Bacteria Flashcards
Cell
Basic unit of life
2 groups based on cellular organisation
Prokaryotes - bacteria
Eukaryotes - Animals, plants, fungi, algae
Why isn’t a virus a group?
It relies on the host’s molecular mechanism
What bacteria does not have a cell wall?
Mycoplasmas - obligates intracellular parasites
Function of cell wall
Define shape, gives rigidity + resists turgor pressure
Cell wall made up of?
Semi - rigid wall composed of peptidoglycan (murein)
Mycobacteria
Cell wall rich in mycelia acid + PDC
What bacteria takes up more gram stain?
Gram-positive
Transpeptidation
process of cross-linking peptidoglycan chains
What does PDC monomer consist of>
NAG = N-acetylglycosamine NAM = N-acetylmuramic acid
What binds NAG + NAM?
Glycosidic acid
Gram-positive
Thickest bacterium = many interconnecting layers of peptidoglycan (20-80nm)
Teichoic + Lipoteichoic acid is embedded in wall
- they help movement of molecules in + out bacterium
Various protein embedded
- Adhesins = adhere to host
- Enzymes = damage host tissues
- Invasins = invade host cells
Cocci
Gram-negative
Thinner bacterium - get layers of PDC (2-3nm)
Outer membrane = rich lipopolysaccharide (LPS)
- LPS linked to PDC by lipoprotein anchor
various proteins in outer membrane
What has an acid fast wall cell wall
Mycobacterium (gram-positive)
What stain does mycobacterium take up?
Ziehl-Neelsen stain
Function of Mycolic acid
Disrupt entry of molecules causing slow growth, giving greater resistance to chemical agents + enzymes
Unique chemical structures in prokaryotic cells
- Fimbriae/pili
- Capsule/slime layers
- Flagella
Fimbriae/pili
involved in attachment of surfaces - other cells
- mainly gram-negative
- coated with proteins
- communication + exchange of genetic information
Capsules/slime layers
Protection from immune evasion (phagocytosis) + attachment
- Biofilms
Biofilms
Collection of microorganism surrounded by the slime they secrete - attached to inert/living species
Flagella
Cells swim through environment
Endospores
major source of infection - produced when starved or adverse environment
Exists in state of dormancy - persist for long periods of time
Highly resistant to extreme pH, temperature, radiation, desiccation, chemical agents
not all gram-positive bacteria form spores
What bacterium form spores?
Bacillus anthraces
Bacillus cereus
Clostridium difficile
Clostridium tetani
Bacterial microflora
The bacteria all over the body may not be damaging but protective or beneficial.
Also called microbiome + commensal bacteria
- tend to be low virulence
- loose interaction with epithelial surfaces ( Skin, GI tract)
- essential for normal wellbeing
- kept in balance by host immune responses
- reduce risk of colonization by pathogenic bacteria
Exotoxin pathogenicity
made by bacteria + secreted out f the bacterium
produce local/systemic infections
different types
Bacteria secrete enzymes + molecules which
- damage immune response molecules
- damage cell + tissue
Different types of exotoxins
Cytolytic toxins - damage cell membrane
A-B toxins - disrupt protein synthesis
Super antigen - activation of T cell response in antigen absence / diversion of immune response
Different types of exotoxins
Cytolitic toxins - damage cell membrane
A-B toxins - disrupt protein synthesis
Super antigen - activation of T cell response in antigen abscence / diversion of immune response
Endotoxins pathogenicity
Lipopolysaccharide in gram-negative (released upon lysis of bacterial cell) + contains - lipid A - core polysaccharide - O-polysaccharide Endotoxins cause: - immune system activation - fever/diarrhoea - release cytokines - inflammation
What has a similar response as endotoxins pathogenicity?
Teichoic acids in gram-positive
Environmental changes where microbes are found to cause bacterial infections
Invasion of wound
Antibiotic therapy
Nosocomial infections
Latrogenic infections
Incidental exposure to cause bacterial infections
GI infections - E.coli - Campylobacter - Vibrio Cholera Person-person - Neisseria meningtidis - Chlamydia trachmatis - Mycobacterium tuberculosis - Neisseria gonorrhoea Environmental - Clostridium retain lives in soil - Legionella = failure to maintain air condition
How do we identify?
Samples
Methods
Methods of identification
Microscopy, culture, serology, molecular
Samples of identification
Timing, biopsy, environmental, body fluids, collection/transport
Symptoms of infection depend on
1) Site of infection
2) No. of pathogens/site of inoculums
3) ability of pathogens to colonise host
4) Virulence factors produced toxins
5) Ability to evade immune response
6) Age/condition of host
Asymptomatic carriers
Carry pathogenic bacteria but no sign of disease
Infectiousness
Ease of spread in a population
Pathogenicity
Ability to cause disease
Pathogenicity factors
e.g. adherence, colonisation, invasion, toxins
Virulence
Power to cause severe disease e.g. toxin, resistance
Intoxication/food-poisoning
Ingestion of bacterial-derived toxin, often in absence of bacterium e.g. toxin in/on food
Infection
Microorganism established, growing and/or spreading on or within host
Attached to each NAM is…
5 amino acids
- but 1 amino acid is removed during assembly = NAM-tetrapeptide
How to reduce risk of colonization by pathogenic bacteria
Modify local pH
Block host binding sites
Secrete toxic metabolites
What can start a systemic cellular responsed
Bacterial derived toxins
Disease
Recognisable + defined damage/injury to host that impairs host function
Biological agent
Any microorganism, cell culture or toxin able to enter human body + cause harm
Typing of E.coli strain O157:H7
Entero-haemorrhagic E.coli
170 O antigens (LPS)
100 K antigens (Capsule)
50 H antigens (Flagella)
How can bacterial infections arise
Incidental exposure/poor or inadequate hygiene/precautions
- GI infections
- person - person
- Environmental
Environmental change where microbe is found
- Wound invasion
- Antibiotic therapy
- Nosocomial infections
- Latrogenic (caused by doctors) infection
How does Clostridium difficile spread
Poor hygiene + inadequate disinfection
How can resistance arise in Clostridium difficile
Inappropriate use of antibiotics + some bacteria have natural resistance (waxy cell wall of Mycobacteria disrupt entry of antibiotics)
Routes of entry of into host, cycling + transmision
1 )Exposure
2) Adherence
3) Invasion
4) Colonisation + growth
5) Toxicity 6) Tissue damage + disease
5) Invasiveness 6) Tissue damage + disease / further exposure back to (1)
Cytolytic toxin
Disrupt cell membrane
A-B toxins
disrupt protein synthesis
Super-antigen toxins
activate T cell response in antigen absence
