Nematodes - Teaching Demo

8/14/2019 Nematodes - Teaching Demo

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An Introduction to theAn Introduction to the

NematodesNematodes

Christian Gallardo, MDChristian Gallardo, MD


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Helminths

Three phyla:

Annelida (Segmented Worms)

Nemathelminthes (Roundworm)

Nematoda

Plathyhelminthes (Flatworms)

Cestoda (Tapeworms)

Trematoda (Flukes)


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Nematodes

Free living and parasitic

More than 80,000 are parasitic to

vertebrates

2mm (Strongyloides stercoralis) to ameter ( Dracunculus medinensis)

Sexes usually separate, male smaller than

female


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Morphology

Elongate cylindrical worm

Symmetrical bilaterally

Body

Outer, hyaline, noncellular cuticle

Subcuticular epithelium

Four longitudinal cords dorsal, ventral

and 2 lateral

Carry nerves and excretory canals

Layer of muscle cells


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Morphology

Alimentray tract

Simple

Mouth: surrounded with lips, some may haveteeth or plates

Esophagus

Intestine: flattened tube, straight course up to therectum

No circulatory system

Hemoglobin, glucose, proteins, salts andvitamins

Nervous system

Ring or commisure of connected gangliasurrounding the esophagus

Sensory organs: Labial, cervical, anal, andgenital regions


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Morphology

Male reproductive organ

Porterior 3rd of the body

Testis, vas deferens, seminal vesicle,and ejaculatory duct

Accessory copulatory apparatus

1 or 2 ensheated spicules Gubernaculum

Copulatory Bursa: winglikeappendedages

Female reproductive organ

Single or bifurcated tube

Ovary, oviduct, seminal receptacle,uterus, ovejector, and vagina

20 200,000 eggs


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Physiology

Excretory system

2 lateral canals that lie in the laterallongitudinal cords

2 Longitudinal muscles for sinuous movement

Thigmotropism penetration of the skin bythe hookworm larvae

Methods of obtaining food Sucking with ingestion of blood (Ancyclostoma)

Ingestion of lysed tissues and blood (Trichuris)

Feeding Intestinal content (Ascaris)

Ingestion of nourishment from the body fluids(filarial worms)


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Physiology

Anaerobic metabolic process

Glycogen content is high

Major portion expended in the production of

large number of ova

Resist digestive juices and tissue invaders Afforded by the cuticle and elaboration of

antienzymes

Life Span:

Trichinella spiralis: 4-16 weeks Enterobius vermicularis: 1-2 months

Ascaris lumbricoides: 12 months

Persist for at least 14 years


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INTESTINAL HELMINTHS

Ascaris lumbricoides (roundworm)

Trichinella spiralis (trichinosis)

Trichuris trichiura (whipworm)

Enterobius vermicularis (pinworm)

Strongyloides stercoralis (Cochin-chinadiarrhea)

Ancylostoma duodenale and Necatoramericanes (hookworms)


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Ascaris lumbricoides(Large intestinal roundworm)


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Epidemiology Annual global morbidity: 1 billion/ year

Mortality: 20,000/ year.

Occur at all ages,

More prevalent: 5 to 9 years age group. The incidence is higher in poor rural

populations

Morphology Female: 22 35 cm; Male: 10 31 cm

Smooth finely straited cuticle Conical anterior and posterior extremities

Ventrally curved papilatted posterior extremity(male)


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Terminal mouth with three oval lips with

sensory papillae

Paired reproductive organs posterior 2/3rd in

(female)

Single long tortuous tubule(male) Eggs


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Symptoms

Usual infection: 5 -10 worms unnoticed by

host

Routine stool examination

Vague Abdominal Pain

Eosinophilia

Loefflers Syndrome migrating Ascaris larvae


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Diagnosis

Identification of eggs (40 to 70 micrometers by

35 to 50 micrometers) in the stool.

Outline of the worm in Upper GI series

Treatment and Prevention Mebendazole, 200 mg (Adults); 100 mg

(Children) for 3 days is effective

Piperazine Citrate, 75mg/kg/day

Good hygiene is the best preventive measure Sanitary disposal of feces and health education

Night soil not be used unless treated with

chemicals


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Trichinella spiralis(Trichinosis)


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Trichinella spiralis (Trichinosis)

Epidemiology

Related to the quality of pork and consumption of

poorly cooked meat

Autopsy surveys: 2 percent infected/ population is

infected

Mortality is low

Morphology

Female: 3.50mm x 0.06 mm, Male: 1.50mm x

0.04mm

A slender anterior end with a small, orbicular,

nonpapillated mouth

Posterior end bluntly rounded in the female

Ventrally curved with two lobular caudal appendages

in male


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A single ovary with vulva in the anterior fifth in

the female

Long narrow digestive tract

Larvae: spearlike burrowing tip at tapering end:

80 120 microns and grows up to 900 to 1300microns


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Life Cycle

Infection occurs by ingestion of larvae, in poorly

cooked meat.

Invade intestinal mucosa and sexually

differentiate within 18 to 24 hours. The female, after fertilization, burrows deeply in

the small intestinal mucosa, whereas the male

is dislodged (intestinal stage).

On about the 5th day eggs begin to hatch in the

female worm and young larvae are deposited inthe mucosa

They reach the lymphatics, lymph nodes and

the blood stream (larval migration).


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Larval dispersion occurs 4 to 16 weeks after

infection.

The larvae are deposited in muscle fiber and, in

striated muscle, they form a capsule which

calcifies to form a cyst.

In non-striated tissue, such as heart and brain,

the larvae do not calcify; they die and

disintegrate.

Persist for several years.

One female worm produces approximately1500 larvae.

Man is the terminal host. The reservoir includes

most carnivorous and omnivorous animals.


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Diagnosis

Early in infection, serologic test: NEGATIVE

Serum levels of muscle enzymes (CPK, LDH)

Muscle Biopsy most definitive diagnosis

3rd to 4th week best time to do biopsy

Treatment and Prevention

Mebendazole: 1000mg/day for 10-14 days

Oral prednisone: 20 40mg daily

Elimination of parasite in hogs Adequate cooking of meat products

Larvae are killed at 55C to 77C


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Trichuris trichiura(whipworm)


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Epidemiology A tropical disease of children (5 to 15 yrs) in

rural Asia (65% of the 500-700 million cases)

Seen in the South Americas,

concentrated in families and groups withpoorer sanitary habits.

Distribution coextensive withA. lumbricoides

Morphology Attenuated whip like anterior, three fifths

traversed by a narrow esophagus resembling astring of beads

A more robust posterior, 2/5th containing theintestine and a single set of reproductiveorgans


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Male: 30-45mm, Female: 35-50mm

Bluntly rounded posterior end of the female

Coiled posterior extremity of the male

single spicule and retractile sheath

Eggs: 3000 10000/ day Lemon shaped with pluglike translucent

polar prominences (lantern shaped)


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Symptoms

Worm burden: less than 10 worms are

asymptomatic.

Heavier infections (e.g., massive infantile

trichuriasis) Chronic profuse mucus and bloody diarrhea

Abdominal pains

Edematous prolapsed rectum.

Malnutrition, weight loss and anemia

Sometimes death.

Diagnosis

Stool exam: Lemon shape eggs in feces


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Treatment and Prevention

Mebendazole, 200 mg (Adults); 100 mg

(Children) for 3 days is effective

Highly endemic and may be prevented by

Treatment of infected individuals Sanitary disposal of human feces

Personal hygiene

Thorough washing of hands

Scalding of uncooked vegetables


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Strongyloides stercoralis(Threadworm)


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Strongyloides stercoralis

(Threadworm)

Epidemiology

Cochin-China diarrhea,

50 to 100 million cases worldwide,

Tropical and subtropical areas with poor sanitation.

Prevalent in the South and among Puerto Ricans.

Morphology

Varies depending on whether it is parasitic or free-

living.

The parasitic female is larger (2.2 mm x 45

micrometers) than the free-living worm (1 mm x 60

micrometers).

Colorless semitransparent


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(Threadworm)

The eggs, when laid are 55 micrometers by 30

micrometers.

Rhabditiform larvae: 225 microns x 16 microns

Long slender, nonfeeding, infective,

filariform larvae


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(Threadworm)

Strongyloides life cycle: complex alternation between free-living and parasitic

cycles

potential for autoinfection and multiplicationwithin the host.

Two types of cycles

Free-living cycle:

The rhabditiform larvae passed in thestool can either molt twice and becomeinfective filariform larvae (direct

development) or molt four times Become free living adult males and

females that mate and produce eggsfrom which rhabditiform larvae hatch.


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(Threadworm)

The latter in turn can either develop intoa new generation of free-living adults orinto infective filariform larvae

The filariform larvae penetrate thehuman host skin to initiate the parasitic

cycle Parasitic cycle:

Filariform larvae in contaminated soilpenetrate the human skin

Transported to the lungs

penetrate the alveolar spaces; Bronchial tree to the pharynx, are

swallowed and then reach the smallintestine


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(Threadworm)

Small intestine: Molt twice and becomeadult female worms

The females: threaded - epithelium ofthe small intestine

Produce eggs which yield

rhabditiform larvae. Rhabditiform larvae

passed in the stool

Autoinfection: become infectivefilariform larvae : can penetrate

either the intestinal mucosa (internalautoinfection) or the skin of theperianal area (externalautoinfection)


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(Threadworm)

Symptoms

Light infections: asymptomatic.

Skin penetration causes itching and red

blotches

During migration: bronchial verminouspneumonia

Duodenum:

Burning mid-epigastric pain and tenderness

Nausea and vomiting.

Diarrhea and constipation may alternate.


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(Threadworm)

Heavy, chronic infections

Anemia, weight loss and chronic bloody

dysentery.

Secondary bacterial infection of damaged

mucosa may produce serious complications. Diagnosis

Examination of feces and duodenal contents

String test: duodenal fluid

Baermann Technique

ELISA (enzyme-linkedimmunosorbent assay)


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(Threadworm)

Treatment and prevention

Thiobendazole: 25mg/kg/BID x 3 days

Alternate: Albendazole and Ivermectin

Sanitary disposal of human feces

Protection of the skin from contact withcontaminated soil


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Enterobius vermicularis(Pinworm, Oxyuriasis)


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Enterobius vermicularis

(pinworm, oxyuriasis)

Epidemiology

Commonest helminthic infection in the US (18 million

cases at any given time).

Worldwide: 210 million.

Urban disease of children in crowded environment

(schools, day care centers, etc.)

The incidence in whites is much higher than in blacks

Morphology

Female:8 mm x 0.5mm; Male: 2mm 5mm.

Female:

Cuticular alar expansion at anterior end

Prominent esophageal bulb

Long pointed tail


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Eggs: 60mm x 27mm

Ovoid

Asymmetrically flat on one side.


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Life Cycle

Eggs are deposited on perianal folds

Self-infection

Transferring infective eggs to the mouth with

hands that have scratched the perianal area Person-to-person transmission

Enterobiasis may also be acquired through

surfaces in the environment that are

contaminated with pinworm eggs (e.g., curtains,

carpeting). Eggs: airborne and inhaled.

Swallowed -- Ingested eggs.


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Larvae: Small intestine

Adults: Colon

The time interval from ingestion of infective eggs to

oviposition by the adult females is about one month

Life span: 2 months

Gravid females migrate nocturnally outside the anus

oviposit while crawling on the skin of the perianal

area

The larvae contained inside the eggs develop in 4 to

6 hours

Retroinfection The migration of newly hatched larvae from the

anal skin back into the rectum, may occur but the

frequency with which this happens is unknown


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(pinworm)

Symptoms

Relatively innocuous and rarely produces serious

lesions.

The most common symptom: perianal, perineal and

vaginal irritation caused by the female migration.

Insomnia and Restlessness.

Gastrointestinal symptoms (pain, nausea, vomiting,

etc.)

Mother Complex

The conscientious housewife's mental distress,

guilt complex, and desire to conceal the infectionfrom her friends and mother-in-law is perhaps the

most important trauma of this persistent, pruritic

parasite.


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(pinworm)

Diagnosis Finding the adult worm or eggs in the perianal area,

particularly at night.

Scotch tape / pinworm paddle

Made upon the morning before bathing or

defecation

Treatment

Pyrental Pamoate: 2 doses (10 mg/kg;

maximum of 1g each) two weeks apart

Very high cure rate. Alternative: Mebendazole.

The whole family should be treated, to avoid

reinfection.


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Necator americanes and

Ancylostoma duodenale

(Hookworms)


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Epidemiology

More than 900 million people worldwide

Cause daily blood loss of 7 million liters

Ancylostomiasis

Most prevalent hookworm infection Second only to ascariasis in infections by

parasitic worms.

N. americanes (new world hookworm)

Most common in the Americas, central and

southern Africa, southern Asia, Indonesia,

Australia and Pacific Islands.


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A. duodenale (old world hookworm) Dominant species in the Mediterranean

region and northern Asia.

Morphology Small cylindrical, fusiform, grayish white

nematodes.

Female: 9 13mm, Male: 5 11mm

Thick cuticle

Bursa

Broad, translucent, membranous caudalbursa with riblike rays at the posterior end ofthe male

Used for attachment to the female duringcopulation


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N. americanes

Buccal capsule is conspicious

Dorsal pair of semilunar cutting plates

Concave dorsal median tooth

Deep pair of triangular subventricularlancets

A. duodenale

2 ventral pairs of teeth

Egg

Sinle thin transparent hyaline shell

2 8 cell stages division in fresh feces


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Life cycle

Eggs are passed in the stool

Under favorable conditions (moisture, warmth,

shade), larvae hatch in 1 to 2 days.

Rhabditiform larvae grow in the feces and/or the soil

After 5 to 10 days (and two molts) they become

become filariform (third-stage) larvae that are

infective.

Infective larvae can survive 3 to 4 weeks in favorable

environmental conditions.

On contact with the human host, the larvae penetratethe skin

Carried through the veins to the heart and then to

the lungs

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Filariform penetrate pulmonary alveoli Ascend the bronchial tree to the pharynx, and are

swallowed

Reach the small intestine, where they reside andmature into adults.

Adult worms live in the lumen of the small intestine, where

they attach to the intestinal wall with resultant blood loss bythe host.

Most adult worms are eliminated in 1 to 2 years, butlongevity records can reach several years.

SomeA. duodenale larvae, following penetration of the hostskin, can become dormant (in the intestine or muscle).

A. duodenale infection

may probably also occur by the oral andtransmammary route.

N. americanus infection

requires a transpulmonary migration phase.


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N t i d


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Intestinal blood loss

Iron deficiency,anemia,hypoproteinemia,edema, cardiacfailure

Hematologic

Attachment of adultworms and injuryto upper intestinal

mucosa

Anorexia, epigastricpain and gastro-intestinal

hemorrhage

Gastro- intestinal

Migration of larvaethrough lung,bronchi, andtrachea

Bronchitis,pneumonitis and,sometimes,eosinophilia

Pulmonary

Cutaneous invasionand subcutaneousmigration of larva

Local erythema,macules, papules(ground itch)

Dermal

PathogenesisSymptomsSite

Table 2. Clinical features of hookworm disease

N t i d


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Diagnosis Identification of hookworm eggs in fresh or

preserved feces.

Species of hookworms cannot be distinguished

by egg morphology. Treatment andcontrol

Mebendazole, 200 mg, for adults and 100 mg

for children, for 3 days is effective.

Sanitation is the chief method of control:

sanitary disposal of fecal material andavoidance of contact with infected fecal

material.

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Nematodes - Teaching Demo