STO's and Neisseria meningitidis Flashcards
1
Q
Treponema pallidum shape and visualization techniques
A
Thin spirochete
- Visualized in fixed tissues by silver stain
- Visualized live by dark field microscope
*Not visible using light microscopy
2
Q
Treponema has a _____ that surrounds the whole cell
It is motile due to…..
A
It has a GAG sheath surrounding the whole cell
Motile due to endoflagella within periplasm (THREE at each end)
3
Q
Treponema envelope composition
A
- No LPS
- Loosely anchored OM containing cardiolipin
- Mostly IM lipoproteins (OM few)
4
Q
Lab culture technique for treponema
A
Can’t culture in lab!
Cultivate in rabbit testes
*has microaerophilic metabolism
5
Q
Primary treponema presentation
A
- Chancre = Ulcerated defined papule at infection site
- Regional lymph node swelling
- heals spontaneously, but organisms remain
6
Q
Secondary treponema presentation
A
- Maculopapular rash anywhere on body (palms/soles)
- Condylomas in moist areas
- Heals spontaneously, recurs for 8 months, then latent for 20 years
7
Q
How many patients progress to tertiary syphillis?
A
About 40%
8
Q
Tertiary syphillis: where’s the lesion?
A
throughout the body
*due to immune response, not bacteria
9
Q
How does tertiary treponema affect particular tissues?
A
Skin: gummas
Bones: porous, fragile
Heart: aorta swells, ruptures
Liver: ??
CNS: paresis in brain, tabes dorsalis in spinal cord
10
Q
Neurosyphillis can occur…
A
during secondary or tertiary stages
11
Q
Vertical transmission of treponema?
A
Yes, it can cross the placenta
- 20% aborted, stillbirth
- 80% congenital defects
12
Q
What does congenital syphillis present as?
A
Hutchinson’s triad
- Interstitial keratitis (blindness)
- 8th nerve deafness
- Hutchinson’s teeth
*also saddlenose, cognitive deficits, and bone deformation
13
Q
Treponema reservoirs and transmission?
A
Only human, only STD
(can artificially infect rabbits, but they don’t progress beyond the Primary stage
14
Q
When is treponema contagious?
A
Only for the first 3-5 years
15
Q
Who should be tested for syphilis?
A
High risk populations
Pregnant women at 28 weeks and at delivery
After any stillbirth
16
Q
Pathogenic factors (4) for treponema
A
Highly infectious (10 organisms)
Hyaluronidase (facilitates spread and invasion)
Motility
Few surface proteins (hide from immune system)
17
Q
______ lesions are full of treponema organisms
A
Primary and secondary
18
Q
(General) control measures for treponema
A
ID sexual contacts
Scrape chancres (only if active infection, not latent)
Serologic testing
19
Q
Indirect serologic tests for treponema
A
induce formation of reagin in host (IgM+IgA)
- add cardiolipin to patients serum
- If positive, the reagin will cause cardiolipin to clump
- ****False positives possible***
FTA test (detect anti-treponema antibodies)
- bind treponema to slide and add patient’s serum
- add a fluorescent anti-human 2’ antibody to detect the 1’ antibody
20
Q
Direct serological tests for treponema
A
FTA test (can also be indirect)
- Fix anti-treponema antibodies to slide, and add patients serum
- Add fluorescent anti-treponema antibodies to detect organisms
21
Q
Syphilis Tx
A
Pen G (2.4 MU)
Early disease = One injection
Latent disease = Three injections
*Salvorsan (arsenic) was used before 1940
22
Q
Neisseria gonorrhea organism shape and location (in cells)
A
Gram (-) , Coffee-bean shaped diplococcus
Intracellular and inside PMN’s
23
Q
N. gonorrhea growth characteristics
A
- Fastidious (grow on MTMor chocolate blood agar)……better with selective media (vanco,colistin)
- Aerobic growth but prefers 5% CO2 (candle jar)
- Cytochrome C oxidase ++
24
Q
Ox+, Gram(-) diplococcus =
A
Neisseria
25
Neisseria genome
Two identical chromosomes (diploid) -- _never heterozygous_
26
Neisseria invades what tissues?
What are the infections that this causes?
invades mucus membranes of the UGT, rectum, eye, throat
Proctitis, pharyngitis, arthritis, dermatitis (rare)
27
Male N. gonorrhea infections
Urethritis
\*40% asymptomatic
28
N. gonorrhea female infections
* Urethritis, vaginitis
* Cervicitis, salpingitis, PID, peritonitis
--\>\> fallopian tube scarring and infertility (even if asymptomatic...60%)
29
Neonatal N. gonorrhea infection
Conjunctivitis
| (from infected birth canal)
30
Animal carriers of N. gonorrhea
None. Exclusively human
31
Infection and coinfectino rates of N. gonorrhea
75% of people who sex an infected person (50% after one time)
40% coinfect with Chlamydia
32
N. gonorrhea diagnosis
Males = gram stain of urethral discharge
Females = culture of cervical/vaginal swab
33
N. gonorrhea virulence factors
1. **Pili**
2. **Proteins 1-3**
1. *Por*
2. *Opa*
3. *Rmp*
3. **IgA protease**
4. **LOS**
5. **Peptidoglycan release**
6. **Fbp**
34
N. gonorrhea virulence factors for ATTACHMENT
_pili_ (initial)
* Antigenic variation via **cassette switching** -- avoid host immune response
* One promoter (**PiliE**), many genes (**PiliS**)
* recombine new piliS gene or part of gene with piliE
OPA protein = "Protein 2" (tight attachment)
* antigenic variation by **DNA slippage of repeats**
* infections in females change Opas during menstrual cycles
35
N. gonorrhea virulence factors for EVASION (3)
_Por_ = protein 1
* Outer membrane **porin**
* **Prevents phagolysosome** fusion
_Rmp_ = protein 3
* **Prevents antibody binding** to Por and LOS in the outer membrane
_IgA protease_
* **prevents complement** activation
* Stops IgA response (first-response Ab in mucus membranes)
36
N. gonorrhea virulence factors for TOXICITY (2)
_Lipooligosaccharide_ (rather than LPS)
* **Lipid A** = toxic in all Gram (-) bacteria (endotoxin)
* **Oligosaccharide** mimics hist cell membrane structure
* **NANA transferase** = sialylates *bacterial LOS with host NANA*
_Peptidoglycan release by autolysins_
* At **low temperature** or **alkaline** pH
37
"Other" N. gonorrhea virulence factor
_Fbp_
**Scavenges iron** from human lactoferrin and transferrin
38
What is PPNG?
Penicillinase-producing N. gonnorhea
\* produces beta-lactamases
39
Other type of resistant gonorrhea?
Pan-resistant NG
\*\*to ALL available antibiotics
40
Tx for N. gonorrhea
**Ceptriaxone** (i.m.) + **Cefixime** (oral)
PLUS
**Doxy** _or_ **erythromycin** for chlamydia co-infection
\*\*NO DOXY DURING PREGNANCY
41
Treat N. gonorrhea sexual partners with...
Cefixime
42
Neonatal N. gonorrhea infection treatment?
Tetracycline drops (for conjunctivitis)
\*\*no longer use AgNO3
43
Neisseria meningitidis structure
Like the gonococcus, but has **polysaccharide capsule**
44
Types of N. meningitidis
12 types
Common: **A, B, C, Y, W135**
45
N. meningitidis initially invades \_\_\_\_\_\_, causing ________ (infection)
It presents as ________ and small hemorrhages. Why?
Invades _bloodstream_--\> _meningococcemia_
_Purpura_ (75%) -- because blood vessels become more permeable in response to the toxic effects of _LOS_ and _soluble peptidoglycan_
46
15% of N. meningitidis cases involve
**_meninges_** (meningococcal meningitis)
* _acute headache, vomiting, stiff neck_
47
Cellular findings in meningococcal meningitis?
This may progress to...
_PMN lymphocytes in CSF_ (d/t increased vascular permeability)
Brain covered in _purulent exudate with PMNL's and N. meningitidis_
--\> may progress to **DIC** and circulatory collapse = **_meningococcal septicemia_**
48
N. meningitidis is ______ in 10% of people
resident flora
49
N. meningitidis spread is helped by \_\_\_\_\_\_\_\_\_\_
_pilin modification_
--with phosphatidylglycerol
--disrupts microcolony and spreads the organism
50
N. meningitidis is chiefly spread by
respiratory droplets, especially in crowded areas and with susceptible populations
51
Common environments (examples) for spread of N. meningitidis
College dorms and military barracks
52
Once N. meningitidis epidemic begins, there is a ____ carrier rate. This necessitates \_\_\_\_\_\_\_\_
**80%** carrier rate
**Prophylaxis** for control of epidemic
53
Most N. meningitidis epidemics are due to...
specific capsular antigen types
54
N. meningitidis virulence factors...
all of the ones from N. g.
PLUS
1. **_Antiphagocytic polysaccharide capsule_**
* Antigen B is **sialylated** = much more disguised
2. **_Special Pili_** that attach to BBB and recruit junction complexes, depleting them in other areas of the BBB (increasing permeability)
3. **_Additional Adhesins_** (in outer membrane)
55
N. meningitidis vaccines
| (current and newly approved)
**NmA** vaccine = general prophylaxis
**ACWY conjugate** vaccine = US use (dorms, army, etc)
**NmB** vaccines = recently approved
* *_Bexsero_ = 3Nm proteins + PorA*
* *_Trumenba_ = 1 recombinant lipidated proteinfrom 2 NmB strains*
56
Preferred N. meningitidis treatment
**3rd gen Ceph**
(may include **acyclovir** too if CSF suggests herpes present (RBC/WBC)
57
Initial treatment of N. meningitidis should be...
broad spectrum antibiotic
including Vancomycin (will penetrate BBB)
58
\_\_\_\_\_ or ______ can be used for prophylactic N. meningitidis treatment in epidemic settings. Why these in particular?
**Rifampin** or **3rd gen Ceph**
\*\* they cross the BBB
\*\*can also use high-dose **ciprofloxacin**
59
Other Neisseria
(Carrier rate, infections in kids and adults, and Tx)
_Moraxella catarrhalis_
* 50% carrier in school aged kids
* infections = opportunistic sinusitis, bronchitis, PNA
* May also present as Otitis Media (3rd most common cause)
* Exacerbates COPD in adults (attach to ECM)
* Produce BETA LACTAMASES = Treat wth **Ceph3** or with **Cipro** (*or not at all?*)
60
Chlamydia trachomatis organism, genome,and structure
* Obligate intracellular parasite
* Small genome (lacks metabolic genes, **steals ATP** from host)
* Cell wall **lacks MurNAC**, but has PBP's
* Susceptible to Penicillin but not to lysozyme (PEN NOT USED TO TREAT)
61
Chlamydia trachomatis has ___ serovariants, baed on \_\_\_\_
15 serovariants
based on LPS antigens
62
Must cultivate Chlamydia trachomatis on \_\_\_\_\_\_\_\_
eukaryotic host cells
(embryonated chicken eggs, McCoy cells in monolayer tissue cultures, mouse brains)
63
Two life cycle forms of Chlamydia trachomatis
_Elementary bodies_
* .3um in diameter, electron dense nucleoid tough membrane (S-S)
* INFECTIVE FORM (the form that enters cell)
_Reticulate bodies_
* 1um diameter, diffuse EM staining, fragile (SH-HS), more ribosomes
* REPLICATIVE FORM (the one that divides)
64
Chlamydia trachomatis life cycle (7 steps)
1. Entry
2. Initial attachment (surface sugars), actin remodeling, induced uptake
3. Vacuole
4. Elementary body metabolism
5. Develops into RB
6. RB matures
7. Release
65
Eye infection of Chlamydia trachomatis
| (Aquisition and symptoms/pathology)
_Trachoma_
* infection at birth or early childhood via flies
* mucopurulent discharge --\> **pannus** forms (keratinized cornea)
* Corneal obscuration and trichiasis
* **Permanent blindness**
Tx = oral **Azithromycin** (mass trial showed reduced infective rate by 50%)
66
Other eye infection of Chlamydia trachomatis (the less severe one)
(who does it infect, and possible complications)
_Inclusion conjunctivitis_
* mostly in neonate (adult from self-innoculation of conjunctiva)
* may be respiratory complications
67
Chlamydia trachomatis neonatal (non-eye) infection
(Symptoms and Dx?)
_Neonatal PNA_
* Shortness of breath
* NO FEVER
* suspect if infant has inclusion conjunctivitis
68
STD version of Chlamydia trachomatis?
Chlamydia
69
Male Chlamydia STD symptoms
* non-gonococcal urethritis
* epididymitis
* prostatitis
(usually self-limiting)
70
Female chlamydia STD symptoms
* urethritis
* cervicitis
* salpingitis/PID (most common cause)
(\*\*Fallopian scarring may lead to infertility or predispose to ectopic pregnancies -- 10 fold increase in likelihood)
71
Most common cause of acquired infertility in females?
Chlamydia induced PID
72
Latent infection of Chlamydia trachomatis?
General infection timeline?
_Lymphogranuloma venereum_
(small abcess--\> heals quickly --\> inguinal buboes later)
\*\*must Ddx from PLAGUE buboes
73
Latent Chlamydia infection may become \_\_\_\_\_\_. This could lead to ______ or ______ due to fibrous restrictions of lymphatic system.
Chronic
elephantiasis or bowel obstruction
74
Specific manifestation of latent Chlamydia depends on...
Serovar of the organism
75
Probability of infection by sex with partner who is infected with Chlamydia trachomatis?
68%
76
Most common Chlamydia trachomatis infections in North/South America and Europe?
What about Asia and Africa?
NA/SA/Eur = STD
Asia/Africa = Trachoma
77
Why do we need to treat both epidemiological localizations of Chlamydia trachomatis the same?
They can cross-infect
78
Chlamydia trachomatis infectiveness is caused by \_\_\_\_\_\_\_
Elementary Bodies
--binding to a host receptor and inducing Pathogen-mediated endocytosis
79
\_\_\_\_\_ remodels the host cytoskeleton in Chlamydia trachomatis pathogenesis
T3SS
80
Chlamydia inhibits ______ so it can proliferate intracellularly
phagolysosome fusion
81
Chlamydia trachomatis induces \_\_\_\_\_\_\_
Cytokine (IL-1) production
82
Chlamydia vaccine?
What is the preferred treatment? Prevention?
_Vax_ = ineffective d/t intracellular location
_Tx_ = **Azithromycin** (one dose oral)
* Can also treat with **Tetracycline** or **macrolides**
_Prevention_ = surgery or epilation for trichiasis to prevent keratinization of the cornea
\*\* ID partners -- expidited partner therapy, legal in 35 states
83
C. pneumoniae may have originated as a _____ from what?
zoonosis from koalas
84
C. pneumoniae infection rate
100%, but mostly asymptomatic
85
C. pneumoniae may progres to....
Walking PNA (like mycoplasma)
86
C. pneumoniae is found in \_\_\_\_\_\_, which suggests...
atherosclerotic plaques
suggests link to atherosclerosis and coronary artery disease
\*\* also associated with asthma, stroke, and late-onset Alzheimer's
87
C. pneumoniae Tx
_usually untreated_
**Tetracycline** may help
88
C. psittaci presentation, transmission, and Tx/control
* **Severe PNA, sepsis** with **patchy, well-defined** lung involvement
* Transmitted via contact with psittacine birds (bites or inhalation of dried feces)
* Control with **tetracycline** and quarantine of imported birds
