Bacteriologycone rete =m oon wows Shame nat emo “rane ! | | es! a Se — | | | | S. aureus Staphylococcal Scalded Skin Syndrome (SSSS) - Exfoliative toxin A ‘Staphylococcal Impetigo — Honey-coloured lesion on face Cutaneous abscesses — Sterile gauze with antibiotics Cellulitis - Pro-inflammatory cytokines ‘Staphylococcal pneumonia — Panton-Valentine Leukocidin Toxic Shock Syndrome - TSST-1 in aerobic (tampon) conditions ‘Staphylococcal food poisoning — Enterotoxin A, B, and C Osteomyelitis - #1 cause in childrencam pactena | FEATURES ‘Agar: Ferment mannitol Hemolysis: Beta-hemolytic TOXINS = Exfollatvo taxi A (ETA) sa heat stable form encoded bya ene | + Surface protein A —evad 7 = Exfoliative toxin B (Era) is a heat labile, plasmic-bome gene. immune system = MECHANISM: BOTH cleave desmoglan-1 wich destroys euprabasal desmosomes. cataese* + Coagulase TEST: postive Nikoleky~ statu corneum detaches wih very sight pressure + Catalase-postive + Aerobic ‘Staphylococcal impotiga ‘conguase = Distinguished from Streptococcus pyogenes (the mast common cause of impetigo) HOW: diferente based on gram-stan morphology + catalase + Honey-coloued lesion on face S eweus Cutaneous abscesses Endocardis ~ Cutaneous abscesses bagn as flict or wound ‘VIRULENCE Aste is folios nthe eyal *Coagulaseto clot Pathogens casing endocarts resi 0 WHO: parenteral drug abusers, whose disease normally denuitis Tight sie of the heart (vicuspid valve) rather than the left ‘Around the abscess ~ has area of inflammation ‘Associated with pro-inflammatory eytokines hylococeal pneumonia ‘CAUSE: Aspiration of oral secretions or from the hematogenous spread ofthe ‘organism trom a DISTANT sito VIRULENCE: Panton-Valentine Leukocidin, a ite protein that specitialy targets white blood cellscoaguse ‘Toxic Shock Syndrome + TOXIN: TSST-1 Is only expressed by S. aureus that have the TSST-1 ger + MECHANISM: Cross link T-cell receptors and MHC-II molecules /when grown in aerobic conditions = signs (OTHER strawberry tongue + Abrupt onset of high fever ra + Hypotension + Diffuse erythematous rash = Swollen “strawberry tongue* + Lead to desquamation ofthe extremities and disseminated intravagcular coagulopathy (DIC), Staphylococcal food poisoning = TOXIN: Entorotoxin A,B, and C = MECHANISM: Intoxication = Enlorotoxin A and B (tigger inflammation in that area fj nausea in vomiting very soon = _ Subsequent heating ofthe food wil kil the bacteria but not inactivate the heat-stable toxin = SOURCE, + Genes are not aways on all the time upregulated by presence of fats (potato salad) : Some - ean ai + Severe vomiting, diarhea, and abdominal pain (OTHER osteomyelitis Staphylococcus aureus - #1 cause Osteomyelitis Inchildren = #1 cause in children ~ Child already had impetigo (S. aureus) + Pseudomonas aeruginosa — = ROUTE: dissemination through the blood i severely IC + LOCALIZATION: involves the growth plate area of long bones, a highly vascularized area of bony growth. + RESULT: Soptic arthritis “+ Nolsseria gonorrheae as the most common cause of septic athits in sexually active persons.Differentiating S. lugcuneneis from other staphylococci. ‘S. saprophytious is the second most common cause of cystitis in young sexually active women. Cystitis is a common inflammatory disease of urinary bladder. PRESENTATION: Cystitis presents with suprapubic pain and dysuria = Including BOTH increased urgency and frequency of urination. - Pyuria (white cells in urine) may be a feature. —w ~ Like 8. aureus, 8. lugdunensis i typically beta-hemolytic, and has synergistic hemolysis with S. aureus. ~ S. lugdunensis grows in tan colonies that have a distinctive odor ike mown grass or hay. + - 5. lugdunensis produces coagulase on the surfaces ofits cells, but does NOT release free coagulase, soit §-Auro will test positive for coagulase using a slide test, but not using a tube test. ‘Secretes coagulase to stiok to + Iteannot ferment mannitol. S.lugdunensis er Differentiating S. epidermicis from other staphylococci. Has coagulas ae = S epidermidis is gamma-hemoiytic i + Coagulase-negative ‘stale = Killed by Novobiogit ae + teannot ferment mannitol.——— canine > care ofa conan ponarbe cheer arent 1, — 1, suc adie linia soi viet Sea at cee Sea ‘ainano ae | | —t_, wg Sepcemas _samocenness [Epes] swymuce genome aun i £ cche ahe senlene ‘Streptococcal Pharyngitis — Cervical lymphadenopathy i Scarlet Fever -(SpeA, Spe8, Spe8—Superantigens rene Streptococcal impetigo ~ young children with poor personal hygiene Rheumatic fever ~ patients WITH severe streptococcal pharyngitis ‘OTHER coluli-related ‘Staphylococcus aureus — towards ‘extremities ‘Streptococcal pyogenes celutis — towards the heart ‘Clostridium perringens - spinor Inoculated, radiates equally Erysipelas — Very clear border ‘Streptococcal pyogenes cellultis— runs towards the heart Streptococcal necrotizing fasctis ~ SpeA, SpeB, SpeB—super-antigens Streptococcal Toxic Shock — toxin is released directly into the tissues Enysipolothix rhusiopathiae Nocardia OTHER necrotizing fancitis Hemophilus inuenza ~ orbit of the [Streptococcus pyogenes oye = Vibrio Vulnificus ‘Acinetobacter baumannll - orange = Pseudomonas aeruginosa ~ severely IC peel colitis = Clostridum perfringens Pasteurella multocida, = Acinetobacter baumannii — middle east soldiers Capnocytophagaram acter Activity Interest cle Hyaluronic acid _Antiphagocytic Same as human hyaluronic acid in | capsule basement membrane; antibody cross- caaae- reactivit pontine M protein Fimbral protein binds Cross reactive epitope with cardiac fibronectin, blocks myosin -— complement etc F protein Adhesin Binds fibronectin, associated with M | protein. S pyasenes Hyaluronidase _Degrades hyaluronic acid Invasion Streptokinase Dissolves fibrin clots “Clot buster” drug FEATURES Pyrogenic Scarlet fever, TSST of GAS, Gi it exotoxins ( P necrotizing fasciitis (flesh-eating batted Exythrogenic © Superantigens bacteria toxi ee Grow in pairs or chains s an erythematous skin reactions, Catalase-negative Pe . pyrogenicity, | Fasticlous growth SpeB Cysteine specific and nonspecific T-cell requirements protease mitogenicity, immunosuppression = Capnophilic conditions (5% >P' coz). StreptolysinO Oxygen labile hemolysin Hemolysis Streptolysin S Oxygen stable hemolysin Responsible for beta hemolysis.VIRULENCE Mprotein = Enable to bind to epithelial cell layers Ab cross-reactive activity with cardiac myosin Streptotysin $ = Non-immunogenic, oxygen-stable ~ Lyse erythrocytes, leukocytes, and platelets. - MECHANISM: Release of lysosomal contents after enguifment subsequent death of the phagocytic cell ~ Responsible for the characteristic B-hemolysis seen on blood agar media. Streptolysin = Oxygen-labile hemolysin capable of lysing erythrocytes, leukocytes, platelets, and cultured cells Streptokinase (A and B) - MECHANISM: Mediate cleavage of plasminogen releasing the protease plasmin {jin turn, cleaves fibrin and fibrinogen = Can lyse blood clots and fibrin deposits and facilitate the rapid spread DNases Ato D = Depolymerize free deoxyribonucleic acid (DNA) present in pus. = Reduces the viscosity of the abscess material fj] facilitates spread of the organisms = Responsible for suppurative diseases ~ Pharyngitis + Softtissue infections + Streptococcal toxic shock SpeA, SpeB, SpeB = TYPE: Superantigens + RESULT: inflammatory effects — toxic shock, fascittis, erythematous rashes, fever, scarlet fever)DISEASES Pang = Enythematous 2 enudete * Cenvcal ympedenepay Soart Fever > CAUSE: Complton of eptoccca pharma * MECHANSNE ocou when th foctng ain ysogerzed by abactriophape @ mediates ‘rodicon ot pyrogeic exotoxin (SpeA. SpeB, Se8—Sunerantgens). OSS Circumorl por 7 = Srenoeryoroie fo + potas = Seen primary ding 2 Loose alo nlcton heumati fever ‘CAUSE: non-suppuratvecomploation ot .pyogenaepharyngtis. Chron, progressive damage to the heat vats may docu + Joint manifestations can ange fom etal frank artis ~ Acute glomeruloneprits: aoe lammaton ofthe rena lomerull WITH edama, hypertension, hematuria, and petra, = WHO: The ease occurs most common in patents WITH severe steptococal phanns| VIRULENCE: Some sein a. pogenss have an outer hyaluronic acd capsule hats _enigencalyindstngushable om hyaluronic acl in mammatan connective tssues. "Because he copsuie cen PROTECT the barter phagocyc dewrance * Encapaustd stein are mare tkaly 0 be response or saver ystmc nections. ‘COMPARE: Unita eres, ‘uboutanecue eave ‘SPREAD: Cems caused by 8. pogeneus runs ‘environment {Fost maths, in young children with poor personal hygiene. ‘Sueptccoocal Tae Shack IESENTATION: localize sin focton with pl, stanmation, mph node ‘enlargement and systemic symptoms. Silat calls * Vary ear border ously seen on ace, but ao on MECHANISM: preceded by nfctions of the respiratory tractor skin with S. yogenos Distinction between infected and na ROUTE tonne ee COMPARE (x opcode asad aces muccel epi We TSS for 8 RESULT: progrestesto shack and organ allure (nay, Iver, ings, heat) Flak tacos for tone shack “Surgery, chil, Wounds (may be Isocuus lke Insect es), NSAIDS, HI, ‘varicella zoster, Influenzacouse catiae =~ coaghiace— hemor “= Roryhomovee “a homobie a a er wore a ‘Scnscne or ae = ‘oreup 9) regatve Sescermas S.sapepnyacis Ss pyogenes — [Eagaacian] grows suscepti» © _optochn ptoenn cEeNacl “SSS NaG sutcoptble reel nen a | | | | 1 Phoumonia Efeecats bovis, S.omeuronae Sang . Meningitis conse - Newborns (OTHER preumoniavlated bm | ‘ Bacitracin “Stsont | [ OTHER Meningits [| |+ Scagalactiae - newooms 8 soasctee |. pneumoniae |L: monocytogenes 'N. meningitis ~ children H.Infuenza ~ 3-18 months unimmunized rustcoloured sputum = Moraxella catarrhalis ~ eldrly = Klebsiella pneumonia — currant red jelly sputum, lobar pneumonia = Francisella tularensis ~dituse pneumonia = Logionelia pneumophila ~ muit-obar consolidation = Mycoplasma pneumoniae atypical + Chlamydiae infant = __Chlamydophita psittaci — interstial pneumonitis E.coli K1 capsule Leptospirosis Intertogans — asepticNeonatal S. agalactiae infection ISEASES. Resistance to bacitracin ‘Synergistic beta-hemolysis, LOCATION: lower Gi, female genital tract, Gram + cocel nd Grow in chains Pe ee Catalase-negative ROUTE: Pneumonia @ from lungs 6] bloodstream (] sepsis (bacterial infection of blood) fj CSF causing meningitis WHO: S. agalactiae is the MOST COMMON CAUSE of septicemia and meningitis in newborns. ‘TRANSMISSION: Can be inhaled while the child is being born DIAGNOSIS, = Culture most sensitive test; a selective broth (.¢., LIM) is needed for optimal detection of vaginal carriage = Polymerase chain reaction-based assays to detect vaginal carriage in pregnant women Baby less than 1 years old with pneumonia progressing to meningitis — overwhelmingly S. agalactiae VIRULENCE: determined primarily by abilty to avoid phagocytosis (mediated by capsule).——— - ——_—____, ofa comttae— ponarbe ce herthonaiic chorohic Seuss novbwcn Tovtiocn tuclacn—— bacacn crows 0% be bie scain Sea at = = ‘Gitun vegan Sencernds S.sapmpnyiis©—««S pyogenes Sagaucrae, = grams sucaymieto nuenn oBinace “Se Nacl”akceple ian | | | | oaecoce Etec sone [Sammenco] _S. mane des Proumocoocal pneumonia —blood-inged (ust) sputum I Endocarditis - damaged heart valves caotso Bacteremia [} meningitis cree Ottis media — young children OTHER pmoumoniareated esr + Staphylococous aureus - PVL ‘OTHER Meningie *Stepococcus agalactiae ~newbom eee rete nevboms £8. pneumonia —rustcoloured sputum coun S.pnounone Moras ctarals~eerty te C reuarosenes {eat preumonia~ cured ly sputin, bar 8 pednonse mening ~ heron proumonia Hi intuenza~ 28 month unimmunized + Frandkela ulrenl tase posuonia Legionella preumopia ~ mutiobarconsollaton Ecol -K1 capsule Leptospirosis Interrogans — aseptic = Mycoplasma pneumoniae ~ atypical ‘Chlamydiae infant ‘Chlamydophila psittaci - interstitial pneumonitissist Endocarditis ‘WHO: can occur in patients with normal or previously damaged heart valves Bacteremia "WHO: 25% to 30% of patients with pneumococcal pneumonia and in more than ‘80% of patients with, meningitis FEATURES Alpha-hemolytic — from production of pneumolysin ‘Susceptible to optochin. Bile-soluble. Elongated gram-positive coce! arranged in pairs (diploct Cell wall includes teichoie acid rich in phosphorylcholine VIRULENCE: strains of S. pneumoniae are covered with a complex polysaccharide capsule + Determined by ability to colonize oropharynx (surface protein adhesions) _—, + Spread into normaly stele tissues pneumaiysin, IgA protease), DISEASES Pneumococcal pneumonia = CAUSE: Most infections are caused by ENDOGENOUS spread from the. oropharynx to distal site + RISK: People with hematologic disorder (e.g., malign risk for fulminant sepsis HOW: Pneumococcal pneumonia develops wih the bacteria multiply in the alveolar spaces. = After aspiration (into lower the bacteria grow rapidly in the nutrient-rich edema fluid, - Erythrocytes, leaking from congested capillaries [] accumulate in the alveoli {followed by the neutrophils then the alveolar macrophages. - SYMPTOMS: = Most patients have a productive cough with biood-tinged sputum = Chest pain (pleursy).. nasupnar iik Br ( cell disease) or functional Asplenia are atDISEASES Endocarditis = WHO: can occur in patients with normal or previously damaged heart valves, Bacteremi = WHO: 25% to 30% of patients with pneumococcal pneumonia and in more than 80% of patients with meningitis ~ Bacteremia meningitis in children/adults; rare in infants Ear infections WHO: leading cause of ear infections in young children, TREATMENT IMMUNIZATION: ~ With 13-valent conjugated vaccine is recommended forall children younger than 2 years of age ~ 28-valent polysaccharide vaccine is recommended for adults at risk for disease = MECHANISM: conjugation of polysaccharides to proteins stimulates a T-helper coll response DRUG: Peniciln is the drug of choice for susceptible strains, although resistance is increasingly ‘common = Vancomycin combined with ceftriaxone is used for empiric therapy;——— canine > Taare aa conan ponarbe cheer arent 1, — 1, suc adie linia soi viet Sea at cee Sea ‘ainano ae | | —t_, wg Sepcemas S.stooonyeca = Spyogenns = Sagnlacae gon mcapmnto _— Oke, UE SES wa | cote che semene [SS OTHER biofiim = S. mutans + EAEC = Pseudomonas aeruginosa =. lugdunensis — normal heart valves = S. pyogenes ~cross reaction with M protein = S. pneumoniae ~ damaged heart valves ~ S. mutans — pre-existing valve defect = Enterococcus faecalis -valve replacement = Coxiella burnetii— Q fever optoctin resistantTellurte in the media prevents the growth of other streptococci, and trypan blue, a dye, stains the bacteria that do grow on the agar differentially based on their metabolism FEATURES Gamma-hemolytic Bile-insoluble Optochin-resistant, DIFFERENTATION between Viridans streptococci by using Mitis-salivarius Agar DISEASES: Streptococci Mutans - Number one cause of cavities, dental plaques - Forms biofilm - THEREFORE must brush teeth - Allows it colonize and stick to heart valves - WHO: with pre-existing valve defect — heart murmur COMPARE = After infection with S. pyogenous — Ab against M proteins @ cross react with myosin in heart @ endocarditis, - S. Aureus - makes coagulase @ endocarditis ‘TREAT: Also, S. mutans have an enzyme, enolase, which is disabled by fluoride——— canine > care ofa conan ponarbe cheer rs oe eer soi viet Sea at = SF ‘ainano ae Sepcemas S.stooonyeca = Spyogenns = Sagnlacae gon mcapmnto _— Oke, UE SES wa bc ! | | | t E fbocais Stove S.pnoumonise © S. mutans. ‘i OTHER cystiis/UTI remove 'S. saprophyticus gon Enterococcus faecalis — bed-ridden patient ‘etl Proteus mirabi C. urealyticum ~ IC Pseudomonas aeruginosa — catheterized eek Burkholderia cepacia complex — catheterize i E. coli- MCC. E tacks UTIs and wound infections — patient that is bed-ridden Endocarditis - severe heart valve defect or valve replacement VanA cassetteeas acre FEATURES t Grow in high salt conditions Break down esculin NOT lysed by bile Resistant to optochin Enterococci are broadly antibiotic resistant Differentiated from related organisms by simple tests (catalase negative, pyrrolidonyl | arylamidase-positive, resistant to bile and optochin). DISEASES Enterococcus faecalis RESULT: cause UTIs and wound infections (patient that is bed-ridden) meee aan = UTI-=similar to S. saprophyticus ae Oe = Non-motile — got there due to wiping error - Endocarditis = ONLY in someone with replacement or severe heart valve defect or valve replacement — since unable to adhere to valves Most infections endogenous + Highly resistant to Vancomycin and many other Atb - Must do Atb susceptibility testing - do test on every single separate sample = VanA cassette ~ makes all alternate version in PG synthesissguebing eae ig anarobe die ‘mene moe = ole note ome Limonocingenes Copiers Beams | Banivect §=— Cicer’ = C.toium Cle Cpertiners = Emetic form — heat-stable enterotoxin, rice = Diarrheal form — heat-labile enterotoxin, meats (Ocular infections ~ Cereolysin + Phospholipase C motte 2 cereus Gram + bacteria baci pore-forming ‘aerobicDISEASES | Bacillus cereus Food Poisoning ~ Gastroenteritis spore bmng + Emetic form characterized by a rapid onset of vomiting and abdominal pain and a short duration; = TOXIN: heat-stable, proteolysis-esistant enterotoxin = _ Not a protein ~ therefore cannot be killed by re-heating rice = SOURCE: rice + Diatheal form — characterized by a longer onset and duration of diarthea and tie ‘abdominal cramps. r = TOXIN: heat-labile enterotoxin + SOURCE: Meats, vegetables & sauces Beceus MECHANISM: Stimulates the adenylate cyclase-cycic adenosine FEATURES ‘monophosphate systom in intestinal pithatia cells leading to VIRULENCE a + Capsule ~ Leading to regional lymphadenopathy, ~ -A-Btoxin edema toxin (PA-+EF) +lethaltoxin (PAs odoma, and sepsis, rey Edema toxin — adenylate cyclase activity ot ‘Pulmonary Anthrax (Woolsorter’s disease) ‘edema toxin is responsible forthe fd + ROUTE: inhalation ‘accumulation ~ MECHANISM: : alveolar macrophages ingest Lethal toxin - zinc metalloprotease activity of the inhaled spores and transport them to lothal toxin stmulatos macrophages to release _the mediastinal Iymph nodes. tumor necrosis factor-a (TNF-a), intrteukin-1B ( - RESULT FEATURES IL-1B), and other prositfammatory cytokines. ~ Massive enlargement of the ~ Capable of cleaving mitogor-activated mediastinal lymph\podes ~ Spore-forming protein (MAP) kinase, leading i colldeath =. Respiratoryfalure Non-motile > Sepsis Nonhemolytic USM: Wound infoctod with anthrax spores = Gramposttve rods. ~ Expressed genes for protective antigen + LF (destroys MAP kinase pathway ~ NO transtation) + EF + RESULT in classic anthrax — PAINLESS necrotic centers (LF) + ring of edema (EF) = Does NOT hurt ~ cannot express genes to send signal your death ‘opaque + outside is glittery = Legionella pneumophilacae ram spacers ball sone =H ig i sgaetinty spe hing {__ oormoie abe tigate mine cohen mie nae wie movade —Loomyiugres— CHET OTHER Bloody dantea | | eo | 2 Bee Eos Ratios = Cid Chin Cae [Cs | otetrincens Cellulitis - splinter deep into tissues, ‘Suppurative myositis — pus WITHOUT muscle necrosis, Myonecrosis and gas gangrene — biister filled with gas Food Intoxication — meat productsDISEASES Collultis: localized edema and erythema with gas formation = CAUSE: Due to splint deep into tissues creating local anaerobic environment = SPREAD ~ Radiate equally in both direction = COMPARE: S. pyogenes (towards trunk/heart) and s aureus (towards extremity) FEATURES Suppurative myositis: aecumulation of pus ( + Beta-hemolyic suppuraton in the muscle planes WITHOUT muscle - Phospholipase C - necrosis accounts orbeta: hemolysis Mygpecrosis and ges gangrene = Rectangular + MECHANISM: Lysis of irtammatory such as ~ Gram-positive rod ‘neutrophil | spread deeper into tissues {J more: Spores rarely observed dad taaues nove spread = Alkaline conditions in the small intestine stimul sporulation PRESENTATION ~ Blister filed with gas ~ gas gangrene = by- product of C. perfringens metabolism = Use fermentation pathway ~ releases gas causing these blisters = Very painful C. perfringens food poisoning = TYPE: Intoxication = SOURCE: contaminated meat products = TOXIN: Enterotexin-producing type A PRESENTATION = Abdominal cramps Watery diarrhea = Necrotizing entertis: acute, necrotizing destruction of jejunum — vomiting, bloody diarrhea, and peritonitis. VIRULENCE Aha toxin, the most important toxin and the one Produced y al ve Yes of C petnge Lecthinase (phospholipase C) Lyses Mediates massive hemolysis Increased vascular permeabilty and bleeding Tissue destruction Hepatic toxicity in s responsible for intestinal stasis. progression to necrotizing enteritis Heat-sensitve enterotoxin The heat-abile toxin is susceptible to pronase Entorotoxin also acts as a Superantigen simulating T- lymphocyte activity.Booms Banco ct Ceti Conan Cie one Cpertiners LimonocingenesDISEASES: Tetanus - TRE AB Toxin = Tetanospasmin is non-conjugative — nontoxic C. tetani strain cannot be converted to a toxigenic — San z = PRODUCTION: Tetanospasmin s produced during the stationary phase of growth, released when the cell Si islyeod FEATURES > MECHANISM Tetanospasmin inactivates proteins that regulate release of the inhibitory neurotransmitters glycine Motile ‘and gamma-aminobutryc acid (GABA) Spore-forming rod = The toxin binding is irreversible, recovery depends on whether new axonal terminals form. Round, terminal spores ~ Toxin bound to nerve endings is protected from antibodies that give it the appearance YN ofadrumaiick + RESULT: spastic paralysis Extremely sensitive to ‘oxygen toxicityGram + pacer sporesorming covtgate anaerobe = Home-canned foods = Honey for infants = Flaccid paralysis Coie = petigerssporesoxming -—— t © bowinun as DISEASE: Botulism = CAUSE: human disease caused by most commonly by ypes A and B - MECHANISM: Botulinum toxin prevents release of the neurotransmitter acetyicholine, thus blocking neurotransmission at peripheral cholinergic synapses ~ Neurotoxin is irreversibly bound = SOURCE - Home-canned foods (types A and B toxins) = Canned food/carrots/potatoes (J creates anaerobic environment in the jar kept at room temperature ~ HONEY for infants ~ ingest spore ~ SIGNS = Blurred vision with fixed, dilated pupils, - Dry mouth Weak and dizzy 1 to 3 days after consuming the contaminated food RESULT + Flaccid paralysis, ~ As with tetanus, recovery of function endings. after botulism requires regeneration of the nerveei tip che mie nie sate ene | | coe! Booms = Banas = Cay Cletus | Cfo pega Pseudomembranous colitis — Exposure to antibiotics spore ming catpae anaeroseDISEASES: Clostridium difficile. ‘CAUSE: Exposure to antibiotics is associated with overgrowth of C. difficile B ‘subsequent disease (ENDOGENOUS infection). soreming TOXIN mga enaerte - Enterotoxin toxin A) is chemotactic for neutrophils + release of cytokines —_ = Cytopathic effect f ~ Resulting in disruption of the tight cell-to-cell junction Lira ve Increased permeability ofthe intestinal wall r -— = Subsequent diarrhea. = Oytotoxin ~ Actin depolymerization = Destruction of the cellular cytoskeleton both in vivo and in vitro - Toxin A +B Interact synergistically . Pseudomembranous MECHANISM. + Toxin A pore-forming toxin eect ~ Pokes holes in cells attract neutrophils, Clostridium dificle. = Toxin B — stops translation = Lysis of cells ] pseudomembranous due to sloughing off inflamed underlying tissues RESULT ~ Small volume of bloody, stingy, mucous diarthea — accompanied by cramping ~ Decreases ability to retain water (diarthea) and nutrient absorption ( malabsorption)Len cee ram + vata ron spe erming ‘Actin-directed intracellular m Tumbling motion Neonatal Disease + Granulomatosis infantiseptica =_Meningitis or meningoencephi with septicemia + S.pneumoniae + Limonocytogenes = Nemeningitis ~ children + Hiinfluenza ~ 3-18 months unimmunized = E.coll=Kt capsule = Leptospirasis interrogans — aseptic + Herpes aseptic meningitis - HSV-2VIRULENCE e — = Attachment factors (intemalins) , = Hemolysins (Listerolysin O, two phospholipase C enzymes) . f + Protein that mediates acti-crected intracellular motlity(ActA) = Type secretion sytom injects actin A lows bacteria to move within the cll = Reason that at human T do not make fagola as they use on sporefoming — DISEASE we MCC ROUTE of infection for adults ~ consumption of contaminated product FEATURES: MCC for neonates ~ mother was infected with Listeria monocytogenes: + Non-branching Neonatal Disease * Gram-positive coccobacilli + Granulomatosis infantiseptica + Facultatively anaerobic - WHEN: Earty-onset disease + Broad temperature range (1°¢ = ROUTE: acquired transplacentally in utero 10.45°c) = Uke Treponema pallidum . concentration of salt + _ PRESENTATION: disseminated abscesses and granulomas in multiple organs + Motile at room temperature = Meningitis or meningoencephaits with septicemia + End-over-end tumbling WHEN: Late-onset disease: acquired at or shortly after birth (2-3 weeks after birth) motion = PRESENTATION: same as GBS + Weak p-hemolysis Disease in healthy adults: influenza-like illness Disease in pregnant women or patients with cell mediated immune defects + Consumption of contaminated {food (contaminated milk and cheese) + PRESENTATION = Febyile bacteremia = Disseminated disease with hypotension and meningitisDIAGNOSIS. - Cerebrospinal fluid (CSF) typically show NO organisms is the most commonly used molecular method for suspected outbreaks - Better diagnosis — take as will have some level bacteremia - Done using a blood culture — take blood sample - More sensitive to grow bacteria uw Microscopy of CSF not diagnostic for meningitisErysipelothrix rhusiopathiae y a i > TT KN / = te Rg Be ee Longer rods ~ pleomorphic Weakly gram+ stain, » Gauses Erysipel / FEATURES + Gram-positive + Non-spore-forming rod + Pleomorphic + Microaerophilic + Neuraminidase — attachment and penetration into epithelial cells * Polysaccharide-like capsule DISEASES Erysipeloid LOCATION: Exclusive to hands and arms PRESENTATION - More purple ~ Painful - burnings throbbing - Clear demarcated Border differ from cellulitis which is more diffuse ‘TRANSMISSION = Alocalized skin infection, loid, (not to be confused with streptococcal erysipelas); ~ Generalized cutaneous disease; + Septicemic. + Pigs COMPARE: Suppuration is uncommon, a feature distinguishing Erysipeloid from streptococcal erysipelasCame ewes Bletiacs Chev Clon © Caio «Cees oa 1 bet nas tats eat ant tierce bie Alsees Nasces N pains OTHER lysogenic bacteriophage = C. Diphtheria OTHER Pseudomembranous = Clostridium difici + C. Diphtheria = Enterohemorthagic E. coli + Vibrio cholera ro sperm 6 aphhere Diphtheria |A-B toxin — binds to EF Lysogeniec bacteriophage Thick pseudomembrane Elok test Palisades Diphtheria toxin repressor (OTR)DISEASE: Diphtheria Cutaneous diphtheria ‘CAUSE: Cutaneous diphtheria is TOXIN: AB toxin acquired through skin contact with ‘A subunit binds to EF G blocks translation painless death other infected persons. with greyish membrane of dead cols +S REGIONS RESULT: The organism colonzes the skin vonhuas | Catalytic rogion on the A subunit ‘and gains entry into the subcutaneous + Receptor-binding region tissue through breaks in the skin. = Translocation region on the B subunit. sete ~ Papule develops first and then an sees eiehine toxit (one) ‘evolves into a chronic, non- FEATURES - "ia loxin repressor (OTs tr = Activated in the presence of high iron smn ane eran healing ulogr, sometimes covered ‘concentrations + Cell wail with arabinose = Can bind tothe toxin gene operator and, galactose, meso- fiaminopimeie acid «Aerobie or facutavely TRANSMISSION: lysogenic bacteriophage, P-phage. araerobie PRESENTATION + Non-matile Se ctive ~_ Exudatve pharyngitis + Ferment carbohydrates” + Some mycolic aid + CULTURE: Rods form palisades aan prevent toxin production. ‘+ Difficy-tetsiodge without making the tissue bleed ‘complications ‘Neuropathy ~ localized to the soft palate and pharynx, later involving oculomotor and ciliary paralysis = Myocarditis DIAGNOSIS: PCR toxin production / ant-toxin antibodies ( Eiek test)Corynebacterium jeikeium — WHO: Immunocompromised patients , ZF predisposing conditions q @ = Prolonged hospitalization = Granulocytopenia 4@ Previous or concurrent antimicrobial therapy or chemotherapy eS + Presence of an intravenous catheter a KEY: Resistant to antibiotics, so antibiotic therapy during hospitalization may foster colonization of the skin C. urealyticum MECHANISM: Lyses urea — alkalizes urine environment RESULT: Causes urinary tract infections producing kidney stones because of strong urease activity RISK + Immunosuppression OTHER cystitis/UTI - Long-term antibiotic therapy = S. saprophyticus Enterococcus faecalis — bed-ridden patient Proteus mirabilis C. urealyticum — Pseudomonas aeruginosa — catheterized Burkholderia cepacia complex - catheterizedGram + actra 1 a Ite olan ats stant >, ———_, whe ci et ote — 1 l ! ne = Tarte Lays ie i i 7 —-ry ots ces tones Cut Chm Cae Cpt see —— vista tierce bie Alsees NascesFEATURES Anaerobic gram-positive rods Not acid-fast Grow slowly in culture Filamentous forms or hyphae Yellow-orange sulfur granules Endogenous infection LOCATION: in oral cavit teeth + gum line DISEASE: Actinomycosis PRESENTATION = Chronic granulomatous lesions - Become suppurative and form abscesses connected by sinus tracts = MCC: Draining sinus tracts along the angle of the jaw and neck (cervicofacial) = Non-healing abscess along the jaw line = Contain bright orange sulfur granule al actinomycosi a os ww = Pelvic actinomycosis — benign form of vaginifis a iy - Colonize intrauterine devi a. S = Central nervous system actinomycosis is a splitary brain abscess » % 3 SasPiee + Suturgraru colectd tom the sus actin apatint wth ‘cthomyenel, + Detcate famertous rds (row) sare seen at the periphery ofthe rushed granuleij i Propionibacterium acnes é |_| LocaTon: Microaerophilic environment at _|root _| MECHANISM: bacteria are phagocytized 8) A release of bacterial hydrolytic enzymes stimulate a localized inflammatory response DISEASE Invasion into blood occurs in one of the following three settings. (1) Transient bacteremia from a genitourinary source (e.g., after childbirth or a gynecologic procedure), (2) Endocarditis (8) Opportunistic septicemia in an immunocompromised patient. FEATURES + Facultatively anaerobic = LOCATION: Normal fiora in mammary glands ~ cow and human + MOST COMMON organism in the urethra - Primary component in normal flora of vagina — key at stopping hyper- + Recovery in urine cultures colonization from other pathogens * Rarely cause infections of the urinary = FUNCTION tract is their inability to grow in urine = Prevent colonizing of agalactiae * Used as probiotics (yogurts) = Prevent neonatal meningitis during the process of birth = Key to prevent from getting vaginal yeast infectionMobiluncus (Gram-stained) CULTURE: Both are gram+ ‘Still stain pink due to thin cell wall LOCATION: Found in vagina of women with other inflammatory conditions -osis = infection with something that may not necessarily cause symptoms = Cause vagina to smell bad - Halitosis = bad breath = CLASSIFIED - Have a gram-positive cell wall = Lack LPS ~ Susceptible to vancomycin, clindamycin, erythromycin, and ampicillin but resistant to colistin |Gardnerella vaginalis, Methylene blue showing “clue cells” with adherent bacteria) Associated with bacterial vaginosisCame wa rong sete . oe vote ae ate ote vee Lewes || —T— | cena Senacs cles Chinn catch cutie oan t vt veces weak segs ‘ae | hes [ramm] |! Pasouota maocca Nese Capnacyophaga Cellulitis — IN patients Cavitary lesion — IC patients Cord factor — interfering with fusion of phagosomes OTHER [BCYE] agar = Francisella tularensis = Legionella pneumopt = Nocardia - _Bordatella Pertussis Catalase and superoxide dismutase ‘Aerial hyphae + acid-fastness Buffered charcoal yeast extract agar= ‘ote ern FEATURES + Strict aerobic rods + Branched filaments + Catalase-positive + GROWTH: is slow, requiting 3 to 5 days of incubation before colonies may be observed on the culture plates + Catalase and superoxide dismutase VIRULENCE AVOIDANCE. = Cord factor — interfering with fusion of phagosomes with lysosomes = Secretion of catalase and superoxide dismutase = Avoiding acid phosphatase-mediated killing by metabolic utilization of the enzyme Cord factor — facilitates intracellular survival. = Interfering with fusion of phagosomes with lysosomes KEY: presence of aerial hyphae + acid-fastness is DISEASE: nocardiosis ROUTE: Exogenous infections acquired by inhalation (pulmonary) or traumatic introduction (cutaneous) PRESENTATION = Mycetoma - suppurative granulomas = Lymphocutaneous infections = Chronic ulcerative lesions = Subcutaneous abscesses + Cellul Cavita people with calsmediatedimmunty defectsRhodococcus OTHER acid-fast stainers FEATURES * Nocardia - Gram-positive + Rhodococcus - Weakly acid-fast + Mycobacterium - Initially appear rod-like agg then revert to coccoid forms Slow growth Accurate identification — genk s oF protein profiling by mass spectrometry WHO - Immunocompromised patients MECHANISM - Survives in macrophages and causes gt = Dissemination in the blood to distal sites.Acid-fast | thin rods, non-motile obligate aerobe —_'—_, M. tuberculosis grows at low temperatures, phenolase + M leprae Early endosomal autoantigen 1 [EEA1] - prevents fusion Interleukin-12 — Increases body temperature ‘Tumor necrosis factor-a — wasting (cachexia) Caseous granulomas Lowenstein-Jensen Media Catalase and SOD ‘Aciotast pacer ‘in reas, nonnotte obligate aero0e M tuberculosisFEATURES + Weakly gram-positive + Stron aly acid-fast + Aerobic rods + HIGH LY Resistant + Catalase+ and SOD -prevent killing by RNI-+ ROL + Plasma membrane are proteins, phosphatidylinositol mannosides and + High lipoarabinomannan (LAM). (619% to 71 mol%) Gc + CULTURE: NaOH Lowenstein Jensen Media (or Middlebrook agar DISEASE: Tuberculosis TOXIN = Prevents fusion of the phagosome with lysosomes (by blocking the specific bridging molecule, early endosomal autoantigen 1 [EEA1] = Catalytically catabolizing the oxidants that are formed RESPONSE + Macrophage infected by M. tuberculosis ‘+ Intracellular replication of Mtb — causing death from necrosis {cell will lyse Mtb will be ingested + Also undergoes apoptosis + Apoptotic parts are ingested by macrophages — will infect more macrophages ‘+ Macrophages secrete interleukin-12 (Increases body temperature by resetting hypothalamus) and tumor necrosis factor-a (Attractant for cytotoxic T-cells, also INCREASES metabolism Inducing T-cell differentiation into TH1 cells (T-helper cells), with subsequent secretion of interferon-y IFNy, the infected macrophages are activated + TNF-a stimulates production of nitric oxide and related reactive nitrogen intermediates, leading to enhanced intracellular killing + Central core of a necrotic mass that is surrounded by a dense wall of macrophages and CD4, CD8, ‘and NKTT cells Granuloma, prevents further spread of the bacteria, + Caseous granulomas become encapsulated with fibrin that effectively protects the bacteria, from macrophage killing(One granulomas inhalation of can lead to Meubereulosis formation of another granuloma F = resulting immediate i king of WT, that (@P0-) gets larger as it 1 a uses with more Tomah = granuloma It ford tissue breaks stabilization localized Be Jal down Bieonsolidation 8 (aterey) disease Bs wall has Broken + (ormary Te) 4 - Called a | i — hollow , ~ SIGN: Coughing os stabilization up (ene) (ening, tery TB) F blood f is stringy — ~ S. pneumonia = J Teactvation faniepinary TB)Acid-fast | thin rods, non-motile obligate aerobe -—_ M. tuberculosis grows at low temperatures, phenolase + M leprae Tuberculoid leprosy - Hypo-pigmented plaques - Enlargement of nerves = Leprosy test positive OTHER acid-fast stainers = Good CMI response (Tht) Nocardia Lepromatous leprosy + Rhodococcus ~ Decrease in CMI (Th2) + Mycobacterium Leonine fascies Anesthesia Armadillos ‘Acid fast bacteria thin rods, non-motte obligate aerobe grows at iow temperatures ‘henoiase + M lepraeee patra DISEASE: Tuberculoid leprosy DISEASE: Lepromatous leprosy = CAUSE: Bacteria intomalized by dermal = WHO: Patient with decrease in CMI will lead ino, on mate progression from Tuberculoid to leprosy oie eo macrophages {will replicate inside macrophages due to same virulence factors as Mtb + RESULT: influx of CTL — will keep infection 705 ato amperes i porlae + localized + MECHANISM: Spread of lesion macrophages ingest bacteria fj travel to lymph nodes but die enroute to lymph node causing more lesions spread = PRESENTATION ~ PRESENTATION + Erythematous macules, papules, or nodules us ~ Hypo-pigmented plaques with flat centers ‘extensive tissue destruction me and raised Diffuse nerve involvement with patchy sensory FEATURES ~ Peripheral nerve damage with loss sensory loss; Lack of nerve enlargement. + Weakly gram-positive = Enlargement of nerves Foamy" macrophages with few lymphocytes ‘and numerous acid-fast rods + UNABLE to be cultured ~ DIAGNOSIS: Lepramin test - similar to PPD test artificial media ~ Leprosy test positive if they Tuberculoid + Cooler temperatures leprosy —have a good CMI response + Manifests on extremities ~ Delayed-type (IV) hypersensitivity reaction + Disease primarily from host let response to infection + 20% HOI + SOURCE: Humans + armadilloavium complex ( kfécrophages have migrated to lymph nodes ] tried to antigen present {failed to kill antigen {J more inflammatory cells arise increased swelling of lymph nodes ‘TREATMENT: May need to debride defective tissue to granuloma LOCATION: Can live in oral activity @ macrophages present antigens FEATURES at cervical lymph node + Strongly aid fast RESULT: slowly-resolving subcutaneous infections + Aerobie rods + Disease primarily from host LOCATION: Wil only grow in cooler site — in cutaneous tissues « Weaey granneetine very well in macrophages and travel through lymph nodes due to *Palnts wth acquired rating macrophages immunodeficiency syndrome ( ADS) + egal primary though ingestion of contaminated ter or ood +__Disominatd 31g macrophages dying enroute — will result in small granuloma along site OFly (4 7x \ i Mycobacterium |JM. chelonae + M. abscessus = fast-growing” mycobacteria marinum + Quicker to develop and quicker to resolve Treatable with standard antbites + Low viulence potential + Following traumatic inoculation of bacteria under the skinGram — orm l diplococci onto! maltose & glucose only glucose oxidase + oxidizer oxidizer ony gone N. meningitidis N. gonorrhoeae| M. catarrhalis soins Pelvic inflammatory disease — women Urethral infection — men Purulent arthritis - MCC in adults (Ophthalmia neonatorum — blindness in children Pilin — attachment to non-cliated human cells Por (protein 1) - intracellular survival Opa (protein 2) - attachment to eukaryotic cell Pilin, PorB, and Opa - attachment and penetration IgA1 protease LOS — inflammatory responses Oxidizing glucose Diplococci OTHER arthritis S. aureus - septic S. pyogenes — rheumatic fever Neisseria gonorthea — septic arthritis in women Chlamydia trachomatis ~ reactive arthri OTHER cystitis/UTI . saprophyticus Enterococcus faecalis - bed-ridden patient Proteus mirabilis, C. urealyticum — IC Pseudomonas aeruginosa ~ catheterized Burkholderia cepacia complex — catheterizedVIRULENCE FACTORS Pin: Proton that mediates nial tachment to nonilated human cols or (protein 1): Poin protein that promotes Inracallular survival by preventing phagolysosome fusion in neutrophils (Opa (protein 2): An adhesion that mediates fm attachment to eukaryte col agess dforentachesins Opa proteins under diferent circumstances adhere to ferent cel ypes Pin, Por, and Opa proteins mediate attachmant and penetration into host cel IgA protease: Destroys lgA~ prevents opsonization 105; Lipotgosaccharide (ess saccharid) Induces inflammatory responses, ny gcose FEATURES + Aerobic + Gram-negative bacteria of saccharide Bl inlammation + tick purulent exudate ‘SEQUENCE: Opa proteins on surace ] bind avidly to surtaco of columnar epithelial cols ross basement membrane | many macrophages has lots of TLAS and bind to lipid A which Is highly exposed due to small amounts + Arranged in pairs (diph + Oxidase positive + Produce catalase +N. gonorrhoeae - oxidizt PRESENTATION - Females ~ony have columnar eptellum in particular part of cervix ths ls ONLY ste where they can be colonies a rest of vagina has squamous epithelium serge ocece ~ iy telecon oman ceicbrase tai tt encarta > ye + Large orice therefore less tkely oft pain ao ha + Pa may anaes btn van tes ong cin 4 < + Men — much of urethra that have right receptors for Opa proteins to bind to much severe symptoms ‘z + Infection in men is primarily restricted tothe urethra folucose id maltose ween “fica mos eae Bo 4 S ~ Septic rts de to being able to travel in blood Grow ingide neutrophilsDISEASE: Gonococcal infections + ROUTE: Spread of infection from genitourinary tract through blood to skin or joints + PRESENTATION + Pustular rash with erythematous base * Disseminated infections with septicemia and infection of skin and joints +N. gonorrhoeae isa MCC of purulent arthritis igfadults ony gcose Ophthalmia neonatorum = CAUSE: Chlamydia tre DIAGNOSIS worldwide = Gram stain of urethral specimens ~ TREAT: administration of silver nitrate is accurate for symptomatic males only ~ Culture on chocolate agar best = SOURCE = Sample of purulent exudate = Inflamed joint = Swab of eye ; B@eQOCUC@ Ut (Oxidase test - reagent will tum purple Therefore able to oxidize glucose but not other CHO bacteria makes oxidase enzyme {Bi produce acid as byproduct on their metabolismGram — l diplococci maltose & glucose only glucose oxidase + oxidizer oxidizer N. meningitidis N. gonorrhoeae M. catarrhalis Disseminated intravascular coagulation with shock | [ OTHER Meningitis Meningitis 'S. agalactiae — newborns Kemnig's sign S. pneumoniae Brudzinski's sign L monocytogenes Diplococci N. meningitis - children cram Atpiccoces matose & goose meningitis Glucose and maltose oxidatively |. influenza — 3-18 months unimmunized Kt capsule is Interrogans — aseptic OTHER IgA protease +S. Pneumoniae - H.influenzae type B + _ NeisseriaDISEASE: Meningitis, ‘TYPE: NOT a sexually transmited disease SEQUENCE: Respiratory pathogens thats encapsulated inhibit phagocytosis) + type IV pil to bind 1o respiratory ‘epithelial calls causing meningitis In children )Transoytosed Bj lick o endothelial calls 9 tavel through bloodstream B cross BBB f} cause meningitis due to LOS has exposed lipid A component ratose &gucsse PROGRESSION: Can continue to travel n blood causing Meningococcemia DISEASE: Meningococcemia Nmenngtts PRESENTATION FEATURES Ptochial rash elo 0 simlar to DIC states since used up coting factors Necrosis on feet and knees if children survive + ramnegatne dplocoes : + Fastidious " ‘+ Thrombosis of small blood vessels and mult-organ involvement 1 Sec Homenmagi lesions 2 Sides + Disseminated itavascular coagulation wit | Gane postive + lateral destruction ofthe acrenal glands + Acid produced trom glucose and maitose * ‘Meningitis symptom ‘oxidatively + Fever Capsule + Nuchal rigicity + Meningococcal ype IV pil ow ‘colonization of nasopharynx a Susnose vo sereanon 7 nasopharynx and Fen me teat Yogen tk ay “ + Endotoxin (LOS) mediates most onical sours when the knee flexes when the head is pushed forward rnnedatone Lisette antiga gat moments Sota ‘Ht maltose & glucose oxidizer N. meningitidis Gram — diplococc’ only glucose oxidase + oxidizer N. gonorrhoeae M. catarrhalis OTHER pneumonia-related = Staphylococeus aureus — PVL = Streptococcus agalactiae — newborn = S. pneumonia - rust-coloured sputum = Moraxella catarthalis — elderly - Klebsiella pneumonia — currant red jelly sputum, lobar pneumonia - Francisella tularensis ~ diffuse pneumonia = Legionella pneumophilia ~ multi-lobar consol - Mycoplasma pneumoniae ~ atypical = Chlamydiae — infant = _Chlamydophila psittaci — interstitial pneumonitis apecceesFEATURES Strictly aerobic Oxidase-positive Gram-negative diplocoogi Elderly patients Resistant to peni WHO: Causes pneumonih in elderly (75+) ‘TREATMENT: Resistant tb 1st generation beta-lactams, susceptible to everything elseTa ecco pooner xavlecrs —_gowhonducoayent pont on etic regiecosne —ikaees caaleve+ ever nprograon tat seated” Sparvinion cracked Sopinedim ‘room ~ Lenmmophia 8 paras Bucele Fens Pmitocite B rensele Meningitis (OTHER Meningitis - = 310 18 months of age 'S. agalactiae — newborns Gram ~ bacteria = Same gram-stain as streptococcus pneumoniae > $. pneumonias = Unimmunized children { L monocytogenes | © ; = N.meningiis~ children Epiglotttis — difficulty swallowing =H. influenza 3-18 months unimmunized Cellulitis - orbit of the eye + E-coli~K1 capsule Coccobacil ~__Leptospirosis interrogans aseptic Bleomorpnic (OTHER celllts-elated + Staphylococcus aureus — towards extremities + Streptococcal pyogenes cellulitis — towards the heart + Clostridium pertingens ~ splinter inoculated, radiates equally x &V actors + Erysipelothix rhusiopathiae required + Nocardia + Hemophilus influenza ~ orbit ofthe eye + Acinetobacter baumanni ~ orange peel cellulitis + Pasteurella multocida 1 Capnecytophaga Hinfluenzae‘Gram ociera_| FUSS ST WTI) DISEASE: H. influenzae meningitis COMPARE ; + Under 1 ~S. agalactiae Retina ® «| WHEN: Typical folows pneumeria + 1-Syears—H. influenza or Neiseria meningitides "gs, + Peak incidence of meningitis was seen in children 3 to 18 months of age shomee PRE Set) QYEULTURE: same gars, sopceocous pneumoniae wl run ogether © © © 25 comPARE: Have LPS, instead LOS — less severe inflammation compared to meningococcus W827 Le 8% | wo: Unimmunized children - ROUTE: Bacteremic spread of the organisms from the nasopharynx mquned E DISEASE: Hemophilus epiglottitis MECHANISM: Bind to epithelia cols in this gots serene X= Hemin FEATURES a WHO: Occurs in children between 2-7 years V=NADH PRESENTATION Both are needed from + Pleomorphic + Chi has dficully swallowing RBCS to grow influenza + Initial pharyngitis, fever, and diffculty breathing, and progressing to cellulitis and swelling of the supra- lotic tissues (Obstruction of the always possible + Gram-negative rods + Lipopolysaccharide with endotoxin activity less severe inflammation + Growth-stimulating factors: + (1) Hemin (also called X factor. DISEASE: Hemophilus influenzae cellulitis for "unknown factor") + @) Nicotinamide adenine dinucleotide (NAD; also called V factor for vitamin"). + Microscopy is a sensitive test + CULTURE: is performed using chocolate agar WHO: Colllts of the orbit of the eye PRESENTATION: Redalsh-blue patches on the cheeks or periorbital areasHaemophilus FEATURES Conjunctivitis WHO: Leading cause of pinkbye in children Easily communicable + Gis Granuom nun + Love -ymphogranuioms veneroum + ore“ Plnese + Fellows Panrul + Hate-Horpes simpx Gandy - Chancrold (Haemophius ducrey) Haemophilus eee y/ Chaneroid — ulcerated lesion on genitalia ‘ainful + bleeds when touched = Typically seen in men to lesion caused by sypl ‘TYPE: Sexually transmitted disease soft chanere, or chancroid CAUSE: Most haemophilus infections are caused by the patient's oropharyngeal flora ( endogenous infections) - EXCEPT Haemophilus ducreyi + Mistaken for primary syp! (OTHER conjunctvis/keratisioindness ‘Bails cereus chancres P. aoruginosa = Neisseria gonomh PRESENTATION - Hives elmanedthamnimbimal ‘+ Women are often asymptomatic = Haemophilus aegiptious + Pain with urination and pain during + Herpes ~ keratitis intercourse are common symptoms + Haemophilus aegyptus + Francis tularensis Chlamydia ~ trachoma, neonatal ~ leading cause of blindness in childrenTa i occas ome r 1 1 t 1 1 xaVhcie —_gowh oncarcoa yet gonkon sethantes cle wet” eine so oon oo ? Hidrzee propia 8 pass ncn ns mice ser “en stn B hancalae ‘Whooping Cough AB toxin Inactivates Gia Charcoal-containing agar Catarthal stage — highest risk to their contacts Paroxysmal stage — whooping cough Convalescent stage OTHER [BCYE] agar Francisella tularensis, Legionella pneumophila Nocardia Bordatella Pertussis Gram nactena coccobacil pleomorphic ‘growth on Bordet-Gengou medium 6. pertussis8 perses FEATURES + Causes whooping cough + Gram-negative respiratory tract pathogen + Adhere to surfaces of epithelial cells + Symptoms CAUSED by + Pertactin + FHA + Fimbriae + Allwill enable bacteria to stick avidly to ciliated upper respiratory epithelium TOXINS + Pertactin and flamentous hemagglutinin binding to sulfated glycoprotein integrins onthe membranes of cltated respiratory epithelium + Phagocytosis ofthe bacteria WITHOUT inating an oxidative burst + Pertussis toxin ~ AB toxin + Inactivates Gia, the inhibitory protein that controls adenylate cytase activity + Leads to an increase in eye adenosine monophosphate (cAMP) levels + Fimbria ~ Mediate the binding to cultured mammalian cells Optimal Timing for Diagnostic Testing + Tracheal Cytotoxin~ affinity for ciliated epithelial cells (weeks) ‘+ Stops beatingflunctioning/making of clia PCR: When ndiual Ras les caugh DISEASE: Whooping Cough =. " MECHANISM: A/B toxin that increases cAMP in epithelial cells, water secretion from cells, stimulation of cough reflex DIAGNOSIS (Optimal diagnostic specimen is a nasopharyngeal aspirate = CULTURE bacteria cultured on Bordet-Gengou or Regan-Lowe or other charcoal-containing agar = The media should be incubated in air at 35°, in a humidified chamber, and for 7 to 12 days + BUT culture takes >7 days, so PCR is a better early test. ‘TREATMENT = Macrolide ~ eradicating organisms and reducing length of infectious stage = Vaccines containing inactivated pertussis toxin, flamentous hemagglutinin, and pertactin are highly effective+ Catarrhal stage + 8 days after exposure + Resembles a common cold + Peak number of bacteria is produced during this stage and the cause of the disease is not yet recognized, patients in the catarthal stage pose the highest risk to their contacts. + Paroxysmal stage + After 1 to 2 weeks + Clliated epithelial cells are extruded from the respiratory tract, and the clearance of mucus is impaired) + Classic whooping cough paroxysms + Convalescent stage + After 2to 4 weeks + Secondary complications can occur + RISK: Non-vaccinated individuals + Human reservoir host +1990 changed formulation of pertussis vaccine = Went from kiled cell vaccine to acceluar pertussis ‘vaccine (does not ect as strong immune response) = Does NOT induce ite long immunity since not {a strong immune response = Thare were side effects of vaccine from killed call vaccineba lactose ameter Tecooe nt fermenter ‘curved sal gowth se ahaerobe! on Campy a ——_| ‘asttermanter coaaee + ‘motles125°C, pola'staining wrease+ urease — —s nar a — ‘otal 37°C 1 Sochanea nds pag HS. natposicn HS wei + uctse + Pasrignosa Yenterbolica — Ypasie I Kcpneumen Statice Precis Vchae Hp a = OTHER bioody darhea |] OTHER nor body darbea Cysts TEES ‘Salmonella enterica com ince Pyelonephritis - EHEC Vibrio cholera neonatal meningi = Schistosoma Vibrio parahaemolyticus. * ‘Septicemia = C.perfringens . jejuni ‘ocose fermenter E. coli O157:H7 B. cereus — heat labile enterotoxin Capsule ETEC tame Resistance to complement ‘Type 3 secretion system (OTHER oystisUTI = _EPEC AB toxins — watery diarrhea | |~ Antibiotic-resistant 2 Pseudomonas aeruginosa ~ catheterized Burkholderia cepacia complex — catheterized S. saprophyticus ince Enterococcus faecalis — bedvidden patient | = Proteus mirabil che = ©. urealyticum IC% Use of cate as carbons at } = EXAMPLE: salmonella Istoseemenar = From groon blue e = Proteus mirabls~ UTIIn = lege healthy 7 nae + Eosin-methylene blue J compare: 0. woayicum | | orange pink = lactose oer plate — also test __/ which atets ea for ry fermentation ‘ / Unease producing bactera FEATURES E. Coll only one that can cause + Gram-negative rods will turn plate + Facultative anaerobes— PUT A At Either highly motle, or no therefore Tan aged tea ec motility * Oxidase-negative wh + Motile with Desc rrmenrs J NontsorFemens} listeria monocytogenes, (uniformly motility distributed over the cell Eq dor == L =]FEATURES Gram-negative Facutatve anaerobic Lactose-fermonter Rods ‘Oxidase negative Lipopolysaccharde consists ot ‘outer somatic © polysaccharide Lipid A (endotoxin) + Mast common aerobic, gram- negative rods inthe ‘gastrointestinal tract + Infections are endogenous + Gastroenterts are generally acquired ‘exogenously VIRULENCE Inflammatory responses due to lipid A, the internal part of LPS (binds to TLR 4, @] TNF, IL-1) ( also = “endotoxin”) Antibody response against O-chain (= the “polysaccharide” in LPS), and against capsule (in bacteria with capsule) and flagellar proteins (in bacteria with flagella) uter carb part of LPs flagellin type Ex: E. coli O157:H7 Phagocyte evasion via capsule (may include lipids as well as carbohydrates) —also poorly antigenic Resistance to complement system killing (anti-C3b) Type 3 secretion system: Structure like flagellum, analogous to a syringe that injects proteins into human cells ANB toxins, lots that increase cAMP @j watery diarrhea, + Some that bind to ribosome @] stop translation fj cell death Hemolysins Pili Broadly antibiotic-resistant.DISEASE: Enteroinvasive E. coli VIRULENCE: Type Ill SS — actin cytoskeleton rearrangement proteins | LOCATION: developing countries CAUSE: ingestion Infectious dose — number of bacteria to be exposed at one time to get sick - Higher infectious dose = es ely to get st elo > Has very high infectious dose oe mgs ieee Sree PRESENTION ac aaa cae ~_Tnvade and destroy the oni ptbeUM saci en Sinton Sr ~ Watery danthes, some bo Sed een comers Er caer ype] ae Pert ae ee ee Eee) ence IEC Fever, eanpng. Oleeasein Insonanddeath of Rebyeaton: Wele/darbes, devoosrg oloncepitebum caret ‘ary Secomes’ runt see dames EHEC Bloody danhes Chis, Elaine Set and Sb Amie a Soler tues Rrasstes mouse aa Sescoene mom (ee)Sanepeacn DISEASE: Enterotoxigenic E. coli i WHO: young children in developing countries or travelers to these areas. see ROUTE: Acquired through consumption of fecally contaminated food or water MECHANISM L_ = ABioxin sntes| = Net effect of this interaction is an increase in cyclic adenosine monophosphate (cAMP) levels | = High infectious dose PRESENTATION: Watery diarrhea ~“v- ‘Wary aannes > E.coli , — wil a pin era the om TT ReaiaySame pace DISEASE: Enteropathogenic E. coli | ucownsa ton rated baci aah cpt ma tee ween: |" Snnoupuntsteanel Ganraon sea mermee + Secretion of proteins into the host epithelial cell occurs by the bacterial type Ill secretion system + Tiresults in polymerization of actin | + Aatin creates pedestal denudes microvll decreasing SA decreased absorption B watery darhea VIRULENCE ones ere raos + Type lll secretion system ‘+ Tirresults in polymerization of actin [ESULT: Infant diarrhea in impoverished countries 2 iyeaarepeuin neces PRESENTATION peer rer ot - Watery diarthea ‘egress anSlmon pa ~ High infectious dose oer ay ry bloody) diarrhea, |everywhere ( {structure due to be useful Roariary ener’ uri Ce mac Stiri es Ma ether =a?DISEASE: Enteroaggregative E. coli MECHANISM = Aggregate on surface of epithelial cells &) denudes villi and effacement j decreased absorption watery diarthea = High infectious dose - Aggregative adherence fimbriae | (AAF1), adhesins that are similar to the BFP responsible for micro -colony formation of EPEC WHO = Developing countries = Daycares - Fecal-oral contact PRESENTATION - Watery diarrhea = High infectious dose Sry Serra ayFEATURES * Bloody diarrhea + Hemolytic urer syndrome (HUS) + Small infectious dose * Developed countries + Undercooked ground beef + Shiga toxin + Acquired by lysogenic bacteriophages DISEASE: Enterohemorrhagic E. coli cause + Consumption of undercooked ground beef or other meat products + Both toxins are acquired by lysogenic bacteriophages. MECHANISM _— = Shiga toxin 1 ~ B subunit binds avidly to surface of intestinal epithelial cells ‘Shiga toxin 2 except B subunit binds avidly to glomerular endothelial cells ‘Stops translation Q] killing intestinal epithelium (j slough off @ bloody + mucous diarrhea. ~ Grain-feeding in stomach - increases acidity in stomach gut of cow @ kills all others bacteria EXCEPT EHEC ( resistant to acids) PRESENTATION * Bloody diarthea, possibly developing to hemolytic uremic syndrome + Hemolytic uremic syndrome (HUS), * Acute renal failure + Thrombocytopenia + Micro-angiopathic hemolytic anemia + HUS has been preferentially associated with the production of Stx-2, which has been shown to destroy glomerular endothelial cells RESISTANCE: Shiga toxin genes are on operon that is tured on by Atb ~ Efflux pump related operon § will increase more Shiga toxin 1 and 2 - THEREFORE Atb will make symptoms worse| E. coli: urinary tract infections VIRULENCE tc ere + P-Piln: Specialized attach very strongly to bladder epithelial cells, prevent E. coli trom being flushed out by flow of urine + Flagelia: Allow E. col to swim in urine, start colonization of ureters + Sbe2: AVB toxin made by some strains of EHEC, causes kidney failure + Homolysin HlyA that lyses erythrocytes MECHANISM: via Shiga-tke toxin = High affinity for receptors on glomerular ‘endothelial cells @ bloody urine, possible kidney failure ROUTE: Ascend into the bladder ] migrate to the kidney PRESENTATION + Oystiis + Pyelonephrtis ‘+ Flank pain — inflammation of kidney + High fever E. coli: neonatal meningitis, septicemia DISEASE: meningitis VIRULENCE: Kt capsular antigen. ‘COMPARE: group B streptococci DIFFERENCE: E. coli make extended spectrum beta lactamase (ESBL) ~ cannot use same Atb PRESENTATION: Onset of symptoms with 1 week PREVENTION: screen mothers for agalactiae or K1 capsule-producing E. coli DISEASE: Septicomia CAUSE: Originates from infections in the urinary or gastrointestinal tract,sa tose mer Toco ohm Toca goa abe coder Soe —— fesemener ciines wei 256 Spastiing wedes wel hans ae SY i i SaaS Mp ERI RIO pe tee Pome vee Hen ca a ma i | Kprebmeniee Ec Smee Press Vctlose ‘Salmonella enterica = Effacement of vill = Non-bloody watery diarthea Salmonella Typhi - Patchy rash on torso Gall bladder chronic colonization M (Microfold) cells, Poultry, eggs, dairy products Hektoen enteric agar — black precipitate Citrate - green g blue ram-tacera C. jejuni Salmonella Typhi prowces HS _l 's nomFEATURES + ldentitied as O-polysaccharide + Invade into the M (Microfold) calls + Type Il secretion system + Gastroenteritis is the most ‘common form of salmonellosis + Nausea, vomiting, and non- bloody diarrhea. + SOURCE: poultry, eggs, dairy products + WHO: reduced gastric acid + 10 patients DISEASE Antibiotic treatment NOT recommended for enteritis because this may prolong the duration of disease ‘Salmonella enterica MECHANISM: Bind to intestinal epithelial cells] njoct cytoskeleton via Type Il SS {leads enguttment by intestinal epithelial cells Q replicate VIRULENCE: Type ll SS PRESENTATION + Effacement of vill + Non-bloody watery diarrhea * Inflammatory response fj cramping + nausea Use of citrate as carbons + Helton enter agar + Symptoms appear 1 week after ingestion ‘source. + Islte Sarmonata HANLE:samonota, Sonam ‘Salmonella Typhi — typhoid fever = From green B blue ‘produces black precintata MECHANISM ~ From intestinal epithelial leads to systemic dissemination and bloodstream infection (septicemia) §) go to liver clearing out most of bacteria &] hepatomegaly J bacteria will o to gall bladder + colonize ~ Enguifed by macrophages PRESENTATION ~ Ten to 14 days after ingestion —high ever (yphold fever) due to TLR 4 recognition ~ Patchy rash on torso = Hepatomegaly = Gall bladder chronic colonizationwd scone omer To ter cad al gar ane Stay Ser —— setae citer wee SG ttf wadies woe ots —S a a 1 i Se mn MR lee ene Faroe vee mae not ca fa es i i | Keprebnone cl Tae] Preis Vehawne tea Gastroenteritis Daycare centers Actin Tenesmus OTHER bloody diarthea EIEC EHEC C. perfringens Blood in the stool Trimethoprim-sulfamethoxazole Mcells Shiga toxin wat oss ripeness rene genteFEATURES Gram-negative Facutatvely anaerobic rods Fermentor ‘Oxidase negative Lipopolysaccharde consists of ‘somatic O polysaccharide Lipid & (endotoxin) Shiga toxin produced bys. dysenteriae disrupts protein ‘synthesis and produces ‘endothelial damage ‘A subunit and the B subunits Primary manifestation of toxin activity Is damage to the intestinal epithelium, ‘Membrane ruffing DISEASE: Shigella Change trom red 3 CAUSE: Fecakorl route yolow = Lactose termentd at WHO: young children in daycare centers bottom of test ube = ONLY tementitin + Uke Enteroaggregative Ecol ONLY fom conations VIRULENCE: Tye $s Highly infectious MECHANISM 4 + Atach to and invade the Mls (ike Saimoneli) + Induce membrane puffing onthe target cell, leading to enguifment of the bacteria, + Rearrangement of actin filaments in the host els cel-o-cell passage occurs + Survive phagocytosis by inducing programmed cel death (apoptosis) PRESENTATION = + Gastroenteritis (shigellosis) ae sie aim + Cardinal feature of shigellosis =} en eS * Lower abdominal eramps i = + Tenesmus (straining to defecate) + Abundant pus + Blood in the stool ‘TREATMENT: Fluoroquinolone or trimethoprim-sulfamethoxazolewd scone omer To ter cad al gar ane Stay Ser —— setae citer wee SG ttf wadies woe ots —S a a 1 i se eon mI ee ene Faroe vee [Ta] nate coe fa ms i | | Kpnalmonee cl Sjmneree Peale chee dace cram -bacera High fever voc Painful bubo — swelling of the lymph nodes in the groin or axilla BLACK PLAGUE Bipolar staining 250C express sigma factor — clots flea blood 370C — genes to spread disease in the human host Flea bite factose nontermenter Dipolar staning Y pestsDISEASE act EY: bipolar staining ~ circles on either end of call, “safety pin bose nan erm ‘Type Il $$ into 20 express sigm factor expression of hem agglutinin clots blood of flea ‘therefore flea is ver)\bitey” and spread bacteria into your bite site 370C ~ express genes pat faclitate spread of other genes to spread disease in the vo na ~< rescuing aan ctcoolton Sopate sie + pt alte macrophage to signal FEATURES for help | macrophages present Yeteinia epitopes at lymph nodes to T-cell enable spread to other macrophages within the fary lymph node «Seta tc PRESTION > eee Pal blood bore infection + Cacete ngaive 1 feted vie oa te (rom pre dog Cpa toon | Aightover an pall bubo (tarry sweting of the mph nodes) inthe goin * Potoneapeultatisante oral phagocytic « Gmeneccraoue 5 Gene tor acheronce, inhibition of platelet ‘aggregationcan wa scone omer To ter cad al gar ane Stay Ser —— setae outa citer wee SG ttf wadies woe ots —S —— >t 1 i wei ie eon mg as oie omens] yma nate ce fa ais mages: i | | Kpnalmonee cl Sjmneree Peale chee dace Gram ~ bacteria Enterocolitis Acute appendicitis Enlarge mesenteric lymph nodes Developed countries — children in day care centers ‘enterocolitica — mimics mimics % enterocenucaFEATURES + CAUSE: Ingestion of contaminated food products or water (unpasteurized milk, pork) + TYPE: Gastroenteritis, + Two thirds of all Y. enterocolitica infections are enterocolitis ‘+ PRESENTATION * Diarrhea not at arc » Fever + Abdominal * Enlarge mesenteric lymph nodes and mi acute appendicitis. + WHO: Y. enterocolitica infection is most common in children, with pseudoappendicitis, * More common in developed countries — children in day care centers + Like Shigella, Enteroaggregative E. coli + CULTURE: organisms can grow at 4° CGam ' sa tacos ma Too at fame ad ot gos oat jl Scary oe ——_| fate ite cies mete 2FG Wl welees elie Bote — —+—_, mare 1 vecinca ales padaseHes mapohon rs wots + gickes Pamghoss Yertottca Ypulse Han a a ‘cpeelnnee) cl Sjmneree Peale chee Klebsiella pneumonia = Lobar pneumonia Currant red jelly sputum Klebsiella granulomatis, = Sexual activity = Beefy lesions = _Donovan bodies OTHER pneumonia-related = Staphylococcus aureus — PVL = Streptococcus agalactiae — newborn = S. pneumonia ~ rust-coloured sputum = Moraxella catarrhalis — elderly - Klebsiella pneumonia — currant red jelly sputum, lobar pneumonia + Francisella tularensis ~ diffuse pneumonia = Legionella pneumophilia ~ multi-lobar consol - Mycoplasma pneumoniae ~ atypical = Chlamydiae — infant = _Chlamydophila psittaci — interstitial pneumonitisDISEASE: Pneumonia VIRULENCE: Capsule = Mucold appearan = Prevent enguifment by macrophages fastener PRESENTATION = Lobar pneumonia = Necrotic destructidtre inca et -- | Cavities | = Production of blood-tinged sputum (cura neurone FEATURES DISEASE: Klebsiella granulomatis CAUSE: trauma of sexual activity PRESENTATION + Lobar pneumonia = Lesion on males penis * Blood-tinged sputum -_Besty lesions ~ Not very painful = Bacteria growing intracellularly ~ Donovan bodies = VERY rare in US and Canada COMPARE: Ducreyi indented lesion + painfulsa tacos ma Too at fame ad ot gos oat Scary oe ——_| taster cies mete 2FG Wl welees elie Bote — —- __, — "mare 1 i outed ites omen mapensihS wees ames Pasiprom Yotouases Ypnse Hiner Cn Kepneumonge E290 coslee [ESS] vedas feats Kidney-stone ‘Swarming” motility Urease OTHER cystitis/UTI 'S. saprophyticus Enterococcus faecalis ~ bed-ridden patient Proteus mirabilis C. urealyticum IC Pseudomonas aeruginosa ~ catheterized Burkholderia cepacia complex - catheterized E.coli MCC ‘Gram bacteria aca lactose fermenter rast fermenter chemical tests 1 pneumoniae‘Gram paca FEATURES 7 RESULT: Ammonium-Mg-Phosphae kdnoy-stone producing UTis sso mr ev sual + Swarming” motility uu —— Normal Gi tract flora wi Fefvoee Proteus mirabilis ~ UTIIn heathy ‘COMPARE: C.urealytcum which Enterobacter, Citrobacter, Morganella, Serratia, Providencia, Erwinia ‘fects Immune-compromised + Septicemia in neonates + Rest cause infection in IC long-term hospitalized patients + Resistance is a particularly serious problem with Enterobacter speciessa tose mer Toco ohm Toca goa abe coder Soe eagle —— fesemener Tete ASG SpcTeing weds wetie-— apis — —- __, a eee MY I | set es gs mpage tes es Pasunrose Verobcleco pecs «Him Gis a ma i | | Kprebmeniee Ec Sjmieree Persie [olen suits ‘Vino shot ‘Vio vuniious “som pana Fice-watrsico Primary septicemia Seawater orbrackish water | | Tissue necrosis necrotizing fasciis | vem OBS agar ‘Shelfsh lactose non fermenter Lysagenie bacteriophage ©. Diphtheria oo ene 8 cAMP - Enterohemorthagic E. coli conte Vibrio cholera ‘Vibrio parahaemolyicus Bacterial gastroenteritis Japan and Southeast Asia Gastroenteritis Seafood-associated ~ US/Canada lucose fermenter ‘Shelfish B-hemolytic colonies with human blood but not sheep blood venberse Enterotoxin — increasing intracellular Ca] chloride ion secretioncove femeer FEATURES Reservoir of seawater or brackish water Require sodium chloride (NaCl) for growth Tolerate a wide range of pH + Susceptible to stomach acids. Grown on TC8s agar — observe fermentation of sucrose ‘Associated with shellfish — colonize their exoskeleton Flagella Curved rod DISEASE: Cholera CAUSE: Contaminated water spread = Infectious dose >108 bacteria but can be much lower if acidity of stomach reduced = Lysogenic bacteriophage VIRULENCE + Polar flagella + Lipid A (endotoxin) + AJB toxin ~ increasing cAMP + Toxin-coregulated pilus (TCP) allows bacteria to adhere to intestinal epithelia @ higher [ toxin] at epithelial surface + Chemotaxis proteins encoded by the cep genes PRESENTATION e-water stool + Similar to the heat-labile enterotoxin of Escherichia coli + Adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP) + Hypersecretion of water and electrolytes. ‘TREATMENT + Fluid and electrolyte replacement + Filtering copepods — sari + DRUGS: azithromycinDISEASE: Vibrio parahaemolyticus CAUSE: Food-borne infection (not intoxication) 24 hours after consuming contaminated raw shellfish, WHO = Seafood-associated gastroenteritis in US/Canada (mast common gastroenteritis overall in Asia) = Most common cause of bacterial gastroenteritis in Japan and Southeast Asia LOCATION: Found in estuarine and marine environments worldwide PRESENTATION FEATURES + Watery diarthea © Cu + Cramps cued + Vomiting + Gram-negative ods + Fermentative + Facultative anaerobic + Require salt for growth + B:hemoiytc colonies on agar media with human blood but not sheep blood + TDHis an enterotoxin that induces chioride ion secretion in epithelial cols by increasing intracellular CaDISEASE: Vibrio vulnificius | OTHER necrotizing fasciitis ‘Streptococcus pyogenes Vibrio Vulnificus FEATURES + Curved, gram-negative rods Pseudomonas aeruginosa - severely IC + Fermentative Clostridum perfringens + Facultative anaerobic + Require salt for growth cove femeer VIRULENCE: Polysaccharide capsule and hydrolytic enzymes voli rresonanou oy Sena tt come caimintedsev oes «Woe ner ter epone ean sxrae «Wome CAUSE: Traumatic inoculation under the skin due to stepping on sea shell ‘SEQUENCE: ingestion § crataging fj septicemia @ spread to LL @ proliferation @ necrotizing fascitiscam aa tata emer Tacos non foment ‘cnved al goth — sc aaerbe on Campy sa" —— ‘eetermenter ost ‘moll 25°C, peor sanng wedse+ ease Fans —_s nar a amare { | i Biocon “re pro HS alpen Seis « ~ Peogross Venteotcs pests Hytn [Gur Keramne cl Sjmneree Peale chee secs Mimicking acute appendicitis Cram —baceria Curved | Damage to jejunum act Contaminated poultry | 42 degrees curved, sai Guillain-Barré syndrome sro on Came agar - O-antigen (0-19) — cross-reactivity in peripheral nerve gangliosides ~_Ascending paralysis OTHER appendicit = Yersinia enterocolitica — mimics = C. jejuni - mimics © unou on Camby aga FEATURES + Thin, curved + Gram-negative rods + Histologic damage to the mucosal ‘surfaces ofthe jejunum + Gastrointestinal infections + Acute enters with diarrhea, fever, and severe abdominal pain *+ Abdominal pain mimicking acute appendicitis = Y, enterocolitica + Inflammatory response + Intense abdominal pain ‘mimicking appendicitis + Cramping + nausea DISEASE: Gastroenteritis CAUSE: Consumption of contaminated food, mi, or water; contaminated poultry = Food products that neutralize gastric acids (e.g., milk) effectively reduce the infectious dose GROWTH: Optimum growth is at 42 degrees, but can stil, - Microaerophilic atmosphere souRCE + Normal flora in Gl of chicken — can also cause systemic infection of chicken just lke salmonella, + Can colonize GI of cattle — but NOT a systemic infection — Just lke listeria monocytogenes ‘SEQUENCE: Ingest bacteria trom contaminated food — undercooked chicken or unpasteurized dairy fj bacteria will colonize intestine by adhering to surface ot vill intestinal epithelial cells ] can invade into tissue and cells and swim between gaps between cells due to being skinny {J reach basement membrane under epithelial cells Q disrupt epithelial cells leading to effacement of vill less absorption and watery diarthea DISEASE: Guillain-Barré syndrome CAUSE: O-antigen (0-19) related to antigenic cross-reactivity in peripheral nerve gangliosides. PRESENTATION: ascending paralysisaa tata emer Tacos non foment ‘cnved al goth — sc aaerbe on Comey aoa —— ‘eetermenter ost wcll 125, bpclarstining esses urease 2 — ——" _, mare 1 I Biocon “re pro HS alpen Seis « ~ Paargnoss Vento Ypests Lipin ] cen Kprebmeniee Ec Sjmneree Peale chee secs ‘Gastric adenocarcinoma Sram pactera Ulcers I Urease baci ‘Vacuolating cytotoxin A (VacA) ~ producing vacuoles after endocytosis | ‘Type VI secretion system — Induce interloukin-8 (IL-8) casved, smal Proton pump inhibitor, macrolide, B-lactam ‘growth on Campy agar Contraindicated antacids OTHER urease rete + C.urealyticum + Proteus mirabilis, +H. pylori 1H. pytonrontnon Cay aa 1 FEATURES + Assume coccoid forms in older cultures + Associated with gastritis, peptic ulcers, gastric adenocarcinoma, and ‘gastric mucosa- associated lymphoid tissue (MALT) B-cell lymphomas + Presence of polar flagella + Do not ferment or oxidize carbohydrates DISEASE VIRULENCE + Highly motile + Urease + Damage is mediated by urease byproducts, mucinase, phospholipases + Lipopolysaccharide (LPS), consisting of pid A ‘+ Establish lifelong colonization n the stomach of untreated humans + Vacuolating cytotoxin A (Vac), a protein that, after endocytosis by epithelial cals, damages the cols by producing vacuoles +” Faciltato thelr survival within our cells ‘+ Type VI secretion system that ats lke a syringe to inject the CagA protein ‘Induce interloukin-8 (IL-8) production, which attracts neutrophils PRESENTATION + Gastts (hats, infitration of neutrophils and mononuclear cells into the ‘gastric mucosa), + Fullness, nausea, vomiting, and hypochlorhydria Evolve ino chronic gastils Ulcers develop at the sites of intense inflammation Antibody tere cannot be used to scriminate ‘TREATMENT + Combined therapy with a proton pump inhibitor (e.g., omeprazole), a Digest mths spec “cl selenion ‘macrolide (eg, clathromycin) and a f-iactam (0g, amoxclin) for 2 weeks osm =r= has had a Noh coceose rate Woon Eterm amt CONTRAINDICATED: Antacids make better environment for Helicobacter cans pylori as do not have to use urease eba lactose ameter Tecooe nt fermenter ‘curved sal gowth se ahaerobe! | i ovo eae ‘asttermentar otaboe coaaee + ‘motle25°C, polar stanng wedse+ urease | 8 Fania — > ——+_, rea ‘otal 37°C biochemical me pro HS alpen Seis « ~ Paccugnoss Ventrocoiica posts «= Han Gent Kprebmenee Ec Sjmneree Peale chee secs cram - bacteria Bacteroides fragilis = Anaerobic peritoneal infections Anti-inflammatory = Post-surgical infections vaca H. hepaticus = _Activator of inflammation strtanaerove BragsDISEASE: Bacteroides fragilis LOCATION: Bacteroids are the MOST COMMON component of human gastrointestinal flora. VIRULENCE : Most pathogenic of the Bacteroids because of its capsule. : But, its capsule is also ant-iflammatory. : REASON: Their LPS is altored so it DOESN'T bind TLRS isk = Post-surgical infections, especially following gastrointestinal surgeries = Brain abscesses in immune compromised patients. FEATURES PRESENTATION = Anaerobic peritoneal infections + Bacteroids are obligately eqn: metronidazole + something realy, relly new (tgecycine) anaerobic + Very fastidious COMPARE: H. hepaticus is a potent activator of inflammation. = VERY antibiotic-resistant. - Associated with inflammation in the intestine and not gastric mucosa. + Those that remain have been selectedbaci Tecooe nt fermenter —_______} otaboe coaaee + biochomical indole + produces H:S notproduca HsS reas + ghonee + ‘rosie non mate ‘mati #125°C, paar staining otal 37°C ly entrbcostica —Ypaste ‘carved sal goth on Campy a ——_| py Cou “et aaeabe 2 fegits Lung infection — MCC in cystic fibrosis patients Bur wounds urinary catheters External Otitis (swimmer’s ear) — alcohol wipes Eye infection — comeal ulcer Ecthyma gangrenosum ~severely IC Osteomyelitis — severely IC Biofilm Pyooyanin + pyoverdin — antibiotic that kill gram-positive 4-42 degrees Organic items like plants Hospital floorPseudomonas gsese aeruginosa p intection ‘WHO: MCC In cystic fbrosis patients Heterozygote advantage ~ resistant to cAMP AB toxin as those disease — lose less wate than normal MECHANISM: Detect in CFTR transport very dense mucous that alow P. aeruginosa to settle tsk groups: IC, patients on mechanical ventilation, burn to pyoverdin + pyocyanin ‘Moist surface on burn wounds Woultis WHEN: after shaving due to open hair follicles LOCATION: hot-ub, swimming poo! un WHO: long-term indwelling urinary cathoters. External Otis (swimmers ear) PRESENTATION: green coloured pus PREVENTION: alcohol wipes: Infection ~ comealuleer| : ‘CAUSE: ina trauma to co reo P. ‘contaminated water Ecthyma gangrenosum — necrotizing fascitis WHO: ini 7 Osteomyelitis ‘WHO: in eeveraly 1c + TREATMENT: must test isolates individually ccBurkholderia cepacia complex * FEATURES * Causes onion rot * DISEASE * Pulmonary infections * WHO: 2nd MCC in cystic fibrosis patients + PRESENTATION * Yellow/White + Smelis like freshly dug dirt * UTI * WHO: catheterized patientsAcinetobacter baumannii * FEATURES wt 4 DISEASE * Strictly aerobic Necrotizing fasciitis : Nowaat reg evengeal fo flora PRESENTATION: Hemofrhagic bullae WHO: immune normal, soldier with war * VIRULENCE — wounds in Middle East * Resistant to antibiotics MECHANISM: inoculated under the skin LOCATION: Soil bacteria - Middle East, North Africa inge peel cellulitis OTHER resistance Enterococci E.coli TREATMENT: Resistant to antibiotics Corynebacterium jeikeium Bacteroides fragilis Pseudomonas aeruginosa Acinetobacter baumanniiCam t coceabecl r r T T t T T aviators growth on charcoal yeast, gow on ‘etic requires cysteine aidase + caalase + teased” — arin crtane eee Ego nea ‘eon H intvencoe L pneumophila B porta Bruce F tronic Price 1 ‘hve impregnation stains B hereeloeEikenella corrodens + FEATURES * Fastidious organism * Non-motile Instigate inflammatory response if traumatically + RESERVOIR: Normal flora in mouth of ‘noculated under the skin humans DISEASE ‘CAUSE: human bite woind or fistfight injury * WHO: children in daycares TREATMENT: penicillinGam i coccabach pooner r T T t T T 1 xavlecors goth on charcoal yeast gonton aevtic—requrestyne —cdae icles ser inprogaon sae rented” — Tyumen ‘ergo f 1 1 H intvencoe L pneumophila B porta Brel F harenio B hereetoe ram bacteria caccobacth eres vidase«, catalase « Pmutociiapearertc Pmutocde Pasteurella multocida * FEATURES + Facultatively anaerobic + Readily cultured from wound — grow into large colonies overnight on blood or chocolate agar + CAUSE: animal (dog or cat) bite wound * RESERVOIR + Normal flora in dog or cat + WHO + IC patients systemic infection + Underlying pulmonary dysfunction exacerbation of chronic respiratory disease DISEASE Cellulitis “ does NOT run in any particular direction Lymphadenitis Respiratory disease — patient with underlying pulmonary dysfunction TREATMENT: PenicillinCam 1 coceobset pleomorphic r T 1 t 1 1 1 Hxaviecors — gouthon charcoal yeast gon on aerobic requfes cysteine ——caidasecalalase+ sve impregnation stains gui ton’ cyclone Badt Gengou medium ‘or goth 1 1 i L preueptila B persis Brel F tarenio Pmatocide B rerosloe Cat scratch fever Bacillary angiomatosis Gram - Chronic regional lymphadenopathy Warty lesions coccobacit Dleomorphic OTHER cat-related Pasteurella multicoda ~ bite Capnocytophaga — bite Bartonella henselae — scratch Rickettsiae typhi - cat fleas ‘ver impregnation stains 8 henselaeBartonella henselae couse FEATURES orem * Most cultures negative soengepwinsins * RESERVOIR * Cats and their fleas Pere * DISEASE * Cat scratch fever PRESENTATION * Chronic regional lymphadenopathy + Warty lesions + Slight fever * Bacillary angiomatosis ‘TREATMENT: self-resolvingBartonella quintana * FEATURES * No animal reservoir + TRANSMISSION: human body lice (louse) * WHO: homeless * DISEASE * Headaches, fevers, myalgias OREN * Continue for OTHER Undulant fever * TREATMENT: self-resolving = Bartonella Quintana - BrucellaFEATURES: + Not easy to culture — unlike P. multicoda + Microaerophilic RESERVOIR: mouths of dogs of cats (DF-2 strains) TRANSMISSION: Dog or cat bite WHO * IC- gastroenteritis DISEASE * Cellulitis — similar to P. multicoda TREATMENT: self-resolving Capnocytophaga (OTHER collultis-related + Staphylococcus aureus — towards extremities + Streptococcal pyogenes cellulitis — towards the heart + Clostridium perfingens — splinter inoculated, radiates equally + Enysipelothrx rhusiopathiae + Nocardia + Hemophilus influenza — orbit of the eye + Acinetobacter baumannii — orange peel cellulitis + Pasteurella multocida +. CapnocytophagaRESERVOIR: mouths of rodents TRANSMISSION: nasopharynx of rat bites CULTURE: blood serum from mammals * Difficult to culture DISEASE * Rash + arthralgias (muscle + joint pain) + PROGRESSION Streptobacillus moniliformis = Treponema palidum + 2:10 days following bite + Rocky Mountain Spotted + Abrupt onset of fever, headach| an upt onset of fever, headach>; meee dnd + 3-4 days after symptoms + Purulent papular rash on hands and feet TREATMENT: penicilin + No reported resistance OTHER rodent-related ‘Streptobacillus moniliformis — bite Leptospirosis Interrogans — urine ‘OTHER rash on hand and feet OTHER arthritis/arthralgias SS. aureus — septic = S. pyogenes — rheumatic fever - Neisseria gonorrhea — septic arthritis in women = Streptobacillus moniliformis + _ Chlamydia trachomatis ~ reactive arthritis in menCam 1 cocci perp f 1 1 t T 1 1 xaviedae gown doa yet gonon pettic requis oinne ates aaa + heringregaon ans taped” — Sgarwiniont.gotane Soda Sogou modu ‘ego i i P Hinfercce __L peenhi 8 pores Bro Uleeroglandular tularemia — necrotic lesion + raised edema Oculoglandular — conjunctivitis Pulmonary tularemia — lab workers Charcoal agar Intracellular pathogen — Inhibits phagosome-lysosome fusion in macrophages OTHER conjunctivitisikeratitis/blindness = Bacillus cereus =P. aeruginosa + Neisseria gonorrheae - Francisella tularensis — Oculoglandular tularemia = Haemophilus aegipticus + Francisella tularensis = Chlamydiae - trachoma, neonatal - leading cause of blindness in children OTHER [BCYE] agar > Francisella tularensis - Legionella pneumophila - Nocardia =_Bordatella Pertussis Price B hereeloe Gram - bacteria coccobacill pleomorphic requires cysteine for arowth F tularensis| Francisella tularensis Uceroglandular tularemia ss + RESERVOIR Painful papule at infected tick bite scone + Lagomorphs (rabbits, hares, deer) Develop into necrotic lesion +9 + Cats the periphery Regional lymphadenopathy ——— ont ‘nays ste 0M + Urceroglandular tularemia tick bite Painful conlungtviis + Oouloplandular— dressing animal + wiping face with infected hands + WHO tone + Lab workers ~ Pulmonary tularemia + FEATURES + Require cysteine for growth + Intracellular pathogen. (- + Strictly aerobic -Ant-phagocyte capsule Intraceluiar pathogen Inhibits phagosome-iysosome fusion in macrophages ‘M.tuberoulosls + Nocardia ~ have proteins to prevent phagesome-tysasome fusion ‘CULTURE: charcoal ‘COMPARE: B, anthracis — willbe ‘easly cultured ‘COMPARE = Pin prick -M. tuberculosis ~ Lobar~S. preumeniaCam coccobac Plan r T T aviators growth on charcoal yeast, gow on sertic oquted ——Sgarwitnton &cyteie Borde Gongou modu 1 t r —— H intvencoe L pneumophila B porta Biucalo T requtes seine ‘organ t F torensio dase +, catalase + Price 1 ‘iver impregnation stains Undulant fever Strict aerobe Reproductive tissue of other mammals (uterus + mammary glands) Inhibiting phagosome-lysosome fusion Catalase and superoxide dismutase (O-chain rRNA sequencing OTHER Undulant fever = Bartonella Quintana + Brucella coceobacill, pleomorphicBrucella FEATURES * Gram-negative coocobaci + Stic aerobe + Intracellular parasite ofthe Reticuloendothelial ‘system RESERVOR, LocaTion, + Replicate in reproductive tissue of other ‘mammals (torus + mammary glands) 1eaoe? a ‘Undulant fever ROUTE: Spread through blood stream infect various cls along the route BJ undulant fever Last for months and years VIRULENCE Inhibiing phagosome-tysosome fusion in macrophages ~ similar to tularemia ‘Suppressing production of TNF-a ~ preventing release of toxic enzymes Catalase and superoxide dismutase f inactivating hydrogen peroxide and superoxide (O-chain ~ much more virulent than those that lack O-polysaccharide DIAGNOSIS: FRNA sequencing ‘TREATMENT: macrolide ‘most senshive and specie Sensi and speicity of Diagnostic Tess for Human Brucellosis 2 sas Bol sa g Blond and bone mara cular s 1 5 100 vy Serum agin tx er = 100 on 1 4 wo x r 7 Eecerrearmmnioet Poe dain ear sarah Nora Nor aaBrucella melitensis — sheep + goats - TRANSMISSION: inhaled while milking goat which aerosolizes Gram - bacteria pooner Brucella abortus — cattle - RESULT: Abortions in cattle aerobic Brucella suis ~ pigs + deer 4 ‘Brucella ) Brucella canis — dogs. RISK - Consume unpasteurized dairy products - Direct contact with infected animals - Laboratory workersCam 1 cocetac porn f 1 1 t 1 1 1 evince gawtnon xcs yast goveion ent agierlstne—cnees aaanes sherpa ete Spa wih ton & cystine Bordat Gengou medium ‘or gow r ( TL preumaphie B porta Bruce Florence Price B hereeloe Legionnaires’ Disease — pneumonia mult-lobar consolidation Pontiac fever - myalgia, fever Gram - bacteria Standing fresh water (ponds, AC) Buffered charcoal yeast extract (BCYE) agar Direct fluorescent antibody (DFA) test Wrap their phagosome with parts of ER OTHER [BCYE] agar Francisella tularensis Legionella pneumophila Nocardia en ee PVL Bordatella Pertussis + Streptococcus agalactiae - newbom +S. pneumonia ~rustcoloured sputum = Moraxella catarhals — elderly Klebsiella pneumonia — currant red ely sputum, lobar pneumonia. Francisella tularensis — tse pneumonia Legionella pneumophila — mul-obar consoldation = Myeoplasma pneumoniae ~ atypical + Chlamyeliae ~ infant * Chiamydophila psitact interstitial pneumonitis ccoceobail pleomorphic: ‘growth on charcoal yeast ‘agar with ron & cystoina L pneumophilaLegionella pneumophila + pears racer bactoa {Reig amoebae au punsnice + pesenvore Phagaysosome fusion sted = Aosba ap phagosome wih pars of Rt poe + TRANSMISSION: ian replete eid macrophages = * LOCATION: standing fresh water (ponds, AC) o1senosk ‘+ WHO: Old male, 60+ long-time smoker + drinker Direct fluorescent antibody (DFA) test Warthn stan = rom palo spam » mease Bred hatcoal yeast ext (YE aoa 1 . Grounds gon oeaese_ Be anthrax * Lejomaie Date ane «TREAT i = - + Photophobia wud + Broumonla = muttobar consoldation ce + Ponte ial ovr + Can dap te prouroia but NOT prod cough fe + TIME: porssted for 2to 5 days + TREATMENT: seltresolve reserani neeFEATURES Non-motile Obligate intracellular pathogen Gram-negative rods Seen best with Giemsa staining Well-Felix positive TARGET ‘+ Endothelial cells and epithelial * G produces petechial rashes * after calls dies + Efichia, Coxiella TARGET: monocytes/granulocytes LOCATION: Arkansas Southern, Midwe: usa WHO: homeless ~ R. prowazeki + SPREAD: by human body lice (louse -bomne) r + Uke Bartonella Quintana R S Ig kettsiae RR. Rickettsiae: Rocky Mountain Spotted Fever| etechial rashes on palms and soles B trunk + High fever + RISK: outdoor sports + DIAGNOSIS: Serology ~ microimmunofluorescence TREATMENT: Doxycycine ppidemic typhus and Brill people with typhoid fever + High fever + RISK: poor hygiene R. typhi: Endemicimurine typhus + SPREAD + Rat flea — principal vector — Important vector for the United States + RISK: poor hygiene + DIAGNOSIS: Indirect fluorescent assay test + TREATMENT: Tetrac 32 mer (OTHER rash on hand and feet = Treponema palidum = Rocky Mountain Spotted Fever = Coxsackie + _Streptobacilus moniiformis sa aa <Erlichia and Anaplasma + FEATURES + DISEASE . pen pest with Glemsa staining + Human monocytic ehrlichiosis / leil Felix positive Human anaplasmosis + RESERVOIR ‘ ° + White-tailed deer, white- + High fever, myalgia footed mouse + Rash — more common in children + TRANSMISSION + Leukopenia * Ixodus tic bites also transmits + Thrombocytopenia Lyme disease + Elevated serum transaminases [Gowpane + LOCATION: South East USA - DIAGNOSIS . ~ Rickettsiae — tick + rash ‘Arkansas + Ingested {] prevent fusion {J replicate |- Erichia/Anaplamsa — tick + no rash inside of cytoplasm of cell ] forms | - Coxiella ~no tick + no rash morula + VIRULENCE: prevent phagosome- lysosome fusion + TREATMENT: doxycyclineCoxiella burnetii FEATURES * Seen best with Giemsa stain TRANSMISSION: inhaled * Unlike Rickettsiae and Erhlichiae via arthropod bite RESERVOIR: Sheep + Cattle * Like Brucella DISEASE * Qfever VIRULENCE Metabolically inactive form — has O-chain that of LPS to protect from environmental stress Metabolically active ~ no O chain — not environmentally stable — can replicated in our bodies (macrophages) Macrophages release pro- inflammatory response (release IL-1, TNF-alpha) Do NOT stop fusion @] acidification of the fusion between phagosome + lysosome will stimulate their growth to make them metabolically active TREATMENT: Doxycycline ase + Pneumonia like symptoms — pneumonitis * Fever + Endocarditis + No rash — unlike Rickettsifi Ehrlichia, Anaplasma ‘entry (OTHER endocaraie a Sane so 12) 5, ugdunensis normal heart 3. vanes 5. pyogones -cross reaction with M protein S. pneumoniae - damaged 1) semanas heart vahes an ‘5. mutans ~pro-isting vale I detect . Enterococou faecal - valve fe replacement = ‘Coxiella burnetii —Q feverSpirochetes l T 1 microaerophilic, Giemsa & silver stains, aerobic, sensitive to high temperatures roaerophil ‘ive tong” appearance T pallidum 8. burgdorferi B. recurrentis L.interrogans “Sprochotes| Lyme disease Erythema migrans — Bulls eye rash ‘Acrodermatitis chronica atrophicans — discoloration and swelling xodus tick - Co-infection with Babesia microti Outer surface protein A - 20-25 degrees Outer surface protein C (OspC) ~ 35 degrees IgM or IgG antibodies Giemsa & siver sans, microaerophiic 8 burgdrienEE EO Borrelia ‘Also caused by Lone star” (A. americanum) ticks’ bite - but do NOT . carry B. burgdorferi burgdorferi .dermatitis chronica atrophicans — discoloration and swelling r surface protein A (OspA) Expressed at 20-25 degrees PURPOSE: allow bacteria to coloniz’ Outer surface protein C (OspC) * FEAT PURPOSE: spread from tic to human host durin * Spiroche' 2 Visualized via dariefeld microscopy few hours to increase its own body temperature + Intemalized flagella — corkscrew movement. Expressed at 35 degrees + us + RESERVOIR: whitefooted mouse, white-talledjaciosis: IgM or IgG at deer + TRANSMISSION: lxodus tick + Corinfection with Babesia microti nr vonaBlgoe-bome Doxycycline ries a orrees cece oriae e eonachusetis to Marne Cefuroxime vera Aseiden — SoSThare + Minnesota and Wisconsin Gus * Norther California and Oregon y + WHO + WHEN: May to August diesSpirochetes l T 1 microaerophilic, Giemsa & silver stains, aerobic, sensitive to high temperatures microaerop! “ice tong” appearance ———_ B. burgetarferi 8. recurrentis L sieepae Spictes Primary syphilis ~ Pain ulcer/chanore ‘Secondary syphilis = Condylomata lata - warty raised lesions in skin folds = Rash all over the body — palms and soles Tertiary syp = Aoritis microacrophii, = Neurosyphils sensitive to tgh omperate = Gummas Congenital syphilis = Peg-shaped teeth + Cartilage destruction =_ Saber shins T pata‘OTHER rash on hand and feet = Treponema pallidum = Rocky Mountain Spotted Fever = Coxsackie Streptobacilus monilformis Treponema pallidum + DISEASE ~ caused by autoimmune reaction in tertiary syphilis + Primary syphils * Pains uloerichanore + Regional lymphadenopathy + Secondary syphiis Rash all over the body ~ palms and soles + Fluslike myalgia ‘+ Lymphadenopathy ae + Sonoma =e + rexrures + Tey seis + RESERVOIR: humane ‘+ TRANSMISSION jeurysm of asco ing are + Neurosyphils * Lesions tem primary Gnas open destruct granulomas and secondary syphilis + CAUSE: own Ab against fibronectin Ab + Viaplacenta deposition granulomatous lesion + Congenital syphilis + 1 week after bith sloughing of skin on ‘soles of baby hands ‘+ Simlarto SSSS Saber shin ~ anterior Blindness, doatness + DIAGNOSIS + Venereal Disease Research Laboratory (VDAL) test “+ Rapid plasma reagn (APR) test + FTAAbs = Test fr lgM-specific for bacteria themselves ~ confirmatory + TREATMENT: penicilinPrimary ype MECHANISM: nected wih bacteria papule develops ulcerated elon wih lod edpos Occurs 10 days ater exposure ~ Lesion pass COMPARE: dury\— pant eson = Chsest regional mph rede swollen “VIRULENCE: Virepthemoaives nour foronactn vada nn estar inthe na tate Alo autoreact wih own bodes that have Rronectn = TIME: Cantaet 13 mone FINAL: Spotancoul rahe ‘Secondary apis prea rom ial leo oer tus "Disord rash incudng pans and oes + GeneraizedImphadenopathy Low ieveltever + Mala Most oar themselves ater this polnt INFECTION TH row of xganisns at ste of infection T.PALLIOUM

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