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Microbiology - Quiz 2 > ALL BACTERIA! > Flashcards

ALL BACTERIA! Flashcards

1
Q

Salmonella (general): Similar to

A

Shigella, E coli (Enterobacteriaceae Family)

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2
Q

Enteroaggregative E. coli (EAEC): Similar to

A

EPEC

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3
Q

Acinetobacter baumanii: At Risk

A

Hospitals

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4
Q

Acinetobacter baumanii: Disease

A

OPPORTUNIST!

Nosocomial infections

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5
Q

Acinetobacter baumanii: Gram stain

A

-

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6
Q

Acinetobacter baumanii: Negative for: (2)

A

Oxidase

Sugar fermentation

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7
Q

Acinetobacter baumanii: Oxygen

A

aerobe

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8
Q

Acinetobacter baumanii: Reservoir

A

Hospital

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9
Q

Acinetobacter baumanii: Shape

A

short rod

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10
Q

Acinetobacter baumanii: Transmission/vector/ habitat

A

Indwelling medical devices

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11
Q

Acinetobacter baumanii: Treatment

A

Multidrug resistant

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12
Q

Acinetobacter baumanii: Virulence Factors (4)

A

Capsular polysaccharides
Adhesins
Proteolytic/lipolytic enzymes
LPS

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13
Q

Bordetella pertussis: At Risk

A

Infants more likely to die

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14
Q

Bordetella pertussis: Diagnosis (3)

A

Contact history, classic cough, lymphocytosis

**Requires fresh, Bordetella-optimized media for growth (not typically used)

PCR for repeat insertion sequences

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15
Q

Bordetella pertussis: Disease

A

Pertussis (whooping cough)

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16
Q

Bordetella pertussis: Epidemiology

A

Major childhood killer pre-1940
–Highest fatality of all among children before vaccine!

Re-emerging now: waning immunity, Agic divergence, decreased vaccination

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17
Q

Bordetella pertussis: Gram stain

A

-

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18
Q

Bordetella pertussis: Incubation Period

A

7-10 days

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19
Q

Bordetella pertussis: Oxygen

A

Obligate aerobe

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20
Q

Bordetella pertussis: Pathogenesis (6 steps)

A
  1. intro via water droplets
  2. interact w/ciliated epithelial cells (trachea/nasopharynx)
  3. adherence
  4. multiplication/toxin production -> local inflammation, mucous secretion, patchy ulcers, cyanosis, pneumonia
  5. host evasion
  6. spread
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21
Q

Bordetella pertussis: Reservoir

A

NONE - only infects humans

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22
Q

Bordetella pertussis: Shape

A

coccobacilli

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23
Q

Bordetella pertussis: Symptoms

A

[Catarrhal stage] runny nose, sneezing, low-grade fever, mild cough

[Paroxysmal stage] whooping cough, vomiting, cyanosis

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24
Q

Bordetella pertussis: Transmission/vector/habitat

A

Aerosol

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25
Q

Bordetella pertussis: Treatment

A

Treat for hypoxia
Erythromycin (alt: tetracycline or chloramphenicol)
–Resistant to penicillin and ampicillin

Treat household contacts prophylactically

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26
Q

Bordetella pertussis: Vaccine

A

DTP (trivalent): side-effects - encephalopathy and permanent neurologic sequelae (not used anymore)

DTaP (acellular trivalent component) introduced mid-90s
-> contains pertussis toxin, FHA, pertactin, and fimbrae

NO lifelong immunity

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27
Q

Bordetella pertussis: Virulence Factors (6)

A

PERTUSSIS TOXIN (inhibits Gi for adenylate cyclase -> adenylate cyclase activated -> cAMP accumulation -> lymphocytosis, histamine-sensitivity, enhanced insulin secretion)

ADENYLATE CYCLASE toxin (catalyzes cAMP from ATP -> impaired leukocyte function and apoptosis)

DERMONECROTIC toxin (VSM contraction => ischemic necrosis of lung tissue)

TRACHEAL CYTOTOXIN (CILIOSTASIS, kills tracheal epithelial cells, proinflammatory)

Endotoxin (LPS)

Several adhesins: pili, Filamentous hemagglutinin, Pertactin, Tracheal colonization factor (-> colonization)

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28
Q

Campylobacter (jejuni): At Risk (3)

A

Infants to young adults in developed
Infants in developing
Immunocompromised, esp. with humoral immunodeficiency (severe)

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29
Q

Campylobacter (jejuni): Diagnosis (4)

A

Gm stain stool specimen
Enrich with filters (very small)
Hippurate positive (very diagnostic)
Culture at 42C in microaerophilic conditions (body temp of poultry)

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30
Q

Campylobacter (jejuni): Disease (2)

A

Diarrhea from inflammatory enteritis

Bacteremia (rare)

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31
Q

Campylobacter (jejuni): Epidemiology (3)

A

MOST COMMON cause of diarrhea in the world

Typically sporadic cases
Multiple simultaneous cases usually point to common contaminated source

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32
Q

Campylobacter (jejuni): Gram stain

A

-

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33
Q

Campylobacter (jejuni): Incubation Period

A

3-5 days

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34
Q

Campylobacter (jejuni): Infectious dose

A

Low infectious dose (500 = 1 drop of raw chicken juice)

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35
Q

Campylobacter (jejuni): Oxygen

A

microaerophilic

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36
Q

Campylobacter (jejuni): Pathogenesis (3 steps)

A
  1. survive gastric barrier
  2. arrive in small/large bowel - inflammation
  3. bloodstream (rare)
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37
Q

Campylobacter (jejuni): Prevention (2)

A

Pasteurization of milk, cooking meat (esp. poultry)

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38
Q

Campylobacter (jejuni): Reservoir

A

Animals (esp. poultry -does not make animals sick)

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39
Q

Campylobacter (jejuni): Shape

A

curved or comma with uni or bipolar flagellum

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40
Q

Campylobacter (jejuni): Symptoms

A

Prodrome (fever, malaise, headache)

fever; abd. pain; diarrhea (few days to a week)

Complications = autoimmunity to nerves (Guilliam-Barre syndrome)

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41
Q

Campylobacter (jejuni): Transmission/vector/ habitat (3)

A

Food (esp. raw chicken), milk, or water

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42
Q

Campylobacter (jejuni): Treatment

A

Oral rehydration therapy

Antimicrobial therapy as indicated (erythromycin; alt - cipro)

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43
Q

Chlamydophilia (general): Diagnosis (4)

A

General Diagnosis

  1. Check for group antigen
  2. Compare acute and convalescent Ab titers
  3. Direct fluorescent Ab exam of appropriate clinical specimens
  4. PCR
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44
Q

Chlamydophilia (general): Gram stain

A

Gm- (by phylogeny)

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45
Q

Chlamydophilia (general): Life Cycle (forms, 3 steps)

A

Elementary Bodies (EB): small, non-multiplying, with a rigid bacterial-like cell wall -> transmits infection

Initial Bodies (IB) [aka reticulate bodies (RB)]: larger, actively multiplying, lack rigid wall, non-infectious

Intracellular growth

  1. EB enter by inducing host phagocytosis (even in non-phagocytotic cells)
  2. EB lose cell wall during first 24h, double in diameter, and synthesize RNA to yield IB
  3. IB divide by binary fission -> some progeny converted back to EB
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46
Q

Chlamydophilia (general): Shape

A

pleomorphic

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47
Q

Chlamydophilia (general): Special growth conditions

A

OBLIGATE intracellular (canNOT make ATP => depends on host ATP)

EB -> IB (RB) in host cell -> divide -> host cell dies and release EBs

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48
Q

Chlamydophilia (general): Treatment

A

Tetracyclines are effective but single high dose azithromycin may be more indicated

Any antibiotic used must enter cells

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49
Q

Chlamydophilia pneumoniae: Diagnosis

A

Antibody assay

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50
Q

Chlamydophilia pneumoniae: Disease

A

Atypical (diffuse) pneumonia

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51
Q

Chlamydophilia pneumoniae: Epidemiology (2)

A

Causes 10% of pneumonia in adults

May play a role in coronary atherosclerosis

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52
Q

Chlamydophilia pneumoniae: Number of serotypes

A

1 serotype

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53
Q

Chlamydophilia pneumoniae: Symptoms (3)

A

Pneumonia/bronchitis
Gradual onset of cough
Little/no fever

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54
Q

Chlamydophilia pneumoniae: Transmission/vector/ habitat

A

Person-to-person via aersol

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55
Q

Chlamydophilia psittaci: At Risk

A

Contact w/birds

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56
Q

Chlamydophilia psittaci: Diagnosis (2)

A

Pathogen in blood or sputum

Antibody assay

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57
Q

Chlamydophilia psittaci: Disease

A

Psittacosis (parrot fever)

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58
Q

Chlamydophilia psittaci: Number of serotypes

A

1 serotype

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59
Q

Chlamydophilia psittaci: Pathogenesis

A

Disseminated infection that targets epithelial cells, endothelial cells, Mos

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60
Q

Chlamydophilia psittaci: Reservoir

A

Birds (induces chronic subclinical infection with constant fecal excretion)

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61
Q

Chlamydophilia psittaci: Symptoms (3)

A

Fever and headache

Severe -> interstitial pneumonia

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62
Q

Chlamydophilia psittaci: Transmission/vector/ habitat

A

Inhalation of bird feces

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63
Q

Chlamydia trachomatis, serotypes L1-3: Diagnosis

A

Ag testing to differentiate between C. trachomatis serotypes

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64
Q

Chlamydia trachomatis, serotypes L1-3: Disease

A

Lymphogranuloma venereum

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65
Q

Chlamydia trachomatis, serotypes L1-3: Symptoms (2)

A

Painless papule progresses to ulcerating vesicle (2 weeks post-exposure)
Can -> painful suppurating disease of regional lymph nodes

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66
Q

Chlamydia trachomatis, serotypes L1-3: Transmission/vector/ habitat

A

STD

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67
Q

Chlamydia trachomatis, serotypes A-C: At Risk (2)

A

Poor hygiene

Asia and Africa

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68
Q

Chlamydia trachomatis, serotypes A-C: Diagnosis (1)

A

Ag testing to differentiate between C. trachomatis serotypes

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69
Q

Chlamydia trachomatis, serotypes A-C: Disease

A

Trachoma (chronic conjunctivitis)

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70
Q

Chlamydia trachomatis, serotypes A-C: Epidemiology (1)

A

World’s leading cause of preventable blindness

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71
Q

Chlamydia trachomatis, serotypes A-C: Pathogenesis

A

Chronic conjunctival reinfection causes infolding of eyelashes => corneal scarring and blindness

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72
Q

Chlamydia trachomatis, serotypes A-C: Prevention (4)

A

Surgery, prophylactic antibiotics, facial cleanliness, environmental improvements/sanitation

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73
Q

Chlamydia trachomatis, serotypes A-C: Special Features: Intra vs extracellular, presence of capsule, invasive or not

A

More invasive serotypes

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74
Q

Chlamydia trachomatis, serotypes A-C: Symptoms (5)

A 
Cloudy cornea
Discharge from eye
Swelling of lymph nodes in front of ears
Swollen eyelids
Turned-in eyelashes
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75
Q

Chlamydia trachomatis, serotypes A-C: Transmission/vector/ habitat (2)

A

Mechanical (finger to eye)

Flies

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76
Q

Chlamydia trachomatis, serotypes A-C: Treatment

A

Annual universal treatment with azithromycin

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77
Q

Chlamydia trachomatis, serotypes D-K (perinatal): At Risk

A

Neonates

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78
Q

Chlamydia trachomatis, serotypes D-K (perinatal): Diagnosis (1)

A

Ag testing to differentiate between C. trachomatis serotypes

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79
Q

Chlamydia trachomatis, serotypes D-K (perinatal): Disease (2)

A 
Inclusion conjunctivitis
Infant pneumonia (usually an extension of ocular disease)
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80
Q

Chlamydia trachomatis, serotypes D-K (perinatal): Epidemiology (2)

A

Inclusion conjunctivitis - most common vertically transmitted neonatal disease

Occasionally seen beyond neonatal age where environ. contamination (swimming pools, etc.) is involved

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81
Q

Chlamydia trachomatis, serotypes D-K (perinatal): Symptoms (3)

A

Large lymphoid follicles
Papillary hyperplasia of the conjunctiva
Red, irritable eye with sticky discharge

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82
Q

Chlamydia trachomatis, serotypes D-K (perinatal): Transmission/vector/ habitat (3)

A

Perinatal
Swimming pools
STD

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83
Q

Chlamydia trachomatis, serotypes D-K: Diagnosis (2)

A

Yearly rapid PCR test of urine for sexually active women

Ag testing to differentiate between C. trachomatis serotypes

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84
Q

Chlamydia trachomatis, serotypes D-K: Disease (2)

A

Non-gonoccocal urethritis

More severe -> epididymytis, salpingitis -> infertility

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85
Q

Chlamydia trachomatis, serotypes D-K: Epidemiology (2)

A

Possibly most common venereal disease

Infection increases chance of HIV transmission

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86
Q

Chlamydia trachomatis, serotypes D-K: Symptoms (2)

A

Males: usually asymptomatic (purulent urethral discharge)

Females: frequently asymptomatic

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87
Q

Chlyamydia trachomatis, serotypes D-K: Transmission/vector/habitat

A

STD

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88
Q

Chlamydia trachomatis, serotypes D-K: Treatment (1)

A

Single high dose azithromycin for BOTH sexual partners

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89
Q

Corynebacterium diphtheriae: At Risk (2)

A

Developing countries w/inadequate pediatric immunization and medical care
Travelers (need booster DTaP)

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90
Q

Corynebacterium diphtheriae: Diagnosis (4)

A

Tentative: tellurite agar, Tinsdale’s medium, and Leoffler media (+ for METACHROMATIC GRANULES)

Definitive:

  • -Toxin production (Elek test)
  • -PCR for toxin gene
  • -Immunoassay of serum
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91
Q

Corynebacterium diphtheriae: Disease (1)

A

Diphtheria: infection of skin and/or throat

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92
Q

Corynebacterium diphtheriae: Epidemiology (3)

A

Once a major cause of death in US -> in pre-immunization era, major fraction of pop. were carriers

Epidemics in poorly immunized pop. w/inadequate medical care

Presents as necrotizing skin infection in the tropics -> spread by contact

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93
Q

Corynebacterium diphtheriae: Gram stain

A

!!+++++++!!

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94
Q

Corynebacterium diphtheriae: Incubation Period

A

2-5 days

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95
Q

Corynebacterium diphtheriae: Life Cycle

A

Do NOT form spores!

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96
Q

Corynebacterium diphtheriae: Other

A

All other corynebacteria (diptheroids) are normal inhabitants of our skin/throat

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97
Q

Corynebacterium diphtheriae: Oxygen

A

aerobe

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98
Q

Corynebacterium diphtheriae: Prevention (2)

A

Immunity depends on presence of Ab against toxin (antitoxin)

Give DTaP booster to travelers

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99
Q

Corynebacterium diphtheriae: Reservoir

A

NONE - only infects humans

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100
Q

Corynebacterium diphtheriae: Shape

A

rod
club-shaped
(pleomorphic)

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101
Q

Corynebacterium diphtheriae: Symptoms (3)

A

Fever, cough, sore throat

Gray PSEUDOMEMBRANE formation in severe cases (thrush)

Inflammation of lymph nodes

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102
Q

Corynebacterium diphtheriae: Transmission/vector/habitat

A

Aerosol

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103
Q

Corynebacterium diphtheriae: Treatment (2)

A

Horse antitoxin immediately (hypersensitivity and anaphylactic shock common)

Penicillin prophylactically or as treatment

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104
Q

Corynebacterium diphtheriae: Vaccine

A

Toxoid - DTaP good for 10 years

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105
Q

Corynebacterium diphtheriae: Virulence Factors (1)

A

DIPHTHERIA EXOTOXIN - blocks eukaryotic cell protein synthesis (inactivates EF2) => produces systemic symptoms)

  • -Lethal to eukaryotic cells
  • -Targets heart, kidney, nervous system
  • -Exotoxin has 2 domains which dissociate within endosome - cell surface receptor (B, promotes endocytosis) and toxin domain (A)
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106
Q

Coxiella burnetii: At Risk (2)

A

Exposure to barn animals, especially birth of barn animals

Cardiac vascular disease can increase risk of endocarditis

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107
Q

Coxiella burnetii: Diagnosis (3)

A

Serologic testing for C. burnetii Ags
Indirect immunofluorescence assay (most dependable)
Immunohistochemical staining and DNA detection methods of infected tissues

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108
Q

Coxiella burnetii: Disease (2)

A

Q fever

Can progress to chronic endocarditis

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109
Q

Coxiella burnetii: Gram stain

A

-

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110
Q

Coxiella burnetii: Prevention (4)

A

Dispose of birth products of sheep and goats
Restrict access to barns/labs housing potentially infected animals
Vaccination
Counseling

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111
Q

Coxiella burnetii: Reservoir

A

Sheep and cattle -> tick and so on

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112
Q

Coxiella burnetii: Special growth conditions

A

Obligate intracellular

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113
Q

Coxiella burnetii: Symptoms (5)

A

Intersitital pneumonia, fever, headache, rash (some patients), elevated LFTs

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114
Q

Coxiella burnetii: Transmission/vector/ habitat (2)

A

Inhaling Coxiella from placental tissue (carcass) of sheep or cattle
Spore-like stage transmits the infection

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115
Q

Coxiella burnetii: Treatment (3)

A

Doxycycline
Quinolone Abx

Chronic endocarditis -> aggressive therapy, surgery

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116
Q

Diffuse adhering E. coli (DAEC): At Risk

A

Older children in developing countries

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117
Q

Diffuse adhering E. coli (DAEC): Diagnosis (2)

A

PCR for virulence genes

Tissue culture -> diffuse adherence

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118
Q

Diffuse adhering E. coli (DAEC): Disease

A

Diarrhea

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119
Q

E. coli (general): Diagnosis (7)

A 
Stool samples
Enrich in Gm- broth
PCR -> virulence factors
Toxin analysis
Antigen testing
Tissue culture assay for adherence
Lac +!
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120
Q

E. coli (general): Gram stain

A

-

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121
Q

E. coli (general): Negative for: (1)

A

Oxidase

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122
Q

E. coli (general): Oxygen

A

fac. Anaerobe

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123
Q

E. coli (general): Positive for: (3)

A

Lactose
Glucose (+gas)
Nitrate

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124
Q

E. coli (general): Prevention (2)

A

Grain fed cattle harbor more acid shock resistant E. coli
–Hay feeding leads to a higher pH => lack of adaptation of pathogenic E. coli

Hygiene

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125
Q

E. coli (general): Shape

A

rod

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126
Q

Ehrlichioses: At Risk (1)

A

Exposure to ticks

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127
Q

Ehrlichioses: Disease (2)

A

Monocytic Ehrlichiosis

Granulocytic Ehrlichiosis

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128
Q

Ehrlichioses: Epidemiology (1)

A

Found in southern US

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129
Q

Ehrlichioses: Gram stain

A

-

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130
Q

Ehrlichioses: Pathogenesis (1)

A

Infects monocytes and granulocytes

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131
Q

Ehrlichioses: Special growth conditions (1)

A

Obligate intracellular

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132
Q

Ehrlichioses: Symptoms (3)

A

Fever, lymphocytopenia, elevated LFTs

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133
Q

Ehrlichioses: Transmission/vector/ habitat

A

Ticks

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134
Q

Ehrlichioses: Treatment (1)

A

Tetracyclines

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135
Q

Enteroaggregative E. coli (EAEC): At Risk

A

Children in developing countries

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136
Q

Enteroaggregative E. coli (EAEC): Diagnosis (2)

A

PCR for virulence genes

Tissue culture -> aggregative adherence

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137
Q

Enteroaggregative E. coli (EAEC): Disease (1)

A

Chronic Diarrhea

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138
Q

Enteroaggregative E. coli (EAEC): Epidemiology (2)

A

Common in developing countries

2012 outbreak in Germany of O104:H4 due to strain that expressed STX

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139
Q

Enteroaggregative E. coli (EAEC): Pathogenesis (1)

A

Aggressive epithelial cell attachment

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140
Q

Enteroaggregative E. coli (EAEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not

A

No A/E lesions

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141
Q

Enteroaggregative E. coli (EAEC): Symptoms (2)

A

Persistent diarrhea

Weight loss

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142
Q

Enteroaggregative E. coli (EAEC): Treatment (1)

A

Fluoroquinolones (travelers and HIV+)

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143
Q

Enteroaggregative E. coli (EAEC): Virulence Factors (3)

A

Heat stable-like toxin (EnteroAggregative stable toxin; EAST)
Plasmid encoded toxin (Pet)
Hemolysin

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144
Q

Enterobacter cloacae: At Risk (1)

A

Hospital setting following antibiotic treatment

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145
Q

Enterobacter cloacae: Disease (4)

A

OPPORTUNIST!

Infections of burns, wounds, respiratory, UT

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146
Q

Enterobacter cloacae: Gram stain

A

-

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147
Q

Enterobacter cloacae: Oxygen

A

fac. Anaerobe

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148
Q

Enterobacter cloacae: Pathogenesis

A

Forms biofilms

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149
Q

Enterobacter cloacae: Positive for: (1)

A

Lactose

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150
Q

Enterobacter cloacae: Shape

A

rod

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151
Q

Enterohemorrhagic E. coli (EHEC): At Risk (2)

A

HUS in ~7% of cases (due to RBC destruction and damage to BV wall lining)
–Acute renal failure (via HUS) in severe cases (children <10; elderly)

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152
Q

Enterohemorrhagic E. coli (EHEC): Diagnosis (3)

A

Sorbitol negative growth (RED on Sorbitol MacConkey Agar)
H7 serology and toxin analysis
PCR/Immunoassay for Shiga-like toxins

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153
Q

Enterohemorrhagic E. coli (EHEC): Disease (2)

A

Bloody diarrhea

Hemolytic uremic syndrome (HUS) if toxin spreads -> due to Shiga-like toxin

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154
Q

Enterohemorrhagic E. coli (EHEC): Incubation Period

A

3 days

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155
Q

Enterohemorrhagic E. coli (EHEC): Infectious dose

A

Low infectious dose (~100)

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156
Q

Enterohemorrhagic E. coli (EHEC): Negative for: (1)

A

Sorbitol**

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157
Q

Enterohemorrhagic E. coli (EHEC): Number of serotypes

A

O157:H7 = most important

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158
Q

Enterohemorrhagic E. coli (EHEC): Pathogenesis (5)

A
  1. COMMON pili-mediated attacment (weak)
  2. T3SS induced formation of attach/efface lesions
  3. other E. coli proteins recruit host cell actin (alter morphology and impact signal transduction pathways in host cell to form A/E lesions)
  4. lesions lead to effacement retraction of host cell microvilli)
  5. interaction of other virulence factors to attach (Tir-intimin) and produce pedestals (actin polymerization; role unclear)
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159
Q

Enterohemorrhagic E. coli (EHEC): Reservoir

A

Cattle (immune - lack host glycolipid for Shiga-toxin binding) but 28% shed EHEC

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160
Q

Enterohemorrhagic E. coli (EHEC): Similar to

A

Shigella

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161
Q

Enterohemorrhagic E. coli (EHEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not

A

Mostly extracellular

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162
Q

Enterohemorrhagic E. coli (EHEC): Symptoms (3)

A

Abd. Pain, bloody diarrhea,
NEVER systemic
HUS

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163
Q

Enterohemorrhagic E. coli (EHEC): Transmission/vector/ habitat (3)

A

Food/water
Animals in petting zoos
Person-to-person

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164
Q

Enterohemorrhagic E. coli (EHEC): Treatment (2)

A

Supportive care

Antibiotics and antimotility agents are contraindicated

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165
Q

Enterohemorrhagic E. coli (EHEC): Virulence Factors (8)

A

T3SS (LEE pathogenicity island)

TIR: T3SS secreted protein delivered to epithelial cell surface for E. coli attachment
INTIMIN: Tir binding protein on E. coli surface
–Facilitates strong attachment

SHIGA-LIKE TOXIN (STX): gene on phage, disrupts euk. protein synthesis (cytotoxic) via RNA cleavage (subunit A), binds to cell (subunit B)

HEMOLYSIN: pore forming protein

Capsule (K-antigen)

LPS

Common pilus

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166
Q

Enteroinvasive E. coli (EIEC): Diagnosis (1)

A

PCR for virulence genes

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167
Q

Enteroinvasive E. coli (EIEC): Disease (1)

A

Diarrhea

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168
Q

Enteroinvasive E. coli (EIEC): Epidemiology (1)

A

Less common in industrialized nations

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169
Q

Enteroinvasive E. coli (EIEC): Pathogenesis (3)

A
  1. attaches to cells of colon via non-fimbrial adhesins
  2. invades mucosal cells
  3. multiplies within cell but does not become systemic.
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170
Q

Enteroinvasive E. coli (EIEC): Similar to

A

Shigella dysentery

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171
Q

Enteroinvasive E. coli (EIEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not

A

Highly invasive

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172
Q

Enteroinvasive E. coli (EIEC): Symptoms (1)

A

Watery diarrhea that can contain blood and mucus (similar to Shigella)

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173
Q

Enteroinvasive E. coli (EIEC): Transmission/vector/habitat (1)

A

Food

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174
Q

Enteroinvasive E. coli (EIEC): Virulence Factors (2)

A

Plasmid encoded genes for invasion, replication, and survival (similar to Shigella)

Attaches via non-fimbrial adhesins

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175
Q

Enteropathogenic E. coli (EPEC): Diagnosis (2)

A

PCR for virulence genes

Tissue culture -> localized adherence

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176
Q

Enteropathogenic E. coli (EPEC): Disease (1)

A

Childhood Diarrhea

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177
Q

Enteropathogenic E. coli (EPEC): Epidemiology (1)

A

Leading cause of childhood diarrhea (developing countries)

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178
Q

Enteropathogenic E. coli (EPEC): Pathogenesis

A

Localized adherence by bundle-forming pili -> A/E lesions -> malabsorption -> diarrhea

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179
Q

Enteropathogenic E. coli (EPEC): Symptoms

A

Diarrhea

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180
Q

Enteropathogenic E. coli (EPEC): Transmission/vector/habitat

A

Person-to-person

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181
Q

Enteropathogenic E. coli (EPEC): Treatment

A

Antibiotics guided by susceptibility testing for severe or protracted cases

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182
Q

Enteropathogenic E. coli (EPEC): Virulence Factors (3)

A

Attaching/Effacing (A/E) lesions
Bundle-forming pili (Bfp)
NO toxins

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183
Q

Enterotoxigenic E. coli (ETEC): At Risk (2)

A

Travelers, infants in developing countries

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184
Q

Enterotoxigenic E. coli (ETEC): Diagnosis (1)

A

PCR for virulence genes

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185
Q

Enterotoxigenic E. coli (ETEC): Disease

A

Traveler’s Diarrhea

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186
Q

Enterotoxigenic E. coli (ETEC): Pathogenesis (3)

A
  1. fimbriae adhere to receptors on enterocytes in SI
  2. net loss of fluid and electrolytes into lumen of gut (LT/ST)
  3. watery diarrhea (LT/ST)
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187
Q

Enterotoxigenic E. coli (ETEC): Symptoms

A

Watery diarrhea

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188
Q

Enterotoxigenic E. coli (ETEC): Transmission/vector/ habitat (2)

A

Food/water

Person-to-person

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189
Q

Enterotoxigenic E. coli (ETEC): Treatment

A

Loperamide (+fluoroquinolone)

Azithromycin or rifaximin (for travelers)

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190
Q

Enterotoxigenic E. coli (ETEC): Virulence Factors (2)

A

Heat-labile toxin (LT): targets adenylate cyclase => increased cAMP levels => excess Cl- secretion and blocked Na+ uptake

Heat-stable toxin (ST): alters cGMP levels -> same effects as LT

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191
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): At Risk (3)

A

6-12 months of age (no more passive immunity)
Complement deficiencies
Developing countries

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192
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Diagnosis (5)

A

History, age of patient

Blood and CSF culture in chocolate agar (will NOT grow on blood agar)

Gm stain CSF

Presence of Type B capsular Ag or PCR detection of capsule genes

Biochemical tests

193
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Disease (~8)

A

Start as nasopharyngitis (+ otitis media, sinusitis)
Meningitis
Bacteremia
Epiglottitis (less comon) and obstructive laryngitis (may be fatal within 24h)
Cellulitis (face) or childhood pyarthrosis (pus in joint)
Pneumonia

194
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Epidemiology (2)

A

Most common encapsulated strain (type B, most virulent) -> decreasing with vaccination

Previously most common cause of bacterial meningitis in children (<4y)

195
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Gram stain

A

-

196
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Oxygen

A

fac. Anaerobe

197
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Pathogenesis (4)

A
  1. respiratory aerosols
  2. colonization (weeks to months)
  3. IgA protease (may aid in immune evasion)
  4. LPS -> systemic infections
198
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Positive for: (3)

A

Urease
Ornithine decarboxylase
Indole production
(maybe not important)

199
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Prevention (1)

A

Prophylaxis in households with young children

200
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Reservoir

A

Carried by 75-80% of the population (5% are encapsulated)

201
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Shape

A

coccobacilli (pleiomorphic)

202
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Special Features: Intra vs extracellular, presence of capsule, invasive or not

A

Capsule present!

203
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Special growth conditions (4)

A

FASTIDIOUS -> MUST use chocolate agar

2 growth factors required (X & V)

  • -X (heat stable): hemin
  • -V (heat labile): NAD or NADP

Susceptible to disinfectants and drying

204
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Transmission/vector/habitat

A

Aerosol

205
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Treatment (4)

A

Meningitis:

  • -3G cephalosporin immediately
  • -Ampicillin/B-lactamase inhibitor if sensitive
  • -Add steroids to reduce damage from inflammation

Contacts: rifampin for prophylaxis

206
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Vaccine

A 
Conjugate capsular (effective) - capsule PRP linked to diphtheria toxoid for increased T-cell dependence
=> more immunogenic in children
207
Q

Haemophilus influenzae (type B and other encapsulated, typeable, systemic): Virulence Factors (4)

A

Capsule (antiphagocytic - ribose for Type B vs hexose for others)
IgA protease
LPS
Adhesins

208
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): At Risk (3)

A

COPD, chronic bronchitis, CF -> respiratory disease

Acute sinusitis or CSF leak -> meningitis

Children

209
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Diagnosis (4)

A

History, age of patient
Blood and CSF culture in chocolate agar (will NOT grow on blood agar)
Gm stain CSF
Biochemical tests

210
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Disease (3)

A

Otitis media
Conjunctivitis
Respiratory disease

211
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Epidemiology (3)

A

50% mortality in neonates

2nd most common cause of otitis media (after Streptococcus pneumoniae)

Most common in children

212
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Gram stain

A

-

213
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Number of serotypes

A

Many

214
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Oxygen

A

fac. Anaerobe

215
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Pathogenesis (2)

A

3 invasion routes (extra- and intracellular)

Can also form biofilms

216
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Prevention (1)

A

Passive immunity from mother only lasts few months

217
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Reservoir

A

Carried by 75-80% of the population (5% are encapsulated)

218
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Shape

A

coccobacilli

219
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Special Features: Intra vs extracellular, presence of capsule, invasive or not (3)

A

No polysaccharide capsule
Both extracellular and intracellular
Non-systemic

220
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Special growth conditions (4)

A

FASTIDIOUS -> MUST use chocolate agar

2 growth factors required (X & V)

  • -X (heat stable): hemin
  • -V (heat labile): NAD or NADP

Susceptible to disinfectants and drying

221
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Symptoms (1)

A

Ear aches

222
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Transmission/vector/habitat

A

Aerosol

223
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Treatment (3)

A

Amoxicillin (otitis media & sinusitis)
Amox w/b-lactamase inhibitor for resistant strains
Can be persistent/recurrent due to biofilm formation and ability to invade cells

224
Q

Haemophilus influenzae (unencapsulated, nontypeable, nonsystemic): Virulence Factors (2)

A

Adhesins -> colonization

LPS

225
Q

Helicobacter pylori: Diagnosis (6)

A 
Radiolabled urea test (Breath test)
Stool culture (campy-BAP with cephalothin [special media])
Rapid urease test
Seroconversion
PCR

Endoscopy + histology (biopsy) -> definitive

226
Q

Helicobacter pylori: Disease (3)

A

Peptic ulcer
Chronic Gastritis
Gastric cancer

227
Q

Helicobacter pylori: Epidemiology (1)

A

Present in 50% of world’s population (highest in developing countries - correlates with greater incidence of gastric cancer)

228
Q

Helicobacter pylori: Gram stain

A

-

229
Q

Helicobacter pylori: Infectious dose

A

ND in humans

10^4 in primates

230
Q

Helicobacter pylori: Oxygen

A

Microaerophilic

231
Q

Helicobacter pylori: Pathogenesis (3)

A
  1. lives in stomach and duodenum mucus -> secretes urease (creates basic environment)
  2. immune cells can’t penetrate mucus -> release superoxide radical upon death => destroy stomach cells
  3. gastritis (days), ulcer (later), metaplasia, cancer
232
Q

Helicobacter pylori: Positive for: (1)

A

Urease (breath test or stool culture)

233
Q

Helicobacter pylori: Shape

A

spiral

234
Q

Helicobacter pylori: Symptoms (2)

A

Recurrent pain in upper abd., GI bleed

235
Q

Helicobacter pylori: Transmission/vector/habitat (2)

A

Fecal matter present in tainted food/water

Stomach-to-mouth by gastro-esophageal reflux (gastritis) => kissing

236
Q

Helicobacter pylori: Treatment (2)

A

Antibiotic treatment [metronidazole, tetracycline] supplemented with bismuth salts (relapses require further treatment)

Contra-indicated for asymptomatic infected except in special circumstances

237
Q

Helicobacter pylori: Virulence Factors (3)

A

–BabA (adhesin - binds to Lewis b Ag on surface of stomach epithelial cell)

–CagA (injected into stomach epithelial cell -> phosphorylated -> disrupts cytoskeleton, adherence to adjacent cells, intracellular signaling, cell polarity)

–VacA (injected - further damages epithelial cell lining)

238
Q

Klebsiella pneumoniae: At Risk (3)

A

Alcoholic, diabetic, lung disease

239
Q

Klebsiella pneumoniae: Diagnosis (1)

A

Capsule production causes mucoid colony morphology

240
Q

Klebsiella pneumoniae: Disease (5)

A 
OPPORTUNIST!
UTI
Bacteremia
Meningitis
Diarrhea
Pneumonia
241
Q

Klebsiella pneumoniae: Gram stain

A

-

242
Q

Klebsiella pneumoniae: Oxygen

A

fac. Anaerobe

243
Q

Klebsiella pneumoniae: Positive for: (1)

A

Lactose

244
Q

Klebsiella pneumoniae: Shape

A

rod

245
Q

Klebsiella pneumoniae: Special Features: Intra vs extracellular, presence of capsule, invasive or not (1)

A

Red currant jelly sputum

246
Q

Klebsiella pneumoniae: Virulence Factors (1)

A

Capsule toxins (reduced phagocytosis, reduced complement activity)

247
Q

Legionella pneumoophila: At Risk (3)

A

Renal transplant, immunocompromised, and elderly

248
Q

Legionella pneumoophila: Diagnosis (4)

A

Culture on charcoal yeast extract with Fe and cysteine

Direct fluorescent Ab test in sputum

Detection of Ag in urine

Analysis of Ab levels in blood samples obtained 3-6w apart (for epigenetics)

249
Q

Legionella pneumoophila: Disease (2)

A

Legionnaires’ disease

Milder form called “Pontiac Fever”

250
Q

Legionella pneumoophila: Epidemiology (3)

A

Significant mortality in original outbreak
Most infections clinically insignificant
Summer/fall outbreaks (increased AC use)

251
Q

Legionella pneumoophila: Gram stain

A

-

252
Q

Legionella pneumoophila: Incubation Period

A

2-10 days

253
Q

Legionella pneumoophila: Oxygen

A

Aerobe

254
Q

Legionella pneumoophila: Pathogenesis (3)

A

Early infection: apoptosis in macrophages/alveolar cells

Second phase: necrosis
–Both processes lead to cell deah in respiratory tract

Rare dissemination -> systemic disease

255
Q

Legionella pneumoophila: Prevention

A

Proper water handling (heating, chlorine, cleanings)

256
Q

Legionella pneumoophila: Reservoir

A

Water of cooling towers, in amoeba or as biofilms

257
Q

Legionella pneumoophila: Shape

A

rod

pleomorphic

258
Q

Legionella pneumoophila: Special Features: Intra vs extracellular, presence of capsule, invasive or not (1)

A

Intracellular growth

259
Q

Legionella pneumoophila: Special growth conditions (1)

A

Nutritionally “fastidious”: grown on charcoal yeast extract with Fe and cysteine

260
Q

Legionella pneumoophila: Symptoms (8)

A

Atypical (diffuse) pneumonia: fever, chills, cough (+/- sputum), muscle aches, headache, tiredness, loss of appetite, and occasionally diarrhea

261
Q

Legionella pneumoophila: Transmission/vector/habitat

A

Airborne from environment

NO human-to-human transmission

262
Q

Legionella pneumoophila: Virulence Factors (1)

A

LPS

263
Q

Mycoplasma pneumoniae: At Risk (4)

A

School-aged kids and teens through young adults

Childhood asthma, chronic lung disease, immunodeficiency

264
Q

Mycoplasma pneumoniae: Diagnosis (4)

A

Sputum gram stain (+monocytes/PMNs) shows no organism

NO CULTURE generally attempted - Throat swab can take 3w (slow growth)

PCR (early results)

**Cold agglutination test (may be + in 50% of patients)

265
Q

Mycoplasma pneumoniae: Disease (2)

A

Atypical (diffuse) pneumonia (gradual onset)

Extrapulmonary infections can occur (CNS, arthritis, autoimmunity) as complication

266
Q

Mycoplasma pneumoniae: Epidemiology (5)

A

Causes 15-50% of pneumonias (50% of summer pneumonias)

Severity correlated with age

Epidemics every 4-8y

Close contact is a factor

Fatalities are rare

267
Q

Mycoplasma pneumoniae: Gram stain

A

variable (no cell wall)

268
Q

Mycoplasma pneumoniae: Number of serotypes

A

1 serotype, but NO lifelong immunity

269
Q

Mycoplasma pneumoniae: Other

A

Have other mycoplasmas, often opportunists

270
Q

Mycoplasma pneumoniae: Pathogenesis (2)

A
  1. attaches to epithelium via adhesins (P1) inducing ciliostasis => necrosis
  2. H2O2 production => oxidative damage and inflammation
271
Q

Mycoplasma pneumoniae: Reservoir

A

NONE - only infects humans

272
Q

Mycoplasma pneumoniae: Shape

A

pleomorphic (NO cell wall)

Smallest replicating bacterium

273
Q

Mycoplasma pneumoniae: Special growth conditions (2)

A

Colonies are small and grow slowly -> fried egg appearance

Needs cholesterol for membrane rigidity

274
Q

Mycoplasma pneumoniae: Symptoms (4)

A

Cough (sputum), weakness, fever, headache

275
Q

Mycoplasma pneumoniae: Transmission/vector/ habitat

A

Aerosol

276
Q

Mycoplasma pneumoniae: Treatment (2)

A

***Resistant to cell wall inhibitors

Sensitive to antibiotics that interfere w/protein synthesis (erythromycin and tetracyclines)

277
Q

Mycoplasma pneumoniae: Virulence Factors (4)

A

Lipoproteins (increase immune evasion and provide rigidity)

P1 adhesin: protein complex at tip of bacterium

H2O2, superoxide: damage host cell membranes, disrupt DNA synthesis & metabolism, -> CILIOSTASIS

278
Q

Neisseria (general): Gram stain

A

-

279
Q

Neisseria (general): Positive for: (2)

A

Oxidase
Glucose (and maltose for N.m.)
**Non-pathogenic Neisseria ferment ALL sugars except sucrose

280
Q

Neisseria (general): Reservoir

A

Humans only

281
Q

Neisseria (general): Shape

A

diplococci (adjacent sides slightly flattened)

THE ONLY Gm- coccus pathogen!

282
Q

Neisseria (general): Special growth conditions (4)

A

FASTIDIOUS
Grow in 5-10% CO2
Need Thayer-Martin selective medium (modified chocolate agar)
Readily killed by drying, heat, disinfectants

283
Q

Neisseria (general): Virulence Factors (4)

A

Pili and OMP (colonization)
IgA1 protease
LOS (LPS w/out O side chains) helps resist serum bactericidal activity

284
Q

Neisseria gonorrhoeae: Diagnosis (4)

A

Gm- stain of purulent exudate (pus)
Present in phagocytic cells
History of exposure
Oxidase-positive Gm- diplococci cultured

285
Q

Neisseria gonorrhoeae: Disease (4)

A

Gonorrhea
Opthalmia neonatorum

Disseminated complications:

  1. Arthritis-dematitis syndrome
  2. Chronic pelvic inflammatory disease (PID; females)
286
Q

Neisseria gonorrhoeae: Epidemiology (4)

A

Most prevalent communicable bacterial disease of humans (along w/C. trachomatis)

Worldwide pandemic

Asymptomatic carrier states are common

Opthalmia neonaturium was once the cause of 50% of blindness in children

287
Q

Neisseria gonorrhoeae: Incubation Period

A

1 hour

288
Q

Neisseria gonorrhoeae: Negative for: (3)

A

Maltose
Lactose
Sucrose

289
Q

Neisseria gonorrhoeae: Number of serotypes

A

100+ serotypes based on antigenicity of pilus protein

Displays ANTIGENIC VARIATION: rearranges pilus genes to express different pili, evade immune system

290
Q

Neisseria gonorrhoeae: Pathogenesis (4)

A
  1. STD via genital contact
  2. pili anchor to epithelium and impair phagocytosis by PMNs
  3. penetrate through surface cells (intracellularly) to reach sub-epithelial CT
  4. inflammation and yellow purulent urethral discharge
291
Q

Neisseria gonorrhoeae: Positive for: (2)

A 
Oxidase
Glucose (G = gonorrhoeae)
292
Q

Neisseria gonorrhoeae: Symptoms (3)

A

Inflammation, yellow purulent urethral discharge (w/pain upon urination)

Males: 2-3 days post-exposure
Females: 10 days (high percentage remain asymptomatic)

293
Q

Neisseria gonorrhoeae: Transmission/vector/habitat (4)

A

STD: direct genital contact, rectal and pharyngeal mucosa, conjunctiva of newborns

294
Q

Neisseria gonorrhoeae: Treatment (3)

A

IM ceftriaxone + oral tetracycline

Silver nitrate or tet/erythromycin ointment to prevent blindness in newborns

High levels of drug resistance

295
Q

Neisseria gonorrhoeae: Virulence Factors (4)

A

Pili, OMP
IgA protease
LOS (but not a major factor in disease state, unlike meningococcus)
NO capsule

296
Q

Neisseria meningitidis: At Risk (3)

A

Crowded conditions: day care centers, military barracks, college dorms

Sub-Saharan meningitis belt (type A) during dry season (Dec-June)

Children 65

297
Q

Neisseria meningitidis: Diagnosis (4)

A

History: URI -> meningitis

**PETECHIAE on skin

Culture/agglutination for capsule Ag in CSF

Blood, CSF (lumbar puncture), nasopharyngeal specimens cultured for G- diplococci

298
Q

Neisseria meningitidis: Disease (4)

A 
Meningitis (high mortality; usually type B)
Septicemia
Mild pharyngitis (in some)

Severe = Waterhouse-Friderichsen (adrenal failure, shock, death)

299
Q

Neisseria meningitidis: Epidemiology (3)

A

Carrier rate varies (5% gen. pop but higher in households with history)
–Carrier state lasts from days to months

Cases usually sporadic

300
Q

Neisseria meningitidis: Incubation Period

A

Days to 1 week

301
Q

Neisseria meningitidis: Negative for: (2)

A

Lactose

Sucrose

302
Q

Neisseria meningitidis: Number of serotypes

A

Serogroups A, B, C, Y, W135 (most important) - based on capsule

303
Q

Neisseria meningitidis: Pathogenesis (4)

A

Muliplies outside of cells, NOT inside
Endotoxin damages small vessels
Bacteria enter blood stream
Organotropism for meninges (but also skin, eyes and lungs)

304
Q

Neisseria meningitidis: Positive for: (3)

A

Oxidase
Glucose
Maltose (M = meningitidis)

305
Q

Neisseria meningitidis: Special Features: Intra vs extracellular, presence of capsule, invasive or not (2)

A

Encapsulated (antiphagocytic)

Extracellular

306
Q

Neisseria meningitidis: Symptoms (9)

A

Meningitis: high fever, vomiting, stiff neck, lethargy, petechial rash

Septicemia: fever, petechial rash, hypotension, WF syndrome

307
Q

Neisseria meningitidis: Transmission/vector/ habitat

A

Lives in nasopharynx, person-to-person aerosol

308
Q

Neisseria meningitidis: Treatment (2)

A

Prompt IV penicillin, 3G cephalosporin, ciprofloxacin

Prophylactic rifampicin or cipro for close contacts

309
Q

Neisseria meningitidis: Vaccine

A

Military and Endemic:
Quadrivalent vaccine for serotypes A, C, Y, and W…(no component for B capsule - sialic acid in capsule)

Africa:
Conjugate vaccine, cheap

310
Q

Neisseria meningitidis: Virulence Factors (5)

A

Capsule
LOS
pili, OMP
IgA protease

311
Q

Proteus mirabilis, vulgaris: Diagnosis (1)

A

Dx with urease test -> alkaline products turn phenol red red (vs yellow with net acid)

312
Q

Proteus mirabilis, vulgaris: Disease (1)

A

OPPORTUNIST!

UTI

313
Q

Proteus mirabilis, vulgaris: Epidemiology (1)

A

Frequent cause of UTI

314
Q

Proteus mirabilis, vulgaris: Gram stain

A

-

315
Q

Proteus mirabilis, vulgaris: Negative for: (1)

A

Lactose

316
Q

Proteus mirabilis, vulgaris: Oxygen

A

fac. Anaerobe

317
Q

Proteus mirabilis, vulgaris: Pathogenesis

A

Urea -[urease]-> NH3 + CO2 -> ALKALINE urine -> salt crystalization and stone formation -> chronic infection

318
Q

Proteus mirabilis, vulgaris: Positive for: (1)

A

Urease

319
Q

Proteus mirabilis, vulgaris: Shape

A

rod

320
Q

Proteus mirabilis, vulgaris: Virulence Factors (2)

A

Flagella (swarming motility), urease

321
Q

Pseudomonas aeruginosa: At Risk (3)

A

Immunocompromised (bacteremia)

COPD and CF (chronic lung infection)

322
Q

Pseudomonas aeruginosa: Diagnosis

A

**Obligate aerobe, no fermentation of sugar

323
Q

Pseudomonas aeruginosa: Disease (5)

A

OPPORTUNIST!
Bacteremia
Pneumonia
Infections of burns, eyes, wounds

324
Q

Pseudomonas aeruginosa: Epidemiology (1)

A

Associated with burns, catheters, implants, ventilator associated pneumonia, implants, eye wounds

325
Q

Pseudomonas aeruginosa: Gram stain

A

-

326
Q

Pseudomonas aeruginosa: Negative for: (1)

A

Sugar fermentation

327
Q

Pseudomonas aeruginosa: Oxygen

A

obligate aerobe (because it does NOT ferment, but technically wrong)

328
Q

Pseudomonas aeruginosa: Pathogenesis (2)

A

Elastase breaks down elastin (lung tissue damage)

Phospholipase breaks down phospholipids in host cell membranes and surfactant

329
Q

Pseudomonas aeruginosa: Shape

A

rod

330
Q

Pseudomonas aeruginosa: Virulence Factors (8)

A

Endotoxin
Exotoxins (elastase, phospholipase)
T3SS-secreted toxins (ExoA, S, T, U)
Pyocyanin (blue-green pigment, generates ROS)

331
Q

Rickettsia (general): Diagnosis (3)

A

Clinical symptoms/history
PCR test
Specific immunohistologic detection of Rickettsiae

332
Q

Rickettsia (general): Gram stain

A

-

333
Q

Rickettsia (general): Life Cycle (3)

A

Growth cycle in human/arthropod cells

  1. enter via phagocytosis (promoted by rickettsia and requires energy) even into non-phagocytic cells
  2. multiply slowly (binary fission - 1x/day)
  3. progeny released via lysis
334
Q

Rickettsia (general): Shape

A

pleomorphic

335
Q

Rickettsia (general): Special growth conditions (1)

A

OBLIGATE intracellular (unclear why: they’re well adapted to intracellular environment but are able to make own ATP)

336
Q

Rickettsia (general): Transmission/vector/habitat

A

Arthropods

337
Q

Rickettsia (general): Treatment (1)

A

Tetracyclines

338
Q

Rickettsia akari: At Risk (1)

A

Exposure to rodents

339
Q

Rickettsia akari: Disease (1)

A

Rickettsial Pox

340
Q

Rickettsia akari: Epidemiology (1)

A

Outbreaks usually confined to single, large apartment buildings

341
Q

Rickettsia akari: Reservoir

A

Mouse

342
Q

Rickettsia akari: Symptoms (3)

A
  1. primary skin lesion (site of bite)
  2. systemic disease 1 week later (fever, chills, headache, rash like chicken pox)
    - -Benign, non-life-threatening
343
Q

Rickettsia akari: Transmission/vector/ habitat

A

Mouse -> mouse mite -> human

344
Q

Rickettsia prowazekii: At Risk (3)

A

Human misery, famine, and war

345
Q

Rickettsia prowazekii: Diagnosis (4)

A

PCR detection
Various serological tests
Elevated LFT
Rise in antibody titers (compare acute and convalescent serum samples)

346
Q

Rickettsia prowazekii: Disease (2)

A

Primary Epidemic Typhus
Endemic Typhus

Brill-Zinsser disease

347
Q

Rickettsia prowazekii: Epidemiology (2)

A

Brill-Zinsser disease (reactivation of latent infection) may reintroduce rickettsia (Russia or eastern Europe)

Often fatal if untreated (except in children)

348
Q

Rickettsia prowazekii: Incubation Period

A

10 days

349
Q

Rickettsia prowazekii: Pathogenesis (6)

A
  1. louse punctures skin to get blood meal - defacates
  2. scratching drives feces (+rickettsia) into wound
  3. multiply first in capillary endothelial cells
  4. incubate
  5. sudden onset of fever and headache
  6. rash (4-7d later)
350
Q

Rickettsia prowazekii: Prevention

A

Louse control (DDT or adequate bath and laundry facilities)

351
Q

Rickettsia prowazekii: Reservoir

A

Flying squirrel and its lice

352
Q

Rickettsia prowazekii: Symptoms (5)

A

Abrupt fever, severe intractable headache, rash, elevated liver enzymes

Frequently fatal

353
Q

Rickettsia prowazekii: Transmission/vector/ habitat (2)

A

Primary Epidemic
Human “body” lice (NOT head/crab lice)

Endemic
Flying squirrel lice

354
Q

Rickettsia rickettsii: At Risk (2)

A

Eastern USA

Exposure to ticks

355
Q

Rickettsia rickettsii: Disease

A

Rocky Mountain Spotted Fever

356
Q

Rickettsia rickettsii: Epidemiology (2)

A

Untreated adult cases have 20% mortality

Mostly cases from April to November

357
Q

Rickettsia rickettsii: Incubation Period

A

<1 week

358
Q

Rickettsia rickettsii: Prevention (1)

A

Avoid ticks (wear suitable clothing)

359
Q

Rickettsia rickettsii: Reservoir (2)

A

Western USA: forest tick

Easten USA: dog tick

360
Q

Rickettsia rickettsii: Symptoms (3)

A
  1. Fever, headache, arthritic pains, abd. pain with nausea and vomiting
  2. Rash from extremities spreads to trunk
  3. Lesions on palm of hand and soles of feet
361
Q

Rickettsia rickettsii: Transmission/vector/ habitat (2)

A

Transovarian -> tick -> human

Mammal -> tick -> human

362
Q

Rickettsia typhi: At Risk (2)

A

Exposure to rats and squirrels

363
Q

Rickettsia typhi: Disease (1)

A

Endemic Murine Typhus

364
Q

Rickettsia typhi: Reservoir (2)

A

Rats and ground squirrels

365
Q

Rickettsia typhi: Symptoms (1)

A

Resembles primary epidemic typhus but milder and less fatal

366
Q

Rickettsia typhi: Transmission/vector/ habitat

A

Rat/ground squirrel flea -> human

367
Q

Salmonella (general): Diagnosis (3)

A

ID with MacConkey/EMB for lac -
Produces H2S - BLACK on Klinger Iron Agar
Serotyping and PCR tests w/ O & H antigens allows species identification

368
Q

Salmonella (general): Gram stain

A

-

369
Q

Salmonella (general): Infectious dose

A

10^3-10^5

370
Q

Salmonella (general): Negative for: (5)

A 
Lactose
Oxidase
Spores
Indole
Urease
371
Q

Salmonella (general): Oxygen

A

fac. Anaerobe

372
Q

Salmonella (general): Positive for: (5)

A 
Glucose (+gas)
Motility (flagella)
H2S (black precipitate)
Nitrate reduction
O & H antigen
373
Q

Salmonella (general): Shape

A

rod

374
Q

Salmonella choleraesius: At Risk (6)

A

Young, malaria, immune dysfunction, steroid use, sickle cell, cancer

375
Q

Salmonella choleraesius: Diagnosis (1)

A

Isolation in blood

376
Q

Salmonella choleraesius: Disease (1)

A

Septicemia

377
Q

Salmonella choleraesius: Epidemiology (1)

A

Rare

378
Q

Salmonella choleraesius: Incubation Period

A

6-72 hours

379
Q

Salmonella choleraesius: Infectious dose

A

10^3

380
Q

Salmonella choleraesius: Number of serotypes

A

1 serotype

381
Q

Salmonella choleraesius: Reservoir

A

Swine

382
Q

Salmonella choleraesius: Symptoms (4)

A

High fever and bacteremia after onset of gastroenteritis

Microabscesses can develop anywhere

383
Q

Salmonella choleraesius: Transmission/vector/ habitat

A

Contaminated food

384
Q

Salmonella choleraesius: Treatment

A

Appropriate antibiotics

385
Q

Salmonella choleraesius: Virulence Factors (3)

A

SPI-1 (invasion, encodes T3SS)
SPI-2 (survival, encodes T3SS)
LPS (endotoxin)

386
Q

Salmonella enteritidis and typhimurium: At Risk (1)

A

Both developed and developing countries

387
Q

Salmonella enteritidis and typhimurium: Diagnosis (1)

A

Isolation in feces

388
Q

Salmonella enteritidis and typhimurium: Disease (1)

A

Acute gastroenteritis

389
Q

Salmonella enteritidis and typhimurium: Epidemiology (4)

A

Most common Salmonella infection in US

Self-limiting
Complications can arise
Death is uncommon

390
Q

Salmonella enteritidis and typhimurium: Incubation Period

A

8-48 hours

391
Q

Salmonella enteritidis and typhimurium: Infectious dose

A

10^3-10^5

392
Q

Salmonella enteritidis and typhimurium: Number of serotypes

A

2200 serotypes

393
Q

Salmonella enteritidis and typhimurium: Pathogenesis (3)

A

LPS release during epithelial cell (intestines) invasion - symptomatic

T3SS mediated invasion

Extracellular cells produce toxins (pertussis-like) - promote inflammation and secretion

394
Q

Salmonella enteritidis and typhimurium: Reservoir

A

Reptiles and poultry

395
Q

Salmonella enteritidis and typhimurium: Symptoms (6)

A

Lasts 1-4 days

Headache, chills, abd. pain, vomiting, diarrhea w/fever

396
Q

Salmonella enteritidis and typhimurium: Transmission/vector/ habitat (4)

A

Poultry, eggs (common), food, water

397
Q

Salmonella enteritidis and typhimurium: Treatment (2)

A

Fluid and electrolyte replacement

Treat patients with predisposing conditions with antibiotics [amp, sulfa, 3G ceph, cipro; resistance is possible]

398
Q

Salmonella enteritidis and typhimurium: Virulence Factors (3)

A

T3SS, LPS, pertussis-like toxin

399
Q

Salmonella typhi: At Risk (1)

A

Developing world

400
Q

Salmonella typhi: Diagnosis (3)

A

Wk1: subclinical, +stool
W2-3: +blood, symptomatic
W3: +stool, gall bladder colonized

401
Q

Salmonella typhi: Disease (1)

A

Enteric (Typhoid) Fever

402
Q

Salmonella typhi: Incubation Period

A

7-14 days

403
Q

Salmonella typhi: Infectious dose

A

High (~10^5)

404
Q

Salmonella typhi: Number of serotypes

A

1 serotype

405
Q

Salmonella typhi: Pathogenesis (9)

A
  1. survives stomach
  2. adhesins attach to intestinal epithelium
  3. endocytosis (invasion of Peyer’s patches)
  4. ingestion by macrophages (T3SS)
  5. survive inside vacuoles (Vi)
  6. kill macrophage and disseminate via thoracic duct to blood, liver, spleen, gall bladder
  7. fever/shock via LPS
  8. reinvade GI via gall bladder
  9. GI bleed and sometimes diarrhea
406
Q

Salmonella typhi: Prevention (4)

A

Control of water/sewage
Food safety
Pastuerization
Carrier screening

407
Q

Salmonella typhi: Reservoir

A

NONE - only infects humans

408
Q

Salmonella typhi: Special Features: Intra vs extracellular, presence of capsule, invasive or not (2)

A

Vi antigen, fac. intracellular pathogen

409
Q

Salmonella typhi: Symptoms (6)

A

Early GI phase (incubation): may be subclinical w/+stool

Bacteremic: episodic fever, bradycardia, skin rash (Rose spot), leukopenia, enlarged liver/spleen

Late GI: intestinal hemorrhage or perforation

Chronic (3%): hide in gallbladder

410
Q

Salmonella typhi: Transmission/vector/ habitat

A

Contaminated food/water

411
Q

Salmonella typhi: Treatment (4)

A

Fluoroquinolones or 3G cephalosporins
–Should penetrate tissue –> macrophages

Chronic carrier states (3%) (gallbladder):

  1. Ampicillin or Cipro
  2. Cholecystectomy
412
Q

Salmonella typhi: Vaccine

A
  1. Ty21a - oral attenuated

2. ViCPS - Vi capsular polysaccharide

413
Q

Salmonella typhi: Virulence Factors (3)

A

SPI-1 (invasion, encodes T3SS)
SPI-2 (survival, encodes T3SS)
LPS (endotoxin)

414
Q

Serratia marcescens: At Risk (3)

A

Infection secondary to broad spectrum antibiotic treatment or instrumentation

Heroin addicts

415
Q

Serratia marcescens: Disease (3)

A

OPPORTUNIST!
Pneumonia (after use of a contaminated respirator)
Joint/tissue infections

416
Q

Serratia marcescens: Gram stain

A

-

417
Q

Serratia marcescens: Negative for: (1)

A

Lactose

418
Q

Serratia marcescens: Oxygen

A

fac. Anaerobe

419
Q

Serratia marcescens: Shape

A

rod

420
Q

Serratia marcescens: Special Features: Intra vs extracellular, presence of capsule, invasive or not (1)

A

Prodigiosins (red pigment)

421
Q

Serratia marcescens: Transmission/vector/ habitat (2)

A

Loves to grow in water

GI tract in neonates

422
Q

Serratia marcescens: Virulence Factors (4)

A

MS-fimbriae
proteases
siderophores
swarming motility (colonization)

423
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): At Risk

A

Children <10y

Also infects adults

424
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Diagnosis (4)

A

Can detect organisms in feces up to 1-4w after recovery -> important for spread

Detect PMN (indicative of invasive process)
Immunochromatographic assay for Shiga toxin
Kliger Iron Agar (+ glucose fermentation)

425
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Disease (1)

A

Dysentery (shigellosis/bloody diarrhea)

426
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Epidemiology (5)

A

Self-limiting, rarely fatal
Dysenteriae: most common species in developing world
Flexneri: common (18%) in US and developing countries
Sonnei: most common species in US (75%)
Bodyii: common in Indian subcontinent

427
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Gram stain

A

-

428
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Incubation Period

A

1-4 days

429
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Infectious dose

A

Low inoculum (<100)

430
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Negative for: (6)

A 
Lactose
H2S
Non-motile
Indole
Urease
H antigen
431
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Oxygen

A

fac. Anaerobe

432
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Pathogenesis (7)

A
  1. acid tolerant
  2. invade intestinal cells (lower ileum and colon)
  3. uptake by macrophages into vacuoles (T3SS)
  4. escape from vacuole into cytoplasm -> cell-to-cell spread (T3SS)
  5. apoptosis of macrophage -> re-infection
  6. IL-1 and TNF from macrophage leads to fever and systemic symptoms
  7. bloody diarrhea + apoptosis of mucosal cells + ulceration (Shiga toxin)
433
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Positive for: (2)

A

Glucose (-gas)

O antigen

434
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Prevention (1)

A

Sanitation

435
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Reservoir

A

NONE - only infects humans

436
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Shape

A

rod

437
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Similar to (2)

A

Salmonella, E coli (Enterobacteriaceae Family)

438
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Special Features: Intra vs extracellular, presence of capsule, invasive or not

A

Fac. intracellular pathogen

439
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Symptoms (6)

A 
Fever (LPS)
Diarrhea, abd. cramps (Shiga toxin)
Bloody diarrhea w/mucus
Bacteremia (rare)
HUS (rare)
440
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Transmission/vector/ habitat

A

4F’s: food, fingers, feces, flies

441
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Treatment (2)

A

Fluid and electrolyte replacement therapy (esp. young children)

Antibiotics in severe cases - increasing resistance

442
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Vaccine

A

Live attenuated vaccine not effective

Not-yet approved O-antigen conjugated to inactivated shiga toxin

443
Q

Shigella (dysenteriae, flexneri, boydii, sonnei): Virulence Factors (3)

A

T3SS (for uptake by/escape from MOs)
LPS
Shiga toxin (exotoxin)
–A subunit: interferes w/60S rRNA function
–B subunit: Binds to receptor on intestinal cells

444
Q

Uropathogenic E. coli (UPEC): At Risk (2)

A

Women via sex (bacterial flora in short urethra) and catheters

445
Q

Uropathogenic E. coli (UPEC): Diagnosis (3)

A

> 10^5 bacteria/ml in urine

Hemagglutination with sensitivity (Type I pili only, P are MR) to mannose testing

446
Q

Uropathogenic E. coli (UPEC): Disease (3)

A

OPPORTUNIST!
UTI
Neonatal meningitis
Bacteremia

447
Q

Uropathogenic E. coli (UPEC): Epidemiology (4)

A

Most common cause of UTIs (95%)
–Reoccurrence is common

Most common neonatal pathogen (K1 - neonatal meningitis)

Major cause of bacteremia, including leading cause of nosocomial bacteremia

448
Q

Uropathogenic E. coli (UPEC): Gram stain

A

-

449
Q

Uropathogenic E. coli (UPEC): Number of serotypes

A

Few are pathogenic

450
Q

Uropathogenic E. coli (UPEC): Oxygen

A

fac. Anaerobe

451
Q

Uropathogenic E. coli (UPEC): Pathogenesis (2)

A

Bacteria + urethra + ascension -> UTI

UTI + blockage -> bacteremia

452
Q

Uropathogenic E. coli (UPEC): Positive for: (1)

A

Lactose

453
Q

Uropathogenic E. coli (UPEC): Shape

A

rod

454
Q

Uropathogenic E. coli (UPEC): Similar to

A

Neisseria meningitidis (K1)

455
Q

Uropathogenic E. coli (UPEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not (2)

A

Replicate intracellularly (epithelial cells)

Serum resistance (evade Complement, correlated w/K1 production) is a critical trait of bacteremia causing strains

456
Q

Uropathogenic E. coli (UPEC): Symptoms (7)

A

Cystitis (dysuria, freqency, urgency, and suprapubic tenderness - typically lower UTI)

Acute pyelonephritis (UTI disseminated to kidney - flank pain, tenderness, fever, dysuria, frequency, urgency)

457
Q

Uropathogenic E. coli (UPEC): Transmission/vector/ habitat (2)

A 
Catheters
Sexual intercourse (spreads bacteria
458
Q

Uropathogenic E. coli (UPEC): Treatment (2)

A

Self-limiting

Treat pyelonephritis with Abx

459
Q

Uropathogenic E. coli (UPEC): Virulence Factors (8)

A 
BACTEREMIA/MENINGITIS:
LPS
K1 capsule (polysialic acid, non-immunogenic, in bacteremia)
motility
Siderophores
UTI:
Pili
--Mannose-binding type 1 (cystitis)
--P (pyelonephritis)
Adhesins -> colonization
Hemolysin
Biofilm formation
460
Q

Vibrio cholerae: At Risk (4)

A

Refugee camps
Poverty
Inadequate sanitation
South-central/southeast Asia

461
Q

Vibrio cholerae: Diagnosis (1)

A

Yellow opaque colonies on TCBS medium (selective and differential for V. cholerae)

462
Q

Vibrio cholerae: Disease (1)

A

Cholera

463
Q

Vibrio cholerae: Epidemiology (1)

A

John Snow + Broad Street Pump

464
Q

Vibrio cholerae: Gram stain

A

-

465
Q

Vibrio cholerae: Infectious dose

A

Infectious dose is source dependent (contaminated rice is highly infectious)

100 to 10^9

466
Q

Vibrio cholerae: Number of serotypes

A

> 250

O1 = epidemic cholera

  • -Classical biotype = old cholera
  • -El Tor biotype = current cholera
467
Q

Vibrio cholerae: Oxygen

A

fac. Anaerobe

468
Q

Vibrio cholerae: Pathogenesis (6)

A
  1. Inactivated by gastric acid, but some survive (rice helps)
  2. Enters small bowel, binds to epithelium
  3. (VF) Toxin Coregulated Pilus -> microcolony formation in intestinal crypts
    - > **Organism remains in intestine and DOES NOT invade
  4. (VF) Cholera toxin: expressed & secreted
  5. B subunit of CT binds ganglioside GM1 -> endocytosis
    - —–(VF) Neuraminidase makes more GM1, increasing binding sites
  6. A subunit is the TOXIN: ADP ribosylation of G protein on AC -> cAMP production -> PKA activation -> increased secretion of electrolytes and water, decreased NaCl absorption
469
Q

Vibrio cholerae: Positive for: (1)

A

Motility (polar flagellum)

470
Q

Vibrio cholerae: Prevention (3)

A

Water: bottle, carbonate, Cl, boil
Ice: beware
Food: dry, steaming hot, special attention to shellfish

471
Q

Vibrio cholerae: Reservoir

A

NONE - only infects humans

472
Q

Vibrio cholerae: Shape

A

comma with polar flagellum

473
Q

Vibrio cholerae: Similar to (2)

A

Vibrio parahaemolyticus (invasive gastroenteritis - shellfish)

Vibrio vulnificus (wound infection - seawater/shellfish - underlying liver disorder)

474
Q

Vibrio cholerae: Symptoms (4)

A

Painless, odorless profuse secretory diarrhea (rice water) -> rapid dehydration -> shock -> potential death

475
Q

Vibrio cholerae: Transmission/vector/habitat

A

Contaminated H2O! shellfish, seafood

476
Q

Vibrio cholerae: Treatment (3)

A

Oral/IV fluid replacement (electrolyte)
Antibiotics (reduce duration of diarrhea)
Doxycycline (adults) or azithromycin (children/pregnant)

477
Q

Vibrio cholerae: Vaccine

A

NONE are highly effective

Inactivated: 2 oral doses (crude suspension, new killed whole cell)
70% effective, not recommended for travel, currently used in Haiti

Live-attenuated: effective in North American clinical trials but not in field

478
Q

Vibrio cholerae: Virulence Factors (5)

A 
O & H antigens
Endotoxin
Enterotoxin (cholera toxin)
Toxin coregulated pilus (TCP) - colonization
Neuraminidase

Microbiology - Quiz 2 (10 decks)

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