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1

Bordetella pertussis

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

nonfermentative

gram- rod

nutrionally fastidious

bordetella pertussis tohama I: causes bronchitis and other respiratory disease.

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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.

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Pathogenesis BP

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.

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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.

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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)

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BP diagnosis

direct fluorscent antibody (DFA) test

advantages: fast.

Disadvantages: may not be specific

polymerase chain reaction

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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.

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Pseudomonas aeruginosa

gram negative rod

non fermenter

motile with flagella

aerobic

simple growth requirement

ubiquitous, soil, river, and hospitals, etc.

green fluorescent pigment (pyoverdin) and a blue pigment (pyocyanin)

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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

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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

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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

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Pseudomonas folliculitis

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

fingernail infection

May become worse in cancer or immunocompormised patients. Ecthyma gangrenosa from P. aeruginosa bacteremia in neutropenic patients.

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contact lenses and p aeruginosa infection

hemolysin

difficult to treat

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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

15

Cystic fibrosis

pseudomonas aeruginosa can create biofims)

bilateral bronchopneumonia

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

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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)

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Longitudinal course of CF lung infections

S. Aureus, H. Influenzae, P. aeruginosa

P eruginosa is intrinsically resistant to all common antibiotics

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clinical manifestations of CF

localized lung infections: excessive neutrophil inflitration

infection confied to and around bronchi and bronchioles

malnutrition

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CF phenotype of PA

Biofilm, mucoid, rough LPS, serum sensitivte, low toxigenicity

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Alginate

D-mannuronic acid and L guluronic acid