MIKROBIOLOGI sistem Urogenital

Bismillahirrahmanirrahiim—

senyum lebar dulu sebelum mulai… sudah lama tak menulis….

 

INFEKSI SALURAN KEMIH (ISK)

Penyakit yang sering mengenai manusia (10% pernah mengalami min satu kali)

Hospital Acquired infection (lebih sering; 35%)

Penyebab sepsis krn gram negatif pasien di RS

ISK adlh komplikasi pada penyakit (Diabetes, transplantasi ginjal, Ginjal ,ggn anatomis sal kemih)

Insidens

Insidens: pria (usia >60 thn= ggn prostat)

Wanita dapat mengalami sepanjang hidupnya

Usia 5-17 thn: insidens 1-3%

Lebih 17 thn menjadi10-20% (50% Wanita usia 20-40 mengalami infeksi berulang -dlm setahun-)

Sexual intercourse

Kehamilan (karena factor anatomis dan hormonal)

Jenis kelamin Wanita lebih sering mengalami ISK karena menurut lokasi anatomis (urethra lebih pendek) dan Dekat daerah perirektal (basah, lembab, banyak mikroorganisme)

Bakteri penghuni Urethra
(bagian distal)

Staphylococcus coagulase negatif (CNS; tidak termasuk Staphylococcus saphrophyticus)

Streptococcus Viridans dan yang nonhemolitik

Lactobacilli

Diphteroids (Corynebacterium spp.)

Neisseria spp. Nonpatogenik

Coccus anaerob

Proponibacterium spp

Basil gram negatif yang anaerob

Mycobacterium spp. & Mycoplasma yang comensal

 

Dikatakan terjadi Infeksi saluran kemih apabila terdapat kolonisasi bakteri dalam urine (bakteriuria) dan adanya invasi bakteri. Karena pada normalnya urine itu steril dan bebas hama.

Kriteria bakteriuria bila terdapat 100.000 (105) atau > per 1 ml urine porsi tengah,  steril  Atau 2 kali pemeriksaan ditemukan bakteri sama.

Penyebab ISK

Community Acquired: E.coli (UPEC), Klebsiella, Staf saprophyticus, enterococci, enterobacteriaceae lainnya

Hospital Acquired: E.coli, Klebsiella spp., Proteus spp., Staphylococci, enterobacteriaceae, Pseudomonas aerogenosa, enterococci dan candida

Lainnya : G- bacilli (acinetobacter), alcaligenes spp., pseudomonas spp., Citrobacter, Gard.vaginalis, Aerococcus urinae, Strepto b hemolitycus.

Bakteri lain yang jarang ditemukan dalam urin (Salmonella : indikator dini pada demam tifoid, Corynebacterium, Leptospira, Hemophylus influenza, Mycobacterium, Chlamydia, Ureaplasma urealyticum, Campylobacter)

Virus dan parasit bukan patogen sal kemih(Trich vaginalis dpt ditemukan dlm urin)

EnterobacteriaceaeEscherechia coli

Staph. saphrophyticus dan Streptococcus grup D

Infeksi ulang/Inf. noso : Proteus spp, Serratia spp dan Pseudomonas spp,

Penderita diabetes: Serratia marcescens

Wanita dgn diabetes atau penderita dng kateter tetap:  (Candida albicans)

Penyebaran hematogen : M. tuberculosis, Strept. pyogenes, Staph. aureus, Corynebacterium dan Lactobacilli

Lanjutan inf. sal. kelamin: Neisseria gonorrhoea, Treponema pallium, Chlamydia dan (Trichomonas).

Bakteri anaerob:  jarang.  Bakteri anaerob paling banyak:  genus Bacteroides terutama B. fragilis.

Kontaminan: Staphylococcus epidermidis dan Streptococcus yang mikroaerofilik.

DIAGNOSIS LAB ISK

PENGAMBILAN URINE

Sebelum pemberian antibiotik

Steril

urine pagi, kecuali u/ M. tb : urine 24 jam

Cara:

    1. Mid stream (cara pengmbilannya: mula2 bersihkan daerah meatus eksternaà urine pertama dibuang, urine berikutnya langsung ditampung dibotol sterilà diberi label)

    2. Punksi suprapubik (merupakan cara yang paling steril, cara pengambilan: bersihkan dan suciamakan daerah sprapubic dg spoit 20ml sterilàurine diisap dari 1 jari diatas os pubisàmasukkan k botol streril)

    3. Kantong urine (digunakan untuk anak- anak atau orang tua yang kurang kooperatif)

4. Kateterisasi (cara ini Sebaiknya dihindari, Pd penderita dgn kateter tetap:pengambilan dari pangkal kateter setelah  dibebas hamakan)

PENULARAN

Penularan ascendens: merupakan penularan yang sering terjadi, sumber penularan berasal dari komersial kulit dan saluran cerna.

Penularan descendens: Sumber penularan bersal dari fokus infeksi di tempat lain. Penularan berupa Bakteri patogen

FAKTOR PREDESPOSISI

Bendungan → kolonisasi bakteri → ISK

  1. Faktor anatomi

       –  urethra ♀  pendek

        –  kelainan kongenital: → bendungan, refluks

  1. Faktor mekanik

       – Iritasi

        – Tumor

       – Kehamilan

3.   Faktor hormonal & metabolisme

      –  Diabetes

       –  Kelainan metabolisme → pembentukan batu

      –  Kehamilan

MANIFESTASI KLINIK

Urethritis

Cystitis

 Pyelonephritis

 Prostatitis (akut dan kronik)

TERAPI

Antibiotik  yang sensitive, masih aktif di sal. Kemih, tidak nefrotoksik

KOMPLIKASI

  1. Bakteriemia
  2. Shok septik
  3. Batu saluran kemih
  4. Pyelonephritis ( jarang)
  5. Kerusakan ginjal

 

 

BAKTERI PENYEBAB PMS (PENYAKIT MENULAR SEKSUAL)

PMS merupakan penyakit yang penyebaran utamanya melalui kontak seksual

PMS disebabkan oleh bbrp agen sprt virus, bacteri, protozoa dan jamur

Masalh yang timbul pada PMS adalah semakin banyak antimikroba yang resisten

PMS ini penting untuk dideteksi dini krn mengenai pasangan seks, terutama untk pnjaja sek komersial

Agen- Agen Penyebab PMS

Caused by Bacteria:

ú  Neisseria gonorrhea

ú  Chlamydia trachomatis

ú  Treponema pallidum

ú  Hemophylus ducreyi

ú  Calymmatobacterium donovani

Virus:

ú  Genital herpes and warts

ú  HIV

ú  Hepatitis B

  • Parasite:

ú  Trichomonas vaginalis

Fungi:

ú  Candida albicans

Infeksi dan Non-infeksi penyebab urethritis

Agen utama

Neisseria Gonorrhea

Chlamydia Trauchomatis

Agen Lainnya

Mycoplasma genitalium

Ureaplasma urealyticum

Trichomonas vaginalis

Herpes simplex virus

Coliform Bacteria

Candida albicans

Treponema pallidum

Human papillomavirus

Non-Infeksi

Karena Iritasi Kimiawi

spermicydes, bath products)

Tumor

Foreign body

Steven Johnson Syndrome

Granulomatosis Wegener

Nieserria Gonorrhea

Human pathogen; does not cause infection in animals

Bacteria is sensitive to drying, do not survive well outside the host à direct/intimate contact

The usual site of entry:

ú  Vagina à spread in cervix

ú  Urethral mucosa of the penis à moves up the urethra

ú  other sexual practice à throat or rectal mucosa

Diplococcus Gram-negative à

Polysaccharide Capsule on the outside of the Meningococcus cell wall

Non motile  and Non spore producing

Non acid fast

Pili  and outer membrane proteinà vary antigenically

Otolysis when not in the host tissue

Aerobic absolute, requires added CO2 and enriched medium à Gonococci are more fastidious than meningococci

Produces oxydase

Penyakit- Penyakit yang disebabkan oleh N. Gonorrhea

Urethritis in men (rarely in women)

Cervicitis in women; PID, sterility, ectopic pregnancy

Anorectal gonorrhea

Proctitis

Ophthalmic neonatorum

Pharyngeal gonorrhea

Disseminated Gonococcal Infection :  arthritis septica dan tendosynovitis, skin lesions

Complication (rarely) endocarditis, meningitis and osteomyelitis

 

Patogenesis

Attaches to columner/cuboid epithelial cells, evading immune response, and multiply in tissue

Supporting components that enables infection:

ú  Porin (part of major outer membrane) à form pores; antigenic; specific serotypes associated with virulence

ú  Rmp (reduction modifiable protein): functions as target of blocking antibodies that prevent antibody binding to porin

ú  LOS = lipooligosacharide à stimulates PMN response (cause purulent exudate)   and blocks antibody mediated killing

ú  Pilin (part of outer membrane prot) à for adherence, and contribute to antigenic diversity in gonococci

ú  Opacity protein (= Opa) (outer memb. Pr) à for adherence

Produces IgA protease à enzyme which is released to destroy IgA1

Capsuleà resist phagocytosis, unless antibody present

Invaded non-ciliated epithelial cells internalize bacteria into vacuoles.

Vacuoles move down to the basement membrane, discharge bacterial contents into subepithelial connective tissues.

No exotoxins

Tissue damage is due to the inflammatory response to N.gonorhoeae à persistent untreated infection results in chronic inflammation and fibrosis à obstruction à infertility (later)

Infection is localized, except in some cases (infrequently), bacteria can invade the bloodstream and other tissues

Manifestasi Klinik

Symptoms develop within 2-7 days; urethral discharge and pain on urination (dysuria) in men; 50% infected women are asymptomatic or with mild vaginal discharge

Women may not be aware of infection until complications occur:

ú  Pelvic Inflammatory Disease (10-20%)

ú  Chronic pelvic pain

ú  Damage to the fallopian tubes

Disseminated infection occurs in women (1-3%), less common in men. Prompt treatment will contain the infection locally (ie. not invasive)

Deteksi Spesimen untuk N. Gonorrhea

Pus and secretions from
urethra, prostat, endocervix, glands

Cotton bud swabs from rectum,
pharynges and conjunctiva.

Synovial and cerebrospinal fluid.

Blood in systemic dissemination.

Laboratoric examinations:

ú  Direct smear/microscopy

                 à Gram staining: increased number of PMNs
à Direct immunofluorescence.

ú  Isolation and identification (Culture, biochemical tests)

ú  Antibiotic sensitivity test

ú  DNA Hybridization.

In male patients: intracellular diplococci in smear of urethral discharge (by Gram staining)

In female patients and asymptomatic men and for specimens obtained from sites other than urethra: culture is essential

Treponema pallidum

Round, thin (0.2µm) coils /spiral with pointed ends

Active motions in unstained preparation

Cannot be stained by anilin dyes

Wet preparation, negative staining, Silver impregnated staining  (biopsy)

Microaerophilic , negative Gram

T. pallidum : cannot be cultivated  in vitro

Quickly dies by drying and heating

Port of Entry

Entrance through abrasions on the skin or mucous membranes à multiply in tissue, slow replication cycle (average incubation period is 3 weeks) à plasma cell, PMN, macrophage infiltration

Horizontal spread (sexual contact)

Vertical spread (transplacental infection of the fetus)

Manifestasi Klinik

  1. A.      Syphilis in Adults: many are infected only as primary-secondary syphilis

Incubation period: 2-10 weeks since initial contact à Primary ulcer : papule changes to painless ulcer (chancre) in the genital organ

  1. Congenital Syphilis (transmission in utero)
  • Acquired after the first 3 months of  pregnancy
  • Results in Intra Uterine Death, congenital abnormalities or silent infection that becomes apparent when about 2 years old.

Penyakit-penyakit yang disebabkan oleh Treponema Pallidum

Sifilis

Adalah infeksi seksual kronis.

Sumber infeksi biasanya lesi aktid pada kulit dan mukosa pasien- pasien sifilis stadium awal(primer dan sekunder)

Organisme ditularkan melalui hubungan seks, menembus luka-luka halus di kulit dan mukosa kelamin dari pasangan yang belum terinfeksi. Tapi pada kasu yang KONGENITAL T.Pallidum ditularkan dengan menembus plasenta dari ibu ke janin, terutama pada tahp infeksi maternal.

Setalah masuk k dalam tbuh, organisme dengan cepat menyebar ke tempat yang jauh sekalipun melalui aliran darah dan limfe. 2-6 minggu setelah awal infeksi akan muncul LESI PRIMER yang disebut CHANCRE ditempat kuman masuk.

Host (tubuh manusia) akan merespon dengan membntuk system imun. Terbentuk 2 antibodi yaitu AB nontreponema dan AB treponema spesifik.

Cancre pada sifilis primer sembuh secara spontan dalam periode 4-6 minggu dan diikuti dengan munculnya sifilis sekunder pada skitar 25% dari pasien sifilis primes yang tdk diobati

sampi pasien sifilis yang tak terobati akan masuk dalam fase llaten lanjut kmudian sifilis tersier, yang manifestasi nya sudah merebet ke berbagai organ spt kardiovaskuler, system saraf pusat. Pada pada fase ini lebih sulit ditemukan karena lebih bersifat asimtomatik.

Primary syphilis: à 1-3 bl à enlarged inguinal nodes (treponemes  entered and multiply in the lymph node, spontaneous healing occur)

Secondary syphilisà 2-6 weeks à flu like illness, myalgia, arthralgia, headache, fever mucocutaneous rash. These are due to multiplication of treponemes in lymph nodes, liver, joints, muscles, skin, mucous membranes

Latent stage: only seroreactive, treponemes are dormant in the liver and spleen à 3-30 years

Tertiary syphilis à NEUROSYPHILIS, CARDIOVASCULAR SYPHILIS, PROGRESSIVE DESTRUCTIVE DISEASE (Gumma in the skin, bone, testis)

Diagnosis Lab

  • Specimen

       ulcer’s secrete and serum, liquor

  • Examination

  a. Dark Field Examination: motile treponemes examined directly after collection. Or Ultraviolet microscopy after staining with fluorescein labeled anti-treponemal antibody

  b. Negative Staining : morphology

  c. Serology

Clamydia Trachomatis

Minute sized bacteria

Cannot grow in artificial medium

Not killed by b– lactam antibiotics.

Obligate intracellular organism

unique life cycle (is infectious as elementary body, and metabolism is active in the form of reticulate bodies)

Major impact in women reproductive tract

70-80% asymptomatic in women; 50% in men

How do Chlamydias evade imune response?

  • Develops/multiply in the fagosome
  • May prevent lisosom fusion with fagosome

Direct cytotoxicity  and host imm resp to Chl. Antigens à clinical manifestation

Repeated infection, and host imm resp à complication (Reyter’s syndrome and scarring of fallopian tube.

Specimens

  • Cervix/urethra secretions
  • Conjunctiva scraping

Examinations performed:

1. Direct smear — Observe inclusion bodies with 10% Giemsa staining

  Eye Secretion/sputum:  lugol (jodium) staining

     to diffrentiate Chl. trachomatis from other Chlamydia

2. Tissue culture and isolation

3. Antigen detection

4. Nucleic acid detection (DNA)

5. Ab detection (serological)

 

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