Exam 3 Flashcards

(290 cards)

1
Q

-Infectious element containing nucleic acid and a protein coat
lacking protein synthesis and energy production machinery
-Replicates within living cells

A

virus

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2
Q

what nucleic acid do viruses use?

A
  • DNA or RNA (only one)
  • single-stranded or double-stranded
  • May be associated with core proteins

*All have some sort of capsid or protein coat, it surrounds the nucleic acid

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3
Q

are viruses free living?

can you see them with a light microscope?

A

no!

No!

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4
Q

do antibodies work against viruses

A

No!

except nitazoxanide in a few circumstances

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5
Q

The _____ is made of lipids and surrounds the ____,

-can be destroyed by acid, alcohol, etc.

A

envelope

capsid

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6
Q

4 features that viruses lack compared to other microorganisms

A

CANNOT:

  1. grow on non-living media
  2. possess both DNA and RNA
  3. possess ribosomes
  4. are not antibiotic sensitive
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7
Q

Protein shell comprised of repeating polypeptide units called capsomeres

A

capsid

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8
Q

2 capsid shapes

A
  1. spherical configuration

2. helical configuration

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9
Q

spherical configuration

A

nucleic acid surrounded by capsid. Usually icosahedral symmetry (20-sided)
– Synonym: cubic symmetry

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10
Q

helical configuration

A

nucleic acid interwoven among protein capsomeres; tubular structure

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11
Q
  • Comprised of protein layer, lipid bi-layer, and glycosylated protein spikes (peplomers)
  • Lipid bi-layer derived from host cell membranes
  • Carbohydrates also host-derived
A

envelope

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12
Q

what viruses have an envelope

A

on ALL animal HELICAL viruses and on some spherical (icosahedral) viruses

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13
Q

Mature viral particle, i.e., nucleo-

capsid +/- envelope

A

virion

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14
Q

how are viruses separated into families?

A
  1. nucleic acid type (RNA/DNA, Single/double stranded, continous/segmented)
  2. size/shape/substructure
  3. presence or absences of envelope
  4. mode of replication
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15
Q

what DNA viruses are single stranded

A

Parvovirus (paroviridae)

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16
Q

what RNA viruses are double stranded

A

Reoviridae (causes rotovirus)

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17
Q

viral cultivation

A
  1. in animals
  2. in eggs (embryonic membranes)
  3. tissue

*requires living cells

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18
Q

virus cultivation endpoint:

visible change to cells

A

cytopathogenic effect (CPE)

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19
Q

virus cultivation endpoint:

RBC clumping to free virus

A

hemagglutination

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20
Q

virus cultivation endpoint:

RBCs adhering to virus

A

hemadsorption

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21
Q

viruses are what type of pathogen

A

obligate intracellular pathogen

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22
Q

4 non-clutivation ways to detect viruses

A
  1. electron microscopy
  2. antigen detection (Fluorescent Ab, radioimmunossay, ELISA)
  3. Nucleic acid detection (PCR, hybridization)
  4. Antibody detection (serology)
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23
Q

Electron microscopy resolution for viruses

A

1-2nm

*visualizes individual virions

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24
Q

Viral infections stimulate what immune response?

A

host antibody responses

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25
describe antibody response to viruses
- Antibody titers rise during the 3-4 weeks following infection - A positive IgM assay or a 4-fold rise in IgG titer signify recent infection - Low titers of IgG persist indefinitely
26
virus-cell infection cycle steps (7)
1. absorption/ attachment of virus to cell membrane 2. penetration and uncoating 3. transcription/translation of early proteins (regulatory proteins and enzymes, host ribosomes) 4. replication of NA 5. transcription/translation of late proteins (ie. structural proteins, enzymes) 6. assembly (nuclear vs. cytoplasmic) 7. release
27
what ways can viruses penetrate and uncoat their viral NA into a cell
- transport across cell membrane via bacteriophage - fusion of envelope with cell membrane - endocytosis (most animal viruses)
28
positive sense replication
RNA directly codes for a protein for a virus
29
negative sense replication
must base pair match to make its complement--> + RNA and then codes to make a protein
30
retrovirus replication
start with RNA--> makes DNA (reverse transcriptase)--> gets incorporated into our genome-->transcribed into RNA--> protein
31
what ways can a virus be released from a cell
1. budding from cell surface (cell intact) | 2. cell rupture (lysis)
32
viral pathogenicity to the infected cell
1. inhibition or acceleration of cell growth 2. alteration in cell membrane antigens and integrity 3. Toxic viral inclusions (accumulation of viral proteins, cellular degenerative materials) 4. cell death/lysis
33
the West hemisphere's largest arboviral meningoencephalitis epidemicwas due to what virus
west nile virus (Flavivirus family-RNA virus) *virus peaks in late summer/early fall
34
arbovirus consists of:
Arthropod-borne viruses
35
what is the major vector for WNV
mosquitos
36
reservoir of WNV and head-end hosts
mosquitos, birds, small mammals humans, horses
37
routes of transmission of WNV
transfusion, transplantation, breastfeeding, transplacental, percutaneous needlestick
38
sx: fever, HA, rash, fatigue (flu-like in the summer) ~80% asypmtomatic
WNV
39
sx: headache, altered MS, muscle weakness, flaccid paralysis, tremor, hyporeflexia, seizures *milder in children
West Nile Meningoencephalitis
40
how do you diagnose WNV?
Serology (IgM, IgG)*** ``` PCR (insensitive) Culture (low yield) Antigen detection (insensitive) ```
41
vaccine for WNV?
equine vaccine
42
tx of WNV
Ribavirin, interferon alpha, high titer IVIG proposed (None proven effective)
43
medically relevant human retroviruses
HIV 1* and 2 | HTLV 1 and 2
44
HIV 1 subtypes
M, N, O (chimp), P (gorilla) - M is the major cause of the current pandemic--> (B is predominant in US, W. Europe and Australis) - N, O and P restricted to W Africa (also HIV-2)
45
major envelope glycoprotein for HIV1 used for: attachment, neutralizing site, diagnosis
GP120
46
major envelope glycoprotein for HIV1 used for: attachment, fusion, neutralizing site, diagnosis
GP41
47
major component of the nuclecapsid for HIV1 used for: diagnosis
P24
48
what NA does HIV1 have
ssRNA
49
what enzymes are essential for HIV1 replication
RT (reverse transcriptase) IN (integrase) P (protease) pre-formed enzymes
50
life cycle: - Attachment: gp120 and CD4 - Entry: gp41 and co-receptors CCR5, CXCR4 and others - Reverse transcription of genomic RNA to dsDNA by the pre-formed RT (cytoplasm) - Integration: pre-formed IN integrates the proviral DNA into the cellular genomic DNA (nucleus) - Latency - Active replication: transcription of the proviral DNA into genomic RNA and mRNA (nucleus) - Translation of viral mRNA into viral proteins (cytoplasm) - Assembly and release - Maturation: P cleaves the viral proteins  cone shape of the nucleocapsid (virion)
HIV
51
main cellular targets for HIV
- CD4+ T cells in blood and tissue (depletion and immune suppression) - Monocytes, macrophages, astrocytes (activation, release of inflammatory factors) - dendritic cells/ APC
52
pathogenesis: main target: CCR5+ activated: CD4+ T cell--> systemic immune activation (adaptive and innate)--> collapse of immune system due to persistence of this process
HIV *results in AIDS
53
how is HIV transmitted
blood, genital and rectal mucosa, gut mucosa (maybe oral in neonates), transplacental transmission
54
factors that increase the risk of HIV transmission
high HIV RNA c/mL of the case index or in semial fluid and cervix - pregnancy for sexual transmission
55
- Rapid rise in plasma RNA c/mL. followed by decrease to steady state - Initial rapid decrease in blood CD4+ T cells followed by partial recovery - Permanent loss of gut CD4+ T cells - Small number of viral quasi species - Establishment of a latent reservoir - Development of the humoral and cellular immune response that results in the control of viral replication and partial recovery of the CD4+ T cells in blood
acute HIV infection
56
- Gradual increase of plasma HIV RNA c/mL - Gradual decrease of CD4+ T cells in blood - Increase in the number of viral quasi species as an immune escape mechanism - Decrease of CD4+ and CD8+ HIV-specific immune responses
Asymptomatic HIV infection
57
sx: fever, adenopathy, pharyngitis, aseptic meningitis and other neurologic manifestations, thrush, rash, mucosal (oro-genital) ulcers
acute retroviral syndrome * infectious-mono-like syndromen * occurs 1-6 weeks after infection
58
6 Early signs of clinical progression of HIV
1. Decrease of CD4+ T cells and hemoglobin**** 2. Enlarged lymph nodes and spleen 3. Thrush 4. Zoster 5. Hairy leukoplakia 6. Lymphocytic interstitial pneumonia (children only)
59
sx: opportunistic infections (ie. Pneumocystis carinii Pneumonia, cerebral toxoplasmosis, CNS lymphoma) neoplasias w/ viral etiology: EBV, HHV-8, HPV (ie.Kaposi's sarcoma) wasting dementia/loss of milestones (young children)
AIDS
60
CD4+ T cell criteria for aids
less than 200 cells/uL, which is less than 15%
61
how is HIV diagnosed
serology *Seroconversion occurs 4 to 8 weeks after acute infection - 4th generation antigen/antibody assays (Detect p24 Ag + IgM + IgG anti-HIV-1 and 2) - Confirmatory tests: Multispot differentiates HIV-1 from 2, Rapid point of care tests or conventional EIA both diagnosis and confirmation * Initial and confirmatory tests have to be from different manufacturers
62
when are antibody-based tests for HIV not useful
- EIA in primary infection - Advanced AIDS - Children 0-1 born to infected mother
63
It may take up to _____ to loose maternal antibodies anti-HIV
24 months
64
What is the preferred diagnostic test for babies who mothers are on antiretroviral therapy (ART) for HIV that includes drugs that cross the placenta -Detects the presence of reservoirs
DNA PCR
65
what diagnostic test do you use for a marker for disease progression and therapeutic response for HIV
RNA PCR
66
treatment of HIV
``` -Combination ART with 3 or more drugs from 2 or more classes: Reverse Transcriptase Inhibitors Protease Inhibitors Fusion inhibitors Co-receptor inhibitors Integrase inhibitors Maturation inhibitors ```
67
prevention of vertical transmission of HIV
- Infant post-exposure prophylaxis for 6 weeks | - Infant pre-exposure prophylaxis if breastfeeding and mother off treatment
68
vaccine and cure for HIV
20% efficacy in 1 vaccine tested -Allogeneic transplantation with HSC that lack CCR5 lead to cure in one individual
69
Family: Picornaviridae
Enteroviruses
70
genera: hepatovirus, parechovirus
enteroviruses
71
types of enteroviruses
1. polioviruses 2. Coxsackieviruses A and B 3. Echoviruses (enteric cytopathogenic human orphan) 4. Numbered EVs *reclassifcation: A, B, C, D and numbered serotypes ie. EV D68
72
cause of the common cold
rhinovirus
73
ssRNA, positive sense Small (25-30 nm) Naked (non-enveloped) Icosahedral protein capsid (VP1, VP2, VP3, VP4)
enterovirus
74
what allows enteroviruses to survive in harsh environments?
lack of envelope and presences on the capsid proteins make them resistant to harsh conditions (can survive the stomach to get to intestines)
75
life cycle: - binds to cell receptor - RNA penetrates into cell - Translation--> polyprotein produced - Replication via (-) strand RNA template - Host cell shutoff within 4 hrs - assembly - cell lysis and virions released
enterovirus
76
when do enteroviruses become clincial
multiplication in reticuloendothelial system
77
what type of shedding do enteroviruses do
pharyngeal and fecal shedding
78
25% of febrile illness in infancy is caused by
enteroviruses *more common in summer/fall
79
transmission of enteroviruses
1. fecal-oral (fecal shedding x7-11 weeks, contaminated food, water, fomites) 2. droplet= secondary (resp. shedding x 1-3 weeks)
80
risk factors for transmission of enterovirsues
1. younger age* 2. SES 3. poor hyigene 4. overcrowded 5. humoral (Ab) immunodeficient)* 6. exercise* 7. viral factors* * severe disease risk - BF is protective
81
what causes: non-specific exanthems non-specific viral lesions/rash
E9 | non-poliovirus enterovirus
82
sx: | vesicles in the POSTERIOR oropharynx w/ high fever
Herpangina caused by: Cox A, enterovirus
83
sx: | blisters in ANTERIOR oropharynx and on extremities
hand-foot mouth disease caused by: Cox A16, A6, and EV 71
84
sx: | respiratory illness: URI, pharyngitis, pleurodynia (mimics chest pain), LRI, wheezing
EV 68 enterovirus
85
sx: hemorrhagic conjunctivitis neurologic signs
EV70, Cox A24, | enteroviruses
86
sx: | myocarditis/pericarditis
Cox B
87
sx: hand-foot-mouth disease and herpangina severe neurologic disease (brainstem encephalitis, acute flaccid paralysis) Pulmonary edema/hemorrhage, pneumonitis, cardiopulmonary collapse
EV 71 entervirus
88
sx: baby with fever ~3 days viral rash sepsis, hepatitis, coagulopathy, myocarditis, meningoencephalitis, pneumonitis
neonatal EV infections
89
ways to diagnose enteroviruses
PCR** | tissue culture and animal inoculation rarely done
90
potential antiviral therapies for EV
Neutralization: Immune Globulin - Attachment & Uncoating: Pleconaril, Vapendavir, Pocapavir (experimental) - replication (in development) - protease (in development)
91
EV prevention
- no non-poliovirus EV vaccine (EV71 showing promise) - good hygiene - poliovirus vaccine (use inactivated/killed/stalked in US) *no herd immunity or associated paralysis
92
ABCs of Hepatitis
``` A-acute (no chronic form) B-blood C-chronic D-disquise E- exotic (also enteric) ```
93
Liver inflammation: increased liver enzymes, decreased liver synthetic function, increased bilirubin
hepatitis
94
``` sx: jaundice hepatomegaly fever anorexia nausea fatigue ```
hepatisis
95
-No envelope, protein capsid (survives in environment, resists acid, and moderate heat) -Picornavirus, related to enteroviruses
hep A
96
transmission of Hep A
1. fecal-oral
97
reservoir of Hep A
contaminated water, food; person to person transmission *No animal reservoir but survives in mollusks
98
``` rate the risks of Hep A transmission by exposure: Grade school Day care Raw vegetables fertilized with night soil Needle stick Travel to Mexico Cake decorated by infected baker Casserole made by infected cook ```
Grade school-lower Day care-higher Raw vegetables fertilized with night soil-higher Needle stick- lower Travel to Mexico- higher Cake decorated by infected baker- higher Casserole made by infected cook- lower *inactivated by cooking heat
99
hep A virus-host interactions
- sx last 2-6 weeks - rare fulminant liver failure - immunity long lasting (no chronic form)
100
how do diagnose Hep A
- clincally based on hx exposure - IgM-acute infection - IgG-past infection - Total Hep A antibody
101
Hep A prevention
-hygiene -Vaccine for: (all children older than 1 yr, travelers, Travelers, Contacts of internationally adopted children, Men having sex with men, Drug users (injecting and non-injecting), Pt with chronic liver disease) -HepA vaccine for post-exposure prophylaxis w/in 2 weeks
102
Envelope dsDNA has its own DNA polymerase inefficient assembly: excess surface antigen
Hep B *Hepadnavirus
103
HBsAg indicates
active Hep B infection
104
transmission of hep B
blood, semen, cervical secretion, breast milk *virus shed into blood and no animal reservoir
105
virus-host interaction of Hep B
- 3 month incubation period (longer than hep A) - sx last 6 weeks (longer than hep A) - 90% resolves spontaneously for ADULTS
106
outcome of HepB
- resolution, life-time immunity - fulminate, fatal course (1%) - chronic infection (80-90% perinatal)
107
what can chronic Hep B result in
- cirrhosis - glomerulonephritis, polyarteritis nodosa - risk of hepatocellular carcinoma
108
what HB antigen or antibody is first detected
HB surface antigen (HBsAg)
109
what HB Ag/Ab is detected next (window period)?
HB core antibody (HBcAb) | IgM and IgG
110
what HB Ag/Ab appears if infection resolves
HB surface antibody (HBsAb)
111
what HB Ag/Ab indicates chronic infection
HB surface antigen persists (HBsAg)
112
HepB prevention
- vaccine - screening blood donors - safer sex - HBIG
113
whats the main indication for liver transplant
Hep C
114
``` Enveloped ssRNA low fidelity replication large numbers of viral particles produced evades immune response ```
Hep C
115
can Hep C be transmitted in breastmilk?
no but avoid cracked nipples *infected infants do well (sever hep is rare)
116
how does perinatal transmission of HCV occur?
transmission only from women HCV-RNA positive at delivery *higher rate (3-4x) if woman is co-infected with HIV
117
chronic Hep C carriers complications
60-70% have intermittent elevated LFTs cirrhosis (increased w/ alcohol consumption) risk of hepatocellular carcinoma
118
hep C diagnosis
Ab screening: enzyme immunoassay look for anti-hep C antibody confirmatory test: NAT (qualitative RT-PCR for HCV RNA in plamsa)
119
when can you get Ab for Hep C in infants
18 months
120
nurse is stuck with a needle used on a pt with known hep C. What test should be dne and when?
wait 7 weeks and test Ab or look for RNA right away
121
hep D requires what for infection and transmission
hep B *uses Hepatitis B surface antigen
122
transmission of hep D
blood, sexual, vertical
123
diagnosis of hep D
serology for Hep D Ab | -NA for Hep D
124
hep D prevention
screen blood for hep B | Hep B vaccine
125
No envelope acid stable, heat stable ssRNA
Hep E
126
reservior of Hep E
swine, boar, deer *only Hep that has an animal reservoir
127
transmission of Hep E
``` -fecal-oral contaminated water (not associated w/ contaminated food) -person-person rare -vertical transmission -risk of blood-borne but rare ```
128
Shed in stool 1 week before symptoms and then for up to 2 weeks Often aysmptomatic Symptoms at 15-60 days if present Laboratory tests normal after 1-6 wks
Hep E
129
how to diagnose Hep E
HepE RNA | serology
130
prevention of HepE
hygiene (clean water supply) | vaccine in research
131
what are the 1st and 2nd most frequent illnesses in the use
1. rhinovirus (common cold) | 2. GE
132
4th leading cause of death in children
diarrhea
133
sx: lethargic sunken eyes poor skin tugor
dehydration
134
is an inflammation of the intestines | Infectious or non-infectious
Gastroenteritis
135
``` sx: diarrhea abdominal cramps nausea/vomiting fever ```
GE
136
3 or more watery or loose stools in a 24-hour period
diarrhea -Acute = lasting 4 weeks Less likely infectious than acute
137
non-infectious causes of diarrhea
``` antibiotic associated IBD/Crohn's, UC Malabsorption celiac IBS toxins ```
138
virsues that cause diarrhea
``` norovirus rotavirus adenovirus 40-/41 Astrovirus Caliciviruis 6. Other small round virus ```
139
what types on the bristol stool chart are considered diarrhea
Type 5, 6, 7
140
small, round dsRNA causes pediatric diarrhea adult food/H2O-borne epidemics
Rotavirus part of calicivirus family
141
- Typically asymptomatic infection, widespread sporadic infection, outbreaks in infants and young children. - 5-10% of GE in children under 2. - Generally mild diarrhea; occasionally severe
Sapoviruses
142
most common viral agents of diarrhea
rotavirus - Norwalk and Norwalk-like viruses = Noroviruses - Sapporo and Sapporo-like viruses = Sapoviruses Enteric Adenoviruses (serotypes 40,41)
143
small, round ssRNA Asymptomatic & relatively mild infections Pediatric diarrhea (2-17% of sporadic GE in young children) Outbreaks: DCC, hospital, nursing home, food-borne, H2O-borne
Astroviruses
144
what type of NA do Torovirus, coronaviruses, rotavirus | picobirnavarius have
Torovirus: ss RNA Coronaviruses: ss RNA Picobirnavirus: ds RNA Rotavirus: ds RNA
145
More associated morbidity and mortality than other viral etiologies of GE
Rotavirus *Globally, most important cause of infantile GE
146
``` Icosahedron no envelope double-shell capid innermost core shell dsRNA cytoplasmic replication; released by cell lysis ```
rotavirus
147
no envelope w/ a capsid means
can survive harsh environments (heat, acidic environment like stomach)
148
Rotavirus Subdivided into 7 groups | Based in immunologic assays related to inner capsid layer
A: frequent human infection; most important human group B: swine; human outbreaks + regional endemic disease C: sporadic and epidemic human disease D-G: rare human disease *A and B mostly cause human disease
149
describe the double shell capsid for rotavirus
- outer capsid contains VP4 and VP7 (which induce neutralzing antibody directed against rotavirus) - inner capids contains VP6 (the major rotavirus group antigen)
150
- Disease of infants and young children (Peak 3 months – 2 years) - Worldwide: epidemic and sporadic - Common! - predominant in autum/winter/spring - Shed in ~20% of outpatient and 35-50% of inpatient children with GE (in absence of vaccine)
rotavirus
151
transmission of rotavirus
fecal-oral transmission* - Water, food, fomite, respiratory transmission less frequent - Possible animal-human transmission (uncommon)
152
pathogenesis: - Affects small intestine - Replicates in villous epithelial cells - Mononuclear inflammation - Villous shortening - Impaired enzymatic and resorptive function - High viral titers shed in stool
Rotavirus
153
sx: - spectrum from asymptomatic to overwhelming - mild fever, early vomiting, diarrhea (watery), dehydration - preceding respiratory sx, abdominal cramps - Illness lasts 3-8 days; shedding for 7-21 days
rotavirus *Deaths secondary to dehydration & metabolic imbalances
154
Ab response to rotavirus
Evidence of both serum and intestinal antibody IgM, IgG, IgA - protective role of breast milk antibody
155
how do you diagnose rotavirus
PCR** - stool usually lacks WBCs, blood - Antigen detection test (EIA, latex aggulination, immunochromotography) - \
156
tx of rotavirus
no viral therapy available - treat/prevent dehydration - immunotherapy - probiotics
157
prevention of rotavirus
RotaTeq or Rotarix vaccines *No. infants and children needing hospitalization or emergency dept. care for rotavirus reduced by ~85%.
158
- Frequent cause of GE outbreaks - 10-50% of all outbreaks - 60%-90% of non-bacterial outbreaks - Important cause of sporadic GE - Outpatient and hospitalized - Affects all ages!!
norovirus
159
``` no envelope ssRNA extensive strain diversity distinct human and animal viruses family Caliciviridae ```
norovirus
160
what is the most common cause of diarrhea in adults
norovirus *2nd most common cause of diarrhea in young children (replacing rotavirus)
161
transmission of norovirus
- fecal-oral, water-borne, food-borne (shellfish) - contaminated environmental surfaces - airborne transmission (vomitus)
162
why does norovirus have high secondary attack rates?
- Prolonged shedding (up to 3-8 wks) - Low-infectious dose - Persistence (environmental surfaces, water, foods)
163
``` pathogenesis: Small intestine Villous BLUNTING PMN and mononuclear infiltrate Impaired enzymatic activity Malabsorption ```
norovirus
164
``` sx: ~1/3 asymptomatic nausea, vomiting, diarrhea, cramps, malaise, HA, myalgia, low grade fever *absence of respiratory symptoms dehydration Typically lasts 24-72 h, up to 8-14 d ```
norovirus
165
antibody repsonse to norovirus
repeated infections, Ab does not confer long lasting protection due to strain diversity and antigenic drift/shift
166
how do diagnose norovirus
usually clinical based on symptoms and epidemiology **PCR (electron microscopy was old gold standard) -stools lack WBCS, blood
167
tx of norovirus
- no antiviral available | - supportive care (fluid therapy, analgesia, antiemetics, bismuth subsalicylate and antimotility agents may decrease sx)
168
norovirus prevention
- Reduce potential for water/food contamination - Personal hygiene - Environmental decontamination - no vaccine yet (research in progress)
169
no envelope ds DNA fiber antigen
adenovirus
170
Determines serotype Mediates attachment Toxic to cells
fiber antigen for adenovirus
171
what causes: | URI, pharyngitis, conjunctivitis, pneumonia, hemorrhagic cystitis, GE
adenovirus
172
- 2-22% of pediatric GE (less than 4 yrs) - 15% of hospitalized GE - peak incidence = less than 2 yrs - no seasonality - incubation period 3-10 days
enteric adenovirus
173
transmission of adenovirus
fecal-oral/person-person
174
``` sx: Asymptomatic infections Watery diarrhea, then vomiting Low-grade fever Paucity of respiratory symptoms Lasts 5-12 days Less dehydration Reinfections can occur ```
enteric adenovirus *less dehydration than rotavirus
175
``` pathogenesis: Small intestine EPITHELIAL damage Villous impairment Malabsorption Electrolyte imbalance ```
enteric adenovirus
176
how do diagnose adenovirus
``` PCR** electron microscopy Antigen detection immunoassays DNA hybridization Difficult to grow in tissue culture ```
177
treatment of adenovirus
no antiviral available (Cidofovir under investigation in immunocompromised hosts) -fluid therapy
178
prevention of adenovirus
hygiene | no vaccine
179
what is the highest cause of death in children less than 5?
pneumonia
180
two important proteins for RSV? and why are they important
F and G | -major factors in virulence, allowing infection. And also the most important targets of the immune system
181
ssRNA, non-segmented F and G proteins A and B subtypes
RSV
182
Fusion of viral envelope to host cell | Fusion of membranes of infected cells to each other “syncytia”
F protein for RSV
183
what protein does the Initial binding of RSV to host cell
P protein
184
-Annual occurrence -occurs highest in winter-spring - Lives on surface for 1 hr 40-60% attack rate less than 2 yrs *most serious illness in very young, specific high-risk populations (premature, CHD, COPD, immunosuppressed, smoking, males)
RSV
185
transmission of RSV
LARGE particle DROPLET
186
tends to emerge earlier in Southern regions of USA | *In more temperate/tropical areas the seasonal effect is much less pronounced
RSV
187
pathophysiology: Invades conjunctiva / nasopharynx 3-5 day incubation period Constriction of smooth muscle in bronchioles Edema / inflammation of airway Ventilation / perfusion mismatch, hypoxia Hyperexpansion by mucous plugging
RSV
188
sx: | Respiratory distress, wheeze/rhonchi, hypoxia, copious secretions: *Bronchiolitis--> pneumonia
RSV
189
immune response for RSV
- Recurrent infections occur - Antibody protection incomplete - Local immunity important for upper airway - Role of cellular immunity unclear - IgE and wheezing
190
vaccine for RSV?
no, but monoclonal Ab (Palavizumab)
191
how to dx RSV
**PCR - cell culture (conventional, shell vial)--> Gold standard but takes a long time - direct antigen detection
192
RNA, Enveloped Genus: Orthomyxovirus Different stains?
Influenza A, B most important flu strains
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structural proteins for influenza
HA (Hemagglutinin) N (Neuraminidase) *HA and N proteins have tremendous capacity for change/mutation
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Negative strand RNA virus encoding 10 genes in 8 separate segments – thus allowing for reassortment. Responsible for yearly epidemics and rarely very severe pandemics (every 10-40 years).
Orthomyxoviruses
195
are irregular spherical particles, of 80 to 120 nm in diameter. Numerous hemagglutinin and neuraminidase “spikes” bristle from their surfaces, and eight other virus-coded proteins have been characterized.
Influenza
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the most abundant protein and the major structural component of the viral envelope of influenza
Matrix or membrane protein (M1)
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- tetrameric protein that acts as an ion channel extending through the viral envelope. - plays an important role in the penetration and release of influenza viral RNA into host cells
M2 of influenza
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__ is associated with the RNA genome of the virus in nucleoprotein complexes of influenza.
nucleoprotein (NP)
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___ are the largest proteins of the virus are designated as either basic (B) or acidic (A) proteins. All three are involved in the synthesis of virus-specific RNAs for influenza
Proteins PB2, PB1, and PA,
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Attachment of flu virus to host cell | - Penetration into cell (early infection)
HA protein *influenza
201
May aid in viral release from infected cell (late infection)
N protein *influenza
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Slight variation in the HA or N protein (ex. Bad response to flu vaccine last yr) -Epidemic strain
Antigenic Drift
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Major/complete antigenic change in the HA or N protein | -Pandemic strain
Antigenic Shift *change in host
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Pathophysiology: Enters through nasopharynx Spreads through epithelial cells down respiratory tract Denudes epithelium Host responds with macrophages, inflammatory mediators Bacterial superinfection
influenza
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how does influenza spread?
SMALL particle (cough, sneeze) *young children best transmitters
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Pediatric Influenza Hospitalizations Highest in
infants less than 6 months
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influenza immune response
- Humoral immunity (antibodies) confer protection to specific strains - Cellular immunity (T cells) may play a role in recovery
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vaccine for influenza?
yes (LAIV, 2-49) (IIV3/IIV4) - Need to be changed annually or biannually as strains drift - Routine influenza vaccination is recommended for all persons aged 6 months and older.
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how to dx influenza
*Multiplex PCR, also rapid flu PCR culture serology
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ssRNA, enveloped Genus: paramyxovirus -Major cause of respiratory illness in young children
parainfluenza
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Four (4) serotypes of parainfluenza virus
**Type 1: Frequent cause of croup (Laryngotracheobronchitis) in children Type 2: Similar to Type 1 but less severe disease Type 3: Important cause of bronchiolitis and pneumonia Type 4: Generally mild disease
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how is parainfluenza spread
``` person-to person LARGE droplets (like RSV) ```
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pathophysiology: Invades nasopharynx Spreads to involve larynx, trachea, bronchi (I, II) Pneumonia (III)
Parainfluenza
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what virus has hemagglutinin neuraminidase structural protein
parainfluenza
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Viral (usually RSV) with Cough, Wheezing and Rales
bronchiolitis *LR tract
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Viral (Usually Parainfluenza) with a Hoarse, Barky Cough and Stridor
croup *LR tract
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Bacterial (Less Often Now Due to H. Influenza vaccine) with Stridor, Fever and Toxicity
epiglottititis *Upper airway
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immune response to parainfluenza
-Recurrent infection may occur -Antibody protection incomplete Better to I, II than III -IgE, histamine release may play local role
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how to dx parainfluenza
**PCR culture
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RNA family: enterovirus more than 100 different subtypes (in 3 groups A, B, C)
rhinovirus
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reservoir of rhinovirus
humans only
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how is rhinovirus spread
aersol/SMALL droplets | *direct inoculation
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``` pathophysiology: -Spreads through local extension -Edema, Hyperemia (nose) -Complications: Otitis, sinusitis, exacerbation of RAD, bronchitis -Pneumonia is rare ```
Rhinovirus
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``` RNA, negative sense paramyxoviridae familiy Causative agent of respiratory tract disease/colds in humans Most children seropositive by age 5 Two genetic lineages ```
Human metapneumovirus (hMPV)
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what is the most common presentation of hMPV
bronchiolitis
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how to dx hMPV
PCR
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Suspected to have originated from masked palm civets-catlike, tree-dwelling animals whose meat is a delicacy in southern China
SARS
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``` pathology: Alveolar damage Hyaline membrane formation Pulmonary congestion Scanty mononuclear infiltrate ```
SARS
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- Multiple hospital outbreaks with transmission to HCW (similar to SARS) - Genomic Analysis: suggests multiple emergent events
MERS (Middle East Respiratory Syndrome)
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reservoir of MERS
unknown Bats, camels??
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In August 2014, _____ caused clusters of respiratory disease in the United States - presents very similar to asthma
 Enterovirus D68
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what are the common names of these influenzas: H5N1 H1N1 H7N9
H5N1- Avian influenza H1N1- pandemic swine flu H7N9- Avian influenza
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species-specific resistance to diseases of other species
natural immunity
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- individual response to exposure to antigen (infecting agent, vaccine)
active immunity
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AKAs of Measless
``` Measles Rubeola Hard measles Red measles 10 day measles ```
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ssRNA, negative sense one serotype paramyxovirdae family *closely related to canine distempter and rinderpest animal viruses
morbillivirus
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cell to cell fusion (syncytia formation and multinucleated giant cells)
Morbillivirus
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Spherical 150-300 nm in diameter Lipoprotein envelope F, H, M glycoproteins
Morbillivirus
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important in development of neutralizing antibodies for morbillivirus
H and M glycoproteins
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causes fusion with cell membrane; enhances cell-to-cell spread of the virus for morbillivirus
F glycoprotein
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hemagglutinin activity for morbillivirus
H glycoprotein
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matrix protein; important for viral assembly for morvillivirus
M glycoprotein
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``` pathogenesis: 0-2 days: respiratory spread 2-3 days: primary viremia 5-7 days: secondary viremia; symptoms 7-11 days: skin, mucous membranes; immune mediated rash (t cell response) ```
Measles *Morbovillivrus
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natural host of measles
humans
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measles immunology
- IgG Ab persists for life (protection against reinfection)
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measles vaccine?
yes, live attenuated MMR Two dose regimen: 12-15 mth; 4-12 yrs
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5 classic childhood exanthems
measles, rubella, roseola, Fifth's disease, chickenpox
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how to diagnose measles
clincial and PCR** | serology
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sx: Fever, erythematous maculo-papular rash (Koplik spots) [begins at hairline spreads caudad], cough, coryza, conjunctivitis
measles
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complications of measles
Otitis, pneumonia, croup, diarrhea, encephalitis
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tx of measles
-No specific antiviral therapy available -invitro susceptible to ribavirin Vitamin A- developing countries -immune globulin w/in 6 days of exposure
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vaccine for measles?
yes, live attenuated MMR
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aka of mumps
Parotitis | Epidemic parotitis
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ssRNA, neg sense paramyxovirus family genus: rubulavirus helical nucleocapsid*
Mumps
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proteins of mumps
Hemolysin, neuraminidase, hemagglutinin
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``` pathogenesis: Incubation 16-18 days Respiratory droplet transmission Multiplies in respiratory tract and exocrine glands (parotid gland) 30-40% of mumps may be asymptomatic ```
mumps
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transmission of mumps
respiratory droplets, saliva, urine, contaminated fomites
258
reservior of mumps
humans
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``` sx: Non-specific prodrome Fever, headache, myalgia, malaise, anorexia Respiratory symptoms in ~40-50% 30-40% of infections may be asymptomatic ```
mumps
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immunology of mumps
- Infection results in antibody and CMI - CMI responsible for recovery - Resistance to infection with IgG
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vaccine for mumps?
yes MMR
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complications with mumps
- orchitis w/ fever (males)- no sterility - Oophoritis (females) - Mastitis, pancreatitis, arthritis, myocarditis, thyroiditis, nephritis
263
tx of mumps
supportive
264
aka of rubella
German measles "light measles" 3 day measles
265
transmission of rubella
droples (humans only)
266
``` RNA, positive sense enveloped -Genus of Togaviridae -Spherical 50-60 nm diameter 3 polypeptides; E1-2, C on surface Fragile virus ```
Rubivirus
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host of rubivirus
humans only
268
pathogenesis: 0-6 days: virus in respiratory epithelium w/ spread to local nodes 6-20: viremia: spread to skin; maximum viremia from 10-17 days 17-22: virus content diminshed
rubella
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sx: Mild symptoms of slight fever, erythematous maculopapular rash, generalized lymphadenopathy (post auricular), transient joint symptoms
rubella
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dx of rubella
clinical, serology
271
tx of rubella
supportive
272
immunology of rubella
resistance to infection with IgG Ab
273
virus causes anomalies in developing fetus | Congenital malformations or fetal death may occur following inapparent maternal infection
rubella
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``` sx: Cataracts and other ocular defects Heart defects blueberry muffin Deafness Intrauterine growth retardation Failure to thrive Mortality within first year Microcephaly Intellectual disability Prolonged excretion of virus ```
CRS
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dx of CRS
ELISA
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``` "celery stalk" long bones Patent ductus arteriosus (PDA) A / V septal defects Purpura HSM Jaundice IDDM (late) ```
CRS
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what infections do parvovirus cause
``` Erythema infectiosum Fifths disease Aplastic crisis in chronic hemolytic anemias Gloves and Socks syndrome Fetal hydrops and death ```
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ssDNA | Naked icoashedral virus
parvovirus *Parvovirus B19 antigenically distinct from all other parvoviruses
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vaccine for rubella?
yes | *vaccine after exposure affords no protection
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what virus infects mitotically active erythroid precusor cells and eventually causes lysis by nuclear and cytoplasmic membrane degeneartion during replication
parvovirus
281
what virus has a side effect of anemia
parvovirus
282
transmission of parvovirus
respiratory and in blood
283
sx: characteristic sudden onset lacy rash on extremities and trunk and “slapped cheek” appearance Adults- arthritis
fifth disease *parvovirus
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infection of parvovirus in pregnancy causes
fetal hydrops
285
sx: | Papular purpura, pruritis, edema of hands and feet, oral lesions
gloves and socks
286
dx of parvovirus
clinical PCR serology
287
pathogenesis: incubation 4-14 days Respiratory entry; massive viremia; entry into RBC Symptoms 17-18 days later (immune mediated) IgM present during rash Crosses the placenta
parvovirus
288
immunology of parvovirus
Antibody probably results in recovery and resistance
289
tx of parvovirus
supportive care no vaccine
290
what family of virus causes rubella
Togaviridae