Stinkwort (Dittrichia graveolens, formerly Inula graveolens; Asteraceae) is an introduced weed that has become naturalised in many parts of southern Australia (Cunningham et al. 1981). Following germination in late spring or summer, it flowers in autumn, producing seeds each with a pappus of numerous bristles, which aid dispersal (Cunningham et al. 1981 ). Although often the only green plant in pasture after periods of dry weather, D. graveolens is highly unpalatable and sheep will only consume it when no alternative feed is available (Cunningham et al. 1981). Following ingestion of D. graveolens seeds, the bristles can become embedded in the mucosa of the intestine, causing enteritis due to mechanical damage (Lang et al. 1952; Schneider and Du Plessis 1980). In addition, contact dermatitis and tainting of milk and meat have been attributed to exposure to D. graveolens (Cunningham et al. 1980). This report describes pyogranulomatous enteritis in sheep due to penetrating seed heads of D. graveolens.
From early April to early May 1991, a flock of 1,000, 10 to 12 month old, mixed sex Merino hoggets at Temora, on the south western slopes of New South Wales, grazed a 60 ha paddock containing D. graveolens. The district was declared drought affected in May 1991 following a very dry summer and autumn and, in April and May 1991, the D. graveolens, which covered an area of approximately 2 ha, was almost the only green feed in the paddock. There was evidence that this plant had been grazed, even though the sheep were supplemented with a light ration of clover hay and oats. In early May 1991, at least 750 sheep (75%) were inappetent, had lost condition and exhibited illthrift and severe diarrhoea. Approximately 200 (20%) died. The arithmetic mean faecal nematode egg count of 10 sheep was 272 eggs per gram. The onset of the problem coincided with the D. graveolens setting seed. Following removal from the D. graveolens on 8 may 1991, there was a general improvement in the appetite of the mob and a reduction in the prevalence and severity of diarrhoea within 1 wk. There were no further deaths after 14 May 1991.
Sheep 1, which died on 8 May 1991, while the flock were still in the paddock containing D. graveolens, had ventral subcutaneous and submandibular oedema and appeared mildly anaemic. The gastrointestinal tract was removed intact for a total nematode count, except for a portion of jejunum which was excised and fixed in formol-saline for histopathology. The abomasum contained 1,100 adult Teladorsagia sp, but no intestinal nematodes were found. No other gross findings, were noted. Sheep 2, which was in poor condition and had diarrhoea, was selected from the flock on 14 May 1991, 6 d after removal from the D. graveolens, and destroyed for necropsy. In the middle third of the small intestine, seed heads were embedded in the jejunal mucosa, which was mildly reddened and thickened. No seed heads were detected in the pharynx, oesophagus, rumen, reticulum, omasum, abomasum or at other sites along the gastrointestinal tract.
Sections of jejunum, liver and kidney from both sheep, as well as spleen from sheep 1 and abomasum, heart, skeletal muscle and brain from sheep 2, were examined histologically. Both sheep had segmental pyogranulomatous enteritis of the jejunum. Vegetable fibres with numerous adherent bacteria, interpreted as ingested bristles of D. graveolens seeds, had entered the crypts of Lieberkuhn where, if the epithelium was intact, neutrophils had exuded to form crypt micro-abscesses. At other sites, the bristles had penetrated the epithelium to lie in the lamina propria and, sometimes, the submucosa. Neutrophils and epithelioid macrophages, including a few multinucleate foreign body giant cells, surrounded the penetrating bristles. Elsewhere, there was a mild diffuse infiltration of mononuclear leucocytes in the lamina propria. The jejunal villi were moderately atrophic and there was mild crypt hyperplasia.
Sheep 1 also had periacinar atrophy of hepatocyte cords, mild vacuolar change of hepatocytes, leucocytosis and serous hepatitis in the liver, as well as haemosiderosis in the kidney and spleen. Along with the gross findings at necropsy, these changes were suggestive of anaemia due to a recent erythrophagocytic episode, the cause of which was not determined, but which possibly was due to Eperythozoon ovis and unrelated to the ingestion of D. graveolens. There were no significant findings in extra-intestinal tissues of sheep 2. No significant bacterial pathogens were, recovered from the jejunum of sheep 1 or the faeces of 2 other sheep from the flock cultured routinely and on media selective for Salmonella sp, Yersinia sp and Campylobacter sp.
Samples of the suspect plant submitted to the Director, Royal Botanic Gardens, Sydney, in May 1991 were identified as D. graveolens (New South Wales Herbarium sheet number 240210). Seeds with bristles were sectioned histologically and compared with the embedded vegetable fibres in sections of affected jejunum. Both the bristles and embedded fibres had a similar core structure. The fresh material had an outer sheath from which small barbs projected. These barbs were less prominent in the embedded fibres, probably due to partial digestion in the intestine.
Enteritis due to penetration of the jejunal mucosa by seed-heads of D. graveolens was diagnosed in the affected sheep. The clinical signs and pathology were similar to those in an outbreak reported by Schneider and Du Plessis (1980), in which 5.3% of 190 sheep died, but the proportion of sheep affected in this outbreak was higher. Schneider and Du Plessis (1980) similarly observed enteritis due to D. graveolens after a dry summer and autumn when winter rains were later than usual and sheep had no alternative feed. The diarrhoea was attributed to increased intestinal permeability and possibly malabsorption resulting from mechanical damage to the intestine and pyogranulomatous enteritis induced by seed-heads of D. graveolens. The enteritis probably contributed to illthrift and mortality in the flock, although other problems, such as undernutrition and anaemia, were also identified.
The penetrating bristles were confined to the jejunum and did not appear to have embedded in the upper alimentary tract, forestomachs, abomasum or at other sites in the intestine. Schneider and DU Plessis (1980) observed reddening and thickening throughout the small intestine, with an increase in the number of bristles and severity of inflammation from proximally to distally. An explanation for the localisation of penetrating bristles in the small intestine could be that the seeds passed through the forestomachs and abomasum largely intact, but the bristles separated from the pappus after partial digestion in the small intestine, allowing them to embed in the mucosa. The barbs on the bristles of D. graveolens appear to facilitate penetration of the intestinal mucosa (Schneider and Du Plessis 1980). Although bristles were still observed in the jejunal mucosa of a sheep examined 6 d after removal from D. graveolens, clinical signs had abated in most sheep by this time. Clinical signs probably resolved as bristles were expelled from the intestinal mucosa with the assistance of the pyogranulomatous inflammatory reaction.
Provided there is adequate alternative feed, pastures containing D. graveolens usually can be grazed without ill effect from this plant, even if it is flowering. However, if other pasture is sparse, sheep should not be allowed to graze D. graveolens because of the risk of enteritis due to ingestion of the seed heads. D. graveolens can be controlled by promoting competition from more vigorous pasture, as well as by cultivation and use of herbicides (Cunningham 1981).
References
Cunningham GM, Mulham WE, milthorpe PL and Leigh JH (1981) Plants of Western New South Wales, New South Wales Government Printing office, Sydney, p 668
Lang PS, Tulloh NM and Fennessy BV (1952) Survey of the Sheep Industry in the Western District of Victoria, University of Melbourne, Melbourne, p 63
Schneider DJ and Du Plessis JL (1980) J. S. Afr. Vet. Assoc. 51:159