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| Journal of the New Zealand Medical Association,
10-August-2007, Vol 120 No 1259
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Heracleum mantegazzianum and
Toxicodendron succedaneum: plants of human health significance in
New Zealand and the National Pest Plant Accord
José G B Derraik
The National Pest Plant AccordThe National Pest Plant Accord (NPPA) is a voluntary and
cooperative agreement between the Nursery and Garden Industry Association,
regional councils, and government departments with biosecurity responsibilities
(primarily the Ministry of Agriculture and Forestry [MAF] and the Department of
Conservation [DOC]).
The NPPA seems to be the only agreement of its kind in
existence (M Newfield, personal communication, 2006). All plant species listed
under the NPPA are automatically declared unwanted organisms under the
Biosecurity Act 1993, pursuant to section 2(1). This prevents their legal sale,
propagation, or distribution within New Zealand.
When listing plants emphasis is given to species that are
invasive, pose the greatest level of threat, are primarily spread by people, and
have limited actual distribution relative to their potential
distribution.39
The NPPA came into effect for the first time on 1 October
2001. It was revised in 2006, with signatory parties renewing their commitment
to the Accord for another five years. Although the Accord is not a binding
contract, it is intended to carry the same effect as a Memorandum of
Understanding between the signatory parties. As a result, these parties share
responsibility to promote compliance with the rules of the Accord, and regional
councils have specific responsibility for actively monitoring compliance (A
Harrison, personal communication, 2006).
There were 202 species initially considered for inclusion in
the NPPA during the 2006 revision of the Accord. The final approved list
includes 109 individual plants species and all the species present in four
genera.40
Following the creation of Biosecurity New Zealand within MAF
in 2004, the Ministry has acquired greater biosecurity accountabilities
including an oversight role for the biosecurity system and explicit
accountability to protect the full range of societal values through its
activities. As a result, MAF aims to ensure that human health values are
adequately considered within its routine activities. Therefore, under this new
role, apart from the potential impact on the environment and the economy, MAF
Biosecurity New Zealand (MAFBNZ) was also accountable for evaluating the
potential human health significance of all plants being assessed for inclusion
in the NPPA.
Several introduced plants species in New Zealand can cause
adverse reactions in humans via skin contact—e.g. Urtica
dioica (perennial nettle) and Ficus carica (fig
tree)—with a number of other species being poisonous if plant parts are
ingested. However, two plant species in particular were evaluated for the NPPA
as a result of their public health significance and the possible need to
officially control them: Heracleum mantegazzianum Sommier et Levier
(Apiaceae) (giant hogweed, cow parsnip, wild parsnip) and Toxicodendron
succedaneum (L.) Kuntze (Anacardiaceae) (rhus tree, wax tree, Japanese wax
tree).
Both species are introduced (i.e. not native) to New
Zealand, and their adverse effects to human health have been widely documented.
They are, for example, included in the list of plants in New Zealand that are
poisonous to children compiled by Landcare
Research.37
In this article, the relevance of these two species to human
health are discussed, including symptoms and treatment, as well as the final
decisions of the NPPA process and some possible management measures.
Heracleum mantegazzianumBackground—Heracleum
mantegazzianum is a giant herb that varies in height from 2.0 to 5.0 m, and
which may live for several years.1 It is a
popular plant in gardens due to its attractiveness (Figure
1).2,3 Heracleum mantegazzianum is
native to Asia, more specifically the western Caucasus but it is now widespread
in Europe1 and North
America.4
In the United States this species escaped from cultivation
and has become a public health hazard—being found in urban, suburban, and
rural settings.5 As a result, H.
mantegazzianum is on the United States federal noxious weed list, which
means that its importation into the country is illegal, as is the interstate and
intrastate movement of this species.6
While H. mantegazzianum appears to be present in
Dannevirke, Napier, Wellington City and in a few scattered localities in
Marlborough, Canterbury, Otago, and Southland,7
its actual current distribution in New Zealand is unknown.
Figure 1. Heracleum mantegazzianum
with its large leaves and flowerheads (Photo courtesy of Rune Aanderaa,
SABIMA)
 Mode of action—The sap of H.
mantegazzianum contains psoralens (furocoumarins) that lead to a relatively
common type of dermatitis: phytophotodermatitis, which is produced by the
interaction of such plant compounds with sunlight on human
skin.8–11 The psoralens are lipid-soluble
and penetrate into the epidermis with ease.12
The photochemical excitation of psoralens is induced by ultraviolet (UV)
radiation, usually within the UVA wavelengths of 320–400
nm.13 Note that the absorption of psoralens
into the skin (and the consequent reaction) is enhanced by high
humidity.14
A detailed study of the mechanisms of phytophotodermatitis
has been provided by Pathak (1986).14 In brief,
two types of toxic reactions occur: one oxygen-independent where the
ultraviolet-activated psoralens bind to RNA and nuclear DNA, and an
oxygen-dependent reaction where the induced compounds cause cell membrane damage
and oedema.11,38
These reactions consequently lead to cell
death.3,11,15,38 This is a phototoxic reaction,
and not an allergic one so there is no immunological response. As a result, no
prior sensitisation is necessary and anybody can be
affected.16 Heracleum mantegazzianum
is one of the main causes of phytophotodermatitis in the United Kingdom and
United States.4
The plant’s clear watery sap is said to exude from all
parts of the plant, so dermatitis is induced via contact with leaves, stem,
seeds, and roots.4 An analysis of furocoumarin
contents indicated that their concentration in H. mantegazzianum plants
was highest in fruit, intermediate in leaves, and low in
stems.15
Nonetheless, touching the plant or brushing against it
appears to be enough to induce exposure to the sap, and all persons that come in
contact with it seem to be affected to some extent. It should be noted that the
content of furocoumarins in the sap of H. mantegazzianum varies with
individual plants, season (being highest in spring), and probably also soil
conditions and climate.2,10,15
Clinical features—The consequent
symptoms of the induced phytophotodermatitis appear usually to have a benign
character, but they can lead to severe blistering and painful burn-like
lesions.5,15 The diagnosis based on the
symptoms displayed by the patient is difficult, and adequate diagnosis is
clinically based on history and physical
examination.13,17 In some cases, the symptoms
of phytophotodermatitis have been mistaken for child
abuse.4
In addition, as a result of the aggressive progression of
the symptoms, phytophotodermatitis induced by H. mantegazzianum is
commonly mistaken for resistant staphylococcal infections or necrotising
fasciitis.5
Contact with the plant sap and exposure to UV light leads to
erythema, oedema, and burn-like lesions within 24 hours and possibly large,
fluid-filled blisters within 48 hours.3,8,10
The occurrence of pruritus is uncommon,18 but
secondary skin infection is a possible
complication.5
The blisters can develop into purplish or blackened scars,
with skin hyperpigmentation remaining visible for months or even years after
exposure.3,4,8,10,16
In addition, the affected areas may remain hypersensitive to
UV light for many years.4,9,16 The occurrence
of systemic manifestations is rare.13 Children
appear to be particularly attracted to playing with H.
mantegazzianum’s large and hollow stems, which are used for play
swords and telescopes.5
It is important to highlight that phytophotodermatitis may
occur via indirect contact with H. mantegazzianum sap. For example, a
woman developed phytophotodermatitis as a result of contact with her cat that
had been playing with a specimen of the plant in the
garden.8 Dogs are also described as being
frequent carriers of the plant’s sap on their fur, which is then
transferred to the owners’ skin.5 It
seems that mammals other than humans may also be affected by
phytophotodermatitis induced by this
plant.19
Treatment—Immediately after exposure,
the skin should be thoroughly washed with soap and cold water to remove plant
sap.5,9 The exposed skin should be protected
from sunlight by covering and/or the application of sunscreen, until at least 48
hours post-exposure even if asymptomatic.3 If
sap enters the person’s eyes, these should be thoroughly flushed with cold
water or irrigation solution.5 Although there
is suggestion that exposure to furocoumarins can cause permanent
blindness,5 there appear to be no cases
documented in the medical literature.
Since most people are unlikely to seek medical attention
prior to the onset of symptoms, management is usually symptomatic and
supportive.3,5 Wet compresses, ice packs, and
paraffin gauze dressings my assist to reduce swelling and
inflammation.3,5
An effective treatment may consist of wound debridement and
daily dressings with silver sulphadiazine, which seems to be effective and
safe.15 In any case, keeping blistered areas
clean with the use of topical antiseptics is advisable to prevent the onset of
secondary infection.13
In some cases, treatment with an oral or topical
anti-inflammatory medication is advised,5,15
with severe cases possibly requiring hospitalisation for analgesia and
supportive care.3,5 Where intense pruritus
occurs, antihistamines may be used.13
The healing process can take up to 2
weeks,15 but in some cases symptoms may last
for over a month.5 Moreover, it is necessary to
monitor the patient for secondary infection, and educate the person to avoid
future exposure.18
Although the subsequent hyperpigmentation requires no
treatment, hydroquinones may be used.18 Since
affected areas may remain hypersensitive to sunlight for months or years, the
continued use of sunscreen is
advisable.3,18
Heracleum mantegazzianum in New Zealand and
NPPA recommendations—Unfortunately there is currently no
information on the number of cases of phytophotodermatitis induced by H.
mantegazzianum in New Zealand.
However, unlike other plants in New Zealand that cause
adverse reactions in humans, H. mantegazzianum stands out as a
particular threat for several reasons, including:
Although the
distribution of H. mantegazzianum is currently limited in New Zealand,
this species has the potential to become widespread along river and stream
banks, especially in areas fenced off from grazing stock.
In addition, the use of H. mantegazzianum as a
garden plant has been promoted in the past, even though current trade in this
plant is very limited. Therefore, due to its significance to human health and
its potential to become an invasive species in New Zealand, Heracleum
mantegazzianum has been included in the list of plants covered by the
Accord.
Toxicodendron succedaneumToxicodendron succedaneum is a relatively small
deciduous tree, native to Eastern Asia, that grows to approximately 12
m.20,21 It has attractive autumn foliage, which
makes it sought after as an ornamental tree (Figures 2 and 3). However, T.
succedaneum is as allergenic as poison ivy (T. radicans), although
it seems to be less of a clinical problem than the latter since it grows as a
tree rather than a creeper (M Rademaker, personal communication, 2005).
Plants in the family Anacardiaceae are the main cause of allergic contact
dermatitis (ACD) induced by plants
worldwide,16,22 with Toxicodendron
spp. being by the far the most common cause.23
Figure 2. Canopy of Toxicodendron
succedaneum showing the characteristic bright reddish colours of its
deciduous autumn leaves (Photo courtesy of DermNet)
 Figure 3. A sapling of Toxicodendron
succedaneum showing green leaves (Photo courtesy of Auckland
Museum)
 In the United States, ACD caused by Toxicodendron
spp. is a significant occupational hazard for agriculture and forestry workers
as well as recreational wilderness users.24
There are substantial associated medical costs, and major economic losses as a
result of the consequent morbidity in particular amongst forestry
workers.24
Mode of action—The sap of
Toxicodendron spp. contains urushiols that are extremely potent
sensitisers, in particular the allergen
catechols.16,21,25,26 Urushiol is described as
colourless or slightly yellow, but once exposed to air it oxidizes and
polymerizes turning black.24
It is estimated that at least 50% (but possibly as much as
75%) of the adult population in the United States is hypersensitive to the
urushiol of Toxicodendron spp. and would likely develop clinical
symptoms.12,23,24,27,28 Note that the
expression of ACD is partially dependent on genetic
factors.12 ACD is a cell-mediated response to
exposure to an antigen of a relatively low molecular weight that can penetrate
the epidermis.23 Toxicodendron induced
dermatitis is more intense in adults, although many severe cases can be observed
in children.12
The antigens of all Toxicodendron spp. are
essentially the same, so cross-sensitivity between different species
occurs.26 Urushiol is found in all parts of the
Toxicodendron plant including stems, leaves, roots, and fruit
skin.24 ACD is induced following exposure to a
damaged part of the plant,24,25 and the latter
is necessary to allow the urushiols (oleoresins) to contact the skin, as the
uninjured plant is innocuous.24,26 In addition,
allergic contact dermatitis can occur following inhalation of the smoke of
burning plants, as the urushiols may be present in the particulate
matter.21,26,29
Inhalation of these particles may therefore result in an
allergic response affecting mucous membranes for example, and ACD may also occur
on skin where particles may settle. In some cases contact with urushiols may
occur via wind transmission.21
Urushiol is non-volatile and dries quickly on
fomites—persisting on clothes and equipment
indefinitely.24 It seems that pets,
particularly long-haired dogs, may be responsible for transmitting the oleoresin
from Toxicodendron plants to
children.12 Aggravating the threat posed by
Toxicodendron spp. is the fact that dermatitis can occur following
contact with dead plant tissue, as urushiol retains its antigenic potential in
the dry state indefinitely.26
Note that most of the literature available on
Toxicodendron refers to North American species, mainly T.
radicans (poison ivy), T. vernix (poison sumac), and T.
diversilobum (poison oak). Nonetheless, since, as previously mentioned, the
antigens of all Toxicodendron spp. are essentially the
same,26 symptoms of exposure, treatment, and
management are applicable to all species.
Clinical features—Although most
contact allergens require repeated exposures to trigger an immune response, the
catechols of Toxicodendron spp. are potent, and susceptible people may
become sensitised after only two exposures.23
After a sensitised person comes into contact with urushiol, the symptoms usually
appear within 2 days.12 However, symptoms may
appear as early as within 6 hours, and may be delayed for as many as 12 days
after contact with the plant’s
urushiol.30
Erythematous papular lesions that itch intensely are usually
the initial symptoms,23 and these may be
associated with an intense burning sensation, and often advance to raised
lesions.30 Pruritus is intense in all stages of
the lesions and is characteristic of Toxicodendron
ACD.23 The severe itching may lead to
scratching with excoriation and secondary lesions, possibly leading to
infection.
Approximately 48 to 72 hours after exposure, vesicular
lesions develop and erupt, releasing plasma that forms a
crust.23 Vesicles are often numerous and small
but bullae can occur in severe reactions.23
Facial oedema with marked periorbital swelling are particularly common in
children.21
In moderately severe cases, oedematous swelling of various
parts of the body may occur, while in severe cases Toxicodendron ACD is
characterised by widespread symptoms and marked oedema of the extremeties and
face.26
The fluid that exudes from vesicles and bullae do not
contain the allergen and therefore the patient cannot spread the dermatitis to
other persons or other parts of the
body.24,26,27,31 However, the rash may grow in
size and new vesicles may develop during the first 2 weeks without further
exposure to urushiol, which leads to the common belief that the serum from the
vesicles contains the antigen.23
The severity of the response will also vary between
individuals, some experiencing mild reddening while other patients may become
temporarily disabled.31 The extent and severity
of the lesions will vary due to a number of factors, especially level of
exposure (area of contact and amount of urushiol involved), patient’s
sensitivity to the allergen, site of contact, and skin
thickness.23,30,31 In addition, lesions may
develop in areas not directly exposed to the plants due to secondary exposure
(via contaminated hands, clothing, tools, etc.), and also due to the
non-specific effect of the cell-mediated
response.23
The ACD induced by Toxicodendron spp. usually
resolves within 3 to 4 weeks,23 but it may last
for 6 weeks in more susceptible individuals.24
Hyperpigmentation may occur in darkly pigmented individuals, which may last for
months.23,24 Although complications and
systemic effects may occur, these appear to be
uncommon.24 Secondary infection, however,
appears to be more common.
Ingestion of Toxicodendron plant material leads to
symptoms that occur mostly within 1 day.32
Chewing or ingestion of the leaves is likely to result in inflammation of the
oral mucous membranes, and may cause severe gastroenteritis—with nausea,
vomiting, diarrhoea, abdominal pain, and
proctitis.12 Other systemic symptoms may
include fever, chills, headache, and fatigue—and, in very serious cases,
hypotensive shock may occur.32
Ingestion of Toxicodendron plant material can also
lead to systemic contact dermatitis, with symptoms as those resulting from
direct skin contact.32
Treatment or management—Following
contact with the sap of Toxicodendron plants, it is important to wash
the affected area immediately with warm soapy
water.25 All clothing, tools, or other objects
or pets that have been exposed to the urushiol should be adequately washed with
common soap or detergent, which renders the urushiol-contaminated areas or
fomites harmless.26
Urishiol may remain under a person’s fingernails,
which must be washed to prevent further self-exposure or contamination of other
individuals.26 Note, however, that the urushiol
binds to skin proteins within a few minutes after exposure, and thorough washing
would only remove the remaining oleoresin yet to
bind.26,30
After approximately 30 minutes post-exposure, all urushiol
is likely to have been absorbed into the
skin.24 However, there are some specific
detergents that seem to optimise the removal of urushiol from human skin, which
may be applied a couple of hours after
exposure.23,24,30
Eruptions may be treated with topical corticosteroids,
although severe cases may require hospitalisation and systemic
administration.25,28 In New Zealand,
three-quarters of the patients confirmed to be affected by Toxicodendron
dermatitis were treated with a reducing dose of prednisone, and the
remaining with potent topical corticosteroids and systemic
antihistamines.33
Note that such corticosteroids may alleviate but not prevent
the development of symptoms.30 Detailed
discussions on the treatment of Toxicodendron ACD have been provided by
other authors.12,23,30
Toxicodendron succedaneum in New Zealand
and NPPA recommendations—Toxicodendron succedaneum is
without doubt the most allergenic plant species in New Zealand causing contact
dermatitis, and one that certainly causes public harm (M Rademaker, Waikato
Hospital, personal communication, 2006). In 1993 alone there were at least 20
cases of allergic contact dermatitis due to T. succedaneum recorded in
the Waikato Hospital.34 There were at least 92
cases of contact dermatitis due to T. succedaneum in the
Waikato region between 1982 and 1994.33
At least 55 cases involved young people (0–20 years)
who were affected during outside play, most of which involved lesions to the
face.21 In contrast, almost all cases involving
those aged 21 or older occurred while
gardening.21
Toxicodendron succedaneum is not yet officially
controlled in New Zealand, but it is classified as a noxious weed in the
Australian states of South Australia35 and New
South Wales,36 where all specimens of this
plant must be destroyed.
In Australia, T. succedaneum was sold for many
years as a garden plant, but since its declaration as a noxious weed it can no
longer be offered for sale;36 a similar
situation to Japan.33,34 In addition, in New
South Wales for instance, public education has assisted in leading to a
considerable reduction in the number of
trees.36
While the potential environmental impact of T.
succedaneum in New Zealand is uncertain, there seems to be no naturalised
population of this plant. However, in Sydney (Australia) T. succedaneum
is considered to be a serious weed problem where birds spread the seeds in their
droppings—and many thousands of seedlings were flourishing in home
gardens, in public areas, and in urban
bushland.36 T. succedaneum can also be
spread by movement of garden soil containing seed, which remains viable for many
years.36
The Steering Group overseeing the NPPA process decided that
there was no justification for including T. succedaneum in the NPPA
list. According to the horticultural industry, “this plant is not a
species that is currently being sold in New Zealand.”
The NPPA's Technical Advisory Group also concluded that
there is no evidence that this species is invasive in New Zealand or is spread
by humans. Therefore, although T. succedaneum warrants some management
due to its potentially serious effects on human health, it did not meet the
criteria for inclusion in the NPPA, and this was consequently deemed not to be
the appropriate mechanism to address the risks to human health associated with
this plant.
Hazard management and conclusionAs a result of the inclusion of H. mantegazzianum
in the National Pest Plant Accord, this plant is now an unwanted organism. As a
result, its sale, propagation, and distribution across the country are illegal.
There is however, no requirement for existing plants to be destroyed.
Due to H. mantegazzianum’s threat to public
health and its potential invasiveness, MAFBNZ encourages the general public,
regional, and local authorities to destroy this plant. Nonetheless, extreme care
should be exercised when removing these plants, and it must be stressed that
contact with dead plant parts and with inanimate objects or pets that have been
in contact with such plants is dangerous.
The use of protective water-resistant clothing and
protective goggles is advisable when dealing with H. mantegazzianum, as
is the simultaneous avoidance of exposure to
sunlight.1,15
A detailed management plan for H. mantegazzianum
was produced by Nielsen et al. (2005) who assessed various control
methods.1 The authors stated that:
“currently used control methods comprise a variety of manual and
mechanical methods, grazing and herbicide application”, and that
“rather than recommending a single control method, a control programme
based on an integrated weed management strategy (IWMS) is preferred”
(p30).
In regards to T. succedaneum, since it has not been
listed in the NPPA, no official measures have been imposed on its sale or
propagation in New Zealand. However, MAFBNZ encourages local and regional
authorities to consider taking action against this species in the interest of
public safety.
Specifically, MAFBNZ recommends that councils promote or
carry out active removal of T. succedaneum (and also H.
mantegazzianum) from public places—including schools, parks,
reserves, and other high public use areas. It seems that the Hamilton City
Council, for example, no longer plants T. succedaneum and has removed
many such trees from public places or other areas on medical
request.34
Regarding the removal of T. succedaneum, like
H. mantegazzianum, dead plant parts or anything that has been in
contact with the plant poses a risk, as ACD can be developed by contacting
tools, pets, or clothing that have been in direct contact with the urushiol
previously.
The removal of Toxicodendron plants consequently
has to be done with care, and as much of the skin area as possible should be
adequately covered. It seems that it is necessary to use heavy-duty vinyl
gloves, as rubber gloves are not very protective as the catechols in urushiol
can penetrate most, if not all, types.12 The
plants removed should be buried or burnt.26
However, as previously pointed out, burning T. succedaneum may also
lead to exposure, and any person in the vicinity should maintain a safe distance
to avoid exposure to urushiol that may be carried in the ashes or smoke.
Finally, medical practitioners that come across cases of
dermatitis as a result of contact with these plant species in private properties
should recommend the removal of the specimen(s). Moreover, when the particular
plant is located on public land, the medical practitioner should inform the
local authorities, as consideration should be given on whether the plant needs
to be removed in the interest of public health.
Competing interests: None.
Author information: José G B
Derraik, Senior Adviser (Human Health), MAF Biosecurity New Zealand, Ministry of
Agriculture and Forestry, Wellington
Acknowledgements: I especially thank Marius
Rademaker (Health Waikato) for his very valuable input. I also thank John
Fountain (National Poisons Centre), Doug Lush (Ministry of Health), Annie
Wright, Sarah Clinehens and Andrew Harrison (MAF Biosecurity New Zealand) for
revising this manuscript and providing feedback, and also Fleur Petricevich and
Melanie Newfield (MAF Biosecurity New Zealand) for their comments.
Rune Aanderaa (SABIMA—The Norwegian Biodiversity
Network), DermNet (www.dermnet.org.nz),
and the Auckland Museum kindly allowed their photographs to be used in this
article.
Correspondence: Dr José G B Derraik,
MAF Biosecurity New Zealand, Ministry of Agriculture and Forestry, PO Box 2526,
Wellington. Fax: (04) 894 0733; email: jose.derraik@maf.govt.nz
References:
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