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Potentially (near) fatal asthma (PFA) defines a subset of patients with asthma who are at increased risk for death from their disease. The diagnosis of PFA should motivate treating physicians, health professionals, and patients to be more aggressive in the monitoring, treatment, and control of this high-risk type of asthma. A diagnosis of PFA is made when any one of the following are present: (1) history of endotracheal intubation from asthma, (2) acute respiratory acidosis (pH < 7.35) or respiratory failure from acute severe asthma, (3) two or more episodes of acute pneumothorax or pneumomediastinum from asthma, (4) two or more episodes of acute severe asthma despite the use of long-term oral corticosteroids and other antiasthma medications. There are two predominant phenotypes of near fatal exacerbations, the "subacute" exacerbation and the "hyperacute" exacerbation. The best way to "treat" acute severe asthma is 3-7 days before it occurs (i.e., at the onset of symptoms or change in respiratory function) and to optimize control of asthma by decreasing the number of symptomatic days and days/nights requiring rescue therapy and increasing baseline respiratory status in "poor perceivers." PFA is treated with a multifaceted approach; physicians should appreciate limitations of pharmacotherapy including combination inhaled corticosteroid/long-acting beta-agonist products as well as addressing nonadherence, psychiatric, and socioeconomic issues that complicate care.

Occupational immunologic lung disease is characterized by an immunologic response in the lung to an airborne agent inhaled in the work environment and can be subdivided into immunologically mediated occupational asthma (OA) and hypersensitivity pneumonitis (HP). Irritant-induced OA, a separate nonimmunologic entity, can be caused by chronic exposure to inhaled irritants or reactive airways dysfunction syndrome, defined as an asthma-like syndrome that persists for >3 months and occurs abruptly after a single exposure to a high concentration of an irritating industrial agent. High-risk fields for OA include farmers, printers, woodworkers, painters, plastic workers, cleaners, spray painters, electrical workers, and health care workers. OA can be triggered by high molecular weight (HMW) proteins that act as complete allergens or low molecular weight (LMW) sensitizers that act as haptens. HMW proteins (>10 kDa) are generally derived from microorganisms (such as molds and bacteria, including thermophilic actinomycetes), plants (such as latex antigens and flour proteins), or animals (such as animal dander, avian proteins, and insect scales) and are not specifically regulated by the Occupational Safety and Health Administration (OSHA). LMW haptens that bind to proteins in the respiratory mucosa include some OSHA-regulated substances such as isocyanates, anhydrides, and platinum. HP can present in an acute, a chronic, or a subacute form. The acute, subacute, and early chronic form is characterized by a CD4(+) T(H)1 and CD8(+) lymphocyte alveolitis. Classically, the bronchoalveolar lavage will show a CD4/CD8 ratio of

Atopic dermatitis (AD), also known as atopic eczema, is a chronic relapsing inflammatory dermatosis characterized by pruritus, xerosis, and a close association with IgE-mediated sensitization to aeroallergens and foods. More than 60% of children with AD are at risk to develop allergic rhinitis or asthma (the atopic march). The distribution of lesions varies by age. Infants tend to have lesions on the cheeks and scalp, and very young children typically have involvement over the extremities cheeks, forehead, and neck. Rash in the diaper area of infants is rarely AD. Lesions in older children and adults are usually located in flexural areas, such as the antecubital and popliteal fossae, along with the head and neck. Acute lesions of AD begin as erythematous papules and serous exudates. Secondary lesions include excoriations and crusted erosions due to scratching. Subacute lesions appear as erythematous scaling papules and plaques. If the itch and rash progress uncontrolled, chronic lichenified AD develops featuring accentuated skin markings with hyperpigmentation. Trigger avoidance, skin hydration, and topical steroids are the first steps for improvement. In acute lesions of AD, the Th2 cells produce IL-4, IL-13, and IL-31, which may potentiate barrier dysfunction and contribute to pruritus. In chronic lesions, the Th1 cells predominate and secrete interferon gamma and IL-12. Barrier dysfunction from filaggrin predisposes patients to AD. Skin superinfection, particularly with Staphylococcus aureus, is common, and cultures of affected lesions help guide therapy. Eczema herpeticum from herpes simplex virus can be life-threatening in AD patients.

The preponderance of clinical data suggest that inhaled corticosteroids (ICSs) are the preferred therapy for the long-term management of asthma, whereas oral or parental corticosteroids and short-acting beta(2)-adrenergic agonists remain the mainstay treatment of acute exacerbations. Allergen and tobacco avoidance are tenets to the practice of allergy-immunology and are beneficial in the treatment of asthma. Failure to avoid animal danders or fungi to which a patient with asthma is allergic is a risk factor for a fatal attack. First introduced in the 1970s, ICSs are the mainstay of pharmacotherapy to control airway inflammation and bronchial hyperresponsiveness in children and adults with asthma. ICSs reduce symptoms, exacerbations, hospitalizations, and deaths while improving quality of life and lung function. When used in combination with an ICS, essentially all clinical trials have indicated that long-acting beta(2)-adrenergic agonists are effective and safe. Leukotriene modifiers (LTMs) are effective in the treatment of persistent asthma, exercise-induced asthma, and aspirin-induced asthma but, in general, are less efficacious than ICSs when used as monotherapy to control asthma symptoms. Nevertheless, some patients respond to LTMs better than ICSs so a personalized approach to asthma pharmacotherapy is recommended. Not only is conventional (subcutaneous) allergen immunotherapy effective in patients with allergic asthma, immunotherapy (subcutaneous or sublingual) administered for rhinoconjunctivitis in children has been shown to reduce the development of asthma.

Leptospirosis is a globally prevalent disease that affects humans, causing systemic illness that may lead to multi-organ involvement. Clinical signs include sudden fever, general malaise, muscular pain, conjunctival suffusion, and jaundice. Disease is caused by pathogenic bacteria including over 200 serologic variants. Most serologic variants have primary reservoirs in wild mammals, which continually infect and colonize domesticated animals. The organism has been recovered from rats, swine, dogs, cattle, and other animals, notably bats. Most studies have focused on domestic animals as reservoir hosts; however, because of their abundance, spatial distribution, and interrelationship with domestic animals, bats are becoming an epidemiologically significant source of leptospires. We present a case of serologically confirmed leptospirosis after bat exposure to add to the growing literature of bats as a possible source of transmission. Recognition of the common presentation of leptospirosis and Weil’s disease, and identification of animal vectors, including bats, allows for the selection of appropriate antibiotic management to aid in resolution of symptomotology.

FEBRUARY 2011 AB60 Abstracts S A T U R D A Y 221 Tranglutaminase 2 Gene Deficiency Results In Decrease Of Airway Resistance And Eosinophilic Inflammation In Murine Asthma Model H. Lee, E. Shim, J. Jung, H. Kang, H. Park, S. Kim, S. Cho, S. Chang, K. Min, Y. Kim; Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, KOREA, REPUBLIC OF, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, KOREA, REPUBLIC OF, Department of Internal Medicine, Sung-Ae General Hospital, Bucheon, KOREA, REPUBLIC OF, Eulji Medical Center, Seoul, KOREA, REPUBLIC OF. RATIONALE:Transglutaminase 2(TG2) is amultifunctional calcium-dependent acyltransferase and ubiquitously expressed in mammalian tissue existing both extracellularly and intracellulary. Recent investigation reported TG2 was highly expressed in the asthmatic airways and augmented the enzymatic activity of phospholipase A2 group 3 which hydrolyzed phospholipid and release arachidonic acids. We hypothesized that TG2 would have some roles in pathogenesis of asthma. METHODS:To evaluate expression of TG2 in asthma patients, we stained lung tissue with anti-TG2 antibody and detected TG2mRNA expression in induced sputum samples of asthmatic patients. To see the effect of TG2 deficiency, wemade a murine ovalbumin (OVA) asthmamodel with TG2 null mice and compared with wild type mice. Airway hyperresponsivenss (AHR) to methacholine, airway inflammatory cells, and cytokines in homogenate of lung tissue were evaluated. RESULTS: TG2 expression in bronchial epithelium and TG2mRNA level in induced sputum samples were increased in asthmatics compared with normal controls. TG2 null mice showed significant reduction in eosinophilic airway inflammation, AHR, serum OVA-specific IgG1/G2a ratio and Th2 cytokines (IL-4, IL-13) in lung homogenates compared with WT mice after OVA challenge. CONCLUSIONS: In human asthmatics, TG2 is highly expressed in airway epithelium and induced sputum. In murine asthma model, TG2 deficiency effectively reverses airway hyperresponsiveness and eosinophilic airway inflammation, Th2 immune responses. These findings suggest that TG2 play important roles in the pathogenesis of asthma.