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Nagasaki Flashcard Extravaganza > More Viruses - polio, rabies, HTLV > Flashcards

More Viruses - polio, rabies, HTLV Flashcards

1
Q

How many carriers of HTLV globally?

A

30 million

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2
Q

What kind of virus is HTLV

A

Delta retrovirus, enveloped RNA

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3
Q

How is HTLV transmitted?

A

Breastfeeding, sexually or parentally

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4
Q

What are the two clinical syndromes of HTLV?

A

1 Adult T-cell leukaemia
* Associated hepatosplenomegaly and
lymphadenopathy
* Frequent cutaneous involvement
* Commonest in young adults infected
perinatally
2 HTLV-associated myelopathy/tropical
spastic paraparesis (HAM/TSP)
* Progressive myelopathy with * spastic/ataxic features
Associated uveitis, arthritis, dermatitis, polymyositis

Association with bronchiectasis, BSIs, strongyloidiasis (esp Aboriginal Australians - likely subtype)

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5
Q

How is HTLV diagnosed?

A

Serology - abx

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6
Q

What areas are endemic for HTLV

A

Japan
Aus - Aboriginal population
S America
Pacific islands
Iran

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7
Q

What type of virus is polio?

A

RNA Picorna->enterovirus. Non enveloped, three serotypes

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8
Q

How is polio transmitted?

A

Human to human, faecal-oral
No animal reservoir (can be eradicated)

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9
Q

what are the clinical syndromes of polio?

A
  • Asymptomatic (70–75%)
  • Flu-like symptoms (25%) ± meningism
  • CNS involvement (0.01–0.5%) - acute flaccid paralysis, encephalitis
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10
Q

what is the treatment for polio

A

supportive

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11
Q

How is polio diagnosed?

A

PCR, serology

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12
Q

What is the virology of rabies?

A

Mononega->Lyssavirus
Enveloped RNA
G protein -> neutralised by vaccine
Negri bodies on histology

Genotypes 1–7 (classical rabies is genotype 1)

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13
Q

What is the epidemiology of rabies?

A
  1. Incidence in the world
    ・ ~55,000 die/yr
    ・ Mainly children are the victims.
  2. Geographic distribution
    ・ 99% in Asia (56%) and Africa(44%) ・ Occurred mainly in rural area
  3. Animals responsible for human rabies
    ・ Domestic animals dog, cat (Asia, Africa)
    ・ Wildlife bat, fox, raccoon… (Europe, America)
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14
Q

What is the transmission of rabies?

A

Saliva via animal bite
Human to human rare
Rare: corneal transplants!
All mammals susceptible
Fast retrograde axonal transport

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15
Q

What are the clinical symptoms of rabies?

A
  1. Incubation periods
    * average 2-3 mo, min 2wk, max 6 yr
  2. Prodromal and early symptoms (2-10 days)
    * Itching, pruritus at bite exposure site, loss of appetite
    3.Acute neurologic period (2-10days)
    * Furious rabies
    – Hydrophobia, Aerophobia, Hypersalivation, Feeling of terror, Hallucination, High
    grade fever
    Paralytic rabies (20%)
    – Urinary incontinence
    - ascending sensorimotor neu- ropathy with ocular, cranial and laryngeal palsies and sphincter disturbances: fasciculation may be seen in muscles. Hydrophobia is rare.
  3. Coma to Death (100% ) or Recovery (?)
    * Aspiration pneumoniae, Respiratory or cardiac arrest
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16
Q

How is rabies diagnosed?

A
  • Clinical diagnosis may be obvious
  • Direct immunofluorescence for rabies antigen from skin biopsy (nape of neck) - gold standard
  • PCR of tissue/CSF/saliva
  • Virus isolation: mouse intracerebral inoculation
    Histopathology: eosinophilic Negri body inclusions
    ELISA for specific antibody (N.B. doesn’t appear for 7–10 days after onset of illness)
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17
Q

How is rabies post exposure managed?

A

WHO:
1. Licking/touching animal - no action
2. Minor - nibble/scratch without bleeding - start vax, stop if animal remains health 10 days or negative animal testing
3. Severe - transdermal bites or scratches, bat exposure, contamination of mucus membrane - administer RIG and vaccine

WHO-> 0- RIG and vax, vax at 3, 7, 14, 28
0,3 if immunised
RIG up to day 7

Antibody titre protective at 0.5

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18
Q

Is rabies PEP effective

A

If commenced within 24 hours of the bite, approved protocols for post-exposure rabies vaccination +/- rabies immune globulin have not had any recorded failures in the developed
world.

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19
Q

What is palliative care in rabies?

A

Resp support
High dose sedation and analgesia
Baclofen

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20
Q

How to prevent and control rabies?

A

Vector control - vax animal, limit bat exposure, control stray dog pop
PREP - vaccinations, titres in high risk pts
PEP availability + vax for staff as saliva v infectious

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21
Q

What type of vaccine is the rabies vax?

A

Purified inactivated cell culture or duck embryo vac- cines are recommended as they are potent and safe.

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22
Q

How should you administer RIG?

A

1/2 injected directly into the wound, 1/2 IM

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23
Q

What are three causes of acute flaccid paralysis?

A

ACUTE HORN CELL DAMAGE
- Polio
- Enterovirus
- Japanese Encephalitis

IMMUNE MEDIATED
- Guillain Barre
- Chinese Paralytic Syndrome (Acute motor axonal neuropathy)

OTHER
- Tick paralysis (removal of tick eliminates symptoms)
- Botox consumption
- toxin exposure
- diptheria neuropathy
- rabies exposure

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24
Q

Compare Polio presentation to GBS

A

Polio:
Paralysis is during or almost immediately after febrile illness
Symmetrical paralysis
2-3 days to reach max. weakness
No sensory involvement
CSF has raised lymphocytes
Limb pain

GBS:
Paralysis several weeks after illness
Symmetrical paralysis
Long duration to develop weakness (7-14 days)
Often sensory invovlemetn
CSF has high PROTEIN
Back pain

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25
Q

An isolated case of neonatal sepsis in a patient from a
nomadic community

What is the likely diagnosis?

A

Listeria monocytogenes; (one of top 3 causes of neonatal
infection)

Gram +ve bacilli (small rods) a contaminant of soft cheeses, meat etc and an important zoonosis in herd animals.

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26
Q

What kind of virus is Mpox?

A

dsDNA
Orthopox
Related to smallpox, and the vaccinia strain

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27
Q

What are the two types of mpox virus?

A

Clade 1 - Congo Basin
Clade 2 - West Africa

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28
Q

What is the clinical syndrome of mpox?

A

Preceding fever and flu-like illness - 2-7 days
Widespread vesicles, 1 to 100s, form scab, heal
Complications: superinfection, pneumonitis, encephalitis, proctitis/genital lesions

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29
Q

Who gets severe mpox?

A

Pregnant women
Children
Advanced HIV - can be IRIS phenomenon

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30
Q

What is the differential for mpox?

A

Common – bacterial folliculitis, MC, syphilis, VZV/shingles, syphilis/HSV

What is your wider differential in advanced HIV? Derm crypto, EO folliculitis, IRIS phenoms eg MC

Anthrax, cutaneous leishmaniasis, can look a bit rickettsial

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31
Q

What is the diagnosis of mpox?

A

PCR

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32
Q

What is the treatment for mpox?

A

Supportive
Analgesia inc suppositories for proctitis
Fluid management
Treat superinfection and conconcurrent STIs

Specific
Tecovirimat – oral, RT emerges quick – low evidence
Cedofovir – low evidence
IV IG vaccinia – no evidence

Stabilize disease if HIV and not on ART – risk severe IRIS-MPOX

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33
Q

What is the vaccinology for mpox?

A

Live, attenuated modified vaccinia strain

Developed for smallpox, but used mpox outbreak

Intradermal

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34
Q

What is the mpox host?

A

African rodents/humans
Reservoir not known

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35
Q

What are the transmission routes for mpox?

A

Zoonotic
Vertical
Human-human (Respiratory and Dermal)

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36
Q

What is the CFR in mpox and what kills them?

A

CFR: West African clade 1%, Congo Basin clade 10% (lower in 2022 – 0.16%)

Sepsis, Cytokine release storm?

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37
Q

What is clinical syndrome of Nipah virus?

A

Usually history of Bangladesh, pigs, bats, date palm juice

Respiratory illness (mild / severe)
Encephalitis

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38
Q

What kind of virus is Nipah?

A

Paromyxovirus (same as measles, Hendra)

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39
Q

How is Nipah virus managed?

A

Supportive only
Ribavarin may have some role

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40
Q

What kind of virus is rabies?

A

ssRNA
Rhabdovirus –> Lyssa virus family
7 serotypes (type 1 = most of disease)
5 proteins, G protein = vaccine target

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41
Q

How is rabies virus transmitted?

A

Transdermal inoculation of virus by bite of infected animal

Corneal transplant

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42
Q

What is clinical syndrome of rabies?

A

First sign = itching at tingling of bite
Two presentations: furious, paralytic

Furious (80%) = hydrophobia, aerophobia, hallucinations, convulsions, autonomic hyperarousal. Death within 1 week

Paralytic (20%) = ascending flaccid paralysis –> paralysis of bulbar and respiratory muscles. Death within 1 month

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43
Q

What is the latency period of rabies?

A

Anywhere from 4 days to 6 years.

Shorter latency if:
Proximal bite
High inoculus
Distal bite but person is short (child / Sarah watch out)

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44
Q

How is rabies diagnosed?

A

Clinically

Gold standard = immunoflourescence of viral antigen on skin biopsy

PCR of saliva / skin biopsy / CSF / brain tissue

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45
Q

How is rabies prevented?

A

Pre-exposure prophylaxis in high risk with vaccination (inactivated) day 0, 7, 21

Avoid bites
Animal control

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46
Q

What is a category 1 rabies exposure?

A

Trick question - doesn’t count as exposure! #lol

  • Intact skin coming into contact with secretions of rabid animal
  • Licking intact skin
  • Feeding / touching animals
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47
Q

What is a category 2 rabies exposure?

A

Scratch / bite not breaking skin (no bleeding)

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48
Q

What is a category 3 rabies exposure?

A
  • Bite / scratch with bleeding
  • Mucosal contamination of saliva
  • Any bat contact
  • Licking broken skin
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49
Q

How is a category 2 rabies exposure managed?

A

Vaccinated: vaccine day 0 and day 3

Unvaccinated: vaccine 4 times in 14 days, RIG into wound and IM once only

(RIG given within 1 day if possible, no point after 1 week)

50
Q

How is a category 3 rabies exposure managed?

A

Vaccinated: vaccinate day 0 and day 3

Unvaccinated: vaccinate 4 times in 14 days. RIG into wound and IM once only within 0-7 days

For all: would management (do not suture closed), tetanus booster, antibiotics

51
Q

What type of virus is polio?

A

Picornavirus –> enterovirus

3 subtypes exist, type 1 causes disease (2 and 3 are eradicated)

52
Q

Where is poliovirus still reported?

A

Afghanistan, Pakistan, Nigeria

53
Q

What is clinical syndrome of poliovirus?

A

Acute flaccid paralysis
Asymmetrical
Usually of legs
Progressive over 3 days
+/- viral prodrome

99% asymptomatic

54
Q

How is polio transmitted?

A

Faecal oral
Food / water contamination
Respiratory droplets

55
Q

Where in the body does poliovirus like to infect?

A

Anterior horn (hence flaccid paralysis)

56
Q

What is the prognosis for those with polio?

A

Death rare, results from bulbar / respiratory paralysis

Flaccid paralysis resolves over weeks / months as anterior horn cells repair, does not resolve entirely

57
Q

What is post polio syndrome?

A

New functional decline years after recovery from polio

58
Q

How is polio diagnosed?

A

Clinically
PCR of stool / throat swab
Convalescent serum

LP –> encephalopathic, viral isolation rare. Limited diagnostic role

59
Q

How is polio managed?

A

Strict bedrest (muscular fatigue worsens paralysis)
Monitor for bulbar / resp paralysis
Analgesia for pain
Tracheostomy may be required in resp paralysis

60
Q

How is polio prevented?

A

WASH (remember faecal oral spread)

Vaccination (live attenuated in endemic areas, killed in other)

61
Q

What are the advantages (3) and disadvantages (2) of live attenuated polio vaccine?

A

ADVANTAGES
Cheap
Easy to administer in mass vaccination (oral)
Prevents transmission to others (GI immunity)

DISADVANTAGES
Vaccine derived polio (mutation back to live form –> shed in stool –> infectious)
Vaccine derived poliomyelitis

62
Q

What are the advantages (2) and disadvantages (2) of killed poliovirus?

A

ADVANTAGES
Safe
Multivalent

DISADVANTAGES
No herd immunity
Does not prevent transmission to others

63
Q

What vaccines are available for polio?

A

Live attenuated (oral, used in endemic settings)

Killed (IM, used in non endemic settings)

64
Q

Name 5 challenges for polio eradication

A

Still endemic in 3 countries

99% infections are asymptomatic

Vaccine hesitancy

Vaccine derived poliovirus (mutation back to live form from live attenuated vaccination)

Poor containment of lab derived polio

65
Q

Name 5 strategies for polio eradication

A

Vaccination

Surveillance for flaccid paralysis

Environmental surveillance for poliovirus

Improved diagnostics of poliovirus

Improved WASH –> reduced transmission

66
Q

What kind of virus is measles?

A

Paromyxovirus
ssRNA
Lipid bilayer

67
Q

How is measles spread?

A

Droplets
Aerosol
Direct contact with respiratory secretions

68
Q

When are patients with measles infective?

A

4 days before rash –> 4 days after rash resolves

69
Q

What is r0 usually in measles?

A

9-18

70
Q

What is the incubation period for measles?

A

10 - 20 days

71
Q

What is the clinical syndrome for measles?

A

Fever + rash + one of 3 C (cough, coryza, conjunctivitis)

Rash = macpap, 4/7 after fever, starts behind ears and spreads to trunk, palmar sparing. Fades to purple, desquamates in malnourished

Koplic spots may be seen 2 days before rash appears

72
Q

How is measles diagnosed?

A

Clinically in unvaccinated

PCR throat swab / urine (only positive day 1-14 of illness)

Serology for IgM after 3 days, or IgG >4x upper limit of convalescent

Multinucleate giant cells with inclusion bodies seen on histology

73
Q

Name 7 complications of measles infection

A
  1. giant cell / bacterial pneumonia
  2. Infective diarrhoea
    (1 and 2 contribute most fatality in measles via reduced cellular immunity for 6/52 following measles infection)

NEUROLOGICAL
3. Measles encephalitis
4. Subacute sclerosing panencephalitis (fatal, occurs years later)
5. Acute demyelinating encephalomyelitis (presents with seizures)

OTHER
6. Keratoconjunctivitis –> blindness in vitamin A deficient
7. Otitis media + hearing loss

74
Q

How is measles managed

A

Supportive
Vitamin A supplementation

75
Q

Tell me about the measles vaccine and its schedule

A

Live attenuated
9 months and 2 years as part of MMR

Contraindicated in pregnancy and advanced HIV

Emergency vaccination of unvaccinated in refugee camps (including babies as young as 6/12)

Revaccinate those initiated on ART

76
Q

What type of viruses are Ebola and Marburg?

A

Filovirus
ssRNA

Ebola = 6 strains, most common = Zaire

(Marburg only 1 strain)

77
Q

What is the distribution of Ebola and Marburg?

A

Ebola = West and Central Africa

Marburg = Central and South Africa

78
Q

What is the reservoir for Ebola and Marburg?

A

Bats for both

79
Q

What are the 4 ways that Ebola and Marburg can be transmitted?

A

INDEX CASE
1. Direct contact with bats (consumption / caves) or their poo

HUMAN -> HUMAN
2. Body fluids (incl at funerals)
3. Sexually
4. Vertically

80
Q

What is the incubation period for Ebola and Marburg?

A

2 - 21 days
2 days = one of shortest for VHF

81
Q

What is the clinical syndrome of Ebola / Marburg?

A

Flu like illness +
Diarrhoea and Vomiting +
Confusion (2ndary to renal and hepatic failure plus hypoglycaemia)

Bleeding: petechial, mucosal, bruising, needle sites. Frank haemhorrage late sign

Vascular permeability: ARDS, oedema, shock

82
Q

What is the mortality rate of Ebola / Marburg?

A

40-90% depending on strain / epidemic

Death usually occurs in 2nd week due to dehydration / haemhorrage / shock / renal failure

83
Q

How is Ebola / Marburg diagnosed?

A

> 3 days: PCR blood for virus isolation

RDT available

Routine bloods: HIGH = LFT, amylase. LOW = WCC, plt, glucose, albumin. DERANGED = renal, clotting

84
Q

How is Ebola / Marburg managed?

A

Convalescent serum if available
No known role for antivirals
Supportive only

85
Q

How can Ebola / Marburg be prevented / controlled?

A
  1. Avoid index contact with bats
  2. Strict isolation of suspected cases
  3. PPE to prevent nosocomial infections
  4. Careful funeral practises
  5. Barrier contraception for up to 6 months to prevent sexual transmission
  6. Avoid contact with POC in labouring women if they had Ebola in pregnancy (compartmentalisation of virus)
86
Q

What kind of virus is Lassa?

A

Arenavirus
ssRNA

87
Q

What is the reservoir for Lassa?

A

Multimammate rat
(Mastomys natalensis)

–> Only found in Nigeria / West Africa

88
Q

What time of year is Lassa virus commonly seen?

A

Dry season (Northern hemisphere winter)

89
Q

How can Lassa virus be transmitted? (3 ways)

A
  1. Contact with rat urine / faeces
  2. Consumption of infected rat
  3. Human to human transmission (after index infection from rat)
90
Q

What is the clinical syndrome of Lassa?

A

Incubation = 1-3 weeks

75% mild flu like / subclinical

25% severe:
“Acute abdomen” + vomiting and diarrhoea + vascular permeability + haemhorrage

Neurological signs = deafness and encephalitis in some

91
Q

How is Lassa diagnosed?

A

RDT / PCR

Routine bloods are usually normal (incl clotting)

92
Q

How is Lassa managed?

A

Ribavarin! Whooo

93
Q

What type of virus is Hantavirus?

A

Bunyavirus
Multiple subtypes

94
Q

What is the reservoir for Hantavirus?

A

Multiple rodents, hence global distribution

95
Q

How is Hantavirus transmitted?

A

Contact with infected rodent faeces / urine / aerosolisation of infected rodent fluids

Human : human transmission not seen

96
Q

What is the incubation period of Hantavirus?

A

1-5 weeks (longer than most VHF)

97
Q

What is the clinical syndrome of Hantavirus?

A

Two types: Pulmonary (USA) + Haemhorragic and renal syndrome (Global)

PULMONARY: severe myalgia + D&V + ARDS + haemhorrage. Death 40%

HAEMHORRAGE + RENAL: hypotension + bleeding + renal failure + conjunctival injection. Mortality = 15%

98
Q

How is Hantavirus diagnosed?

A

Serology
Virus undetectable by PCR after 3 days of illness

99
Q

How is Hantavirus managed?

A

Haemhorragic + renal syndrome: ribavarin may have some effect

Otherwise supportive only

100
Q

What type of virus is Rift Valley?

A

Bunyavirus

101
Q

What is the reservoir and vector for Rift Valley?

A

Reservoir = livestock

Vector = mosquitos, sandfly

102
Q

What is the mode of transmission for Rift Valley?

A
  1. Contact with unwell animals
  2. Animal:human / human:human via mosquito / sandyfly bite
103
Q

What is the clinical syndrome of Rift Valley fever?

A

Flu like / asymptomatic in most

Eye: –> retinal lesions, blurred vision
CNS: –> meningoencephalitis
VHF: –> rare, requires hepatic involvement

Mortality <1%

104
Q

How is Rift Valley fever managed and prevented?

A

Manage with ribavarin

Prevent with animal vaccine, avoid contact with unwell animals, bite prevention

105
Q

How is Rift Valley fever diagnosed?

A

PCR / serology

106
Q

What kind of virus is CCHF?

A

Bunyavirus

107
Q

What is the distribution of CCHF?

A

East Europe
Middle East
Africa

108
Q

What is the reservoir and vector for CCHF?

A

Reservoir = livestock

Vector = tick

109
Q

How can CCHF be transmitted? (3 ways)

A
  1. Tick bite
  2. Contact with infected animal
  3. Vertical
110
Q

What is the incubation period for CCHF?

A

1-3 days (v short!)

111
Q

What is the clinical syndrome for CCHF?

A

SUDDEN onset
fever, myalgia, neck stiffness
bleeding / petechiae / bruising
hepatorenal failure

Recovery / death after 7/7 illness
Mortality = 10%

112
Q

How is CCHF diagnosed?

A

PCR / serology in combination
Many serotypes makes it tricky

113
Q

How is CCHF managed and prevented?

A

Ribavarin (evidence unclear)

Vaccine available but not widely used
Prevent tick bites and contact with unwell animals

114
Q

What kind of virus is HTLV?

A

Retrovirus
ssRNA
HTLV 1 = 5 clades (disease causing)
HTLV 2 = 2 clades

115
Q

How is HTLV transmitted? (4 ways)

A
  1. Sexual contact
  2. Vertically (incl breast feeding)
  3. Infected blood transfusion
  4. Needle sharing in IVDU
116
Q

Where is HTLV found, what is the prevalence?

A

Prevalence = 20 million
Most in Japan
Also in Caribbean, South America, Iran

117
Q

What is the clinical syndrome of HTLV?

A

4% increased risk of T cell lymphoma / leukaemia

4 presentations:
1. Acute type (2/3)
2. Chronic / smouldering
3. Lymphoma type
4. HAM / TSP (HTLV associated myelopathy / tropical spastic paresis)

118
Q

How is HTLV diagnosed?

A

Serology for HTLV

Leukaemia / lymphoma bone marrow / LN biopsy. Ca may be high, WCC often >30

119
Q

How is HTLV managed?

A

No way to eradicate HTLV infection

Manage as per leukaemia / lymphoma

Steroids if HAM / TSP

120
Q

How can HTLV be prevented?

A

Barrier contraception
Screening of blood donation
Safe needle exchange

Nagasaki Flashcard Extravaganza (34 decks)

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