Chlamydia trachomatis, Mycoplasma, Ureaplasma, and other Non-Gonococcal urethritis: Chlamydia trachomatis: Microscopy and culture:
- Small unicellular round-to-ovoid bacteria that cannot
stained by Gram’s stain.- Some inclusion bodies retain Iodine or the counter
stain safranin. - Rigid Cell wall .
- The cell envelope has two lipid bilayers with cell wall
material (but not peptidoglycan nor muramic acid).
n
- Obligatory intracellular parasite.- It depends on the host cellular energy compounds ATP,
and NAD.- Cultivated in yolk sac of embryonated egg or tissue
culture.
Chlamydia inclusion :R. bodies. Chlamydia inclusion .
Pathogenesis and life cycle:-Transmission: Sexual route.-Infectious part: The elementary body.-The elementary bodies taken by phagocytosis into susceptible host cell (Columnar epithelial cells).-Once inside the cell, the elementary body prevents fusion of the phagosome and lysosomes.
-It will converted into metabolically active dividing Reticulate body. (non-infectious body).-Inclusion bodies. -After 48 hours, rupture of infected cell to release many elementary bodies.-Host cell death, and infection of another cell.
Chlamydia life cycle:N
Tissue damage induced by Chlamydia trachomatis:1-Nongonococcal urethritis: -Caused by: Serovars: D,E, F,.., to K. - In male : Urethritis, infection could extend to epididymitis and prostatitis but rarely to testicles; (Orchitis: very rare). -One-third of patients have Reiter Syndrome (HLA-B27); Acute aseptic arthritis and urethritis. - In Female: Cervicitis and Pelvic inflammatory disease: Endometritis, Salpingitis. -Exposure to Antibiotics or Interferone-Gamma results in persistence infection. - Tubal factor infertility and Ectopic pregnancy.
N
2-Lymphogranuloma venereum:(LGV): more invasive infection
-Caused by Serovars: L1, L2, and L3.
-Enters small skin breaks of external genitalia.
-Papules in the external genitalia.(for one to two months).
-Herpetic-like Ulcer of genitalia.
-More invasive infection.
-Painful swelling of inguinal and perirectal lymph nodes.
- Lymphatic Obstruction; Elephantiasis of Genitalia.
Clinical picture of Chlamydia trachomatis: N
Clinical picture of Chlamydia trachomatis:
Urethral discharge : (more mucoid with fewer pus cell). Chlamydial Cervicitis.
Diagnosis of Chlamydia trachomatis infection: Clinical specimens:Urethral discharge, HVS, urine, and Scraping of infected epithelial cells or Squamocolumnar junction swabs. 1- Direct microscopy: A-Immunofluorescent microscopy. B-Electron microscopy. 2-Detection of Chlamydia genetic material by PCR.
3-Serology: Serologic testing for specific antibodies is not helpful except in suspected Lymphogranuloma venereum. 4-Antibiotic sensitivity: Doxycycline, azithromycin, and Erythromycin.
Laboratory diagnosis:
Immunofluorescent staining of inclusion body. Electron microscopy and immuno-electrone microscopy for inclusions.
Mycoplasma hominis, Mycoplasma genitalium, and Ureaplasma urealyticum:- The smallest prokaryotic microbe capable of growth on cell-
free media. - Because of their extremely small size (0.1-0.3 micrometer), Mycoplasma species pass through sterilization filters.
- Lacking cell walls, all species are enclosed instead by lipid
bilayer membrane containing sterols.
- Due to the absence of Cell walls (No peptidoglycan cell wall): 1-The bacteria are plastic, pleomorphic in nature, and cannot be classified as either cocci nor bacilli. 2-The bacteria are resistance to penicillin and cephalosporins.
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- Double-stranded DNA genomes measure less than one million Kilodaltons.
Cultural characteristics and colony morphology: - Facultative anaerobes, and some species are strict anaerobes.- Fastidious for external source of cholesterol (serum).- Given appropriate supplementation, they can be grown in cell-
free media.- Colonies are visualized microscopically by 30 to 100 x
magnification.- Colonies show a characteristics (fried egg) appearance.
Biochemical activities of Mycoplasma and Ureaplasma:-Mycoplasma hominis and Ureaplasma urealyticum grow more rapidly than Mycoplasma pneumoniae.-They can be distinguished by their carbon utilization patterns; -M. hominis degrades arginine. -U. urealyticum hydrolyses urea; ammonia can destroy the epithelial cells.
In female:-The major clinical condition associated with M. hominis is postabortal fever.-M. hominis is recovered locally in cases of Pelvic inflammatory disease.-All M. hominis species are Erythromycin resistance.
n
- Ureaplasma urealyticum and Mycoplasma genitalium are associated with cases of PID; Endometritis and vaginosis.
- Tetracycline is the drug of choice for treatment of M. hominis infection. - Other species are sensitive to azithromycin.
In male:- Ureaplasma urealyticum and Mycoplasma genitalium are
associated with cases of Urethritis. - The infection could be disseminated to other tissue in immunocompromised patients.
Bacterial vaginosis and PID:-The most common vaginal infection worldwide.-Disruption of vaginal normal flora (Lactobacillus species).-Causative agents: 1-Gardnerella vaginalis. Gram-variable-staining facultative anaerobic Coccobacilli.
2-Mycoplasma species or other bacterium.
-Other causes of vaginal infection: -Fungal infection: Candidiasis. -Protozoan infection.
Vaginal Candidiasis:
-Most commonly encountered opportunistic mycoses worldwide.
-Cellular immunity protects against mucocutaneous candidiasis,
neutrophils protect against invasive candidiasis
-They are members of the normal flora.
-More than 150 species of Candida known.-Only ten species cause disease in humans.
-The most common species of medical significance are:
1-Candida albicans.
2-Candida tropicalis.
Morphology and cultural characteristics: Candida is thin-walled, small yeasts (4 to 6 microns) that reproduce by budding.Microscopically: Candida albicans is a dimorphic fungi, in addition to budding yeast cells, pseudohyphae, it also can produce true hyphae.Asexual Germination of Candida occurs by production of Blastospores or Chlamydiospores.
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-Macroscopically: on agar media they produce creamy colonies within 24 hours at 37 C or room temperature.
-Candida species produce a small ,white, rounded colonies with feet projection and regular margin.
Germ tube test: -Candida species must be incubated with serum for 90 minutes at 37 C;
-yeast cells of C. albicans will produce true hyphae or germ tube.
Clinical presentation of Candida albicans:
- Candida albicans causes almost 100% of cases of
oropharyngeal candidiasis and at least 90% of cases of
Candida vulvovaginitis.
- Vaginal candidiasis presents as itching and burning pain of
the vagina.
- Thick or thin white discharge.
- HVS, and discharge should be examined for differential
diagnosis.
- Candida albicans can cause urethritis in male.
Trichomoniasis: (Vaginal and Urethral infection): Trichomonas vaginalis: Classification: Urogenital Mastigophora. Morphology:
20-30 um ,oval or pyriform in shape ,with short undulating membrane ,
axostyle and four free flagella.Transmission: sexual intercourse, and contaminated clothes.
Pathology and Clinical picture: Vaginitis - itching, copious- yellowish offensive discharge. Urethritis in male and female. Prostatitis and seminal vesiculitis in male.
Diagnosis: finding the trophozoite in smears from vaginal or urethral discharge.
Trichomoniasis:n
Congenital and Perinatal infections:
Congenital (intrauterine or prenatal) infections are those transmitted during fetal life by transplacental route from mother to fetus.
The causative agents are:1-Cytomegalovirus.2-Herpes simplex virus.3-HIV.4-Parvovirus B19.5-rubella virus.6-Treponema pallidum.7-Toxoplasma gondii.
The effect of intrauterine infection on fetus:Three types of effects on the growing fetus may result from this infections:1-Abnormal organogenesis: rubella :structural abnormalities in tissue and organs; defects in retina, pulmonary artery stenosis. 2-Inflammatory response results in tissue damage: CMV and T.gondii: cause Cerebritis; so cerebral atrophy and intracranial calcification.3-Placental insufficiency: low birth weight, premature birth, fetal death.
N
Perinatal infections are acquired from mother at birth or during the first four weeks after birth fromMaternal or non-materinal sources.
Causative agents:1-E.coli and other Enterobacteriaceae.2-Group B Streptococci.3-Listeria monocytogenes.4-Gonococci and Chlamydia5-Viruses and Candida.
Effects: Bacterial sepsis: Mortality rate is 10-40%.Meningitis: Significant neurological damage: in 20-50% of survivors.
