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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:
 Some medically important orders of class insecta
include:
Order Diptera
Order Heteroptera
Order Phthiraptera (reading assignment)
Order Siphonaptera (reading assignment)
Class Insecta
2
 Medically important families of order Diptera include:
 Family Culicidae,
 Family Simulidae,
 Family Psychodidae,
 Family Glossinidae ,
Class insecta
3
Order Diptera
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
Life cycle: Complete metamorphosis:
Egg --- larva ---- pupa ---- adult
Class insecta . . . Diptera . . .
5
Family Culicidae: The mosquitoes
Class insecta . . . Diptera . . .
6
Culicidae: The mosquitoes
Diptera . . . Culicidae . . .
7
Morphology
Aedes aegypti
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
Diptera . . . Culicidae . . .
9
Culex quinquefasciatus
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
 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:
Diptera . . . Culicidae . . .
12
 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
Diptera . . . Culicidae . . .
14
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.
Diptera . . . Culicidae . . .
16
Malaria Life cycle; vector part
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.
Diptera . . . Culicidae . . .
18
Migratory routes & developmental sites within the
mosquito for malaria parasites and filarial worms
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),
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,
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,
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 . . .
Diptera . . . Culicidae . . .
23
Malaria vectorial system . . .
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 . . .
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,
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,
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
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 . . .
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
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 . . .
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:
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
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 . . .
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,
INSECTICIDE RESISTANCE . . .
35
3. Reduced toxicant uptake
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)
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
38

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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
  • 7. Diptera . . . Culicidae . . . 7 Morphology Aedes aegypti
  • 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
  • 9. Diptera . . . Culicidae . . . 9 Culex quinquefasciatus
  • 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:
  • 12. Diptera . . . Culicidae . . . 12
  • 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
  • 14. Diptera . . . Culicidae . . . 14
  • 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 . . .
  • 23. Diptera . . . Culicidae . . . 23 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,
  • 35. INSECTICIDE RESISTANCE . . . 35 3. Reduced toxicant uptake
  • 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
  • 38. 38