PARASITOLOGY LECTURE Batch 2021

CHAPTER 3: NEMATODES INFECTIONS

Intestinal Nematodes
A – Ascaris lumbricoides
C – Capillaria philippinensis
H – Hookworms
E – Enterobius vermicularis
S – Strongyloides stercoralis
T – Trichuris trichiura

Ascaris lumbricoides
Common names: Giant round worms, Pink worm, Giant intestinal roundworm, and
roundworm
Most common (MC) Soil-Transmitted Helminth (STH) as well as the MC intestinal
nematode infection.
PARASITE BIOLOGY
● Cream colored roundworm that’s parasitic in the human intestines.
● Have a terminal mouth with three lips and sensory papillae
● Adults reside but do not attach to the mucosa wall of the small intestines.
● Shown to produce:
o pepsin inhibitor 3 (PI-3) protects worms from digestion
o phosphorylcholine suppresses lymphocyte proliferation

MORPHOLOGY (ADULT)
Male Female
● 10-31 cm in length ● 22-35 cm in length
● Ventrally curved posterior end ● Paired reproductive organs in the
with two spicules posterior two-thirds
● Produces 200,000 eggs per day,
decrease when worm load increases.

MORPHOLOGY (OVA)
 Unfertilized Egg Fertilized egg Embryonated Egg
● 88-94 by 39-44 µm ● 45-70 by 35-50 µm ● Infective stage
● Longer and ● Thick, transparent, ● When ingested, larvae
narrower than hyaline shell hatches in the small
fertilized eggs. ● Thick outer layer as intestine’s lumen to
● Thin shell and a supporting release the larvae.
irregular structure ● It’s very distinct due to its
mammilated ● Delicate vitelline, very circular shape and
coating filled with lipoidal, inner having a thick shell.
refractile granules. membrane (highly
impermeable)
● Larvae develops in
14 days in the
protoplasm.

EPIDEMIOLOGY

● Due to its wide cosmopolitan distribution, Ascariaris lumbricoides is the Most

Common (MC) Soil-Transmitted Helminth (STH) and as well as being the MC
intestinal nematode infection.
● Affecting the world wide areas with warm, moist climates. The disease remains
endemic in countries of Southeast Asia, Africa, Central and South America.
Estimates reveal that the high number of cases of ascariasis is found in East
Asia and Pacific Island.
● Children are particularly vulnerable to ascariasis infections, ages between 5 to 15
years old have the highest intensities compared with other age groups.
● Like many other in-come countries like the Philippines, the prevalence may reach
80-90% in certain high-risk groups like children in public elementary schools.
● STH depends more on socioeconomic factors more than physical factors. Main
factors such as: dense human population, involvement in agriculture, illiteracy,
and poor sanitation.

MODES OF TRANSMISSION
● Fecal-oral route, MC mode of transmission
• Inhalation of contaminated dust
• Transplacenta may occur

PATHOGENESIS & CLINICAL MANIFESTATIONS

Majority of Ascaris infections are asymptomatic, the usual 10-20 worms may not show
symptoms thus may go unnoticed by the host unless it is discovered by stool
examination or spontaneous passing of worms in the stool.
During lung migration, the larvae may make the host react to something that previously
had no effect (etc. difficulty breathing).
In heavy infections, worms may be lodged in the appendix or occlude in the pancreatic
duct, resulting appendicitis and pancreatitis, respectively. Worm burden can go as high
as 1-4,999 epg for light infection, 5,000-49,999 epg for moderate intensity, and more
than 50,000 epg for heavy intensity.
Concerns for complication, the continuous biting and prickling of intestinal mucosa by
Ascaris adult may irritate the mucosa nerve endings and result in intestinal spasm
leading to intestinal obstruction.
DIAGNOSIS
Signs and symptoms of ascariasis are quite vague and indistinguishable from other
nematode infections or non-parasitic infections.
Hence, clinical diagnosis of ascariasis should be confirmed by microscopic examination
of a stool sample.
TREATMENT
Individual infections are cured by a single dose of any broad-spectrum anthelminthics
such as:

Drug of choice Adult dose Pediatric dose

Albendazole 400mg PO once 400mg PO once,

200mg PO once (for ages 12-
23 months old )
Mebendazole 100 mg bid x 3d or 100 mg bid x 3d or
500mg once 500mg once
Ivermectin 200 µm/kg PO once
Pyrantel pamoate 10mg/kg (max. 1g)
Nitazoxanide 500 mg bid x 3d

PREVENTION AND CURE

Mass & Targeted Treatment
● DOH Administrative Order 2006-0028 (Integrated Helminth Control Program)
o STH Control Program
o Administered twice a year
o Goal after 3 years, worm prevalence below 50%
● DOH Administrative Order 2010-0023(Adverse Events Following Deworming)
o MDA
o Twice a year or every 6 months
o ages 5 and 12 above
● Environmental Sanitation

Individual
● Practice proper hand washing with antiseptic soap
● Wash fruits and vegetables before consumption
 Capillaria Philippinensis
Common name: Pudoc Worm

One of the four species of capillaries known to infect humans. It is a zoonotic disease,
characterized by abdominal pain, chronic diarrhea, and gurgling stomach. May also be
associated with protein-losing enteropathy, electrolyte imbalance, and intestinal
absorption.
(The illness typically results in severe enteropathy, diarrhea, and malabsorption
syndrome when nutrient absorption in the small intestine is limited (intestinal disease).
Reason behind the common name of C. philippinensis? The name “Pudoc worm” was
based on the name of the place where the illness and related worm were initially found,
which was Pudoc West, Tagudin, Ilocos Sur.

PARASITE BIOLOGY
● Both have an esophagus with secretory cells called STICHOCYTES
● The esophageal structure is called STICHOSOME
● Characteristic, thin and filamentous anterior end and a slightly thicker and
shorter posterior end.

MORPHOLOGY (ADULT WORM)

Male Female
• 1.5-3.9 mm in length • 2.3-5.3 mm in length
• Spicule is 230-300 µm long, • Vulva located at the junction of
characterized by caudal alae and anterior and middle thirds.
long, non-spiny sheaths
Body divided into 2:

(Anterior)

• Esophagus
• Esophageal glands

(Posterior)

• Intestine
• Reproductive system w/ slightly
prominent vulva
 MORPHOLOGY (OVA)

Immature Egg Embryonated Egg

● 36-45 µm by 20 µm
● eggs are peanut-shaped or barrel-shaped; Oval in shape
● Thick and striated shells
● flattened ends, and flattened to slightly prominent bipolar
Morphology mucoid plugs.

(Ova)

• Unembryonated when • Infective stage

passed in feces
• Becomes embryonated in
water

LIFE CYCLE
 PATHOGENESIS & CLINICAL MANIFESTATIONS
Patients initially experience intermittent diarrhea (progresses to 8-10 volumes/day).
After a few weeks, noticeable weight loss, anorexia, vomiting, edema, and malaise.
Laboratory findings will show severe protein-losing enteropathy and hypoalbuminemia;
malabsorption of fats and sugars; low serum potassium, sodium, and calcium.
(malabsorption syndrome when nutrient absorption in the small intestine is limited)
The large number of worms is responsible for the severe pathology
If the disease is not treated soon after symptoms occurs, severe manifestations of the
disease will develop with a potentially fatal outcome.

DIAGNOSIS
● Finding eggs in the excreted feces
● Laboratory methods:
a) DFS
b) Stool concentration methods
c) Enzyme-linked immunosorbent assay (ELISA)

TREATMENT
For severe cases, patient is treated with electrolyte replacement and a high protein diet.
While also be given anthelminthic drugs.
Drug of choice Adult dose Pediatric dose

Albendazole 400mg PO daily x 10d 400mg PO daily x 10d

Mebendazole 200mg PO bid x 20d 200mg PO bid x 20d

EPIDEMIOLOGY

• First discovered in Northern Luzon, Philippines. In 1966, Pudoc West, Tagudin,

Ilocos Sur, Capillariasis outbreak occurred which caused a massive spread of the
disease and resulted more than 1,000 cases and 77 deaths.

• It is reportedly common in the endemic regions, particularly in Philippines and

Thailand, among people who consume freshwater fish without cooking. Ingestion
of infected fish leads to intestinal infection by the parasitic larva causing
associated symptoms that may be life-threatening without treatment.

• Sporadic cases have been reported from other East and Southeast Asian
countries.

• “Mystery disease” in 1998 resulted in deaths of villagers due to misdiagnosis.

• 17% in cases of chronic diarrhea

• Zamboanga del Norte is a recent endemic area

PREVENTION & CONTROL

Population Treatment
• DOH Administrative Order 2009-0021
o Food and water-borne diseases
• Education on the importance of proper hand washing and hygiene
• Latrines should be set out of reach from water and food supply

Individual
• Do not eat raw or undercooked fish
• Practice proper hand washing

Ref:
https://www.dovemed.com/article-synonyms/capillaria-philippinensis-infection/
https://www.chegg.com/flashcards/parasitology-nematodes-b2a799ba-d500-4450-
a93c-8125adb75e59/deck
https://www.cdc.gov/dpdx/ascariasis/index.html
Nematode Infections: Intestinal Nematodes
HOOKWORMS: Necator americanus and Ancylostoma duodenale

GENERAL CHARACTERISITCS:
• soil-transmitted helminths (STH)
• blood-sucking nematodes attach to the mucosa of the small intestine
• commonly found in tropical & subtropical
• where they occur as single and mixed infections
• all hookworms have the meromyrarian type of somatic cell w/ 2 to 5 cells
arranged per dorsal or ventral half.

MORPHOLOGY:
Necator americanus Ancylostoma duodanale
Adults are: Adults are:
• small cylindrical • slightly larger than N.
• Fusiform Americanus
• grayish-white nematodes
Head: curved opposite to the curvature Head: same direction as the curvature of
of the body the body.
• like a hook at the anterior
end.
Buccal capsule: ventral pair of semilunar Buccal capsule: has 2 pairs of curved ventral
cutting plates teeth.

SHAPE SHAPE

BUCCAL SHAPE: BUCCAL SHAPE:

Male Female Male Female

5 to 9 mm by 0.30 9 to 11 mm by 0.35 8—12 mm long approximately

mm mm 10—15 mm long

Posterior end: Mature cells Adults has single pair Adults has single
broad, membranous produces = 5000 of reproductive organ pair of reproductive
caudal burse with to 10,000 eggs organ
rib-like rays – used
for copulation
 BUCCAL SPEARS:

Necator americanus Ancylostoma duodanale

Filariform larva: Filariform larva:
• conspicuous and parallel • inconspicuous
• Conspicuous transverse striations • Transverse striations on the sheath in
present on the sheath in the tail region the tail region

FILARIFORM

Filariform (L3) hookworm larva in a wet

mount Close-up of the posterior
Filariform (L3) hookworm larva end of a filariform (L3)
hookworm larva.

RHABIDITFORM LARVAE
N. americanus and A. duodenale

● are distinguishable
● they resemble those Strongyloides stercoralis there are larger, more attenuated
posteriorly and have longer buccal cavity
● Genital primordium: smaller in hookworms compared to S. stercoralis
 A, Hookworm rhabditiform
larva

C.Hookworm rhabditiform,
B, Hookworm rhabditiform larva. larval form buccal capsule
Note: long buccal capsule and lack of prominent
genital primordium.

EGGS

● Difficult to distinguish the eggs of A. duodanale from those N. americanus

● Eggs have:
o bluntly rounded ends and a single thin
o transparent hyaline shell
o unsegmented at oviposition
o 2 to 8 cell stage of division when passed out with fresh feces
o Measures: 60-75 µm by 35-40 µm

Hookworm egg in an Hookworm egg in an Hookworm egg in a wet mount

unstained wet mount, Taken unstained wet mount, Taken under UV fluorescence
at 400x magnification. at 400x magnification. microscopy; image taken at
200x magnification.

HOOKWORM LIFE CYCLE

Eggs are passed in the stool
Larvae will hatch 1 to 2 days become a free living in contaminated soil.
5 to 10 days (and two molts) they become filariform (3rd stage) larvae that are infective
The infective larvae can survive 3 to 4 weeks in favorable environmental conditions
Bare feet: Larvae penetrate the skin & carried through the blood vessels to
the heart and then to lungs.
Swallowed: Penetrate into the pulmonary alveoli, ascemd the bronchial tree
to the pharynx.
Larvae reach the jejenum of the small intestine
Adult worms live In the lumen of the small intestine (distal jejenum)
Attach to the intestinal wall = blood loss by the host
Most adult worms are eliminated in 1 to 2 years
Longevity may reach several years.
PATHOGENESIS AND CLINICAL MANIFESTATIONS:

Pathology (a) skin at the site of entry of the filiform larvae

of (b) lung during larval migration
Hookworms (c) small intestine – the habitat of the adult worms
infection:
Penetration Maculopapular lesions and localized erythema
of the
filariform
through
skin
produces:
Itching: - Often severe
- Known as “ground rich” or “dew itch”
- Related to contact with soil especially in dewy morning
Itching, edema, erythema, and later papulovesicular eruptions can last for 2 weeks.
Larvae Result: abundant, bronchitis or pneumonitis
migrating
through
lungs:
In the stage Result: abdominal pain, steatorrhea, sometime diarrhea w/ blood and mucus, as well
of eosinophilia
maturation
of the worm
in the
intestine:
Hookworm infection is usually chronic, hence patient often show no acute symptoms.
Chronic Result: progressive, secondary, microcytic, hypochromic anemia of the iron-deficient typ
moderate due primarily to continuous loss of blood
or heavy
hookworm
infection:
Hyboalbum ● Low level of albumin due to combined loss of blood, lymph and protein.
eania
(another Symptoms: exertional dyspnea, weakness, dizziness, and lassitude
manifestati Signs: rapid pulse, edema, and albuminuria.
on of ● compared to Ascariasis – quite mild and remedial measures -
hookworm)

In general, the prognosis of hookworm infection is good

During ● Parasite continuously presents diverse immunogenic challenges to the host.
migration ● Extensive humoral responsesproduced against the larva and the adult hookworm
of the larva which share many antigens.
in human
body:

Cellular mediated by eosinophils, mast cells, and Th2 cells.

Immune
Response:
Despite of all, there has no clear evidence that host develops perpetual immunity against; however:
Polyvalent IgE antibodies have been suggested to provide some protective roles.
DIAGNOSIS
Final Diagnosis depends on the identification of parasite ova in the feces. The following
techniques are inexpensive and can be applied to both individual and mass screening:
FINAL DIAGNOSIS:
1. Direct Fecal Smear (DFS)
a. Only when infection is quite heavy
b. Not detect the parasite in light infections
2. Kato Thick or Kato-Katz method
a. Increase detection rates since more tools examined.
b. Quantitative: determined the intensity of infections # of helminths egg
per gram of feces
c. Disadvantage: rapid clearance of hookworms eggs after 30 to 60
minutes with the use of glycerine as a clearing agent.
3. Concentration method - like zinc sulfate centrifugal flotation and the formalin-
ether/ethyl acetate concentration method
a. Use greater quantity of stool that contribute the increase in sensivity
b. FLOTAC – centrifugal flotation method- shown higher sensivity for the
diagnossi of soil-transmitted helminths compared to mult. Examin. Of
Kato-Katz smears
4. Culture methods: Harada Mori :
a. Allow hatching of larvae from egg on strips of filter paper w/ on end
immersed in water
b. Culture methods are recommended for species identification.

MOLECULAR:
 1. PCR-based
a. Detection of hookworm DNA in feces
2. Enzyme-linked immunosorbent assay (ELISA)
a. Detection of secretory/excretory coproantigens

EPIDEMIOLOGY

INFECTED PERSONS

576 to 740 million Tropical and subtropical countries

• Either A. duodanale or N. Americanus

50, 000 deaths Associated anemia

In the world:

A. duodanale or N. Americanus

A. duodanale Prevalent in Europe and Southwestern Asia

N. Americanus Prevalent in tropical Africa and the Americas

BOTH SPECIES: WIDELY DISTRIBUTED THROUGHOUT THE TROPICS AND SUBTROPICS

RIGID DAMARCATIONS: NO LONGER PRESENT

Geographical distribution of two hookworms:

In the Philippines;

LOCAL STUDIES
Out of 1,958 Samples positive for hookworms in cultures
97% N. Americanus
1% A. duodenae
2% Mixed infections
LOCAL DISTRIBUTIONS
(agricultural areas)- Famers (affected)
50% - more than (late 1990’s) Compestela Valley province

HIGH-RISK GROUPS
(prevalence of hookworm infection- high)
5.5% and 2.8% Pregnant women and adolescent females

46.9% Among military and para-military personnel had

infection
13.6% Indigenous people communities (Davao del Norte)
• School children (infected)

22.7% Food Handlers (Metro Manila)

14.8% Food Handlers (Cebu)

TREATMENT AND PREVENTION:

TREATMENT PREVENTION AND CONTROL

● All diagnosed cases of hookworms ● Regular mass drug administration
infection should be treated (national program in school)
● Mass screening before treatment ● deworming
impractical ● WASHED approached to comprehensive
● soil-transmitted helminth infection control STH Infection (in PH)
control- mass drug administration ● Improved clean water and sanitation
● Albendazole – (larvicidal and ● Discouraged: Open Defecation
ovicidal) ● Advised: Wearing of shoes, slippered,
o 400 mg single dose for adults boots and sanitary disposal of human
and children over 2 years old feces
● Mebendazole – 100 or 500 mg ● Hookworm Vaccine Initiative – Sabin
● Anemia and hypoproteinemia - iron Vaccine Institute
supplementation & adequate diet

Nematode Infections: Intestinal Nematodes

HOOKWORMS: Enterobius vermicularis

GENERAL CHARACTERISITCS:

Associated Diseases: Enterobiasis or oxyuriasis (Human pinworm)

• Classified as: Meromyarian – based on the arrangement of the somatic
muscles where 2 to 5 cells per dorsal or ventral half.
• Human pinworm – most common helminth parasite in temperate regions.
• Infection: Perianal itching or pruritus ani
• Less attention: given to pinworm in tropical areas
• - no usual cause of significant morbidity or mortality
• Migrating worms – go beyond the perianal region
• cause complications in ectopic areas

MORPHOLOGY
Adult Worms:
● cuticular alar expansions at the anterior end
 ● a prominent posterior esophageal bulb
● Found: in the cecum and adjacent portions of the small & large intestines

Male Female
-2 to 5 mm by 0.2 mm -8 to 13 mm by 0.4 mm
-curved tail and single spicule - long pointed tail
- rarely seen because they die after -Uteri of gravid females: distended with
copulation. eggs
- Single female produces = more than
10,000 eggs
SHAPE SHAPE

RHABIDITIFORM LARVA:
• 140 μm to 150 μm by 10 μm
• Charateristics: esophageal bulb no cuticular expansion on the anterior end

EGGS:
• D-shaped eggs
• From 50 to 60 μm by 20 to 30μm
• Size averaging: 55 by 36 μm

Translucent shells
• outer: triple albuminous covering for
mechanical
• Inner: embryonic lipoidal membrane for
chemical protection
LIFE CYCLE:
Gravid adult female E.
Vermicularis deposit eggs on perianal
folds
Infection occurs via self
innocilation
Following ingestion of infective eggs, the
larvae hatch in the small intestines
Adults establish themselces: in colon
(cecum)
The time interval from ingestion of
infective eggs to oviposition by the adult
females is about one month.
Full maturity adult Adult life
span is 2 months
Female: 8 to
33mm
Male: 2 to 5
mm
Gravid females migrate
nocturnally outside the anus and
oviposit while crawling on the skin of
the perianal area.
Larvae contained inside the eggs develop
(the egg become infective) – 4 to 6 hours
under optimal conditions

PATHOGENEIS AND CLINICAL MANIFESTATIONS:

Enterobius vermic: innocuous parasire & rarely produces any serious lessons
Mild catarrhal inflammation of the Result: from the attachment of the worms
intestinal:

Mechanical irritation and secondary Result: Inflammation of the deeper layers of

bacterial invasion: the intestines

Invasion of the appendix: Not usual

It can cause of appendicitis (not
usual)
Migration of egg-laying females to Result: causes irritation of the perineal
the anus: region
Children infected: Result: suffer from insomnia due to the
pruritus.

Other signs of infection:poor appetite, weight loss, irritability, grinding of teeth, and
abdominal pain.
Aberrant adult worm migration Complications: appendicitis, vaginitis,
endometritis, salpingitis, and peritonitis.

Pinworm or their eggs: Ectopic sites such as in liver and

lung

The prognosis of enterobiasis or oxyuriasis

is good.

DIAGNOSIS: Enterobiasis should be suspected in: children and adults who shows
perianial itching

● By only vigorous scratching

MICROSCOPIC EXAMINATION - Diagnosis is confirmed by finding adult worms or

eggs
- Adult worms may seen in feces or in the perianal
region
- Eggs found in feces only about 5% of infected
persons/
Laboratory Method: - -Gives highest percentage (%) of positive results and
Graham’s scotch adhesive tape greatest number of eggs seen.
swab
(Perianal cellulose tabe swab)
Diagnostic Method - easy to perform and very sensitive and specific

EPIDEMIOLOGY:
Enterobiasis
● Occurs in both temperature and tropical regions of the world
● High prevalence in both developed and developing countries
o Only intestinal nematode infection that cannot be controlled through
sanitary disposal of human feces.
● Eggs: usually contaminated underwear and beddings.
● Route of Infection: Mouth, Respiratory System, Anus
● Risk Factors for infection: Overcrowding, Thumb-sucking, nail biting, & lack of
parental knowledge on pinworms

INFECTED PERSONS
208.8 million In the world
18 million Canada and the United States
of America
12 to 41% Washington, D.C

In the world:
INFECTED PERSONS
Prevalence level
29% Schoolchildren
● Exclusive Private schools

56% Public schools

Local:
16% Female
9% Male

In the Philippines:
TREATMENT AND PREVENTION & CONTROL

TREATMENT PREVENTION AND CONTROL

• Mebendazole: 100 mg PO • Personal cleanliness & hygiene
single dose or • Hand washing should be done
after using
• Albendazole : 400 mg PO • the toilet, as well as before and
single dose after meals
• Use of showers rather than
• bathtubs is suggested
• Pyrantel pamoate:11 • Infected persons should sleep
mg/kg base PO single alone until adequately treated.
dose (max. of 1 g)- • Vacuum cleaning around beds
secondary drug of choice. and contaminated areas will be
useful.
• E. vermicularis is quite • Familial disease, chemotherapy
susceptible to these of the entire family is
drugs, with reported cure recommendedthe control of the
rates of over 90% disease
• Underwear, night clothes,
blankets, and bed sheets should
be handled with care and
washed in hot soapy water
Trichuris trichiura
▪ Whipworm
▪ Is a soil transmitted helminth
▪ Classified as holomyarian
▪ T. Trichuria causative trichuriasis agent
▪ It is a very common intestinal helminthic infection, and about one quarter of the
world’s population is thought to carry the parasite

PARASITE BIOLOGY
A. Morphology

a) Eggs
- Less resistant to desiccation than A. lumbricoides
Basis Eggs

Size 50 – 54 um by 23 um

Shape Lemon/football-shaped;
barrel-shaped, thick-shelled and possess
a pair of polar “plugs” at each end.
Shell Yellowish outer;
transparent inner shell

Type of Eggs Description Picture

Unembryonated Passed down in stools
Eggs

Atypical An atypical category of

Unembryonated unembryonated egg, contained an
Eggs incompletely developed larva
an abnormal larva, or granular
components
was common among the LEs.

The abnormalities observed

included
a. great variation in shape,
size, and color.
b. similar atypical whipworm
eggs have been reported in
patients after treatment
with mebendazole,
thiabendazole,
tetracloroethylene, and
dithiazanine.

b) Larva
- the larvae escape and penetrate the intestinal vili where they remain for 3 to
10 days
 c) Adult

Basis Female Male

Size 35 – 50mm 30 – 45mm
Appearance colorless slightly shorter than
female

Esophagus narrow ; resembling string

of beads

Reproductive Organs single set single spicule

Posterior End Blunt posterior end Coiled posterior end;

retractile sheath
B. Life Cycle
→ Female T. trichiuria lays 3000 – 20,000 eggs per day; produces about 60 million
eggs over an average lifespan of 2 years
→ Infectious form maturation
● Unembryonated egg passage in stool > soil deposition > eggs embryonate
within 2 – 3 weeks, become infectious in 15-30 days
→ Human stages
● Egg ingestion > eggs hatch into larvae in small intestine > undergo four
larval stage > larvae mature into adult worms, embed in cecum, ascending
colon
→ Life span: 1-3 years

Pathogenesis & Clinical Manifestations

A. Complications
→ Heavy infections > Trichuris dysentery syndrome
● Embedded worm quantity in colon and rectum
● Manifested by chronic dysentery, rectal prolapse
→ Light infections > moderate anemia
→ Petechial hemorrhages
● Embedded worm quantity in mucosa
→ Intestinal bleeding is common
→ Appendicitis/Granuloma formation
● Lumen filled with worms, irritation, inflammation Rectal Prolapse
→ Anemia
● Heavy intensity trichuriasis, blood loss
→ Children
● Impaired growth, cognitive development

B. Signs & Symptoms

Infection/Disease Signs & Symptoms
Trichuriasis Poor appetite, wasting, stunting,
reduced intellectual and
cognitive development (children)

Light infections Usually, asymptomatic

Heavier chronic trichuriasis infection Blood-streaked diarrheal stools,

abdominal pain, tenderness,
nausea, vomiting, weight loss
C. Prognosis
→ Trichuriasis prognosis is very good
● No larval migration thru. lungs
● no lung pathology occurs

DIAGNOSIS

Laboratory Techniques Description

Direct Fecal Smear (DFS) With a drop saline solution
Kato thick smear method Used for egg counting to
determine cure rate (CR), egg
reduction rate (ERR), and intensity
of infection

Kato-Katz techniques High sensitivity & specificity for

detection Trichuris eggs

Other Diagnosis: Diagnosing Trichuris

✔ Acid-ether technique
✔ Formalin-ether/ethyl
acetate concentration
✔ FOTAC technique

TREATMENT
Medications Dosage Contraindications Adverse Effects
Mebendazole 100 mg Hypersensitivity Mild and transient
2x/day for 3 Early pregnancy may present as
days headache, nausea,
vomiting,
Single Dose: gastrointestinal
discomfort,
500 mg used itchiness
for mass
treatment
Albendazole 400 mg once Hypersensitivity Mild and transient
for 3 days Early pregnancy may present as
headache, nausea,
vomiting,
gastrointestinal
discomfort,
itchiness
Benzimidazole
Ivermectin

Combination of
albendazole exhibit
better cure rate &
err

→ Deworming (children)
● shown to contribute to improved motor and language development, reduced
malnutrition
● nutritional status and intellectual development have shown to improve after
deworming

EPIDEMIOLOGY
→ Trichuriasis
● occurs temperate and tropical climate; widely distributed in warm, moist areas
of the world
● 604 – 795 million are infected globally
● Most prevalent in East Asia, Pacific Island Regions
→ Age Groups
● Children 5 – 15 years of age are most frequently infected, have highest
intensities of infection
→ In Philippines
● Prevalence ranged from 4.5 – 55.1% in preschool children
● 8.1 – 57.9% in school-age children
→ Distribution is similar to A. lumbricoides
→ Prevalence of coinfections with 2 helminths is 19.1%

PREVENTION & CONTROL

→ WHO recommended biannual mass drug administration
● Mebendazole 500 mg/ albendazole 400 mg
● among school-age children where STH infections prevalence is ≥50%
● High-risk groups: preschool children, women of childbearing, pregnant women
(2nd & 3rd trimesters), lactating women
● Once a year treatment in communities with STH prevalence <50%
→ Other strategies:
● Provision of safe water, environmental sanitation, hygienic education
Strongyloides stercoralis
▪ Strongyloides stercoralis is a human parasitic roundworm, commonly known as
threadworm
▪ Characterized by free-living rhabditiform, parasitic filariform stage
▪ Soil-transmitted helminth
▪ only species of this genus that is naturally pathogenic to humans
▪ major causative agent of strongyloidiasis in humans

PARASITE BIOLOGY
❖ Morphology
▪ Strongyloides stercolaris exist in both parasitic and free living form.
▪ In the parasite phase, the females are readily discovered but not the males.

a) Eggs

Basis Eggs Image

Size Measures 50-58 um by 30um-
34um

Color Clear thin shell

Appearance similar of those of hookworms
except in measurement
Deposition Parasitic eggs: intestinal
mucosa
Free-living eggs: soil

b) Larva
Larva Basis Rhabditiform larva Infective Filariform larva
Size 225 um by 16 um 550 um

Color colorless colorless

Appearance Slighty smaller, less smaller
attenuated
posteriorly from
hookworm
Tail blunt tail end Distinct cleft (notched) at
tip of the tail
Buccal Cavity Shorter buccal
capsule
Esophagus Elongated with
pyriform(pear-
shaped) posterior
bulb (also called the
median bulb)
Intestine Straight cylindrical Non-feeding
tube
Reproductive Organs Larger genital
primordium
Image
 c) Adult

Basis Parasitic/ Filariform Female Parasitic Male

Size 2.2 mm by 0.04mm
Color Colorless;
Semi-transparent

Appearance Finely striated cuticle

Tail Short conical pointed tail
Buccal Cavity Short has four small lips
Esophagus Long slender
Intestine Continuous to the
subterminal anus
Reproductive Organs Vulva located in 1/3 length
of the body

paired uterus, oriduct and

ovaries constitute the female
genital organs

Ova (for female) Single ova

8-12 thin-shelled
Transparent
Segmented
50-58um by 30-34um

Ends Anterior end: slender

tapering
posterior end: extremely
pointed
Basis Free-living Female Free-living Male
Size 1mm by 0.06mm 0.7mm by 0.04mm

Color
Appearance Smaller than Smaller than female;
parasitic female:
No caudal alae
Tail Ventrally curved
Buccal Cavity
Esophagus Muscular double-
bulbed esophagus
Intestine Straight cylindrical
tube
Reproductive Organs 2 copulatory spicules:

Gubernaculum:
 A. Parasitic
Female
B. Free-Living
Male
C. Free-Living
Female

B. Life Cycle

a) Free-Living Cycle
1. Female worm lays embryonated eggs;
2. developed into rhabditiform larvae;
3. transforms into free-living adults ;
4. reproduced;
5. rhabditiform larvae hatch;
6. conditions became unfavorable develops into filariform larvae.
b) Parasitic Cycle
1. Filariform larvae penetrate human skin;
2. enter circulation;
3. pass thru lungs;
4. migrated to larynx;
5. swallowed;
6. larval maturation in duodenum;
7. reproduction by parthenogenesis;
8. deposits eggs in intestinal mucosa;
9. rhabditiform larvae maturation;
10. fecal excretion.

→ Autoinfection
● Occurs when rhabditiform larvae pass down the large intestine and
develop into filariform larvae

PATHOGENESIS & CLINICAL MANIFESTATIONS

▪ 3 Phase of Acute Infection of Strongyloides
(a) Invasion of the skin by filariform larvae
(b) Migration of larvae through the body
(c) Penetration of intestinal mucosa by adult female worms

A. First Phase
 Larval invasion of skin produces erythema and pruritic elevated hemorrhagic
papules
B. Larval Migration Phase
Lungs are destroyed causing lobar pneumonia with hemorrhage, cough,
tracheal irritation, mimicking bronchitis
C. Third Phase
Intestinal mucosa migration from pylorus, rectum, greatest numbers found in
duodenal regions, upper jejunal regions

A. Complications
→ Light Infection
● Asymptomatic
→ Moderate Infection
● Causes diarrhea alternating with constipation
→ Heavy Infection > Cochin China diarrhea
● Intractable, painless, intermittent diarrhea , episodes of watery and
bloody stools
→ Hyperinfection
● Syndrome of accelerated autoinfection, manifests with exacerbation of
gastrointestinal and pulmonary symptoms and increased numbers of
larvae in stool/sputum
● Immunocompromised
→ Other complications:
a) Edema
b) Emaciation
c) Loss of appetite
d) Anemia
e) Lobar pneumonia
f) Ileus
g) Intestinal obstruction
h) Gastrointestinal bleeding
i) Malabsorption leading to cachexia

B. Signs & Symptoms

Infection/Disease Signs & Symptoms

Chronic strongyloidiasis Often asymptomatic;

Intermittent vomiting, diarrhea,

constipation, borborygmi, anal
pruritis, urticaria, larva currens
rashes, recurrent asthma,
nephritic syndrome
 C. Prognosis
→ Light Infections: good
→ Moderate/Heavy Infections: high mortality rates
→ Disseminated Infections
● Patients with cancer, malnutrition, HIV/AIDS, HTLV-1, using
immunosuppressive drugs after organ transplant

DIAGNOSIS
Laboratory Techniques Description
Baermann funnel gauze method Operates on the principle that the
nematode larvae wiggle out of the
biological material, cannot swim
against gravity and will fall through
the water to the area of clamped off
tubing.
Harada-Mori culture Positive stool is applied to filter
paper and placed into a test tube w/
about 7ml of boiled/distilled water
Beale’s string test or Doudenal aspiration “Entero Test” or String Test, where
capsulated yarn is swallowed by the
patient to reach the duodenum
Small bowel biopsy Diagnostic procedure in which a
portion of the small bowel lining is
removed for examination
Serologic testing A laboratory test that checks for the
presence of antibodies or other
substances in a blood sample.
Nutrient Agar Plates Nutrient medium used for the
cultivation of microbes supporting
growth of a wide range of non-
fastidious organisms.

TREATMENT

Medications Dosage Contraindications Adverse Effects

Albendazole 400 mg daily for 3 days Hypersensitivity (in transient
pregnant) gastrointestinal
discomfort,
headache
Thiabendazole Hypersensitivity (in give rise to
pregnant) dizziness,
gastrointestinal
irritation,
drowsiness,
pruritus, headache
lasting for several
hours
Ivermectin 200 mg/kg daily for 2
days
Provides best
results in chronic
uncomplicated
strongyloidiasis
EPIDEMIOLOGY
→ Strongyloides stercoralis
● Found throughout the world; follows distribution pattern similar to hookworm
in tropics and subtropics as wells as Europe and USA
● 50 – 100 million people estimated to be infected

→ In Philippines
● Strongyloides is relatively rare
● Prevalence fluctuates between 0 – 2.3%
● Infection is more frequent in 7 – 14 years old male children
→ Risk Factors
● Poor sanitation
● Indiscriminate disposal of human feces

PREVENTION & CONTROL

Strongyloidiasis can be prevented by:
→ Prevention of contamination of soil with feces.
→ Avoiding contact with infective soil and contaminated surface waters
→ Provide health education
● Personal Family, community hygiene
→ Treatment of infected individuals
→ Serologic evaluation
● Solid organ transplant donors
Lymphatic filariasis

• Is caused by WUCHERERIA BANCROFTI, BRUGIA MALAYI and BRUGIA TIMORI

• Disease is transmitted by blood-feeding arthropod vectors, mainly mosquitos and

blackflies

These worms causes:

LYMPHEDEMA

LYMPHANGITIS

chronic case;

3. ELEPHANTIASIS

Scientific classification:

● KINGDOM- Animalia

● SUBKINGDOM- Metazoan

● PHYLUM- Nematoda

● FAMILY- Filaridae

● GENUS- Wuchereria

● SPECIES- W. bancrofti

Types of Hosts:

Definitive host:

5. Humans are the definitive host for the worms that cause lymphatic filariasis

Intermediate hosts:

6. Transmitted by Culex, Aedes, and Anopheles species

7. B.malayi is transmitted by Anopheles and Mansonia species

Morphological difference between W. bancrofti and B. malayi microfilariae

PARASITE LOCATION LOCATION OF MICROFILARIA VECTOR EPIDEMIOLOGY
S OF ADULT MICROFILARIA PERIODICITY

LYMPHATIC FILARIASIS

W. Lymphatic Blood Nocturnal Culex, Cosmopolitan (S.

Bancrofti Tissue (mostly) Aedes America, S. Asia,
Africa)

B. malayi Lymphatic Blood Nocturnal Monsonia, South-East Asia,

Tissue (mostly) Anopheles Indonesia and
India

B. timori Lymphatic Blood Nocturnal Anopheles South-East Asia

Tissue (mostly)
PATHOGENESIS AND CLINICAL FINDINGS

D. Adult worms in the lymph nodes cause inflammation that eventually obstructs the
lymphatic vessels, causing edema. Massive edema of the legs is called elephantiasis.

E. Note that microfilariae do not cause symptoms

F. Early infections are asymptomatic.

i. Later, fever, lymphangitis, and cellulitis develop. Gradually, the obstruction leads to
edema and fibrosis of the legs and genitalia, especially the scrotum

ii. Elephantiasis occurs mainly in patients who have been repeatedly infected over a long
period

iii. Tropical pulmonary eosinophilia is characterized by coughing and wheezing,

especially at night

iv. These symptoms are caused by microfilariae in the lung that elicit an immediate
 hypersensitivity reaction characterized by a high immunoglobulin E (IgE)
concentration and eosinophilia

Diagnosis:

• Due to nocturnal periodicity of most W.Bancroti stains, wet smears or thick blood
smears are taken between 8 p.m – 4 a.m

1. Demonstration of microfilarae in the peripheral blood

a. Thick blood smear: 2-3 drops of free flowing blood by finger prick method, stained
with JSB-II

b. Membrane filtration method: 1-2 ml intravenous blood filtered through 3µm pore
size membrane filter

c. DEC provocative test (2mg/Kg): After consuming DEC, mf enters into the
peripheral blood

in day time within 30 - 45 minutes.

Treatment:

→ Remarkable advances in the treatment of LF have recently been achieved focusing

not on individual but on community with infection, with the goal of reducing mf in the
community, to levels below which successful transmission will not occur.

→ The World Health Organization (WHO) in the 50th World Health Assembly has
targeted LF for elimination by the year 2020. The Global Programme to Eliminate
Lymphatic Filariasis has two major goals:

- to interrupt transmission of the parasite via preventive chemotherapy,

- and to provide care for those who suffer from the clinical manifestations of
LF through hygiene education programs.

D. The goal for endemic communities is to eliminate the presence of microfilariae in the
blood in order to prevent transmission of the disease by vectors.

E. According to the WHO, single doses of DEC in combination with another drug such
 as albendazole or ivermectin is 99% effective in removing microfilariae from the
blood for up to one year from treatment.

Epidemiology:

120 million are affected worldwide

1 billion are at risk

WUCHERERIA BANCROFTI BRUGIA MALAYI

Affects more than 100 million people in the tropical Affects 12.5 million people in SOUTHEAST ASIA
areas of INDIA, SOUTHEAST ASIA, PACIFIC
ISLANDS, AFRICA, and SOUTH and CENTRAL
AMERICA

Philippines:

45 provinces are endemic for LF;

REGION IV

REGION VIII

REGION IX

REGION X

REGION XI

REGION XII

CARAGA
Parastrongylus contonensis
Pathogenesis and Clinical manifestation:

● Incubation period is 6 to 15 days, but may vary 17-47 days.

common symptoms include:

● Stiffness of the neck,

● Paresthesia

● Vomiting,

● Fever, nausea

● Blurred vision or diplopia

● Body or muscle pain,

● Fatigue.

● Confusion,

● Incoherence,

● Disorientation,

● Memory lapses

● Coma have also been observed during illness.

● Intraocular hemorrhage and retinal detachment as associated complications have

also been reported.

Diagnosis:

Diagnosis of parastrongyliasis in humans is relatively difficult, since the primary site of

infection is the brain. Presumptive diagnosis may be made based on travel and exposure
history, correlated with clinical symptoms, medical history, laboratory findings, brain

imaging results, and serological tests.

• Examination of blood may reveal a high proportion of eosinophils, comprising 7 to

36% of the white blood cell (WBC) count.

• Examination of CSF may contribute to increased sensitivity in the diagnosis of

parastrongyliasis.

• CSF eosinophilia of greater than 10% in proportion to WBC will exclude other
common causes of meningitis.

• The CSF protein level in most patients is mildly elevated, while the CSF glucose is
normal. However, other infections (e.g., cysticercosis, trichinosis, visceral larva
migrans, schistosomiasis, paragonimiasis, and gnathostomiasis) involving the
central nervous system must first be ruled out.
Treatment:

• No anthelminthic treatment is recommended at present, although mebendazole and

albendazole have been demonstrated to effectively treat parastrongyliasis in China,
Taiwan, and Thailand.

• Anthelminthic therapy has been shown to relieve symptoms and reduce the duration
of the disease.

• Ocular parastrongyliasis may require surgical removal of worms from the eyes.
Symptomatic treatment with the use of analgesics and lumbar puncture can relieve
the headaches experienced by the patient with eosinophilic meningitis.

• Prednisone 30 mg daily is recommended, particularly in severe cases with cranial

nerve involvement.

• The anti-inflammatory and immunosuppressive effects of steroids are helpful in

mitigating the disease process.

Prevention and control:

● The main preventive strategy against parastrongyliasis is through awareness and

education on proper eating habits and safe food preparation.

● The public should be discouraged from eating raw or poorly cooked mollusks or
unwashed vegetables.

● Hand washing after gardening should also be advised.

● Farmers occasionally use molluscicides, such as metaldehyde or iron phosphate

food bait pellets to control intermediate hosts.

● Copper barriers against snails and slugs are also utilized by farmers to prevent
contamination of vegetable and fruit crops.

● Health workers in endemic areas should also be educated on the diagnosis,

treatment, control, and prevention of parastrongyliasis.

Epidemiology:

● Human infection with P. cantonensis was first reported in 1945 by Nomura and Lin in
Taiwan.

● As a human parasite, P. cantonensis has also been documented in approximately 30

countries including Thailand, China, Tahiti, French Polynesia, USA, Cuba, New
Caledonia, Japan, Australia, Vanuatu, India, and the Philippines.

● In the Philippines, Nishimura and Yogore reported the presence of Parastrongylus in

rats.

● Further studies showed that its prevalence in rats is less than 7%. The presence of P.
cantonensis as a parasite of rats and/or snails has been reported in the following
provinces of Luzon: Batangas, Bulacan, Cavite, Ilocos Norte, Laguna, Mountain
 Province, Nueva Ecija, Pampanga, Pangasinan, Quezon, Rizal, Sorsogon, Tarlac, and
Metro Manila.

● Two cases of ocular parastrongyliasis have been reported from the East Avenue
Medical Center.

● The patients were blood relatives coming from Isabela who have eating history of
improperly cooked snails.

● The worms were identified at the College of Public Health, University of the
Philippines Manila.

Trichinella Spiralis
Trichinella spiralis is a nematode parasite, occurring in rats, pigs, bears and humans,
and is responsible for the disease trichinosis. It is sometimes referred to as the "pork
worm" due to it being found commonly in undercooked pork products.
Brief History
- First described by Tiedemenn in 1822
- First observed in 1835 in the muscles of a patient at autopsy by James Paget
who was a first year medical students at St Bartholomew’s Hospital London.
- Owen in 1835 describe the encysted larva form in the muscle and named it
Trichina spiralis.
- Leuckart, Virchow and Zenker independently proved the infectivity of the
encysted larvae when fed to experimental animals.
- They traced the life cycle of the worms from the encysted larvae in muscles,
to adult in the duodenum and then again encystement in muscles.
- Trichinella derived from minute size of adult (Gr.trichos-hair ella spiralis refers
to spirally coiled appearance of larva in muscles.
- They traced the life cycle of the worms from the encysted larvae in muscles,
to adult in the duodenum and then again encystement in muscles.
- Trichinella derived from minute size of adult (Gr.trichos-hair ella spiralis refers
to spirally coiled appearance of larva in muscles.’
- Host: humans, rats, pigs, bears, foxes, walrus or any other carnivore or
omnivore serves as both the final and intermediate host.
Scientific Classification:

● Kingdom: Animalia

● Phylum: Nematoda

● Class: Adenophorea
 ● Order: Trichurida

● Family: Trichinellidae

● Genus: Trichinella

● Species: spiralis

● Name: Trichinella spiralis

● There are eight know species and genotypes under the genus: Trichinella.

o Trichinella spiralis
o Trichinella britovi
o Trichinella native
o Trichinella murrelli
o Trichinella nelson
o Trichinella papuae
o Trichinella pseudospiralis
Morphology:

● T. spiralis is white roundworm with an un- segmented body and is visible to

naked eye and inhabit small intestinal.

● The adult male has a body size ranges from 0.62 to 1.58mm, has one testis
located on the posterior end of its body and adult females are 1.26 to 3.35mm
by 0.029- 0.038mm one ovary located on the posterior end.

● Larvae measures 80-120μm by 5 μm.

Life Cycle:
After humans ingest the cysts from infected undercooked meat, pepsin and
hydrochloric acid help free the larvae in the cysts in the stomach.
B. Thirty to 34 hours after the cysts were originally ingested, the adults mate,
and within five days produce larvae.
C. The larvae then use their piercing mouthpart, called the "stylet", to pass
through the intestinal mucosa and enter the lymphatic vessels, and then enter
the bloodstream.
D. Then burrow into the sub-epithelium of the vili.
E. The infective stage is the encysted larva found in the muscle of pigs and other
animals.
 F. The larvae then migrate to the small intestine, where they molt four times
before becoming adults.
G. The larvae travel by capillaries to various organs, such as the retina,
myocardium, or lymph nodes; however, only larvae that migrate to skeletal
muscle cells survive and encyst.
The larval host cell becomes a nurse cell in which the larvae will be encapsulated.
The development of a capillary network around the nurse cell completes encystation
of the larvae

Pathogenesis and Clinical features

● The clinical conditions are divided into three phases:

● Enter phase > Incubation and intestinal invasion

● Invasion phase > Larval migration and muscle invasion.

 ● Covalence phase > Encystment and encapsulation.

Enter phase > Incubation and intestinal invasion

● Resembles attack of acute food poisoning

o Diarrhea
o Constipation
o Vomiting
o Abdominal cramps
o Malaise
o Nausea

● Stage of intestinal: the larvae encyst, invade the intestinal epithelium in the
duodenum and jejunum and develop into adult.

● Symptoms: nausea, diarrhea, abdominal cramps and sometimes vomiting.

This is diagnosed as food poisoning. The onset of illness may be from 2 to 30
hours of ingestion of infective food.

Invasion phase > Larval migration and muscle invasion.

Resulting to metabolites lead to:

Immonological

Pathological

Metabolic

● Inflammatory reactions results to eosinophilia> release of Histamines.

j) Histamines, serotonin, bradykinins, and postaglandyns contribute to an

increase in vascular permeability > tissue edema.
k) Severe mayalga, periorbital edema.

Covalence phase > Encystment and encapsulation.

a. Fever, weakness, pain and other symptoms starts to abate.
b. Expect full recovery
 c. Neurologic signs arising from brain damage may persist.
l) Muscle phase: this occurs during the release of larvae, their migration,
deposition and encapsulation in muscle.
m) Typical presentation with fever, oedema of face, swelling and weakness
affected muscles. Eosinophilia is constant feature
n) Myocarditis and encephalitis are serious and potentially fatal complication.
Respiratory symptoms may occur,
o) This stage appears usually one to four weeks after infection.
p) Encapsulation phase: lasting one to eight months after infection, the fever
and other symptoms subside. After the stage the cyst begin to calcify.

Symptoms
• A large burden of adult worms in the intestines promote symptoms such as
nausea, heartburn, dyspepsia, and diarrhea from two to seven days after
infection.
• As the larvae migrate through tissue and vessels, the body's inflammatory
response results in edema, muscle pain, fever, and weakness.
• A classic sign of trichinosis is periorbital edema, swelling around the eyes,
which may be caused by vasculitis.
• Splinter hemorrhage in the nails is also a common symptom.
• Most dangerous case is worms entering the central nervous system. Cannot
survive there, but they may cause enough damage to produce serious
neurological deficits (such as ataxia or respiratory paralysis), and even death.
• Trichinosis can be fatal depending on the severity of the infection; death can
occur 4– 6 weeks after the infection, and is usually caused by myocarditis,
encephalitis, or pneumonia.
Diagnosis

● The most definitive diagnostic examination is the demonstration of the larva

through muscle biopsy.

● Muscle biopsy is done through histological examination of 0.2 to 0.5 g of

muscle tissue.

● Digestion of muscle samples with pepsin and hydrochloric acid can also be
done to determine the number of larvae per gram of muscle, or to isolate
larvae for molecular characterization.

● The digestion technique, however, is limited to muscle larvae that are about
10 to 12 days old (about 2-3 weeks post infection) since younger larvae may
 be destroyed by the digestion fluid.

● Non-specific laboratory tests to detect eosinophilia, muscle enzymes

(creatine phosphokinase, lactate dehydrogenase, and myokinase), and total
IgE in serum may be useful in diagnosis.

● Currently, enzyme-linked immunosorbent assay (ELISA) is recommended for

the diagnosis of trichinellosis.

● Confirmation of ELISA positive samples may be done through Wester blot

technique.

● Latex agglutination technique may be utilized for rapid (<1 hour) confirmation
of trichinellosis.
Treatment:
• The treatment of choice for trichinellosis is mebendazole 5 mg/kg body
weight daily, or albendazole 15 mg/kg body weight per day in two divided
doses, for 10 to 15 days.
• For children 2 years and older, albendazole should be given at 10 mg/kg body
weight.
Epidemiology:

Trichinella infections in humans have already been documented in 55

countries worldwide. There are about 10,000 cases reported each year, 0.2%
resulting in mortality. Human trichinellosis occurs wherever meat is a part of
the diet. Outbreaks have been reported in Argentina, Bosnia-Herzegovina,
China, France, Laos, Romania, Spain, Sweden, Thailand, Turkey, Ukraine,
Uzbekistan, and Vietnam.

Trichinella infection has never been documented in a small number of island

countries, including the Philippines.
Prevention and Control:

● Health education is an important component of prevention and control

measures against this parasitic infection. It is recommended that meat be
cooked at a minimum of 77°C (170°F). Freezing is another way to kill larvae.

● Storage at –15°C for 20 days or –30°C for six days is suggested.

● Smoking, salting, or drying meat is not effective.

Other control measures include regular animal monitoring (meat inspection or

detection of circulating antibodies), keeping pigs in rat-free pens, and proper
disposal of suspected carcasses.

Anisakis spp.
 D. Anisakids are nematode parasites of whales, dolphins, porpoises, walruses,
seals, sea lions, and other deep marine mammals.
E. Like any nematode, anisakids have elongated vermiform bodies without
segmentation.
F. They have a complete digestive tract, and the sexes are separate. Although
they are parasites of marine mammals, they can cause gastrointestinal
infections and allergic reactions in humans with the consumption of raw and
undercooked squid and fish containing the 3rd stage larvae of the parasite.
G. Commonly involved infective species are Anisakis simplex and
Pseudoterranova decipiens.

Parasite Biology:
C. The 1st stage larvae that develop inside the eggs molt into the 2nd stage
larvae that hatch out of the egg.
D. The free swimming 2nd stage larvae are ingested by micro-crustaceans,
where the 3rd stage larvae develop.
E. Going up the predatory food chain, the third stage larvae are transported to
various paratenic hosts, like squid and several species of fish.
F. 3rd stage larvae are more concentrated in fish viscera but may occasionally
be found in the fish muscles.
G. Anisakis simplex are milky white in color, measuring 19 to 36 mm in length,
with a long stomach, and a blunt tail with mucron, and are referred to as Type
I larvae.
H. Following ingestion by marine mammals, the 3rd stage larvae molt twice and
develop into adult worms.
Life Cycle:

Pathogenesis and Clinical Manifestation

● Humans may ingest the 3rd stage larvae from raw or improperly cooked
infected fish.

● The 3rd stage larvae, however, do not develop into the adults in the human gut.

● Larval infection with anisakids is called anisakiasis or, more recently,

anisakidosis. It may result in gastric and intestinal pathology.

● A second manifestation of morbidity brought about by the parasites is an

allergic reaction to the chemicals secreted by the worms.

● Ingested larvae invade the submucosa of the stomach or the intestines,

resulting in:
o hemorrhage
o Inflammation

● Anisakiasis involves acute abdominal symptoms, usually within hours after

ingestion of larvae. This nonspecific abdominal distress can be mistaken for
other conditions such as peptic ulcers, food poisoning, and appendicitis.
Occasionally, the larvae are coughed up.

● If the larvae pass into the bowel, a severe eosinophilic granulomatous

response may also occur 1 to 2 weeks following infection, causing symptoms
mimicking Crohn’s disease, and rarely, intestinal perforation can occur. Rare
 cases of ectopic infection are known, in sites such as the peritoneal cavity,
mesentery, esophagus, and tongue.

● Most infections are self-limiting as larvae are unable to survive for long
periods in the human host, but the associated tissue damage can cause
longer lasting symptoms.

● Antigens that remain in the fish muscle after the larvae are killed (e.g. after
freezing) can cause allergic reactions in some individuals.
Diagnosis:
• Anisakidosis should be highly suspected if there is a recent history of eating
raw or improperly cooked fish or squid prior to the acute onset of symptoms.
• Through gastroscopic/endoscopic examination, the larvae can be visualized
and removed for identification.
• Intestinal anisakidosis is more difficult to establish, and may be diagnosed
only after surgery.
• Serological procedures to detect specific antibodies have been employed with
good results, such as enzyme-linked immunosorbent assay (ELISA), and
radioallergosorbent test (RAST).
Treatment:
The treatment for anisakiasis may require removal of the worm from the body by
endoscopic removal. By using endoscopic forceps.
A. Corticosteroids
b. Albendezole

Prevention and Control:

● Marine fish, squid and shellfish must be Cooked prior to consumption.

● Raw and undercooked preparation, fish an shellfish must undergo blast
freezing at -35 degrees for at least 15 hours.
● Freezing at -20 degrees c for seven days has been found to be effective.
 Toxocariasis
Brief History

● Human infection with Toxocara spp. was first described by Wilder in 1950.

● He identified a nematode larva of unknown species within a retinal granuloma of a child.

Toxocariasis is an infection transmitted from

animals to humans (zoonosis) caused by the
parasitic roundworms commonly found in the
intestine of dogs (Toxocara canis) and cats (T.
cati)

Scientific Classification

❖ Kingdom: Animalia

❖ Phylum: Nematoda

❖ Class: Chromadoria
 ❖ Order: Ascaridida

❖ Family: Toxocaridae

❖ Species: Canis, Cati

❖ Genus: Toxocara

❖ Name : T.cati (Cat roundworm)

❖ T.canis (Dog roundworm)

Two types of roundworms that's causes toxocariasis:

• Toxocara Canis - Found in dog

• Toxocara Cati - Found in cat

Morphology

T.canis

Males: 10cm

Female: 18cm

and easily visible to the naked eye. Males and females have two long
andnarrow lateral cervical alae and three “lips” at the anterior end.

T.cati

Males: 6cm

Female: 10cm

Both male and females have two broad arrowhead-shaped

lateral cervical alae and three “lips” at the anterior end.
 Toxocara eggs are golden in color, spherical to slightly pear shaped,
thick-shelled.

→ The size range for different species varies slightly; T.

canis is slightly larger (80—85 µm) than T. cati (65—75 µm).

Toxocara
canis larva
hatching.
Toxocara spp.
develop to third
stage (L3)
larvae in ovo.
When hatched,
L3 larvae are
about 350—400
µm long and
about 15—20 µm in maximum width, with a straight esophagus extending about a third of the
body length.

Adult Toxocara spp.measure approximately 4—6 cm long (males) and 6—10 cm long (females).
Like all ascarids, Toxocara have three “lips” on the anterior end of the worm. They also possess
large, spear-shaped cervical alae, which are broader in T. cati than T. canis.
-Toxocara sp. in tissue sections stained with hematoxylin and eosin.
In tissue, Toxocara spp. larvae are 15—20 µm wide in lateral sections and are often found
surrounded by a granulomatous reaction. Two large excretory columns are present and single-
pointed lateral alae are conspicuous along most of the body length.

HOSTS

Definitive: Dogs and cats

Paratenic and Accidental -Humans and others usually small mammals

LIFE CYCLE

• Eggs embryonate over a period of 1 to 4 weeks in the environment and become infective,
containing third-stage (L3) larvae

• Ingestion by dog

• Eggs hatch and larvae penetrate the gut wall

• Migrate into various tissues encyst if dog older than 5 weeks

• Younger dogs larvae migrate through lungs, bronchial tree, esophagus, and move back
 into the small intestine about 60 to 90 days after hatching

Older Dogs

• Encysted Stages reactivate during pregnancy

• Infection spread by transplacental and transmammary routes

• Infective eggs spread through lactating bitche

Accidental Host

• Infected by ingestion of infective eggs from contaminated soil.

• Eggs hatch and larvae penetrate the intestinal wall

• Carried by Circulatory System to various tissues

• Larvae dont undergo further development but can cause reactions in tissue (toxocariasis)

Transmission
▪ Ingestion of infective larval eggs

● Eggs are passed in dog or cat feces

● Can also be found in soil ( Don't eat Dirt)

• Eating undercooked rabbit sheep or chicken

→ Accidental hosts that have eggs encysted and their muscle

● Toxocara canis infections are more common than toxocara Cati infections because of
the defecation habit of dogs

SYMPTOMS

In dogs usually asymptomatic

In Puppies

Noisey breathing

Vomiting

Diarrhea

Pot belly

May cause death in heavy infection

In humans usually asymptomatic

● Abdominal pain

● Decreased appetite

● Fever
● Hives

● Restlessness

● Various other symptoms depend on what organ the larvae infect

Three different toxocariasis syndrome;

• Visceral larva migrants

• - Concerned with major organs

• Covert Toxocariasis

• - Milder version of VLM

• Ocular larvae migrants

• - Affects only the eye and optic nerve

Visceral larva migrants ( VLM )

Is the result of migration and subsequent death of the larvae in the different
tissues and organs producing an intense inflammatory response manifested as
eosinophilic granulomas.

Caused from larvae wondering throughout various organs of the body ( Brain,
Lungs, Liver ( most common),Heart, Muscle)

Caused by high parasite load

Migration of the larvae causes inflammation of internal organs and something the
CNS

- CNS inflammation - Meningitis

• Sometimes subcutaneous migration tracks of the larva can be seen

• Death can occur in patient with hypersensitivities to allergens

 - Rarely in other patients

● Patients can present with a variety of signs and symptoms: Wheezing is a common
sign of VLM

→ Weight loss

→ Fatigue

→ Asthma

→ Vomiting

→ Headache

→ Irritability

→ Rash

→ Fever

D. Can also cause chronic eosiphilia

- abnormally high amount of eosinophils in the blood and tissue

→ Part of the causes of the abdominal pain fever and rash

- Treated with corticosteroids

● VLM is found In approximately 73% of the children and the US age of 4 to 8

Covert Toxocariasis ( CoTOX )

• Least severe

- This is believed to be due to chronic exposure

7. Most patient are asymptomatic and eosinophilia is less frequent

• Signs and symptoms:

a) Coughing

b) Wheezing

c) Fever

d) Abdominal pain

e) Headache

f) Behavioral changes

c) Upon clinical examination hepatomegaly and lymphadenitis are found

Ocular larvae migrants.

• Signs and symptoms restricted to the eyes and optic nerve

- larva migrating to posterior segments of the eyes

▪ Rare when compared to VLM

- OLM and VLM very rarely happen of the same time

✔ Light toxocara burden is though to induce a lower immune response

✔ This allows the larva to easily enter the eye

✔ Usually only one is infected by a single larva

✔ Loss of vision occurs over days to weeks

✔ Other symptoms: red eye, white pupil, strabismus, fix pupil an retinal detachment

✔ Ocular granulomas conform around the larva and are commonly misdiagnosed
retinoblastoma

✔ Toxocara damage in the eye is permanent and can cause blindness if not threaten

✔ Toxocara cati has been particularly implicated in OLM

 ✔ Blindness is also common

(d) Another syndrome

- Neurological Toxocariasis

- one of causes of encephalitis

- larva migrate to the: brain, meninges and may be found in the cerebrospinal fluid
( CSF)

Diagnosis

- Fecalysis

- Biopsy

- Clinical and Serologic test

- ELISA (enzyme-linked immunosorbent assay)

- PCR ( polymerase chain reaction)

- Blood test

- CT ( computed tomography)

- MRI ( magnetic resonance imaging

Treatment

● Toxocariasis is often self resolving within weeks

● Toxocara larva cannot mature within human host

 ● If a patient is diagnosed with vlm or olm

- Corticosteroids are given

● Antihelmentics such as Albendazole

- are given a second line defense

- Granulomas can also be removed via surgery or laser photocoagulation

- Antiparasitic drugs:

- Albendazole or mebendazole combination with anti - inflammatory medication

Loose ends

● No current vaccine available or even under development

● However the genome for both varieties of toxocara have been sequence

● This could lead to breakthroughs in treatment and prevention

● Not many larvae needed to cause and effect 100 to 200

● Eggs found in up to 88% of the soil worldwide

Epidemiology

Human toxocariasis is primarily a Soil transmitted zoonosis with the infection more
commonly found in Children than adults.

- Cases are more frequently seen in Children living in homes and neighborhoods where dogs
and puppies are not dewormed and poor personal hygiene.

Number of surveys around the world demonstrated high rates of contamination of soil with
the parasite eggs in parks ,play grounds and other public places ( 10-30 %).

- In Western countries, the prevalence of infection in dogs was reported to be about 25% but
may be as high as 30 to 60 %.
- Studies have also demonstrated contamination of soil samples taken from gardens of
homes where clinical case of toxocariasis has been found.

Prevention and Control

• Make sure to treat your dogs, more important regularly for worms

• Wear gloves when working with possible contaminated soil

• Do not allow children to ingest or play in possibly contaminated soil

• Wash hands after playing with pets

• Clean up after your pets

• Have your pets dewormed

• Cover sandboxes when not in use

• Cook meat well

• Teach your kids not to look with their eyes not their mouths

• Contamination of soil

• Dogs and cats source of infection, treatment program starting at 2 to 3 weeks of age should
implemented