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Aphasmids

This document discusses several nematode parasites including Trichuris trichiura (whipworm), Capillaria philippinensis, and others. It covers the biology, life cycles, pathogenesis, clinical manifestations, diagnosis, treatment and epidemiology of these parasites. Trichuris trichiura inhabits the large intestine and can cause rectal prolapse in heavy infections. Capillaria philippinensis resides in the small intestine and was responsible for an epidemic in the Philippines in the 1960s that led to over 1,000 cases and 100 deaths. Diagnosis is based on finding eggs in stool samples and treatment involves antiparasitic drugs like albendazole.

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0% found this document useful (0 votes)
500 views60 pages

Aphasmids

This document discusses several nematode parasites including Trichuris trichiura (whipworm), Capillaria philippinensis, and others. It covers the biology, life cycles, pathogenesis, clinical manifestations, diagnosis, treatment and epidemiology of these parasites. Trichuris trichiura inhabits the large intestine and can cause rectal prolapse in heavy infections. Capillaria philippinensis resides in the small intestine and was responsible for an epidemic in the Philippines in the 1960s that led to over 1,000 cases and 100 deaths. Diagnosis is based on finding eggs in stool samples and treatment involves antiparasitic drugs like albendazole.

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Ritz Celso
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NEMATODES:

APHASMIDS
DR. HALIDE ABELLA-TANGARORANG
TRICHURIS
TRICHIURA
HABITAT: LARGE INTESTINE
INTRODUCTION

•  Another name: Whipworm


•  Disease: Trichuriasis
•  Soil transmitted
•  Frequently observed occurring together with Ascaris
•  Similar distribution
•  Similar mode of transmission
•  3rd most common roundworm infection
•  1st: ascariasis
•  2nd: hookworm infection
PARASITE BIOLOGY

•  Male
• 30-35mm
• Shorter than the female
• Coiled posterior end
• A single spicule and
retractile sheath
•  Female
•  35-50mm
•  Bluntly rounded posterior
end
PARASITE BIOLOGY

•  Anterior three-fifths of the body


•  Attenuated
•  Traversed by a narrow
esophagus
•  2/3 of the body length
•  Thin-walled tubed
surrounded by
stichocytes
•  The whole structure is
called stichosome
•  Resembles a string of
beads
PARASITE BIOLOGY

•  Posterior two-fifths of the body


•  Robust or fleshy
•  Contains the intestine
•  A single set of reproductive
organs
•  Male
•  Single spicule
surrounded by a spiny
spicule sheath
•  Female
•  Lays approximately
3,000-10,000 eggs/day
PARASITE BIOLOGY

•  Larvae
•  Released soon after the ingestion of
the embryonated eggs
•  Penetrate the intestinal villi
•  Remain for 3-10 days
PARASITE BIOLOGY

•  Egg
•  50-54 um x 23 um
•  Lemon-shaped with plug-like
translucent polar prominences
•  Yellowish outer shell
•  Transparent inner shell
•  Unsegmented when laid
•  Embryonic development occurs in
the environment
•  Clayish soil
•  More susceptible to dessication
compared to Ascaris eggs
PARASITE BIOLOGY

•  Habitat
•  Large intestine: most common-cecum
•  2nd most common site: ascending
colon
•  Attenuated anterior end
•  Whiplike portion
•  Deeply embedded into the intestinal
wall
•  Fleshy posterior end
•  Protrudes into the intestinal lumen
PARASITE BIOLOGY
•  After copulation, female lays egg
•  Passed out with the feces and deposited in the soil
•  Under favorable condition
•  Egg develops and becomes embryonated within 2-3
weeks
•  Once swallowed
•  Infective eggs go to the small intestine
•  Undergo 4 larval stages
•  Become adult worms
•  No heart-lung migration
•  Lifespan
•  Average for females
•  2 years
•  Can produce a total of over 60 million eggs over its
lifespan
LIFE CYCLE
PATHOGENESIS AND CLINICAL
MANIFESTATIONS

•  The anterior portion of the worm


•  Embedded in the mucosa
•  Cause petechial hemorrhages – lead to anemia
•  May predispose to amoebic dysentery
•  The ulcers provide a suitable site for E. histolytica
invasion.
•  Manifestations
•  Mucosal appearance
•  Hyperemic and edematous
•  Enterorrhagia is common
PATHOGENESIS AND CLINICAL
MANIFESTATIONS
•  Rectal prolapse may occur: in heavy
infection
•  A hallmark of whipworm
infection
•  Rare
•  Rectum loses internal support
•  Worms bury their thin heads
into the intestinal lining
•  Loosening of the elastic
epithelium
•  Weakening of the
surrounding muscles
•  Appendicitis may occur
•  Lumen may be filled with worms
•  Irritation and inflammation
PATHOGENESIS AND CLINICAL
MANIFESTATIONS
•  Symptomatic infection
•  5,000 eggs/gram of feces
•  Dysenteric syndrome
•  20,000 eggs/gram of feces
•  Severe diarrhea
•  Light infections
•  No clinical manifestations
•  Parasite is discovered only in routine S/E
•  Heavy infections
•  Worms found throughout the colon and rectum
•  Marked by frequent blood-streaked diarrheal stool,
abdominal pain and tenderness, nausea and vomiting,
anemia and weight loss.
PATHOGENESIS AND CLINICAL
MANIFESTATIONS

•  Prognosis
•  Very good
•  No lung pathology occurs
•  No larval migration through the lungs as in Ascaris
and hookworms
DIAGNOSIS
•  Clinical diagnosis
•  Possible only in very heavy chronic infection
•  Frequent blood-streaked diarrhea, abdominal pain
and tenderness
•  Rectal prolapse
•  Adult worms attach to the rectal mucosa
•  Laboratory diagnosis
•  Essential in light infections where symptoms are absent
•  Direct Fecal Smears
•  Kato Katz Technique
•  Quantitative method
•  Used for egg counting
•  Determine cure rate, egg reduction rate and
the intensity of the infection
TREATMENT

•  Mebendazole: treatment of choice


•  500mg single dose
•  Contraindications: hypersensitivity and early pregnancy
•  Albendazole: alternative
•  500mg single dose
•  Contraindication: pregnancy
•  In moderate and heavy infection
•  Needs 2-3 days of consecutive treatment
•  Adverse effects of both drugs
•  Transient gastrointestinal discomfort
•  headache
EPIDEMIOLOGY

•  Trichuriasis
•  Occurs both in temperate and tropical countries
•  More widely distributed in the tropics
•  Prevalence
•  Temperate countries: 20-30%
•  Tropical countries: 60-85%
•  Philippines: 80-84%
•  Age more frequently infected: 5 to 15 years old
•  Distribution and prevalence of trichuriasis is co-extensive
with that of A. lumbricoides.
EPIDEMIOLOGY

•  Factors affecting transmission of trichuriasis


•  Same as that with A. lumbricoides
•  Indiscriminate defecation of children around yards
•  Frequent contact between fingers and soil among
children at play
•  Poor health education
•  Poor personal, family and community hygiene
•  Unhygienic behavior and eating habits should be
corrected
PREVENTION AND CONTROL

•  Mass treatment
•  Indicated if infection rates are greater than 50%
•  Prevention of infection in highly endemic areas
•  Treatment of infected individuals
•  Sanitary disposal of human feces by construction of
toilets and their proper use.
•  Washing of hands with soap and water before and after
meals
•  Health education on sanitation and personal hygiene
•  Thorough washing and scalding of uncooked vegetables
especially in areas where night soil is used as fertilizer.
CAPILLARIA
PHILIPPINENSIS
HABITAT: SMALL INTESTINE
INTRODUCTION

•  Disease: intestinal capillariasis


•  Abdominal discomfort
•  Chronic diarrhea
•  Gurgling stomach
•  1963
•  Described first in the Philippines
•  1967-1968
•  An epidemic occurred
•  More than 1,000 cases
•  Almost 100 individuals died
PARASITE BIOLOGY
•  A tiny nematode that resides in
the small intestine of humans.
•  Male
•  1.5 to 3.9mm in length
•  Spicule is 230-300um long
•  Unspined sheath
•  Female
•  2.3 to 5.3mm in length
•  Body is divided into 2 almost
equal parts
•  Anterior: esophagus
•  Posterior: intestine and
reproductive system
•  Prominent vulva
PARASITE BIOLOGY

•  Eggs
•  Peanut-shaped with striated
shells and flattened bipolar
plugs
•  36-45um x 20um
•  Passed in the feces
•  Unembryonated when passed
out
•  Embryonates in the soil or
water
PARASITE BIOLOGY
•  In the water
•  Ingested by small species
of freshwater or brackish
water fish
•  In the intestine of the small
fish
•  Eggs hatch
•  Grows into infective larvae
•  When the small fish is
eaten uncooked
•  The larvae escape from the
fish intestine
•  Develops into adult worms
in human intestine
PARASITE BIOLOGY
•  In the human intestine
•  1st generation female
worms
•  Produce larvae to
build up the
population
•  Subsequent generations
•  Predominantly
produce eggs
•  A few produce both
larvae and eggs or
larvae only
•  Some of the larvae are
retained in the gut lumen
and develop into adults
PARASITE BIOLOGY

•  Leads to hyperinfection
and autoinfection
•  Produce very large number
of worms
•  An autopsy was done
on one expired patient
•  200,000 worms in 1
liter of bowel fluid
PATHOGENESIS AND MANIFESTATIONS
•  Initial clinical manifestations
•  Abdominal pain
•  Borborygmus: most constant feature
•  Diarrhea
•  After a few weeks
•  Weigh loss, malaise, anorexia, vomiting and edema
•  Laboratory findings
•  Severe protein-losing enteropathy
•  Malabsorption of fats and sugars
•  Decreased excretion of xylose
•  Low electrolyte levels (potassium)
•  High levels of IgE
•  If not treated, it leads to death.
PATHOGENESIS AND MANIFESTATIONS

•  Large number of worms that develop in humans


•  Responsible for the pathology
•  Do not invade intestinal tissues
•  Cause micro-ulcers in the epithelium
•  Cause compressive degeneration and mechanical
compression of cells
•  Ulcerative and degenerative lesions in the intestinal
mucosa
•  Responsible for the malabsorption of fluids and
electrolytes
DIAGNOSIS

•  Based on finding the characteristic eggs in the feces.


•  Direct Smear or Wet Mount
•  Stool Exam with concentration method
•  With these 2 tests various larval stages and adult
worms may be seen
•  The uterus of the adult female may contain eggs and
sometimes larvae.
•  Recovery of the parasite from the small intestine by
duodenal aspiration
TREATMENT

•  Electrolyte replacement and high protein diet


•  In severe cases of electrolyte and protein loss
•  Antidiarrheals
•  Antihelminthics
•  Albendazole
•  400mg OD x 10D
•  Drug of choice
•  Destroys larval stages more readily
•  Mebendazole
•  200mg BID x 20D
•  Relapse may occur if the regimen is not followed.
EPIDEMIOLOGY

•  First recorded capillariasis


•  Northern Luzon, Philippines
•  Countries where it was later reported
•  Thailand, Iran, Japan, Egypt, Korea, Taiwan and India
•  In these countries, small fishes have been implicated
•  Natural hosts
•  Fish-eating birds
•  Mode of Infection
•  Eating uncooked small freshwater/brackish water fish
•  Endemic areas in the Philippines
•  Zambales, Southern Leyte, Ilocos, Compostela Valley and
Zamboanga del Norte
EPIDEMIOLOGY

•  1998
•  Outbreak in Monkayo, Compostela Valley
•  Called a “mystery disease”
•  Resulted in death of villagers due to misdiagnosis
PREVENTION AND CONTROL

•  Discourage people in endemic areas from eating raw fish


•  Good sanitary practice should be followed
•  1967-1968
•  Epidemic in the Philippines
•  Washing of fecally contaminated bedsheets in
lagoons in the Tagudin area of Ilocos Sur
•  All infected persons should be treated quickly
•  Their feces disposed of in a sanitary manner
•  Health education
•  Inform populations at risk about the hazards of eating
uncooked fish
TRICHINELLA
SPIRALIS
HABITAT: SMALL INTESTINE
INTRODUCTION
•  1828 in London
•  First found in the muscles of patients that were autopsied
•  1835
•  Richard Owen
•  The first investigator to describe and name the encysted
larvae
•  Before the turn of the century
•  German investigators were able to prove that raw or
insufficiently cooked meat (pork) was responsible for
trichinosis in humans
•  3 subspecies that can infect humans
•  T. spiralis spiralis -temperate regions
•  T. spiralis nativa -arctic regions
•  T. spiralis nelsoni -Africa
PARASITE BIOLOGY
•  Adult worm
•  Whitish in color
•  Male
•  1.5mm x 0.04mm
•  Single testis located near the
posterior end of the body
•  Joined in the midbody by the
genital tube
•  Extends back to the cloaca
•  Cloaca
•  A pair of caudal appendage
•  Copulatory pseudobursa
•  Two pairs of papillae
•  No copulatory spicule
PARASITE BIOLOGY

•  Females
•  3.5mm x 0.06mm
•  Single ovary
•  Posterior part of the body
•  Oviduct, a seminal receptacle, coiled
uterus, vagina and a vulva
•  Vulva is found on the anterior
fifth on the ventral side of the
body
•  Viviparous female
•  Lives for 30 days
•  Capable of producing 1,500 larvae or
more in her lifetime
PARASITE BIOLOGY
•  Larva
•  Measures 80-120um x 5.6um at
birth
•  Max: 900-1,300um by 35-40um
after it enters a muscle fiber
•  Has a spear-like burrowing
anterior tip
•  Encysted larvae
•  The digestive tract resembles
that of the adult worm
•  The reproductive organs are not
yet fully developed
•  It is possible to identify the sex
of the parasite
PARASITE BIOLOGY

•  Trichinella infection
•  The host serves as both the final
and intermediate host
•  Humans, rats, dogs, cats, pigs,
bears, and foxes
•  The host harbors both the adult
and the larval stages
•  Infective stage
•  Encysted larvae
•  Seen in the muscle fiber of the
host
PARASITE BIOLOGY

•  Mode of transmission
•  Ingestion of the encysted larvae through raw
or insufficiently cooked meat (usually pork).
•  Once ingested
•  The cysts are digested in the stomach
•  The larvae excyst either in the stomach or in
the small intestine
PARASITE BIOLOGY
•  Larvae
•  Burrows into the subepithelium of the villi where they
mature
•  Adult worms
•  Mate
•  After fertilization
•  Female begins to produce eggs that grow into larvae
in the uterus
•  Female worms deposit larvae in the mucosa after a
few days
•  Larvae
•  Penetrates the mucosa
•  Pass through the lymphatic system into the circulation
•  Finally ending in the striated muscles
PARASITE BIOLOGY

•  In the muscles
•  Larvae grow and develop
•  After about 3 weeks, they start to coil into individual
cysts
PARASITE BIOLOGY

•  Encapsulation
•  Is consummated 4-5 weeks after infection
•  The larva in the cyst remains viable for many years
•  Calcification
•  May occur in humans
•  May take place 6-12 months after infection
•  May lead to the destruction or death of the larva
•  Average lifespan is 5-10 years
PARASITE BIOLOGY

•  When a carnivore or
omnivore consumes
meat containing infective
larvae
•  The larvae break out
through gastric
digestion of the cysts
•  The cycle continues
PATHOGENESIS AND MANIFESTATIONS

•  The severity of symptoms


•  Depends on the intensity of infection
•  Light infection
•  Patients harboring up to 10 larvae
•  Asymptomatic
•  Moderate infection
•  50-500 larvae
•  Symptomatic
•  Severe infection
•  More than 1,000 larvae
•  Potentially fatal
PATHOGENESIS AND MANIFESTATIONS

•  Clinical manifestations
•  Vary depending on the stage of the parasite
•  3 phases: corresponds to the stage of the parasite
•  Enteric phase: incubation and intestinal invasion
•  Invasion phase: larval migration and muscle invasion
•  Convalescent phase: encystment and encapsulation
•  Enteric phase
•  May resemble an attack of food poisoning
•  Diarrhea or constipation
•  Vomiting and abdominal cramps
•  Malaise and nausea
•  Red blotches on the skin
PATHOGENESIS AND MANIFESTATIONS

•  Invasion phase
•  Cardinal signs and symptoms
•  Severe myalgia
•  Periorbital edema
•  Eosinophilia
•  Other typical signs and symptoms
•  High remittent fever
•  Dyspnea and dysphagia
•  Difficulty in chewing
•  Sometimes some paralysis of the extremities
•  Occasional signs and symptoms
•  Splenomegaly
PATHOGENESIS AND MANIFESTATIONS
•  In severe cases
•  Gastric and intestinal hemorrhages
•  Myocardial complications
•  Myocarditis: most common grave manifestation
•  Pericardial effusion
•  Congestive heart failure
•  Neurological complications
•  Meningitis, meningoencephalitis
•  Cerebral lesions may develop
•  In heavy infection
•  Ocular disturbances
•  Diplegia, deafness, epileptic attacks
•  Coma
PATHOGENESIS AND MANIFESTATIONS

•  Convalescent phase
•  The following will start to abate:
•  Fever, weakness, pain and other symptoms
•  Full recovery is expected.
•  Trichinosis is a self-limiting disease.
•  Prognosis
•  Good in mild infection
•  Death is uncommon except in cases of heart failure,
encephalitis and other complications such as pneumonia
and septicemia
•  Indicative ofe poor prognosis
•  Low grade or absent peripheral blood eosinophilia
DIAGNOSIS

•  Diagnosis is usually based on


•  History of exposure
•  Physical examination
•  Laboratory exams
1.  Demonstration of larva in muscle biopsy
•  Most definitive diagnostic exam
•  Done only when encystment has started
•  Usually 7 days after infection and onwards
•  Most parasitized muscles
•  Diaphragm, pectorals, gluteus, deltoid, biceps and
gastrocnemius
DIAGNOSIS

•  The likelihood of demonstrating the parasite larva


depends on
•  Mainly the intensity of the infection
•  Partly on chance
•  A negative biopsy does not necessarily mean that the
patient is negative for trichinosis.
2.  Biochemical tests -will strengthen the diagnosis
•  Elevated creatine phosphokinase, lactate
dehydrogenase and myokinase levels
•  Chemical evidence of muscle damage
DIAGNOSIS
3.  Serology: provide confirmatory diagnosis
•  Look for a rise in antibody titer
•  Starts 3-4 weeks after a light infections
•  Starts to rise as early as 2 weeks in heavy infection
•  Bentonite Flocculation Test (BFT)
•  Latex Flocculation Test (LFT)
•  IFAT
•  ELISA
4. Beck’s Xenodiagnosis
•  Done on meat suspected of harboring the encysted larva of
Trichinella
•  Involves feeding the meat to albino rats
•  Observe for 14 days
•  Look for the presence of the female worm in the duodenum
and larvae in the muscles of the experimental animal.
TREATMENT

•  Usually managed through bed rest and supportive


treatment
•  Drugs used
•  Analgesics and antipyretics to control symptoms
•  Adenocorticosteroids
•  Prednisone 20mg TID tapered over a period of 2-3
weeks
•  Inhibits the severity of the disease
•  For the allergic reaction to the death of the parasite
TREATMENT

•  Thiabendazole
•  25mg/kg body weight BID x 7D
•  If done during the 1st week of infection
•  Expel the adult worm from the GIT
•  No effect on the migrating larvae
•  Useless for infections detected 2 weeks after
exposure
•  Mebendazole: larvicidal
•  20mg/kg body weight q6H for 10-14D
EPIDEMIOLOGY

•  Trichinosis occurs whenever meat is part of the diet


•  Countries where infection is reported
•  Canada, Mexico, Holland, Ukraine, Lithuania, Yugoslavia,
Spain, Egypt, Lebanon, Syria, Brazil, Uruguay, Chile,
Ecuador, Vietnam, Malaysia and Thailand.
•  Countries where infection is absent or rare
•  India, Australia, New Zealand, New Guinea and some
islands in the Pacific.
•  It’s possible to acquire the disease anywhere in the world.
•  More than a hundred species of carnivores and
omnivores harbor the parasite.
EPIDEMIOLOGY

•  Trichinosis
•  Primarily a zoonotic disease
•  Mode of infection
•  Ingestion of raw or insufficiently cooked meat of infected
animals
•  Human infection
•  A dead-end infection for the parasite.
•  The infection is maintained in pig-pig or pig-rat-pig cycle
EPIDEMIOLOGY
•  2 distinct types of the life cycle
•  Domestic life cycle
•  Involves pigs, rats
around human habitation
•  More important to
humans
•  Infected pork is the most
common source of
infection
•  Important to cook pork
thoroughly before being
eaten
•  Meat is considered safe
when all traces of pink
have disappeared
•  Rat to tat infection
occurs by cannibalism
EPIDEMIOLOGY

•  2 distinct types of the life cycle


•  Sylvatic life cycle
•  Involves wild animals
•  Humans may possibly be infected
•  When domestic animals have been fed with
infected wild game
•  When humans rely on wild games for food
PREVENTION AND CONTROL

•  Health education
•  Recommendations
•  Cook meat at 77C (177F)
•  Freezing can kill the larvae
•  15C for 20 days
•  30C for 6 days
•  Smoking, salting, and drying meat is not effective
•  Other control measures
•  Meat inspection
•  Keeping pigs in rat-free farm.

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