The Nematodes Tabulated

THE NEMATODES
Ascaris lumbricoides (Giant intestinal worm)

ADULT MORPHOLOGY OVA MORPHOLOGY
MALE FEMALE DIFFERENTIATION UNFERTILIZED FERTILIZED
Size 15-30cm Size 20-45cm by Size 88 – 94 μm 45-75 μm by 35-
by 3mm 5mm 45 μm
Tail Ventrally Reproductive Paired Shape Larger, longer, Broadly ovoid
curved tail System Reproductive elongated,
organs irregular shape
No. of Spicules 2 Number of 200,000 per day Membrane Thin shelled Thick shelled
copulatory Eggs Vitelline is absent Vitelline is
Produced present
Characteristics large creamy white or pinkish worm is cylindrical, Characteristics Difficult to Golden brown
elongated, tapering gradually at the anterior end. identify
terminal mouth with trilobate lips and a small Embryonation in No Yes
triangular buccal cavity Soil
DESCRIPTION FIGURES OF ASCARIS LUMBRICOIDES
• Disease: Human Ascariasis MORPHOLOGY
• Largest and most common nematode of man.
• 3 layers of shell of fertilized ova:
o Vitelline membrane – innner non-
permeable, lipoidal layer
o Glycogen membrane – thick,
transparent middle layer
o Albuminous/Mammillary coat –
outermost layer
• Occasionally, mammillary coat maybe absent
or removed in some eggs and they are
referred to as “decorticated”, while eggs with
albuminous layer are referred to as
“corticated”.
LIFE CYCLE
Diagnostic Stage: Adult worm
Infective Stage: Embryonated egg
1. Adult worms image live in the lumen of the
small intestine. A female may produce
approximately 200,000 eggs per day, which
are passed with the feces
2. Unfertilized eggs may be ingested but are not
infective. Larvae develop to infectivity within
fertile eggs after 18 days to several weeks
3. depending on the environmental conditions
(optimum: moist, warm, shaded soil). After
infective eggs are swallowed
4. the larvae hatch UNFERTILIZED EGG DECORTICATED
5. invade the intestinal mucosa, and are carried
via the portal, then systemic circulation to the
lungs
6. The larvae mature further in the lungs (10 to
14 days), penetrate the alveolar walls, ascend
the bronchial tree to the throat, and are
swallowed
7. Upon reaching the small intestine, they
FERTILIZED EGG CORTICATED
develop into adult worms. Between 2 and 3
months are required from ingestion of the
infective eggs to oviposition by the adult
female. Adult worms can live 1 to 2 years.
ANIS, C.J., ARANGCO, R., GECALE, C.D., GOLEZ, M.D., LEONOR, G., MANGILIT, A.J., POBRE, C.M., SY, K.C | BSMT 1
TRANS: THE NEMATODES
LARVA HATCHING FROM AN EGG ADULT WORM TRILOBATE LIPS
DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CONTROL

Finding the eggs in the feces, • Piperazine Ascaris lumbricoides, a common parasite • Mass treatment
fertilized or unfertilized by: citrate found in warm countries with poor although ideal may not be
• Direct Fecal Smear (DFS) • Pyrantel sanitation, causes ascariasis, a prevalent practical because of the
• Kato-Thick pamoate infection affecting people of all ages but high costs of anti-
• Kato-Katz • Mebendazole particularly widespread among children helminthiases.
• Concentration Technique • Albendazole aged 5 to 9, especially those in preschool. • Selective treatment
Fecalysis may give a negative • Levamisole Children who frequently come into contact refers to treating only a
in following conditions: Note: Piperazine with contaminated soil, often due to group usually those found
• Patient free from Ascaris and Pyrantel open defecation in yards and houses positive for eggs after
infection. pamoate are used with earthen floors, are the primary stool examination.
• Worms still mature in these days because source of soil contamination with the • Preventive aspect, health
lumen. these drugs have a parasite's eggs. These eggs can survive in education, sanitary
• During larval migration neuromuscular the environment for long periods. disposal of human
Ascariasis is the most common excreta, proper personal
• Only male worm is present blocking effect on the
parasite causing helminth infection globally, with around hygiene, refrain from
in intestine
paralysis. 1 billion individuals affected. In the using human excreta as
Ascaris-specific antibodies can
Philippines, rural areas and impoverished fertilizer and thorough
be detected by Ascaris-specific
urban sections have a prevalence ranging cooking of food.
peptides in dot EIA, a method
from 80-90%. Additionally, domestic pigs
with satisfactory sensitivity and
can carry Ascaris, potentially transmitting it
specificity for helminth
to humans, further complicating the control
diagnosis
of the disease.
PATHOLOGY
The pathology of Ascaris lumbricoides maybe grouped into those • Serious and sometime fatal effects of Ascariasis are due
caused by the larval stage and those caused by the adult: to the erratic migration of the adult worms. They maybe
• Pathology due to Larval Migration: regurgitated and vomited and may escape through the
o Larval migration to the lungs – can cause pneumonitis nostrils.
resembling an asthmatic attack accompanied by marked • Vomited Ascaris may pass the larynx and may lead to
eosinophilia Ascaris pneumonitis of Loeffler’s syndrome. suffocation or may reach the lungs and produce
The clinical manifestations are asthmatic type of pulmonary gangrene or may enter the eustachian tube
respiration, cough, urticaria, rash, edema of the lips and and provoke otitis media. Fever and certain drugs are the
eosinophilia. two of the causative factors of Ascaris migration.
o Occasionally, ectopic larva may initiate granulomatous • The adult may invade the bile duct, gall bladder, liver and
reactions in organs like the brain, spinal cord and kidneys. appendix. They may occlude the ampulla of vater and
• Pathology due to the Adult Worm: cause acute hemorrhagic pancreatitis. The worm may
o The adult worm usually feeds on the intestinal contents, the penetrate the intestinal wall, migrate into the peritoneal
liquid nutrients. cavity and produce peritonitis. Some worms may
o Small numbers of adult worms in the intestine (10 – 20 become entangled resulting in intestinal obstruction.
worms) may not show symptoms and go unnoticed by the • Even when the worms cause little or no traumatic
host. damage, the by-product of living or dead worms may
o Symptoms such as abdominal pain, diarrhea, nausea and rarely produce marked toxic manifestations such as
loss of appetite maybe experienced by the host. edema of the face and urticaria, accompanied by loss
of appetite and weight.
Toxocara canis and Toxocara cati (Dog ascaris and Cat ascaris)
DESCRIPTION DIFFERENTIATION OF SPECIES
Toxocara canis and Toxocara cati are Ascaris worms naturally POINT OF TOXOCARA TOXOCARA
parasitic in the intestines of dogs and cats that accidentally infect DIFFERENTIATION CANIS CATI
human, an aberrant host, producing a disease called visceral Common Name Dog ascaris Cat ascaris
larval migrans (VLM) or toxocariasis. VLM is a clinical syndrome Diseases Toxocariasis or Visceral Larva Migrans
resulting from the invasion of human visceral organs by nematode Intermediate Host Man Man
larvae of the genus Toxocara. Definitive Host Dog Cat
Infective Stage Eggs Eggs
Mode of Ingestion Ingestion
Transmission
Habitat Tissue, Organs, esp. subcutaneous
LIFE CYCLE FIGURES OF TOXOCARA CANIS AND TOXOCARA CATI
• In dogs and cats, the worm exhibits the same TOXOCARA SPP. EGGS TEASED TOXOCARA SP.
life cycle as the human Ascaris. FROM AN ADULT WORM EGG APPROX 75μm
• The adult female worms are 10 – 12 cm in
length and pass numerous eggs into their
host’s feces.
• In moist soil, the eggs become embryonated
in several weeks.
• When ingested by dogs and cats, the larvae
hatch in the small intestine, migrate to the
intestinal mucosa and by way of blood stream TOXOCARA CANIS LARVA HATCHING
reach the liver, lungs, bronchial tree and
trachea, swallowed again and mature in the
small intestine of these animals.
• The embryonated eggs on the other hand,
when ingested by human, larvae will hatch
and cannot follow its normal course of
development as seen in their natural hosts.
T. canis adult male T. cati broad alae
• The larvae penetrate the intestinal mucosa
and female T. canis 3 lips w/striations
and are carried by the blood stream to the
liver, lungs and other organs.
• Here they wander for weeks and months or
become dormant and they do not develop
beyond the migrating larval forms.
PATHOLOGY
• Larval migration – may produce
hemorrhage, necrosis and granuloma at the
site.
• Eosinophilia, liver damage, pulmonary
inflammation and ocular problems have also
been observed.
• A number of children have exhibit anemia
accompanied by a high WBC count.
DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CTRL
The diagnosis of toxocariasis in Because the clinical Wherever infected dogs Prevention and control: Small children
human is usually established on course of VLM is so and cats are present, the should be protected against contact
clinical grounds with triad of variable, it is very difficult eggs are threat to human. with infected dogs and cats. Animal
marked: to evaluate efficacy of any This is especially true for under 6 months should be dewormed
• Eosinophilia treatment. In addition, children who are exposed with piperazine every month and
• Hepatomegaly since the infection is to contaminated soil and older one every 2 months. Worms
• Hyperglobulinemia. usually self-limited, only who tend to put objects in passed, as a result of treatment should
Examination of stool from severe cases need to be their mouth. be destroyed. Dogs and cats’ stools
infected patients is not useful treated. passed in children’s play areas should
because egg-laying adults are not be buried and sandboxes, which offer
present. However, examination Thiabendazole appears an attractive defecating area to cats,
of fecal material from infected to shorten the course of should be covered when not in use.
pets often supports the the disease. There is no satisfactory chemical for
diagnosis. killing the eggs in soil.
Trichuris trichuria (Whipworm)

DIFFERENTIATION MALE FEMALE Size 50-54 by 22-23 μm
Size 3 – 4.5 cm 3.5 – 5 cm Shape barrel shaped, lemon shaped,
football shaped or Japanese
lantern
Reproductive Testes are sacculate Single set of Membrane Thick with three layers
Organs (saclike) reproductive organ
No. of Spicules 1 sheathed spicule None Color Yellowish outerlayer
Transparent inner layer
Characteristics Attenuated, Robust; Bluntly rounded, Vulva, Characteristics Prominent bipolar plugs on both
thick, posterior coiled straight posterior end ends
360o
No. of Eggs None 3,000-10,000/day Embryonation Soil
Produces 60 million in lifespan
2yrs
DESCRIPTION FIGURES OF TRICHURIS TRICHIURIA
• Disease: Trichuriasis ADULT MORPHOLOGY: a. female b. male T. trichiuria ova
• The human whipworm lives attached to
the wall of the caecum.
• Man is the principal host of Trichuris, but
it has also been reported in monkeys
and hogs.
LIFE CYCLE
Diagnostic Stage: Unembryonated eggs
passed in feces
Infective Stage: Embryonated eggs are
ingested.
1. The unembryonated eggs are passed
with the stool. In the soil, the eggs
develop into a 2-cell stage.
2. Advanced cleavage stage
3. And then they embryonate
4. eggs become infective in 15 to 30 days.
After ingestion (soil-contaminated hands
or food), the eggs hatch in the small
intestine, and release larvae
5. That mature and establish themselves
as adults in the colon
6. The adult worms (approximately 4 cm in
length) live in the cecum and ascending
colon. The adult worms are fixed in that
location, with the anterior portions
threaded into the mucosa. The females
begin to oviposit 60 to 70 days after
infection. Female worms in the cecum
shed between 3,000 and 20,000 eggs
per day. The life span of the adults is
about 1 year.
Demonstration of the • Albendazole Trichuriasis is a common parasitic • Treatment of infected
characteristic of barrel-shaped • Mebendazole infection found mostly in warm, moist individuals
ova through: • Pyrantel regions, with prevalence rates as high as • Sanitary disposal of human
• Direct Fecal Smear (DFS) pamoate 80-90% in some tropical countries like feces
• Kato-Thick the Philippines. It often occurs alongside • Washing of hands before
• Kato-Katz Ascaris infection and is most prevalent in meals
• Concentration Technique areas with heavy rainfall, subtropical • Proper instruction to children
climates, and polluted soil. Children are on sanitation and proper
more prone to infection, especially personal hygiene
young children who frequently play on • Thorough washing and
contaminated ground and ingest the cooking of food
parasite's eggs through contaminated • Avoid using human excreta as
hands, food, or water. fertilizer
PATHOLOGY
Light infections usually do not give rise to recognizable clinical manifestations and the presence of the parasite is discovered only on
routine stool examination.
Patient with heavy Trichuriasis, the worms maybe found throughout the colon and rectum. The characteristic clinical picture includes
frequent small blood-streaked diarrheic stool, abdominal pain and tenderness, nausea and vomiting, anemia (hypochromic
anemia), weight loss and rectal prolapse.
Enterobius vermicularis (Pinworm or Seatworm)

DIFFERENTIATION MALE FEMALE Size 50–60 by 20–30 μm
Size 2 – 5 mm in length 8 – 13 mm in length Shape D shaped or lopsided
Color Whitish or brownish Embryo Tadpole-like
Tail Strongly curved Long pointed Membrane Outer (Thick hyaline
No. of Spicules 1 copulatory spicule None albuminous)
No. of Lips Trilobate lips Inner (lipoidal)
Characteristics Rarely seen (after Cephalic alae (also in male) Embryonat fully embryonated when
copulation it dies easily) Prominent esophageal bulb (also in ion laid and will mature
male) within six hours after
Easily disintegrated body with eggs oviposition of gravid
No. of Eggs None 4,672 – 16,888 a day female
Produces
DESCRIPTION FIGURES OF ENTEROBIUS VERMICULARIS
Disease: Enterobiasis or Oxyuriasis MORPHOLOGY OF ADULT WORM:
Cephalic Alae – a pair of lateral cuticular A. MALE B. FEMALE
wing-like expansion at the anterior end.
Eggs are resistant to disinfectant and under
cool, moist condition may remain viable for
13 days.
Eggs fully embryonated are already infective.
LIFE CYCLE
Diagnostic Stage: Eggs on Perianal Folds
Infective Stage: Embryonated eggs
ingested by human
1. Gravid adult female Enterobius
vermicularis deposit eggs on perianal
folds. Infection occurs via self-
inoculation (transferring eggs to the
mouth with hands that have scratched
the perianal area) or through exposure to
eggs in the environment (e.g.
contaminated surfaces, clothes, bed
linens, etc.).
2. Following ingestion of infective eggs, the
larvae hatch in the small intestine.
3. And the adults establish themselves in
the colon, usually in the cecum.
4. The time interval from ingestion of EGGS IN SCOTCH TAPE TEST OVA OF E. VERMICULARIS
infective eggs to oviposition by the adult
females is about one month. At full
maturity adult females measure 8 to 13
mm, and adult males 2 to 5 mm; the adult
life span is about two months. Gravid
females migrate nocturnally outside the
anus and oviposit while crawling on the
skin of the perianal area.
5. The larvae contained inside the eggs
develop (the eggs become infective) in 4
to 6 hours under optimal conditions.
1. Rarely, eggs may become airborne and
be inhaled and swallowed.
Retroinfection, or the migration of newly
hatched larvae from the anal skin back CEPHALIC ALAE MORPHOLOGY OF THE OVA
into the rectum, may occur but the
frequency with which this happens is
unknown.
DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

CONTROL
• Pinworm infection signs: • Mebendazole Enterobius vermicularis, a type of • Proper personal
o Perianal itching • Albendazole parasitic infection, is widespread globally hygiene especially
o Insomnia • Pyrantel but more common in colder regions where hand washing before
o Restlessness pamoate bathing and changing clothes are less and after meals and
• Diagnosis is made by finding the frequent. In warmer, moist areas, like the cutting of fingernails.
characteristic eggs using Cellulose Infection is self- tropics, where children often go • Things used by
tape anal swab technique (Scotch limited and in the unclothed, the infection is less prevalent. infected individuals
Tape Test). absence of It spreads easily in crowded places like like clothes and
• About 5% infected patients are reinfection, ceases daycares and schools, regardless of bedlinens should be
eggs found in the feces. without treatment. economic status or education level. sterilized by boiling.
• Sample collection soon after the • General cleanliness
patient awakens in the morning To avoid In the Philippines, it affects both private in the house should
and before take a bath or reinfection in the (29%) and public school (56%) children, always be practice.
defecates, since oviposition family since it is with higher rates in public schools. • When one member
usually takes place at night. easily spread of the family or
• Repeated examinations on 7 within the family, The infection is often transmitted institution
consecutive days are necessary hence it is termed through hand-to-mouth contact due to • proved positive for
before the patient is considered a “familial scratching around the anus, inhaling Enterobiasis, all
free from infection. disease”; it is airborne eggs from dust, or self-infection members should be
• Occasionally, adult worms maybe customary to treat through the anus. treated irregardless
seen crawling from the anus at the entire family of whether each one
night, after the child has been put simultaneously. Retro infection and autoinfection play has
to sleep. In such cases, the worms roles in sustaining the infection within • been examined by
should be placed in alcohol and individuals. Studies in the Philippines perianal swab or not.
brought to the laboratory for have found eggs under fingernails and
identification. fingertips, indicating common modes of
transmission.
PATHOLOGY
Many children and adults show no recognizable symptoms and usually serve only as carriers. At the site of attachment, there
may be minute ulcerations or abscesses especially in the ceacal mucosa. The most significant pathologic conditions are produced
by migrating gravid female wherein the migration of the female from the caecum to the perianal region to oviposit cause crawling
sensation. During this period, there may be intense itching in the perianal region or pruritus ani which will result to scratching of
the itchy area until it is scarified. Pruritus ani more often may give rise to hemorrhage, eczema and pyogenic infection of the
anal and perianal region.
A number of signs and symptoms has been attributed to the presence of pinworm like poor appetite, disturbed sleep, insomnia,
weight loss, irritability, grinding of teeth, nausea and vomiting, but these symptoms are often difficult to establish its correlation
with pinworm infection.
Migrating worms may enter the appendix and produce appendicitis. In female patients the migrating worm may oviposit in the
genital causing vulvovaginitis with mucoid vaginal discharge or may enter the reproductive tract up to the fallopian tubes and
either become encysted or produce symptoms of salpingitis.
HOOKWORMS
SCIENTIFIC NAME COMMON NAME DISEASE
Necator americanus New World Hookworm, American Hookworm Necatoriasis, Uncinariasis, Tropical anemia,
“Laziness”
Ancylostoma duodenale Old World Hookworm Ancylostomiasis, Miner’s anemia
Ancylostoma braziliense Cat Hookworm Cutaneous Larva Migrans, Creeping eruption
Ancylostoma caninum Dog Hookworm Cutaneous Larva Migrans, Creeping eruption
MORPHOLOGY FORMS
POINT OF DIFFERENTIATION N. americanus A. duodenale
Male (applies to all hookworms) They have fan-like organelle at the posterior portion known as copulatory bursa or bursa
copulatrix.
Female (applies to all hookworms) Larger than males
Shape S-shaped C-shaped
Color (applies to all hookworms) Grayish-white
Head Curved opposite to the curvature of the Continues in the same direction as the
body curvature of the body
Tail Conspicuous transverse striations present Inconspicuous (small) buccal spears and
on the sheath transverse striations
Copulatory Bursa Longer, with a bdigitate or bipartile dorsal Short and broad with a tripartite or tridigitate
ray, and long, slender copulatory spicule dorsal ray and with a pair of simple, long,
that are fused at the tip to form a delicate bristle-like copulatory spicule, plain and
barb free at the tip.
Buccal Capsule Pair of semi-lunar cutting plates Two pairs of ventral teeth almost similar in
size
A. braziliense A. caninum
Buccal Capsule A pair of large teeth and a pair of Wide buccal capsule bearing three pairs of
inconspicuous median teeth ventral teeth
Copulatory Bursa Almost as broad as long and is supported Long, moderately slender rays
by relatively short lateral rays.
LARVAE OVA
Rhabditiform Larvae Hatches in 24 – 48 hours. short, stout with a long, narrow buccal chamber • Ovoidal
(1st stage larvae) and a flask-shaped muscular or bulbous esophagus and an inconspicuous • Thin-shelled
genital primordium. Mouth is open, and they feed on bacteria and • Colorless
organic matter present in the soil or feces, hence they are considered • 56 – 60 μm by 34 – 40 μm
as the feeding stage of Hookworm. • Unsegmented at
Filariform Larvae Develops in the soil within 5 – 8 days. It grows longer and slender with oviposition
(3rd Stage Larvae) a pointed posterior end. Mouth closes, the esophagus elongates and • Usually 2-8 stages of cell
has a protective sheath as covering. This is the non-feeding stage and the division in fresh feces.
infective stage of hookworm.
LIFE CYCLE FIGURES OF HOOKWORM
Diagnostic stage: Eggs in feces MORPHOLOGY OF HOOKWORM
Infective stage: Filariform larva
1. Eggs are passed in the stool, and under
favorable conditions (moisture, warmth,
shade), larvae hatch in 1 to 2 days and
become free-living in contaminated soil.
These released rhabditiform larvae grow
in the feces and/or the soil.
2. And after 5 to 10 days (and two molts)
they become filariform (third-stage)
larvae that are infective
3. These infective larvae can survive 3 to 4
weeks in favorable environmental
conditions. On contact with the human
host, typically bare feet, the larvae
penetrate the skin and are carried
through the blood vessels to the heart
and then to the lungs. They penetrate
into the pulmonary alveoli, ascend the
bronchial tree to the pharynx, and are
swallowed.
4. The larvae reach the jejunum of the small
intestine, where they reside and mature
into adults. Adult worms live in the lumen
of the small intestine, typically the distal
jejunum, where they attach to the
intestinal wall with resultant blood loss by
the host,
5. Most adult worms are eliminated in 1 to OVA OF HOOKWORM

2 years, but the longevity may reach
several years.
A. duodenale
N. americanus
RHABDITIFORM LARVAE FILARIFORM LARVAE
A. caninum A. braziliense

CONTROL
• DFS (finding the Drugs of Choice: Prevalence of hookworm infection • Proper personal
characteristics of eggs in • Mebendazole depends on: hygiene
the feces) • Albendazole • The continuous presence of infection • Sanitary disposal of
• Concentration Technique • Flubendazole in the human population, human excreta
(recover the eggs) • Defecation habits ensuring the eggs • Wearing of shoes
o Zinc Sulfate Mebendazole and are deposited in favorable locations and slippers to
Floatation Albendazole are both for extrinsic development of parasites, avoid skin contact
o Formalin Ether benzimidazole derivatives • Favorable environmental conditions with filariform larvae
Concentration that block the uptake of and in contaminated soil
• Harada-Mori – to glucose by most intestinal • Opportunity of the filariform larvae to • Treatment of
differentiate the eggs and and tissue nematodes. infect humans infected individuals
rhabditiform larvae in S. • Mass treatment
stercoralis. If significant anemia is Factors determining the geographic when incidence is
• Egg Counting Methods present, the first distribution prevalence of the two- greater than 50%
(useful in surveys) consideration is the common species of human • Correction of
o Stoll Egg Count treatment of anemia. hookworms: anemia by giving
o Kato thick smear • Temperature adequate diet and
• Recovery of the Larvae Iron therapy is indicated • Pattern of rainfall iron therapy
from soil we can use: to raise hemoglobin level • Burying action of dung beetles
o Baermann Funnel to normal.
Method In the Philippines, the overall prevalence
o Damp Gauze Pad Thiabendazole – either rate of hookworm infection is about 5 –
Method of Beaver topical or systematic has 45% wherein the dominant specie is
• Occasionally, larvae are been successful for Necator americanus.
recovered in skin biopsy or creeping eruption. 96% - Necator americans
following freezing of the 2% - Ancylostoma
skin. 2% - mixed infections
PATHOLOGY
Due to the Larval Stages Due to Adult Worms
• Ground Itch or Dew Itch • Hookworm anemia
o Percutaneous entry of the infective filariform larvae is o Adult worms suck the host’s blood and mucosal
often characterized by an itching sensation or substances. An anticoagulant secretion facilitates blood
dermatitis. Itching is often severe, and it is known as sucking. Another factor that should be considered is the
“ground itch” or “dew itch”, as it is related to contact with presence of bleeding raw areas of mucosa left by the
soil, especially on a dewy morning. Within several hours, adult worms when they transfer to a new site. The blood
allergic reactions to the worms or their products causes picture is “Microcytic hypochromic anemia”. The signs
pruritus, erythematosus papular rash that may and symptoms of chronic infection are those of profound
become vesicular. Scratching may lead to secondary iron deficiency anemia. The essential damage
bacterial infection. produced in intestinal hookworm infection is
hemorrhage from the intestinal wall.
• Pulmonary lesion (Wakana Disease) • Hypoalbuminemia

o Syndrome caused by the massive pulmonary migration o There is a low level of albumin due to combined loss of
of larval stages of hookworms. This may be due to blood, lymph and protein.
allergic reaction to the migrating larvae and may
produce symptoms similar to Ascaris pneumonitis.
• Creeping eruption or Cutaneous Larva Migrans
o Dermatitis characterized by serpiginous intracutaneous
lesions caused by migration of the filariform larvae or
nematode larvae that normally do not infect the human
host like A. caninum and A. braziliense. The infective
larval stage can enter the human skin but cannot pass
below the stratum germinativum producing instead a
serpiginous tunnel in this stratum. There will be no further
development in human host, the larvae remain trapped
in the skin of the wrong host for weeks or months,
wandering through subcutaneous tissue. The larvae
move at a rate of several millimeters to a few centimeters
per day.
Strongyloides stercoralis (Threadworm)

MORPHOLOGY FORMS
ADULT WORM (PARASITIC FEMALE) LARVAE
Length 2 – 7 mm Rhabditiform Larvae Filariform Larvae
Width 30 – 4 μm Mouth Short buccal cavity Not present
Size Small Esophagus Muscular elongated long
with pyriform posterior
bulb
Color Colorless Others Relatively conspicuous Forked or notched
genital primordium. tail
Buccal Cavity Short Facts Passed out in the
feces.
Esophagus Long, slender cylindrical extending through OVA
the anterior third or two-fifths of the body Size 50 – 58 by 3 – 34 μm
Shape Chinese lantern
Membrane Single file of thin-shelled
FACTS FREE LIVING FEMALE
Known for its extra ordinary conditions. It is the most documented facultative • Shorter than the parasitic female
parasite capable of leading both a free living and parasitic existence. People are • Stouter
the principal host of S. stercoralis, but dogs and monkeys have a similar parasite. • Double bulb muscular esophageal pharynx
Similar specie, Strongyloides fuellerborni, can infect higher primates and humans. • Broadly fusiform,
• Parasitic female being parthenogenetic is capable of self-fertilization without • Pointed tail that is curved ventrad.
the participation of the male.
• No male form of this parasite has been reliably identified, possibly because it
is not essential in the life cycle of the parasite
LIFE CYCLE
FREE-LIVING CYCLE PARASITIC CYCLE
Diagnostic Stage – Rhabditiform larvae 6. Filariform larvae in contaminated soil penetrate human skin
Infective Stage – Filariform larvae when skin contacts soil, and migrate to the small intestine.
1. Rhabditiform larvae are passed in the stool of an infected 7. It has been thought that the L3 larvae migrate via the
definitive host, develop into either infective filariform larvae bloodstream and lymphatics to the lungs, where they are
(direct development) eventually coughed up and swallowed. However, L3 larvae
6. or free-living adult females appear capable of migrating to the intestine via alternate routes
2. that mate and produce eggs (e.g. through abdominal viscera or connective tissue). In the
3. from which rhabditiform larvae hatch small intestine, the larvae molt twice and become adult female
4. and eventually become infective filariform (L3) slarvae worms.
5. The filariform larvae penetrate the human host skin to initiate 8. The females live embedded in the submucosa of the small
the parasitic cycle. intestine and produce eggs via parthenogenesis (parasitic males
6. This second generation of filariform larvae cannot mature into do not exist)
free-living adults and must find a new host to continue the life 9. which yield rhabditiform larvae. The rhabditiform larvae can
cycle. either be passed in the stool
1. Go to free living cycle
10. can cause autoinfection
FIGURES OF STRONGYLOIDES STERCORALIS
MORPHOLOGY OF STRONGYLOIDES STERCORALIS RHABDITIFORM LARVAE
STRONGYLOIDES STERCORALIS FREE-LIVING ADULTS FILARIFORM LARVAE

• Harada-Mori – used to recover • Albendazole Strongyloides stercoralis is • Improved sanitation
the larvae. • Thiabendazole especially prevalent in the tropical • Proper personal hygiene
Note: 3 stool samples, 1 per day. and subtropical areas where warm, • Prompt treatment of
• Duodenal Aspiration moisture and lack of sanitation favor existing infections
• String test. its free-living existence. • Use of shoes and
• Duodenal Intubation slippers to avoid contact
• Serologic Testing with contaminated soil
o ELISA are good preventive
o IHA measures.
PATHOLOGY
In great majority of cases of Strongyloidiasis, infections are light and go unnoticed by their human hosts, as they produce no significant
symptoms. The only objectively discerned abnormality is peripheral eosinophilia.
The types of diseases caused by Strongyloides may be classified as cutaneous, pulmonary and intestinal:
• Cutaneous Infection
o The initial penetration of the skin by the filariform larvae of Strongyloides provokes little or no reaction, although if the number
of larvae is usually large, there may be pruritus and erythema at the site of penetration. In highly sensitized individuals
(repeatedly infected), an allergic response to the penetrating larvae may develop. The larva may not be successful in
promptly carrying out their pulmonary migration, instead they may migrate in the skin causing a type of creeping eruption
or larva migrans characterized by a rapidly progressing linear urticarial lesion termed as larva currens (racing larva).
• Pulmonary Infection
o Pneumonitis may develop as a result of larval migration to the lungs.
• Intestinal Infection
o In heavy infection, the mucosa maybe honeycombed by the adult worms and larvae and sloughing of extensive patches
may occur. Long- standing and heavy infections result in weight loss and chronic dysentery accompanied by
malabsorption and steatorrhea.
CAPILLARIA PHILIPPINENSIS (PUDOC WORM)

DIFFERENTIATION MALE FEMALE DIFFERENTI TYPICAL ATYPICAL
ATION
Size 2.13 – 3.17 mm in length 2.5 – 4.3 mm in length Producer Typical Typical
Extra ordinary long, Anterior: esophagus Color Yellow
and stichosomes
Characteristics Shape Peanut or Guitar
Posterior: Intestine and
reproductive organs Size 42 by 20 μm 36 – 45 by 20 μm
1 smooth spicular sheath Membrane Moderately Thin Shelled
No. of Spicules Thick, Striated
Bipolar Flattened None
TWO TYPES OF FEMALE
Plugs
DIFFERENTIATION TYPICAL ATYPICAL Development 1–2 Multisegmented
8 – 10 eggs arranged in a 40 – 45 eggs segmented or Embryonated
Eggs in Uterus
single row arranged in 2 – 3 rows stages Eggs will hatch
while in still in
Classification Oviparous Larviparous
utero into the first
gives rise to typical Capillaria Hatch while still in the stage larvae
Hatching
egg uterus
DESCRIPTION FIGURES OF Enterobius vermicularis
• Disease: Intestinal Capillariasis & Pudoc’s ADULT WORM MORPHOLOGY
Disease
• Habitat: Small intestine
• parasitic infection causes by two species of
nematodes, Capillaria hepatica, which
causes hepatic capillariasis, and
Capillaria philippinensis, which causes
intestinal capillariasis
• C. hepatica is transferred through the fecal
matter of infected animals and can lead to
hepatitis. C. philippinensis is transferred
through ingesting infected small freshwater
fish and can lead to diarrhea and
emaciation.
• Intermediate Host: Fish (Bagsang, Bastu,
Birut, Ipon)
• Discovered by: Nelia Salazar at Brgy.
Pudoc Ilocos Norte
LIFE CYCLE
Diagnostic Stage: Unembryonated thick-
shelled eggs passed in feces
Infective Stage: Larvae develop in tissue of
intermediate host
1. Typically, unembryonated, thick-shelled
eggs are passed in the human stool and
become embryonated in the external
environment in 5—10 days.
2. After ingestion by freshwater fish, larvae
hatch, penetrate the intestine, and migrate
to the tissues.
3. Ingestion of raw or undercooked fish results
in infection of the human host. OVA MORPHOLOGY
4. The adults of Capillaria philippinensis are
very small (males: 2.3 to 3.2mm; females:
2.5 to 4.3 mm) and reside in the human
small intestine, where they burrow in the
mucosa.
5. In addition to the unembryonated, shelled
eggs which pass into the environment, the
females can also produce eggs lacking
shells (possessing only a vitelline
membrane).
6. Which become embryonated within the
female’s uterus or in the intestine. The
released larvae can re-invade the intestinal
mucosa and cause internal autoinfection.
7. This process may lead to hyperinfection (a
massive number of adult worms).

CONTROL
The specimen of choice is stool. • Mebendazole The first case of human infection with Since infection is acquired
• DFS • Albendazole Capillaria philippinensis occurred in by eating raw or improperly
• Conc. Technique 1963 from Ilocos Norte and since then, cooked fish, fish should be
o AECT In severe cases with there have been 2,000 confirmed cases thoroughly cooked to
o FECT electrolyte and protein and 108 deaths. There are more prevent disease in man.
▪ reveal eggs and loss, electrolyte reported cases of male infection than Proper sanitary practices
larvae and replacement should be female with ratio of 2:1. Man acquires should also be practice. All
sometimes even given to the patients. the parasite by ingestion of raw or infected individuals should
adult worms. insufficiently cooked fish harboring the be treated immediately,
infective stage. In the Philippines, and feces should be
transparent fishes like bagsang, bagsit disposed properly.
and ipon may harbor the parasite.
Capillaria philippinensis is a parasite of
fish-eating birds and there is a fish-bird
cycle in nature ensuring the continuity of
its life cycle. The ability to infect fish-
eating birds suggest that this parasite
maybe widely distributed throughout
Asia and possibly elsewhere.
The provinces endemic in the

Philippines are Ilocos Norte, Ilocos Sur,
Cagayan, La Union, Pangasinan,
Zambales, Agusan del Norte and Leyte.
PATHOLOGY
The clinical manifestations of the disease are extreme and persistent diarrhea that may lead to dehydration, rapid weight loss,
abdominal pain, gurgling of stomach (borborygmus), muscle wasting, anorexia, vomiting and edema. There is malabsorption
of fats and sugar (intestinal malabsorption) and low plasma levels of Potassium, Calcium, carotene, and total protein. If the disease is
not treated immediately severe manifestations of the disease may develop like hypotension and cardiac failure and may lead to the
death of the patient.
Trichinella spiralis (Trichina worm)

ADULT MORPHOLOGY LARVAE
DIFFERENTIATION MALE FEMALE Size at Birth 80 – 120 μm
Size 1.5 by 0.04 mm in length 3.5 by 0.06 mm in length Size reaches 900–1,300 μm by 35–40 μm
Color Whitish Anterior tip Spear-like burrowing
Tail Ventrally curved tail Mature Has digestive tract similar to
Reproductive Single testis near posterior Single ovary at very Encysted adult. Reproductive organs
System end posterior part Larva are still immature
Female None Viviparous or larviparous
Classification
Characteristics Body consisting of esophagus filled with stichosomes Others A.K.A Juvenile Larvae
No. of Larvae None 1, 500 larvae
Produces
DESCRIPTION FIGURES OF TRICHINELLA SPIRALIS
Disease: Trichinosis, Trichiniasis ADULT MORPHOLOGY
• Accidental to Human
LIFE CYCLE
Diagnostic Stage: Encysted larvae
Infective Stage: Encysted larvae
• Depending on the classification used,
there are several species of Trichinella:
T. spiralis, T. pseudospiralis, T. nativa,
T. murelli, T. nelsoni, T. britovi, T.
papuae, and T. zimbabwensis, all but the
last of which have been implicated in
human disease. Adult worms and
encysted larvae develop within a single
vertebrate host, and an infected animal
serves as a definitive host and potential
intermediate host. A second host is
required to perpetuate the life cycle of
Trichinella.
• The domestic cycle most often involved
pigs and anthropophilic rodents, but
other domestic animals such as horses
can be involved. In the sylvatic cycle, the
range of infected animals is great, but
animals most often associated as
sources of human infection are bear,
moose and wild boar.
• Trichinellosis is caused by the ingestion
of undercooked meat containing
encysted larvae (except for T.
pseudospiralis and T. papuae, which do
not encyst) of Trichinella species.
1. After exposure to gastric acid and
pepsin, the larvae are released from the
cysts.
2. And invade the small bowel mucosa
where they develop into adult worms.
3. Females are 2.2 mm in length; males 1.2
mm. The life span in the small bowel is
about four weeks. After 1 week, the
females release larvae
4. That migrate to striated muscles where
they encyst
5. Diagnosis is usually made based on
clinical symptoms, and is confirmed by
serology or identification of encysted or
non-encysted larvae in biopsy or autopsy
specimens.

CONTROL
• Muscle biopsy – • Thiabendazole – maybe given Prevalence of trichinosis in • The general public
demonstration of the during the first week of infection to humans is associated with should be
encysted larvae. expel the adult worm from the GI consumption of pork and continuously
• Serological tests – tract. This drug has no effect on pork products, hence informed through
CFT, ELISA, BFT migrating larvae and may prove to this is common in pork eating educational
(Bentonite be useless 2 weeks adter exposure. countries like Europe and campaigns regarding
Flocculation Test), • Mebendazole – is larvicidal when United States than in tropics pork and bear
Bachman intradermal give 20mg per kg body weight 6 and the Orient. transmission.
test using antigen hourly for 10-14 days. • It is recommended
prepared from T. spiralis • Patients with symptomatic trichinosis Trichinosis is a zoonosis. that meat be cooked
diluted 1:5,000 or should be confined to bed and given Man acquires the infection at 77ºC (177ºF).
1:10,000. Reaction is general supportive treatment. from inadequately cooked or Freezing is another
observed after 30 mins. • Salicylates – are usually enough to improperly processed way to kill larvae.
Positive result is a relieve headache and muscular infected lean pork or bear Storage at -15ºC for
blanched wheal pain. meat. Two hosts are required 20 days or -30ºC for
surrounded by an area • Fluids and electrolytes balance to complete the life cycle. six days is effective.
of erythema should be watched since impaired There are two maintenance • Smoking, salting or
• Beck’s Xenodiagnosis capillary permeability can lead to cycle: drying of meat are
– make use of general edema and later • Pig to pig not effective.
experimental animals mobilization of fluid. • Rat to rat
like Albino rats
PATHOLOGY
The variability and severity of the clinical symptoms depend upon the number of worms, the size and the age of the patient, the tissues
invaded and the general resistance of the patient.
Except for the early intestinal lesions caused by the adult worms, pathology is concerned with the presence of the larvae in the muscles
and vital organs. Five larvae/gram of muscle could result to death.
The disease is commonly divided into three phases corresponding to the periods of:
• Incubation and intestinal invasion
o Symptoms: diarrhea or constipation, vomiting, abdominal cramps, malaise and nausea.
• Larval migration and muscle invasion
o Signs and Symptoms: fever, facial edema, urticaria, pain and swelling and weakness.
o Severe cases: there may be splenomegaly, gastric and intestinal hemorrhages.
• Encystment and encapsulation
o This is the convalescent stage, wherein fever, weakness, pain and other symptoms start to disappear. Full recovery is
expected since trichinosis is a self-limiting disease.
Wuchereria bancrofti (Bancrofti’s filarial worm)

ADULT MORPHOLOGY DESCRIPTION
DIFFERENTIATION MALE FEMALE Disease: Bancroftian filariasis,
Size 2 – 4 cm in length 8 – 10 cm in length Wucheriasis, Elephantiasis
Color Creamy white
Characteristics Long, filiform in shape, tapering at both ends with smooth cuticula The worm being a tissue invading
Identifying Feature When stained, the central axis shows dark-staining nuclei nematode is found inhabiting the
Other Feature Body nuclei, Sheathed, Terminal nuclei, Tail lymph vessels and lymph glands
of the vertebrate host.
MICROFILARIA MORPHOLOGY
Size 244 – 196 μm in length by 7.5 – 10 μm in diameter
Coumns of Dark Staining 2 -3 rows and distinctly conspicuous and discrete
Nuclei
Periodicity Nocturnal, except South Pacific type, which is subperiodic
Excretory Cell Near the excretory pore is small while
G cells Located toward the posterior end are small, similar in size and
usually flat on one side.
Tail Tapering to a delicate point with no nuclei terminal
LIFE CYCLE FIGURES OF WUCHERERIA BANCROFTI
Diagnostic Stage: Microfilariae MORPHOLOGY OF MICROFILARIA
Infective Stage: Human (L3 Filariform),
Vector (microfilariae)
During a blood meal, an infected mosquito
introduces third-stage filarial larvae onto the
skin of the human host, where they penetrate
into the bite wound
1. They develop in adults that commonly
reside in the lymphatics.
2. The female worms measure 80 to 100
mm in length and 0.24 to 0.30 mm in
diameter, while the males measure
about 40 mm by 1 mm. Adults produce
microfilariae measuring 244 to 296 μm
by 7.5 to 10 μm, which are sheathed and
have nocturnal periodicity, except the
South Pacific microfilariae which have
the absence of marked periodicity. The
microfilariae migrate into lymph and
blood channels moving actively through
lymph and blood.
3. A mosquito ingests the microfilariae
during a blood meal.
4. After ingestion, the microfilariae lose
their sheaths and some of them work
their way through the wall of the
proventriculus and cardiac portion of the
mosquito’s midgut and reach the
thoracic muscles.
5. There the microfilariae develop into first-
stage.
6. larvae and subsequently into third-stage
infective larvae.
7. The third-stage infective larvae migrate
through the hemocoel to the mosquito’s
prosbocis.
8. and can infect another human when the
mosquito takes a blood meal

CONTROL
• Demonstration of microfilaria in the • Diethylcarbamazine The disease has a worldwide • Education regarding
blood. citrate (DEC) distribution in tropical and filarial infections
o Microfilaria of W. bancrofti exhibits subtropical countries. At least • Control of mosquito
nocturnal periodicity chiefly present 48 species of mosquitoes vector
in the blood during the night from including Aedes, Anopheles, • Use of protective
8:00 PM to 4:00 AM. Culex and Mansonia are clothing and insect
o Best Time to Collect Blood natural or experimental repellants
Specimen is 10PM – 2AM (peak vectors. The prevalence of • treatment of
hours). filariasis is correlated with the infections to prevent
• Thich Blood Smear about the size of 25 density of population and poor further transmission
centavo coin (2 thick smear/slide) sanitation, since mosquito are essential in the
dehemoglobinized and stained with vectors breed mainly in water prevention and
Giemsa or Wright’s or Delafield’s contaminated with sewage control of
Hematoxylin stain. and decaying organic matter. bancroftian filariasis.
o Dehemoglobinization is necessary The principal vector in the
before staining the blood smear and Western hemisphere is Culex
this is accomplished by immersing quinquefasciatus and in the
the smear in distilled water for a few South pacific, Aedes
minutes until the color of the smear polynesiensis. The former is a
turns into white. night-biting, sylvatic, non-
• Wet smear may also be done by placing domesticated mosquito. In the
one drop of blood in a slide and adding Philippines, there are two
one drop of acetic acid in order to lyse types of Bancroftian filariasis
the RBC. Movement of the microfilaria is namely, the urban type which
observed in this method. is most prevalent in abaca
• Heparinized capillary method is also raising areas of the country
useful in the diagnosis. These is done by and the rural type prevailing
filling up the heparinized tube with blood, rather away from the houses
then centrifuge and get the buffy coat towards the mountains and
and place it in a slide and stain with hills. In urban type, the
Giemsa or Wright’s. mosquito vector is Aedes
• If negative in these methods, poecilus, which breeds in the
concentration methods maybe useful water, accumulated in the
such as Knott’s concentration and axils of abaca and banana
the Millipore or Membrane Titration plants. In the rural type, the
method. In Knott’s concentration vector is Anopheles minismus
technique, acetic acid and Formalin are flavorostris, a night biting
used. Aside from blood, urine and scrotal mosquito that breeds in
fluid can also be used in the laboratory mountain streams. The
diagnosis of this infection. provinces endemic for W.
• In many chronic infections, microfilaria bancrofti are the ff.: Romblon,
may not be demonstrated in the Camarines Sur and Norte,
peripheral blood because of the Albay, Sorsogon, Mindoro,
following factors: Quezon, Masbate, Samar,
o low intensity of infection Leyte, Bohol, All provinces in
o dead worms Mindanao, Palawan, Sulu and
o obstructed lymphatics Mt. Province (Bondoc)
PATHOLOGY
Filarial symptoms are caused mainly by the adult worms. These adults maybe living, dead or degenerating. Microfilaria apparently
causes less pathology although they have been associated with Tropical Pulmonary Eosinophilia (TPE), granuloma of the spleen
and allergic reactions following their destruction by drugs.
TPE is a classic example of occult filariasis in which classical clinical manifestations are not present and microfilaria are not found in
the blood but maybe found in the tissues.
The adult worms lying in the dilated lymphatics or in the sinuses of the two lymph nodes, provoke a pseudotubercular granulomatous
reaction which becomes more pronounced on their death. It results to occlusion of the small lymphatics and narrowing of the
larger ones, which may give way to edema, vascular and lymphatic hyperplasia, fibrosis and caseation.
Prolonged obstruction of the lymph glands will eventually lead to marked fibrosis giving rise to elephantiasis, the degenerating worms
being absorbed and replaced by hyalinized or even calcified scar tissues.
The most commonly encountered clinical manifestations are hydrocoele and chylocoele with accompanying enlargement of the
inguinal and lymph nodes and elephantiasis of the scrotum and vulva. Enlargement of the genitals and lower lymphatics are
common.
Brugia malayi (Malayan filarial worm)

DIFFERENTIATION MALE FEMALE Disease: Malayan filariasis
Size 13 – 23 mm in length 43 – 55 mm in length
Color whitish The adult B. malayi bears a
Characteristics Thread like filaria general resemblance to those of
Identifying Feature When stained, the central axis shows dark-staining nuclei W. bancrofti.
Other Feature Body nuclei, Sheathed, Terminal nuclei, Tail
Size 177 – 230 μm in length
Characteristics Enclosed in a sheath, have angular curvature with secondary kinks
Column of Nuclei 2 rows indistinct or confluent
Excretory Cell Large
G cells Larger than those of W. bancrofti and are ovoidal in shape
Tail Presence of 2 nuclei at the tip of the tail
LIFE CYCLE FIGURES OF WUCHERERIA BANCROFTI
Diagnostic Stage: Microfilariae MORPHOLOGY OF MICROFILARIA
Infective Stage: Human (L3 Filariform),
Vector (microfilariae)
During a blood meal, an infected mosquito
(typically Mansonia spp. and Aedes spp.)
introduces third-stage filarial larvae onto the
skin of the human host, where they penetrate
into the bite wound
1. They develop into adults that commonly
reside in the lymphatics.
2. The adult worms outwardly resemble
those of Wuchereria bancrofti but are
smaller. Female worms measure 43 to
55 mm in length by 130 to 170 μm in
width, and males measure 13 to 23 mm
in length by 70 to 80 μm in width. Adults
produce microfilariae, measuring 177 to
230 μm in length and 5 to 7 μm in width,
which are sheathed and have nocturnal
periodicity (in some regions B. malayi
may be sub-periodic, and note that
microfilariae are usually not produced in
B. pahangi infections). The microfilariae
migrate into lymph and enter the blood
stream reaching the peripheral blood.
3. A mosquito ingests the microfilariae
during a blood meal.
their sheaths and work their way through
the wall of the proventriculus and cardiac
portion of the midgut to reach the
thoracic muscles.
stage larvae.
6. and subsequently into third-stage larvae.
7. The third-stage larvae migrate through
the hemocoel to the mosquito’s
proboscis.
mosquito takes a blood meal
CONTROL
• Identification of microfilaria • Diethylcarbamazine Epidemiology: B. malayi is primarily • The prevention and
in the blood. present in India, Thailand, Vietnam, Sri control are similar to
o Microfilaria have a Lanka, Indonesia, Philippines, China, W. bancrofti.
subperiodic Korea and small focus in Japan. Animal
periodicity and reservoir such as cats and monkeys are
although they are recognized. The typical vector is Mansonia
also present during but in Japan, Korea and coastal China, it is
the day. Aedes togoi. Mansonia is most prevalent in
o Best time to collect low regions, where numerous ponds are
blood specimen infested with water plants of the genus
should be during the Pistia, which are essential for the breeding
night where they are of these mosquitoes. In the Philippines, B.
present in greater malayi was found to be restricted to areas
number in the of freshwater swamps, whereas W.
peripheral blood bancrofti has a wider distribution. There
circulation. seems to be only one type of malayan
• Laboratory methods used filariasis in the Philippines with modified
for W. bancrofti also apply periodicity (subperiodic nocturnal). The
to B. malayi. The knotting of mosquito vectors are Mansonia bonneae,
microfilaria, an agonal which breeds in freshwater swamps and
phenomenon during drying Mansonia uniformis, which breeds in rice
of the films maybe fields. The province endemic for malayan
prevented by adding filariasis are: 1. Palawan 2. Sulu (Bongao
chloroform or methanol to in Tawi-tawi) 3. Agusan 4. Eastern Samar
the blood.
PATHOLOGY
The pathogenic mechanism of human filariasis due to B. malayi are essentially the same as those of W. bancrofti except that the
deformity produce in infected cases is not as severe as in the latter. Malayan filariasis is characterized by superficial lymphadepathy
and high eosinophilia (7 – 20%).
Loa loa (African eyeworm, Loa worm)

DIFFERENTIATION MALE FEMALE Disease: Loiasis,
Size 30 - 34 mm in length 40 - 70 mm in length Calabar or fugitive
Color No Information swellings.
Characteristics Cylindrical, thread-like
Arrangement of Nuclei in Distinct continuous row tail of nuclei; extend tip of tail Live in the
Tail subcutaneous fat
Other Feature Note: Similar to the microfilaria of B. Malayi under the skin
The optimum site for the microfilaria during their non-circulation phase is the
lung; they appear only in the peripheral blood during the day.
Size 250 – 300 μm in length by 6 – 8 μm in width
Characteristics Sheathed. Sheath stains poorly in ordinary blood films and is usually
overlooked.
Column of Nuclei Terminal (distinct continuous row)
Excretory Cell Similar to microfilaria of B. Malayi
G cells Similar to Microfilaria of B. Malayi
Tail Tapering gradually, caudal nuclei continuous with those of the trunk.
LIFE CYCLE FIGURES OF LOA LOA
Diagnostic Stage: Presence of microfilaria MORPHOLOGY OF MICROFILARIA
worm
Infective Stage: Larvae
The vector for Loa loa filariasis are flies from
two species of the genus Chrysops, C.
silacea and C. dimidiata. During a blood
meal, an infected fly (genus Chrysops, day-
biting flies) introduces third-stage filarial
larvae onto the skin of the human host, where
they penetrate into the bite wound.
1. The larvae develop into adults that
commonly reside in subcutaneous
tissue.
2. The female worms measure 40 to 70 mm
in length and 0.5 mm in diameter, while
the males measure 30 to 34 mm in length
and 0.35 to 0.43 mm in diameter. Adults
produce microfilariae measuring 250 to
300 µm by 6 to 8 μm, which are sheathed
and have diurnal periodicity. Microfilariae
have been recovered from spinal fluids,
urine, and sputum. During the day they
are found in peripheral blood, but during
the noncirculation phase, they are found
in the lungs.
3. The fly ingests microfilariae during a
blood meal.
their sheaths and migrate from the fly’s
midgut through the hemocoel to the
thoracic muscles of the arthropod The
number
stage larvae.
6. and subsequently into third-stage
infective larvae.
to the fly’s proboscis.
fly takes a blood meal.
• Identification of microfilaria • The surgical removal Loa loa is confined to the equatorial • Education regarding the
in the peripheral blood of adult when rain forest of Africa and is endemic infections and its vectors,
during the day, or by accessible is an in Tropical West Africa, the Congo especially for persons
removal of the adult worms accepted method of basin, and parts of Nigeria. Infection entering the known
from the skin of the treatment. A is most prevalent in small endemic areas is
conjunctiva. favorable time is settlements situated in or at the essential.
during their migration margin of the forests and is favored • Protection from fly bites
across the nose of by the presence of rubber along with treatment of
conjunctiva. plantations cases is also helpful in
• Chemotherapy with reducing the incidence of
diethylcarbamazine the infection. However,
is effective but the presence of disease
several courses of in animal reservoir
treatment may be (monkeys) limits the
needed. feasibility of controlling
the disease
PATHOLOGY
The adult worms normally live in the subcutaneous tissue through which they migrate back and forth provoking a temporary
inflammatory reaction known as “fugitive” or “Calabar” swellings regarded as local reactions to sudden liberation of the worm’s
metabolites. Adults are particularly troublesome when passing in the orbital conjunctiva or across the bridge of the nose. Under the
conjunctiva, it can produce irritation, edema of the eyelids and impaired vision. In Uganda, there are three types of ocular
manifestations, namely:
1. conjunctiva granulomata - present as non-painful, itchy solitary of small yellow nodules about 2 mm in length.
2. painless edema of the eyelids known as “bung eye”.
protopsis – edema of the orbital cellular tissue which is also called “bug eye” or “bulge eye”.
Onchocerca volvulus (Convulated filaria)

DIFFERENTIATION MALE FEMALE Disease: Onchocerciasis,
Size 19 - 42 mm in length 33.5 - 50 mm in length River blindness
Color White, Opalescent, Transparent
Characteristics Distinct transverse striations of the cuticula.
Arrangement of Nuclei in Do not extend to tip of tail.
Tail
Other Feature Filiform and blunt at both ends. Coiled within the nodules. No sheath
and nuclei in tail.
Size 315 – 360 μm in length by 6 μm in width
Characteristics anterior and posterior ends being nuclei free.
FEMALE WORM
give birth to unsheathed microfilaria which are typically found in the lymphatics of connective tissues
and cutaneous layers in the vicinity of the parent worm, as well as in the stratum germinativum and
corneal conjunctiva, rarely in blood or internal organs.
LIFE CYCLE FIGURES OF LOA LOA
Diagnostic Stage: Presence of microfilaria MORPHOLOGY OF ADULT WORM
worm
Infective Stage: Larvae
During a blood meal, an infected blackfly
(genus Simulium) introduces third-stage
filarial larvae onto the skin of the human host,
where they penetrate into the bite wound.
1. In subcutaneous tissues the larvae.
2. Develop into adult filariae, which
commonly reside in nodules in
subcutaneous connective tissues.
3. Adults can live in the nodules for
approximately 15 years. Some nodules
may contain numerous male and female
worms. Females measure 33 to 50 cm in
length and 270 to 400 µm in diameter,
while males measure 19 to 42 mm by
130 to 210 µm. In the subcutaneous
nodules, the female worms are capable
of producing microfilariae for
approximately 9 years. The microfilariae,
measuring 220 to 360 µm by 5 to 9 µm
and unsheathed, have a life span that
may reach 2 years. They are
occasionally found in peripheral blood,
urine, and sputum but are typically found
in the skin and in the lymphatics of
connective tissues.
4. A blackfly ingests the microfilariae during
a blood meal.
5. After ingestion, the microfilariae migrate
from the blackfly’s midgut through the
hemocoel to the thoracic muscles.
stage larvae.
7. and subsequently into third-stage
infective larvae
to the blackfly’s proboscis.
fly takes a blood meal.

• Aseptic removal of skin snip • Surgical removal of O. volvulus is endemic in many parts • Education regarding the
of the subcutaneous the encapsulated of Africa especially in the Congo disease and its black fly
nodules. nodule is often basin and Volta River basin. In transmission is
• Microscopic examination of performed to remove America, it occurs in many parts of essential.
this tissue in a coverslipped the adult worms and Central and South American • Protection from black
drop of NSS to detect the countries. Several species of the bites by use of
presence of unsheathed stop production of black fly genus Simulium serve as protective clothing,
microfilaria. microfilaria. vectors, but none so appropriately screens, and insect
• O. volvulus microfilaria is • Treatment with named as principal vector except repellants, as well as
not found in blood specimen Diethylcarbamazine Simulium damnosum (the damned prompt diagnosis and
but maybe found in urine followed by Suramin black fly). The disease is confined to treatment of infections
specimens because is recommended with neighborhood of rapidly flowing are critical.
nodules are often located an alternative drug streams where the black flies or
near the genitalia. mebendazole. buffalo gnats breed. There is greater
prevalence of infection in men than in
women because of greater
occupational exposure. It has been
shown by studies in endemic areas in
Africa that 50% of men will be totally
blind before they reach 50 years of
age. This account for the common
term “river blindness” applied to the
development of onchocerciasis
PATHOLOGY
The usual clinical manifestations of the disease are fever, eosinophilia and urticaria. As the worm mature, mate, and begin
producing microfilaria, the subcutaneous nodules begin to appear and can occur on any part of the body. These nodules are most
dangerous when present on the head and the neck because the microfilaria may migrate to the eyes and cause severe tissue
damage leading to blindness.
A number of skin conditions are related to the presence of this parasite including pruritus, hyperkeratosis, myxedematous
thickening and hanging groin wherein the nodules are located near the genitalia.
MANSONELLA SPECIES
Filarial infections caused by Mansonella species are less important than those previously discussed. All of the species produce non-
sheathed microfilaria in blood and subcutaneous tissue, and all are transmitted by biting midges (Culicoides). Infection caused by
these species can be treated with DEC as for previous filarial infections. Species identification can be accomplished with blood smear,
noting the structure of microfilaria. It causes serous cavity filariasis in the abdomen.
MANSONELLA SPECIES MORPHOLOGY
Common The adults are creamy white, elongated, cylindrical with smooth cuticle
Persistent filaria and bluntly rounded anterior and posterior end curved ventrally in both
name
Mansonella body cavities (peritoneal sexes. The male measures 45 mm by 60 microns while the female
Habitat
perstan cavity and Pleural cavity) measures 70 to 80 by 120 microns. The microfilaria appears in the
blood both day and night (non-periodic) with nuclei extending up to the
Disease Dipetalonemiasis tip of the blunt tail.
Common The female measures 65 to 81 mm in length and 0.21 to 0.25 mm in
Ozzard’s filaria diameter. The male species are known only from a posterior segment
name
33-mm in length and 0.2 mm in diameter. The whole male worm has
Mansonella body cavities not yet been seen. The non-periodic microfilaria which is unsheathed
Habitat
ozzardi (subcutaneous tissue) somewhat resembles that of M. perstans in size but differs in the
appearance of the tail, which tapers to a thin filament, contains a column
Mansonelliasis or of 4 to 6 ovoid or bar-like nuclei and the tail itself beyond the nuclei is
Disease
Ozzard’s filariasis somewhat basophilic.
The non-sheathed microfilaria measures 180 to 240 microns. The
cephalic space is slightly longer than wide, and the first 4 to 5 nuclei are
elongated and tend to be quadrate, arranged in a single column of 9 to
Mansonella streptocerca
12 which extend to the rip of the tail. When fixed, the microfilaria is
relatively straight except at the posterior end which, is strongly bent in
a shepherd’s crook curve.
LIFE CYCLE FIGURES OF MANSONELLA SPECIES
Mansonella perstans MANSONELLA PERSTANS
• Diagnostic stage: microfilariae
• Infective stage: filariform larva
• During a blood meal, an infected midge introduces third-
stage (L3) larvae onto the skin of the human host, where
they penetrate into the bite wound
1. They develop into adults that reside in body
cavities, most commonly the peritoneal cavity or
pleural cavity, and less frequently in the
pericardium.
2. The size range for female worms is 70 to 80 mm in
length and 120 µm in diameter, and the males
measure approximately 45 mm by 60 µm. Adults
produce unsheathed, subperiodic microfilariae
(200 µm long, 4.5 µm wide) which enter peripheral
circulation.
3. A midge vector ingests microfilariae during a blood
meal.
4. After ingestion, the microfilariae migrate from the
midge’s midgut through the hemocoel to the
thoracic muscles of the arthropod.
5. There the microfilariae develop into first-stage
larvae.
6. and subsequently into third-stage infective larvae.
7. The third-stage infective larvae migrate to the
midge’s proboscis.
8. and can infect another human when the midge
takes a blood meal
Mansonella ozzardi
• Diagnostic stage: microfilariae
• Infective stage: filariform larva
• During a blood meal, an infected arthropod (midges,
genus Culicoides, or blackflies, genus Simulium)
introduces third-stage filarial larvae onto the skin of the
human host, where they penetrate into the bite wound.
1. They develop into adults that commonly reside in
subcutaneous tissues.
2. Adult worms are small and slender, measuring
about 49 mm long and 150 µm wide (females) or
26 mm long and 70 µm wide (males). Adults
produce unsheathed and non-periodic microfilariae
that reach the blood stream.
3. The arthropod ingests microfilariae during a blood MANSONELLA OZZARDI

meal.
arthropod’s midgut through the hemocoel to the
thoracic muscles.
larvae
6. and subsequently into third-stage infective larvae.
7. The third-stage infective larvae migrate to
arthropod’s proboscis
8. and can infect another human when the arthropod
takes a blood meal.
Mansonella streptocerca
• Diagnostic Stage: Microfilariae
• Infective Stage: Filariform larva
• During a blood meal, an infected midge introduces third-
stage filarial larvae onto the skin of the human host,
where they penetrate into the bite wound.
1. They develop into adults that reside in the dermis,
most commonly less than 1 mm from the skin
surface.
2. The females measure approximately 27 mm in
length and are 50 µm wide at the level of the vulva
(anteriorly) and ovaries (near the posterior end),
and up to 85 µm at the mid-body. Males measure
50 µm in diameter. Adults produce unsheathed and
non-periodic microfilariae, measuring 180 to 240
µm by 3 to 5 µm, which reside in the skin but can
also reach the peripheral blood. MANSONELLA STREPTOCERCA
3. The midge vector ingests the microfilariae during a
blood meal.
midge’s midgut through the hemocoel to the
thoracic muscles.
larvae
6. and subsequently into third-stage larvae.
7. The third-stage larvae migrate to the midge’s
proboscis
8. and can infect another human when the midge
takes another blood meal.
EPIDEMIOLOGY
Human infection is produced by bites of infected Culicoides which, breed in jungles and swamps. The infective stage is filariform larva.
Man is the final host and some of the monkeys in Africa and South America have been found as reservoir hosts.
Angiostrongylus cantonensis (Rat lungworm or Rodent lungworm)

DIFFERENTIATION MALE FEMALE Size 46 – 48 by 86 – 74 μm
Length 15.9 – 19 mm 21 – 25 mm Appearance Elongated, ovoidal with
delicate hyaline shell
Diameter 0.26 mm 0.30 – 0.36 mm Shell Hyaline shell, Thin shelled
Tail Ventrally curved tail Others Unembryonated when laid
Spicules and Eggs Long Spicule 15, 000 eggs/day L3 - two well-developed
Other Feature Single lobed caudal bursa Barber’s pole uterine tubule chitinous rods below its
which is kidney, pale, and • more likely visible buccal cavity.
filiform • easy to diagnose
Posterior end is shaped like a
bluntly ending horn
DESCRIPTION FIGURES OF ANGIOSTRONGYLUS CANTONENSIS
• Disease: Angiostrongyliodiasis or ADULT MORPHOLOGY
Eosinophilic Meningoencephalitis in
man
• Habitat: lungs of rats; brain
• Definitive host: Rats
• Intermediate Hosts: Snails (Achatina
fulica or giant African snail, Hemiplecta
sagittifera, Helicostyla macrostoma,
Vaginilus plebeius, and Veronicella
altae)
• Incubation period: 6 to 15 days or 12 to
47 days
LIFE CYCLE
Diagnostic Stage: Larvae
Infective Stage: L1
MOT: Ingestion or active penetration
Adult worms of A. cantonensis live in the
pulmonary arteries and right ventricle of the
normal definitive host.
1. The females lay eggs that hatch in the
terminal branches of the pulmonary
arteries, yielding first-stage larvae. The
first-stage larvae migrate to the pharynx,
are swallowed, and passed in the feces.
They penetrate or are ingested by a
gastropod intermediate host.
2. After two molts, third-stage larvae are
produced
3. which are infective to mammalian hosts.
When the infected gastropod is ingested
by the definitive host, the third-stage
larvae migrate to the brain where they
develop into young adults.
4. The young adults return to the venous
system and then the pulmonary arteries
where they become sexually mature. Of
note, various animals act as paratenic
(transport) hosts: after ingesting the
infected snails, they carry the third-stage
larvae which can resume their
development when the paratenic host is
ingested by a definitive host. Humans
can acquire the infection by eating raw or
undercooked snails or slugs infected with
the parasite; they may also acquire the
infection by eating raw produce that
contains a small snail or slug, or part of
one.
5. There is some question whether or not
larvae can exit the infected gastropods in
slime (which may be infective to humans
if ingested, for example, on produce).
Infection may also be acquired by
ingestion of invertebrate paratenic hosts
containing L3 larvae (e.g. crabs,
freshwater shrimp). In humans, larvae

migrate to the brain, or rarely to the
lungs, where the worms ultimately die
6. Larvae may develop to fourth or fifth
stage in the human host but seem to be
incapable of maturing fully.

CONTROL
• It is difficult to • No anti- The final host of A. cantonensis is the rat, Rattus • Preventive
diagnose the infection helminthic rattus and Rattus norvegicus. The intermediate measures include
because the adults lay treatment can hosts commonly found in our country are careful washing and
primarily in the brain. be recommended Achatina fulica (giant Japanese snails), Pila cooking of
In areas where the at present. luzonica (kuhol), Parathelpusa mistio (talangka), vegetables, thorough
disease is endemic, • Surgery may be Brotia asperata (suso), garden slugs and even cooking of prawns
people showing brain needed when it freshwater prawns or water and vegetables and crabs.
dyscrasia and has a is lodged in the contaminated with third stage larva. Man, usually • avoidance of
moderate or high anterior chamber gets the infection through the following: ingestion of raw
eosinophilic count in of the eye. 1. ingestion of raw mollusk containing the Achatina fulica
the CSF should be third stage larvae. snails and slugs.
considered as potential 2. ingestion of raw leafy vegetable • Elimination of the
victim. History of the contaminated with mucus secretions of snail and slug
patient as to ingestion of the mollusks containing the third stage intermediate host.
possible intermediate larvae. Rodent eradication
hosts should be 3. drinking water contaminated with the may help prevent
considered. infective larva. human infection.
• No immunologic test 4. ingestion of paratenic hosts such as
has been developed freshwater prawns and crabs
yet for infection. containing the infective larva.
• Post-mortem In the Philippines, A. cantonensis has been
examination must be reported in rats with a prevalence rate of 7%. It
done on persons was reportedly present in the following places:
suspected of dying with 1. Batangas 8. Bulacan
the infection to search 2. Cavite 9. Ilocos Norte
for the worms. 3. Laguna 10. Mountain Province
4. Nueva Ecija 11. Pampanga
5. Pangasinan 12. Quezon
6. Rizal 13. Sorsogon
7. Tarlac 14. Metro Manila
PATHOLOGY
The incubation period for this infection is from 12 – 47 days. The clinical picture of eosinophilic meningoencephalitis is one of
acute onset of severe headache, low grade fever, nausea, and vomiting. Other clinical manifestations include stiffness of the
neck, weakness of the hands and legs and abdominal pain. During the illness the patient may exhibit increasing confusion or
incoherence, disorientation and impairment of memory or profound coma. Clinical and laboratory results maybe negative.
Autopsy of the brain may show leptomeningitis, encephalomalacia and ventricular dilation. It also shows the worm in vascular
and perivascular tissues. Infection due to Angiostrongylus is self-limiting and the prognosis is good. The disease is occasionally fatal.
Dracunculus medinensis (Guinea worm, Medina worm, Dragon worm, Fiery Serpent worm of the Israelites)
MORPHOLOGY FORMS
ADULT WORM
FIGURES OF Dracunculus Medinensis
FEMALE
Length 70 – 120 cm
Diameter 0.7 to 1.7 mm
Lifespan 12 to 18 months
Others elongated, cylindrical, bluntly rounded at the
anterior end
has no vagina and present only prior to being
gravid.
Adult worm – inhabit the cutaneous and subcutaneous
tissue.
DESCRIPTION
• Common name: Guinea worm, Medina worm, Dragon Guinea worm disease, a neglected tropical disease (NTD), is caused
worm, Fiery Serpent worm of the Israelites by the parasite Dracunculus medinensis. The disease affects poor
• Disease: Dracontiasis, Dracunculiasis communities in remote parts of Africa that do not have safe water to
• Habitat: Subcutaneous tissue drink. There is neither a drug treatment for Guinea worm disease nor a
• Largest and longest nematode. vaccine to prevent it. Great progress has been made towards
• Dracunculus medinensis is a tissue invading elimination of Guinea worm disease; the number of human cases
nematode of medical significance. annually has fallen from 3.5 million in the mid-1980s to 15 in 2021.
LIFE CYCLE
Humans become infected by drinking unfiltered water
containing copepods (small crustaceans) which are infected
with larvae of D. medinensis.
1. Following ingestion, the copepods die and
release the larvae, which penetrate the host
stomach and intestinal wall and enter the
abdominal cavity and retroperitoneal space.
2. After maturation into adults and copulation, the
male worms die and the females (length: 70 to
120 cm) migrate in the subcutaneous tissues
towards the skin surface.
3. Approximately one year after infection, the
female worm induces a blister on the skin,
generally on the distal lower extremity, which
ruptures. When this lesion comes into contact
with water, a contact that the patient seeks to
relieve the local discomfort, the female worm
emerges and releases larvae.
4. The larvae are ingested by a copepod
5. and after two weeks (and two molts) have
developed into infective larvae
6. Ingestion of the copepods closes the cycle

Diagnosis is established by The ancient method of D. medinensis occurs in many Education regarding the life cycle
observation of the typical slowly wrapping the worm on parts of Asia and equatorial Africa. of the worm and avoidance of
ulcer and flooding the the stick is still used in many Human infection results from water contaminated with cyclops
ulcer with water to recover endemic areas. Surgical ingestion of water from so-called is critical. Protection of drinking
the discharge of larvae. removal is also a practical “stepwells” where people stand water by prohibiting bathing and
Occasionally X-ray and reliable procedure for the and bathe in water at which time washing of clothing in wells is
examination reveals worms patient. The drug of choice is the gravid female worm discharges essential. Treatment of water
in various parts of the body. Niridazole, with alternative larvae from lesions on the arms, with chemicals and the use of
drugs being metronidazole legs, feet, and ankles to infect fish that consume cyclops as
and thiabendazole. Cyclops in water. Ponds and food are also helpful.
standing water are occasional
sources of infection when human
uses these for drinking water.
PATHOLOGY
Symptoms of infection usually occur one year after the initial exposure when the gravid female creates vesicular lesions and ulcer in
the skin for the liberation of the larval worms. At the site of the ulcer, there is erythema and pain, as well as an allergic reaction to the
worm. There is also the possibility of abscess formation and secondary bacterial infection leading to further tissue destruction and
inflammatory reaction, with intense pain and sloughing of skin. If the worm is broken in attempt to 61 remove it, there may be toxic
reactions and if the worm dies and calcifies, there may be nodule formation and some allergic reaction.

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THE NEMATODES

Ascaris lumbricoides (Giant intestinal worm)

LARVA HATCHING FROM AN EGG ADULT WORM TRILOBATE LIPS

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CONTROL

Trichuris trichuria (Whipworm)

Enterobius vermicularis (Pinworm or Seatworm)

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

5. Most adult worms are eliminated in 1 to OVA OF HOOKWORM

RHABDITIFORM LARVAE FILARIFORM LARVAE

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

• Pulmonary lesion (Wakana Disease) • Hypoalbuminemia

Strongyloides stercoralis (Threadworm)

STRONGYLOIDES STERCORALIS FREE-LIVING ADULTS FILARIFORM LARVAE

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CONTROL

CAPILLARIA PHILIPPINENSIS (PUDOC WORM)

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

The provinces endemic in the

Trichinella spiralis (Trichina worm)

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

Wuchereria bancrofti (Bancrofti’s filarial worm)

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

Brugia malayi (Malayan filarial worm)

Loa loa (African eyeworm, Loa worm)

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CONTROL

Onchocerca volvulus (Convulated filaria)

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CONTROL

3. The arthropod ingests microfilariae during a blood MANSONELLA OZZARDI

Angiostrongylus cantonensis (Rat lungworm or Rodent lungworm)

freshwater shrimp). In humans, larvae

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION &

DIAGNOSIS TREATMENT EPIDEMIOLOGY PREVENTION & CONTROL

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