Clinically important Spirochaete infections Flashcards
spirochetes:
1- are —
* — in periplasmic space (i.e. between the — and – membranes)
2- Lab diagnosis:
* — to see on light microscopy
* Treponema pallidum won’t — at all in the lab
* Leptospira interrogans and Borrelia burgdorferi only grow on — culture media
* — microscopy
*—
* Serology: Test – or — for
evidence of an — response
- Most spirochaete infections are
diagnosed by —
motile
flagella
outer ad inner
too thin
won’t grow
specialised
Fluorescent
PCR
blood or CSF
immune
serology
syphilis epidemiology:
-Infection progresses in — and may become — if untreated. i.e., episodes of – disease interrupted by periods of—
Transmission:
1. —
2. — (in utero from infected pregnant woman via — spread to her fetus)
- Incubation period average — (10-90d)
Period of Infectiousness:
- Primary and secondary stages (infectious — or – present)
- — infectious in subsequent stages.
- High-income countries: – mainly– concentrated clusters in groups with multiple partners
- Low- and middle-income counties: — levels, congenital –
- clinical course if untreated:
day 0 : exposure
day 21: chancre —–
the incubation period is between —
4-10 weeks we will have;
then the latent syphilis takes — ( early is less than a year and late is more than 1 year)
stages
chronic
acitve
latent infection
sexual
vertical
hemotogenous
3 weeks
lesions or rash
less
STI
endemic
congenital syphilis
primary syphilis
10-90
2ndary syphilis
years/decades
( from exposure to primary is
10-90 days while primary to 2ndary is 4-10 weeks)
syphilis pathogenesis:
1- portal of entry: —- between – membrane ad infected — or by — spread
2- incubation period: Disseminates from inoculation site through the —
3- attach to cells: Binds to — cells&
goes between —
4- defeat/envade; Structure of – membrane “hides” the spirochaete from the host immune response
5- cause damage: Primary chancre:
Proliferates in the – walls causing — leading to –
6- get out: Lesions of primary
and secondary syphilis are —
direct contact
mucous membrane
lesions
trans placental
bloodstream
vascular endothelial cells
tight junctions
oute
blood vessels
tissue necrosis
ulceration
highly infectious
( check slide 10)
1- primary syphilis is — chancre
by which it ca cause:
1-Penile chancre
(Taylor, Mosby-Wolfe)
2-Extragenital chancre (CDC)
3-Labial chancre (Springer
Images)
2- secondary syphilis:
* Approx. — after primary infection
– — syndrome (fever/ headache/ bone and joint pains)
* Rash appears – later
- these are —
- they include condylomata lata n mucous patch
- other manifestations are:
3- latent syphilis:
-“Early” latent syphilis (the – period after the – of the lesions of — syphilis)
* May get — of infectious lesions
* — risk
-“Late” latent syphilis ( — after —
syphilis)
* Patient — & —
painless
8 weeks
influenza like
3-4
highly contagious
manifestations:
* Splenomegaly
* Lymphadenopathy
* CNS involvement
e.g. aseptic meningitis
1 year
resolution
2ndary
recurrence
transmission
>1 year
asymptomatic n. not infectious
4- tertiary syphilis:
* — lesions ( — )
– Bone, skin
* —
* — syphilis
BUT presentation can be very – “The Great Imitator”
5- congenital syphilis:
If primary or secondary syphilis goes untreated in pregnancy:
* Approx. 25% risk of –
* – can also occur after delivery
* Affected babies can present with:
– — (“syphilitic snuffles”), poor
feeding, rash, –
– – complications
– – abnormalities on x-ray
granulomatous
gummata
neurosyphilis
cardiovascular
non specific
stillbirth
death
Rhinorrhoea
hepatosplenomegaly
neurological
bone
1-lab diagnosis of syphilis:
* Who should be tested for syphilis?
– — patients
– – patients ( — )
* Patients at — medicine
(GUM) clinic/ patients presenting with other —
* — patients
* — donors
2- testing in primary syphilis ( chancre):
Exudate from chancre:
* —
* —- microscopy
Blood
* — (occasionally false negative)
-Remember T. pallidum can’t survive outside the human host & — is not possible
3- syphilis serology:
- Non-treponemal tests e.g.
RPR ( — but — )
* Rise in – infection
* Fall after –
- monitor — to treatment.
-Detect – / — (rise in– )
- Treponemal tests e.g.
TPPA ( — )
-Rise in – infection
-REMAIN –
-EVEN AFTER THE INFECTION HAS BEEN—
symptomatic
asymptomatic by screening
genito-urinary
STI
antenatal
blood
PCR
dark feild
serology
culture
sensitive but not specific
active
treatment
response
relapse n reinfection
titres
specific
acitve
high
treated
syphilis treatment:
* — is the treatment of choice
– – can be used in penicillin allergy
* Only penicillin can be used for –
* — reaction may occur
prevention n control:
* No – available
* Safe – ( – use)
* Contact – of sexual partners
* Antenatal — and treatment of mothers with – serology (to prevent – syphilis)
penicillin
doxcilcin
neursyphils
Jarisch-Herxheime
vaccies
sex
condom
tracing
screening
+ve
congenital
borrelia ssp causing infection:
1- Lyme disease :
- organsim —
- reservoir —
- vector —-
2- Louse-borne Relapsing
Fever (LBRF):
- organism —
- reservoir —
- vector —
3-Tick-borne Relapsing
Fever (TBRF):
- organism —
- reservoir —
- vector –
Borrelia burgdorferi
Rodents , birds
Hard ticks (Ixodes spp.)
Borrelia recurrentis
Humans
Human body louse
Other Borreliaspp.
Rodents
Soft tick
Lyme disease pathogenesis:
* — , –,— pathogen
* Little is known re mechanisms of pathogenesis
* – of immune response
epidemology:
* Zoonosis
* Reservoir: — (e.g. mice), –
* Transmission to human: — (in –)
– — of attachment of tick to human host influences likelihood of transmission
– Ixodes ricinus is the vector in Europe; Ixodes scapularis in the US
* Incubation period: —
* Seasonal variance (incidence highest in May-August) individuals who are – at highest risk
Invasive, nontoxigenic, persistent
evasion
rodents n birfs
tick bite
in saliva
duration
3-30 days
active outdoors
Lyme disease clinical features:
-Early Signs and Symptoms: — , – , —
- Target lesion - central – with clearing and outer – ring
-May have – symptoms
-Later Signs & Symptoms which takes days to weeks later: — , — , — , —
-Weeks to months later: — - —-
(Facial nerve palsy, mononeuritis,
meningitis) , — - Lyme carditis
Lyme — – often knees
erythema migrans n rashes
redness
erthematous
mild systemic
Headache, fever, conjunctivitis,
myalgia
weeks to months:
neurological as ndueroborelliosis
cardiac
arthritis
chronic Lyme:
* Lots of misinformation about this – possibly some — symptoms (post-lyme syndrome) but not due to –
* Once treated appropriately – lyme disease does not require further courses of –
* Important to rule out other diseases causing these symptoms
* Some persistent symptoms may occur e.g. — damage done to a joint due to lyme arthritis prior to treatment
-N.B. Ensure you consult reliable resources e.g. IDSA, ESCMID
guidelines, HPSC, NICE
- lab diagnosis:
—- : No laboratory testing required - treat
Later stage Lyme disease:
* – (used most commonly for diagnosis)
– Carried out on – or –
– — (early), – (late)
Arthritis/ Skin manifestations
* – on joint fluid or tissue (if available) in addition to –
post ifectious
active infection
antibiotics
irreversible
Erythema migrans
serology
serum or csf
IgM or IgG
PCR +seroloogy
Lyme disease treatment:
* Early manifestations
– Adults: — 10 days
– Pregnancy & young children: — 14-21 days
* — :
– Intravenous (IV) ceftriaxone x 14 days
– PO options if —
N.B. — symptoms do not
require retreatment
prevention:
* Protectiveclothing
* Tick repellente.g. DEET
* Remove ticks –carefully!
doxyclins
amoxicillins
neuroborreliosis
ambulatory
presistent
leptosprososis pathogenesis:
get in : Penetrates skin through
— in the epidermis OR crosses intact —membranes
attach to cell: Organisms disseminate from site of entry through — and penetrate various —
damage:
In severe disease: – with blood
vessel –
* — : diffuse tubulointerstitial
inflammation and tubular necrosis
* Lungs: intra-alveolar —
* – : damage to hepatocytes
get out n spread: not relevent spread by –
minor breaks
mucous
blood stream n tissue
vasuclrties w blood vessel necrosis
kidney
hemorrage
liver
rats
leptospirosis epidemiology:
* Zoonosis, reservoir: wild & domestic mammals
Transmission to human:
* Contact of – membranes or ( – ) skin withwater, moist soil or vegetation contaminated with the urine of infected animals
* No — transmission
Risks:
* — exposure to cotaminated water including “adventure tourism”
* — exposure to infected animals
* Flooding/ rainy season esp. in – countries
Incubation period: —
— distribution
mucous
break
human to human
recreational
occupational
developing
7-12
worldwide
leptospirosis clinical manifestations:
* 90% have a — illness
* 10% have a – illness
* — illness
1. —- (fever, headache, muscle
pains, conjunctivitis)
2. May resolve after —
OR
May progress to — phase:
- — or
- — (severe form)
lab diagnosis:
* Serology (mainstay of diagnosis in clinicalpractice):
– — positive in – infection
– Repeat to confirm trend
* – (only available in reference laboratories)
– Blood — in illness (1st 7 days)
– — stays positive for longer
treatment:
Severe: —
Mild: – or –
prevention:
* Rodent — & surveillance
* Avoid— sources, especially if skin abrasions orcuts
There is no – available for humans
mild febrile
severe
biphasic
initial spirochaemtaemia
5-7 days
immune
aseptic meningitis or weils disease
IgM
acute
NAAT
early
urine.
iv penicillin
oral amoxilin or doxyclicins
control
water
no vaccines
weils disease:
* — form of leptospirosis associated with L. interrogans serovar Icterohaemorrhagiae
* — illness
– Headache, fever
– Rash
– Shock
– Thrombocytopenia (low platelets),
haemorrhage
– Abnormal liver function, jaundice
– Acute kidney injury
* 10-15% mortality
severse
generalised
