Immunology Exam 6: Infectious Agents Flashcards

1
Q

Non-treponemal testing methods for Syphilis

A

RPR, VDRL

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2
Q

Treponemal testing methods for Syphilis

A

FTA-ABS
TP-PA
T. pallidum Ab for ELISA
T. pallidum Ab by western blot

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3
Q

What is the purpose of the RPR? How to interpret?

A

Cardiolipin reacts with Reagin (a non-treponemal antibody) to detect syphilis –> Flocculation assay with charcoal agglutination

Reactive = small tiny dots
Non-reactive = one condensed button that looks like a comet tail

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4
Q

Primary stage of Syphilis

A

Development of a chancre

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5
Q

Secondary stage of Syphilis

A

Rashes on soles of feet and palms of hands

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6
Q

Latent stage of Syphilis

A

Non-infectious state that occurs after untreated secondary syphilis, may last for years

More likely to develop into late-stage syphilis than spontaneous recovery

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7
Q

Tertiary (late) syphilis

A

Appearance of gummas
Neurodegenerative

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8
Q

What are signs of Congenital syphilis?

A

Hutchisonian Triad –> deafness, keratitis, hutchinson’s teeth

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9
Q

Early to latent infections are _____ antibody positive

A

IgM

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10
Q

Late or chronic infections are _____ antibody positive

A

IgG

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11
Q

Non-treponemal antibodies are a _____ test for syphilis

A

Screening (RH does this backwards)

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12
Q

Treponemal antibodies are a ______ test for syphilis

A

confirmatory (RH does this backwards)

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13
Q

Cardiolipin

A

Lipid made from damaged cells, cholesterol, and lecithin that reacts with Reagin (non-treponemal antibodies)

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14
Q

Limitations of TP-PA

A

Uses serum and CSF only, cannot differentiate between IgM or IgG

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15
Q

In what stages of Syphilis will the RPR/VDRL (non-treponemal tests) be positive?

A

Primary and secondary
*Starts to decline during latent stage and tertiary stage

*Untreated infections will be better detected than treated infections after latent stage

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16
Q

In what stages of Syphilis will the Treponemal antibody tests be positive? (TP-PA, FTA-ABS, etc)

A

All stages of Syphilis, with more patients testing positive the later the stage

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17
Q

What is Syphilis treated with?

A

Penicillin in early stages

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18
Q

Etiology of Lyme’s disease

A

Transmission of Borrelia burgdorferi by Ixodes ticks

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19
Q

Diagnosis of Lyme’s disease

A

Bull’s eye rash,

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20
Q

What group of people may be at increased risk of Lyme disease induced arthritis?

A

People with HLA DRB104 and DRB102

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21
Q

Possible lab diagnosis of Lyme’s

A

May be grown using Barbour-Stoenner-Kelly medium
Testing includes serum, skin lesions, and CSF for antibody and PCR methodologies

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22
Q

What is the two-step process of Lyme’s disease diagnosis?

A

Step 1: positive result on EIA or an IFA

Step 2: if signs or symptoms persist for 30 or more days, perform IgG western blot. If signs or symptoms persist for 30 days or less, perform both IgM and IgG western blot

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23
Q

Explain the diagnosis of Lyme’s disease and the western blot

A

(+) IgM –> must have 2 of 3 characteristic bands

(+) IgG –> must have 5 of 10 characteristic bands

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24
Q

Reverse vs forward algorithm for Syphilis

A

Forward: start with non-treponemal Ab, then go to treponemal to confirm

Reverse (what RH does): start with treponemal Ab, then do RPR to confirm

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25
Q

What are the 3 stages of Lyme’s?

A
  1. Localized bulls eye rash
  2. Early Dissemination
  3. Late dissemination with arthritis involvement if untreated
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26
Q

What type of virus is EBV? How is it transmitted? What spectrum of diseases does it cause?

A

DNA herpes virus transmitted through intimate contact with salivary secretions

Causes infectious mononucleosis, lymphoproliferative disorders, and certain malignancies (Burkitt Lymphoma)

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27
Q

Lab findings with EBV

A

20% or more atypical lymphocytes, absolute lymphocytosis, heterophile antibodies

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28
Q

Paul-Bunnell test

A

Old method of detection for heterophile antibody titer to diagnose IM/EBV

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29
Q

Early antigens for EBV infections

A

EA-D: found in nucleus/cytoplasm

EA-R: restricted to cytoplasm only

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30
Q

Late antigens for EBV infections

A

VCA (viral capsid antigens)

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31
Q

Latent-phase antigens for EBV infections

A

EBV nuclear antigens (EBNA)

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32
Q

When does Anti-EBNA appear in EBV?

A

During convalescent mononucleosis

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33
Q

When does IgM anti-VCA vs IgG anti-VCA appear in EBV?

A

IgM anti-VCA: acute IM
IgG anti-VCA: acute or past IM

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34
Q

When does Anti-EA-D appear in EBV?

A

acute IM

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35
Q

What virus uses the viral escape mechanism, latency?

A

VZV remaining latent in nerve cells

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36
Q

What virus uses the viral escape mechanism, altering immune function?

A

EBV stimulating polyclonal B cell activation

37
Q

What virus uses the viral escape mechanism, suppression of immune response?

A

CMV reducing MHC I expression

38
Q

What virus uses the viral escape mechanism, blocking action of immune system components?

A

HCV binding C3b

39
Q

What virus uses the viral escape mechanism, mutations resulting in production of new viral antigens?

A

Influenza

40
Q

What hepatitis viruses are transmitted by fecal-oral route?

A

A and E

41
Q

What hepatitis viruses are transmitted via parenteral route?

A

B, D, C

42
Q

RNA hepatitis’s

A

A, C, D, E

43
Q

DNA hepatitis

A

B

44
Q

What is the HBV marker for active infection?

A

HBsAg

45
Q

What is the only HBV marker that will be present if vaccinated?

A

Anti-HBs (surface antibody)

46
Q

What is the HBV marker for active viral replication and indicates a high degree of infectivity?

A

HBe Antigen

47
Q

What does presence of Anti-HBe in HBV indicate?

A

Recovery from Hep B

48
Q

Chronic vs Acute exposure to HBV (what markers will be present)

A

Chronic: Only have anti-HBc, antigens will persist

Acute: Antigens will go away over time, will have Anti-HBe, Anti-HBs, Anti-HBc

49
Q

How to detect CMV

A

Viral culture incubated with human fibroblast cell lines and presence of CPEs

Molecular tests for DNA, CMV antigens

Serology

50
Q

Rubella standout features

A
  • German Measles
  • Can cause congenital abnormalities, miscarriage, stillbirth
  • Prevented by MMR vaccine
51
Q

Rubeola standout features

A
  • Measles
  • Subacute sclerosing panencephalitis
  • Prevented by MMR
52
Q

Mumps standout features

A
  • RNA virus transmitted through respiratory droplets
  • Causes parotitis
  • Prevented by MMR
53
Q

Which HIV is the cause of most HIV infections worldwide?

A

HIV-1, subtype C

54
Q

Which HIV is the cause of most HIV infections in the US?

A

HIV-1, subtype B

55
Q

HIV-2

A

originated in west africa, less prevalent

56
Q

What does pol gene in HIV code for?

A

Viral enzymes
Includes p51: reverse transcriptase enzyme

57
Q

What does gag gene in HIV code for?

A

Nucleocapsid and core proteins
Includes p24

58
Q

What does env gene in HIV code for?

A

Viral envelope proteins
Includes gp41 and gp120: attachment to host cell (envelope)

59
Q

What is the main target of HIV?

A

CD4 receptor, uses gp120 to bind

60
Q

What is the criteria for AIDS diagnosis from HIV?

A

<200 cells/uL of CD4

61
Q

Treatment for HIV

A

CART (combined antiretroviral therapy)

62
Q

Current testing algorithm to diagnose HIV

A

Perform screening for HIV-1 and HIV-2 antibodies and p24 antigen

Confirm positive antibody results to differentiate 1 and 2

If the differentiation immunoassay is negative, perform PCR. If PCR is then positive, it is acute HIV infection

63
Q

What does this indicate for HIV: p24 positive, but HIV-1/2 negative

A

Acute/active infection

64
Q

What does this indicate for HIV: p24 negative, but HIV-1/2 positive

A

Chronic or past infection

65
Q

What does this indicate for HIV: p24 and HIV-1/2 positive

A

Positive, immune system keeping it in check

66
Q

What is a GOOD result for HIV monitoring?

A

> 200 CD4 cells/uL
<500 RNA copies/mL

67
Q

Quantitative viral load assay for HIV

A

Uses qPCR to measure amount of HIV RNA circulating in patient plasma; primers target gag or pol genes

68
Q

What does a significant increase in HIV viral load indicate?

A

A need for drug resistance testing and a possible change in CART

69
Q

Infectivity

A

Organism’s ability to establish an infection

70
Q

Pathogenicity

A

Ability of an organism to cause disease

71
Q

Virulence

A

Extent of pathology caused by an organism when it infects a host

72
Q

What does Group A strep pyogenes cause?

A

Pharyngitis (Strep Throat)

73
Q

What does Group B strep pyogenes cause?

A

Pyoderma

74
Q

What does Group C strep pyogenes cause?

A

Scarlet Fever

75
Q

What are the clinical manifestations of acute group A streptococcal infection?

A

Toxic shock syndrome
Necrotizing fasciitis
Post streptococcal glomerularnephritis
Acute rheumatic fever

76
Q

What is Strep pyogenes M antigen associated with?

A

Hyaluronic capsule for virulence

77
Q

Streptolysin O vs Streptolysin S

A

Streptolysin O = antigenic, oxygen labile

Streptolysin S = non-antigenic, oxygen stable

78
Q

Hyaluronidase

A

Helps break down host connective tissue

79
Q

Streptokinase

A

Enzyme to dissolve clots by activating plasmin

80
Q

Group B strep

A

S. agalactiae

81
Q

What does S. agalactiae cause?

A

Pneumonia and meningitis in neonates

82
Q

What does S. dysgalactiae cause?

A

Pharyngitis and pyogenic infections in humans

83
Q

What is Group C strep?

A

S. equii
S. dysgalactiae

84
Q

What bacteria is associated with gastric/duodenal ulcers?

A

Helicobacter pylori

85
Q

Which bacteria is rapidly urease positive?

A

H. pylori

86
Q

Three life cycle stages of T. gondii

What is the definitive host?

A

Definitive host = cats

Tachyzoite (seen in humans and cats)

Bradyzoite (seen in tissue biopsy)

Sporozoite (found in oocysts in feces)

87
Q

What is Cryptococcus neoformans associated with? How to diagnose?

A

Pigeon poop
India Ink stain

88
Q

What is Histoplasma capsulatum associated with?

A

Cave dwellers, bird/bat poop
Ohio River/Mississippi River valley regions
Infects mononuclear phagocytes