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.