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In this lecture educator explains about Mycoplasma. They are the wall-less organisms. Without a cell wall, they are unaffected by many common antibiotics such as penicillin or other beta-lactam antibiotics that target cell wall synthesis. They can be parasitic or saprotrophic.
Mycoplasma pneumoniae is the major pathogen.
- M. pneumoniae causes “atypical” pneumonia.
- It is recognized as one of the most common causes of community-acquired pneumonia in otherwise healthy patients younger than 40 years.
- Causes upper and lower respiratory illness in all age groups.
- Ability to mimic host cell membrane allows infection to persist even after treatment.
Important Properties: Mycoplasmas are the smallest free-living organisms; many are as small as 0.3 mm in diameter. Their most striking feature is the absence of a cell wall. Consequently, mycoplasmas stain poorly with Gram stain, and antibiotics that inhibit cell wall (peptidoglycan) synthesis (e.g., penicillins and cephalosporins) are ineffective. Their outer surface is a flexible cell membrane; hence these organisms can assume a variety of shapes. Theirs the only bacterial membrane that contains cholesterol, a sterol usually found in eukaryotic cell membranes. Mycoplasmas can be grown in the laboratory on artificial media, but they have complex nutritional requirements, including several lipids. They grow slowly and require at least 1 week to form a visible colony. The colony frequently has a characteristic “fried-egg” shape, with a raised centre and a thinner outer edge.
M. pneumoniae infections occur worldwide, with an increased incidence in the winter. This organism is the most frequent cause of pneumonia in young adults and is responsible for outbreaks in groups with close contacts such as families, military personnel, and college students. It is estimated that only 10% of infected individuals get pneumonia. Mycoplasma pneumonia accounts for about 5% to 10% of all community-acquired pneumonia.
M. pneumoniae, a pathogen only for humans, is transmitted by respiratory droplets. In the lungs, the organism is rod-shaped, with a tapered tip that contains specific proteins that serve as the point of attachment to the respiratory epithelium. The respiratory mucosa is not invaded, but ciliary motion is inhibited, and necrosis of the epithelium occurs. The mechanism by which M. pneumoniae causes inflammation is uncertain. It does produce hydrogen peroxide, which contributes to the damage to the respiratory tract cells. M. pneumoniae has only one serotype and is antigenically distinct from other species of Mycoplasma. Immunity is incomplete, and second episodes of disease can occur. During M. pneumoniae infection, autoantibodies are produced against red cells (cold agglutinins) and brain, lung, and liver cells. These antibodies may be involved in some of the extrapulmonary manifestations of infection.
Mycoplasma pneumonia is the most common type of atypical pneumonia. It was formerly called primary atypical pneumonia. (Atypical pneumonia is also caused by Legionella pneumophila [Legionnaires’ disease], Chlamydia pneumoniae, Chlamydia psittaci [psittacosis], Coxiella burnetii [Q fever], and viruses such as such as influenza virus and adenovirus. The term atypical means that a causative bacterium cannot be isolated on routine media in the diagnostic laboratory or that the disease does not resemble pneumococcal pneumonia.) The onset of Mycoplasma pneumonia is gradual, usually beginning with a non-productive cough, sore throat, or earache. Small amounts of whitish, non-bloody sputum are produced. Constitutional symptoms of fever, headache, malaise, and myalgias are pronounced. The paucity of findings on chest examination is in marked contrast to the prominence of the infiltrates seen on the patient’s chest X-ray. The disease resolves spontaneously in 10 to 14 days. In addition to pneumonia, M. pneumoniae also causes bronchitis. The extrapulmonary manifestations include Stevens-Johnson syndrome, erythema multiforme, Raynaud’s phenomenon, cardiac arrhythmias, arthralgias, haemolytic anemia, and neurologic manifestations such as Guillain-Barré syndrome.
Laboratory Diagnosis, Treatment and Prevention
Laboratory Diagnosis: Culturing: is usually not made by culturing sputum samples; it takes at least 1 week for colonies to appear on special media. Culture on regular media reveals only normal flora. Serologic testing is the mainstay of diagnosis. A cold-agglutinin titer of 1:128 or higher is indicative of recent infection. Cold agglutinins are IgM autoantibodies against type O red blood cells that agglutinate these cells at 4°C but not at 37°C. However, only half of patients with Mycoplasma pneumonia will be positive for cold agglutinins. The test is nonspecific; false-positive results occur in influenza virus and adenovirus infections. The diagnosis of M. pneumoniae infection can be confirmed by a fourfold or greater rise in specific antibody titer in the complement fixation test.
Treatment: The treatment of choice is either a macrolide, such as erythromycin or azithromycin, or a tetracycline, such as doxycycline. The fluoroquinolone levofloxacin is also effective. These drugs can shorten the duration of symptoms, although, as mentioned earlier, the disease resolves spontaneously. Penicillins and cephalosporins are inactive because the organism has no cell wall. Prevention: There is no vaccine or other specific preventive measure.
There are about 200 types of mycoplasma bacteria, but most of them are harmless. Following are the important types:
- Mycoplasma pneumoniae
- Mycoplasma genitalium
- Mycoplasma hominis
- Ureaplasma urealyticum
- Ureaplasma parvum Mycoplasma hominis has been implicated as an infrequent cause of pelvic inflammatory disease. Ureaplasma urealyticum may cause approximately 20% of cases of nongonococcal urethritis. Ureaplasmas can be distinguished from mycoplasmas by their ability to produce the enzyme urease, which degrades urea to ammonia and carbon dioxide.