER HEALTHY OR WITH RESPIRATORY DISEASE IN VARIOUS SITUATIONS (IN PART FROM WARDLEY, GASKELL AND POVEY, 1974)
Percentage of sample virus pos.
Situation Veterinary hospital, respiratory symptoms Breeding colony, endemic respiratory disease Pet population, healthy Cat show survey, healthy Breeding colony, no endemic respiratory disease
0.6 1.0 1.8
40.9 8.0 24.0
357 100 974
either the rhinotracheitis (FVR) virus or one of the feline caliciviruses, and occasionally combined infections in which both of these viruses are present are encountered, although there is no good evidence that such dual infections are more severe than FVR alone. The rest of this review will concentrate on these two viruses and the diseases associated with them. Both viruses are of widespread distribution throughout the world, and serological surveys have shown specific antibodies present in 80% or greater of adult cat populations. Isolations of FCV are made more frequently than FVR from healthy cats particularly in cats kept in population dense situations (Table II). This difference is to be expected considering the frequency of continuously shedding FCV carriers, which will be discussed later, and the number of FCV strains some of which are nonpathogenic. However from cases of respiratory disease, the isolation rate of FVR virus rises sharply, particularly from the more severe
The above is the first, and a major point, in the differentiation of these infections. FVR is regularly a more severe condition than FCV disease, although factors such as size of infecting dose and specific and nonspecific host resistance will modify the severity of the infection in either disease. With the caliciviruses there is the added complication of many strains being mildly pathogenic or nonpathogenic. The prodromal signs of impending respiratory disease are typically a degree of lassitude accompanied by a febrile response which may be as high as 41°C. With FVR particularly, sneezing and clear ocular and nasal discharges follow within a day or so, the overall incubation period for the disease being as short as two days but more typically four to eight days or occasionally as long as 17 days. The same incubation periods apply to FCV disease. Severe ocular signs including chemosis, diffuse keratitis and comeal ulceration are seldom seen with
FCV. Involvement of lung tissue seemingly frequently, at least with experimental FCV infections, and may occur with FVR, but in the absence of complicating bacterial bronchopneumonia may go undetected and apparently heals fairly quickly. X Involvement of systems other than the res;piratory tract can occur with both FCV and z - _ , FVR, the latter however only in young, old -' or immuno-depressed animals, where symptoms \;4 of central nervous dysfunction, or liver disease may be seen. Incidentally the role of FCV in the feline urological syndrome (FUS), does not seem to be a primary one and the herpes ^l N tX} virus which has been reported as inducing urolithiasis is apparently quite distinct from the FVR herpesvirus. FVR virus has been associated with ulceration of the skin and an FCV virus has been isolated from paw lesions in a kitten. Pregnant animals frequently abort during or immediately after the respiratory infection, this being regularly the case with FVR. Experimentally FVR virus has produced genital tract lesions but these have not yet been described occurring naturally. occurs
FIGURE 1. Mouth of cat infected with FVR showing four punctate ulcers of the type occasionally seen with this disease.
FCV, but are not infrequent sequels to FVR particularly in the younger or somewhat debilitated animal. The change in character of ocular and nasal discharges from clear to purulent signifies an increasing amount of secondary bacterial activity. Textbooks on feline medicine have referred to ulcerative glossitis as a distinct condition, but we now know that it is a direct consequence of viral damage to the tongue epithelium. Although FVR virus can produce such damage (Figure 1), it is much more commonly associated with FCV disease, and indeed may be the only clinical sign in some cases. The ulcers, starting as vesicles which rapidly rupture, are usually seen on the anterior dorsal margin of the tongue (Figure 2) but they may occur on the hard or soft palates, fauces of the throat, lips or even external nares. Very severe ulceration of the pharynx has been seen associated with both FVR and FCD and rarely severe ulceration of the esophagus has occurred with FVR. Coughing associated with marked to severe tracheitis is an indicator of FVR rather than
FIGuRE 2. Mouth of cat showing very typical extensive ulceration of the anterior dorsal surface of the tongue associated with feline caliciviral disease. 95
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TABLE III POINTERS TO CLINICAL DIFFERENTIATION OF FELINE RESPIRATORY INFECTIONS Aetiological Agent Chlamydia
Symptoms Nasal Discharge Epithelial Ulcerations
Primary infection typically severe Conjunctivitis often prominent maybe keratitis
Variable mild to moderate Conjunctivitis mild to absent
Often profuse Very occasionally tongue or pharynx
Scanty to moderate Very frequently tongue, also hard palate, pharynx, external nares Rare if ever
Mild Chronic and marked conjunctivitis Scanty to moderate Not associated
Rare if ever
port media and in that way will survive for up to three days in transit. Alternative transport media are also available for chlamydia or bacterial isolation attempts. Serological tests particularly serum neutralization, or for FCV and chlamydia, complement fixation, can be used to determine the existence of the diseases in a colony situation, or for determining relative susceptibility or protection of an individual or group.
Reference should be made to feline chlamydial disease (pneumonitis) because of former overestimates of its importance. It is now apparent that it is not the problem it was once thought, and when the infection does occur the disease process is predominantly ocular rather than general respiratory. Severe persisting conjunctivitis is most frequently described. The role of reoviruses and mycoplasma organisms in cat respiratory disease has still to be clarified. They are probably most significant in mixed infections and alone cause mild, if any, disease with conjunctivitis likely the most prominent symptom.
Treatment of feline respiratory infections is aimed at maintaining a patency of airways, ensuring adequate oxygenation of blood, restoring fluid balance, combating secondary bacterial infections, and aiding healing processes. The presence of copious thick discharges in the respiratory tract can occasionally be responsible for a severe dyspnoea. A steam vaporizer may give considerable relief but the use of antihistamines (e.g. phenylephrine HCl1) to reduce the volume of secretion, combined with a mucolytic agent such as a tyloxapol compound2 by nebulizer (e.g. de Vilbiss No. 40) may be more satisfactory. In severe cases, usually FVR, dehydration can be very marked, equivalent to a water loss of 6% or greater of body weight. The clinical estimate of dehydration can be supported by a packed cell volume and total protein estimation. In general lactated Ringers solution is suitable and in all but the most urgent cases can be given subcutaneously or
DIAGNOSIS Some pointers to making a specific etiological diagnosis or at least a differentiation between FVR and FCV disease have been given. They are summarized in Table III. Confirmation of diagnosis becomes most important with advent of specific vaccines and increasing knowledge of the different epidemiology of the etiological agents. Fortunately both FVR and FCV grow readily and produce characteristic cytopathic changes in tissue culture cells of cat origin, making a confirmatory diagnosis possible within three days and in some cases within 24 hours. For success in isolation, the prerequisites are vigorous sterile swabbings of the tonsil region, ideally taking also a conjunctival swab. Best results are obtained with swabs taken within the first seven days of illness. It is not necessary to send the samples to a laboratory frozen in dry ice providing a suitable transport media is used. This can be supplied by the laboratory and held in readiness. The cotton tip of the swab can be broken off into a small (2-5 ml) vial of trans-
lNeo-synephrin, Winthrop Laboratories, Aurora, Ontario.
2Alevaire, Winthrop Laboratories, Aurora, On-
to recurrent attacks of conjunctivitis, rhinitis or sinusitis. These are usually bacterial in origin, their invasion made possible by the usual chronic damage to areas of mucous membrane from the time of viral infection. Antibiotics give temporary relief and autogenous bacterins are successful in some cases. The symptoms are usually more irritating to the owner than they are to the cat. The use of rhinectomy in these cases indicates promising results.
intraperitoneally as frequently as twice daily. Five percent dextrose in 0.85% saline is a good altemative. Specific antiviral drugs are slowly appearing but the use of the antiherpetics such as the deoxyuridines has not been fully evaluated for the cat. The antibiotics are not antiviral but are indicated for the chlamydial and secondary bacterial infections. In adult cats, oxytetracycine (12 mg/day/kg) in four divided doses gives a broad coverage, as does chloramphenicol which is useful even in the younger cat of three months plus. In kittens, ampicillin at 50 mg/kg/day every six hours may be helpful. Antibiotic therapy should be continued for at least five days even if there is early response. Before antibiotic treatment is instigated, cultures for an antibiotic sensitivity test should be performed. The healing process is hastened by an adequate intake of nutrients. Particularly in the purebreds it seems total anorexia persists even after the clearing of nasal discharges which might have interfered with olfactory stimulation of appetite. However, strong smelling for instance fish-based foods, can be helpful. Baby foods fed by spoon sometimes are accepted but the injection of a complex of the B vitamins supplemented with extra B-12 followed within two hours or so with an offering of thin strips of raw liver dipped in milk and semi-force-fed will often succeed where other attempts have failed. Vitamin C (up to 1 gram daily) and vitamin A (10,000 i.u. daily) may aid mucosal tissue repair and shorten recovery time. The use of aspirin in the cat can be helpful in reducing high fever and improving the attitude of the animal providing the dose is carefully restricted to 5 mg/kg and is given for no more than three days. Last, but not least, attentive nursing with cleaning of discharges, applying ophthalmic solutions or ointments with antibiotic if indicated, helping with grooming, together with a liberal supply of tender loving care are of inestimable assistance to a successful outcome.
EPIDEMIOLOGY Both FVR virus and the feline caliciviruses are unable to survive outside of the cat for more than a few days (three for FVR, no more than ten for FCV). Thus to perpetuate themselves, which they do very successfully, these viruses depend on direct transmission from cat to cat and on persistence within cats. Transmission occurs most readily where there is opportunity for direct nose to nose contact or at least only short (less than four feet) separating distances between shedding and recipient cat. The hands of attendants may be an important vehicle for spread, more significant than clothing and other potential fomites, whereas widespread airborn infection does not seem important. When exposed to virus, even cats that are clinically immune to FVR or FCV disease will often show transient viral multiplication and shed virus for a day or several days. In initial infections the period of shedding is generally longer (one to two weeks with FVR) and with an initial FCV infection shedding of virus often persists for several months and occasionally for years. Thus "carriers" of FCV are frequently found. Although sometimes there may be more or less coincidental chronic or recurrent respiratory signs such carriers are usually symptom free. With the majority of cats sooner or later there is a cessation of virus excretion which is seemingly permanent. The mechanisms involved in this persistence and eventual elimination of FCV are as yet poorly under-
stood. The FVR virus also has a mechanism for persistence which recent work indicates is a sequel to at least 69% of FVR infections (14). This parallels the situation with other members of the Herpes family such as the virus producing cold sores in man. Unlike FCV, where during the persistence virus is continuously demonstrable particularly in the pharynx, with FVR carriers virus is seldom isolatable but instead seems to have a truly latent phase, details of which are slowly being elucidated. Stimulation of translation from the
In uncomplicated cases, animals will be near recovery within a week or ten days. However, it is by no means uncommon for the severe cases to persist for several weeks. Mortality is not high when viewed overall but young kittens, the older cat or the cat with intercurrent disease such as panleukopenia, are more often victims. It is well appreciated that a number of recovered cats, particularly those which have experienced severe FVR are prone 97
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longer than eight weeks with FVR and 12 weeks with FCV antibody. The degree to which such maternal antibody is protective or capable of interfering with the vaccine is not known.
latent stage to overt virus replication and shedding can be achieved regularly by the use of corticosteroids. When a combination of prednisolone (2.25 mg) and dexamethasone (0.75 mg) is given intramuscularly on each of days 0, 2 and 4, virus shedding may be expected from carriers between four and 11 days after the start of the injections with a duration of shedding varying between one and 13 days. In the natural situation, a variety of stimuli which may be regarded collectively as "stress", for example change of housing and going into board, have been shown to produce such shedding. As with FCV carriers, the persistently infected FVR cat may be symptomless but careful observation often shows a unilateral or sometimes bilateral ocular or nasal discharge associated with virus re-excretion. It is not known with certainty whether FVR carriers ever eliminate the virus, but it seems likely that in many cases the virus is so well adapted to its site or sites of persistence in the cat that shedding is most unlikely and that cat becomes epidemiologically unimportant.
Vaccines against feline chlamydial disease have been available for many years but their supporters are outnumbered by their critics. The recent introduction of an FVR vaccine3 undoubtedly heralds the beginning of a new and welcome era. The recommendation is for vaccination at nine and 11 or 12 weeks of age with six-monthly boosters. It is too soon to properly evaluate the performance of this product in the field. The author has occasionally identified FVR virus from respiratory disease cases in cats which had received FVR vaccine but the clinical impression was of a somewhat milder disease than would have been expected in a nonvaccinated animal. The instruction to give the currently available vaccine intramuscularly should be followed with care, avoiding the possibility of intranasal instillation as even one-tenth dose may produce disease by that route. With the demonstrated cross-protection between feline caliciviruses vaccine development for this disease also has been possible and a combination of FVR and FCV in a single vaccine is now available in the United States. There is likely to be a real advantage from using an intranasal route of administration of a suitable product thus best stimulating local antibody. This may need to be supplemented with a parenteral inoculation also to best stimulate circulating and cell-mediated immunity.
Traditionally the immunity following viral respiratory infections has been regarded as being of short duration. This is only partly true. Following initial FCV infection antibodies appear in the serum after a week or so and often rise to levels of 1/1024 (SN50) or greater within six to 12 weeks and fall gradually. The antibody levels against FVR are initially much lower (1/4 to 1/64) and tend to fall more quickly. However, even when such antibody is no longer detectable, challenged cats show no or much reduced clinical signs. It is apparent that for FVR, serum neutralizing antibody levels and indeed all markers of humoral antibody are only a guide to the immune state of the cat. Cell-mediated immunity may be more important although the role of locally secreted antibody has not been properly evaluated either. Another misconception has been that the many strains of FCV are immunologically distinct and thus have the potential for producing a succession of infections in any one cat. Recent work (25, 33) has shown that at least for a number of strains and in the short term, there is clinical cross-protection between them, although as mentioned earlier, this clinical protection does not prevent transient virus multi-
CONTROL BY MANAGEMENT In the absence of, or as an adjunct to, a comprehensive vaccination policy several points of advice can be given particularly to the larger breeder or cattery owner as regards
control of respiratory disease. In the face of endemic respiratory disease, minimizing population density and maximizing ventilation to above 12 air changes an hour are desirable. Where the successful rearing of kittens is being ruined by respiratory infection, the provision of separate kittening accommodation and routine hygiene (particularly of hands) is advocated. Where mothers are carriers (and the development of the corticos-
plication. Maternal antibody is almost entirely colostrally transferred to the kittens and persists for rather irregular periods of time but seldom
3FVR Vaccine, Pitman-Moore Ltd., 690 Progress Road, Toronto, Ontario.
teroid test may be useful for detecting FVR carriers) kittens can be early weaned at five weeks, before maternal antibody has declined. For the boarding cattery, the provision of completely segregated caging, not allowing any direct contact, should be advised, with the disinfection of gloved hands between cages being very desirable. Ultraviolet lighting is probably only effective over a short distance and can be deleterious to eyesight. The use of enclosed cages fitted with glass wool air filters was successful in maintaining healthy cats in a conditioning laboratory in the face of respiratory disease and panleukopenia infection in the same room (16).
sion. Plusieurs souches des calicivirus f6lins ne provoquent qu'une infection subcinique; d'autres produisent par ailleurs une ulceration caracteristique de la langue, avec ou sans ecoulement oculaire et nasal ou eternuement. Le traitement aide 'a reduire consid6rablement la mortalite, sauf chez les sujets tres jeunes ou tres ages; les chats gueris peuvent cependant manifester des signes cliniques chroniques ou devenir porteurs. Le developpement de vaccins et une meilleure connaissance de la transmission de ces virus devraient faciliter la lutte contre les infections qu'ils provoquent. REFERENCES
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Feline respiratory disease still poses many questions but armed with all available knowledge and with the prospect of useful vaccines, we are in a position to successfully diagnose, treat, and control this important complex.
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1971. 3. BITTLE, J. L. and W. J. RUBIc. Immunogenic and protective effects of the F-2 strain of feline viral rhinotracheitis virus. Am. J. vet. Res. 36: 89-91. 1975. 4. BuRKi, F. Picornaviruses of cats. Arch. ges. Virusforsch. 15: 690-696. 1965. 5. BURKI, F. Virologic and immunologic aspects of feline picomaviruses. J. Am. vet. med. Ass. 158: 916-919. 1971. 6. CELLO, R. M. Microbiological and immunologic aspects of feline pneumonitis. J. Am. vet. med. Ass. 158: 932-938. 1971. 7. CELLO, R. M. Clues to differential diagnosis of feline respiratory infections. J. Am. vet. med. Ass. 158: 968-973. 1971. 8. CHAPPUIS, G. and C. STELLMAN. Biomathematical system of relationship and dominance for the classification of feline picomavirus. J. biol. Stand. 2: 319-328. 1974.
The widely distributed and common feline viral rhinotracheitis virus and feline caliciviruses which were formerly called feline picornaviruses, are responsible for the major part of the feline respiratory disease complex. Feline viral rhinotracheitis is regularly the more severe infection with typically marked conjunctivitis, copious ocular and nasal discharges, and marked depression. Feline calicivirus infection is subclinical with many strains, and others characteristically show ulceration of the tongue, with or without ocular and nasal discharges and sneezing. Treatment reduces mortality to low levels in all but very young and old, but recovered cats may have chronic symptoms or be persistently infected with virus (carriers). The development of vaccines and newer knowledge on the transmission of these viruses provides a basis for control of their infections.
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