CONTENT

O PROTOZOA
INTRODUCTION
STRUCTURE
CLASSIFICATION
DISEASE CAUSED BY PROTOZOA
O MALARIA
INTRODUCTION
CAUSES
SIGNS AND SYMPTOMS
LIFE CYCLE OF MALARIA PARASITE
TREATMENT
PREVENTION
O AMOEBIASIS
INTRODUCTION
LIFE CYCLE
MODES OF TRANSMISSION
CLINICAL MANIFESTATIONS
CLINICAL FEATURES
TREATMENT
METHODS OF PREVENTION

INTRODUCTION
Unicellular, chemoheterotrophic, eucaryotic organisms of kingdom
Protista (3-2000 mm).
Protozoan means first animal.
20,000 species, only a few are pathogens. Most are free-living
organisms that inhabit water and soil. Some live in association with
other organisms as parasites or symbionts.
Reproduce asexually by fission, budding, or schizogony.
Some exhibit sexual reproduction (e.g.: Paramecium).

Trophozoite: Vegetative stage which feeds upon bacteria and

particulate nutrients.

Cyst: Some protozoa produce a protective capsule under adverse

conditions (toxins, scarce water, food, or oxygen).

STRUCTURE
Most parasitic protozoa in humans are less than 50 m in size. The
smallest (mainly intracellular forms) are 1 to 10 m long, but Balantidium
coli may measure 150 m. Protozoa are unicellular eukaryotes. As in all
eukaryotes, the nucleus is enclosed in a membrane. In protozoa other than
ciliates, the nucleus is vesicular, with scattered chromatin giving a diffuse
appearance to the nucleus, all nuclei in the individual organism appear
alike. One type of vesicular nucleus contains a more or less central body,
called an endosome or karyosome. The endosome lacks DNA in the
parasitic amebas and trypanosomes. In the phylum Apicomplexa, on the
other hand, the vesicular nucleus has one or more nucleoli that contain
DNA. The ciliates have both a micronucleus and macronucleus, which
appear quite homogeneous in composition.

CLASSIFICATION
In 1985 the Society of Protozoologists published a taxonomic scheme that distributed the
Protozoa into six phyla. Two of these phyla the Sarcomastigophora and the Apicomplexa-contain the most important species causing human disease. This scheme is based on
morphology as revealed by light, electron, and scanning microscopy. Dientamoeba fragilis,
for example, had been thought to be an ameba and placed in the family Entamoebidae.
However, internal structures seen by electron microscopy showed that it is properly placed in
the order Trichomonadida of flagellate protozoa. In some instances, organisms that appear
identical under the microscope have been assigned different species names on the basis of
such criteria as geographic distribution and clinical manifestations; a good example is the
genus Leishmania, for which subspecies names are often used. Biochemical methods have
been employed on strains and species to determine isoenzyme patterns or to identify relevant
nucleotide sequences in RNA, DNA, or both. Extensive studies have been made on the
kinetoplast, a unique mitochondrion found in the hemoflagellates and other members of the
order Kinetoplastida. The DNA associated with this organelle is of great interest. Cloning is
widely used in taxonomic studies, for example to study differences in virulence or disease
manifestations in isolates of a single species obtained from different hosts or geographic
regions. Antibodies (particularly monoclonal antibodies) to known species or to specific
antigens from a species are being employed to identify unknown isolates. Eventually,
molecular taxonomy may prove to be a more reliable basis than morphology for protozoan
taxonomy, but the microscope is still the most practical tool for identifying a protozoan
parasite.

DISEASE CAUSED BY PROTOZOA

MALARIA
INTRODUCTION
Malaria is a mosquito borne infectious disease of humans and other animals
caused by eukaryoticprotists of the genus Plasmodium. The disease results from
the multiplication of Plasmodium parasites within red- blood cells, causing
symptoms that typically include fever and headache, in severe cases progressing
to coma or death. It is widespread in tropical and sub-tropical regions, including
much of Sub-Saharan Africa, Asia, and the Americas.
Five species of Plasmodium can infect and be transmitted by humans. Severe
disease is largely caused by P.falciparum while the disease caused by P.vivax,
P.ovale and P.malarai is generally a milder disease that is rarely fatal.
P.knowlesi is a zoonotic species that causes malaria in macaques but can also
infect humans.

CAUSES
Malaria is caused by a parasite that is passed from one human to another by the bite of
infected Anopheles mosquitoes. After infection, the parasites travel via the
bloodstream to the liver, where they mature and infect red blood cells present in the
bloodstream.
The parasites multiply inside the red blood cells, which then break open within 48 to
72 hours, infecting more red blood cells. The first symptoms usually occur 10 days to
4 weeks after infection, though they can appear as early as 8 days or as long as a year
after infection. The symptoms occur in cycles of 48 to 72 hours.
Most symptoms are caused by:

The release of merozoites into the bloodstream

Anemia resulting from the destruction of the red blood cells

Large amounts of free hemoglobin being released into circulation after red
blood cells break open.

Malaria can also be transmitted from a mother to her unborn baby (congenitally) and
by blood transfusions. Malaria can be carried by mosquitoes in temperate climates, but
the parasite disappears over the winter.
There are five types of malarial parasites:
P. falciparum- Account for about 90% of deaths from malaria.
P. vivax- Responsible for the largest number of malaria infections worldwide.
P.ovale
P.malarai
P.knowlesi- Recently discovered, has been causing malaria in Malaysia and
areas of Southeast Asia.
Another type, falciparum malaria, affects more red blood cells than the other types
and is much more serious. It can be fatal within a few hours of the first symptoms.

SIGNS AND SYMPTOMS

Symptoms of malaria include:
Fever,
Shivering,
Arthralgia (joint pain),
Vomiting,
Muscle pain
Nausea
Sweating
Coma
Anemia (caused by hemolysis),
Jaundice,
Hemoglobinuria,
Retinal damage, and
Convulsions.

Malaria has been found to cause cognitive impairments, especially in children.

It causes widespread anemia during a period of rapid brain development and
also direct brain damage. Cerebral malaria is associated with retinal whitening,
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which may be a useful clinical sign in distinguishing malaria from other causes
of fever.
Severe malaria is almost exclusively caused by Plasmodium falciparum, and
usually arises 614 days after infection. Consequences of severe malaria include
coma and death if untreatedyoung children and pregnant women are
especially vulnerable.
Complications include:

Brain infection (cerebritis)

Destruction of blood cells (hemolytic anemia)

Kidney failure- feature of blackwater fever, where hemoglobin from

lysed red blood cells leaks into the urine.

Liver failure

Meningitis

Respiratory failure from fluid in the lungs (pulmonary edema)

Rupture of the spleen leading to massive internal bleeding (hemorrhage)

Splenomegaly (enlarged spleen)

Hepatomegaly (enlarged liver)

Hypoglycemia

Hemoglobinuria

Severe malaria can progress extremely rapidly and cause death within hours or
days. In the most severe cases of the disease, fatality rates can exceed 20%,
even with intensive care and treatment. In endemic areas, treatment is often less
satisfactory and the overall fatality rate for all cases of malaria can be as high as
10%.

LIFE CYCLE OF MALARIA PARASITE

The parasite's secondary hosts are human and other vertebrates, female
mosquitoes of the Anopheles genus are the primary, i.e. definitive hosts and act
as transmission vectors. If a mosquito pierces the skin of an infected person, it
potentially picks up gametocytes within the blood. Fertilization and sexual
recombination of the parasite occurs in the mosquito's gut. (Because sexual
reproduction of the parasite defines the definitive host, the mosquito is the
definitive host, whereas humans are the intermediate host.) New sporozoites
develop and travel to the mosquito's salivary gland. This produces an ookinete
that penetrates the gut lining and produces an oocyst in the gut wall. When the
oocyst ruptures, it releases sporozoites that migrate through the mosquito's body
to the salivary glands, where they are then ready to infect a new human host.
This type of transmission is occasionally referred to as anterior station transfer.

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TREATMENT
When properly treated, a patient with malaria can expect a complete
recovery. The treatment of malaria depends on the severity of the disease;
whether patients can take oral drugs or must be admitted depends on the
assessment and the experience of the clinician. Uncomplicated malaria is
treated with oral drugs.
The most effective strategy for P. falciparum infection recommended by
WHO is the use of artemisinins in combination with other antimalarials
artemisinin-combination therapy (ACT) to avoid the development of drug
resistance against artemisinin-based therapies.
Severe malaria requires the parenteral administration of antimalarial
drugs. Until recently the most used treatment for severe malaria was
quinine but artesunate has been shown to be superior to quinine in both
children and adults. Treatment of severe malaria also involves supportive
measures.
Infection with P. vivax cases should be treated with chloroquine in full
therapeutic dose. For prevention of relapse, primaquine should be given
at a dose of 14days.

PREVENTION
Methods used to prevent the spread of disease, or to protect individuals in areas
where malaria is endemic, include prophylactic drugs, mosquito eradication and
the prevention of mosquito bites. The continued existence of malaria in an area
requires a combination of high human population density, high mosquito
population density and high rates of transmission from humans to mosquitoes
and from mosquitoes to humans. If any of these is lowered sufficiently, the
parasite will sooner or later disappear from that area, as happened in North
America, Europe and much of the Middle East. However, unless the parasite is

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eliminated from the whole world, it could become re-established if conditions

revert to a combination that favors the parasite's reproduction.
1) Chemoprophylaxis: Several drugs, most of which are used for treatment
of malaria, can be taken preventively.
Chloroquine may be used where the parasite is still sensitive.
However, due to resistance one of three medications, mefloquine
(Lariam), doxycycline, and the combination of atovaquone and
proguanil hydrochloride (Malarone) is frequently needed.
Doxycycline and the atovaquone and proguanil combination are
the best tolerated; mefloquine is associated with higher rates of
neurological and psychiatric symptoms.
Quinine was used historically; however, the development of more
effective alternatives such as quinacrine, chloroquine, and
primaquine in the 20th century reduced its use. Today, quinine is
not generally used for prophylaxis. The use of prophylactic drugs
where malaria-bearing mosquitoes are present may encourage the
development of partial immunity.
2) Vector control:
Before DDT, malaria was successfully eradicated or controlled in
several tropical areas by removing or poisoning the breeding
grounds of the mosquitoes or the aquatic habitats of the larva
stages, for example by filling or applying diesel oil to places with
standing water.
Another technique was to replace the fresh water in the breeding
grounds with salt water.
Sterile insect technique is emerging as a potential mosquito control
method. Progress towards transgenic, or genetically modified,
insects suggest that wild mosquito populations could be made

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malaria-resistant. Researchers at Imperial College London created

the world's first transgenic malaria mosquito, with the first
Plasmodium-resistant.

Successful

replacement

of

current

populations with a new genetically modified population relies upon

a drive mechanism, such as transposable elements to allow for nonMendelian inheritance of the gene of interest. However, this
approach contains many difficulties and success is a distant
prospect.
Another way to reduce the malaria transmitted to humans from
mosquitoes has been developed in Arizona. They have engineered a
mosquito to become resistant to malaria. This was reported on 16
July 2010 in the journal PLoS Pathogens. It is another step on the
journey towards potentially assisting malaria control through GM
mosquito release.

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AMOEBIASIS
INTRODUCTION:
Amoebiasis protozoal infection of human beings initially involves the
colon, but may spread to soft tissues, most commonly to the liver or lungs, by
contiguity or hematogenous or lymphatic dissemination.
Amoebiasis is the third leading parasitic cause of death worldwide,
surpassed only by malaria and schistosomiasis. On a global basis, amoebiasis
affects approximately 50 million persons each year, resulting in nearly 100,000
deaths.

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Pathogenic amoeba, which produce condition of a great clinical variation:

1. Acute Amoebic Dysentery

stools contain blood and mucus, which may give rise to amoebic
hepatitis or liver abscess.

2. Chronic Amoebic Dysentery

with recurrent attack of diarrhea or relatively mild dysentery.

3. Amoebic Colitis
characterized by periods of constipation and diarrhea and episodes of abdominal
discomfort frequently stimulating appendicitis.
Etiologic Agent: Enatamoeba Histolytica

Prevalent in unsanitary areas

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Common in warm climate

Acquired by swallowing

Cysts survives a few days outside of the body

Cyst passes to the large intestine and hatch into trophozoites. It passes
into the mesenteric veins, to the portal vein, to the liver, thereby forming
amoebic liver abscess.

Entamoeba Histolytica has two developmental stages:

1. Trophozoites/vegetative form

Trophozoites are facultative parasites that may invade the tissues or

may be found in the parasitized tissues and liquid colonic contents.

2. Cyst

Cyst is passed out with formed or semi-formed stools and are resistant
to environmental conditions.

This is considered as the infective stage in the cycle of E. histolytica

Source: Human Excreta

Incubation Period:

The incubation period in severe infection is three days. In subacute

and chronic form it lasts for several months. In average cases the
incubation period varies from three to four weeks

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Period of Communicability:
The microorganism is communicable for the entire duration of the illness.

MODES OF TRANSMISSION:
1. The disease can be passed from one person to another through fecal-oral
transmission.
2. The disease can be transmitted through direct contact, through sexual
contact by orogenital, oroanal, and proctogenital sexual activity.
3. Through indirect contact, the disease can infect humans by ingestion of
food especially uncooked leafy vegetables or foods contaminated with
fecal materials containing E. histolytica cysts.
Food or drinks maybe contaminated by cyst through pollution of water
supplies, exposure to flies, use of night soil for fertilizing vegetables, and
through unhygienic practices of food handlers.

CLINICAL MANIFESTATIONS:
a. Acute amoebic dysentery

Slight attack of diarrhea, altered with periods of constipation and often

accompanied by tenesmus.

Diarrhea, watery and foul smelling stool often containing blood-streaked

mucus

Colic and gaseous distension of the lower abdomen

Nausea, flatulence, abdomnal distension and tenderness in the right iliac

region over the colon

b. Chronic amoebic dysentery

Attack dysentery that lasts for several days, usually succeeded by

constipation

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Tenesmus accompanied by the desire to defacate

Anorexia, weight loss, and weakness

Liver may be enlarged

The stool at first is semifluid but soon becomes watery, bloody, and
mucoid

Vague abdominal distress, flatulence, constipation or irregularity of bowel

Mild toxemia, constant fatigue and lassitude

Abdomen loses its elasticity when picked up between fingers

On sigmoidoscopy, scattered ulceration with yellowish and erythematous

border

The gangrenous type (fatal cases) is characterized by the appearance of

large sloughs of intestinal tissues in the stool accompanied by
hemorrhage.

CLINICAL FEATURES:
1. Onset is gradual
2. Diarrhea increases and stool
becomes bloody and mucoid
3. In untreated cases:

TREATMENT:
1. Metronidazole

(Flagyl)

800mg

TID X 5 days
2. Tetracyline 250 mg every 6 hours
3. Ampicillin, quinolones sulfadiazine

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4. Streptomycin SO4, Chloramphenicol

5. Lost fluid and electrolytes should be replaced
Several antibiotics are available to treat amoebiasis. Treatment must be
prescribed by a physician. You will be treated with only one antibiotic if
your E. histolytica infection has not made you sick. You probably will be
treated with two antibiotics (first one and then the other) if your
infection has made you sick.

METHODS OF PREVENTION:
1. Health education
2. Sanitary disposal of feces
3. Protect, chlorinate, and purify drinking water
4. Observe scrupulous cleanliness in food preparation and food handling
5. Detection and treatment of carriers
6. Fly control (they can serve as vector)
PUBLIC HEALTH PREVENTION

One important public health strategy is to make sure to treat infected

individuals who appear asymptomatic, since these people also pass cysts
in their stool and thus contributed to spreading the disease.

Good sanitation and water facilities are also important in preventing the
disease.

Food handlers, childcare workers, and health care workers with

amoebiasis should not be allowed to work until their symptoms are gone.

If children have symptoms, they should not attend childcare centers or

schools until their symptoms are gone.

In general, people should practice good hygiene, since the fecal matter
from those infected could contaminate food and water that is then
transferred to others. This includes careful hand washing with soap and
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hot running water for at least 10 seconds after going to the toilet, as well
as practice frequent hand washing in general to eliminate any parasite that
one may have picked up throughout the day.

Travelers should take precaution

Clean bathrooms and toilets often.

Boil water

Avoid uncooked foods

Practice safe food storage and handling: thoroughly cook all raw foods,
thoroughly wash raw vegetables and fruits, and reheat food until the
internal temperature of food reaches at least 167F.

HOME PREVENTION

Avoidance of drinking unboiled or unbottled water in endemic areas.

Uncooked food such as fruit and vegetables that may have been washed
in local water should also not be consumed.

Amoebic cysts are resistant to chlorine at the levels used in water

supplies, but disinfection with iodine may be effective.

Wash hands with soap and warm water after going to the toilet and before
eating or preparing food.

Proper food storage and preventing its contamination with feces, flies,
and contaminated water

Avoiding sexual practices that may lead to fecal-oral contact.

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