casereport congenital microphthalmic syndrome in a swine

Case ReportCongenital Microphthalmic Syndrome in a Swine

Radka Andrysikova 1 Titus Sydler2 Dolf Kuumlmmerlen3 Wolfgang Pendl3

Robert Graage3 RomanaMoutelikova4 Jana Prodelalova4 and Katrin Voelter1

1Equine Department Section of Ophthalmology Vetsuisse Faculty University of Zurich Winterthurerstrasse 2608057 Zurich Switzerland2Institute of Veterinary Pathology Vetsuisse Faculty University of Zurich Winterthurerstrasse 270 8057 Zurich Switzerland3Department for Farm Animals Division of Swine Medicine Vetsuisse Faculty University of Zurich Winterthurerstrasse 2708057 Zurich Switzerland4Veterinary Research Institute Hudcova 29670 621 00 Brno Czech Republic

Correspondence should be addressed to Radka Andrysikova andrysikovagmailcom

Received 24 March 2018 Accepted 28 May 2018 Published 21 June 2018

Academic Editor Franco Mutinelli

Copyright copy 2018 Radka Andrysikova et al This is an open access article distributed under the Creative Commons AttributionLicense which permits unrestricted use distribution and reproduction in any medium provided the original work is properlycited

A 17-week-old crossbred finishing pig was presented for lameness of approximately one week Clinical evaluation includingophthalmologic examination revealed ataxia partial flaccid paresis of the pelvic limbs skin lesions at feet and claws andseverely reduced visionblindness Both eyes had multiple persistent pupillary membranes (iris-to-iris and iris-to-lens) andhypermature cataracts Histopathological examination of the eyes revealed microphthalmia microphakia with cataract formationmyovascularisedmembrane in the vitreous retinal detachment and retinal dysplasia Microscopic examination of tissues collectedpostmortem demonstrated nonsuppurative polioencephalomyelitis with the most prominent inflammatory lesions in the lumbarspinal cord Subsequently presumed TeschenTalfan disease was confirmed by porcine teschovirus identification in the spinalcord using the reverse transcription-polymerase chain reaction (RT-PCR) To the authorsrsquo knowledge this is the first case reportdescribing in detail histopathological changes in the porcine congenital microphthalmic syndrome

1 Introduction

Several congenital ocular defects in pigs such as anoph-thalmia macro- and microphthalmia and cyclopia havebeen documented in the veterinary literature [1]

Microphthalmia which is frequently associated withmultiple malformation has been described in both domesticand nondomestic species including several canine breeds(eg Doberman Pinscher Saint Bernard and MiniatureSchnauzer but more frequently as part of the collie eyeanomaly) horses cattle (Angus Shorthorn Hereford) Texelsheep pigs camel white-tailed deer and raptors [2] How-ever microphthalmia may be seen as sporadic finding in anyspecies [3]

Microphthalmia syndromes may arise early in organo-genesis caused by abnormal development of the optic vesi-cle (either deficiency in the optic vesicle or later becauseof retarded growth and expansion of the optic cup)

Microphthalmia can also occur at later developmental stagesas a result of insufficient early intraocular pressure [2]If microphthalmia originates at the stage of the neuralplateoptic sulcus it is frequently associated with multipleocular malformations (eg anterior segment dysgenesiscataract retinal dysplasia and persistent hyaloid artery) [2]Microscopic abnormalities typically include microphthal-mos opaque and pigmented cornea aphakia ormicrophakiaand absence of a normal anterior chamber Histologicalchanges are represented by missing Descemetrsquos membraneandor normal corneal endothelium disorganized cysticciliary and iridal epithelium and heterotopia (eg stratifiedsquamous epithelium glandular tissue or cartilage in theanterior segment) [3]

A long-established cause of microphthalmia in swine ishypovitaminosis A [4ndash6] Other known or suspected causesinclude gestational-acquired infections drugs and environ-mental pollutant toxicities [7 8] More recently various

HindawiCase Reports in Veterinary MedicineVolume 2018 Article ID 2051350 6 pageshttpsdoiorg10115520182051350

2 Case Reports in Veterinary Medicine

(a) (b)

Figure 1 Macroscopic postmortem photograph of the left eye (a) and the right eye (b) Multiple persistent pupillary membranes (iris-to-irisand iris-to-lens) and hypermature cataracts are present in both eyes

genetic aberrations ranging from chromosomal duplicationsto mutations in a single gene SOX2 [8] were identified to beimplicated in microphthalmia development in humans andother animal species

TeschenTalfan disease is caused by the ubiquitousTeschovirus A (previously classified as Serogroup 1 porcineenterovirus) a nonenveloped ssRNA(+) virus in the orderPicornavirales family Picornaviridae There are 13 serotypes(PTV-1 to -13) [9] of different pathogenicity but all of themexhibit gastrointestinal and neurotropism Both domesticpigs and wild boars are the only known hosts [10]

The disease manifests itself clinically as fever diarrheaand pneumonia with subsequent paresisparalysis of pelviclimbs The most severely ill pigs may succumb to the diseaseafter 3-4 days [11] Chorioretinal lesions have been reported ininfected pigs [1] Histopathologically necrosis perivascularcuffing neuronophagia and gliosis are hallmarks of nonsup-purative polioencephalitis [10]

TeschenTalfan disease has been documented in CentralEurope Denmark Great Britain Canada USA and Aus-tralia It is a reportable disease in Switzerland as well as inother European countries under the Teschen Disease Orderin domestic and European Union legislation [10] Over thelast decade there have been reported 4-5 outbreaks per yearin Switzerland (personal communication Dr Xaver Sidler)

This report documents the most complex case of porcinecongenital microphthalmic syndrome to the authorsrsquo knowl-edge characterized by microphthalmia multiple persistentpupillary membranes (PPMs) which consisted of both iris-to-iris and iris-to-lens microphakia with cataract formationmyovascularised membrane in the vitreous retinal detach-ment and retinal dysplasia

2 Case Presentation

A 17-week-old Large White x Landrace crossbred fatten-ing pig weighing 55 kg was presented to the Division ofSwine Medicine Vetsuisse Faculty University of Zurich for

evaluation of lameness The pig was housed on a finishingfarm along with other 94 fattening pigs The first symptomoccurred a week prior to the consultation with eight animalsaffected with lameness (morbidity ca 8) The initial treat-ment by the referring veterinarian consisting of Metacam (20mgml meloxicam) and Betamox (150 mgml amoxicillin)failed to achieve improvement Subsequently the Swiss PigHealth Service (SGD) transported two finishing pigs to theDivision of Swine Medicine of the Vetsuisse Faculty Onepig exhibited only ataxia and the other exhibited both ataxiaand vision loss The visual pig was not included in thisreport

The blind pig was calm andmentally alert but ataxic withpartial flaccid paresis of the pelvic limbs although able tostand up with help There were several skin lesions of thefeet and claws with the joints within normal limits Pan-niculus and interdigital reflexes were normal and the rectaltemperature was 395∘C The pig appeared to be blind It wasable to urinate and defecate without problems

The ophthalmologic examination revealed normal palpe-bral and dazzle reflexes and negative pupillary light reflexes(PLR) in both eyes (OU) Vision was considered questionablebased on reducedquestionable menace response OU Exam-ination with a portable slit-lamp biomicroscope (Kowa SL-15 Kowa Co Ltd Tokyo Japan) revealed bilateral multiplePPMs (iris-to-iris and iris-to-lens) and bilateral hypermaturecataracts (Figure 1) Adnexal structures and the rest of theanterior segment structures were normal OU The posteriorsegment could not be examined due to the opacity of the opticmedia OU

Because of the progressive worsening of neurologic signsno treatment was attempted and the pig was humanelyeuthanized and submitted to the Institute of VeterinaryPathology Vetsuisse Faculty University of Zurich for patho-logical examination which found no gross lesions in any ofexamined organ systems other than both eyes Brain spinalcord and both globes were submitted for histopathologicalexamination

Case Reports in Veterinary Medicine 3

Figure 2 (A) Low power magnification image of the microphthalmic globe with microphakic cataractous lens and complete retinaldetachment Hematoxylin and eosin stain bar = 5 mm (B) High power magnification of persistent pupillary membrane (a) anterior portionof themyovascularisedmembrane (b) cataractous lens (c) with calcium crystals (d) and posterior portion of themyovascularisedmembrane(e) Hematoxylin and eosin stain bar = 500 120583m (C) High power magnification image of dysplastic retinal layers with rosettes (f) in the innernuclear layer Hematoxylin and eosin stain bar = 250 120583m

At necropsy brain spinal cord and both globes wereremoved and fixed for several days in 10 buffered formalindehydrated in a descending alcohol series then paraffin-embedded cut in 2-3 120583m sections mounted on glass slidesand stained using hematoxylin and eosin

From the central nervous system histological slides wereprepared from cranial cortex with basal ganglia cortex withhippocampus and thalamic regions midbrain cerebellumpons medulla oblongata cervical thoracic and lumbarspinal cord Craniospinal ganglia were not examined

Histologically a nonsuppurative polioencephalomyelitiswas present from the hypothalamus to the lumbar spinalcord However concerning the grade of inflammatory cellcontribution the processmust be declared as verymild in thebrain whereas inflammatory lesions were more prominentin the lumbar spinal cord Additionally the entire spinalcord exhibited a high grade of Wallerian degeneration Indiencephalic regions there were few vessels with few lym-phocytes in the Virchow-Robin spaces and few small foci ofintrameningeal lymphocytes present In the mesencephalonfew foci of lymphocytes were found in themeninges few oneslayered cuffed vessels and some degenerated neurons show-ing vacuolation at themargin of the soma and dilatedmyelinsheaths in the surrounding areaswere visible Cerebellumanditsmeningeswere not affected andmedulla oblongata showedsparse small glial nodules Lesions in the spinal cord weremuch more prominent showing prominent glial nodulesperivascular cuffing and neuron degeneration and mostlyshrunken hypereosinophilic neurons in the grey matter andhigh grade Wallerian degeneration in the white matterWallerian degeneration was more prominent in the ventralspinal cord columns however lateral and dorsal columns

were also affected Even in spinal roots Wallerian degener-ation was present as well as few infiltrating lymphocytesUnfortunately spinal ganglia as well as trigeminal gangliawere not collected Altogether the histopathological picturewas compatible with a subacute TeschenTalfan disease con-dition

Ocular lesions included microphthalmia multiple PPMs(iris-to-iris and iris-to-lens) microphakia with cataractformation myovascularised membrane surrounding thecataractous lens and expanding into the vitreous towards theretina retinal detachment and retinal dysplasia (Figure 2)Moreover Wallerian degeneration was identified in the opticnerve In spite of the widespread ocular changes the ciliarybodywas large and prominentThedetached retina containedonly indistinctivelypoorly developed different cellular layersrosette formation was occasionally observed in the innernuclear layer These findings were classified as congenitalmicrophthalmic syndrome Since there was no histologicalevidence of inflammation in any of the examined oculartissues including the uveal tract and retina the ocularchanges were presumed to be of another cause than acuteinflammatory disease

Based on history clinical examination course of thedisease and histopathologically confirmed nonsuppurativepolioencephalomyelitis a tentative diagnosis of TeschenTalfan disease was suspected and samples of brain and spinalcord were subjected to laboratory examination to test for thepresence of the porcine teschovirus

RNA extractions from both brain and spinal cordwere performed using TRI Reagent (Sigma Aldrich StLouis MO USA) according to the manufacturerrsquos instruc-tions The negative control consisted of nuclease-free water


(Top-Bio Prague CzechRepublic) instead of biologicalmate-rial Porcine teschovirus strain VIR 46088 (CAPM V ndash 647)obtained from the Collection of Animal PathogenicMicroor-ganisms (CAPM Veterinary Research Institute Brno) wasused as a positive control

Isolated RNA was used for a one-step reverse trans-cription-polymerase chain reaction (RT-PCR) (TranscriptorOne-step RT-PCR Kit Roche Mannheim Germany) usingspecific primers (PEV-1a-F 51015840-AGTTTTGGATTATCT-TGTGCCC-31015840 PEV-1e-R 51015840-CGCGACCCTGTCAGGCAG-CACndash31015840) targeting the highly conserved 51015840-nontranslatedregion (51015840-NTR) [12] Used primers generated 316 bp productcharacteristic to members of the genera Teschovirus Finallyto further increase specificity of our PCR reaction secondldquonestedrdquo PCR was performed (Aptamer Hot Start MasterMix Top-Bio Prague Czech Republic) (158 bp PEV-1c 51015840-TGAAAGACCTGCTCTGGCGCGAG-31015840 PEV-1d 51015840-GCT-GGTGGGCCCCAGAGAAATCTC-31015840) [12] Both obtainedamplicons were sequenced commercially (SeqMe PrıbramCzech Republic) and data were analyzed using BLAST andaligned with GenBank sequences

Porcine teschovirus was detected in spinal cord but notin the brain sample Comparison of acquired 316 bp sequencefrom 51015840-NTR locus with teschovirus sequences available inGenBank showed 96 nucleotide similarity with porcineteschovirus strain BL7792 (GenBank no GQ293236)

3 Discussion

Among congenital globe abnormalities reported in pigssuch as anophthalmiamacro- andmicrophthalmia cyclopiaand retinal dysplasia microphthalmia is the leading ocularanomaly [1 7] The most frequent cause of the congeni-tal globe abnormalities is maternal vitamin A deficiencyInsufficient levels of vitamin A in farm animals have beenreported in populations with limited access to natural sourcesof vitamin A and inadequate or no vitamin supplements[6 13ndash16] If hypovitaminosis A resolves before the 12th dayof gestation no malformation in newborn piglets is observedand eye organogenesis is normal in piglets when dams receivevitamin A supplement at earlier stages of pregnancy [17]On the contrary if malnutrition persists up to day 90abnormalities of spinal cord brain skin and tail arise [18]These changes are well documented in piglets born to vitaminA-deficient dams receiving subnormal doses of vitamin Auntil at least 18 days after conception In the same study itwas found that mesenchymal tissue (eg iris and primaryvitreous body) and not ectoderm was the primary targetof the hypovitaminosis A Failed closure of the fetal opticfissure abnormal mesenchymal proliferation anterior andposterior to the lens and decreased rate of globe growthduring the last two-thirds of pregnancy were hallmarks inpiglets of vitamin A-deficient sows [17] However oculartissue development observed in the case reported here aswell as lack of other hallmarks associated with early to mid-gestation hypovitaminosis A (eg spinal cord brain skinand tail abnormalities) suggests that either hypovitaminosisA in late gestation period or other teratogenic insults were themain causes of microphthalmia

Apart from hypovitaminosis A several other causes ofmicrophthalmia were reported including suspected drugtoxicities and high levels of selenium in diet [7] Hereditarymicrophthalmos has been reported in Yorkshire pigs [1]White Shorthorn cattle Jersey calves and Hereford cattle (asa part of encephalopathy-microphthalmos syndrome) Thepattern of heritability seems to be autosomal recessive traitin all cases listed above [7]

The globes evaluated in this case had PPM strandsPersistent pupillary membranes represent remnants of thevessels andmesenchymeof the tunica vasculosa lentis anterior(so called pupillary membrane) in the developing eye Thisprimitive vascular system reaches maximal development byday 45 in the dog then begins to regress as the aqueoushumor takes over this metabolic function [2] and completelydisappears in dogs within the first weeks after the birth [2 319] Pupillary membrane tunica vasculosa lentis and hyaloidartery undergo first apoptosis later cellular necrosis untilcomplete atrophy [2] When these mechanisms fail PPMspersistent hyperplastic primary vitreous (PHPV) and per-sistent hyperplastic tunica vasculosa lentis (PHTVL) remain[20] The normal age of pupillary membranersquos regression inswine is not known [1]

Although rarely reported in swine PPMs are reportedoccasionally in dogs and horses and inheritability has beenrecognized in several canine breeds [20]

One report documented a very high frequency of PPMsoccurrence inYucatanmicropigs reaching 661ofmicropigsbetween 7 and 12 months of age Similar to the case reportedin this study other associated pathologies including presenceof hyaloid remnants congenital cataracts nuclear opacitiesand suture line abnormalities were diagnosed in up to 80 ofexamined Yucatan micropigs [21]

Lenticular abnormalities such as cataract or micro-phakia are common hallmarks of the anterior segmentdysgenesis Although congenital cataracts are found in manyspecies only few of them are linked to maternal exposureto toxins infection (eg rubella virus in humans) or otherin utero insults during the critical stages of lenticular devel-opment [3] Congenital perinuclear (at the nuclearcorticaljunction) cataracts developed in piglets whose mothers hadbeen treated with alloxan [1] Juvenile cataract which isbelieved to be inherited has been described in Vietnamesepot-bellied pigs [1]

The retinal abnormalities (retinal dysplasia with occa-sional rosettes) observed in our fattening pig representthe disorganized development of retinal tissue that maybe accompanied by pigment disturbance or evidence ofassociated retinal degeneration [22]

Retinal dysplasia is an important hereditary abnormalityin many breeds of dogs [2] but is seldom encountered as agenetic disease in other species [3] Retinal dysplasia may beassociatedwithmaternal infection eg infectionwith bovineviral diarrheandashmucosal disease (BVD-MD) virus (pestivirus)later than 76 days but before 150 days of gestation or intrau-terine infection with feline panleukopenia virus among oth-ers [3]

In the swine described in this case report the exactcause of the clinically apparent and histologically confirmed


congenital microphthalmic syndrome was not determinedSince there were no other reported instances of microph-thalmia in the swine herd or siblings of the affected pighypovitaminosis A seems to be less likely cause of microph-thalmia in this case Moreover other symptoms observed inthe animal (eg multiple PPM and retinal detachment) areusually not linked to hypovitaminosis A On the contraryother characteristic symptoms of hypovitaminosis A includ-ing abnormalities of brain spinal cord tail and skin wereabsent in the examined pig Sporadic genetic mutation andmaternal exposure to toxic or infectious Noxa were consid-ered to bemore likely etiologyThe histological changes in thecentral nervous system and presence of porcine teschovirusdetected in spinal cord by theRT-PCRwhile the brain samplewas assessed negative confirmed previous TeschenTalfaninfection explaining the clinical symptoms for which thefinishing pig had been originally presented to the Division ofSwineMedicine of theVetsuisse Faculty University of ZurichThere were no apparent inflammatory changes neither inretina nor in choroid therefore the authors assume that theocular pathology was solely caused by a harmful event inutero in the last third of gestation (based on the retinalstratification) and the later infection had no (or minimal)influence on these changes

In conclusion we present a case of complex microph-thalmic syndrome in pig involving structural changesof anterior chamber (multiple iris-to-iris and iris-to-lensPPMs) lens (microphakia hypermature cataract) and pos-terior segment (vitreal myovascularised membrane retinaldysplasia with occasional rosettes in the inner nuclear layerand retinal detachment) The probable etiology seems to beeither sporadic genetic mutation or maternal exposure totoxic compound or infection

Disclosure

Dr Andrysikovarsquos current address is Animal Eye Center PC215 W 67th Ct Loveland CO 80538 USA

Conflicts of Interest

The authors declare that they have no conflicts of interest

Acknowledgments

The authors would like to thank Dr Maja Ruetten Dr medvet DECVP FVH (Pathology) PathoVet AG TagelswangenZH Switzerland for performing histopathologic examina-tion of ocular specimens and also the Swiss Pig HealthService (SGD) for technical support Special thanks are dueto Dr Steven M Roberts DVM MS DACVO Animal EyeCenter PC Loveland Colorado USA for kind proofreadingof the manuscript The study was supported by Ministry ofEducation Youth and Sports of the Czech Republic (Grantno LO1218)

References

[1] J W Pearce and C P Moore ldquoFood Animal OphthalmologyrdquoinVeterinary Ophthalmology K N Gelatt B C Gilger and T J

Kern Eds pp 1610ndash1674Wiley-Blackwell Oxford 5th edition2013

[2] C S Cook ldquoOcular Embryology and Congenital Malforma-tionsrdquo in Veterinary Ophthalmology K N Gelatt B C Gilgerand T J Kern Eds pp 3ndash38 Wiley-Blackwell Oxford 5thedition 2013

[3] R R Dubielzig K Ketring G J McLellan and D MAlbert ldquoCongenital developmental or hereditary abnormal-ities in animalsrdquo inVeterinary Ocular Pathology A ComparativeReview pp 29ndash57 Saunders Elsevier Edinburgh 2010

[4] H C Bendixen ldquoLittery occurrence of anophthalmia or micro-phthalmia together with other malformations in swine - pre-sumably due to vitamin A deficiency of the maternal dietrdquo ActaPath Microb Scand vol 54 pp 161ndash179 1944

[5] S Berge ldquoThree hereditary anomalies in pigsrdquoHereditas vol 27no 1-2 pp 176ndash192 1941

[6] F Hale ldquoThe relation of vitamin A to anophthalmos in pigsrdquoAmerican Journal of Ophthalmology vol 18 no 12 pp 1087ndash1092 1935

[7] D J Maggs P E Miller and R Ofri ldquoDevelopment and con-genital abnormalitiesrdquo in Slatterrsquos Fundamentals of VeterinaryOphthalmology pp 13ndash26 Elsevier Saunders St Louis 5thedition 2013

[8] A S Verma andD R FitzPatrick ldquoAnophthalmia andmicroph-thalmiardquo Orphanet Journal of Rare Diseases vol 2 no 1 articleno 47 2007

[9] E J Lefkowitz D M Dempsey R C Hendrickson R J OrtonS G Siddell and D B Smith ldquoVirus taxonomy the database ofthe International Committee on Taxonomy of Viruses (ICTV)rdquoNucleic Acids Research vol 46 no D1 pp D708ndashD717 2018

[10] D J Taylor ldquoVirus Diseasesrdquo in Pig Diseases D J Taylor Edpp 18ndash108 St Edmundsbury Press Ltd Bury St EdmundsburySuffolk 1999

[11] K-O Eich U Schmidt and M de Jong Handbuch Schweinek-rankheiten VerlagsUnionAgrar Landwirschaftsverlag GmbHMunster 2000

[12] A Krumbholz RWurm O Scheck et al ldquoDetection of porcineteschoviruses and enteroviruses by LightCycler real-time PCRrdquoJournal of Virological Methods vol 113 no 1 pp 51ndash63 2003

[13] SAC C VS disease surveillance report ldquoRange of ocular defor-mities in calves due to hypovitaminosis Ardquo Veterinary Recordvol 174 no 10 pp 244ndash247 2014

[14] J Bouda P Jagos V Dvorak and V Hamsık ldquoVitamin Aand Carotene Metabolism in Cows and their Calves Fed fromBucketsrdquoActa Veterinaria Brno vol 49 no 1-2 pp 45ndash52 1980

[15] M J Carrigan J R Glastonbury and J V Evers ldquoHypovita-minosis A in pigsrdquo Australian Veterinary Journal vol 65 no5 pp 158ndash160 1988

[16] Y Millemann H Benoit-Valiergue J-P Bonnin J-J Fontaineand R Maillard ldquoOcular and cardiac malformations associatedwith maternal hypovitaminosis A in cattlerdquo Veterinary Recordvol 160 no 13 pp 441ndash443 2007

[17] B Palludan ldquoThe influence of vitamin A deficiency on foetaldevelopment in pigs with special reference to eye organogen-esisrdquo International Journal for Vitamin and Nutrition Researchvol 46 pp 223ndash225 1976

[18] R Neundorf P Kielstein and V Bergmann ldquoErnahrungs-bedingte Erkrankungen Erkrankung infolge eines Mangelsoder Uberschusses an Vitaminen Vitamin Ardquo in Schweinek-rankheiten Atiologie - Pathogenese - Klinik - Behandlung -Bekampfung R Neundorf P Kielstein and V Bergmann Eds


pp 110ndash115 Ferdinand Enke Verlag Stuttgart Jena 3rd edition1987

[19] D J Maggs P E Miller and R Ofri ldquoUveardquo in Slatterrsquos Fun-damentals of Veterinary Ophthalmology pp 220ndash246 ElsevierSaunders St Louis 2013

[20] R R Dubielzig K Ketring G J McLellan and D M AlbertldquoThe Uveardquo in Veterinary Ocular Pathology a comparativereview pp 245ndash322 Saunders Elsevier Edinburgh 2010

[21] G Saint-Macary and C Berthroux ldquoOphthalmologic observa-tions in the young Yucatan micropigrdquo Laboratory Animals vol44 no 4 pp 334ndash337 1994

[22] R R Dubielzig K Ketring G J McLellan and D M AlbertldquoThe Retinardquo in Veterinary Ocular Pathology a comparativereview pp 349ndash397 Saunders Elsevier Edinburgh 2010

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Advances in

Virolog y

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Cell BiologyInternational Journal of



Case Reports in Veterinary Medicine

Submit your manuscripts atwwwhindawicom


(a) (b)

Figure 1 Macroscopic postmortem photograph of the left eye (a) and the right eye (b) Multiple persistent pupillary membranes (iris-to-irisand iris-to-lens) and hypermature cataracts are present in both eyes

genetic aberrations ranging from chromosomal duplicationsto mutations in a single gene SOX2 [8] were identified to beimplicated in microphthalmia development in humans andother animal species

TeschenTalfan disease is caused by the ubiquitousTeschovirus A (previously classified as Serogroup 1 porcineenterovirus) a nonenveloped ssRNA(+) virus in the orderPicornavirales family Picornaviridae There are 13 serotypes(PTV-1 to -13) [9] of different pathogenicity but all of themexhibit gastrointestinal and neurotropism Both domesticpigs and wild boars are the only known hosts [10]

The disease manifests itself clinically as fever diarrheaand pneumonia with subsequent paresisparalysis of pelviclimbs The most severely ill pigs may succumb to the diseaseafter 3-4 days [11] Chorioretinal lesions have been reported ininfected pigs [1] Histopathologically necrosis perivascularcuffing neuronophagia and gliosis are hallmarks of nonsup-purative polioencephalitis [10]

TeschenTalfan disease has been documented in CentralEurope Denmark Great Britain Canada USA and Aus-tralia It is a reportable disease in Switzerland as well as inother European countries under the Teschen Disease Orderin domestic and European Union legislation [10] Over thelast decade there have been reported 4-5 outbreaks per yearin Switzerland (personal communication Dr Xaver Sidler)

This report documents the most complex case of porcinecongenital microphthalmic syndrome to the authorsrsquo knowl-edge characterized by microphthalmia multiple persistentpupillary membranes (PPMs) which consisted of both iris-to-iris and iris-to-lens microphakia with cataract formationmyovascularised membrane in the vitreous retinal detach-ment and retinal dysplasia

2 Case Presentation

A 17-week-old Large White x Landrace crossbred fatten-ing pig weighing 55 kg was presented to the Division ofSwine Medicine Vetsuisse Faculty University of Zurich for

evaluation of lameness The pig was housed on a finishingfarm along with other 94 fattening pigs The first symptomoccurred a week prior to the consultation with eight animalsaffected with lameness (morbidity ca 8) The initial treat-ment by the referring veterinarian consisting of Metacam (20mgml meloxicam) and Betamox (150 mgml amoxicillin)failed to achieve improvement Subsequently the Swiss PigHealth Service (SGD) transported two finishing pigs to theDivision of Swine Medicine of the Vetsuisse Faculty Onepig exhibited only ataxia and the other exhibited both ataxiaand vision loss The visual pig was not included in thisreport

The blind pig was calm andmentally alert but ataxic withpartial flaccid paresis of the pelvic limbs although able tostand up with help There were several skin lesions of thefeet and claws with the joints within normal limits Pan-niculus and interdigital reflexes were normal and the rectaltemperature was 395∘C The pig appeared to be blind It wasable to urinate and defecate without problems

The ophthalmologic examination revealed normal palpe-bral and dazzle reflexes and negative pupillary light reflexes(PLR) in both eyes (OU) Vision was considered questionablebased on reducedquestionable menace response OU Exam-ination with a portable slit-lamp biomicroscope (Kowa SL-15 Kowa Co Ltd Tokyo Japan) revealed bilateral multiplePPMs (iris-to-iris and iris-to-lens) and bilateral hypermaturecataracts (Figure 1) Adnexal structures and the rest of theanterior segment structures were normal OU The posteriorsegment could not be examined due to the opacity of the opticmedia OU

Because of the progressive worsening of neurologic signsno treatment was attempted and the pig was humanelyeuthanized and submitted to the Institute of VeterinaryPathology Vetsuisse Faculty University of Zurich for patho-logical examination which found no gross lesions in any ofexamined organ systems other than both eyes Brain spinalcord and both globes were submitted for histopathologicalexamination














3 Discussion













Disclosure




Acknowledgments


References






























Microbiology












Volume 2018



Agronomy







Volume 2018

Zoology






Volume 2018


Advances in

Virolog y




















3 Discussion













Disclosure




Acknowledgments


References






























Microbiology












Volume 2018



Agronomy







Volume 2018

Zoology






Volume 2018


Advances in

Virolog y










Disclosure




Acknowledgments


References






























Microbiology












Volume 2018



Agronomy







Volume 2018

Zoology






Volume 2018


Advances in

Virolog y

















Microbiology












Volume 2018



Agronomy







Volume 2018

Zoology






Volume 2018


Advances in

Virolog y







casereport congenital microphthalmic syndrome in a swine

Documents