Lecture 10 Flashcards
Staphylococcus Aureus
main bacterial threat to New Zealanders mild disaese most humans get during lifetime potential for death -jack of all trades: cause wide range of illnesses -most common form of food poisoning
Staphylococcus Aureus Scenarios:
Fever and a new murmur Osteomyelitis Skin and Soft tissue Infection Pneumonia Infectious Disease Outbreak(rest home residents vomitting- most common cuase of food poisoning) Post-operative complications Child with red swelling around one eye
Staphylococcus Aureus
thick peptidoglycan cell wall
purple round circles, form clusters
“coccus” = round circle
“staphylo-“= grape like
“clusters of grape like circles”
purple= takes purple stain into cell wall (thick peptidoglycan cell wall)
Bacteria cells have poles. divide at poles. can form chain if daughter cell remains attached to parent cell.
Normally daughter and parent cell break off and become individuals. But big bacteria/ particularily bacteria with thick cell walls, remain adherent.
Staphylococcus Aureus has 3x poles, North, south and East/West pole.
-divides in multiple planes. therefore can form clumps. cells stack up ontop of one another (cell division)
-enzyme pumps separate DNA and proteins to different ends of cells so can bud off
A 55 year old man, is overweight, attends his GP practice with a painful red rash across his left foot. His foot is warm and swollen and he has an antalgic gait
over weight= risk factor for skin and soft tissue infection
Antalgic gait= hurts when walks
Hair follicle: bacteria attempts to invade e.g. in hair follicle. and associated with sweat gland.
Most skin bacteria lack capacity to damage hair/sweat cells, and may actually rather be protective. But some bacteria have ability to interact with and/or damage epithelial cells lining the sweat gland (e.g. using toxins/cytolitic/cytotoxic proteins)
-most bacteria dont, as most bacteria on the skin DO NOT interact with human cells
Damaged cells(before death) release chemicals (CYTOKINES) (proteins) that recruit immature cells to the site (CHEMOTAXIS)
-Tissue WBC roam and sample tissues, in skin they have starlike projections (dendritic cells). Sniff chemicals being released by damaged sweat gland/skin cells. Chemotactic (dendritic cells follow gradient, to high conc, to get to site of infection)
-more Cytokines are released. (augment process, release more WBC)
-Nearby capillaries a) become sticky/ various molecules to make BV lining (endothelium) sticky. P-selectin. trap WBC(bounce, roll and stop at highest conc of P-selectin, which is nearest to site of infection b)open up and allow more WBC to squeeze out of the vessel (diapedis) and move to the infection (chemotaxis).
WBC phagocytose/engulf bacteria
Process continues to augment until everything is under control
Cytokines irritate nerve fibres = pain (cytokines intiate pain)
Blood flow changes = swelling, warmth, redness
The ingested bacteria fuses with enzyme factories inside the neutrophil WBC. Phagocytose to have bacteria in phagosome (encircling membrane). Toxic granules inside neutrophil, bind to the phagosome, and form a lysosome. Toxic granules infect toxic substances(bleach) into sphere to dissolve bacteria. (create oxygen free radicals to damage bacteria) and the enzymes release chemicals to kill the bacteria (lysosome and toxic granule)
Visual results of Staphylococcus Aureus
-shows all Cardinal signs (localised swelling, purilence/puss in middle(bacteria, WBC, dead bacteria, expired WBC, protein goo), red (tiny BV in skin opened to increase BF to deliver more immune agents to site of infection), painful upon touch (nerve fibres in skin area aggrevated by chemicals, protein, goo, sending pain messages to brain) - could be sufficiently painful to make child unable to walk and therefore loss of function
Scaley, itchy (irritable>painful), school sores, inpatiganous rash. usually caused by Strep. Pyogenes (causes rheumatic fever). Non-dangerous legions(no fever) but highly contageous.
Car bunkles, assoc. with hair follicles (therefore on back of neck). volcano like (deep pot of puss/infection, with multiple heads emerging to surface). Difficult to treat, sometimes surgery to cut volcano out - leads large deficit which takes large amount of time to heal. No death but cause illness
- cardinal signs of inflammation + purilence/puss, centred on hair follicles (boils)= furuncle/ skin abccess/ folliculitis (infection centred on multiple hair follicles)
-diffuse redness of leg (not just around skin abccess). possible lesion/blister (think white tail spider) Cellulitis (infection in superficial layers of skin. Bacteria entered through hair follicle, but spread out under the skin. Most commonly cuased by group A strep. pogenes. but also Staphylococcus Aureus. Occasionally very severe, spreads entire limb, into lymphatics, causing painful infected lymph nodes in groin. sometimes lead to intensive care unit ICU admission. Mostly just annoyed at painful, hot, swollen leg
Epidemic of Meningococcal disease in 1990s
Niceria Meningitisis
Alot of cases in 1990s and early 200s
-Epidemic- more cases that expected to see (big uprising)
-serious Staphylococcus Aureus in Auckland ontop override epidemic of meningococcal
-Mortality of Bacteria Meningitis: 4% (risk of death)
- if have Staphylococcus Aureus in blood, death rate/mortality = 1/5. frail elderly at risk
==>
Therefore Staphylococcus Aureus is not only more common, but alot more deadly than other diseases such as meningitis (which have had public health campaigns)
Number of cases in NZ of invasive disease per head of popn
Invasive disease: disaese in bone/spine/ abccess in brain/infection of heart/ germs in blood stream
- dwarfed/much less than the number of cases of Skin infection requiring hospital admission/and or surgery (e.g. Staphylococcus Aureus)
- Increasing rate
- Burden on population and healthcare system both
Distribution of Staphylococcus Aureus
Not evenly spread (non-uniform distribution) over NZ
Epidemiology: make sensible deductions
- of invasive and with skin infection
-Less in south island vs upper north island
-Population density. Rates per popn (potentially more easily transmittable in a city environment than in a small community)
-greater levels of poverty in upper north island than south island
-climate, more hot and sweaty (decreased hygiene)
-seasonal variation of cases (more in summer than winter)
Where does Staphylococcus Aureus come from?
Predominantly human pathogen (spreads from human to human. probably through touch)
Human transmission to domestic animals (animals suffer same but with subtle differences)
Bovine mastitis( England/europe 200 years ago, when dairy was intensified. From humans to cow, adapted to cow to cuase disease)
Broiler chicken bone (infection in feet. Poland 1968, from humans–> chickens) and soft tissue infection
- AUS and NZ not affected by b. chicken. as have own poultry flock (never taken poultry stock from other parts of world). Europe rel. small number of genetic varients spread on planes and ships around world)
*Animals also get infected by this disaese. but it has been transmitted from humans
No environmental reservoir known (found consistently on humans)
Bovine Mastitis
massive problem for dairy industry (esp when dairy create's country's GDP) Pain and suffering Reduced milk production Reduced milk quality Reduced growth in young contagious -difficult to treat costs \$\$$
Colonisation of Staphylococcus Aureus
Prevelance (% at one point in time) Colonisation 20-25% (1/5)
-likes to live in Nose
-over semester, number of new cases of colonisation/Incidence= around 50-60%
-therefore remaining 80% likely to be infected over 3month period
(= Bacterial factors, Host factors, Environmental factors(e.g. south vs north island), Exposure)
Colonisation PRECEDES the major illnesses
Exposure of some sort, leads to colonisation, in an at risk host (especially if there is a mis-match between the germ and the hosts immunity) disease may develop
Staphylococcus Aureus does not have a “mild” and “dangerous” version. across whole species they have a similar capacity to cause disease (except a few rare cases)
Host factors: Some hosts dont get Staph- some immune and genetic factors that possibly contribute to protecting the host
-colonisation/carriage is common
-Peak incidence in the first year of life. Declines with old age (less than 20%). (if mum is staph. aureus carrier at time of delivery, baby will become infected in first few hours of life (almost immediately)
Nasal Carriers: Persistent =15%. Intermittent. Non- (25%)
Prevalance vs Incidence
Prevalance: % at one point in time
Incidence: number of new cases over time (more difficult to measure)
Staphylococcus Aureus locations on body
Carrier: almost always in nose
Tolerate salts (noses are high salt environment. therefore lots of other bacteria cant tolerate and wont live there)
-Staphylococcus as genus and Staphylococcus Aureus as species enjoy it.
-Nose immune system is highly developed: in permanent contact with outside world
-Staphylococcus Aureus has ways of avoiding nasal immune system
Salts good Antiseptic (keeps meat e.g.)
Nasal Carriers of Staphylococcus Aureus
Non-(20%) never ever pick up Staphylococcus Aureus. “super humans” . Born that way/genetic. Lower risk of getting Staphylococcus Aureus disease. Beta3Defensin, protein located all around body. high concentrations on skin and in nose. Multiple forms. Capacity to kill/break/destroy bacteria such as Staphylococcus Aureus.
Intermittent: pick up/comes and goes every 4 weeks
Persistent (15%) always have Staphylococcus Aureus. changes every 3-4 months. increased risk of disease(as always around them). reduced risk of death
Various forms of disease and illness that Staphylococcus Aureus can cause
N symptoms- 60% over a year
Food poisoning/emmicis- common. (not direct infection. not Staphylococcus Aureus getting into gut and causing vomiting. is indirect, replication in food, releasing toxin (toxic shock syndrome toxins). Ingestion of toxin/protein. 6hours later if sufficient levels of toxin will wake up and vomit a few times. end.
-food poisoning has rapid onset and rapid onset. no diarohea as doesnt interact with rest of bowel. just vomiting. not bacteria themselves, is toxin produced in food(food poisoning)
Skin infection- 3% over a year
Serious- 0.02% (1 per 5000)
