1.0 pneumoniae colonisation or asymptomatic infection. (Chaudhry, Ghosh

1.0
| Microbe Classification

 

Mycoplasma pneumoniae belongs to the class
Mollicutes and family Mycoplasmataceae. Mycoplasma pneumoniae cells have an elongated shape that
is approximately 0.1–0.2 µm (100-200 nm) in width and 1-2 µm (1000-2000 nm) in length. The bacteria lacks a cell wall making it
insensitive to beta-lactam anti-microbial agents (which target cell wall
synthesis), prevents gram staining, and contributing to their pleomorphic nature.
(Kashyap & Sarkar, 2010) Mycoplasma pneumoniae is a strict aerobe
compared to other mycoplasma which tend to be facultative anaerobes.

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2.0
| Mechanisms of Virulence

 

2.1 |
Cytadherence

M. pneumoniae is an extracellular pathogen that has evolved a specialized
attachment organelle for close association with host cells. M.
pneumoniae’s attachment is paramount to the survival and existence of the
bacterium within the host. (“Mycoplasma pneumoniae infection”, 2016)
The close association between M. pneumoniae and the host cells
prevents the bacterium from being removed by the host’s mucociliary clearance
mechanisms. (Waites & Talkington, 2004) The bacterium attaches to
and damages the respiratory epithelial cells at the base of cilia, activating
the innate immune response and producing local cytotoxic effects.

 

2.2 | Virulence Factor

M. pneumoniae produces a unique virulence factor known as Community Acquired
Respiratory Distress Syndrome (CARDS) toxin. The CARDS toxin most likely aids
in the colonization and pathogenic pathways of M. pneumoniae,
leading to inflammation and airway dysfunction. (Waites & Talkington, 2004)
 While M. pneumoniae primarily
lives on the surface of the respiratory epithelial cells, it has also been
shown to invade tissues and replicate intracellularly.

 

 

 

 

 

2.3 | Associated Host Independent factors

 

2.3.1 | Immunopathogenesis:  Cytotoxicity and Inflammation

A major pathway of M. pneumoniae pathogenesis
is induction of inflammation via the TLR-mediated cytokine release and
generation of free radicals. In addition an exaggerated innate immune response
in M. pneumoniae infection can be due to a positive feedback
effect of previous M. pneumoniae colonisation or asymptomatic
infection. (Chaudhry, Ghosh & Chandolia, 2015) Hydrogen peroxide and superoxide is produced locally, which has a
cytopathic effect on airway epithelium and cilia and is responsible for
persistent cough. (Mayer, 2016) Current evidence from human and animal studies suggests that cytokine
production and lymphocyte activation may either minimize disease through the
enhancement of host defense mechanisms or exacerbate disease through
immunological lesion development. It also causes an immune repose monopolizing
the immune systems but through antigenic variations it capable of avoiding
being phagocytized. By monopolizing the immune system, the pathogen is capable
of making the host susceptible to other pathogens.                                     

 

3.0
| Clinical outcome and Disease presentation

 

Mycoplasma
pneumoniae infections can occur in the upper or lower respiratory
tract. Disease presents itself with several
symptoms

–       Fever

–       Malaise

–       Persistent, slowly worsening dry cough

–       Headache

–       Sore throat

–       Sore chest and tracheal tenderness

The most common
clinical syndrome following infection with M. pneumoniae is
tracheobronchitis, which is seen in 70-80% of the infections. Approximately one
third of infected persons will develop pneumonia which is usually mild but of
long duration. (Mycoplasma pneumoniae infection – including symptoms, treatment
and prevention, 2016)

Extrapulmonary complications involving all of the major organ
systems can occur in association with M. pneumoniae infection as
a result of direct invasion and/or autoimmune response. The extrapulmonary
manifestations are sometimes of greater severity and clinical importance than
the primary respiratory infection. (Waites & Talkington, 2004)

 

4.0
| Mode of Transmission

 

Mycoplasma is
a communicable disease spread through contact transmission: droplet
transmission and common vehicle transmission: airborne transmission. The reservoir
of infection is the human body where the portal of entry is the mucous
membranes of the upper respiratory tract. Mycoplasma Pneumoniae can be spread
by direct contact with nose and throat (portal of exit) discharges of the infected
persons through coughing, sneezing or talking. Alternatively, one can become
infected indirectly by touching a person or a fomite that is contaminated and then
allowing the infectious particles to enter the nose or mouth.  (Mycoplasma,2011) The organisms are
carried over a droplet and inhaled directly into the respiratory tract of new
person. Transmission is thought to require prolonged close contact with an
infected person. Spread in families, schools and institutions occurs
slowly.

 

4.1
| Associated precautions

Tier two
precautions are always used in conjunction with Standard Precautions for
clients with known or suspected infections that are spread through: airborne
and droplet transmission.

Airborne
and Droplet Precautions – These precautions are put into play when patients are
known or suspected of having serious illnesses transmitted by airborne droplet.

In admitting
and caring for patients:

Place the patient in a private room with negative air
pressure controls.

Limit movement of the patient outside the room and make
sure they wear a surgical mask when out and about.

Use of personal
protective equipment and hand hygiene before and after touching patients and/or
their surroundings preventing (indirect) transmission of disease through
fomites.

 

 

5.0
| Impact on healthcare system

 

 Despite the
availability of potent new antimicrobials and effective vaccines,1an estimated 5.6
million cases of CAP occur annually in the United States. (Fine MJ et al, 2000) The estimated
total annual cost of health care for CAP in the United States is $8.4 billion.
(Goss CH et al, 2003) The price includes the antibiotics and
diagnostics for pneumonia management. Choosing between outpatient and
inpatient treatment is a crucial decision because of the possible risk of death. This
decision not only influences diagnostic testing and medication choices, it can
have a psychological impact on patients and their families. On average, the
estimated cost for inpatient care of patients with CAP is $7,500. Outpatient
care can cost as little as $150 to $350.17–19 Hospitalization
of a patient should depend on patient age, comorbidities, and the severity of
the presenting disease. The growing resistance of S. pneumoniae to penicillin. This pattern of resistance
increases the cost of treatment because of prolonged hospitalization, relapses,
and the use of more expensive antibacterial agents. (Kuti JL, Capitano B, Nicolau DP, 2002)

 

 

 

 

 

 

7.0
| Control mechanism

 

7.1
| Treatment

Mycoplasmas in general are bacteria that
lack a cell wall, so they require residence in a host organism, such as a human
or animal for survival. Therefore, all are inherently resistant to beta-lactam
antibiotics (e.g., penicillin, which target cell wall synthesis.  Effective treatment includes macrolides, the
antimicrobial of choice and tetracycyclines and fluoroquinolones. 
Although resistance to quinolones or tetracyclines among clinical isolates
of M. pneumoniae has not been reported, considering the side
effects of tetracycline therapy and fluoroquinolones not being recommended for
use in children, an effective vaccine against M. pneumoniae is
desirable. Inactivated vaccines have been tested in clinical trials and the
summarised efficacy was only 40% approximately against M. pneumoniae associated
pneumonia. (Linchevski, Klement & Nir-Paz, 2009)

 

7.2
| Overcome the spread of disease

The spread of disease is
overcome through antimicrobial stewardship and precautionary steps in
healthcare facilities.  Antimicrobial stewardship denotes coordinated
interventions to improve and measure the appropriate use of antibiotics by
encouraging the selection of optimal drug regimens. (Viasus D,
Vecino-Moreno, De La Hoz & Carratalà, 2016)

The problem of macrolide resistant M. pneumonia is emerging. Antibiotic
stewardship is needed to inhibit the inappropriate use of macrolide and new
antibiotics with a more acceptable safety profile for all ages need to be
explored. Physicians should practice prudent use of macrolide drugs due
to the emergence of macrolide-resistant strains of M. pneumoniae. (Cao, Qu, Yin & Eldere, 2015)

In the healthcare setting
compliance to standard and contact precautions, environmental disinfection
using chlorine-based solution, hand hygiene and educating staff and
patients/visitors on measures of infection prevention – which is all crucial in
preventing environmental contamination and/or indirect transmission between patients
via healthcare workers.

Consider establishing
prospective surveillance for pneumonia in affected areas Transmission of the
disease may sometimes continue despite control measures. Active surveillance
can enable public health officials to characterize the possible continuing circulation
of the disease and identify the potential need for adjustments to control
measures. (Mycoplasma pnuemoniae (Mp), 2011)

1.0
| Microbe Classification

 

Mycoplasma pneumoniae belongs to the class
Mollicutes and family Mycoplasmataceae. Mycoplasma pneumoniae cells have an elongated shape that
is approximately 0.1–0.2 µm (100-200 nm) in width and 1-2 µm (1000-2000 nm) in length. The bacteria lacks a cell wall making it
insensitive to beta-lactam anti-microbial agents (which target cell wall
synthesis), prevents gram staining, and contributing to their pleomorphic nature.
(Kashyap & Sarkar, 2010) Mycoplasma pneumoniae is a strict aerobe
compared to other mycoplasma which tend to be facultative anaerobes.

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2.0
| Mechanisms of Virulence

 

2.1 |
Cytadherence

M. pneumoniae is an extracellular pathogen that has evolved a specialized
attachment organelle for close association with host cells. M.
pneumoniae’s attachment is paramount to the survival and existence of the
bacterium within the host. (“Mycoplasma pneumoniae infection”, 2016)
The close association between M. pneumoniae and the host cells
prevents the bacterium from being removed by the host’s mucociliary clearance
mechanisms. (Waites & Talkington, 2004) The bacterium attaches to
and damages the respiratory epithelial cells at the base of cilia, activating
the innate immune response and producing local cytotoxic effects.

 

2.2 | Virulence Factor

M. pneumoniae produces a unique virulence factor known as Community Acquired
Respiratory Distress Syndrome (CARDS) toxin. The CARDS toxin most likely aids
in the colonization and pathogenic pathways of M. pneumoniae,
leading to inflammation and airway dysfunction. (Waites & Talkington, 2004)
 While M. pneumoniae primarily
lives on the surface of the respiratory epithelial cells, it has also been
shown to invade tissues and replicate intracellularly.

 

 

 

 

 

2.3 | Associated Host Independent factors

 

2.3.1 | Immunopathogenesis:  Cytotoxicity and Inflammation

A major pathway of M. pneumoniae pathogenesis
is induction of inflammation via the TLR-mediated cytokine release and
generation of free radicals. In addition an exaggerated innate immune response
in M. pneumoniae infection can be due to a positive feedback
effect of previous M. pneumoniae colonisation or asymptomatic
infection. (Chaudhry, Ghosh & Chandolia, 2015) Hydrogen peroxide and superoxide is produced locally, which has a
cytopathic effect on airway epithelium and cilia and is responsible for
persistent cough. (Mayer, 2016) Current evidence from human and animal studies suggests that cytokine
production and lymphocyte activation may either minimize disease through the
enhancement of host defense mechanisms or exacerbate disease through
immunological lesion development. It also causes an immune repose monopolizing
the immune systems but through antigenic variations it capable of avoiding
being phagocytized. By monopolizing the immune system, the pathogen is capable
of making the host susceptible to other pathogens.                                     

 

3.0
| Clinical outcome and Disease presentation

 

Mycoplasma
pneumoniae infections can occur in the upper or lower respiratory
tract. Disease presents itself with several
symptoms

–       Fever

–       Malaise

–       Persistent, slowly worsening dry cough

–       Headache

–       Sore throat

–       Sore chest and tracheal tenderness

The most common
clinical syndrome following infection with M. pneumoniae is
tracheobronchitis, which is seen in 70-80% of the infections. Approximately one
third of infected persons will develop pneumonia which is usually mild but of
long duration. (Mycoplasma pneumoniae infection – including symptoms, treatment
and prevention, 2016)

Extrapulmonary complications involving all of the major organ
systems can occur in association with M. pneumoniae infection as
a result of direct invasion and/or autoimmune response. The extrapulmonary
manifestations are sometimes of greater severity and clinical importance than
the primary respiratory infection. (Waites & Talkington, 2004)

 

4.0
| Mode of Transmission

 

Mycoplasma is
a communicable disease spread through contact transmission: droplet
transmission and common vehicle transmission: airborne transmission. The reservoir
of infection is the human body where the portal of entry is the mucous
membranes of the upper respiratory tract. Mycoplasma Pneumoniae can be spread
by direct contact with nose and throat (portal of exit) discharges of the infected
persons through coughing, sneezing or talking. Alternatively, one can become
infected indirectly by touching a person or a fomite that is contaminated and then
allowing the infectious particles to enter the nose or mouth.  (Mycoplasma,2011) The organisms are
carried over a droplet and inhaled directly into the respiratory tract of new
person. Transmission is thought to require prolonged close contact with an
infected person. Spread in families, schools and institutions occurs
slowly.

 

4.1
| Associated precautions

Tier two
precautions are always used in conjunction with Standard Precautions for
clients with known or suspected infections that are spread through: airborne
and droplet transmission.

Airborne
and Droplet Precautions – These precautions are put into play when patients are
known or suspected of having serious illnesses transmitted by airborne droplet.

In admitting
and caring for patients:

Place the patient in a private room with negative air
pressure controls.

Limit movement of the patient outside the room and make
sure they wear a surgical mask when out and about.

Use of personal
protective equipment and hand hygiene before and after touching patients and/or
their surroundings preventing (indirect) transmission of disease through
fomites.

 

 

5.0
| Impact on healthcare system

 

 Despite the
availability of potent new antimicrobials and effective vaccines,1an estimated 5.6
million cases of CAP occur annually in the United States. (Fine MJ et al, 2000) The estimated
total annual cost of health care for CAP in the United States is $8.4 billion.
(Goss CH et al, 2003) The price includes the antibiotics and
diagnostics for pneumonia management. Choosing between outpatient and
inpatient treatment is a crucial decision because of the possible risk of death. This
decision not only influences diagnostic testing and medication choices, it can
have a psychological impact on patients and their families. On average, the
estimated cost for inpatient care of patients with CAP is $7,500. Outpatient
care can cost as little as $150 to $350.17–19 Hospitalization
of a patient should depend on patient age, comorbidities, and the severity of
the presenting disease. The growing resistance of S. pneumoniae to penicillin. This pattern of resistance
increases the cost of treatment because of prolonged hospitalization, relapses,
and the use of more expensive antibacterial agents. (Kuti JL, Capitano B, Nicolau DP, 2002)

 

 

 

 

 

 

7.0
| Control mechanism

 

7.1
| Treatment

Mycoplasmas in general are bacteria that
lack a cell wall, so they require residence in a host organism, such as a human
or animal for survival. Therefore, all are inherently resistant to beta-lactam
antibiotics (e.g., penicillin, which target cell wall synthesis.  Effective treatment includes macrolides, the
antimicrobial of choice and tetracycyclines and fluoroquinolones. 
Although resistance to quinolones or tetracyclines among clinical isolates
of M. pneumoniae has not been reported, considering the side
effects of tetracycline therapy and fluoroquinolones not being recommended for
use in children, an effective vaccine against M. pneumoniae is
desirable. Inactivated vaccines have been tested in clinical trials and the
summarised efficacy was only 40% approximately against M. pneumoniae associated
pneumonia. (Linchevski, Klement & Nir-Paz, 2009)

 

7.2
| Overcome the spread of disease

The spread of disease is
overcome through antimicrobial stewardship and precautionary steps in
healthcare facilities.  Antimicrobial stewardship denotes coordinated
interventions to improve and measure the appropriate use of antibiotics by
encouraging the selection of optimal drug regimens. (Viasus D,
Vecino-Moreno, De La Hoz & Carratalà, 2016)

The problem of macrolide resistant M. pneumonia is emerging. Antibiotic
stewardship is needed to inhibit the inappropriate use of macrolide and new
antibiotics with a more acceptable safety profile for all ages need to be
explored. Physicians should practice prudent use of macrolide drugs due
to the emergence of macrolide-resistant strains of M. pneumoniae. (Cao, Qu, Yin & Eldere, 2015)

In the healthcare setting
compliance to standard and contact precautions, environmental disinfection
using chlorine-based solution, hand hygiene and educating staff and
patients/visitors on measures of infection prevention – which is all crucial in
preventing environmental contamination and/or indirect transmission between patients
via healthcare workers.

Consider establishing
prospective surveillance for pneumonia in affected areas Transmission of the
disease may sometimes continue despite control measures. Active surveillance
can enable public health officials to characterize the possible continuing circulation
of the disease and identify the potential need for adjustments to control
measures. (Mycoplasma pnuemoniae (Mp), 2011)

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