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Blood, Immunity and Infection > Infection > Flashcards

Infection Flashcards

(93 cards)

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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
How does ARF lead to RHD?
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
26
Streptococcal titres
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
27
ARF treatment
Bed rest System inflammation monitoring Family testing Penicillin IM injections every 4 weeks for the next 10 years, or until 21, whichever is longer
28
Main component of bacterial cell wall
Peptidoglycan
29
Most common causes of pharyngitis
50% S. pyogenes 40% rhinoviruses/other viruses 10% other (e.g., influenza, EBV)
30
Partial haemolysis
Alpha haemolysis Green By viridans streptococci
31
Complete haemolysis
Beta haemolysis Completely disappears S. pyogenes
32
No haemolysis
Gamma haemolysis | Enterococcus faecalis
33
Sinusitis aetiology
90%–98% of the time viral | Rest of the time bacterial
34
Types of LRTI
Pneumonia Pleurisy Empyema Lung abscess
35
What is the only bacteria that has been shown to cause bronchitis?
Bordatella pertussis
36
S. penumoniae virulence factors
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
37
Transformation
Bacteria commit suicide and release their DNA | Other individuals take up this DNA nad express it
38
Primary investigation for pneumonia
CXR | If normal, antibiotics not required
39
Following pneumonia tests
Nasopharyngeal swab Sputum culture Blood culture
40
Macrolides target
Ribosomal 50S transpeptidation subunit
41
Chloramphenicol target
Ribosomal 50S peptidyl transferase subunit
42
Aminoglycosides target
Ribosomal 30S initiation subunit
43
Tetracyclines target
Ribosomal 30S tRNA binding
44
Macrolide example
Erythromycin | Broad spectrum bacteriostatic antibiotic active against strep, staph and chlamydia bacteria
45
Adverse effects of macrolides
Increased peristalsis therefore GI upset Sudden death due to QT interval prolongation Drug–drug interactions
46
Two types of penumonia
Community acquired Healthcare associated Determines treatment
47
Treatment of healthcare-associated pneumonia
Cefuroxime +/- Gentamicin
48
Treatment for bronchitis
Treatment for cough with NSAIDs or sedating antihistamines | Antibiotics have been shown to potentially reduce cough duration but no other significant improvement
49
Possible routes of osteomyelitis infection
Trauma e.g., joint replacement Spread from local area of infection e.g., SSTI Haematogenous route e.g., bacteraemia
50
Pathogenesis of osteomyelitis
Bacteria infect bone Leukocytes infiltrate infected site Inflammation and pus Devacularisation, dead bone and abscess
51
Pathogenesis of chronic osteomyelitis
Bacteria might invade bone cells and evade immune response and drugs
52
Patients at risk for osteomyelitis
``` Diabetics with foot ulcers Patients with traumatic infections Patients undergoing root canals SSTI patients Chickpox-infected children ```
53
Osteomyelitis pathogens
S. aureus S. pyogenes GBS
54
Diagnosis of osteomyelitis
Radiology Bone biopsy Blood sample if associated with bacteraemia
55
B-lactam resistant penicillins
Methicillin Flucloxacillin Augmentin (amoxicillin + clavulanic acid)
56
Endocarditis
Infection of the endocardium and heart valves leading to leakiness and eventual heart failure Death by stroke or crashing pulmonary oedema
57
Endocarditis pathogenesis
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
Outcomes of endocarditis
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
Three types of bacteraemia
True Contaminant Transient
60
Investigations for endocarditis
1) Blood cultures looking for continuous bacteraemia | 2) Investigate valvular function (auscultation, echo, look for evidence of emboli in distant arterioles)
61
Bactericidal antibiotics
Penicillins Cephalosporins Gentamicin
62
Bacteriostatic antibiotics
Macrolides | Tetracyclines
63
MIC
Minimum inhibitory concentration | Minimum amount of drug that bacteria will be killed by
64
Main cause of endocarditis
Viridans streptococci | Then S. aureus
65
Endocarditis treatment
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
Why are bactericidal antibiotics necessary for endocarditis?
Neutrophils cannot enter vegetations, therefore just using a bacteriostatic antibiotic will only prolong the infection
67
Prevention of endocarditis
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
Endocarditis vs ARF
Splinter haemorrhages = emboli from vegetations Continuous bacteraemia = infection in vascular tree Echo may show vegetations
69
Gastroenteritis
Syndrome of diarrhoea and/or vomiting
70
Diarrhoea
3+ loose stools in the past 24 hours
71
Acute diarrhoea
<14 days
72
Persistent diarrhoea
14–30 days
73
Chronic diarrhoea
>30 days
74
M cells
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
Clostridium difficile
Opportunistic bacteria that causes gastroenteritis when the normal microbiome of the gut is disrupted, e.g., after antibiotic usage
76
Non-inflammatory diarrhoea
Mucosal disruption affects absorption/secretion | Watery, no blood or pus
77
What causes non-inflammatory diarrhoea?
Exotoxin ingestion Enterotoxin-producing organisms Viruses
78
Inflammatory diarrhoea
Normally in the large bowel | Acute mucosal inflammation causing bloody/pussy diarrhoea
79
What are some organisms that cause inflammatory diarrhoea?
Shigella | Campylobacter
80
Salmonella enterica
``` Gram -ve motile bacteria Infects the ileum and colon Long and variable incubation period Low infectious dose Typhoidal (headache) vs. non-typhoidal (diarrhoea) ```
81
Salmonella treatment
Intrinsically resistant to cephalosporins and aminoglycosides, with resistance spreading to other antibiotics Generally, if antibiotics can be avoided then they should be
82
Giardia lamblia
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
Metronidazole
Inert drug that requires activation Inhibits DNA synthesis No activity against aerobic bacteria because prodrug not activated
84
Viral gastroenteritis
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
Shigella
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
Campylobacter
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
Primary peritonitis
Spontaneous | Bacterial spread without GI perforation
88
Secondary peritonitis
Bacterial spread from GI or urogenital tracts
89
Nosocomial
Hospital-acquired infection
90
Pathophysiology of peritonitis
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
What antibiotics could you use for enterococci?
Cephalosporins e.g., amoxicillin Ceftrioxime + Metronidazole Amoxicillin + Gentamicin + Metronidazole
92
Gentamicin adverse effects
Nephrotoxicity Ototoxicity Neuromuscular blockade
93
Gentamicin dose
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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