NEMATODES

MARK M. CALBAN, MD, MPM

CSU
College of Medicine & Surgery

PHYLUM NEMATODA
Nematodes/True Roundworms
Unsegmented, Elongated, Cylindrical in
shape
Sexes are separate
Females are LARGER than males
Life Cycle includes:
Egg Stage
4 Larval Stages
Adult Stage
2

Ascaris lumbricoides
(large intestinal roundworm)
Disease Caused: Ascariasis,
the most common human helminth
infxn; 70% from Asia
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ASCARIS LUMBRICOIDES Male

Cross Section
1.
2.
3.
4.
5.
6.
7.

Cuticle and Hypodermis

Longitudinal Muscle
Layer
Vas Deferens
Testis
Lateral Line w/
Excretory Canal
Intestine
Pseudocoelom

ASCARIS LUMBRICOIDES Female

Cross Section
1.
2.
3.
4.
5.
6.

Cuticle and
Hypodermis
Longitudinal
Muscle Layer
Ovary
Oviduct
Uterus
Intestine

ASCARIS LUMBRICOIDES Lips

The THREE (3)
lips & sensory
papillae are seen at
the anterior end.
The margin of each
lip is lined with
minute teeth which
are NOT visible at
this magnification.

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What is the lifespan of the adult

ascaris worm?
A.
B.
C.
D.
E.

1 year
2 years
5 years
10 years
NONE OF THE ABOVE

The female ascaris worms lays approx

how many eggs/day?
A.
B.
C.
D.
E.

100,000
200, 000
300,000
400,000
NONE OF THE ABOVE

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PATHOLOGY
Reactions of tissues to invading larvae.
Irritation of the intestine by the mechanical and toxic action
of the adult.
Complications arising from the parasites extra intestinal
migration.

PATHOLOGY
Tissue phase:
With heavy or repeated
infection, pneumonia,
cough, low-grade fever,
30% to 50% eosinophilia
(Lfflers syndrome) result
from migration of larvae
through the lungs (1 to 2
weeks after ingestion of
eggs).
Allergic asthmatic reaction
may occur with reinfection.

Intestinal phase:
Intestinal or appendix
obstruction results from
migrating adults in heavy
infections.
a. Vomiting and abdominal pain result
from adult migration.
b. Protein malnutrition can occur in
children with heavy infections and poor
diets.
c. Some patients are asymptomatic.

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PATHOLOGY
LARVA:
Ascaris Pneumonitis/
Loefflers Syndrome
Difficulty of breathing,
cough, fever, lung
infiltration.
May become ERRATIC

ADULT:
Diarrhea
Malnutrition
Villous Atrophy
Worm bolus/obstruction

Pathogenesis & Clinical Findings

The major damage occurs during larval migration rather
than from the presence of the adult worm in the intestine.
The principal site of tissue reaction are the lungs, where
inflammation with an eosinophilic exudate occurs in
response to larval antigens (Loefflers Syndrome)
Because the adults derive their nourishment from ingested
food, a heavy worm burden may contribute to
malnutrition, especially in children in developing
countries.

PATHOLOGY
Complications from
intestinal obstruction are
caused by tangling of the
large worms or migration
of adults to other sites, such
as the appendix, bile duct,
or liver (detectable by
radiograph).

PATHOLOGY
Migrating adults (22
to 35 cm long) may
exit by the nose,
mouth, or anus.
They are large,
creamy, and white and
have a cone-shaped
tapered anterior; the
male has a curved tail

Intestinal Ascariasis
Protruberant Abdomen
Intermittent Colicky
Cramps
Loss of Appetite
Jejunal Mucosa
broadening and
shortening of villi,
elongation of crypts,
decrease in villus crypts
ratio, round cell
infiltration of lamina
propria

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Laboratory Diagnosis
DIRECT FECAL SMEAR
2mg of Feces + 1 gtt NSS
LPO/MPO
KATO TECHNIQUES
20-60mg feces
qualitative tech, MASS
examination
KATO KATZ TECHNIQUE
Quantitative
Egg counts/gram feces
determine egg reduction after
treatment
Determine intensity of ascaris
infection.

TREATMENT

Albendazole - Drug of Choice; 400mg SD

Mebendazole - 500mg SD
Pyrantel Pamoate - 10mg/kg
Ivermectin - 200ug/kg SD

PREVENTION
HANDWASHING
Proper disposal of human wastes
Health Education
Mass Chemotherapy done periodically

Trichuris trichiura
(Whipworm/)
Disease Caused: Trichiuriasis
Cousin of Ascaris
Trichocephalus trichiura
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Trichiuris trichiura
Common Name: Whipworm
Holomyarian Type of Somatic Muscle Arrangement.
Final Host: Man
Habitat: Large Intestine
Diagnostic Stage: Ova
Infective Stage: Embryonated Ova; MOT: Ingestion
Portal of Entry: Mouth

Anterior 2/3 attenuated & Thin

Posterior 1/3 fleshy & robust

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Bipolar Plug
Foot Ball Shape
Lemon-Shaped
Barrel-Shaped

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MAJOR PATHOLOGY AND SYMPTOMS

Persons with slight infection are asymptomatic, with no
treatment required.
Heavy infection (500 to 5,000 worms) simulates
ulcerative colitis in children
inflammatory bowel disease in adults
Histology reveals eosinophil infiltrations but no decrease
in goblet cells

MAJOR PATHOLOGY AND SYMPTOMS

The surface of the colon may be matted
with worms. Patients will have:
a. Bloody or mucoid diarrhea
b. Weight loss and weakness
c. Abdominal pain and tenderness
(colitis may be seriously debilitating)
d. Increased peristalsis and rectal
prolapse, especially in children
Chronic infections in children
Growth stunting
Stool is loose with mucus (and obvious
blood) in heavy infection.

 Enterrorhagia,

RECTAL
PROLAPSE
(increased
peristalsis that
occurs in an effort
to expel the
worms.,
Appendicitis

NOT cause significant

anemia, unlike the
hookworms. !

Diff fr Ascaris: No
heart & Lung
migration

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Notes:
Adult worms
live in the cecum and ascending colon.
Anterior portion is threaded into the mucosa.
Female worms shed between 3,000 20,000 eggs/day
Lifespan is 1 year

Laboratory Diagnosis
Needed to confirm your
suspicion based on History
& PE.
1. Direct Fecal Exam
2. Kato Technique
(qualitative) & Kato-Katz
Technique (quantitative)
3. Concentration Techniques
(Sedimentation/Flotation
Mx)

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Laboratory Diagnosis
DIRECT FECAL SMEAR
2mg of Feces + 1 gtt NSS
LPO/MPO
KATO TECHNIQUES
20-60mg feces
qualitative tech, MASS
examination
KATO KATZ TECHNIQUE
Quantitative
Egg counts/gram feces
determine egg reduction after
treatment
Determine intensity of ascaris
infection.

TREATMENT
DOC: MEBENDAZOLE
500mg SD - light infxns
500 mg x 3 doses - heavy infxns

PREVENTION

Treatment of infected individuals

Sanitary disposal of human wastes by construction of toilets
and their proper use
Frequent handwashing
Health Education
Thorough scalding and washing of uncooked vegetables

Enterobius vermicularis
(pinworm/seatworm)

Oxyuris vermicularis

MORPHOLOGY ADULT WORM

MORPHOLOGY EGGS

LIFE CYCLE

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 The eggs are distributed in the environment.

Infection can be acquired by ingestion/inhalation of eggs.
The adult worm invades the colon.
At around 12mn-4am, the gravid female migrates to the
perianal area. Here, the female worm ruptures to release
eggs causing pruritis (thats why affected individuals
scratch their perianal area at night.

 Fully gravid female migrates down the colon and anus

(crawls on perianal and perineal skin) 15-43 days after
ingestion of infective stage ova. (rupture of eggs caused
pruritus)
Eggs found in the environment
Transmission: anus to mouth by finger contamination
(by scratching; contamination by carriers on soiled bed
linen; airborne eggs; retrofection (female worm after
laying eggs will crawl back making it difficult to cure)

PATHOLOGY

CELLOPHANE/SCOTCH TAPE
SWAB

CELLOPHANE/SCOTCH TAPE
SWAB

TREATMENT

PREVENTION AND CONTROL

Strongyloides stercoralis
(threadworm)
Rhabditiform Larvae - Free Living form
Filariform Larvae Parasitic Form

STRONGYLOIDES STERCORALIS
Common Name:
THREADWORM;
Smallest Nematode of
Man
Habitat: Small Intestine
Cochin China
Diarrhea

EPIDEMIOLOGY
Tropics, especially in Southeast Asia.
Its geographic pattern is similar to that of hookworm because
the same type of soil is required.
More of a focally transmitted worm than a soil transmitted
helminth because it is infective shortly after passage w/ the
feces

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LIFE CYCLE

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MAJOR PATHOLOGY AND SYMPTOMS

1. Major clinical features are
abdominal pain, diarrhea, and
urticaria, with eosinophilia.
2. Skin shows recurring
allergic, raised, itchy, red
wheals from larval penetration.
3. Migration of larvae:
Primary symptoms are in the
lungs; bronchial verminous
(from worms) pneumonia.

MAJOR PATHOLOGY AND SYMPTOMS

4. Intestinal symptoms include abdominal pain, diarrhea,
constipation, vomiting, weight loss, variable anemia,
eosinophilia, and protein-losing enteropathy.
Light infections are often asymptomatic; gross lesions are
usually absent.
The bowel is edematous and congested with heavy infection.
5. S. stercoralis has caused sudden deterioration and death in
immunocompromised persons because of heavy
autoinfection and larval migration throughout body
(hyperinfection), with bacterial infection secondary to larval
spread and intestinal leakage.

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BAERMANN TECHNIQUE

LAB DIAGNOSIS
1. Recovery of the rhabditiform (noninfective) larvae is
normally from the stool concentrate. Caution: Filariform
(infective) larvae can also be recovered in the stool.
A minimum of four (4) stools are recommended before
indicating that the patient is not infected (routine formalin,
ethyl acetate sedimentation concentration);
2. If the stool specimens are negative, examination of duodenal
contents is recommended (duodenal aspirates, Entero-Test
capsule); however, the overalL sensitivity of the method varies.

LAB DIAGNOSIS

LAB DIAGNOSIS
3. Various concentrates (Baermann) and cultures (HaradaMori, petri dish) can also be used for larval recovery.
4. Eggs are rarely seen in the stool but may be recovered
from duodenal contents.

LAB DIAGNOSIS
5. In very heavy infections, eggs (less common), larvae (both
types), and adult worms may be recovered in the stool.
6. If agar plates are used (culture, method of choice), they
must be dried sufficiently to eliminate free water on the agar
prior to use.

PREVENTION
Similar to hookworm infection

TRICHINELLA SPIRALIS
(TRICHINA WORM)

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MAJOR PATHOLOGY & SYMPTOMS

1. Intestinal phase shows small intestine edema
and inflammation, nausea, vomiting, abdominal pain,
diarrhea, headache, and fever (1st week after infection).
2. Migration phase shows high fever (104F), blurred
vision, edema of the face and eyes, cough, pleural
pains, and eosinophilia (15% to 40%) lasting 1 month in
heavy infection; death can occur during this phase in 4th to
8th week after infection.

MAJOR PATHOLOGY & SYMPTOMS

3. Muscular phase shows acute local inflammation with
edema and pain of the musculature. Other symptoms vary
depending on the location and number of larvae present.
Larvae encyst in skeletal muscles of limbs, diaphragm, and
face, but they invade other muscles as well. Weakness and
fatigue develop.
4. Focal lesions show periorbital edema, splinter
hemorrhages of fingernails, retinal hemorrhages, and rash.

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METHOD OF DIAGNOSIS
DIAGNOSTIC CRITERIA
Identification of encysted larvae in biopsied muscle;
Serologic testing (ELISA) 3 to 4 weeks after infection.
A history of eating undercooked pork or bear
Fever, muscle pain, bilateral periorbital edema, and rising
eosinophilia

DIAGNOSTICS

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Capillaria philippinensis
(pudoc WORM)

Capillaria philippinensis
(Pudoc Worm)

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PATHOLOGY
The first proven case of human infection with Capillaria
philippinensis occurred in 1963 in a patient from the
Philippines who died 3 days after admission to the
hospital with a diagnosis of malabsorption syndrome.
Although the significance was not recognized until 4 years
later, C. philippinensis eggs were found in the stools and
autopsy showed parasitism of the large and small
intestines.

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LIFE CYCLE
Although the exact mode of transmission is unknown,
experimental infection is transmitted through small fish that serve
as the intermediate host; often, whole, small fish may be ingested.
Development to the infective stage in the fish takes at least 3
weeks.
In areas of the Philippines where this infection occurs, people also
eat raw shrimp, crabs, and snails.
They also tend to defecate in the fields or water where the fish,
shrimp, crabs, and snails are obtained, thus completing the life
cycle.
The worms live burrowed into the mucosa of the small bowel,
mainly the jejunum.

PATHOGENESIS
Symptoms are related to the worm burden; with large numbers
of worms, there may be intestinal malabsorption and fluid loss
along with electrolyte and plasma protein imbalance.
Most of the abnormality is found in the small intestine, where
the wall is thickened and indurated and contains many larval
and adult worms.
Watery stools are passed (up to eight per day), with fluid loss
of several liters.
Patients lose weight rapidly and develop muscle wasting,
abdominal distention, and edema.
Death from pneumonia, heart failure, hypokalemia, or cerebral
edema may occur within several weeks to a few months.

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PATHOGENESIS
In some cases, patients reported chronic abdominal pain
and diarrhea over a period of many months prior to
diagnosis.
On gastroduodenoscopy and subsequent histology, the
jejunal mucosa revealed flattened villi, crypt proliferation,
acute inflammation, and eosinophilic granulomata.

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The harder the

struggle, the
greater the glory.
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