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Year 2 clinical pathology > week 2. viral infection, prevention and immunisation > Flashcards

week 2. viral infection, prevention and immunisation Flashcards

1
Q

what is the immunology testing done for viral infections?

A

test for IgG and IgM
IgM will indicate that the patient has currently a disease
While IgG can indicate that they had the disease in the past.
IgM is produced instantly while IgG develops later on

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2
Q

does a negative immunology test always indicate that the patient does not have the disease?

A

No some disease take a while to act and become apparent. So have to redo the test within a week to confirm

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3
Q

what is the maternal antibody?

A

IgA in breast milk

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4
Q

what are the types of disease that are presented with a rash?

A

Parvovirus
Measles
Chickenpox
Rubella
Non-polio enterovirus infection
EBV –> glandular fever (with ampicillin)
g bacterial causes such as Staphylococcus aureus, N. meningitidis

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5
Q

what disease causes measles, how is it transmitted and for how long is the patient infected for?

A

Virus –> Paramyxovirus + Enveloped single stranded RNA virus

Transmission Person to person droplet spread–> can last in the air for 2 hours

Infectivity From start of first symptoms (4days before rash to 4 days after disappearance of rash

Incubation 7-18 days (average 10-12)

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6
Q

what is the host for measles?

A

Humans are the only natural host. Distribution is worldwide

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7
Q

What are the symptoms of measles?

A

Early symptoms–> Fever, malaise, conjunctivitis, coryza and cough (3’c’s)

Rash–> Erythematous, maculopapular, head – trunk,

Koplik’s spots –>1-2 days before rash.

Fever

Infection in the immunocompromised

Rash + fever + cough/coryza/conjunctivitis

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8
Q

what are the complications of measles?

A

Otitis media (inflammation of the ear) (7-9%)
Pneumonia (1-6%)  this is what kills you
Diarrhoea (8%)
Acute encephalitis – rare but fatal (1 in 2000)
Subacute sclerosing panencephalitis (SSPE)

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9
Q

What is Subacute sclerosing panencephalitis (SSPE)?

A

Rare, fatal, late (7-30 years after measles)

chronic form of progressive brain inflammation

Death – highest in

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10
Q

what is the diagnosis of measles?

A

Clinical , Leukopenia
Oral fluid sample
Serology swab

Notifiable (on suspicion)
Public Health England
Oral fluid for IgM/viral RNA

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11
Q

what infections are suppose to be notified to public health England?

A 
Acute meningitis
Acute poliomyelitis
Measles
Mumps
Rubella
Smallpox
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12
Q

what is the treatment of measles?

A

Supportive
Antibiotics for superinfection

Prevention
Vaccine – live MMR
- 1 year / pre-school
Human normal immunoglobulin

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13
Q

what causes shingles?

A

chicken pox virus

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14
Q

what is the characteristic of chicken pox?

A

starts small then gets bigger and bigger –>entire body –> even inside the mouth and so forth

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15
Q

what happens to chicken pox once you recover from chicken pox?

A

Then the virus hides in your dorsal root ganglia

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16
Q

how is shingles caused and what is the symtpoms?

A

chicken pox virus comes out again as shingle –> affect a single dermatome –> can be painful and is localized –> only can get it if you have chicken pox
Shingles –> is shredding virus –> can give other people chicken pox

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17
Q

what virus causes chicken pox, how is it transmitted and for how long is the patient infected for?

A

Virus –> Varicella Zoster virus, Herpes virus – DNA virus

Transmission Respiratory spread/personal contact (face to face/15mins)

Incubation period 14-15 days

Infectivity –> 2 days before onset of rash until after vesicles dry up

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18
Q

what host is invovled in chicken pox?

A

human host only

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19
Q

what are the symptoms of chicken pox? (VZR)

A

Fever, malaise, anorexia
Rash – centripetal
macular > papular > vesicular > pustular
spots are red and crusted over

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20
Q

what are the complications with chicken pox?

A 
Pneumonitis (risk increased for smokers)
Central nervous system (CNS) involvement
Thrombocytopenic purpura
Foetal varicella syndrome
Congenital varicella
Zoster
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21
Q

what is Congenital varicella ?

A

 affected infants have distinctive abnormalities at birth due to mother having chicken pox

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22
Q

what is the diagnoses of chicken pox?

A

Diagnosis
Clinical
PCR –vesicle fluid/CSF

Serology
Immunity
IgG in pregnant women in contact with VZV and no history of chickenpox

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23
Q

Treatment for chicken pox?

A

Symptomatic adults and immunocompromised children

Aciclovir oral, iv in severe disease or neonates.

Chlorpheniramine can relieve itch (>1 yr olds)

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24
Q

what is the prevention of chicken pox?

A

Vaccine – live, 2 doses (USA/Japan)
Health care workers
Susceptible contacts of immunocompromised pts

VZ Immunoglobulin (VZIG) given if:

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25
Q

when is VZ immunoglobulin given to prevent chicken pox?

A

significant exposure
a clinical condition that increases the risk of severe varicella e.g. immunosuppressed patients, neonates and pregnant women
no antibodies to VZ virus
Ig does not prevent infection in all, reduces severity
pregnant women who has not had chicken pox

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26
Q

what virus causes rubella, the transmision, incubation period and infectivity of rubella?

A

Virus –>Togavirus, RNA virus

Transmission –>Droplet spread – air-bourne
Less contagious

Incubation period –>14-21 days

Infectivity –> One week before rash to 4 days after.

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27
Q

What are the symptoms of rubella?

A

Early symptoms– non-specific

Lymphadenopathy – post-auricular (in ear), suboccipital

Rash–> very non specific–> transient, erythematous, behind ears and face and neck.

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28
Q

what are the complications of rubella?

A

Complications –>thrombocytopenia; post infectious encephalitis;
arthritis.
50% of infectious children are asymptomatic.

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29
Q

what is casued when a pregnant women has rubella?

A

Congenital rubella syndrome (CRS)

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30
Q

what are the complications of Congenital rubella syndrome (CRS)?

A

cataracts and other eye defects
deafness
cardiac abnormalities
microcephaly
retardation of intra-uterine growth
inflammatory lesions of brain, liver, lungs and bone marrow.
CRS more severe when infection contracted earlier in pregnancy.
Foetal damage rare after 16/40; only deafness reported up to 20/40

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31
Q

what is the risk intra uterine transmisison of rubella at different weeks of pregnancy?

A

less than 11 weeks –> 90%
11-16 weeks –> 20%
16-20 weeks–> very minimal –> deafness only
>20 weeks –> no risk

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32
Q

what is the name of the vaccine against measles, rubella and mumps?

A

MMR vacine

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33
Q

what is the clinical sign of Parvovirus B19 ?

A

’slapped cheek’

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34
Q

What virus cauases Parvovris B19?

How is it transmitted, its incubation period and complications?

A

B19 – DNA virus.
Transmitted by respiratory secretions or from mother to child
Incubation period 4 to 14 days.
Risk of miscarriage in early pregnancy - but low
Asymptomatic in 20%

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35
Q

what feotal disease can be caused by Parvovris B19?

A

Anaemia

Hydrops

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36
Q

what is hydrops?

A

feotal anemia

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37
Q

what are the clinical features of Parvovris B19?

A 
Minor respiratory illness
              	Rash illness ‘slapped cheek’
        	Arthralgia
        	Aplastic anaemia
		Anaemia in the immunosuppressed
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38
Q

what is the diagnosis and treatment of Parvovirus?

A

Diagnosis
Serology IgM/IgG – 90% have IgM at time of rash
Amniotic fluid sampling
PCR in immunocompromised.

Treatment

None if self limiting illness
Blood transfusion
No vaccine available

Infection control – difficult as infectious prior to arrival of the rash and significant number of cases are subclinical.

Pregnant HCWs should avoid chronic cases.

Not a notifiable disease

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39
Q

what symtpoms are caused by Enteroviral infections?

A

Coxsackie, entero, echoviral infections.
Hand, foot and mouth disease.
Fever-rash syndromes.
Meningitis

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40
Q

How common is the enteroviral infections?

How is it transmitted and prevented

A

Worldwide, prevalent in under 5 year olds.
90% asymptomatic.
Transmission is faecal-oral and by skin contact.
Supportive management and good hygiene to prevent transmission.

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41
Q

what diseases cause respiratory symptoms?

A 
Respiratory Syncytial Virus 
Parainfluenza
Influenza
Adenovirus
Metapneumovirus
Rhinovirus
42
Q

what does Respiratory Syncytial Virus cause?

A 
Bronchiolitis
Under 1 year olds (0-24 months)
Annual winter epidemics, incubation 4-6 days.
Can be life threatening
Reinfections common
43
Q

what is the diagnosis and treatment of bronchiolitis?

A

diagnoses –>PCR on secretions from nasopharyngeal aspirate

Treatment –> O2, manage fever and fluid intake.
immunoglobulin and monoclonal antibodies - Palivizumab

44
Q

are bronchiodilators or steroids used in treatment of bronchiolitis?

A

they used to be but not any more –> don’t work

45
Q

what does Metapneumovirus cause and what family is it in?

A

Causes respiratory illness similar to RSV – ranges from mild upper respiratory tract infection to pneumonia.

Of the family Paramyxovirus

46
Q

how is Metapneumovirus diagnosed and treated?

A

diagnosis –> – PCR

treatment – supportive only

47
Q

what does Adenovirus cause?

A

Accounts for 10% childhood respiratory infection.
Clinical disease mild URTI (occ. Severe pneumonia)
conjunctivitis
(diarrhoea – serotypes 40/41)

48
Q

what is diagnosis and treatment of Adenovirus ?

A

Diagnosis –> Respiratory panel PCR
Eye swab PCR
Serology possible

Treatment –> None/ cidofovir in immunocompromised

49
Q

what does Parainfluenza cause and how is it transmitted?

Also how is it diagnosed and treated?

A

Transmission – person to person; inhalational
Clinical croup/bronchiolitis/URTI
Dx –>Multiplexed PCR
Rx –>none

50
Q

what is the rhino virus and what others virus’s have similar clinical features?

A

the common cold –> Found in approximately 70% children with mild upper respiratory tract symptoms.

Similar clinical features – coronavirus, human bocavirus, enterovirus, adenovirus

51
Q

what two virus’s causes children to have diarrhoea?

A

Rotavirus

Norovirus

52
Q

How is Rotavirus transmitted, incubdation period and epidemiology?

A 
Reovirus (RNA virus)
Transmission – faecal-oral and occasionally respiratory
Low infective dose
Incubation period 1-2days
Epidemiology
Seasonal in UK (winter/spring)
Worldwide
440 000 deaths/yr
53
Q

clinical features of rotavirus?

A

Diarrhoea and vomiting

Increased mortality in poorer countries
Seasonal variation

54
Q

what is diagnosis, treatment and prevention of rotavirus?

A

Dx PCR
Rx rehydration
Prevention oral live vaccine – UK introduction 2013. Given at 2 and 3 months of age

55
Q

Where does norovirus occurs, how does it spread, what is its course?
Also its diagnosis and treatment?

A 
AKA ‘winter vomiting bug’
Outbreaks - nurseries, hospitals, cruise ships
Foodborne
Person to person spread
High incidence of vomiting (>50%)
Short course - 12-60 hours
Dx		PCR
Rx		Rehydration
56
Q

what is the virus that causes mumps? How is it transmitted, how long is it infective for and how long is the incubation period?

A

Paramyxoviridae family,
Transmission - direct contact,
droplet spread,
fomites

Infectivity – several days before parotid swelling to several days after.

Incubation – 2-4 weeks (mostly 16-18 days)  so don’t realise you have had the infection

57
Q

what are the clinical manifestation of mumps?

A

Early symptoms – nonspecific e.g. low-grade fever, anorexia, malaise, and headache

Next 24 hours – earache, tenderness over ipsilateral parotid

Next 2-3 days – gradually enlarging parotid with severe pain

Normally bilateral but can be unilateral in at least 25%.

Pyrexia up to 40°C.

After peak swelling, pain, fever and tenderness rapidly resolve, and the parotid gland returns to normal size within 1 week

58
Q

What are the rare clinical manifestation of mumps?

A 
Submandibular and/or sublingual sialadenitis 
Epididymo-orchitis 
Oophoritis 
Meningitis 
Encephalitis 
Renal function abnormalities (mild) 
Pancreatitis

CNS involvement is the most common extrasalivary gland manifestation of mumps
Epididymo-orchitis is the most common extrasalivary gland manifestation in the adult
Infection in first trimester - increased foetal death

59
Q

Investigations/Diagnosis/Treatment of mumps?

A 
Normal WCC
Raised serum amylase (salivary or pancreatic)
Normally clinical diagnosis
Serology (IgM)
Blood
Saliva
(PCR)
Treatment – symptomatic only.
Vaccine preventable – live attenuated vaccine.
60
Q

what are the acitivities undertaken to break the cycle of pathogen transmission?

A 
Eliminate pathogenic organism
Remove source/reservoir
Minimise transmission
Eliminate exit and entry
Reduce susceptibility to infection
61
Q

what process are undertaken for eliminating pathogenic organisms?

A

Environmental cleaning and decontamination –>H2O2 room decontamination, Spillage management, Laundry

Equipment–> decontamination, Sterilisation,Disinfection

Antisepsis –>Surgical skin prep,MRSA decolonisation,

Antibiotic prophylaxis –>Perioperative,Post-exposure

62
Q

what action is taken to remove source/resevoir?

A

Hand hygiene

Environmental cleaning and decontaminatio

63
Q

what actions are taken to minimise transmission?

A 
Hand hygiene
Personal protective equipment 
Equipment decontamination
Source and protective isolation
Use of disposable equipment
64
Q

what is involved in personal protection equipment?

A

Aprons
Gloves
Masks

65
Q

what is involved in eliminating entry and exit?

A 
Antisepsis
Asepsis
Air handling
Sharps management
Patient management
66
Q

how do you Reduce susceptibility to infection?

A

Antibiotic stewardship “Start smart – then focus

Immunisation

67
Q

how can infections/disease be Surveillance ?

A

Process of gathering information to ensure that disease outbreaks are pre-empted or identified early

Hospitals
Infection Prevention & Control (IPC) tea

Community
Legislation on reportable/notifiable diseases

68
Q

what are the hospitals Surveillance?

A

Passive surveillance: clinical reporting and laboratory records
Active surveillance: seeking out trouble e.g. Surgical Site Infection Surveillance (SSIS) programmes

69
Q

what is sterilization?

A

Complete killing or removal of all types of micro-organisms

70
Q

what is the difference between vegetative bacteria and spores of bacteria?

A

vegetative is active bacteria

while spores are just small particles of bacteria that are alive but do not grow or replicate

71
Q

what are the sterilization methods?

A

Heat –> Moist, dry

Chemical –>Gas, liquid
Filtration

Ionising radiation –>Used for single use disposable equipment

72
Q

what are the two types of sterlization by year?

A 
Moist heat
Autoclave --> sterilise surgical equipment
Delivery of steam under high pressure
Specific pressure and temperature cycles
more commonly used

Dry heat
Oven
Controlled temperature cycles
160C for 2 hrs or 170 C for 1 hr

73
Q

what is Disinfection?

A

Removal or destruction of sufficient numbers of potentially harmful micro-organisms to make an item safe to use

74
Q

what are the properties to consider in disinfections?

A

Effects on micro-organisms –> Antimicrobial spectrum, sporicidality

Chemical properties
Shelf life, in-use concentration, compatibility with other chemicals

Physical effects –>Corrosiveness

Harmful effects –>Irritant potential, toxicity

75
Q

what is the process for surgical reprocessing?

A

Risk of infection
High

Physical properties
Metal construction
Paper/cloth packaging

Decontamination level
Sterilization

Decontamination method
Moist heat

76
Q

what is the process of cleaning fo Flexible endoscope?

A

Risk of infection
High

Physical properties
Metal/plastic construction
Fragile, sensitive parts

Decontamination level
“High level” disinfection

Decontamination method
Chemical

Several alternative agents
Delivered via “washer-disinfector”

77
Q

what is the process of cleaning involving Syringe needle?

A

Risk of infection
High

Physical properties
Plastic/metal construction
Paper packaging

Decontamination level
Sterilization

Decontamination method
γ-irradiation pre-use
Disposal after use

78
Q

what are the risk and process of Central venous catheter (CVC) insertion site?

A

Physical properties
Living tissue

Decontamination level
Disinfection (antisepsis)

Decontamination method
Chemical
2% chlorhexidine in 70% isopropyl alcohol1

79
Q

what are the process of cleaning of Surgeon’s hands?

A

Physical properties
Living tissue

Decontamination level
Washing

Decontamination method
Surgical scrub

80
Q

what are the non specific defences of the body against infection?

A

unbroken skin

- mucous membrane of gut, lung
- acid & enzymes of gut
- non-specific metabolism / inactivation
81
Q

what is the innate immune system?

A
  • complement, WBC & cytokines
82
Q

give examples of passive immunity?

A

transfer from mother to baby –> maternal antibodies last up to a year
blood transfusion which contain antibodies but only last several weeks

83
Q

what is active immunity?

A

Active immunity is usually long-lasting immunity produced by the immune system in response to antigens.
These antigens can be from natural infection or from vaccination

The immune system makes antibodies to help destroy antigens.
The benefit of vaccination is that active immunity occurs without disease or disease complications.

84
Q

what is immunological memory?

A

The persistence of protection for many years after natural infection or vaccination

85
Q

what part of the antigen does antibodies interact with?

A

An epitope

86
Q

what is primary immune response?

A

it develops in the weeks following first exposure to an antigen
- mainly IgM antibody

87
Q

what is involved in secondary immune response?

A

response is faster and more powerful - mainly IgG antibody

88
Q

how do antibodies produce immunity?

A

Antigen binds non-specifically to variable region of antibody (Ig) molecules –> This triggers clonal expansion

1st wave of IgM production, followed by IgG production

IgG binds tightly to antigen and through simultaneous complement binding facilitates the destruction of the antigen-bearing micro-organism

When infection resolved levels of IgG decline

However one set of the IgG producing B lymphocytes persist with the ability to recognise that specific antigen = Immunological memory

89
Q

what is active immunity?

A

Natural infection

Inactivated or attenuated live organisms

90
Q

give example of live vaccines?

A

MMR, BCG, Yellow fever, Varicella

Act like the natural infection

91
Q

give example of inactivated vaccine?

A

pertussis, typhoid, IPV

92
Q

give example of vaccine that contains components of organisms

A

influenza, pneumococcal

93
Q

give example of a vaccine that contains inactviated toxins?

A

diphtheria, tetanus

94
Q

give examples of disease that are vaccinated using Injection of human immunoglobulin?

A

tetanus, botulism, hep B, rabies, varicella

95
Q

what type of immunisation is the transfer of antibodies from mother to foetus?

A

Passive Immunity

Vertical transmission of auto-antibodies from mother to foetus & breastfeeding

96
Q

what is the advantages and disadvantages of live vaccines?

A

Advantages
Single dose often sufficient to induce long-lasting immunity
Strong immune response evoked
Local and systemic immunity produced

Disadvantages
Potential to revert to virulence
Contraindicated in immunosuppressed patients
Interference by viruses or vaccines and passive antibody
Poor stability
Potential for contamination

97
Q

what is the advantages and disadvantages of inactivated/killed vaccines?

A

Advantages
Stable
Constituents clearly defined
Unable to cause the infection

Disadvantages 
Need several doses
Local reactions common 
Adjuvant needed 
keeps vaccine at injection site
activates antigen presenting cells
Shorter lasting immunity
98
Q

what is the type of reactions you get against vaccines?

A

Local - pain, swelling or redness at injection site; small nodules may form at injection site

General - fever, irritability, malaise, fatigue, headache, nausea, vomiting, diarrhoea, loss of appetite

99
Q

what are the timing of the reactions to the live and inactivated vaccines?

A

Inactivated vaccines
generally within 48hrs following vaccination

Live vaccines:
occur according to time taken for virus to replicate

100
Q

how does the frequency of the reaction to the vaccine differ between live and inactivated vaccines?

A

Live vaccines
Freq of reactions decreases with no of doses - ab produced in response to live vaccine neutralises the small amount of vaccine virus in subsequent vaccine dose

Inactivated vaccines
Freq of reactions increases with no of doses - if ab levels are good from earlier vaccination, ab binds to the vaccine antigen in a subsequent dose leading to inflammatory response

Year 2 clinical pathology (21 decks)

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