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
20
Q
Symptoms of gonorrhoea in men
A
- burning or pain when urinating
- white, yellow, green discharge from penis
- painful/inflamed testes
21
Q
Symptoms of gonnorhoea in women
A
- burning sensation when urinating
- vaginal bleeding between periods
- increased vaginal discharge
22
Q
Symptoms of gonorrhoea begin … after contact
A
1-14
23
Q
Complications of Gonorrhoea in just women
A
- pelvic inflammatory disease
- symptoms include abdominal pain/fever, chronic pelvic pain, internal abscesses, ectopic pregnancy, formation of scar tissue in fallopian tubes causing infertility
24
Q
Complications of gonorrhoea in just men
A
- scrotal swelling
- narrowing of urethra
- painful inflammation in epididymis (tube exiting back of each testicle) can cause infertility
25
Q
In men and women, where can gonorrheoa spread to?
A
- blood, skin, joints
- meninges as desseminated gonococcal infection
- increase change of getting and spreading HIV
26
Q
Dental relevance of Gonorrhoea
A
- cause infection in oropharynx
- key part in development of antibiotic resistance due to presence of Neisseria species with these genes
- oropharyngeal infection is hard to treat as antibiotic concs are too low when reaching this site
- contribute to oral sex/saliva exchange in sexual activity
- most patients are asymptomatic but can experience sore throat, pain, discharge, difficulty swallowing
27
Q
Characteristics of Legionella pneumophilia
A
- gram negative
- flagellated
- aerobic
- non spore-forming
- thin
- waterborne
- appears green in water
- fastidious
- small short rod but in culture, filamentous bacillus
28
Q
How do L. pneumophilia grow?
A
- commensal heterotroph with 2 main obtaining methods
- directly from other microorganisms within associated biofilm or by infecting and replicating inside eukaryotes
- the former can obtain nutrients from living and decaying organic matter in matrix for example remnants of gram-neg bacteria like E.Coli
- the latter can reproduce in various eukaryotes like protists and animal cells. Key macromolecules are broken down and used in bacteria
29
Q
2 diseases caused by L. pneumophilia
A
- Legionnaires disease
- Pontiac fever
30
Q
Prevalence of Legionnaires
A
- 2-10 day incubation period
- worldwide but uncommon
- in Europe, Australia and USA, about 10-15 cases per million
- in 2020, 27 countries confirmed 7712 cases
- 75-80% are over 50 yrs and 60-70% are male
31
Q
Prevalence of Pontiac fever
A
- short incubation of 1-3 days
- not often reported as mild/non-specific manifestations
- no fatalities reported and cases resolve spontaneously without treatment
- high attack rate - people exposed up to 95%
- affects age medians of 29-32
32
Q
Outbreaks of Legionella pneumophilia
A
- 1976 in late summer Philadelphia in a group at a convention for American Legion. Those affected had a pnuemonia eventually called Legionnaires
- first fatality in an AirForce veteran, further 221 infected and 34 deaths by mid-August
- later episode in 2001 - largest outbreak of Legionnaires Disease in Murcia Spain. 800 cases and 449 confirmed from infection of cooling tower
- most recent in Japan, from host springs and public baths. in 2015, 7 patients of spa house - related strains caused severe disease
33
Q
Aetiology of L. pneumophilia
A
- found in natural water sources like lakes, resevoirs
- possible for it to be found within water systems where it can thrive in favourable conditions
- when people breathe in small droplets of water or accidentally swallow water containing Legionella in lungs
34
Q
Symptoms of Legionnaires Disease
A
- fever
- headache
- loss of appetite
- muscle pain
- diarrhoea
- nausea
- coughing
35
Q
Symptoms of Pontiac disease
A
- fever
- chills
- headaches
- muscle aches
36
Q
Treatment of Legionnaires disease
A
- antibiotics directly into vein and 1-3 week course at home on healing
- oxygen via face mask or tube
- possibly ventilator
37
Q
Treatment for Pontiac fever
A
- none generally
- recover without
38
Q
Pathogenicity of L. pneumophilia
A
- bacteria prefer intracellular environments to multiply and target alveolar macrophages
- these macrophages consume bacteria and bacteria inhibit fusion of lysosomes within preventing bacteria break down
- multiply within macrophage, releasing new neutrophils and monocytes causing destructive alveolar inflammation
- cell dies and releases microbes, repeating process
39
Q
Dental relevance of L. pneumophilia
A
- can colonise in oropharynx for up to 8 weeks
- contaminate dental unit water systems
- increased risk of respiratory infection from inhaling infected aerosols
- infection risk minimised through infection control guidelines and modern water distribution systems
- in dental settings, waterline flushing, water resevoir systems, deionised or sterilised water, disinfection by chemicals
40
Q
What is Clostridioides difficile?
A
- gram positive
- toxin producing
- obligate anaerobe
- key microbe in hospital infections
- vegetative cells can’t grow in aerobic conditions
- transmissible and infectious in form of spores
41
Q
Epidemiology of C.difficiles
A
- infections after normal microbiota is upset via use of antibiotics
- major cause of Antibiotic Associated Diarrhoea in hospital patients
- in vulnerable patients, spores germinate in colon to produce more vegetative cells which produce toxins providing symptoms of disease
- sporulation pathway initiated by bacteria creates spores which are infectious and transmissible between hospitalised patients
- spores are dormant so immune system resistant - resistant to antibiotics, disinfectant in hospital
42
Q
Incidence of C. difficiles
A
- 22.2 per 100,000
- mainly immunocompromised children with cancer - 10-30% of them get it
- transplant patients
- previously infected patients
- certain medications - antibiotics and acid suppressing agents
43
Q
Links of C.difficiles
A
- to proton pump inhibitors - gastric acid inhibits survival but suppressing it increases it
- importance of ribotype - certain ones are associated with increased antibiotic resistance, mortality rate 2-6% depending on ribotype, highest in IBD and intensive care units
44
Q
Symptoms of C. difficile infections
A
- diarrhoea
- abdominal pain
- fever
- nausea
- appetite and weight loss
45
Q
Another issue C. difficile can cause and symptoms
A
- Pseudomembranous Collitis - swelling and/or inflammation of large intestine due to overgrowth of C.difficile
- causes diarrhoea, abdominal pain, fever, dehydration
46
Q
Treatments of C. difficile infection
A
- stop taking antibiotic that is suspected to cause infection
- take antibiotics to kill C. difficile - around 10-14 day course like vancomycin or fidamoxin
- surgery is rare but can be used to remove diseased section of colon
47
Q
Relevance of C. difficile to dentistry
A
- dental practices responsible for 10% of antibiotic prescriptions
- need to help control over-prescription of antibiotics
- can use antibiotic stewardship to measure it and minimize resistance and harm in patients
- dentists can weigh up risk and benefits of antibiotics
- can live on contaminated surfaces for months/years - need to ensure they use effective disinfectants
48
Q
Pathogenicity of C. difficile
A
- have TcdA and TcdB bacterial toxins
- examples of glucosyltransferases
- toxins interact with cell surface carbohydrates, enter cells via endocytosis and inactivate small GTP-binding proteins through glucose transfer
- leads to cell death by disrupting actin cytoskeleton, tight cell junctions and causing apoptosis
- toxins induce intestinal injury and inflammation by disrupting epithelial barrier, inducing proinflammatory mediators and causing cell death, contributing to mucosal damage
