Helminthology Final Examination (Nematodes)

Nematodes

Unsegmented, free living or parasitic, usually cylindrical & elongate

False

True of False:

Tegument is w/ circular annulations can readily available to the naked eye

True

alimentary canal is present in Nematodes

Roundworm

Nematodes AKA as?

Microvilli in the guts

where does absorption of nutrients does happen?

1. Cortical zone

2. Median zone

3. Basal zone

Parts of the cuticle?

Epicuticle

Cortical Zone is covered by a thin layer known as?

Cuticulin

Cortical zone contains highly resistant protein called?

Ala/Alae

These are cuticular wing like expansions of nematodes

Phasmids

are sensory pits on each side near the end of the tail of nematodes

Amphids

• These are sensory organs on each side of the head of the nematode

• are innervated invaginations of cuticle in nematodes. They are usually found in the anterior (head) region of the animal, at the base of the lips.

• are the principal olfactosensory organs of nematodes

12

amphid is made up of ___ sensory neurons with ciliated dendrites

Somatic muscle | Hypodermal Cords

• muscles that are present below the cuticle and hypodermis.

• They are attached to the hypodermis and separated into four sections by ________. They are obliquely striated unlike mammalian muscles and have dense bodies.

Six

How many Lips are there in Nematodes?

False

True or False:

Buccal capsule is not present in the mouth of NEMATODES.

Esophagus

Serve as the pumping organ that sucks food into the alimentary canal & forces it into the intestines

Intestine

Simple, tube-like structure

1. Direct (with IH)

a. Eggs outside the host hatch to larvae, then develops to infective larvae which are active.

b. Eggs develop outside the host to infective larvae but do not hatch or remain inside egg. Entry to host only thru ingestion of embryonated egg

c. Entry to definitive host, or in some specie they penetrate the skin.

Direct Life cycle of Nematodes

a. Eggs hatch to larvae from viviparous worm, enter IH, then IH eaten by DH

b. Eggs do not hatch but eaten by IH, then IH eaten by DH.

c. Worms viviparous, larvae in blood of DH from which infective larva develops. Infective larvae is introduced to DH when infected IH sucks blood from the former

Indirect Life Cycle of Nematodes with IH

Large Roundworm of pigs

Aka as Ascaris suum (suis)

15-25cm by 3mm

Size of the male A. suum

41cm by 5mm

size of the female A. suus

Ascaris suum

Eggs of this specie is oval, have thick shells, the albuminous layer bears prominent projections and they are brownish-yellow in colour.

200,000-2,000,000

How many eggs are layed in A. suus?

True

True or false:

Eggs of the A. suus are resistant to adverse conditions (drying and freezing). They remain viable to 5 years or longer.

Infection is thru ingestion of the infected egg present in contaminated food and water or from soiled skin of the dam in case of sucking pigs.

How does A. suus infection occur?

Ingested eggs hatch in the intestine and the larva burrow into the wall of gut,is released in small intestines, then to peritoneal cavity, to the liver, and then carried by blood to the lungs which will break out then going to bronchioles, bronchi then swallowed and will mature in the intestines.

After ingestion of the egg of the A. suus, what will happen next?

False

True or False:

Prenatal infection does occur in A. suus

Migration in the liver

destruction of tissue, hemorrhage causing milk spots leading to condemnation.

Lungs

lesions resembles asthma condition due to presence of oedema, emphysema, and hemorrhage. Death may occur in heavy infections.

Presence of adult

when they are numerous in numbers, they become twisted in bundles and causes obstruction. They may wander in the stomach and causes vomition, when present in bile ducts it can cause stasis in man, and they can perforate intestines causing peritonitis.

• Pneumonia, presence of cough & exudates in lungs

• Diarrhea in heavy infections of adults which affects their growth.

Clinical signs of A. suus

clinical signs and demonstration of eggs in the feces.

How to diagnose A. suus?

1. Levamisole, Cambendazole, Parbendazole, Fenbendazole

2. Tetramizole, Piperazine, Dichlorvos

3. Morantel tartrate

Treatment for A. suus

1. Treat sow before farrowing. Wash and scrub sows thoroughly to remove eggs adhering to the body.

2. Place in a farrowing pen previously cleaned (with boiling water and soda).

3. Within 10 days of farrowing, remove sow and litter to a clean pasture free of ascaris.

4. After weaning, remove sow and young pigs.

Management of A. suus

Parascaris equorum

➢ occurs in small intestines of equines

➢ life cycle is similar to A. suum

➢ egg is globular with a thick pitted shell

Equine Roundworm

AKA Parascaris equorum

1. cause catarrhal enteritis and diarrhea (fetid in odor and pale in color), flatulence and fat bellied.

2. Cause obstruction

presence of adult worms cause_____?

Treatment

1. Cambendazole

2. Thiabendazole

3. Fenbendazole

Treatment for P. equorum

thru clinical signs and demonstration of eggs in the feces.

Diagnosis of Parascaris equorum

Toxascaris leonina

➢ Occurs in dogs, cats, foxes, even wild canidae & felidae

➢ The infective stage is the egg containing 2nd stage larva w/c moult inside the host for 3rd stage larva up to 4th & 5th stage larva.

➢ Migration of larva does not occur as compared to T. canis

Toxocara canis

➢ Occurs in small intestines of dogs & fox.

➢ Larger than T. leonina,male is 10cm long and female is 18cm long).

➢ Life cycle exemplifies somatic and tracheal route of migration

True

True or False

May involve prenatal and colostral transmission

Toxocara cati

➢ Occurs in SI of cats & fox & wild felidae

➢ Prenatal infection does not occur, but transmammary transmission occur.

Ascariasis in dogs and cats

➢ Heavy infection is common in poor hygiene

➢ Heavy prenatal infection may lead to death of whole litter

➢ There’s diarrhea and vomiting as worms mature in the stomach and intestines.

➢ Pneumonia is uncommon.

➢ for less severe infections, there’s unthriftiness, potbellied appearance, intermittent diarrhea and possible anemia.

➢ Adult worms migrate to aberrant sites like the bile ducts.

➢ Coat is dull, harsh, there’s restlessness.

➢ Thiabendazole, Mebendazole, Fenbendazole

➢ Pyrantel pamoate, Dichlorophen, trichlorphon

Treatment for Ascariasis in dogs and cats

➢ Characterized by chronic granulomatous eosinophils lesions associated with larva in the inner organs of children especially liver, lungs, brain and eye.

➢ Larva migrates in somatic manner.

➢ There would be large number of larvae in repeated infections. Infection is usually seen in children 1-5 years old due to direct eating habit

Visceral Larva Migrans

Larvae that reenter the alveolar blood vessels travel to the muscles or organs, where they become encysted and their development is arrested

Somatic Migration of Larvae Meaning

Toxocara vitulorum

➢ Occurs in the small intestines of cattle, zebu, and Indian buffalo

➢ Its cuticle is not thick which make it soft & translucent.

➢ Transplacental & transmammary transmission occurs

➢ CS includes diarrhea accompanied by colic

➢ Diarrhea presents as mud colored evil smelling stoo

Family Heterakidae

Genus Heterakis

Heterakis gallinarum

➢ Occurs in the ceca of fowls, guinea fowl, pea fowl, turkey, duck, goose & numerous other birds.

➢ Male is 7 -13mm long, female is 10-15 mm long

➢ Large alae extending some distance down the sides of the body.

➢ Eggs develop in the open & reach the infective stage at 14 days.

➢ Eggs are resistant & may remain viable in the soil for months

➢ Host swallows the egg & the larva hatches in the intestines after 1-2 hours.

➢ Production of eggs manifested after 24-30 days

➢ Earthworm may serve as transport host (2nd Larval stage)

Life cycle of Heterakis gallinarum

➢ Direct effects of these worms are slight & only in heavy infection may there be thickening of the cecal mucosa w/ a number of petechial hemorrhages.

➢ Carrier of Histomonas meleagridis, the causal agent of blackhead disease in turkeys

Pathogenesis & Clinical Signs of Heterakis gallinarum

➢ Thru fecal examination

➢ Direct examination of feces in cecum

➢ Phenothiazine

➢ Phenothiazine w/ piperazine

➢ tetramizole

Diagnosis and Treatment of Heterakis gallinarum

Genus Ascaridia

Occurs in the small intestine of the fowl, guinea fowl, turkey, goose, & various wild birds

➢ Most serious infection occurs in 3 months old chickens

➢ They cause hemorrhage & enteritis

➢ Birds become anemic & suffer from diarrhea

➢ Cause of decreased egg production

➢ In heavy infection, may cause intestinal obstruction

➢ Piperazine

Pathogenesis and Treatment of Genus Ascaridia

Family Oxyuridae

Genus Enterobius

Enterobius vermicularis

AKA as human pinworm or seatworm

Oxyuris vermicularis

Enterobius vermicularis is foremerly known as?

➢ is a nematode (roundworm) and a common human intestinal parasite, especially in children. The medical condition associated with pinworm infestation is known as enterobiasis, or less precisely as oxyuriasis in reference to the family Oxyuridae.

Enterobius vermicularis

• The pinworm appears as a white, small and delicate nematode.

• The adult female has a sharply pointed posterior end, is 8 to 13 millimeters long, and 0.5 millimeter thick.

• The adult male is considerably smaller, measuring 2 to 5 millimeters long and 0.2 millimeter thick, and has a curved posterior end.

• The eggs are translucent and have a surface that adheres to environmental objects.

• The eggs measure 50 to 60 micrometers by 20 to 30 micrometers, and have a thick shell that is flattened on one side.

• The small size and colorlessness of the eggs make them invisible to the naked eye, except in barely visible clumps of thousands of eggs.

• Eggs may contain a developing embryo or a fully developed pinworm larva.

• The larvae grow to 140–150 micrometers in length.

Morphology of pinworm (Enterobius vermicularis)

• The pinworm has a worldwide distribution, and is the most common helminth (i.e., parasitic worm) infection in the United States and Western Europe.

• Pinworms are particularly common in children, with prevalence rates in this age group having been reported as high as 61% in VPAR22 NB: ELCT India, 50% in England, 39% in Thailand, 37% in Sweden, and 29% in Denmark.

DISTRIBUTION OF ENTEROBIUS VERMICULARIS

1. Eggs being ingested (hatched in duodenum)

2. larvae grow rapidly to a size of 140 to 150 micrometers and migrates thru small intestine towards the colon

3. during migration they moult twice and become adults. The female survive for 5-13 weeks and males about 7 weeks

4. The male and female pinworms mate in the ileum, where after the male usually die, and are passed out with stool.

5. The gravid female pinworms settle in the ileum, caecum (i.e., beginning of the large intestine), appendix and ascending colon, where they attach themselves to the mucosa and ingest colonic contents.

6. Almost the entire body of a gravid female becomes filled with eggs. The estimations of the number of eggs in a gravid female pinworm ranges from about 11,000 to 16,000. The egg-laying process begins approximately five weeks after initial ingestion of pinworm eggs by the human host.

7. The gravid female pinworms migrate through the colon towards the rectum at a rate of 12 to 14 centimeters per hour

8. They emerge from the anus, and while moving on the skin near the anus, the female pinworms deposit eggs either through (1) contracting and expelling the eggs, (2) dying and then disintegrating, or (3) bodily rupture due to the host scratching the worm.

9. After depositing the eggs, the female becomes opaque and dies. The reason the female emerges from the anus is to obtain the oxygen necessary for the maturation of the eggs.

life cycle of Enterobius vermicularis (pinworm)

• Pinworms spread through human-to-human transmission, by ingesting (i.e., swallowing) infectious pinworm eggs and/or by anal insertion.

• The eggs are hardy and can remain viable (i.e., infectious) in a moist environment for up to three weeks. They do not tolerate heat well, but can survive in low temperatures: two-thirds of the eggs are still viable after 18 hours at −8 degrees Celsius (18 °F)

• After the eggs have been initially deposited near the anus, they are readily transmitted to other surfaces through contamination

TRANSMISSION OF PINWORM (ENTEROBIUS VERMICULARIS)

A pinworm infection or enterobiasis is a human parasitic disease and one of the most common childhood parasitic worm infections in the developed world.

Infection usually occurs through the ingestion of pinworm eggs, either through contaminated hands, food, or less commonly, water.

The chief symptom is itching in the anal area

The incubation time from ingestion of eggs to the first appearance of new eggs around the anus is 4 to 6 weeks.

Pinworms are usually considered a nuisance rather than a serious disease.

what is enterobiasis?

• One third of individuals with pinworm infection are totally asymptomatic.

• The main symptoms are pruritus ani and perineal pruritus, i.e., itching in and around the anus and around the perineum.

• The itching occurs mainly during the night, and is caused by the female pinworms migrating to lay eggs around the anus

Signs and symptoms of Enterobiasis

The benzimidazole compounds albendazole (brand names e.g., Albenza, Eskazole, Zentel and Andazol) and mebendazole (brand names e.g.,Ovex, Vermox, Antiox and Pripsen) are the most effective

Treatment for Enterobiasis?

Family Strongyloididae

Genus Strongyloides

mammals, birds, reptiles and amphibians.

Strongyloides infects?

Strongloides stercoralis

(has a cosmopolitan distribution in tropical and subtropical regions)

Strongyloides fuelleborni

occurs in African primates where infection can be shared with humans

Srongyloides fuelleborni kellyi

occurs exclusively in humans in New Guinea

Strongyloides raati

infects humans (strongyloides)

• The parasitic females are approximately 2mm in length, with blunt-ended tails, and an elongated, straight-sided (filariform) oesophagus, occupying approximately one third of the body length.

• The ovary is didelphic and opens at the vulva which is positioned approximately two thirds along the body length.

• The free-living adults stages are approximately 1mm in length, with the female slightly larger than the male.

• Both sexes have a rhabditiform oesophagus; the free-living female has a didelphic ovary and a vulva at the mid-point of the body

Morphology of Strongyloides

(1) a sex determination event;

(2) a female-only developmental switch. Numbered larval stages are shown as L.

The progeny of the parasitic females have two developmental switches of Strongyloides ratti

Strongyloidiasis

• an intestinal infection caused by 2 species of the parasitic nematode Strongyloides

• The most common and clinically important pathogenic species in humans is S stercoralis. S fuelleborni is found sporadically in Africa and Papua New Guinea.

• Distinctive characteristics of this parasite are its ability to persist and replicate within a host for decades while producing minimal or no symptoms (individuals with an intact immune system) and its potential to cause life-threatening infection (hyperinfection syndrome, disseminated strongyloidiasis) in an immunocompromised host (60-85% mortality rate).

• Infection is clinically characterized by watery diarrhea, abdominal cramping, and urticarial rash. In malnourished children, strongyloidiasis remains an important cause of chronic diarrhea, cachexia, and failure to thrive.

During chronic uncomplicated infections, the larvae may migrate to the skin

known as larva currens because of the quick migratory rate of the larva

what causes cutaneous strongyloidiasis?

caused by the nematode (roundworm) Strongyloides stercoralis.

What causes Strongyloidiasis

Strongyloides stercoralis. Other species may include: Strongyloid myopotami and Strongyloides procyonis

What is the most common human pathogen?

65 years

The longest documented asymptomatic infection of strongyloidiasis?

strongyles

AKA palisade worms?

Buccal capsule is well developed with median thickening on the dorsal wall of the dorsal gutter which carries the duct of the dorsal esophageal gland.

Anterior margin of the buccal capsule bears leaf like cuticular structure called the leaf crowns or corona radiate.

Anterior margin of buccal capsule does not bear teeth or cutting plates but teeth may be present in the depth of the buccal capsule.

Describe the buccal capsule of he palisade worms (Strongyles)

True

True or False

Male copulatory bursa is well developed and has typical eye. Head is for attachment at region of vulva with expanded posterior end.

Direct and Segmented

True or False

Life cycle is indirect and eggs when laid are unsegmented strongyles

Strongyles equinus

It occurs in the cecum and colon of equines including zebra

worms are fairly rigid and dark grey in color, males are 26-35 mm long and females are 40-56 mm long.

external and internal leaf crowns are present and buccal capsules with one large tooth with bifid tip and two short sub ventral teeth.

Strongyles dentatus

• occur in the large intestines of equines

• resembles S. equinus grossly but head is wider than the rest of the body.

Strongyles asini

• occur in large intestines of ass and horses

S. equinus

, the infective larvae penetrate the mucosa of the colon and cecum and enter subserosa where they cause nodule formation then migrate to the peritoneal cavity, enter the liver (wander in it for about 4 months) then return to the lumen of large intestines to mature via wall penetration. Eggs are produced in about two months after infection.

S. dentatus

the infective larvae enter the wall of the intestine then pass to the liver via the portal system,in the liver the larvae wander for up to 9 weeks then reach the connective tissue underlying the peritoneal lining of the abdominal cavity where they form hemorrhagic nodule. About three months, they migrate between the layers of the mesocolon to the walls of the cecum and colon where the hemorrhagic nodules are also formed. Eventually young worms go to the lumen of the large intestine tomature. Eggs are produced on about 10-11 months post infection

Strongyles vulgaris

infective larvae penetrate the intestinal wall then penetrate the intima of arterioles. They will migrate towards the anterior mesenteric artery where they produce aneurysms and thrombi in about 4-5 days post infection. Then they enter the lumen and reach maturity. Eggs are produced 6-7 months post infection. Some larvae may linger in the mesenteric artery. Note that equine strongyles have long prepatent periods of 11 months post infection.

1. Eggs are passed out in the early stage of segmentation.

2. Under suitable environmental condition of moisture, oxygen and temperature, first stage larvae develop in 24 hours, then hatches into free living rhabditiform larvae which feed on bacteria and grow

3. Larvae molt into 2nd stage then become 3rd stage infective larvae in 5-6 weeks. Infective larvae do not feed and exist on reserve food granules, and when exhausted larvae die

4. Infective larvae are negatively geotropic because they crawl up blades of grasses and positively phototropic because they are attracted to mild light.

5. At night, larvae descend to the soil, Larvae are also active in warm than in cold weather. Moisture favors larvae migration because of the above habits and response to the stimuli, their possibility of getting a host is increased. Infection is by the ingestion of infective larvae with herbage of water

LIFE CYCLE IN GENERAL OF STRONGYLES

ANEMIA, ULCERS AT THE SITE OF ATTACHMENT

All the three adult strongyles of equine are blood suckers causing?

SEVERE LESION IN THE ARTERY

Larval stage of S. vulgaris causes

THROMBUS FORMATION AND ANUERYSMS IN ARTERIAL VESSELS ESPECIALLY IN THE ANTERIOR MESENTERIC ARTERY

Larvae of S. vulgaris cause

s destruction of the liver tissue which may be fatal.

S. equinus larvae causes

thrombus

clot of blood formed within the blood vessel and reaining attached to its place of origin.

Anuerysm

an abnormal blood filled bulge of a blood vessel and an especially an artery resulting from weaking of the vessel wall

embolism

sudden blocking of an artery by a clot of foreign materials that has been brought to its site of lodgement by the blood current.

cardiac arrest

sudden and often unexpected stoppage of effective heart action

Anaemic infarction

one due to sudden interruption of flow of arterial blood to the area