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DTM&H 2024 > Virus > Flashcards

Virus Flashcards

1
Q

Alphavirus Example

A

EEE, WEE, Venezuelan EE, RRV, Chikungunya

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2
Q

Flavivirus Example

A

Dengue, Zika, JEV, MVE, West Nile, Yellow Fever, St Louis Encephalitis

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3
Q

Bunyavirus Example

A

California encephalitis, La Crosse, Rift Valley Fever

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4
Q

Rabies Transmission

A

Terrestrial mammals (99% dogs), Bats (Americas only), rare reports of tissue/organ transplant

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5
Q

Rabies Virology

A

Bullet-shaped RNA wrapped in five proteins - matrix, envelope, nucleo, phospho and RNA polymerase

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6
Q

Rabies Pathogenesis

A

Exposure -> centripetal retrograde axonal transport to brain along motor neurons, evades immune surveillance > CNS transynaptic spread, replication, inclusion (Negri) body formation, neurons intact but dysfunctional > centrifugal neuronal transport to salivary glands (viral excretion) carried to skin, heart, muscle tongue, but no viraemia

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7
Q

Rabies Natural history

A

Once clinical signs evident, there is no treatment or survival

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8
Q

Rabies Deaths per annum

A

60,000 (21,000 India)

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9
Q

Rabies Furious rabies

A

80% cases - brain stem, cranial nerves, limbic system higher centres

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10
Q

Rabies Paralytic rabies

A

20% cases - medulla, spinal cord, spinal nerves

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11
Q

Rabies Prodromal symptom

A

Pruritus

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12
Q

Rabies Clinical furious

A

Phases of arousal and lucid, CN II, VII, VIII, autonomic stimulation, arrhythmia, priapism, survive <7d

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13
Q

Rabies Hydrophobic spasm

A

Provoked by drinking > Inspiratory spasm, becomes more severe, can cause oesophageal tears and pneumothorax

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14
Q

Rabies Clinical paralytic

A

Ascending paralysis (?GBS) loss of reflexes, bulbar sx, survive <30d

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15
Q

Rabies Differential diagnosis

A

Post-vaccinal, paralytic polio, Flavivirus, Herpes B virus

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16
Q

Rabies Clinical care

A

Palliative, barrier nursing (low evidence, but improves anxiety), vaccination of staff and household, inform public health authorities

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17
Q

Rabies Diagnosis

A

Nuchal biopsy - immunofluorescence rabies Ag on innervation of hair follicle; saliva PCR (variably released); viral tissue culture; brain biopsy Negri bodies (inclusion in cytoplasm of Purkinje cells)

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18
Q

Rabies Treatment

A

Only if American bat virus, early Ab response, ICU available - Milwaukee protocol discredited

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19
Q

Rabies Pre-exposure vaccination

A

Endemic area, rabies lab worker, endemic animal handlers, travellers to dog rabies enzootic areas (esp children), HCW looking after rabies pt - at least 2 (WHO) ideally 3 (UK) vaccines

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20
Q

Rabies Vaccine administration

A

IM deltoid (NOT gluteal), intradermal improves availability, accessibility and affordability in LMIC

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21
Q

Rabies Post-exposure management

A

Cat 2+ Scrub with soap and water 15min, avoid suturing, give vaccine x2 (RIG and vax x4 if cat 3 AND unvaccinated)

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22
Q

Rabies Category 1 exposure

A

Touching or feeding animals. Licks intact skin, includes drinking milk from rabid cow

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23
Q

Rabies Category 2 exposure

A

Nibbling of uncovered skin, minor scratches or abrasions without bleeding, treat as cat 3 if bat exposure, bites on head/neck/face/hands/genitals (highly innervated) - stop Rx if animal well after 10d/proven negative

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24
Q

Rabies Category 3 exposure

A

Single or multiple transdermal bites/scratches, contamination of mucous membranes or broken skin with saliva, exposures due to bats, includes raw meat of rabid animal - stop Rx if animal well after 10d/proven negative

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25
Q

Rabies Immunosuppressed

A

PrEP x3, Ab response 2-4w later, PEP x5 and RIG for cat 2+

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26
Q

Rabies Prevention

A

Mass dog vaccination (IM or oral), educate children, vigorous washing of all bites, vaccination

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27
Q

Rabies PEP

A

RIG up to 1y after, but not if vax given >7d ago

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28
Q

JEV Outcome

A

1/3 die 1/3-1/2 longterm disability

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29
Q

JEV Epidemiology

A

Asia/Pacific. Main cause of viral encephalitis in Asia >3 billion people at risk

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30
Q

JEV Transmission

A

Arbovirus, Culex

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31
Q

JEV Amplifying host

A

Pigs, Water birds also involved, vaccination will not eradicate due to animal reservoir

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32
Q

JEV Symptoms

A

> 99% asymptomatic, acute meningoencephalitis syndrome with seizures, Parkinsonism (basal ganglia predilection) - CFR 30% in encephalitis

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33
Q

JEV Diagnosis

A

Gold standard seroneutralisation - paired, and not available outside large reference centres, ELISA available poor spec in serum, also perform on CSF

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34
Q

JEV Vaccination

A

Ixiaro (UK - inactivated), Imojev (Aus - live chimeric). WHO recommended strategy in endemic setting: one-time campaign in the primary target population as defined by local epidemiology (typically children <15), followed by incorporation of JE vaccine into routine immunisation program. WHO recommended strategy in travellers: JE vaccination is recommended for travellers to endemic areas with extensive outdoor exposure during the transmission season

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35
Q

HPV WHO 2030 Targets

A

90% fully vaccinated by 15y, 70% women screened by 35-45, 90% CaCx receive treatment and care

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36
Q

HPV Genotype

A

CaCx 16/18, Anogenital warts 6/11

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37
Q

HPV Epidemiology

A

Most infections will clear within 8m

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38
Q

HPV Ab response

A

50% women develop no measurable Ab response following infection

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39
Q

HPV HIV co-infection

A

Increase CaCx x6, Anal cancer x10, increased anogenital warts, HPV is RF for HIV acquisition, HIV decreases HPV clearance

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40
Q

HPV CaCx diagnosis

A

Visual inspection (VIA) and HPV diagnostics have lower sens/spec in WLHIV compared with general population

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41
Q

HPV WHO HPV screening

A

General HPV DNA from 30 every 5-10y; WLHIV HPV DNA from 25 every 3-5y

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42
Q

HPV WHO Vaccine recommendation

A

2 doses from 9yo, option for 1-dose 9-20yo - aim before sexual debut

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43
Q

Dengue Epidemiology

A

40-50% world population at risk, 70% cases in Asia, most abundant vector-borne viral disease globally, steadily increasing burden with urbanisation and climate change (increasing and longer wet seasons) Explosive outbreaks in Sth America not predictable and can cripple healthcare systems, mortality increases when healthcare systems compromised. Mortality relatively low, morbidity through economic and health burden is significant with lost productivity in young fit healthy workers

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44
Q

Dengue Vector

A

Aedes aegypti (violin white markings) feed off multiple people in a day, do not fly far, Aedes albopictus (white line) forest mosquito adapted to urban environment, spread from Asia in used-tyre trade, eggs can withstand desiccation, hatch when rains

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45
Q

Dengue Virology

A

DENV ssRNA flavivirus, 4 serotypes, 3 structural proteins (C M E), 7 non-structural proteins (NS)

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46
Q

Dengue Clinical presentation

A

Incubate 5-7d, ~75% asymptomatic, ‘break bone fever’ Fever, retroorbital headache, maculopapular rashes, myalgia, joint pain, only a quarter of those infected have symptoms

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47
Q

Dengue Rash

A

Petechiae acute, islands of white in a sea of red recovery

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48
Q

Dengue Disease phases

A

Febrile, Critical, Recovery. Febrile is high viraemia, start of inflammatory host response (high fever, severe myalgias) vast majority go to recovery phase, some however to Critical where capillary leakage occurs, days 4-6 with maximal host inflammatory response, risk for shock, bleeding, organ impairment, and recovery phase usually >d7 where host inflammatory response resolves

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49
Q

Dengue Warning signs

A

Abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleed, lethargy/restlessness, liver enlargement >2cm, increase HCT with concurrent rapid decrease in Plt

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50
Q

Dengue Severe dengue

A

Plasma leakage, haemorrhage, organ impairment AST or ALT >=1000, CNS impaired consciousness, heart/other organ impairment

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51
Q

Dengue Tourniquet test

A

Take blood pressure, inflate cuff again to midway between sBP and dBP, maintain 5min, deflate, wait 2min, count petechiae at antecubital fossa, likely dengue >=10 petechiae

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52
Q

Dengue Probable dengue

A

Epi risk, fever and 2 of: N&V, rash, aches/pains, tourniquet test positive, leukopaenia, any warning sign

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53
Q

Dengue Host risk factors for severe disease

A

Pregnant, Comorbidities esp DM & uncontrolled HTN, >60, over and undernutrition

54
Q

Dengue Viral factors for severe disease

A

DENV2, high viral load

55
Q

Dengue Host immune response for severe disease

A
56
Q

Dengue Adaptive humoral immune response

A

Primary infection usually non-severe, invokes homotypic (long-lasting) and heterotypic immunity (wanes after 1-2y). Strong association between secondary infection with heterotypic serotype and severe disease. Infants of dengue immune mothers at greater risk for severe disease during first year (while maternal Ab waning)

57
Q

Dengue Antibody dependent enhancement

A

Heterotypic non-neutralising IgG from previous dengue binds to dengue virus, recognised by Fcg receptor on macrophage/monocyte -> massively increased uptake and replication -> increased viral load -> enhanced immunopathogenic cascade (cytokine release) - the secondary infection causes expansion of the T cells with low avidity, this fails to obtain viral control, but with high cytokine production and excess proinflammatory cytokines causes severe clinical phenotype of tissue damage and vascular leakage. Hyperinflammation is self-fulfilling upregulated macrophage activity similar to HLH, adds weight to consideration of immunomodulation as future treatment options (JAK1/2 bari, IL-6 toci) +/- N-AC to minimise liver damage

58
Q

Dengue Plasma leak

A

Breakdown of glycocalyx structure, disruption of osmotic barrier, exposes adhesion molecules and activation of endothelial cells with leakage of protein-rich fluid through paracellular gaps, this result sin extravascular fluid accumulation (hypovolaemia, shock, pulmonary oedema, pleural effusions)

59
Q

Dengue Thrombocytopaenia cause

A

Multifactorial: bone marrow suppression, platelet dysfunction, peripheral destruction (immune clearance of Ab coated Plt, complement-mediated plt lysis, plt consumption by DIC, plt apoptosis) - plt transfusion not indicated unless bleeding. Nadir usually d4-6

60
Q

Dengue Diagnosis

A

1st week PCR or NS1Ag, 2nd week IgM, RDT often combine NS1 and Ab testing

61
Q

Dengue Febrile phase management

A

Supportive Clinical: look for warning signs, Lab: monitor Hb/HCT & Plt, AST & ALT, US: to identify early fluid accumulation from plasma leakage, including GB wall thickening, ascites and pleural effusions

62
Q

Dengue Critical phase management

A

Clinical: haemodynamic Ax, clammy, tachycardia, narrow PP precede hypotensive shock, assess fluid & mucosal bleeding, Lab: rising HCT suggests significant plasma leakage, coagulopathy shows prolonged APTT and low fibrinogen with normal PT, US to assess serosal fluid accumulation, TTE to assess cardiac function in fluid refractory shock or if myocarditis suspected

63
Q

Dengue Recovery phase management

A

Clinical: significant risk of fluid overload if IV fluids continued, Lab: most lab parameters normalise, Hb may fall temporarily below baseline as extravasated fluid is reabsorbed, ALT & AST gradually normalise by often lag, Bradyarrhythmias may occur but are usually benign

64
Q

Dengue Treatment

A

Supportive, no antiviral or adjunctive therapies have shown benefit, meticulous fluid balance, oral paracetamol (avoid NSAIDs). Dengue-specific/host directed treatment awaited

65
Q

Dengue Vaccine

A

Dengvaxia efficacious and safe in seropositive persons 72-80% against dengue, >90% against severe dengue. Dengvaxia increases risk of severe dengue in seronegative persons RR2-3 -> Ab dependent enhancement, overall population level benefit favourable but huge loss of vaccine confidence, Qdenga in pipeline no safety concerns in seronegative

66
Q

Dengue Vector control

A

Environmental management: elimination of containers (piped water systems, mosquito-proofing water storage, disposal of waste), Chemical control with larvicides, insecticides, indoor residual spraying, biological control (Wolbachia)

67
Q

Dengue Wolbachia

A

Intracellular bacteria, introduced to Aedes can reduce dengue transmission

68
Q

Arbovirus Definition & key concepts

A

Arthropod borne virus. Resurgence of arbovirus due to urbanisation, climate change, increased population mobility. Most of the diseases have high asymptomatic rate and short incubation time. Difficult diagnostics with short-lived PCR positivity and high serological cross-reactivity among flavivirus. No specific treatment drugs available. Difficult vector control. Need for more research into therapeutics and vaccines

69
Q

VHF Family

A

Filoviridae -Ebola (Zaire, Sudan, Bundibugyo, Tai Forest) and Marburg, Arenaviridae - Lassa, Nairoviridae - Crimean-congo haemorrhagic fever

70
Q

VHF Burden of disease

A

~36,000 cases per year, not all lab confirmed, likely significantly underestimated

71
Q

VHF Transmission zoonotic

A

Initial trigger almost always zoonotic - spillover to humans (animal/vector and human overlap) - unpredictable combination of factors - shedding patterns, land use, human-vector interface. Exception is human reservoirs where viable virus persists in survivors after recovery (ie Ebola sexual transmission).

72
Q

VHF Transmission person to person

A

Person-to-person transmission drives outbreaks. R0 estimates 1.34-4.7. Direct contact with contaminated body fluids or objects through broken skin or mucous membranes. High potential for exposure in households due to caring practices and late presentation to healthcare due to fear. Super-spreading events: funeral ceremonies, markets, cultural obligations. Increased population movement: shift into more dense urban environments changes exposure risk. Nosocomial transmission due to poor IPC - pregnancy is very high risk, undetected cases, slow diagnosis of suspect cases. Ongoing exposure to a common zoonotic transmitter can resemble person-to-person spread (eg Lassa with ongoing exposure to same rodent)

73
Q

VHF Spectrum of illness

A

Asymptomatic Ebola 3-6%, CCF 70% Lassa 80%, Marburg unknown. Difficulty identifying due to non-specific common symptoms and case definition. Asymptomatic are unlikely to transmit due to lack of body fluids and low viral load. Pauci-symptomatic transmission potential may depend on type of symptoms (dry vs wet). Symptomatic - extent of exposure to a symptomatic case and whether that case is dry or wet is strongly associated with risk of infection. Ebola - many contacts with high exposure do not become infected

74
Q

VHF Prevention and control

A

Prevention of VHF outbreaks is difficult due to unpredictability of spillover, challenging control of hosts. Curtailing onward transmission in humans is feasible: interventions to achieve shorter, less severe outbreaks. Critical foundation is community confidence and involvement

75
Q

VHF Epidemiology of interventions

A

Reduce exposure, break transmission, speed care for infected, reduce severity and fatality. Active case detection (reduce delay from onset to isolation, speed care provision), earlier and more rapid isolation and care (improve outcome, reduce exposure), triage and suspect management (avert undetected cases in routine services, also confidence in safety in healthcare setting), faster more frequent testing (reduce time to care, better management of suspect and quarantine), IPC healthcare facilities (prevent transmission, avert amplification), IPC household (human and animal - prevent/reduce exposure), IPC community (adapt public health measures - avert exposure), contact tracing (early detection, break transmission), quarantine (reduce time to detection, reduce unwitting transmission but risk of opposite effect). Community collaboration is essential

76
Q

VHF Community engagement

A

Engaging with the sociocultural dimensions of epidemics is critical to mounting an effective outbreak response - take the time to establish trust (despite feeling the need to ‘save time’, failing to engage community is likely to have the reverse effect) “If the community are kept outside, they will not come inside for treatment”

77
Q

VHF Key points

A

Global burden of VHF is likely underestimated and transmission missed. Zoonotic spillover is unpredictable and hard to prevent. Curtailing human-human transmission and transmission at the human-animal interface is feasible and more effective if communities are involved at a deeper more functional level from the beginning. Outbreak response interventions aim to break transmission through reducing exposure using IPC, earlier detection, diagnosis, isolation and treatment to achieve shorter, less severe outbreaks. Forethought, preparedness, organisation is important. One size does not fit all and adaptation by, and integration of, affected populations are critical to successful outbreak control.

78
Q

Ebola Epidemiology

A

> 20 Ebola outbreaks since 1976 >33,000 infections, >15,000 deaths. CFR EBOV 40-80%, SUDV 40-55%, BDBV 35-40%, TAFV 0%

79
Q

Ebola West Africa

A

Post conflict environment, porous borders, no institutional memory of Ebola (HCW initially not trained to respond and protect themselves, community resistance to the Ebola outbreak response). Multiple factors leading to severe consequences: magnitude of outbreak, multiplication of foci and need for multiple ETCs, delayed community response, care delays, burial practices, high number of HCWs infected

80
Q

Ebola Virology

A

ssRNA virus, NP and GP are targets for PCR and vaccines. Lipid envelope easily destroyed by soap, chlorine, UV light. Incubation 2-21d

81
Q

Ebola Pathogenesis

A

Virus infects dendritic cell, travels throughout body, immune system dysregulation -> death of lymphocytes and excessive cytokine release -> Circulatory system (capillary leakage and third spacing, coagulopathy, endothelium damage, low BP). Multiple organ dysfunction: Brain (encephalopathy), Liver (hepatocyte injury or dysfunction -> raised ALT/AST, reduced clotting factors, hypoalbuminaemia, hypoglycaemia), GIT (vomiting and diarrhoea -> fluid and electrolyte imbalance, disrupted acid base), spleen (cytokine dysregulation, death of lymphocytes), kidney (AKI, fluid electrolyte and acid-base derangement), skeletal muscle (injury with elevated CK)

82
Q

Ebola Differential diagnosis

A

Clinical manifestations are non-specific. Consider malaria, typhoid, diarrhoeal diseases (Shigella, Cholera), Rickettsioses, other VHFs

83
Q

Ebola Phases of illness

A

Early (fever, asthenia, headache, myalgia, arthralgia, anorexia)- > GI (diarrhoea, emesis) >Terminal (fever and GI Sx subside, confusion and delirium worsen -> comatose, olig/anuric, death either gradual or sudden from arrhythmia)

84
Q

Ebola Longterm sequelae

A

Neurologic (headache, seizures, peripheral neuropathy), Ophthal (intraocular inflammation), MSK (arthralgia/arthritis), Sexual (ED, testicular pain, dysmenorrhoea, pelvic pain), Abdo (pain, N&V), Hearing loss/tinnitus, Mental health (depression, anxiety, PTSD)

85
Q

Ebola Clinical management

A

Supportive (but aggressive) GI loss from diarrhoea and vomiting (aggressive fluids to keep up with losses), Monitor and replace electrolyte abnormalities (potassium, glucose, bicarb), septic shock physiology (aggressive fluids, but monitor for vascular leak, pulmonary oedema), symptomatic management (N&V, diarrhoea, seizures, myalgia, abdominal pain), prophylactic abx (gut translocation). ALIMA ‘Cube’ - clear box for care

86
Q

Ebola Therapeutics

A

Remdesivir, MBP134 used in Uganda. Investigational: Zmapp, MAb114, Regeneron

87
Q

Ebola Key points

A

EBOV disease is an important high consequence infectious disease. Orthoebolavirus has a weak lipid envelope that is easily susceptible to robust IPC measures. EBOD mimics many other tropical diseases (especially when early in patient course) -> know epidemiology. Treatment and prevention (vaccine) options exist (only for EVD), when available, they need to be provided alongside optimised supportive care

88
Q

Lassa Epidemiology

A

Zoonosis (multimammate rodent - Mastomys natalensis) - household contacts usually have same zoonotic exposure, less common to have human-to-human transmission. Highest numbers in Nigeria during Dec-May. Suspected case = malaise, fever, headache, sore throat, cough, N&V&D, myalgia, chest pain, HEARING LOSS (much more common in Lassa than other VHF) and either history of contact with rodent excreta/urine OR with probable/confirmed human case, Confirmed is suspected case + lab confirmation (IgM, PCR or viral culture), Probable is suspected case who died or absconded without collection of specimen

89
Q

Lassa Management

A

Supportive care (fluid, renal, haem, resp), antiviral (ribavirin). Research into various agents, and experimental vaccines - no approved vaccine at present

90
Q

CCHF Epidemiology

A

Tick-borne, characterised by fever, thrombocytopaenia and haemorrhage. Treatment is mainly supportive +/- ribavirin. Russians discovered it and passaged it through psychiatric patients for 20 years until they had the ability to culture it (!). Significant spectrum of disease severity - mild cases present minimal risk of nosocomial transmission as does standard laboratory management of patient samples.

91
Q

CCHF Transmission

A

Large ruminants (cattle, camels) do not become unwell despite viraemia, migratory birds are a risk for transmitting infected ticks to new countries. Less person-to-person transmission than EBOV or Lassa, rare in the community, but in a highly viraemic patient within the hospital is a risk for nosocomial transmission

92
Q

CCHF Children

A

Rare to get severe disease or death, generally fever, anorexia, N&V and abdominal pain, less likely haemorrhagic manifestations

93
Q

CCHF Treatment

A

Supportive, ribavirin (most effective if given in first 6d of illness), side effect is dose-dependent haemolytic anaemia (evidence for ribavirin is weak) - large-scale multi-country trials of therapeutics are urgently required

94
Q

CCHF Diagnosis

A

PCR, LFA in development

95
Q

Yellow fever Virology

A

SSRNA + virus, Flavivirus, incubation 3-6d (max 15d), endemic in Africa and South America. Transmitted A aegypti

96
Q

Yellow fever Transmission cycle

A

Sylvatic: non-human primates - mosquitoes. Urban: human - mosquito. Intermediate (Savanna): human or non-human primate - mosquito

97
Q

Yellow fever Clinical

A

Most asymptomatic, Mild fever, headache, chills, muscle pain, nausea - most self-limiting for 1 week. 10-25% haemorrhagic manifestation, kidney and liver damage. CFR 20-50%

98
Q

Yellow fever Vaccine

A

Live attenuated YFV. Pros: safe, massively used since 1938, fast neutralising immune response, one dose has long-lasting protection 10d post administration if >2yo. Cons: need for embryonated egg, need for strict cold chain. AE 1:100,000 hypersensitivity. 1:200-400,000 vaccine-associated viscerotropic disease, 1:150-250,000 vaccine-associated neurotropic disease

99
Q

Yellow fever Vaccine contraindications

A

<6m, anaphylaxis to previous dose or to any component of vaccine (including egg), thymus disorder, acquired immunodeficiency, immunosuppressed, first degree relative with vaccine-derived viscero or neurotropic disease (that was not related to a known medical risk factor), >60 and travelling to low risk location

100
Q

Yellow fever Vaccine precautions

A

6-8m, >60, Pregnant or breastfeeding, low dose steroid or non-biological oral immunomodulators, HIV (even with CD4>200 and suppressed VL)

101
Q

Yellow fever Fractional dose vaccine

A

Minimum potency 1000 IU/dose (20% of vax) - consider fractional dose in response to an emergency situation in which current vaccine supply is insufficient, but this will not provide durable response

102
Q

Dengue Vaccine challenges

A

Existence of 4 DENV types each capable of causing infection, disease, and death. No validated immune correlation of protection. Immunologic assays are unable to precisely define DENV type specific immune responses. Requirements for very large efficacy trials to demonstrate benefit across diverse populations and clinical endpoints

103
Q

Dengue Prevention in travellers

A

Mosquito prevention (day time), risk highest during and shortly after rainy season. Vaccination Qdenga may be offered to >4yo and older who have had dengue infection in the past and are planning to travel to areas where there is a risk of dengue infection or areas with an ongoing outbreak

104
Q

Zika Virology

A

ssRNA+ flavivirus

105
Q

Zika Congenital

A

Risk T1 8% T2 6% T3 4%. Medium and longterm sequelae: seizures, hearing loss, visual impairment, dysphagia, developmental delay

106
Q

Zika Sexual transmission

A

1% of ZIKV in Europe and US acquired through sexual transmission. M to F&raquo_space; F to M/M to M. Persistence of virus in semen 54d, likely non-infectious at 30d. Male traveller if female partner pregnant - use condoms for rest of pregnancy, if female not pregnant avoid conception (and use barrier) for 3 months. Female traveller if pregnant - use condoms 2 months (if male travelled with her - for the rest of pregnancy), if not pregnant avoid conception for 2-3 months

107
Q

Zika Clinical

A

50-80% asymptomatic, 20-50% mild disease, <1% complications - include neurologic (GBS, acute myelitis, meningoencephalitis), ocular (uveitis), TTP, transient myocarditis

108
Q

Chikungunya Virology

A

Alphavirus, Togaviridae, incubation 2-6d. Viraemia usually lasts 5-7d, IgM detectable 3-8d after sx onset, persist 1-3m, IgG detectable 4-10d after sx onset, persists for years

109
Q

JEV Virology

A

Flavivirus

110
Q

Zika Epidemiology

A

South America, South/SE Asia, Sub-Saharan Africa

111
Q

Chikungunya Epidemiology

A

Asia, Africa, Americas

112
Q

Chikungunya Clinical

A

incubation 2-6d, then 1w of fever, myalgia, rash. Polyarthralgia/polyarthritis can last weeks to months

113
Q

Chikungunya Vaccine

A

Recommended >18y travelling to country/territory where there is an outbreak. Consider >65, particularly those with underlying medical conditions, or persons staying for a cumulative period of 6 months or more

114
Q

Oropouche Virology

A

Orthobunyavirus

115
Q

Oropouche Epidemiology

A

Northern South America - Brazil. Transmitted by midges (Culicoides paraensis) and mosquitoes (Aedes). Reservoir pale-throated sloths, non-human primates, birds. Most infections are mild (similar to dengue), approx 4% develop neuroinvasive disease

116
Q

BBV/TB Epidemiology

A

New diagnoses 2023: HCV 1.1mil HBV 1.2mil, HIV 1.3mil, TB 2.2mil. Living with…in 2023: HIV 40mil, HCV 50mil, TB 10.6mil (1.8bil inc LTBI), HBV 254mil. Deaths in 2023: HCV 290,000, HIV 630,000, HBV 820,000, TB 1.3mil

117
Q

Hepatitis Epidemiology

A

Greatest number of deaths to viral hepatitis in SE Asia. Huge impact made with HIV care, hepatitis lacking behind

118
Q

Hepatitis WHO targets

A

2030: 95% reduction in new cases, 65% reduction in deaths. Previous: 30% reduction in HBV cases, 10% reduction in HBV-related deaths by 2020

119
Q

Hepatitis Differential diagnosis

A

HAV, HBV +/- HDV, HCV, HEV, Leptospirosis, YF, VHF, CMV/EBV, Alcohol and other toxins, ischaemia, autoimmune, NAFLD (accumulaton of NCDs in LMIC is one of leading causes of chronic liver disease, affects 25% of the population), Malaria. ALT in 1000s think autoimmune or acute viral hepatitis

120
Q

HAV Summary

A

Faecal-oral (inc frozen foods). Incubation 4-8w <6yo asymptomatic, >6yo symptomatic jaundice 70%. Spontaneous resolution over 1-2 weeks, liver failure rare, no chronic HAV. Diagnosis by serology (IgM/IgG). Vaccine effective in ~95% of cases and lasts for at least 20 years (cannot give in under 6m population. LMIC most are exposed and infected in childhood -> immune

121
Q

HBV Summary

A

Blood/body fluid exposure. Incubation 1-6m. Course: 30% symptomatic, 95% of cases in adults will resolve, liver failure may occur (1%) Children much higher risk of chronic infection 95% infants. Diagnosis serology (acute cIgM, chronic sAg/cAb, immune sAb) Recombinant HBsAg is the vaccine 3 doses 95%effective in healthy people. HBV is a neglected tropical disease, 91% undiagnosed, no idea of those who have it know how many are linked to care, engaged with care, on treatment, or suppressed. Mismatch between what people need and what is happening

122
Q

HCV Summary

A

Blood/body fluid exposure (Chemsex is RF, but sexual transmission not as pronounced as HIV/HBV). Incubation 2w-6m. Course <30% symptomatic, most cases become chronic (75-80%), liver failure may occur (1-2%). Diagnosis HCV Ab, RNA (Ag tests also available). No vaccine, reinfection common in high-risk groups. Treatment: acute and chronic HCV can be treated with DAAs upon initial diagnosis (based on detectable HCV RNA)

123
Q

HEV Summary

A

Faecal-oral GT1-2 drinking water GT3-4 animal (raw pork liver sausage - Mikhail Surenovich Balayan). Incubation 4-8w often preceded by prodrome and diarrhoeal illness. Course mild or symptomatic, typically resolves spontaneously over 1-2 weeks, liver failure rare except in pregnancy (acute liver failure 20%) chronicity recognised in immunocompromised. Diagnosis by serology (IgM/IgG) and molecular testing (HEV RNA). HEV vaccine licensed in China, global trials underway in women of childbearing age. Chronic HEV can occur in transplant, probably happens in HIV but not well described

124
Q

HBV Antivirals in acute HBV

A

RCTs have not demonstrated efficacy but have confirmed safety. Consider TDF/3TC if two of (in HIC): hepatic encephalopathy, Bili >171, INR >1.6

125
Q

HIV/HBV Coinfection

A

Common, 7.4% globally, much more likely to develop chronic HBV (30%), used TDF or 3TC backbone. Without treatment progression to cirrhosis can be rapid. Treatment does not completely prevent disease progression - likely had a period of significant disease activity

126
Q

HBV Prevention of MTCT

A

Maternal TDF from 30/40 to 4w post partum. Infant HBV and HBIg on first day of life

127
Q

HCC Epidemiology

A

In UK, >90% of those with HCC are asymptomatic at diagnosis. In West Africa, late presentation with weight loss, abdominal pain, abdominal swelling, jaundice. Late presentation = poor outcomes. Can develop HCC without cirrhosis. Length of time from HBV infection is the greatest risk. 50% of HCCs are due to HBV

128
Q

HBV Treatment

A

Contol viraemia by stopping reverse transcription, but cannot (at the moment) get rid of what is in the nucleus. Therefore, if immunosuppressed later in life, will reemerge

129
Q

HDV Summary

A

Blood/body fluid exposure (MTCT is rare). 5% of HBsAg carriers (high seroprevalence in Middle East, Centra Asia and South America, and high risk groups IVDU, MSM, SW (a/w HCV, HIV) - up to 80%). Incubation up to 3m. Usually found on screening of acute hepatitis or progressive chronic liver disease. Virion/parasite - dependent on replicating architecture of other viruses, predominantly HBV. If coinfected simultaneously generally acute self-limiting. If D adds to chronic B, 5% acute liver failure 80-100% develop chronicity. HDV suppresses both HBV and HCV replication (DNA/RNA levels do not predict outcome). Diagnosis serology IgM/IgG or molecular testing (RNA) - guidelines for testing are inconsistent (EASL: low HBV DNA and high ALT). Treatment IFNa <30% SVR at 6 months

130
Q

HCV Treatment

A

Natural hx 15% resolve, 85% chronic, of those 20% develop cirrhosis, and of those 75% slowly progressive with 25% HCC (transplant or death). Revolutionary treatment - short courses of oral therapy cure rates 95%. However, risk of reactivation of HBV infection during or following HCV treatment up to 24% - including those who have isolated HBV cAb - mechanism is not well understood, but clearly some interaction between the two viruses. Egypt have done an amazing job targeting their population and treating

DTM&H 2024 (32 decks)

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