Lesser loosestrife (Lythrum hyssopifolia) is a widely distributed weed being recorded in SA, NSW, Vic and QLD. It prefers wetter areas and is considered to be relatively unpalatable (1).
It has previously been recorded as causing significant mortalities in sheep in this district with reports published by local DPI field and laboratory staff in 1991.
Since I began in Wagga in 1990, I have also seen substantial sheep mortalites (up to 200 head) especially where loosestrife represented the only available green feed in a stubble paddock. I have also seen cases where it only occupied a wet corner of a paddock and as I recall there was other feed available.
The last 10 years have been drier than normal and thus have not favoured loosestrife. The abnormally wet late spring and early summer of 2010 were ideal for its resurgence.
An excellent review of sheep poisonings in Victoria from this weed can be found in the AVJ Vol 87, No 12, Dec 2009.
While reports of cattle poisonings are apparently not common, they would not be unexpected. In the case described in this paper, sixteen cows died from a mob of forty eight – a significant loss. The enormous publicity and subsequent awareness we were able to create appeared to prevent further losses over a wide area. From my point of view, unlike private practitioners, we deliver value to rate payers by making them aware of potential problems and preventing loss.
On 12 January 2011, I received a call from a producer who had a case of what sounded like grain poisoning. Cows with large calves at foot had been introduced into a pasture paddock with good dam water and then four days before I was contacted, had been given access to wheat stubble with a wide variety of weeds and also plenty of areas where grain was down and could not be harvested. By January 12th, there were three dead cows (one in the dam), another recumbent, two obviously ill and probably another ten affected.
A necropsy was conducted. Findings included: dehydration, yellow fat (probably due to the age of the cow), extensive sub-epicardial petechial haemorrhages and pulmonary congestion. There was inflamed/congested omentum but the rumen appeared normal and contained negligible grain. The abomasum was very congested/inflamed but not oedematous. The small intestine and caecum mucosa had small haemorrhages and congestion. There was a moderately enlarged gall bladder but the liver was grossly normal. The kidney cortex was a cream colour which explained the unusual odour of the cow (ureamic).
Lesser loosestrifte was common in both paddocks and sorrel was also present. Both plant species are capable of causing the kidney damage seen at necropsy.
The recumbent cow was sampled for serum biochemistry.
Differential Diagnosis – Lesser loostrife toxicity, oxalate toxicity, arsenic toxicity, salmonellosis.
Serum biochemistry (recumbent cow)
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Comments: Marked elevation in serum urea and creatinine, along with hyponatraemia, hypochloraemia, hypocalcaemia and hyperphosphataemia is consistent with renal damage and dysfunction. Urea and creatinine at this level is unlikely due solely to dehydration.
The section of kidney is characterised by multifocal renal tubular necrosis which are characterised by loss or attenuation of the tubular epithelial and accumulation of hyaline to granular, dark eosinophilic material in the affected tubules which is consistent with severe proteinuria. The tubular degeneration is accompanied by severe multifocal leucocytic infiltration which is predominated by lymphocytes, with some h8istiocytes and neutrophils. The glomeruli are moderately congested but are otherwise minimally changed.
In the renal medulla there is a moderate to marked congestion with few focal aggregates of lymphocytes. Highly proteinaceous fluid is present in majority of the tubules.
The section of liver is characterised by moderate congestion and scattered foci of hepatocyte loss, degeneration and accumulation of mononuclear leucocytes. One focus of haemorrhage is evident in the section which is not accompanied by any erythrocyte breakdown products.
Rumen, abomasum, caecum
Rare dilated abomasal glands with accumulation of secretory material are in the section of abomasum. Modest numbers of lymphocytes are in the mucosal layer of the caecum. No significant lesion noted in the section of rumen.
Laboratory Report Comments:
Preliminary findings with serum biochemistry appear consistent with kidney damage and insufficiency.
The diffuse nature of the gross and histopathologic lesions is consistent with nephrotoxicity, which may be due to a variety of causes. Whilst Lesser Loosestrife (Lythrum hyssopifolia) toxicity can cause renal lesions seen in the case, the hepatic lesions are not quite consistent. Lesser Loosestrife toxicity usually results first in hepatocyte damage, which is followed by renal damage from the metabolites, the hepatic changes in this case and their distribution are more likely a legacy of previous bacterial hepatitis. Other plant toxins known by nephrotoxic include Ameranthus retroflexus (pigweed), Iostropis, and lantana sp. The lack of typical crystalline structures in the kidney suggest oxalate toxicity is unlikely the cause of renal lesions.
Lesions in the abomasum and caecum are unlikely to be clinical significance in this case.
It was the plant poisonings season and I prepared a press release on loosestrife, witchgrass and lupinosis and emailed it straight to our local contacts. The relevant section was:
Loosestrife Kills Cattle
Heavy cattle losses on a farm near Wagga Wagga have been caused by eating the poisonous plant loosestrife District Veterinarian Tony Morton said today.
Initial thoughts that the losses in a stubble paddock were from grain poisoning quickly changed when evidence of massive kidney damage was seen and there was no evidence of grain poisoning in the rumen.
Eliz Braddon SDV at Young is seeing similar problems in sheep.
Loosestrife loves wet conditions and chemical farming, this year has been ideal for its reappearance as a problem weed so it's important to check lower lying areas of paddocks for its presence and keep stock off it if found.
Little of it has been seen over the run of drought years.
Prior to that it had caused repeated heavy losses of sheep especially in the wetter areas of the old Wagga Boarde.g. The Rock-Mangoplah, Tarcutta but had also been seen sporadically elsewheree.g. Ganmain in localised wet areas.
Similarly Steve Whittaker SDV at Albury has also seen substantial losses in wet years.
Sorrel is another weed often found in similar areas and it too is a potential cause of kidney damage and death.
The media showed instant interest.
I was interviewed 18 January 2011 on the affected producer's farm by Prime TV and it was broadcast in the first 5 minutes of that evening's local news. WIN TV did an interview at the office which also made it into their evening news. The ABC interview made it to the Country Hour, and the press release was also in 'The Rural' a weekly insert in many local papers. A deluge of enquiries followed resulting in us having to have handouts in the office with photos of the plant and scans ready for those who wanted an electronic version.
I believe that the diagnosis of loosestrife poisoning based on the kidney pathology is correct. In my experience with loosestrife and sheep, the kidney pathology is far more striking than the liver pathology. It was abundant especially in the wetter areas of the pasture paddock and stubble paddock. The pasture paddock grazed by the cattle before release into the stubble was well chewed down with the loosestrife clearly eaten. It had also been extensively eaten in the wetter area of the stubble paddock. Alternative nephrotoxic plants were not present except for sorrel in very small quantities.
The owner reported that new cases and deaths continued through January despite removing the cows from the at risk paddock on 12 January 2011. Near the end of the outbreak he weaned the calves (as recommended) and thinks that may have helped as no calves were affected.
It did not surprise me to find that loosestrife would kill cattle and, as with sheep, could cause heavy losses.
What I found gratifying was that the press were very interested and as a result of extensive TV, radio and newspaper coverage we were subjected to a deluge of enquiries for the next two weeks from as far away as the western districts of Victoria, Young and West Wyalong. Some of these enquiries were from agronomists and farm advisors who in turn were receiving numerous enquiries from their clients.
I saw no further losses. Helen McGregor (DV Hume LHPA) anecdotally had one suspected sheep case at Temora between the diagnosis and press release. Steve Whittaker (SDV Hume LHPA) made a sheep case diagnosis in his area. Prior to the press release, a practitioner diagnosed the problem on another cattle property in the same locality. With the abundance of loosestrife and wide distribution and lack of awareness by many farmers prior to the publicity I think we had a major impact in preventing heavy losses of both sheep and cattle. In other wet years there have been extensive and at times heavy losses.
From my point of view the take home message is: If you want to deliver the ratepayers a bang for their buck, doesn't be shy about writing and sending out your own press releases and regard reporters as one of your best assets. You need the message to hit the print, radio and TV to get the maximum awareness. Having a farmer who is willing to let the TV cameras onto his property usually guarantees good coverage.