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2nd Repro > GU infections > Flashcards

GU infections Flashcards

1
Q

Double stranded DNA (large), enveloped alphaherpesvirus. DNA is encapsidated, space between capsid and envelope is filled with viral and cellular proteins - termed tegument.

A

Herpes Simplex virus (HSV-1 and 2

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2
Q

Defense mech of female tract:

A
  • Epithelial cells
  • Provide a mechanical barrier
  • Produce/secrete antimicrobial molecules
  • Transport IgA
  • Process and present antigen
  • Communicate with underlying immune cells
  • Normal microbial flora
  • Lactobacillus lowers vaginal pH to 4.2-5.0
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3
Q

The Five P’s

A
  • Partners
  • Prevention of pregnancy •Protection from STI’s •Practices
  • Past history of STI’s
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4
Q

Test for chlamydia and gonorrhea simultaneously

A
  • Voided urine PCR probe
  • First urine after no urination x 1 hour
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5
Q

Dx for trichomas

A
  • Trichomonas
  • Microscopic exam of discharge
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6
Q

Dx of ureaplasma

A
  • Ureaplasma
  • PCR or culture
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7
Q

Understand lytic replication phase of HSV

A

associated with active transcription of numerous virus genes, viral DNA replication, assembly and release of infectious virions. virus mostly replicates in the mucosal epithelium during primary infection or following reactivation.

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8
Q

Latent infection -

A

limited to neurons – trigeminal or sacral ganglion; virus is quiescent, very limited virus gene expression, no viral DNA replication, no production of virions; viral DNA is maintained as an episome (extra “chromosome”) in latently infected neurons

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9
Q

sheds infectious particles frequently (25% chance daily), transmission can effectively occur in the absence of genital lesions. Virus is not stable in the environment – transmission is most efficient upon direct mucosa-mucosa contact.

A

Untreated HSV-2 carrier

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10
Q

Genital herpes is most often due to____ (termed recurrent infection clinically) of HSV-2, but can also be HSV-1 in some cases.

A

reactivation

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11
Q

HSV: Transplacental transmission is rare, but fetus can pick up the virus during natural delivery,leading to

A

neonatal herpes – a serious disease with some mortality and significant long-term sequelae in survivors.

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12
Q

Dx of HSV

A

Clinical presentation (vesicles), detection of virus in the lesions (culture, IFA, PCR), detection of HSV-1 or HSV-2 specific antibodies (determines infection status independent of the presence of genital lesions).

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13
Q

Pt has painless lesios on vagina, she said she had a headache and fever a few days ago. Dx?

A

HSV

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14
Q

Tx for HSV

A

Famciclovir, nucleoside analogs that are processed by viral (but not host) DNA polymerase and lead to chain termination during viral DNA synthesis.

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15
Q

Why can’t we create a vaccine for HSV

A

Treatment inhibits virus replication, but does not affect viral latency – this is why current treatments cannot clear HSV. No vaccine is available.

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16
Q

Linear double stranded DNA (very large) fused at both ends. Virion is ovoid to brick shaped; complex structure of the virion includes lateral bodies, core, and several membranes.

A

Molluscum Contagiosum – poxvirus

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17
Q

How is Molluscum a unique DNA virs?

A

Unlike any other DNA virus, poxviruses replicate exclusively in the cytoplasm – virus encodes and carries all proteins necessary for replication.

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18
Q

Transmission of molluscum

A

** direct contact or via fomites** (towels, etc) and virus is reasonably stable in the environment. Humans are the only known reservoir. Virus is usually cleared (can take up to 12 months). Virus replicates in the dermis.

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19
Q

Nodular to wart-like skin lesions, begin as papules and become umbilicated with central caseous plug; occur in cluster of 5-20 nodules

A

Molluscum Contagiosum

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20
Q

How do we Dx molluscum contagiousum

A

Based on the presentation of lesions (that may not be associated with inflammatory response) and histologically (large eosinophilic cytoplasmic inclusions – molluscum bodies).

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21
Q

Tx of MOlluscum contigiosum

A

If clearance of virus is delayed, nodules can be removed by scraping, application of liquid nitrogen, or iodine treatment. More severe disease in immunocompromised patients – can be treated with ritonavir or cidofovir. No vaccine is available.

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22
Q

papovavirus family, small circular double stranded DNA, icosahedral capsid, not enveloped, more than 100 subtypes – about a third of subtypes infect genital tract.

A

HPV

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23
Q

Viral cycle of HPV

A

Virus replication in the skin (infection occurs at the basal layer of epithelium by direct inoculation of a damaged skin), active replication is mostly in the upper epithelium layers to escape immune system. Throughout replication, viral DNA is maintained as an episome in the nucleus.

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24
Q

Replication is local and produces a wart. Most anogenital warts are caused by_____ Infection is self-limiting in most cases, but can take many months to years to clear.

A

HPV 6 and 11.

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25
Q

In some cases integration of HPV event leads to cancer. Cancer is associated with certain strains of HPV

A

(high risk, 16, 18, 31, and 45).

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26
Q

Explain pathology of HPV causing cancer

A

Further, most pathogenic integration events disrupt the expression of viral E2 gene which is a _negative regulator of viral E6 and E7 o_ncogenes. Due to high prevalence of infection (> 20 million in U.S.), HPV-induced cervical cancer is the second leading cause of cancer deaths in women.

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27
Q

Dx of HPV

A

Diagnosis: Clinical presentation of the wart. Pap smear for cancer screening, typing of HPV by PCR.

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28
Q

How does Guardasil work?

A

Vaccine is available against high risk strains (Gardasil) – recombinant capsid proteins (L1) self-assemble into empty virion like-particles that elicit protective humoral response.

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29
Q

Pleomorphic gram negative rods (coccobacilli), bacteria in this family are frequently found associated with mucous membranes, facultative anaerobes.

Cause Chancroids

A

Haemophilus ducreyi

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30
Q

Painful ulcerated lesion with lymphadenopathy adn pleomorphic gram Neg rods

A

Haemophilus ducreyi

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31
Q

Dx of Haemopholus Ducreyi

A

culture or nuclear acid based detecgtion

32
Q

YOu ahve a patient with a painful single ulceration on his penis. What you do tx w?

A

H.Ducreyi

tx with Azithromycin, Cefriaxone or Ciprofloxacin

33
Q

Pleomorphic gram negative rods, similar to H. ducreyi. Separated from the Haemophilus genus as it is not dependent on X-factor or V-factor for growth.

A

Gardnerella vaginalis

34
Q

Part of normal vaginal flora in many sexually active women – disturbance of normal flora leads to outgrowth, causing disease (i.e. following antibiotic treatment for an unrelated infection or menses). Vaginal Lactobacillus keeps this in check.

A

Gardnerella vaginalis

35
Q

Vaginitis, pruritis, dysuria, foul smelling copious vaginal discharge with a fishy odor.

A

Gardnerella vaginalis

36
Q

Presence of ‘Clue Cells’

+ Whiff test

A

Gardnerella vaginalis

37
Q

Treament for Gardenella vaginitis

A

MEtranidazole or clindamycin

38
Q

Belongs to a mycoplasma family – no cell walls –

B-lactam antibiotics do not work – neither does Gram stain!

Pleomorphic shape, produces urease to break down urine into ammonia resulting in alkaline urine.

A

Ureaplasma urealyticum

39
Q

Symptoms include dysuria and yellow mucoid discharge. Carried by 60% of healthy women, disease is due to infection of lower urinary tract (urethritis, prostatitis).

A

Ureaplasma urealyticum

40
Q

Dx and Tx for Ureasaplasma urelyticum

A

Diagnosis: PCR or culture - requires cholesterol and urea for growth, extremely tiny colonies (T-strain).

Treatment: Erythromycin or tetracycline.

41
Q

Gram negative spirochete, extra outer membrane, periplasmic flagella. Disease is thought to be primarily driven by host’s immune response.

A

Treponema pallidum or syphillis

42
Q

Painless chancre at the site of inoculation – highly infectious, continuous shedding of bacteria. Chancre resolves within 4-6 weeks, but bacteria is never cleared.

A

Primary syphillis: treponema pallidum

43
Q

Hematogenic systemic spread of bacteria leads to rash, fever, lymphadenopathy, patchy alopecia, and infection of multiple organs, including CNS. Condyloma latum: highly contagious lesion at moist sites

A

Secondary Syphillis

44
Q

At least 6 years to develop, 30% of untreated; result of slow, inflammation-driven damage to organs over a long time.

Gummatous syphilis: localized granulomatous lesions within skin or bones, non-infectious. Cardiovascular syphilis: aneurysm in the ascending aorta or aortic arch – due to destruction ofsmall arterioles supplying the aorta. Neurosyphilis: asymptomatic - clinically normal

Subacute - fever, stiff neck, headache
meningovascular - infarction due to damage of blood vessels in the brain Tabes dorsales - spinal cord is affected

A

Tertiary syphillis

45
Q

Can a baby get syphillis while in utero

A

Disseminated infection of the fetus, high mortality rate; infants that survive develop early or late congenital syphilis.

46
Q

baby born and soon after has rash, fever, lymphadenopathy, patchy alopecia, and infection of multiple organs, including CNS.

Condyloma latum: highly contagious lesion at moist sites

A

baby has congenital syphillis

47
Q

Congenital infection does not damage the fetus until

A

4th month of pregnancy – antibiotic therapy given in the first 4 months of pregnancy can prevent congenital syphilis.

48
Q

What is the challenge of dx syphillus?

A

ard to diagnose – cannot be cultured in ordinary medium, too small to be seen on light microscope. Direct examination of a specimen from chancre, rash, or the condyloma latum by darkfield microscopy. Serologic testing for asymptomatic stages:

49
Q

What is used to Dx syphillus

A

darkfiled microscopy, serology and nucleic acid-based approaches

50
Q

Tx for syphillius

A

Benthazine penicillin,

**immunity doesn’t protect against re-infection

51
Q

When would we use serology to dx:

A

don’t really, not very helpful

52
Q

Herpes, chancroid, lyphogrnauloma venerum are all

A

PAINFUL lesions

53
Q

Syphillis, molluscum, warts are all

A

Non painful lesions

54
Q

Most common bacterial STD in US

Gram Negative, obligate intracellular bacteria

A

Chlamydia trachomatis

55
Q

Hard to visualize on gram stain; don’t have peptidoglycan layer or muramic acid

Cell wall contains LPS

A

Chlamydia trachomatis

56
Q

Bacteria targets columnar epithelial cells at mucous membranes – causes conjunctivitis, cervicitis, and pneumonia. Infection acquired during birth causes inclusion conjunctivitis and infant pneumonia.

A

Chlamydia trachomatis

57
Q

Metabolically inactive,canno treplicate,but infectious and stable in the environment

A

Elementary body (EB) of Chylmida

58
Q
  • Forms intracellular inclusions
  • Metabolically active,intracellular non-infectiousform, can divide and make more of itself

also known as reticulate bodies

A

Initial body (IB) of chlamydia

59
Q

How do we dx chlamydia?

A

Requires cell culture to grow – diagnosis primarily based on nucleic acid approaches

60
Q

How do we tx Chlamydia

A

Azithromycin and doxycycline are antibiotics of choice

61
Q

Gram negative oxidase positive diplococci. Virulence factors include pili (adhesion to host cell, prevention of phagocytosis, antigenic variation), outer membrane porins (invasion into epithelial cells), opa proteins (adherence and invasion into epithelial cells), IgA protease (aids in cellular uptake).

A

Neisseria gonorrheae

62
Q

How do you tx chlamydia/gonorrhea

A

Azithromycin OR

Doxycycline and Ceftriaxone

63
Q

Adhesion to non-ciliated epithelial cells allows LPS-mediated destruction of cilia on neighboring cells. Bacteria can be taken up by endocytosis and released into subepithelial space enabling invasion.

A

Neisseria gonorrheae

64
Q

Males: urethritis with painful urination and purulent discharge (similar to C. trachomatis), epididymitis, prostatitis, urethral strictures.
Females: urethritis, endocervicitis, can progress to PID.

Both: ever, joint pains, skin lesions on extremities

A

Neisseria gonorrheae

65
Q

Can gonorrhea be transmitted to baby? What happens?

A

usually transmitted during delivery, causes ophthalmia neonatorum – eye infection of the neonate that damages the cornea and can cause blindness.

66
Q

How do you Dx gonorrhea

A

now nucleic acid-based diagnostic approaches are routinely used

67
Q

why aren’t there vaccines for gonorrhea?

A

Bacteria “switches” surface antigens to prevent lasting immunity – reinfection is possible, effective vaccine does not exist

68
Q

tx of choice for gonorrhea

A

Ceftriaxone is the treatment of choice

69
Q

Motility driven by four flagella and undulating membrane. Trophozoite is the only stage of this organism, replication is by longitudinal binary fission. Colonizes urethras, vaginas, or prostate (5-10% of population).

A

Trichomonas vaginalis

70
Q

Transmission of trichonoma vaginalis

A

Transmission is via direct contact, rarely by fomites; infants can be infected during birth.

71
Q

Most infected males are asymptomatic, urethritis and prostatitis is rare. Symptoms of infection are generally mild in females (scant watery discharge), but infection can also lead to vaginitis associated with itching, burning, and painful urination.

A

Trichomonas vaginalis

72
Q

Dx trichonomas vaginalis

A

Microscopic examination of vaginal or urethral discharge, frequently the organism is also found in urine, highly motile. A nucleic acid probe is also available.

73
Q

Tx for trichonomas vaginalis

A

Treatment: Metronidazole (Flagyl) is the drug of choic

74
Q

Vaginitis (“yeast infection”) – outgrowth of endogenous population. Increased incidence of vaginitis is due to antibiotics, oral contraceptives, menses, pregnancy. Symptoms include vaginal itching and thick copious discharge.

A

C. albicans

75
Q

Dx of yeast infection

A

Diagnosis: KOH preparation of skin scrapings.

76
Q

Tx for yeast infection

A

Treatment: Imidazole vaginal suppositories or a single dose of oral fluconazole.

77
Q

consequences of STI

A
  • Spontaneous abortion
  • Pelvic inflammatory disease (PID) • Ectopic pregnancy
  • Infertility in women
  • Urethral strictures in men
  • Cervical/penile carcinoma
  • Death

2nd Repro (16 decks)

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