Infectious Bovine Keratoconjunctivitis

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Moraxella bovis
Kingdom Bacteria
Phylum Proteobacteria
Class Gammaproteobacteria
Order Pseudomonadales
Family Moraxellaceae
Genus Moraxella
Species M. bovis

Also Known As: IBK — New Forest Eye — New Forest Disease — Pinkeye — Pink-eye — Infectious Opthalmia — Blight

Caused By: Moraxella bovis

Contents

Introduction

Infectious bovine keratoconjunctivitis or New forest eye disease is an ocular disease of cattle caused by the gram negative, β-haemolytic, aerobic rod shaped bacterium, Moraxella bovis . The bacterium is non-motile and occurs in pairs.

This disease is the most common and important ocular disease seen in cattle worldwide. It is not zoonotic.

Distribution

IBK is seen worldwide but mainly in areas with high temperature climates and thus is widespread in Asia, Africa and all American continents. It is also seen in parts of Europe and the UK. In seasonal countries, disease is most prevalent in the summer months and is usually seen in young animals. During the warmer months, fly numbers are higher and intense sunlight and dust predispose the eye to infection.

Disease is transmitted by biting flies, including Haematobia irritans, Musca domestica, Stomoxys calcitrans and Musca autumnalis . It can also be transmitted by infected animals, via contact with mucous membranes and their secretions, and also by asymptomatic carrier individuals. Carrier animals often carry avirulent, non-pathogenic strains of M. bovis.

Signalment

Bos taurus and Bos indicus cattle can be affected; disease is not documented in any other species.

Young cattle are often, but not exclusively, affected.

A similar disease is seen in horses, caused by a different Moraxella species.

Pathogenesis

M. bovis invades the lacrimal and tarsal glands of the eye, causing keratitis, opacity, uveitis, aqueous flare and corneal ulcers.

The bacterium adheres to the cells via its fimbriae and pili proteins, and produces β-haemolysin toxins which lyse the corneal epithelial cells.[1] M. bovis also secretes cytotoxic toxin and pathogenic fibrinolysin, phosphatase, hyaluronidase and aminopeptidases.

The bacterial membrane proteins and LPS are also pathogenic.[2]

Clinical Signs

Inflammation of the cornea caused by the bacterium and its toxins causes pain, blepharospasm, lacrimation, photophobia and conjunctivitis. Ocular discharge begins serous and may become mucopurulent. Corneal ulcers may be visible on physical examination. Affected animals are often also inappetant and may lose weight and productivity.

Severe or untreated cases can lead to panophthalmitis and permanent blindness.

Age related immunity often develops after exposure when young.

Diagnosis

Pathology remains confined to the eye and does not reach the bloodstream. Diagnosis is usually based on clinical signs.

On clinical examination (and necropsy if incidentally found), early disease is detectable as a raised area of cloudiness in the cornea[3] indicating keratitis. This then spreads and corneal oedema develops giving the eye a blue tint. Conjunctivitis is evident by oedema, erythema and vascular congestion of the scleral vessels. Corneal ulcers may be visible on gross examination and are more obvious with administration of fluoroscein dye. They may be superficial or deep and may leave stromal scars behind after healing.

Season and history of infection and presence of flies will raise suspicion of IBK before an animal is examined.

Lacrimal swabs can be taken and the bacterium can then be cultured on media impregnated with blood or serum where it forms small, round, shiny, friable colonies. It will not grow on MacConkey agar. Fluorescent antibody testing (FAT) is also available for identification. The bacterium may be visible on smears of lacrimal secretions.

Treatment

Sub-conjunctival injections of appropriate antibiotics such as procaine penicillin are most effective, but treatment can also be given systemically, e.g. oxytetracycline, tulathromycin, tilmicosin or florfenicol. Early acute cases may respond to regular application of ophthalmic ointments such as those containing cloxacillin. Withdrawal periods must be adhered to, so selecting a drug licensed for the preferred method of administration is advised.

Anti-inflammatory therapy may also improve demeanour during recovery.

Recovery time ranges from days to months depending on the severity of infection and ulcer formation.

If possible, animals should be housed indoors during treatment so that flies can be controlled and irritation minimised.

Severe cases may require surgery such as temporary third eyelid closure or conjunctival pedicle grafts to facilitate ulcer healing.

Control

Eradiation is not possible due to the ubiquitous nature of M. bovis. Fly control is valuable but rarely practical. Early detection, treatment and isolation of affected individuals may restrict spread of an outbreak.


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References

  1. Billson, F. M., Harbour, C., Michalski, w. P., Tennent, J. M., Egerton, J. R., Hodgson, J. L (2000) Characterisation of haemolysin of Moraxella bovis using a hemolysin-neutralising monoclonal antibody. Inf. and Immun., 3469-3474
  2. Prieto, C. I., Aguilar, O. M., Yantorno, O. M. (1999) Analyses of lipopolysaccharides, outer membrane proteins and DNA fingerprints reveal intraspecies diversity in Moraxella bovis isolated in Argentina. Veterinary Microbiology, 70(3/4):213-223; 36
  3. Bedford, P. G. C (1992) Ocular diseases. Bovine medicine: diseases and husbandry, Wiley-Blackwell, Oxford, pp712-721; 27


CABIlogo

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 28 July 2011.








Haskell, S (2008) Blackwell’s Five-Minute Veterinary Consult: Ruminant. Wiley-Blackwell, Oxford

Merck Veterinary Manual, Infectious Keratoconjunctivitis, accessed online 24/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/30500.htm




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