10 malaria and filariasis


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10 malaria and filariasis

  1. 1. MOSQUITOES-BORNE DISEASES1 Part 1: Malaria
  2. 2.  Mosquitoes as a vector for malaria - Biology – Life cycle - Transmission - Symptoms - Treatment - Prevention and control 2
  3. 3. Every minute 2 people die of malaria. By the time we will finish this lecture malaria would have killed120 more people 3
  4. 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 4
  5. 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. 5
  6. 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. 6
  7. 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 7
  8. 8. BIOLOGY 8
  9. 9. SOME IMPORTANT ANOPHELES SPECIES INMALAYSIA An. aconitus An. nigerrimus An. balabacensis An. subpictus An. dirus An. sundaicus An. donaldi An. flavirostris An. letifer An. leucosphyrus An. maculatus An. minimus 9
  10. 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. 10
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  15. 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. 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. 17. MALARIA: LIFE-CYCLE 17 http://www.cdc.gov/
  18. 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. 18
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  28. 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. 29differencebetween.net
  30. 30. MALARIA: TREATMENT Commonly used antimalarial drugs and the high cost and toxicity of alternative drugs. e.g - Chloroquine; - Primaquine; - Quinine; - Tetracycline; - Sulphadoxine-Pyrimethamine 30
  31. 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 31
  32. 32. MOSQUITOES-BORNE DISEASES32 Part 2: Lymphatic Filariasis
  33. 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 filariasis2. brugian filariasis 33
  34. 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. 34
  35. 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. 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 36
  37. 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. 37
  38. 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
  40. 40. AGENT FACTORSOrganism VectorsW. bancrofti CulexB. malayi Mansonia, AedesB. timori Anopheles 40
  41. 41. FILARIAS Wuchereria bancroftiApproximately 90% of infections are caused by W. bancrofti, while most of theremaining infections are caused by B. malayi (~9%) and B. timori (~1%). 41
  42. 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. 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. 43
  44. 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. 45. FILARIASIS: LIFE-CYCLE 45 http://www.cdc.gov/
  46. 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 46
  47. 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 47
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  49. 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. 49
  50. 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. 50