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infectious disease > 7 STDs > Flashcards

7 STDs Flashcards

1
Q

what causes syphilis?

A

treponema pallidum

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2
Q

what is treponema pallidum

A

a spirochete that has never bee ncultured

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3
Q

primary syphillis

A

localized disease

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4
Q

secondary syphillis

A

systemic disease

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5
Q

tertiary syphillis

A

long-term inflammation of the CNS, aorta, brain, skin, spine, eye

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6
Q

congenital syphillis

A

systemic, chronic, inflammation

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7
Q

those with syphillis often have

A

HIV, other STDs

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8
Q

can syphilis go through skin if someone shakes your hand?

A

yes

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9
Q

transmission of syphilis

A

humans are only known hosts

-transmission almost always by direct contact with infectious lesions

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10
Q

highest incidence of syphillis

A

20-29 year olds, sexually active adults

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11
Q

what percent of exposed people contract the disease

A

30%

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12
Q

how many cases of primary or secondary syphilis diagnosed per year in US

A

30,000

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13
Q

how many cases of early latent syphilis, diagnosed per year in US

A

30,000

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14
Q

primary syphillis

A
  • chancre appears 10-90 days (3 wks) after exposure at inoculation site; heals in 3-6 weeks (up to 26 weeks)
  • regional adenopathy (painless, rubbery)
  • larger the inoculum, larger the chancre
  • serological testing during this stage is negative and the disease is essentially local
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15
Q

chancre

A

hard, indurated, highly infectious, painless (genitalia or orally)

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16
Q

primary syphillis can be diagnosed with what kind of microscopy

A

darkfield

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17
Q

secondary syphilis

A

lesions begin 6-8 (“2-24”) weeks after initial chancre, may overlap with time when chancre is present, especially with HIV

  • systemic disease
  • lasts 2-6 weeks
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18
Q

skin + mucous membranes are sites of

A
  • principal manifestations
  • macular to papular
  • occasionally pustular or nodular rash
  • palms and soles
  • patchy alopecia
  • mucous patches
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19
Q

-alopecia

A

bald spot

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20
Q

systemic syphillis

A

malaise, anorexia, headache, sore throat, arthralgias, low fevers, adenopathy

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21
Q

adenopathy

A

enlargement of lymph nodes anywhere in your body

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22
Q

secondaria syphillis

A

high bacteremia + very

contagious

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23
Q

nicekl/dime lesions

A

secondary syphilis

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24
Q

verrucous papules

A

syphillis

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25
Q

latent syphilis—> tertiary syphilis

A

-25% experience a relapse of secondary syphlis

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26
Q

duration of latent syphilis

A

variable

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27
Q

how many people with secondary syphilis will progress to tertiary syphilis

A

1 in 3, 1 to 30 years later

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28
Q

hallmark of latent syphilis

A

positive serological test in the absence of any clinical disease or symptoms

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29
Q

spirochetes

A

syphillis

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30
Q

tertiary syphilis contagious?

A

no, but highly destructive and usually takes years to occur

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31
Q

tertiary syphilis: late benign or gummatous syphilis

A

develops in 15% of cases 1-10 years after infection

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32
Q

gummas

A

nodular lesions with granulomatous inflammation , can be any organ

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33
Q

cardiovascular tertiary syphili

A

10% of cases develop this 10-40 years after infection

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34
Q

what occurs during cardiovascular tertiary syphii

A

arteritis (vasuclitis) results in thickening/hardening of the vasa vasorum; aortic regurgitation; aneurysms, obstruction

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35
Q

neurosyphilis during tertiary syphilis

A

8% untreated cases, 5-25 y after infection; dementia, general paresis, tabes dorsal

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36
Q

ulcerating gumma occurs in

A

late syphilis

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37
Q

if mother infective with syphilis, , child will be

A

still born or present with fulminant syphilis

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38
Q

fulminant syphilis

A

rhitinis, snuffles followed by skin lesions

  • osteochondritis (inflamed bone, cartilage)
  • hepatosplenomegaly and adenopathy
  • immune complex glomerulonephritis
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39
Q

congenital syphilis death in infant

A

in first 2 years with pulmonary hemorrhages, bacterial infecitons, hepatitis

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40
Q

Hutchinsons’s teeth**

A
  • occurs in congenital syphilis
  • notched, narrow edged permanent incisors
  • mulberry molars
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41
Q

congenital syphilis

A

develop lesions similar to tertiary syphilis

  • symmetric hydrarthrosis of knee joins
  • deafness
  • hutchinson’s teeth
  • saddle noses
  • saber shinsrhagades
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42
Q

rhagades

A

fissures, cracks, fine linear dermal scars especially around the mouth, and areas subjected to frequent movement

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43
Q

perforation of the hard palate caused by

A
  • syphilitic gumma

- gummas are granuloma like lesions seen in tertiary syphilis

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44
Q

screwdriver shaped incisors with notching

A

hutchinson’s teeth-congenital syphillis

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45
Q

saddle nose

A

deformities of the nasal cartilage due to congenital, untreated syphilis

46
Q

diagnosis + treatment of primary syphillis

A
  • presenting signs and symptoms, history
  • dark field examination of exudate in lesion, direct fluorescent antibody
  • seronegative
47
Q

diagnosis + treatment of secondary syphlis

A

screenig test using nontreponemal antigen (cardiolipin lecithin)

48
Q

what percentage develops relapses of secondary syphilis

A

25%

49
Q

what percent develops late syphilis

A

30%

50
Q

treatment during what stages of syphilis cures the disease

A

primary or secondary

51
Q

changes of what stage of syphilis are not reversible after treatment, except for gummas

A

tertiary

52
Q

penicillin

A

if latent, 2-3 weekly doses, primary or secondary 1 dose; tertiary 3 doses; congenital 10 days

53
Q

mothers with congenital syphilis

A

before 16th week, no congenital syphillis in child; after 16th week, cannot prevent all manifestations with peniillin

54
Q

what causes gonorrhea

A

neisseria gonorrhoeae

55
Q

neisseria gonorrhoeae gram stain

A

-gram negative diplococcus

56
Q

neisseria gonorrhoeae infects

A

-mucus secreting epithelial cells

57
Q

neisseria gonorrhoeae evades host thorugh

A

alteration of cell surface

58
Q

men with neisseria gonorrhoeae

A

> 95% symptomatic

59
Q

women with neisseria gonorrhoeae

A

no symptoms

60
Q

skreet

A

urethral scarring in men with gonorrea

61
Q

pelvic inflammamtory disease with abscesses, subsequenct ectopic pregnancies or sterility in

A

women with gonorrhea

-can be lethal

62
Q

more gonorrhea symptoms

A
  • dissemintated bacteremia occurs with rash and arthritis

- gonorrheal pharyngitis

63
Q

what is common with gonorrhea?

A

gonorrhea pharyngitis

64
Q

twists?

A
  • antigenic variation via gene rearrangement
  • protease cleaves IgA1 but not IgA2
  • can attach to, and invade, nonciliated epithelial cells, where they can multiply and either cause local inflammation or disseminated disease
  • in contrast, GC LPS kills epithelial ciliated cells, which might otherwise “sweep” them away
65
Q

GC

A

the clap

66
Q

GC= the clap

A

-1 million reported cases/year but 2/3 mill per year

-

67
Q

1/3rd of all urethritis in US males have

A

THE CLAP= GC

68
Q

after a single exposure, risk for women and men

A

50% risk of acquisition for women, 20% for men after a single exposure

69
Q

pharyngeal infection with GC common cause of sore throat

A

pharyngitis, tonsillitis, gingivitis- in men who have sex with other men and is principle origin of gonococcemia

70
Q

epipidiymis enlarges in

A

gonorrhea

71
Q

gonoccocal ophtlamia

A

eye is red

72
Q

GC rash

A

lesions are not raised, but instead are depressed and not bullous

73
Q

GC in women

A

30% GU tract infected with with GU are completely asymptomatic; others have vague symptoms that are nonspecific, treatment not sought (if pharynx may have sore throat)

74
Q

usual site of infection for women with GC is in the

A

cervix, which gets inflamed; contiguous spread to rectum, urethra, bartholin’s glands

75
Q

10-20% GC women develop

A

pelvic inflammatory disease (PID)- endometritis, salpingitis, tubovarian abscesses, peritonitis

76
Q

tubo-ovarian abscess secondary to

A

gonorrhea in females

77
Q

gonorrhea tx

A
  • cetriaxone + other agent
  • quinolones nor cefixie alone are acceptaple therapy
  • there is increasing resistance to antibiotics
78
Q

neisseria gonorrhea located i

A

cervix, urethra, rectum

79
Q

do not use these drugs in pregnant women

A

quinolones or tetracyclines

80
Q

principle origin of gonococcemia

A

men who have sex with other men

81
Q

bacteria of chlamydiae

A

C. trachomatis, psittaci, pneumoniae

82
Q

chlamydiae bactera are

A

intracellular

83
Q

two stages of chlamydiae

A

reticulate body (Active metabolism) and the elementary body (transit form that goes from one cell to another)

84
Q

what are the most common causes of urethritis and cervicitis in the US

A

chlamydiae

->50% in males

85
Q

what causes PID

A

chlamydiae

86
Q

what causes trachoma, which leads to blindness

A

trachomati

87
Q

3rd most common STD in the US

A

chlamydiae

88
Q

genital C. trachomatis uses what as a precursor for Trp

A

indole

89
Q

C. trachomoatis servovars D-k causes (chlamydiae)

A

urethritis, cervicitis, endometritis, salpingitis, pelvic inflammatory disease, epididymitis, prostatitis, proctitis, arthritis, conjunctivitis, pneumonoitis

90
Q

C. trachomoatis servovars L1, L2, L3 cause

A

lympgranuloma vernereum (LGV), abscesses of the inguinal lymph nodes, and painful genital lesions

91
Q

C. psittaci causes

A

pneumonia in humans and birds

92
Q

C. pnuemonieae causes

A

upper and lower respirtaroy tract infections in humans, very comong (1/2 young adults have had)

93
Q

chlamydia genome

A 
small
15% size of E.coli
-encodes 500 proteins
-cannot generate ATP
-no oxidative enzymes, flavoproteins, or cytochromes
-can make their own proteins
94
Q

chlamydia genome endocytosis leads to

A

colonies within phagosomes (intracytoplasmic inclusions)

-lysosomes do not fuse with phagosomes and so bacteria survive

95
Q

evidence for chlamydia type III secretion

A

inject proteins into cytoplasm avoiding lysosomes

96
Q

chlamydia diagnosed more in women than men because

A

women get screened often

97
Q

lymphogranuloma granuloma LGV serovars L1, L2, L3

A
  • primary sore small, painless
  • swellign 1-4 weeks later
  • LNs may ulcerate, go undetected if in urethra, vagina, or rectum (proctitis)
  • scarring in rectum, abscesses in perineum
98
Q

diagnosis of chlamydia

A

direct fluorescent assays used; gene probe methods like nucleic acid ammplicfication tests (NAAT)

99
Q

tx of chlamydia

A

tetracylcines, macrolides, quinolones, sulfonamides, - are all active against active form (Reticulate bodies)-must penetrate the host cell and make their way to the intracellular bacteria

100
Q

*what are the tx of choice

A

doxycycline or azithromycin

-erythromicin is alternative for children or pregnant women

101
Q

tx LGV

A

doxycycline 100mg 2x a day for 21 days

102
Q

clamydia urethritis/cervitis

A

1g azithromycin 2x daily doxy 100mg for a week

103
Q

Papillomavirus

A

noneveloped, shed with skin, hearty

  • cutaneous and ano-genital warts and cervical cancer
  • juvenile onset recurrent respiratory papillomatosis (JORRP) + focal oral hyperplasia
104
Q

respiratory pap

A

death by suffocation-during vaginal delivery, infant’s oropharynx infected

105
Q

papilloma virus vaccine

A

prevents HPV6, 11, 16, 18

106
Q

complications of genital infection

A
  • aseptic meningitis

- rare complicatoins

107
Q

-aseptic meningitis-of herpes

A
  • more common in primary than recurrent infection

- generally no neurological sequelae

108
Q

rare complications of genital infection- herpes

A

stromatitis, pharyngitis

  • radicular pain
  • sacral parathesias
  • transverse myelitis
  • autonomic dysfunction
109
Q

oral herpes

A

soft palate

110
Q

first clinical episode of genital herpes

A

may become severe or prolonged

-antiviral therapy should be used-especially if symptoms

infectious disease (7 decks)

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