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micro immuno 2 > Legionella and Coxiella Plague and other bacterial zoonotic diseases (3/6/18) > Flashcards

Legionella and Coxiella Plague and other bacterial zoonotic diseases (3/6/18) Flashcards

1
Q

when was legionnaires disease was found

A

legionnaires conveion in 1979 and 130 got sick and 25 died with similar sympotms

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2
Q

morphology of legionella pneumophila

A

gram neg
aerobic
small pleomorphic bacilli
non capsule

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3
Q

catalase response to legionella

A

positive

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4
Q

where is legionella pneumophila found

A

in water and in soil

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5
Q

what is infected by legionella pneumophila

A

facultative intraceullar bacteria(infects protozoa_

opportunistic pathogen

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6
Q

how does legionella pneumophila infect protozoa

A

requires special media to isolate (buffered charcoal yeast extract (CYE)

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7
Q

how is legionella pneumophila opportunistic pathogen

A

only smoked and immunocompromised hosts with bad cell mediated immunity

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8
Q

what does legionella pneumophila

A

atypical pneumonia due to aerosols by humidifies and cooling systems

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9
Q

legionella pneumophila virulence factor

A 
Pili (fimbriae
Flagella
LPS
type 4 secretion (Icm/Dot)
legionell-containing vacuole in macrophages
low metabolic state
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10
Q

LPS of legionella pneumophila toxicity

A

less toxic than other gram-neg

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11
Q

how does legionella pneumophila enter a low metabolic state

A

biofilm-imbedded cells resist stress

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12
Q

what happens because legionella pneumophila is a Facultative intraceullar bacteria

A

can multiply inside free-living amoebas, other protozoa and alveolar macrophages

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13
Q

pathogenisis of legionella pneumophila

A

aerosolized drops breathed in

grow in macrophages, causing inflammation, producing necrotizing multifocal pneumonia

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14
Q

action of legionella-containg vacuole

A

made by mitochondiea, ribosomes, and ER proteins make the LCV to block the lysosomes and bacteria replicate inside of them

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15
Q

how does legionella pneumophila resist immunity

A

intracellular multiplcation

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16
Q

immunity against legionella pneumophila

A

innate and adpative mechanism
TLR in macrophages and dendritic cells recognize Legionella LPS
Th1 adaptive immune response: INF-gamma, Il-2, and Il-18 are produced and activate macrophages and intracellular killing
little use of antibodies

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17
Q

cases of legionellosis

A

5000 in US

25000 in world

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18
Q

how does legionellosis transmit

A

not person to person but via large complex manmade water systems (Hotel, hospitals, nursing homes, cruise ships)

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19
Q

forms of legionellosis

A

Legionannaires disease: sever - pneumonia

Pontiac fever: mild self-limited form with flu-like symptoms (no pneumonia

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20
Q

how are both forms of legionellosis spread

A

both by water and pontiac fever by sontaminiated soil

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21
Q

why do we have an increase in legionellosis

A

climate change
aging US pop
Aging plumbing
increase of at risk patients

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22
Q

leionnaires disease affects who

A

5% exposed mostly middle age or elderly smokers, and with chronic diseases of immunosuppression

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23
Q

legionnaires disease leads to

A

shock, respiratory failure or both

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24
Q

mortality rate of legionnaires disease

A

15%, and higher with health-care association (46%)

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25
Q

symptomes of legionnaires disease

A 
myalgia and headach
rising high fever
dry cough on 2nd/3rd day and chest pain
chills vomiting diarrhea confusion and delirium
hepatic dysfunction
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26
Q

time between exposure and legionnaires disease

A

2-10 days

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27
Q

diagnosis of legionnaires disease

A

difficult:
direct fluorescent antibody with culture of infected tissue
PCR

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28
Q

how direct fluorescent antibodies are used to diagnose legionnaires disease

A

L. pneumophila- specific monoclonal antibodies that recognize all serogroups
use high-quality specimes (recognizes 25-50% o culture-proven cases

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29
Q

gram staining for legionnaires disease

A

bad staining

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30
Q

culturing for legionnaires disease

A

Buffered Charcoal est extract agar with vitamin, L-cystein, ferric pyrophasphate

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31
Q

treating legionnaires disease

A

Fluoroquinolone or axithromycin are preferred
erythromycin can treat infection
not penicillin: most legionella produce beta-lactamases)

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32
Q

how to prevent legionnaires

A

minimize aerosole in public places from contaminated water

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33
Q

why is preventing legionnaires complicated

A

resist chlorine and head

forms biofilms

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34
Q

how to prevent legionnaires

A

dont use tap water in aerosolizing water

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35
Q

infection in humans acquired by direct or indirect contact with animals

A

Zoonoses

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36
Q

types of Zoonoses

A

Coxiella burnetii- Q-fever
Yersina pestis: Bubonic Plague
Brucella: undulant fever
Fancisella: Tularemia (similar to plague)
Pasteurella Multocida: soft tissue infection

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37
Q

how to get coxiella burnetii

A

inhalatino of soil and dust contaminated after birth of infected animals

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38
Q

how to get yersina pestis

A

exposure to flease from infected rodents

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39
Q

how to get brucella

A

direct contact with animal infected

ingested of contaminated diary

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40
Q

how to get Fancisella

A

direct contact with infected mammal
inhalation
bite of infected tick

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41
Q

how to get paseurella multocida

A

cat or dog bite

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42
Q

what was Coxiella first seen as

A

a new type of Rickettsia

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43
Q

what is Coxiella related to

A

LEgionella

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44
Q

Morphology of Coxiella burnetti

A

gram-

small coccobacilli

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45
Q

pathogen as Coxiella burnetii

A

obligate intracellular pathogen (macrophages and phagocytic cells)

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46
Q

where does coxiella burnetii grow well

A

placental tissues contaiminating soil after birth

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47
Q

who is most at risk for coxiella burnetii

A

vets, famers, slaughter house workers, animal researchers

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48
Q

infectious dose foc coxiella burnetii

A

1-10 organisms cuase disease in 50% (id50=1)

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49
Q

Virulence factors for coxiella

A 
LPS
Type IV secretion (Dot/Icm)
Resistant to low pH and enzymes of phagolysomes
Coxiella-contain vacuole
Biphasic life cycle
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50
Q

what happens to coxiella when phagosome and lysosome fuse

A

continues to multiple

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51
Q

a phagolysosome-like compartment where Coxiella replicates

A

Coxiella-containing Vacuole

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52
Q

The lifecycle of Coxiella

A

Small Cel variants: not metabolically active (like spore)

Large cell variant: metabolically active- switches to this when enters into host cell

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53
Q

how does Coxiella become a pathogen

A

Aerosol transmission- Inhaled into lungs
• Binds to alveolar macrophages and is passively taken up hrough phagocytosis
• Affinity for reticuloendothelial system (macrophages and monocytes)
• Can also invade non-phagocytic cells - epithelial and endothelial cells

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54
Q

intracellular trafficking of Coxiella burnetii

A

Once in a phagosomelysosomal
fusion occurs normally, creating a phagolysosome (pH 5.4)
• Then Coxiella expands the compartment size creating the Coxiella containing vacuole (CCV),
• Transitions to the metabolically active LCV and begins to replicate –ntakes up to 6 days

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55
Q

when symptomes of Q-fever occur

A

about 20 days after inhalation

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56
Q

symptoms of Q-fever

A

flu like-abrupt fever, chills, muscle aches and headache
Stomach pain, nausea, vomiting and diarrhea
non-productive cough
Hepatosplenomegaly and abnormal liver function common

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57
Q

symptoms of severe cases of !-fever

A

Pneumonia or hepatitis

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58
Q

comlications due to Q-fever

A

myocarditis, pericarditis, encephalitis (rare)

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59
Q

chronic infects of Q-fever are associtated with

A

endocarditiis

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60
Q

how to treat Q-fever

A

recover without antibiotcs

maybe 2 week with doxycycline

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61
Q

how did the plague occure

A

non-immune rats lead to bacteremia
fleas feed on rats and get Y pestis
bacteria block intestines so fleas vomit up Y pestis into a bite wound

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62
Q

when did the black plauge occure the most

A

high rat population and rat mortality

63
Q

when flease leae an infected rodent and pass the infection to other in the population, not to humans

A

sylvatic cycle

64
Q

masses of rats in close contact with humans, infected with flease-that bite huam

A

Urban cycle

65
Q

how did pneumonic plague occure

A

when humans infected Y. Pestis develop bacteremia, infecting the lungs leading to person to person spread (No fleas needed)

66
Q

exististance of sylvatic plauge

A

most continents
common in south east asian
not in western europe or australia
15 cases in the US

67
Q

morphology of Yersinia pestis

A

Gram-neg
bacillus (pleomorphic)
non-motile
Enterobacteriaceae family

68
Q

what part of yersinia pestis is needed for pathogenesis

A

virulence plasmids

69
Q

how does Y pestis turn on and off virulence factors

A

regulatory systems that sense temp, calcium, and otehr envirnomental triggers

70
Q

how does Y petsis multiply in flea foregun

A

low temp virulence factors

phospholipase D- resists antibacterail factors in flea midgut

71
Q

who does Y pestis blocause vomitting by the flea

A

Coagulase

Polysaccharide biofilm

72
Q

flea bite does what to Y pestis

A

temp shift shows new envirnoment so virulence changes

73
Q

virulence of Y pestis upon biting

A

Differ LOPS
F1 capsule
Plasminogen activator (Pla)
Yops

74
Q

LPS of Y. pestis upon flea bite

A

not recognized by TLR (immune evation

75
Q

F1 capsule of Y pestis

A

gel like capsule antiphagocytic

76
Q

role of plasminogen activator in Y pestis

A

spread through tissues - enzymatic and adhesion to matrix proteins

77
Q

Roll of Yops

A

destroy host cell

deisrutpt host cell

78
Q

how does yops secreted by type III secretion affect professional phagocytes onces inside

A

disrupt signalling path, estroy cytoskeleton structures, trigger apoptosis, inhibit cytokine production and acidifiaction of phagosome

79
Q

what does Y pestis do when it enters the blood stream

A

reaches regional lymph nodes, lyses ost cell, multiply’s rapidly and produces bubo

80
Q

what is bubo

A

hemorrhagic suppurative lymphadenitis

81
Q

Bacteremia of Y pestis leads to

A

Toxic shoeck - LPS endotoxin, yops, proteases, and aextracellular products

82
Q

incubation of bubonic plauge

A

2-7 days after flea bite

83
Q

what does bubonic plauge do

A

fever and painful bubo in groin or axilla
50-70% process to bacteremia and may die from gram-negative septic shock (hours to days after dubo)
5% develop pneumonic plauge, mucoid or bloody sputum

84
Q

Incubation period of pneumonic plauge

A

2-3 days after exposion

85
Q

what does Pneumonic play do to you

A

fever, malaise, tighten chest
cough,sputum, dyspnea (trouble breathing), and cyanosis(blue lips) later
death on 2-3rd day
no one survives without antibiotics within 24hurs

86
Q

diagnosis of Plague

A

gram-stained smears of aspirates from bubo show bipolar-staining gram-negative bacilli
Immunofluroescence techniquie in public heath labs

87
Q

how to isolte Plague

A

blood agar or MacConkey agar (takes a while though so patient may die)

88
Q

treating plague

A

Gentamicin or strptomycin withor without doxycycline

Also ciprofloxacin or Chloramphenicol if meningitisis presently

89
Q

if treat plague early, what is the mortality

A

less than 10%

90
Q

morphology of Brucella abortus

A

Gram negative rods
small coccobacili
non-motile
Aerobe

91
Q

Brucella abortus tests positive to

A

catalse, oxidase, and urease

92
Q

can brucella abortus ferment sugar

A

no

93
Q

envelope of brucella abortus

A

unusual, phosphatidylcholine like eukaryotic cells

94
Q

growth rate of brucella abortus

A

slow (2-3 days to culture

95
Q

where does Brucellosis occur

A

persist for life in animals reproductive organs

96
Q

what does Brucellosis cause

A

abortion, sterility, decreased milk production in cattle, goats and hogs

97
Q

how does Brucellosis spread

A

direct contact with infected tissues and ingestion of contaminated feed
not person to person

98
Q

how to control brucellosis

A

systematic control: vaccination, eradication of infected animals

99
Q

how many people get brucellosis

A

100/year

100
Q

how do humans get brucellosis

A

consumption of unpasteurized dairy and health products from mexico
cuts in skin, mucous membrean, inhalation ingestion

101
Q

occupational exposures to brucellosis

A

Vets, livestock, slaughterhouse owkres, lab workers

102
Q

what kind of pathogen is brucella

A

Facultative intracellular parasite of epithelial cells and phagocytes

103
Q

waht can brucella evade once past skin or mucous membran

A

evade innate immunity, specifically TLR because outer membrane looks like eukaryotes

104
Q

where doe Brucella multiply

A

macrophages in liver sinusoids, spleen, bone marrow, and reticuloendothelial systemto orm granulomes

105
Q

how does brucela live within a cell

A

inhibit myeloperoxidase system, phagosome-lysosome fusion and apoptosis of host cell

106
Q

what secretion system does Brucella have

A

type 4 like legionella

107
Q

what in cows, sheep,pigs, and goats stimulates brucella growth

A

erythritol (because human placents don’t have this, Brucella can’t infect human placentas

108
Q

immunity to brucella

A

antibodies formed, not protective

T-cell mediated immune response critical using TH1-type response with cytokines to clean Brucela from macrophages

109
Q

symptoems of brcellosis (undulandt fever)

A

7-21 days after infection
malaise, chills, fever, headache, weight loss
periodic denching night sweats

110
Q

how long does brucellosis occure

A

weeks-to 1-2 years

111
Q

physical findings of brucellosis and localizing signs

A

few : less than 25 % show detectable englagement of lymph nodes
spelenomegaly most common but also lymphadenopathy and hepatomegaly

112
Q

diagnosiing brucella

A

isolate from blood of biopsy of liver,bone marrow or lymph nodes
slow to grow in plates, but modern tech speeds it up
serological test are available, but may not indicated current disease

113
Q

treating brucella

A

Doxycycline in combo with rifampin or gentamicin

no vaccine

114
Q

effectiveness of brucella treatment

A

2-7 days for fever to break

10% relase within 3 months

115
Q

Morphology of Francisella tularensis

A

GRam-negative
non-motile
Coccobacilli - small rod
Aerobic

116
Q

whay is needed for francisella tularensis to grow

A

cystein

117
Q

what kind of parasite is francisella tularensis

A

facultative intraceullular parsite of macrophages

118
Q

what does francisella tularensis cause

A

Tularemia ie rabbit fever

119
Q

why is francisella tularensis classified as a tier 1 select again

A

low dose
ease of spread
high virulence

120
Q

Virulence of F. tularensis

A

lipid rich capsule

unusual LPS

121
Q

LPS immune response of F. tularensis

A

induce protective antibodies

but not stimulate innate immunity (not recognized by TLR)

122
Q

natural infections of F. tularensis results in what for immunity

A

long lasting immunity as antibody titers remain high for years

123
Q

how is Tularemia spread

A

contact with infected mammal of blood feeding arthropod (tick bite)
rabbits, squirrels, muskrats, beaver, and deer can be infected without symptons
minor skin abrasion
inhalation

124
Q

Cases of Tularemia in the us

A

100-200 cases with high tick and rabiit associated strains

125
Q

where is tularemia not found

A

british isles, africa, S. america or australia

126
Q

how long does tularemia grow

A

unimpeded until phagocytes are enountered

127
Q

where do lessions occure for tularemia

A

near site of infection with ulceration

128
Q

what happens to tularemia upon macrophages ingestion

A

reside in phagosome, resists lysomome fusion and escape from host cytoplasm

129
Q

where can tularemia multiply

A

hepatocytes, kidneys, and alveolar epithelial cells

130
Q

a type of inflammation due to a college of immune cells ie macrophages found in many disease

A

Granuloma

131
Q

when does Granuloma occur

A

when the body attempts to wall off a foreing substance that it cannot eliminate

132
Q

incubation of tularemia

A

2-5 days

133
Q

what does tularemia progression depend on

A

site of inoculation and extendt of spread

134
Q

how does tularemia begin

A

acute onset of high fever (grater than 104 degrees F), chills, and malaise

135
Q

most common tularemia

A

ulceroglandular due to tick bite or infected animal

136
Q

ulceroglandular form of tularemia results in

A

ulcer and swollen lymph nodes

137
Q

Oculoglandular form of tularemia

A

inoculation through the ye, when butchering an infected animal

138
Q

oropharyngeal form of tularemia

A

ingestion of large dose (> 10^8) rsulting in sore thraot, mouth ulcer, tonsillitis, and swelling of lymph glands

139
Q

most serious Tularemia

A

Pneumonic form

140
Q

Pneumonic form of Tularemia reuslts in

A

inhalation of dust or aerosols result in pneumonic tularemia or infection like typhoidal from

141
Q

what can tularemi pneumonia develop hrough

A

bacteremia or inhalation

142
Q

typhoidal form of tularemia

A

combination of genreal symptoms without locatlizing or other syndroms

143
Q

diagnosisng tularemia

A

diffisult because symptoms like other more common illnesses
use pateint history (tick, der fly bites, sick/dead animal contact)
serologic tests used: agglutinating antibodies usually present by week 2 of illness

144
Q

how to culture tularemia

A

hard to grow and must use choclate agar and sulfhydryl compounds

145
Q

treating tularemia

A

antibioics: gentamicin and streptomycin

also doxycycline and ciprofloxacin, but may relapse

146
Q

who gets vaccine for tularemia

A

high risk population gets live attenuated vaccine

147
Q

Morphology of pasteurela multocida

A

small coccbacillary
gram-
facultative anaerobe

148
Q

why is pasteurella multocida a facultative anaerobe

A

oxidase positive

149
Q

what can pasteurella multocida ferment

A

variety of carbs

150
Q

penicillin susceptibility of pasteurella multocida

A

is, unline most gram-negaive rods

151
Q

where is pasteurella multocida found

A

normal respiratory flora of domstic mammals (Dogs an cats)

152
Q

most common cuas of infected dog or cat bite

A

pasteurella multocida

153
Q

when does pasteurella mutlocida occure

A

24 hrs of animalbite or scratch

154
Q

what does pasteurella mutlocida cause

A

diffuse cellulties with a well defined erythematous border

micro immuno 2 (8 decks)

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