Mycoplasma Pneumoniae and Atypical Pneumonia

 Introduction • • Mycoplasma are the smallest prokaryotic microbes present in nature. Because of their small size (150 to 250 nm) and deformable membrane, they are able to pass through filters with pore sizes that retain other bacteria. • Contain a 600–1,350 kbp genome And 23–35% GC. • Have a tendency to form ‘fried egg’ colonies in solid culture media. • Seven species of mycoplasma have been found to be pathogenic to humans, including : • M. pneumoniae, U. urealytium, M. genitalium, M. hominis, M. fermentans, M. penetrans and M. pirum  Description of the Organism • They require many exogenous nutrients for growth, including: vitamins, amino acids, nucleic acid precursors and, in particular, lipids. o (addition of serum or cholesterol to growth medium) • Energy is supplied by carbohydrate metabolism. • Some non fermenting mycoplasmas derive energy from amino acid (arginine) metabolism. The family Mycoplasmataceae is composed of two genera: 1) Mycoplasma : Has more than 13 species that infect humans 2) Ureaplasma : (T-strain mycoplasmas ) • Consist of 2 species that infect humans (U. urealyticum, U.parvum)  Pathogenesis • Mycoplasmas are extracellular parasites • They attach to the surface of ciliated and non-ciliated epithelial cells ◦ Some mycoplasmas, such as: M. pneumoniae, M.penetrans, and M. genitalium, have special attachment organelles containing adhesin molecules but many that effectively penetrate cells, such as M. fermentans and M. hominis, do not. Mycoplasma pneumoniae and Atypical Pneumonia  Introduction  Some cases of pneumonia did not respond to sulfonamides and penicillins.  The condition was designated as “primary atypical pneumonia” (PAP) The atypical pneumonia syndrome can be caused by ◦ influenza virus, adenovirus, respiratory syncytial virus, cytomegalovirus, Chlamydophila sp., Legionella sp., Pneumocystis jirovecii, Mycoplasma pneumoniae, SARS, and …. M. pneumoniae • In addition to primary atypical pneumonia and community-acquired pneumonia, M. pneumoniae can also induce autoimmune hemolytic anemia and other diseases in the blood, cardiovascular system, gastrointestinal tract, and skin, and can induce pericarditis, myocarditis, nephritis and meningitis's. • M. pneumoniae was detected in approximately 12% of all CAP cases. • Most common atypical bacteria isolated. • In paediatric population, M. pneumoniae account for approximately 10–40% of all lower respiratory tract infections.  Description of the Organism M. pneumoniae : 1) Growth on cell-free defined medium 2) Grows well aerobically 3) Ferments glucose 4) Lyse RBC Photomicrograph of colonies of mycoplasma growing on agar medium Mycoplasma salivarium colonies growing with fried egg appearance Mycoplasma pneumoniae colonies with mulberry colony formation  P1-adhesin • Transmembrane protein • Mutant strains lacking P1-adhesin fail to adhere to animal cells • Involved in gliding motility (in cell to cell transfer) • Repeated gliding motility allows the organism to bind and release itself from the attaching surface which eventually increases the infective surface area. • Anti-P1 monoclonal antibody had inhibitory effects on gliding motility and adherence to tracheal rings by M. pneumoniae  Epidemiology • The highest attack rates are in individuals 5 to 20 years old • There appears to be an age-related incidence of upper versus lower respiratory tract infection caused by M. pneumoniae. ◦ Whereas those 5 to 20 years old tend to develop bronchitis and pneumonia ◦ In older infected adults, pneumonia is relatively common  Transmission • M. pneumoniae infection is spread by respiratory droplets • Incubation period : 2 to 3 weeks  Clinical Disease 1. RESPIRATORY INFECTION ◦ M. pneumoniae infections involve only the upper respiratory tract ◦ The disease has an insidious onset manifested by fever, malaise, headache, cough 2. EXTRAPULMONARY INVOLVEMENT  DERMATOLOGIC INVOLVEMENT  RAYNAUD PHENOMENON  CARDIAC COMPLICATIONS  NEUROLOGIC COMPLICATIONS  MUSCULOSKELETAL, RENAL, AND HEMATOPOIETIC COMPLICATIONS  CARDIAC COMPLICATIONS • Most commonly reported extrapulmonary manifestations of M. pneumoniae infection • The signs and symptoms ◦ Arrhythmia, congestive failure, chest pain, and electrocardiographic abnormalities ◦ A loud third heart sound may be the only clue to cardiac involvement • The mechanism of heart damage is unknown, but M. pneumoniae has been isolated from the pericardial fluid of one patient  NEUROLOGIC COMPLICATIONS • Encephalitis • Aseptic meningitis and meningoencephalitis • Transverse myelitis • Brain stem dysfunction • Guillain-Barré Syndrome • Peripheral neuropathy •Are most often noted in hospitalized patients MUSCULOSKELETAL, RENAL, AND HEMATOPOIETIC COMPLICATIONS • Poly arthralgias are common in M. pneumonia, but arthritis is rare • Renal complications associated with immune complex deposition and high-titer cold agglutinins have been reported  Diagnosis • Culture of the organism from respiratory secretions or body fluids should be the gold standard for diagnosis. • If culture is successfully performed, M. pneumoniae grown on agar produces a “mulberry” colony • Culture requires 1 to 2 weeks for definitive results • Enzyme-linked immunoassays have been developed to detect IgM and IgG directed against M. pneumoniae  Con . . . • Detection of M. pneumoniae antigens directly in sputum specimens has been accomplished with the use of an antigen-capture, indirect enzyme immunoassay. • The cold agglutinin assay is neither very sensitive (50% to 70%) nor specific. • The real-time PCR, performed on sputum, nasopharyngeal aspirate, or throat swab material, suggest that this test could serve as a specific and rapid diagnostic method  Treatment • Antimicrobial therapy is not necessary for mycoplasmal upper respiratory tract infection. • Pneumonia due to mycoplasma is self-limited and not life-threatening in most cases. • The mainstays of treatment for M. pneumoniae respiratory tract infection are macrolides and tetracyclines.