Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology - Quiz 2 > ALL BACTERIA! > Flashcards

ALL BACTERIA! Flashcards

1
Q

Salmonella (general): Similar to

A

Shigella, E coli (Enterobacteriaceae Family)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Enteroaggregative E. coli (EAEC): Similar to

A

EPEC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acinetobacter baumanii: At Risk

A

Hospitals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acinetobacter baumanii: Disease

A

OPPORTUNIST!

Nosocomial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acinetobacter baumanii: Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acinetobacter baumanii: Negative for: (2)

A

Oxidase

Sugar fermentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acinetobacter baumanii: Oxygen

A

aerobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acinetobacter baumanii: Reservoir

A

Hospital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acinetobacter baumanii: Shape

A

short rod

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acinetobacter baumanii: Transmission/vector/ habitat

A

Indwelling medical devices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acinetobacter baumanii: Treatment

A

Multidrug resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acinetobacter baumanii: Virulence Factors (4)

A

Capsular polysaccharides
Adhesins
Proteolytic/lipolytic enzymes
LPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bordetella pertussis: At Risk

A

Infants more likely to die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bordetella pertussis: Disease

A

Pertussis (whooping cough)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bordetella pertussis: Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bordetella pertussis: Incubation Period

A

7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bordetella pertussis: Oxygen

A

Obligate aerobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bordetella pertussis: Reservoir

A

NONE - only infects humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Bordetella pertussis: Shape

A

coccobacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Bordetella pertussis: Symptoms

A

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

[Paroxysmal stage] whooping cough, vomiting, cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bordetella pertussis: Transmission/vector/habitat

A

Aerosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Bordetella pertussis: Treatment

A

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

Treat household contacts prophylactically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Campylobacter (jejuni): At Risk (3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Campylobacter (jejuni): Disease (2)

A

Diarrhea from inflammatory enteritis

Bacteremia (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Campylobacter (jejuni): Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Campylobacter (jejuni): Incubation Period

A

3-5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Campylobacter (jejuni): Infectious dose

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Campylobacter (jejuni): Oxygen

A

microaerophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Campylobacter (jejuni): Pathogenesis (3 steps)

A
  1. survive gastric barrier
  2. arrive in small/large bowel - inflammation
  3. bloodstream (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Campylobacter (jejuni): Prevention (2)

A

Pasteurization of milk, cooking meat (esp. poultry)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Campylobacter (jejuni): Reservoir

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Campylobacter (jejuni): Shape

A

curved or comma with uni or bipolar flagellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Campylobacter (jejuni): Treatment

A

Oral rehydration therapy

Antimicrobial therapy as indicated (erythromycin; alt - cipro)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Chlamydophilia (general): Gram stain

A

Gm- (by phylogeny)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Chlamydophilia (general): Shape

A

pleomorphic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Chlamydophilia (general): Treatment

A

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

Any antibiotic used must enter cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Chlamydophilia pneumoniae: Diagnosis

A

Antibody assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Chlamydophilia pneumoniae: Disease

A

Atypical (diffuse) pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Chlamydophilia pneumoniae: Epidemiology (2)

A

Causes 10% of pneumonia in adults

May play a role in coronary atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Chlamydophilia pneumoniae: Number of serotypes

A

1 serotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Chlamydophilia pneumoniae: Symptoms (3)

A

Pneumonia/bronchitis
Gradual onset of cough
Little/no fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Chlamydophilia pneumoniae: Transmission/vector/ habitat

A

Person-to-person via aersol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Chlamydophilia psittaci: At Risk

A

Contact w/birds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Chlamydophilia psittaci: Diagnosis (2)

A

Pathogen in blood or sputum

Antibody assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Chlamydophilia psittaci: Disease

A

Psittacosis (parrot fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Chlamydophilia psittaci: Number of serotypes

A

1 serotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Chlamydophilia psittaci: Pathogenesis

A

Disseminated infection that targets epithelial cells, endothelial cells, Mos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Chlamydophilia psittaci: Reservoir

A

Birds (induces chronic subclinical infection with constant fecal excretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Chlamydophilia psittaci: Symptoms (3)

A

Fever and headache

Severe -> interstitial pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Chlamydophilia psittaci: Transmission/vector/ habitat

A

Inhalation of bird feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Chlamydia trachomatis, serotypes L1-3: Diagnosis

A

Ag testing to differentiate between C. trachomatis serotypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Chlamydia trachomatis, serotypes L1-3: Disease

A

Lymphogranuloma venereum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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

A

STD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A

Poor hygiene

Asia and Africa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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

A

Ag testing to differentiate between C. trachomatis serotypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Chlamydia trachomatis, serotypes A-C: Disease

A

Trachoma (chronic conjunctivitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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

A

World’s leading cause of preventable blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Chlamydia trachomatis, serotypes A-C: Pathogenesis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

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

A

More invasive serotypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

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

A

Mechanical (finger to eye)

Flies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Chlamydia trachomatis, serotypes A-C: Treatment

A

Annual universal treatment with azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

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

A

Neonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

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

A

Ag testing to differentiate between C. trachomatis serotypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

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

A 
Inclusion conjunctivitis
Infant pneumonia (usually an extension of ocular disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

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

A

Perinatal
Swimming pools
STD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

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

A

Non-gonoccocal urethritis

More severe -> epididymytis, salpingitis -> infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

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

A

Possibly most common venereal disease

Infection increases chance of HIV transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

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

A

Males: usually asymptomatic (purulent urethral discharge)

Females: frequently asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

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

A

STD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

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

A

Single high dose azithromycin for BOTH sexual partners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Corynebacterium diphtheriae: At Risk (2)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Corynebacterium diphtheriae: Disease (1)

A

Diphtheria: infection of skin and/or throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Corynebacterium diphtheriae: Gram stain

A

!!+++++++!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Corynebacterium diphtheriae: Incubation Period

A

2-5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Corynebacterium diphtheriae: Life Cycle

A

Do NOT form spores!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Corynebacterium diphtheriae: Other

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Corynebacterium diphtheriae: Oxygen

A

aerobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Corynebacterium diphtheriae: Prevention (2)

A

Immunity depends on presence of Ab against toxin (antitoxin)

Give DTaP booster to travelers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Corynebacterium diphtheriae: Reservoir

A

NONE - only infects humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Corynebacterium diphtheriae: Shape

A

rod
club-shaped
(pleomorphic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Corynebacterium diphtheriae: Symptoms (3)

A

Fever, cough, sore throat

Gray PSEUDOMEMBRANE formation in severe cases (thrush)

Inflammation of lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Corynebacterium diphtheriae: Transmission/vector/habitat

A

Aerosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Corynebacterium diphtheriae: Treatment (2)

A

Horse antitoxin immediately (hypersensitivity and anaphylactic shock common)

Penicillin prophylactically or as treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Corynebacterium diphtheriae: Vaccine

A

Toxoid - DTaP good for 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Coxiella burnetii: Disease (2)

A

Q fever

Can progress to chronic endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Coxiella burnetii: Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Coxiella burnetii: Reservoir

A

Sheep and cattle -> tick and so on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Coxiella burnetii: Special growth conditions

A

Obligate intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Coxiella burnetii: Symptoms (5)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Coxiella burnetii: Treatment (3)

A

Doxycycline
Quinolone Abx

Chronic endocarditis -> aggressive therapy, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Diffuse adhering E. coli (DAEC): At Risk

A

Older children in developing countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

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

A

PCR for virulence genes

Tissue culture -> diffuse adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Diffuse adhering E. coli (DAEC): Disease

A

Diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 +!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

E. coli (general): Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

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

A

Oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

E. coli (general): Oxygen

A

fac. Anaerobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

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

A

Lactose
Glucose (+gas)
Nitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

E. coli (general): Shape

A

rod

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Ehrlichioses: At Risk (1)

A

Exposure to ticks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Ehrlichioses: Disease (2)

A

Monocytic Ehrlichiosis

Granulocytic Ehrlichiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Ehrlichioses: Epidemiology (1)

A

Found in southern US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Ehrlichioses: Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Ehrlichioses: Pathogenesis (1)

A

Infects monocytes and granulocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Ehrlichioses: Special growth conditions (1)

A

Obligate intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Ehrlichioses: Symptoms (3)

A

Fever, lymphocytopenia, elevated LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Ehrlichioses: Transmission/vector/ habitat

A

Ticks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Ehrlichioses: Treatment (1)

A

Tetracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Enteroaggregative E. coli (EAEC): At Risk

A

Children in developing countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

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

A

PCR for virulence genes

Tissue culture -> aggregative adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

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

A

Chronic Diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

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

A

Aggressive epithelial cell attachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

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

A

No A/E lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

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

A

Persistent diarrhea

Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

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

A

Fluoroquinolones (travelers and HIV+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Enterobacter cloacae: At Risk (1)

A

Hospital setting following antibiotic treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Enterobacter cloacae: Disease (4)

A

OPPORTUNIST!

Infections of burns, wounds, respiratory, UT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Enterobacter cloacae: Gram stain

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Enterobacter cloacae: Oxygen

A

fac. Anaerobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Enterobacter cloacae: Pathogenesis

A

Forms biofilms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Enterobacter cloacae: Positive for: (1)

A

Lactose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Enterobacter cloacae: Shape

A

rod

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

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

A

Bloody diarrhea

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Enterohemorrhagic E. coli (EHEC): Incubation Period

A

3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Enterohemorrhagic E. coli (EHEC): Infectious dose

A

Low infectious dose (~100)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

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

A

Sorbitol**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Enterohemorrhagic E. coli (EHEC): Number of serotypes

A

O157:H7 = most important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Enterohemorrhagic E. coli (EHEC): Reservoir

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Enterohemorrhagic E. coli (EHEC): Similar to

A

Shigella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

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

A

Mostly extracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

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

A

Abd. Pain, bloody diarrhea,
NEVER systemic
HUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

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

A

Supportive care

Antibiotics and antimotility agents are contraindicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

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

A

PCR for virulence genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

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

A

Diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

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

A

Less common in industrialized nations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Enteroinvasive E. coli (EIEC): Similar to

A

Shigella dysentery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

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

A

Highly invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

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

A

Food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

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

A

PCR for virulence genes

Tissue culture -> localized adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

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

A

Childhood Diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

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

A

Leading cause of childhood diarrhea (developing countries)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Enteropathogenic E. coli (EPEC): Pathogenesis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Enteropathogenic E. coli (EPEC): Symptoms

A

Diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

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

A

Person-to-person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Enteropathogenic E. coli (EPEC): Treatment

A

Antibiotics guided by susceptibility testing for severe or protracted cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

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

A

Travelers, infants in developing countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

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

A

PCR for virulence genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Enterotoxigenic E. coli (ETEC): Disease

A

Traveler’s Diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Enterotoxigenic E. coli (ETEC): Symptoms

A

Watery diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

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

A

Food/water

Person-to-person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Enterotoxigenic E. coli (ETEC): Treatment

A

Loperamide (+fluoroquinolone)

Azithromycin or rifaximin (for travelers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

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

213
Q

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

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)

222
Q

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

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

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

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

242
Q

Klebsiella pneumoniae: Oxygen

A

fac. Anaerobe

243
Q

Klebsiella pneumoniae: Positive for: (1)

244
Q

Klebsiella pneumoniae: Shape

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

252
Q

Legionella pneumoophila: Incubation Period

253
Q

Legionella pneumoophila: Oxygen

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)

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

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

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

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

315
Q

Proteus mirabilis, vulgaris: Negative for: (1)

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)

319
Q

Proteus mirabilis, vulgaris: Shape

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

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

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

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

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

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

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

369
Q

Salmonella (general): Infectious dose

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

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)

378
Q

Salmonella choleraesius: Incubation Period

A

6-72 hours

379
Q

Salmonella choleraesius: Infectious dose

380
Q

Salmonella choleraesius: Number of serotypes

A

1 serotype

381
Q

Salmonella choleraesius: Reservoir

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

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

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

417
Q

Serratia marcescens: Negative for: (1)

418
Q

Serratia marcescens: Oxygen

A

fac. Anaerobe

419
Q

Serratia marcescens: Shape

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

428
Q

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

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

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

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)

453
Q

Uropathogenic E. coli (UPEC): Shape

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)

463
Q

Vibrio cholerae: Epidemiology (1)

A

John Snow + Broad Street Pump

464
Q

Vibrio cholerae: Gram stain

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions