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Microbiology test 3 > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

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1
Q

What do hepatitis viruses do?

A

infect and damage the liver
cause icteric sxs of jaundice
release of liver enzymes due to tissue damage

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2
Q

Acute hepatitis types

A

hepatitis A

hepatitis E

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3
Q

Possible courses of viral hepatitis (4)

A
  1. Subclinical
  2. Typical acute icteric hepatitis (incubation period, prodrome, icteric, convalescent)
  3. Fulminant hepatitis
  4. Chronic hepatitis
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4
Q

Typical acute icteric hepatitis phases

A
  1. Incubation Period (dif. length dpnding on type)
  2. Prodrome/pre-icteric: fatigue, malaise, anorexia
  3. Icteric phase: jaundice, dark urine, elevated ALT, AST
  4. Convalescent phase: disappearance of jaundice & other sxs
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5
Q

Fulminant hepatitis description

A

rapid progression, high fatality rate

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6
Q

Chronic hepatitis (which types)

A

ONLY B, C and D type viruses

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7
Q

Hepatitis A virus causes what?

A

causes infectious hepatitis

does NOT become chronic

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8
Q

HAV epidemiology

A

Virions excreted in feces
food and water born transmission
major risk factor for dz-contact with infected family member

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9
Q

HAV Clinical Manifestation

A

Entry of virus is through intestine after ingestion.

The disease is typically mild, but the course may be prolonged

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10
Q

HAV dx

A

in laboratory
IgM antibody demonstration by ELISA
many asymptomatic infections occur, finding antibody is common

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11
Q

HAV Tx

A

(HAV=acute viral hepatitis)
bed rest, reduction of activities
stay hydrated
avoid hepatotoxins (EtOH, drugs, anesthesia)
if liver deterioration or IV fluids needed->hospitalize

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12
Q

HAV prevention (4)

A
  1. Proper handwashing
  2. avoidance of contaminated food (uncooked shellfish) & water chlorination
  3. Post exposure prophylaxis with immune serum globulin, early in infection
  4. killed virus vaccine is available
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13
Q

Hepatitis B Virus is:
the most common & widespread cause what?
and
can be an infectious cause of what?

A

most (C) cause of CHRONIC HEPATITIS

infectious cause of PRIMARY HEPATOCELLULAR CARCINOMA

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14
Q

Which viral molecules are imp in dx and state of HPV-infected patient

A

HBsAg – HBV surface antigen
HBcAg - HBV core antigen
HBeAg - surface antigen fragment – presence indicates patient is infectious

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15
Q

Which antigen remains high in chronic hepatitis B but not acute HBV?

A

HBsAg

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16
Q

What is the major reservoir of HBV?

A

Chronic hepatitis patients are a major reservoir of HBV
Serological screening of blood has reduced risk of infection from blood and blood products
Virus is shed during asymptomatic periods

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17
Q

How is HBV spread?

A

needle sharing, acupuncture, ear piercing tattooing, (peri-natal-congenital infection also possible with HBeAg positive mother)

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18
Q

HBV is present in:

A

serum, blood, semen

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19
Q

High Risk patients HBV infection (6)

A 
Healthcare workers 
IV drug users 
Homosexuals 
Promiscuous heterosexuals 
Institutionalized persons 
Family contacts of infected individuals
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20
Q

Where does HBV replicate

A

almost exclusively in the liver

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21
Q

HBV incubation period

A

50-180 days

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22
Q

HBV clinical manifestation

A

slow and insidious onset
Prodrome: fever, rash (urticarial), arthralgias (symmetrical)
Subclincial HBV infection possible, recognized only by presence of anti- HBsAg
Self-limited infection is normal

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23
Q

Complications of HBV

A

Chronic HBV (5-10%)-(U) after innaparent infection &detected by increased serum liver enzymes

10% of chronic HBV will develop cirrhosis & liver failure

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24
Q

Dx of HBV is based on

A

Clinical symptoms

Serum – presence of liver enzymes from destruction of hepatic cells; course of the disease may be followed by serology

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25
Q

Which viral antigens are secreted into the blood stream during HBV infections

A

HBsAg and HBeAg

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26
Q

What does IgM anti-HBc indicate?

A

hallmark of a new, ongoing HBV infection if present with HBsAg

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27
Q

What does IgG anti-HBc indicate?

A

past infection, if present with HBsAg indicates chronic infection

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28
Q

What is the best correlate to the presence of infectious HBV?

A

detection of HBeAg

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29
Q

What indicates probably chronic HBV state?

A

continued detection of HBeAh & HBsAg or both without antigens to these

30
Q

What is the fate of most HBV cases

A

spontaneous resolution & do not require early tx

31
Q

Tx of chronically infected HBV patients

A

may be given PEG-interferon and other agents to inhibit the viral polymerase including nucleoside and nucleotide analogues.
Not a cure, but antagonizes viral replication

32
Q

How to prevent transmission of HBV

A

A subunit vaccine is available and widely used to prevent infection
Anti-HBV immunoglobulin can prevent transmission within 1 week of exposure (used w/newborn infants of HBsAg positive mothers (plus vaccination) )

33
Q

Hepatitis D Virus description

A

The delta agent – a viral parasite of HBV that uses HBsAg for its capsid
HDV replication requires the presence of HBV for helper functions

34
Q

How can one get HDV?

A
  1. Coinfection with HBV (both at same time)

2. Superinfection in patients with an established chronic HBV hepatitis

35
Q

What does HDV do?

A

increases the severity of HBV infections
fulminant hepatitis is more likely
more rapid & severe outcome when HDV coinfects with HBV in a previously uninfected individual
superinfection may exacerbate a previously stable chronic condition or accelerate chronic cirrhosis

36
Q

HDV epidimiology

A

Parallels HBV, worldwide distribution Spread by same routes as HBV Chronic infection is common with HDV Individuals persistently infected with HBV and HDV are reservoirs

37
Q

HDV dx

A

ELISA for delta antigen or antibodies

38
Q

HDV prevention

A

HBV vaccine will prevent any replication of HDV as well

39
Q

HCV basics

A

HCV causes 90% of NANB Hepatitis
Dx doesn’t seem as bad as HBV but likely to ESTABLISH CHRNOIC INFECTIONS which often progress to CIRRHOSIS & LIVER FAILURE years later

40
Q

HCV Epi

A

transmission not well understood

In many cases , exact source of infection not known & many at-risk patients have no idea they should be tested

41
Q

Recognized Risk Factors for HCV Infection (6)

A 
IV drug use
Hemodialysis
Tattoos 
Blood transfusions 
Organ transplants 
Contact with health care providers
42
Q

How many acute HCV infections become chronic?

A

~85% of individuals with an acute HCV infection ultimately develop chronic disease

43
Q

Developed countries peak transmission years

who is affected?

A

Peak transmission 1960- 1980.

1 in 33 baby boomers may be infected and could begin showing up with cirrhosis and/or cancer soon

44
Q

HCV Dx

A

ELISA detection of patient antibody followed by confirmatory tests

  • Seroconversion occurs slowly (abt 24 weeks post-infection), so CHRONIC STATE/VIREMIC PTS OFTEN ESCAPE DETECTION IF CLINICIAN RELIES ONLY ON STANDARD ELISA
  • rapid tests (OraQuick HCV) available
45
Q

HCV Tx (2)

A
  1. alpha interferon & ribavirin combined with virus-specific protease inhibitors telaprevir, boceprevir or simeprevir
    (better than standard treatment without protease inhibitors, demands careful monitoring to avoid selection of drug resistant viruses )
  2. Solvadi (nucleotide analog polymerase inhibitor) plus ribavirin and interferon for the genotype 1 virus
46
Q

HCV types

A 
6 genotypes (at least 50 subtypes) of HCV exist w/varying degrees of sensitiviety to tx
-protease inhibitors are intended for type I HCV
47
Q

HCV prevention

A

blood screening
{preventative vaccine may be difficult to produce & test, HCV suppresses innate immune system, masks itself from neutralizing antibodies & spreads directly from cell to cell}

48
Q

HIV onset clinical manifestations

A

onset may be asymptomatic or a/w self-limited mononucleosis-like condition
-duration of asymptomatic period is variable (up to 15 years)

49
Q

Does HIV go away? Does its infectiousness fo away?

A

Nope, all pateints are considered lifelong carriers and continuously infectious

50
Q

When can you dx AIDS?

A

when CD4 T cell counts fall below 200 uL & severe damage to immune system becomes evident (AIDS indicator dz emerge, such as Kaposi’s sarcoma, MAC, pneumocystis pneumonia, CMV dz & others)

51
Q

Name 4 HIV indicator dzs?

A
  1. Kaposi’s sarcoma
  2. MAC infection
  3. pneumocystis pneumonia
  4. DMV dz
    (& others)
52
Q

HIV/AIDS temporal relationship

A

Development of AIDS lags behind HIV infection by about a decade The existence of HIV-resistant and slow-responding individuals is now recognized

53
Q

HIV description

A

Human retrovirus (lentivirus)
RNA genome
Enveloped virion
Reverse transcriptase (RNA dependent DNA polymerase) enzyme encoded by virus

54
Q

HIV-1 origins

A

Retrospective studies have found virus in samples of serum dating to the 1950’s and an origin in chimpanzees is postulated.
Human population entry through bushmeat exploitation?

55
Q

How does HIV-1 replication occur? (5 steps)

A
  1. Infection of cells with CD4 and a chemokine co-receptor molecule displayed at surface (helper T (TH), monocytes, macrophages)
  2. Reverse transcription of viral genome, integration into host chromosome
  3. Viral replication occurs using this copy
  4. Latency is established (may be very short term)
  5. Activation of latent virus follows & progeny production begins
56
Q

Cytopathic effects of HIV transmission

A

TH (helper T) cell loss occurs in the pt & results in profound immunosuppression
precise mechanism of viral host cell killing is uncertain at this point

57
Q

HIV transmission mechanisms (5)

A
  1. Sexual contact (HSV lesions, syphilis increase risk)
  2. Parenteral (IVDU, needle sticks)
  3. Perinatal (in utero, post partum, high risk w/infected mother)
  4. organ transplant
  5. occupational (low, but exists)
58
Q

How is HIV NOT transmitted

A

not by insect bites

casual contact is highly unlikely to result in infection

59
Q

HIV epidemiology

A

worldwide (2 distinct types: HIV-1 & HIV-2 as well as many subtypes in circulation)
>Developed nations - homo & bisexuals, IVDUs & their sex partners, babies born to infected mothers
>Sub-Saharan Africa & some regions of Latin America, Caribbean islands - heterosexual transfer dominates (mother-to-child infection is big >problem)
In the U.S., the heterosexual population is presently showing greatest rates of increase.

60
Q

HIV infection pattern

A
  • pt is maximally infectious at initial infection stage, before antibody response is evident
  • virus load follows a pattern of RISE, DIP, RETURN as infection initiates, pt. responds w/antibodies & the immune system ultimately collapses
61
Q

HIV 2 step test

A

2 step system to minimize false positives:
1. EIA screen to reveal anti-HIV antibodies in patient serum
2. Western blot for confirmation: a more specific test that confirms the antibodies observed in first tests specifically bind to defined HIV virion antigens
WILL NOT RELIABLY REVEAL PTs w/RECENT INFECTIONS

62
Q

2 other HIV dx test

A
  1. Nucleic acid tests (NAT): PCR-based test allows viral RNA to be detected directly & enable virus loads to be quantified
  2. HIV-1 antibody rapid tests are in use – hoped that more infections will be recognized sooner
63
Q

How do you screen donor blood for HIV`

A

Donated blood is screened directly for the presence of HIV antigens (p24) or with RNA NAT

(These are detectable earlier than the patient will initiate an antibody response, so ppl. giving blood early in infection are detected)

64
Q

How do we tx HIV

A

Combinations of antiviral agents (HAART)

-Simultaneous treatment with multiple agents is required since HIV has such a high mutation rate

65
Q

Name 3 main categories of antiviral agents

A
  1. Reverse transcriptase inhibitors
  2. Protease inhibitors
  3. Fusion-penetration inhibitors
66
Q

Describe two types of reverse transcriptase inhibitors and why dz are these used in anyway?

A
  1. Nucleoside/tide analogs – inhibit reverse transcriptase production of DNA by premature chain termination (NRTI)
  2. Non-nucleoside reverse transcriptase inhibitors – bind to reverse transcriptase and inhibit enzyme (NNRTI)

these are a part of HAART to tx, NOT CURE, HIV

67
Q

What to protease inhibitors do?

When are we using these?

A

stop maturation/viral assembly

use these as part of HAART for HIV

68
Q

What do fusion-penetration inhibitors do?

When are we using these?

A

interfere w/HIV entry into host by inhibiting the fusion of virus & host membranes
used as a part of HAART for HIV

69
Q

How well does the combo antiviral agent (HAART) approach work?

A

-made a remarkable difference, virus sinks to undetectable levels
Therapy is difficult for patients, but compliance is essential to avoid emergence of drug-resistance
This therapy is not a cure

70
Q

What does the future of HIV tx hold? (2)

A

MATURATION INHIBITORS that block virus release from infected cell
INTEGRASE INHIBITORS that halt virus genome integration into host genome

71
Q

HIV infection prevention method

A

Best method now is prevention of spread

  • Education
  • Clean needle programs
  • Condoms

Microbiology test 3 (8 decks)

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