Mycoplasma pneumoniae

Mycoplasma pneumoniae 

GENERAL CHARACTERISTICS

·       Mycoplasma pneumoniae are the Smallest free-living bacteria.

·    Mycoplasma pneumoniae are unique among bacteria because they do not have a cell wall and their cell membrane contains sterols. In contrast, other cell wall – deficient bacteria (called L - forms) do not have sterols in their cell membrane and can form cell walls under the appropriate growth conditions.

·   The absence of the Cell wall renders the Mycoplasma pneumoniae resistant to Penicillin, Cephalosporins, Vancomycin and other antibiotics that interfere with synthesis of the cell wall.

·       Shape – Pleomorphic

·       Motility – Non-motile 

·       Capsule – Absent 

·       Endospores – Absent

·       Respiration – Aerobic

·       Optimum Temperature -  37 °C

·       Optimum pH – 7.8 to 8.0. Mycoplasma pneumoniae may die when pH becomes below 7.0.

·      Habitat – Mycoplasma pneumoniae are found in the mucosa of Upper Respiratory Tract (UTR) and Urogenital tract of humans. Also found in oral cavity. They are also present in sewage, plants, animals and insects.

·      Mycoplasma pneumoniae is a type of “atypical” bacteria that commonly causes mild infections of the respiratory system. In fact, pneumonia caused by Mycoplasma pneumoniae is sometimes referred to as “Walking pneumonia” since symptoms tend to be milder than pneumonia caused by other germs.

·  Mycoplasma pneumoniae was discovered by Nocard and Roux in 1989 in animals with Contagious bovine pleuropneumonia. In 1937, Dienes and Edsall isolated the first pathogenic Mycoplasma, Mycoplasma hominis from a Bartholin’s gland abscess. In 1944, Eaton isolated another Atypical pneumonia and in 1962 Chanock named as Mycoplasma pneumoniae.   

PATHOGENICITY OF Mycoplasma pneumoniae

DISEASE TRANSMISSION

·       Mycoplasma pneumoniae causes Respiratory infection that spreads easily through contact with respiratory fluids. 

INCUBATION PERIOD

1 to 3 Weeks.

VIRULENCE FACTORS OF Mycoplasma pneumoniae

i.       Adhesin Proteins (P1 Adhesins)

ii.     Lipoproteins (evades host Immune system)

PATHOGENESIS OF Mycoplasma pneumoniae

·    Mycoplasma pneumoniae is an extracellular pathogen that adheres to the Respiratory epithelium by means of a complex of Adhesions proteins (P1 Adhesin).

·    The adhesions interact specifically with Sialated Glycoprotein Receptors at the base of Cilia on the epithelial cell surface (and on the surface of erythrocytes).

·       Ciliostasis then occurs, after which first the cilia, then the ciliated epithelial cells, are destroyed.

·     The loss of these Cilia cells interferes with the normal clearance of the upper airways and permits the Lower respiratory tract to become contaminated with microbes and mechanically irritated. This process is responsible for the Persistent cough present in patients with symptomatic disease.

·       Mycoplasma pneumoniae functions as a Superantigen ( antigens that result in excessive activation of the immune system), stimulating inflammatory cells to migrate to the site of infection and release Cytokines, initially Tumor Necrosis Factor-α and Interleukin-1 (IL-1) and later, IL-6. This process contributes to both the clearance of the bacteria and the observed disease.

·    A number of Mycoplasma pneumoniae are able to rapidly change expression of surface lipoproteins, which is believed to be important for evading the host immune response and establishing persistent or chronic infections.     

CLINICAL DISEASES CAUSED BY Mycoplasma pneumoniae

·       Exposure to Mycoplasma pneumoniae typically results in asymptomatic carriage.

·   The most common clinical presentation of Mycoplasma pneumoniae infection is Tracheobronchitis (Lower respiratory tract infection particularly in Windpipe and Bronchi).

·   Low grade fever, Malaise, Headache, and a dry, non-productive cough develop 2 to 3 weeks after exposure.

·       Acute Pharyngitis (Inflammation of the pharynx) may also be present.

·       Symptoms gradually worsen over the next few days and can persist for 2 weeks or longer.

·       The Bronchial passages primarily become infiltrated with Lymphocytes and Plasma cells.

·      Pneumonia (referred to as Primary Atypical Pneumonia or Walking Pneumonia) can also develop, with a patchy Bronchopneumonia.

·       Myalgias and Gastrointestinal tract symptoms are uncommon.

·   Secondary complications include Neurologic abnormalities (e.g., Meningoencephalitis, Paralysis and Myelitis), Pericarditis, Hemolytic anemia, Arthritis and Mucocutaneous lesions.

LABORATORY DIAGNOSIS OF Mycoplasma pneumoniae

MICROSCOPIC EXAMINATION

·       Microscopy is of no diagnostic value because Mycoplasma pneumoniae have no cell wall.

COLONY MORPHOLOGY ON EATON’S AGAR

·     Unlike other Mycoplasmas, Mycoplasma pneumoniae is a strict aerobe.

·     The Mycoplasma pneumoniae grow slowly in culture, with a generation time of 6 hours.

·  Colonies of Mycoplasma pneumoniae are small and have a homogeneous granular appearance (“Mulberry shaped”), unlike the fried-egg morphology of other Mycoplasmas.

SEROLOGY (Antibody detection)

i.       Enzyme Immunoassay (EIA)

ii.     Complement fixation test (CFT)

iii.   Cold Agglutination test

MOLECULAR DIAGNOSIS

a)     16S rRNA Sequencing

b)     Polymerase Chain Reaction (PCR)

TREATMENT AND PREVENTIVE MEASURES

·       Drug of choice is Erythromycin, Doxycycline or Fluoroquinolones

·       Immunity to reinfection is not lifelong, and vaccines have proved ineffective