CHLAMYDIA Trichomonas Vaginalis Candidaiasis د. حامد الزعبي

Transcription

1 CHLAMYDIA Trichomonas Vaginalis Candidaiasis د. حامد الزعبي

2 Chlamydia

3 Epidemiology Risk factors and transmission are similar to other STDs In USA over 900,000 cases are reported each year, which is more than gonorrhea The asymptomatic cases among males and females are higher than in gonorrhea Risk is more Pregnant s and menstruating women Reinfection is frequent Reported Sexually Transmitted Diseases, United States, 2004

4 Family: Chlamydiaceae Genus: Chlamydia C. trachomatis - Urogenital infections, trachoma, conjunctivitis, pneumonia and lymphogranuloma venerium (LGV) Genus: Chlamydophilia C. psittaci - Pneumonia (psittacosis) C. pneumoniae - Bronchitis, sinusitis, pneumonia and possibly atherosclerosis

5 Chlamydia- Microbiology Small obligate intracellular parasites Inner and outer membrane LPS but no peptidoglycan Cell wall not well characterized Energy parasites Can t make ATP

6 Physiology and Structure Elementary bodies (EB) Extracellular form Rigid outer membrane Disulfide linked proteins Resistant to harsh conditions Non-replicating, non-metabolically active form Infectious form Bind to columnar epithelial cells (macrophages)

7 Physiology and Structure Reticulate bodies (RB) Intracellular form Fragile membrane Fewer disulfide bonds Metabolically active form Replicating form Non-infectious

8 Developmental Cycle of Chlamydia EB bind to host cells Epithelial Macrophage Internalization Endocytosis Phagocytosis Inhibition of phagosomelysosome fusion Reorganization into RB Growth of RB and release

9 Chlamydia curriculum Chlamydial Morphologies and life cycle Noninfectious reticulate body Infectious Elementary body Inclusion body Infectious Elementary body Host cell Host cell -Chlamydia induced cell apoptosis -Infect the neighboring cells

10 fe cycle Chlamydia curriculum hr

11 Pathogenesis Chlamydiae have a tropism for epithelial cells of the endocervix and upper genital tract of women, and the urethra, rectum and conjunctiva of both sexes. Once infection is established, there is a release of proinflammatory cytokines by infected epithelial cells. This results in early tissue infiltration by PMNs, later followed by lymphocytes, macrophages, plasma cells and eosinophils. If the infection progresses further (because of lack of treatment and/or failure of immune control), aggregates of lymphocytes and macrophages (lymphoid follicles) may form in the submucosa; these can progress to necrosis, followed by fibrosis and scarring.

12 C. trachomatis - Serovars

13 C. trachomatis Ocular infections Worldwide Poverty and overcrowding Endemic in Africa, Middle East, India, SE Asia United States - American Indians Infection of children Transmission: droplets, hands, contaminated clothing, flies, contaminated birth canal

14 Clinical Syndrome -Trachoma From: G. Wistreich, Microbiology Perspectives, Prentice Hall

15 Clinical Syndrome -Trachoma (C.trachomatis biovar: trachoma) Chronic or repeated infection Follicle formation on conjunctiva Scarring of the conjunctiva

16 Eyelids turn in and abrade cornea Ulceration Scarring Blood vessel formation

17 Flow of tears impeded Secondary infections

18 Urethritis The most common cause of nongonococcal urethritis (NGU) in men (40 to 96 percent) Majority (>50%) are asymptomatic The incubation period is variable but is typically 5 to 10 days after exposure Symptoms mucoid or clear urethral discharge dysuria Sometimes the discharge is so scant. This is in contrast to the more copious and purulent urethral discharge and shorter (two to seven days) incubation period for gonococcal urethritis Prostatitis Epididymitis Clinical syndromes In Men

19 Clinical syndromes Urethritis Cervicitis Majority (70%-80%) are asymptomatic Local signs of infection, when present, include: mucopurulent endocervical discharge In woman cervical edema with erythema and friability Normal Cervix Cervicitis

20 Complications in Women Pelvic Inflammatory Disease (PID) Salpingitis Endometritis Clinical syndromes In woman Perihepatitis (Fitz-Hugh-Curtis Syndrome)

21 Clinical Syndrome - Lymphogranuloma Venereum C. trachomatis (biovar: LGV) First stage Small painless vesicular lesion at infection site Fever, headache and myalgia Second stage Inflammation of draining lymph nodes Fever, headache and myalgia Buboes (rupture and drain) Proctitis Ulcers or Elephantiasis

22 Patient with LGV Bilateral inguinal buboes (arrows)

23 C. trachomatis - Diagnosis Histo Cytology: Iodine-staining inclusions Not sensitive Culture: Iodine staining inclusions Most specific Iodine-stained inclusion bodies

24 C. trachomatis - Diagnosis Antigen detection (ELISA or IF) Group specific LPS Strain specific outer membrane proteins Nucleic acid probes Several kits available May eventually replace culture

25 C. trachomatis - Treatment Doxycycline ; alternatives are erythromycin and sulfonamides Treatment of patients and their sexual partners

26 Trichomonas vaginalis Trichomonas vaginalis is flagellated protozoan and the causative agent of trichomoniasis. Women are usually symptomatic, while infections in men are usually asymptomatic. Trichomonas vaginalis exists only as a trophozoite (no cysts stage)

27 Trichomonas vaginalis It is pear-shaped, with a short undulating membrane lined with a flagellum and 4 anterior flagella. It moves with wobbling and rotating motion. In females it causes low-grade inflammation limited to vulva, vagina and cervix, causing frothy yellow or creamy discharge. In males it may infect the prostate, seminal vesicles and urethra.

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29 Pathogenesis It is causative agents of persistent vaginitis. The histological features are non- specific & include increased vascularity & congestion. Several studies showed that T. vaginalis produce a cell- detaching factor that causes detachment & sloughing of vaginal epithelial cells.

30 Diagnosis Specimen used : urine/vaginal discharges (female) prostatic secretions/urine (male) Clinical diagnosis is based on symptoms of burning, a frothy creamy discharge, hyperemia of the vagina.

31 Microscopic examination in a drop of saline for motile trichomonas of the fresh vaginal discharge Motile pear-shaped

32 Cultures will reveal the organism when negative microscopic examination result was obtained. Example :diamond's medium Incubated aerobically for 96 hours at 35ºC. Showing turbidity in lower portion of tube. Treatment: metronidazole

33 CANDIDIASIS Candida albicans (budding yeast) How common is genital candidiasis? Nearly 75% of all adult women have had one genital infection ( yeast infection ) in their life time. On rare occasions, male may also experience genital candidiasis. Candidiasis is opportunistic infection & there are some conditions that may put a women at risk for genital infection e.g: Diabetes mellitus, General debilitating disease Immunodeficiency, Pregnancy & contraceptive pills.

34 Transmission CANDIDIASIS Most of the cases of candida infection are caused by the person ' s own candida (endogenous infection). It is usually live in mouth, gastrointestinal tract & vagina without causing symptoms. Symptoms can develop only when Candida overgrown in these sites. Rarely, Candida can be passed from person to another, such as sexual contact Clinically: Vulvo- vaginitis or vaginal thrush Manifested by a thick yellow a white (cheesy- like) discharge, burning sensation, itching

35 CANDIDIASIS Diagnosis : Vaginal discharge examined by: 1-Direct microscopy Candida yeast can be detected in un- stained or gram stained film 2- Culture C. albicans grows well on sabouraud, s agar. After hours incubation at 37c or at room temp., colonies appear as cream, pasty with yeast smell 3- Differential Germ tube tests To diff. between C.albicans & non- pathogenic species of Candida e.g C. tropicalis& C. peudotropicalis

36 Treatment A-Topical antifungal Nystatin Canestan Miconazol ( Dactarine ) B-Systemic antifungal Ketoconazol ( oral ) Amphotericine - B I.V

37 The End