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Med Micro Final Exam > From notes > Flashcards

From notes Flashcards

1
Q

HIV is a ____ which is its genus name

A

lentivirus

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2
Q

Where is HIV2 mostly found?

A

in africa

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3
Q

how does HIV2 differ from HIV1?

A

tends to develop more slowly and to be milder; less infectious early

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4
Q

HIV is NOT a ___ genome so instead it just has:

A

NOT a segmented genome; just has 2 copies of the same RNA

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5
Q

gp120 of HIV binds to what?

A

a CD4 T lymphocyte

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6
Q

In HIV, where does translation into viral proteins occur?

A

cytoplasm

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7
Q

What is the most opportunistic infection in HIV patients?

A

pneumocystis

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8
Q

What is another name for kaposi’s sarcoma which is often a clinical consequence of HIV/AIDS?

A

malignant neoplasms

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9
Q

What is the first step in diagnosing HIV?

A

conducting a rapid test

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10
Q

What does a rapid HIV test look for?

A

looks for Ab that binds to HIV (b/c there are HIV antigens on the filter of the test)

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11
Q

If a rapid HIV test is positive, what must be done?

A

a western blot confirmatory test

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12
Q

If a rapid HIV test is negative, what must be done?

A

nothing; pt doesn’t have HIV

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13
Q

What are the two types of specimens you can use for a western blot test?

A
  1. venipuncture for whole blood

2. oral fluid specimen

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14
Q

What must be done after an initial western blot test for HIV?

A

if the patient is negative or there are indeterminate western blot results, must do follow-up testing after 4 weeks

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15
Q

new HIV guidelines from the CDC requires routine HIV screening for who?

A

all people between 15-64

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16
Q

HIV screening is now based on ___ and NOT based on ___

A

age; risk

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17
Q

During L&D, a woman with undocumented HIV status should have what done?

A

rapid testing

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18
Q

If the rapid HIV test conducted on a woman during L&D is positive, what should be done?

A

initiate ARV prophylaxis on basis of rapid test result

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19
Q

Rapid HIV testing of the newborn is recommended if:

A

mothers HIV status is unknown at delivery

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20
Q

If a rapid HIV test on a newborn is positive, what should be done?

A

initiate ARV prophylaxis within 12 hours of birth

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21
Q

What are the 4 targets/treatment strategies for HIV?

A
  1. reverse transcriptase
  2. protease inhibitors
  3. fusion inhibitors
  4. integrase inhibitors
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22
Q

What are 2 co-receptors on lymphocytes that can also help HIV bind?

A

Chemokine Receptors: CCR5 & CXCR4

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23
Q

What happens with HIV’s positive-sense RNA strand?

A

It is not translated to make the nucleocapsid proteins!!! Instead, Reverse Transcriptase makes a DNA copy of the RNA strand. This DNA copy then enters the nucleus & is integrated into the genome of the host cell via integrase. As long as this host cell lives, it will be infected with viral DNA.

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24
Q

How does replication of HIV affect the rest of the body?

A

Replication of HIV causes a gradual decrease in CD4+ cells.

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25
Q

Why is a decrease in CD4+ cells bad?

A

This allows more opportunistic infections to arise; Body can’t fight off microbes that you encounter every day and usually have no problem killing.

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26
Q

What’s the difference between HIV and AIDS?

A

HIV – is when the virus in the body (Pt makes Ab’s specific to HIV).
AIDS – is when opportunistic infections start occurring; doesn’t necessarily have to be caused by HIV.

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27
Q

How long does it take before AIDS begins to present in HIV patients?

A

Usually takes at least 7 years before opportunistic infections begin to occur. • Patient usually dies from an opportunistic infection.

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28
Q

How are HIV-1 and HIV-2 similar?

A

Both have the same mode of transmission and both are associated with similar opportunistic infections and AIDS.

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29
Q

How do HIV-1 and HIV-2 differ?

A

HIV-2 tends to develop more slowly and is an overall milder disease. It’s also less infectious early. HIV-2 is mostly found in Africa; not much HIV-2 in US.

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30
Q

how is HIV diagnosed?

A

anti-HIV antibodies (seroconversion) by ELIA or rapid test

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31
Q

Is HIV a tough virus?

A

No; easily killed by drying, high level detergents, household bleach, alcohol, formaldehyde, and heat (56˚C for 30 minutes)
Dried blood won’t even transmit it

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32
Q

what do HIV fusion inhibitors do?

A

Blocks entry into the host cell by not allowing gp120 to bind to the CD4+ receptors.

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33
Q

What are the 2 life stages of protozoan parasites?

A
  1. trophozoite (soft, fragile, growing in the body)

2. cyst (hard, non replicating, able to survive outside of the body) tends to be the part thats transmitted

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34
Q

What do species of the Plasmodium family cause?

A

malaria

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35
Q

Plasmodium are parasites of the:

A

red blood cells

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36
Q

How are Plasmodium species transmitted?

A

transmitted via Anopheles species

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37
Q

How many types of Anopheles species are there? How many transmit malaria?

A

430 species of Anopheles; 30-40 transmit malaria.

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38
Q

Plasmodium require what 2 hosts to survive throughout a population?

A
  1. mosquito (for sexual reproduction; must have an Anopheles mosquito in order to transmit malaria)
  2. human (or other animal) for asexual reproduction
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39
Q

Transmission of malaria is usually found in what type of climate?

A

Tropical and subtropical areas

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40
Q

What makes P. falciparum cause such a severe infection?

A

P. falciparum infects all RBCs (no preference whether the RBC is young, mid-, or old). Therefore, parasitemia is usually higher.

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41
Q

Where malaria is endemic, what do doctors do for patients with a fever?

A

The patient is usually given a presumptive diagnosis of malaria without lab confirmation. (So, treatment can start early!)

42
Q

Why do patients infected with Plasmodium vivax or Plasmodium ovale often experience relapses (several additional attacks) months or years without symptoms?

A

Relapses are due to dormant liver stage parasites, or hypnozoites, that may reactivate.
***Treatment to reduce the chances of such relapses should follow the treatment of the first attack.

43
Q

What is the gold standard for diagnosing malaria?

A

microscopy of blood

44
Q

What is the drug of choice to treat parasites in the blood?

A

chloroquine

45
Q

What is the drug of choice to treat dormant liver forms of parasites & to prevent relapses?

A

primaquine

46
Q

Which 2 Plasmodium species don’t have dormant liver stages?

A

P. falciparium and P. malariae

47
Q

What causes sickle cell anemia?

A

sickle cell anemia is a single amino acid mutation in the hemoglobin gene; if a child receives 2 mutated hemoglobin genes, they’ll end up with sickle cell anemia

48
Q

The number of heterozygous (good copy & bad copy) sickle cell anemia cases are highest where:

A

where P.falciparum is found

49
Q

Where is sickle cell anemia highly prevalent/common?

A

Africa

50
Q

Toxoplasma gondii is a protozoan that infects and grows inside of:

A

animals (MOSTLY CATS)

51
Q

How is toxoplasma gondii transmitted?

A

fecal-oral ingestion of the oocytes (female gametocyte) that are in the cats feces

52
Q

Why is Toxoplasma gondii especially dangerous to pregnant woman?

A

Pregnant woman can ingests the oocytes and have tissue cysts that form in the fetus’s eye, which may lead to blindness.
***Tissue cysts are generally not a problem if they grow anywhere else.

53
Q

What is Giardia lamblia and what disease does it cause?

A

Giardia lamblia is a single-cell flagellate protozoan that causes giardiasis or “Hiker’s Diarrhea.”

54
Q

What symptoms present with giardiasis?

A

Mild diarrhea & severe malabsorption (difficulty digesting or absorbing nutrients from food)

55
Q

What asymptomatic (~50%) animal is giardia often found in?

A

beavers

56
Q

How do you treat giardia?

A

metronidazole

57
Q

How can you diagnose giardia?

A

both the cysts and trophozoites can be found in stool sample

58
Q

Trichomoniasis vaginalis differs from giardia mainly in that:

A

it DOES NOT have a cyst form

59
Q

What are they symptoms of Trichomoniasis for men? Women?

A

Men – usually asymptomatic

Women – frothy, yellow-green discharge with a strong odor

60
Q

How is Trichomoniasis treated?

A

Metronidizole

61
Q

Where is the parvovirus found?

A

in respiratory secretions: saliva, sputum and nasal secretions

62
Q

Where does the parvovirus grow?

A

grows in red blood cell precursors

63
Q

What is another name for parvovirus B19?

A

fifth disease; erythema infectiosum; slapped face rash

64
Q

How is the parvovirus diagnosed?

A
  1. characteristic rash
  2. serology
    - look for IgM in pregnant women (newly exposed)
    - may shift to IgG later (when blood is drawn relative to when virus is in the body
65
Q

What kind of cells does HPV target?`

A

HPV infects the epithelial cells of the skin and mucous membranes

66
Q

Where does HPV replicate?

A

HPV must replicate near the skin’s surface with all the dead keratin cells. (Development of the epithelium is essential for the development of the viral particles.)

67
Q

How fast is HPV replication?

A

viral replication of HPV is slow

68
Q

What does HPV cause?

A

warts

69
Q

HPV virus types are roughly ____ which means genital types have ___

A

roughly tissue specific

genital types have affinity for genital skin and mucosa

70
Q

How is HPV on the surface of the skin spread?

A

spread by skin to skin contact

71
Q

There are about ___ serotypes of HPV that cause genital infections

A

40

72
Q

what are the two serotypes of HPV that are associated with cervical CA?

A

16 and 18

73
Q

How is a persistent HPV infection characterized?

A

by persistently detectable type-specific HPV DNA

74
Q

What is the most important risk factor for precancerous cervical cellular changes and cervical cancer?

A

persistent oncogenic HPV infection

75
Q

HPV is thought to be responsible for about ___% of anal cancers

A

90%

76
Q

HPV is thought to be responsible for about ___% of vaginal cancers

A

65%

77
Q

HPV is thought to be responsible for about ___% of vulvar cancers

A

50%

78
Q

HPV is thought to be responsible for about ___% of penile cancers

A

35%

79
Q

Recent studies show that about ___% of oropharyngeal cancers are linked to HPV

A

60%

80
Q

Babies born to a mother with genital warts occassionally develop warts in the ____

A

respiratory tract

81
Q

How do you treat genital warts?

A

warts can be removed by patient applied topicals, provider applied topicals, surgery, or freezing (laser); this doesn’t necessarily cure the infection; recurrences are frequent, especially in the first few months

82
Q

What are the usual symptoms of HPV?

A

usually has no signs or symptoms

83
Q

The most common manifestation of HPV infection in men is ____

A

genital warts

84
Q

High risk HPV types seldom cause ___

A

genital warts

85
Q

Detection of high risk HPV infection in a woman doesn’t mean she’s been cheating b/c:

A

HPV infection can be present for many years before it is detected; no method can determine when HPV infection was acquired

86
Q

GARDASIL contains:

A

capsid protein antigens that were made in yeast.

87
Q

How does the GARDASIL vaccine work?

A

it contains capsid protein antigen. The capsid proteins then self-assemble to “look” like the virus but can’t replicate

88
Q

What are the 4 serotypes contained in the GARDASIL vaccine?

A

6, 11, 16, 18

89
Q

HSV1 causes:

A

fever blisters

90
Q

HSV2 causes:

A

genital herpes

91
Q

Varicella Zoster virus causes:

A

chickenpox and shingles

92
Q

Epstein-Barr Virus (EBV) causes:

A

infectious mononucleosis and some cancers

93
Q

Cytomegalovirus causes :

A

mono-like illness

94
Q

What causes roseola?

A

HHV 6 & 7

95
Q

What does the herpes virus bring with it that is important for drug targets?

A

brings the gene for its own polymerase

96
Q

What makes the herpes virus so fragile?

A

its an enveloped virus that can’t survive if it dries out

97
Q

What type of cells does HSV1&2 infect?

A

epithelial cells

98
Q

In patients with HSV1 or 2, epithelial cells are destroyed by:

A

the replication of the virus

99
Q

How are the lesions seen in those with HSV1 or 2 described?

A

vesicular lesions

100
Q

In those with HSV1 or 2, host defenses resolve ___ but DO NOT resolve ___

A

resolve the local lesion; does NOT resolve latency

101
Q

Herpes infection: during primary infection, the virus enters the _____ and migrates along axons to ____ in the CNS

A
  • enters peripheral sensory nerves

- sensory nerve ganglia

102
Q

When the herpes virus becomes a latent infection in the nerve cells, the viral DNA is considered a ___ and is NOT integrated

A

episome

Med Micro Final Exam (3 decks)

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