St. John's wort (Hypericum perforatum), a native to many areas of Europe, western Asia and North Africa, was introduced Australia in 1873 as a garden plant. By 1893, St. John's wort was recognised as a weed in Victoria and has since become a major invasive weed especially in the Central and Southern Tablelands and slopes of NSW. In NSW, it is listed as a declared noxious weed under the NSW Noxious Weeds Act 1993 (Naughton & Bourke, 2007).
St John's wort causes primary photosensitisation in livestock with unpigmented skin. This report describes a case of photosensitisation in Dorper and Australian White ewes with lambs-at-foot caused by the ingestion of St. John's wort. This report also discusses control options for St John's wort.
In late November 2022 a sheep producer of the Central Tablelands reported skin lesions in 50% of 400 Dorper and Australian White ewes with lambs-at-foot. The lesions were more severe and prevalent in the lambs. The lesions were erythematous, swollen, and crusty, and most apparent on the muzzle, periorbita, pinna, and dorsal regions. In the flock, the pinna was the worst affected area, and ten ewes were also found with a severely affected dorsum (Image 1).
The sheep were being used to graze St. John's wort (primarily the broad-leafed form) to control it before flowering. The producer had observed that some of the ewes seemed to eat the weed preferentially. The pasture consisted of native and introduced grasses with an infestation of St. John's wort and some blue heliotrope (Heliotropium amplexicaule). The producer commented that St. John's wort was more prevalent in wet years whereas the heliotrope was more prevalent in dry years.
The producer used his flock in part for weed control. This approach had been successful in previous years and now some paddocks were clear of the St. John's wort. Previously, Merinos had been used to graze the St. John's wort in winter (when the plant was inactive) without causing photosensitisation. Some of Merino flocks on the property had been affected this year (with erythematous faces) but not to the same extent as the Dorper and Australian White flock. The producer sprayed the St. John's wort by helicopter in the summer when the plant was flowering.
The producer moved the sheep to unaffected pasture and the lesions primarily resolved within a month but approximately 10-15 ewes had died as well as some lambs. The owner treated the most severely affected sheep, especially the lambs, with topical zinc cream applied to the exposed and affected skin. The sheep remained off the affected pasture during summer. The mob was later moved back onto the affected pasture and had not had a recurrence of photosensitisation. The producer planned to monitor the flock closely, moving them if there were any signs of photosensitisation.
St. John's wort poisoning is common in sheep, goats and pale-skinned cattle grazing infested pastures on the Central Tablelands of NSW. It is almost always diagnosed based on the history and clinical signs, as it was in this case. None of the plants causing crystal-associated cholangiohepatopathy (Tribulus spp. and Panicum spp. in particular) were known to occur in significant quantities and clinically the affected sheep were otherwise bright and alert. Some pastures on this property were also infested with blue heliotrope, which is also potentially toxic. Blue heliotrope intoxication was unlikely to have contributed to this case as it causes chronic liver damage, usually without photosensitisation (Bourke 2005). However, the sheep were not blood tested for evidence of liver disease.
The leaves and flowers of St. John's wort contain the toxin hypericin, which causes the clinical signs observed in livestock (Csurhes & Zhou, 2016). On sunny days, clinical signs can be observed within five hours of grazing pastures heavily contaminated with St. John's wort (Naughton & Bourke, 2007). Acute clinical signs include pruritus (restlessness, head rubbing) and red, swollen and painful skin lesions on the eyes, lips, ears, nose, white blazes, coronary bands and other pale hairless areas. Affected livestock will avoid the sun and may become inappetent, anorexic, dehydrated and reluctant to move.
Acute St. John's wort poisoning can result in livestock deaths (NSW DPI, 2023). This is usually due to starvation or misadventure (Chase et al., 2017). St. John's wort is estimated to cause production losses of $22.5 million per year in NSW (Csurhes & Zhou, 2016).
There is no specific treatment for primary photosensitisation. Keeping stock in a shed or shady paddock whilst they are showing clinical signs is critical (Chase et al., 2017). Livestock usually require sun protection for a minimum of four to seven days whilst the toxin is excreted from the body (Naughton & Bourke, 2007). Affected stock can be let out onto unaffected pasture at night, and young stock may need to be supplemented with milk whilst udder lesions heal.
If the photosensitisation is not due to a hepatopathy, NSAIDs may be used for analgesia and antibiotics for secondary bacterial infections. Caution is required for medical treatment that requires hepatic metabolism if secondary photosensitisation is suspected.
The prognosis of animals with primary photosensitisation is generally good if they are removed from the source and provided sun protection. Skin lesions will begin to resolve in 24-48 hours after cessation of exposure, but severe lesions may present for up to six months (Chase et al., 2017).
Management and control of declared noxious weeds is the responsibility of the land occupier (Noxious Weeds Act, 1993). St. John's wort can be spread by seed or plant parts. Seeds can be transported on animals, inside digestive tracts, on clothing and equipment, in water and via the wind. Seeds can then remain dormant in the soil for up to 10-12 years. Therefore, it is important to reduce movement from affected to non-affected paddocks. St. John's wort can also grow from plant fragments. When cultivating affected fields, roots that are not fully extracted from the ground and dried out may result in future weed growth (Naughton & Bourke, 2007).
St. John's wort, a perennial plant, grows prolifically when it is lightly or rotationally grazed but fails to thrive when heavily grazed. As recommended by Naughton and Bourke (2007), stock can be used to control the weed. Grazing is safest when concentrations of hypericin are lowest, between July and August when the plant is not rapidly growing and before flowering. Wool sheep with at least four months of wool growth are better protected than bare-shorn or shedding sheep. In wetter years, St. John's wort will have increased hypericin concentrations and grazing periods may need to be shortened (NSW DPI, 2023). Pregnant or lactating livestock should not be used to graze heavily infested paddocks as hypericin can cross the placenta and enter the mammary gland meaning that lambs risk a double dose. Adults are more tolerant of the toxin compared to young sheep. Shade should always be available for any class of livestock grazing St. John's wort (Naughton & Bourke, 2007).
A range of biological control agents including Chrysolina beetles, gall midges, green aphids and St. John's wort stunt mites have been released in Australia. Herbicides are also used but are most effective when the St. John's wort is actively growing and flowering. Once the flowers begin to brown, the weed is less susceptible to chemical control. Effective control may require chemical application over two consecutive years.
Unfortunately, all these herbicides have a moderate risk of developing resistance. When choosing a chemical, it is also important to aim for a selective herbicide as competitive ground cover will reduce the opportunity for future weed development (NSW DPI, 2023).
The authors would like to thank the producer for sharing this case and for allowing it to be published in Flock & Herd.