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Viruses Flashcards

1
Q

What is good about ELISA?

A

Remember in low incidence setting most positives are false positives
Excellent sensitivity but more limited specificity
Technically simpler, automatable and objective readout

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2
Q

Western Blot Assay pros and cons?

A

Limited sensitivity but excellent specificity
Interpretation of results leads to subjective element
Often requires multiple bands to be positive

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3
Q

Antigen detection Assay pros and Cons?

A

Amenable to multiple point of care formats
Can be very robust
Element of subjectivity in reading result

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4
Q

PCR assays pros and cons?

A

Very good sensitivity and specificity
Assay can be over sensitive
Sampling error can occur
Needs sophisticated equipment
Isothermal amplification now possible

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5
Q

What is wrong with crude antigen tests?

A

False positive rates higher

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6
Q

Where do you need to test a specificity and sensitivity

A

In endemic areas
Negatives need to come from an endemic area

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7
Q

What does IgG 4 positive mean?

A

It means active disease
IgG

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8
Q

How long are you immune positive for following infection?

A

Antibodies last several years

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9
Q

When are you trichinella positive?

A

Not when you are symptomatic
Only have antibodies later on

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10
Q

Where is hep A and who is infected?

A

It’s worldwide, more common in LMIC
In LMIC most children >90% have been infected before the age of 10

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11
Q

How is hep A transmitted?

A

Faecal-oral, contaminated food or water
Person to person contact

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12
Q

How does hep A present in adults? Phases

A

Incubate 14-28 days
Prodromal phase lasts 7 days and includes fever, malaise, anorexia, nausea, vomiting and abdo pain
Icteric Phase: Jaundice, clerical icterus, dark urine and pale stools

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13
Q

How does hep A present in children?

A

Usually asymptomatic

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14
Q

Lab abnormalities in hep A?

A

Elevation of ALT>AST (>1000)
Elevation of serum bilirubin and ALP (Up to 400)
ALT and AST rise precedes bilirubin elevation and peaks 1 month after exposure
Hyperbilirubinaemia peaks 7-10 days

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15
Q

What is the general clinical course of hep A?

A

Usually self-limiting
Rarely causes chronic disease

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16
Q

What are the unusual cx of hep A?

A

Acute hepatic failure
Relapsing hepatitis
Prolonged cholestasis
Autoimmune hepatitis

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17
Q

What are some of the extra-hepatic manifestations?

A

Arthralgias, arthritis, Rash, immune complex disease

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18
Q

What antibody becomes positive first?

A

IgM, lasts several weeks or months
IgG increases later, but provides lifelong protection

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19
Q

How do you diagnose Hep A?

A

Acute infection: IgM anti-HAV
Total anti HAV antibodies measures both IgG and IgM, therefore cannot tell difference between acute and chronic

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20
Q

What is treatment and prevention of hep A?

A

Supportive therapy for tx
Vaccine for prevention: Inactivated HAV, 2 doses
A live attenuated vaccine which is 1 dose is available in some countries

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21
Q

What do you do for post-exposure prophylaxsis of hep A?

A

HAV vaccine or immunoglobulin within 2 weeks of exposure

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22
Q

How many genotypes of HEV?

A

4 genotypes that affect humans (HEV1-HEV4)

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23
Q

Where is HEV1 and HEV2 found?

A

LMIC such as Africa and Asia, some outbreaks in Mexico

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24
Q

Where is HEV3 and HEV4 found?

A

More higher income countries, China especially

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25
What is reservoir for HEV1 and 2 vs HEV3 and HEV4?
Humans for HEV1 and 2 Mainly swines in HEV3 and HEV4
26
What is tx of HEV1 and HEV2?
Contamination of drinking water supplies with human faeces Iatrogenic
27
What is tx of HEV3 and HEV4?
Consumption of contaminated animal meat or contact with infected animals Iatrogenic
28
How is HEV transmitted?
Large waterborne transmission with HEV-1 and HEV-2 Zoonotic transmission of HEV 3 and HEV 4
29
What are the clinical manifestations of hep E?
Incubate for 2-6 weeks Get Acute Icteric hepatitis: occurs in 5-30% of cases, more commonly assoc with HEV1 and 2 lasts 2-6 weeks, Prodromal phase of 7 days
30
What are the extra-hepatic manifestations of hep E?
GBS, encephalitis and myelitis Renal cx such as IgA nephropathy, membranoproliferative glomerulonephritis, cryglobulinaemia
31
What is the clinical course of Hep E?
In immunocompetent patients HEV usually resolves spontaneously Chronic infection occurs more common with HEV 3 and HEV4, this is mainly in immunocompromised patients Pregnant women get higher risk of symptomatic disease and acute liver failure with HEV1 and HEV2
32
How do you Dx acute hep E? chronic hep E?
Detection of anti-HEV IgM Chronic HEV infection- detect HEV RNA in serum
33
Tx of Hep E?
Most immunocompetent individuals do not require antivirals Ribavirin can lead to faster recovery times but is CI in pregnancy
34
How do you prevent hep E?
Boil and chlorinate water Heat food >2 mins Screen blood banks Recombinant vaccine only available in China
35
What genotype os responsible for most HCV infections?
Genotype 1 accounts for 44% of all HCV infections Genotype 3: More common in LMIC especially south Asia Genotype 4: North Africa and Middle East
36
How is HCV transmitted?
Medical procedures Tattoing IVDU Needlstick injuries Mother to child and sexual transmission is possible, HIV infection increases risk of HCV transmission
37
What is the acute course of HCV?
Not typically clinically apparent Fulminant hepatitis is rare
38
How does chronic HCV present?
Majority of patients develop chronic hep C (75-80%) DEtect HCV RNA after 12 weeks Common symptoms are fatigue, weight loss and joint pains, RUQ discomfort 75% develop extra-hepatic manifestations
39
Some examples of extra-hepatic hep c?
Vasculitis T2DM Thyroid disease Eye disease
40
How do you Dx HCV?
Anti-HCV antibodies emerge within 12 weeks of infection HCV RNA detects early and chronic infection
41
What do you check if positive anti HCV antibodies?
detect HCV RNA Diagnosed with chronic heo C if HCV RNA remains positive for 6 months
42
Tx of HCV? Who are priority groups
Interferon free DAA are the first line therapy All adults with acute or chronic HCV Priority groups: substantial fibrosis, cirrhosis, high risk populations, patients with extra hepatic manifestations, liver transplant patients
43
What is defined as cure from Hep C?
Sustained virologic response at 12 weeks after end of therapy
44
What do you need to assess for before starting tx in Hep C?
Assess for liver fibrosis with non-invasive testing
45
What is tx in patients without cirrhosis vs cirrhosis?
Without cirrhosis: sofosbuvir/velapastir usually 12 weeks or sofosbuvir/daclatsavir 12 weeks With cirrhosis: sofostbuvir/daclatsavir 24 weeks
46
What are the major forms of influenza that infect humans?
Two major types-- A and B
47
What are the main reservoirs of A type of influenza?
Ducks, pigs, cats, whales
48
genetic drift vs shit?
Genetic drift-- the more immunity in the community, the faster the mutation of the virus Genetic shift-- from zoonotic to humans
49
What four subtypes of influenza cause disease?
H1N1 H1N2 H2N2 H3N2 Usually only one type circulates actively
50
What flu viruses are worst in young children?
B viruses
51
Where does influenza morbitidy and mortality shows periodicity?
In temperate regions, not tropical!
52
What are some of the rare complications of influenza?
Viral Pneumonia and ARDs Encephalopathy Pericarditis Rhabdomyolysis GBS
53
Who is presentation of flu not obvious in?
Typically older people do not develop a fever Infants often present with GI symptoms
54
What diseases coincide with peak of influenza?
IHD Diabetes Stroke
55
How does influenza link to strep Pneumoniae?
Strips the cilia on the epithelium Much worse infection with S Pneumoniae
56
What do you need antibodies to protect from?
Enteroviruses Pneumococcus Meningococcus Giardia
57
What are the classes of antivirals?
1) M2 ion channel blockers such as amatidine and rimantidinie. Need to start fast, but high levels of resistance, resitant to one, will be resitant to the other. Significant toxicity, especially in elderly. 2) Neuroaminidase inhibitors, do not get class resistant. Such as oseltamavir. 3) Polymerase acidic endonuclease drugs such as baloxavir
58
What are most vaccines based on? Other than live attenuated
A haemoglutination response
59
What are some of the issues with egg based vaccines?
Delays in adapting strains to eggs Issues with scale up in the event of pandemic Side effects such as GBS Can probably give vaccines to kids that are allergic to eggs
60
Which vaccines work best in which groups of people?
LAIV work best in healthy young adults Split vaccines work least well in elderly
61
What does finding HBsAg and HBeAg mean in serology?
Highly virulent
62
What is the clinical picture of HBV?
Only small % develop clinical symptoms acutely which is just general hepatitis picture
63
Who is at highest risk of chronic hep B?
90% of infants <1yr
64
How is chronic hep B defined?
Presence of HBsAg on 2 occasions measured at 6 months apart
65
What is the risk of chronic hep B?
25% will go on to develop cirrhosis Of these, some will go on to develop HCC Some people directly develop HCC without cirrhosis
66
Interpret these results: HBsAg positive Anti HBs negative Anti HBC positive HBV DNA detected
Hepatitis B infection is HBsAg present for more than 6 months, then this is chronic In acute infection Anti HBc is in the form IgM
67
What is the window period of hep B?
24-30 weeks HBsAg and anti HBsAg is negative Only thing that is positive is Anti HBc IgM
68
What is APRI? what is the cut off for cirrhosis?
Aspartate amino transferase to platelet ratio index If More than 2 means cirrhosis
69
Who do you treat for Hep B?
If cirrhosis present, treat ALL patients and treat lifelong If cirrhosis not present, take into account age- older than 30? Look at ALT and HBV DNA
70
Who can you stop tx in Hep B in?
Patients who have been on therapy for a year If LFTs normal, viral load undetectable and HBeAg converted to anti-HBe
71
Tx of Hep B?
Tenofovir or Entecavir For kids entecavir Alternative is Pegylated interferon for 1yr, but SE profile include bone marrow toxicity
72
How do you tx pregnant women with Hep B?
Tenofovir recommended at 30-32 weeks until 3 months post partum to reduce risk of VT Recommended in women with HBV DNA>20,000 C-Section not recommended
73
What is defined as cure?
Virologic cure: • Eradication of HBV DNA from blood and liver • Continued positive anti-HBc with or without anti-HBs • Unattainable at present Functional cure: • HBsAg loss • Undetectable levels of HBV DNA in peripheral blood • Sustained indefinitely after a finite course of therapy Partial cure: • Detectable HBsAg • Low (<2000 IU/mL) to undetectable level of HBV DNA • Maintained indefinitely after treatment is stopped
74
How do you prevent Hep B? What is acquired immunity defined as?
Recombinant vaccine 3 dose series Administer first dose within 24hrs of birth Acquired immunity is individuals with anti-HBs levels >10
75
Why does hep D coinfect with Hep B?
It has to envelope itself with Hep B surface antigen Hep D has no envelope and no enzymes itself
76
What is the most frequent route of transmission of hep D?
Is parenteral typically IVDU
77
How does Hep D infect someone?
Either at the exact same time as Hep B, cotransmission Typically this will present with more acute infection as have 2 viruses Or.. it can superinfect in someone with chronic hep B This makes progression towards cirrhosis and flares much more aggressive It seems to suppress hep B so viral load goes down, but it takes over causing cirrhosis etc
78
How do you Dx Hep D?
HBsAg must be present HDV RNA is a marker of replication, used for monitoring treatment Anti HDV IgM is present in acute infection then become IgG
79
Tx for Hep D?
Pegylated Interferon for at least 48weeks TDF not recommended
80
What is the indication for treatment of hep D?
Persistent HDV replication
81
Clinical picture of Yellow Fever
15% of people develop severe disease which is jaundice, bleeding, hepatomegaly Epistaxsis, coffee ground vomitus Proteinuria
82
What are lab results of Yellow fever?
Albuminuria Transaminase Elevation
83
When is the highest RPR seen in syphillis?
In secondary syphillis, can be subject to prozone phenomenon causing RPR negative
84
What is luese maligna?
Severe Rash seen in malignant syphilis
85
Stages and natural course of syphillis? Stages
Primary: Get exposed, about 10 days to 3 weeks develop chancre. Not everyone develops a chancre or is a very dismissable lesion. Secondary: 3weeks to 3 months later see secondary syphillis which is Rash fever, neuro symptoms Latent: This stage is asymptomatic. Can be early latent if <1yr Tertiary: Gumma (Granulomatous response to treponema), bones, cardiac, nerve disease It is unclear how many people go on to develop tertiary syphillis
86
Primary Stage of syphillis clinical manifestation?
Classical chancre, heaped up border with clean base, not necrotic or purulent PAINLESS RPR is positive in 70% of cases Cannot be distinguished from herpes clinically Direct inoculation can happen anywhere eg mouth or fingers Very difficult to diagnose in females as is Painless so will typically be unaware lesion present
87
What is clinically

GORGAS (33 decks)

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