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| Journal of the New Zealand Medical Association,
10-August-2007, Vol 120 No 1259
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Phytophotodermatitis
caused by contact with a fig tree (Ficus carica)
José G B Derraik, Marius
Rademaker
Plant dermatitis
(phytodermatitis) is caused by a reaction in the skin following contact with
certain plants or plant parts. They can be irritant such as cactus spine
injuries, urticarial (e.g. from stinging nettles), allergic from plants such as
Primula obconica or Toxicodendron succedaneum, or they can be
phytophototoxic in nature.1
Phytophotodermatitis is
generally a toxic reaction due to direct skin exposure to certain plants or
plant parts, followed by exposure to ultraviolet (UV) light. The most common
plants to cause phytophotodermatitis belong to the Apiaceae (Umbelliferae)
family.1 Other plant families that can cause
phytophotodermatitis include Rutaceae, Moraceae, and Fabaceae.
Case reportTwo male arborists were cleaning
up storm damaged limbs from a large fig tree, Ficus carica, which was
heavily laden with fruit (e.g. Figures 1 and 2). The work took place in Auckland
between 10:30 am and noon, on a dry, relatively clear summer day (80% relative
humidity, temperature 24°C, total UV exposure in 1.5 hours 3.58 mJ).
Both workers were dressed in
short-sleeved shirts or singlets. During the removal of the storm damage, they
wrapped their arms (predominantly their right arms) around the fig tree branches
when dragging them to the wood chipper.
Some 9 hours later, the first
arborist noted a burning sensation on his right arm, which he attributed to
sunburn. However, over the next 12 hours, the skin on this arm became swollen,
erythematous, and was sore to touch. Within 24 hours of contact with fig tree
parts, bullae appeared on the forearm, wrist, and back of the hand
Figure 3. Second arborist’s forearm
approximately 36 hours (A), 48 hours (B), 72 hours (C), 12 days (D), and
35 days (E) after contact with Ficus carica tree branches and
exposure to sunlight.
(Photos courtesy of Alex White and Gerald Collett)
Note: In the photos a
‘ring’ can be observed in the wrist region where an armband
presumably prevented exposure to sunlight and the consequent occurrence of
phototoxic reaction.
These symptoms on the first
arborist persisted for over 2 weeks despite the use of alternative remedies,
including a mixture of lavender oil and Aloe vera gel. As the acute
erythema settled, post-inflammatory pigmentation developed, which slowly
resolved over a month.
The second worker also
experienced a burning sensation on his right forearm some 9 hours after working
with the fig tree. Blistering of skin was noticed approximately 31 hours after
contact with the fig tree (Figure 3), at which point the arborist covered the
blisters and bullae with manuka honey. His condition progressively worsened with
swelling and formation of large bullae on the affected arm (Figure 3). Circa 51
hours after contact with the plant, he attended the accident and emergency
(A&E) department at the local hospital. Initially the pain and blistering
were restricted to the arm which had been wrapped around the fig
branches—but subsequently he developed pain and swelling on the left arm,
chest, and legs which had also been in contact with the fig tree. The discomfort
progressed such that he was unable to work for approximately 10 days.
He responded slowly to topical
corticosteroids and oral non-steroidal anti-inflammatories. The symptoms
gradually resolved over 4 to 6 weeks (Figure 3).
DiscussionThe history and clinical
appearances was pathognomonic of a phytophotodermatitis which, in these two
cases, was secondary to contact with the fig tree. Phytophotodermatitis is the
interaction of plant compounds, most often psoralens, with sunlight on human
skin; this results in an acute dermatitis.1 It
is usually a phototoxic reaction, as opposed to a photoallergic reaction. As a
result, no prior sensitisation is necessary and anybody can be
affected.2 Other types of phytodermatitis
include urticarial dermatitis, irritant contact dermatitis, and allergic contact
dermatitis.
The eruption of
phytophotodermatitis usually begins 24 hours after exposure and peaks at
48–72 hours. Phytophototoxicity may be amplified by both humidity and
perspiration. It typically manifests as a burning erythema that may subsequently
blister, and post-inflammatory hyperpigmentation lasting weeks to months may
ensue. In some patients, the preceding inflammatory reaction may be mild and go
unrecognised by the patient.
Phytophotodermatitis occurs most
commonly in the spring and summer when furocoumarins are at their highest
concentration in plants, and when UV levels are also at their peak. The
incidence of phytophotodermatitis is unknown, but will vary according to the
risk of exposure to psoralens. Because furocoumarins are found in a wide range
of wild and domestic plants (Table 1), a variety of patient groups may become
exposed.
Table 1. Examples of plants known to cause
phytophotodermatitis, and the main sensitising compounds associated with
them
5-MOP = 5-methoxypsoralen, 8-MOP = 8-methoxypsoralen.
The two cases presented were at
very high risk of developing phytophotodermatitis because of their prolonged and
significant contact, high summer levels of furocoumarins in the plant, peak
summer UV levels, exposed skin, warm temperature, and perspiration.
Whilst photoallergic reactions
are a cell-mediated immune response in which the antigen is the light-activated
photosensitising agent, phototoxic reactions result from direct damage to tissue
caused by light activation of the photosensitiser.
The main photosensitisers in
plants are furocoumarins and consist of psoralens (5-methoxypsoralens,
8-methoxypsoralens), angelicin, bergaptol, and xanthotal (Table
1).1–3
The photochemical excitation of
these furocoumarins is induced by UV radiation, usually within the UVA
wavelengths of 320–400 nm (peak activity is around 335
nm).13
Two types of toxic reactions
occur: one oxygen-independent, where the UV-activated furocoumarins bind to RNA
and nuclear DNA; and the other: an oxygen-dependent reaction where the induced
compounds cause cell membrane damage and
oedema.1,3–6 These reactions consequently
lead to cell death (sunburnt cells and apoptotic keratinocytes).
Ficus carica, which is
believed to have originated in western Asia, was brought to the Mediterranean as
early as 5000 BC. In New Zealand, it is commonly cultivated as a fruit tree in
home gardens and appears to be widespread in the North Island (particularly in
northern regions); it can also be found in some areas of the South Island,
particularly in those areas that experience long, hot summers (Melanie Newfield,
personal communication, 2007).
Ficus carica belongs to
the Mulberry family (Moraceae). The leaves and unripened fruit of figs contain
the furocoumarins, psoralen, and bergapten, as well as the coumarins,
umbelliferone, 4',5'-dihydropsoralen, and marmesin. The furocoumarins are
lipid-soluble and can penetrate the epidermis with
ease.7–10
There are a number of other
Ficus species which may cross react with F. carica including
Weeping fig (F. benjamina), Cluster fig (F. racemosa), and
Sycamore Fig (F. sycomorus).
Eating figs does not cause
photosensitisation, unless the juice is smeared onto the face. However,
anaphylaxis has been reported after eating figs; in some of these cases, this
may represent a cross-reaction with natural rubber
latex.11–12
Although phytophotodermatitis
from Ficus carica has been previously reported, it is often poorly
recognised. As the cases reported here illustrate, contact with fig and other
plant sources of furocoumarins can cause severe local reactions.
It is important that awareness
is raised amongst the general public—especially those people whose
occupations lead to a greater likelihood of exposure: arborists, orchardists,
forestry workers, and gardeners.
Author information:
José G B Derraik, Senior Adviser (Human Health), MAF Biosecurity
New Zealand (NZ), Ministry of Agriculture and Forestry, Wellington; Marius
Rademaker, Hon Associate Professor, Department of Dermatology, Waikato
Hospital, Hamilton
Acknowledgements:
We are grateful to Gerald Collett, Alex White, and Ian Barnett (Treecare
Services Ltd, Auckland) for providing us with the precise details of the case as
well as the very useful photographs, which made this case report possible. We
also thank Petr Kocna for allowing us to include his photographs in this
article, and Melanie Newfield (MAF Biosecurity NZ) for relevant information.
Climate data were kindly supplied by National Institute of Water and Atmospheric
Research (NIWA).
Correspondence:
Dr José G B Derraik, MAF Biosecurity NZ,
Ministry of Agriculture and Forestry, PO Box 2526, Wellington. Fax: (04) 894
0733; email: jose.derraik@maf.govt.nz
References:
This case report was corrected on 7 September 2007
to reflect the Erratum at http://www.nzma.org.nz/journal/120-1261/2720
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