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ESA 3 > Infection 3 > Flashcards

Infection 3 Flashcards

1
Q

What are the clinical features of someone presenting as an emergency case with suspected severe infection?

A

Sudden onset

High temp (>38) and chills (Fever)

Tachycardic and hypotensive

High resp rate

Headache

Nausea

Weakness and generalised muscle pain

Abdominal pain

Photophobia

Pale, cool extremities

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2
Q

What is SIRS?
Give a defintion, why it occurs and the clinical criteria

A

Systemic inflammatory response syndrome

Response to non-specific insult (Ischaemia, trauma, infection)

Clinical criteria = two or more of:

Temperature = <36 or >38

HR = >90bpm

RR = 20/min or pCO2 of <4.3kPa

WBC = <4x10^9/L or >12x10^9/L

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3
Q

Give the definition of bacteraemia

A

Presence of bacteria in blood (+/- clinical features)

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4
Q

Define sepsis

Define septicaemia

A

Sepsis:

Systemic response to infection defined as:

SIRS + documented or presumed infection

Septicaemia:

Generalised sepsis

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5
Q

Define severe sepsis

A

SIRS

+

Organ dysfunction/hypoperfusion

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6
Q

How can we assess if bodily organs are hypo-perfused

A

Hypotension, decreased urine output

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7
Q

Define Septic shock

A

Severe sepsis

+

Persistent hypotension despite IV fluid administration

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8
Q

Label the white boxes with name of stucture and function regarding infection

Black boxes an be labelled with structure only

A

White, top left to bottom:

Lipopolysaccharide - Endotoxin, triggers inflammation

Pilus - Enhances attachment

Polysaccharide capsule - Promtes adherance, prevents phagocytosis

Black, top to bottom:

Outer membrane

Inner membrane

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9
Q

Give the inflammation cascade that occurs after endotoxins bind to macrophages

Asume homeostasis cannot be restored

A

Local:

Cytokines (TNF and ILs)

Stimulates inflammatory response to promote wound repair and recruit the reticuloendothelial system

Systemic:

Cytokines released into circulation

Stimulates growth factor, macrophages and platelets

Goal is homeostasis restoration

SIRS:

Homeostasis not restored

Cytokines activate humoral cascades and RE system leading to ciculatory insult/damage

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10
Q

Describe how sepsis can lead to microvascular insult/damage

A

Cytokines promote production of thrombin therfore coagulation

Cytokines also inhibit fibrinolysis

Coagulation cascade leads to microvascular thrombosis

Can lead to organ ischaemia, dysfunction and failure

Microvascular injury is the major cause of shock and multiorgan failure

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11
Q

What investigations might you perform for someone with suspected infection/sepsis?

A

FBC

Urea and electrolytes

Blood sugar

Liver function tests

CRP testing

Clotting studies

Blood gases

EDTA for PCR

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12
Q

What is the ‘sepsis six’?

A

6 actions to be performed within an hour of a patient going septic or a patient coming in in suspected sepsis

As follows:

High flow oxygen administration

Take blood cultures + other cultures, consider source control

Administer empirical IV antibiotics

Measure serum lactate

Start IV fluid resuscitation

Commence accurate urine output measurement

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13
Q

What are some specific features of a patient with Nesseria menigitidis infection?

A

Non blanching (purpuric) rash

Neck stiffness

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14
Q

What is the most common cause of meningitis?

A

Bacterial

Nesseria menigitidis

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15
Q

How is Nesseria meningitidis spread?

A

Direct contanct with infected respiratory secretions (droplets, aerosols)

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16
Q

Is Nesseria meningitidis normally pathogenic?

A

No, in most it is a harmless commensal bacteria

In the unlucky few it is pathogenic

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17
Q

What antibiotic is best suited for treatment of bacterial meningitis and why?

A

Ceftriaxone:

Penetrates CSF

Active against Nesseria meningitidis

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18
Q

Give some of the serious complications of severe infection/meningitis

A

Irreversible hypotension

Resp failure

AKI (renal failure)

Raised intercranial pressure

Ischaemic necrosis of hands and feet

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19
Q

What tests are required for confirmation of bacterial meningitis infection

A

Blood culture

PCR of blood

Lumbar puncture (if safe) - Culture and PCR of CSF

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20
Q

What examinations can be carried out on CSF?

A

Glucose and protein estimation

M,C&S:

Appearance - Normal, cloudy, blood stained

WBC and RBC count

Gram staining

PCR

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21
Q

What conditions can cause the CSF to appear normal, cloudy/turbid or blood stained?

A

Normal:

Normal conditions, Viral meningitis

Cloudy/Turbid:

Bacterial meningitis, Tuberculous meningitis

Blood-stained:

Sub-Arachnoid haemorrhage

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22
Q

Give some details on the structure and variation of Nesseria meningitidis

A

Gram negative diplococcus

Polysaccharide capsular antigen (prevents phagocytosis)

Outer membrane acts as an endotoxin

Numerous Serogroups (A, B, C, W-135)

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23
Q

Of the different serogroups of Nesseria meningitidis which is most prevalent

  • In UK
  • Worldwide
A

UK:

B

Worldwide:

A

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24
Q

Describe the prevention of meningitis

A

Vaccination:

N. meningitidis C vaccine available

ACWY vaccines used for immunocompromised patients and travel protection

B vaccine not routine

Prophylaxis:

Notifiable disease

Report cases to local health protection unit

Close contacts can be given antibiotic prophylaxis and considered for vaccination

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25
Q

What are the major factors contributing to the outcome of the host-pathogen relationship?

A

Virulence

Number of organisms

Host’s immune response

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26
Q

Define Immune system

A

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

27
Q

Define infectious disease

A

When the pathogen succeeds in invading and/or overwhelming the host’s immune defenses

28
Q

What are the key roles of the immune system?

Give a very brief description of each

A

Pathogen recognition:

Cell surface and soluble receptors

Containing/eliminating the infection:

Killing and clearance mechanisms

Regulating itself:

Causing minimum damage to host (resolution)

Remembering pathogens:

Preventing re-occurence

29
Q

What are the key features of innate immune response?

A

Fast (within seconds)

Recognises groups of pathogens

Lack of memory

No change in intensity w/repeat exposure

30
Q

What are the key features of the adaptive immune system?

A

Slow (3-4 days)

Response specific to one pathogen

Immunologic memory

Variable intensity (increases with repeat exposure)

31
Q

What are the first lines of defense in the innate immune system?

What is their overall function?

A

Barriers:

Physical barriers

Physiological barriers

Chemical barriers

Biological barriers

Function:

Factors that limit entry and growth of pathogens

32
Q

Give examples of physical barriers of the innate immune system

Their collective immune function?

A

Skin

Mucous membranes

Bronchial cilia

Function:

Prevent ingress of pathogens

33
Q

Give examples of physiological barriers of the innate immune systems

What is their collective function?

A

Diarrhoea

Vomiting

Coughing

Sneezing

Function:

Mechanical ejection of pathogen/irritant

34
Q

What are the chemical barriers of the innate immune system?

Give functions of each factor

A

Low pH:

Skin (5.5)

Stomach (1-3)

Vagina (4.4)

Number of pthogens sensitive to low pH

Antimicrobial molecules:

IgA - Prevents microorganism binding (tears, saliva)

Lysozyme (sebum, perspiration, urine)

Mucous - Traps pathogen

B-Defensins - Antiviral (epithelium)

Gastric acid + Pepsin

35
Q

What is the main biological barrier of the innate immune system?

Functions?

A

Commensal microbes:

Nasopharynx
Mouth/throat
Skin
GI tract
Vagina (lactobacillus)

Absent in internal organs (where they would cause disease)

Functions:

Compete with pathogens for attachment sites and resources

Produce antimicrobial chemicals

Synthesise Vit K, B12 and other B vitamins

36
Q

Give some skin and nasopharynx commensal species

A

Skin:

Staph aureus + Staph epidermidis

Strep pyogenes

Candica albicans

Clostridum perfringens

Nasopharynx:

Strep Pneumoniae

Nesseria meningitidis

Haemophilus spp

37
Q

In what situations do clinical problems arise regarding commensal displacement?

A

When normal flora is displaced

Breaching skin:

Skin loss (burns)

Surgery

IV drug use (endocarditis)

IV lines

Faeco-oral

Fecal-perineal-urethral route:

UTI

Poor dental hygiene/dental work:

Dental extraction

Gingivitis

Flossing

38
Q

Describe the clinical concequences of poor dental hygiene/dental work

A

Common cause of harmless bacteraemia

Serious infection risk:

Hypo or asplenic patients

Damaged or prosthetic heart valves

Previous infective endocarditis

Serious consequences:

Infective endocarditis

39
Q

What are the causes and clinical consequences of decrease or increase in normal flora?

A

Normal flora overgrowth can occur in immunocompromised patients:

Can be caused by:

Diabetes

AIDS

Malignancy

Chemotherapy

Normal flora depleted by antibiotics:

Allows pathogens to grow

Can cause:

Severe colitis (Clostridium difficile)

Thrush (Candica albicans)

40
Q

What are the second line innate barriers of the immune system?

What is their collective function?

A

Phagocytes

Chemicals

Inflammation

Function:

Contain and clear infection

41
Q

What is the main function of phagocytes?

A

Recognition and killing (phagocytosis etc) of microbes

42
Q

What are the phagocytic cells of the innate immune system?

A

Macrophages

Monocytes

Neutrophils

43
Q

What is the immune function of macrophages?

A

Present in all organs

Ingest and destroy microbes (phagocytosis)

Present microbial antigens to T cells

Produce cytokines/chemokines (chemoattractants)

44
Q

What is the immune function of monocytes?

A

Present in blood

Recruited to infection site to differentiate to macrophages

45
Q

What is the immune function of neutrophils?

A

Presnt in blood

Increased during infection

Recruited by chemokines (chemoattractants) to site of infection

Ingest and destroy pyogenic bacteria (E.g. Staph aureus and Strep pyogenes)

46
Q

What are the non-phagocytic cells of the innate immune system?

A

Basophils / Mast cells

Eosinophils

Natural killer cells

Dendritic cells

47
Q

What are the functions of Basophils / Mast cells?

A

Early actors of inflammation

Vasomodulation

Important to allergic response

48
Q

What is the function of Eosinophils?

A

Defense against multicellular parasites (worms)

Release IgE (binds to parasite)

49
Q

What is the function of Natural killer cells?

A

Kill all abnormal host cells (malignant or virally infected)

50
Q

What is the innate immune function of the dendritic cells

A

Present microbial antigens to T cells

The messengers between innate immune system and adaptive

51
Q

How does the innate immune system recognise pathogens?

A

PAMPS:

Pathogen-associated molecular patterns

Membrane structures of the pathogen that can be recognised

Can be proteins, nucleaic acids, carbohydrates, lipids etc

Thse are recognised by Pathogen recognition receptors (PRRs) which bind

Opsonins:

Opsonins coat microbial surfaces leading to enhances attachment of phagocytes and clearance of microbe

Less specific than PAMPS-PRR

52
Q

Give some examples of different PAMPS and their PRR

A

Gram negative bacteria:

Lipopolysaccharide - TLR4

Lipoproteins and lipopeptides - TLR2

Gram positive bacteria:

Peptidoglycan - TLR2

Lipoteichoic acids - TLR4

Mycobacteria:

Lipoarabinomannan - TLR2

Bacterial flagella:

Flagellin - TLR5

53
Q

Give examples of Opsonins

A

Complement proteins:

C3b

C4b

Antibodies:

IgG

IgM

Acute phase proteins:

CRP

Mannose binding lectin

54
Q

What type of bacteria are opsonins particularly important in clearing?

Give some examples

A

Encapsulated bacteria

E.g.

Nesseria Meningitidis

Strep Pneumoniae

Haemophilus influenzae

55
Q

Describe the process of phagocytosis

A
  1. Chemotaxis and adherence to microbe
  2. Ingestion of microbe
  3. Formation of phagosome
  4. Fusion of phagosome with lysomsome to form phagolysosome
  5. Digestion
  6. Formation of residual body
  7. Discharge of residual body
56
Q

What are the phagocyte intracellular killing mechanisms?

A

Oxygen dependent pathway:

Toxic O2 products damage pathogen

E.g. Superoxide, Hydrogen peroxide, Nitric oxide, O-, Hypohalite

Oxygen independent pathways:

Lysozyme

Lactoferrin or transferrin

Cationic proteins (cathepsin)

Proteolytic an hydrolytic enzymes

57
Q

Describe the complement system

A

Proteins C1 to C9

Activation:

Alternative pathway

Initiated by cell surface constituents

OR

MBL pathway

Initiated when mannose binding lectin binds to mannose containing residues of proteins found on salmonella spp./Candica albicans

58
Q

Give the functions of the important complement proteins

A

C3a and C5a:

Recruitment of phagocytes

C3b - C4b:

Opsonisation of pathogens

C5 - C9:

Killing of pathogens

Membrane attack complex (Forms pore in cell membrane leading to cell lysis)

59
Q

Apart from the complement system what is the other chemical defense system of the second line innate immune system?

A

Cytokine/Chemokines

60
Q

What cytokines/chemokines are produced by the liver and what is their function?

A

TNF-a, IL-1, IL-6

Functions:

Liver:

CRP and MBL release

Bone Marrow:

Neutrophil mobilisation

Inflammation:

Vasodilation

Vascular permaeability

Adhesions molecules (attract neutrophils)

Hypothalamus:

Increase body temp

61
Q

How can over-reaction of the innate immune system lead to clinical problems

A

Infection (E.g. Gram negative bacteria)

Overreaction of the TLR4 receptor and complement lead to overrecruitment of phagocytes and excessive tissue reaction

Excessive systemic inflammatory response

Cytokine shower

Coagulopathy

Vasodilation

Capillary leak

All reduce tissue/organ perfusion

Sepsis and multi-organ failure

62
Q

Why are hypo or asplenic patients at greater risk of infection?

A

Spleen hold half the body monocytes

Polysaccharide encapsulted bacteria resist opsonisation by complement proetins

Natural antibodies produced in the spleen required for successful immune response (opsonisation)

63
Q

Give some conditions that can cause reduced phagocytosis

A

Decreased spleen function:

Asplenic or hyposplenic patients

Decreased neutrophil number:

Cancer chemotherapy

Other drugs

Leukaemia and lymphoma

Decreased neutrophil function:

Chronic granulomatous disease (no oxidative burst)

Chediak-Higashi syndrome (no phagolysosome formation)

ESA 3 (54 decks)

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