microbio Flashcards
commensal
Living on or within another organism, deriving
benefit without injuring or benefiting the other
individual
saprophyte
An organism that takes nourishment from
dead organic matter
opportunist
An organism that usually does not cause
disease but, under circumstances such as
immune deficiency, can become a pathogen.
colonisation
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.
infection
Term indicating that microorganisms have
entered and replicated in the body – may be
local or systemic
clinical disease
An impairment of health or a condition of
abnormal functioning
gram stain
- blue/purple (Gram positive) - cocci or rods
- red (Gram negative) cocci or rods
GRAM POSITIVE cell wall
thick, formed of peptidoglycan
has lipoteichoic acid, teichoic acid
has surface proteins
cytoplasmic membrane is beneath
GRAM NEGATIVE cell wall
thin
has an outer membrane, thin petidoglycan in between and cytoplasmic membrane beneath
outer membrane has LPS, O polysaccharide, lipid A, proteins, porins
in general gram positives
- survive well on drying
- some produce spores
- produce exotoxins
- have teichoic acid in their cell wall
in general gram negatives
- do not survive drying
- no spores
- have endotoxin in their cell wall
mycobacterium cell walls
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)
bacteria that infect humans
• Opportunist – from normal
flora
• Opportunistic – from
environment
• Obligate pathogen
staph aureus
gram positive
coagulase positive
• Wound infections, septicaemia, food poisoning,
endocarditis, pneumonia, osteomyelitis, t_oxic shock
syndrome_
- A Gram positive coccus that forms clusters
- Grows easily on blood agar – golden/gray colonies
- _ Coagulase positive, protein A in cell wall_
- Produces alpha beta gamma delta haemolysins, enterotoxins & toxic shock syndrome toxin
- Some produce PVL (Panton Valentine leucocidin)
gram postivie cocci
– 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)
streptococci GPC in pairs
‘Alpha’ (partially-) -haemolytic streps Strep pneumoniae
• Non haemolytic streps e.g enterococci, anaerobic
streptococci
gram positive rods
– Spore-forming e.g. Bacillus anthracis,
Clostridium tetani, Clostridium
botulinum
– Non spore-forming e.g. Corynebacterium diphtheriae, Listeria
gram negative cocci
Neisseria meningitidis
– Neisseria gonorrhoeae
gram engative rods
– E. coli, Klebsiella, Proteus
Pseudomonas
– Haemophilus
– Legionella,
– Salmonella, Shigella, Campylobacter
anaerobes
e.g Bacteroides: grow only in
absence of oxygen & sensitive to
metronidazole
mycobacteria
e.g. M. tuberculosis: acid fast
bacilli, most slow growing on special media
Chlamydia
e.g. C trachomatis - needs cell
culture or indirect detection
spirochaetes
Treponema pallidum
(causes syphilis) does not grow in the
laboratory
nucleic acid studies
Diagnosis of culture negative meningitis
post Rx
Meningococcal serotype (vaccination)
Mycobacterium tuberculosis resistance,
speciation, typing
Typing of other outbreak bacteria in
general (esp. MDR)
future methods
MALDI-TOF and mass spectrometry
derivatives
Proteomics & genomics
Better point-of-care diagnostics
Microarrays (nucleic acid,
protein/antigen)
pathogenic factors in Staph aureus
- Coagulase – deposits fibrin around the bacteria in tissues
- Protein A – binds the Fc portion of IgG
- Produces alpha beta gamma delta toxins – damage red cell & othermembranes to gain nutrients
- Enterotoxins – damage gut cells, cause vomiting & diarrhoea (food poisoning) & toxic shock
- T_oxic shock syndrome toxin_ – a superantigen, switches on cytokine production of T cells directly
- PVL – kills leucocytes esp neutrophils
- _ Exfoliatin_ – damages skin cells
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
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
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_
Toxic shock syndrome
Infection of medical devices e.g.
catheters, prosthetic joints
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*
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
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
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
rheumatic fever
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_
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 – clindamycin switches off toxin production.
Vancomycin – very occasionally used if serious
infection and multiple allergies
streptococcus pneumoniae
A Gram positive coccus that forms pairs
Alpha-haemolytic – ‘pneumolysin’ partially
lyses haemoglobon e.g. in an agar plate culture
Polysaccharide capsule - >80 types
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
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_
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
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
coagulase negative staph (eg epidermidis) features
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
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
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
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
Bacillus species
Aerobic GPR, forms spores
B anthracis - anthrax
B. cereus – food poisoning
corynebacterium
Aerobic GPR, no spores
C diphtheriae diphtheria toxin, membrane,
(cardiac, nervous system, local damage)
‘Diphtheroids’ – various harmless species of
Corynebacteria colonise skin, throat
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
pathogenic factors in E. coli
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.
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
infections due to E. coli
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
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
coliforms
Klebsiella
Enterobacter
Proteus
Serratia
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)
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 types – in patients with cystic fibrosis
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
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
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
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
pathogenic factors in H influenzae
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
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
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
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
Nisseria species
SURVIVE AND REPLICATE INSIDE NEUTROPHILS
Gram negative cocci
Mucous membranes;
Die off rapidly in environment
N. meningitidis (meningococcus)
N. gonorrhoeae (gonococcus)
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
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
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
