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
future methods
 MALDI-TOF and mass spectrometry derivatives  Proteomics & genomics  Better point-of-care diagnostics  Microarrays (nucleic acid, protein/antigen)
26
pathogenic factors in Staph aureus
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. **_Enterotoxin_**s – **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_ – k**ills leucocytes esp neutrophils** 7. _ Exfoliatin_ – d**amages skin cells**
27
Staph aureasu carried in
 Carried in nose of 20-30% of the population  Also throat, groin, perineal and rectal carriage  Broken skin colonised e.g. eczema
28
staph aureaus transmission
 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
infections caused by staph aureus
 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_  T**oxic shock syndrome**  Infection of medical devices e.g. catheters, prosthetic joints
30
antibiotics against staph aureus
 **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
STREPTOCOCCUS PYOGENES
**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
streptococcus pyogenes carried in
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
infections cuased by strep pyogenes
 *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
rheumatic fever
antibody-mediated damage to the host causes pharyngitis * antibodies raised against organism in throat antibody cross-reacts with cardiac antigens* (**molecular mimicr**y) _ permanent heart damage ensues + severe_ _illness with fevers, joint pains (Rheumatic Fever)_ **Glomerulonephritis** is similar- due to a_ntigenantibody complexes depositing in kidney_
35
antibiotics against strep pyogenes
 **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 – c**lindamycin switches off toxin productio**n.  Vancomycin – very occasionally used if serious infection and multiple allergies
36
streptococcus pneumoniae
A Gram positive **coccus that forms pairs**  **Alpha-haemolytic – ‘pneumolysi**n’ _partially lyses haemoglobon_ e.g. in an agar plate culture  **Polysaccharide capsule - \>80 types**
37
pneumococcus carried in
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
pneumococcus infections
 **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
antibiotics for pneumococcus
**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
staph epidermidis
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
coagulase negative staph (eg epidermidis) features
 A **Gram positive coccus that forms clusters**  **Low virulence** – d_oes not produce coagulase_  **Colonises the ski**n ~ 104/sq cm  Produces **biofilm glycocaly**x (‘slime’) - _Infection of plastic devices_
42
effects of foreign bodies in a wound
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
plastic and metal implants
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
Clostridium species
**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
Bacillus species
**Aerobic GPR, forms spores** ** B anthracis - anthrax**  B. cereus – food poisoning
46
corynebacterium
**Aerobic GPR, no spores**  **_C diphtheriae_** diphtheria toxin, membrane, (cardiac, nervous system, local damage)  **_‘Diphtheroids_**’ – various *harmless species of Corynebacteria colonise skin, throat*
47
endotoxin
 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
pathogenic factors in E. coli
**endotoxin**  _Iron binding proteins_  A small p**olysaccharide 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. col_***i (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
e.coli carried in and transmission
 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
infections due to E. coli
 **Urinary tract infection**s – 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
antibiotics for E coli
**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
coliforms
Klebsiella   Enterobacter  Proteus  Serratia
53
pseudomonas aeruginosa
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
pathogenic factors in pseudomonas aeruginosa
Endotoxin – as previously for E. coli ** Exotoxin A, leucocidins  Iron binding proteins**  **Secreted toxins & enzymes** – various e.g. **elastase**  **Mucoid type**s – in patients with cystic fibrosis
55
pseudomonas aeruginosa carried in transmission
** 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
infections caused by pseudomonas aeruginosa
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
antibiotics agains pseudomonas aureginosa
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
haemophilus influenzae
**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
pathogenic factors in H influenzae
 **Endotoxin** – as previously for E. coli  S**ome strains** have a l**arge polysaccharide capsul**e:  _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
H influenza carried and transmitted
 _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
infections due to H influenza
_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
antibiotics for H influenzae
**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
Nisseria species
**SURVIVE AND REPLICATE INSIDE NEUTROPHILS**  **Gram negative cocci**  Mucous membranes;  *Die off rapidly in environment*  N. meningitidis (meningococcus)  N. gonorrhoeae (gonococcus)
64
Legionella pneumophila
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
SALMONELLA SPECIES
**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
HELICOBACTER PYLORI
**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*