Chapter 215 Mycoplasma pneumoniae
Among the 5 Mycoplasma species isolated from the human respiratory tract, Mycoplasma pneumoniae is the only recognized human pathogen and is a major cause of respiratory infections in school-aged children and young adults.
Etiology
Mycoplasmas are the smallest self-replicating biologic system and are dependent on attachment to host cells for obtaining essential precursors such as nucleotides, fatty acids, sterols, and amino acids. They are distinguished by the complete absence of a cell wall, double-stranded DNA, and small genomes ranging from 577 to 1,380 kb. M. pneumoniae is fastidious, and growth in commercially available culture systems is too slow to be of practical clinical use.
Epidemiology
M. pneumoniae infections occur worldwide and throughout the year. In contrast to the acute, short-lived epidemics of some respiratory viral agents, M. pneumoniae infection is endemic in larger communities, with epidemic outbreaks occurring every 4-7 yr. In smaller communities, infections are sporadic, with long-lasting and smoldering outbreaks occurring at irregular intervals. Community outbreaks can spread largely through school contacts, but up to 40% of household members of an infected student also develop mycoplasma infection.
The occurrence of mycoplasmal illness is related, in part, to age and pre-exposure immunity. Overt illness is unusual before 3 yr of age. Children <5 yr of age appear to have mild illness associated with upper respiratory tract involvement, vomiting, and diarrhea. The peak incidence of lower respiratory illness occurs in school-aged children. M. pneumoniae accounts for 7-40% of all community-acquired pneumonias among children 3-15 yr of age. Recurrent infections occur infrequently but are well documented to occur in adults at intervals of 4-7 yr.
Transmission
Infection occurs through the respiratory route by large droplet spread. The incubation period is 1-3 wk. High transmission rates have been documented within families, with a high percentage of secondary cases developing lower respiratory tract infections. Outbreaks can occur in closed settings (military recruits, institutions, summer camps for children) or can occur as community-wide epidemics.
Pathology and Pathogenesis
Cells of the ciliated respiratory epithelium are the target cells of M. pneumoniae infection. The organism is an elongated snakelike structure with an attachment tip characterized by an electron-dense core and a trilaminar outer membrane. Attachment to the ciliary membrane is mediated by a complex network of interactive adhesion and adherence-accessory proteins localized to this specialized attachment tip (P1/B/C, P30, P65, P24, and P41). These proteins cooperate structurally and functionally to mobilize and concentrate adhesion proteins at the tip and permit mycoplasmal colonization of mucous membranes. Avirulent phenotypes that arise through spontaneous mutations at high frequency cannot synthesize specific cytoadherence-related proteins or are unable to stabilize them at the tip organelle.
Virulent organisms attach to ciliated respiratory epithelial cell surfaces through sialated glycoprotein or sulfated glycolipid receptors and burrow down between cells, resulting in ciliostasis and eventual sloughing of the cells. Mechanisms of cytopathology have not been determined completely; one possibility is the transmission to cells of various cytotoxins such as hydrogen peroxide. M. pneumoniae can also produce a protein similar to the S1 subunit of pertussis toxin. Intracellular organisms have not been found in vivo, and M. pneumoniae rarely invades beyond the respiratory tract basement membrane. However, M. pneumoniae can invade certain cell lines in vitro and survive in the cytoplasm or perinuclear regions for prolonged periods. M. pneumoniae has been detected by polymerase chain reaction (PCR) in many nonrespiratory sites. These observations suggest that M. pneumoniae causes more extrapulmonary infections and chronic disease than appreciated.
A possible mechanism of M. pneumoniae disease is the release of various proinflammatory and anti-inflammatory cytokines. M. pneumoniae infection may induce numerous interleukins, interferons, tumor necrosis factor-α, and other cytokines. The disease produced by M. pneumoniae is complex; the immunologic response of the host may be responsible for the manifestations of disease itself as well as for protection against infection, depending on the qualitative and quantitative balance of humoral and cellular immunity. Although it is well documented that specific cell-mediated immunity and antibody titers against M. pneumoniae increase with age (and therefore probably follow repeated infections), the immune mechanisms that protect against or clear infection are not defined. Patients with immunodeficiencies such as hypogammaglobulinemia and sickle cell disease can have more-severe mycoplasmal pneumonia than do immunocompetent hosts. M. pneumoniae can persist for years in the respiratory tract of patients with hypogammaglobulinemia despite multiple courses of antibiotics. M. pneumoniae is a common infectious cause of acute chest syndrome in sickle cell disease, but it is not prevalent in patients with AIDS.
Clinical Manifestations
Tracheobronchitis and bronchopneumonia are the most commonly recognized clinical syndromes associated with M. pneumoniae infection. Although the onset of illness may be abrupt, it is usually characterized by gradual onset of headache, malaise, fever, and sore throat, followed by progression of lower respiratory symptoms, including hoarseness and cough. Coryza is unusual with M. pneumoniae
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