Case report — Gevalverslag

Acute Lantana camara poisoning in a Boer goat kid

Annalize Idea and C L C Tuttb

INTRODUCTIONLantana camara, a member of the

Verbenaceae, is an exotic ornamentalshrub2–4,6 that is of particular importancein South Africa as a cause of cattle intoxi-cation in the moist eastern parts of thecountry2–4,6. It was originally introducedfrom Central and South America andoccurs commonly in many tropical andsubtropical regions of the world6,14,15,17.The most important toxic principle ofLantana camara is lantadene A, a pentacy-clic triterpene acid2–4,6,7,18. This substancehas been shown to cause injury to the bilecanalicular membranes, with subsequentcholestasis and hepatocellular damage12.Ingestion of the plant by cattle and sheepresults in secondary photosensitivity,icterus and constipation, or in some cases,diarrhoea1–5,10,12,15. Two other members ofthe Verbenaceae, Lippia rehmannii andL. pretoriensis, also contain pentacyclictriterpene acids and may cause photosen-sitivity when dosed to ruminants4,5,13.

Reports of naturally occurring Lantanacamara poisoning in goats are rare10.Munyua et al. reported a case of acute

L. camara poisoning in Kenya, when agroup of calves, sheep and East Africangoats on zero-grazing were inadvertentlyexposed to the plant9. The clinicopatho-logical features of acute and chronic low-dose L. camara poisoning in indigenousZimbabwean goats were investigated byObwolo et al.10,11. Acute poisoning wasclinically characterised by anorexia,dehydration, ruminal stasis and severeicterus within 1–4 days of consuming theplant , but no photosensit isat ionoccurred9–11. The necropsy findings in thiscase included severe icterus, dehydration,constipation, hepatosis, distention of thegall-bladder and nephrosis. Moderatehepatosis with single-cell necrosis andbile stasis, as well as acute renal tubularnecrosis, were confirmed histologically.

CASE HISTORYDuring May 1996, a farmer near

Pretoria, Gauteng, reported 3 mortalitiesin a flock of approximately 35 Boer goatsrecently introduced from the Kurumanarea in the Northern Cape province.Necropsy of a 5-month-old Boer goat kidrevealed icterus, dehydration, anenlarged, brown liver and a distendedgall-bladder with multiple subserosalpetechial haemorrhages at the gall-bladder neck. The kidneys were pale witha yellow, glistening appearance andbulged at the cut surfaces. Moderate,diffuse pulmonary congestion waspresent. The colon and rectum were

impacted with putty-like faeces. No skinlesions consistent with photosensitisationwere present.

Specimens of the liver, kidneys, lungand spleen were collected in 10 %buffered formalin for histology. Sectionswere routinely prepared and stainedwith haematoxylin and eosin, andMasson’s trichrome8 method for connec-tive tissue. Hepatocytes were diffuselyand moderately swollen and possessedfinely granular cytoplasm, with distinctcell borders. Some cells contained largeintracytoplasmic vacuoles (Fig. 1). The cellnuclei varied in size and were hypochro-matic, occasionally multinucleate, withfinely stippled chromatin and one ormore prominent nucleoli (Fig. 1). Severalof the hepatocytes contained intracyto-plasmic, yellowish-green bile pigmentglobules. Scattered hepatocytes exhibitedcoagulative necrosis in which karyorr-hexis, karyopyknosis or karyolysis werevariably present in addition to cytoplasmcondensation and hypereosinophilia(Fig. 1). Hepatic cell plates were generallydisrupted and the spaces of Dissemoderately dilated. Mild bile ductproliferation and portal fibroplasia werepresent. Inflammatory cell infiltrates,consisting mostly of small numbers ofneutrophils, lymphocytes and plasmacells, were present in the portal tracts andscattered throughout the parenchyma(Fig. 1).

Kidney lesions comprised areas ofcoagulative necrosis of the proximaltubules, predominantly in the cortex, butextending into the medulla (Fig. 2). Mostof the remaining tubular epithelial cellswere swollen, with finely granularcytoplasm (Fig. 2). Some proximal anddistal convoluted tubules were dilated,while scattered tubules, especially at thecortico-medullary junction, containedyellowish-pink granular casts (Fig. 2).Other lesions included moderate, diffusepulmonary congestion and multifocalatelectasis. The spleen was moderatelydiffusely congested.

During a farm visit, numerous Lantanacamara shrubs were found in thegarden and surrounding camps of thesmallholding. The farmer had noticedsome of the goats consuming Lantana

ABSTRACTAcute Lantana camara poisoning in a Boer goat kid is described. The animal was part of aflock of boer goats that was introduced from the Kalahari thornveld, where the plant doesnot occur, to an area where the plant grew abundantly. At necropsy, the animal was severelyicteric, dehydrated and constipated, with hepatosis, distention of the gall-bladder andnephrosis, but no skin lesions. Histopathological findings of the liver confirmed moderatehepatosis with single-cell necrosis and bile stasis. The pathology is consistent with thatdescribed in acute Lantana poisoning in cattle, sheep and goats. The absence of photosen-sitisation may be attributed to relatively mild liver damage, or the rapid course of thistoxicosis.

Key words: Boer goat, constipation, hepatosis, icterus, Lantana camara, nephrosis,photosensitisation.

Ide A, Tutt C L C Acute Lantana camara poisoning in a Boer goat kid. Journal of the SouthAfrican Veterinary Association (1998) 69(1): 30–32 (En.). Department of Pathology, Faculty ofVeterinary Science, University of Pretoria, Private Bag X04, Onderstepoort, 0110, SouthAfrica.

aDepartment of Pathology, Faculty of Veterinary Science,University of Pretoria, Private Bag X04, Onderstepoort,0110 South Africa.

bDepartment of Medicine, Faculty of Veterinary Science,University of Pretoria, Private Bag X04, Onderstepoort,0110 South Africa. Present address: ‘Rye’, Park Road,Swanley, Kent, BR8 8AH, United Kingdom.

Received: October 1997. Accepted: January 1998.

30 0038-2809 Tydskr.S.Afr.vet.Ver. (1998) 69(1): 30–32

camara plants in the garden and on closerexamination it was clear that the plantshad been browsed. Another species, iden-tified by the National Botanical Institute,Pretoria, as Lantana mearnsii Moldenkevar. latibracteola Moldenke, was also grow-ing on the premises, although in far lowernumbers than L. camara. This is an indige-

nous Lantana sp. of uncertain toxicity. Atthe time of the visit, the rest of the flockappeared to be in good health.

DISCUSSIONThe clinical signs, gross and histopatho-

logical findings in this case are compatiblewith those described for acute L. camara

poisoning in catt le , sheep andgoats2,3,5,9,11,16–18. The fact that photosensiti-sation was not present in this casecorrelates with previously described casesof experimental toxicity in goats inZimbabwe10,11. It is believed that this maybe attributed to relatively mild liverdamage, insufficient to prevent elimina-tion of phylloerythrin10. Alternatively, thecourse of the toxicosis may have been tooacute for the animal to have beensufficiently exposed to sunlight.

Other toxic or infectious causes for thepresence of icterus in the case examinedwere ruled out on the basis of thenecropsy and histopathological findings.Although only 1 goat was presentedfor examination, it is possible that theother mortalities in the flock could alsobe attributed to L. camara poisoning,especially when the epidemiology of thiscase is taken into account.

To our knowledge, this is the 1st reportof naturally occurring Lantana camarapoisoning in goats in South Africa. Goatsusually avoid eating these unpalatableplants. An important predisposing factoris the introduction of goats from an areawhere L. camara does not occur to a small-holding where the plant grew abun-dantly. In addition, the pasture was ofpoor quality at the time of introduction.Subsequent to our diagnosis, the premiseswere cleared of all L. camara shrubs and nofurther cases were reported.

ACKNOWLEDGEMENTSWe thank the National Botanical

Institute, Pretoria, for assisting with plantidentification and Mrs H. Smit of thephotographic division of the Faculty ofVeterinary Science, Onderstepoort, forprocessing of the photographs.

REFERENCES1. Black H, Carter R G 1985 Lantana poisoning

of cattle and sheep in New Zealand. NewZealand Veterinary Journal 33: 136–137

2. Fourie N, Van der Lugt J J, Newsholme S J,Nel P W 1987 Acute Lantana camara toxicityin cattle. Journal of the South AfricanVeterinary Association 58: 173–178

3. Kellerman T S, Coetzer J A W 1985 Hepato-genous photosensitivity diseases in SouthAfrica. Onderstepoort Journal of VeterinaryResearch 52: 157–173

4. Kellerman T S, Coetzer J A W, Naudé T W1988 Plant poisonings and mycotoxicoses oflivestock in southern Africa (1st edn). OxfordUniversity Press, Cape Town

5. Kelly W R 1993 The liver and biliary system.In Jubb K V F, Kennedy P C, Palmer N (eds)Pathology of domestic animals (4th edn).Academic Press, California: 319–406

6. Louw P G J 1943 Lantanin, the activeprinciple of Lantana camara L. Part I. –Isolation and preliminary results on thedetermination of its constitution. Onderste-poort Journal of Veterinary Science 18: 197–202

Fig. 1: Liver: hepatocytes are swollen with finely granular cytoplasm, distinct cell borders(arrowhead), and occasional large intracytoplasmic vacuoles. Occasional hepatocytes aremultinucleate (short arrow). Randomly scattered hepatocytes show coagulative necrosis(long arrow). Note the portal cellular infiltrate (P). HE ×400.

Fig. 2: Kidney: necrosis of epithelial cells in some proximal tubules is present (arrowhead).The remainder of the tubular epithelial cells show degenerative changes. There is alsodilation of occasional tubules, some of which contain cellular casts (short arrow). HE ×400.

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7. Louw P G J 1948 Lantadene A, the activeprinciple of Lantana camara L. Part II. –Isolation of lantadene B, and the oxygenfunctions of lantadene A and lantadene B.Onderstepoort Journal of Veterinary Science 23:233–238

8. Luna L G (ed.) 1968 Manual of the histologicalstaining methods of the Armed Forces Instituteof Pathology (3rd edn). McGraw Hill, NewYork

9. Munyua S J M, Njenga M J, Karitu T P,Kimoro C, Kiptoon J E, Buoro I B J 1990 Anote on clinical-pathological findings andserum enzyme activity in sheep, goats andFriesian calves with acute Lantana camarapoisoning. Bulletin of Animal Health andProduction in Africa 38: 275–279

10. Obwolo M J, Odiawo G O, Goedegebuure

S A 1990 Clinicopathological features ofexperimental Lantana camara poisoning inindigenous Zimbabwean goats. ZimbabweVeterinary Journal 21: 1–7

11. Obwolo M J, Basudde C D K, Odiawo G O,Goedegebuure S A 1991 Clinicopathologicalfeatures of experimental acute Lantanacamara poisoning in indigenous Zimbab-wean goats. Bulletin of Animal Health andProduction in Africa 39: 339–346

12. Pass M A 1986 Current ideas on the patho-physiology and treatment of lantanapoisoning of ruminants. Australian Veteri-nary Journal 63: 169–171

13. Rimington C, Quin J I 1935 The isolation ofan icterogenic principle from Lippiarehmannii (Pears). South African Journal ofScience 32: 142–151

14. Sanders D A 1946 Lantana poisoning incattle. Journal of the American VeterinaryMedical Association 109: 139–141

15. Seawright A A 1963 Studies on experimentalintoxication of sheep with Lantana camara.Australian Veterinary Journal 39: 340–344

16. Seawright A A 1964 Studies on the pathol-ogy of experimental lantana (Lantana camara)poisoning in sheep. Pathologia Veterinaria 1:504–529

17. Seawright A A, Allen J G 1972 Pathology ofthe liver and kidney in lantana poisoning ofcattle. Australian Veterinary Journal 48: 323–331

18. Seawright A A, Hrdlicka J 1977 The oraltoxicity for sheep of triterpene acids isolatedfrom Lantana camara. Australian VeterinaryJournal 53: 230–235

Book review — Boekresensie

Proceedings of a symposium on lions and leopards asgame ranch animals

Edited by J van Heerden

1997. South African Veterinary Association Wildlife Group, Onderstepoort, South Africa, 265pp. Price R100 (excl. postage).ISBN 1 875088 09 1.

The proceedings were made available todelegates at the annual Wildlife Group symposiumheld on the 24 and 25 October 1997. People from anumber of disciplines and all experts in their fieldhave made contributions to the proceedings. Thetopics covered included sociality and ecology oflions and leopards in the wild, lion genetics,census and capture techniques, handraising andveterinary management, a disease overview,parasites and trophy hunting.

The proceedings open with a biblical overview oflions by Pastor R Schmid. An international contri-bution by Dr Linda Munson (world-renownedveterinary pathologist with a special interest inwild carnivores) discusses the canine distempervirus outbreak in lions in the Serengeti and whatthe implications are for wild felid populations inSouth Africa and elsewhere. Prof. J du P Bothmagives us a glimpse into the life and times of theleopard, elusive creature that it is. He reiterated theimportance of the leopard, and other largecarnivores, in attracting tourists to Africa. KarenTrendler shares information on handrearing largecarnivores and emphasises that they pose a uniqueset of problems especially once they have grown a

‘little’ and their hunting instincts become stronger.Dr Dewald Keet’s paper discusses the role of thelion and cheetah in the epidemiology of tubercu-losis in the Kruger National Park. This disease isbecoming a serious threat to one of the largestnatural lion populations in the world and hasimplications for the private landowner.

The proceedings provide a good source ofup-to-date information on lions and leopards. Itis a worthwhile acquisition for researchers,veterinarians, game ranchers or lay persons withan interest in large carnivores. After reading theseproceedings one realises that the stability ofAfrica’s natural lion and leopard populations isunder threat, not only from ‘man the predator’ andloss of habitat but also from exotic and emergingnew diseases like tuberculosis and caninedistemper virus. While other species are effectivelyprotected on smaller, private lands, largecarnivores are not really suited to the gameranching scenario, emphasising the importance oflarge protected areas for the conservation of thesespecies.

L RasmussenJohannesburg Zoological Gardens

32 0038-2809 Tydskr.S.Afr.vet.Ver. (1998) 69(1): 30–32