Transcript Mycoplasma and Ureaplasma

Mycoplasma and Legionella
Ziad Elnasser, MD, Ph.D
Mycoplasma and Ureaplasma
No cell wall.
 The smallest of free living organisms.
 Associated with human disease:
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Mycoplasma pneumoniae.
 Mycoplasma hominis.
 Ureaplasma urealyticum.
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Microbiology
0.2 – 0.3 μ pleomorphic, filamentous.
 No cell wall, triple membrane contains
sterols from tissue.
 No stains, small genome.
 Aerobic to facultative anaerobe, grows on
Mycoplasma agar, inverted fried egg.
 Binds to RBC’s on agar (Hemadsorption).
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Mycoplasma pneumoniae
Pneumonia in young, any season.
 Atypical pneumonia, scattered patches.
 10% of all Pneumonias.
 Droplets, low infectious dose, temperate
climates, 5-15y of age.
 Sporadic endemic illness in families.
 IP 2-15 days, infectivity 60%.
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Pathogenesis
Trachea, bronchi, bronchioles and alveoli.
 Cytadhesin (P1) binds to oligosaccharides
containing sialic acid.
 I Ag on surface of RBC’s.
 Destroys cillia and causes desquamation.
 Shedding 2-8 days before symptoms to 14
weeks after infection.
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Immunity
Local and systemic.
 CF antibodies, IgA antibodies 2-4 weeks.
 Cold agglutinins IgM binds to I Ag on
surface of RBC’s in 66% of cases.
 Reinfection could occur.
 Symptoms related to immune response,
more severe in adults.
 Raynaud’s phenomena.
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Clinical Aspect
Mild tracheobronchitis, fever, cough,
headache and malaise.
 Less severe pneumonia (walking
pneumonia).
 X-ray shows patchy pneumonia, lower
lobe.
 Pleural effusion in 25%
 Pharyngitis with fever, sore throat.
 Otitis media, myringitis, and pneumonia.
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Diagnosis
Clinically overlaps with viral and bacterial.
 PMN’s in gram stain, bacteria not seen.
 Isolation in special media, incubation for
one week or longer.
 Serology 4 fold increase in titre.
 Cold agglutinins not specific, adenovirus,
Epstien barr virus.
 Immune assays, DNA hybridization, PCR.
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Treatment
Erythromycin, Tetracycline.
 Clarthromycin, Azithromycin.
 Flouroquinilone.
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Legionella
Gram negative bacilli, American legion
convention.
 Environmental pathogen.
 Thin 0.5-0.7μm, filamentous 20μ long.
Poor staining with gram but silver
impregnation is used (Dieterle).
 3 flagella, motile, non spore former.
 Outer membrane LPS but less compared
to other g- bacteria.
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Growth and Classification
L-cysteine, ferric ions, acidic pH.
 2-5 days needed for growth,ground glass
colonies.
 Catalase, oxidase, β lactamase.
 14 serogroups, L.bozemanii, L.dumoffii,
L.micdadei.
 Non infects humans.
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Legionellosis
Inhalation, destructive pneumonia.
 1976 American Legion convention.
 Other stored sera proved of previous
pneumonia caused by Legionella.
 Water reservoirs of large buildings.
 No person to person transmission.
 Not present in healthy people.
 Low virulence to humans.
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pathogenesis
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Necrotizing multifocal pneumonia.
Alveoli and terminal bronchioles.
Inflamatory exudate contains fibrin, PMNs,
macrophages, and erythrocytes.
Facultative intracellular pathogen→alveoli
→alveolar macrophages→OMP binds C3
facilitates phagocytosis→Macrophage invasion
potentiator OMP→cell entry→coiling
phagocytosis→apoptosis and pore forming
toxin.
Immunity
Virulence because it is intracellular.
 CMI is the key.
 Inhibition of MHC antigens.
 Humoral immunity is less important.
 Antibodies only enhancing phagocytosis.
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Clinical aspects
Toxic pneumonia, myalgia, headache,
fever, dry cough.
 Chills, delirium, pleuritic chest pain,
vomiting diarrhea.
 Patchy infiltrates in chest x-ray.
 Hepatic dysfunction.
 Mortality is about 15%.
 Pontiac fever.
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Diagnosis
DFA.
 Culture of infected tissues.
 Lung aspirates, bronchoalveolar lavage,
lung biobsy.
 Buffered Charcol Yeast Extract (BCYE).
 PCR.
 Ag detection.
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Treatment
Erythromycin.
 Most legionella produces beta lactamases.
 Tetracycline, rifampin, newer quinolones.
 Azithromycin, clarithromycin.
 Prevention:Hyperchlorination of water.
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Heating water to more than 70C.
 Silver and cupper ionization systems
 Mists of water.
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Pseudomonas
Gram negative bacillus.
 Colonizers and contaminants,
apportunistic diseases.
 Bacteremia, arthritis, abscesses, wounds,
conjunctivitis, UTI.
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Ps. aerugenosa
Aerobic motile, g- rod, pale staining.
 Colourfull water soluble pigments.
 The most resistant to antimicrobial agents.
 Simple growth requirements.
 20 – 40 C, Oxidase +, fruity odor.
 Pyocyanin, Flourescin.
 Lps , pili, polar flagellum, alginate
(mannoronic and glucoronic acid) CF pts.
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Extracellular products
Exotoxin A ( lecithinase, hemolysis,
collagenase).
 ADP-ribosylation of EF-2.
 Exoenzyme S ADP-ribosylates vimentin
acts as adhesin.
 Elastases.
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Diseases
Environment, throat, stool, > in hospitals.
 Leukemia, Cystic fibrosis, and burns.
 Humidifiers, inhalators, contact lenses
sloutions, medications, disinfectans, sinks.
 Food and water no problem.
 CF chloride ion transport defect, thick
mucus.
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pathogenesis
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Attachment favored by loss of fibronectin.
Exotoxin A, exotoxin S, and elastin.
Hemorragic destruction of blood vessles.
CS pts cells are less sialated increases
receptors for the organism.
Biofilm (glycocalyx), alginate over produced.
Interfers with antibiotics and Immune
mechanisms.
CMI deficient patients.
Clinical aspects
Apportunists.
 pnemonia and in CF is chronic.
 Otitis externa, swimmers ear, in DM.
 Ecthyma gangrenosum.
 Diagnosis is simple.
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Treatment
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Most resistant to penicillin, ampicillin,
cephalothin, tetracyclin, streptomycin,
chloramphenicol, sulfonamide.
New aminoglycosides.
Third and fourth generation cephalosporins.
Carbapenems and flouroquinolones.
CF aerosolized tobramycin.
Vaccines tried in CF some improvement.
Burkholderia, Acinetobacter, aeromonas and
pleisomonas.