BIO 120.3 Second Exam Reviewer PDF
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Summary
This document reviews Gram-positive cocci, including Streptococcus and Staphylococcus species. It covers their classification, pathogenesis, virulence factors, and clinical findings related to various infections like impetigo, pyoderma, and toxic shock syndrome, as well as neonatal meningitis. The document also discusses diagnostics and treatments.
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○ onsidered to be the norm for C ODULE 3: Pathogenesis, Epidemiology, and M cla...
○ onsidered to be the norm for C ODULE 3: Pathogenesis, Epidemiology, and M classifying Control of Medically Important Microorganisms Hemolysis and Other Infectious Agents Biochemical reactions Growth characteristics Genetic studies Other antigenic reactions Gram-Positive Cocci Morphology ofStreptococcus spp. Grouped based on presence of catalase ○ Catalase test: presence of catalase indicates bubbles when hydrogen peroxide is put on the bacterial slide Streptococci (catalase positive, chained arrangement) ○ Group A ○ Group B ○ Group D ○ Viridans group atalase negative C ○ S. pneumoniae Cell Structure Staphylococci (catalase negative, ○ Cocci arranged in chains clustered/grape-like arrangement) Culture ○ S. aureus ○ Hemolytic ○ S. epidermidis B-hemolytic: complete, clear ○ S. saphrophyticus zone A-hemolytic: partial, greenish Classification of Streptococci discoloration G-hemolytic: non-hemolytic Lancefield classification ○ Presence ofantigeniccharacteristicsof the C-carbohydrate (cell wall) ○ More than 18 groups (groups A-S) High dose of penicillin with clindamycin ○ ○ Eryhtromycin Diagnostics include gram stain, culture, and throat swab Clinical Findings of Skin Infection roup A: Streptococcus pyogenes G Culture Catalase-negative Microaerophilic B-hemolysis caused by Streptolysin O and S ○ O: oxygen-labile ○ S: oxygen-stable Pathogenesis/Virulence Factor M-protein ○ Adherence factor, anti-phagocytic, antigenic Lipoteichoic ○ Adhered factor irect invasion D Streptolysin O and S Impetigo, pyoderma, cellulitis, necrotizing Streptokinase fasciitis Hyaluronidase Progression of Necrotizing Fasciitis Exotoxins ○ S.pyogenesutilizesexotoxinstotarget ○ Eryhtrogenic or pyrogenic toxin the fascia Responsible for scarlet fever Toxic shock syndrome Stimulates overproduction of cytokines Clinical Findings of Throat Infection Fournier’s Gangrene ○ Affects the scrotum, anus,andprivate parts of the male Treatment ○ Surgery ○ Penicllin G ○ Clindamycin Clinical Findings on Scarlet Fever Direct invasion ○ Pharyngitis Symptoms and signs ○ Fever, dry throat ○ Pus on the tonsils, thus “pyogenes” Treatment Clinical Findings - Neonatal meningitis - Neonatal pneumonia - Neonatal sepsis Treatment - Penicillin Diagnositics - Gram stain of CSF or urine - Culture of CSF, urine, or blood Pathogens that cause Neonatal Meningitis - treptococcus agalactiae S irect invasion D - Escherischia coli Hallmark: strawberry tongue - Listeria monocytogenes ○ Other symptoms include rashes withi the body, flushed face, fever Group D: Enterococcus and non-enterococci May arise from untreated strep throat Enterococcus Treatment ○ Enterococcus faecalisandE. faecium ○ Surgery ○ Can grow in 40% bile, 6.5% NaCl ○ Penicillin G ○ Second cause of nosocomial infections ○ Clindamycins Non-enterococci ○ Streptococcus bovisands. Equinis Clinical Findings on Toxic Shock Syndrome ○ Can grow in40%bilebutnotin6.5% Direct invasion NaCl Treatment ○ Penicillin (erythromycin) Culture ○ Amoxicillin - Catalase-negative ○ Clindamycin - Facultative anaerobe Diagnostics - Usually G-hemolytic but may be A-hemolytic ○ Gram stain ○ Culture Clinical Findings - Subacute bacterial endocarditis linical Findings on Delayed Antibody-Mediated C - Biliary tract infections Disease - UTI (esp. enterococci) Targets the heart AntigensofS.pyogenesandhearthavesimilar Treatment features, so the immune system mayconfuse - Ampicillin + aminoglycoside (emerging the two and attack the heart resistance) Rheumatic fever - Vacomycin (emerging resistance) ○ Hallmark symptom: St. Vitus dance - There is a possibility for the resistant gene vanA to be passed off toS. aureus roup B: Streptococcus agalactiae G Culture Diagnostics Catalase-negative Gram stain Facultative anaerobe Culture B-hemolytic ○ Enterococci in 40% bile, 6.5% NaCl Can be acquired by babies during delivery ○ Non-enterococci in bile only Causes neonatal meningitis, pneumonia, sepsis ○ Neonatal: 1 day to 3 months treptococci: Viridans Group S ○ Swabbing during the 35th week of Viridans pregnancy is administered to detect - Normal flora of oral cavity and nasopharynx Group BStreptococcus - Mitis, Salivarius, Mutans, Anginosus groups - Anginosus is B-hemolytic - Vaccine (pneumovax) - omprise of 30% of dental plaques C - Usually start off as dental carries, but can Diagnostics travel through the heart Culture - Catalase-negative - Facultative anaerobe, may be microaerophilic - A-hemolytic, may also be G-hemolytic Pathogenesis/Virulence Factor ram stain G Extracellular dextran Culture ○ Adhesion to heart valves ○ Does not grow with optochin and bile Positive Quellung reaction Clinical Findings - Subacute bacterial endocarditis (S. viridans) - Dental carries (S. mutans) Staphylococcus spp. - Brain or liver abscesses (S. intermedius) Morphology/Metabolism Cocci, grape-like clusters Treatment Catalase positive - Penicillin B-hemolytic (S. aureus) Coagulase (+) (onlyS. aureus) Diagnostics ○ S. epidermidis and S. saprophyticus - Gram stain are coagulase (-) - Culture Staphylococcus is penicillin-resistant, while Streptococcusis susceptible Streptococcus pneumoniae ○ Gram staining, catalase, cultures Primary cause of bacterial pneumonia and meiningitis in adults, otitis media in children taphylococcus aureus S Arranged in pairs (diplococci) Pathogenesis/Virulence Factors ○ Lancelet-shaped Catalase-negative Facultative anaerobe A-hemolytic athogenesis and Virulence Factor of S. P pneumoniae Capsules ○ Antigenic, can be recognized and neutralized by antibodies Pneumolysin ○ Binds to cholesterol in host-cell membranes Clinical Findings Pneumonia Meningitis ○ Stiff neck in adults Clinical Findings Sepsis Due to exotoxins Otitis media (in children) ○ Gastroenteritis Bacterial endocarditis ○ TSS ○ Scalded skin syndrome Treatment AKA Ritter disease - Penicillin (many strains resistant) Direct invasion - Erythromycin (emerging resistance) ○ Pneumonia - Ceftriaxone ○ eningitis M Bacillus anthracis ○ Acture bacterial endocarditis Primarily affects herbivores (goats, cattle, ○ UTI sheep) ○ And more Humans infected via contact with diseased animals Treatment ○ 95% cutaneous, 5% inhalation of - Cleaning of the wound spores, GI anthrax rare - Penicillinase-resistant penicillins In animals, portal of entry via mouth - 1st gen cephalosporins - Clindamycin Pathogenesis Diagnostics Endospores - Gram stain Capsule (poly-D-glutamic acid) - Culture (B-hemolytic, golden yellow pigment) ○ Prevents phagocytosis - Catalase (+), coagulase (+) Exotoxins ○ Protective antigen (PA) - promotes entry of EF; similar to B subunit Spore-forming Gram Positive Bacilli ○ Edema factor (EF) - active A subunit; - acillus:B. anthracisandB. cereus B impairs neutrophil function causing - Clostridium: C. botulinum, C. tetani, C. massive edema perfringens, C. difficile ○ Lethal factor (LF) - stimulates release of tumor necrosis factor Capsules andexotoxinscanonlybeexpressed Bacillus spp. upon entry of suitable tissue via plasmids Clinical Findings Cutaneous ○ Painless, black vesicles Morphology Pulmonary Cell structure GI ○ Cells arranged in long chains ○ Abdominal pain, vomiting, blood ○ Central spores diarrhea Culture ○ Aerobic Treatment ○ Hemolysis inB. cereus - Ciprofloxacin ○ Gelatin liquefied in gelatin stabs, - Doxycycline inverted tree - Raxibacumab (pulmonary) - Vaccines Diagnostics - ram stain, culture, serology G Clostridium botulinum - PCR of nasal swab - Foundinsoil,cannedorbaggedfoodproducts, smoked fish, and honey Bacillus cereus - Causes flaccid paralysis - Adult botulism, infant botulism, and wound botulism Pathogenesis - otile, non-encapsulated M - Causes food poisoning when spores are ingested Pathogenesis Endospores Enterotoxins ○ Heat-labile toxin - causes nausea, abdominal pain, diarrhea ○ Heat-stable toxin - causesnauseaand vomiting, limited diarrhea Toxins Clinical Findings ○ N eurotoxin: inhibits release of - Food poisoning: nausea, vomiting, diarrhea acetylcholine from peripheral nerves - Bacteremia/endocarditis: rare ○ Released upon death of bacterium Treatment Clinical Findings - Vancomycin ➔ Foodborne botulism - Clindamycin ◆ GI symptoms - No treatment for food poisoning ◆ Cranial nerve palsies ◆ Muscle weakness Diagnostics ◆ Respiratory paralysis - Culture from contaminated food ➔ Infant botulism ◆ Constipation Clostridium Spp. ◆ Flaccid paralysis ◆ Difficulty in swallowing (dysphagia) Morphology ➔ Wound botulism Cell structure ◆ Similar to FB but without GI symptoms ○ Rod-shaped ○ Central, subterminal, or terminal Treatment spores Antitoxinn (FB and WB) ○ Petrichously-flagellated BIG-IV (IB) Culture ○ Bot immunoglobulin-IV ○ Anaerobes, few aerotolerant ○ Fewer complications and side effects ○ Grows well on blood-enriched media Penicillin ○ B-hemolytic Intubation and vent Surgical debridement (WB) - ound in soil F Diagnostics - Spore-former - Gram stain, culture - Anaerobic and produces gas - Rampant and one of the primary causes of Clostridium tetani death in soldiers before penicillin Skin trauma by any spore-contaminated object - May enter existing trauma, causing Found in soil and animal feces further infection Hallmark symptom: Risus sardonicus ○ As soon as this symptom manifests, Pathogenesis morbidity follows Toxins Gamma-aminobutyric acid (GABA) ○ Alpha-toxin - lecithinase ○ responsible for inhibition of muscle ○ Other tissue-destructive enzymes contraction Clinical Findings Pathogenesis ➔ Cellulitis/wound infection Toxins ◆ Necrotic skin exposed ○ Tatanospasmin: sustained contraction ◆ Crepitus - moist, spongy crackling of skeletal muscles called “tetany” consistency due to pocket of gas ○ Inhibits release of Renshaw cell ➔ Clostridial myonecrosis interneurons,preventingthereleaseof ◆ Destroys muscles GABA and glycine which areinhibitory ➔ Diarrheal illness neurotransmitters, leading to high ◆ Ingested contaminated food frequency impulses to the muscle cells ◆ Watery diarrhea Clinical Findings Treatment - Muscle spams - Surgery (may include amputation) - Lockjaw - Penicillin - Risus sardonicus - Hyperbaric oxygen - Respiratory muscle paralysis Diagnostics Treatment - Gram stain, culture - Tetanus toxoid (part of DTaP vaccine) - Antitoxin (human tetanus immune globulin) Clostridioides difficile - Clean the wound Causes pseudomembranous colitis - Metronidazole or penicillin Responsible for antibiotic-associated pseudomembranous colitis Dignostics ○ Red, inflamed mucosa and areas of - Gram stain, culture white exudate Opportunistic pathogen Clostridium perfringens ○ Prolonged use of wide-spectrum antibiotics causes proliferation due to gut microflora being wiped out by the medicine, thus encouraging growth of C. difficile Pathogenesis Toxins ○ Toxin A- causes diarrhea ○ Toxin B- cytotoxic to the colonic cells Binary toxin CDT ○ Newly discovered in 2002 ○ Produced 15 to 20 times more toxin Clinical Findings - Causes gas gangrene - Pseudomembranous colitis (antibiotic-associated) Treatment Morphology - Discontinued antibiotics - Coccobacillus/pleomorphic rods - Colonoscopy - Club-shaped - Fidaxomicin - Vancomycin Culture - Metronidazole - Facultative anaerobe - Fecal transplantation - Catalase-positive - Non-motile Diagnostics - PCR for toxin detection, EIA for antigens to Pathogenesis toxins A and B Toxins ○ Exotoxin A subunit blocks EF-2, Non-spore-Forming Gram-Positive Bacilli inhibiting protein synthesis B subunits provide entry into cardiac and neural tissues Diagnostics - orynebacterium diptheriae C - Listeria monocytogenes Corynebacterium diptheriae ram stain G Cultureonpotassium-telluriteagar(darkblack colonies) on potassium-tellurite agar Loeffler’s coagulated blood serum ○ Reddish granules stained with methylene blue after 12h growth Clinical Findings Diphtheria - ound in soil, water,humanskin,andmucous F ○ Mild sore throat + fever membrane ○ Pseudomembrane on pharynx - Respiratory droplets from the carrier - Causes diphtheria Treatment - Affects the pharynx - Antitoxin - Forms a grayish pseudomembrane (composed - Penicillin or erythromycin of fibrin, leukocytes, necrotic epithelial cells, - Vaccine: DTaP andC. diptheriaecells) Gram-Negative Pathogens Listeria monocytogenes Also known as facultative intracellular bacteria ○ Can live inside WBC, creating a protective shell around it ○ Opportunistic in the sense that it infects immunocompromised individuals Found in a wide range of environments Survives at low temperatures (4C), low pH, high salt Associated with dairy products or pre-packed raw produce (fruits, vegetables, meats) Causes listeriosis Morphology Neisseria spp. Morphology ○ Gram negative diplococci Culture ○ Facultative anaerobe ○ Optimal growth in high CO2 ○ Nesseria meningitidis Maltose and glucose fermenter Can become systemic ○ Neiiseria gonorrheae Glucose fermenter - Short rods Culture - Facultative anaerobe - Catalase-positive - Motile - B-hemolytic Pathogenesis Listeriolysin O and phospholipases ○ Evades intracellular killing Clinical Findings - Septicemia in pregnant women - Third trimester - Neonatal meningitis - Meningitis in immunosuppressed patients and elderly Treatment - Ampicillin - Trimethoprim/sulfamethoxazole Diagnostics - Gram stain, culture N. meningitidis 13 serotypes found on the capsules Biochemical Classification of Enterics ○ Groups A, B, and C mainly cause Lactose fermentation → gas and acid meningitis ○ E. coliand others – lactose (+) Petechiae: Blood vesseldestruction,exhibiting ○ Salmonella, Shigella, Pseudomonas – visible red rashes on the skin Lactose (-) IgA Protease H2S production ○ Cleaves immunoglobulin A Urea hydrolysis ○ Found in pathogenic strains of this Gelatin liquefaction bacteria Amino acid decarboxylation Pilus for adherence ○ Nasopharyngeal cells Differential and Biochemical Tests ○ Extract iron from hosts IMVIC tests Treatment includes TSIA in slant/butt tubes ○ Vaccines against group B serotype ○ Triple sugar iron agar ○ Pen G, ceftriaxone ○ K = alkaline = red ○ Rifampin or ciprofloxacin for close ○ A = acid = yellow contacts Use of differential media (Ex. EMB, MAC, XLD) Thayer-Matin VCN Media (chocolate agar base) ○ Differentiates between lactose and ○ Vancomycin (selective for G-) non-lactose fermenters ○ Colistin (selective against all other G- MPN test except Neisseria) ○ Nystatin (antifungal) N. gonorrhea - Pilus - Help cells undergo multiple recombinations so antigenicproperties are ever-changing - Adherence - Can cause ectopic pregnancies and sterility The Enterics erycommonpartofthenormalgutmicroflora V or may cause GI infections ○ Difficult to eradicate ○ Affects theimmunocompromised,such Antigenic Classification as the elderly and infants Enterobacteriaecaeae, Vibrionaceae, Bacteroidaceae, Pseudomonadaceae Morphology ○ Gram-negative rods ○ Some are motile with peritrichous flagella; some are nonmotile Transmission ○ Fecal-oral ○ Migration up the urethra ○ Colonization of catheters in hospitalized patients Metabolism Outer membrane ○ Catalase-positive ○ LPS O-side chains (O) ○ Oxidase-negative Capsules (K) ○ Facultative anaerobic (except Flagella (H) Pseudomonas spp.) Degrees of Intestinal Invasion - TI U 1. No cell invasion - Neonatal meningitis a. Bacteria binds only to the cell - Sepsis b. Exotoxins (enterotoxins) cause diarrhea E. coliinfections c. Water diarrhea: ETC andV. cholerae 2. Invasion of intestinal epithelial cells a. Binding and invasion occurs; resulting to cell death b. Fever, bloody diarrhea, pus c. Systemic immune response d. EIEC,Shigella,Salmonella enteritidis 3. Invasion of lymph nodes and bloodstream a. Fever, headache, WBC count elevated b. Bacteremia, sepsis c. Salmonella typhi, Yersinia enterocolitica, Campylobacter jejuni TI is primarily seen in women and patients U Family Enterobacteriaceae hooked to catheters for a long time ○ Dysuria: burning sensation when - ery common: part of the normal gut V peeing microflora or may cause GI infections ○ Hematuria: blood found in urine - 63 genera; 20-25 species are clinically ○ Pyuria: elevated WBC in urine significant Sepsis is secondary to UTI Morphology Types of Diarrhea caused byE. coli - Gram-negative rods - Some motile with peritrichous flagella; some nonmotile Culture and Biochemical Properties - May grow aerobically or are facultative anaerobes - Glucose fermentation with gas production - Catalase positive - Oxidase negative - Reduce nitrate to nitrite - E. coli: circular, convex, andsmoothcolonies; some may be hemolytic - Enterobacter: mucoid colonies - Klebsiella: large and mucoid colonies - Salmonella and Shigella: colonies like E. coli but do not ferment lactose scherichia coli E Virulence Factors Pilus ○ Epithelial cell invasion (colonization) Exotoxin production ○ LT and ST ○ Shiga-like toxin PEC and ETEC produce the same kind of E Endotoxin (Lipid A) diarrhea Iron-binding siderophores ○ Described as rice water stools ○ EAF: EPEC adherence factor Clinical Findings - Diarrhea ○ PEC: Pilusattachestoepithelialcells, E ○ Same toxin as EIEC (Shiga toxin) causing microvilli of the intestine to Fecal-oral transmission efface, thus resulting in watery diarrhea Morphology ○ Both EPEC and ETEC are stage 1, no - Slender rods; non-motile cell invasion occurs - Cocco-baccillus in young cultures ETECE. colimay have both LT and ST ○ LT is a type of AB toxin, where the Culture B-subunit binds to the intestine - Aerobes/facultative anaerobe allowing the A-subunit to enter and - Glucose fermenters causing the continuous secretion of - Non-lactose fermenter cyclic AMP - No H2S production ○ Hypersecretion of cAMP → - Acid production, rare gas production overproduction of fluids → fluids cannot be reabsorbed by intestinal Virulence Factors lumen - Shiga toxin (same as EHEC and EIEC) ○ ETECE. coliaka traveler’s diarrhea - Low infectious dose (10^2) ○ Can cause fluid loss of upto20%per - Only need a few cells to cause infection day - Translation is disrupted,leadingtocell EHEC E. coli exhibits bloodydiarrhea,hascell death invasion - Salmonella and vibrio have a higher ○ Stage 2 infectious dose; ○ Largest outbreak recorded in 2011 in Germany Clinical findings ○ Associated with contaminated food Fever products, particularly with meat Abdominal pain EIECE.coliissimilartoEHEC,butalsohasthe Bloody diarrhea with mucus and pus presence of pus and WBCs in stool and fever ○ Hypersecretion of fluids, and EAEC E. coli contains ST, enterotoxin, and reabsorption cannot occur due to the hemolysin invasion of intestinal mucosal cells Shigellaspp. Treatment - No flagella - Oral fluid replacement - No lactose production - IV fluid - No H2S production - No anti-diarrheal drugs - Rare gas production - Antibiotics for severe infections (TMP-SMX, CFT, AZT) Shigella dysentriae Diagnostics Gram stain Culture on MAC or EMB, HE, XLD ○ Xylosetysine-deoxycholate: to differentiate salmonella and shigella K/A on TSIA, no gas or H2S Salmonella Commensal and pathogenic ○ Found in animals, pathogenic to humans Transmission viacontaminatedwaterandfood or animal products Causes enteritis, enteric fever, and systemic infections Associated with typhoids, with 2200 serotypes I ntestinal tracts of humans and primates ○ Typhoidal Causes bacillary dysentery Typhi Paratyphi - K/A, gas, and H2S on TSIA ○ Non-typhoidal Enterotytis Other Enterobacteriaceae Morphology - Bacillus-shaped - Motile Culture - Facultative anaerobe - Non-lactose/sucrose fermenter - Acid production, gas, and H2s production Virulence Factors Capsule (Vi antigen) ○ The immune system of a host can recognize capsules, which can phagocytose them ○ Cansurvivemacrophages,hencebeing a facultative intracellular bacteria ○ Macrophages and neutrophils come from the spleen Motile Siderophores Clinical findings Typhoid (enteric) fever ○ Caused bySalmonella typhi ➔ K lebsiella pneumoniae and Klebsiella oxytoca ○ Fever, headache, abdominal pain,rose are associated with hospital infections spots on chest, and abdomen ➔ Proteus mirabilitis would appear to be ○ Abdominal pain can be reminiscent of spreading on agar due to their high motility appendicitis pain ◆ Splits urea in NH3 and CO2, creating ○ Invades intestinal epithelium alkaline urine ○ Can be systemic Enterocolitis Vibrio cholerae ○ Most common manifestation of non-typhoidal salmonella ○ Nausea, headache, vomiting, watery diarrhea(somemaycontainmucousor blood), abdominal cramping, fever Carrier state ○ Happens to individuals who are recovering from typhoid fever ○ Salmonella may reside in the gallbladder Sepsis Treatment - TF: Ciprofloxacin/ceftriaxone - EC: fluid and electrolyte replacement Diagnostics - Gram stain - Blood, stool, or urine culture on MACorEMB, auses cholera C HE, XLD Fecal-oral route (usually contaminated water) - Hektoen Enteric Agar ETEC-like but more severe ○ ttachment of organism to intestinal A ○ Watery diarrhea eipthelial cells ○ Produces a toxin similar to LT toxin Thecausativeagentofcholera,associatedwith Clinical Findings poor sanitation Watery diarrhea ○ Contaminated sources of food or water ○ Fluid loss of 1L/hr South America: Poor disposal of sewage ○ No pus Bangladesh: monsoon floods containing feal ○ Sunken eyes matter mixed with potable water ○ Low pulse V. parahaemolyticus acquired through ○ Poor skin turgor ingestion of raw seafood ○ Predominant in Japan Treatment Prefers brackish and marine waters for growth - Fluid and electrolyte replacement Only pathogenic to humans - Doxycycline ○ Lower infectious dose of around - Fluoroquinolone 10^2-10^4 for individuals with low concentration of gastric juices Diagnosis - Microscopy Morphology - Culture on TCBS agar - Comma-shaped, curved rods - Motile with polar flagellum Helicobacter pylori Culture - erobes A - Sucrose-fermenter - Halophilic, requires 0.5-4.5% NaCl - Grows at pH 8.509.5 - TCBS culture medium (Thiosulfate-Citrate-Bile Salts-Sucrose agar) - Yellow colonies against a dark green background of the medium color Virulence Factors - auses peptic (duodenum) and gastric C Toxin choleragen (AB toxin) (stomach) ulcers, gastritis (inflamed stomach) ○ Same mechanism as LT toxin in ETEC - Leadingcauseisassociatedwithuseofaspirin ○ Induces cAMP production which products stimulates fluidsecretionandprevents reabsorption Morphology ○ Encoded in the chromosome of the - Gram-negative and microaerophilic organism, unlike ETEC whose LT is - Spiral, curve-shaped rods plasma-encoded - Motile: single or tufts of polar flagellum Fimbriae Culture ○ iema or silver stains show curved G rods ulture on TCBS agar C Common HAIs Pseudomonas aeruginosa Gram-negative, obligate anaerobes that are almost resistant to almost every antibiotic Pyoverdin and pyocynanin gives colonies on agar media a greenish-blue coloration ○ Apparent on wound dressing if it is infected Give off a fruity, grape-like scent ○ Important diagnostic feature, cultures and wounds give off this scent BE PSEUDO ○ Burns, En docarditis, Pn eumonia, Sepsis,Externalmalignantotitismedia - icroaerohphilic M UT I,DiabeticOs teomyelitis - Longer incubation of 14 days - Media enriched with blood (e.g. chocolate Virulence Factors agar) or antibiotics Exotoxin A - Oxidase and catalase positive ○ Similar to t oxin produced by C. - Urease-positive diphtheriae, p rotein synthesis is - Gray to translucent, pinpoint colonies inhibited - Optimal pH growth at 6-7 - Best isolated using gastric biopsy specimens Acinetobacter and exhibits better growth under long - Aerobic, gram-negative coccobacillus or incubation of3-6days,butincreasesrecovery diplococci after 14 days - Can be mistaken forNeisseria - Foundinsoilandwaterandmaycauseawide Virulence Factors range of infections in the hospital Adhesion factors Mucinase, phospholipase for tissue damage To prevent HAIs: Survives at neutral pH, which are capable of - Handwashing growing and colonizingthestomachwherepH - Limiting use of invasive devices is low - Prudent use of antibiotics ○ H. pylori utilizes urease activity to neutralize the acid ○ Flagella allows them to move through Respiratory Infections gastric mucus towards the epithelium Haemophilus influenzae - Aerobic, gram-negative, non-motile bacillus Clinical Findings often foundinthlungsofpeopleinfectedwith - Chronic duodenal and stomach ulcers flu virus - Can cause meningitis, influenza, and sepsis Treatment - Bismuth, tetracycline, metronidazole Virulence Factors - Clarithromycin, amoxicillin - 6 types of capsules (a, b, c, d, e, f) - Proton pump inhibitors - Btypeismostassociatedwithinvasive infections in children Diagnostics Microscopy with stains Bordetella pertussis ○ Hemotoxylin and eosin stains Causes whooping cough, high-risk groups are demonstrate gastritis infant less than 1 year old lso a highly contagious disease typucally A found in play schools and daycare facilities ○ Cases decreased dramatically since development of vaccines ○ Disease resurgence observed with 15-20,000 cases per year between 2005 and 2017 Pertussis: violent cough ○ Production of pertussis toxin (AB toxin) ○ The tracheal toxin (kills ciliated eipthelial cells) ○ FHA facilitates binding to ciliated epithelial cells Stages of Whooping Cough Catarrhal stage: most contagious ○ Resemble upper RT infection with low gradefever,runnynose,sneezing,and mild cough Paroxysmal stage: primary symptom of whooping cough is apparent ○ Fever subsides, bursts of non-productive coughing begins ○ May become blue from low oxygen, tongue protrudes, eyes bulge, neck veins engorge, vomiting may occur Mycobacterium - Causes TB and leprosy Morphology - Acid-fast bacillus - Obligate anaerobes (particular for Mt) → can be found in lungs - Non-motile, no capsule - Catalase positive Culture Growth is slow, takes up to 6 weeks Acid Fast Bacteria Staining ○ Carbol-fuschin (red-pink color) Morphology combined with little heat so dye penetrates cells ○ Mycolicacidlayerispresent→difficult for nutrients and dye to penetrate ○ Acid aclochol (combination of HCl) ○ Background of the sample is stained blue, AFB will appear red or pink in color Mycobacterium leprae Causes leprosy ○ Lepromatous leprosy ○ Tuberculoid leprosy LL is the most severe form, with no cell-mediated immunity ○ The immune system cannot recognize the bacteria and goes unchecked ○ Affects the nerves, eyes, and testis in men ○ Can be isolated from any sample ○ Inability to feel the fingers and toes and resemble claws, blindness,lossof nose cartilage TL is a milder form of leprosy ○ Self-limiting disease due to cell-mediated response ○ Cannot grown on culture media Hyphae ○ Ceoneocytic or septate MODULE 3: Medically-important Fungi ○ Mycelium: mat of hyphae General Characteristics Yeast Eukaryotic ○ Single-celled fungi Cell wall Dimorphic fungi ○ Chitin, glucans, mannans ○ Fungi with yeast and hyphal form Cytoplasmic membrane ○ Triggered by temperature or nutrients ○ Ergosterol - major sterol present in the environment ○ Antifungals mainly target ergosterol ○ C. immitis is capable of yeast and Metabolism hyphal form ○ Heterotrophic ○ The yeast form is aka as spherules, Saprophytic which form at 37C Parasitic ○ The hyphal form moves at room Ubiquitous in terrestrial and aquatic temperature environments ○ Yeast-like cells are easy to move ○ Less prominent in marine around environments Pseudohyphae Distribution is cosmopolitan ○ Hyphae with constrictions at each septum ○ Hyphae only structure is straight in apperance ○ Pesudohyphae may be pinching and oval-y Spores ○ Conidia-asexualspores,formedoffof a hyphae (most common) Aspergillus Virulence Factors Mucor 1. Morphological transformation ○ Blastoconidia - buds on yeast 2. Genetic switching of metabolic processes in Type of spore made by yeast response to the host environment cells 3. Production of surface adhesins ○ Arthroconidia - asexual spores formed 4. Cell wall components that resist phagocytosis bysegmentationofhyphae,candetach 5. Secretion of enzymes that attack host itself substrates ○ Sporangia - sac that contains the 6. Formation of biofilms sporangiospores Secretes enzymes, not toxins Establishinfectionviagrowth,leadingtotissue Diagnostics death Microscopy Mold growing on tissues is destructive, where ○ KOH wet mount (10-30%) the hyphae can penetrate the said tissue ○ Silver, India ink, Giemsa staining, etc. causing spores to grow out Culture ○ OnSDA(SabouraudDextroseAgar)or Mycoses PDA (Potato Dextrose Agar) with antibiotics - utaneous and superficial C PCR - Subcutaenous Serology - Systemic ○ Isolation and detection - Opportunistic Antifungal Drugs ➔ Amphotericin B Superficial Mycose ◆ Used for systemic fungal infections Malassezia furfur ◆ Via IV Normal skin flora ◆ Side effects: renal toxicity, fever, Lipophilic anemia Infections ◆ MOA: destroys ergosterol ○ Dandruff (mildest) ➔ Flucytosine ○ Pityriasis versicolor ◆ Inhibits DNA/RNA synthesis ○ Follliculitis ◆ Best with amphotericin B ○ Chronic infections include hypo- and ◆ Via IV hyperpigmentation ◆ Side effects: bonemarrowdepression, nausea, vomiting, diarrhea ◆ MOA: inhibits DNA/RNA synthesis ➔ Azoles ◆ Most commonly available antifungals ◆ Imidazoles (ketocanazole, miconazole, clotrimazole) ◆ Triazoles (itraconazole) ◆ MOA: inhibits Cytochrome P-450 (ergosterol synthesis) ➔ Nystatin ◆ Too toxic for IV use ◆ Not absorbed via GI tract so can be used to treat mouth and esophageal infections ◆ MOA: destroys ergosterol een on the back, chest, and sometimes the S ➔ Griseofulvin neck or face ◆ Slow cure of skin infections Also known as furfuraceous scales ◆ MOA: inhibits spindle formation ➔ Terbinafine ◆ Best for treating fungal nail infections ◆ MOA: blocks fungal cell wall synthesis Hortaea (Exophiala) weneckii ○ All genera infect skin, hair, or nails Infections ransmission is more direct, more susceptible T ○ Tinea nigra (palmaris) to infection when exposed to infected people ○ Prevalent in women across coastal ○ Can also be acquired in moist surfaces areas, fungi thrive in warm and moist Diseases environments ○ Tinea (ringworm) - characterized primarily by itching Diagnosis I mage above shows M. furfur after K OH staining ircular patterns indicate active inflammation C Acquire skin scrapings – “Spaghetti a nd White centers mean infection has healed meatballs” Person-to-person contact ○ Hyphal structures - spaghetti ○ Spores - meatballs Superficial Mycoses Treatment Shampoo ○ Dandruff shampoo with selenium sulfide Azoles ○ Imidazoles Cutaneous Mycoses inea capitisoccursmostlyinchildrenbutcan T Dermatophytes affect adults too Filamentous fungi infecting only skin, hair, Tinea unguium is characterized by nails that and/or nails are thickened, discolored, and brittle Lives on dead skin layer Secretes keratinase Diagnosis 3 genera ○ Trichophyton- skin, hair, and nails ○ Microsporum -hair and skin ○ Epidermophyton- nails and skin porothrix schenckii S Also known as Gardener’s disease ○ Found in soil and plants, associated with rose thorns in particular ○ Subcutaneous nodule can necrotize, new ulcers can appear in the arms ○ Dimorphic fungi Sporotrichosis Treatment Azoles ○ Triazoles Chromoblastomycosis - richophyton spp. T - KOH staining digest keratin in the samples, revealing hyphal structures of the fungi - Wood’s light: use of UV light (365 nm) by pointing it to the infected area - Green spots indicate infection in humans Cutaneous Mycoses Treatment Keep skin dry, usual treatments are topical Azoles ○ Imidazoles ○ Triazoles ○ Oral antifungals for severe or chronic cases Terbinafine ?
