Trypanosoma

Brucei

Rhodesiense
Geraldez, Bea Fae A.
group 3
Trypanosoma Brucei Rhodesiense in a blood smear (Giemsa-stained

light photomicrograph).

Disease on Human
Trypanosomiasis, human African
(sleeping sickness)

Human African trypanosomiasis, also known as

sleeping sickness, is a vector-borne parasitic disease.
It is caused by infection with protozoan parasites
belonging to the genus Trypanosoma. They are
transmitted to humans by tsetse fly (Glossina genus)
bites which have acquired their infection from human
beings or from animals harboring human pathogenic
parasites.
 Morphology
1. Long thin form
2. Short stumpy form
3. In blood film they appear C or U or

S shape.
4. Amastigote form
5. Oval bodies.
6. Nucleus.
7. Kinetoplast.
8. Habitat: Striated muscle in heart,

skeletal, neurological cells and cells

of reticuloendothelial system. Tissue

Blood
Life Cycle:

a.Definitive host:
Man, wild and domestic animals.
b.Intermediate host (if any):
Triatomine bugs (reduviid bugs)
c.Mode of transmission:
Tsetse flies can transmit T. brucei. Both forms of sleeping sickness are

transmitted by the bite of the tsetse fly (Glossina species). Tsetse flies

inhabit rural areas, living in the woodlands and thickets that dot the East

African savannah.
d.Infective stage:
Infection occurs in two stages, an initial haemolymphatic stage followed

by a meningoencephalitic stage after the trypanosomes invade the central

nervous system.
e.Vector (if any):
Only known vector for each is the tsetse fly (Glossina spp.).
 The epidemiology of the disease is
mediated by the interaction of the
parasite (trypanosome) with the vectors

(tsetse flies), as well as with the human
and animal hosts within a particular

Epidemiology
environment.

Found in 13 countries in

eastern and southern Africa.

 Symptoms

Headache, malaise, weakness, fatigue,

pruritis, and arthralgia. First-stage signs
can include hepato-splenomegaly,
weight loss and intermittent fevers
lasting one day to one.
 Diagnosis
Diagnosis requires confirming the presence

of the parasite in any body fluid.

Made by identifying trypanosomes in fluid

from a chancre, lymph node aspirate, blood

 Treatment
Suramin is recommended for the

hemolymphatic stage of T. brucei

rhodesiense infection, and melarsoprol

is used in those with CNS involvement.

Melarsoprol, an organoarsenic

compound, is the only drug available.

Melarsoprol is the only option.

Melarsoprol is as effective (95%) as in

trypanosomiasis but even more toxic.

Adverse reactions to melarsoprol can

be severe and life-threatening.

REFERENCES
Trypanosoma Brucei

Rhodesiense - an overview |

ScienceDirect Topics. (n.d.).

Www.sciencedirect.com.

https://www.sciencedirect.com/t

opics/immunology-and-

microbiology/trypanosoma-

brucei-rhodesiense
Trypanosoma
cruzi
Presented by : Yvonne E. Ico
 Table of contents
02

01 Morphology 03

Disease on human Life Cycle

04

Epidemiology
05 07

Symptoms
06 Treatment

Diagnosis
 named after the Brazilian physician Carlos Chagas, who
discovered the disease in 1909

Trypanosoma cruzi

CHAGAS DISEASE •
found only in the Americas (mainly, in rural areas of Latin America where
poverty is widespread). Chagas disease

American trypanosomiasis
Trypanosoma cruzi
Chagas disease is caused by the parasite Trypanosoma cruzi, which
is transmitted to animals and people by insect vectors

The Trypanosoma cruzi, the causative agent of a neglected tropical disease,

Causal Agent:
The protozoan parasite, Trypanosoma cruzi, causes Chagas disease, a zoonotic
disease that can be transmitted to humans by blood-sucking triatomine bugs.
Morphology
Trypanosoma cruzi is a hemoflagellate protozoan parasite. T. cruzi has

three main forms, amastigotes, epimastigotes and trypomastigotes.

Trypomastigotes are long and

slender measuring between 12
and 30µm.

The epimastigote is similar in

appearance to the
trypomastigote, but the
kinetoplast is located anterior to
the nucleus.

The amastigotes are round and the flagellum is not apparent.

LIFE CYCLE
Definitive Humans are considered the main
host reservoir for Trypanosoma

armadillos, opossums,
raccoons, woodrats, some
Intermediate other rodents, and domestic
host dogs.

Triatomine bugs

The bugs become infected during blood

feeding. The parasites develop
in the gut of the bug and leave in the feces
 • food borne
Mode of transmission
•Blood by blood
•Mother to child

Transmitted by kissing bugs , Infection usually occurs

after bugs defecate on the bite site and are rubbed
into the wound by the host scratching

Infective Stage

Initial haemolymphatic stage followed by

meningiencephalitic stage after trypanosomes invade
the CNS

VECTOR- Triatomine bugs | Kissing bugs

 Parasitic infection that is commonly spread
through contact with the poop of an
Epidemiology infected triatomine bug a blood sucking
insect that feeds in humans and animals

Symptoms
Acute phase Chronic phase

Fever heart failure

Fatigue

Rash Irregular heartbeat

Swelling eyelid
Stomach pain or constipation

due to enlarged colon

Nausea or Vomiting Muscular pain
Diagnosis

Observation of
parasite in a blood
smear by microscopic
examination,
Anthick and thin
blood smear are
made and stained
for visualization of
parasites
 Treatment:
Treatment for Chagas disease is
recommended for people diagnosed
early in the course of infection
(acute phase), babies with congenital
infection, and for those with
It works by killing the suppressed immune systems. Many
organism patients with chronic infection may
also benefit from treatment.
Nifurtimox

Benznidazole
effective in early disease this decreases
in those who have long-term infection
 Tips to prevent this disease:

• Avoid sleeping outdoors

•Practice safe food and water precaution
• Avoid getting blood transfusion or organ transplant where
chagas
disease is found
•Use insecticide if sleeping outdoors
Thank you!
 REFERENCES:

https://www.cdc.gov/parasites/chagas/gen_info/detailed.html

https://www.cdc.gov/parasites/chagas/treatment.html

https://www.canada.ca/en/public-health/services/diseases/chagas-disease-
american-trypanosomiasis/prevention-chagas-disease-american-
trypanosomiasis.html
 TRIVIA DAY PRESENTATION

TRYPANOSOMA
BRUCEI
GAMBIENSE

DATA GATHERED FROM SCIENCEKIDS.CO.NZ

TRYPANOSOMIASIS,
HUMAN AFRICAN
(SLEEPING
SICKNESS)
 FACT 1

Human African
trypanosomiasis, also
known as sleeping sickness,
is a vector-borne parasitic
disease.
Caused by infection with
protozoan parasites
belonging to the genus
Trypanosoma.
THEY ARE TRANSMITTED TO HUMANS
BY TSETSE FLY (GLOSSINA GENUS)
BITES.
FACT 2

DISEASE ON HUMAN

Trypanosoma brucei
gambiense

Trypanosoma brucei
rhodesiense

American trypanosomiasis or
Chagas disease
LIFE CYCLE
FACT 6

MODE OF TRANSMISSION
Cyclical transmission
Mechanical transmission
Per-orale and vertical transmission
FACT 3

Major human epidemics

There have been several epidemics in Africa
over the last century:
one between 1896 and 1906, mostly in
Uganda and the Congo Basin;
one in 1920 in a number of African
countries; and
the most recent epidemic started in 1970
and lasted until the late 1990s.
IN 1998, ALMOST 40 000 CASES WERE
REPORTED, BUT ESTIMATES WERE
THAT 300 000 CASES WERE
UNDIAGNOSED AND THEREFORE
UNTREATED.

HEADING
DURING THE LAST EPIDEMIC THE
PREVALENCE REACHED 50% IN
SEVERAL VILLAGES IN ANGOLA, THE
DEMOCRATIC REPUBLIC OF THE
CONGO, AND SOUTH SUDAN.
SLEEPING SICKNESS WAS THE FIRST
OR SECOND GREATEST CAUSE OF
MORTALITY IN THOSE COMMUNITIES,
EVEN AHEAD OF HIV/AIDS.
IN 2009, AFTER CONTINUED CONTROL
EFFORTS, THE NUMBER OF CASES
REPORTED DROPPED BELOW 10 000 (9
878) FOR THE FIRST TIME IN 50 YEARS.
THIS DECLINE IN NUMBER OF CASES
HAS CONTINUED WITH 992 AND 663
NEW CASES REPORTED IN 2019 AND
2020 RESPECTIVELY, THE LOWEST
LEVEL SINCE THE START OF
SYSTEMATIC GLOBAL DATA-
COLLECTION 80 YEARS AGO. THE
ESTIMATED POPULATION AT RISK IS 55
MILLION PEOPLE FOR THE PERIOD
2016–2020; WITH ONLY 3 MILLION
PEOPLE AT MODERATE OR HIGHER
RISK.
CURRENT DISEASE DISTRIBUTION
THE DISEASE INCIDENCE DIFFERS FROM ONE
COUNTRY TO ANOTHER AS WELL AS IN
DIFFERENT PARTS OF A SINGLE COUNTRY.
IN THE LAST 5 YEARS, OVER 70% OF
REPORTED CASES OCCURRED IN THE
DEMOCRATIC REPUBLIC OF THE CONGO,
WITH AN AVERAGE OF LESS THAN 1,000
CASES DECLARED ANNUALLY.
ANGOLA, CENTRAL AFRICAN REPUBLIC,
CHAD, CONGO, GABON, GUINEA, MALAWI
AND SOUTH SUDAN DECLARED BETWEEN
10 AND 100 NEW CASES IN 2019, WHILE
CAMEROON, CÔTE D'IVOIRE, EQUATORIAL
GUINEA, UGANDA, UNITED REPUBLIC OF
TANZANIA, ZAMBIA AND ZIMBABWE
DECLARED BETWEEN 1 AND 10 NEW CASES.
COUNTRIES SUCH AS BURKINA FASO, GHANA,
KENYA AND NIGERIA, HAVE REPORTED
SPORADIC CASES IN THE LAST 10 YEARS.
COUNTRIES LIKE BENIN, BOTSWANA,
BURUNDI, ETHIOPIA, GAMBIA, GUINEA
BISSAU, LIBERIA, MALI, MOZAMBIQUE,
NAMIBIA, NIGER, RWANDA, SENEGAL, SIERRA
LEONE, SWAZILAND AND TOGO HAVE NOT
REPORTED ANY NEW CASES FOR OVER A
DECADE. TRANSMISSION OF THE DISEASE
SEEMS TO HAVE STOPPED IN SOME OF THESE
COUNTRIES BUT THERE ARE STILL SOME
AREAS WHERE IT IS DIFFICULT TO ASSESS
THE EXACT SITUATION BECAUSE THE
UNSTABLE SOCIAL CIRCUMSTANCES AND/OR
DIFFICULT ACCESSIBILITY HINDER
SURVEILLANCE AND DIAGNOSTIC
ACTIVITIES.
FACT 4

Infection and symptoms

The disease is mostly transmitted through the bite
of an infected tsetse fly but there are other ways
in which people are infected:
Mother-to-child infection
Mechanical transmission through other
blood-sucking insects is possible.
FACT 5

In the first stage, the

trypanosomes multiply in
subcutaneous tissues, blood and
lymph. This is also called haemo-
lymphatic stage, which entails
bouts of fever, headaches,
enlarged lymph nodes, joint pains
and itching

In the second stage the parasites

cross the blood-brain barrier to
infect the central nervous system.
This is known as the neurological
or meningo-encephalic stage.
FACT 6

Disease management: diagnosis

Disease management
is made in 3 steps:

Screening for potential infection. This involves

using serological tests (only available for T.
b.gambiense) and checking for clinical signs -
especially swollen cervical lymph nodes.
Diagnosing by establishing whether the
parasite is present in body fluids.
Staging to determine the state of disease
progression. This entails clinical examination
and in some cases analysis of the
cerebrospinal fluid obtained by lumbar
puncture.
FACT 7

Drugs used in the treatment of first stage:

Pentamidine: discovered in 1940, used for the

treatment of the first stage of T. b. gambiense sleeping
sickness. Despite non-negligible undesirable effects, it
is in general well tolerated by patients.
Suramin: discovered in 1920, used for the treatment of
the first stage of T. b. rhodesiense. It provokes certain
undesirable effects, including nephrotoxicity and
allergic reactions.
 FACT 8

Drugs used in the treatment of second stage:

Melarsoprol: discovered in 1949, it is used for the treatment of both
gambiense and rhodesiense infections. It is derived from arsenic
and has many undesirable side effects, the most dramatic of
which is reactive encephalopathy (encephalopathic syndrome)
which can be fatal (3% to 10%). It is currently recommended as
first-line treatment for the rhodesiense form, but rarely used in the
gambiense form.
Eflornithine: much less toxic than melarsoprol, registered in 1990
is only effective against T.b. gambiense. It is generally used in
combination with nifurtimox (as part of the Nifurtimox-
eflornithine combination therapy, NECT) but can be used also as
monotherapy. The regimen is complex and cumbersome to apply.
FACT 8

Nifurtimox: The Nifurtimox-eflornithine

combination therapy, NECT, was introduced in
2009. It simplifies the use of eflornithine by
reducing the duration of treatment and the
number of IV perfusions, but unfortunately it
has not been studied for T.b. rhodesiense.
Nifurtimox is registered for the treatment of
American trypanosomiasis but not for human
African trypanosomiasis. Both drugs are
provided free of charge by WHO to endemic
countries with a kit containing all the material
needed for its administration.
Drugs used in the treatment of both stages:
Fexinidazole is an oral treatment for gambiense human
African trypanosomiasis It was included in 2019 in the WHO
Essential medicines list and WHO human African
Trypanosomiasis treatment guidelines. This molecule is
indicated as first line for first stage and non-severe second
stage. It should be administered for 10 days within 30 minutes
after a solid meal and under supervision of trained medical
staff. Currently a clinical trial for its use in rhodesiense HAT is
ongoing.
 TRIVIA DAY PRESENTATION

THANK YOU FOR LISTENING!

 •END•

DATA GATHERED FROM SCIENCEKIDS.CO.NZ

REFERENCES

https://images.fineartamerica.com/images-medium-large/1-
trypanosoma-brucei-gambiense-lm-eric-v-grave.jpg

https://ph.images.search.yahoo.com/search/images;_ylt=AwrKEaYK
3vBjkScoQqOzRwx.;_ylu=Y29sbwNzZzMEcG9zAzEEdnRpZAMEc2Vj
A3BpdnM-?p=tsetse+fly&fr2=piv-
web&type=E210PH91215G0&fr=mcafee#id=3&iurl=https%3A%2F%2
Fi.pinimg.com%2Foriginals%2Fc1%2F0b%2Fc1%2Fc10bc1cea586c2
aea99ec4f2ae5d24fb.jpg&action=click

https://www.cdc.gov/parasites/sleepingsickness/biology.html
LEISHMANIA
DONOVANI
PRESENTED BY: JUSTINE JEWEL C. MANUEL

FEBRUARY 21, 2023

CLINICAL PARASITOLOGY
2ND YEAR-BS MLS

A. Y. 2022-2023
 What is it?
Disease in human
Life cycle
Definitive host
Intermediate host
Mode of

SCOPE
transmission
Infective stage
Vector
Life Cycle (image)
LEISHMANIA DONOVANI

Epidemiology
Symptoms
Diagnosis
Treatment
 LEISHMANIA DONOVANI

Named after William Leishman, who

discovered microbes on splenic swabs, and
Charles Donovan, who discovered microbes
on splenic puncture biopsies.

a PROTOZOA; an infectious pathogen (class

WHAT IS IT? Kinetoplastida) that targets humans.

A species of intracellular parasite belonging

to the genus Leishmania, a group of haemo
flagellate kinetoplastids. (Wikipedia)

This parasite belongs to a family named

"Trypanosomatidae" (that belongs to the
order Kinetoplastida and includes free-living
and parasitic species).
 DISEASE IN HUMAN
LEISHMANIASIS
A parasitic disease found in tropical,
subtropical, and parts of southern Europe.
It is classified as a neglected tropical
disease (NTD).

A vector-borne illness that is transmitted

with the aid of using sand flies and due to
obligate intracellular protozoa of the genus
Leishmania.

The disease is caused by infection with the

Leishmania parasite, which is transmitted
by the bite of a sand fly.

LEISHMANIA DONOVANI
 DISEASE IN HUMAN

CUTANEOUS
LEISHMANIASIS
The most common form of
leishmaniasis.
caused by more than 15 species of
the protozoan parasite Leishmania,
transmitted by infected female
sandflies.

MUCOCUTANEOUS
LEISHMANIASIS
LEISHMANIA DONOVANI
Appears as a complication of cutaneous
leishmaniasis and can occur months or
years after the skin ulcer has healed.
 LIFE CYCLE
DEFINITIVE
INTERMEDIATE

HOST HOST
Us, the humans infected female

phlebotomine

sand flies

MODE OF

VECTOR TRANSMISSION
bite (from the
phlebotomine
intermediate host)
sand flies
Human to human
INFECTIVE
sexual contact
STAGE blood transfusion
contaminated
promastigote (A stage of
syringe
the unicellular life cycle
in which the flagellum is
in front of the nucleus
and separated from the
cell body, typically in
trypanosomes.)

LEISHMANIA DONOVANI
LIFE CYCLE

LEISHMANIA DONOVANI
 MORPHOLOGY
LEISHMANIA DONOVANI

AMASTIGOTE PROMASTIGOTE
(2.4 µm-3.5 µm wide) (15-25 µm long
flagellum: 15-30 µm long.)
MORPHOLOGY
LEISHMANIA DONOVANI

PROMASTIGOTE

AMASTIGOTE
 MICROSCOPE VIEW
SOURCE: https://w1.med.cmu.ac.th/parasite/prorozoa-flagellates/1154/

AMASTIGOTE PROMASTIGOTE
LEISHMANIA DONOVANI
ORIGIN OF THE PARASITE
The genus Leishmania may be originated
in South America, but diversified after
moving to Asia.

HOW DID IT START

SPREADING? EPIDEMIOLOGY
Number of infected sand flies bite their
hosts and start spreading.

HOW MANY ARE AT RISK?

350 million people in 88 countries in

total.

LEISHMANIA DONOVANI
 EPIDEMIOLOGY
LEISHMANIA DONOVANI

In 2016, leishmaniasis affected people in focus areas of about 90

countries in tropical, subtropical, and southern Europe. Ecological
environments varied from tropical rainforests to deserts.
 EPIDEMIOLOGY
LEISHMANIA DONOVANI

Back in 2002, the disease was endemic to tropical and

subtropical regions in 88 countries. There were an estimated
12 million cases worldwide. There were 1.5 to 2 million new
cases each year. The cutaneous form was the most common
(1-1.5 million cases per year) and accounted for 50-75% of all
new cases, with 0.5 million cases of visceral leishmaniasis (VL)
occurring annually. (Sundar et al., 2002)

But as of 2018, nearly 100 endemic countries reported

700,000 to 1 million new cases of leishmaniasis annually. The
number of cases of this deadly disease continued to rise in East
Africa. (Burza et al., 2018)
 SYMPTOMS

CUTANEOUS
LEISHMANIASIS
skin lesions (lasting for months or years)
scabs

MUCOCUTANEOUS
LEISHMANIASIS

LEISHMANIA DONOVANI
stuffiness or bleeding of the nose
 VISCERAL SYPTOMS

MOST COMMON:
Fever

Weight loss (cachexia /kuh·kek·see·uh/)

Hepatosplenomegaly (usually the spleen protrudes

beyond the liver)

Pancytopenia – namely Anemia, Leukopenia, and

Thrombocytopenia

LEISHMANIA DONOVANI
High total protein and low albumin levels due to
hypergammaglobulinemia
DIAGNOSIS

LEISHMANIA DONOVANI
SOURCE: REMIAO ET AL., 2020
 LEISHMANIA DONOVANI

WE MUST...
apply insect repellent

PREVENTION wear loose and protective

clothing
use insecticides
stay in air-conditioned or in a
room with screen door/windows

SOURCE: CDC
 LEISHMANIA DONOVANI

MILTEFOSINE

good for adults and adolescence

(like 12 yrs. old)
one 50-mg oral capsule twice a day
for 28 consecutive days

TREATMENT
 LEISHMANIA DONOVANI

AMPHOTERICIN B
DEOXYCHOLATE

TREATMENT
 LEISHMANIA DONOVANI

PENTAMIDINE ISETHIONATE

TREATMENT
 LEISHMANIA DONOVANI

“AZOLES” (KETOCONAZOLE,
ITRACONAZOLE, AND
FLUCONAZOLE)

TREATMENT
 LEISHMANIA DONOVANI

PAROMOMYCIN

TREATMENT
Thank you for

listening 🤍🤍
QUESTIONS? COMMENTS?
SUGGESTIONS? REACTIONS?
 REFERENCES
Akhoundi, M., Downing, T., Votýpka, J., Kuhls, K., Lukeš, J., Cannet, A., Ravel, C., Marty, P., Delaunay, P., Kasbari, M., Granouillac, B., Gradoni, L., & Sereno, D. (2017).
Leishmania infections: Molecular targets and diagnosis. Molecular Aspects of Medicine, 57, 1–2. https://doi.org/10.1016/j.mam.2016.11.012

American Association of Veterinary Parasitologists. (n.d.). Leishmania donovani. American Association of Veterinary Parasitologists. Retrieved February 21, 2023, from
https://www.aavp.org/wiki/catprotozoa/coccidia-apicomplexan/sarcomastigophora/trypanosomes-leishmanial-organisms/leishmaniasis/leishmania-donovani/

Burza, S., Croft, S. L., & Boelaert, M. (2018). Leishmaniasis. The Lancet, 392(10151), 951–970. https://doi.org/10.1016/s0140-6736(18)31204-2

Creative Commons Attribution-NonCommercial-Share Alike 3.0. (2022, March). Symptoms, transmission, and current treatments for cutaneous leishmaniasis: Dndi. Drugs
for Neglected Diseases initiative (DNDi). Retrieved February 19, 2023, from https://dndi.org/diseases/cutaneous-leishmaniasis/facts/

Editors of Stopleishmania.org. (n.d.). Leishmaniosis in humans. Stopleishmania.org. Retrieved February 16, 2023, from http://www.stopleishmania.org/leishmaniosis-
humans.php#:~:text=Leishmania%20transmission%20in%20humans&text=The%20sandfly%20becomes%20infected%20after,but%20they%20are%20exceptionally%20r
are.

Editors of Wikipedia. (2023, January 28). Leishmania donovani. Wikipedia. Retrieved February 16, 2023, from https://en.wikipedia.org/wiki/Leishmania_donovani

G., M. (2016, October 20). Leishmania Donovani (With Diagram) | Zoology. Zoology Notes. Retrieved February 19, 2023, from
https://www.notesonzoology.com/parasitology/leishmania-donovani-with-diagram-zoology/4673

Global Health, & Division of Parasitic Diseases and Malaria. (2020, February 18). CDC - Leishmaniasis - Biology. Centers for Disease Control and Prevention. Retrieved
February 16, 2023, from https://www.cdc.gov/parasites/leishmaniasis/biology.html#:~:text=Leishmaniasis%20is%20a%20vectorborne%20disease,donovani%2C%20L.

Lukeš, J., Mauricio, I. L., Schönian, G., Dujardin, J.-C., Soteriadou, K., Dedet, J.-P., Kuhls, K., Tintaya, K. W., Jirků, M., Chocholová, E., Haralambous, C., Pratlong, F., Oborník,
M., Horák, A., Ayala, F. J., & Miles, M. A. (2007). Evolutionary and geographical history of the Leishmania donovani complex with a revision of current taxonomy.
Proceedings of the National Academy of Sciences (PNAS), 104(22), 9375–9380. https://doi.org/10.1073/pnas.0703678104

Reimão, J. Q., Coser, E. M., Lee, M. R., & Coelho, A. C. (2020). Laboratory Diagnosis of Cutaneous and Visceral Leishmaniasis: Current and Future Methods. Microorganisms,
8(11), 1632. https://doi.org/10.3390/microorganisms8111632

Sundar, S., & Rai, M. (2002). Laboratory Diagnosis of Visceral Leishmaniasis. Clinical and Vaccine Immunology, 9(5), 951–958. https://doi.org/10.1128/cdli.9.5.951-
958.2002

U.S. Department of Health & Human Services / Global Health, Division of Parasitic Diseases and Malaria. (2017, December 14). Leishmaniasis. Centers for Disease Control
and Prevention. Retrieved February 19, 2023, from https://www.cdc.gov/dpdx/leishmaniasis/index.html#print

U.S. Department of Health & Human Services / Global Health, Division of Parasitic Diseases and Malaria. (2023, February 13). CDC - Leishmaniasis - resources for Health
Professionals. Centers for Disease Control and Prevention. Retrieved February 19, 2023, from
https://www.cdc.gov/parasites/leishmaniasis/health_professionals/index.html#tx

U.S. Department of Health & Human Services / Global Health, Division of Parasitic Diseases and Malaria. (2023, February 13). CDC - Leishmaniasis - Treatment. Centers for
Disease Control and Prevention. Retrieved February 19, 2023, from
https://www.cdc.gov/parasites/leishmaniasis/health_professionals/index.html#:~:text=In%202014%2C%20FDA%20approved%20the,other%20species%20(e.g.%2C%20L.
Leishmania Major
Leishmania Spp.
Syrelle M. Nocido
BS MLS 2
 DISEASES

This affects the SKIN (wet ulcer)

Leishmania major (rural).
Multiple small red papule covered
with serous exudate; possible
intense itching; ulceration of
papule occurs early

MORPHOLOGY

Amastigote
Promastigote
5 by 3 μm long
9-15μm Long and slender
Round to oval
Nucleus located in or near center
Nucleus located usually off center
Kinetoplast, located in anterior end
Round to oval Kinetoplast present, consisting of dotlike
Single free flagellum, extending from anterior end
blepharoplast from which emerges a small axoneme
Parabasal body located adjacent to the blepharoplast
L
I C
F Y
E C
L
E
 Intermediate host
Female Sandflies
(Phlebotomus)

Mode of transmission
Definitive host
Vector (Female Sand Fly Bite)
Humans as the definitive
Blood transfusion
host Lab accident
Sexual intercourse
Congenital infection
EPIDIMIOLOGY
the Eastern Hemisphere
Northern Africa, the Middle East
Northwestern China
Northwestern India.
It affects as many as 12 million people worldwide, with 1.5–2.0
million new cases each year.
SYMPTOMS
Some people have a silent
infection, without any symptoms
or signs. People who develop
clinical evidence of infection
usually have fever, weight loss,
enlargement (swelling) of the
spleen and liver, and abnormal
blood tests.
Leishmaniasis Major

DIAGNOSIS
Our Picture

Giemsa-stained slides of
aspiration of fluid
underneath the ulcer bed for the
typical amastigotes, culture of
ulcer tissue and Serologic Tests
Leishmaniasis Major
TREATMENT

Fluconazole Paromomycin Intralesional

injections
References
LEISHMANIA

MEXICANA
Presented by:
Paulite, Kimberly Joy R.
Leishmania Mexicana
also referred to as American cutaneous leishmaniasis.
affects either the skin/mucosae or internal organs.
Leishmania mexicana is an intracellular parasite that
causes two polarly opposed diseases: One is a self-
limited disease, characterized by ulcerative lesions
associated with a low infectious load, as found in
patients with localized cutaneous leishmaniasis (LCL).
Cutaneous leishmaniasis (CL)
Leishmaniasis is caused by protozoan parasites which
are transmitted by the bite of infected female
phlebotomine sandflies.
the most common form and causes skin lesions, mainly
ulcers, on exposed parts of the body.
These can leave life-long scars and cause serious
disability or stigma. About 95% of CL cases occur in the
Americas, the Mediterranean basin, the Middle East and
central Asia.
Morphology
Amastigotes of Leishmania are spherical to ovoid and
measure 1-5 µm long by 1-2 µm wide.
They possess a large nucleus, a prominent kinetoplast,
and a short axoneme, the last of which is rarely visible
by light microscopy. The organisms reside in
macrophages of the host and can be found throughout
the body.
Morphology
Morphology
Life Cycle
Definitive host

Human
Intermediate host

Infected female
phlebotomine sand flies.
 Mode of Transmission

Vector-borne Disease

Vector

Lutzomyia olmeca olmeca

Infective stage
Leishmaniasis is transmitted by the bite of infected
female phlebotomine sand flies. The sand flies inject the
infective stage from their proboscis during blood meals .
Epidemiology
Leishmaniasis is found in people in focal areas of
approximately 90 countries in the tropics, subtropics,
and southern Europe. The ecologic settings range from
rain forests to deserts. Leishmaniasis usually is more
common in rural than in urban areas, but it is found in
the outskirts of some cities.
Symptoms
Breathing difficulty.
Skin sores, which may become a skin ulcer that heals
very slowly.
Stuffy nose, runny nose, and nosebleeds.
Swallowing difficulty.
Diagnosis
Laboratory diagnosis of leishmaniasis can be made by the
following:
demonstration of parasite in tissues of relevance by
light microscopic examination of the stained specimen,
in vitro culture, or animal inoculation;
detection of parasite DNA in tissue samples
 Diagnosis
Laboratory diagnosis of leishmaniasis can be made by the
following:
immunodiagnosis by detection of parasite antigen in
tissue, blood, or urine samples, by detection of
nonspecific or specific antileishmanial antibodies
(immunoglobulin), or by assay for leishmania-specific
cell-mediated immunity.
Treatment
The skin sores of cutaneous leishmaniasis usually heal
on their own, even without treatment. But this can take
months or even years, and the sores can leave ugly
scars.
Conventional amphotericin B deoxycholate
Reference
Centers for Disease Control and Prevention. (2017, December 14). CDC - dpdx - leishmaniasis. Centers for Disease
Control and Prevention. Retrieved February 20, 2023, from https://www.cdc.gov/dpdx/leishmaniasis/index.html
Centers for Disease Control and Prevention. (2020, February 18). CDC - Leishmaniasis - Biology. Centers for Disease
Control and Prevention. Retrieved February 20, 2023, from
https://www.cdc.gov/parasites/leishmaniasis/biology.html
Centers for Disease Control and Prevention. (2020, February 18). CDC - Leishmaniasis - Epidemiology & Risk
Factors. Centers for Disease Control and Prevention. Retrieved February 20, 2023, from
https://www.cdc.gov/parasites/leishmaniasis/epi.html
Centers for Disease Control and Prevention. (2023, February 13). CDC - Leishmaniasis - resources for Health
Professionals. Centers for Disease Control and Prevention. Retrieved February 20, 2023, from
https://www.cdc.gov/parasites/leishmaniasis/health_professionals/index.html
Eiras, D. P., Kirkman, L. A., & Murray, H. W. (2015, March 1). Cutaneous leishmaniasis: Current treatment
practices in the USA for returning travelers. Current treatment options in infectious diseases. Retrieved February
20, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360962/
González C;Rebollar-Téllez EA;Ibáñez-Bernal S;Becker-Fauser I;Martínez-Meyer E;Peterson AT;Sánchez-Cordero V;
(n.d.). Current knowledge of Leishmania vectors in Mexico: How geographic distributions of species relate to
transmission areas. The American journal of tropical medicine and hygiene. Retrieved February 20, 2023, from
https://pubmed.ncbi.nlm.nih.gov/22049037/
Moore, E. M., & Lockwood, D. N. (2010, May). Treatment of visceral leishmaniasis. Journal of global infectious
diseases. Retrieved February 20, 2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2889655/
THANK YOU FOR
LISTENING!
Bachelor of Science in Medical Laboratory Science
Clinical Parasitology

Leishmania tropica
Leishmania tropica (Wright 1903)
• Protozoan heterogenous species complex
• The vector of this parasite is sandfly
HISTORY: The first person to describe the
organism was Wright in 1903 who saw
them in the cutaneous lesion of an
Armenian patient undergoing treatment in
Boston
Zoonotic L. tropica
• is a parasite of dogs and rodents and is
associated with rural disease
Anthroponotic L. tropica
• is a parasite of humans and occurs in
urban environments
Sandfly ( Lutzomyia longipalpis)
• The common vector for L. tropica disease
( zoonotic and anthroponotic)
Leishmaniasis recidivans
• The disease carried by L. tropica
• is a rare, cutaneous form of
leishmaniasis, occurring in patients with
a good cellular immune response. It is
also known as lupoid leishmaniasis.
Cutaneous Leishmaniasis
-Common form which
causes sore at the bite
site, which heals for weeks
or months, leaving
unpleasant looking scar
L. tropica morphology

Infective stage
Life Cycle
Epidemiology
• Anthroponotic L. tropica infection was
formerly common in many large cities of
the Middle East (Baghdad, Teheran,
Aleppo, and Damascus) leading to it
being known as “urban” cutaneous
leishmaniasis. It is also found in
southern Italy, Greece, Pakistan, and
north-western India.
Epidemiology
• Endemic to those countries of Europe and
northern Africa bordering the Mediterranean
Sea and to the Asian countries of Syria,
Israel, southern Russia, China, Vietnam, and
India. L. mexicana has been reported from
Peru, Bolivia, Brazil, the Guianas, and
Mexico.
Epidemiology
• A variant clinical form of cutaneous
leishmaniasis occurring in South and Central
America and Ethiopia is referred to as diffuse
cutaneous leishmaniasis (DCL). DCL never
heals spontaneously and there is a tendency
to relapse after treatment.
Laboratory Diagnosis
• Amastigotes may be detected
microscopically in biopsy tissues, smears
or secretions before or after culture.
Parasites are best visualized using
Giemsa’s or Leishman’s stains, and
suitable culture media include
conventional nutrient agar-blood
mixtures
 L. tropica diagnosis
using giemsa stain

L. tropica diagnosis
using Wright’s
stain
Treatments
• Amphotericine B • Ketoconazole
Treatments
• Antimonial medications are often effective
by intramuscular injections for 10 days.
Resistant infections may require repeated
treatments.
Prevention
• No vaccines or drugs to prevent infection
are available.
• controlling the sand fly populations by
destroying the vectors and by controlling
rodents in endemic areas where the sand
flies may also find hosts.
When outdoors (or in unprotected quarters):

• Minimize the amount of exposed (uncovered)

skin.
• Apply insect repellent to exposed skin and
under the ends of sleeves and pant legs.
When indoors:

• Stay in well-screened or air-conditioned

areas.
• Keep in mind that sand flies are much
smaller than mosquitoes and therefore can
get through smaller holes.
• Spray living/sleeping areas with an
insecticide to kill insects.
Sources:
• https://dermnetnz.org/topics/leishmaniasis
• https://www.cdc.gov/dpdx/leishmaniasis/index.html
• https://pubmed.ncbi.nlm.nih.gov/14971592/
• Parasitology for Medical and Clinical Laboratory
Professionals, John W. Ridley, Ph.D.
Leishmania Species:

LEISHMANIA
BRAZILIENSIS
COMPLEXES
CLINICAL PARASITOLOGY
Reporter: Rivera, Darell R.
DISEASES
Mucocutaneous Leishmaniasis (espundia)
Causes oral and nasal lesions causing severe
damage to the mucus membranes.

About 1 to 10% in Brazil and Peru caused by

Leishmania braziliensis progress to a
metastatic infection of the mucosa of the
oral/nasal cavity or larynx, often 1 to 5 years
after healing of the initial simple cutaneous
lesion.
MORPHOLOGY

Amastigote Promastigote
round or oval long slender spindle shape
2-6 x 1-3 micrometer bodies
delicate cell membrane 15-20 x 1-2 micrometer
round or oval nucleus thick cell membrane
flagellum is absent round or oval nucleus
flagelum is present
LIFE
CYCLE
Sandfly
Human
DEFINITIVE HOST
Human
INTERMEDIATE HOST
Sandflies
MODE OF TRANSMISSION
via the bite of sandflies (female
vector)
Person-to-person transmission by
sexual contact, blood transfusions
and the use of contaminated
syringes has also been described,
but they are exceptionally rare.
EPIDEMIOLOGY
occurs mostly in Brazil and Central America
primarily in forestry and construction
workers.
Latin American countries consisting of
Brazil, Bolivia, and Peru account for nearly
90% of the cases; other nations include
Colombia, Paraguay, and Venezuela.
African countries including Ethiopia, Sudan,
Kenya, and Namibia
EPIDEMIOLOGY

According to the World Health Organization

(WHO), certain socio-economic indicators point to a
higher risk of infection. These include:
Poverty
Malnutrition
Famine
Illiteracy
Lack of sanitation and proper hygiene
Large-scale migration and settlements
DIAGNOSIS
Certain blood tests to detect antibodies against
the parasite
Montenegro skin test: It is generally not a very
effective method to aid in the diagnosis
DNA testing (hybridization) and PCR
Biopsy of skin lesion
Detection of pathogen using staining methods
Examining tissues under a microscope to detect
the parasite
TREATMENT
The treatment for Mucocutaneous Leishmaniasis differs from one
individual to another. Proper consultation with the infectious disease
consultants and public health officers are generally recommended
before treatment starts. The treatment measures include:
Oral medicines and topical ointments/applications for skin
lesions: The ulcers do not go away on their own without suitable
treatment
If the ulcers heal and cause cosmetic disfigurement, then plastic
surgery may be performed. A restorative surgery may be required
for the face and nose
Intravenous medications (that may include intramuscular
injections)
For fungal (secondary) infections that develop due to
Leishmaniasis, antifungal medication are prescribed.

The medications administered vary depending upon the type of

Leishmania species causing the infection.
MEDICATIONS:
Imidazole antifungal
Ketokonazole
Itraconazole
Fluconazole **