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Path and therapeutics > Viral infections > Flashcards

Viral infections Flashcards

1
Q

Influenza viral family

A

Orthomyxovirus family

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2
Q

Influenza familut genera

A

Orthomyxovirus family genera A, B, C

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3
Q

Influenza genome

A

single stranded negative RNA

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4
Q

how many ribonucleoprotein segments in influenza?

A

–8 separate ribonucleoprotein segments

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5
Q

does influenza have envelope?

A

yes,
•Lipid envelope with two surface glycoprotein species
–Hemagglutinin H
–Neuraminidase N

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6
Q

what are the subtypes of influenza A based on?

A

Influenza A subtypes are based on H & N genes

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7
Q

influenza proteins NA, M1 and M2: where>

A
  • Matrix protein (M1) on inner surface
  • Pores composed of M2 protein

Major antigenic determinants of influenza
•Haemagglutinin (HA)
–HA binds to sialic acid residues on cell surface
•Neuraminidase (NA)
–NA catalyses cleavage of glyosidic linkages to sialic acid bonds facilitating exit of new progeny viruses from the cell

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8
Q

how many subtypes of H and N in influenza?

A

–15 known variants of haemagglutinin

–9 known variants of neuraminidase

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9
Q

what is the reserve for all subtypes of influenza?

A

wild birds

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10
Q

what inflouenza is currently circulating in humans?

A

H3N2

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11
Q

1957 influenza pandemic strain

A

H2N1

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12
Q

Antigenic drift

A

•Virus encodes RNA-dependent RNA polymerase
–Lacks proof reading ability
–RNA replication error accumulation
•Continuously evolving antigenic sites – Immune response less effective
–Hence need for ANNUAL influenza immunisation with updated vaccine strains

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13
Q

Antigenic SHIFT

A
  • Genetic segment re-assortment – (influenza A only)
  • New virus emerges into the population – Primed immune response ineffective
  • Hence origin of influenza A PANDEMICS
  • To cause a pandemic, the new virus must have the capacity for spread directly from human to human
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14
Q

Can influenza Vaccinees URT symptoms and shed vaccine virus ?

A

YES

•Vaccinees may have URT symptoms and shed vaccine virus

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15
Q

bronchiolitis statistics

A

–90% of children 0-2 yrs. are infected with RSV; –20% have LRTI; –3% hospitalized; –0.002% mortality

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16
Q

age at presentation with bronchiolitis

A

Peak age 2-5 mnths –Rare in 1st mnth

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17
Q

aetioogy of bronchiolitis

A

Respiratory syncytial virus (RSV): 70%
•Metapneumovirus 10-20%
•Influenza 10-20%
• Parainfluenza, Adenovirus, Bocavirus

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18
Q

Immunity to RSV>?

A

New intra-nasal vaccine undergoing trials
•Passive immunity via hyperimmune globulin
•Monoclonal antibody to F protein (palivizumab)

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19
Q 
Primary varicella zoster virus infection (chickenpox) in pregnancy 
more common where?
complications
prevention
treatment
A

• More common in women born in tropical regions – Approx 50% non-immune
• Significant risk of varicella pneumonia – Up to 20% – Case fatality rate is high
Interventions
•Prevention –Varicella Zoster Immunoglobulin (VZIG)
•Treatment –Antivirals (Aciclovir)

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20
Q 
CMV
compliations
risk groups 
treatment
prevention
A

•Pneumonitis occurs most commonly in solid organ transplant or stem cell transplant recepients
•Highest risk group is seronegative RECEPIENT (pre-transplant) and receives a CMV seropositive organ from the DONOR
CMV interventions : •Prophylaxis •Pre-emptive therapy
•Treatment: Antivirals –Valgancilovir –Ganciclovir

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21
Q

Maculopapular or macular rash with fever: possible causes

A 
Measles
Rubella
Parvovirus B19
Human herpes virus-6, -7
Epstein-Barr virus \_\_ post antibiotics
Enteroviruses
HIV seroconversion
Scarlet fever
Rheumatic fever (E marginatum)
Secondary syphilis
Toxic shock syndrome
Rickettsial infections
Typhoid
Dengue fever
Kawasaki’s disease
Drug reaction
Still’s disease
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22
Q

petechial/purpuric rash with fever: possible causes

A 
Meningococcaemia
Infective endocarditis
Severe bacterial sepsis with DIC
Leptospirosis
Rickettsial infections
Viral haemorrhagic fevers
Vasculitis
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23
Q

nodular rash with fever, possible causes:

A 
Erythema nodosum
Pseud. aeruginosa*
Cryptococcosis*
Histoplasmosis*
Lepromatous leprosy*
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24
Q

vesicular/pustular rash with fever

A 
Herpes simplex virus
Varicella zoster virus
Enteroviruses (incl HFM)
Staph. aureus
Strep. pyogenes
N. Gonorrhoeae
Stevens-Johnson syndrome
25
Q

Erythema chronicum migrans

A

Erythema chronicum migrans

Lyme disease

26
Q

epidemic viral rashes in children, typical features:

A
  • All except mumps are characterised by feverand generalised rash
  • Highly infectious - >90% infected in childhood
  • Lifelong immunity following natural infection
  • Childhood infection _ occasional complications
  • Adult infection - more often severe, complicated
27
Q 
MUMPS
incidence
incubation period
Featues
Complicaitons
A 
• Peak incidence in 5-9y (pre-vax era)
• Incubation period:15-24d
• 30% sub-clinical
• Clinical mumps
– Non-specific prodrome x 1-2 d
– Unilateral → bilateral parotid swelling/tenderness.
• Complications
– Orchitis in 20%  postpubertal young 
– Oophoritis in 5%
– Aseptic meningitis in 15%
– Rarely encephalitis, permanent unilateral deafness
28
Q 
MEASLES
Infectiousness
Peak incidence
INcubation period
Features
Complications
Prognosis
A

•Highly infectious: R0 = 11-14
•Eliminated from some countries
•Developed countries: peak incidence in 3-5 year olds (pre-MMR)
•Developing countries: high incidence in <2y, high fatality rate
Clinical features
• Incubation period 10-14 days.
• Prodromal symptoms – coryza and conjunctivitis, Koplik’s spots in the buccal mucosa.
• Fever (40C) and maculopapular rash. Rash appears first on the face and spreads to the trunk and limbs within 2 days.
• Complications: pneumonia (bacterial or viral) encephalitis
• High morbidity and mortality in the immunocompromised host

29
Q

RUBELLA
Features
Pregnancy

A

Rubella and Its Complications
• Mild illness with fine red maculopapular rash in childhood.
• Arthralgia/arthritis in ~60% adult women.
• Infection in first trimester of pregnancy - Congenital rubella syndrome

30
Q

PARVOVIRUS B19
Features
Prevention? Treatment in pregnancy?

A

• Causes mild illness “slapped cheek syndrome” in young school children. Fine rash.
• Like rubella causes arthropathy in women
• Virus infects nucleated red cells
→ sig. anaemia in immune compromised. Rx IVIg
→ aplastic crisis in haemolytic anaemia
→ fetal infection may cause hydrops fetalis due to heart failure. Treated by intruterine transfusion
• No vaccine available

31
Q

Herpes viruses
Genome
Surface?

A
  • Identical on Electron microscopy (fried egg)
  • Large double-stranded DNA genome
  • Icosahedral capsid
  • Lipid envelope
32
Q

Herpesviridae classification

A

Classification
• Over 100 herpesviruses have been identified
• Biological properties and genomic structure
®Sub-families alpha-, beta-, gamma- herpesvirinae
• Viruses of each species are numbered in chronological order of discovery
• Eight human herpes viruses have been identified to date

33
Q

Latency and lytic infection with herpes?

A
  • During lytic infection, host cells are productively infected. New virions ®cell lysis.
  • After primary infection, viruses are not eradicated but persist by establishing latent infection in host cells, when no new virions are made
  • Latency genes may be expressed.
  • Reactivation of virus may occur, with production of infectious virions
34
Q

Natural history of infection

A
  • Primary infections are frequently asymptomatic
  • Virus is not cleared but persists in a latent state
  • Reactivation may be clinical or sub-clinical
  • Infection is usually widespread in the natural host
35
Q

Host response to infection,

treatment

A
  • Seropositive status indicates infection, not immunity
  • Cell-mediated responses are critical in controlling infection
  • Both primary and recurrent infection threaten individuals with defective cell mediated immunity
  • Anti-viral agents, e.g. Aciclovir, Ganciclovir can control productive herpes virus infections but cannot eradicate/control latent infection
36
Q

Varicella
Clinical features
VaccinatioN?

A

Clinical Features
• Incubation period 10-21d
• Asymptomatic infection uncommon
• Prodromal symptoms: fever, pharyngitis, malaise
• Itchy/painful lesions appear in crops
• Macules -papules - vesicles - pustules - crusts
• Virus is not cleared following primary infection but
establishes latency in sensory dorsal root and cranial nerve
ganglia
• More severe in adults / immunocompromised
• Maternal varicella - risk of congenital/neonatal varicella
• Varicella vaccine is a live attenuated vaccine, now licensed
in UK

37
Q

ZOSTER

clinical features

A

Clinical Features
• Reactivation of latent VZV
• Pain at site may precede eruption of painful vesicles
• Unilateral; 1-2 unilateral dermatomes involved
• Thoracic in >50% cases
• Ophthalmic division trigeminal nerve - eye in 50%
• Immunocompetent rarely suffer > 2 attacks/lifetime
• Post-herpetic neuralgia especially in the elderly

• Incidence PHN increases with age and in the i.c. host

38
Q

HSV 1, HSV 2

Clinical features

A

• HSV1 and HSV2 are distinct serotypes
• Painful vesicular lesions
• Latent infection of sensory ganglia by retrograde
spread
• Primary infection and reactivation frequently
asymptomatic
• Multiple symptomatic recurrences may occur in
immunocompetent individuals
• More severe in immunocompromised host

39
Q

Orofacial herpes
transmission
clinical features

A 
Pirmarily HSV 1
• Transmitted by salivary contact
• 10 infection -fever & gingivostomatitis
• Recurrent oral herpes > cold sores
• Can spread to other areas of skin, eye
– Herpetic whitlow,
– Eczema herpeticum,
– Corneal ulceration
• Herpes encephalitis can occur at any age
-usually due to HSV1 reactivation
40
Q

Genital herpes
clinical features
detection

A

Typically HSV 2
• Sexually transmitted disease, HSV1 increasingly
common
• Primary/initial infection may cause constitutional illness
with fever, aseptic meningitis/ urinary retention
• Multiple painful ulcers on genitals/adjacent skin +/-
urethritis cystitis cervicitis proctitis
• Recurrent attacks less severe
• Lifelong viral shedding regardless of symptoms
• Risk of neonatal herpes
• Genital HSV increase risk of HIV transmission
• Control of troublesome recurrences:
prophylaxis or pre-emptive Rx

Detection of primary/ reactivated HSV/VZV in skin lesions:
•Electron microscopy
•Immunofluorescence
•Tissue culture
•PCR
41
Q

ANTI-VIRAL AGENTS LICENSED IN UK FOR MANAGEMENT HHV INFECTIONS

HSV and VZV

A
  • Aciclovir
  • Valaciclovir→aciclovir
  • Famciclovir→penciclovir
42
Q

ANTI-VIRAL AGENTS LICENSED IN UK FOR MANAGEMENT HHV INFECTIONS
CMV

A
  • Ganciclovir
  • Valganciclovir → ganciclovir
  • Foscarnet
  • Cidofovir
43
Q

CMV
clinical features
prevalence

A

• Adult seroprevalence 50% (­1% pa)
• Congenital infection in <1% – majority asymptomatic
• Occasional cause of “glandular fever” / mononuclear syndrome
• Life-threatening disease in patients with defective cellular immunity
– AIDS
– Bone marrow Tx
– Organ Tx recipients
Not associated with malignancies

44
Q

EBV
prevalence
features
asssociated in what diseases?

A

• Adult seroprevalence 95%
• Primary infection sub-clinical in childhood
• Symptomatic in 50% adolescents/young adults Infectious mononucleosis “kissing disease”
– fever
– lymphadenopathy
– pharyngitis
• Cause/co-factor in several malignancies inc
Burkitts lymphoma
Nasopharyngeal carcinoma
Hodgkin Disease
HIV-associated lymphoma
Post Transplant lympohoproliferative disease

45
Q

Glandular fever

mONONUCLEAR SYNDROME

possible aetiologies

A

features suggestive of infectious mononucleosis including fever, pharyngitis lymphadenopathy
• “Mononuclear syndrome” – means that increased mononuclear cells ( lymphocytes and/or monocytes) are present in the peripheral blood
• Several possible aetiologies depending on age, clinical setting, travel etc
• In the teenager, young adult in UK first consider:
– Primary infection with EBV, CMV or toxoplasma gondii
– HIV seroconversion
– Streptococcal throat infection

46
Q

aetiologies of ACUTE VIRAL MENINGITIS

A
  • Enteroviruses (including polio)
  • Mumps virus
  • Herpes simplex viruses (genital herpes)
  • HIV seroconversion illness
  • Other herpes viruses eg varicella zoster virus
  • Epstein Barr virus
47
Q

HHV8
Assocaited with what condition
Family
Encodes what?

A
  • Epidemiology suggested Kaposi’s sarcoma (KS) caused by a sexually transmitted agent
  • HHV-8 sequences identified in KS (1993)
  • Gamma herpes virus
  • No recognised illness associated with primary infection
  • Encodes oncogenes
  • HHV-8 is present in KS tumour cells
  • Primary effusion lymphomas (PELs)
  • Castleman’s disease in AIDS
48
Q

Infections in the immunocompormised host

A
  • requires modified diagnostic skills -
    • The usual cardinal features may be absent eg no fever or rash
    • More than one cause - not necessarily a single unifying diagnosis
    • Agents of acute infection may cause chronic disease
    • Delayed/absent serological responses
    • Interpretation of serology complicated by passive acquisition of AB in blood/blood products
    • “Timetable” modified by prevention strategies
49
Q

clinical features of acute VIRAL MENINGITIS
prognosis
treatment
aetiologies

A

Headache Photophobia Vomiting
+/-Neck stiffness
•No LOC. No Δ behaviour. No Δ intellectual function.
•Patient appears generally well – unlike bacterial meningitis.
•Benign self-limiting condition
•Mild pleocytosis – Predominantly lymphocytes
Aetiology:
•Enteroviruses (including polio)
•Mumps virus
•HSV (genital herpes) , EBV, VZV
•HIV seroconversion illness

50
Q

Enteroviruses
classify
spread
Clinical features

A

Non-enveloped RNA viruses
Faecal-oral spread → lymphoid tissue → viraemia
Vast majority of infections asymptomatic
Potential for CNS invasion and neurological disease
Neurological Manifestations:
•Aseptic meningitis
•Meningoencephalitis
•Paralytic poliomyelitis

51
Q

Mumps meningitis
epidemiology
features
course of the illness

A
  • Complicates 10% cases with parotitis
  • 50% cases occur in absence of any parotid swelling
  • Presents before, during or after parotid swelling
  • Usually CSF lymphocytosis, ↑protein, normal glucose but ↑ polys, low glucose can confuse picture
  • 10 day illness with complete recovery as a rule
  • Subclinical CNS infection is common
  • CSF Pleocytosis present in 50% mumps cases without meningitis
52
Q

HSV meningitis
aetiology
associations?

A

•Distinct from HSV encephalitis
•Complication of primary genital herpes (HSV2 or HSV1)
•↑frequency due to HSV’s changing epidemiology
•NB Enquire re genital symptoms
More common in females
•Implicated in Mollaret’s meningitis

53
Q

Acute encephalitis

Clinical features
aetiology

A

meningoencephaltis/encephalomyelitis
Clinical features c/w brain tissue disease
•Altered personality/behaviour (ΔMS)
•Seizures
•Focal neurological signs
Risk of permanent disability or death.
Inflammatory cells may be present in CSF

Aetiology:
•Herpes simplex 
•Enteroviruses (including polio) 
•Varicella zoster virus 
Travel-related: •Rabies 
•Arthropod-borne “Arboviruses”  –eg West Nile virus 
•Post-infectious (ADEM)
54
Q 
herpes encephalitis
epidemiology
features
prognosis
treatment
A
  • Commonest sporadic cause of encephalitis
  • Usually HSV1, recurrent or primary
  • HSV spreads to brain, esp temporal lobe
  • Usually no associated HSV skin lesions
  • Untreated → 70% mortality; neuro sequelae
  • Early aciclovir Rx →↓ morbidity/mortality
  • High index of suspicion → empiric Rx until Dx ruled out
  • Beware false negative HSV on PCR
55
Q 
RABIES
clinical features
course of the disease
prevention
treatment
A

•Zoonosis – man is incidental host
•Endemic in wild mammals in many countries
•Transmission via bite from infected animal
•Neuronal spread: bite → CNS → salivary glands → limbic system → aggression → t/m by bite
•Incubation period reflects site of bite (4w-6m)
•Human cases “Paralytic” or “dumb”
Rx and prevention: c 0% survival
•National animal importation policies , Vaccination of pets and wild animals
• Routine prophylaxis: vaccine
•Post-exposure vaccine: vaccine + immune globulin

56
Q

ADEM
description
clinical features
aetiology

A

ACUTE DEMYELINATING ENCEPHALOMYELOPATHY - ADEM
•Clinical features suggest acute encephalitis -but no infectious agent or local antibody response in the CNS.
•Auto-immune phenomenon
•Systemic infection→demyelination & inflammation.

  • White cells and protein may be present in the CSF
  • Diagnosis of exclusion
  • complication following measles, mumps, rubella, varicella zoster virus infections
57
Q

polyomyelitis
clincial featurs
epidemiology

A

POLIOMYELITIS
• Infrequent complication of poliovirus infection
•Asymp –aseptic meningitis
•Poliomyelitis develops in 1%: Infection of anterior horn cells →flaccid paralysis → Respiratory failure (bulbar)
•Now eliminated from most countries.WHO targets eradication

58
Q

Less acute/ insidious cns infections

A 
TB meningitis* 
•Cerebral malaria 
•Spongiform encephalopathy (eg vCJD) 
•SSPE – measles virus 
–Sub-acute sclerosing panencephalitis 
* More common in immunocompromised host
59
Q

oppurtunistic cns infections

A 
Opportunistic CNS Infections 
•HIV encephalopathy 
•Primary CNS lymphoma/PTLD (EBV) 
•CMV Encephalitis 
•Progressive multifocal leukoencephalopathy (JV virus) 
•Cryptococcus neoformans** meningitis 
•Cerebral toxoplasmosis 
•Nocardia 
•Aspergillus

Path and therapeutics (14 decks)

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