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The internal parasites that still infect our pigs

Monday, December 5, 2011

In the second of two articles on parasitic diseases, a swine specialist reviews four parasitic diseases that, though reduced, remain of clinical and economic importance


by S. ERNEST SANFORD

I'll start by saying that the move to total indoor, confinement-rearing of pigs has reduced the prevalence of most internal parasites in our domestic pig population. However, unlike the external parasites, which are almost all gone and definitely miniaturized in importance, most internal parasites are still present and important in our pigs.

The internal parasites that I will discuss here include: round worms (Ascariasis); nodular worms (Oesophagostomiasis); lung worms (Metastrongylosis); and whip worms (Trichuriasis).

Because the remaining internal parasites are very different from the above, I'll leave the following four for a later discussion: Coccidiosis (Isospora suis); Cryptosporidiosis (Cryptosporidium spp.); Trichinosis (Trichimella spirilis); and Eperythrozoonosis (Mycoplasma [formerly Eperythrozoon] suis)

Round worms (Ascarids-Ascariasis)
The pig roundworm, Ascaris suum, infects pigs of all ages, worldwide. Although infection occurs in any age of pig, it is most common in the grow-finish pig.

Life cycle. Ascarid eggs, passed out in pigs' feces, hatch in the intestines after being eaten by a pig. Hatched larvae penetrate the intestinal wall and travel to the liver, lungs and other organs via the bloodstream. They reach the liver and lungs in two to four and 10 days, respectively.

Larvae are coughed up from the lungs, swallowed and reach the intestines in 14-20 days after initial ingestion of the eggs, then mature in the intestines in about two months. The entire time from ingestion of eggs to maturity to lay eggs in the feces (called the pre-patent period) is about eight weeks. Eggs mature for another two to four weeks in the environment before they become infective.

Ascarid eggs are extremely hardy, lasting up to 15 years in the environment. Once a barn is contaminated, ascariasis persists in that pig population indefinitely.

Clinical signs. Unthriftiness, failure to gain weight, rough hair coat and pendulous abdomen are common clinical signs of ascariasis in growing pigs. Thumping respiration and coughing occur especially in naïve gilts and feeder pigs placed in a barn contaminated with ascarid eggs. This can be easily misdiagnosed as a viral pneumonia.

Gross lesions and diagnosis. Scarring of the liver, producing gray to white "milk spots" caused by migrating ascarid larvae, is the most obvious gross lesion seen. Milk spots occur seven to 14 days after exposure to the eggs and, in less severe infestations, can heal and disappear in 30-60 days. Acute, multiple pinpoint hemorrhages in the lung occur in acute infections.

Diagnosis is made on seeing roundworms in pens or in intestines on post mortem. Ascarid eggs are identified under the microscope in fecal samples six to eight weeks after initial ingestion of eggs.

Control. Many dewormers given at the appropriate time of the ascarid life cycle are available to remove ascarids (see Table 1). Prevention, though difficult, is better.

Washing sows to remove eggs prior to placement in sanitized farrowing rooms, early weaning at two to three weeks of age before eggs are infective, all-in/all-out production and deworming sows about one week before placement are all measures used to control roundworms.

Nodular worms (Oesophagostomiasis)
Nodular worms (Oesophagostomum spp.), like roundworms, have defied our attempts to eradicate them and are still very much present in our pig population today. Infection occurs in all ages but is most common in grow-finish pigs and adults. It is common in outdoor pigs but has persisted in confinement-reared, indoor pigs also.

Life cycle. Larvae hatch from eggs in pigs' feces, persist in the environment for up to a year until ingested as third stage larvae (L3) which invade the wall of the cecum and colon, moult to L4 larvae and return to the intestinal lumen in six to 20 days. There, they mature to adults and lay large numbers of eggs as early as three weeks after initial infection. 

Gross lesions and diagnosis. Larvae become encysted in the intestinal wall and can be seen grossly from the serosal (outer) surface of the intestines. Eggs are identified through microscopic examination of fecal samples.

Treatment and control.
Several anthelminthics are available for control (Table 1). Deworming sows prior to farrowing reduces exposure of piglets to worm eggs in the farrowing room and prevents proliferation of the worm cycle.

Lung worms (Metastrongylosis)

I can say, with confidence, that the lungworm, Metastrongylus elongatus, is one internal parasite that was eliminated from our domestic pig population when we moved to total indoor, confinement pig rearing. Lungworms, however, still infect and are of importance to outdoor pigs. 

Life cycle. Lungworms use the common earthworm as an intermediate host. Adult lungworms lay eggs that leave the pig in its feces. First stage larvae (L1) hatch from eggs in feces and can survive in feces or soil for long periods of time. After ingestion by earthworms, larvae develop into the infective L3 stage in about 10 days and can remain dormant for up to 18 months.

Larvae penetrate the intestines of pigs which eat infected earthworms during the pigs' rooting behaviour. The larvae localize in the lungs and mature to adults that lay eggs in about 25 days after ingestion. Eggs are coughed up, swallowed and passed out in feces.

Clinical signs, gross lesions and diagnosis. Clinical signs consist of unthriftiness and possible "thumping" respiration similar to that caused by roundworm migration.
Some larvae that migrate to the liver cause gray or white scarring similar to roundworm milk spots. Most larvae reach the back of the lung, creating a localized parasitic pneumonia.

Diagnosis is best made by post-mortem examination. Microscopic examination of feces will also reveal the embryonated eggs of lungworms.

Treatment and control. Removal of pigs from contaminated pastures prevents infection. There are several effective anthelminthics (Table 1). Deworming sows prior to farrowing reduces exposure of piglets to worm eggs.

Whipworms (Trichuriasis)
We can add whipworm infections, trichuriasis, caused by Trichuris suis, to the list of internal parasites eliminated by moving to indoor, totally confined pig production. All ages can be infected but outdoor-reared, grow-finish pigs are most commonly infected. Infection in adult swine is often subclinical but serves as a source of infection for young pigs.

Life cycle. Mature female whipworms lay eggs that are passed in pig feces. Eggs become infective in three to four weeks and remain infective in the environment for up to six years. Eggs, ingested by a pig, hatch and L3 larvae invade the small intestines.

Larvae eventually re-enter the intestinal lumen and move down to the large intestines, where they bury themselves into the mucosa of the cecum and colon, causing a hemorrhagic inflammation.

Clinical signs, gross lesions and diagnosis. Mucoid to hemorrhagic diarrhea is the classical sign of whipworm infection and has to be differentiated from swine dysentery, salmonellosis and ileitis, three other hemorrhagic diarrheas seen in grow-finish pigs, any and all of which can be concurrently present in the same pig.

At postmortem, mature whipworms are readily seen buried in the mucosal surface of the cecum and colon. Laboratory fecal examination will identify the characteristic eggs, but clinical signs and gross lesions are present long before eggs are laid.

Treatment and control. Table 1 shows the anthelminthics that are effective against whipworms. As mentioned before, however, once removed from contaminated pastures and brought indoors, whipworms and several other internal parasites have been eliminated from domestic pigs.

In short, most parasitic diseases of pigs, very common in the last century, have been eradicated or reduced to very low prevalence in today's swine herds.

Of the external parasites, lice are virtually nonexistent and sarcoptic mange occurs rarely. Most internal parasites, though much reduced in prevalence, are still present and are still of clinical and economic importance. BP

S. Ernest Sanford, DVM, Dip. Path., Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington. Email: ernest.sanford@boehringer-ingelheim.com

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