Microbiology - Final Exam - Mayi

Front 1

Viruses belonging to paramyxoviridae

Which lacks NA/HA activity

Back 1

Mumps virus
Measles virus
RSV (Resp Syncytial Virus)
HPIV

- RSV

Front 2

Clinical manifestations of mumps

Back 2

1. Swollen parotid glands
2. Swelling painful, b/L w/ fever
3. Asymptomatic

Front 3

What % of mumps infection shows parotitis?

Can complications occur if parotitis is not present?

If so, which demographic of people?

Back 3

30-40%

Yah

MC in people who reached puberty

Front 4

Are Abs sufficient to control mumps?


CMI? What happens w/ CMI and mumps?

Back 4

No, not sufficient
-- virus spreads from cell to cell
-- serum Igs don't offer protection

CMI controls infection
-- causes some of the symptoms

Front 5

What are the types of complications due to mumps virus?

Back 5

- epididymo-orchitis following parotitis (inflammation of epididymis/balls)

- meningoencephalitis

- oophoritis (inflam. of ovaries) or mastitis (inflam. of breasts)

Front 6

Can mumps be definitively dx'd based on clinical manifestations?

How can mumps be definitely dx'd?

Back 6

Nah, b/c parotitis may be caused by other diseases (non-viral/autoimmune)

RT-PCR or ELISA to look for Abs (IgM/IgG)

Front 7

How is the mumps virus transmitted?

What kind of shedding occurs?

Back 7

Direct contact w/ respiratory secretions/saliva/fomites

Asymptomatic shedding

Front 8

Who is at risk for contracting mumps?

Back 8

- Unvaccinated people
- Immunocompromised people
- People who received only 1 dose of vaccination
- Some who received >1 dose

Front 9

What kind of immunity does the mumps vaccine confer?

Back 9

Elicit only partial immune response against the virus in circulation

**More effective vaccine required**

Front 10

Commonalities b/w measles, mumps and rubella?

Back 10

- enveloped virus: easily inactivated by dryness & acid
- infectious period precedes symptomatic period
- limited to humans
- only 1 serotype exists
- immunity life long

Front 11

Where are we seeing mumps outbreaks?

Back 11

Seen in saliva, CSF & urine

NO antiviral drugs

Front 12

Rotavirus morphology

Back 12

Naked, double-shelled w/ segmented genome

-- one of the proteins is viral enterotoxin
-- wheel like appearance

Front 13

What is the virus resistant to?

How many antigenic groups does it have?

Which antigenic groups are linked to human disease?

Back 13

Drying, detergents, acidic pH

7 distinctive antigenic groups - A-G

A, B, C linked to human disease

Front 14

What is rotavirus group A the MCC of in the US?

What 2 serotypes is rotavirus group A divided into?

Back 14

-- MCC of diarrhea

-- G (glycoprotein) and P (protease sensitive) serotypes

Front 15

- What age group are most affected by severe diarrhea by group A rotavirus?

- Clinical course of disease?

- Immunity?

Back 15

- children

- vomiting and watery diarrhea for 3-8 days

- immunity after infection incomplete; repeat infection less severe

Front 16

Lab diagnosis of rotavirus?

Back 16

ELISA detection (in feces or rectal swabs) of rotavirus specific antigen

Latex agglutination test for rotavirus

RT-PCR

- cell culture NOT used b/c difficult to cultivate virus from clinical specimen

Front 17

- Where are large amounts of rotavirus found?

- When is the disease mostly seen in temperate climates?

- Transmission?

Back 17

- Feces
** released even in ASYMPTOMATIC**

- winter months - "winter vomiting disease"

- fecal-oral route and possibly respiratory route

Front 18

Viruses transmitted by inhalation and ingestion?

Back 18

the PR CLAN (pulmonary, rectal)

Poliovirus
Rotavirus

Coronavirus
Lassa fever virus
Adenovirus
Norovirus

Front 19

Rotavirus:
1. Mostly seen in children less than what age?
2. By what age are almost all children infected?
3. What age group is the maximum incidence of rotavirus gastroenteritis seen?
4. What is this max. susceptibility corelated with?

Back 19

1. <5 yoa
2. By 3rd year of life
3. 6-24 mos
4. Decline of maternally acquired immunity

Front 20

Control of rotavirus:
1. Resistant to most disinfectant but...?
2. Prevention/control?

Back 20

1. Chlorine
2. Strict adherence to handwashing measures
-- putting all infected babies together
-- vaccination

Front 21

Rotavirus: Vaccination

1. What kind of vaccine? How many?
2. What are they?

Back 21

1. 2 live, oral, attenuated vaccines

2
a. Rotashield - pulled from market due to problems of intussuspection (intestinal flooding)
**Therapy includes rehydration**
b. Children w/ immunodeficiency disorders - tx'd w/ rotavirus-specific Ig preperation

Front 22

Noravirus
1. What percent of foodborne illness outbreaks caused by this?
2. MCC of what?
3. Somtimes called?

Back 22

1. 50%
2. non-bacterial cause of acute gastroenteritis for all ages worldwide
3. "stomach flu"

Front 23

Noravirus:
Symptoms?

Back 23

n/v/d/abd cramps, sore throats for 12-60 hrs
-- sudden onset

-- self limiting in most people

-- dehydration problem w/ very young, elderly and immunocompromised

Front 24

Noravirus
1. Transmission
2. Single/multiple strains?
3. Immunity?
4. Consumption of what food usually leads to outbreak?

Back 24

1. consumption of fecally-contaminated food or water & by person-person spread or contaminated fomites
2. multiple
3. NO lifelong immunity
4. raw (less frequently - steamed) shellfish

Front 25

Where is the spread of noravirus particularly high in incidence?

Why?

How long can viral shedding occur?

Back 25

1. Cruise ships
2. frequent change in passenger population, crowding, difficulty in adequate decontamination during short periods on shore
3. 2-3 wks after symptom resolution

Front 26

What 3 factors help the rapid spread of infection of noravirus?

Back 26

1. Fecal-oral route of transmission
2. Low infectious dose (< 100 viral particles)
3. High environmental stability

Front 27

Noravirus:
Lab dx?

Back 27

1. Clinical diagnosis
2. Detection of viral RNA by RT-PCR
--food, water, stool samples
3. ELISA

Front 28

Noravirus: Transmission

1. Contact w/ what and who?
2. Vomit?
3. Why highly contagious?
4. Temp of survival?

Back 28

1. sick person, contaminated food, and water
2. aerosolized vomit can transmit virus
3. only 100 viral particles to initiate infection
4. Freezing and heating to 140F

Front 29

Why is it hard to develop long-lasting immunity to noravirus?

Back 29

Many different strains
-- can occur throughout a person's lifetime

Front 30

Noravirus:
Control

Back 30

1. Handwashing
2. Wash produce
3. Bleach to decontaminate surfaces immediately after episode
4. Wash contaminated clothes immediately
5. Infected persons should not prepare food until 3 days after recovery

Front 31

Astrovirus:
1. morphology
2. treatment
3. prevention and control

Back 31

1. Star-like
2. no antiviral drug for treatment; no vaccine
3. Improved personal hygiene; proper disinfection of contaminated surfaces

Front 32

Astrovirus

Symptoms are frequently _______

Back 32

Asymptomatic

Front 33

MCC of acute hepatitis?
MCC of chronic hepatitis?

Back 33

1. HAV
2. HCV

Front 34

Diagnosis of hepatitis A?

Back 34

1. symptoms
2. ELISA for serological detection of alpha-HAV IgM
3. shed in stool ~10-14 days before symptoms
4. canNOT initiate chronic infection
5. Ab protection for life
6. NOT a/w hepatic cancer

Front 35

Transmission of Hep A

Back 35

1. ingestion of contaminated food/water
2. sharing contaminated utensils
3. sexual contact w/ infected person

Front 36

Control of Hep A

Back 36

1. prevent fecal/oral tranmission of HAV
2. avoid potentially contaminated food or water, ESP uncooked shellfish
-- hand washing is crucial
-- chlorine treatment kills the virus
3. Immune serum globulin given w/in 2 weeks of exposure can prevent clinical illness

Front 37

HAV treatment/vaccination?

Back 37

1. HAV vaccine (killed vaccine) prevents infection
-- only 1 serotype and infects only HUMANS
2. Ig as prophylaxis for travelers
-- may prevent or attenuate household outbreaks

Front 38

Hep B (HBV) genetics

Back 38

- partially dsDNA of only 3200 bases
- encodes RT
- replicates via RNA intermediate

Front 39

Structure of Hep B

Back 39

core - DNA, a protein kinase, DNA pol w/ RT and ribonuclease H activity

**surrounded by capsid**

capsid - contains core Ags (c & e)

envelope - HBsurface Ag

Front 40

HBsAg

Back 40

- Immunogenic and is released by virus

- in serum: can bind to and block action of neutralizing Ab
-- limits body's ability to resolve infection

Front 41

What is needed to resolve Hep B infection and prevent it form becoming chronic?

Back 41

Effective CMI

Front 42

Jaundice?

Back 42

Too much biliruben circulating in blood
- degree of yellowing depends on level of biliruben
- first face, and progresses downward to feet
- too much - stool turns dark brown; urine darkens from buildup

Front 43

Other symptoms a/w jaundice?

Back 43

Pruritis - severe to point where it causes sleep disruption and emotional distress

Front 44

Clinical outcome of Hep B in children/neonates?

Back 44

- Less severe for children b/c of immature immune system

- 95% infected neonates develop chronic infections

Front 45

Diagnosis of Hep B

Back 45

1. symptoms
2. elevated liver enzymes
3. serological profile
4. ground-glass hepatocyte cytopathology (histological hallmark of chronic HBV infection)

Front 46

Hep B tests?

Back 46

1. HBsAg (Hep B surface antigen)
2. anti-HBcAg (IgM/G vs. hep core antigen)
3. HBeAg & anti-HBe

Front 47

Of the 3 Hep B tests, which one is a key marker?

Back 47

HBsAg - seen in serum 2-6 wks before biochemical damage to liver is evident

Front 48

Which hep B test appears 2-4 wks after HBsAg and becomes undetectable in a few months?

Back 48

IgM anti-HBcAg

Front 49

When is HBeAg found in the patient's blood?

What does the presence indicate?

What are the mutants?

Back 49

- When virus is replicating at a high rate

- active hepatitis

- HBeAg-minus mutants

Front 50

Which test reveals presence of HBV DNA (as few as 20 copies/mL serum)?

What significant does this test have?

Back 50

- Quantitative real time PCR

- management of chronic HepB infection; IDs patients at high risk of progression; allows patients to f/up after therapy

Front 51

What is needed to resolve Hep B infection and prevent it form becoming chronic?

Back 51

Effective CMI

Front 52

Jaundice?

Back 52

Too much biliruben circulating in blood
- degree of yellowing depends on level of biliruben
- first face, and progresses downward to feet
- too much - stool turns dark brown; urine darkens from buildup

Front 53

Other symptoms a/w jaundice?

Back 53

Pruritis - severe to point where it causes sleep disruption and emotional distress

Front 54

Clinical outcome of Hep B in children/neonates?

Back 54

- Less severe for children b/c of immature immune system

- 95% infected neonates develop chronic infections

Front 55

Diagnosis of Hep B

Back 55

1. symptoms
2. elevated liver enzymes
3. serological profile
4. ground-glass hepatocyte cytopathology (histological hallmark of chronic HBV infection)

Front 56

Hep B tests?

Back 56

1. HBsAg (Hep B surface antigen)
2. anti-HBcAg (IgM/G vs. hep core antigen)
3. HBeAg & anti-HBe

Front 57

Of the 3 Hep B tests, which one is a key marker?

Back 57

HBsAg - seen in serum 2-6 wks before biochemical damage to liver is evident

Front 58

Which hep B test appears 2-4 wks after HBsAg and becomes undetectable in a few months?

Back 58

IgM anti-HBcAg

Front 59

When is HBeAg found in the patient's blood?

What does the presence indicate?

What are the mutants?

Back 59

- When virus is replicating at a high rate

- active hepatitis

- HBeAg-minus mutants

Front 60

Which test reveals presence of HBV DNA (as few as 20 copies/mL serum)?

What significant does this test have?

Back 60

- Quantitative real time PCR

- management of chronic HepB infection; IDs patients at high risk of progression; allows patients to f/up after therapy

Front 61

What is difficult during the HBsAg window and why?

When is the patient considered chronic?

Back 61

Routine serodiagnosis b/c HBsAg and anti-HBsAg are undectable

when anti-HBsAg is (+) for 6 mos

Front 62

Transmission of HepB?

Back 62

1. Neonatal from mother's infected blood
2. sexual activity (50% cases)
3. IVD use (20% cases)
-- 50% of IVDU are infected
4. 1 HBV transmission occurs/250,000 individuals transfused
-- screen for HBcAg
5. 27% cases - cause unknown

Front 63

When can HepB Ig be administered to prevent spread of disease?

Difference b/w recovery of infected adults and babies/children?

Back 63

>1wk - prevent spread of disease

Adults - usually recover; most babies/children develop chronic infection

Front 64

HBV vaccine

Back 64

- recommended for infants, children & high risk people
- given in series of 3 injections (IM); contains HBsAg (subunit vaccine)
- single serotype & limited host range ensure success

Front 65

Why is HepB vaccine considered the 1st anti-cancer vaccine?

Back 65

Prevents hepatitis B disease and serious consequences, such as: hepatocellular carcinoma

**does NOT cause or worsen MS/other demyelinating disease**

Front 66

Therapy for chronic hepB infection

Back 66

- INF-alpha - for 4 mos
- Lamivudine (target is polymerase) - for 1 year
- nucleoside analogues: ATE
---Adefovir dipivoxil
---Telbivudine
---Entecavir

Front 67

1. Size of HepD virus?
2. What is part of HDV envelope and necessary for infection?
3. What is HepD considered to be a satellite virus of?

Back 67

1. smallest human pathogen known
2. HBsAgs
3. HepB

Front 68

1. What does coinfection or superinfection of HepB/D increase risk of?
2. Tx for HepD
3. What is HDV RNA?

Back 68

1. fulminant hepatitis and liver cirrhosis
2. NO specific tx
3. ribozyme

Front 69

1. What % of fulminant hepatitis caused by HDV?

2. How is HDV spread?

3. In what people can HDV replicate and cause disease

Back 69

1. 40%
2. blood, semen, vaginal secretions
3. people with active HBV infection

**prevention of HBV PREVENTS HDV**

Front 70

HepC:
1. Who does it infect?
2. What family does it belong to?
3. How is it different from other viruses in the same family?

Back 70

1. humans and chimps
2. Flavivirus
3. Not transmitted by anthropod vector (mosquito)

Front 71

Clinical symptoms:

1. Acute hepC
2. chronic hepC
3. What % of cases have severe, rapid progression to cirrhosis
4. predominant symptom?

Back 71

1. resolution and recovery in 15% cases
2. disease later in life in 70% cases
3. 15% of cases
4. chronic fatigue

Front 72

Lab detection of HepC

Back 72

1. ELISA for alpha-HCV
2. RT-PCR for RNA in serum of seronegative patients w/ hepatitis-like symptoms
3. Abs produced 7-31 wks s/p initial infection

Front 73

Pathogenesis of HepC

Back 73

1. infects hepatocytes
2. can remain cell associated and prevent cell death
3. inhibits apoptosis of INF-alpha action, promotes persistent infection
4. Progresses to liver disease in 85% of patients
5. continual liver repair - risk of carcinoma

Front 74

Spread of HepC?

Back 74

1. blood products, organ transplants
2. HCV contamination in blood banks
3. shared needles
4. tattoos
5. body piercing
6. circumcision in developing places
Less frequent:
1. sex
2. perinatal transmission

Front 75

Treatment of HepC

Back 75

- INF-alpha
- pegylated INF-alpha +/- Ribavirin
---Rebetron
---Hemolytic anemia (monitor Hb)

Front 76

HepE:
1. general
2. transmission
3. At risk
4. Epidemics where?

Back 76

1. enteric non A, non B
2. Fecal/oral transmission
3. Pregos (30% mortality); developing countries
4. India, Pakistan, Nepal, Burma, North Africa, Mexico

Front 77

HepE:
treatment, detection, prevention/vaccination

Back 77

1. No Ig available pre-/post-exposure prophylaxis
2. clinically indistinguishable from HAV
---ELISA for IgM
3. self-limiting infection
4. prevention most effective w/ NO vaccinations

Front 78

Adenovirus
1. serotypes
2. gastroenteritis and diarrhea serotypes
3. which cause gastroenteritis in children

Back 78

1. 100 serotypes; 51 infect humans
2. 40, 41, 42
3. 40 and 41

Front 79

Adenovirus:

Epidemiology

Back 79

1. endemic throughout the year
2. survives for long periods outside host
3. ubiquitous in humans & animals
4. can cause asymptomatic shedding
5. shedding can occur mos-yrs

Front 80

Adenovirus:
1. Transmission
2. Prevention

Back 80

1. direct contact; indirect w/ fomites; fecal-oral route; waterborne; inhalation of aerosolized droplets: pharyngitis & ARDS

2. strict asepsis (in closed communitites); hand washing; adequate chlorination