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Tropical Medicine > Viruses > Flashcards

Viruses Flashcards

1
Q

Hepatitis A transmission

A

fecal-oral route, potential sources of transmission and outbreaks -daycare, IVDU, travel

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2
Q

clinical manifestations of hep A

A

Incubation period: 14-28 days, prodromal phase 7 days, fever, malaise, anorexia, nausea, vomiting; Icteric phase: jaundice, scleral icterus, dark urine

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3
Q

Lab abnormalities in hep A

A

ALT>AST, Bili <10 but elevated. Usually ALT and AST elevate first and then the bili. Peak 1 month after the exposure

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4
Q

How to diagnose Hepatitis A

A

HAV in the stool avail 1 week after, the ALT will increase immediately, the IgM anti-HAV will increase at week 1, IgG will start to increase at Week 2
*IgM anti-HAV is to diagnose acute HAV infection

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5
Q

Prevention of Hep A

A

Vaccine: inactived HAV 2 dose vax (age>1year)
Or PEP: HAV vaccine/immunoglobulin after exposure within 2 weeks

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6
Q

4 genotypes of Hepatitis E that affect humans

A

HEV1, HEV2, HEV3, HEV4

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7
Q

Epidemiology of HEV1, 2, 3, 4

A

All in developing regions
HEV1 and 2-humans are the reservoir
HEV3 and HEV4-ANimals are the reservoir

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8
Q

Clinical Manifestations of Hep E

A

Incubation period: 2-6 weeks
Acute icteric hepatitis: occurs more frequently in HEV1 and 2 (usually about 2-6 weeks)
Extrahepatic manifestations: GBS, Neuralgic amyotrophy, encephalitis, myelitis
Renal: IgA nephropathy ,MPGN

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9
Q

Extrahepatic manifestations of Hepatitis E

A

GBS, neuralgic amyotrophy, encephalitis, myelitits
IgA nephropathy, MPGN, cryoglobulinemia

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10
Q

which Hep E type causes chronic infection

A

HE3 and 4 -usually immunocompromised, chronic hepatitis, fibrosis, cirrhosis

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11
Q

Diagnosis of HEV

A

-Acute: anti-HEV IgM or HEV RNA
-Chronic: IgG (several years) ; HEV RNA in serum>6 months

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12
Q

Treatment of HEV

A

ribavirin usually used for immunosuppressed

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13
Q

how do you prevent HEV

A

there is only a recombinant vax 3 dose series in china

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14
Q

epidemiology of hepatitis C genotypes

A

1: Most common, High/middle income countries
3: 25%, in south asia
4: 15% in Africa, middle east
2, 6, 5, 7, 8: not as common

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15
Q

transmission of HCV

A

Percutaneous exposure to blood, IVDU, needle stick, tattoos. Vertical or MSM less common

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16
Q

diagnosis of HCV

A

Anti-HCV Abs (12 weeks of infection); HCV RNA quantification/detection; HCV Core Antigen; genotype important for treatment

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17
Q

Priority groups for treatment chronic HCV infection

A

substantial fibrosis (F2 or F3), Cirrhosis (F4), liver transplant patients

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18
Q

how to treat HCV

A

Interferon free direct acting antiviral
(NS3/4 protease drugs (PREVIR)
(NSSA INhibitors (ASVIR))
(NSSB polymarse inhibitor (BUVIR))

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19
Q

Typical treatment regimen for HCV with or without cirrhosis

A

Sofosbuvir/velpatasvir 12 weeks

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20
Q

which 4 subtypes of influenza have caused most human disease

A

H1N1, H1N2, H2N2, H3N2

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21
Q

is influenza a or b worse in children

A

B

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22
Q

what things can you die from if you cannot make antibodies i.e. if you are agammaglobulinemic

A

-enterovirus
-s. pneumo, h influenza, n meningitis (encapsulated)
-Giardia

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23
Q

three types of anti-virals

A
  1. M2 ion channel blocker (amatidine, rimantidine)
  2. Neuroaminidase inhibitor (oseltamavir)
  3. Inhibition of polymerase acidic endonuclease (xofluza)
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24
Q

which influenza strain causes worse disease in the elderly

A

H3N2

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25
Q

what are the enteroviruses

A

polio, coxsackie, echovirus, enterovirus

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26
Q

how do enteroviruses enter body, what diseases do they cause

A

entry via aerosol or ingestion, replication in the oro-pharynx and in the peyers patches–>primary and secondary viremia–>
POLIO, Coxsackie–BRAIN
ECho, Polio, Cox–>Meningitis
Hep A–>Liver
Echo, Coxsackie–>SKIN (hand foot mouth)
echo, cox A and B–>Muscle (myocarditis, pericarditis, pleurodynia)

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27
Q

EV 68

A

rhinovirus, primary respiratory diseases (sometimes pneumonia, CN palsies, acute flaccid paralysis)

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28
Q

EV 71

A

aspetic meningitis, encephalitis including brainstem encephalitis, polio like syndrome

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29
Q
A

eczema coxsackie

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30
Q

what virus causes myocarditis

A

coxsackie B -causes cardiomyopathy

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31
Q

Treatment of Enteroviruses

A

Ribavirin, Amantidine, Pleconaril, IVIG

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32
Q

Transmission of polio, reservoir

A

Fecal-oral route; humans are the only reservoir
TYpe 1 is the main one

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33
Q

two polio vaccines

A

IPV-inactived (Salk)
Oral vaccine (Sabin)

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34
Q

OPV
IPV
VAPP
cVDPV
WT

A

Oral polio vaccine (sabin)
Inactived polio vaccine (Salk)
VAPP (Vaccine associated paralytic polio)
cVDPV -Circulating, vaccine-derived polio
WT-Wild type virus

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35
Q

VAPP

A

Vaccine associated paralytic polo (type 3)

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36
Q

what are the types of polio that are concerning

A

type 3-VAPP
But now Type 2-cVDPV

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37
Q

Clinical spectrum in a high resource setting of measles

A

diarrhea, otitis media, pneumonia, encephalomyelitis

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38
Q

immunocompromsed hosts with measles

A

progressive, giant cell encephalitis, pneumonitis

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39
Q

in low resource settings, what does measles look like

A

blindness (vitamin A deficiency), diarrhea, pneumonia

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40
Q

conjunctivitis, coryza, koplicks spots

A

measles

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41
Q
A

koplik spots

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42
Q

Measles treatment

A

normally, self limiting –>Vitamin A for 2 days
Immunocompromised-ribavirin , immune serum
neonates- immune serum

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43
Q

what protective/immunity factors in measles

A

Antibodies are good (a lot of IgG1-passed to the fetus)
Neutralizing antibodies
Early ADCC (Boys do this better-androgen)
Strong T cell immunity is critical

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44
Q

What is the measles vaccine

A

live attenuated vaccine

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45
Q

fever malaise partotitis orchitis

A

mumps

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46
Q

transient arthralgia, viremia, mild febrile illness with rash

A

rubella

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47
Q

what is the risk of rubella vaccine in post pubertal women

A

bad arthralgias

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48
Q

what are the Congenital rubella clinical sx

A

deafness, heart disease, CNS defect, neonatal purpura, cataract

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49
Q

if you don’t achieve 90% of rubella coverage, what happens

A

you will paradoxically increase the amount of the rubella because the women will be getting rubella at a later age (i.e. when they are child bearing age)

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50
Q

Natural history of Hepatitis B

A

1)Incubation: 4-7 weeks before HBV DNA and HBsAg become detectable
2) Acute HBV infxn: 1/3 of adults develop symptoms (fever, fatigue, malaise, abdominal pain)
3) Progression to Chronic HBV Infection

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51
Q

chronic HBV Infection definition

A

detection of HBsAg on 2 occasions measured 6 months apart

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52
Q

What are the common extrahepatic manifestations of Hep B

A

Renal: MGN, MPGN
Rheum: Polyarteritis Nodosa
Aplastic Anemia
Vasculitis

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53
Q

Positive HBsAg, Anti-HBs, Anti-HBc, HBV DNA detected positive

A

Infected with Hep B: cant tell if it is chronic or acute though; unless HBsAg>6 months

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54
Q

HBsAg negative, Anti-HBs Positive, Anti-HBc positive, HBV DNA not Detected

A

Resolved infection (the presence of HBsAg is no longer detected)

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55
Q

HBsAg negative, Anti-HBs Posivite, Anti-HBc, HBV DNA not detected

A

immunity-vaccination

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56
Q

if the core protein is isolated positive

A

false positive

57
Q

What is host immunity in Chronic HBV infection

A

the phase when HBV target and destroy infected liver cells; intermittent process (patients can transition between the phases)

58
Q

What are the phases of chronic HBV Infection

A

Immunotolerance, HBeAg positive immunoactive disease, HBeAg negative inactive disease, HBeAg-negative immunoreactive disease

59
Q

What is HBeAg

A

its a marker of high viral HBV

60
Q

What is the difference between perinatal infection labs and infection in adults labs HBV

A

ALT is normal in Perinatal infection, ALT is >2 times upper limit of normal when adult; You have none to mild inflammation of the liver histology when perinatal; asymptomatic and treatment is not indicated in perinatal

61
Q

Draw out the graph of HBV antigen concentrations and weeks after exposure

A
62
Q

What are the ways to assess liver damage with HBV in a non-invasive way

A
63
Q

What is the APRI cut off for cirrhosis? Fibrosis?

A

2.0 cirrhosis=METAVIR F4=Fibro Scan?11-14kPa
Fibrosis=1.5, METAVIR>F2=Fibroscan >7-8.5

64
Q

Patient with HBsAg, APRI >2. What do you do

A

Treat with tenofovir or entecavir

65
Q

45year old patient with HBsAg positive, ALT is elevated, HBV >20,000

A

Treat with tenofovir or entecavir

66
Q

50year old patient with HBsAg Positive , APRI<1.5, ALT normal

A

Defer treatment, monitor

67
Q

18 year old with HBsAg positive, ALT normal

A

Defer treatment and monitor

68
Q

What is theh monitoring for +HBV infection

A

Every 6 months, look for HCC; Every 12 months, check Labs and APRI or fibro scan

69
Q

What are the treatments for HBV in children

A

entecavir

70
Q

What are the treatments for HBV in Pregnancy

A

antiviral therapy to reduce the risk of perinatal transmission in HBsAg-positive pregnant women with an HBV DNA Level>200,000 IU/mL; TDF starting at 30-32 weeks, until 3 weeks pp

71
Q

What is the definition of virological cure

A

eradication of HBV DNA from Blood and liver, continued positive anti-HBc

72
Q

What is the definition of functional cure

A

HBsAg loss, undetectable levels of HBV DNA in peripheral blood

73
Q

What is the definition of Partial cure

A

Detectable HBsAG, Low <2000 to undetectable HBV DNA

74
Q

What is the vaccine schedule for Hep B

A

3 doses, first dose within 24 hours of birt

75
Q

How to transmit Hepatitis D

A

Perenteral transmission, Sexual Transmission, Intrafamilial transmission, perinatal transmission (very rare)

76
Q

Diagnosis of Hep D:

A

HDAg: Indicator of acute infection, short lived
HBsAg: Must be present for HDV Infectivity -correlates with HDV RNA
HDV RNA-Marker of HDV replication -positive in chronic infection, used for monitoring
Anti-HDV IgM: Acute infection
Anti-HDV IgG: Long term, even after the viral clearance

77
Q

What is the only drug that is properly studied in HDV

A

PEG-IFN alpha 48 weeks, If HCV, add ribavirin, if HBV, add tenofovir

78
Q

Genotypes of yellow fever and where are they located

A

IA West Africa,
IB South America,
II Central and East Africa

79
Q

Vector of yellow fever

A

aedes aegypti

80
Q

What is the incubation period of yellow fever and what is the clinical preentation?

A

3-6 days, asymptomatic (5-50%), 60-80%, hemorrhagic fever 5-10%

81
Q

Describe the 2 periods of yellow fever

A

3-6 days after bite–>fever with headache, conjunctival injection, bradycardia, leukenia and neutropenia.
for hte next 2-24 hours, you may feel better and have symptoms abate.
After 3-8 days: Headache, epigastric pain, vomiting, hypotension, shock, hemorrhage, thrombocytopenia

82
Q

What is the LFT pattern in yellow fever?
What about other labs?

A

AST>ALT
Wide range of WBC
Albuminuria
Transaminase elevation AST
Direct bili incr to 10 max
May have thrombocytoenia and prolonged PT/TT

83
Q

DDx of patients with fever, headache, LFT elevation from the jungle

A

Malaria
Hepatitis
Dengue
Yellow Fever
salmonella
Brucella
Hemorrhagic fevers (Typhoid)
Lepto

84
Q

How do you diagnose yellow fever?

A

Serology-IgM, IgG

85
Q

Pt visited forested area in sub-sarahan Africa, had an acute onset of fever, chills, myalgia, lumbosacral pain. Patient has gingival hemorrhage. Labs show AST>ALT. PT/PTT increased. On histology, councilman body found.

A

Yellow fever

86
Q

What are the vaccines in yellow fever?

A

live attenuated virus vaccine

87
Q

What is YEL-AND? When does it happen?

A

Yellow fever vaccine associated neurotropic disease, onset 11 days after vaccination (2-28 days) ; meningoencephalitis due to direct viral invasion of CNS

88
Q

Who experiences the most side effects from yellow fever vax?

A

Thymus disease, immunosuppression (but not AIDS),

89
Q

What is YEL-AVD?

A

yellow fever vaccine-associated neurotropic disease. after yellow fever vaccine, headache, malaise, myalgias, sometimes rhabdo

90
Q

Transmission of Mpox

A

Entry via broken skin, respiratory tract, mucous membranes (incubation period 7-10)-prairie dog

91
Q

what are the different clades of Mpox

A

Clade I: Central African Clade
Clade II: West African Clade

92
Q

what is the suspected case definition for Mpox

A

A person of any age presenting since 01/22 with an unexplained acute rash or one or more acute skin lesions AND
one of theh following-
HA, Fever, LAD, Myalgia, Back pain, Asthenia
AND
No explanation of the rash

93
Q

What is the definition of a probable Mpox infection

A

A person who meets the case definition for suspected cases (acute rash, lesions AND Ha, fever, LAd, myalgia, back pain, or asthenia) AND
has an epi link, direct physical contact with skin or skin lesions; has had multiple sexual partners 21 days before symptoms or has detectable levels or orthopoxvirus IgM antibody

94
Q

rapid Mpox diagnosis

A
95
Q

clinical presentation of Mpox

A

Incubation period 5-21 days, invasive phase (1-5 days) fever, flu like ililness, LAD, then the erruptive phase (macules–>papules–>vesicles–>pustules–>scabs)

96
Q

DDx of monkey pox like skin rash

A

Chickenpox, molluscum contangiosum, disseminated gonoccoal infection, Orf, enterovirus, measles, syphilis

97
Q

difference between monkeypox and chickenpox

A

biggest difference is the rash distribution (face/palms and soles in mpox) v. absent on palms and soles on chicken pox

98
Q

when can you end isolation in mpox

A

No new lesions x 48 hours/crusted over, avoid contact with immunosuppressed, pregnant; use condoms for 8 weeks

99
Q

complications of mpox

A

secondary bacterial infections, bronchopneumonia, sepsis, encephatitis, keratitis

100
Q

Infection control with mpox

A

negative pressure room, antichamber for donning and doffing

101
Q

Treatment of mpox

A

brincidofovir (FDA approved), DNA polymerase inhibitor (can cause transaminitis)/ Tecovrimat (emergency approved)

102
Q

What type of virus is Mpox

A

Orthopoxvirus: enveloped double stranded DNA virus that replicates in hte cytoplasm (large genome!)

103
Q

Which clade has higher mortality in mpox

A

Clade I -central African countries
Pregnancy complications

104
Q

LAD, rash on palms/soles, peripheral>central rash

A

Mpox

105
Q

Who has the highest rates of complications in Mpox

A

HIV CD4<100

106
Q

How do you diagnose Mpox

A

PCR swabbing of the lesions

107
Q

What are the VHF

A

zoonoses, enveloped RNA viruses, biosafety level 4

108
Q

30yoM from Sierra Leone (W Africa) who presents with fatigue, headache, joint paints, vomiting, nausea, diarrhea, abdomen pain. abdomen diffusely tender. No bleeding, no rash. Looks unwell

A

ssRNA zoonotic filovirus EBOLA

109
Q

What are the top strains of ebola

A

zaire, sudan, bundibugyo

110
Q

How do you get ebola? Incubation? Case fatality rate?

A

Human-to-human contact with bodily fluids, NOT aerosolized, not via mosquitos
Incubation period: 2-21 days
Case fatality rate 30-90%

111
Q

clinical features of ebola (case definition)

A

sudden onset fever, HA, vomiting, abdominal pain, diarrhea, anorexia, lethargy

112
Q

how to diagnose ebola

A

RT-PCR

113
Q

Treatment of ebola stages:

A

Stage1-Ha, fever, myalgia; tx analgesia, zinc
Stage 2: vomiting/nausea; Tx abx, PPI, IVF, antiemetic
Stage 3: Hiccups, seizures, hemorrhage, coma; Tx Vitamin K, TXA, FFP

114
Q

Ebola Zaire treatment

A

mAb 114 or REGN EB3

115
Q

Vaccines for ebola zaire

A

rVSV-EBOV (single dose)
Ad26-MVA-Filo

116
Q

what is clinically indistinguishable from Ebola

A

Marburg virus-no approved vaccines or treatment

117
Q

what type of virus is lassa? Reservoir lassa

A

arena virus-Reservoir: Mastomys Natalensis (rodent)

118
Q

transmission of lassa

A

spillover-contamination of food, water, environment, Dry season; incubation 3-21 days (human to human spread)

119
Q

patient from nigeria with sore throat, vomiting, high fever, facial swelling ; low plt, proteinuria, renal failure, AST>ALT; non-malarial disease

A

Lassa Virus

120
Q

What is a comlication of lassa

A

sensorineural hearing loss

121
Q

What is the treatment of lassa fever

A

ribavirin, favipiravir, mAb

122
Q

What is hantavirus

A

ssRNA virus, bunyavirus

123
Q

old world Hanta Virus

A

RENAL syndrome ; proteinuria, polyuric

124
Q

NEW world Hantavirus

A

cardiopulmonary syndrome: pulmonary edema, leaky syndrme

125
Q

Andes orthohantavirus

A

Patagonia, long tailed pygmy rice rat -peak in spring/summer, in Argentina and Chile

126
Q

Andes orthohantavirus incubation–>prodrome–>sx

A

9-40days; flu like, fever, headache –>severe sx respiratory compromise, pulmonary edema, encephalopathy

127
Q

patient who sacrified cattle and had a tick bite/crushing

A

Crimean-Congo Hemorrhagic Fever

128
Q

Vector of CCHF

A

Hyalomma tick

129
Q

Clinical course of CCHF

A

3-7 incubation
Pre-hemorrhagic period 7-14 days (myalgia, fever, nausea, vomiting)
Hemorrhagic period (15-16) bleeding, bruising

130
Q

Treatment of CCHF

A

ribavirin

131
Q

What kind of virus is Nipah Virus

A

Zoonotic, SS RNA, henipavirus (paramyxo)

132
Q

Reservoir of Nipah
Intermediate host

A

Pteropus bat–>eats the date palm sap
Intermediate host: Pig, Horse, (anmials)

133
Q

Clinical course Nipah

A

Acte-nonspecific fever, behavioral changes
Subacute/late onset: Encephalitis
Long term: relapse of encephalitis

134
Q

DDx of encephalitis in Asia

A

HSV, VZV, JEV, Dengue, Rabies
Rickettsia, T,
Cerebral malaria, Neurocysticercosis

135
Q

What kind of virus is rabies

A

lyssa

136
Q

Route of infection of rabies

A

Broken skin, intact mucosa –>virus binds to motor or sensory nerve ending

137
Q

CSF findings in rabies encephalomyelitis

A

pleocytosis, leukocytes <100, mononuclear, rabies virus +, rabies Ab, Negri Bodies

138
Q

What are the strategies for personal protection against rabies?

A
  1. Post exposure PPx (Bite, then get rabies immunoglobulin)
  2. Pre-exposure + post exposure (Pre-exp get the rabies vax, if you get bite, post exposure booster -no RIG, vaccine only)
139
Q

Treatment of wound after dog bite

A
  1. clean wound
  2. tetanus
  3. don’t suture
    4.PEP-vaccine Rig if dont have vaccine (4 dose IM over 21-28 days or 3 or 2 dose multisite ID over 7 days)

Tropical Medicine (19 decks)

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