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Nematode Infections
Clark Cleo B. Badilles

Learning Objectives
To describe several intestinal nematode parasites
To identify their biology, infective stages, their
mode of transmission, pathogenesis, diagnosis,
and epidemiology
To make plans for the prevention and control of
these intestinal nematodes
To familiarize with the morphological structure of
each intestinal nematodes since microscopy is the
main diagnostic technique.
Intestinal Nematodes
Ascaris lumbricoides
== The most common intestinal nematode of man.
== Commonly called “giant round worm”, which
occur frequently in the tropics.
== It is estimated that more than 1 billion
individuals are infected, 70% of whom are from
Asia.
== Is a soil-transmitted helminth, which means that
the soil plays a major role in the development and
transmission of the parasite.
== It causes varying degrees of pathology:
1.) Tissue reaction to the invading larvae
2.) Intestinal irritation to the adult
3.) Other complications due to the extraintestinal
migration.
== Soil-transmitted helminth infections like acariasis

are diseases of poverty. They contribute to
IMPAIRMENT OF COGNITIVE PERFORMANCES and
GROWTH OF CHILDREN.
== REDUCE WORK CAPACITY AND PRODUCTIVITY
OF ADULTS.
This worm has a so-called “POLYMYARIAN TYPE”
of somatic muscle arrangement in which cells are
numerous and project well into the body cavity.
== The worm has terminal mouth with three lips
and sensory papillae.
== The adult Ascaris lumbricoides reside in but do
not attach to the mucosa of the small intestine.
Larva morphology is similar to adult.
== FEMALES:
1.) 22 to 35 cm in length, with smooth striated
cuticles.
2.) Have paired reproductive organs in the posterior
two-thirds.
== MALES:
1.) 10 to 31 cm in legnth
2.) Ventrally curved posterior end with two spicules.
3.) Reproductive organ is a single, long, tortuous
tubules.
EGGS:
== Infertile eggs: measure 88 to 94 um to 39 to 44 um, longer
and narrower than fertile eggs, with a thin shell and irregular
mammilated coating filled with refractile granules.
= Difficult to identify and are found not only in the absence of
males. They are found in about two of five infections.
== Fertile eggs: measures 45 to 70 um by 35 to 50 um. There

is no outer coarsely, mammilated albuminous covering which
may be absent of lost in “decorticated eggs”.
= Has a thick, transparent, hyaline shell with a thick outer
layer as a supporting structure and a delicate vitelline,
lipoidal, inner membrane, which is highly impermeable.
= At oviposition, the fertile eggs have an ovoid mass of
protoplasm, which will develop into larvae in about 14 days.
== Embryonated egg: the infective stage.
= Ingestion of these eggs, the larvae hatch in the lumen
of the small intestine and penetrate the intestinal wall.
= These larvae then enter the venules to go to the liver
through the portal vein, on to the heart and pulmonary
vessels where they break out of capillaries to enter the
air sacs. In the lungs, larvae undergo molting before
migrating to the larynx and oropharynx to be swallowed
into the DIGESTIVE TRACT.
= MIGRATION PHASE and MOLTING in LUNGS: take
about 7 to 10 days
= PREPATENT PERIOD: takes about 60 to 70 days.
= The EGGS ARE DEPOSITED IN THE SOIL WHEN THE
PERSON WITH ASCARIS INFECTION DEFECATES
INDISCRIMINATELY.
== In soil, it takes about two to three weeks for eggs
to develop into the infective stage (embryonation)
under favorable conditions with suitable
temperature, humidity, and moisture.
== The larvae reach their third stage when they
molt within the egg and become embryonated.
Only when this infective stage is swallowed can
humans become infected with Ascaris lumbricoides.
== Embryonated eggs CAN SURVIVE in moist shaded
soil for a few months to about two years in tropical
and sub-tropical areas, but for much longer in
temperate regions.
PATHOGENESIS and CLINICAL MANIFESTATIONS:
== The usual infection of 10 to 20 worms may not show
symptoms, hence, may go unnoticed by the host unless
it is discovered by stool examination or the
spontaneous passing of worms in the stools.
== DURING LUNG MIGRATION: the larvae may cause
host sensitization resulting in allergic manifestations
such as LUNG INFILTRATION, ASTHMA ATTACKS, and
EDEMA OF THE LIPS. Symptoms similar to PNEUMONIA
may result due to the penetration of lung capillaries by
several larvae as they enter the air sacs.
== ABDOMINAL PAIN
== INCREASE EOSINOPHILIA
== Moderate infections may produce lactose intolerance
in pre-school children. Heavy infections are likely to
cause bowel obstruction.
== SERIOUS, and at time, FATAL effects of ascariasis are due to
erratic migration of adult worms. They may be REGURGITATED
and VOMITED, may escape through the nostrils or rarely,
inhaled into the trachea. (The ADULT worms may invade the
BILE DUCTS through the ampulla of Vater and enter the
GALLBLADDER or LIVER.)
== Once in the bile duct: patients may experience severe
COLICKY ABDOMINAL PAIN, which is brought by the
movement of the worms inside the biliary tract.
== Once in the pancreas or appendix: patient may experience
acute appendicitis or pancreatitis, respectively.
== Intestinal bacteria may be carried to these
EXTRAINTESTINAL SITES producing ABSCESSES.
== Penetration of the worm through the intestinal wall into
the peritoneal cavity may occur and produce PERITONITIS.
== Intestinal volvulus, intussusception, and
Intestinal OBSTRUCTION may also result from
Ascaris infection. High fever may cause Ascaris
migration.
== Complications brought about by the larvae and
adult worms are a cause for concern. The
continuous biting or pricking of the intestinal
mucosa for food by a few Ascaris adults may irritate
nerve endings in the mucosa and result in
INTESTINAL SPASM leading to INTESTINAL
OBSTRUCTION.
DIAGNOSIS
== Clinical diagnosis of ascariasis is rather inaccurate
because the signs and symptoms are quite vague
and are indistinguishable from those of other
intestinal nematode infections or from non-parasitic
infections.
== The clinical diagnosis of ascariasis should be
confirmed or established by MICROSCOPIC
EXAMINATION OF A STOOL SAMPLE. The disease
should be highly suspected in a child who reportedly
passed out the worm with his/her feces.
== In the laboratory, the usual techniques used to diagnose
ascariasis consist of finding eggs in the feces using the
following techniques.
1.) direct fecal smear (DFS) – About 2 mg feces are emulsified
in a drop of NSS on a glass slide. A coverslip is placed and the
sample is examined under a microscope using a LOW POWER
MICROSCOPIC LENS.
2.) Kato technique or cellophane thick smear method- The
amount of fecal sample used is from 20 to 60 mg. A purely
QUALITATIVE METHOD, and is recommended for mass
examination of feces for diagnosis of Ascariasis infection.
3.) Kato-Katz technique- This is a modified Kato technique
because the amount of feces used is being measured. Hence,
it may be used to quantify the amount of eggs found in a
measured fecal sample. IT IS THEREFORE A QUANTITATIVE
TECHNIQUE. Can be used to enable one to make egg counts of
the parasite per gram of feces and to determine egg reduction
rate after treatment.
TREATMENT:
== Individual infections are cured by a single dose of any of the
broad-spectrum antihelminthics such as ABENDAZOLE,
MEBENDAZOLE, and PYRANTEL PAMOATE.
= ABENDAZOLE: the drug of choice, 400 mg single dose (200
mg for children under 2 years old).
= MEBENDAZOLE: 500 mg single dose
= PYRANTAL PAMOATE: 10 mg/kg (max. 1 g) also as a single
oral dose.
= IVERMECTIN: has recently been shown to be as effective as
albendazole if given at a dose of 200 ug/kg single dose.
== THESE DRUGS HAVE CURE RATES OF CLOSE TO 100% FOR

ASCARIASIS!!
== Reinfection, is usually observed four months post-
treatment and full reinfection appears at six or seven
months after treatment. This situation may be
remedied by giving treatment at least twice a year at
an interval of four or six months among
schoolchildren.
EPIDEMIOLOGY AND PREVENTION AND
CONTROL
== Ascaris has a cosmopolitan distribution. Over
one billion people globally are estimated to have
ascariasis, and of these, at least 20,000 die annually,
mostly young children. THE RISK OF INFECTION
EXISTS WHEREVER FECAL DISPOSAL IS IMPROPER!!
== REMAINS EPIDEMIC in many countries of
Southeast Asia, Africa, and Central and South
America.
== Children are particularly vulnerable since they are
at risk of INGESTING EMBRYONATED ASCARIS EGGS
while PLAYING IN SOIL CONTAMINATED WITH
HUMAN FECES.
== Ascariasis is one of the soil-transmitted
helminthiases but the level of transmission from soil to
humans depends more on socio-economic factors than
on physical factors.
== The main factors appear to be highly density of
human population, involvement in AGRICULTURE ( the
use of night-soil as fertilizer)
1.) PROPER DISPOSAL OF HUMAN FECES

2.) HEALTH EDUCATION (PERSONAL, FAMILY and
COMMUNITY HYGIENE)
3.) MASS CHEMOTHERAPHY DONE PERIODICALLY, ONCE,
TWICE, THRICE A YEAR WITH CHILDREN AS THE TARGET
POPULATION.
HOOKWORMS:
== Necator americanus
== Ancylostoma duodenale
= These are the two hookworms that infect human.
Which are also soil-transmitted helminths.
= Blood-sucking nematodes that attach to the
mucosa of the small intestine.
= They are most commonly found in TROPICAL and
SUBTROPICAL COUNTRIES where they OCCUR AS
SINGLE OR MIXED INFECTIONS.
All hookworms have the MEROMYARIAN TYPE of
SOMATIC MUSCLE ARRANGEMENT where the cells
are few in number- two to five per dorsal or ventral
half.
== Necator americanus ADULTS: small, cylindrical,
fusiform, grayish-white nematodes.
FEMALES: 9 to 11 mm by 0.35mm, and are larger than
males.
MALES: 5 to 9 mm by 0.30 mm, The posterior end has a
BROAD, MEMBRANOUS CAUDAL BURSA WITH A RIB-
LIKE RAYS, which are used for COPULATION.
== The BUCCAL CAPSULE has a ventral pair of semilunar
cutting plates. The head is curved opposite to the
curvature of the body, which is like a HOOK AT THE
ANTERIOR END.
== Ancylostoma duodenale adult is slightly larger
than the N. americanus
== Single-paired male and female reproductive
organs.
== The shape of the A. duodenale adult is such that
the head continues in the same direction as the
curvature of the body.
== The BUCCAL CAPSULE has two pairs of curved
ventral teeth.
== RHABDITIFORM LARVAE of N. americanus and A.
duodenale are indistinguishable.
== EGGS are difficult to distinguish too. Both eggs
have bluntly rounded ends and a single thin
transparent hyaline shell. Unsegmented at
oviposition, and in the 2- to 8-cell stages of division
in fresh feces.
== FILARIFORM LARVAE: N. americanus filariform
larvae are conspicuous and parallel throughout their
lengths. In contrast, the filariform larvae of A.
duodenale has inconspicuous buccal spears and
traverse striations on the sheath in the tail region.
== THE INFECTIVE STAGE TO HUMANS. INFECTION
IS BY PENETRATION THROUGH THE EXPOSED SKIN.
== The hookworm life cycle is direct and begins with
the adult worms copulating while attached to the
mucosa of the small intestines. Female worms
oviposit into the intestinal lumen and the eggs are
passed out with the human feces.
== In the soil, the embryo within the egg develops
rapidly and hatches after one to seven days into the
RHABDITIFORM LARVAE.
== After 7 to 10 days, the larva is transformed into
the non-feeding FILARIFORM LARVA, which is now
INFECTIVE TO HUMANS.
== 1.) FILARIFORM LARVAE, penetrate the skin.
== 2.) Enter the venules and migrate to the HEART
and LUNGS then into the ALVEOLI.
== 3.) The larvae then ascend to the trachea and are
finally swallowed, passing down to the small
intestine.
== 4.) After another month, the worms become
sexually mature and start laying eggs.
PATHOGENESIS and CLINICAL MANIFESTATIONS
== PENETRATION OF FILARIFORM LARVAE:
produced MACULOPAPULAR LESIONS and
LOCALIZED ERYTHEMA. Itching is often severe, and
it is known as “ground itch” or “dew itch” AS IT IS
RELATED TO CONTACT WITH SOIL, ESPECIALLY ON A
DEWY MORNING.
== If the larvae migration through the lungs are
ABUNDANT, BRONCHITIS or PNEUMONITIS may
RESULT. (produces minute hemorrhages, with
eosinophilic and leukocytic infiltration, but rare in
the tropics).
== In the stage of MATURATION OF THE WORM IN
THE INTESTINE, there is ABDOMINAL PAIN,
STEATORRHEA, or sometimes DIARRHEA with BLOOD
AND MUCUS, and BLOOD EOSINOPHILIA of 30 to
60%.
== Hookworm infection is usually chronic, hence
patients often show no acute symptoms. Chronic
moderate or heavy hookworm infection results in
progressive, secondary, microcytic, hypochromic
anemia of the iron-deficiency type due to
PRIMARILY TO CONTINUOUS LOSS OF BLOOD.
== Hypoalbuminemia is another manifestation of
hookworm infection. There is low level of ALBUMIN
due to combined loss of BLOOD, LYMPH, and
PROTEIN.
== OTHER SYMPTOMS: Exertional dyspnea,
weakness, dizziness, and lassitude, while signs
include rapid pulsem edeme and albuminuria.
== Unlike ascariasis, the complications of hookworm
infections are quite mild, and remedial measures
are readily applied.
== PROGNOSIS is GOOD vs ASCARIASIS
DIAGNOSIS
== FINAL DIAGNOSIS depends on finding parasite eggs in the
feces.
== The following techniques are inexpensvie and can be
applied to both individual and mass screening.
1.) Direct Fecal Smear (DFS) = is of value only when the
infection is quite heavy. It may not detect the parasite in light
infections. (egg count of <400 eggs per gram feces)
2.) Kato technique or Kato-Katz method = may increase
detection rates since more stool is examined. The latter
technique may also provide quantitative diagnosis allowing
egg counts to be made.
3.) Concentration methods like ZnSO4 centrifugal flotation
and the formalin-ether concentration method increase
positive findings several folds.
4.) Culture methods like the HARADA-MORI allow hatching
of larvae from eggs on strips of filter paper with one end
immersed in water
== The concentration method is recommended for
determining whether the stool is POSITIVE or
NEGATIVE for EGGS of HOOKWORMS.
== CULTURE METHOD is used only for SPECIES
DETERMINATION of HOOKWORMS.
TREATMENT
== Treatment of hookworm infection is a must.
Prioritize for pregnant women, children, and patients
with malnutrition, pulmonary tuberculosis, or anemia.
== BROAD-SPECTRUM ANTIHELMENTHICS, such as
MEBENDAZOLE and ALBENDAZOLE are preferred in
areas where namatode infections are endemic.
== These drugs are called BENZIMIDAZOLE DERIVATIVES
that block the uptake of glucose by most intestinal and
tissue nematodes.
== 400 mg dose for adults and children over two years
old.
== Mebendazole not recommended for children below
2 years of age.
EPIDEMIOLOGY
== Over 900 million people in tropical and
subtropical countries are estimated to be infected
with either A. duodenale or N. americanus.
== Associated anemia causes at least 50,000 deaths
annually.
== Geographical distribution of the two human
hookworms used to be regarded as relatively
distinct. A. duodenale was prevalent in Europe and
South-western Asia, while N. americanus was
prevalent in tropical Africa and Americas.
== Greater in AGRICULTUREAL AREAS.
== FARMERS are more prone to the infection because they
work in ricefields and vegetable gardens, and they are not
properly protected from contact with infective soil.
== In COMPOSTELLA VALLEY PROVINCE, infection rates have
been shown to be more than 50% in the late 1990’S.
FACTORS THAT CONTRIBUTE TO THE TRANSMISSION OF
HOOKWORMS
1.) Suitability of the environment for eggs or larvae; damp,
sandy, or friable soil with decaying vegetation, and
temparature of 24 to 32 Degree celsius.
2.) Mode and extent of fecal pollution of the soil (unsanitary
disposal of human feces or the use of night soil as fertilizer).
3.) Mode and extent of contact between infected soil and skin
or mouth.
PREVENTION AND CONTROL
1.) Sanitary disposal of human feces
2.) Wearing of shoes, slippers, and boots so that
skin contact with infective larvae in contaminated
soil is avoided.
3.) Health education on personal, family and
community hygiene
4.) Treatment of infected individuals
5.) Mass chemotherapy when prevalence is higher
than 50%
6.) Protection of susceptible individuals by
improving household income and consequently,
improving diet to prevent malnutrition.
Trichuris trichiura
== Whipworm, is a also a soil-transmitted
helminth. Ascaris and Trichuris are frequently
observed as occurring together. (mode of
transmission and distribution are quite similar)
== Classified as HOLOMYARIAN, based on the
arrangement of somatic muscle in cross-section
where the cells are small, numerous, and closely
packed in a narrow zone.
== MALES: measure 30 to 45 mm, slightly shorter than
the female.
= COILED POSTERIOR with a SINGLE SPICULE and
RETRACTILE SHEATH.
== FEMALES: measure 35 to 50 mm long, has blunty
ROUNDED POSTERIOR END.
= A female LAYS approximately 3,000 to 10,000 eggs
per day
== The worms have an attenuated anterior three-fifths
traversed by a narrow esophagus resembling a string of
beads.
== LARVA: ARE NOT USUALLY DESCRIBED PROBABLY
BECAUSE SOON AFTER EMBRYONATED EGGS ARE
INGESTED, the LARVA escape and penetrate INTESTINAL
VILLI where they remain for three to ten days.
== EGGS: measures 50 to 54 um by 23 um.
= LEMON-SHAPED with PLUG-LIKE TRANSLUCENT
POLAR PROMINENCES.
= yellowish outer layer and transparent inner shell.
Fertilized eggs are unsegmented at oviposition and
embryonic development takes place outside of the
host when eggs are deposited in CLAYISH SOIL.
Compared to Ascaris, Trichuris eggs in soil are more
susceptible to desiccation.
== Trichuris worms inhabit the LARGE INTESTINE.
Their entire WHIP-LIKE portion is deeply embedded
into the intestinal wall of the CECUM.
== After copulation, the female worm lays eggs,
which are passed out with the feces and deposited
in the soil. UNDER FAVORABLE CONDITIONS, the
eggs develop and become embryonated within two
to three weeks. If swallowed, the INFECTIVE
EMBRYONATED EGGS go to the SMALL INTESTINE
and UNDERGO FOUR LARVAL STAGES to become
adult worms.
== There is no heart-lung migration.
== Each female worm can produce a total of over 60
million eggs over an average lifespan of 2 years.
== The anterior potions of the worms, which are
embedded in the mucosa, cause PETECHIAL
HEMORRHAGES.
== The MUCOSA is hyperemic and edematous;
enterorrhagia is common and there may even be
RECTAL PROLAPSE among the heavily infected.
== The lumen of the appendix may be filled with
WORMS, and consequent irritation and
inflammation may lead to APPENDICITIS OR
GRANULOMAS.
== Infections with over 5,000 T. trichiura eggs per
gram of feces are usually symptomatic.
== 20,000 eggs per gram feces often develop severe
diarrhea or dysenteric syndrome.
== In heavily parasitized individuals, the worms may
be found throughout the colon and rectum. Such
cases of heavy chronic trichuriasis are often marked
by frequent blood-streaked diarrheal stools,
abdominal pain and tenderness, nausea and
vomiting, anemia, and weight loss.
= PROGNOSIS : VERY GOOD, because there is no
larval migration through the lungs as in Ascariasis
and hookworm infections, no lung pathology occurs.
DIAGNOSIS
== Possible only in very heavy chronic Trichuriasis
where the patient suffers from frequent blood-
streaked diarrhea, abdominal pain and tenderness,
and rectal prolapse.
== Direct Fecal Smear (DFS) = with a drop of saline
== Kato thick smear method using about 20 to 60
mg of stool sample (used for egg counting to
determine cure rate (CR), egg reduction rate (ERR),
and intensity of infection)
== Concentration technique, such as acid-ether,
and formalin-ether methods.
TREATMENT
== MEBENDAZOLE, the drug of choice
== ALBENDAZOLE may be used as an alternative drug
== 400 mg single dose (ALBENDAZOLE)= light infections
== 500 mg single dose (MEBENDAZOLE)= light infections
== MODEARATE AND HEAVY INFECTIONS, two to three
days of consecutive treatment may be required.
== EGG REDUCTION RATE, CURE RATES, REINFECTION

RATES, and EGG COUNTS should be determined pre-
and post- treatment.
EPIDEMIOLOGY
== Occurs both in temperate and tropical countries,
but is more widely distributed in warm, moist areas
of the world.
== Hundred of millions of people are infected.
== Prevalence in temperate countries ranges from
20 to 30% while in tropical countries, it ranges from
60 to 85%.
== Children 5 to 15 years of age are more
frequently infected!!
== In the Philippines, the prevalence is from 80 to
84%. Distribution and prevalence are co-extensive
with that of A. lumbricoides.
== TRANSMISSION are the same as that of
Ascaris lumbricoides , indiscriminate defecation of
children around yards, frequent contact between
fingers and soil among children at play, poor health
education, and poor personal, family, community
hygiene.
PREVENTION and CONTROL
== Mass treatment may be indicated if infection rates
are greater than 50%. Due to high reinfection rates
periodic treatment may be necessary.
1.) TREATMENT OF INFECTED INDIVIDUALS
2.) SANITARY DISPOSAL OF HUMAN FECES BY
CONSTRUCTION OF TOILETS AND THEIR PROPER USE
3.) WASHING OF HANDS WITH SOAP AND WATER
BEFORE AND AFTER MEALS.
4.) HEALTH EDUCATION ON SANITATION AND
PERSONAL HYGIENE
5.) THOROUGH WASHING AND SCALDING OF
UNCOOKED VEGETABLES ESPECIALLY IN AREAS WHERE
NIGHT SOIL IS USED AS FERTILIZER.
Enterobius vermicularis
== HUMAN PINWORM
== causes enterobiasis or oxyuriasis, which is
characterized by perianal itching or pruritus ani.
== Although not usually fatal, migrating worms
could go beyond the perianal region and thus,
might cause pathology elsewhere.
== This intestinal nematode is classified as
MEROMYARIAN, based on the arrangement of the
somatic muscles where there are two to five cells
per dorsal or ventral half.
== Adult worms have CUTICULAR ALAR EXPANSIONS at
the anterior end and prominent posterior esophageal
bulb. Found in the LOWER ILEUM and CECUM
== FEMALES: measures 8 to 13 mm by 0.4 mm and has a
long pointed tail.
= Has a long POINTED-TAIL
= The uteri of gravid females are distended with eggs
= Gravid Females: migrate down the intestinal tract and
exit through the anus to deposit eggs on the perianal
skin.
= A SINGLE FEMALE LAYS 4,672 TO 16,888 EGGS PER
DAY; after DEPOSITION THE FEMALE DIES!!
== MALES: measure 2 to 5 mm by 0.1 to 0.2 mm has a
curved tail and a single spicule.
= RARELY SEEN, because they usually die after
copulation.
== RHABDITIFORM LARVAE: measures 140 to 150um by
10 um, has the characteristic esophageal bulb has NO
CUTICULAR EXPANSION ON THE ANTERIOR END.
== EGGS: are asymmetrical, with one side flattened and

the other side convex, and range from 50 to 60 um by 20
to 30 um in size averaging 55 by 36um.
== The translucent shell consist of an outer, triple
albuminous covering for mechanical protection and an
inner embryonic lipoidal membrane for chemical
protection.
== EGGS become infective outside the host in four to
six hours.
== Resistant to disinfectants but succumb to
dehydration in dry air within a day. However, in mooist
conditions, these eggs may remain viable for 13 days.
== Relatively innocuous parasite and rarely produces
any serious lesions.
== Mild catarrhal inflammation of the intestinal
mucosa may result from the attachment of the worms,
and mechanical irritation and secondary bacterial
invasion may lead to inflammation of the deeper layers
of the intestines.
== MIGRATION OF EGG-LAYING FEMALES lead to the
anus causes irritation of the perineal region.
== Intense itching leads to scratching and eventually
secondary bacterial infection.
== Children infected with this parasite may suffer from
insomnia due to the PRURITUS.
== Other signs of infection are POOR APETITE,
WEIGHT LOSS, IRRITABILITY, GRINDING OF TEETH,
and ABDOMINAL PAIN.
== THE PROGNOSIS OF ENTEROBIASIS or
OXYURIASIS is GOOD EXCEPT THAT THIS PARASITIC
DISEASE is easily spread within the family, hence it
may be described as a FAMILIAL DISEASE.
DIAGNOSIS
== Suspected in CHILDREN and ADULTS who show
PERIANAL ITCHING relieved only by vigorous
scratching.
== ADULT WORMS may be seen in the feces in only
about 5% of infected person.
== THE METHOD OF LABORATORY DIAGNOSIS IS
GRAHAM’S SCOTCH ADHESIVE TAPE SWAB ,
which gives the highest percentage of positive
results and the greatest number of eggs seen.
 https://www.youtube.com/watch?v=-JB9Fm_9tQs
TREATMENT
== The drug of choice is PYRANTEL PAMOATE (10
mg/kg with a second dose 2 to 4 weeks later).
== ALBENDAZOLE ( 400 mg chewable tablet single
dose)
== MEBENDAZOLE (500 mg chewable tablet single
dose)
== CURE may be considered only after
SEVEN PERIANAL SMEARS using the SCOTCH-
TAPE SWAB method are all found to be
negative.
EPIDEMIOLOGY
== occurs both in temperate and tropical regions of the
world and has a high prevalence in both developed
and underdeveloped countries.
== It is the ONLY NEMATODE INFECTION that cannot be
controlled through sanitary disposal of human feces
because eggs are deposited in the perianal region
instead of the intestinal lumen.
== EGGS usually contaminate underwear and
beddings. The route of infection is through the mouth,
the respiratory system, and finally through the anus.
(INHALATION OF DUST CONTAINING THE EGGS OR
HATCHED LARVAE ENTER THE ANUS AND CAUSE
RETROINFETION WHEN THEY GO BACK INTO THE
LARGE INTESTINE)
== Personal cleanliness and persona hygiene are
essential.
== FINGERNAILS should be cut short and hand
washing should be done after using the toilet, as
well as before and after meals
== INFECTED PERSON SHOULD SLEEP ALONE!!
== Underwear, night clothes, blankets, and
bed sheets should be handled with care,
BOILED AND LAUNDERED
Strongyloides stercolaris
== This group of nematodes is characterized by free-
living rhabditiform and parasitic filariform stages.
== S. stercolaris is the only species naturally
pathogenic to humans. Several species have been
reported in mammals and in birds. THE INTESTINE IS
THE PARASITE’S HABITAT.
== PARASITIC OR FILARIFORM FEMALE: 2.2 mm by
0.4mm, colorless, semi-transparent, with finely,
striated cuticle.
== IT HAS SLENDER TAPERING ANTERIOR END AND A
SHORT CONICAL POINTED TAIL.
== The SHORT BUCCAL CAVITY has FOUR
INDISTINCT LIPS.
== THE LONG SLENDER ESOPHAGUS extends to the
anterior fourth of the body, and the intestine is
continuous to the subterminal anus.
== THE VULVA is located one-third the length of the
body from the posteri.or end.
== THE UTERI contain a single file of eight to twelve
thin-shelled, transparent, segmented ova, 50 to 80
um by 30 to 40um.
== FREE-LIVING FEMALE: measures 1 mm by
0.06mm and is smaller than the parasitic female.
== It has muscular double-bulbed esophagus and
the intestine is a straight cylindrical tube.
== FREE-LIVING MALE: measure 0.7mm by

0.04mm, is smaller than the female, and has a
ventrally curved tail, two COPULATORY SPICULES, A
GUBERNACULUM BUT NO CAUDAL ALAE.
== PARASITIC MALES HAVE NOT BEEN RELIABLY
IDENTIFIED.
== RHABDITIFORM LARVAE: measures 225um by
16um. It has an elongated esophagus with a
pyriform posterior bulb. This species differs from
hookworm from in being slightly SMALLER and LESS
ATTENUATED POSTERIORLY.
== INFECTIVE FILARIFORM LARVAE: IS NON-

FEEDING, and slender, about 550 um in length. It is
similar to the hookworm filariform larva but usually
is smaller, with a distinct cleft at the tip of the tail.
== EGGS: have clear thin shell and are similar to
those of hookworms except that they measure only
about 50 to 58 um by 30 to 34 um.
== FREE-LIVING Strongyloides stercolaris are
FOUND IN THE SOIL. THE FEMALE WORMS LAYS
EMBRYONATED EGGS, which develop into
RHABDITIFORM LARVAE after a few hours. When
conditions in the soil BECOME UNFAVORABLE,
RHABDITIFORM LARVAE DEVELOP INTO
FILARIFORM LARVAE, which are INFECTIVE TO
HUMANS.
== THE PARASITIC LIFE CYCLE BEGINS when
FILARIFORM LARVAE infect humans THROUGH THE SKIN.
(enter the circulation, pass through the lungs, and
migrate into the larynx where they are subsequently
SWALLOWED)
== Females generally reproduce by PARTHENOGENESIS.
Invade the intestinal mucosa where they deposit their
eggs. Eggs hatch into rhabditiform larvae, migrate into
the lumen and pass out into the feces.
== AUTOINFETION: occurs when the rhabditiform larvae
pass down the large intestine and develop into
FILARIFORM LARVAE. Then these filariform larvae will
reinvade the intestinal mucosa and enter the circulation
to start another parasitic cycle WITHOUT LEAVING THE
BODY OF THE HOST!!!
PATHOGENESIS AND CLINICAL MANIFESTATIONS
== 3 PHASES OF INFECTION
1.) Invasion of the skin by filariform larvae
2.) Migration of larvae through the body
3.) Penetration od the intestinal mucosa by adult female
worms. (The #2 and #3 phases may occur simultaneously)
== In the first phase of infection, SKIN PRODUCES ERYTHEMA,
and PURITIC ELEVATED HEMORRHAGIC PAPULES.
== DURING MIGRATION PHASE: LUNGS ARE DESTROYED!

Causing LOBAR PNEUMONIA WITH HEMORRHAGE.
== THIRD PHASE OF INFECTION, Adult female worms may be

found in the intestinal mucosa from the pylorus to the rectum,
but the greatest numbers are found in the DUODENAL and
UPPER JEJUNAL REGIONS.
== Light infection does not cause intestinal
symptoms.
== Moderate infection causes diarrhea alternating
constipation.
== Heavy infection produces INTRACTABLE,
PAINLESS, INTERMITTENT DIARRHEA ( COCHIN
CHINA DIARRHEA ) characterized by numerous
episodes of watery and bloody stools.
== SOME COMPLICATIONS are EDEMA,

EMACIATION, loss of apetite, anemia, lobar
pneumonia, and malabsorption leading to
CACHEXIA.
== PROGNOSIS is GOOD IN LIGHT INFECTIONS, but
moderate and heavy infections have
HIGH MORTALITY RATES DUE TO MASSIVE
INVASION OF TISSUES by ADULTS and LARVAE.
DIAGNOSIS
== The finding of unexplained eosinophilia in a patient
may be a clue pointing to strongyloidiasis.
== HARADA-MORI CULTURE, BAERMANN FUNNEL
usually leads to detection of the infection.
RECOMMENDED FOR USE IN THE FIELD.
== BAELE’S STRING TEST
== DUODENAL ASPIRATION
== SMALL BOWEL BIOPSY
== In, disseminated strongyloidiasis, LARVAE may be
found in sputum or urine.
== SEROLOGY may not be useful in filarial endemic
areas since there are cross-reactions between
Strongyoides and filarial worms antigens.
TREATMENT
== All individuals should be treated. The drug of choice
is ALBENDAZOLE, 400 mg administered or three
consecutive days.
== Albendazole, appears to eradicate up to 80% of
infections.
== THIABENDAZOLE, which is given at 50 mg per kg.
(max 3 grams per day) in 2 divided doses daily for 2
consecutive days after meals.
== EGG REDUCTION RATE (ERR) cannot be determined
because eggs are not passed out in the feces but are
oviposited in the intestine and other tissues of the host.
REINFECTION RATE IS DIFFICULT TO CALCULATE
BECAUSE OF AUTOINFECTION!!
EPIDEMIOLOGY
== Strongyloides stercolaris , is found throughout
the world and follows a distribution pattern similar
to hookworm in the tropics and subtropics as well as
in EUROPE and U.S.A.
== It is more of a FECALLY-TRANSMITTED BECAUSE it
is infective shortly after passage with the feces.
==INFECTION and DISEASE RATES as well as

MORBIDITY and MORTALITY figures are not well
documented !!!
Capillaria philippinensis
== is characterized by abdominal pain, chronic diarrhea, and
GURGLING STOMACH.
== It was described in the Philippines in 1963, after the death
of the first human case.
== AN EPIDEMIC OCCUR: between 1967 to 1968 WHERE
MORE THAN 1,000 CASES WERE REPORTED AND ALSMOST
100 INDIVIDUALS DIED.
== A TINY NEMATODE residing in the small intestines of
humans.
== Member of the superfamily TRICHUROIDEA, which
characteristically have a thin filamentous anterior end and a
slightly thicker and shorter posterior end.
== The ESOPHAGUS has rows of secretory cells called
STICHOCYTES, and the entire esophageal structure is called
STICHOSOMES.
==MALES: measures 1.5 to 3.9 mm, SPICULE is 230 to
300 um long and has an unspined sheath.
==FEMALES: measures 2.3 to 5.3mm, Produce
characteristic eggs, which are peanut shaped with
straited shells and flattened bipolar plugs.
== EGGS: measures 36 to 45 um by 20um, are passed in
the feces and embryonated in the soil or water.
== They MUST REACH THE WATER IN ORDER TO
BE INGESTED BY SMALL SPECIES OF FRESHWATER
OR BRACKISH WATER FISH. Hatch in the intestine
of the fish and grow into the infective stage larvae.
When the fish is eaten uncooked, the larva escape
from the fish intestines and develop into adult
worms in human intestines.
== The first generation of FEMALE WORMS,
produces larvae to build up the population.
Subsequently generations predominantly produce
eggs although there are always a few female worms
that produce both eggs and larvae or larvae only.
== Abdominal pains, gurgling stomach
(BORBORYGMUS), and diarrhea.
== After few weeks, there is a noticeable weight loss,
malaise, anorexia, vomiting, and edema.
== Laboratory findings show SEVERE PROTEIN-LOSING
ENTEROPATHY, malabsorption of fats and sugars,
decreased excretion of xylose, low electrolyte levels
(especially potassium), and high levels of
immunoglobulin E.
== If disease is not treated soon after the symptoms
occur and severe manifestations of the disease develop,
infected patients USUALLY DIE!!
== Histologically, the intestines also show
FLATTENED AND DENUDED VILLI and DILATED
MUCOSAL GLANDS.
== The LAMIA PROPIA is infiltrated with plasma
cells, lymphocytes, macrophages, and neutrophils.
DIAGNOSIS
== Based on finding characteristic eggs in the feces
by DFS or wet mount as well as stool concentration
methods.
== Larval or Adult worm presence on the stool
specimens too.
== DUONDENAL ASPIRATIONS from the small
intestines
TREATMENT
== In severe cases with electrolyte and protein loss,
patients should be given electrolyte replacement
and a high protein diet.
== ANTIDIARRHEA AND ANTIHELMENTHIC DRUGS
should also be given:
= MEBENDAZOLE 200mg twice a day for 20 days
= ALBENDAZOLE 400 mg once daily for 10 days
= Relapses may occur if the treatment regimen is
not followed.
EPIDEMIOLOGY
== First recorded in Northern Luzon in the Philippines.
== It was later found in Thailand, Iran, Japan, Egypt,
Korea, Taiwan, and India.
== Migratory fish eating birds are considered the
NATURAL HOSTS.
== In Philippines, nearly 2,000 cases have been
documented from the Northern Luzon provinces,
Zambales, and Southern Leyte.
== Infections occur from eating uncooked small
freshwater/brackish water fish!!
== In Monkayo, Compostella Valley Province, an
outbreak described as a “mystery disease” in 1998.
== 2012, Mindoro “OUTBREAK”
==
== Infections can be prevented by discouraging
people in endemic areas from eating raw fish.
== Good sanitary practices should be followed.
== It is believed that the 1967 to 1968 Philippine
epidemic was due to washing of FECALLY
CONTAMINATED BED SHEETS IN LAGOONS in the
TAGUDIN AREA OF ILOCUS SUR.
== All infected person should be treated
immediately!
THE END, THANK YOU!
Cestode Infections
Learning Objectives
To Describe the most prevalent Intestinal
Cestodes Infections.
To Familiarize the parasite’s biology, clinical
manifestations and pathology, diagnosis,
treatment, epidemiology, and prevention and
control.
To make plans for the prevention and control of
Cestode infections.
To familiarize the morphological structure
especially the scolex and the size of proglottids of
each Cestode parasite since it is one used for
microscopic species identification.
Intestinal Cestodes
Taenia saginata
== Is known as the beef tapeworm of humans.
== Human serve as definitive host and never as
intermediate host.
== The ADULT WORM inhabits the upper jejunum
and may live for up to 25 years. It derives
nourishment from intestinal contents.
== ADULT WORMS: measure 4 to 10 m in length
and may have 1,000 to 4,000 proglottids.
== The CUBOIDAL SCOLEX measure 1 to 2 mm in
diameters and has FOUR (4) prominent ACETABULA.
== IT IS DEVOID OF HOOKS OR ROSTELLUM
== Attached to the SCOLEX is a short neck from which a
chain of immature, mature, and gravid proglottids
develop.
== MATURE PROGLOTTIDS: are approximately square in
shape, and they contain mature male and female
reproductive organs.
== FOLICULAR TESTES: numbering 300 to 400 are
scattered throughout the proglottid.
== VAGINA: has a sphincter. / The UTERUS: is distended
with OVA and has 15 to 20 lateral branches.
== Gravid proglottids are longer than they are wide and
are most distal from the NECK.
== The genital pores of proglottids are irregularly
alternate.
== OVA: are spherical or subspherical in shape,
measuring 30 to 45 um in diameter.
= Brownish in color, with a thick embryophore which
appears striated because of numerous pits. Inside
the eggshell is the oncosphere or embryo provided
with three pairs of hooklets.
== GRAVID PROGLOTTID: contain 97,000 to
124,000 OVA. Annually, a worm may pass out
594,000,000 OVA.
= it would undergo APOLYSIS and are either passed
out with the feces or actively crawl out of the bowel
to the external environment
= With APOLYSIS of the gravid segments, EGGS are
released and they remain viable in soil for weeks. UPON
INGESTION OF T. saginata eggs by cattle, the
oncosphere is released.
== INSIDE THE CATTLE, the ONCOSPHERE actively
penetrates the intestinal mucosa and enters a venule
from which it is carried to other parts of the body.
== It is typically enters a muscle fiber and develops into
an INFECTIVE STAGE CALLED CYSTICERCUS BOVIS
in TWO MONTHS.
== CYSTICERCUS: Ovoidal, milky white, about 10 mm in
diameter, and has a single scolex invaginated into a
fluid-filled bladder.
== Humans readily become infected when these
ENCYSTED LARVAE are INGESTED FROM RAW OR
IMPROPERLY COOKED BEEF!!!
== INSIDE THE HUMAN: the LARVAE is digested out
of the meat, and the SCOLEX EVAGINATES TO
ATTACH TO THE MUCOSA OF THE SMALL
INTESTINES, where it will become mature in about
12 weeks!!!
== Usually ONE ADULT tapeworm is present in T.

saginata infections!!
== T. saginata causes mild irritation at the site of the
attachment.
== Patients with taeniasis may experience non-specific
symptoms, such as epigastric pain, vague discomfort,
hunger pangs, weakness, weight loss, loss of appetite, and
pruritus ani (PERIANAL ITCHING).
== RARELY, tangled proglottids may result in
INTESTINAL OBSTRUCTION!!
== Individual T. saginata proglottids, are actively
motile and they have been documented to cause
OBSTRUCTION IN BILE and PANCREATIC DUCTS, as
well as APPENDIX.
== But most active proglottids are in the PERIANAL
AREA and in the UNDERGARMENTS may result in
ANXIETY and DISTRESS.
DIAGNOSIS
== Specific diagnosis rests on identifying the
characteristics proglottids, eggs, or scolex.
== Specimen is usually brought in by patients are
the GRAVID PROGLOTTIDS, either SINGLE or in
CHAIN. After they are passed out with the feces or
may be recovered in the patient’s
UNDERGARMENTS.
= Pressed or flattened in between two glass slides
and are examined against the light. This will allow
one to HAVE A ROUGH COUNT OF THE LATERAL
BRANCHES from the main uterus.
= STAINING is also used like INDIA INK
== EXAMINATION OF THE STOOL can be done for the
presence of eggs, but eggs are IRREGULARLY PASSED
OUT WITH THE STOOLS.
== Concentration techniques like the formalin-ether
concentration technique will be useful in increasing
the chance of demonstrating the eggs.
== PERIANAL SWABS may also be helpful because
the eggs are left in the PERIANAL SKIN as the
GRAVID segment squeeze out of the anal opening.
TREATMENT
== The drug of choice is PRAZIQUANTEL.
= Given at a dose of 5 to 10 mg per Kg as a single
dose for both adults and children.
= It is not necessary to collect the scolex unless
species diagnosis is needed.
== CRITERIA FOR CURE:
1.) Recovery of the scolex!!
2.) Negative stool examination 3 months after
treatment!!
Taenia solium
== Is known as the PORK TAPEWORM OF MAN.
== It has a cosmopolitan distribution.
== MAN serves as BOTH A DEFINITIVE AND AN
INTERMEDIATE HOST!!
== both INTESTINAL and TISSUE INFECTIONS
OCCUR IN MAN!
== THE ADULT WORM inhabit the UPPER SMALL
INTESTINES. Like other intestinal cestodes, it derives
NOURISHMENT FROM INTESTINAL CONTENTS OF
THE HOST.
== IT IS SHORTER THAN T. saginata and has a less
number of proglottids. The ADULTS measure 2 to 4 m
in length and may have 800 to 1,000 proglottids.
== SCOLEX: has four ACETABULA, but it smaller
(1mm) and more SPHERICAL than that of T. saginata
= The scolex carries a cushion-like rostellum with a
double crown of 25 to 30 large and SMALL HOOKS,
which are absent in T. saginata
= The general morphology of the proglottids
resembles that of T. saginata the difference lies in
the presence of an accessory ovarian lobe, the
absence of a vaginal sphincter, and the smaller
number of follicular testes (100 to 200) in the mature
proglottid of T. solium
== EGGS: are indistinguishable from that of T. saginata. They
measure 30 to 45 um and have a thick brown striated
embryophore surrounding a HEXACANTH EMBRYO.
== GRAVID PROGLOTTID: contains approximately 30,000 to
50,000 OVA. LESS ACTIVE than proglottids of T. saginata ,
they do not observe to actively crawl about.
== These eggs are ingested by the HOGS/PIGS and the
ONCOSPHERES are released in the intestines!!
= The oncosphere penetrates the intestinal mucosa to
typically encyst in the muscles as CYSTICERCUS
CELLULOSAE. (MUSCLES, TONGUE, HEART,
DIAPHRAGM, LIVER, SPLEEN, AND MESENTERY)
= INFECTED PORK MEAT/MEAT IS TERMED AS “MEASLY
PORK”
== INGESTION OF THIS MEASLY PORK, the larva is
liberated and the scolex attaches to the intestinal
mucosa of the human. Maturity is attained in
APPROXIMATELY 12 WEEKS from time of ingestion
of the cysticercus.
== MAN may also be an intermediate host of T.
solium , eggs are very resistant and when the eggs
are ingested, development to cysticerci ensues as
it does in pigs (It will then spread to
different organs through the
bloodstream).
== Human infection with cysticercus cellulosae
can be acquired through the fecal-oral route by
ingesting Taenia solium eggs from contaminated
food or drink. Individuals harboring the adult Taenia
solium can infect THEMSELVES
(AUTOINFECTION) due to poor hygienic
practice.
== IT IS USUALLY ENCAPSULATED WITH
ADVENTITIOUS HOST TISSUE. However, in the
vitreous humor and in the BRAIN of the HUMAN, it
may be encapsulated. A FULL SIZE OF 5 mm may be
attained in 10 weeks.
== Intestinal Infection
= Mild- nonspecific abdominal complaints. Unlike in T.
saginata, proglottids are not as active, and therefore,
obstruction of the bile and pancreatic duct and
appendix is UNLIKELY!!
== Cysticercus
= Cysticerci are often multiple and can develop in any
organ or tissue. Most commonly, they are located in
striated muscles and in the brain, but the subcutaneous
tissues, eye, heart, lung, and peritoneum have all been
involved.
= PRODUCE INFLAMMATION, and can survive up to 5
years. Upon death, the cystic fluid increases and there is
a pronounced tissue response to the parasite. THE
PARASITE IS EVENTUALLY CALCIFIED.
== SYMPTOMATOLOGY is dependent on the
number, size, and location of the lesion.
== The most serious manifestation is
NEUROCYSTICERCOSIS (NCC), which is considered as
one of the most serious ZOONOTIC DISEASE
WORLDWIDE.
== The death of the larva leads to inflammation of
the affected region. CALCIFICATION is the end-result
of the cellular reaction. CONVULSION are the most
common manifestations of CEREBRAL
CYSTICERCOSIS and MOTOR DEFICITS, HEADACHE,
and VOMITING may OCCUR!!!
== IN THE EYES, cysticerci are often RETINAL or
SUBRETINAL IN LOCATION. They may float freely in
the vitreous or aqueous humors. VISION IS USUALLY
AFFECTED due to CHORIORETINITIS and
VASCULITIS!!! (BLURRING AND LOSS OF VISION)
DIAGNOSIS:
== INTESTINAL
= Specific diagnosis of Taeniasis rests on identifying the
characteristic proglottids, eggs, or the scolex as
described for T. saginata
== CYSTICERCUS
= NEUROCYSTICERCOSIS may be suspected in a patient
with EPILEPTIC SEIZURES without associated systemic
symptoms but living in an endemic area.
= COMPUTED AXIAL TOMOGRAPHY (CAT) scans and
NUCLEAR MAGNETIC RESONANCE IMAGING (MRI) are
useful for localizing cysticerci and evaluating the
PATHOLOGY BEFORE and AFTER TREATMENT.
== OPTHALMIC CYSTICERCOSIS can be diagnosed
through the visualization of the cysticerci using
OPTHALMOSCOPY but the procedure may induce
movement and/or evagination of the scolex.
== MUSCULAR and SUBCUTANEOUS CYSTICERCI are
usually palpable and can be recovered through
tissue biopsy for histophatologic processing.
== SEROLOGIC TESTS include serum and CSF
(cerebrospinal fluid) enzyme-linked
immunosorbent assay (ELISA) and Electro-
immuno transfer blot (EITB) or WESTERN BLOT
for specific IgG and IgM anticysticercal
antibodies. (75 tp 100% sensitivity) .
TREATMENT:
== INTESTINAL
= The drug of choice is PRAZIQUANTEL and NICLOSAMIDE.
Because of the theoretical possibility of autoinfection and
subsequent cysticercosis, treatment should not be delayed.
= PRAZIQUANTEL is given at 5 to 10 mg per kg, single dose for
both adults and children.
== CYSTICERCOSIS
= PRAZIQUANTEL at a dose of 50 to 75 mg per kg divided into
three doses for 30 days or ALBENDAZOLE at a dose of 400 mg
twice daily for 8 to 30 days. (Steroids are then given either
80 mg of PREDNISOLONE or 10 mg of IM dexamethasone) 4
HOURS AFTER THE LAST DOSE.
 EPIDEMIOLOGY
== The distribution of T. solium and T. saginata
infections is highly related to the habit of eating raw or
improperly cooked meat.
== Abstinence from beef as part of the religious beliefs
among the Hindus prevent T. saginata infections, while
among the Moslems, prevention of T. solium infections
happens because of abstinence of from pork.
== Taenia solium = especially common in Slavic
countries, Latin America, Southeast Asia, China, and
India.
== Taenia saginata = has high endemicity in Ethiopia and
East Africa. It has been reported from Japan, Southeast
Asia, Europe, Australia, Canada, and the United States of
America.
== In Philippines, T. saginata infections are more
common than T. solium infections. Surveys of animal
intermediate hosts however showed that pigs are
infected more than the cow or the cattle.
= Many of the identified cases were adult males
who came from the Northern Luzon provinces,
where eating raw or undercooked meat while
drinking alcohol is a delicacy. Neurocysticercosis has
been reported on several literature.
== May appear simple but difficult to implement.
Thorough cooing of meat is a primary measure.
FREEZING at -20 degree Celsius for 10 days kills the
CYSTICERCI.
== SANITARY INSPECTION of all the slaughtered pigs,
cows, and cattle should be done.
Hymenolepis nana
== Commonly know as the DWARF TAPEWORM
because it is the smallest tapeworm infection
HUMANS.
== It is found worldwide, mainly among children.
== It is the ONLY HUMAN TAPEWORM, which can
complete its entire life cycle in a single host,
indicating that it does not require an obligatory
intermediate host.
== Man can both harbor both the adult and the
larval stages of the parasite.
== ADULT WORMS: found in the ileum. It has a delicate
strobila measuring from 25 to 45 mm in length and 1
mm in width.
== SCOLEX: subglobular with four cup-shaped suckers.
There is a retractable rostellum armed with a single row
of 20 to 30 Y-shaped hooklet.s.
== The neck is long and slender.
== The anterior proglottids are short and the posterior
ones are broader than long.
== No more than 175 to 220 segments compose the
entire length of the strobilia.
== The proglottids measure 0.15 to 0.3 mm in length
and 0.8 to 1.0 mm in width.
== THE GENITAL PORES: are found along the same side
of the segments.
== Mature proglottids contain three ovoid testes
and one ovary in a more or less straight across the
segment. When become GRAVID, the testes and
ovary DISAPPEAR while the uterus hollows out and
becomes filled with eggs. SEPARATED from the
strobila and disintegrate as they pass out of the
intestines, releasing eggs in the stool.
== EGGS: are spherical or subspherical, measuring
30 to 47 um in diameter. The oncosphere has a thin
outer membrane and a thick inner membrane with
conspicuous bipolar thickenings, from each of which
arise 4 to 8 hair-like polar filaments embedded in
the inner membrane.
== The LIFE CYCLE has a dual pathway; a DIRECT and an
INDIRECT DEVELOPMENT.
1.) IN DIRECT CYCLE, the host ingest eggs which hatch
in the duodenum. The liberated embryos penetrate the
mucosal villi and develop into the infective cysticercoid
larvae. After 4 to 5 days, the larvae break out of the villi
and attaches to the intestinal mucosa to develop into
adults.
2.) INDIRECT DEVELOPMENT, Through the accidental
ingestion of infected ARTHROPOD intermediate host
like the RICE and FLOUR BEETLES (Tenebrio sp.) = the
cysticercoid larvae are released and will eventually
develop into the adult tapeworm in the intestines of
the host. It takes 20 to 30 days from time of ingestion,
for the eggs to appear in the feces.
== AUTOINFECTION can occur through the
fecal-oral transmission or within the small bowel,
ONCOSPHERES from the eggs are released and they
invade the host villi to start a new generation.
PATHOGENESIS and CLINICAL MANIFESTIONS
== The symptoms are generally produced because of the
patient’s immunological response to the presence of the
parasite. Light worm burden is generally ASYMPTOMATIC!
== CLINICAL MANIFESTIONS: include headache, dizziness,
anorexia, pruritus of the nose and anus, diarrhea, abdominal
pain, and PALLOR.
== CHILDREN: exhibit sleep disturbances that would stunt
growth.
== Rarely, convulsions would occur
== HEAVY INFECTIONS, may result in enteritis due to necrosis
and desquamation of the intestinal epithelial cells.
== With time, if the infected person is healthy, regulatory
immunity may limit or eventually clear the H. nana population
spontaneously.
DIAGNOSIS
== Specific diagnosis is made by demonstration of the
characteristics eggs in the patient’s stool.
== Concentration technique of the stool specimens
== Proglottids are not recovered because they undergo
DEGENERATION prior to passage with stools.
TREATMENT
== PRAZIQUANTEL 25 mg/kg single dose. The drug doses
is HIGHER than that for taeniasis because of the
relatively resistant CYSTICERCOIDS in the intestinal
tissue.
== Treatment is usually repeated two weeks to cover for
the worms emerging from the remaining viable
cysticercoids.
EPIDEMIOLOGY
== Found in countries with WARM CLIMATE like
Southern USA, Latin America, the Mediterranean, East
Asia and the Philippines (Southeast Asia).
== An estimated 20 million people are infected.
== Transmission generally occurs where there is poor
sanitation, overcrowding, and poor personal hygienic
practices.
== IT IS A FAMILIAL AND INSTITUTIONAL INFECTION
common in orphanages, day care centers and mental
institutions.
== In the Philippines, two independent surveys of Jueco
in 1983 and Cross et al. in 1984 showed a prevalence of
less than 1% in humans.
== The life cycle involves a single host and
transmission is direct. This makes prevention more
difficult especially in crowded dwellings. Emphasis
should be placed on personal hygiene and
environmental sanitation.
== INFECTED CASES should be thoroughly treated.
== FOOD must be properly stored and protected
from possible infestation with GRAIN BETTLE.
Dipylidium caninum
== is a very common intestinal parasite of dogs and cats
worldwide.
== Dipylidiasis in human is accidental
== ADULT WORM: PALE REDDISH 10 to 70 cm in length.
= SCOLEX is small and globular with four deeply cupped
suckers and a protrusible rostellum, which is armed with
1 to 7 rows of rosethorn shaped hooklets.
== PROGLOTTIDS: are narrow with two sets of male and
female reproductive organs and bilateral genital pores,
earning for this parasite the common name double-
pored tapeworm
== GRAVID PROGLOTTIDS have the size and shape of a
pumpkin seed and are filled with capsules or packets of
about 8 to 15 eggs enclosed in an embryonic membrane.
= Upon detachment, they either migrate out of the anus
or passed out with the feces.
= EGGS = are spherical, thin-shelled with a HEXACANTH
EMBRYO. Some of the eggs may remain in the fur of the
host’s resting place.
= LARVA of Ctenocephalides canis (dog flea),
Ctenocephalides felis (cat flea), Pulex irritans (human
flea), and Trichodectes canis (dog louse) INGEST THE OVA
AS THEY FEED ON EPIDERMAL DEBRIS.
= Inside the body of these arthropod, the HEXACANTH
EMBRYO develops into the CYSTICERCOID LARVAE,
which is able to survive the flea’s development.
INFECTION START when dogs, cats, and humans
accidentally ingest the flea.
== Infection is rarely multiple and symptoms are minimal.
== Slight intestinal discomfort, epigastric pain, diarrhea,
anal pruritus, and allergic reactions have been reported.
SOME ARE EVEN ASYMPTOMATIC
DIAGNOSIS
== Diagnosis is established upon recovery of the
characteristic gravid proglottids passed out or in chain.
== Proglottids should be pressed or flattened between
two glass slides for examination.
== STOOL EXAMINATION for the presence of egg IS NOT
RECOMMENDED, since the gravid proglottids do not
disintegrate in the intestines but in the environment.
TREATMENT
== Treatment consist of PRAZIQUANTEL 5 TO 10 mg/kg
given as a single dose.
EPIDEMIOLOGY
== Human infection is rare but has been reported in
European countries, USA, Argentina, Rhodesia, China,
and the Philippines,
= INFANTS and VERY YOUNG CHILDREN are usually
infected because of their close contact with their pet
cats and dogs.
= In the Philippines, the first human infection was
reported as early as 1912 by M.P. Mendoza-Guanzon in
a child.
= SURVEYS of dogs in the city of Manila showed a
prevalence of 5.19 to 36% while dissection of dog and
cat fleas for cysticercoids showed only a prevalence of
2.4%
== Periodic deworming of pet cats and dogs is
recommended.
== Insecticide dusting of dogs and cats are effective
against fleas
== The POTENTIAL DANGER of playing with pets
must be included in the health education of
children.
Diphyllobothrium latum
== It is commonly called the “FISH TAPEWORM” or
the “BROAD TAPEWORM”.
== DIPHYLLOBOTHRIASIS refers to the intestinal
infection with the ADULT WORM.
== ADULT TAPEWORM: measures from 3 to 10 m in
length and may have 4,000 proglottids.
== SCOLEX is spatulate and measures 2 to 3 mm in
length by 1 mm in diameter. It has two brothia or
sucking grooves which are located dorsally and
ventrally.
== NECK: long and attenuated and is followed by
immature proglottids. The terminal four-fifths of the
worm is composed of mature and gravid proglottids.
== Unlike in taeniasis, the proglottids of D. latum
disintegrate only when the segment has completed
reproductive function.
= with the distention of the uterus, the uterine pore
is relaxed and unembryonated ova are discharged
from the proglottid. Approximately 1,000,000 OVA
may be released daily.
== OVA: Complete their development in water and
release the free-swimming coracidium, a ciliated
embryo, which is ingested by freshwater COPEPODS
of the genera Cyclops and Diaptomus
= The larva develop inside the copepod becoming
PROCERCOID LARVA
= The copepod is in turn ingested by the FISH.
= Inside the FISH, the PROCERCOID LARVA migrates
through fish tissues and develops into a
plerocercoid larva in the muscles and viscera.
= This fish is ingested raw or improperly cooked by
man, dog, cat, and other mammals which is the
definitive host of the D. latum
= AMONG FISH INTERMEDIATE HOSTS are perch,
trout, salmon, and pike.
== Infections are usually limited to one worm,
although there have been reports of mechanical
obstruction due to a large number of worms.
= Infected individuals may show no sign of disease.
Some, however, may experience nervous
disturbances, weight loss, weakness, and anemia.
= SYMPTOMS may be due to absorbed toxins or
byproducts of degenerating proglottids or due to
mucosal irritation.
= Vitamin B12 deficiency, the parasite consumes so
much of this vitamin that it is though to have 50%
times more B vitamins than that of T. saginata
DIAGNOSIS
= DEFINITE DIAGNOSIS is made on finding the
characteristic operculated eggs or on occasion,
proglottids in stools. Sometimes, proglottids may be
vomitted. Since eggs are usually numerous, direct fecal
smears usually suffice.
TREATMENT
== The drug of choice is PRAZIQUANTEL as 5 to 10 mg/kg
single dose.
== THE CRITERION FOR CURE is the recovery of SCOLEX
IN FECES AFTER TREATMENT. If it is not recovered , a
repeat stool examination is done after three months to
be certain that the patient is no longer infected.
EPIDEMIOLOGY
== Human infection is dependent on the presence of
human or animal definitive hosts, the presence of
suitable intermediate hosts, dietary habits, and amount
of pollution of fresh waters.
== The preference of consuming raw fish dishes and the
lack of sanitary toilet facilities contribute to the
transmission of the parasite.
== D. latum is prevalent in the temperate zones where
members of the population are avid fish-eaters. It is
present in the BALTIC countries, Switzerland, Romania,
and the Danube Basin.
= In ASIA, Russia, Turkistan, Israel, Northern Manchuria,
and Japan.
= In the Americas it can be found in CHILE, Argentina
and in some North American states and Canada.
THE END, THANK YOU!
COCCIDIANS and
PLASMODIUM
Coccidians
Coccidian parasites are members of the Class
Sporozoea in the Phylum Apicomplexa.
The phylum name comes from the apical

complex that is present at some stage of the
parasite and is made up of elements, such as the
polar rings, rhoptries, micronemes, conoid, and
subpellicular microtubules. (But can only be
viewed under ELECTRON MICROSCOPY)
Life cycle: is characterized by an alternation of
generations one SEXUAL and one ASEXUAL
(occurring in the same host or in another host)
== ASEXUAL REPRODUCTION: Multiplication is by

SCHIZOGONY
== SEXUAL REPRODUCTION: Multiplication is by
SPOROGONY
Isospora belli
Infection with Isospora belli develops after
ingestion of an OOCYST containing two sporocysts
with each containing four sporozoites.
== Excystation occur in the SMALL INTESTINE, and
the released sporozoites enter the EPITHELIAL CELLS
of the DISTAL DUODENUM and PROXIMAL ILEUM.
== TROPHOZOITES develop into merozoites inside
the cells by SCHIZOGONY (as the number of
SCHIZONTS rupture it releases new trophozoites,
merozoites, and schizonts)
== These new organisms eventually would undergo
sexual cycle and the development of micro- and
macrogametocytes occur. (Microgametocytes
would fertilize macrogametocytes with the
formation of ZYGOTES).
== Zygotes develop into OOCYSTS that would
eventually leave the intestinal cells and enter the
FECAL STREAM.
== OOCYSTS: are elongate and ovoidal in shaoe,
measuring 20 to 33 um by 10 to 19 um, attains
maturity within 48 HOURS following evacuation
with the STOOLS.
PATHOGENESIS and CLININAL MANIFESTATIONS
== Often asymptomatic, even with presence of
oocysts in stools
== If symptomatic, diarrhea usually occur but may
be intermittent for months.
== There may be fever, malaise, anorexia, abdominal
pain, and flatulence.
== “MALABSORPTION SYNDROM”
== AIDS patients, dissemination of the parasites into
other organs.
DIAGNOSIS
== Oocysts from stools detected using microscopy
after formalinethyl accetate concentration
addition.
== ENTERO-TEST
== DUODENAL ASPIRATE EXAMINATIONS
== MOLECULAR BASED TECHNIQUES
TREATMENT
== For asymptomatic, bed rest and a bland diet.
== Symptomatic, especially occurring in AIDS
patient, can be treated with TRIMETHOPRIM-
SULFAMETHOXAZOLE 160/800 mg 4X/D for 10 days.
EPIDEMIOLOGY
== FECAL-BORNE Parasite, so TRANSMISSION is
usually VIA FOOD AND WATER CONTAMINATION
== Poor Sanitary Conditions
== Good Sanitary Practices
== Washing and cooking of food properly
== Drinking safe water (boiling it first, if the area you
are visiting does not have a proper water system)
Cryptosporidium hominis
OOCYSTS: round and measure 4 to 5 um in
diameter. Each contains four sporozoites which
are present at the time of passage into the feces.
After ingestion, the oocysts would undergo
excystation and the sporozoites will attach to
the surface of the epithelial cell of the
gastrointestinal tract, where it will develop into
TROPHOZOITES and become Intracellular but
extracytoplasmic and attach to the brush borders.
== The TROPHOZOITE would divide by
SCHIZOGONY producing merozoites which enter
other cells to repeat the cycle.
MACROGAMETOCYTES and MICROGAMETOCYTES
are produce, which will the macrogamete will be
fertilized by microgamete.
== A ZYGOTE, develops later an OOCYTS which will
eventually pass in the feces.

== Cryptosporidiosis hominis was a little recognized
disease prior to the occurrence of AIDS.
== Immunocompetent host, Self-limiting diarrhea of
2 to 3 weeks and less commonly abdominal pain,
anorexia, fever, nausea, and weight loss.
AIDS patient, diarrhea becomes so severe that the
patient might eventually die. Bile duct and gall bladder
may become heavily infected and LEAD TO ACUTE AND
GANGRENOUS CHOLECYSTITIS.
== The parasite can also go to the respiratory system,
which will lead to chronic coughing, dyspnea,
bronchiolitis, and pneumonia.
DIAGNOSIS
== Stool examination: It could be Sheather’s sugar
flotation(commonly used) OR formalin-ethyl-acetate
concentration technique.
== INDIRECT FLUORESCENT ANTIBODY
== ENZYME IMMUNOASSAY
== DNA PROBING
== ACID-FAST STAINING: the quickest and cheapest method of
diagnosis
TREATMENT
== NITAZOXANIDE
== BOVINE COLUSTRUM
== PARANOMYCIN
== CLARITHROMYCIN
== AZITHROMYCIN
EPIDEMIOLOGY
== Universal distribution
== FAULTY WATER PURIFICATION SYSTEM most of
the time
== In Philippines, low 2.6% (a study conducted at
San Lazaro Hospital)
== SYNERGISTIC EFFECT of multiple disinfectants and
combined water treatment processes may reduce
the prevalence of C. hominis oocyst in drinking
water.
== When swimming to natural water and swimming
pools especially stagnant, avoid swallow the water.
Cyclospora cayatanensis
Originally called the cyanobacterium-like body
(CLB), but upon careful study, it was found to be a
coccidian parasite.
OOCYST: 8 to 10 um in diameter and pass in the
feces. (UNSPORULATED) when passed but after 5
or more days, two SPOROCYSTS develop.
WHEN INGESTED, the sporozoites are released
and enter intestinal cells to go through schizogony
and gametogony.
== The onset of symptoms may occur 12 to 24 hours
after exposure.
== CHRONIC INTERMITTENT WATERY DIARRHEA
occurs early in the infection and may alternate with
constipation (6 to 7 weeks with 6 or more stools per
day)
== FATGIUE, ANOREXIA, WEIGHT LOSS, NAUSEA,
VOMITING, ABDOMINAL PAIN, FLATULENCE,
BLOATING and DYSPNEA may develop.
== “D-XYLOSE MALABSORPTION”
== However, IMMUNITY MAY RESULT WITH
REPEATED INFECTIONS.
DIAGNOSIS
== Microscopic examination of the stool
== Acid-fast staining (Kinyoun’s stain)
== Autofluorescent
== Fluorescent microscopy
== PCR (used to differentiate Cyclospora from Eimeria
spp. Closely related protozoans)
== Safranin staining technique
TREATMENT
== The disease is self-limiting and treatment is not
necessary if the symptoms are mild.
== CO-TRIMOXAZOLE 160/800 mg twice daily for 7
days.
EPIDEMIOLOGY
== Found in many countries, but are thought to be
endemic in HAITI, PERU, NEPAL.
== Raspberries imported from Guatemala were
incriminated in the INFECTIONS IN THE UNITED
STATES.
== CONTAMINATED WATER
== ATTACH ITSELF TO LEAFY VEGETABLES (OOCYST
FORM)
== NO ANIMAL RESERVOIRS
Toxoplasma gondii
A coccidian parasite that belongs to the phylum
Apicomplexa.
Worldwide distribution and that infects human
and many species of animals.
INFECTIVE STAGES: TACHYZOITE, BRADYZOITE,
AND OOCYST
== COMPLETE LIFE CYCLE occurs only in the
members of the cat family (Felidae) which serve as
definitive host.
== The EXTRAINTESTINAL STAGES are the ASEXUAL
STAGES: TACHYZOITES and BRADYZOITES.
== CAT INTESTINAL EPITHELIUM (MEROZOITES multiply
(schizogony) and are then followed by differentiation
into macrogametes and microgametes.
== FERTILIZATION: give rise to an OOCYST: OVOIDAL in
shape, has thin wall and measures 10 to 13 um by 9 to
11 um.
== OOCYSTS are passed out with the feces of the cat in
the unsporulated stage. (which will undergo sporulation
within 3 to 4 days)
== Ingestion of mature OOCYSTS leads to infection
through contamination of food and water.
== When the mature oocyst reaches the intestine of the
new host, it undergo EXCYSTATION, liberating four
SPOROZOITES which can PENETRATE THE LAMINA
PROPIA OF THE INTESTINE.
== THEN, the parasites gain entry to the LYMPHATIC
SYSTEM, then spread to the different organs, fluid,
tissues of the BODY.
== TOXOPLASMA: INTRACELLULAR PARASITE, which
infected different kinds of nucleated cells including
macrophages.
== As the sporozoites enter the new cell, it transforms
into a TACHYZOITE; which will eventually give rise to
slow multiplying BRADYZOITE that form CYST (ONLY
THIS STAGES ARE PRESENT IN HUMANS & OTHER
HOST)
== ASEXUAL MULTIPLICATION: by variation of binary
fission called ENDODYOGENY, which will
eventually burst LIBERATING trophozoites which will
invade neighboring or other cells.
== Because of this, the parasite can be transferred
through GRANULOCYTE BLOOD TRANSFUSION,
ORGAN TRANSPLANT, BONE MARROW TRANSPLANT,
and the BRADYZOITES can be acquired by eating
meat of infected animals, herbivores and carnivores.
PATHOGENESIS and CLINICAL MANIFESTATION
== Commonly asymptomatic as long as the immune
system of the patient is functioning well.
== Immune system quickly responds to the
presence of the parasite, which in turn, adapt by
transforming into BRADYZOITES that are protected
by CYST WALL and PROLIFERATE AT A SLOW RATE.
(Cyst: can be found in brain, skeletal, heart, and
retina)
== Clinical manifestation become apparent when the
immune system is suppressed as in old age, drug-
induced immunosuppression after organ transplant,
or patient with AIDS.
== ENCEPHALITIS: most common manifestation
== MYOCARDITIS and FOCAL PNEUMONIA, have
also been reported
== RETINOCHOROIDITIS, LYMPHORETICULAR
HYPERPLASIA WITH ENLARGEMENT OF THE
POSTERIOR CERVICAL LYMPH NODE, HEPATITIS,
SPLENOMEGALY, PNEUMONIA, EXTRAMEDULLARY
HEMATOPOIESIS, AND FAILURE TO GAIN WEIGHT.
== STILLBIRTH and ABORTION may result when
mother acquire the infection during the first
TRIMESTER of pregnancy.
DIAGNOSIS
== Identification of the parasite can be done through
examination of tissue imprint stained with GIEMSA.
== TISSUE SECTIONS can be processed and stained with
HEMATOXYLIN and EOSIN.
== SERODIAGNOSTIC METHODS to detect antibodies
against T. gondii
== PCR
== Indirect Hemagglutination test
== Indirect Fluorescent Antibody Test
== ELISA (Enzyme Linked Immunosorbent Assay)
== Latex Agglutination
TREATMENT
== PYRIMETHAMINE (25 to 100 mg daily) and
SULFADIAZINE (1 to 1.5 g qid daily) used in
combination for one month. (These drugs do not kill
Toxoplasma but keep it under control)
== These drugs have serious side effects and one of
that is it LOWER BLOOD COUNRS IN MOST PEOPLE,
so it should be given together with LEUCOVORIN
(FOLIC ACID).
EPIDEMIOLOGY
== ENDEMIC WORLDWIDE in humans and
domesticated and wild animals as well.
== In Philippines, only 2.4% of the population is
seropositive for Toxoplasma gondii
== Food should be protected from contamination by
cat feces.
== Meat and Eggs should be cooked well.
== Unpasteurized milk should be avoided.
== Pregnant should avoid contact with cats
PLASMODIUM
Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
== The causative agent of Malaria, which is still
considered the most important parasitic disease
affecting man as it is responsible for 1.5 to 2.7
million deaths annually.
== It has been identified by WHO as one of the three
major infectious disease threats, along with HIV and
TUBERCULOSIS.
TRANSMITTIED by the BITE of an infected
FEMALE MOSQUITO belonging to the genus
Anopheles.
== P. falciparum and P. vivax responsible for the
90% of all the cases of human malaria.
Various processes comprise the life cycle of the
parasite. The ASEXUAL CYCLE IN HUMANS consists of
SCHIZOGONY, and GEMOTOGONY, which leads to the
formation of GAMETOCYTES.
== THE SEXUAL CYCLE IN THE MOSQUITO, involves
SPOROGONY, which leads to the formation of
SPOROZOITES.
== 1.) The infected FEMALE MOSQUITO bites and sucks
blood from the human host. In the process, salivary
fluids containing sporozoites are also injected.
== 2.) The parasite are immediately carried to the liver
and enter the parenchymal cells. The parasite then
commence EXOERYTHROCYTIC SHIZOGONY, which
produces merozoites in varying duration and amounts
depending on the species of the Plasmodium.
== 2.) Merozoites proceed to the PERIPHERAL BLOOD
to enter the erythrocytes (RBC). P. vivax and P. ovale re-
invade the livers cells forming HYPNOZOITES, while the
other species do not.
== 3.) With in the red blood cell, the merozoite grows as
a ring form developing into a TROPHOZOITE, which will
further divided to form more merozoites.
== 4.) P. falciparum merozoites can alter the structural
and antigenic properties of these red cells.
== 5.) The malarial parasites feed on the hemoglobin
resulting in the production of pigment. Which will soon
after rupture and the merozoites are released into the
blood, ready to enter new erythrocytes. (THIS
ASEXUAL LIFE CYCLE IS SYNCHRONOUS, PERIODIC, AND
SPECIES-DETERMINED)
== 6.) Some MEROZOITES develop into
MICROGAMETES (male) or MACROGAMETES (female)
which are picked up by feeding female mosquitoes for
COMPLETION OF THE LIFE CYCLE.
== 7.) In the gut of the female mosquito, the male
gametocytes exflagellate and produce eight sperm-like
microgametes which may fertilize the female
macrogametes to form a ZYGOTE.
== 8.) The ZYGOTE, becomes motile and PENETRATES
the mosquito’s GUT as an OOKINETE, which then
develops into an OOCYST.
== 9.) OOCYST, grows and produces sporozoites, which
escape from the oocyst and enter the SALIVARY
GLANDS OF THE MOSQUITO. (WHICH WILL THEN BE
INJECTED TO A NEW HUMAN HOST, when the
mosquito takes a blood meal)
== MORPHOLOGICALLY: early trophozoites form is a
RING-SHAPED STAGE with a RED CHROMATIN dot
and A SMALL AMOUNT OF BLUE CYTOPLASM when
stained with GIEMSA or WRIGHT’S STAIN.
== HAS A LARGE AMEBOID CYTOPLASM, which is
spread through the erythrocyte.
== GAMETOCYTES: fill the entire RBC, large
chromatin mass and a blue cytoplasm with pigment.
It is round to BANANA-SHAPED.
== The interval of time from sporozoite injection to
detection of parasites in the blood is the PREPATENT
PERIOD (DEPENDING ON THE SPECIES).
== P. falciparum = 11 to 14 days
== P. vivax = 11 to 15 days
== P. ovale = 14 to 26 days
== P. malariae = 3 to 4 weeks
== The time between sporozoite injection and the
appearance of clinical symptoms is typically 8 to 40
days, depending again on the species involved.
(INCUBATION PERIOD)
== THERE ARE NO ABSOLUTE DIAGNOSTIC CLINICAL
FEATURES OF MALARIA EXCEPT FOR THE REGULAR
PAROXYSMS OF FEVER WITH ASYMPTOMATIC
INTERVALS.
== PRODROMAL SYMPTOMS may include a FEELING
OF WEEKNESS AND EXHAUSTION, A DESIRE TO
YAWN AND STRETCH, ACHING BONES, LIMBS, AND
BACK, LOSS OF APPETITE, NAUSEA AND VOMITING,
AND SENSE OF CHILLINESS.
== EPIGASTRIC DISCOMFORT.
== THE CLASSICAL MALARIA PAROXYSM HAS THREE
STAGES
1.) Cold Stage= starts with a sudden inappropriate
feeling of coldness and apprehension (VIOLENT TEETH
CHATTERING and SHAKING OF THE WHOLE BODY)
2.) Hot Stage = Patient becomes hot and manifests with
headache, palpitations, tachypnea, epigastric
discomfort, thirst, nausea and vomiting. The
temperature may reach a peak of 40 to 41 degree
Celsius. (skin is flushed and hot)
3.) Sweating Stage = Defervescence or diaphoresis
ensues with the patient manifesting with profuse
sweating. The temp lowers over the next 2 to 4 hours,
and symptoms diminish.
== The total duration of the typical attack is 8 to 12
hours.
DIAGNOSIS
== PROMPT and ADEQUATE diagnosis of malaria is
necessary for the disease to be managed effectively
thus preventing the life threatening complications.
== MICROSCOPIC IDENTIFICATION using Giemsa or
WRIGHT’S stain
== QUANTITATIVE BUFFY COAT (QBC) method uses a
specially prepared capillary tube coated with
acridine orange.
== Malaria RAPID DIAGNOSTIC TEST (malaria RDTs)
== PCR
TREATMENT AND PREVENTION
== ANTIMALARIAL DRUGS (causal prophylactic drugs,
blood schizonticidal drugs, tissue shizonticides,
gametocytocidal drugs,
== THE MAIN USES OF ANTIMALARIAL DRUGS ARE:
1.) PROTECTIVE (prophylactic)
2.) CURATIVE (therapeutic)
3.) PREVENTIVE
== CHLOROQUINE
== SULFADOXINE-PYRIMETHAMINE COMBINATION OF
QUININE
== ARTEMISININ AND ITS DERIVATIVES (Qinghaosu
derivatives)
== ATOVAQUONE, PYRONARIDINE, DESFEROXAMINE
(new generation of antimalarial drugs)
== Personal protection measure against
mosquito bites are also very helpful.
== The use of insecticide-treated nets (ITNs)
== The use insecticide on areas where there
are a lot of stagnant water
THE END, THANK YOU!
Protozoan Infections
LEARNING OUTCOMES
To describe the classification of protozoan
parasite with great medical and public
importance
To understand the Biology of each protozoan
parasite, its infective stage, and transmission to
human
To familiarize the Epidemiology of each
protozoan parasite
To describe the treatment and prevention of the
spread of protozoan infection
Protozoan Classification
All protozoan fall under the KINGDOM PROTISTA
DIVIDED into two several phyla but the major

organisms causing disease in man belong to
these phyla.
1.) PHYLLUM SACROMASTIGOPHORA
2.) PHYLLUM CILIOPHORA
3.) PHYLLUM APICOMPLEXA
4.) PHYLLUM MICROSPORA
PHYLLUM SACROMASTIGOPHORA
2 SUBPHYLLA:
1.) Subphyllum Mastigophora = organelles
responsible for the organism locomotion are WHIP-
LIKE structures arising from the ectoplasm called
FLAGELLA.
 These includes HEMOFLAGELLATES namely,

Giardia, Chilomastix, Trichomonas, Dientamoeba,
Trypanosoma, and Leishmania.
2.) Subphyllum Sarcodina = organelles responsible
for the organism locomotion are HYALINE FOOT-
LIKE extrusions from the ectoplasm called
PSEUDOPODIA.
 Amebae, namely, Entamoeba, Endolimax,

Iodamoeba, Acanthamoeba, and Naegleria.
PHYLLUM CILIOPHORA
= Organelles responsible for the organism locomotion
are HAIR-LIKE projections from the ectoplasm called
CILIA.
= Includes only one parasite of medical and public

health interest, Balantidium coli.
PHYLLUM APICOMPLEXA
= have an APICAL COMPLEX at the anterior end
which consist of POLAR RINGS, SUBPELLICULAR
TUBULES, CONOID, RHOPTRIES, and MICRONEMES.
= These structures are involved in the PENETRATION
and INVASION of target cells.
= All members are parasitic
= CLASS SPOROZOA, namely, Plasmodia, Babesia,
Toxoplasma, Isospora, Cryptosporidium, and
Cyclospora.
= These parasites have been reportedly practically
from ALL ORGAN SYSTEMS both in human and
animals.
PHYLLUM MICROSPORA
= Consists of spore-forming parasites of both
vertebrates and invertebrates.
= Contains 100 more genera
= Members are similar in that they posses a unique
EXTRUSION APPARATUS which enable them to
INSERT INFECTIVE MATERIAL TO THE HOST CELL;
HIGHLY COILED POLAR FILAMENT.
= Enterocytozoon binuesi and Encephalitozoon spp.
CLASSIFICATION OF PROTOZOAN PARASITES
SACROMASTIGOPHORA
SARCODINA Acanthamoeba castellani

Endolimax nana
Entamoeba coli
Entamoeba dispar
Entamoeba gingivalis
Entamoeba histolytica
Iodamoeba butschlii
Naegleria fowleri
MASTIGOPHORA Chilomastix messnili
Dientamoeba fragilis
Giardia lamblia
Trichomonas hominis
Trichomonas tenax
Trichomonas vaginalis
Leishmania braziliensis
Leishmania donovani
Trypanosoma brucei complex
Trypanosoma cruzi
CILIOPHORA Balantidium coli
APICOMPLEXA Babesia spp.

Cryptosporidium hominis
Cyclospora cayetanensis
Isospora belli
Plasmodium spp.
Toxoplasma gondii
MICROSPORA Enterocytozoon bineusi

Encephalitozoon spp.
Vittaforma cornea
Trachipleistophora hominis
Pleistophora spp.
Brachiola vesicularum
Microsporidium spp.
PROTOZOAN PARASITES are provided with
NUCLEUS/NUCLEI, CYTOPLASM, an OUTER
LIMITING MEMBRANE, and CELLULAR
ELABORATIONS called ORGANELLES.
MANY of these protozoans require a WET

ENVIRONMENT FOR FEEDING, LOCOMOTION,
OSMOREGULATION, and REPRODUCTION.
INFECTIVE STAGE: CYSTS, which are relatively

resistant to environmental changes compared to
its vegetative stages called TROPHOZOITES
Intestinal Amebae
Seven species of amebae are commonly found in
human fecal specimens.
THESE ARE: Entamoeba histolytica, E. dispar, E.
hartmanni, E. coli, E. polecki, Endolimax nana, and
Iodamoeba butschlii .
Trophozoites divide by binary fission.
Most of cysts-forming amebae go through

nuclear division, and then divide again after
EXCYSTATION IN A NEW HOST.
Entamoeba histolytica
Subphyllum: Sarcodina
Superclass: Rhizopoda
Class: Lobosea
Order: Amoebida
Family: Entamoebidae
Genus: Entamoeba
 Two morphologically INDUSTINGUISHABLE species

of Entamoeba histolytica, one the was capable of
causing DISEASE (Entamoeba histolytica) and the
other is a harmless commensal called Entamoeba
dispar
Pseudopod-forming nonflagellated protozoan
parasite.
CAUSE invasive intestinal and extraintestinal
disease.
LIFE CYCLE: 2 STAGES
i. INFECTIVE CYSTS
ii. INVASIVE TROPHOZOITE
No other host than human is implicated in the

life cycle, although natural infection of primates
has been reported.
The QUADRINUCLEATE CYST is resistant to gastric
acidity and desiccation and can survive in a moist
environment for several weeks.
TROPHOZOITES multiply by binary fission; then

encyst producing uninucleate cyst, which then
undergo two successive nuclear divisions to form
characteristic quadrinucleate cysts
Infection starts with ingestion of fecally-

contaminated material. (food or water) or direct
colonic inoculation through contaminated enema
equipment (water thermomter, gloves, apron,
surgical equipment)
SIGNS AND SYMPTOMS
= Amebic colitis clinically presents as gradual onset of
ABDOMINAL PAIN and DIARRHEA with or without blood
and mucus in the stools. (incubation period of 8 to 10
days)
= ADULTS: intermittent diarrhea alternating with
constipation
= CHILDREN: may develop fulminant colitis with severe
bloody diarrhea, fever, and abdominal pain
= OCCURS less than 1% of intestinal infections.

= It can be mistaken for CARCINOMA (mass-like lesion)
= Asymptomatic may also occur especially to
areas/communities where it is considered endemic.
AMEBIC LIVER ABSCESS (ALA) is the most
common extraintestinal form of amebiasis.
= FEVER(77%) and RIGHT UPPER QUADRANT (RUQ)
pain (83%); in a study of 206 adults with ALA for
acute cases (less than 2 weeks duration).
= Chronic disease (more than 2 weeks duration) in
adults involves wasting disease with significant
weight loss rather than fever.
= Only 30% of ALA cases have concurrent diarrhea
= MORTALITY: uncomplicated ALA is less than 1%.

PATHOLOGY
= E. histolyitca was named by Schaudinn in 1903
because of its ability to lyse human tissues.
= its invasive process is initiated when the
TROPHOZOITE STAGE is able to PENETRATE through
the mucus layer covering the COLONIC
EPITHELIUM.
= These penetration is facilitated by expression of
virulence factors (3 FACTORS), three of which have
been extensively studied and characterized up to the
molecular level.
1.) Gal/Gal Nac lectin which mediates adherence to
host cells. (it cause thinning of the MUCIN LAYER)
2.) Amebapores which form pores in host cell
membranes (Shortening of the villi)
3.) CYSTEINE PROTEINASES, which are cytopathic for
host tissues. (Breakdown of extracellular matrix).
From the primary site of the colon, E. histolytica

trophozoites reach the liver through THE PORTAL
VEIN and cause PERIPORTAL INFLAMMATION.
(amoebic hepatitis)
 Once in the liver, the trophozoites lyse both
inflammatory and liver cells and the abscess
becomes filled with NECROTIC, PROTEINACEOUS
DEBRIS, described as ANCHOVY SAUCE-LIKE
ASPIRATE.
COMPLICATIONS:
= The most serious complication of amebic colitis is
perforation and secondary bacterial peritonitis.
= Colonic perforation occurs 60% of fulminant colitis
cases.
= in ALA, the most serious complications are rupture
into the pericardium with a mortality rate of 70%,
RUPTURE into the pleura with mortality rate of 15 to
30% and super infection, Intraperitoneal rupture which
occurs in 2 to 7.5% cases in the second most common
complication.
= Secondary AMEBIC MENINGOENCEPHALITIS occurs in
1 to 2% and it should be considered in cases of
amebiasis with abnormal mental status.
IMMUNITY:
= Activated T cells kills E. histolytica by:
1.) Directly lysing trophozoites in a contact-
dependent processes
2.) Producing cytokines which activate macrophages
and other effector cells (neutrophils and
eosinophils). (INTERFERON (IFN-) and ITERLEUKIN
(IL-2) may have a role in activating macrophages
and amebicidal activity)
3.) Providing helper effect for B cell antibody
production.
HOWEVER, amebiasis have shown to suppress
the immune system of human and animals
(immunosuppression) during the acute stage of
amebiasis. CHARACTERIZED BY THESE STATE.
= T cell HYPORESPONSIVE
= SUPPRESSED proliferation and CYTOKINE
PRODUCTION.
= DEPRESSED DELAYED TYPE HYPERSENSITIVITY
(DTH).
= Macrophage suppression
DIAGNOSIS
= Microscopic Diagnosis
== The standard method of parasitologic diagnosis is microscopic
detection of the trophozoites and cysts in stool specimens.
(IDEALLY: minimum of 3 stool specimens collected in diff days
should be examined)
== Fresh stool, should be examined within 30 minutes from
defecation. (DFS or Direct fecal smear, with saline solution alone,
the microscopists can observe trophozoites motility
(UNIDIRECTIONAL MOVEMENT FOR E. histolytica)
= STAINING: using saline and methylene blue,

Entamoeba species(will stain BLUE) will differentiate
from WBC.
PCR, ELISA, and ISOENZYME ANALYSIS: are use
dor differentiation of E. histolytica and E. dispar
Serology: Detection of antibodies in the serum is
still the key in the diagnosis of amebic liver
abscess (ALA). Microscopic detection cannot be
done because aspiration is an invasive procedure
and trophozoites are missed because they are
located in the periphery of the abscess.
Radiographic Studies: Ultrasound, computerized
tomography (CT scan), and Magnetic resonance
imaging (MRI) are non invasive and sensitive
methods in early detection of ALA.
TREATMENT AND PROGNOSIS:
= The treatment of amebiasis has two objectives
1.) To cure invasive disease at both intestinal and
extra-intestinal sites
2.) To eliminate the passage of cysts from the
intestinal lumen.
== METRONIDAZOLE is the drug of choice.
== TINIDAZOLE and SECNIDAZOLE are also effective.
== DILOXANIDE FUROATE for asymptomatic cysts
passers.
DISEASE DRUG OF CHOICE ADULT DOSE PEDIATRIC DOSE
ASYMPTOMATIC CYST - DILOXANIDE - 500 mg tid (THREE - 20 mg/kg/d in 3

PASSER FUROATE TIMES A DAY) X 10 doses X 10 days (max
- METRONIDAZOLE days 1500 mg/d)
AMEBIC COLITIS - TINIDAZOLE - 500 - 700 mg tid X - 35 – 50 mg/kg/d in

- METRONIDAZOLE 7 – 10 d 3 doses X 7-10
- 2 grams/day days
divided tid X 3 - 50 mg/kg/d
Days divided tid X 3 d
AMEBIC LIVER - TINIDAZOLE - 750 MG tid X 10 d - 35 – 50 mg/kg/d in

ABSCESS (ALA) - 2.5 g orally once 3 doses x 7 – 10 d
- 600 mg bid or 800 - 60 mg/kg/d
mg tid X 5 d divided tid (max 2
grams) X 3 d
PREVENTION AND CONTROL:
= One of the best estimates suggested the existence
of 500 million cases in the world (more prevalent in
tropics).
= DEPENDS on INTEGRATED and COMMUNITY-
BASED efforts to IMPROVE ENVIRONMENTAL
SANITATION and TO PROVIDE FOR SANITARY
DISPOSAL OF HUMAN FECES, SAFE DRINKING WATER,
AND SAFE FOOD.
= ACHIEVED ONLY through HEALTH EDUCATION
AND PROMOTION.
Commensal Amebae
The presence of commensal amebae in the stool of
an INDIVIDUAL is significant for two reasons:
1.) They may be mistaken for the pathogenic E.
histolytica
2.) They are indication of fecal contamination of food
or water.
== ACCURATE diagnosis of the commensal amebae is
crucial!!
 ALL SPECIES have the following
stages:
1.) TROPHOZOITES
2.) PRECYST
3.) CYST
4.) METACYSTIC TROPHOZOITE
= Except for Entamoeba gingivalis which has no cyst
stage and does not inhibit the intestine
 Metacystic trophozoites colonize the large
intestines and live on the mucus coat covering the
intestinal mucosa. These amebae are non-invasive
and do not cause disease.
Entamoeba dispar
= Morphologically similar to E. histolytica, but their DNA
and ribosomal RNA are different. Isoenzyme analysis is
different from E. histolytica
Entamoeba hartmanni
= This is also similar to E. histolytica except that it is
much smaller, and does not ingest RBC.
= more SLUGGISH in movement
= Adult cyst measure from 5 to 10 um, are
quadrinucleated and have a coarse cytoplasm
= Immature cyst usually have chromatoidal bars, which
may be short with tapered ends, or thin and bar-like.
Entamoeba coli
= is cosmopolitan in distribution and is a harmless
inhabitant of the colon.
= The Trophozoite can be differentited from E.
histolytica by the following features:
1.) More vacuolated or grannular endoplasm with
bacteria and debris but no RBC.
2.) A narrower, less differentiated ectoplasm
3.) Broader and blunter pseudopodia
4.) More sluggish undirected movements
5.) Thicker, irregular peripheral chromatin with large
eccentric karyosome in the nucleus
= E. coli cyst may be differentiated from E.
histolytica by:
1.) ITS LARGER SIZE
2.) GREATER NUMBER OF NUCLEI ( 8 VERSUS 4 in E.
histolytica)
3.) MORE GRANULAR CYTOPLASM
4.) SPLINTER-LIKE CHROMATOIDAL BODIES
Entamoeba polecki
= is a parasite of pigs and monkeys
= Rarely, it may infect humans
= It can be distinguished from E. histolytica in that
its CYST is consistently UNINUCLEATED.
= It stained fecal smears, the nuclear membrane,
and karyosome are very prominent.
Entamoeba gingivalis
= can be found in the MOUTH
= lives on teeth surface, gum, in gum pockets, and
sometimes TONSILLAR CRYPTS.
= It moves quickly and has numerous blunt
PSEUDOPODIA
= Food vacuoles that contain cellular debris and
bacteria are numerous
= NO CYST STAGE HAS BEEN DOCUMENTED
= TRANSMISSION: kissing, droplet spray, or by
sharing utensils.
Endolimax nana
= Characterized by its small size of 6 to 15 micrometer
= SLUGGISH MOVEMENT
= Nucleus: Irregular karyosome
= CYST: are about 6 to 12 micrometer in diameter and
QUADRINUCLEATE when mature.
Iodemoeba butschlii
= Identified by its characteristic large vesicular NUCLEAR
with a large endosome surrounded by achromatic
granules.
= CYST: UNINUCLEATED and has a large glycogen body
which stain deeply with IODINE.
EPIDEMIOLOGY:
= In single stool examinations of over 30,000
FILIPINOS. The PREVALENCE of:
= Entamoeba coli was about 21%
= Endolimax nana about 9%
= Iodomoeba butschlii about 1%
 Protozoan cyst were observed in 13.5% of

overseas Filipino workers (OFW) screened by UP
Manila back in 1998.
A study on intestinal parasitic infections among
FOOD SERVICE WORKERS in TERTIARY HOSPITAL in
MANILA revealed that 20.3% were infected with
Endolimax nana and 13.6% with Entamoeba coli.
Another study of food handlers in selected school

canteens in Manila showed infection rates of
22.8% for Endolimax nana, 0.8% each for
Entamoeba hartmanni and Iodomoeba butschlii
FREE-LIVING PATHOGENIC
AMEBAE
Acanthamoeba sp. A small free-living ameba
characterized by an active trophozoite stage and a
dormant cyst stage.
Sluggish movement of its trophozoites which feed

on gram-negative bacteria, blue green algae, or
yeasts.
Reproduce by Binary Fission; and ENCYST if the

environment is favorable.
MORPHOLOGICALLY: trophozoites exhibit
characteristically single and large nucleus with a
centrally-located, densely staining nucleolus, a
large endosome, finely granulated cytoplasm, and
a large contractile vacuole.
EXHIBITS SMALL, SPINY FILAMENTS for
locomotion known as ACANTHAPODIA. It
MOVES SLUGGISHLY WITH POLYDIRECTIONAL
MOVEMENT.
= Acanthamoeba has been definitely established as the
CAUSATIVE AGENT of GRANULOMATOUS AMEBIC
ENCEPHALITIS (GAE).
= Especially to chronically ill patients, people
undergoing immunosuppressive therapy or patients
with AIDS.
= PREDOMINANT SIGNS and SYMPTOMS: destructive

encephalopathy and associated meningeal irritation.
= NONSPECIFIC CONSTITUTIONAL manifestation:
FEVER, CHILLS, FATIGUE, and WEIGHT LOSS.
= Headache, Confusion, Somnolence, coma,

hallucinations, and seizures are cmmon.
NEUROLOGIC SYMPTONS: Focal hemiparesis,
cranial nerve palsies, visual disturbances or
ataxia, Increased intracranial pressure can cause
papilledema.
SKIN LESIONS are also an important diagnostic of
the infection
INCUBATION: 10 DAYS, with subacute and
chronic clinical course of infection that lasts for
several weeks.
= CLINICAL MANIFESTATIONS: Mental
abnormalities, meningism, localized neurological
signs and symptoms, and coma.
 Acanthamoeba has also been recognized as an
ocular surface pathogen, causing AMEBIC KERATITIS.
Associated with the use of soft contact lenses
(contaminated), immunocompromised PATIENTS.
SIGNS AND SYMPTOMS KERATITIS: CORNEAL
ULCERATION, Progressive corneal infiltration,
clouding, iritis, and scleritis, severe pain,
hypopyon, and LOSS OF VISION.
DIAGNOSIS:
= Acanthamoeba encephalitis is made only after
death in the majority of cases.
= has a fatal outcome in 3 to 40 days.
= Specific diagnosis depends on demonstrating the
trophozoites or cysts in TISSUES using
HISTOPATHOLOGIC STAINS and MICROSCOPY.
= Can be isolated from Cerebrospinal fluid(CSF) ad
cultured for further studies.
= Epithelial biopsy
= PCR, using specific primer pairs
TREATMENT and MANAGEMENT:
= 5-FLUOROCYTOSINE
= KETOCONAZOLE
= ITRACONAZOLE
= PENTAMIDINE
= AMPHOTERICIN B
= CLOTRIMAZOLE in Combination with Pentamidine,
Isethionate, and Neosporin
SURGICAL excision of the INFECTED CORNEA
EPIDEMIOLOGY:
= Acanthamoeba can be found anywhere freshwater,
seawater, ocean sediments, bottled mineral water,
swimming pools, soil, medicinal pools, contact
lenses, etc. In humans, found in throat, nasal cavity,
intestines, cerebral tissue, lung tissue, skin wounds,
cornea.
= More hygienic practices could be a practical for
prevention and control.
= Contact lens wearers are advised to disinfect their
lenses regularly
Naegleria spp.
= a free-living ameboflagellate, so called because the
organism can exist as an ameba (trophozoite form)
and as a flagellate form (swimming form)
= Naegleria fowleri, causes fatal
meningoencephalitis in humans and laboratory mice
as well.
= It can cause degenerative or cytopathic effects in
mammalian cell cultures.
= Isolates: thermally-polluted stream, an artificially-
heated swimming pool, and from a brain aspirate of
a young patient.
TROPHOZOITE: can easily be characterized by
LOBOSE MONOPSEUDOPODIUM and a very
prominent nucleus with a centrally-located
nucleolus.
CAUSES: human disease ranging from gastritis

and diarrhea to a rapidly fatal primary amebic
meningoencephalitis (PAM), a rare disease that
leads to inflammation of the brain and
destruction of brain tissues.
DIAGNOSIS:
= based on the actual presence of the trophozoites in
the brain and cerebrospinal fluid.
= ASPIRATES from suspected infections, when
introduced into bacteria-seeded agar culture medium,
exhibit trophozoites within 24 hours of culture.
= Under the microscope the trophozoites can be
identified by the presence of blunt, lobose
pseudopodia and directional movement.
= PCR and ELISA
TREATMENT:
= POLYTENE ANTIBIOTIC AMPHOTERICIN B is the
drug of choice for PAM.
= CLOTRIMAZOLE exhibits amebicidal activity in
vitro but has no similar effects in vivo.
= AZITHROMYCIN additional drugs to treat PAM
EPIDEMIOLOGY:
= Naegleria spp. Have been isolated from samples
obtained from chlorinated swimming pool,
freshwater lakes, thermal springs, domestic water
supplies, thermally polluted water, sewage, soil, air,
humidifier systems, cell cultures, and human throat
and nasal cavities.
PREVENTION AND CONTROL:
= There is NO KNOWN MEANS OF PREVENTION and
CONTROL.
= Avoid swimming on stagnant swimming pools,
unchlorinated pools, mud-like lakes and ponds.
CILIATES and FLAGELLATES
Balantidium coli (ciliates)
= The CAUSATIVE AGENT of Balantidiasis or
Balantidial dysentery.
Giardia lamblia (flagellates)
= lambliasis
Balantidium coli
= exhibits both trophozoite and cyst stages
= TROPHOZOITE: measure 30 to 300 um long and 30 to
100 um wide.
= It has a cystostome through which it acquires food,
and cytophyge through which it excretes waste.
= It has two dissimilar nuclei (MACRO and
MICRONUCLEUS) and two contractile VACUOLES
= CYST: measures 40 to 60 um in diameter
= spherical and ovoid, covered with thick cell walls.
= Unlike amebae, ENCYSTATION DOES NOT RESULT IN
AN INCREASE IN NUMBER OF NUCLEI.
Trophozoites inhabit the lumen, mucosa, and
submucosa of the large intestines, primarily the
cecal region.
= Multiply through BINARY FISSION and cause
PATHOLOGIC CHANGES in the COLONIC MUCOSAL
WALL AND MUCOSA
 CYSTS are formed principally as protection for

survival outside the host.
PATHOGENESIS and CLINICAL
MANIFESTATIONS
== TISSUE INVADER
== trophozoite capable of attacking epithelium and
creating characteristic ULCER with rounded base and
wide neck, in contrast to flasked shaped, narrow necked
ulcers of amebiasis.
== Can invade/spread to the MESENTERIC NODES, the
PLEURA, and THE LIVER.
== Majority of the symptomatic patients complain of
diarrhea and dysentery associated with abdominal
discomfort or pain with nausea and vomiting for acute
cases may have 6 to 15 episodes of diarrhea per day.
== Many infected individuals are asymptomatic.
In chronic disease, diarrhea may alternate with
constipation, and may be accompanied by anemia
and cachexia.
= also associated with non-specific abdominal
pain/symptoms.
= Fulminant diseases (SEVERE) occur in
immunocompromised or malnourished patients.
= COMPLICATIONS: include INTESTINAL
PERFORATION and ACUTE APPENDICITIS
DIAGNOSIS: Microscopic demonstration of
trophozoites and cysts in the feces using direct
examination or concentration techniques.
= BIOPSY specimens from lesions obtained from
SIGMOIDOSCOPY.
TREATMENT:
= TETRACYLINE 500 mg 4X/d
= METRONIDAZOLE 750 mg three times daily for 5
days
= IODOQUINOL 650 mg 3x/d
EPIDEMIOLOGY:
= Uncommon in temperate climates
= It is found associated with pigs throughout the
tropics.
= It is also associated with 56 mammalian species
several of which belongs to families of primates.
= HIGHER PREVALENCE: Poor environmental
sanitation.
= exposure to swine is seen in about 25% of human
cases.
= Human infections in the Philippines have been few
and sporadic. The prevalence is less than 1%.
= proper sanitation, safe water supply, and
protection of food from contaminations.
= Cyst may be resistant to environmental conditions
and may survive for long periods of time, they easily
inactivated by heat and by 1% sodium hypochlorite.
= Ordinary chlorination of water may not be
effective.
Giardia lamblia
= intestinal parasitic flagellate of worldwide
distribution.
= known to cause endemic and epidemic diarrhea
= G. intestinalis, G. duodenalis, Lamblia duodenalis,
or L. intestinalis
= It was first discovered by Anton van Leeuwenhoek
in his own stools and was first described by Lambl in
1859 who called it Cercomonas intestinalis
Lives in DUODENUM, JEJUNUM, UPPER ILEUM
OF HUMANS.
It has a simple asexual life cycle that includes
binucleated flagellated trophozoites and
quadrinucleated infective cyst.
TROPHOZOITES: measure 9 to 12 um long by 5 to
15 um wide.
== PYRIFORM or TEARDROP SHAPED, POINTED
POSTERIORLY, with A PAIR OF OVOIDAL NUCLEI, ONE
ON EACH SUDE OF THE MIDLINE.
== It is BILATERALLY SYMMETRICAL, with a distinct
medial line called the AXOSTYLE.
CYSTS: ovoid and measure 8 to 12 um long by 7
to 10 um wide.
== YOUNG CYSTS: 2 nuclei
== MATURE: 4 nuclei
= Characterized by flagella retracted into
axonemes(the median body), and deeply stained
curved fibrils surrounded by a tough hyaline cyst
wall secreted from condensed cytoplasm.
PATHOGENESIS and CLINICAL
MANIFESTATION
== infection occurs when the host/person ingest food
contaminated with the mature cyst.
== IT TAKES ABOUT ONE TO FOUR WEEKS ( 9 days average) for
disease to manifest
== abdominal pain, described as cramping associated with
diarrhea
== EXCESSIVE flatus with an ODOR of hydrogen sulfide
“ROTTEN EGGS”
== The ability of the parasite to cause disease can be traced to
its ability to alter mucosal intestinal cells once it has attached
to the apical portion of the enterocyte.
== The ATTACHMENT: done VIA THE ADHESIVE DISC LOCATED
ON ITS VENTRAL SIDE.
UPON ATTACHMENT to the INTESTINAL CELLS, the
parasite is able to cause alterations in the VILLI
such as VILLOUS FLATTENING and CRYPT
HYPERTROPHY (THESE ALTERATIONS LEAD TO
DECREASE ELECTROLYTE, GLUCOSE, FLUID
ABSORPTION, MALNUTRITION)
== MALABSORPTION and MALDIGESTION,
which in turn cause the SIGNS and SYMPTOMS of
the patient.
== BACTERIAL colonization of the area may further
worsen the damage already caused by the parasite.
It also shows to REARRANGE CYTOSKELETON in
human COLONIC and DUODENAL MONOLAYERS.
(Suggested to cause ENTEROC.YTE APOPTOSIS)
== It is also increases EPITHELIAL PERMEABILITY,
thus leading to the loss of BARRIER and FUNCTION,
causing more damage to the intestinal tissue.
= CHRONIC INFECTION: steatorrhea, or the passge

of greasy, frothy stools that float on toilet water.
= In undeveloped countries, it has been described
as a cause of the “FAILURE TO THRIVE SYNDROME”
DIAGNOSIS:
== Demonstration of G. lamblia trophozoites and/or
cyst in stool specimens.
== Spotty shedding of cysts requires at least three
examinations on alternate days.
== DUODENAL ASPIRATIONS; more effective
== ENTERO-TEST may demonstrate Giardia
trophozoites, where the patient swallows a gelatin
capsule containing a nylon string, with one end of the
string attached to the patients cheek. After about six to
eight hours, the string is removed and any ADHERENT
FLUID IS OBSERVED FOR MICROSCOPIC EXAMINATION.
IMMUNOFLUORESENCE TEST
DIRECT FLUORESCENT ANTIBODY ASSAYS
TREATMENT:
== Metronidazole 250 mg 3x/d for 5 to 10 days.
(cure rate of 90%)
== Tinidazole single dose 2 grams for adults or 50
mg/kg in children
== FURAZOLIDONE 100mg 4x/day daily for 7 to 10
days
EPIDEMIOLOGY:
== ASSOCIATED WITH POOR ENVIRONMENTAL
SANITATION.
== In Philippines, a series of parasitological surveys
revealed an overall prevalence of 6%.
== COMMON OUTBREAK EXCLUSIVELY WATER-
BORNE.
== Important risk factors include: POOR HYGIENE,
POOR SANITATION, OVERCROWDING,
IMMUNODEFICIENCY, BACTERIAL and FUNGAL
OVERGROWTH IN THE SMALL INTESTINES, and
HOMOSEXUAL PRACTICES “GAY BOWEL SYNDROME”
PREVENTION and CONTROL:
== Proper sanitary disposal of human excreta to
prevent contamination of food and water supply.
== Environmental control: FLIES
== Food handler must be properly educated with
regards to sanitation and the whole food
establishment.
== Safe and Protected sex
THE END, THANK YOU!

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Nematode Infections

Clark Cleo B. Badilles

== Soil-transmitted helminth infections like acariasis

== Fertile eggs: measures 45 to 70 um by 35 to 50 um. There

== THESE DRUGS HAVE CURE RATES OF CLOSE TO 100% FOR

1.) PROPER DISPOSAL OF HUMAN FECES

== EGG REDUCTION RATE, CURE RATES, REINFECTION

== EGGS: are asymmetrical, with one side flattened and

== FREE-LIVING MALE: measure 0.7mm by

== INFECTIVE FILARIFORM LARVAE: IS NON-

== DURING MIGRATION PHASE: LUNGS ARE DESTROYED!

== THIRD PHASE OF INFECTION, Adult female worms may be

== SOME COMPLICATIONS are EDEMA,

==INFECTION and DISEASE RATES as well as

== Usually ONE ADULT tapeworm is present in T.

The phylum name comes from the apical

== ASEXUAL REPRODUCTION: Multiplication is by

PATHOGENESIS and CLINICAL MANIFESTATIONS

DIVIDED into two several phyla but the major

 These includes HEMOFLAGELLATES namely,

 Amebae, namely, Entamoeba, Endolimax,

= Includes only one parasite of medical and public

SARCODINA Acanthamoeba castellani

APICOMPLEXA Babesia spp.

MICROSPORA Enterocytozoon bineusi

MANY of these protozoans require a WET

INFECTIVE STAGE: CYSTS, which are relatively

Trophozoites divide by binary fission.

Most of cysts-forming amebae go through

 Two morphologically INDUSTINGUISHABLE species

No other host than human is implicated in the

TROPHOZOITES multiply by binary fission; then

Infection starts with ingestion of fecally-

= OCCURS less than 1% of intestinal infections.

= Only 30% of ALA cases have concurrent diarrhea

= MORTALITY: uncomplicated ALA is less than 1%.

From the primary site of the colon, E. histolytica

= STAINING: using saline and methylene blue,

ASYMPTOMATIC CYST - DILOXANIDE - 500 mg tid (THREE - 20 mg/kg/d in 3

AMEBIC COLITIS - TINIDAZOLE - 500 - 700 mg tid X - 35 – 50 mg/kg/d in

AMEBIC LIVER - TINIDAZOLE - 750 MG tid X 10 d - 35 – 50 mg/kg/d in

 Protozoan cyst were observed in 13.5% of

Another study of food handlers in selected school

Sluggish movement of its trophozoites which feed

Reproduce by Binary Fission; and ENCYST if the

= PREDOMINANT SIGNS and SYMPTOMS: destructive

= Headache, Confusion, Somnolence, coma,

CAUSES: human disease ranging from gastritis

 CYSTS are formed principally as protection for

= CHRONIC INFECTION: steatorrhea, or the passge

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