Biology 216 - Lect 33 - Chlamydia
I. Chlamydia in General
A. Bacteriology - Obligate intracellular (Induce phagocytosis
by all cell types (epithelia, phagocytes))
Grow within phagosome (inhibit phago/lysosome
fusion or escape lysosomal contents).
Degenerative evolution:
Use host ATP, enzymes, nucleic acids.
Developmental cycle - differentiate into two forms.
1. Elementary body - extracellular
infectious stage (small than bacteria)
Attach to host cells (tropism for columnar
epithelial cells of mucus membranes) -
Basis of Ag tests
2. Reticulate body - metabolically active;
Multiply into colony in cell (Membrane bound inclusion)
Many infectious elementary body progeny
produced and released upon cell
rupture or exocytosis
B. Diagnosis
1. Direct exam - Iodine or Giemsa stain for inclusion body
(not easy to find) - Stain glycogen coat of retic body
Old way - Culture in McCoy cells (egg, tissue culture)
48 hours - look for inclusion (amplified)
2. Antigen detection - Fluorescent antibody for
elementary body (Microtrak); ELISA
3. Serodiagnosis - not routine since most surface;
Only with invasive C. psittaci; C. trach serology does exist.
4. DNA probes available and widely accepted.
II. C. trachomatis (misleading name since many serovars
and disease - TRIC Agents)
A. Trachoma - keratoconjunctivitis (inflammation of cornea) ->
partial or total blindness (millions)
1. Pathogenesis - high virulence serovar (A - C); Person ->
person clothing, towels -> eye.
Local infection - inflammation (pyogenic);
Neovascularization and hypertrophy.
Single infection is mild; Chronic -> opacity, ulceration,
secondary infection. Progressive damage over years
Scaring of conjuctiva -> pebbly appearance
2. Diagnosis - Clinical picture; Inclusions in epithelia of eyelid
and pebbly appearance; Fl-Ab
3. Treatment (local antibiotics); 4. Prevention - personal hygiene.
B. Inclusion conjunctivitis - lower virulence serovar (D - K)
1. Pathogenesis - Adults (unchlorinated pools and direct);
Neonate from birth canal.
Local inflammation and inclusions. Problem if chronic.
Also mild pneumonia
C. Non-gonococcal urethritis (NGU) -
Same serovar as inclusion conjunctivitis
NGU - 50 % Chlamydia. Remainder Mycoplasma, Ureaplasma,
1992 reportable to CA State Dept not CDC.
Estimated 4 million/yr in US; 1/2 million PID;
Reportable nationally 1996
1. Pathogenesis - STD, Local colonization,
Most asymptomatic,
Same as GC including complications
2. Diagnosis - Clinical suspect GC or NGU.
Direct smear PMN w/o Gm negative intracellular diplococci
Ag detection: ELISA (Chlamydiazyme); Fl-Ab (Microtrak)
No culture (Used to inoculate McCoy cells); DNA probe to rRNA
3. Treatment - antibiotics.
4. Prevention - Erythromycin in eye of neonate 1 hour after birth.
III. C. psittaci - zoonosis in bird populations (crowding/stress) -
parrot fever, ornithosis, psittacosis; Reportable
A. Pathogenesis - 100 cases/yr; From secretion of
infected birds (parrots, turkey....)
Birds - respiratory or diarrhea (most severe in parrots,
asymptomatic in others)
Human - Inhalation, lung and systemic multiplication
(2 week incubation)
Lung - Edema, exudate, hemorrhage,
bloody sputum, consolidation, anoxia.
Systemic - Granulomatous liver/spleen, endocarditis,
fever, headache, myalgia
Lasts few weeks; Mortality 20 % w/o treatment, 5 % with.
B. Diagnosis - History (bird handlers); Lab serodiagnosis.
C. Treatment - antibiotics
IV. TWAR (Taiwan Acute Respiratory) -
A. Chlamydia pneumoniae - similar to Mycoplasmal pneumonia.
Sequenced 2000
B. Role in Atherosclerosis?
1. Correlation between C. pneumoniae and atherosclerosis
Fl-antibody analysis of plaque material (strong correlation)
2. Other evidence: Antibody titer, PCR, culturable.
3. In vitro endothelial cell response to C. pneumoniae
- Release coagulation factors
- Release of inflammatory cytokines
4. Conclusion:
- Strong correlation
- Cause or effect?
- Initiate or contribute?