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Microbiology PCCWQ3

QuestionAnswer
What is the shape, stain, O2 req and formation of staphylococci - gm+,cocci,clustersincellsof20ormorelikeagrapebunch,facultativeanaerobes
What is a common diplococci - nieserriaagm-bacteria
What are the three clinically important species of the Staph genus and what do they cause - s.aureus: staph infxn, s.epidermidis: UTI and subacute bacterial endocarditis and s.saprophyticus: UTI and cystitis
What is unique about the morphology of of s.aureus - some times it may have a capsule
What are the hemolytic characteristics around staph colonies - s.aureus has blood agar colonies surrounded by zones of hemolysis, s.epidermidis some produce hemolysis, s. saprophyticus is non-hemolytic
What is the presence of coagulase in the species of staph - s. aureus: coagulase+, s. epidermidis/saprophyticus -
The presence of what NZ helps differentiate staph and strept - catalase is present in staph but not strept
What does the word aureum from Aureus mean - it means gold because it is the color of staph aureus strain in colony
What is the function of superoxide dismutase - converts 2H+ and O2- to 2 H2O2 which is an oxidizing agent converted by catalase into H20 and O2
What are the specific antigens of the staph cell walls - s.aureus: ribitol teichoic acid, s. epidermidis: glycerol teichoic acid, s.saprophyticus: has both types of teichoic acid
What 2 proteins contribute to the cell wall virulence of staphylococci - protien A that interacts with IgG and activates the complement system and Fibroectin-binding protein (FnBP) that facilitates mucosal and tissue matrices
Where does one commonly find staph epidermidis - in ant nares (nasal passages), possibly in mouth and all over rest of body and in urogential orifices.
What bacteria may become dangerous in the event of lack of urine flow - s.epidermidis and e.coli found in the anal region will slowly ascend urinary tract causing UTI and eventually bladder infection
Who typically gets UTI - the elderly b/c their hygiene gets worse when they have to wear diapers
Who typically has s.saprophyticus - considered a normal part of vaginal flora. Known to be a common cause of UTI in adolescent females particularly those whom are sexually active
How is staph aureus differentiated from the other staph species - coagulase +, ferments mannitol [alcohol substrate], secretes ribitol teichoic acid
How do you tell the difference between saprophyticus and epidermidis - epi has glycerol teichoic acid and saprophyticus has both glycerol and ribitol acid
What 5 toxins are produced by the staphylococcus genus - exfoliatin, enterotoxin, pyrogenic toxin, panton-valentine and hemolysis
What is produced by exfoliatin and enterotoxin - ex: scalded skin syndrome, entero: poisoning colitis
What is the result of pyrogenic, panton-valentine and hemolysins - pyro: toxic shock syndrome, p-v: damages leukocytes, hemolysins: lyse membranes
What enzymes are produced by S.aureus to destroy tissue - staphylokinase, lipase and hyaluronidase
What will staphylokinase do - will cut through blood clots (scabs) to gain entrance to the bloodstream)
What is the role of lipase - used for lipid metabolism at the site of infected wounds
How does a-proteins increase virulence of Staph - antiphagocytic protein that will bind to fixed portion of ab inhibiting phagocytosis
Microbiology Study Aid Page 11 of 22 What is the fnx of m-proteins in the cell wall - antiphagocytic as well like a protein
What is a superantigen - a molecule that provokes the immune receptor to nearly a full t cell response
How can staph have a superantigenic effect - by secreting TSS [pyrogenic] and enterotoxins that are heat labile and heat stabile
What is alpha hemolysis or alphatoxin - most frequently detected hemolysis in s.aureus causing partial RBC lysis
What is beta hemolysis - complete RBC lysis resulting in a clear ring around the colony
What is gamma hemolysis - absolutely no color change around the colonies due to no RBC lysis
What are leukocidal proteins and what do they do - protein-A and p-val toxin destroy leukocytes and neutrophils
What is hyaluronic acid - a chief component of connective tissue
What is hyaluronidase and where does it come from - causes epithelial bacteria to spread from skin to CT to organs being formed by staph
What is the role of neutrophilia - primary defense against bacterial infections
What is lymphocytosis - primary defense against viral infections as a general rule
What type of pathology is stimulated by superantigen exotoxin - binds to MHC class II Ag complex enhancing T cell response causing cytokin (IL-2, IFN, TNF) mediated toxic shock
When is IgA formed by the body - in response to mucosal infections
When is IgE formed in the body - formed in response to eosinophilia and all parasitic infections
When does eosinophil count increase - in the case of parasitic infections and allergic reactions
What type of antibody is IgE - its a reaginic antibody causing allergic rxns resulting in histamine secretion
Which 2 types of infections are produced by staph aureus - toxigenic [involving toxin] and invasive [creates abscess]
What are the 3 main toxigenic infexns and what produces them - Scalded skin syndrome: exfolliative toxin, toxic shock syndrome: pryogenic enterotoxin F, food poisoning: enterotoxin
What happens in scalded skin syndrome - epithelia undergoes degredation at stratumgranulosum level
Who gets scalded skin and what are the signs - infants and newborns, pastialines [red lines at joints], nikolskis sign[texture is rough]
What are the two major antigenic characteristics of Toxic Shock Syndrome - heat stabile enterotoxins and superantigens stimulating cytokine release
What are the signs and symptoms of toxic shock - slight fever, hypotension and rash that will begin to peel due to hemolysis
How else would we classify TSS besides entero and why - pyrogenic [fever producing] stim's IL 1, IL 6, and TNF
What is the difference between the heat labile and stabile toxins - labile will be destroyed at 60 degrees celsius and stabile will presist
What are the invasive s.aureus skin infections in order of depth and danger - folliculitis, impetigo/pyoderma, boil or furnuncle, carbuncle
What is an impetigo/pyoderma - encrusted pustule beyond accessory glands
What are the three main disseminated infections [bloodstream/lymph] - acute bacterial endocarditis, osteomyelitis, pyoarthritis
Who typically gets bacterial endocarditis and where do it begin and end - commonly in drug abusers beginning in heart valves and ending in the CNS
Microbiology Study Aid Page 12 of 22 What are the main symptoms of acute endocarditis - Jane way lesions, oslers nodes[more tender than lesions], rothspots
Who gets osteomylitis and what are the signs and symptoms - in boys under 12 has inflammation over bone, fever, chills and shakes
What are the symptoms and clinical tests for pyoarthritis -inflamed and infected synovial it with blood demonstrating inc'd WBC count
What are they invasive staph infxns of the eyes - blepharitisis inflammation of the eye lid called conjunctivitis
What is MRSA - methicillin resistant staphaureus, plasma mediated resistance acquired in hospital
What is caused by MRSA - devastating consequences and sometimes n.gonorrhea
What is the invasive staph infxn of the lungs and what does it cause - sever pneumonia in elderly resulting in cavitation due to parenchymal cell dstrxn
What is hydrantis suppurativa and what causes it - recurrent pyrogenic abscess in apocrine sweat gland caused by staph
What is caused by staph eperdimidis and what are some of its properities - UTI in the elderly, has a capsule and is considered a beta hemalytic [total lysis]
How do we prevent staphylococcus - washing hand and formites especially in hospitals
What are the general features of streptococci - single, paired or chained Gm+ cocci, microaerophilic and attached to suface pili
What mimics strep pharyngitis and how do we differentiate - n.gonorrhia the gm- diplococci produces yellow instead of white exudate and is a capnophil
What are some of the antigenic properties of strept - non-motile, catalase-, hyaluronic acid capsule and fibronectin binding protien F
What is the mode of metabolism for strept - facultative anaerbore fermenting cho into lactic acid
What are the symptoms of strep-pharyngitis - white exudate in mouth, sore throat persisting longer than 72 hours
What can be some of the secondary consequences to strep -pharyngitis - rheumatic fever, tonsillitis, septicemia and nephritis
What causes cellulitis and erysipelas - in fxn usually through a small cut in the skin
What is s.cellulitis - rapidly spreading inflammation, usually of the skin and subcutaneous tissue
What is strept erysipelas - erythematous cellulites with defined border seen on the face or limbs[butterflyrashorerysipeloidlesion]
What is scarlet fever [streptopyrogenic] - similar to strep.pharygitis, causing rash in superantigenic exotoxin expressed response to erythrogenic toxin
Who gets cellulitis and erysipelas - woman who have birth, causes uteral infection in post parturition leading to septicemia
What is puerperal sepsis and what does it cause - post partum uterine endometrial infxn. causing purulent vaginal discharge
What is rheumatic fever and what doe it cause - an autoimmune response of superantigenic exotoxins called cystine protease [flesh eating bacteria]
Which strept groups are beta hemolytic - groups A and B
What are the 7 diseases associated with strept GroupA and their prototype - pharyngitis, scarlet fever, impetigo, cellulitis/erysipelas, rheumatic fever, glomerulonephritis and endocarditis. Prototype: Strept pyrogens
What are the 5 distinguishing features of group a streptococci - mprotein, catalase-beta hemolytic, produce erythrogenic exotoxin and produces streptolysins type S and O
What is the group B prototype - streptagalactiae Microbiology Study Aid Page 13 of 22 What are the associated diseases of Group B
Where do we find strept group B - normal oral and vaginal flora in %15 of women
What are the distinguishing features of group B - is a beta-hemalytic and has a sialic acid capsule
What is produced by strept group D and what type of bacteria
Where do we find strept group D - part of normal oral and intestinal flora
What are the grup D enterococci - e.fecalis and e.faecium
What is peptostreptococci and where is it found - obligate anaerobe in mucosal membranes of GI tract
What is caused by strept viridens and where is it found - implicated in dental endocarditis and is the main oral floral
What is the general feature of strept pneumoniae - Gm+, alpha hemolytic that is lancet shaped and precipitated by C reactive protein
What are the pathogenic characteristics of s.pneumoniae - autolysin in bacterial cell wall releases virulent factor "pnuemolysin" which causes lysis of cell membranes
What are the quelling positive organisms - s.pneumoniae, n.meningitidis, h.influenzae, klebsiella
What is the role of s.pneumoniae as a disease and in who - rarely occurs as the primary infection but usually secondary in the very young and very old as well as drug addicts
Who gets acute bacterial pneumoniae and what does it result in - mostly present in older people that results in viral flu
What are the causative pathogens of pneumonia - s.pnumoniae 60%, H.influenzae 9%, s.aureus 8%, viruses 10%
What are the symptoms of strept pneumonia - sensitive to bile and quinine, begins in resp tract producing brown sputum
What produces blue green sputum - psuedomonia
What are the characteristics of Neisseria and it location - gm-, diplococci located in the mucus membrane
Describe the pathogenic characteristics of Neisseria
- produces IgAase and has pili to stick to membrane surfaces w/ no flagella and has capsule in n.gonorrhorea and n.meningitidis. Capnophils!
How do we treat Neisseria - vancomyosin and nystatin
What are the general characteristics of n.gonorrhea - gm- pyogenic and pus producing
What are the symptoms of N.Gonorrhea - erythamados lesions in the glans of penis and labia of vagina and rarely an inflamed absess
What are the pathogenic characteristics of N.gonorrhea - has LPS molecules, capable of penicillase prod, IgAase prod, pili
What 7 diseases are caused by n.gonorrhea - urethritis, exudate secretion as dead WBCs, opthalmia neonatorum, rectal infections, pyoarthritis, septic arthritis and pelvic inflammatory disease
What are the PID shuffles (pelvic inflammatory disease)
- chandliers sign+ Chandliers sign + shows very short shuffling steps
What are the symptoms of PID - endometriosis, scarring in both sexes causing permanent changes after inflam
How do we treat gonhorrea - penicillin, prevention and encouraged use of condoms
What is opthalmia neonatorum - bilateral purulent conjunctivitis contracted in birth canal
What are the general characteristics of N.meningitidis
 - quelling +, capsule, extracellular parasite, LPS molecules are highly toxic
What is the location of n.meningitidis - natural reservoir of meningococci in human nasopharynx
What are the symptoms - fever with a rash (particular pinhead rash or macular rash) and neck rigidity
What is kernigs sign and what does it implicate - positive sign is pain in slow extension of limb due to meningeal inflammation putting pressure on cranial nerve roots causing pain
What is the result of n.meningitidis - fatal fulminant meningococcemia or waterhouse-friderichsen syndrome which includes hemorrhaging
What is the direction of lab diagnosis of n.menin
 - culture csf sample and find elev num of WBC's but no bacteria. Also high levels of glucose and maltose resulting in acid production
What is waterhouse-friderichsen syndrome - circulatory failure and adrenal insufficiency resulting in CN 8 nerve deafness and severe skin necrosis
What is moxarella catarrhalis - similar to neisseria: gm - diplococci and is thus misinterpeted. Does not form sugars
What other diseases are associated with moxarella - otitis media, maxillary sinusitis, pulmonary disease, meningitis
What are the general features of haemophilus - gram rod, need heme- or hematin, pyogenic and is a secondary invader
What are the 3 classifications of haemophilus - h.influenza, h.aegyptius and h.drucreyi
What are the characteristics of h.influenzae - small gm- with pleomorphic tendency, facultative anaerobe and grows best in aerobic conditions.
What are the 2 necessary growth factors for h.flu in the blood - x factor (hematin) to sythesize catalase NZ and V-factor
What is the pathogenicity of h.flu - polysaccharide capsule that is antiphagocytic and immunosuppresive, IgAase
Who primarily gets h.flu - common cause of infection in children
What are some secondary consequence of acute bacterial meningitis - otitis media, sinusitis, bronchitis and acute bacterial epiglottitis
What are the more serious infections that can occur in bacterial meningitis - pneumonia in the very old/young and immunocompromised, respiratory arrest in children and cellulitis/pyarthrosis
What are the way we diagnosis acute bact. meningitis in the lab - gm- coccobacillus, CSF contains a lot of organisms and quelling reaction
How do neonates deal with infections - passive immunity provided by mother and natural immunity at age 8
What is caused by h.aegyptius - bacterial conjunctivitis and is a highly contagious childhood disease
What is the key to lab diagnosis - purulence and response to tetracycline as a topical ointment
What is haemophilus ducreyi - soft painful chacres (Chancroids) in the genital tract as opposed to hard chacre of syphillis.
What is the symptoms and mode of transmission for h.ducreyi - lymphadenitis(swollenpustularnodes),is a sexually transmitted disease
How do you diagnose h.ducreyi in the lab - microscopy reveals no spiral shaped organisms b/c is a gm- coccobasillary rod
What are the general features of bordatella - gm- rod that is small coccobacilli growing in singles or in pairs
What are the classifications of bordatella and their roles as a pathogen - b.pertussis (whooping cough), b.parapertussis (mild form of whooping cough), b.bronchiseptica (primarily an animal
What are the primary pathogenic characteristics of bordatella - pertussis toxin (lymphocytosis promoting factor), hemagglutimin pili
What type of bacteria is b.pertussis - obligate human parasite
What are the 3 stages of symptomology of brucella - catarrhal stage, paroxysmal stage and convalescent stage
What is the catarrhal stage - mild flu like symptoms, cough, most contagious period lasting 1-2 weeks
What is the paroxysmal stage and how long does it last - whoop develops in cough, may cause cyanosis, vomiting, convulsions and total exhaustion. Lasts for 1-6 weeks
What is the convalescent stage and how long does it last - characterized by gradual decrease in symptoms lasting 2-4 weeks
How does one id bordatella in the lab - reveals lymphocytosis, will culture on a Bordet Gengon agar and a Regan Lowe agar
How do we treat bordatella - erythromycin to eradicate b.pertussis and antibiotics prevent secondary bacterial infections
What is a zoonotic disease - infections disease, naturally transmitted between vertebrate animals and humans
What are the most common sources of zoonotic disease - domestic animals like pets and farm animals
How do zoonotic diseases achieve entry into the human body - skin penetration, inhalation and ingestion
What are the general characteristics of brucella [stain,shape, movemnt, O2 use] - gm- rods (small coccobacilli arranged singly or in pairs), non motile, non encapsulated intracellular parasites and is strictly aerobic
What are the primary antigentic characteristics and in what species - A antigen in b.abortus and M antigen in B.melitensis
Where are the 4 strains of brucella found - b.abortus in cattle, b.melitensis in goats, b.suis in swine and b.canis in dogs
What are the symptoms of acute brucella infections - fever weakness and myalgia
How do we treat brucella - tetracycline and streptomycin for3-6weeks
What is Yersinia - an enterobacteriaciae meaning it has O, H and other surface antigens.
What are the 3 main species of yersinia - y.pestis, y.enterocolitica and y.pseudotuberculosis
How do enterocolitica and pseudotuberculosis establish infection - through massive invasion
What is y.pestis - highly virulent and can be transmitted by infected flea bites and able to replicate in nonactivated macrophages as bubonic plague
What is genetically different about Y.pestis in terms of virulence - has 2 genes (Fra1) that codes for antiphagocytic capsule and (Pla) plasma activator gene which degrades complement component C3b and C5a [preventing opsonization]
What is another role of Pla gene - degrades fibrin clots thus allowing the spread of Y.pestis
Which antigen is universally possessed by yersinia - O antigen, lipopolysaccharide protein complex w most being toxic to animals
What is caused by yersinia - zoonotic infxns w humans being accidental hosts, plague, bubonic plague and pneumonic plague
What is plague (black death), where does it occur and who transmits it - highly contagious and fatal, transmits via rat flea(xenopsylla cheopis) west of the mississippi.
What is bubonic plague - from infected rat flea bites w fatality being about 75% and death in 3-5 days
What is pneumonic plauge and how is it transmitted - results from human to human transmission via respiratory droplets and results in fatality 100% of the time
What is the clinical picture of pneumonic plague playing out - purulent pneumonia, DIC, septic shock to cutaneous hemorrhage, hypotension and DIC complication including plague meningitis
How do we treat plague - quarantine patient and apply streptomycin. Pneumonic is untreatable after 12-15 hours of the first symptom appearing
What is caused by y.enterolitica - enterocolitis, necrotizing enterotitis involving terminal ileum and mesenteric lymph node enlargement
What type of disease mimics this - acute appendicitis and camplyobacter jejuni
Who gets y.enterocolitica and what are the symptoms - common among young children: abdominal pain and diarrhea and fever
What are the symptoms of Y. pseudo tuberculosis - causes enterocolitis and swollen tender lymph nodes
What is the clinical expression of bubonic plague and how much bacteria causes it - clinical xpression is buboes:swollen lymph nodes in inguinal and axial region which only requires 1-10 organisms to bring about illness
What is yersiniosis - lesions develop in walls of SI causing severe GI disease w/ mesenteric lymphdentitis
What are the 2 clinical courses of yersiniosis - acute lympadenitis, terminal ileitis or septicemia w abscesses in organs [death]
What are the general characteristics of francisella tularensis - gm-rods, nonmotile, thin lipid capsule, aerobic
What are the zoonotic bacteria and their common characteristic - brucella, yersinia, francisella, pasturella and botanell all are intracellular residents
What are the other diseases associated with francisella tularemia - rabbit fever, glandular fever, tick fever, or deer fly fever
How is f.tularensis acquired - insect bites or direct contact with blood and tissue of effected animals
What is the most common type of tularensis - ulceroglandular tularemia
What are the various diseases associated w f.tularensis and their entry point - ulceroglandular: skin infxn, oculoglandular: in eye, glandular pneumonic if inhaled, typhoidal tularemia if ingested.
What are the initial manifestations - fever head ache, adenopathy, backpain, anorexia, chills and sweats
What is the treatment for francisella - streptomycin w relapses occurring fairly frequently
how do we prevent francisella - meat should be cooked thoroughly and sheep handlers and trappers should get vacc
What is pasturella - indigenous flora of respiratory tract and oropharynx in animals and birds
What are the resulting infxns from pasturella and how are they caused - pneumonia and septicemia as a result of stress (shipping fever and fowl cholera)
How is pasteurella likely transmitted to humans - humans get it from cat bites where the site doesn't heal and becomes more septic and shared foods
What are the 3 forms of diseases are associated with pasteurella - localized cellulitis and lymphadentis, exacerbation of COPD symptoms, systemic infections in immunocompromised patients esp those with hepatic disease
What are the general characteristics of bartonella - facultative, intracellular, slightly curved rods, zoonotic
What are the 3 primary forms of bartonella - b.henselae, b.quitana, b.bacilliformis
What is caused by b.henslae - causes cat scratch fever producing mild inflammation and angiomatosis
What is produced by b.quintana - trench fever mild and relapsing fever with maculopapular rash transmitted by louse [pediculus humanus parasites present in states of poor hygiene]
What is caused by B.baciliformis - oroya fever clinically presented as infectious anemia known as carrions disease
What is the effect of B.bacilliformis on the body - pathogenic RBC destruction and liver/spleen damage followed by verruga peruana scalp rash
Where do people get B.bacilliformis - endemic in S. America Peru, Ecuador and Colombia transmitted by the sand fly
What is caused by Listeria monocytogens - abscesses of granulomas in different tissue w/mortality rate 30-80%
What is the body's response to L.monocytogens - typically neutrophilic leukocytosis with development of monocytosis
How does organism enter the body - through ingestion and disseminates from GI tract
What is the precursors for adults - affects host already compromised by purulent meningitis
What is the most common entry for neonates - from a mild genital tract infection of the mother
What is the typical consequence of in utero and during delivery infections - tend to kill baby during delivery or 1-4 weeks afterwards
How is L.monocytogens diagnosed in clinic - gm+coccobacillus, catalase+, tumbling motility in liquid medium and facultative growth on enriched media
How do blood agar and antons test determine the presence of L.monocytogens - agar: demonstrates hemolysis, antons: involves rabbits eye inoculation producing purulent conjunctivits with keratitis
How do we treat L.monocytogens - ampicillin but highly fatal in newborns
How do we prevent L.monocytogens - mild pasteurization kills organism and its associated w/ cream cheese and milk
what is caused by bacillus and how - zoonois in sheep and cattle with spore playing important role in transmission
What are the medically important species of bacillus - B.anthracis causing anthrax and B.cereus causing food poisoning
How is bacillus diagnosed in the clinic - Gm+, large rods, occur in pairs or long chains, nonmotile, facultative aerobic
What is caused by B.anthracis - profound toxemia exotoxin in blood resulting in death in 2-5 days
What is the mechanism of cutaneous B.anthracis manifestation - 95% of anthrax cases, spore enter through cuts or abrasions forms small pustules (Eschar) killing 10% of people
What is the Pulmonary manifestation - known as wool sorters disease, 5% or anthrax, spores enter into lungs
What are the symptoms that characterize pulmonary anthrax - abrupt onset of fever, malaise, cough, hemorrhagic necrosis of lymph nodes, respiratory distress and cyanosis
What is the gastrointestinal manifestation of anthrax - caused by ingestion of spore leading to nausea
What are the pathogenic characters of B.anthrax - capsular polypeptide of D-glutamic acid that inhibits phagocytosis and produces exotoxin causing CNS distress and respiratory failure/anoxia
What is the exotoxin composed of - lethal proteases that cleave kinase and activates MAPK/mitogen inhibiting cell growth
How do we treat B.anthracis - penicillin and early detection
What bacteria express super antigneicity - staphaureus [morecommon]and strept groupA
How do we prevent B.antracis Microbiology Study Aid Page 18 of 22 - kill infected animals and sterilize wool and apply effective vaccines to animals
What is B.cereus - produces an enterotoxin that causes gastroenteritis, food poisoning esp reheated fried rice
What are the 2 types of gastroenteritis from B.cereus - emetic gastroenteritis[severe nausea/vomiting], diarrheal gastroenteritis watery stool
What are the important bacterial zoonoses
- L.monocytogenes, y.pestis, f.tularemia, brucella, B.anthracis
What are the characteristics of clostridium - spore forming Gm+ rods, obligate anaerobes that infect unhealthy low redox tissue
What are the 4 types of clostridium and what do they cause - perfringes: food poisoning/soft tissue infxn, botulinum: botulism, tetani: tetanus, difficile: gastroenteritis
What is the primary pathogenicity of clostridium perfringens - produces 12 identifiable toxins in addition to enterotoxin of which alpha toxin ismost important
What is the role of alpha toxin in c.perfringes - lecithinase production breaks down cell walls resulting in necrosis and gas gangrene
What is the general location of c.perfringes - widely distributed in the environment, in gunshot wounds, enteritis infections, GI distress, septic abortions, cellulites and other inflammatory diseases
What is the most severe forms of c.perfringes tissue invasion - necrotitis and enteroticans prevelant in New guinea turning infection blue/black
What is the role of enterotoxin secreted by c.perf - toxin is a protein and is heat labile produced in Large intestine
What is the overall metabolic activity of c.perfringes - ferments glucose, maltose, lactose and sucrose producing H2S and proteolytic NZ
What are the distinguishing characteristics of C.perfringens from other clostrideums - nitrate reduction, lack of motility, sporulation, lactose fermentation and lecithinase prod
What are the 2 consequence of lactic acid accumulation in c.prefringes - anaerobic cellulitis and myonecrosis [gas gangerene]
What is the recommended vaccination schedule for whooping cough - vaccine given at 2 months, boosters at 4, 6 and 18 months and admission to school
What causes mild food poisoning - enterotoxin of type A c.perf strain occuring in very old and malnourished child
What causes enteritis necroticans - caused by beta toxin of type C strains resulting in intestinal lesions
What is caused by c.tetani - agentoftetanus(lockjaw)
What is produced by C.tetani - exotoxin: tetanospasmin (neurotoxic), attacking brainstem and ant horns of spinal cord inhibiting neuroinhibiters resulting in massive contractions
What is tetanolysin - a second toxin that is hemolytic but of minor importance to pahtogenesis of tetanus
What is the general characteristics of c.tetani - slenderGm+rod, motile, strict anaerobe, spores, shape is drum stick or tennis racket
What are the metabolic products of c.tetani - acids: acetric, butyric, propionic, ethanol
When does infection w c.tetani commonly happen - minor trauma like laceration, puncture or thru retrograde neuronal transport
What are the symptoms of c.tetani infection - muscle stiffness, tetano spasms of lockjaw(trismus), risuss ardonicus, back arching, short frequent spasms of voluntary muscles and then death from exhaustion/respiratory fail
How do you treat c.botulinum - antitoxin and penicillin, debride tissue and perform a tracheotomy to aid breathing
What is the gen characteristics of C.botulism - large motile, gm+ rods w subterminal oval spores
What is produced by c.botulinim - produces 7 serologically distinct neurotoxins, gelatinase and H2S
What does the exotoxin secreted by c.bot do - acts on NMJ's producing flaccid muscle paralysis
What are the symptoms of food poisoning due to C.bot - nausea, dizziness, cranial palsy, double vision, muscle weakness, respiratory paralysis
What is floppy baby syndrome - intestinal infant botulism occurring after spore ingestion and subsequent germination in GI tract disseminating causing constipation and muscle weakness losing limb control
How do we treat food poisoning due to c.bot - antitoxin, stomach lavage, enema but NOT antibiotics
How do we treat intestinal (infantile) botulism - only supportive care needed
How do you prevent the spread of botulism - give antitoxin to everyone who ate the contaminated food, heat food to 80-100 deg C for 10 min and proper sterilization bacteria
What are the general characteristics of C.difficile and where are they located - gm+rods with terminal spores in colon of 20% of people as normal flora
What is produced by C.difficile - enterotoxin and cytotoxin that kills mucosal cells
What are the clinical manifestations of C.difficile - severe gastro enteritis or pseudomembranous colitis
What are the symptoms of C.difficile - abrupt onset of acute abdominal pain with watery and profuse diarrhea and circulatory collapse leading to death in 30% of cases
How do you treat c.difficile - vancomycin or metronidazole and monitor fluid electrolyte status
What is erysypelothrix rhusiopathiae (e.rhu) and who has it - gm+rod causing cellulitis in fish handlers and butchers
What are the 8 general of entero bacteriaceae - escherichia, enterobacter, klebsiella, proteus, serratia, salmonella, shigella, yersinia
What are the general characteristics of enterobacteriaciae - gm- non spore forming rods, facultative anaerobes, oxidase negative
Enterobacteriaciae cause what 2 major syndromes - nosocomial infxns and gastrointestinal disturbances
What is the antigenic composition of enterobacteriaciae - all have somatic O antingen, flagellar H and capsular K antigens
What is the O antigen for - associated with LPS of outer membrane of all Gm- bact making colonies rough [avirulent]
What is function of K antigen and who has it the most - polysaccharides in capsules covering O antigens in k.pneumoniae/s.typhi
How do we separate the two groups of enterobacteriaciae - lactose fermenters and non
What is the media used for separation of lactose groups - Eosi-methylene blue(EMB)agar and MacConkey agar
What does EMB agar differentiate and in what colors - non path E.coli is green and inhibits Gm+ organisms, pathogenic non lactose fermenting is transluscent: salmonella and shigella
What does MacConkey Agar differentiate - E.coli becomes pink vs. pathogenic translucent ones. Inhibits others by contents of bile salts
What is the pathogenicity of enterobacteriaciae - capsule suppresses/evades phagocytosis and enterotoxins(exo), cause transduction of fluid into ileum
Describe the enterotoxins of enterobacteriaciae - under genetic control, heat labile one and a heat stable one produced by E.choli/vibrio
What are the roles of the 2 heat labile toxins - SubunitA: activates cAMP causing H20 and Cl- secretion and Subunit B: attaches to brush border and facilitates entrance of subunit A
What does the heat stable toxin of enterobacteriaciae do Microbiology Study Aid Page 20 of 22 - activates granylate cyclase to stim fluid secretion via cAMP
What is the endotoxin of enterobacteriaciae made of - LPS complex and a lipidA-core
What does the Lipid A-core cause - hypotension from endogenous hypotensive agents from platelets and fever Il1-6
What is a local schwartzman reaction and where do they occur - hemorrhage at the site of injection and thrombus formation in adrenal/heart/intestine/kidney
What is a generalized schwartzman reaction and where do they occur - bilateral renal cortical necrosis after 2nd xposure to LPS in adrenal/hrt/intestine/kidney
What causes a hemorrhage - single exposure to endotoxic bacteria during pregnancy or cortisone treatment
What is an adjutant action in hemorrhage - on the immune response by increasing antibody response to other unrelated antigens
What is mediator release in hemorrhage - macrophage etc. release many other physiologically active molecules
What is the effect of hemorrhage on blood cells - neutropenia within minutes of exposure to LPS followed by leukocytosis
How does a hemorrhage occur in pregnancy - LPS may cause hemorrhage in placenta thru serotonin release stim by LPS
What is the general characteristics of E.coli - gm-, short rods, facultative anaerobe, catalase+, oxidase-
What are the 4 distinct syndromes of E.coli - entero-toxigenic, entero-pathogenic, entero-invasive, entero-hemorrhagic syndrome
What is enterotoxigenic syndrome - travelers' diarrhea caused by enterotoxigenic e.coli, oral fecal bacteria colonize inhibiting Na reabsorption and Cl- production causing watery diarrhea for several days
What is enteropathogenic syndrome - diarrhea of infants, bacteria attaches to mucosal cells causing inflammation of GI What is enteroinvasive sndrome
What is the leading causes of meningitis in neonates - group B strept and e.coli due to lack of IgM and susceptible to E.Coli sepsis
What other disease does e.coli cause and in whom - very common cause of UTI especially in women
What are the symptoms of e.coli - dysuria, frequent urination, hematuria, pyuria
What is the general characteristics of Salmonella - gm- motile rods, indistinguishable from other enterobacteriaceae
What are the human salmonella diseases - s.typhi, s.enteritidis, s.typhimurium, s.parathyphi A, s.schottmuller
What antigens are present in salmonella - O and H antigens and most virulent strains possess a capsular polysaccharide
Where is salmonella primarily found - poultry products and roast beef, pet turtles and vegetables as well.
What are the 3 major categories of salmonella - enteric fever, septicemia and gastroenteritis
What causes enteric fever - s.typhi [typhoid fever], invasive intestinal inflammation invading mucosal epithelium
What is a likely site of infection reservoir for enteric fever - gall bladder and regional lymph nodes
What are the symptoms of enteric fever - headache, continuous fever, splenomegaly, rose colored spots in skin due to bacterial multiplication
What are some complications associated with enteric fever - GI hemorrhage of bowel with perforitis and 3% of patients become carriers permanently
How is enteric fever controlled Microbiology Study Aid Page 21 of 22 - chloramphenicol is the drug of choice and ampiciliin
What is septicemia - a fulminant disease independent of intestinal symptoms
What are the frequent agents of septicemia - s.choleraesuis and entero-bacteriaciae spread through the blood
What people have higher risk of septicemia and what would happen - people with sickle cell anemia are at a hi risk for developing osteomyelitis
What is gastroenteritis and what causes it - most common cause of salmonellosis due to S.enteritidis
What are the symptoms of gastroenteritis - nausea, vomiting, abdominal cramps diarrhea and headache for 2-7 days
How would you diagnose gastroenteritis in a lab - s.typhi: isolated from blood and stools, s.choleraesuis isolated from blood and s.enteritidis isolated from stools
What do we treat gastroenteritis with - no therapy needed and antibiotics may INCREASE the carrier rate
What are the characteristics of shigella - gm- rod, non motile, facultative anaerobe, pathogenic to humans
What does shigella cause and how is it transmitted - causes bacillary dysentery and shigellosis transmitted thru flies and fecal oral infection
What are the symptoms of shigella - bloody stool for first few days, fever and rash together
Describe the characteristics of shigella dysenteriae - secretes exotoxin that is heat labile, causes diarrhea and neurotoxin
How do you treat S.dysenteriae - antibiotics only in severe infection, combination of sulfamethoxazole, fluid replacement
What is edwardsiella - lactose fermenting enteric rod resmbling salmonella
What is citrobacter - resembles salmonella antigenically and is opportunistic pathogen in immunocompromised patients
What does citrobacter cause and in who - UTI, wound infection, osteomyelitis, gastroenteritis in the elderly and hospitalized
Where is klebsiella usually found and what is its antigenicity - indigenous flora of the intestinal and respiratory tracts and is QUELLING+
What is klebsiella pneumoniae - has antiphagocytic capsule, usually secondary invader, primary cause of nosocomial UTI and linked to diarrhea of the newborn
Where do one find K.enterobacter - indigenous intestinal flora that is also on plants
What is helicobacter pylori - gm-rods, curved or spiral rods, multiple flagella gives rapid corkscrew motility, micro aerophyllic, ureae+
How is helicobacter pylori transmitted - person to person, non-invasive but recruits and activates inflammatory cells in mucosa
What kind of conditions are caused by H.pylori - acute gastritis as initial infection causing duodenal ulcers, chronic gastritis and gastric ulcers. RISK FACTOR FOR: gastric carcinoma and gast b-cell lymphoma
How do we treat H.pylori - bismuth salts, metronidazole, ampicillin/tetracycline
What are pseudomonads - obligate anaerobic gm- rods with small polar flagellated pili, oxidase+
Where do we see the presence of pseudomonads and what are they doing - seen in lungs of cystic fibrosis patients in a slimelayer(mucoid-polysaccglycocalyx)
What is produced by pseudomonads that help id them clinically - pyoverdin[green]pigment, pyocanin[bluepigment], bluegreen pus is p.aeruginosa
What is pseudomonad aeruginosa - common etiological agent of human disease in 30% of hospitalized people
What are the 5 pathogenic properties of pseudomonad aeruginosa Microbiology Study Aid Page 22 of 22 - pili, slimelayer, hemolysin, collagenase elastase and flagella
What are the pathogenic virulence factors of P.aeruginosa - LPS, exotoxin A and Exotoxin S:inhibits protein synthesis
What are the 4 clinical signs of P.aeruginosa bacteria - cellulits, pneumoina [esp cystic fibrosis patients], septicemia and endocarditis
What are the other species of pseudomonas - burkholderia mallei, Burk.cepacia, Burk.seudomallei and Burk.gladioli
What are the general characteristics of bacteroides - obligate anaerobic gm- rods, non motile and pleomorphic
Where do we see bacteroids and what type primarily - accounts for 99% of fecal flora and B.fragilis most common in colon
Where else are bacteroides isolated from - normal oropharynx, vagina and external genitalia
What is the major pathogenic factors of B.fragilis - polysaccharide capsule, collagenase, hyaluronidase and weak endotoxin
What does B.fragilis cause - GI abscesses, PID [leading cause], cellulitis esp in diabetics
What may be caused by B.fragillis - postoperative peritonitis, gynecological infxns, lung/brain abscesses
How do we treat B.fragillis - debridement and drainage in cellulitis cases
What is Bacteroides melaninogenicus and what does it cause - part of the normal flora of mouth causing putrid sputum, infxn of female genital tract and lung abscess
How do we treat bacteroides melaninogenicus - same as B.fragilis, debridement and drainage
what is prevotella - obligate anaerobe, slender gm-rods, pigmented black colonies like pseudomonads
What is porphyromonas - anaerobic Gm- rods
What are the types and cause of Porphyromonas - P.gingivalis, P.endodontalis causes peridontal disease, dental abscess, gingivitis
What is proteus - Gm-rods, non lactose fermenters, motile
What are the types and consequences of Proteus - P.mirabilis, P.vulgaris cauing UTI
What is enterobacter - Gm- rods, ferment lactose cause UTI, pneumonia in hospitalized patients.
Created by: lerch