anirugh singh (2/20./18) Flashcards

1
Q

morphology of Corynebacterium diphteriae

A

gram+
aerobic
pleomorphic club-shpared rods

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2
Q

catalase reaction with Corynebacterium diphteriae

A

possitive

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3
Q

what does Corynebacterium diphteriae grow on

A

on rich media enrich with blood or animal material

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4
Q

where does Corynebacterium live

A

live oropharynx as a pathogen

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5
Q

what does Corynebacterium diphteriae produce

A

diphtheria toxin encoded on a lysogenic bacteriophage

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6
Q

what are non-commensal Corynebacterium called

A

diphteriae

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7
Q

where do Corynebacterium diphteriae live

A

pharynx, nasopharyn, distal urethra, and skin

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8
Q

what is diphteria

A

disease caused by the local and systemic effects of siphtheria toxin

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9
Q

local disease of Diphtheria

A

pharyngitis or tonsillitis, with plaque -like psuedomembrane in throat and trachea

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10
Q

Diphtheria toxin in blood can affect

A

multiple organs, heart=produces myocarditis

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11
Q

what type of toxin is Diphtheria toxin

A

A-B endo toxin

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12
Q

how does Diphtheria toxin work

A

B binds to cell
internalized by endocyctic vacuole
low pH of vacuole caused toxin to unfold
A subunit goes to cytoplasm A subunit (ADP-ribosylate elongation factor-2 (EF-2)) leads to inhibition of protein synth

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13
Q

how is Corynebacterium diphteriae spread

A

droplet, direct contact with cuatneous infection
lesser extent by fomites
carriers through pharyngeal or nasal to harbor the organism for a long time

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14
Q

commonality of Corynebacterium diphteriae disease

A

rare where immunication is practiced (10 cases per year

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15
Q

diagnosis of Corynebacterium diphteriae

A

clinical

cutulure on selective medium containgin potassium tellurite (tinsdale medium)

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16
Q

how body tried to fight the Diphtheria toxin

A

Diphtheria toxin is antigenic, stimulating production of neutralizing antitoxin antibodies during natural infection

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17
Q

what is formalin

A

inactivated toxin, remaining natigenic to stimulate neutralizing antibodies

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18
Q

treating diphtheria

A

diphtheria antitoxin

penicillins, cephalosporins, erythrocymcin, tetratcyclin

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19
Q

how is diphtheria antitoxin made

A

antiserum produced in horses

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20
Q

immunization of diphtheria

A

with diphtheria toxoid by stimulating production of neutralzing antibodies

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21
Q

how immunity gained for diphtheria

A

first year of life with 3-4 shots

booster every 10 years to maintian immunity

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22
Q

morphology of Listeria monocytogenes

A

aerobic, gram + rod

features resembling both corynebacteria and streptococci

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23
Q

how to distinguish Listeria monocytogenes from streptococci

A

Listeria monocytogenes

is catalase positive

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24
Q

growing Listeria monocytogenes

A

rich media

can grow at low temp (0degrees C)

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25
Q

how distinguish Listeria monocytogenes from corynebacteria

A

tumbling motility in fluid media at low temp (below 30 C)

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26
Q

what Listeria is pathogenic to human

A

Listeria monocytogenes

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27
Q

stereotypes of Listeria

A

13 serotypes (most common 1/2a. 1/2b. 4b)

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28
Q

how Listeria monocytogenes is a pathogen

A

intracellulat

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29
Q

when does Listeriosis show it self

A

until dissemination

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30
Q

foodborne outbreaks of Listeriosis leads to

A

GI primary infection leading to nausea, ab pain, diarrhea, and fever

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31
Q

Disseminated infection in adults of Listeriosis leads to

A

fever, malaise, occasional bacteremia

can cause encephalitis and meningitis

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32
Q

a fetus getting Listeria monocytogenes leads to

A

still burth or fulminant neonatal sepsis

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33
Q

major virulence factors of L. monocytogenes

A

Internalin and Lysteriolylis O

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34
Q

what does L. monocytogenes infect

A

phatgocytes by endocytosis to replicate there and eventually infects neighboring cells by actin polymerization

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35
Q

how does L. monocytogenes attach to host cell

A

Internalins (InIA, and InIB)

36
Q

what lyses the endocytic vacuole for L. monocytogenes

A

Listeriolysin O (LLO)

37
Q

where is L. monocytogenes foudn

A

ubiquitous in nature: soil, water, GI of animal

Food born: deli meat, dairy, n-cooked food at low temp

38
Q

why is it hard to eliminate L. monocytogenes

A

forms biofilms

39
Q

who is most susceptible for L. monocytogenes

A

infacts under 1 month and the elder over 60

40
Q

diagnosis of L. monocytogenes

A

Blood and CSF culture show beta-hemolytic gram positive rods

41
Q

immunology to L. monocytogenes

A

innate( neutrophil kills bacterial) and adaptive immune(T cell mediated for resolution of infection and long term protetion response

42
Q

preventing L. monocytogenes

A

No vaccine
avoid unpasteurized dairy and cooking food
don’t be immunocompromised

43
Q

treating L. monocytogenes

A

Ampicillin and trimethoprim/sulfamethoxaole

44
Q

considered the treatment of

choice for fulminant cases and in patients with severe compromise of T-cell function for L. Monocytogenes

A

ampicillin with gentamicin

45
Q

Morphology of Bacillus anthrasis

A

gram+, aerobic, spore forming long chain rods

non-motile

46
Q

growing bacillus anthrasis

A

on rich media

47
Q

spores of Bacillus anthrasis

A

extremely hardy and live for a long wall

48
Q

where does Bacillus anthrasis live

A

soil, zonnotic

49
Q

what does Bacillus anthrasis

A

Antrax A

50
Q

what is human anthrax

A

lly an ulcerative sore on an exposed part of

the body, which usually resolves without complications

51
Q

how to get Bacillus anthrasis spore to germinate

A

rich encironment of human tissue

52
Q

role of capsule in Bacillus anthrasis

A

antiphagocytic effect of glutamic acid capsule for virulence

53
Q

how does the anthrax toxin cause edema at site of infection

A

Adenylate cyclase activity

54
Q

what happens if anthrax spores are inhales

A

fulminant pneumonia leading to respiratory failure and death

55
Q

who gets anthrax

A
primariliy herbivors (get B anthraxis from pastures)
Humans contant is from contacting these animals
56
Q

Diagnosis of Bacillus anthrasis

A

Culture of skin lesions, sputum, blood, and CSF
smears with large gram+ rods usually are anthrax
hemolysis and motility exclude B anthracis
sputum and blood culture are positive in pneumonia

57
Q

how do we fight B anthracis

A

unknown: antibody directed against the toxin complex

capsular glutamic acid is immunogneic but antibody doesnt fight it

58
Q

treating Bacillus anthrasis

A

ciprofloxacin and doxycyclin
eradication of animal anthrax
live and inactivated vaccines

59
Q

morphology of mycoplama and ureaplasma

A

smallest free living micro organisms(.2-.3 micrometers)
with no cell wall
plastic and pleomorphic as:
coccoid bodies, filaments, and bottle-shaped forms
Mycoplasma pneumoniae is an aerobe, but others are facultative anaerobix

60
Q

how Mycoplasma and Ureaplasma cells bind

A

a single trilaminar membrane, with host derived exogenous sterols

61
Q

growth of Mycoplasma and Ureaplasma

A

enriched liquid culture medium and on special mycoplasma agar to produce minute colonies that look like fried eggs

62
Q

what disease does Mycoplasma pneumoniae cause

A

walking pneumonia

63
Q

where does Mycoplasma pneumoniae infect to cause walking pneumonia

A

trachea, bronchi, bronchioles, and peribronial tissue

also alveoli and alveolar walls

64
Q

walking pneumoniae symptoms

A

nonproductive cough, fever, and headache

radiographic scatter pneumonia

65
Q

who gets walking pneumoniae real bad

A

immune deficiences
sickle cell
downs

66
Q

what is common with Mycoplasma pneumoniae

A

pharyngitis and ototis

67
Q

roll of CARDS toxin in wlaking pneumoniae

A

interferes with ciliary action and causes nuclear vacuolization and fragmentation of tracheal epithelial cells leading to inflammation and desquamation the mucosa
(ADP-ribosylating)

68
Q

commonality of Mycoplasma pneumoniae pneumonia

A

10%

69
Q

who is Mycoplasma pneumoniae infection spread

A

droplet with a small dose (100 orgs)

70
Q

who gets Mycoplasma pneumoniae

A

teenagers
families and closed communites
throughout the year

71
Q

immune response to Mycoplasma pneumoniae

A

T and B cell - mediate to help stop reinfection

72
Q

when complement-fixing serum antibodies titers reach their peak

A

2-4 weeks after infection and disappear over 6-12 months

73
Q

what does the • Nonspecific immune responses to the glycolipids of the
outer membrane of the organism from mycoplasma pneumoniae cause

A

cold agglutinins, IgM, hemolysis and

Raynaud phenomena

74
Q

diagnosis of mycoplasma pneumoniae

A

culture and staiing doesnt work: slow growth and n cell wall
serologic test using complement fixation( • Single high CF or cold hemagglutinins IgM-specific antibody titer
supports diagnosis, however, cold hemagglutinins are nonspecific)
PCR for rapid and specific diagnosis

75
Q

when doing culture and staining, if there is none, what do you have

A

viral or mycoplasma etioloty

76
Q

treating mycoplasma pneumoniae

A

macrolides
doxycyclin
fluoroquinolones
no vaccine

77
Q

what other mycoplama and ureaplasma can cause STD’s

A

Mycoplasma genitaliumand two species of Ureaplasma are leading
candidates to join Neisseria gonorrhoeae and Chlamydia trachomatis
as causes of sexually transmitted` genital infection

78
Q

morphology of Mycobacterium tuberculosis

A
slim, poor staining bacilli
whave acid fastness (red carbol fuchsin through the decolorization setp
obliagte aerobe
no spores
nonmotile
79
Q

where do Mycobacterium tuberculosis live

A
animal host (pathogen)
environment (no pathogen)
80
Q

why are Mycobacteria unique

A

lipid rich cell wall

81
Q

how does TB manifest

A

systemic , but only shown in the most exposed people

shows after a long period of asymptomatic

82
Q

symptoms of active TB

A

chronic pneumonia, fever, cough, bloody sputum, and weight loss

83
Q

What does TB do once it leaves the Lung

A

central nervous gets fucked up

84
Q

how does one get TB

A

inhalation of droplet nuclei carying the organism

1 cough can generate 3000 infected droplet nuclei, and you only need 10 bacilli to initate a pulmonary infection

85
Q

imunity against TB

A

High initate immunity
TH1 immunity important
Cytotoxic CD8+ lymphocytes also

86
Q

diagnosis of TB

A

acid fast stains
PCR
Tubercullin test
Qauntiferon gold

87
Q

drugs for TB

A

first line: isoniazide, ethambutol, rifampin,pyrazinamine
second line: para-aminosalicylic acid, ethionamide, cycloserine, fluorquinolones
BCG vaccine protetive afainst meningeal TB and Efficacy angainst pulmonary TB varies