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Hormonal & Reproductive Week 4 - WLB > STDs - Diebel > Flashcards

STDs - Diebel Flashcards

1
Q

What are the four most common types of infections that people with STDs present clinically?

A

Urethritis
Cervicitis
Vaginitis and vaginosis
Genital ulcers

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2
Q

What are the common causes of Urethritis?

A

N. gonorrhoeae, C. trachomatis

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3
Q

What are the common causes of Cervicitis?

A

C. trachomatis

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4
Q

What are the common causes of Vaginitis?

A

T. vaginalis, C. albicans

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5
Q

What are the common causes of Vaginosis?

A

Gardnerella spp.

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6
Q

What are the 5 types and major causes of Genital Ulcers (Nonexudative Infections)?

A 
Syphilis – T. pallidum
Herpes – HSV-1 and HSV-2
Chancroid – H. ducreyi
Lymphogranuloma venereum – C. trachomatis
Genital warts – HPV
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7
Q

What are the common causes of Pelvic inflammatory disease (PID)?

A

Polymicrobic; N. gonorrhoeae, C. trachomatis, anaerobes

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8
Q

What are the clinical symptoms that are suggestive of particular genital diseases (Chlamydia, Gonorrhea, HPV/MCV, HSV-2, Syphilis)?

A

Anogenital malignancy – should be ruled out

Chlamydia – significant discharge usually present

Gonorrhea – significant discharge usually present

HPV / MCV – often leads to wart-like growths

HSV-2 – painful vesicles and shallow ulcers usually present

Syphilis – often painless, no wart lesions

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9
Q

What two diagnostic tests are used in HPV?

A

Pap smear - looking for giant cells

PCR tests for certain HPV types

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10
Q

What is the treatment for HPV?

A

warts or precancerous tissue can be removed to prevent spread, but virus is not treatable (incurable)

can self-resolve, but takes 1-2 years

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11
Q

Human Papilloma Virus classification:

A

dsDNA, Group I

Circular Genome

Icosahedral Nucleocapsid

Nonenveloped

Papovaviridae

Papillomavirus

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12
Q

What are the most common types of HPV that present as warts?

A

6 and 11

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13
Q

How does HPV replicate and cause cancer?

A

Warts: Tumorigenic => Carcinomas

Virus introduced to skin through foreign body or microabrasion => Get through mucosal barriers/layers => get into stem cells => use host DNA polymerase expressed by stem cells (no viral DNA polymerase)

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14
Q

What are the important proteins involved in HPV tumorgenesis?

A

E1 = binds to host DNA and uses ATP to create replication bubble => unwind DNA => recruit host DNA polymerase

E2 = loader protein, helps E1 attach to DNA

E6 = enhances the ability of host cells to move through the cell cycle by binding to E6AP and p53 to form a trimeric complex => p53 gets ubiquinated which targets it for degradation => stops DNA damage monitoring/repair/apoptosis => tumor cell progression

E7 = binds to Rb => Rb cannot bind to E2F => unbound E2F => uncontrolled transcription factor promotion of S-phase => persistent replication => tumor cell progression

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15
Q

What for organisms can cause urethral discharge in sexually active men?

A

Chlamydia trachomatis – typically clear discharge
Mycoplasma hominis – typically clear discharge
Neisseria gonorrhoeae – typically purulent discharge
Ureaplasma urealyticum – typically clear discharge

***In sexually active men, purulent discharge is highly suggestive of gonorrhea

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16
Q

What diagnostic tests confirm Gonorrhea?

A

Gram Stain: Gm (-) diplococci intracellular bacteria

Can also do DNA probes for PCR or ELISA, but less common clinically

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17
Q

Neisseria gonorrhoeae classification

A

Bacteria

Gram (-)

Diplococci

Oxidase (+)

Only Glucose Oxidizer

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18
Q

What virulence factors help N. gonorrhoeae cause infection?

A

Specialized pili – allows attachment to mucosal surface, antigenic variation to evade host defenses, prevents killing by phagocytosis.

Endotoxin.

Capsule.

IgA protease.

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19
Q

What is the treatment for N. gonorrhoeae?

A

ceftriaxone (+ doxycycline for probable concurrent Chlamydia infections)

Prophylactic erythromycin eye drops for neonates.

Vaccine development difficult.

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20
Q

What unique culture does N. gonorrhoeae grow on?

A

Thayer-Martin media:

Media inhibits the growth of most other microorganisms.

Contains the following antibiotics:
Vancomycin – kills most G (+)
Colistin – kills most G (-)
Nystatin – kills most fungi
SXT – inhibits G (-) organisms, particularly swarming Proteus

Nutrients = chocolate sheep’s blood, beef infusion, casein hydrolysate, and starch.

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21
Q

How do you differentiate between N. gonorrhoeae and N. meningiditis?

A

N. meningitidis oxidizes both maltose and glucose.

N. gonorrhoeae only oxidizes glucose.

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22
Q

What is the clinical presentation of and N. gonorrhoeae Local infection (genital tract or anorectal infections)?

A

asymptomatic, urethritis, dysuria (men), cervicitis (women), opthalmia neonatorum (eye infections caused to exposure to the pathogen during birth).

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23
Q

What is the clinical presentation of and N. gonorrhoeae systemic infection?

A

septic arthritis

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24
Q

What are the complications of N. gonorrhoeae if left untreated?

A

Pelvic inflammatory disease (PID), ectopic pregnancy, sterility, Fitz-Hugh-Curtis Syndrome

In women, the infection can progress to the uterus, fallopian tubes, ovaries (PID) which can lead to an increased risk for ectopic pregnancies. From the fallopian tubes the bacteria can spill into the peritoneal cavity causing peritonitis. This can lead to an infection of the liver capsule (Fitz-Hugh-Curtis Syndrome).

In neonates, it can inoculate the conjunctiva during passage through the birth canal causing opthalmia neonatorum  risk for blindness.

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25
Q

What is the pathology of N. gonorrhoeae infection?

A

Attach via pili to mucosal cells of the urethra and vagina. Evades mucosal IgA antibodies via IgA protease. Endocytosed by many cell types including urethral epithelial cells. Kills ciliated cells. Together this leads to inflammatory response leading to urethritis (men) and cervicitis (women).

26
Q

What etiologies should be considered in any patient with genital lesions?

A

Haemophilus ducreyi (chancroid) – painful ulcers

Klebsiella granulomatosis (Donovanosis) – generally painless, rare in the U.S.

***HSV-2 (less commonly, HSV-1) (Genital herpes) – painful ulcers

Chlamydia trachomatis (Lymphogranuloma venereum (LGV) – painless ulcers, rare in the U.S.

Treponema pallidum (Syphilis) – painless ulcers

27
Q

What is the treatment for Herpes simplex infection?

A

Acyclovir (Chain terminator for cells undergoing active lytic replication)

28
Q

Why is Acyclovir ineffective at killing Latent Herpes?

A

Needs viral Thymidine Kinase to become active

***This enzyme is only active when the virus is actively undergoing lytic replication

29
Q

What special smear and cultures are used diagnostically for HSV-2 and Haemophilus ducreyi?

A

Viral cultures can be taken from the base of the vesicles

Tzanck smear looking for giant multinucleated cells (suggestive of HSV, HPV has one giant nucleus).

Pap smear

PCR and/or serology could be used to confirm virus type.

30
Q

Is Herpes Simplex (HSV-1/HSV-2) alpha, beta, or gamma viruses?

A

Alpha viruses

HSV-1, HSV-2, Varicella = Alpha
(CMV = Beta)
(EBV = Gamma)

31
Q

What is a potential serious complication of Herpes Simplex Infection?

A

Encephalitis

via viremia after invasion of mucosal surfaces

32
Q

What immune functions can mediate Herpes Simplex?

A

CD8 T-cells

33
Q

Classification of HSV-1/HSV-2

A

DNA virus

Icosahedral Nucleocapsid

Enveloped

DS DNA Linear Genome (Class I)

Herpesviridae

34
Q

How does HSV replicate in host cells?

A

Encodes many proteins that serve to modulate the host cell and host immune response

Encode for several proteins that are required to promote viral DNA replication (including a viral DNA-dependent DNA polymerase).

These proteins are the major targets of current antiviral chemotherapy against herpesvirus infections.

35
Q

Acyclovir is used to treat what infections?

A

treatment of HSV and VZV infections (alphaherpesviruses). Encephalitis, disseminated herpes, etc?

36
Q

What forms of resistance may develop against Acyclovir?

A

Resistance to the drug comes from mutations to the thymidine kinase and/or the viral DNA polymerase.

37
Q

What drug is used to treat Beta and Gamma Herpes viruses?

A

Gancyclovir

38
Q

What are the three causes of abnormal vaginal discharge? What symptoms differentiate them?

A

Gardnerella and Mobiluncus (bacterial vaginosis) – discharge typically white to gray, moderate amount, very malodorous.

Candida albicans (candidiasis) – itchiness present, discharge typically white, small amount, clumped.

Trichomonas vaginalis (trichomoniasis) – itchiness present, discharge typically yellowish, in large amounts.

39
Q

What is the diagnostic work up for abnormal vaginal discharge?

A

Diagnostic work-up included determining the vaginal pH and performing the “KOH amine test”. The results suggested either trichomoniasis or bacterial vaginosis as the likely causes of infection.

Further examination included a wet mount of the vaginal discharge and a Gram stain of the vaginal discharge.

40
Q

What does the finding of clue cells on gram stain suggest?

A

Epithelial cell covered by bacteria => Bacterial Vaginosis

41
Q

What pathogen is diagnosed by a wet mount of the vaginal discharge revealing large, motile (flagellated) organisms in low-power fields?

A

Trichomonas vaginalis

42
Q

What are the symptoms of Trichomonas vaginalis infection?

A

Many cases are asymptomatic, and men seldom have symptoms.

Women often have vaginitis symptoms, which can include a white to yellowish-green frothy discharge. Women who become infected during pregnancy are predisposed to premature labor andlow-birth-weight infants.

Chronic infection may also lead to infertility.

43
Q

What is the drug of choice for Tx of Trichomonas vaginalis?

A

Treatment with metronidazole is recommended for both the infected patient and their sexual partner.

Metronidazole typically gets activated through partial reduction during anaerobic respiration. Good drug for anaerobic cells, little effect on human cells or aerobic bacteria.

44
Q

What pathogen is diagnosed with a wet prep revealing a few yeast cells and pseudohyphae (yeast is growing rapidly)?

A

Candida albicans

The presence of pseudohyphae in the smear is a clear indication that the yeast is growing rapidly and causing a yeast infection.

45
Q

What is the most common cause in vaginitis?

A

Candida albicans

46
Q

What situations cause high susceptibility of Candida albicans?

A

Vaginal infections with this organism are nearly always opportunistic. Disruptions of the normal bacterial biota or even minor damage to the mucosal epithelium in the vagina can lead to overgrowth by this fungus. Diabetics and pregnant women are also predisposed to vaginal yeast overgrowths. Some women are prone to this condition during menstruation.

Women with HIV infection experience frequently recurring yeast infections. Also, a small percentage of women with no underlying immune disease experience chronic or recurrent vaginal infection withCandidafor reasons that are not clear.

47
Q

What is the treatment for Candida Albicans?

A

No vaccine is available forC. albicans.

***Topical and oral azole drugs are used to treat vaginal candidiasis, and some of them are now available over the counter.

48
Q

What cell types does HIV infect, and why does it have such an impact on the patient’s immune response?

A

Can infect T cells and macrophages.

Need CD4, CXCR4, or CCR5.

49
Q

How does the HIV virus replicate?

A

Reverse transcription.

50
Q

What other opportunistic infections is a patient with HIV susceptible to?

A
51
Q

What are the risk factors for infection in individuals with HIV?

A

Unprotected sexual intercourse, contaminated blood

52
Q

A 33-year-old woman presented with a low-grade fever, malaise, and a rash. She recalled having had painless ulcers, which appeared on the vulva 6 weeks before this current episode. Physical examination revealed a temperature of 100.6°F (38.1°C), inguinal lymphadenopathy, a generalized rash on palms and soles, and pustular cutaneous lesions and condylomata lata on her face. Blood work came back normal.

What is the likely cause of infection?

A

Treponema pallidum (Syphilis)

53
Q

What is the diagnostic work up for Syphilis?

A

Herpes can be ruled out by Tzanck smear (a cytologic examination to detect HSV-infected cells) (not likely, ulcers usually painful).

Additional tests for confirmation of the clinical diagnosis may include serologic tests (useful for the diagnosis of syphilis) and culture (to rule out chancroid) (not likely, ulcers usually painful).

Here a rapid plasma regain (RPR) serologic test was positive and diagnosis was confirmed by a specific serologic test.

54
Q

What is the clinical course of Syphilis?

A

Untreatedsyphilisis marked by distinct clinical stages designated as primary, secondary, andtertiarysyphilis.

The disease also has latent periods of varying duration during which it is quiescent.

The spirochete appears in the lesions and blood during the primary and secondary stages and, thus, is transmissible at these times. Syphilisis largely not transmissible during the latent and tertiary stages.

55
Q

What is the earliest indication ofsyphilisinfection?

A

appearance of a hard chancreat the site of entry of the pathogen

The chancre appears after an incubation period that varies from 9 days to 3 months

begins as a small, red, hard bump that enlarges and breaks down, leaving a shallow crater with firm margins

The base of the chancre beneath the encrusted surface swarms with spirochetes.

Most chancres appear on the internal and external genitalia, but about 20% occur on the lips, oral cavity, nipples, fingers, or around the anus.

56
Q

About 3 weeks to 6 months after the chancre heals in Syphilis, the secondary stage appears. What are the clinical features of Secondary Syphilis?

A

Signs and symptoms are more profuse and intense:

Initial symptoms are fever, headache, and sore throat, followed by lymphadenopathy and a peculiar red or brown rash that breaks out on all skin surfaces, including the palms of the hands and the soles of the feet. A person’s hair often falls out.

57
Q

What are the clinical features/complications of Tertiary Syphilis?

A

During latency antibodies to the bacterium are readily detected but the bacterium itself is not.

Cardiovascular syphilis results from damage to the small arteries in the aortic wall. As the fibers in the wall weaken, the aorta is subject to distension and fatal rupture. The same pathologic process can damage the aortic valves, resulting in insufficiency and heart failure.

painful swollen syphilitic tumors calledgummasdevelop in tissues such as the liver, skin, bone, and cartilage

Neurosyphilis can involve any part of the nervous system, but it shows particular affinity for the blood vessels in the brain, cranial nerves, and dorsal roots of the spinal cord. The diverse results include severe headaches, convulsions, atrophy of the optic nerve, blindness, dementia, and a sign called theArgyll-Robertsonpupil—a condition caused by adhesions along the inner edge of the iris that fix the pupil’s position into a small irregular circle.

58
Q

What are the symptoms of Congenital Syphilis?

A

Early congenital syphilis encompasses the period from birth to 2 years of age and is usually first detected 3 to 8 weeks after birth. Infants often demonstrate such signs as profuse nasal discharge, skin eruptions, bone deformation, and nervous system abnormalities.

59
Q

Classification of Treponema pallidum

A

a spirochete bacteria

regularly coiled cell with a Gram (-)cell wall

Strict parasite with complex growth requirements that necessitate cultivating it in living host cells

60
Q

How is Treponema pallidum infection diagnosed?

A
  1. detecting the bacterium in patient lesions: wet mount/dark-field microscopy of a suspected lesion

***A single negative test is not enough to exclude syphilis because the patient may have removed the organisms by washing, sofollow-uptests are recommended.

  1. antibodies in the patient’s blood: rapid plasma reagin (RPR), VDRL, Kolmer, and the Wasserman test.

***Two kinds of antibodies are formed: those that specifically react with treponemal antigens and those that are formed against nontreponemal antigens.

(also the presence of these cardiolipin antibodies)

PCR test

61
Q

What is the treatment for Syphilis?

A

Penicillin G is used in the treatment of all stages and forms of syphilis. It is given parenterally in large doses with benzathine or procaine. The goal is to maintain a blood level lethal to the spirochete for at least 7 days.

Alternative drugs (tetracycline and erythromycin) are less effective, and they are indicated only if penicillin allergy has been documented. It is important that patients be monitored for successful clearance of the spirochete.

Hormonal & Reproductive Week 4 - WLB (8 decks)

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