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Blood, Immunity and Infection > Infection > Flashcards

Infection Flashcards

1
Q

SSTI inflammation process in response to bacterial infection

A

1) Bacteria and other pathogens enter wound
2) Platelets from blood release blood-clotting proteins at wound site
3) Mast cells secrete factors which increase delivery of blood, plasma and cells to injured area
4) Neutrophils secrete factors that kill and degrade pathogens
5) Phagocytosis by neutrophils and macrophages
6) Macrophages secrete cytokines that attract immune cells to site to activate tissue repair
7) Inflammatory response continues until foreign material eliminated

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2
Q

Role of IL-8 in infection

A

Pro-inflammatory cytokine release by macrophages that help neutrophils find site of infection

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3
Q

PAMPs

A

Pathogen-associated molecular patterns found on pathogen surfaces

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4
Q

PRRs

A

Pattern recognition receptors found on host cell surfaces

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5
Q

LPS PAMPs are found on gram ____ bacteria

A

Negative

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6
Q

LTA PAMPs are found on gram ____ bacteria

A

Positive

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7
Q

NfkB

A

Tissue factor that activates proinflammatory cytokine production

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8
Q

Organisms that cause SSTI

A

Mainly S. aureus and S. pygogenes

Also some other bacteria, fungi (tinea) and viruses (chickenpox)

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9
Q

Streptococcus identification

A 
Gram positive cocci
Catalase negative (as opposed to staph)
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10
Q

Group A streptococcus

A

S. pyogenes
Presents a “group A” antigen which is recognised by a specific antibody
Show beta haemolysis on blood agar

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11
Q

MSCRAMMs

A

Microbial surface components recognising adhesive matrix molecules
Large protein family expressed on bacteria e.g., S, pyogenes which specifically bind to host ECM proteins e.g., collagen, elastin, fibronectin

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12
Q

Ways that S. pyogenes can evade an immune response

A

1) Hyaluronic acid capsule
2) M protein (binds factor H which prevents opsonisation with C3b and therefore resists phagocytosis)
3) Secretion of toxins
4) Spreading factors

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13
Q

4 types of toxins that S. pyogenes secretes

A

1) streptolysins (which lyse immune cells)
2) C5a peptidase (breaks up C5a to prevent neutrophil chemotaxis)
3) DNases (degrade neutrophil extracellular traps)
4) SpyCEP (destroys IL-8 to prevent neutrophil chemotaxis)

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14
Q

4 types of spreading factors that S. pyogenes secretes

A

Proteases
Lipases
Hyaluronidase
Streptokinase

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15
Q

Streptokinase

A

Anticoagulant that activates plasminogen to plasmin which degrades fibrin

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16
Q

Main classes of B-lactam antibiotics

A

Penicillin
Cephalosporins
Carbapenems

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17
Q

How does penicillin work?

A

Binds to transpeptidase enzyme which prevents formation of peptide cross-links in bacterial cell wall
Results in weak cell wall and eventually cell lysis

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18
Q

3 types of penicillin

A

Penicillin G (IV, aqueous, rapid excretion)
Benzathine penicillin G (IM, low concentration, slow excretion)
Penicillin V (oral, absorbed well from GI tract on empty stomach)
Amoxycillin

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19
Q

Septic arthritis

A

Presence of infection from bacteria in bone/marrow/joint space
Occurs most frequently in childhood
General systemic symptoms including fever and malaise, as well as swelling, erythema, and tenderness around the infected joint

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20
Q

Nonsuppurative GAS disease

A

Delayed sequelae following uncomplicated infection with GAS

Non-pus-forming

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21
Q

Treatment of septic arthritis

A

First, bacteria needs to be isolated by aspirating the joint and gram staining/growing/catalase staining
Drainage and washout of the joint required
Intravenous antibiotics needed initially then longer course of oral antibiotics

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22
Q

Major Jones criteria of ARF

A 
Carditis
Polyarthritis
Sydenhams chorea
Erythema marginatum
Subcutaneous nodules
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23
Q

Minor Jones criteria of ARF

A 
Fever
Polyarthralgia
History of rheumatic fever
Raised acute phase reactants
Prolong PR interval
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24
Q

ARF diagnosis

A

2 major criteria OR 1 major and 2 minor
PLUS evidence of preceding strep infection either by rising or elevated strep antibody titres OR positive GAS throat culture

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25
Q

How does ARF lead to RHD?

A

Antibodies cross-react with collagen or cardiac valvular endothelia antigens, then T cells infiltrate leading to inflammation or long-term damage
Recurrent ARF attacks due to repeated strep infection lead to increased scar formation in the valve. After the attack of ARF and carditis, the valve scars and is neurovascularised, perpetuating RHD

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26
Q

Streptococcal titres

A

antistreptolysin O and antiDNase B titres
Can be elevated even when throat culture is normal
ASO titre level highest about 3–6 weeks after infection, which is about when children will present with ARF

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27
Q

ARF treatment

A

Bed rest
System inflammation monitoring
Family testing
Penicillin IM injections every 4 weeks for the next 10 years, or until 21, whichever is longer

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28
Q

Main component of bacterial cell wall

A

Peptidoglycan

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29
Q

Most common causes of pharyngitis

A

50% S. pyogenes
40% rhinoviruses/other viruses
10% other (e.g., influenza, EBV)

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30
Q

Partial haemolysis

A

Alpha haemolysis
Green
By viridans streptococci

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31
Q

Complete haemolysis

A

Beta haemolysis
Completely disappears
S. pyogenes

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32
Q

No haemolysis

A

Gamma haemolysis

Enterococcus faecalis

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33
Q

Sinusitis aetiology

A

90%–98% of the time viral

Rest of the time bacterial

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34
Q

Types of LRTI

A

Pneumonia
Pleurisy
Empyema
Lung abscess

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35
Q

What is the only bacteria that has been shown to cause bronchitis?

A

Bordatella pertussis

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36
Q

S. penumoniae virulence factors

A

1) Pneumococcal surface protein A (binds epithelial cells and prevents C3b deposition)
2) PspC (prevents complement activation)
3) Pili (contributes to colonisation and cytokine production)
4) Choline binding protein (binds to Ig receptors on epithelial cells and allows transport into cells)
5) Pneumolysin (lyses neutrophils and epithelial cells)
6) Polysaccharide capsule

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37
Q

Transformation

A

Bacteria commit suicide and release their DNA

Other individuals take up this DNA nad express it

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38
Q

Primary investigation for pneumonia

A

CXR

If normal, antibiotics not required

39
Q

Following pneumonia tests

A

Nasopharyngeal swab
Sputum culture
Blood culture

40
Q

Macrolides target

A

Ribosomal 50S transpeptidation subunit

41
Q

Chloramphenicol target

A

Ribosomal 50S peptidyl transferase subunit

42
Q

Aminoglycosides target

A

Ribosomal 30S initiation subunit

43
Q

Tetracyclines target

A

Ribosomal 30S tRNA binding

44
Q

Macrolide example

A

Erythromycin

Broad spectrum bacteriostatic antibiotic active against strep, staph and chlamydia bacteria

45
Q

Adverse effects of macrolides

A

Increased peristalsis therefore GI upset
Sudden death due to QT interval prolongation
Drug–drug interactions

46
Q

Two types of penumonia

A

Community acquired
Healthcare associated
Determines treatment

47
Q

Treatment of healthcare-associated pneumonia

A

Cefuroxime +/- Gentamicin

48
Q

Treatment for bronchitis

A

Treatment for cough with NSAIDs or sedating antihistamines

Antibiotics have been shown to potentially reduce cough duration but no other significant improvement

49
Q

Possible routes of osteomyelitis infection

A

Trauma e.g., joint replacement
Spread from local area of infection e.g., SSTI
Haematogenous route e.g., bacteraemia

50
Q

Pathogenesis of osteomyelitis

A

Bacteria infect bone
Leukocytes infiltrate infected site
Inflammation and pus
Devacularisation, dead bone and abscess

51
Q

Pathogenesis of chronic osteomyelitis

A

Bacteria might invade bone cells and evade immune response and drugs

52
Q

Patients at risk for osteomyelitis

A 
Diabetics with foot ulcers
Patients with traumatic infections
Patients undergoing root canals
SSTI patients
Chickpox-infected children
53
Q

Osteomyelitis pathogens

A

S. aureus
S. pyogenes
GBS

54
Q

Diagnosis of osteomyelitis

A

Radiology
Bone biopsy
Blood sample if associated with bacteraemia

55
Q

B-lactam resistant penicillins

A

Methicillin
Flucloxacillin
Augmentin (amoxicillin + clavulanic acid)

56
Q

Endocarditis

A

Infection of the endocardium and heart valves leading to leakiness and eventual heart failure
Death by stroke or crashing pulmonary oedema

57
Q

Endocarditis pathogenesis

A

Turbulent flow through abnormal valve
Platelets and fibrin attach to damaged valvular epithelium, forming sterile vegetations
Transient bacteraemia arising from mouth, skin, gut, urinary tract etc. seed bacteria onto sterile vegetations
Infected vegetation enlarges and sheds infected emboli
Valve destruction

58
Q

Outcomes of endocarditis

A

Impaired valve function leading to heart failure and crashing pulmonary oedema as the lungs rapidly accumulate fluid
Emboli due to broken off vegetations leading to infarcts (more common)

59
Q

Three types of bacteraemia

A

True
Contaminant
Transient

60
Q

Investigations for endocarditis

A

1) Blood cultures looking for continuous bacteraemia

2) Investigate valvular function (auscultation, echo, look for evidence of emboli in distant arterioles)

61
Q

Bactericidal antibiotics

A

Penicillins
Cephalosporins
Gentamicin

62
Q

Bacteriostatic antibiotics

A

Macrolides

Tetracyclines

63
Q

MIC

A

Minimum inhibitory concentration

Minimum amount of drug that bacteria will be killed by

64
Q

Main cause of endocarditis

A

Viridans streptococci

Then S. aureus

65
Q

Endocarditis treatment

A

Antibiotics (dependent on organism), IV, high dose, at least 2 weeks (often 4 weeks)
Cure rate 70%–90%
Could use penicillin plus flucloxacillin plus gentamicin to cover all common bases

66
Q

Why are bactericidal antibiotics necessary for endocarditis?

A

Neutrophils cannot enter vegetations, therefore just using a bacteriostatic antibiotic will only prolong the infection

67
Q

Prevention of endocarditis

A

Reduce risk of bacteraemia in persons known to have abnormal heart valves (e.g., past RHD, congenital abnormalities)
E.g., antibiotic prophylaxis at time of dental work
Luckily, endocarditis is now so rare that this is barely necessary

68
Q

Endocarditis vs ARF

A

Splinter haemorrhages = emboli from vegetations
Continuous bacteraemia = infection in vascular tree
Echo may show vegetations

69
Q

Gastroenteritis

A

Syndrome of diarrhoea and/or vomiting

70
Q

Diarrhoea

A

3+ loose stools in the past 24 hours

71
Q

Acute diarrhoea

A

<14 days

72
Q

Persistent diarrhoea

A

14–30 days

73
Q

Chronic diarrhoea

A

> 30 days

74
Q

M cells

A

Specialised capture cells of the immune system present in the gut which capture foreign particles and transport them to dendritic cells
Allows IgA influx to gut

75
Q

Clostridium difficile

A

Opportunistic bacteria that causes gastroenteritis when the normal microbiome of the gut is disrupted, e.g., after antibiotic usage

76
Q

Non-inflammatory diarrhoea

A

Mucosal disruption affects absorption/secretion

Watery, no blood or pus

77
Q

What causes non-inflammatory diarrhoea?

A

Exotoxin ingestion
Enterotoxin-producing organisms
Viruses

78
Q

Inflammatory diarrhoea

A

Normally in the large bowel

Acute mucosal inflammation causing bloody/pussy diarrhoea

79
Q

What are some organisms that cause inflammatory diarrhoea?

A

Shigella

Campylobacter

80
Q

Salmonella enterica

A 
Gram -ve motile bacteria
Infects the ileum and colon
Long and variable incubation period
Low infectious dose
Typhoidal (headache) vs. non-typhoidal (diarrhoea)
81
Q

Salmonella treatment

A

Intrinsically resistant to cephalosporins and aminoglycosides, with resistance spreading to other antibiotics
Generally, if antibiotics can be avoided then they should be

82
Q

Giardia lamblia

A

Parasite of small bowel transmitted through the faecal–oral route
Non-invasive, but causes loss of brush border therefore decreased absorption and diffuse villous shortening
Fatty and malabsorptive diarrhoea, but non-inflammatory
Slow onset, good at surviving in cyst form in water reservoirs therefore can be a recurrent source of infection

83
Q

Metronidazole

A

Inert drug that requires activation
Inhibits DNA synthesis
No activity against aerobic bacteria because prodrug not activated

84
Q

Viral gastroenteritis

A

Most important are rotavirus, norovirus and enteric adenovirus
Infection of enterocyte epithelium with adherence to mucosa and disruption of absorption/secretion
No acute inflammation or mucosal destruction

85
Q

Shigella

A

Gram -ve
Very low infectious dose, very pH resistant
Ulceration and inflammation of colon but doesn’t penetrate past lamina propria therefore no bacteraemia
Incubation period 1–4 days but can shed weeks after infection

86
Q

Campylobacter

A

Inflammatory colitis of ileum, jejunum and colon
Enters through M cells and spreads, producing a local inflammatory response
Susceptible to gastric acid, slow growing
Normally transmitted via infected food
Antibiotics used in people with high risk of transmission or complications e.g., chefs, HIV patients

87
Q

Primary peritonitis

A

Spontaneous

Bacterial spread without GI perforation

88
Q

Secondary peritonitis

A

Bacterial spread from GI or urogenital tracts

89
Q

Nosocomial

A

Hospital-acquired infection

90
Q

Pathophysiology of peritonitis

A

Bacteria enter peritoneum
Local inflammatory response
Greater omentum is a physical barrier and tries to contain the bacteria
Rapid neutrophil deployment and generalised inflammation

91
Q

What antibiotics could you use for enterococci?

A

Cephalosporins e.g., amoxicillin
Ceftrioxime + Metronidazole
Amoxicillin + Gentamicin + Metronidazole

92
Q

Gentamicin adverse effects

A

Nephrotoxicity
Ototoxicity
Neuromuscular blockade

93
Q

Gentamicin dose

A

5 mg/kg lean body weight daily up to 500 mg

3 mg/kg lean body weight daily in renal impairment

Blood, Immunity and Infection (5 decks)

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