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DJ - ESA 3 - Infection > Travel-related Infections / Adaptive Immunity > Flashcards

Travel-related Infections / Adaptive Immunity Flashcards

1
Q

What are rigors?

A

Sudden feeling of coldness with shivering accompanied by a temperature (fever), sweating.

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2
Q

What are the key aspects of the Patient (determinant of disease) when considering tavel-related infections?

A

Time:
Calendar Time - When time of year did they go (seasonal)?Relative Time - How recently were you there (incubation period)?

Place:
Recent Place is important; (Africa? Where in Africa? Where exactly in Africa?)

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3
Q

What are the key aspects of the travel history?

A
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4
Q

Why is the travel history important?

A

Different strains of pathogen - may be antigenically different (resulting in different antibodies/different immune response - will affect protection & detection), have antibiotic resistance

‘Imported’ diseases - some are rare/unknown in the UK

Infection prevention - on the ward and in the lab

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5
Q

What is the pathogen that causes malaria?

A

Plasmodium - a parasite. There are four species:
Falciparum, vivax, ovale, malariae

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6
Q

How is malaria transmitted?

A

Through a vector - the female Anopheles mosquito.
Once the mosquito has bitten (during the night) an infected individual, they then have the parasite (once it has moved from their gut to their salivary gland). If they bite again, when the parasite has moved to their salivary glands, the recipient will become infected.

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7
Q

Where is malaria common? What about the UK?

A

The tropics (near the equator). There are 250 million cases a year. ~1500 people present with malaria in the UK in a year.

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8
Q

What is incubation period? For malaria it is…

A

The time elapsed between the entry of the infective pathogen and first signs and symptoms of the disease.
7 - 21 days after mosquito bite (can be slightly longer).

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9
Q

What is a typical presentation of a malaria sufferer?

A

Headache, cough, fatigue, malaise, arthralagia, myalgia

Rigors which eventually cycle every 3rd (tertian) or 4th (quartan) day.

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10
Q

What are these tertian and quartan fevers indicative of?

A

Tertian (every 48h)
Benign: P. ovale, P. vivax
Malignant: P. falciparum

Quartan (every 72h)
P. malariae

Due to the cyclic lysis of RBCs as trophozites (growing stage of the Plasmodium parasite) finish their cycle every 2 or 3 days.

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11
Q

What may be visible on examination of a malaria sufferer?

A

Sometimes just fever.

Occasionally splenomegaly, coma (P. falciparum), respiratory distress (metabolic acidosis, pulmonary oedema).

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12
Q

What investigations should be carried out on possible malaria cases?

A 
Blood smear (detect parasites),
FBC, U&Es, LFTs, Glucose,

If CNS symptoms a Head CT.

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13
Q

How do we treat malaria?

A

Malignant (P. falciparum) - Quinine or Artemisinin

Benign (P. ovale/vivax/malariae) - Chloroquine + Primaquine (for exo-erythrocytic phase - infection in liver)

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14
Q

How do we prevent malaria? (Hint: ABC)

A

Assess risk - knowledge of at risk areas

Bite prevention - nets, adequate clothing, repellant,

Chemoprophylaxis - start before (~1 week) and continue after return (~4 weeks) - must be specific to region.

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15
Q

What is the causative pathogen of typhoid and paratyphoid fever (enteric fever)? Classify it.

A

Salmonella typhi/paratyphi (A, B or C),
Gram negative aerobic, bacilli - known as enterobacteriaceae.

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16
Q

What is the mechanism of infection for enteric fever?

A

Faecal oral route - from contaminated food/water.
Source - cases or carriers (only found in humans).
It is a systemic disease (incubation of 1-2 weeks).

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17
Q

Is enteric fever common in the UK?

A

No. Although it is widely distributed (it is due to poor sanitation) it is found mainly in ‘3rd world’ countries. There are 21 million cases a year, mainly children. Most cases in the UK are travel-related (rather than through transmission) - ~500 cases a year.

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18
Q

How can salmonella typhi/paratyphi be differentiated from other gram negative bacilli?

A

Using MacConkey’s agar.

Lactose fermenting bacteria: make the agar hazy due to production of acid (uses lactone) - E. Coli, Klebsiella

Non-lactose fermenting bacteria: agar will become pink will produce alkali (uses peptone) - Salmonella, Shigella

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19
Q

How does salmonella typhi/paratyphi cause infection?

A

Gram-negative endotoxin (LPS)
Invasin - allows intracellular growth
Fimbriae (short hair-like processes) adhere to epithelium over ileal lymphoid tissue (Peyer’s patches - histological feature), which recruits the reticuloendothelial system.

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20
Q

What are the signs and symptoms of enteric fever?

A

Fever & headache,
Abdominal discomfort, constipation, dry cough
Hepatosplenomegaly, ~rash
~Bradycardia

Increased risk of intestinal haemorrhage and perforation

Paratyphoid is normally milder.

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21
Q

What investigations would you carry out in a possible enteric fever sufferer?

A

M, C & S on blood and faeces culture.
FBC, U&Es, LFTs: would show moderate anaemia, relative lymphopenia and raised LFTS (for transaminase and bilirubin)

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22
Q

What antibiotic do we usually use to treat enteric fever?

A

Ceftriaxone (as for meningitis) or azithromycin for 1-2 weeks.

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23
Q

How can we prevent the transmission of enteric fever?

A
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24
Q

Are there other species of Salmonella that do not cause enteric fever?

A
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25
Q

What are the symptoms of salmonella typhimurium infection?

A

Diarrhoea, vomiting, fever, abdo pain.
It is generally self-limiting.

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26
Q

What are brucellosis?

A

It is a zoonosis - diseases that can be transferred from animals to humans.

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27
Q

Name a few brucella - how are they transmitted?

A

Brucella abortus (cattle), Brucella melitensis (goats & sheep) are gram negative coccobacillus.

Can be transmitted through breaks in skin or GI tract (milk).

28
Q

What are the signs and symptoms of infection with brucella?

A

Non-specific febrile illness (undulant fever), bone/joint involvement.

29
Q

How is brucella diagnosed?

A

From blood culture - must be careful it is very contagious.

30
Q

How is brucella treated?

A

Doxycycline and rifampicin.

31
Q

What do we do with patients who may have a disease that is highly infectious?

A

Consider isolation pending diagnosis (individual room/negative pressure room).

Not all conditions are spread from case-to-case.

Take precautions: specimens may be high risk for laboratory staff (PPE?)

32
Q

What type of virus caused SARS? Classify it.

A

A coronavirus - RNA, enveloped +ve strand.

33
Q

What conditions do the filoviridae family of viruses cause? What is the vector?

A

Ebola and Marburg haemorrhagic fever. The vector is believed to be a bat.

34
Q

What are the signs and symptoms of Ebola?

A

Flu-like illness with diarrhoea, vomiting, headaches, confusion, rash and potentially coma. There is internal and external bleeding at 5-7 days.

35
Q

How is Ebola transmitted?

A

Direct contact with bodily fluids (blood, excretions etc.) of those WITH symptoms. People can be infected even from those that are deceased.

36
Q

What is the treatment for Ebola?

A

Experimental. Zmapp - … low stocks…; Anti-virals; a vaccine is under development.

37
Q

What are the key players in the adaptive immune response?

A

T cell (CD4+ and CD8+), Pathogen, Antigen presenting cells.

38
Q

Where are antigen presenting cells found?

A

SALT (skin), GALT (gastrointestinal), NALT (nasopharyngeal), BALT (broncho) - associated lymphoid tissue.

Lymphoid organs (lymph nodes, spleen).

Blood circulation (plasmacytoid and myeloid dendritic cells).

39
Q

What do cells have to be able to do in order to be antigen presenting?

A

Have to be able to carry out phagocytosis (ingest the whole microbe) and micropinocytosis (endocytosis where small, soluble particles are brought into the cell).

40
Q

Are viruses intracellular or extracellular microbes? What about bacteria? Why is this significant for antigen presenting cells?

A

Viruses are intracellular; bacteria are extracellular

Antigen presenting cells will have specific PRRs (pathogen recognition receptors).

41
Q

What are some of the antigen presenting cells? Where are they found and what do they present to?

A 
('Interdigitating') Dendritic Cells - lymph nodes;
Langerhan's cells - SALT; Macrophages - various;
B Cells (BCR) - lymphoid tissue

All present to T cells.

42
Q

What sort of immunity will exposure to extracellular pathogens develop?

A

Humoral immunity - antibodies and complement are involved.

43
Q

What sort of immunity will exposure to intracellular pathogens develop?

A

Cell-dependent immunity - cytotoxic T cells (CD8+), macrophages, antibodies are heavily involved.

44
Q

What are MHCs and HLAs?

A

They are major histocompatibility complexes and human leukocyte antigens. There are 2 classes of MHCs which HLAs fall under - they are the molecules responsible for antigen presentation.

45
Q

How many classes of MHCs are there? What does each class do? Where are they found?

A

MHC Class 1: HLAs present peptides from intracellular pathogens (viruses) which CD8+ respond to. Found on all nucleated cells.

MHC Class 2: HLAs present peptides from extracellular pathogens (bacteria) which CD4+ respond to. Found on dendritic cells, macrophages, B cells.

46
Q

How do we acquire MHC molecules?

A

Hereditary - with a co-dominant expression - maximising numbers of different MHC molecules.

There are lots of different alleles (polymorphic genes) meaning there is an increased presentation of different antigens/microbes.

47
Q

Structurally, how do MHC molecules have gene polymorphism?

A

They have a peptide binding cleft - a variable region with highly polymorphic residues. Many of these peptides are presented by the same class of MHC molecules giving them broad specificity.

48
Q

Why can MHC molecules cause clinical problems in patients who have had organ transplants?

A

There may be HLA molecule mismatch between the donor and recipient - leading to graft-vs-host reaction.

49
Q

What are some conditions which have an HLA association?

A

Ankylosing spondylitis - HLA-B27 –> 90% of AS sufferers will have this HLA molecule present (in raised concentrations).

Diabetes (Insulin-dependent) - HLADQ2 –> 50-75% of patients

50
Q

Where are T cells produced? Where do they mature?

A

Bone marrow. Mature in the thymus gland.

51
Q

What are the functions of CD4+ cells? How do they achieve this?

A

Help the immune response against both extracellular and intracellular microbes. Their T-cell (CD4+) receptors will bind to the MHC 2 molecules. They produce cytokines (Interleukins, e.g. IL-4; IL-7; TNF-a)

52
Q

What are the main functions of the cytokines (Interleukins, TNF-a) produced by CD4+ cells?

A

Interleukins (and TNF-alpha) promote development and differentiation of B cells, T cells as well as some other haematopoietic cells.

53
Q

Outline how humoral immunity is obtained.

A

Extracellular microbes (bacteria, parasites - worms, fungi) –> ingested by macrophages/dendritic cells/B cells –> present peptides via MHC 2 molecules to CD4+ T cells (specifically TH2 and TH17!) –> results in: 1. Antibody production (B-cells); 2. activates the Complement system

54
Q

What is the complement system?

A

It is active in the innate immune response. It complements the ability of antibodies and phagocytic cells to clear infection.

55
Q

What are the four fuctions of the Complement System?

A

Opsonisation - enhancing phagocytososis of antigens
Chemotaxis - attracting macrophages and neutrophils
Cell lysis - rupturing membranes of foreign cells

Agglutination - clustering and binding of pathogens together (sticking)

56
Q

Outline how cell-dependent immunity is obtained.

A

Intracellular microbes (viruses, bacteria and protozoa) are ingested by antigen presenting cells (macrophages, dendritic cells, B cells) –> the T-cell receptor of the CD4+ cells (specifically TH1!) binds to the MHC 2 on the APC. This process activates the naive CD4+ cell.

Now - a CD8+ cell binds to the APC - this time to the MHC 1! This cell can now become a cytotoxic T lymphocyte (CTL) which will target infected cells - killing them with perforins and granzymes.

57
Q

In the adaptive immune response to intracellular microbes, how else can TH1 cells help the response?

A

TH1 cells (in addition to activating CD8+ cells into CTLs) will also:

Allow B cells to isotype switch - producing IgG (antibodies).

Increase number of macrophages (mature monocytes) which kill opsonised microbes via phagocytosis.

58
Q

Why is the IgG antibody better than IgM?

A

G = good; M = meh.

IgM is highly involved in the primary response.

IgG is a result of isotype switching during the adaptive immune response (active in secondary response)

The response it gives is faster, stronger and has a greater duration.

59
Q

What antibodies do B cells produce?

A

IgG4: opsonisation
IgA: mucosal production
IgG, IgE: Antibody-dependent cell cytotoxicity

IgE…: Allergies…

60
Q

What cell and antibody are heavily involved in allergies?

A

Mast cells - activated by TH2 cells in response to extracellular microbes - produce IgE in the case of allergies. Their intention is to achieve local inflammation!

61
Q

What cell is heavily involved in killing parasites?

A

Eosinophils kill parasites. They are activated by TH2 CD4+ cells (NOT TH17) in response to extracellular microbes - parasites.

62
Q

What cell stimulates the increase of neutrophils in infection?

A

TH17 cells will stimulate the production of neutrophils in response to extracellular microbes. Neutrophils act on the pathogens via phagocytosis.

63
Q

What are the 2 types of immunisations (broadly speaking)?

A

Active: inoculate small amount of antigen (may have lost/decreased virulence).

Passive: antibody transfer.

64
Q

What do we measure to diagnose and also manage HIV infection?

A

Diagnosis: HIV-1 (/2) p24 antibody and p24 antigen.

*Measuring both will help diagnose HIV - initially p24 antigen increases - during initial infection - before the p24 antibody is detectable - early diagnosis possible*.

Management: CD4+ and CTL counts are important in managing the condition.

65
Q

What is HAART?

A

Highly active anti-retroviral therapy It is commonly used in AIDS patients when their HIV is advanced, their CD4+ T cell count has fallen dramatically and they are symptomatic.

66
Q

How can HLA typing be used to determine anti-HIV responses?

A

The presence of certain HLA types (HLA-B27, 51 etc) will suggest slow progression of HIV - here the antigen presented is of a key peptide for the survival of the virus - therefore there is an effective T cell response.

Others (HLA-B35; homzygote in HLA-1 alleles) will indicate rapid progression - antigen presents less critical peptides from the virus (due to its mutation - therefore less effective T cell response.

DJ - ESA 3 - Infection (12 decks)

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