Difficulty passing urine (urinary retention): Taking jimson weed might make this condition worse.
Rissech, Payret M. and Garcia, Tornel S. [Datura stramonium poisoning]. Med.Clin.(Barc.) 11-25-1979;73(9):397. View abstract.
How does it work?
Thompson, H. S. Cornpicker’s pupil: Jimson weed mydriasis. J Iowa Med.Soc. 1971;61(8):475-477. View abstract.
The appropriate dose of jimson weed depends on several factors such as the user's age, health, and several other conditions. At this time there is not enough scientific information to determine an appropriate range of doses for jimson weed. Keep in mind that natural products are not always necessarily safe and dosages can be important. Be sure to follow relevant directions on product labels and consult your pharmacist or physician or other healthcare professional before using.
Lopez, I. A. Intoxication by datura stramonium. Ohio.State Med.J 1978;74(5):300-301. View abstract.
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Datura stramonium(jimson weed)
Jimson weed is a plant from the Solanaceae family
characterised by its malodorous leaves, large tubular flowers
and ovoid spiny fruit capsules. Jimson weed may be grown as
an ornamental plant or found as a weed across Europe
(Anadón et al. 2012). The plant is entirely toxic and contains
tropane alkaloids which possess strong anticholinergic
properties (Soler-Rodríguez et al. 2006). Because Jimson weed
is rarely consumed by horses in the pasture due to poor palatability, poisoning usually occurs when the plantcontaminates hay (Naidoo 2012). Toxicity in horses usually
results soon after ingestion and is related to the amount
ingested and the alkaloid concentration (Naidoo 2012).
Common clinical signs include tachycardia, mydriasis, dry
mucosae and convulsions, but severe, intractable impaction
colic is the predominant sign of horse intoxication (Botha and
Naudé 2002; Naidoo 2012). In an equine centre in Toledo, Spain, a jimson weed
poisoning episode occurred as a result of ingestion of hay
grossly contaminated (up to 51% by weight) with the prickly fruit
and stem of the plant. Colic was the most remarkable clinical
sign observed in affected horses and one horse died from acute gastric dilatation and rupture (Soler-Rodríguez et al.
2006). In Bulgaria, an outbreak of jimson weed poisoning
involving 34 horses after ingestion of harvested ensiled corn heavily contaminated with freshly cut jimson weed, was
reported (Binev et al. 2006a). Clinical signs included mild
hyperthermia, mydriasis, dry mucosae, tachycardia, polypnoea, dyspnoea, acute gastric distention and severe
intestinal gas accumulation due to adynamic ileus, anorexia,
lack of defaecation, thirst and urination (Binev et al. 2006a).
Specific haematological changes such as
hyperchromaemia, erythrocytosis, increased haematocrit
value and low erythrocyte sedimentation rate were observed
and a normalisation of these parameters within 4–5 days of exposure was indicative of the favourable issue of intoxication
(Binev et al. 2006b). Post mortemanalysis revealed toxic liver
dystrophy and extensive dystrophic and necrotic changes in
the kidneys and myocardium (Binev et al. 2006a).
Taxus baccata(European yew)
European yew (Fig 3) is an evergreen tree or shrub from the
Taxaceae family found across much of Europe. In France and Belgium, European yew is the most significant poisonous plant
for horses (Chandes 2002; Berny
et al. 2010; Vandenbroucke
et al. 2010) and cases have also been recorded in Italy (Caloni
et al. 2013) and Switzerland (Curti et al. 2009). With the
exception of the fleshy red aril around the seed, all parts of the
plant contain taxine alkaloids and are extremely poisonous. Irritant volatile oils are also found throughout the plant
(Anadón et al. 2012). Taxine alkaloids are cardiotoxic and
capable of causing hypotension, bradycardia and depressed
atrioventricular conduction (Anadón et al. 2012). Horses are
suspected to be the most susceptible species to European
yew toxicosis. Ingestion of 200–400 mg/kg bwt of yew leaves
has been reported to be the minimum lethal dose for horses
(Ogden 1988; Tiwary et al. 2005; Wilson and Hooser 2012).
Clinical signs of poisoning include nervousness, trembling,
dyspnoea resulting from severe colitis, ataxia, diarrhoea,
bradycardia, convulsions and collapse, but sudden death
(24 h or less depending on the amount ingested) due to acute
cardiac arrest is usually the most common result (Tiwaryetal.
2005; Anadón et al. 2012).
Robinia pseudoacacia (black locust)
Black locust (Fig 4) is a fast-growing deciduous tree from the
Fabaceae family, native to North America, but widely
cultivated and naturalised in Europe. Horses are the animals most susceptible to the effects of black locust (Vanschandevijl
et al. 2010). Poisoning may result from the ingestion of roots,bark, sprouts, seeds and pods (Anadón et al. 2012). The
primary toxic principle is the toxalbumin robin (Botha and
Naudé 2002). The glycoside robitin and alkaloid robinine are also found throughout the plant (Vanschandevijl et al. 2010).
Clinical signs usually develop 1–2 h after ingestion and seem to be dose-dependent as small amounts lead to a
gastrointestinal upset and higher doses cause CNS signs
(hyperexcitability) to appear (Uhlig et al. 2008; Vanschandevijl
et al. 2010). The following clinical signs have been reported:
anorexia, lethargy, abdominal pain, diarrhoea (which may be
bloody) or dark and firm faeces, laminitis, weakness to
posterior paralysis, head pressing and absence of menace
response and pupil reflexes (Botha and Naudé 2002; Uhlig
Fig 3: Taxus baccata (European yew). Photograph by C. Cortinovis. Fig 4:Robinia pseudoacacia (black locust). Photograph by C.
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