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Species Characteristics Epidemiology Diagnosis Escherichia (E. coli) Facultative Anaerobe Motile (peritrichous) Fecal-Oral – leads to gastroenteritis Vigorous lactose fermintation Gram Negative Bacilli ROD SHAPED Direct Contact - UTI Reduces nitrate Can form a coliform 2nd most common cause of neonatal meningitis Enteropathogenic E. Coli EPEC Gram Negative Bacilli Facultative Anaerobe Motile (peritrichous) Vigorous lactose fermintation Pathogenesis Major Disease Small Intestine Gastroenteritis - Infants < 1 year in developing countries EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape Attachment: Bundle-forming pili (BFP) Afimbrial adhesions Reduces nitrate Can form a coliform 2nd most common cause of neonatal meningitis ROD SHAPED Locus of enterocyte effacement (LEE) proteins - Attaching & Effacing (A/E ) lesions T3SS – type 3 secretion system Tir/Intimin binding for firm attachment SPATE (EspF, Tir, EspC) reorganizes cell actin and cytoskeleton to make a pedicle - EspF a LEE protein that allows interstitial fluid to leak out Can bind to Monocytes and Macrophages to block signaling & prevent phagocytosis Watery diarrhea Nausea & vomiting Abdominal cramps Enterohemorrhagic E. Coli. EHEC STEC VTEC Facultative Anaerobe Motile (peritrichous) Gram Negative Bacilli Reduces nitrate Can form a coliform Vigorous lactose fermintation EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape ROD SHAPED Gram Negative Bacilli Facultative Anaerobe Motile (peritrichous) Vigorous lactose fermintation Reduces nitrate Can form a coliform 2nd most common cause of neonatal meningitis Attachment: Plasmid-encoded pili & intimin-Tir A/E mediated diarrhea that leads to hemorrhagic colitis Verotoxins: - Shiga-like Toxin-1 (STX or STL) - Shiga-like Toxin 2 (STX or STL) Binds to GB3 – expressed on endothelial cells of kidneys, intestines produce microthrombi & Lifethreatening Illness (HUS) = site that gets toxin dies and activates coagulation = coagulation leads to distal ischemic necrosis = and you get RBC fragmentation =leads to Hemolytic Uremic Syndrome 2nd most common cause of neonatal meningitis Diffusely Adherent E. Coli (DAEC) Small & Large Intestine EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape Small Intestine Afa-Dr adhesions binds to DAF activates the immune system and recruits PMNs diffuse adherence pattern on cultured epithelial cells HeLa or HEp-2 Sat SPATE that disrupts tight junctions can cause diarrhea Type 1 Pili binds to PMNs to promote it’s action. Gastroenteritis All Ages – US Hemorrhagic colitis ‘ Bloody diarrhea Nausea & vomiting Abdominal cramps Gastroenteritis Traveler’s diarrhea Water diarrhea Nausea & vomiting Abdominal cramps Enterotoxigenic E. Coli ETEC Gram Negative Bacilli ROD SHAPED cells PMN’s produce DAF which enhances it’s binding Facultative Anaerobe Motile (peritrichous) EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape Small Intestine Vigorous lactose fermintation Reduces nitrate Can form a coliform Plasmid-encoded pili Enterotoxins - Heat-Stable Toxin (ST) activates cGMP Gastroenteritis All Ages – Travelers into US Watery diarrhea Nausea & vomiting Abdominal cramps - Heat-labile Toxin (LT) activates cAMP 2nd most common cause of neonatal meningitis ROD SHAPED Enteroinvasive E. Coli EIEC Gram Negative Bacilli Facultative Anaerobe Motile (peritrichous) Vigorous lactose fermintation EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape Small Intestine diarrhea EIEC Dysentery Infants & Children Large Intestine Dysentery Diarrhea Watery diarrhea, Cramps, Reduces nitrate Can form a coliform Plasmid-encoded pili or Macropinocytosis 2nd most common cause of neonatal meningitis Invasion Plasmid Ags (IPA) lyse endosome so bacteria can escape ROD SHAPED mobilize actin for horizontal transmission – lysing enterocyte and causing bloody diarrhea Dysentery Mucoid diarrhea with blood Fever Abdominal pain May lead to ulcerations Enteroaggregative E. Coli EAEC) Gram Negative Bacilli Facultative Anaerobe Motile (peritrichous) Vigorous lactose fermintation EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape PMN infiltrate causing inflammation and increasing mucus secretion Large Intestine Aggregative adherence fimbriae (AAF) forms a biofilm and you find on salad leaves Reduces nitrate Can form a coliform Dispersin neutralizes negative charge of LPS 2nd most common cause of neonatal meningitis Pic induces mucus hypersecretion & # of goblet cells ROD SHAPED Pet get endocytosed and cleaves cytoskeleton protein – host cells round and detach Uropathogenic E. Coli UPEC Gram Negative Bacilli Facultative Anaerobe Motile (peritrichous) 2nd most common cause of neonatal meningitis Reduces nitrate MOST COMMON CAUSE OF UTI 2nd most common cause of neonatal meningitis ROD SHAPED Vigorous lactose fermintation Can form a coliform EMB (EosinMethylene Blue) Agar – Get’s a metallic green shape EAST-1 activates cGMP Bladder Attachment: Type 1 pili - the key to virulence. It recruits PMNs to come and kill bacteria. Releases it’s compounds which destroy cells and exfoliate, but bacteria travels and escapes Gastroenteritis Infants & children in developing countries Fever Watery to mucoid diarrhea Nasuea & vomiting Abdominal cramps MOST COMMON CAUSE OF UTI Urethral Infection & Cystitis polyuria dysuria cloudy urine Pyelonephritis (upper ureter to kidney) fever polyuria hematuria Salmonella enterica Facultative Anaerobe Salmonellosis: Fecal-oral – contaminated food (eggs, poultry, dairy) Culture: SalmonellaShigella Agar (SS-Agar) Small & Large Intestine Attaches to enterocyte surface Gram Negative Bacilli Motile (peritrichous) No lactose or sucrose fermentation Food-borne Taken up by DC sampling the gut Reduces sulfate to hydrogen sulfide Colonizes GI tract of animals Hektoen Enteric Agar (HEK) – look for fish eye VACCINE FOR TYPHOID FEVER Shigella Facultative Anaerobe Gram Negative Bacilli Nonmotile All species produce Shiga toxin S. dysenteriae is most potent Typhoid Fever: Fecal-oral – contact with contaminated fomites Fecal-oral – contaminated food and water DOES NOT Ferment lactose DOES reduce sulfur NO lactose fermentation No sulfate reduction Greatest risk group in US are children < 15 years – 70% of cases Attaches to M cell surface S. enterica enteritidis: Salmonellosis Low-grade fever Water diarrhea can be bloody diarrhea if severe Nausea & vomiting Abdominal cramps Can reside in M cells via S-CV using SPI-2 In Macrophage or DC, it can disseminate to bone marrow, lymphatics, spleen, liver Small and Large Intestine Bacteria enter M cells Apoptose macrophages Invade basolateral side of enterocytes using IPS S. enterica typhimurium Typhoid Fever Fever Headache Bloody diarrhea Lethargy Delirium Abdominal cramps Rose spots on abdomen Shigellosis Fever Tiredness Water diarrhea Abdominal pain Tenesmus Enterocyte invasion activate cAMP Shiga Toxin Inhibits protein synthesis Cytotoxic Klebsiella pneumonia Facultative Anaerobe Agar plate Stringy? Has Polysaccharide capsule is most important virulence factor Pneumonia thick blood with sputum Nonmotile Gram Negative Bacilli capsule Puffy and shiny? Has a capsule Has a mucoid capsule lung necrosis and abscess Most common in ventilator associated pneumonia Opportunistic Wound and soft tissue infections HIGH RESISTANCE TO MICROBIALS Second leading cause of UTI Septicemia – bacteria in blood Yersinia Facultative Anaerobe Fecal-oral Blood agar has robust growth Not pestis T3SS Y. pestis Bubonic Plague Gram Negative Bacilli Nonmotile Encapsulated Three species: Pestis bubonic & Pneumonic Plague Pestis flea bite Pestis contaminated respiratory droplets Pestis person to person Psuedotuberculosis & enterocolitica gastroenteritis Spiked RBCs – there are lipid problems Bipolar staining with Giemsa staining looks like a hairpin apparently Can grow at 4 celcius – loves growth on blood agars Yersinia outer membrane proteins – YOPS YPM = super antigen Pestis Phospholipase Protein capsule Ymt – bacteria can survive in flea Forms clots in GI tract so it’s hungry and it feeds Intestines, Skin, Lungs Macrophages engulf bacteria (YOPS) allows them to live and replicate inside – and move them to lymphatics Have a capsule that allows them to escapde phagocytosis T cells produce IFN-y and promote killing of enterolitica but no pestis Proteus mirabilis Facultative Anaerobe Gram Negative Bacilli Motile (peritrichous) Rapid Urease production Swarming motility - form clusters of flagellated cells. Sulfur reduction Fever Chills Myalgia Nausea Sore Throat Headache Painful bubo (groin or axella) – lesions due to lymphadenopathy Septic shock – 50-75% of cases Pneumonic Plague When it disseminates to the lungs High fever Shortness of breath Coughing Hemoptysis Lethargy Respiratory failure Septicemia - High fever, hypotension and shock, delirium, organ damage UTI infections transmitted from contaminated catheters Bladder and kidney infections Swarming motility Urease activity can raise pH which precipitates kidney stones Pseudomonas aeurginosa Strict Aerobe Find it in soil, and it can survive high Oxidase positive (Along with Has many virulence factors Respiratory Infections Motile (Monotrichous) Gram Negative Bacilli Oxidase-positive Notable antimicrobial resistance temperatures and in all environments 10% of hospital acquired infections Brucella and cholera) and antimicrobial resistance Produces lots of ATP and has a fruit smell Opportunistic bacteria Biofilms on soil and water Has a turquoise colored agar Eye and ear infections Elastases – degrade ECM IgG proteases C3b proteases Exotoxin A – Inactivates EFII Phospholipase – cell membrane damage Pyocyanin – kills leukocytes Exoenzyme S – for adhesion Can lead to endocarditis Small Intestine Cholera Voluminous watery diarrhea no blood large loss of electrolytes - dehydration, metabolic acidosis (bicarbonate loss), hypokalemia (K loss), hypovolemia (cardiac arrhythmia and renal failure) Open wound and soft-tissue infections Adapts to nearly all environments Adapts to nearly all environments #1 Disease in CF patients Vibrio Cholerae Facultative Anaerobe Fecal-Oral Gram Negative Bacilli Motile (Monotrichous) Multiples freely in water and found in waters worldwide Oxidase positive Can get from chitinous shellfish Thiosulfate Citrate Bile Salts Agar (TCBS) – grows well in high salinity Cholera Toxin - Activates cAMP Oxidase positive (Along with Brucella and Pseudomonas) Rice water stool Low bp Vomiting Rapid heart rate and feeble pulse GramNegative, GramNegative, GramNegative, GramGram-Negative, Negative, Fastidious Bacteria Gram-Negative, Fastidious Fastidiou Fastidious s Bacteria Bacteria Fastidious Fastidiou Bacteria sBacteria Neisseria Aerobe GRAM NEGATIVE DIPPLOCOCCI Nonmotile Sexual Contact (gonococcus) replicates in GU, rectum, eyes, throat bacteremia spreads to skin and joints of knees, ankles, and wrists (arthralgia) Diplococcus #1 CAUSE OF MENINGITIS Bordatella pertussis DOES NOT ferment carbs Aerobe Nonmotile GRAM NEGATIVE Coccobacillus Ferments glucose & lactose Contaminated respiratory droplets (Meningococcus) replicates in epithelial tissue of nasopharynx bacteremia spreads to lungs, then joints, brain and heart 100% respiratory droplets replicates in the lungs cilia become immobilized, destroyed, get patches of no ciliated cells which causes irritation Bacteria Thayer-Martin agar 5% chocolate agar+antibiotics Mucosa 1. Bacteria attach to epithelial cells N. gonorrhoeae N. meningitides 3. LOS (lipooligosaccharide) stimulates cytokine production (can function as an endotoxin) Catalase positive 2. Porin I (POR) induces endocytosis 4. PMNs get active, destroy tissue Gonorrhea Males THICK urethral discharge Dysuria Females cervical discharge dysuria severe pain Meningococcal Meningitis Initially – mild pharyngitis Sudden onset headache Fever Vomiting Stiff neck Petechial rash (DIC) necrotic lesions, loss of limbs, brain covered with exudate, 100% mortality Bordet-Gengou media, or potato-bloodglycerol Requires nicotinamide and charcoal Respiratory mucosa Attach via FHA, P69, and Pertussis toxin (PTX) PTX impairs ciliary action and activates cAMP which causes mucus secretion causes tracheal cytotoxin to kill cilia Cell debris + mucus + impaired ciliary action = severe, persistent cough Whooping Cough Catarrhal (1-2 wks) mucoid rhinorrhea nasal congestion sneezing Paroxysmal (1-6 wks) Intense bouts of cough Convalescent (3 wks – months) Persistent cough Secondary infections Haemophilus influenza Facultative anaerobe Nonmotile Direct contact OR Contaminated respiratory droplets GRAM NEGATIVE Number 2 cause of meningitis Coccobacillus Normal flora H. influenza are NOT encapsulated Hib vaccine Gets into nasopharynx, replicates in epithelial cells, and bacteremia gets in lungs, then to joints, skin and brain Hemin (X Factor) & Nicotinamide adenine dinucleotide (NAD, V factor) Look for shiny, smooth, thick growth Respiratory mucosa bacteria colonize nasopharynx Hib capsule responsible for virulence - composed of ribose, ribitol, phosphate (PRP) – impairs ciliary action protects bacteria from phagocytosis anti-PRP response important for bacterial clearance Meningitis (Type B capsular form) pharyngitis headache stiff neck fever lethargy irritability vomiting Epiglottitis Inflamed epiglottis & surrounding tissue Airway obstruction Cellulitis & arthritis Tender red swelling Pain in large joints Brucella spp. Strict aerobe Nonmotile GRAM NEGATIVE Coccobacillus Replication occurs in DC and Macs Direct contact with infected animal (feces, urine, tissues) Ingestion of contaminated foods (unpasteurized dairy) Oxidase, catalase, urease positive (Oxidase positive along with Pseudomonas and Cholerae) Gets in skin or mucosa Replicates in Reduces sulfur and nitrate Skin, Oral, Respiratory OMP allows to bind Variable bacteria are directed to ER and develop ER vacuole and replicate Activation of the macrophage by the bacteria can generate granulomas Brucellosis Acute Flue-like illness (fever, sweats, malaise, headache, joint/muscle/back pain, fatigue) Undulant Fever during the day Drenching sweats at night Can form arthritis, endocarditis, Francisella tularensis Strict aerobe Nonmotile GRAM NEGATIVE Coccobacillus Macs, DCs cell bacteremia in spleen, heart, bone, lymph nodes Chocolate agar Bite Tick Dog tick, wood tick, lone star tick Direct contact with infected animal Medias added with cysteine Skin, Oral, Respiratory mucosa OMP to bind Oxidase negative Pathogenicity island allows to escape phagosome and replicate in cytosol Two groups: Type A occurs only in N. America (Most lethal) Type B Occurs in Europe, Asia, N. America (Not as lethal) Gets in skin or mucosa and replicates in DC and Macs Replication occurs in DC and Macs Rabbits are the main resovoirs Anaerob Anaerobic ic & & Atypical Atypical Bacteria Bacteria Actinomyces Gram positive Gram positive Facultative or strictly Cell bacteremia in spleen, heart, bone, lymph nodes Anaerobi c& Atypical Bacteria hepatomegaly splenomegaly Mac undergoes apoptosis release it to infect another mac It can go through lemphatics and cause lymphadenopathy It can disseminate and cause granulomas Tularemia Ulceroglandular Disease (UGD) fever, headache, chills, malaise pain in bite areas lesion ulcerates (necrotic death of Macs) Oculoglandular Disease sames as above but with conjunctivitis Oropharyngeal or Typhoidal Disease same as above but ulcers are in oral cavity or in intestine Pneumonic Disease Same as above but you get respiratory ulcerations Sepsis Anaero Anaerobic & bic & Atypical Bacteria Atypical Bacteria REALLY ONLY PRESENT AFTER SOME SORT OF TRAUMA TO SURGERY Anaerobic & Atypical Bacteria Actinomycosis chronic granulomatous lesions cervicofacial-most common anaerobic thoracic abdominal pelvic CNS colonies called sulfur granules Found in mouth, gut, and GI Clostridium botulinum Anaerobe Motile Gram positive Spore-forming Ingestion of toxincontaminated foods (Canned foods) – TOXINS ARE PREFORMED Or Direct contact with spores (in a wound) – SPORES DON’T HAVE PREFORMED TOXIN Botulism Toxin A, B, & E 1. binds to receptors on presynaptic membranes of motor neurons 2. Botulism toxin cleaves SNARE proteins to inhibit Ach from binding to it’s receptor 3. Botulism neurotoxin enters 4. Can’t contract muscles and you get paralysis Foodborne Botulism 18-36 hours Weakness, dizziness, expressionless face Two main toxins: A toxin – disrupts tight junctions and gives diarrhea Pseudo membranous colitis: get from intense inflammation that forms the pseudomembrane Often seen in infants who don’t have an established flora in their gut Clostridium difficile Anaerobe Spore-forming Gram positive Normal flora of 5% of INFECTION ENDOGENOUS ampicillin and clindamycin treatment CAUSES THIS SINCE IT’S AN B Toxin – Cytotoxic Progressively: IN MUSCLE Nausea and vomiting Blurred vision inability to swallow Difficulty in speech weakness of skeletal muscles respiratory panalysis the population Clostridium perfringens Gram positive Anaerobe Nonmotile Spore-forming OPPORTUNISTIC BACTERIA Direct contact with Spores in open wound OR Ingestion of spores/bacteria Endospores get into intestines and skin - Replicates and makes the 3 toxins - Grows into deep muscle tissue and toxins induce edema and necrosis (SHOCK) Clostridium tetani GRAM POSITIVE ROD Gram positive Strict anaerobe Motile Spore-forming Direct contact with spores Look for zone of hemolysis Antibiotics allows the bacteria to take over Alpha Toxin Phospholipase dissolves RBC, leukocyte and muscle cell membranes Theta Toxin Pore-forming toxin that alters capillary permeability and is toxic to the heart muscles Gas Gangrene Severe pain at the site of wound Edema, tenderness, discoloration, hemorrhage bullae (Large, red blisters) CO2 and hydrogen released at wound as a gas and it smells terrible Enterotoxin Activates Calcium levels and you lose fluids and macromolecules Clostridial Food Poisoning Nausea, abdominal pain, diarrhea Tetanospasmin – toxin Degrades synaptobrevin required to dock on presynaptic membrane blocks glycine and GABA, motor neurons are not inhibited and you get continues voluntary muscle contraction Tetanus Early: Severe painful spasms, Rigidity of voluntary muscles, Lockjaw Progressively Rigidity and violent spasms of trunk and limb muscles Spasms of pharyngeal muscles, difficulty swallowing Respiratory spasms which leads to death Bacteroides fragilis Gram NEGATIVE Enzymes – catalase and SOD helper tolerate ROS Anaerobic Gram Negative Major cause of intrabdominal infections Virulence Factors Adhesions Enzymes – catalase and SOD helper tolerate ROS Toxins – Heat labile zinc metalloprotease toxin – damages epithelium, causes fluid loss and PMN recruitment Abscess formation in normally sterile sites Bacteremia Intra-abdominal Infections (80%) Gynecological infections Chlaymdia Trachomatis NO GRAM STAIN NO GRAM STAIN Direct contact with contaminated secretions ACID FAST STAIN Chlamydia gets into genitals, replicates, Th1 response leads to acute inflammation and chronic infection IFN-y can halt replication, but RB can resist it. Legionella pneumophila NO GRAM STAIN COCOO-BACILLI Flagellated Inhalation of airborne, aerosolized microbes – it lives in water supplies in Gimenez and Dieterle silver stain EB (Elemenarty Bodies) enters conjunctiva or urogenital tracts and infects epithelium. EB = metabolically inactive, but infectious Enters lysosome but doesn’t die – it then becomes a RB (Reticulate Bodies) RB is metabolically active, but NONinfectious TSS3 allow for nutrient uptake. Once there are a lot, RB EB and infectious part bursts from cell Virulence Factors Peptide toxin inhibits respiratory burst Catalse detoxifies residual H2O2 Skin and soft-tissue infections Follicular Conjunctivitis person to person Leading cause of blindness in the world Corneal Scarring Eyelid turns inward eyelashes abrasive to cornea corneal ulcerations Urogentical Infection Dysuria THIN, urethral discharge Legionnaire’s Disease – a type of pneumonia Fever, chills, headache, NONPRODUCTIVE COUGH buildings Mycobacterium leprae Tuberculoid Th1 response NO GRAM STAIN Lepromatous Th2 response Survives in macs. contaminated respiratory droplets Need cysteine for growth exotoxins DETECT with an ACID-FAST STAIN Tuberculosis Intracellular Persistence Evades lysosomal fusion with phagosome Catabolizes NO and ROS Activates Macs to produce IL-1, TNF, IL-12 to form a granuloma Tuberculosis Primary TB Fever, night sweats, anorexia, weakness, bloody cough Secondary TB Immunosupression triggers reactivation, granulomas dissolve, get TB again Lepromatous Rickettsia NO GRAM STAIN Obligate, intracellular, aerobic, GRAM NEGATIVE COCCOBACILLI Arthropod vector Rickettsia rickettsia – vector – tick Resovoir – dog or rodent Virulence Factors Adherance: OMP A binds to endothelial cells Pathogenesis: due to destruction of infected cells (endothelial) by bacteria Rickettsia prowazekii Vector – louse Resovoir – Human Endemic Typhus (Prowazekii) Sudden fever, chills, headache, myalgia, arthralgia, maculopapular rash (trunk then to extremities) Myocarditis, stupor, delirium Rickettsia typhi Vector – flea Resovoir - rodent Treponema pallidum SYPHILIS Gram-negative Person-to-person Sexual contact (STD) Congenital (in utero) Rocky Mountain Spotted Fever (Rickettsii) Sudden Fever, then Chills, headache, myalgia Rash on hands and feet and spreads toward trunk widespread vasculitis – GI, respiratory and renal failure, coma and seizures Outer Membrane Proteins minimal expression (100-fold less than gram-negative bacteria) adherence to nearly all body tissues Primary Painless, ulcerative lesion at site of entry (chancre) Gram-negative coat with fibrin to avoid phagocytosis also shown to bind Ig and complement proteins as a “disguise” Little ag exposure on bacterial surface (limited if any host response initially) Hyaluronidase Gets into your genitals, replicates in epithelium (PRIMARY SYPHILIS) Tertiary (5-20 years later – due to a hypersensitivity reaction) Multiple organs develop inflammatory lesions Arteritis Meningitis (with hallucinations and psychosis) - Gummas Bacteremia to lymphatics and bloodstream Spreads to heart, brain, liver, bone (SECONDARY AND TERTIARY SYPHILIS) Borrelia burgdorferi SPIROCHETES SPIROCHETES 7-20 periplastic flagella VECTOR: Hard tick Secondary Rash (trunk, palms of hands, soles of feet), and flu-likesymptoms hepatitis arthritis nephropathy GI disease Giemsa or Wright stain LPS is toxic Peptidoglycan is inflammatory Antigen can change, making for a prolonged immune response Lyme Disease Erythema migrans-annular lesion with a clear or necrotic center and a raised order neurologic and cardiac symptoms arthiritis CAN CAUSE CARDIAC SYMPTOMS GRAM +++++++ +++++++ BACTERI A GRAM +++++++++ +++++BACT ERIA GRAM +++++++ +++++++ BACTERI A GRAM GRAM ++++++ ++++++++++++++ ++++++ BACTERIA ++BACT ERIA GRAM ++++++++++++ ++BACTERIA Staphylococcus Facultative anaerobe Coagulase positive – autoinfection, direct contact, contaminated food, fomite Catalase positive Adhesion techoic acid binds to nasal epithelial Protein A binds to Fc portion to prevent opsonization S. aureus Furuncle (Boils) & Carbuncles Lesions of hair follicles, sebaceous glands, sweat glands Mannitol Salt Agar (MSA) - it contains a 7.5% NaCL which inhibits growth of other normal flora Pyrogenic toxins Enterotoxins Heat-stable superantigens resistant to gut enzymes - Micro dilution or Disk diffusion susceptibility test – add antibiotics and see if it’s susceptible Beta, delta, gamma hemolysins Beta = degrades sphingomyelin Gamma = Combine with PV proteins that lyse WBC Delta = disrupts cell membranes Impetigo Forms large blisters and rupture and crust Scalded Skin Syndrome (SSS) – Ritters Disease Causes erythema and epidermal desquamation at remote sites from staph infections You see this in babies usually Nonmotile Irregular clusters Bacteria gets into mucus and skin, replicates, and gets into different types of tissue causing necrosis of tissue S. epidermidis (Opportunistic, from indwelling equipment) S. aureus (most virulent) S. saprophyticus (agent of UTI) Coagulase negative – autinfection LOOKS LIKE GRAPES Catalse positive = STAPH Toxic Shock Syndrome Toxin (TSST-1) Superantigen – cytotoxic Leukocidins Toxin that lyses WBC by forming pore Exfoliatin – SUPER ANTIGEN A = heat stable, B = heat-labile Toxic Shock Syndrome High fever, vomiting, diarrhea, sore throat and myalgia – you get this crazy rash everywhere Food poisoning You ingest one of the enterotoxins, NOT THE BACTERIA, and you get BOTH cause desquamation of skin Coagulase positive = S. aeureus Novobicin sensitive = S. epidermidis Novobicin resistant = S. saprophyticus GAS (S. pyogenes) Bacteria gets into skin and mucus membranes, replicates, enters lymphatics, and release toxins and enzymes which causes necrosis in tissues – possibly SHOCK GAS = Direct contact, fomites, or contaminated respiratory droplets MRSA – MethicillinResistant S. Aureus is on the rise Ag Detection Rapid detection kit for Group A Carbs Culture Beta Hemolysis Bacitracin sensitive Enzymes Coagulase Protects from phagocytosis binds to fibrinogen and fibrin nausea, vomiting, and diarrhea. Toxins are heat-stable so reheating food does no inactive toxins. SALTED MEATS< CUSTARD< ICE CREAM< SALAD BARS It’s explosive and fast Hyaluronidase/staphylokinase Permits invasion of tissues dissolves fibrin clots M protein/ Lipoteichoic Acids / Protein F Adherance to nasopharynx and skin epithelia Streptodornase / Streptokinase DNase and Fibrinolysin to break up PMS’s NET Pyrogenic Exotoxin A, B, C Superantigens TSS and Scarlet fever are produced by these Diphopyridine Nucleotidase Lyse WBC Streptolysin O & S – only need a little Strepococcal Pharyngitis (Strep Throat) Sore throat, fever, headache Tonsil, soft palate, and uvula are red, swollen, and covered with yellow exudate Impetigo Small vesicle surrounded by erythema on face or lower extremities Enlarges, develops into a pustule, and breaks into a form crusted lesion Erysipelas Spreading area of erythema / edema (face), pain, fever, bit O = Anaerobic Hemolysin S = aerobic hemolysin induces upon bacteria exposure to serum BOTH DAMAGE TISSUE AND LYSE PHAGOCYTES lymphadenopathy Strep TSS myalgia, severe pain, necrotizing fasciitis, myonecrosis, nausea, vomiting, diarrhea Scarlet fever Buccal mucosa, temples, cheeks are deep red STRAWBERRY TONGUE and SANDPAPER RASH on chest Acute Rheumatic Fever (ARF) 3 weeks after strep throat – due to recurrent infections Fever, carditis, chorea, arthritis GBS (S. agalactiae) LEADING CAUSE OF SEPSIS AND MININGITIS IN THE 1st FEW DAYS OF LIFE Bacteria gets into the mucus membrane and quickly spreads to the lungs and CNS Normal resident of GI tract GBS = Direct contact with nasal secretions or contaminated respiratory droplets Detect Group B Ag in blood agar Capsule can bind Serum Factor H to inhibit alternative pathway for complement Beta Hemolysis Bacitrant resistent Acute Glomerulonephritis (AGN) 6 wks after strep throat – lesions of glomerulii Onset in first few days leads to: Respiratory distress Fever Lethargy Irritability Hypotension Pneumonia Meningitis (5 – 10%) If it gets into the CNS, there is a 20% mortality rate and a 20-30% brain damage rate S. Pneumoniae Treat with PCV13 Bacteria get into Gram-positive Choline Binding Protein Pneumococcal Pmeumonia 3RD LEADING CAUSE OF MENINGITIS Gram-positive diplococcic vaccine – Pneumococcal conjugate vaccine Do this in children – it’s conjugated to a protein and it generates a stronger immune response Pneemococcal Polysaccharide Vaccine (PPSV23) Do this in adults over 65. It’s only a polysaccharide vaccine so it only generates an IgM response and isn’t as strong Bacillus anthracis Aerobic or facultative anaerobe GRAM POSITIVE Nonmotile Spore-forming Protein capsule PREVENTION: Anthrax Vaccine Absorbed (AVA, Biothrax) vaccine requires an aluminum hydroxide adjuvant your lungs because of impaired host defense – smoking, pollution, drugs, alcohol. It replicates, the pneumolysin toxin is released and it causes DIC so you die B. anthracis Direct contact with spores through spores B. cereus and B. subtilis Cause infections of the eye, soft-tissue and lung associated with immunosuppression, trauma, indwelling catheters or contaminated medical equipment diplococcic Susceptible to Optochin Binds phosphocholines of bacteria with Carbs of nasopharynx Capsule Prevents C3b opsoniation Blocks phagocytosis Pneumolysin Directly cytotoxic to endothelial cells (so it can disseminate into the bloodstream) Impairs ciliary action Suppresses phagocytic activity Increases anti-inflammatory cytokines (Like IL-10 and TGF-beta) Triggers platelet activation (Can cause DIC) Take skin lesion, sputum, CSF or blood specimen and inoculate onto blood agar get nonhemolytic growth, gram positive stain Add penicillin and you get a stringof-pearls kind of look. Protein capsule allows for adherence Anthrax Toxin PA (Protective Antigen) clusters ATR on a lipid raft which then binds either to EF (Edema Factor) which activates cAMP or LEF (Lethal Factor) which cleaves MAPKK pathway and leads to macrophage and endothelial cell death (Necrosis) Endospore into lungs, intestine or skin, replicates then spreads via macrophages and lymphatics, spreads to different tissues and causes necrosis A leading cause of pneumonia in the world 5 million children die each year Shaking chills, high fever, cough, chest pain Pneumococcal Meningitis One of the leading causes of bacterial meningitis H. Influenza and N. Meningitidis are the others Headache, stiff neck, photophobia, irritability Other infections Otitis Media sinusitis bacteremia Cutaneous Anthrax Erythematous papule vesicular lesion Ulcerative lesion Scab (Black Eschar) Pulmonary Anthrax Mild fever, nonproductive cough which leads to respiratory distress, causing cyanosis (alveoli die) Bacteremia can occur, it seeds to every organ and you die. Coryanebacteriu m diphtheria Facultative anaerobe Club-shaped bacillus GRAM POSITIVE B. Cereus Causes diarrhea (cAMP) Contaminated respiratory droplets PREVENTION DTaP vaccine Anitmicrobials and Diphtheria antitoxin Swabs of nose or throat inoculated onto Blood agar (eliminate Strep) and Cystin-Tellurite agar – should form a black colony PCR for DTX Listeria monoctogenes GRAM POSITIVE Diptheria Toxin (DTX) encoded by a lysogenic phage B subunit serves as ligand for host receptor Inactivates EF-II and kills the cells Bacteria in pharynx, larynx, or tonsils. Replicates and resides in pseudomembrane providing DTX. Toxemia develops with necrosis of heart muscle (MYOCARDITIS), liver, kidneys, adrenals, neuronal and endothelia (hemorrhaging) Contaminated food (unpasteurized milk, ice cream, raw vegetables, cold cuts) PALCAM agar with a food source Internalin Actin reorganization allows to move to another cell. Or Double-Membraned Vacuole Babies can get it during labor/delivery Mueller-Hinton Agar - Gram + - Catalase + - Small zone of hemolysis Listeriolysin O Degrades endosome/phagosome/vacuole so it can escape into cytosol and avoid being fused with a lysosome Diphtheria: First, as an exudative pharyngitis - Sore throat, low-grade fever, malaise Second, exudate on tonsils, pharynx, and larynx evolves into a pseudomembrane (necrotic epithelia embedded in fibrin, RBC and WBC, - active bacteria Lymphodenopathy Breathing obstruction Myocarditis Cardiac arrhythmia Coma Listeriosis Nausea, abdominal pain, watery diarrhea, fever Can disseminate to CNS and cause meningitis Characteristic S. aereus S. epidermidis S. saprophyticus Color of Colonies Often yellow White White to pale grey Hemolysis Most isolates A few isolates Non-hemolytic Coagulase production Yes No No Mannitol fermentation Yes No Yes Novobiocin Sensitive Sensitive Resistant Characteristics • Facultative Anaerobes; Nonmotile • Blood agar is preferred because satisfies growth requirements and can differentiate groups based upon hemolysis patterns • Catalase-negative (Staphylococcus catalase-positive) • Classification by Group-Specific Surface Carbohydrate (which C-protein): − Group A (S. pyogenes) – Beta Hemolysis − Group B (S. agalactiae) – Beta Hemolyis − Group C (S. dysgalactiae) − Group D (S. bovis, Enterococcus) − Non-Groupable (S. pneumoniae, Viridans) – Non-hemolytic (S. pneumoniae is alpha-hemolytics) • Classification by Hemolysis Pattern: − Alpha (Group D and Non-groupable) − Beta – most destructive (Groups A, B, C, F, G) − Non-hemolytic (Some Group D and Non-Groupable) Epidemiology • Transmission – Direct contact, Fomites or Contaminated respiratory droplets (GAS); In utero or during birth (GBS); Direct contact with nasal secretions or Contaminated respiratory droplets (S. pneumoniae or Pneumococcus) • Lancefield’s Groups • Species • Sub-Types • Characteristics • Group A • S. pyrogenes • >80 subtypes based on M protein • • Beta-hemolytic Highly pathogenic • Group B • S. agalactiae • 5 sub-groups • • Beta-hemolytic Pathogenic for neonates • Group D • Enterococci, including E. faecalis and E. faecium • • Ungroupable • Viridans streptococci • • Ungroupable • S. pneumoniae • • • • Alpha, beta, or gamma hemolytic Grow in 6.5% NaCl Opportunistic S. mutans, S. sanguis, S. salivarius, etc • Alpha-hemolytic; often associated with dental cavities and endocarditis Smooth (capsulated) and rough • • • Mostly alpha-hemolytic Bile soluble, optochin sensitive Highly pathogenic Optochin sensitive Characteristic bactitracent Group A Streptococcus Group B Viridans Streptococcus Enterococci Streptococcus pneumoniae Streptococcus Hemolysis in agar b b a a, o, r, g a Growth in 6.5% NaCl - - - + - Bacitracin sensitivity + - - - - Bile solubility - - - - + Optochin sensitivity - - - 1. 2nd most common cause of neonatal meningitis a. E. Coli 2. Most common cause of UTI a. E. Coli, mainly UPEC nd 3. 2 most common cause of UTI a. Klebsiella pneumonia 4. Most common cause of UTI from a catheter a. Proteus mirabilis 5. #1 disease along with cystic fibrosis a. Pseudomonas aeuroginosa 6. #1 most common cause of meningitis a. Neisseria 7. #2 most common cause of meningitis a. H. influenza 8. #3 most common cause of meningitis a. Strep. Pneumonia 9. #1 most common cause of neonatal meningitis and sepsis in the first few days of life a. GBS 10. Leading cause of pneumonia in the world - + a. Step. Pneumonia 11. Most common cause of intra-abdominal infections a. Bacterioides Fragilis 12. Most ubiquitous bacteria in hospitals a. Pseudomonas Auerginosa 13. Oxidase Positive? a. Vibrio, Brucella, Neisseria, Pseudomonas 14. Acid Fast Stain a. Chlamydia b. Mycobacterium 15. Forms spores? a. Bacillus, Anthracis, Clostridium 16. Gram (+) Coccus a. Staph b. Strep 17. Gram (+) Bacillus a. Bacillus anthracis b. Clostridium c. Corneybacterium diphtheria d. Listeria e. Mycobacterium tuberculosis 18. Gram (+) Anaerobes a. Actinomyces b. Clostridium 19. Gram (-) Anaerobes a. Bacteriodes fragilis 20. Gram (-) Enterobacteriaceae NON-FASTIDIOUS a. E. Coli – Facultative Anaerobe b. Salmonella – Facultative Anaerobe c. Shigella – Facultative Anaerobe d. Klebsiella – Facultative Anaerobe e. Yersinia – Facultative Anaerobe f. Proteus – Facultative Anaerobe g. Pseudomonas – Obligate Aerobe h. Vibrio - – Facultative Anaerobe 21. Gram (-) Bacteria FASTIDIOUS a. Coccus i. Neisseria 1. Thayer-Martin b. Coccobacillus 1. Bordatella a. Bordet-Gengou 2. Haemophilus a. Factor V and X (NAD and Hemin) b. Chocolate Agar 3. Brucella a. Reduces sulfur, nitrate b. Chocolate Agar 4. Francisella Tularensis a. Agars that contain cysteine 22. Gram negative has what for virulence? a. Capsule 23. Where are E. Coli normally found? a. Digestive tract 24. Where is Staph. Aeurus normally found? a. The nose 25. What are obligate pathogens a. Organisms always associated with disease 26. Are skin flora more gram + or gram -? a. Gram + 27. Are internal flora more gram – or gram +? a. Gram – 28. Anaerobes outnumber anaerobes by how much? a. 100:1 29. What is an example of mutualistic relationship? a. E. Coli synthesize Vitamin K and complex B vitamins. In return, we provide a warm, moist, nutrient rich environment for E. coli 30. How can E. Coli be an opportunistic infection? a. It can leave it’s normal home of the digestive tract and gets into the urinary tract and cause UTI infections 31. How Can S. aureus be an opportunistic infection? a. S. aureus is commonly found in the upper respiratory tract, but if it gets into a wound it can cause problems 32. Which type of bacteria normally colonize the skin? a. Gram positive bacteria 33. Which type of bacteria normally colonize the internal flora? a. Gram negative bacteria 34. What is the ratio of anaerobes to aerobes? a. 100:1 35. What are some beneficial roles of bacteria? a. Stimulate the host immune response b. Prevent adherence and colonization of pathogens c. Produce vitamins d. Produce substances which kill other bacteria e. Stimulate the lymphatic tissue of GI tract 36. What are specific mechanisms of commensal bacteria that aid us? a. Outcompete for space and nutrients b. Secrete mucins that prevent attachment c. Secrete metabolic products that inhibit pathogens d. Produce antibiotic substances 37. What are the characteristics of Lactobacillus? a. Gram (+), anaerobic b. Found in mouth, stomach, intestines and GU c. Used as probiotics 38. What are the factors that affect microflora location and composition? a. Nutrients b. Physical and chemical factors c. Mechanical factors d. Variation in age, diet, hygiene, stress 39. Major flora of the skin? a. S. epidermidis b. Propionibacterium acnes 40. What two species are important pathogens in implant-related infections a. P. acnes and P. granulosum 41. Major flora of the anterior nares? a. S. epidermidis b. S. aureus c. P. acnes 42. Major flora of the posterior nares? a. Corynebacterium species b. Strep. pneumonia c. Haemophilus influence 43. Major flora of the saliva and oral mucosa? a. Bacteria: i. S. epidermidis ii. S. aureus iii. S. salivarius iv. H. influenza v. Lactobacillus b. Yeast: i. Candida albicans c. Protozoa i. Trichomonas tenax ii. Entamoeba gingivalis 44. Major flora of the teeth a. Streptococcus mitis, mutans, and sanguis 45. How do S. mutans stick to the surface of you teeth? a. They convert sucrose to a polysaccharide and stick to the dental pellicle 46. What do S. mutans and Lactobacillus do to damage your teeth? a. They metabolize sugars to lactic acid and cause cavities 47. What is the pathogenicity of S. sanguis? a. They can enter the bloodstream from minor trauma and adhere to the heart causing endocarditis 48. Significant cause of peptic ulcers and gastritis? a. Helicobactor pylori 49. What two categories of phyla compose most of the large intestine flora? a. Bacteroidetes (Gram -) i. Bacteroides (fragilis) ii. Proteobacteria b. Fermicutes (Gram +) i. Bacilli 1. Peptostreptococci 2. Enterococci 3. Lactobacilli 4. Clostridia 50. What ratio of large intestinal flora determined obesity in mice? a. Fermicutes/bacteroidetes ratio. i. A higher bacteroidetes vs. fermicutes lead to weight loss 51. What is the normal vaginal flora ratio of anaerobes:aerobe? a. 4:1 52. What is the most common cause of meningitis and sepsis in new newborns? a. Women infected with Group B. Streptococcus 53. Full-term pregnancy, vaginal delivery, breastfeed a. Bifidiobacterium 54. Full-term pregnancy, vaginal delivery, bottle-feed a. Facultative and obligate anaerobes 55. C-section? a. Coliforms 56. Premi? a. BAD STUFF 57. Post-menopause? a. Gram (-) increase and decrease in lactobacillus 58. Old? a. Candida albicans 59. 4 Steps to a Gram stain a. Stain with crystal violet b. Precipitate c. Decolorize with an alcohol d. Counterstain with safranin e. Purple = positive f. Red = Negative 60. Coccus example a. Staph (diplococcus) 61. Bacillus example a. E. Coli 62. Spirillum example a. Borrelia Burgoderfi 63. Vibrio example a. Cholera 64. Coccobacillus example a. Chlamydia 65. What is a plasmid that has integrated into the DNA? a. Episome 66. What is conjugative plasmid a. F plasmid b. Encodes for genetics transfer enzymes and sex-pilis gene c. This kind can be transferrable to other similar bacteria 67. What are non-conjugative plasmids? a. Don’t code for transfer enzymes b. Can be transferred to other similar bacteria only if the other bacteria already has an F-plasmid 68. What’s significant about plasmids? a. They transfer antibiotic resistance, virulence factors, and can alter key antigens 69. What are 3 ways the plasmid can replicate? a. On it’s own and get passed to a daughter cell b. By fusing with the DNA and replicating that way c. Replication for conjugation to pass on it’s plasmid to another bacteria 70. What’s important about the operon? a. It’s essential for regulating the coding all the necessary genes for a given function 71. Pathogenicity island a. A group of genes that coordinate their own control (Francisella tularensis) b. They often are surrounded by transposon-like elements that encode for virulence properties 72. Inducible operons – positive or negative control? a. Positive control – it’s silenced until the activator binds 73. Repressor operons – positive or negative control? a. Negative control – It’s active until the repressor binds 74. How do you get genetic variability? a. DNA mutations b. Transposons 75. What is transduction? a. The transfer of DNA between bacterial cells using a bacteriophage 76. What is Generalized transduction a. Involves the lytic cycle, no integration, and there is no control over transferrable elements 77. What is Specialized transduction a. Involves the lysogenic stage b. There is an integration step c. More control over where it’s inserted 78. What is transformation? a. Bacteria eat dead bacteria DNA and the DNA incorporates into their DNA 79. Bacteria who can do transformation has what ability> a. Competence 80. What are the four stages of bacterial growth a. Lag phase i. Cells are adapting to the environment and are no dividing b. Log phase i. Cells divide quicker than they die c. Stationary phase i. Cells die and duplicate at an equal rate d. Decline phase i. Cells die quicker than they duplicate 81. Bacteria that undergo aerobic respiration remove toxic oxygen byproducts by what enzymes a. Catalase, peroxidase, SOD 82. Obligate aerobes a. Require oxygen b. Has catalase and SOD 83. Obligate anaerobes a. Cannot grow in the presence of oxygen b. Does not have catalase or SOD 84. Facultative anaerobes a. Can grow with or without oxygen, but like oxygen b. Has catalase and SOD 85. Microaerophiles a. Can grow in little oxygen concentrations b. Does not have Catalase or SOD 86. Aerotolerant Anaerobes a. Oxygen doesn’t affect this organism b. Does not have catalase, but does have SOD 87. Bacteria need iron for growth How do they get free iron? a. Cytotoxins cause cells to release ferritin, and then hemolysins break up RBCs to release hemoglobin 88. How do PMN’s respond to the above question a. They release lactoferrin to sequester iron again 89. Temperature and pH can affect bacterial growth, T/F a. T 90. What are the five steps to bacterial suvivial a. Colonization b. Spreading Factors (Invasins) c. Accessing nutrient sources d. Production of endo and exotoxins e. Escaping the host defense 91. How do bacteria spread – what three enzymes a. Hyaluronidase b. Collagenase c. Streptokinase / Staphylokinase 92. What does Hyaluronidase do? a. Attacks connective tissue and opens the extracllular matrix 93. What bacteria use this? a. Strep, Staph, Clost 94. What does collagenase do? a. Breaks collagen, especially muscle tissue 95. What bacteria uses this? a. Clost. Perf 96. What do Licthinases do? a. They degrade phosphotidylcholine in membranes 97. What kind of enzyme cleaves immunoglobulins a. Proteases 98. What kinds of enzymes are used to escape PMN’s NETs a. Nucleases and Catalases 99. Endotoxins are a part of Gram (-) cell wall that are released when a bacteria dies 100. Exotoxins are a part of Gram (+) bacteria that are released and secreted 101. Penicillin a. Beta-lactam drugs b. Interfere with peptidoglycan synthesis by preventing cross-bridge formations – blocks PBP (penicillin binding protein) or transpeptidases c. Penicillin G and V d. Used for: i. S. pyogenes (GAS), (Neiserria) meningococcus, pneumococcus e. Disadvantages i. Most bacteria now have Beta-lactamases ii. Allergies 102. Cephalosporins a. Beta-lactam drugs b. Does the same as penicillin, but it has a longer half-life and is more resistant to Beta-lactamases c. Used for: i. Gram (+) bacteria and bacteria resistant to penicillins d. Disadvantages i. Bacteria still have beta-lactamases ii. Allergies 103. Glycopeptide (VANCOMYCIN) a. Complex glycopeptide that disrupts synthesis of peptidoglycan synthesis of Gram (+) b. Binds to D-alanine of the pentapeptide side chain c. Used for: i. Super Beta-lactam resistant Gram (+) bacteria d. Disadvantages: 104. a. b. c. 105. 106. a. b. a. b. c. d. 107. a. b. 108. c. a. i. S. Aeureus are beginning to have a plasmid to resist this. ii. It’s damaging to the kidneys Bacitracin It interferes with bactoprenol for peptidoglycan synthesis Used for: i. Skin infections by Gram (+) bacteria, usually Staph and GAS You find this in Neosporin Polymyxins Cyclic polypeptides that insert into membranes and dissociate LPS and phospholipids in Gram (-) bacteria Used for: i. External ear, eye, and skin infections Tetracyclines Reversibly bind to 16S of 30S ribosomal subunit Bacteriostatic Used for: i. UTI, eye and respiratory infections caused by Chlamydia, mycoplasma (pneumonia), rickettsia (fever) ii. Spirochetes infections (Borrelia and Treponema), Yersinia, brucellosis, and tularemia Tetracycline and Doxycycline i. Better GI absorption and longer half-life ii. Amingoglycosides Irreversibly binds to 30S subunit by inserting incorrect amino acids i. Bacteriocidal Treats severe Gram +/- bacteria i. Strep, E. Coli, Streptomycin, Kanamycin, Gentamicin Macrolides Reversibly binds to peptidyl transferase of 50S subunit and inhibits protein elongation i. Bacteriostatic 109. 110. 111. 112. b. Used for: i. Staph, strep, chlamydia, corynebacterium (diphtheria), Treponema, Borrelia ii. DOC for mycoplasma, Legionella, Bordatella, iii. Erythromycin, Azithromycin, Clarithomycin, Roxithromycin Clindamycin a. Binds reversibly to peptidyl transferase and can bind to charged tRNA to block elongation i. Bacteriostatic b. Used for: i. Staph and Strep, Anaerobic Gram (-) bacteria Quinolones (Fluoroquinnolones) a. Inhibits the action of bacterial DNA topoisomerase (DNA Gyrase) b. Used for: i. Broad spectrum of Gram +/- bacteria ii. DOC for UTI cause by E. Coli and enterobacteria c. Ciprofloxacin, Levofloxacin, Moxifloxacin Sulfonamide a. Antimetabolite drug b. Competes with PABA to block synthesis of folic acid c. Mammals do not synthesize folic acid so low sideeffects d. Used for: i. UTI of gram-negative ii. Otitis media (pneumococcus) iii. Chronic bronchitis (pneumococcus) iv. Shigellosis v. Traveler’s diarrhea e. Sulfamethoxazole, sulfanilamide Trimethoprim a. Inhibits DHRP to block synthesis of folic acid b. Combined with Sulfamethoxazole CIPRO for UTI (Quinolone) Erythromycin (MACROLIDE) for A-typical pneumonia for mycoplasma