Veterinary Parasitology: basic concepts

Veterinary Parasitology: basic concepts

1.1 Introduction

The primary aim of this book is to provide a ‘student-friendly’ introduction to Veterinary Parasitology for those aspiring to become veterinarians, veterinary nurses or veterinary scientists. It also offers an accessible resource for those already qualified and wishing to refresh or expand their general knowledge of the topic. Others engaged in the many and varied facets of animal health and veterinary public health will also find information relevant to their interests.

This first chapter explores the nature of parasitism while Chapters 2–7 examine clinically relevant relationships and interactions between the parasite, its host and the environment. Finally, Chapters 8 and 9 recognise that, in the real world, veterinarians and animal health workers are not usually presented with a parasite as such, but with a problem concerning some bodily dysfunction affecting a flock, herd or individual.

To fulfil the aims of this book, the emphasis throughout has a clinical bias. Academic information is restricted to that necessary to gain a broad understanding of the pathogenesis, epidemiology, diagnosis and control of the commonest parasitic diseases. Key words are defined in the text or, if printed in a blue typeface, explained in a nearby ‘Help box’. A glossary is provided on the website that accompanies this book.

Wherever possible, concepts are described in straightforward language, and unnecessary jargon or detail is avoided. Further aids to learning are provided in ‘Help boxes’, while ‘Extra Information Boxes’ offer additional insights for more advanced readers. Cross-references within the book are given in the format (see Section 9.2.3), (see Table 9.10) etc. These are to assist readers who may wish to follow up on particular points, but they can otherwise be ignored.

The emphasis with regard to parasite identification and the diagnosis of associated disease is on ‘how it’s done’ rather than ‘how to do it’. Latin names and taxonomic relationships are introduced only where these provide a useful foundation for comprehension, learning or further reading. The number of parasites that might be encountered in veterinary practice is so great that to mention them all would transform this ‘guide to learning’ into an encyclopaedia, which would defeat the purpose of the book. Selected examples are therefore given to provide an understanding of underlying principles and to illustrate the range and diversity that exists within the wonderful world of Veterinary Parasitology.

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1.1.1 What is Veterinary Parasitology?

Animal disease can have noninfectious or infectious origins. Noninfectious diseases result from genetic defect, physiological abnormality, structural dysfunction or external factors such as injury, radiation or poisoning. In contrast, infectious diseases are associated with invasive self-replicating agents that have evolved to occupy an animal body as their ecological niche in just the same way as a koala bear has become adapted for life in a particular species of Eucalyptus tree.

By convention, the study of infectious agents is divided into Microbiology, which embraces noncellular and prokaryotic organisms, like viruses and bacteria, and Parasitology, which is concerned with eukaryotic life-forms. Fungi are an anomaly in this scheme as, although they are eukaryotes, they are traditionally taught as part of Microbiology in most veterinary schools and so have been omitted from this book.

Veterinary Parasitology is a composite of three distinct disciplines, each with its own set of host–parasite interactions, clinical considerations and vocabulary. The three topics that make up the bulk of Veterinary Parasitology are:

  1. Veterinary entomology: the study of parasitic arthropods, including insects, ticks and mites (see Chapters 2 and 3);
  2. Veterinary protozoology: a subject that embraces the wide range of single-celled eukaryotic organisms that comprise the parasitic protozoa (see Chapter 4);
  3. Veterinary helminthology: which covers three main groups of parasitic worms – trematodes (flukes), cestodes (tapeworms) and nematodes (roundworms), as well as some minor groups such as the thorny-headed worms (see Chapters 5–7).

1.2 Parasitism and parasites

1.2.1 Parasitism

Parasitism is part of a spectrum of intimate zoological relationships between unrelated organisms which includes:

  1. Commensalism: two species living together for the benefit of one or both, but without detriment to either party, and without any metabolic dependence (e.g. cattle egrets and cattle).
  2. Symbiosis: two species living together, each dependent on the other for their mutual well-being and survival (e.g. cellulose-digesting organisms in the caecum of a horse).
  3. Parasitism: two species living together, where one of the pair (the parasite) is living at the expense of the other (the host).
  4. Parasitoidism: two species living together as in parasitism except that the host invariably dies (or is at least rendered incapable of functioning) once the parasitoid has extracted the sustenance it needs for that stage of its development. Familiar examples include parasitoidal wasps used in horticulture that lay their eggs on or in other insects to provide a food-source for their larvae.

Parasitism implies nutritional dependence on the host for at least part of the life-cycle. It also involves a high degree of specialised adaptation as the animal body is not a passive ecological niche (like a rotten tree-trunk harbouring beetles, for example) but is responsive and hostile to foreign invasion. A parasite must be able to overcome host defences and evade immunological attack. Mechanisms must also be in place to ensure transfer of infection, both geographically from host to host (‘horizontal transmission’) and temporally from generation to generation (‘vertical transmission’). This often entails an intricate integration of the life-cycle of the parasite with that of its host.

Parasites can themselves be victims or beneficiaries of invading organisms. Fleas, for example, are exploited by larval stages of both tapeworms and nematodes, while the canine heartworm, Dirofilaria, is metabolically dependent on a symbiotic bacterium, Wohlbachia.

1.2.2 Classification

The unwise student could approach every parasitic infection as a separate entity, but this would be an enormous task and a very inefficient approach to learning. It would soon become apparent that similarities exist between some diseases and this would prompt the question: ‘what are the common factors?’ So, classification is an inherent attribute of human curiosity. It has been noted already that Veterinary Parasitology embraces at least three types of arthropod, several types of protozoa and at least three types of parasitic worm, and so the value of classifying aetiological agents of disease is already becoming apparent.

Taxonomy is a powerful and essential component of biological understanding, although, from a clinician’s viewpoint, it is a tool rather than an end in itself. Knowledge of the relationship between parasites often allows similarities in life-cycle, epidemiology, pathogenesis and drug susceptibility to be predicted. Thus, if used intelligently, classification provides a valuable framework for learning and reduces considerably the amount that has to be committed to memory. The classification in this book is kept at the simplest level compatible with this objective.

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The identity of every organism is defined by using a combination of its genus and species names. Thus, the protozoan parasite that causes redwater fever in northern European cattle is Babesia divergens, while the related species Babesia bovis and Babesia bigemina cause similar diseases in warmer regions. By international agreement, the ending -osis is placed on a parasite name to indicate the disease caused by that parasite, e.g. babesiosis. By tradition, the ending -iasis is sometimes preferred in human medicine and may occasionally be found in veterinary publications.

It is sometimes useful in Veterinary Parasitology to refer to the common characteristics of a larger grouping of parasites such as a family, which always has a technical name ending in -idae (e.g. the Ixodidae, which is anglicised as ‘ixodid ticks’), or even a superfamily with the suffix -oidea (e.g. the Trichostrongyloidea, which becomes ‘trichostrongyloid worms’).

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1.2.3 Host–parasite relationships

Parasites and their hosts have evolved together over many millions of years. Every host is vulnerable to infection by several, if not many, parasitic species. Thus, there are many more parasitic species on this planet than host species! It is not surprising, therefore, that a great diversity of host–parasite relationships exists. These are often amazingly intricate and are part of the fascination of parasitology, as will become apparent when the life-cycles of individual parasites are described in later chapters.


Parasites can be broadly categorised according to their location on or in the body of their host:

  1. Ectoparasites: live or feed on the surface of the host, or embed themselves into superficial or adjacent underlying tissues. Ectoparasites engage in host–parasite associations ranging from flies that land fleetingly to feed on secretions from the eyes, nose or other orifices to mites that spend nearly their whole lives in skin tunnels.
  2. Endoparasites: live within the body of the host. Parasites may be found in every body tissue except, perhaps, bone and keratin. Those free in the lumen of the gastrointestinal tract are, technically speaking, lying outside of any host tissue (see Figure 1.1), but they are nevertheless included in this category.

Figure 1.1 Gastrointestinal parasites such as the worms depicted here in black are technically ‘outside’ of any body tissue.

A fundamental distinction that influences both the pathogenesis of infection and options for control is the relationship of the parasite to the tissue it inhabits:

  1. Extracellular parasites: these live on or within host tissues but do not penetrate into host cells. Examples include almost all metazoan and also many protozoan parasites.
  2. Intracellular parasites: these live inside a host cell modifying its genomic expression to cater for their needs, e.g. many protozoan parasites and at least one nematode genus (Trichinella).

Parasites can also be differentiated on the basis of their reproductive behaviour in the final host (see Figure 1.2). This distinction is useful as it points towards fundamental biological differences that influence pathogenesis, epidemiology, control and treatment:

  1. Microparasites: these multiply within their host. Consequently, each organism that enters the body is capable of initiating a massive infection if not checked by host defences or by chemotherapy. This category includes the parasitic protozoa (as well as microorganisms such as bacteria).
  2. Macroparasites: these do not generally increase in number while they are on or within the final host. They may produce eggs or larvae but these are dispersed into the environment. Thus, the number of mature parasites on or in the final host never exceeds the number of infective units that originally invaded the body. This category includes arthropods and helminths, although there are a few species that break the general rule by multiplying on or in the host (for example: lice, mites and a few nematodes, e.g. some Strongyloides species).
  3. Microcarnivores: these visit the host transiently to feed but leave again before undergoing any development or producing offspring. Many parasitic arthropods, such as mosquitoes, can be included in this designation.

Figure 1.2 Microparasites (above) multiply their numbers within the host; whereas the number of mature macroparasites (below) never exceeds the number that invaded the host (with a few exceptions).

With such a diverse spectrum of host–parasite associations, there are inevitably some organisms that do not fit conveniently into these broad groupings.


Some parasites require just one host to complete their developmental cycle and produce progeny. Others utilise two or more animals. Hosts can be exploited in different ways and the following terminology is used to differentiate between these:

  1. Final (or definitive) host: a term used to identify the host in which sexual reproduction of the parasite takes place.
  2. Intermediate host: this is a host in which only immature stages grow and develop. Asexual replication may occur (but not sexual reproduction).
  3. Transport and paratenic hosts: no parasitic development of any kind takes place in these and they are not a necessary part of the life-cycle. The parasite takes advantage of another animal by using it as a vehicle to increase its chances of reaching its next essential host. The word ‘paratenic’ implies an intimate relationship in which the parasite becomes embedded within the tissues of its host. The corresponding association with a transport host is more casual and often passive in nature. The two terms are sometimes used interchangeably with less precision.
  4. Reservoir host: as the name suggests, this depicts a host population that acts as a source of infection for other animals.
  5. Vector: this is a vague term for an insect, tick or other creature that carries (transmits) a disease-causing organism from one host to another.

Life-cycles are described as being:

  1. Indirect (or heteroxenous): if an intermediate host is involved; or
  2. Direct (or homoxenous): if there is no intermediate host.


Parasitic zoonoses are diseases of mankind associated with animal parasites (see Section 9.3). They can be classified according to the various biological pathways that lead to human infection (see Figure 1.3):

  1. Direct zoonoses: direct transfer from animal to human, e.g. Cheyletiella mites from an infested lap-dog.
  2. Cyclozoonoses: where humans infect animals and vice versa in strict rotation, e.g. the beef tapeworm.
  3. Metazoonoses: these involve a vector as intermediary, e.g. phlebotomine sandflies carrying Leishmania from dogs to humans.
  4. Saprozoonoses: indirect transfer via the environment, e.g. children playing on ground contaminated with Toxocara eggs from a dog or fox.

Figure 1.3 Ecological relationships that expose humans to zoonotic parasites: a – direct zoonoses; b – cyclozoonoses; c – metazoonoses; d – saprozoonoses (further explanation in text which uses same lettering as shown above). Sandfly redrawn after Mönnig from Lapage, 1962 with permission of Wolters Kluwer Health – Lippincott, Williams & Wilkins.

1.3 Host–parasite interactions

Hosts rarely gain any benefit from the presence of parasites and are often harmed by them. Defence mechanisms have therefore evolved which, if totally effective, would have extinguished parasitism as a lifestyle. But the continued existence of an abundance of parasites indicates that successful counter-strategies have arisen through natural selection. These in turn have driven the development of further protective measures and so the cycle known as the ‘parasitic arms-race’ continues. Coevolution has resulted in host–parasite interactions of such complexity that they can be reviewed only at a superficial level in an introductory text such as this.

1.3.1 Host defences

Hosts have evolved many behavioural and other strategies to reduce the risk of succumbing to parasitism. Herbivores, for example, will not eat the lush grass close to a faecal deposit where the greatest concentration of infective worm larvae occurs (the ‘zone of repugnance’). The most powerful form of defence, however, is the immune system. This comprises a battery of chemical and cellular weaponry used to combat invasive organisms. Immune reactions may completely or partially disable the attacker or they may alleviate the clinical consequences of infection.

Ideally, immunity should protect against reinfection after the invading parasites have been eliminated. This is called ‘sterile immunity’. It can last for a lifetime but often wanes with time. Sometimes, however, such protection persists only as long as a few parasites survive to continually boost the immune processes. This is known as ‘premunity’.

In some cases, parasite evasion has gained an evolutionary advantage that renders host immunity relatively ineffective, so the host remains vulnerable despite being repeatedly exposed to infection (e.g. sheep with liver fluke). Some immune reactions directed at a parasite can produce collateral damage to host tissues. Hypersensitivity and allergy are well-known examples.

Innate and acquired immunity

Vertebrates have evolved two separate but closely linked systems to provide protection against invasive pathogens. These are known as innate and acquired immune responses.

Innate immunity

The innate (or nonspecific) immune response is the body’s first line of defence. It functions similarly whatever the nature of the invader and whether or not the host has experienced similar attack before. It comprises a series of natural physical, chemical and cellular barriers that are either permanent features (such as the integrity of skin and mucosae or the acidity of the stomach) or that can be quickly mobilised. The latter include a variety of cell-types with different modes of attack as well as humoral factors such as complement. A spectrum of communication molecules (cytokines andchemokines) released by white blood cells (leukocytes) enables the innate immune system to interact with the acquired immune system.

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Acquired immunity

Acquired (also called ‘adaptive’ or ‘specific’) immune res-ponses come into action more slowly than innate reactions as they are tailor-made to combat the particular nature of each new challenge. A quicker response occurs when an animal is subsequently re-exposed to the same pathogen as the system is already primed for that specific reaction. Acquired immunity starts with the detection of foreign molecules (antigens) and the processing of these by antigen- presenting cells. This process generates two forms of adaptive response which are strongly linked to each other:

  1. a cellular response characterised by T-lymphocyte participation, and
  2. humoral immune reactions mediated by B-lymphocytes and antibody-producing plasma cells.

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Sep 7, 2017 | Posted by in GENERAL | Comments Off on Veterinary Parasitology: basic concepts
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