Bacteria Chapter 22-18-19 Helicobacter- Pseudomonas - Bordetella - Corynebacterium Flashcards
describe helicobacter pylori
- gram negative vibrio
what chemical reaction does helicobacter pylori cause
urea + H2O -> CO2 + ammonia
what are the virulence factors for helicobacter pylori and what do they do
-urease: urea-> ammonia -> pH increase, neutralization of stomach acid
- VacA: protein that acts on gastric mucosal epithelia and promotes flow of urea into stomach
- CagA: protein injected into host epithelia -> cells change
- mucinase
- flagella
how do organisms survive the acidity of stomach juices
by producing a powerful urease
- upon reaching the layer of mucus they penetrate to the epithelial surface where bacterial products incite an inflammatory response
- thinning of mucus layer occurs and 10 to 20% of infected individuals develop ulcerations
- only small percentage develop cancer but more than 90% of individuals with stomach cancers are infected with H pylori
how are gastric ulcers treated
- no preventative
- 2 antibiotics plus a medication to suppress stomach acid
what is the initial infection immune response of gastric ulcers
IgM followed by IgA and IgG which suppresses bacterial growth and leads to the typical low level persistent infection which remains symptom free for 80-90% of carriers
what are the symptoms of helicobacter pylori
no symptoms in most people
describe pseudomonas aeruginosa
gram negative rods
- polar flagella
- obligate aerobe
- simple nutrient requirements
- broad temperature range 20-43 Celcius
how are pseudomonas aeruginosa cells arranged
pairs
what are the virulence factors for pseudomonas aeruginosa
- alginate: adherence, protection from dehydration and immune evasion
- lipopolysaccharide: lipid A is endotoxic; core interacts CFTR; O antigen protects from complement- mediated killing
what is alginate’s possible contribution to virulence
biofilm formation
describe opportunistic pathogens
-common in environment
- resistance to many chemical disinfectants
- R-plasmid based resistance to many antibiotics
what types of pathogens are major problems in hospitals
opportunistic pathogens in nosocomial infections
where are opportunistic pathogens seen in hospitals
- lungs: artifical ventilators, cystic fibrosis
- skin: burn victims, folliculitis
- bladder infections
- ear infections
- eye infections
what characterizes pseudomonas aeruginosa
soluble blue green dye pyocyanin and pyoverdin
describe the clinical features and epidemiology for pseudomonas aeruginosa
- pulmonary (CF patients)
- nosocomial infection
what are the antibiotic resistance mechansisms for penicillins, aminoglycosides, chloramphenicol, fluoroquinolones
- penicillins: beta lactamase, altered binding or uptake
- aminoglycosides: hydrolysis, altered uptake
- chloramphenicol: hydrolysis, altered uptake
- fluoroquinolones: change in DNA gyrase, altered uptake
describe bordetella pertussis
gram negative
- strict aerobe
- non motile, capsule
what illness is caused by bordetella pertussis
whooping cough
what does Bordetella pertussis show
dense surface growth in the lower respiratory tract (bronchi and bronchioli) without cell invasion and with strong mucus secretion
what is the virulence factors in whooping cough
- adhesion to ciliated respiratory tract cells but NOT invasive
- toxins
what toxins are virulence factors for pertussis
- pertussis toxin ptx
- secreted invasive adenylate cyclase/hemolysin
- tracheal cytotoxin: NO release
what does pertussis toxin ptx do
ADP-ribosylation of G protein: cAMP increase -> increase mucus and other secretions
what does secreted invasive adenylate cyclase/hemolysin do
increase cAMP
what does tracheal cytotoxin do
-NO release
- kills ciliated cells
-toxin is a component of peptidoglycan
what is the bordetella pertussis treatment and epidemiology
- DTaP vaccine
- aerosol transmission, children’s disease, mild symptoms in adults who are the resevoir
describe corynebacterium diptheriae
- gram positive pleiomorphic rods
- opportunistic pathogen
- oral pathogen with systemic effects
what are the characteristics of diptheria and mechanism of action
- pseudomembrane in the throat, heart, kidney damage
- inhibits protein synthesis by inactivation an elongation factor of eukaryotic cells. kills local cells in the throat but can also be carried in the bloodstream to various organs
what chemical reaction is caused by diptheria
NAD + EF2 -> ADP ribose EF2 + nicotinamide
what are the virulence factors for diptheria
-throat adhesion
- diptheria toxin (ADP ribosylation of EF2 causing translation to stop)
what are local and systemic disease risks from diptheria toxin
local: suffocation and paralysis - impaired swallowing, peripheral neuritis
systemic: cardiac arrhythmia and kidney failure
what is the treatment and epidemiology for diptheria toxin
- prevent by toxoid vaccination
- spread by saliva droplets
what illnesses does the DPT vaccine protect against
-diptheria
- pertussis (whooping cough)
- tetanus
