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Phase 2a NEW > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Pathogen

A

An organism capable of causing disease

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2
Q

Commensal

A

An organism which colonises the host but causes no disease in normal circumstances

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3
Q

Opportunist pathogen

A

A microbe that only causes disease if host defences are compromised

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4
Q

Virulence/pathogenicity

A

The degree to which an organism can cause disease

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5
Q

Asymptomatic change

A

When a pathogen is carried harmlessly to a tissue or site where it causes no disease

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6
Q

Bacterial nomenclature

A

Genus
Species
Streptococcus (genus) pyogenes (species)

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7
Q

Mucosal surfaces tend to be

A

colonised

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8
Q

Bacterial morphology

A 
Cocci - round
Bacilli - rod shaped
Diploccocus, chain, cluster (cocci shapes)
Filamentous/branching (rod shapes)
Spirochaetes (spiral shaped)
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9
Q

Stains

A

Purple - gram positive

Pink - gram negative

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10
Q

Protect bacteria from the host immune system

A

Polysaccharide capsule

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11
Q

Allow bacteria movement

A

Flagella

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12
Q

Allow bacteria to attach and colonise to host

A

Pili

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13
Q

Ziehl-neelsen stain

A

Stain for TB (mycobacterium tuberculosis)

Acid fast bacilli

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14
Q

Bacterial cell envelope

A

Gram-positive - single PL membrane containing peptidoglycan

Gram-negative - inner cytoplasmic with peptidoglycan and outer lipopolysaccharide membrane (double-membrane)

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15
Q

Spores

A

A hardened structure which is resistant to desiccation and harsh conditions within bacteria

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16
Q

Bacterial environemnt

A

Extreme temps
Low pH
Months without water
UV light

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17
Q

Growth rate of bacteria

A

Rapid

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18
Q

Bacterial toxins

A

Endotoxin - component of the outer membrane of bacteria - lipopolysaccharide in gram-negative bacteria, non-specific, stable under heat
Exotoxin - secreted proteins of gram-positive and gram-negative bacteria, can convert to toxoid, specific, unstable under heat

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19
Q

Tetanus

A

Clostridium tetani - causes muscle spasms due to nerve hosting

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20
Q

Bacterial plasmids

A

Provide resistance

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21
Q

Bacterial conjugation

A

‘bacterial sex’

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22
Q

Bacterial genetic variation

A

Mutation

Gene transfer

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23
Q

Impetigo

A

Crusty lesion on the face

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24
Q

Gram-positive bacteria

A

Streptococcus

Staphylococcus

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25
Q

Bacteria can be

A

Aerobic

Anaerobic

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26
Q

Gram pos bacteria

A

peptidoglycan only

Purple on gram stain

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27
Q

Staph aureus treatment

A

Flucloxacillin

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28
Q

Staphylococcus species

A

40
Coagulase positive or negative
Coagulase - enzyme produced that clots blood plasma and this fibrin clot formed around bacteria protects it from phagocytosis
S aureus is coag pos
Normal habitat - nose and skin
Spread by air and touch
MRSA - resistant to B-lactams, gentamicin, erythromycin, tetracycline. Resistance transferred by MecA gene between bacteria

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29
Q

Staph aureus

A

Virulence factors - Pore-forming toxins (PVL causes hemorrhagic pneumonia), Proteases (exofoliatin - attacks joints between desmosomes in the skin), Toxic shock syndrome toxin (stimulates cytokine release), Protein A (surface protein)

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30
Q

Staph aureus associated conditions

A

Wound infections
Abscesses
Septicaemia

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31
Q

Coagulase negative staphylococci

A

S epidermis - infections in catheters (opportunistic), main virulence factor is ability to form persistent biofilms)
S saprophyticus - Acute cystitis (urease - kidney stones)

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32
Q

Strep pyogenes

A

Chains of gram positive cocci
B haem
Penicillin sensitive (treatment)

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33
Q

Haemolysis

A

Strep
Alpha haem - partial greening, S intermedius,
Beta haem - S pyogenes, clear zone
Non haem - no lysis

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34
Q

Streptoccoci classification

A

Hemolysis
Lancefield typing
Biochemical properties

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35
Q

Sero-grouping (Lancefield grouping)

A

Method of grouping catalase negative, coagulase negative bacteria based on

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36
Q

Sero-grouping

A

Carb cell surface antigens - Lacefield A-H and K-V
Antiserum to each group added to a suspension of bacteria - clumping indicates recognition
Group A - strep pyogenes
Group B - strep agalactiae

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37
Q

Strep pyogenes infections

A 
Wound infections lead to cellulitis 
Tonsillitis and pharyngitis 
Otitis media 
Impetigo 
Scarlet fever
Compllications of strep pyo infection - rheumatic fever, glomerulonephritis (both inflammatory)
Anti-SLO titre test
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38
Q

S pyogenes virulence factors

A

Capsule - hyaluronic acid (protection)
M protein - surface protein (encourages complement degradation)
Exported factors - streptokinase (breaks down clots)
Toxins - Streptolysins O and S (binds cholesterol helping to adhere to human cells)

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39
Q

Draughtsman colonies indicate infection by

A

S.pneuoniae

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40
Q

S pneumoniae

A

Normal commensal in oro-pharynx
Causes - Pneumonia, meningitis, sinusitis
Predisposing factors - impaired mucus trapping (viral infection)

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41
Q

S pneumoniae virulence factors

A

Capsule - polysaccharide (antiphagocytic)
Polyvalent vaccine available
Inflammatory wall constituents (peptidoglycan)
Cytotoxin - pneumolysin

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42
Q

Viridans streptococci

A

Collective name for oral streptoccoci
Oral infections such as caries and abscesses
Important in infective endocarditis (S oralis)
Cause deep organ abscesses (brain and liver)
Most virulent are the Milleri group

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43
Q

Optochin test

A

Resistant

Sensitive (S pneumoniae)

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44
Q

Diphtheria treatment

A

Anti-toxin

Erythromycin

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45
Q

C diphtheria

A

Toxin - inhibit protein synthesis

Prevention - vaccination (toxoid - inactivated toxin)

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46
Q

C difficile

A

anaerobic gram pos

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47
Q

Important gram pos bacteria

A 
S aureus
S epidermidis
S pyogenes
S pneumoniiae
Viridans streptocoocci 
C diphtheria
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48
Q

Gram positive vs negative

A

Gram pos - peptidoglycan wall is thicker than gram neg
Gram neg - has inner and outer membrane (PL bilayer), outer part is composed of LPS (lipopolysaccharide)
LPS - Lipid component is toxic (endotoxin)

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49
Q

Pathogenecity determinants

A

Colonisation factors - adhesins, invasins, nutrient acquisition, defence against host
Toxins - secreted proteins which cause damage
Protein secretion system - translocate toxins across PL bilayer

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50
Q

Proteobacteria

A

Enterobacteria - Rods, motile (flagella), facultatively anaerobic (both aerobic and anaerobic)
Some species colonise the intestinal tract (can be good or bad)

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51
Q

3 Important enterobacteria

A

Shigella - not motile
E coli - can use lactose as a carb source of energy, but the other 2 cannot, motile
Salmonella enterica - motile

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52
Q

Enterobacteria testing

A

MacConkey-lactose agar
Stool sample
Lac positive (Lactose-fermenters produce red patches) (E.coli)
Lac negative (Shigella and salmonella)
Agglutination test - distinguish between salmonella and shigella

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53
Q

Cell surface antigens of gram neg bacteria

A 
K antigen (exopolysaccharide capsule)
H antigen (flagellum)
O antigen (LPS)
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54
Q

E coli

A

Enterobacteria
Commensal
Most abundant facultative anaerobe in gut
Flagella
Infections caused are wound infections (surgical), UTIs (cystitis), catheterisation, gastroenteritis, traveller’s diarrhoea, bacteraemia which can lead to sepsis syndrome, meningitis (rare)

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55
Q

E coli

A 
Several pathovars (pathogenic strains)
Common 'core genome' as well as blocks of genes (pathogenicity islands) which are acquired via lateral gene transfer
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56
Q

Shigella

A

Very closely related to E coli except it contains a virulence plasmid
4 species
Severe bloody diarrhoea
Acid-tolerant bacteria which means it has a small infective dose
Person to person, contaminated water and food
Entry through colonic macrophage cells (where colonic mucosa is invaded by shigella), leading to apoptotic macrophages and release of inflammatory cytokines, this results in the destruction of the gut epithelium, ulitmately bloody diarrhoea due to tissue damage

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57
Q

Shigella virulence determinant

A

Shiga toxin - cleaves a bond in rRNA, this inhibits protein synthesis. Complication includes kidney failure

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58
Q

Salmonella

A

2 species - enterica, bongori (v rare, don’t need to know it)
A frequent cause of food poisoning (milk, poultry, meat and eggs)
Infections caused include - Gastroenteritis, enteric fever( Typhoid)

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59
Q

Salmonella

A

Ingestion of contaminated food/water

High infective dose required

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60
Q

Salmonella pathogenesis

A 
Bacterial mediated endocytosis 
Induction of chemokine release
Neutrophil recruitment and migration
Neutrophil induced tissue injury
Fluid and electrolyte loss (diarrhea)
Inflammation/necrosis of gut mucosa
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61
Q

Vibrio cholerae

A

Facutative anaerobe
Saline environments
Most severe dirrhoeal disease - Cholera
Pandemics

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62
Q

Cholera

A

Faecal-oral route (faecal contaminated water - poor sanitation or unndercooked shellfish)
High infective dose
Acid-sensitive (difficult to cross gastric barrier)
Vominous watery stoolds (secretory diarrhoea)
Deydration/death due to hypovolaemic shock
No blood, pus or fever (not dysenteric)
No invasion or damage to mucosa

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63
Q

Cholera virulence determinants

A

TCP pili - required for colonisation

Cholera toxin - works in same way as heat labile toxin except even more potent.

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64
Q

Pseudomonas aeruginosa

A

Motile
Aerobe
Opportunistic
very difficult to treat due to multiple antibiotic resistance

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65
Q

Pseudomonas aeruginosa infections

A

Acute - burn/surgical wounds, UTI (catheters), neutropenic patients can become septic due to bacteremia
Chronic - Cystic fibrosis patients

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66
Q

Cystic fibrosis and pseudomonas aeruginosa

A

thick mucus, difficult to clear, becomes home for various pathogen which can’t be cleared, pseudomonas aeruginosa will not be cleared once trapped in this

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67
Q

Haemophilus influenzae

A

Exclusively human parasite
Mostly nasopharyngeal carriage
Opportunistic infections mainly in young children or adult smokers - Meningitis, bronchopneumonia, epiglottitis, bacteraemia, pneumonia
Fastidious - requires lots of nutrients

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68
Q

Chocolate agar is

A

Heated blood agar which allows H influenzae to grow

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69
Q

H influenzae virulence determinants

A

Capsule - invasive strains are capsulates

LPS

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70
Q

Legionella pneumophila

A

Severe inflammatory pneumonia
Immunocompromised patients affected
Man made aquatic environments - shower heads
Fastidious - charcoal agar
Can infect alveolar macrophages - upregulates pro-inflam genes in alveolar macrophages

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71
Q

Bordetella pertusis

A

Whooping cough
Person-to-person transmission (airborne)
Low infective dose, highly contagious
Non-specific flu-like symptoms, then followed by paroxysmal coughing

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72
Q

Hypersynthesis of cyclic AMP (cAMP) leads to

A

Suppression of innate immune functions (immunosuppression)

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73
Q

Neisseria

A

Non-flaggellated diplococci
Fastidious
2 important species - N meningitidis, N gonorrhoeae
Person to person contact

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74
Q

N meningitidis

A

Nasopharynx

Person to person (airborne)

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75
Q

N meningitidis pathogenesis

A

Crosses nasopharyngeal epithelium and enters blood stream
Lowe level bacteraemia (asymptomatic) or septicaemia (sepsis)
Meningitis - Invasion of meninges - bacteria enters CSF from blood stream after crossing BBB

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76
Q

N meningitidis - Virulence dterminants

A

LPS - Cytokine cascade, sepsis (DIC)

Capsule - anti-phagocytic

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77
Q

N Gonorrhoeae

A

2nd most common STD
Person to person
can be asymptomatic especially in women
Urethritis and PID if infection ascends

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78
Q

N Gonorrhoeae - Virulence dterminants

A

LPS

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79
Q

Campylobacter

A

2 types - Jejuni, Coli
Spiral rods
Most common cause of food poisoning - undercooked poultry, unpasteurised milk
Mild to severe diarrhoea often with blood

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80
Q

Helicobacter pylori

A

Spiral shaped

Gastritis and peptic ulcer disease

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81
Q

Bacteriodetes

A

Non motile
Rods
Found in large intestine (most abundant of all)
Commensal flora
Anaerobe
Opportunistic - Tissue injury during surgery or perforated appendix

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82
Q

Chlamydiae

A

Small
Non-motile
Obligate intracellular parasites

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83
Q

Chlamydia life cycle

A

Elementry body - small, robust, non-replicative
Endocytosed by a host cell
Reprogrammed vacuole
Differentiates into the reticulate body
Replicates within vacuole
Once vacuole is full it redifferentiates back into the elementary body and released

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84
Q

Chlamydia diseases

A

Trachoma biovar leads to irreversible blindness
Genital tract biovar - most common STD, infects epithelial cells of mucous membranes of urethra and vagina, can ascend to uterus and ovaries (PID, Infertility)

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85
Q

How to prevent and control infections

A

Education
Policy development - hand washing
Surveillance - screening

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86
Q

Infection

A

Requires harm to be done to the individual - invasion, toxin, host response

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87
Q

Routes of transmission

A

Risk factors - E.g. recent return from sierra leone with fever
Screening - MRSA admission screening
Clinical diagnosis - Cough and cavity on CXR
Lab diagnosis - Urinalysis (CPEs)

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88
Q

CPEs

A

Carbapenemase-producing enterobacteriaceae

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89
Q

Broadest spectrum beta-lactam antibiotics

A

Carbapenems (serious infections, often last resort ab)

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90
Q

How to stop transmission routes in the clinical environment

A

Isolation - barrier or protective ward design

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91
Q

Common skin and nasal commensal (colonisation)

A

Staph aureus

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92
Q

Infection prevention - Environment

A

Isolation
Cleaning
Ward design

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93
Q

Norovirus

A

Uncontained Vomiting and diarrhoea
During winter
Tends to be in children
Low infective dose
Difficult to clean - resistant to usual cleaning products and alcohol gel
Traditional hand washing is the ideal method

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94
Q

Hand hygiene

A

Single most effective method of preventing cross-infection - can be hand-washing or alcohol gel

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95
Q

C Difficile

A

Hand washing required
Transmitted via spores
Spores germinate, cells multiply, C diff adheres to mucus and enterocytes, colonisation, toxin production, manifestations

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96
Q

Personal protective equipment

A

Gloves
Apron
Masks

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97
Q

Disposal of sharps

A

Prevent needle stick injuries

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98
Q

Virus

A

Infectious, obligate intracellular parasite, comprising genetic material (DNA/RNA) surrounded by a protein coat and/or membrane

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99
Q

Viral shapes

A

Helical
Complex
Icosahedral

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100
Q

Virus structure

A

No cell wall, organelles, only can have DNA or RNA - not both at once
Not living as they do not feed or respire

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101
Q

Viral replication

A

Attachment to a specific receptor on the host cell (glycoproteins on the surface)
Cell entry
Host cell interaction and replication (using host cell machinery)
Translation of viral mRNA to produce proteins
Assembly of virions
Release of new viral particles

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102
Q

How do viruses cause disease

A

Direct destruction of host cells - host cell lysis (lysis of neurons leads to paralysis in poliovirus)
Modification of host cell - rotavirus causes villi of the gut to atrophy which decreases small intestine surface area, nutrients not absorbed effectively, and ultimately diarrhoea
Over-reactivity of immune system - HepB (Cytotoxic T cells against hepatocytes) - Jaundice, pale stool, dark urine, RUQ pain, fever and malaise, itching
Damage through cell proliferation - HPV causes cervical cancer (anti-tumour genes switched off)
Evasion of host defences - Antigenic variability, cell-to-cell transport, downregulation of interferon and other host defence proteins. Herpes simplex virus (oral manifestations), Herpes zoster (chickenpox - vesicular rash (fluid filled) - reactivation will lead to shingles

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103
Q

Fungi forms

A

Yeast
Mould
Dimorphic fungi - some fungi exist as both yeasts and mould, switching between the 2 when conditions suit

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104
Q

Yeasts

A

Divide by budding

Less than 1% of fungi

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105
Q

Moulds

A

Multicellular hyphae and spores

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106
Q

Fungal diseases

A 
Tinea pedis (athlete's foot)
Onychomycosis (fungal nail infections)
Candida spp
Pneumocystis
Invasive aspergillosis
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107
Q

Fungal disease - Diagnosis

A

Cultures of nail clippings/scrapings
Microscopy and histology performed on cultures
Serology

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108
Q

Onychomycosis - Differential diagnosis

A

Psoriasis
Eczema
Yellow nail syndrome

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109
Q

Onychomycosis - Treatment

A

Terbinafine

Itraconazole

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110
Q

Mucosal candidiasis

A

Thrush
White adherent plaques on oral or genital mucosa
Associated with diabetes, dentures and poorly ventilated underwear

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111
Q

Mucosal candidiasis - Treatment

A

Topical antifungals

Oral fluconazole

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112
Q

Mucosal candidiasis - Diagnosis

A

Clinical

Culture

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113
Q

Invasive aspergillosis and Galactomannan

A

Severely immunocompromised patients typically but also post-influenza disease
Galactomannans - family of molecules found on cell wall of aspergillus

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114
Q

Invasive aspergillosis - Treatment

A

Amphotericin

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115
Q

Pneumocystis pneumonia

A

Immunocompromised patients - HIV often presenting illness

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116
Q

Pneumocystis pneumonia - Diagnosis

A

PCR of sputum

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117
Q

Pneumocystis pneumonia - Treatment

A

Co-trimoxazole

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118
Q

1,3 - B-D Glucan (1-3BDG)

A

Non-specific indicator for individual fungi

Released into serum during invasive infection

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119
Q

Fungi vs bacteria

A

Generally much more difficult to treat fungi than bacteria because they are eukaryotic

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120
Q

Fungal cell

A

Components not present in human cells but present in fungal cells - cell wall mannoproteins, plasma membrane contains ergosterol (human pm contains cholesterol)

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121
Q

Anti-fungals

A

Amphotericin and terbinafine - targets ergosterol in plasma membrane by inhibiting its synthetic pathway
Echinocandins - targets cell wall mannoproteins

122
Q

Summary of activity of Azoles

A

Fluconazole - Candida
Itraconazole - Aspergillus
Voriconazole - Invasive aspergillosis

123
Q

Azole adverse events

A

Relatively safe
Rare SEs
Voriconazole - severe hepatitis, visual disturbances, skin maligancy (photosensitivity)

124
Q

Azole resistance

A

Mutations in ERG11 gene

125
Q

Polyenes

A

Pore formation in ergosterol containing membranes - fungicidal
Amphotericin
Toxic SEs - nephrotoxicity

126
Q

Echinocandins

A

Inhibitors of 1,3-BG synthase
Caspofungin
Few SEs/interactions
Excellent anti-candida activity

127
Q

Protazoa classification

A

Amoeboids
Ciliates
Sporozoa
Flagellates

128
Q

Amoeboids

A

Caused by entamoebia histolytica
many entamoebia colonise the gut in humans
E histolytica causes severe dysenteric illness
Faecal-oral transmission - ingestion of cysts from faecally contaminated food and water
Can spread through the blood to liver, brain and lungs
Treatment - Metronidazole

129
Q

Trypanosomiasis - African

A

Flagellate
Vector - tetse fly
Fever, headaches, extreme fatigue,
Diagnosis - Blood film, CSF

130
Q

Trypanosomiasis - American

A

Flagellate
Vector - Triatomine bug
Headache, fevers, chagoma, romana’s sign
Later disease - cardiac manifestations

131
Q

Leishmaniasis

A

Flagellate
Vector - Female sand fly
3 types - cutaneous (skin), muco (oral), visceral (abdo - hepato-splenomegaly is main sign of this)

132
Q

Giardia lambia

A 
Giardiasis 
Diarrhoea, cramps, bloating
Faecal-oral spread (travel, close-contact)
Diagnosis - Stool microscopy (cysts)
Treatment - Metronidazole
133
Q

Trichomonas vaginalis

A 
Flagellate
STI
Trichomoniasis 
Women - purulent discharge, abdo pain, dysuria
Men - often asymptomatic, prostatitis 
Treatment - Metronidazole
134
Q

Cryptosporidiosis

A

Contaminated food/water - ingestion of cysts
Watery diarrhoea, no blood, vomiting, fever and fatigue
Stool sample - Oocytes seen (acid-fast stain)

135
Q

Taxoplasmosis

A

Taxoplasma gondii
Ingestion of undercooked meat
Taxoplasma encephalitis
Retinochoroiditis

136
Q

Trimethoprim

A

UTI

137
Q

Congo

A

One of the highest cases of malaria

138
Q

Thrombocytopenia

A

Low platelets

139
Q

Fever after traveling tends to be

A

Malaria

140
Q

Malaria

A

5 species

Vector - Female anopheles mosquito

141
Q

Malaria - Liver stage (growth)

A

Mosquito takes blood meal and injects sporozoites
Travel to liver and infect liver cells
Mature into shizonts
Shizonts rupture releasing merozoites into blood

142
Q

Malaria - Blood stage (rupture)

A

Merozoites enters the circulation and infects RBCs
Trophozoites mature into schizonts
Shizonts rupture releasing more merozoites (cycles of this continue)
Some differentiate into sexual stage - gametocytes
Blood stage gives rise to all manifestations

143
Q

Malaria - Vector stage

A

Another mosquito takes a blood meal ingesting gametocytes
Mature into an oocyst which ruptures releasing sporozoites
Sporozoites are injected into the host during the next blood meal

144
Q

Malaria - Symptoms

A 
Fever and chills
Flue-like illness
Headache
Nausea
Vomiting
145
Q

Severe malaria

A

P Falciparum is responsible for most malaria related deaths
Cycloadherence - Leads to cerebral malaria (haemorrhage)
Rosetting
Sequestration

146
Q

Malaria - hematological changes

A

Anaemia
Jaundice
Haemaglobinuria
Thrombocytopenia

147
Q

Complicated malaria

A

Cerebral malaria - vascular occlusion (drowsy, raised ICP, seizures and coma)
Renal failure - vascular occlusion (proteinuria, haemturia)
ARDS (lungs) - hypoxia
Bleeding - thrombocytopenia (DIC, bleeding, anaemia, sepsis)
Shock is the ultimate result of all these

148
Q

Diagnosis of malaria

A

Thick and thin blood films

3 repeats over 24hr period

149
Q

Malaria - Treatment

A 
IV Artesunate (quinine + doxycycline)
Primaquine (used to eliminate hypnozoites which may be living dormant in liver - prevention)
150
Q

Sore throat

A

Infection so treat with antibiotic

151
Q

Sore throat

A

Laryngitis - viral

Tonsilitis - viral/bacterial

152
Q

Antimicrobials

A

Wider umbrella term which includes antifungals, antibacterials, antiprotazoals and antivirals

153
Q

Antibiotic

A

Work by binding a target site on a bacteria

Antibiotic class - determined by binding point on bacterium

154
Q

Penicillin

A

Beta-lactam

Inhibits cell wall synthesis

155
Q

Beta lactams

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

156
Q

Beta-lactams

A

Target peptidoglycan

Work better on gram-pos than gram-neg bacteria

157
Q

Beta-lactams

A

Disrupt peptidoglycan production

158
Q

Antibiotics - Nucleic acid synthesis

A

Rifampicin

Quinolones

159
Q

Antibiotics - Protein synthesis

A

Aminoglycosides - gentamicin
Tetracyclines - Doxycycline
Macrolides - Clarithromycin (important alternative to penicillin for allergies to it)

160
Q

Antibiotics - Folate synthesis

A

Trimethoprim

161
Q

Antibiotics - function

A

Give time and support for the immune system to respond

162
Q

How are bacteria pathogenic

A 
Attach and enter
Local spread
Multiply
Evade host defences
Shed from body
163
Q

Toxins produced by body

A

Exotoxin - protein production

Endotoxin - gram-neg

164
Q

Gut bacteria symptoms

A

Diarrhoea

165
Q

Bacteriostatic antibiotics

A

Prevent bacteria multiplying
Inhibitory to growth
Reduce toxin production

166
Q

Bacteriocidal antibiotics

A

Agent that kills the bacteria
Antibiotics that tend to inhibit cell wall synthesis
Useful in infections more serious such as endocarditis and meningitis where an intervention is needed quickly

167
Q

Minimum inhibitory concentration (MIC)

A

Determines how much antibiotic is needed to stop the bacteria growing
Lowest MIC = best antibiotic (in theory)

168
Q

2 major determinants of anti-bacterial effects

A

Concentration (one or two big doses)

Time (multiple doses)

169
Q

Time-dependent killing

A

Beta-lactams

170
Q

Conc-dependent killing

A

Aminoglycosides

Quinolones

171
Q

Elimination of drugs

A

Liver (metabolism)

Kidney (excreted)

172
Q

How bacteria resist antibiotics

A

Change antibiotic target - changes to the molecular configuration
Destroy antibiotic - beta-lactam ring is hydrolysed by beta-lactamase
Prevent antibiotic excess
Remove antibiotic from bacteria - efflux pumps

173
Q

Bacterial resistance to antibiotics

A

Intrinsic - natural resistance
Acquired - spontaneous gene mutation changes cell structure and enzymes. Horizontal gene transfer (transduction - bacteriophages transfer DNA) , transformation, conjugation - plasmids containing resistance)

174
Q

Resistant bacteria - Gram positive

A

MRSA - Methicillin resistant staph aureus (resistant to all beta-lactams). Treatment tends to be with glycopeptides
VRE - Vancomycin-resistant enterococci

175
Q

Resistant bacteria - Gram-negative

A

Beta-lactamase enzymes hydrolysing penicillins

176
Q

Cephalosporins

A

Broad-spec antibiotics

177
Q

Co-amoxiclav

A

Amoxicillin

Clavulanate (beta-lactamase inhibitor)

178
Q

Gram negative bacteria - Further resistance

A

ESBL

179
Q

Carbapenem-resistant Enterobacteriaceae (CRE)

A

Produce carbapenemases which provide resistance

180
Q

Beta-lactams

A

All contain beta-lactam ring
Penicillins
Cephalosporins

181
Q

Cephalosporins

A

Good for people with penicillin allergy

182
Q

Gram-pos bacteria

A

Beta-lactams

thick cell wall

183
Q

Cellulitis

A

Skin and soft tissue infection
S aureus is the causative organism
Flucloxacillin

184
Q

Pharyngitis

A

Strep is causative
Oral penicillin
IV benzylpenicillin

185
Q

Pneumonia

A

S pneumoniae is causative
Oral amoxicillin
IV benzylpenicillin

186
Q

Glycopeptides

A 
Target cell wall
Vancomycin IV only 
Gram positive only
Treat MRSA
Used when there are penicillin allergies 
SE - Renal impairment
187
Q

Gram neg

A

Thin cell wall

188
Q

Gram positive vs negative bacteria

A

Pos - Thick cell wall

Neg - Thin cell wall

189
Q

Antibiotic pathways

A 
Cell wall synthesis inhibition
Prevent protein synthesis 
Prevent DNA synthesis 
Anti-metabolites
Inhibitors of membrane function
190
Q

Macrolides

A 
Protein synthesis inhibitors
Clarithromycin and erythromycin (bioavailability is same for both Oral and IV)
Target gram-positive
Used in penicillin allergy 
Treats severe pneumonia
191
Q

Lincosamides

A 
Protein synthesis inhibitors
Clindamycin (oral and IV)
Gram positives
Treats cellulitis if penicillin allergy
Also treats necrotising fasciitis
192
Q

Tetracyclines

A

Protein synthesis inhibitors
Doxycycline (Oral only)
Broad spec
Treats cellulitis and pneumonia

193
Q

Aminoglycosides

A 
Inhibits protein synthesis 
Gentamicin - IV only
Gram-negatives but also staphs
Treat UTIs and infective endocarditis 
However, it is very nephrotoxic which can be irreversible
194
Q

Quinolones

A 
Inhibits DNA synthesis 
Ciprofloxacin (oral and IV)
Gram negative but some gram positive
UTIs and Intra-abdo infections
Pencillin allergies also
195
Q

Trimethoprim

A

Folate antagonist
mainly gram negs but is broad-spec
UTIs

196
Q

Nitrofurantoin

A

UTIs

gram negs and pos

197
Q

Lower UTI

A

Nitrofurantoin
E coli
Urine culture

198
Q

Cellulitis

A 
Lower limbs 
Unilateral
Red, hot, painful, tender skin
Spreading
Systemic symptoms
S aureus 
Blood cultures
Oral or IV flucloxacillin
Clarithromycin if pen allergy
199
Q

Mycobacteria

A

TB

200
Q

Ziehl-Nielson acid-fast stain

A

Mycobacteria
High lipid content in cell wall makes mycobacteria resistant to gram stain
Acid fast bacilli

201
Q

Tuberculosis of spine

A

Gibbus formation

202
Q

Fish tank granuloma

A

Mycobacterium marinum
Fish tank granuloma
Lesion on hand/arm
Tend to be caused by fish bites

203
Q

Buruli ulcer

A

M ulcerans

First presents as a nodule which develops into an ulcer which grows and deforms, results in done destruction

204
Q

Leprosy

A

M leprae

205
Q

Mycobacteria

A

Aerobic, non-spore forming, non motile bacillus
Gram-pos
Cell wall - high molecular weight lipids (protective coat) - survive inside macrophages
Slow reproduction and slow growth - gradual onset of Slow response to treatment (6 months) disease
Slow growth means takes much longer to culture in lab

206
Q

Immunology of mycobacterial disease

A

Mycobacteria are phagocytosed by macrophages and traffic to a phagolysosome
Antigen presentation on macrophage occurs
Adaptive immunity activated with T cell-mediated cytokines such as interferon
Some macrophages fuse with each other to form giant multinucleated cells (Langhans giant cells)
Cytotoxic T cells infiltrate the mycobacterial lesion
Central tissue may necrose and form a granuloma
If this works mycobacteria shut down metabolically in order to survive (dormancy)
If it fails then it results in a cavity full of mycobacteria and in the lungs this is dangerous

207
Q

Granulomata

A

Lesions that arise in response to trying to contain mycobacteria

208
Q

Erythema nodosum

A

Hypersensitivity reactions to mycobacterial antigen

Inflammatory response

209
Q

Mantoux test

A

Tuberculin skin test

210
Q

Immunology of tuberculoid leprosy

A

Tissue hypersensitivity and granulomata
Tissue damage - nerves
Interferon production

211
Q

Primary TB

A

Bacilli taken in lymphatics to hilar lymph nodes
Cell mediated immune response from T cells
Latent TB - no clinical disease formed
Pulmonary TB - Granuloma forms around bacilli that settled in apex

212
Q

TB

A

Can be systemic

213
Q

Main 2 mycobacterial illness

A

TB

Leprosy

214
Q

HIV

A

Sexually transmitted
Has a dormancy period
Attacks the immune system
High ability to mutate

215
Q

HAART

A

Highly active antiretroviral therapy

216
Q

HIV Phases

A

Acute primary infection
Asymptomatic phase
Early symptomatic HIV
AIDS

217
Q

Markers used to monitor HIV infection

A

CD4 and T cell count

HIV viral load (RNA copies)

218
Q

AIDS

A

Acquired immune deficiency syndrome

Rapid progression in elderly and children

219
Q

AIDS-defining conditions

A 
Candidiasis 
Pneumonia 
Dementia/encephalopahy 
TB
Non-hodgkin's lymphoma 
Aseptic meningitis
220
Q

HIV presenting symptoms

A 
Fever
Sweats
Headache
Diarrhoea
Hepatosplenomegaly
Weight loss
Lethargy
221
Q

Fever and rash differential diagnosis other than HIV

A

Syphillis

222
Q

Patient with fever, rash and non-specific symptoms - Protocol for investigation

A

Take sexual history
HIV seroconversion illness
Tell lab - check for antigen

223
Q

Shingles - Treatment

A

Aciclovir

224
Q

AIDS CD4 count indicator

A

Less than 200 units

225
Q

Early symptomatic HIV

A

Recurrent shingles

Candidiasis

226
Q

AIDS

A

PCP - Pneumonia
Oesophageal candida
TB
Dementia

227
Q

HIV - Respiratory diseases

A 
TB
Pneumonia
Lung cancer
Emphysema/COPD
Lymphoma
228
Q

Pneumocystis - Treatment

A

Treatment - Co-trimoxazole

229
Q

TB

A

Diagnosis - Sputum sample sent to a lab and stained under a microscope with Ziehl-Nielson stain - acid-fast bacilli
All patients with TB require HIV test in UK

230
Q

Resp disease in HIV

A

Bacterial pneumonia
TB
PCP

231
Q

Cerebral toxoplasmosis

A

Latent HIV
Space occupying lesion in the brain
Treat with sulphadiazine

232
Q

HIV related neoplasms

A

Lymphoma - Non-hodgkin’s

Kaposi’s sarcoma (mostly causes skin lesions)

233
Q

Site of action of HIV drugs

A

Protease inhibitors

Reverse transcriptase inhibitors

234
Q

HAART

A

Highly active antiretroviral therapy - HIV treatment

3 drugs

235
Q

AIDS

A

Many opportunistic infections and neoplasms which occur when CD4 falls below 200 units

236
Q

UNAIDS 90/90/90 goals

A

Global target to be achieved by 2020:
90% diagnosed
90% diagnosed on ART (antiretroviral therapy)
90% viral suppression for those on ART

237
Q

HIV

A

Chronic treatable condition

238
Q

HIV prevention

A 
Antiretroviral treatment (Undetectable = untransmittable)
Circumcision 
Vaccines
HIV diagnosis/partner notification
Behavioural - condom use
Needle exchange programmes
239
Q

U=U

A

Undetectable = untransmittable

240
Q

Prep

A

Pre-exposure prophylaxis (pre-sex)

241
Q

Pep

A

Post-exposure prophylaxis (post-sex)

242
Q

Infections which need to be tested for HIV

A

Unexplained lymphadenopathy
Unexplained oral candida
Unexplained weight loss
Multi-dermatomal shingles

243
Q

Rash on palms of hands and feet can be due to either

A

Secondary syphilis

HIV

244
Q

Gradually increasing shortness of breath and cough

A

Pneumocystis

245
Q

HIV screening test

A

Venous blood sample - 4th generation includes p24 antigen
Takes 4 weeks
High sensitivity and specificity
Salivary antibody screening tests also available

246
Q

Retroviruses

A

Enveloped viruses

Have to turn their RNA into DNA

247
Q

Lentiviruses

A

Genus of slow viruses with a long incubation period

248
Q

HIV

A

An enveloped virus with glycoproteins
Inside is a protein capsid which houses nucleic aid and enzymes
Glycoproteins - GP41, GP120
Targets CD4 helper cells - HIV fuses to CD4 receptor and passes its contents into the CD4 cell

249
Q

HIV receptors

A

HIV infects cells that express CD4
The interaction between CD4 and GP120 is conserved among all primate lentiviruses
The co-receptors are chemokine receptors (CCRS)

250
Q

Cell tropism - cells which become infected

A

CD4 T cells

Macrophages (have CD4 and CCRS receptors too)

251
Q

Immune system response to HIV

A

Humoral - Antibodies

Cell-mediated - CD8, CD4

252
Q

Immune system consequences of HIV

A

Progressive decline in number and function of CD4 T cells characterises HIV infection and leads to susceptibility to infection

253
Q

Mechanisms of CD4 T cell depletion

A 
Direct cytotoxicity 
Activation-induced death
Decreased production 
Redistribution 
Ultimate drop in the number of CD4 T cells
254
Q

Reservoirs of HIV replication

A

Genital tract
CNS
GI system
Bone marrow

255
Q

HIV1

A

Retrovirus evolved from simian immunodeficiency virus in chimpanzees

256
Q

Who is at risk of HIV

A 
Men who have sex with men
Injecting drug users
Commercial sex workers
Heterosexual women
Migrant workers
257
Q

Preventing HIV transmission

A

PrEP
PEP
Circumcision
Condom

258
Q

Risk of mother to child transmission - HIV

A

Less than 1% with HAART intervention and no breastfeeding

35% with no intervention

259
Q

How to stop mother to child HIV transmission

A

Antenatal screening

Life-long antiretroviral treatment for mother

260
Q

Helminths

A

Worms

Mostly resident in bowel

261
Q

Helminths - 3 groups

A

Nematodes (roundworms) - Intestinal
Trematodes (flatworms, flukes) - Blood
Cestodes (tapeworms) - Invasive or non-invasive

262
Q

Pre patent period

A

Interval between acquiring infection and appearance of eggs/larvae in the stool

263
Q

Intestinal nematodes

A

Soil-transmitted
Faecal-oral spread
Transmitted from human to human via eggs or larvae

264
Q

Ascariasis

A

Ascaris lumbricoides

Large roundworms

265
Q

Loeffler’s syndrome - Symptoms and signs

A

Cough
Fever
CXR infiltrates
Wheeze

266
Q

Asacariasis - Diagnosis

A

Stool microscopy for eggs

267
Q

Ascariasis - Treatment

A

Mebendazole

268
Q

Hookworm

A

2 species - Anycylostoma duodenale, Necator americanus

Small size

269
Q

Hookworm - Clinical features

A

Ground itch

270
Q

Hookworm - Diagnosis

A

Stool microscopy for eggs

271
Q

Hookworm - Treatment

A

Mebendazole

272
Q

Pinworm/Threadworm

A

Common in UK

Enterobius vermicularis

273
Q

Pinworm/Threadworm - Clinical features

A

Pruritus ani

Appendicitis

274
Q

Whipworm

A

Trichuris trichiura

275
Q

Whipworm - Clinical features

A

Bloody diarrhoea

276
Q

Strongyloidiasis

A

Strongyloides stercoralis

277
Q

Hyperinfection syndrome

A

Auto infection

Immunocompromised state

278
Q

Larva migrans

A

Toxocara canis/cati

Causes ocular toxocariasis (granulomatous reaction) which leads to blindness

279
Q

Cutaneous larva migrans

A

Itchy skin eruption due to dog hookworm

280
Q

Anisakiasis

A

Due to raw fish (sushi)
Anisakidae
Sea creature which invades fish bodies

281
Q

Tissue nematodes

A

Filaria

Causes elephantiasis

282
Q

Tapeworm

A

Taenia saginatum

Due to uncooked beef

283
Q

Neurocysticercosis

A

Pork tapeworm

284
Q

Schistosomiasis

A

Schistosoma
Swimmer’s itch
Infection can cause bladder cancer

285
Q

Liver flukes

A

Invade liver by biliary tree

286
Q

Bacterial enzymes

A

Deconjugate compounds within enterohepatic circulation aiding reabsorption back across the intestinal wall (bilirubin, cholesterol, bile)

287
Q

If normal bowel barriers are breached by bacteria this leads to

A

Peritonitis

288
Q

Gastric acid

A

First defence against pathogens trying to colonise gut

289
Q

Disruption to normal flora by antibiotics causes

A

C difficile

290
Q

Diarrhoea

A

Main drug cause is Antibiotics

291
Q

Diarrhoea - stool charactertics

A

Blood, mucus, watery, fat content

292
Q

Viral diarrhoea

A

The commonest cause of diarrhoea is viral
Rotavirus - children
Norovirus - all ages
Damage mucosal architecture - villi, inflamamtory exudate
Watery diarrhoea

293
Q

Bacterial diarrhoea - Types

A

Enterotoxin mediated - Cholera, Colonise upper bowel, water diarrhoea, dehydrated v quickly, mucosal architecture remains intact
Invasive - Lower colon, shigella, salmonella, damages architecture, bloody mucoid stools

294
Q

Cholera

A

Faeco-oral spread
Watery diarrhoea, vomiting, rapid dehydration
Treatment - Doxycycline, fluids

295
Q

Travellers diarrhoea

A

3 or more unformed stools in 24hrs

Fever, N/V, cramps, bloody stools

296
Q

Diarrhoea - Investigations

A

Bloods - Blood cultures

Stool tests - Microscopy, culture

297
Q

Diarrhoea - Management

A

Antibiotics
Fluids
Electrolytes (prevent arrhythmias)

298
Q

Peptic ulcer disease

A 
LUQ/RUQ pain
H.pylori infection 
Causes gastritis and ulceration 
N/V, indigestion 
Increased RF for gastric cancer
Treatment - Antibiotics (Clarithromycin, amoxicillin),  PPI (Omeprazole)
299
Q

Ascending cholangitis/biliary sepsis

A

Jaundice
Fever
RUQ pain
Treat with antibiotics

300
Q

Cholecystitis vs cholangitis

A

Cholecystitis - Gall bladder

Cholangitis - Tract

301
Q

Liver abscess

A

RUQ pain, fever
Aspirate sample - E coli
USS/CT
Antibiotics and drainage

302
Q

Enteric fever

A

Salmonella (typhoid)
RLQ pain, fever, bradycardia, headache, myalgia, constipation or diarrhoea
Diagnosis - Blood cultures
Treatment - IV antibiotics (Ceftriaxone)

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