Ascasris suum is a parasitic nematode from the family of Ascarididae. It is a widespread parasitic nematode which causes infection in swine that has high prevalence rates in the host population (Dold and Holland, 2010). The adult males are about 15 cm to 31 cm long and 2 mm to 4 mm in diameter. Its posterior end is curved ventrally, and its tail is bluntly pointed. Females are larger than males, measuring 20 cm to 49 cm long and 3 mm to 6 mm wide. The female can lay up to 200,000 eggs per day, and its uteri can contain up to 27 million eggs at a time but are shed intermittently (Roberts and Janovy, 2008). The eggs remain dormant in temperate regions and resume its development when the temperature rises. Eggs are highly resistant to chemical agents, but conditions with high temperature, direct sunlight, and low humidity, significantly reduce their survival. Within 3-4 weeks, the eggs can develop to an infective stage (eggs containing L3 larva), under optimal conditions (MSD Veterinary Manual, n.d.).
Adult worms live in the lumen of the small intestine of its host. Eggs around 200,000 produced by the female are passed through the feces. The unfertilized eggs can be ingested by the host but are not able to infect it. Depending on environmental conditions, the eggs can mature into an infective form after 18 days, but may take several weeks to do so. After the ingestion of the infective eggs, larvae will hatch in the small intestine and will then migrate to the cecum and proximal colon where it will penetrate the mucosa. The larvae then migrate through the portal circulation to reach the liver. After a short period in the liver, it will be then carried to the lungs by circulation. It will further develop in the lungs in which it will penetrate the alveolar space and move to the pharynx where it can be swallowed by the host. The larvae will return to the small intestine 10 to 15 days after the infection. Upon reaching the small intestine, the larvae will mature and reach sexual maturity (Dold and Holland, 2010; CDC, 2017).
Pathogenicity and distribution of Ascaris suum
Ascaris spp. affects a wide range of hosts including humans, poultry and livestock. An estimated 1.2 billion humans are infected with Ascaris lmbricoides with majority of the infection on sub-saharan Africa, Latin America and Asia (Nejsum et al, 2012). According to CDC, infections in humans are found in association with poor hygiene, poor sanitation, and in places where human feces are used as fertilizers. The study of Nejsum et al, 2012 also discussed the distribution of Ascaris suum in pigs with an emphasis on the effect of farming practices and geographic distribution on the said distribution and frequency of infection.
Heavy infestation of Ascaris spp. may cause vomiting, impaction of the bowel due to the obstruction of intestinal lumen by worms, anemia, emaciation and pendulous abdomen. The presence of the larvae in the lungs may cause pneumonia which would result in coughing with some exudation (Stewart and Hoyt, 2006). The piglets may show neurological signs. At post-mortem examination, apart from the presence of adult worms in the intestines, pathological lesions are found in the liver and the lungs as white spots caused by the granulation tissue due to migration of the larvae. Adult Ascarids in moderate number are relatively non pathogenic but it compete with its host for food and can therefore markedly reduce feed efficiency. Infections of A. suum may stimulate the development of strong protective immunity which depends on the level and length of exposure period. (Vlamink et al, 2014).
Biology and life cycle of Trichuris suis
T suis is also a parasitic nematode of swine. They are also known as whipworm because of having a broad short posterior end and a very long narrow whip-like anterior end which give the parasite a whip-like appearance (Pittman et al., 2010). The adult whipworms are white in color and about 3-5 cm long. The male adult tail is coiled and has a single spicule in a protrusible sheath while the female adult tail is curved. The adult worms are rarely recovered from the stool since they are embedded in the wall of the large intestine (Taylor et al, 2016). The eggs are lemon-shaped, measuring 50-70 µm in length by 25-35 µm in width, have a distinct plug at each pole and contain a single cell which are not infective. Eggs leave the host in manure and are able to survive for long periods in the environment (Bowman, 2014). The eggs of T suis are comparable to Ascaris eggs for they are also highly resistant to chemicals and may remain ineffective for 3-4 years (MSD Manual, n.d.).
The life cycle of T suis are direct (Zajac and Conboy, 2012), in which the eggs are being passed out into the feces where they become infective within 3-4 weeks, the eggs will develop into a 2-cell stage, an advanced cleavage stage, and then they differentiate in to a fertilized egg. The infection will start after the ingestion of eggs containing an infective first stage larva. The larvae hatch out and penetrate the intestinal wall to develop further before moving to the large intestine and cecum where they mature into adults. The adult worms live in the cecum and ascending colon and are fixed in that location with its anterior portions embedded into the mucosa. The adult female begins to lay eggs after 60-70 days of infection. It produces eggs up to 3,000 to 20,000 per day in the cecum. The lifespan of the adult worms is approximately 1 year (MSD Manual, n.d. & CDC, 2013).
Pathogenicity and distribution of Trichuris suis
According to the site of Centers for Disease Control and Prevention, an estimated 604-795 million people in the world are infected whipworm. As discussed in the study of Pitman et al., 2010 Trichuris suis is a parasite of swine but the infections can also be established in humans. The infection occurs by ingesting infective eggs through contaminated food, water or when rooting in contaminated soil. The infection induces strong immunity. Heavy infections may lead to the inflammation of the intestinal wall leading to weakening of the host and emaciation. During post mortem, very little damage is usually observed. However, in heavy infections, necrosis, oedema, and hemorrhage of the mucosa may be seen. Ulcer like lesions may be present in the cecum and colon. There may be nodule formation which are ganuloma like and contain anterior portion of the worms and eggs. The mucosa of the large intestines may be replaced by a necrotic diphtheritic membrane. (Stewart and Hoyt, 2006)
The incidence, rate, and intensity or severity of nematode infection can be influenced by factors such as age, breed, nutrition, and physiological state (Kusiluka and Kambarage, 2006). The prevalence of nematodes is generally thought to be higher in young animals than in adults (Kagira et al, 2003). This is due to higher immunogenicity of helminths which is important in the generation of acquired immunity in older animals. The physiological status of the animal may influence susceptibility to nematode infections. Hormonal changes during late pregnancy and lactation lower the resistance of the host to nematodes and consequently result in the establishment of higher worm burdens (Bethony et al., 2006; Mpairwe et al., 2014 )
Poor nutrition lowers the resistance of the animal thus enhancing the establishment of worm burdens and increasing the pathogenicity of the parasites. Worm burdens tend to be higher in poorly fed than in properly fed animals. Similarly, if animals are fed on helminth free diet, the chance of helminth infection decreased. Management structures for the animals affect the epidemiology of nematodes. High stocking density will increase the contamination of the environment with nematode eggs. This makes the infective stages to be more accessible to prone animals (Ghanem et al, 2009). Tethering animals during wet season may result in increased environmental contamination with the infective larvae and other clinical diseases (Kagira et al., 2003; Nissen et al., 2011)