Chapter 6 Parasitic zoonoses.
Cutaneous Larva Migrans
Cutaneous larva migrans (CLM), also known as larva migrans cutanea and creeping eruption, is an acute skin syndrome caused by migrating larvae of parasitic nematodes. CLM manifests as an erythematous (red), serpiginous (twisting), pruritic skin eruption caused by accidental skin penetration and migration of nematode larvae. A variety of nematodes cause CLM, including hookworms (named for their shepherd's hook appearance as adults) and Strongyloides worms (strongylo is Greek for round). CLM is the most commonly acquired tropical skin disease whose earliest description can be found more than 100 years ago. Hookworm infection occurs predominantly among the world's poorest people (Mohandas Gandhi had hookworm infection in the later part of his life). Infection caused by Ancylostoma duodenale, the nonzoonotic hookworm that causes diseases known as ground itch worldwide and sandworms in the southern United States, was described as early as the 1840s during the building of the St. Gotthard tunnel between Switzerland and Italy. The post civil war era in the United States (1870s-1880s) led to poor conditions in the south where people were thought to be lazy until it was discovered that hookworm infection (caused by Necator americanus) caused anemia in these southerners. In the southern United States hookworm infection was believed to be a contributing factor in the slowing of this region's economic development during the early part of the 20th century. In the late 1800s and early 1900s many homes in rural American states did not have indoor plumbing and were often plagued with diseases such as hookworm that were directly linked to improper sanitary facilities. Before 1900, few American physicians were aware of hookworm disease until Dr. Charles Wardell Stiles learned about hookworms while assisting with animal autopsies in Europe in the late 19th century. When Stiles returned to the United States, he worked for the Bureau of Animal Industry of the Department of Agriculture in Washington, D.C., and taught at Johns Hopkins School of Medicine, spreading information about the parasite and health problems associated with this nematode. In 1910, Dr. Stiles convinced John D. Rockefeller to donate $1 million to found the Rockefeller Sanitation Commission for the Eradication of Hookworm Disease and worked state by state to establish ways to combat hookworm disease through health education (building of enclosed outhouses), patient treatment (thymol, enemas, and tetrachloroethylene), and community cooperation. As a result of these efforts, hookworm prevalence is lower in the southern United States. Worldwide the disease is still a major health problem.
Stro. stercoralis was first discovered in 1876 in French soldiers who had been in Vietnam (then known as Cochin China). It was considered to be a harmless parasite for years; however, in the last 40 years it has been known to cause severe inflammatory and ulcerative bowel disease in people. It is now widespread in tropical and temperate countries (especially in institutions with poor hygiene). It is one of the few worms that is more prevalent in adults than in children.
Nonzoonotic parasites such as Ancylostoma duodenale (ankylo is Greek for bent and stoma is Greek for mouth) and Necator americanus (American killer) can also cause CLM in people.
CLM is caused by a variety of juvenile nematodes. The main nematode genus that causes CLM is Ancylostoma. Ancylostoma nematodes are stout with a curved anterior end giving the worm a hook-like appearance. There are two plates in their buccal capsule each with two large teeth that are fused at the base. A pair of small teeth is also found in this capsule (Figure 6-47). Adult males are about 8 to 11 mm in length and adult females are 10 to 13 mm in length. Each species has a unique bursa. Its normal life span is 1 year. Eggs are 50 x 30 [micro]m and have a thin, smooth, colorless shell with two-to eight-cell stage of cleavage (Figure 6-48). Zoonotic species include:
* An. braziliense (the canine and feline hookworm) is the most important zoonotic species causing CLM and is common in dogs and cats of the Gulf Coast and tropical areas in the Americas. It is also found in wild felines and various carnivores. An. braziliense is a parasite of dogs and cats whose third stage larvae can penetrate the superficial layers of human skin yet are unable to pass through the skin. Beaches, yards, and playgrounds frequented by infected dogs and cats may become heavily infested with larvae. An. braziliense is smaller than An. caninum and has only 2 ventral teeth on each side of the buccal cavity. The males are 5.0 to 7.5 mm long; females are 6.5 to 10.6 mm long. Eggs are 75 to 95 [micro]m in length.
* An. caninum (the canine hookworm) is the most common hookworm of domesticated dogs, especially in the Northern Hemisphere. An. caninum is also found in foxes, coyotes, wolves, bears, wild carnivores, and cats. It is also an important cause of eosinophilic enteritis in northeastern Australia and the United States. An. caninum is stout-bodied, grayish or reddish in color, and has 3 pairs of ventral teeth in the buccal cavity (Figure 6-1B). Males are 11 to 13 mm long; females are 14.0 to 20.5 mm long. Eggs are 56 to 75 [micro]m long.
* An. ceylonicum is a parasite found in dogs and cats in Sri Lanka, Southeast Asia, and the East Indies.
* An. tubaeforme (the feline hookworm) is a parasite found in cats and is generally distributed worldwide and throughout the United States. An. tubaeforme is intermediate in size between An. caninum and An. braziliense and has three teeth on each side of the buccal cavity. Males are 9.5 to 11.0 mm long; females are 12 to 15 mm long. Eggs are 55 to 76 [micro]m long.
CLM in people is caused by invasive juvenile nematodes that normally mature in animals other than humans.
[FIGURE 6-47 OMITTED]
[FIGURE 6-48 OMITTED]
Another genus of nematode that causes CLM is Strongyloides. Species of Strongyloides are among the smallest nematodes and can maintain parasitic life cycles with only the female of the species as a result of its parthenogenetic (without fertilization of the male) nature. Parthenogentic females are 2 to 2.5 mm in length; nonparasitic males are up to 0.9 mm in length. Both sexes have a small buccal capsule. Eggs are 50 to 58 [micro]m in length and are thin-shelled containing partially embryonated eggs. Zoonotic species include:
* Stro. stercoralis is the most common species worldwide and infects primates, dogs, cats, and other mammals. Stro. stercoralis is a small, slender nematode that is almost transparent and virtually impossible to see grossly at necropsy.
* Stro. fuelleborni occurs in Africa and is the hookworm of primates.
* Stro. papillosus is the hookworm of sheep, goats, and cattle.
* Stro. westeri is the hookworm of horses (known as the threadworm) and can cause bleeding and respiratory problems. In untreated foals it may cause diarrhea, weakness, weight loss and poor growth.
Other genera of nematodes that cause CLM include:
* Uncinaria stenocephala (the northern canine hookworm) is found in Europe. It can also be found in Canada and the northern parts of the United States (primarily in foxes and wolves). Its life cycle is similar to An. caninum. Percutaneous infection is rare with U. stenocephala in which 95% of the larvae fail to develop. U. stenocephala is a small hookworm, which does not have teeth, but two cutting plates in its mouth cavity. Males are 5 to 9 mm long; females are 7 to 13 mm long. Eggs are 63 to 76 [micro]m long.
* Bunostomum phlebotomum is the cattle hookworm. The adult male is about 9 mm and the female is up to 18 mm in length. Infection in cattle is by ingestion or skin penetration of the distal limbs. It is a stout worm (about 20 mm) with a large mouth and a body that may be hook-shaped. It may cause diarrhea, anemia, and sore feet in cattle.
* Gnathostoma spp. (cat, dog, and pig roundworms), Capillaria spp. (whipworms found in rodents, cats, dogs, and poultry), and Stro. myopotami (found in the small intestine of mammals) are rare causes of CLM. These are summarized in the less common nematode zoonoses chart.
Epizootiology and Public Health Significance
Ancylostoma and Strongyloides spp. occur worldwide with the greatest number of cases occurring in Asia and sub-Saharan Africa. Ancylostoma parasites live in sandy or loamy soil and cannot exist in clay or muck. Ancylostoma needs warm moist conditions where rainfall averages are more than 40 inches per year and the average temperature is greater than 50[degrees]F. An. braziliense is found mainly in tropical and subtropical areas; An. ceylanicum is found in Asia and the Middle East; An. caninum is found in the Northern Hemisphere and in northeastern Australia; An. tubaeforme is found in the United States. Stro. fuelleborni occurs more commonly in Africa. Uncinaria parasites are found mainly in Europe. Bunostomum parasites are found worldwide.
Strongyloides larvae move more quickly than other nematodes in human skin and produce a disease sometimes referred to as larva currens (racing larva).
The prevalence of hookworm CLM in the United States is unknown; but approximately 7% of travelers to clinics specializing in travel-related disease present with CLM. In the United States, most cases occur in eastern and southern coastal areas from New Jersey to Texas with the highest incidence in Florida. Worldwide CLM is indigenous to the Caribbean, Central and South America, Africa, and Southeast Asia.
The prevalence of Stro. stercoralis is likely underestimated because infection is often asymptomatic. Strongyloides is endemic in the Appalachian United States, especially in eastern Tennessee, Kentucky, and West Virginia. Worldwide prevalence is estimated as 2% to 20% in endemic areas. At-risk people include those who have recently traveled to or immigrated from endemic areas and veterans of World War II and Vietnam. Currently 100 to 200 million people are estimated to be infected worldwide in 70 countries. The mortality rate for patients requiring hospitalization with Strongyloides infection is approximately 17%. In disseminated strongyloidiasis, the mortality rate can be as high as 70% to 90%.
The prevalence of CLM caused by the other genera of nematodes is less frequent than those listed above and varies by region.
Hookworm (Ancylostoma, Uncineria, and Bunostomum) larvae of animals live in infected soil and penetrate human skin on contact (such as walking barefoot). In animals, transmission routes are percutaneous, prenatal, and transmammary. Young animals can be infected by ingestion of infective larvae from the environment or via the colostrum or milk of infected bitches (An. caninum). Infective larvae penetrate animal skin and migrate through the blood vessels to the lungs, enter the trachea, are coughed up, swallowed, and pass to the intestine where they complete their development. Colostral and lactogenic infection are also possible. In pregnant females, migrating larvae may pass to the placenta and enter the fetus. Transmission of U. stenocephala is similar to that of An. caninum except that dogs probably do not become infected by the prenatal or colostral routes.
CLM usually presents as one of three scenarios: barefoot children in areas frequented by hookworm-infested pets; travelers on exotic vacation who walk barefoot on their travels; and laborers (plumbers, masons, and electricians) working in hookworm-infected crawl spaces and dirt.
Infection with Strongyloides nematodes occurs by the percutaneous route with filariform third-stage larvae. In animals, autoinfections and transmammary infections also occur. Infection can also occur when a horse ingests larvae when eating grass. Mares can pass the nematode in their milk.
The life cycle of Ancylostoma starts when infected animals defecate thin-walled, unembryonated eggs with the feces. In warm, moist, sandy soil the eggs hatch to rhabditiform larvae in 1 to 2 days and molt twice to become infective filariform (third-stage) larva after 5 to 10 days. Filariform larvae may remain viable in the environment for up to 3 weeks. The infective filariform larvae live in the top one-half inch of the soil, with their ends projecting upward from the surface, waiting for people or animals to pass by. Larval skin penetration requires skin contact with contaminated soil for 5 to 10 minutes. Using proteases, the larvae penetrate through follicles, fissures, or intact skin of the new host (another animal or human). After penetrating the stratum corneum layer of the epidermis, the larvae shed their natural cuticle. Larvae typically begin migration in four days. In animal hosts, the larvae are able to penetrate into the dermis and are transported via the lymphatic and venous systems to the lungs. They break through into the alveoli and migrate to the trachea, where they are coughed up and swallowed. In the intestine they mature sexually, and the cycle begins again with secretion of their eggs. A hookworm produces an anticoagulant in its saliva so the animal host's blood does not clot at the site the hookworm attaches. If the worm moves from that site to reattach itself at another, the first site may continue to bleed, sometimes seriously. Humans are accidental hosts, and the larvae lack the collagenase enzymes required to penetrate the epidermal basement membrane to invade the dermis. Therefore, in humans, the disease remains limited to the skin (Figure 6-49). Only An. duodenalis (nonzootic) spreads beyond the skin.
Strongyloides is the only helminth to secrete larvae (and not eggs) in feces.
The Strongyloides life cycle is more complex than most nematodes because it alternates between free-living and parasitic cycles. In the free-living cycle rhabditiform larvae are passed in the stool and can either molt twice and become infective filariform larvae (direct development) or molt four times and become free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch. The filariform larvae penetrate the skin to initiate the parasitic cycle (ingestion, transmammary, and autoinfection are other transmission routes of Strongyloides but will not be discussed here). In the parasitic cycle filariform larvae in contaminated soil penetrate skin (the CLM manifestation) and are transported to the lungs where they penetrate the alveolar spaces. From the alveolar spaces they are carried through the bronchi to the pharynx, are coughed up, and are swallowed. Upon reaching the small intestine, they molt twice and become adult female worms. The females live in the epithelium of the small intestine and by parthenogenesis produce eggs (which yield rhabditiform larvae). The rhabditiform larvae can either be passed in the stool or cause autoinfection (rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection)) (Figure 6-50).
[FIGURE 6-49 OMITTED]
The life cycle of Uncinaria begins when the host ingests an infective third stage larva. The larva matures in the small intestine where adults produce eggs that are passed out with the feces. The eggs hatch in the soil and the larvae molt twice to reach the infective third stage. Infective larvae penetrate skin and cause disease as described for Ancylostoma.
The life cycle of Bunostomum begins when larvae penetrate the principal host and are transported via the blood to the lungs before proceeding to their preferred sites where they mature.
Clinical Signs in Animals
Parasites that cause CLM in people have the ability to mature into adult worms in animals. These adult parasites tend to cause gastrointestinal disease, whereas juvenile parasites may cause cutaneous and systemic disease.
[FIGURE 6-50 OMITTED]
Ancylostoma nematodes in dogs can cause an acute normocytic, normochromic anemia followed by hypochromic, microcytic anemia in young puppies and may be fatal. Debilitated and malnourished animals may continue to be unthrifty and suffer chronic anemia. Mature, well-nourished dogs may harbor a few worms asymptomatically; they are of primary concern as the direct or indirect source of infection for pups. Diarrhea with dark, tarry feces may accompany severe infections. Anemia, anorexia, emaciation, and weakness develop in chronic disease. Anemia rarely develops with An. braziliense or U. stenocephala. Dermatitis as a result of larval invasion of the skin may be seen with any hookworm but has been seen most frequently in the interdigital spaces with U. stenocephala; however, both genera can cause gastrointestinal disease including diarrhea and protein-losing enteropathies. Pneumonia may develop from overwhelming infections in puppies. In cats, An. tubaeforme causes weight loss and a regenerative anemia. Death can occur with heavy infestations. An. braziliense is less pathogenic in cats producing very little hemorrhage at the sites where adults attach. In cattle, Bunostomum adult worms can cause anemia, rapid weight loss, and alternating bouts of diarrhea and constipation. Hypoproteinemia may also be seen. Death can occur in calves.
Larval hookworms may cause clinical signs such as dermatitis where larvae penetrate the skin or from larval migration. The lesions may produce erythema, pruritus, and papules and are typically found on the feet and interdigital spaces. In most cases, these lesions resolve approximately 5 days after they appear. Some infections can be severe and result in self-inflicted trauma. Larval penetration of the distal limbs of cattle can cause them to stamp and there may be local skin lesions, edema, and scabs.
Heavy infection with Strongyloides may produce a blood-streaked, mucoid diarrhea typically in young animals (horses, cattle, dogs, and cats) during hot humid weather. Emaciation (even with good appetite) and reduced growth rate may be early signs of disease. In advanced stages, animals may develop shallow, rapid breathing and fever. Autoinfection may be induced by the use of corticosteroids.
Clinical Signs in Humans
CLM in people presents with a stinging sensation upon initial penetration of the larvae in the skin that develops into an erythematous papule or a nonspecific dermatitis hours after penetration. Larval penetration occurs most commonly in the feet (39%), followed by the buttocks (18%) and the abdomen (16%). Larvae migrate to produce a 2-to 4-mm wide erythematous, elevated, vesicular serpiginous track. Migration of the larvae through the skin varies with the nematode and ranges from a week to several months after initial penetration. The rate of larval migration ranges from 2 mm to 2 cm per day. An allergic response to the larvae or their byproducts may cause the pruritic, erythematous track. The actual location of the larvae is usually 1 to 2 cm beyond the tract (Figure 6-51).
[FIGURE 6-51 OMITTED]
Most Strongyloides infections are asymptomatic and can be present for decades undiagnosed. If symptoms occur they typically involve the gastrointestinal, pulmonary, and integumentary systems. Specific signs of disease by body system include:
* Skin penetration by larvae typically occurs on the feet and can produce cutaneous eruptions that are pruritic and vesicular. Larva currens (racing larvae) is the rash produced by Strongyloides infection that can creep 5 to 15 cm per hour. This rash is most likely an allergic response to the migrating larvae and looks like a pruritic wheal or linear urticaria. This skin manifestation may last hours to days.
* Gastrointestinal symptoms occur after larvae enter crypts of intestinal mucosa where they mature and invade tissue. Symptoms are vague and include anorexia, weight loss, nausea, chronic diarrhea, constipation, and bloating. Malabsorption may occur in chronic infections. As eggs hatch in the intestine, autoinfection is possible.
* Pulmonary symptoms occur when larvae migrate to and damage lung tissue. Initial symptoms are wheezing and a mild cough. Disseminated disease is associated with wheezing, dyspnea, cough, tachypnea, and hemoptysis.
Diagnosis in Animals
Ancylostoma, Uncinaria, and Bunostomum infections are diagnosed by identification of thin-shelled, oval eggs on flotation of fresh feces from infected animals.
Unlike in animals, the larvae are unable to penetrate the epidermal basement membrane of human skin resulting in the roaming of larvae haphazardly in the epidermis because they are unable to complete their life cycle.
Strongyloides larvae are identified from fresh fecal material using the Baermann technique to separate larvae from fecal material. Adult female worms can also be identified by scraping the mucosa of the small intestine (the presence of eggs in the uterus easily differentiates them from larvae of other nematodes). An ELISA test is also available.
Diagnosis in Humans
Diagnosis of hookworm CLM in people is based on the classic clinical appearance of the eruption. A minority of people demonstrates peripheral eosinophilia on a CBC and increased IgE levels on serum immunoglobulin tests. A skin biopsy sample, taken just ahead of the leading edge of a tract, may show a larva using periodic acid-Schiff stain.
Strongyloides larvae are seen in stool approximately 1 month after skin penetration. Baermann technique (larvae migrate from stool samples to warmed water and are detected in the centrifuged fluid), agar plate culture, direct fecal smear, or using Harada-Mori filter paper are recommended techniques for identification of Strongyloides. Larvae can be found in extraintestinal sites such as sputum, bronchoalveolar lavage, urine, semen, ascites, gastric biopsy, skin biopsy, and cerebrospinal fluid. ELISA tests are also available.
Treatment in Animals
In dogs, An. caninum and U. stenocephala infections can be treated with a variety of antinematodal drugs such as dichlorvos, fenbendazole, mebendazole, piperazine, pyrantel, pyrantel/febantel, and praziquantel/pyrantel/febantel. Milbemycin is also licensed for treatment of An. caninum infections. If anemia is severe, blood transfusions or supplemental iron and a high-protein diet may be needed until the hemoglobin levels are normal. Heartworm prevention with milbemycin, milbemycin/ lufenuron, and diethylcarbamazine/oxibendazole controls An. caninum, whereas pyrantel/ivermectin controls An. caninum, An. braziliense, and U. stenocephala. In cats, drugs approved for treatment of An. tubaeforme include dichlorvos, mebendazole, milbemycin, piperazine, pyrantel, pyrantel/praziquantel, and selamectin. Dichlorvos, mebendazole, and piperazine are also approved for treatment of U. stenocephala. Heartworm prevention with ivermectin, milbemycin, and selamectin controls An. tubaeforme, whereas ivermectin also controls An. braziliense. Bun. phlebotomum in cattle can be treated with febantel or ivermectin-based products.
Stronglyoides infections in dogs can be treated with ivermectin or thiabendazole. In cats, fenbendazole is used.
Treatment in Humans
Thiabendazole is currently considered the agent of choice for treating hookworm CLM in people. Topical application is used for early, localized lesions and oral treatment is used for widespread lesions or unsuccessful topical treatment. Other effective alternative treatments include albendazole, mebendazole, and ivermectin. Antibiotics are indicated if secondary bacterial infections are present. Untreated lesions resolve after the larvae die typically within weeks to months.
In all animals, feces should be examined posttreatment to confirm efficacy of the treatment.
Strongyloides infections should be treated even in the absence of symptoms with ivermectin or thiabendazole. Disseminated strongyloidiasis requires treatment for at least 7 days or until the parasite can no longer be identified in clinical samples.
Management and Control in Animals
Bitches should be free of hookworms prior to breeding and should be kept out of potentially contaminated areas during pregnancy. Whelping should occur in sanitary quarters. Concrete runways that can be washed are best for housing dogs. Prompt isolation of healthy dogs from dogs that appear unhealthy can prevent infection. Thorough washing of surfaces with steam or concentrated salt or lyme solutions, followed by rinsing with hot water, effectively destroys Strongyloides. In areas where both ascarids (nematodes in genera such as Ascaris, Toxocara, Toxascaris, and Baylisascaris) and hookworms are common, puppies and their mothers should be treated with an age-appropriate anthelmintic at 2, 4, 6, and 8 weeks of age (some recommend extending this to 12 weeks and then treating monthly until the pet is 6 months old). Because prenatal infection does not occur in kittens, preventive treatment should begin at 3 weeks of age, and be repeated at 5, 7, and 9 weeks. Nursing dogs and queens should be treated concurrently with their offspring because they often develop patent infections along with their young.
Management and Control in Humans
Human can prevent CLM by avoiding skin to soil contact (do not walk barefoot), defecating in proper facilities, avoiding the use of human and animal excrement or raw sewage as manure/fertilizer, deworming pets and livestock, and seeking medical care if mosquito-like bites on the sole of the foot turn into lines.
Cutaneous larva migrans (CLM) is caused by a variety of juvenile nematodes mainly in the genus Ancylostoma. Zoonotic species include An. braziliens, An. caninum, An. ceylonicum, and An. tubaeforme. Another genus of nematode that causes CLM is Strongyloides. Species of Strongyloides include Stro. stercoralis, Stro. fuelleborni, Stro. papillosus, and Stro. westeri. Other genera of nematodes that cause CLM include Uncinaria, Bunostomum, Gnathostoma, and Capillaria. Ancylostoma and Stronglyoides spp. occur worldwide with the greatest number of cases occurring in Asia and sub-Saharan Africa. Ancylostoma parasites live in sandy or loamy soil and cannot exist in clay or muck. Ancylostoma needs warm moist conditions where rainfall averages are more than 40 inches per year and the average temperature is greater than 50[degrees]F. Strongyloides parasites are found worldwide, although some species are found in higher proportions in certain regions. Uncineria parasites are found mainly in Europe. Bunostomum parasites are found worldwide.
Ancylostoma and Uncineria larvae live in infected soil and penetrate human skin on contact (such as walking barefoot). In animals, transmission may result from skin penetration, ingestion of infective larvae from the environment or via the colostrum or milk of infected dams (An. caninum) and transplacentally. Transmission of U. stenocephala is similar to that of An. caninum except that dogs probably do not become infected by the prenatal or colostral routes. Infection with Strongyloides nematodes occurs by the percutaneous route with filariform thirdstage larvae. Autoinfections and transmammary infections also occur. Infection can also occur when a horse ingests larvae when eating grass.
Ancylostoma nematodes in dogs can cause an acute normocytic, normochromic anemia followed by hypochromic, microcytic anemia in young puppies that may be fatal. In cats, An. tubaeforme causes weight loss and a regenerative anemia. Heavy infection with Strongyloides may produce a blood-streaked, mucoid diarrhea typically in young animals during hot humid weather. CLM in people presents with a stinging sensation upon initial penetration of the larvae that develops into an erythematous papule or a nonspecific dermatitis hours after penetration. Larval penetration occurs most commonly in the feet, followed by the buttocks, and the abdomen. Most Strongyloides infections are asymptomatic and can be present for decades undiagnosed. If symptoms occur they typically involve the gastrointestinal, pulmonary, and integumentary systems. Ancylostoma, Uncinaria, and Bunostomum infections are diagnosed by identification of thin-shelled, oval eggs on flotation of fresh feces from infected animals. Strongyloides larvae are identified from fresh fecal material using the Baermann technique to separate larvae from fecal material. Diagnosis of hookworm CLM in people is based on the classic clinical appearance of the eruption. Baermann technique, agar plate culture, direct fecal smear, or using Harada-Mori filter paper are recommended techniques for identification of Strongyloides.
In dogs, An. caninum and U. stenocephala infections can be treated with a variety of antinematodal drugs. In cats, many antinematodal drugs are approved for treatment of An. tubaeforme. Bunostomum infections in cattle are treated with febantel and ivermectin products. Stronglyoides infections in dogs can be treated with ivermectin or thiabendazole. In cats, fenbendazole is used. Thiabendazole is currently considered the agent of choice for treating hookworm CLM in people. Topical application is used for early, localized lesions and oral treatment is used for widespread lesions or unsuccessful topical treatment. Strongyloides infections should be treated even in the absence of symptoms with ivermectin or thiabendazole. Many control measures are recommended for these nematodes including testing bitches for hookworms prior to breeding, allowing whelping only in sanitary quarters using concrete runways for housing dogs, and isolation of healthy dogs from dogs that appear unhealthy can prevent infection. Humans can prevent CLM by avoiding skin to soil contact, defecating in proper facilities, avoiding the use of human or animal excrement or raw sewage as manure/fertilizer, deworming pets and livestock, and seeking medical care if mosquito-like bites on the sole of the foot turn into lines.
Visceral Larva Migrans
Visceral larva migrans (VLM), also known as larva migrans visceralis, is a syndrome caused by invasion of internal organs of the paratenic host (transport host where larvae do not undergo any development) by second-stage nematode larvae. When nematode larvae gain entry into an improper host, they do not complete the normal migration but instead have arrested development and begin an extended, random wandering through various body organs. VLM is caused by a variety of nematodes, but common species include Toxocara canis, To. cati, Baylisascaris procyonis, and Ascaris suum. To. canis is by far the most common species causing VLM and for many years it was believed that dog and cat nematodes could not infect humans. This was proven false in the early 1950s when Wilder discovered nematode larvae in eye tissue while performing histological studies at the Armed Forces Institute of Pathology. Wilder named the disease nematode endophthalmitis and concluded that it was an unrecognized cause of childhood blindness. Two years later Beaver demonstrated the larval form of To. canis as the causative agent of systemic disease causing cough, fever, and chronic eosinophilia in three children. As a result of the internal organ involvement the disease was termed visceral larva migrans to differentiate it from cutaneous larva migrans; however, an ocular form is also recognized.
Bay. procyonis is a common intestinal parasite of raccoons in North America with other species of this genus found in bears, skunks, and badgers. Baylisascaris was first described as As. procyonis by Stefanski and Zarnowski in 1951, but was later reclassified by Sprent in 1968 (named after H. A. Baylis of the British Museum). In many regions of the United States large populations of raccoons infected with Bay. procyonis live in close proximity to humans. Although documented cases of human baylisascariasis remain relatively uncommon, environmental contamination by infected raccoons suggests that the risk of exposure and human infection is substantial.
Ascaris worms, named from the Greek asketos meaning fidgety describing their movement, are among the largest nematodes and have been known since the times of Ancient Greece and Rome, Mesopotamia, and China. Descriptions of this parasite were recorded on papyrus in 1550 B.C. by the ancient Egyptians. When swine were domesticated and began living in close association with humans, the adaptation of the swine parasite into people was presumed to occur. The life cycle of Ascaris was not known until 1916 and is cosmopolitan in distribution especially prevalent in poor children in tropical countries with overcrowded slums and poor sanitation.
VLM is caused by a variety of juvenile nematodes. The main nematode genus that causes VLM is Toxocara. Zoonotic species include:
* To. canis. This species is the most important species causing VLM with dogs and other canines serving as definitive hosts. Mature worms are found in the intestines of the definitive host that sheds large numbers of unembryonated eggs into feces. Eggs become embryonated in the environment in about 9 to 15 days under optimal humidity and temperature (25[degrees]C to 30[degrees]C). To. canis adult males are about 4 to 6 cm in length and females are up to 15 cm in length. The tail of the male decreases in diameter and has five papillae on each side. Three lips and prominent cervical alae (cuticle expansion) are present in the adult worm. Eggs are 90 x 75 [micro]m long and are brownish, almost spherical with thick, finely pitted shells, and are unembryonated when laid.
* To. cati is widely distributed among domestic cats and other felines. The cervical alae of To. cati are shorter and broader than those of To. canis and the eggs are slightly different in their appearance. To. cati is more commonly seen in cases of human ocular larva migrans.
* To. vitulorum is a parasite found in cattle, is believed to be a low level zoonosis, and mainly affects children in the tropics. Young calves are infected by their mother's milk.
* To. pteropodis is a parasite of fruit bats (flying foxes) in Australia and is passed by the transmammary route.
Toxocara species with no reported zoonotic potential include To. tanuki, To. alienate, and To. mackerrasae. Two newer species with unresolved zoonotic status are To. malayasiensis (domestic cats) and To. lyncus (caracals).
Another genus of nematode that causes VLM is Bay. procyonis, also known as the raccoon roundworm. Bay. procyonis is the most common and widespread cause of clinical larva migrans in animals. Adult male worms are about 12 cm in length and females are 23 cm in length. Eggs are smaller than Toxocara eggs and are about 62 to 70 [micro]m long. Paratenic hosts (animals acting as substitute intermediate hosts of a parasite) include rodents, birds, and rabbits with human infections being rare. Other species of Baylisascaris are found in skunks (Bay. columnaris), badgers (Bay. melis and Bay. columnaris), bears (Bay. transfuga), fishers (Bay. devosi), and martins (Bay. devosi); no human infections have been reported from these species.
Another genus of nematodes that cause VLM is Ascaris. As. lumbricoides is a human parasite and As. suum is an intestinal nematode of pigs. Adults have three prominent lips and do not have alae. Adult males are between 15 to 30 cm in length and females are between 20 and 49 cm in length. Fertilized eggs are oval to round, are 45 to 75 [micro]m long, and have a thick, bumpy outer shell.
As. suum is morphologically identical to As. lumbricoides and are considered by some to be the same species.
Epizootiology and Public Health Significance
To. canis and To. cati occur worldwide in soil. To. vitulorum is found mainly in the tropics (also is present in the United States), whereas To. pteropodis is found in Australia. The prevalence of Toxocara VLM in the United States is unknown because it is not a reportable disease; but it is believed that approximately 10,000 human cases occur annually. Most cases are seen in children ages 1 to 7 years. Antibody titers to Toxocara in U.S. children are 4.6% to 7.3% (compared to 83% in the Caribbean). Titers are highest in the southeastern United States and Puerto Rico. Antibodies to To. canis worldwide are between 2% and 14%. Toxocara in dogs in the United States has been reported between 2% and 79% (10% to 85% in cats).
Baylisascaris parasites have been reported only from the United States and Europe. In the United States infected raccoons are more commonly found in the mid-Atlantic, northeastern and Midwestern states, and in parts of California. The prevalence of Baylisascaris is rare with only 25 cases reported in the United States in 2003. Five of the 25 cases were fatal and many survivors have permanent neurologic damage.
As. suum parasites are found worldwide, but particularly affect people living in warm, moist environments. Ascaris infections were estimated to be 643 million in 1947 and by 1979 between 800 million and 1 billion people were infected (it ranked third among human infections). Ascaris infections are common throughout Asia and are prevalent in Africa. Endemic regions exist in Canada and the Gulf Coast and southern Appalachian states of the United States (30% of the people may be infected).
To. canis infection in humans and dogs occurs by ingestion of embryonated eggs. Sources of embryonated eggs include sandboxes and playgrounds contaminated with dog feces. Dogs can also become infected by eating tissues containing hypobiotic (dormant) larvae found in prey (these larvae mature in the dog's intestines but do not migrate). Hypobiotic larvae also serve as a reservoir of infection in pregnant dogs as they become reactivated during the last third of pregnancy. Larvae enter the uterus or mammary glands where they can infect the fetus or puppy. To. cati infection in humans and cats occurs by ingestion of embryonated eggs. Cats can become infected after ingesting hypobiotic larvae. To. cati is not transmitted to cat fetuses through the placenta; however, kittens can be infected through the milk or colostrum. Humans can be infected with To. vitulorum by ingestion of embryonated eggs. To. vitulorum in cattle occurs by ingestion of embryonated eggs; calves become infected mainly through milk (larvae are in high numbers in milk during the first week after calving).
Baylisascaris infections in humans and raccoons occur from ingestion of embryonated eggs in soil, water, or on fomites. Raccoons can acquire the disease by ingestion of larvae in tissue of intermediate hosts (rodents).
Ascaris infections in humans and pigs occur from ingestion of embryonated eggs usually eaten with contaminated food and water.
The life cycle of Toxocara starts when the embryonated eggs are ingested and larvae hatch in the intestine (it takes unembryonated eggs 14 to 35 days to become embryonated eggs). Larvae invade the intestinal wall and are spread by the blood to the liver, heart, and lung. In young dogs the larvae penetrate the alveolar wall; migrate to the bronchioles, bronchi, and trachea; reach the pharynx; are swallowed into the esophagus, and reach the small intestine. When the larvae reach the intestines the second time, they develop into adults, mate, and produce eggs that are passed in the feces. Occasionally immature larvae may also be found in feces. In older puppies and adult dogs, many larvae do not complete migration to the lungs and the larvae travel to the muscles, liver, kidneys, and other viscera where they become dormant. In humans, larval migration ends on route to the lung or ends in the lung or the larvae enter the arterial system and are disseminated throughout the body. Larvae leave the blood vessels where they generally become encapsulated by connective tissue. Encapsulated larvae may survive for years and may become reactivated. Larvae can be transmitted between people by cannibalism.
Adult To. canis nematodes survive approximately 4 months in the intestines and most of the parasites have been expelled in the feces within 6 months of infection.
Any age of dog can also develop patent infections if they ingest tissues (rodent or other mammal) containing hypobiotic larvae. These larvae mature in the dog's intestines without further migration. Hypobiotic larvae may also serve as a reservoir of infection in pregnant dogs. Hypobiotic larvae become reactivated during the last third of pregnancy, enter the uterus or mammary glands, and infect the fetus or puppy. Fetuses acquire the parasites in utero where they then enter the liver, migrate through the lungs, and develop into adults (in about 3 weeks). Larvae acquired through milk do not migrate through tissues instead they complete their development in the intestines. Bitches can acquire infections during lactation from movement of hypobiotic larvae to the intestines or from ingestion of larvae from contaminated puppy feces. These infections in bitches spontaneously resolve in 4 to 10 weeks after parturition (Figure 6-52).
The life cycle of To. cati is similar to To. canis except that To. cati is not transmitted in utero.
Raccoons become infected with Bay. procyonis by ingesting embryonated eggs or larvae in tissue of intermediate hosts. Larvae hatch in the intestine, develop in the intestinal wall, and complete their maturation in the intestinal lumen. Extraintestinal migration does not appear to occur in raccoons. Unembryonated eggs are excreted in raccoon feces, develop for at least 2 to 4 weeks in the environment, and become infective. Humans become infected when they ingest embryonated eggs. Migrated larvae may be found in the liver, heart, lungs, CNS, and eyes. Bay. procyonis is different from other nematodes that cause larva migrans because of its aggressive tissue migration and invasion of the CNS, its continued growth of larvae to a large size within the CNS, and its resistance to dying once in the paratenic host (Figure 6-53).
[FIGURE 6-52 OMITTED]
Ascaris infection is acquired through ingestion of embryonated eggs that hatch in the cecum and proximal colon, penetrate the intestinal wall, and enter lymphatics or venules. The larvae pass through the right side of the heart, enter the pulmonary circulation, penetrate the alveolar wall, move to the bronchioles to the bronchi to the trachea, reach the pharynx, are swallowed, and reach the small intestine where they mature. In humans, As. suum larvae can enter the liver and lungs producing an eosinophilic pneumonia and liver lesions (Figure 6-54).
[FIGURE 6-53 OMITTED]
Clinical Signs in Animals
Toxocara nematodes in young puppies can cause poor growth, an enlarged abdomen, diarrhea, constipation, vomiting, flatulence, and coughing. Chronic enteritis can produce intestinal wall thickening or intussusception. In severe cases, gall bladder obstruction, bile or pancreatic duct obstruction, or intestinal rupture may occur. As the larvae pass through the liver and lungs inflammation and respiratory distress may be observed. Elevated liver enzymes may be seen during larval migration and ocular signs such as retinal disease have been described. Clinical signs are rare in adult dogs.
[FIGURE 6-54 OMITTED]
In cats, To. cati infection does not occur in utero; therefore, kittens are older when larvae are migrating. Many infections in kittens are asymptomatic, but heavy infections can cause abdominal distension, rough coat, diarrhea, and dehydration. Adult cats tend to be asymptomatic. In calves, To. vitulorum causes anorexia, abdominal pain, diarrhea, constipation, dehydration, weight loss, and poor gain.
As the primary hosts, raccoons appear to tolerate Bay. procyonis in their small intestine, and extensive migration of the parasite beyond the intestinal lumen does not seem to take place. Heavy infections in young raccoons can cause intestinal obstruction. In dogs, infection does not cause overt clinical signs and is typically discovered on routine fecal examinations.
Young pigs infected with As. suum may show clinical signs of reduced growth rate and in heavy infections may have intestinal obstruction. Adult worms can migrate into the bile ducts producing icterus especially in hogs in transit to slaughter who have long periods of time between feedings. Larval migration to the liver can cause hemorrhage and fibrosis; in the lungs pulmonary edema may occur.
Clinical Signs in Humans
Larva migrans as a result of Toxocara, also known as toxocariasis, in people presents in three forms:
* Visceral. Most cases of VLM are asymptomatic and are discovered via routine blood work demonstrating persistent eosinophilia. Signs in children include lethargy, fever, hepatomegaly, and cranial abdominal pain. Less common signs include nausea, vomiting, wheezing, coughing, dyspnea, pruritic rashes, lymphadenopathy, muscle pain, and neurologic signs. Symptoms may persist for months with deaths being rare.
* Ocular. Cases of ocular larva migrans can cause a variety of clinical disease including retinal granulomas, retinal detachment, uveitis, keratitis, vitreous abscesses, and endophthalmalitis. Infection is typically unilateral and a single larva is responsible for the symptoms. Vision loss may be progressive or sudden and may be permanent.
* Covert. In the covert form, antibodies to Toxocara cause symptoms that cannot be related to the other syndromes. The most common clinical sign is abdominal pain followed by hepatomegaly, coughing, sleep alteration, headaches, rash, pruritus, and respiratory distress. The covert form is not always associated with eosinophilia and this form can last for months or years.
Two syndromes have been described for people with Baylisascaris infections:
* Visceral. Bay. procyonis visceral larva migrans (also called neural larva migrans or cerebrospinal nematodiasis) presents as acute fulminant eosinophilic meningoencephalitis producing symptoms that include incoordination, ataxia, torticollis, nystagmus, and mentation changes. These symptoms may lead to stupor and coma. Once invasion of the CNS has occurred, the prognosis is grave with or without treatment.
* Ocular. Ocular larva migrans is typically unilateral and occurs when larvae migrate to the eye. Clinical signs include photophia, retinitis, and blindness.
Clinical signs in humans caused by Ascaris infections include pneumonitis (as a result of hemorrhage at the site causing blood to pool in the alveoli), abdominal pain, rashes, ocular pain, and restlessness. Heavy infections can cause intestinal blockage that may become fatal.
Diagnosis in Animals
All nematodes causing VLM can be diagnosed via fecal floatation and identification of eggs. Toxocara eggs are between 90 and 75 [micro]m in length, contain a single dense cell mass and a thick, brown outer shell. The shell has distinctive fine pits in its proteinaceous coat. Larvae may also be seen in feces or vomitus. Eggs may be shed intermittently in dogs. Baylisascaris eggs are similar to Toxocara eggs but are smaller (62 to 70 [micro]m in length). Ascaris eggs are oval to round, 45 to 75 [micro]m in length and have a thick, bumpy outer shell (Figure 6-55).
A single To. canis female worm can produce 200,000 eggs per day.
[FIGURE 6-55 OMITTED]
An ELISA test has been used to detect nonpatent Toxocara infections in dogs. Baylisascaris is difficult to diagnose in live animals, but the larvae may be found in tissue biopsy. Baylisascaris larvae are 50 to 70 [micro]m in diameter and have a prominent single lateral alae. Ascaris larvae may be found in sputum.
Diagnosis in Humans
People with Toxocara infections are typically diagnosed by clinical signs, ophthalmic examination, and routine blood tests (eosinophilia). Histopathology is not routinely used for diagnosis. Humans infected with VLM do not produce or excrete eggs; therefore, fecal examination is not a useful diagnostic tool. Serologic tests such as ELISA and immunoblot assays are used in humans. PCR tests have been developed but are not currently used in the United States.
Baylisascariasis is diagnosed by complete blood count (CBC) and CSF examination and biopsy. Serologic tests are not commercially available but are available in research laboratories (ELISA, indirect immunofluorescence, and immunoelectrotransfer).
Ascariasis is diagnosed by fecal floatation and identification of eggs. Larvae may be seen in sputum, but are difficult to accurately identify by most technicians.
Treatment in Animals
In dogs and cats, Toxocara infections can be treated with a variety of antinematodal drugs such as fenbendazole, mebendazole, and piperazine. Treatment of puppies/kittens and nursing bitches/queens should be done at the same time. Because most antinematodal drugs kill the adult worm, these drugs should be repeated at 2-to 4-week intervals. The CDC recommends puppies receive anthelmintic drugs at 2, 4, 6, and 8 weeks of age. The Companion Animal Parasite Council recommends year-round treatment with broad-spectrum heartworm anthelmintics that also have activity against parasites with zoonotic potential.
Dogs or raccoons infected with Baylisascaris can be treated with a variety of antinematodal drugs including piperazine, pyrantel, ivermectin, moxidectin, albendazole, and fenbendazole. Ascaris infections in swine can be treated with piperazine, dichlorvos, fenbendazole, and pyrantel.
Treatment in Humans
Anthelmintic drugs such as thiabendazole, mebendazole, and albendazole can be used to treat severe cases of VLM caused by Toxocara. Anti-inflammatory drugs such as corticosteroids may be needed to counteract the severe hypersensitivity reactions caused by dying larvae. Treatment of ocular disease may require surgery.
Baylisascaris infections can be treated with thiabendazole, fenbendazole, levamisole, and ivermectin, but the clinical outcome is poor. Corticosteroids can be used to counteract hypersensitivity reactions. Laser photocoagulation has been used for ocular larva migrans. Ascaris infections are treated with mebendazole, ivermectin, or pyrantel pamoate.
Management and Control in Animals
Puppies and kittens should be dewormed to eliminate shedding of Toxocara eggs. Puppies should begin deworming programs at 2 weeks of age, repeated at 2-week intervals. In kittens, prenatal infection does not occur and egg excretion begins later than in puppies. Deworming for kittens can begin at 3 weeks of age and repeated at 5, 7, and 9 weeks. Removal of feces and cleaning of kennels is essential in preventing Toxocara infections. Sand boxes should be covered when not in use.
Baylisascaris infections in dogs can be reduced by avoiding contact with raccoons and their feces (eggs may remain infective for years under ideal conditions). Raccoons should be discouraged from visiting backyards and farms, including preventing access to food, garbage, attics, and basements. Sand boxes should be covered when not in use. Removal of brush may discourage raccoons from making a den on someone's property.
Ascaris infections in swine can be reduced by strategic deworming and waste removal. The antibiotic hygromycin has been effective as a feed additive in reducing Ascaris levels.
Management and Control in Humans
Humans can prevent VLM caused by Toxocara by having pets strategically dewormed, removing feces from the environment before they become embryonated, enforcing leash laws and collection of feces by pet owners, proper hygiene (washing hands and raw foods), controlling pica in children, and public education. Families may want to consider not getting a pet until children are past the toddler stage.
VLM as a result of Baylisascaris infections can be reduced by avoiding contact with raccoons and their feces (not feeding raccoons, removing brush near homes, keeping food and garbage in raccoon-proof containers). Raccoons tend to use latrines where they regularly defecate (usually at the base of trees, near fallen logs, large rocks, woodpiles, decks, and rooftops). Raccoons should not be kept as pets (even very young raccoons are often infected with Baylisascaris).
VLM as a result of Ascaris infections can be reduced by limiting contact with pigs, strategic deworming of pigs, and proper hygiene.
Visceral larva migrans (VLM) is a syndrome caused by invasion of internal organs of the paratenic host by second-stage nematode larva. VLM is caused by a variety of nematodes, but common species include To. canis, To. cati, Bay. procyonis, and As. suum. To. canis is the most important species causing VLM with dogs and other canines serving as definitive hosts. Mature worms are found in the intestines of the definitive host that shed large numbers of unembryonated eggs into feces. To. cati is widely distributed among domestic cats and other felines. Bay. procyonis is the most common and widespread cause of clinical larva migrans in animals. As. lumbricoides is a human parasite and A. suum is an intestinal nematode of pigs. To. canis and To. cati occur worldwide in soil. Baylisascaris parasites have been reported only from the United States and Europe. As. suum parasites are found worldwide, but particularly affect people living in warm, moist environments. To. canis infection in humans and dogs occurs by ingestion of embryonated eggs. Dogs can also become infected by eating tissues containing dormant larvae found in prey. In pregnant dogs reactivation of dormant larvae may occur during the last third of pregnancy and larvae may enter the uterus or mammary glands where they can infect the fetus or puppy. To. cati infection in humans and cats occurs by ingestion of embryonated eggs. Cats can become infected after ingesting dormant larvae (To. cati is not transmitted to cat fetuses through the placenta). Kittens can be infected through the milk or colostrum. Baylisascaris infections in humans and raccoons occur from ingestion of embryonated eggs in soil, water, or on fomites. Raccoons may also acquire the disease by ingestion of larvae in tissue of intermediate hosts. Ascaris infections in humans and pigs occur from ingestion of embryonated eggs usually eaten with contaminated food and water. Toxocara nematodes in young puppies can cause poor growth, an enlarged abdomen, diarrhea, constipation, vomiting, flatulence, and coughing. Chronic enteritis can produce intestinal wall thickening or intussusception. Many infections in kittens are asymptomatic, but heavy infections can cause abdominal distension, rough coat, diarrhea, and dehydration. Adult cats tend to be asymptomatic. Larva migrans as a result of Toxocara in people presents in three forms: visceral, ocular, and covert. As the primary hosts, raccoons appear to tolerate Bay. procyonis in their small intestine, and extensive migration of the parasite beyond the intestinal lumen does not seem to take place. Two syndromes have been described for people with Baylisascaris infections: visceral (mainly neurologic) and ocular. Young pigs infected with Ascaris suum may show clinical signs of reduced growth rate and in heavy infections may have intestinal obstruction. Clinical signs in humans caused by Ascaris infections include pneumonitis, abdominal pain, rashes, ocular pain, and restlessness.
All nematodes causing VLM can be diagnosed via fecal floatation and identification of eggs. An ELISA test has been used to detect nonpatent Toxocara infections in dogs. Identification of larvae may be helpful in diagnosis. People with Toxocara infections are typically diagnosed by clinical signs, ophthalmic examination, and routine blood tests (eosinophilia). Serologic tests such as ELISA and immunoblot assays are used in humans. PCR tests have been developed but are not currently used in the United States. Baylisascariasis is diagnosed by CBC and CSF examination and biopsy. Ascariasis is diagnosed by fecal floatation and identification of eggs. In dogs and cats, Toxocara, Baylisascaris, and Ascaris infections can be treated with a variety of antinematodal drugs. Anthelmintic drugs can be used to treat severe cases of human VLM. Anti-inflammatory drugs such as corticosteroids may be needed to counteract the severe hypersensitivity reactions caused by dying larvae. To prevent VLM, puppies and kittens should be dewormed to eliminate shedding of Toxocara eggs. Removal of feces and cleaning of kennels is essential in preventing Toxocara infections. Sand boxes should be covered when not in use. Baylisascaris infections in dogs can be reduced by avoiding contact with raccoons and their feces. Ascaris infections in swine can be reduced by strategic deworming and waste removal. Humans can prevent VLM caused by Toxocara by having pets strategically dewormed, removing feces from the environment before they become embryonated, enforcing leash laws and collection of feces by pet owners, proper hygiene, controlling pica in children, and public education. VLM as a result of Baylisascaris infections can be reduced by avoiding contact with raccoons and their feces. VLM as a result of Ascaris infections can be reduced in people by limiting contact with pigs, strategic deworming of pigs, and proper hygiene.
Dracunculiasis, also known as Guinea worm infection, is a disease characterized by inflammation and cutaneous ulcers in the distal limbs as a result of the presence of Dracunculus medinensis (the Guinea worm) in the subcutaneous tissue. Dracunculus comes from the Greek drakontion meaning little dragon, which describes the serpent-like appearance of the worm in cutaneous tissue. For centuries, D. medinensis was associated with the cities of Medina (Saudi Arabia) and Guinea (West Africa), whose populations had an unusually high incidence of the disease and where the species and common names of the nematode are derived. The Guinea worm has been known since ancient times when the disease and its treatment were described in the Ebers papyrus around 1550 B.C. Calcified Guinea worms were found in Egyptian mummies and the description of the plague of the fiery serpents during the Hebrews' exodus from Egypt referred to Guinea worm infection. Early Greek and Roman physicians associated Guinea worm infection with particular water sources. During the Middle Ages a Persian physician identified the worm and during the 11th century Avicenna described dracunculiasis, its treatment, and complications. Drawings of the worm were made in 1598, winding the worm out on a stick as a cure was described in 1674 by Velschius, descriptions of the adult worm were made by Linnaeus in 1758, and by 1871 its detailed life cycle was identified by Fedchenko. European physicians were not aware of the Guinea worm until the 19th century when the British army medical officers started to see signs of the worm in soldiers serving in India. Slaves transported from the Gulf of Guinea to the New World from the 17th century onward were often infected with Guinea worms; however, dracunculiasis never became a problem in the Americas with only a few areas in northern South America establishing the disease. Dracunculiasis has been identified in the early 1980s by the WHO as a disease on its eradication list and by 1996 eradication has been 97% completed. In 1947 there were an estimated 48 million people infected with D. medinensis; in 1998 there were an estimated 70,000 people infected with the Guinea worm. If global elimination of Guinea worm infection is achieved, dracunculiasis will be the third disease eradicated in world history (smallpox was the first; SARS was the second).
Dracunculiasis is caused by D. medinensis, one of the largest known nematodes, and is a parasite of humans, dogs, horses, cattle, wolves, leopards, monkeys, and baboons. Males may reach a length of 4 cm and females may reach a length of 120 cm. The adult worm has a small, triangular mouth without lips and has both dorsal and ventral papillae. In females the gravid uterus has an anterior and posterior branch containing hundreds of thousands of embryos. Males are typically 12 to 40 mm long with unequal spicules. Larvae are 500 to 700 [micro]m long. D. medinensis is ovoviviparous with larvae developing within eggs that remain within the female until they hatch (larvae are provided with a sheltered environment). Eggs are not used in the identification of this organism.
D. medinensis is also known as the Medina worm, Guinea worm, serpent worm, dragon worm, pharaoh worm, and Avicenna worm.
D. insignis is the Guinea worm of North American wildlife in which the male worm is approximately 20 mm long and the female is 300 mm long. D. insignis has been reported in the raccoon, mink, striped skunk, fox, muskrat, fisher, short-tailed weasel, opossum, badger, Bonaparte weasel, and dog in the United States and Canada. Raccoons are the most favorable definitive host for D. insignis in North America. This species was first described by Leidy in a short account in 1858 and confirmed as a separate species by Chitwood in 1950; however, this species is not accepted by all authorities.
D. lutrae is the species of Guinea worm that has only been found in river otters in Ontario, New York, and Michigan. Other species of Dracunculus are summarized in Table 6-8.
Epizootiology and Public Health Significance
Dracunculiasis was widespread in Africa and Asia prior to eradication programs begun by the WHO in 1986. Dracunculiasis is currently reported in 13 countries in Central, East, and West Africa. In 1986, there were an estimated 3.5 million cases of dracunculiasis in 20 countries, with 120 million persons at risk for contracting the disease. By the end of 2004, Asia was free from dracunculiasis. The remaining countries where dracunculiasis is endemic are all in Africa; however, there has been a reported 50% reduction in the number of cases from 2003 to 2004 (from 32,193 to 16,026). In 2005, Ghana and Sudan have reported 95% of the world's cases; however, Ghana reduced its cases by 53% during the first half of 2005.
Infection with D. medinensis in people occurs by ingestion of the intermediate host (the crustacean Cyclops spp.) in water. Dogs and other animals can become infected with D. insignis by ingestion of contaminated water or a paratenic host (frogs or fish). Transmission of D. insignis in raccoons is confined to only a few weeks of the year. Adult worms are usually patent in late spring or early summer corresponding with changes in the raccoon's food habits. Mink infections are not as seasonal as raccoon infections as a result of the mink's year-round feeding on aquatic life.
In general, Guinea worms in mammals are regarded as D. medinensis in the Old World and South America and as D. insignis in North America.
D. lutrae is transmitted to river otters through ingestion of contaminated water or a paratenic host, but there is not the seasonal infection rate because of the river otter's year-round food habits.
Inside the definitive host (human, dog, raccoon), the ingested Cyclops is destroyed by stomach acids. Once the larvae are freed they penetrate the duodenal lining, enter the lymphatic system, and migrate to subcutaneous tissues. Larvae molt at about 20 days postinfection and molt a final time at approximately 43 days. Once in subcutaneous tissue the worms mature slowly, reaching full maturity in one year. After the adults mate (by the third month after infection), the male dies, becomes encysted, and degenerates. Gravid females migrate to the skin between the eighth and tenth months (embryos in the uterus are fully mature) causing an allergic reaction as a result of the release of metabolic wastes into the skin. Between 10 and 14 months postinfection the female worm produces a pruritic blister in the skin (90% of lesions are found in the feet and legs). When these blisters are exposed to water (such as a river or lake) the female's uterus ruptures and releases large numbers of larvae into the water. The larvae can live for 6 days in clean water and 2 to 3 weeks in muddy water. Larvae are ingested by the crustacean Cyclops. Once ingested, the larvae mature into their infective stage in approximately 14 days and can then reinfect humans (Figure 6-56).
Dracunculus infections in domestic animals in endemic areas are possibly of human origin.
[FIGURE 6-56 OMITTED]
Clinical Signs in Animals
D. medinensis infections although rare have been reported in dogs in endemic regions. The main clinical sign in dogs is the development of cutaneous ulcers. D. insignis, a species found in North America, can infect the subcutaneous connective tissues of the legs of raccoons, mink, opossums, muskrats, and other animals, including dogs. They produce 3 to 5 cm cutaneous, nonhealing ulcers through which the female worm's anterior end is protruded upon contact with water. Infections in animals are rare but are occasionally found in animals that spend time around small lakes and shallow, stagnant water. Lesions are typically found on the limbs. Dehydration, vomiting, diarrhea, and dyspnea are also common symptoms of infection.
Dracunculus is the only parasite known to be solely transmitted by water consumption.
Clinical Signs in Humans
D. medinensis infections are asymptomatic in people until the female worm reaches the skin approximately 10 to 12 months after acquiring the worm. Once the worm is near the skin surface people develop a blister in the epidermis and may develop a fever. Prior to blister formation, allergic-type symptoms, such as wheezing and pruritus, are often present. As the blister grows it becomes erythematous at the edges, edema occurs, and inflammation causes pruritus and a burning sensation (Figure 6-57). Typically the blister ruptures in a few days (relieving the pain and swelling) and the female worm releases larvae-containing fluid.
[FIGURE 6-57 OMITTED]
After the blister ruptures an ulcer forms around the blister site as the adult worm continues to emerge. Secondary bacterial infections can occur as bacteria are drawn under the skin by a retreating worm. Worms that fail to reach the skin can cause complications in deeper tissues when they begin to degenerate and release antigens. Complications include aseptic abscesses and arthritis. Other worms that do not reach the skin may calcify or be resorbed. Calcified worms can cause problems as a result of the pressure they can put on tissues.
D. insignis does not parasitize humans; although some people believe that D. medinensis infections in the United States may actually be caused by D. insignis.
Diagnosis in Animals
Dracunculiasis is typically diagnosed by palpation of the worm in a skin nodule or by examination of larvae from an ulcerated skin nodule.
Diagnosis in Humans
Clinical diagnosis of dracunculiasis in people is made when larvae can be found in ulcers and identified by microscopic examination. When the adult female worm emerges from the ruptured nodule, it can be identified as a probable Guinea worm infection.
Treatment in Animals
Treatment in animals is by careful extraction of the parasite. Repeated wetting of the wound helps release most of the larvae. Administration of anthelmintics such as niridazole or benzimidazole may be useful in facilitating the worm's removal.
Treatment in Humans
Treatment in people is by winding the anterior end of the worm around a stick (Figure 6-58). One to 2 weeks is necessary to complete removal. Rupturing of the worm during extraction may cause severe inflammation. Metronidazole or niridazole can be used in treating Dracunculus infections although these drugs do not kill the worm but rather facilitate its removal. Analgesics and wound care are also advised.
[FIGURE 6-58 OMITTED]
Management and Control in Animals
Although dracunculiasis is rare in animals, preventing animals from using or coming in contact with contaminated water may help prevent this disease. Controlling wildlife infections is more difficult and has not been attempted in a large scale way.
Management and Control in Humans
The WHO declared in early 1980s that one of its goals was the eradication of dracunculiasis by 1995. Although the disease is not eradicated, it had a rapid and sustained reduction in all countries other than Sudan. Strategies for controlling this disease include providing safe drinking water (boiled and filtered), preventing infected persons from entering the water of ponds and stepwells, health education (including instruction on the use of cloth water filters), early treatment and bandaging of lesions, and vector control using temephos that kills Cyclops crustaceans.
Dracunculiasis, also known as Guinea worm infection, is caused by D. medinensis, one of the largest known nematodes, and is a parasite of humans, dogs, horses, cattle, wolves, leopards, monkeys, and baboons. Males may reach a length of 4 cm and females may reach a length of 120 cm. D. medinensis is ovoviviparous with larvae developing within eggs that remain within the female until they hatch (larvae are provided with a sheltered environment). Dracunculiasis was widespread in Africa and Asia prior to eradication programs begun by the WHO in 1986. Dracunculiasis is currently reported in 13 countries in Central, East, and West Africa. Infection with D. medinensis occurs by ingestion of the intermediate host (the crustacean Cyclops spp.) in water. Dogs and other animals can become infected with D. insignis (which is not believed to be zoonotic) through ingestion of contaminated water or a paratenic host (frogs or fish). Inside the definitive host (human, dog), the ingested Cyclops is destroyed by stomach acids, larvae are freed and penetrate the duodenal lining, enter the lymphatic system, and migrate to subcutaneous tissues. Between 10 and 14 months postinfection the female worms produces a pruritic blister in the skin and these blisters are exposed to water (such as a river or lake) the female worm's uterus ruptures and releases large numbers of larvae into the water. Larvae are ingested by the crustacean Cyclops and mature into their infective stage in approximately 14 days and can then reinfect humans. D. medinensis infections although rare have been reported in dogs in endemic regions producing cutaneous ulcers. D. medinensis infections are asymptomatic in people until the female worm reaches the skin approximately 10 to 12 months after acquiring the worm. Once the worm is near the skin surface people develop a blister in the epidermis and may develop a fever. Typically the blister ruptures in a few days and the female worm releases larvae-containing fluid. Dracunculiasis in animals and people is typically diagnosed by palpation of the worm in a skin nodule or by examination of larvae from an ulcerated skin nodule. Larvae can be found in ulcers and identified by microscopic examination. Treatment in animals and people is by careful extraction of the parasite. Administration of anthelmintics (niridazole or benzimidazole) may be useful in facilitating the worm's removal. Preventing animals from using or coming in contact with contaminated water may help prevent this disease. Strategies for controlling this disease in people include providing safe drinking water, preventing infected persons from entering the water of ponds and stepwells, health education, early treatment and bandaging of lesions, and vector control using temephos that kills Cyclops crustaceans.
[FIGURE 6-59 OMITTED]
Filarial Nematode Zoonoses
Filarial nematodes are a group of parasitic worms found in the blood and tissue of its host. Filarial nematodes rely on an arthropod vector (intermediate host) to complete its life cycle and to be transmitted to another animal (Figure 6-59). Larval filarial nematodes are known as microfilariae and are found in the blood or in subcutaneous tissue (Figure 6-60). There are many human or primate only filarial nematodes such as Onchocera volvulus (river blindness), Wuchereria bancrofti (elephantiasis), and Loa loa (loiasis). Zoonotic filariasis occurs when humans are infected with larva that normally infect animals and cannot complete their life cycle in humans. Zoonotic filarial nematodes are summarized in Table 6-9.
[FIGURE 6-60 OMITTED]
Trichinosis, also known as trichinellosis, trichinelliasis, and trichina infection, is caused by the intestinal nematode Trichinella spiralis. Trich. spiralis is named from the Latin tricho meaning hair and spira meaning coil used to describe the appearance of the nematode in muscle tissue. Trichinosis is common in carnivorous mammals primarily on North American and Eurasian continents. Humans typically acquire trichinosis by eating pork infected with the encysted larvae and may be the basis for the tradition of avoiding pork in Mosaic and Islamic religions. The association between Trichinella infections and pigs has been recognized for a long time; however, the encysted larvae in the muscle were not seen until 1821. The discovery of the worm in humans in 1835 was made by James Paget, a first-year medical student at St. Bartholomew's Hospital in London and later knighted as a distinguished physician. Paget described Trichinella infection in muscle tissue of the diaphragm in a paper presented at the Abernethien Society February 6, 1835. Richard Owen, who is attributed with the discovery of trichinosis, actually presented Paget's paper to the Zoological Society 18 days after Paget's presentation. Adult Trichinella worms were discovered by Rudolf Virchow in 1859. In 1860, Friedrich Zenker demonstrated the clinical significance of eating infected raw pork and the development of Trichinella infection. By the late 1860s, trichinosis was well recognized as a disease spread through infected pigs, leading to a cultural aversion to certain pork products such as German and Dutch sausage. Since 1895 the causative agent of trichinosis was known as Trich. spiralis, but since then there have been several species, subspecies, or strains of Trichinella; however, no morphological differences exist among some of these different Trichinella strains. Trichinosis is easily prevented by thorough cooking of meat and is uncommon in countries such as the United States and France where there are laws prohibiting the feeding of raw meat scraps to hogs. In the United States most cases of trichinosis are attributed to ingestion of undercooked wild game. In 1990, one of the last large outbreaks of trichinosis in the United States occurred in Southeast Asian immigrants who ate raw pork sausage at a wedding reception.
Trichinella spp. are the smallest parasitic nematodes of humans. Adult males are between 1.4 and 1.6 mm in length with a more slender anterior portion. Males do not have a copulatory spicule. Adult females are twice the size of males with a more slender anterior portion. Females have a vulva located approximately one-third of the body length from the anterior end. Larvae are approximately 0.1 mm in length.
Trichinella nematodes are unique in that the same animal serves as both definitive and intermediate host (larvae and adults are located in the same animal, but in different organs).
Trichinella spp. are considered to be a complex of species, with a variety of genotypes identified by DNA analysis. There are few distinct morphologic differences between species and species identification is based on characteristics such as reproductive isolation, infectivity to certain hosts, and resistance to freezing. The species of Trichinella include:
* Trich. spiralis; the primary species associated with domesticated animals.
* Trich. britovi; the species seen frequently in wild boars, horses, and free-ranging swine. Trich. britovi has also been reported in bear (Japan) where it has been given a separate classification by some (T9).
* Trich. nelsoni; the species seen in various large carnivores of tropical Africa.
* Trich. nativa; the species documented in cougars, walruses, whales, and bears causing more prolonged diarrhea and fewer muscle symptoms.
* Trich. pseudospiralis; the species documented in birds that does not form a capsule in the muscle therefore causing less muscle inflammation and pain.
* Less common species are summarized in Table 6-10.
Epizootiology and Public Health Significance
Trichinosis occurs worldwide (Australia does not have any documented cases that have originated within its borders), but is seen more frequently in temperate climates than in the tropics. Trichinosis has relatively high rates of infection in the United States and Europe as a result of the ethnic customs of eating raw or rare pork dishes or wild animal meats.
Tasting of raw homemade pork sausage for proper seasoning is a common source of Trichinella infection.
In the United States trichinosis is largely limited to sporadic cases or small clusters related to consumption of home-processed meats from noncommercial farm-raised pigs and wild game. Trichinosis has been a reportable disease in the United States since 1966. The CDC surveillance system has data as far back as 1947 demonstrating a significant decrease in cases from a peak of nearly 500 in 1948 to the current rate of fewer than 50 per year. The fatality rate of trichinosis in the United States is 0.003. The USDA conducts periodic surveillance of farm-raised pigs to monitor diseases such as trichinosis.
Over the past 20 years, there has been an increase in the number of trichinosis outbreaks in developing countries. International trade of meats and rising affluence in countries without well-established monitoring systems has contributed to the increasing incidence of trichinosis. Trichinosis is rare in countries with laws prohibiting the feeding of raw garbage/animal byproducts to commercially raised pigs and in countries with well-managed slaughterhouse surveillance systems. Home raising of pigs, with feeding of raw garbage instead of grain, is still a common practice in the developing world. China has some of the highest recorded case numbers worldwide.
Although trichinosis is generally considered a disease of omnivorous or carnivorous animals, herbivores have become infected most likely from prepared feed that contained remnants of infected animals. In France, imported horse meat has become the most common source of trichinosis (more than a dozen outbreaks infected more than 3,000 people since 1976). Mutton and goat meat have become a recognized source of infection in countries where pig consumption is restricted for religious or economic reasons.
The life cycle of Trichinella is spent entirely in the mammalian body host. In nature, the parasite is maintained in an encysted (encapsulated) larval form in the muscles of animal reservoirs and is transmitted when other animals prey on them. Human trichinosis infections are established by consumption of insufficiently cooked infected meat, typically pork or bear (other animal species have also been implicated). Humans are dead-end hosts (unless the practice of cannibalism occurs). Most mammals are susceptible to trichinosis through consumption of meat containing the encysted larvae. Rats are important in maintaining Trichinella cycles because farm pigs will eat rats, which are commonly found near garbage sites.
Trichinella is the world's largest intracellular parasite.
Trichinella infection occurs by ingestion of encysted larvae in muscle. The cyst wall is digested by gastric acid and pepsin in the stomach, allowing freed larvae to penetrate the duodenal and jejunal mucosa. In approximately 4 days, the larvae develop into sexually mature adults that begin mating. After mating, females penetrate deeper into the mucosa and discharge living larvae (up to 1,500) over a 4- to 16-week period. After mating, noninfective adult males are expelled in the stool. Eventually the females die and pass out of the host. Larvae migrate into the lymphatic system, are carried by the portal circulation to the peripheral circulation, reach striated muscle, and penetrate individual muscle cells. The diaphragm, tongue, masseter, and intercostal muscles are among the most common muscles involved in pigs. Larvae grow rapidly and begin to coil within the cell. Capsule formation begins approximately 15 days after infection and is finished by 4 to 8 weeks postinfection. Once capsule formation is complete the larvae are infective. The muscle cell will degenerate as the larva grows, at which time calcification begins. If immature larvae pass through the intestine and are eliminated in the feces, they are infective to other animals (Figure 6-61).
Encysted (encapsulated) Trichinella larvae survive and remain infectious for years (maybe greater than 30 years) even if the capsule is calcified. Trichinosis requires two hosts in its life cycle: female worms produce larvae that encyst in muscle of the first host and the new, second host becomes infected when muscle is eaten.
[FIGURE 6-61 OMITTED]
Clinical Signs in Animals
Most Trichinella infections in domestic and wild animals are asymptomatic.
In trichinosis, there is typically one larva per muscle cell.
Clinical Signs in Humans
In humans, the usual incubation period of trichinosis is 8 to 15 days. Heavy Trichinella infections may produce serious illness with 3 successive clinical phases:
* Intestinal. The first signs of trichinosis occur between 12 and 48 hours after ingestion of infected meat with initial symptoms as a result of the invasion of the intestinal wall by the juvenile larvae. In this phase vague symptoms such as nausea, vomiting, and diarrhea are seen. Dyspnea and red blotchy rashes may erupt on the skin. At the end of this phase facial edema and fever is seen 5 to 7 days after the first appearance of symptoms.
* Muscle invasion. This phase is caused by the migration of numerous larvae into muscle. Clinical signs include periorbital edema (classic sign), intense muscle and joint pain, and shortness of breath. Neurologic complications such as deafness and seizures may be seen. A pronounced eosinophilia is seen during this phase.
* Convalescent. Clinical signs may resolve after a few days, but may persist for 5 to 6 weeks. In severe infection, muscle pain can lead to difficulty swallowing, speaking, breathing, and chewing. The most frequent cause of death is myocarditis as a result of invasion of cardiac muscle and heart failure. If acute signs go into remission most people become asymptomatic even without treatment and with the existence of larvae in the musculature. Late sequelae include rheumatoid arthritis and continued muscle pain.
Diagnosis in Animals
Trichinosis in animals may be diagnosed by microscopic examination of a muscle biopsy sample (usually tongue). A negative muscle biopsy does not necessarily rule out trichinosis. Serologic testing using ELISA technique is a reliable test to detect anti-Trichinella antibodies. Seroconversion in animals may occur with as few as 0.01 larvae per gram of meat, but may not occur for weeks after infection.
[FIGURE 6-62 OMITTED]
Diagnosis in Humans
Trichinosis in people may be suspected in patients with eosinophilia (CBC), myoglobinuria (UA), and elevated creatine kinase values (serum chemistry). Calcified densities in muscles may be seen on radiographs, but are not present in acute infections. CT brain scans may show focal defects in the cerebral cortex if neurologic involvement is present. Parasite-specific indirect IgG ELISA titers are approximately 100% accurate in diagnosing trichinosis. Anti-larvae antibodies are also available and are approximately 30% accurate. Western blot analysis is used to confirm positive ELISA results. Muscle biopsy is the definitive diagnostic test and is done by crushing a portion of muscle tissue between two slides and viewing directly (Figure 6-62).
Treatment in Animals
Treatment in animals is generally impractical. Symptomatic and supportive care to alleviate pain until the infection is resolved may be attempted.
Treatment in Humans
In human cases of trichinosis anthelmintic therapy is considered effective only during the intestinal phase of infection. Thiabendazole and mebendazole are commonly used in people. Corticosteroid treatment can reduce the immunologic response to the larvae.
Management and Control in Animals
Control of trichinosis in pigs is accomplished with good management (controlling rodents, cooking garbage for 30 minutes at 212[degrees]F if feeding to it to pigs, and preventing cannibalism (tail biting) and access to wildlife carcasses).
Management and Control in Humans
Trichinosis in people is preventable by thoroughly cooking meat. Most developed countries have surveillance programs to monitor meats entering the commercial market; however, these controls have been documented to fail. Inspection of meat at the time of slaughter, either by microscopic examination of muscle or by digestion methods, is effective in preventing human infection. In North America, commercial products that are labeled ready to eat must be processed by adequate heating, freezing, or curing to kill Trichinella before marketing. Pork should be cooked to an internal temperature of 137[degrees]F (58[degrees]C) or greater. Freezing pork is also effective at 5[degrees]F (-15[degrees]C) for 20 days, -9.4[degrees]F (-23[degrees]C) for 10 days, or -22[degrees]F (-30[degrees]C) for 6 days. Freezing cannot be relied on to kill Trichinella organisms in meat other than pork. Pickling and smoking meat does not kill the larvae.
Trichinosis is caused by Trichinella spp., a parasitic nematode with adult males measuring between 1.4 and 1.6 mm in length and adult females measuring twice the size of males. Trichinella spp. are considered to be a complex of species, with a variety of genotypes identified by DNA analysis. The species of Trichinella include Trich. spiralis, Trich. britovi, Trich. nelsoni, Trichi. nativa, Trich. pseudospiralis, and a few less common species. Trichinosis occurs worldwide and is seen more frequently in temperate climates than in the tropics. The life cycle of Trichinella is spent entirely in the mammalian body host. In nature, the parasite is maintained in an encysted (encapsulated) larval form in the muscles of animal reservoirs and is transmitted when other animals prey on them. Trichinella infection occurs by ingestion of encysted larvae in muscle. Most Trichinella infections in domestic and wild animals are asymptomatic. In humans, heavy Trichinella infections may produce serious illness with three successive clinical phases, which include intestinal (nausea, vomiting, diarrhea, dyspnea, red blotchy rashes, facial edema, and fever), muscle invasion (periorbital edema (classic sign), intense muscle and joint pain, and shortness of breath), and convalescent (resolution of clinical signs, death, or chronic infection). Trichinosis in animals may be diagnosed by microscopic examination of a muscle biopsy sample (usually tongue). Serologic testing using ELISA technique is a reliable test to detect anti- Trichinella antibodies. Trichinosis in people is diagnosed with parasite-specific indirect IgG ELISA titers. Anti-larvae antibodies are also available and are approximately 30% accurate. Western blot analysis is used as to confirm positive ELISA results. Muscle biopsy is the definitive diagnostic test and is done by crushing a portion of muscle tissue between two slides and viewing directly.
Treatment of trichinosis in animals is generally impractical. In human cases of trichinosis anthelmintic therapy using thiabendazole or mebendazole is considered effective only during the intestinal phase of infection. Control of trichinosis in pigs is accomplished with good management. Trichinosis in people is preventable by thoroughly cooking meat and meat inspection.
Trichuriasis, also known as whipworm infection, is caused by a variety of Trichuris nematodes commonly called whipworms. Trichuris nematodes are named from the Greek trichos meaning hair and oura meaning tail because the anterior two-thirds of the worm is thin and hair-like, whereas the posterior one-third is fat like the handle of a whip. Evidence of whipworm infection can be traced to ancient civilizations. Trichuris eggs have been found in the fossilized feces of stone-age humans from 10,000 years ago. Mummified bodies dated around 2400 B.C. from Nubia (Northeast Africa) had Trichuris eggs in visceral contents kept in Canopic jars during the mummification process. As Egyptians and Nubians maintained trade during this time period whipworm infections were probably a common infection in Egyptians as well. Eggs of Tric. trichiura, the primate parasite, have been found in glacier mummies more than 5,000 years old. Trichuris eggs were found in the Neolithic wetland villages in Western Europe. Otzi the Iceman, found on September 19, 1991 in the Alps, believed to have lived around 3200 B.C. and had been infected with whipworms. Today, Tric. trichiura is one of the most common human intestinal parasites in parts of the world where sanitary conditions are poor.
Most human cases of trichuriasis are caused by Tric. trichiura, the nematode of humans and nonhuman primates. Tric. trichiura is about 30 to 50 mm in length, with males being shorter than females. Its mouth is tiny, lacks lips, and contains a small spear. Adult worms have a long esophagus, an anus near the tip of the tail, and lack an excretory system. Both sexes have a single gonad; males have a single spicule surrounded by a sheath and females have a uterus that contains many unembryonated, lemon-shaped eggs with an operculum at each end.
The cat whipworm, Tric. campanula, is not found in the United States.
Zoonotic species of Trichuris include Tric. vulpis (the dog whipworm, which is commonly found in the United States yet is difficult to detect at times because low numbers of eggs are shed and are shed in waves) and Tric. suis (the pig whipworm). There are approximately 60 to 70 other species of Trichuris in a variety of animals, but their zoonotic potential has not been proven. For example, Tric. ovis is an important pathogen of sheep and cattle and Tric. muris is found in rats and mice.
Epizootiology and Public Health Significance
Trichuriasis is found worldwide, but is rarely found in arid, extremely hot, or extremely cold regions of the world. For trichuriasis to become a serious health problem in a region, two requirements are needed: proper environmental conditions (a warm climate, high rainfall and humidity, dense shade (allows for egg survival and development), and moisture-retaining soil) and poor sanitation.
In the United States, whipworm infection is rare with the highest incidence occurring in the rural Southeast, where 2.2 million people are infected. Internationally there are more than 500 million people infected with Tric. trichiura nematodes. The prevalence of zoonotic trichuriasis is unknown, but is typically associated with poor socioeconomic standards of living. In the United States, approximately 10% to 20% of dogs are positive for Tric. vulpis (40% in stray dogs). Tric. suis occurs in 2% to 5% of adult swine and 15% to 40% of nursing piglets.
Trichuris nematodes have a direct life cycle and mature in a single host that becomes infected when it ingests embryonated eggs from contaminated soil. Trichuris eggs are sticky and may be carried to the mouth by hands, other body parts, fomites, or foods. Using manure as a fertilizer can be a source of whipworm infection. House flies can serve as mechanical vectors of whipworms.
Trichuris eggs are unembryonated and noninfectious when they are excreted. Development to an egg containing first-stage larvae (the infectious form) takes 10 to 14 days. The host ingests the embryonated eggs from soil (mainly in children who eat dirt) or soil-contaminated objects (typically food or water) and the eggs hatch in the small intestine. In the small intestine the larvae penetrate the cells in the base of the crypts, begin to develop, and tunnel in the intestinal epithelium back toward the luminal surface. This development in the small intestine lasts for up to 14 days with final maturation occurring in the large intestine. Adults are found in the cecum and colon where the thinner, anterior end of the worm burrows into the large intestine and the thicker, posterior end hangs into the lumen and mates with nearby worms. Eggs are produced and shed with the feces. Tric. vulpis females produce eggs in approximately 70 to 90 days in dogs; Tric. suis females produce eggs in approximately 41 to 45 days in pigs; Tric. trichiura females produce eggs in 30 to 90 days in primates. Adult females lay eggs for up to 5 years (Figure 6-63).
[FIGURE 6-63 OMITTED]
Both larval and adult whipworm are found only in the intestines and do not undergo tissue migration.
Clinical Signs in Animals
Tric. vulpis is found in dogs and wild canines. Most cases of trichuriasis are asymptomatic with occasional signs being poor condition or performance. Heavy parasite loads can cause weight loss, anemia, and diarrhea that may be mucoid or bloody. Chronic infections causing intestinal irritation may lead to intussusceptions.
Tric. suis is found in pigs and wild boars with a shorter incubation period than the other species (10 to 12 days). Most cases of trichuriasis are asymptomatic in adult swine. In pigs up to 3 months of age, severe diarrhea containing mucus and blood, anorexia, and death may be seen. Pigs with Tric. suis may be more prone to other intestinal infection especially Ca. jejuni.
Tric. trichiura is found in humans, nonhuman primates, and rarely swine. Most cases in animals are asymptomatic. Heavy infections can lead to diarrhea.
Clinical Signs in Humans
People with trichuriasis are typically asymptomatic. Heavy infections tend to be seen in small children or people who eat a lot of dirt. Symptoms in people with heavy infections include chronic bloody diarrhea, abdominal pain and distension, nausea, vomiting, flatulence, headache, weight loss, and anemia. Children with severe trichuriasis may develop dystenery, anemia, growth retardation, finger clubbing, and rectal prolapse. Extremely rare cases of visceral larva migrans caused by Tric. vulpis have been reported in humans.
Diagnosis in Animals
Trichuriasis is diagnosed by identifying Trichuris eggs by fecal examination (Figure 6-64). Eggs can be seen using fecal flotation, but centrifugation is the preferred method. Eggs are oval, yellowish-brown, thick-shelled, and contain two polar plugs. Eggs vary in size with Tric. vulpis eggs approximately 72 to 90 [micro]m x 32 to 40 [micro]m (twice the size of the other two species); Tric. suis eggs approximately 50 [micro]m x 25 [micro]m; Tric. trichiura eggs approximately 50 [micro]m x 23 [micro]m (Tric. suis and Tric. trichiura eggs are very similar in their appearance). Trichuris eggs can be shed intermittently making repeated fecal testing or proctoscopy helpful in identifying positive cases.
[FIGURE 6-64 OMITTED]
Diagnosis in Humans
Trichuriasis in people is diagnosed by fecal identification of eggs as described for animals. Fecal examination can detect eggs and charcot-leyden (C-L) crystals (crystals are formed from the breakdown of eosinophils and may be seen in the stool or sputum of animals/people with parasitic disease).
Treatment in Animals
Trichuriasis can be treated with a variety of anthelmintics such as fenbendazole, febantel, mebendazole, and dichlorvos. Milbemycin alone or in combination with heartworm preventative is effective treatment in dogs. Hygromycin as a feed additive is used to control Tric. suis in pigs.
Treatment in Humans
Trichuriasis in people can be treated with mebendazole, alendazole, and oxantel, but may be difficult to treat as a result of the worm's location in the cecum and colon.
Management and Control in Animals
Trichuriasis can be prevented in animals by conducting regular fecal examinations in domestic pets, properly treating positive animals, and utilizing proper hygiene in positive animals. Sanitation and eliminating moist areas in the environment can reduce the survival of Trichuris worms. Pigs should be housed on slatted concrete floors to aide in sanitation of their housing. Regular pen cleaning and disinfection between use is recommended. Outdoor lots and pastures should be well-drained so that moisture cannot increase in the environment. Land rotation is also recommended. Dogs should be housed on cement or gravel runs in contrast to dirt runs. Runs should be cleaned daily and regularly disinfected. Lawns should be kept short and not over watered if dogs are allowed to defecate on them.
Management and Control in Humans
Trichuris infections in humans can be avoided by proper disposal of human feces, educating people about the problems associated with eating dirt or crops fertilized with night soil, preventing animals from having access to children's playground areas, practicing good hygiene, washing raw foods before eating them, boiling or filtering drinking water, and postponing acquiring new pets until children are past toddler age.
Trichuriasis, also known as whipworm infection, is caused by species of the nematode Trichuris. Most human cases of trichuriasis are caused by Tric. trichiura. Zoonotic species of Trichuris include Tric. vulpis (the dog whipworm) and Tric. suis (the pig whipworm). Trichuriasis is found worldwide, but is rarely found in arid, extremely hot, or extremely cold regions of the world. Trichuris infection occurs when embryonated eggs are ingested. Trichuris eggs are sticky and may be carried to the mouth by hands, other body parts, transport hosts, fomites, or foods. Trichuris eggs are unembryonated and noninfectious when they are excreted. Development to an egg containing the infectious first-stage larvae takes 10 to 14 days. Tric. vulpis, found in dogs and wild canines, is typically asymptomatic with occasional signs being poor condition or performance. Heavy parasite loads can cause weight loss, anemia, and diarrhea that may be mucoid or bloody. Chronic infections causing intestinal irritation may lead to intussusception. Tric. suis is found in pigs and wild boars causing severe diarrhea in young pigs, whereas adults may be asymptomatic. Tric. trichiura is found in humans, nonhuman primates, and rarely swine and is usually asymptomatic. Heavy infections can lead to diarrhea. People with trichuriasis are typically asymptomatic. Symptoms in people with heavy infections include chronic bloody diarrhea, abdominal pain and distension, nausea, vomiting, flatulence, headache, weight loss, and anemia. Children with severe trichuriasis may develop dystenery, anemia, growth retardation, finger clubbing, and rectal prolapse. Trichuriasis is diagnosed by identifying Trichuris eggs by fecal examination. Trichuriasis can be treated with a variety of anthelmintics. Trichuriasis in people can be treated with mebendazole, alendazole, and oxantel. Trichuriasis can be prevented in animals by conducting regular fecal examinations in domestic pets, properly treating positive animals, and utilizing proper hygiene in positive animals. Infection in people can be avoided by proper disposal of human feces, educating people about the problems associated with eating dirt or crops fertilized with night soil, preventing animals from having access to children's playground areas, practicing good hygiene, washing raw foods before eating them, boiling or filtering drinking water, and postponing acquiring new pets until children are past toddler age. (See Table 6-11 for less common zoonotic hematode.)
Table 6-7 Less Common Zoonotic Cestodes Predominant Cestode Disease Signs in People Dipylidium Dipylidiosis Infection is typically caninum asymptomatic; heavy infections may cause abdominal pain, bloody diarrhea, and weight loss Hymenolepis nana Hymenolepiasis Large numbers of cestodes can cause atrophy of the intestinal villi and inflammation causing abdominal pain and diarrhea Spirometra spp. Sparganosis Slow growing, tender, painful nodule formation that typically occurs near the eye, producing edema Bertiella studeri Intestinal Clinical signs rare; and Bertiella cestode heavy infestations mucromata infections cause abdominal pain, diarrhea, and nausea Raillietina Intestinal Clinical signs rare; dermerariensis and cestode heavy infestations Raillietina asiatica infections cause abdominal pain, diarrhea, and nausea Inermicapsifer Intestinal Clinical signs rare; madagascariensis cestode heavy infestations infections cause abdominal pain, diarrhea, and nausea Mesocestoides Intestinal cestode Clinical signs rare; variabilis and infections heavy infestations Mesocestoides cause abdominal pain, lineatus diarrhea, and nausea Diplogonoporus Intestinal cestode Clinical signs rare; grandis infections heavy infestations cause abdominal pain, diarrhea, and nausea Clinical Signs Cestode in Animals Transmission Dipylidium * Dogs and cats * Ingestion of caninum show unthriftiness, cysticercoids lethargy, increased (infective stage) appetite, and mild when the hand is diarrhea licked by dogs with this stage in their mouth or ingestion of infected fleas Hymenolepis nana * Rodents are * Ingestion of eggs asymptomatic (rarely ingestion of infected intermediate hosts such as beetles) * Person-to-person autoinfection also possible (no intermediate host needed) Spirometra spp. * Dogs, cats, and * Ingestion of larvae other carnivores in the second are final hosts and intermediate hosts are asymptomatic (fish, frogs, reptiles) Bertiella studeri * Nonhuman primates * Ingestion of and Bertiella are asymptomatic infected mucromata intermediate hosts (Oribatidae mites) Raillietina * Rats and primates * Ingestion of dermerariensis and are asymptomatic infected Raillietina asiatica intermediate hosts (beetles and cockroaches) Inermicapsifer * Small rodents are * Ingestion of madagascariensis asymptomatic infected intermediate hosts (Oribatidae mites) Mesocestoides * Carnivores are * Ingestion of variabilis and natural hosts and undercooked Mesocestoides are asymptomatic infected lineatus * First intermediate intermediate hosts hosts are oribatid mites * Second intermediate hosts are rodents, birds, amphibians, and reptiles Diplogonoporus * Marine mammals * Ingestion of grandis (especially whales) infected raw or are final hosts undercooked * Larvae are found in saltwater fish saltwater fish Geographic Cestode Distribution Diagnosis Dipylidium * Worldwide (the most Identification of caninum common cestode of proglottids or dogs in Europe) eggs that are 40 [micro]m in size in feces Hymenolepis nana * Worldwide Fecal examination demonstrating colorless eggs that are 40 to 50 [micro]m Spirometra spp. * Worldwide, CT and MRI can especially China, identify lesions in Japan, and the brain Southeast Asia Bertiella studeri Africa, Asia, and Identification of and Bertiella South America proglottids mucromata Raillietina Worldwide Identification of dermerariensis and proglottids Raillietina asiatica Inermicapsifer Africa, Madagascar, Identification of madagascariensis and the Caribbean proglottids Mesocestoides Africa, Asia, and Identification of variabilis and South and North proglottids Mesocestoides America lineatus Diplogonoporus Japan Identification of grandis proglottids and eggs in fecal samples Cestode Treatment and Control Dipylidium Niclosamide and caninum praziquantel Avoid hand licking by dogs or cats; routine fecal examinations for dogs and cats and appropriate treatment if positive Hymenolepis nana Praziquantel Rodent and insect control; good personal hygiene Spirometra spp. Effective drugs not available Proper cooking of fish, frogs, and snails; avoid potentially contaminated water Bertiella studeri Praziquantel and Bertiella Proper food hygiene mucromata such as thorough cooking of intermediate hosts and cleaning vegetables Raillietina Praziquantel dermerariensis and Proper food hygiene Raillietina asiatica such as thorough cooking of intermediate hosts and cleaning vegetables Inermicapsifer Praziquantel madagascariensis Proper food hygiene such as thorough cooking of intermediate hosts and cleaning vegetables Mesocestoides Praziquantel variabilis and Proper food hygiene Mesocestoides such as thorough lineatus cooking of intermediate hosts and cleaning vegetables Diplogonoporus Praziquantel grandis Proper food hygiene such as thorough cooking of intermediate hosts and cleaning vegetables Table 6-8 Different Species of Dracunculus Geographical Species Host Distribution Dracunculus alii Snakes India Dracunculus coluberensis Snakes India Dracunculus dahomensis Snakes West and Central Africa Dracunculus doi Snakes India Dracunculus houdemeri Snakes Vietnam Dracunculus ophidensis Snakes Italy, U.S. Dracunculus oesophageus Snakes Italy, Madagascar Dracunculus globocephalus Turtles U.S. Dracunculus fuellebornius Opossums Brazil Dracunculus insignis Dogs, wild Canada, U.S. carnivores Dracunculus lutrae Otters Canada Dracunculus medinensis Many mammals Africa, Americas, Asia Source: Cairncross, S., Muller, R., and Zagaria, N. Dracunculiasis (Guinea Worm Disease) and the Eradication Initiative, American Society for Microbiology, Clin. Microbiol Rev. 2002, April; 15(2). Table 6-9 Filarial Zoonotic Nematodes Predominant Signs Nematode Disease in People Brugia malayi, Brugia Often asymptomatic; Brugia timori filarias; clinical signs include lymphatic lymphangitis mainly in filariasis; the legs and groin area; Malayan fever, headache, and filariasis backache may also be seen Dirofilaria Dirofilariasis Typically asymptomatic; immitis occasionally localized vasculitis and pulmonary infarcts are found producing chest pain, cough, and hemoptysis. Granulomas around the dead worm may be seen as a nodule in the lung on radiography and needs to be differentiated from cancer Dirofilaria Dirofilariasis; Typically asymptomatic; repens, connective occasionally settle Dirofilaria tissue in subcutaneous tissue tenuis, dirofilariasis producing painful, Dirofilaria pruritic nodules ursi, and Dirofilaria striata Nematode Clinical Signs in Animals Brugia malayi, * Dogs and cats are main reservoirs Brugia timori of the nocturnally periodic strain of Brugia malayi (intermediate hosts are Aedes and Mansonia mosquitoes) * Dogs, cats, and wild felines are reservoirs of subperiodic strain of Brugia malayi (transmitted by Mansonia mosquitoes) Dirofilaria * Dogs show weight loss, decreased immitis exercise tolerance, and cough; in advanced cases dyspnea, fever, ascites, cyanosis, and periodic collapse may occur Dirofilaria * Dirofilaria repens is in dogs who may repens, show weight loss, cough, or may be Dirofilaria asymptomatic tenuis, * Dirofilaria tenuis is in raccoons in the Dirofilaria southern United States and is ursi, and typically asymptomatic Dirofilaria * Dirofilaria ursi is found in bears and striata lynxes in the United States and is asymptomatic * Dirofilaria striata is found in felines in the United States and is asymptomatic Geographic Nematode Transmission Distribution Brugia malayi, Infected mosquitoes * South, Brugia timori transmit infective, Southeast, third-stage larvae Adult and East Asia worms live in lymph (India, Burma, vessels and lymph nodes; Thailand) females release first-stage larvae (microfiliariae) that circulate in blood, are taken up by mosquitoes, and develop to third-stage larvae. After transmission larvae migrate to an area and develop into adult worms within 3 months Dirofilaria Third-stage larvae are * Worldwide immitis transmitted by infected especially in mosquitoes and warm climates blackflies. Microfilariae (southern are not found in humans. United States, Central and South America, Mediterranean) Dirofilaria Third-stage larvae are * Worldwide repens, transmitted by infected especially in Dirofilaria mosquitoes and warm climates tenuis, blackflies. Microfilariae (southern Dirofilaria are not found in humans. United States, ursi, and Central and Dirofilaria South America, striata Mediterranean) Nematode Diagnosis Treatment and Control Brugia malayi, Identification of Diethylcarbamazine and Brugia timori microfilariae measuring ivermectin 220 [micro]m in length Mosquito repellents and from Giemsa-stained nets should be used to blood smears; filtration prevent mosquito bites techniques may be used to concentrate larvae; serologic tests are available but in some endemic areas positive titers can be seen in over 50% of people Dirofilaria Radiographs Surgical excision of immitis Serologic assays parasite Animals are treated with adulticide (melarsomine) followed by microfilaricide (ivermectin, milbemycin, or levamisole) Insect repellents to protect from biting insects Preventative drugs such as ivermectin, milbemycin, selamectin, or diethyl-carbamazine is given to serologically negative dogs Dirofilaria Radiographs Surgical excision of repens, Excision and parasite Insect Dirofilaria identification of repellents to protect tenuis, parasites from nodules from biting insects Dirofilaria Serologic assays ursi, and Dirofilaria striata Table 6-10 Different Species and Genotypes of Trichinella Species Distribution Major Host Reservoir Trichinella Worldwide; most common Swine, wild boar, spiralis (T1) species affecting bear, horse, fox humans Trichinella Arctic Bear, horse nativa (T2) Trichinella Temperate; southern Wild boar, horse britovi (T3) Europe Trichinella Worldwide; lacks cyst Birds, omnivorous pseudospiralis (T4) in muscle mammals Trichinella Temperate, near Bear murreli (T5) arctic; United States T6 Northern temperate; Bear arctic and subarctic regions Trichinella Tropical; southern Warthog; wild nelsoni (T7) hemisphere; Africa carnivores south of the Sahara T8 South Africa Lion T9 Japan Bear Trichinella Papua New Guinea; not Pigs, wild boars papuae (T10) encapsulated larvae Trichinella East Africa Crocodiles zimbabwensis (T11) Resistance Species Infectivity to Humans to Freezing Trichinella High Low to none spiralis (T1) High infectivity for pigs and rodents Trichinella High High nativa (T2) Low infectivity to rats and pigs Trichinella Moderate Low britovi (T3) Moderate infectivity for pigs Trichinella Moderate None pseudospiralis (T4) Moderate infectivity for pigs Trichinella Low Low murreli (T5) Low infectivity for pigs T6 Low High Low infectivity for pigs Trichinella High None nelsoni (T7) Low infectivity for rats and pigs T8 Low None T9 Low None Trichinella ? ? papuae (T10) Moderate infectivity for pigs Trichinella ? (zoonotic potential ? zimbabwensis (T11) unknown) Moderate infectivity for animals Adapted from Murray, C. and Lowry, K. Trichinosis, www.emedicine.com, December 16, 2005 and Krauss, H. Weber, A. et al., Zoonoses infectious diseases transmissible from animals to humans, 3rd ed., American Society of Microbiology, 2003. Table 6-11 Less Common Zoonotic Nematodes Predominant Nematode Disease Signs in People Angiostrongylus Angiostrongyliasis; Severe headache, cantonensis Cerebral fever, vomiting, neck angiostrongyliasis; stiffness, seizures, Eosinophilic and occasionally meningoencephalitis; paresis. Accumulation Eosinophilic of eosinophils in meningitis cerebrospinal fluid causing increased pressure. Symptoms persist for days to months; may be lethal. Anisakis simplex Anisakiasis; herring Abdominal pain, and Pseudoterranoa worm disease nausea, and vomiting; decipiens may lead to gastric ulceration and intestinal perforation; pruritus and urticartia; may be self-limiting Capillaria hepatica; Hepatic capillariasis Light infections are renamed Calodium asymptomatic; heavy hepatica infections cause acute liver disease (death possible in children). Capillaria Intestinal Abdominal pain, philippinensis: capillariasis anorexia, diarrhea; in renamed severe cases vomiting, Paracapillaria weight loss, diarrhea philippinensis with electrolyte and protein imbalances Capillaria aerophila; Pulmonary Bronchitis, coughing, renamed Eucoleus capillariasis bloody sputum, dyspnea aerophila Ancylostoma caninum; Eosinophilic enteritis Ulceration and dog hookworm strictures of ileum, abdominal pain, vomiting, and diarrhea Gnathostoma Gnathostomiasis Abdominal pain, spinigerum pruritus, development of painful, red, migrating swellings of skin (subcutaneous gnathostomiasis); larvae may break through skin, inflammation of internal organs (visceral gnathostomiasis); CNS invasion can be fatal Oesophagostomum Oesophagostomiasis Infections may be bifurcum, inapparent; nodules in Oesophagostomum the intestinal wall aculeatum, and may lead to large Oesophagostomum bowel obstructions. stephanostomum Multinodular oesophagostomiasis produces hundreds of small nodules in the large intestine. Uninodular oesophagostomiasis, also called Dapaong tumour, produces painful granulomatous masses in the abdominal wall or within the abdominal cavity. Thelazia callipaeda Thelaziasis Inflammation of and Thelazia conjunctiva; most californiensis frequent in small children Trichostrongylus spp. Trichostrongylidiasis People are usually asymptomatic or have mild gastrointestinal signs; severe infections cause diarrhea and abdominal pain Clinical Signs Nematode in Animals Transmission Angiostrongylus * Cardiopulmonary * Ingestion of raw or cantonensis disease in rats undercooked Mature worms live in paratenic hosts pulmonary arteries of (crabs, crayfish, or infected rats. Eggs freshwater fish) hatch, larvae * Ingestion of penetrate the alveoli, intermediate host are coughed up, and (snails) are passed in feces. * Ingestion of free Larvae invade snails, infectious larvae develop into infective larvae, and intermediate or paratenic hosts ingested by final hosts. Anisakis simplex * Final hosts (whales, * Ingestion of and Pseudoterranoa seals, and dolphins) undercooked decipiens are asymptomatic. saltwater fish and * Intermediate hosts squid (herring, mackerel, * Killed larvae can cod, and flounder) cause anaphylactic are asymptomatic. reactions Capillaria hepatica; * Rodents (can be as * Ingestion of renamed Calodium high as 80%) develop embryonated eggs hepatica liver infection. from environment Capillaria * Fish are * Ingestion of raw or philippinensis: asymptomatic undercooked renamed intermediate hosts. freshwater or Paracapillaria * Fish-eating birds brackish water fish philippinensis are asymptomatic definitive hosts. Capillaria aerophila; * Young dogs and cats * Ingestion of renamed Eucoleus may develop chronic, embryonated eggs; aerophila nonresponsive cough. after ingested larvae hatch, invades intestinal wall, migrates through lymph and blood to lung and finally reside in trachea or bronchi Ancylostoma caninum; * Young dogs show * Third-stage larvae dog hookworm patent infection (infective form) (diarrhea, weight from dog feces are loss). transmitted to people via skin penetration Gnathostoma * Dogs and cats are * Ingestion of third spinigerum asymptomatic final stage larvae of hosts. second intermediate * Freshwater fish, host (freshwater frogs, and snails fish, frogs, and are asymptomatic snails) or paratenic second intermediate hosts (chickens); hosts. ingestion of * Chickens are liberated stages or asymptomatic stages in first paratenic hosts. intermediate hosts (water fleas); third-stage larvae can be acquired Oesophagostomum * Primates have * Ingestion of third bifurcum, caseous stage larvae Oesophagostomum granulomatous adhering to aculeatum, and lesions in the vegetation; first Oesophagostomum colon. stage larvae develop stephanostomum in the egg, hatch, and develop into third-stage larvae (the remnant of the second stage is sheath) Thelazia callipaeda * Dogs and wild * Transmission of and Thelazia canines are main Thelazia californiensis hosts with clinical californiensis is by signs of increased the face fly, Fannia tear production, canicularis. light sensitivity, * Transmission of and occasionally Thelaziacallipaea is conjunctivitis. by Musca and Fannia * Cats, cattle, flies. The adult badgers, rabbits, female worm lays her foxes, and monkeys eggs in the tears, may also be eggs develop into affected. larvae that are ingested by the fly. Larvae develop in the fly, move to the mouth of the fly, and when the fly feeds near the eye, the larvae move from the fly's mouth to the eye of the new host. Trichostrongylus spp. * Ruminants carry * Ingestion of the worm in their infective third- abomasums and small stage larvae that intestine. has contaminated * Trichostrongylus plant material. Eggs axei is the small are excreted by stomach worm of infected ruminants cattle, sheep, and (most kept on goats. It causes pasture are young calves, lambs, infected). Third- and kids to develop stage larvae develop watery diarrhea. within one to several weeks depending on temperature. Geographic Nematode Distribution Diagnosis Angiostrongylus * Australia, China, Eosinophilia in cantonensis India, Southeast CSF; serologic tests Asia, and Oceana available (also reported in southern United States) Anisakis simplex * Worldwide, Endoscopic exam and Pseudoterranoa especially Spain, demonstrating decipiens Japan, France, the larvae; ELISA and Netherlands, and immunoblotting North America techniques Capillaria hepatica; * North and South Liver biopsy show renamed Calodium America, Africa, eggs 30 to 50 [micro]m hepatica Asia, and central Europe Capillaria * Southeast Asia Fecal examination philippinensis: (endemic in shows bipolar, renamed Philippines) and thick-shelled eggs; Paracapillaria Western pacific larvae and adults philippinensis areas may also be found in feces Capillaria aerophila; * Worldwide Fecal examination renamed Eucoleus or airway cytology aerophila specimens show double-operculated eggs Ancylostoma caninum; * All tropical and ELISA, dog hookworm subtropical immunoblots, fecal regions, but examination higher rates in Australia Gnathostoma * Southeast Asia, Excision and spinigerum Central America, examination of and Australia larvae; serologic tests available Oesophagostomum * West Africa Identification of bifurcum, (Ghana and Togo) 40 to 90 [micro]m oval, Oesophagostomum thin-shelled eggs; aculeatum, and ELISA; laparoscopy Oesophagostomum can show nodules in stephanostomum intestinal wall Thelazia callipaeda Thelazia callipaeda is Visual identification and Thelazia in Southeast Asia of worm in californiensis Thelazia conjunctival sac californiensis is in western United States Trichostrongylus spp. Worldwide; human Identification of infection is high thin-shelled eggs in the Middle East 50 x 90 [micro]m; (25%). third-stage larvae can also be identified Treatment Nematode and Control Angiostrongylus Mebendazole and cantonensis corticosteroids Avoid ingestion of raw or undercooked snails, crabs, or crayfish; proper cleaning of vegetables; avoid ingestion of raw or undercooked internal organs of animals. Anisakis simplex Endoscopic extraction and Pseudoterranoa of larvae; mebendazole decipiens In endemic areas avoid ingestion of saltwater fish; cook fish to hygiene when handling fish. Capillaria hepatica; Mebendazole renamed Calodium Avoid food hepatica contamination by rats; proper hygiene when handling food and utensils that may be exposed to rodents; disposal of animal livers. Capillaria Mebendazole philippinensis: Avoid consumption renamed of undercooked fish Paracapillaria or crustaceans from philippinensis endemic areas. Capillaria aerophila; Thiabendazole or renamed Eucoleus fenbendazole aerophila Proper food hygiene by washing soil- contaminated food; avoid areas with animal feces Ancylostoma caninum; Mebendazole dog hookworm Avoid walking barefoot in areas containing dog feces; treat infected dogs. Gnathostoma Surgery; albendazole spinigerum Avoid raw or undercooked fish, frog, or poultry meat; boil water. Oesophagostomum Mebendazole, bifurcum, albendazole, or Oesophagostomum surgery Personal aculeatum, and hygiene following Oesophagostomum handling of primates stephanostomum or potentially contaminated material Thelazia callipaeda Removal of worm and and Thelazia irrigation californiensis Fly control Trichostrongylus spp. Mebendazole and albendazole are effective; pyrantel pamoate is used in the United States Proper personal hygiene; rinsing and proper cooking of vegetables
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||Part 4: NEMATODE ZOONOSES|
|Author:||Romich, Janet Amundson|
|Publication:||Understanding Zoonotic Diseases|
|Article Type:||Disease/Disorder overview|
|Date:||Jan 1, 2008|
|Previous Article:||Chapter 6 Parasitic zoonoses.|
|Next Article:||Chapter 6 Parasitic zoonoses.|