Ragweed
Seasonal allergies due to ragweed: After examining the flowers, you recognize the bloom with the small flowers (middle of the image) as a chive, Allium schoenoprasum. The plant with the bright yellow blossoms (right) is goldenrod, Solidago species, and the remaining plant with greenish yellow, bell-shaped flowers (left, 10-o'clock position) is ragweed, Ambrosia artemisiifolia.
Chives grow in clumps to 6-12 inches high. They form a semisphere of purple,
pink, or white flowers. Chives are used for cooking but are not allergenic.
Goldenrod blooms from late summer through mid fall. Its bright yellow
flowers attract insects and birds. Because the pollen grains are heavy, bees,
butterflies, birds, and ants are needed to pollinate this plant. Goldenrod and
ragweed bloom at the same time of year and commonly grow side by side. Despite
its vibrant color and attraction by insects and birds, goldenrod is not
responsible for seasonal allergies. Named for the shape of its ragged leaves,
ragweed is a common source of seasonal allergies. Unlike goldenrod, ragweed
requires the wind to release pollen and initiate fertilization; therefore, its
flowers are not as brilliant as those of the goldenrod plant.
Ragweed is a common cause of allergy
symptoms from late summer to mid fall (August through November). Avoiding
ragweed pollen is the most effective method for decreasing ragweed allergy.
Closing windows in the car and home minimizes exposure to the pollen. Decreasing
time spent outdoors, especially on dry and windy days, can be helpful as well.
Allergic rhinitis is often caused
by exposure to environmental or occupational factors, including perennial
allergens (eg, dust mites, mold, grains, wood dust, latex) and seasonal
allergens, mainly tree, grass, and weed pollen such as ragweed, as in this case.
Typical physical findings include
allergic shiners, or dark circles around the eyes; swollen and boggy nasal
turbinates;
and cobblestoning
of the posterior oropharynx
due to exuberant lymphoid tissue.
Management of allergic rhinitis consists of both
allergen avoidance and pharmacologic
management. Environmental control includes
avoiding the specific allergen to
which the patient has immunoglobulin E (IgE)–mediated hypersensitivity,
reducing outdoor exposure during specific seasons, cleaning indoor environs, and
avoiding nonspecific triggers such as smoke, strong perfumes, and fumes.
Treatment with oral antihistamines and decongestants is the cornerstone of the
pharmacologic management of allergic rhinitis. Because of their favorable
adverse-effect profile, newer
second-generation, nonsedating
antihistamines, such as cetirizine (Zyrtec),
fexofenadine (Allegra), and
loratadine (Claritin), are
preferred over older first-generation antihistamines, such as diphenhydramine
(Benadryl) and chlorpheniramine (Chlor-Trimeton). In addition, many commercial
formulations of the second-generation antihistamines include a decongestant for
complete symptom relief.
Nasal steroids can be used to control
chronic symptoms; initiating these steroids 1-2 weeks before the beginning of
ragweed season offers the best results. Other symptomatic agents, such as
vasoconstrictors (eg,
oxymetazoline
hydrochloride), provide fast-acting relief of nasal drainage and congestion.
However, these products cannot be used
for more than 3 days without a risk of rebound symptoms. Immunotherapy
and systemic steroid treatment may be required in extreme cases of allergic
rhinitis, including ragweed allergy.
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