Plasmodium and Babesia Species Overview for Medtech Students

Plasmodium and Babesia Species Overview for Medtech Students

Plasmodium and Babesia species are critical topics in clinical parasitology, focusing on the life cycles, transmission, and clinical manifestations of these pathogens. This resource is designed for second-year Medtech students, providing essential insights into malaria caused by Plasmodium and babesiosis caused by Babesia. Key aspects include the various species of Plasmodium that infect humans, their geographical distribution, and the clinical implications of infections. The document also covers diagnostic methods, treatment options, and preventive measures relevant to these parasitic diseases.

Key Points

  • Explains the life cycle of Plasmodium species, including P. falciparum and P. vivax.
  • Covers the transmission modes of Babesia and its clinical manifestations.
  • Details diagnostic techniques such as blood smears and rapid diagnostic tests.
  • Discusses treatment options for malaria and babesiosis, including drug resistance issues.
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C L I N I C A L P A R A S I T O L O G Y
LEC 11: PLASMODIUM AND BABESIA SPECIES
MS. MARTINA DEANNE C. MENDOZA, RMT
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PLASMODIUM SPP.
Malaria remains the leading parasitic disease that causes
mortality worldwide.
This disease is caused by malaria parasites which are
micro-organisms that belong to the genus Plasmodium that
is transmitted by the bite of an infected female mosquito
belonging to the genus Anopheles.
The known species infecting humans:
P. falciparum
P. vivax
P. ovale
P malariae
P. knowlesi
P. vivax the widest geographic distribution and is the
species most likely to be found in temperate climates.
P. vivax and P. falciparum cause more than 95% of
infections.
P. ovale primarily confined to western parts of Africa.
P. knowlesi causes malaria in the macaque monkey, has
also been implicated in cases of zoonotic human malaria in
Malaysia and the Philippines.
In general, infections caused by P. vivax, P. ovale, and P.
malariae are less severe than those caused by P.
falciparum.
Life Cycle
Ring-Form Trophozoite (early trophozoite) In human
infections, this is the earliest stage, in which the organism
has a prominent, red to purple chromatin dot and a small
blue ring of cytoplasm surrounding a vacuole.
Growing Trophozoite (Late Trophozoile) characterized
by an increase in the amount of cytoplasm, the
disappearance of the vacuole, and the appearance of
malarial pigment in the organism's cytoplasm.
Immature Schizont (Multinucleate Stage)
characterized by a splitting of the chromatin mass.
Mature Schizont contains merozoites, which are
individual chromatin masses, each surrounded by
cytoplasm.
Microgametocytes (Male) have pale blue cytoplasm and
a diffuse chromatin mass that stains pale pink to purple.The
chromatin may be surrounded by a clear halo.
Macrogametocytes (Female) show a well-defined,
compact chromatin mass that stains dark pink; the
cytoplasm stains a darker blue than microgametocytes
Exoerythrocytic Phase
Humans serve as intermediate hosts and acquire the
infection when the female mosquito takes a blood meal and
injects the infective sporozoites with salivary secretions.
The sporozoites enter the human circulation and take
approximately 60 minutes to reach the liver, where they
begin the exoerythrocytic phase by penetrating
parenchymal cells.
Maturation through the trophozoite and schizont phases
results in the production of hepatic merozoites.
The release of mature merozoites from liver cells and
invasion of RBCs signal the beginning of the erythrocytic
phase.
Generally, only one cycle of merozoite production occurs in
ther liver before RBCs are invaded.
P. vivax and P. ovale, however, may persist in the liver in a
dormant stage known as hypnozoites, which accounts for
the relapse (recurrence) of the disease within 1 to 3 years
after the primary infection.
Erythrocytic Phase
Merozoites have structures and proteins (e.g., erythrocyte-
binding antigen) that selectively adhere to receptors on the
RBC membrane.
P. vivax, as well as P. knowlesi, use antigens of the
Duffy blood group as receptors for attachment to
and internalization into the RBCs, whereas P.
falciparum may simply attach to receptors that are
integral parts of the RBC membrane itself.
When merozoites have attached, endocytic invagination of
the RBC membrane allows the organism to enter the RBC
within a vacuole.
Once inside the RBC, the organism feeds on hemoglobin and
initiates the erythrocytic phase.
Malarial pigment (hemozoin), which is composed of iron
deposits, is formed in the growing trophozoite as a result of
incomplete metabolism of hemoglobin.
Once the organism has reached the mature trophozoite
stage, the chromatin begins to divide (developing schizont).
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When the chromatin split has been completed (mature
schizont); each chromatin mass is surrounded by its own
small amount of malarial cytoplasm (merozoite).
When the RBC ruptures, merozoites are released to invade
other RBCs.
Two outcomes are possible:
1. One is that the merozoite enters a cell and repeats
development into a schizont
2. The other enters a cell and develops into one of the
sexual stages, the microgametocyte or
macrogametocyte.
Sexual Phase
Sporogony, which takes place in the mosquito, results in the
production of sporozoites infective for humans.
Both the microgametocyte and the macrogametocyte are
infective for the female mosquito when she takes a blood
meal.
In the insect's stomach, exflagellation by the male and
subsequent fertilization of the female result in formation of
an ookinete that migrates through the gut wall and forms
an oocyst on the exterior gut wall.
Sporozoites are produced within the oocyst. Mature
sporozoites are released into the body cavity of the
mosquito and migrate to the salivary glands.
The female then injects sporozoites into a human as she
takes her blood meal.
SPOROGONY Sexual reproduction
The formation of oocysts containing sporozoites that
results from the division of a zygote.
Takes place in mosquitoes
SCHIZOGONY Asexual reproduction
Produces merozoites by the process of multiple fission.
Occurs in humans, has an exerythrocytic phase that
takes place in the liver and an erythrocytic phase that
takes place in erythrocytes.
The female Anopheles mosquito serves as the biological vector
and definitive host.
Pathogenesis & Clinical Manifestations
Modes of Transmission:
Bite of an Anopheles mosquito
Blood transfusion and infected needles
Transplacental
The organism is sequestered in the placenta and
can compromise because fetal development
because it affects transplacental transport
nutrients
Pre-Patent Period the interval from sporozoite injection
to detection of parasites in the blood; ranges from 11 days
to 4 weeks
P. falciparum 11 to 14 days
P. vivax 11 to 15 days
P. ovale 14 to 26 days
P. malariae 3 to 4 weeks
Incubation Period the time between sporozoite injection
and the appearance of clinical symptoms is typically 8 to 40
days
P. falciparum 8 to 15 days
P. vivax 12 to 20 days
P. ovale 11 to 16 days
P. malariae 18 to 40 days
Malarial Paroxysm begins 10 to 15 days after the bite of
an infected mosquito
Associated with the growth of the parasites in RBCs
and high levels of cytokines
Symptoms are linked to the rupture of RBCs and
release of merozoites, malarial metabolites, and
endotoxin-like substances into the bloodstream
Three Stages Of Malaria Paroxysm:
Involves headache, bone pain, nausea, and/or flulike
symptoms
The total duration of the attack is 8 to 12 hours
1
st
stage Cold Stage
Sudden inappropriate feeling of coldness and
apprehension.
Mild shivering quickly turns to violent teeth chattering
and shaking of the entire body.
Lasts for 15 to 60 minutes.
2
nd
stage Hot Stage or Flush Phase
The patient becomes hot and manifests with headache,
palpitations, tachypnea, epigastric discomfort, thirst,
nausea, and vomiting.
The temperature may reach a peak of 41°C or more.
The patient may become confused or delirious, and the
skin may be notably flushed and hot
Lasts for 2 to 6 hours.
3
rd
stage Sweating Stage
Defervescence or diaphoresis (fever subsides) ensues
with the patient manifesting with profuse sweating
The temperature lowers over the next 2 to 4 hours.
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The interval between attacks is determined by the length of the
erythrocytic cycle
P. falciparum 48 hours (3
rd
day), malignant tertian
malaria
P. vivax and P. ovale recur every 3
rd
day, benign tertian
malaria
P. malariae every 72 hours (4
th
day), causing paroxysm
on days 1 and 4, hence the term, quartan malarta
Due to the lack of an exoerythrocytic stage, fever caused by P.
knowlesi follows a quotidian pattern (24-hour erythrocyte cycle),
or is noted to be non-relapsing.
Age Of Infected Erythrocytes
P. vivax and P. ovale infect only young red blood cells
P. malariae infects only aging cells
P. falciparum and P. knowlesi infects all ages of
erythrocytes
Recrudescence
The renewal of parasitemia or clinical features arising from
persistent undetectable asexual parasitemia in the absence
of an exoerythrocytic cycle.
Relapse
Renewed sexual parasitemia following a period in which
the blood contains no detectable parasites.
Occurs with vivax and ovale malaria
Results from the reactivation of hypnozoite forms of the
parasite in the liver
Long-term infection with any malarial organism may result
in damage to the liver and spleen caused by deposits of
malarial pigment (hemozoin).
P. vivax and P. ovale mostly invades the reticulocytes;
there is generally low-tevel parasitemia (2% - 5%).
P. malariae infections can lead to nephrotic syndrome,
which arises from the deposition of circulating immune
complexes of malarial antigen and antibody on the
basement membrane of the glomeruli.
Severe form of malaria - caused by P. falciparum
Up to 50% of erythrocytes may be infected
Cerebral malaria may develop
The infected RBCs demonstrate sticky knobs that mediate
adhesion to the endothelial cells of the capillary walls.
The parasite protein P. falciparum erythrocyte
membrane protein 1 (PfEMP-1) is involved in
mediating the attachment.
Other proteins: rosettins, riffins, and histidine-rich
proteins (HRP).
In addition, complement receptor 1 on the surface of
erythrocytes may help infected cells bind with other
erythrocytes to form rosettes that can abstruct small
capillaries.
Rosettins and PfEMP-1 are the ligands for rosette
formation.
HRP localize to the cytoadherence ligands making the
adhesion more effective.
Blackwater Fever less common complication of infection with
P. falciparum
A condition characterized by hemoglobinuria.
Develops in patients with repeated infections and those
undergoing quinine therapy.
Hemoglobinuria appears black in acid urine.
o The black appearance of the urine is due to
massive intravascular hemolysis.
Protection Against Malaria parasite cannot replicate or exist
in these RBCs
Duffy Antigen Receptor for Chemokines (DARC)
The Duffy blood group antigen serves not only as blood
group antigen, but also as a receptor for chemokines, and as
a receptor for Plasmodium vivax malaria parasites.
Individuals with the Duffy-negative phenotype are resistant
to P. vivax invasion
Duffy null phenotype, Fy (a-b-) is found in 68% of Blacks
Patients with hemoglobinopathies such as
Sickle cell disease
Hemoglobin C disease
Glucose-6-phosphate dehydrogenase (G6PD)
deficiency
Diagnosis
MICROSCOPIC EXAMINATION
Thick and thin blood smears stained with Giemsa or
Wright's stain Definitive & Gold Standard
Giemsa is the preferred stain, as it allows for detection of
certain morphologic features (e.g., Schüffner's dots,
Maurer's clefts, etc.).
Thick smears are used to detect the presence of
parasites
Thin smears are used for species-level identification.
Specimens may be taken any time and all blood stages of
the parasite may be found.
In P. falciparum malaria, only the ring & gametocytes are
found
Obtaining smears every 6 to 8 hours is usually appropriate
Malarial Rapid Diagnostic Tests
These tests make use of immunochromatographic methods
to detect Plasmodium-specific antigens in a finger prick
blood sample.
Antigens being targeted by these RDTs include
Histidine rich protein I| (HRP Il) a water soluble
protein produced by trophozoites and young
gametocytes of P. falciparum
Plasmodium lactate dehydrogenase (pLDH)
produced by both sexual and asexual stage and can
distinguish between P. falciparum and non-P.
falciparum
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FAQs of Plasmodium and Babesia Species Overview for Medtech Students

What are the main species of Plasmodium that infect humans?
The main species of Plasmodium that infect humans include P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. P. falciparum is responsible for the majority of severe malaria cases, while P. vivax has the widest geographic distribution. Each species has unique characteristics and clinical implications, with P. vivax and P. falciparum causing over 95% of infections globally. Understanding these species is crucial for effective diagnosis and treatment.
How is malaria transmitted and what are its symptoms?
Malaria is primarily transmitted through the bite of infected female Anopheles mosquitoes. Other transmission modes include blood transfusions, organ transplants, and transplacental transfer. Symptoms of malaria typically include fever, chills, headache, and malaise, which can escalate to severe complications if left untreated. The clinical presentation varies depending on the Plasmodium species involved, with P. falciparum often leading to more severe manifestations.
What diagnostic methods are used for malaria and babesiosis?
Diagnostic methods for malaria include microscopic examination of Giemsa-stained blood smears, which allows for the identification of Plasmodium species based on their morphological features. Rapid diagnostic tests (RDTs) are also employed to detect specific antigens related to the parasites. For babesiosis, similar blood smear techniques are used to identify Babesia species, often revealing characteristic ring forms or Maltese cross formations. These methods are essential for timely and accurate diagnosis.
What treatment options are available for malaria?
Treatment options for malaria focus on eradicating the blood parasites and may include drugs like chloroquine, quinine, and artemisinin-based combination therapies. The choice of treatment depends on the Plasmodium species, severity of the disease, and local drug resistance patterns. For instance, P. falciparum has developed resistance to many antimalarial drugs, necessitating alternative treatment strategies. Prophylactic measures may also be recommended for travelers to endemic areas.
What are the clinical manifestations of babesiosis?
Babesiosis is characterized by symptoms such as fever, chills, fatigue, and hemolytic anemia. The disease is often more severe in immunocompromised individuals and can lead to complications like splenic rupture. The clinical presentation can vary based on the species of Babesia, with B. divergens typically causing more severe illness compared to B. microti. Early diagnosis and treatment are crucial to prevent serious outcomes.

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