14. Microbial Pathogenicity Flashcards
1
Q
Properties of Staph Aureus
A
- gram positive
- single membrane with no LPS and thick layer of peptidoglycan
- coccus shape
- commensal
- colonise nostrils and skin
- facultative anaerobe
- non-spore forming - can’t enter dominant state in harsh conditions
- largest genome of staph genus
2
Q
Growth of staph aureus
A
- form biofilms - adhesion to human matrix proteins via cell anchored and other surface proteins
- grow in clusters, pairs and sometimes short chains
- transduction most common horizontal form
- virulence factors - coagulase binds to prothrombin in host, forms staphylothrombin complexes, fibrinogen to fibrin, coagulation cascade activated, blood clots formed
3
Q
Epidemiology of Staph Aureus
A
- most common cause of bloodstream infections - up to 50 per 100,000 per year
- around half of adults are thought to be colonised
- around 15% of adults persistently carry S. aureus in anterior nares
- forms biofilms on medical devices/prosthetics and tissue surfaces
- some strains have resistance to antibiotics e.g MRSA
4
Q
Explain MRSA
A
- methicillin resistant staphylococcus aureus
- methicllin antibiotic used when S.aureus resistant to penicllin, which 80% are
- methicillin resistance is due to acquisition of mecA-gene, primarily from horizontal transfer
- 2% of population have MRSA but may be asymptomatic carriers
5
Q
Relevance of S.aureus to dentistry
A
- can form biofilms on dental prostheses due to them being a non-shedding surface
- most predominant pathogens in people with oral infection
- important pathogen that can cause carious teeth and abscesses
- found in oral rinse of 33% of sample group
- MRSA found on tongue swab of 25% of sample group
6
Q
Diseases caused by staph aureus
A
- skin issues like acne, boils, pimples, impetigo, cellulitis
- toxic shock syndrome (fever, rash, vomiting, death)
- pulmonary infections like pneumonia, emphysema
- blood stream infections like sepsis
- bone and joint infections like arthritis, osteomyelitis
7
Q
Treatment of staph aureus infections
A
- antibiotics e.g penicllin, flucloxacillin, fusidic acid
- surgical drainage of abscesses
- fluid replacement for dehydration and food poisoning
- intravenous antimicrobial therapy
8
Q
Prevention of staph aureus issues
A
- cleanliness
- handwashing
- aseptic management of lesions
9
Q
MRSA is treated by what?
A
- clindalycin
- various tetracycline antibiotics
10
Q
Do dentists have to treat MRSA?
A
- not directly but
- can spread through cuts in mouth and cause issues
- mucositis is inflammation of oral mucosa, angular chelitis is inflammation of corners of mouth, parotitis is inflammation of parotid glands
- can cause implant failure with peri-implant infections
- MRSA transmitted in healthcare setting called HA-MRSA from invasive procedures like surgery
11
Q
Pathogenicity mechanism of S-.aureus
A
- evades host immune system by forming biofilms and blocking chemotaxis of leukocytes
- coagulase forms clots by converting soluble glycoprotein fibrinogen to insoluble fibrin
- clotting stops phagocytosis as prevents immune cells from reaching bacteria
- leukocidins are released by S.aureus and these toxins destroy phagocytes and leukocytes, also cause pus accumulation in skin infections
- protein A (cell wall protein) causes immunoglobulin-G to bind in wrong orientation on surface of cells, thought to disrupt opsonization and phagocytosis
- fibronectin-binding proteins A and B have roles in endothelial cell invasion and inflammation
12
Q
What is N. gonnorhoeae?
A
- diplococcus bacteria that causes sexually transmitted disease gonorrhoea
- aerobic and nutritionally fastidious
- gram-negative so has LPS in outer membrane, middle layer of peptidoglycan and cytoplasm in inner membrane
13
Q
Features of N. gonorrheae that affect function
A
- type IV pili allow it to adhere to and move along surfaces and allow exchange of genetic material between cells
- accessory gene pool has 247 genes - bacteria contains regulatory transcription networks allowing N. gon to adapt to changing environment
- different pumps allow bacteria to acquire iron and removal of antibiotics
- ROS/reactive oxygen species generated by neutrophils in immune response but detoxified by enzymes within N. gon in order to protect bacteria
14
Q
Prevalence of gonorrhoea
A
- second most common bacterial STI worldwide
- more in men who have sex with men, sex workers and transgender women
- highest cases ever in 2022 - increases of 50%
- in 2016, 86.9 million new cases worldwide
- most common in Africa, Americas and lowest in Europe
15
Q
Risk factors for N. Gonorrhoea
A
- young (15-24)
- new sexual contact in last year or more than one partner
- inconsistent condom use
- certain sexual preferences, having HIV, commercial sex work
- current or prior history of STI
- deprivation
16
Q
Process of N. gonorrhoea attaching and adhering the body
A
- pilli formation from pili like structures previously discussed extend from bacteria cell surface
- specific adhesins then occur at tips of pilli which have higher affinity for specific receptors (made of glycoproteins and proteoglycans) on the mucosal linings of urogenital tracts
- bind and form a complex , most well known of these is PiLC
- binding interaction complex is formed and forms a tight bond between bacteria and tissue lining
- strong bonds withstand strong forces like fluid motion and passing of urine in urogenital tracts to allow bacteria to stick to host
- now bacteria can establish itself in the host and begin its infectious process
17
Q
What happens once N. gonorrhoeae had attached in host?
A
- tissue penetration occurs by activating host cell signalling pathway that causes changes in cells composition and physiology
- bacteria causes change in host cell cytoskeleton by modifying cell protein structures, forming structures called filopodia surrounding and protecting bacteria undergoing transytosis through epithelial lining
- also bacteria manipulates endosomes that usually break down in pathogens, allows them to go undetected by host cell, furthering ability to infect host cell
- can induce inflammatory response as host immune response releases cytokines causing rash, pain, discharge
- in rare cases, dissemination and spread through bloodstream can cause Disseminal Gonoccal gonnorrhoea causing further complications like joint and organ problems
18
Q
How is N. gon pathiogenic?
A
- lives inside membrane-bound compartment called phagosome in host cell
- offers bacteria a secure setting, protected from host immune system
- has access to nutrients and can replicate using host tools
- functions metabolically and can reproduce, creating bacteria population inside phagosome
- can create a chronic infection due to internal lifestyle, shielded from external influence
19
Q
How does N. gon develop resistance?
A
- acquires mutations in genes that encode target site of antibiotics
- acquire plasmids carrying genes conferring resistance to specific antibiotics
- these plasmids can transfer between bacteria, allowing spread of resistance within bacterial populations
- creation of new antibiotics has been slow compared to rising resistance
