Transcript pinta

Lectures
mycoplasma,ureaplasma
spirochetes-borrelia,
leptospira,treponema
chlamydia, rickettsia
Mycobacterium att
Spirochetales
Genus : TREPONEMA, BORRELIA, LEPTOSPIRA,
Species:
Treponema pallidum – spp.pallidum - syfilis,
-ssp.pertenue, ssp.endemicum
Treponema carateum – pinta
Borrelia recurrentis – epidemic reccurent fever
Borrelia species. – endemic recurent fever
Borrelia burgdorferi – borreliosis
Leptospira interrogans, L. icterohemorhagicus ...... – leptospirosis
Common properties – helical gram negative, not cultivable
Treponema
Morphologically identical
common serological respond in man – (VDRL, FTA),
PNC susceptibility Different epidemiology and clinical signs
T.pallidum ssp.pallidum – veneric disease syfilis
T.pallidum ssp.endemicus – bejel,
T.pallidum ssp. pertenue – framboisie,
non veneric
T.carateum – pinta
Physiology and structure - Tr.pallidum
„ Spirochete “ = curled hair, strictly human pathogen not cultivable Slow
replication (time of replication = 30 hrs) Too thin to be visible in light
microscope ( darkfield, fluorescence)
Patogenesis and immunity
OMP – outer membrane protein – adherence,
hyaluronidase – only virulent – perivascular infiltration.
Host cells are covered by fibronectin – produced by T.p. – anti
phagocytal properties
Immune answer of patient = tissue destruction
Clinics – 3 phases
1) skin in the place of penetration – ulcus durum –
primary site of replication (multiple T.sp in ulcus )
endarteritis a periarteritis, infiltration of ulcer with PMNL and
makrophages, fagocytosis – spirochets are able to survive it
2) disseminated disease – generalised skin lesions multiple T.sp in
blood
Spontanneous remmission
possible
3) Late manifestation in any organ or tissue
Laboratory dg
Microscopy – early dg - in darkfield in the 1st., 2nd., stadium and
congenital syfilis – not appropriate for oral lesion – not pathogenic
spirochetes
- fluorescence,
- impregnation with silver
Cultivation – not cultivable on artificial media
Serological diagnosis
– non treponemal tests – IgG or IgM antibodies cross reactivity with
antibodies against lipid ( antigen ) from destructed cells cardiolipin VDRL, RRR test – floculation of cardiolopin antigen with patien sera
with antitreponemal antibodies, VDRL j the only appropriate test for
CSF testing and for control of efficiency of therapy
- treponemal tests – specific, confirmation FTA-ABS fluorescence
absorption test, TPHA – treponema pallidum hemagglutination test
False positive Not treponemal – viral infections, colagenosis of
vascular system, gravidity, recent immunisation, IM,application of
feroin, lepra, malaria
Treponemal – pyodermia, skin neoplasma, akne, mycosis, ulcus cruris,
reumatoid arthritis, psoriasis, SLE, gravidity, herpes genitalis,
autoimmune diseases
Sensitivity of test in non treated syphilis
VDRL
FTA
TPHA
primary secundary
59-87%
100%
86-100
99-100
64-87
99-100
latent
73-91%
96-99
96-100
late
39-94%
96-100
94-100%
Interpretation of serological tests
Nontreponemal tests
positive later in the 1 st stadium ,present during not treated lues during the 2nd stadium,
25% of not treated are negat. in the 3rd st.., appropriate for therapy control
Treponemal tests
less influenced by therapy, specificity 98% Positive in newbornes of inficated mothers ?
Congenital syphilis or passive transfer of maternal antibodies
Therapy
PNC (!Herxheimer reaction! , V PNC for later stadia
G PNC for congenital and late, TTC, ERY, CMP – in the case of
allergy, for neurosyphilis only PNC or CMP
Prevention and control
vaccine is not available, therapy of sexual partners,
promiscuity a iv drug abusers, AIDS
Epidemiology world wiede spread
- direct contact
- congenital
- transfussion of blood
Infectivity – low (30%),
Infection of fetus soon after infection of mother-bacteraemia in early
stages – not treated mother – spontanneous repeated bacteraemias 8
years
Other treponematoses
T.pallidum ssp.endemicum – bejel, endemic syphilis,
interhuman transmission, nonveneric disease
3 stages:
inicial oral lesions,
sec. oral defects
late gumatas
T.pertenue – framboisie (yaws) –
granulomatouse disease
direct contact with ill skin
eatly stage – skin
late stage– destruction od skin, lymphatic nodes and bones
T. carateum – pinta – primary skin
Small papuls, spreading, persisting for years reccurent, disseminating
hypopigmentation
Therapy: PNC, TTC, CMP
Dg: clinical, Mi from lesions, VDRL
Geografical spread of bejel (blue), framboisie (red) a pinta (yellow
Borrelia
B.recurrentis- Reccurent fever
– epidemic
- endemic
B.burgdorferi – Lymes diseases– borreliosis – 1977
typical morphology of spirochetales
faible staining (anillin stain),
flagella, motile,
Not cultivable
nutritional requirements, replication time 18 hrs,
Lab.diagnostic:
*Mi in blood smear(reccurent fever),
...........biopsie of skin (borreliosis)
*serologic (borreliosis) – IgM, IgG, CSF – Ab index
Borrelia burgdorferi–Lyme disease – borreliosis
1977 arthriis in children
tick borne - Ixodes ricinus... (spring, fall
differeent species of borrelia - B. garini, B.afzeli...
different clinical signs
present in skin, isolation in later stages (? symptoms – caused by living
borrelia or immunopathological mechanismus?)
Clinics: INKT 3-30 days,
1) erytema chronicum migrans +nonspecific signs - 4 weeks
2) late manifestation (80% non treated)
*neurological and cardial symptoms
*arthralgies a arthritis
Dg : Mi – scarecly
serology and clinical (ECM )
Therapy:PNC – longtime, DOXY, AMOX,
in combination
Serology – only in positive history and clinic
IFT ,ELISA tests – all stages
Nontreated:
IgM 2-4 weaks after appearence of ECM , (MX 6-8w),
longlasting in persistent infection
IgG MX after 4-6 months., persistent during late manifestation
Radical and early threatment: - no IgG formation
dg neuroboreliosis – detection of Ab in CSF –
antibody index – detection of intrathecal production of IgG ab
IgG posit. in CSF can be trasfered pasively from blood via HE
barriere, IgM cannot be – pentamer molecules
Confirmation – Western blot – detection of antibodies against unique
antigens (41 kD – flagellar – IgM.,
31kD OspA, 34kD OspB, 60kD – in later stages, IgG
DNA amplification PCR
Leptospires
L.interrogans ? – 19 serogroups and 172 serotypes
(ssp.icterohemorhagica)
L.biflexa – 38 serogroups and 65 serotypes
Pathogennic for annimals
spread by urine, canals – surviving 6weeks
22 serotypes responsible for human diseases (diseases are not serotype
specific)
Clinics:
subclinical disease,
fever, systemic disease (Weil disease)
Pathogenesis: Spread via intact mucus and small skin injuries, infection
of skin and small vessels and all organs (meningitis, hepatal a renal
dysfunction, hemorrhagies)
Dg. microscopy, agglutiantion
Mycoplasma 69 serotypes and ureaplasma 3 serotypes
Common properties, commonly present in the nature,
3 human pathogens, different clinical entities,
ethiopathogenesis not exactly clear
Mycoplasma pneumoniae, M. hominis, Ureaplsma urealyticum
The smallest bacteria without cell wall living free in nature PNC resistant, Gram negative, formerly classified as viruses
Cultivation media with sterols, colonies of ox eyes
generation time 1-6 hrs,
Cross reactitivty (main Ags are proteins and glycoproteins)
extracelular pathogens , respiratory infections in summer and
fall (epidemies in 4-8 years cycles, most commonly school age
children
Transmission - inhalation and sexually
Clinical picture:
M.pneumoniae – infections of respiratory tract, atypical pneumonia
M.hominis- pyelonefritis, pelvicitis, post delivery fevers,
Ureaplazma – uretritis
Diagnosis:
microscopy – faintly stainable – no cell wall
cultivation:
M. pneumoniae – specific media, ox eyes colonies,
medium with glucose – change of color indicator when pH chnged
because od metabolism of glc to acid – indication of the growth
Ureaplasma –
detection by metabolicsm of urea
and ATB resistance – rapid test
serology : detection of IgM against M. pneumoniae
Therapy
ERY, TTC – M. pneumoniae
M. hominis – resitence for ERY
Chlamydiae
• Formelly classified as big viruses because of their i.c.
parasitism, they have special growth cycle, do not have
peptidoglycan in the cell wall
• - both DNA and RNA (they are bacteria),
- external and internal membrane like G- (LPS),
- they are susceptible to some ATB
C. trachomatis, C. psittaci, C.pneumoniae
Present in 2 morphological formes:
- Elementar body- EB – small, infectious, not dividing
- Reticular body -RB – bigger noninfectious, dividing,
i.c., metabolical activity – energetic parazitism – can
synthetise proteins, cannot produce energy
Chlamydiae – growth cycle
• Elementar body (EB) is attached on the surface of
the target cell by receptors, internalised by
phagocytosis. The cell wall of chlamydia does not
allow bacteria to unify the phagosome with
lysosome – i.c. surviving. EB is reorganised to
reticular body, that can divide by binnary fission –
24 hrs, than reorganised again to EB, the cell
crashes and EB are transformed to the living the
cell (48-72hrs after infection)
Chlamydia trachomatis
• 3 serovars – trachomatis (12 serotypes), LGV (3 serotypes)
and annimal
• C.trachomatis – A,B,Ba,C – trachom – blindness
B, D-K – in women – cervicitis, uretritis, proctitis,
conjunctivitic + coomplications
– in men uretritis, proctitis, conjunctivitis + complications
– in children – conjunctivitis, pneumonia, - infection during
delivery – farygeal carriage and presence at GIT
• LGV- L1, L2, L3 -Lymfogranuloma venereum +
complication
• Pathogenesis – enter via minimal injury - direct destruction
of epithelial cells + inflammatory reaction. In LGV
infection is localised in lymphnodes– abscess, rupture,
fissures, fistulas
Clinical presentation,diagnosis, therapy
• Trachom – chronical keratoconjunctivitis – strictures, chronical
irritation of cornea via the lid that is deformed, panus, blindness –
transmission via hands, towel, fleas, carriage in respiratory tract and
GIT in children.
• Inclussion conjunctivitis- adult - folicular - mucopurulent pus,
keratitis, infiltation of cornea – in connection swith earlier genital
infection, autoinnoculation
• Neonatal conjunctivitis and pneumonia – inoculation at birth during
delivery – hyperaemia and copious pus, interstitial pneumonia,
rhinitis, not fever, staccato cough
• Urogenital infection – sexually transmitted non gonococcal uretritis –
mucopurulent discharge, hypertrofic ektopium, in men assymptomatic
• Reiter syndrome – uretritis, conjunctivitis, polyartritis,
mucockutaneous lessions – younger men – sequaelae of uretritis
• Therapy: i.c. – ERY, TTC, AZI
• LVG - Chronic sexually transmitted disease, more often in
men, primary lession – small no aches discrete. Heeling –
headaches, fever, myalgia. Secudarye stadium – inflamtion
of lyphnodes – aches, fluctuation, bubo, growing, drenaige
via fistules Systemic manifestation – fever, anorexia,
meningismus, arthralgia. Chronical LVG – genital
ulceration, fistuls, strictures, genital elephantiasi
• Laboratory diagnosis
– cytology – Giemsa stainning
– cultivation – on tissues
– detection of antigen (OMP or LPS) – ! In cells! –
sampling of epitelial cells
– detection of Nucleic acid -PCR – detection of viable and
non viable cells – is not usefull for monitoring the success
of therapy
– serology – in endemic area – IgG positive
C. psittací, C. pneumoniae
Chlamydophila
• Respiratory infection – transmitted from parrots and spread
via RES and blood. Lung infection. Immune response :
mostly lymphocytes. – oedema,thickness of alveolar wall,
cyanosis, anoxia – involevement of CNS GIT, systemic
(rash, carditis, hepatomegalia, keratoconjunctivitis)
• Conjunctivitis of children in Thaiwan – pharyngeal carriage
– TWAR strains – bronchitis, pneumonia, sínusitis....,
atypical pneumonia,
• Dg – serological
• TH – ERY, TTC
Rickettsiacae
• Aerobic, i.c. or e.c. parasits, G-,
growing only in eucaryotic cells – formerly described as
viruses,
surviving
phagocytosis, spread to cytoplasma where they divide by
binary fission
• 4 genuses
– Rickettsia,
– Coxiella (e.c. survive outside the cell) , no vector
– Rochalimea – e.c.,
– Ehrlichia (forms elementary and initial bodies and morula
- all forms are i.c.)
• Transmitted by insects – (with exeption of Coxiella)
Rickettsiae
• Rickettsia rickettsii –Rocky mountains fever – tickborne –
transovarial transmission, reservoir – rodents – spotted
fever. Dg – Giemsa staining, tissue clutures - Weil Felix
test – cross reactivity with Proteus sp. antigens.
Th: TTC, CMP
• Rickettsia prowazekií – spotted fever – human louse vector
– man is reservoire (bad living conditions) . Louse dies
for infection – not transovarial transmission – epidemic
typhus – macular exantem. Reactivation after years Brill
Zinser´s disease.
• Rickettsia typií – endemic typhus – vector :Xenophylla
cheopsis, reservoires - rodent . Maculopalar rash. Not
complicated.
• Ricketsia Tsutsugamushi – Pacific
Coxiella, Ehrlichia, Rochalimaea
C. burnetti – Q fever – inhalation of infectious particules
from contaminated environment, no insect vector.
Proliferation in respiratory tract – dissemination –
pneumonia, granulomatous hepatitis. Infection of wild
annimals and insect, spred via urine, milk, stool – raw milk,
vegetable Acute infection – rapid development, flu disease,
respiratory infection, hepatosplenomegalia. Chronic infection
– diffuse granulomatosis – chronic endocarditis. Dg –
difficult by serology – antigenic variation od phases I and II
Ehrlichia – Paul Ehrlich – leucocytar rickettsiae, parasitism
on lymphocytes, neutrophils a monocytes. Not ery.
Ehrlichiosis – tick borne – flu signs, leucopenia,
trombocytopenia. Rash only in 20%. Good prognosis
R.quintana, R. henselae