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Microbiology test 3 > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

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
Which viral antigens are secreted into the blood stream during HBV infections
HBsAg and HBeAg
26
What does IgM anti-HBc indicate?
hallmark of a new, ongoing HBV infection if present with HBsAg
27
What does IgG anti-HBc indicate?
past infection, if present with HBsAg indicates chronic infection
28
What is the best correlate to the presence of infectious HBV?
detection of HBeAg
29
What indicates probably chronic HBV state?
continued detection of HBeAh & HBsAg or both without antigens to these
30
What is the fate of most HBV cases
spontaneous resolution & do not require early tx
31
Tx of chronically infected HBV patients
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
How to prevent transmission of HBV
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
Hepatitis D Virus description
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
How can one get HDV?
1. Coinfection with HBV (both at same time) | 2. Superinfection in patients with an established chronic HBV hepatitis
35
What does HDV do?
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
HDV epidimiology
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
HDV dx
ELISA for delta antigen or antibodies
38
HDV prevention
HBV vaccine will prevent any replication of HDV as well
39
HCV basics
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
HCV Epi
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
Recognized Risk Factors for HCV Infection (6)
``` IV drug use Hemodialysis Tattoos Blood transfusions Organ transplants Contact with health care providers ```
42
How many acute HCV infections become chronic?
~85% of individuals with an acute HCV infection ultimately develop chronic disease
43
Developed countries peak transmission years | who is affected?
Peak transmission 1960- 1980. | 1 in 33 baby boomers may be infected and could begin showing up with cirrhosis and/or cancer soon
44
HCV Dx
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
HCV Tx (2)
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
HCV types
``` 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
HCV prevention
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
HIV onset clinical manifestations
onset may be asymptomatic or a/w self-limited mononucleosis-like condition -duration of asymptomatic period is variable (up to 15 years)
49
Does HIV go away? Does its infectiousness fo away?
Nope, all pateints are considered lifelong carriers and continuously infectious
50
When can you dx AIDS?
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
Name 4 HIV indicator dzs?
1. Kaposi's sarcoma 2. MAC infection 3. pneumocystis pneumonia 4. DMV dz (& others)
52
HIV/AIDS temporal relationship
Development of AIDS lags behind HIV infection by about a decade The existence of HIV-resistant and slow-responding individuals is now recognized
53
HIV description
Human retrovirus (lentivirus) RNA genome Enveloped virion Reverse transcriptase (RNA dependent DNA polymerase) enzyme encoded by virus
54
HIV-1 origins
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
How does HIV-1 replication occur? (5 steps)
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
Cytopathic effects of HIV transmission
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
HIV transmission mechanisms (5)
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
How is HIV NOT transmitted
not by insect bites | casual contact is highly unlikely to result in infection
59
HIV epidemiology
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
HIV infection pattern
- 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
HIV 2 step test
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
2 other HIV dx test
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
How do you screen donor blood for HIV`
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
How do we tx HIV
Combinations of antiviral agents (HAART) | -Simultaneous treatment with multiple agents is required since HIV has such a high mutation rate
65
Name 3 main categories of antiviral agents
1. Reverse transcriptase inhibitors 2. Protease inhibitors 3. Fusion-penetration inhibitors
66
Describe two types of reverse transcriptase inhibitors and why dz are these used in anyway?
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
What to protease inhibitors do? | When are we using these?
stop maturation/viral assembly | use these as part of HAART for HIV
68
What do fusion-penetration inhibitors do? | When are we using these?
interfere w/HIV entry into host by inhibiting the fusion of virus & host membranes used as a part of HAART for HIV
69
How well does the combo antiviral agent (HAART) approach work?
-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
What does the future of HIV tx hold? (2)
MATURATION INHIBITORS that block virus release from infected cell INTEGRASE INHIBITORS that halt virus genome integration into host genome
71
HIV infection prevention method
Best method now is prevention of spread - Education - Clean needle programs - Condoms

Microbiology test 3 (8 decks)

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