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123 Cards in this Set
- Front
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E. coli
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Gram Neg
Family: Enterobacteriaceae Ferments lactose. Humans major reservoir (except EHEC) Virulence Factors: 1.) Specific Pili (fimbrial): UTI, most common cause. 2.) K capsular: neonatal meningitis, gram neg scepticaemia. 3.) Wound infections w. bacteroides fragilis, group D strep. |
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Proteus/Providencia/Morganella
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Gram Neg
Family: Enterobacteriaceae Virulence Factors: 1.) Urease: splits urea and ↑pH, promotes struvite stone formation. Stones obstruct flow, act as nidus for persistent infxn. Notes: motile; swarm solid media. |
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Klebsiella (K. pneumoniae)
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Gram Neg
Family: Enterobacteriaceae Virulence Factors: 1.) capsule: high level of antibiotic resistance. 2.) Community-acquired lobar pneumonia, in alcoholic men 40+ yrs old. 3.) Nosocomial infxns of lower resp. tract, urinary tract, surgical wounds. Notes: major opportunist |
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Enterobacter
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Gram Neg Rod
Family: Enterobacteriaceae Virulence: Opportunist;, burn, wound, resp., urinary (UTI) infxns, bacteraemia. |
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Citrobacter
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Gram Neg
Family: Enterobacteriaceae Virulence: 1.) Nosocomial infxn in pts with compromised immune sys 2.) Meningitis, brain abscess in neonates. |
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Serratia
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Gram Neg
Family: Enterobacteriaceae Virulence: Nocosomial infxns, UTI, wound, pneumonia, septicaemias. Notes: produces red pigment in culture. |
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Yersinia
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Gram Neg
Family: Enterobacteriaceae Virulence: Y. pestis: plague Y. enterocolitica: severe diarrhoea, local abscess. Y. pseudotuberculosis: severe enterocolitis. |
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Gastroenteritis
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Sxs: vomiting, nausea, diarrhoea, abdominal discomfort
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Diarrhoea
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Disease of the small intestines; ↑'d fluid/electrolyte loss, frequent and/or fluid stool.
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Dysentery
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Inflammatory disease of large intestines. Frequent passage of small volume stools with blood, mucus, pus, severe abdominal cramps, tenesmus.
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Salmonella
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Gram Neg
Class: enterobactericiaea Notes; only salmonella enterica (6 subspecies, 5 serogroups) infect humans. Do not ferment lactose. Virulence factor (enteritis): 2 salmonella pathogenicity islands for Type III secretion systems. Vi antigen. Stomach pH activates transcription of factors. 1.) PhoP/PhoQ: Typhoid fever 2.) gastroenteritis Dx: black colonies on HEA. |
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Enteric/Tyhoid Fever
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Agent: Salmonella Typhi; ingestion of food/water contaminated with human faeces/urine.
Path: Crosses intestinal epithelial via M cells, invades macs, disseminates via lymphatics. Sxs: prolonged, step-wise ↑g fever, diarrhoea, constipation, rose spots (rash), hepatosplenomegaly, GI preforration/haemorrhage(late). Notes: Immunity requires cell and humoral responses. |
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PhoP/PhoQ
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Important virulence factor of S. Typhoid; two regulatory systems that senses the intracellular environment and induces transcription of genes necessary for survival inside macs.
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Gastroenteritis
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Agent: S. Typhimurium, S. Enteritidis.
Path: Ingestion of contaminated foodstuffs (chicken, eggs). Invades both M cells and macs (unlike typhoid). Induces electrolyte fluxes, cytoskeletal rearrangements, mem. rffling, bacterial internalisation, syn. of IL-8, prostaglandin-induced inflammation. Virulence Factors: SPI encoding type III secretion system. Sxs: loose, non-bloody stools of moderate volume. Many leukocytes in stool. Usu. actue, self-limiting infxn. |
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Type III secretion system
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Key virulence factor of salmonellas causing gastroenteritis, encoded by Salmonella Pathogenicity Islands (SPI). Mediates translocation of secreted effector proteins into target epithelial cells necessary for invastion and sxs.
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Bacteraemia
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Most common in infants, elderly, immunosuppressed, sickle-cell anaemia.
Common Agents: S. choleraesuis, S. Dublin. |
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Salmonella osteomyelitis
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an infection rarely seen in pts. without sickling disorders. Asplenic state of these pts. give ↑'d susceptibility to infxn.
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Shigella
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Gram negative rods
Class: enterobacteriaceae Does not ferment lactose or produce H2S. Nonmotile. 4 species. Humans are only reservoir, not part of normal flora. Virulence Factors: Shigella PAI on virulence plasmid (codes for Type III secretion), shiga toxin (s. dysenteriae type I), stomach acid resistence (small # cause disease). Diseases: shigellosis Dx: green, transparant colonies on HEA. |
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S. sonnei
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Late lactose fermentor (unlike most other shigellas that don't ferment). Most common isolate in developed countries.
Transmission: P2P dir. contact, water sports, faecal contamination. Sxs: watery diarrhoea |
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S. flexneri
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Most common shigella in developing countries.
Transmission: food/water faecal contamination. |
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S. dysenteriae Type I
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aka Shigella bacillus; cause of Classic Bacillary Dysentery, a severe dysentery in distal colon. Virulence: Shiga toxin
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S. boydii
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Shigella seen only in India
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Shigellosis
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Sxs: watery diarrhoea or dysentery (cytokine-mediated inflamm. of distal colon). Onset 12-48 hrs post-ingestion. Most infxns self-limiting.
Tx: Rehydration. No vaccine. |
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Actin Propulsion System
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Actin tail "pushes" shigella into adjacent enterocyte. This occurs after shigella gets through M cell, then into mac, stimulates mac apoptosis, and gets into enterocyte.
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Shiga Toxin
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Produced by S. dystenteriae type I. A subunit acts on 60S, stops protein syn. 5 identical B subunits fxn in binding to host cell.
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Enterotoxigenic E. Coli (ETEC)
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Disease: Traveller's Diarrhoea.
Site: Small intestines. Transmission: faecal-oral. Sxs: rapid onset watery diarrhoea 1-5 days. Virulence: Colonising Factor Antigens (CFA), enterotoxins (cholera-like). |
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Enteroinvasive E. Coli (EIEC)
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Disease: similar but less severe than shigellosis
Site: colonic mucosa. Sxs: watery diarrhoea followed by dysentery. Virulence: large plasmid. |
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Enteropathogenic E. Coli (EPEC)
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Disease: infant diarrhoea in developing countries.
Virulence: pilus-mediated (bundle-forming pilus); attaches to and effaces brush border. |
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Enteroaggregative E. Coli (EAEC)
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Disease: watery diarrhoea in developing countries, esp. young children.
Virulence: interferes with transport properties of target cells. |
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Enterohaemorrhagic E. Coli (EHEC)
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Most common strain in developed countries.
Disease: uncomplicated diarrhoea, Haemorrhagic colitis, HUS. Common in warm months. Transmission: bovine origin; undercooked hamburgers. Sxs: bloody diarrhoea, abdominal pain. Virulence: Bundle-forming pili (A/E lesion), SLT-II (Shigella-like toxin). Dx: sorbital negative |
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Haemolytic Uraemic Syndrome (HUS)
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Sxs: haemolytic anaemia, throbocytopaenia, acute renal failure.
Pop.: young children, eldery. Agent: EHEC; due to SLT-II |
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Pyelonephritis
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Agent: small # of O-serotype E. coli, ones that produce haemolysin and siderophore (aerobactin). 80% produce P fimbriae, a marker for pyelonephritic strains.
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Meningitis
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Agent: Most common E. coli. Second group B strep (S. agalactiae), 3rd Listeria, Neisseria meningitidis.
Virulence: 75% have K1 surface polysaccharide Ag for bloodstream survival. |
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Campylobacter
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Family: campylobactereceae
slender, curved/spiral gram negative rods, motile, microaerophilic, slow-growing. Reservoir: animals (zoonosis) Diseases: C. jejuni enteritis. Dx: grows on Campy Blood Agar. (Highly selective) |
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C. jejuni
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Disease: common cause of bacterial gastroenteritis in developed countries.
Epidemiology: peaks in summer/early fall. Infants highest infxn. Transmission: poultry Sxs: fever, bloody diarrhoea, abdominal pain, >10 BM/day, ulceration. |
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C. fetus
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Disease: extra-intestinal diseases; diarrhoeal illness similar to C. jejuni, replasing systemic diseases.
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Helicobacter pylori
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Spiral gram neg rod; highly motile.
Colonises human stomach Diseases: peptic ulcer disease, gastric malignancy. Reservoir: unknown Virulence factors: urease (neutralises gastric pH), flagella, adhesins, VacA (vacuolating cytotoxin), cag PAI (inflamm.) Tx: antimicrobial + proton pump inhibitor |
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Vibrio cholerae
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curved, motile, gram neg rod
Disease: cholera (usu. serogroup-O1) Reservoir/habitat: salt water. Virulence: Cholera Toxin (ADPribosyltransferase A/B toxin), mucinase (helps penetrate mucous layer of S.I.) Dx: yellow colonies on TCBS (thiosulfate citrate bile sucrose) |
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Cholera
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Agent: v. cholerae
Sx: rice water stool; hypovolaemic shock/death Tx: rehydration. Vaccine: killed whole-cell, ctxB subunit toxoid combo; or live attenuated |
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V. parahaemolyticus
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Marine organism found in esturaries
Disease: self-limiting diarrhoea, mild cholera-like ilness. Transmission: contaminated seafood (esp. shellfish). Dx: blue-green colonies on TCBS (thiosulfate citrate bile sucrose). |
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V. vulnificus
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Disease: rapid progressive wound infxn, fulminant bacteraemia.
Transmission: exposure to contaminated seawater, consumption of raw oysters. |
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Aeromonas
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Family: enterobacteria
name-recognition only; gram neg, implicated in diarrhoeal/extraintestinal diseases |
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Plesiomonas
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Family: enterobacteria
name-recognition only; gram neg, implicated in diarrhoeal/extraintestinal diseases |
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Neisseria
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Gram negative dipploccoci; non motile.
Oxygen: obligate aerobes, facultative if KNO2 present. Host: only humans Fastidious, grows only on CBA. |
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N. Gonorrhoeae
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Grows in glucose, not maltose. Oxidase positive
Disease: gonorrhoea, PID, DGI Virulence: pilli, OMP, LOS, penicillin resistence common in Asia/Africa, Tetracyclin resistence found. Vaccine: none, due to antigenic/phase variation of pili/OMPs. |
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Gonorrhoea
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2nd most common STD.
Incubation: 2-7d Sxs: male: acute urethritis Sxs (female): cervicitis, urethritis, vaginal discharge, abdominal pain, dysuria, progression to PID (sterility, ectopic pregnancy) Male Dx: GNC in urethral exudate with PMNs Female Dx: culture isolation of oxidase-pos, GNC from cervix/anal canal Tx: ceftriaxone+tetracycline |
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Gonococcal arthritis-dermatitis syndrome
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Manifestation of disseminated gonoccocal infxn (DGI).
Sxs: tenosynovitis (joint inflamm.), suppurative arthritis (jnt. infxn.) |
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Outer Membrane Protein
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Chief virulence factor in N. gonorrhoeae; fxn in adherence, controlled by opa genes. Phase variation switches gene on/off with frameshifts, antigenic variation changes AA composition.
OMP-I: surivial inside phagocytes OMP-II: homologous recomb. involving slipped-strand mispairing. |
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Lipooligosaccharide (LOS)
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Virulence factor of N. gonorrhoeae, containing sialic acid (found on RBCs) that may mask it the bacteria from Abs. Triggers TNF-α, scars oviducts. Required for binding to sperm.
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Transferrin/Lactoferrin Binding Proteins
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N. gonorrhoea uses to steal iron from transferrin/lactoferrin.
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Neisseria Meningitidis
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Gram neg dipplococci
Diseases: nasopharyngeal infxn, meningococcaemia, meningitis. Virulence: capsule (grp A/C immunogenic, grp B not.), pili, endotoxin, OMP, IgA protease. Pathogenic serotypes: B, C, Y Tx: rifampin, ciprofloxacin |
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Moraxella (Branhamella catarrhalis)
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Gram neg dipplococci; confused for Neisseria
Diseaese: otitis media, lower resp. tract infxns. |
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Meningococcal Disease
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Stages:
1.) nasopharyngeal infxn - usu. asymptomatic. 2.) colonisation of mucous mem. - pili 3.) Haematogenous dissemination - metastatic lesions; febrile to systemic. Sxs: petechiae to ecchymoses; meningococcaemia/meningitis possible. Dx: CSF gram stain; culture on choc. agar is definitive. |
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Pseudomonas Aeruginosa
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Gram neg rod; motile, oxidase+, ferment-. Anaerobic if nitrate available. Non fastidious.
Diseases: bacteraemia, pneumonia (CF), UTIs, ecthyma gangrenosum, wound sepsis, endocarditis, meningitis, otitis externa, keratitis, corneal ulcer, blood/jnt infxns (IV drug users). Virulence: cell-associated and extracellular. |
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ecthyma gangrenosum
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Skin manifestation of Ps. aeruginosa infxn, esp. in bacteraemic pts. Haemorrhagic lesion due to destruction of elastin by elastase. Can occur w. other gram- bac.
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Nonbacteraemic Pneumonia aka 1° Pneumonia
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Acute Ps. aeruginosa infxn; due to aspiration of URT secretions. Associated w. ventilator use.
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Bacteraemic Pneumonia
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Fulminant ps. aeruginosa infxn associated w. neutropaenia (post-chemotherapy).
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Cell-associated Virulence Factors of Ps. Aeruginosa
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1.) Pili
2.) Mucoid exopolysaccharide (MEP/alginate). Helps colonise in CF, also allows biofilms. 3.) LPS - protects from complement, Abs. 4.) flagella - motility, attachment |
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Extracellular Virulence factors of Ps. Aeruginosa
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1.) proteases - elastases, alkaline protease.
2.) exotoxin A: ADP ribosyltransferase, ~diphtheria toxin. 3.) Type III cytotoxins 4.) pyochelin, pyoverdin - scavenger iron siderophores 5.) pyocyanin - blue-green; induces production of toxic O2 free radicals to kill resp. epithelial cells. |
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Burkholderia cepacia
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GNB, ferment-, formerly pseudomonas. Opportunist.
Disease: nosocomial resp. infxns in pts. w. CF or chronic granulomatus disease. UTIs in catheterised pts. Septicaemia. |
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Bacteroides fragilis
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GNB anerobic. Main species in wound infxns.
Virulence: pili, capsule (abscess formation), succinic acid (inhibits PMNs, superoxide production). Tx: metronidazole. |
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Legionella pneumophilia
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Slender, pleomorphic obligate aerobic intracellular GNR. Stains v. poorly. Fastidious, slow growing on BCYE. Flagellated, motile.
Habitat: aquatic protozoan parasite or biofilms; must be aerosolised for transmission. No P2P, humans are dead end hosts. Life cycle has transmission, replication phase. Possible manifestations: asymptomatic, Legionnaire's Disease, Pontiac Fever. Dx: culture in BCYE, urinary Ag testing, many PMNs but no bacteria seen. |
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Legionnaire's Disease
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Agent: L. pneumophilia
Time: summer to fall. Pts: >55, smokers, chronic pulm. disease. Sxs: myalgia, heachache, rapidly rising fever, non-productive cough w. 2-10d onset (atypical pneumonia). Can end in shock, resp. failure. Mortality: 15% Tx: Macrolides, eg. azithromycin. |
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Legionella Virulence Factors
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1.) Invasion proteins: entry & survival inside mac, no lysosomal fusion. (mip, dot/icm)
2.) Iron extraction from host. 3.) (-)n of oxidative killing by PMNs. 4.) Pore-forming toxin. |
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Pontiac Fever
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Agent: L. pneumophilia
Non-pneumonic manifestation of Legionella. Nonfatal, self-limiting. Sxs: rapid onset of fever, chills, headache, sever mm aches. Flu-like. Always epidemic form. |
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Mycoplasma
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Smallest known free-living bacteria; require sterols for growth. Extracellular. No cell wall, triple layer mem. Fried egg appearance. Will not gram stain.
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M. pneumoniae
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Reservoir: humans
Transmission: aerosolised droplets (cf. Legionella). Diseases: walking pneumonia: acute resp. disease; tracheobronchitis, atypical pneumonia (most common cause, esp. school-aged chilren, teenagers). Virulence: P1 (attachment to resp. epithelium in between cilia), H2O2 (tissue toxin against ciliary fxn; loss of escalator) Dx: serologic tests; cold haemagglutinin test. PCR. Many monos, but no bacteria seen (can't gram stain) Tx: tetracyclines, macrolides. |
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M. hominis, U. urealyticum
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Energy: Mycoplasma (glucose), Ureaplasma (urea).
Disesaes: BV, PID, resp. infxns (newborns), NGU. |
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Treponema spp
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High motile, helically coiled spirochetes. Axial fibrils wind around cylinder. Does not stain, visualised by Dark Field Microscopy or immunoflurescence. Cannot be cultured
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Syphilis (general)
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Agent: T. pallidum
Reservoir: humans Transmission: sexual contact w. infectious lesions (chancre, rash, condyloma lata, mucous patches). Path: slow evolving, chronic systemic infxn in stages. Systemic infxn occurs long before 1° lesion appears. Dx: Darkfield detection of spirochetes, serology, non-treponemal serology tests, Wasserman test (complement-fixation). Tx: penicillin G (no vaccine), watch for Jarisch-Herxheimer rxn. |
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1° syphilis
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Onset: 3-4wks after contact
Sx: Indolent, hard, indurated chancre at site of inoculation filled w. treponema. Regional lymphadenopathy. Heals spontaneously. |
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2° syphillis (disseminated syphillis)
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Onset: 2-8 wks after healing of chancre.
Sxs: generalised indolent, non-pruritic mucocutaneous rash (condyloma lata) or highly infectious erhthematus plaques (warm moist areas) |
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Latent Stage (syphilis)
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Time: yrs to life.
Spirochetes sparse, but may spread to foetus or seed blood stream intermittently. Treponemal/nontreponemal tests all positive. |
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3° syphillis (late syphilis)
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Onset: yrs after initial infxn.
Sx: slowly progressive inflammatory disease. Neurosyphilis, cardiovascular syph., gummas (liver granuloma). |
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Early Syphilis
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Stages of syphilis that occur within first year of acquisition (1°, 2°, early latent).
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Congenital Syphilis
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T. pallidum readily crosses the placenta.
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Specific (Treponemal) Serologic Tests
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FTA-ABS and MHA-TP. Detect specific treponemal Abs. Remain positive even after successful Tx, unlike non-treponemal tests.
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Leptospira interrogans
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Zoonotic organism, looks like question mark.
Disease: Leptospirosis, Weil's Disease. Ts: rat urine-contaminated water. Sx: mild, flu-like. Rare severe 2nd phase (Weil's Disese) has hepatic/renal impairment, jaundice, prostration, circ. collapse, meningitis-like Sxs. |
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Borrelia burgdorferi
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Weakly staining gram- spirochete; difficult to culture.
Disease: Lyme Disease Reservoir: mouse Vector: Ixodes tick Vaccine: no longer available. |
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Lyme Disease
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Agent: B. burgdorferi
Stage 1: localised infxn, erythema migrans (bull's eye). Stage 2: disseminated infxn; 2° skin infxns, fever, neurologic, cardiac, musculoskeletal sxs. Stage 3: persistent infxn: arthritis. Dx: exposure to endemic area, erythema migrans, serologic ELISA. Tx: doxycycline |
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Relapsing fever
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Agents: B. recurrentis (louse-borne), other Borellia spp. (tick-borne)
Path: organism undergoes multiple cyclic antigenic variations Sxs: cyclic pattern of fever followed by sweating weakness. |
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Bartonella
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GNB; fastidious, slow-growing.
Reservoir: B. henselae (cats), B. quintana (humans, via lice). Diseases: cat scratch disease, bacillary angiomatosis |
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Cat Scratch Disease (CSD)
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Agent: B. henselae
Vector: loveable cats Sx: regional lymphadenopathy. Typically benign infxn in children. |
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Bacillary Angiomatosis (BA)
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Agent: B. quintana, B. henselae
Pts: HIV Sx: unique vascular lesions of skin. |
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Bordetella pertussis
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Small aerobic GNR; fastidious.
Adults reservoir for infants, P2P via aersol. Oddities: strong tissue tropism; only attaches to ciliated cells of trachea, bronchi. Disease: Whooping cough Virulence: Pertussis toxin, AC toxin, dermonecrotic toxin, tracheal toxin, adhesins. |
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Pertussis (Whooping Cough)
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Agent: B. pertussis
path: toxin-mediated paralysis of cilia, causing inflammation of resp. tract. Escalator lost, pneumonia likely. Onset: 7-10d Stages: catarrhal, paroxysmal cough, convalescent. Complications: 2° bacterial pneumonia, seizures, encephalopathy. Dx: elevated WBC w. lymphocytosis, PCR, culture (difficult), DFA/ Tx: 1°ly supportive. Erythromycin, vaccine. |
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Pertussis Toxin
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Classic A/B toxin targets immune effector cells, preventing bacterial clearance. Causes lymphocytosis (blocked migration to lymph nodes)
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Adenylate Cyclase Toxin
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Virulence Factor of B. pertussis. Targets early immune defences (neutrophils). Lyses RBCs. Confuses neutrophils, blocking chemotaxis, phagocytosis, superoxide generation, and microbial killing.
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Dermonecrotic Toxin
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Virulence Factor of B. pertussis.
Effect: blue-black lesions, death at high doses. Modifies ρ-protein. Exact role uncertain, possibly (-)s phagocytosis. |
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Tracheal Cytotoxin
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B. pertussis toxin, derived from peptidoglycan.
Effect: induces toxic levels of IL-1, analogous to endotoxin. Causes ciliastasis, destruction. |
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B. Pertussis adhesins
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1.) FHA: aggregation of RBCs, rod-like sxr.
2.) fimbriae/pili: expression variable & varied. 3.) pertactin: attachment to human cells via RGD tripeptide (consensus seq. of integrin family) 4.) BrkA: protects bacteria from complement. Has 2 RGD sequences. |
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Catarrhal Stage of Pertussis
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First stage.
Onset: insidious Sx: coryza (runny nose), sneezing, low-grade fever, mild occasional cough. Cold-like. |
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Paroxysmal Cough Stage of Pertussis
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2nd stage, 1-2wks after catarrhal stage.
Sx: bursts of numerous, rapid coughs, ended by characteristic high-pitched whoop. Attacks more at night. Lasts 1-6 wks. |
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Convalescent Stage of Pertussis
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3rd stage; recovery graduatl. Cough disappears over 2-3 wk period. Paroxysms often recur.
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Pertussis Vaccine
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Whole-cell: not sued in US anymore. Very effacacious, but expensive, risk of acute encephlopathy.
Acellular: purified, inactivated components. Primary given 2, 4, 6 months. Booster at 18 months and before school, then age 10. |
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Haemophilis Influenzae
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Mostly aerobic GN coccobacillus. Capsular type b (Hib) virulent. Requires X, V factors (chocolate agar).
Reservoir: man. Virulence Factors: PRP capsule (unencapsulated forms normal nasopharyngeal flora) Disease: meningitis in children <5 yrs, epiglottitis, osteomyelitis, pericarditis. Nontypable: otitis media, acute bronchitis. Dx: gram stain, culture, latex agglutination, CIE. Tx: chloramphenicol or 3rd gen. ceph. Prophylaxis w. rifampin. |
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Hib vaccine
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Pure Polysaccharide Vaccine (HbPV): not effective in children <18 months (when needed the most), due to T-independent nature.
Polysaccharide-protein conjugate vaccine: T-dependent vaccine works in young children. |
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Yersinia pestis
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Small, gram- coccobacillus w. bipolar staining. Enterobacteriaceae. Intracellular.
Dieases: bubonic plague, pneumonic plague. Virulence: endotoxin, Pla, F1 antigen, V antigen, YadA, lcr, yop. Factors turned on only at 37ºC, low Ca2+. Allows survival in macs, not PMNs. Vector: fleas. Tm: sylvatic via nonurban animals, urban via rats. Notes: progression to 2º disease allows P2P spread. Dx: Bipolar staining bacilli. Detect F1 antigen. Tx: streptomycin. |
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1º Bubonic Plague
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Most common form of plague.
Sx: sudden onset fever, painful bubo (enlarged lymph node) in groin area, bacteraemia, death by septic shock. |
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1º Pneumonic Plague
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Agent: Y. pestis.
Deadliest form of plague (100% mortality w/o Tx). Death by 2-3d. Tm: P2P via droplet. |
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1º Septicaemic Plague
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Sxs: DIC, haemorrhages in skin, necrosis of small vessels, no obvious buboes. Mortality 100% w/o Tx.
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Yersinia enterocolitica
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Reservoir: cattle, pigs.
Tm: pork products. Sx: enterocolitis. Can mimic appendicitis. Pt.: children > adults, more in winter. Virulence: grows at low temps (25°C) |
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Yersinia pseudotuberculosis
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Zoonotic infxn that occasionally causes human disease.
Tm: contaminated food/drink Sx: acute mesenteric lymphadenitis, disseminated infxns. |
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Franciscella tularensis
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Very small faintly staining gram- coccobacillus. Nonmotile, nopiliated, fastidious. Facultative intracellular parasite in macs. Highly infectious.
Tm: rabbits, muskrats via ticks. No P2P spread. Cat. A biological weapon. Endemic area: AR, MO, OK |
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Tularaemia
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Agent: F. tularensis
Path: enters thru skin abrasions, bites. 3-5d incubation, invades RE organs, forms granulomas (ulceroglandular tularaemia). Sx: fever, chronic ucerative skin lesion, large tender lymph nodes. Dx: clinical+geographic. Tx: Avoidence, CMI. Vaccine v. dangerous. |
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Brucella spp.
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Small, nonmotile, nonencapsulated gram- coccobacilli. Fac. intracellular.
Area: CA, TX. Reservoir: goats/sheep (B. melitensis), cattle (B. abortus), hogs (B. suis), dogs (B. canis). Tm: ingestion of contaminated product or direct contact (no insect vector). |
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Brucellosis
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Agent: brucella spp
Path: fac. intracellular parasite of RES, multiply in macs. Block degranulation. Sx: malaise, chills, undulant fever (cf. borreila relapsing fever), chronic illness. Dx: hx of exposure. Serologic test presumptive. Isolation of brucellae definitive. Tx: avoidance, vaccine, pasteurisation. |
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Chlamydia spp.
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Obligate intracellular small gram-. No peptidoglycan layer! MOMPs basis for serotyping. Unique biphasic development cycle: Elementary Body (EB) is spore-like, Reticulate Body (RB) is vegetative, intracellular. RB converts back to EB before exiting a cell.
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Chlamydophilia psittaci
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Disease: human ornithosis; zoonoitc inhalation of aerosolised bacteria from birds. Human infxns rare.
Sx: atypical pneumonia. Dx: serologic. |
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Chlamydophilia pneumoniae
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Tm: human only pathogen. P2P via resp. route.
Sx: pharyngitis to severe pneumonia. Dx: no good tests available! |
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Chlamydia trachomatis
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Obligate intracellular gram-, replicates in endosomes.
Diseases: trachoma, inclusion conjunctivitis, LGV, genital tract infxns, NGU, neonatal pneumonia/conjunctivitis. Dx: NAAT techniques, DFA, EIA. Tx: azithromycin |
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Trachoma
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Agent: C. trachomatis, serovars A, B, Ba, C.
Chronic conjunctivitis, seen usu. in Africa. Path: persistent ocular infxns starting in childhood, leading to blindness from mechanical scratching of cornea by disfigured eyelids. |
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Inclusion Conjunctivitis
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Agent: C. trachomatis, serovars D, E, F, H, I, J, K.
Path: babies born to mothers infected with C. trachomatis may develop this conjunctivitis. Does not cause blindness. |
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Lymphogranuloma venerum (LGV)
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Agent: C. trachomatis, serovars L1, L2, L3.
Range: S.A., Africa. Sx: 1° lesion followed by lymphadenopathy, systemic sxs. |
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Genital Tract Infections of C. trachomatis
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Most common bacterial STD, by serovars D, E, F, H, I, J, K (same as inclusion conjunctivitis)
Reservoir: asymptomatic pts. Sx: unlike N. gonorrhea, less acute, more chronic complications. Mild purulent inflammation, septic arthritis (Reiter syndrome). Can lead to PID, infertility, ectopic pregnancy. |
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Rickettsia rickettsii
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GNB, obligate intracellular energy parasite, lives in cytoplasm, utilises F-actin polymerisation.
Epidemiology: tick is reservoir and vector. April-Sept. Appalachian Mts. 2/3 pts. <15yo. However, older pts have more severe disease. Disease: Rocky Mountain Spotted Fever. |
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Rocky Mountain Spotted Fever
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Agent: R. rickettsii
Sx: acute fevers, headache, myalgia. Then disseminates via blood, replicates in endothelial cells. Centripetal spread of rash (palm→trunk) Path: 1° lesion is vasculitis (rash, petechial lesions). Dx: clinical/epidemiologic. Rising Ab titer. Indirect fluorescent Ab test (pos. 2-3 wks after onset) Mortality: 20-25%, 3% w. Tx |
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Rickettsia prowazekii
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Disease: louse-borne typhus.
Tm: no P2P, only via louse. However, humans 1° reservoir. Sx: fever, headache, rash. Centrifugal spread (trunk→palm). Complications: recrudescent typhus (Brill's disease), a relapse. Notes: seen in times of misery. Epidemic disease (cf. R. typhus, endemic disease) |
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Rickettsia typhi
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Diseases: endemic/murine typhus.
Tm: rat to flea to human. |
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Orienta tsutsugamushi
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Disease: scrub typhus.
Notes: major cause of undiagnosed febrile illness in soliders in Vietnam. |
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Coxiella burnettii
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Very hardy obligate intracellular gram-; grows in lysosomes. Extremely infectious.
Disease: Q fever Sx: acute pneumonia, chronic endocarditis. Tm: inhalation of particles from animals. Very hardy. Notes: undergoes antigenic variation of LPS. |
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Ehrlichia chaffeensis
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Obligate intracellular gram-, lives in vacuoles.
Disease: human monocytic erlichiosis. Tm: tick-borne, deer reservoir Path: Enters through break in skin (cf. RMSF), infects monocytes. Sx: febrile, rash in 10-35%, often asymptomatic. |
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Anaplasma phagocytophilum
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Obligate intracellular gram-, lives in vacuoles.
Disease: human granulocytic anaplasmosis Tm: tick-borne, white-footed mouse reservoir Path: Enters through break in skin (cf. RMSF), infects monocytes. Sx: febrile, rash in 10-35%, often asymptomatic. |