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MYCOPLASMA:
STRUCTURE:
**In contrast, other cell wall deficient bacteria = L-forms, don’t have sterols in their cell membrane
and can form cell walls under appropriate growth conditions
1. M.Genitalium:
Attachment organelle
Intracellular growth
2. M.pneumonia:
Extracellular obligate human pathogen
Contains complex adhesion proteins
Most important adhesion protein= P1 adhesine
Phase and antigenic changes cause ciliostasis
Exotoxin = pertussis tx like toxin which causes vacuolisation
Polyclonal T and B cell stimulation = cytocine = auto antibody
PATHOGENESIS:
1. M.Pneumonia:
Extracellular pathogen
Adheres to respiratory epithelium
Attachment structure forms at one end of the cell
Attachment structure: adhesion proteins+P1 adhesin
Adhesions interact specifically with sialated glycoprotein receptors:
at the base of the cilia on epithelial surface
on the surface of erythrocytes
Cilia and ciliated epithelial cells are destroyed – ciliostasis
Loss of these ciliated epithelial cells:
interferes with normal clearance of upper airways
permit the bacteria to spread to lower respiratory tract
Cilia and epithelial cell loss and interaction with sialated glycorpoteins result in persistant cough
**Ciliostasis test – evaluates ciliary activity of trachea
M.pneumonia functions as super antigen – stimulates inflammatory cells to migrate to site of
infection = release of cytokines:
Initially TNF-alpha+IL-1
Later IL-6
Formation of these inflammatory cytokines contributes to clearance of bacteria and observed
disease
Mycoplasma species can change expression of surface lipoproteins rapidly:
important for evading host immune responses
establishing persistent or chronic infections
BRIEF:
EPIDEMIOLOGY: GENITOURINARY:
CLINICAL: RESPIRATORY:
Genitourinary tract is colonized with other mycoplasma species, it is difficult to determine role
of these organisms in disease
M.genitalium cause nongonococcal urethritis, cervicitis, pelvic inflammatory disease
M.hominis cause pyelonephritis, postpartum fevers, and systemic infections in
immunocompromised patients.
LAB: MYCOPLASMA
Microscopy has no diagnostic value (mycoplasmas stain poorly with gram stain)
Antigen tests have poor sensitivity and specificity = not recommended
NUCLEIC ACID AMPLIFICATION TESTs = most sensitive diagnostic tests
CULTURE – M.pneumonia – can be isolated in cultre from throat washings, bronchial washings,
sputum;
BUT organisms grow slowly and require special media supplemented with:
Serum (provides sterols)
Yeast extract (for nucleic acid precursors)
Glucose
Ph indicator
Penicillin (to inhibit other bact)
Serology tests are available for M.pneumonia – enzyme immunoassays for detection of IgM and
IgG
Serology tests are more sensitive than culture
Disadvantage with serologic tests is that they have to be collected early in the course of disease
and then after 3 to 4 weeks to demonstrate a rise in antibody levels
MYCOFAST:
TREATMENT:M.PNEUMONIA:
Macrolides (azithromycin)
Tetracyclines (doxycycline)
Fluoroquinoles are effective in M.pneumonia
although the tetracyclines and fluoroquinolones are reserved for use in adults.
Azithromycin is widely used for treating M. pneumoniae
TREATMENT: SEXUALLY
Ureaplasma urealyticum
Mycoplasma genitalium
Mycoplasma hominis
UREALYTICUM:
Urease(+)
differentiated from mycoplasmas wirh urease positivity
rapid growth in culture
colonized at genitourinary system in adults
diseases:
nongonococcal urethritis
low weight birth
Chorioamnionitis
Urinary infection (urolithiasis)
Transmitted with sexually and vertical route