Chapter 15 Flashcards

1
Q

What is the causative agent of syphilis?

A

Trepnema pallidum
Pallidum pallidum (corkscrew shape)
Cannot be cultivated in laboratory media

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2
Q

Why was it changed from STD’s to STI’s?

A

To include those who are asymptomatic

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3
Q

What are among the top reportable diseases in Canada?

A

Chlamydia, Gonorrhea

If you find an incident, you must report it to Health Canada

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4
Q

What is the incubation time of pallidum pallidum?

A

1-90 days, which makes it difficult to track

Occurs more in males

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5
Q

What is the clinical manifestation of primary phase syphilis?

A

Chancres (skin lesions) at the site of inoculation

Usually painless and heals spontaneously but highly infectious

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6
Q

What are the clinical manifestations of secondary phase syphilis?

A

The disease can begin to be disseminated (all over body) 2-12 weeks after infection
Skin lesions on trunk, palms, soles of feet with highly infectious fluid
Other organ involvement
Symptoms with disappear in 3-12 weeks

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7
Q

What can the secondary phase of syphilis be followed by?

A

An asymptomatic latent phase (3-30 years) with antibodies present

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8
Q

What are the 3 outcomes of an untreated syphilis patient in the latent phase?

A

Relapse, no relapse or move to the tertiary phase

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9
Q

What are the clinical manifestations of tertiary phase syphilis?

A

Neurologic, cardiovascular symptoms
Possibly with Gummas (nonspecific deep granulomatous lesions)
Organism is eating skin up from beneath it

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10
Q

How does congenital syphilis occur?

A

When mothers have untreated/improperly syphilis

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11
Q

How does congenital syphilis present?

A

As secondary syphilis at birth (lesions all over the body), miscarriage, may not appear until age 2

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12
Q

How can we prevent congenital syphilis?

A

If women are screen in early pregnancy and treated with penicillins

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13
Q

How can syphilis be diagnosed using microscopy?

A

Using dark field or fluorescent microscopy

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14
Q

What is the first step to diagnosing syphilis using serology?

A

VDRL (Venereal Disease Research Laboratory Test), RPR (Rapid Plasma Reagin test)
First do non-specific (non-treponemal) test to look for non-tremponemal antibodies against the antigens released from destroyed cells.
If the test if negative, true negative. If the test is positive, look for treponemal antibodies

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15
Q

What is the second part of diagnosing syphilis using serology?

A

Look for the treponemal antibodies released from pallidum
FTA-ABS (fluorescent treponemal antibody absorption)
MHA-TP (microhemagglutination test)
TP-PA test (Treponema pallidum particle agglutination test)

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16
Q

How is syphilis treated?

A

Using penicillin and doxycycline

Can prevent secondary and tertiary syphilis by early diagnosis and treatment

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17
Q

What is the causative agent of gonorrhoea?

A

Neisseria gonorrhoeae (gram negative diplococci) capnophile (CO2 loving) with humid atmospheres

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18
Q

Where does neisseria gonorrhoeae colonize?

A

Female reproductive tract (cervix, uterus, fallopian tubes), urethra, mouth, throat, eyes and anus

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19
Q

What is the chance of each gender acquiring gonorrhoea post single encounter?

A

Females have a 50% chance

Males have a 20% chance

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20
Q

What is ophthalmia neonatorum?

A

The vertical transmission of gonorrhoea from an infected mother to her baby during childbirth

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21
Q

What are the virulence factors of neisseria gonorrhoeae?

A

Pili aiding in attachment to human mucosal epithelium (constant and hypervariable regions)
Por proteins (form pores)
Opa proteins (assist binding to epithelium)
LOS (endotoxin)
IgA protease
Capsule (resists phagocytosis)
Rmp proteins (inhibits cidal activity of serum)

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22
Q

What are the clinical manifestations of gonorrhea in females?

A

Often asymptomatic, but if they are present they will develop in 2-7 days (vaginal discharge)

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23
Q

What are the complications of untreated gonorrhea in females?

A

Pelvic inflammatory disease (PID), chronic pelvic pain and infertility

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24
Q

What are the clinical manifestations of gonorrhea in males?

A

Purulent urethral discharge and painful discharge

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25
Q

What are the other conditions that can result from gonorrhea infection?

A

Purulent anorectal discharge, sore throat, ophthalmic infection

26
Q

How is gonorrhea infection diagnosed in men?

A

A direct Gram stain of the urethral discharge from symptomatic males with urethritis showing gram negative diplococci inside PMN’s

27
Q

How is gonorrhea infection diagnosed in females?

A

Can use direct gram stain like in men because the normal vaginal and rectal flora contains gram negative coccobacilli
Must confirm using culture

28
Q

How is gonorrhea infection treated?

A

Using antibiotics, but resistant to many so must know where it was picked up to determine what it may be susceptible to
No immunity

29
Q

Which gender is chlamydia more common in?

A

Females

30
Q

What is chlamydia trachomatis?

A

An obligate intracellular bacterium. Cannot survive outside of the host, can’t culture in artificial media and too small to see under the gram stain

31
Q

What are the serotypes of chlamydia trachomatis and what do they cause?

A

L1, L2, L3 (maybe D-K?) cause STIs (lymphogranuloma venereum-LGV, genital chlamydiosis, nongonococcal urethritis-discharge with no organism present), ocular and respiratory infection
A-C causes trachoma (non-traumatic blindness due to rubbing lesions)

32
Q

What is the life cycle of chlamydia trachomatis?

A

The elementary body attaches to a specific receptor on the host cell and forces it to take it in via endocytosis, differentiates to reticulate body, replicates by binary fission, differentiates into elementary bodies and is released to adjacent cells

33
Q

How does presumptive diagnosis of chlamydia work?

A

Clinical suspicion based on symptoms (urethritis, epididymitis, conjunctivitis)
Positive nonculture result (EIA, DFA or nucleic acid detection)

34
Q

How does definitive diagnosis of chlamydia work?

A

Culture and ID of inclusion bodies (dark bodies) or

Combination of 2 nonculture methods (EIA, DFA or nucleic acid detection)

35
Q

What are two other causes of vaginitis and urethritis?

A

Candidiasis due to C. albicans

Trichomoniasis due to Tichomonas vaginalis (protozoan parasite)

36
Q

What is the clinical manifestation C. albicans infection?

A

Can be part of the normal vaginal microflora (carrier) or can cause infection (itching, erythema, none or thick, cheesy discharge)
Lactobacillus will be missing from normal microflora

37
Q

How is candidiasis treated?

A

Using oral antifungals but resistance is a possibility

38
Q

What is the clinical manifestation of trichomoniasis?

A

Profuse, offensive yellow-green discharge or asymptomatic

39
Q

How is trichomoniasis treated?

A

Metronidazole

40
Q

What causes genital herpes?

A

Herpes simplex virus 2 primarily (HSV-1 and 2)
Herpes simplex 1 sometimes
Each used to be at separate sites but now have become mixed

41
Q

Where is HSV-1 primarily found?

A

In saliva, causing oropharyngeal infections in children and cold sores after reactivation

42
Q

Is there cross immunity for the herpes simplex viruses?

A

No

43
Q

What are the clinical manifestations of genital herpes?

A

Ulcerating vesicles with the first lesion appearing 3-7 days post infection that break down to form painful ulcers (swollen lymph nodes, fever, headache, malaise)
2 weeks to heal

44
Q

How does genital herpes become latent and reactivate?

A

The virus/lesion is on a sensory nerve ending, becomes latent in the dorsal root ganglion neurons then when reactivated, they travel down the same route to cause recurrent lesions (genital cold sores)

45
Q

What happens when a herpes infected mother gives birth?

A

The neonatal will have disseminated herpes or encephalitis

46
Q

How is genital herpes diagnosed?

A

By finding the viral DNA in vesicle fluid or ulcer swabs

Can use PCR, immunofluorescence

47
Q

How is genital herpes treated? How is recurrent genital herpes treated?

A

Antivirals

Reccurent infections are treated with 6-12 months of low dose antiviral to stop/reduce frequency of recurrences

48
Q

What can human papilloma virus (HPV) cause?

A

Papillomas/warts and cervical cancer (contagious cancer)

120 distinct types (>40 genital types with varying risks)

49
Q

How can HPV be detected?

A

Using cytology sections (Pap smears for koilocytes)

Nucleic acid detection using PCR

50
Q

How can HPV be prevented?

A

Using the quadrivalent vaccine (good for HPV 6, 11, 16 and 18) at an early age in both males and females

51
Q

What infection is pneumocystis pneumonia an indication of?

A

HIV

52
Q

What is human immunodeficiency virus (HIV)?

A

A retrovirus (RNA as the genome that codes for reverse transcriptase to DNA)
Isolated from blood lymphocytes in 1983
Likely started in Africa in 1950s

53
Q

Where did HIV-1 and HIV-2 come from?

A

Arose from closely-related primate viruses that jumped to humans

54
Q

What are the 3 groups of HIV-1?

A

Main (A-J): B is most common in north america europe. A and C in africa
New (N) and Outlier (O) in west central africa
Travel is changing this geographical distribution

55
Q

What is the pathogenesis of HIV?

A

Infects T helper cells (CD4) and enters from the binding of viral gp120 envelope glycoprotein to CD4 receptor.
Chemokine co-receptor (CCR5) or CXCR4 (progression) involved in establishing infection
Viral replication halts after integration of provirus (latent)

56
Q

How can someone be resistant to HIV?

A

Have CCR5 gene deletions

57
Q

How do the routes of HIV transmission differ between resource rich and resource poor countries?

A

Resource rich sees more due to homosexual intercourse

Resource poor sees more due to heterosexual intercourse and via in utero transmission

58
Q

What is the clinical definition of a HIV patient?

A

CD4 count is 200/mm3 (>1000 mm3)

Immune system is still functioning

59
Q

What is the clinical definition of a HIV/AIDS patient?

A

CD4 count

60
Q

How is HIV treated?

A

Using HAART (highly active antiretroviral therapy) which is a cocktail of drugs due to mutations that could cause virus to bypass one mechanism of action

61
Q

What are the drawbacks of HIV treatment?

A

Mitochondrial toxicity and altered fat distribution
HIV inhabits CSF and GU tract, which is hard for drugs to reach
Resistance

62
Q

How is HIV diagnosed?

A

Serological (HIV-1 and HIV-2 antibodies)
Molecular analysis (detect HIV-1 RNA or proviral DNA)
Measuring load of HIV-1 RNA (RT-PCR)