The feline herpesvirus I (FHV-1) is one of the most common viral infections in cats, and is responsible for the clinical disease known as feline viral rhinotracheitis, an upper respiratory tract infection known colloquially as Cat Flu.

FHV-1 has the ability to persist in latent form in the trigeminal nerve, making reccurrence (or recrudescence) of infection common. Eighty percent of cats become carriers following primary infection and vaccinated cats may become chronic carriers without evidence of clinical disease. Recrudescence may be associated with stress, surgery, lactation, corticosteroid therapy, and immunosuppression from Feline Leukemia Virus (FeLV) or Feline Immunodeficiency Virus (FIV) infection.

Ulcerative nasal dermatitis (cold sores) in an FHV-infected cat that also suffered chronic FLUTD, sinusitis and conjunctivitis. The 2 y.o. cat first suffered catflu as an 8-week-old kitten. Clinical response recorded with broad spectrum antibiotics and long-term lysine supplementation orally. Courtesy Dr Jim Euclid

 

Virology

FHV-1 is a member of the subfamily Alphaherpesvirinae, and as such develops neuronal latency following primary infection. The trigeminal and vestibular ganglia are known sites of FHV latency and recrudescent ocular infections may occur by reactivation of the virus and travel via the axons of the ophthalmic branch of the trigeminal nerve to the eye[2]. Herpesvirus DNA has been detected using PCR assays in feline ocular tissues, both diseased and clinically normal. Recovery rates of viral DNA from the cornea of asymptomatic cats have ranged from 5.9 – 49%. Recovery rates of viral DNA from the conjunctiva of asymptomatic cats have ranged from 2.6 – 31%[3].

FHV-1 propagates readily in the epithelium of the respiratory tract and the conjunctiva[4]. The course of infection in the conjunctival epithelium is self limiting. Epithelial damage is evident in two days and is most pronounced in seven to ten days post infection. Intranuclear inclusion bodies are readily identified in histologic section of affected tissue, but they are less readily identified on cytological examination of conjunctival scrapings.

Clinical signs

Clinically, it is difficult to distinguish herpes virus from Calicivirus infection and requires PCR isolation of FHV-1 DNA to make a confirmatory diagnosis. However, this is complicated by the fact that there is no a priori cause and effect between FHV-1 infection and the presenting clinical signs.

Acute FHV-1 infection usually occurs in neonatal and young adult cats, resulting in a plethora of clinical signs as a consequence of viraemia.

Respiratory disease including chronic sinusitis and rhinotracheitis (Cat Flu), pharyngitis, asthma-like symptoms and chronic obstructive lung disease. The upper respiratory signs predominate with sneezing and nasal and ocular discharge being most notable.

Ophthalmological disease, including conjunctivitis, blepharitis, eosinophilic keratitis[5], keratoconjunctivitis sicca (dry eye), symblepharon (conjunctival to corneal adhesions) and corneal sequestrum. KCS may occur as a result of lacrimal adenitis or it may be due to ductule obstruction in cats with FHV-1 conjunctivitis. The sicca tends resolve when the inflammation subsides. Symblepharon may occur wherever there is significant damage to the conjunctival epithelium, and as such may occur follow FHV-1 conjunctivitis. Feline sequestrum may occur whenever there is chronic damage or irritation of the corneal stroma, and may follow FHV-1 keratitis[6].

Gingivitis

Chronic gastrointestinal disease, with a plausible correlation with irritable bowel disease
Skin diseases, including FHV dermatitis, and a plausible correlation with eosinophilic granuloma complex[7][8].
Correlation with Feline lower urinary tract disease (FLUTD), including urolithiasis and chronic idiopathic cystitis.

Diagnosis

The diagnosis of FHV-1 ocular infections is based upon the clinical history, the findings on clinical examination and the results of the appropriate diagnostic tests. Corneal dendrites may be very subtle, and it is necessary to use Rose Bengal, a vital stain to detect them. Since full thickness epithelial erosions generally occur only in advanced disease, fluorescein stain may not be helpful.

Virus isolation which for many years was the most sensitive means of making a positive diagnosis of feline herpesvirus ocular disease, has for the most part been replaced with the Polymerase Chain Reaction (PCR) test. A commercial virus collection swab is moistened with transport medium and rolled in the conjunctival fornix. The swab is then placed into the transport medium and submitted to the lab.

Conjunctival cytology is not a reliable method of diagnosing FHV-1 ocular disease. Intranuclear inclusion bodies are readily seen in histologic section of affected tissue, they are often not apparent on conjunctival smears. Intracytoplasmic inclusion bodies characteristic of chlamydial infection are more apparent with Giemsa staining of conjunctival smears. Conjunctival cytology is therefore of value in ruling out chlamydial conjunctivitis. It is unusual for chlamydia, mycoplasma or calicivirus ocular infections to cause corneal lesions.

Treatment

The treatment of acute FHV-1 infection in young cats when upper respiratory involvement is present includes broad spectrum antibiotics such as doxycycline or amoxicillin/clavulanate. General support may be required in compromised neonates and this may include fluids, heat and the use of a vaporizer.

If corneal involvement is present, topical antivirals are prescribed. In the adult cat with recrudescent FHV-1 infection topical antivirals are best used aggressively early in the course of the disease before stromal involvement progresses. Three antiviral medications are available.

– Famciclovir[9] – Idoxuridine
– Adenine arabinoside
– Omega interferon

Other strategies to assist in the treatment of eosinophilic keratitis reported in the last few years include topically applied interferon, oral administration of l-lysine and oral administration of cimetidine.

Orally administered l-lysine has been reported to inhibit herpesvirus growth by competitive inhibition of the uptake of arginine which is required for viral multiplication. It is given to cats at a dosage of 125 mg twice daily.

Cimetidine has been shown to generally stimulate cell mediated immunity. It is given at a dosage of 50 mg once daily. Anecdotal reports suggest that maintenance of cats on one or more of these medications during periods of quiescence, will result in a longer period of time before recrudescence of infection occurs, and that when recrudescence occurs, the infection in milder and of shorter duration.

Corticosteroids may be used in the treatment of chronic herpetic stromal keratitis to suppress the potentially scarring immune response if used carefully and in conjunction with an antiviral agent. Steroids are contraindicated if epithelial or conjunctival involvement is still active, because they delay re-epithelialization, prolong virus shedding and may allow conjunctival and corneal epithelial infection to involve the corneal stroma. Alternatively, topical Cyclosporine may be used with caution to reduce the scarring associated with herpesvirus stromal keratitis.

Vaccination

A three year protection has been shown with core vaccines delivered to cats at 8 and 12 weeks of age[10].

References

↑ L. Munson, R. Wack, M. Duncan, R. J. Montali, D. Boon, I. Stalis, G. J. Crawshaw, K. N. Cameron, J. Mortenson, S. Citino, J. Zuba and R. E. Junge (2004) Chronic Eosinophilic Dermatitis Associated with Persistent Feline Herpes Virus Infection in Cheetahs (Acinonyx jubatus) Vet Pathol 41:170-176
↑ Parzefall B et al (2010) Evidence of feline herpesvirus-1 DNA in the vestibular ganglion of domestic cats. Vet J 184(3):371-372
↑ Zicola, A et al (2009) Feline herpesvirus 1 and feline calicivirus infections in a heterogenous cat population of a rescue shelter. JFMS 11:1023-1027
↑ Gonzalez-Mariscal L et al (2009) Virus interaction with the apical junctional complex. Front Biosci 14:731-768
↑ Eye vet
↑ Barnett, KC & Crisoin,SM (2002) Feline ophthalmology. Elsevier, London
↑ Lee, M Bosward, KL & Norris, JM (2010) Immunohistological evaluation of feline herpesvirus-1 infection in feline eosinophilic dermatoses or stomatitis. JFMS 12:72-79
↑ Holland JL, Outerbridge CA, Affolter VK, Maggs DJ. (2006) Detection of feline herpesvirus 1 DNA in skin biopsy specimens from cats with or without dermatitis. J Am Vet Med Assoc. 229(9):1442-6.
↑ Malik R et al (2009) Treatment of feline herpesvirus-1 associated disease in cats with famciclovir and related drugs. J Feline Med Surg 11(1):40-48
↑ Gore TC, Lakshmanan N, Williams JR, Jirjis FF, Chester ST, Duncan KL, Coyne MJ, Lum MA, Sterner FJ. (2006) Three-year duration of immunity in cats following vaccination against feline rhinotracheitis virus, feline calicivirus, and feline panleukopenia virus. Vet Ther. 7(3):213-22.