Submitted to:

Mr. Jo Hanes D. Contemprato, RMT

Group 4:
Briones, Maria Reinalyn
Camacho, Milieka Faye
Castro, John Carlo
Erni, Cherlyn
Blood and tissue Flagellates
Trypanosoma brucei subsp. rhodesiense
Introduction
It is a protozoan subspecies causing Rhodesian trypanosomiasis;
it is transmitted by tsetse flies, especially Glossina morsitans in
humans; various game animals can act as reservoir hosts.

Morphology
T. brucei is a typical unicellular eukaryotic cell, and measures 8
to 50 μm in length. It has an elongated body having a streamlined
and tapered shape. Its cell membrane (called pellicle) encloses
the cell organelles, including the nucleus, mitochondria, endoplasmic reticulum, Golgi apparatus,
and ribosomes. In addition, there is an unusual organelle called the kinetoplast, which is made up
of numerous circular DNA (mitochondrial DNA) and functions as a single large mitochondrion.
The kinetoplast lies near the basal body with which it is indistinguishable under microscope. From
the basal body arises a single flagellum that run towards the anterior end. Along the body surface,
the flagellum is attached to the cell membrane forming an undulating membrane. Only the tip of
the flagellum is free at the anterior end.The cell surface of the bloodstream form features a dense
coat of variant surface glycoproteins (VSGs) which is replaced by an equally dense coat of
procyclins when the parasite differentiates into the procylic in the tsetse fly midgut.
Trypanosomatids show several different classes of cellular organisation of which two are adopted
by Trypanosoma brucei at different stages of the life cycle:
 Epimastigote, which is found in tsetse fly. Its kinetoplast and basal body lie anterior to the
nucleus, with a long flagellum attached along the cell body. The flagellum starts from the
centre of the body.
 Trypomastigote, which is found in mammalian hosts. The kinetoplast and basal body are
posterior of nucleus. The flagellum arises from the posterior end of the body.
These names are derived from the Greek mastig- meaning whip, referring to the trypanosome's
whip-like flagellum. The trypanosome flagellum has two
main structures. It is made up of a typical flagellar
axoneme which lies parallel to the paraflagellar rod, a
lattice structure of proteins unique to the kinetoplastida,
euglenoids and dinoflagellates.
The microtubules of the flagellar axoneme lie in the
normal 9+2 arrangement, orientated with the + at the
anterior end and the - in the basal body. The a cytoskeletal
structure extends from the basal body to the kinetoplast.
The flagellum is bound to the cytoskeleton of the main cell body by four specialised microtubules,
which run parallel and in the same direction to the flagellar tubulin
The flagellar function is twofold — locomotion via oscillations along the attached flagellum and
cell body, and attachment to the fly gut during the procyclic phase.
Life Cycle
Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites
throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the
replication by binary fission . The entire life cycle of African Trypanosomes is represented by
extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when
taking a blood meal on an infected mammalian host ( , ). In the fly’s midgut, the parasites
transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and
transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and continue
multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Humans are
the main reservoir for Trypanosoma brucei gambiense, but this species can also be found in
animals. Wild game animals are the main reservoir of T. b. rhodesiense.

Epidemiology
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
environment. Related to these interactions, the disease is confined in spatially limited areas called
“foci”, which are located in Sub-Saharan Africa, mainly in remote rural areas. The risk of
contracting HAT is, therefore, determined by the possibility of contact of a human being with an
infected tsetse fly. Epidemics of HAT were described at the beginning of the 20th century;
intensive activities have been set up to confront the disease, and it was under control in the 1960s,
with fewer than 5,000 cases reported in the whole continent. The disease resurged at the end of the
1990s, but renewed efforts from endemic countries, cooperation agencies, and nongovernmental
organizations led by the World Health Organization succeeded to raise awareness and resources,
while reinforcing national programs, reversing the trend of the cases reported, and bringing the
disease under control again. Since rhodesiense HAT is a zoonosis, where the animal reservoir plays
a key role, the interruption of the disease’s transmission is not deemed feasible.
Diagnosis
The diagnosis of African Trypanosomiasis is made through
laboratory methods, because the clinical features of infection
are not sufficiently specific. The diagnosis rests on finding
the parasite in body fluid or tissue by microscopy. The
parasite load in T. b. rhodesiense infection is substantially
higher than the level in T. b. gambiense infection.
T. b. rhodesiense parasites can easily be found in blood.
They can also be found in lymph node fluid or in fluid or
biopsy of a chancre. Serologic testing is not widely available
and is not used in the diagnosis, since microscopic detection
of the parasite is straightforward
Symptomatology
A bite by the tsetse fly is often painful and can develop into a red sore, also called a chancre. Fever,
severe headaches, irritability, extreme fatigue, swollen lymph nodes, and aching muscles and joints
are common symptoms of sleeping sickness. Some people develop a skin rash. Progressive
confusion, personality changes, and other neurologic problems occur after infection has invaded
the central nervous system. If left untreated, infection becomes worse and death will occur within
months.
Treatment
Treatment for African sleeping sickness depends on the stage of the disease. For the first stage,
intravenous suramin sodium for both T. gambiense and T. rhodesiense, and intramuscular
pentamidine for the Gambian form can be used. These drugs have side effects, which include fever,
rash, renal insufficiency, muscle pain, and paresthesia for suramin; and tachycardia, hypotension
and hypoglycemia for pentamidine. These drugs do not cross the blood-brain barrier, and so, they
cannot be used for the CNS stage of the disease.
Once CNS involvement occurs, intravenous melarsoprol is the drug of choice for both types of
sleeping sickness. This arsenic-containing drug can cause fatal arsenic encephalopathy (usually
prevented by coadministration of corticosteroids), and resistance to the drug has also been
observed. A febrile episode called a Jarisch-Herxheimer reaction due to trypanosome lysis may
occur following melarsoprol treatment.
A second-line drug, nitrofurazone, is used in cases of melarsoprol treatment failure. A newer drug
eflornithine, is less toxic than melarsoprol, and can also be used during the hemolymphatic stage;
however it is only effective against T. brucei gambiense. Recent evidence ahs shown that a
combination treatment of oral nifurtimux and intravenous eflornithine is of similar efficacy
compared to longer intravenous monotherapy with either agent. Combination therapy is
advantageous due to the relative ease in administration and a decreased risk of developing drug
resistance. Although nifurtimox is currently registered as a drug against American
trypanosomiasis, its use in the nifutimox-eflornithine combination treatment (NECT) has been
included in the WHO List of Essential medicine.

Prevention and Control

Wear protective clothing, including long-sleeved shirts and pants. The tsetse fly can bite through
thin fabrics, so clothing should be made of medium-weight material.

1. Wear neutral-colored clothing. The tsetse fly is attracted to bright colors and very dark colors.
2. Inspect vehicles for tsetse flies before entering. The flies are attracted to moving vehicles.
3. Avoid bushes. The tsetse fly is less active during the hottest period of the day. It rests in bushes
but will bite if disturbed.
4. Use insect repellant. Though insect repellants have not proven effective in preventing tsetse
fly bites, they are effective in preventing other insects from biting and causing illness.

Trypanosoma cruzi
 The etiologic agent of Chagas’ disease or American
trypanosomiasis.
 The only parasite that was discovered and studied before
it was known to cause a disease.
 Transmitted to humans by blood-sucking triatomine bugs.
Carlos Chagas
 Found out that the trypanosomes he dissected from the
intestine of a triatomid were the same parasites found in the blood of a child suffering from
fever and enlargement of the lymph nodes.

Parasite Biology

T. Cruzi
 Belongs to the trypanosome group Stercoararia
 Is an intracellular parasite (with myocytes- particularly myocardial tissues and cells of
the reticuloendothelial system being the most heavily infected cells).
o Other tissues that get infected includes:
 Skin
 Gonads
  Intestinal mucosa
 Placenta
 Arthropod vector – responsible for propagating this parasite
are the reduviid bugs, belonging to the genera Triatoma,
Panstrongylus, and Rhodnius.
 Zoonotic mammalian reservoir hosts have been identified,
including domestic animals, armadillos, raccoons, rodents,
marsupials, and eve some primates.
 Exhibits all four stages of development: amastigote,
promastigote, epimastigote, and trypomastigote.

o Trypomastigote- found in the bloodstream

o Amastigotes- found in tissue cells of humans

 Inside its vector, amastigote, promastigote, epimastigote forms in triatomine bugs occurs
in the midnight and trypomastigote in the hindgut.
Amastigotes
o Develop in muscles and other tissues
o Round or ovoid in shape
o Measures 1.5 to 4 µm in diameter
o Usually found in small groups of cyst-like collections in tissues.

Life Cycle
An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases
trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through
the wound or through intact mucosal membranes, such as the conjunctiva . Common triatomine
vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus.
Inside the host, the trypomastigotes invade cells near the site of inoculation, where they
differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and
differentiate into trypomastigotes, and then are released into the circulation as bloodstream
trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into
intracellular amastigotes in new infection sites. Clinical manifestations can result from this
infective cycle. The bloodstream trypomastigotes do not replicate (different from the African
trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by
another vector. The “kissing” bug becomes infected by feeding on human or animal blood that
contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the
vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into
infective metacyclic trypomastigotes in the hindgut .

Diagnosis
 Chagas’ disease may be suspected when general and cardiac symptoms are present in
patients coming from endemic regions.
 Electroencephalogram of these patients may show ventricular extrasystole and atrial
fibrillation.
 Diagnosis is by demonstration of trypanosomes in blood, cerebrospinal fluid, fixed tissues,
or lymph.
 Only in the first two months of acute disease can T. cruzi be seen by direct examination or
thick blood smears.
 Parasite concentration methods increase the probability of detecting parasitemia.
 Blood cultures and xenodiagnoses are useful for detecting low levels of T. cruzi.
 In xenodiagnoses, laboratory-reared triatomine bugs are allowed to feed on patients
suspected of being infected.
 The bugs are later examined for the presence of T. cruzi.
 Serological methods, such as immunofluorescent antibody test, complement fixation test,
and indirect hemagglutination essay are effective in demonstrating chronic disease.
 ELISA tests, which are more sensitive and specific are now used to demonstrate antibodies
to T. cruzi.
 Dot- immunobinding assays using antigen bond to nitrocellulose paper may show promised
for use under field conditions since it offers the advantage of using only small amounts of
fluid with no need for sophisticated and expensive equipment.
 The polymerase chain reaction can also be used in amplifying DNA from the kinetoplast.
Syptomatology
Chagoma
o An focal inflammation that is produced at the site of inoculation
o A small, painful, reddish nodule.
o Followed by acute and chronic phases
o Fever and generalized lymphadenopathy are features of the acute disease.
o Trypanosomes may enter through the conjunctiva of the eye and cause edema
of the eyelid and conjunctiva, a condition known as Romaña’s sign.
o Chronic disease has no characteristic symptoms and may last for 20 years or more.
o Manifestations of chronic disease include cardiomyopathy related to
congestive heart failure, cardiospasm, megaesophagus, and megacolon
(conditions may be fatal and can lead to death).
o Many asymptomatic cases are unrecognized.
o Chagas’ disease is serious and often fatal in young children but is less severe
and tends to be chronic in older children and adults.
Chagas disease has an acute and a chronic phase. If untreated, infection is lifelong.
Acute Chagas disease occurs immediately after infection, may last up to a few weeks or months,
and parasites may be found in the circulating blood. Infection may be mild or asymptomatic. There
may be fever or swelling around the site of inoculation (where the parasite entered into the skin or
mucous membrane). Rarely, acute infection may result in severe inflammation of the heart muscle
or the brain and lining around the brain.
Following the acute phase, most infected people enter into a prolonged asymptomatic form of
disease (called “chronic indeterminate”) during which few or no parasites are found in the blood.
During this time, most people are unaware of their infection. Many people may remain
asymptomatic for life and never develop Chagas-related symptoms. However, an estimated 20 –
30% of infected people will develop debilitating and sometimes life-threatening medical problems
over the course of their lives.
Complications of chronic Chagas disease may include:

 heart rhythm abnormalities that can cause sudden death;

 a dilated heart that doesn’t pump blood well;
 a dilated esophagus or colon, leading to difficulties with eating or passing stool.

In people who have suppressed immune systems (for example, due to AIDS or chemotherapy),
Chagas disease can reactivate with parasites found in the circulating blood. This occurrence can
potentially cause severe disease.

Treatment
 There is no entirely suitable drug available for treatment of Chagas’ disease.
  Nifurtimox (side effect: weight loss , anorexia, behavioral changes, antabuse effect bone
marrow suppression peripheral neuropathy and benznidazole (Side effect: rashes, bone
marrow suppression, and peripheral neuropathy ) are only partially effective in acute
disease.
 Allopurinol and itraconazole – halt the progression into cardiomyopathy (although no form
of treatment has been shown to reverse damage caused by the disease.
 Triazole derivatives (posaconazole, ravuconazole) and cruzipain inhibitors are currently
under development
 Cardiac manifestations are controlled by pacemakers and antiarrhythmic drugs
(amiodarone) while megasyndromes aare managed via special diets and surgical
procedures.

Epidemiology
 Chagas’ disease exists only in the American continent
 Approximately 16 to 18 million people are infected, and 100 million (25% of the
population of Latin America) are at risk of acquiring the infection.
 The overall incidence of the disease is about 200 000 cases a year.
 Mortality rate is unknown due to many unrecognized asymptomatic cases.
 Serologic surveys show that 15 to 50% of the population in the endemic areas is infected.
 Prevalence is highest in rural areas and among the poorer classes.
 Acute disease usually affects children, but is often unrecognized.
 Chronic disease is more common than acute disease.
 The highest incidence occurs in the fifth decade of life with males more than affected than
females.
 American trypanosomiasis is a zoonosis transmitted from rodents and burrowing animals.
 Unsanitary housing conditions contribute to transmission because vectors adapt to living
and breeding in human habitations.
 In endemic countries, bugs generally are found within cracks in the walls and thatched
roofs.
Prevention and Control
 Prevention of Chagas’ disease is based on vector control, screening and sterilization of
transfusion blood, and health education.
 Control of the vectors of the disease has centered mainly on insecticide spraying and
housing improvement to reduce breeding sites of the triatomine bugs.

Leishmania braziliensis
Leishmania spp. are digenetic or heteroxenous parasites, whose life cycle involves two hosts,
a vertebrate and an invertebrate, the sandfly.

MORPHOLOGY
Two developmental stages are formed:

amastigotes and promastigotes.

The amastigotes are small spherical non-flagellated cells ranging from 2-4µm in diameter. The
nucleus and kinetoplast are surrounded by small ring of vacuolated cytoplasm and the cells are
among the smallest nucleated cells known.
- the intracellular form in the vertebrate host
-The amastigote is also called the Leishman-Donovan (LD) body.
- literally “without a flagellum,”

Promastigotes are thin elongate cells with an anterior kinetoplast and an emergent free flagellum.
They are generally lancet-like in shape and range in size from 5-14µm in length by 1.5-3.5µm in
width.
-the extracellular form in the sandfly (Phleobotomus spp. and Lutzomyia spp.) vector
- literally the body form with “an anterior flagellum”

Different parasite species are generally not differentiated by morphological differences, but rather
on the basis of geographical, biological and clinical features.

Site of infection: Amastigotes invade

macrophage cells of the reticuloendothelial
and lymphoid systems of the skin,
nasopharynx or viscera depending on the
parasite species. The parasites survive within
phagosomes but resist digestion by lysosomal
enzymes. They multiply and grow, ultimately
rupturing the host cell and releasing stages to
infect new macrophages, including those
which circulate in the blood (monocytes)
Amastigotes are taken up from the blood of an infected host when the female sandfly bites, and
in the sandfly gut they develop into promastigotes where they multiply by binary fission;
promastigotes move anteriorly into the proboscis, and are introduced into the vertebrate host when
the sandfly bites again. The promastigotes injected by the sandfly during feeding are phagocytized
and develop into intracellular amastigotes.
Host range: All Leishmania spp. infect mammals and are most commonly found in humans, dogs
and rodents. Infections are confined to tropical areas, different parasite species being found in the
Old World (Middle-East and Africa) and the New World (Central and South America).

Life Cycle

Leishmaniasis is transmitted by the bite

of infected female phlebotomine
sandflies. The sandflies inject the
infective stage (i.e., promastigotes)
from their proboscis during blood
meals . Promastigotes that reach the
puncture wound are phagocytized by
macrophages and other types of
mononuclear phagocytic cells.
Promastigotes transform in these cells
into the tissue stage of the parasite (i.e.,
amastigotes) , which multiply by
simple division and proceed to infect other mononuclear phagocytic cells . Parasite, host, and
other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral
leishmaniasis results. Sandflies become infected by ingesting infected cells during blood meals (
, ). In sandflies, amastigotes transform into promastigotes, develop in the gut (in the
hindgut for leishmanial organisms in the Viannia subgenus; in the midgut for organisms in
the Leishmania subgenus), and migrate to the proboscis .

Mode of transmission: All species are transmitted by small blood-sucking sandflies,

notably Phlebotomus spp. in the Old World and Lutzomyia spp. in the New World. Only the
females feed on blood. Amastigotes ingested during feeding transform in the midgut or hindgut
into promastigotes which multiply by binary fission. The parasites migrate forward to the foregut
and proboscis where some become swept away by saliva into the bite site when the fly feeds.
Differential 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. Serological
tests have been developed but there are difficulties in distinguishing between recent and chronic
infections and between infections by different parasite species, although a delayed-type
hypersensitivity (DTH) skin test has shown good promise as a marker of cured symptomatic or
asymptomatic visceral infection. Modern molecular characterization techniques have used the
polymerase chain reaction (PCR) to amplify parasite DNA from host tissues.
Pathogenesis: The parasites cause three distinct types of clinical disease, cutaneous,
mucocutaneous and visceral leishmaniasis. Old World cutaneous leishmaniasis is caused by L.
tropica and L. aethiopica while New World cutaneous leishmaniasis is caused by L.
mexicana and L. braziliensis. Infections generally involve only one or a few lesions at the bite
site; they do not spread to other sites. Active lesions appear as open sores/ulcers with pronounced
inflammation. Most lesions heal spontaneously, leaving the host with solid protective immunity
to re-infection. However, under certain conditions (esp. immuno-compromised hosts), some L.
aethiopica infections may spread giving rise to disseminated cutaneous leishmaniasis (not unlike
leprosy in appearance). Infections by L. braziliensis are also often confined to single skin lesions,
but sometimes they spread to the mucocutaneous junction in the pharynx and may cause severe
destructive nasopharyngeal lesions. Visceral leishmaniasis is caused by L. donovani whereby
infected macrophages congregate in the viscera, notably the liver and spleen, producing
hepatosplenomegaly, oedema and anaemia. It is a slow but progressive illness, with bouts of
irregularly recurring fever, and is invariably fatal, unless treated.
Treatment and control: Some cutaneous infections require no treatment as lesions may heal
within several months. Systemic therapy with pentavalent antimonials (sodium stibogluconate or
meglumine antimonate) is the treatment of choice for disfiguring and visceral infections. The
development of antimonial drug resistance, however, is a growing problem in many endemic
areas, including South America, India and the Middle-East. Pentamidine or amphotericin B can
be used if antimonials are ineffective, and miltefosine and aminosidine (paromomycin) have
shown promise as treatment options, especially when combined with immunotherapy using the
tumour-necrosis factor-alpha (TNF-?) inhibitor pentoxifylline. Preventive measures include
protection from sandfly bites but this can be difficult as they are so small that they can penetrate
most mosquito nets. Reducing the size of reservoir host populations (especially dogs) has proven
beneficial in many endemic urban areas. Many cutaneous infections, however, are acquired in
forests away from human habitation, as the reservoir hosts are wild animals (esp. rodents). The
prevention of sandfly bites in forest areas is almost impossible but may be minimized by the use
of protective clothing, insect repellants and insecticidal sprays in houses.
Leishmania donovani
Introduction
It is a species that is the causal agent of visceral leishmaniasis in Mediterranean and adjacent
countries, the south central section of western Asia, eastern India, northern China, Kenya,
Ethiopia, and the Sudan; also found in Brazil, Argentina,
Colombia, and Venezuela; in the Old World, it is
transmitted by various species of Phlebotomus; New World
vectors are species of Lutzomyia; dogs and other carnivores
are known as reservoir hosts in some areas. The intracellular
amastigote form multiplies in macrophages and produces a
reticuloendothelial hyperplasia grossly affecting the spleen
and liver, with other lymphoid tissues being involved as
well, resulting in severe hepatosplenomegaly, which usually
is fatal if untreated.
Morphology

Leishmania donovani is a unicellular eukaryote having a

well-defined nucleus and other cell organelles including a
kinetoplast and a flagellum. Depending on its host it exists
in two structural variants, as follows:

Amastigote Promastigote

Amastigote form found in the mononuclear
phagocyte and circulatory systems of humans.
It is an intracellular and non-motile form,
being devoid of external flagellum. The short
flagellum is embedded in the anterior end
without projecting out. It is oval in shape, and
measures 3–6 µm in length and 1–3 µm in
breadth. The kinetoplast and basal body lie
towards the anterior end.
Promastigote is formed in the alimentary tract
of the sandfly. It is an extracellular and motile
form. It is considerably larger and more
highly elongated, measuring 15–30 µm in
length and 5 µm in width. It is spindle-
shaped, tapering at both ends. A long
flagellum (about the body length) is projected
externally at the anterior end. The nucleus lies
at the centre, and in front of which are
kinetoplast and basal body.

Life Cycle
In man the intracellular parasites undergo repeated binary fission resulting over crowdedness
inside the host cell. The host cell ultimately bursts and parasites are released. The fly ingests
Leishmanias along with the blood of man.
The parasites after reaching the midgut of the
fly increase in size, develop flagellum and
becomes metamorphosed into leptomonad
form. The leptomonads multiply by
longitudinal binary fission and reach the
proventriculus of the fly.

Repeated multiplication inside the

proventriculus causes complete obstruction of
the organ. In this condition when the fly tries
to ingest fresh blood, the meal can go no
further than the oesophagus. This causes a
regurgitation of the sucked blood during bite.
Along with the regurgitated blood leptomonad forms are introduced in the blood stream of man.

Epidemiology
In Kenya, where Phlebotomus martini is the probable vector, epidemics of visceral leishmaniasis
occurred in the 1950s and 1970s, suggesting a human reservoir, but domestic dogs have
occasionally been found infected with L. donovani. In the Sudan, between the epidemics in the
1950s and the current, ongoing, one, visceral leishmaniasis usually occurs sporadically in
nomads who occupy temporary villages in the dry season near patches of scrub that harbor the
vector Plebotomus orientalis. Leishmania donovani has been isolated from rodents in the Sudan;
rodents may be important in maintaining enzootic foci in interepidemic periods. Parasite isolates
from East Africa are more closely related biochemically to L. donovani.
 Laboratory Diagnosis
Laboratory diagnosis of leishmaniasis can be made by the following: (i) demonstration of
parasite in tissues of relevance by light microscopic examination of the stained specimen, in vitro
culture, or animal inoculation; (ii) detection of parasite DNA in tissue samples; or (iii)
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.

Symptomatology

 Fever
 Weight loss (cachexia; wasting)
 Hepatosplenomegaly (usually, the spleen is more prominent than the liver)
 Pancytopenia—i.e., anemia, leukopenia, and thrombocytopenia
 A high total protein level and a low albumin level, with hypergammaglobulinemia

Treatment
Visceral disease always requires treatment. Several medications are available. Commonly used
medicines include sodium stibogluconate (Pentostam), amphotericin B, paromomycin, and
miltefosine (Impavido).

Prevention and Control

Follow these steps to help prevent being bitten by a sand fly:

 Wear clothing that covers as much skin as possible. Long pants, long-sleeved shirts tucked
into pants, and high socks are recommended.
 Use insect repellent on any exposed skin and on the ends of your pants and sleeves. The most
effective insect repellants contain DEET.
 Spray indoor sleeping areas with insecticide.
 Sleep on the higher floors of a building. The insects are poor fliers.
 Avoid the outdoors between dusk and dawn. This is when sand flies are most active.
 Use screens and air conditioning indoors when possible. Using fans might make it more
difficult for the insects to fly.
 Use a bed net tucked into your mattress. Sand flies are much smaller than mosquitos, so you
need a tightly woven net. Spray the net with insecticide containing pyrethroid if possible.
 Buy bed nets, insecticides, and repellents before traveling to high-risk areas.