parasite toxocara - dmuparasitology.dmu.ac.uk/learn/modules/toxocara/story... · 2017. 7. 11. ·...

Toxocara

The Toxacara Parasite: The DMU e-Parasitology Project – A European Collaboration. Funded by the De Montfort University (DMU) Teaching Innovation Project Fund. Copyright 2016 De Montfort University. All rights reserved.

Toxocara Parasite

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Authors: Dr. M.D. Ollero, Dr. A. Magnet, Dr. F. Izquierdo, Dr C. Hurtado, Dr. F.J. Carrillo, Dr. S. Fenoy, Prof. C. del Águila.

http://parasitology.dmu.ac.uk/http://parasitology.dmu.ac.uk/http://parasitology.dmu.ac.uk/http://www.dmu.ac.uk/

Toxocara


1. Infectious Agent and Morphology

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Toxocara



1.1 Genus The genus Toxocara belongs to the family Ascarididae and phylum Nematoda (roundworm). This genus includes three important species:

– T. canis (dog roundworm), – T. cati (cat roundworm), – T. vitulorum (cattle roundworm).

Humans are accidental hosts (paratenic host) infected by accidental ingestion of embrionated Toxocara eggs, the larvae hatch in the human body and can travel into organs and other tissues (larvae are known as larvae migrans).

Human toxocariasis is an infection caused by the larvae of T. canis, and less frequently by T. cati and T. vitulorum. Toxocara is the principal cause of visceral larva migrans in humans and can also produce both eye and brain diseases.

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Toxocara

Scientific classification

Domain Eukaryuota

Kingdom Animalia

Phylum Nematoda

Class Secernentea

Order Ascaridida

Family Toxocaridae

Genus Toxocara


Toxocara



1.2 Adult Forms T. canis is smaller than most of the other species in the family Ascarididae.

It is dioecious, i.e. males and females have different morphologies. Males are smaller than females.

– Males: 4 cm to 6 cm. They are a ventrally curved at their posterior end with a simple spicule. They have a single tubular testis.

– Female worms are 6.5 cm to 16 cm. The vulva is about one-third of the body length from the anterior end; the ovaries are very large and extensive. The uterus emits 200.000 ova per day.

Both, males and females are white in colour. Lateral hypodermal cords are visible to the naked eye. There are prominent cervical alae in both sexes. They have three prominent lips each with a dentigerous ridge, the oesophagus is strongyliform (Brunaska et al., 1995).

Figure: 1.1 a, b: Adults, male and female in saline solution. Picture property of Parasitology Laboratory, Universidad San Pablo CEU.

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1.3 Eggs T. canis’ eggs are almost spherical and roughly 75 µm x 85 µm, dark brown (Soulsby,1987). Its cover is thick and ornate.

It comprises four layers which protect the egg against physical, chemical and mechanical environmental conditions (Bouchet and Leger, 1986).

Infertile eggs present more irregular and poorly defined layers.

The inside of the egg is globular and not segmented. When they are laid, they are not embrionated.

Fertile eggs are passed within the faeces of infected dogs. To be infective they need to mature in the environment under suitable conditions: temperature, humidity, light and oxygen.

Depending on the environmental conditions they develop inside the egg of juvenile larvae (J)1, J2 varies from 2-5 weeks (Nichols, 1956; Schacher, 1957; Sprent, 1958).

Figure1.2: immature egg, not embrionated. Figure copied with permission from (Ollero, 2004)

Figure1.3: infective eggs containing the larvae. Figure copied with permission from (Ollero, 2004)

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Toxocara



1.4 Larvae Larvae have a length of 400 µm.

The infective juvenile larvae develops inside the fertile egg and is known as J2 (Nichols, 1956). However other authors claim that larvae moult again, inside the egg, to J3 (Brunasca et al., 1995; Miyazaki, I. 1991; Xi and Jim., 1998).

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Figure1.4: Light microscopy of a larvae J1 inside the fertile egg. Figure copied with permission from (Ollero, 2004)

Figure1.5: Light microscopy of a larvae J2 inside the fertile egg. Figure copied with permission from (Ollero, 2004)

Figure 1.6: Light microscopy of a larvae J2 hatches out the fertile egg. Figure copied with permission from (Pons, 2009)

Figure 1.7: Light microscopy of a larvae J2 outside egg. Figure copied with permission from (Ollero, 2004)


Toxocara


2. Life Cycle

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Toxocara


2. Life Cycle

2.1 Life Cycle Overview 1 The life cycle of T. canis is complex. The definitive host is the dog and other canids. However, the migration in the dog is different depending on the age, sex and history of previous contact with the parasite.

– In puppies the larvae has enteric-pneumo-enteric migration, completing the cycle (A). Puppies are major source of environmental egg contamination (Webster, 1958) as they host the adult in the small intestine (B).

– In dogs, older that six months, the larvae has enteric-pneumo-somatic migration (C) (Sprent, 1958).

– Humans and other small mammals and birds can be accidental hosts (D) (paratenic host), developing different pathologies due to an enteric-pneumo-somatic migration.

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Figure 2.1: Toxocara canis life cycle.


Toxocara


2. Life Cycle

2.2 Life Cycle Overview 2 Fertile eggs passed in faeces of infected dogs. To be infective they need to mature in the environment under suitable conditions:

– temperature between 15-35ºC, – high humidity (85%), – light and oxygen.

After 5-9 days under these conditions first stage J1 can be observed inside the egg (E) (Schacher, 1957). Depending of the environmental conditions the second molt (inside the eggs) will require between 2-5 weeks to develop J2 (E) (Nichols, 1956; Schacher, 1957; Sprent, 1958). The ova can be viable for up to 1 year under optimal environmental conditions.

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Figure2.2: Toxocara canis life cycle.


Toxocara


2. Life Cycle

2.3 Adult Dogs and Puppies Adult dogs

If adult dogs ingest this infective egg (4) or a paratenic host (8), an enteric-pneumo-somatic migration occurs. Larvae are carried by the circulatory system to a wide variety of tissues (liver, heart, lungs, brain, muscle or eyes)(6).

Puppy

If a puppy ingests this egg (1), the larvae migrate through the lungs, bronchial tree, and oesophagus. They are then are swallowed and the adult worms develop in the small intestine where they can lay the eggs (enteric-pneumo-enteric migration) (A). The eggs are passed with the host´s faeces and this contaminates the environment (B).

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Toxocara


2. Life Cycle

2.4 Puppy Infection Puppies can be infected by different routes:

– Pre-natal transmission (5): if a larva is in the tissues of a female dog it may activate during pregnancy, migrate across the placenta to the foetal liver, and remain in the liver until birth. After birth, the larvae migrate to the lungs, undergo tracheal migration, and arrive at the gut.

– Trans-mammary transmission (7): if a larva passes with the milk it may develop to the adult form in the gut without any migration in the puppy.

Paratenic host transmission (3): It may occur when a puppy eats a paratenic host with larvae encysted in its muscle (rabbit, mouse).

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Toxocara


2. Life Cycle

2.5 Human and Other Animals Humans and other animals such as mice, rabbits and monkeys are paratenic hosts who become infected when:

– ingesting infective eggs from contaminated soil, contaminated vegetables or by touching dogs’ or cats’ hair (2) (Fan et al., 2013; Wolfe and Wright, 2003).

– consuming raw meat from infected paratenic hosts such as chicken and duck liver (Hoffmeister et al., 2007; Fan et al., 2013).

After ingestion, larvae hatch out into the small intestine and penetrate the gut wall, then; via blood circulation reach the liver and lungs and then start migrating to different tissues (D) (liver, heart, lungs, brain, muscle, eyes).

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Toxocara


2. Life Cycle

2.6 More on Paratenic Hosts In paratenic hosts, such as humans, Toxocara larvae:

– do not develop to maturity – do not moult – do not grow – do not replicate – wander through internal organs (Larva

Migrans) (Fan, 2013).

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Toxocara


3. Host Parasite Relationship and

Immune Response

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Toxocara


3. Host-Parasite Relationship and Immune Response

3.1 Histology When the larvae of T. canis migrate through the human tissues, a wide spectrum of histological responses can occur.

The typical histological lesion associated with human toxocariasis is the presence of the larva surrounded by a granuloma of eosinophils, epithelial cells, foreign body giant cells and fibrous tissue. Haemorrhage necrosis and inflammation can also be observed due to the migration of the larvae.

Toxocara larvae might be destroyed inside the granuloma but can also survive in the tissues for many years because they have a remarkable ability to avoid the host’s immune responses (Smith et al., 1981).

The host immune response to migrating larvae appears to be mounted against the larval excretory-secretory antigens (TES-Ag).

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Toxocara


4. Clinical and Pathological Features

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Toxocara



4.1 Overview In humans, T. canis larvae move through the blood to various organs, including liver, heart, lungs, kidneys, brain, muscle and eyes. The disease manifestations depend on:(Fan et al., 2013).

– the intensity of infection, – the organs involved, – the duration of migration, – immune mediated host responses – the host age.

The migration is often associated with haemorrhage, necrosis, inflammation and elevated eosinophilia. Larvae might be destroyed inside the granuloma but can also survive in the tissues for many years. Toxocariasis currently is classified clinically into (Fan et al., 2013):

– visceral larva migrans (VLM) – ocular toxocariasis (OT) – neurotoxocariasis (NT) – covert toxocariasis (CT)

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Toxocara



4.2 Visceral Larva Migrans (VLM) VLM comprises a group of symptoms associated with eosinophilic granulomas containing Toxocara sp. larvae in the liver, lung, heart, and other tissues.

The acute signs and symptoms associated with hepatic and pulmonary larval migration often include: abdominal pain, decreased appetite, hepatomegaly, fever, coughing, asthma, bronchiolitis, hypereosinophilia, leucocytosis and hipergammmaglobulinemia (Magnaval et al., 2001).

– It is more common in young children (2-7 years) – There are also cases in adults – It is dependent on the history of geophagia, pica and/or exposure

to puppies. (Yoshikawa et al., 2008; Akao and Ohta, 2007).

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Figure 4.1: Pulmonary lessions in a puppy infected with T. canis (Prieto, 1995)


Toxocara



4.3 Ocular Larva Migrans (OLM) or Ocular Toxocariasis (OT) Ocular larva migrans (OLM) is better known as Ocular Toxocariasis (OT). It is typically a unilateral ocular disease resulting from the haematogenous invasion of the eye by one or more T. canis larvae.

The most common symptoms are loss of vision, strabismus, leukocoria or red eye. Other signs are uveitis, endolphthalmitis, papillitis, retinal granulomatous lesions or inflammatory mases in the peripheral vitreous. This symptomatology is similar to that of retinoblastoma (Magnaval et al., 2001)

OT affects mainly children (Glickman and Shofer, 1987; Arevalo el al., 2013)

OT patients show normal or slightly high blood eosinophil numbers. Low or negative titters of anti-Toxocara IgE are observed in serum, but high titters of anti-Toxocara IgG are detected in aqueous humour (Arevalo et al., 2013; Benitez del Castillo et al., 1995).

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Figure 4.2: Light microscopy of larvae in mouse’s eye. Figure copied with permission from (Ollero, 2004)


Toxocara



4.4 Neurological Toxocariasis Toxocara larvae can migrate to cerebrospinal fluid, brain tissue, meninges and the spinal cord (Bardón et al.,1994).

The main clinical signs are encephalitis, meningoencephalitis, epilepsy, myelitis, neuropsychologic deficits, lethargy, and sleep and behaviour disorders.

Blood eosinophilia can be observed in only 65% of cases and pleocytosis in cerebrospinal fluids in 62% with eosinophils as the predominant type (Fan et al., 2013; Magnaval et al., 2001).

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Figure 4.3: Light microscopy of a larvae in mouse’s brain. Figure copied with permission from (Ollero, 2004)

Figure 4.4: Light microscopy of a larvae in the retina of an experimentally infected gerbil (Pons, 2009)


Toxocara



4.5 Covert or Common Toxocariasis (CT)

Covert Toxocariasis is associated with seropositive adults and children who are asymptomatic or have mild or nonspecific symptoms.

The most common symptoms are fever, abdominal pain, rash, pruritus, weakness, cough, headache, abnormal blood eosinophil or slightly high and elevated total IgE levels (Fan et al., 2013; Magnaval et al., 2001).

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Toxocara


5. Diagnosis

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Toxocara


5. Diagnosis

5.1 Overview The diagnosis of human toxocariasis is based on the clinical manifestations, laboratory test and sero-diagnostic techniques. The diagrams below are examples of methods of diagnosis; Enzyme-Linked Immunosorbent Assay and Western Blot.

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Figure 5.1: Enzyme-Linked Immunosorbent Assay (ELISA) for confirmed diagnosis from T. canis.

Figure 5.2: Western Blot (WB) for confirmed diagnosis from T. canis.


Toxocara


5. Diagnosis

5.2 Medical History and Examination Toxocariasis can be difficult to diagnose because the symptoms and signs are similar to other infections. It is important to know the patient´s history of geophagia or pica and their exposure to puppies.

The diffuse symptoms make necessary to follow the below criteria during the clinical diagnostic. The patient could be diagnosed with toxocariasis if they meet 5 to 6 of the following nest conditions; however, it would be unclear if only 3 or 4 were met (Glickman et al., 1978).

– Leukocytosis ≥10.000 mm3 – Eosinophilia ≥ 10 % – Anti- A isohemagglutinin titters ≥1 :400 and Anti-B isohemagglutinin titers ≥1:200 – IgG in serum double than normal – IgM in serum double than normal – IgE in serum ≥ 500 UI/ml – Hepatomegaly

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Toxocara


5. Diagnosis

5.3 Serology – VLM and CT

Enzyme-Linked Immunosorbent Assay (ELISA) with Toxocara excretory/secretory Antigens (TES-Ag) from larvae maintained in vitro, can be used to measure anti-Toxocara spp. antibodies. However, this assay can produce cross-reactivity with antibodies against other human roundworms. A positive ELISA for Toxocara can be confirmed by western blot (WB). The detection of lower molecular weight bands from 24 to 35 kDa confirms the diagnosis

Moreover, the detection of IgG subclasses in particular, IgG2 and IgG4, is more effective for the immunodiagnosis of toxocariasis.

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Figure 5.3: ELISA and WB for confirmed diagnosis from T. canis. Figure copied with permission from (Pons, 2009)

kDa - +


Toxocara


5. Diagnosis

5.4 Serology – VLM and CT Continued The increase in serum of IgE specific for TES-Ag in patients with clinical signs can suggest toxocariasis too (Magnaval et al., 1991; Boldis and Ondriska, 2015).

Recently, a capture-ELISA assay with monoclonal antibodies has been described (Rodriguez-Caballero et al., 2015). This type of test doesn´t produce the cross-reactions described by the ELISA test

One problem of the diagnosis is that positive serological results cannot distinguish between current and past infections. This is because T. canis larvae persist during prolonged periods within paratenic hosts maintaining the high levels of immunoglobulins (Fenoy et al.; 1992). However, the study of the avidity of specific IgG –TES-Ag in the state of infection: high IgG avidity is observed in the chronic phase and low IgG avidity in recently acquired toxocariasis (Hubner et al., 2001).

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Toxocara


5. Diagnosis

5.5 Serology – OT In the patients with Ocular Toxicariasis (OT), Toxocara antibody levels in serum can be low.

However, the detection of Toxocara antibody levels (with ELISA with TES-Ag from T.canis) in the aqueous or vitreous humour samples from the affected eye may be helpful to confirm OT cases (Benitez del Castillo et al,, 1995). See example ELISA test below.

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Figure 5.4: ELISA to detect Toxocara antibody levels in the aqueous or vitreous humour samples.


Toxocara


5. Diagnosis

5.6 Imaging (X-RAY, scans, ultrasound)

Computerised Tomography and Nuclear Magnetic resonance can be used to detect eosinophilic granulomas containing Toxocara sp. larvae in different human tissues.

However images observed are not specific and granuloma biopsies are needed in order to confirm the presence of the larva.

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Figure 5.5: Liver CT scan showing a low-density area (circled) due to toxocariasis. (Magnaval et al. 2001)


Toxocara


6. Treatment and Prevention

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Toxocara



6.1 Chemotherapeutic Agents

Albendazole or mebendazole is the most common treatment given to humans with VLM and OT.

– Albendazole: 400 mg orally, twice a day for five days (both adult and paediatric dosage). – Mebendazole: 100-200 mg orally, twice a day for five days (both adult and paediatric dosage).

For OT the goal of treatment is to minimize damage to the eye. Treatment of OT with albendazole or mebendazole is used at the same doses as for VLM.

Steroids are also prescribed to control the eye inflammation. Sometimes, surgical intervention to prevent chronic inflammation or enucleation is necessary.

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Toxocara



6.2 Prevention and Control

Intervention programmes such as controlling Toxocara infections in dogs and cats will reduce the number of infectious eggs in the environment and thus, reduce the risk of infection. These actions are (CDC, 2016):

– Clean the pet’s living area by throwing animal faeces in the bin. – Not allowing children to play in areas where pets or other animals defecate. – Washing hands with soap and warm water after playing with pets or other animals. Not forgeting to

scrub under the nails. – Teaching children the importance of washing hands to prevent infection. – Teaching children that it is dangerous to eat dirt or soil. – Deworming pets periodically.

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Toxocara


7. Public Health Risks

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Toxocara


7. Risk Factors

7.1 Overview Toxocara canis has a worldwide distribution. It is prevalent in all locations that have domestic cats, dogs, and other canids. It is also associated to places with other mammals such as mice, pigs, foxes; birds or humans that act as paratenic hosts (Soulsby, 1987).

The ranges of infection by T. canis in dogs are 86 to 100% in puppies and 1 to 45% in adults.

In humans seroepidemiological studies by IgG anti-body level reveal that human toxocariasis is among the most frequently occurring helminthiases. In Wester countries, seroprevalence is higher in rural areas (35% to 42%) than in semi-rural (15% to 20%) and urban (2% to 5%) areas respectively. In developing countries, seroprevalences tend to be higher (Fan et al., 2015).

People are at a higher risk of getting toxocariasis if they (CDC 2016): – own a dog – have contact with soil (gardeners, farmers, etc.) – Are children with geophagy and pica; socioeconomically disadvantaged populations and some

minority groups.

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Toxocara


References

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References

A-Fan – Akao, N., & Ohta, N. (2007). Toxocariasis in Japan. Parasitolog. Int, 87-93. – Arevalo, J., Espinoza, J., & Arevalo, F. (2013). Ocular toxocariasis. 50(2), 76-86. – Bardón, R., Cuellar, C., & Guillén, J. (1994). Larval distribution of Toxocara canis in BALB/c

mice at nine weeks and one year post-inoculation. Journal of Helminthology, 68(4), 359-360. – Benitez del Castillo, J., Herreros, G., Guillén, J., Fenoy, S., Bañares, A., & García, J. (1995).

Bilateral ocular toxocariasis demonstrated by aqueous humor enzyme-linked inmunosorbent assay. Am. J. Ophtharmol, 119(4), 514-516.

– Boldis, V., Ondriska, F., Spitalska, E., & Reiterova, K. (2015). Immunodiagnostic approaches for the detection of human toxocarosis. Exp Parasitol, 159, 252-258.

– Bouchet, F., & Leger, N. (1986). Ultrastrutural studies of alterations induced by microwaves in Toxocara canis eggs: prophylactic interes. Zeitschirift fur Parasitenkunde(72), 755-764.

– Brunasca, M., Dubinsky, P., & Reiterova, K. (1995). Toxocara canis: Ultrastructural aspects of larval moulting in the maturing eggs. International Journal for Parasitology, 25(6), 683-690.

– CDC. https://www.cdc.gov/parasites/toxocariasis/ (2016). Toxocariasis (also known as Roundworm Infection). Prevention & Control. In.

– Fan, C., Holland, C., Loxton, K., & Barghouth, U. (2015). Cerebral Toxocariasis: Silent progression to neurodegenerative disorsders? Clinical Microbiology Reviews, 663-686.

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References

Fan- Magnaval – Fan, C., Liao, C., & Cheng, Y. (2013). Factors affecting disease manifestation of toxocarosis in

humnas: genetics and envirnmental. Vet. Parasitol.(193), 342-352. – Fenoy, S., Cuellar, C., Aguila, C., & Guillén, J. (1992). Persistence of Immune response in

human toxocariasis as measured by ELISA. Int. J. Parasitol., 22(7), 1037-1038. – Glickman, L., & Shofer, F. (1987). Zoonotic visceral and ocular larva migrans. Vet Clin North

Am Small Anim Pract, 17(1), 133-143. – Glickman, L., Schantz, P., Dombroske, R., & Cypess, R. (1978). Evaluationof serodiagostic

tests for Visceral Larva Migrans. American Journal of Tropical Medicine and Hygiene, 27(3), 492-498.

– Hoffmeister, B., Glaeser, S., Flick, H., Pornschlegel, S., Suttorp, N., & Bergmann, F. (2007). Cerebral toxocariasi agter consumption of raw duck liver. Am J Trop Med Hyg., 76(3), 600-6002.

– Hubner, J., Uhlikova, M., & Leissova, M. (2001). Diagnosis of the early phase of larval toxocariasis using IgG avidity. Epidemiol. Mikrobiol. Inmunol., 67(70), 67-70.

– Magnaval, J., Fabre, R., Maurieres, P., Charlet, J., & de Larrad, B. (1991). Application of the western blotting procedure for the immunodiagnosis of human toxocariasis. Parasitol Res., 77(8), 697-702.

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References

Magnaval-R – Magnaval, J., Glickman, L., Dorchies, P., & Morassin, B. (2001). Highlights of human

toxocariasis. The Korean Journal of Parasitology, 39(1), 1-11. – Miyazaki, I. (1991). Helminthic Zoonoses. International Medical Foundation of Japan. – Nichols, R. L. (1956). The etiology of visceral larva migrans. Diagnostic morphology of infective

second stage larvae. Journal of Parasitology, 42(4), 349-361. – Ollero, M. (2004). Toxocara canis: Estudio de factores biológicos e inmunológicos

relacionados con su migración y desarrollo de técnicas de diagnóstico molecular. Universidad San Pablo-CEU.

– Pons, E. (2009). Estudio de factores biológicos relacionados con la migración cular y cerebral de Toxocara canis y aplicación de nuevas alternativas en su diagnóstico. Universidad San Pablo CEU.

– Prieto, M. (1995). Desarrollo de Toxocara canis en peros beable infectados experimentalmente: respuesta inmunológica en los hosteadores y estudio de diversos parámetros sero-hematológicos y lesionales. Universidad de Santiago de Compostela.

– Rodriguez-Caballero, A., Martinez-Gordillo, M., Medina -Flores, Y., Medina-Escutia, M., Meza-Lucas, A., Correa, D., . . . Ponce-Macoela, M. (2015). Successful capture of Toxocar acanis larva antigens from human serum samples. Parasit. Vectors, 8(8), 264.

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References

S-Y – Schacher, J. (1957). A contribution to the life history and larva morphology of Toxocara canis.

Journal of Parasitology(43), 549-612. – Smith, H., Quinn, R., Kusel, J., & Girdwood, R. (1981). The effectr of temperature and

antimetabolites on antibody binding to the outer surface of second stage Toxocara canis larvae. Mol. Biochem. Parasitol., 4(3), 183-193.

– Soulsby, E. (1987). Parasitología y enfermedades parasitarias de los animales domésticos. México DF: Nueva Editorial Interamericana.

– Sprent, J. (1958). Observations on the development of Toxocara canis in the dog. Parasitology(48), 184-209.

– Webster, J. (1958). On prenatal infection and the migration of Toxocara canis Werner 1782, in dogs. Canadian Journal of Zoology(36), 435-440.

– Wolfe, A., & Wright, I. (2003). Human toxocariasis and direct contact with dogs. Vet. REc, 152, 419-422.

– Xi, W., & Jim, J. (1998). A novel method for the recovery of Toxocara canis in mice. Journal of Helminthology, 72, 183-184.

– Yoshikawa, M., Nishiofuku, M., Moriya, K., Ouji, Y., Ishizaka, :. K., Mikasa, K., . . . Akao, N. (2008). A familial case of visceral toxocariasis due to consumption of raw bovine liver. 57(4), 525-529.

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8. Glossary

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Paratenic host: It is a host that is not necessary for the development of a particular species of parasite, but nonetheless may happen to serve to maintain the life cycle of that parasite. In contrast to its development in a secondary host, a parasite in a paratenic host does not undergo any changes into the following stages of its development. Strongyliform: oesophagus type characterized by a “bat” shape.

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Start1. Infectious Agent and Morphology1.1 Genus1.2 Adult Forms1.3 Eggs1.4 Larvae

2. Life Cycle2.1 Life Cycle Overview 1 2.2 Life Cycle Overview 22.3 Adult Dogs and Puppies2.4 Puppy Infection2.5 Human and Other Animals2.6 More on Paratenic Hosts

3. Host Parasite Relationship and �Immune Response3.1 Histology

4. Clinical and �Pathological Features4.1 Overview4.2 Visceral Larva Migrans (VLM)4.3 Ocular Larva Migrans (OLM) or Ocular Toxocariasis (OT)4.4 Neurological Toxocariasis4.5 Covert or Common Toxocariasis (CT)

5. Diagnosis5.1 Overview5.2 Medical History and Examination 5.3 Serology – VLM and CT5.4 Serology – VLM and CT Continued5.5 Serology – OT5.6 Imaging (X-RAY, scans, ultrasound)

6. Treatment �and Prevention6.1 Chemotherapeutic Agents6.2 Prevention and Control

7. Public Health Risks7.1 Overview

ReferencesA-FanFan- MagnavalMagnaval-RS-Y

8. GlossaryGlossary

parasite toxocara - dmuparasitology.dmu.ac.uk/learn/modules/toxocara/story... · 2017. 7. 11. ·...

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