hemoflagellates winifreda u. de leon asmph yl6. hemoflagellates blood and tissues trypanosoma...
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HEMOFLAGELLATES
WINIFREDA U. DE LEON
ASMPH YL6
HEMOFLAGELLATES
BLOOD AND TISSUES TRYPANOSOMA
LEISHMANIA
ARTHROPOD BORNE
KINETOPLASTIDA- differ from other protozoan because they provide with DNA in their nuclues
EXTRA NUCLEAR DNAKINETOPLAST
STAGES OF DEVELOPMENT
CURRENT OLD
AMASTIGOTE - LEISHMANIA
PROMASTIGOTE LEPTOMONAD
EPIMASTIGOTE CRITHIDIA
TRYPOMASTIGOTE TRYPANOSOME
STAGES OF DEVELOPMENT
audio• Amastigote stage:
– Different because they are providedof Kinetoplast which is composed axonem, blepharoplast, and para basal body
– Intracellular in location
– Most of the time invade the cells of reticuloendothelial system
– These amastigote multiply and Continue to multiply until the cell is filled by amastigote
– Amastigote will be released once the host cell is filled up with the stage of development and will eventually released amastigote into the circulation
– The amastigote is supposed to develop and become promastigote
Promastigote stage
– From promastigote there is epimastigote stage which is an elongated organism with nucleus and kinetoplast
– In this stage:
– Epimastigote differs in the sense promastigote stage that it does not carry the undulating membrane
Epimastigote stage
– From the epimastigote it willbecome trypomastigote, there is nucleus and flagellum
– Longer undulating membrane
How does trypomastigote differes:
- Very long undulating membrane connected to the kinetoplast
- The kinetoplast moved posterior to the nucleus in this stage
TRYPANOSOMA CRUZI- SOUTH AMERICA
Audio• Tryponosoma cruzi
– Prevalence in human has infection rate of 7/100 people
TRYPANOSOMA CRUZI
VECTORREDUVIID BUGS
3 genera identified:TRIATOMAPANSTRONGYLUSRHODNIUS
Common names:-KISSING BUG- habit of biting in the face mainly near the mouth-ASSASIN BUG- neck-CONE NOSED BUG- latest board exam for pharmacy
Are these bugs exclusive to south america ?No- Bed bugs localy; but are smaller- Causes nuisance bites on humans and causes allergic reaction due to sensitivity to the bite of
these bugs- Amastigote stage are found on the tissues of the patient- If the cell ruptures trypamastigotes develops- Animal reservoir: epimastigote develops until they become metacyclic trypomastigotes
infective stage- Infective stage passed out with the feces due to metacyclic trypanosomes’ posterior method of
development- Bad habit: biting while defecating
VECTOR
LIFE CYCLE
• If it is cruzi or Chagas disesase by dr carlos chagas
• Amastigotes are found inside the cell and when the host cells burst that is when they are releases and developed into trypomastigote stage
• Palpebral edema- romana sign• Both young and old populatios are equally
affected
ROMANA SIGN
MAIN PATHOLOGY
DECREASES NERVE GANGLIA- supplying HOLLOW ORGANS when it relaxed it causesENLARGEMENTMEGA DISEASE
There is involvement of:
ESOPHAGUS
INTESTINES
HEART
MEGA- ESOPHAGUS
PATHOLOGY
• Enlarged intestines
• Cardiomegaly- in chronic chagas disease– Enlargement of the ventricles– Apical aneurysm is pathognomonic of chagas
involving the heart
HEART IN CHAGAS DISEASE
DIAGNOSIS
BLOOD, LYMPH FLUID, BUFFY COAT
TRYPOMASTIGOTES
C OR S SHAPED
PROMINENT KINETOPLAST
Characteristic feature: prominent kinetoplast
TISSUES - AMASTIGOTES
• A heart muscle filled up with amastigotes
• Audio for next slide:– They have to be fed with patients blood– In africa, when there is high susp[icion, bug
will be fed with patients blood and after 3 weeks, bugs will be dissected.
DIAGNOSIS
CULTURE- jews doctor Dr warman who cul;tures organism in the philippines
XENODIAGNOSIS- animal inoculation testPATIENT’S BLOOD
BUG
METACYCLIC TRYPANOSOMES(INFECTIVE STAGE)
CONTROL/ PREVENTION
TREATMENT
NIFURTIMOX
BENZNIDAZOLE
PREVENTION
PROPER BLOOD DONOR SCREENING
BETTER HOUSING
HOUSING CONDITION
AFRICAN TRYPANOSOMES
TRYPANOSOMA BRUCEI COMPLEX
3 species:
T. b. BRUCEI - non pathogenic 8in humans, only in animals NAGANA
CAUSATIVE: SLEEPING SICKNESS
T. b. RHODESIENSE
T. b. GAMBIENSE
• RHODISIENCE- occur only in mid-eastern part of africa
• Gambiense- western hemisphere
• Derived where they were identified
• Rhodiseince-rapid and fatal
• Gambiense- chronic form
• Few cases now identified
OCCURENCE
TRYPANOSOMA RHODESIENSE
MID EASTERN AFRICA
RAPID FATAL FORM
TRYPANOSOMA GAMBIENSE
WESTERN HEMISPHERE
CHRONIC
OCCURENCE
FLY BELT
TSE TSE FLIES
( GLOSSINA)
-Fly belt of africa- African
tryponosomiasis occur- No amastigote stage- Only trypomastigotes-
pleomorphic
• What they found are that trypomastigotes are pleomorphic:– Some are short, some are long, static when
recovered from patient– Infective stage: metacyclic trypomastigote– Have anterior stage of development: salivary
gland– Introduced when they bite the host
LIFE CYCLE
PATHOLOGY
WINTERBOTTOM’S SIGN
KERANDEL’S SIGN
PROGRESSIVE CNS INVOLVEMENT
SOMNOLENT
APATHETIC
COMA
• Winterbottom sign- At the site of the bite there could also be lesion
• There is a delayed response to pain- kerandel’s sign
• Progressive CNS involvement and detected by doctor when the patient becomes somnolent, they are apathetic coma death
SITE OF TSE TSE BITE
Site of Tse tse fly• Site of the bite toxic products by the
tsetse fly• Increasing involvement of the CNS• They can fall asleep in the street while
walking• Medical movie: while patients are dining
they could simply fall asleep the patient was already in deep coma
Immune evasion
• There are spikes which correspond sto fever, acts when glycoproteins are released, numbered 1, 2, 3. Actually there are hundred released
• Hypergammaglobulinemia
• Another surface glycoproteind will be in circulation
• Even the patient have high titer of Ab, stil its not protective
• When antigen have different codes,
• The parasites are able to hide sndevade from the protective nature of the antibodies
PATHOLOGY
PATHOLOGY
IMMUNE EVASION – VARIANT SURFACE
GLYCOPROTEIN
Immune evasion• There are spikes which correspond to fever, acts when glycoproteins are released,
numbered 1, 2, 3. Actually there are hundred different glycoproteins when they released in circulation
• Hypergammaglobulinemia• When there are released, Another surface glycoprotein will be in circulation• Even the patient have high titer of Antibody, still it’s not protective• When antigen have different codes, even antibodies developed they are not
protective• The parasites are able to hide and evade from the protective nature of the antibodies
• In Africa they believe they thought they actually decreased the number of cases but in this figure, 1999, re-emergenvce environmental changes worldwide
DIAGNOSISBLOOD, LYMPH FLUID, BUFFY COAT
CSF
only the trypomastigotes
SEROLOGY - CATT
Card agglutination test for trypanosomiasis- rapid dx’c procedure to identify the condition
Lumbar tap- should be in strict aseptic technique
TRYPOMASTIGOTES- pleomorphic (short,
long, or longitudinal)
TREATMENT
PENTAMIDINE- first line of drug
MELARSOPROL
EFLORNITHINE- widely use now in africa
LEISHMANIA
L. TROPICA SKIN CUTANEOUS
ORIENTAL SORE
L. BRAZILIENSE SKIN/ MUCOUS MEMBRANE
MUCO-CUTANEOUSESPUNDIA
L. DONOVANI VISCERAL ORGANS LIVER/ SPLEEN
KALA AZAR
• Leishmania• 3 species
– L. tropica• Affects only the skin• Cutaneous leishmaniasis• Oriental sore in India
– Braziliense• Skin/mucous membrane• Initially not only the mouth also, ears, nose
– Donovani• Viceral leishmaniasis• Liver and spleen
VECTOR
SANDFLIES- under phlebotomous species
-In Phil there are about a hundred species of phlebotomous flies
PHLEBOTOMINE FLIES
TERMITE HILLS
• Vector– Sandflies
• Phlebotomous• In Phil there are about a hundred species of phlebotomous flies
– Termite hills• Host
– Rats– There are rat holes under the termite hills
• Other hosts– Canid families– Not only humans are infected but also the family canidae– Infected individual has amastigotes in tissues—they are found Inside the macrophages, once it is filled it
will bvurst and release amastigotes– When sandflies bite the patoient, it will get the promastigote promastigote
2 stages• Promastigote in sandflies• Promastigote in patient
Is it only acquired thru bite of cutaneous leishmaniasis?• Mechanical vectors may transmit parasite to other • Our overseas Filipino workers are going to these countries where Leishmaniasis are
rampant• Cutaneous lesion- weeping lesions• These are typical lesions and dermatologist are not yet so much familiar from these
lesions
HOSTS
OTHER HOSTS
FOX
JACKAL
WOLVES
DOGS
LEISHMANIASIS
AFRICA
CHINA
SOUTHERN EUROPE
SOUTH AMERICA
Brazil/ Honduras
MIDDLE EAST
SITE OF BITE
CUTANEOUS
CUTANEOUS LESIONS
• Muco-cutaneous– Not only the mouth but also the nose– Highly disfiguring
• Visceral leismani• Kala-azar: hepatosplenomegaly
– Post kala-azar– Post kala-azar dermal lesion
• Amastigotes onside the lesion• Initially diagnosed as leprosy• When pricked the lesion found to have amastigotes of leishmania• Histoplasma are also occupying macrophages
MUCO-CUTANEOUS
VISCERAL
POST KALA AZAR
DIAGNOSIS
NEEDLE ASPIRATIONSMEAR – GIEMSA
CULTURE
Novey
MCNeal
Nicolle
LEISHMANIN SKIN TEST
TREATMENT
ANTIMONY COMPOUNDSSTIBOGLUCONATE
AMPHOTERICIN BGLUCANTINEPENTAMIDINEMILTEFOSINE
CRYOTHERAPY
• Diagnosis
• Smear stained with giemssa
• Cultuire
• What is the choice of culture medium for leishmania
– Novey, mcneal, Nicole NMN
• Leishmanin skin test
• Treatment
• Antimony compounds
• Amphotericin B:
• Glucatine
• Arytherapy- like cold compress—freeze and kill the organisdm
PUBLIC HEALTH CONCERNS
HEAVY INTERNATIONAL TRAFFIC
OFWS
PHILIPPINE SPECIES OF PHLEBOTOMINES
PHILIPPINE SPECIES OF REDUVIID BUGS
POSSIBILITY OF LOCAL TRANSMISSION??
• Public health concerns
• Everybody are going out of the country, however, t may also be good to find out that majority of Flipino csn be found to the contries where these [parasoites are endemic—thay can be infected
• Phlebotomins- vectrors of leishmania
• American t: reduvid bugs
FINGER PRICK BLOOD SAMPLE
THIN BLOOD FILMS
audio– Select the finger to puncture (usually the third or fourth finger) (Maam prefers the ring finger)– Puncture the side of the ball of the finger. Do not make the puncture too close to the nail bed. If the blood
does not well up immediately, put pressure. Normally, it should well up immediately. Not too much since it will be plasma.
– Touch the blood with the slide – THIS IS VERY IMPORTANT.– To conserve glass slides, prepare thick and thin smears on the same slide. – For thin blood film, hold another slide about 30 degrees on the blood drop. Gently press then push to the
other side of the slide.– Thick smear – for rapid diagnosis– Thin smear – to know the species of the filarial; usually the hemoglobin is removed first but this is already
not the concern of the doctor.
AFTER STAINING
THANK YOU AND GOOD DAY
THANK YOU