illustrations of bacterial pathogenicity - respiratory tract Flashcards
p 31 - (34 cards)
what causes diphtheria?
a gram positive rod Corynebacterium diphtheriae
an extracellular toxinogenic bacterium
- an effective toxoid vaccination is used.
how is the diphtheria toxin (DTX) controlled?
carried on a bacteriophage integrated into the bacterial chromosome.
- controlled by the TF DtxR, suppresses expression when bound by iron. hence DTX produced in host as iron is low.
pathogenesis of diphtheria?
- colonisation of the nasopharyngeal epithelium
- secretes AB type toxin.
- intense local inflammation, mucosal cell damage, bacteria growth in inflammatory exudate.
- pseudomembrane formation, occludes airway and asphyxiates
- toxin can also cause irregular heartbeat, coma and death
how does the DTX work?
B part of AB binds HEGF (heparin- binding epidermal growth factor)
- toxin endocytosed. endosome acidified and disulphide bridge between A and B breaks.
- B forms a pore and the A part is released into the cell.
- A will ADP-ribosylate translation elongation factor-2 (EF-2) and block protein synthesis
what causes pharyngitis?
streptococcus pyogenes - a gram positive cocci of Lancefield group A.
- haemolytic due to production of streptolysin
- pyogenic (pus forming) that causes other acute suppurative infections (pus forming) such as tonsillitis, scarlet fever, puerperal fever, erysipelas, impetigo and in animals mastitis.
the last 3 can also be caused by staphylococcus aureus
what’s impetigo (well, the most common form)?
Impetigo contagiosa - This common form of impetigo, also called nonbullous impetigo, most often begins as a red sore near the nose or mouth which soon breaks, leaking pus or fluid, and forms a honey-colored scab, followed by a red mark which heals without leaving a scar. Sores are not painful, but may be itchy. Lymph nodes in the affected area may be swollen, but fever is rare. Touching or scratching the sores may easily spread the infection to other parts of the body
what’s erysipelas?
an acute streptococcus bacterial infection[2] of the upper dermis and superficial lymphatics
streptococci and staphylococci are?
both often called pyogenic cocci. staph aureus in particular causes opportunistic infections ie hospital acquired MRSA
how does streptococcus pyogenes colonise?
numerous adhesins. colonises throat epithelium
streptococcus pyogenes methods of spread, survival and damage?
1 - capsule - poorly immunogenic
2 - surface M protein - antigenic variation and binds complement
3 - C5a peptidase - inhibits chemotaxis
4 - streptolysins O and S - pore forming toxins (beta haemolysis)
5 - pyogenic toxins - superantigens (toxin shock syndrome)
6 - hyaluronidase - breaks down tissue
7 - streptokinase - lyses clots
8 - DNAse - depolymerises DNA in pus to reduce viscosity
later complicatind toxic shock like syndrome ons of strep pyogenes infection?
1 - rheumatic fever - heart, joint grnulomas plus fever, may caused rheumatic heart disease
2 - glomerulonephritis - type 3 hypersensitivity - AbAg complexes lodge in glomeruli
3 - necrotizing fasciitis and toxic shock like syndrome (multiorgan failure similar to LPS endotoxin)
what causes toxic shock syndrome?
staphylococcus aureus. superantigen cause. similar to strep pyogenes. secreted at site of colonisation and gets into the blood
what causes pneumonia?
an inflammatory disease often caused by strep pneumoniae
- most common cause of community acquired pneumonia
strep pneumoniae colonizaton?
adhesins for nasopharmynx, resists removal by pneumolysin (a pore ofrming toxin) that damages ciliated cells. IgA protease
strep pneumoniae migration?
to lower respiratory tract. avoids phagocytosis wit pneumolysin and its capsule. capsule prevents opsonisation and aids survival in droplets during dissemination.
strep pneumoniae damages?
lung tissue with pneumolysin primarily and also some inflammation.
legionaire’s disease?
first identified in 1976 at convention of US legion of veterans.
- typically contracted from aircon units ie a point source not propagated. any device that makes a fine mist of water droplets ie water cooler or shower head.
legionaire’s disease caused by ?
legionella pneumophila. multiples in alveolar macrophages. prevents phagosome-lysosome fusion.
stimulates cytokine release and lung damage appears to reflect a vigorous inflammatory response.
- a facultative intracellular parasite of amoebae. perhaps how it survives.
cause of whooping cough?
bordatella pertussis. acute severe disease in young children.
- diphtheria/pertussis/tetanus vaccine is effective. outbreaks due to vaccine drop. kills over 200,000 pa in the developing world.
colonisation of whooping cough?
aerosol inhalation. adhesins to respiratory epithelium (pili, pertactin, filamentous haemagglutinin (FHA)) multiplies in the mucosa.
whooping cough damage?
destroy ciliated epithelia and mucosal cells by LPS lipid A acute inflammation. plus an array of exotoxins such as pertussis toxin (adp-ribosylator) and an adenylate cyclase toxin.
pathogenesis of whooping cough?
accumilation of mucous, inflammatory cells, dead epithelia and bacteria in the airway.
- fever and bronchitis.
- this and possible toxin action on neurones promotes paroxysms of coughing. life threatening in infants with underlying cardiac/pummonary disease and can lead to neurological sequelas.
cause of pneumonic plague?
yersinia pestis. highly virulent with death of around 50% of some cities in 14th century.
over half die in 10 days. death rate closse to 100%. spreads rat to human via fleas to give bubonic plague which spreads via lymphatics (huge nodes) blood to the lungs to give pneumonic pague. can then be exhaled in droplets causing rapid person to person spread.
- necrotic lesions ie of fingers may hvae given the name “the black death”.
virulence factors of yersinia pestis?
antiphagocytic capsule, protein toxins inc injected effector proteins that subvert macrophage function. also LPS lipid A as gram negative.
