Flashcards in bordetella pertussis lecture 17 Deck (20):
capable of invading the respiratory tract causing pertussi or whooping cough
clinical symptoms: recurrent, violent cough that can last up to 6 weeks.
small (0.2 to 0.5 x I um), encapsulated coccobacillus
strictly aerobic, oxidase positive
bordetella pertussis tohama I: causes bronchitis and other respiratory disease.
BP virulence factors
adhesisn: filamentous hemagglutinin. Pertussis toxin (6 subunits: S1-S3, 2 S-4, S5. Pili pertactin
toxins: pertussis toxin. Invasive adenylate cyclase. Dermonecrotic toxin (lethal toxin). Tracheal cytotoxin peptidoglycan fragments. LPS: lipid A and Lipid X.
inhalation of aerosols
Bacterial adhere to ciliated epithelial cells. Toxins produced. Damage to mucosal cells or acts on neurons. Leads to paroxysmal cough
bacteria adhere to phagocytes and is ingested. Intracellular phase is unknown.
Ptx and Invasive ACase BP
S1 catalyzes ADPR rxn of Gi, leading to activate the host ACase thus causing increased level of cAMP
bacterial invasive ACase, directly activates conversion of ATP to cAMP.
Clinical presentation of BP
Incubation: 7-10 days
Catarhal 1-2 wekks: Rhinorrhea, malaise, fever, sneezing, anorexia
paroxysmal: 2-4 weeks. Repetitive cough with whoops, womiting, leukocytosis
convalescent 3-4 weeks or longer. Diminished paroxysmal cough, development of secondary complications (pneumonia, seizures, encephalopathy)
direct fluorscent antibody (DFA) test
Disadvantages: may not be specific
polymerase chain reaction
Treatment and prevention of BP
erythromycin is effective in eradicating the organisms and can reduce the duration of infectivity, however, with limited value because illness is usually unrecognized during peak of contagiousness
the introduction of the whole cell pertussis vaccine in the late 1940s led to a dramatic decline in disease incidence. Since the 1970s, however, the number of reported cases has been steadily rising. The newer accellular pertussis vaccines appear to be less efficacious than the whole cell vaccines used previously.
gram negative rod
motile with flagella
simple growth requirement
ubiquitous, soil, river, and hospitals, etc.
green fluorescent pigment (pyoverdin) and a blue pigment (pyocyanin)
Bacterial biofilms (pseudomonas aeruginosa)
exopolysaccharide matrix enclosed bacterial community, different from bacteria in suspension.
100-1000 fold more resistant to antibiotics
one of the causes for chronic infections
biofilms are ubiquitous
Biofilm formation in CF lungs
Virulence factors of pseudomonas aeruginosa
exotoxin A: similar mode of action as diptheria toxin- ADP riboslylation of EFII. controlled by transcriptional activator subject to iron regulation
exoenzyme S: may be required for dissemination from burn wounds and for tissue destruction in chronic lung infections. In vitro, it adp ribosylates several proteins (fimentin, ras). Type III secretion
elastase: breaks down elastin, collagen, immunoglobulins, complement components. ELastase rpdouction is controlled by transcriptional activator, LasR, which senses the presence of other P. Aeruginosa cells in a process called quorum sensing. Iron regulated
Phosopholipase C and heat stable phosopholipase: hydrolysis of phosoplipds leading to tissue damage
alkaline phosphatase: proteolysis leading to tissue damage
alginate: promotes adherence to respiratory epithelium, interfers with effective phagocytosis and my be immunostimulatory
type of infection pseudomonas aeruginosa
pneumonia: CF, Surgery, Trachostomy
Osteomyelitis: IV drug use, diabetic, trauma
Septicemia: Neutropenia, neonates. Burns
Meningitis: neurosurgery, neonates
endocarditis: IV drug use
UTI: kidney stones, catheterization
panophthalmitis: corneal injury (contacts)
malignant otitis extrna: diabetes
resulting from immersion in contaminated water such as hot tubs, whirlpools, swimming pools
a secondary infection in people who have acne or who depilate their legs
May become worse in cancer or immunocompormised patients. Ecthyma gangrenosa from P. aeruginosa bacteremia in neutropenic patients.
contact lenses and p aeruginosa infection
difficult to treat
Treatment of P. aeruginosa
resistant to many antibiotics
tx must be tailored to the sensitivity of each isolate and monitored frequently.
resistant strains often emerge during therapy
combination terapy: antipseudomonas penicillin, ticarcillin or piperacillin, plus an aminoglycoside, eg. gentamicin or amikacin
pseudomonas aeruginosa can create biofims)
most common genetic disease in caucasians
autosomal recessive, affecting 1 in 2500 live births in N. america
5% of white populations carry one defective gene with homozygotes expressing the symptoms of the disease
the gene is located on chromosome 7
the gene produce is called CF transmembrane conductance regulator CFTR
Cystic fibrosis 2
Mutations in CFTR are responsible for the disease
various types of mutations have been identified but also 70% of such mutations are a three nucleotide deletion resulting in a deltion of a single amino acid, delta F508.
major organs affected: lung and exocrine glands (pancrease and small intestines)
85% of CF patients are pancreatic insufficiency, 15% of them suffer from intestinal blockage (meconium ileus)
Longitudinal course of CF lung infections
S. Aureus, H. Influenzae, P. aeruginosa
P eruginosa is intrinsically resistant to all common antibiotics
clinical manifestations of CF
localized lung infections: excessive neutrophil inflitration
infection confied to and around bronchi and bronchioles
CF phenotype of PA
Biofilm, mucoid, rough LPS, serum sensitivte, low toxigenicity