Ascarids - Intestinal Roundworms

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Ascarids - Intestinal Roundworms

Taxonomy, Common Name, Disease

 

* CLASS: SECERNENTEA

* SUBCLASS: SPIRURIA

* ORDER: ASCARIDIDA

* SUPERFAMILY: ASCARIDOIDEA

* FAMILY: ASCARIDIDAE

Scientific name - Ascaris lumbricoides (humans)

 

* FAMILY: TOXOCARIDAE

Scientific name - Toxocara canis (dogs and cats)

Scientific name - Toxascaris leonina (dogs and cats)

Scientific name - Toxocara cati (cats)

 

Historical

Ancient Greeks and Romans were familiar with Ascarids, and they were

mentioned in the Ebers Papyrus. There is a very closely related

species Ascaris suum which occurs in pigs. There has been much

speculation over the years as to whether or not the two were

originally the same parasite which has " recently " evolved into two

separate species

Hosts

Humans, dogs, cats, foxes, coyotes, primates, cattle, horses,

chickens, turkeys, quail, pheasant, ducks, grouse, fish, sheep, goats

are some of the common hosts of various Ascarid species.

Human ascarids:

Ascaris lumbricoides

Distribution

Worldwide

Life Cycle

These are large worms (males 15-25 cm; females 20-40 cm) that occur in

the small intestine. They feed upon the intestinal contents, competing

with the host for food. The life cycle is direct (no intermediate

hosts are involved). Unsegmented eggs are passed in the feces. The

first-stage juveniles develop and molt to the second-stage within the

egg. This is the infective stage (second-stage juveniles). Eggs do not

hatch until ingested by a host. The eggs hatch in the intestine and

the second-stage juveniles migrate through tissues to the hepatic

portal system where they are carried to the liver. The juveniles molt

and become third-stage in the liver; this requires 4 or 5 days. They

go from the liver to the heart and then to the lungs by way of the

blood stream. In the lungs they molt to the fourth-stage in 5 or 6

days. These juveniles are coughed up and swallowed; they become adults

in the small intestine. The nematodes main food is liquid contents of

the intestinal lumen. Egg laying begins 50 to 60 days after the eggs

are ingested.

Symptoms-Pathogenicity

If large numbers of juveniles are present in the lungs they may cause

pneumonia. Juveniles entering the liver or other organs induce

inflammatory reactions. If large numbers of migrating juveniles are

present they may cause serious symptoms, especially if present in the

brain. A few adults in the intestine cause no serious symptoms. Larger

numbers compete with the host for food and may cause intestinal

discomfort, nausea, vomiting and diarrhea. In children the worms may

cause poor growth, loss of weight and abdominal symptoms. Rarely the

adult worms rupture the intestinal tract and enter the peritoneal

cavity causing peritonitis and may obstruct the bile ducts. Adult

worms are reported to wander either upstream (to the pancreatic and

bile ducts, or stomach), or downstream to the appendix causing various

problems.

Management

Sanitation - avoid eating food contaminated with the infective eggs.

Satisfactory anthelmintics are available for treatment of infected

individuals and other Ascarids of domesticated animals. Treatment -

Mebendazole, pyrantel pamoate, Vermox . Diagnosis is based on

identifying eggs in the stool by fecal smears.

Importance

It is estimated that about 1 billion persons, almost one quarter of

the world population, are infected.

Characteristics

Three large prominent lips, each with a dentigerous ridge, and no

interlabia or alae. Lateral lines are visible grossly. Males are 15 to

31 cm long and 2 to 4 mm at greatest width. The posterior end is

curved ventrad, and the tail is bluntly pointed. Spicules are simple,

nearly equal, and measure 2 to 3.5 mm long. No gubernaculum. Females

are 20 to 49 cm long and 3 to 6 mm wide. The vulva is about one third

the body length from the anterior end. The ovaries are extensive, and

the uteri may contain up to 27 million eggs at a time, with 200,000

being laid per day. Fertilized eggs are oval to round, 45 to 75 um

long by 35 to 50 um wide, with a thick, lumpy outer shell that is

contributed by the uterine wall. When the eggs are passed in the

feces, the layer is bile stained to a golden brown.

References

 

1. Georgi, J.R. and M.E. Georgi. 1990. Parasitology for

Veterinarians. W.B. Saunders Company. Philadelphia. 411 pages.

2. Read, C.P. 1972. Animal Parasitism. Prentice Hall. New Jersey.

182 pages.

3. Schmidt, G.S., and L.S. Roberts. 1989. Chapter 27. Order

Ascaridata: Large Intestinal Roundworms. in Foundations of

Parasitology. Times Mirror/Mosby College Publishing. St. Louis. 750 pages.

4. Maggenti, A.R. 1981. General Nematology. Springer-Verlag, New

York. 372 pages.

5. Chandler, A.C. and C.P. Read. 1961. Introduction to

Parasitology. John Wiley & Sons, Inc. New York. 822 pages.

6. Noble, E.R. and G.A. Noble. 1973. Parasitology The Biology of

Animal Parasites. Lea & Febiger, Philadelphia. 617 pages.

 

Dog and cat ascarids:

Toxocara canis (dog and cat)

Toxocara cati (cat)

Toxascaris leonina (dog and cat)

Distribution

Worldwide.

Life Cycle

In young dogs (3 months) infection is by ingesting eggs containing

second-stage juveniles. The eggs hatch in the duodenum; the

second-stage juveniles penetrate the intestinal wall and eventually

reach the liver where they increase in size but do not molt. Leaving

the liver they go to the heart, and then to the lungs. They molt to

the third stage in the lungs, trachea or esophagus. They molt to

fourth stage in the stomach and to adults in the intestine.

Unembryonated eggs are passed in the feces and develop to the

infective stage on the ground (second-stage juveniles within the egg).

Some juveniles do not go from the lungs to trachea but get into the

blood returning to the heart and are distributed to somatic tissue.

 

In older dogs (6 or more months) most infective juveniles do not go

from lungs to the trachea but get into the pulmonary system and are

transported to somatic tissue via blood.

 

In adult dogs none of the juveniles return to the intestine, but got

to somatic tissue and remain in second stage for as long as 6 months.

Puppies are commonly infected prenatally by reactivation of latent

juveniles in the somatic tissues of females. These juveniles migrate

to the fetus via the placenta. They remain as third-stage juveniles

until birth of the puppies when they mature in the intestine of the

pups. With Toxocara cati (cats) prenatal infection does not occur.

 

Toxocara canis infects a wide variety of animals but does not develop

to maturity, remaining in the second juvenile stage. Some animals may

serve as a transport host (e.g. mouse). In children (16-36 months old)

T. canis can cause viseral juveniles migrans. The symptoms are general

poor health and pulmonary involvement. In older children there may be

ocular involvement.

 

The life cycle of T. leonina is simple. Ingested eggs hatch in the

small intestine, where the juveniles penetrate the mucosa. After a

period of growth, they molt and return directly to the intestinal

lumen, where they mature. Although they are mildly pathogenic, their

main importance is a diagnostic one because T. leonina is considered

of little importance as a source of visceral larva migrans.

Management

Sanitation; treatment of puppies with anthelmintics. Avoid ingesting

the infective egg. Mebendazole (vermox) is drug of choice.

Importance

A large proportion of puppies and kittens are infected at birth. Young

children can easily become infected by ingesting eggs from play areas

utilized by both humans and pets.

 

Characteristics

Except for the cervical alae, the biology and morphology of T. canis

and T. cati are similar. The alae of T. canis are long and narrow,

whereas those of T. cati are short and broad. Adults look basically

like Ascaris, only they are much smaller. Three lips are present.

Unlike Ascaris, however, Toxocara has prominent cervical alae in both

sexes. Males are 4 to 6 cm, and females are 6.5 to more than 15 cm

long. The brownish eggs are almost spherical, with superficial pits.

The body of Toxascaris tends to flex dorsally while that of Toxocara

flexes ventrally. The alae of T. cati are short and wide, whereas they

are long and narrow in T. canis and T. leonina; the surface of the egg

of T. leonina is smooth but pitted in Toxocara spp.; and the tail of

male Toxocara is constricted abruptly behind the anus, whereas it

gradually tapers in Toxascaris.