Prevention and Treatment:

Antibiotics such as erythromycin, clarithromycin (Biaxin) or azithromycin (Zithromax) are effective treatment. However, because mycoplasma infection usually resolves on its own, antibiotic treatment of mild symptoms is not always necessary. The doctor will recommend bedrest, plenty of fluids, therapeutic coughing, breathing exercises, proper diet, cough suppressants, pain relievers and fever reducers such as aspirin or acetaminophen. Home care includes rest and a high-protein diet with adequate fluids. With proper treatment, full recovery is expected.

Since there is no vaccine available, to prevent the occurrence of the disease, we need to apply good and hygiene daily life by cleaning and disinfect common touched surfaces regulary. Do not share cup, toothbrush, eating utensils to prevent exchange of saliva that may have carried the pathogen. Limit eating “community” food that may have been contaminated by someone’s hands. Stay home and always avoid crowding environment if you have a fever. Lastly, do not smoke.

Diagnosis:

To diagnose pneumonia, the doctor begins with a medical history and physical examination. By placing a stethoscope on the chest, the doctor may be able to hear crackling sounds, coarse breathing, wheezing and/or the breathing may be faint in a particular area of the chest. Additionally, the doctor may order a chest x-ray, a sputum gram stain and a blood test. The chest x-ray may show a blotchy-white area, where fluid and pus has accumulated in the lung's air sacs. The sputum grain stain and the blood test may determine the cause and severity of the condition.

A positive blood test for cold-hemagglutinins in 50-70% of patients after 10 days of infection (cold-hemagglutinin-test should be used with caution or not at all since 50% of the tests are false-positive), lack of bacteria in a gram-stained sputum sample, and a lack of growth on blood agar. Mycoplasma atypical pneumonia can be complicated by Stevens-Johnson syndrome, hemolytic anemia, encephalitis or Guillain-Barré syndrome.

Other serology tests include complement fixation which detects both IgG and IgM specific to M.pneumoniae, enzyme-linked immunoassay for M. pneumonia specific IgM, and indirect hemagglutination. All of these have acceptable sensitivity and specificity.

Pathogenesis:

The pathogenesis of the microorganism has two properties: The first is a selective affinity for respiratory epithelial cells, and the second is the ability to produce hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes. Colonization of the respiratory tract by M. pneumoniae results in the cessation of ciliary movement. The normal clearance mechanisms of the respiratory tract do not function, resulting in contamination of the respiratory tract and the development of a dry cough.

Mycoplasma pneumonia cause infection primarily as extracellular parasites, attaching to the surface of ciliated and nonciliated epithelial cells. This is done by the P1 adhesin protein that localizes themselves at the tips of the bacterial cells and binds to sialic acid residues on host epithelial cells. The attachment site, or receptor, is a complex carbohydrate structurally akin to antigen I of red blood cells. Following attachment, mycoplasmal organisms may cause direct cytotoxic damage to epithelial cells because of hydrogen peroxide generation or cytolysis via an inflammatory response mediated by mononuclear cells or antigen-antibody reactions.

Mycoplasma pneumoniae is also thought to be involved in mediating other diseases and infections in its monopolization of the immune response. Some patients have developed severe bacterial and viral infections just after or during a M. pneumoniae infection. This is thought to occur by the creation of an environment that is anatomically, physiologically, and/or immunologically conducive to other organisms for invasion as well as for cellular damage.

The diagram above illustrates mycoplasmas (red) infecting epithelial cells (black). The mycoplasmas form a small structure called a "tip" by which they adhere to the epithelial cells. If the mycoplasmas are prevented from adhering to the epithelial cells, they are avirulent.

Virulence Factor:

* You may click on the table to view a bigger size image.

Reservoir and Transmission:

The children are an important M. pneumoniae reservoir. Mycoplasma pneumoniae is transmitted from person-to-person contact through respiratory secretions during coughing and sneezing which is respiratory droplet transmission. Hence, close contact is required for transmission, and the bacteria are more commonly found among members of the same family and in schools and day-care institutions. The contagion requires a continuous contact because of the sensitivity of M. pneumoniae to changes in temperature and humidity levels. There is little point in isolating someone infected with the virus since some people carry the infection without feeling ill.

Once attached to the mucosa of a host organism, M. pneumonia extracts nutrients, grows and reproduces by binary fission. Attachment sites include the upper and lower respiratory tract, causing pharyngitis, bronchitis and pneumonia. The infection caused by this bacterium is called atypical pneumonia or “walking pneumonia” because of its protracted course and lack of sputum production and wealth of extra-pulmonary symptoms.

Mycoplasma pneumoniae has an incubation period of about 1 to 4 weeks, which means it may take up to four weeks after exposure to get Mycoplasma pneumonia. They symptoms of infection are headaches, muscle pain, scratchy aching throat, worsening dry cough, fever, chills, vomiting, slow heartbeat, breathlessness, bluish color to lips and nail beds, diarrhea and rash. The most common clinical syndrome following with M. pneumonia is tracheobronchitis. However, over this time period, symptoms may slowly begin to appear. An epidemic occurs every three to five years.

Its Biological Characteristics:

Mycoplasma pneumoniae is the smallest (range from 0.2-0.8 micrometers) free-living bacteria and it is member of the class Mollicutes. This class of organisms lack of peptidoglycan cell wall. Instead, it has a cell membrane which incorporates sterol compounds, similar to eukaryotic cells. It obtains sterols from host serum, allowing it to retain the cell’s structure. Since it has no cell wall, it is resistance to penicillins and other beta-lactam antibiotic which are designed to disrupt the bacterial cell wall. And so, they can be parasitic and saprophytic.

Mycoplasma pneumonia are extracellular, mucous membrane pathogen that do not invade other tissues. They have a low GC-content (18-40 mol%). The analysis of 16S ribosomal RNA sequences suggest that this kind of bacteria is classified under gram-positive since they are too small to be stained. They may induce cellular changes including changes in metabolism and cell growth and infection.

M. pneumonia has the smallest genome size and as a result, lack of many metabolic pathways and so they need to extract nutrient especially glucose from host’s cells and metabolize it in order to get energy for survival and reproduction. M. pneumonia is strict aerobes. They grow slowly by binary fission and the colonies may take up to 3 weeks to develop and so the physical sign of infection of the patient will present for several days to weeks.

Introduction

After blasting for the nucleotide sequences, we found that the gene that responsible to the sequences is Mycoplasma pneumoniae adhesin protein (P30) gene. It was found in Mycoplasma pneumonia. The gene coded for adhensin protein P30 which is required for cytoadherence and associated with cell development of M.pneumoniae. Loss of P30 caused a mutation and the morphological abnormalities like change in cell shape. It indicates P30 plays a role in mycoplasma cell development and support adhesin P1’s receptor-binding function that enhance the attachment to host cells.

Mycoplasma pneumonia