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Listerial Keratoconjunctivitis and Uveitis (Silage Eye)

Article  in  Veterinary Clinics of North America Food Animal Practice · November 2010

DOI: 10.1016/j.cvfa.2010.09.003 · Source: PubMed

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 Author's personal copy

Listerial
Keratoconjunctivitis
and Uveitis
(Silage Eye)
Hidayet Metin Erdogan, DVM, PhD

KEYWORDS
 Cattle  Listeria  Keratoconjunctivitis  Uveitis  Silage eye
 Silage feeding

Listeriosis is a bacterial zoonotic disease caused by the genus Listeria, especially Lis-
teria monocytogenes.1–4 The disease is manifested by 3 distinct clinical patterns,
which are encephalitis, abortion, and septicemia in both humans and animals.5,6 In
addition, mastitis,7 iritis, and/or keratoconjunctivitis6,8–15 have also been associated
with L monocytogenes infection in ruminants in recent years.
Listeria has attracted considerable attention owing not only to increased reports of
clinical disease in animals2,6,16 and people3 but also to its implication as a foodborne
pathogen.1,4

ETIOLOGY

The origin of keratoconjunctivitis comprises many infectious agents, including

L monocytogenes.15,17 Listerial keratoconjunctivitis or silage eye is always associated
with L monocytogenes and silage feeding.2,10,11,14,15,18
L monocytogenes is a gram-positive, non–spore-forming, noncapsular, short,
regular rod. Listerial organisms can multiply from around 0 C to around 50 C, with
optimal growth being between 30 C and 37 C.19,20 L monocytogenes can also tolerate
a wide range of pH (3.8–9.2).21 The tolerance to this broad range of temperatures and
pH enables L monocytogenes to survive and grow indefinitely in the environment.
Listeria spp are aerobic or facultatively anaerobic organisms.2 In anaerobic conditions,
L monocytogenes cannot survive at a pH of less than 3.8,18,22 but exposure to oxygen
makes it possible for L monocytogenes to survive even if the pH is as low as 3.8.18
Therefore, anaerobic conservation of silage is important, as silage has long been asso-
ciated with L monocytogenes infection and is thought to be the source of the
organism.2,5,16,20,22

Division of Veterinary Clinical Science, Department of Internal Diseases, Faculty of Veterinary

Medicine, University of Kafkas, 36100 Kars, Turkey
E-mail address: hmerdogan@hotmail.com

Vet Clin Food Anim 26 (2010) 505–510

doi:10.1016/j.cvfa.2010.09.003 vetfood.theclinics.com
0749-0720/10/$ – see front matter Ó 2010 Elsevier Inc. All rights reserved.
 Author's personal copy
506 Erdogan

PATHOGENESIS

The ways in which L monocytogenes reaches and causes systemic illness have long
been the subject of interest. The existence of different forms of clinical listeriosis and
their irregular distribution in animals suggest that L monocytogenes gains entry in
several ways.2 The pathogenesis is thus poorly defined.23
Experimental and clinical cases disclosed the main portal of entry as the oral route,
bruised mucosa (oral or conjunctival), inhalation, and direct or indirect contact with
contaminated materials.23,24 Studies have supported the hypothesis that L monocyto-
genes–contaminated forages, such as grass, silage, grain awns, straw, and hay, can
break up the integrity of the mucosal membranes and allow L monocytogenes to
penetrate.2,24
Erdogan2 found a strong association between silage eye and the use of big bale
silage and silage feeding in ring feeders, as it is already reported that animals eating
silage in ring feeders and from big bales were at a greater risk of exposure to the agent
and physically damaging their conjunctival membranes,2,9,14,15,18,25 because there is
a continuous exposure of the eye to silage in such feeding methods, which may lead to
infection of epithelial cells of the cornea and conjunctiva by L monocytogenes,26
resulting in eye inflammation. Although listerial keratoconjunctivitis has long been
reported, the pathogenesis of the disease remains to be fully described.15

EPIDEMIOLOGY

Keratoconjunctivitis is a widespread disease of the ruminants, causing distress to

animals and economic losses to farmers. The epidemiology of listeriosis has exten-
sively been studied in general, but the epidemiology of listerial keratoconjunctivitis
has not yet been studied in detail. The disease has been reported from different parts
of the world, especially Europe and the United Kingdom, where silage feeding is
a common practice.6,8–15
Outbreaks of listerial keratoconjunctivitis have occasionally been reported.8–15 The
morbidity rate may vary between 25% and 100%,18 the farm prevalence was 8.6%,
and the incidence rate in all herds and affected herds were reported as 3.4% and
66.5%, respectively, by Erdogan and colleagues.6 Erdogan2 also reported that the
most common clinical sign was the silage eye (83.7%) and that most cases occurred
in late autumn, winter, and spring when animals were housed and silage feeding was
exercised.
Silage and farm environment are thought to be the sources of the infection, as
contamination of the agricultural ecosystem with L monocytogenes is well docu-
mented and L monocytogenes is thought to be a saprophytic organism living in
a plant-soil environment. Carrier humans and animals are thought to play an essential
role in the contamination of their environment (eg, vegetation, soil, water).2,27–32
Listerial keratoconjunctivitis has always been related to silage feeding.14,18 This
suggestion was supported by the findings of a PhD study performed by Erdogan.2 In
that study, unconditional logistic regression analyses of survey data revealed a signifi-
cant relationship between silage and the disease. Use of big bale silage, silage feeding
in ring feeders during the indoor period, ad libitum silage feeding from clamp during the
outdoor period, improper silage making (soil contamination), unsuitable housing condi-
tions (overcrowding), and presence of other animals with clinical listeriosis on the farm
significantly increased the risk of listerial keratoconjunctivitis.2 In addition, other factors
that may increase the susceptibility of animals to listeriosis, possibly to listerial kerato-
conjunctivitis as well, include poor nutritional state, sudden changes to very cold and
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Listerial Keratoconjunctivitis and Uveitis 507

wet weather, stress of late pregnancy and parturition, and overcrowded and unsanitary
conditions with poor access to feed supplies and poor herd or flock management.33,34

Clinical Signs
The disease is named as listerial keratoconjunctivitis,15 iritis,10,35 uveitis,18,36 silage
eye,6,25 and ophthalmitis.37 Lesions are located unilaterally or bilaterally, but most
lesions are unilateral. Morgan9 reported 2 outbreaks of the disease; the lesions were
a catarrhal conjunctivitis with epiphora and photophobia, moderate ophthalmitis with
hydrophthalmus and hypopyon, and keratitis in the first outbreak and severe ophthal-
mitis with marked hydrophthalmus, hypopyon and iridocyclitis, and conjunctivitis and
moderate involvement of the cornea in the second. The course of the disease was about
7 to 10 days in these outbreaks, and no residual lesions were reported. Staric and
colleagues15 reported keratoconjunctivitis manifested by excessive lacrimation,
blepharospasm, photophobia, blindness, yellowish anterior chamber fluid and corneal
opacity of varying degree, turbidity of anterior chamber, anterior uveitis, and hyperemic
conjunctiva. Keratitis manifested by punctate abscesses, peripheral clouding, and epi-
phora and iritis have also been associated with L monocytoegens infection in cattle.12
Uveitis/anterior uveitis or iritis was reported in deer, sheep, and cattle.10,11,14,18,25,35–37
Sargison18 described the signs of uveitis as excessive lacrimation, blepharospasm,
photophobia, miosis, and iridocyclitis followed by swelling and undulating folds in the
iris and ciliary body; severe inflammatory changes with bluish white corneal opacity
starting at the limbic border and spreading centripetally within 2 to 3 days; accumulation
of focal aggregation of fibrin in the anterior chamber attached to the inner surface of the
cornea; accumulation of white material beneath the cornea, hypopyon, and mild
conjunctivitis at the period of inflammation; pannus with widespread corneal opacity;
and vascularizations spreading from the limbus in more severe cases. The course
was reported to be 1 to 3 weeks if not treated.18 Similar clinical signs and inflammatory
changes in the eyes of cattle and sheep were also reported by other
researchers.10–12,35,36,38
Listerial keratoconjunctivitis and uveitis have been reported as primary conditions,
which are not associated with other clinical signs of listeriosis.10,14,15,18 No report of
nervous listeriosis following anterior uveitis exists except for that of Ohshima and
colleagues,38 in which cerebral listeriosis was reported to be present along with
uveitis.

Diagnosis
Clinical signs involving the uvea are typical, and history of silage feeding may help in
diagnosis, but the exact diagnosis is based on the demonstration of L monocytogenes
from the samples collected from the affected eye. Conventional or molecular techniques
(eg, polymerase chain reaction) are sufficient to detect Listeria in affected materials.2
Differential diagnosis of listerial keratoconjunctivitis may include infectious bovine
keratoconjunctivitis (IBK) associated with Moraxella bovis and other agents. Uveal
changes make the disease distinct from IBK because IBK produces severe conjunc-
tivitis, lacrimation, blepharospasm, photophobia, intense corneal changes, and
corneal ulceration in more severe cases and occurs most commonly in summer and
autumn when flies are active.9,18,34,35

Treatment
Treatment of listerial keratoconjunctivitis includes parenteral and/or topical use of
antibiotics. Morgan9 reported the use of chloramphenicol powder with less effect.
Sargison18 and Blowey35 reported the success of the subconjunctival use of the
 Author's personal copy
508 Erdogan

combination of oxytetracycline and dexamethasone. Walker and Morgan37 used

topical oxytetracycline in sheep but found it ineffective; they then administered paren-
teral ampicillin plus topical ceprovin, which led to the recovery of cases within 2
weeks. Mee and Rea36 also reported the recovery of cows with uveitis within 2 weeks
of administration of systemic antibiotics and antibiotic-corticosteroid ophthalmic oint-
ment, although they did not mention the names of the drugs used. Evans and
colleagues12 reported the recovery of 3 cases after the use of topical antibiotic oint-
ment in one case, atropine and oxytetracycline plus polymyxin B sulfate ophthalmic
ointment in the second case, and subcutaneous injection of procaine penicillin G in
the third case. Staric and colleagues15 also reported complete healing after systemic
and topical antibiotic use but did not mention the name of the antibiotics used.
Reports revealed that systemic or topical use of antibiotics or a combination of both
with or without corticosteroid resulted in complete recovery within 2 weeks in almost
all cases. Recovery without any treatment was also reported.9,12

Control
Because the elimination of L monocytogenes from the farm environment is not
possible because of its ubiquitous occurrence in nature, the lack of reliable and rapid
methods of detecting the organism when it is present in low numbers, and the lack of
understanding of the epidemiology of listeriosis and L monocytogenes infection,
attempts can be made only to prevent listerial organisms from multiplying to the level
of an infectious dose, minimize its presence in the farm environment by improving
hygiene and cleanliness of the farm, and minimize its intake by animals by preparing
foodstuff such that L monocytogenes does not grow.2 The most important risk factor
of listerial keratoconjunctivitis is silage feeding, as all clinical cases were linked to
silage feeding, especially big bale silage, and problems ceased after removing silage
from the diet.2,9,15 Wherever silage is implicated, some recommendations can be
made. The proportion of silage in the ration can be reduced, silage feeding can
be introduced to the animals gradually, and more attention can be paid to silage
making. Spoiled and moldy silage should be removed from the feed. When making
silage, additives should be used, soil contamination should be avoided, and the silo
or clamp should be sealed off as quickly as possible so that an anaerobic condition
is maintained and the pH is kept low.2,34,39 The method of silage feeding should be
changed so that eye contact can be minimized, that is, not using ring feeders, direct
feeding from clamps, and big bale silage.2 Better farm management practices, such as
the improvement of nutritional status of animals, better housing conditions, and good
hygiene and cleanliness, can also be of some value in preventing the disease.2,34

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