Arthropod-born infections

Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases.

Many such vectors are haematophagous, which feed on blood at some or all stages of their lives.

1. ARTHROPOD BORNE DISEASES Dr. Dalia El- Shafei Assistant Professor , Community Medicine Department, Zagazig University

2. Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases. Many such vectors are haematophagous , which feed on blood at some or all stages of their lives.

3. Arthropod-borne Viral Hemorrhagic Diseases

4. Acute febrile diseases with extensive external & internal hemorrhage, usually serious & may be associated with shock & liver damage with high case fatality. The most important of these fevers are Yellow fever, Dengue fever, Rift valley fever & West Nile fever.

5. YELLOW FEVER

6. A communicable arthropod-borne viral hemorrhagic quarantinable acute disease of short duration & varying severity . Causative agent: Y ellow fever virus .

7. Endemic in Africa & South America in zone between 15° north & 100° south latitude of equator ( yellow fever belt) .

8. How Egypt is protected from Yellow Fever: Absence of yellow fever in Egypt & its rarity in other areas such as Eastern Africa despite wide spread of vector aedes Egypti may be due to cross immunity from other flavi virus (e.g. dengue, west Nile, Japanese encephalitis) in population which may be providing an ( ecological barrier ).

9. Reservoir : Sylvatic or Jungle yellow fever: main reservoir in forest area is vertebrates other than human mainly monkeys & vector is forest mosquitoes ( haemagogus species). Human has no essential role in transmission of yellow fever. { Sylvatic is a scientific term referring to diseases or pathogens affecting only wild (sylvan means forest-dwelling) animals. The word "sylvatic" is also simply a synonym for "sylvan" = "of the forest“}. Urban yellow fever: reservoir is human & vector is Aedes aegypti mosquitoes .

10. Period of communicability: No man-to-man transmission. B lood of man is infective to mosquito shortly during late IP & during first 3-5 days of disease . In mosquitoes after biting an infected person there is 9-12 days extrinsic IP, then the mosquito becomes infective all over its life. T here is also trans-ovarian transmission which may contribute to maintenance of infection.

11. Mode of transmission: Urban yellow fever: bite of infective female Aedes aegypti mosquitoes . Sylvatic or jungle yellow fever: bite of several species of genus Haemagogus . IP: 3-I0 days ( 6 days in international health regulation).

12. Virus Transmission Zoonotic virus flaviviridea

13. Susceptibility & resistance: 1-Age & sex: all ages & both sexes are susceptible . 2.Immunity : infection is followed by absolute immunity, 2 nd attacks are unknown. Transient passive immunity to inborn infant of immune mother occurs for up to 6 ms. 3.Occupation : W oodcutter , H unter.

14. IP 3- 10 days Symptoms Influenza like Hepatic Hemorrhagic illness Death 20-50%

15. Clinical features: - Mild form: sudden onset, FHMA, chills, muscle pain, prostration, nausea & vomiting. - Faget sign: slow pulse out of proportion of elevated temperature. - Jaundice is moderate early in disease & intensified later. - Albuminuria or anuria may occur, leucopenia. - Most of the manifestations resolve after 5-7 days. - After a brief remission of hours to a day some cases progress to severe form (hemorrhagic symptoms including epistaxis, gingival bleeding, haematemesis (coffee ground or black) melena, liver & renal failure). - Fatality rate of jaundiced cases may reach 20-50%.

16. Diagnosis: 1. Isolation of virus from blood by inoculation of suckling mice, mosquito or cell culture. 2. ELISA “viral antigen in blood”. 3. PCR “viral genome in blood & liver tissue”. 4. Serologic diagnosis “specific IgM in early sera or rise in titre of specific antibodies”.

17. Prevention & control Vaccine 17 D vaccine Personal protective measures

18. Prevention: General : 1) Environmental sanitation: A) Eradication or control of Aedes Aegypti : i. Anti-larval & anti- pupal measures ii. Anti-adult measures iii. Jungle mosquitoes “impractical”. B) Human protection against mosquitoes: e.g. protective clothing, bed nets, repellents. 2) Health education : modes of transmission.

19. Individual measures for control of mosquito bite

20. Specific: 1 ) Immunization: a) Active Immunization: “ most effective preventive measure” - 17 D vaccine: ■ Live attenuated vaccine “non virulent strain cultivated on chick embryo & subsequently freeze dried”. Vaccine is stored at -25°C. ■ Single dose, 0.5ml, S.C. injection . ■ 99 % immunity: International health regulation considered vaccine effectiveness to start after 10days & persists for 10 years & then re-immunization is required. ■ No or minimal reaction “1 st 4 ms of life....vaccine associated encephalitis”. ■ Given to: - International travelers coming from or going to endemic countries. - Since 1989 WHO has recommended that at risk countries in Africa that fall in the endemic belt should incorporate it into their routine childhood immunization program after 6 month.

21. Dakar vaccine: - Live attenuated neurotropic virus. - It is produced in mouse brain & administered by cutaneous scarification. - It is not approved by WHO for international use as it leads to encephalitis .

22. International measures: It is one of quarantinable diseases & following measures should be done to prevent introduction of yellow fever from endemic area (Yellow Fever belt) into receptive area (areas free of yellow fever, but the vector is present & population is susceptible e.g. in Egypt): * Notification within 24 hs by governments to WHO.

23. * Valid vaccination certificate: a . Is required from all international travelers including children coming from or going to endemic areas "Yellow Fever belt". b . Validity starts 10 days after primo-vaccination & lasts for 10 ys . c. Validity starts on same day after re-vaccination & lasts for 10 ys . d. If no certificate is available: traveler is isolated for 6 days from date of leaving endemic area. e. If traveler arrives before 10 days of vaccination, i.e. certificate is not valid yet: traveler is isolated until certificate becomes valid or until end of international IP calculated from day of leaving last endemic area. f. Traveler is quarantined in mosquito-proof accommodation in airport. g. This certificate is required by many countries including Egypt.

24. Disinfection of any aircraft leaving an endemic area for receptive area, by aerosol spray of suitable insecticide, shortly before departure and also on arrival . Quarantine of imported monkeys.

25. DENGUE FEVER (Break Bone Fever)

26. C ommunicable arthropod-borne viral hemorrhagic acute febrile disease of short duration & varying severity. It is endemic in south Asia. Dengue 1, 2, 3, 4 are now endemic in Africa. In recent years outbreaks of dengue fever has occurred on east coast of Africa from Mozambique to Ethiopia to Saudi Arabia.

27. Causative agent: viruses of dengue fever: 1, 2, 3 & 4 types. Reservoir: Man-mosquito cycle in tropical urban centers. A monkey-mosquito cycle may serve as a reservoir in south Asia & West Africa . Mode of transmission: bite of infective Aedes aegypti mosquito.

28. Clinical picture: S udden onset of fever for 3-5 days, intense headache, rash early generalized erythema & maculopapular rash. Minor bleeding “epistaxis , gum bleeding and peteachia ”. Generalized bleeding & lymphadenopathy.

29. Prevention & control: 1 . Environmental sanitation: b. Eradication or control of mosquito vector. c. Human protection against mosquitoes. 2 . Health education.

30. RIFT VALLEY FEVER

31. C ommunicable arthropod-borne viral zoonotic disease. It was introduced to Egypt from East & South Africa in1977, causing outbreak in animals, that was transmitted to man. Causative agent: Rift valley fever virus. Reservoir: Cattle, sheep, goats. Mode of transmission: - bite of some infective Aedes & Culex species. - Handling diseased animals & their tissues.

32. Aborted animals from infected cow with RVF

33. Clinical picture: Disease is usually mild & self-limited: fever, influenza like picture (FHMA) & recovery. Severe cases show hemorrhagic fever, liver necrosis, damage of retina & encephalitis May be fatal.

34. Prevention and control: 1 . Measures for animal reservoir: • Prevention & control in animals “vaccination”. • Quarantine of imported animals from endemic areas. 2 . Eradication or control of mosquito vector. 3 . Measures for man: • Human protection against mosquitoes

35. VIRAL ENCEPHALITIS

36. A n endemic disease in different parts of world . U sually mild but serious outbreaks have been reported with involvement of brain , spinal cord and meninges. Occurrence:  West Nile virus encephalitis: Africa & Middle East.  Eastern equine encephalitis: East U.S.A  Western equine encephalitis: West U.S.A Japanese B encephalitis: Japan , Korea, Philippines & India.

37. Agent: specific arbovirus Reservoir: Birds & some wild & domestic animals. Vector: Mostly by mosquitoes & some by ticks. In Egypt, WNV is transmitted by culex .

38. Prevention: 1. Eradication or control of vector . 2 . Protection of man from vector 3 . Quarantine measures for imported birds & animals.

39. Other viral haemorrhagic fevers

40. Such as: Lassa fever, Marburg disease & Ebola virus disease H ighly fatal & manifested by hemorrhagic maculo-papular rash & bleeding from all orifices of body in case of Ebola virus disease.

41. Eating the bush meat is behind the outbreak

42. Will Ebola ever end in Africa??? WHO confirms new Ebola case in Liberia On April 1, 2016

43. EPIDEMIC TYPHUS (louse - borne typhus)

44. Causative organism : - Rickettsia prowazeki . Reservoir of infection:- - Man, case , organisms are found in blood throughout febrile stage. - Vector: louse , " pediculus humanus ". Modes of transmission:- 1- Contamination of skin with faeces of infected louse. The organisms find entry through skin abrasions by scratching. 2- Inhalation of dried faeces of infected louse. N.B.: 1- The louse bite is not infective. 2- There is no transovarial transmission from louse to its generations.

45. Clinical picture:- I.P .: 12-14 days. Abrupt onset of high fever, rigors, body aches. Face becomes flushed then cyanotic & patient soon becomes dull & confused. Skin rash appears on the 5 th day on folds of axilla, anterior part of forearms then trunk & back. Complications: Bronchopneumonia , thrombotic changes, gangrenes of fingers, toes and genitalia. Diagnosis : C/P & confirmed by lab investigation as weil-felix reaction (agglutination test).

46. Prevention:- 1- Community development. 2- Health education “ personal cleanliness” . 3- Measures against lousiness :- - Providing washing facilities: - Delousing of population “washing facilities & dusting with a suitable insecticide”. 4- Specific prevention: - Typhus vaccine (live attenuated vaccine), Madrid E typhus vaccine “single IM dose, immunity for 5 years”.

47. Control: * Cases:-  Notification to LHO.  Isolation in hospital after dusting .  Terminal disinfection by dusting (to kill any lice) & steam disinfection for clothes & bedding (to kill rickettsia).  Treatment by tetracycline 500 mg / 6hs for seven days.  Release after clinical recovery of the case. *Contacts:-  Delousing by bathing & dusting.  Surveillance for 2 weeks, for case-finding.

48. *Epidemic measures:-  Delousing of confined groups & underdeveloped communities by washing facilities & dusting.  Vaccination of high risk groups.  Searching for the source of infection.

49. ENDEMIC (MURINE) TYPHUS (flea-borne typhus)

50. Causative organism: R . mooseri . Reservoir of infection: Rat & vector is rat flea. Mode of transmission: Contamination of skin with faeces of infective fleas. Organisms find entry through skin abrasions.

51. Clinical picture: I . P. : 8 - 14 days. Resembles mild epidemic typhus. Diagnosis: Weil- felix reaction. Prevention : - Eradication & control of rats. - Control of fleas. N.B.: No specific prevention. Control of cases & contacts: as usual.

52. Q-FEVER

53. A cute febrile rickettsial disease, with minimal clinical manifestations mainly in form of atypical pneumonia . Agent: Coxiella Burnetti is an organism which has an unusual stability; it survives adverse physical conditions such as dryness, pasteurization & many disinfectants. Reservoir: T icks , human body lice, small wild mammals, cattle, sheep, goats, birds and man. Period of communicability: Direct transmission from person to person is rare.

54. Modes of transmission: - Occupational: direct contact with domestic animals . - Air borne: dust contaminated by placental tissues, birth fluids & excreta of infected animals . - Ingestion of raw milk - Trans- conjunctival - From person to person.

55. Case presentation: Incubation Period: 14-21 days Clinical Picture: Onset is sudden with chills, headache, malaise, weakness and severe sweats. Infection may be in apparent or non-specific. Pneumonitis is found in X-rays. Spontaneous recovery is common.

56. Diagnosis: - Culture in eggs or animal inoculation from blood after onset of disease . - Serological tests may show a rising titre . - Weil-Felix reaction is negative .

57. Control: A - Preventive measures: 1- Animal control: - Vaccination or antibiotics . - Milk pasteurization at high. 2-Health education: A dequate disinfection & disposal of animal products. 3- Immunization: Inactivated vaccine Q 34, “1ml SC”. For high risk workers as lab workers & workers in contacts with animals & animal products.

58. B-Control of cases and contacts: 1- Cases : a- Notification: to LHO. b- Isolation: none c- ttt : Tetracycline or Chloramphenicol is effective. d- Disinfection: Concurrent of sputum, blood & articles 2- Contacts: no special measures, Search for cases. C - Epidemic and International measures: No specific measures.

59. RELAPSING FEVERS

60. TICK- BORNE RELAPSING FEVER “TBRF” A systemic spirochetal disease due to infection with Borrelia duttoni Transmitted by ticks

61. Agent: spirochete Borrelia duttoni “many different strains according to areas of isolation and or vector rather than biological differences”. Reservoir : In most areas, it affects rodents & accidentally man but in Central Africa , it primarily affects man. Period of communicability: Ticks remain infective for several years & pass infection transovarially to their progony . Mode of transmission: B ite (through the saliva) or coxal fluid of an infected tick.

62. Case presentation : IP: 3-10 days - Periods of fever lasting 2-9 days alternating with afebrile periods of 2-4 days - The number of relapses varies from 1 to 10 or more. Each febrile period terminates by crisis & disease lasts for more than 16 days. - Transitory petechial rashes are common. - Bronchitis , nerve palsies, hepatosplenomegaly & renal fever can occur. - Fatality rate: 2-10 %.

63. Diagnosis: Blood films show circulating Borrelia duttoni . Specimen must be taken during the febrile attack.

64. Control: A-Preventive Measures: 1) Control of ticks & rodents: treating interiors of houses by benzene hexachloride or dieldrin to prevent ticks from infesting human habitations. Cracks & proper housing construction are very important. 2) Protection of susceptible: Use personal protection measure including use of repellents & protective clothes. Also, chemoprophylaxis with tetracycline after exposure (tick bite) is used when risk of acquiring the infection is high. 3) International measures: notification to W.H.O.

65. B-Control of cases & contacts: 1) Cases: Notification: to LHO Isolation: precautions with blood & body fluids. Concurrent disinfection : none Treatment : tetracycline 2) Contacts: Case findings. C- Epidemic measures: apply insecticides to clothes & houses.

66. LOUSE BORNE BELAPSING FEVER “LBRF” S pirochetal disease caused by Borrelia recurrentis & transmitted by human louse. 1 or 2 & never more than 4 relapses. Death is often in the 1 st attack . Agent : Gram negative spirochete ( Borrelia recurrentis ). Reservoir: Man is the only reservoir.

67. Period of communicability: Louse becomes infective 4-5 days after ingestion of blood from an infected person & remains infective for life (20-40 days) Mode of transmission :Transmitted from infected person to new individuals by human louse; Pediculus humanus . Infection occurs by contamination of wound with louse's body fluid, following crushing of louse on skin . N.B .: (1) No transovarian transmission. (2) Neither bites nor faeces of louse cause infection.

68. Case presentation: - IP: 2-10 days - C/P: FHMA, skeletal & abdominal tenderness with palpable liver & spleen, jaundice & purpura occur. Hyperpyrexia, hypotension & cardiac failure can be fatal.

69. Diagnosis: Blood should be taken during febrile period & examined by dark ground illumination or stained blood films. Intraperitoneal inoculation or culture in lab animals can be used to recover the spirochetes.

70. Control: A-Preventive measures: 1) Delousing: residual insecticide powder. 2 ) Protection of susceptible: use of repellents & protective clothes. Also, chemoprophylaxis with tetracycline after exposure is used when risk of acquiring the infection is high. 3 ) International measures: notification to WHO

71. B- Control of cases and contacts: 1) Cases: - Notification : to LHO - Isolation: precautions with blood & body fluids. - Concurrent disinfection : none - ttt : procaine penicillin injection followed by oral tetracycline 2) Contacts: Case findings. C ) Epidemic measures: Apply insecticides to clothes & houses.

72. FILARIASIS ( BANCROFTIAN FILARIASIS)

73. Filarasis in Egypt: It is endemic in Egypt. Nile Delta: Qalyobia ( Sandanhour ), Menoufia ( Kafr al Hemma & Shenawaii ), Sharkia (El korain village), Dakahlia , Kafr el sheikh, Gharbia Upper Egypt: Giza ( Badrashin ) & Assuit . A program for elimination of lymphatic filariasis started in 2002 & showed successful results.

74. Causative agent: Nematode : Wuchereria bancrofti & other long thread-like worm (male 4 cm & female 7cm). Adult worm normally resides in lymphatic of infected people. Female worms produce microfilaria that reach blood stream 6-12 months after infection. The microfilaria appears in large number during night with maximum density in blood between 10 p.m & 2 a.m ( nocturnal periodicity ).

75. Reservoir of infection: Human with microfilaria in their blood. Man is definitive host & mosquito is intermediate host . Period of communicability: Human can infect mosquito when microfilaria is present in peripheral blood. They can persist for 5-10 ys or longer after infection, mesquite becomes infective after about 2 weeks.

76. Mode of transmission: Bite of infective mosquito: in Egypt: female Culex pipiens , but it could be transmitted by bite of Anopheles gambia & Aedes . Mosquito cycle begins when microfilaria are ingested by female mosquito during feeding. Microfilaria penetrates stomach wall of insect & develops in thoracic muscles into elongated infective filariform larva that migrate to proboscis. When mosquito bites an individual, larvae can enter punctured skin, then passes via lymphatic where they molt & become adult.

77. Susceptibility & resistance: General susceptibility : Filarial disease appears only in small % of infected persons. Immunity : Man may develop resistance only after many years of exposure to infection. Environment : Unsanitary planning with inadequate sewage disposal, where breeding places of culex & collection of water for other species.

78. Clinical feature: Asymptomatic A cute form: fever , lymphangitis & lymphadenitis Chronic obstructive form: due to fibrosis & obstruction of lymphatic vessels after repeated attacks, 10 years later, leading to elephantiasis of limbs, breast & genitalia, hydrocele, chyluria , paroxysmal nocturnal asthma & severe eosinophilia.

79. Diagnosis: D etection of microfilaria in blood during maximum presence (nocturnal). Live microfilaria can be seen in a drop of blood, geimsa smears.

80. Prevention: General : 1. Environmental sanitation: a. Eradication or control of mosquito vector b. Human protection against mosquitoes: e.g. protective clothing, bed nets, repellents . 2. Health education: M odes of transmission & Protection against mosquito bites.

81. Specific “Mass drug administration (MDA )”: WHO recommends MDA in Endemic areas A nnual single dose, diethylcarbamizine citrate (DEC) 6mg/kg BW + 400 mg albendazole for 4-6 years, or regular use of DEC-medicated cooking salt for 1-2 years . - 2 fold purpose: preventing future cases of lymphatic filariasis & helping those people who are already suffering from disease .

82. Control: Control of cases: 1. Notification : to LHO. 2. Isolation : not practical. As far as possible, patients with microfilaria treated with anti-filarial drugs should be protected from mosquitoes to reduce transmission.

83. 3. Specific ttt : DEC ( Banocid , Hetrazan ). ttt results in rapid suppression of most or all MF from blood , but may not destroy all adult worms. Low level of MF may reappear after ttt . Therefore, ttt must usually be repeated at yearly interval, & lab follow up should be done for treated cases.

84. Elimination of lymphatic filariasis in Egypt WHO has launched a global program for elimination of lymphatic filariasis worldwide. Elimination of lymphatic filariasis means a reduction of disease incidence close to zero as a result of continued & coordinated activities. WHO's strategy comprises 2 components: interruption of transmission, & care for those who already have disease . To interrupt the transmission, the entire population at risk must be covered by MDA for a period long enough to ensure that level of MF in blood remains below that which is necessary to sustain transmission. Egypt started the program for elimination since 2000 following WHO recommendation of administering DEC & Albendazole .

85. LEISMANIASIS

86. G roup of diseases due to infection with Leishmania which is transmitted by sandflies . Reservoir: man, dogs, wild rodents & foxes . Vector: several species of sandflies.

87. Leismaniasis In Egypt: A focus of visceral leishmaniasis was discovered in El Agamy , in 1982 . The last case there was reported in 2005. O nly one more case of visceral leishmaniasis was reported, in the Suez region in 2008. However , due to a lack of awareness among medical practitioners, visceral leishmaniasis is suspected to be underreported. Import of cases from Libya and Sudan may occur regularly & go unnoticed.

88. Cutaneous leishmaniasis has been an increasing problem in Egypt. Known foci are among nomads in North Sinai. R eported number of cases is estimated to be 4-5 times lower than the real number of cases. People at risk are soldiers, laborers, & immunocompromised adults.

89. CUTANEOUS LEISHMANIASIS (Oriental sore) New world cutaneous Leishmaniasis : L. mexicana . Old world cutaneous Leishmaniasis : L . tropica , L. major & L. aethiopica . Modes of transmission: 1. Bites of infective sandfly . 2. Contact with skin lesions of case . Occurrence: L . Mexicana: Mexico & Peru. L . tropica : Central Asia, India & West Africa. In Egypt it is found in Alexandria region. L . major: Mediterranean & Southwest Asia. L . aethiopica : Ethiopia & Kenya.

90. Clinical picture: Starts with a papule & enlarges to become an indolent ulcer on exposed parts of body which either heals or lasts for many years.

91. MUCOCUTANEOUS LEISHMANIASIS Causative agent: L. braziliensis “central & south America”. C/P: nasopharyngeal destruction & deformities.

92. VISCERAL LEISHMANIASIS (Kala Azar ) Causative agent: L. donovani C/P: C hronic infection with fever, hepatosplenomegaly , lymphadenopathy & anaemia . There is progressive emaciation & weakness with generally fatal outcome if not treated

93. Diagnosis of Leishmaniasis : 1 . Demonstration of Leishmania bodies in stained smear of ulcer, organ or blood. 2. Culture if necessary.

94. control : Prevention : General:  Vector control e.g. by insecticides.  Protection of man from sandflies: e.g. repellents, protective clothes.  Proper control of domestic animals especially dogs  Rodent control  Health education .

95. Specific :  Active immunization: live attenuated vaccine to minimize severity of disease in some endemic areas.  International measures: non

96. Control of cases & contacts: Cases : - Early case finding & treatment. - Skin lesions must be covered to avoid infection of vector & contact infection of exposed individuals. Contacts : - Health education. - Examination.

97. MALARIA

98. A parasitic re-emerging disease 1 million deaths/year in world “mostly young African children” Recently multiple foci of drug resistant malaria are encountered in different areas. Tropical & subtropical areas .

99. Tropical Africa Southwestern Pacific Forested areas of South America Southeastern Asia Indian sub-continent

100. Causative agent: Protozoan parasites with asexual & sexual phase “Plasmodium vivax , P. falciparum, P. ovale & P. malaria. Mixed infections are not infrequent in endemic areas.

101. Reservoir: Humans: only important reservoir of human malaria. Case may have several plasmodia species at same time. I nfective stage to vector is gametocytes which have to be mature, both sexes, sufficient density & viable . A ntimalarial drugs lose viability of gametocytes. Female anopheline mosquito is definitive host Infective stage to man is sporozoite .

102. Period of communicability: As long as infective macro gametes are present in blood of patients. This varies with parasite species. In untreated cases it may reach up to 3 years, however, with antimalarial drugs the period is shortened greatly. Humans may infect mosquitoes as long as infective gametocytes are present in the blood, this varies with parasite species and with response to therapy. Untreated or insufficiently treated patients may be a source of mosquito infection for one to several years. Transfusion transmission may occur as long as asexual forms remain in the circulating blood. Stored blood can remain infective for at least a month.

103. Mode of transmission: 1- Bite of infective female anophiline mosquito, where sporozoite are present in salivary glands. Most species feed at night; some important vectors also bite at dusk or in the early morning. 2- Infection or transfusion of infected blood or use of contaminated needles & syringes (e.g. injecting drug users) may also transmit malaria. 3- Congenital transmission occurs rarely. However, pregnant women are vulnerable than others to falciparum malaria (and possibly other plasmodium species).

104. Incubation period: Time between infective bite & appearance of clinical symptoms is 9-40 days according to type of malaria species . With infection through blood transfusion, IP depend on the number of parasites infused & are usually short, but may range up to about 2 months.

105. Susceptibility: It is universal except in human with specific genetic traits. Age : - All ages are affected. -Tolerance to clinical disease is present in adults in highly endemic areas where exposure to infective anopheline is continuous over many years. Sex: -Males are more exposed usually due to outdoor life. Immunity: - no natural immunity. -Infection induces species specific immunity. -Some sort of active immunity develops in endemic areas.

106. Genetic: Most indigenous populations of Africa show a natural resistance to infection with P.vivas which is associated with absence of Duffy factor on their erythrocytes. Persons with sickle cell trait ( heterozyotes ) show relatively low parasitaemia when infected with P. falciparum, so relatively protected from severe disease; homozygote's suffering from sickle cell disease are at increased risk of severe falciparum malaria especially anemia. HIV infection: increased risk of symptomatic falciparum malaria & its severe manifestations. Sociocultural & environmental factors: Low socioeconomic standard, outdoor sleeping, agricultural societies & vitiated air contribute to spread of infection. Suitable environment for mosquito breeding “ hot+humid+rainfall ”

107. Clinical picture: slowly rising fever, chills, malaise, headache, nausea, lassitude, muscle & joint pain, then rigor sensation & rapidly rising temperature ending by profuse sweating. The cycle of fever, chills, sweating is repeated either daily or every other day or every 3 rd day or irregularly according to malaria species. Relapses may occur after a period of cure without parasitaemia at irregular interval up to 5 years.

108. Complications: - Anemia. - Splenomegaly. - Abortion & fetal infection. - Falciparum malaria may be associated with respiratory distress, jaundice, liver failure, encephalopathy, pulmonary & cerebral edema, coma & death.

109. Diagnosis: • M alaria parasites in thick blood film . • Repeated microscopic examination every 12-24 hs may be necessary to cover all parasite species . • Several tests have been developed: The most promising are: - Rapid diagnostic tests: plasmoidal antigens in blood . - PCR: most sensitive method. - Demonstrating antibodies which appear after 1 st week of infection but may persist for years denoting past malaria infection.

110. Prevention: 1 . General preventive measures: of arthropod borne disease. - Environmental sanitation, vector control and Health education: * Elimination of the breeding sites of mosquito. * Eradication of larval stages by spraying crude oil & larvicides on water surface. * Destruction of adult mosquitoes by using suitable insecticides (liquid aerosol, pyrethrium ). - Human protection : * Screening of windows and doors, using bed nets and animal barrier between breeding places and human habitation. - using protective cloths. - Apply of repellents to exposed skin between dusk - Avoid going outdoors & down when anopheline mosquitoes commonly bite. - Health education: public , at risk groups and travelers. - Avoid taking blood from any individual giving history of malaria or a history of travel to, or residence in, a malarious area.

111. 2. Specific measures: Chemoprophylaxis for international travelers going to endemic areas. ■ Chloroquine or hydrroxy chloroquine 5 mg /kg/week or chloroquine phosphate (500 mg for average adult). ■ C ontinued for 4-6 weeks after leaving endemic areas. ■ In areas with chloroquine -resistant P. falciparum, mefloquine is recommended (5mg/kg/week) for adults, 1-2 week before travel, during stay & 4 weeks after leaving endemic area.

112. Control: Case : Early case finding: * By lab examination of clinically suspected persons. * By periodic survey. * Through malaria campaign. ttt : Using antimalarial drugs as chloroquine or mefloquine etc. Contacts : ■ Investigation for early case findings. ■ Investigation for source of infection or exposure.

113. Malaria Survey F ield study in endemic areas to find out magnitude of problem, ecological factors & to plan for prevention and control. Planning : ■ Mapping area to identify water channels, collections, cultivated lands, houses & climatic conditions. ■ Study population characteristics e.g age, sex, occupation, habits etc. ■ Study vector; types of mosquitoes, density, species, life span, breeding places, resistance to insecticides. ■ Choose the suitable representative sample. Preparation of: ■ Team of work. ■ Equipments (microscope , slides ect ) ■ Transportation facilities. Investigation: Clinical &lab examination. Statistical analysis: to show malariometric indices.

114. Human Indices: 1-Splenic index (non-specific): % of children between 2-6ys showing splenomegally “excluding other causes”. Interpretation: - Below 10% low endemicity . -10-25% moderate endemicity . -25-50 % hyperendemic . 2-Parasitic index (specific): % of infants below one year showing malaria parasites in their blood, it is most sensitive index of recent infection. Gametocytic index; is % of those having gametocytes in their blood. 3-Vector index: Oocytic index is % of oocytes or ookinetes in stomach wall of female anopheles. 4-Sporozoite index is %of female anopheles having sporozoites in salivary glands.

115. Malaria Eradication Eradication is the highest level of disease control A iming at elimination of reservoir of infection, complete cure of cases & prevention of disease transmission by destruction of vectors. To eradicate malaria in certain area 4 phases have to be done: 1. Preparatory phase: preparation , planning surveying to study vector & magnitude of problem. 2. Attack phase: complete coverage of area by insecticides. D.D.T. is applies twice a year during period of malaria transmission. 3. S urveillance system for early case finding & presumptive treatment with chloroquine of any case with fever & completion of treatment in + ve blood film cases. 4. Consolidation phase: insecticides are stopped & continue with presumptive & radical treatment.