Mcim Lecture 11 Flashcards

0
Q

Gastrointestinal (enteric) viruses

  • 70% of all cases of human gastroenteritis are due to viruses( rest are bacteria, parasitic infections)
  • many different types of enteric viruses( but 4 types are responsible for the most cases of disease) what are they?
A

1) rotavirus: most common cause of diarrhea in kids under 5yr (can occur in adults, but with milder symptoms)
2) adenovirus: mainly kids under 2yr; occurs year round
3) astrovirus- all ages, mostly in winter months
4) calicivirsus( large group that inc. norivirus )- all ages, all the time

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1
Q

Representative viral diseases(6)

A
  1. Skin( and beyond)
    - herpes simplex virus
    - human papilloma virus
  2. Gastrointestinal viruses
  3. Viruses of the central nervous system
  4. “Blood-borne” viruses
  5. Respiratory viruses
  6. Emerging viral diseases (Ebola)
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2
Q

Different types of enteric viruses all share some common features, what are they? (2)

A
  1. Mainly transmitted by fecal-oral route ex) contact with, and ingestion of, fecal material containing virus
  2. Similar disease progression: 1-3 days from 1st contact to symptoms ex. The “incubation period”
    - similar symptoms (vomiting, diarrhea, nausea, abdominal pain)
    - usually a self- limiting infection(3-4 days) in otherwise healthy humans

therefore- determining which virus is actually causing a GI disease can only be done by laboratory testing

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3
Q

What is Norovirus? Aka. Norwalk virus

A

naked RNA virus; identified in 1972 after outbreak of GI disease in Norwalk, Ohio

  • other viruses with similar features were later identified and called “Norwalk-like” therefore, general term is “Norovirus”

very stable in the environment- survives 10ppm chorine, freezing, heating to 60C

  • fecal- contaminated food/water Is usual source of injection
  • can’t tell by looking at/smelling food that it carries Norovirus
  • low infectious dose- 10-100 virus able to cause disease
  • long term close-quarter contact is a major risk factor ex) hospitals, nursing care homes, day cares, cruise ships etc
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4
Q

How does Norovirus cause disease?

A
  • ->viruses attach, enter, and replicate in intestinal epithelial cells
  • ->lyric infection cycle destroys host cells
  • new viruses released into feces: re transmission
  • localized damage to gut epithelium: nausea, vomiting, abdom.pain, also: loss of absorptive capacity(diarrhea)
  • recovery via immune response( but no long term immunity)
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5
Q

Typical clinical features of Norovirus?

A
  • 2-3 day incubation period prior to symptoms
  • 1-5 days of watery diarrhea + nausea/vomiting/ abdominal pain
  • severe dehydration is the main clinical concern: tachycardia, hypotension
  • supportive therapy only ex) no effective anti vitals: fluid replacement to prevent dehydration
  • can continue to shed virus for 2 weeks after symptoms disappear: most likely source of new infections
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6
Q

Viruses of the CNS?

A

aka “neurotrophic” viruses( viruses able to infect nerve cells)

  • ->encephalitis(inflammation of the brain)
  • ->meningitis( inflammation of protective membrane covering brain)
  • ->poliomyelitis ( destruction of motor neurone in brain, spine)

wide variety of viruses–>mumps, measles, rabies, herpes, enterviruses, Etc

Infection usually starts somewhere else 
Ex) poliovirus (fecal-oral transmission) 
-->enters intestinal epithelial cells 
-->enters intestinal lymphoid tissues
-->absorbed into blood 
-->Crosses blood-brain barrier 
-->enters neurons
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7
Q

West Nile virus (wnv)

A
  • small enveloped RNA virus
  • ex, of a “vector-borne” virus: a virus whose primarily(but not only) mode of transmission is via a living carrier( a vector)- usually an insect
  • first seen in 1937 in west Nile region of Uganda and remained mostly localized to Africa, west Asia, Middle East: sporadic outbreaks over past 70 years
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8
Q

West Nile cycle transmission cycle?

A
  • natural host for WNV is birds(mainly crows, but others also)
  • primary transmission cycle is from Bird to bird via culex tarsalis mosquito
  • humans(and other animals) are “incidental” hosts
  • -> acquire virus after bite from infected mosquito
  • -> infected human now becomes a “dead-end” host- cannot re-transmit WNV to other humans via mosquito bite
  • NO evidence of transmission through casual contact with birds and cannot be spread person to person via casual contact– but: other ways for direct human to human transmission: mother to child during birth, organ transplants, blood transfusion
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9
Q

West Nile Virus clinical presentation

A
  • 80% of WNV-infected people Have no symptoms
  • 20% develop mild “west Nile fever”
  • -> 3 to 4 days after bite
  • -> fever headache, body ache, rash, swollen glands
  • -> lasts 3 to 4 days, then recovery w/o long term effects
  • 1% develop more severe encephalitis (usually pt. >50yr)
  • viral replication in the brain leads to inflammation–> headache, high fever, neck stiffness, disorientation
  • paralysis, seizures (leading to death in severe cases)
  • symptoms subside over time, but neurological damage may be permanent
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10
Q

West Nile clinical presentation

A
  • no effective anti-viral therapy; no human vaccine
  • immunity after natural infection is probable(short or long term??)
  • best preventative measure is to avoid mosquito exposure
  • Saskatchewan: 1st appeared in 2003: –> 947 confirmed cases: 10 without symptoms, 868 with west bile fever, 62 with encephalitis, 7 deaths
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11
Q

“Blood borne” viruses

A
  • viruses which infect various organs or cells, but whose presence can routinely be seen in the bloodstream (& other bodily fluids)–> transmitted by direct contact with blood/bodily fluids
  • major BBVs: hep B, Hep C, HIV
  • minor BBVs: hep A & D, West Nile virus, cytomegalovirus
  • your biggest worry as a health care provider ex) hep B: 1 in 3 risk of infection when in direct contact with blood from an infected person(ex. Needle stick injury)
  • hep c: 1 in 30
  • HIV: 1 in 300
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12
Q

Hep C virus

A

Hepatitis= inflammation of the liver

  • -> jaundice, poor appetite & weight loss, fatigue, muscle & joint pain
  • -> progressive loss of liver function over time, often requiring liver transplants to avoid death( = 40% of liver transplants are due to HCV)
  • note: HCV is only one possible cause of “hepatitis”
  • -> first described clinically in early 1970s ( non- A, non-B hep)
  • -> identified as a unique virus in 1989
  • Canada– 250, 000
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13
Q

Hepatitis C virus

A
  • enveloped RNA virus with a small ( 10 genes) genome
  • very rapid replication rate–> up to 10^12 new viruses produced per day during an active infection
  • 7 different “genotypes” (plus> 50 sub types) –> different in RNA sequence of “non- structural” genes
  • note: the different HCV genotypes are differently thoughout the world (ex. North America- geno. 1: Middle East & Africa- geno 4; etc) and differ in how they respond to anti-viral therapy
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14
Q

Transmission of HCV?

A
  • blood-borne ex) via exchange of blood or body fluids):
  • -> IV drug use with shared needles:65% of new cases
  • -> blood transfusion, organ transplants: < 0.1% (vs 4% pre- 1990)
  • -> occupational exposure to blood (ex. Health care workers): 3%
  • -> hemodialysis: 1%
  • other known routes( although relative risk is low or unknown):
  • -> household exposure or unprotected sex with HCV partner
  • -> mother- fetus transmission( occurs in= 5% of HCV mothers)
  • -> body piercing, tattooing, etc with improperly sterilized equipment
  • HIV is NOT transmitted by:
  • coughing, sneezing, hugging, kissing & other casual contact
  • sharing eating utensils or via food or water
  • Mosquitos or other biting insects
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15
Q

Progression of clinical disease (after first contact) HCV

A
  • HCV is carried by the blood to liver; enters and replicates in the liver cells (= “acute” infection)
  • -> typical “hepatitis” symptoms appear in 5-10 weeks in 30% of people ex. 70% of people with acute HCV have no symptoms
  • -> 20% of people with acute infection spontaneously eliminate the virus within several week and have no further problems
  • -> 80% of people with acute infection progress to “chronic” disease
  • HCV persists in the person for at least 6 months
  • rate of virus replication slows & severity of symptoms declines
  • but: if not treated:
  • -> 60-70% develop cirrhosis(scarring) of liver & liver failure
  • -> 2-5% develop liver cancer( hepatocelluar carcinoma)
16
Q

Diagnosis of HCV via blood test(2)

A
  • -> antibodies against HCV(positive= acute or chronic disease or past exposure to the virus)
  • -> HCV nucleic acid by PCR( positive = virus is present & therefore patient has active disease)
17
Q

Anti-viral therapy for HCV

A
  • “pegylated” interferon(INF+ polyethylene glycol= pegasys)
  • -> PEG increases half life of INF and reduces clearance rate
  • -> one subcutaneous injection per week
  • +ribavirin
  • -> inhibits virus replication
  • -> orally-2x per day
  • +- telaprevir, boceprevir(approved do use in 2011)
  • -> inhibits viral protease enzyme required for assembly
  • -> 2 tablets every 8hr
  • duration of treatment partly depends on HCV genotype ex) geno 1-48 weeks(up to 72 weeks), geno. 2-3–> 24 weeks
  • very costly( = 65000 for 48 weeks) and many side effects
18
Q

Can HCV infection be cured( &/ or prevented)?

A
  • “cure” defined as no virus detectable after 24 wks treatment
  • overall success rate after therapy=75%
  • factors impacting success:
    1. Overall health of patient
    2. Genotype of the virus (geno. 1 is harder to treat)
    3. Patients compliance with dosing instructions–> therapy must be continuos to fully suppress virus and avoid possible emergence of drug resistance
  • vaccine prospects( for prevention)
  • no vaccine to date
  • -> numerous genotype & sub-types
  • -> no suitable animal model on which to do testing