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Exam II

Exam Ii

by KristiLavin, Mar. 2015

Subjects: Lectures 6-12

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153 Cards in this Set

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	What are the Gram Negative Rods/Coccobacillis	Haemophilus Aggregatibacter Cardiobacterium Eikenella corrodens Capnoctophaga Pasteurella multocida Brucella Francisella Legionella Brodetella Enterobacteriaceae
	What are the Gram positive rods/coccobacilli	Bacillus Listeria Corynebacterium Erysipelothrix Nocardia Actinomycetes Streptomycetes Arcanobacterium Gardenella Rhodococcus Mycobacterium Clostridium
	Non-sporeforming Gram positive rods	Corynebacterium Listeria Erysipelothrix Lactobacillus Arcanobacterium Gardenella Nocardia Rhodococcus Mycobacterium
	Spore forming Gram positive rods	Bacillus (aerobic) Clostridium (anaerobic)
	Corynebacterium species that are pathogenic:	Pathogen: diphtheria
	Opportunistic Corynebacterium	jeikeium- infections prosthetic devices striatum- common pathogen normal flora pseudodiphtheriticum- endocarditis pseudotuberculosis- , dermonecrotic toxin ulcerans- unpastuerized milk urealyticum: urine pathogen xerosis: valve endocarditis, septicemia, pneumonia
	Other coryneform bacteria	Rohtia dentocariosa- normal oral flora R. mucilagnosa- endocarditis
	Gram Stain morphology of: C. diphtheria C. jeikeium C. pseudodiphtheriticum	small, pleomorphic GPR (club shaped) small, pleomorphic GPR small, pleomorphic GPR (chinese letters)
	General Characteristics of all Corynebacterium	Free living saprophyte Usual Flora of humans Catalase Positive Non-motile Facultative anaerobic Babes-Ernst Granules-polymerized phosphates
	What make C. diphtheriae pathogenic	Exotoxin; Diphtheria toxin Two Fragments (A+B); linked by disulfide bonds A: Active fragment, inhibits protein synthesis B: binds to cell mem. protein allowing for entry of A
	Conditions for C. diphtheriae toxin production	Alkaline pH Oxygen concentration Iron concentration (inversely proportional)
	What other groups can produce diphtheria toxin?	C. ulcerans C. pseudotuberculosis -Must be lysogenized with beta-phage containing tox gene
	Clinical Symptoms of C. diphtheria:	Via Respiratory route 2-4 days Low-grade fever, malaise, mild sore throat Systemic: toxin in blood stream effects kidneys, heart, and nervous system Death from cardiac failure due to toxin
	Treatment for Diphtheria	Antitoxin and antibiotics
	Agar used to visualized Babes-Ernst granules	Loeffler's serum agar
	Cystine-tellurite blood agar (CTBA)	Modified Tinsdale: Selective- inhibits many non-corynebacterium differential- brown or black halos around colonies
	Toxigenicity testing	Elek- immunodiffusion PCR- for tox gene
	How to confirm Corynebacterium	Fermentation reactions Urease Nitrate Toxigenicity testing
	Nitrate reaction for Corynebacteria	+ C. diphtheria C. pseudodiphtheriticum = C. jeikeium
	Urease Reaction for Corynebacterium	+ C. pseudodiphtherticium = C. diphtheria C. jeikeium
	C. diphtheria unique characteristics	Sucrose + beta-hemolytic
	Two Pathogenic species of Listeria	L. monocytogenes- human L. ivanovii- animal
	General Listeria characteristics and clinical infections	Widespread Associated with diary products, deli meat Immunocom, neonates, elderly: septicemia/meningitis Adults: penetrate intestines and systemic spread Can be fatal to fetus
	Virulence factors of L. monocytogenes	Hemolysin (listeriolysin O) Catalase Superoxide dismutase Phospholipase C Surface protein 60
	Differentiate L. monocytogenes from Group B strept	Catalase + CAMP test: block is produced
	L. monocytogenes	Catalase + CAMP + Motility at 25 deg Grows at 4 deg Bile esculin + Hippurate Hydrolysis + Narrow zone of beta hemolysis
	Who is at high risk for Erysipelothrix rhusiopathiae?	Fish handlers: self-limiting to site of inoculation painful swelling, usually hands or fingers Endocarditis (valve replacements)
	Erysipelothrix rhusiopathiae biochemicals	Catalase = K/K H2S+ Requires CO2 May have alpha hemolysis pleomorphic thin GPR, long filaments
	Acranobacterium haemolyticum	Indistinguishable form Grp A strept; resembles scarlet fever Catalase = Narrow zone of Beta hemolysis
	Lactobacillus characteristics	Aerotolerant anaerobe Normal vaginal flora Does not survive in urine Use antibiotics- typically inhibited not killed alpha hemolytic
	Gardenella vaginalis characteristics	Gram-variable Bacterial vaginosis? Treat: metronidazole, clindamycin Do direct examination of vaginal secretions Look for clue cells
	Clue cell	Epithelial coated with gram variable bacilli
	Nugent score	Scoring system used for diagnosing bacterial vaginosis GPR (0-4) small gram variable rods G. vaginalis (0-4) curved gram-variable rod (0-2) 7-10: bacterial vaginosis
	Bacteria with short chain mycolic acid	Corynebacteria 22-36 carbon atoms
	Bacteria with medium chain mycolic acid	Norcardia and related organims 50-62 carbon atoms
	Bacteria with long chain mycolic acid	mycobacteria 70-90 carbon atoms
	Acid fast bacteria	Primary stain: carbol fuchsin Decolorizer ("acid fast" organism resist) Nocardia is partially acid fast
	Modified acid fast	Shorter decolorization step: Allows for ID of Nocardia
	Counter stain in acid fast	methylene blue
	MAF positive	Myobacteria Nocardia Rhodococcus Gordonia Tsukamurella
	MAF negative	Actinomyces Streptomyces Actinomadura Nocardiopsis
	Nocardia general characteristics	Aerobic GPR, thin filamentous rods, gram variable weakly acid fast slow growers resemble fungi ubiquitous in envirnoment Peptidoglycan wall containing: meso-diaminopimelic acid, arabinose, and galactose
	Transmission of Nocardia	Cutaneous infection Not considered communicable
	Actinomadura	Actinomycotic mycetoma forms granules with branched filaments effects lower extremity subcutaneous tissue A. madurae can produce acid from cellobiose A. pelletieri cannot
	Streptomyces	Aerobic Peptidoglycan GP Catalase + Produce one more antibiotics can invade bone cause fungus tumor
	Gordonia bronchialis	"nocardioform"= mycelial forms that fragment into rods or coccoid Reduce nitrate (Nocardia does not) Antibiotic susceptible Closely related to Rhodococcus
	Tsukamurella paurametabola	Chronic lung infections, subcutaneous abcesses, cutaneous lesions, catheter associated bacteremia, peritonitis, prosthesis Susceptible to Beta-lactams, aminoglycosides
	Rhodococcus	Red (salmon-colored) pigment R. equi weakly acid fast necrotizing pneumonia Immunocompromised host
	Tropheryma whipplei	Whipple's Disease: diarrhea, weight loss, arthralgia, abdominal pain, treat with Trimethorpim-sulfamethoxazole (1 yr) Facultative intracellular pathogen
	Group 1 bacillus	Oval cylindrical spores central or terminal location does not distend vegetative cell
	Group 2 bacillus	oval spores central or terminal location causes the vegetative cell to swell
	Group 3 bacillus	round spores terminal location swollen spore
	Bacillus anthracis virulence factors	Polypeptide capsule (pX02) Potent exotoxin (Edema factor, protective antigen, lethal factor) Vaccine is avaliable
	Infections of Anthrax	Most infections cutaneous-malignant pustule/black eschar GI anthrax- from raw meat Pulmonary anthrax- mild symptoms 2-5 days, sudden respiratory distress: less than 24 hours death Treat with penicllin
	B. anthracis morphology	Macroscopic: Non-hemolytic "medusa head Microscopic: Large, square-ended GPR Bamboo appearance In blood: filmentous rods
	B. cereus	Food poisoning: Entertoxins Emetic form: associated with fried rice Beta hemolytic weakly motile
	Haemophilus species General biochemicals	Catalase + Oxidase + Nitrite+ GNR pleomorphic Non-motile Aerobic to facultatively anaerobic
	Haemophilus influenzae requires	both x and v factors
	Haemophilus parainfluenzae	requires v factor produced it's own x factor
	Satellitism	Growth around another organism that produces the necessary growth factors Exceptions H. aphrophilus and H. ducreyi
	H. influenzae colonize	10% of normal flora of the upper respiratory tract
	H. influenzae virulence factors	Capsule (HiB)- meningitis in children IgA protease LPS adherence
	Clinical Manifestation of H. influenzae	Encapsulated Strain- meningitis Epiglottitis Bacterial tracheitis Cellulitis Pharyngitis pneumonia No capsule (non typable strain)-pneumonia, otitis media, sinusitis
	H. aegyptius	Resembles H. influenzae Pinkeye (Conjunctivitis) Brazilian purpuric fever (70% mortality rate)
	H. ducreyi	STD: chancroid (soft chancre) Incubate 4-14 days: painful lesion irregular edge
	Miscellaneous Haemophilus	H. parainfluenzae-endocarditis, insidious onset H. parahaemolyticus-pharyngitis H. aphrophilus- bite wound infections
	Nairobi biplate used for	For H. ducreyi Colony: school of fish
	Determining X and V factor requirements	Mueller-Hinton agar plate X and V strips 5-10% CO2 18-24 hours
	Porphyrin test	+ If organism makes X factor Convert Delta-aminolevulinic acid to porphyrins Kovacs reagent Wood UV lamp
	Treatment of Haemophilus	Cefotaxime or ceftriaxone Trimethoprim sulfamethoxazole Drug-resistant: Beta-lactams H. ducreyi: erythromycin
	Biochemical profiles of H. influenzae and H. para influenzae	Both: GNR (coccobacilli), grey round colonies No growth on: SBA, MAC Satellitism Influenzae: Required V and X strip Parainfluenzae: Only required V strip
	What does HACEK stand for?	H- Haemophilus (includes Aggregatibacter aphrophilus A- aggregatibacter actinomycetemcomitans C- cardiobacterium hominis E- Eikenella corrodens K- Kingella
	HACEK general characteristics	GNR Increased CO2 Causes endocarditis Usual flora of the oral cavity Opportunistic in immunocompromised
	Which HACEK organism is Catalase +	Aggregatibacter actinomycetemcomitans
	Which two HACEK are oxidase V and which one is Negative?	V: Haemophilus, Aggregatibacter = Capnocytophaga spp
	Which HACEK is glucose and maltose negative	Eikenella
	Which HACEK are Sucrose +	Haemophilus Cardiobacterium hominus
	Which HACEK are lactose postive	Haemophilus
	Aggregatibacter Biochemicals	Sucrose = Lactose = Urease= Indole = Esculin= Citrate = Catalase + Oxidase V
	Cardiobacterium hominins	Pleomorphic GNR "rosette" morphology Pits agar Capnophilic Oxidase + Catalase- Indole +
	Eikenella corrodens	Capnophilic Require hemin (X factor) GN coccobacilli bleach like odor, pits agar Non-motile Nonfermenter Oxidase + Catalase= LDC +, ODC +, ADC =
	Kingella	Infections mainly in children Grows on MTM: does not pit, GNR Glucose, Nitrate + Urease, Indole, Esculin, Gelatin, Citrate = Beta-hemolytic Can be confused with N. gonorrhoeae
	Capnocytophaga	Was called DF-1 DF-2 often fusiform Common in septicemia Facultatively anaerobic
	Pasteurella multocida	Serogroups A-F (5) Non hemolytic, narrow green on brown halo Colonizes URT and GI Non motile Catalase, Oxidase+ Glucose fermentation
	Brucella	Category B select agent Zoonotic brucellosis or undulant fever (mon.-yrs) most common lab associated infection aerobe nonspore forming GNR nonmotile intracellular parasite
	Brucella biochemicals	Oxidase + Catalase + H2S and urease + help to differentiate Blood and BM cultures: acute and convalescent sera- serology tests safer
	Francisella species	Facultative intracellular parasite Non-motile Small GN coccobacilli aerobe zoonotic infection- tularemia granulomatous disease, A select agent, diagnose from serology Type A most virulent asso with rabbits
	Legionella pneumophila	Legionnaire's disease, Pontiac fever 14 serogroups Asymptomatic to deadly Inhalation of aerosols from environmental sources Epidemics from AC units Nosocomial infections in immunocomp. Top 4 acquired pneumonias
	Legionnaires' Clinical Manifestations	Incubation 2-10 days Nonproductive cough, fever, headache, myalgia Progresses to bloody or purulent sputum, rales Dissemination via circulatory system Mortality (15-30%) Most cases serogroup 1
	Pontiac fever	Nonpneumonic form of legionnellosis Incubation 2 days Flu like symptoms Spontaneous recovery
	Legionella enter and multiply within	Bronchoalveolar macrophages Predisposition: Immunocompromised Patients with chronic lung disease Alcoholics and heavy smokers
	Culturing requirements of Legionella	Aerobic L-cysteine BCYE (with L-cysteine)- long thin GNR Grow at 35-37 deg Grayish white or blue green convex, wet looking colonies
	Urine Antigen testing Legionella	Binax now 15 min- 97% sensitive RIA EIA
	Legionella Serology	IFA Cross reactivity: GNR, Chlamydia, mycoplasma Sensitivity Specificity Paired Serum: 4-fold rise in IFA titer (acute/convalescent)
	Major Pathogens of Bordetella	B. pertussis-whooping cough B. parapertussis- whooping cough B. bronchiseptica- opportunistic
	Infection of Bordetella	Breathing in aerosols Highly contagious (90%) Whooping cough: incubation 1-2 weeks, flulike symptoms, whoop cough, serious in young children
	Diagnosis and Isolation of Bordetella	Nasopharynx-aspirate or fluid, calcium alginate swab Inoculate to Regan-lowe media (transport) or Media (Bordet-Gengou potato infusion agar with glycerol and sheeps blood) Incubate aerobically, moistened for 7 days
	Bordetella colony morphology	GNR mercury droplets DFA or agglutination Biochemicals differentiate species
	Bordetella biochemicals	B. pertussis: oxidase and catalase + B. parapertussis: oxidase, citrate, urease, growth on blood free peptone + B. bronchiseptica: + growth on blood free peptone, urease, nitrate, motility, citrate, oxidase, catalase
	All enterics	Ferment glucose reduce nitrate oxidase negative (except plesiomonas) Motile at body temp (except Klebsiella, Shigella, Yersinia) Large moist, grey-while colonies (Klebsiella mucoid) Facultative anaerobic
	Virulence and Antigenic factors of Enterics	Adherence Toxins Invasive enzymes O antigen-lps H antigen- flagellar K antigen- capsular
	Primary pathogens of the Enterics	Salmonella Shigella Yersinia enterocolitica
	E. coli	Dry pink colonies on MAC Beta-hemolysis Motile Sex pili, fimbriae Posses O, H, and K antigens Ferments: glu, lac, trehalose, xylose IMViC ++-- Citrate - Does not produce H2S, PAD, DNase or urease
	Five categories of E. coli Diarrheal disease	EPEC- enterpathogenic E. coli ETEC- enterotoxigenic E. coli EIEC- enteroinvasive E. coli EHEC-enterohemorrhagic E. coli EaggEC- enteroaggregative E. coli
	EPEC	Multiple serotypes Fecal-oral transmission infantile diarrhea Characterized by attaching and effacing lesion TTSS (Type III secretion system) Injector system
	Type III secretion system	Bundle forming pilus allow contact with cell, destroying microvilli Cell comes closer to contact TTSS is activated and inserts into epithelial cell Secrete effector molecules, cell signal tranduction pathway activated Causes cytoskeletal arrangement to create a pedestals; causing diarrhea
	ETEC	Traveler's diarrhea 1-5 days, large inoculum Colonize small intestines; release toxins: Heat liable (LT: A and B subunits) causing hypersecretion due to activation of adenyl cyclase and Heat stable (ST)- stimulate guanylat cyclase causing hypersecretions
	ETEC vaccine	Anti fimbrial response prevents attachment: killed or attenuated Mucosal response improtant Anti-LT response may offer short term protections
	EIEC	Affects children and adults dysentery; direct penetration and invasion of intestinal mucosa watery diarrhea, scant stool pus mucus and blood Nonmotile and do not ferment lactose
	EHEC	Hemorrhagic diarrhea, colitis Hemolytic-uremic syndrome Watery diarrhea progesses to bloody diarrhea without pus O157:H7: Shiga toxin: Verotoxin I (cytotoxin) and II (not neutralized by shiga toxin antibodies) Screen for with a SMAC plate
	Shiga toxin (STEC)	A/B structure: 5 copies of B unit A subunit is enzymatic: N-glycosidase, inactivates ribosomal RNA, inhibits protein synthesis This results in hemolytic anemia can result in acute renal failure if confined to kidneys
	EHEC treatment and vaccine	Antibiotics may worsen the disease Monoclonal antibodies Vaccines composed of shiga toxoid, killed bacteria, attenuated bacteria
	EAggEC	Diffusely adherent (DAEC) Watery diarrhea lasting two weeks commensals form colon with special adherence for the urinary tract
	Extraintestinal E. coli infections	UTIs- catheterizations and UTI defects Septicemia and meningitis
	Klebsiella spp	Non motile IMVC --++ Citrate + PAD = H2S =
	Klebsiella pneumoniae virulence	Capsule: Antiphagocytic resists antimicrobial absorption mucoid appearance of colonies
	Klebsiella infections	nosocomial infection Hospital acquired infection: LRT, pneumonia, wound infections, UTI, bacteremia Often antibiotic resistant
	Differentiate K. pneumoniae and K. oxytoca	K. oxytoca is indole +
	Other Klebsiella species	K. ozaenae: nasal secretions and cerebral abcesses K. rhinoscleromatis: Africa and South America
	Enterobacter Species	Enterobacter: E. cloacae E. aerogenes Pantoea agglomerans: motile, formerly Enterobacter Cronobacter sakazakii: Formerly Enterobacter MR -, VP+ ODC +, LDC + (except E. cloacae) Infection site: wound, urine, blood, CSF
	Serratia species characteristics	ONPG + DNases + Resistant to antimicrobials
	Serratia species	Serratia marcescens: red pigment at RT Serratia liquefaciens Serratia rubidaea: some red pigment at RT Serratia odorifera: dirty mouse odor
	Serratia pathogenicity	opportunistic pathogens colonize respiratory tract and UTI Causes 2% of nosocomial infections of the bloodstream, LRT, UTI surgical wounds, and skin and soft tissue of adult patients
	Beer wort	Hafnia: delayed citrate reaction
	Tribe Proteeae is composed of	Proteus Providencia Morganella
	General Characteristics of Tribe Proteeae	Normal intestinal flora opportunistic NLF PAD + ODC+
	Proteus species	From wounds, urease +, swarming P. mirabils Indole -/ODC + K/A H2S + P. vulgaris Indole +/ODC = A/A H2S+
	Proteus species virulence	Fimbriae Hemolysin Flagella IgA protease Urease Ammonia production: kidney stones
	Morganella morgani	Found in GI tract of humans and reptiles Associated with snake bites
	Providencia species	Providencia stuartii (most common)- nosocomial burn unit outbreaks Providencia rettgeri: UT pathogen, occasionally nosocomial infection
	Providencia: Pathogenesis	Providencia stuartii: persists in urine due to adhesin, can proceed to blood stream P. alcalifaciens associated with diarrhea
	Salmonella species	GNR, facultatively anaerobic Clear, colorless, NLF colonies Neg: Indole, VP, PAD, urease, Potassium cyanide
	Subgroup I of Salmonella	Human infections: S. typhi, S. choleraesuis, and S. parathypi Differentiate by: LDC-rules out S. parathypi ODC rules out S. typhi Trehalose fermentation rules of S. choleraesuis
	Typhoid v. Nontyphoid	Typhoid: S. typhi, S. paratyphi, ingest but not from animal host, not self-limiting diarrhea, antibiotics indicated Non-typhoid: diarrhea (inflammatory), caused by many serotypes, self-limiting, animal host, no antibiotics
	Salmonella typhi	Systemic syndrom- typhoid fever diarrhea is not prominent humans only Mortality due to intestinal hemorrhage and perofration Vi antigen Carriers (1-6%) Associated with gall stones
	S. thyphi immunity	natural infection protective immunity Vaccines oral live attenuated Cross protection with S. paratyphi
	Paratyphi A	Causes enteric Fever Human specific emerging as prominent typhiodal pathogen in some regions
	Pathogenesis of Salmonellosis	All are invasive and inflammatory: Start in small intestines Invades epithelial cells of intestinal tract (TTSS) Bacteria are engulfed Cause transient disruption of host cell membrane, effects actin dynamic Bacteria get through to other side to lymph system
	Salmonella virulence factors	TTSS (SPI 1 (uptake) and SPI 2 (intracellular survival) Adherence fimbriae Vi in S. typhi many pseudogenes
	Shigella	Causes shigellosis, dysentry S. dysenteriae (group A)- serious infection S. flexneri (group B)- ass in gay men and young adults S. boydii (group C)- most common in developing countries S. sonnei (group D)- most common isolate in US
	Characteristics of Shigella	Non motile NLF H2S = (except S. flexneri) - Urease, LDC S. sonnei: + ONPG and ODC S. flexneri: = ONPG and ODC
	Clinical infection of Shigella	Nonfatal self-limiting Low inoculum 10-200 organisms infection from penetration of the mucosal epithelium no animal reservoir transmitted person to person
	Pathogenesis of shigellosis	Infection in large intestines invasive and inflammatory involves intestinal lymph tissue induces apoptosis of macrophages damage can persist after infection is resolved
	Shigella infection mechanism	Invade intestinal epithelium through M cells Pass through lamina propria some ingested by macrophages; induce inflammatory response invade basolateral side of epithelial cells Induce endocytosis of host escape vacuole released into cytoplasm spread to other cells
	S. dysenteriae	Secretes shiga toxin GNR ferment lactose slowly More virulent than others more infectious than others
	Differentiating Shigella species	ONPG and ODC are both S. sonnei (+) and S. flexneri (=) S. boydii: mannitol (+), ONPG (V), ODC (=) S. dysenteriae: mannitol (=), ONPG (V), ODC (=)
	Yersinia	GNR, Motile at 25 deg Y. pestis - bubonic plague (Agent A) Y. pseudotuberculosis- systemic flu-like symptoms Y. enterocolitica- inflammatory diarrhea
	Y. pestis	Category A select agent Plague Transmitted via flea bite GN coccobacilli, safety pin Bubonic, pneumonic: secondary
	Y. pestis biochemical tests	flocculent or "stalactite" growth in broth Non-motile Catalase positive Oxidase, urease, and indole negative
	Y. entercolitica	Infection from contaminated food self limiting diarrhea, fever, abdominal pain, mimics appendicitis Model for TTSS
	Yersinia Pathogenesis	Virulence plasmid prevents phagocytosis actively suppresses inflammatory response
	Edwardsiella tarda	Urea- LDC+ H2S+ Indole + Citrate - Bacteremia and wound infection
	Cirtobacter freundii	Lactose + (50%)- looks like E. coli, citrate + (E.coli =) Lactose - (50%)- looks like salmonella, = for LDC All: weak urease, ferment lactose, citrate +, MR +

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