Blood born protozoans

• Blood protozoa of major clinical significance
include members of genera Trypanosoma (T.
brucei and T. cruzi); Leishmania (L.
donovani, L. tropica and L. braziliensis);
Plasmodium (P. falciparum, P.
ovale, P. malariae and P. vivax); Toxoplasma
gondii; and Babesia (B. microti

African trypanosomiasis (Sleeping
sickness)

• Etiology
There are two clinical forms of African
trypanosomiasis:
– 1) a slowly developing disease caused by
Trypanosoma brucei gambiense
– 2) a rapidly progressing disease caused by T.
brucei rhodesiense.

• Epidemiology
T. b. gambiense
– predominant in the western and central regions of
Africa, whereas
• T. b. rhodesiense
– restricted to the eastern third of the continent (figure
2E). 6,000 to 10,000 human cases are documented
annually. 35 million people and 25 million cattle are at
risk. Regional epidemics of the disease are cause of
major health and economic disasters.

Chaga's disease: Countries in which
American trypanosomiasis is endemic

• Morphology
– T. b. gambiense and T. b. rhodesiense are similar in
appearance:
– The organism measures 10 - 30 micrometers x 1-3
micrometers.
– It has a single central nucleus and a single flagellum
originating at the kinetoplast and joined to the body
by an undulating membrane
– The outer surface of the organism is densely coated
with a layer of glycoprotein, the variable surface
glycoprotein

Trypanosoma cruzi, trypomastigote
form, in a blood smear (Giemsa stain)

Figure 7C. Trypanosoma cruzi.
Leishmanial form

Riduvid bug, the vector of American
trypanosomiasis

Ramana's sign: unilateral conjunctivitis
and orbital edema

Leishmania tropica amastigotes from a skin touch preparation. In A, a still
intact macrophage is practically filled with amastigotes, several of which
have clearly visible a nucleus and a kinetoplast (arrows); in B,
amastigotes are being freed from a rupturing macrophage. Patient with
history of travel to Egypt, Africa, and the Middle East. Culture in NNN
medium followed by isoenzyme analysis identified the species as L.
tropica minor.

Life cycle
• During a blood meal on the mammalian host, an infected tsetse fly (genus
Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites
enter the lymphatic system and pass into the bloodstream . 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.

Structure of Trypanosome brucei

Figure 1B Forms of Trypansoma brucei obsreved in the tstese fly and in the human blood
stream
T. brucei is transmitted by tsetse flies of the genus Glossina. Parasites are ingested by the fly
when it takes a blood meal on an infected mammal. The parasites multiply in the fly, going
through several developmental stages in the insect gut and salivary glands (procyclic
trypanosomes, epimastigotes, metacyclic trypanosomes). The cycle in the fly takes
approximately 3 weeks. When the fly bites another mammal, metacyclic trypanosomes are
inoculated, and multiply in the host's blood and extracellular fluids such as spinal fluid.
Humans are the main reservoir for T. b. gambiense, but this species can also be found in
animals. Wild game animals are the main reservoir of T. b. rhodesiense

Two areas from a blood smear from a patient
with African trypanosomiasis. Thin blood
smear stained with Giemsa. Typical
trypomastigote stages (the only stages found
in patients), with a posterior kinetoplast, a
centrally located nucleus, an undulating
membrane, and an anterior flagellum. The two
Trypanosoma brucei species that cause human
trypanosomiasis, T. b. gambiense and T. b.
rhodesiense, are undistinguishable
morphologically. The trypanosomes length
range is 14-33 µm

• Blood smear from a patient (a U.S. traveler)
with Trypanosoma brucei rhodesiense. A
dividing parasite is seen at the right. Dividing
forms are seen in African trypanosomiasis, but
not in American trypanosomiasis (Chagas'
disease)

Blood smear from a patient with
Trypanosoma brucei gambiense

Life cycle
The infective, metacyclic form of the trypanosome is injected into
the primary host during a bite by the vector, the tsetse fly (figure 3).
The organism transforms into a dividing trypanosomal
(trypomastigote) blood form (figure 1B) as it enters the draining
lymphatic and blood stream. The trypanosomal form enters the
vector during the blood meal and travels through the alimentary
canal to the salivary gland where it proliferates as the crithidial
form (epimastigote) and matures to infectious metacyclic forms
(Figure 1B). Trypomastigotes can traverse the walls of blood and
lymph capillaries into the connective tissues and, at a later
stage, cross the choroid plexus into the brain and cerebrospinal
fluid. The organism can be transmitted through blood transfusion.

Symptoms
•
The clinical features of Gambian and Rhodesian
disease are the same, however they vary in
severity and duration. Rhodesian disease
progresses more rapidly and the symptoms are
often more pronounced. The symptoms of the
two diseases are also more pronounced in
Caucasians than in the local African population.
Classically, the progression of African
trypanosomiasis can be divided into three stages:
the bite reaction (chancre), parasitemia (blood
and lymphoid tissues), and CNS stage.

Bite reaction:
• A non-pustular, painful, itchy chancre (Figure 4
A and B) forms 1-3 weeks after the bite and
lasts 1-2 weeks. It leaves no scar.

Parasitemia:
• Parasitemia and lymph node invasion is marked by
attacks of fever which starts 2-3 weeks after the bite
and is accompanied by malaise, lassitude, insomnia
headache and lymphadenopathy and edema (figure
4E). Painful sensitivity of palms and ulnar region to
pressure (Kerandel's sign) may develop in some
Caucasians. Very characteristic of Gambian disease is
visible enlargement of the glands of the posterior
cervical region (Winterbottom's sign) (Figure 4C).
Febrile episodes may last few months as in Rhodesian
disease or several years as in Gambian disease.
Parasitemia is more prominent during the acute stage
than during the recurrence episodes.

CNS Stage:
• The late or CNS stage is marked by changes in character
and personality. They include lack of interest and
disinclination to work, avoidance of acquaintances,
morose and melancholic attitude alternating with
exaltation, mental retardation and lethargy, low and
tremulous speech, tremors of tongue and limbs, slow
and shuffling gait, altered reflexes, etc. Males become
impotent. There is a slow progressive involvement of
cardiac tissue. The later stages are characterized by
drowsiness and uncontrollable urge to sleep. The
terminal stage is marked by wasting and emaciation.
Death results from coma, intercurrent infection or
cardiac failure

The leg of a teenage girl who has sleeping sickness, showing the chancre at
the site of the tsetse fly

The partially healed chancre on the arm of a
female patient in a ward of a rural clinic.

Neurological complications can occur as a result
of infection and, as seen here, patients may be
immobilised for their own safety.

Tsetse fly. The vector of African
trypanosomiasis

A male sleeping sickness patient with
myxoedema. WHO

The damaged brain of a patient who
had died from African trypanosomiasis
(or sleeping sickness).

The clinical features of Rhodesian
disease are similar but briefer and
more acute. The acuteness and
severity of disease do not
allow typical sleeping sickness. Death
is due to cardiac failure within 6-9
months.

Pathology and Immunology
• An exact pathogenesis of sleeping sickness is not known, although
immune complexes and inflammation have been suspected to be
the mechanism of damage to tissues. The immune response against
the organism does help to eliminate the parasite but it is not
protective, since the parasite has a unique ability of altering its
antigens,the VSG (see the chapter on Molecular Biology of
Trypanosomes). Consequently, there is a cyclic fluctuation inthe
number of parasites in blood and lymphatic fluids and each wave of
parasite represents a different antigenic variant. The parasite
causes polyclonal expansion of B lymphocytes and plasma cells and
an increase in total IgM concentration. It stimulates the
reticuloendothelial function. It also causes severe depression of cell
mediated and humoral immunity to other antigens.

Diagnosis
• Detection of parasite in the bloodstream, lymph
secretions and enlarged lymph node aspirate
provides a definitive diagnosis in early (acute)
stages. The parasite in blood can be concentrated
by centrifugation or by the use of anionic support
media. Cerebrospinal fluid must always be
examined for organisms. Immuno-serology
(enzymelinkedimmune
assay, immunofluorescence) may be indicative
but does not provide definite diagnosis.

Treatment and Control
• The blood stage of African trypanosomiasis can be
treated with reasonable success with Pentamidine
isethionate or Suramin. These drugs have been
reported also to be effective in prophylaxis although
they may mask early infection and thus increase the
risk of CNS disease. Cases with CNS involvement should
be treated with Melarsoprol, an organic arsenic
compound. The most effective means of prevention is
to avoid contact with tsetse flies. Vector eradication is
impractical due to the vast area involved. Immunization
has not been effective due to antigenic variation.

American trypanosomiasis
(Chagas' disease)

Etiology
• Chagas' disease is caused by the protozoan
hemoflagellate, Trypanosoma cruzi.

Epidemiology
• American trypanosomiasis, also known as Chagas'
disease, is scattered irregularly in Central and
South America,
• stretching from parts of Mexico to Argentina
(figure 6). Rare cases have been reported in
Texas, California and
• Maryland. It is estimated that 16-18 million
people are infected by the parasite and 50 million
are at risk. About
• 50,000 people die each year from the disease.

Morphology
• Depending on its host environment, the
organism occurs in three different forms
(Figure 7 and 9B).
– The trypanosomal (trypomastigote) form (figure
7A), found in mammalian blood, is 15 to 20
microns long and morphologically similar to
African trypanosomes.
– .

– The crithidial (epimastigote) form (figure 7B) is
found in the insect intestine.

• The leishmanial (amastigote) form (figure 7C), found
intracellularly or in pseudocysts inmammalian viscera
(particularly in myocardium and brain), is round or
oval in shape, measures 2-4 microns and lacks a
prominent flagellum

Life cycle
• The organism is transmitted to mammalian host by many species of kissing (riduvid) bug (figure 8), most
• prominently by Triatoma infestans, T. sordida, Panstrongylus megistus and Rhodnius prolixus. Transmission
• takes place during the feeding of the bug which normally bites in the facial area (hence the name, kissing bug)
• and has the habit of defecating during feeding. The metacyclic trypamastigotes, contained in the fecal material,
• gain access to the mammalian tissue through the wound which is often rubbed by the individual that is bitten.
• Subsequently, they enter various cells, including macrophages, where they differentiate into amastigotes and
• multiply by binary fission. The amastigotes differentiate into non-replicating trypomastigotes and the cells rupture
• to release them into the bloodstream. Additional host cells, of a variety of types, can become infected and the
• trypomastigotes once again form amastigotes inside these cells. Uninfected insect vectors acquire the organism
• when they feed on infected animals or people containing trypomastigotes circulating in their blood. Inside the
• alimentary tract of the insect vector, the trypomastigotes differentiate to form epimastigotes and divide
• longitudinally in the mid and hindgut of the insect where they develop into infective metacyclic trypomastigotes
• (figure 9C). Transmission may also occur from man to man by blood transfusion and by the transplacental route.

Symptoms
• Chagas' disease can be divided into three stages: the
primary lesion, the acute stage, and the chronic stage.
• The primary lesion, chagoma, appearing at the site of
infection, within a few hours of a bite, consists of a slightly
raised, flat non-purulent erythematous plaque surrounded
by a variable area of hard edema. It is usually found on
• the face, eyelids, cheek, lips or the conjunctiva, but may
occur on the abdomen or limbs. When the primary
• chagoma is on the face, there is an enlargement of the pre-
and post- auricular and the submaxillary glands on
• the side of the bite. Infection in the eyelid, resulting in a
unilateral conjunctivitis and orbital edema (Ramana's
• sign) (figure 9A), is the commonest finding.

Acute Stage:
• The acute stage appears 7-14 days after infection. It is
characterized by :
– Restlessness
– sleeplessness, malaise, increasing exhaustion, chills, fever and
bone and muscle pains.
– Other manifestations of the acute phase are
• cervical, axillary and iliac adenitis, hepatomegaly,
• erythematous rash and acute myocarditis.
• There is a general edematous reaction associated
withlymphadenopathy. Diffuse myocarditis, sometimes accompanied
by serious pericarditis and endocarditis, is very frequent during the
initial stage of the disease.
– In children, Chagas' disease may cause meningo-encephalitis
and coma. Death occurs in 5-10 percent of infants..

Chronic Stage:
• The acute stage is usually not recognized and
often resolves with little or no immediate
damage and the infected host remains an
asymptomatic carrier. An unknown proportion
(guessed at 10-20%) of victims develop a
chronic disease
– Disturbances of peristalsis lead to megaesophagus
and megacolon

Pathology and Immunology
• The pathological effects of acute phase Chagas' disease largely result from direct damage to infected cells. In
• later stages, the destruction of the autonomic nerve ganglions may be of significance. Immune mechanisms, both
• cell mediated and humoral, involving reaction to the organism and to autologous tissues have been implicated in
• pathogenesis.
• T. cruzi stimulates both humoral and cell mediated immune responses. Antibody has been shown to lyze the
• organism, but rarely causes eradication of the organism, perhaps due to its intracellular localization. Cell mediated
• immunity may be of significant value. While normal macrophages are targeted by the organism for growth,
• activated macrophages can kill the organism. Unlike T. brucei, T. cruzi does not alter its antigenic coat. Antibodies
• directed against heart and muscle cells have also been detected in infected patients leading to the supposition
• that there is an element of autoimmune reaction in the pathogenesis of Chagas' disease. The infection causes
• severe depression of both cell mediated and humoral immune responses. Immunosuppression may be due to
• induction of suppressor T-cells and/or overstimulation of macrophages.

Diagnosis
• Clinical diagnosis is usually easy among
children in endemic areas.
• Cardiac dilation, megacolon and
megaesophagus in individuals from endemic
areas indicate present or former infection.
• Definitive diagnosis requires the
demonstration of trypanosomes by
microscopy or biological tests (in the insect or
mice).

• There is no curative therapy available. Most drugs
are either ineffective or highly toxic. Recently two
experimental drugs, Benznidazol and Nifurtimox
have been used with promising results in the
acute stage of the disease, however their side
effects limit their prolonged use in chronic cases.
• Control measures are limited to those that
reduce contact between the vectors and man.
Attempts to develop a vaccine have not been very
successful, although they may be feasible.

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, Rhodinius, and Panstrongylus.
Inside the host, the trypomastigotes invade cells, 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 .
Trypanosoma cruzi can also be transmitted through blood transfusions, organ
transplantation, transplacentally, and in laboratory accidents.

Etiology
• Several species of Leishmania are pathogenic
for man:
– L. donovani causes visceral leishmaniasis (Kala-
azar,black disease, dumdum fever);
– L. tropica (L. t. major, L. t. minor and L. ethiopica)
cause cutaneous leishmaniasis(oriental sore, Delhi
ulcer, Aleppo, Delhi or Baghdad boil);
– L. braziliensis (also, L. mexicana and L. peruviana)
are etiologic agents of mucocutaneous
leishmaniasis (espundia, Uta, chiclero ulcer).

Many children suffering from visceral
leishmaniasis develop a noticeable
thickening, stiffening and darkening of
the eyelashes and eyebrows.

Epidemiology
• Leishmaniasis is prevalent world wide: ranging
from south east Asia, Indo-
Pakistan, Mediterranean, north and central
Africa, and south and central America.

Morphology
• Amastigote (leishmanial form)
– is oval and measures 2-5 microns by 1 - 3 microns

• Leptomonad
– measures 14 - 20 microns by 1.5 - 4 microns, a
similar size to trypanosomes

Crater lesion of leishmaniasis

Leishmania donovani, leptomonad
forms.

Leishmania donovani in bone marrow
cell. Smear.

Bone marrow smear showing
Leishmania donovani parasites in a
bone marrow histiocyte from a dog

Giemsa stained leishmanial promastigotes from a
culture in which the bar-shaped kinetoplast in the
organism closest to the center of the group "rosette“
may be seen.

Life cycle
promastigote
• The organism is transmitted by the bite of several species
of blood-feeding sand flies (Phlebotomus) which carry
• the in the anterior gut and pharynx. The parasites gain
access to mononuclear phagocytes where
• they transform into amastigotes and divide until the
infected cell ruptures. The released organisms infect other
• cells. The sandfly acquires the organisms during the blood
meal; the amastigotes transform into flagellate
• promastigotes and multiply in the gut until the anterior gut
and pharynx are packed. Dogs and rodents are
• common reservoirs (figure 11F).

Leishmaniasis is transmitted by the bite of female phlebotomine sandflies.
The sandflies inject the infective stage, promastigotes, during blood meals .
Promastigotes that reach the puncture wound are phagocytized by
macrophages and transform into amastigotes . Amastigotes multiply in
infected
cells and affect different tissues, depending in part on the Leishmania
species . This originates the clinical manifestations of leishmaniasis. Sandflies
become infected during blood meals on an infected host when they ingest
macrophages infected with amastigotes ( , ). In the sandfly's midgut, the
parasites differentiate into promastigotes , which multiply and migrate to
the proboscis .

Symptoms
• Visceral leishmaniasis (kala-azar, dumdum fever):
– L. donovani organisms in visceral leishmaniasis are rapidly
eliminated from the site of infection, hence there is rarely a
local lesion, although minute papules have been described in
children. They are localized and multiply in the mononuclear
phagocytic cells of spleen, liver, lymph nodes, bone marrow,
intestinal mucosa and other organs. One to four months after
infection, there is occurrence of fever, with a daily rise to 102-
104 degrees F, accompanied by chills and sweating. The spleen
and liver progressively become enlarged (figure 11B, C and E).
With progression of the diseases, skin develops hyperpigmented
granulomatous areas (kala-azar means black disease). Chronic
disease renders patients susceptible to other infections.
Untreated disease results in death.

Profile view of a teenage boy suffering from
visceral leishmaniasis. The boy exhibits
splenomegaly, distended abdomen and severe
muscle wasting.

A 12-year-old boy suffering from visceral
leishmaniasis. The boy exhibits splenomegaly
and severe muscle wasting

Jaundiced hands of a visceral
leishmaniasis patient.

Enlarged spleen and liver in an autopsy
of an infant dying of visceral
leishmaniasis

18 October 2001
'Leishmaniasis' is a deadly tropical
disease which affects around 2 million
people a year. It has become
increasingly resistant to drugs. A
chance discovery showed a cancer
drug undergoing tests had some
extremely useful properties.

Cutaneous leishmaniasis (Oriental
sore, Delhi ulcer, Baghdad boil):
• In cutaneous leishmaniasis, the organism (L.
tropica) multiplies locally, producing of a
papule, 1-2 weeks (or as long as 1-2 months)
after the bite. The papule gradually grows to form
a relatively painless ulcer. The center of the ulcer
encrusts while satellite papules develop at the
periphery. The ulcer heals in 2-10 months, even if
untreated but leaves a disfiguring scar (figure 12).
The disease may disseminate in the case of
depressed immune function.

• Mucocutaneous leishmaniasis (espundia,
Uta, chiclero): The initial symptoms of
mucocutaneous leishmaniasis are the same as
those of cutaneous leishmaniasis, except that
in this disease the organism can metastasize
and the lesions spread to mucoid (oral,
pharyngeal and nasal) tissues and lead to their
destruction and hence sever deformity (figure
12E). The organisms responsible are
L. braziliensis, L. mexicana and L. peruviana.

Pathology
•
Pathogenesis of leishmaniasis is due to an
immune reaction to the organism, particularly
cell mediated immunity. Laboratory examination
reveals a marked leukopenia with relative
monocytosis and lymphocytosis, anemia and
thrombocytopenia. IgM and IgG levels are
extremely elevated due to both specific
antibodies and polyclonal activation.
•

Diagnosis
•
Diagnosis is based on a history of exposure to
sandfies, symptoms and isolation of the
organisms from the lesion aspirate or biopsy,
by direct examination or culture. A skin test
(delayed hypersensitivity: Montenegro test)
and detection of anti-leishmanial antibodies
by immuno-fluorescence are indicative of
exposure.

Sodium stibogluconate (Pentostam) is the drug
of choice. Pentamidine isethionate is used as
an alternative. Control measures involve
vector control and avoidance. Immunization
has not been effective.

Skin ulcer due to leishmaniasis, hand
of Central American adult.

Scar on skin of upper leg representing
healed lesion of leishmaniasis

Non-healing cutaneous leishmaniasis
lesion on ear lobe

Girl with diffuse mucocutaneous
leishmaniasis of the face which is
responding to treatment

Cutaneous leishmaniasis skin lesion. The lesion
measured about 1 inch in diameter and was moist with
raised borders. There was no drainage;
however, the lesion did appear to be infected

• Etiology
Four Plasmodium species are responsible for
human malaria
– P. falciparum,
– P. vivax,
– P. ovale
– P. malariae.

• Epidemiology
There are an estimated 200 million global cases
of malaria leading a mortality of more than one
million people per year.
– P. falciparum (malignant tertian malaria) and P.
malariae (quartan malaria) are the most common
species of malarial parasite and are found in Asia and
Africa.
– P. vivax (benign tertian malaria) predominates in Latin
America, India and Pakistan
– P. ovale (ovale tertian malaria) is almost exclusively
found in Africa (figure 12G).

Malaria generally occurs in areas where environmental conditions allow parasite
multiplication in the vector. Thus, malaria is usually restricted to tropical and subtropical
areas (see map) and altitudes below 1,500 m. However, this distribution might be
affected by climatic changes, especially global warming, and population movements.
Both
Plasmodium falciparum and P. malariae are encountered in all shaded areas of the map
(with P. falciparum by far the most prevalent). Plasmodium vivax and P. ovale are
traditionally thought to occupy complementary niches, with P. ovale predominating in
Sub-Saharan Africa and P. vivax in the other areas; however these two species are not
always distinguishable on the basis of morphologic characteristics alone; the use of
molecular tools will help clarify their exact distribution.

• Morphology
– ring shaped, 1-2 microns in size
– other forms (ameboid and band) may also exist.
The sexual forms of the parasite (gametocytes) are
much larger and 7-14 microns in size.
– P. falciparum is the largest and is banana shaped
while others are smaller and round.
– P. vivax causes stippling of infected red cells).

• The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female
Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and
mature into schizonts , which rupture and release merozoites . (Of note, in P. vivax and P. ovale a
dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream
weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ),
the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ).
Merozoites infect red blood cells . The ring stage trophozoites mature into schizonts, which rupture
releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes)
. Blood stage parasites are responsible for the clinical manifestations of the disease.
The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an
Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known
as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate the
macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes)
which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow,
rupture, and release sporozoites , which make their way to the mosquito's salivary
glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle

• Life_cycle_of_malaria_Part_1_Human_hostx.
mp4
• Malaria in the 21st century
x[www.keepvid.com].mp4
• malaria lifecycle x[www.keepvid.com].mp4

Plasmodium falciparum: Blood Stage
Parasites:
• Thin Blood Smears
Fig. 1: Normal red cell; Figs. 2-18: Trophozoites
(among these, Figs. 2-10 correspond to ring-
stage trophozoites); Figs. 19-26: Schizonts (Fig.
26 is a ruptured schizont); Figs. 27, 28: Mature
macrogametocytes (female); Figs. 29, 30:
Mature microgametocytes (male)

Plasmodium falciparum: Blood Stage
Parasites: Thick Blood Smears

Plasmodium malariae: Blood Stage Parasites:
Thin Blood Smears
Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (rings); Figs. 6-13: Trophozoites; Figs.
14-22: Schizonts; Fig. 23: Developing gametocyte; Fig. 24: Macrogametocyte (female); Fig.
25: Microgametocyte (male)

• Plasmodium malariae: Blood Stage Parasites:
Thick Blood Smears

Plasmodium ovale: Blood Stage Parasites: Thin Blood Smears
Fig. 1: Normal red cell; Figs. 2-5: Young trophozoites (Rings); Figs.
6-15: Trophozoites; Figs. 16-23: Schizonts; Fig. 24:
Macrogametocytes (female); Fig. 25: Microgametocyte (male)

Plasmodium vivax: Blood Stage Parasites: Thin
Blood Smears
Fig. 1: Normal red cell; Figs. 2-6: Young
trophozoites (ring stage parasites); Figs. 7-18:
Trophozoites; Figs. 19-27: Schizonts; Figs. 28
and 29: Macrogametocytes (female); Fig. 30:
Microgametocyte (male)

Plasmodium falciparum: Gametocytes
Figs. 27, 28: Mature macrogametocytes (female); Fig. 29, 30: Mature microgametocytes
(male)

Plasmodium malariae: Gametocytes
Fig. 23: Developing gametocyte; Fig. 24:
Macrogametocyte (female); Fig. 25:

Plasmodium falciparum: Gametocytes: An
asplenic, 41 y.o. woman, immigrant from
Haiti, who returned to the US 2 days ago; high
P. falciparum parasitemia; the presence of such
young gametocytes in the peripheral blood is
exceptional

Plasmodium falciparum: Gametocytes: A
patient from Haiti; mature gametocytes

Plasmodium malariae: Gametocytes: Smear
from patient:
56 y.o. man who had traveled to Kenya

Plasmodium malariae: Gametocytes: Smear
from patient: 56 y.o. man who had traveled to
Kenya

Plasmodium ovale: Gametocytes
Fig. 24: Macrogametocyte (female); Fig. 25:
Microgametocyte (male).

Plasmodium vivax: Gametocytes
Fig. 28 and 29: Nearly mature and mature
macrogametocyte (female); Fig. 30:

Gametocytes
Smears from patients: Note the Schüffner's
dots in A, and the fimbriation of the
erythrocyte in B. The erythrocytes in P. ovale
infections are less enlarged than with P.
vivax, and are not as deformed.
A, B: Male patient born in Nigeria, who came
to the US 5 days ago

C Plasmodium vivax: Gametocytes
Smears from patients:
Note the variability in Schüffner's dots.
A: A pregnant woman who visited India 6 months ago
(specimen contributed by New Jersey SHD)
B,C: 50 y.o. woman 3 months ago from a 1-month visit to
India

Ring stages
• VILMA SANTOS
• MAZINGER Z
• ORANGE JUICE
• FERDINAND MARCOS

• VILMA SANTOS – SCHUFFNER’S DOTS
• MAZINGER Z – ZIEMANN’ DOTS
• ORANGE JUICE – JAMES DOTS
• FERDINAND MARCOS – MAURER’S DOTS

Plasmodium falciparum: Ring Stage Parasites.
Fig. 1: Normal red cell; Figs. 2-10: Increasingly
mature ring stage parasites.

Plasmodium malariae: Ring Stage Parasites
Fig. 1: Normal red cell; Figs. 2-5: Rings

Appliqué form
Ring with double chromatin dot
Older ring stage parasite
Doubly infected erythrocyte
Multiple infections, 6 rings in 2 erythrocytes

Plasmodium malariae: Ring Stage Parasites
Smears from patients: 56 y.o. man who had
traveled to Kenya

Plasmodium ovale: Ring Stage Parasites
Fig. 1: Normal red cell; Figs. 2-5: Ring stage
parasites

Plasmodium ovale: Ring Stage Parasites Smears from patients:
Note the relatively large chromatin dots. A, C: 54 y.o. man who returned the
previous month from a visit to Kenya and Malawi. P. ovale, confirmed by PCR
(specimen contributed by New Mexico SHD). B: 20 y.o. man who returned 10
months ago from a visit to Mozambique, Zimbabwe and Swaziland; this attack is
thus a relapse

Plasmodium vivax: Ring Stage Parasites
Fig. 1: Normal red cell; Figs. 2-6: Ring stage
parasites (young trophozoites)

Plasmodium vivax: Ring Stage Parasites Smears from patients:
A: Rings in 2 slightly enlarged RBCs; 17 y.o. man with a relapse due to P. vivax (PCR confirmed), 6
months after returning from a visit to Papua New Guinea (specimen contributed by Virginia SHD)
B: Double infection with rings, RBC enlarged and deformed, Schüffner's dots beginning to
become visible; 69 y.o. woman born in India who was symptomatic on the day of arrival to the
US (specimen contributed by Pennsylvania SHD) C: Late ring in a RBC with Schüffner's dots; 60
y.o. man who returned 2 months ago from a 3 month trip to Laos and North Korea (

Plasmodium falciparum: Schizonts
Figs. 19-25: Increasingly mature schizonts; Fig.
26: Ruptured schizont

Plasmodium malariae: Schizonts. Increasingly
mature schizonts

Plasmodium falciparum: Schizonts. Smears from patients: Schizonts are seen only rarely
in P. falciparum malaria. An asplenic, 41 y.o. woman, immigrant from Haiti, who returned
to the US 2 days ago; high P. falciparum parasitemia
A: Young schizont with 10 nuclei;
B: Mature schizont with 24 nuclei, ready to rupture (“segmenter”)

Plasmodium malariae: Schizonts.Smears from patients:
The parasites are compact and the infected erythrocytes are not enlarged. In C and
D, the merozoites are arranged in a rosette pattern.
A, B, C, D: 56 y.o. man who had traveled to Kenya

Plasmodium ovale: Schizonts
Increasingly mature schizonts

Plasmodium vivax: Schizonts
Figs. 19-27: Increasingly mature schizonts

Plasmodium ovale: Schizonts
Smears from patients: A, B: 54 y.o. man who
returned the previous month from a visit to
Kenya and Malawi. Infection with P. ovale,
confirmed by PCR

Plasmodium vivax: Schizonts Smears from patients: Note that in these patients, the Schüffner's
dots are not conspicuous. (This happens in many of the smears received at CDC; it is probably
related to variability in staining.)
A, C, D, E:

Plasmodium falciparum: Trophozoites
Figs. 11-18: Increasingly mature trophozoites

Plasmodium malariae: Trophozoites
Figs. 6-13: Increasingly mature trophozoites;
Fig. 13 is a "band form".

Thin smears from two patients with high parasitemias: A: An asplenic, 41 y.o. woman,
immigrant from Haiti, who returned to the US 2 days ago; high P. falciparum
parasitemia (specimen contributed by Florida SHD) CDC
B: A patient who acquired malaria by blood transfusion and died with extremely high
parasitemia; PCR confirmed P. falciparum; one of the 2 RBCs contains 3 young
trophozoites, which have begun to accumulate pigment

Plasmodium malariae: Trophozoites Smears
from patients:
The infected erythrocytes are not enlarged
(sometime they even appear smaller than non-
infected ones). C is a "band form" trophozoite.
A, B, C: 56 y.o. man who had traveled to Kenya

Plasmodium ovale: Trophozoites
Increasingly mature trophozoites. Note the
fimbriated red cells (Figs. 8, 13)

Plasmodium vivax: Trophozoites
Figs. 8-18: Increasingly mature trophozoites of
P. vivax

Plasmodium ovale: Trophozoites Smears from patients: Note the lack
of ameboidicity in the older trophozoites (B,C) and the fimbriation of
the erythrocyte in C. The erythrocytes in P. ovale infections are less
enlarged than with P. vivax, and are not as deformed. The Schüffner's
dots are visible in A, but not B and C.
A: 20 y.o. man who returned 10 months ago from a visit to
Mozambique, Zimbabwe and Swaziland (specimen contributed by
New York SHD). CDC
B, C: 23 y.o. man who arrived to the US 5 months ago after having
been in Liberia and Ivory Coast

Plasmodium vivax: Trophozoites
Smears from patients: Increasingly mature trophozoites. The RBCs are enlarged and
deformed, the parasites are ameboid, and the Schüffner's dots vary in intensity.
A, B: 26 y.o. woman who spent 2 weeks in Papua New Guinea 5 months ago (specimen
contributed by Pennsylvania SHD) CDC
C, E: 60 y.o. man who returned 2 months ago from a 3-month visit to Laos and North Korea
(specimen contributed by Hawaii SHD)
D: 28 y.o. woman who returned 3 months ago from a 2 weeks visit to Kenya

Life cycle
Malarial parasites are transmitted by the infected female anopheline mosquito
which injects sporozoites present in the saliva of the insect (Figure 18). Sporozoites
infect the liver parenchymal cells where they may remain dormant (hypnozoites)
or undergo stages of schizogony to produce schizonts and merogony to produce
merozoites (meronts). When parenchymal cells rupture, thousands of meronts are
released into blood and infect the red cells. P. ovale and P. vivax infect immature
red blood cells whereas P. malariae infects mature red cells. P. falciparum infects
both. In red cells, the parasites mature into trophozoites. These trophozoites
undergo schizogony and merogony in red cells which ultimately burst and release
daughter merozoites. Some of the merozoites transform into male and female
gametocytes (figure 19) while others enter red cells to continue the erythrocytic
cycle. The gametocytes are ingested by the female mosquito, the female
gametocyte transforms into ookinete, is fertilized, and forms an oocyst (figure 20)
in the gut. The oocyte produces sporozoites (sporogony) (figure 20) which migrate
to the salivary gland and are ready to infect another host. The liver
(extraerythrocytic) cycle takes 5-15 days whereas the erythrocytic cycle takes 48
hours or 72 hours (P. malariae). Malaria can be transmitted by transfusion and
transplacentally.

Sexual stages of the malaria parasite
Plasmodium falciparum

Stage II (central) and stage III (bottom right)
immature gametocytes

Stage IV immature gametocyte, located
centrally

Stage V mature gametocyte, showing
characteristic sausage-shaped
morphology, located centrally (blood film, wet
mount, x1000 magnification under oil
immersion)

Male (micro)gametocyte exflagellation -
extrusion of motile, flagella-like microgametes
with vigorous movement (blood film, wet
mount, x1000 magnification under oil
immersion) (an unusually clear picture of this
metabolically dynamic and visually striking
event)

Plasmodium_exflagellationx.mp4

Figure 20 Developmental stages of
Plasmodium falciparum in the
Anopheles mosquito vector

Two oocysts, dissected from the outer wall of
the Anopheles stephensi midgut, 10 days post
infection of the mosquito

Single oocyst, dissected from the outer wall of
infection of the mosquito

Single oocyst, dissected from the outer wall of
infection of the mosquito (wet mount, x1000
magnification under oil immersion)

Isolated bow-shaped sporozoite, dissected
from the salivary glands of Anopheles
stephensi, 17 days post infection of the
mosquito (wet mount, x1000 magnification
under oil immersion)

Symptoms
• The symptomatology of malaria depends on the parasitemia, the presence of the organism in
different organs and the parasite burden. The incubation period varies generally between 10-30
days. As the parasite load becomes significant, the patient develops headache, lassitude, vague
pains in the bones and joints, chilly sensations and fever. As the disease progresses, the chills and
fever become more prominent. The chill and fever follow a cyclic pattern (paroxysm) with the
symptomatic period lasting 8-12 hours. In between the symptomatic periods, there is a period of
relative normalcy, the duration of which depends upon the species of the infecting parasite. This
interval is about 34-36 hours in the case of P. vivax and P. ovale (tertian malaria), and 58-60 hours in
the case of P. malariae (quartan malaria). Classical tertian paroxysm is rarely seen in P. falciparum
and persistent spiking or a daily paroxysm is more usual.
• The malarial paroxysm is most dramatic and frightening. It begins with a chilly sensation that
progresses to teeth chattering, overtly shaking chill and peripheral vasoconstriction resulting in
cyanotic lips and nails (cold stage). This lasts for about an hour. At the end of this period, the body
temperature begins to climb and reaches 103-106 degrees F (39- 41degrees C). Fever is associated
with severe headache, nausea (vomiting) and convulsions. The patient experiences euphoria, and
profuse perspiration and the temperature begins to drop. Within a few hours the patient feels
exhausted but symptom-less and remains symptomatic until the next paroxysm. Each paroxysm is
due to the rupture of infected erythrocytes and release of parasites.
• Without treatment, all species of human malaria may ultimately result in spontaneous cure except
with P. falciparum which becomes more severe progressively and results in death. This organism
causes sequestration of capillary vasculature in the brain, gastrointestinal and renal tissues. Chronic
malaria results in splenomegaly, hepatomegaly and nephritic syndromes.

• Sierra_Leone_Treating_Children_with_Malaria
_-x_WMD_Videoblog.mp4
• Mine_Action_Technology_Workshop_-
_Malariax.mp4

• Pathology and immunology
Symptoms of malaria are due to the release of massive
number of merozoites into the circulation. Infection results
in the production of antibodies which are effective in
containing the parasite load. These antibodies are against
merozoites and schizonts. The infection also results in the
activation of the reticuloendothelial system (phagocytes).
The activated macrophages help in the destruction of
infected (modified) erythrocytes and antibody-coated
merozoites. Cell mediated immunity also may develop and
help in the elimination of infected erythrocytes. Malarial
infection is associated with immunosuppression.

• Diagnosis
Diagnosis is based on symptoms and detection
of parasite in Giemsa stained blood smears.
There are also antibody tests (Figure 20B).
• .

• Treatment and Control
Treatment is effective with various quinine
derivatives (quinine sulphate, chloroquine,
meflaquine and primaquine, etc.). Drug
resistance, particularly in P. falciparum and to
some extent in P. vivax is a major problem.
Control measures are eradication of infected
anopheline mosquitos. Vaccines are being
developed and tried but none is available yet
for routine use

Etiology
•
Babesia microti is the only member of the
genus that infects man.

Morphology
•
The trophozoite is very similar to the ring form
of the Plasmodium species (figure 21A and B).

• Life cycle
The organism (sporozoite) is transmitted by a
tick and enters the red cell where it undergoes
mitosis and the organisms (merozoite) are
released to infect other red cells. Ticks acquire
the organism during feeding on an infected
individual. In the tick, the organism divides
sexually in the gut and migrates into the
salivary gland (figure 21C).

• Symptoms
Babesiosis is associated with hemolytic
anemia, jaundice, fever and
hepatomegaly, usually 1-2 weeks after
infection.

• Diagnosis
Diagnosis is based on symptoms, patient
history and detection of intraerythrocytic
parasite in the patient or transfer of blood in
normal hamsters which can be heavily
parasitized.

• Treatment and Control
Drugs of choice are clindamycin combined
with quinine. The patient may recover
spontaneously. One should avoid tick
exposure and, if bitten, remove the tick from
the skin immediately.

Babesia microti infection, Giemsa-stained thin
smear. The organisms resemble Plasmodium
falciparum; however Babesia parasites present
several distinguishing features: they vary more
in shape and in size; and they do not produce
pigment. A 67 year old woman, status post-
splenectomy, infection probably acquired in
Long island (New York)

Infection with Babesia. Giemsa-stained thin
smears. Note the tetrad (left side of the
image), a dividing form pathognomonic for
Babesia. A 6 year old girl, status post
splenectomy for hereditary
spherocytosis, infection acquired in the US.

The Babesia microti life cycle involves two hosts, which includes a rodent, primarily the white-footed mouse, Peromyscus leucopus. During a blood meal, a
Babesia-infected tick introduces sporozoites into the mouse host . Sporozoites enter erythrocytes and undergo asexual reproduction (budding) . In the blood,
some parasites differentiate into male and female gametes although these cannot be distinguished at the light microscope level . The definitive host is a tick, in
this case the deer tick, Ixodes dammini (I. scapularis). Once ingested by an appropriate tick , gametes unite and undergo a sporogonic cycle resulting in
sporozoites . Transovarial transmission (also known as vertical, or hereditary, transmission) has been documented for “large” Babesia spp. but not for the
“small” babesiae, such as B. microti . Humans enter the cycle when bitten by infected ticks. During a blood meal, a Babesia-infected tick introduces
sporozoites into the human host . Sporozoites enter erythrocytes and undergo asexual replication (budding) . Multiplication of the blood stage parasites is
responsible for the clinical manifestations of the disease. Humans are, for all practical purposes, dead-end hosts and there is probably little, if any, subsequent
transmission that occurs from ticks feeding on infected persons. However, human to human transmission is well recognized to occur through blood transfusions
. Note: Deer are the hosts upon which the adult ticks feed and are indirectly part of the Babesia cycle as they influence the tick population. When deer
populations increase, the tick population also increases, thus heightening the potential for transmission.

Thin blood film of B. microti ring forms with a
typical Maltese Cross (four rings in cross
formatio

• Etiology
Toxoplasma gondii is the organism responsible
for toxoplasmosis

• Epidemiology
Toxoplasma has worldwide distribution and
20%-75% of the population is seropositive
without any symptomatic episode.
However, the infection poses a serious threat
in immunosuppressed individuals and
pregnant females.

• Morphology
The intracellular parasites (tachyzoite) are 3x6
microns, pear-shaped organisms that are
enclosed in a parasite membrane to form a
cyst measuring 10-100 microns in size. Cysts in
cat feces (oocysts) are 10-13 microns in
diameter (figure 22).

Life cycle
•
The natural life cycle of T. gondii occurs in cats and small rodents, although the
parasite can grow in the organs (brain, eye, skeletal muscle, etc.) of any mammal
or birds (Figure 22). Cats gets infected by ingestion of cysts in flesh. Decystation
occurs in the small intestine, and the organisms penetrate the submucosal
epithelial cells where they undergo several generations of mitosis, finally resulting
in the development of micro- (male) and macro- (female) gametocytes. Fertilized
macro-gametocytes develop into oocysts that are discharged into the gut lumen
and excreted. Oocysts sporulate in the warm environment and are infectious to a
variety of animals including rodents and man. Sporozoites released from the
oocyst in the small intestine penetrate the intestinal mucosa and find their way
into macrophages where they divide very rapidly (hence the name tachyzoites)
(figure 23) and form a cyst which may occupy the whole cell. The infected cells
ultimately burst and release the tachyzoites to enter other cells, including muscle
and nerve cells, where they are protected from the host immune system and
multiply slowly (bradyzoites). These cysts are infectious to carnivores (including
man). Unless man is eaten by a cat, it is a dead-end host.

reservoirs of infection. Cats become infected
with T. gondii by carnivorism (1). After tissue
cysts or oocysts are ingested by the cat, viable
organisms are released and invade epithelial
cells of the small intestine where they undergo
an asexual followed by a sexual cycle and then
form oocysts, which are then excreted. The
unsporulated oocyst takes 1 to 5 days after
excretion to sporulate (become
infective). Although cats shed oocysts for only
1 to 2 weeks, large numbers may be
shed. Oocysts can survive in the environment
for several months and are remarkably
resistant to disinfectants, freezing, and
drying, but are killed by heating to 70°C for 10
minutes.
Human infection may be acquired in several
ways: A) ingestion of undercooked infected
meat containing Toxoplasma cysts (2); B)
ingestion of the oocyst from fecally
contaminated hands or food (3); C) organ
transplantation or blood transfusion; D)
transplacental transmission; E) accidental
inoculation of tachyzoites. The parasites form
tissue cysts, most commonly in skeletal

• Symptoms
Although Toxoplasma infection is common, it rarely produces symptoms in
normal individuals. Its serious consequences are limited to pregnant
women and immunodeficient hosts. Congenital infections occur in about
1-5 per 1000 pregnancies of which 5-10% result in miscarriage and 8-10%
result in serious brain and eye damage to the fetus. 10-13% of the babies
will have visual handicaps. Although 58-70% of infected women will give
birth to a normal offspring, a small proportion of babies will develop
active retino-chorditis or mental retardation in childhood or young
adulthood. In immunocompetent adults, toxoplasmosis, may produce flu-
like symptoms, sometimes associated with lymphadenopathy. In
immunocompromised individuals, infection results in generalized
parasitemia involvement of brain, liver lung and other organs, and often
death.
•

Immunology
• Both humoral and cell mediated immune
responses are stimulated in normal
individuals. Cell-mediated immunity is
protective and humoral response is of
diagnostic value.

• Diagnosis
Suspected toxoplasmosis can be confirmed by
isolation of the organism from tonsil or lymph
gland biopsy.

• Treatment
Acute infections benefit from pyrimethamine
or sulphadiazine. Spiramycin is a successful
alternative. Pregnant women are advised to
avoid cat litter and to handle uncooked and
undercooked meat carefully

Toxoplasma gondii in the bronchoalveolar lavage (BAL) material from an
HIV infected patient. Numerous trophozoites (tachyzoites) can be
seen, which are typically crescent shaped with a prominent, centrally
placed nucleus. Most of the tachyzoites are free, some are still
associated with bronchopulmonary cells.

Toxoplasma gondii in tissue from a cat.

PNEUMOCYSTIS PNEUMONIA
• Pneumocystis jiroveci (formerly known as Pneumocystis carinii)
• Pneumocystis jiroveci was formerly thought to be a protozoan but is
now known to be a fungus. It is included here because
pneumocystis pneumonia is often described as an opportunistic
parasitic disease.
• Pneumocystis pneumonia is an infection of immunosuppressed
individuals and is particularly seen in AIDS patients. The organism is
pleomorphic, exhibiting, at various stages of its life cycle: 1-2
micron sporozoites, 4-5 micron trophozoites and 6-8 micron cysts. It
spreads from person to person in cough droplets. Infection in
immunosuppressed individuals results in interstitial pneumonia
characterized by thickened alveolar septum infiltrated with
lymphocytes and plasma cells. Pneumonia is associated with
fever, tachypnea, hypoxia, cyanosis and asphyxia. Diagnosis is based
on isolation of organisms from affected lungs. Trimethoprim-
sulphamethoxazole is the treatment of choice (figure 24).

Pneumocystis jiroveci trophozoites in broncho-
alveolar lavage (BAL) material. Giemsa stain.
The trophozoite are small (size: 1-5 µm), and
only their nuclei, stained purple, are visible
(arrows). AIDS patient seen in Atlanta, Georgia

This is a generalized life cycle proposed by John J. Ruffolo, Ph.D. (Cushion, MT,
for the various species of Pneumocystis. These fungi are found in the lungs of
mammals where they reside without causing overt infection until the host's immun
system becomes debilitated. Then, an oftentimes lethal pneumonia can result. A
phase: trophic forms replicate by mitosis to . Sexual phase: haploid trophic fo
conjugate and produce a zygote or sporocyte (early cyst) . The zygote underg
meiosis and subsequent mitosis to produce eight haploid nuclei (late phase cyst)
. Spores exhibit different shapes (such as, spherical and elongated forms). It is
postulated that elongation of the spores precedes release from the spore case. I
believed that the release occurs through a rent in the cell wall. After release, the
spore case usually collapses, but retains some residual cytoplasm . A trophic
stage, where the organisms probably multiply by binary fission is also recognized
exist. The organism causes disease in immunosuppressed individuals.

FACULTATIVE PARASITIC PROTOZOA
• These are free-living amebae that occasionally
cause serious human disease. They are of
particular significance in
immunocompromised hosts.

Negleria fowleri
•
This organism is a flagellate that may inhabit
warm waters (spas, warm springs, heated
swimming pools, etc.) and gain access via the
nasal passage to the brain and cause
encephalitis (figure 25)

characteristically large nuclei, with a
large, dark staining karyosome. The
amebae are very active and extend
and retract pseudopods. Trichrome
stain. From a patient who died from
primary amebic meningoencephalitis
in Virginia

Naegleria fowleri trophozoite in spinal fluid.
Trichrome stain. Note the typically large
karyosome and the monopodial locomotion.
Image contributed by Texas SHD.

Free-living amebae belonging to the genera Acanthamoeba, Balamuthia, and Naegleria are important
causes of disease in humans and animals. Naegleria fowleri produces an acute, and usually lethal, centra
nervous system (CNS) disease called primary amebic meingoencephalitis (PAM). N. fowleri has three
stages, cysts , trophozoites , and flagellated forms , in its life cycle. The trophozoites replicate by
promitosis (nuclear membrane remains intact) . Naegleria fowleri is found in fresh water, soil, thermal
discharges of power plants, heated swimming pools, hydrotherapy and medicinal pools, aquariums, and
sewage. Trophozoites can turn into temporary flagellated forms which usually revert back to the trophozo
stage. Trophozoites infect humans or animals by entering the olfactory neuroepithelium and reaching th
brain. N. fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while flagellated forms are
found in CSF.
Acanthamoeba spp. and Balamuthia mandrillaris are opportunistic free-living amebae capable of causing
granulomatous amebic encephalitis (GAE) in individuals with compromised immune
systems. Acanthamoeba spp. have been found in soil; fresh, brackish, and sea water; sewage; swimming
pools; contact lens equipment; medicinal pools; dental treatment units; dialysis machines;
heating, ventilating, and air conditioning systems; mammalian cell cultures; vegetables; human nostrils an
throats; and human and animal brain, skin, and lung tissues. B. mandrillaris however, has not been isolate
from the environment but has been isolated from autopsy specimens of infected humans and
animals. Unlike N. fowleri, Acanthamoeba and Balamuthia have only two stages, cysts and trophozoites
, in their life cycle. No flagellated stage exists as part of the life cycle. The trophozoites replicate by mitos
(nuclear membrane does not remain intact) . The trophozoites are the infective forms and are believed to
gain entry into the body through the lower respiratory tract, ulcerated or broken skin and invade the centra
nervous system by hematogenous dissemination . Acanthamoeba spp. and Balamuthia mandrillaris cys
and trophozoites are found in tissue

Acanthemeba
•
Several species of free-living Acanthemeba are
pathogenic to man. They normally reside in soil
and can infect children who swallow dirt while
playing on the ground. In normal individuals, the
infection may cause mild disease (pharyngitis) or
remain asymptomatic, but in immunodeficient
individuals, the organism may penetrate the
esophageal mucosa and reach the brain where it
causes granulomatous encephalitis

Summary
Organism Transmission Disease/symptoms Diagnosis Treatment
Trypanosoma
brucei
Tsetse fly. Sleeping sickness; cardiac
failure.
Hemoflagellate in blood or
lymph node.
Blood stage: Suramin or
petamidine isethionate;
T. cruzi Reduvid (kissing)
bug.
Chagas disease:
megacolon, cardiac failure.
Hemoflagellate in blood or
tissue.
CNS: melarsoprol
Nifurtimox and
Benzonidazole.
Leishmania
donovani
Sand fly Visceral leish-maniasis,
granulo-matous skin
lesions.
Intracellular
(macrophages) leishmanial
bodies.
Pentosam; Pentamidine
isethionate.
L. tropica Sand fly. Cutaneous lesions. As for L. donovani. As for L. donovani.
L. braziliensis Sand fly Mucocutaneous lesions. As for L. donovani. As for L. donovani.
Plasmodium
falciparum P. ovale,
P. malariae and P.
vivax
Female anopheline
mosquito.
Malarial paroxysm: chills,
fever, headache, nausea
cycles.
Plasmodia in rbc, typical of
the species involved.
Quinine derivatives Proguanil
Lariam
Babesia microti Tick Hemolytic anemia,
Jaundice and fever
Typical organism (Maltese
cross) in rbc.
None; self resolving.
Toxoplasma gondii Oral from cat fecal
material;
or meat
Adult: flu like;
congenital: abortion,
neonatal blindness and
neuropathies.
Intracellular (in
macrophages) tachyzoites.
Sulphonamides,
pyemethamine, possibly
spiramycin (non-FDA).
Pneumocystis
jiroveci
Cough droplets Pneumonia Pneumocystis in sputum.
Trimethoprim and
sulphamethoxazole.

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