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Semester 3 > Infection 1-6 > Flashcards

Infection 1-6 Flashcards

1
Q

What are the 4 steps of the Koch Henle Postulates?

A
  1. Isolate the organism from every case
  2. Propagate in pure culture in vitro
  3. Re-inoculate and produce disease
  4. Re-isolate
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2
Q

What are the key differences between Koch’s postulates and diagnosis?

A

Koch’s - Isolates SAME organism from MANY patients and isolates able to reproduce disease in model

Diagnosis - ONE isolate from ONE patient. Identify if the organism is a recognised pathogen.

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3
Q

How can microbes be classified biologically?

A

Prokaryote
Eukaryote
Viruses

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4
Q

How can microbes be classified medically?

A

Pathogen
Non-pathogen
Opportunistic pathogen

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5
Q

What are the main differences between eukaryotes and prokaryotes?

A

Eukaryotes have membrane bound organeles and multiple chromosomes. Prokaryotes only have one and transcription/translation is coupled (compartmentalised in eu.). Ribosomes - 30+50S=70S pro. 40+60S=80S eu.

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6
Q

How do viruses infect the host?

A

Obligate intracellular parasites that multiply using the host cell’s biosynthetic machinery.

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7
Q

What is a bacteriophage?

A

Virus which infects bacteria

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8
Q

What are the principle characteristics of innate immunity?

A

Rapid response
Invariant
Limited number of specificities
Constant during response

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9
Q

What are the principle characteristics of adaptive immunity?

A

Slow response
Variable
Numerous highly selective specificities
Improve during response

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10
Q

How do neutrophils act?

A

Phagocytosis and killing of microorganisms. Granules contain numerous bactericidal substances.
Phagocytosis particles opsonised by IgG or compliment and functions as effector cell of humoral immunity

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11
Q

How do eosinophils act?

A

Killing of antibody-coated parasites through release of granule contents - highly basic or ‘cationic’ proteins
Bind avidly to IgE-coated particles

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12
Q

Describe the nucleus of a neutrophil (polymorph)

A

multilobed

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13
Q

What type of white blood cells are common at the site of an allergic reaction?

A

Basophils and eosinophils

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14
Q

What is a basophil and how does it work?

A

A leucocyte with large basophilic granules which contain heparin, histamine and other vasoactive amines. Granules released at the site of inflammation and in immediate hypersensitivity (allergic) reactions
Express high affinity receptors for IgE - interaction causes the release of basophil granules

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15
Q

What is a mast cell?

A

A tissue cell which is not bone marrow derived but otherwise similar to its circulating counterpart, the basophil

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16
Q

What is the largest nucleated cell of the blood?

A

Monocyte - 16-20 micrometers.

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17
Q

What is a macrophage?

A

Antigen presenting cell
Mature monocytes
Strongly phagocytic
Receptors for Ig and complement

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18
Q

What are natural killer cells?

A

Type of lymphocyte able to kill virus infected cells and certain types of cancer cells
Large cytoplasmic granules distinguish them microscopically

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19
Q

How do NK cells and cytotoxic T cells act differently?

A

NK act independently of antigen presentation and recognition, which is necessary for the action of T cells

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20
Q

What are dendritic cells?

A

Antigen presenting cells. Possess long processes which interdigitate between lymphoid cells and interdigitate between lymphoid cells and present antigens to them.

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21
Q

What is a B lymphocyte and where is it derived?

A

Precursor of antibody-forming cells. Bone marrow derived

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22
Q

What is a plasma cell?

A

The B lymphocite in its high-rate antibody secreting state. Rarely seen in the blood, but found in spleen, lymph nodes etc whenever antibody is being made.

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23
Q

From where are T lymphocytes derived?

A

Thymus

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24
Q

What are the primary lymphoid organs?

A

Bone marrow where T and B lymphocytes are made. Thymus where T lymphocytes mature/are selected

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25
Q

What are the secondary lymphoid organs?

A

Eg. Spleen, lymph nodes nad peyers patches. Contain T cells, B cells, antigen presenting cells

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26
Q

What cells constitute the bone marrow stroma?

A 
Fibroblasts (reticular connective tissue)
Macrophages
Adipocytes 
Osteoblasts
Osteoclasts
Endothelial cells forming the sinusoids
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27
Q

What are the 3 types of stem cells present in bone marrow?

A

Haematopoietic - wbc, rbc and platelets
Mesenchymal - gatekeeper cells of marrow
Endothelial stem cells

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28
Q

What is aplastic anaemia?

A

Bone marrow does not produce sufficient new cells to replenish blood cells. Deficient in all blood cell types.
Idiopathic or autoimmune - wbc attack bone marrow

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29
Q

Describe the development of T cells.

A

Precursors arrive at thymus from bone marrow. Cortex and medulla educate thymocytes into mature competent T cells. Mature T cells are released into the peripheral.

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30
Q

What are thymocytes?

A

Precursor lymphocytes from the bone marrow which enter the thymus via blood vessels. Proliferate and mature in the thymus. 1-3% survive the selection process that allows mature T cells to enter the peripheral circulation.

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31
Q

Name 2 diseases associated with Thymus disease.

A

Severe combined Immunodeficiency - SCID

DiGeorge Syndrome - genetic disorder causesd by deletion of a small setion of chromosome 22

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32
Q

What type of cells are CD3,4,8,16 and 19?

A 
CD3 T cells
CD4 Helper T cells
CD8 Cytoxic T cells
CD16 Macrophages
CD 19 B cells
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33
Q

Describe the path of B cells through lymph nodes.

A

Travel from the blood stream entering the cortex via high endothelial venules. Leave via efferent lymph.

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34
Q

What happens when a B cell encounters an antigen?

A

Forms primary foci from which proliferating cells migrate to the primary follicle forming a secondary follicle with a germinal centre. A few weeks after it forms, the germinal centre reaction dies down.

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35
Q

What may cause lymph nodes to enlarge?

A 
Infection
Virus
Inflammation
Cancer
Caner of the blood
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36
Q

What is GALT?

A

Gut Associated Lymphoid Tissue

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37
Q

What is MALT?

A

Mucosa Associated Lymphoid Tissue

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38
Q

What is SALT?

A

Skin Associated Lymphoid Tissue

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39
Q

What are tonsils?

A

Mass of lymphoid tissue in submucosa of oropharynx. Many lymphoid follicles, mostly with germinal centres

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40
Q

What are Peyers patches?

A

Organised patches of lymphoid follicles int he submucosa of the gut, mainly the ileum

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41
Q

What is an infection?

A 
Invasion of a host's tissues by microorganisms
Disease caused by:
- microbial multiplication 
- toxins
- host response
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42
Q

What is microbiota?

A

“commensals”
Microorganisms carried on skin and mucosal surfaces
Normally harmless or even beneficial
transfer to other sites can be harmful

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43
Q

How may infections be spread?

A 
Physical contact
Airborne 
Vector may be necessary
Ingestion 
Inhalation
Mother to child - vertical transmission
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44
Q

What determines the disease caused by an infection?

A 
Pathogen:
- virulence factors
- inoculum size
- antimicrobial resistance
Patient:
- site of infection
- co-morbidities
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45
Q

How do you determine if a patient has an infection?

A

History - symptoms/exposure
Examination
Investigations - specific/supportive

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46
Q

How do microorganisms cause disease?

A

Exposure -> adherence -> Invasion -> Multiplication -> Dissemination

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47
Q

What are virulence factors?

A

Factors of viruses that cause disease - exotoxins e.g.. cytolytic, AB toxins, Superantigens, enzymes and endotoxins

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48
Q

What are some supportive investigations?

A 
Full blood count
C reactive protein
Blood chemistry
Imaging
Histopathology
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49
Q

Name some tests you might use to determine specific infection bacteriology.

A

Specimen type
M, C & S - microscopy, culture and sensitivity (antibiotic susceptibility)
Antigen detection
Nucleic acid detection

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50
Q

Name some tests you might use to determine specific infection virology

A

Antigen detection
Antibody detection
Detecting viral nucleic acid

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51
Q

What are the 2 semi-independent parts of the lymphatic system?

A

Lymphatic capillaries and vessels

Lymphoid tissues and organs

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52
Q

What is the function of the lymphatic system?

A

Fluid balance
Fat absorption
Defence

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53
Q

What is the lymphatic system?

A

A network of vessels that assist in circulating fluids - excess fluid away from interstitial spaces to the blood stream

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54
Q

What is the structure of lymphatic capillaries?

A

Tiny closed end vessels consisting of simple squamous epithelium. More permeable than blood vessels because they lack a basement membrane.
Resemble small veins, one way valves

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55
Q

How are lymphatic vessels compressed?

A

Contraction of surrounding smooth muscle
Periodic contraction of smooth muscle in lymphatic vessel wall
Pressure changes in the chest during breathing

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56
Q

Where does the right lymphatic duct converge and empty into?

A

Upper right limb and right half of head, neck and chest and empties into right subclavian vein

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57
Q

Where does the thoracic duct converge and empty into?

A

Rest of body (compared to right lymphatic duct) and empties into the left subclavian vein

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58
Q

What are the lymphoid organs?

A

Lymph nodes
Tonsils
Spleen
Thymus gland

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59
Q

Describe the structure of lymph nodes.

A

Rounded structures distributed along the lymphatic vessels
Outer part - cortex. Follicles with germinal centre (contains dividing lymphocytes)
Inner part - medulla. Contains phagocytic macrophages.

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60
Q

What are lacteals?

A

Special lymphatic vessels located in the lining of the small intestine -. fat enters lymphatic vessels and then venous circulation

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61
Q

What is chyle?

A

Lymph that is milky in appearance due to fat.

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62
Q

How does the lymphatic system act in the bodies defensive mechanisms?

A

Removes organisms and foreign substances from the lymph

Associated with activation of the immune system.

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63
Q

What is the collective term for lymph node enlargement?

A

Lymphadenopathy - may be due to lymphadenitis (painful and responding to foreign antigen) or metastatic cancer (usually painless and firm)

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64
Q

What is the function of tonsils?

A

Trap and remove bacteria and other foreign materials

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65
Q

How is tonsillitis caused?

A

Congestion of bacteria.

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66
Q

What is the spleen?

A

The largest lymphatic organ containing sinuses filled with blood. 2 tissue types - red and white pulp.

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67
Q

What is red pulp?

A

Receives arterial blood which passes into venous sinuses. Lined by macrophages - removes old red cells and recycles iron

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68
Q

What is white pulp?

A

T and B cell compartments with macrophages and other immune cells.

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69
Q

What is the function of white pulp?

A

Recognise pathogens, remove pathogens and activate T cells and B cells

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70
Q

How does age affect the thymus?

A

Largest at infancy and during puberty, small in an adult and replaced by fat and connective tissue in the elderly.

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71
Q

What is the function of the thymus?

A

Site of T lymphocyte production

Secretes protein hormones called thymosins

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72
Q

What are the main types of fungi?

A

Yeast

Mould

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73
Q

What are the 2 most common types of pathogenic parasites in humans?

A 
Protozoa
Helminth (worm)
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74
Q

How does age affect immunity?

A

Different antibodies at different ages - inter-uterine from mother etc

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75
Q

How does gender affect immunity?

A

Hormones

Anatomy - UTI

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76
Q

How do social factors affect immunity?

A

What you are exposed to.

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77
Q

How does time affect disease?

A

Calendar time - weather, temperature etc

Relative time - time since being somewhere (?)

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78
Q

How does where a patient has been affect their chances of disease?

A

Some diseases are more common in different countries/places and people who have visited are less likely to have immunity than those that live there. Therefore, where they currently live and have recently visited can affect their health

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79
Q

Name some mechanisms of infection

A 
Contiguous spread
Inoculation
Haematogenous
Ingestion
Inhalation
Vector 
Vertical transmission
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80
Q

What 3 things is a diagnosis based on?

A

History
Examination
Investigation

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81
Q

What specific treatments might be given for an infection?

A

Antimicrobials

Surgery - drainage, debridement, dead space removal

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82
Q

What supportive treatment might be given for an infection?

A

Symptom relief

Physiological restoration

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83
Q

What is a purpuric rash?

A

The appearance of red or purple discolouration on the skin that does not blanch on applying pressure. Looks like bleeding under the skin. 3-10 mm diameter of spots

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84
Q

What are the clinical features of sepsis?

A 
Systemic inflammatory response syndrome
A response to a non-specific insult
Two or more of:
- Temperature 38
- Heart rate >90
- Resp. rate >20/min
WBC 12x10^9/L
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85
Q

What is bacteraemia?

A

Presence of bacteria in the blood

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86
Q

What is septicaemia?

A

Clinical term meaning generalised sepsis

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87
Q

What is sepsis?

A

The systemic response to infection - SIRS + documented/presumed infection

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88
Q

Define severe sepsis.

A

SIRS + organ dysfunction/hypoperfusion (hypotension, decreased urine output)

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89
Q

Define septic shock.

A

Severe sepsis + persistently low blood pressure despite administration of intravenous fluids

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90
Q

What is the common bacterial pathogen to cause meningococcal meningitis in a teenager and how is it spread?

A

Neisseria meningitidis.
Spread by direct contact with respiratory secretions. Most people are harmlessly colonised but in the unlucky few, rapidly progressive.

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91
Q

How is low blood pressure caused in a septic patient despite the high pulse rate?

A

Endotoxins that the bacteria release cause vasodilation, decreasing total peripheral resistance. Mean arterial blood pressure = Total peripheral resistance + Cardiac output

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92
Q

What is the role of a pilus on a bacterial cell?

A

Enhances attachment to other cells

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93
Q

What does the polysaccharide capsule on a bacterial cell do?

A

Promotes adherence

Prevents phagocytosis

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94
Q

In the inflammatory cascade, what are the local effects of cytokines?

A

Stimulate inflammatory response to promote wound repair and recruit RE system

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95
Q

In the inflammatory cascade, what are the systemic effects of cytokines?

A

Stimulating growth factor, macrophages and platelets. Goal is homeostasis. Lead to activation of humoral cascade and RE system

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96
Q

How can the release of cytokines cause organ ischaemia, dysfunction and failure?

A

Cytokines initiate the production of thrombin and also inhibit fibrinolysis
Coagulation cascade leads to microvascular thrombosis…
Microvascular injury is the major cause of shock and multiorgan failure

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97
Q

What urgent investigations would you order on someone with sepsis?

A 
Full blood count, urea and electrolytes
EDTA bottle for PCR
Blood sugar
Liver function test
C-reactive protein
Clotting studies
Blood gases
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98
Q

What are the sepsis 6 and when must they be delivered?

A

Within 1 hr:
Deliver high flow oxygen
Take blood cultures and other cultures and consider source
Administer empirical IV antibiotics
Measure serum lactate
Start IV fluid resuscitation
Commence accurate urine output measurement

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99
Q

What are the requirements for an antibiotic for meningitis?

A

Active against the pathogen that penetrates the CSF

Empiric choice is ceftriaxone

100
Q

What are some life threatening complications of sepsis?

A 
Irreversible hypotension
Respiratory failure
Acute kidney injury
Raised intracranial pressure 
Ischaemic necrosis of digits/hands/feet
101
Q

How is a diagnosis of sepsis confirmed?

A

Blood culture
PCR of blood
Lumbar puncture (if safe) - culture of CSF and PCR

102
Q

What is the cerebrospinal fluid examined for in sepsis?

A

Appearance - turbidity and colour
Microscopy - WBCs and RBCs
Gram stain
Referral for PCR

103
Q

Describe Neisseria meningitidis.

A

Gram-negative diplococcus
Numerous serogroups based on polysaccharide capsular antigen - evades immune response by preventing phagocytosis
Outer membrane acts as an endotoxin

104
Q

What % of adults may be carriers of meningococcal disease?

A

25%

105
Q

How is meningococcal disease spread?

A

aerosols and nasopharyngeal secretions. Acquired by clearance, carriage or invasion

106
Q

What is the most common group of meningococcal disease?

A

In England, 1000 cases/yr mainly group B, fatality rate approx 10% but elsewhere, group A predominates. ‘Meningitis belt’ across Africa.

107
Q

Describe some preventions of meningitis.

A

Meningococcal C conjugate vaccine
ACWY vaccines available for immunocompromised patients and travel protection
People in close contact to patients can be given antibiotic prophylaxis and considered for vaccinations

108
Q

Why is there no vaccine in routine use for meningococcal group B?

A

B capsule poorly immunogenic and similar to neural tissue.

Vaccine developed after screening candidate proteins from genome

109
Q

Define the immune system.

A

Cells and organs that contribute to immune defences against infectious and non-infectious substances

110
Q

Define infectious disease.

A

When the pathogen succeeds in evading and/or overwhelming the host’s immune defences.

111
Q

What are the roles of the immune system?

A

Pathogen recognition
Containing/eliminating the infection
Regulating itself
Remembering pathogens

112
Q

What type of barriers can the innate immune system form?

A 
Physical barriers
Physiological barriers
Chemical barriers
Biological barriers
(limit entry and growth of pathogens)
113
Q

What physical barriers does the innate immune system provide?

A

Skin
Mucous membranes
Bronchial cilia

114
Q

What physiological barriers does the innate immune system provide?

A

Diarrhoea
Vomiting
Coughing
Sneezing

115
Q

What are the chemical barriers of the innate immune system?

A

Low pH - skin, stoomac, vagina

Antimicrobial molecules - IgA, lysozyme, mucous, beta-defensins, gastric acid and pepsin

116
Q

What are some biological barriers of the innate immune system?

A

Normal flora - non pathogenic microbesin strategic locations eg nasopharynx, mouth, skin, GI tract, vagina etc. Absent from internal organs

117
Q

What are the benefits of normal flora?

A

Compete with pathogens for attachment site and resources
Produce antimicrobial chemicals
Synthesize vitamins

118
Q

What are some examples of normal flora that inhabit the skin?

A 
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus pyogenes
Candida albicans
Clostridium perfingens
119
Q

What are some examples of normal flora that inhabit the nasopharynx?

A

Streptococcus pneumoniae
Neisseria meningitidis
Haemophius species

120
Q

How might normal flora be displaced from its normal location to a sterile location?

A

Breaching the skin integrity - skin loss, surgery, injection drug users, IV line
Fecal-oral route - food borne infection
Fecal-perineal-urethral route - urinary tract infection (women)
Poor dental hygiene/dental work (most common) - dental extraction, gingivitis, flossing

121
Q

Who are considered to be high risk patients for infection?

A

Asplenic (and hyposplenic)
Patients with damaged or prosthetic valves
Patients with previous infective endocarditis
Would be given antibiotic prophylaxis

122
Q

When might normal flora overgrow and become pathogenic?

A

When host is immune-compromised - diabetic, AIDS, malignant disease, chemotherapy

123
Q

When might normal flora be depleted by antibiotics?

A

Intestine -> severe colitis (Clostridium difficile)

Vagina -> thrush (Candida albicans)

124
Q

What is the second line of defence in innate immunity?

A

Phagocytes and chemicals -> inflammation (factors that will contain and clear the infection)

125
Q

How are pathogens recognised?

A

Microbial structures: Pathogen-associated molecular patterns (PAMPs): carbohydrates, lipids, proteins, nucleic acids recognised by:
Phagocytes: Pathogen Recognition Receptors (PRRs): Toll like receptors

Opsonins might bind to the microbial surfaces leading to an enhanced attachment of phagocytes and clearance of microbes

126
Q

What are some examples of PAMPs and PRRs for gram negative bacteria?

A

Lipopolysaccharide (LPS) -> TLR4
Lipoprotein and lipopeptides -> TLR2
Porins

127
Q

What are some examples of PAMPs and PRRs for gram positive bacteria?

A

Peptidoglycan -> TLR2

Lipoteichoic acids -> TLR4

128
Q

What are some examples of PAMPs and PRRs for all mycobacteria?

A

Lipoarabinomannan -> TLR2

Mannose-rich glycans

129
Q

What is an example of a PAMP and PRR for Bacterial flagella?

A

Flagellin -> TLR5

130
Q

Give some examples of opsonins.

A

Complement proteins eg C3b and C4b
Antibodies - IgG, IgM
Acute phase proteins - C-reactive protein (CRP), manose-binding lectin (MBL)

Theses are essential in clearing encapsulated bacteria

131
Q

How do phagocytes act?

A

Recognise PAMPs/opsonins, engulf and degrade infectious microbes

132
Q

What are the 2 pathways by which phagocytes might kill pathogens?

A

Oxygen-dependent pathway (respiratory burst)

Oxygen-independent pathways

133
Q

How does the oxygen dependent pathway by which phagocytes may kill pathogens work?

A

Produces toxic O2 products for teh pathogens: Hydrogen peroxide, hydroxyl radical, nitric oxide, singlet oxygen, hypohalite

134
Q

What are the oxygen independent pathways by which a phagocyte might destroy a pathogen?

A

Lysozyme
Lactoferrin or transferrin
Cationic proteins
Proteolytic and hydrolytic enzymes

135
Q

What are the 2 activating pathways of the complement system?

A

Alternative pathway - initiated by cell surface microbial constituents
MBL pathway - Initiated when MBL binds to mannose containing residues of proteins found on Salmonella app. Candida albicans

136
Q

What do serum proteins C3a and C5a do?

A

Recruit phagocytes

137
Q

What do serum proteins C3b -C4b do?

A

Opsonisation of pathogens

138
Q

What do serum pathogens C5-C9 do?

A

Kill pathogen’s membrane and attack complex

139
Q

What do cytokines/chemokines do?

A

chemoattraction
phagocyte activation
inflammation

140
Q

What are the anti-microbial actions of macrophage-derived TNF/IL-1/IL-6?

A

Liver (opsins) - CRP and MBL (-> complement activation)
Bone marrow - Neutrophil mobilisation
Inflammatory actions - Vasodilation
Vascular permeability
Adhesion molecules -> attraction of neutrophils
Hypthalamus - increased body temperature

141
Q

How does an infection cause sepsis and multi-organ failure?

A

Infection activates microbial toxins (LPS) which can cause overreaction of TLR4 receptor and complements. This can cause an excessive inflammatory response which leads to sepsis and multi-organ failure.

142
Q

How does an excessive inflammatory response lead to decreased tissue/organ perfusion?

A

cytokine shower
coagulopathy
vasodilation
capillary leak

143
Q

Why might phagocytosis be reduced?

A

Decrease spleen function (asplenic/hyposplenic)
Decrease neutrophil number (cancer chemo, certain drugs, leukaemia and lymphoma)
Decrease neutrophil function (chronic granulomatous disease (no reps burst), Chediak-Higashi syndrome (no phagolysosome formation))

144
Q

What are the 5 stages of innate immunity?

A
  1. Innate barriers
  2. Compliment, mast cells and macrophages activation (PRR)
  3. Vascular changes and chemoattraction
  4. Hypothalamus and liver are involved
  5. Redness, heat, swelling and pain - local inflammation
145
Q

What is the mechanism of action of the first line of defence in innate immunity?

A

Limit entry and growth of pathogens at portals of entry

146
Q

What is the mechanism of action of the second line of defence in innate immunity?

A

Contain and eliminate the infection

147
Q

What are healthcare infections?

A

Infections arising as a consequence of providing healthcare. In hospital patients neither present nor incubating at time of admission. For practical purposes, this means onset is at least 48 hrs. Also includes infections in hospital visitors and healthcare workers

148
Q

Why are healthcare infections important?

A

Frequent - prevalence = 8% of in-patients
Impact on health
Impact on healthcare organisations
Preventable
Av of 1 day extra in hospital (not everyone gets them but can stay in hospital for 10 days…)

149
Q

What type of HCAI is most common(roughly)?

A

GI - 21%
UTI - 20%
Varies across hospitals and departments

150
Q

How might you prevent infection?

A

Prevent pathogen entering
Prevent the mechanism of infection
Prevent infection occurring

151
Q

What are some common healthcare infection viral pathogens?

A

Blood borne (Hep. B/C, HIV)
Nonovirus
Influenza
Chicken pox

152
Q

What are some common healthcare infection bacterial pathogens?

A

Staph aureus inc. MRSA (MSSA more common than MRSA)
Clostridium difficile
Escherichia coli, Klebsiella pneumoniae
Pseudomonas aeruginosa
Mycobacterium tuberculosis - histopathologists

153
Q

What are some common healthcare infection fungi pathogens?

A

Candida albicans

Aspergillus species

154
Q

What are some common healthcare infection parasites?

A

Malaria

155
Q

What risk factors are common in patients that make them more susceptible to infection?

A 
Extremes of age
Obesity/malnourished
diabetes
cancer
immunosuppression
smoker
surgical patient
emergency admission
156
Q

What are the 4 Ps of infection, prevention and control?

A

Patient - risks/interactions with other people
Pathogen - virulence/ecological factors
Practice (of the hospital and staff)
Place - fixed and variable features (beds in a bay, patients:toilets

157
Q

How can we prevent patients becoming infected?

A 
General:
optimise patient's condition
Antimicrobial prophylaxis
Skin prep
Hand hygiene

Specific:
MRSA screens
Mupirocin nasal ointment
Disinfectant body wash

158
Q

How might we halt patient to patient transmission of HCAI?

A

Physical barriers:
Isolation of infected patients
Protection of susceptible patients

159
Q

How can HCAI be prevented from transferring from healthcare professionals to patients?

A

Healthcare workers should be disease free and vaccinated
Good practice:
Good clinical techniques (eg. sterile non-touch)
Hand hygiene
PPE - personal protective equipment
Antimicrobial prescribing

160
Q

What are some environmental features that may contribute to HCAI?

A 
-Built environment:
space/layout
Toilets
Wash hand basins
- Furniture and furnishings
- Cleaning:
- Medical devices  
- Appropriate kitchen and ward food facilities -must have good food hygiene practice
- Theatres/patient rooms - positive/negative pressure rooms.
161
Q

How must the hospital be cleaned?

A

Disinfectants
Steam cleaning
Hydrogen peroxide vapour - v toxic to vapour and humans - whole, empty room.

162
Q

How must medical devices be cleaned to prevent HCAI?

A

Single use equipment
Sterilisation
Decontamination

163
Q

Why is travel history important?

A

Imported disease
Different strains of pathogen - antigenically different, impacts on protection and detection, antibiotic resistance
Infection prevention - on the ward and in the lab

164
Q

What are the key aspects of the travel history?

A 
Where
When
How (direct or via)
Accommodation
How long
Specific risks (including sexual contacts)
Preventive measures
165
Q

What are the 4 main species of malaria?

A

Plasmodium falciparum, vivax, ovals and malariae

166
Q

How many deaths does malaria cause each year?

A

1 million (250 million cases)

167
Q

How is malaria spread?

A

Vector - female Anopheles mosquito (contained in salivary gland)
No case-to-case spread but cryptic and iatrogenic cases rarely reported

168
Q

What is the incubation period of malaria?

A

1-3 weeks after bite

169
Q

What will the presenting history of a patient with malaria be?

A

Starts non-specific - headache, cough, fatigue, malaise, athralgia, myalgia
Fever chills and sweats which eventually cycled every 3rd or 4th day

170
Q

What would you expect to see on examination of a patient with malaria?

A

Other than fever often few signs (+/- splenomegaly)
Cerebral features - coma
Respiratory distress - metabolic acidosis, pulmonary oedema

171
Q

What investigations would be done to confirm malaria?

A

Blood smear to detect parasite
FBC, U&Es , LFT, glucose
Head CT if CNS symptoms

172
Q

What treatment would be given to a patient with malaria?

A

Dependent on species:
P. falciparum (‘maignant’) - quinine or artemisinin
P. ovale, vivax malariae (‘benign’) - chloroquine +/- primaquine ( for exo-erythrocytic phase)

173
Q

Hw can malaria be prevented?

A

Assess risk
Bite prevention
Chemoprophylaxis

174
Q

What is the mechanism of infection of typhoid?

A

Faecal-oral from contaminated food/water source is cases or carrier. Widely distributed in some countries due to poor sanitation

175
Q

Who is typhoid most common in?

A

Children

176
Q

What organisms might cause Typhoid?

A

Salmonella enterica serovar Typhi/paratyphi A, B or C
Entericobacteriaceae, aerobic gram - rod
Non-lactose fermenter

177
Q

What is the virulence of salmonella?

A

Gram - endotoxin, VI antigen
Invasion which allows intracellular growth
Fimbriae adhere to epithelium over ileal lymphoid tissue (Peyers patches) -> RE system

178
Q

What are the 2 phases of malaria?

A

Exo-erythrocytic (liver - asymptomatic) and erythrocytic (RBCs - fever etc)

179
Q

What are the signs and symptoms of enteric fever (typhoid)?

A 
Systemic disease with fever and headache
Incubation period 7 - 24days
Abdominal discomfort
Constipation
Dry cough
Hepatosplenomegaly
Occasionally rash
Relative bradycardia
Complications include intestinal haemorrhage and perforation
Paratyphoid is generally milder
180
Q

What would be seen on investigation of an enteric fever?

A

Moderate anaemia
Relative lympopenia
Raised LFTs (transaminase and bilirubin)
Culture of blood and faeces taken
Serology (antibody detection) no longer used

181
Q

What treatment would be given to someone with enteric fever?

A

Antibiotics - usually ceftriaxone or azithromycin for 7 - 14 days

182
Q

How might enteric fever be prevented?

A

Food and water hygiene precautions
Typhoid vaccine to high risk travellers and lab personnel - Vi capsular polysaccharide antigen or live attenuated vaccine
Protective effect - 50 - 75%

183
Q

Other than typhoid, what else might a salmonella infection cause?

A

‘Food-poisoning’ eg. Salmonella typhimurium or Enteritidis
Widespread distribution
Diarrhoea, fever, vomiting, abdominal pain
Generally self limiting but bacteraemia and deep-seated infections may occur

184
Q

What type of organism is Brucellosis?

A

A zoonosis - primary animal pathogen eg B. abortus (cattle), B. melitensis (goats and sheep)
Gram negative coccobacillus

185
Q

How is Brucellosis transmitted?

A

Through skin breaks/GI tract

186
Q

What are the signs and symptoms, how is a diagnosis made and what is the treatment of Brucellosis?

A

Non-specific febrile illness - undulant fever
Bone/joint involvement, epidydimitis
Diagnosis from blood culture
Treat with doxycycline and rifampicin

187
Q

What is the virion of a virus?

A

Genome (nucleic acid) + capsid (protein surrounding genome)

188
Q

What are the stages of replication of a virus?

A 
Adsorption
Entry
Uncoating
Transcription
Virion synthesis
Assembly
Release
189
Q

How might you detect an infection (what do you look for)?

A

Antibodies
Antigen
By PCR

190
Q

How are blood borne viruses transmitted?

A

Blood
Sex
Therefore if they have one, may have another so must check for all

191
Q

How does silent transmission of BBVs occur?

A

Asymptomatic period so may transfer then

192
Q

Describe the pathogen of HIV.

A

Retrovirus
Single stranded RNA
HIV-1 from chimpanzee
HIV-2 from sooty mangabey

193
Q

How do HIV affect the host cell?

A 
Attach to CD4 cell
Reverse transcriptase makes DNA from teh RNA
Integration into host nucleus
Reproduction of viral components
Assembly of new HIV viruses
Released
194
Q

What are the symptoms of primary HIV illness?

A 
Fever
Rash
Flu-like
Weight loss
Pharyngitis
Generalised lymphadenopathy
Immune system deteriorates so other disease present
195
Q

What is classified as AIDs?

A

CD4 count less than 200

196
Q

What tests would you do for HIV?

A 
Standard - CVS, resp, abdomen, neurology...
MOuth
Eye
Skin
Genitals
Lymphs
197
Q

How is HIV diagnosed?

A 
HIV 1&2 comined ab/ag test (window period) 2 week
Immunoblot
HIV viral load
Resistance profile
CD4
198
Q

What investigations are ordered for a patient with known HIV?

A

General organ systems
Status of HIV/immune system
Infections - other BBV, opportunistic infections, past history
Underlying co-morbidities

199
Q

What can you do for a person with HIV? How can you iproce their life?

A 
Prevent related disease - undetected viral load, increase CD4
Reduce co-morbidity and mortality
Improve quality of life
Prevent resistance
Prevent transmission
200
Q

How do you treat HIV?

A

3 drugs acting in defferent parts of the lifecycle
HAART
patient must be compliant

201
Q

How can you prevent HIV?

A 
No sex
Use condoms
Know who you are having sex with
No IVDU
Use clean needles if you are
Screened negative blood for transfusions
202
Q

How can you reduce the risk of HIV transmission?

A

Don’t breast feed if safer - if not, only 6 months
Circumcision
Pre exposure drugs
Post exposure drugs - antiretroviral drugs
Vaccination not yet established

203
Q

Describe the Hepatitis virus.

A

Hepadnaviridae
double stranded DNA virus
Genotype A-D

204
Q

What is the difference between acute and chronic Hep B?

A

Acute - fever, surface antigen, antibody produced -> cured
Chronic - body doesn’t heal itself - liver cirrhosis

Both can also cause liver failure

205
Q

What signs will a patient with Hep B present with?

A

Jaundice

Signs of chronic liver disease

206
Q

What is practice-staging of Hep B?

A

Combination of different specific antigens/antibody tests

  • acute
  • chronic
  • past
  • vaccinated
207
Q

WHat investigations will be done on a patient with suspected hep B?

A 
General state
Liver function
Other BBV/STI
Cancer screening
Other causes of liver disease
Image liver - biopsy/ultrasound
endoscopy for oesophageal viruses
Any complications from liver damage
208
Q

What should be done for a patient with hep B?

A

Monitor viral load, liver function and complications
Decide when to give antivirals
Monitor antiviral side effects
Prevent other liver disease

209
Q

What is given for Hep B?

A

Usually single drugs - supression rather than cure

Follow NICE 2013 guidelines - interferon, tenofovir

210
Q

How can the transmission of hep B be prevented?

A 
Vaccination - generalised/targeted
Safe sex
Mother to child interventions
Screening blood/products
Post exposure prophylaxis - needlestick injury
211
Q

Describe the pathogen of Hep C.

A

Single stranded RNA
Flavivirus
6 genotyeps

212
Q

How is hep C mostly transmitted?

A

Injecting drug use most common

Also through sexual transmission but less common (more common for B and HIV)

213
Q

How can Hep C be fatal?

A

Cause liver cancer

214
Q

What type of Hepatitis is curable?

A

Hep C

215
Q

Where are antigen presenting cells present?

A 
Skin (SALT)
Mucu membrane (GALT, NALT, BALT)
Lymphoid organs (lymph node, spleen)
Blood circulation (plasmacytoid and myeloid DCs)
216
Q

How are pathogens captured?

A

Phagocytosis (whole microbe)

Micropinocytosis (soluble particles)

217
Q

How do pathogen sensors differ?

A 
Extracellular pathogens (bacteria) -present to  CD4+ T cells  - humoral immunity
Intracellular pathogens (viruses) - present to CD8+ T cell - cell dependent immunity
218
Q

Where do interdigitating dendritic cells exist?

A

Lymph nodes - present to T and B cells

219
Q

Where are langerhans’ cells present?

A

Skin - present to T cells

220
Q

What class of molecules are found on all nucleated cells?

A

Class I

221
Q

Where are class II molecules found?

A

Dendritic cells
Macrophages
B cells

222
Q

What are the key features of MHC class I and class II molecules?

A

Co-dominant expression - Both parental genes are expressed -> increase number of different MHC molecules
Polymorphic genes - different alleles among different individuals -> increase presentation of different antigens/microbe

223
Q

What ain the main function of MHC class I molecules?

A

Present viral peptides

224
Q

What is the main function of MHC class II molecules?

A

Present bacterial peptides

225
Q

What is the structure of MHC class I and class II molecules?

A 
Peptide binding cleft - variable region with highly polymorphic residues
Broad specificity - Many peptides presented by the same MHC molecule
Responsive T cells - MHC class I: CD8+ T cells, class II: CD4+ T cells
226
Q

What are Elite Suppressors?

A

Long term nonprogressors (LTNP) can control viral replication. Dependent on MHC molecule presen - HLA-B27, B51, B57 present key peptides for teh survival of the virus causing an effecting T cell response
Rapid progressors have HLA-B35 and are homozygotes in HLA-1 alleles. This icauses a mutation in the less critical peptides presented by MHC I causing weak T cell response

227
Q

What molecule is mismatched in a rejected transplant organ?

A

HLA molecule. Graft-versus-host reaction

228
Q

How is HLA associated with autoimmune disease?

A

Ankylosing spondylitis - HLA-B27 in 90% of patients

Insulin-Dependent Diabetes Mellitus - HLADQ2 -> 50-75% of patients

229
Q

What is a common problem with MHC molecules? Give examples.

A

Cross reactivity between microbial and host antigens
Rheumatic heart disease - Streptocoocus progenies and antigen in cardiac muscle
Guillain-Barre syndrome - Campylobacter jejuni and Myelin-associated gangliosides
Type 1 diabetes - Coxsakieviruses (A2, A5 and A9) and pancreatic islet cells

230
Q

What type of T cells are there?

A

CD3+, CD4+ (TH1 and TH2 cells)

CD3+, CD8+ (cytotoxic T cells or TC)

231
Q

What is the function of CD8+ T cells?

A

Protect against intracellular pathogens

232
Q

What is the function of CD4+ T cells?

A

Provide help for antibody production and regulate immune response

233
Q

What cytokines are produced by CD4+ cells?

A

TH1 cells: TNFalpha, IFNgamma

TH2 cells: IL-4, IL-5, IL-10

234
Q

How are naive CD4 T cells activated?

A 
Professional antigen presenting cells engulf foreign material and bring to lymph nodes. Here they begin to present antigens which are bound to MHC class II allowing CD4+ cells that express the specific TCR cells against the peptide/MHC complex to activate.
Verification that it is a foreign cell and not self, must then come from CD28 on the T cell and B7 on the APC (co-stimulatory molecules).
235
Q

What happens to a CD4+ T cell that is not verified?

A

It becomes anergic - will not respond to any foreign cells in the future. Eventually apoptose

236
Q

How are naive CD8 cells activated?

A

Same as CD4+ BUT MHC I instead of MHC II are presented by APC

237
Q

What are the functions of CD4+ TH1 cells?

A

Cell-mediated immunity against intracellular microbes
Killing of infected cells - cytotoxic T cells, natural killer cells
Phagocytosis - macrophages (IFNgamma)
Antibody production (B cells) - IgG1-3

238
Q

What do CD8+ cells produce that kill infected cells?

A

Perforins

Granzymes

239
Q

What are the functions of TH2 CD4+ T cells?

A

Humoral immunity against extracellular microbes
Killing of parasites - eosinophils (IL-5)
Antibody production - B cells (IgG4)
Mast cell activation - IgE
Mucosal protection - IgA

240
Q

How are naive B cells activated?

A

By CD4+ T helper cells through immunological synapse.
T cell independent - Type 1 - B cell binds to antigen and receives secondary activation by toll-like receptors. Then limited to IgM antibodies that are specific TLR-binding antigen
Type 2 - Antigens that are expressed on the surface of pathogens with an organised and repetitive form can activate B cells by cross-linking of antigen receptors in a multi-valent fashion. Many bacteria have repeating carbohydrate epitopes that stimulate B cells, cross linking their IgM antigen receptors, leading to IgM synthesis in the absence of T cell stimulation.

241
Q

What are some characteristics of the humoral response?

A 
Fast
Strong
Long duration
High affinity
Isotype switch
242
Q

What are the functions of IgG antibodies?

A

Fc-dependent phagocytosis
Complement activation
Neonatal Immunity
Toxin/virus neutralisation

243
Q

What is the function of IgA antibodies?

A

Mucosal immunity

244
Q

What are the functions of IgE antibodies?

A

Immunity against helmiths

Mast cell degranulation (allergies)

245
Q

What is the function of IgM antibodies?

A

Complement activation

246
Q

What medical achievements have been derived from study of the adaptive immune system?

A 
Disease prevention - vaccination/active immunisation
Immunoglobulin therapies - immune deficiencies
Immediate protection - passive immunity (antibody transfer)
Diagnostic tests (antibody based) - infectious diseases, autoimmune diseases, blood type and HLA types

Semester 3 (19 decks)

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