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micro immuno 2 > Chlamydia, Rickettsial Diseases and Spirochetes (3/8/18) > Flashcards

Chlamydia, Rickettsial Diseases and Spirochetes (3/8/18) Flashcards

1
Q

morphology of chlamydia

A

Small (.3-1micrometer)

gram-

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2
Q

how does chlamydia act as a pathogen

A

obligate intracellular bacteria relying on host amino acids and atp

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3
Q

cell wall of chlamydia

A

no peptidoglycan

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4
Q

life cycle of chlamydia

A 
biphasic:
Elementrary bodies (EB)-small rigid cell wall, infectious form
Reticulate bodies (RB)- large fragile, metabolically active replicative form
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5
Q

where can chlamydia live

A

diverse tissue tropism and disease

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6
Q

major difference between EB and RB chlamydia

A

EB: isolated orgnism infectious, adaptived for extracellular survival
RB: Isolated organisms not infectious, adapted for intracellular growth

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7
Q

lifecycle of C. trachomatis

A

Attaches and induces endocytosis (TARP-translocated actin recruiting protein)
Using stored ATP, EB converts to replicative RB
Inhibition lysosomal fusion in host cell by forming its own membrane-bound vesicle (the inclusion where replication takes place)
Once a threshold of RB, convert to EB
CPAF (Chlamydia protease-like activity factor)- regulated cellular apoptosis signals
EBs are released

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8
Q

where replication takes place for RB CC. trachomatis

A

in an inclusion

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9
Q

reservoid for C. trachomatis

A

humans

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10
Q

where does C. trachomatis cuase disease

A

conjunctiva (eye and Genitals

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11
Q

commonality of C. trachomatis

A

most common disease in world (100 mill new cases)

most common bacterial STI worldwild

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12
Q

what is the commmon cause of neonatal conjunctivitis

A

contact with C. trachomatis with infected cervical secretions during vaginal delivery

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13
Q

how many does Chronic follicular conjunctivites affect

A

500 mill world wide

blinds 7-9 million (africa)

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14
Q

when does one get chronic follicular conjunctivities

A

in infancy or early childhood from mom vis contact with infected secretions (fomites, fingers, flies)

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15
Q

Chlamydia affects how much in urethral infection

A

5% general pop in US men and women

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16
Q

Conagiousness of Urethral chlamydia

A

Very (1/3 of male sex contacts of women with chlamydia cervicitis develop urethritis)
Asymptotic infection in men are more common than with gonorrhea

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17
Q

incubation period for urethral infection via chlamydia

A

2-6 weeks

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18
Q

tissue tropism of chlamydiae

A

columnar epithelial cells of endocervic and upper Genital tract of women
urethra, rectum, and onjunctiva of both sexes
depending on biovar other cell types can also be infected: endothelium, S. muscle, lymph, and macrophages

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19
Q

what mediates initial attachment of chlamydiae

A

MOMP (major outer membrane protein) followed by endocytosis

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20
Q

how can chlamydia enter

A

LGV biovars enter through breaks in skin/mucosa or endocytosis

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21
Q

what is the source of primary injury due to chlamydia

A

inflammation: (also cuased by Chlamydial LPS

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22
Q

what are the pro-inflammatory cytokines for chlamydia inflammation

A

IL-8 releasedby epithelial cells

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23
Q

inflammation by chlamydia leads to

A

early tissue inasion by PMN, then lymphocytes, macrophages, plasma cels, and eosinophils

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24
Q

If the immune system fails to control chlamydia infection what happens

A

aggregates of lymphocytes and macrophages in submucosa leading to necrosis and fibrosis and scarring: lead to infertility and blingness of eye

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25
Q

immuniy to chlamydia

A

incomplete (50% of women still shedd aftera a year)

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26
Q

what response is the most protective for chlamydia

A 
TH1 response (CD4+ t cells)
also Th2 directed at MOMP may participate, but antibody is associated with injury in chronic forms of the disease trachoma
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27
Q

chronic inflammation of eyelids that can lead to scaring of cornea often leading to blindness

A

Trachoma

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28
Q

acute infection presnt in newborns as mucopurulent eye discharge, but does not lead to blindness

A

Inclusion conjuctivitis

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29
Q

how does inclusion conjunctivities get to baby

A

from morther to infant at birth to affect newborns and adults

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30
Q

what may inclusion conjunctivies turn into

A

can lead to infant pneumonia sydrome (cough and difficulty feeding)

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31
Q

eye infections of chlamydia trachomatis

A

trachoma and inclusion conjunctivites

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32
Q

Genital infections of chlamydia trachomatis

A

Urethritis and epididymitis in men
cervicitis, salpingitis, and urethral syndrom in women
Lymphogranuloma venereum (LGV)

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33
Q

characteristics of urethritis and epididymitis

A

dysuria(diffficult urination) and thin urethral dischage

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34
Q

characteristics of cervicits, salpingitis, and urethral syndrome

A

asymptomatic Vaginal dischage

5-30 of women get pelvic inflammatory disease leading to sterility and ectopic pregnancy

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35
Q

inflamed fallopian tubes

A

salpingitis

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36
Q

where is LGV found

A

STD of S. america, africa, SE asia, india and caribbean

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37
Q

what causes LGV

A

invasice biovars: L1, L2 or L3

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38
Q

how does LGV get into body and what does it cause

A

entery through breaks in skin causing transient genital lesion, invades inguindal lymph notes to create bubos(swollen gland in groin)
also cuases hemorrhagic ulcerative proctitis

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39
Q

How to diagnose Chlamydia historically

A

collect epithelial cells from site of infection (urethral swab collection hurts men)

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40
Q

how do we diagnose chlamydia now?

A

Nucleic acid Amplifcation test (NAAT) to detect chlamydia and N gonorrhoeae DNA using first void urin sample for genital infections

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41
Q

treating C. trachomatis

A

Azithromycin for non-LGV (oral)

Doxycyclin for LGV

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42
Q

morphology of Rickettsiae

A

small with small genone
Gram-negative
aerobic coccobacilli
non-motile

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43
Q

parasite type for rickettsiae

A

obligate intracellular parasites

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44
Q

how do we get Rickettsiae

A

arthropod-borne to humans via arthrodpod vectors (ticks, fleas, mites, and sandflies)

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45
Q

cell envelope of Rickettsiae

A

LPS and 2 other OM proteins

Cell wall of peptidoglycan

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46
Q

why does Rickettsiae need to depend on host

A

reductive evolution requires host co-factors, amino acids, phosphorylated sugars, and ATP

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47
Q

how does Rickettsiae metabolize host glutamate

A

aerobic respiration and TCA cycle

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48
Q

grwoth of Rickettsiae

A

slow- in host cytoplasm or nucleus

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49
Q

entery of Rickettsiae

A

enter host via endocytosis-attachment of OMP
escape phagosome using phopholipase
grow in host cell cytoplasm

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50
Q

where is Rickettsiae transmitted from

A

trick salivary glands

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51
Q

locatl spread of rickettsiae leads to

A

necrotic eschar (Black sore)

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52
Q

tissue tropism for Rickettsiae leading to

A

vascular endothelium infection leads to vasculitis(inflammation of Blood vessel)
vascular lesions
increase vascular permeability: hypopvolemai and hypotension

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53
Q

Thrombosis cuase by

A

focal areas of endothelial proliferation and perivascualr infiltration

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54
Q

leakage of rBC by Rickettsiae leads to

A

rash and petechial lesions

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55
Q

CAtegories of Rickettsiosis

A

Spottered Fever group- US

typhus group- EU

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56
Q

symptoms of both types of Rickettsiosis

A

Fever, headache, myalgia, and rash

may be fatal due to severe vascular collapse

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57
Q

where spotted fever group comes from

A

Tick -borne rickettsia

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58
Q

what causes Rocky Mountain spotted fever

A

Rickettsia rickettsii

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59
Q

who does Rickettsia Rickettsii SF normally parasite

A

ticks, spreading to tick offspring

only slightly more than 500 cases a year in the US

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60
Q

when is Rickettsia Rickettii SF highest

A

between april and september, betwween age 60-69 and killing in children less than 10

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61
Q

what type of tick transmitts R. Rickett SFi?

A

Adult feamle ticks(but diff speicies) transmit because they need blood meal to lays egs

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62
Q

how long can infected adult tricks live without blood meal

A

4 years

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63
Q

R. Ricketti SF ticks across the US

A
  • Western states - wood tick
  • Eastern states - dog tick
  • Southwest and Midwest- lone star tick
  • Ubiquitous- Brown dog tick
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64
Q

incubation period for R. rickettsii SF

A

6-7 days

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65
Q

symptoms of R. rickettsii SF

A

fever headache, RASH, toxicity, mental confusion, Myalgia (muscle pain)

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66
Q

travel of rash from Rickettsia Rickettsii SF

A

begins on arm and ankles, spreads to extremities of trunk within hours

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67
Q

what parts of the rach from Rickettsi aSF are used for diagnostic test

A

rash on palsm an d soles

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68
Q

complications if RMSF is leaft untreated

A 
Intravascular coagulatoin
thrombocytopenia (low platelets)
Encephalitis (brain inflammation
Vascular collapse
Renal and heart failure
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69
Q

diagnosis of Rickettsia SF

A

hard/hazardous to culture
how to diagnosis in early stages (antibodies appear 6-7 days after illness onset)
clinical signs
serologic diagnosis is perferred

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70
Q

when to start therapy for Rickettsia SF

A

based on clinicl sings and aymptoms and epidemiologic considerastions

71
Q

how is seologic diagnoisis of Rickettisa SF done

A

Indirect fluoresent antibody(IFA)-reference labs

skin lesion biopsy- immunofluorescent antibody used for rapid confirmation

72
Q

treating Rickettisae SF

A

Doxycyclin-first wek of illness
if delayed, can’t use it (complications
Sulfonamides make the situation worse

73
Q

disease caused by Typhus group

A

Epidemic Thyphus fever
Endemic (murine) Typhus
Scrub typhus

74
Q

how to get epidemic typhus fever

A

R. prowazekii spread by body lice(often by times of misery where lots of people get lice)

75
Q

how to get Endemic (murine) typhus

A

R. typhi spread by rat flease

76
Q

how get Scrub typhus

A

orintia tsutsugamush spread by chiggers

77
Q

the only epidemic ricketsial disease

A

Typhus fever

78
Q

where is typhus found

A

africa, latin america and asia, homeless population

NOT in the US for 50 years

79
Q

typhus fever pathogenisis

A

R. Prowazekii circulates in patients blood during aute febril infection
human body louse gets infected during feeding (Blood meal)
louse die 7-21 days after infection
lice poop has R. prowazekii after 5-10 days

80
Q

how does humans eveutally get typhus fever

A

louse poop while they food, so bacteria enter blood stratm when a human scratches the bite ( can also infect through mucous membrane of eyes and respiratory tract

81
Q

Incubation period of Epidemic Typhus

A

1-2 weeks

82
Q

symptoms of epidemic Typhus

A

maculopapular rash: on trunk then to extremities (opposite from RMSF)
headache, Malaise, and Myalgia common
complication: myocarditis and CNS dysfunction

83
Q

fatality rate of Epidemic Typhus if untreated

A

10-60%(increases with age)

84
Q

diagnosising Epidemic typhus

A

serology used to confirm, clinicla history to justify

85
Q

treating Epidemic Typhus

A

immeidate with Doxycyclien

86
Q

how to prevent Epidemic Typhus

A

louse control

no vaccine

87
Q

how humans get Endemic(Murine) typhus

A

incidental - urban rodents are natural reservoir (rat flea with R. typhi)

88
Q

occurange of Endemic (murine typhus

A

world wide (50-100 case in US)

89
Q

pathogenesis of endemic (Murine) typhus

A

similar to louse-orne typhus but with expose to rats and rat flease

90
Q

serologic tests to separate Endemic and Epidemic Typhus

A

can’t separate

91
Q

what does intital lesion of scrub typhus decelop as at the bite

A

necrotic eschar

92
Q

symptomes of scrub typhus

A

fever slowing increase

headache Maculopapular rash, mental change, general lymphadenopathy

93
Q

length of maculopapular rash

A

shorter duration than louse borne or murine typhus

94
Q

trating scrub typhus

A

Doxycycline

95
Q

Morphology of Bartonella

A

Gram-neg coccobacili

96
Q

parasite of bartonella

A

facultative intraceullar parasite as an opportunistic pathogen

97
Q

primary niche and infection of bartonella

A

endothelial cells to be released into the blood stream to infect eryhtocytes
eventually taken up by arthropod

98
Q

vectors for bartonella

A

ticks, fleas, sand flies, and mosquitoes

99
Q

what can bartonella casuse co-infections with

A

lyme’s disease

100
Q

Bartonella henselae

A

Cat-scratch disease

101
Q

cases of Bartonella henselae (cat-scratch disease)

A

25k in the US mostly children

102
Q

how is Bartonella henselae (cat-scratch disease) spread

A

cat scratch, bites, or cat flease

103
Q

preventing Bartonella henselae (cat-scratch disease)

A

flea control

104
Q

symptomes of Bartonella henselae (cat-scratch disease)

A

swollen lymph nodes skinrash, conjunctivites, encephalities, prolongued fever

105
Q

how is affected by bartonella quintana (trench fever)

A

homeless alcoholic me in france and US by body louse

106
Q

bartonella quintana (trench fever) severity

A

mild subclinical diease

107
Q

symptomes of bartonella quintana (trench fever)

A
  • sudden onset of chills, headache, relapsing fever, maculopapular rash
108
Q

morphology of spirchetes

A

spirals (loose coils to rigid corkscrew)
Motile via rotation and flexion
fexible peptidoglycan cell wall with axial fibrils
outer bi-layered membrane (like gram neg)

109
Q

seeing spirochetes

A

hard to see with routing microscopy

110
Q

medically important genera of spirochetes

A

trponema
leptopria
borrelia

111
Q

normal flora for spirchetes

A

oral cavity and dental crevice

112
Q

Trench mouth (Vincent infection or ANUG-acuter necrotixing ulcerative gingivites) gets it name from

A

WWI

113
Q

how does Trench mouth (Vincent infection or ANUG-acuter necrotixing ulcerative gingivites) infect

A

opportunistic, correltaed with immunocompromised sever malnutrition and neglect of basic oral hydien

114
Q

what do spirochetes and anaerobic flora cuase

A

necrotizing, ulceration infection of the gums, oral cavity, or pharynx (bleeding gums, bad breath, metallic taste, sudden onset, pain)

115
Q

Morphology of treponema pallidum

A

motile
Slim spirochete
corkscrew shape
no lps

116
Q

how to kill treponema pallidum

A

easy: dry, heat, detergenet, disinfected

117
Q

what odes Trponema pallidum cuse

A

syphilis

118
Q

studying treponema pallidum

A

hard to culutre and can only be grown in animals

119
Q

what does T. Pallidum need from host

A

Minimalist pathogen: basic nutreitns and metabolites

120
Q

can T. Pallidum detox O2

A

no (no catalse or oxidase)

121
Q

Energy pathways for T. pallidum

A

lacks : no TCA of Electron transport

122
Q

growth speed of T. pallidum

A

slo (30 hours)

123
Q

who does syphilis pathogen

A

only human

124
Q

how do you get syphilis

A

sexual contact with person with active primary or seconday lesion
also non-genital contact

125
Q

how to get syphilis without touching genitals

A

congenital syphilis - transplacental transmission

Needles

126
Q

is tertiary syphilis contagious

A

no

127
Q

problwm of syphilis

A

world wide, as lesions cause HIV to enter

128
Q

rise of syphilis

A

on the riase (Up 18% in the US) 27,814 primary and secondary syphilis in US most with dudes who bang dudes)
628 people with congenital syphilis (minorities)

129
Q

Pathogeneisis of spirochete

A

reaches subepithelial tissue via small breaks in skin or mucous membranes
multiplty in submucos iwthout detection
spread to bloodstreat and establish infection in distant tissues

130
Q

the primary lesions of T. Pallidum is what and results in what

A

endarteritis-inflammation of inner lining of an artery and a necrotic ulceration forms
dense granulomatous cuffs of lymphocytes, monocytes, and plasms sound vessels

131
Q

how does T. pallidum evade

A

unkown

132
Q

when does Primary syphilis occure

A

3-90 days after exposure

133
Q

what first appears from primary syphilis

A

primary lesion (chancre) at point of contact
single painless, non-itchy skin ulceration
lymph node englangement 7-10 days after chancre
heals after 4-6 weeks

134
Q

when does secondary syphilis occure

A

2-8 weeks after primary infection in 1/3 of patients

135
Q

what does secondary syphilis involve

A

skin ,mucous membranes, and lymph nodes

gives a symmetrical, red-pink, non-itchy rask on trunk and extremities, including palms and soles

136
Q

what fills the lesion of seconadry syphilis

A

bacteria (highly infectious)

137
Q

after xeconday syphilis what occures

A

latent syphilis (1/3 spontanously clear infection)

138
Q

symptoms of latenet syphilis

A

no clinical symptoms but serolgical tests are positive

139
Q

what can happen with latent syphilis

A

relapse to secondary

transmit to others or feus

140
Q

what odes tertiary syphilis result in

A

tissue distrcution

141
Q

how common is tertiary syphilis

A

1/3 of untreated secondar syphilis, after infection 15-20 ears

142
Q

how tertiary syphilis manifests itself

A

neeurosyphils
Ocular syphilis
Cardiovascular syphilis
GUmma

143
Q

when syphilis invades the nervous system

A

neurosyphilis

144
Q

symptomes of neuosyphilis

A

headache, altered behavior, loss of coordination, paralysis, Tabes dorsalis,
sensory deficits and dementia (most common in HIV positive patients)

145
Q

symptomes of ocular syphilis

A

vision change

146
Q

symptomes of cardiovascular syphils

A

aortis - leads to aneurysms

147
Q

where is gumma

A

in skin, bone, joints, organs

148
Q

diagnosis of syphilis

A

serologically: detection of antibodies aginst treponeal antigens

149
Q

treponemal vs non-treponemal

A

looks for treponemal antigen (FTA- ABD, MHA-TP)

cardiolipin based test that is non-specific and cross reaction possible when autoimmune disaes present

150
Q

treating ssyphilis

A

penicillin at all stages

151
Q

morphilogy of borrelia burgdorferi

A 
long slender psirochetes
axial flagella (many)
outer membrane without LPS
stains with Giemsa or Write
Microaerophilic
152
Q

grow speed of Borrelia Burgdorferi

A

slow (24-48 doubleing time hours)

153
Q

what genes does Borrelia Burgdorferi lack

A

essential nutrients(amino acids, fatty acids, nucleic acids

154
Q

genome type of Borrelia burgdorferi

A

partitioned genome- many circular and linear plasmids

155
Q

disease from borrelia burgdorferi

A

Lyme

other Borrelia cause relapseing fever

156
Q

species of Borrelia burgdorferi

A

18 diff subspecies: differ in geographic distribution and clinical manifestation

157
Q

OMP’S OF bORRELIA BURGDORFERI

A

MULTIPLE CLASSES,that undergo antigenic variation (outer surface proteins)(Osps)

158
Q

what do Osps do

A

OspA and OspC are differentially expressed dpening on state of tick or mammalian infection
other bind fibrongectin and serum factor H

159
Q

the primary reservoid of B. burgdorferi

A

rodernts

160
Q

how do ticks get B. burgdorferi

A

tick larvae food on mice

161
Q

when lyme’s disaes occures

A

in spring and summer when nymphs feed on vertebrate hosts as part of life cycle

162
Q

inoculum of B burgdorferi

A

low (less than 20)

163
Q

enxootic cycle of B. Burgdorferi

A

larve hatch fro m uninfected eggs and feed on infected host
larve molt into myphs, feed and transmited B. Burgdorferi to vertebrae host
Nymphs mold into adults which feed on deer and mate

164
Q

where is lyme disease present

A

where deer are present

165
Q

symptomes of primary lyme diease

A

bull’s eye pattern -macule or papule rash at bite site (erythema migrans)
Fever, Fatigue, Myalgia, headache, joint pain, mild neck stiffness

166
Q

who doesnt get seconday lyme disease

A

50% of patietns develop like primary

167
Q

when does secondary(Chronic) lyme disease occure

A

days to months after primary rash

168
Q

what happens in seconary lyme diease

A

Fluctuating meningitis, cranial nerve palsies, and peripherneuropathay
heart conducting problems - atrioventricular block - myocarditis leading to caridac englandment
arthrits

169
Q

what is chronic lyme diease from

A

autoimmune state

170
Q

diagnosis of Lyme diease

A

expose and clinical finds

later statge can use serology for antibodies

171
Q

how to culture Lyme disease

A

from erythema migrans skin lesion, blod, joins, CSF.

but very hard

172
Q

can you see lymes disease with a microcope

A

no

173
Q

treating lyme’s diase

A

Doxycycline and BEta- lactam: early lyme and arthristis

but slow response

174
Q

preventing lymes disease

A

wear protective clothing

remove tick fast (ned 48-72 hours to reansmit bacteria

micro immuno 2 (8 decks)

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