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ESA 3 - Infection and Immunity > Session 5 - Travel related infection and adaptive immune system > Flashcards

Session 5 - Travel related infection and adaptive immune system Flashcards

1
Q

Why is taking a travel history important?

A

Could involve:

  • Different strains of pathogen
  • Antigenically different – Impacts on detection
  • Antibiotically resistant pathogens – Impacts on protection
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2
Q

What are the key questions to ask in a travel history?

A
  • Where did you go?
  • When did you go?
  • How did you get there? Direct or via another country?
  • Where did you stay accomodation wise? Tent? Hotel? Etc
  • How long were you there for?
  • Specific risks such as sexual contact or animal contact
  • What preventative measures did you take?
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3
Q

What causes malaria and how does it spread?

A

Plasmodium parasite.

Spreads via vector, the mosquito. Non transmissable between humans.

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4
Q

What is the incubation period for malaria and what are the presenting complaints?

A

Incubation period 1-3 weeks

  • Presents with headache, cough, fatigue, malaise, arthralgia (joint pain), myalgia (muscle pain)
  • Fever chills and sweats occur which cycle every 3rd or 4th day.
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5
Q

What would be revealed upon examination of a patient with malaria?

A
  • May have splenomegaly
  • Cerebral features in extreme cases, e.g. coma
  • Respiratory distress – metabolic acidosis and pulmonary oedema may occur.
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6
Q

What investigations would you undertake to diagnose malaria?

A

Blood smear to detect parasites - reveals RBCs with ring shaped parasites

FBC

Serum Glucose

Liver function test

Urea and electrolytes

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7
Q

How would you treat malaria?

A

Quinine for the p falciparum species

Chloroquine for every other species

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8
Q

Briefly describe the pathogenesis of malaria

A

1) mosquito injects plasmodium parasite.
2) Parasite travels to liver and infects hepatocytes
3) Hepatocytes rupture and release parasite into blood. Parasite infects RBCs.
4) Parasites rupture from RBCs and infect others, resulting in ‘fever waves’ when simultaneous rupturing of RBCs occur.

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9
Q

How can malaria be prevented?

A

1) Avoid risk
2) Bite prevention - repellant, nets
3) Chemoprophylaxis - start before and continue after return for about 4 weeks

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10
Q

What is enteric fever?

A

General term for fever which comprises typhoid and paratyphoid fever

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11
Q

What pathogen causes enteric fever?

A

Salmonella enterica

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12
Q

What are the characteristics of the enteric fever pathogen and how does this allow it to invade?

A
  • It is a Enterobacteriaceae (family of gram negative bacteria), aerobic
  • Produces an endotoxin and is classified as an Vi antigen (Vi for virulence)
  • Invasin allows the bacteria to penetrate into cells
  • Fimbriae adhere to the epithelium over ileal lymphoid tissues (known as Peyer’s Patches
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13
Q

What is the presenting complaint for enteric fever?

A
  • Presents with fever and headache. Abdominal discomfort, constipation, dry cough
  • Hepatosplenomegaly
  • Possible intestinal haemorrhage and perforation
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14
Q

What would investigations for enteric fever reveal?

A
  • Moderate anaemia
  • Relative lymphopenia (low level of lymphocytes in blood)
  • Raised LFT (transaminase and bilirubin)
  • Culture blood and faeces for pathogen
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15
Q

How do you treat enteric fever?

A

Ceftriaxone for 1-2 weeks

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16
Q

How do you prevent enteric fever?

A

1) typhoid vaccine
2) food and water hygiene precautions

17
Q

What is non-typhoidal salmonella infection? What might it lead to?

A
  • ‘Food poisoning’ salmonellas
  • Results in diarrhoea, fever, vomiting, abdominal pain
  • May result in deep seated infections and bacteraemia.
18
Q

What is brucellosis? what are its characteristics and how is it transmitted? How is it treated?

A
  • Gram negative coccobacillus.
  • Transmitted through skin breaks or infected milk.
  • Results in non specific febrile illness (fever)
  • Diagnosed via blood culture
  • Treat with doxycycline and rifampicin.
19
Q

What is travellers’ diarrhoea? What is the pathogen which usually causes it? What is the route of infection? How can it be prevented?

A
  • Defined as 3 or more unformed stools in 24 hours, associated with cramps, nausea and bloating
  • Can indicate a more serious diarrhoea if blood or mucus found in stool or a high fever results.
  • Pathogen rarely identified but usually enterotoxigenic E. coli
  • Source of infection usually faecal-orale route Prevented with good hygiene.
20
Q

What are the characteristics of Legionella pneumophila? Why is it clinically important?

A
  • Gram negative, aerobic, flagellated bacteria.
  • Causes Legionnaire’s disease – a form of pneumonia.
  • May be found in hospital water systems.
21
Q

What are antigen presenting cells?

A

APCs are cells that capture, process and present pathogenic antigens to T cells

22
Q

Where can APCs be found?

A
  • In skin – SALT (Skin associated lymphoid tissue)
  • In mucous membrane - GALT (Gut associated LT), NALT (Nasal associated LT), BALT (Bronchus associated LT).
  • Lymphoid organs
  • Blood circulation
23
Q

What types of cells are APCs?

A

Most cells can present an antigen to T cells Macrophages are the ‘professionals’

24
Q

What 2 methods do APCs use to capture a pathogen?

A
  • Phagocytosis (whole microbe)
  • Micropinocytosis (soluble particle capture)
25
Q

How can an APC distinguish between intracellular and extracellular microbes?

A

Extracellular PAMPs detected by APC and antigen presented on MHC (major histocompatibility complex) - Results in humoral immunity.

Intracellular PAMPs detected and presented on MHC. Results in cell-dependent immunity to destroy cell.

26
Q

What is the major histocompatability complex?

A

A cell surface molecule that presents antigens on the surfaces of the cells which can either be PAMP or self antigens.

27
Q

Where are the 2 classes of MHCs located?

A

o Class 1 – Located on all nucleated cells

o Class 2 – Found on dendritic cells, macrophages, B cells (Antigen presenting cells)

Class 1 + 2 located on dendritic cells, macrophages and B cells

28
Q

What is the main function of class 1 and class 2 MHCs?

A

o Class I – Presents peptides from intracellular PAMPs

o Class II – Presents peptides from extracellular PAMPs

29
Q

What is the structure of an MHC?

A
  • Peptide Binding cleft – Variable region with highly polymorphic residues
  • Broad specificity – Many peptides can be presented by same MHC molecule
30
Q

Which T cells respond to which MHC classes?

A

o Class I – CD8+ T cells (cytotoxic t cells)

o Class II – CD4+ T cells (mature T helper cells – help for immune response)

Rule of 8s – 1x8 = 8, 2x4 = 8

31
Q

Why are some patients long term non progressors for HIV?

A

Due to certain MHC molecules located on the cells of CD4 cells which present key peptides for the survival of the virus, allowing an effective T cell response to viral invasion. Rapid progressors present a less critical peptide by their MHC and therefore results in a weak T cell response.

32
Q

What clinical problems can occur with MHC molecules?

A
  • Major cause for organ transplant rejection due to MHC mismatch
  • People with certain HLA genes are more likely to get an autoimmune diseases
33
Q

What is the function of T cell receptors on CD8 cells with regards to intracellular microbes?

A
  • These recognise and attach to MHC molecules on APCs, activating the T cell
  • The T cell can then recognise antigens presented on infected cells and release perforins and granzymes to destroy the cells.
34
Q

What is the function of T cell receptors on CD4 cells with regards to intracellular microbes?

A
  • Recognise the MHC molecules on APCs and cells, activating the T cell
  • T Cell turns on B cells which produce antibodies and opsonise and neutralise the cells.
  • T cell turns on macrophages which phagocytose the opsonised microbes.
35
Q

What is the function of T cell receptors on CD4 cells with regards to extracellular microbes?

A
  • Recognise the MCH molecules on APCs and cells and activates the T cells
  • TH2 (T helper cell 2) cells can then:
        o Activate eosinophils which kill the parasites o Activate B cells which release antibodies

     o Activate Mast cells which produce local inflammation

• TH17 cells activate neutrophils which phagocytose the microbes

36
Q

What are the 4 types of antibodies B cells produce and what is each useful for?

A

1) IgG4 - opsonisation
2) IgA - mucosal protection
3) IgG and IgE - antibody dependent cell cytotoxicity
4) IgE - Detects allergen molecules and recruits inflammatory molecules

ESA 3 - Infection and Immunity (11 decks)

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