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MBBS - Y1 > Week 6 - viral disease > Flashcards

Week 6 - viral disease Flashcards

1
Q

List some common viral infections in primary care. (LO1)

A
  • Influenza.
  • HPV - Human Papillomavirus.
  • HHV - Human Herpes Virus.
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2
Q

Describe some features of influenza. (LO1)

A
  • Seasonal disease - peak in late december.
  • Acute viral infection of the respiratory tract.
  • 3 types: A, B and C.
  • Type B is most common.
  • Type A can also infect and be transmitted by birds.
  • Highly infectious.
  • Incubation period of 1-3 days before symptoms present.
  • Morbidity and mortality to particularly vulnerable - older people, pregnant women, people with chronic illnesses, immunosuppressed people.
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3
Q

When do influenza cases peak? (LO1)

A

Late December. It is a seasonal disease.

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4
Q

Why do we need to develop a new flu vaccine every year? (LO1)

A

The influenza virus undergoes frequent antigenic changes.

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5
Q

List some complications of influenza. (LO1)

A
  • Lower respiratory tract infection.

- This can lead to hospitalisation and even death.

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6
Q

List the types of vaccine given for influenza. (LO1)

A
  • Live attenuated quadrivalent - children.
  • Inactivated quadrivalent.
  • Inactivated trivalent - over 65s.
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7
Q

Describe the management for influenza. (LO1)

A

Antiviral drugs - neuraminidase inhibitors:

  • Oseltamivir.
  • Zanamivir.
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8
Q

What symptoms can be caused by human papilloma virus (HPV)? (LO1)

A
  • Hand and foot warts (commonly).

- Genital warts (women).

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9
Q

What diseases can human papilloma virus (HPV) lead to? (LO1)

A
  • Cervical cancer.
  • Head and neck cancer.
  • Penile cancer.
  • Anal cancer.
  • Vaginal cancer.
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10
Q

What protection is available against human papilloma virus (HPV)? (LO1)

A

Gardasil vaccine:

  • Old one protects against strains 6, 11, 16 and 18.
  • UK is now moving to Gardasil 9 which protects against strains 31, 33, 45, 52 and 58 as well as the previous strains.
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11
Q

Which strains of human papilloma virus (HPV) cause cervical cancer? (LO1)

A

16 + 18

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12
Q

Which strains does the old human papilloma virus vaccine (Gardasil-4) protect against? (LO1)

A

6, 11, 16, 18.

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13
Q

Which strains does the new human papilloma virus vaccine (Gardasil-9) protect against? (LO1)

A

6, 11, 16, 18, 31, 33, 45, 52, 58.

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14
Q

How many types of human herpes virus (HHV) exist and what is common between them? (LO1)

A
  • 8 types.

- All of them are retained for life once infected.

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15
Q

What are the 8 types of human herpes virus (HHV)? (LO1)

A
  1. Herpes simplex virus type 1 (HHV-1).
  2. Herpes simplex virus type 2 (HHV-2).
  3. Cytomegalovirus (HHV-3).
  4. Varicella Zoster virus (HHV-4)
  5. Epstein-Barr virus (HHV-5).
  6. Human herpes virus 6 (HHV-6).
  7. Human herpes virus 7 (HHV-7).
  8. Kaposi’s sarcoma herpes virus (HHV-8) - more recently.
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16
Q

Describe herpes simplex virus type 1 and 2. (LO1)

A
  • Highly infectious.

- Cause of cold sores and genital herpes.

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17
Q

Describe cytomegalovirus. (LO1)

A
  • Retained for life.
  • Rarely causes issues in healthy people.
  • Can cause issues in pregnant women as it can be transmitted to their babies who may develop symptoms.
  • Immunocompromised people can also experience symptoms or comorbidities such as interstitial pneumonia.
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18
Q

Describe Varicella Zoster virus. (LO1)

A
  • Cause of chicken pox.
  • Cause of shingles upon reactivation.
  • Causes shingles in those who are vulnerable - over 65 or immunocompromised people, etc.
  • Can be fatal in vulnerable people.
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19
Q

Describe Epstein-Barr virus. (LO1)

A
  • Can cause glandular fever - “The main symptoms of glandular fever include extreme tiredness, swollen glands in your neck and a high temperature.”
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20
Q

Describe Epstein-Barr virus. (LO1)

A
  • Can cause glandular fever - “The main symptoms of glandular fever include extreme tiredness, swollen glands in your neck and a high temperature.”
  • Initial infection of oral epithelial cells.
  • Spreads to B lymphocytes.
  • Can cause a range of diseases.
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21
Q

Describe human herpes virus 6 (HHV-6). (LO1)

A

Can cause Roseola Infantum in children - rash.

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22
Q

Describe human herpes virus 7 (HHV-7)/reactivated HHV-6. (LO1)

A
  • Can cause Pityriasis Rosea.

- Can be itchy but usually resolves itself.

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23
Q

Describe what is meant by immunisation. (LO2)

A

The process by which a susceptible individual is rendered immune to an infection.

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24
Q

What are possible aims of immunisation? (LO2)

A
  • Preventing symptoms.

- Eradicating disease.

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25
Q

What is meant by passive immunisation? (LO2)

A

The transfer of pre-formed antibodies to a susceptible individual giving temporary protection from infection.

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26
Q

Give some examples of passive immunisation. (LO2)

A
  • Occurring naturally - e.g. mother to baby via placenta and breastmilk.
  • Normal immunoglobulin - e.g. hep A, measles.
  • Specific immunoglobulin - e.g. hep B, rabies, varicella zoster, tetanus.
  • Monoclonal antibodies - e.g. respiratory syncytial virus (RSV), SARS-CoV-2 (COVID-19).
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27
Q

What is meant by a live attenuated vaccine? (LO2)

A
  • A vaccine that is traditionally generated by serial passage in tissue culture.
  • Weakened pathogen due to how they are cultured.
  • Using serial passage means the pathogen adapts to that type of medium so has difficult replicating in other mediums such as human tissue.
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28
Q

Give some examples of live attenuated vaccines. (LO2)

A
  • BCG TB vaccine.
  • MMR vaccine.
  • Chickenpox and Zostavax shingles vaccine (VZV).
  • Rotavirus vaccine (oral).
  • Sabin vaccine (oral polio).
  • Yellow fever vaccine.
  • Typhoid vaccine (oral).
  • Influenza vaccine (intranasal).
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29
Q

What are the advantages of live attenuated vaccines? (LO2)

A
  • The pathogen replicates in the recipient and so triggers an excellent immune response compared to other types of vaccine.
  • The vaccine closely resembles the infection - e.g. the polio and rotavirus vaccines are given orally and so trigger immune responses in the mucosal tissue of the GI system which prepares the body for infection as these are the tissues usually infected by the pathogen.
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30
Q

What are the disadvantages of live attenuated vaccines? (LO2)

A
  • Potential for reversion - the pathogens, especially in oral polio and oral rotavirus vaccines replicate and can be shed in faeces and spread to other individuals.
  • Potential for sustained vaccine strain infection.
  • Not suitable for everyone - contraindications for immunocompromised people, e.g. HIV positive patients, undergoing active cancer treatment, organ transplant immunosuppression, chronic autoimmune disease, pregnant women (risk of neonatal infection).
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31
Q

What is meant by an inactivated whole cell vaccine? (LO2)

A

A pathogen killed by chemical or physical process before being introduced in people.

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32
Q

Give some examples of inactivated whole cell vaccines. (LO2)

A
  • Inactivated polio (Salk).
  • Hepatitis A.
  • Rabies.
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33
Q

What are the advantages of inactivated whole cell vaccines? (LO2)

A
  • There is NO risk of infection since the pathogen is dead and no potential for replication.
  • Therefore, can be given in immunocompromised individuals and pregnant women.
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34
Q

What are the disadvantages of inactivated whole cell vaccines? (LO2)

A
  • Since the pathogen cannot replicate, the pathogenic load is reduced and there is a weaker immune response to the vaccines.
  • Therefore, immunity is not as strong compared to live vaccines.
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35
Q

What is meant by an inactivated toxin (toxoid) vaccine? (LO2)

A

Toxins from the pathogen chemically treated (e.g. with formaldehyde) to eliminate toxicity whilst maintaining immunogenicity.

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36
Q

Give some examples of inactivated toxin (toxoid) vaccines. (LO2)

A
  • Diphtheria.

- Tetanus.

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37
Q

List the two types of subunit vaccines. (LO2)

A
  • Recombinant subunit vaccines.

- Chemically purified subunit vaccines.

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38
Q

What is meant by a recombinant subunit vaccine? (LO2)

A

A specific viral protein produced in a heterologous expression system (artificially produced in either yeast cells or insect cells).

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39
Q

Define heterologous. (LO2)

A

Having a different relation, relative position or structure.

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40
Q

Give some examples of recombinant subunit vaccines. (LO2)

A
  • Hepatitis B.

- Papillomavirus (HPV).

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41
Q

What is meant by a chemically purified subunit vaccine? (LO2)

A

Certain proteins are extracted directly from the pathogen and purified.

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42
Q

Give some examples of chemically purified subunit vaccines. (LO2)

A
  • Acellular pertussis.

- Influenza.

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43
Q

What is meant by a polysaccharide vaccine? Why is it not an ideal vaccine and what is given instead? (LO2)

A
  • The polysaccharide is a long repeated chain which generates a T cell independent immune response due to the length of the polysaccharide chain.
  • When B cell receptors bind the polysaccharide chain, multiple receptors from the same B cell can bind due to the chain being so long.
  • This leads to cross-linking of the B cell receptors and an immune response leading to antibody production.
  • T cell involvement is required for memory cell formation and due to the cross-linking, there is no T cell action so there’s a reduced production of memory cells.
  • To combat this, conjugated polysaccharide vaccines were produced.
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44
Q

Give some examples of polysaccharide vaccines. (LO2)

A
  • Some meningococcal vaccines.
  • Some pneumococcal vaccines.
  • Salmonella.
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45
Q

What is meant by a conjugated polysaccharide vaccine? (LO2)

A
  • A T cell dependent immune response is required for memory cell production.
  • To attract T cells, the polysaccharide chain is conjugated to proteins which can trigger a T cell response.
  • This converts the immune response to the polysaccharide vaccine to a T cell dependent response which gives better LONG-TERM immunity.
  • An example of a conjugated protein is the diphtheria toxoid.
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46
Q

Give some examples of conjugated polysaccharide vaccines. (LO2)

A
  • H. influenzae.
  • Pneumococcal.
  • Meningococcal.
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47
Q

Why are polysaccharide vaccines not given to children and what is given in its place? (LO2)

A
  • Polysaccharide vaccines are poorly immunogenic in children due to the T cell independent immune response.
  • A conjugated polysaccharide vaccine is given instead.
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48
Q

What types of vaccines have been made for the SARS CoV-2 (COVID-19) virus? (LO2)

A
  • Adenovirus vector.

- mRNA vaccine.

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49
Q

What is meant by an adenovirus vector vaccine (COVID-19)? (LO2)

A

An adenovirus is engineered to remove the replication genes and are implanted with a transgene of interest.

The transgene used is the gene for the spike protein which has been seen in almost all variants of COVID-19 (except omicron which has a mutated spike protein).

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50
Q

Give an example of the adenovirus vector vaccine (COVID-19). (LO2)

A

AstraZeneca COVID-19 vaccine.

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51
Q

Explain how the adenovirus vector vaccine (COVID-19) is made and how it works. (LO2)

A
  1. Replication genes removed from adenovirus molecule so it cannot replicate in humans.
  2. Viral transgene (gene from the pathogen of interest) is inserted into the adenovirus nuclear material so transgene proteins are produced by adenovirus.
  3. When vaccine is given, the adenovirus produces COVID proteins but doesn’t replicate.
  4. When an immune response destroys the adenovirus, it also produces antibodies to the COVID proteins.
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52
Q

Give some examples of the mRNA vaccine (COVID-19). (LO2)

A
  • Pfizer COVID-19 vaccine.

- Moderna COVID-19 vaccine.

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53
Q

What are adjuvants and what is their role in vaccines? Give some examples. (LO2)

A
  • Adjuvants are agents that stimulate the immune system.
  • Their role in vaccines is to increase the number of antibodies and the longevity of immunity.
  • Commonly used adjuvants: aluminium, hydrogen peroxide.
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54
Q

Explain how the mRNA vaccine (COVID-19) is made and how it works. (LO2)

A
  • The vaccine contains lipid nanoparticules carrying the COVID protein mRNA.
  • The mRNA can escape into the cytosol of the host cells and can be translated to make the COVID-19 spike protein.
  • The COVID spike protein is exposed on the host cell surface which triggers an immune response, producing antibodies to the COVID antigen.
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55
Q

Why are adjuvants beneficial? (LO2)

A
  • The function of adjuvants is linked to theit ability to sequester/isolate antigens and cause inflammation.
  • More recent examples include monophosphoryl iipid A, oil-water emulsion of squalene and phosphoguanine.
  • The development of new adjuvants allows for modulation of the type of immune response to a vaccine.
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56
Q

Describe the common adverse effects linked to vaccines. (LO2)

A
  • Related to either the pathogen or other components of the vaccine.
  • Most commonly local reactions, e.g. pain, swelling, redness.
  • General systemic effects: headaches, fever, malaise.
  • Some vaccines cause rashes - MMR, VZV.
  • Anaphylaxis is rare.
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57
Q

List some more severe side effects of vaccines. (LO2)

A
  • Yellow fever - encephalitis.
  • Rubella - arthropathy, thrombocytopenia.
  • BCG vaccine - osteitis.
  • Rotavirus vaccine - risk of intussusception.
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58
Q

List some more severe side effects of vaccines. (LO2)

A
  • Yellow fever - encephalitis.
  • Rubella - arthropathy, thrombocytopenia.
  • Osteitis - from BCG vaccine.
  • Risk of intussusception from rotavirus vaccine - parents are encouraged to maintain good hand hygiene when changing nappies since they can catch the virus through faeces causing a GI infection.

Intussusception is the twisting of the bowel, leading to obstruction.

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59
Q

List some containdications for vaccinations. (LO2)

A
  • History of anaphylaxis to previous vaccine/vaccine component.
  • Immunosuppression.
  • Pregnancy.
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60
Q

Why would an immunisation be deferred? (LO2)

A
  • If the patient is acutely unwell.
  • If other vaccines have been given recently.
  • If the patient is on immunoglobulin therapy.
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61
Q

What are two types of immunisation failures? (LO2)

A
  • Primary vaccine failure.

- Secondary vaccine failure.

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62
Q

What is meant by primary vaccine failure? (LO2)

A

No immune response to the vaccine.

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63
Q

List some possible reasons for primary vaccine failure. (LO2)

A 
Vaccine factors:
- Administration error.
- Manufacturing error.
- Incomplete strain coverage.
Host factors:
- Immunodeficiency.
Inappropriate vaccine schedule.
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64
Q

What is meant by secondary vaccine failure? (LO2)

A

Immunity develops initially but wanes with time.

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65
Q

Briefly describe the innate immune response to vaccination. (LO2)

A
  • 1st line defence.
  • Not specific.
  • No memory.
  • Relies on interactions between pattern recognition receptors (PRR) and PAMPs.
  • Comprises of mechanical barriers, proteins, cells (APCs, NK cells).
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66
Q

Briefly describe the adaptive immune response to vaccination. (LO2)

A
  • Delayed.
  • Specific to the pathogen.
  • Has memory.
  • Comprises of B cells (antibodies), T cells (CD4 helper, CD8 cytotoxic).
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67
Q

What is the function of booster vaccinations? (LO2)

A

Increases the number of antibodies and memory cells by reintroducing the pathogen and triggering a second immune response.

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68
Q

Viruses have mainly been classified according to which three properties? (LO3)

A
  • Historical classification by host - e.g. humans, plants, animals.
  • Classification according to disease or target organ - e.g. respiratory, enteric, hepatitis.
  • Classification according to vector - e.g. arboviruses, avian viruses.

N.B. Arbovirus - vector is an arthropod, e.g. mosquito, ticks, etc.

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69
Q

Molecular biology allows us to classify viruses according to which properties? (LO3)

A

Genetic sequence and biophysical structure.

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70
Q

How are viruses classified according to taxonomy? (LO3)

A
  • Virus Order.
  • Virus Family.
  • Virus Subfamily.
  • Type species.
  • Morphology.
  • Genetic material (DNA vs RNA).
  • Envelope.
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71
Q

List some important viral species. (LO3)

A
  • Human herpes virus.
  • Human papillomavirus.
  • Human adenovirus.
  • Hepatitis viruses.
  • Human rotavirus.
  • Measles.
  • Influenza.
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72
Q

By which property does the Baltimore system classify viruses? (LO3)

A

This system classifies by nuclear material.

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73
Q

BONUS QUESTION*:
Describe the Baltimore classification of viruses. (LO3)

*Don’t need to know this.

A

I - Double-stranded DNA - e.g. herpes simplex virus.
II - Single-stranded DNA - e.g. human parvovirus.
III - Double-stranded RNA - e.g. rotavirus.
IV - Positive sense single-stranded RNA - e.g. hep C, SARS CoV-2.
V - Negative sense single-stranded RNA - e.g. influenza.
VI - RNA reverse-transcribing - e.g. HIV (the only member of this group).
VII - DNA reverse-transcribing - e.g. Hep B (the only member of this group).

74
Q

How do we differentiate between bacterial vs viral disease? (LO3)

A
  • Can be difficult since most symptoms are the same.
  • However, some symptoms are pathognomonic (specific to a disease).
  • E.g. in respiratory disease - productive cough is usually bacterial, non-productive cough is usually viral.
  • Viral infectious don’t persist as long.
  • Higher fevers with viral infections.
75
Q

List some methods of diagnosing viral infections. (LO3)

A
  • Serology.
  • Nuclear acid-based techniques, e.g. PCR.
  • Next generation sequencing.
  • Monoclonal antibodies.
  • Enzyme immune assays.
76
Q

Briefly describe point of care testing (POCT). (LO3)

A

Rapid screening test for common viral infections which is done for all patients who are admitted/present to hospital.

  • Bedside test.
  • Tests for influenza A, influenza B, RSV.
  • PCR-based.
  • 20 minutes from start to finish.
  • Can dictate the patient’s management, admission, isolation, etc.
77
Q

List some notifiable viral infections. (LO3)

A
  • Acute poliomyelitis.
  • Acute Hep A.
  • Acute Hep B.
  • Measles.
  • MERS (Middle East Respiratory Virus).
  • Mumps.
  • Rabies.
  • Rubella.
  • COVID-19.
  • Viral haemorrhagic fever.
  • Yellow fever.
78
Q

List examples of infectious body fluids for viruses. (LO3)

A
  • Blood.
  • Amniotic fluid.
  • Vaginal fluid.
  • Semen.
  • Human breast milk.
  • Cerebrospinal fluid (CSF).
  • Peritoneal fluid.
  • Pleural fluid.
  • Pericardial fluid.
  • Synovial fluid.
  • Saliva (likely due to blood contamination, not always visible to naked eye).
  • Unfixed tissues and organs.
  • Exudate or tissue fluids from skin.
  • Any body-fluid visibly stained with blood.
79
Q

List examples of non-infectious body fluids for viruses. (LO3)

A
  • Urine.
  • Vomit.
  • Saliva - if it’s not blood-stained.
  • Faeces - if it’s not blood-stained.
80
Q

What is a needlestick injury? (LO4)

A
  • In a clinical setting, it’s a piercing of the skin (percutaneous injury) with a sharp instrument (often a hypodermic needle).
  • The sharp has been contaminated with the blood of another (usually a patient).
  • This allows the blood of a patient to come into contact with the blood of a healthcare worker.
    This could potentially transmit blood-borne diseases.
81
Q

Give some examples of blood-borne viruses and state their transmission rate in a susceptible individual. (LO4)

A
  • Hepatitis B - 30% transmission rate in susceptible recipient.
  • Hepatitis C - 3% transmission rate in susceptible recipient.
  • HIV - 0.3% transmission rate in susceptible recipient.
  • Hep B is the most infectious, followed by Hep C, followed by HIV.
82
Q

What are some factors to consider when a needlestick injury occurs? (LO4)

A
  • Does it involve significant fluid? - blood, semen, vaginal secretions, saliva, internal body fluids. (NOT urine or faeces).
  • Is the source high risk? - IV drug user, sex industry worker, originally from Sub-Saharan Africa, regularly has unprotected sex with any of the aforementioned groups, child of mother with HIV, currently under investigation for AIDS defining illness.
  • If source risk is unknown, assume low risk exposure.
83
Q

What is meant by the term source with regards to a needlestick injury? (LO4)

A

The individual who is the source of the blood/body fluid which made contact with the recipient.

84
Q

What is meant by the term recipient with regards to a needlestick injury? (LO4)

A

The individual who has been exposed to the possibility of acquiring the blood-borne virus as a result of an incident.

85
Q

List some factors associated with increased risk of needlestick injury acquired HIV infection. (LO4)

A
  • Is it a deep injury?
  • Is there visible blood on the device?
  • Is the injury from a needle that has entered the source’s blood vessel?
  • Does the source have terminal HIV-related illness?
86
Q

Describe the immediate management of a needlestick injury, regardless of source risk. (LO4)

A
  1. Wash the site liberally with soap and running water - do not use antiseptics or skin washes as we don’t know the effect of these on local immunological defenses.
  2. Encourage the wound to bleed - pinch and squeeze, DO NOT SUCK.
  3. Any exposed mucous membranes should be irrigated liberally with water - for conjunctivae, wash before and after removing contact lenses.
  4. Report the incident to your supervisor.
  5. Immediately seek medical treatment - usually Occupational Health, site nurse or A&E.
  6. Inform source and do appropriate tests on source and recipient.
  7. PEP.
87
Q

Describe the post-exposure prophylaxis (PEP) procedure for HIV. (LO4)

A
  • PEP should be started if the source is known to be HIV positive or high risk.
  • National risk after transmission after exposure is 0.3%. Consider this before exposing the patient to anti-retro viral drugs.
  • Low viral load (<200 copies HIV RNA/ml) - PEP not recommended as extremely low risk of transmission.
  • PEP can be offered to those anxious about risks.
88
Q

Describe the prescription of HIV PEP. (LO4)

A
  • As soon as possible, ideally within 1 hour.
  • Not recommended beyond 72 hours post-exposure.
  • 245mg tenofovir/emtricitabine 200mg) once daily + Raltegravir 400mg twice daily or 1200 once daily.
  • HIV PEP should not be taken with rifampicin and at least 4 hours should pass after using vitamin supplements, calcium, iron or magnesium, before taking PEP.
89
Q

Describe the post-exposure prophylaxis (PEP) for hepatitis B. (LO4)

A
  • Establish recipient’s Hep B immunisation status.
  • An accelerated course or booster dose of a Hep B vaccine.
  • May need Hep B Ig (HBIG) intramuscular injections - for passive immunity, immediate but temporary protection.
90
Q

Describe the post-exposure prophylaxis (PEP) for hepatitis C. (LO4)

A
  • There is no PEP for Hep C.
  • If the source is known to be Hep C positive, Occupational Health services will follow up with the needlestick injury recipient.
  • Regular checks and blood tests to detect any transmission.
  • If seroconversion is detected - referral to Viral Hepatitis Clinic.
91
Q

List some key considerations for testing the source’s blood. (LO4)

A
  • Must gain consent before sending off bloods.
  • Recipient exposed healthcare worker should NOT approach the source patient.
  • Be sensitive when discussing the process - whom test results will be shared with, positive result impacts future health and life insurance policies.
92
Q

What is the procedure for sending the source’s blood for testing if they lack capacity? (LO4)

A
  • If they’re expected to regain capacity within the timeframe for decision on testing, MUST wait for consent.
  • If there is no advanced decision to refuse treatment/send off test results, then assess whether testing is in patient’s best interests.
  • If no clinical benefit to testing source patient, in England, Wales and NI can assume the patient would want to “do the right thing”.
  • There is no legislation to support this in Scotland.
  • If patient source regains capacity, they must be informed of the procedure and provided all the info to decide on if they want the results.
93
Q

What tests are conducted on the source’s blood after a needle-stick injury? (LO4)

A
  • HIV antibodies and p24 antigen test.
  • Hep B surface antigen test.
  • Hep C antibody and core antigen test.
94
Q

List some of the common and important viral diseases. (LO5)

A
  • Influenza.
  • Respiratory Syncitial Virus (RSV).
  • SARS CoV-2
  • Human Immunodeficiency Virus (HIV).
  • AIDS.
95
Q

What are the three types of influenza? (LO5)

A
  • A (birds and human).
  • B (primary human).
  • C (primary human).
96
Q

Briefly describe the influenza virus. (LO5)

A
  • A and B are responsible for most clinical illnesses.
  • Highly infectious.
  • Usual incubation period of 1-3 days.
  • Frequent antigenic changes.
  • They have a specific seasonality.
  • Large impact on the general population.
  • Substantive outbreak and morbidity and mortality rate, especially within people with chronic diseases.
97
Q

Describe the course of infection of influenza in antenatal women. (LO5)

A
  • 5-10% of antenatal women have serological evidence of infection with influenza.
  • HSA recommends annual immunisation of antenatal women.
  • Excess mortality during pregnancy is primarily due to overwhelming pulmonary disease.
  • Increasing rate of ITU admissions and hospital admissions.
  • 2-4 fold increased risk of complications with increasing stage of pregnancy: viral pneumonia, pre-term delivery, perinatal mortality, foetal distress.
98
Q

Describe the management of influenza in ‘at-risk’ groups. (LO5)

A
  • Immunisation with inactivated influenza vaccine.
  • Exposure prophylaxis has its role in prevention.
  • Clinicians managing immunosuppressed patients are also ‘at-risk’.
  • Empirical treatment should be considered pending results of viral PCR screen.
  • Lower respiratory tract infection should always have influenza as a differential in addition to others.
99
Q

List the types of influenza vaccines. (LO5)

A
  • The live attenuated vaccine (LAIV) quadrivalent in children.
  • Inactivated influenza vaccine (quadrivalent: H1N1, H3N2, influenza B two subtypes).
  • Trivalent adjuvanted inactivated vaccine for over 65s.
100
Q

List the general at-risk groups for influenza. (LO5)

A
  • Antenatal women.
  • Immunosuppressed patients.
  • Morbidly obese people.
  • Over 65s.
  • People with a certain set of conditions, especially those compromising respiratory functions.
101
Q

List the conditions that would make a person part of the at risk group for influenza. (LO5)

A
  • Chronic respiratory system diseases.
  • Cardiovascular system diseases.
  • Endocrine system diseases.
  • Hepatic system diseases.
  • Renal system diseases.
  • Neurological/neuromuscular conditions.
102
Q

What is meant by at risk group with regards to influenza? (LO5)

A

At risk groups are more likely than others to develop severe disease if they should be infected.

WHO and most countries prioritise specific ‘at risk’ groups for immunisation.

103
Q

List the risks of influenza infection complications. (LO5)

A
  • Lower respiratory tract infection.

- Admission to hospital.

104
Q

Describe respiratory syncitial virus (RSV). (LO5)

A
  • Major cause of severe respiratory infection in infants, leading to 3.4 million hospitalisations and 66,000 deaths worldwide.
  • Major cause of upper and lower respiratory tract infections in older children and adults leading to morbidity.
  • Elderly can also be severely affected with mortality approaching that of influenza A in >65s.
  • Very infectious and spreads with ease.
105
Q

List some predisposing factors for RSV infection. (LO5)

A
  • Prematurity.
  • Low birthweight.
  • Congenital cardiopulmonary disease.
  • Immunodeficiency.
  • Maternal smoking (tobacco exposure).
  • Male sex.
  • Day care attendance.
  • Overcrowding.
  • Lack of breastfeeding.
  • Low socio-economic status.
  • Admission to hospital during RSV season.
106
Q

Describe the virology of RSV. (LO5)

A
  • RSV belongs to the paramyxoviridae family.

- RSV comprises of two genetically distinct subgroups - RSV/A and RSV/B.

107
Q

Describe the transmission of RSV. (LO5)

A
  • Small inoculum is necessary to infect.
  • By respiratory secretions:
    1. Direct contact.
    2. Via fomites.
    3. By large droplets.
  • RSV has been recovered from environmental surfaces near infected patients for up to 6 hours.
  • Entry occurs through contact with nasal mucosa or eyes.
  • The incubation period varies from 2-8 days.
108
Q

Describe the pathogenesis of RSV. (LO5)

A
  • Infants and young children shed RSV in nasal secretions for 7 days, maximum 3 weeks.
  • Almost all hospitalised infants shed RSV during the first 7 days of hospital stay.
  • Majority still shed the virus at the time of discharge.
  • High virus titre of 10⁵⁻¹⁰ to the 7 PFU/ml in secretions from the upper and lower respiratory tract in young children.
  • RT-PCR confirmed RSV shedding for about 10 days.
109
Q

List the clinical manifestations of an RSV infection. (LO5)

A

Clinical symptoms of bronchiolitis:

  • Expiratory wheezing.
  • Cough and coryza.
  • Air trapping.
  • Nasal flaring.
  • Subcostal retractions.
  • Cyanosis.
  • Fever only in 50% of infants requiring admission.
110
Q

List the investigations for an RSV infection. (LO5)

A
  • Nucleic acid detection.
  • Antibody test.
  • Lab:
    1. Nasopharyngeal aspirate.
    2. Nasal swab.
    3. Endotracheal aspirate/BAAL from those intubated.
111
Q

Describe the prophylaxis for an RSV infection. (LO5)

A
  • Passive immunoprophylaxis.
  • Humanised monoclonal antibody specific for antigenic epitope A at the F protein of RSV.
  • Palivisumab/synagis produced using recombinant DNA technique in mouse myeloma against RSV.
  • Provides passive immunity against RSV.
  • Has been approved for use in high-risk children since 1998.
112
Q

What are the recommendations for the use of passive immunisation against RSV? (LO5)

A
  1. High risk due to bronchopulmonary dysplasia.
  2. High risk due to congenital heart disease (CHD).
  3. High risk due to severe combined immunodeficiency syndrome (SCID).
113
Q

Describe the treatment for an RSV infection. (LO5)

A

Supportive treatment:

  • Healthy children and immunocompetent adults require supportive treatment only.
  • Hypoxia, apnoea and poor oral intake in children <1 year old - require hospitalisation.
  • Inspired O2 concentration and IV fluid may be required.
  • No recommendations for glucocorticoids or bronchodilators - antibiotics only if bacterial superinfection.

Antiviral treatment:

  • Ribavarin - aerosol for treatment of RSV in children and mechanically ventilated patients.
  • Ribavarin has efficacy concerns in children and drug administration issues mean it’s rarely used except in immunocompromised patients.
  • Duration of therapy in immunocompromised is about 5 days.
114
Q

What is SARS CoV-2? (LO5)

A
  • Causative agent of the current coronavirus pandemic.
115
Q

Describe the transmission of the SARS CoV-2 virus. (LO5)

A
  • Aerosol droplets.
  • Incubation 2-10 days.
  • Symptoms onset median: day 4-5 from exposure.
  • High viral shedding occurs early in disease course even those with mild symptoms.
  • Prolonged shedding noted.
  • Reinfection possible.
  • Asymptomatic cases.
116
Q

List the symptoms of a SARS CoV-2 infection. (LO5)

A
  • Fever or chills.
  • Shortness of breath.
  • Fatigue, muscle ache, body aches.
  • Headaches.
  • Loss of taste or smell.
  • Sore throat.
  • Congestion or runny nose.
  • Nausea or vomiting.
  • Diarrhoea.

Week 2:
- About 15-20% develop severe dyspnoea due to viral pneumonia, requiring hospitalisation, supportive cart, oxygen.

Week 2-3:
- 1/3 of hospitalised patients need ITU care.

117
Q

List the risk factors for a severe SARS CoV-2 infection. (LO5)

A
  • Age - >65.
  • Hypertension.
  • Diabetes mellitus.
  • Coronary heart disease.
  • Cerebrovascular disease.
  • COPD.
  • Malignancy.
  • Immunosuppression.
118
Q

Describe the treatment of a SARS CoV-2 infection. (LO5)

A
  • No treatment for asymptomatic/mild symptoms (absence of viral pneumonia and hypoxia).
  • Hospitalised patients:
    1. Antiviral therapy: molnupiravir, remdesivir.
    2. mAB: Ronapreve.
    3. Glucocorticosteroid, oxygen.
  • Severe disease management: pneumonia.
119
Q

Describe the diagnosis of a SARS CoV-2 infection. (LO5)

A
  • Presenting symptoms: fever, cough.
  • O/E chest: rales or rhonchi.
  • Tachycardia and tachypnoea.
  • Severe asthma or COPD exacerbation.
  • Hypoxia.
120
Q

Describe the findings of an FBC for a SARS CoV-2 infection. (LO5)

A

FBC:

  • Lymphopenia.
  • Neutrophilia.
  • Deranged D-dimers.
  • Elevated ALT.
  • Elevated LD.
  • High CRP.
  • High ferritin levels.
121
Q

Describe the spread of SARS CoV-2 infection. (LO5)

A
  • Hand to mucous membrane - sticks to skin easily, specifically the T zone (eyes, nose, mouth).
  • Viable for 3 days on solids, 24 hours cardboard, dependent on temperature/humidity/3 hours if aerosolised.
  • Airborne - cough, talking, intubation, non-invasive positive pressure ventilation, high flow O2, nebuliser, suctioning.
  • Faecal/oral - viral shedding present in stool and diarrhoea is common.
122
Q

What is HIV? (LO5)

A
  • HIV-1 and HIV-2 are enveloped RNA viruses.
  • Family: retroviridae.
  • Genus: lentivirus.
  • They reverse transcribe their genome to form DNA which integrates into the host genomic DNA.
  • 4 genetic groups of HIV-1 (M, N, O and P).
  • HIV-1 group M viruses (subtypes A-K) dominate the epidemic.
123
Q

Describe the interaction of HIV with the cells of our bodies. (LO5)

A
  1. HIV approaches a human CD4 T-lymphocyte.
  2. Binding: virus binds with glycoproteins to a CD4 receptor and either a CCR5 or CXCR4 co-receptor protein.
  3. Fusion: the virus fuses to the host cell and releases RNA into the cell.
  4. Reverse transcription: HIV enzyme reverse transcriptase converts single-stranded HIV RNA into double-stranded HIV DNA.
  5. Integration: HIV DNA enters host nucleus and is integrated into host DNA, using an enzyme called integrase creating a provirus.
  6. Transcription: the provirus becomes active and uses RNA polymerase to create copies of HIV genomic material, as well as mRNA. The mRNA is used as a blueprint to make long chains of HIV proteins.
  7. Assembly: the enzyme protease cuts the long changes of HIV into individual proteins and assemble a virus particle containing HIV RNA.
  8. Budding: the newly assembled virus buds from the host cell, taking with it a part of the cell’s outer envelope. This covering is a mixture of protein and sugar, forming the HIV glycoproteins.
  9. The immature virus breaks free of the infected cell.
  10. Maturation: protease completes cutting the HIV protein chains into individual proteins and the newly formed copy of HIV can now infect other cells.
124
Q

List the modes of HIV transmission. (LO5)

A
  • Blood.
  • Semen.
  • Vaginal secretions.
  • Breast milk.

If any of these come into contact with mucous membranes, damaged tissue or if injected into the body:

  • Vaginal, oral or anal sex.
  • Contaminated needles.
  • IV drug use.
  • Perinatal transmission during pregnancy, labour, delivery or breastfeeding.
  • Occupation exposure, e.g. needle stick or exposure to eye/nose/wound.
  • Blood transfusion/organ donation from HIV infected donor (extremely rare).
125
Q

List the key populations most at risk of contracting HIV. (LO5)

A
  • Male anal sex.
  • People who inject drugs.
  • Prisons.
  • Sex workers and clients.
  • Transgender people.
126
Q

List the clinical manifestations of HIV. (LO5)

A
  • Symptomatic primary infection occurs in 30-70% of infected individuals.
  • Fever.
  • Pharyngitis.
  • Myalgia.
  • Arthralgia.
  • Malaise.
  • Non-puritic, macupapular rash on the face and trunk.
  • General lymphadenopathy.
  • Organ specific manifestations.
127
Q

Describe the investigations for HIV. (LO5)

A
  • Virological tests - serological diagnosis (‘HIV test’).
  • 4th generation test combines antibody/antigen detection.

HIV-1 RNA virus load after serology:

  • Detects the amount of virus present.
  • Monitors the effectiveness of anti-retroviral therapy (ART).
  • Used during acute infection to detect the virus.
  • Measured by HIV-1 RNA RT-PCR.
128
Q

State the WHO recommended principles for HIV testing services (the 5 Cs). (LO5)

A
  1. Consent.
  2. Confidentiality.
  3. Counselling pre- and post-testing.
  4. Correct test results.
  5. Connection (linkage to care, treatment, etc.)
129
Q

Describe the management of HIV. (LO5)

A
  • There’s no cure.
  • Anti-retroviral therapy (ART) can control the virus and help prevent transmission.
  • Adherence to effective ART can reduce risk of transmission to sexual partner by 96%.
  • Oral PrEP of HIV is the daily use of ART by HIV-negative people to block the acquisition of HIV.
  • PEP is the use of ART within 72 hours of exposure to prevent HIV infection.
130
Q

List the types of anti-retroviral treatment (ART). (LO5)

A

There are 6 classes:

  • Nucleoside reverse transcriptase inhibitors (NRTIs).
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs).
  • Protease inhibitors (PIs).
  • Integrase inhibitors (INSTIs).
  • Fusion inhibitors (FIs).
  • Chemokine receptor antagonists (CCR5 antangonist).

Always use 3 or more different ART medications for therapy.

131
Q

What is meant by AIDS? (LO5)

A
  • HIV can lead to AIDS in the absence of treatment.
  • Median time from acquisition of HIV-1 to AIDS: 8-10 years.
  • Average is a loss of 30-60 CD4+ cells/μl per year in the absence of treatment.
  • Accompanied by several systemic and organ specific manifestions.
  • Primarily characterised by certain opportunistic infections that take advantage of the weakened immune system.
  • A diagnosis of AIDS is made when an HIV positive patient has a CD4+ count of <200 or 14%, or the patient is diagnosed with an AIDS defining condition.
  • Combined treatment with 3 ARTs is essential in preventing the onset of AIDs.
132
Q

Give some examples of systemic and organ specific manifestations of AIDS. (LO5)

A
  • Opportunistic infections.
  • Oncological complications.
  • Cardiovascular complications.
  • CNS complications.
133
Q

Define homeostasis. (LO6)

A
  • A self-regulating process by which biological systems maintain stability while adjusting to changing external conditions.
  • A condition in which body functions, fluids and other internal factors are maintained within a usually narrow range of values suitable for supporting life.
  • The body is in a dynamic state of equilibrium.
134
Q

Define what is meant by a sensor with regards to homeostasis. (LO6)

A

A receptor that detects, monitors and responds to changes in a variable in the external environment.

135
Q

Define what is meant by a control centre with regards to homeostasis. (LO6)

A
  • An area that sets the physiological range for the variable and determines the necessary response for bringing the variable back to the set point.
  • In humans, control centres are usually located in the brain.
136
Q

Define what is meant by an effector with regards to homeostasis. (LO6)

A

Tissues and organs that have to respond to changes in the relevant variable to bring it back to the set point.

137
Q

Briefly explain the general steps of homeostasis. (LO6)

A
  1. Sensor is stimulated by a stimulus and sends signals to control centre.
  2. Control centre is alerted and sends signals to relevant effectors to enable corrective mechanism.
  3. Effectors carry out actions and the variable is corrected to the range for homeostasis.
138
Q

What are two types of feedback mechanism for homeostatic control? (LO6)

A
  • Negative feedback mechanism.

- Positive feedback mechanism.

139
Q

Describe how the negative feedback mechanism works to maintain homeostasis. (LO6)

A
  • The effectors act to have an opposing effect on the variable.
  • Most homeostasis in the body occurs by the negative feedback mechanism
  • E.g. rise in body temperature –> effectors act to decrease temperature.
140
Q

Describe how the positive feedback mechanism works to maintain homeostasis. (LO6)

A
  • The effectors have a positive effect.
  • Small deviations from original values become amplified.
  • There is no set point so it can continue indefinitely if unchecked.
  • Normally a self-limiting mechanism once the desired physiological outcome has been achieved.
  • E.g. breastfeeding - sucking of the baby stimulates increase in lactation while there is already lactation occurring.
141
Q

List some examples of positive feedback mechanisms in homeostasis. (LO6)

A
  • Coagulation cascade (blood clotting).
  • Uterine contractions during childbirth.
  • Production of an action potential.
  • Production of gene transcription factors - one transcription factor regulates another and they both regulate the target gene.
142
Q

Which parts of the body are involved in thermoregulation? (LO6)

A
  • Human body temperature range: 36oC - 38oC.
  • Hyperthermia: >40oC.
  • Hypothermia: <35oC
  • Sensor: thermoreceptor.
  • Control centre: hypothalamus.
  • Effectors: depends on the situation.
  • N.B. Peripheral thermoreceptor: skin.
  • Central thermoreceptor: hypothalamus - detects temperature of blood passing through.
143
Q

Explain the process of restoring homeostasis during a temperature increase. (LO6)

A
  1. Thermoreceptors on skin/hypothalamus detect rise in temperature.
  2. The hypothalamus processes this information.
  3. Effectors receive instructions to restore normal temperature:
    - Smooth muscle in walls of blood vessels to the skin - vasodilation.
    - Sweat glands - release sweat.
144
Q

Explain the process of restoring homeostasis during a temperature decrease. (LO6)

A
  1. Thermoreceptors on skin/hypothalamus detect fall in temperature.
  2. The hypothalamus processes this information.
  3. Effectors receive instructions to restore normal temperature:
    - Skeletal muscle - shivering.
    - Smooth muscles in walls of blood vessels to the skin - vasoconstriction.
    - Brown and adipose tissue (brown fat) - fat burning.
    - Piloerection - insulation.
145
Q

What is economic evaluation and why is it used by NICE? (LO7)

A
  • Using analytic methods to identify measure, value or compare cost and consequence of one or more alternative programs or interventions.
  • NICE employ this to decide on different health technologies.
146
Q

List the three economic evaluation techniques used. (LO7)

A
  • Cost-effective analysis (CEA).
  • Cost-utility analysis (CUA).
  • Cost-benefit analysis (CBA).

These 3 techniques allow for comparison of interventions to decide which has a better outcome at lower cost.

147
Q

What are the key steps for cost analysis. (LO7)

A
  1. Identify - what resources are affected by the programme of treatment?
  2. Measure - how would we measure resource use - quantify? (hours of work/amount of drug used per week.
  3. Value - how much is the resource worth?
148
Q

How is cost usually measured? (LO7)

A
  • Usually measured in monetary value.

Net cost = programme cost - cost of the illness.

149
Q

What is the cost of illness defined as? (LO7)

A

The cost of illness is defined as the value of resources that would be used as a result of that illness, including health sector costs, lost productivity by the patient and intangible costs such as pain and suffering.

150
Q

How is outcome measured? (LO7)

A
  • CEA - clinical effectiveness/health outcomes - i.e. cases prevented/years of life saved.
  • CUA - clinical effectiveness but includes quality of life as an adjustment to health outcome (QALYs) - i.e. disability, mental health, ability to travel, work, etc.
  • CBA - monetary outcomes/benefits (consider societies willingness to pay (WTP)).
151
Q

What are the two approaches to cost-effectiveness analysis and how do they differ? (LO7)

A
  1. Average cost effectiveness ratio (ACER).
  2. Incremental cost effectiveness ratio (ICER).

ACER - compares a single treatment against no/a lack of treatment.
ICER - compares two or more treatments.

152
Q

How is average cost-effectiveness ratio calculated? (LO7)

A

ACER = cost (C)/effectiveness (E)

153
Q

How is incremental cost-effectiveness ratio calculated? (LO7)

A

ICER = ΔC/ΔV

ΔC = cost of new programme - cost of current programme

ΔE = effectiveness of new programme - effectiveness of current programme.

154
Q

What is meant by non-dominance? (LO7)

A
  • When a new intervention costs more but is also more effective.
  • When a new intervention costs less but is also less effective.

We then need to work out which is more economical.

155
Q

How do we deal with non-dominance? (LO7)

A
  1. The mean cost is calculated in monetary value using the cost of the new programme subtracted from the cost of the current programme. The mean effect is calculated using QALYs.
  2. Once the means are worked out, we rank them least to most costly.
  3. Exclude the dominant interventions (those that have a clearly higher cost or effect).
  4. Using the equation, calculate ICER for the 2 interventions we are comparing against - mean cost divided by mean effect.
  5. Once ICER has been calculated, compare it against the cost-effectiveness threshold.
156
Q

What is meant by the cost-effectiveness threshold and what is the current threshold in the UK? (LO7)

A

This threshold is based on society’s willingness to pay for the addition of this treatment and a number of factors are considered here because public funds are used.

In the UK, the current threshold is £20,000-£30,000/QALY.

157
Q

Example:
Treatment A has a mean cost of £10,000 and mean effect (QALY) of 2.
Treatment B has a mean cost of £18,000 and mean effect (QALY) of 1.8.
Treatment C has a mean cost of £20,000 and mean effect (QALY) of 2.8.

By calculating the ICER and using the cost-effectiveness threshold, state which treatment is the best option. (LO7)

A
  1. Treatment B is less effective than A and C and more expensive. Hence, it is excluded as a dominant intervention.
  2. ICER = (20,000-10,000)/(2.8-2) = 10,000/0.8 = £12,500/QALY gained.
  3. As the current threshold in the UK is £20,000-30,000/QALY gained, treatment C is the ideal intervention as £12,500 is below the threshold.
158
Q

What is meant by the service development policy? (LO7)

A
  • This sets out NHS England’s approach for decision-making about which new treatments and interventions to commission.
  • It aims to ensure funding is allocated fairly and appropriately.
  • The service development has three phases.
159
Q

What are the three phases of the service development process? (LO7)

A
  1. Clinical build.
  2. Impact analysis.
  3. Decision.

Using all the information from these phases, NHS England carry out biannual relative prioritisation process to determine which services will be routinely commissioned.

160
Q

What is the purpose of the clinical build phase of the service development process? (LO7)

A
  • Where new or amended clinical commissioning policies are proposed and developed.
  • A clinical evidence review by NHS England’s specialised services Clinical Panel challenges and confirms whether the proposition has a sound evidence base.
161
Q

What is the purpose of the impact analysis phase of the service development process? (LO7)

A
  • Identifies the financial and operational impacts of moving from current to proposed pathways of care in the draft policy proposition or service specificiation proposition.
  • The proposed policy or service specifications then are also subject to stakeholder testing, and public consultation.
162
Q

What is the purpose of the decision phase of the service development process? (LO7)

A
  • Cost-neutral or cost-saving interventions will be decided whether to be approved based on an assessment of clinical benefit.
  • For propositions which require additional investment and where there is not sufficient funding available to cover all interventions being proposed, the policy propositions are assessed on their likely relative clinical benefit and relative value for money.
163
Q

What is meant by individual funding requests (IFR). (LO7)

A
  • These are made by clinicians when they believe a patient’s clinical circumstances are exceptional and because of this, they would benefit from a treatment that isn’t usually available on the NHS.
  • Example: immunoglobulin vaccine or certain cancer treatments.
  • Applications are considered by an independent panel.
  • The IFR team have been working on online application forms to make this request process easier.
164
Q

Define what is meant by reservoir of infection. (LO8)

A

Any person or animal, arthropod, plant, soil, substance in which the disease agent lives and multiplies.

165
Q

Define what is meant by transmission pathway. (LO8)

A

Mechanism by which an infectious agent is spread from the source/infection reservoir to a susceptible individual.

166
Q

List some common routes of infection of communicable diseases from human-to-human. (LO8)

A 
Direct:
- Droplet - e.g. influenza, COVID.
- Aerosol - e.g. tuberculosis, COVID.
- Faecal-oral - e.g. dysentery.
- Close contact - e.g. meningococcal meningitis, chickenpox.
- Sexual - e.g. STDs, HIV.
Indirect:
- Food - e.g. staphylococcus food poisoning.
- Waterborne - e.g. cryptosporidium.
- Fomites - e.g. dysentery.
- Needles - e.g. HBV, HCV, HIV.
- Vector-borne - e.g. malaria.
167
Q

List some common routes of infection of communicable diseases from animals. (LO8)

A
  • Livestock via food - e.g. salmonella, E.coli.
  • Domestic pets - e.g. campylobacter, toxocariasis in faeces.
  • Wild animals - e.g. lyme disease.
168
Q

What is it known as when you develop an infection of an organism from your own body. (LO8)

A

Commensal infection.

169
Q

Some communicable diseases have more than one transmission pathway. Give some examples of these and how they are transmitted. (LO8)

A

Cholera:
- Environmental reservoir with person-to-person.
- Foodborne.
- Waterborne.
Campylobacter:
- Environmental and animal reservoirs with animal-to-human and human-to-human spread.

170
Q

List some techniques used to prevent community acquired infections? (LO8)

A
  • Reduce susceptible population - active and passive immunisation.
  • Reduce infectious population - diagnosis and treatment of infected individuals.
  • Reduce person to person spread - education (hand hygiene, safe sex, needle exchange, isolation (COVID)).
  • Reduce animal to human spread - eradication of infectious animals, immunisation and treatment of animals, milk pasteurisation.
  • Reduce environmental transmission - general sanitation and hygiene.
  • Disaster response - climate induced disasters, major disasters affecting health services, refugee settings.
  • Prevention/control of highly infectious and dangerous diseases - notifiable diseases.
171
Q

List the key bodies involved in infection control in a UK healthcare setting. (LO8)

A 
UK Health Security Agency:
- Consultant in Communicable Disease Control (CCDC)
- Consultant epidemiologist.
Local Authority:
- Consultant in Public Health.
- Environmental Health Officer.
- Community Infection Control Nurse.
Acute Trust:
- Medical microbiologist.
- Consultant in genito-urinary medicine.
172
Q

Explain the role of the CCDC in infection control. (LO8)

A
  • Employed by Public Health England (PHE).
  • Surveillance of notifiable and other infectious disease.
  • Lead in control of outbreaks and other incidents.
  • Management of contacts of certain infectious diseases.
  • Provide advice on the control of communicable disease.
  • Ensuring that other healthcare providers comply with guidance on infection control.
173
Q

Explain the role of the medical microbiologist in infection control. (LO8)

A
  • Employed by Acute NHS Trust.
  • Management of diagnostic laboratory.
  • Diagnosis and management of patients with infections.
  • Control of hospital infection.
  • Specialist advice to CCDC.
174
Q

Explain the role of the environmental health officer in infection control. (LO8)

A
  • Employed by the Local Health Authority.
  • Monitor food and other premises.
  • Investigate cases of possible food poisoning.
175
Q

Explain the role of the consultant epidemiologist in infection control. (LO8)

A
  • Employed by the UK Health Security Agency (UK HSA).
  • Involved in regional surveillance.
  • Assist the CCDC when necessary.
  • Manage incidents affecting more than one district.
176
Q

What is a notifiable disease? (LO9)

A

Any disease which, by law, is required to be reported to the government.

177
Q

Why do notifiable diseases need to be reported by law? (LO9)

A
  • It is a form of biosurveillance.
  • Allows authorities to monitor disease spread and possibly predict epidemics or pandemics.
  • In cases of notifiable disease, HCPs can break confidentiality to allow proper tracking of the infection.
178
Q

List the current notifiable diseases in the UK. (LO9)

A
  • Acute encephalitis.
  • Acute infectious hepatitis.
  • Acute meningitis.
  • Acute poliomyelitis.
  • Anthrax.
  • Botulism.
  • Brucellosis.
  • Cholera.
  • COVID-19.
  • Diphtheria.
  • Enteric fever (typhoid/paratyphoid fever).
  • Food poisoning.
  • Haemolytic uraemia syndrome (HUS).
  • Infectious blood diarrhoea.
  • Invasive group A streptococcal disease.
  • Legionnaires’ disease.
  • Leprosy.
  • Malaria.
  • Measles.
  • Meningococcal septicaemia.
  • Mumps.
  • Plague.
  • Rabies.
  • Rubella.
  • Severe acute respiratory syndrome (SARS).
  • Scarlet fever.
  • Smallpox.
  • Tetanus.
  • Tuberculosis.
  • Typhus.
  • Viral haemorrhagic fever (VHF).
  • Whooping cough.
  • Yellow fever.
179
Q

Explain the process of notification once a notifiable disease diagnosis is suspected. (LO9)

A
  • The healthcare practitioner must not wait for laboratory results to confirm the diagnosis.
  • A form must be filled and send within 3 days of diagnosis.
  • If urgent, a call must be made within 24 hours of diagnosis followed by written notification within 3 days.
180
Q

Why is there a timeframe for when you should notify the government about a notifiable disease? (LO9)

A

There is usually a window of time within which effective measures can be put in place.

181
Q

What factors are considered with regards to public health once the notification form has been sent? (LO9)

A

Various factors are considered:

  • Significant contacts who may have been exposed.
  • Vaccination history.
  • Epidemiologically linked cases.
  • Factors that make contacts more vulnerable.
  • Source of infection/contamination.
  • Wider public health context.
182
Q

What advice may be given once the notification form has been sent? (LO9)

A
  • Isolation of patient to prevent further spread.
  • Further lab-testing.
  • Post-exposure prophylaxis/immunisation.

MBBS - Y1 (14 decks)

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