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Microbiology PCCWQ3
| Question | Answer |
|---|---|
| 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. |
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