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Filarial Nematode

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Filarial nematodes
Scientific classification
Kingdom:	Animalia
Phylum:	Nematoda
Class:	Secernentea
Order:	Spirurida
Superfamily:	Filarioidea
Family:	Onchocercidae
Subfamily:	Onchocercinae

Filarial nematodes (or filariae or filarids) are parasitic nematodes transmitted by haematophagous arthropods to terrestrial vertebrates. In humans, they cause a broad spectrum of symptoms that vary according to the filarial species and the individual's immune reactions to various developmental stages of the parasite. According to the World Health Organisation, lymphatic filariasis alone (excluding other forms grouped under cutaneous filariasis) puts 1.2 billion people at risk, and 120 million are infected in Asia, Africa, the Western Pacific and the Americas. Filarial nematodes are a major focus of medical and scientific research. However, as the human parasites are very difficult to study for ethical reasons, laboratories have had to develop experimental models. The species used for research are or have been either parasitic of humans although transmitted to laboratory rodents (Brugia malayi [1] for instance), dogs, cats or monkey filariae or naturally parasitic of rodents transmitted to laboratory mice (such as Litomosoides sigmodontis [2]).

Biology

Filarial nematodes require two hosts (dixenous life cycle): a haematophagous arthropod as intermediary host (called vector in epidemiological vocabulary) and a terrestrial vertebrate as final host in which reproduction occurs. They have no free phase, but the developmental stages that pass from one host to the other (microfilariae transmitted to the arthropod, and infective third stage larvae transmitted to the definitive host – see below) are the more resistant forms.

Life cycle

The adults live in body cavities, the subcutaneous tissue or in peripheral or central lymphatic vessels of the mammalian host. Males and females mate, and the females lay motile eggs, which are first stage larvae (L1) inside their egg shell, called microfilariae. The microfilariae make their way to peripheral lymphatic and/or blood vessels in order to be taken up by the intermediary host during its blood meal. The microfilariae of some species (called periodic) migrate synchronously from the central circulation to the periphery, coinciding with the feeding times of the vector. In the arthropod, the microfilariae migrate through the gut walls to the hemocoel, into cells and form a syncytium in which they develop to the third larval stage (L3). The infective L3 will wait for another blood meal before perforating the arthropod’s tissues in order to reach, and escape through, its mouth parts. This is most often lethal to the vector. Once in the skin of their definitive host, the L3 migrates in the subcutaneous connective tissue to the lymphatic vessels, through the lymphatic system, to its final niche. It will then moult twice, growing rapidly (from a couple of millimetres as an L3 to several centimetres as a sexually mature adult). The final niche of a filarial nematode is characteristic of each species. Onchocerca volvulus forms subcutaneous nodules (collagenous formations in modified lymphatic vessels); Wuchereria bancrofti, Brugia malayi reside in lower lymphatic vessels, Loa loa remains mainly in the subcutaneous tissue, Litomosoides sigmodontis migrates to the pleural cavity. However, Wenk in 1926 and several authors since, have suggested that all filarial nematodes may have a primary localisation in the lymphatics and even the subcutaneous nodules formed by some may be formed from within lymphatic vessels. As they live inside another organism filarial nematodes have developed highly specialised mechanisms in order to maximise their transmission from one host to the other.

Morphology

Until the advent of phylogenetics the taxonomy of filarial nematodes relied entirely on combining and comparing morphological traits of several stages, or both sexes. It became apparent that their morphology is highly adapted to their life history, both in their phylogeny and their development. Extensive observation of filarial nematodes of amphibians, reptiles, birds and non-human mammals have provided vast insight into the anatomical adaptations of these parasites to their life style.

Microfilariae

Filarial nematodes, being trapped inside their host’s tissues, cannot expel their progeny via its excrements. However, transmission is enabled by the capacity of the microfilarial stage to meet its next host in the peripheral blood of lymphatic vessels. To achieve this, the microfilariae have to be small enough to travel through the host’s capillaries (on average, 100 µm long and 5 µm wide), but must have sufficient musculature and energy to migrate to the zones where the arthropod is most likely to feed, for instance on the ears, or the lower limbs, especially for periodic species. Such tropisms have been observed in genera such as Onchocerca, Monanema and Cercopithifilaria. This requires the use of sensory organs, called amphids, that inform the microfilariae of the physicochemical characteristics of their environment. In many species the microfilariae are either laterally or dorsoventrally flattened, or can be coiled or their cuticle ridged, which enhances their grip on their environment.

Larval stages

Little is known about the habits of the larvae in the arthropod host. The microfilariae migrate through the gut walls to the hemocoel, into cells and form a syncytium. They remain curled up in the syncytium during most of their development until the third larval stage. Their morphology has little specificity, and their interactions with the intermediary host, although complex, are little studied. One can only assert that they are able to detect when the arthropod is feeding, and migrate to the mouth parts to be transmitted. The infective larvae (L3) is a resistant form (comparable to the third larval dauer stage in Caenorhabditis elegans), that must be small enough to pass through the arthropods mouth parts, yet resistant enough to survive the extreme differences between the two hosts’ physiologies, not to mention the immune reactions this process induces in the definitive host. The cells in the infective stage have a reduced cytoplasm