Mycoplasma hominis - Introduction, Classification, Morphology, Clinical Syndrome

Last Modified: June 12, 2026 by Reshma Maharjan

Classification of Mycoplasma hominis

Classification of Mycoplasma hominis can be done phenotypically.

Domain: Bacteria

Phylum: Mycoplasmatota

Class: Mollicutes

Order: Mycoplasmatales

Family: Mycoplasmataceae

Genus: Mycoplasma

Species: hominis

Introduction to Mycoplasma hominis

Mycoplasma hominis is a facultative anaerobe that is fast-growing (within 1-4 days) and is able to metabolize arginine but does not utilize glucose. It produces a large fried egg appearance colony on Mycoplasma media.

It inhabits the mucosa of the urogenital tract. To differentiate it from other genital Mycoplasma spp., inhibition of the growth of the bacteria with specific antisera is done.

Morphology of Mycoplasma hominis

The common morphological features of Mycoplasma hominis include:

  • gram-negative (very poorly stained)

  • size 0.3x0.8 micrometer (passes through 0.45micrometer filter)

  • lack cell wall

  • the cell membrane is 3 layered and contains sterols (eg. Cholesterol) which are supported by cytoskeleton and protein networks

  • two forms – filamentous and granular

  • lacks flagella or pilli but exhibits gliding motility

  • multiplication by binary fission

Fig: Mycoplasma hominis morphology (Source: iStock)

Clinical syndrome of Mycoplasma hominis

Clinical manifestations of Mycoplasma hominis, also known as Genital mycoplasma, vary depending on the type of infection.

  • It causes urogenital infections resulting in manifestations such as salpingitis (infection of the fallopian tube), pelvic abscess, puerperal (postpartum) infection, septic abortion, prostatitis, PID, amnionitis, non-gonococcal urethritis, acute pyelonephritis.

  • It may also cause primary atypical pneumonia, meningitis in newborns, arthritis, peritonitis, thrombophlebitis, and brain abscess.

  • Incidence of colonization by genital mycoplasmas increases after puberty as a result of sexual contact

  • In neonates, transmission occurs from colonized mother by ascending route to the newborn infant (urogenital tract), by crossing the placenta by delivering through a colonized birth canal, or postnatally from mother to infant. Meningitis, abscess, bacteremia, and pneumonia can be observed

  • In immunosuppressed patients, it takes an invasive form. Bacteremia, arthritis, pneumonia, peritonitis, abscesses, and other wound infections.

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