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AccessibleShark275

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University of South Carolina

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microbiology gram-negative bacteria bacterial identification pathogens

Summary

This document provides an overview of gram-negative aerobic bacteria, including their characteristics, classification, pathogenesis, and common resistance mechanisms. It also touches upon identification techniques.

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**[Gram Negative Aerobes: Antosz]** **[Objectives]** - Compare key feature of gram-negative aerobic bacteria including morphology, growth characteristics, and classification - Interpret biochemical tests used to identify gram-negative aerobic bacteria - List clinically relevant spe...

**[Gram Negative Aerobes: Antosz]** **[Objectives]** - Compare key feature of gram-negative aerobic bacteria including morphology, growth characteristics, and classification - Interpret biochemical tests used to identify gram-negative aerobic bacteria - List clinically relevant species of gram-negative aerobic bacteria - Describe the pathogenesis and clinical syndromes associated with each of these pathogens - Recognize resistance mechanisms gram-negative express against common antibiotic classes **[Enterobacterales]** - Order of gram-negative bacteria - Share an enterobacterial common antigen - Prev classified under the family Enterobacteriaceae - Rod-shaped - Facultative anaerobes - Can survive with or without oxygen - Characteristics - Ferment glucose - Reduce nitrate to nitrite - Catalase pos - Oxidase neg - Some resistant to bile salt **[Gram-positive Vs. Gram-negative]** **Gram Positive Bacteria** **Gram Negative Bacteria** ---------------------------------------- --------------------------------------- Thick peptidoglycan layer in cell wall Thin peptidoglycan layer in cell wall No lipopolysaccharide membrane Lipopolysaccharide membrane Produces exotoxins Produces endotoxins Stained purple by gram-staining Stained red/pink by gram staining **[Pathogenesis and Immunity]** - Common virulence factors associated with enterobacterales - Endotoxin - Lipopolysaccharides in the outer membrane od gram-neg bacteria - Capable of causing lethal shock to cell - Activation of complement system, release of cytokines, leukocytosis, thrombocytopenia, fever, decreased peripheral circulation, shock, death - Capsule - Encapsulated enterobacterales are protected by phagocytosis by hydrophilic capsular antigens - Antigens interfere with the binding of antibodies to the bacteria - Protective role of capsule is diminished if patient develops specific anticapsular antibodies - Antimicrobial resistance - Extended-spectrum beta-lactamases (ESBLs) - DNA gyrase and topoisomerase mutations **[Common Enterobacterales]** - Escherichia coli - Named after Escherich; coli, of the colon **[How Can We Identify Organisms?]** - Gram stain - Growth media - Sterile specimens: non-selective media - Blood agar - Non-sterile specimens: selective media - MacConkey agar - Biochemical tests - Automated systems - Benchtop tests (spot indole, oxidase) - Rapid Diagnostic Tests - Multiplex PCR - MALDI-TOF MS **[MacConkey Agar]** - **Selective** and **differential** agar - **Selective:** only grows gram neg bacteria - Ingredients: bile salts and crystal violet dye - Limit growth of gram pos bacteria - **Differential**: can further differentiate organisms based on lactose metabolism - Ingredients: lactose - Lactose fermentation decreases pH vibrant pink/ red colors - **Lactose-Fermenters** - Escherichia Coli - Klebsiella spp. - Enterobacter spp. - Citrobacter spp. (except C. koseri) - **Nonlactose -Fermenters** - Salmonella spp. - Shigella spp. - Serratia spp. - Proteus spp. **[Spot Indole Test]** - Detects ability of bacteria to metabolize tryptophan to produce indole 1. Drop indole reagent onto filter paper 2. Using inoculating loop, pick up fresh colonies of bacteria and rub colonies over reagent on paper 3. Observe color change (within 20 sec) - **Indole (-)** - Enterobacter cloacae - Klebsiella aerogenes - Klebsiella pneumoniae - Citrobacter fredundii - **Indole (+)** - Escherichia coli - Klebisella oxytoca **[Oxidase Test]** - Used to identify bacteria that produces cytochrome c oxidase, and enzyme of the bacterial electron transport chain 1. Drop reagent (tetramethyl-p-phenylenediamine) onto filter paper 2. Using inoculating loop, pick up fresh colonies of bacteria and rub colonies over reagent on paper 3. Observe color change (within 10 seconds) - **Oxidase (+)** - Pseudomonas spp. - Vibrio spp. - Aeromonas spp. - Moraxella spp. - **Oxidase (-)** - Salmonella spp. - Acinetobacter spp. - Shigella spp. - Proteus spp. - Providenceia spp. - Serratia spp. - Morganella spp. **[Escherichia Coli]** - Most common and clinically significant Enterobacterales - Part of the normal flora of GI tract, may colonize lower end of urethra/vagina - Associated with - Urinary tract infections (UTI): \#1 leading organism - Gastroenteritis - Meningitis (leading cause in neonatal meningitis) - Sepsis - Different serotypes with varying virulence - Also member of normal intestinal microbiota **[E. Coli Morphology]** - Circular, smooth, flat, nonviscous colonies with distinct edges - Hemolysis on blood agar - Metallic sheen on different agars - Lactose fermenter - Indole positive **[Clinical Syndromes: UTI]** - Treatment - Antimicrobials that only achieve concentrations in urine are recommended - Fosfomycin, nitrofurantoin - Bactrium, fluoroquinolones for more complicated/ resistant infections **[Clinical Syndromes: Escherichia Coli Diarrhea]** - Very common - Strains of E. Coli that cause gastroenteritis are divided into several groups - Enterotoxigenic (ETEC) - Enteropathogenic (EPAC) - Enteroaggregative (EAEC) - Shiga toxin-producing (STEC) - Enteroinvasive (EIEC) **[Enterotoxigenic Escherichia Coli (ETEC)]** - Traveler's diarrhea - Infant diarrhea in developing countries - Transmission: Consumption of fecally contaminated food or water - Symptoms: watery non-bloody diarrhea, abdominal cramps, N/V - Pathogenesis: plasmid-mediated enterotoxins (heat-stable and heat-liable) that stimulate hypersecretions of fluids and electrolytes **[Enteropathogenic Escherichia Coli (EPEC)]** - Rare in US; Infant diarrhea in developing countries - Transmission: Fecal-oral exposure to contaminated food/surfaces - Symptoms: watery diarrhea, vomiting - Pathogenesis: plasmid-mediated attachment and effacement (disrupts normal microvilli structure, causing malabsorption and diarrhea) - Invades epithelial cells lining the colon with destruction of normal mucosal epithelial cells **[Enteroaggregative Escherichia Coli (EAEC)]** - Infant diarrhea (developing and some developed countries) - Can be chronic growth retardation - Traveler's diarrhea - Transmission: Fecal-Oral - Symptoms: Persistent water diarrhea, vomiting, dehydration, low-grade fever - Pathogenesis: - Autoagglutination: adherence of rods ("stacked bricks") over epithelium of small intestine cytokine release, shortening of microvilli, hemorrhage, decreased fluid absorption **[Shiga Toxin-Producing Escherichia Coli (STEC)]** - Consumption of undercooked ground beef/meat products, water, unpasteurized milk/fruit juices - \ 90% of these species - Biggest risk with Enterobacter Spp. exposed to third-generation cephalosporins - Include E. cloacae complex and K.aerogenes - Citrobacter: mainly species C. freundii or C. youngae - Rare acquisition: Plasmid-mediated AmpC genes - Always resistant even in the absence of antibiotics - Aka "stability derepressed AmpC" **[Proteus Spp, Morganella Spp., Providencia Spp.]** - Motile, slow/non-lactose3 fermenters - Proteus can swarm on media due to its motility - Proteus and Morgangella: Urease (+) - Generates CO2 and ammonia (distinctive ammonia smell) - Increases urine pH Mg + Ca precipitate Kidney stones - Providencia: Urease (-) - Associated with UTIs, pneumonia, bacteremia **[Salmonella Spp.]** - Motile - Fermented glucose and Mannose - Resistant to bile salts - Non-lactose/non-sucrose fermenter - Produces H2S - Not generally part of the human microbiome - Transmission: fecal to oral spread, ingestion of contaminated foods - Person-to-person with low inoculum possible for Salmonella Typhi - Associated with gastroenteritis, bacteremia, enteric fever asymptomatic colonization **[Hekaton Enteric Agar]** - ![](media/image3.png)Represents both selective and differential media - Divides Salmonella, Shigella,... - Selective ingredients: bile salts, lactose, sucrose, salicin, peptone - Bile Salts: limit the growth of gram pos bacteria - Lactose, sucrose, salicin: preferred by other gram-neg bacteria - Not used by Salmonella and Shigella - Peptone: for Salmonella and Shigella - Differential ingredients: - Lactose, sucrose, and salicin fermentation decreases pH vibrant yellow-orange color - Thiosulfate or ferric ammonium citrate black peptide with H2S production **[Salmonella Classification]** **[Salmonella: Gastroenteritis]** - Most common form of salmonellosis - AKA "Food poisoning" - Transmission: contaminated food/water - Highest incidence in summer/fall (outdoor gatherings) - Common sources: poultry, eggs, dairy, contaminated cutting boards - Symptoms: N/V, non-bloody diarrhea, fever, cramps, myalgias, headaches - Onset: 6-48 hours - Duration 2-7 days **[Salmonella: Bacteremia]** - Most common: Salmonella Typhi, Salmonella Paratyphi, and Salmonella choleraesuis - Higher risk in peds and immunocompromised - Clinical presentation: - Similar to other gram-neg infections; localized suppurative infections (osteomyelitis, endocarditis, arthritis) can occur - Transmission: Contaminated food or water **[Salmonella: Enteric Fever (Typhoid Fever)]** - Severe systemic illness - Caused by Salmonella Typhi or Salmonella Paratyphi - Less frequently seen in developed countries; most associated with foreign travel - Reservoir: Humans - Transmission: Contaminated food or water - Symptoms: Fever, headache, myalgias, malaise, anorexia GI symptoms Bacteremic phase Colonization of gall bladder Reinfection of intestines **[Salmonella: Asymptomatic Colonization]** - Chronic colonization: Salmonella detected in the bodily specimens (stools, urine) \> 12 months after acute infection - Normally occurs with Typhoid and Paratyphoid - Gallbladder is typical reservoir - Recurrent infection unlikely - Can shed high amounts of bacteria and infect others **[Salmonella]** - Typhoid Vaccines (2 Types) - Inactivated typhoid vaccine, injection: ViCPS - Timing of last dose before possible exposure: 2 weeks - Live typhoid vaccine, oral: Ty21a - 1 capsule by mouth - Timing of last dose before possible exposure: 1 week - Recommended for: - Travelers to parts of the world where typhoid is common - People in close contact with typhoid carrier - Laboratory workers who work with Salmonella typhi bacteria - Treatment - Rehydration antibiotics Check susceptibilities **[Salmonella Prevention]** - Hand washing - Boil it, cook it, peel it, or forget it - Skip ice water - Peel fresh fruit and veggies after washing hands - Avoid street vendors **[Shigella Spp]**. - Slender, non-motile bacilli - Convex, circular, transparent colonies - Resistant to bile salts - Non-lactose fermenter - Doesn't produce H2S - Most clinically important: - S. dysenteriae (most serious) - S. sonnei (most common in US) - S. flexneri (most common in underdeveloped countries) - Transmission Fecal-Oral - Low inoculum can cause disease (100-200 bacteria) - Daycares, children, close quarters - Pathogenesis: invade M cells in Peyer's patches of intestine, engulfed by cell, replicate within cell, undergo cell-to-cell passage, eventually leads to cell apoptosis - Symptoms: watery diarrhea mucous/bloody diarrhea, fever, cramps tenesmus (cramping rectal pain, feeling of incomplete defecation) - Treatment: usually self-limiting, rehydration, antibiotics if severe **[S. dysenteriae]** - Produces Shiga toxin (exotoxin) disrupts protein synthesis - Primary manifestation of toxin activity is damage to the intestinal epithelium - Can also damage glomerular endothelial cells, resulting in renal failure (HUS) - Causes dysentery (bloody diarrhea) - Most severe form, mortality rate 5-15% **[Yersinia Spp.]** - Zoonotic infection - Usually associated with contact with rats/rodents - Most clinically important - Y. Pestis: highly virulent pathogen, causes the plague - Y. entercolitica, Y. pseudotuberculosis: primarily enteric pathogens, relatively uncommon **[Yersinia pestis: Plague]** - Bubonic Plague (Black Death) - Transmission: bite from infected flea - Incubation: 7 days - Affects the lymphatic system, inflammation in lymph nodes, high fever bacteremia - If not treat: 75% of Pts die - Most fatal in human history - Pneumonic Plaque - Transmission: respiratory droplets, doesn't have to involve fleas/animals - Incubation: 2-3 days - More virulent and rare than bubonic plaque (1 bacilli can cause disease) - Pulmonary symptoms, fever, sever hemorrhaging (death in hours) - If not treated: 95% of Pts die **[Yersinia entercolitica]** - Enterocolitis - Transmission: ingestion of contaminated food/water - Incubation: 1-10 days, average 4-6 days - Symptoms: diarrhea, fever, abdominal pain, "pseudo-appendicitis" - Chronic form of the disease can develop and persist for months **[NON-FERMENTERS]** **[Pseudomonas Spp.]** - Most clinically important non-fermenter - \> 200 species - Pseudomonas aeruginosa most important species - Obligate aerobes - Can grow virtually in any environment, especially in water - Found in soil, water, decaying matter, vegetation - Moist hospital environments (sinks, ventilators, toilets) - Small, motile rods with polar flagella **[Pseudomonas aeruginosa: Morphology]** - Water-soluble pigments on agar - Pyocyanin (blue), most common - Pyoverdin (yellow-green, fluorescent) - Pyorubin (reddish-brown), less common - Some have mucoid appearance - Thick polysaccharide capsule, aka alginate, as a biofilm - Especially found in cystic fibrosis Pts - B-hemolytic on blood agar - Non-lactose fermeneter - Oxidase (+) - Catalase (+) **[Pseudomonas aeruginosa: Morphology]** - Adhesins (4 surface components facilitate adherence to host cells) - Flagella and Pili - Mediate motility - Lipopolysaccharide (LPS) - Responsible for endotoxin activity (inflammation) - Alginate - Mucoid exopolysaccharide - Forms capsule on the bacterial surface - Protects organisms from phagocytosis and antibiotic-killing - Gene-controlling production of alginate can be activated in Pts with CF or chronic respiratory diseases who are exposed to long-term colonization with mucoid strains - Toxins and Enzymes - Exotoxin A: disrupts protein synthesis - Pyocyanin, pyoverdine: form toxic oxygen compounds - Elastases (LasA, LasB): degrade elastin damage to elastin containing tissues, lung parenchymal damage - Phospholipase C; breaks down lipids and lecithin tissue destruction - Exoenzymes S and T: destroy tissues ![](media/image5.png)**[Pseudomonas aeruginosa: Resistance]** **[Pseudomonas aeruginosa: Epidemiology]** - Not part of normal human flora - Opportunistic pathogens - After antibiotic exposure: typically restricted to Pts receiving broad-spectrum antibiotics that suppress normal intestinal bacterial population - Immunocompromised Pts - Hospitalized Pts **[Clinical Syndromes: Pulmonary Disease]** - Tracheobronchitis, pneumonia (especially hospital-acquired and ventilator-associated), pulmonary exacerbations in cystic fibrosis - Asymptomatic colonization severe necrotizing bronchopneumonia - Colonization common (cystic fibrosis Pts, chronic lung diseases, neutropenia) - Mucoid strains are commonly isolated and difficult to eradicate - Associated with an increase in acquired antibiotic resistance and expression of adaptive resistance **[Clinical Syndromes: Skin and Soft Tissue]** - Most commonly seen with diabetic foot infections and burn wounds - Colonization of wounds localized vascular damage tissue necrosis bacteremia - Folliculitis - Immersion in contaminated water (hot tub, pools) **[Clinical Syndromes: Other]** - UTIs - Primarily nosocomial - Catheter-related - Ear Infections - Outer ear infections: Swimmer's ear - Eye infections - Bacteremia - Resistance to Pseudomonas is increasing; combination of antimicrobials may be indicated in serious infections **[Acinetobacter Spp.]** - Strictly aerobic - Gram variable: can appear gram-neg or gram-pos - Ubiquitous Saprophytes - Found in moist and dry surfaces (rare for gram-neg) - Most common species - A. baumannii - Non-lactose fermenter - Oxidase (-) **[Acinetobacter Spp.]** - Part of normal human flora of oropharynx in some humans - Associated with: - Hospital-acquired infections, especially after **antibiotic exposure** - Pulmonary infections - Wound infections - UTIs - Bacteremia - Resistance similar to Pseudomonas - BLs: B-lactamases (ESBLs, AmpC, carbapenemases), Porin mutations, efflux pumps - AGs: aminoglycoside modifying enzymes - FQs: gyrA and parC mutations **[Stenotrophomonas Spp.]** - Genus formerly classified as Pseudomonas Xanthomas Stenotrophomas - Small, motile, polar flagella - Ubiquitous in water, soil, plants - Moist prosthetic surfaces (catheters, ventilators) - Most common clinical species: S. maltophilia - Non-lactose fermenter - Oxidase (-) - Catalase (+) **[Stenotrophomonas maltophilia]** - Low pathogenicity, rarely infectious - Increased risk in debilitated Pts with impaired host defenses - Ventilation, catheters, chronic pressure ulcers - Long-term antibiotic exposure - Clinical Syndromes: - Asymptomatic colonization - Hospital-acquired infections, especially after antibiotic exposure - Pneumonia - Wound infections - Bacteremia - Resistant to many antibiotics, including carbapenems - DOC: Bactrim - Alternatives: ceftazidime, levofloxacin, minocycline **[Moraxella Spp.]** - Short, non-motile GN coccobacilli - Except M. catarrhalis (diplococci) - Most common clinical species: M. Catarrhalis - Non-lactose fermenter - Oxidase (+) - Catalase (+) - Associated with sinusitis, otitis, bronchitis, pneumonia - Resistant to penicillin **[Burkholderia Spp.]** - Obligate GN aerobe, motile with flagella - Most common: - B. cepacian complex (9 species), B. pseudomallei - B. mallei in animals - Everywhere in environment and moist surfaces - Non-lactose fermenter - Most: oxidase (+) - Catalase (+) **[Burkholderia cepacian complex]** - Opportunistic pathogen - Low virulence, except in pulmonary infection - Increased risk in CF and chronic granulomatous disease - Colonization is contraindicated to lung transplant in CF Pts - Associated with - Pneumonia, cepacia syndrome, Catheter infections (UTI, bacteremia) - **B. cepacia Selective Agar (BCSA)** - Selective: crystal violet, vanc, polymyxin B, gentamicin - Differential: sucrose, lactose, phenol red (pH indicator) - Appears green/brown with yellow halos - **Oxidative-Fermentative Polymyxin-Bacitracin-Lactose (OFPBL) Agar** - Selective: polymyxin, bacitracin - Differential: Tryptone, lactose, bromothymol blue (pH indicatior) - Appears yellow with yellow halos **[Burkholderia pseudomallei]** - Diagnosis: - Gram stain: bipolar staining "safety pin" appearance - Ashdown's media: crystal violet, gentamicin, neutral red - Cornflower head,, metallic colonies, earthy odor - Causative pathogen in melioidosis - Endemic in Southeast Asia, Africa, Australia - Soil, water, vegetation - Transmission: inhalation, ingestion, direct contamination of wounds - Symptoms: skin lesions, fever, malaise, bronchitis/pneumonia sepsis - Used in biological weapons **[Burkholderia Spp.]** - Resistant to many antibiotics - DOC: Bactrim - Ceftazidime, minocycline, meropenem **[Vibrio Spp.]** - Short, curved, motile GN rods - Facultative anaerobes - Salt-loving (halophile; think shellfish/seawater) - Requires NaCl for growth - Most common: - V. cholerae, V. parahaemolyticus, V. vulnificus - Most are non-lactose fermenters - Oxidase (+) **[Vibrio cholerae]** - Causative pathogen of Cholera - O1 and O139 produce cholera toxin epidemics - Commonly seen in African/SA - Transmission: consumption of fecally contaminated water, ingestion of shellfish that has not been adequately cooked - Symptoms: watery diarrhea ("rice-water stools"), vomiting, electrolyte imbalances, hypovolemic shock - Cholera toxin - Complex A-B toxin - Ring of 5 B subunit: internalized and interacts with G proteins that control adenylate cyclase catabolic conversion of ATP to cAMP - Result in hypersecretion of water and electrolytes - Able to adhere to mucosal cell layer **[Vibrio Cholerae: Treatment]** - Rehydration: decreases mortality - IV replacement - Severely dehydrated: 10% of body weight replented within 2-4 hours - If severe or hospitalized -- antibiotics - Doxy, z-pak, cipro - Zinc therapy in children **[Vibrio Cholera: Prevention]** - Wash hands - Boil it, cook it, peel it, or forget it - Vaccine - Single dose, live oral cholera vaccine (Vaxchora) - Ages 2-64; traveling to area of active cholera transmission - Admin 10 days prior to travel **[Vibrio vulnificus]** - Virulent species - Highest risk in those with liver disease, renal disease, immunocompromised... - Marine bacteria found in sea water of Atlantic, Pacific, and Gulf Coast - Transmission: consumption of raw/inadequately cooked shellfish - Skin lesions while handling shellfish, exposure to contaminated seawater - Wound infections - Wounds may become infected in association with contact with shellfish - Progress rapidly with redness, swelling, and formation of necrotic tissue - Primary bacteremia - Occur as result of dissemination from enteritis after consumption of contaminated oyster - Fever, chills, N/V/D, abdominal pain - Treatment: Doxy/minocycline + ceftriaxone, wound care **[Vibro parahaemolyticus]** - Acute outbreaks of diarrhea with seafood - Transmission: consumption of contaminated raw oysters/shellfish exposure to contaminated seawater - Associated with gastroenteritis, wound infections; self-limiting **[Fastidious, Non-Enterics]** **[Haemophilus Spp.]** - Small, pleiomorphic, GN coccobacilli - Most common: - **H. influenzae**, H. aegyptius, H. ducreyi - Fastidious growth requires either hemin or nicotinamide adenine dinucleotide (NAD) - Growth on chocolate agar - Loves heme because nutritional requirements **[Heamophilus influenzae]** - Virulence factors - Many have antiphagocytic polysaccharide capsule - Contains ribose, ribitol, and phosphate (polyribitol phosphate PRP) - Classified as typeable or nontypeable based on presence of capsule - Serotype b (hib) - Antibodies directed against the capsule stimulate bacterial phagocytosis and compliment-mediated bactericidal activity - Develop via natural infection, vaccine, transfer of maternal antibodies - Transmission: person to person; colonize respiratory mucosa **[Heamophilus influenza: Clinical Syndrome]** - Otitis media, sinustitis, bronchitis - Pneumonia - Epiglottitis - Meningitis - Treatment - Cephalosporins, macrolides **[Heamophilus influenzae: Prevention]** - Conjugated H. influenzae type B vaccine - Routine administration of conjugate Hib vaccine series beginning at 2 months - Booster recommended at age 12-15 months **[Campylobacter Spp]** - Zoonotic infections - Animal serve as reservoirs - Transmission through zoonosis by ingestion of contaminated foods - Poultry contributes to majority of infections in US - Associated with - Gastroenteritis - Occurs 2-5 days after ingestion of contaminated food/water - Self limiting - Small infectious dose (400-500 bacteria) - Guillain-Barre syndrome - Reactive arthritis - Vascular infections, bacteremia, meningitis - Treatment: macrolides, Augmentin **[Helicobacter Spp.]** - Small, thin, motile, spiral-shaped GN rod - Rapid, corkscrew movement - Grow in microaerophilic atmosphere (low O2, High CO2) - Unable to ferment or oxidize carbohydrate - Most common - **H. pylori**, H, cinaedi, H. finnelliae **[H. pylori: Pathogenesis]** - Can establish lifelong colonization in the stomach - Blocks acid-production - Neutralizes gastric acid (via urease) - Adheres to gastric epithelial cells (surface adhesion proteins) - Evades immune system - Virulence factors local tissue damage - Damage to protective lining gastritis, peptic ulcer, gastric carcinoma, MALT B-cell lymphoma **[H. pylori]** - Colonizes the stomach with increasing frequency with age - Diagnosis - Antibody detection (non-invasive) - Tissue exam of gastric biopsy - Urease testing via biopsy or breath test - Culture is difficult since H. pylori adheres to gastric mucosa - Treatment (symptomatic Pts) - Combination therapy consisting of clarithromycin, amoxicillin, and PPI - OR bismuth subsalicylate, tetracycline, metronidazole, PPI **[Gram Negative: Cocci]** **[Neisseria Spp.]** - Short, GN diplococci - Most common: - N. gonorrhoeae, N. meningitides - Oxidase (+) - Catalase (+) **[Neisseria: Virulence Factors]** - Pili - Attachment to host cells, transfer of genetic material - Porin proteins - Outer membrane proteins that form pores or channels for nutrients to pass into cells and waste products to exit cell - PorA and PorB - N. gonorrhoeae only has PorA - Opa proteins - Membrane proteins that mediate binding to epithelial and phagocytic cells - Important for cell-to-cell signaling - Rmp Proteins - Stimulate antibodies that interfere with serum bactericidal activity - Protein receptors for transferrin, hemoglobin... to scavenge iron - Immunoglobulin A1 protease - Inactivates IgA1 - Some strains of N. gonorrhoeae can produce B-lactamase - N. meningitidis has polysaccharide capsule to protect from antibody-mediated phagocytosis **[N.gonorrhoeae]** - Causative pathogen of gonorrhea - 2^nd^ most common STD - Reservoir: exclusively humans - Transmission: sexual contact - Most common sites of inoculation - Females: cervix/vagina - Males: Urethra or Penis - Men: - Symptomatic urethritis - Epididymitis (most frequent complications) - Anorectal infections - Women: - Cervicitis - Anorectal infections - Pelvic inflammatory disease - Dissemination can occur if untreated septic arthritis, endocarditis, dermatitis, meningitis - Diagnosis: - Nucleic acid amplification tests (NAATs) - Superior to culture and gram stain - Stain: not sufficient to rule out infection in some cases - Culture: no longer diagnostic standard; empiric treatment needed before 24-48 hours - Treatment: ceftriaxone IM **[N. meningitidis]** - Common causative pathogen of meningitis or meningococcemia - 6 serotypes: A, B, C, W135, X, Y - Transmission: respiratory droplets among prolonged close contact (household, soldiers in barracks) - Symptoms: fever, headache, vomiting, neck stiffness, myalgia, petechial skin lesions - Prevention: - Close contacts: chemoprophylaxis with rifampin, cipro, and ceftriaxone - Vaccines: - Meniginococcal A,C,W,Y: 11-12 years with booster at 16 - Meningococcal B: 10 years and older and high risk

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