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ESA 3 > Infection 5 > Flashcards

Infection 5 Flashcards

1
Q

What are the relevant patient factors to travel related infections?

A

Calendar and relative time

Recent places

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2
Q

Why is a patient’s travel history important?

A

Imported diseases that are rare or unkown in the UK can occur, Infection DDx must be broadened to include infections endemic to areas travelled recently by patient

Different strains of pathogen are/have potentially:

Antigenically different

Impacting on protection and detection

Antibiotic resistance differences

Guides necessary ward and lab based infection prevention

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3
Q

What are the key aspects of a patients travel history?

A

Where? (Be exact)

When?

How (Direct or via?)

Accomodation

How long?

Specific risks (including sexual contact)

Preventative measures taken (E.g. Doxycycline)

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4
Q

What are the 4 main species of micro-organism that can cause malaria?

A

Plasmodium:

  • Falciparum
  • Vivax
  • Ovale
  • Malariae
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5
Q

escribe the spread of malaria

A

Female mosquitos are the vector

No case to case spread

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6
Q

Where does malaria occur?

A

The tropics:

Africa, Asia, Middle east, South and Central America

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7
Q

Describe a typical malaria history

A

Headache

Cough

Fatigue and Malaise

Arthralgia (joint pain)

Myalgia

Fever, Chills and Sweats which cycle every 3rd or 4th day

All occuring 1-3 wks after bite (incubation period)

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8
Q

What might be the common findings of an examination of patient with malaria?

A

Fever

Possible Splenomegaly

Coma

Resp distress (metabolic acidosis, pulm oedema)

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9
Q

Who is responsible for treatment of malaria?

A

Infectious disease physician

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10
Q

Describe malaria management

A

Blood smear to detect parasites

FBC, Urea and Electrolytes, LFTs, Glucose

Head CT if CNS symptoms

Treatment is species dependent:

    • P. falciparum - quinine or artemisinin*
    • P. vivax, ovale, malariae - chloroquinine +/- primaquine*
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11
Q

Describe a cycle of Malaria transmission/infection beginning from a mosquito biting an infected human

A

Mosquito acts as vector, infected blood passes into the mosquito gut and can be passed on via the mosquitos saliva

A mosiquto bites a human and the malarial parasite enters the blood through mosquito saliva

Parasite takes root in the liver (Exo-erythrocytic phase)

Parasite is released into the blood (Erythrocytic phase)

Mosquito can bite newl infected human and further pass it on

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12
Q

Outline the prevention of malaria

A

ABC

Assess risk:

  • Knowlegde of risk areas for regular or returning travellers

Bite prevention:

  • Repellant, aqequate clothing, nets
  • Chemoprophylaxis before travel

Chemoprophylaxis:

  • Specific to region

Stats and continues before/after return

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13
Q

What is enteric fever?

A

General term for Typhoid and Paratyphoid fever

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14
Q

Describe the epidemiology of enteric fever worldwide and in the UK

A

Worldwide:

Widespread in areas with poor sanitation

21 million cases per year, mostly children

UK:

500 cases/yr (travel related - mainly India)

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15
Q

What is the mechanism of infection of enteric fever?

A

Faeco-oral

Source is cases or carriers only

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16
Q

What is the causative organism for enteric fever?

A

Salmonella enterica serotypes

Commonly Salmonella typhii/paratyphii A, B or C

Aerobic gram negative rods

Non-lactose fermenting

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17
Q

What are the virulence factors of Salmonella enterica subsp. that commonly cause enteric fever?

A

Gram negative endotoxin (VI antigen)

Invasin (to allow intracellular growth)

Fimbriae (small hairlike processes) allow adherence to ileal peyer’s patches

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18
Q

What are the symptoms and signs of enteric fever?

A

Systemic disease w/ fever and headache

Abdominal discomfort

Constipation

Dry cough

Rash

Hepatosplenomegaly

Bradycardia

Complications can include haemorrhage and perforation of bowel

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19
Q

What investigation might be performed in a patient with suspected enteric fever?

What would be found in a patient with enteric fever?

A

Investigations:

FBC, WBCC, Urea and Electrolytes, LFTs, Blood and stool culture

Results:

Moderate anaemia

Relative lymphopenia

Raises LFTs

Bacteria in blood and stool culture (S. Enterica subsp.)

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20
Q

What is the current treatment for enteric fever?

A

Ceftriaxone or azithromycin for 7-14 days

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21
Q

Describe the preventative measures for enteric fever

A

Hygiene:

Food and water hygiene precautions (boil water etc)

Vaccine:

Used for high risk travel and lab personnel

VI capsular polysaccharide antigen or live attenuated virus

50-75% protective

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22
Q

Apart from enteric fever, what other common disease is caused by salmonella spp.?

Give common causative organisms, symptoms and complications

A

Food poisoning

Widespread distribution including UK (non-travel related)

Organisms:

Commonly caused by S. typhirium/enteritidis

Symptoms:

Diarrhoea

Fever

Vomiting

Abd. pain

Complications:

generally self limiting but bacteriaemia and deep seated infection may occur

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23
Q

What is zoonosis?

A

Any process whereby an infectious disease is transmitted from animal to human

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24
Q

Give an example of a zoonosis disease

Include the common causative organisms and it’s distribution worldwide

A

Brucellosis

Organisms:

Brucella abortus (cattle) and B. melintensis (goats and sheep)

Gram negative coccobascillus

Distribution:

S. Europe

Africa

Asia

C&S America

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25
Q

With regards to brucellosis describe the:

  • Transmission
  • Symptoms
  • Diagnosis
  • Treatment
A

Transmission:

Through skin breaks or the GI tract (Milk)

Symptoms:

Non specific, febrile (undulant fever, rising and falling)

Bone/Joint involvement

Epidydimitis

Diagnosis:

Generally from blood culture

Treatment:

Doxycycline and rifampicin

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26
Q

Why is travel history important in a patient that potentially has a severe/high risk disease?

A

Assessment of travel guides possible diagnosis

Also allows us to assess possibility of high risk infection being present

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27
Q

What precautions might be taken with someone with a suspected high risk of a travel related infection?

A

Requirement to consider isolation

Additional protections afforded to clinicians/lab staff handling high risk specimens

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28
Q

Give an example of two types of novel emergent viruses that caused pandemics

A

Influenza:

E.g. H1N1 swine flu in 2009

Coronavirus:

E.g. SARS-CoV in 2003 (severe acute respiratory syndrome)

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29
Q

Give examples of viruses, vectors and diseases that cause haemorrhagic fevers

A

Your examples may vary

Filoviridae - Bat - Ebola haemorrhagic fever

Flaviviridae - Mosquito - Dengue and Yellow haemorrhagic fever

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30
Q

What are the symptoms of Ebola?

A

Flu-like

Vomiting

Diarrhoea

Haedaches

Confusion

Rash

Internal/external bleeding at 5-7 days

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31
Q

Describe the transmission of Ebola

A

Through direct contact with infected bodily fluids

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32
Q

What are the potential causes of traveller’s diarrhoea?

What is the relevance of organism type/species to the symptoms experienced?

A

Bacteria

Parasites

Viruses

Different organisms can cause differnt types of stool found in diarrhoea

33
Q

Name some web resources that you might use to look for information regarding any potential outbreaks of infections in areas your patient might have travelled?

A

www. cdc.gov
www. who.int

34
Q

What is influenza A and how is it spread/

A

A virus

Spreads via droplets/aerosols (commonly from a cough or sneeze)

35
Q

What are the common symptoms of Infuenza A infection?

A

Fever

Cough

Sore throat

Muscle aches

Conjunctivitis

In severe cases Pneumonia

36
Q

Describe how Infuenza A might be subtyped

A

Subtyped based on two proteins found on the surface of the viral envelope

Haemagglutinin:

Protein that causes RBCs to agglutinate (clump together)

Neuraminidase:

A protein that cleaves the glycosidic bonds of neuraminic acid monosaccharides

Subtype of each (H and N) gives the overall subtype (E.g. H1N1)

37
Q

Describe how Influenza A can cause pandemics

A

Antigenic drift:

Gene mutation of antigens on envelope

Antigenic shift:

The process by which two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains.

Pandemics:

These two processes in tandem produce new subtypes of virus that are occasionally highly virulent and +/- deadly, this leading to a pandemic

38
Q

How would you manage a patient with Influenza A?

A

Oseltamivir (First ever Neuraminidase inhibitor)

Only in high risk patients (elderly, young, infirm) that present with onset of symptoms less than 48hrs ago

Only supportive treatment for otherwise healthy adults

39
Q

What are the common symptoms of Legionella pneumophilia infections?

A

Bacterium causes Legionnairres’ disease

A form of pneumonia

Symptoms also include:

Fever

Headache

Chills

Cough (dry or productive)

Musle aches

Ataxia

Confusion

Diarrhoea and vomiting

40
Q

What might be the labratory findings of a standard blood workup (FBC, WBCC, U&E, LFTs and Culture)?

A

Urea and electrolytes deranged (commonly hyponatraemia)

Impaired Liver function

Culture would reveal gram negative bascilli of L. pneumophilius

41
Q

How is L. pneumophilia spread?

What is the source?

A

Spread via aerosol

Sources = Cases and soil

42
Q

How does L. pneumophilia derange noraml innate immune function to aid in replication?

A

Once phagocytosed by macrophages lysosymes are unable to bind

L. pneumophilia remains in the macrophage where it can replicate

43
Q

What are the common antibiotic clasess used to treat L. pneumophilia?

A

Macrolides

Fluoroquinolones

44
Q

What is the response of a Naive T cell to a pathogen?

A

No response

45
Q

What are the two types of microbe as for as adaptive immune response is concerned?

A

Intracellular microbes (replicate intracellularly):

Viruses

Some bacteria

Protozoa

Extracellular microbes (replicate extracelullarly):

Most bacteria

Parasites

Worms

Fungi

46
Q

What is the initial cellular interaction of the adaptive immune system?

A

Antigen presenting cells react with T lymphocytes

47
Q

What are the 3 processes involved in APC function?

A

Capture of microbe

Processing of microbe

Presentation of antigen to T lymphocytes

48
Q

Where are APCs found?

A

Within lymphoid tissue:

Skin - SALT (Skin associated lymphoid tissue)

Mucous membranes (GastricALT, NasalALT, BronchialALT etc)

Lymphoid organs (Lymph nodes, spleen)

Circulation (Plasmacytoid and myeloid Dendritic cells)

49
Q

How do APCs capture antigens?

A

Phagocytosis (whole microbe)

Micropinocytosis (Soluble particles - random process)

50
Q

How do APCs recognise pathogenic cells?

A

Extracellular pattern recognition receptors (PRRs) recognise extracellular pathogens via pathogen associated molecular patterns

Intracellular PRRs recognise intracellular pathogens via PAMPs

51
Q

Give some types of APCs and where they are found

A

Dendritic cells - Lymph nodes

Langehans’ cells - Skin

Macrophages - various tissues

B cells (recognise antigen in native form) - Lymphoid tissues

52
Q

What are the differences in response of an APC when it encounters intracellular or extracellular microbes?

A

Extracellular:

Extracellular PAMP is recognised by extracellular PRR leading to activation of humoral immunity (Antibodies and complement)

Intracellular:

Intracellular PAMP is recognised by PRR leading to activation of cell-dependent immunity (Cytotoxic T cells, macrophages and antibodies)

53
Q

What class of molecules do APCs present to T lymphocytes?

A

Present Major Histocompatibility Complex (MHC) class I/II

Also known as Human Leukocyte Antigens (HLA)

54
Q

Describe the differences between MHC I and MHC II molecules

A

Presenting cell:

Class I presented by all nucleated cells

Class II presented by professional APCs (dendritic cells, macrophades, B cells etc)

Function:

Class I molecules presented when peptides from intracellular microbes are detected by APC

Class II molecules presented when peptides from extracellular microbes are detected by APC

Responsive T cells:

Class I molecules present to CD8+ T cells (Extrcellular)

Class II molceules present to CD4+ T cells (Intracellular)

55
Q

What are the key genetic features of the HLA genes?

A

Co-dominant expression:

Both parental genes expressed

Increases the number of MHC molecules we can express, stregthening immunity

Polymorphic genes:

Different alleles among different individuals

Increases presentation of different antigens in the population

56
Q

Outline the differences in structure of MHC Class I and II molecules

A

Class I:

Two peptides

Alpha 1, 2 and 3 regions on peptide 1

Beta 2 microglobulin subunit on peptide 2

Peptide binding site between Alpha 1 and 2 units on peptide 1

Class 2:

Two peptides

Alpha 1 and 2 units on peptide 1

Beta 1 and 2 units on peptide 2

Peptide binding site is between the two peptides

57
Q

How specific is the binding of MHC molecules to processed peptides?

A

Broad specificity (can present a large number of peptides)

58
Q

Outline the process of MHC Class I presentation on cell surface from the entry of a virus into the cell

A

Endogenous pathway:

Virus wil replicate and produce proteins

These proteins are recognised as useless and directed to proteasomes where they are cleaved into small peptides

These peptides are transported to the ER where MHC class I molecules can be found, if there is a match, the two form a complex

This complex is exported to cell membrane to await recognition by CD8+ T cell

59
Q

Proteasome action is not confined to viral proteins, it can cleave self proteins, why does this not lead to autoimmune disease in a health person?

A

Self proteins are recognised by MHC Class I molecules but the complex is not recognised by CD8+ T cells and do not lead to activation

60
Q

Outline the process of MHC class II presentation on the cell surface from entry of Exogenous antigens into the cell

A

Exogenous pathway:

Exogenous antigen from extracellular microbe is endocytosed

Lysosome fuses with endosome and antigen is digested into small peptides

MHC class II bearing vesicle exported from ER fuses with endosome

If MHC II recognises a peptide the complex is exported to the cell membrane to be recognised by a CD4+ cell

61
Q

Describe why patients with HIV might vary in their disease progression

A

Slow progressors:

Exhibit HLA genes such as B27, B51 and B57

These are linked to the presentation of not mutating peptides that are key to virus survival

This leads to a sustained and effective CD4+ response to HIV as the virus cannot mutate these key peptides without losing the ability to replicate/infect cells etc

These patients are also known as Elite controllers or long term non-progressors due to this ability to effectively control viral replication

Rapid progressors:

Exhibit HLA genes such as B35 and are commonly homozygotes for HLA-I alleles

Linked to the presentation of non-key peptides that the virus can readilty mutate

This leads to decreased recognising of the HIV virus and hence decreased CD4+ response hence rapid progression of disease

62
Q

What is the relevance of HLA molecules to medical treatment?

A

Transplant:

HLA mismatch between donor organ and recipient leads to recipient immune system attacking donor tissue (Organ rejection)

Graft versus host:

Grafted tissues such as skin begins to attack recipient cells

63
Q

Give some conditions in which there is an HLA type link

A

Ankylosing spondylitis:

HLA-B27 found in 90% of patients

Insulin dependent Diabetes Mellitus:

HLA-DQ2 found in 50-75% of patients

64
Q

Dendritic cells can present MHC molecules unusually in response to certain stimuli, explain this

A

Intracellular microbes can trigger a dendritic cell to present with MHC class I and II molceules hence activating CD4+ and CD8+ cells

CD4+ cells activated in this way are a differnt type of CD4+ cells to that seen in humoral immunity

Mechanism unknown

65
Q

Where do T cells mature?

A

Thymus gland

66
Q

Describe the T cell receptor

A

Used to recognise MHC I and II molecules

Huge genetic diversity required to recognise all MHC molecules

Genetic diversity comes about via a process called gene rearrangement

Creates a variable region within the TCR protein that binds to MHC

67
Q

What are the types of T cell?

A

CD4+:

Called T helper cells

TH-1

TH-2

TH-17

CD8+:

Cytotoxic T lymphocytes (CTL)

68
Q

What are the common immune features on a T cell membrane?

A

All:

T Cell receptor - For binding to processed peptide on MHC

CD3 - Co-receptor involved in signal transduction

CD4+:

CD4 protein - Recognises MHC class II molecules directly conferring specificity

CD8+:

CD8 protein - Recognises MHC class I molecules directly conferring specificity

69
Q

Describe the activation of Naive CD4+ cells

A

Naive TH-0 CD4+ cells bind to an APC presenting MHC class II molecules in 3 ways:

CD4 bind directly to MHC II

TCR binds to the peptide presented by MHC II

CD28 on the T cell binds to B7 protein on the APC

APC releases cytokines that stimulate one of two outcomes:

If the MHC II is presenting extracellular microbe fragments then the TH-0 lymphocyte becomes TH-2 or TH-17 for best humoral response

If the MHC II is presenting intracellular microbe fragments (such as in the case of dendritic cells) then the TH-0 lymphocyte becomes TH-1 for best cellular immune response (TH-1 goes on to interact with CD8+ which is activated in tandem with CD4+)

70
Q

What is co-stimulatory activation of T cells?

A

Binding of TCR and CD4+/8+ is not enough to fully activate a T cell and therefore an extra recptor/ligand binding pair is required to bind to fully activate

E.g. B7 and CD28 for CD4+ cells

71
Q

Describe the T cell response to intracellular microbes

A

APC (Dendritic cell) presents MHC I and II molecules and acessory activation proteins such as B7 that activate both CD4+ (into TH-1) and CD8+ cells

CD8+ cells are not fully activated and require interaction with TH-1 cells to fully activate

CD8+ cells are now fully activated CTLs that will bind to infected MHC class I presenting cells and release cytotoxic proteins that lead to death of the infected cell (E.g. Perforins and Granzymes)

72
Q

Label the boxes

Describe what is demonstrated by this graph

A

Top then bottom:

CD4+ cells

Viral Load

Interpretation:

HIV Viral load is dependent on CD4+ number

The higher the CD4+ the better the body can control viral replication and hence lower viral load

73
Q

What is concept is demonstrated by these two graphs?

A

Shows that long term survivors of HIV (on the left) have a consistently higher level of CD8+ cells which combat the HIV infected cells

In patients which cannot control the virus the CD8+ cells drop rapidly and viral load rises quickly

74
Q

Apart from activation of CD8+ T cells what is the response to intracellular microbes?

A

TH-1 cells which activate CD8+ cells also activate:

B cells:

    • Produces antibodies*
    • Leads to opsonisation, neutralisation, complement activation*

Macrophages:

    • Phagocytic activity*
    • Kills opsonised microbes*
75
Q

Describe the typical primary and secondary antibody reactions to infection

A

Primary

Antibodies are largely pentameric IgM and small amount of IgG

IgM contributes to opsonisation

Reflects naivety to the pathogen

Secondary:

Antibodies are largely IgG with some IgM

IgG is a more effective antibody, it opsonises, activates complement and initiates antibody dependent cell cytotoxicity

Larger total amount of antibody

Reflects a learned response to pathogen, high amount of specific IgG

76
Q

Apart from activation of CD4+ cells, what is the adaptive immune response to extracellular microbes?

A

TH-2 Cells activate:

Eosinophils - Killing of parasites

B Cells - Release antibodies

Mast Cells - Mediate local inflammation, can trigger allergic reaction

TH-17 Cells activate:

Neutrophils - Phagocytosis of bacteria

77
Q

Outline the range of Antibodies relesed in reaction to etracellular microbe and give their functions

A

IgG4:

Opsonisation

IgG, IgE:

Antibody dependent cell cytotoxicity

IgE specifically:

Mediation of allergic reaction

78
Q

Give some examples of medical advances derived from study of the adaptive immune system

A

Vaccination

Ig Therapy:

Treatment of immune deficiency

Immediate protection:

Passive immunisation (antibody transfer)

Antibody based diagnostic testing:

Infectious disease

Autoimmune disease

Blood type and HLA typing

ESA 3 (54 decks)

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