Mold Allergy Clinical Presentation
- Author: Shih-Wen Huang, MD; Chief Editor: Harumi Jyonouchi, MD more...
History
Allergic rhinitis and conjunctivitis
Because molds can grow in indoor environments, many children are exposed to them from birth. How early children can become allergic to mold Ags is unclear; however, nearly 40% of children with allergic rhinitis have positive skin test or radioallergosorbent testing (RAST) reactivity to mold allergens.
Symptoms of allergic rhinitis include runny nose, itchy nose, sneezing, nasal congestion, sniffling, sore throat, cough, itchy eyes, and runny eyes and may be worse when patients are indoors. Symptoms may be most severe in hot and humid seasons, but some molds are prevalent throughout the year. The most characteristic symptoms are injected conjunctivae, headache, and fatigability.
Children typically have a history of recurrent respiratory infections (including sinus infections) and otitis media.
One study revealed that mold allergy may be most prevalent in winter secondary to the airtight insulation used in homes built in recent years.[13, 14] History of prolonged cold symptoms that last for more than 2 weeks in winter may indicate mold allergy.
Although uncommon, sinusitis or lower respiratory tract disease (eg, allergic bronchitis, bronchial asthma) subsequently develops in some patients.
An increased prevalence of adenoid hypertrophy is reported in children with mold allergy.
Allergic asthma
The history of mold-induced asthma may not differ from that of any other allergic asthma. The onset may be acute or insidious. The patient's history usually includes cough, wheezing, and tachypnea with dyspnea with prolonged expiration.
Symptoms may be precipitated by exposure to molds, viral infections, or exposure to any irritants, especially when patients have become hyperresponsive.
Allergic bronchopulmonary aspergillosis (ABPA), allergic bronchopulmonary mycosis (ABPM), and extrinsic allergic alveolitis (EAA)
Molds are ubiquitous microorganisms; therefore, unless the prevalence of the offending fungi is known, eliciting a history of fungal exposure leading to chronic inflammation and disease development is difficult.
In EAA, because of the relationship between the disease and exposure to specific fungi in particular professions, the diagnosis can be suspected at an early stage. The period from exposure to onset of disease may be months to years in EAA.
The frequency of familiar occurrence of ABPA was determined in 164 patients with ABPA diagnosed over a period of 22 years in one study.[15] The familiar occurrence of ABPA was found only in 4.9% of the 164 patients.
Allergic fungal sinusitis (AFS)
This disease appears to be most common in areas with hot, humid climates and high ambient mold-spore counts. Most AFS cases caused by Bipolaris spicifera are reported in Texas, Louisiana, and Georgia. At least 6 cases of allergic Aspergillus sinusitis were reported in the state of Texas.[10]
Physical
Clinical manifestations of mold allergies are primarily limited to the upper and lower respiratory tracts.
Allergic rhinitis and/or allergic conjunctivitis
Signs include allergic shiners, Dennie lines (the accentuated lines below the margin of lower eyelids), frequent otitis media, and pale and swollen turbinates.
The conjunctivae are often injected, with prominent palpebral conjunctivae and/or frequent tearing.
Persons who chronically breathe through their mouth typically have narrow and elevated palates, enlarged tonsils, and a cobblestone appearance of the posterior pharyngeal wall.
Children often have elongated adenoid facies with signs of overbite. They often speak with heavily nasal voices.
Allergic asthma
Signs include cough, wheezing, prolonged expiration, and tachypnea.
A deformed chest wall (eg, pigeon breast, barrel chest) is sometimes observed in children, especially in those with chronic allergic asthma.
Depending on the frequency of wheezing in the daytime and nighttime, asthma can be classified as mild intermittent, mild persistent, moderate persistent, or severe persistent according to the National Asthma Education and Prevention Program Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma published by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH).[16]
In murine model of chronic fungal asthma, toll-like receptor 2 (TLR2) mediated signaling was shown to be a major contributing factor to maintain type 2 T-helper (Th2)-cytokine driven, anti-fungal innate response.
ABPA and ABPM
Cough, purulent sputum, dyspnea, wheezing, low-grade fever (< 38.5°C), chest pain, hemoptysis, and malaise are common.
In the acute stage, symptoms can be minimal or can be accompanied by occasional crackles. In chronic cases, clubbing, cyanosis, tachypnea, and cor pulmonale are common. In children with cystic fibrosis (CF), ABPA may cause rapid weight loss, lethargy, fever, and productive cough.
AFS
AFS generally produces a subacute or chronic course of sinus involvement. All pediatric patients presented with nasal polyposis and progressive facial deformity.
Patients may report dull pressure on the face or head. Persistent, sometimes unilateral, nasal stuffiness, hyposmia, purulent and postnasal secretion, sore throat, fetid breath, and malaise are always present. The secretions often pool in the nasopharynx at night. The increasing postnasal drainage with resultant cough may be accompanied by wheezing.
EAA
EAA may occur in an acute, intermediate, or chronic form.
In the acute stage, patients may have flulike illness accompanied by coughing and undue breathlessness hours after exposure. Malaise, fever, chills, widespread aches and pains, anorexia, and tiredness may also be present.
In the chronic form, EAA is a slowly progressive illness causing undue breathlessness, dry cough but no wheeze, possible weight loss, and, in rare cases, clubbing. Patients gradually have respiratory failure, pulmonary hypertension, or right heart failure.
Causes
All of the clinical disorders related to mold allergy are caused by repeated exposures to molds and the immune responses of susceptible individuals. The relationships between specific molds and particular disorders are discussed in Pathophysiology.
Molds are potential problems in outdoor and indoor environments. Nearly 20 allergenically important molds are related to the household environment. Among them, Alternaria and Hormodendrum species are the most well recognized.
Favorite habitats include damp, dark places (eg, cellars, bathrooms, garages, attics); rotting leaves or vegetation, indoor plants, and organic plant containers (eg, wicker, straw, hemp); old foam-rubber pillows and peeling wallpaper; furniture stuffed with decaying kapok or cotton; rubber gaskets on old refrigerator doors; dishwashers, drainage sinks, and washing machines; and garbage cans. Water-damaged areas, such as leaky roofs, walls with dry rot, and wet carpets, or areas with poor drainage are also prime habitats for mold (see the images below).
Moisture is trapped in the wall behind a vinyl wall covering. 
Large amounts of moisture support fungal growth, as is the case with this dry wall covering. 
Glues can collect mold. 
Soapy shower doors collect fungi. 
Wet drywall collects mold. 
Wall coverings can pucker because of mold. Depending on the areas where surveys are conducted, sterile mycelia and the fungi of the genera Cladosporium, Penicillium, Alternaria, Epicoccum, Aspergillus, Pullularia, and Drechslera are most commonly encountered. Studies have also shown that poorly maintained landscaping, high shade levels, and large amounts of organic debris near the home (including ivy, compost, and bark chips) are highly correlated with the accumulation of indoor molds. Also, the development of mold in room-air humidifiers, cold-mist vaporizers, and air-conditioning systems has received much recent attention.
When mold allergens bind to specific IgE on mast cells of susceptible individuals, mast-cell activation causes an immediate reaction, leading to the early release of histamine. As in the case of other airborne allergens, a delayed allergic reaction is expected to follow, with infiltration of various inflammatory cells that serve to magnify the inflammatory process, which may last for days. Immediate and late mucosal inflammatory processes lead to the development of the signs and symptoms of allergy (see Pathophysiology).
Although genetic factors are known to influence the development of allergies, the exact genetic transmission of each disorder listed in Pathophysiology is currently unknown. Environment plays an important role. In addition to the presence of mold allergens, smoking increases the frequency of allergic rhinitis and asthma. A child with CF is at increased risk for ABPA. Many cases of EAA occur as occupational diseases among individuals working in environments infested with specific molds.
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