INTRODUCTION TO PARASITOLOGY POSSIBLE SOURCES OF PARASITIC

INFECTIONS
Parasite 1. Soil
- Greek words: “para” = near & “sites” = a. Embryonated eggs which are present in
food soil may be ingested, e.g. roundworm,
- a living organism which for the purpose of whipworm.
procuring food & shelter take up their b. Infective larvae present in soil may enter
abode temporarily, on or within another by penetrating exposed skin, e.g.
living organism hookworm
- the one organism, usually the physically 2. Water
smaller of the two (the parasite) benefits a. Infective forms present in water may be
and the other (the host) is harmed swallowed
- This relationship can be loose or mostly b. Water containing the intermediate host
intimate, and for the parasite, it is usually may be swallowed
obligatory. c. Infective larvae in water may enter by
penetrating exposed skin
Macroparasites - multicellular parasites d. Free-living parasites in water may enter
that are visible to the naked human eye, through vulnerable sites such as the
such as helminth parasites (parasitic nasopharynx
worms, such as flukes, tapeworms, and 3. Food
roundworms, or nematodes). a. Contamination with human or animal
feces
b. Meat containing infective larvae
4. Insect Vectors
i. Biological vectors
a. Mosquito—malaria, filariasis
Microparasites - small, generally, b. Sandflies—kala-azar
unicellular and invisible to the naked eye, c. Tsetse flies—sleeping sickness
such as protozoan parasites. d. Reduviid bugs—Chagas’ disease
e. Ticks—Babesiosis
ii. Mechanical vectors
a. Housefly—amoebiasis
5. Animals
i. Domestic
a. Cow, e.g. beef tapeworm, sarcocystis.
The parasite causes harm to the host in b. Pig, e.g. pork tapeworm, Trichinella
many ways: spiralis
1. depriving the host of digested food; c. Dog, e.g. hydatid disease, leishmaniasis
2. erecting mechanical blockades of food, d. Cat, e.g. toxoplasmosis, opisthorchis
blood, lymph, and bile passages; and ii. Wild
3. causing tissue damages by rupture, a. Wild game animals, e.g.
enzymatic digestion, induction of autolysis, trypanosomiasis.
or secretion of toxins. b. Wild felines, e.g. Paragonimus
westermani
iii. Fish, e.g. fish tapeworm 4) INTERMITTENT PARASITE
iv. Molluscs, e.g. liver flukes - visits and leaves their hosts at intervals
v. Copepods, e.g. guinea worm like that during its feeding time, a.k.a.
6. Other Persons temporary parasite
Carriers and patients - leeches, bed bugs visit their host only for
7. Self (autoinfection) a short period of time
a. Finger to mouth transmission
b. Internal reinfection CLASSIFICATION BASED ON
PATHOGENICITY
KINDS OF PARASITES 1) Pathogenic – capable of causing disease
1) ECTOPARASITE 2) Non-pathogenic - incapable of causing
- lives on surface of the host disease
- have elaborate mechanisms and
strategies for finding hosts
- some aquatic leeches, e.g., locate hosts by
sensing movement and then confirm their
identity through skin temperature and
chemical cues before attaching
Examples: Ticks, Lice, Leeches, Mites &
Fleas
2) ENDOPARASITE
- lives within the host
- many endoparasites acquire hosts
through entrance of the tissue, as well as
through consumption of raw foods
Examples: Roundworms & Tapeworms in
the Gut

CLASSIFICATION BASED ON THE NEEDS

FOR A HOST
1) OBLIGATORY PARASITE
- majority of parasites are obligatory
parasites and are totally dependent on the
host for food, shelter, and/or protection;
- they cannot survive without the host
2) FACULTATIVE PARASITE
– one capable of choosing either a free-
living or a parasitic existence
3) SPURIOUS PARASITE
- a parasite of another animal which pass
through the human body without further
development or without causing any injury
or damage
CLASSIFICATION BASED ON WHERE THEY
ARE FOUND
1) Coprophilic parasite – able to live and
multiply in moist fecal matter outside the
body
2) Hematozoic parasite – a parasite living
inside a red blood cell
3) Cytozoic Parasite – a parasite living
inside the cell or tissue
4) Coelozoic parasite – the parasite living in
body cavities
5) Enterozoic parasite – the parasite living
inside the lumen of the intestines
OTHER TERMS
1) HYPERPARASITEOR SECONDARY
PARASITE
- parasite within a parasite; i.e. malaria in
mosquitoes, tapeworm larvae in fleas.
- sometimes referred to as
"hyperparasitoidism"
2) PSEUDOPARASITE
- an object that is mistaken for a parasite
3) WANDERING OR ABBERANT PARASITE
- one which is never transmitted from man
to man & which develops abnormally in
man.
- instead of arriving at the site of infection
in the definitive host, reach an unusual
place as a dead end, becoming unable to
complete the life cycle. For example, the
tapeworm Taenia solium may migrate to
the brain and remain there unless removed
via an operation.
4) MONOXENOUS – these parasites have
only one host, rest of the cycle being spent
outside the host (e.g. Entamoeba
histolytica; a.k.a. monogenic parasites)
5) HETEROXENOUS – these parasites have
two or more hosts, usually belonging to
parasite widely separated taxonomic
groups (e.g. Taenia, various flukes)
- a.k.a. digenetic parasite needs, in addition
to a primary host, also a secondary host to
complete the entire life cycle. Plasmodium
vivax (malaria parasite) completes its
asexual part of life cycle in people and the
sexual part in the female Anopheles
mosquito.
6) DIOECIOUS – having female & male
reproductive organs in different
individuals; or separate sexes (e.g.
nematodes, schistosomes)
7) MONOECIOUS – having female and male
reproductive organs in same individual;
hermaphroditic (e.g. tapeworms)
VECTORS – transmit parasites from host to
host
a) Biological Vector - essential in the life
cycle of a parasite.
b) Mechanical Vector - unessential in the
life cycle of a parasite (e.g. cysts of
intestinal protozoa carried over to food by
legs of vectors.
c) Anthropophilic Vector – when the vector
prefers human blood when it is available.
d) Zoophilic Vector – when the vector
prefers animal blood when it is available.
ZOONOSIS – literally means “diseases of
animals”
– now used to describe those diseases of
animals, which are transmittable to
humans.
TYPES OF HOSTS
1)DEFINITIVE OR FINAL HOST
- host in which parasite reaches sexual
maturity & reproduces.
- is usually the main host. For digenetic
parasites, it is the host for the adult stage
and for the completion of sexual part of life
cycle.
- e.g. humans (Schistosomes), mosquito
(Plasmodium vivax)
2) INTERMEDIATE HOST/SECONDARY HOST
- Some development in host, but does not
reach sexual maturity; often asexual
stages.
- a temporary environment, but one that is
essential for the completion of a particular
parasite's life cycle.
- true for digenetic parasites
- e.g. snails (Clonorchis sinensis)
3) PARATENIC HOST - an IH in which no
development of the parasite occurs,
although its presence may be required as
an essential link in the completion of the
parasite's life cycle
- e.g. the successive fish hosts that carry
the plerocercoid of D. latum, to larger food
fish eventually eaten by humans or other
final hosts.
4)RESERVOIR HOST
- Non-human animals that serve as sources
of infection to humans.
- It can harbor a pathogen indefinitely with
no ill effects.
- are permissive host alternatives to
definitive hosts, such that the infective
stage can be passed from the host to the
population of the definitive host.
The Roof rat (Rattus rattus) is a reservoir
host of bubonic plague with the oriental rat
fleas that infest them being a prime vector
of the disease.
5)SUSCEPTIBLE HOST - one that is readily
infected by a particular parasite
6)PERMISSIVE HOST - is either a definitive,
intermediate, or accidental host that
allows the parasite to complete its life cycle
in part or the whole.
7)NON-PERMISSIVE HOST - is a host
organism other than a true definitive host,
which receives the parasite but the
parasite finds itself in a dead end.
PHASES OF PARASITISM
- For a parasite to establish itself in its host,
it must undergo various stages/ phases:
i. Contact and entry to the host
ii. Migration of the parasite in the
host to its habitat
iii. Maturation and reproduction
A. Contact & Entry to the Host:
- This involves EXPOSURE (the act/ process
of introduction of the parasite to its host)
from one or more sources as:
1) Contaminated soil – oral ingestion
2) Contaminated water – oral ingestion
3) Food containing the immature infective
stage of the parasite
4) Skin penetration from bites of arthropod
vector or from direct penetration of
infective forms.
5) A domestic or wild animal harboring the
parasite
6) Another person, his clothing, bedding, or
immediate environment which he has
contaminated.
7) Airborne transmission
8) Transplacental (i.e. congenital)
9) Blood transmission
10) One’s self – autoinfection
B. Migration of parasite in the host to its
habitat.
C. Maturation & Reproduction
- involves the parasite’s use of the host’s
nutrients for growth, energy and
multiplication.
Biological Incubation Period
- period related to the development of the
parasite.
- starts w/ the entry of the parasite to its
host & ends as soon as the parasite or their
products can be demonstrated in the feces
or other excreta or in the circulating blood
(parasitemia), by aspiration, biopsy or
other diagnostic procedure.
Clinical Incubation Period
- refers to the interval between exposure &
the earliest evidence of symptoms
produced as a result of the infection (or
infestation).
Infection Epidemiology - the branch of medicine
- is the entry & development or which deals with the incidence,
multiplication of a pathogen in the body of distribution, and possible control of
man or animals. diseases and other factors relating to
Infestation health.
- is the lodgment, development & Epidemiologic studies will:
reproduction of arthropods on the surface ✓ provide info on the prevalence of
of the body or in the clothing of man, or the parasites in a population;
fur of animals. ✓ indicate whether the infections are
endemic, hyperendemic, epidemic &
THE ENVIRONMENT sporadic;
- The presence or absence of a number of ✓ provide clues as to the sources of
biological, chemical & physical factors in exposure; and
the environment directly or indirectly
✓ direct attention to the amount of illness
affects the densities & distribution of
in the community for the application of
parasites. These are:
control/preventive measures
1) Flora – vegetation that serves as food &
• PREVALENCE RATE - the frequency of
shelter for hosts, both definitive &
occurrence of a disease in a population in a
intermediate, greatly influences parasite
certain period of time. It includes old &
population.
new cases; & is usually expressed in %.
2) Fauna – animal population constitute
• INCIDENCE RATE - the frequency of
potential hosts for parasites so that the
occurrence of a disease (involving new
latter can maintain themselves.
cases only) in a popl’n for a certain pd of
3) Water – some infective forms of
time. (%)
parasites are free-swimming & requires
• MORTALITY RATE – expresses the
water to migrate & reach its host.
frequency of deaths among those having
4) Host population density & behavior
the disease in a community. It is expressed
- population densities of transport,
in deaths per 100,000 per year.
intermediate & definitive hosts affect
• MORBIDITY RATE – expresses the
parasite population densities.
frequency of being sick of the disease; & is
5) Influence of Seasons/ Climate/
commonly reported as cases of notifiable
Temperature/ Humidity
disease per 1,000 per year.
• ENDEMIC – when disease in the human
DIAGNOSIS, TREATMENT, PREVENTION
population maintains a relatively steady,
AND CONTROL OF PARASITOSES
moderate level; always present
Diagnosis has 2 methods of approach:
• HYPERENDEMIC – if prevalence is high
1) Clinical (based of medical signs and
• EPIDEMIC – if there is a sharp rise in the
reported symptoms, rather than diagnostic
incidence or an outbreak of considerable
tests)
intensity occurs
2) Laboratory (based significantly on
• SPORADIC – if it appears only occasionally
laboratory reports or test results, rather
in one or at most a few members of the
than the physical examination of the
community.
patient.
• EPIDEMICITY – typically results from
introduction of an agent or a new strain
into a community.
Once accurate specific diagnosis has been
made the following points must be
considered before proceeding with
treatment:
1) severity, duration & intensity of infection
& the probability of reinfection
2) efficacy, availability, toxicity, &
acceptability of the treatment.
- chemotherapy, surgical intervention (e.g.
lesions found in the brain or eye produced
by Cysticercus cellulosae
CONTROL
- of a disease means its restraint
- in the patient = may constitute
symptomatic relief or repression of the
activities of the causative agent but not its
elimination.
PREVENTION
- in public health = a check to sufficiently
remove the likelihood of further
dissemination of an epidemic or to reduce
the prevalence of disease in a population.
- implies interception, so that the
individuals in a community are no longer
exposed to the hazards of the disease.
A prerequisite to control & prevention of
the parasitoses is a clear understanding of
the epidemiology of each causative
organism such as:
a) the distinctive characteristics of the
parasite.
b) the conditions under which it survives
&propagates.
c) the means of exposure & transmission to
man & other hosts.
The practicing physician can contribute to
their control in the following ways:
a) the detection, accurate diagnosis &
evaluation of the clinical importance of the
disease in the patient;
b) adequate treatment of the patient;
c) search for & treatment of other cases in
the patient’s family;
d) determination, if possible, of the source
of the infection, prompt reporting to health
officials;
e) advise to patients & their families as to
how they can avoid further exposure;
f) support& cooperation in community
preventive measures; and
g) education of patients in ways utilizing &
strengthening local health depts.
Methods applicable to the control &
prevention of parasitic diseases are
directed to anyone or all of the
components of parasitism and are
designed to cut a link in the parasitic cycle.
a) Measures directed to the HOST
- prompt examination & treatment of
human cases
b) Measures directed against the PARASITE
- use of synthetic & natural chemical
preparations that are parasiticidal
c) Measures directed against the VECTOR,
RESEVOIR HOSTS, AND OTHER
ENVIRONMENTAL FACTORS
- application of chemicals to eradicate or
kill arthropod vectors.
- application of molluscides on bodies of
fresh to brackish H2O to kill snails.
- control thru environmental sanitation&
sanitary waste disposal.
MODULE 2 HISTORY-ALTERING
MICROORGANISMS
HISTORY-ALTERING MICROBES:
BACTERIA
Thermus aquaticus
• discovered by Thomas Brock in 1969 at
the Yellowstone National Park, USA
• heterotrophic, rod-shaped, immotile,
often filamentous, Gram (-) bacteria
• thermophilic hot spring bacterium
• the DNA polymerase (Taq polymerase)
used in Polymerase Chain Reaction (PCR) is
isolated from this species
→ stable & functional at 95°C through
multiple cycles = unaffected by the
denaturation step employed in the PCR;
incredibly accurate!
Yersinia pestis
• nonmotile, aerobic, Gram (-) bacilli or
coccobacilli
• caused the infamous Plague that killed
millions of people especially in the
Americas, Africa & Eurasia
• may cause five principal forms of plague:
(a) bubonic, (b) septicemic, (c) pneumonic,
(d) meningeal, and (e) pharyngeal plague
Y. pestis on proventricular spines lining the
digestive tract of an Oriental rat flea.
(a)Bubonic Plague
- incubation period: 2-8 days
- patients develop fever, headache, chills,
and weakness and one or more swollen,
painful lymph nodes (buboes)
- bite of an infected flea
- bacteria multiply in a lymph node near the
portal of entry.
(b) Septicemic Plague
- incubation period: poorly-defined; likely
within days of exposure
- patients develop fever, chills, extreme
weakness, abdominal pain, shock, and
possibly bleeding into the skin and other
organs
- bite of an infected flea or from handling
infected animals
- can occur as the first symptom of plague
or may develop from untreated bubonic
plague
(c) Pneumonic Plague
- incubation period: 1-3 days
- patients develop fever, headache,
weakness, and a rapidly developing
pneumonia with shortness of breath, chest
pain, cough, and sometimes bloody or
watery mucous
- from inhalation of infectious droplets or
may develop from untreated bubonic or
septicemic plague after the bacteria spread
to the lungs = person-to-person
transmission
HISTORY-ALTERING MICROBES: BACTERIA
Yersinia pestis
• PPE: long robes, high boots, gloves, hats
& beak-shaped masks
→Why the beak-shaped masks? – space for
natural, aromatic herbs that “filter” the
bad air (miasma)
→Cane = measure of distance from
patients
• Etiology was resolved in 1894 in Hong
Kong by Alexandre Yersin (also contributed
to resolving part of the transmission cycle)
HISTORY-ALTERING MICROBES: FUNGI
Candida albicans
• Yeast, a natural inhabitant of the body
• Overgrowth = Candidiasis
• Common infections:
(a)Vaginal yeast infection
(b) Thrush
(c) Invasive candidiasis
• Not an STI: The balance of yeast could
change as a result of sexual activity but
having sex does not cause infection.
(a)Vaginal candidiasis (or Vaginal yeast
infection)
- hormones, medicines, or changes in the
immune system can make infection more
likely
- Symptoms: itching/soreness, pain during
sexual intercourse, pain/discomfort when
urinating, abnormal vaginal discharge
- Prevention: wearing cotton underwear;
take antibiotics exactly as prescribed
(b) Invasive candidiasis
- a serious infection that can affect the
blood, heart, brain, eyes, bones, and other
parts of the body
- Candidemia, is a common infection in
hospitalized patients
- Symptoms: fever and chills that don’t
improve after antibiotic treatment
- Prevention: antifungal medication, be a
safe patient: speak up & keep hands clean
(c) Thrush: Infections of the mouth, throat
& esophagus
- common in cancer, diabetic, HIV/AIDS
patients and other immunocompromised
- Symptoms: white patches on the inner
cheeks, tongue, roof of the mouth, throat;
redness/soreness; cotton-like feeling in the
mouth, loss of taste, pain while
eating/swallowing, cracking & redness at
the corners of the mouth
- Prevention: maintaining good oral health,
rinsing after inhaled corticosteroids
Penicillium sp.
• Genus of blue or green mold
• Found on foodstuffs, leather and fabrics
•Of economic importance = antibiotic
(penicillin), and cheese production
(a) Antibiotic production
• Penicillium chrysogenum
• it inhibits the bacterial enzymes
responsible for cell wall synthesis in
replicating microorganisms and by
activating other enzymes to break down
the protective wall of the microorganism
(esp. Gram +)
• Penicillins: treatment of throat infections,
syphilis, meningitis, etc.
(b) Cheese production
• Penicillium roqueforti
• Used in making blue cheese
• asexual spores (conidia) are inoculated
into the cheese curd at the beginning of the
cheese-making process
• initially collected from naturally-rotten
bread
• Common spoiling agent in food (e.g.,
bread, fruits)
ACELLULAR ENTITIES: VIRUSES
• acellular parasitic entities
• lack most of the components of cells,
such as organelles, ribosomes, and the
plasma membrane
• not classified within any domain or
kingdom
• vary in their structure, their replication
methods, and in their target hosts
Virions: Very small (~ 20–250nm) virus
particles outside of the cell; the infectious
form of a virus outside the host cell
The shapes and sizes of viruses vary and
are distinct for each family.
Structures:
• nucleic acid core
• outer protein coating or capsid
• outer envelope made of protein and
phospholipid membranes derived from
the host cell (sometimes, notably among
viruses that infect animal cells)
complexity of the host ≠ complexity of the
virion
VIRUS LIFE CYCLE
1. Attachment (adsorption) of the virion to
the host cell
2. Penetration (entry, injection) of the
virion nucleic acid into the host cell
3. Synthesis of virus nucleic acid and
protein by host cell machinery as
redirected by the virus
4. Assembly of capsids and packaging of
viral genomes into new virions
5. Release of new virions from the cell
THE PLAQUE ASSAY
VIRUSES: TOBACCO MOSAIC VIRUS
TMV is usually transmitted from plant to
plant by mechanical means (e.g., worker's
hands, cultivation, etc.)
Symptoms:
• smaller than normal size
• mosaic of dark and light green areas on
foliage
• vein-banding (darker green tissue
following along veins)
• distorted or puckered foliage tips
• necrosis or browning = “mosaic burn”
VIRUSES: THE RABIES VIRUS
• Order Mononegavirales, Rhabdoviridae
Family
• Mature virion appears either as bullet
shaped particles with one rounded and one
flattened end or as bacilliform particles.
• generally acquired from the bite of an
infected animal.
• The domestic dog (Canis familiaris) is the
most important vector but may also occur
in bats, raccoons, skunks, and foxes
TRANSMISSION:
1. Bite of infected rabid animal
2. Contact of saliva with broken skin, with
mucous membrane, or with lesions
3. Corneal transplant

ACELLULAR ENTITIES: VIROIDS & PRIONS
• small, circular, infectious ssRNA
molecules
• differ from viruses: they lack protein
• Size range: 246 to 399
• cause a number of important plant
diseases and can have a severe agricultural
impact
• A few well-studied viroids include
coconut cadang-cadang viroid (246
nucleotides) and potato spindle tuber
viroid (359 nucleotides).
• No viroids are known that infect animals
or microorganisms.
ACELLULAR ENTITIES: VIROIDS
Viroid movement inside plants
• After entry into a plant cell, viroids
replicate either in the nucleus or the
chloroplast.
• Viroids can move between plant cells via
the plasmodesmata.
• On a larger scale, viroids can move
around the plant via the plant vascular
system.
VIROID DISEASE
• Viroid-infected plants can be
symptomless or develop symptoms that
range from mild to lethal.
• Most are growth related, and it is
believed that viroids mimic or in some way
interfere with plant small regulatory RNAs
ACELLULAR ENTITIES: VIROIDS & PRIONS
• The opposite extreme from that of viroids
• infectious agents whose extracellular
form consists entirely of protein = lacks
both DNA and RNA.
• cause several neurological diseases e.g.,
scrapie in sheep, bovine spongiform
encephalopathy (BSE or “mad cow
disease”) in cattle, chronic wasting disease
in deer and elk, and kuru and variant
Creutzfeldt–Jakob disease in humans.
• No prion diseases of plants are known,
although prions have been found in yeast.
• Collectively, animal prion diseases are
known as transmissible spongiform
encephalopathies.
If prions lack nucleic acid, how is prion
protein encoded?
• The host cell itself encodes the prion.
• The host contains a gene, Prnp (“Prion
protein”), which encodes the native form
of the prion, known as PrPC (Prion Protein
Cellular).
• This is primarily found in the neurons of
healthy animals, especially in the brain.
• The pathogenic form of the prion protein
is designated PrPSc (prion protein Scrapie),
because the first prion disease to be
discovered was that of scrapie in sheep.
• PrPSc is identical in amino acid sequence
to PrPC from the same species, but has a
different conformation.
PRIONS: BOVINE SPONGIFORM
ENCEPHALOPATHY
• “mad cow disease”
• progressive neurological disorder of
cattle
• possibly originated as a result of feeding
cattle meat-and-bone meal that contained
BSE-infected products from a
spontaneously occurring case of BSE or
scrapie-infected sheep products.
PRIONS: CREUTZFELDT–JAKOB DISEASE
• rapidly progressive, invariably fatal
neurodegenerative disorder that leads to
dementia
• very rare: 1-2 cases in per million people
each year
SYMPTOMS:
1. Personality changes
2. Memory loss
3. Impaired thinking
4. Blurry vision or blindness
5. Insomnia
6. Problems with coordination
7. Trouble speaking
8. Trouble swallowing
9. Sudden, jerky movements
 f) methods of reproduction.
• The protoplasmic unit that constitute the
organism consists essentially of a nucleus
lying within the cell cytoplasm, &
containing the chromosomes essential for
life, reproduction, & transmission of
genetic constitution of the species.

INTRODUCTION PROTOZOANS

CHARACTERISTICS OF PROTOZOA in the endoplasm = food synthesistakes

• Eukaryotic
• Unicellular
✓mostly 5-250um (0.5um – 7 mm)
✓Few are multicellular but this is a derived
character
• No collagen or chitin in cell walls
• Heterotrophic
✓Ancestral state is non-photosynthetic
✓Few groups are photosynthetic but is a
derived character
• Most are motile (except Apicomplexa:
Plasmodium, Toxoplasma, Gregarines)
place; food is stored in the form of glycogen
or protein called chromatoidal bodies.
ectoplasm = envelopes the cell; functions
as the locomotor apparatusfor the
procurement & ingestion of food, in
respiration, discharge of metabolic wastes
& protection of the organism.
Locomotory organelles arising from the
ectoplasm may vary:
Pseudopodia
– false feet; in amoebae (crawling
movement)
Flagella
– in flagellates; hair-like projections
Cilia
– in ciliates; numerous short threads
distributed over the surface of the body.

Locomotory organelles
- Absorb liquid nutrient from the medium
or ingest bacteria & cells at any site of the
• exhibit considerable variation in
body surface.
a)size and shape
- Others have specialized cell mouth called
b)locomotory organelles
CYTOSTOME usually located in anterior
c)behavior
end of the body.
d)life history
e)nutritional mode
- Ciliates have in addition a cell anus or
CYTOPEGE at the posterior end of the body
and through which particulate food wastes
are discharged.

2) SEXUAL – via: a) syngamy/gametomy or

b) conjugation
a) Syngamy/Gametogony – sexually
differentiated cells called gametes unite
permanently & complete fusion of the
nuclear materials takes place. = zygote
(among sporozoans)

MODES OF REPRODUCTION (ASEXUAL)

1) ASEXUAL – via: a) simple binary fission or
b) schizogony/multiple fission
a) Simple Binary Fission - division into 2
equal parts
✓ In flagellates = longitudinal
✓ In ciliates = transverse

b) Schizogony/multiple fission
- where 2 or more products of division
result
- nucleus of the parent cell 1st undergo
repeated division & then the cytoplasm
collects around them.
b) Conjugation
- e.g. 2 Paramecia (Ciliates) unite along
their oral surfaces, the macronuclei
disintegrate & the micronuclei in each
organism divide twice.
- All the daughter nuclei disintegrate except
one.
2. Enzymatic action of the enclosed
organism on the inner surface of the cyst
wall.
3. Favorable pH & enzymatic action of the
host tissues.

b) Encystation – formation of cyst from

trophozoites
Favorable factors possibly involved in this
process:
1. Deficiency or overabundance of food
supply.
2. Excess of catabolic products of the
organism or of associated bacteria.
3. Marked change in pH.
4. Dessication of the medium.
5. Depletion or excess O2 supply.

In other protozoans, there may be

alternation of generations involving
sexual & asexual developments w/in 1
host or involving 2 or more hosts. This
includes the schizogonic, gametocyte-
gamete production, zygote formation.

TWO BASIC EVENTS IN THE LIFE CYCLE OF

MOST PROTOZOANS

a) Excystation – cyst stage becomes

trophozoites

Favorable factors possibly involved in this

process:
1. Osmotic changes in the medium.
Amoebae Protozoans

Amoeba (Greek word = "to change")

• any of several tiny, one-celled protozoa in
the phylum (or primary division of the
animal kingdom) Sarcodina*.
• Amoebae live in freshwater and salt
water, in soil, and as parasites in moist
body parts of animals.
• Amoebae may have one or more nuclei,
depending upon the species.
• solitary cells that move and capture food
by means of pseudopods, flowing
temporary extensions of the cell.
• Most sarcodines are free living; others
are parasitic.
E. histolytica Protozoans: Amoeba

Entamoeba histolytica

• Feder Losch (1875) in St. Petersburg,

Amoebiasis is more prevalent in the tropics
and subtropics, and in unsanitary places
regardless of climate.
Russia found amoebae in fecal samples but
only regarded them as responsible for
maintaining the inflammatory process, not
as a cause of dysentery.
• Fritz Schaudinn (1903) established the
differentiation between Entamoeba
histolytica and Endamoeba coli, Schaudinn
decided to call it E. histolytica because of
its ability to cause tissue lysis.
• the only species of the different intestinal
amoebae which has the potential for tissue
invasion.

Morphology of cyst:
It is composed of a cytoplasm (cellular
fluid) that is divided into 2 parts:
1.Ectoplasm – a thin, clear, gel-like outer
layer that acts as a membrane
2.Endoplasm – an inner, more watery,
grainy mass containing the organelles
Infectious Dose - Theoretically, the • Food vacuoles: contain
ingestion of one viable cyst can cause an leucocytes-bacteriai may be
infection. RBCs.

the causative agent of amoebiasisandis

globally considered a leading parasitic
cause of human mortality.

Morphology of Trophozoite (vegetative

form):
• 10-60 X 15-30 μ average (20-50
μ)
• Cytoplasm is clearly
differentiated into:
• Ectoplasm: is clear with well • infects predominantly humans other
developed pseudopodia. primates.
• Endoplasm: dense & fine • Diverse mammals (dogs & cats) can
granular enclosing. become infected but usually do not shed
• Nucleus: spherical containing cysts with their feces, thus do not
central karyosome & peripheral contribute significantly to transmission.
evenly distributed small
chromatin dots. Amorphous: changes shape constantly

Contamination is through:
- direct contact with dirty hands or objects.
- fecal contamination of drinking water &
foods.
• Droppings of flies
• Through food handlers
• Sexual contact
• Use of night soil as fertilizer in vegetable
farms.
Cysts survive outside the host in water
and soils, and on foods, especially under
moist conditions on the latter.
Excystation – occurs in the lower portion of
the ileum with the liberation of
trophozoites which may colonize the colon
if conditions are favorable.
- The dehydration of the bowel contents
stimulates encystation (trophozoites to
cysts).
- Cysts are passed out from the host
through the feces.
- Trophozoites can also be passed in
diarrheal stools, but are rapidly destroyed
once outside the body, and if ingested
would not survive exposure to the
gastric environment.
Non-invasive infection – trophozoites
remain confined to the intestinal lumen of
individuals who are thus asymptomatic
carriers and cysts passers (in most cases).
AMEBIASIS: CLINICAL PRESENTATION
• most infections restricted to the lumen of
the intestine (luminal amebiasis) are
asymptomatic.
• AMEBIC COLITIS or INVASIVE
INTESTINAL AMEBIASIS occurs in the
intestinal mucosa.
Symptoms include:
✓ Peritonitis – redness and inflammation of
the lining of the intestine
✓ Perforations – formation of holes
✓ Formation of amebic granulomas
(ameboma)
• AMEBIC LIVER ABSCESS = most common
extraintestinal amebiasis manifestation.

Amoebic abscess in the brain also occurs
which is hematogeneous in origin but
usually arises from or is concomitant with
amoebiasis of the liver or lungs.
Amoebiasis cutis/cutaneous amoebiasis
involves extension of lesions on the skin of
the abdominal cavity & that of the perianal
area.
E. hystolytica: Laboratory Diagnosis
• Microscopic identification of
cysts and trophozoites in the
stool
-Fresh stool
Wet mounts, with or without
iodine stain
Permanently stained
preparations (e.g., trichrome)
-Concentrates from fresh stool
Wet mounts, with or without
iodine stain
*Concentration procedures,
however, are not useful for
demonstrating trophozoites
-aspires or biopsy samples
obtained during colonoscopy or
surgery.
• Serology (IFA, IHA, ELISA)
• Isoenzymes
• Monoclonal antibody (antigen
detection)
• PCR
Symptoms, history and epidemiology are
the keys to diagnosis.
Treatment
• Invasive amebiasis is treated
with a nitroimidazole such as
metronidazole or tinidazole or
Secnidazole and then a luminal
amebicide such as paromomycin
(which is preferred)
• Diloxanide furoate can also be
used in children >2 yr of age.
Tissue:
• Metronidazole
• Tinidazole
• Secnidazole
• Dehydroemetine
• Chloroquine
Bowel lumen:
• Paromomycin
• Iodiquinol
• Diloxanide furoate
Treatment and prevention of E. hystolytica
Metronidazole – penetrates deeper tissues
and destriys amoeba present in liver, brain,
lungs etc. The organism’s metabolism
converts the drug into its lethal form.
A second drug is used to eradicate the
amoeba present in the intestinal lumen
(paromomycin)
Prevention: When traveling to areas where
E. hystolytica is epidemic or endemic.
AVOID drinking water also ice cubes
Filter and boil water
Thoroughly wash unpeeled fruits and raw
vegetables

Prevention & Control

Primary prevention Entamoeba coli

-safe excrete disposal • The complete name is typically used to
-safe water supply avoid confusion with Escherichia coli
-hygiene • It is larger than E. histolytica about 20–
-health education 50 μm with sluggish motility and contains
Secondary ingested bacteria.
-early diagnosis • Non-pathogenic luminal commensal
-treatment amoebae without tissue invasion
PROGNOSIS: • Life cycle is similar to that of E. histolytica
- If diagnosed early & treated but does not have an infective stage and
promptly, the prognosis is good. does not ingest red blood cells.
• Global in its distribution, with the highest
prevalence in regions with inadequate
sanitation, typically in rural areas.

• The nucleus is clearly visible in unstained

films and has a large eccentric karyosome
and thick nuclear membrane lined with
coarse granules of chromatin (A and B).
• Cysts are large, 10–30 μm in size, with a
prominent glycogen mass in the early
stage (immature). The chromatoid bodies
are splinter-like and irregular. The mature
cyst has 8 nuclei (C)
Entamoeba coli: Cyst

Entamoeba coli: Trophozoite

• Blunt-shaped
• 10-50um in size
Endoplasm:
✓Dirty-looking, honeycomb appearance
✓more vacuolated/granular with bacteria,
yeast, debris but NO RBCs
Pseudopodia:
✓Broader and blunter
✓Function more to ingest food
✓Sluggish, non-directional motility
Nucleus:
✓1
✓Thicker, irregular, coarsely granular Entamoeba coli
peripheral chromatin with a large eccentric
karyosome GEOGRAPHICAL DISTRIBUTION:
Cosmopolitan & worldwide. Man is the
most common if not the exclusive source of
human infection.
PATHOGENESIS: E.coli is only a lumen
parasite of the large intestine & is non-
Differential Features of E. histolytica and pathogenic.
E. coli DIAGNOSIS: Definitive diagnosis is the
same as for E.histolytica, i.e. direct fecal
smear for diarrheic stools containing the
trophozoites.
TREATMENT: not necessary since it is non-
pathogenic.
FREE-LIVING AMOEBA
• Comprise a large group of protozoa living
in moist soil, decaying vegetation and in all
types of water, especially water containing
bacteria
• Several species have been observed as
human symbionts without pathological
consequence, although some of them may
result in severe disease.
• Two genera are known to be pathogenic
in man:
1.Naegleria fowleri (brain-eating ameba)
2.Acanthamoeba
1. Naegleria fowleri
History and Distribution
• N. fowleri is named after Fowler, who
along with Carter described it first from
Australia in 1965.
• N. fowleri is a heat-loving (thermophilic)
amoeba that thrives in warm water at low
oxygen tension and is commonly found in
warm freshwater (e.g. lakes, rivers,
• and springs) and soil.
• It is world wide in distribution.
• From 2002 to 2011, 32 infections were
reported in the US, and in India, a total of
17 cases have been reported so far.
Morphology
N .fowleri occurs in 3 forms:
a. Cyst
b. Amoeboid trophozoite form
c. Flagellate trophozoite form
Morphology: Trophozoite Stage
- The trophozoites occur in 2 forms:
amoeboid and flagellate
➢ Amoeboid form
- about 10–20 μm, showing rounded
pseudopodia (lobopodia), a spherical
nucleus with big endosome, and pulsating
vacuoles.
• With electron microscopy, vacuole
appear to be densely granular in contrast
to highly vacuolated body of amoeba and
are called as amoebostomes.
• They are used for engulfing RBCs and
WBCs and vary in number, depending on
the species.
• Amoeboid form is the feeding, growing,
and replicating form of the parasite, seen
in CSF and tissues.
• It is the invasive stage of the parasite and
the infective form of the parasite.
a) Transmission electron micrograph (TEM)
of Naegleria fowleri trophozoites
illustrating the prominent nucleus with a
centrally located electron-dense nucleolus.
(b) Scanning electron micrograph (SEM) of
trophozoites exhibiting ‘food-cups’ (arrow).
➢ Flagellate form
- The biflagellate form occurs when
trophozoites are transferred to distilled
water.
• This transformation of trophozoites to
biflagellate pear-shaped form occurs
within a minute.
• The flagellate can revert to the amoeboid
form, hence N. fowleri is classified as
amoeboflagellate.
• Non-feeding and non-
Dividing
Morphology: Cyst Stage
- Trophozoites encyst due to unfavorable
conditions like food deprivation,
dessication, cold temperature, etc.
- The cyst is 7–10 μm in diameter and has a
smooth double wall.
- They are the resting or the dormant form
and can resist unfavorable conditions,
such as drying and chlorine up to 50 ppm.
- The trophozoites can withstand moderate
heat (45°C), but die at chlorine levels of 2
ppm and salinity of 0.7%.
- Cysts and flagellate forms of N. fowleri
have never been found in tissues of
cerebrospinal fluid (CSF).
Life Cycle
• Typically, infection occurs when people
go swimming or diving in warm freshwater
river or ponds and poorly maintained
swimming pools or nasal irrigation using
• contaminated tap water.
• The life cycle of N. fowleri is completed in
the external environment.
• The trophozoites replicate by promitosis.
• Flagellate form of trophozoite helps in
the spread of N. fowleri to new water
bodies.
• Since the amoeboid form is the invasive
stage, hence, the flagellate forms revert to
amoeboid forms to become infective to
man.
Under unfavorable conditions, it forms a
cyst and which undergoes excystation in
favorable conditions.
Pathogenicity and Clinical Features
• Patients are mostly previously healthy
young adults or children.
• Human infection comes from water
containing the amoebae and usually
follows swimming or diving in ponds.
• The amoebae invade the nasal mucosa
and pass through the olfactory nerve
branches into the meninges, and brain to
initiate an acute purulent meningitis and
encephalitis, called as primary amoebic
meningoencephalitis (PAM).
• The incubation period varies from 2 days
to 2 weeks. In the incubation period, the
patient experiences anosmia.
• The disease advances rapidly, causing
fever, headache, vomiting, stiff neck,
ataxia, seizure, and coma.
• Cranial nerve palsies have also been
documented.
• The disease almost always ends fatally
within a week (average 5 days).
Laboratory Diagnosis
The diagnosis of PAM is based on the
finding of motile Naegleria trophozoites in
wet mounts of freshly-obtained CSF.
Cerebrospinal Fluid Examination
The CSF is cloudy to purulent, with
prominent neutrophilic leucocytosis,
elevated protein, and low glucose,
resembling pyogenic meningitis.
• Wet film examination of CSF may show
trophozoites.
• Cysts are not found in CSF or brain.
• At autopsy, trophozoites can be
demonstrated in brain histologically by
immunofluorescent staining.
Treatment
The drug of choice is amphotericin-B
intravenously. It can also be instilled
directly into the brain.
• Treatment combining miconazole and
sulfadiazine has shown limited success,
only when administered early.
• More than 95% cases of PAM are fatal
despite of treatment.
2. Acanthamoeba
- genus of free-living amoebae
- present almost ubiquitously in the
environment, they are commonly found in
dust, soil and freshwater environments
- they have also been isolated from
swimming pools, cooling towers, air-
conditioning systems and domestic tap
water.
• Mostspecies are free-living bacterivores,
but some are opportuniststhat can cause
infectionsin humans and other animals.
• Approximately, 400 cases have been
reported worldwide.
Acanthamoeba in its two forms:
(A) trophozoite, (B) impenetrable cyst
Morphology
• The trophozoite is large, 20–50 μm in size
and characterized by spine- like
pseudopodia (acanthopodia).
• It differs from Naegleria in not having a
flagellate stage and in forming cysts in
tissues.
CYST
• The dominant, polygonal double- walled
cysts are highly resistant.
• The cysts are present in all types of
environment, all over the world
TROPHOZOITE
• feeding and dividing stage
• cyst forming
Life Cycle
• Both trophozoites and cysts are
infective. Human beings acquire by
inhalation of cyst or trophozoite, ingestion
of cysts, or through traumatized skin or
eyes.
• After inhalation of aerosol or dust
containing trophozoites and cysts, the
trophozoites reach the lungs and from
there, they invade the central nervous
system through the blood stream,
producing granulomatous amoebic
encephalitis (GAE).
Pathogenicity and Clinical Features
• Infection usually occurs in patients with
immunodeficiency, diabetes, malignancies,
malnutrition, systemic lupus
erythematosus (SLE), or alcoholism.
• The parasite spreads hematogenously
into the central nervous system.
• Subsequent invasion of the connective
tissue and induction of proinflammatory
responses lead to neuronal damage that
can be fatal within days.
• A postmortem biopsy reveals severe
edema and hemorrhagic necrosis.
Clinical Disease
It presents chiefly as 2 chronic
conditions—keratitis and encephalitis.
ACANTHAMOEBA KERATITIS
• An infection of the eye that typically
occurs in healthy persons and develops
from the entry of the amoebic cyst
through abrasions on the cornea.
• associated with the use of contact lenses
• Unilateral photophobia, excessive
tearing, redness and foreign body
sensation are the earliest signs and
symptoms; disease is bilateral in some
contact lens users.
• Keratitis and uveitis can result in
permanent visual impairment or blindness.
GRANULOMATOUS AMOEBIC
ENCEPHALITIS(GAE)
• serious infection of the brain and spinal
cord that typically occurs in persons with
a compromised immune system.
• GAE is believed to follow inhalation of the
dried cysts.
• The incubation period is long and the
evolution of the illness is slow.
• Clinical picture is that of intracranial
space-occupying lesions with seizures,
paresis, and mental deterioration.
• Due to the rarity of this parasite and a
lack of knowledge, there are currently no
good diagnoses ortreatmentsfor
Acanthamoeba infection.
Laboratory Diagnosis
• Diagnosis of amoebic keratitis is made by
demonstration of the cyst in corneal
scrapings by wet mount, histology and
culture.
• Diagnosis of GAE is made by
demonstration of trophozoites and cysts
in brain biopsy, culture, and
immunofluorescence microscopy using
monoclonal antibodies.
a. CSF shows lymphocytic pleocytosis,
slightly elevated protein levels, and normal
or slightly decreased glucose levels.
b. CT scan of brain provides inconclusive
findings.
Due to the rarity of this parasite and a lack
of knowledge, there are currently no good
diagnoses or treatmentsfor
Acanthamoeba infection.
FLAGELLATES AND CILIATES
THE FLAGELLATES
• Parasitic protozoa, which possess whip-
like flagella as their organs of locomotion
are called as flagellates and classified as:
Phylum: Sarcomastigophora
Subphylum: Mastigophora
Class: Zoomastigophora (mastix: whip)
• Depending on their habitat, they can be
considered under:
A. Lumen-dwelling flagellates
- in the alimentary tract and urogenital
tract
- have multiple flagella, no kinetoplast
B. Hemoflagellates
- in blood and tissues
- have only 1 flagellum, possess kinetoplast
• Most luminal flagellates are
nonpathogenic commensals.
• Two of them cause clinical diseases:
✓ Giardia lamblia - can cause diarrhea
✓ Trichomonas vaginalis - can produce
vaginitis and urethritis.
Giardia lamblia
• It is one of the earliest protozoan parasite
to have been recorded.
• Formerly Lamblia intestinalis and also
known as Giardia duodenalis and G.
intestinalis.
• Endemicity is very high in areas with low
sanitation, especially tropics and
subtropics
• causes Giardiasis or backpackers fever
“Old man wearing glasses”
Giardia lamblia: Morphology
TROPHOZOITE
- the vegetative form of the parasite
- shape of a tennis racket
- dorsal: convex; ventral: has a concave
sucking disc (helps in its attachment to the
intestinal mucosa)
- The trophozoite is motile, with a slow
oscillation about its long axis, often
resembling a falling leaf
- possess:
• 1 pair of nuclei
• 4 pairs of flagella
• Blepharoplast from which the flagella
arise (4 pairs)
• 1 pair of axostyles (midline)
• 2 sausage-shaped parabasal/median
bodies = transversely posterior to the
sucking disc
• It exists in 2 forms:
A. Trophozoite (vegetative form)
B. Cyst (infective form)
CYST
- the infective form of the parasite
- The cyst is small and oval, measuring 12
μm x 8 μm and is surrounded by a hyaline
cyst wall.
- Its internal structure includes 2 pairs of
nuclei grouped at one end. A young cyst
contains 1 pair of nuclei.
- The axostyle lies diagnonally, forming a
dividing line within cyst wall.
- Remnants of the flagella and the sucking
disc may be seen in the young cyst.
Giardia lamblia: Life Cycle
• Giardia passes its life cycle in 1 host.
• Infective form: Mature cyst
• Infective dose is 10–100 cysts
• There may be 200,000 cysts passed per
gram of feces.
• It does not invade the tissue, but remains
tightly adhered to intestinal epithelium by
means of the sucking disc.
• Mode of transmission:
1.Man acquires infection by ingestion of
cysts in contaminated water and food.
2.Direct person to person transmission
may also occur in children, male
homosexuals, and mentally ill persons.
Giardia lamblia: Transmission
Zoonotic transmission is also possible, and
therefore Giardia infection is a concern for
people camping in the wilderness or
swimming in contaminated streams or
lakes, especially the artificial lakes formed
by Beaver dams (hence the popular name
for giardiasis, "Beaver Fever").
Giardia lamblia: Epidemiology
• Man is the primary host although dogs,
cats, beavers, bears, pigs and monkeys are
also infected and serve as reservoirs.
• In the Philippines, it is the most widely
distributed intestinal flagellate with a
prevalence rate of 5-20%.
• Cysts also survive in water, e.g. in
freshwater lakes & streams
• has occurred as outbreaks from
recreational water sources such as
swimming pools, water parks, & hot tubs,
most likely because of an infected user
rather than a source of water that was
contaminated
Giardia lamblia: Clinical Features
Often, they are asymptomatic but in some
cases may lead to:
• Diarrhea (sudden, explosive and watery)
• Steatorrhea (pale, foul smelling, greasy
stools = fat malabsorption)
• Flatulence
• Stomach cramps
• Nausea
• Bloating, foul sulfuric belching
• Incubation period is variable, but is
usually about 2 weeks
If not treated, giardiasis can last for
months, or even years!
Giardia lamblia: Laboratory Diagnosis
Stool Examination
A. Macroscopic examination: fecal
specimens containing G. lamblia may have
an offensive odor, are pale colored and
fatty, and float in water.
B. Microscopic examination: cysts and
trophozoites can be found in diarrheal
stools by saline and iodine wet
preparations. In asymptomatic carriers,
only the cysts are seen.
Enterotest or String Test
• A coiled thread inside a small weighted
gelatin capsule is swallowed by the
patient, after attaching the free end of the
thread in the cheek.
• The capsule passes through the stomach
to the duodenum.
• After 2 hours, the thread is withdrawn,
placed in saline, and is mechanically
shaken.
• The centrifuged deposit of the saline is
examined for Giardia.
Giardia lamblia: Treatment and Prevention
• Metronidazole (250 mg, thrice daily for
5–7 days) and tinidazole (2 g single dose)
are the drugs of choice.
Giardiasis can be prevented by following
measures:
1. Proper disposal of waste water and
feces.
2. Practice of personal hygiene like
handwashing before eating and proper
disposal of diapers.
3. Prevention of food and water
contamination. Community chlorination of
water is ineffective for inactivating cysts.
4. Boiling of water and filtration by
membrane filters are required.
Trichomonas
• Trichomonas differs from other
flagellates, as they exist only as
trophozoites. Cystic stage is not seen.
• Genus Trichomonas has 3 species, which
occur in humans
1. T. vaginalis - associated with human
pathology and disease
2. T. hominis - non-pathogenic commensal
of the large intestine
3. T. tenax - in the tartar and around the
gums, and in the nasopharynx-geal region;
not pathogenic, but indicative of poor oral
hygiene.
Trichomonas vaginalis
• T. vaginalis was first observed by Donne
(1836) in vaginal secretion.
• Prevalence of trichomoniasis varies from
5% patients at hospitals to 75% in sexual
workers.
MORPHOLOGY
• pear-shaped/ovoid with a short
undulating membrane reaching up to the
middle of the body
• 4 anterior flagella + fifth running along
the outer margin of the undulating
membrane, which is supported at its base
by a flexible rod, costa.
• A prominent axostyle runs throughout
the length of the body and projects
posteriorly like a tail.
• The cytoplasm shows prominent
siderophillic granules, which are most
numerous alongside the axostyle and
costa.
• Motile with jerky or twitching type
movement.
Trichomonas vaginalis: HABITAT
• T. vaginalis, despite its name, infects both
men and women.
•In females the organism inhabits the
vagina.
•In males it is usually found in the urethra,
prostate, seminal vesicles or epididymis.
"strawberry cervix"
Trichomonas vaginalis: LIFE CYCLE
Life cycle of is completed in a single host
either male or female.
Infective form: trophozoite
Incubation period: 10 days
Mode of transmission:
• transmitted directly by sexual
transmission is the usual coexists with
other STDs like candidiasis, gonorrhea,
syphillis, or HIV
• Babies may get infected during birth.
• Fomites such as towels have been
implicated in transmission.
Trichomonas vaginalis: TRICHOMONIASIS
• The epidemiology of trichomoniasis
exhibits features similar to other STDs and
incidence correlates with the number of
sexual partners.
• co-infection with other STDs is common.
- Disease is produced when normal cell
destruction in the infected vagina is unable
to provide glycogen for normal
populations of Bacillus. These bacteria
metabolize glycogen to lactic acid thus
keeping the normal pH acid. With this
change in pH, opportunist bacteria &
trichomonads can survive.
• a "strawberry cervix" due to
trichomoniasis.
• The term "strawberry cervix" is used to
describe the appearance of the cervix due
to the presence of T vaginalis protozoa.
• The cervical mucosa reveals punctate
hemorrhages along with accompanying
vesicles or papules.
Trichomonas vaginalis: DIAGNOSIS &
TREATMENT
DIAGNOSIS
• In females: Direct smear of sedimented
urine vaginal secretions or scrapings
• In males: Direct smear of sedimented
urine & prostatic secretions
TREATMENT
• Simultaneous treatment of both partners
is recommended.
• Metronidazole 2 g orally as a single dose
or 500 mg orally twice a day for 7 days is
the drug of choice.
Chilomastix mesnili
a nonpathogenic intestinal commensal of
humans.
• This occurs as trophozoites and cysts.
• The trophozoite is pear-shaped.
• At the anterior end, it has a spherical
nucleus.
• Distinct spiral groove is seen on one side
of the nucleus.
• The cysts are lemon-shaped surrounded
by a thick cyst wall.
• Both trophozoites and cysts are
demonstrated in the semiformed stool.
• The organism feeds on bacteria and food
debris.
• Since infection is acquired through
ingestion of cysts, prevention depends on
improved personal hygiene.
Chilomastix mesnili: LIFE CYCLE
• Trophozoites live on bacteria found in the
lumen.
• Divides by simple binary fission.
PATHOGENESIS:
- A harmless commensal & does not cause
any symptoms.
DIAGNOSIS/TREATMENT/PREVENTION:
- Direct fecal smear flotation technologies
are applicable. Treatment is not indicated.
Preventive measures follow those for
amoebiasis.
Balantidium coli
•It is the only ciliate protozoan parasite of
humans
•It is the largest protozoan parasite of
humans.
•B. coli resides in the large intestine of
man, pigs, and monkeys.
Balantidium coli: MORPHOLOGY
B. coli occurs in 2 stages – trophozoite and
cyst
Trophozoite
• lives in the large intestine, feeding on cell
debris, bacteria, starch grains, and other
particles.
• Very large ovoid cells, measuring up to
200 μm are sometimes seen
• cell has 2 nuclei—a large kidney-shaped
macronucleus and lying in its concavity a
small micro nucleus
• actively motile and is invasive stage of the
parasite found in dysenteric stool
• The motility of trophozoite is due to the
presence of short delicate cilia over the
entire surface of the body.
Cyst
• The cyst is spherical in shape and
measures 40–60 μm in diameter.
• It is surrounded by a thick and
transparent double-layered wall.
• The cytoplasm is granular. Macronucleus,
micro nucleus, and vacuoles are also
present in the cyst.
• The cyst is the infective stage of B. coli.
• It is found in chronic cases and carriers.
Balantidium coli: LIFE CYCLE
B. coli passes its life cycle in one host only
(monoxenous)
Natural host: Pig.
Accidental host: Man.
Reservoirs: Pig, monkey, and rat.
Infective form: Cyst.
Mode of transmission:
• Balantidiasis is a zoonosis.
• Human beings acquire infection by
ingestion of food and water contaminated
with feces containing the cysts of B. coli.
• Infection is acquired from pigs and other
animal reservoirs or from human carriers.
Balantidium coli: CLINICAL SIGNS
• After ingestion of an infective
Balantidium coli cyst days to weeks may
pass before infection occurs.
• Common symptoms of Balantidiasis:
– chronic diarrhea
– occasional dysentery
– nausea
– foul breath
– colitis
– abdominal pain
– weight loss
– deep intestinal ulcerations
– possibly perforation of the intestine
Balantidium coli: DIAGNOSIS
Stool Examination
• Diagnosis of B. coli infection is
established by demonstration of
trophozoites and cysts in feces.
• Motile trophozoites occur in diarrheic
feces and cysts are found in formed stools.
• The trophozoites can be easily recognized
by their large size, macronucleus, and
rapid-revolving motility.
• The cysts can also be recognized in the
formed stools by their round shape and
presence of large macronucleus.
Biopsy
When stool examination is negative, biopsy
specimens and scrapings from intestinal
ulcers can be examined for presence of
trophozoites and cysts.
Balantidium coli: TREATMENT &
PREVENTION
Treatment
Tetracycline is the drug of choice and is
given 500 mg, 4 times daily for 10 days.
Alternatively Doxycycline can be given.
Prevention
• Avoidance of contamination of food and
water with human or animal feces.
• Prevention of human-pig contact.
• Treatment of infected pigs.
• Treatment of individuals shedding B. coli
cysts.