#6 Respiratory Tract Infections III – Flashcards
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| What is causes Legionnaires' disease? |
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| Legionella pneumophila which is a rod shaped, gram negative bacteria that requires special charcoal containing medium for growth, difficult to gram-stain, flagella may be present (motile) |
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| What special requirement does L. pneumophila require for growth? |
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| Must be grown on charcoal medium, requires L-cysteine, ferric ions, and slightly acidic conditions |
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| How is legionnaires' disease transmitted? |
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| Not via person to person, is resistant to chlorine and hence survives well in the water system of buildings, usually transfered through breathing contaminated aerosolized water |
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| What are the symptoms of Legionnaires' disease? |
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| Headache, muscle ache, fever w/chills and rigors, dry cough, chest pain, shortness of breath, abdominal symptoms in some cases (diarrhea, pain, vomiting) |
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| How does Legionnaires' disease infect hosts? |
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| Confined to lungs, lodges in the alvoeli and phagocytosed by macrophages, macrophage invasion potentiator (Mip) and porin proteins binding to complement component C3b aid in phagocytosis, multiplies in the cell and released after death |
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| How is Legionnaires' disease diagnosed? |
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| Direct fluorescent antibody smears combined with culture of infected tissues (high quality specimen required), PCR and immunoassay of urine are also useful |
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| How is Legionnaires' disease prevented and treated? |
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| Prevention aimed at controlling source of infected water, beta-lactamase produced by L. pneumophila makes penicillin and cephalosporins ineffective, treated with erythromycin and rifampin |
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| What is Mycoplasma pneumoniae? |
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| The smallest known self-replicating microorganism, irregularly shaped due to lack of cell wall (making them penicillin resistant), require special medium to grow and grows slowly in aerobic conditions, grows down to make a fried egg appearance |
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| How is Mycoplasma pneumoniae transmitted? |
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| Causes pneumonia, infection is acquired by droplet spread, 2-15 day incubation, uncommon in children <6 months, does not inflict acute illness and is ambulant, hence called "walking pneumonia" |
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| What are the symptoms of pneumonia? |
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| Fever, headavhe, malaise, sore throat, unproductive cough, develops into runny nose, chest pain, earache, early symptoms are easy to overlook |
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| How does Mycoplasma pneumoniae infect hosts? |
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| Binds to bronchial epithelial cells in lower respiratory tract, binding mediated by mycoplasma protein (cytadhesin) that binds to an oligosacharride moiety on ciliated epithelial cells, interferes with ciliary action, initiates desquamation and inflammatory reaction, thickens walls of bronchioles and alveoli |
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| How is Mycoplasma pneumoniae diagnosed? |
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| Gram staining is not helpful, isolation and culture may be done in special medium but is slow, diagnosis is usually serologic, single high complement fixation of IgM-specific antibody titer is suggestive of recent infection |
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| How is Mycoplasma pneumoniae treated? |
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| Erythromycin and tetracyclin usually used, azithromycin and quinolones are also effective |
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| How is Mycoplasma pneumoniae immunity established? |
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| Local and systemic immune responses, immunity is not complete, fades within 6-12 months, reinfection is common |
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| What is Klebsiella pneumoniae? |
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| Enterobacteria (non-motile), gram negative, has large polysaccharide capsule which interferes with complement deposition, colony is strikingly mucoid |
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| What demographic is most susceptible to Klebsiella pneumoniae? |
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| Very old and very young, more prevalent among debilitated patients, colonizes the oral cavity and is often antimicrobial resistant due to readily acquiring R factors which contain transposons |
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| What are the symptoms of Klebsiella pneumonia? |
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| Cough, fever w/chills and rigors, chest pain, red gelatinous sputum (characteristic feature), mortality is high when untreated |
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| How does Klebsiella pneumonia infect patients? |
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| Via lungs from oral cavity, has virulent capsule, interferes with phagocytosis, causes host cell death and forms lung abscess, can permanently damage lung, metastatic spread to distant organs is not uncommon, can induce shock via endotoxin |
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| How is Klebsiella pneumonia diagnosed? |
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| Culture is primary method on MacConkey agar which demonstrates lactose fermentation (pink coloration of colony) |
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| How is Klebsiella pneumonia treated? |
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| No vaccine, most are resistant to penicillin and derivatives, ciprofloxacin or combination of cephalosporin and aminoglycosides are effective |
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| What is Pseudomonas spp.? |
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| P. aeruginosa is the most important strain (all other cause opportunistic infections, is an aerobic, non spore forming, gram negative rod, motile, can grow in a variety of solutions and high salt content, is faculative anerobe and can grow in a wide range of temps, produces colorful water and soluble pigments, produces flourescent yellow and blue pigment to produce green color |
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| What is the structure of Pseudomonas aeruginosa? |
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| LPS and porin proteins present on outer cell mmebrane, pili extends from cell surface and composed of repeated monomers of pilin subunits, flagelum, alginate is secreted which creates a mucoid exopolysaccharide slime layer |
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| What are the extracellular products of Pseudomonas aeruginosa? |
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| Exotoxin A, exoenzyme S, elastase, and other enzymes |
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| What is the function of exotoxin A secreted by Pseudomonas aeruginosa? |
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| Is immunogenic, enters cell via receptor mediated endocytosis, enters low pH vesicles, translocates and reaches target molecule, elongation factor-2 inactivated by ADP ribosylation, shuts down protein syntehsis and initiates cell death |
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| What is the function of Exoenzyme S secreted by Pseudomonas aeruginosa? |
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| ADP-ribosylates several intracellular proteins including cytoskeleton filament vimentin, also functions as surface bound adhesin |
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| Describe the epidemiology of P. aeruginosa |
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| Widespread, found in water, soil, and vegetation, nosocomial infections may be fatal in patients with underlying disease, may grow in humidifiers for respirators, solutions, sinks, etc, neonates and IV drug usuers at special risk |
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| Describe the pathogenesis of P. aeruginosa |
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| Infects via wound, intratracheal tube, indwelling catheter, attaches to receptors on epithelial cell surface glycolipids mediated by pilli, flagella, and the extracellular polysaccharide slime |
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| What are the virulence factors for exotoxin A, exotoxin S, and elastase? |
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| Exotoxin A is cytoxic and locally destructive, exotoxin S is destructive to cell cytoskeleton, elastin is important due to its ability to digest elastin |
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| Describe P aeruginosa immunity |
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| Not well understood, both cellular and humoral immune response is important, individuals with defective CMI responses are at high risk of developing infection |
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| How is P. aeruginosa diagnosed? |
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| Grows readily in culture, produces hemolytic colony on blood agar, oxidase positive, produce pyocyanin, grows at 43C, may have a fruit odor |
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| Describe P. aeruginosa's resistance to antimicrobials |
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| Resistant to penicillin, ampicillin, cephalothin, tetracycline chloramphenicol, sulfonamides, and earlier generations of aminoglycosides, resistance is mediated by porin proteins on cell wall restricting entry, resistance is also mediated by mutations and plasmid mediated mutations |
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| How is P. aeruginosa treated? |
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| Primarily with beta-lactam antibiotics pipracillin (w/tazobactam) and ticracillin (w/clavulanic acid) |
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| How is P. aeruginosa prevented? |
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| A vaccine is available for special group of hosts (burn patients, CF patients, immunocompromised patients) which contains somatic antigens from multiple P. aeruginosa serotypes, still very experimental |
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| What is Chlamydia pneumoniae? |
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| Obligate intracellular bacteria, lacks a rigid cell wall, has 3 species: C. trachomatis (genital infections and conjunctivitis), C. psittaci (respirator), and C. pneumoniae (respiratory) |
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| How is clamidia transmitted? |
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| C. psittaci is transmitted by birds, others by human |
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| Describe the epidemiology of C. pneumoniae |
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| Adults most affected w/past infections, important cause of bronchitis, pneumonia, and sinusitis, trasmited via respiratory secretions |
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| How is C. pneumoniae diagnosed? |
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| Difficult, must be grown in living cells (HEp2 cell line), PCR is reliable method, immunoflurosence microscopy using antibody directed against EB antigen is specific |
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| How is C. pneumoniae treated? |
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| Non preventable since bacterium is ubiquitous, treated with macrolides (erythromycin, clarithromycin, azithromycin), tetracycline/doxycycline, levoflaxin, given for 10-14 days |
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| How is C. pneumoniae and atherosclerosis related? |
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| Can grow in smooth muscle cells, endothelial cells of the coronoary artery, and macrophages, has been isolated in atherosclerotic lesions |
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| Describe the epidemiology of C. psittaci |
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| Causes psittacosis (parrot fever) or ornithosis (disease of birds), transmitted to humans via inhalation of respiratory secretions or dust from bird droppings, usually latent in natural host, seem mostly as occupational hazzard |
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| Describe the pathogenesis of C. psittaci |
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| After infecting the respiratory tract epithelium, bacteria spreads to RE cell sof the liver and spleen, multiplies at sites and causes focal necrosis, then disseminated by hematogenous route to lungs and other organs, alveolar wall thickens due to edema and cellular infiltration, mucus plugs occur in small airways |
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| What are the symptoms of C. psittaci? |
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| Fever, headache malaise, myalgia, dry cough, liver and spleen are often enlarged, occasional systemic complications |
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| How is C. psittaci treated? |
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| No vaccine, macrolide and tetracyclin are effective |
