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NADIS disease bulletins are written specifically for farmers, to increase awareness of prevalent conditions and promote disease prevention and control, in order to benefit animal health and welfare.

Farmers are advised to discuss their individual farm circumstances with their veterinary surgeon.

 

Listeriosis

 

There were several NADIS reports during January  of listeriosis in silage fed ewes.  While some cases were associated with feeding of poor quality silage bales, others were due to secondary fermentation in feed rings or bunkers.   

 

The bacterial cause of listeriosis, Listeria monocytogenes, proliferates in soil, faeces and rotting vegetation and can replicate at low environmental temperatures.  L. monocytogenes can also tolerate the high temperatures which are sometimes generated during aerobic fermentation of poor silage.  In anaerobic conditions, L. monocytogenes cannot survive below pH 5.6 but in poorly consolidated silage with some oxygen present it can survive at pH levels as low as 3.8. 

 

Poor quality big bale silage presents a particular risk for listeriosis because it is usually made later in the season than conventional clamp silage, from grass with lower sugar and higher dry matter contents.  The combined effects of a high pH, due to inefficient lactic acid fermentation, inadequate consolidation and failure to totally exclude air from such silage, enable the proliferation of L. monocytogenes.  These principles also apply to poorer quality clamp silages.  These conditions also favour the growth of certain moulds, so mouldy silage generally presents a high risk for listeriosis.

 

MOULDY SILAGE PRESENTS A HIGH RISK FOR LISTERIOSIS

 

Entry of air into baled silage during storage permits the slow growth of aerobic bacteria and a slow rise in pH allowing L. monocytogenes, already present from soil contamination, to multiply.  In tightly packed, hard centred bales, or well-consolidated clamp silage, aerobic deterioration tends to be superficial, being confined to the site of entry of air, but in soft centred bales, or poorly-consolidated clamp silage, such as whole crop silages, the aerobic deterioration and subsequent multiplication of L. monocytogenes may occur throughout the bale or clamp. 

 

A ROUGH SILAGE FACE, REMOVAL OF A LARGE SECTION OF PLASTIC SHEETING AND SLOW PROGRESS THROUGH THE CLAMP ENABLE SPOILAGE AND PROLIFERATION OF L. MONOCYTOGENES

 

A TIDY SILAGE FACE, CUT WITH A BLOCK CUTTER AND ONLY REMOVING SUFFICIENT SHEETING TO GAIN ACCESS, RESTRICTS THE PROLIFERATION OF L. MONOCYTOGENES

 

Secondary fermentation of previously stable silage, associated with failure to regularly remove stale feed from bunkers or feed rings, also enables proliferation of L. monocytogenes.

 

SPOILAGE AND SECONDARY FERMENTATION OCCURS IN SILAGE WHICH CANNOT BE REACHED IN THE CENTRE OF A RING FEEDER OR REMAINS ON THE FLOOR WHEN BUNKERS ARE REFILLED, PROVIDING AN OPPORTUNITY FOR PROLIFERATION OF L. MONOCYTOGENES

 

The feeding of listeria-contaminated silage to sheep can result in several clinical diseases.  The most commonly encountered is meningo-encephalitis, but anterior uveitis (silage eye), abortion and neonatal septicaemia are sometimes seen.  It is unusual for different forms of listeriosis to occur simultaneously in a flock.

 

Listerial meningo-encephalitis is caused by formation of micro-abscesses in the brainstem.  The clinical signs vary in severity depending upon the degree and precise location of the abscesses, and include fever, anorexia, profound depression and various specific neurological signs.  Affected animals frequently drool saliva and have unilateral drooping of the eyelid, lip and ear.  Some sheep show deviation of the head and walk compulsively in circles.  Severely affected animals may become frenzied or comatose and die in 10-14 days.  The important differential diagnoses are scrapie, pregnancy toxaemia and brain abscessation.

 

RECUMBENCY, HEAD DEVIATION, DROOLING OF SALIVA AND UNILATERAL FACIAL PARALYSIS IN A MULE EWE HOGG

 

HEAD DEVIATION AND CIRCLING IN A TEXEL-CROSS HOGG

 

The route of infection is thought to be via abrasions in the mouth and spread to the brain along nerves, thus the incidence of infection is highest in two year old animals as permanent cheek teeth are erupting.  Most cases occur 4 - 6 weeks after feeding of L. monocytogenes contaminated silage.  Cases are usually sporadic, but outbreaks can occur associated with the feeding of particularly poor quality silage. 

 

When cases are recognised early, treatment with high doses of antibiotics can be effective.  Control is aimed at ensuring that only good quality silage is fed to sheep.  

Neil Sargison BA VetMB DSHP FRCVS

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