Chlamydia, Rickettsial Diseases and Spirochetes (3/8/18) Flashcards
(174 cards)
1
Q
morphology of chlamydia
A
Small (.3-1micrometer)
gram-
2
Q
how does chlamydia act as a pathogen
A
obligate intracellular bacteria relying on host amino acids and atp
3
Q
cell wall of chlamydia
A
no peptidoglycan
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
5
Q
where can chlamydia live
A
diverse tissue tropism and disease
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
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
8
Q
where replication takes place for RB CC. trachomatis
A
in an inclusion
9
Q
reservoid for C. trachomatis
A
humans
10
Q
where does C. trachomatis cuase disease
A
conjunctiva (eye and Genitals
11
Q
commonality of C. trachomatis
A
most common disease in world (100 mill new cases)
most common bacterial STI worldwild
12
Q
what is the commmon cause of neonatal conjunctivitis
A
contact with C. trachomatis with infected cervical secretions during vaginal delivery
13
Q
how many does Chronic follicular conjunctivites affect
A
500 mill world wide
blinds 7-9 million (africa)
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)
15
Q
Chlamydia affects how much in urethral infection
A
5% general pop in US men and women
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
17
Q
incubation period for urethral infection via chlamydia
A
2-6 weeks
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
19
Q
what mediates initial attachment of chlamydiae
A
MOMP (major outer membrane protein) followed by endocytosis
20
Q
how can chlamydia enter
A
LGV biovars enter through breaks in skin/mucosa or endocytosis
21
Q
what is the source of primary injury due to chlamydia
A
inflammation: (also cuased by Chlamydial LPS
22
Q
what are the pro-inflammatory cytokines for chlamydia inflammation
A
IL-8 releasedby epithelial cells
23
Q
inflammation by chlamydia leads to
A
early tissue inasion by PMN, then lymphocytes, macrophages, plasma cels, and eosinophils
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
25
immuniy to chlamydia
incomplete (50% of women still shedd aftera a year)
26
what response is the most protective for chlamydia
```
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
```
27
chronic inflammation of eyelids that can lead to scaring of cornea often leading to blindness
Trachoma
28
acute infection presnt in newborns as mucopurulent eye discharge, but does not lead to blindness
Inclusion conjuctivitis
29
how does inclusion conjunctivities get to baby
from morther to infant at birth to affect newborns and adults
30
what may inclusion conjunctivies turn into
can lead to infant pneumonia sydrome (cough and difficulty feeding)
31
eye infections of chlamydia trachomatis
trachoma and inclusion conjunctivites
32
Genital infections of chlamydia trachomatis
Urethritis and epididymitis in men
cervicitis, salpingitis, and urethral syndrom in women
Lymphogranuloma venereum (LGV)
33
characteristics of urethritis and epididymitis
dysuria(diffficult urination) and thin urethral dischage
34
characteristics of cervicits, salpingitis, and urethral syndrome
asymptomatic Vaginal dischage
| 5-30 of women get pelvic inflammatory disease leading to sterility and ectopic pregnancy
35
inflamed fallopian tubes
salpingitis
36
where is LGV found
STD of S. america, africa, SE asia, india and caribbean
37
what causes LGV
invasice biovars: L1, L2 or L3
38
how does LGV get into body and what does it cause
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
39
How to diagnose Chlamydia historically
collect epithelial cells from site of infection (urethral swab collection hurts men)
40
how do we diagnose chlamydia now?
Nucleic acid Amplifcation test (NAAT) to detect chlamydia and N gonorrhoeae DNA using first void urin sample for genital infections
41
treating C. trachomatis
Azithromycin for non-LGV (oral)
| Doxycyclin for LGV
42
morphology of Rickettsiae
small with small genone
Gram-negative
aerobic coccobacilli
non-motile
43
parasite type for rickettsiae
obligate intracellular parasites
44
how do we get Rickettsiae
arthropod-borne to humans via arthrodpod vectors (ticks, fleas, mites, and sandflies)
45
cell envelope of Rickettsiae
LPS and 2 other OM proteins
| Cell wall of peptidoglycan
46
why does Rickettsiae need to depend on host
reductive evolution requires host co-factors, amino acids, phosphorylated sugars, and ATP
47
how does Rickettsiae metabolize host glutamate
aerobic respiration and TCA cycle
48
grwoth of Rickettsiae
slow- in host cytoplasm or nucleus
49
entery of Rickettsiae
enter host via endocytosis-attachment of OMP
escape phagosome using phopholipase
grow in host cell cytoplasm
50
where is Rickettsiae transmitted from
trick salivary glands
51
locatl spread of rickettsiae leads to
necrotic eschar (Black sore)
52
tissue tropism for Rickettsiae leading to
vascular endothelium infection leads to vasculitis(inflammation of Blood vessel)
vascular lesions
increase vascular permeability: hypopvolemai and hypotension
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Thrombosis cuase by
focal areas of endothelial proliferation and perivascualr infiltration
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leakage of rBC by Rickettsiae leads to
rash and petechial lesions
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CAtegories of Rickettsiosis
Spottered Fever group- US
| typhus group- EU
56
symptoms of both types of Rickettsiosis
Fever, headache, myalgia, and rash
| may be fatal due to severe vascular collapse
57
where spotted fever group comes from
Tick -borne rickettsia
58
what causes Rocky Mountain spotted fever
Rickettsia rickettsii
59
who does Rickettsia Rickettsii SF normally parasite
ticks, spreading to tick offspring
| only slightly more than 500 cases a year in the US
60
when is Rickettsia Rickettii SF highest
between april and september, betwween age 60-69 and killing in children less than 10
61
what type of tick transmitts R. Rickett SFi?
Adult feamle ticks(but diff speicies) transmit because they need blood meal to lays egs
62
how long can infected adult tricks live without blood meal
4 years
63
R. Ricketti SF ticks across the US
* Western states - wood tick
* Eastern states - dog tick
* Southwest and Midwest- lone star tick
* Ubiquitous- Brown dog tick
64
incubation period for R. rickettsii SF
6-7 days
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symptoms of R. rickettsii SF
fever headache, RASH, toxicity, mental confusion, Myalgia (muscle pain)
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travel of rash from Rickettsia Rickettsii SF
begins on arm and ankles, spreads to extremities of trunk within hours
67
what parts of the rach from Rickettsi aSF are used for diagnostic test
rash on palsm an d soles
68
complications if RMSF is leaft untreated
```
Intravascular coagulatoin
thrombocytopenia (low platelets)
Encephalitis (brain inflammation
Vascular collapse
Renal and heart failure
```
69
diagnosis of Rickettsia SF
hard/hazardous to culture
how to diagnosis in early stages (antibodies appear 6-7 days after illness onset)
clinical signs
serologic diagnosis is perferred
70
when to start therapy for Rickettsia SF
based on clinicl sings and aymptoms and epidemiologic considerastions
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how is seologic diagnoisis of Rickettisa SF done
Indirect fluoresent antibody(IFA)-reference labs
| skin lesion biopsy- immunofluorescent antibody used for rapid confirmation
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treating Rickettisae SF
Doxycyclin-first wek of illness
if delayed, can't use it (complications
Sulfonamides make the situation worse
73
disease caused by Typhus group
Epidemic Thyphus fever
Endemic (murine) Typhus
Scrub typhus
74
how to get epidemic typhus fever
R. prowazekii spread by body lice(often by times of misery where lots of people get lice)
75
how to get Endemic (murine) typhus
R. typhi spread by rat flease
76
how get Scrub typhus
orintia tsutsugamush spread by chiggers
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the only epidemic ricketsial disease
Typhus fever
78
where is typhus found
africa, latin america and asia, homeless population
| NOT in the US for 50 years
79
typhus fever pathogenisis
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
how does humans eveutally get typhus fever
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
Incubation period of Epidemic Typhus
1-2 weeks
82
symptoms of epidemic Typhus
maculopapular rash: on trunk then to extremities (opposite from RMSF)
headache, Malaise, and Myalgia common
complication: myocarditis and CNS dysfunction
83
fatality rate of Epidemic Typhus if untreated
10-60%(increases with age)
84
diagnosising Epidemic typhus
serology used to confirm, clinicla history to justify
85
treating Epidemic Typhus
immeidate with Doxycyclien
86
how to prevent Epidemic Typhus
louse control
| no vaccine
87
how humans get Endemic(Murine) typhus
incidental - urban rodents are natural reservoir (rat flea with R. typhi)
88
occurange of Endemic (murine typhus
world wide (50-100 case in US)
89
pathogenesis of endemic (Murine) typhus
similar to louse-orne typhus but with expose to rats and rat flease
90
serologic tests to separate Endemic and Epidemic Typhus
can't separate
91
what does intital lesion of scrub typhus decelop as at the bite
necrotic eschar
92
symptomes of scrub typhus
fever slowing increase
| headache Maculopapular rash, mental change, general lymphadenopathy
93
length of maculopapular rash
shorter duration than louse borne or murine typhus
94
trating scrub typhus
Doxycycline
95
Morphology of Bartonella
Gram-neg coccobacili
96
parasite of bartonella
facultative intraceullar parasite as an opportunistic pathogen
97
primary niche and infection of bartonella
endothelial cells to be released into the blood stream to infect eryhtocytes
eventually taken up by arthropod
98
vectors for bartonella
ticks, fleas, sand flies, and mosquitoes
99
what can bartonella casuse co-infections with
lyme's disease
100
Bartonella henselae
Cat-scratch disease
101
cases of Bartonella henselae (cat-scratch disease)
25k in the US mostly children
102
how is Bartonella henselae (cat-scratch disease) spread
cat scratch, bites, or cat flease
103
preventing Bartonella henselae (cat-scratch disease)
flea control
104
symptomes of Bartonella henselae (cat-scratch disease)
swollen lymph nodes skinrash, conjunctivites, encephalities, prolongued fever
105
how is affected by bartonella quintana (trench fever)
homeless alcoholic me in france and US by body louse
106
bartonella quintana (trench fever) severity
mild subclinical diease
107
symptomes of bartonella quintana (trench fever)
- sudden onset of chills, headache, relapsing fever, maculopapular rash
108
morphology of spirchetes
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
seeing spirochetes
hard to see with routing microscopy
110
medically important genera of spirochetes
trponema
leptopria
borrelia
111
normal flora for spirchetes
oral cavity and dental crevice
112
Trench mouth (Vincent infection or ANUG-acuter necrotixing ulcerative gingivites) gets it name from
WWI
113
how does Trench mouth (Vincent infection or ANUG-acuter necrotixing ulcerative gingivites) infect
opportunistic, correltaed with immunocompromised sever malnutrition and neglect of basic oral hydien
114
what do spirochetes and anaerobic flora cuase
necrotizing, ulceration infection of the gums, oral cavity, or pharynx (bleeding gums, bad breath, metallic taste, sudden onset, pain)
115
Morphology of treponema pallidum
motile
Slim spirochete
corkscrew shape
no lps
116
how to kill treponema pallidum
easy: dry, heat, detergenet, disinfected
117
what odes Trponema pallidum cuse
syphilis
118
studying treponema pallidum
hard to culutre and can only be grown in animals
119
what does T. Pallidum need from host
Minimalist pathogen: basic nutreitns and metabolites
120
can T. Pallidum detox O2
no (no catalse or oxidase)
121
Energy pathways for T. pallidum
lacks : no TCA of Electron transport
122
growth speed of T. pallidum
slo (30 hours)
123
who does syphilis pathogen
only human
124
how do you get syphilis
sexual contact with person with active primary or seconday lesion
also non-genital contact
125
how to get syphilis without touching genitals
congenital syphilis - transplacental transmission
| Needles
126
is tertiary syphilis contagious
no
127
problwm of syphilis
world wide, as lesions cause HIV to enter
128
rise of syphilis
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
Pathogeneisis of spirochete
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
the primary lesions of T. Pallidum is what and results in what
endarteritis-inflammation of inner lining of an artery and a necrotic ulceration forms
dense granulomatous cuffs of lymphocytes, monocytes, and plasms sound vessels
131
how does T. pallidum evade
unkown
132
when does Primary syphilis occure
3-90 days after exposure
133
what first appears from primary syphilis
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
when does secondary syphilis occure
2-8 weeks after primary infection in 1/3 of patients
135
what does secondary syphilis involve
skin ,mucous membranes, and lymph nodes
| gives a symmetrical, red-pink, non-itchy rask on trunk and extremities, including palms and soles
136
what fills the lesion of seconadry syphilis
bacteria (highly infectious)
137
after xeconday syphilis what occures
latent syphilis (1/3 spontanously clear infection)
138
symptoms of latenet syphilis
no clinical symptoms but serolgical tests are positive
139
what can happen with latent syphilis
relapse to secondary
| transmit to others or feus
140
what odes tertiary syphilis result in
tissue distrcution
141
how common is tertiary syphilis
1/3 of untreated secondar syphilis, after infection 15-20 ears
142
how tertiary syphilis manifests itself
neeurosyphils
Ocular syphilis
Cardiovascular syphilis
GUmma
143
when syphilis invades the nervous system
neurosyphilis
144
symptomes of neuosyphilis
headache, altered behavior, loss of coordination, paralysis, Tabes dorsalis,
sensory deficits and dementia (most common in HIV positive patients)
145
symptomes of ocular syphilis
vision change
146
symptomes of cardiovascular syphils
aortis - leads to aneurysms
147
where is gumma
in skin, bone, joints, organs
148
diagnosis of syphilis
serologically: detection of antibodies aginst treponeal antigens
149
treponemal vs non-treponemal
looks for treponemal antigen (FTA- ABD, MHA-TP)
| cardiolipin based test that is non-specific and cross reaction possible when autoimmune disaes present
150
treating ssyphilis
penicillin at all stages
151
morphilogy of borrelia burgdorferi
```
long slender psirochetes
axial flagella (many)
outer membrane without LPS
stains with Giemsa or Write
Microaerophilic
```
152
grow speed of Borrelia Burgdorferi
slow (24-48 doubleing time hours)
153
what genes does Borrelia Burgdorferi lack
essential nutrients(amino acids, fatty acids, nucleic acids
154
genome type of Borrelia burgdorferi
partitioned genome- many circular and linear plasmids
155
disease from borrelia burgdorferi
Lyme
| other Borrelia cause relapseing fever
156
species of Borrelia burgdorferi
18 diff subspecies: differ in geographic distribution and clinical manifestation
157
OMP'S OF bORRELIA BURGDORFERI
MULTIPLE CLASSES,that undergo antigenic variation (outer surface proteins)(Osps)
158
what do Osps do
OspA and OspC are differentially expressed dpening on state of tick or mammalian infection
other bind fibrongectin and serum factor H
159
the primary reservoid of B. burgdorferi
rodernts
160
how do ticks get B. burgdorferi
tick larvae food on mice
161
when lyme's disaes occures
in spring and summer when nymphs feed on vertebrate hosts as part of life cycle
162
inoculum of B burgdorferi
low (less than 20)
163
enxootic cycle of B. Burgdorferi
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
where is lyme disease present
where deer are present
165
symptomes of primary lyme diease
bull's eye pattern -macule or papule rash at bite site (erythema migrans)
Fever, Fatigue, Myalgia, headache, joint pain, mild neck stiffness
166
who doesnt get seconday lyme disease
50% of patietns develop like primary
167
when does secondary(Chronic) lyme disease occure
days to months after primary rash
168
what happens in seconary lyme diease
Fluctuating meningitis, cranial nerve palsies, and peripherneuropathay
heart conducting problems - atrioventricular block - myocarditis leading to caridac englandment
arthrits
169
what is chronic lyme diease from
autoimmune state
170
diagnosis of Lyme diease
expose and clinical finds
| later statge can use serology for antibodies
171
how to culture Lyme disease
from erythema migrans skin lesion, blod, joins, CSF.
| but very hard
172
can you see lymes disease with a microcope
no
173
treating lyme's diase
Doxycycline and BEta- lactam: early lyme and arthristis
| but slow response
174
preventing lymes disease
wear protective clothing
| remove tick fast (ned 48-72 hours to reansmit bacteria
