60 Q&A on Bovine Parasitology by Grupo Asís

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60 Q&A on Bovine Parasitology Technical details Author: Aránzazu Meana Mañes

and Francisco A. Rojo Vázquez.

Format: 22 x 28 cm. Number of pages: 232. Number of pictures: 260 with biological cycles. Binding: Hardcover.

Through 60 cases of questions and answers (Q&A), in which real situations in the veterinary profession are reflected, an entirely practical review of bovine endoparasites and ectoparasites is carried out. The book is divided into four chapters dedicated to endoparasites of the digestive and respiratory apparatus, systemic endoparasites and cutaneous parasites. Its more than 260 images and diagrams, give this work an atlas character of bovine parasitology.

Aimed at veterinary surgeons, students, teachers and other professionals in the veterinary sector.

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Aránzazu Meana Mañes Curriculum vitae She obtained a degree and doctorate from Veterinary Medicine from the Complutense University of Madrid (CUM) and is a university professor in the Department of Animal Health of the Faculty of Veterinary Science of the CUM. She is also a Diplomate of the European Veterinary Parasitology College. She has worked as a small animal veterinarian in private practice. Her research focuses on the physiopathology and epidemiology of the most important parasitic diseases in domestic animals (liver and gastrointestinal helminthosis of herbivores, equine and bovine piroplasmosis) as well as control methods (chemoprophylaxis and anthelmintic resistance and genetic resistance) of parasitic diseases in domestic animals and wildlife. She has published numerous research papers on parasitic diseases of animals in international parasitology and veterinary journals. She has also given numerous presentations at national and international parasitology conferences. She has worked in the Departments of Veterinary Clinical Science of the Veterinary Medicine Faculty of Cambridge University and the University of Glasgow (UK). She has been Deputy Director of the Department of Animal Health of the Veterinary Medicine Faculty of Complutense University of Madrid (CUM), a Member of the Experts Committee of the Ministries of Health, Education and Science, Agriculture, Fisheries and Food, a Member of the Spanish Society of Parasitology (SSP), a Member of the World Association for the Advancement of Veterinary Parasitology and Diplomate of the European Veterinary Parasitology College (EVPC).

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Francisco A. Rojo Vázquez Curriculum vitae He obtained a degree and doctorate from the Veterinary Medicine Faculty of Leon and the University of Oviedo. He is a university professor at the Universities of Salamanca (Faculty of Pharmacy), Madrid (Faculty of Veterinary Medicine) and Leon (Faculty of Veterinary Medicine), and Diplomate of the European Veterinary Parasitology College. He has collaborated as a scientist at the CSIC and as a visiting professor at the School of Veterinary Medicine of Philadelphia (USA) and has been the Director of the Centre for Animal Health Research (CAHR), Valdeolmos (Madrid), Deputy Director General of Research and Technology of the INIA, Ministry of Science and Innovation. He is also a researcher at the Mixed Institute (CISC-ULE) of Mountain Livestock (IGM) in Leon. His research activity focuses on the physiopathology, epidemiology, immunology and control (chemoprophylaxis and anthelmintic resistance, genetic resistance) of parasitic diseases of domestic animals. He is the author of several research papers on various aspects of parasitic diseases in animals and humans, published in international parasitology and veterinary journals, as well as presentations at national and international parasitology conferences. He is also author and co-author of several textbooks and monographs on parasitic veterinary pathology. He has worked at the Department of Parasitology, Central Veterinary Laboratory of the Ministry of Agriculture, Fisheries and Food, Weybridge (UK) in the Department of Parasitology, Moredun Research Institute, Edinburgh (Scotland) and in the Department of the Hospital for Large Animals, Philadelphia School of Veterinary Medicine, University of Pennsylvania. He has held numerous university positions and is a member of the most important parasitology and veterinarian associations. He is a Founder Diplomate of the European Veterinary Parasitology College (EVPC).

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60 Q&A ON Bovine Parasitology TABLE OF CONTENTS 1. Q&A about digestive endoparasites Introduction 1. How are Strongyloides transmitted to calves? 2. Can calves be born parasitised by ascarids? 3. What are the implications of Toxocara infection in bovids? 4. What is type II ostertagiosis? 5. Can Ostertagia infection be detected in milk tanks? 6. What factors influence the onset of clinical ostertagiosis? 7. How can economic losses due to ostertagiosis be avoided? 8. Are all small worms in cows Trichostrongylus? 9. Is it the same thing to detect eggs in faeces than diagnose gastroenteritis caused by Trichostrongylus? 10. What Trichostrongylus do bovids share with other animals? 11. Have any helminth populations resistant to antiparasitic drugs been detected? 12. Is climate change influencing the life cycle of Fasciola hepatica? 13. How is fasciolosis diagnosed in cows? 14. What losses are caused by Fasciola hepatica on a dairy farm? 15. Are there parasites of the rumen? 16. What are bovine cestodes like? 17. Does age make a difference in cestode infections? 18. Are adult animals resistant to Cryptosporidium? 19. What measures can be taken to prevent outbreaks of cryptosporidiosis? 20. What is the impact of Giardia infection in bovines? 21. How many Eimeria species exist in cows? 22. Why are some species of Eimeria more pathogenic? 23. How do you prevent losses due to coccidiosis? 24. Is there a nematode that is located in the oesophagus?

2. Q&A about respiratory endoparasites Introduction 25. What are Dictyocaulus like? 26. What parasite causes bronchitis with a dry and constant cough? 27. Are hydatid cysts frequent?

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3. Q&A about systemic endoparasites Introduction 28. Can piroplasms cause death? 29. How is piroplasmosis diagnosed? 30. How is Theileria transmitted in the absence of ticks? 31. Are animals infected but asymptomatic after piroplasmosis? 32. Are infections caused by Sarcocystis frequent? 33. How is infection caused by Sarcocystis detected? 34. In what organs can hydatid cysts be located? 35. What species of cysticerci parasitise bovids? 36. Can cows have coenurosis? 37. Is it possible to find trypanosomes in Europe? 38. Can toxoplasmosis be transmitted to humans by eating beef? 39. Which parasites cause abortions in cattle? 40. How is neosporosis diagnosed? 41. Why are calves with trichomoniasis not diagnosed? 42. How is trichomoniasis detected? 43. How is besnoitiosis transmitted? 44. Is it possible to find cattle schistosomes in Europe? 45. What Filariae infect cattle? 46. What fly larvae are found in the oesophagus? 47. What risk is there to treating hypodermosis in winter?

4. Q&A about cutaneous parasitoses Introducton 48. What scabies can be detected in cattle? 49. How are scabies transmitted? 50. Is it possible to eradicate scabies mites? 51. What indicates the presence of lice in cattle? 52. Are there ticks in the cold months? 53. What are the warbles? 54. What are the differences among the species of Hypoderma? 55. Are screwworms common in cattle? 56. Are there any allergic problems caused by mosquito bites? 57. What measures can be taken against flies? 58. Are there nematodes in the skin of bovids? 59. What parasite causes blindness in cows in pasturage? 60. What parasite remains as ocular nodules?

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

Most important parasites of the bovine respiratory apparatus

What are Dictyocaulus like? At the end of the summer, in a beef cattle farm in Asturias (Spain), a group of two-year-old calves develops clinical symptoms characterised by a bad general appearance; rough, dull hair; a constant dry cough and rapid weight loss. During the veterinarian’s visit it is found that some animals remain inactive and lying down and they have clear signs of dyspnoea and decay. The owner confirms the recent deaths of two animals with the same signs. During the necropsy, long white worms were observed in the lungs. According to the laboratory report, the animals also had an infection caused by Pasteurella multocida.

1. What are Dictyocaulus like and how are they transmitted to animals? 2. What is the population at risk? 3. During what time is there an increased risk of parasitic bronchitis?

Dictyocaulus: trachea, bronchi and bronchioles

2. Echinococcus: lung cysts

What are Dictyocaulus like and how are they transmitted to animals?

They are worms that in the adult state are found in the trachea and bronchi. They are a whitish colour and are thin and threadlike. Males are between 3.5 and 5.5 cm long. At the rear end, they have a small copulatory bursa supported by their ribs and short, thick, dark spicules which are all the same size (about 200 μm). Females are twice as big as males, between 6 and 8 cm long, and they are oviparous. The vulva is located at their rear end which is short and pointed. After mating, they lay eggs of about 55-85 μm which contain fully developed first stage larvae (L1).

The L1 D. viviparous measure between 390 and 450 μm long. They have several intestinal cells and dark granules. Their oesophagus is rhabditiform. Their front end is rounded and devoid of a cephalic button. The L1 hatch in the bronchi, they are released quickly, and, aided by the vibratile epithelium of the bronchi, they ascend to the trachea. Thanks to fits of coughing, larvae reach the nasopharyngeal space and are swallowed with mucous or expelled to the outside through the nasal flow. The egg hatching finishes in the digestive apparatus and the L1 are expelled with the faeces. The development of the different larval stages takes

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

Most important parasites of the bovine respiratory apparatus

1. What are Dictyocaulus like and how are they transmitted to animals? 2. What is the population at risk? 3. During what time is there an increased risk of parasitic bronchitis?

Dictyocaulus: trachea, bronchi and bronchioles

2. Echinococcus: lung cysts

What are Dictyocaulus like and how are they transmitted to animals?

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

actively from the faeces or are helped by the sporangia of the fungi of the genus Pilobolus to move towards the grass. Generally, transmission occurs when animals ingest the L3 with grass. The parasitised animals eliminate the L1 with the faeces. If environmental conditions (temperature and humidity) are suitable, in about 6-7 days they become L3, although it may be longer (several weeks). Normally, the L3 leave the faecal mass with the help of the sporangia of the fungi Pilobolus that grow in cow dung, which serves to disperse larvae across the grass.

During the early stages of infection, the larvae migrate and block the bronchioles until obstructing the distal alveoli. In about two weeks, sick animals manifest polypnoea, dyspnoea and abdominal breathing, as well as fits of coughing and decreased appetite. They adopt a characteristic posture with separated limbs, the head extended, open mouth and dilated nostrils. Lesions mainly affect the respiratory tract. In the trachea and bronchi, a large amount of viscous mucous, frothy and sometimes purulent, is observed, in which the parasites form real tangles that can obstruct the light of the bronchioles, including the bronchi.

place in the environment, which in appropriate conditions takes about 6-7 days, although it can be extended to a few weeks. If temperature and humidity are favourable, the larvae change twice inside the faecal mass and become L3, the infective stage for bovines. The L3 measure between 0.9 and 2.7 mm. They maintain the previous phase cuticle and clearly display the intestinal cells. In this stage, the larvae emerge

What is the population at risk?

The animals with a higher risk of suffering dictyocaulosis, also called verminous bronchitis, are those animals without any prior antigenic stimulation. Therefore, the disease is more common in young animals than in adults and usually occurs in the autumn months, although in warm, humid areas outbreaks also appear during the winter. However, clinical outbreaks may also arise throughout the year. In the United Kingdom, since the 50s and for several decades, dictyocaulosis has been controlled well by means of vaccines based on irradiated L3. It is important that after vaccination the animals maintain a certain level of immune protection through natural exposure to infection.

D. viviparus has a direct life cycle. The L1 is excreted in the faeces and in favourable conditions of humidity, temperature and oxygenation they change twice without losing a cuticle. In the laboratory, after 5-7 days they become L3, at which time they are already infective and are maintained at the expense of the reserves accumulated in the previous phases. In field conditions, development time increases. The L3 are of the strongylida type. At their ends, cuticles from the previous phases are observed and inside, intestinal cells are oddly coloured. Their size ranges between 0.9 and 2.7 mm.

In the decades of the 80s and 90s of the 20th century, the marketing of a long-acting anthelminthic meant a drastic drop in sales of the vaccine against dictyocaulosis, as breeders adopted chemoprevention as a control method. However, with this method the animals do not receive sufficient antigenic stimulation (insufficient exposure to the parasite) to develop their own protection, so they remain “receptive” to the disease when exposed to infection by D. viviparous. The confirmation of this fact is the increase in the outbreaks of dictyocaulosis in the United Kingdom in the past 20 years, especially in adult animals and in the second grazing season.

During what time is there an increased risk of developing parasitic bronchitis?

Bovine dictyocaulosis is more common in humid and temperate regions. These factors favour the survival of a sufficient number of L3 in the grass for a long time, so that contaminated pastures in the autumn remain a risk the following spring. Said larval population is responsible for the infection of calves coming out to pasture for the first time. Following natural infection with L3, animals develop certain protective immunity against reinfection. However, if the animals have not experienced prior antigenic stimulation (by vaccination or natural infection contact) or if they receive anthelmintic treatment that prevents the establishment of larvae ingested with the grass, they will be susceptible to the disease. Among the factors implicated in the appearance of clinical outbreaks of dictyocaulosis in a herd, the following stand out: the history of verminous bronchitis on the farm and the presence of sufficient humidity to facilitate migration of L3 from the faecal mass to the grass (wet summers, preceded by dry periods which also favour the growth of fungi Pilobolus in bovine faeces). Little or no migration of the L3 to the grass in the dry months causes an “immunity gap”, resulting in increased susceptibility by the animals in the next grazing season. In conclusion, dictyocaulosis is more common in humid areas and when susceptible animals are introduced into a farm where the levels of contamination of the grass are insufficient to produce clinical symptoms in the original herd. Moreover, the latter situation sets off high contamination of the grass through the defecations.

Adult Dictyocaulus are thin, whitish, threadlike worms. The male is between 3.5 and 5.5 cm long and the female is longer, between 6 and 8 cm. Their mouth is surrounded by four small lips and a small cavity with a chitinous rear ring. They are nematodes with a small copulatory bursa.

D. Viviparous larvae present in faeces can be spread by coprophilous fungi Pilobolus spp., often growing in bovine droppings. When the sporangium of Pilobolus opens, spores of the fungus are propelled to some distance, along with D. Viviparous. larvae When there is no Pilobolus, pasture contamination by Dictyocaulus larvae is greatly reduced. Also contributing to larval dispersal: the wind, birds, manure, vehicle tyres, footwear, etc.

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

What is the population at risk?

During what time is there an increased risk of developing parasitic bronchitis?

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

Characteristic lesions of chronic catarrhal tracheobronchitis are observed with cellular infiltration (lymphocytes and eosinophils) and fibrin deposits. The inflamed bronchial mucous becomes a pinkish-greyish colour and is thickened.

What parasite causes bronchitis with a dry and constant cough?

Histologically, epithelial hyperplasia of the bronchi is observed with loss of vibratile cilia due to the irritative action of the larvae that migrate towards the upper bronchi. In addition, peribronchiolitis is observed with areas of atelectasis and consolidation of alveoli with infiltration of lymphocytes and compression of the alveoli.

On a dairy farm in southern England, twenty high production cows were imported from Spain. During the quarantine period, they remain isolated in a field in which previously replacement heifers of the year before have been. At 25 days of isolation, half of the females have a high temperature, as well as severe respiratory symptoms and a continuous, dry cough that prevents them from even resting. The decline in milk production has been very marked.

1. What pathological repercussions does dictyocaulosis have?

observed. These symptoms are gradually accentuated until the breathing becomes laboured to the point that the calves adopt typical positions (separated limbs, head extended) and an anguished expression. On the other hand, in mild cases, cough usually occurs when animals do some exercise or are forced to do so. Most affected animals recover from an outbreak, but some (above all the younger ones) can develop severe respiratory signs which usually lead to death within a few days (1-4 days).

2. Are there vaccines to prevent dictyocaulosis? 14

3. What happens to the dead worms?

What pathological repercussions does dictyocaulosis have?

As in the majority of infections by helminths, the severity and duration of clinical manifestations in animals affected by dictyocaulosis depends mainly on the infective dose (number of ingested L3, age of the animals and various environmental and management factors). Typically, primary infections result in chronic conditions, especially in 6-10 month-old calves. On the other hand, when reinfections occur with a high dose of L3 in young bovines, and also in adults, the evolution is acute.

In general, clinical signs are associated to the degree of infection, but also to the age of the animals and the coexistence of other pathological processes of infectious or parasitic aetiology (ostertagiosis, fasciolosis, etc.). Loss of appetite and weight is observed in the sick animals. Manifestations vary with the stage of infection; cough appears and the respiratory rate increases while appetite is reduced. These early symptoms occur at 10-12 days of infection, coinciding with the migration of the larvae and the consequent blocking of the small bronchi and bronchioles. In this phase of the disease, polypnoea, dyspnoea and abdominal respiration are

irradiation, before going out to the pastures. This vaccine is given orally in two separate doses with a four week interval. Between both doses the animals should remain stabled to prevent infection before the administration of the second dose. It should be borne in mind that although vaccination results are good, this procedure does not prevent the development of some parasites that continue to contaminate the pastures. In practice, that means that if there is a serious

Are there vaccines to prevent dictyocaulosis?

Preventing dictyocaulosis is based on developing the immunity of the animals themselves, either through vaccination or exposure to natural infection, provided it is controlled by strategic anthelmintic treatments. Vaccination of dairy cattle before the first grazing season gives good and long immunity to most of the animals. Acquired immunity and the corresponding strategic planning for deworming treatments is a good tactic to control the disease, although errors may occur. Failures in the treatment carried out or its management at inappropriate times mean an increased risk of clinical presentation of dictyocaulosis. On the other hand, well developed strategic anthelmintic treatments prevent mild infections in the first grazing season, but the animals are â&#x20AC;&#x153;helplessâ&#x20AC;? when they go out to pasture for the second time. Vaccination is a good prophylactic measure in high-risk areas, however it should be accompanied by general preventive measures (avoid grazing in dangerous areas and times). Hence, there is the possibility of vaccinating calves of over two months with a vaccine containing L3 attenuated by

From an economic standpoint, vaccination is applicable to control dictyocaulosis in endemic areas with a high risk. The immunity persists for about four months; although, if the animals thereafter remain in slightly contaminated pastures, mild reinfections occur and consequently, new stimulus for the protective immunity to last. Correct vaccination protects well, but does not prevent the development of a small number of nematodes that continue to contaminate the pastures, which is why the entire herd should be vaccinated each year.

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

What parasite causes bronchitis with a dry and constant cough?

1. What pathological repercussions does dictyocaulosis have?

2. Are there vaccines to prevent dictyocaulosis? 14

3. What happens to the dead worms?

What pathological repercussions does dictyocaulosis have?

Are there vaccines to prevent dictyocaulosis?

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

Dictyocaulus cycle

process of risk, the animals should be vaccinated annually. In non-endemic areas or in pastures with a low level of contamination that do not pose a serious risk to the animals, vaccination makes less sense. In these cases, it is more useful to carry out a strategic treatment with a high efficiency anthelmintic immediately before grazing or long term administration of drugs that reduce the number of treatments needed for control.

What happens to the dead worms?

The success of the treatment depends on the choice of the appropriate anthelmintic and using it at the right time. Most animals recover after administering an appropriate anthelmintic, although some may have a slight growth delay. It is recommended to treat the animals with symptoms and let the rest develop immune resistance. Most of the affected bovines overcome the dictyocaulosis, especially after treatment, but complete recovery takes weeks and for some time they become carriers, and therefore the source of new infections. With regard to the anthelmintic treatment, and regardless of the clinical manifestations due to the presence of live worms in the respiratory apparatus, it is important to

Post mortem diagnosis can be established to identify the pulmonary lesions (purulent catarrhal bronchitis and bronchiolitis, reddish consolidated areas on the pulmonary lobes flow rates, emphysema and atelectasis due to obstruction). By examining the scraping samples from the epithelium of the trachea and the bronchi, eggs or L1 can be seen. The adult worms are in the light of the trachea, bronchi and bronchioles, surrounded by a large amount of mucous. In pre-patency phases, immature forms can only be seen with a magnifying glass when examining the mucous. In post-patency phases of the infection, there are no adult worms anymore, although the lesioned pulmonary areas make us suspect infection.

The differential diagnosis should be made with other sporadic processes, specific to the cold months, and that occur with an acute temperature rise, although these processes are often with less cough and dyspnoea. Often some bacterial pathologies, such as pasteurellosis or pulmonary tuberculosis, coincide with dictyocaulosis, the same as viral infections such as BvD, IBr, etc., in which case a specific diagnosis is required.

Adult

L4 L1 in faeces

consider the possible consequences of the accumulation of dead parasites in the tracheobronchial tree. For example, a pneumonia through inhalation which may be significantly more serious. Because of this, it may happen that prior to observing an improvement some animals worsen and even die. Precisely, some antiparasitics such as ivermectin cause the mass death of worms, which carries the potential risk of anaphylactic shock, especially when the parasite loads the animals bear are very high. If there is no concern for the period of milk suppression, and in cows that are very parasitised, an alternative is the administration of an imidazothiazole, such as levamisole, which acts by paralysing the worms. In short, the aim is to avoid a significant accumulation of dead parasites in the respiratory apparatus. The worms paralysed by the anthelmintic are expelled by natural organic defences (bronchial epithelium and cough), leaving the lungs free of parasites. If necessary, after the first treatment another anthelmintic of a different group can be administered one or two weeks later to remove the worms that have survived the first treatment and prevent worsening of the sick animals due to the massive destruction of worms.

Ingestion of L3 Fungus Pilobolus

Dictyocaulus

Q&A Of rESpIrATOry EnDOpArASITES

Dictyocaulus cycle

What happens to the dead worms?

Adult

L4 L1 in faeces

Ingestion of L3 Fungus Pilobolus

Echinococcus

Q&A Of rESpIrATOry EnDOpArASITES

Are hydatid cysts frequent? During the periodic medical check that is performed on staff working at a slaughterhouse in Zamora (Spain), the presence of cystic formations were detected in the lungs of three of the twenty employees. Their medical history confirmed that they had previously shown nonspecific respiratory signs, such as dyspnoea, fever, chronic cough and even bronchospasm and haemoptysis symptoms. As all of them were smokers, not much importance had been given to this, because it had been associated to smoking problems. One of them reported that in a fit of coughing something that looked like egg whites that had not curdled and with a salty taste was expectorated. All of them only take part in the tasks of slaughtering the cattle, which includes removal of the viscera, such as the lungs with hydatid cysts.

1. What are the characteristics of hydatidosis in Spain? 2. Is there a risk of transmission to humans at the slaughterhouse? 18

3. What size and where are the cysts in the lungs of bovids? And in humans? 4. When are cysts fertile or infertile?

In Spain, hydatidosis was a compulsory notifiable disease between 1982 and 1996. The official Spanish data indicated that in 1982 the incidence of human hydatidosis was 2.52 cases per 100,000 inhabitants. Control and eradication programmes began in 1986 and were developed for several years. They were based on routine treatment of dogs with praziquantel. Strict control of corpses from the emergence of animal diseases such as bovine spongiform encephalopathy and catarrhal fever (bluetongue disease) in ovines, together with the measure of the treatment of domestic dogs resulted in a decrease of human hydatidosis to values of 1.01 cases per 100,000 inhabitants in 1996. From that year, the cases of human hydatidosis registered in Spain are those which were “voluntarily” declared by the authorities in different regions or Autonomous Communities, which in the opinion of some posed a problem. The comparison of reported cases to hospital data shows that the number of cases of human hydatidosis has clearly been underestimated in the past 10 years. For example, in the Autonomous Community of Castile and Leon the number of reported cases was 2.69 per 100,000 inhabitants, while the estimate from hospital records is four times higher. The official prevalence of hydatidosis in domestic animals in Spain in 2000 was 0.98% in ovines and caprines, but data obtained by the personnel involved in the control programmes are 20 times higher in ovines in specific areas such as La Rioja. Official data shows that between 2000 and 2008 bovine hydatidosis fell from 0.97% in 2000 to values of about 0.5% in 2008. In any event, the prevalence data is higher in animals bred extensively than in intensive farming systems.

2 1

What are the characteristics of hydatidosis in Spain?

Hydatidosis is a serious process whose prognosis depends on the location and type of cyst. One of the main risks is the rupture of the hydatid cyst with the subsequent seeding of vesicles and the release of anaphylactic substances. One of the most striking features of hydatidosis is the fact that

the presence of large cysts may be completely asymptomatic. Furthermore, there is no parasite that produces lesions in as many organs as Echinococcus granulosus. Oncospheres can develop in the liver, lung, kidney, spleen, muscle tissue, brain, etc.

Is there a risk of transmission to humans at the slaughterhouse?

Species of the genus Echinococcus have an indirect life cycle involving definitive and intermediate hosts. The definitive hosts (carnivores) become infected by ingesting hydatid cysts that contain viable protoscolices. The vesicles are released through mastication and the action of pepsin in the stomach. After about six hours of infection, the majority (85% carnivores) of protoscolices evaginate and attach themselves to the intestinal epithelium of the small intestine, where they reach the adult stage. After 30 days of infection, egg production begins. Each Echinococcus produces between 34 and 58 eggs per day. Most (70% carnivores) are released in the intestines and are eliminated with the faeces.

The metacestode of E. granulosus is typically unilocular and has a subspherical shape. It grows expansively by concentric elongation between 1-5 cm per year, depending on the strain, the host species and the degree of infection. The cyst of E. granulosus is composed of two elements: vesicular larva and a fibrocellular cover produced by the host (white, adventitia membrane of variable thickness, depending on the inflammatory reaction). From the structural viewpoint, it is a large parasitic granuloma subsequent to an inflammation process, which is initially subacute and chronic later.

Intermediate hosts, including humans, become infected when they ingest parasite eggs in contaminated food or water. The oncosphere which is located inside the egg is released, evaginates and penetrates the crypts of the villi of the upper ileum and jejunum, until it reaches a small haematic or lymphatic vessel, from where it passively reaches various organs. Most oncosphere are retained in the liver, others pass to the lung and some can be located in the kidneys, spleen, muscle tissue, brain, bone, etc. At 10-14 days post infection, the parasite begins to reorganise itself to give rise to a hydatid cyst. After the ingestion of eggs by an appropriate intermediary, the number of oncospheres that settles is about one in 70, but only one in 250 manages to survive and develop into a cyst.

Echinococcus

Q&A Of rESpIrATOry EnDOpArASITES

1. What are the characteristics of hydatidosis in Spain? 2. Is there a risk of transmission to humans at the slaughterhouse? 18

3. What size and where are the cysts in the lungs of bovids? And in humans? 4. When are cysts fertile or infertile?

2 1

What are the characteristics of hydatidosis in Spain?

Is there a risk of transmission to humans at the slaughterhouse?

Echinococcus

Q&A Of rESpIrATOry EnDOpArASITES

The species of the genus Echinococcus have an indirect life cycle. The definitive hosts (carnivores) become infected by ingesting hydatid cysts that contain viable protoscolices. The vesicles are released by mastication, and are subsequently subjected to the action of pepsin in the stomach. It is not known what the exact stimulus that induces evagination is, although it could be due to variations in temperature and osmotic pressure, as well as agitation phenomena. Complete evagination can last between 3 and 8 days. Then, protoscolices attach themselves to the intestinal epithelium by the suckers and hooks, and develop into adult worms. Adult forms are limited to a specific region of the small intestine. Specifically, the crypts of Lieberkühn are a location of particular nutritional significance.

When the cysts rupture, either spontaneously or secondary to a traumatism or surgery, seeding and formation of new cysts (multiple secondary hydatid disease) can occur. In addition, hosts can become infected or suffer anaphylactic reactions. Humans only become infected through ingestion of water or food, which is contaminated with the parasite eggs or by close and careless contact with parasitised dogs (being licked, giving kisses). In this sense, childhood is the stage of life when infection usually occurs. 20

What size and where are the cysts in the lungs of bovids? And in humans?

Studies show that adult animals present a higher amount of visceral cysts than young ones and they are usually also larger. The preferable pulmonary location of hydatid cysts in younger animals does not have a logical explanation, since the liver is the first organ which oncosphere larvae go through. The reason for the relative increase of hepatic cysts in older animals is also unknown. In 67% of young animals, cysts with a diameter smaller than 10 mm were found, but not in adults. In all older animals and in 33% of young animals cysts with a diameter greater than 10 mm were found. Some studies have corroborated the hypothesis that hydatid cysts generate protoscolices when they reach a diameter of 15-20 mm at 5 or 6 months of the cestode eggs being ingested, finding that all small cysts in young bovines were infertile. For this reason, pragmatically, cysts of a diameter smaller than 10 mm are considered infertile. The fact that all older animals do not present small cysts can be due to the development of immunity against the parasite, and therefore formations of new cysts and constant reinfections are avoided.

Possibly, the largest cyst and greatest accumulation of cysts described in humankind is the case of a farmer in the Otago area of New Zealand. When he was six, he fell on a large stone and probably ruptured his hydatid cyst, since he was seriously ill for a few weeks, although little by little he recovered. However, after two or three years his abdomen began to grow slowly, increasing greatly in size for 30 years. At 39 he weighed 108 kg and his abdominal circumference was 145 cm. His physical condition went on deteriorating until he needed surgery, in which cysts of various sizes were removed. Their total content was 50 litres. 2-3 years after the surgery, he was diagnosed with two more cysts, which were removed in a new operation performed 13 years later, when their size was about the same as the head of a human fetus. Regarding cystic development, the most notable case is probably that of an 11-year-old English boy who had an abdominal hydatid cyst removed at St. Bartholomew’s Hospital in London in 1882. Later, he moved to the USA and when he was 67 years old (56 years after the first surgery) he underwent surgery again for two hepatic cysts! The most common human hydatidosis is precisely the hepatic one, which affects both lobes of the liver equally, although according to some authors it is more frequent in the right one (54-90%) than in the left one (29-40%). The size of hydatid cysts is important for several reasons. Regardless of the relationship to the pathology that can be produced, size, shape and location of cysts notably influence the success of treatment. Regarding the size it seems like the greatest therapeutic successes have been obtained when the cysts are smaller or equal to 5 cm in diameter, while only a fifth of those that measure more than 12 cm are resolved.

When Echinococcus eggs are eliminated in the faeces, most are already embryonated, they are spherical or elliptical and their size ranges between 30-50 μm and 22-44 μm. The main layer is the embryophore, consisting of 54 cells which provide physical protection. The vitelline layer (outer casing) becomes detached from the egg before being released. The embryophore is relatively thick and impermeable and is formed of polygonal blocks composed of a protein similar to keratin. After a suitable intermediate host ingests the viable eggs, dissolution of the embryophore cover occurs in the stomach and intestine, as this process requires the action of proteolytic enzymes (although it does not depend on a specific enzyme). Subsequently, activation of the oncosphere and the release of its membrane occur. The oncosphere evaginates its three pairs of hooks and, through penetration glands (which lyse the tissue while protecting the parasite from the digestive enzymes of the host) and rhythmic movements of the body; it penetrates the crypts of the villi of the upper ileum and jejunum, reaching a small haematic or lymphatic vessel, from where it passively reaches various organs.

Layers of the cyst (a) and hydatid sand (b). fertile and viable cysts have live protoscolices over the proligerous membrane or in its interior and also in the hydatid fluid, called “hydatid sand”.

Hydatid cysts are composed of three membranes: adventitia, laminar and germinal. The adventitia membrane is fibrous and is composed of three layers that are formed as a consequence of the host’s reaction in the initial stages of development of the oncosphere. Inside the cyst, and from the fifth month, brood vesicles are formed by asexual proliferation of the germinal layer. Inside it, the asexual budding process is repeated and leads to the formation of thousands of protoscolices which can remain viable for six years.

Echinococcus

Q&A Of rESpIrATOry EnDOpArASITES

What size and where are the cysts in the lungs of bovids? And in humans?