**1. Introduction**

Listed as a Neglected Tropical Disease (NTD) by the WHO, lymphatic filariasis (LF) is a debilitating infectious disease of the developing world. This disease is caused by three species of lymph-dwelling filarial nematodes, *Wuchereria bancrofti*, *Brugia malayi* and *Brugia timori* (see **Table 1**). These worms are transmitted by mosquitoes and infections can lead to severe clinical manifestations such as elephantiasis, hydrocele, and lymphedema. It is these serious outcomes, which makes LF one of the leading causes of disability in the endemic regions, ultimately impairing life quality and stunning economic growth. Due to the massive negative effect LF has on public health, the WHO coordinates programmes with the aim to eliminate LF as a public health problem in 80% of the endemic countries by 2030 [1].


*Overview of the human filarial diseases, their causative agents with the nematode-transmitting arthropod vectors as well as estimations of currently infected people and the endemic regions for the disease.*

#### **Table 1.**

*Overview of the human filarial diseases.*

#### **1.1 Biology of the parasites**

The three species of filarial nematodes causing LF are transmitted to its human host by different mosquito species. *W. bancrofti* is transmitted by mosquitos of the genera *Aedes*, *Anopheles*, *Culex* and *Mansonia*. *B. malayi* by *Mansonia* and *Anopheles spp*., and *B. timori* is transmitted by *Anopheles barbirostris* [2–4]. To date, no reservoir host is known, but subperiodic forms have been found in domestic and wild animals such as cats and monkeys. Development and replication of the filarial nematodes requires both the mammalian host and the arthropod vector. During the blood meal of the mosquito infective L3 larvae are transmitted into the mammalian host. These L3 larvae reach lengths up to 1.5 mm and 18–23 μm in diameter. Within their host, the L3 larvae migrate to the lymphatics, where they molt and become adult worms within 5–18 months. In these filarial nematodes display sexual dimorphism with females being longer than their male counterparts. Females of *W. bancrofti* are 8–10 cm long and between 0.24–0.30 mm in diameter, while males reach 4 cm in length and up to 1 mm in diameter. Compared to *W. bancrofti*, *Brugia ssp*. adult worms are smaller in length with females measuring 4.3–5.5 cm in length and 130–170 μm in diameter and males reaching 1.3–2.3 cm in length and 70–80 μm in width. When gravid, female worms release sheathed microfilaria (MF) in the lymphatic vessels that drain into the blood stream. The MF of *W. bancrofti* are larger in size compared to those of *Brugia ssp*.. *W. bancrofti* MF are 244–296 μm long and 7.5–10 μm wide, while *Brugia* MF are 177–230 μm and 5–7 μm wide (see **Table 2**). MF release by female worms follows a nocturnal or diurnal periodicity that is in tune with the biting behavior of the mosquito vector in the endemic area [5]. While *W. bancrofti* and *B. malayi* mostly follow a nocturnal periodicity with peak MF blood counts around midnight, diurnal patters have been observed in the Pacific regions, where *Aedes* mosquitoes (e.g. *Aedes polynesiensis*) are the common vector [6]. This coordinated behavior between parasite and vector is a

*Biology of the Human Filariases DOI: http://dx.doi.org/10.5772/intechopen.102926*


*This table gives an overview over the discussed filarial nematodes species with facts about their biology, size and associated disease pathology.*

#### **Table 2.**

*Overview of the human-pathogenic filarial nematodes.*

great example of co-evolution. Estimations for the life span for adult female worms of the aforementioned filarial nematode species range between 5 and 10 years, MF have a lifespan of 6–24 months [7, 8]. Female worms produce up to several thousand MF per day which remain in the lymphatics or in blood vessels, preferably under the skin. During a blood meal, MF are ingested by the female mosquitos. The MF penetrate the midgut and thereby shed their sheaths and migrate on to the thoracic muscles, where they molt twice and develop to the infective L3 stage. The L3 migrate through the haemocoel to the mosquito's proboscis and from there is transmitted to the mammalian host during a blood meal of the mosquito. The development rate of the larvae within the mosquitoes is temperature-dependent and takes between 10 and 12 days [3, 9–11]. Of note, no sexual reproduction or replication occurs within the arthropod vector.
