**2. Disease transmission by** *Aedes aegypti*

*1.4.1. Physiological resistance in Aedes spp.*

46 Dengue Fever - a Resilient Threat in the Face of Innovation

pyrethroid and DDT [29, 34, 37, 38].

conferring resistance to insecticides.

*1.4.2. Behavioral resistance in Aedes spp.*

In Tanzania, like many other African settings, there is limited information on the *Ae. aegypti* resistance, most of the resistance data were collected mainly in the Americas and Asia. Our recent study in Dar es Salaam [24] demonstrated that the majority of *Ae. aegypti* strains were resistant to pyrethroid class of insecticide; mortality ranging from 83 to 92% in Dar es Salaam City. Data on molecular markers of resistance are scarce; however, studies elsewhere have correlated the occurrence of the knockdown resistance (kdr) mutations and resistance to

The mechanism of action of the pyrethroid compounds is through their toxic effect and subsequent disruption of the VGS channels in the insect nervous system [32]. The evidence suggests that *Ae. aegypti* resistance to pyrethroids is conferred by the *kdr* mutations in the VGS channel [29, 39]. Nonsynonymous mutations in *kdr* gene are associated with insecticide resistance to DDT and pyrethroids on codon V1016I and F1534C in domains II and III of the VSG channel in *Aedes* spp. [40]. Other studies demonstrated the role of *kdr* gene mutation I1011M/V and F1269C in association with *Ae. aegypti* resistance [33, 34, 41]. In African settings, the occurrence of F1534C in concurrence with the V1016I mutation was also observed in Ghanaian *Ae. aegypti* population [42]. The more recent study demonstrated the significant role of *kdr* mutation V410L alone or in combination with the F1534C in reducing the sensitivity of *Ae. aegypti* to both type

In addition to the *kdr* mutations, metabolic resistance is also know to lead to a physiological resistance due to the increase in the synthesis of detoxifying enzymes or in their specificity to metabolize the insecticide, both resulting in an enhancement of the insect detoxifying capacity of the vector [43, 44]. The P450 monooxygenases were shown to play a significant role in modulating resistance as revealed by high-throughput assays, by comparing the overall profile at genomic and transcriptome levels between resistant and susceptible populations [37]. A study that characterized several P450s, four CYP's, 9 J32, 9 J24, 9 J26, and 9 J28, conferring insecticide resistance in *Ae. aegypti* [37]. The CYPs were shown to be capable of metabolizing deltamethrin and permethrin; two common pyrethroid-based insecticides are widely used in vector interventions. Furthermore, there is evidence on the role of glutathione transferase (GST) enzymes in conferring resistance to several classes of insecticides [45]. In *Ae. aegypti*, the GST occurs as a cluster of genes in chromosome 2 and is shown to play a significant role in the metabolism of DDT [46]. Over expression of the GST enzyme is associated with DDT and pyrethroid resistant in *Ae. aegypti* populations. We, therefore, characterized additional members of this class in *Ae. aegypti* and provide evidence for a role of two additional GSTs in

Thus is defined as the ability of a vector to detect and escape from an insecticide-treated area and avoid the toxin. This type of resistance has been shown in different classes of insecticides, including organochlorines, organophosphates, carbamates, and pyrethroids [47]. It has been shown that vectors are capable of avoiding feeding if they come across certain insecticides or escape the area sprayed with the insecticides. There are currently limited studies exploring this mechanism of resistance in *Ae. aegypti.* This paucity of information could hamper control

I (e.g., permethrin) and type II (e.g., deltamethrin) pyrethroids [32].

*Ae. aegypti* mosquito is a major vector of dengue virus represented by four closely related serotypes called dengue 1, 2, 3, and 4 cause different illness including dengue fever, dengue shock syndrome, and dengue haemorrhagic fever. Dengue virus (DENV) belonging to the family Flaviviridae and genus *Flavivirus* [48].

Transmission of dengue fever (DF) occurs when a female *Aedes* spp. mosquito obtains its blood meal from an infected person during the period of viraemia. Mosquito-borne viruses multiply in both invertebrate and vertebrate cells where they cause cytopathic effects and cell destruction. Vector mosquitoes become infected when they feed on blood of a viremic vertebrate host in which there are sufficient circulating viral particles to provide an infectious dose to the mosquito.

A mosquito with salivary gland infection may transmit infectious virions during salivation as it probes the tissues of another vertebrate host. Transovarial transmission of virions occurs from the female mosquito to her progeny, and females of the next generation can transmit the virus orally without having been infected through blood feeding. There is also a venereal transmission of some arboviruses from male to female mosquito as observed and reported by Amarasinghe and others [49] (**Figure 2**).

**Figure 2.** Arboviral transmission cycle vectored by *Aedes* mosquitoes.

Transmission of dengue virus occurs in 3 cycle, namely, enzootic cycle, epizootic cycle, and epidemic cycle. The enzootic cycle involves monkey-Aedes-monkey cycle, and this cycle is primitive and has been reported in South Asia and Africa [50]. The second is epizootic cycle, which involves the transmission of dengue virus from nonhuman primates to the next human in epidemic cycles by Aedes mosquito. Lastly, the epidemic cycle where the transmission cycle is through human *Ae. aegypti* contact, human cycle with periodic, or cyclical epidemic (**Figure 2**).

**4. Control and surveillance**

needs of the people in the community.

**4.3. Adult control of** *Aedes aegypti*

**4.4. Use of repellents**

active hours of the day.

**4.5. Surveillance**

**4.2. Larval mosquito control**

This can be done by professionals by giving the public awareness, which can help to empower people to take control of mosquito breedings around their surroundings and adult control. The public can be provided with the tools needed to reduce mosquito annoyance. This is when the community, families, and individuals involved in planning and implementation of local vector control activities in order to ensure that the program meets priorities and the

Ecology of *Aedes* Mosquitoes, the Major Vectors of Arboviruses in Human Population

http://dx.doi.org/10.5772/intechopen.81439

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Frequent larval breeding sites should be searched and treated as frequent as possible by trained field technicians and trained community members. Mosquito elimination in larval stages before emerging to adults will reduce the adult mosquito population. Reduction of mosquito breeding sites such as jars, barrels, pots, vases, bottles, tins, water coolers, and tyres can be done by environmental management, removing of solid waste and managing artificial manmade habitats. All domestic water storage containers should be cleaned and covered daily.

This should aim to control *Ae. aegypti* population. The use of insecticides such as lambda cyhalothrin- or deltamethrin-treated material by hanging them on windows and used as water jar covers may reduce *Ae. aegypti* population [53]. The use of insecticide space spraying,

Application of repellents such as DEET, DIMP, and of like is of paramount importance in reducing or controlling human to vector contact. The application should be done during

Surveillance is important detect mosquito species in a certain area and changes in populations. By having valuable data, we are capable of more successfully time larvicide applications and more correctly target the adulticide activities. The WHO recommends of regular household surveys of *Aedes* spp. collecting evidence on the ecological and epidemiological indices to guide prevention and control strategies. This involves determining the habitat productivity, preference of the breeding sites, containers for the presence of egg, larvae and pupae as well as the collection of adult mosquitoes for further identification. Larval surveys involve identifying the presence of immature mosquitoes in breeding sites such as discarded tyres,

coils, and vaporizers in the community may reduce the mosquito population.

**4.1. Community education**

In this life cycle (human-to-*Ae. aegypti* mosquito-to-human cycle), the main dengue virus transmission is through mosquito that usually acquires the virus after feeding on the blood of an infected person. Replication of the virus occurs in the epithelial lining of the mosquito's midgut and then the virus move to haemocoele to infect the salivary glands. The virus can be transmitted though saliva during probing or blood feeding. The extrinsic incubation period may take 8–12 days, and this mosquito remains infected in all her life [50].

Infected humans are the major carriers of the virus where mosquito can acquire the virus through biting. The incubation time varies from virus to virus, but generally, arboviruses exhibit between 2–15 days from inoculation to development of clinical symptoms. During this period, *Aedes* mosquito can acquire the virus after feeding this person.

The reemergence of dengue disease in other places may be associated with the transovarial (via the eggs) transmission of dengue virus by *Ae. aegypti.* Dengue fever cannot spread directly from one person to another. Usually, *Ae. aegypti* prefers to feed mammalian hosts and will like to feed on humans, and even in the presence of other hosts (anthropophilic behavior), this behavior together with multiple feeding habit and highly domesticated behavior can make it an efficient vector.
