CLINICAL MICROBIOLOGY

MEDICAL PARASITOLOGY

BY
Dr. (Mrs.) Linda B. Debrah

Course Code SMS 294

 Learning Objectives
By the end of this course, students should be able to:

• Demonstrate detailed knowledge and understanding

of the;
– Biology, life cycle, pathogenesis and diagnosis of
parasites in humans and their relevance to human health

– Prevention, control and treatment of medically important

parasites

• Determine the socio-economic impacts of parasites

of medical importance
 Parasitology

Protozoa Helminths Arthropods

(worms)

A parasite: A pathogen that simultaneously injures and derives sustenance from

its hosts
 Protozoa
Kingdom Protista
• Protozoans are unicellular organisms
– may infect the digestive tract
• duodenum
• small bowel
• colon
• urogenital tracts of humans
• Many belong to the Amoebae (Amebae),
and flagellates
• Transmitted mainly by fecal-oral route
 Protozoa

Sarcodina Zoomastigophora Ciliophora Apicomplexa

(Ameba group) (Flagellates) (Ciliates) (Sporozoa)

1. Intestinal 1. Gastrointestinal Eg. Balantidium 1. Blood-

1. Girdia lamblia coli • Plasmodium spp
Eg. Entamoeba
2. Urogenital 2. Tissue-
species . Toxoplasma gondii
Trichomonas vaginalis
3. hemoflagellates 3. Lungs-
Trypanosoma species, . Pneumocystic carini
Leishmania species
4. Intestinal –
. Cryptosporidium
 Protozoa
• Morphology
• Distribution
• Life cycle
• Pathogenesis/clinical manifestation
• Laboratory diagnosis
• Prevention, Treatment and control
• Etc.
 Flagellates
Intestinal/digestive tract
• There are 4 common species of intestinal
flagellates:
– Giardia lamblia
– Dientamoeba fragilis
– Chilomastix mesnili
– Trichomonas tenax/ Trichomonas hominis
 Giardia lamblia
• Also called
– Giardia intestinalis
– Giardia duodenalis

• Causes a common intestinal disease,

giardiasis
 Morphology of Giardia
Trophozoites:
• Shaped like a pear cut in half lengthwise (or human
face)
• About 15 µm x9 µm
• It has a concave sucking disc for attachment to the
intestinal mucosa
• Has 2 nuclei that resemble eyes
• Structures called median bodies that resemble
mouth
• Has 4 pairs of flagellae that look like hair
Cyst:
• Cyst is the infective form of the parasite
• It is oval, measuring 12 μm -8 μm
• A young cyst contains 2 nuclei
• A mature cyst contains 4 nuclei
• The axostyle lies diagonally
• Remnants of the flagella may be seen in
the cyst
Diagram of Giardia lamblia
 Life cycle of G. lamblia
• Cyst is acquired by ingestion of food or water
contaminated with feces

• Excystment occurs in the small intestine to release the

trophozoite

• Highly motile trophozoite gets attached to the mucosa of

the duodenum and proximal jejunum and begins to
multiply by binary fission

• Life cycle is completed by encystment of trophozoites in

the bowel and colon, followed by excretion into the
external environment
 Life cycle of Giardia lamblia

https://www.cdc.gov/dpdx/giardiasis/index.html
• Both cyst and trophozoite may be shed by
an infected individual
– But trophozoites survive poorly outside the
host
– Whereas cyst may remain viable for weeks
under moist conditions

• Man is the only known reservoir

 Pathogenesis and Clinical
manifestations
• Trophozoites remain adhered to intestinal
epithelium by means of the sucking disc
causing stunting and shortening of the villi

• Giardia Infection can result in

– asymptomatic condition (50% of infected
people)
– or symptomatic disease ranging from mild
diarrhea to severe malabsorption syndrome.
• Incubation period is 1-4 weeks
• Intestinal infestation in children
• Diarrhea or loose, fowl-smelling stools
• Stools are pale, bulky with no blood or
mucus
• Steatorrhea (fatty stool)
• Abdominal cramp
• Excessive flatulence, vomiting, loss of
appetite, weight loss, etc.
 Diagnosis
Microscopy
• Stool is the preferred specimen
– Formed stools contain oval cysts but diarrheal
specimen may contain both cysts and
trophozoites

• Stools can be examined by either Wet

method or concentrated method

Molecular diagnosis
• PCR on stool specimen
 Wet mount method

– Take 1gm of stool

– Emulsified with physiological saline (0.9%)
– Put a drop on a slide
– Cover with coverslip
– Examine under X10 objective
– Confirm with X40.
– A typical "falling leaf" movement indicates the
presence of the trophozoite
Concentration method
 Prevention and control
• Giardiasis occurs mainly in areas where
sanitation is poor;
– Therefore good personal and group hygiene
must be observed
– Proper environmental hygiene such as
provision of KVIP toilets
– Proper disposal of human excreta to prevent
contamination of soil, water and food by the
cyst
– Avoidance of oral-anal sex
• In endemic areas,
– Drinking water from streams and lakes must
be properly boiled before drinking
• (cyst can survive in water for 2-3 months).
– Filtration of water can also eliminate the
organism
– Fruits and vegetables must be properly
washed before eating
 Dientamoeba fragilis
• Initially classified as ameba
• But others think, it is flagellate
• Has only trophozoite
 Morphology
• Oval in shape
• Trophozoite is 5-12µm
• Has 1 or 2 nuclei
 Life cycle
• Mode of transmission is not clear
• But believed to be through fecal-oral
route.
• May be carried by eggs of Enterobius
vermicularis??
 Clinical manifestation
• Most infected people remain
asymptomatic
• It is mildly symptomatic in about 25% of
infected individuals
• Symptoms such as
– abdominal discomfort
– intermittent diarrhea
– flatulence
– weight loss
 Diagnosis
• Presence of trophozoites in the stool
– Eg. wet method
 Control and prevention
• Reservoir for the parasite and its life cycle
are not known
– So specific recommendations are difficult
• However,
– Maintenance of good and adequate sanitary
conditions will help
 Chilomastix mesnili
• It is non-pathogenic
• An intestinal commensal protozoa of
human
• Its diagnosis is normally confused with
Trichomonas. It can however be
differentiated by its spiral motion
 Morphology
• Exists in both trophozoites and cyst forms
• Exists as lemon-shaped in the cyst form
– About 5-7µm long
– Has 1 nucleus
– Has 3 flagellae at the anterior end
– Has large anterior cytostome
– Sharply pointed at the posterior end
• Acquired through contaminated drinking
water or food
• Occurs normally in the colon
• Non-pathogenic
 Trichomonads
• There are 3 forms of Trichomonads:
– Trichomonas vaginalis
– T. hominis
– T. tenax
• Only T. vaginalis is pathogenic
– Found in cervix , vagina urethra and urinary
bladder of female
– And urethra and prostrate glands of male
 Trichomonas tenax
• Occurs in human oral cavity
– In tartar, cavities and gingival margins
• Associated with poor oral hygiene
• Can be transferred through
– Oral droplets
– kissing or
– fomites such as eating utensils
• It is non-pathogenic
 Trichomonas hominis
• Inhabits the intestinal tract around the
cecum
• Non-pathogenic
 Flagellates of urogenital tract
Trichomonas vaginalis

• It is distributed worldwide
• Causes urogenital infections
• It is estimated that 180 million women worldwide
acquire this disease annually
• 25% of sexually active female become infected
sometime in their life
• Sexually active males are also parasitized at
least transiently
 Morphology

• Exists only as trophozoite

– Found in the cervix, vagina, urethra and
urinary bladder vaginas of female
– Urethra and prostrate glands of male
– Pear-shaped
– 25 µm in length with 4 anterior flagella
– A short undulating membrane
Trichomonas vaginalis
 Life cycle
• By sexual intercourse
T. vaginalis
 Pathogenesis
• Trichomonas vaginalis infects the vagina
and secretes cysteine, proteases, lactic
acid and acetic acid
• which disrupt the glycogen levels and lower the pH
of the vaginal fluid

• Trophozoite does not invade the vaginal

mucosa
• The infection can range from mild irritation
to severe inflammation
 Clinical manifestation
• Transmitted by sexual intercourse
• Sometimes transmitted by fomites such as
– towels,
– toilet seats, etc
• Infection rate is about 5-20% in women
and less than 5% in men
 Clinical manifestation
• In females, it starts with;
– Greenish, yellow, frothy vaginal discharge
– Dysuria (painful urination)
– Abdominal pain

• There may be erosion of epithelial lining of the

vagina which is associated with
– Itching
– Burning sensation
– Dyspareunia ( painful sexual intercourse )

• Vulvar and cervical lesions

• Associated with adverse pregnancy
outcomes, including;
– premature rupture of membranes
– pre-term labor,
– pelvic inflammatory disease,
– increased risk for HIV infection
• Most men with trichomoniasis generally
have no symptoms
– but can infect their sexual partners
– May cause up to 11%-13% of nongonococcal
urethritis (NGU)
– Occasionally, epididymitis, and prostatitis can
occur

• 10% of infected males have thin, white

urethral discharge
 Diagnosis
Microscopic examination
• A fresh specimen of vaginal or urethral secretion
is mixed with physiological saline solution and
examined under microscope
• In males secretions from the end of the penis
should be obtained in the morning before
urination
– The presence of globular-shaped trophozoite with
jerky and wavelike motility indicates presence of T.
vaginalis
• Direct microscopic examination of smears
– From vaginal discharge
– Or smears from high vaginal swab (HVS)

• Fixed smears can be stained with acridine

orange or Giemsa stains

• Direct fluorescent antibody (DFA) is another

method of parasite detection
Culture
• Culture of clinical specimens diamond‘s
medium or knuferberg‘s medium is
recommended

Molecular diagnosis
• PCR on clinical specimens
Giemsa stain- X40
 Control and prevention
• Simple ABC
– Avoid sexual intercourse
– Be faithful to your partner
– Condom use
• Treatment of sexual partner
• Patients should be advised to abstain from
sexual intercourse until they and their partners
have completed treatment and follow-up
 Giard/a Jamb/la
- - - -\ - INTESTINAL
Trypanosoma pp.
BLOOD -)-..- - - -

Trichomonas tenax
ORAL FLAGEL S

Lelshmanla spp
TrJchomonas vaglnal TISSUE
/s
- - - - ---1- GENITAL
 Hemoflagellates (Blood flagellates)
• Called hemoflagellates because
– the organisms require hematin obtained from blood hemoglobin
for respiration
• Family Trypanosomatidae has 2 genera:
– Trypanosoma
– Leishmania

– The major difference between the 2 genera is that the primary

diagnostic form found in Leishmania is amastigote whereas that
of Trypanosoma is the trypomastigote

• Their life cycle involves 2 hosts:

– an insect and
– a vertebrate
 Trypanosomes
• Trypanosome causes 2 distinctly different
forms of disease
– African trypanosomiasis (sleeping sickness)

– American trypanosomiasis (Chagas disease)

 African trypanosomiasis
• Caused by
– Trypanosoma brucei gambiense
– And Trypanosoma brucei rhodesiense

• Both are transmitted by tsetse fly (Glossina)

• Gambian sleeping sickness occurs in Central

and West Africa (accounts for 97% of reported cases
of sleeping sickness)

• Rhodesian sleeping sickness occurs in Eastern

part of Africa
Tsetsefly-Glossina
Species of tsetse fly (Glossina)
• T. b. gambiense is transmitted by
– Glossina palpili
– Glossina tachinoides
– Glossina fuscipes
The flies breed in shaded areas along stream
banks
• T.b. rhodesiense is transmitted by
– Glossina pallidipes
– Glossina morsitans
 African trypanosomiasis
• Man is the reservoir for Gambian sleeping
sickness

• Wild and domestic animals such as

antelope, deer, cattle, etc. are reservoirs
for Rhodesian sleeping sickness
 American trypanosomiasis
• Caused by Trypanosoma cruzi

• Transmitted by the true bugs (triatomids

and reduviids)

• Found in South, Central and Latin America

Triatomids
 Morphology
• Both species cannot be distinguished morphologically

– Have elongated bodies shaped like 'C' or 'S'.

– Single flagellum arises from the kinetoplast (part of

mitochondrion) and extends forward along the outer margin of
the undulating membrane

– Small dot-like parabasal body of the Kinetoplast stains darkly

• Has a centrally placed nucleus which stains
dark-mauve (Blue)

• Has cytoplasm which stains palely and contains

granules
 Life cycle
• The life cycle is the same for both spp but
different intermediate hosts or vectors are
involved
 Life cycle
• The tsetse fly takes bloodstream trypomastigote from an
infected person or reservoir host in the blood

• The bloodstream trypomastigote transforms into procyclic

trypomastigote then migrates to the mid-gut of the fly where
they multiply by binary fission

• In about 2 weeks time, the procyclic trypomastigotes

transform into epimastigote and migrate to the salivary gland
of the fly

• The epimastigote transform into infective metacyclic

trypomastigote and moves to the proboscis of the fly
 Life cycle
• When the fly bites another person, it injects metacyclic
trypomastigote into the new person

• At the site of the bite, a lesion called trypanosomal

chancre develops

• The Trypanosoma then multiplies by binary fission at this

site and enter the blood, lymph nodes, and the central
nervous system
Life cycle of Trypanosoma brucei
 Pathogenesis and
Clinical manifestations
• An initial chancre is formed at the site of bite
– characterized by a localized tender reddish swelling

• After a period of multiplication, the Trypanosoma enter general

circulation through the lymphatics
• Macroglobulinemia microvascular damage, coagulopathy, and
perivascular inflammation. Fever and headache then appear
– Repeated antigen-antibody cycle

• The acute stage will last for about 1 month or 1 year depending on the
spp

• T. b. rhodesiense usually cause acute systemic disease

• Any lymph node may be infected but those
of the posterior cervical regions are most
involved

• Enlargement of these nodes is known as

Winterbottom's sign
• In chronic stage,
– Trypomastigotes may spread into the CNS
– This may be followed by mental retardation, tremors,
meningoencephalitis, and character changes may
occur
– Results in sleeping sickness

• T. b. gambiense usually causes chronic disease

 • In the final stage, the patient becomes somnolent, the
nervous system retards and eventually goes into coma
and die

• The incubation period for T.b. rhodesiense is between

3-21 days and T.b. gambiense is 1 year.
• T.b. gambiense does not cause epidemic
• but T.b. rhodesiense causes epidemic

• It is difficult to control T.b. rhodesiense

• because some domestic animals (cattle, sheep)
• and wild game animals act as reservoir hosts
 Life cycle of T.cruzi
• When the ruduviid bug vector defecates infective
trypomastigotes near the site of its blood meal

• The presence of the bite produces an itching sensation

in the host. As the host scratches the bite area
typomastigotes gain entry into the host by being rubbed
into the wound

• Following entry into the wound the trypomastigote invade

surrounding cells where they transform into amastigotes

• The amastigotes then multiply and destroy host cells

(such as heart muscles, liver, brain etc.) and convert
back to trypomastigotes
• The trypomastigotes are transmitted back to the
reduviid bug when it takes another blood meal

• Upon ingestion, trypomastigote transform into

epimastigotes in the midgut. Multiplication of the
epimastigotes produces thousand of additional
parasites that convert back into trypomastigote
when they reach the hindgut

• The trypomastigotes are then passed with the

feces when the bug defecates near the site of its
next blood meal and thus the cycle begins again
Life cycle of Trypanosoma cruzi
 Pathogenesis and Clinical
Manifestation
• Acute form
• Redness at the skin infection site (chagoma)
– High fever, Swollen face, marked edema of the eyelids
(Romana’s sign) and keratitis

• Lasts for 20-30 days

• Lymphadenopathy, hepatosplenomegaly,
myocarditis
• Incubation period is one week
 The chronic form
• Symptoms are associated with damage sustained during
the acute phase
• Chronic abdominal pain, chronic constipation
• When motor sensors are destroyed
– Paraplegia (impairment of motor sensory function)
– Diplegia (paralysis of the lower extremities) and
– Spastic paralysis (muscular weakness caused by damage of
brain)

• Cardiomyopathy may be a complication

– Palpitations, dizziness, pericardial discomfort
– Stroke, sudden death
 Laboratory diagnosis
Microscopic examination
– Direct detection of trypanosomes in the blood,
lymph node aspirate and in cerebrospinal fluid
– Can be fixed and stained with Giemsa thin preparation
and in thick blood films

Serodiagnosis
– Specific antibodies or antigens can be
detected in serum and CSF
Molecular diagnosis
– PCR on clinical specimens
 Prevention and control of
trypanosomiasis
• Control of the breeding sites of the tsetse fly by clearing
bushes around homes

• People going to endemic areas should wear protective

clothing, use bed nets and insect repellants

• Use of insecticide to spray infected areas (fly belts)

• Treatment of human cases to reduce transmission

Other Blood and Tissue
dwelling flagellate
 Leishmania

• Leishmania are intracellular parasites of

both blood and tissues

• Present as
– amastigotes in humans and other vertebrates

– and as promastigotes in the intestine of sand fly

 Leishmania
• Zoonotic infection affecting 12million people worldwide in 88
countries

• 3-4% Reported cases in the Ho municipality

• 12-32% suspected cases in the Ho municipality (Kweku et

al.,2011)
• There are 4 main spp of Leishmania of
medical importance
– Leishmania tropica
– Leishmania braziliense
– Leishmania mexicana
– Leishmania donovani
 Vector
• They are all transmitted by
– Sand fly (genera Phlebotomus or Lutzomyia)
 Morphology of Leishmania
• Amastigotes
– Small, round-oval bodies (2-4µm) depending on the
species
– Can be seen in groups inside macrophages or lying
freely between cells
– Nucleus and kinetoplast stain dark reddish mauve
– Cytoplasm stains palely

• The morphology of amastigotes are the same for

all the Leishmania
 Leishmania tropica
• Causes cutaneous leishmaniasis or
Oriental sore
• Occurs in the old world
– Africa, Asia, and the Middle East
• The vector is Phlebotumus sandfly
• Reservoir hosts are
– Dogs, foxes, and rodents
• Other species which cause cutaneous
leishmaniasis or oriental sore are
– L. aethiopica
– L. major
– L. infantum (minor), etc

• L. mexicana also causes cutaneous (bay

sore and chiclero ulcer) in the new old
 Life cycle
• All the 4 have the same life cycle
• Promastigote is the infective stage
• Promastigote is present in the saliva of the
sandfly
• When an infected sandfly bites a human
being, it injects the promastigote into the
skin
• The promastigotes lose the flagella to
become amastigotes
• The amastigotes are then picked up by
macrophages and other reticuloendothelial cells

• The amastigotes then multiply leading to the

rapture of cells and tissues

• These lead to destruction of visceral organs

such as liver and lungs

• When the sandfly bites an infected person, it

picks up the amastigotes, which transform into
promastigote stage
• The promastigotes again multiply by
binary fission in the midgut of the sandfly

• They then migrate to the proboscis of the

sandfly

• A new person can be infected by this

infected sandfly
Life Cycle of Leishmania
 Clinical manifestations
• The incubation period is 2-8 weeks
• A red papule appears at the site of the bite
• It becomes itchy
• The papule enlarges and ulcerates
• The ulcer becomes hard, crusted, and
exudes serous materials
• Lesions may heal in a few months but
leave disfiguring scars
 Lab diagnosis
• Microscopic examination
– Demonstration of amastigotes in blood smears and tissue
aspirates (bone marrow, spleen, lymph nodes) is the gold
standard for diagnosis.
– Smears from the ulcer biopsy specimen
• Fixed smears can be stained with Giemsa to demonstrate amastigotes

• Culture
– Tissue specimens or blood are cultured in NNN medium.
– Animal inoculation
– Serodiagnosis
• Molecular diagnosis
– PCR on clinical specimens
• Skin test
– Leishmanin skin test (Montenegro test)
 Serological test
• ELISA- Enzyme-linked immunosorbent
assay
• to detect either
– antibodies to the parasite or
– the antigen of the parasite
.,
 L. braziliensis
• Causes mucocutaneous leishmaniasis
(Chiclero ulcer)
• Occurs in the new world (Central and
South America)
• Common among workers working in chicle
sap farms –used for making chewing gum
• The vector is Lutzomyia sandfly
• Reservoir hosts are dogs
 Clinical manifestations
• Incubation period is 2-8 weeks for the papules
to appear
• There is metastatic spread of promastigotes
from the site of the bite via the lymphatics which
involves the nose, pharynx, palate and lips
• Destruction of mucus and membranes and
related tissue structures
• Invasion of the pharynx may result in loss of
speech
• Severe disfiguring and facial mutilation
 L. donovani
• Causes visceral leishmaniasis or kala-azar
• It affects the internal organs such as liver,
lungs, intestine, etc
• Occurs in Africa, Asia, South and Central
America
• The vector is Phlebotomus sandfly
• Reservoir host: dogs, foxes, porcupines,
etc.
 Clinical manifestations
• Incubation period is several weeks-1 year

• First, the patients experience fever, diarrhea,

anemia

• Intermittent chills and sweating like malaria may

follow
• As the organism multiplies, they invade the cells
of the liver and spleen.
• These organs become enlarged

• Weight loss and emaciation may occur

• Advanced stages result in kidney damage and

granulomatous areas of skin

• The skin may become darkened and is referred to as

"kala-azar" meaning black fever

• Chronic cases usually lead to death in 1-2 years if not

treated
 Lab diagnosis
• Amastigote stage can be observed in
tissue biopsy, bone marrow and lymph
node aspirates
– Make smears from the aspirates
– Stained with Giemsa and observed under oil
immersion
• Promastigote stage can be seen in blood,
bone marrow and tissue culture
 Prevention and control
• Protection from sandfly bites through
– The use of screening, protective clothing and
repellents
– The use of bed nets impregnated with
insecticide
– Netting of windows and doors

• All infected people should be treated

promptly and the ulcers eradicated to
reduce transmission
 Treatment
• Treatment of mucocutaneous leishmaniasis is
usually ineffective
• Secondary bacterial infections are treated with
antibiotics
• In visceral leishmaniasis:
– Pentavalent antimonials compound given intravenously
or intramuscularly. Sodium stibogluconate (20 mg/kg
daily for 28 days) and meglumine antimoniate are the
drugs of choice.
• Amphotericin B
• Paromomycin
• Miltefosine
 Amoebae
• Amoebae are unicellular organisms common in the
environment
• Many are parasitic in vertebrates and invertebrates
• The following species of amoeba are found in/on
humans:
1. Entamoeba histolytica
2. Entamoeba dispar
3. Entamoeba coli
4. Entamoeba hartmanni
5. Entamoeba gingivalis
6. Endolimax nana
7. Iodamoeba buetsschlii
8. Dientamoeba fragillis
 Worldwide incidence
• Has cosmopolitan distribution but more commonly in the
tropics and subtropics

• World prevalence is about 0.2-50%

• Estimated that 10% of world's population may be infected

• 50 million cases of invasive amoebiasis/year

• 100 000 deaths/year

 Entamoeba histolytica
(tissue destroying)
• No animal reservoir is known

• Facultative pathogens

• Most people clear the infection spontaneously in

6-12 months with mild or no symptoms

• Can cause serious invasive diseases such as

ulcers on the skin and abscesses in the liver,
lungs, spleen and the brain
 Morphology
• E. histolytica exists in 2 forms

– Trophozoite stage

– Cyst stage
 Trophozoite
• This is the actively motile feeding stage
• The organism is oval at the anterior end and
pointed at the posterior end
• They are amoeboid in shape and are constantly
changing
• Has 1 nucleus in the cytoplasm and has chromatin
dot
• Ingested red blood cells may be found in the
cytoplasm of the trophozoite
– indicating the amoebic trophozoites are pathogenic
• Trophozoites form directional pseudopodia
(false feet) and move in one direction in fresh
warm specimen

• The amoebic trophozoites remain actively

motile as long as the environment is favourable,
and the cyst forms when the environmental
temperature or moisture drops

• Trophozoites live in the mucosa and

submucosa of the human large intestine
 Cyst
• The cyst is the dormant, resistant and the
infective stage

• It is round or oval, measuring 10-15 µm

• The immature cyst has 1 or 2 nuclei and

chromatoid bars in the cytoplasm

• The mature cyst has a cyst wall and 4 nuclei.

The nuclei stain brown with iodine preparation
 Life cycle
• The life cycle of amoebae does not involve intermediate
hosts or non-human reservoirs

• After ingestion of the cyst in contaminated food or water,

the cyst passes through the stomach where exposure to
gastric acid in the stomach stimulates the release of the
pathogenic trophozoites in the duodenum

• The trophozoites are carried to the colon where they

mature and reproduce by binary fission

• The trophozoites may lead a commensal life in the crypt

of the colon mucosa

• They may also cause ulceration of the large intestine

• Under desiccation in the colonic region,
the trophozoites encyst and passed out in
the feces

• The cyst is the infective stage and can

survive for several weeks in the
environment
Life cycle of
Entamoeba histolytica
• Successful colonization depends on a
number of factors including

– the size of inoculum ingested

– intestinal motility
– presence of specific intestinal flora
– the host's diet
 Pathogenicity/Clinical
manifestations
• Most people infected with E. histolytica
remains asymptomatic
– However a few people develop clinical
symptoms

• E. histolytica has 3 forms of clinical

manifestation:
– 1. Intestinal
– 2. Extraintestinal
– 3. Cutaneous
 1. Intestinal amoebiasis
• Most people infected with E. histolytica remains
asymptomatic carriers

• However, a few people develop intestinal

amoebiasis

• Only the cyst stage is infectious

• The trophozoite stage dies out readily once passed

out of the body

• The trophozoite will be killed by stomach acids if

ingested
• In the intestine, the trophozoites of the virulent
E.h. are capable of penetrating intact intestinal
mucosa
– by releasing an enzyme that lyses the tissues, hence
their name histolytica (tissue-histo and dissolving-
lysis)

– The histolytic enzyme allows the amoebae to

penetrate into the intestinal mucosa, where
subsurface lesions develop

– These lesions may coalesce into extensive ulcerative

areas, thus leading to severe dysentery with stools
containing bloody mucus
• Clinical presentation of the intestinal infections
depends on degree of ulceration and mucosal
damage

• When ulcerations are small and infrequent,

symptoms may be absent.

• As the involved area of mucosa increases in

size, primary diarrhea with cramping pain occurs
 Symptoms
– Abdominal pains
– Cramping
– Colitis with diarrhea may occur

• In advanced stage
– Numerous bloody stools may be passed in a day
– Vomiting, weakness, and dehydration may also occur

• The stool is usually fowl smelling or fishy

smelling with blood, and/or pus and mucus

• Mortality is high if not treated

2. Extra-intestinal amoebiasis
• In a small percentage of cases, the pathogenic
amoeba or the trophozoite can enter the
bloodstream and be disseminated to various
internal organs

• In such cases, abscesses usually occur in

– the liver
– heart
– brain
– lungs
– or any other organ
 Amoebic pulmonary abscess
• Symptoms
– Fever
– Cough
– Dyspnea (short of breath)
– Pain
• Sudden pain
– Like peptic ulcer (ruptured abscess)
– Vomiting
 3. Cutaneous amoebiasis
• Amoebiasis of the skin occurs when damaged skin
comes in contact with amoeboid trophozoites eg.
– when amoebic liver abscess drains through the
skin as a result of
• spontaneous rupture of the liver abscess
• or through surgical drainage of amoebic liver
abscess
• If not treated, perianal ulcers may occur

• Urogenital ulcers could also occur

– The vagina and the labia could be infected

– Men then become infected with penile

amebiasis after experiencing unprotected sex
with a woman who has vaginal amebiasis

– The penis could be affected, especially

among homosexuals during anal intercourse
 Diagnosis
Intestinal
• Stool examination
– Cysts and trophozoites
• Sigmoidoscopy for mucosal scrapings
– Direct wet mount and iron haematoxylin staining to
demonstrate trophozoites

• Sigmoidoscopy
– Lesions, aspirates, biopsy
• Serodiagnosis
– Serological test is positive only in invasive amoebiasis
• Molecular diagnosis
 Diagnosis
Extraintestinal diagnosis
Microscopic examination
– Demonstration of trophozoites in pus aspirated from
the wall of liver abscess.
• Molecular diagnosis
– PCR of pus aspirated from ALA
• Serodiagnosis
– helpful in diagnosing disseminated amebiasis
•Imaging (ultrasound, X-rays)
– Look for a pleural effusion, and elevation of the right dome of his
diaphragm (80%).
•Abscess aspiration
– Only selected cases
 Microscopy-stool
• Specific diagnosis is made by observing the
trophozoite or cyst of amoeba in the feces
– Take about 1gm of the stool
– emulsified with physiological saline
– put a drop on a slide
– add 1 drop of iodine solution
– cover with coverslip and
– examine under X10
– trophozites are seen with movement and ingested
RBCs
 Prevention and control
• E. histolytica occurs mainly in the tropics and subtropics
where sanitation is very poor

• Human infection results from

– The ingestion of the cyst through hand-to-mouth contamination
and food and water contaminated with human excreta
– E. histolytica may be transferred through unprotected sex
– Flies and cockroaches may also serve as vectors by depositing
infective cysts on unprotected food
– Improper treatment of water supplies is another source of
possible infection
Control methods include
• Avoid fecal-oral route
– Good personal hygiene must be observed
– Proper disposal of human excreta
– Eating of cold food such as salad should be
avoided in endemic areas
– Where there is no potable water, the water
should be filtered or boiled
– Adequate sanitation such as construction of
KVIP and provision of good drinking water
must be pursued by public health authorities
 Non-pathogenic amoebae
1. Entamoeba coli
2. Entamoeba hartmanni
3. Entamoeba gingivalis
4. Endolimax nana
5. Iodamoeba buetsschlii
6. Dientamoeba fragillis

– All these are non-pathogenic

– Their presence is an indication of contamination
with fecal matter
CILIATES
 Ciliate protozoan
• Balantidium coli, is the only ciliate in this group
• It is the largest intestinal pathogen of man
• It causes the disease called balantidiasis
• Common in areas where pigs are reared as
scavengers
• Pigs are the reservoir host
– but it affects monkeys, and man
• It is very common in areas where personal and
group hygiene are poor, eg. mental homes,
prisons, etc.
 Morphology
• The organism exists in 2 forms:
– Trophozoite stage
– Cyst stage
 Trophozoite
• The trophozoites are
– Broadly rounded at the posterior end and conical shaped at the
anterior end
– It is about 50-200µm
– At one end of the organism there is a funnel-like structure called
peristome

• Has 2 nuclei:
– a big one shaped like the kidney called macronucleus
– and a smaller one called micronucleus which is close to the
bigger one

• The organism is covered with numerous cilia

• It has food and contractile vacuoles

 Cyst
• The cysts are round (40-60µm in diameter)
• Has a cyst wall
• Has macro- and micronucleus
• Has no food vacuole
 _._,- •I "•- ■- ■ I ■ ..., ., I

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IPe
Cytosto e
Cyst w

Mtoronuc eus
crooucleus
Pellicle

!Food vacuore _
Contracti e
1

vacuole
 Life cycle
• Human acquires the infection by ingestion of
food or water contaminated with mature cyst

• The cysts are released upon digestion

• Excystation occurs in the small intestine

• The trophozoites invade the mucosal lining of

the large intestine, cecum and terminal ileum

• The actively motile trophozoites undergo

asexual reproduction to produce more
trophozoites.
• The trophozoites use the cilia for motility

• When conditions become unfavourable, the trophozoites

empty their food vacuoles and secrete a cyst wall around
them to become cysts

• The cysts are then passed out in the feces into the
environment

• The cysts may survive several weeks in the environment

and will continue the cycle when ingested through
contaminated food or water
 .- "/
. . {. ..
• :I

.,
Balantidium coli ·THIN l 62·
• •

I
 Clinical manifestations
• Asymptomatic condition can occur

• Symptomatic disease includes:

– Abdominal pain
– tenesmus (inability or difficulty to empty the bowel at
defecation)
– Nausea
– Watery stools with blood and pus
– Ulceration of the intestinal mucosa can occur

• The symptoms are like those of amoebiasis

except
– the lack of extra-intestinal invasion of other organs.
 Laboratory diagnosis
• Microscopic examination of feces for trophozoites
and cysts

• Trophozoites are usually seen in bloody mucoid

diarrhea and cysts are found in formed stool

• A loop full of specimen including the bloody

mucoid stool is taken
– emulsified with saline
– transferred onto the slide
– a drop of iodine is added
– cover with cover slip.
– Examine under X10 and confirm with X40 magnification
 Control and prevention
• Similar to those of amoebiasis.
– Good personal hygiene must be observed
– Proper sanitary disposal of human excreta
– Eating of cold food such as salad should be avoided
in endemic areas.
– Where there is no potable water, bottled water should
be taken, or the water should be filtered or boiled.
– Adequate sanitation such as construction of KVIP and
provision of good drinking water must be pursue by
public health authorities
– Avoid eating unwashed fruits and cold salad
 Treatment
• Medications normally used are;
– Tetracycline
– Metronidazole
– Iodoquinol
Intestinal and Tissue Coccidian
parasites
 Intestinal and tissue Coccidian
parasites (Sporozoa)
• Coccidians belong to the
– Phylum-Apicomplexa
– Subclass- Sporozoa

• There are 4 main genera of intestinal and tissue Coccidia

which affect man
– Cryptosporidium
– Isospora
– Sarcocystis (The 3 species that can infect humans
• Sarcocystis hominis (transmitted through cattle),
• Sarcocystis suihominis (transmitted through pig) and
• Sarcocystis lindemanni (unknown mode of transmission).

– Toxoplasma
• The taxonomic position of Pneumocystis is
equivocal
– Some authors think it belongs to the yeast
and others think, it is a sporozoan

• They typically have asexual and sexual

reproduction in their life cycle
 Isosporiasis/
cystoisosporiasis
• It is a human intestinal disease caused by
the parasite Isospora belli

• It is found worldwide especially in the

tropical and subtropical areas

• Infection often occurs in immuno-

compromised individuals eg AIDS patients
and outbreaks have been reported in united
states
• Coccidian parasites have male gametocyte
(microgametocytes) and female gametocytes
(macrogametocytes)

• The female gametocytes produce single

macrogametes whilst the male gametocytes
produce multiple microgametes

• After fertilization of the female macrogamete by

the male microgamete, a zygote is formed

• The zygote develops into an oocyst

• The oocyst is the infective stage

• The oocyst of the Isospora species and
Sarcocystis hominis develop 2 sporocysts
and each contains 4 sporozoites

• In Cryptosporidium, the sporocyst stage is

absent
Sarcocystis Spp
and
Isospora belli
 Morphology
• S. homonis and I. belli have oocyst

• The oocyst is oval, measuring about 32 X 16μm

• Has a thick cyst wall

• Usually contain a central undivided mass of protoplasm

(zygote)

• The oocyst of the S. hominis and I. belli are similar except

that the oocyst of the S. hominis is half the size of I. belli.

• Oocyts of S. homonis is very delicate and sometimes the

cyst wall may rupture
– As a result, sporocysts of the S. hominis are found in stool
specimen
– Sometimes, immature oocysts are passed in the stool
 Life cycle of I. belli
• Sarcocystis and I. belli have almost similar cycle

• The life cycle of both involve sexual and asexual stage in man

• Man is infected with I. belli by ingesting infective oocyst in

contaminated food, water, fruits and unwashed vegetables

• After ingestion of the oocyst there is excystation in the intestine to

release sporozoites which invades epithelial cells and develop into
trophozoites

• The trophozoites undergo asexual reproduction to produce

merozoites which invade new intestinal cells
• Some of the merozoites instead of undergoing more
asexual reproduction develop into male and female
gametocytes

• The male gametocyte fertilizes the female gametocyte to

produce fertilized immature oocysts containing the
zygote (sporoblast)

• This is then passed out into the environment

• The immature oocysts with sporoblasts develop into

mature oocysts with sporozoites which can infect
another person
Life cycle of I. belli
 Life cycle of Sarcocystis
Humans

• Sarcocystis is acquired by eating raw or undercooked

meat containing these sarcocysts.

• After ingestion of the oocyst, bradyzoites are released

from ruptured cyst in the small intestines and they invade
the lamina propria of the intestinal epithelium
• They then differentiate into macro and microgametocytes
they fuse and form oocyst
• Oocysts sporolates in the intestinal epithelium and are
shed from hosts in feces
• Due to the fragile nature of the oocyst wall individual
sporocysts may also be detected in feces
 Life cycle of Sarcocystis
Intermediate host

• Sporocysts ingested by intermediate host (cattle for S. hominis and

pigs for S. suihominis) are excysted in the intestine to release
sporozoites

• These sporozoites invade endothelial cells of the blood vessel and

undergo schizogony resulting in first generation schizonts
(merozoites)

• Merozoites derived from first generation invade small capillaries and

blood vessels becoming second generation schizonts

• The second generation merozoites invade muscle cells and develop

into sarcocysts containing bradyzoites which are the infective stage of
the definitive host

• When human eats raw or undercooked meat, he gets the infection

and the cycle continues
Life Cycle

..
'
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 Pathogenesis and clinical
manifestations
• Infected individuals may be asymptomatic carriers

• Or may experience mild to severe gastrointestinal

disease which resembles that of giardiasis

• The symptoms include low grade fever, abdominal

cramp, nausea, chills, chronic diarrhea, weight loss,
malaise, etc

• These symptoms may be mild and transient lasting for

less than a month or may be severe and chronic
• Isospora infection is predominantly an
infection of people in developing world

• Can be a common presentation of

immunocompromised patients such as
those with HIV/AIDS
 Diagnosis
Stool specimen for diagnosis
• Formalin-ether concentration method is used
• All stages of Isospora, from immature oocysts to
fully developed sporozoites may be found in the
stool
• Unless stained with iodine the oocysts and its
contents are transparent and difficult to recognize

• Molecular diagnosis
• PCR of the stool sample
 Prevention and control
• Improvement in sanitary and hygienic conditions, by
providing enough public toilets

• Efficient disposal of human excreta

• Boiling of untreated water before drinking

• Washing fresh fruits and vegetables before eating

• Meat, eg. pork, beef, etc, should be well cooked before

eating

• All infected persons should be treated

 Treatment
• Isospora belli
• Infection is self-limiting, hence, no treatment is indicated in
immunocompetent persons.
• Immunosuppressed patients with diarrhoea are treated with co-
trimoxazole (160 mg trimethoprim/800 mg sulfamethoxazole
orally or i.v. 4 times/day for 10 days).
• Relapses can occur in persons with AIDS and co-trimoxazole is
given for maintenance therapy

• Sarcocystis
• No specific treatment is available for sarcocystosis. For
myositis, albendazole, metronidazole
• and co-trimoxazole have been used. Corticosteroids have been
used for
• symptomatic relief
Cryptosporidium parvum
 Cryptosporidium parvum
• Cryptosporidial species are distributed worldwide

• Infection is found in mammals, reptiles, and fish

• The life cycle of Cryptosporidium parvum is typical of

coccidians

• The life cycle is similar to I. belli

– except that the sporocyst stage is absent

• In cryptosporodiasis, large numbers of oocysts are

passed in the stool
 Morphology
• The oocysts are small and round (5µm) which
stains pink-red

• Within the oocysts, are 4 sporozoites

• No sporocyst in C. parvum

• May look like yeast cells

– But yeast and fecal debris often stain dull red and
can be distinguished from the oocysts
 Mode of transmission
• Waterborne transmission:
– Cryptosporidium is resistant to the usual water-
purification methods, eg. chlorination, etc.
– Runoff of local waste water and surface water into
municipal water supplies is an important source of
contamination
• Zoonotic spread from animal reservoirs to
humans
• Fecal-oral-route
Pathogenesis/clinical manifestations
• Like all protozoan infections, it can be asymptomatic

• Disease in healthy people can be mild, self-limiting

– enterocolitis characterized by watery diarrhea, without blood

• Spontaneous remission after 10 days is typical

• Contrary, disease in immunocompromised patients like

AIDS patients can be very chronic characterized by 50 or
more stools per day and tremendous fluid loss
– This can last for months to years
 Control and prevention
• Same as for amoebiasis and giardiasis.
 Tissue coccidian parasites
(Toxoplasma gondii)
• Toxoplasma gondii causes toxoplasmosis

• Toxoplasma gondii is an obligate intracellular

parasite that inhabits all types of nucleated cells
including brain, eyes, skeletal and cardiac muscles

• Both asexual and sexual stages take place in the

domestic cat and other members of the cat family
– but only asexual cycle occurs in other carnivorous and
omnivorous mammals including man and birds.
– Cats are the definitive host
 Morphology
• The major morphological forms of the parasites are
– oocyst
– tachyzoite
– Tissue cyst

• Oocyst:
– oocysts are oval with thick cyst wall
– Inside the oocyst are 2 sporocyts and
– inside each sporocyst are 4 sporozoites

• Tachyzoites- rapidly multiplying form- are seen during acute

stage of the disease
• Bradyzoites-slow developing form- are seen at the chronic
stage
 Mode of transmission
• There are 3 modes of transmission
1. By direct ingestion of the mature oocyst in food or
water contaminated with an infected cat feces.
2. By eating undercooked or raw meat eg. beef, cat, rat
meat, etc, infested with the tissue oocyst (tachyzoite
or bradyzoite).
3. By Congenital infection: transmitted from an infected
mother to the fetus during pregnancy.
– This has a devastating effect on the fetus (eg.
blindness).
 Life cycle
• The sexual and asexual cycles occur in the domestic cat
and other members of the cat family

• Cats acquire the infection by ingesting oocyst from food or

water contaminated with cat feces or tissue cyst in meat,
pork, rat, mouse

• After the ingestion of the cysts by the cat, the cyst wall is
dissolved by the proteolytic enzymes in the stomach and
the small intestine

• The released sporozoites from oocyst and bradyzoites

from tissue cysts enter the intestinal mucosa and multiply
asexually to form tachyzoites.
• The released tachyzoites may enter the resting stage,
the tissue cyst

• Cysts are formed most commonly in the brain, liver and

muscles

• A cyst may contain hundreds of bradyzoites

• Cysts usually cause no host reaction and may remain for

a long period in the host.
 Sexual stage
• The zoites released in the small intestine undergo asexual
multiplication (schizogony) leading to formation of merozoites. Some
merozoites are carried to extra intestinal tissues or organs and form
tissue cysts.

• Some merozoites transform into male and female gametocytes and

initiate sexual cycle (gametogony) with the formation of microgamete
and macrogamete.

• After the male gamete fertilizes the female gametes, a zygote is

formed

• It secretes a cyst wall around itself and becomes an oocyst

• It matures and contain 2 sporocysts,

• Each sporocyst contains 4 sporozoites which are
then passed out in the feces of the cat to the
environment.

• The sporulated cysts can survive in soil for

months

• The asexual reproduction in man is the same as

that in cat but sexual stages do not occur in
humans, mice or other non-feline hosts
Life cycle of Toxoplasma gondii
 Clinical manifestation
• The incubation period is 1-3 weeks

• The acquired infection is usually asymptomatic

• Symptoms of acute disease include chills, fever,

headache, myalgia, fatigue, etc.

• Congenital infection also occurs in infants born

to mothers infected during pregnancy
• If the infection occurs in the first trimester,
it results in spontaneous abortion, stillbirth
or severe disease

• Congenital infection after first trimester

results in epilepsy, encephalitis,
hydrocephalus, chronic retinitis, blindness,
anemia, brain damage, etc
 Diagnosis
• There are several serologic tests for
diagnosis of toxoplasmosis
– ELISA test (Enzyme-linked immunosorbent
assay)
– Florescent haemagglutination test (FHA)
– Indirect haemagglutination test (IHA)
– Complement fixation test (CFT)
• PCR method (the use of DNA probes)
 Prevention and control
• Avoid eating raw and undercooked meat
• Heating meat to 660c degree Cel. for 4-6 minutes will kill
the tissue cysts
• Pregnant women should not have intimate contact with
domestic cat
• Pregnant women should avoid handling cat litters
• Wash hands with soap and water after handling meat
• Never feed raw meat to cats; feed only canned food or
cooked meat
• Keep cats indoors
• Change litter boxes everyday
• Flush cat feces down the toilet or burn them
• Use gloves while working in garden
 Blood Coccidian Parasites

Malaria

• Phylum -Apicomplexa
• Genera - Plasmodium
• Class -Sporozoa-no structure for
motility
• 200 known species

• 10 ability to cause infection in man

• 4 clinically relavant to man

– Plasmodium vivax
– Plasmodium ovale
– Plasmodium falciparum
– Plasmodium malariae
 Malaria is a life-threatening
disease

It is the most important infectious disease and

the leading cause of morbidity and mortality
in developing world
As at 2020
Globally
• About 241 million cases compared to 227 million cases reported
in 2019
• The estimated number of malaria deaths stood at 627 000 in
2020.
• An increase of 69 000 deaths over the previous year
• In sub Saharan Africa
95% of global malaria cases
96% of malaria deaths
Children under 5 accounted for about 80% of all malaria
deaths in the Region.
 Types of malaria
Classification based on clinical features

• Quotidian fever- 24 hours cycles of fever- P.

falciparum

• Tertian fever- 48 hours cycles of fever - P. vivax/ P.

ovale

• Quartan fever -72 hours cycles of fever- P. malariae

 Classification based on name of
agent

• Malignant tertian/sub tertian-falciparum

malaria-Plasmodium falciparum

• Benign tertian-Vivax malaria- Plasmodium

vivax

• Quartan malaria-malariae malaria-

Plasmodium malariae
• P. vivax is the most widely distributed of
the 4 species

• P. falciparum is the dominant form in the

tropics

• P. ovale is very rare and found only in

Africa
 Major Morphologic forms
There are about 24 morphologic forms

• Ring forms (Early Trophozoites)

• Developing Trophozoites
• Immature Schizonts
• Mature Schizonts
• Microgametocytes
• Macrogametocytes

All six forms occur following the invasion of the red blood
cell
 Life cycle
Mosquitoes of the genus Anopheles are responsible
for malaria transmission

The life cycle of these four species of malarial

parasites are the same

1.It involves the sexual development phase

(Sporogony)- female anopheles mosquitoes

2.Asexual development phase (schizogony) -

human/vertebrate
 Sexual Phase
• During a blood meal of the female anopheles
mosquito from an infected person,

• the mosquito picks up both male (micro) and female

(macro) gametocytes into its stomach

• In the stomach of the mosquito, the male gametocyte

fertilizes the female gametocyte to form a motile
zygote

• The zygotes migrate to the outer part of the stomach

and are known as Ookinettes

• The Ookinette secretes a cyst wall around itself to

become oocyst
 Sexual Phase continued
• The oocyst then undergoes maturation to become
sporozoites in the oocyst

• When the oocyst ruptures, thousands of sporozoites

are released
– which move to the salivary gland and the proboscis

• When the mosquito takes the next blood meal, the

sporozoites are injected into the new person

• The length of the development cycle depends on the

Plasmodium, the vector as well as the ambient
temperature
 Asexual phase
• The asexual phase is divided into two stages

1. Pre-erythrocytic /exo-erythrocytic /stage-Liver (8-

25days)

2. Erythrocytic stage

The process of development of malaria parasites at

asexual phase is called schizogony (asexual
multiplication)
 Pre-erythrocytic /exo-erythrocytic
stage
• Sporozoites injected into the blood stream leaves the
blood in about 30mins and subsequently invade the
parenchymal cells of the liver (hepatocytes)

• Inside the liver the sporozoite divide asexually to form a

cyst-like organism known as pre-erythrocytic schizonts
which contains thousands of merozoites (8-25 days)

• The infected liver cells eventually raptures and releases

merozoites into the circulating blood

• The merozoites feed on hemoglobin and become

trophozoites
 Erythrocyctic stage
On formation of merozoites one of three pathways are taken

1.Infected RBCs rapture leasing these forms to target and infect new RBCs

2.Development into microgametocytes and macrogametocytes

3. Destruction by the immune system by otherwise healthy individual

4. Hypnozoites (dormant plasmodium infected liver cells may form during

infection with P. vivax or P. ovale

•The period between infection with the parasite and appearance of malaria
parasites in the red blood cells without signs and symptoms is called pre-patent
period
.6 ·= 1n s
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 Other forms of Transmission
• Blood transfusion from infected person

• Sharing of contaminated needles and syringes

mainly from infected drug addict to another

• Organ transplant-liver

• Congenital malaria- from mother to baby

 Clinical manifestation
• Clinical manifestation starts as the RBC rupture, the resulting
merozoites, hemoglobin and toxic cellular waste products
initiate the first in a series of paroxysms

1. Irregular fever: the pattern of fever occurs in about a week

after infection

2. Anemia:
• anemia can occur in all, but severe in P. falciparum
infection, partly because the P. falciparum attacks red
blood cells of all stages which will undergo hemolysis
• The type of anemia is hemolytic
4. Splenomegaly:
• there is enlargement of the spleen, especially
very early in the acute phase.

• In the chronic phase, after several rounds of

attacks, there is enlargement of the spleen and
liver leading to Hepatosplenomegaly.

5. Jaundice:
• A mild jaundice may occur due to hemolysis in
all types of malaria.

• But severe jaundice may occur in P. falciparum

infection
Specific malaria parasites
 Plasmodium vivax
• P. vivax is the most widely distributed. It occurs in tropics,
subtropics as well as temperate regions

• P. vivax infects only young immature erythrocytes

– Infected cells become enlarged and distorted

• The incubation period is usually 10-17 days

• Paroxysm follows the rupture of the RBC liberating

merozoides which sometimes infects new RBC

• The infection start with flu-like symptoms such as

headache, muscle pains, chills, shivering, anorexia,
nausea and vomiting
• This cold stage will last for about 1 hour and the temperature
will begin to rise

• The hot stage will follow lasting for about 3-6 hours, during
which there is high temp, fever, headache, malaise, vomiting
and thirst

• The sweating stage follows lasting for 1-2 hrs during which the
temp drops to normal

• Paroxysms occur every 48hrs in untreated patients- tertian

malaria

• Chronic P. vivax can lead to brain, kidney, and liver damage

due to the malarial pigment, cellular debris and capillary
plugging of these organs by masses of adherent erythrocytes

• Dormant hypnozoites may cause relapses months to years

following initial infection
• In blood smear majority of stages in asexual cycle
may be present including gametocytes

• Within the first few hours of paroxysm, many of the

infected cells contain very early forms of the
parasite called trophozoites

• The best time for diagnosis will be halfway

between paroxysm

• The stages depends on the time samples are

taken
 Plasmodium ovale
• P. ovale is primarily found in tropical Africa, Asia and South
America

• P. ovale infects only young immature erythrocytes

– The RBCs become enlarged and distorted

• Incubation period is same as P. vivax

• Paroxysm and relapse caused by the reactivation of hypnozoites is

the same as P. vivax

• However untreated patient in P. ovale experience infections that

last about a year where as P. vivax may remain asymptomatic for
years

• All stages of development are seen in P. ovale infection however

distinguishing the various stages is difficult because of similarities
 Plasmodium malariae
• P. malariae is found in sub tropic and template regions

• P. malariae infects only mature erythrocytes

– Infected cells are normal in size and not distorted

• Incubation period is from 18-40 days

• The type of fever is similar to those of P. vivax and P. ovale,

but occurs 72 hrs instead of 48hrs

• The frequently encountered stages are the developing trophozoites and

schizonts

• Gametocytes are not distinguishable from those of P. vivax

• Dormant hypnozoites are not associated with P. malariae there are no

known relapse
 Plasmodium falciparum
• Present in the tropics and sub tropical regions
accounting for about 50% of all malaria cases

• P. falciparum infects RBCs of all ages reaching high

parasitemia levels quickly (deadly)
– Infected RBCs are normal in size and not distorted

• Incubation period is between 7-10 days

• The clinical manifestations are usually acute forms and

it terminates fatally

• Most common clinical manifestations includes

headache, photophobia, muscle aches and pains,
anorexia, nausea and vomiting
• Severe anemia

• Cerebral malaria- when plugs form in the associated

capillaries of the brain
– patients often falls into coma which may result in death
(>80% )

• Renal disease- black water fever- infection of the

kidney resulting in hemoglobinuria,
– acute renal failure, tubular necrosis, nephrotic syndrome
and death may result

• Liver involvement- Abdominal pain, Vomiting of bile,

Dysentery
– Rapid dehydration

• Pulmonary edema

• Tropical splenomegaly syndrome

• Peripheral blood smears reveals mostly ring
forms and gametocyte forms

• Trophozoites and schizonts are only visible

in peripheral blood of patient with severe
infection
 Laboratory Diagnosis
1. Giemsa stained peripheral blood films
– Thick films-identifying the presence of malaria parasites
slides
– Thin films-differentiating plasmodium species

– All blood films should be studied under oil immersion

2. Wrights stain

3. Polymerase chain reaction (PCR)

The various morphologic forms observed at any stage is

dependent on the time of sample collection
 Laboratory Diagnosis
• Note: To rule out malarial infection
– multiple sets of blood films-thick and thin films
are necessary

– Blood should be collected every 6 to 12

hours for up to 48 hours
 Laboratory procedure
• The procedure is as follows:
– One of the fingers is disinfected with 70% alcohol

– Let it dry and prick with sterile lancet

– Discard the first drop of blood and prepare both thick

and thin blood films.

– Stain the films with, eg. Giemsa stain, Leishman's stain

(thin film only) or Field stain (for only thick film).

– Examine under oil immersion and look for characteristic

rings of P. falciparum.
•

•
•

•
Prevention and control
 Prevention and control
• Chemoprophylaxis and prompt eradication of infection
are necessary for breaking the mosquito-human cycle

• Control of mosquito breeding sites

• Protection of individuals by screening, netting, protective

clothing, spraying of rooms with insecticide, and the use
of insect repellents

• Travelers to endemic areas can take prophylactic drugs,

eg. doxycycline, malarone, etc.

• Pregnant women should be properly treated to avoid

congenital transmission
Treatment
• Ensure a rapid and complete elimination of
the Plasmodium parasite from the patient’s
blood

– in order to prevent progression of

uncomplicated malaria to severe disease or
death,
– chronic infection that leads to malaria-related
anaemia
 Treatment
• The following treatment options are available
– Suppressive: prophylactic drugs aimed at avoiding infection
and clinical symptoms eg. malarone

– Therapeutic: aimed at eradicating the erythrocytic cycle

– Radial cure: aimed at eradicating the exo-erythrocytic cycle

in the liver

– Gametocidal: destruction of gametocytes to prevent

transmission by mosquitoes
• Malaria should be treated first before tackling the complications
associated with it
• .
 Research and Monitoring
• The development of potential malarial
vaccines have been an area of research that
has yielded some results. Yet more needs to
be done
– Mosquirix (RTS,S/ASO1)-Partial protection
against children

• Continuous efficacy monitoring is needed to

inform treatment policies and to ensure early
detection of drug resistance