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.

BLOOD SMEARSTHICK/ THIN

AFTER STAINING

THANK YOU AND GOOD DAY

THANK YOU