Microbiology and parasitology Final lecture
Protozoa

Definition of terms:
Infective stage – refers to the stage of the
parasite that enters the host or the stage
that is present in the parasite’s source of
infection.


Pathogenic stage – refers to the stage of
the parasite that is responsible for
producing the organ damage in the host
leading to the clinical manifestations.
Encystation – process by which
trophozoites differentiate into cyst forms.
Excystation – process by which cysts
differentiate into trophozoite forms
General Properties of Protozoa






The Kingdom Protozoa consists of
single celled eukaryotic organisms
that are spherical to oval or
elongated in shape.
classification of these organisms is
mainly based on the organ of
locomotion utilized.
Some are facultative parasites
capable of a free-living state (e.g.,
Acanthamoeba and Naegleria).
- normally reside in the soil
or water but can cause
severe illness when they
gain entrance into the
central nervous system or
the eyes.
Majority of protozoa divide by
means of binary fission (flagellates,
ciliates, and amebae).
Sporozoans reproduce through both
sexual and asexual means.
- Asexual reproduction is
achieved through a process
called merogony or
schizogony.
- Sexual recombination can
occur, leading to antigenic
and genomic variation.
They are small in size

Protozoan infections are most often
diagnosed through microscopic
examination of body fluids, tissue
specimens, or feces.
Special stains may be used to
demonstrate the different protozoa.
Parasitic protozoa infections are
diagnosed by demonstrating the
motile, feeding, dividing stage of
the parasite called trophozoite, or
- The trophozoite is the
motile (with pseudopods
or “false feet”) and feeding
form and is the pathogenic
stage.
The dormant, non-motile form
called the cyst.
- The cyst is the non-motile
form and is the infective
stage for most intestinal
protozoan parasites, except
for
- Trichomonas vaginalis
where cyst forms are not
found.
Intestinal and Urogenital Protozoa
Subphylum Sarcodina: Entamoeba
histolytica
 Important properties and life cycle
 An intestinal and tissue ameba and
is the only known pathogenic
intestinal ameba
 Life cycle consists of two stages
- the non-motile cyst
(infective stage) and
- the motile trophozoite
(pathogenic stage).
 The trophozoite is found within the
intestinal and extra intestinal
lesions, and in diarrheal stools.
 Cysts are usually found in nondiarrheal, formed stools.
development of abscess in
the liver.
 Epidemiology and Pathogenesis
 Entamoeba histolytica is found
worldwide but is more common
in tropical countries, especially
in areas with poor sanitation.
 Primarily transmitted by the
fecal oral route through
ingestion of the cyst from
contaminated food and water.
 Water serves as the major
source of infection of the
parasite.
 Sexual transmission may also
occur in unprotected sex with a
woman who has vaginal
amoebiasis or through anal
intercourse.
 Ingested cyst undergoes
excystation in the ileum where
it differentiates into a
trophozoite (pathogenic stage)
proceeds to colonize the cecum
and colon.
 Trophozoites undergo
encystation and become
converted into cysts, which are
then passed out with the feces.
- Trophozoites are usually
recovered in the feces of
patients with active
infection (diarrheic stools)
while cysts are found in
formed, non-diarrheic
stools.
- Trophozoites of E.
histolytica secrete enzymes
that cause local necrosis
producing the typical
“flask shaped” ulcer
associated with the
parasite. Invasion of the
portal circulation may
occur leading to the
Once we going to ingested the infective cyst and we
get it from the contaminated food or water. Once
ingested this parasite will take residency or find a
habitat either in the intestinal tract or in the liver. And
that infective stage will transform into pathogenic
stage. From cyst they will then form into a
trophozoites. The trophozoites is what we consider the
motile or pathogenic stage clinical signs and
symptoms will be manifested here. This is only a
cycle any individual infected with this kind of
protozoa. Once they pass out a urine especially due to
no proper disposal very common on slum areas, they
can pass the infection to other individuals. From a
cyst which is the infective stage once they will find a
phylum especially in our gastrointestinal tract it will
transform into trophozoite and this is the pathogenic
stage which we are going to experience the clinical
signs and symptoms especially the diarrhea. It can
even migrate to other organs such as our liver and it
can cause a hepatic abscess or abnormal condition of
the liver due to the toxin produce by these protozoa.
 Disease: Amoebiasis
1. Acute intestinal amoebiasis
- presents as bloody, mucus
containing diarrhea
(dysentery) accompanied
by lower abdominal
discomfort, flatulence
(release of gas), and
tenesmus (feeling of
incomplete defecation).
- Chronic infection may
occur, with symptoms such
as occasional diarrhea,
weight loss, and fatigue.
- Lesion called an
amoeboma may form in
the cecum or in the
rectosigmoid area of the
colon, which may be
mistaken for a malignant
tumor in the colon.
2. Extraintestinal amoebiasis
- Occurs when the parasite
enters the circulatory
system.
- Most common
extraintestinal form of
amoebiasis is the amoebic
liver abscess.
Characterized by right
upper quadrant pain,
weight loss, fever, and a
tender, enlarged liver.
- Abscess found on the right
lobe of the liver may
penetrate the diaphragm
and cause lung disease
(amoebic pneumonitis).
- Other organs that may
become infected include
the pericardium, spleen,
skin, and brain
(meningoencephalitis).
3. Asymptomatic carrier state
- Occurs under the following
conditions:
(a) if the parasite involved
is a low virulence strain;
(b) if the parasite load is
low; and
(c) if the patient’s immune
system is intact
- The patient presents with
no symptoms but the
parasite reproduces and is
passed out with the
patient’s feces.
 Laboratory Diagnosis
 Intestinal amoebiasis is
confirmed by the finding of
trophozoites in diarrheic
stools or cysts in formed
stools.
 Trophozoites
characteristically contain
ingested red blood cells.
 Stool specimen is
examined within one hour
of collection to see the
motility of the trophozoites.
 Serologic testing may be
useful for the diagnosis of
invasive amoebiasis.
 Treatment
 Metronidazole - for
symptomatic intestinal
amoebiasis or hepatic
abscess
 Alternative drug tinidazole
- for both intestinal and
extraintestinal amoebiasis.
 Diloxanide furoate,
metronidazole, or
paromomycin – for
asymptomatic carriers.
 Surgical drainage of
amoebic liver abscess may
be necessary if there is no
improvement with medical
therapy.
 Prevention and Control
 Most important preventive
measure observance of
good personal hygiene. This
includes:
1. Proper hand washing,
especially for food
handlers.
2. Proper waste disposal
should be observed to
avoid fecal
contamination of
water sources.
3. Use of “night soil”
(human feces) for
fertilization of crops
must be avoided.
4. Adequate washing
and cooking of
vegetables should be
observed.
Subphylum Mastigophora:Giardia lamblia
(Giardia intestinalis)
 Important Properties and Life Cycle
 Giardia lamblia is an
intestinal protozoan that
was initially known as
Cercomonas intestinalis.
Another name used is
Giardia duodenale.
 Also exists in a cyst form
and a trophozoite form.
 Trophozoite is pear shaped
or teardrop shaped with
four pairs of flagella and
has a motility likened to a
falling leaf. Described as
resembling an old man with
whiskers (“old man
facies”).
 Possesses a sucking disc
which the parasite uses to
attach itself to the intestinal
villi of the infected human.
 Cyst is typically oval and
thick walled with four
nuclei. The fully mature
cyst contains four nuclei
with four median bodies. It
divides through binary
fission.
 Each cyst gives rise to two
trophozoites during
excystation in the intestinal
tract.
 Epidemiology and pathogenesis
 Giardia lamblia has a
worldwide distribution
through contaminated water
sources.











Disease can occur in
outbreaks related to
contaminated water
supplies
50% of infected individuals
do not present with
symptoms and serve as
carriers.
Other than humans, many
species of mammals may
act as reservoirs.
Infection is also common
among individuals
engaging in oral anal
contact.
High incidence has been
seen in daycare centers
and among patients in
mental hospitals.
Life cycle
The parasite is transmitted
through ingestion of the
cyst from fecally
contaminated water and
food.
Cyst enters the stomach
and is stimulated by the
gastric acid to undergo
excystation in the
duodenum.
Trophozoites attach
themselves to the duodenal
mucosa through the sucking
disks.
Damage to the intestines is
not due to invasion of the
parasite but because of
inflammation of the
duodenal mucosa, leading
to diarrhea with
malabsorption of fat and
proteins.
Trophozoites may also
infect the common bile duct
and gallbladder.
These may include
deficiencies in fat soluble
vitamins, folic acid, and
proteins.
- A self-limiting infection,
lasting one to two weeks.
Relapses may occur,
especially in patients with
IgA deficiency.
 Laboratory diagnosis
 The demonstration of the
cyst or trophozoite (or both)
in diarrheic stools.
 Only cysts are isolated
from the stools of
asymptomatic carriers.
 If microscopic examination
of the stool is negative,
string test may be
performed which consists
of making the patient
swallow a weighted piece
of string until it reaches the
duodenum.
 Trophozoites adhere to the
string and can be
visualized after
withdrawal of the string.
 Treatment
 Metronidazole, tinidazole,
and nitazoxanide - primary
choice of treatments for G.
lamblia infection. As per
recommendation of the
Centers for Disease Control
and Prevention in the
United States,
 Prevention and control
1. Avoidance of fecal
contamination of water
supplies through proper waste
disposal.
2. Drinking water should be
boiled, filtered, or iodine
treated especially in endemic
areas.
3. Proper hand washing is also
recommended.
-
 Disease: Giardiasis
1. Asymptomatic carrier state
- Infection with the parasite
is usually completely
asymptomatic.
- Infected individual
unknowingly passes out
the parasite with the feces
which can then
contaminate water.
2. Giardiasis (Traveler’s
diarrhea)
- infection is characterized
by a non-bloody, foul
smelling diarrhea
accompanied by nausea,
loss of appetite, flatulence,
and abdominal cramps.
- The symptoms may persist
for weeks or months.
- Malabsorption of fat may
lead to the presence of fat
in the stool (steatorrhea).
- Patients are usually
afebrile. Manifestations
may vary depending on
which nutrient becomes
deficient due to the
resulting malabsorption.
Subphylum Mastigophora: Trichomonas
vaginalis
 Important properties and Life cycle
 The parasite is a pearshaped organism with a
central nucleus, four
anterior flagella, and an
undulating membrane.
 exists only in the
trophozoite form (infective
and pathogenic).
 Epidemiology and pathogenesis
 Trichomonas vaginalis is
not an intestinal pathogen.
 Causes urogenital
infections
 The main mode of
transmission is through
sexual intercourse.
 isolated from the urethra
and vagina of infected
women as well as the
urethra and prostate gland
of infected men.
 Infection is highest among
sexually active women in
their thirties.
 Lowest in postmenopausal women.
 Parasite may be transmitted
through toilet articles and
clothing of infected
individuals.
 Infants may be infected as
they pass through the
infected birth canal during
delivery.
 Parasite invades the vaginal
mucosa of infected women.
They multiply through
binary fission.
 Trophozoites feed on local
bacteria and leukocytes.
 In men, the most
common infection site is
the prostate gland and the
urethral epithelium.
 Disease: Trichomoniasis
 Infection in men
- Usually asymptomatic and
men serve as the reservoir
for infection in women.
- In men who develop
symptoms, the
manifestations are those
related to development of
prostatitis (inflammation of
the prostate), urethritis
(manifest as discharge),
and other urinary tract
involvement.
- Persistent or recurring
urethritis is the most
common symptomatic
form of the infection.
 Infection in women
- Also asymptomatic, some
women may present with
scant, watery vaginal
discharge.
- In more severe cases, the
discharge may be foul
smelling and greenish
yellow in color.
- May be accompanied by
itching (pruritus) and a
burning sensation in the
vagina.
- The cervix appears very
red, with small punctuate
hemorrhages, giving rise to
a strawberry cervix.
- Other common symptoms
include dysuria and
increased frequency of
urination.
 Infection in infants
- occurs as the infant passes
through the infected birth
canal of the mother during
vaginal delivery.
- The infected infants may
manifest conjunctivitis or
respiratory infection.
 Laboratory Diagnosis
 Diagnosis is made by the
finding of the characteristic
trophozoite in a wet mount
of vaginal or prostatic
secretions, urine, and
urethral discharges.
 Treatment
 Metronidazole - The drug
of choice for treatment of
trichomoniasis.
 All sexual partners
of an individual with the
infection must be
simultaneously treated to
prevent “ping pong”
infections.
 Prevention and Control
1. Practice safe sex
2. Use of condoms can limit the
transmission of the parasite.
3. Health and sex education are
important
4. Maintenance of the acidic pH
of the vagina may also be
helpful.
Phylum Ciliophora: Balantidium coli
 Important Properties and Life cycle
 Balantidium coli is
morphologically more
complex than E. histolytica.
 It has a primitive mouth
called a cytostome, a
nucleus, food vacuoles, and
a pair of contractile
vacuoles.
 The infective stage: cyst
 The pathogenic stage:
trophozoite
 Invades the mucosal lining
of the terminal ileum,
cecum, and colon.
 It is the largest protozoan to
infect humans.
 The trophozoites typically
exhibit:
- Rotary
- Boring motility (through
cilia)
- contain two nuclei (a small
dot like micronucleus
adjacent to a kidney bean
shaped macronucleus).
 The cyst also contains two
nuclei although the
micronucleus may not be
readily observable.
 Epidemiology and pathogenesis
 Parasite has a worldwide
distribution
 Most common and most
important reservoir is the
pig.
 Monkeys may occasionally
act as reservoirs of the
parasite.
 Main source of infection is
water contaminated by pig
feces and the mode of
transmission is through the
fecal oral route.
 Person to person
transmission via food
handlers has been implicated
in outbreaks.
 Cysts are found in
contaminated water, which
when ingested, undergoes
excystation in the small
intestines.





The trophozoites travel to
the large intestines where
they produce ulcers similar
to those seen in amoebiasis.
However, extra intestinal
involvement is not seen.
Disease: Balantidiasis
 Most infected individuals
are asymptomatic
 A dysenteric type of
diarrhea resembling amebic
dysentery may occur in
patients with high parasite
load.
 Acute infections manifest
with liquid stools
containing pus, blood, and
mucus.
 Chronic infections may
manifest with a tender
colon, anemia, wasting
(cachexia), and alternating
diarrhea and constipation.
 Extraintestinal infection is
rare and may involve the
liver, lungs, mesenteric
nodes, and urogenital tract.
Laboratory Diagnosis
 Diagnosis is based on the
finding of trophozoites and
cysts in the stool specimen.
 Due to its large size, the
parasite can be readily
detected in fresh, wet
microscopic preparations.
Treatment
 Oxytetracycline and
iodoquinol - The current
recommended treatment of
patients with balantidiasis
 Metronidazole - may also
be used as alternative to
treat infected patients.
Prevention and Control
1. Maintenance of sanitary
hygiene, proper disposal of
pig feces.
2. Boiling of drinking water.
Blood and Tissue Protozoa
Subphylum Sarcodina: Acanthamoeba
(Free living Amoeba)
 Important Properties and Life cycle
 Acanthamoeba Castellani,
together with Naegleria, is a
minor protozoan pathogen
but unlike Naegleria,
Acanthamoeba usually
causes infection in
immunocompromised
patients
 A free-living amoeba that
causes inflammation of the
brain substance and its
meningeal coverings
(meningoencephalitis).
 Parasite is found widely in
soil, contaminated
freshwater lakes, and other
water environment.
 Able to survive in cold
water. Like E. histolytica,
 Infective stage: is the cyst
 Pathogenic stage: the
trophozoite.
 Epidemiology and pathogenesis
 Two ways by which the
parasite can be acquired
- Through aspiration or nasal
inhalation.
- Through direct invasion in
the eye.
 People acquire the infection
usually while swimming in
contaminated water.
 Inhalation of the cysts from
dust has also been shown to
occur.
 The trophozoites enter
through the lower
respiratory tract or through
ulcers in the mucosa or
skin.
 Parasite then migrates
through the bloodstream


and invade the central
nervous system.
Eye infection with
Acanthamoeba occurs
primarily in patients who
wear contact lenses.
Tap water contaminated
with the parasite is the
source of infection for
contact lens users.
 Disease
1. Granulomatous amebic
encephalitis
- infection occurs primarily
in immunocompromised
individuals.
- The parasite produces a
granulomatous amebic
encephalitis and brain
abscesses in
immunocompromised
patients.
- Symptoms develop slowly
and may include headache,
seizures, stiff neck, nausea,
and vomiting.
- The brain lesions may
contain both the
trophozoites and the cysts.
- In rare instances, the
parasite may spread and
produce granulomatous
lesions in the kidneys,
pancreas, prostate, and
uterus.
2. Keratitis
- infection of the cornea of
the eye.
- Symptoms include severe
eye pain and vision
problems.
- Loss of vision may occur
due to perforation of the
cornea.
 Laboratory Diagnosis
 By finding of both
trophozoites and cysts in
the cerebrospinal fluid as


well as brain tissue and
corneal scrapings.
Histologic examination of
corneal scrapings may also
be done.
Calcofluor white, a stain
usually used to
demonstrate fungi, may be
used to demonstrate the
parasite in corneal
scraping specimens.
 Treatment
 Pentamidine,
Ketoconazole, or
Flucytosine - effective in
the treatment of infection,
however, prognosis is poor
even with treatment.
 Topical miconazole,
chlorhexidine,
itraconazole,
ketoconazole, rifampicin,
or propamidine - for eye
and skin involvement.
 Propamidine - has been
documented to have the
best success record.
 Prevention and Control
1. Adequate boiling of water.
2. Regular disinfection of
contact lenses is also advised.
3. Contact lens wearers are also
advised to avoid using
homemade non sterile saline
solutions.
Subphylum Sarcodina: Naegleria
 Important Properties and Life Cycle
 Similar to Acanthamoeba,
the parasite Naegleria is
also classified as a freeliving protozoan.
 It shares many
characteristics with
Acanthamoeba.
 Parasite is also found
worldwide in soil and
contaminated water
environment.
 Naegleria can survive in
thermal spring water.
 The known pathogen
worldwide is Naegleria
fowleri, which is the only
amoeba with three
identified morphologic
forms
- trophozoite,
- flagellate,
- and cyst forms.
 The trophozoite exhibits the
typical amoeboid motility
which is described as “slug
like.”
 Flagellate form is pear
shaped and is equipped
with two flagella that is
responsible for the
parasite’s jerky or spinning
movement.
 The non motile form is the
cyst
 Amoeboid trophozoite form
is however the only form
that is known to exist in
humans.
 Epidemiology and pathogenesis
 Naegleria infection is
usually acquired trans
nasally when swimming in
contaminated water.
 Parasite penetrates the nasal
mucosa and cribriform
plate, enters the central
nervous system, and
produces a rapidly fatal
meningitis and encephalitis
(primary amoebic
meningoencephalitis.
 The parasite produces
infection in otherwise
healthy individuals, usually
children.
 The parasite may be
acquired through inhalation

of dust containing the
parasite.
Entire life cycle of the
parasite (amoeboid
trophozoite → flagellate
trophozoite → amoeboid
trophozoite → cyst form)
occurs entirely in the
external environment.
 Disease
1. Asymptomatic infection – the
most common clinical
presentation in patients with
colonization of the nasal
passages.
2. Primary amoebic
meningoencephalitis (PAM) –
the result of colonization of
the brain by the amoeboid
trophozoites leading to rapid
tissue destruction. Patients
initially complain of sore
throat, nausea, vomiting,
fever, and headache. Patients
eventually develop signs of
meningeal irritation (e.g.,
Kernig’s sign) as well as
alterations in their senses of
smell and taste. If untreated,
the patients may die within
one week after onset of
symptoms.
 Laboratory Diagnosis
 Diagnosis is based on the
finding of the amoeboid
trophozoites in the
cerebrospinal fluid.
 Treatment
 Treatment is ineffective
because of its rapidly fatal
course. However, some
patients have been shown
to recover from infection
due to early detection and
initiation of treatment.
 Treatment of choice is
Amphotericin B in
combination with
miconazole and
rifampicin (Murray,
2014).
 Prevention and Control
 There is no known means
of preventing Naegleria
infection other than the
prevention of
contamination of water
sources.
 Adequate chlorination of
swimming pools and hot
tubs is recommended.
Subphylum Mastigophora:
Hemoflagellates Leishmania spp.
 Important Properties and Life Cycle
 The life cycle of the
parasite involves a vector,
the female sandfly of the
Phlebotomus and
Lutzomyia genera.
Leishmania specie. are
obligate intracellular
parasites.
 It has three morphologic
forms
1. the amastigote
2. promastigote and
3. epimastigote.
 The infective stage is the
promastigote. The
promastigote form may
be seen only if a blood
sample is collected and
examined immediately
after transmission.
Epimastigotes are found
primarily in the vector.
 The pathogenic stage
and diagnostic form is
the amastigote which is
found primarily in tissue
and muscle, as well as the
central nervous system
within macrophages and
in cells of the
reticuloendothelial
system.
 The amastigote is:
- Round to oval in shape and
contains a nucleus
- A basal body structure
called a blepharoblast
- a small parabasal body
located adjacent to the
blepharoblast.
- Both the blepharoblast and
parabasal body are
collectively known as the
kinetoplast.
 The promastigote is:
- Long and slender with a
kinetoplast located in its
anterior end
- a single free flagellum
extending from the anterior
portion.
 Epidemiology and Pathogenesis
 The parasite has a
worldwide distribution.
Natural reservoirs
include rodents, ant
eaters, dogs, and cats.
 In endemic areas, the
parasite may be
transmitted in a human
vector human cycle.
 There are three major
strains of Leishmania
which differ in the
tissues affected and the
resulting clinical
manifestations.
 These are:
- Leishmania donovani
(visceral leishmaniasis)
- Leishmania tropica
(cutaneous leishmaniasis)
- Leishmania braziliensis
(mucocutaneous
leishmaniasis).

Leishmania donovani complex

L. donovani is the causative agent
of visceral leishmaniasis (also
known as kala azar or dumdum
fever).
 The complex consists of:
1. L. donovani chagasi which is
mainly seen in Central America
(mainly Mexico, West Indies,
and South America)
Transmitted by the Lutzomyia
sandfly;
2. L. donovani found in parts of
Africa and Asia (Thailand, India,
China, Burma, and East
Pakistan) and is transmitted by
the Phlebotomus sandfly;
3. L. donovani infantum, also
transmitted by the
Phlebotomus sandfly and is
found mainly in
Mediterranean Europe, Near
East, and Africa.
 The promastigote is injected into
the human host through bite of the
sand fly. After entry into the host, it
loses its flagella, is engulfed by
macrophages, and transforms into
amastigotes.
 The organs of the
reticuloendothelial system (liver,
spleen, and bone marrow) are the
most severely affected.
 Disease: Visceral Leishmaniasis(Kala
azar, Dumdum Fever)
After an incubation period of 2
weeks to 18 months, the disease
begins with intermittent:
- Fever
- Weakness
- weight loss.
 Massive enlargement of the spleen
(splenomegaly) is characteristic,
leading to:
- hypersplenism and
resulting anemia.
- Hepatomegaly or
enlargement of the liver
- In light skinned patients,
hyperpigmentation of the
skin may be seen (kala azar
means “black sickness” or
“black fever”).
 Involvement of the bone marrow
leads to :
- destruction of the cellular
components with the
corresponding clinical
effect.
- anemia due to destruction
of red blood cells
- bleeding tendencies due to
reduction of platelets
(thrombocytopenia)
- increased risk for
secondary infection
because of reduction of
white blood cell
(leukopenia).
- Glomerulonephritis or
inflammation of the
glomeruli of the kidney
 The disease may be fatal if
untreated.
 Laboratory Diagnosis
 The screening test is called the
Montenegro skin test. This test is
similar to the tuberculin skin test
for the diagnosis of tuberculosis. It
is used as screening for large
populations at risk but is not used
for diagnosis.
 Definitive diagnosis is done by
demonstration of the amastigote
from Giemsa-stained slides of
specimen from blood, bone
marrow, lymph nodes, and biopsies
of infected areas.
 Culture of blood, bone marrow,
and other tissues may also be done,
which will show the promastigote
forms.
 Serologic tests are now also
available such as indirect
fluorescent antibody (IFA)
 Enzyme linked immunosorbent
assay (ELISA), or direct
agglutination test (DAT).
 Treatment
 liposomal amphotericin B
(Ambisome) - The present
recommended drug of choice
 Sodium stibogluconate has also
been found to be effective but the
development of resistance may
occur.
 gamma interferon in combination
with pentavalent antimony - Other
patients have shown favorable
responses.
 Prevention and Control
1. The use of insect repellents
2. protective clothing
3. installation of screens may be
helpful.
4. Prompt treatment of infected
humans is essential to help
halt the spread of the disease.
Leishmania braziliensis complex



L. braziliensis is the causative
agent of mucocutaneous
leishmaniasis which involves skin,
cartilage, and mucous membranes.
Infection with L. braziliensis
occurs most commonly in Brazil
and Central America, primarily in
construction and forestry workers.
The complex consists of:
- L. panamensis (Panama
and Colombia),
L. peruviana (Peruvian
Andes), and
- L. guyanensis (The
Guianas, parts of Brazil
and Venezuela).
 Infection is transmitted by
sandflies (Lutzomyia and
Psychodopigus) through skin bite.
 The promastigotes invade the
reticuloendothelial cells where they
transform into amastigotes
(diagnostic stage).
 Reproduction of the amastigotes
result in tissue destruction.
 The amastigotes are taken up by
the vector during a blood meal and
are transformed into promastigotes.
 Disease: Mucocutaneous
Leishmaniasis
 Mucocutaneous leishmaniasis, also
called espundia, begins with a
papule at the site of insect bite,
then forms metastatic lesions,
usually at the mucocutaneous
junction of the nose and mouth.
 Disfiguring granulomatous,
ulcerating lesions destroy the
nasal cartilage (tapir nose) but
not the adjacent bone.
 Death can occur from secondary
infections.
 Laboratory Diagnosis
 Diagnosis is confirmed by
demonstration of amastigotes in
clinical specimen.
- Ulcer biopsy specimens
are used for the diagnosis
of mucocutaneous
leishmaniasis.
- Microscopic examination
of Giemsa stained ulcer
biopsy specimens reveals
the diagnostic amastigotes.
- Culture of infected
material may show the
promastigotes.
- Serologic testing may
also be done
-
 Treatment
 Sodium stibogluconate - the most
widely used drug for the treatment
of mucocutaneous leishmaniasis
Due to resistance has been shown
to develop.
 Alternative drugs include
- liposomal Amphotericin
B
- oral anti fungal drugs
(fluconazole,
ketoconazole, and
itraconazole).
 Prevention and Control
1. The most important
preventive measure is the
control of the insect vector. If
this cannot be done, measures
should be undertaken to
protect individuals from
sandfly bites
2. Using netting
3. Window screens
4. Protective clothing
5. Insect repellents.
6. Prompt treatment can also
help prevent spread of the
disease.
Leishmania tropica complex
 Important Properties and Life Cycle
 The complex consists of L. tropica,
L. aethiopica, and L. major. These
are the causative agents of what is
referred to as Old World cutaneous
leishmaniasis.
 The life cycle of L. tropica is
similar to that of L. braziliensis.
 All three members of the complex
are transmitted by the Phlebotomus
sandfly and primarily attacks the
human lymphoid tissue of the skin.
 Disease: Old World Cutaneous
Leishmaniasis
 The disease is also known as
oriental sore, and Baghdad or
Delhi boil.

It is characterized by one or several
pus containing ulcers that may
heal spontaneously.
 The initial lesion is a small, pruritic
red papule at the bite site.
 In patients with anergy and
hypersensitivity responses,
spontaneous healing does not
occur.
 Thick skin plaques with multiple
nodules may develop, especially on
the limbs and face.
 Laboratory Diagnosis
 Microscopic examination of
Giemsa stained slides of fluid
aspirated from beneath the ulcer
bed is the usual diagnostic
procedure of choice. Microscopic
examination reveals the typical
amastigotes.
 Culture of specimen will show the
promastigote form.
 Serologic tests are also available.
 Treatment
 The drug of choice is sodium
stibogluconate. Steroids with
application of heat to the infected
lesions may be used.
 Other alternative drugs are
meglumine antimonite,
pentamidine, and oral
ketoconazole.
 Paromomycin ointment may be
helpful in the healing of the ulcers.
 Prevention and Control
1. Preventive measures are the
same as those for the different
forms of leishmaniasis.
2. However, unlike the other
Leishmania, a vaccine has
been developed against L.
tropica which is currently
undergoing clinical trials.
Trypanosoma spp.
 Important Properties and Life Cycle
 The trypanosomes are also
hemoflagellates like Leishmania.

The major difference between the
two lies in their diagnostic stages –
- Which is the amastigote for
Leishmania
- the trypomastigote for the
trypanosomes. The
trypomastigotes are
curved, assuming the shape
of the letters C, S, or U.
- Unlike Leishmania, the
kinetoplast of the
trypomastigote is
posteriorly located, with
the single large nucleus
located anterior to it.
- The trypomastigotes are
visible in the peripheral
blood.
Trypanosoma cruzi
 Epidemiology and Pathogenesis
 The parasite is found primarily
in South and Central America
 Transmitted by the bite of the
reduviid or triatomid bud
(Triatoma or “cone nose” bug
or “kissing bug”).
 Usually transferred to a human
host when the feces of the bug
containing the infective
trypomastigotes is deposited
near the bite site.
 The feces are then introduced
into the bite site when the host
scratches the bite area.
 Other routes of transmission
include:
- Blood transfusion
- Sexual intercourse
- Transplacental
transmission
- Through the mucous
membranes when the bite
site is near the eye or
mouth.
 Humans and animals
(domestic cats and dogs,
and wild species such as
armadillo, raccoon, and
rat) serve as reservoir
hosts.
 The trypomastigotes
invade the surrounding
cells and transform into
amastigotes.
 The amastigotes then
reproduce leading to
destruction of host cells.
 Then transformed back
into trypomastigotes,
which invade the blood,
penetrate other cells in
the body, and transform
back into amastigotes.
 Different cell types may
be affected. However
glial cells,
reticuloendothelial cells,
and especially
myocardial cells are the
most frequently affected.
 The disease is primarily
seen in rural areas
because the reduviid bug
lives in the walls of rural
huts and feeds at night.
 Acute infection is rarely
seen in the United States.
 Chronic infection is
now seen with increasing
frequency among
immigrants from Latin
America.
 Disease: Chagas Disease
(American Trypanosomiasis)
 The acute phase of the disease
begins with a nodule
(chagoma) near the bite site and
unilateral swelling of the eyelid
with conjunctivitis (Romana’s
sign).
 The eyelid swelling may be
due to the bug feces being
accidentally rubbed into the
eye.

Accompanied by fever, chills,
malaise, myalgia, and fatigue.
 Patients may recover or may
enter the chronic phase.
 Characterize the chronic phase
of Chagas disease:
- Hepatosplenomegaly
- Enlargement of lymph
nodes (lymphadenopathy)
- Myocarditis with cardiac
arrhythmia. Cardiac
muscle is the most
frequently and most
severely affected tissue.
- Loss of tone of the colon
and esophagus due to
destruction of the
Auerbach’s plexus may
lead to abnormal dilatation
of these organs, called
megacolon and
megaesophagus,
respectively.
 CNS involvement may also be
seen in the form of
meningoencephalitis and cysts.
 Death may occur due to cardiac
failure and arrhythmias.

Other diagnostic methods that
can be used include:
- bone marrow aspiration,
- muscle biopsy,
- culture on special medium,
and
- xenodiagnosis.
 Xenodiagnosis entails allowing
an uninfected laboratory raised
reduviid bug to feed on an
infected patient. After several
weeks, the intestinal contents of
the bug are examined for the
presence of the parasite.
 Serologic tests can also be
helpful.
 Both xenodiagnosis and
serologic tests are useful in the
chronic form of the disease.
 Treatment
 benznidazole and nifurtimox
- The drugs of choice for
treatment are but these are less
effective during the chronic
phase of the disease.
 Alternative agents are
allopurinol and ketoconazole
 Prevention and Control
1. Prevention involves
protection from the bite of the
reduviid bug
2. Improvement of housing
conditions, and insect control.
3. Education regarding the
disease and its transmission is
also helpful.
Trypanosoma brucei gambiense and
Trypanosoma brucei rhodesiense
 Laboratory Diagnosis
 Acute disease is diagnosed by
the finding of trypomastigotes
in thick or thin films of the
patient’s blood.
 Epidemiology and Pathogenesis
 The two species are similar in
morphology and life cycle.
 Their life cycles involve the
tsetse fly (Glossina) as the
vector.
 Humans are the reservoir for T.
brucei gambiense, while
domestic animals (especially
cattle) and wild animals serve
as the reservoir for T. brucei
rhodesiense.
 The infective and pathogenic
stage is the trypomastigote.
 The trypomastigotes spread
from the skin to the blood then
to the lymph nodes and the
brain.
 A demyelinating encephalitis
occurs leading to the
characteristic manifestations of
the disease.
 T. gambiense infection (West
African or Gambian Sleeping
Sickness) is chronic while
 T. rhodesiense infection (East
African or Rhodesian Sleeping
Sickness) is more rapidly fatal.
 The disease is endemic in sub–
Saharan Africa which is the
natural habitat of the tsetse fly.
 T. gambiense causes disease
along the water courses in West
Africa while
 T. rhodesiense causes disease
mostly in the arid regions of
East Africa.
 Disease: African Sleeping Sickness
 The initial lesion is an
indurated ulcer called chancre
at the site of the insect bite.
 Intermittent weekly fever and
lymphadenopathy then develop.
Enlargement of the posterior
cervical lymph nodes
(Winterbottom’ssign) is
commonly seen.
 Other manifestations seen
during this stage include:
- red rash accompanied by
pruritus
- localized edema, and
- a delayed pain sensation
(Kerandel’s sign).
 The encephalitis is
characterized by:
- Headache
insomnia, and
mood changes.
Muscle tremors
slurred speech, and
apathy follow, progressing
to somnolence (sleeping
sickness) and coma.
 Untreated disease is fatal.
 Trypanosoma brucei
rhodesiense is more virulent
than Trypanosoma brucei
gambiense.
 Infection with the parasite has a
shorter incubation period.
 Winterbottom’s sign may not
be seen. There is no
lymphadenopathy and CNS
involvement occurs early in the
course of the disease.
 A rapid and fulminating disease
may follow with the parasite
spreading in the blood.
 Death is seen usually within 9–
12 months following infection
in untreated patients and may
be due to glomerulonephritis
and myocarditis.
 Laboratory Diagnosis
 Microscopic examination of
Giemsa-stained slides of the
blood, lymph node aspirations
and CSF will reveal the
trypomastigotes during the
early stages of the disease.
 Aspiration of the chancre or
enlarged lymph nodes may
also reveal the parasites.
Parasites are isolated from the
CSF of patients with CNS
involvement.
 Serologic tests can also be
helpful as well as detection of
the presence of IgM and
proteins in the CSF of patients.
The presence in the serum
and/or CSF of IgM is
considered diagnostic.
-




 Treatment
 Several drugs are available for
the treatment of both East
African and West African
Sleeping Sickness, which
include melarsoprol, suramin,
pentamidine, and eflornithine
(Zeibig, 2013).
 The choice of drug will depend
on whether the patient is
pregnant or not, the age of the
patient, and the stage of the
disease.
 Prevention and Control
 Preventive measures involve
protection against the bite of
the fly.
1. Use of netting and protective
clothing are recommended.
2. Use of fly traps
3. Insecticides may be helpful.
4. Clearing the forest around the
villages are also helpful
measures.
Subphylum Apicomplexa:Plasmodium spp.
 Important Properties and Life Cycle
 Malaria is caused by five
plasmodia species:
- Plasmodium vivax,
- Plasmodium malariae,
- Plasmodium ovale,
- Plasmodium knowlesi, and
- Plasmodium falciparum.








The vector and definitive host
is the female Anopheles
mosquito.
The sexual cycle (sporogony)
occurs primarily in mosquitoes,
and
The asexual cycle (schizogony)
occurs in humans (intermediate
hosts).
The infective stage is the
sporozoite from the saliva of
the biting mosquito, which is
taken up by the liver cells. This
is called the exoerythrocytic
phase.
Multiplication and
differentiation of sporozoites
into merozoites occur during
this stage. P. vivax and P. ovale
produce a latent form (called
hypnozoite or sleeping form) in
the liver, which is the cause of
the relapse or recrudescence
seen in vivax and ovale
malaria.
Merozoites (pathogenic stage)
are released from liver cells and
infect the red blood cells.
The parasite’s life cycle now
enters the erythrocytic phase.
These merozoites multiply and
are eventually released to infect
other red blood cells.
The periodic release of
merozoites causes the typical
recurrent symptoms seen in
malaria patients.
Some merozoites then develop
into microgametocytes (male
gametocytes) and
macrogametocytes (female
gametocytes).
The gametocyte containing red
blood cells are ingested by the
mosquito during feeding.
Sexual reproduction then
ensues.




 Epidemiology and Pathogenesis
 Infection with plasmodia occurs
worldwide.
 It occurs primarily in tropical and
subtropical areas, especially in
Asia, Africa, and Central and South
America. Sixty nine percent (69%)
of cases in the Philippines are due
to Plasmodium falciparum while
the remaining 31% are due to

Plasmodium vivax (World Malaria
Report 2013).
The primary vector is Anopheles
flavirostris, which breeds in clear,
slow flowing streams near foot
hills and forests.
In the 2014 Asia Pacific Malaria
Elimination Network (APMEN) VI
held in Makati City, Philippines.
Secretary of Health Doctor
Enrique Ona reported an 83%
reduction in malaria cases from
2005 to 2013, with a 92% decrease
in malarial deaths.
Secretary Ona also reported that of
53 known provinces that are
endemic for the disease, 27 have
already been declared malaria free,
which are:
- Cavite
- Batangas
- Marinduque
- Catanduanes
- Alba
- Masbate
- Sorsogon
- Camarines Sur
- Iloilo
- Aklan
- Capiz
- Guimaras
- Bohol
- Cebu
- Siquijor
- Western Samar
- Eastern Samar
- Northern Samar
- Northern Leyte
- Southern Leyte
- Biliran
- Camiguin
- Surigao del Norte
- Benguet
- Romblon
- Batanes
- Dinagat Islands.
The main mode of transmission of
malaria is the bite of the female
mosquito vector.









The parasite can also be
transmitted through blood
transfusion (transfusion malaria),
intravenous drug abuse with
sharing of IV needles (“main line
malaria”), and transplacental
transmission (congenital malaria).
Most of the pathologic findings
result from the destruction of red
blood cells.
P. falciparum and P. knowlesi can
infect both young and old red
blood cells leading to high levels of
parasitemia.
P. vivax and P. ovale mainly infects
young red blood cells,
while P. malariae infects old red
blood cells.
Plasmodium knowlesi is a natural
parasite of macaque monkeys
throughout the Southeast Asia
region.
Cases of infection have been noted
in Thailand, Singapore, Brunei,
Indonesia, Myanmar, Vietnam, and
the Philippines (Murray, 2014).
The red blood cells infected by P.
knowlesi have normal morphology.
All developmental stages of the
parasite may be seen in the
peripheral blood.










 Disease: Malaria
 Paroxysms of malaria are divided
into three stages:
1. cold stage
2. hot stage, and
3. the sweating stage.
These paroxysms are considered
partially as allergic responses to the
schizonts and to the antigens
released following the release of
the merozoites.
A malarial paroxysm presents with
abrupt onset of chills (rigors)
accompanied by headache, muscle
pain (myalgia), and joint pains
(arthralgia).
This stage lasts for approximately
10–15 minutes or longer.
Spiking fever lasting 2–6 hours
follows, reaching up to 41 °C,
accompanied by shaking chills,
nausea, vomiting, and abdominal
pain. This is then followed by
drenching sweats.
Patients usually feel well between
febrile episodes. Splenomegalyis
often present and anemia is
prominent.
The timing of the fever cycle is 72
hours for P. malariae, in which
symptoms recur every 4th day
(quartan malaria).
Malaria caused by P. vivax, P.
ovale, and P. falciparum recure
every 3rd day (tertian malaria).
P. falciparum causes malignant
tertian malaria since it causes
severe infection which is
potentially life threatening due to
extensive brain (cerebral malaria)
and kidney damage.
The dark color of the patient’s
urine is due to kidney damage
giving rise to the term “black water
fever.”
P. vivax and P. ovale cause benign
tertian malaria that is characterized
by relapses that can occur up to
several years after the initial illness
and is due to the latent hypnozoites
in the liver.

Most cases of P. knowlesi infection
resembles infection in patients by
other malarial parasites. A small
number of cases of patients
develops severe infection.
 The severity of the infection is due
to the high parasitemia levels
produced due to its ability to infect
all stages of red blood cells and its
24 hour erythrocyte cycle
(quotidian malaria).
 Laboratory Diagnosis
 The diagnosis of malaria is based
on examination of Giemsa stained
or Wright stained thick and thin
smears of the blood.
 The thick blood smears are used for
screening purposes
 The thin blood smears are used to
differentiate the various
Plasmodium species.
 The best time to take blood films is
midway between paroxysms of
chills and fevers or before the onset
of fever.
 This is the time when the greatest
number of intracellular organisms
are present.
 Characteristic trophozoites will be
seen within the infected red blood
cells. P. falciparum will show
characteristic crescent shaped or
banana shaped gametocytes.
 Infection with P. falciparum is
highly considered if there are > 10
infected red blood cells consisting
only of ring forms.
 For P. malariae and P. knowlesi,
demonstration of the characteristic
rosette schizont is diagnostic.
 P. knowlesi should be suspected if
there is a higher average merozoite
count of 16/red blood cell as
compared to 10–12/red blood cell
of P. malariae.
 The presence of early trophozoite
forms and two to three parasites per
red blood cell (similar to P.
falciparum) is more suggestive of
P. knowlesi infection.
 Treatment
 chloroquine or parenteral quinine The drugs of choice for acute
malaria infection.
 Chloroquine does not affect the
hypnozoites of P. vivax and P.
ovale. For vivax and ovale malaria,
 Primaquine is given to destroy the
hypnozoites. For chloroquine
resistant strains of P. falciparum
 Other agents may be used
including mefloquine + artesunate,
artemether lumafantrine,
atovaquone proguanil, quinine,
quinidine, pyrimethamine
sulfadoxine (Fansidar), and
doxycycline (Murray, 2014).
 Artemisin based combination
therapies (ACTs) are now
recommended for uncomplicated
malaria and for chloroquine
resistant vivax malaria.
 Artesunate is the drug of choice for
severe malaria, in combination
with either amodiaquine,
mefloquine, or sulfadoxine
pyrimethamine.
 P. knowlesi infection is managed
similar to P. falciparum due to its
potential to produce severe
infection
 Prevention and Control
 Chemoprophylaxis of malaria for
travelers to endemic areas consists
of mefloquine or doxycycline.
1. Travelers to areas where the
other plasmodia are found
should take chloroquine
starting two weeks before
arrival and continued for 6
weeks after departure,
followed by a 2-week course
of primaquine if exposure
was high.
 Other preventive measures include:


2. Avoidance of the bite of the
vector through the use of
mosquito netting
3. Window screens
4. Protective clothing, and
5. insect repellants.
The mosquitoes usually bite from
dusk to dawn, so protection is
important during the night.
Reduction of mosquito population
is also helpful, including the use of
insecticide sprays, as well as
drainage of stagnant water in
swamps and ditches.
Phylum Apicomplexa:Toxoplasma gondii
 Important Properties and Life Cycle
 The definitive host of the parasite
is the domestic cat or other felines
 Humans and other mammals serve
as the intermediate hosts.
 The parasite develops in the
intestinal cells of the cat and passes
to the tissues through the
bloodstream. These are then passed
in the cat’s feces and mature into
infective oocysts in the external
environment.
 Infection in humans begins with
the ingestion of oocysts (infective
form) in undercooked meat or from
contact with cat feces.
 In the small intestines, the oocysts
rupture into trophozoites
(tachyzoites or bradyzoites).
 Tachyzoites are the rapidly
multiplying forms responsible for
the initial infection
 Bradyzoites are shorter, slow
growing forms seen in chronic
infections.
 Epidemiology and Pathogenesis
 Infection by T. gondii occurs
worldwide.
 Infection is usually sporadic but
outbreaks associated with ingestion
of raw meat or contaminated water
can occur.
 Individuals who are severely
immunocompromised are more
likely to develop severe disease.
 The parasite can be transmitted in
two ways:
1. ingestion of improperly
cooked meat of animals that
serve as intermediate hosts,
and
2. ingestion of oocyst from
contaminated water.
 Transplacental transmission may
occur:
1. with severe
consequences on the
fetus.
2. Sharing of needles by
IV drug abusers
3. blood transfusion are
less common modes
of transmission of the
parasite.
 Disease: Toxoplasmosis
1. Infection in immunocompetent
individuals
- usually asymptomatic.
- Acute infection may
manifest non specific
symptoms such as chills,
fever, headache, and
fatigue. This may be
accompanied by
inflammation of lymph
nodes (lymphadenitis).
- Chronic infection may
manifest with
lymphadenitis, hepatitis,
myocarditis, and
encephalomyelitis.
Chorioretinitis leading to
blindness may also occur
2. Congenital infection
- occurs in infants born to
mothers who were infected
during pregnancy.
- The manifestations vary
depending on when the
infection was acquired.
- Infection during the first
trimester of pregnancy may
result to miscarriage,
stillbirth, or severe
infection (encephalitis,
microcephaly,
hydrocephalus,mental
retardation, pneumonia).
- If the infant acquires the
infection during the last
trimester, symptoms may
not develop until months to
years after delivery.
- The most common
manifestation is
chorioretinitis with or
without blindness.
3. Infection in
immunocompromised hosts
- usually manifest with
neurologic symptoms
similar to patients with
diffuse encephalopathy,
meningoencephalitis, or
brain tumors.
- Reactivation of latent
toxoplasma infection is
common. Other sites of
infection include the lungs,
eye, and testes.
 Laboratory Diagnosis
 Demonstration of high antibody
titers through immunofluorescence
assay is essential for the diagnosis
of toxoplasma infection.
 Microscopic examination of
Giemsa stained preparations will
show the crescent shaped
trophozoites during the acute
infection. Cysts may be seen in the
tissues.
 Prenatal diagnosis can be done
through ultrasonography and
amniocentesis with PCR analysis
of the amniotic fluid (method of
choice).
 Treatment
 Infection in immunocompetent
hosts is usually self-limiting and
does not require specific therapy.
The regimen of choice for
immunocompromised patients,
especially those with AIDS, is
initial high dose pyrimethamine
plus sulfadiazine given for an
indefinite period.
 Alternative regimen for those who
develop symptoms of drug toxicity
is clindamycin plus
pyrimethamine.
 For pregnant women, clindamycin
or spiramycin may be given.
 Prevention and Control
1. The most effective preventive
measure is through adequate
cooking of meat.
2. Pregnant women should refrain
from eating undercooked meat
3. Should avoid contact with cats
and refrain from handling litter
boxes. Cats should not be fed
raw meat.
Microbiology and parasitology Final lecture







Cestodes
 General Properties of Cestodes
 Cestodes are classified under the
subkingdom Metazoa, phylum
Platyhelminthes.
 These parasites are considered as
primitive worms.
 They do not possess a digestive
system nor a nervous system.
 They absorb nutrients and
eliminate waste products through
their outer surface called the
tegument. Commonly known as
tapeworms
 These parasites are flat and consist
of three distinct regions—the head,
neck, and body (proglottids).
 The head contains an organ of
attachment called the scolex, which
may consist of either hooks,
suckers, or sucking grooves.
 In some species, the scolex has a
fleshy extension called a rostellum
to which hooks may be attached.





The body is divided into multiple
segments (hence, the name
tapeworm) called proglottids.
A series of proglottids is called
strobila (plural strobili).
All cestodes are hermaphroditic
(self fertilizing) with each
proglottid containing both male
and female reproductive organs.
Each proglottid, therefore, is
capable of laying eggs (now called
a pregnant proglottid or gravid
segment).
The neck serves as the region of
growth and connects the head to
the body of the worm.
The worm grows by adding new
proglottids from the neck. The
oldest proglottids are found at the
most distal part of the body of the
parasite.
A typical cestode life cycle is
divided into three stages:
- Egg
- Larva
- adult worm.
For the majority of cestodes, the
egg contains an embryo called the
oncosphere, which represents the
first larval or motile stage.
It is equipped with small hooks
(called hooklets) that eventually
enable the parasite to pierce the
wall of the intestines.
The eggs are excreted in the feces
of infected hosts and are
transmitted to the intermediate
hosts (cattle, pig, or fish).
Infection in humans is usually
acquired through ingestion of the
undercooked or raw flesh of the
intermediate host containing the
infective larvae.
After ingestion, the ingested larvae
are transformed into adult worms
in the intestines of the infected
host.

The adult worm then undergoes
self-impregnation with the gravid
segment rupturing to release the
eggs in the intestines. These eggs
are then passed out to the external
environment during defecation.
Intestinal Cestodes
Taenia saginata (Beef Tapeworm)
 Important Properties and Life Cycle
 The intermediate host is cattle
where the eggs enter the blood
vessels within the cattle’s
intestines.
 The eggs are then transported to the
skeletal muscles of the cattle where
they develop into cysticerci
(larvae).
 Infection with the beef tapeworm is
acquired by ingestion of
improperly cooked or raw beef
containing the infective larva
(called cysticercus).
 These larvae then mature into adult
worms (pathogenic stage) in the
small intestines within a period of
approximately three months.
 These tapeworms are known to
achieve a length of as much as 10
meters. Humans serve as the
definitive hosts.
 The eggs of Taenia saginata are
usually indistinguishable from the
eggs of the pork tapeworm Taenia
solium.
 Both species may be differentiated
by the appearance of their scolices
and the structures of their
proglottids.
 The scolex of Taenia solium
contains a rostellum while that of
Taenia saginata does not. Taenia
saginata proglottid is rectangular
and contains more uterine branches
(about 15–30) in comparison with
Taenia solium which is square in
appearance containing about 7–15
uterine branches.
 Epidemiology and Pathogenesis
 Taenia saginata infection is
common in areas of the world
where beef is routinely eaten,
especially undercooked beef.
 It has been found to be endemic in
Eastern Europe, Russia, Eastern
Africa, and Latin America (Centers
for Disease Control and
Prevention).
 The adult worms do not produce
significant damage in the small
intestines.
 Disease: Taeniasis
 Majority of patients are
asymptomatic. Those with high
worm burden may complain of
diarrhea, abdominal pain, loss of
appetite with resultant weight loss,
and body malaise.
 The gravid proglottids may reach
the anus where egg laying may
occur resulting in itchiness in the
anal region (pruritus ani).
 Laboratory Diagnosis
 Examination of fecal specimen
from infected patients is the
procedure of choice.
 Eggs or gravid proglottids may be
recovered from the stool although
eggs are less often found than the
proglottids
 Treatment
 Praziquantel- The drug of choice
against the adult worm
 Prevention and Control
1. Proper waste disposal and
sanitation practices as well as
the adequate cooking of beef
are the main preventive
measures for taeniasis.
2. Freezing of beef meat for
approximately 10 days may
kill the encysted larvae.
Prompt treatment of infected
persons help prevent spread
of the disease.
Taenia solium (Pork Tapeworm)
 Important Properties and Life Cycle
 Infection with the pork tapeworm
is acquired through ingestion of
improperly cooked or raw pork
meat which contains the infective
larva called cysticercus cellulosae.
 Unlike the beef tapeworm, Taenia
solium infection can also occur
following the ingestion of food or
water contaminated with human
feces that contain the eggs of the
parasite.
 Therefore, unlike the beef
tapeworm, Taenia solium has two
infective stages
- eggs
- larvae
 Autoinfection may also occur.
 Pigs serve as the intermediate host
while humans serve as both
intermediate and definitive hosts.
 There are two scenarios that can
occur depending on which infective
stage entered the human host.
 In cases where infection is acquired
through ingestion of undercooked
or raw pork meat, the infective
stage is the larval form which
transforms into adult worm in the
intestines of infected individuals.
In this instance, humans serve as
the definitive hosts.
 On the other hand, ingested worm
eggs hatch in the small intestines,
burrow through the wall of the
intestines into a blood vessel, and
disseminate to various organs. In
this instance, humans serve as
intermediate hosts.
 Epidemiology and Pathogenesis
 T. solium infection is more
prevalent in underdeveloped
communities with poor sanitation
and where people eat raw or
undercooked pork.
 Higher rates of illness have been
seen in people in Latin America,
Eastern Europe, sub–Saharan
Africa, India, and Asia (Centers for
Disease Control and Prevention).
 Adult worms produce little damage
in the intestines.
 Encysted larvae may produce
damage in the tissues where they
disseminate. For instance, in the
brain, they may manifest as space
occupying lesions. Although the
larvae may encyst in various
tissues of the body, they evoke
little inflammatory response.
 When the encysted larvae die, they
may release substances that may
induce an allergic reaction in the
host which may potentially be fatal
due to the development of
anaphylactic shock.
 Disease
1. Taeniasis
- the disease produced by the
adult worm.
- Most cases are
asymptomatic but in the
presence of high worm
burden, manifestations
may be similar to beef
tapeworm infection.
2. Cysticercosis
- the result of larval
encystation in various
tissues of the body. The
most common involvement
is that of the skeletal
muscles where patients
may complain of muscle
pain.
- Cyticercosis of the brain
(neurocysticercosis) is the
most feared and most
severe involvement.
- It may present with
symptoms associated with
increased intracranial
pressure such as seizures,
headache, and vomiting.
- Ocular cysticercosis may
lead to visual disturbances
due to development of
inflammation of the uvea
(uveitis) and retina
(retinitis).
 Laboratory Diagnosis
 Microscopic examination of stool
specimen from infected persons is
the diagnostic procedure of choice
in patients with taeniasis.
Demonstration of ova or
proglottids may help establish the
diagnosis.
 The demonstration of the typical
morphology of the scolex can
differentiate pork tapeworm from
beef tapeworm. For cysticercosis,
diagnostic procedure depends on
demonstration of the cyst in tissue,
through biopsy or CT scan.
 Treatment
 Praziquantel - The drug of choice
for treatment of intestinal infection
 For cysticercosis, praziquantel may
also be effective but it is usually
not recommended for ocular and
CNS involvement.
 Alternative drugs include
albendazole, paromomycin, and
quinacrine hydrochloride.
 Surgical removal of the larvae may
be necessary.
 Cases of neurocysticercosis- Anti
convulsants may be given,
 Prevention and Control
 Important preventive measures for
pork tapeworm infection are the
same as that for beef tapeworm and
include:
1. proper waste disposal
2. sanitary measures thorough
cooking of pork meat, and the
prompt treatment of infected
persons to prevent the spread
of the parasite.
Diphyllobothrium latum (Broad Fish
Tapeworm)
 Important Properties and Life Cycle
 The longest of the tapeworms, the
fish tapeworm can reach a length of
about 13 meters.
 Its eggs consist of ciliated larvae
called coracidia (s. coracidium).
 One end of the egg is occupied by a
lid structure called an operculum.







Its scolex contains a pair of long
sucking grooves.
The gravid segments contain a
uterine structure that is centrally
located and assumes a rosette
formation.
Human infection with D. latum is
through ingestion of improperly
cooked or raw fish containing the
plerocercoid (infective stage), the
precursor larval stage.
After ingestion, the plerocercoid
attaches to the intestinal mucosa
and matures into the adult worm.
The adult worm self-fertilizes and
the eggs are passed out with the
stool. If the eggs come to contact
with fresh water, the coracidium
hatches and is ingested by the first
intermediate host, a tiny crustacean
called a copepod (Cyclops sp.).
After ingestion, the coracidium
develops into the larval stage called
the procercoid.
The copepod is then eaten by a
freshwater fish (second
intermediate host) where the
procercoid develops into the
plerocercoid.
Definitive hosts for the parasites
are humans and other fish eating
mammals such as dogs, cats, bears,
and seals.





 Epidemiology and Pathogenesis
D. latum infection occurs in
countries where raw freshwater fish
is consumed.
 Little damage is produced in the
small intestines of the human hosts.
In some individuals, the parasite
may compete with the host for
vitamin B12, leading to a
deficiency of this vitamin.
Disease: Diphyllobothriasis
1. Asymptomatic disease – the
most common presentation
among most individuals infected
with the parasite.
2. Diphyllobothriasis– may
manifest with symptoms of
gastrointestinal involvement,
which may include diarrhea and
abdominal discomfort. When the
adult worm attaches itself to the
jejunum and ileum, the patient
may develop deficiency of
vitamin B12, leading to anemia
similar to pernicious anemia and
is characterized as megaloblastic
anemia resulting from lack of
maturation of red blood cells.
Laboratory Diagnosis
 Diagnosis is based on finding of
the characteristic eggs and/or the
proglottids (less frequent) in a stool
specimen.
Treatment
 The drug of choice for the
treatment of diphyllobothriasis is
praziquantel.
 An alternative drug is niclosamide.
Prevention and Control
 Preventive measures include:
1. Proper sanitary procedures,
thorough cooking of fish prior
to consumption, and the
prompt treatment of infected
individuals to
2. Prevent spread of the parasite.
Freezing of the fish for 24–48
hours at –18 °C can kill all
larvae.
Hymenolepis nana (Dwarf Tapeworm)
 Important Properties and Life Cycle
 H. nana is different from the other
tapeworms because it does not
require an obligatory intermediate
animal host.
 The eggs are directly infectious
and humans get the infection after
the accidental ingestion of the eggs
of the parasite.
 This may occur after ingestion of
fecally contaminated food or water.
One may also acquire the eggs by
touching one’s mouth with
contaminated fingers or through
ingestion of contaminated soil.
 Accidental ingestion of rice or
flour beetles containing the
infective larvae and that may have
gotten into food is another way by
which the infection may be
acquired.
 Rodents serve as additional source
of infection.
 Once the eggs (infective stage)
gain entrance into the human host
after ingestion of contaminated
food and water, the eggs transform
into cysticercoid larvae.
 The larvae mature into adult worms
capable of self-reproduction.
 Eggs are released after
disintegration of the gravid
segments.
 There are two pathways for the
eggs
- the eggs may be passed to
the outside environment
through the feces or some
of the eggs may remain
inside the human host.
- Those that remain inside
the human host hatch into
larvae and mature into
adult worms, thereby
starting a new cycle within
the human host. This type
of re infection is called
autoinfection.
 Epidemiology and Pathogenesis
 The dwarf tapeworm is the most
common tapeworm recovered in
the United States.
 It has a worldwide distribution and
is also found in East Asia and the
Philippines.
 It is common in areas with
inadequate sanitation and hygiene.
Children and persons living in
crowded areas are at risk of
developing infection.
 The parasite produces little damage
in the small intestines
 Disease: Hymenolepiasis
 Most patients are asymptomatic. In
cases of high worm burden,
patients may complain of :
- Nausea
- Weakness
- loss of appetite
- diarrhea, and
- abdominal pain.
- In young children with
heavy infection, anal
itchiness (pruritus ani) may
occur leading to headaches
due to difficulty sleeping.
 It can be confused with a pinworm
infection. Autoinfection may lead
to hyper infection syndrome which
can result in secondary bacterial
infection and spread of the worms
to other tissues of the body.
 Laboratory Diagnosis
 Diagnosis is established by finding
of the characteristic eggs in stool
specimen.
 Treatment
 Praziquantel is the drug of choice.
 Niclosamide can be an alternative
drug.
 Prevention and Control
 Important preventive measures
include:
1. Proper hygiene
2. Waste disposal
3. control of transport host
population
4. Rodent control
5. Proper storage of grains
6. Flour must be observed to
prevent infestation with
flour and grain beetles.
7. Prompt treatment of
infected individuals must
be instituted to prevent the
spread of the parasite.



and water contaminated by dog
feces or through contact with
contaminated dog feces.
Eggs transform into larvae in the
intestines, penetrate the intestines,
and migrate through the
bloodstream to different tissues in
the body, particularly the liver
and the lungs.
The hydatid cyst (pathogenic stage)
then develops in the infected
tissues.
Dogs acquire the parasite by eating
the visceral organs of the
intermediate host.
Extra Intestinal Cestode
Echinococcus granulosus (Dog Tapeworm
or Hydatid Tapeworm)
 Important Properties and Life Cycle
 Infection with E. granulosus is
primarily a zoonotic type of
infection.
 Dogs are the most important
definitive hosts
 Sheep are usually the intermediate
hosts.
 Humans are considered as
accidental and dead end hosts.
 The eggs of E. granulosus are
identical to those of Taenia spp.
and are thus not diagnostic.
 The diagnostic stage of the parasite
is its larval form, which is encased
in a cyst wall and is called the
hydatid cyst.
 Infection is acquired after ingestion
of eggs (infective stage) from food
 Epidemiology and Pathogenesis
 E. granulosus infection is common
in Africa, Europe, Asia, the Middle
East, Central and South America,
and in rare cases, North America
(Center for Disease Control and
Prevention).
 The embryos develop into large,
fluid filled hydatid cysts, which act
as space occupying lesions.
 In addition, the cyst fluid contains
antigens that can sensitize the host.
Rupture of the cyst, either
spontaneously or during trauma or
surgical removal, may lead to the
release of these antigens leading to
anaphylaxis and widespread
dissemination of the parasite.
 Disease: Echinococcosis, Hydatid
Cyst Disease, Hydatid Disease,
Hydatidosis

Most patients are asymptomatic
during the early stages of the
disease. However, as the cysts
enlarge, necrosis of the infected
tissues occur.
 Involvement of the liver may result
in obstructive jaundice.
 Patients with lung involvement
may manifest with cough, chest
pain, and shortness of breath.
 Other organs that may be infected
include the spleen, kidneys, heart,
bone, and central nervous system,
including the brain and eyes
(Center for Disease Control and
Prevention).
 Cyst rupture may lead to
anaphylactic shock leading to death
of the patient.
 Laboratory Diagnosis
 There are several ways by which E.
granulosus infection can be
diagnosed. These include:
1. examination of biopsy
specimen;
2. serologic tests (e.g., ELISA
or indirect
hemagglutination test); and
3. radiography to demonstrate
the hydatid cysts (e.g., CT
scan or ultrasound).
 Care should be exercised when
doing biopsy to prevent rupture of
the cyst.
 Treatment
 In cases when surgery is possible,
removal of the cyst has been
considered as the treatment of
choice. However, medical
management alone may prove
effective, especially if the cyst is
located in inaccessible areas.
 Drugs that have been proven
effective include mebendazole,
albendazole, and praziquantel.
 Prevention and Control
1. Improvement of personal
hygiene practices
2. prevention of
contamination of food and
water with dog feces
3. avoidance of feeding pet
dogs with contaminated
viscera
4. the prompt treatment of
infected canines and
humans are some measures
to prevent the spread of the
parasite.
5. Chemoprophylaxis should
be given to dogs in endemic
areas.
6. Health education is
essential.