Microbiology 3: bacteria COPY COPY Flashcards
structural difference in organisation of cell contents between bacteria and eukaryotic cells
Bacteria do not have organelles (different to eukaryotes)
Outline the location of DNA in bacteria
hey just have their genetic material and ribosomes floating in the cytoplasm, as well as a cell wall
What kind of appendages coul dbacteria have? Does this affec virulence
Hypha/stalks Yes may do
Normal 3 tpes of naceria
Cocci, bacilli, spiral
List the common virulence features for bacteria
Diverse secretion systems, Flagella (movement, attachment), Pili (important adherence factors), Capsule (protect against phagocytosis) i.e. Streptococcus pneumoniae ,Endospores (metabolically dormant forms of bacteria) heat, cold, desiccation and chemical resistant i.e. Bacillus sp. and Clostridium sp. Biofilms Exotoxin Endotoxin
How does flagella and pili contribute to virulence
Flagella (movement, attachment) Pili (important adherence factors)
How does capsule contribute to virulence Example
Capsule (protect against phagocytosis) i.e. Streptococcus pneumoniae
How does endospores contribute to virulence Examle
Endospores (metabolically dormant forms of bacteria) heat, cold, desiccation and chemical resistant i.e. Bacillus sp. and Clostridium sp.
How does biofilms contribute to virulence. Examples
(organized agregrates of bacteria embedded in polysaccahride matricesi. e. Pseudomonas aeruginosa i.e. Staphylococcus epidermidis
3 types of exotoxin
Neurotoxin Enterotoxin Tissue invasive exotoxin Miscellaneous exotoxin Pyrogenic exotoxin
Outline neurotoxin wiht examples
act on nerves or motor endplate i.e. Tetanus or Botulinum toxins
Outline 2 types of enterotoxin withexamples
- Infectious diarrhea Vibrio cholera, Escherichia coli, Shigella dysenteriae and Campylobacter jejuni 2. Food poisoning Bacillus cereus or Staphylcoccus aureus
THEY ACT ON THE GI TRACT
Outline pyrogenic exotoxins
Stimulate cytokine release Staphylcoccus aureus or Streptococcus pyogenes
Outline Tissue invasive exotoxin
allow bacteria to destroy and tunnel through tissue i.e. Staphylococcus aureus, Streptococcus pyogenes Clostridium perfringens
Which enzymes might tissue invasive exotoxin involve
enzymes that destroy DNA, collagin, fibrin, NAD, red or white blood cells
Examples of miscellaneous exotoxin, and what is different about them
specific to a certain bacterium and/or function not well understood Bacillus anthracis and Corynebacterium diphtheriae
What is endotoxin released by
Only produced by Gram-negative bacteria
What is endotoxin
Not a protein but it’s the the lipid A moiety of LPS
Differentiate gram positive and gram negative
Gram +ve= big cell wall, 1 lipid bilayer Gram -ve= small cell wall, 2 lipid bilayers
What is seen on the lipid bilayer of
On the lipid bilayer of gram negative bacteria, we see LPS and sugars – these are endotoxins
What can happen if lots of the LPS is shed
Then it can cause endotoxic shock Normally shed in steady amounts
Why can giving antibiotics to gram neg bacteria be dangerous
when bacteria lyse they release large quantities of LPS/ Endotoxin Leads to septic shock
Define septic shock
Sepsis that results in dangerous drops in blood pressure and organ dysfunction is called septic shock. It is also referred to as endotoxin shock because endotoxin often triggers the immune response that results in sepsis and shock.
Differentiate endotoxin shock and septic shock
different effectors molecules in Gram-positive bacteria or even fungi can trigger this adverse immune response – so the term septic shock is inclusive (of endotoxin shock and other shocks too)
What is haemolytic-uraemic syndrome
triad of acute renal failure, hemolytic anemia and thrombocytopenia
What usually causes haemolytic-uraemic syndrome
Shiga toxin producing E. coli strain
Define outbreak
An outbreak is a greater-than-normal or greater-than-expected number of individuals infected or diagnosed with a particular infection in a given period of time, or a particular place, or both.
What are E.coli strains which release shiga toxin known as
EHEC enterohemorrhagic E. coli
Reservoirs for EHEC
reservoir are normally ruminants – mostly cattle
When does human infection with EHEC often occur
occurs through the inadvertent ingestion of fecal matter and secondary through contact with infected humans
Who does HUS affect more
usually the hemolytic-uremic syndrome is very rare in adults
What can be done with genetics in an outbreak
You can sequence the gene in the bacteria to find the virulent genes You can then do PCR on people to confirm this e.g on stool samples
Give an example of how bacteriophage transfer can cause increased virulence
E.g. EHEC contains shiga toxin causing HUS enteroaggregative E. coli (EAEC) contains 2 plasmids Baceriophage can infect the EHEC and transfer the shiga toxin genetic info to the EAEC
What 2 plasmids are contained in EAEC
pAA-type plasmids - contains the aggregative adhesion fimbrial operon ESBL plasmid - harbors the genes encoding for extended-spectrum b-lactamases (i.e. beta lactam resistant)
What is the result of transfer of EHEC to EAEC
EAHEC Now the bacteria which was aggregating and beta-lactam resistant (EAEC) also contains a shiga toxin
Composition of shiga toxin
have an AB5 subunit composition Subunit a (StxA) is non-covalently associated with a pentamer of protein B (StxB).
What is the function of subunit A and the B subunits in shiga toxin
StxA is enzymatically active domain. StxB pentamer is responsible for binding to host cell receptors.
Mechanism of subunit A action
enzyme that cleaves the 28S ribosomal RNA in eukaryotic cells ,,, inhbits protein synthesis
Why can a shiga toxin bacteria infection affect gut microbiota
Bacterial ribosomes are also a substrate for StxA and this will result in decreased proliferation of susceptible bacteria might affect the commensal microflora in the gut
Why is shiga toxin a mobile genetic element
Shiga toxins are encoded on a bacteriophage highly mobile genetic elements and contributes to horizontal gene transfer Toxins are highly expressed when the lytic cycle of the phage is activated (so that the gene can be taken up by lots of E coli)
When are shiga toxins highly expressed
Toxins are highly expressed when the lytic cycle of the phage is activated (so that the gene can be taken up by lots of E coli)
Where is EHEC and EAEC found in the GI
EHEC= large bowel EAEC= large bowel and small bowel (the new virulence of the EAHEC may have been because there was now shiga toxin in the small bowel because of shiga in EAEC)
Where is aggregative adherence fimbriae (AAF) located
genes encoding for AAF are on a plasmid mobilized between strains
Funciton of AAF
Allows binding to enterocytes AND allows binding to eachother to make biofim
What is the impact of AAF bunding to enterocytes with regard to human immune response
AAF stimulate a strong IL-8 response
What happens to the cell when AFF binds
Lead to the disruption of actin cytoskeleton leading to exfoliations
Communicable diseases occurring in Europe
1) Respiratory tract infections 2) Sexually transmitted infections, including HIV and blood-borne viruses 3) Food- and waterborne diseases and zoonoses 4) Emerging and vector-borne diseases 5) Vaccine-preventable diseases 6) Antimicrobial resistance and healthcare-associated infections
Give example of BACTERIAL resp tract infections
Legionnaires’ disease (legionellosis) Legionella pneumophila (Gram -) Tuberculosis Mycobacterium tuberculosis (Gram +)
What type of bacteria are TB and legionella pneumophilia
TB=gram +ve Legionella=gram -ve
Where is legionella pneumophilia commonly found and what is the route of infection
Lives in amoeba in ponds, lakes, air conditioning units Infection route: inhalation of contaminated aerosols
What cells are affected in humans by legionella pneumophilia
In humans L. pneumophila will infect and grow in alveolar macrophages Human infection is “dead end” for bacteria – the bacteria can’t survive here on
What virulence factor is involved in L pneumophilia
Type IV secretion system There is a large protein spanning the 2 cell membranes and cell wall allows the bacteria to secrete effector proteins inside to out They are able to survive and replicate in macrophage vacuoles, because it can release special virulence factors due to the type IV system, and
Why is TB difficult to treat
Because it is grouped with gram +ve bacteria, but it has a very different cell wall Lots of lipids attached to the cell wall
What is latent TB
M. tuberculosis can enter a dormant state Latent TB - evidence of infection by immunological tests but no clinical signs and symptoms of active disease
What is the treatment for TB
with antibiotics BUT TAKES at least 6 months
Success rate of treatments for TB
72% success rate of treatment of new cases Treatment success rate for second infection is 54% Multi drug resistant (MDR) treatment success rate in is 32%
List common bacterial STI
Chlamydia trachomatis infection Gonorrhoea Syphilis
What bugs cause gonorrhoea and syphilis
(Neisseria gonorrhoeae) and (Treponema pallidum) for syph
What type of bacteria is each of Chlamydia trachomatis Neisseria gonorrhoeae Treponema pallidum
Gram neg
Outline the replication of Chlamydia trachomatis
Obligate intracellular pathogen Cannot culture outside of cell
What is most common STI in europe
Chlamydia
What other disease can Chlamydia trachomatis cause
Other parts of the world –> Eye infection Blindness
What is the structure of Neisseria gonorrhoeae
Diplococcus (pairs of cocci, can remember as looks like two balls and gonorhea is an STI……)
What cells does N gonorrhoeae interact with
Establishes infection in the urogenital tract by interacting with non-ciliated epithelical cells
What is the important virulence of N gonorrhoeae
pili and antigenic variation escape detection and clearance by the immune system
Most common food- and waterborne diseases
Campylobacteriosis (Campylobacter sp. mostely C. jejuni) Salmonellosis (- Salmonella sp.) Cholera (Vibrio cholerae) Listeriosis (Listeria monocytogenes)
T/f shigella releases shiga toxin
Can do! Shigella dysenteriae
T/F campylobacter sp. (mainly C jejuni) is usually a cause of epidemics What is the highest risk group
F Usually sporadic cases and not outbreaks Small children 0-4 years – highest risk group
How can you acquire a Campylobacter sp. mostly C. jejuni infectin
Infection most likely through undercooked poultry
Virulence factor of Campylobacter sp. mostly C. jejuni
Adhesion and Invasion factors, Flagella motility, Type IV Secretion system, Toxin
T/f salmonella sp. is associated with outbreaks
T
Where can salmonella sp. be acquired What is main risk group
Undercooked poltry Highest infection rate in small children (0-4 years)
What is the virulence associated with salmonella sp
Type III secretion systems encoded on pathogenicity islands (SPI)
Outline type III secretion system with the bug using it
Salmonella sp. uses it I think this is the injectisome, can inject proteins into the cell SPI1: is required for invasion SPI2: intracellular accumulation
What disease does vibrio cholera cause
Cholera is an acute, severe diarrheal disease Without prompt rehydration, death can occur within hours of the onset of symptoms
Important virulence factor with vibrio cholerae
type IV fimbria cholera toxin carried on a phages
How did cholera acquire cholera toxin
It was infected with a first bacteriophage which gave it a gene to code for a receptor (type IV fimbria) The type IV fibria then allowed binding of a second bacteriophage The second bacteriopage gave the gene for the cholera toxin
How does the cholera toxin work
Binds to enterocyte Through b pentamer to the GM1 ganglioside receptor on enterocyte A/B cholera toxins cleves A1 domain from A2 domain, activating A1. A1 faragment enters cytosol, activates Gsa, continually stimulating AC to produce cAMP. High cAMP activates CFTR… efflux of ions (esp chloride) and water from infected enterocytes Leads to diarrhoea
How can cholera toxin be treated
Enkephalins bind to the opioid receptors on enterocytes, which act through G proteins to inhibit the stimulation of cAMP synthesis induced by cholera toxin, thereby directly controlling ion transport
Risk group for listeria monocytogenes
Risk group immuno-compromised, elderly, pregnant and their fetus
How does listeria infect
Listeria can enter non-phagocytic cells and cross three tight barriers Intestinal barrier, Blood / brain barrier and Materno / fetal barrier
What is special about listeria
Can infect cell to cell without exiting and then re-entering It polyermises actin using profilin *see tutorial* Important for immunology and for research
What are the bacterial emerging and vector borne diseases and hat are they caused by
Plague (Yersinia pestis; Gram-) Q fever (Coxiella burnetti; Gram –)
Which vaccine preventable diseases are bacteria
Invasive Haemophilus influenzae disease Diphtheria Invasive meningococcal disease Invasive pneumococcal disease Pertussis Tetanus
What are these vaccine preventable disease cause by and what gram type: Invasive Haemophilus influenzae disease Diphtheria Invasive meningococcal disease Invasive pneumococcal disease Pertussis Tetanus Diphtheria Invasive meningococcal disease Invasive pneumococcal disease Pertussis Tetanus
Haemophilus influenzae (-ve) Clostridium diphtheriae (Gram +) Neisseria meningitidis (gram -ve) Streptococcus pneumoniae Gram + (Bordetella pertussis Gram -) (Clostridium tetani Gram +)
Define Antimicrobial Antibacterial Antibiotic
Antimicrobial interferes with growth & reproduction of a ‘microbe’ Antibacterial commonly used to describe agents to reduce or eliminate harmful bacteria Antibiotic is a type of antimicrobial used as medicine for humans, animals originally referred to naturally occurring compounds
What are the most frequent types of HAI
surgical site infections, urinary tract infections, pneumonia, bloodstream infections and gastrointestinal infections.
What about a hospital can cause infection
Interventions Dissemination Concentration
Outline intervention as a hospital source of infection
LINES (iv, central, arterial, CVP) CHEMO CATHETERS INTUBATIN PROSTHETICS Prophylactic antibiotics Inappropriate prescribing
Outline dissemination for Hospitals as a source of infection
hospital personnel can spread infection from one patient to another
Outline concentation for Hospitals as a source of infection
there are more people with infection in the environment, increasing risk
Which pathogens ar ea major problem in hospitals Gram neg or pos
Enterococcus faecium (+ve) Staphylococcus aureus (+ve) Clostridium difficle (+ve) Acinetobacter baumanii (-ve_ Pseudomonas aeruginosa (-ve) Enterobacteriaceae (-ve)
Give examples of Enterobacteriaceae
E.coli, Klebsiella pneumoniae, Enterobacter sp.
State the drug resistance of the following Enterococcus faecium (+ve) Staphylococcus aureus (+ve) Clostridium difficle (+ve) Acinetobacter baumanii (-ve_ Pseudomonas aeruginosa (-ve) Enterobacteriaceae (-ve): -E.coli, Klebsiella pneumoniae, Enterobacter sp.
Enterococcus faecium (vancomycin resistance) Staphylococcus aureus (methicillin resistant - MRSA) Clostridium difficile (can establish infection because of previous antibiotic treatment) Acinetobacter baumanii (highly drug resistant) Pseudomonas aeruginosa (multi drug resistant i.e fluoroquinolone-resistant) Enterobacteriaceae pathogenic E. coli (multi drug resistant) Klebsiella pneumoniae (multi drug resistant) Enterobacter species (multi drug resistant)
What happens as more bacteria become drug resistant
Clinicians are forced to use older, previously discarded drugs, such as colistin, that are associated with significant toxicity and for which there is a lack of robust data to guide selection of dosage regimen or duration of therapy
Outline pathogenic e. coli
Most frequent cause of bacteraemia by a Gram-negative bacterium Most frequent cause of community and hospital acquired UTI
What is the main problem with the escape pathogens?
They are antibiotic resistant
Which antibiotics is E. coli resistant to in many countries?
Cephalosporins
Which antibiotics is E. coli still sensitive to?
Carbapenems
State the target proteins and the method of resistance to the following classes of antibiotics:
a. Cephalosporins
b. Carbapenems
c. Methicillin
d. Vancomycin
a. Cephalosporins
Target: Penicillin binding proteins (PBP)
Resistance: Extended-Spectrum Beta-Lactamase (ESBL)
b. Carbapenems
Target: PBP
Resistance: Carbapenemase enzymes
c. Methicillin
Target: PBP
Resistance: alternative target (PBP2A), which has low affinity for methicillin and can function in its presence
d. Vancomycin
Target: peptidoglycan precursor
Resistance: synthesis of a different peptidoglycan precursor
