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71 Cards in this Set
- Front
- Back
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Tell me about Streptococcus?
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Gram positive bacteria, Strep A never a normal flora, Strep B is normal flora in intestines, Group D (enterococcus) normal flora of intestines.
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Which Strep is the main cause of neonatal meningitis?
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Strep Group B (agalactiae), transmission occurs during birth, in vagina from intestines.
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Which strep is normal flora of intestines, skin, vagina and URT can lead to nosocomial problems?
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Strep Group D (Enteros)
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What group of strep is a common cause of pneumonia and is normal flora of the URT?
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Strep pneumonia,
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What is the major virulence factor of Strep?
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Protein M. It prevents complement fixation, resistance to phagocytosis.
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What are some of the exotoxins of Strep?
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Streptolysin O: Not functional in Oxygen (labile). Streptolysin S: Oxygen Stable. Pyrogenic exotoxins (fever producers), only present on 25% of all strep. come from bacterioges.
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What is the Colonization, transmission, and epidemiology of Strep?
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Not part of normal flora even though often not infectious. respiratory droplets. URT and skin infections mostly in children 5-15 years old. can cause invasive disease.
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What are the clinical manifestations of Group A Strep (pyogenes)?
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Pharyngitis, Scarlet Fever (Strep throat complicated by exotoxins) with characteristic sand paper rash. Invasive disease - pneumonia. can lead to bloodstream invasion causing sepsis endocarditis.
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What group of Strep can lead to Rheumatic heart disease?
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Strep group A (pygones). Causing initially pharyngitis.
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What kind of immue hypersensitivity disorder is acute glomerulonephritis and what causes it?
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It is type 3 and caused by Strep pyogenes (group A). Originating from a pharyngitis or a skin infection.
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What bacteria causes PANDA?
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Group A Strep (pyogenes) can have symptoms of OCD, likely caused by inappropriate reaction to GAS.
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How do you initially treat Strep infections?
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Penicillin, in cases of invasive disease, use higher doses of penicillin with clindamyocin and erythromycin. Prevention: No vaccines available, prophylaxis with antibiotics to prevent sequelae.
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What is the main pathogen in the corynebacteria group?
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C. diphtheriae which causes diphtheria. A URT infection with systemic toxemia. Other bacteria in group are diphtheroids and do not cause dyphtheria and are normal flora. However, can become infectious in immunocompromised groups.
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What bacteria used to be considered corynebacteria, now no longer grouped in it?
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Arcanobacterium haemolytican which leads to pharyngitis, Beta hemolytic in blood agar can be treated with penicillin. Confused with Strep A often.
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What are corynebacterium diphtheriae's virulence factors?
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Cell wall glycolipids most important, similiar to Mycobacteria, but not acid-fast staining. They are club shaped and form Chinese characters (V and L forms).
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What is Diphtheria's Exotoxin status?
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It has a lethal exotoxin that is required for the disease state. Comes from bacteriophage genome, binds to susceptable cells, especially heart. Leads to inhibition of protein synthesis results in cell death, antibodies are completely protective, (vaccine).
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What are the most infectious bacteria?
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1. Botulinum 2. Dyphtheriae
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What is the habitat, transmission, and epidemiology of Dyphtheria?
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normal flora in non-toxigenic strains. On skin and URT. Transmitted through respiratory droplets. Historically common disease in children. "strangling angel of children". Disease not common in US or Europe, but occassional cases in adults due to waning vaccine protection. Still common in children in countries without vaccine
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What is the clinical sign of diphtheria?
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Grayish white exudate (pseudomembrane) in throat and on tonsils. Leading to respiratory obstruction in children. Bacteria stay in throat but toxins spread to heart and other organs. Neck Edema.
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Diagnosis, Treatment, and Prevention of Diphtheria?
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Grows well on standard media. Treat with antitoxin therapy (inactivates circulating toxins), Antibiotics: penicillin and erythromycin. Prevention: vaccine- made from toxoid of diphtheria toxin (immunogenic and non-toxic). DTP (DTaP at 2 months), Tdap in teens primarily for pertussis, lower does of diphtheria toxoid. Td: standard tetanus booster with a little diphtheria every 10 years.
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What are some of the gram positive bacteria?
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Strep and Corynebacterium Diphtheria
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What is gram stain is Haemophilus?
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Haemophilus is a gram negative coccobacilli. H. Influenza is responsible for URT infections like Otitis media, LRT infections (pneuomia), and Bacterial Meningitis.
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What Haemophilis strain is in HACEK causing endocarditis?
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H. Parainfluenza
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What clinical features are associated with Moraxella Catarrhalis?
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Actually classified with Nisseria, however more similiar in infection to H. Influenza. Normal URT flora, 3rd most common cause of otitis media in children, and common cause of chronic bronchitis.
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What is unique about Haemohilis and what are its virulence factors?
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Extremely hard to grow in culture. Must use special Media, with blood-derived products (factor X and V). Best at 37 C with CO2 incubator. Antigens: LPS (endotoxic, cytotoxic), Capsule (major, antiphagocytic, 6 serotypes: b most virulent). Many strains non-encapsulated, thus not infectious (nontypable). Possess IgA proteases, and may have Beta-lactamase- 25% do in US.
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What is Diphtheria's Exotoxin status?
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It has a lethal exotoxin that is required for the disease state. Comes from bacteriophage genome, binds to susceptable cells, especially heart. Leads to inhibition of protein synthesis results in cell death, antibodies are completely protective, (vaccine).
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What are the most infectious bacteria?
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1. Botulinum 2. Dyphtheriae
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What is the habitat, transmission, and epidemiology of Dyphtheria?
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normal flora in non-toxigenic strains. On skin and URT. Transmitted through respiratory droplets. Historically common disease in children. "strangling angel of children". Disease not common in US or Europe, but occassional cases in adults due to waning vaccine protection. Still common in children in countries without vaccine
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What is the clinical sign of diphtheria?
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Grayish white exudate (pseudomembrane) in throat and on tonsils. Leading to respiratory obstruction in children. Bacteria stay in throat but toxins spread to heart and other organs. Neck Edema.
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Diagnosis, Treatment, and Prevention of Diphtheria?
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Grows well on standard media. Treat with antitoxin therapy (inactivates circulating toxins), Antibiotics: penicillin and erythromycin. Prevention: vaccine- made from toxoid of diphtheria toxin (immunogenic and non-toxic). DTP (DTaP at 2 months), Tdap in teens primarily for pertussis, lower does of diphtheria toxoid. Td: standard tetanus booster with a little diphtheria every 10 years.
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What is the Habitat/transmission, and epidemiology of Haemophilis?
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Habitat: normal flora of nasopharynx (nontypable). Transmission: via airborne droplets and shared secretions. Epid: Meningitis and invasive disease most common in children bet: 6mon-2years (due to low anti-capsule antibody). Was most common meningitis in children before vaccine for strain b. Otitis medica and sinisitis are caused by unencapsulated strains
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What are the 3 most common causes of otitis media?
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1. Strep pneumoniae 2. haemophilis 3. M. Catarrhalis
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What are the clinical manifestations of surface infections with Haemophilis?
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Otitis media, sinusitis, conjuctivitis (H aegyptius), Chronic bronchitis, and pneumonia (dibilitated adults)
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What the clinical manifestations of invasive infections with haemophilis?
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Mainly type b strains: Epiglotitis, Cellulitis, Pneumonia, Systemic spread: 2 mon-2 yr, Septicemia (DIC), Meningitis (uncommon). Nontypable strains in adults from sinusitis and trauma.
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What is the dx, treat, and Prev. of Haemophilis?
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Dx: direct exam of CSF w/ gram stain, with culture on Chocolate agar. Treat: 25% maybe Beta-lactamase positive use third generation cephalosporins (Ceftriaxone and cefotaxime) for invasive disease. Prevention: Hib vaccine, purified type b capsular polysaccharide conjugated to protein. Can us Rifampin prophylaxis in high risk pop.
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What are the smallest prokaryotes capable of self replication?
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Mycoplasmas, they do not have cell walls. They have a pleomorphic shape, but possess structural features unlike amoebas. Their cell membrane has cholesterol (unusual for bacteria). Must be grown in a special media with sterols. Form fried egg colonies.
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What are the virulence factors for mycoplasmas?
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No cell wall (so no peptidoglycan, no teichoic acids, no LPS, etc). Has a P1 protein which uses to adhere to the respiratory epithelial cells. No exotoxins.
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What is the Habitat, transmission and epidemiology of mycoplasmas?
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Habitat: found in URT in absence of disease but still pathogen. Transmission: via respiratory secretions. Epidemiology: school aged children and young adults. community acquired no nosocomial disease.
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What is the clinical manifestions fo mycoplasmas?
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Respiratory disease in varying degrees. Gradual onset of pharyngitis, tracheobronchitis, ear pain (membrane infection myringitis), mild pneumonia (atypical, walking pneumonia). No invasion of tissues, stimulates inflammation on mucosal surface.
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What is the Dx., treatment, and prevention of Mycoplasmas?
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Dx: Routine culture and Gram stain both Negative. Serology is what is useful: Cold agglutinins, DNA assays. Treatment: Erythromyocin ( or newer macrolides) no cell wall antibiotics. Often resolve spontaneously. Prevention: no vaccine.
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What strains of Mycoplasma cause urogenital infections?
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M. Hominis, M. genitalium, and U. urealyticum. Opportunistic infections: common in normal vaginal flora, and urethra of sexually active men. hominis: can cause pelvic inflammatory disease. Genitalium and urealyticum are STD's may co-infect with gonorrhea and chlamydia. Cause Non-gonococcal urethritis.
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What are the two fungi that are apart of the normal human flora?
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Candida and Malazzezia yeast.
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The two Candida that are the most important clinically?
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Candida albicans and Glabrata ( is more resistant to AmphoB and azole than C. albicans).
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What are the unique characteristics of Candida albicans and its virulence factors?
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Dimorphic morphology: yeast and hyphal forms. Both in host.
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What are the habitat, transmission, and epidemiology of C. Albicans?
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Normal flora on skin, most mucosal membranes of healthy persons. Moist areas especially. Transmission: Normally from one's own flora over growing due to host's resistance lowered. Neonates from mother. Epidemiology: Very common in immune deficient pop.
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What are the clinical manifestations of C. albicans?
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They are opportunistic infections with varying ranges: mild to life threatening. Thrush (oro-pharyngeal infection), skin (form of diaper rash), nail, Urogenital infection, GI infection, and Systemic disseminated infection. Intertrigo in obese people. Vulvovaginitis is common in women, can spread to sexually active men and cause Balanitis. Diabetics and other immune depressed can get GI neoplastic diseases can lead to disseminated disease. Candidemia is 4th most common positive blood culture. Associated with fever and shock. Is the invasive, disseminated, and systemic form.
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How do you Dx, treat, and prevent C. Albicans infections?
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Dx: Direct microscopic exam. Culture is very slow. Can ID with Germ Tube, biochemical tests. Treatment is with Amphotericin B and other azoles like fluconazole, lower toxicity. Long term treatment is required (4-6 weeks). C. Glabrata: has better drug resistance so it is hard to treat. Prevention: no vaccines, only prevention of inculating suseptible patients.
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What is the Bordetella bacteria cause?
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Pertussis (whooping cough), it is a small gram-negative coccobacilli. B. Pertussis- whooping cough- humans. B. parapertussis- mild, whooping cough- like disease.
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What are the distinctive properties and virulence factors of B. Pertussis?
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LPS (endotoxin), acellular vaccine components (agglutinogens and pertactin), Fimbrial hemagglutinin (F-HA): major component of new acellular vaccines. What are some of the extracellur products? Tracheal cytotoxin: inhibits ciliated cells, triggers inflammation. Pertussis toxin: inhibits monocyte and neutrophil activation/killing, increases levels of intracellular cAMP, and another major component of new vaccine. Adenylate cyclase: inhibits monocyte and neutrophil activation/killing by increased incellular cAMP.
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What is the habitat, transmission, and epidemiology of Bordetello pertussis?
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Habitat: Nasopharynx of humans w disease, not normal flora so no carrier state. Transmission: p to p: via respiratory droplets, highly communicable. Epidemiology: Newborn is very susceptable (no maternal antibody to pass on). Increased outbreaks in older adults w. mild chronic cough. epidems every 3 to 5 years.
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What are the clinical manifestations of Pertussis?
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There is a Catarrhal stage: symptoms follow a 7 to 10 day incubation period after exposure. Mild symptoms of a an uncomplicated URT infection. Spreads from pharynx, trachea, then to Bronchi. Very infectious phase. The Paroxysmal stage is when the progression to a classical paroxysmal whooping cough occurs. Maybe life threatening in infants. Can have seizures and other infections of ear, sinuses, or lower respiratory tract. Infection may be 10x more common than we realize.
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How do you Dx., treat, and prevent pertussis?
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Culture can be done on pernasal swabs, but must be grown on modified Bordet-Gengou agar for 3 to 4 days, not sensitive. PCR is becoming more common, because of speed and sensitivity. Treatment: Erythromycin, treatment of secondary infection, and supportive care. Prevention: Vaccine: Acellular vaccine (DTaP)- contains purified F-HA, PT toxoid and minor components. Decreased effectiveness after 5 years, leads to milder disease. New! Booster Immunization= Tdap, recommended for adults and adolescents. Erythromycin prophylaxis for susceptable individuals exposed.
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Is pneumonia a common outcome of pertussis?
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No. However, can result.
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What are some of the common pseudomonas bacteria?
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Pseudomonas aeruginosa, stenotrophomonas maltophilia, Burkholderia cepacia. Pseudomonas are often found in water and soil. They are gram negative rods. Many are common only to cystic fibrosis patients and immunocompromised patients.
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What are some other pseudmonas like Gram-negative environmental pathogens?
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Aeromonas Hydrophila- common cause of wound infections contaminated with fresh water. Elizabethkingia meningosepticum- unusual cause of wound infections (water), and meningitis.
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Explain what Acinetobacter baumannii is?
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It is an emerging pathogen. Antibiotic resistance is high. Initially a compat wound in US soldiers in Iraq, transmitted via soil and water. Emerging major nosocomial problem in US hospitals. Can lead to pneumonia, UTI, woud infections, etc. Colonization not same as disease.
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What can you usually expect with unusual Gram-negative organisms?
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1. Expect to be only found in compromised hosts, surgery, or wounds. 2. Expect the source to be from the environment (usually water, hospital). 3. Expect antibiotic resistance.
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What are the distinctive properties and virulence factors of Pseudomonas aeruginosa?
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It has a capsule, it can be grown in almost any medium including antibacterial soup. It is a Strict aerobe, Cannot perform fermentation at all. Can be grown in water easily, and very resistant to chemical disinfectants and antibiotics. Cellular Antigens: LPS- (endotoxin). Capsule (glycocalyx) Slime layer- polysaccharide, antiphagocytic. Mucoid capsule= alginate, nearly exclusive for CF strains. Exotoxins and enzymes: know that they kill phagocytic cells.
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What is the Habitat, transmission, and epidemiology of pseudomonas aeruginosa?
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Habitat: Environment= water in hospital reservoirs. Transmission: hands of hospital personel and direct contact. Epidemiology: Nosocomial or community acquired disease. but needs a defect in host to cause infection.
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What are the clinical manifestations of pseudomonas aeruginosa?
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Nosocomial pneumonia: defect immunocompromised hospital patients. Acute onset pneumonia, invasive and sepsis is common, 70% mortality even with treatment, with Slime capsule (non-mucoid). Cystic fibrosis pneumonia: Defect mucocilliary clearance mechanism. Chronic progressive lung destruction, change to mucoid capsule, no bloodstream invasion. Burn or wound Defect break in skin integrity, immunocompromised as a result of the burn trauma. spreads to blood stream 80%mortality. Other wounds with green pus. UTI's= urinary catheter (direct contamination). Dermatitis: Defect=moist skin from extended exposure to contaminated water, more severe in diabetics and immunocompr.. Swimmer's ear as well. Corneal infections: defect scratch in the cornea. Endocarditis Defect: injection of Bacteria in blood (IV drug users).
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What is the Dx, treatment and prevention for pseudomonas aeruginosa?
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Dx. Culture from appropriate clinical specimens. Blood agar, other media. Based on biochemical tests. Antibiotic sensitivity testing is Critical!!! Treatment is with antibiotics it is sensitive to, very resistant to many. Monotherapy and combination therapy for life threatening infections. Prevention: cannot get rid of it in hospitals however, prohibit fresh flowers with some patients. Hand washing! No vaccines, some in research.
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What is a Legionella bacteria?
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They are gram-negative rods that grow in fresh water environments. Can cause Legionare's disease (acute pneumonia) and Pontiac fever (mild self limiting). Most caused by Legionella pneumophilia serogroup 1 (normal individuals). Other serogroups are common in transplant patients (nosocomial).
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What are the distinctive properties and virulence factors of legionella?
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Gram negative rods, stain poorly with gram-stain and other stains. Strict aerobes. Intracellular growth in human macrophages and protozoa in environment.
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What is the habitat, transmission, and epidemiology of Legionella?
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Found in fresh water surfaces all over world. Grow best in building water systems (warmer). Highest numbers in surface biofilms. Intracellular growth in amoebae and other free-living protozoa. Transmission: Inhalation of aerosols from contaminated building water sources, like water cooling towers, can travel a km or more. Community acquired disease, but no human to human transmission!! Epidemiology: Community acquired usually from cooling towers, and nosocomial from hospital water supply. about 25,000 cases a year.
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What are the clinical manifestations of legionella?
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Legionare's disease= acute pneumonia, extreme quick. Pathogenesis associated with intracellular multiplication in alveolar macrophages, monocytes. Pontiac fever- mild self-limited respiratory disease, no pneumonia or fatalities.
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How do you Dx, treat, and prevent legionella?
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Dx: Urine Antigen test usually performed, after no response to penicillin. Will only detect serogroup 1. Treatment: Erythromycin or newer macrolides, or fluoroquinolones are helpful with survival. Prevention: No vaccine, monitor and dissinfect water reservoirs.
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What are Mycobacterium?
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They are a group of rod-shaped aerobic bacteria that stain "acid-fast." They are all slow growing, taking weeks to grow in agar. Person to person transmission. Bovis is from cows, tuberculosis is humans.
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What is atypical mycobacterium?
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Free living in soil and water, growth within amoebae. Transmission only from environment. Cases increasing in AIDS patients. TB like disease in some species.
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What about related Acid-fast pathogens?
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Partially acid-fast blotchy Gram positive staining. Nocardia: long rods, filaments with branching. Can resemble TB with granulomas, and intracellular growth within macrophages. Can disseminate to brain with absesses. Rhodococcus: Short rods and cocci, chronic lung disease, common in AIDS patients.
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What are the distinctive properties and virulence factors of Mycobacterium Tuberculosis?
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Considered gram positive cell wall does not stain. Acid-fast stain. Obligate aerobe, upper lungs, growth is slow, weeks to grow on agar media. Capable of intracellular growth in macrophages. Cellular antigens: Cell wall has glycolipids (fat) containing mycolic acids, wax like. Proteins: PPD= purified protein derivative (tuberculin).
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What is the habitat, transmission, and epidemiology of Mycobacterium TB?
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Habitat: Pathogens of humans, cattle, and several other animals. Transmission: p to p. inhalation of respiratory droplets 1 to 5 um. Epidemiology: Worldwide 1/3 of world is infected. highest incidence is 20 to 40 year olds. US: 13,000 cases a year w 600 deaths. Common in those with loss of cell mediated immune response. Extremely infectious via aerosol dissemination leading to epidemic spread.
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