Pathogen case studies Flashcards
Gonorrhoea info
strict pathogen, no animal reservoir
non-motile
can be grown in pure culture
needs intimate mucosal contact
syphilis info
T. pallidum - strict pathogen
spiral -flagella in periplasm
fragile + slow growing p
helped by minute tissue abrasions
CHRONIC
30-50% mortality
stages
very sensitive to penicillin - but high level needed for several weeks
STIs public health
they are linked to human behaviour - easier to control
Viagra, the pill
changes in public attitude to sex
antibiotic resistance
Gonorrhoea virulence factors
order of stage of infection
good adhesion - pili, protein II (adhesin)
capsule - avoid phagocytosis
protein I (porin protein - damage)
IgA proteases
Tbp (transferrin binding protein - nutrient acquisition)
LPS (add sialic acid - molecular mimicry of host tissue)
antigenic variation of proteins to avoid immune system
Gonorrhoea intreated leads to
pelvic inflammatory disease
infertility (infect fallopian tubes)
baby blindness
Gonorrhoea symptoms
M: thick urethral discharge, pain on urination
F: vaginal discharge, up to 50% women asymptomatic
syphilis stages
primary - chancre sores
secondary - rash fever neuro
latent - no symptoms
tertiary - gumma tumour like growth, bone, cardiac, nerve disease
how does syphilis evade the immune system
lack exo and endotoxins
invade privileged tissues, less likely to be attacked by the immune system eg. CNS, eyes, placenta
can maintain infection with few organisms
low iron requirement
lack surface antigens
chlamydia info
chlamydia trachomatis
small, wall-less
intracellular pathogen - obligate
2 cell forms of chlamydia
elementary body - survives outside the host cell - initiates infection
reticulate body - differentiates from the EB - responsible for intracellular growth
chlamydia strains D and K symptoms
M: cause urethritis
F: cervicitis
chlamydia symptoms
M: painful urination, thin water discharge
F: infection of cervix, infection of urinary tract, infertility, ectopic pregnancy
can be symptomatic in both
chlamydia treatment
beta-lactams don’t work, no PG, wall-less
tetracycline, azithromycin but have side effects
what factors lead to the emergence of “new” pathogens and re-emergence of “old” ones
globalisation and environmental change
new ways of growing and handling food
natural disasters and other breakdowns in public health eg. political
changes in pathogens eg. antibiotic resistance
recognition of “new” pathogens eg. helicobacter pylori
in 1984 h. pylori was confirmed to be the cause of most cases of…
gastritis
gastric ulcers
duodenal ulcers
some types of gastric cancer
why is h. pylori a “new pathogen”
was overlooked for decades
the key to isolating it was prolonged incubation on rich media in an atmosphere of low oxygen and increased carbon dioxide.
properties of h. pylori
spiral shaped
strict pathogen
microaerophilic
highly motile and chemotactic - polar flagella
urease enzyme to protect against stomach acid
pathogenicity island - region of the genome which encodes key virulence factors
how does h. pylori cause stomach ulcers
motility and chemotaxis
adhere and colonise
urease enzyme converts urea to ammonia - bubble of neutral pH - form microcolony
virulence factors cause damage to epithelial layer and break down mucosal layer allowing acid and pepsin to damage epithelial - pain
h. pylori key virulence factors
flagella
LPS -adherence
VacA - pore forming toxin - punch holes in cell membranes
type IV secretion system - inject protein effectors, take control of host cell
eg. CagA - models host cytoskeleton to help pathogens grow
urease
exotoxins
h. pylori symptoms
80% asymptomatic
10-15% duodenal ulcer
2-5% gastric ulcer/cancer
h. pylori treatment
2 antibiotics + drug to stop acid production: 2-3 weeks
90% successful
Legionella pneumophila – Legionnaires’ Disease
spread by air conditioning system - now biocides used
type IV secretion system
