CASE NOTES
Vetch toxicosis (Vicia villosa ssp dasycarpa)
Andrew Thompson, District Veterinarian, Northern Slopes RLPB
Posted Flock & Herd February 2011
Introduction
Woolly pod vetch (and Namoi variety Vicia villosa ssp. Dasycarpa cv. Namoi) is a self-regenerating legume, selected from imports from Turkey in 1951 by the CSIRO. It is an autumn-winter-spring growing annual which flowers in late spring to early summer producing many 2-5 seeded pods. The flower is purple and pea-like. When moisture is adequate and temperatures not too high, it will grow on into summer months. Cattle have been poisoned by grazing woolly pod and popany vetch (V benghalensis) and it has been reported in the literature as being associated with grazing Hairy Vetch in various countries. Poisoning is normally associated with grazing the plant at full maturity and when it is the dominant species. Angus and Murray grey cattle (as well as Friesian etc) have been over-represented in poisoning incidents.
Intoxication may be manifest in a number of other syndromes. The seeds and vegetative portion have been reported to contain cyanogenetic glycosides as well as containing substances which induce toxic hepatitis or haemolytic anaemia. Photosensitisation has accompanied the ingestion of common vetch (Vicia sativa L.). In one incident reported of cattle grazing hairy vetch seed, signs of nervous derangement signs included bellowing, sexual excitement, locomotor difficulties, convulsions and death.
A similar syndrome has been reported in association with cattle consuming citrus pulp for 6 weeks and concentrates containing 3% di-ure-ido-isobutane (DUIB).
In citrus pulp toxicosis, the toxic principal also is not known, but like hairy vetch toxicosis, the character of the inflammation in the organs suggests a type IV hypersensitivity reaction, with a lectin acting as an immunostimulant. Alternatively, vetch lectins may bind to and activate a variety of T lymphocyte functions, stimulating lymphokine production, cytotoxicity, and the granulomatous inflammatory response that characterizes the disease (Panciera, Mosier, and Ritchey 1992 referring to Tollefsen, Kelly and Spackman, 1978),
Pathogenesis
The syndrome which is reported in cattle results in multisystemic disease with high mortality rates. The underlying pathogenesis of this syndrome is poorly understood and has been reproduced experimentally in a cow which had previous exposure to hairy vetch before being force fed cuttings from hairy vetch (Panciera, Mosier and Ritchey, 1992). An imunologically mediated pathogenesis for vetch toxicosis has been suggested, but not confirmed. The cattle need to have grazed the vetch in abundance for at least 2 weeks and usually 6 weeks. It occurs both when the vetch is a major and minor component of the pasture.
Pathological changes consist of extensive infiltration of many organs by lymphoreticular cells, plasma cells, multinucleated giant cells and eosinophils (Panciera 1978)
Insects that parasitise vetch have been suggested as possible aetiological agents of ‘vetch toxicosis’, but this has not been substantiated (Panciera 1978)
Clinical Signs
Include dermatitis, conjunctivitis, diarrhea and illthrift mainly in adult cattle. Other reported signs include: anorexia, +/- fever, reduced milk production, weight loss, extensive pruritic exudative dermatitis involving BOTH pigmented and unpigmented skin and melaena.
Mortality generally approaches 50% of those cattle recognized as ill, but varies from 0 to 100% (Panciera). Most die after a course of illness from 10-20 days.
Diagnosis
Distinctive histopathology — extensive granulomatous inflammation of many organs including renal cortex, dermis, myocardium, adrenals, lymph nodes, hepatic portal triads (macrophages, plasma cells and small numbers of eosinophils, multinucleated giant cells in renal, myocardial and lymph node lesions) and renal tubular fibrosis Skin biopsy histo — dermal inflammation, esp. around vessels and adnexal structures, some have degeneration and cellular infiltration of sebaceous and sweat glands, mononuclear cells and acute lesions had large numbers of eosinophils, oedema and vasculitis, crusting and ulceration.
Blood biochemistry — increased serum urea, creatinine, elevated GGT and AST.
Haematology — eosinophilia, anaemia.
Dermatitis — affecting pigmented & non-pigmented skin (head and shoulders, tail head and mammary gland) - biopsy.
Gross pathology
Multiple skin foci with exudation, matting, crusting and fissuring (some changes due to rubbing); haemorrhages (s/c and serosal eccymoses); kidneys finely mottled with multiple pale foci up to 5mm diameter visible on the capsular surface extending through the renal cortex as pale streaks or nodules; enlarged nodes, pale areas in endocardium, pneumonia?
Differential Diagnosis
- Photosensitisation
- Dermatomycosis
- Cutaneous arthropod infestations
- Pox and other viral dermatoses
- Allergic urticarias
Treatment
Nil
Control
Woolly pod and popany vetch must be regarded as potentially toxic to some breeds of cattle when grazed in its actively growing phase.
Remove from the pasture at first sign of disease.
Grazing vetch pastures for only 1 week in every 4.
Case histories
See attached reports.
RVL Wollongbar search revealed 8 cases of possible vetch toxicosis (including my case to follow)
These cases in NSW occurred mainly in Spring and Summer.6/8 were coastal.
Differentials included: renal lymphosarcoma (usually unaccompanied by histiocyte proliferation with syncitial cell formation and eosinophil infiltration).
References
- PAW Harper, RW Cook, PA Gill, GC Fraser, LM Badcoe, JM Power — Australian veterinary journal Vol 70 No 4 April 1993
- RJ Panciera, DA Mosier, JW Ritchey — journal of veterinary Diagnostic Investigation 4:318-325 (1992)
- Case IV — 98 — 1045 (AFIP 2641073)
- B Johnson, J Moore, LW Woods, F.D Galey — Journal of veterinary Diagnostic Investigation 4:362-363 (1992)
- RJ Panciera, l Johnson, B Osburn — JAVMA Vol 148 No. 7
- BR McGufficke, PD Cregan, WJ McDonald — Agfact P2.5.9 1987
- Panciera RJ — in effects of poisonous plants on livestock (1978)
- GK Saunders, DJ Blodgett, TA Hutchins, RM Prater, JL Robertson, PA Friday, WK Scarratt — Journal of veterinary Diagnostic Investigation 12: 269-271 (2000)
- RL Peet, JJ Gardner — AVJ Vol 63, No. 11, November 1986
- HJ Brewkink — the Veterinary Record, September 2, 1978 11. GW Thomas — In practice November 1979
Vetch Case report #1: Gum Flat
History
29/7/03 previously healthy big fat homebred Black Angus — on woolly pod vetch, clover and dry natives for 2 months (paddock has been shut up since March and now they have the run of the property — gates left open) — property supered and was previously a piggery.
Had been significant autumn rain during March. Moved location 2 months previously (came from bundarra during the drought when they had been poor); 5/32 dead cattle so far — unresponsive to antibiotics (Penicillin) — die with haemorrhage from rectum following period of recumbency and weight loss.
Was sudden death 8-10 weeks ago (3rd calf cow) when feed was coming on in February, but cases since then have been younger.
Clinical signs
Agitated, aggressive; RR 32; HR 80; T 40; hair loss and pruritis around face, neck, tail head and udder — progressing to tarry diarrhoea, visual impairment, staggering, weight loss.
Gross pathology
Excoriated, raw lesion tail head, multiple dermal lesions planum nasale; PM: enlarged, firm pale appearance of liver with rounded borders; rumen full of dam water (where it was found); very jaundiced carcase; kidney cortex pale with dark corticomedullary junction; heart enlarged and pale; lungs emphysaematous and oedema interlobular; congestion and numerous raised areas.
Laboratory Results
Chemistry
Elevated GLDH, urea, Creatinine, Phosphorus.
Decreased protein, albumin, globulin; anaemia.
Histology
Eosinophilic granulomatous interstitial nephritis, myocarditis and portal hepatitis consistent with vetch poisoning.
Dermatitis, eosinophilic, granulomatous, chronic-active, severe.
Treatment Options
NIL — once cattle show these symptoms they invariably die. May die after subsequent exposure to the vetch pasture.
Control Options
Problems have been avoided in some cases by grazing vetch pastures for only one week in every 4.
Vetch Case report #2 Gravesend
History
11/11/03 Mixed herd of cows strip grazing paddocks containing Lucerne, ‘Russian vetch (later identified as Vicia villosa ssp eriacarpa)’,natives, liverseed grass and Patterson’s curse seen (green cestrum and Turkey bush had also been observed); owner reports orange urine with one beast.
One poll Hereford cow found dead after moving into a paddock containing Bishops weed (and this was thought to have caused photosensitization by the owner). Vaccinated 3 months prior and drenched 6 months prior.
Post-mortem beast #1
Autolysed: Bloody lungs, blood at nostril, gall bladder enlarged, necrotic, purulent material in mammary gland and uterus (purulent material oozing from teat canal); liver swollen with rounded edges?; spleen enlarged with some haemorrhages under capsule and autolysed consistency; dry omasum with some haemorrhage; liver multiple small yellow foci; kidney red at one pole; uterus contained brown purulent material — bladder empty and no signs of scouring.
Laboratory beast #1
Haemogram within normal range. Acute necrotizing mastitis (probably staphylococcal). Acute granulomatous cortical adrenallitis (degenerate granulocytes).
Clinical signs beast #2
(black and white cow ’ dairy?):
Elevated temperature, scouring 9contains mucus), tendency to charge, galloping heart rate, drooling at the mouth, depression, bug-eyed appearance, shade-seeking and inflamed non-pigmented skin (photosensitization?); polyuria, dyspnoea, hair loss and dermatitis; inflamed and full mammary gland; epiphora, conjunctivitis?; shade seeking ; lethargy progressing to recumbency.
Gross pathology beast #2
Orange s/c fat, enlarged orange heart, marked pulmonary emphysema (+/- fibrosis); distended gall bladder, liver swollen with thick capsule (pale) bladder wall thickened and inflamed?; dry rumen and omasum; inflamed lining intestines (linear pattern); kidney deep red and mottled; hair loss over mainly limbs and face.
Laboratory beast #2
Acute and chronic mastitis. Granulomatous nephritis. Vascular neutrophilia. Skin showed moderate orthokeratotic hyperkeratosis.
Outcome
Other animals (including shorthorns) with diarrhea and mild illness.
Comment
Sounds very similar to ‘Pyrexia with dermatitis in dairy cows’ by Gruffydd Wyn Thomas In Practice 1979.