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- Toxicodendron Mill.
The 15 species of trees and shrubs in this genus are native to eastern Asia and to North and South America.
Plants in this genus have formerly been considered to be species of Rhus L., and this nomenclature is still to be found in the literature. Several members of the genus, particularly Toxicodendron radicans Kuntze and Toxicodendron diversilobum Greene are noted for their variability that is due in part to a presumed reversion to an ancestral condition, and in part to a tendency to hybridise with other species of Toxicodendron growing in the vicinity (Gillis 1971).
The genus Toxicodendron is the most common cause of contact dermatitis in the USA. The species most commonly encountered is Toxicodendron radicans, the poison ivy, but other species may be more important locally.
The sap from crushed leaves of poison ivy and related species, when applied to white paper, will darken on drying. Blackened exudation may also be noticed on bruised plant material. These observations form the basis of the "black spot test" described by Guin (1980a) as an aid to the recognition of these plants.
- Toxicodendron borneense Gillis
- (syn. Rhus borneensis Stapf)
This very rare species has only been found in the state of Sabah in northern Borneo. Gillis (1971) presumes that it contains an urushiol because of his observation that it possesses a resin that darkens with age.
- Toxicodendron diversilobum Greene
- (syns Rhus diversiloba Torrey & A. Gray, Rhus lobata Hook., Rhus toxicodendron L. ssp diversiloba Engl.)
- Western Poison Oak
This species occurs on the west coast of N. America, ranging from Baja California to British Columbia. It is less common in the northern areas of its range. Some hybridisation with T. rydbergii Greene occurs in northern areas (Gillis 1971).
It is recognised as a cause of contact dermatitis (Legge 1921, Curtis 1960, Gross et al. 1975, Craig et al. 1978). The principal constituents of its urushiol are 3-n-penta- and 3-n-heptadec(en)ylcatechols (Corbett & Billets 1975, Gross et al. 1975).
- Toxicodendron nodosum Gillis
- (syns Rhus nodosa Blume, Rhus perakensis Scortech.)
This is quite a rare species occurring in Indonesia and Malaysia. It possesses a toxic effluvium (Gillis 1971).
- Toxicodendron radicans Kuntze
- (syns Rhus toxicodendron L., Rhus radicans L.)
- Poison Ivy, Poison Vine, Markweed, Three-leaved Ivy, Poor Man's Liquid Amber
Several sub-species of poison ivy are recognised, the taxa being distributed in fairly well defined areas. Much of the early research work was carried out on plant material described simply as Toxicodendron radicans, or, more usually, Rhus radicans or Rhus toxicodendron, but at this time many of the sub-species were still considered to be separate species. Listed below are the names of the sub-species together with their previously accepted names and their distribution (Gillis 1971):
- Toxicodendron radicans ssp barkleyi Gillis
- (syn. Rhus villosum Sessé & Moçiño)
This taxon occurs in Mexico and Guatemala.
- Toxicodendron radicans ssp divaricatum Gillis
- (syns Rhus divaricata Greene, Toxicodendron divaricatum Greene)
This taxon occurs in Mexico and the south-eastern corner of Arizona, USA.
- Toxicodendron radicans ssp eximium Gillis
- (syns Toxicodendron eximium Greene, Rhus eximia Standley)
This is one of the more unusual and rare sub-species which is found in south-western Texas and into Mexico.
- Toxicodendron radicans ssp hispidum Gillis
- (syns Rhus toxicodendron L. var hispida Engl., Rhus intermedia Hayata)
Known as Taiwan tsuta-urushi, this sub-species may be found in western and central China and in Taiwan.
- Toxicodendron radicans ssp negundo Gillis
- (syns Toxicodendron negundo Greene, Toxicodendron aboriginum Greene)
This taxon is found in the southern lobe of Ontario, in the Great Lake States, and in the central states and Midwest of the USA.
- Toxicodendron radicans ssp orientale Gillis
- (syns Toxicodendron orientale Greene, Rhus orientalis Schneider, Rhus ambigua Lavallée)
Known as tsuta-urushi, this taxon occurs in Japan and on the Kurile Islands and Sakhalin region of the (former) USSR.
- Toxicodendron radicans ssp pubens Gillis
- (syn. Rhus toxicodendron L. var pubens Engelm.)
This taxon occurs in southern central USA between the Lower Mississippi Valley and eastern Texas.
- Toxicodendron radicans ssp radicans
- (syns Toxicodendron radicans Kuntze, Rhus radicans L., Toxicodendron radicans var littoralis F. Barkley)
This taxon occurs in eastern and south-eastern USA, and in Bermuda and on the Bahama Islands. Specimens have also been found in Nova Scotia.
- Toxicodendron radicans ssp verrucosum Gillis
- (syns Toxicodendron verrucosum Greene, Rhus verrucosa Scheele)
This sub-species occurs in Texas and Oklahoma, USA.
Poison ivy is the most common and widespread species of the Anacardiaceae. It may be found in southern Canada, all of the USA, throughout Mexico, in Bermuda, in the western Bahamas, in Japan, Taiwan, and western and central China, and on the Kurile Islands and in the Sakhalin region of the USSR (Gillis 1971). The early literature refers to the plant as Rhus toxicodendron L. It was introduced into Britain (Nicholson 1899, Nott 1910, Shadbolt 1916) and, according to Anon (1908), was grown in a fairly considerable number of gardens, but instances of trouble rising from it were somewhat rare and scattered. Anon (1908) further noted that most cases seemed to occur in the south-east of England where summers are hottest. Poison ivy is now likely to be found in Britain only in botanic gardens. It has also been introduced into western Europe (Giuseppe 1928, Beurey 1980b), South Africa (Ross 1959), Australia (Aplin 1966), New Zealand, Tasmania (Cleland 1914b, Maiden 1914, Nurse 1966, Turner 1972, Apted 1978), Bulgaria (Topalov 1957), Poland (Lukowska 1971), and Russia (Solomatin 1962). However, the plant has not yet developed a reputation as a common noxious weed outside the North American continent, except perhaps in Australia, where it has been planted for the colour of its autumn (fall) foliage and has caused dermatitis in homeowners (Nurse 1966, Apted 1978), and in eastern USSR Dermatitis in the USSR is produced by T. radicans ssp orientale (Khlebovich 1960, Emeliyanov 1974).
Poison ivy as a cause of contact dermatitis has been described on many occasions (McNair 1923, Curtis 1960, Maibach & Epstein 1964, Whiting 1971, Ducombs & Texier 1974, etc.). Even an anecdotal biographical history of poison ivy has been published (Rostenberg 1955). It is estimated that in excess of 50% of the population of the USA is sensitive to poison ivy (Kligman 1958a), this being either a primary sensitivity to T. radicans or a cross-sensitivity to the almost identical sensitisers in other locally common Toxicodendron species.
The allergenic material, termed urushiol, is contained within intercellular secretory canals in the stems, leaves, and petioles (Eggers 1974). On exposure to the air, the sap turns black, the reaction requiring oxygen, moisture, and an oxidase (McNair 1923). Blackening of the sap does not render it inert (Kligman 1958a). Heavy contamination of the skin (or fomites) with sap can produce a black lacquer deposit within a few hours (McNair 1923, Mallory et al. 1982). The urushiol is also found on the surface of the leaves and is thus readily accessible. In contact with the eye, it may cause swelling of the eyelid and conjunctivitis. If the cornea is involved, pain, photophobia, and blepharospasm may be experienced (Grant 1974). Brushing past the foliage with unprotected skin may result in a delayed reaction exhibiting a highly typical linear pattern of vesicular dermatitis. One close encounter of this sort is usually sufficient to induce sensitivity. It has been demonstrated that young leaves contain greater quantities of urushiol than do older leaves (Craig et al. 1978, Baer et al. 1980).
Direct skin contact with plant material is not a necessary prerequisite. The urushiol, if allowed to contaminate articles of clothing, animals, tools, etc. may subsequently be transferred to human skin. Even burning the plant material may be hazardous if unburnt particles of the plant, or vapourised urushiol is carried away in the smoke.
The chemical nature of the urushiol has been well studied. The major constituents are 3-n-pentadec(en)ylcatechols, but small amounts of 3-n-heptadec(en)ylcatechols are also present (Gross et al. 1975, Craig et al. 1978, Baer et al. 1980). There is evidence that the relative proportions of the individual constituents vary with the source of the plant material, but this may be in part the inevitable consequence of incomplete identification of the sub-species being studied.
Cross-sensitivity reactions have been demonstrated to many other plants in the genus and family (Keil et al. 1945a, 1945b, 1946, Howell 1959) and to some extent to resorcinol, and to hydroquinone and its monobenzyl ether (Kligman 1958a). Resorcinol sensitive persons are also known to cross-react to hydroquinone (Van der Walle et al. 1982).
- Toxicodendron rydbergii Greene
- (syns Toxicodendron radicans Kuntze var rydbergii Erskine, Rhus toxicodendron L. var rydbergii Garnett, Rhus rydbergii Small)
- Rydberg's Poison Ivy
This is the most northerly ranging species in the family Anacardiaceae. It ranges from 52° Lat. in the southern provinces of Canada into the northern latitudes of the USA, but also occurring down through the central and southern states of the USA to north-eastern Arizona and western Texas. Hybrids with Toxicodendron diversilobum Greene and with certain sub-species of T. radicans Kuntze may also be observed (Gillis 1971).
This species is noted as a cause of delayed contact dermatitis (Gross et al. 1975).
- Toxicodendron striatum Kuntze
- (syns Rhus striata Ruiz & Pavón, Rhus juglandifolia Willd.)
- Poison Sumac, Manzanillo, Hinchador, Amché, Palo de Compadre
This small tree grows in Central America and in northern South America. The common name manzanillo is applied both to the tree and its timber. The name manzanillo is also applied to the botanically unrelated Hippomane mancinella L. (fam. Euphorbiaceae). Hinchador is the name used in Costa Rica, and means "the sweller". The shrub is of the right height to brush easily against the face and hands (Standley 1927).
It has caused severe allergic contact dermatitis with blistering and oedema (Dahlgren & Standley 1944, Standley & Steyermark 1949, Hurtado 1965). In one case (Hurtado 1965), the dermatitis developed two days after sawing the wood and persisted for two weeks. von Reis Altschul (1973) found an herbarium note attributing a case of dermatitis to a specimen of Rhus juglandifolia collected in Guatemala.
Sprague (1921) wrote that Humboldt and Bonpland were sceptical as to the alleged ill-effects of remaining under the tree without actual contact taking place: "Lac aquosum, quod arbor stillat, in cute post 2 vel 3 dies ejicit pustulas similes variolis, quamobrem incolae non solum succum sed etiam umbram arboris metuunt, fabulantes eam noxiam esse, praesertim quando post pluvias sol arborem calefecit. Sunt tamen, qui nec post contactum, nec post tritum ullum sentiunt effectum adversum." Triana, on the other hand, was satisfied that the popular idea of the shade of the tree being dangerous was well-founded: "Le Rhus juglandifolia exerce une actione curieuse sur l'homme: l'ombre seulement de l'arbre ou ses émanations, son contact, son approche, la fumée de son bois, produisent, suivant les individus, une irritation avec gonflement accompagné de démangeaisons. L'intensité de ces accidents est presque nulle pour certaines personnes, plus ou moins grave pour l'autres. L'un de nous (Triana) a éprouvé ces effects en récoltant et en desséchant la plante; même action sur une autre personne qui l'avait touchée. Les gens du pays combattent ces affections en faisant des frictions avec de la graisse ou avec de la crème" (Ann. Sc. Nat. sér. 5, xiv. 289;1872). Triana's evidence as to the poisonous nature of Rhus juglandifolia seems to have been overlooked (Kew Bull. 1898, 100).
The urushiol of this species has been shown to contain a mixture of 3-pentadec(en)ylcatechols (Nakano et al. 1970). The oleoresin shows haemolytic activity on human red blood cells (Hurtado et al. 1965).
Cross reactions have been reported to Toxicodendron radicans Kuntze, Lithraea caustica Hook. & Arn., Mauria puberula Tul., and Toxicodendron vernicifluum F. Barkley (Hurtado 1968).
- Toxicodendron succedaneum Kuntze
- (syn. Rhus succedanea L.)
- Wax Tree, Japanese Wax Tree
Native to China and Japan, this plant is cultivated locally for the fruits from which a wax (sumach wax, Japan tallow, vegetable wax) is extracted for use in varnishes, polishes, ointments, and plasters (Usher 1974). The plant is listed as a popular species for cultivation as a bonsai, a Japanese art form produced by artificially stunting the growth of a tree (Murata 1964).
The leaves, fruit, and bark can cause dermatitis (Burry 1969, Guimaraes et al. 1960, Behl et al. 1966. The sap is vesicant (Chopra et al. 1949). The wax has caused dermatitis in workers handling fabrics waterproofed with it (Schwartz et al. 1957). This plant, and not T. radicans, is the commonest cause of "poison ivy dermatitis" in Australia (Czarnecki et al. 1982). The Japanese wax tree was voluntarily withdrawn from sale by several South Australian nurserymen after six or seven workers in one nursery developed dermatitis through handling the plant (Aplin 1976).
Majima (1922b) isolated laccol from this species, and identified it as a 3-heptadec(en)ylcatechol.
- Toxicodendron toxicarium Gillis
- (syns Toxicodendron quercifolium Greene, Rhus toxicodendron L., Rhus toxicarium Salisb., Rhus quercifolia Steudel)
- Eastern Poison Oak, Oak Leaf Ivy
This species occurs widely in south-eastern USA. Taxonomically, it has been the most misunderstood species of the poison ivy complex. Hybrids with certain sub-species of Toxicodendron radicans Kuntze may be found (Gillis 1971).
It is recognised as a cause of delayed contact dermatitis (Gross et al. 1975, Craig et al. 1978).
- Toxicodendron vernicifluum F. Barkley
- (syns Rhus verniciflua Stokes, Rhus vernicifera DC.)
- Chinese Lacquer Tree, Japanese Lacquer Tree
Lacquer from this tree, known variously as Chinese lacquer, Chinese shellac, Japanese lacquer, or ningpo varnish, was used in China as early as 2255 BC but the art of lacquering was not introduced into Japan until about 250 BC (Toyama 1926). The tree was distributed in Japan before 701 AD. At one time, every farmer in certain parts of Japan was obliged to establish plantations of the tree, and taxes were paid in lacquer (White 1887).
The lacquer is obtained by tapping the trees. Incisions are made in the bark, just deep enough to reach the wood. Some lacquer is extracted from felled trees, under water. The latex flowing from the incised trees darkens on exposure to the air. As the quality is highest when the lacquer is light in colour, it is stored in bamboo tubes. A volatile substance is associated with the fresh latex which, because of its poisonous nature, is eliminated from the latex by stirring for several hours in open vessels. The procedures followed in Japan, China, and Burma differ in some particulars (Burkill 1935).
Lacquer dermatitis was described in China as early as 453 BC. A good description was given by Ping-yuan-hon-lun (605–609 AD) in China, and later in Wamyo-rui-ju-sho (923–930 AD) in Japan (Toyama 1918), and also by Zan Yun Fang (c. 600 AD) (Toyama 1926). An early European account of lacquer dermatitis was published by Kaempfer (1712). According to Burkill (1935), the risk of dermatitis to tappers is reduced by the fact that they are a special class or caste of highly skilled workmen.
Toxicodendron vernicifluum and its lacquer can give rise to dermatitis at all stages from the initial collection of the latex to the final application of the lacquer, and even, it appears, a thousand years later - lacquer from a Chinese jar, which had been buried for about a millenium, caused dermatitis (Toyama 1918). Contact dermatitis from handling the plant itself has been reported by Buraczynski (1903), by Bauer (1940), and by Rost (1914). A girl in North Vietnam developed dermatitis after wearing shoes made of the wood (Holcik 1959). Bullous occupational dermatitis with systemic illness was reported by Antonev et al. (1964). Contact dermatitis from the lacquer has been far more frequently reported because so many such cases have occurred in Western Europe or North America, and because the sources of contact are sometimes exotic and unexpected. Men engaged in hanging embossed Japanese wallpaper are said to have been affected (White 1887). Some individuals become so sensitive that they cannot pass a furniture shop where articles are being varnished without being affected. Others, less sensitive, react only on contact with freshly varnished furniture (Allen 1887). In Hawaiian pineapple factories, cans that were passing through a bath containing one part of lacquer to five parts of gasoline caused dermatitis in those handling the cans (Wayson 1923). A seller of canes used for toy flags developed dermatitis that was attributed to the lacquer on incomplete evidence (Pusey 1923). Lacquered lamp shades have also been incriminated, but inconclusively (Weber 1937). Lacquered bracelets and boxes have caused dermatitis in woodworkers and others (Goldstein 1968). The lacquer on Japanese rifles caused dermatitis in American servicemen sensitive to poison ivy (Toxicodendron radicans Kuntze) (Hinman 1946, Coomber 1947). Contact with a recently varnished bar in Japan caused dermatitis in 12 American officers; it is possible that some were previously sensitised to poison ivy (Etler 1951). In Scotland, subjects sensitive to poison ivy developed dermatitis after contact with varnished boxes (Murrell 1896). Lacquer used as a spray has caused dermatitis (Anon 1931). For 15 years, a woman had suffered a recurrent dermatitis of the fingers, palms, and wrists; the cause was proved to be lacquered soup bowls (Hollander & Shelton 1937).
When used for firewood, the smoke contains highly irritating particles (Holcik 1959).
The clinical features are almost infinitely variable, according to the mode and sites of contact, and the degree of sensitivity. A study of affected workers in a factory (Riedel 1940) illustrated some of the problems. Little (1924) noted that those who work with the varnish seem to acquire immunity to its actions. She also recorded that the oil expressed from Thea sasanqua (tea oil; see Camellia sasanqua Thunb., fam. Theaceae) relieves the itching and is used by lacquer workers each evening to remove every trace of the varnish from their hands and arms.
Majima (1922a) found the lacquer to contain 3-pentadec(en)ylcatechols, the individual constituents of which were characterised by Sunthankar & Dawson (1954). The urushiol constitutes 35–70% of Chinese lacquer, and a somewhat greater proportion of Japanese lacquer (Toyama 1923, 1926, Toyama & Usuba 1926).
Cross-sensitivity to other anacardiaceous plants has been mentioned above. It has been investigated by Howell (1959); the range is wide but variable. Sturua (1963) found sensitivity to T. vernicifluum to be specific with no cross-sensitivity to T. succedaneum or T. radicans; tests were carried out with slices of twigs of the plant.
- Toxicodendron vernix Kuntze
- (syns Rhus vernix L., Rhus venenata DC.)
- Poison Sumac, Poison Dogwood, Poison Elder, Poison Tree, Poison Wood, Poison Ash, Swamp Sumac
This species occurs on the North American continent from southern Quebec through the USA to Florida, in the eastern third of the country (Gillis 1971). Stevens & Warren (1907) noted that on wounding the tree, a pale cream-coloured thick poisonous juice exudes in abundance, which begins to darken at once and finally becomes black.
T. vernix is recognised as a cause of contact dermatitis (Ducombs & Texier 1974, Gross et al. 1975, Craig et al. 1978). Gross et al. (1975) have shown that the urushiol contains a series of 3-n-pentadec(en)ylcatechols.
The clinical features of the dermatoses caused by members of the Anacardiaceae have been described in the individual monographs above. However, the syndromes induced by the more potent sensitisers share certain distinctive features. In previously unsensitised individuals, exposure is followed by a latent period of 9–14 days before dermatitis appears (Biberstein 1929, Field & Sulzberger 1935). In sensitised individuals, symptoms develop from a few hours to several days after contact; Guin (1980b) reports that he observed reactions as early as 4 days and as late as 15 days after identical applications of the sap of Toxicodendron radicans ssp negundo to various parts of his own forearm. Inadvertent application of the sap from T. radicans ssp divaricatum on a pair of contaminated sunglasses to parts of the face elicited a reaction within 5.5 hours.
The first symptom is intense pruritus; papules soon appear, often in a linear pattern in the case of poison ivy contact, and these evolve into vesicles or bullae. Any and all parts of the body may be affected in severe cases, the allergenic material being easily carried by the fingers to sites remote from the points of initial contact. The allergenic material is not, however, present in the vesicle fluid. Areas of thicker skin are less susceptible. Except in regions well protected by hair, oedema may be considerable, and particularly so on the eyelids and male genitalia.
The evolution of the eruption occurs in crops, affecting firstly the sites where most allergen has been absorbed, and then successively the less heavily contaminated sites or sites of thicker skin. The dermatitis has commonly reached its full extent after 48 hours. Healing occurs within 2–3 weeks unless there is re-exposure to the offending allergen. Scarring does not occur unless secondary infection has been introduced. Hyperpigmentation is a common complication of poison ivy dermatitis in black skin, uncommon in Caucasian skin (Fisher 1977, Taub 1965); hypopigmentation can also occur (Kligman 1958a).
Perianal dermatitis from eating poison ivy leaves was described by Dakin (1829). If plant material is ingested, there may be vomiting, diarrhoea, and neurological symptoms simulating atropine poisoning - drowsiness or stupor, convulsions, delerium, fever, and pupillary dilatation. Sensitive patients challenged with an extract of poison ivy orally developed degranulation of circulating basophils within an hour (Shelley & Resnik 1965). Nephritis too may complicate poisoning, either following ingestion or after massive cutaneous vesiculation (Templeton et al. 1947, Rytand 1948). Acute or chronic glomerulonephritis has occurred during Toxicodendron dermatitis (Devich et al. 1975, Schaffer et al. 1951, Rytand et al. 1948); glomerular deposits of complement and the presence of circulating immune complexes suggested a type III hypersensitivity mechanism. One case of erythema multiforme associated with poison ivy contact dermatitis has been reported by Schwartz & Downham (1981). This complication was not associated with any systemic symptoms, and the possibility of it arising from the treatment of the dermatitis with antihistamine was considered.
Contact sensitivity to Toxicodendron is most commonly acquired in childhood or early adult life, and tends to decline in later life. Ninety percent of those exposed become sensitised, and such exposure is the commonest cause of contact dermatitis in the USA. There is no evidence for familial predisposition to acquiring sensitivity, but atopic individuals may be less susceptible (Jones et al. 1973). It has been estimated that perhaps 50% of the population of the USA has acquired sensitivity to poison ivy and other urushiols (Kligman 1958a), and only 10–15% of the population is truly immune (Epstein 1973). There is no evidence that children are any more or less susceptible than adults; incidence of sensitivity in all the younger age groups is a measure of exposure to the allergenic material (Straus 1931, Epstein 1961). Immunity in Asiatics has been ascribed to exposure to Mangifera in early life (Epstein & Claiborne 1957).
Various methods of hyposensitisation have been advocated, including the application of gradually increasing doses to the skin (Maisel 1932), and graduated dosage orally of 10% cashew nut oil (Kligman 1958b). A patient's attempts to desensitise himself by chewing poison ivy leaves caused stomatitis, and dermatitis of the face and perianal skin (Silvers 1941). Oral hyposensitisation was demonstrated in some individuals (Kligman 1958b) and confirmed in a study of larger groups (Epstein et al. 1974). An adequate quantity of purified urushiol must be administered during a sufficiently long period of time, and observation is required for cutaneous and systemic complications (Shelmire 1941, Schaffer et al. 1951).
Experiments in guinea pigs (Baer et al. 1966) showed that the capacity of the urushiols to induce delayed contact sensitivity depends on the nature of the ring substituents. Catechol and 3-n-alkylcatechols were equally effective in inducing sensitivity, but the degree of sensitivity as well as cross-reactivity depended upon the length of the alkyl chain. Dermal toxicity was unrelated to sensitising capacity (Baer et al. 1967). Further studies (Baer et al. 1968) emphasised the importance of the alkyl chain in determining antigenic specificity and non-reciprocal cross-reactivity. Cross-reactivity within the Anacardiaceae was studied in guinea pigs by Lima (1953) who used the oleoresin from Lithraea molleoides Engl. as the primary sensitiser. The guinea pigs were tested with the oleoresins of 12 species from 7 genera. Only Lithraea brasiliensis Marchand, Lithraea caustica Hook. & Arn., and Toxicodendron radicans Kuntze gave definite cross-reactions. In a clinical study involving both open and closed patch tests in patients primarily sensitised to poison ivy (Howell 1959), all patients showed cross-sensitivity to poison oak, whilst cross-sensitivity to other genera occurred frequently in open patch tests, and very frequently in closed patch tests. Cross-sensitivity within this family must be considered to be general unless it has been positively excluded. Cross-sensitivity to Ginkgo biloba L. (fam. Ginkgoaceae) and to various members of the family Proteaceae should also be considered to be distinctly possible. More obscure sources of cross-sensitivity might be found among certain phenolic materials used medicinally, including resorcinol, hexylresorcinol, Castellani's Paint, etc. (compare Kligman 1958, Caron & Calnan 1962, Keil 1962, Cronin 1973a, Marks & West 1978, Waddell & Finn 1981, Burrows & Irvine 1982), wheat bran (Wenkert et al. 1964), and also certain alkyl quinones (Hausen 1981).
The following suggestions for treatment of poison ivy and other urushiol-elicited dermatoses are adapted from Mitchell (1982). The aim of the treatment is to make the patient comfortable whilst the dermatitis resolves:
Mild to moderate dermatitis
1. Provide continuous cold, wet compresses of tap water or Burow's solution 1:40. A modified Burow's solution may be prepared conveniently by dissolving one Domeboro(TM) Tablet in 1 quart (a little over 1 litre) of water. When the eruption is widespread, three 10 minute cool baths daily have a soothing effect.
2. As the vesiculation subsides, change to topical applications of calamine lotion mixed in equal parts with water.
3. As the skin begins to dry, change to topical application of a corticosteroid cream. Such creams, however, have little more that a placebo effect in poison ivy and similar dermatoses.
The simpler the topical therapy is kept, the better. Avoid calamine lotions with additives, topical antihistamines, and "-caine" compounds, otherwise surprisingly violent exacerbations may ensue. Relief of pruritus by oral medication is notoriously difficult and varies in efficacy from one patient to another. Aspirin in divided doses to a total of 3000 mg per 24 hours is often helpful and is probably not prescribed often enough for the relief of itching. The antipruritic effect of antihistamines appears to be in proportion to their sedative effects. There are many types of antihistamines to choose from - the oral administration of diphenhydramine hydrochloride 50 mg at night and in addition chlorpheniramine maleate 8–12 mg three times daily is recommended. It is important to warn the patient of the sedative effect of this treatment, particularly in respect to driving a motor vehicle, working with moving machinery, etc. If antihistamines are taken, alcohol should not be taken.
Localised oedema, which may result from involvement of the face, neck, and anogenital area, may indicate a need for oral corticosteroid therapy (see below).
The patient suffers agonising discomfort. He should rest at home in loose-fitting clothing and avoid overheating, caffeine, and alcohol. Compresses or bathing, as noted above, should be used for 10 minutes every 2–3 hours. A dose of 40 mg prednisolone daily, in divided doses, is prescribed, to be taken with milk between small, frequent meals. This is adequate treatment for some cases. For severe cases, experienced dermatologists have recommended an even larger dose of corticosteroid (80 mg of prednisolone) in the first 24 hours. In order to obtain response in 98% of patients, a daily dose of 80–100 mg is required. The dose is gradually reduced during 7–10 days. Flare-ups are frequent if withdrawal is too rapid, or if alternate day dosage is used. It is better to taper the dose during 20 days. Such short courses of corticosteroid therapy carry the usual risks, but the risks of such short-term therapy in otherwise healthy individuals are negligible compared with the risks of prolonged corticosteroid therapy for skin diseases. In the treatment of acute dermatitis with systemic corticosteroids, one should be concerned principally about the patient who may have peptic ulceration. A significant complication is central nervous stimulation - the patient cannot sleep.
No-one should administer poison ivy or similar such extracts in the management of the acute disease. This is ill-advised and immunologically unsound. Such administration may produce no effect, or the dermatitis may be aggravated.
The symptoms of severe ocular involvement may be relieved by topical use of atropine and corticosteroids (Grant 1974).
The patient is usually better off at home. Pyoderma secondary to the dermatitis, and principally consisting of boils, may be managed by standard methods including appropriate systemic antibiotic therapy with culture organism sensitivity control.
Many methods have been devised to destroy the offending plants (Chesnut 1896, Byram 1931, Crooks & Klingman 1968, Maibach & Epstein 1964, Gillis 1975) or to otherwise protect the patient, but none is wholly effective (Howell 1943, Birmingham 1969). Recurrence or prolongation of the dermatitis is caused by re-exposure to urushiol or possibly to some other immunochemically related material. Instruct the patient to have potentially contaminated clothing, including shoes, towels, sheets, sleeping bags, and other items washed or cleaned. A pet dog should also be washed several times. The allergenic oleoresins of poison ivy and related plants are non-volatile oils which oxidise very slowly, if at all, in the absence of moisture. Children, animals, rocks, vegetation, tools, athletic or hiking equipment, furniture, automobiles and their accessories, etc., may transfer allergen to sensitive persons. Instruction on the nature and botanical distribution of poison ivy and other relevant members of the families Anacardiaceae, Ginkgoaceae, and Proteaceae is a vital prophylactic measure. A physician would, therefore, benefit by possessing a book or reprint of a paper with coloured pictures of locally suspect species to show to patients (two examples of useful papers: Guin & Beaman 1980, Guin et al. 1981). Avoidance of exposure may, nevertheless, prove to be impossible.
Barrier creams, topical detoxicants, and the like give inadequate protection. Thorough washing after exposure does not prevent a severe dermatitis in highly sensitive persons; it may, however, reduce the reaction in those who are less sensitive. Harsh soaps and vigorous scrubbing offer no advantage over simple soaking in cool water. The popular "herbal" remedy for the prevention of poison ivy dermatitis in the USA involves application of the sap of the jewelweed (Impatiens biflora Walt., fam. Balsaminaceae). This has been shown to be no more effective than water alone in preventing dermatitis (Guin & Reynolds 1980).
Immunological prophylaxis is sometimes possible. It is however a rigorous procedure demanding supervision by a physician since the danger of untoward effects is considerable. Large quantities of active allergens must be ingested over long periods of time, and, when therapy is stopped, sensitivity rapidly returns. This form of treatment should be reserved for very sensitive persons who, for reasons of work or environment, cannot avoid exposure to the allergens. Of the experimentally proven agents (crude poison ivy oleoresin, synthetic pentadecylcatechol, and cashew nut shell oil), only the crude poison ivy oleoresin is available at this time. Many companies supply it in over-the-counter preparations, but these are either wholly inactive or are so dilute as to be valueless for prophylaxis. A reliably active oleoresin is supplied by Hollister-Stier Laboratories (107 South Division Street, Spokane, Washington 99202). The standard desensitisation kit contains 15 ml each of 1:100, 1:50, and 1:25 dilutions of oleoresin in corn oil (a total of 1050 mg of allergen). Instruction sheets are enclosed in the package. The important point is to increase the dose of the allergen in a dropwise fashion as rapidly as the patient's tolerance allows. Onset of itching means that the increment is too great. When this happens, reduce the dose by 2–5 drops; after pruritus subsides, increase it again. Other untoward reactions such as dermatitis, urticaria, or pompholyx may occur if the cardinal symptom of pruritus is ignored or is not recognised. Little is known about the systemic toxicity potential of such regimens. The preparation may occasionally cause pruritus ani; dividing the dose tends to reduce this complication. The total dose for hyposensitisation varies between 2000 and 3000 mg. After the first set is completed, 1:25 dilutions should be used in doses of 1–1.5 ml daily. Adequate hyposensitisation is determined by patch test responses (experimental) and clinical observation (practical). The procedure may be started in late winter and continued as a maintenance dose until July. Clinically, patients have some protection until September or October, when the opportunity for exposure usually dwindles. Sensitivity requires about 6 months to return to pre-treatment levels. Some persons must remain on therapy all the year round.
In general, "treatment is worse than the disease", and thoughtful, educated avoidance of exposure to the offending material is the mainstay of prophylaxis.
The possibility of an improved method of prophylaxis being developed has arisen following publication by Watson et al. (1981) of some immunologic studies on guinea pigs. It was found that the development of contact sensitivity to poison ivy urushiol was inhibited by intravenous injection of the diacetate esters of poison ivy and poison oak urushiols two weeks prior to attempted sensitisation. By a similar technique, sensitised guinea pigs were rendered hyposensitised by injection of urushiol diacetates. Concomitant hyposensitisation to poison sumac urushiol and cashew nut shell liquid was also observed.