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Take 2: Electric Boogaloo > Phase 2 - Microbio > Flashcards

Phase 2 - Microbio Flashcards

1
Q

Define pathogen

A

Organism that causes or is capable of causing disease

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2
Q

Define commensal

A

Organism which colonises the host but causes no disease in normal circumstances - e.g. bacteria from throat can cause pneumonia in lungs

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3
Q

Define opportunist pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Define virulence/pathogenicity

A

The degree to which a given organism is pathogenic

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5
Q

Define asymptomatic carriage

A

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

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6
Q

Resolving power of naked eye

A

100μm

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7
Q

Resolving power of light microscope

A

0.2μm

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8
Q

Typical size of protazoa like entamoeba histolytica

A

~30μm

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9
Q

Common size of spirochetes like borrellia recurrentis

A

~15μm

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10
Q

Common size for bacilli like e. coli

A

~2-3μm

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11
Q

Common size of cocci

A

~1μm

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12
Q

Which is the biggest virus we learn of

A

Rotavirus

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13
Q

What is the typical size of viruses

A

All smaller than 1μmBigger viruses ~0.3-0.8μmSmaller virus <0.1μm

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14
Q

What is the smallest virus we learn of

A

poliovirus

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15
Q

What is unique about the nature of Chlamydia trachomatis

A

It is a bacteria but it is an obligate intracellular organism - it’s smaller than rotavirusRickettsia and Coxiella are also obligate intracellular bacteria

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16
Q

Define serovar/serotype

A

a distinct variation within a species of bacteria/viruses/among immune cells of different individuals

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17
Q

Which areas are open to bacterial colonisation

A

Mucosal surfacesBacteria can also get into many organs and cause inflammation

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18
Q

What do the colours of the gram stain signify

A

Purple - gram positivePink/red - gram negativepurPle - Positive; piNk - Negative

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19
Q

Basic shapes of bacteria

A

Coccus (round berry-like)diplococcus (2 cocci)streptococcus (chain of cocci)staphylococcus (cluster of cocci)Bacillus (rod)Chain of rodsVibrio (curved rod)Spirochete (spiral rod)Filamentous/branching bacteria

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20
Q

Typical structures that a bacterium is composed of

A

Chromosome of circular double ctranded DNA (free in cytoplasm)Inner membraneOuter membranePili/fimbriaeCell wallSome bacteria also have - a capsule made from polysaccheride- flagella- plasmids, which can be transferred from bacterium to bacterium

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21
Q

On which bacteria are capsules more common and why

A

On bacteria which get into blood/lungsIt helps protect them against the immune system

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22
Q

What is the purpose of pili/fimbriae

A

Recepting/sensing the environment

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23
Q

Which stain is commonly used for mycobacteria; what colour does it stain?

A

Ziehl-Neesen stain - stains red

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24
Q

How does the ziehl-neelsen stain only stain non-gram bacteria? What is the term used for this kind of bacteria?

A

There is a stage in the Ziehl-Neelsen stain where the bacteria are bathed in alcohol/acid. Regular gram bacteria are decolourised at this stage but certain organisms like mycobacteria resist the acid.These are called acid/alcohol fast bacteria (AFB or AAFB)

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25
Q

Describe the cell envelope of a gram positive bacterium

A

Thin cytoplasmic membraneThick layer of peptidoglycan with lipoteichoic acid strands within itPotentially a capsule

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26
Q

Describe from inside to out the cell envelope of a gram negative bacterium

A

Cytoplasmic membrane:- Thin inner membrane- Very thin layer of peptidoglycan- (piller-like) Lipoproteins within periplasmic space- Thin outermembraneLipopolysaccerides (ENDOTOXIN) - composed of:- Lipid A- O antigen- Terminal sugarspotentially a capsule

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27
Q

What is the peptidoglycan in bacteria

A

Crosslinked sugers and amino acids

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28
Q

What causes the difference in staining between gram positive and negative bacteria?

A

Gram positive bacteria are able to resist decolouration (usually a mix of ethanol and acetone) due to their thick peptidoglycan layersGram negative have a thin peptidoglycan layer so the stain is easily lost and they have to be counterstained (with safranin or basic fuchsin stain)

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29
Q

What is a spore

A

Small oval or spherical structures with thick walls which are very resistant to high temperatures, radiation, desiccation and chemical agents. They are involved in reproduction and are used by certain bacteria to defend themselves. They can last for a long time in the environment

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30
Q

What environment can bacteria survive in?

A

Temperature: <-800C to + 80CpH: <4 - 9Water/desiccation: 2 hours - 3 monthsLight: could be killed by UV

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31
Q

What environment can spores survive in

A

Temperature: <-800C to 1200C pH: <4-9Water/desiccation: >50 years

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32
Q

Growth rate of bacteria (give doubling time)

A

Common bacteria like E. coli or S. aureus:- In a broth or solid media: 20-30 minMycobacterium tuberculosis in broth or media:- 24 hoursMycobacterium leprae in broth or media:- 2 weeks

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33
Q

What is typically done now to test for mycobacteria in a culture

A

Grow too slowly for regular agar plate techniques ao using nucleic acid boosting techniques/PCR can be useful

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34
Q

Types of bacterial toxins

A

ENDOTOXINComponent of the outer membrane of GRAM NEGATIVE bacteria, eg lipopolysaccharidesEXOTOXINSecreted proteins of Gram positive and Gram negative bacteria

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35
Q

What is an example of a condition caused by bacterial exotoxins

A

Tetanus - causes simultaneous, prolonged, severe muscle contraction

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36
Q

Differences between Endo- and Exotoxins (bacterial)

A

Exotoxins are composed of protein, endotoxins are composed of lipopolysacherride.Exotoxins have specific action while endotoxins are non-specificexotoxins are labile in heat, endotoxins remain stableexotoxins have strong antigenicity, endotoxins have weak antigenicityexotoxins are produced by both gram positive and gram negative; endotoxins are only found on gram negative (LPS)exotoxins can be converted to toxoid; endotoxins cannot

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37
Q

How many chromosomes do bacteria normally contain

A

1typically 2-4 x10^3 kb (kilobase - 1kb= 1000 bases)

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38
Q

How many RNA polymerases do bacteria have

A

1

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39
Q

What type of ribosomes do bacteria contain

A

30s/50s

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40
Q

What does much of bacterial antibiotic resistance result from

A

Point mutations. Commonly:- base substitution- deletion- insertion

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41
Q

How many bases typically in a plasmid

A

10-60 kb

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42
Q

Name some sections commonly found in a plasmid

A
  • Transfer promotion genes- plasmid maintenance genes- antibiotic/virulence determinant genes
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43
Q

How are plasmids typically transferred between bacteria

A

Bacterial conjugation

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44
Q

How can gene transfer occur in bacteria

A
  • Transformation (gain from environment) eg via plasmid- Transduction eg via bacteriophage- Conjugation eg via sex pilus
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45
Q

Where does most bacterial variation come from

A

Gene transfer - lateral transfer of genes

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46
Q

Name the main obligate intracellular bacteria

A

Genus Rickettsia:- R. rickettsii - R. prowazekii- R. conorii- etc.Genus Chlamydia:- C. trachomatis- C. psittaci- C. pneumoniaeGenus Coxiella:- C. burnetii

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47
Q

Which notable illness is caused by the Rickettsia genus of bacteria

A

Rickettsia rickettsii causes:- scrub typhus/rocky mountain spotted fever- transferred via tick

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48
Q

Which notable illnesses are caused by the Chlamydia genus

A

Chlamydia trachomatis can cause:- the STI- trachoma (eye infection)Chlamydia psittaci causes:- bird related pneumonia (can get from kissing pet parrots)Chlamydia pneumoniae:- associated with respiratory tract infections

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49
Q

Name the bacteria that may be cultured on artificial media AND has NO cell wall

A

Mollicutes:- Mycoplasma pneumoniae (atypical pneumonia)- M. hominis (STIs and infertility)- Ureaplasma urealyticum

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50
Q

Name the bacteria that may be cultures on artificial media AND has a cell wall AND grow as filaments

A

Genus ACTINOMYCES e.g. A. israeliiGenus NOCARDIA e.g. N. asteroidesGenus STREPTOMYCES (important source of antibiotics)

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51
Q

Name the bacteria that may be cultures on artificial media AND has a cell wall AND grow as single cells AND are cocci AND gram negative

A

Anaerobic: Genus VEILLONELLAAerobic: Genus NEISSERIA- N. meningitidis- N. gonorrhoeae

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52
Q

What diseases are caused by the genus Neisseria

A

N. meningitidis causes:- meningitis in late teens/early twentiesN. gonorrhoeae causes:- gonorrhoea (2nd most common bacterial STI)- has increased bacterial resistance

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53
Q

Name the bacteria that may be cultures on artificial media AND has a cell wall AND grow as single cells AND are cocci AND gram positive

A

Anaerobic:- PEPTSTREPTOCOCCUS- ENTEROCOCCUS (E. faecalis)Aerobic:- STAPHYLOCOCCUS- STREPTOCOCCUS

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54
Q

How can Staphylococcus be further divided up

A

Coagulase positive:- S. aureus(- S. intermedius)Coagulase negative:- S. epidermidis(- all other staph species)

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55
Q

How can Streptococcus be further divided up

A

Alpha-haemolytic:- Viridans streptococcus- S. pneumoniae- S. sanguis- S. oralisetc.Beta-haemolytic:- S. pyogenes- S. agalactiaeetc.Non-haemolytic:- S. bovis

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56
Q

What do different haemolytic reactions look like

A

Alpha-haemolytic partially lyses blood (via production of hydrogen peroxide) so makes the bacterial colonies look greenBeta-haemolytic fully lyses haem (via production of 2 pore-forming toxins) so turns blood agar clearNon-haemolytic can’t lyse blood (also known as gamma-haemolysis)

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57
Q

What is the Lancefield classification? Give names of relevent bacteria.

A

It classifies bacteria from group A to group G based on which antibody they have - S. pyogenes is Lancfield group A- S. agalactiae is Lancefield group B- Enterococcus faecalis (a different genus, NOT a strep) is Lancefield group D

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58
Q

Diseases caused by staph

A

S. aureus - associated with skin infections; also sometimes endocarditis, particularly after dental surgeryS. epidermis is oppertunistic, normally lives on skin but can cause infection if the human is compromised (e.g. due to catheter, plasters etc.)

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59
Q

What diseases are caused by strep

A

S.pyogenes:- associated with pus, - causes scarlet fever- strep throatS. pneumonia causes:- common pneumonia- meningitis in older peopleAlpha-haemolytic strep - esp. viridans- associated with infective endocarditis

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60
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND acid fast

A

MYCOBACTERIA:- M. tuberculosis (TB)- M. leprae (leprosy)- M. avium-intracellulare- M. ulcerans- M. kansasii- etc

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61
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND gram positive

A

Anaerobic:- CLOSTRIDIUM* C. tetani (tetanus)* C. difficile (diarrhea)* C.perfringens* C. botulinumetc.- PROPIONIBACTERIUM* P. acnesAerobic:- CORYNEBACTERIUM* C. diphtheriaeetc- LISTERIA * L. monocytogenesetc- BACILLUSB. anthracis (Anthrax)B. cereus (food poisoning)etc

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62
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND gram negative

A

Anaerobic:- BACTEROIDES* B. fragilisAerobic:- ‘Coliforms’ (gut bacteria - non-spore forming)- ‘Pseudomonads’ (belonging to pseudomonas genus)- ‘Vibrio’ (curved rod)- ‘Parvobacteria’ (small, fastidious, non-spore forming coccobacilli)

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63
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND gram negative AND are coliforms

A

ESCHERICHIA- e.g. E. coli KLEBSIELLA SALMONELLA - e.g. S. typhi SHIGELLA - e.g. S. sonnei CITROBACTER PROTEUS YERSINIA- e.g. Yersinia pestis etc

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64
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND gram negative AND are Pseudomonads

A

PSEUDOMONAS- e.g. P. aeruginosa

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65
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND gram negative AND are vibrio bacteria

A

VIBRIO- e.g. V. choleraeCAMPYLOBACTER- e.g. C. jejuniHELICOBACTER

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66
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are bacilli AND gram negative AND are parvobacteria

A

HAEMOPHILUS- eg H. influenzae BRUCELLABORDETELLA- e.g. B. pertusissPASTEURELLA

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67
Q

Name the bacteria that may be cultured on artificial media AND has a cell wall AND grow as single cells AND are spirochaetes

A

LEPTOSPIRA- e.g. L. icterohaemorrhagiae (Leptospirosis)TREPONEMA- e.g. T. pallidum (syphilis)BORRELIA- B. burghdorferi (lyme disease)- B. recurrentisetc

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68
Q

Which antigenic groups of strep are Beta-haemolytic?

A

A, B, C, G

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69
Q

How do you differentiate between viridans strep and S. pneumoniae?

A

Optochin test- Viridans strep is resistant to optochin; S. pneumonia is sensitive to optochin- On agar culture - optochin sensitivity looks like an area around the optochin disk that is clear of bacteria

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70
Q

How do you differentiate between S. aureus and other staphylococcus

A

Coagulase/DNAse test- S. aureus is coagulase positive (also s. intermedius)- rest are negative

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71
Q

What is a go-to antibiotic for staph infections

A

Flucloxacillin

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72
Q

How many species of staph are there

A

at least 40

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73
Q

What is coagulase? Why might this be produced?

A

Enzyme produced by bacteria that clots blood plasma- Fibrin clot formation around bacteria may protect from phagocytosis

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74
Q

Where is the normal habitat of staph

A

nose and skin

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75
Q

Are coagulase +ve or -ve staph more likely to cause problems

A

Coagulase +veCoagulase -ve species (e.g. S. epidermidis) only important as opportunistic infections

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76
Q

How is staph aureus spread

A

Aerosol and touch- some people are carriers/shedders

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77
Q

What are S. aureus’ virulence factors

A

Pore-forming toxins (in some strains)- α - haemolysin (low levels: apoptosis, high levels: mass necrosis)- Panton-Valentine Leucocidin ‘PVL’ (causes hemorrhagic pneumonia)Proteases - Exfoliatin (exotoxin - scalded skin syndrome)Toxic Shock Syndrome toxin (super antigen)- (stimulates cytokine release)Protein A - (surface protein which binds antibodies in wrong orientation)

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78
Q

What is MRSA?

A

Methicillin (aka flucloxacillin) Resistant S. aureus- resistant to major antibiotics- break open beta-lactam ring of certain antibiotics- resitant to gentamicin, erythromycitetracycline

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79
Q

Types of S. aureus infections

A

Pyogenic:- wound infections- causes:* abscesses* Impetigo* Septicaemia* Osteomyelitis* Pneumonia* EndocarditisToxin mediated:- Scalded skin syndrome- Toxic shock syndrome- Food poisoning

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80
Q

Name the main coagulase -ve staph species

A
  • S. epiderimidis- S. saprophyticus
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81
Q

Characteristics of S. epidermidis

A
  • Oppertunistic infections* common in immunocompromised and people with prostheses- Main virulence factor - ability to form persistant biofilms (clusters of bacteria that are attached to a surface and/or to each other and embedded in a self-produced matrix)
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82
Q

Characterictisics of S. saprophyticus

A

Causes acute cystitis (UTI)- commonly comes from skin contact in sexual intercourseVirulence factors:- haemagglutinin for adhesion- urease

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83
Q

Is S. pyogenes aerobic or anaerobic?

A

It’s facultatively anaerobic (can grow anaerobically or aerobically)

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84
Q

Is S. pyogenes penicillic sensitive?

A

Yes

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85
Q

Where is s. pyogenes most likely to infect?

A

Throat, skin, post partum infections

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86
Q

What kind of infections are s. agalactiae associated with

A

Neonatal infections - passed from mother to child

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87
Q

How are Lancefield groups tested? Describe the procedure.

A

Lancefield microbead agglutination test:- Antiserum (solution of antibodies) made that recognise each specific group- The antiserum is tagged to tiny plastic beads- These are added to a suspension of bacteria- If the bacterial antigen is complementary to the antiserum, they bind together and cause the beads to clump together- this is visible to the naked eye

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88
Q

Virulence factors of S. pyogenes

A

Exported factors:- Enzymes* Streptokinase (important) ** breaks down clots * Hyaluronidase ** spreading * C5a peptidase ** reduces chemotaxis- Toxins* Streptolysins O&S (Important) ** binds cholesterol* Erythrogenic toxin (Importnat) ** Streptococcal pyrogenic toxin e.g. SPeA – exaggerated response ** Can lead to scarlet fever in childrenSurface factors:- Capsule - hyaluronic acid - M protein – surface protein (Important) (encourages complement degradation) * can cause scarlet fever in children

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89
Q

Infections caused by S. pyogenes

A

Respiratory- Tonsillitis & pharyngitis (most common)- Otitis mediaSkin and Soft tissue- Wound infections- Impetigo- cellulitis - puerperal feverScarlet fever- SPeA and M typeComplications- rheumatic fever- glomerulonephritis

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90
Q

Characteristic appearances of S. pneumonia in culture/tests

A
  • “draughtsman” colonies (depressed central part with raised edges)- α- haemolytic- Gram positive cocci in pairs- Optochin sensitive
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91
Q

Where is S. pneumonia often found (non-pathogenically)

A

Found as a commensal in oro-pharynx of 30% of population

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92
Q

What does S. pneumoniae cause pathogenically

A

PneumoniaOtitis medis (middle ear infection)SinusitisMeningitis

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93
Q

What factors predispose to S. pneumoniae infection

A
  • Impaired mucus trapping (e.g. viral infection)- Hypogammaglobulinaemia (problems making antibodies)- Asplenia (absence of spleen)- HIV
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94
Q

S. pneumonia virulence factors

A

Capsule- polysaccharide (84 types), antiphagocytic Inflammatory wall constituents- teichoic acid (choline)- peptidoglycanCytotoxin- pneumolysin (pore-forming)

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95
Q

Which vaccines are there for S. pneumoniae infection

A
  • polysaccharide vaccine ‘PPV’ - contains 23 types of pollysaccheride antigens from s. pneumoniae capsule- conjugate vaccine ‘PCV’ - contains 13 types of pollysaccheride antigens from s. pneumoniae capsule
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96
Q

Who are S. pneumoniae vaccines given to and why

A

Only at risk people over 2 y/oThe immune response to polysaccheride antigens is poor in the very young

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97
Q

Who is at risk for S. pneumoniae infection

A

People with:- sickle cell disease, - asplenia, - renal disease, - immunodeficiency, - diabetes - chronic liver disease

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98
Q

How does pneumolysin form pore

A

Subunits assemble into a ring structure on host cell surface thus forming a pore in the membrane

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99
Q

Characteristics of Viridans group strep

A

α- haemolytic (or non-haemolytic)Optochin resistant

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100
Q

What diseases can Viridans group strp cause

A
  • Some cause dental caries & abscesses - typically live in mouth- Important in infective endocarditits (difficult to diagnose and treat)- Cause deep organ abscesses (e.g. brain, liver)
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101
Q

Which strep species are typically associated with infective endocarditis? What is a typically presentation of this?

A
  • S. sanguinis- S. oralisVery typical for people to get endocarditis after having dental surgery - they get into the blood from the mouth
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102
Q

Most virulent group of Viridans group strep

A

‘milleri group’S.intermedius, S.anginosus, S.constellatus

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103
Q

Main aerobic Gram positive bacilli

A
  • Listeria monocytogenes - Bacillus anthracis- Corunebacterium diphtheriae
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104
Q

What does listeria monocytogenes cause?

A

causes listeriosis (starts as type of food poisoning - grows in moist areas)- usually self-limiting- can cause issues in immunocompromised people and pregnant women

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105
Q

What does bacillus anthracis cause?

A

Anthrax- associated with cattle- spore forming so can be around for a long time3 syndromes depending on route of acquisition:- Cutaneous - blister with black centre (‘eschar’)- Inhalation - respiratory sepsis- Ingestion - severe gasteroenteritis

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106
Q

What does corynebacterium diphtheria cause

A

Diphtheria- infectin of pharynx* thick greyish pseudo membrane on tonsils can be a characteristic of it- involves infection of immune cells- involves metachromatic granules

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107
Q

Main anaerobic gram positive bacilli

A

All main are types of CLOSTRIDIA- C. tetani- C. botulinum- C. difficile

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108
Q

What does C. tetani cause? Associated symptoms and characteristics.

A

Tetanus- muscle contractions and stiffness progressing from head to body (neck stiffness, sore throat, difficulty opening mouth) - rictus grin- Get from infected wounds- Toxin inhibits GABA

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109
Q

What does C. botulinum cause?

A

Botulism- paralysis spreading from head to body (from Botulinum toxin)- from contaminated food or infected wounds

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110
Q

What does C. difficile cause?

A

Antibiotic associated diarrhea (as it kills off good bacteria and leaves C. difficile able to colonise more of the gut)- pseudomembranous colitis (destroys coloon)

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111
Q

What are the components of LPS

A
  • Lipid A - the toxic portion that is anchored in the outer leaflet of outer membrane- Core (C) antigen (AKA core oligosaccheride) - short chain of sugars, some are unique to LPS- Somatic (O) antigen (O-polysaccheride) - highly antigenic repeating chain of oligosaccherides
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112
Q

Why do mycobacteria or mycoplasmas not stain with Gram stain? Are they considered gram positive or negative?

A

Mycobacteria outer lipid bilayer is composed of Mycolic acidsMycoplasmas don’t have peptidoglycan- They are phylogenetically considered Gram positive

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113
Q

The two types of virulence factors/pathogenicity determinants

A

Colonisation factorsToxins (‘effectors’)

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114
Q

Name colonisation factors

A

Adhesins, invasins, nutrient acquisition, defence against the host

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115
Q

What are toxins/’effectors’ released by gram bacteria?

A
  • Usually secreted proteins that cause damage and subversion- In gram neg bacteria the protein secretion system spans both layers on the cell membrane - proteins are translocated from inside cytoplasm and secreted
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116
Q

Which bacteria are within the Phylum proteobacteria

A

Enterobacteriaceae or Enterobacteria FAMILY (contains Shigella, salmonella, escherichia etc.)Vibrio (e.g. vibrio cholerae)PseudomonansHaemophilus (e.g. H influenza)Legionella (e.g. Legionella pneumophila)Bordetella (e.g. bordetella pertussis)NeisseriaCampylobacterHelicobacter (e.g. Helicobacter pylori)

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117
Q

Characteristics of Enterobacteria

A

RodsMost are motile (have peritrichous flagella - flagella over their entire surface, like around the perimeter)Some species colonise the gut (commensals and pathogenic)Facultatively anaerobic

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118
Q

Name main members of enterobacteria?

A

ShigellaEscherichia (esp E. coli)Salmonella (e.g. S. enterica)Proteus (e.g. P. mirabilis)Klebsiella (e.g. K. pneumoniae)Less relevent according to lecturer:Serratia (e.g. S. marcenescens)Yersinia pestisEnterobacter spp.

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119
Q

Which main enterobacteria are lactose use positive?

A

E. coliKlebsiella pneumoniae

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120
Q

Which main enterobacteria are motile

A

E. coliSalmonella entericaSerratia marcensens (is this important??)Yersinia pestis at 25 degrees C (NOT motile at 37 degrees so NON-MOTILE inside humans)Proteus mirabilis

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121
Q

Which main enterobacteria are NOT motile?

A

Shigella flexneriKlebsiella pneumoniaeYersinia pestis at 37 degrees C

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122
Q

How do you test Lactose phenotype?

A

On MacConkey agarSelective for gram-negative bacteria (contains bile salts and crystal violet)Contains indicator so Lactose metabolising positive organism colonies turn red

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123
Q

Which antigen is associated with flagella

A

H antigen

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124
Q

How do you discriminate between similar bacteria like Salmonella and Shigella

A

Serology(in this case, no H (flagella) antigen pressent for Shigella)

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125
Q

What is serotyping

A

Differentiating between specieses/strains by identifying cell surface antigens

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126
Q

What is a serovar

A

Antigenically distinct varients of a single species

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127
Q

What are the 3 main antigenic determinants for serotyping in gram negative bacteria

A

K antigen (exopolysaccheride ‘capsulel’)H antigen (flagella)O (somatic) antigen (LPS)

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128
Q

What is Escherichia coli normally

A

Commensal gram -ve bacteria - most abundant facultative anaerobe in gut (10^7-10^8/g faeces)Has peritrichous flagella

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129
Q

Principal infections caused by pathogenic E. coli

A

(i) Wound infections (typically post-surgical)(ii) UTIs (cystitis; 75-80% of female UTIs - faecal source or sexual activity; * catheterisation - most common type of nosocomial (originating in hospital) infection)(iii) Gastroenteritis(iv) Travellers’ diarrhoea(v) Bacteraemia (can be asymptomatic - sometimes leading to sepsis syndrome)(vi) Meningitis (infants) - rare in UK

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130
Q

What are the species’ of Shigella

A

S. dysenteriae, S. flexneri, S. boydii, S. sonnei

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131
Q

What does shigella cause

A

Shigellosis: severe bloody diarrhoea (bacillary dysentery)- S. dysenteriae causes most severe form.BUT - S. sonnei most prevalent in developed world.

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132
Q

Where is Shigella infection often found

A

Endemic in developing countries where sanitation is poor – mainly in children.

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133
Q

Symptoms of shigellosis

A

Frequent passage of stools (>30/day)Small volume, pus and blood, prostrating cramps, pain in straining, feverUsually self-limiting (in adults)

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134
Q

Pathogenesis of Shigella infection

A

Acid-tolerant (low infective dose, ~10^2)Person-to-person, or contaminated water & food(fresh/raw vegetables used in salads)Entry through colonic M cells (antigen sampling cells - lie over lymphoid follicles and deliver antigens to underlying immune cells)Induced uptakeImportant virulaence factor: Shiga toxin

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135
Q

Pathology of Shigella

A
  • lands on M cell apical surface- gets taken to basolateral surface- phagocytosed by macrophage (but rmains unharmed)- Shigella induces apoptosis of macrophage- moves laterally, destroying tissue- Macrophages also release cytokines to attract polymorphoneuclear leukocytes to the site of in fection causing more tissue damage
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136
Q

What are the 2 specieces of Salmonella

A

S. enterica (has >2 500 serovars, including Salmonella enterica serovar Typhi)S. bongori (rare - contact with reptiles)

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137
Q

What does S. enterica cause

A

salmonellosis (usually from contaminated food/drink)3 forms:1. Gastroenteritis/enterocolitis2. Enteric fever3. Bacteraemia (bacteria in blood)

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138
Q

Pathogenesis of salmonellosis

A

Ingestion of contaminated food/water - high I.D. (infective dose)(~10^6) (‘faecal-oral route’)→ Invasion of gut epithelium (small intestine)→ Transcytosed to basolateral membrane→ Enters submucosal macrophages→ Intracellular survival/replicationIn Serovars Enteritidis and Typhimurium:- intestinal secretion and inflammatoryresponse are LOCALISED- DO NOT produce toxinsIn serovar Typhi:- Infection is SYSTEMIC due to dissemination within macrophages (macrophages migrate to reticuloendothelial organs via lymph and blood)- produces TYPHOID TOXIN (has DNAse activity - a genotoxin)

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139
Q

Gastroenteritis/enterocolitis - causes and characteristics

A

Caused by serovars Enteritidis and TyphimuriumFrequent cause of food poisoning (milk, poultry meat & eggs)Second highest no. of food-related hospitalisations/deaths (UK)6-36 hr incubation period, resolves (~7 days) Localised infection, only occasionally systemic

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140
Q

Enteric fever - causes/characteristics

A

Typhoid/paratyphoid fever - caused by serovars Typhi and ParatyphiLinked to poor quality drinking water/poor sanitation Systemic disease ~20 million cases, ~200,000 deaths/year (globally)

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141
Q

What causes Bacteraemia

A

Serovars Cholerasuis and Dublin- it is uncommon

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142
Q

Steps of gastroenteritis pathogenesis

A
  1. Bacterial-mediated endocytosis 2. Induction of interleukin-8 release →3. Neutrophil recruitment and migration4. Neutrophil-induced tissue injury →5. Fluid and electrolyte loss → diarrhoeaInflammation/necrosis of gut mucosa
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143
Q

Steps of enteric/typhoid fever pathogenesis

A
  1. Bacterial-mediated endocytosis2. Transcytosis to basolateral membrane3. Survival in macrophage (MΦ) → systemic spread Initially, little damage to gut mucosa
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144
Q

What % of people become carriers of S. enterica serovar Typhi

A

~10% are carriers for < or = 3 months (bacteria shed in faeces)~ 1-4% become chronic carriers (at least a year or more)

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145
Q

Notable characteristic of Proteus mirabilis

A

Can differentiate into an elongated hyperflagellated form → gives it surface motility (ability of ‘swarming’) over solid surface

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146
Q

What does Proteus mirabilis cause

A

Catheter-associated UTIs (~30% of cases)- can ascend and cause pyelonephritis (kidney infection)Formation of bladder/kidney stones, can block catheter- does this by producing urease (increasing urine pH) which forms ammonia and leads to calcium phosphate precipitation

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147
Q

Characteristics of Klebsiella pneumoniae

A
  • environmental (it is an enterobacteria but more common in environment)- opportunistic, nosocomial infections (neonates, elderly, compromised)- colonisation of gastrointestinal tract (normal) and oropharynx (less frequently) is often benignMulti-drug resistant (resistant to carbapenems)
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148
Q

What does Klebsiella pneumoniae cause

A

UTI, pneumonia (aspiration from oropharynx), surgical wound infections from gut, bacteraemia → sepsis (high mortality).

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149
Q

Characteristics of Vibrio cholerae

A
  • Facultative anaerobe- Normally from Saline environments: commensal to planktonic crustaceans such as copepods → ingestion by shellfish → contamination of drinking water due to flooding of coastal areas or poor sanitation (faecal contamination)- characteristic curved rod shape
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150
Q

What does vibrio cholerae cause

A

Cholera: Most severe diarrhoeal diseaseAssociated with LPS O1 serotype → epidemics (and occasionally O139 variant)Characterised by pandemics (7 recorded since 1817)

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151
Q

History of Choleral pandemics

A

1P-6P, Indian subcontinent;7P began in Sulawesi (1961) → SE Asia (1963) → Africa (1970) → Latin America (1991) → Caribbean (2010)1.4-4.0 million cases/year, 20,000-140,000 associated deaths

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152
Q

General pathology of Cholera (aquisition, incubation, consequence)

A

Faecal-oral route (not person-to-person) - high infective dose required (not acid resistant)(faecal contaminated water (poor sanitation) or undercooked shellfish from risk areas) ↓Incubation, few hours to 5 days (V.c. multiplies in small intestine) ↓Voluminous watery stools (‘secretory’ diarrhoea - rice water stool)Can lose 20 litres fluid/day plus electrolytes → dehydration/death (hypovolaemic shock) → 50-60% mortality if untreatedNo blood, pus or fever (i.e. not dysenteric)i.e. no invasion or damage to mucosa

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153
Q

What can most cases of Cholera be treated by

A

Oral re-hydration therapy (ORT)

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154
Q

What is the main virulence factor of V. cholerae

A

Cholera toxin

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155
Q

Pathogenesis of Cholera (mechanism of cholera toxin)

A

CT binds to a glycolipid receptor on epithelial cell (B subunits)A subunit ADP-ribosylates G-protein (Gs) → locked in ‘ON’ stateUncontrolled cAMP productionProtein kinase A activatedPhosphorylates CFTR (cystic fibrosis transmembrane conductance regulator) anion transporterCFTR activity modified (loss of Cl- & Na+ into gut lumen) → massive loss of H2O

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156
Q

Characteristics of Pseudomonas aeruginosa

A

Ubiquitous, free-living (in environment), motile (single polar flagellum), rod-shaped.Opportunistic (serious cause of nosocomial infections)Resistant to multiple antibiotics (& disinfectants) - very difficult to treat

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157
Q

Infections caused by P. aeruginosa. Can it cause acute or chronic?

A

Acute infections:(i) Localised - burn/surgical wounds - UTI (catheters) - Keratitis (infection of cornea - requires some kind of scratch etc.)(ii) Systemic (bacteraemic → sepsis - hard to treat) - affects neutropenic patients - low white blood cell count (leukaemia, chemotherapy, AIDS)(iii) affects ICU patients (ventilator acquired pneumonia) - leading cause of nosocomial pneumoniaChronic infections:(i) In Cystic fibrosis (CF) patientsCommon denominator to all infections - compromised host defences

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158
Q

What happens in cystic fibrosis (general overview)

A

Defective CFTR (chloride ion transporter)→ thick mucus produced in lungs.- Lungs prone to microbial infection

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159
Q

Most problematic source of infection for CF patients

A

P. aeruginosa

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160
Q

Types of P. aeruginosa

A

P. aeruginosa ‘wild-type’ (non-mucoid)P. aeruginosa ‘CF’ phenotype (mucoid) = mutants that secrete a thick coating of exopolysaccharide (i.e. hyper-produce capsule): provides additional protection against host defences in the lung

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161
Q

What leads to the progressive lung damage following infection of CF lung by P. aeruginosa

A

Mainly due to effect of host immune system trying to clear infection

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162
Q

Characteristics of Haemophilius influenzae

A

Exclusively human parasite (obligate/ no environmental reservoir):Nasopharyngeal carriage in 25-80% population (non-capsulate strains)- transient carriage of capsulate strains occurs in 5-10% (more dangerous as they are invasive - can move around body)Oppertunistic

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163
Q

Who are particularly susceptible to H. influenzae infection

A

Young children and adult smokers

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164
Q

What infections can Haemofilius influenza cause

A
  • Meningitis* (age <5 yrs), 5-10% of adult cases ∙ Bronchopneumonia ∙ Epiglottitis, sinusitis, otitis media ∙ Bacteraemia (often associated with pharyngitis) ∙ Pneumonia in CF, COPD, HIV patients* infections caused by capsulate strains (invasive) – uncommon in healthy adults
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165
Q

Diagnostic characteristics of H. influenxae

A

Fastidious - requires ‘factor X’ (haem) and ‘factor Y’ (NAD) - requires chocolate agar (lysed/oxidised blood)Non-motile

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166
Q

Virulence determinants of H. influenzae

A

(i) Capsule - invasive strains are capsulate (‘encapsulated’) → can penetrate nasopharyngeal epithelium → resistance to phagocytosis and complement system - 6 different capsule serotypes (a-f) (type b strains are the main cause of meningitis)Commensals and upper respiratory tract pathogens are non-capsulate referred to as ‘non-typeable’ H. influenzae (NTHi)(ii) LPS (‘endotoxin’) → inflammation → complement resistance

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167
Q

Which vaccine has reduced the cause of H. influenza caused meningitis

A

Hib vaccine (HH. influenza type b)

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168
Q

What does Legionella pneumophila cause, source of acquisition and who does it usually affect

A

Legionnaires’ disease - severe inflammatory pneumonia (1-3% of all pneumonias) - 15-20% mortalityInfection from man-made aquatic environments (air-conditioning cooling towers, shower heads, nebulisers, humidifiers etc.) - never person-to-person transmission - replicate within freshwater protozoa- can repliacte in alveolar macrophages tooAffects immunocompromised (elderly, alcoholics, smokers etc.)

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169
Q

What does Bordetella pertussis cause

A

Pertussis (whooping cough)Non-specific flu-like symptoms (~7 d), followed by paroxysmal coughing(https://www.youtube.com/watch?v=l5SHtdczSBc)(B. parapertussis causes mild pharyngitis)

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170
Q

Characteristics of B. pertussis

A

Humans - only known reservoir (obligate human pathogen)Highly contagious (low I.D.) - aerosol transmission(- produces pertussis toxin and Adenylate cyclase-haemolysin toxin (CyaA))Non-invasive

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171
Q

Diagnostic characteristics of B. pertussis

A

Short (sometimes oval) rods (coccobacilli)FastidiousGram negative

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172
Q

Diagnostic characteristics of Neisseria

A

Non-flagellated diploccociFastidiousGram -ve

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173
Q

Where can Nessieria be found in the environment

A

Humans are the only known reservoir

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174
Q

Characteristics of N. meningitidis

A

Nasopharyngeal carriage in 5-10% population (asymptomatic) Rises to 20-90% during outbreaksPerson-to-person (aerosol) transmission (universities, barracks, Haj)

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175
Q

Pathogenesis of N. meningitidis

A

crosses nasopharyngeal epithelium and enters bloodstream → low level - bacteraemia (asymptomatic) or high level - septicaemia (sepsis - high mortality if not treated) → meningitis: invasion of the meninges - bacteria enter CSF of subarachnoid space after crossing blood-brain barrier(second most frequent cause of meningitis in young children)

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176
Q

Virulence determinants of N. meningitidis

A

(i) Capsule is major virulence determinant (serogroup B - 90% cases) → anti-phagocytic(noncapsulated N.m. only found in nasopharynx - not pathogenic)(ii) LPS (membrane ‘blebs’) → cytokine cascade → sepsis

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177
Q

What are non-blanching petechial pr purpuric rashes associated with

A

Meningococcal sepsis(capillary damage - bleeding - ecchymosis AKA bruising)

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178
Q

What does N. gonorrhoeae cause

A

Gonorrhoea - second most common STD worldwide

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179
Q

How is gonorrhoea transmitted

A

Person-to-person only

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180
Q

How often can N. gonorrhoeae infection be asymptomatic

A

~10% men, ~50% women

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181
Q

Characteristic infection presentation of gonorrhoea

A

Urethritis with additional infection of female genitalia. Serious complications in women - can lead to salpingitis (fallopian tubes) and/or PID (pelvic organs) if infection ascends.Proctitis, gingivitis, pharyngitis depending on sexual preferenceCan transmit as conjunctivits to newborns

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182
Q

Are gonococci capsulated or not

A

They are non-capsulated

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183
Q

Helicobacter pylori appearance

A

spiral shape, tuft of polar flagella

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184
Q

Where are H. pylori found in the body

A

Discovered in gastric mucus (1982) which was previously thought to be sterile

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185
Q

Incidence of H. pylori in global population

A

Present in ~50% global population, but onlya fraction develop disease

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186
Q

Which diseases are H. pylori associated

A

Major role in gastritis and peptic ulcer disease (80-90% of ulcers)Implicated in ~10% cases of gastric adenocarcinoma & mucosa-associated lymphoid tissue lymphoma (linked to production of VacA and CagA toxins)

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187
Q

Name of main bacteria in Phylum bacteroidetes

A

Bacteroides

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188
Q

Characteristics of Bacteroides

A

Non-motile rodsObligate anaerobesCommensal flora of colon (most abundant organism in gut - 30-40% of total)Opportunistic

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189
Q

What amount per g of faeces is Bacteroides? Population ratio compared to E. coli?

A

> 10^10/g faeces (outnumbers E. coli 20:1)

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190
Q

What infections can infections can Bacteroides cause

A

Infection of tissue injury (surgery, perforated appendix or ulcer) → predominantly peritoneal cavity infections (peritonitis, intrabdominal abscesses are most common) can lead to bacteraemiaMost frequent cause of banaerobic infectionsOften present in polymicrobial infections with enterobacteria - presence of facultative anaerobes depletes O2, allowing anaerobes such as Bacteroides to proliferate

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191
Q

Which Bacteroides species is most commonly responsible for infections

A

B. fragilis(although it is only 0.5-1.0% of total commensal Bacteroides)

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192
Q

Which genuses are in Phylum Chlamydiae

A

Chlamydia and Chlamydophila

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193
Q

Characteristics of Chlamydia and Chlamydophila

A

Very small, non-motile.Obligate intracellular parasites.Many species within this group live asymptomatically as endosymbionts in amoebae, invertebrates and vertebrates.Cannot culture in bacteriological media - detect by serum Abs (antibodies - tho these could be due to previous infection so anleternate confirmatory test must also be done) or PCR (AKA NAA or NAAT)

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194
Q

Life cycle of Chlamydia and Chlamydophila

A

2 developmental stages:(i) Elementary bodies (EBs) - rigid, extracellular form, ~0.3 μm, dormant infectious enter cell through endocytosis prevent phagosome-lysosome fusion ↓ differentiates into…(ii) Reticulate bodies (RBs) - fragile, intracellular form, ~1.0 μm, metabolically active replicative non-infectious acquire nutrients from host cell

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195
Q

How many developmental stages in life cycle of Chlamydia/Chlamydophila

A

2- Elementary body stage- Reticulate body stage

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196
Q

Form/characteristics of Chlamydia/Chlamydophila Elementary bodies

A

Rigid, dormant extracellular form~0.3 micrometers

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197
Q

What occurs during the elementary body phase of Chlamydia/Chlamydophila life cyle

A

InfectiousEnter cell throughendocytosisprevent phagosome-lysosome fusion (so it can’t be destroyed by host defence of cell)

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198
Q

What happens in reticulate body phase of Chlamydia/Chlamydophila life cycle

A

Non-infectiousReplicationAcquire nutrients from host cell

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199
Q

Characteristic of Chlamydia/CHlamydophila reticulate body

A

fragile, metabolically active, intracellular formpleiomorphic~1.0 micrometers

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200
Q

Medically important members of genus Chlamydia

A

C. trachomatis (has 3 biovars):- trachoma biovar (serotypes A-C)- gentital tract biovar (serotypes D-K)- lympho granuloma venereum (LGV) biovar

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201
Q

What disease does the Chlamydia trachomatis biovar trachoma cause

A

Trachoma → blindness (eye-to-eye transmission via hands, fomites (innanimate objects like mascara brushes) or flies)Largest cause of preventable blindness caused by infectius organismsEasily treated if caught early but often not recognised till later

202
Q

What does C. trachomatis biovar genital tract cause

A

Chlamydia STI- most common STD in UK - infects epithelial cells of mucous membranes of urethra (both sexes) and vagina- can ascend to uterus and ovaries (PID, infertility)- usually asymptomatic (i.e. 70-80% cases in women)Conjunctivitis (hand-to-eye transmission OR mother-to-child during delivery)

203
Q

What does the lympho granuloma venereum (LGV) biovar of Chlamydia trachomatis cause

A

LGV (an STD) - invasive urogenital/anorectal infection- endemic to the tropics, cases rising in Europe/North America

204
Q

Medically important members of Chlamydophila

A

C. pneumoniaeC. psittaci

205
Q

What does C. pneumoniae cause

A

Resp tract infection (mild/’walking’ pneumonia)Causes ~10% community acquired pneumonias

206
Q

What does C. psittaci cause

A

Psittacosis (severe pneumonia)Mainly affects bird owners (zoonotic)Uncommon

207
Q

Spirochaete physical form

A

Long, slender, helical, highly flexible

208
Q

Characteristics of Spirochaetes

A

Most are free-living and non-pathogenicPathogenic varieties difficult to cultureHas a modified outer membrane (Treponema and Borrelia lack LPS, have a different glycolipid instead)

209
Q

Where is the spirochaete endoflagella located

A

Between peptidoglycan and outer membranePeriplasmic flagellaFixed at each end of bacterium and confers shapeOverlap in centre of bacterium

210
Q

Characteristics of spirochaete endoflagella function

A

Propels in corkscrew motionSwims faster in high viscosity medium (i.e. normal environment of spirochaetes)‘Hides’ antigenic flagellum

211
Q

What are the 3 medically important members of Spirochaetes

A

Borrelia burgdorferiLeptospira interrogansTreponema pallidum

212
Q

What does Borrelia burgdorferi cause

A

Lyme disease

213
Q

How is Lyme disease transmitted

A

Via ticksB.b. infects small mammels (e.g. rodents)Tick larvae feeding on the infected animal acquire B.b.Usually transmitted to humans by tick nymphs (adults easier to spot)

214
Q

Symptoms of Lyme disease

A

Bull’s eye rashFlu-like symptoms (fever, fatigue, headache)(neurological problems in 10-15% patients, joints → arthritis)Most symptoms arise as consequence of immune response

215
Q

How can lyme disease spread within the human body

A

dissemination via lymphatics/blood to other organs

216
Q

What does leptospira interrogans cause

A

Leptospirosis (zoonosis) - rare in UKSymptoms of leptospirosis:- Flu-like- Severe form (Weil’s disease) in 10-15% infected individuals * jaundice, acute renal and hepatic failure, pulmonary distress, haemorrhage

217
Q

How is leptospirosis acquired?

A

Contact of infected animal urine with mucous membrane or abraded skin

218
Q

What does treponema pallidum cause

A

Syphilis

219
Q

How many stages of syphilis (treponema pallidum infection)

A

3Primary stageSecondary stageTertiary stage

220
Q

What occurs in primary stage syphilis (treponema pallidum infection)

A

Localised genital infection (chancre)Defined as days-weeks post-infection (i.e it is in the primary stage if it is occuring within days/weeks of being infected)

221
Q

What occurs in secondary stage syphilis (treponema pallidum infection)

A

Systemicskin (rash), swollen lymph nodes, joint pains, muscle aches, headache, feverOccurs at 1-3 months post-infectionHighly transmissible~50% of cases are at secondary stage

222
Q

What occurs in tertiary stage syphilis (treponema pallidum infection)

A

‘Gummas’ (granulomas) in bone and soft tissueCardiovascular syphilis (affects aorta)Neurosyphilis (affects brain and spinal cord)Occurs several years post-infectionNon-infectious

223
Q

How can syphilis be treated

A

All stages can be treated with antibiotics but treatment is longer for tertiary stage syphilis and tertiary-related damage can’t be reverted

224
Q

Name mycobacteria of medical importance and their relevant medical condition

A

M. tuberculosis - tuberculosisM. leprae - LeprosyM. avium complex (MAC) - Disseminated infection in AIDS, chronic lung infection (oppertunistic - doesn’t usually affect humans)M. kansasii - Chronic lung infection (oppertunistic - doesn’t usually affect humans)M. ulcerans - Buruli ulcer (west africa/ australia - often affects kids - doesn’t usually kill but maims)Rapidly growing mycobacteria (AKA M. fortuitum complex) - Skin/soft tissue infectionsM. marinum - fish tank granuloma (asymptomatic in tropical fish - skin conditions in humans)

225
Q

Are most mycobacteria environmental or human organisms

A

Most are environmentalTB evolved to infect humans and some other mammals like bovines

226
Q

How is leprosy (m. leprae) communicated

A

Through respiratory mediums Only infectious in early respiratory period

227
Q

What effect does leprosy have on humans

A

Skin hypopigmentation - some lesions presentNeural lesion - loss of sensation and pain response

228
Q

What socioeconomic factor is leprosy associated with

A

poverty

229
Q

Stages of Buruli ulcer (m. ulcerans infection)

A

NoduleSmall ulcerLarge ulcerBone destruction (causes deformation)

230
Q

What is severe Buruli ulcer associated with

A

Poverty - don’t have resources to seek medical help until sever, late stagesIt is treatable if found at an early stage

231
Q

Characteristics of TB

A

Infects people over a long period of timePeople put large amount of bodies resources into fighting off TB thus causing consumptive appearanceLeading cause of death by infectious disease

232
Q

Mycobacteria physical appearance

A

Slightly curved, beaded bacilli

233
Q

What makes mycobacteria resistant to gram stain?

A

High lipid content with mycolic acid in cell walls

234
Q

Ziehl-Neelsen stain process

A

Red Carbol fuchsin addedWashed with acid/alcohol (mycobacteria are acid fast so resistant to destaining)Add Methylene blue

235
Q

How many bacilli are needed for a diagnosis

A

10 000 bacilli per ml of sputum

236
Q

Characteristics of mycobacteria

A

Aerobic, non-spore forming, non-motileCell wall has high molecular weight lipids

237
Q

Key components of mycobacteria cell wall

A

Mycolic acidsLipoarabinomannan

238
Q

How fast do mycobacteria grow

A

M. tuberculosis generation time is 15-20h vs. 1h for common bacterial pathogens - Have to wait at least 48 hours before you can declare no M. tuberculosis is growing in a culture - Slows down diagnosis

239
Q

What is generation time?

A

Time taken for bacterial population to double in number

240
Q

How is TB transmitted

A

aerosol transmission

241
Q

What occurs in primary TB?

A

Initial contact made by alveolar macrophagesBacilli taken in lymphatics to hilar lymph nodes

242
Q

What is latant TB

A

Where Primary infection is controlled but cell mediated immune response from T cells persitsNo clinical disease (as immune system is strong enough to keep bacilli trapped in granulomas)Cell mediated immune response to TB can still be detected via tuberculin skin testCan remain in the body in this form for decades

243
Q

What occurs in Pulmonary TB

A

Can be post-primary (immediately after primary infection) or after reactivationGranulomas form around bacilli that have settled in the apex of lungs * more air and less blood supply (fewer white blood cells)Necrosis occurs in granuloma/tubercles (looks kasiated - like cheese) resulting in abscess formation and caseous material coughed upMay spread in lungs causing other lesions

244
Q

What are granulomas dependant on

A

A sufficient number of CD4 cells and TNF alpha being present

245
Q

What increases risk of TB becoming active

A

ImmunosuppressionAnti-TNF therapies (given for chronic inflammation)

246
Q

What is a primary complex in TB

A

Consists of granuloma, lymphatics and lymph nodes

247
Q

What issues can TB cause when it spreads beyond lungs

A

TB meningitisMiliary TBPleural TBBone and joint TBGenito-urinary TB

248
Q

How can TB be spread beyond lungs

A

Carried by macrophages which then move around body

249
Q

What does TB of spine cause?

A

Bent gibbus formation

250
Q

Immunological response to mycobacteria

A

Mycobacteria phagocytosed by macrophages and attempted to phagolysosomeMycobacteria have adapted to intracellular environment and aims to withstand phagolysosomal killing and escape to cytosol

251
Q

What does effective immunity to M. TB require

A

CD4 T-cells (this immune response is t cell and macrophage mediated)CD4 generate interferon gamma (IFN-y) - this helps activate intracellular killing by macrophages; and other cytokines like TNFa

252
Q

What does the granuloma consist of

A

Macrophages and Th1 lymphocytes capable of synthesysing IFN-y and other cytokines like TNF alpha

253
Q

What happens if TB granuloma works? What happens if it doesn’t work?

A

Mycobacteria shut down metabolically in order to survive - dormancyBut if fails, e.g. in the lung, this can result in the formation of a cavity full of live mycobacteria and eventual disseminated disease (can lead to abcesses eventually)

254
Q

What needs to be done first when trying to culture mycobacteria

A

Decontamination to kill off other rapid growing bacteria (lipid coat protects mycobacteria)

255
Q

What methods can be used to culture mycobacteria

A

Solid cultures- Egg based Lowenstein Jensen- Agar based Middlebrook 7H11- Take 2-8 weeksLiquid culture- Automated systems BACTEC- Mycobacterial growth indicator tube (MGIT).- Fluorometric detection in liquid media- Takes 1-3 weeks

256
Q

What allows more rapid diagnosis of mycobacteria

A

Nucleic acid detection (with PCR)(GeneXpert MTB/RIF cartridge based test)

257
Q

Name of Nucleic acid detection test used for mycobacteria

A

GeneXpert MTB/RIF cartridge based test(learn name, was highlighted by lecturer)

258
Q

What does the GeneXpert MTB/RIF cartridge based test do

A

Purifies and concentrates MTB, sonicates to release genomic material and then performs PCR Detects Rifampicin resistance using fluorescence

259
Q

How many bacilli/ml (minimum) can GeneXpert MTB/RIF cartridge based test for mycobacteria detect?

A

131 bacilli/ml

260
Q

How sensitive and specific is GeneXpert MTB/RIF cartridge based test for mycobacteria?

A

Sensitivity 88%, Specificity 98%(learn the sensitivity, it was highlighted by lecturer)

261
Q

Is M. TB fastidious?

A

yes

262
Q

When may nucleic acid detection of TB not pick up on TB

A

if TB is latent

263
Q

How can latent TB be recognised

A

Via tuberculin/Mantoux testBit of TB protein is injected into skin (intradermal)If previously infected TB memory cells will be present so skin will become inflamedSimilar test can be done with blood in solution

264
Q

What is the downside of tuberculin/Mantoux test

A

Can pick up on the person having had a TB vaccination (presence of antibodies doesn’t necessarily mean they were infected)

265
Q

How quickly is T cell response stimulated after exposure to M. TB

A

3-9 weeks

266
Q

Positive and negative effects of T cell response stimulation in TB

A

+ve effects; - macrophage killing of mycobacteria ,- containment of infection, - formation of tissue granulomata.-ve effects; - hypersensitivity reactions with skin lesions, - eye lesions - swelling of joints

267
Q

Standard drug therapy for TB

A

isoniazid (INH), rifampicin (RIF), pyrazinamide (PZA) and ethambutol (ETH) x 2 months followed by isoniazid and rifampicin for further 4 months

268
Q

Second line treatment for TB

A

Injectable agents (streptomycin, cycloserine, capreomycin)- Severe side effects, including liver damage

269
Q

How long does TB treatment take

A

4-9 months of combination therapy

270
Q

What are the resistance mechanisms of M. TB to drugs

A

Drug inactivation:- Mtb produces beta- lactamaseDrug titration:- Target overproductionAlteration of drug target:- Missense mutationsAltered cell envelope:- Increased permeability and drug efflux

271
Q

Multi-drug resistant TB: cause and characteristic

A

Resultant from inadequate TB therapy and failure to clear patients of bacteriaXDR-TB: resistant to four commonly used TB drugs. 6% of all TB cases

272
Q

Treating XDR-TB

A

Lengthy and expensiveBPaL regimen:- Bedaquiline - Pretomanid - Linezolid- All orally administered for 6 monthsBPaL can also fail with totally drug resistant TB- No known solution

273
Q

How do viruses cause disease

A
  • Direct destruction of host cells- Modification of host cell- “Over-reactivity” of immune system- Damage through cell proliferation- Evasion of host defences
274
Q

What is the leading cause of death world wide

A

Lower resp tract infection (e.g. can be caused by Respiratory Syncytial Virus)

275
Q

Importance of viral infections in the UK

A
  • Outbreaks (e.g. Influenza, Measles, Mumps, Norovirus)- Cancer (e.g. EBV and lymphoma, Hep B/C and hepatocellular carcinoma, HPV and cervical/anal cancer, HIV and many resulting infections)- Immunosuppressed patients (Reactivation of latent viruses)- Miscarriage and birth defects (e.g. CMV, VZV, HSV, Rubella)- Morbidity and mortality (Psychological and physical)
276
Q

Which viruses can lie latent and reactivate upon immunosuppression

A

All herpes class viruses:- EBV,- CMV,- human herpesvirus 6 (HHV6),- human herpesvirus 7 (HHV7),- JC virus (human polyomavirus 2),- BK virus (human polyomavirus 1

277
Q

Which viruses are herpes class

A
  • Herpes simplex virus 1 - Herpes simplex virus 2- Varicella-zoster virus- Cytomegalovirus- Epstein-Barr virus- Human Herpesvirus 6 (varients A and B)- Human Herpesvirus 7- Kaposi’s sarcoma virus AKA human herpesvirus 8
278
Q

What is a virus?

A

An infectious, obligate intracellular parasite comprising genetic material (DNA or RNA) surrounded by a protein coat and/or a membraneAll also have a receptor binding protein to “dock” to cells

279
Q

Range of sizes of human viruses

A

20 to 260nm in diameterPoxviruses are some of the biggestParvovirus is the smallest

280
Q

Viruses vs Bacteria

A
  • Bacteria have cell wall, viruses don’t- Bacteria have organelles, viruses don’t- Bacteria have DNA and RNA, viruses only have DNA or RNA- Viruses are always dependant on a host cell, bacteria are not- Bacteria are living organisms, viruses are typically considered not living
281
Q

Are DNA or RNA viruses typically hardier

A

DNA viruses

282
Q

What are virions

A

The complete, infective form of a virus outside a host cell consisting of genetic material (DNA or RNA) and a protein coat/capsid

283
Q

Different shapes of viruses

A
  • Helical (spiral shaped genetic material)- Icosahedral (cubic? Looks like those regular 3D shapes they make with paper for maths class)- Complex (e.g. bacteriophage looks like a weird spider creature)
284
Q

Different types of viral external structure

A
  • Non-enveloped (e.g. adenovirus, parvovirus)- Enveloped (e.g. Influenza, HIV)
285
Q

What would you examine when detecting a new virus

A

Genetic sequence

286
Q

Stages of viral replication

A
  1. ATTACHMENT to specific receptor2. CELL ENTRY3. HOST CELL INTERACTION and REPLICATION4. ASSEMBLY OF VIRION5. RELEASE OF NEW VIRUS PARTICLES
287
Q

What does the attachment receptor of a virus dictate

A

Dictates the type of cells the virus can infect- E.g. gp120 receptor on HIV allows it to attach to CD4 cells with CCR5 or CXCR4 chemokine receptors as coreceptors

288
Q

What happens during cell entry by a virus

A

Virion is uncoated within the cellOnly central viral “core” (nucleic acid and some associated proteins) is used for replication

289
Q

What happens during host cell interaction and replication of a virus

A
  • Viral genome migrates to cell nucleus- Viral genome is transcribed to mRNA using host material (enzymes, amino acids, nucleotides)- Subverts host cell defence mechanism (as it is using own resources)
290
Q

What does translation of viral mRNA produce

A
  • Structural proteins- Viral genome- Non-structural proteins e.g. enzymes
291
Q

Where can assembly of virion occur within host cell

A
  • Nucleus (e.g. like herpes viruses)- Cytoplasm (e.g. like poliovirus)- At cell membrane (e.g. influenza virus)
292
Q

How can new virus particles be released from host cell?

A
  • Particles can burst out causing cell death e.g. like rhinovirus- Particles can bud off/exocytose, taking some of cell membrane with it e.g. HIV, Influenza
293
Q

Example of direct destruction of host cells by a virus

A

Poliovirus - causes host cell lysis and death after viral replication period of 4 hoursAs polio affects neurons - this neuronal lysis/death leads to paralysis

294
Q

Example of virus causing disease by modification of host cell

A

Rotavirus - atrophies villi and flattens epithelial cells- Decreases small intestine SA- Nutrients including sugar not absorbed- Hyperosmotic state- Profuse diarrhoea

295
Q

Example of a virus causing disease via “over-reactivity” of immune system

A

Hep B- Causes hepatocytes to be attacked by cytotoxic T lymphocytesResults in: - Jaundice- Pale stool- Dark urine- RUQ (right upper quadrant abdominal) pain- Fever and malaise- Itching (from release of bile salts)When Hep B is chronic the sustained viral replication and hepatocyte destruction occurs at a lower level so has fewer clinical symptoms(also SARS-Cov-2)

296
Q

Example of virus causing damage through cell proliferation

A

HPV causes cervical cancer- After acquisition through direct contact there is partial viral replication and expression of some HPV proteins- Viral DNA is integrated into host chromosome- This leads to continuous expression of oncoproteins causing cellular DNA mutations- And so we get dysplasia and neoplasia

297
Q

Example of virus causing damage through evasion of host defences

A

At a cellular level:- Latency e.g. herpesviridae- Cell-cell spread e.g. measles, HIVAt molecular level- Antigenic variability e.g. Influenza, HIV, rhinovirus- Prevention of host cell apoptosis e.g. herpesviridae- Downregulation of interferon and other intracellular host defence proteins (many viruses do this)- Interference with host cell antigen processing pathways e.g. herpesviridae, measles, HIV

298
Q

Where does each of the main herpes viruses lie dormant

A
  • HSV 1 and 2 and VZV lie latent in Nerve root ganglion- EBV and HHV-8 (AKA Kaposi sarcoma virus) - Lymphoid cells- HHV-6, HHV-7, CMV - lie latent in Myeloid cells
299
Q

What are the advantages of direct cell-cell spread

A
  • Avoids random release into environment- Increased speed of spread within tissues- Avoiding immune system
300
Q

What is antigenic variability

A

Ability to change surface antigens to evade host immune systemThrough mutations during replication

301
Q

How does prevention of host cell apoptosis by virus cause damage

A

Prevention of host cell apoptosis allows the virus to continue replicating within it, so more virus is produced and then released. It also has an essential role into how some viruses are oncogenic

302
Q

How does downregulation of interferon and other intracellular host defence proteins by viruses cause damage

A
  • Normally interferon is synthesised and allows messaging to other cells to activate their antiviral state - When interferon synthesis is blocked, it leaves the neighbouring cells susceptible to infection
303
Q

How can viruses interfere with host cell antigen processing pathways

A

Can down regulate MHC class 1 so the viral antigen is not identified quickly by immune system

304
Q

Why can viruses vary in the range of clinical syndromes they cause

A
  • They can infect different host cells and tissues- They have different methods of interaction with the host cell
305
Q

What symptoms can they cause: Herpes simplex virus vs JC virus

A

HSVSkin: - Orofacial herpes- Genital herpes- Herpetic whitlow- Erythema multiforme- Herpes gladiatorumVisceral:- Oesophagitis- Pneumonitis- HepatitisCNS: - Meningitis- Encephalitis- Transverse myelitisEye: - Conjunctivitis- KeratitisJC virus:CNS - Progressive multifocal leukoencephalopathy

306
Q

Which viruses can cause common cold

A
  • Rhinovirus- Parainfluenza virus- Respiratory syncytial virus
307
Q

Which viruses can cause eye infections

A
  • Herpes Simplex- Adenovirus- CMV
308
Q

Which viruses can cause Encephalitis/meningitis

A
  • JC virus- Measles- LCM virus- Arbovirus- Rabies
309
Q

Which viruses can cause pharyngitis

A
  • Adenovirus- EBV- CMV
310
Q

Which viruses can cause gastroenteritis

A
  • Adenovirus- Rotavirus- Norovirus- Astrovirus- Coronavirus
311
Q

Which viruses can cause skin infections

A
  • VZV- HHV-6- Smallpox- Molluscum contagiosum- HPV- Parvovirus B19- Rubella- Measles- Coxsackie A virus
312
Q

Which viruses cause sexually transmitted diseases

A

Herpes simplex type 2HPVHIV

313
Q

Which viruses can cause gingivostomatitis

A

Herpes simplex type 1Gingivostomatitis = Infection of mouth and gums that leads to swelling and sores

314
Q

Which viruses can cause pneumonia

A

Influenza virus type A and BParainfluenza virusResp syncytial virusAdenovirusSARS coronavirus

315
Q

Which viruses can cause Myelitis

A

Poliovirus(HTLV-I)

316
Q

Which viruses cause pancreatitis

A

Coxsackie B virus

317
Q

Which virus can cause cardiovascular infection

A

Coxsackie B virus

318
Q

What are the diagnostic tests for detecting viruses

A
  • PCR (detects presence of genetic material and the initial size of viral load - doesn’t work for novel viruses)- Serology (Checks for viral exposure. Is there immune memory to the virus)- Histology (any features of viral infection present?)- Viewing a viral culture through light microscopy (structure of infected cells visibly changes) - Limited clinical use- Electron microscopy - Limited clinical use * Too much time/effort, too expensive
319
Q

Key points about viruses

A
  • Viruses are a COMMON AND SIGNIFICANT cause of human disease globally and nationally (in UK)- Viruses are very SMALL and consist of GENETIC MATERIAL surrounded by a PROTEIN COAT- A virus is COMPLETELY DEPENDANT on host cell machinery to replicate- Recognising how viruses cause disease allows us to: - Understand transmission and natural history - Know who is most at risk - Develop treatments and “preventative” drugs- Viruses vary wildly in range of clinical syndromes they can cause (infect diff cells/tissues AND diff methods of interaction with host)
320
Q

What does the Varicella Zoster Virus cause

A

Varicella “chickenpox” - primary infectionHerpes zoster (HZ) “Shingles” - secondary reactivation* Very infectious

321
Q

What does a VZV particle consist of

A
  • Double strand DNA genome- Nucleocapsid- Tegument (cluster of proteins lining space between envelope and neucleocapsid)- Lipid envelope- Glycoprotein spikes
322
Q

Infection timeline of VZV

A
  • VZV enters body- Incubation period (1-3 weeks)- Rash- High infectivity period occurs 1-2 days before rash appears to when the blisters have crusted over
323
Q

When is chickenpox most infectious

A

1-2 days before rash appears to when the blisters have crusted over

324
Q

Where does VZV replicate in body

A

Nasopharynx - present in nasal secretions

325
Q

How can VZV be transmitted

A
  • Nasal secretions e.g. sneezing- Contact with vesicular matter
326
Q

Epidemiology of chickenpox

A
  • Common in childhood- Highly contagious, (90% in household hit rate)- Usually benign but can be serious in certain groups 90% of adults raised in the UK have had chickenpox
327
Q

Risk groups for chickenpox

A
  • Immunocompromised and patients who have had transplants - Adults- Pregnant women- Smokers- Infants
328
Q

Socioeconomic issue of endemic/chronic illnesses

A

Lots of lost school days and sick days from workDecrease productivity

329
Q

Progressive stages of chickenpox blister

A
  • Macule - red spot, not prominently raised- Papule - slight raised bump- Vesicle - small blisters- Pustule - pus-filled, white blisters- Crust - rougher, scabbing
330
Q

Distribution of chickenpox rash

A
  • More central - rash forms in warmer areas so sparser on extremities- Lesions at different stages of progression can appear on body
331
Q

Characteristics of smallpox rash

A
  • Centrifugal distribution - more appears on face and extremities (away from centre)- All lesions evolve at same time (so all at same stage of progression)- Deeper lesions, affecting deeper layers of skin - some have central umbilication (dip in middle
332
Q

What is something that is pathognomonic to chickenpox

A

Cropping - having lesions at different stages but in the same area of body

333
Q

Diagnosis of chickenpox

A
  • Pop lesion with sterile needle- (DON’T wipe with alcohol swab first - can denature virus)- Absorb vesicle contents onto swab- Replace swab in cassette and send for VZV/HSV PCR
334
Q

Complications of chickenpox

A
  • Dehydration- Haemorrhagic change to the rash- Cerebellar ataxia (common) - unsteady gait- Encephalitis - confused, diorientated, loss of motor function, possible sizure- Varicella pneumonia- Bacterial empyema (pockets of pus collected inside body cavity - esp pleural space)- Skin and soft tissue infection typically with group A strep- Bone and joint infections: deep sepsis-osteomyelitis/pyomyositis- Congenital (foetal) varicella syndromeRARE in children - MORE COMMON in adults
335
Q

What is the most common complication of chickenpox in adults

A

Chickenpox pneumonitisAffects 15% of healthy adults30% risk in lung disease/smoker30% mortality untreated6% mortality even with treatment

336
Q

Treatment for Varicella pneumonitis

A
  • Antiviral - Acyclovere (10mg per kg, 3 times a day - IV*) * doesn’t work well orally- Valacyclovere (valine sidechain) when getting better (can be taken orally)
337
Q

How common is foetal infection of VZV in pregnancy

A

10-15%~2% develop FOETAL VARICELLA SYNDROME (FVS) when mother contracts chickenpox in FIRST HALF of pregnancy (v rare)

338
Q

Characteristics of foetal infection of chickenpox

A
  • Usually transient (only lasts short amount of time) and asymptomatic- If any manifestations - usually shingles in first year of life
339
Q

Potentially severe defects that can occur as complications of FVS

A
  • Cicatricial skin scarring (scarring from formation + contraction of fibrous tissue in wound)- Limb hypoplasia (poorly developed limbs)- Visceral/ocular lesions- Microcephaly (small head) and growth retardation
340
Q

How are serum samples collected

A
  • Blood sample taken- Tube contains gel to separate cells from serum once centrifuged- Small sarstedt (name of brand) tubes kept for around 3 years (archive samples)
341
Q

When are initial serum samples taken in pregancy

A

~10-12 weeks pregnant

342
Q

Why are archived serum samples useful

A

Can compare archived serum sample when taking sample later to check for stuff

343
Q

How does shingles reactivate as a unilateral rash

A
  • First - primary infection of widespread chickenpox- VZV goes dormant in dorsal root (or cerebral) ganglion- Localised reactivation - singles (only affects that dermatome unilaterally as virus can’t cross over midline to other side of spine)
344
Q

What type of viruses is dormancy and reactivation more common in

A

DNA viruses

345
Q

Characteristic onset of shingles

A

Most common in elderlyCan go from no rash to horrible rash in day or so

346
Q

Pain relief for shingles rash

A
  • Regular analgesia doesn’t work properly - Have to use drugs that dampen nerve tips (normally used for epilepsy)- E.g. Gabapentine
347
Q

Sites of shingles reactivation

A
  • Thoracic region (50-70% of all cases)- Cervical, lumbar and sacral - less frequent- Ophthalmic (10-20%) - affecting ophthalmic division of trigeminal nerve - particularly problematic as shingles can affect every layer of eye + cause vision problems
348
Q

Long term complication of shingles (even after the infection is resolved)

A

Post-herpetic neuraligia- Nerve endings stay irritated for 2 years or so after the rash is gone

349
Q

What is the Hutchinson sign and what does it indicate

A

A lesion on the tip of the nose- Indicates the shingles probably has corneal involvement

350
Q

Complications/signs of shingles becoming complicated

A
  • Dissemination- Haemorrhagic change- Shingles in peripheral dermatomes - means immune system isn’t controlling things wellIn Immunocompromised - can get SECONDARY infection (e.g. bacterial)
351
Q

Complications of herpes virus in people with atopic dermatitis/eczema

A

Eczema herpeticum- Rash looks like it’s never quite come under control- Seems like a combination of herpes virus and rapidly worsening eczema

352
Q

What do enteroviruses cause

A

Hand foot and mouth disease- Shed enteroviruses in stool

353
Q

What pathologies cause rash on palms and soles of feet

A
  • Enteroviruses (hand, foot, mouth disese)- Secondary syphilis (bacterial)- Part of an immune response to drugs - toxic erythema (erythema is just like bruising)
354
Q

What does Parvovirus B19 target and basic method of action for how they do this

A

Immature red cells- They attach to P antigens displayed by immature red cells which prevents normal maturation

355
Q

Complications of parvovirus B19

A

Profound anaemia - blood cells not replaced as older cells die* Better prognosis in childrenComplications in pregnant women:- Hydrops fetalis - severe swelling in foetus

356
Q

Treatment for hydrops fetalis

A

Can give trans umbilical transfusion to increase chance of survival till birth - then supportive measures e.g. assited breathing, removal of excess fluid via needle- Intervention only works in early stages

357
Q

How do you test for hydrops fetalis

A

Middle cerebral artery dopplers (detects resistance of flow in foetal brain circulation)

358
Q

Characteristics of parvovirus B19 rash

A
  • Reticular rash (net-like pattern) - Flares up in higher temperatures e.g. in hot bath
359
Q

What rash does HHV-6 cause

A

Roseola - larger, more spread-out patches of slightly raised, darker skin

360
Q

Characteristics of HSV rashes

A
  • Vesicular rashes - Lesion on vermillion border of lip - common sight of herpes rash - Rashes below belt as well
361
Q

Typical locations of HSV1 and HSV2 rashes

A
  • HSV1 - both above and below belt- HSV2 - typically only below belt
362
Q

Complications of HSV in immunosuppressed patients

A

Mucositis- Sore areas in mouth - mucosal epithelium is shedBugs can target these shed areas - secondary infectionsE.g. candida plaques

363
Q

Name a common pox virus, especially in children

A

Moluscum contagiosum- CAN ALSO BE BE SEXUALLY TRANSMITED (in genital areas)

364
Q

How can moluscum contagiosum be treated

A
  • Pop vesicle and remove white centre- However, if too rough, can cause further skin damage and it can come back
365
Q

Which part of moluscum contagiosum often reactivates in immunosuppressed people

A

Lesions around eyes

366
Q

Which age group is primary cytomegalovirus infection most common in

A

Teens and 20s

367
Q

Diagnostic appearance of Primary CMV

A

Macular rashLymphadenopathy- Atypical lymphocytes (sticky, destructive, spread out)

368
Q

Complications of CMV reactivation

A
  • Retinitis - pizza pan retina - sight threatening- CMV pneumonitis (most viral pneumonitis look very similar/same) - dangerous- Colitis with CMV on top
369
Q

Histological hallmark of CMV

A

Owl’s eye intranuclear inclusions- NORMALLY TREATED WITH PCR tho

370
Q

How is CMV treated

A

IV ganciclovir- Or Valganciclovir can be orally taken in less severe case (val is just valine group which allows oral consumption)

371
Q

What does measles cause

A
  • Cough, coriza (runny nose), conjunctivitis, diarreah- Maculopapular rash (dry feel)- Salt grain-like lesions in mouth- Febrility- Otitis media (can cause hearing loss in severe cases)- Potential pneumonia- Potential encephalitis
372
Q

What do the local health protection unit control

A

Cough, coriza, conjunctivitis, diarreah, immune control

373
Q

How transmissible is measles

A

R0 = 16 (very high)100 in unvaccinated population

374
Q

Characteristic skin presentation of Dengue shock syndrome

A

Significant bruises/swelling from internal bleeding

375
Q

Which gram +ve bacteria can cause cellulitis

A

S. aureus and Group A (pyogenes), C, G strep

376
Q

Which gram +ve bacteria can cause pharyngitis/strep throat

A

Group A, C, G strep

377
Q

Define protozoa

A

Single cell with nucleus - is eukaryotic>30, 000 specieses

378
Q

What are the 5 major groups of protozoa

A

FlagellateAmoebaSporozoaMicrosporidiaCiliate

379
Q

List main flagellate protozoa

A
  • Trypanosoma brucei gambiense (African trypanosomiasis - sleeping sickness)- Trypanosoma brucei rhodesiense (African trypanosomiasis - sleeping sickness)- Trypanosoma cruzi (American Trypanosomiasis - Chagas Disease)- Leishmania spp. (Leishmaniasis)- Trichomonas vaginalis (Trichomoniasis - STI)- Giardia lamblia (Giardiasis)
380
Q

Which protozoa cause African trypanosomiasis?

A
  • Trypanosoma brucei gambiense- Trypanosoma brucei rhodesiense(Batman puts you to sleep by stabbing with a needle in gambia or rhodes)
381
Q

Which organism transmits African trypanosomiasis

A

Tsetse fly (via bite)

382
Q

What does African trypanosomiasis cause

A
  • Chancre- Flu like symptoms- CNS involvement (sleepy, confusion, personality change)- Coma and Death
383
Q

How is African Trypanosomiasis diagnosed

A

Via blood film or CSF

384
Q

Which protazoa causes American trypanosomiasis (Chagas disease)

A

Trypanosoma cruzi(Jesus got nailed to a cross - people felt ill)

385
Q

How is american trypanosomiasis spread

A
  • Through contact with faeces of triatomine “kissing” bug (found around/in mud huts in South America)- Through blood- Vertically acquired- Eating contaminated food
386
Q

Symptoms of American Trypanosomiasis (Chagas disease)

A

Acute:- Flu like symptoms- Lymphadanopathy - (Romaña sign - swollen eyelid - if faeces rubbed into eye)- (Chaga means fester/disease in Portuguese)Chronic:- Cardiomyopathy (harder to pump - walls of heart: stretched, thickened or stiff)- Megaesophagus (oesophagus dilates and loses motility)- Megacolon (dilation)

387
Q

How is Chagas disease diagnosed

A
  • By visualising trypomastigotes (the type of flagellate protozoa that causes Chagas) on blood film- OR amastigotes (the protozoa have no visible flagellum!) on biopsy (for CHRONIC)Remember as: they need flagella (masti) to move around if only temporary (i.e. acute) but Chagas requires maturity in life which causes you to keep most of your potential inside so trypomastigote not promastigote. When it is chronic the -mastigotes get comfortable and stop moving around (thus no VISIBLE flagella - promastigote)
388
Q

Important types of trypanosomatida

A
  • Amastigote - no visible flagella (but potential for flagella still there)- Promastigote - anterior flagella (cell itself looks like cover of edamame beans/pea pod) with flagellum STICKING MOSTLY out of the cell- Trypomastigote - Still bean pod looking cell with anterior flagella but most of the flagellum is now INSIDE the cell but at the edge i.e ATTACHED PARALLELY TO CELL MEMBRANE
389
Q

Can Chagas disease be treated

A

Can be treated effectively if acuteCANNOT effectively treat once chronic - can only provide supportive treatments e.g. pacemaker, antiarrhythmias etc.

390
Q

Which organisms cause Leishmaniasis

A

Leishmania! Spp. (means specieses - >20 affect humans) - protazoa(Lesion mania - in the sand)

391
Q

How is leishmaniasis spread?

A

Via bite of sand fly

392
Q

How is Leishmaniasis diagnosed

A
  • Via biopsy (can see amastigotes)- Via serology combined with clinical signs- Can be diagnosed with PCR
393
Q

What are the 3 clinical pictures of Leishman

A
  • Cutaneous- Mucocutaneous- Visceral(baso increasing severity from superficial to deep - also gets more virulent with increasing severity)
394
Q

What does cutaneous Leishmaniasis cause

A

Most commonUlcers on exposed body parts e.g. face, arms, legsMay be large number of lesions (can be up to 200 - can cause serious disability)Risk of superadded infectionsCauses scarring -> social prejudice (thus better to get bitten in less exposed areas)

395
Q

What does mucocutaneous Leishmaniasis cause

A

Partial/total destruction of mucous membranes of:- Nose- Mouth- Throat cavities- And tissues surrounding these sitesSocial stigma and rejection!Increased risk of recurrent bacterial pneumonia (people can subsequently die of sepsis) due to destruction of nose/palate

396
Q

What does Visceral Leishmaniasis cause

A

Affects lymph system so:- Irregular bouts of fever- Weight loss- Massive splenomegaly- Hepatomegally- Anaemia (secondary)- High fatality if untreated (100% within 2 years)

397
Q

Which organism causes trichomoniasis

A

Trichomonas vaginalis - protozoaSTI ENDEMIC TO UK

398
Q

Trichomoniasis signs/symptoms

A
  • Often asymptomatic- Dysuria- Yellow, frothy discharge
399
Q

How can Trichomoniasis be treated

A

With metronidazole - antibiotic

400
Q

What organism causes Giardiasis + type of spread

A

Giardia lambliaFaeco-oral spread esp linked to contaminated water

401
Q

Giardiasis signs/symps

A

DIarrhoeaKEY FEATURES: Cramps, bloating, flatulenceCan become lactose intolerant after infection

402
Q

Where is giardiasis more likely to occur

A

In a traveller In childcare settings e.g. nurseriesThese are KEY FEATURES

403
Q

How can giardiasis be diagnosed

A

Trophozoites (active - jellyfish with face)/cysts (inactive - round, thick wall) seen in stoolIdentifying clinical features

404
Q

How is giardiasis treated

A

Metronidazole - antibiotic

405
Q

What is the name of the main medically relevant amoeba? What disease does it cause? + spread

A

Entaemoeba histolytica (Amoeba that affects gut and destroys cells)Causes Amoebiasis (Amoebic dysentry! Bloody diarrhoea!)FAECO-ORAL SPREAD

406
Q

What does amoebiasis cause?

A

IMPORTANT:- Dysentry- Colitis- Liver and lung abscesses- Can live in gut asymptomatically

407
Q

How do amoeba move

A

They use pseudopoda - temporary projections of the cell - kinda just reach out with protrusions and squirm along like macrophages

408
Q

Why do entamoeba histolytica cause intestinal issues

A

The amoeba invades colon and consumes RBCs

409
Q

Risk factors for Amoebiasis

A
  • Poor sanitary conditions/tropical countries- MSM (men who have sex with men)
410
Q

How can amoebiasis be diagnosed

A

Trophozoites/cysts seen in stool

411
Q

How is amoebiasis treated

A

METRONIDAZOLE

412
Q

Name the main sporozoa

A
  • Cryptosporidium spp (Spore-like protozoa that affects crypts in intestine)- Toxoplasma gondii (remember as Toxic in plasma?)- Plasmodium spp (need to learn individual spp. - related to blood plasma)
413
Q

What disease does Cryptosporidium spp cause? Which species in particular are relevant in humans

A

Cryptosporidiosis (diarrhoeal)- C. Hominis and C. parvum (Homo species affecting and ‘small’ respectively)

414
Q

What are the symptoms of Cryptosporidiosis

A
  • DIARRHOEA (watery but no blood)- Vomiting- Fever- Weight loss- Usually self-limiting but can be fatal in - immunocompromised
415
Q

How can cryptosporidiosis be diagnosed

A

Acid fast oocysts seen in stool

416
Q

How is Cryptosporidiosis spread

A

Waterborne (e.g. Fresh water swimming)

417
Q

How long does cryptosporidiosis last in healthy individuals

A

Usually 1-2 weeks

418
Q

What is cryptosporidiosis treated with in more severe cases

A

Nitazoxanide - antimicrobial

419
Q

What organism causes Toxoplasmosis?

A

Toxoplasma gondii (toxic plasma gon’ die?)

420
Q

How is Toxoplasmosis acquired?

A
  • Ingestion of food contaminated with bradyzoits (tissue cysts) - e.g. rare beef/lamb, shellfish, unpasturised goats milk- Ingestion of oocysts via contact with FELINE faeces
421
Q

Toxoplasma gondii - what are their definitive hosts and intermediate hosts

A
  • Only cats are definitive hosts (full cycle occurs, ingestion to excretion)- Other mammals including humans are intermediate hosts (parasite can be ingested but it becomes a tissue cyst so isn’t excreted)
422
Q

What occurs when toxoplasma gondii oocysts/bradyzoites are ingested

A
  • Haematogenous spread- Invasion of tissues- Tissue cysts develop, primarily in muscles and neurons
423
Q

What can toxoplasmosis cause in immunocompromised

A
  • Disseminated disease - Toxoplasma Encephalitis (inflammation of brain)- Chorioretinitis (inflammation of choroid lining of retina)- Can have devastating consequences in pregnancy: - Worst in first trimester - Causes congenital toxoplasmosis - Microcephaly - Hydrocephalus - Interuterine growth retardation - Miscarriage - Can be treated if picked up early enough - Counselling for termination may be offered
424
Q

Presentation of acute toxoplasmosis in healthy individual

A
  • 90% often asymptomatic- 10% - glandular fever type illness
425
Q

Which organism causes Malaria?

A

Plasmodium spp - sporazoa protozoa- Plasmodium falciparum (most SEVERE, high mortality if untreated - through blood plasma - falciparum = small scythe)- Plasmodium ovale- Plasmodium vivax- Plasmodium malariae- Plasmodium knowlesi

426
Q

Incubation period for common malaria causing sporozoa

A
  • Plasmodium falciparum - typically a month- Plasmodium ovale and vivax - up to a year
427
Q

Which organism transmits malaria

A

Female Anopheles mosquito

428
Q

How is malaria diagnosed?

A
  • Light microscopy of blood film - will contain trophozoite- Thick and thin film done- Three blood films done on consecutive days (length of lifecycle)- First smear probs +ve in 95% of cases- Can also used rapid diagnostic tests that detect plasmodium antigens in blood
429
Q

Thick vs. thin blood films

A
  • Thick film is sensitive but low res (e.g. for deciding if person has malaria or not)- Thin film higher res so can identify different species AND is used to work out parasitaemia percentage
430
Q

Symptoms of malaria

A
  • FEVER!!- Chills- Headache- Myalgia- Fatigue- Diarrhoea- Vomiting- Abdo painCan be variable in diff people but fever is most common
431
Q

Malaria signs

A
  • Anaemia- Jaundice- Hepatosplenomegaly- ‘Black water fever’ (haemoglobinuria) - from haemolysis products in urineSome people may not LOOK ill
432
Q

Who are most at risk of getting the most unwell from malaria

A

Travellers and pregnant women

433
Q

Life cycle of malaria

A
  • Mosquito ingests plasmodium gametocytes from biting infected human (is infected for rest of its 4 week lifespan)- Gametocytes develop in mosquito midgut and end as sporozoites in salivary glands - MOSQUITO BITES next human and injects sporozoites- Sporozoites now in human blood infect HEPATOCYTES - Infected hepatocytes develop into SCHIZONTS, which burst and infect RBCs causing ABDO PAIN- Plasmodium becomes trophozoite within RBC- Trophozoite develops into schizont which ruptures and re-infects more RBCs (causes CYCLICAL FEVER)- Causes HAEMOLYSIS so ANAEMIA and JAUNDICE (from BILIRUBINEMIA) and HAEMOGLOBINURIA- Blood stage usually lasts 48 hours- Some trophozoites develop into gametocytes which are taken up by another mosquito!
434
Q

What additional ability makes Plasmodium falciparum infection more severe + it’s complications

A
  • Causes OBSTRUCTED MICROCIRCULATION (typically in big organs) - Mostly due to PROINFLAMMATORY CYTOKINE CASCADE - stimulates endothelial activation which causes rolling of RBCs and endothelial cytoadherence - Also causes ROSETTING - clumping together of RBCs and plateletsResults in “Complicated Malaria”- Cerebral malaria, - ARDS, - Renalfailure- Bleeding/Anaemia- Sepsis/Shock- Possibly other organ failure including heart - esp because of anaemia -> anaerobic -> LACTIC ACIDOSIS + HYPOGLYCAEMIA (reduced gluconeogenesis from liver damage + parasite uses up glucose)
435
Q

Causes and signs/symptoms of Cerebral malaria

A

VASCULAR OCCLUSION causes:- DROWSINESS- RAISED INTRACRANIAL PRESSURE- SEIZURES- COMA -> deathDrowsiness can also be due to hypoglycaemia so check that too

436
Q

Causes and signs/symptoms of Acute Respiratory Distress Syndrome (ARDS!) due to complicated malaria

A

Direct effect of VASCULAR OCCLUSION:- Compensatory TACHYPNOEA due to ANAEMIA and LACTIC ACIDOSIS- INCREASED VASCULAR PERMEABILITY causing PULMONARY OEDEMA- All contribute to SOB and HYPOXIA

437
Q

Causes and signs/symptoms of Renal failure in complicated malaria

A

Directly due to VASCULAR OCCLUSION- Secondary HYPOPERFUSION due to DEHYDRATION from fever (which causes HYPOTENSION)- HAEMOLYSIS products can be NEPHROTOXICSubsequently:- PROTEINURIA- FATIGUE- HAEMATURIA

438
Q

Causes of Bleeding in complicated malaria

A
  • Platelet aggregation occurs which causes THROMBOCYTOPENIA- Generalised inflammation -> activation of coagulation cascade -> clotting factors used up -> DISSEMINATED INTRAVASCULAR COAGULATION (DIC) -> micro clots in blood and abnormal bleeding e.g. ABNORMAL EPISTAXIS (nose bleed)Worsening anaemia also contributes
439
Q

Causes of Shock in complicated Malaria

A
  • PRO-INFLAMMATORY CASCADE occurs which causes VASODILATION- SEVERE ANAEMIA can cause CARDIOGENIC SHOCK- INCREASED VASC PERMEABILITY in the bowel can allow gram -ve bacteria from bowel into bloodstream -> causes GRAM -VE SEPSIS- Increased vascular permeability can also cause intravascular fluid leakage into “3rd space”- BLEEDING can cause HYPOVOLEMIA
440
Q

Signs and symptoms of shock

A
  • HYPOTENSION- TACHYCARDIA- DROWSY- PALE
441
Q

Treatment for Complicated malaria?

A

IV ARTESUNATE (combination of quinine and doxycycline)

442
Q

Supportive measures for the extra complications of Complicated malaria

A
  • Cerebral: antiepileptics- ARDS: oxygen, diuretics, ventilation- Renal failure: fluids, dialysis- Sepsis: broad spectrum antibiotics- Bleeding/Anaemia: blood products- Exchange transfusion if huge parasite burden
443
Q

How can relapses of malaria occur

A

P. ovale and vivex can form HYPNOZOITES in liver which can reactivate up to years later

444
Q

What additional treatment is given to eliminate hypnozoites after p. ovale/vivex infection

A
  • PRIMAQUINE - CONTRAINDICTED in G6PD (glucose-6-phosphate dehydrogenase) DEFICIENCY - can cause HAEMOLYSIS
445
Q

Example of drug to treat acute malaria (uncomplicated)

A

Chloroquine

446
Q

When should you consider a possibility of malaria?

A

FEVER + RECENT TRAVEL

447
Q

What is the key principle of antibiotics

A

Only use antibiotics if they are actually needed

448
Q

What is an antibiotic

A
  • Agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high dilution- Work by binding to a target site on a microorganism- Most agents used now are semi-synthetic derivatives of antibiotics so the more correct term is antimicrobials
449
Q

Define target site (on a bacterium)

A

Points of biochemical reaction crucial to the survival of the bacterium

450
Q

Where can antibiotics bind to bacteria and what defines where they bind

A
  • Crucial binding site varies with the ANTIBIOTIC CLASS- Some bind to ribosomes (affects protein synthesis)- Some bind to DNA or associated components (affects nucleic acid synthesis)- Some bind to cell wall (affect cell wall synthesis)
451
Q

Which classes of antibiotics affect cell wall synthesis

A

Beta lactams (contains beta lactam rings)- Penicillins- Cephalosporins- Carbapenems- MonobactamsGlycopeptides

452
Q

Name the important penicillins

A
  • Penicillin V- Penicillin G (Benzylpenicillin)- Flucloxacillin- Amoxicillin/Ampicillin- Piperacillin
453
Q

Name the important Cephalosporins

A
  • Cefuroxime- Cefotaxime- Ceftriaxone- (Cefalexin)- (Ceftazidime
454
Q

Name the important carbapenams

A
  • Meropenem- (Ertapenem)- (Imipenem)
455
Q

Name a relevant Monobactam

A

Aztreonam

456
Q

Name some important glycopeptides

A

VancomycinTeicoplanin

457
Q

Which type of bacteria are more susceptible to beta lactams and glycopeptides

A

Beta lactams and glyopeptides work best on gram +ve as they have big cell wall

458
Q

Mechanism of action of beta lactams

A
  • Bind covalently (and thus irreversibly) to PENICILIN BINDING PROTEINS- Cell wall synthesis (specifically peptidoglycan production) is disrupted - lysis occurs- Results in HYPO-OSMOTIC or ISO-OSMOTIC environment (fluid moves into cell and causes it to burst)- Only active against rapidly multiplying organisms
459
Q

Why are gram -ve bacteria less susceptible to beta-lactams

A
  • Beta-lactams have to diffuse through the bacterial cell wall first to bind to the PBPs- Gram negative organism have additional LPS layer that decreases antibiotic penetration
460
Q

What causes the differences in the spectrum and activity of beta-lactam antibiotics

A

It is due to their relative affinity for different PBPs

461
Q

Which antibiotics affect nucleic acid synthesis/DNA functioning

A
  • Rifampicin - METRONIDAZOLE- Fluoroquinolones (acts on DNA gyrase (and topoisomerase IV)) - CIRPROFLUXACIN - Levofluxacin - Moxifloxacin
462
Q

Which antibiotics affect protein synthesis (at ribosomes)

A
  • Aminoglycosides (30s subunit)- Tetracyclines (works on 30s subunit)- Lincosamides (50s subunit)- Macrolides- Chloramphenicol
463
Q

What is the main aminoglycoside

A

GENTAMICIN- used for lots of different serious bacterial infections

464
Q

What is the main tetracycline

A

DOXYCLINE (also an antiprotozoal - used against malaria)- commonly used for chlamydia

465
Q

What is the main Lincosamides

A

CLINDAMYCIN - commonly used for patients allergic to penicillin

466
Q

What are the main Macrolides and what are they used for

A

ErythromycinCLARITHROMYCIN (also used for H. pylori infections)Azithromycin (also used for chlamydia)- commonly used for resp. And throat infections- also in uncomplicated skin infections and otitis media in paediatrics

467
Q

Which antibiotics affect Folate synthesis

A
  • Sulphonamides (e.g. sulphamethoxazole)- TRIMETHOPRIM - Commonly used for UTIs- CO-TRIMOXAZOLE (combination of sulphamethoxazole and trimethoprim)
468
Q

What are bactericidal antibiotics

A

Agent that KILLS BACTERIA by INHIBITING CELL WALL SYNTHESISKill >99.9% in 18-24 hours

469
Q

What are bactericidal antibiotics useful for

A
  • In infections where penetration to site of bacterial growth is poor (e.g. endocarditis)- In difficult to treat infections (e.g. in immunosuppressed patients)- Or infections that need to be eradicated quickly (e.g. meningitis and encephalitis, sepsis)
470
Q

Why does endocarditis require bactericidal antibiotics

A
  • Infection is in a site where patient’s own immune system is unable to deal with bacteria- Bacteria are working alone - Bacteria within cardiac vegetations are at high concentrations, have lower rates of metabolism/cell division/are dormant- Surrounded by fibrin, platelets and possibly calcified material
471
Q

What is a negative side effect of bactericidal antibiotics

A
  • Can lead to release of endotoxin from gram negative bacteria- Resulting increase in antigenic load causes an aggressive and dangerous inflammatory response - gram negative bacterial sepsis- Jarisch-Herxheimer reaction from spirochetes (e.g. in syphilis, leptospirosis etc.)- Also can cause toxin production -> Toxic Shock Syndrome (s. aureus) and Pneumolysin release (s. pneumonia)
472
Q

What do bacteriostatic antibiotics do

A

Inhibit bacterial growthKill >90% in 18-24 hour

473
Q

How are bactericidal and bacteriostatic antibiotics defined (in terms of MBC and MIC)

A
  • If the ratio of Minimum Bactericidal Concentration (MBC) to MINIMUM INHIBITORY CONCENTRATION (MIC) is >4 - the drug is defined as bacteriostatic- If the ratio of MBC to MIC is <4 the drug is defined as Bactericidal
474
Q

What types of antibiotics are bacteriostatic

A

Antibiotics that inhibit protein synthesis, DNA replication or metabolism

475
Q

How is MIC determined

A
  • Test in tube dilution in lab- INCUBATE for 24 HOURS- Determine MIC based on TURBIDITY (how clear or cloudy the solution is)
476
Q

What does an antibiotic need to be able to do to work effectively

A
  • It needs to attach to its binding target AND occupy an adequate number of binding sites (related to its conc within microbe) - CONCENTRATION present- It needs to remain at the binding site for a sufficient period of time for bacterial metabolic processes to be sufficiently inhibited - TIME it remains
477
Q

Two types of bacterial killing functioning by antibiotics

A

Time dependant killingConcentration dependent killing

478
Q

What is the key parameter for time dependent killing for antibiotics

A
  • The TIME for which serum concs remain ABOVE the MIC during the dosing interval- t>MIC
479
Q

Which antibiotics use time dependant killing

A

Beta-lactamsClindamycinMacrolidesOxazolidinones (synthetic - used against resistant bacteria e.g. vancomycin resistant enterococcus, MRSA, M. tb)

480
Q

What is the key parameter in concentration dependent killing

A

How HIGH the conc is ABOVE the MICPeak conc/MIC ratio

481
Q

Which antibiotics use conc-dependent killing

A

AminoglycosidesQuinolones

482
Q

Define pharmacokinetics

A

The activity of drugs in the body over a period of time. It is a function of:- Its RELEASE from dosage form, - ABSORPTION from site of administration into bloodstream, - DISTRIBUTION to various parts of the body, including site of action- its rate of ELIMINATION from body via metabolism (via liver) or excretion (via kidney) of unchanged drug

483
Q

Questions to ask when considering appropriateness of antibiotics for a certain site

A
  • Which antibiotics will penetrate that site? - E.g. if pus has collected around the infected site there will be no direct blood supply and it will be difficult to get antibiotic to the site. Or in endocarditis as the bacteria is on the valves which depend on blood flowing past so hard to get antibiotic to stick- What is the pH of the site?- Is the antibiotic lipid soluble?
484
Q

What does dosage interval/duration of antibiotic depend on

A

Half life + elimination time

485
Q

How do bacteria resist antibiotics

A
  • Change antibiotic target- Destroy antibiotic- Prevent antibiotic access- Remove antibiotic from bacteria
486
Q

Give examples of bacterial resistance due to changed antibiotic target

A

IMPORTANT- Flucloxacillin no longer able to bind to PBP of certain staph aureus (MRSA)- Wall component changes in enterococci reduce vancomycin binding (VRE)- Rifampin activity reduced by changes to RNA polymerase in M. TB (Multi drug resistant TB - MDR-TB)

487
Q

Examples of bacterial resistance via destroying/inactivated antibiotic

A
  • Some bacteria have ‘BETA LACTAMASE’, an enzyme which HYDROLYSES the BETA LACTAM RING of penicillins and cephalosporins etc.- Staphylococci produce ‘penicillinase’ - inactivates penicillin (BUT NOT flucloxacillin)- Gram -VE bacteria PHOSPHORYLATE AND ACETYLATE Aminoglycosides (e.g. gentamicin)
488
Q

How do bacteria prevent antibiotic access

A

Modify the bacterial membrane porin channel size, numbers and selectivity

489
Q

Examples of bacterial resistance via preventing antibiotic access

A
  • Pseudomonas aeruginosa against imipenem, - Gram negative bacteria against aminoglycosides
490
Q

Give examples of bacterial resistance via removal of antibiotic from bacteria

A
  • S. aureus or S. pneumoniae resistance to fluoroquinolones- Enterobacteriacae resistance to tetracylines
491
Q

How do bacteria develop resistance

A

Intrinsic resistanceAcquired resistance:- spontaneous gene mutation- horizontal/lateral gene transfer ** conjugation ** transduction ** transformation

492
Q

Characteristic of intrinsic resistance

A

All subpopulation of a species will be equally resistant

493
Q

Examples of intrinsic resistance

A
  • Aerobic bacteria CANNOT reduce metronidazole to its active form (requires anaerobic pathway)- Vancomycin CANNOT penetrate outer membrane of GRAM NEGATIVE bacteria- Anaerobic bacteria lack oxidate metabolism which is required for aminoglycoside uptake- PBP in enterococci are not effectively bound by cephalisporins
494
Q

Example of resistnace via spontaneous gene mutation

A

M. TB - point mutation in the rifampin-binding region rpoB

495
Q

What occurs in conjugation (bacterial lateral gene transfer) + example

A

Sharing of extra-chromosomal DNA plasmids (via “bacteria sex”)New Delhi metallo-beta-lactamase, ESBLs (extended spectrum beta-lactamases)

496
Q

What occurs in transduction (bacterial lateral gene transfer) + example

A

Insertion of DNA via organisms like bacteriophagesmecA genes for MRSA are acquired via a mobile genetic element called “staphylococcal cassette chromosome”

497
Q

What occurs in transformation (bacterial lateral gene transfer) + example

A

Picking up naked DNA from the environmentForeign DNA from S. mitis to S. pneumoniae conferring penicillin resistance

498
Q

Mode of resistance of MRSA

A
  • Contains mecA gene - on Staphylococcal cassette chromosome mec (SSCmec) - acquired via transduction mediated by bacteriophage- Encodes PBP2a (penicillin binding protein 2a)- Confers resistance to all beta-lactams including flucloxillin
499
Q

Resistance acquisition of VRE

A
  • Plasmid mediated - of gene encoding altered amino acid which prevents vancomycin binding- Promoted by cephalosporins
500
Q

Mode of aquisition + action of ESBL

A

Acquired via random mutation at active siteHydrolyse OXYIMINO side chains of CEPHALOSPORINS (cefotaxime, ceftriaxone, ceftazidime) and MONOBACTAMS (aztreonam)

Take 2: Electric Boogaloo (20 decks)

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