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microbio Flashcards

1
Q

commensal

A

Living on or within another organism, deriving
benefit without injuring or benefiting the other
individual

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2
Q

saprophyte

A

An organism that takes nourishment from
dead organic matter

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3
Q

opportunist

A

An organism that usually does not cause
disease but, under circumstances such as
immune deficiency, can become a pathogen.

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4
Q

colonisation

A

The presence, growth and multiplication of an
organism on internal or external body surfaces
body without observable clinical symptoms or
immune reaction in a patient.

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5
Q

infection

A

Term indicating that microorganisms have
entered and replicated in the body – may be
local or systemic

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6
Q

clinical disease

A

An impairment of health or a condition of
abnormal functioning

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7
Q

gram stain

A
  • blue/purple (Gram positive) - cocci or rods
  • red (Gram negative) cocci or rods
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8
Q

GRAM POSITIVE cell wall

A

thick, formed of peptidoglycan

has lipoteichoic acid, teichoic acid

has surface proteins

cytoplasmic membrane is beneath

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9
Q

GRAM NEGATIVE cell wall

A

thin

has an outer membrane, thin petidoglycan in between and cytoplasmic membrane beneath

outer membrane has LPS, O polysaccharide, lipid A, proteins, porins

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10
Q

in general gram positives

A
  1. survive well on drying
  2. some produce spores
  3. produce exotoxins
  4. have teichoic acid in their cell wall
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11
Q

in general gram negatives

A
  1. do not survive drying
  2. no spores
  3. have endotoxin in their cell wall
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12
Q

mycobacterium cell walls

A

have a waxy cell wall containing _mycolic
acids_

It is Gram positive in structure but does not stain with Gram’s stain;

therefore we use a special stain –

the Ziehl- Neelsen stain (ZN).

This group are also called AFB (acid-fast bacilli)

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13
Q

bacteria that infect humans

A

• Opportunist – from normal
flora
• Opportunistic – from
environment
• Obligate pathogen

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14
Q

staph aureus

A

gram positive

coagulase positive

• Wound infections, septicaemia, food poisoning,
endocarditis, pneumonia, osteomyelitis, t_oxic shock
syndrome_

  1. A Gram positive coccus that forms clusters
  2. Grows easily on blood agar – golden/gray colonies
  3. _ Coagulase positive, protein A in cell wall_
  4. Produces alpha beta gamma delta haemolysins, enterotoxins & toxic shock syndrome toxin
  5. Some produce PVL (Panton Valentine leucocidin)
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15
Q

gram postivie cocci

A

– Streptococci GPCs in pairs & chains Beta-haemolytic streptococci

• GROUP A (=Streptococcus pyogenes)
• GROUP B (=Streptococcus agalactiae )
• GROUP D (e.g. Enterococcus faecalis – NB
may be non-haemolytic)

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16
Q

streptococci GPC in pairs

A

‘Alpha’ (partially-) -haemolytic streps Strep pneumoniae
• Non haemolytic streps e.g enterococci, anaerobic
streptococci

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17
Q

gram positive rods

A

– Spore-forming e.g. Bacillus anthracis,
Clostridium tetani, Clostridium
botulinum
– Non spore-forming e.g. Corynebacterium diphtheriae, Listeria

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18
Q

gram negative cocci

A

Neisseria meningitidis
– Neisseria gonorrhoeae

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19
Q

gram engative rods

A

– E. coli, Klebsiella, Proteus
Pseudomonas

– Haemophilus
– Legionella,
– Salmonella, Shigella, Campylobacter

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20
Q

anaerobes

A

e.g Bacteroides: grow only in
absence of oxygen & sensitive to
metronidazole

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21
Q

mycobacteria

A

e.g. M. tuberculosis: acid fast
bacilli, most slow growing on special media

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22
Q

Chlamydia

A

e.g. C trachomatis - needs cell
culture or indirect detection

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23
Q

spirochaetes

A

Treponema pallidum
(causes syphilis) does not grow in the
laboratory

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24
Q

nucleic acid studies

A

Diagnosis of culture negative meningitis
post Rx
 Meningococcal serotype (vaccination)
 Mycobacterium tuberculosis resistance,
speciation, typing
 Typing of other outbreak bacteria in
general (esp. MDR)

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25
Q

future methods

A

 MALDI-TOF and mass spectrometry
derivatives
 Proteomics & genomics
 Better point-of-care diagnostics
 Microarrays (nucleic acid,
protein/antigen)

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26
Q

pathogenic factors in Staph aureus

A
  1. Coagulase – deposits fibrin around the bacteria in tissues
  2. Protein A – binds the Fc portion of IgG
  3. Produces alpha beta gamma delta toxins – damage red cell & othermembranes to gain nutrients
  4. Enterotoxins – damage gut cells, cause vomiting & diarrhoea (food poisoning) & toxic shock
  5. T_oxic shock syndrome toxin_ – a superantigen, switches on cytokine production of T cells directly
  6. PVL – kills leucocytes esp neutrophils
  7. _ Exfoliatin_ – damages skin cells
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27
Q

Staph aureasu carried in

A

 Carried in nose of 20-30% of the population
 Also throat, groin, perineal and rectal carriage
 Broken skin colonised e.g. eczema

28
Q

staph aureaus transmission

A

 Endogenous infection in a nasal carrier
 Hand & environmental transfer of bacteria between
families, partners, in public areas
 In hospitals - MRSA on staff hands, environment,
fomites (contaminated inanimate objects), from
draining pus.
 Importance of soap & water hand cleansing,
alcohol hand rubs, surgical scrub

29
Q

infections caused by staph aureus

A

 Wound infections – traumatic, surgical
 Skin infections – impetigo,
boils/carbuncles
 ENT infections – otitis media, sinusitis
(not sore throat but occasionally
peritonsillar abscess)
 Septicaemia / sepsis syndrome
Infective endocarditis – e_sp. injecting drug
users_

Pneumonia especially post-influenza
Septic arthritis & osteomyelitis
 F_ood poisoning – toxin – 2 to 6 hours
later_
 Toxic shock syndrome
 Infection of medical devices e.g.
catheters, prosthetic joints

30
Q

antibiotics against staph aureus

A

Penicillin – 80-90% resistance now due to betalactamase production
Flucloxacillin
Co-amoxiclav (‘Augmentin’)
Erythromycin or clindamycin – esp if allergy to
the penicillins
Vancomycin – if MRSA*

31
Q

STREPTOCOCCUS PYOGENES

A

GROUP A STREP

A Gram positive coccus that forms chains

Beta-haemolytic – completely lyses red cells
e.g. In an agar plate culture -zone of haemolysis

Produces streptolysins, streptokinase

 M Protein in cell wall

32
Q

streptococcus pyogenes carried in

A

Carried in nose & throat of 1-5% of the
population especially children

 Transmitted through close contact, on
hands, from septic lesions

 Importance of soap & water hand
cleansing, alcohol hand rubs, surgical
scrub

 Easily cultured in the laboratory from
throat and wound swabs, blood cultures

33
Q

infections cuased by strep pyogenes

A

Sore throat (Pharyngitis) +/- abscess
_Scarlet fever rheumatic
fever, fever & glomerulonephritis after strep sore throat_
 Wound infection
Cellulitis, impetigo, erysipelas
 Septicaemia
Streptococcal toxic shock
Necrotising fasciitis
 Other infections e.g. Sinusitis, otitis media

34
Q

rheumatic fever

A

antibody-mediated damage to the host

causes pharyngitis

  • antibodies raised against organism in throat antibody cross-reacts with cardiac antigens*

(molecular mimicry)

_ permanent heart damage ensues + severe_ illness with fevers, joint pains (Rheumatic Fever)

Glomerulonephritis is similar- due to a_ntigenantibody complexes depositing in kidney_

35
Q

antibiotics against strep pyogenes

A

Penicillin – 100% sensitive (i.e sensitive to
amoxicillin and all other penicillins
 Erythromycin or clindamycin* – esp if allergy to
the penicillins (10% resistant)  *esp used if patient shocked – clindamycin switches off toxin production.

 Vancomycin – very occasionally used if serious
infection and multiple allergies

36
Q

streptococcus pneumoniae

A

A Gram positive coccus that forms pairs

Alpha-haemolytic – ‘pneumolysin’ partially
lyses haemoglobon e.g. in an agar plate culture

Polysaccharide capsule - >80 types

37
Q

pneumococcus carried in

A

Carried in nose & throat of 20-40% of
children 5-10% adults, highest in
wintertime

 Transmitted through prolonged close
contact via respiratory secretions

 Easily cultured in the laboratory from
sputum, blood cultures, etc

38
Q

pneumococcus infections

A

Pneumonia – e.g. Lobar
 Exacerbation of chronic bronchitis
 Meningitis - infants & elderly
 Sinusitis, otitis media, conjunctivitis
 Septicaemia (usually from one of the
above)
Rare – endocarditis, spontaneous
bacterial peritonitis
_Splenectomised / sickle cell patients at
special risk of serious infection_

39
Q

antibiotics for pneumococcus

A

Penicillin – 95% sensitive (i.e also sensitive to
amoxicillin and all other penicillins)

_NB penicillin resistance is not due to betalactamase
enzyme (unlike Staph aureus) – but
penicillin-binding protein mutations_

  • * Erythromycin** – esp if allergy to the penicillins –
  • *but NOT for meningitis**
  •  Ceftriaxone –for meningitis*

Vancomycin – very occasionally used if serious
infection and multiple allergies

40
Q

staph epidermidis

A

coagulase negative

 A Gram positive coccus that forms clusters
 Low virulence – does not produce coagulase
 Colonises the skin ~ 104/sq cm
 Produces biofilm glycocalyx (‘slime’) - Infection of
plastic devices

41
Q

coagulase negative staph (eg epidermidis) features

A

 A Gram positive coccus that forms clusters
Low virulence – d_oes not produce coagulase_
Colonises the skin ~ 104/sq cm
 Produces biofilm glycocalyx (‘slime’) - Infection of
plastic devices

42
Q

effects of foreign bodies in a wound

A

make it easier for bacteria to cause infection
- especially the coagulase-negative
staphylococci such as Staph epidermidis

10^6 staph aureus bacteria on wound without foreign stuff

10^2 staph bacteria with foreign stuff needed to cause infect

43
Q

plastic and metal implants

A

Prosthetic hip & knee joints, indwelling IV lines,
replacement valves, peritoneal dialysis etc
 Plastic & metal facilitate infection - ?neutrophils
unable to function; low pathogenicity bacteria
e.g. Staphylococcus epidermidis adhere to
material
Difficult to eradicate infection, risk of severe
sepsis, device must be replaced

44
Q

Clostridium species

A

Gram positive rod, anaerobic, forms
spores

 e.g. C. difficile – potent toxin affects
colon; antibiotic-associated diarrhoea or
(severe cases) pseudomembranous
colitis – esp in hospitals

C. tetani – tetanospasmin – blocks
neuromuscular transmission (upper
motor neurone)
 Minor wound in a non-vaccinated
individual

C. perfringens – multiple toxins
 Gas gangrene
 Food poisoning

45
Q

Bacillus species

A

Aerobic GPR, forms spores

 B anthracis - anthrax

 B. cereus – food poisoning

46
Q

corynebacterium

A

Aerobic GPR, no spores
C diphtheriae diphtheria toxin, membrane,
(cardiac, nervous system, local damage)
‘Diphtheroids’ – various harmless species of
Corynebacteria colonise skin, throat

47
Q

endotoxin

A

 Endotoxin – also called lipopolysaccharide (LPS)
very potent – activates cytokine release,

• Binds to Toll like receptors (esp TLR4 )
• Binds to LPS binding protein
• Activates cytokine release e.g. TNF & other proinflammatory mediators

• Cell recruitment, fevers, shock (if severe)

• Outer sugars (O antigen) highly variable – means
there are many strains
•Sugars interfere with immune response

48
Q

pathogenic factors in E. coli

A

endotoxin

Iron binding proteins

 A small polysaccharide capsule – avoid phagocytosis

Fimbriae for adhesion (& special ones for transfer of plasmids (circles of DNA bearing resistance genes)

Enterotoxins – certain strains of E. coli that cause diarrhoea; can inject toxins into cell:

Enterohaemorrhagic E. coli (e.g. E. coli O157 – an enterohaemorrhagic toxin, can cause bloody diarrhoea, and haemolytic uraemic syndrome

(HUS)

Enterotoxigenic E. coli – ETEC - traveller’s diarrhoea

Enteropathogenic E. coli - EPEC – infantile diarrhoea

 There are other types also.

49
Q

e.coli carried in and transmission

A

 Carried in the gut esp the colon about 107/gram
faeces, 100% of the population
 Can colonise perineum, vagina, wounds,
sometimes respiratory tract e.g. ITU patients

Transmission:
Endogenous – e.g. into urinary tract, peritoneum if
gut perforation
Exogenous - contaminated medical equipment,
food & drinking water, hands, farm animals
 Importance of clean water supplies, hand hygiene

50
Q

infections due to E. coli

A

Urinary tract infections – cystitis,
pyelonephritis
Diarrhoeal disease - esp. travellers,
infants, contact with animals
 Septicaemia / sepsis syndrome
(secondary to an infected focus such as
peritonitis, severe UTI, cholecystitis)
 Nosocomial pneumonia
 Neonatal meningitis
 Miscellaneous e.g. bone, joint infection

51
Q

antibiotics for E coli

A

Amoxicillin – 50% resistance due to betalactamase
production
 Trimethoprim & oral cephalosporins for UTI
Co-amoxiclav (‘Augmentin’) for UTI,
community-acquired severe sepsis
 ‘Tazocin’ for hospital-acquired severe sepsis
Gentamicin added to above for severe sepsis
 Increase in multi-drug-resistant (MDR) strains
even in the community

52
Q

coliforms

A

Klebsiella
  Enterobacter
 Proteus
 Serratia

53
Q

pseudomonas aeruginosa

A

Grows easily on blood agar & produces a distinctive
green pigment
 Like all Gram negatives- have an outer membrane
containing endotoxin, porin channels, various
proteins
Large genome – adapts to environment
Also has fimbriae; flagellae (motile)

54
Q

pathogenic factors in pseudomonas aeruginosa

A

Endotoxin – as previously for E. coli

 Exotoxin A, leucocidins
 Iron binding proteins
Secreted toxins & enzymes – various e.g. elastase
Mucoid types – in patients with cystic fibrosis

55
Q

pseudomonas aeruginosa carried in transmission

A

 Ubiquitous in environmental water and soil

Can replicate in distilled water and some
disinfectant solutions
 Can colonise patients especially – compromised,
ITU (respiratory tract), urinary catheters, burns
Transmission:
 Contaminated medical equipment and fluids,
uncooked food & poor quality drinking water
 Some survival on hands
 Pools and baths/spas if not chlorinated

56
Q

infections caused by pseudomonas aeruginosa

A

Septicaemia / sepsis syndrome
(secondary to an infected focus such as
IV catheter/Hickman line)
 Pneumonia – especially ICU, neutropenic;
cystic fibrosis
 Urinary catheter infection
 Eye infection – contaminated contact
lenses
 Otitis externa, burns, other skin & soft
tissue infection

57
Q

antibiotics agains pseudomonas aureginosa

A

Intrinsically much more resistant to antibiotics

 ‘Tazocin’ (piperacillin-tazobactam) for hospitalacquired
severe sepsis
 Gentamicin added to above for severe sepsis
Ciprofloxacin the only oral agent
 Some MDR strains in hospitals, CF patients

58
Q

haemophilus influenzae

A

Small Gram negative rod (‘cocco-bacilli’)

 Needs special heated blood agar as it requires
blood factors [X & V] to grow (hence the genus
name);
 Used to be thought to be the cause of ‘flu (hence the
species name)
 Outer membrane containing endotoxin, porin
channels, various proteins

59
Q

pathogenic factors in H influenzae

A

Endotoxin – as previously for E. coli
 Some strains have a large polysaccharide capsule:
Capsular types a to f (type b most important –
hence Hib vaccine for children)

Non-capsular strains – less virulent
IgA-ase – destroys IgA on mucous membranes
Adhesins– for adhesion

60
Q

H influenza carried and transmitted

A

 _Only lives on mucous membrane_s – requires host
factors
Mainly found in the upper respiratory tract

Transmission:
 Close contact / respiratory droplet
 Capsulate type survives better

61
Q

infections due to H influenza

A

Mainly H. flu type b - children under 5 y
 Meningitis, bacteraemia
Epiglottitis, cellulitis, septic arthritis

Mainly H. flu non-typable (no capsule)
 Otitis media, sinusitis
 Conjunctitivis
 Pneumonia – community-acquired
pneumonia especially exacerbation of
chronic bronchitis

62
Q

antibiotics for H influenzae

A

Amoxicillin – 15% resistance due to betalactamase
production - for URTI
Co-amoxiclav (‘Augmentin’) for URTI
Ceftriaxone for meningitis (or a similar agent) or
other severe Hib infections
 Prophylaxis for a close contact child

NB conjugate vaccine for Hib

63
Q

Nisseria species

A

SURVIVE AND REPLICATE INSIDE NEUTROPHILS

Gram negative cocci
 Mucous membranes;

Die off rapidly in environment

 N. meningitidis (meningococcus)
 N. gonorrhoeae (gonococcus)

64
Q

Legionella pneumophila

A

SURVIVES AND REPLICATES INSIDE MACROPHAGES

 Gram negative rod, needs iron
 Environmental waters – esp inside amoebae
 Difficult to grow in lab – do urinary antigen test

 Cooling towers of air con; screen wash(!)

 Severe community acquired pneumonia,
Pontiac fever

65
Q

SALMONELLA SPECIES

A

Gram negative rod, does not ferment lactose

 _Food poisoning type_s – poultry & other
farm animals – hundreds of species (S.
enterica var Typhimurium) – mild to
severe diarrhoea, occ. septicaemia

Enteric fever types: ‘Salmonella typhi’, ‘S.
paratyphi’ – Typhoid fever - severe
invasive infection of gut& RE system
diarrhoea, occ. septicaemia

66
Q

HELICOBACTER PYLORI

A

Small curved microaerophilic gram
negative rod

 Colonises the stomach
 CagA protein associated with virulence
 Gastritis, duodenal (& some gastric)
ulceration
Gastric lymphoma (MALT-type B cell)
association
Dual or triple combination
antibiotic/proton pump inhibitors for
eradication

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