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INF: Infections > Bacteria (Bugs) > Flashcards

Bacteria (Bugs) Flashcards

1
Q

description of clostridium difficile

A

Description: gram positive rod, anaerobic, tissue-damaging exotoxin, spore-forming

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2
Q

Pseudomonas aeruginosa

A

Description: gram negative bacillus, obligate aerobe; exotoxin A

Encounter/ Entry: oxidase & catalase positive; motile; pilli for adhesion to epithelial; drug efflux pumps on outer membrane

Establish Infection: capsule & tight outer membrane; toxin ribosylates target- inhibits protein synthesis; type III secretions

Multiplication/Tissue Damage: biofilm production (antiphagocytosis); proteases; can get to bone & joint ; membrane damaging toxins;

Common Disease Types: otitis externa, hot tub dermatitis/folliculitis, endocarditis (esp IV drug users); keratitis, bone & joint infections; CF much more susceptible; NOSOCOMIAL INFECTIONS; sneaker osteomyelitis (especially in diabetic); often complication of burn injuries; number one cause of nosicomial pneumonia; respiratory failure in CF

Transmission: thrives in aquatic environments; found in soil; occasionally on skin: ear canal; hot tubs, sneakers

Other Notes: produces blue/green pigment & fruity odor; affects diabetics, burn victims, IV drug users; catheter/UTI infections; hot tub folliculitis; ecythema gangrenosum

Diagnosis/treatment: pip/tazo (maybe fluoroquinolones or aminoglycosides); has beta-lactamase (resistant to B-lactams); diagnosis via culture

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3
Q

transmission of treponema pallidum

A

Transmission: human-human; close sexual contact; can transmit mother-fetus if mother has bacteremia

cause of syphilis

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4
Q

identifying qualities of staph epidermidis

A

Other notes: catalase positive; coagulase negative

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5
Q

immunization for bordetella pertussis

A

Immunization: DTaP toxoid

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6
Q

description of pseudomonas aeruginosa

A

Description: gram negative bacillus, obligate aerobe; exotoxin A

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7
Q

description of haemophilus influenzae

A

(most importantly: encapsulated type B- Hib)

Description: gram negative coccobacillus

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8
Q

Disease types associated with borrelia burgdorferi

A

Disease Types: LYME DISEASE; characteristic target rash- erythema migrans; neurologic symptoms (Bell’s Palsy, confusion)

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9
Q

bordetella pertussis

A

Description: gram negative coccobacillus, aerobe, 3 exotoxins: pertussis toxin, adenylate cyclase; tracheal cytotoxin

Encounter: inhaled from cough-generated droplets from infected person

Infection: attaches to ciliated cells of respiratory epithelium

Spread/Damage: toxins kill epithelial cells, increase cAMP

Transmission: only found in humans with active disease

**spasmodic, Whooping Cough, abx don’t cure symptoms if epithelial damage is done

Immunization: DTaP toxoid

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10
Q

how is c diff encountered

A

Encounter: part of normal flora of intestine; often less competition when normal flora wiped out by abx

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11
Q

how is treponema encountered?

A

Encounter/Entry: human is only known host—enters mucous membranes or small abrasions in skin via sexual contact

cause of syphilis

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12
Q

other notes about mycobacterium leprae

A

Other Notes: thrives in cold temps (explains why it favors extremities)

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13
Q

how does bordetella pertussis infect?

A

Infection: attaches to ciliated cells of respiratory epithelium

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14
Q

diagnosis/treatment of brucella

A

Diagnosis/treatment: dx: blood or tissue biopsy (but not all cases are bacteremic); tetracyclines (doxy); rifampin; need multiple trugs & long course since such slow growth rate

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15
Q

encounter/entry of pseudomonas aeruginosa

A

Encounter/ Entry: oxidase & catalase positive; motile; pilli for adhesion to epithelial; drug efflux pumps on outer membrane

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16
Q

transmission of mycoplasma pneumoniae

A

Transmission: occurs in young adults in close quarters (only human-human); occurs in outbreaks/communities

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17
Q

multiplication/tissue damage from yersinia pestis

A

Multiplication/Tissue Damage: major virulence due to suppression of early inflammatory response (type III secretion system + plasminogen activator); able to travel systemically- sudden onset of severe symptoms; have

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18
Q

vaccination of mycobacteria TB

A

Vaccination: diagnose: TST or blood test, CXR; positive skin test if T cell is responding to TB– give induration; all patients with active TB should be offered directly observed therapy (DOT) because partial treatment leads to resistance; treatment: RIPE (rifampin, isoniazid, pyraxinamide, ethambutol); INH for latent TB

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19
Q

common disease types associated with chlamydia trachomatis

A

Common Disease Types: sexually transmitted: GU trac, recurrent– PID, (serovars D-K), trachoma (eye infection)– main cause of blindness (serovars A,B,C); lymphogranuloma venereum LGV (serovars L1-L3)- also STD; passed on to fetus during birth

Reiter’s syndrome: uveitis, urethraitis, arthritis

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20
Q

diagnosis/treatment of listeria monocytogenes

A

Diagnosis/treatment: diagnose: blood or CSF culture; treat: ampicillin or penicillin

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21
Q

transmission of bacillus anthracis

A

Transmission: normal pathogen of grazing ungulates (encountered in soil)– cause a lot of bleeding so that in nature, can exit host as blood & sporulate; **can be aerosolized (biothreat)

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22
Q

how does haemophilus influenzae spread/damage the host?

A

Spread/Damage; local infection: sinusitis, otitis media, epiglottitis

systemic: capsule, LPS causes proinflammatory damage (most damage due to inflammatory response)

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23
Q

description of chlamydia trachomatis

A

Description: poor gram stain (cell wall doesn’t have muramic acid); obligate intracellular

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24
Q

encounter/entry of EIEC

A

EIEC: enteroinvasive e. coli

Encounter/ Entry: not motile, lactose negative, binds to shigella antigens, contains virulence plasmid

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25
Q

multiplication/tissue damage from campylobacter jejuni

A

Multiplication/Tissue Damage: can be invasive leading to bacteremia

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26
Q

salmonell enterica

A

Description: gram negative rod, facultative anaerobe (intracellular: macrophages)

Encounter/ Entry: (typhoid fever: only human-human); GI (food-human)

Establish Infection: invades epithelium via membrane ruffles & type III secretion system; remains in phagosomes; capsule, motile

Multiplication/Tissue Damage: strong inflammatory response & type III secretions; recruit neutrophils); thypoid: seeding of gall bladder –> common shedding/infection

Common Disease Types: gastroenteritis (salmonellosis)- most common foodborne illness in US-inflammatory diarrhea (leukocytes in stool), enteric (typhoid) fever– only human-human pathogen, rose spots; sustained bacteremia (vascular infection), often in aorta; #1 cause of osteomyelitis in sickle cell disease; pea soup diarrhea

Transmission: enteric bacteria (colonizer) - but NOT component of human normal flora; food-human (can be human-human)

Host Defense: invades lymphatics in colon (in macrophages); inflammatory responses possible (reactive arthritis, IBS)

Other Notes: acid labile (degraded in stomach)–need high dose to cause infection; closely related to E. coli

Vaccination: vaccination against typhoid fever (maybe 20% effective)

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27
Q

transmission of brucella

A

Transmission: direct contact with livestock or unpasteurized dairy (zoonic– accidental pathology in humans)

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28
Q

host defense with salmonella enterica

A

Host Defense: invades lymphatics in colon (in macrophages); inflammatory responses possible (reactive arthritis, IBS)

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29
Q

how is neisseria gonorrhoeae encountered/enter

A

Encounter/ Entry: human only known host; enters through vagina (sexually transmitted); mediated by (type IV) pilli & opacity(opa) proteins

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30
Q

diagnosis/treatment of helicobacter pylori

A

Diagnosis/treatment: diagnosis: endoscope/urea breath test, serology, fecal antigen test, C-urea breath test; treatment for cancer/peptic ulcers: combo of PPI, amox & macrolide (clarithromycin)

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31
Q

transmission of shigella

A

Transmission: enteric bacteria; fecal-oral (person-person) *most contagious bacterial diarrhea

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32
Q

helicobacter pylori

A

Description: gram negative comma (curved rod); facultative anaerobe with cytotoxins

Encounter/ Entry: commensal of human stomach

Establish Infection: slow growing; adhesins help bind to gastric epithelia; urease– lyses & increases pH so it can survive better; motile with flagella

Multiplication/Tissue Damage: persistent infection (infeced for decades); urease; non-inflammatory LPS sometimes

Common Disease Types: chronic gastritis, cause of most duodenal ulcer, gastric ulcer; risk for gastric adenocarcinoma & MALToma

Transmission: pathogen/commensal of human stomach (pylorus); gastric-oral/fecal-oral/oral-oral

Other Notes: urease positive; oxidase positive

Diagnosis/treatment: diagnosis: endoscope/urea breath test, serology, fecal antigen test, C-urea breath test; treatment for cancer/peptic ulcers: combo of PPI, amox & macrolide (clarithromycin)

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33
Q

how does listeria monocytogenes establish infection

A

Establish Infection: B hemolytic; motile (comet-like tails); facultative intracellular; projections into neighbor cells

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34
Q

multiplication/tissue damage caused by neisseria meningitidis

A

Multiplication/Tissue Damage: inflammation–> leaky capillaries; meningococcemia; meningitis, bacteremia;able to survive in bloodstream; can lead to shock; phase & antigenic variation

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35
Q

other notes about bacteroides fragilis

A

Other Notes: contributes to beneficial role of normal flora

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36
Q

host defense with listeria monocytogenes

A

Host Defense: after initial entry, bacterium remains intracellular (usually controlled by cell-mediated immunity & CD8 T Cells- antibody response is irrelevant)

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37
Q

treatment of rickettsia rickettsi

A

Treatment: doxycycline

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38
Q

description of neisseria meningitidis

A

Description: gram negative diplococcic, facultative intracellular

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39
Q

treatment for chlamydia trachomatis

A

doxy, use ceftriazone to also treat comorbid gonorrhea (

often found together, thru sexual contact)

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40
Q

diagnosis of treponema pallidum

A

Diagnosis: through PCN

cause of syphilis

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41
Q

common disease types of klebsiella

A

Common Disease Types: common cause of nosocomial infections; can cause lobar pneumonia (currant jelly sputum); UTI

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42
Q

how is clostridium tetani encountered?

A

Encounter: infection via contamination of wound

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43
Q

how does bordetella pertussis spread/cause damage?

**spasmodic, Whooping Cough, abx don’t cure symptoms if epithelial damage is done

A

Spread/Damage: toxins kill epithelial cells, increase cAMP

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44
Q

what is the representative gram negative rod we think of first in nosocomial (hospital-acquired) infections?

A

pseudomonas aeruginosa

why?

-resistant to many abx due to tight porin channels & efflux pumps

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45
Q

description of neisseria gonorrhoeae

A

Description: gram negative, diplococci, facultative intracellular

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46
Q

other notes about mycobacteria TB

A

Other Notes: symptoms: cold sweats, cachetic,; fear of young people with TB developing meningitis

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47
Q

multiplication/damage of ETEC

A

ETEC: enterotoxigenic e coli

Multiplication/Tissue Damage: increased cAMP lead to watery diarrhea, dehydration, electolyte imbalance

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48
Q

transmission of yersinia pestis

A

Transmission: highly transmissable when aerolized (biothreat); usually arthropod (fleas)

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49
Q

description of mycoplasma pneumoniae

A

Description: gram indeterminate (no cell wall; cell membrane has sterols); pleomorphic shape; small size & small genome

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50
Q

how is clostridium botulinum encountered?

A

Encounter: infants: spores in food (honey); adults: toxin in food (canned or seafood)

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51
Q

chlamydia trachomatis

A

Description: poor gram stain (cell wall doesn’t have muramic acid); obligate intracellular

Encounter/entry: sexual contact; elementary body encounter epithelium

Establish infection: epithelial cells- reticular bodies directly damage epithelial barriers; type III secretion system ; RBs convert to Ebs and infect more

Multiplication/Tissue damage: type III secretion; induce inflammation

Common Disease Types: sexually transmitted: GU trac, recurrent– PID, (serovars D-K), trachoma (eye infection)– main cause of blindness (serovars A,B,C); lymphogranuloma venereum LGV (serovars L1-L3)- also STD; passed on to fetus during birth

Transmission: can be transmitted to fetus during birth (conjunctivitis & pneumonia); Reiter’s syndrome: uveitis, urethraitis, arthritis

Notes: bacteria exist as elementary (transmissable/infectious) form and reticular form (replicative within cells); cell wall lacks muramic acid

Treatment: doxy; use ceftriaxone to also treat gorrorhea (often found together, thru sexual contact)

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52
Q

encounter/entry of listeria monocytogenes

A

Encounter/ Entry: oral transmission; uptake by antigen-sampling M cells & macrophages, ruptures macrophages

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53
Q

neisseria gonorrhoeae

A

Description: gram negative, diplococci, facultative intracellular

Encounter/ Entry: human only known host; enters through vagina (sexually transmitted); mediated by (type IV) pilli & opacity(opa) proteins

Establish Infection: mucosal colonization (women)-attaches to columnar epithelial in cervix ; ascends from cervix (women have higher risk of ascendance)

Multiplication/Tissue Damage: salpingitis, PID; persistent infection leading to systemic bacteremia- can spread to skin/joints; IgA protease, iron acquisition, evade phagocytes; can do phase variation & antigenic variation; serum resistant (resistant to serum complement)

Common Disease Types: can have asymptomatic carriage; PID- white pirulent vaginal discharge; PID can spread to peritoneum (Fitz Hugh Curtis Syndrome via violin string adhesions); congenital pirulent conjunctivitis is mother pass to baby (EARLY ONSET); DCI (disseminated gonocococcal infection– bacteremia); can also cause proctitis, conjunctivitis, pharyngitis

Transmission: human only host (asymptomatic infection possible); sexually transmitted

Host Defense: barriers of cervical infection: cervical canal, mucus plug, hormones

Other Notes: growth on VPN agar & chocolate agar; oxidase positive

Diagnosis/treatment: ceftriaxone (but also administer macrolide or doxy to cover chlamydia too)

Vaccination: no

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54
Q

Transmission of streptococcus pneumoniae

A

Transmission: reservoir= nasopharynx

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55
Q

immunization for corynebacterium diptheriae?

A

Immunization: DTaP toxoid

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56
Q

Common disease types associated with legionella pneumophila

A

Common Disease Types: Legionaires: walking pneumonia, patchy CXR with consolidation in one lobe, paired with diarrhea, hyponatremia, neuro symptoms (HA/confusion); pontiac fever

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57
Q

how does francisella tularenis establish infection

A

Establish Infection: short survival in air but low dose required for infection; highly invasive

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58
Q

other notes about listeria monocytogenes

A

Other Notes: pregnant women (1/3 of infections); catalase positive; survive in cold environments

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59
Q

how does corynebacterium diphtheriae spread/cause damage?

A

Spread/damage: all of pathology due to toxin; blocks protein synthesis; toxin spreads systemically– pseudomembranes & edema (bull’s neck)

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60
Q

ETEC (enterotoxigenic e. coli)

A

Description: (E COLI) gram negative rod, facultative anaerobe; heat labile toxin & heat stable toxin

Encounter/ Entry: contaminated food/water; adheres to epithelium via pili

Establish Infection: colonizes intestinal tract; toxin cause increased cAMP

Multiplication/Tissue Damage: increased cAMP lead to watery diarrhea, dehydration, electolyte imbalance

Common Disease Types:“traveler’s” diarrhea; watery diarrhea; self-limited

Transmission: enteric bacteria; transmitted via water (Mexico)

Host Defense: develop immune response to the heat labile toxin; if in endemic area- can form immunity

Other Notes: like less virulent v. cholerae (heat-labile toxin)

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61
Q

treatment of mycoplasma pneumoniae

A

Treatment: (No cell wall) macrolides

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62
Q

description of bacillus anthracis

A

Description: gram positive rods (in chains); obligate aerobe; spore-former (2 toxins: Lethal Factor & Edema Factor); since makes spores– biothreat

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63
Q

encounter/entry of mycoplasma pneumoniae

A

Encounter/entry: human only known reservoir; droplets

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64
Q

other notes about EHEC

A

EHEC: enterohemorrhagic e coli

Other Notes: only e coli that doesn’t ferment sorbitol; 0157:H7 serotype causes outbreaks; occurs in US!

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65
Q

how is the host defense involved in borrelia burgdorferi

A

Host Defense: complement activated, chemokines released by skin cells, antibody response (against surface lipoproteins—helps with diagnosis); phase variation can occur in lipoproteins

cause of Lyme Disease

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66
Q

transmission of rickettsia rickettsi

A

Transmission: spread by dermacentor tick; primary mammal host of these ticks: rodents, dogs

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67
Q

multiplication/tissue damage from klebsiella

A

Multiplication/Tissue Damage: growth can trigger necrosis, inflammation & hemorrhage

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68
Q

common disease types of neisseria meningitidis

A

Common Disease Types: asymptomatic carriers spread the disease; Waterhouse-Friederichson Syndrome (adrenal hemorrhage); common to see petichiae rash (due to hemorrhage); one of principle bacterial agents of CNS disease; can cause otitis media, conjunctivitis,s eptic arthritis, urethritis, purulent pericarditis

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69
Q

encounter/entry of EHEC

A

EHEC: enterohemorrhagic e coli

Encounter/ Entry: low infectious dose; contaminated food (beef); can transmit human-human; adheres to epithelium of large bowel

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70
Q

how does yersinia pestis establish infection?

A

Establish Infection: highly invasive , can survive in macrophages (intracellular & extracellular bug); can really cause bacteremia; peptide capsule

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71
Q

how does mycobacterium leprae establish infection?

A

Establish Infection: tuberculoid leprosy: within macrophages (strong TH1 response); lepromatous leprosy: (TH2 cells involved)bacteria not maintained in macrophage

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72
Q

corynebacterium diphtheriae

A

Description: gram positive rod, anaerobe, AB exotoxin; no spores

Encounter: oral secretions

Infection: colonizes pharyngeal epithelium

Spread/damage: all of pathology due to toxin; blocks protein synthesis; toxin spreads systemically– pseudomembranes & edema (bull’s neck)

Transmission: only reservoir: throat of man

Immunization: DTaP toxoid

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73
Q

klebsiella

A

Description: gram negative rod

Encounter/ Entry: often intro by medical manipulation (IV, cath); normal GI flora

Establish Infection: capsule (K antigen), immotile; diverse antigens

Multiplication/Tissue Damage: growth can trigger necrosis, inflammation & hemorrhage

Common Disease Types: common cause of nosocomial infections; can cause lobar pneumonia (currant jelly sputum); UTI

Transmission: enteric bacteria (GI tract); common in skin, pharynx

Other Notes: mutli-drug resistance (some produce extended spectrum beta lactamase ESBL); ferment lactose; urease positive

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74
Q

description of streptococcus pneumoniae

A

aka Pneumococcus

Description: gram positive, diplococci

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75
Q

stages of lyme disease

A

(due to borrelia burgdorferi)

3 phases of Lyme Disease: Stage 1 (early infection, localized); Stage 2 (early infection, disseminated infection); Stage 3 (late infection; persistent infection; post-lyme (“chronic”)

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76
Q

description of francisella tularenia

A

Description: gram negative coccobacillus, facultative intracellular; **biothreat

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77
Q

Rickettsia rickettsi

A

Description: gram negative (but poorly stained), coccobacillus, obligate intracellular

Encounter/entry: arthropod vector for transmission

Establish Infection: pathogen of endothelium- spread by ticks, lysis of vascular endothelium (lead to leaky vessels), use host actin to provide motility & transfer to other cells

Multiplication/tissue damage: infection of endothelial cell, spread to neighboring cells- affected blood vessels hemorrhage

Common Disease Types: headache, fever, vasculitis; Rocky Mountain Spotted Fever: rash (due to hemorrhage) spreads from limbs to central; myalgias; disseminated coagulopathy

Transmission: spread by dermacentor tick; primary mammal host of these ticks: rodents, dogs

Other notes: geography plays a role- most prevalent in southeast US

Treatment: doxycycline

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78
Q

description of yersinia pestis

A

Description: gram negative; facultative anaerobe, no spores/toxins; **biothreat (plague)

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79
Q

common disease types from yersinia pestis

A

Common Disease Types: plague; ataxia caused by pain of bubos; can penetrate lungs (when human-human transmission occurs) causing bloody sputum (late stage); sepsis syndrome is primary COD; bubos (enlarged lymph node with tons of bacteria usually in axilla or groin)

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80
Q

how streptococcus pneumoniae encounters host

A

Encounter: nasopharyngeal colonization via respiratory droplets

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81
Q

how is clostridium perfringens encountered?

A

Encounter: contamination of wound (especially after abdominal surgery)

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82
Q

common diseases associated with chlamydia pneumoniae

A

Common disease types: pharyngitis, bronchitis, atypical pneumonia

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83
Q

other notes about helicobacter pylori

A

Other Notes: urease positive; oxidase positive

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84
Q

encounter/entry of salmonella enterica

A

Encounter/ Entry: (typhoid fever: only human-human); GI (food-human)

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85
Q

disease types involved with staph epidermidis

A

Disease Types: UTI, nosocomial bacteremia, endocarditis (especially on prosthetic valves), infections of prostheses/shunts/implants

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86
Q

how does chlamydia pneumoniae establish infection

A

Establish Infection: epithelial cells- reticular bodies directly damage epithelial barriers; type III secretion system ; RBs convert to Ebs and infect more

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87
Q

how does bacteroides fragilis multiply/cause tissue damage

A

Multiplication/Tissue Damage: produce B-lactamase

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88
Q

host defense involved in mycobacteria tuberculosis

A

Host Defense: environmental & genetic factors can predispose to TB; TNF inhibitor drugs can reactivate TB

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89
Q

description of salmonella enterica

A

Description: gram negative rod, facultative anaerobe (intracellular: macrophages)

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90
Q

description of EIEC

A

EIEC: enteroinvasive e. coli

Description: gram negative rod, facultative anaerobe, no toxins

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91
Q

how does clamydia trachomatis establish infection

A

Establish infection: epithelial cells- reticular bodies directly damage epithelial barriers; type III secretion system ; RBs convert to Ebs and infect more

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92
Q

description of staph aureus

A

Description: gram positive, clusters of cocci, aerobe

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93
Q

how does staphylococcus aureus establish infection?

A

Establish Infection: colonizes skin & nose, enters through break in skin

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94
Q
A
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95
Q

transmission of mycobacteria tubercluosis

A

Transmission: infectious aerosols (droplets) human-human

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96
Q

transmission of campylobacter jejuni

A

Transmission: zoonotic infections (fecal-oral); commensal of domestic animals’ GI tract; foodborne especially in summer

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97
Q

description of shigella

A

Description: gram negative, facultative anaerobe (cytoplasmic pathogen), shiga toxin

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98
Q

host defense & francisella tularenis

A

Host Defense: cell-mediated immunity (T cells) necessary to clear intracellular infection

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99
Q

Staphlococcus epidermidis

A

Description: gram positive, clusters of cocci

Encounter: normal skin flora (only pathogenic if on foreign body)

Establish Infection: biofilm, infections on prosthetic material/catheters

Disease Types: UTI, nosocomial bacteremia, endocarditis (especially on prosthetic valves), infections of prostheses/shunts/impants

Transmission: normal skin flora

Other notes: catalase positive; coagulase negative

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100
Q

disease/pathology seen with staphlyococcus aureus

A

Disease Types:

think pus: folliculitis, furuncles, impetigo, cellulitis, wound infetions– inflammatory response due to superantigens

  • SSSS toxin: staph scalded skin syndrome
  • TSST toxin: toxic shock syndrome
  • enterotoxin: food poisoning (2-6 hours after ingestion)
  • leukocidin toxin: factor seen in community- acquired MRSA
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101
Q

other notes about campyobacter jejuni

A

Other Notes: thermophilic; oxidase positive; bile salt resistant

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102
Q

how does campylobacter jejuni establish infection?

A

Establish Infection: motile, slow growing; grows in bile

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103
Q

treatment of infection of clostridium perfringens?Treatment: debridement, hyperbaric chamber

A

Treatment: debridement, hyperbaric chamber

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104
Q

listeria monocytogenes

A

Description: gram positive rod, cytoplasmic pathogen (intracellular)

Encounter/ Entry: oral transmission; uptake by antigen-sampling M cells & macrophages, ruptures macrophages

Establish Infection: B hemolytic; motile (comet-like tails); facultative intracellular; projections into neighbor cells

Multiplication/Tissue Damage: damage due to host resposne; spread via blood & macrophages

Common Disease Types: flu-like symptoms; can produce meningitis, sepsis;

Transmission: can contaminate refrigerated food (milk, soft cheese, meat); also in stool

Host Defense: after initial entry, bacterium remains intracellular (usually controlled by cell-mediated immunity & CD8 T Cells- antibody response is irrelevant)

Other Notes: pregnant women (1/3 of infections); catalase positive; survivie in cold environments

Diagnosis/treatment: diagnose: blood or CSF culture; treat: ampicillin or penicillin

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105
Q

Staphylococcus aureus

A

Description: gram positive, clusters of cocci, aerobe

Encounter: colonizes skin & nose

Establish Infection: colonizes skin & nose, enters through break in skin

Damage/Spread: B-hemolysis, IgG binding protein A in cell wall; secretes antigens

**catalase positive, coagulase positive (latex assay, clumping factor, Protein A)

Disease Types:

think pus: folliculitis, furuncles, impetigo, cellulitis, wound infetions– inflammatory response due to superantigens

  • SSSS toxin: staph scalded skin syndrome
  • TSST toxin: toxic shock syndrome
  • enterotoxin: food poisoning (2-6 hours after ingestion)
  • leukocidin toxin: factor seen in community- acquired MRSA
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106
Q

transmission of clostridium tetani?

A

Transmission: common in soil, spores survive for years

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107
Q

common disease types of neisseria gonorrhoeae

A

Common Disease Types: can have asymptomatic carriage; PID- white pirulent vaginal discharge; PID can spread to peritoneum (Fitz Hugh Curtis Syndrome via violin string adhesions); congenital pirulent conjunctivitis is mother pass to baby (EARLY ONSET); DCI (disseminated gonocococcal infection– bacteremia); can also cause proctitis, conjunctivitis, pharyngitis

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108
Q

how does borrelia burgdorferi establish infection?

A

Establish Infection: endoflagellum allows penetration of endothelium; motile; penetrate blood vessels

cause of Lyme Disease

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109
Q

diagnosis/treatment of mycobacteirum leprae

A

Diagnosis/treatment: lepromin skin test; treatment: multidrug therapy tuberculoid: dapsone & rifampin 6 months; lepromatous: these 2 + clofazamine for 2-3 years

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110
Q

treatment for streptococcus pyogenes

A

Treatment: penicillin, beta lactams, clinda, macrolides

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111
Q

Stages of Pneumococcal Pneumonia

A

(due to infection by streptococcus pneumoniae)

Exudative phase: alveoli fill with exudate

Early consolidation phase: chemotaxis

Hepatization phase: lung looks like a liver

Resolution phase: macrophages clear debris

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112
Q

description of mycobacterium leprae

A

Description:gram positive & acid fast (mycolic acid in waxy coat) rod; aerobe

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113
Q

how does treponema pallidum establish infection?

A

Establish infection: local infection (primary syphilis); motile

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114
Q

description of EHEC

A

EHEC: enterohemorrhagic e coli

Description: (E. COLI) gram negative rod, facultative anaerobe, shiga-toxin that inhibits translation

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115
Q

transmission of mycobacterium leprae

A

Transmission: human-human; nasal secretions; main reservoir is the armadillo in the US, grows in footpads of immunodeficient mice too

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116
Q

description of ETEC

A

ETEC: enterotoxigenic e coli

Description: (E COLI) gram negative rod, facultative anaerobe; heat labile toxin & heat stable toxin

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117
Q

common disease types from listeria monocytogenes

A

Common Disease Types: flu-like symptoms; can produce meningitis, sepsis;

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118
Q

transmission of borrelia burgdorferi

A

Transmission: deer/mice to tick à humans; can pass transplacentally (congenital)

cause of Lyme Disease

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119
Q

description of vibrio cholerae

A

Description: gram negative comma (curved rod), facultative anaerobe; toxin-mediated disease via enterotoxin

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120
Q

how does neisseria gonorrhoeae multply/cause tissue damage?

A

Multiplication/Tissue Damage: salpingitis, PID; persistent infection leading to systemic bacteremia- can spread to skin/joints; IgA protease, iron acquisition, evade phagocytes; can do phase variation & antigenic variation; serum resistant (resistant to serum complement)

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121
Q

host defense & bacillus anthracis

A

Host Defense: inflammation suppressed

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122
Q

encounter/entry of neisseria meningitidis

A

Encounter/ Entry: human only host; enter through upper respiratory tract(requires close contact) ; pili and opa mediated attachment

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123
Q

transmission of e coli

A

Transmission: enteric bacteria- COMMENSAL; fecal-oral transmission

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124
Q

other notes about e coli

A

Other Notes: can ferment lactose; most abundant facultative anaerobe in the gut

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125
Q

EPEC (enteropathogenic e. coli)

A

Description: gram negative rod, facultative anaerobe, no toxins

Encounter/ Entry: adheres to epithelium via pili in small intestine

Common Disease Types: diarrhea (not bloody) with mucus; malaise; vomiting

Other Notes: just like EHEC, but happens in small intestine without toxin

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126
Q

host response involved with legionella pneumophila

A

Host Response: host response/ inflammation is much of damage

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127
Q

how does mycoplasma pneumoniae establish infection?

A

Establish Infection: adhere to respiratory epithelium; slow growing (1-3 week incubation); stays localized in upper respiratory tract

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128
Q

how does streptococcus pneumoniae spread/cause damage?

A

Spread/Damage: spreads to lower respiratory tract, attaches via adhesins, can undergo phase variation (less susceptible to immunity)

*most common cause of community acquired pneumonia; can cause pneumococcal meningitis

*bile sensitive

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129
Q

diagnosis/treatment of borrelia burgdorferi

A

Diagnosis/Treatment: diagnosis through clinical presentation & serology; treatment with doxy, amoxicillin, ceftriaxone

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130
Q

mycoplasma pneumoniae

A

Description: gram indeterminate (no cell wall; cell membrane has sterols); pleomorphic shape; small size & small genome

Encounter/entry: human only known reservoir; droplets

Establish Infection: adhere to respiratory epithelium; slow growing (1-3 week incubation); stays localized in upper respiratory tract

Multiplication/tissue damage: no capacity for invasive disease; blocks ciliary action; mononuclear (monocyte) infiltrate – typical pneumonia show neutrophil infiltrate ;IgM Cold agglutinins

Common Disease Types: walking pneumonia, patchy CXR that looks worse than clinical manifestation

Transmission: occurs in young adults in close quarters (only human-human); occurs in outbreaks/communities

Treatment: (No cell wall) macrolides

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131
Q

Mycobacterium tuberculosis

A

Description: acid fast rod; aerobe

Encounter/ Entry: infectious aerosols, reach alveoli; interacts with alveolar macrophage

Establish Infection: lives within macrophage in alveoli- don’t allow phago-lysosome fusion; slow-growing within macrophages (no symptoms yet)

Multiplication/Tissue Damage: replicate in lungs, can spread via RES; grows slowly; cell envelope has thick waxy layer (lipids, porins); secretion system (not Type III or iV, but similar) (damage is immune mediated) ; able to eat host membranes

Common Disease Types: TB; Many outcomes after infection (infection is not the same as active disease): Acute Infection (pre-symptomatic); stable control of infection (latent) (never symptoms, skin test positive- Cell-mediated immunity-CD4T cells & granuloma); primary disease (pathology after months); latent can be reactivated;Miliary TB disseminated to body, lesions look like millet seeds) ;active TB (caseous necrosis of granuloma)

Transmission: infectious aerosols (droplets) human-human

Host Defense: environmental & genetic factors can predispose to TB; TNF inhibitor drugs can reactivate TB

Other Notes: symptoms: cold sweats, cachetic,; fear of young people with TB developing meningitis

Diagnosis/treatment: diagnose: TST or blood test, CXR; positive skin test if T cell is responding to TB– give induration; all patients with active TB should be offered directly observed therapy (DOT) because partial treatment leads to resistance; treatment: RIPE (rifampin, isoniazid, pyraxinamide, ethambutol); INH for latent TB

Vaccination: diagnose: TST or blood test, CXR; positive skin test if T cell is responding to TB– give induration; all patients with active TB should be offered directly observed therapy (DOT) because partial treatment leads to resistance; treatment: RIPE (rifampin, isoniazid, pyraxinamide, ethambutol); INH for latent TB

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132
Q

encounter of staphylococcus aureus

A

Encounter: colonizes skin & nose

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133
Q

Brucella

A

Description: gram negative, coccobacillus, facultative intracellular

Encounter/entry: ingestion (usually unpasteurized dairy product)/direct contact with animal

Establish Infection: grows within macrophages, but can spread very quickly; inhibits fusion of endosome & lysosome

Multiplication/damage: noncaseating granulomas; can cause systemic disease; spreads through RES

Common disease types: undulant fever; anorexia, liver & splenic involvement; osteomyeltis;

Transmission: direct contact with livestock or unpasteurized dairy (zoonic– accidental pathology in humans)

Diagnosis/treatment: dx: blood or tissue biopsy (but not all cases are bacteremic); tetracyclines (doxy); rifampin; need multiple trugs & long course since such slow growth rate

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134
Q

escherichia coli

A

Description: gram negative rod; facultative anaerobe; LPS exotoxin **serotyping antigens is helpful for pathogenic straings (antigens: O, H, K)

Encounter/ Entry: fecal-oral; doesn’t enter cytoplasm; pili, hemolysin,

Establish Infection: capsule with K antigen; pili

Multiplication/Tissue Damage: #1 cause UTI, #1cause gram negative sepsis; neonatal meningitis due to bacteremia in infants

Common Disease Types: E coli is most frequent cause of UTI (UPEC species); also cause neonatal meningitis

Transmission: enteric bacteria- COMMENSAL; fecal-oral transmission

Other Notes: can ferment lactose; most abundant facultative anaerobe in the gut

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135
Q

how does helicobacter pylori establish infection

A

Establish Infection: slow growing; adhesins help bind to gastric epithelia; urease– lyses & increases pH so it can survive better; motile with flagella

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136
Q

yersinia pestis

A

Description: gram negative; facultative anaerobe, no spores/toxins; **biothreat

Encounter/ Entry: human-human when aerosolized; bite of infected fleas (vector/arthropod)

Establish Infection: highly invasive , can survive in macrophages (intracellular & extracellular bug); can really cause bacteremia; peptide capsule

Multiplication/Tissue Damage: major virulence due to suppression of early inflammatory response (type III secretion system + plasminogen activator); able to travel systemically- sudden onset of severe symptoms; have

Common Disease Types: plague; ataxia caused by pain of bubos; can penetrate lungs (when human-human transmission occurs) causing bloody sputum (late stage); sepsis syndrome is primary COD; bubos (enlarged lymph node with tons of bacteria usually in axilla or groin)

Transmission: highly transmissable when aerolized (biothreat); usually arthropod (fleas)

Host Defense: inflammation suppressed

Diagnosis/treatment: treatment has to be inititated within 24 hours from onset of symptoms

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137
Q

how is corynebacterium diptheriae encountered?

A

Encounter: oral secretions

138
Q

streptococcus pneumoniae

A

aka Pneumococcus

Description: gram positive, diplococci

Encounter: nasopharyngeal colonization via respiratory droplets

Infection: antiphagogenic capsule, alpha hemolysis, pneumolysis breaks pore in host tissue

Spread/Damage: spreads to lower respiratory tract, attaches via adhesins, can undergo phase variation (less susceptible to immunity)

*most common cause of community acquired pneumonia; can cause pneumococcal meningitis

*bile sensitive

Transmission: reservoir= nasopharynx

Treatment: penicillin

139
Q

Campylobacter jejuni

A

Description: gram negative comma (curved rod), facultative anaerobe; enteroxins & cytotoxins

Encounter/ Entry: zoonotic infections (fecal-oral); commensal of domestic animals’ GI tract; foodborne especially in summer

Establish Infection: motile, slow growing; grows in bile

Multiplication/Tissue Damage: can be invasive leading to bacteremia

Common Disease Types: boody diarrheal disease, gastroenteritis, post-infectious sequelae: Guillain-Barre syndrome (demyelination of nerves– ascending paralysis), reactive arthritis

Transmission: zoonotic infections (fecal-oral); commensal of domestic animals’ GI tract; foodborne especially in summer

Host Defense: resistant to antibodies & complement

Other Notes: thermophilic; oxidase positive; bile salt resistant

140
Q

how does clostridium difficile spread/cause damage?

A

Spread/damage: sloughing of epithelium & pseudomembranes (pseudomembranous colitis

141
Q

description of clostridium botulinum

A

Description: gram positive rod, anaerobic, neurotoxic exotoxin, spore-forming

142
Q

Transmission of chlamydia trachomatis

A

Transmission: can be transmitted to fetus during birth (conjunctivitis & pneumonia)

143
Q

encounter of bordetella pertussis

A

Encounter: inhaled from cough-generated droplets from infected person

144
Q

how does e coli establish infection

A

Establish Infection: capsule with K antigen; pili

145
Q

common disease types of shigella

A

Common Disease Types: severe: dysentery, parallels Chrohn’s (due to shigatoxin); *most contagious bacterial diarrhea

146
Q

immunization for clostridium

A

Immunization: Tdap toxoid

147
Q

how does staph epidermidis establish infection

A

Establish Infection: biofilm, infections on prosthetic material/catheters

148
Q

how is bordetella pertussis transmitted?

A

Transmission: only found in humans with active disease

149
Q

how is clostridium botulinum often transmitted?

A

Transmission: ingested

150
Q

enterococcus

A

aka Group D Strep

Description: gram positive, cocci that form short chain, anaerobic

Encounter: often catheter-related infections, wound infections

Transmission: part of normal fecal flora of humans & animals; often spread by healthcare workers

*VRE (vancomycin resistant enterococci) has been established

-bile resistant

151
Q

other notes about salmonella enterica

A

Other Notes: acid labile (degraded in stomach)–need high dose to cause infection; closely related to E. coli

152
Q

how does clostridium perfringens infect?

A

Infection: alpha toxin hydrolyzes cell membranes

153
Q

treatment/diagnosis of legionella pneumophila

A

Treatment/Diagnosis: urine antigen tests for dx; often treat upon suspicion; macrolides, fluoroquinolone

154
Q

encounter/entry of rickettsia rickettsi

A

Encounter/entry: arthropod vector for transmission

155
Q

Vibrio cholerae

A

Description: gram negative comma (curved rod), facultative anaerobe; toxin-mediated disease via enterotoxin

Encounter/ Entry: contaminated water/food; fecal-oral

Establish Infection: polar flagellae; adhesins allow adherence to intestinal mucosa; release enterotoxin, inserts into cell membrane, stimulates adenyl cyclase & increase cAMP (increase Cl secretion, causing secretions)

Multiplication/Tissue Damage: enterotoxin ; biofilm; adhesins

Common Disease Types: toxin mediated diarrhea; wound infections; systemic infections in compromised host; toxin mediated diarrheal (rice water stool)– hypokalemia & met. acidosis; wound infections; can get other infections from raw shellfish– sepsis, cutaneous bullae

Transmission: environmental- survive in fresh and salt water; bile salt resistant, oxidase positive, halophilic – survives as colony (biofilm) in environment

Other Notes: bile salt resistant (able to survive in GI tract); oxidase positive

Diagnosis/treatment: Therapy: REHYDRATE (fluid & K loss; glucose & Na); IV Ringer sol’n; Abx: tetracycline & fluoroquinolones

156
Q

encounter/entry of chlamydia trachomatis

A

Encounter/entry: sexual contact; elementary body encounter epithelium

157
Q

common disease types associated with mycoplasma pneumoniae

A

Common Disease Types: walking pneumonia, patchy CXR that looks worse than clinical manifestation

158
Q

transmission of chlamydia pneumoniae

A

Transmission: aerosols from coughing

159
Q

other notes about neisseria gonorrhoeae

A

Other Notes: growth on VPN agar & chocolate agar; oxidase positive

160
Q

Bacteroides fragilis

A

Description: gram negative bacillus, anaerobe (opportunist)

Encounter/ Entry: component of normal flora on skin ; enters epithelial/cutaneous barrier

Establish Infection: synergy in polymicrobial infections; often form abscesses

Multiplication/Tissue Damage: produce B-lactamase

Common Disease Types: endogenous infections ;bacterial vaginosis; but NOT increased susceptibility with immunodeficient states because part of normal internal flora; often cause putrid odor & gas (crepitus)

Transmission: normal flora of GI tract; somewhat in female genital tract

Other Notes: contributes to beneficial role of normal flora

161
Q

outcomes of streptococcus pyogenes

A

Pyogenic Infections: impetigo, pharyngitis, cellulitis, erysypilis

Toxigenic effects (streptogenic exotoxin): scarlet fever, strep TSS, necrotizing fasciitis

Complications after infection: Rheumatic Fever, glomerulonephritis

162
Q

multiplication/tissue damage of mycobacteria

A

Multiplication/Tissue Damage: replicate in lungs, can spread via RES; grows slowly; cell envelope has thick waxy layer (lipids, porins); secretion system (not Type III or iV, but similar) (damage is immune mediated) ; able to eat host membranes

163
Q

transmission of klebsiella

A

Transmission: enteric bacteria (GI tract); common in skin, pharynx

164
Q

how does brucella establish infection?

A

Establish Infection: grows within macrophages, but can spread very quickly; inhibits fusion of endosome & lysosome

165
Q

description of bacteroides fragilis

A

Description: gram negative bacillus, anaerobe (opportunist)

166
Q

diagnosis/treatment of yersinia pestis

A

Diagnosis/treatment: treatment has to be inititated within 24 hours from onset of symptoms

167
Q

how does EHEC establish infection

A

EHEC: enterohemorrhagic e coli

Establish Infection: acid stable (stomach); causes attaching & effacing lesions, dissolves microvilli & forms pedestals via type III secretion system

168
Q

description of campylobacter jejuni

A

Description: gram negative comma (curved rod), facultative anaerobe; enteroxins & cytotoxins

169
Q

EHEC (enterohemorrhagic e. coli)

A

Description: (E. COLI) gram negative rod, facultative anaerobe, shiga-toxin that inhibits translation

Encounter/ Entry: low infectious dose; contaminated food (beef); can transmit human-human; adheres to epithelium of large bowel

Establish Infection: acid stable (stomach); causes attaching & effacing lesions, dissolves microvilli & forms pedestals via type III secretion system

Multiplication/Tissue Damage: remains localized in intestine (doesn’t cause bacteremia); shiga toxin damage cells by inhibiting protein synthesis

Common Disease Types: local damage: hemorrhagic colitis- bloody diarrhea, abdominal pain; systemic (damage kidney, brain): hemolytic uremic syndrome (HUS): hemolytic anemia, thrombocytopenia, renal failure

Transmission: undercooked meat, fresh produce (spinach)

Host Defense: mostly secretory issues not involving inflammatory response

Other Notes: only e coli that doesn’t ferment sorbitol; 0157:H7 serotype causes outbreaks; occurs in US!

Diagnosis/treatment: supportive treatment for HUS; thoroughly cook meet

170
Q

description of mycobacteria tuberculosis

A

Description: acid fast rod; aerobe

171
Q

streptococcus agalactia

A

aka Group B Strep

Description: gram positive cocci in chains, anaerobic

Transmission: in normal flora of vagina; spread to babies during delivery, can cause sepsis

-bacitracin resistant, B-hemolytic

172
Q

vaccination for salmonella enterica

A

Vaccination: vaccination against typhoid fever (maybe 20% effective)

173
Q

common disease types of bacteroides fragilis

A

Common Disease Types: endogenous infections ;bacterial vaginosis; but NOT increased susceptibility with immunodeficient states because part of normal internal flora; often cause putrid odor & gas (crepitus)

174
Q

encounter/entry of francisella tularenis

A

Encounter/ Entry: no direct transmission between humans; ticks/rabbits- tick bite causes ulcer

175
Q

encounter/entry of bacteroides fragilis

A

Encounter/ Entry: component of normal flora on skin ; enters epithelial/cutaneous barrier

176
Q

common disease types of vibrio cholerae

A

Common Disease Types: toxin mediated diarrhea; wound infections; systemic infections in compromised host; toxin mediated diarrheal (rice water stool)– hypokalemia & met. acidosis; wound infections; can get other infections from raw shellfish– sepsis, cutaneous bullae

177
Q

description of listeria monocytogenes

A

Description: gram positive rod, cytoplasmic pathogen (intracellular)

178
Q

transmission of francisella tularenis

A

Transmission: occurs in many animals (main reservoir: rabbit); direct contact with infected mammals; bites of infectious arthropods-tick (dermacentor) (no person to person); can be aerosolized (warfare)

179
Q

encounter/entry of campylobacter jejuni

A

Encounter/ Entry: zoonotic infections (fecal-oral); commensal of domestic animals’ GI tract; foodborne especially in summer

180
Q

how does mycobacteria tuberculosis establish infection

A

Establish Infection: lives within macrophage in alveoli- don’t allow phago-lysosome fusion; slow-growing within macrophages (no symptoms yet)

181
Q

description of clostridium tetani

A

Description: gram positive, rod, anaerobe, neurotoxic exotoxin + spores

182
Q

how does corynebacterium diphtheriae cause infection?

A

Infection: colonizes pharyngeal epithelium

183
Q

host defense & yersinia pestis

A

Host Defense: inflammation suppressed by type III secretions

184
Q

transmission of EHEC

A

EHEC: enterohemorrhagic e coli

Transmission: undercooked meat, fresh produce (spinach)

185
Q

description of chlamydia pneumoniae

A

Description: poor gram stain; obligate intracellular; spore-like infectious form

186
Q

how does ETEC establish infection?

A

ETEC: enterotoxigenic e coli

Establish Infection: colonizes intestinal tract; toxin cause increased cAMP

187
Q

how does vibrio cholerae establish infection?

A

Establish Infection: polar flagellae; adhesins allow adherence to intestinal mucosa; release enterotoxin, inserts into cell membrane, stimulates adenyl cyclase & increase cAMP (increase Cl secretion, causing secretions)

188
Q

diagnosis/treatment of pseudomonas aeruginosa

A

Diagnosis/treatment: pip/tazo (maybe fluoroquinolones or aminoglycosides); has beta-lactamase (resistant to B-lactams); diagnosis via culture

189
Q

host defense involved in mycobacterium leprae

A

Host Defense: 2 forms of leprosy solely based on host immune respone: tuberculoid form (pacudibacillary): few bacteria, abudant lymphocytes with well-formed granuloma vs lepromatous form (multibacillary) with numerous bacteria, few lymphocytes, without well-formed granuloma; inflammatory T cells & macrophages are critical host response

190
Q

spread/damage due to clostridium tetani?

A

Spread/Damage: all of symptoms are due to toxin inhibitin interneurons & relaxation signals

191
Q

shigella

A

Description: gram negative, facultative anaerobe (cytoplasmic pathogen), shiga toxin

Encounter/ Entry: enters cytoplasm, invade COLON epithelium & destroy (basolateral surface)

Establish Infection: invades M cell; not motile, taken into vacuole & dissolves- is in cytoplasm and invades neighbor cells

Multiplication/Tissue Damage: releases cytokines (type III secretion system); bloody/inflammatory diarrhea; shigatoxin inhibits translation (60s); inflammatory response

Common Disease Types: severe: dysentery, parallels Chrohn’s (due to shigatoxin); *most contagious bacterial diarrhea

Transmission: enteric bacteria; fecal-oral (person-person) *most contagious bacterial diarrhea

Other Notes: acid stable (easily passes stomach); 95% identical to e coli (but lactose non-fermenter)

Diagnosis/treatment: stool culture; treat: fluid replacement, abx

192
Q

how does chlamydia trachomatis multiply/cause tissue damage

A

Multiplication/Tissue damage: type III secretion; induce inflammation

193
Q

host defense with ETEC

A

ETEC: enterotoxigenic e coli

Host Defense: develop immune response to the heat labile toxin; if in endemic area- can form immunity

194
Q

atherosclerosis and chlamydia pneumoniae

A

Notes: epidemiological association with atherosclerosis

195
Q

clostridium difficile

A

Description: gram positive rod, anaerobic, tissue-damaging exotoxin, spore-forming

Encounter: part of normal flora of intestine; often less competition when normal flora wiped out by abx

Infection: toxin kills epithelium

Spread/damage: sloughing of epithelium & pseudomembranes (pseudomembranous colitis

Detection: toxin in feces

Treatment: discontinue first abx, administer vanco or metronidazole

196
Q
A
197
Q

how does klebsiella establish infection?

A

Establish Infection: capsule (K antigen), immotile; diverse antigens

198
Q

transmission of vibrio cholerae

A

Transmission: environmental- survive in fresh and salt water; bile salt resistant, oxidase positive, halophilic – survives as colony (biofilm) in environment

199
Q

transmission of legionella pneumonphila

A

Transmission: outbreaks (Classic Legionaire’s in 1976)

200
Q

description of corynebacterium diphtheriae?

A

Description: gram positive rod, anaerobe, AB exotoxin; no spores

201
Q

borrelia burgdorferi

A

Description: spirochete

Encounter: lives within ticks, come from mice or deer, enter via tick bite

Establish Infection: endoflagellum allows penetration of endothelium; motile; penetrate blood vessels

Multiplication/Tissue Damage: binds to plasminogen; inhibits complement; disseminates through blood stream (induces inflammatory response)

Disease Types: LYME DISEASE; characteristic target rash- erythema migrans; neurologic symptoms (Bell’s Palsy, confusion)

Transmission: deer/mice to tick à humans; can pass transplacentally (congenital)

Host Defense: complement activated, chemokines released by skin cells, antibody response (against surface lipoproteins—helps with diagnosis); phase variation can occur in lipoproteins

Diagnosis/Treatment: diagnosis through clinical presentation & serology; treatment with doxy, amoxicillin, ceftriaxone

202
Q

vaccination of neisseria meningitidis

A

Vaccination: vaccine (type B capsule not included)

203
Q

how does neisseria meningitidis establish infection?

A

Establish Infection: mucosal colonization in pharynx, spread systemically & to lower respiratory tract & can cross blood-brain barrier (meningitis); capsule; makes IgA protease; iron acquisition

204
Q

description of helicobacter pylori

A

Description: gram negative comma (curved rod); facultative anaerobe with cytotoxins

205
Q
A
206
Q

description of clostridium perfringins

A

Description: gram positive rod, anaerobe, tissue damaging exotoxin, spore forming

*only clostridium with a capsule

207
Q

how is the host defense involved in treponema pallidum infection

A

Host Defense: can evade immunity (waxy coat); induces prostaglandin E2; resists phagocutosis

cause of syphilis

208
Q

treatment for clostridium difficile?

A

Treatment: discontinue first abx, administer vanco or metronidazole

209
Q

how is borrelia burgdorferi encountered?

A

Encounter: lives within ticks, come from mice or deer, enter via tick bite

cause of Lyme Disease

210
Q

how does haemophilus influenzae encounter host?

A

Encounter: mucosal colonization in nasopharynx via respiratory secretion droplets

211
Q

multiplication/tissue damage of rickettsia rickettsi

A

Multiplication/tissue damage: infection of endothelial cell, spread to neighboring cells- affected blood vessels hemorrhage

212
Q

how does haemophilus influenzae infect host?

A

Infection: attaches to epithleium, uses IgA protease to fend off immune response, LPS initiates immue response, capsule protects

213
Q

diagnosis/treatment of mycobacteria TB

A

Diagnosis/treatment: diagnose: TST or blood test, CXR; positive skin test if T cell is responding to TB– give induration; all patients with active TB should be offered directly observed therapy (DOT) because partial treatment leads to resistance; treatment: RIPE (rifampin, isoniazid, pyraxinamide, ethambutol); INH for latent TB

214
Q

diagnosis & treatment of neisseria meningitidis

A

Diagnosis/treatment: prohylaxis of exposed (abx- rifampin) can be preventive; treatment with ceftriaxone

215
Q

other notes about shigella

A

Other Notes: acid stable (easily passes stomach); 95% identical to e coli (but lactose non-fermenter)

216
Q

EIEC (enteroinvasive e. coli)

A

Description: gram negative rod, facultative anaerobe, no toxins

Encounter/ Entry: not motile, lactose negative, binds to shigella antigens, contains virulence plasmid

Common Disease Types: diarrhea, fever, dysentery

Other Notes: think of as less virulent shigella

217
Q

multiplication/damage from bacillus anthracis

A

Multiplication/Tissue Damage: toxin Edema Factor: increase cAMP, cause edema and inhibit phagocytosis; Lethal Factor acts as protease; causes necrosis (seen in eshcar)

218
Q

common disease types of rickettsia rickettsi

A

Common Disease Types: headache, fever, vasculitis; Rocky Mountain Spotted Fever: rash (due to hemorrhage) spreads from limbs to central; myalgias; disseminated coagulopathy

219
Q

transmission of bacteroides fragilis

A

Transmission: normal flora of GI tract; somewhat in female genital tract

220
Q

diagnosis/treatment of francisella tularenis

A

Diagnosis/treatment: treat: aminoglycoside (streptomycin)

221
Q

multiplication/tissue damage of psuedomonas aeruginosa

A

Multiplication/Tissue Damage: biofilm production (antiphagocytosis); proteases; can get to bone & joint ; membrane damaging toxins

222
Q

diagnosis & treatment for shigella

A

Diagnosis/treatment: stool culture; treat: fluid replacement, abx

223
Q

other notes about pseudomonas aeruginosa

A

Other Notes: produces blue/green pigment & fruity odor; affects diabetics, burn victims, IV drug users; catheter/UTI infections; hot tub folliculitis; ecythema gangrenosum

224
Q

encounter/entry of klebsiella

A

Encounter/ Entry: often intro by medical manipulation (IV, cath); normal GI flora

225
Q

how does bacillus anthracis establish infection

A

Establish Infection: capsule (poly D glutamic- protein); 3-part protein toxin (both toxins have to be present): protective factor, edema factor (increase cAMP), lethal factor –> works anti-inflammatory response

226
Q

multiplication/damage of chlamydia pneumoniae

A

Multiplication/damage: type III secretion; induce inflammation

227
Q

common disease types of EHEC

A

EHEC: enterohemorrhagic e coli

Common Disease Types: local damage: hemorrhagic colitis- bloody diarrhea, abdominal pain; systemic (damage kidney, brain): hemolytic uremic syndrome (HUS): hemolytic anemia, thrombocytopenia, renal failure

228
Q

how does neisseria gonorrhoae establish infection

A

Establish Infection: mucosal colonization (women)-attaches to columnar epithelial in cervix ; ascends from cervix (women have higher risk of ascendance)

229
Q

Disease types associated with treponema pallidum

A

Disease Types: SYPHILLIS: chancre ulcer; years after initial infection: chronic infection; gummas; condyloma lata

cause of syphilis

230
Q

enctounter/entry of legionella pneumophila

A

Encounter/Entry: natural parasite of protozoa; inhaled from environmental source (contaminated water aerosolized)

231
Q

other notes about neisseria meningitids

A

Other Notes: growth on VPN agar & chocolate agar’ oxidase positive

232
Q

encounter/entry of mycobacteria tuberculosis

A

Encounter/ Entry: infectious aerosols, reach alveoli; interacts with alveolar macrophage

233
Q

multiplication/tissue damage of vibrio cholerae

A

Multiplication/Tissue Damage: enterotoxin ; biofilm; adhesins

234
Q

how does clostridium perfringens spread/cause damage?

A

Spread/Damage: toxin continues to kill tissue (gas gangrene develops); toxin can form short term food poisoning

235
Q

Immunization for haemophilus influenzae?

A

Immunization: capsular conjugate vaccine (to form antibodies to type B capsule); bound to diphtheria toxoid vaccine

236
Q

encounter/entry of ETEC

A

ETEC: enterotoxigenic e coli

Encounter/ Entry: contaminated food/water; adheres to epithelium via pili

237
Q

multiplication/damage of brucella

A

Multiplication/damage: noncaseating granulomas; can cause systemic disease; spreads through RES

238
Q

common disease types of mycobacterium leprae

A

Common Disease Types: Leprosy ( Hansen’s Disease): tuberculoid leprosy: well demarcated hairless lesions/plaques- small amts of bacteria; well formed granulomas; lepromatous leprosy: glove & stocking neuropathy (in extremities);lesions on extensor surfaces- large amts of bacteria; leonine facies

239
Q

common disease types of ETEC

A

ETEC: enterotoxigenic e coli

Common Disease Types: “traveler’s” diarrhea; watery diarrhea; self-limited

240
Q

bartonella henselae

A

Description: gram negative (but need silver stain to visualize)

Pathology: cat scratch disease: fever, axial lymphnodes; bacillary angiometosis: fevers, chills, HA; raised red vascular lesions; both caused by cat scratch

241
Q

common disease types of mycobacteria tuberculosis

A

Common Disease Types: TB; Many outcomes after infection (infection is not the same as active disease): Acute Infection (pre-symptomatic); stable control of infection (latent) (never symptoms, skin test positive- Cell-mediated immunity-CD4T cells & granuloma); primary disease (pathology after months); latent can be reactivated;Miliary TB disseminated to body, lesions look like millet seeds) ;active TB (caseous necrosis of granuloma)

242
Q

transmission of neisseria gonorrhoeae

A

Transmission: human only host (asymptomatic infection possible); sexually transmitted

243
Q

how to diagnose a clostridium difficile infection?

A

Detection: toxin in feces

244
Q

how is streptococcus pyogenes spread/cause damage?

A

Spread/Damage: skin infection remains localized; deep infections spread quickly– M proteins & hyaluronic acid capsule prevent phagocytosis; beta-hemolysis

245
Q

treponema pallidum

A

Description: no gram stain (although seen with dark staining); spirochete

Encounter/Entry: human is only known host—enters mucous membranes or small abrasions in skin via sexual contact

Establish infection: local infection (primary syphilis); motile

Multiplication/spread: infection can spread systemically; lipoproteins induce cytokines (damage caused is due to inflammatory respone)

Disease Types: SYPHILLIS: chancre ulcer; years after initial infection: chronic infection; gummas; condyloma lata

Transmission: human-human; close sexual contact; can transmit mother-fetus if mother has bacteremia

Host Defense: can evade immunity (waxy coat); induces prostaglandin E2; resists phagocutosis

Diagnosis: through PCN

246
Q

EAEC: enteroaggregative e. coli

A

Description: gram negative, rod, facultative anaerobe, no toxins

Encounter/ Entry: fimbriae, serine protease , puts dispersin coat on host cells

Establish Infection: stacked brick pattern of adherence to epithelial cells

Common Disease Types: can systemically cause HUS ; “traveler’s diarrhea;” diarrhea in HIV patients ; inflammatory diarrhea

Other Notes: often found with traveler’s diarrhea; recently discovered

247
Q

other notes about francisella tularenis

A

Other Notes: a lot on Martha’s Vineyard (often associated with yardworkers- survive in soil/animal carcas– if run over with lawnmower, can aerosolize)

248
Q

how does streptococcus pyogenes infect?

A

Infection: M protein promotes adherence extracellularly, colonizes

249
Q

description of escherichia coli

A

Description: gram negative rod; facultative anaerobe; LPS exotoxin **serotyping antigens is helpful for pathogenic straings (antigens: O, H, K)

250
Q

how does bacteroides fragilis establish infection?

A

Establish Infection: synergy in polymicrobial infections; often form abscesses

251
Q

K1 e. coli

A

Description: (E COLI) gram negative rod, facultative anaerobe

Establish Infection: identical K1 capsule as group B meningococcal

Common Disease Types: can pass to fetus to cause neonatal meningitis & bacteremia

Transmission: many women carry K1 in vaginal tract

252
Q

Transmission of neisseria meningitidis

A

Transmission: human only host (asymptomatic carriage), easily spread in close quarters

253
Q

other notes about ETEC

A

ETEC: enterotoxigenic e coli

Other Notes: like less virulent v. cholerae (heat-labile toxin)

254
Q

bacillus anthracis

A

Description: gram positive rods (in chains); obligate aerobe; spore-former (2 toxins: Lethal Factor & Edema Factor); since makes spores– biothreat

Encounter/ Entry: no direct transmission between humans; only spores can inititate infection (via ingestion, inhalation or thru skin breaks)

Establish Infection: capsule (poly D glutamic- protein); 3-part protein toxin (both toxins have to be present): protective factor, edema factor (increase cAMP), lethal factor –> works anti-inflammatory response

Multiplication/Tissue Damage: toxin Edema Factor: increase cAMP, cause edema and inhibit phagocytosis; Lethal Factor acts as protease; causes necrosis (seen in eshcar)

Common Disease Types: 3 forms of anthrax: cutaneous: rarely fatal; eschar/lesions; gastrointestinal:intestinal hemorrhage inhalation: associated with sheep wool (Wool Sorter’s Disease); high mortality; widened mediastinum on CXR; hemorrhagic mediastinitis, hemorrhagic meningitis

Transmission: normal pathogen of grazing ungulates (encountered in soil)– cause a lot of bleeding so that in nature, can exit host as blood & sporulate; **can be aerosolized (biothreat)

Host Defense: inflammation suppressed

Diagnosis/treatment: abx for cutaneous; diffucult to treat pulmonary (fluoroquinolones, doxy)

255
Q

how does rickettsia rickettsi establish infection

A

Establish Infection: pathogen of endothelium- spread by ticks, lysis of vascular endothelium (lead to leaky vessels), use host actin to provide motility & transfer to other cells

256
Q

transmission of enterococcus

A

Transmission: part of normal fecal flora of humans & animals; often spread by healthcare workers

*VRE (vancomycin resistant enterococci) has been established

-bile resistant

257
Q

encounter/entry of helicobacter pylori

A

Encounter/ Entry: commensal of human stomach

258
Q

transmission of helicobacter pylori

A

Transmission: pathogen/commensal of human stomach (pylorus); gastric-oral/fecal-oral/oral-oral

259
Q

description of bordetella pertussis

A

Description: gram negative coccobacillus, aerobe, 3 exotoxins: pertussis toxin, adenylate cyclase; tracheal cytotoxin

260
Q

streptococcus pyogenes

A

aka: Group A Strep

Description: gram positive cocci in chains, no spores, anaerobe, exotoxins

Encounter: person-person via droplets

Infection: M protein promotes adherence extracellularly, colonizes

Spread/Damage: skin infection remains localized; deep infections spread quickly– M proteins & hyaluronic acid capsule prevent phagocytosis; beta-hemolysis

Transmission: lives on human skin & in mucous membranes

Treatment: penicillin, beta lactams, clinda, macrolides

  • Pyogenic Infections:* impetigo, pharyngitis, cellulitis, erysypilis
  • Toxigenic effects (streptogenic exotoxin):* scarlet fever, strep TSS, necrotizing fasciitis
  • Complications after infection:* Rheumatic Fever, glomerulonephritis
261
Q

common disease types of bacillus anthracis

A

Common Disease Types: 3 forms of anthrax: cutaneous: rarely fatal; eschar/lesions; gastrointestinal:intestinal hemorrhage inhalation: associated with sheep wool (Wool Sorter’s Disease); high mortality; widened mediastinum on CXR; hemorrhagic mediastinitis, hemorrhagic meningitis

262
Q

clostridium perfringens

A

Description: gram positive rod, anaerobe, tissue damaging exotoxin, spore forming

*only clostridium with a capsule

Encounter: contamination of wound (especially after abdominal surgery)

Infection: alpha toxin hydrolyzes cell membranes

Spread/Damage: toxin continues to kill tissue (gas gangrene develops); toxin can form short term food poisoning

Transmission: common in soil, intestinal flora

Treatment: debridement, hyperbaric chamber

263
Q

encounter/entry of brucella

A

Encounter/entry: ingestion (usually unpasteurized dairy product)/direct contact with animal

264
Q

encounter/entry of yersinia pestis

A

Encounter/ Entry: human-human when aerosolized; bite of infected fleas (vector/arthropod)

265
Q

how does campylobacter jejuni affect host defense

A

Host Defense: resistant to antibodies & complement

266
Q

how does clostridium botulinum spread/cause damage?

A

Spread/Damage: all pathogenic effects are due to botulinum toxin (inhibits nerve conduction at cholinergic synapses)– flaccid paralysis

267
Q

multiplicaiton/tissue damage from francisella tularenis

A

Multiplication/Tissue Damage: enters through ulcer, goes into macrophages, goes thru lymph to RES organs & causes granulomas with caseating necrosis (palpable lymph nodes)

268
Q

transmission of staph epidermidis

A

Transmission: normal skin flora

269
Q

transmission of salmonella enterica

A

Transmission: enteric bacteria (colonizer) - but NOT component of human normal flora; food-human (can be human-human)

270
Q

how does borrelia burgdorferi cause damage/spread?

A

Multiplication/Tissue Damage: binds to plasminogen; inhibits complement; disseminates through blood stream (induces inflammatory response)

cause of Lyme Disease

271
Q

transmission of clostridium perfringens?

A

Transmission: common in soil, intestinal flora

272
Q

Neisseria meningitidis

A

Description: gram negative diplococcic, facultative intracellular

Encounter/ Entry: human only host; enter through upper respiratory tract(requires close contact) ; pili and opa mediated attachment

Establish Infection: mucosal colonization in pharynx, spread systemically & to lower respiratory tract & can cross blood-brain barrier (meningitis); capsule; makes IgA protease; iron acquisition

Multiplication/Tissue Damage: inflammation–> leaky capillaries; meningococcemia; meningitis, bacteremia;able to survive in bloodstream; can lead to shock; phase & antigenic variation

Common Disease Types: asymptomatic carriers spread the disease; Waterhouse-Friederichson Syndrome (adrenal hemorrhage); common to see petichiae rash (due to hemorrhage); one of principle bacterial agents of CNS disease; can cause otitis media, conjunctivitis,s eptic arthritis, urethritis, purulent pericarditis

Transmission: human only host (asymptomatic carriage), easily spread in close quarters

Other Notes: growth on VPN agar & chocolate agar’ oxidase positive

Diagnosis/treatment: prohylaxis of exposed (abx- rifampin) can be preventive; treatment with ceftriaxone

Vaccination: vaccine (type B capsule not included)

273
Q

description of brucella

A

Description: gram negative, coccobacillus, facultative intracellular

274
Q

encounter/entry of bacillus anthracis

A

Encounter/ Entry: no direct transmission between humans; only spores can inititate infection (via ingestion, inhalation or thru skin breaks)

275
Q

how does clostridium difficile infect?

A

Infection: toxin kills epithelium

276
Q

transmission of listeria monocytogenes

A

Transmission: can contaminate refrigerated food (milk, soft cheese, meat); also in stool

277
Q

common disease types of salmonella enterica

A

Common Disease Types: gastroenteritis (salmonellosis)- most common foodborne illness in US-inflammatory diarrhea (leukocytes in stool), enteric (typhoid) fever– only human-human pathogen, rose spots; sustained bacteremia (vascular infection), often in aorta; #1 cause of osteomyelitis in sickle cell disease; pea soup diarrhea

278
Q

how does mycoplasma pneumoniae multiply/cause damage?

A

Multiplication/tissue damage: no capacity for invasive disease; blocks ciliary action; mononuclear (monocyte) infiltrate – typical pneumonia show neutrophil infiltrate ;IgM Cold agglutinins

279
Q

treatment of EHEC

A

Diagnosis/treatment: supportive treatment for HUS; thoroughly cook meet

280
Q

description of staphlococcus epidermidis

A

Description: gram positive, clusters of cocci

281
Q

Encounter/entry of chlamydia pneumoniae

A

Encounter/Entry: aerosols from coughing

282
Q

Other notes regarding chlamydia trachomatis

A

Notes: bacteria exist as elementary (transmissable/infectious) form and reticular form (replicative within cells); cell wall lacks muramic acid

283
Q

transmission of streptococcus agalactia

A

Transmission: in normal flora of vagina; spread to babies during delivery, can cause sepsis

-bacitracin resistant, B-hemolytic

284
Q

clostridium tetani

A

Description: gram positive, rod, anaerobe, neurotoxic exotoxin + spores

Encounter: infection via contamination of wound

Infection: tissue damage/anaerobic encourages germination & growth

**spastic paralysis, lockjaw, opisthotonis

Spread/Damage: all of symptoms are due to toxin inhibitin interneurons & relaxation signals

Transmission: common in soil, spores survive for years

Immunization: Tdap toxoid

285
Q

multiplication/tissue damage of shigella

A

Multiplication/Tissue Damage: releases cytokines (type III secretion system); bloody/inflammatory diarrhea; shigatoxin inhibits translation (60s); inflammatory response

286
Q

common disease types of francisella tularenia

A

Common Disease Types: tularemia; variable based on route of transmission; fever, chills, fatigue, HA, sore joints, diarrhea, lymphadenopathy

287
Q

how does staphylococcus aureus spread & cause damage?

A

Damage/Spread: B-hemolysis, IgG binding protein A in cell wall; secretes antigens

**catalase positive, coagulase positive (latex assay, clumping factor, Protein A)

288
Q

description of treponema pallidum

A

Description: no gram stain (although seen with dark staining); spirochete

cause of syphilis

289
Q

transmission of corynebacterium diphtheriae

A

Transmission: only reservoir: throat of man

290
Q

how does streptococcus pneumoniae infect host?

A

Infection: antiphagogenic capsule, alpha hemolysis, pneumolysis breaks pore in host tissue

291
Q

diagnosis/treatment for bacillus anthracis

A

Diagnosis/treatment: abx for cutaneous; diffucult to treat pulmonary (fluoroquinolones, doxy)

292
Q

multiplication/tissue damage of e coli

A

Multiplication/Tissue Damage: #1 cause UTI, #1cause gram negative sepsis; neonatal meningitis due to bacteremia in infants

293
Q

diagnosis/treatment of neisseria gonorrhoea

A

Diagnosis/treatment: ceftriaxone (but also administer macrolide or doxy to cover chlamydia too)

294
Q

mycobacterium leprae

A

Description:gram positive & acid fast (mycolic acid in waxy coat) rod; aerobe

Encounter/ Entry: human-human; nasal secretions

Establish Infection: tuberculoid leprosy: within macrophages (strong TH1 response); lepromatous leprosy: (TH2 cells involved)bacteria not maintained in macrophage

Common Disease Types: Leprosy ( Hansen’s Disease): tuberculoid leprosy: well demarcated hairless lesions/plaques- small amts of bacteria; well formed granulomas; lepromatous leprosy: glove & stocking neuropathy (in extremities);lesions on extensor surfaces- large amts of bacteria; leonine facies

Transmission: human-human; nasal secretions; main reservoir is the armadillo in the US, grows in footpads of immunodeficient mice too

Host Defense: 2 forms of leprosy solely based on host immune respone: tuberculoid form (pacudibacillary): few bacteria, abudant lymphocytes with well-formed granuloma vs lepromatous form (multibacillary) with numerous bacteria, few lymphocytes, without well-fromed granuloma; inflammatory T cells & macrophages are critical host response

Other Notes: thrives in cold temps (explains why it favors extremities)

Diagnosis/treatment: lepromin skin test; treatment: multidrug therapy tuberculoid: dapsone & rifampin 6 months; lepromatous: these 2 + clofazamine for 2-3 years

295
Q

how does shigella establish infection?

A

Establish Infection: invades M cell; not motile, taken into vacuole & dissolves- is in cytoplasm and invades neighbor cells

296
Q

transmission of haemophilus influenzae

A

Transmission: human only known host (aerosol transmission)

297
Q

how does treponema pallidum multiply/spread?

A

Multiplication/spread: infection can spread systemically; lipoproteins induce cytokines (damage caused is due to inflammatory response)

cause of syphilis

298
Q

common disease types of e coli

A

Common Disease Types: E coli is most frequent cause of UTI (UPEC species); also cause neonatal meningitis

299
Q

other notes about klebsiella

A

Other Notes: mutli-drug resistance (some produce extended spectrum beta lactamase ESBL); ferment lactose; urease positive

300
Q

how does salmonella enterica establish infection

A

Establish Infection: invades epithelium via membrane ruffles & type III secretion system; remains in phagosomes; capsule, motile

301
Q

multiplication/damage from listeria monocytogenes

A

Multiplication/Tissue Damage: damage due to host resposne; spread via blood & macrophages

302
Q

how does legionella penumohpila establish infection

A

Establish Infection: establishes niche in lung; interacts & grows within macrophage in alveoli; modifies phagosome (delays phagosome/lysosome fusion)

303
Q

description of borrelia burgdorferi

A

Description: spirochete

cause of Lyme Disease

304
Q

description of legionella pneumophila

A

Description: gram negative (need silver stain to see); bacillus

305
Q

francisella tularenis

A

Description: gram negative coccobacillus, facultative intracellular; **biothreat

Encounter/ Entry: no direct transmission between humans; ticks/rabbits- tick bite causes ulcer

Establish Infection: short survival in air but low dose required for infection; highly invasive

Multiplication/Tissue Damage: enters through ulcer, goes into macrophages, goes thru lymph to RES organs & causes granulomas with caseating necrosis (palpable lymph nodes)

Common Disease Types: tularemia; variable based on route of transmission; fever, chills, fatigue, HA, sore joints, diarrhea, lymphadenopathy

Transmission: occurs in many animals (main reservoir: rabbit); direct contact with infected mammals; bites of infectious arthropods-tick (dermacentor) (no person to person); can be aerosolized (warfare)

Host Defense: cell-mediated immunity (T cells) necessary to clear intracellular infection

Other Notes: a lot on Martha’s Vineyard (often associated with yardworkers- survive in soil/animal carcas– if run over with lawnmower, can aerosolize)

Diagnosis/treatment: treat: aminoglycoside (streptomycin)

306
Q

how is streptococcus pyogenes encountered?

A

Encounter: person-person via droplets

307
Q

haemophilus influenzae

A

(most importantly: encapsulated type B- Hib)

Description: gram negative coccobacillus

Encounter: mucosal colonization in nasopharynx via respiratory secretion droplets

Infection: attaches to epithleium, uses IgA protease to fend off immune response, LPS initiates immue response, capsule protects

Spread/Damage; local infection: sinusitis, otitis media, epiglottitis

systemic: capsule, LPS causes proinflammatory damage (most damage due to inflammatory response)

Transmission: human only known host (aerosol transmission)

Immunization: capsular conjugate vaccine (to form antibodies to type B capsule); bound to diphtheria toxoid vaccine

Treatment: beta lactams (rifampic for prophylaxis for close contacts)

308
Q

notes about EIEC

A

enteroinvasive e coli

Other Notes: think of as less virulent shigella

309
Q

other important points with legionella pneumophila

A

Other notes: oxidase positive; 2 forms: exponential phase (nonvirulent, just growing); post-exponential phase (virulent)

310
Q

common disease types of brucella

A

Common disease types: undulant fever; anorexia, liver & splenic involvement; osteomyeltis;

311
Q

legionelle pneumonphila

A

Description: gram negative (need silver stain to see); bacillus

Encounter/Entry: natural parasite of protozoa; inhaled from environmental source (contaminated water aerosolized)

Establish Infection: establishes niche in lung; interacts & grows within macrophage in alveoli; modifies phagosome (delays phagosome/lysosome fusion)

Multiplication/Tissue Damage: elicits intense host response (immune mediated damage); type IV secretion system; doesn’t spread outside of lung

Common Disease Types: Legionaires: walking pneumonia, patchy CXR with consolidation in one lobe, paired with diarrhea, hyponatremia, neuro symptoms (HA/confusion); pontiac fever

Transmission: outbreaks (Classic Legionaire’s in 1976)

Host Response: host response/ inflammation is much of damage

Other notes: oxidase positive; 2 forms: exponential phase (nonvirulent, just growing); post-exponential phase (virulent)

Treatment/Diagnosis: urine antigen tests for dx; often treat upon suspicion; macrolides, fluoroquinolone

312
Q

common disease types of pseudomonas aeruginosa

A

Common Disease Types: otitis externa, hot tub dermatitis/folliculitis, endocarditis (esp IV drug users); keratitis, bone & joint infections; CF much more susceptible; NOSOCOMIAL INFECTIONS; sneaker osteomyelitis (especially in diabetic); often complication of burn injuries; number one cause of nosicomial pneumonia; respiratory failure in CF

313
Q

how does pseudomonas aeruginosa establish infection?

A

Establish Infection: capsule & tight outer membrane; toxin ribosylates target- inhibits protein synthesis; type III secretions

314
Q

transmission of ETEC

A

ETEC: enterotoxigenic e coli

Transmission: enteric bacteria; transmitted via water (Mexico)

315
Q

how is staph epidermidis encountered

A

Encounter: normal skin flora (only pathogenic if on foreign body)

316
Q

how is host defense involved in neisseria gonorrhea infection

A

Host Defense: barriers of cervical infection: cervical canal, mucus plug, hormones

317
Q

encounter/entry of shigella

A

Encounter/ Entry: enters cytoplasm, invade COLON epithelium & destroy (basolateral surface)

318
Q

multiplication/tissue damage of helicobacter pylori

A

Multiplication/Tissue Damage: persistent infection (infeced for decades); urease; non-inflammatory LPS sometimes

319
Q

description of streptococcus agalactiae

A

aka Group B Strep

Description: gram positive cocci in chains, anaerobic

320
Q

diagnosis/treatment of vibrio cholerae

A

Diagnosis/treatment: Therapy: REHYDRATE (fluid & K loss; glucose & Na); IV Ringer sol’n; Abx: tetracycline & fluoroquinolones

321
Q

common disease types of helicobacter pylori

A

Common Disease Types: chronic gastritis, cause of most duodenal ulcer, gastric ulcer; risk for gastric adenocarcinoma & MALToma

322
Q

treatment of chlamydia penumoniae

A

Treatment: doxy

323
Q

cother notes about rickettsia rickettsi

A

Other notes: geography plays a role- most prevalent in southeast US

324
Q

how does clostridium botulinum infect?

A

Infection: most cases, no live bacteria involved

(ingestion)

325
Q

host defense involved in EHEC infection

A

EHEC: enterohemorrhagic e coli

Host Defense: mostly secretory issues not involving inflammatory response

326
Q
A
327
Q

encounter/entry of vibrio cholerae

A

Encounter/ Entry: contaminated water/food; fecal-oral

328
Q

description of Klebsiella

A

Description: gram negative rod

329
Q

description of enterococcus

A

aka Group D Strep

Description: gram positive, cocci that form short chain, anaerobic

330
Q

common disease types of campylobacer jejuni

A

Common Disease Types: boody diarrheal disease, gastroenteritis, post-infectious sequelae: Guillain-Barre syndrome (demyelination of nerves– ascending paralysis), reactive arthritis

331
Q

common symptoms of EIEC

A

EIEC: enteroinvasive e. coli

Common Disease Types: diarrhea, fever, dysentery

332
Q

transmission of psuedomonas aeruginosa

A

Transmission: thrives in aquatic environments; found in soil; occasionally on skin: ear canal; hot tubs, sneakers

333
Q

encounter/entry of e. coli

A

Encounter/ Entry: fecal-oral; doesn’t enter cytoplasm; pili, hemolysin,

334
Q

clostridium botulinum

A

Description: gram positive rod, anaerobic, neurotoxic exotoxin, spore-forming

Encounter: infants: spores in food (honey); adults: toxin in food (canned or seafood)

Infection: most cases, no live bacteria involved

Spread/Damage: all pathogenic effects are due to botulinum toxin (inhibits nerve conduction at cholinergic synapses)– flaccid paralysis

Transmission: ingested

335
Q

multiplication/damage of EHEC

A

EHEC: enterohemorrhagic e coli

Multiplication/Tissue Damage: remains localized in intestine (doesn’t cause bacteremia); shiga toxin damage cells by inhibiting protein synthesis

336
Q

description of streptococcus pyogenes

A

aka: Group A Strep

Description: gram positive cocci in chains, no spores, anaerobe, exotoxins

337
Q

encounter/entry of mycobacterium leprae

A

Encounter/ Entry: human-human; nasal secretions

338
Q

other notes about vibrio cholerae

A

Other Notes: bile salt resistant (able to survive in GI tract); oxidase positive

339
Q

description of rickettsia ricketsii

A

Description: gram negative (but poorly stained), coccobacillus, obligate intracellular

340
Q

multiplication/tissue damage of legionella pneumophila

A

Multiplication/Tissue Damage: elicits intense host response (immune mediated damage); type IV secretion system; doesn’t spread outside of lung

341
Q

multiplication/tissue damage of salmonella enterica

A

Multiplication/Tissue Damage: strong inflammatory response & type III secretions; recruit neutrophils); thypoid: seeding of gall bladder –> common shedding/infection

342
Q

how is streptococcus pyogenes trasnmitted?

A

Transmission: lives on human skin & in mucous membranes

INF: Infections (5 decks)

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