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INTRODUCTION

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Mycoplasmas are bacteria that make up 1 genus of a special class called Mollicutes. The species are widespread in nature and can affect humans, plants, and animals. They are the smallest self-replicating microorganisms (0.2 μm) and are capable of a cell-free existence. A small genome and limited biosynthetic capabilities are responsible for their biological characteristics and requirements for complex growth media.

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Mycoplasmas are unique from other bacteria due to their lack of cell wall around the cell membrane. Lack of rigid cell walls allows them to be presented in pleomorphic shapes not susceptible to antibiotics that inhibit cell wall synthesis like penicillins and other β-lactam antibiotics, and they are unaffected by the Gram staining method. There are over 120 Mycoplasma species, of which 14 have been isolated in humans. The most common species causing disease in humans include Mycoplasma pneumoniae, Mycoplasma hominis, and Mycoplasma genitalium.

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The best-characterized human Mycoplasma disease is respiratory tract infection due to M pneumoniae, a prominent cause of the atypical pneumonia syndrome. M hominis, another member of the genus, is associated with a variety of genitourinary and perinatal conditions, including postpartum maternal sepsis, neonatal skin infections, meningitis, and bacteremia. Problems associated with M genitalium include pelvic inflammatory disease, salpingitis, and nongonococcal urethritis in sexually active individuals.

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MYCOPLASMA PNEUMONIAE

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PATHOGENESIS AND EPIDEMIOLOGY

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The most common route of transmission of M pneumoniae from person to person is by inhalation of respiratory droplets expelled through coughing. During infection, M pneumoniae can be found within the mucosal secretions from the nose, throat, and trachea. Upon reaching the respiratory tract epithelium, it attaches to the host cell using a specialized terminal tip structure. P1 and other supporting proteins (eg, P30, P40, and P90) promote adhesion and binding to host cells via sialic acid receptors. Damage to host cells is related to hydrogen peroxide and superoxide radicals interacting with host cell toxins leading to deterioration of epithelial cells and their associated cilia and, ultimately, cell lysis. A potential candidate protein of M pneumoniae that may be involved in causing direct damage to the respiratory tract is a pertussis toxin–like protein termed community-acquired respiratory distress syndrome (CARDS) toxin.

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Various reports state that the most distinguishable pathologic feature is an increase of plasma cell–rich lymphocytic infiltration in the peribronchovascular areas with accumulation of macrophages, neutrophils, and lymphocytes in the alveolar spaces. The immunologic response following infection and the immunity of the host generate an inflammatory reaction that plays an important role in the progression of M pneumoniae pulmonary and extrapulmonary manifestations.

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M pneumoniae infection can occur throughout life and mainly infects the upper and lower respiratory tracts of children and adults worldwide. It is most common in school-aged children and young adults. Gender and race do not appear to play a role. M pneumoniae causes an estimated 20% to ...

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