Micro Flashcards

1
Q

Primary syphilis

A

Within first few weeks of infection
- initial replication at site of infection –> forms an ucler, “chancre” and initiates bacteremia

“chancre” is the defining characteristic

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2
Q

Secondary syphilis

A
  • **macropapular rash on palms and soles **
  • moist papules on skin and mucous membranes
  • patchy alopecia
  • maybe constitutional symptoms of low fever, malaise, anorexia, weight loss, headache, myalgia, lymphadenopathy.
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3
Q

Tertiary syphilis

A
  • granulomas
  • CNS involvement (including meningitis)
  • neurosyphilis
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4
Q

Congenital syphilis

A

spirochetes easily cross placenta
40-50% miscarriage/stillbirth/neonatal death
survivals develop several secondary syphilis and physical abnormalities

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5
Q

Syphilis (pathogenesis)

A

Transmits via intimate contact

  • sexually w/ low infectious dose ~57
  • transplacental
  • rarely via blood-blood

Infects endothelium of small blood vessels

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6
Q

SARS

A

Started in China ~2003
Attributed to the Civet animal coronavirus
~8000 infections worldwide (800 deaths)

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7
Q

Swine flu

A

Started in Mexico ~2009
Attributed to triple-recombination between human and animal influenza viruses
~250k deaths worldwide

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8
Q

MERS

A

Started in Saudi Arabia (2012-2014)
Attributed to one coronavirus that appeared in humans in 2011.
~100 deaths worldwide

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9
Q

Conditions of unknown etiology (may be due to infectious agents)

A

Alzheimer’s disease
MS
T2Diabetes (transmission resembles infectious condition, but no pathogen found)

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10
Q

Condylomata lata

A

infectious moist lesion on genitals.

indicative of secondary syphilis

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11
Q

Percentage of syphilis that enters tertiary syphilis

A

1/3 resolve, 1/3 latency and 1/3 progress onto tertiary syphilis

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12
Q

Diagnosis of syphilis

A

Chancre (primary), maculapapular rash on soles or palms (secondary), condylomata lata (secondary), CNS symptoms (tertiary), Argyll-Robertson pupil (tertiary)

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13
Q

Argyll-Robertson pupil

A

One of both pupils fails to constrict in response to light, but does constrict to focus on a near object.

Indicative of neural syphilis

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14
Q

Microscopy staining for syphilis

A

too small to see by standard microscopy

silver or dark field (no gram stain)

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15
Q

Reagin

A

Nonspecific antibodies produced by treponema.
Detectedable by flocculation tests with cardiolipin (VDRL or RPR)

Also generated by other bugs (not used for diagnosis of syphilis)

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16
Q

Serology for syphilis

A

Generates a lot of reagin (nonspecific antibodies) – disappears after infection.

Also has specific antibodies detectable by IF or hemagglutination – Remains positive for life.

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17
Q

Syphilis treatment

A

penicillin G for primary and secondary
slow release enhances effectiveness

No known resistance

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18
Q

Yaws

A

aka Treponema pertenue
Tropical disease of overcrowding and poor sanitation.
Three phase like syphilis, but no neuro- or cardio- involvement

Reagin positive
Treat with penicillin

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19
Q

Treponema pertenue

A

aka Yaws
Tropical disease of overcrowding and poor sanitation.
Three phase like syphilis, but no neuro- or cardio- involvement

Reagin positive
Treat with penicillin

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20
Q

Pinta

A

aka Treponema carateum
Central and South America, rarer than yaws
No constitutional symptoms, just hypo- and hyper-pigmented skin plaques
Spread by direct contact

Reagin positive
Treat with penicillin

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21
Q

Pediculosis

A

caused by 3 types of lice: head, body and pubic

head - school kids, itchy behind ear
body - homeless, itchy at night
public - promiscuous, itchy groin

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22
Q

syphilis virulence

A

immune evasion - low inflammation

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23
Q

syphilis bacteria name

A

Treponema pallidum

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24
Q

N. gonorrhoeae virulence factors

A

IgA protease - clears mucosal surfaces to facilitate colonization
pili - attachment and antiphagocytic
LOS (not LPS) - less immunogenic than LPS
Porins - confer serum resistance, enhance cell entry
Opa - enhance cell adherence &entry

25
Q

N. gonorrhoeae diagnosis

A

NAAT (nucleic acid amplification testing)

26
Q

N. gonorrhoeae

A
Gram (-)
diplococci
human-restricted
oxidase(+)
catalase (+)
aerobic/facultative
27
Q

N. gonorrhoeae culture

A

Thayer-martin if normal flora (it has antibiotics)

chocolate agar if sterile (CSF, blood)

28
Q

Complement deficiency

A

predisposes to N. gonorrhoeae and its complications

29
Q

untreated gonococcus in women

A

results in PID

30
Q

N. gonorrhoeae complications

A

DGI (disseminated gonococcal infection)
septic arthritis
meningitis
endocarditis

31
Q

N. gonorrhoeae infection in newborns

A

Bilateral conjunctivitis
generally infected at birth (can happen postpartum or in utero)

Eye pain, redness, discharge

If untreated –> permanent blindness follows quickly

32
Q

N. gonorrhoeae treatment

A

Ceftriaxone
cefotaxime

admit if complications

33
Q

C. trachomatis

A

obligate intracellular bacteria

must use drugs that can penetrate human cell membrane

34
Q

Reticular bodies

A

“ret”ain inside the body
larger intracellular inclusions that are visible on microscopy.

Large machinery for replication

35
Q

Elementary bodies

A

smaller entities that are formed when C. trachomatis is looking to spread.

Very infectious

36
Q

C. trachomatis virulence factors

A

T3SS used for entry & establishing inclusion body

37
Q

C. trachomatis serovars

A

A – C: blinding trachoma
D – K: genital tract infections
L1 – L3: lymphogranuloma venereum

38
Q

Reiter Syndrome

A

aka Reactive Arthritis

usually secondary to an immune-mediated response – chlamydia is known to trigger it

Triad: Can’t see (conjunctivitis), can’t pee (urethritis), and can’t climb a tree (arthritis)

80% positive for HLA-B27

39
Q

C. trachomatis diagnosis

A

initiated based on physical findings

NAAT preferred, but culture also works.

40
Q

C. trachomatis treatment

A

tetracyclines (doxycycline) EXCEPT for pregnant/pediatric/allergic patients who get erythromycin or other alternatives.

41
Q

RNA viruses

A

Tend to carry onco-genes

42
Q

DNA viruses

A

Tend to activate proto-oncogenes (ie disrupt normal cell cycle processes)

43
Q

Proto-oncogenes

A

myc - transcription factor
sis - platelet derived growth factor
erb B - growth factor receptor

44
Q

Oncogenes

A

p53

RB

45
Q

retroviruses

A

Can contain oncogenes

Can cause expression of regional oncogenes

46
Q

HPV low-risk types

A

HPV-2, -4: causes warts

Most common is -6,-7

47
Q

HPV high-risk types

A

HPV-16,-18,-31,-33

causes squamous cell carcinomas of the cervix, penis and oropharynx

Carries the E6, E7 genes

48
Q

E6 gene

A

Carried by high risk HPV types

-binds p53 –> leads to degradation of ubiquitin pathway

49
Q

E7 gene

A

Carried by high risk HPV subtypes

- binds nonphosphorylated Rb –> prevents its interaction with E2F

50
Q

Epstein-Barr virus

A

Herpes virus that causes mononucleosis

Associated with Burkitt’s lymphoma. Tumors express latent viral antigen of uncertain function and have overexpressed myc genes.

51
Q

HBV and HCV (hepatitis)

A

Chronic hepatitis predisposes to cirrhosis and liver cancer after many years

52
Q

HTLV-1 and -2 (Human T-cell Lymphotropic virus)

A

RNA virus with no oncogene. Causes leukemia and lymphoma

53
Q

Kaposi sarcoma herpes virus

A

associated with Karposi’s sarcoma in patients with HIV

54
Q

HIV protease

A

An essential enzyme that is translated at the rough ER and matures in the golgi.
It is then packaged in the virion where it MUST cleave Gag into its three subunits to form infectious particles.

This cleavage process results a change from an indistinct core the typical trapezoidal core of the mature HIV-1

55
Q

Stages of HIV infection

A
  1. Exposure (transmission)
  2. Primary HIV infection (acute phase)
  3. Seroconversion
  4. Clinical latent period
  5. Early symptomatic HIV infection
  6. AIDS (CD4 count
56
Q

Receptors that HIV targets

A

CD4 receptor and the CCR5 initially (CCR5+ cells = macrophage)

Mutates later on to infect also the CXCR4 (CXCR4+ cells = Helper T cells)

57
Q

Acute HIV infection

A

Occurs over the initial first few week.
Anti-HIV antibodies develop
Possible acute syndrome –> wide spread dissemination of virus via seeding of lymphoid organs

58
Q

NAAT

A

Nucleic acid amplification testing