The pathology of kidney diseases in sheep : a thesis presented in partial fulfilment (30 %) of the requirements for the degree of Master of Philosophy in Veterinary Pathology at Massey University

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(2) THE PATHOLOGY OF KIDNEY DISEASES IN SHEEP. A t,hesis presented in partial fulfilment. (3Cf/o). of the. requirements for the degree of l\laster of Philosophy. in VP.tcrinary Pathology at T·1asse y University.. Pavlos G-eorgiou Toum.azos. 1981.

(3) ii. ACKNOWLEDGEMENTS. I would l ike cor dially to thank Dr A.C. J ohns tone , for his c ontj.nuous and untiring guida�1ee, a ss i sta n ce throughout this study.. a dvic e ,. my supervisor,. encouragemei:t and. Spec ia l thanl�s are a lso clue to. 1-Tr. G. V.. Peter s en for his advice and assist a n c e in tbe stat i s t i c a l a na lys i s of data and for his arrangements for visits at Longburn freezing >·rorks . JI'Ia.ny th anks ar·e expr e s sed to the veterinary and meat in s pe c tion st<;.ff of the 1:-or-thvlick' s f reez�_ ng works at L ong burn, for t:he i r co:Llaboration. duT.Lng. .. :·llection peri od.. Professor B.\if. MankteloH, Dr M.R. A l ley and Dr R.D. Jcl.J.y gELJe helpf1}.1 advice during tbe w-c . iting and preparation. of this thRsis.. I am grateful for te chnical a s sis t a n ce provided by I.Jrs P I : .. and her. ·. .. Slack. "team" for the prep ara ti on of tissues for histopathological. examination; Hr T.G.. Law and tne staff of the };asse y University }':cintc;:y. for the pr eparat i o n of the photographs and 1·qJrod.u.ction of the figures. present e d in this thesis. I a l s o extend my sinc e re st gra t:•... /3. to many other fri ends. frcg. this and other D e pa rtment s of the Ji'ncu.lty of Yeteri:nary Science who v:erc a lw ays keenly receptive to my enquiries and request s and have directly or ind i rec tly helped me in my work. I would like to sinc ere ly thank my wife Vaso for typing tl:is thesl.s and the p.::l.tience,. understa ndin g and sacrifices :Jade by her and our. children Hiranda and Nestoras du:ring preparation of the manusc:cipt.. This inves ti ,:':a tion -vms partly suppor te d by a C ommor.vre a l th Scholal·ship. I am most gratefull to the administrators of this Gran t , especially the secretary Miss D.L.. Anderson ..

(4) iii. ABSTRACT. Renal diseases in sheep form a di verse spectrum of pathology and an extensive literature revievr of spontaneously occurring and e':per i ­ mentally induced diseases of the 3hecp of this t he s i s survey. of. to. pr o v i de a c ompa r is on vri th. ki dneys jn slaughter-house �illed. the l esion s h. s e ep. of results of this survey form the major p ar t provide s information on sheep. uhich. these. . The. 1980.. at the. The p r evalen ce. 13,988. Borth-v;ick'. of. re na. signif icant variat i on ( p ( 0. 05) in the. l. sheep a. t otal. of. vre re ca t e gor i z ed into s even. le si on in each.. In. a. p resentation. The abnormal kidneys. sheep sl ughter e d over a. a. s. free z ing \lOrks,. disease. vras 3 . 1 8. prevalence of. 830 dise11sed ki dne ys. Longburr1. :per cen� and. lesions. ";as. of sheep ex&11ined.. l•rere founrl. groups according to the major. s ome kidneys. in. to large populati ons of. found beh1eE:n the various lines, chains and da ily totals. From t he se. found. thesis and. this. is only s pa rsely re po r t e d elsevrhere.. consecuti ve five day per i o d. no. of. diseases relative. under study were obtained from 444- of. in January. presented in Chapter l. �Kidney is. ancl. these. pathologic&.l. addi b onB-1 m nor lesions vrere present,. i. ma king a total of 1212 macroscopic le sio n s identified.. White finding in and. 179. spots and strealr..s . c on G t i tuted the major. 188. kidneys;. respectively;. Abscesses,. pale,. red and. gross p8.thological. brovm discolourati on in 174,. 120. scars in 107; cysts in 37 and nodules in 25 kidneys.. neoplasms and focal space occupying lesions of uncertain. aetiology 1.vere included under the category of nodule.. Pieces of tissue selected from. 181 kidneys. to represent the vario·LtS. lesions seen at gross examination were examined histologically. were identified,. These. recorded and graded accor ding to the anatomical location,. pattern of distribution, tissue changes and degree of severity.. The main histopathological feature of the white spotted kidneys vras.

(5) iv. chronic, mainly multifocal inflammation of the cortical interstitium. Similar. but. r a dially disposed inflammatory lesions with marked fibrosis. occurred in the. scarred kidneys .. pattern of these lesions suggested. The. a haematogenous di::;tribution of a. pathog en. the scarred k idneys were. the result of ascending inflammation. or infarctive. processes.. Kidneys vli. nephrosis. probably. discolouration showed mild to. th pale. of the cortical. emosi derin deposition .. t o areas of scarring.. moderately. severe. epithelial cells� while kidneys vlith brovm. discolouration shovred corticotubular ha. in the spotted kidney.s vJhile. In some. intracyt oplasmic. kidneys. and intralumenal. haemosiderosis wa::: restricted. Red discoloured kidneys. shm·red. patchy. or d iffuse. congestion.. Cystic lesions were either retention. parasitic or. caused by blockage of tubules .. the. In the. result of urinary latter,. tha block�ge. ,._,.as either congenital or associate d with chronic inflammation.. With the exception of. were chronic. nephrosis. in nature and for most of. diagnosis vras not esta blished.. Echinococcus. and conges-tion all the. granulosus hy. them. In fact,. datid cysts. lesions. a definitive aetiological. in only those lesions containing. could such. a. diagnosis. be. made.. Additional studies are indicated for the provision of further information on. (a). the prevalence of renal diseases in different. gevgraphical locations, and. (c). ( b). variation of disease types from area to area. the causes of the lesions identified from this type of. investigation..

(6) V. TABLE OF CONTENTS Page ACKNOWLEDGEMENTS. iii. ABSTRACT LIST OF ILLUSTRATIONS CHAPI'ER l:. CHAPTER 2:. ii. Review o f the liter atur e Introduction ( I) Diseases of the glomerulus l. Spontaneous glomerulonephropathies 2. Experimental autoinrnune glo merulo neph:ritis' ( II) Diseases of renal tubules l. Inflammatory 2. Degenerative ( III ) Diseases o f the renal pelvis ( IV ) Renal Neoplasms ( v ) Renal Cysts ( VI ) Uro lithiasi:::: A survey of diseased sheep kidneys Introduction Mater ials and Ne tho ds Results Gr o ss Pathology l. Abnormal shape 2. Increased size 3 . Reduced 8ize 4 . Disco louration 5 . Spots and streaks 6. Scars 7. Cysts 8. Nodules Histopathology l. Discolouration 2. Spots and str ealm 3 . Scar s 4. Cysts 5 . Nodules Discussion Conclusion. vi l l. 2. �. 7 10 10 15 24 25 25 27 30 30 30 31 34 37 37 37 37 38 38 38 39 40 41 42 45 47 49 52 60. BIBLIOGHAPHY. 62. APPENDICES. 72.

(7) vi LIST OF ILLUSTRATIONS Follovling Figure 2.1. Figure 2.2. Figure 2.3. Figure 2 .4. Figure 2 .5. Figure 2 .6. Histogram showing the distribution in weight of 8)0 l.i< dne y s collected from 444 sheep 1·ri th renal l esio ns .. Hi st ogra m shovTing the gross pathological fe at ur es of 12 12 lesions recorded in 830 diseased k idneys . Misshapen kidney (No. 23 4). a) Capsular surface shmving dumbbell sha pe caused by seve r e s carring in .central area. Less extensive sc a rr ing is pr esen t over the c a psular surface of the poles. b ) The cut surface of the same k idn ey shovring the scar:J:'ed tissue extending from capsule to pelvis.. Pale shrunken kidney ( No. 30·t) The reduct i on in size is due to di f fus e scarring of the renal parenchyma. The incised surface of this kidney is shovm. 34. 34. 37. •. in f igure 2 .14 .. 37. region.. 37. Pale Slwllen kidney (No . 99). No te the pallor of the outer c ortex c ontrasting with the c ong es ted corticowodullary Pa tch:y red discolouration of kidneys ( No. 5 ) due t o c onge stio n. The change is less severe and. res tricted t o t1w right po le in the ki dney on the righ t .. 37. Figure 2 . 7. Diffuse red discolov.ra cion of a kidney ( No. 2 5 4) due to conge sti on .. Yl. Figure 2.8. Diffuse dark brovm discolouration of a kidney ( No. 201) due to haemosiderosis.. 37. Figure 2.9a Dark brown discolouration of kidneys ( No.l33 ) distr ibuted in scarred and depressed areas of renal cortex. The pale raised areas are the r emaining functional kidney tissue. Figure 2.9 b. Cut section of kidneys showing radial brown str eaking of scar tissue extending from capsular surface to medulla.. 38. 38. rJage.

(8) vii Following page Figure 2.10. Figure 2.1 1. Figure 2.12. a) Severe diffuse spotting of subcapsular cortical tissue ( kidney No. 119 ) . b) The same kidney on cut section showing ill-defined, white streaks extending radially into iriller cortical parenchyma.. 38. a) llioderEt.tely severe vrhi te spotting of the subcapsular c ortical tissue ( kidney No.2) b) The cut section of t he same ki dne y showing ill-defined v1hi t e streaks vrhich are most prominent in the outer cortical paren chyma .. 38. a ) M ult ip le , slightly depr e s se d ill­ defined s cars in the subcap sular tissue ( kidney No . 4) . b) Cut section of the s a me kidney showing poorly defined linear vrhite hands of scar tis3ue in the cortex.. Figure 2.13. Extensive scarring of the subca psular tissue (kidney No. 130).. Figure 2.14- Cut secti on of a sma l l scarred kidney ( no. 304) shovr in g diffuse fibr osis affecting all areas o f the kidney. Note the d i sto rt ed renal papilla. The capsular surface of trLis kidney is shovm in figure 2.4. Figure 2.1 5. Figure 2.16. Figure 2. 17. Congenital cysts. a) Capsular surface showing numerous well d efine d cortical depressions overl r ing the cystic parench:yma ( J:..idney. )8. 38. 38. No.5 5 ) . b) Cut secti on of the same kidney shovring four well defined c ortical cysts.. 39. Hydatid cysts in kidney ( No. 198) . a) Cyst of Ec hi no co ccu s grnulosus in parahilar cortical tissue. b) The cut section shov;ing the multilo­ culated cyst.. 39. Renal abscessation ( No. 5 9 ) . a ) The cortical surface of a ki��ey containing an organized abscess in the left pole. Note the deformity caused by depressed, scarred tissue in paracentral areas. b) Cut section of the same kidne�r showing the or� anizing abscess ( large arrovr ) and scars \ small arrow) extending from the cortex to the pelvis.. 33.

(9) viii Following page Figure 2.18. Renal abscessation. a). ( No. 200) .. The kidney conLa:i.ns an e n ca ps u l ate d. caseous abscess bnlging from the capsular surface.. b). Figure. 2.19. The. cut section of the. carcinoma (Ho. 237) . o of the left pole of the kidney by a renal co.J:cinoma. b) Cut sectior-1 of the kidney shmving the s l ightly encaps-..11a·�ccl lobulated tumour. Renal a. ). Di s t � t i on. with extensive. hae m or rhage .. Figure. 2.20. areas. Renal lymphoma. of. and. necrosis. 39. (lTo. 236).. a) Di s t orti on of a kidney by a lymphoma occupyin& the l(�f L polar >;tnd hilar zones.. b). The. incised. surf:>.ce. focal twnour mnssec in. Figure 2.21. sho1·1ing. the. additional tissue.. cor tical. Figur�. 2.22. 2 . 23. the. l e s i on upon sectionJ.ng.. 40. Chronic parasitic noJule (kidl1cy No. 20). a) Appearance on capsular surface. On i n c ision the.� uell defined cortical b) nodule was hard and contained gritty mate rial.. 40. Hassive renal infarct. kidney on left. ( no. 2 49 ) . 'rhe. l. is swo le n ,. haemorrhagic and necrotic.. thrombus. is. p1·esent in the. diffusely An orga ni z i ng renal vein.. The right kidney is normal. l<'igure. 2 .24.. Nep h ros i s .. Moderately severe. de ge nera tive. pyknotic nuclei tubules contain. Figure 2.26. Figure 2 .27. Ne phros is .. t. � ca t ere. 40. d. changes in epithelial cells. of proximal convoluted. Fi.gure 2.25. 39. Nodule of undctcr:r;.Lr_ed cause ( k idney No. 12 ) . a) A fib r ous no:iclle elei.Tated slightly above the cap::;ular surface. b) Note the concentric lamination of. Figure. 39. sam8 kidney.. t ub ule s .. and cell loss. hyaline. Lesions. severe than those. in. Note dil ate d casts. HE x 3 2 0 41. The. gran ula r. ar e similar but less figure 2 .24. HE x 4 00. 41. Haemosiderosis. "ifuole mount" section of kidney stained by Perls' method for iron showing extensive cortical accumulation of r�emosiderin ( x 7).. 42. Haemosiderosis. Extensive deposition of haemosiderin in cytoplasm of epithelial cells of proximal convoluted tubules ( arrovm). Granular casts are present in the tubular lumena. HE x 320. 42.

(10) ix Follmring page Figure. 2.28. Haemosiderosis.. Haemosiderin deposition. in inflamed and scarred tis sue of a. HE x. kidney.. 42. 50. Detail o f inset in figure. 2.28. sho-,ring. haemosiclerin granules in epith8lial cells of tubules. ( broad. ) and interstitial ( narrow arrovm ) .. arrow. inflammatory reaction. HE Figure. 2.30. X. 150. Kidney vii th spots and streaks.. 2.31. Focal. mainly l ymp ocyti c infiltration of renal. h. HE x. cortical interstitium. Figure. 42. 125. Kidney vri th spots and streak s .. 45 Interstitial. infiltration by lymphocytes and pl asma cells.. Note the degenerative change in epit he li al cells of tubule s and formation of proteina­. ceous casts 1·1i thin lumena.. Figure. 2 . 32. 320. HE x. 45. Glomerulus within an area of c·hronic inflammation in a "spotted" kidney.. the prolife ra t ion of cells tufts,. Note. in glomerular. the obliteration of glomerular. capillari es an d �rinary space and fibrosis. of Bomn.:ln 1 s capsule.. The entire field has. been infiltrated by plasma cells and phagocytes.. Figure. 2.33. HE x. Scarred kidney.. Small linear zone of. fibrosis v!ith lymphocyte and plasma cell. infiltr ation in the outer cortex. Figure. 2.34. 4-5. 32 0. Scarred J:r.idney.. HEx. 125. 45. An extensive iveclgeshaped. cortical scar associated 'lri th marked. tubular and glomerular atrophy . Figure. 2 . 35. Renal papilla right. ). left. ). and pelvis. 50. 4'7. ( on. of a kidney vli th extensive radial. scarring. tubules, arrows. ( on. HE x. ). Note the reduced numbers of several containing casts. ( broad. and others with calcification of. basement membrane and epithelial cells. ( narrovT. arrows. ).. The interstitial ti s sue. of the papilla i s fibrotic and infiltrated by lymphocytes.. lightly. The pelvic. epithelium is slightly hyperplastic and shows mild infiltration of subepithelial. HE. ti ssue by lymphocytes. Figure. 2 . 36. Renal papilla right. ). ( on. left. ). x 50. and pelvis. 47. ( on. of a severely scarred kidney showing. extensive replacement of tubules by fibrosis.. Remaining tubules are atrophied.. There i s extensive fibrosis of the renal pelvis.. HE x. 125. 47.

(11) X. Following page Figure 2.37. Figure 2.38. Degeneration of pelvic and papillary epithelia associated with fibrosis, lymphocytic and plasmacytic infiltrations. HE X320. 47. Renal cortex of a scarred kidney showing tubular atrophy, dilatation of tubules 1vith accumulation of highly eo sino :philic material in lumena (thyroidiza tion ) , interstitial fibrosis and infiltration by lymphocytes and plasma cells. T1v0 atrophied glomeruli are present narrow arrmvs . HE x 125. 47. Glomeruli in area of inflamm�tion and s carring sho-vring gradation in the severity of basement membrane thickening due to membranous deposition. Note the segmental lesion in one glomerulus (arrow). PAS x 125. 47. Glomerulus in an area of chronic inflamma­ tion shmving severe sclerosis of Bo1:nnan' s capsule 1vi th collagenous adhesion arroi·r to the adjacent glorneru.lar tuft. HE x 320. 47. associated -vrith qhronic of lymphocytes and plasma cells in adjacent renal tiDsue. HE X 320. 47. (. ). Figure 2.39. Figure 2.40. (. Figure 2.4-l. Renal cyst. ). (c). inflammatory exudate. Figure 2.42. Figure 2.43. (c). Renal cyst vrith no inflammatory changes in the adjacent renal parenchyma. HE x 125 Echinococcus granulosu: cyst shm·Iing laminated cuticle adjacent to the collagenous tissue in the second layer of the cyst. Figure 2.44. Figure 2.45. Figure 2.46. 48. (cc).. (Le). HEx320. 48. Carcinoma. Acinar and tubuloacinar arrangement of neoplastic cells supported by a slight reticu�ar stroma. The cells are polyhedral to ovoid vrith abundant, slightly vacuolated, eosinophilic cytoplasm. RE X320. 49. Carcinoma. A more densely, cellular area of tumour to that shovrn in figure 2.44 showing greater cellular pleomorphlsm. HE X320. 49. Carcinoma showing v1hite arrow and representative of into lobules. HE. 49. (. ). dystrophic calcification a band of fibrous tissue that dividing the tumour x320.

(12) xi. Following page Figure 2 .47 Rene.l a denoma . The tumou:r is well encapsulated and the neoplastic cells are arranged in acinar, tubular and papillary f ormations. HE x 125. 49. Figure 2. 4 8 Nal igPant l�'Tllphoma. Monotonous regularity of lymphoid cells with round,ov0id or indented pachychromatic nuclei and inapparent nucle oli . llli x 500. 50. Figure 2.49 Focal granuloma in renal cortex, probably of parasitic origin, shoHing central area of case ous necrosis and eosinophilic debris (N). Surrounding this material are several polykaryons ( arrovis ) . The adjacent tissue is heavily infiltrated by lymphocytes, plasma cells, phago cyte s and occasional eosinophils. HE x 320. 50.

(13) l. CHAPrER. REVIE\f OF I,ITERATURE IHTR ODU C'r I O�'T. KnoHledee of natur all y occuring diseases in th e ovine the. k idne y. in. last de c ade has increased mnrkedly in parallel to the appl ication. of investigA.iive teclmiques such and the recogni i i on of. as those r ep ort ed. in. the stucljos of. Lan drace sheep and the. affecting the ovine Prevalence of. into the. recognition of. other. rovievJ as models of diBease in. in this chapter. glomerulopathies. tbe. avail able. kidney. ::uch. 1977 I and II ) ,. c:ats (Os born e , Hammer, Stevens. and. 1977) have influe nc e d research. later in this. prim�ry. do gs (Peddinghaus and T rauhre in ,. horses ( Sla1won ancl Le1·1is, 1979), et al,. renal biopsy and immunofluorescence. entit ies resulting f rom cross species. no1·1. comparison. For i nstan c e ,. as. gl ome r ul opa th y. of. Finnish. glomerulopathies discussed. man.. literature on pathology. of diseases. is revievwd.. disease _in ovine k idn:..:ys. Reports on the p r eva len ce of. ren a l. diseases in sheep are few. and. of limited value as indicators of r en al disease in lar ge populat1ons. The only report relating. specifically t. o re nal disease in. slaughterecl sheep is that of Zhir ik (1974).. abattoir. In this study 1 .72 per cent. of 119,046 sheep slaughtered in a Moldavian abattoir had kidney lesions. Of the 196 lesions 194 \vere chronic although the cr iteria for cbxonicity were not stated. renal lesions.. In. 433. emergency-slaughtered sheep 46 had. These were examined histologically and inflammat or y. changes 1'fe:re present in 3 6 of whic!:. one glomerulonephr itis.. 35. were inter stitial nephritis. and. The degenerative changes of cloudy sv;elling,. hydropic degeneration, lipidosis and melanosis occur�ed in four other sheep..

(14) 2. E chinococcal cysts , granulomata , urolithiasis and hydronephrosis were also noted although exact numbers were not given. Diseases 0f the ovine kidney. ( I). Diseases of the glomerulus. (1). Snon t ane ou s. glomcrulonephropathies. erular. Proliferative glom. common. lesions have been noted as a. finding in routine post mortem material from sheep. Le 1vis , 1979),. but. to. date the glomerulopathy. of. rel ati vely (S la'l'rson. and. the li'innish Landrace. the only one in which the cause and pathogenesis has been. breed is. determined. a. ). Finnish Landrace__g,lomerulopathy. Thomson,. Davidson and. Angus , (1973). reported a spontaneous. glomerulopathy of Finnish Landrace sheep affecting. in 1971. and. 16. of. 5 of. 40 lambs born in the following year.. showed diffuse lesions. of. 33 lambs. born. The kidneys. mesangiocapillary glomerulonephritis upon. post mortem or biopsy examination.. Five lambs >·rhich died with acute. renal failure shovred a brief clinic:�l illness in i'lhich there 'iTaS enlargement and tenderness su g s ive. g e t. of. ki dne y s of. all sheep. 150. g.. in the kidney region and behaviom:·al signs. central nervous. s y s tem. v1ere pale ar..d. The renal capsule stripped. dysfunction.. greatly enl readily. At necropsy bcth. arged ,. weighing up to. t o reveal a smoo th. surface containing circular red or s ometimes yellow spots 1-2 diameter .. unp tt d. i. mm. e. in. When cut transversely the cortices were t ough and the spots. noted superficially were seen throughout the en�ire cortical width . Softening and petechial haemorrhages in cerebral gyri adjacent t o miiline were pre se n t. in. four of the lambs.. Histological examination of the kidneys revealed a severe diffuse glomerular lesion characterized by proliferation of mesangial cells , thickened capillary basement membranes and florid epithelial crescents..

(15) 3 Accompanying these changes was a mild vasculit i s and irregula,r inters tit ial infiltration of lymphocytes .. Discrete granular sub8ndo -. thelial d e p o s its con t aining immuno gl obul i n were demoustrated b y ele ctron microscopy and immunofluorescence. Lambs. (Ane;us,. G-ardir-'er, Norgan e t al ,. 1974).. shov1ing ne rv o us signs had l e sion s of e x t o !1S ive s p onei o sis at. the junction of t he cortical grey matter o.nd the sub c ortical vrhi te mat ter of the d ors omedial, which,. frontal ,. \•rhile bil ate r al ,. parietal and occipita l lobes of cerebrum. were n o t c om plet e ly symmetrical.. p le xu s e s showed moderate to severe interstitial oedema.. were demonstrated by immunofluorescence. in. 'rhe choroid Dep o s its of IgG­. the interstitium of the. choroid. plexu s of lateral ventric les and als o in l; e r pos ed behJeen choroidal. (Hor e;an , 19'77).. epithelial cells. I n one sheep there. vms. endotheLal. separation vJi th f ormo.tion of subendotllelj.al electron-lucent space:-',. The early work o f Thomson et. al_ had. suge;ested the aetiology vras. due to colostral t r ansmis s i on of an infectiou.s agent,. but t his l , ,n)o t he s is. was shmm u n tenable by a c ros s-f o s t e rin e; exper iment carried out by Angus et al. (1975). using no1.,rborn Finnish Landrace and Cheviot lambs.. Severe me san g io capill a ry gl omerul one phritis o ccurred in four nev1born Finnish Landrace lambs reared by t lo eir Landrace lambs,. O\m dams .. One of six Finnish. a ll reared by Cheviot e\o�es also deve loped focal lE:s i ons. of milder degree.. N o gl ome r ul onephri t i s oc curred in any of the four. Cheviot lambs reared by F innis h Landrace ewe s, lambs died of the d is ease .. whose naturall y reared. An art i f i c iall y reared colos trum-free Finnish. Landrace lamb was als o affected .. The experiment shov1ed that the disease was familial,. s ince i t s. prevalence in the pr ogeny of the high risk gr oup allocated o n the basis of an affected progeny in previous lambings ,. (x2. =. 5.1 4 ,. P. Gardi ner. =. 0.05 ). (1976). was significantly higher. than that in the balance of the fl ock.. f ound that the third e omponent of complement. (C,' 3).

(16) 4. in serum o f newborn , subsequently affected l ambs v<as. 5. per cent of that. in unaffe c t e d lambs and persisted at lovr leve ls unt il renal failu.re o c cur re d at around. 6-8. v re e ks of age.. Examination of. renal c ortex by. immunofluorescence using spe cific c:mtise�a for IgG, IgH,. IgA,. C 13 and. f ibrin supported pr evi o 1s morphological evidence indicating a strong. 1. s imilarity b etvre P. n this disea:Je and hypocomplementaernic glornerulone­ phri t i s in humans.. IID!llune complexes. c onta inin g IgG, IgM and C 1 3 vrere. al so pr ese n t in the choroidal in t ers t i t i um b. ). .. nephropathy. Copper deficiency associated. Ric::hard s on , Terlecki and Gwynoth,. -. (1979). a nephropat]:ly in. reported. ewes and lambs fed a s e mi pur i fie d cliet of low copper contenJc. ma in di e t ary compon ent s w-ere casein, li!ilk pov1d er. , d ex t r o s e ,. s t ar ch. na t e. ,. m iner a l. ve ge t ab l. (omi t tin g. e. ,. vThi te fish meal,. fat, potessium bi c arbonat e. copper sulphate. ). The. ,. maize. sod:Lum bicRrb:)--·. and vHamin mixes.. With a fevr ex c e p t ions the sevex i ty of the renal lesions varied w ith the l en gth of the time t h e diet vras fed and r ang e d from glomerular· b asement. membrane. e. t hi c k ning and hypercellularity to glomerular anr1. tubular at roph y , degeneration, intorstitial fibrosis and mineralization.. e. In m odera t e l y and se ve r l y affected cases, arteriosclerosis and lymphocytic. infiltration were also a featur e. .. Arterial changes in c lud e d. int imal thickening vri th redu c t i on and oc cas ion a l ly almost total occlusion o f the lumena particularly in the small arteries and arterioles. There was a dis orde rly proliferati on of t he media s ometimes acc ompanied by calcifica t i on. vessels.. Periadvent i t ial fibrosis was present in the larger. T he authors presume d that the arte rial changes le ading t o. /. partial renal ischaemia and or hyper tension were the major causal factors. in this neph.ropathy. c. ). Spontaneous gl omerulone�hri tides of unknown aet i olQgy. i. ). Langham and Hallman ,. (194 1). report e d glomerulone ph.rit is in a.

(17) 5. five months old Hampshire ram that had been sick and showed marked dyspnoea due to Oestrus ovis infection for several weeks. ex. ami nat i on the renal. surface due. small. to. p. ca sul e stripped. j unc ti on on. the. seve r e thi c ke ning of a d d. n. the. glomerular. changes,. basement. Occasiona l. to the corticomedul lary. examination. membrane s. due. shmv-ed very t o fibrosis. The �ubules shovJed s e c ondary n. atrophy and gradua l replac e me t of epithelial. cells by c01me ctive t is sue. vrere. Nicrosc opical. surface.. rt i ca l. Nume rous narrovr grey. -. ep osit ion of hyaline material .. degenerative. a. periphery of the cortex. the. incised. r e ve l in e a 1nottJ.ecl co. grey v!h i te vesicle s .. raised.. streaks extencled from. easily. On post mortem. and conta.ined g. ranu l ar. and. interstitial accumulations of l ym phocytes. hyaline an. d. casts.. mac r p age s. o h. pr esent . ii). The. kidneys. 7 m ont hs and 3. 347. in 312 of. years sl a u ght. ere d. gra pni c l ocations in USA and one g lome rulonephritis. ( Lerner. sheep. mon. t hs of. age. be tvre en. age was. in ab a t t o irs from six in England shol'red. and Dixon,l966a. examinations vrere performed 80. clinically normal sheep. in. 10. n:::'. 34'1. e xami ned by fluorescence. different ge o­. pos t. Kidney. and from 15 mi cros. g d beh1een. a proliferative. Complete. animals.. 7 mont hs and 3 year s. micro�copic examin ati on. ).. a e. r t em. mo. tissue from. sheep under. copy .. E lectron. was made on renal tissue of 10 of the. sheep and blood and urine. s am. 3. a du lt. pl e s were collected from 50 adult sheep .. Gl omerul onephritis was associated with mild prote inuria and azotaemia in about a third of the sheep and by heavy deposition of IgG and c0mplement along the glomerular capillary walls in all sheep examined.. In spite of severe proliferative changes in most glomeruli ,. the prevalence of scarring was relatively l ow. '·rere absent.. Basement membrane changes. The severity of disease increased vri th age.. nephritis was not seen in lambs less than3 months old .. Gl omerulo­.

(18) 6 Fluorescent antibody testing f or 't globulin and j3 1C gl obul i n deposition showed a s imilar aged. related pattern .. age. l ambs. l e s s tha!1 3 months ,.;ere affe c t e d , bu t fluore s ce n c;c; 1-ras pos i t ive. for all In. .s.nimals. 90. pe r. be hreen 7. months. and. 3 :y ears .. cent of the latter group of animals the r e vras intense. s taining -wi th host. t{ gl obul in. and. � lC. in a. gl obulin. dis tribu t i on al ong the glomerul ar cap i ll a r y. 10. None of the. "1-Ialls .. unif orm membranous. In. the remaining. p e r cent fluore s cent local i zn t i on of t he s e prote ins Has c onfined. predominan t ly to the me sangial. cells .. The disease was characte r i z e d. ultrastru c t urally b y marked end othel ial and rne sangial c e l l pr ol iferat ion and swe l l ing .. gl ome r ular. There v1a s occasi onal irre gul ar. of the. basement memb r ane , &s vre l l as smudging and Svie l l ing of the. epithel ial cell f o o t pr o ce s se s .. were. t hicke ning. In s ome s e c t i ons c oll agen fibr ils. n o t e d. in the me s angial cell s .. bac t e rial infe c t i ons ,,,ere f ound in. Al tho'.l . gh vari ous parasi t i c and. the. she ep under stu.dy. no. c orre lat i on. betv1een infe ct i on by any one par t i cular organism and the degree of gl omerul one phr i t i s -vra s es tablishe d .. L erne r , Dixon and Lee. over a pe r i od of 15 rapi dl y. pr o gre s s ive .. m o nt h s. In. ( 1968) showed. by. from 12. s he ep. adult. this s tudy. kidneys. nephritis were eluted vrith acid citrate .. renal biops i e s taken. s e r ially. that t he d i s e ase -vras n o t. from. sheep \'ri t h. gl ome ru l o ­. The eluted material vms. characterized by density gradieut ultracentrifugation and immunoelectro­ phoresis and shown t o consist predominantly of ?S/IgG . Fluoroscein conjugated e luate from sheep with spontane ous glomerul onephritis did not attach in vitro to normal lamb kidney .. The eluates were shovrn to. have a very short half life in the circulati on when trace labelled with 2 1 5 r and inj ected int o sheep , rabbits and mice and did not fix in vivo. to normal lamb or 11nephritic11 adult sheep kidneys .. They concluded. that spontane ous glomerulonephritis in sheep was not associated with.

(19) 7. antibodies against the glomerular b asement membrane , and vl'as presumed t o be mediat e d by antigen-antib ody c omplexes .. iii. .An apparent a s sociat ion behleen g_ampyohact e r fetus. ). and p r o lifera t ive glomerul on e ph ritis has be en reported in. i nfection. 83. per cent of. 243. range she ep by Den Boe r. microscopic studies of t he kidneys occasional. Light an d e lect ron. shovred glome rular hype rcel lula rity,. f o cal t hicke ning of the glomerular bas eme nt membranes,. marked endot helial and me sangia l ce ll epit helial. (1969 ) .. Fluoresce nce microscopy showed she e p I gG. foot proce sse s .. and complement. pro l i fe ra tion and smu dging of t he. deposi t ed in a nodula r pa t t e rn on the. glomer�lar hasement. The numbers o f nuclei in gl ome r uli and blood pressure value s. membrane s .. increase d in direct proportion t o t he severity of t he morphological Thirty seve n of. c hange s . of. 1 : 50. or. h ighe r. 105. aga inst C .. she ep i n t his group ha d ant ibody t i t res fe tus and the quant it ative valu e s of t hese. we re in dire ct proportion to t he his t ol ogic gra ding glomerulonephritis .. of s eve rity oi the. Pre liminary t e st s using t he indire ct immunofluo­. r escen c e t e chnique showe d. C.. fe tus and relat e d antigens on t he. glo!I!e rulaT bas ement membranes .. H a e ma gglu tina t ion t ests shm-re d a n. antigen ic cross reactivity betw ee n s oluble. extracts o f s he ep glome rular. basement me mbrane and C . fetus antibody .. Slavrs on and L ewis. (1979 ). found that proliferative glomerular. lesi ons , s ome times advance d , are re p orted as common in ruminant kidneys and c onsider that further work is ne e de d t o c onfirm the ass o ciat i on bet1-re en. (2). C.. fe tus infe c t i on and spon t ane ous glome rulonephritis .. E xperimental Aut oimmune Gl omerul onephri t i s F:xperimental aut oimmune gl omerul onephri t is. ( EAG ). has b e en indu c e d. by several workers using he terol ogous gl omerular basement membrane. ( GBM ). and Freund ' s c omplete adjuvant. ( S te blay , 1962, 1963. and. 1966 ;.

(20) 8. Lerner and Dixon , l966b ; Rudofsky and Steblay , 19 66 ;. and Rudofsky ,. S t e blay. 1968 ; 1'/elsh , G o l o ff and Smith , 1971 ; ltlelsh and Smith , 1972; Batsford and Hard1vick, 1 977 ;. 1978) .. Jame z ,. Steblay. every tw o 1ve e ks wi t h he t e r o l ogou s GBH. one or c o m b i nat i ons. ( 1962) and. i n t r amu s cula r ,. of the. shov;e d tha t s he e. Freund 1 s. p. inj e cte d. c o mp l e t e a dj uvan t. by. subcutane ous or i n tr a derma l. l. rout e s deve l oped a f u mi n a t i ng e x t ra capi l lary el ome ru l one phr i t i s v<hi ch. 27-80. ca11se d dea t h VTi thin. change s. days of. the f i r s t. i n j e c t i on .. i n glomeruli : e sul t e d i n increased g l oDeru l ar p e rme abil i t y and r. pr ogr8 s s e s. to fibr oepi t helial proliferat i on. of the gl ome rular t u f t s and. f orma t i on of cre s cents with eventual s carifi c a t i o n . degene ra t i on and i n t e r s t i t i a l fibr o t i c change. glome rula r l e s i ons .. Ki dneys. vr e r e unaff e c te d . fatal ma t e r na. c o l os trum , kidney .. l. This. sugge s te d e i ther. o c curre d s e c ond ar y t o the. t ha t. last. third. p. to. Lerner and Dix on. he t e r o l o gou s. or. ( 1966b). de. m o ns t rat e d. h om o l o gou s GBH. and (3 1C globulins ,. which. that. 1966 ) . EAG i ndu c e d b y i n j e c t i on. vTe.s due t o the p r. o du c t i o n. s he e p. caused. with induced EAG. c. o n t aine d. S e ru m. l n. e l obu i. an anti-kidney. The nephritogenic property of. absorb t i on in. the. serum could. vitro with sheep GBM .. Steblay and Rudofsky ( 1968) reported GBM. t. an immediate , although transient glomerulonephritis. when inje cted int o lambs .. of human. of a n i -GBI1. were deposited in a linear fashion along. the basement membrane of the glomeru lar ca pi ll ar i e s . from ne phre c t omi z e d. foe tal or n e o nai.:al. nornal s he e p by ar t e r y t o. ar t e ry c r o s s -cir·cula t i on ( Ru d o f s ky and S t eb lay ,. be removed by. t b e i:r.' pre gn an cy. the cau s a l a gent of the. of affe c t i n g the. \-ra s t ransfcre d from affP. c t e d. antibody which. of. gl ome rul onephr i t i s vJ..: s n o t t ransm:L tted in u t e r o or in the. or t hat i t was in c a a b l e. EAG. l11arke d tubul&r. of f oe cuse s and ne\·J born l ambs de riveJ. f r om. s he e p vTi th glomerul onephri t i s induce C. in the. of. earlie s t. 'rhe. EAG. in sheep after injections. cells and Freund ' s a djuvant characterised. by a. continuous.

(21) 9. linear deposit of I gG s pe ci f ic t o GBI"l al ong the GBM . o f au t oant ibo d y in k i dney e luates. was d e t. erm ine d by i ndi re c t. R e a c t ivity w <:t s demOl1 S lrat e d with B o'\'rman '. fluore s c e n c e .. and t ub ul a r baseme!lt membrane of kidney as vrel l membr::mes in. The specificity. b oth man. aYJ.d s he e p. as. s. immuno­. GBH ,. c "l p s ul e ,. pul monary basement. .. The pa t te r n of distribut ion of immunol ogi cal reactants in the se .. lesions is cons idered by. L erner. and D ix on ( 196�) and Steblay ( 1966 ) t o. closely resemble those seen in the. ri t i s o f G o odpas ture ' s syndro�e ,. ne ph. nephrotox i c serum nephritis and s ome other poorly define d n e phr i t i d e s of. man ,. post s t r ep t o c o c ca l ( 1966 ) no t e d. but >·ras. infe c t i on. that this. v1hich aut oantib ody had J q:.ne s re j e c t i on. ( 1978). not char:;.c ieri s t i c of or lupus. appeared t o be. been demons tra t e d. i nve s t iga t e d the. det ermine. to. m e d i a t e di s e a s e .. pa� h o ge n i c. the structural. and. necks of. el. Steblay et. firs t experimental mode l in. me chanisms of. a ff e c ting transplanted kidneys using sheep .. a l l o gr8 f t s were p l a c e d int o t he. of acute. nephr i t ide s. erythema t os-...t s . the. chr or1ic. cr aft. Renal. aut o-and. ne phre c t omi s G d s h e e p. to. funct i onal effe cts of transplantati on ,. re current gl omerul onephritis and the i nflu e n ce of immunosuppre ssive drugs .. An experimental autoimmune gl omerul onephritis was. indu ced. in. 12 of 37 sheep by repeated injections of human GBH in Freund ' s c omplete adjuvant .. The se re ce ived all ografts and immunosuppre s sive. after the onset of haematuria and proteinuria .. t he r a y. p. During the gra f t ing. procedure and at 30 minutes , tl1ree , six and ten days after transplanta­ tion snrgical biopsies were collected from the donor kidneys and examined by light , e le ctron and immunofluorescent microscopy. Allografts in immunosuFpressed �ecipients functioned well during the first post-operative week, but their function deteriorated rapidly during the next week.. The non-immunosuppre ssed allografts funct i oned.

(22) 10. only br ie fly and in most the gl omerular filtration rate fell 2-3 days after t r ans plant at i on . infil t r a t i on of lymphoid c e l l s ,. and. rapi d ly. A l l the a l l o grafts shm-1ed extensive wide spre e:d. oedema and s w e l l ing of tubular. The a l l o gr a f t s in she e p vTi th EAG shmwd. gl omer-u.lar c e ll s .. a. l inear. depos i t i on of ant i -GBiVI antil) od i e s in t h e ir gl o:::n e r u l i vli thin 30 minu t e s. of. transplanta t i on .. This was f o l l ovTe cl by the. progre s s iv e re currant gl omc rul onc phri tis .. d eve l opment of a rapidly. By the s eventh d 9.y a f t e r. t rans plant a t i on m o s t gl omerul i. i n the s e gra f t s had deve l ope d ls.rge cre s cent s which c on tained nume r ous phae-ocyt i c cells .. The author. c. c oncluded t hat in EAG-affe c t e d r e c ipien t s of normal kidneyR the prin ipal cause. of. graft failure was a r e currence. of pre -ex i s t ing aut o i nwn.J.ne. gl omerul one phri t i s .. ( II). (l). Diseases. of Renal Tubul:_e s. Infl� 'T!..TTlat ory. Cyt omegal ovirus irrfe c t i on. a). Har t l e y and D one. (1963). inclu s i on b ody d i s e a s e. of. re p o r t e d two unre lated c a s e s. the. kidne�. in l am� s .. his t o l ogical feature was a mul t i f o cal , cell. inf i l t ration mainly of the. e xtens ive. d amage. of. the. tubul e s. l e s i ons w i t h epi the l ial swe l l ing. proteLnace ous casts which often s catter. pred ominant ly lymphore t i. cular. areas. adjacent t o. and de s qu amat i on. There wa s. t he. and. inter s t i tial. fo rmat i on of. c ontaine d d i s integrat ing c e ll s .. of glomerul i shov1ed marked. llary collagen deposition .. The m o s t not a b l e. c o r t i cal in t e r s t i t ium .. in. of cyt omegal i c. th i cke n in g of. the. GBM. and. A. extracapi­. One or more eosinophilic t o amphophilic ,. homogene oas , granular , intranuclear inclusi on bodies were frequently present in epithelial cells of the thick ar:m of the l oop of Henle , distal convoluted and the collecting tubules .. Some times the inclusion. b ody occupied the v1hole of the dis tended nucleus . cells of glomeruli or blood vessel s .. N one. vrere found in. Occasi onal faintly staining.

(23) 11. cytoplasmic b). \'lere also present .. inclus i on s. J.:!e]t Q.'ill_:h_ro s i s. L e p t ospir osis is r e c ogni z e d a s n disease c.f f e c t in g m o st d ome s t i c spe c ie s and. is impor tant v.rorld vlide. 1974- ; Smith. and AJ:·ms tr ong ,. in. s he e p has. 1954 ;. 'de bs ter. b e en. and. r e p orted from N e w Z e aland. Hirsh , 1980 ) ,. 180. of. as a cau s e. b·u.t darkfield. abor t e d foetus c on t a i ne d by. five. haematuria .. agglutinat ion lys is. Benders on ,. l e p t o 2 :p i r o s i s. 1974 ; Narshall . 1974) and N orril ,. 1 95 3 ;. and t he Dav ids on. a b or t i on or fever , hae molyt i c anaemia. in I llin ois .. post mort e m examinat i on of. kidney sections. of. and. 1952 ; Salisbury ,. Beamer �a.l d e s cribed an ou t b r eak. pre gnant e -�/e s. kidn e y s af1d marke d. IIodge s ,. ( llar t ley ,. ( Beamer , HardenbrQok. Amer i ca.. and haEomogl obinuri a .. 19. z o on o s is ( Blood. Spontaneously occurring. 1975) .. and Reynolds , 195 5 ;. Un i_ted States of. as a. Sixteen. of abortion in. of the she e p. died. and. of. the. No. lept os pirae w e r e d e m on s tr a t e d_ L 1. evre s shovred i c t e ru s , Sl'i' O l l e n. examination. of s t omach c ontents of. spir ochae tes and 9 of ll. t e s t in g t o l e p t ospirae .. one. e1ve B had s er a � n c i t ive. 'rhe or gan i s m was. transmi t t e d t o a guinea l)ig by inoculat i on of foe tal s t o:nacl1 c onter,t s .. T he. and sudden. anae:nia reve a l e d blood ,. r e mainin g reports d e ath .. e s se nt ially. s i gns. of fever ,. Pat h o l o g_L cal e xam i nat i on. s imi lar. ha em oglob i nuria ,. SH Ollen. de scribe. chan ge s of generalized. yel l ovr. -br mm. d is co l ouration. j aundic e , hae m oly ti c. of t he s e. ar1imals. i c terus ,. thin. of l iver. and. vmtery. brown. kidneys .. His t ol ogical. change s in kidneys. indicated recent haemoglobinuric. nephrosis , with haemoglobin and haemosiderin casts in tubules and yellow-brown granular pigment ( haemosiderin ) in the cytoplasm of epithelial cells of the. tubule s .. Focal areas of inf18.I!Iffia tion were. present in the interstitium and varied from lymphocytes , pla sma cells and neutrophils. in. acute lesions t o a predominance of lymphocyte s and. plasma cells in subacute lesions .. Silver s taining techniques revealed.

(24) 12 in. l e pt ospiral organisms. Observat i ons on the mortem fea ture s. re ported by. the tubule s and inters titium in s ome case s .. c lini c a l ,. haematologica.l , s er o l o gi cal and po s t. of experiment ally induced ovine leptospir o s i s were. Langham ,. N orse and Il[ ort e n ,. 1958 ;. Hodge s ,. 1974 ;. Narshall ,. 1 974 . Langham , e t al reporte d extens ive l e s i ons in t he ki dneys lambs at. experimentally. intervals. ranging. Lept os-p:i.ra pomona vrhich were killed. infe c t e d >fi th. from 8 t o 72 da.)Ts after. i nfect i on .. c i rcumsc r ibe d foci and s treaks measuring from one in diame ter \fer e note d gr os sly in. 1'- hc r osr:: op i c a l l y these lymphocyte s , although. cells. the ki dne ys. macrophages , mostly. only. reGeneration. secti ons of. me dulla .. in the. -;ortex. Although. s with inflan:rLtat ory. in one case ,. of tubular e pi t he l i a l. Pr ate inace ous ma te ri a l. the urinary s paces of half the infe c t e d animal.3 , s tain o f. infe cted l am bs .. of t he tub1.1_ la r e pithe l ia in area. vrere f ound in five l ambs ,. 'lfaS pre sent. mi l l ime t ers. c hara c t e ri s ed by infiltra ti ons of. plasm::J. c e l l s ar.d fe>·r. necrosis. Grey-white. to f ou r. of all. sea t tered foci vrere observed also in the. a t rop hy and. c hanges. s ome. areas were. of 10. the ki dne y of. f our l amb s. 'l'he. vras. found in. Warthin-Sta:c ry. which were ba c t e r i o l o gi cally. positive at time of ne cropsy sho-vred leptospirae. in t he tubules cf one. l amb onl y .. Similar observati ons were reporte d by H odges i n ei gh t l ambs experimentally inoculat e d with a culture of _l:,_eptospira interr ogans. serotype pom ona.. Mar shall al s o de s cri b e d s imi:l_ar gross and l i ght. micros c op i c l e sions in kidneys of she e p 3 4 days after experimental inf e c t i on with Lept ospi ra interrogans serotype_pQ.!!!.9l!§.:. .. E l e c tr on. mi cro� copic e xamination of areas with damage d tubule s showe d l e pt o s pirae c oncentrated around the periphery of c e lls of the proximal c onvoluted tubules and intermingl e d with the brush border.. The number of microvil l i.

(25) 13. in the brush b orders was s ome times great ly reduced and many of the microvilli had bulbws ends .. Necrotic epithelial cells -vrithin the tubular. tu�)ules -v;ere observed and the se 1- r ere s ometimes found free in the ltunen . c ) �throz. Q_onosis Infection of sheep by. EJ?e rythr o z o on. ovis 1-ras first reported from. South Africa by Neitz , Alexander and du Toit in 1934 .. It has since. been reported from England , Bulgaria and o � her European countries , U . S . A . , Iran , Australia , Ne-vr Zealand and Kenya ( Sutton , 1974 ) .. main clinical f inding is anaemia . vary depending. on. L e s i on s. The. seen a t post mortem examination. the stage and severity of infection and may include. icterus , thin 1·r atery blood, pall or of muscles , excess peri cardial. and. per i tc"leal fluid, splenic enlargement , emaciation , and bro-vmish disco­ l ouration of the kidneys ( Neitz et al , 1934 ) .. �y::.s. infe ction are variable.. Y.idn8ys. T he renal lesions in. often appear grossly normal but. they may be discoloured bro1m by haemosiderin .. Deposition of haemosiderin. may be extensive and o ccurs in the cyt oplasm cf epi thelial cells , the tubular lumena and the connective tissue beh1een the proximal convoluted tubules . These changes are most pronounced in animals shmring prolonged haemogl obinuria.. �eras , ( 1969 ) obse1�ed subacute to chronic nephrosis. with glomeYular sclerosis in extreme cases .. Chroni� focal interstit ia]. inflammatory changes were most prominent in areas with the heaviest haemosiderin deposits .. Inflammatory lesions in association vri th renal. haemosiderosis have not been reported by others ( Foggie and lhsbet , 1964 ; Rouse and Johnso� 1966 ; Jolly, 1967; Sutton, 1974 ) .. �eras. s uggested that high level s of haemoglobin i;1 plasma may cause rena l vas oconstricti0n and lead ·'· o the erlens'i'v=e tubula!' de-ge-ne:r-at i oh . d ) T oxoplasmosis Renal lesions have not been reported in spontaneously occurring •i.

(26) 14 ovine t ox oplasmosis .. Howe verJ Sharma and Gaut3.m. ( 19 78). repor t e d. extensive ne crosis involving glomerul i , tubules and c om1e ctive t issue s tr oma in she ep experiment ally infe c t e d vri th rr ox opJ. asma gond i i e. Q. ). .. Ri cke t t s i_os i s. Belchev a n d Pavlov. ( 1977 ). reported the clini cal >3yiDpt oms and. pathomorphological changes f ound in five. ewe s and tvro vre aned l amb s. e xam in e d after having na tura l l y c ontra c t e d Q fever infe c t i on . diagn o s i s of Q_. f e ve r. v,ras based on s e r o l o gi_cal examinat i on .. De finit ive. A t n e cr opsy. the kidneys l o oked normal but on his t o l O g'J showed va cu olar degeneration � or t i c o tubular e pi the l i a l ce l l s and s cat t ered areas of fi.broblas t i c. of the. and l ymph o cy t i c pr o l Hera t i on i·fi th moderEl. t e diffuse hyperaentia o f the medul l a . f. ). Sarc o cys t o s i s. Renal l e s i on s have n o t b e e n n o t e d i n s pontane ou s ly o ccuTring case s of sarc o cys t os i s 1. h o1·1 ever several report s. s ar c o cy s t o s i s re c or d l e s i ons. ( 197 7 ). Fayer and J ohns on nephr i t i s in e i gh t. s p o r o cys t s. .. The. of experimentally indu <.: C 'l. in the ki dneys of affe c t e d animal s .. des cribed a m i l d ,. a cut e. ,. di ffuse gl orr.e . rul o -... lamb s inoculated orally vri th Sar c o cys tis. gl omeruli vfere enlarge d ,. thi ckened b aseme nt membrane s .. 1 8 ek ,. o v i c :mis. hype r c e llular and s"hm·re d. S chi z on t s ue re fre quently obse rve d �o1i thin. enlarge d endothe l i a l cells in the gl om e rul i and lymph o c y t e s and m on o c y t e s vere f ound in capil lary lumena .. Renal i n t e rst i t i mn c ontained sma l l. f o cal aggre gates of lymphoid cells .. The r enal medulla was c onge s t 8 d .. ln a further s tudy L e e k and Fayer ab orti ons in she e p . with. 50 , 000 , 100 , 000. ( 1 978). r e por t e d the indu c t i on of. E l even pregnant ewe s were experimentally i n o culat e d or. 500 , 000. Sarc o cvs t i s ov�canis spor ocysts f r om. dogs.. Fhght ei'res e ither ab orted , died or became moribund before l ambing.. Of the. .15. foe tuses , ll were of normal appearance and f our autolyse d. •. .T.issues .from all f oe tuses examined were n e gative for schiz onts and cysts ..

(27) 15. At ne cropsy. 27. to. 33. days after inoculat i on the acutely ill e wes h ad. severe haemorrhagic pe r i c ardit i s , epi card i t i s and myocardi t i s . Haemorrhages of l e s s e r severi ty we re al s o pr e s e nt in the kidney s , spleen ,. l iver and ske l e tal mus cle s .. kidney s e c t i ons of thre e. S chi z on t s were demons t rat e d in. Evre s SlJrviving the acute. of the s e animals .. illness appeared unthr i f t y .. were moderately haemorrhagi c .. At p o s t mor tem the kidneys '. No. of t h e s e evm s. s ar c o c y s t s were found in the bdneys. of the s e animal s .. (2). Dege�e r a t ive. T oxic T ubular Nephr o s i�I T h i s term is u s e d in l it e r ature in re f e r e n ce t o a rather he t 3 r o gene ous group of degenerat ive changes affe c t ing the e p i thelial. of the renal tubu l e s. .. cells. M o s t r e na l d i s e ase s have a s s o c ia t e d d e ge n e ra t ive. chanee s in the tubule s and thu s the term t ox i c tubular nephr o s i s i s usual ly empl oye d vrhere. In. proce s s .. �his. tubular dege nera t i on i s. review such d i s e ase s are. under the headings of c he m i cal , a. ). the primary or prj_ncipal. c ons idered by ae t i o l o gy. plc: :1t and e n d o genous t oxins .. Chemi cal t oxins. 'l ox i c tubular nephr o s i s has been d e s crib e d in North De rbyshire. ( Clegg. and Rylands ,. R ober tson ,. 1957). mining areas .. 1 9 66). and S ou t hern S c ot land. in y oung lamb s r e ared in the. ( Butl e r ,. Nisbe t and. vicinity of old lead. The striking post mortem features of e ight lambs e x amined. by Clegg and Rylands were carcass emaciat i on) ost e oporosis and enlarge d , pale kidneys .. On se c t i on the kidneys had marke d hydrone phr osis and a. dark haemorrhagic band behreen c ortex and m e dulla. hydr onephrosis in only 3 of the the other. 17. 20. dnimals e xamined .. Butler et al reported The kidneys of. lambs , while normal in size, showe d diffuse faint ye l l ow. mottling of the external surface ..

(28) 16 The his t o logi cal change s in kidneys were s imilar in b oth reports and included extens ive ne c r o s i s of t he proximal a n d dis tal c onvolu t e d tu bular epi the l ia and de ge ne r a t ive ch ange s 1vhich ranged f r om cellul ar. enlargement w i th granu l ar cy t o pl a sm and l a r e;e ve s i cular nuc l e i t o ne cros i s. .. In s ev e ral ld dneys e o sin ophi l i c int ranucl ear inclusi on. b od i e s vrere nume r ous in the e p i th e l i al c e l l s of proximal conv o lu t e d tubul e s .. H i l d t o severe ,. f o ca l or d i f fuse gl om e r ular l e s i on s vJe r e. pr e s e n t and mo s t p romi ne n t i n t h e ou t e r z one cha nge s vre r e. pr ogre s sive w i t h t he p ar i e t a l. of the. corte x .. The. layer of B ov/Tilan ' s c ap s u le. e p i t he l ium underg o ing cub o i d a l or in s om e ca s e s c olullll1a r me ta11l a s ia . T hi s w a s acc ompani e d by varying d e gre e s of atr ophy , fibr ous repl a c ement of the glomerular t uf t s a n d peri glomerul a r fibro s i s .. C oppe r. In a revi e-vr of chr onic c o pper p o i s oning in s he e p , T od d at t e n ;i on t o tw o ph a s e s of t he di s e a s e . '. a ccumul ati on of c opper in t he. t i ssue s ,. c opp e r r e l e a s e i'lh i ch prc c i p i tates. t oxi c tub ul a r ne phr os i s .. The and. first ,. 16. drei·J. a p e r i o d. of. s e c ond ly a phase of sudden. a hae m. o l y t i c crisi s re sul t i ng in. G opinath � Hall a nd H ovJe l l. e ffe ct of c opper sulphate in. ( 1909). ( 1974). she G p given daily d o s e s. body weight over a ni ne w e e k per iod .. Se ver1. of. reported. 20. the. /. mg kg. she e p i'le r e ki lle d af t e r. thre e , five , seven and nine weeks o f t re a t me n t and the remainder all ov1ed t o develop a hae m o lytic cris i s .. N o gross abnormal ities were seen in any. of t he kidneys c o l lected from the se ven sheep kil le d before haemolysis o c curred.. The only his t ol ogi cal change o c cu.rred in the epithe l i a l cells. of proximal c onvo luted tubule s which shm1e d the pre sence of intracyt o­ plasmic e osinophil i c granul e s , which i-rere PAS +ve , diastase r e s i s tant and s t ained f o r l i p ofuscin.. The n�ber and size of granules we re. dire ctly proporti onal t o the cumulative c opper dose . The kidneys of animals i-rhich died or ·were kil l e d id th haemolysis.

(29) 17. were swolle n , dark brmm to black and showed l oss of demarcation b e twe e n c ortex. and me dul la .. Kidne ys from t h o s e animalB whi<ili had. unde r g one tw o pe r i ods of hae m o ly s i s 1·1ere blue - b l a ck in c o l our with p i np o int black f o c i s t reaks. on. on the surface e xt e n d i n g as f ine black c or t i cal. transve rse se c t i o n .. H i. s t o l o gi c a lly the prox imal c onv olut e d. tubular e p i t h e l i a shovre d in c reas E:: d e os i n op�·li l i a a:r.d abundant c y t oplasm i c gra nu le s .. di ::J.S t a s e. In all kidne ys t he maj or i ty of the granul e s 1·1ere PAS +ve , re sistant and s ome of thel.!l s t a i ne d f or haemogl obin ,. ir on and l i p ofus c i n . ph il i c hy al ine. C or t i cal and llledul l ary t ubule s. or granu lar. c a s t s s ome. c oppe r ,. c ont aine d e os in o ­. of vrh i ch '"e re p os i t ive f ol'. hae m o gl o b i n .. The ki dneys. of t1·1 0 anima l s vrh i c h vre r e ki l l e d i n the pos thaemol y t -i.. r::. pha s e v:ere svr o l l e n and b l v.e -b la ck in c ol our .. His t ol o gi ca lly ther e l"ras. d e ge ne ra t i on , vacuola t i on , f o cal ne c r o s i s and d e s quama t i on of e p i the l ial c e l l s vrhi ch ;·ms m o s t pr omine n t in the proximal c onv oluted tubule s . J , a rge nwnbers s im i l ar. o f g l obular or granul a r intracy t opl asmi c granul e s. H:i . th. s taining prope r t i e s t o those de s cr ib e d ab ove we re pre s e nt .. E o s i n ophi li c hyal i ne and granular cas t s c o n t ai ning hae moglobin were freque:1t. in the c or t i cal a nd medullary tubul e s .. reported. by H ovre l l and. S imilar stud i e s were. Gopinath (1977 ) .. Me rcuric C h l o r i de Naturally o c curring mercurial pois oning has not been reported i n she e p , but R obins on and He ske th. ( 1976 ). and R obins on. and Trafford ( 1 977 ). have des cribe d t he early his t ol ogical , his t o chemical and urinary e nzyme change s in shee p kidneys with experimentally induced mercuric chl o ride nephr o t oxicity.. Six adult c r o ss-bred ewe s divided int o groups of two were &iven a. s ingle intravenous dose of mercuric chl oride ; 0 . 1, 0 . 25 and 0 . 5 m g/kg.

(30) 18. b ody weight re s pe �tiv e l y . for. three h ou rs. Urine samples were taken and. after dosage. alkaline phosphatase ,. transpeptidasc , l eu c inE::: amin op e pt id a s e. tbe same. On e. in the. b). in. increase. cell. mg/kg. body 1·re i ght. hei.ght in many. of. pr oximal. cyt oplasmic {f.c anul ar i ty in groups. i n c r e a s e d e x cre ,; i on of. t rausr)(�pti da se over the. l e uci ne aminope p t i d a s e. remaine d. in. c on t r o l .. Change s. she ep IWre l e s s marked .. All sheep s}J 01·red. 0 glutamyl. r e du c t i on i.n t he. 0.5. The nu c l e i vrere denser than th o s e in the. o ther. d.. sample Has. and d e stroye d. samp l e d. kidneys of sl1c cp given. chl oride sh m·r e d a. tubul e s .. t glutamyl. the d osed sheep .. 1·ray as. conv o lu t e d tubule s vri th an of. f inal urine. untre atE: d c on tr ol s:b e o p 1-ras. Hi s t ol og ically the mercur i c. hourly intervals. and p-glucur onida s e 1·rere a s s ay e. The sheep vrere de str oyed at the t ime the c o l le c t e d .. at. n or llla l. vras al s o. In the. c ontr o l .. e le 1r[1 c e d .. alkal ine phosphatase. O t her. highe s t. and. dosage group. urinary enzyr.1es. .. t oY. ins. Plan t. 'r ribul osis ov i s and e nz o o t i c i c t c_:r.!:3:_� 'r r ibulus range s in. t e r r e s tris. a. plant v.rhi ch groNs abundantly. S outh Africa and whi ch has been. of ge e ld ikkop (T r i bu l o sis 1962 ) .. is. ov i s ). r e p orted. as. i. in m ount a no u s. the dire c t. c aus e. in sheep ( Br ovm ,. and enz ootic icterus. Numer ous analyses ind i c a t ed that T . terre stris c ont a ins more. than five parts. per mil l i on. considered t o be. a. ,. of s e l e nium thus both disease entities v1ere. l ow grade subclini cal selenium int oxication .. of these. syndromes nephrosis is a proffii nent. feature. In both. and causes death due. t o uraemia. The changes in geeldikkop are less severe than those of enzootic icterus but in both diseases. h kidne ys are swollen.. t e. case the sv;elling may be up t o tvro. or. In the latter. three times normal size and the.

(31) 19. kidneys are othenfise of similar appearance grossly t o those in chr on i c c opper t ox i cit y. .. Micros c opic a l ly the change s are those of. d i ffuse nephr o s is vrhi ch i s s om e t imes a c c ompan:i_e d h y a cute glomr> .cu.l o-·. ne phr i t i s. .. The e p ithe l i a l cells. of bilirubin. and iron. of. tubule::; c o nt a ined larg3 f]_Uantities. containing p igmen t and the. tub ular lumena c·rere. filled vri th haemogl obin and ce llular casts . Oxala. t:e s. -------. Oxalate. nephrosis ha::; been. repor t e d. in sheep graz ing pastures. containing plants such as Hal oge t on (Hal oget on p;lomerulatus ) , pigl'reed fa. (Amara}1thus retroflexus ) ,. t hen ( Chen Q_Qod ium al bum) , s ours ob. ( Oxal is cernua) an•i orchard s orrel (!l:ldme-r.: c oncer:trat i ons of. oxa l a t e s. .. Affected. introduce•l to s u ch pas tures ( Bl o od. a c ot o c o lla ). animals. and. which have high. are usually re cently. Hendcrs on , 1974 ; Ande r s on. o.nd. Huffman , 1957 ) . Anders on and Huffman re po rt e d severe losses in. sheep grazing pastures r i ch in H . regioP cf the U . S .A .. fl o cks of. gl omeru l a t u s i n the. Grossly the kidneys. Nere. Rocky l'l ountain. pale vrith patchy. c onge s t i on and histol ogically t he y demonstrated heavy de p o s i t i on. calciu..m oxalat e crys t a l s were affe cted .. 1'li thin. the tubular lumena .. of. Nearly all nephrons. r-iany casts vrere present in the prox ima l and distal. convoluted tubules and urinary spaces co�tained a p ink staining precipitate .. Wilson and Wilson ( 1961 ) suggested that fungi such as. Peni cill ium spp. might be capable of producing significant amounts of calcium oxalate poisoning.. in. feeds and could thus contribute to ou.tbreaks of. One such outbreak in young lambs was reported by Linklate r. and Angus ( 1979 ) .. The source o f oxalate was not clearly indentified. but mr.y have been from mould-contaminated c oncentrates fed to both evres and lambs .. Quite heavy grov;ths of Penicillium. SRP.. ·. vTere is olated from. crushed oats and the c oarsemix fed to the ewes and lambs. in. this.

(32) 20. outbreak.. Five of sixty purebred Suffolk lambs died ¥Then four t o six. weeks old and had hi s t o l o gi cal change s. c onsistent \'Ti th reports of. e x p e r imental p o i s oning of she e p by oxalate. Jame s , 1969) and. ammonium. oxalate ( Jame s ,. Sem'lri ght. T e re nal corti ces shmv ed nu... l'Jlerous d i l a t e d. h. cells .. Heavy d e p o s i t s o f oxalate. hyaline. or gr an. ul ar. in. and. Steele ,. tubul e s l ined by. crys tal s. casts vrere pre s e nt. ( Shupe. c ontaining plants. a s He ll. as. 1971 ) .. flattenei. e osinophil i c. many tubule s and a few crys t a l s. cry s t al s \·l ere. were. a l s o seen in t h e urinary s p a c e s. mo s. pr ofuse in the dis tal c onvolute d tubttle s in ass o c ia t i o� 1·rith. t. int ox i ca t i on. in. gl o:nerc1li .. T he. c onne � t ive tis sue .. pr o l i ferat i on of intertubular. Oxalate. of. and. s heep. has. a l s o been. induced. exper imei1 t aily. by intravenous or intrarumenal s oclium or p otas s ium oxalate inj e c t i ons. (Wat ts , 1957 and 1959 ) . J g,mes e t. al ( 1 971). 10 s he e p dosed weight ,. Nine. kidJJ. e ys of all. int. reported experimental oxalat e int oxj cat i on. rarumi na l l y. sheep. died wi thin. a!limal s. p l r than norma l. a e. I'Tith amm.on iu. l're re. and the. 12-22. swollen. m. h ours. and. up on. oxalate at 5 5 0 of. d os ing .. incision. me dulla was very hyperaemic .. mg/kg. in. b o dy. the. At n e cropsy. the. c or t e x. a ppe f:J-re d. H i s t ol o gi c a l. c rys t al s. examination of. the. kidneys s h m'le d. the tubules of. the. cortex partictllarly of the corticomedullary j unct i on .. Ele ctr on microscopic. ob serva t i ons. extensive. of. de p os i t i on. of. in. kid ne ys indi c a t e d tha t oza l a t e i on. rather than calc ium oxalate crystal masses caused the main renal damage and that pre cipitation of calciLl.IIl. oxalate takes place in the tubular lumena rather than the cytoplasm of tubular epithelial cells . T.he principal cause of death in sheep with subacute oxalate poisoning , v1hen the kidney damage I'TaS lnsu:fficicnt t o cause renal failure is acute rumenoreticulitis resulting from direct injury of epithelium leading t o inflammation and necrosis ..

(33) 21. ( 1976 ). Schie fe T , Hewitt and Milligan. i lllm. ed i a t e ly after. pre enant. 98. in du c e abor t i on in. oxa l i c. e1._re s fed. that although oxa l i c a c i d i ons cross the. the. admini s tere d to. of the. in. the second half. levels. h. subsequent. and. :Y...idneys a t the t ime. fed.. from evJes. in mos t lambs. Seve ral hundred p is :1 i n g by. o o. s pe c i es. s :lgge s t e d. tha t. oak. the. t ox i. results from the. but. i n ge s t i n of the. o. all. leafing. ugh. to. c rys t al s. thr oughout. and or. /. been re c ognised. e. �orm. and yo'J.Ilg. p o i s on ous t. of. for. a. ( Sm i t h , Jon.es. ha s been. i ;:; tanni c -ac id. oa k. poisoning. leaves ( B o"'...l gh t on. han others and. and. to what. more p o i s o c1 ou s during the budd ing and. early. s t a ge , and how this may be related to a c on current sh or t a ge. other feeds et al ,. the doses. an imal s .. unders tood. u s o.al. buds. e x e n t s ome. e. are. fully. the. S ome s p e c i s are m or. oaks. en o. s}10"1·red. of ewes fed l o1·r. in oak p o i s oning. l. Hardy , 19 3 6 ) . or. severe. bark i s r i ch in tannic a c id i t. princ i p e. c. t h or s. of oak tre e s and shrubs are knm.,rn .<md. ( Has ce l , 1662 ; C ornevin , 1893 ). t. lambs. s ome. and in. long t ime but i t s pa th oge ne si s is not Since. au. barrie r in. oxa l i c acid. members of the genus Q�� r.� has. and H.1.nt , 1972 ) .. 'I'he. of birth revealed oxalate. but not in tJ.1e co1.1trol. sp. ( Oaks ). The lambs ki lle d. Hi s t o l o gi c a l. abor t i o n .. high levels of. of pregnancy. o f o xa l i c a c i d ,. Que r cus. pl9.cental. ewe s , the int oxi ca t i on -vras n o t. cause intra-ute rine de at examinat i on. acid .. no:rmal ki.dtteys .. had grossly. birth. att e mp t ed unsuc e s sfull y t o. or an appe t ite for the. oak:B. are unansv1ered que s i on s. t. o:f. ( S:ni th. 1972 ) .. B ought on. and Hardy. re p orte d. 90-95. pe r cent mor tality in range. she ep pois one d by eating the buds , green shoots and young l ea-ve s of the common shin oak. ( Que�cus. brevileba) which i s ahundan t on the range s of. the Edward's Plateau region of "\'le s t "l'exas . sheep on. 38. Four hundred and twenty six. different properties d i e d within a period of f our weeks .. At necropsy the kidneys were pale and studded with pinpoint haemorrhages ..

(34) 22. ( 1959 ) n o te d similar. Smith. hi s t ol ogi cal In. the s e ,. ce lls. ch ange s in his series. and i n add i t i on. changes affe c t ing ma inly the pr oximal convolut e d tubu l e s .. nume r ous. of albu.min admixed �-li t h n e cr o t i c e pi ths l i a l. ca:::; t s. f or m a d e nse homogene ous ma s s l imitGcl by the b as e me n t membr :1ne .. ( 1955 ). :t-1ull ins ma t e l. gr oss. r e por t e d ten cas e s of a c orn p o i o oning i n appr oxi­. 200 e \ve s in Ne1v Z e aland. v:hi c h ue re moved into an area v1he re. y. the re 1·ras an. ". avenue " of oak tre e s .. Deaths. o c curre d from 4-10 days. a ft e r a c c: e s s t o and up to five day s after removal from acorn . mo. r t em. examina t i on v;as made. examination c. ). on only one of the e VTe s .. Post. H i s t o l ogi cal. reve. a l e d ne c r o s i s of the proximal c onv oluted tubul e s .. E n d o�enous t oxaemias. PTegnang_y t oYc_ae:ni�. Pre gnan cy toxaemia. i n she e p i s a comm on ,. usually fe.tal me t c:b o l i c. di s e as e vrhi ch o ccur s i n t h e l a s t tr ime ster o f ge s t at i on and u s ual l y in e1>J"e s carrying tHins. imp ortan ce. or t r iple t s .. ( r·1 cCausl a:.'ld ,. O ' Hara ,. Al though of c onsiderable e c on omi c H e rd s on et. C}.:!,_, 1 974 ) its. pa th o gc no si. s. h a s no�; b e e n elu cidate d d e pi t e ext ensive b i ochemi cal in.ve ::; t i ga t i on. s. ( R e id , 1968) . pre gnancy ,. as. The primary pre d i s pos ing cause i s 1.mdernutri t i on in J ate. H i t b over-fat e-vr e s being more sus ceptible .. n r onme n t al. change. e vi. e x c e ss ive he at also. be grossly normal. pale ( M cC ausl and. play. ,. ( Ferris , e t al,. short periods of fas ting an d. transpor t ,. ( S ie gmund. a role . H. erd s on. ,. Smi th e t al ). Stre s s e s such. e t al ,. Dunnil e t a l , .. The. t he kidney is severe diffuse lipi d o si s. 1975 ) . 1969 ). or. Ki dne y s may. slightly. ma in histological change in. of c o r t i cal tubule s. ( Smi th. et a l ,. 1972 ) . Repor ts relating t o glomerular changes in pregnancy toxaemia are c ontroversial.. Ferris e t. al. pregnant ewes by the stress. induced of f o od. environment late in pregnancy.. t oxaemia in 13 of. 20. deprivation and a change in. All the glomeruli appeared enlarged.

(35) 23. with c apillary tuf t s vrh i ch virtually f i l l e d Bovnnan ' s space .. PAS. i. staine d se ct i ons s h owe d f o cal thickening of the cap l lary baseme nt membrane s but there was n o s i gni f i c ant. increase in c e l l ularity .. E l e c tr o � mi cr o s c opy r·evealed endo the l ial. c e ll s -vr e ll in g. pli cat i on of gl omerular basement membran e s ,. ,. f ocal redu­. vride spr e ad f o cal fus i o�1 of. e pi the l ial f o ot pr o ce s se s and extens ive v i l l ous t ransf ormati on of The morphol ogi cal change s we re a s s o ci a t e d w i t h. e pi the lial c e ll s . az otaemi a. �. pr o t e inuria 1. rkCaus l and e t al ,. and incre a s e d p l a s ma renin a c t ivi ty .. ''�"ere unab l e t o shm-r any gl omeru lar abnor.maJ. i t i e s hy. l i ght and ele ctr on m i cr os c o pi c examinat i on in ll she e p >·rith spontane c'..l s pregnancy t oxae mia .. All t oxaemi c she e p had sign if can t impairment. i. renal func t i on "l'rhi c h vras shown f r om the. of. clinica_l.. c l e a ran c e and incre ased_ s e r LJ.rn. abnonna l i i;y by de c r e a s e d crea-Linine creat inine and bl o od urea ni tr oge n . vre :rP. f i r s t s i gns. of. The kidneys of t oxaemi c she e p. sl ightly pal e , but otherwi se g1· o s s l y normal ani no his t ol ogi c:;,.l. l e s i ons vrere found in the kidneys of t oxaemic or c ontr ol she e p . Mc Cau3lancl e t a l s ugce ste d that s ome. o f the shee1) u s e d b y Ferris �t al. may have had pre -e x i s t ing gl omerular d i s e a s e and >·rhen s t re s s e d had. pre f e r ent ially dev e l oped pregnancy d. ). t oxaemi a .. E n t e r o t o��e mia. Enterot oxae m i a caused by the epsil on t oxin of C l o s t ridium. perfr inge n s. type. D and referre d to p opularly as " pulpy kidney " i s an. imp ortant disease wherever she ep are raised .. The d i se ase has a. pre d i l e ction f or su ckling lambs and c on c entrate-fed v1eaners in f e e d lots .. The kidney s. and bulge a l i t t l e. of re cently dead animal s are c on ge s t e d on the. wi thin an hour or two arE. Gardner. ( 1971 ). cut. surface .. ,. swol l en. S oftening o c curs rapidly and. -. dark re� and j e lly l ike .. f ound no det e c table. his t o chemical alterations in the kidneys. gr o s s ,. his tol ogi cal or. of intoxi cat e d la�bs obtained.

(36) 24. The reduction in hist ochemically demonstrable. immediately after death . alkaline phosphatase and the renal. pr oximal tub u l ar epithelium in. a s s o ci a t ed had. staining affinity in the brush. PAS. 1·i i t h. int oxi cated an m a l s wa s. i. nu clear d e ge ner a t i o n and did n ot o c c ur unt i l. el ap s e d after death .. lesion rather than a. dire ct e ffe c t o f e p s i l on t oxin .. cated anim 9. l s o c curs as. a p ost h. This lesion Gardner. en t ero t ox aem ia in sheep . change s. c or t e x of. change a s s ociated 1-Ti th. t e r e l e r;;. s e of. allov;rs. interstitial tissue .. mor tem. r e nal. Fur thermore. is. t he. i n t ox i­. the. The pos t mortem breakdown of the. ante -mortem vas cular damage . d a ma ge d capillari e s. some t i rue. vras the r e f ore , he c onclude d , an aut o l y t i c. It. characteristic interstitial haemorrhage in the. of dee,snerative. b ord e r of. already. intact erythrocyte s into t he. c onsi de r e d pathognomonic of. c un c lude d. tha t. the. rapidity. of. onset. in the ki d n,� y s of in t ox i c a t e d animal s aft e r. death may b e d us t o the c om"b ina t i on o f high b ody t e mp erature re sult in g fr o:a. c...n temortem. r e nal tubular. ( II I ). convul s i ons. and a d i r�ct. e f fe c t. o f e ps i l o n t oxin up o:1. epithelium or in t e rs ti t ium .. Diseases. of t h e renal pe lvis. Pye l onephr i t i s. There are. few re p or t s. of pyelonephritis in sheep .. descr i b e d a pyelonephritifl in a tv1elve. m onth s. Hahafey. old wether .. ( 194 1 ). Both ld dney s. were swollen and the thickened capsule vras adherent t o the v1hole Many pale nod'.l lar areas of varying sizes v.rere visible. cortical surface .. extending from the cortex to the medul la .. In the left kidney suppur9.­. tion was marked , with extensive cortical and medullary necrosis and pus in the renal pelvis . severe lesions .. A. small. The right kidney showed similar but less quant ity of. bladder and in the pelv ic portion chronic inflammatory changes. of. ...;£". pus was also present in the the urethra .. Both kidneys sho·,;ed. variable severity throughout .. The. gl omerular epithelium was necrotic and large numbers of neutrophils.

(37) 25. had infiltrated B owman • s capsule and urinary space s .. Bacterial c o l onie s. were pre s e nt in t he gl omerul ar t uf t s o f s o me glome ru l i .. The c onvoluted. tubule s nnd as cending l oops of Henle s ho-,re d ep i th e lia l desquamat i on and ne c r o s i s .. There vms moder a t e l y dense neutrophi l i c inf i l tr at i o n of. tubular lumena and inter s t i t ium . numbers of h i s t i o c y tc s ,. 'l'rere pre sent . medulla .. In the medullary in t e r s ti tium large. lymph o cyte s ,. plasma c e l l s and fibrob l a s t s. Only a small numbe r of intac t tubul e s remained in t he. The renal pe lvis sho1-rG d severe f i b r o s i s and sma l l numb e r s of. neutropb il s ,. The urinary b ladde r vms h i ::; t o l ogi ca lly n ormal .. gr mvt h s o:L Ci tr obacter f reund i i \·Tere. cul t ure d .. Pure. The author c onsid e re d. organism rea c he d the kidney by the ha e ma t o ge n ous. that the ca<J.s at ive r ou t e. the. . Ki·ishna ,. Palivfal. and KuL:3hre s tha. ( 1 974 ). de scribed suppurat i·.re. pye l o n e phr t i s i n tHo sheep i n Hhich t he renal le sions vrere i dent i cal. i. to that des cribe d by :f.1 ahafey . i s o l a t e d from b oth .. In one. E s che ri chi a c o l i serotype 06 'I'TaS. of the she e p. cyst i t i.s v� ere als o present i ndi ca t i v e. ( IV). suppurative pye li t i s and. of as cend.i:1g infe c t i on .. ,. Renal N o opl a =; ms. Primary rena l ne oplasms in she e p have main ly been repor t e d f r om survey material c o ll e c ted in s laugh t e r -h ou s e s or diagn o s t i c s t a t i on material .. T able l . I. l i s t s the renal. tumours diagnos e d by various. author s .. In addit i on , lymphoma. (V). the kidney is a c ommon s i te of me tastasis. ( i-le b s te r , 1966. and. 196 7 ;. Johns t one and Mankt e l ow. of mal. ignant. 1978 ) .. Renal Cys t s. A case o f c ongenital cys t ic kidney i n seven month o l d lamb 'l'Tas reporteQ by Parame ta ,. 1970 .. The animal was in good c ondit i on b u t with.

(38) 26. TABL:S l . I Ovine renal ne.Q.£.l asms diagno s e d by v ar i ous authors. T ype of ne o p a sm. l. Numb e rs. Au thor. ( 1952-5 3 ). Ad.en oma. 1. Ji'lii'. C arc inoma. 4. Sandison and AndeTs on. 2. Smith and J one s. 1. Corde s and Shortridge. Carcinoma ( Re nal pelvis ). 2. W e b& t e r. ( 19 66 ). Nephroblast o'Jla. 2. Ja cks o�1. ( 1936 ). 1. Pamucku. ( 1956 ). 1. Brandly and N.igni...i. Haemangi oendo theli oma. *. Pers onal communicat i on. ( 1 9 63 ). ( 1968). ( 1961 ). ( 1971 ). ( 1�63 ). -¥-·. 2. Ma.nkte l mv. 3. C ordes and Shortridge. 1. Harcourt and Spice. 1. Feld:n3.n. 3. Fl ir. 1. Web ster. 2. Smith and Jone s. 1. Flir. 2. Smith and J one s. ( 1971 ). ( 1968). ( 1933 ). ( 1952-5 3 ) ( 1967 ). ( 1961 ). ( 1952-53 ) ( 1961 ).

(39) 2.7. m o de r a t e e nl ar gen;.e n t of the abd ome n due t o ki dn e y 1.;e ighing 3 . 860 kg .. a.. ve ry large polycy s t i c. T he other kicLYJ.ey vras. 75. g.. On disse c t i on. the large kid.ney sho1·ie d mul tiple cys t s throughout cut surfac e and contained 2 , 63 5 ml. (VI ). of fluid .. _1Jr olith·i asj& Ur olit hias is is the format i on of st ony pre cipi tat e s an;y'l.;here in. t he urinary pas sage: s and cnn b e of c on s i d c re.b l e e c onomic importance in she ep a l t h ough the pre·iraleHcc of obs tnwt ive dis eas e is much l e s s than tha t o f s t one f orm at. i on. ( Jvbb and Y.. c nnedy ,. obs t ruc t i on in vTC thors may be c ornmon a s. 1970 ) .. Uretlu·al. t he result of the r e l a t ively. smal l d ial!le tcr of t h e ure thra in the se animals and may occur a t ar:y. s i t e be hreen the pro c e s su s ure t hrae and the sphin c t e T of the urinar y. bladder ( He•·rs on , 193? ) .. T he m o s t t.; Ommon s i t e s of obs tru c t i on arc at. the vermif orm appenjaGe or narroHe s t. ( Udall. The gr o s s v ari ab l e. .. the. sigmo:i. d. the ur e thr a i s. and Je!lsen , 1958 ) .. and hi s t o l o g i ca l. renal f indings in uroli t hia s i s are. T he J.r..idneys may be enlurged ( Nc\•/ S on) , hydr onep:h...r o t i c. ( C ornelius , J·1 oul t on and HcGovran ,. 1959 ). only slight ly o e de11at ous and suol l e n. e t al ,. f l c zure Hhere. 1971 ). or gr o s s ly normal. wet a n d flabby ( \·!�aver ,. ( L alov ,. Ant on ov ,. 1963 ) ,. Popchri s t ov. ( S t a cy , 1 9 69 ) .. Histol ogi cal c ha n ges are variable in s e ve ri ty wi th inf l amma t o ry , degenerative and s ome times dy s tr ophi c change in all part s of the. kidne y and the pre sence o f ac cumulat e d often calcidied material vTi thin tubul e s .. ( Lal ov. T h e numb e r ,. et al ; Newson ; vle av e r ;. C ornelius e t. al ) .. physical and chemical characteristics of c a lculi 7ary. c ons iderably depending l a r g e ly on the d i e t ary intake of the she ep . S il i cat e s ,. oxalat e s and xanthine crys t al s o c cur i n acid urine. ( Jubb. e t al ;.