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123 Cards in this Set

  • Front
  • Back
E. coli
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.
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.
Klebsiella (K. pneumoniae)
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
Gram Neg Rod
Family: Enterobacteriaceae
Virulence: Opportunist;, burn, wound, resp., urinary (UTI) infxns, bacteraemia.
Gram Neg
Family: Enterobacteriaceae
1.) Nosocomial infxn in pts with compromised immune sys
2.) Meningitis, brain abscess in neonates.
Gram Neg
Family: Enterobacteriaceae
Virulence: Nocosomial infxns, UTI, wound, pneumonia, septicaemias.
Notes: produces red pigment in culture.
Gram Neg
Family: Enterobacteriaceae
Y. pestis: plague
Y. enterocolitica: severe diarrhoea, local abscess.
Y. pseudotuberculosis: severe enterocolitis.
Sxs: vomiting, nausea, diarrhoea, abdominal discomfort
Disease of the small intestines; ↑'d fluid/electrolyte loss, frequent and/or fluid stool.
Inflammatory disease of large intestines. Frequent passage of small volume stools with blood, mucus, pus, severe abdominal cramps, tenesmus.
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.
Enteric/Tyhoid Fever
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.
Important virulence factor of S. Typhoid; two regulatory systems that senses the intracellular environment and induces transcription of genes necessary for survival inside macs.
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.
Type III secretion system
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.
Most common in infants, elderly, immunosuppressed, sickle-cell anaemia.
Common Agents: S. choleraesuis, S. Dublin.
Salmonella osteomyelitis
an infection rarely seen in pts. without sickling disorders. Asplenic state of these pts. give ↑'d susceptibility to infxn.
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.
S. sonnei
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
S. flexneri
Most common shigella in developing countries.
Transmission: food/water faecal contamination.
S. dysenteriae Type I
aka Shigella bacillus; cause of Classic Bacillary Dysentery, a severe dysentery in distal colon. Virulence: Shiga toxin
S. boydii
Shigella seen only in India
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.
Actin Propulsion System
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.
Shiga Toxin
Produced by S. dystenteriae type I. A subunit acts on 60S, stops protein syn. 5 identical B subunits fxn in binding to host cell.
Enterotoxigenic E. Coli (ETEC)
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).
Enteroinvasive E. Coli (EIEC)
Disease: similar but less severe than shigellosis
Site: colonic mucosa.
Sxs: watery diarrhoea followed by dysentery.
Virulence: large plasmid.
Enteropathogenic E. Coli (EPEC)
Disease: infant diarrhoea in developing countries.
Virulence: pilus-mediated (bundle-forming pilus); attaches to and effaces brush border.
Enteroaggregative E. Coli (EAEC)
Disease: watery diarrhoea in developing countries, esp. young children.
Virulence: interferes with transport properties of target cells.
Enterohaemorrhagic E. Coli (EHEC)
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
Haemolytic Uraemic Syndrome (HUS)
Sxs: haemolytic anaemia, throbocytopaenia, acute renal failure.
Pop.: young children, eldery.
Agent: EHEC; due to SLT-II
Agent: small # of O-serotype E. coli, ones that produce haemolysin and siderophore (aerobactin). 80% produce P fimbriae, a marker for pyelonephritic strains.
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.
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)
C. jejuni
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.
C. fetus
Disease: extra-intestinal diseases; diarrhoeal illness similar to C. jejuni, replasing systemic diseases.
Helicobacter pylori
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
Vibrio cholerae
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)
Agent: v. cholerae
Sx: rice water stool; hypovolaemic shock/death
Tx: rehydration.
Vaccine: killed whole-cell, ctxB subunit toxoid combo; or live attenuated
V. parahaemolyticus
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).
V. vulnificus
Disease: rapid progressive wound infxn, fulminant bacteraemia.
Transmission: exposure to contaminated seawater, consumption of raw oysters.
Family: enterobacteria
name-recognition only; gram neg, implicated in diarrhoeal/extraintestinal diseases
Family: enterobacteria
name-recognition only; gram neg, implicated in diarrhoeal/extraintestinal diseases
Gram negative dipploccoci; non motile.
Oxygen: obligate aerobes, facultative if KNO2 present.
Host: only humans
Fastidious, grows only on CBA.
N. Gonorrhoeae
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.
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
Gonococcal arthritis-dermatitis syndrome
Manifestation of disseminated gonoccocal infxn (DGI).
Sxs: tenosynovitis (joint inflamm.), suppurative arthritis (jnt. infxn.)
Outer Membrane Protein
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.
Lipooligosaccharide (LOS)
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.
Transferrin/Lactoferrin Binding Proteins
N. gonorrhoea uses to steal iron from transferrin/lactoferrin.
Neisseria Meningitidis
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
Moraxella (Branhamella catarrhalis)
Gram neg dipplococci; confused for Neisseria
Diseaese: otitis media, lower resp. tract infxns.
Meningococcal Disease
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.
Pseudomonas Aeruginosa
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.
ecthyma gangrenosum
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.
Nonbacteraemic Pneumonia aka 1° Pneumonia
Acute Ps. aeruginosa infxn; due to aspiration of URT secretions. Associated w. ventilator use.
Bacteraemic Pneumonia
Fulminant ps. aeruginosa infxn associated w. neutropaenia (post-chemotherapy).
Cell-associated Virulence Factors of Ps. Aeruginosa
1.) Pili
2.) Mucoid exopolysaccharide (MEP/alginate). Helps colonise in CF, also allows biofilms.
3.) LPS - protects from complement, Abs.
4.) flagella - motility, attachment
Extracellular Virulence factors of Ps. Aeruginosa
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.
Burkholderia cepacia
GNB, ferment-, formerly pseudomonas. Opportunist.
Disease: nosocomial resp. infxns in pts. w. CF or chronic granulomatus disease. UTIs in catheterised pts. Septicaemia.
Bacteroides fragilis
GNB anerobic. Main species in wound infxns.
Virulence: pili, capsule (abscess formation), succinic acid (inhibits PMNs, superoxide production).
Tx: metronidazole.
Legionella pneumophilia
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.
Legionnaire's Disease
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.
Legionella Virulence Factors
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.
Pontiac Fever
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.
Smallest known free-living bacteria; require sterols for growth. Extracellular. No cell wall, triple layer mem. Fried egg appearance. Will not gram stain.
M. pneumoniae
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.
M. hominis, U. urealyticum
Energy: Mycoplasma (glucose), Ureaplasma (urea).
Disesaes: BV, PID, resp. infxns (newborns), NGU.
Treponema spp
High motile, helically coiled spirochetes. Axial fibrils wind around cylinder. Does not stain, visualised by Dark Field Microscopy or immunoflurescence. Cannot be cultured
Syphilis (general)
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.
1° syphilis
Onset: 3-4wks after contact
Sx: Indolent, hard, indurated chancre at site of inoculation filled w. treponema. Regional lymphadenopathy. Heals spontaneously.
2° syphillis (disseminated syphillis)
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)
Latent Stage (syphilis)
Time: yrs to life.
Spirochetes sparse, but may spread to foetus or seed blood stream intermittently.
Treponemal/nontreponemal tests all positive.
3° syphillis (late syphilis)
Onset: yrs after initial infxn.
Sx: slowly progressive inflammatory disease. Neurosyphilis, cardiovascular syph., gummas (liver granuloma).
Early Syphilis
Stages of syphilis that occur within first year of acquisition (1°, 2°, early latent).
Congenital Syphilis
T. pallidum readily crosses the placenta.
Specific (Treponemal) Serologic Tests
FTA-ABS and MHA-TP. Detect specific treponemal Abs. Remain positive even after successful Tx, unlike non-treponemal tests.
Leptospira interrogans
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.
Borrelia burgdorferi
Weakly staining gram- spirochete; difficult to culture.
Disease: Lyme Disease
Reservoir: mouse
Vector: Ixodes tick
Vaccine: no longer available.
Lyme Disease
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
Relapsing fever
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.
GNB; fastidious, slow-growing.
Reservoir: B. henselae (cats), B. quintana (humans, via lice).
Diseases: cat scratch disease, bacillary angiomatosis
Cat Scratch Disease (CSD)
Agent: B. henselae
Vector: loveable cats
Sx: regional lymphadenopathy. Typically benign infxn in children.
Bacillary Angiomatosis (BA)
Agent: B. quintana, B. henselae
Pts: HIV
Sx: unique vascular lesions of skin.
Bordetella pertussis
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.
Pertussis (Whooping Cough)
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.
Pertussis Toxin
Classic A/B toxin targets immune effector cells, preventing bacterial clearance. Causes lymphocytosis (blocked migration to lymph nodes)
Adenylate Cyclase Toxin
Virulence Factor of B. pertussis. Targets early immune defences (neutrophils). Lyses RBCs. Confuses neutrophils, blocking chemotaxis, phagocytosis, superoxide generation, and microbial killing.
Dermonecrotic Toxin
Virulence Factor of B. pertussis.
Effect: blue-black lesions, death at high doses. Modifies ρ-protein. Exact role uncertain, possibly (-)s phagocytosis.
Tracheal Cytotoxin
B. pertussis toxin, derived from peptidoglycan.
Effect: induces toxic levels of IL-1, analogous to endotoxin. Causes ciliastasis, destruction.
B. Pertussis adhesins
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.
Catarrhal Stage of Pertussis
First stage.
Onset: insidious
Sx: coryza (runny nose), sneezing, low-grade fever, mild occasional cough. Cold-like.
Paroxysmal Cough Stage of Pertussis
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.
Convalescent Stage of Pertussis
3rd stage; recovery graduatl. Cough disappears over 2-3 wk period. Paroxysms often recur.
Pertussis Vaccine
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.
Haemophilis Influenzae
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.
Hib vaccine
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.
Yersinia pestis
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.
1º Bubonic Plague
Most common form of plague.
Sx: sudden onset fever, painful bubo (enlarged lymph node) in groin area, bacteraemia, death by septic shock.
1º Pneumonic Plague
Agent: Y. pestis.
Deadliest form of plague (100% mortality w/o Tx). Death by 2-3d.
Tm: P2P via droplet.
1º Septicaemic Plague
Sxs: DIC, haemorrhages in skin, necrosis of small vessels, no obvious buboes. Mortality 100% w/o Tx.
Yersinia enterocolitica
Reservoir: cattle, pigs.
Tm: pork products.
Sx: enterocolitis. Can mimic appendicitis.
Pt.: children > adults, more in winter.
Virulence: grows at low temps (25°C)
Yersinia pseudotuberculosis
Zoonotic infxn that occasionally causes human disease.
Tm: contaminated food/drink
Sx: acute mesenteric lymphadenitis, disseminated infxns.
Franciscella tularensis
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
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.
Brucella spp.
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).
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.
Chlamydia spp.
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.
Chlamydophilia psittaci
Disease: human ornithosis; zoonoitc inhalation of aerosolised bacteria from birds. Human infxns rare.
Sx: atypical pneumonia.
Dx: serologic.
Chlamydophilia pneumoniae
Tm: human only pathogen. P2P via resp. route.
Sx: pharyngitis to severe pneumonia.
Dx: no good tests available!
Chlamydia trachomatis
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
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.
Inclusion Conjunctivitis
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.
Lymphogranuloma venerum (LGV)
Agent: C. trachomatis, serovars L1, L2, L3.
Range: S.A., Africa.
Sx: 1° lesion followed by lymphadenopathy, systemic sxs.
Genital Tract Infections of C. trachomatis
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.
Rickettsia rickettsii
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.
Rocky Mountain Spotted Fever
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
Rickettsia prowazekii
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)
Rickettsia typhi
Diseases: endemic/murine typhus.
Tm: rat to flea to human.
Orienta tsutsugamushi
Disease: scrub typhus.
Notes: major cause of undiagnosed febrile illness in soliders in Vietnam.
Coxiella burnettii
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.
Ehrlichia chaffeensis
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.
Anaplasma phagocytophilum
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.