Slide Deck 2 Flashcards
What is the disease? What does it look like? Patients who die with this disease typically die from?
Corynebacterium diphtheria (you can see pseudomembranous pharyngitis, gray-white membrane)
asphyxia or cardiomyopathy (the cells get killed)
How does the shown bacteria cause its efffects.
What characteristic in this picture helps you reocgnize it?
ADP-ribosylation of Elongation Factor 2, inhibiting protein synthesis
Metachromatic granules (blue and red),
They form irregular, club-shaped or V-shaped arrangements in normal growth. They undergo snapping movements just after cell division, which brings them into characteristic forms resembling Chinese letters or palisades.
How do you treat diphtheria patients? How do you prevent it?
Prevent with DTaP, toxoid vaccine Diptheria, Tetanus, and acellular Pertussis
treat with antitoxin
Bordatella pertussis, or whooping cough, is fatal for 1% of infants–but they don’t have the musculature that is conducive for hearing characteristic whooping cough. How do we diagnose them? (Three ways) What are the characteristics of the illness?
- culture isolation on Bordet-Gengou agar, up to 2 weeks after onset
- positive PCR test from nasopharyngeal swab, up to 4 weeks after onset
- serological test (anti-pertussis toxin antibodies, 2-12 weeks after onset)
cough illness lasting more than 2 weeks with a) paroxysms of coughing, b) inspiratory whoop c) posttussive vomiting, or d) apnea (infants)
What does bordatella pertussis do to infants that is responsible for why it can be fatal?
It causes necrotizing bronchiolitis. extreme lymphocytosis: pulmonary hypertension, respiratory failure, and death. Antibiotics can’t treat it because by then it’s already within the cell–only preventative measures
During which of the four clinical stages: incubation, catarrhal (malaise, fever, anorexia, sneezing), paroxysmal (whooping cough), and convalescent (less coughing, complications), do we see the highest bacterial load? What is the ramificaiton of this?
catarrhal – no cough, so you don’t even know the patient has whooping cough! then it spreads so rapidly (via respiratory droplets)
B. pertussis is a __ (aerobic/anaerobic, Gram ____, ____ (shape). If it does not contain the pertussis toxin, which functions by ______, then it will be called B. parapertussis and be associated with milder whooping cough symptoms.
B. pertussis is an aerobic Gram negative coccobacilli. If it does not contain the toxin, which functions by inhibiting Gi via ADP ribosylation, blocking cAMP and pro-inflammatory cytokine production, then it will be called B. parapertussis and be associated with milder whooping cough symptoms.
Does the acellular pertussis vaccine work?
It protects against severe disease, but not against transmission or colonization (neithe does the whole cell pertussis vaccine, which was removed from the market because protesting mommies were full of wrong data). However, aP is less effective than wP.
What is the natural habitat for legionella pneumophila, and how is it transmitted?
aquatic bodies: it only transmits from aerosol from water bodies, not from person-to-person!
What is happening here, and what is it a sign of?
Coiling phagocytosis: Legionella pneumophila enters macrophages in this manner
What type of pneumonia would make you suspect legionella pneumophila, and what agar would you use to culture? On culture, you see gram _____ ___ (shape).
Until the 3-5 days before you see visible colonies, what lab diagnosis can you use?
single lobar pneuomnia, hyponatremia, associated with neurologic systems, fever
grow on charcoal, use a silver stain, will be gram negative bacilli
Urinary antigen detection, direct fluorescent antibody staining, ELISA
What are the major causes for ventilator associated pneuomonia?
Pseudomonas aeruginosa (20-40%), S. aureus/MRSA (15-30%)
What drugs do you use for ventilator acquired pneumonia suspicion?
Antibodies that bind to ____ has promise to control pseudomonas aeruginosa
PcrV
If you see slime-producing strains in cystic fibrosis patients, this makes you suspicious of ____. Why does this disease targets CF patients, and what age of those patients?
Pseudomonas Aeruginosa
>5yo
Several hypotheses related to the underlying molecular defects in CF have been suggested to explain this high rate of prevalence. These include abnormalities of airway surface liquid leading to impaired mucociliary clearance or malfunction of antibacterial peptides, increased availability of bacterial receptors, reduced ingestion of pathogens by CF cells and impaired defence related to low levels of molecules such as nitric oxide or glutathione. Further work is needed to identify which of these mechanisms is important in the early stages of infection. Once the organisms have gained a foothold in the CF airway they have a wide array of properties that enhance their survival and allow them to evade host defences and antibiotic agents successfully. Conversion to mucoidy and the formation of biofilms are two of the main mechanisms by which this is achieved.
