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Life Protection > Week 15 - Bacterial infections, immunology > Flashcards

Week 15 - Bacterial infections, immunology Flashcards

1
Q

What is an antibiotic? How are they derived

A

Fights bacterial infections Largely natural products of fungi and bacteria - derived by fermentation Some newer ones completely synthetic

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2
Q

Relationship between commensal and pathogens

A

Commensal organisms - live at various parts of body, but don’t cause issues Pathogen organism - when commensal organisms move and cause issues

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3
Q

Outline principle of selective toxicity in antibiotics

A

Best antibiotics target specific microorganism, but do not damage the host But can also cause loss of natural flora

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4
Q

What is antibiotic colitis?

A

Some antibiotics lead to C.diff overgrowth

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5
Q

What is the ‘therapeutic margin’?

A

Active dose vs their toxic effect Ex. narrow means low flexibility of dose before toxic effects, may need monitoring

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6
Q

How are antibiotics classified? (3)

A

Structure Target site for activity Type of activity

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7
Q

Key part of chemical structure in penicillins and cephalosporins - and significance

A

B-lactam ring Large group of antibiotics have this active component in common

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8
Q

What’s the difference between a gram positive and gram negative organism?

A

Gram positive - Large, porous peptidoglycan Gram negative - small strip of peptioglycan in periplasmic space - MORE difficult to treat

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9
Q

Where do antibiotics work in bacteria? TARGETS (6 with 2 examples each)

A

Cell wall synthesis - B-lactam, vancomycin Folic acid metabolism - Trimethoprim, sulfonamides Cell membrane - Colistin, deptomycin DNA and RNA processing - Quinolones, rifampin Protein synthesis - Erythomycin, tetracycline, doxycycline Free radicals - metronidazole, nitrofurantoin

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10
Q

Describe bactericidal vs bacteriostatic antibiotics

A

Bactericidal - kill bacteria (used when host immunity is impaired, or VERY severe infections) Bacteriostatis - inhibits bacteria (use when host defence mechanisms are intact so body can finish the job), used in many infectious diseases

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11
Q

Describe broad vs narrow spectrum antibiotics

A

Effective vs many vs few types Broad ex. cefotaxime Narrow ex. penicillin

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12
Q

Types of penicillins and examples

A

Basic - benzylpenicillin, penicillin V - fights strep,pneum, menin, treponemes BUT NOT staph aureus Anti-staph penicillin - flucloxacillin - narrow spectrum, Gram+, Broader spectrum penicillin - amoxicillin - also works on some Gram- and enterococci Antipseudomonal penicillin - piperacillin - extended spectrum for Gram+ and Gram- B-Lactam inhibitor combinations - Augmentin (clavulanic acid mixed with amoxycillin) binds and inactivates beta-lactamases (and then amoxycillin kills it)

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13
Q

Genetic mechanisms of antibiotic resistance (2)

A

Chromosome mediated / spontaneous mutation Plasmid-mediated exchange - transferable, carry genes for resistance

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14
Q

Examples of mechanisms by which antibiotic resistance can occur

A

Altered or new target Drug inactivation Metabolic by-pass Efflux pumps Overproduction of target Intrinsic impermeability

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15
Q

Supplementary treatments of bacterial infections (aside from antibiotics) (2)

A

Surgery (drainage) Immunological (rare)

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16
Q

Factors that inform the choice of antibacterial (5)

A

Sensitivity More than one agent required? Site of infection Contraindications Cost

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17
Q

What factors determine the dose of antibiotics?

A

Age, weight, renal / liver function, severity of infection

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18
Q

What is the minimum inhibitory concentration

A

Minimum amount that will inhibit or kill the organism at the site of infection

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19
Q

Potential routes of antibiotics (5)

A

Oral, intramuscular, intravenous, topical, rectal

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20
Q

Describe determining the duration of therapy

A

Depends on nature of infection, clinical response, but optimum duration is not known

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21
Q

Why is CSF cloudy in meningitis?

A

Increased protein and white cells

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22
Q

Shapes and gram status of most common types of bacterial meningitis (3)

A

Neisseria meningitidis Gram-, diplococci Hib Gram-, bacillus Strep. pneum Gram+, diplococci

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23
Q

What is staph aureus (gram status, shape)

A

gram positive cocci growing in clusters

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24
Q

Alpha vs beta haemolysis on blood agar

A

Alpha - greenish discoloration indicates Strep pneumonia Beta - clearing around colonies (looks like glowing), Strep pyogenes and some strains of Staph aureus

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25
Q

What are the antigen detection tests?

A

PCR Latex agglutination tests

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26
Q

In suspected case of meningitis, speticaemia what is the first step?

A

Injection of penicillin i/m or i/v unless SEVERE reaction

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27
Q

What is the innate immune system?

A

Born with it, developed through evolution, in place before infection, responds in the same to to repeated infections, present in plants, insects, all animals

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28
Q

What is the adaptive immune system?

A

Triggered by exposure to microbes There is a lag time following exposure Combats pathogens that evade/overwhelm IIS Specific, remembers pathogens so better/faster with repeated exposure

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29
Q

Components of the innate immune system (barriers, cells and soluble molecules)

A

Barriers - physical (ex. skin and mucosa) and chemical (antibacterial enzymes in tears / saliva, antibac peptides Cells - phagocytes (neutrolphils and macrophages) and natural killer cells, mast cells, eosinophils Soluble molecules - effector proteins and cytokines

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30
Q

Types of granulocytes

A

Neutrophil, mast cell, basophil, eosinophil

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31
Q

Types of granulocytes / granular leucocytes (4)

A

Neutrophil, mast cell, basophil, eosinophil

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32
Q

Describe basophils

A

Main role in hypersensitivity type 1 reaction Blue granules when stained

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33
Q

Describe mast cells

A

Granules contain inflammatory mediators, degranulate Roles in hypersensitivity type 1 reaction and parasites

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34
Q

Describe eosinophils

A

Role in response to parasite and allergies Release granule content Pink stained

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35
Q

Types of phagocytes (3)

A

neutrophils, macrophages, dendritic cells

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36
Q

Describe neutrophils

A

Most abundant WBC in blood Early response (inflammation) Phagocytosis Killing of microbes

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37
Q

Define phagocytosis, roles

A

Cell ‘Eating’ Pathogens, damaged cells, dead cells, nutrients Very important of function of IIS to prevent infection, protect from pathogens, get rid of garbage

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38
Q

Steps of phagocytosis

A

Chemotaxis - movement to site of injury Recognition and attachment Engulfment Digestion

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39
Q

Describe process of chemotaxis

A

Movement of cells to site of infection guided by chemoattractants (that are released by bacteria, inflammatory cells such as chemokines, damaged tissues)

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40
Q

Types of lysosomes and their roles (4)

A

Proteolytic ensymes - Degrade microbes Lysozyme - break bacterial walls Lactoferrin - bind iron so not enough left for bacteria Defensins - destroy bacterial wall

41
Q

Oxygen dependent vs oxygen independent killing of pathogens

A

Oxygen dependent - Phagocyte oxidase creates superoxide, hydrogen peroxide, hydroxl radicals, nitric oxide, peroxynitrite radicals Oxygen independent - lysosomes

42
Q

Describe outputs of oxygen dependent killing pathogens

A

Phagocyte oxidase creates superoxide, hydrogen peroxide, hydroxl radicals, nitric oxide, peroxynitrite radicals

43
Q

Describe opsonization, why is it important

A

Makes phagocytosis more efficient by coating pathogens with opsonins - faster recognition, faster phagocytosis Important because some microbes (ENCAPSULATED) will not be broken down without it

44
Q

Describe opsonization, why is it important

A

Makes phagocytosis more efficient by coating pathogens with opsonins (antibodies and complements) - faster recognition, faster phagocytosis Important because some microbes (ENCAPSULATED) will not be broken down without it

45
Q

Describe natural killer kills

A

Kill virus-infected cells Kill malignant cells (tumour cells) Express cytotoxic enzymes

46
Q

What is the complement system?

A

System of plasma proteins (C1-C9) activated by microbes, helps to coat them and stimulates inflammation

47
Q

Components of adaptive immune system

A

Cells - T lymphocytes, B lymphocytes Soluble molecules - antibodies, cytokines

48
Q

Types of T cells and role

A

Cellular immunity T Helper - express CD4, activate macrophages, help B cells produce antibodies Cytotoxic - express CD8, attacks microbes / tumour cells Regulatory - inhibit function of other T cells and immune cell / control of immune repsonse

49
Q

Types of B lymphocytes (3)

A

Follicular B Cells - spleen, lymph nodes, IgG high-affinity, PROTEIN Marginal zone B cells- spleen, lymph nodes, IgM, LIPID B-1 cells - Peritoneal cavity, mucosa, IgM low affinity, LIPID

50
Q

What is needed to ensure protection? (4 steps)

A

Recognise danger Act (effector function) Control (regulation) Remember (memory)

51
Q

Describe Pathogen Associated Molecular patterns (PAMPs)

A

Patterns that are recognised on pathogens / microbes generally. Such as lipoteichoic acid, LPS Recognised by Pattern recognition receptors

52
Q

Describe pattern recognition receptors and list examples (4)

A

Part of innate immune system, recognise molecules on pathogens / detect invaders Toll-like receptors C-type lectin receptors NOD-like receptors RIG-like helicase receptors Scavenger receptors

53
Q

Describe process of immune recognition in adaptive immune system

A

Antigen receptors on B and T cells can recognise microbial structures (failure can lead to autoimmune diseases)

54
Q

Summary of cells, response, receptors, range, specificity, memory of IIS and adaptive IS

A
55
Q

What is acute inflammation?

A

Initial QUICK response to tissue injury Minutes/hours to develop Short duration Innate immune response Relatively non-specific (several types of injury)

56
Q

Triggers of acute inflammation

A

Infection Tissue damage - physical (frost bite, burns), chemical (chemical burns, irritants), mechanical & ischaemia (trauma, reduced blood flow) Foreign bodies - splinters, dirt, sutures

57
Q

What is the purpose of acute inflammation?

A

Alert Limit spread of infection / injury Protect from infection Eliminate dead cells/ tissue Create conditions for healing

58
Q

The process of acute inflammation (the 5 Rs)

A

Recognition of injury Recruitment of leucocytes Removal of injurious agents Regulation Resolution /repair of affected tisuse

59
Q

5 signs of acute inflammation

A

Redness (rubor), swilling (tumor), heat (calor), pain (dolor), loss of function

60
Q

Systemic changes in response to acute inflammation

A

Fever (caused by endogenous or exogenous pyrogens), neutrophilia (high neutrophils) Increase in acute phase reactants - CRP, fibrinogen, complement, serum amyloid A protein RARE = sepsis

61
Q

What are the vascular responses to acute inflammation? (3)

A

Vasodilation of small vessels Increased blood flow Increased vessel permeability to allow leucocytes and plasma proteins to enter inflammation site

62
Q

Inflammatory exudate vs transudate

A

Exudate - water, salts, small plasma proteins, inflmmatory celsl and RBCs that go to site of inflammation Transudate - fluid leak due to altered osmotic / hydrostatic pressure, not due to inflammation

63
Q

Types of inflammatory exudate (4)

A

Serous - few cells, plasma based, often seen in skin blisters (burns, viral) Purulent (fibrino-purulent) - Pus ex. acute appendicitis and abscess Fibrinous - Fibrin deposition, large vascular leaks, can lead to scarring Haemorrhagic - RBC predominate offten following blood vessel rupture, trauma

64
Q

Describe the series of cellular events in acute inflammation (3)

A

Migration and accumulation of cells Removal of pathogens / injured / dead cells Migration and accumulation of monocytes

65
Q

Steps of neutrophil recruitment during acute inflammation (5)

A

Margination Rolling Integrin activation by chemokines Firm adhesion to endothelium Transmigration through endothelium into tissue Chemotaxis to inflamed site

66
Q

Describe Integrin activation by chemokines

A

chemokines released by activated endothelium which act on integrins to make them higher affinity so the neutrophil is now much more stronlgy bound to cell

67
Q

Describe margination and rolling

A

Margination - neutrophil moves closer to endothelium Rolling - selectins bind to ligand of cells which roles them along endothelium (P-selectin always there and e-selection appears in response to inflammation)

68
Q

Describe Chemotaxis to inflamed site

A

Chemoattractants (largely proteins) released to lead cell to site (like bread crumbs)

69
Q

How do the types of cells at inflammation site change over time?

A

Neutrophils (6-24hr) Monocytes (change into macrophages in tissues) (24-48hr)

70
Q

What kind of cells show up in allergies or parasite infection?

A

Eosinophils

71
Q

What type of cells show up in viral infections

A

lymphocytes

72
Q

Different mechanisms to destroy pathogens (4)

A

Release of granule content Phagocytes Generation of reactive oxygen / nitrogen species Formation of Neutrophil Extracellular Traps (NETs)

73
Q

What are the outcomes of acute inflammation?

A

Complete resolution Repair (scarring, fibrosis) Chronic inflammation - cannot be resolved

74
Q

Describe regeneration ability of cells (how good are different types of cells at regenerating)? (3 types)

A

High regeneration - labile like skin Intermediate regeneration - Stable tissues are normally in G0/G1 but may regenerate when injured *liver, kidney, pancreas) No/little regeneration ability - permanent tissues with heal with fibrosis, loss of function - neurons, myocardium, skeletal muscles

75
Q

Factors that favour tissue resolution (7)

A

Minimal destruction Minimal cell death Good regeneration ability of injured tissue Fast clearance of infection Quick removal of dead tissue Removal of foreign materials Immobilisation of wound edges

76
Q

Factors that prevent tissue healing (10)

A

Infection Diabetes Poor general health / nutrition Old age Drugs (steroids) Extensive injury Poor vascular supply Extensive bleeding Foreign bodies Pressure / torsion / movement of wound

77
Q

Outline GREEN warning signs (low risk) - colour, activity, resp, hydration

A

PICTURE

78
Q

Outline AMBER warning signs (intermediate risk) - colour, activity, resp, hydration, other

A

PICTURE

79
Q

Outline RED warning signs (high risk) - colour, activity, resp, hydration, other

A

PICTURE

80
Q

What is included in a septic screen?

A

Blood, urine, CSF, swabs

81
Q

In what cases would you not do an LP? (2)

A

Signs of high intercranial pressure, low platelet count

82
Q

Treatment for Septicaemia and meningitis

A

IV ceftriaxone (slightly higher dose for suspected meningitis) Also give IV dexamethasone for meningitis to protect hearing

83
Q

What do you give children with underlying disease?

A

TAZ plus gentamicin (or vancomycin)

84
Q

How do you treat a child with pneumonia?

A

Oxygen FLuid IV anitibiotics - or oral amoxycillin if possible (if not IV Augmentin or IV Cefuroxime)

85
Q

Describe epiglottitis and treatment

A

Swollen epiglottis, often bracing and drooling Do not examine, keep them calm, waft oxygen, get ENT to intubate if necessary, IV antibiotics

86
Q

Describe Kawasaki disease and treatment

A

Persistent high temperature, rash, cracked lips, swollen lymph nodes High dose IVIG, Aspirin (despite risk of Reye’s), echo to rule out coronary artery aneurysms In young babies or children who don’t respond, give high dose steroids

87
Q

Potential complications of varicella (5)

A

Secondary bacterial infection Pneumonitis Encephalitis Severe haemorrhagic varicella (when immunocompromised) Reye’s

88
Q

Most common organisms under three months

A

Group B Streptococcus E Coli Other Listeria

89
Q

What should you consider in a child with a fever over 5 days?

A

Kawasaki disease

90
Q

Aims of clinical diagnostic microbiology (5)

A

Presence / absence of pathogen AMR testing Pathogenic potential Rationale for treatment Public health concerns

91
Q

How do we look for a pathogen? (3)

A

Look for presence of pathogen itself Look for presence of product of pathogen (antigen, polysaccharide, toxins, DNA) Patients immune response to pathogen

92
Q

How to take a proper sample

A

Aseptic techniques Correct specimen (s) Timing (during disease) Handling the specimen Quick transport of specimen Transport medium (temp, preserve viability and sterility) Communication between lab/Dr

93
Q

Type of stain used for TB

A

Ziehl Nielsen Auramine is better to determine severity as you can more easily count the bacteria

94
Q

Gram negative, gull wing shape - what is it?

A

campylobacter

95
Q

What type of tests need to be done under selective atmosphere?

A

Anaerobic culture for Clostridium tetani, botulinum, difficile

96
Q

Difference in urine samples for STIs vs UTIs

A

STIs - first catch urine UTIs - mid stream urine

97
Q

Describe staph aureus

A

Gram positive cocci that clumps Lives on skin Different staph infections have different significance, severity

98
Q

What is staph aureus - How do you identify staph aureus in the lab - and best antibiotic to treat it?

A

Gram-positive cooci that vlumps, aerobic Produces coagulase enzyme (most other staphs do not) Lives in nose / skin normally and can be AMR

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