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B. vector Biology 2nd class.pdf
1. 1. Class Insecta:-
Contains the majority of medically important species
Mosquitoes, tsetse flies, sand flies, black flies, etc.
2. Class Arachnida:-
ticks, mites, etc.
3. Class Crustaceans:
copepods, shrimps, crabs, lobsters, water fleas, crayfish, etc.
PHYLUM ARTHROPODA
1
Medically important Classes of Phylum Arthropoda:
2. Some medically important orders of class insecta
include:
Order Diptera
Order Heteroptera
Order Phthiraptera (reading assignment)
Order Siphonaptera (reading assignment)
Class Insecta
2
3. Medically important families of order Diptera include:
Family Culicidae,
Family Simulidae,
Family Psychodidae,
Family Glossinidae ,
Class insecta
3
Order Diptera
4. Some Medically important Genus of family Culicidae include:
Aedes
Aedes aegypti : vector for yellow fever & dengue viruses,
Culex
Culex quinquefasciatus: vector of filarial worms & arboviruses,
Anopheles
Anopheles mosquitoes: important vectors of malaria,
Class insecta . . . Diptera . . .
4
Family Culicidae: The mosquitoes
5. Life cycle: Complete metamorphosis:
Egg --- larva ---- pupa ---- adult
Class insecta . . . Diptera . . .
5
Family Culicidae: The mosquitoes
6. Class insecta . . . Diptera . . .
6
Culicidae: The mosquitoes
8. Aedes aegypti
The main vector for yellow fever and Dengue virus,
Maintains, across generations, & transmits yellow fever virus
Vector of the four serotypes of Dengue virus (DENV1-4),
There are ~50–100 million DENV infections each year,
The mosquito populations exhibit a large amount of genetic
variation in their ability to become infected with, propagate,
and eventually transmit DENV1–4.
Diptera . . . Culicidae . . .
8
10. The main vector of filarial worms
Wuchereria bancrofti
Endemic in 83 countries,
1.2 billion people are at risk of infection,
Around 120 million people are infected,
Transmission of filarial worms:
The bite of female mosquitoes,
L3 deposited on human skin during blood meal,
L3 enter into human body via bite puncture wound,
Diptera . . . Culicidae . . .
10
Culex quinquefasciatus
11. Mosquitoes ingest L1 during the blood meal,
L1 penetrates the mosquito’s stomach,
Enter the body cavity (hemocoel),
Migrate to flight muscles for growth,
After 2 molts, L1 develops to L3,
L 3 migrate to the mosquito’s head,
L 3 (infective stage) reach the proboscis,
L3 infects a man at the next blood meal,
Diptera . . . Culicidae . . .
11
Culex quinquefasciatus
Transmission of filarial worm to a mosquito vector:
13. Are vectors of malaria
Malaria:
Major health problem in 100 countries,
Active transmission in 97 countries,
1.2 billion are at high risk,
≈ 216 million global incidences,
A remarkable decrease in cases and
deaths currently,
Diptera . . . Culicidae . . .
13
Anopheles mosquitoes
15. Diptera . . . Culicidae . . .
15
Malaria vectorial system
Around 40 species of Anopheles
mosquitoes are vectors of malaria,
Malaria transmission depends on:
The mosquitoes:-
Occurrence,
Feeding preference,
Susceptibility to infection,
Socioeconomic & environmental factors,
Availability of matured gametocytes.
16. Diptera . . . Culicidae . . .
16
Malaria Life cycle; vector part
17. Diptera . . . Culicidae . . .
17
Pathogen development in Anopheles mosquitoes
Developmental sites include:
mid-gut,
Malpighian tubules,
thoracic musculature, and
salivary glands,
• These sites are appropriate
environments to initiate parasite
gene expression,
• Permit post-translational
modifications of previously
expressed gene products that
are required for development.
18. Diptera . . . Culicidae . . .
18
Migratory routes & developmental sites within the
mosquito for malaria parasites and filarial worms
19. Diptera . . . Culicidae . . .
19
Developmental sites and migratory routes
Malaria parasites:
Infected blood meal (A),
Enter into the mid-gut (B),
Escape the peritrophic matrix (C),
Replicate in the mid-gut epithelial cells (D),
Travel through the haemocoel (E),
Replicate & reside in the salivary glands (H),
20. Diptera . . . Culicidae . . .
20
Developmental sites and migratory routes
The filarial worms:
Infected blood meal (A),
Enter into the mid-gut (B),
Escape the peritrophic matrix (C),
Penetrate the mid-gut epithelium (D),
Develop in the thoracic musculature (G),
L3 break out & enter the haemocoel (E),
L3 migrate to the head region,
L3 actively emerge from the head region,
21. Diptera . . . Culicidae . . .
21
Migratory steps pose potential barriers:
Blood coagulation inhibit pathogens movement,
The proteolytic enzymes, secreted into the lumen
for blood digestion, kill parasites,
The pharyngeal armature can cause physical damage
to microfilariae (~250-300mm),
Blood feeding initiates the formation of peritrophic matrix,
which eventually surrounds the blood meal and physically
separates it from the mid gut epithelium.
The mosquitoes innate immune system kills the parasites,
22. Diptera . . . Culicidae . . .
22
In Americas:
An. albimanus,
An. darlingi,
In South America:
An. darlingi,
An. aquasalis,
An. albitarsis,
An. bellator,
An. cruzii,
In Asia:
An. sacharovi,
An. superpictus,
An. stephensi,
An. arabiensis,
An. culicifacies
Malaria vectorial system . . .
24. Diptera . . . Culicidae . . .
Sub Sahara
Principal vectors:-
An. gambiae s.s.,
An. arabiensis,
Secondary vectors:-
An. pharoensis,
An. funestus,
An. rivurolum,
An. nili
In Ethiopia
Principal vector:-
An. arabiensis,
Secondary vector:-
An. pharoensis,
An. funestus,
An. nili,
24
Malaria vectorial system . . .
25. VECTOR CONTROL
25
Malaria control would be achieved by:-
Preventing humans from the bit of vector,
Selectively destroying vector species,
Clearing gametocytes in all carriers,
Previous control efforts led to the rapid
selection of insecticide-resistant strains
of mosquitoes,
26. VECTOR CONTROL . . .
26
Measures directed against vectors designed to:
Limit reproduction of vectors,
Reduce the longevity of vectors,
Minimize vector-human contact,
Wider mechanisms have been used,
Biological agents,
Bacterial toxins,
Insect growth regulators,
Botanical repellents,
Immunological,
Chemical insecticides,
27. VECTOR CONTROL . . .
27
Four groups have been used extensively:-
Organochlorine (DDT),
Organophosphates,
Carbamates,
Pyrethroids,
Organochlorine (DDT) for agriculture:
Introduced in 1934,
Banned in 1983,
DDT in malaria control:
Launched in 1949 as IRS,
Completely removed in 2000,
CHEMICAL INSECTICIDES
28. VECTOR CONTROL . . .
28
Organophosphates as IRS:
Malathion,
Fenitrothion,
Pirimiphos-methyl,
Pyrethroids as LLINs,
Most popular in malaria
control due to:
Low cost
Low mammalian toxicity,
Higher efficiency to
invertebrates,
Permethrin,
Deltamethrin,
Cypermethrin
Cyfluthrin,
Etofenprox,
Lambda-cyhalothrin
Synthetic Pyrethroids:
CHEMICAL INSECTICIDES . . .
29. VECTOR CONTROL . . .
29
Have their own mode and site of action,
Active molecules:-
Quickly infiltrates through the integument,
Reach the site of action,
Bind with the action sites such as:-
vital enzyme,
nerve tissue,
receptor proteins,
kill insects at the threshold concentration,
MODE OF ACTION OF INSECTICIDES
30. VECTOR CONTROL . . .
30
Properties of chemical insecticides:-
Lethal,
Sub-lethal,
Excitation/repellent,
Insecticides efficiency is affected by:-
Insecticide resistance,
Inadequate resources,
Poor quality,
Operational failure:
• overuse or misuse,
MODE OF ACTION OF INSECTICIDES . . .
31. INSECTICIDE RESISTANCE
31
It is a decrease in sensitivity to a given chemical:-
The resistance should be
Statistically defined,
Heritable to the progeny,
Evaluated relative to the susceptible population,
Insecticide resistance in insects occur due to
one or the combined effect of the following:-
1. The physiological resistance,
2. Behavioral resistance,
3. Reduced toxicant uptake:-
Due to altered cuticle,
Selection of resistant forms,
Evolution of resistant populations,
For a given insect population, insecticide resistance means:
32. INSECTICIDE RESISTANCE . . .
32
I. Metabolic resistance:
Modification of the three enzyme groups:
i. Cytochrome P450 Mono-oxygenases (CYP450s),
ii. Carboxyl/cholinesterases,
iii. Glutathione-S-transferases (GSTs),
• Results in over production of detoxifying enzymes,
II. Target site modification:
Mutational changes in neuronal VGSC,
(e.g., kdr mutation),
In these case insecticides no longer bind to target sits,
1. THE PHYSIOLOGICAL RESISTANCE
33. INSECTICIDE RESISTANCE . . .
33
Example: Pyrethroid resistance have been developed
in An. gambiae population b/s of two mechanisms
1. Metabolic resistance:
Due to elevated level of detoxifying enzymes,
2. Altered target site (kdr):
Two point mutations at VGSC,
∆ leucine to phenylalanine (L1014F), W. African type,
∆ leucine to serine (L1014S), East African type,
PHYSIOLOGICAL RESISTANCE . . .
34. INSECTICIDE RESISTANCE . . .
34
2. THE BEHAVIORAL RESISTANCE
Insects move away from insecticide-treated areas,
Often without lethal consequences,
Changes the insects customary behavior,
Movement of insects is of two types:-
Direct contact or excitation (irritancy),
after making physical (tarsal) contact,
Non-contact or spatial repellency,
without making physical contact,
An. gambiae s.s. ,for example, is changing its behavior in Africa:
Its endophilic nature is changing to exophilic,
shifting from human to animal feeding pattern,
36. INSECTICIDE RESISTANCE . . .
36
I ) Biotic factors:-
Rapid reproduction of insects,
The inherent nature of insect species,
Abundant progeny,
Migration of insects & wide host range,
II ) Abiotic factors:-
Dosage of insecticides,
Period and frequency of applications,
Insecticides with similar mode of action,
Factors for resistance development (IRD)
37. INSECTICIDE RESISTANCE . . .
37
Makes insecticide use ineffective,
Limits the available vector control options,
In most cases, resistance confers cross-resistance,
i.e. Resistance to one insecticide confers resistance to
another insecticide,
Previous selection with an insecticide can confer
resistance to new materials, even without the pre-
exposure to the new one,
IMPACT OF INSECTICIDE RESISTANCE