Bacterial STI Flashcards by Christopher Hauglid

Which groups of people have the highest and lowest rates of STIs?

Highest: Men who have sex with men (MSM)

Lowest: Women who have sex with women (WSW)

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Contact Tracing

Evaluation, treatment, and counseling of sex partners of persons who are infected

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Chlamydia: Unique Features (Two of them)

1) Replicate only within cells (Obligate Intracellular Parasites)
2) Lack peptidoglycan

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Family Chlamydiaceae (Characteristics)

Small cocci

Obligate intracellular parasite (cannot make own ATP)

Gram negative-like envelope, EXCEPT with No peptidoglycan

LPS only has weak endotoxin activity

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Family Chlamydiaceae (Life Cycle Stages)

Elementary Bodies (EB): Infectious form
-Adapted for EXTRACELLULAR survival

Reticulate Bodies (RB): Replicative form
-Adapted for INTRACELLULAR growth

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Family Chlamydiaceae (Life Cycle)

1) EB infects cell
2) EB converts to RB
3) RB undergoes binary fission (Inclusion)
4) Phagosome and plasma membrane are lysed, releasing EBs to infect other cells

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Chlamydia trachomatis (Host, Biovars, Serovars, Tropism)

Host: Humans only

Biovars:

1) Trachoma (Conjunctivitis and Genital Infections)
2) LGV (More invasive)

Serovars: Multiple based on major outer membrane protein MOMP

Tropism: for nonciliated, columnar, cuboidal, and transitional epithelial cells of urethra, endocervix, endometrium, fallopian tubes, anorectum, respiratory tract, and conjunctivae

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Chlamydia trachomatis (Disease)

Trachoma, inclusion conjunctivitis, infant pneumonia…

1) STI/urogenital infections
2) Lymphogranuloma venereum
3) INFERTILITY IF UNTREATED

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Which serovars of C. trachomatis cause Trachoma?

A, B, Ba, C

“ABBa C Track”

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Which serovars of C. trachomatis cause Urogenital Tract Disease?

D-K

“Donkey Kong”

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Which serovars of C. trachomatis cause Lymphogranuloma venereum (LGV)?

L1, L2, L2a, L2b, L3

**All start with “L” **

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Which serovars of C. trachomatis are the most invasive?

LGV serovars

-They replicate in mononuclear phagocytes

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Chlamydia trachomatis: Trachoma (Disease and Transmission)

Disease: Chronic conjunctivitis of the eye

Transmission: eye to eye by droplets, hands, contaminated clothing, and FLIES

Leading cause of preventable blindness in the world

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Chlamydia trachomatis: Conjunctivitis (Acute vs Neonatal)

Acute (in sexually active adults):
-Mucopurulent discharge, keratitis, corneal infiltrates, and occasional corneal vascularization

Neonatal (exposed at birth):
-5 to 12 day incubation followed by swelling of eyelids, discharge. Can last 12 months if not treated (Erythromycin)

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Chlamydia trachomatis: Urogenital Infections (Men vs Women)

Men:

Most are SYMPTOMATIC
Dysuria and thin MUCOPURULENT discharge (mucus and pus)
Complications: epididymitis, prostatitis, fever
May progress to REITER SYNDROME

Woman:

80% are ASYMPTOMATIC (Huge RESERVOIR for infection)
MUCOPURULENT discharge
PELVIC INFLAMMATORY DISEASE (can cause sterility)

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Chlamydia trachomatis: Lymphogranuloma venereum (LGV) (Serovars, Symptoms)

Serovars: L1, L2, L3 MORE INVASIVE
“L1, 2, and 3 cause L-G-V”

Symptoms:

Primary (PAINLESS) lesion/papule at site of infection
Inguinal lymphadenopathy*
Nodes become supurative (i.e. buboes), rupture, and form FISTULAS
Proctitis*

Chlamydia trachomatis: Lymphogranuloma venereum (LGV) (Endemic to)

Sporadic in the U.S.

Highly prevalent in AFRICA, ASIA, and SOUTH AMERICA

Chlamydia trachomatis (Diagnosis)

Culture of cells followed by staining with IODINE identifies glycogen in RBs –> note INCLUSIONS

EBs noted via immunofluorescence (ELISA)

Requires sample of epithelial cells SCRAPINGS of cervix, urethra (men), or conjunctiva

Nucleic Acid Amplification Tests (NAATs) from urine or urethral discharge

CANNOT culture with liquid media, as it does not live outside of cells (Require cell monolayer***

Chlamydia trachomatis (Treatment and Prevention)

Treatment: Doxycycline or Macrolides

Prevention: Control re-infection, safe sex, early detection and treatment of symptomatic patients and their sexual partners

What is the mechanism of action of Doxycycline and Macrolides?

Inhibit protein synthesis

Neisseria gonorrhoeae (Characteristics, Appearance, Host)

Gram negative, aerobic, diplococci
-Gonococcus, meningococcus

Kidney bean appearance

Host: Humans only

How do you distinguish between N. gonorrhoeae and N. meningitidis?

Sugar Fermentation test

N. gonorrhoeae DOES not ferment maltose

N. meningitidis FERMENTS MALTOSE

Biologic effect of Pilin

Attachment, anti-phagocytic

Biologic effect of Por protein (Porin)

Promotes intracellular survival

Biologic effect of Opa protein (Opacity protein)

Attachment to eukaryotic cells

Biologic effect of Lipooligosaccharide (LOS)

Lipid A and core oligosaccharide, lacks O-antigen. Endotoxin. ***Antigenic variation of LOS helps evade immune system***

What are the four virulence factors of N. gonorrhoeae that undergo antigenic variation to avoid immune response?

Opa protein (Opacity protein), Por protein (Porin), Pilin, Lipooligosaccharide (LOS) "Oprah Pours Pills in her Lips"

What are the other three virulence factors of N. gonorrhoeae?

Outer membrane blebs (Contain LOS and OM proteins, enhance toxicity and absorb antibodies) IgA1 protease (Destroys IgA) B-lactamase (Hydrolyzes B-lactam ring in penicillin)

Neisseria gonorrhoeae (Epidemiology)

- Carriage can be asymptomatic, especially in WOMEN | - Most common in African Americans (aged 15-24), Southeastern U.S., and people with multiple sexual encounters

Who has the highest risk of disseminated disease in patients infected with N. gonorrhoeae?

Those with deficiences in late components of complement e.g. C5b to 9 (lysis via the attack complex)

Neisseria gonorrhoeae (Pathogenesis and Immunity)

1) Gonococci attach to MUCOSAL CELLS (Pili, PorB, Opa) 2) Penetrate into cells and multiply 3) Pass through cells to subepithelial space where infection is established * **Primary site of infection for women is CERVIX (bacteria infect endocervical columnar epithelial cells)*** 4) LOS stimulates inflammation: chemokines and TNFa (proinflammatory cytokine) which is responsible for symptoms

Which species of Neisseria has a capsule?

N. gonorrhoeae DOES NOT have a capsule, so is engulfed immediately; also does not spread often N. meningitidis HAS A CAPSULE

Neisseria gonorrhoeae (Disease)

* **Gonorrhea*** - Characterized by MUCOPURULENT DISCHARGE and DYSURIA after 2-5 day incubation period - Approximately 95% of infected men have acute symptoms vs. 50% of women

Neisseria gonorrhoeae (Complications)

Men: epididymitis, prostatitis, periurethral abscesses Women: salpingitis, tuboovarian abscesses, PID in 10-20% of women, infertility, ectopic pregnancy

Neisseria gonorrhoeae (Disseminated Infections, i.e. Gonococcemia)

1) SEPTICEMIA and Infection of skin and joints (1-3% of women; lower in men) 2) Fever, migratory arthralgias, SUPPURATIVE ARTHRITIS in the wrists, knees, and ankles, PUSTULAR RASH on an erythematous base over the extremities but not on head or trunk ***Leading cause of purulent arthritis in adults***

Neisseria gonorrhoeae (Other Diseaes: 3 of them)

1) Purulent conjunctivitis (Newborns; OPHTHALMIA NEONATORUM) 2) Anorectal gonorrhea (common in women and MSM) 3) Pharyngitis (almost always accompanies genital infection)

Neisseria gonorrhoeae (Diagnosis)

1) Direct smear: Gram negative, bean-shaped diplococci ***IN NEUTROPHILS*** (less accurate in women due to commensal flora) 2) Culture (scrapings or throat/rectal swabs) - Fastidious --> Chocolate Agar (Nonselective) Thayer-Martin media (Selective) 3) NAAT(Nucleic Acid Amplification) - Can combine with test for chlamydia

Neisseria gonorrhoeae (Treatment and Prevention)

Treatment: * **CEFTRIAXONE plus DOXYCYCLINE or AZITHROMYCIN to treat Chlamydia (presumed with Gonorrhea) - Neonates --> prophylaxis with erythromycin drops; opthalmia neonatum is treated with Ceftriaxone Prevention: -Patient education, screenings, condoms