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Host and Defense > Week 14 > Flashcards

Week 14 Flashcards

1
Q

What is the malignant species that causes malaria?

A

Plasmodium falciparum

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2
Q

Name three benign plasmodium species.

A

Pl. Vivax

Pl. ovale

Pl. malariae

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3
Q

What species of mosquito is malaria typically spread by (pl. falciparum)?

A

Anopheles species

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4
Q

True or false… there is an increasing trend for malaria in the unites states since 1973

A

True

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5
Q

What are some symptoms of cerebral malaria?

A

Seizures

Acidosis

Anemia (coma with eyes open, may lead to heart failure)

Skin becomes lighter

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6
Q

What four groups of people are at risk for death if they get malaria?

A

Children 6mo to 6 years

Non-immune adults

Pregnancy - especially primigravida

Emigrants returning from home visits

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7
Q

Severe Malaria rarely occurs in what groups of people?

A

Sickle cell trait (heterozygous)

People from endemic areas (become immune)

Note that these people can still get malaria, just not severe malaria

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8
Q

Describe the life cycle of plasmodium falciparum

A

Parasite develops in mosquitos. The sporozoites are released into the mosquito saliva. Mosquito bites a human host. Sporozoites enter the blood and in the liver. Note that there is no latent stage in the liver, here they are called hypnozoites. When they infect RBCs they are called merozoites. The life cycle in the RBCs is called shizogany

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9
Q

Describe shizogany. The life cycle of pl. falciparum in the RBCs.

A

Ring trophozoites

Rings with Maurer’s clefts

Rings: appliqué forms

Maturing trophozoites

Shizont (early stage)

Mature shizont (looks like a RBC filled with stuff)

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10
Q

Where are the mature shizonts located?

A

Adhered to the microvessels of the brain. (Cytoadhesion)

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11
Q

Explain why malaria shizonts are sequestered to the microvasculature of the brain

A

Malaria parasite secrete a complex of proteins that incorporate into the membrane of RBCs called ‘knobs’ pf-EMP-1 is expressed through the membrane so it is in contact with the plasma. This will bind to receptors of endothelial cells in the brain.

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12
Q

What is opisthotonos?

A

This is a hyperextended position the body takes due to severe cerebral malaria because of its effect on the CNS

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13
Q

What are the benefits to the parasite of sequestration?

A

Evades splenic clearance - free intravasculature replication

Post capillary venue blood ph is low which favors replication

Post capillary venue pco2 is high which also favors replication

The parasite infects RBCs of any age.

All lead to enormous parasite mass in severe malaria

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14
Q

What is the three pronged approach for combating malaria?

A

Incesticide impregnated bed nets

Residual insecticide spraying

Preimptive treatment with ACT (artemisinin based combination therapy

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15
Q

True or false… bacteremia with septic shock results in multiple organ failure, whereas malaria results in selective organ pathology

A

True

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16
Q

What are some ways to prevent malaria?

A

Prophylaxis with anti-malarials

Mosquito repellent

Permethrin-impregnated bed nets

Permethrin-treated clothing

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17
Q

What is the difference between antigenic drift and antigenic shifts?

A

Antigenic drift - antigens involve a few mutations that reduces the hosts immune system’s ability to recognize the virus

Antigenic shifts - drastic changes to the antigen via mutation that frequently results in viral resistance, leading to epidemics

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18
Q

Describe how Antivirals for DNA-encoded viruses, like Herpes virus, work

A

They inhibit viral transcription via inhibiton of DNA polymerase

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19
Q

How do Antivirals for RNA-encoded viruses, like rhinoviruses, work?

A

Inhibitors of viral uncoating (M2 protein )

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20
Q

HSV-1 typically resides in the ___ ganglion. HSV-2 typically resides in the ___ ganglion

A

Trigeminal

Sacral

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21
Q

Name the following…

HSV-1
HSV-2
HHV-3
HHV-4
HHV-5
A

Herpes simplex 1 (oral herpes)

Herpes simplex 2 (genital herpes)

HHV-3 also known as VSV (varicella zoster virus (chicken pox))

HHV-4 - EBV (Epstein Barr virus)

HHV-5 - CMV (cytomegalovirus)

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22
Q

What are some triggers that can cause latent herpes infections to become active?

A

Stress, fatigue, sun, surgery, fever, menstrual periods, immunocompromised

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23
Q

What is immunosenescence?

A

Age-related decline in immune function

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24
Q

Name four antiviral drugs for HSV and/or VSV

A

Acyclovir

Valacyclovir

Penicyclovir

Famcyclovir

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25
Q

Acyclovir is 10x more potent against ___ than ____. It is typically inexpensive. It can be administered oral, IV, or topical

A

HSV-1 or HSV-2

VZV

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26
Q

What is valacyclovir?

A

It is administer orally only but then is converted in the body to acyclovir to levels that are 3-5x greater than oral acyclovir

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27
Q

Which antiviral drug for HSV is administered topically only?

A

Penicyclovir

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28
Q

Which drug is administered orally only but is metabolized into penicyclovir? It is mainly used for VZV

A

Famcyclovir.

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29
Q

Patients must always hydrate well while on any -cyclovir drug to avoid ____

A

Crystalline nephropathy (damage to kidneys)

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30
Q

Name two drugs that are used to trear HSV and or CMV infections

A

Gamcyclovir

Foscarnet

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31
Q

Gancyclovir is used for prophylaxis or treatment of ___ or ___

A

CMV

HHV-6

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32
Q

What are some contraindications or adverse effects of gancyclovir?

A

Contraindicated during pregnancy and in males (shrinks testes 😵)

Due to its high risk of cytotoxicity, it must be administer in a clinical setting and monitored closely

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33
Q

True or false…. both gancyclovir and foscarnet can only be administered via IV

A

True

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34
Q

Foscarnet is used to treat…

A

CMV and viral induced retinitis in immunocompromised patients.

Useful in acyclovir or gancyclovir resistant HSV or CMV infections

Note that this drug is much safer than gancyclovir although it has possible nephrotoxic effects

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35
Q

What is the method of action for Foscarnet?

A

Selectively inhibits viral DNA polymerase enzymes (not kinases)

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36
Q

The cyclovir drugs depend on___. Why is this an issue?

A

Viral enzymes.

Herpes simplex uses thymadine kinase and DNA polymerase

This is an issue because these enzymes can mutate

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37
Q

What is the method of action of oseltamivir? Is it active against influenza A, B, or both? Why is early administration crucial?

A

Neuroaminidase inhibitor. Prevents cleavage of cell receptor keeping virus particle bound to host

***active against both influenza A and B

Early administration is crucial because replication peaks at 24-72 hours after the onset of illness. (When a 5 day course of treatment is initiated within 2 days of onset, the duration of flu symptoms are decreased by up to 1-2 days

note that there may be a disulfuram like reaction

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38
Q

What is the mechanism of zanamivir? What is its clinical use? How is it administered? What are its contraindications?

A

It is a neuraminidase inhibitor

Clinical use: treatment and prophylaxis of influenza A and B

Administer via inhaler only

Contraindications: sever asthma, COPD, severe allergies to milk proteins

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39
Q

What is the mechanism of amantadine? Is it used to treat influenza A, B, or both? Contraindications/adverse effects?

A

Antiviral: interferes with viral M2 protein and thus blocks the uncoating in the host (not used anymore cause it has 100% resistance)

Anti Parkinson’s disease: a weak antagonist of the NMDA receptor, increases dopamine release and prevents its reuptake

Only active against influenza A!!!

Contraindications: patients with renal impairment, epilepsy, pregnancy, glaucoma

Adverse effects: ataxia, dizziness, anxiety, slurred speech

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40
Q

Th17 cells release ___ and ___ which induces the epithelial cells to produce ___

A

IL-17

IL-22

Antimicrobial peptides

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41
Q

What are the three purposes of antimicrobial peptides?

A

Destroy pathogens

Select commensal communities

Initiate inflammation

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42
Q

What does cathelicidin do?

A

Disrupts membranes of bacteria. Additional toxic effects intracellularly. Kill cells and disable viruses

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43
Q

Barriers are sites of ongoing innate and adaptive immunity. ___, ___, and ___ monitor tissue health

A

Macrophages

Dendritic cells

Gamma-delta T cells

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44
Q

What are some things that granulocytes release?

A

Elastase

Histamine

Proteases

Antimicrobial peptides

Etc.

-Note that they do not release perforin or granzyme

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45
Q

How long does it take a single lymphocyte to completely circulate?

A

~24 hours

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46
Q

Macrophages promote an inflammatory response. List 5 cytokines they release to promote inflammation and briefly describe what they do.

A

IL-1b: activates vasculature, tissue destruction to allow access of effector cells

TNF-a: activates vasculature (permeability)

IL-6: induces acute-phase protein production in liver. Increase antibody production

CXCL8: attracts neutrophils, basophils, T cells

IL-12: activates NK cells. Induces differentiation of CD4 cells to Th1

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47
Q

Which cytokine stimulates the liver’s acute phase response? What are some proteins produced in this phase?

A

IL-6

C-reactive protein
Mannose binding lectins
Serum amyloid protein

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48
Q

What are the three killing mechanisms of neutrophils?

A

Phagocytosis

Degranulation

Nets

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49
Q

After the establishment of a viral infection the cells produce interferons. Which attacks first, NK cells or CD8 T cells?

A

Typically, NK cells kill first, then CD8 T cells

50
Q

What are the three effects of interferons?

A

Induce resistance to viral replication in all cells

Increase expression of ligands for receptors on NK cells

Activate NK cells to kill virus-infected cells

51
Q

Name the three classical APCs. Name one other APC

A

Dendritic cells
Macrophages
B cells

Gamma-delta T cells can also be APCs

52
Q

When the cognate pair first moves to the primary focus, proliferation of ___ secreting plasma cells occurs driven by interleukins ___ and ___

A

IgM

IL-5
IL-6

53
Q

When the cognate pair moves to the secondary focus, B cells rapidly divide every 6 hours to form ___ and ___ driven by ___, ___, and ___

A

Centroblasts

Germinal centers

IL-6

IL-15

BAFF

54
Q

What four interleukins do Th17 cells release? What is the overall function?

A

IL-17
IL-21
IL-22
IL-26

enhance the neutrophil response to fungal and extracellular bacterial infections

55
Q

What five cytokines are released by Th1 cells? What is the overall function?

A 
IFN-gamma
GM-CSF
TNF-a
LT
IL-2

Help macrophages to suppress intracellular infections

56
Q

What five cytokines do Th2 cells release? What is the overall function?

A 
IL-4
IL-5
IL-10
IL-13
TGF-beta

Help basophils, mast cells, eosinophils, and B cells respond to parasite infections

57
Q

What three cytokines do TFH cells release? What is the overall function?

A

IL-21
IL-4
IFN-gamma

Help B cells become activated, switch isotype, and increase antibody affinity

58
Q

What three cytokines do Treg cells release? What is the overall function?

A

TGF-beta
IL-10
IL-35

Suppress the activities of other effector T cell populations

59
Q

Immune responses resolve and tissue is repaired by what four ways?

A

Reduction in proinflammatory cytokines

Increase in anti-inflammatory cytokines

Treg cell signaling and development

T cell CTLA4 expression

60
Q

True or false… inhibiton of peripheral Th17 cells by IL-4 or IFN-gamma induces Treg cell development

A

True

61
Q

___ and ___ act to inhibit activation and growth of Th1 cells

A

TGF-beta

IL-10

62
Q

____ acts on Th2 cells to inhibit proliferation

A

IFN-gamma

63
Q

What are the differences in the presentations of acute hepatitis vs. chronic hepatitis?

A

Acute: incubation = several weeks. Flu-like symptoms. Jaundice, enlarged, painful liver. Resolves spontaneously

Chronic: *often asymptomatic. Physical exam can show problems with liver. Persists for years/decades

64
Q

Out of HepA, B, C, and E, which cause acute or chronic hepatitis?

A

A and E cause acute hepatitis

B can cause both

C causes chronic

65
Q

What type of a virus is hepatitis A? How is it trasmitted? What is its incubation period?

A

Non-enveloped ssRNA virus

Transmission = fecal-oral route

Incubation period = 28 days

66
Q

Incidence of HepA in children in developing countries reaches ___%. Footborne Hep A outbreaks are commonly related to…

A

100

Overcrowding

Poor sanitation

Polluted water sources

67
Q

What is the most common cause of acute hepatitis? What are its risk factors?

A

Hepatitis A

No known risk factors

68
Q

Shedding of Hep A occurs ___prior to acute hepatitis and ___ after onset of jaundice

A

1-3 weeks

1 week

69
Q

True or false.. in regards to Hep A, most children have symptoms while most adults are asymptomatic

A

False. Its the opposite. Most adults have symptoms while 70% of children are asymptomatic

70
Q

True or false… Hep A is a self-limited illness with rare complications. Once you’ve had Hep A and recovered, it usually 100% cleared.

A

True

71
Q

True or false… the hepatitis A vaccine is really effective

A

True. Everyone should get vaccinated

72
Q

What kind of a virus is Hep E? How is it transmitted? How are its clinical presentations different from Hep A? What is its incubation time?

A

Non-enveloped ssRNA

Spread via fecal-oral route (fecal contamination of water) person to person spread is rare

Acute hepatitis is clinically indistinguishable from Hep A

Incubation = 40 days

73
Q

What is the smallest DNA virus that infects humans?

A

Hep B

74
Q

What kind of a virus is Hep B? What are some things it’s genome codes for?

A

Enveloped DNA virus. DsDNA/ssDNA

Compact, overlapping reading frames produce..

HBsAg (surface antigen)
HBcAg (core nucelocapsid protein)
DNA pol
HBxAg (no known function)

75
Q

What is the most common blood-borne virus in a hospital setting? Describe the rule of 3s.

A

HepB

If you are not vaccinated and get pricked by a patient who has the virus, you have a 30% chance of getting HBV, 3% chance for HCV, and 0.3% for HIV

76
Q

Describe the ways hepatitis B is transmitted

A

Perinatal: infants who are born to mothers who have HBV are 90% likely to get it (if mother is HBeAg+). However the neonatal vaccine has 95% efficacy

Parenteral: most common blood-borne virus in health care settings

Sexual: most common mode of transmission in low-prevalence areas

77
Q

What is the most common mode of transmission of HBV in low-prevalence areas?

A

Sexual

78
Q

___% of newly infected adults will have acute hepatitis from Hep B

A

30

79
Q

True or false.. perinatal/childhood primary infections of hepB is asymptomatic

A

True

80
Q

The rate of progression to chronic hepatitis B ____ correlates with age

A

Inversely

81
Q

True or false… chronic HepB always results in severe symptoms

A

False. It is a broad spectrum of illness form asymptomatic to cirrhosis and liver cancer

82
Q

True or false… men are more likely to have acute flares of hepB when they have chronic HepB. Also alcohol consumption worsens it

A

True

83
Q

What are some lab predictors of poor outcomes of chronic hepB?

A

HBeAg positivity (means the virus is replicating a lot)

HBV serum DNA level (>2000 IU/mL)

High titer HBsAg

Necrosis-inflammation on liver biopsy

84
Q

Describe how HBV surface antigen is used to diagnosis HepB

A

HBsAg, if persistent for > 6mo, its a chronic infection

Clearance of HBsAg followed by development of anti-HBs confers life-long immunity

HBsAg positive indicates you have HepB. anti-HBs indicates you have had it in the past but are over it. HBsAg and anti-HBs indicate chronic

85
Q

Other than HBV surface antigen, what is other ways to diagnose HepB?

A

HBV core antigen (HBcAg) (Note-however that this is intracellular and never detected in serum)

HBV e antigen (HBeAg is a marker of replication and infectivity)

HBV serum DNA PCR

86
Q

In regards to HBV what is the first antigen our immune system sees and produces antibodies for?

A

surface antigen (HBsAg)

87
Q

What is the treatment for HepB?

A

Two types of Antivirals: IFN and nucleoside analogs

Tenofovir and entecavir are first lines of defense in US

88
Q

When should you treat HepB?

A

When there is HBV DNA > 20,000 (HBeAg+) or >2,000 HBeAg-)

AND

Disease

89
Q

True or false.. there is a vaccine for HepB and everyone should be vaccinated

A

True

90
Q

What kind of a virus is HepD? What is special about this virus?

A

Defective ssRNA

It is a passenger virus accompanying HBV

It infects 10% of those with HBV

91
Q

What do simultaneous infections with HBV and HDV look like?

A

Looks like HBV alone

92
Q

How do you diagnose and manage HepD?

A

Diagnosis: PCR or anti-HDAg IgM/IgD

Management: IFN-a is the only approved treatment (low success rate)

93
Q

What kind of a virus is HepC? How is it transmitted?

A

Enveloped RNA virus in Flavivirus family (related to yellow fever, dengue west Nile.

Blood borne transmission

94
Q

There are ___major genotypes of HCV worldwide. genotype #___ is most prevalent in the US

A

6

1a

95
Q

What are the two tests available for HepC diagnosis? How do you interpret these?

A

HCV antibody:
Negative HCV ab = no infection
Positive HCV ab = past or present infection, need to check for virus

HCV RNA:
Positive = active infection
Negative = cleared infection

96
Q

Who should be tested for HepC?

A

Everyone born between 1945 and 1965

IV drug users

Transfusion recipients

HIV infection

Etc.

97
Q

What are some things you do to manage HepC?

A

Always test for HIV and HepB

Determine genotype (important for drug selection)

Evaluate for liver damage

98
Q

What are the treatment guidelines for HpepC?

A

They are continually updated

Antivirals for HCV polymerase and protease

99
Q

What is the worldwide prevalence of TB (latent and active)

A

33%

More than 2 billion people worldwide

2nd most common infectious cause of death in adults worldwide

100
Q

Mycobacteria have cell membranes composed of ___ which makes it acid fast. Doubling time in culture is about every ~___hours, which is slow

A

Mycolic acid

24

101
Q

True or false… humans are the only known reservoirs of M. Tuberculosis

A

True

102
Q

What are the four possible outcomes of TB exposure?

A

Clearance

Latent infection

Primary disease (active on first exposure)

Reactivation disease (most common form of active disease)

103
Q

Although most adults will contain primary TB infection in a latent form (asymptomatic) primary TB is most common in what groups of people?

A

Children <4 years of age

Immune compromised

104
Q

If you have latent TB, it is asymptomatic with a __% lifetime chance of reactivation

A

10

105
Q

What are some high risk factors for reactivation of latent TB?

A

HIV (100% chance)

Jejunoileal bypass (60%)

IV drug use (30%)

Lots of others

106
Q

Describe the pathogenesis and host response of TB

A

MTB replicate in the phagosomes of macrophages (prevent lysosome fusion with phagosome)

Granulomas form to wall off the infection

107
Q

What are the clinical manifestations of latent TB?

A

No symptoms!

108
Q

What are the clinical manifestations of active TB?

A

Pulmonary symptoms: cough, hemoptysis, lung collapse, chest pain

“Consumption”: fevers, fatigue, weight loss, night sweats

TB can be present in virtually any organ

109
Q

Why is it that you should only test for LTBI in low incidence settings if the population is high risk?

A

Only test people with the intention of treating them if they are positive. So only test people who are at risk and would need treatment

110
Q

What groups of people are considered high risk of exposure?

A

Known contacts of active TB case

Immigrants from endemic areas

Residents/employees of institutions with high risk of TB

111
Q

Who is at a high risk of disease for LTBI?

A

HIV infection

IV drug use

Medical conditions such as diabetes, chronic renal failure, and malignancy

Immune suppressed

(Note that TNF-alpha blocking drugs for treatment of inflammatory diseases are likely to crack open granulomas to bring it to reactivation)

112
Q

What are the two ways to diagnosis LTB? What is a flaw with this system?

A

There are no current means to test directly the presence of latent infection so we rely on surrogate measures of the host immune response.

PPD: skin test looking for hypersensitivity

IGRA: look for IFN-gamma release when blood cells are exposed to TB antigens in vitro

113
Q

What is a key difference between the IFN-gamma test and the skin test for TB?

A

IFN-gamma test is either positive or negative while the skin test has some more grey area

114
Q

What is the preferred regimen for treating LTBI?

A

Isoniazid daily for 9 months

115
Q

What are the ways to diagnose active TB?

A

Combination of exposure history, signs and symptoms, and imaging (remember that the skin tests or IFN-gamma tests wont work well because the immune system isn’t working well)

AND

Lab evidence of TB: granulomas, AFB stain on smear

116
Q

Name four anti-TB drugs and their roles in combination therapy

A

Rifampin - target slowly dividing mycobacterial persisters

Isoniazid - efficient cleared of rapidly dividing mycobacteria

Pyrazinamide - target slowly dividing mycobacterial persisters

Ethambutal - prevention of resistance

117
Q

What are the treatment guidelines for treating active TB?

A

4 four 2,2 for 4

Isoniazid, rifampin, pyrazinamide, and ethambutal for two months.

Rifampin and isoniazid for four more months

118
Q

What is the difference between MDR TB (multi-drug resistant) and XDR TB?

A

MDR TB: resistant to INH and RIF

XDR TB: resistant to INH, RIF, all fluoroquinolones, and any injectable

119
Q

___ is the most powerful known risk for reactivating latent TB. TB is the most common cause of death for ___ patients

A

HIV

AIDS

-risk of TB reactivation in HIV patients is 5-8% every year

120
Q

If a patient has HIV and TB… ___ should not be given with ___. ___ should be used instead

A

RIF

Pls

RAL (rifabutin)

Host and Defense (17 decks)

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