This presentation deals with a major and common presenting clinical sign rather than a specific plant or group of toxins.
As such rather than cover many individual possible plant poisoning the presentation will take a finger food approach of photosensitisation cases that I have personal experience with.
From this I hope to be able to demonstrate a few key maxims with photosensitisation
Since 1993 some twenty-nine cases which database suggests had photosensitisation as a major sign.
Seawright has an excellent section on this.
One definition is ‘dermatitis and/or conjunctivitis on exposure to sun’ (post-shearing dermal necrosis?)
A better definition from Seawright ‘specially heightened susceptibility to sunlight caused by the deposition in the skin (or other integumental structures such as the cornea or visible mucus membranes) of molecules that are able to absorb solar wave lengths and thereby become activated.’
In summary, sunlight acting on the particular photosensitive molecules (present in higher levels as an end result of consumption of or contact with toxic substances) triggers a free radical cascade that damages cellular membrane systems.
‘As a result there is enhanced capillary permeability, cell necrosis, vascular occlusion and acute inflammation.’
This damage is reduced or blocked by pigment and hair covering.
Death can result occasionally from shock. However illness/death due more to liver damage.
The above mentioned photosensitive molecules can either be their primarily from ingested substances (eg St John’s wort, Buckwheat), or far more commonly, secondary as a result of liver damage.
The photosensitising substance in liver damage cases is phylloerythrin, derived from chlorophyll (via microbial activity).
Removed from the liver and excreted in the bile.
Level of photosensitisation is not always related to degree of liver damage. Where the liver damage is generalised it is, but where damage is zonal (eg Eremophilia deserti) death or other severe signs such as CNS affects may be more prevalent than photosensitisation.
Cattle differential diagnoses include Pestivirus, Bovine Malignant Catarrh, and Vesicular Diseases.
Note primary contact photosensitisation from fungal related furocoumarins in parsnips, parsley and celery. Lesions can resemble vesicular diseases. Look for signal of cloudy cornea that indicates furocoumarins.
Awareness of conditions that can lead to poisonings and then vigilance so that can remove etc before severe consequences.
Major outbreak in spring 1991 affecting almost all sheep flocks on black soil.
After a wet and mild winter with lush burr medics (Medicago polymorpha) pastures heavily infested with the native Cow Pea Aphid.
Lambs worst affected, swollen ears. Few deaths or severe clinical cases.
Problem was significant in the 50s and 60s but has not been seen since 1991.
Graziers indicate always associated with the ingestion of aphids but whether these are indicators or contributors (stress the plants) or the primary cause is open to debate. Cases are recorded without aphids.
Treatment difficult as usually no safe paddock to remove sheep to.
Secondary or primary — no liver pathology on samples taken personally.
The major cause of photosensitivity at Narrabri. Cases in most years where good cereal fodder crops. S
eep are more susceptible.
Occurs as grouping of cases when the following conditions apply
Cases seemed to more prevalent on
Secondary (toxins produced as result of stress) or primary (furocoumarins). The latter has cloudy cornea and this has been seen personally in at least one case.
Number of cases summer 1993 -94. Few cases since.
1993-94 cases occurred when early summer rains on bare drought affected pastures produced Tribulus dominated pastures. Cases began as the Tribulus became stressed with no further rain besides sporadic minor storm showers.
Saponins are primary toxin (also in Panics and variety other plants). Pithomyces chartarum can increase toxicity of Tribulus.
Both T.terristris and T.micrococcus.
Dramatic liver gross pathology, jaundice etc.
Single grouping of cases in late 2004. No other cases prior despite large number of lambs grazed on lucerne in district.
Followed flood rains of 200-300 mm and then sunny conditions.
Clinical signs similar to medics.
Liver enzymes elevated on samples taken personally.
Have single property that gets cases most winters with wethers grazing country containing regrowth. Other nearby sheep eat with impunity (is regrowth the critical factor).
Single case with cattle during winter.
Deaths and nervous signs before photosensitisation.
Major deaths recorded cattle on TSR in north-west.
Outbreak on four properties nearby properties grazing cattle in spring 1996.
Crops had started well but hayed off early due to lack of rains, leaving good cover dry mulch.
Sporadic 50 mm storm wet the dry oats and cases followed two weeks later.
Deaths and severe photosensitisation.