A sheep producer from the Yeoval area reported problems with severe sunburn in one mob of 350 adult Merino ewes with 200 lambs at foot in late November 2011. The owner first noticed droopy ears and scabby faces on a Saturday. The animals were examined by me on the following Tuesday morning. The owner reported having a sunny weekend followed by ongoing rain and a drop in temperatures.
About half of the lambs had been marked the month prior. The other lambs had not yet been marked as they were late dropped and due to severity of sunburn, marking was further delayed for welfare reasons. Lambs and ewes are routinely vaccinated with 5-in-1. The mob had been grazing one paddock for the past 4-5 months. This paddock had a cover of 40-50% St. John's wort (Hypericum perforatum), native grasses, and a few Patterson's curse (Echium plantagineum) plants. The paddock offered approximately 30% shade cover with mature native trees. A few red and white coloured cattle also grazed this paddock but none showed any clinical abnormalities.
At the time of examination, no stock had died and none were sacrificed for necropsy. Lambs and ewes were examined in the yards. About 30% of adult ewes and 30-40% of lambs at foot were affected. Ewes remained bright despite having extensive skin lesions on the face (Figures 1a and 1b).
Lambs, however, demonstrated a range of signs from severe depression to extreme irritation, often manifested by incessant head shaking. The skin lesions of lambs and ewes consisted of severe crusting of the nose, face, muzzle, eyelids and pinnae (Figures 1a 1b, 2a and 2b).
The epithelium underlying the scabs was ulcerated. Some of the affected animals had severe alopecia around the eyes and muzzle. This was especially apparent in the affected ewes. The muzzle, eyelids, ears and sometimes the lips were oedematous and swollen. The ears often drooped and had crusty blackened tips (Figure 2a).
One lamb had a completely blackened face and muzzle. This affected lamb had green pus oozing from the skin lesions of the eyelids and face. In addition, lambs in particular tended to have 5-6 discrete nodular crusting lesions on the surface of the nose and upper and lower lips. Rectal temperatures ranged from 39.9 to 40.1 degrees Centigrade.
The differentials considered in this case were primary photosensitisation due to St. John's wort, dermatophilosis, scabby mouth and bluetongue. Five jugular blood samples were collected in plain vacutainer tubes and four scab samples were submitted from affected animals for biochemistry and virology. Tests for liver enzymes, cytology and virus identification in scabs and for bluetongue were specifically requested to rule out other causes of photosensitisation (e.g. secondary to liver damage) and to exclude bluetongue, a notifiable disease, that can manifest with similar signs as seen in this case.
All blood samples were negative for bluetongue virus on PCR testing and for bluetongue virus antibody cELISA. One out of 4 scab samples were positive for orf virus on electron microscopy. Biochemistry results demonstrate mild elevations of GGT and AST. Two of four samples demonstrated marked elevations of CK (Table 1). All other biochemistry values were within normal range.
The affected mob was moved to another paddock with trees, shade cover and no St. John's wort. Lambs with severe secondary infections were treated with oxytetracycline.
The history of paddock access to St. John's wort, grazed young shoots mixed in with native grasses, appearance of characteristic skin lesions confined to the less wooly areas (e.g. ears, nose, face, etc.), exclusion of other diseases by diagnostic tests confirmed that photosensitisation due to St. John's wort was the most likely cause of dermatitis in this case. Secondary photosensitisation (e.g. secondary to liver damage) was unlikely given that there was only mild changes in liver enzymes. GLDH, a liver specific enzyme, was within normal limits. GGT was only mildly elevated and tends to have higher normal ranges especially in young ruminants.1 AST, a non-specific indicator of tissue damage, was only mildly elevated and when combined with CK (creatine kinase), a tissue specific enzyme for muscle damage, indicates muscle damage/myopathy.1 There were marked elevations in CK in two samples (lamb and ewe). These marked elevations could be due to muscle mass loss from injury or loss of condition over lambing in the ewe. The marked elevations of CK in the lamb could be due to recent marking the month prior. The orf virus was likely an additional though incidental finding in this case. Perhaps the discomfort associated with the skin lesions and subsequent damage to the skin triggered orf viral shedding. Alternatively, the virus could have been spread during lamb marking.
One month after the initial visit, there was almost complete resolution of skin lesions in the mob. Only a few remained with skin lesions, but they were all in the healing stages. (Figures 3a,3b and 3c). No animals died and only two lambs required treatment with oxytetracycline for secondary skin infections.
St. John's wort, was originally introduced into Australia in 1875 as a garden plant.6 It is a hairless perennial weed 60-100 cm high producing yellow flowers with five petals. It can be uniquely identified by the oil glands in the leaves that appear as perforations when held up to the sun.6,7 It favours temperate regions and is traditionally found along the coast, slopes and tablelands of NSW.6,7 St. John's wort contains a toxic fluorescent red pigment called hypericin, which is found concentrated within the oil glands of the leaves.6,7 In Australia, there are two types of St. John's wort, a narrow leaf (leaves 7-9mm wide) and a broad leaf type (leaves 10-12mm wide).6 Both are toxic, but the narrow leaf is more toxic as it contains more oil glands in the leaves.6 The St. John's wort type in this case was identified as the narrow leaf type. This type was also found in a neighbour's paddock.
Hypericin remains intact after ingestion and passes from the liver to the bloodstream.6,7 With repeated grazing, hypericin levels can persist in the blood and can even cross into foetal-placental blood circulation or into the milk during lactation.6,7 Hyerpicin in the blood produces its toxic effect by increasing the sensitivity of the animal's body to light wavelengths and subsequently producing sunburn in the less wooly parts of the sheep (e.g. nose, face, ears, etc.).7
Options to keep this weed under control include use of a combination of selective grazing based on leaf variety, sheep type and chemical control. When grazing, use older sheep that are not pregnant nor lactating (e.g. dry ewes or wethers) and carrying a fleece of a minimum of 4 months wool growth. 6,8 Merino sheep with fine wool (less than 20 microns) are also less susceptible. 6,8
Broadleaf St. John's wort can be initially grazed from 1 May to 14 October (24 weeks) and narrow leaf can be grazed from 1 July to 14 September (10 weeks.)6,8 It is imperative however, that all sheep be removed off wort contaminated paddocks before the new season flower shoots reach 50-100mm in height as poisonous levels of hypericin peak rapidly.6,8
St. John's wort can be controlled with a variety of effective chemicals including fluoroxypyr, triclopyr, picloram, glyphosate, glyphosate and metsulfuron-methyl.8 It is best to check label recommendations and with agronomists or noxious weeds officers for optimal control strategies. Some of the chemicals have to be applied at flowering, or other plant growth stages, and they may kill other pasture species as well.
Although the sheep in this case were reported to have been grazing on the contaminated paddock for 4-5 months, it is possible that cloud cover, tree cover in paddock, wool growth and fibre type may have delayed the onset of photosensitisation. In this case, the ewes were carrying 6 months wool growth and were of superfine wool type (17 micron).
An Australian study found that sheep carrying four months of wool growth or greater were 3 to 4 times more tolerant of hypericin than recently shorn sheep.5 Superfine Merinos in contrast to medium wooled types were also able to ingest more hypercin without suffering deleterious effects.2,5 The amount of skin protection against sunlight was likely the determining factor in the ability of sheep to ingest wort safely as opposed to the differences in hypericin metabolism and excretion.2 This study further confirmed previous studies3,4 of the absolute requirement of bright sunlight in order to activate circulating blood hypericin before the effects of hypericin poisoning develop manifested by hyperthermia, facial/ear swelling and skin lesions. The increased consumption of St John's wort as the available paddock feed declined led to elevated blood levels of hypericin. The onset of a few sunny days were likely to have led to the development of skin lesions.
The author of this article wishes to thank Andrew Hansen for his generous time and assistance, Ian Lugton for his editorial assistance and EMAI Menangle veterinary laboratory for their diagnostic testing services.