What do you understand by the term atypical pneumonia?
Is atypical pneumonia a 'community acquired pneumonia' or 'hospital acquired pneumonia' ?
Which organisms are responsible for atypical pneumonia?
The pathogens causing atypical pneumonia include:
Viruses including influenza A and B, parainfluenza, adenovirus and respiratory syncytial virus
What is the source of these infections? What is their habitat?
Mycoplasma pneumonia / human
Chlamydia psittaci / Birds
Chlamydia pneumoniae /
Coxiella burnetii /
Francisella tularensis /
Legionella pneumophila / Water
Viruses including influenza A and B, parainfluenza, adenovirus and respiratory syncytial virus./ human
Describe the clinical picture (mode of presentation) of atypical pneumonia, mycoplasma pneumonia as an example.
Commonly between 5-15 years
Scratchy throat (tracheitis)
Refractory dry cough (bronchitis)
Low grade fever
Do not seek medical help
What are the physical findings of atypical pneumonia?
No signs of consolidation
Diffuse small airway obstruction
Bullae in tympanic membrane (bullous myringitis) in mycoplasma pneumonia
What are the radiological findings of atypical pneumonia?
Describe morphological and cultural characteristics of mycoplasma pneumonia.
Mycoplasma pneumonia is one of the smallest free-living microorganisms
It lacks a cell wall, and hence stains poorly on usual bacterial stains
It grows aerobically and produces tiny colonies on special agar that have an "inverted fried egg" appearance
Hemabsorption of red blood cells on the surface of agar plates is a feature of mycoplasma pneumonia
How does mycoplasma pneumonia produce the damage?
Mycoplasma pneumonia attaches to the cilia and microvilli of cells lining the bronchial epithelium
Attachment is mediated by a surface adhesion, the P1 protein, which binds to oligosaccharides containing sialic acid in the bronchial epithelial cells
Ciliary action is stopped followed by loss of cilia and desquamation of epithelial cells into the lumen
Oligosaccharide receptors (1-F1) are not found in non-ciliated cells or mucus
Describe the pathological findings of mycoplasma pneumonia.
Sloughing of cells into the lumen is responsible or the cough that defines the clinical presentation
The inflammation conspicuously involves the interstitial space or alveolar wall with mono-nuclear cells
The inflammatory process involves the trachea, bronchioles, and peribronchial tissues
The lumen is filled with purulent exudate containing polymorphonuclear leukocytes
Bronchial and bronchiolar walls are infiltrated with monocytes and plasma cells
There is widening of peribronchial septae and hyperplasia of type II pneumocytes
Organisms are shed in respiratory secretions for 2-8 days after onset of symptoms, and shedding can continue for as long as 14 weeks after infection
Other pathogens producing atypical pneumonia produce similar pathologic changes.
How does our defenses respond to mycoplasma pneumonia?
Immunity to Mycoplasma pneumonias:
Local and systemic specific immune responses occur
IgA antibody wanes 2-4 weeks after onset of infection
Complement-fixing serum antibodies peak at 2-4 weeks and disappear in 6 to 12 months
Nonspecific immune response to the outer membrane also develop e.g., cold hemagglutinins (IgM antibodies that react with I antigen of human RBCs)
Immune mediated mechanisms play a role in M. pneumonia infection
Reinfections is associated with quicker development of inflammatory changes in experimental animals
High levels of IgG immune complex are found in the acute phase of illness and correlate with degree of pulmonary involvement
M. pneumonia can stimulate B and T lymphocyte mitogenic activity
Do you get immunity for re-infection with mycoplasma pneumonia?
Immunity to M. pneumonia is not complete, and re-infection is common
Clinical disease is more severe in older children, suggesting that many clinical manifestations are due to cellular immune responses
How can we diagnose mycoplasma pneumonia?
Definitive diagnosis is made by the following:
Isolation of the organism
takes 2-3 weeks and is too expensive and time consuming
Detection of M. pneumonia antigens or nucleotide sequences in clinical specimens by enzyme immunoassay or per DNA hybridization is under development
Demonstration of an antibody response
the compliment fixation test detects specific antibody and is commonly used
antibody rises 7-9 days after infection, peaks at 3-4 weeks and lasts for 6-12 months
a four-fold rise or decline in titer is necessary for diagnosis
Two thirds of patients with symptomatic M. pneumonia will develop high titers of cold agglutinins
these are not specific and are seen in other viral infections (adenovirus, EBV)
this test is simple and can be performed at the bedside
New assays include indirect immunofluorescence and ELISA and detect IgM as well as IgG. An ELISA using adhesion PI protein is being developed.
Antigen detection and culture of sputum for specific pathogens helps establish the diagnosis in other cases of atypical pneumonia. Serology is useful but acute convalescent titers are needed.
How do you treat mycoplasma pneumonia?
Erythromycin and tetracycline are equally effective in treatment of M. pneumonia infection
they shorten the course of infection but do not eliminate the carrier state
therapy is generally continued for 2-3 weeks, as relapses can occur in up to 10% cases
Clarithromycin and azithromycin are also effective but much more expensive
Quinolones such as ciprofloxacin have in vitro efficacy against mycoplasma, but are expensive and contra-indicated in children
Can we use beta-lactum antibiotics to treat mycoplasma pneumonia?
Since mycoplasmas lack a cell wall, beta-lactam antibiotics are ineffective for treatment
How can we prevent infections with agents causing atypical pneumonia?