Research Paper on Mycoplasma Pneumonia: Atypical Bacteria Causing Mild Pneumonia

Introduction

Mycoplasma Pneumonia is an atypical bacterium that does not color on a Gram stain; it remains colorless; hence, Gram staining is not recommended. The bacterium causes pneumonia, which is different from pneumonia caused by other bacteria as the symptoms that are depicted are mild (Kliegman, Stanton, Schor, Behrman, & Nelson, 2016). Some of the signs in people infected with the bacteria include sore throat, fever, headache, and fatigue, among other clinical presentations. Although it is mainly seen to cause pneumonia, it can also cause myriad other conditions and illnesses in children, such as chest cold (tracheobronchitis). The recommended staining method is methylene blue stain or Dienes (Kliegman et al. 2016). The structure of the bacterium ranges from a spherical shape to a filamentous one and has no cell walls (Nir-Paz, 2017). With about 500 to 1000 genes, Mycoplasma Pneumonia is among the smallest, self-replicating bacteria possessing only ribosomes, double-stranded circular DNA, and plasma membrane for cell growth and replication (Nir-Paz, 2017). They are surrounded by a plasma membrane that protects the cytoplasm from the environment (Nir-Paz, 2017). Culturing Mycoplasma Pneumonia involves broth and agar medium coupled with glucose and phenol red at a pH of 7.8 (Nir-Paz, 2017). Mycoplasma Pneumonia produces acid that changes the color of the medium from purple to yellow. These bacteria cause illnesses by damaging the lining of the respiratory system, which includes the lungs, throat, and windpipe. Mycoplasma Pneumonia is a communicable disease that is spread from person to person through coughing or sneezing. Therefore, it is more likely to break from crowded places such as schools, military barracks, hospitals, and college residences.

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Virulence Factors

Mycoplasma Pneumonia is aided by a virulence factor known as Community-Acquired Respiratory Distress Syndrome toxin (CARDS), which is an ADP-ribosyltransferase exotoxin. The CARDS toxin that helps in the inflammation and dysfunction of the respiratory tract by causing cytotoxicity (Zander, 2008). CARDS toxin is known to cause reduced lung function as well as histological changes. CARDS toxin leads to the heightened presence of Th-2 cytokines and Th-2 chemokines that results in inflammation of eosinophilis, mucous metaplasia, and increased presence of T and B cells. The bacterium attaches itself to the epithelial cells with the help of a 160 kDa type 1 pilli (Zander, 2008). Mycoplasma Pneumonia creates colonies that lead to the production of superoxides and hydrogen peroxide that destroy the epithelial layer of the cell and the adjacent cells. The destruction causes ciliary motion to cease, which leads to coughing, sore throat, and fever. The bacterium, on attaching itself to a host cell, inserts microtubules that use up the host nutrients and oxygen as it is unable to self-synthesize damaging the host cell. Mycoplasma Pneumonia can avoid detection by the phagocytes through antigenic variations that cause the host susceptible to other diseases.

Immunity

Mycoplasma Pneumonia triggers an immune response by causing lymphocyte multiplication and the release of several types of cytokines. This causes a humoral immune response that targets the bacteria; however, Mycoplasma Pneumonia can evade the immune response by inducing molecular imitation, hiding within the cells, and phenotypic plasticity. The bacterium can also effect a change in the lipoprotein deposits to evade the immune response and survive environmental changes (Zander, 2008). Immunosuppression is found in severe cases. Incubation periods can be of up to 4 weeks before symptoms of the disease appear. Mycoplasma Pneumonia is mostly asymptomatic and is hard to identify as it portrays symptoms similar to other respiratory diseases.

Pathology

Mycoplasma Pneumonia causes mild symptomatic indications such as headache, fever, and malaise. An unproductive cough and sore throat can also be witnessed in some cases, and fulminant pneumonia does not usually occur. Mycoplasma Pneumonia can cause extra-pulmonary infections to occur, including dermatological, neurological, gastronomical, musculoskeletal, and cardiac symptoms (Zander, 2008). Mycoplasma Pneumonia can bring respiratory diseases such as bronchitis, tonsillitis, aggravated asthma, and pharyngitis. Although most of the infections affect the respiratory tract, infections related to the bacterium can be found in the tissue of the brain, blood, heart, skin, and joints. Skin conditions such as the Stevens-Johnson syndrome, toxic epidermal necrolysis, and erythema multiforme are associated with Mycoplasma Pneumonia. The Stevens-Johnson syndrome is a major skin condition that manifests due to Mycoplasma Pneumonia. SJS can be severe with the appearance of blisters that show the bloodstream has been infected (Zander, 2008). Mycoplasma Pneumonia can cause anorexia, abdominal pain, vomiting, and diarrhea.

Central nervous system (CNS) complications are the primary manifestations of extra-pulmonary infections. In most cases, CNS infections are preceded by a show of respiratory disease. Common signs such as aseptic meningitis, encephalitis, meningoencephalitis, and polyradiculitis appear in Mycoplasma Pneumonia infections (Kliegman et al. 2016). Some of the severe complications of Mycoplasma Pneumonia infection are acute disseminated encephalomyelitis and acute transverse myelitis. Mycoplasma Pneumonia caused encephalitis is common in children under the age of 10 when compared to adults, with 30% of the cases being severe. Mycoplasma Pneumonia has been known to cross the barrier separating the brain and blood, leading to brain abscesses (Kliegman et al. 2016). The presence of Mycoplasma Pneumonia in the brain tissue causes damage to neurons as the immune systems attack the bacteria. Mycoplasma Pneumonia can also cause intravascular coagulation and thrombosis. Patients with sickle cell are more susceptible to suffering cold agglutination caused by Mycoplasma Pneumonia.

Epidemiology

In the Public Health England, there is a total of 16,878 culture, serological, and other unspecified diagnostics of Mycoplasma Pneumonia (Brown, et al. 2016). The figure 1 below shows the laboratory reports that have been reported of the virus infection and detection from 1995 to 2015. Chen et al. (2015) presented that in the current demonstration, there are about 16 known species of the Mycoplasma Pneumonia. Some of these species are isolated from human beings, without including some of the species that have been isolated from the animals. According to the researchers, Mycoplasma Pneumonia is considered to be the smallest known free-living microbe. In the initial demonstrations, Mycoplasmas were associated with the widening of the clinical spectrum, that have been associated with respiratory tract infections, especially in children. The study by Chen et al. (2015) indicated that Mycoplasmas are present in about 40% of children who are infected with CAP. In this population, 18% of them require hospitalization.

Figure 1: Laboratory Reports for Mycoplasma Pneumonia since 1995-2015 (Brown et al. 2016)

Presentations

Robert decides to share a cab with his friends as they leave a party, they are rowdy, and one of them has a dry cough that is not too noticeable since he tries to suppress it. A fortnight later, Robert can feel a sore throat causing discomfort, so he buys medicine, but that only provides a short-lived reprieve, as now he wakes up sneezing and having chills. Robert is a senior in high school, just around the age that Mycoplasma Pneumonia is common. The pharyngitis worsens together with sinus congestion, and now a dry cough that is not so pronounced has started. Robert has asthma, though he can go days without needing to use his inhaler, he has had to use it twice in the morning hours. By evening Robert has to see the school nurse who advises his parents to take him to the doctor. The doctor opts to conduct a chest radiograph, but that does not provide much information on the actual cause. The blood works come back with elevated levels of IgM antibodies that are produced to combat Mycoplasma Pneumonia initially.

Prevention

There is no vaccine currently available for the prevention against Mycoplasma Pneumonia. Some of the prevention tips recommended are covering your mouth and nose when sneezing or coughing and washing hands with soap. The bacteria survive in humid conditions and so opening windows when in public transport is recommended. There is no immunity formed against the bacteria from previous infections, and subsequent infections are likely to happen in the future (Kliegman et al. 2016). When coughing without a handkerchief, it is not advisable to cover your mouth with your hands, instead use the elbow joint to ensure that the bacteria do not move to your hands and get spread as you interact with people.

Treatment

Antibiotics that destroy bacterial walls such are ineffective against Mycoplasma Pneumonia. Beta-lactam antibiotics such as penicillin are under this category. Mycoplasma Pneumonia has no cell wall, so antibiotics that disrupt protein synthesis or modification of DNA are recommended. Tetracyclines, fluoroquinolones, and macrolides are effective in in-vivo and in-vitro elimination of Mycoplasma Pneumonia. Macrolides are the best option, and they work by binding to a particular set of ribosomes, thus preventing the formation of proteins vital for the survival of the bacteria and have an anti-inflammatory effect (Kliegman et al. 2016). The action of binding to the ribosomes prevents cell growth and in high concentrations death of the cell. Macrolides are transported to the site of the infection by leukocytes as they respond to the threat.

Clinical Relevance

There have been reported cases of drug-resistant Mycoplasma Pneumonia from around the year 2000. In Asia, the resistance is as high as 90% with rising numbers in Europe (Berger, 2019). Resistance is high against erythromycin and azithromycin that are used to treat the bacteria. Macrolide resistance is also on the rise where there have been over usage of the drug. Macrolide resistance was reportedly higher in children since Mycoplasma Pneumonia affects them most; however, there was no noticeable increase in virulence of the bacteria in light of the resistance. The P1 strain has not shown evidence of resistance to macrolides suggesting a polyclonal basis for the resistance.

The available alternatives to macrolides are tetracyclines, fluoroquinolones, and systemic corticosteroids. The replacements, however, are known to cause contraindications and are not recommended for children in countries like Korea (Berger, 2019). The PIDS and IDSA bodies recommend initial administration of azithromycin in infants and children three months and older as of the first line against Mycoplasma Pneumonia resistance. Doxycycline is recommended for children under the age of 7 and below and levofloxacin or moxifloxacin for young adults and teenagers.

References

Berger, S. (2019). Mycoplasma Pneumoniae Infection. Los Angeles: Gideon Informatics, Incorporated.

Brown, R., Nguipdop-Djomo, P., Zhaom H., Stanford, E., Spiller, O., & Chalker, V. (2016). Mycoplasma pneumoniae Epidemiology in England and Wales: A National Perspective. Frontiers in Microbiology, 7, 157. doi: 10.3389/fmicb.2016.00157

Chen, Z., Yan, Y., Zhu, H., Shao, X., & Ji, W. (2013). Epidemiology of community-acquired Mycoplasma Pneumoniae respiratory tract infections among hospitalized Chinese children, including relationships with meteorological factors. Hippokratia, 17(1), 20-26. https://www.ncbi.nlm.nih.gov/pubmed/23935339