The document discusses mosquito-borne diseases malaria and lymphatic filariasis, outlining their causative agents, life cycles, symptoms, treatment and prevention. Malaria is caused by Plasmodium parasites and transmitted by Anopheles mosquitoes, killing over 1 million people annually. Lymphatic filariasis is caused by parasitic worms transmitted by Culex and Mansonia mosquitoes and can lead to severe swelling of limbs.

1. MOSQUITOES-BORNE DISEASES
1 Part 1: Malaria

2.  Mosquitoes as a vector for malaria
- Biology – Life cycle
- Transmission
- Symptoms
- Treatment
- Prevention and control
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3. Every minute 2 people die of malaria. By the time we
will finish this lecture malaria would have killed120
more people
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4. PART 1: MALARIA
 Malaria kills at least 1.1 million people per year, and
probably more due to incomplete reporting in many of the
countries on which it imposes the greatest burdens
 Malaria is present in more than 100 countries, and
imposes an economically significant burden on the
populations of at least 80
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5. MALARIA: INTRODUCTION
 Malaria is caused by single-celled protozoan parasites of
the genus Plasmodium.
 The parasites are transmitted from person to person by
anopheline mosquitos.
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6. SOME HISTORY ON MALARIA
 Malaria is an ancient disease and references to what was
almost certainly malaria occur in a Chinese document
from about 2700 BC, clay tablets from Mesopotamia from
2000 BC, Egyptian papyri from 1570 BC and Hindu texts
as far back as the sixth century BC.
 The early Greeks, including Homer in about 850 BC,
Empedocles of Agrigentum in about 550 BC and
Hippocrates in about 400 BC, were well aware of the
characteristic poor health, malarial fevers and enlarged
spleens seen in people living in marshy places.
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7.  1880 – Alphonse Laveran in Algeria found the
parasit in red blood cells
 1894 – Patrik Manson suggested mosquitoes as a
carrier
 1890 – Grassi and Feletti  Plasmodium vivax
and Plasmodium malariae
 1897 – Welch Plasmodium falciparum
 1898 – Ronald Ross reported the life-cycle of bird
malaria in Culex fatigans
 1922 – Stephens  Plasmodium ovale
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8. BIOLOGY
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9. SOME IMPORTANT ANOPHELES SPECIES IN
MALAYSIA
 An. aconitus An. nigerrimus
 An. balabacensis An. subpictus
 An. dirus An. sundaicus
 An. donaldi
 An. flavirostris
 An. letifer
 An. leucosphyrus
 An. maculatus
 An. minimus
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10.  Four species of malaria parasite infect humans:
— Plasmodium falciparum occurs throughout tropical
Africa and in parts of Asia, the Western Pacific, South
and Central America, Haiti and the Dominican Republic;
— Plasmodium vivax is almost absent from Africa but is
the predominant malaria parasite in Asia and South and
Central America;
— Plasmodium malariae is found worldwide but has a
very patchy distribution;
— Plasmodium ovale occurs mainly in tropical West
Africa and rarely in the Western Pacific.
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11. MALARIOUS REGIONS OF THE WORLD
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WHO, 2010

12. 12

13. 13

14. 14

15. PLASMODIUM: LIFE-CYCLE
 Infection begins when sporozoites, the infective stages, are injected
by a mosquito and are carried around the body until they invade liver
hepatocytes
 Where they undergo a phase of asexual multiplication
(exoerythrocytic schizogony) resulting in the production of many
uninucleate merozoites.
 These merozoites flood out into the blood and invade red blood cells
where they initiate a second phase of asexual multiplication
(erythrocytic schizogony) resulting in the production of about 8-16
merozoites which invade new red blood cells.
 This process is repeated almost indefinitely and is responsible for the
disease, malaria.
 As the infection progresses, some young merozoites develop into
male and female gametocytes that circulate in the peripheral blood
until they are taken up by a female anopheline mosquito when it 15
feeds.

16.  Within the mosquito the gametocytes mature into male
and female gametes,
 Male gametes  microgametocyte
 Female gametes  macrogametocyte
 Fertilization occurs and a motile zygote (ookinete) is
formed within the lumen of the mosquito gut, the
beginning of a process known as sporogony.
 The ookinete penetrates the gut wall and becomes a
conspicuous oocyst within which another phase of
multiplication occurs resulting in the formation of
sporozoites that migrate to the salivary glands of a
mosquito and are injected when the mosquito feeds on a
16
new host.

17. MALARIA: LIFE-CYCLE
17
http://www.cdc.gov/

18. Stages of P. falciparum in thin blood smears.
Fig. 1: Normal red cell;
Figs. 2-18: Trophozoites (among
these, Figs. 2-10 correspond to ring-
stage trophozoites);
Figs. 19-26: Schizonts
(Fig. 26 is a ruptured schizont);
Figs.27, 28: Mature
macrogametocytes (female);
Figs. 29, 30: Mature
microgametocytes (male).
Illustrations from: Coatney GR, Collins WE,
Warren M, Contacos PG. The Primate
Malarias. Bethesda: U.S. Department of Health,
Education and Welfare; 1971.
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19. RING FORMS: EARLY TROPHOZOITES
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20. RING FORMS: EARLY TROFOZOITES
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21. DEVELOPING TROPHOZOITES
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22. IMMATURE SCHIZONTS
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23. MATURE SCHIZONTS
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24. MICROGAMETOCYTES
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25. MACROGAMETOCYTES
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26. 26

27. 27

28. MALARIA: SYMPTOMS
 Malaria begins as an influenza-like illness with attacks of fever
eight days or more after the bite of an infected mosquito
 Cycles of fever, shaking chills, drenching sweats and
headaches may develop.
 The frequency and severity of the fever depends on the malaria
species involved but it usually lasts 2–3 days
 The attacks of fever coincide with waves of parasite
multiplication and the destruction of red blood cells.
 Long-lasting infections often result in enlargement of the liver
and spleen.
 It is the most severe type of malaria and, if untreated, may
progress to shock, kidney and liver failure, coma or death 28

29. 29
differencebetween.net

30. MALARIA: TREATMENT
 Commonly used antimalarial drugs and the high
cost and toxicity of alternative drugs.
 e.g
- Chloroquine;
- Primaquine;
- Quinine;
- Tetracycline;
- Sulphadoxine-Pyrimethamine
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31. MALARIA: PREVENTION AND CONTROL
 Protective measures include the wearing of protective
clothing, the use of repellents on exposed skin, mosquito
coils and other insecticide vaporizers, sleeping under
mosquito nets, and improving dwellings.
 Visitors to malarious areas should use prophylactic drugs
to prevent the development of the disease in the event of
receiving an infective bite.
 Indoor application of residual insecticides to the walls and
ceilings of houses.
 Control or elimination of breeding sites
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32. MOSQUITOES-BORNE DISEASES
32 Part 2: Lymphatic Filariasis

33. INTRODUCTION
 Lymphatic filariasis is caused by three species of
parasitic worm which occur in the lymph vessels and may
cause huge swellings of the limbs and other parts of the
body.
 Although the disease causes much suffering and
disability it is rarely life-threatening.
 2 types:
1. bancroftian filariasis
2. brugian filariasis 33

34. BANCROFTIAN FILARIASIS
 Cause by Wuchereria bancrofti
 In rural areas, bancroftian filariasis is mainly transmitted
by some Anopheles species that are also malaria vectors,
and by Aedes.
 Urban bancroftian filariasis typically occurs in slums in
developing countries.
 It is transmitted by Culex quinquefasciatus, which breeds
in polluted water in drains, cesspits and ditches.
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35.  In 1996, it was estimated that some 107 million people were
infected in parts of China, India, other parts of south-east Asia,
the Pacific Islands, tropical Africa, and South and Central
America
 Bancroftian filariasis occurs in two forms: in the most common
form the microfilariae circulate in the blood at night, whereas in
the second form they occur continuously in the blood but
increase in number during the day.
 The vectors of the first form are Culex quinquefasciatus and
certain Anopheles species (which bite at night).
 The second form is found in the South Pacific and in some
rural areas in south-east Asia where the main vectors are
35
daytime-biting mosquitos such as certain Aedes species.

36. BRUGIAN FILARIASIS
 Brugian filariasis, caused by Brugia malayi and B. timori.
 In 1996, it was estimated to infect some 13 million people
mainly in south-east Asia.
 Its main vectors for B. malayi are the Mansonia species.
 B. malayi has been found in Macaques, leaf monkeys,
cats and civet cats
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37.  Brugian filariasis, caused by B. malayi, occurs in two
forms, of which the most common is transmitted at night
and the other during both day and night.
 The first form occurs in rural populations in rice-growing
areas in Asia.
 It is transmitted by night-biting Anopheles species and by
Mansonia species which breed in swamps and ponds
with aquatic vegetation.
 The second form is mainly a parasite of monkeys living in
swamps.
 Mansonia species breeding in swampy forests in
Indonesia and Malaysia may infect people living nearby.
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38.  B. timori is the least common, and therefore least studied
species of filaria known to cause lymphatic filariasis.
 B. timori also has no known animal reservoir.
 B. timori occurs on the islands of Flores, Timor and Alor,
to the east of Java, and is transmitted by Anopheles
barbirostris.
 Anopheles barbirostris, a vector that feeds at night. As a
result, high levels of B. timori microfilariae are found in the
blood at night. 38

39. LYMPHATIC FILARIASIS ENDEMIC COUNTRIES AND
TERRITORIES
39

40. AGENT FACTORS
Organism Vectors
W. bancrofti Culex
B. malayi Mansonia, Aedes
B. timori Anopheles
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41. FILARIAS
Wuchereria bancrofti
Approximately 90% of infections are caused by W. bancrofti, while most of the
remaining infections are caused by B. malayi (~9%) and B. timori (~1%).
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42. FILARIASIS: LIFE-CYCLE
 In the human host, the adult worms concentrate in the vessels
and nodes of the lymphatic system.
 Gravid females release motile sheathed microfilariae, which
migrate to the peripheral circulation.
 It takes approximately 6 to 12 months from initial infection to
the time when the microfilariae begin to appear in the
periphery.
 These peripheral microfilariae exhibit a fascinating circadian
rhythm, wherein they migrate at night into the peripheral blood
via the circulation, returning to the arterioles in the lungs during
the day.
 This migration to the periphery aids in the transmission of the
microfilariae to the vectors, which are primarily, though not
exclusively, night-biting mosquito species. 42

43.  After the microfilariae are ingested by the mosquito, the
sheath is lost and they migrate out of the mosquito
stomach and into the flight muscle tissues of the thorax.
 At this location, the microfilariae will molt three times,
developing into the infectious 3rd stage larvae (L3) after
approximately 10 to 20 days.
 The exact time required is dependent on the density of
infection in the mosquito and the local climate conditions
at the time of development.
 Infectious L3 larvae migrate to the proboscis of the
mosquito.
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44.  The larvae are not directly injected into the human host by the
mosquito, but rather are deposited on the skin and migrate into
the bite wound.
 The L3 larvae then migrate through subcutaneous tissues to
gain the lymphatic system, where they will develop into adults
over the course of approximately 1 year.
 Male and female adults will mate soon after reaching maturity
and gravid females subsequently release their motile
microfilariae.
 The chance of an infection being established from a single bite
by an infected mosquito is very low.
 The adult worms can live for many years, giving rise to large
44
numbers of microfilariae in the blood.

45. FILARIASIS: LIFE-CYCLE
45
http://www.cdc.gov/

46. FILARIASIS: CLINICAL SYMPTOMS
 People do not know they have lymphatic filariasis unless
tested
 The clinical symptoms and signs are mainly determined
by the duration of the infection.
 The adult worms, which live in the lymphatic vessels, can
cause severe inflammation of the lymphatic system and
acute recurrent fever.
 Secondary bacterial infections are a major factor in the
progression towards lymphoedema and elephantiasis,
the characteristic swelling of the limbs, genitalia and
breasts
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47.  Hydrocele is another common clinical manifestation of
chronic infection with W. bancrofti.
 This condition results from the accumulation of fluid in the
serous membrane surrounding the testes.
 Swelling increases over the period of the chronic infection
and, when left untreated, leads to very large growth of the
scrotum.
 This can be very painful and another severe impediment
to mobility
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48. 48

49. FILARIASIS: TREATMENT
 People who are infected can be treated with
diethylcarbamazine (DEC).
 This has been used in some areas for the mass treatment
of infected people to reduce morbidity and transmission.
 DEC is much more lethal to the microfilariae than to the
adult worms, which may only be killed after prolonged
treatment.
 The death of microfilariae due to the action of DEC may
cause nausea and other unpleasant, but not dangerous,
side-effects, which sometimes discourage people from
completing courses of treatment.
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50. FILARIASIS: PREVENTION AND CONTROL
 Control or elimination of breeding sites in polluted water is
possible by improving sanitation systems and hygiene in
general
 Indoor residual spraying
 To remove or destroy the aquatic vegetation to which the
larval and pupal stages are attached.
 Sometimes, as for instance in swamp forests in parts of
Indonesia and Malaysia, larval control measures are
impracticable because of the large extent of the breeding
areas.
 In such situations the main emphasis should be on the
prevention of mosquito bites by means of self-protection.
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