[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 50.16.107.222. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Download PDF
Figure 1.
Portrait of James Wardrop as ayoung man in the early 19th century. Copy of an engraving believed to havebeen made from a portrait by Andrew Geddes. Illustration courtesy of DanielM. Albert, MD, MS. (Digitally processed image.)

Portrait of James Wardrop as ayoung man in the early 19th century. Copy of an engraving believed to havebeen made from a portrait by Andrew Geddes. Illustration courtesy of DanielM. Albert, MD, MS. (Digitally processed image.)

Figure 2.
Chronic equine recurrent uveitisin a horse. Subluxated lens and striae indicate glaucoma with globe stretching.(Digitally processed image.)

Chronic equine recurrent uveitisin a horse. Subluxated lens and striae indicate glaucoma with globe stretching.(Digitally processed image.)

Figure 3.
Chronic equine recurrent uveitisin a horse. Severe posterior synechiae and anterior cortical cataracts arepresent. (Digitally processed image.)

Chronic equine recurrent uveitisin a horse. Severe posterior synechiae and anterior cortical cataracts arepresent. (Digitally processed image.)

Figure 4.
Photomicrograph of the pars plicataof the ciliary body in a horse with equine recurrent uveitis. Infiltrationof aggregates of lymphoplasmacytic inflammation is evident (hematoxylin-eosin,original magnification ×200). (Digitally processed image.)

Photomicrograph of the pars plicataof the ciliary body in a horse with equine recurrent uveitis. Infiltrationof aggregates of lymphoplasmacytic inflammation is evident (hematoxylin-eosin,original magnification ×200). (Digitally processed image.)

Figure 5.
Photomicrograph of a portion ofthe ciliary process in a horse with equine recurrent uveitis. Linear eosinophilicintracytoplasmic inclusions are located within the nonpigmented ciliary epithelium(NCE) (arrows). Lymphoplasmacytic inflammatory infiltrate affecting and internalto the NCE is seen (Masson trichrome, original magnification ×400).(Digitally processed image.)

Photomicrograph of a portion ofthe ciliary process in a horse with equine recurrent uveitis. Linear eosinophilicintracytoplasmic inclusions are located within the nonpigmented ciliary epithelium(NCE) (arrows). Lymphoplasmacytic inflammatory infiltrate affecting and internalto the NCE is seen (Masson trichrome, original magnification ×400).(Digitally processed image.)

Figure 6.
Fundus photograph of a horse witha classic, peripapillary "butterfly" typical of equine recurrent uveitis.The winglike altered fundus reflectivity on both sides of and inferior tothe optic disc represents previous chorioretinitis. Wardrop did not describesuch lesions, as his observations were made before the origin of the ophthalmoscope.(Digitally processed image.)

Fundus photograph of a horse witha classic, peripapillary "butterfly" typical of equine recurrent uveitis.The winglike altered fundus reflectivity on both sides of and inferior tothe optic disc represents previous chorioretinitis. Wardrop did not describesuch lesions, as his observations were made before the origin of the ophthalmoscope.(Digitally processed image.)

1.
Albert  DMRobinson  N Wardrop Lecture, 1974: James Wardrop: a brief review of his life andcontributions. Trans Ophthalmol Soc U K. 1974;94892- 908
PubMed
2.
Wardrop  J Essays on the Morbid Anatomy of the Human Eye.  Edinburgh, Scotland George Ramsay & Co1808;
3.
Millar  GT James Wardrop (1782-1869): from Whitburn to Windsor Castle. J R Coll Surg Edinb. 2001;46225- 233
PubMed
4.
Wardrop  J An Essay on the Diseases of the Eye of the Horse.  London, England McMillan1819;
5.
Dwyer  AECrockett  RSKalsow  CM Association of leptospiral seroreactivity and breed with uveitis andblindness in horses: 372 cases (1986-1993). J Am Vet Med Assoc. 1995;2071327- 1331
PubMed
6.
Jones  TC Equine periodic ophthalmia. Am J Vet Res. 1942;345- 71.
7.
Whitley  RDMiller  TRWilson  JH Therapeutic considerations for equine recurrent uveitis. Equine Pract. 1993;1516- 23
8.
Deeg  CAEhrenhofer  MThurau  SRReese  SWildner  GKaspers  B Immunopathology of recurrent uveitis in spontaneously diseased horses. Exp Eye Res. 2002;75127- 133
PubMedArticle
9.
Brooks  DE Equine ophthalmology. Gelatt  KNed.Veterinary Ophthalmology. Philadelphia,Pa Lippincott Williams & Wilkins1999;1053- 1116
10.
Moore  CPHeller  NMajors  LJWhitley  RDBurgess  ECWeber  J Prevalence of ocular microorganisms in hospitalized and stabled horses. Am J Vet Res. 1988;49773- 777
PubMed
11.
Moore  CPFales  WHWhittington  PBauer  L Bacterial and fungal isolates from Equidae withulcerative keratitis. J Am Vet Med Assoc. 1983;182600- 603
PubMed
12.
Moore  CPCollins  BKFales  WH Antibacterial suspectibility patterns for microbial isolates associatedwith infectious keratitis in horses: 63 cases (1986-1994). J Am Vet Med Assoc. 1995;207928- 933
PubMed
13.
Andrew  SEBrooks  DESmith  PJGelatt  KNChmielewski  NTWhittaker  CJ Equine ulcerative keratomycosis: visual outcome and ocular survivalin 39 cases (1987-1996). Equine Vet J. 1998;30109- 116
PubMedArticle
14.
Kershaw  Ovon  Oppen TGlitz  FDeegen  ELudwig  HBorchers  K Detection of equine herpesvirus type 2 (EHV-2) in horses with keratoconjunctivitis. Virus Res. 2001;8093- 99
PubMedArticle
15.
Lavach  JD Ocular manifestations of systemic diseases. Vet Clin North Am Equine Pract. 1992;8627- 636
PubMed
16.
Moore  CP Eyelid and nasolacrimal disease. Vet Clin North Am Equine Pract. 1992;8499- 519
PubMed
17.
Albert  DM The ophthalmoscope and retinovitreous surgery. Albert  DMEdwards  DDedsThe History ofOphthalmology. Malden, Mass Blackwell Publishers1996;177- 202
18.
Magrane  WG Early history. Magrane  WGed.A History of Veterinary Ophthalmology. Elkhart, Ind Franklin Press Inc1988;1- 16
19.
Miller  TRBrooks  DESmith  PJSapienza  SJ Equine glaucoma: clinical findings and response to treatment in 14horses. Vet Comp Ophthalmol. 1995;5170- 182
20.
Smith  PJGum  GGWhitley  RDSamuelson  DABrooks  DEGarcia-Sanchez  GA Tonometric and tonographic studies in the normal pony eye. Equine Vet J Suppl. 1990;1036- 38
PubMedArticle
21.
Schwink  KL Equine uveitis. Vet Clin North Am Equine Pract. 1992;8557- 574
PubMed
22.
Parma  AESantisteban  CVillalba  JBowden  R Eperimental demonstration of an antigenic relationship between Leptospira and equine cornea. Vet Immunol Immunopathol. 1985;10215- 224
PubMedArticle
23.
Halliwell  REBrim  TAHine  MTWolf  EDWhite  FH Studies on equine recurrent uveitis, II: the role of infection with Leptospira interrogans serovar Pomona. Curr Eye Res. 1985;4:1033- 1040
PubMedArticle
24.
Parma  AEFernandez  ASantisteban  CBowden  RCerone  S Tears and aqueous humor from horses inoculated with Leptospira containing antibodies which bind to cornea. Vet Immunol Immunopathol. 1987;14181- 185
PubMedArticle
25.
Morter  RLHerschler  RCFessler  JFLavignett  A Experimental equine leptospirosis (Leptospira pomona). Proc Annu U S Anim Health Assoc. 1964;68147- 152
PubMed
26.
Williams  RDMorter  RLFreeman  MJLavignette  AM Experimental chronic uveitis: ophthalmic signs following equine leptospirosis. Invest Ophthalmol. 1971;10948- 954
PubMed
27.
Roberts  SJ Sequelae of leptospirosis in horses on a small farm. J Am Vet Med Assoc. 1958;133189- 194
PubMed
28.
White  LMcCoy  RTait  BEbringer  R A search for gram-negative enteric micro-organisms in acute anterioruveitis: association of Klebsiella with recent onsetof disease, HLA-B27, and B7 CREG. Br J Ophthalmol. 1984;68750- 755
PubMedArticle
29.
Sahly  HPodschun  RKekow  JNolle  BGross  WLUllmann  U Humoral immune response to Klebsiella capsularpolysaccharides in HLA-B27–positive patients with acute anterior uveitisand ankylosing spondylitis. Autoimmunity. 1998;28209- 215
PubMedArticle
30.
Cooley  PLWyman  MKindig  O Pars plicata in equine recurrent uveitis. Vet Pathol. 1990;27138- 140
PubMedArticle
31.
Dubielzig  RRRender  JAMorreale  RJ Distinctive morphologic features of the ciliary body in equine recurrentuveitis. Vet Comp Ophthalmol. 1997;7163- 167
32.
Miller  TRWhitley  RD Uveitis in horses. Mod Vet Pract. 1987;68351- 357
33.
Wilcock  RP The eye and ear. Jubb  KVFKennedy  PCPalmer  Neds.Pathologyof Domestic Animals. 1 Orlando, Fla Academic Press Inc1993;441- 529
34.
Deeg  CAKasper  BGerhards  HThurau  SRWollanke  BWildner  G Immune responses to retinal autoantigens and peptides in equine recurrentuveitis. Invest Ophthalmol Vis Sci. 2001;42393- 398
PubMed
35.
Linford  RL Laminitis (founder). Smith  BPedLarge Animal InternalMedicine. St Louis, Mo Mosby–Year Book Inc1996;1300- 1309
36.
Gilger  BCWilkie  DADavidson  MG  et al.  Use of an intravitreal sustained-release cyclosporine delivery devicefor treatment of equine recurrent uveitis. Am J Vet Res. 2001;621892- 1896
PubMedArticle
37.
Fruhauf  BOhnesorge  BDeegen  E  et al.  Surgical management of equine recurrent uveitis with single port parsplana vitrectomy. Vet Ophthalmol. 1998;1137- 151
PubMedArticle
Special Article
August 2004

James Wardrop and Equine Recurrent Uveitis

Author Affiliations

From the Department of Clinical Sciences, School of Veterinary Medicine,University of California–Davis (Dr Paglia); and the Departments of SurgicalSciences (Dr Miller) and Pathobiological Sciences (Dr Dubielzig), School ofVeterinary Medicine, University of Wisconsin–Madison. The authors haveno relevant financial interest in this article.

Arch Ophthalmol. 2004;122(8):1218-1223. doi:10.1001/archopht.122.8.1218
Abstract

James Wardrop should be remembered not only as one of the founders ofocular pathology but also for his contributions to the field of comparativeophthalmology. He described a "specific inflammation" that veterinarians todayknow as equine recurrent uveitis. As described by Wardrop in the 19th century,this condition is known today to eventually lead to blindness.

In 1782, James Wardrop was born in Linlithgow, Scotland, a small townshipnear Edinburgh (Figure 1). He hadextensive training as a general surgeon, and by the age of 22 years had completeda 4-year surgical apprenticeship in Scotland; a 2-year appointment as housesurgeon in London, England; part of a year at a prestigious Paris, France,medical school; and a year under Georg Joseph Beer in Vienna, Austria. Beerhad established the first clinic limited to the practice of ophthalmologyin Europe some 17 years earlier. In 1823, Wardrop was appointed Surgeon Extraordinaryto the Prince Regent, who later became King George IV. Wardrop's reputationas one of the foremost surgeons in his day, however, rested more on the accuracyof his diagnoses, his ability to be an original and forceful thinker, andthe number and value of his publications rather than on his technical skills.1

Although Wardrop was considered a general surgeon, his greatest contributionsincluded establishing the foundations for ophthalmic pathology and being thefirst to classify ocular diseases according to the anatomical parts involved.1 One may speculate that at least some of his interestin ophthalmology was fostered by his having an exotropic left eye as a child.1 In 1808, he published one of his most important works,entitled Essays on the Morbid Anatomy of the Human Eye,2 and in it he coined the term keratitis. He also had a passion for hunting and horse racing and was considered"one of the best judges of horseflesh in the Kingdom."3 In1819, he combined his fascination for ocular pathology with his extensiveknowledge of horses in An Essay on the Diseases of the Eyeof the Horse.4 This important workhelped to build a foundation for equine ophthalmic anatomy and aided in thedifferentiation of inflammatory diseases of the equine eye based on the tissueof origin. More specifically, the essay is notable because it is among thefirst to differentiate a form of ocular inflammation that Wardrop termed specific inflammation from other forms of ocular inflammatorydisease in horses. Today this condition is called equine recurrent uveitis(ERU), and it affects 10% to 15% of all horses, making it the leading causeof blindness in horses then and now.58 Theessay is also noteworthy for its allusion to the notion of sympathetic inflammationbetween the 2 eyes and its description of several surgical techniques fortreating ocular disease in horses, including the use of glass eyes to preventdeformity in horses that have lost an eye.3

Wardrop's interest in equine ophthalmology appears to stem from thecritical economic role horses played in his day, his innate scientific curiosity,and an aesthetic appreciation for the animal's strength and beauty. In 19th-centuryGeorgian society, human productivity and physical safety were heavily dependenton the animal having good vision. Wardrop recognized that chronic ERU wasthe most common cause of visual loss in horses and, hence, was of great economicimportance, because it often rendered the animal useless for its intendedpurpose and sometimes bankrupted its owner in the process. However, Wardropwas also insightful because as a physician-scientist, he saw human and veterinarymedicines as a single medicine in which a better understanding of the diseasesof one species would benefit the other, and vice versa. Although he erroneouslybelieved horses had fewer and more uniform ocular diseases than humans4 (perhaps in part because horses have a much more floridinflammatory response than do humans), his appreciation for the linkage betweenspecies allowed him to make significant contributions to both human and veterinarymedicine. It was also Wardrop's hope that differentiation between the varioustypes of ocular inflammation based on anatomy would facilitate improving theselection and breeding of quality animals.4

In An Essay on the Diseases of the Eye of the Horse, Wardrop elucidated 2 principal forms of ocular inflammation.4 The first form, which he called simple or common inflammation, was a keratoconjunctivitisthat was characterized by swollen eyelids, conjunctival hyperemia, oculardischarge, and diffuse or focal loss of "pellucidity and lustre" of the cornea.4 In advanced stages, corneal perforation and loss of"appearances and utility" of the eye occurred.4 Thecritical observation, however, was that anterior uveitis was secondary tocorneal disease. Systemic signs such as fever, loss of appetite, thirst, "frequencyof the pulse," unhealthy appearance of the coat, and alternate "heat and chills"often accompanied this form.4 Trauma was acommon cause, but it was also seen as a consequence of colds and fevers. Younghorses and those in "high condition" were more commonly affected,4 as they were under the greatest amount of stress.We can assume by "high condition" he meant horses that were used for racingpurposes and, hence, may have also been more commonly treated because of theirvalue.

Today's veterinary ophthalmologist would easily recognize the patientsthat Wardrop describes, and in addition to traumatic keratitis would includeas possible causes sterile corneal stromal abscesses, corneal foreign bodies,bacterial keratitis (especially due to Streptococcus species, Staphylococcus species, Acinetobacter species, and Pseudomonas species), fungalkeratitis (due to Aspergillus species and Fusarium species), viral keratitis (equine herpesvirus 2, equine influenzavirus A2, and adenovirus), ocular parasites such as Onchocerca cervicalis and Thelazia species,and allergic and chemical irritations.916 Thesimilarities between these causes and those seen in humans are striking andspeak to the validity of Wardrop's concept of applying medical principlesacross species lines.

Although the methods of treating these disorders have improved greatlyfrom the "bleeding, purging, and blistering" of Wardrop's day,4 herecognized that the outcome often depended on the immediate and aggressivetreatment of the inflammation if the course of the disease was not to be protractedor to result in long-term damage to the globe. As today, he also recognizedthe importance of "paying attention to the air of the stable; for this isoften impure." In addition, he recommended avoiding exposure to light andnot feeding the animal a large amount of grain.4 Modernequine medicine has recognized that housing in a stable increases fungal contaminationof the equine conjunctiva10 and that sunlightinduces intense ocular pain and photophobia in horses with keratitis. Wardropcorrectly argued against a common practice at the time of scarifying the eyesand removing the third eyelid, although in some circles in the United Statesthis unfortunate practice persisted until well into the 1900s. He advocatedextreme caution in draining a hypopyon and emphasized careful surgical techniquewhen doing so.4 Today, rather than trying totreat an obvious clinical sign of the condition (eg, ocular surface vascularinjection) by limiting ocular blood flow by means of therapeutic bleedingand inducing systemic hypotension with purgative balls, the veterinary ophthalmologistuses many of the same antimicrobial agents familiar to the physician, alongwith systemic and topical anti-inflammatory medications.

Wardrop was among the first to clearly differentiate in horses the primarilycorneal origin of simple inflammation from the uveal origin of the secondform of ocular inflammation that he called specific inflammation.4 Although the 2 forms appear superficiallysimilar, the latter has more serious consequences for vision and is the "mostdangerous disease of the Eye of the Horse." Unlike the corneal origin of simpleinflammation, he noted that the uveal origin of specific inflammation wasalso more frequent in "particular lines of blood."4 Thisobservation was later borne out in studies that found certain horse breedssuch as the Appaloosa to have an 8-fold increased frequency of ERU.5 It affected animals of all ages, all classes, andall states of condition, although horses that were "high bred" or in highcondition were believed to be more commonly affected. Dark, ill-ventilatedstables were thought to have a great influence on the incidence of the disease.4

Wardrop noted that specific inflammation usually develops very suddenly,that it is characterized by swelling of the eyelids and copious tearing, butthat the conjunctival injection is not as great as in simple inflammation.4 A key differentiating feature, however, is lack ofa "distinct speck on the cornea," and the whole anterior chamber is "dim andclouded."4 As in simple inflammation, thisform may exhibit varying degrees of hypopyon.4 Thecondition is often, at least initially, unilateral and may be quite asymmetricalin severity. He described spontaneous resolution of the inflammation overa period of a few weeks and observed that the eye may then look quite normalor may have adhesions that distorted the pupil (posterior synechia). He astutelynoted that inflammatory episodes typically recur at varying and sometimesquite distant intervals, and that ultimately the accumulated damage leadsto a cataract and visual loss.4 Well beforethe introduction of the ophthalmoscope in 1850,17 Wardropdescribed dissecting the eyes of these horses and finding a collection offluid "between the choroid coat and retina," condensation of the vitreal elements,and a retina that is detached and compressed "into a chord or bundle."4 Finally, as some of today's horse buyers can stillattest, Wardrop marveled at how astute some dealers in horses were in identifyinghorses that have had an episode of specific inflammation and how the dealerswould sell an animal (often during a period of quiescence) before the animal'svalue was lost owing to blindness.4

As with simple inflammation, Wardrop's description of specific inflammationis easily recognized by today's veterinary ophthalmologist. It is most commonlyknown as ERU but has also been referred to as periodic ophthalmia, recurrentiridocyclitis, relapsing uveitis, and "moon blindness." The latter term purportedlyoriginated with Vegetius in the fourth century AD, who thought that the cyclicnature of the inflammatory outbreaks was associated with changes in the phasesof the moon.18 In Wardrop's essay, he divergedfrom this traditional use of the term moon blindness andinstead used it to describe a dense white cataract that perhaps resemblesa brightly illuminated moon. Nevertheless, his description of recurring boutsof epiphora, photophobia, anterior chamber opacification, ocular vascularinjection, and the visually devastating sequelae of synechiae, cataract, andretinal detachment could be easily found in today's textbook descriptionsof horses with ERU (Figure 2 and Figure 3). With the comparatively recentadvent of tonometers such as the Mackay-Marg and Tono-Pen (Mentor Ophthalmics,Norwell, Mass) that are suitable for use in horses, glaucoma also has beenfound to be a sequelae of ERU.19 Equine recurrentuveitis is the most common cause of glaucoma in horses, although glaucomaitself is relatively uncommon in horses, perhaps because of their very largeuveoscleral outflow pathway.20

Today ERU is regarded as an umbrella term for a diverse set of diseasescharacterized by episodes of active uveitis alternating with varying intervalsof clinical quiescence.9 It undoubtedly remainsone of the leading causes of blindness in horses worldwide.58 Thetypical initial episode consists of severe anterior uveitis, but subsequentepisodes are less severe and more chronic in nature. Ultimately, the accumulatedeffects of the inflammation lead to progressively more destructive pathologicchanges and visual loss. Causes believed to be important today include thespirochetes Leptospira interrogans and Borrelia burgdorferi; other bacterial infections that include brucellosis,salmonellosis, streptococcus hypersensitivity, Escherichiacoli, and Rhodococcus equi; the parasites Onchocerca cervicalis, Toxoplasma gondii, and various other intestinal parasites; and viral agents that includeequine influenza virus, equine herpesvirus 4, equine arteritis virus, andpossibly equine anemia virus.9,21 Inaddition, blunt or penetrating trauma may play an inciting role by breakingdown the relatively labile equine blood-aqueous barrier. Wardrop's admonitionto consider the environment proved to be prescient, since it is clear thatmany of the infectious causes of ERU in horses are acquired through less-than-optimalhusbandry practices.9 Again, the striking similaritiesbetween the recognized causes of ERU in horses and the causes of uveitis inhumans speaks to Wardrop's insight into comparative ophthalmology.

The pathophysiology of ERU is unclear, but the disease undoubtedly hasan immune-mediated basis.9 It has been speculatedthat a common theme of all of these inciting causes is that they disrupt therelatively unstable blood-aqueous barrier of the equine eye and allow immunologicallyreactive components to enter the eye. Hypersensitivity to L interrogans serovars (especially pomona)is commonly implicated as a cause, and the equine cornea and lens have beenshown to share antigenic properties with this organism.22 Althoughanti-Leptospira antibodies are found in the serum,tears, and aqueous humor of horses infected with Leptospira, living organisms are not necessary for ERU to occur.23,24 Frequently,uveitis may not be seen until 15 months after systemic infection with Leptospira,25 and the factthat it can resolve with only anti-inflammatory drugs again suggests thatit is primarily immune-mediated in nature.

Although horses that are seropositive for antibodies to L interrogans serovar pomona are 13.2 timesmore likely to have uveitis than seronegative horses,5 notall seropositive horses will develop uveitis.26,27 thisfinding, in conjunction with the recognized heritable nature of ERU, has ledsome to suggest that ERU in horses occurs in a manner analogous to that inhumanswho posses the tissue marker HLA-B27 and develop uveitis in assiciationwith Klebsiella species.28,29 Thatis, uveitis develops only if the horse possesses an as yet undefined specifictissue antigen and is also exposed to L interrogans. Nevertheless,a significant number of horses with uveitis are seronegative to all serovarsof L interrogans, indicating that this organism aloneis not the sole cause of ERU in horses.

The histopathological changes in ERU have built on Wardrop's descriptions,and today ERU is characterized as a uveal lymphoplasmacytic inflammatory infiltratethat most commonly affects the nonpigmented ciliary epithelium of the ciliaryprocesses7,3033 (Figure 4). Other histologically identifiablelesions involving the nonpigmented ciliary epithelium include linear eosinophilicintracytoplasmic inclusions that may be located within mitochondria and thickacellular hyaline membranes closely adherent to the inner aspect of the nonpigmentedciliary epithelium31 (Figure 5). In patients with chronic ERU undergoing an acute episode,a perivascular lymphoplasmacytic inflammatory infiltrate within the choroid,retina, optic nerve, and anterior uveal tract is often identifiable.33 An exudative retinal detachment may result from thechorioretinitis. These retinal detachments may focally reattach because offibrous organization or may progress to total separation.33 Vitreousopacities, chorioretinitis, retinal detachment, and optic nerve atrophy arefrequently observed in chronic ERU (Figure6).

Although Wardrop viewed specific inflammation as usually incurable,he thought there was some benefit from bleeding (≤2.9-4.8 L from the jugularvein closest to the affected eye), administering purgative balls, feedinga "cooling diet" (less high-energy feedstuffs such as grain), and improvingthe ventilation of the stable.4 Given thatERU frequently resolves spontaneously (at least initially), and that chronicforms may require slitlamp biomicroscopy to identify that they are active,it is highly likely that many treatment strategies—perhaps even thoseused today—are erroneously believed to be effective. He also applieda "vinous tincture of opium" with a brushlike camel's-hair pencil to the globe2 to 3 times daily, meaning he applied medicine that stained the eye, usinga whiskerlike instrument for its application. He believed that this procedurewas helpful in some cases,4 although the realvalue of this therapy may simply have been to provide some degree of painrelief.

Of interest is Wardrop's observation that, as in humans, ERU is ofteninitially unilateral. He questioned whether destroying the first eye wouldarrest the progress of the disease in the fellow eye, and so he treated avaluable race horse with unilateral disease by incising the cornea and expressingthe lens, vitreous, and other intraocular contents. He reported that the animaldid not experience an episode in the opposite eye for up to 6 years later.He noted that others before him used less refined techniques for destroyingthe diseased eye such as putting quicklime between the eyelids or by thrustinga nail into the eye in hopes of preventing the disease in the opposite eye.4 Obviously, such therapy would be considered crueltoday.

Although there is some suggestion that severe ERU might allow the exposureof immunologically isolated antigenic constituents such as interphotoreceptorretinoid-binding protein or retinal S antigen34 and,hence, could result in disease in the contralateral eye, to date no studyhas demonstrated a benefit to destroying the affected eye; in addition, thehistological changes seen in ERU are not consistent with sympathetic ophthalmia.Currently, ERU is not regarded as a variant of sympathetic ophthalmia butinstead as a disease that often affects both eyes asymmetrically. The slitlampbiomicroscope, a tool not available to Wardrop, has allowed the detectionof low-grade inflammation in the fellow eye of a substantial number of horsesthat have what appears to the naked eye to be unilateral disease.

Today's veterinary ophthalmologist uses many of the same medicationsthat the physician uses to treat humans with recurrent uveitis. Because itmay be difficult to safely approach the eye of a very large animal that hasconsiderable ocular pain, a subpalpebral lavage system is occasionally placedto facilitate treatment of fractious animals. This system consists of a tubethat is placed into the dorsal or ventral conjunctival fornix and out throughthe skin of the upper or lower lid, respectively. This tube connects witha port that is secured near or through the mane of the horse and allows medicationto reach the corneal surface safely through the opening in the fornix. Thetreatment of ERU is also complicated by the fact that even topical atropinesulfate can induce gastrointestinal tract stasis and colic (which can be fatalto large herbivores), and that systemic corticosteroid therapy may resultin the keratinized hoof separating from the underlying bone (laminitis), therebypotentially permanently crippling the animal.35 Recentlytopical and intravitreal cyclosporine (administered as a sustained-releaseintravitreal implant) has shown promise in reducing the severity of the diseaseand the frequency of attacks.36 Although parsplana vitrectomy has been suggested as another avenue to prevent recurrentepisodes,37 this approach requires longer-termfollow-up and replication at other centers before it can be widely advocated.

As evident, our understanding of ERU has come a long way since JamesWardrop differentiated between the various forms of ocular inflammation inthe horse. Nevertheless, ERU remains the most common cause of blindness inhorses, and much more needs to be done if we are to address the economicallyimportant and aesthetically disfiguring condition effectively. Unfortunately,despite potent modern immunosuppressive drugs and broad-spectrum antibiotics,today's veterinary ophthalmologist would have to agree with Wardrop's observationin 1819 that "however beneficial these remedies may be in diminishing theseverity of the symptoms, yet they never prevent the repetition of attacks,and the ultimate destruction of the organ."4

Back to top
Article Information

Correspondence: Paul E. Miller, DVM, Department of Surgical Sciences,School of Veterinary Medicine, University of Wisconsin–Madison, 2015Linden Dr, Madison, WI 53706-1102 (millerp@svm.vetmed.wisc.edu).

Submitted for publication July 1, 2003; final revision received October26, 2003; accepted December 11, 2003.

References
1.
Albert  DMRobinson  N Wardrop Lecture, 1974: James Wardrop: a brief review of his life andcontributions. Trans Ophthalmol Soc U K. 1974;94892- 908
PubMed
2.
Wardrop  J Essays on the Morbid Anatomy of the Human Eye.  Edinburgh, Scotland George Ramsay & Co1808;
3.
Millar  GT James Wardrop (1782-1869): from Whitburn to Windsor Castle. J R Coll Surg Edinb. 2001;46225- 233
PubMed
4.
Wardrop  J An Essay on the Diseases of the Eye of the Horse.  London, England McMillan1819;
5.
Dwyer  AECrockett  RSKalsow  CM Association of leptospiral seroreactivity and breed with uveitis andblindness in horses: 372 cases (1986-1993). J Am Vet Med Assoc. 1995;2071327- 1331
PubMed
6.
Jones  TC Equine periodic ophthalmia. Am J Vet Res. 1942;345- 71.
7.
Whitley  RDMiller  TRWilson  JH Therapeutic considerations for equine recurrent uveitis. Equine Pract. 1993;1516- 23
8.
Deeg  CAEhrenhofer  MThurau  SRReese  SWildner  GKaspers  B Immunopathology of recurrent uveitis in spontaneously diseased horses. Exp Eye Res. 2002;75127- 133
PubMedArticle
9.
Brooks  DE Equine ophthalmology. Gelatt  KNed.Veterinary Ophthalmology. Philadelphia,Pa Lippincott Williams & Wilkins1999;1053- 1116
10.
Moore  CPHeller  NMajors  LJWhitley  RDBurgess  ECWeber  J Prevalence of ocular microorganisms in hospitalized and stabled horses. Am J Vet Res. 1988;49773- 777
PubMed
11.
Moore  CPFales  WHWhittington  PBauer  L Bacterial and fungal isolates from Equidae withulcerative keratitis. J Am Vet Med Assoc. 1983;182600- 603
PubMed
12.
Moore  CPCollins  BKFales  WH Antibacterial suspectibility patterns for microbial isolates associatedwith infectious keratitis in horses: 63 cases (1986-1994). J Am Vet Med Assoc. 1995;207928- 933
PubMed
13.
Andrew  SEBrooks  DESmith  PJGelatt  KNChmielewski  NTWhittaker  CJ Equine ulcerative keratomycosis: visual outcome and ocular survivalin 39 cases (1987-1996). Equine Vet J. 1998;30109- 116
PubMedArticle
14.
Kershaw  Ovon  Oppen TGlitz  FDeegen  ELudwig  HBorchers  K Detection of equine herpesvirus type 2 (EHV-2) in horses with keratoconjunctivitis. Virus Res. 2001;8093- 99
PubMedArticle
15.
Lavach  JD Ocular manifestations of systemic diseases. Vet Clin North Am Equine Pract. 1992;8627- 636
PubMed
16.
Moore  CP Eyelid and nasolacrimal disease. Vet Clin North Am Equine Pract. 1992;8499- 519
PubMed
17.
Albert  DM The ophthalmoscope and retinovitreous surgery. Albert  DMEdwards  DDedsThe History ofOphthalmology. Malden, Mass Blackwell Publishers1996;177- 202
18.
Magrane  WG Early history. Magrane  WGed.A History of Veterinary Ophthalmology. Elkhart, Ind Franklin Press Inc1988;1- 16
19.
Miller  TRBrooks  DESmith  PJSapienza  SJ Equine glaucoma: clinical findings and response to treatment in 14horses. Vet Comp Ophthalmol. 1995;5170- 182
20.
Smith  PJGum  GGWhitley  RDSamuelson  DABrooks  DEGarcia-Sanchez  GA Tonometric and tonographic studies in the normal pony eye. Equine Vet J Suppl. 1990;1036- 38
PubMedArticle
21.
Schwink  KL Equine uveitis. Vet Clin North Am Equine Pract. 1992;8557- 574
PubMed
22.
Parma  AESantisteban  CVillalba  JBowden  R Eperimental demonstration of an antigenic relationship between Leptospira and equine cornea. Vet Immunol Immunopathol. 1985;10215- 224
PubMedArticle
23.
Halliwell  REBrim  TAHine  MTWolf  EDWhite  FH Studies on equine recurrent uveitis, II: the role of infection with Leptospira interrogans serovar Pomona. Curr Eye Res. 1985;4:1033- 1040
PubMedArticle
24.
Parma  AEFernandez  ASantisteban  CBowden  RCerone  S Tears and aqueous humor from horses inoculated with Leptospira containing antibodies which bind to cornea. Vet Immunol Immunopathol. 1987;14181- 185
PubMedArticle
25.
Morter  RLHerschler  RCFessler  JFLavignett  A Experimental equine leptospirosis (Leptospira pomona). Proc Annu U S Anim Health Assoc. 1964;68147- 152
PubMed
26.
Williams  RDMorter  RLFreeman  MJLavignette  AM Experimental chronic uveitis: ophthalmic signs following equine leptospirosis. Invest Ophthalmol. 1971;10948- 954
PubMed
27.
Roberts  SJ Sequelae of leptospirosis in horses on a small farm. J Am Vet Med Assoc. 1958;133189- 194
PubMed
28.
White  LMcCoy  RTait  BEbringer  R A search for gram-negative enteric micro-organisms in acute anterioruveitis: association of Klebsiella with recent onsetof disease, HLA-B27, and B7 CREG. Br J Ophthalmol. 1984;68750- 755
PubMedArticle
29.
Sahly  HPodschun  RKekow  JNolle  BGross  WLUllmann  U Humoral immune response to Klebsiella capsularpolysaccharides in HLA-B27–positive patients with acute anterior uveitisand ankylosing spondylitis. Autoimmunity. 1998;28209- 215
PubMedArticle
30.
Cooley  PLWyman  MKindig  O Pars plicata in equine recurrent uveitis. Vet Pathol. 1990;27138- 140
PubMedArticle
31.
Dubielzig  RRRender  JAMorreale  RJ Distinctive morphologic features of the ciliary body in equine recurrentuveitis. Vet Comp Ophthalmol. 1997;7163- 167
32.
Miller  TRWhitley  RD Uveitis in horses. Mod Vet Pract. 1987;68351- 357
33.
Wilcock  RP The eye and ear. Jubb  KVFKennedy  PCPalmer  Neds.Pathologyof Domestic Animals. 1 Orlando, Fla Academic Press Inc1993;441- 529
34.
Deeg  CAKasper  BGerhards  HThurau  SRWollanke  BWildner  G Immune responses to retinal autoantigens and peptides in equine recurrentuveitis. Invest Ophthalmol Vis Sci. 2001;42393- 398
PubMed
35.
Linford  RL Laminitis (founder). Smith  BPedLarge Animal InternalMedicine. St Louis, Mo Mosby–Year Book Inc1996;1300- 1309
36.
Gilger  BCWilkie  DADavidson  MG  et al.  Use of an intravitreal sustained-release cyclosporine delivery devicefor treatment of equine recurrent uveitis. Am J Vet Res. 2001;621892- 1896
PubMedArticle
37.
Fruhauf  BOhnesorge  BDeegen  E  et al.  Surgical management of equine recurrent uveitis with single port parsplana vitrectomy. Vet Ophthalmol. 1998;1137- 151
PubMedArticle
×