Primary Atypical Pneumonia ("walking pneumonia" – there are other causes of this too), URIs in children
Characteristics:
Mycoplasmae are the smallest free-living life forms (0.2-0.3 nm diameter, several times longer)
bacteria without cell wall (not gram stainable, not affected by beta-lactam antibiotics) – sterol-containing cell membrane
require complex growth medium with sterols – slow growing (3+ days), produce small (50-500nm) "fried egg" colonies
filamentous morphology with a terminal organelle, gliding motility
Pathogenesis:
requires close contact for transmission (e.g., within families)
penetrate mucociliary blanket of respiratory mucosa, then non-invasively attach between and parallel to cilia
ciliotoxic – produce H2O2 and superoxide (overwhelm host cell defense mechanisms against peroxidative injury)
induces T-cell memory but only humeral immunity, so progressively worse immune response with each reinfection
Clinical Features:
like strep pneumonia, except later onset (weeks not days) and fewer symptoms (malaise, then cough)
minimal findings on chest exam but chest x-ray shows patchy bronchopneumonia (not lobar as in strep)
autoimmune manifestations – cold agglutinins (antibodies that agglutinate group O RBCs at 4° C), rashes, arthritis
Management:
Diagnosis by IgM (IgG takes too long) – treat with a macrolide or a tetracycline
Prevention:
Protective immunity is incomplete, and reinfections are frequent
autoimmune effects make vaccination impossible (immunosuppression prevents disease, vaccination makes it worse)
Related to:
Ureaplasma urealyticum
– causes urethritis caused due to NH3 produced from urea by urease
Mycoplasma hominis
– causes placental infection that interferes with fetal nutrition (lack of growth)
Chlamydia trachomotas
Disease:
Chlamydia
Characteristics:
very small bacteria – obligate intracellular bacterial parasite; STD; specialized bacteria
have cell wall during part of life cycle, multiply by binary fission
infectious particle is 0.3 nm elementary body, metabolically inactive with an impermeable cell wall (no peptidoglycan)
Pathogenesis:
affects any transitional or columnar epithelium – upon phagocytosis, lysosomal fusion is inhibited
reducing atmosphere in vesicle breaks disulfide bonds, so cell wall becomes permeable – forms 1.0 nm reticulate body
reticulate bodies are metabolically active and replicate – metabolism produces oxidizing atmosphere, reforming cell wall
utilization of cell nutrients and enlarged phagosome cause problems – eventually, elementary bodies lyse the cell
Clinical Features:
(1) conjuctivitis – from contact with infected secretions, usually congenitally – can lead to trachoma ("dry eye") blindness
leading preventable cause of blindness
(2) pneumonia – in infants from congenital infection
(3) urethritis in males – often complicated by epididymitis
(4) cervicitis in females – often complicated by salpingitis (infection of fallopian tubes) – causes infertility
(5) proctitis – inflammation of the rectum
(6) lymphogranuloma venereum – invasive serotypes spead from urethra causing suppuration and scarring of regional lymph nodes and contiguous tissues (such as the rectum) or formation of draining fistulas
Management:
Diagnosis by direct culturing, IgM, immunofluorescence, ELIZA, or in situ DNA hybridization
treat with a macrolide or a tetracycline (sensitive to sulfonamides and erythromycin too) – no b -lactam antibiotics
Prevention:
Vaccination unlikely since protective immunity is transient and serotype specific (18 serotypes altogether)
Related to:
Chlamydia psittaci
– natural hosts are birds and animals, causes pneumonia when transmitted to humans
Chlamydia pneumoniae
– recently identified species, causes upper and lower respiratory disease
Rickettsia prowazekii and Rickettsia rickettsii
Diseases:
Epidemic Typhus (R. prowazekii) – carried by body louse, common with poor hygiene
Rocky Mountain Spotted Fever (R. rickettsii) – carried by deer or wood tick, may be confused with meningococcemia
Characteristics:
small (0.3x0.5 nm) cocco-bacilli bacteria with permeable membrane – requires insect vector for trans.
obligate intracellular parasites have glycolytic enzymes, cytochromes, and most of Krebs cycle, but need cofactors
Pathogenesis:
enter into small blood vessel at site of vector bite and infect vascular epithelial cells
attach to cell membrane and initiate phagocytosis with rickettsial phospholipase on host cell membrane
immediate escape of Rickettsia from phagosome by phospholipase action, followed by replication
replication in cytoplasm or nucleus, then release from cell by lysis or via cell membrane filopodia (depends on species)
reactive hyperplasia of infected cells leads to cell destruction and micro-thrombus formation
perivascular extravasation of RBC and attraction of inflammatory cells produces vasculitis of small blood vessels
survival of host depends on extent of vasculitis and number of organ systems involved