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79 Cards in this Set
- Front
- Back
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What are general characteristics of the Enterobacteriacaea family of bacteria?
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G- bacilli
glucose fermentors oxidase negative reduce nitrate to nitrites |
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What are the three antigens used to classify strains of Enterobacteriaceae?
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O-antigen - LPS
H-antigen - flagella K-antigen - capsule |
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Enterobacteriaceae species can be split into 2 groups: lactose fermentors and lactose non-fermentors. What are the species that occupy these 2 groups?
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Lactose fermentors - CEEK
Citrobacter Enterobacter Escherichia Klebsiella Lactose non-fermentors - ShYPS Shigella Yersinia Proteus Salmonella |
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What virulence factors are shared by all the Enterobacteriaceae?
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Endotoxin (Lipid A of LPS) - causes overproduction of cytokine resulting in endotoxic shock
Capsule - interfere with binding of antibody and action of complement Antigenic phase variation - altered expression of various H or K antigens Siderophores - iron-chelating protein to acquire iron, which is essential for bacterial growth Exotoxins - exported from bacterium and can alter specific cell function leading to disease Type III secretion systems - directly inject bacterial proteins into host cell cytoplasm, secreted proteins have cytopathic activities |
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What are the subtypes of E.coli and what diseases do they cause?
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UPEC (Uropathogenic E.coli) - cystitis (bladder infections) and pyelonephritis (kidney infections)
MNEC (meningitis associated E.coli) - neonatal meningitis ETEC (Enterotoxigenic E.coli) - traveler's diarrhea EPEC (Enteropathogenic E.coli) - childhood diarrhea EHEC (Enterohemorrhagic E.coli) - bloody diarrhea EIEC (Enteroinvasive E.coli) - diarrhea similar to invasive Shigella EAEC (Enteroaggragative E.coli) - persistent diarrhea in children, traveler's diarrhea |
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What is the mechanism of pathogenicity of UPEC?
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UPEC = Uropathogenic E.coli
Adhesins bind to bladder (Type I pili) and kidney (P pili) to initially colonize and protect bacteria from being flushed away during urination alpha-hemolysin - this exotoxin forms a pore that disrupts the plasma membranes of cells |
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What is the mechanism of pathogenicity of MNEC?
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MNEC = meningitis associated E.coli
75% of isolates have K1 capsular antigen Adhesins - IbeA and OmpA facilitate adherence and invasion of endothelial cells, facilitating crossing of blood-brain barrier Serum resistance - OmpA interacts with complement binding protein to protect bacteria from complement mediated killing |
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What is the mechanism of pathogenicity of ETEC?
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ETEC = Enterotoxigenic E.coli
cause of most Traveller's diarrhea spread through food and water contaminated with human waste incubation of 24-72 hours colonize epithelium of small intestine and deliver exotoxins that elicit diarrhea Exotoxins: Heat labile toxin (LT) - plasmid encoded A-B toxin that causes secretory diarrhea by increasing intracellular cAMP levels Heat stable toxin (ST) - small plasmid encoded peptide that stimulates guanylate cyclase in gut epithelial cells resulting in secretory diarrhea from increased intracellular cGMP Adhesins - colonization factor antigens (CFA/I, CFA/II, CFA/III) are fimbriae important for adherence to jejunum and ileum epithelial linings |
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What is the mechanism of pathogenicity of EPEC?
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EPEC = Enteropathogenic E.coli
cause of childhood diarrhea in developing countries bacteria bind to intestinal epithelial cells and disrupt overlying mucous gel, causing fever and bloody diarrhea colonize epithelium of sm.intestine and subsequently destroy microvilli Adhesins: Bundle-forming pili (BFP) - responsible for initial attachment to the intestinal epithelium Type III Secretion (T3SS) - responsible for attachment and effacement lesions, loss of microvilli structure, pedestal formation at point of bacterial attachment, secretes Tir protein that inserts into host cell membrane and acts as a receptor for intimin, enabling tight adherence |
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What is the mechanism of pathogenicity of EHEC?
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EHEC = Enterohemorrhagic E.coli
causes bloody diarrhea, abdominal pain, but no fever or only low-grade fever; in 10% of cases leads to hemolytic-uremic syndrome (HUS) most frequent serotype is O157:H7 cattle are reservoir - infection acquired from ingesting undercooked meat, unpasteurized milk or juices Adhesins - Type III Secretion System (T3SS) forms attachment and effacement lesions Exotoxin - Shiga-like toxin is an A-B subunit toxin that inhibits protein synthesis, often the cause of HUS |
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How is E.coli diagnosed?
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growth on routine media
differentiate from other Enterobacteriaceae by biochemical tests ETEC cannot be practically diagnosed microbiologically because it is difficult to differentiate from commensal E.coli EHEC can be differentiated from commensal E.coli because EHEC does not ferment sorbitol |
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How are E.coli infections treated?
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ETEC - rehydration, tetracycline/doxycycline, TMP-SMX, bismuth subsalicylate, ciprofloxacin
EHEC - no antibiotics because they increase incidence of HUS |
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What are the general characteristics of Salmonella?
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G- bacilli with flagella
facultative intracellular pathogen common cause of diarrhea causes 15% of food-borne illnesses in US reservoirs are farm animals, chickens, turtles, other reptiles |
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What bacteria causes typhoid fever?
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Salmonella enterica serovar typhi
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What are the mechanisms of pathogenicity of Salmonella enterica?
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secrete Salmonella pathogenicity island 1 (SPI-1) type III secretion system in intestines to induce ruffling on surface of enterocytes, leading to bacterial internalization
within enterocytes, bacteria survive and multiply in phagosomes SPI-2 type III secretion system aids in dissemination of Salmonella to bloodstream |
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What is the clinical presentation of a patient infected with Salmonella enterica?
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diarrhea, nausea, vomiting occur 24-48 hours after ingestion
usually self-limited, lasts 7 days fever occurs in 50% of cases Typhoid fever - prolonged fever, persistent bacteremia, constipation or diarrhea |
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How is Salmonella infection diagnosed?
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Growth in agar with routine stool culture
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How is Salmonella infection treated?
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Diarrhea need not be treated unless immunocompromised patient or severe infection
Typhoid fever and bacteremia treated with antibiotics |
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What are the general characteristics of Shigella?
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G- bacilli
4 important species: S.dysenteriae S.flexneri S.boydii S.sonnei Causes dysentery - cramps, painful straining to pass stood, frequent bloody mucoid stools |
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What are the medically important species of Yersinia?
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Yersinia enterocolitica - causes infectious diarrhea due to consumption of contaminated milk, meat, or water
Yersinia pseudotuberculosis - causes infectious diarrhea, bacteria can spread to mesenteric lymph nodes Yersinia pestis - cause of the bubonic plague |
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What are the mechanisms of pathogenicity of Yersinia pestis?
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once in bloodstream, bacteria travel to nearest lymph node
bacteria in lymph node leak into bloodstream, where cell lysis releases LPS endotoxin causing septic shock Adhesins - Ail, chromosomally encoded T3SS on plasmid confers resistance to phagocytosis via secretion of effector proteins that intoxicate host cell: YopE - disassembly of actin cytoskeleton YopH - dephosphorylation of proteins required for phagocytosis YopJ/P - causes apoptosis of phagocytes Fra1 - antiphagocytic protein that forms part of a capsule around Y.pestis |
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What clinical diseases are caused by Yersinia pestis?
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Bubonic plague - transmission from rats via flea bites, 2-6 day incubation period, bubo develops near site of flea bite, becomes progressively enlarged, painful, and erythematous, 75% mortality
Pneumonic plague - aerosol spread from person to person, 1-4 day incubation period, sudden onset of chills, fever, headache, myalgias, weakness, productive cough, dyspnea, 90% mortality Primary septicemic plague - direct inoculation of organism into bloodstream, nausea, vomiting, diarrhea, abdominal pain |
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How is Yersinia pestis diagnosed?
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blood cultures
bubo aspirates and sputum samples grow on sheep blood agar Giemsa stain - characteristic bipolar appearance (closed safety pins) |
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How is Yersinia pestis treated?
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streptomycin
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What are general characteristics of Klebsiella?
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plump G- bacilli
prominent capsule causes mucoid appearance of isolated colonies 2 medically important species: K.pneumoniae K.oxytoca opportunistic pathogens cause community-acquired pneumonia, UTI, sepsis, wound infection |
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What are the mechanisms of pathogenicity of Klebsiella?
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LPS
Pili for adherence Polysaccharide capsule prevents complement deposition and phagocytosis |
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Why is Klebsiella difficult to treat?
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often very resistant to antibiotics
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What are some general features of Enterobacter, Citrobacter, and Serratia marcescens?
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part of Enterobacteriaceae family
cause nosocomial respiratory infections, UTIs, abdominal infections often resistant to beta-lactam antibiotics, especially cephalosporins |
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What are general features of Proteus?
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common cause of nosocomial and community-acquired UTI
2 important species: P.mirabilis P.vulgaris contains urease that splits urea into ammonium hydroxide, causing increase in urine pH and promoting formation of struvite kidney stones hundreds of flagella per cell cause hypermotility |
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What are general features of Pseudomonas?
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G- bacilli
aerobic 4 medically relevant species: P.aeruginosa P.fluorescens P.putida P.stutzeri |
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What diagnostic test can distinguish Pseudomonas from Enterobacteriaceae?
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Catalase test - Pseudomonas is catalase positive and Enterobacteriaceae is catalase negative
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What are some general features of P.aeruginosa?
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live in moist environments
capable of growing in many different organic compounds opportunistic common cause of nosocomial infection |
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What are the mechanisms of pathogenicity of P.aeruginosa?
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pili at end of bacteria function as adhesins
capsule of P.aeruginosa in CF patients convers to mucoidy phenotype, these cells overproduce alginate, an exopolysaccharide that is antiphagocytic exotoxins - Exotoxin A acts similarly to diphtheria toxin - ADP ribosylates EF-2 and disrupts protein synthesis LasA and Las B (elastase) are two proteases that act to degrade elastin T3SS - transfers up to 4 effector proteins (ExoS, ExoT, ExoU, ExoY) into host cells causing disruption of actin cytoskeletons and/or cell lysis endotoxin |
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What bacteria colonizes a majority of adult CF patients and what disease does it cause?
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P.aeruginosa
pneumonia |
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What clinical diseases are caused by P.aeruginosa?
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Pneumonia in CF patients
nosocomial pneumonia in ventilated patients bacteremia and sepsis in cancer patients skin infections in burn patients catheter associated UTIs skin lesions called ecthyma gangrenosum hot tub folliculitis |
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How can P.aeruginosa be diagnosed?
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grows on many types of lab media
produces grape-like odor produce fluorescent pigments oxidase positive |
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How is P.aeruginosa treated?
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P.aeruginosa has intrinsic and acquired resistance to multiple antibiotics
aminoglycosides used in conjunction with an agent active against bacterial cell walls (piperacillin, ceftazidime, imipenem, aztreonam) |
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What are general properties of Legionella?
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thin G- bacilli
aerobic L.pneumophila is most medically significant species |
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What are general features of L.pneumophila?
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cause of Legionairre's Disease
inhabits natural bodies of water as well as cooling towers where they parasitize amoebae greater than 10 serogroups exist, but serogroup 1 causes 80% of disease facultative intracellular pathogen primarily infects macrophages |
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What are the mechanisms of pathogenicity of L.pneumophila?
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attaches to macrophages and provokes coiling phagocytosis - formation of long thin pseudopod by macrophage that wraps around bacterium and engulfs it in a coiled vesicle
dot genetic locus (defect in organelle trafficking) - necessary for blockage of phagolysosome fusion and ribosome recruitment |
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What are the clinical diseases caused by Legionella pneumophila?
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transmission via aspiration of water or inhalation of aerosol, no human-to-human transmission occurs
nosocomial and community-acquired pneumonia opportunistic infection - immunocompromised, smokers, alcoholics, and elderly are more susceptible high fever, respiratory symptoms, headache, change in mental status, nausea, vomiting, diarrhea, hyponatremia (low blood sodium) |
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How can L.pneumophila be diagnosed?
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Dieterle silver staining
poorly stained by Gram staining grows on buffered charcoal-yeast extract (BCYE) agar, which contains L-cysteine, a required AA direct fluorescent antibody (DFA) test Urinary antigen test - detects only L.pneumophila serogroup 1 |
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How is L.pneumophila treated?
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high dose of erythromycin - associated with side-effects
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What are general characteristics of Vibrio?
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G- comma-shaped rod
infections spread via exposure to seawater 3 medically important species: V.cholerae - causes cholera, a severe form of diarrhea V.parahaemolyticus - causes gastroenteritis V.vulnificus - causes gastroenteritis and wound infections in cuts exposed to seawater |
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What are some general characteristics of Campylobacter jejuni?
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curved G- rod
frequent cause of gastroenteritis leading to diarrhea most common bacterial enteric pathogen in the world |
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What are general characteristics of Helicobacter pylori?
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G- curved rod
grows best under microaerophilic conditions (low oxygen) possibly the only pathogen of the stomach |
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What properties of Helicobacter pylori enable it to survive in the stomach?
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acid inhibitory protein - blocks production of acid secretion
urease - splits urea into ammonium hydroxide to raise pH, creating an alkaline microenvironment for the organism |
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What are the mechanisms of pathogenicity of Helicobacter pylori?
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acid inhibitory protein blocks acid secretion
urease creates alkaline microenvironment flagella allows motility through mucous that lines the stomach, facilitating adherence to gastric epithelial cells exotoxins - VacA, a cytotoxin, causes vacuolation of cultured epithelial cells Type IV secretion - effector proteins transferred directly to cells, stimulating inflammation |
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What clinical diseases are associated with Helicobacter pylori?
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infection usually asymptomatic
gastric inflammation peptic ulcer disease risk factor for adenocarcinoma, non-Hodgkin's lymphona, low-grade B cell mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach |
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How is H.pylori diagnosed?
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histologic examination of tissue biopsy obtained via endoscopy
Giemsa or silver stains Urease test - biopsy specimens assayed for urease activity Urea breath tests - pt drinks radio-labeled urea solution, presence of urease causes exhalation of radio-labeled CO2 serological tests for IgG |
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How are H.pylori infections treated?
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2 popular regimens:
Bismuth subsalicylate + tetracycline + metronidazole Omeprazole (PPI) + clarithromycin + metronidazole |
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What are general characteristics of Haemophilus?
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small G- coccobacilli
facultative anaerobe 2 medically important species: H.influenzae - causes otis media, sinusitis, bronchitis, epiglottitis, pneumonia, meningitis H.ducreyi - causes STD similar to syphilis |
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What are general characteristics of Bordetella?
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tiny G- coccobacilli
strict aerobes 3 important species: B.pertussis - causes whooping cough B.parapertissus - causes less severe respiratory disease in humans B.bronchiseptica - causes mild disease in animals |
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What are the mechanisms of pathogenicity of Bordetella pertussis?
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adhesins - pili and filamentous hemagglutinin (FHA) allow adherence to ciliated epithelial cells in upper airway
FHA binds galactose residues on epithelial cells and CR3 on PMNs bacteria survive inside phagocytes endotoxin capsule - only the encapsulated organisms of Bordetella are virulent Exotoxins: Adenylate cyclase toxin - produces cAMP in presence of host cell calmodulin, resulting in inhibition of leukocyte function Dermonecrotic toxin - may be responsible for localized tissue destruction seen during infection Tracheal cytotoxin - peptidoglycan fragment that inhibits or kills ciliated cells, pro-inflammatory Pertussis toxin - A-B subunit toxin, one subunit has enzymatic activity - ADP-ribosylation of host cell G protein, which ultimately causes a rise in cAMP levels |
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What are the stages of Pertussis disease?
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1. Incubation (2 weeks)
2. Catarrhal stage - mild coughing and sneezing, patient very infectious 3. Paroxysmal stage - explosive cough followed by whooping during inhalation, cough may lead to exhaustion, cyanosis, vomiting, and convulsions; resolution is very slow |
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What are some factors that have lead to an increase in Bordetella pertussis infections?
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under-vaccination in infants
under- or misdiagnosis of classic and mild pertussis incidence of pertussis among older children, adolescents, and adults, who serve as reservoirs for the disease have become an important source of disease transmission to infants and young children who are more susceptible to disease complications |
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How is Bordetella pertussis diagnosed?
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samples for culture collected from nasopharynx and grown on Bordet-Gengou medium or charcoal-containing medium
after 4 weeks, cultures are rarely positive, indicating that symptoms are due to inflammatory response, and not bacteria |
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How should B.pertussis be treated?
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erythromycin is treatment of choice, but should be given before onset of paroxysmal stage because after this stage it is mostly immune response that causes the symptoms
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How can B.pertussis infections be prevented?
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Whole-cell killed vaccine:
immunity wanes after 2 years no protection after 12 years CNS side effects Acellular vaccines: fewer side-effects currently licensed for children |
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What are some general characteristics of Neisseria?
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G- diplococci
2 important species: N.gonorrhoeae - causes the STD gonorrhea N.meningitidis - causes meningitis and sepsis |
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What are general characteristics of Neisseria meningitidis?
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5 major serogroups based upon polysaccharide capsule: A,B,C,W-135,Y
types B,C,Y common in the US most disease in US is sporadic or occurs as part of small epidemics |
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What are the determinants of pathogenicity of Neisseria meningitidis?
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endotoxin
pili antigenic variation polysaccharide capsule iron acquisition |
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What is the role of pili in the pathogenicity of N.meningitidis?
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antigenic variation of the pili can help bacteria avoid host immune response
pilE is the locus on the N.gonorrhoeae chromosome that leads to transcription and translation of pili at low rates of recombination, silent pil genes reassort with pilE genes, creating DNA recombination to lead to brand new pili genes |
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What feature of N.meningitidis protects the bacteria from phagocytosis?
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antibodies on the polysaccharide capsule
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What clinical diseases are associated with Neisseria meningitidis?
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Meningococcemia - sudden onset of fever, chills, nausea, vomiting, rash (maculopapular, petechial, or ecchymotic), myalgia, and arthralgias; fulminant meningococcemia patients present with very rapidly progressive illness characterized by shock, disseminated intravascular coagulation (DIC), and multiple organ failure
Meningitis - associated with meningococcemia, but may also occur alone; symptoms include severe headache, confusion, lethargy, vomiting, coma, seizures, focal neurologic signs |
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How is Neisseria meningitidis diagnosed?
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G- diplococci can be seen in samples of CSF
blood or CSF sample culture counterimmunoelectrophoresis or latex agglutination assays |
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How is N.meningitidis treated?
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Penicillin G
Cephalosporins also very active against N.meningitidis Chloramphenicol for pts with penicillin allergy |
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How can N.meningitidis infections be prevented?
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vaccine exists for serogroups A,C,W-135,Y
no vaccine exists for serogroup B |
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What are general characteristics of Bartonella?
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G- bacilli that invade endothelial cells and erythrocytes
2 medically important species: B.quintana B.henselae zoonotic infection |
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What are general characteristics of B.quintana?
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transmitted person to person via body louse
causes trench fever and bacillary angiomatosis |
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What are characteristics of B.henselae?
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zoonotic infection - reservoir is household cats
transmitted by cat flea, cat scratch, or cat bite causes cat-scratch disease - enlargement of lymph nodes following cat scratch or bite |
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What are general characteristics of Brucella?
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small G- coccobacilli
aerobic cause disease in humans, cattle, goats, and hogs infection acquired through contact with mucous membranes, cuts, inhalation, consumption of unpasteurized milk or dairy products survive inside macrophages due to type IV secretion system |
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What clinical diseases are associated with Brucella?
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nonspecific symptoms - fever, malaise, sweats, nonproductive cough
B.abortis - disease of cattle, infection is mild and self-limiting B.canis - disease of dogs, foxes, coyotes, infection is mild and self-limiting B.melitensis - disease of goats and sheep, infections are more serious and tend to be prolonged B. suis - disease of swine and reindeer, infection can become chronic |
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How is Brucella diagnosed and treated?
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Diagnosis - isolate organism from blood or biopsy specimens, serological tests
Treatment - tetracycline or doxycycline |
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What are general characteristics of Francisella tularensis?
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small G- coccobacillus
facultative anaerobe infects rabbits, squirrels, muskrats, beavers, and deer humans infected via contact with infected animal (skin, mucous exposure, ingestion, inhalation, tick bite) intracellular pathogen replicates in macrophages by inhibiting phagolysosomal fusion |
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What are the clinical diseases associated with Francisella tularensis?
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Tuleremia - 5 clinical presentations
1. cutaneous ulcer and swollen lymph node at site of tick bite 2. direct eye infection results in conjunctivitis and swollen lymph node 3. sepsis 4. pulmonary infection occurs from inhalation of infected aerosols, high mortality rate 5. GI disease after consumption of infected meat |
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How can Francisella tularensis be treated and prevented?
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Treatment: streptomycin
Prevention: vaccine |
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What are general characteristics of Pasteurella multocida?
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small G- coccobacillus
part of normal mouth and respiratory flora of cats and dogs human infection from cat or dog bite |
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What clinical diseases are associated with Pasteurella multocida?
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cellulitis after 24hr incubation period
chronic respiratory disease in pts with pulmonary dysfunction systemic infection in immunocompromised patients |
