Vector borne diseases

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1. MALARIA 2. What is Malaria?ã You know it. Well done.ã And for those who think they know little about malaria, follow us for next 35 minutes and go through your…
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  • 1. MALARIA
  • 2. What is Malaria?• You know it. Well done.• And for those who think they know little about malaria, follow us for next 35 minutes and go through your book at home.
  • 3. MALARIATHE PARASITE
  • 4. • Plasmodium falciparum• Plasmodium vivax• Plasmodium ovale – Tropical Africa• Plasmodium malariae – Karnataka
  • 5. MALARIATHE VECTOR
  • 6. Some species• An. culicifacies• An. fluviatilis• An. stephensi• An. minimus• An. philippinensis• An. sundaicus• An. maculatus
  • 7. Factors which determine vectorial importance of mosquitoes• DENSITY – Critical density- below which effective transmission cannot be maintained in a community • An. culicifacies- high density • An. fluviatilis- low density• LIFE SPAN
  • 8. • CHOICE OF HOST – Anthrophilic species like An. fluviatilis are better vectors of malaria than zoophilic species• RESTING HABITS – Endophily – Exophily• BREEDING HABITS• TIME OF BITING• RESISTANCE TO INSECTICIDES
  • 9. MALARIATHE DISEASE
  • 10. Reservoir of infection• Human reservoir – Harbors the sexual forms (gametocytes) of the parasite• P. malariae – Chimpanzees in tropical Africa
  • 11. • A patient can be a carrier of several plasmodia species at the same time• Children are more likely to be gametocyte carriers than adults. The child is thus epidemiologically a better reservoir than the adult.
  • 12. Conditions that must be met before a person can serve as a reservoir• Both male and female gametocytes are present in blood• Gametocytes are mature• Gametocytes are viable• Gametocytes are present in sufficient density to infect mosquitoes (at least 12/cumm of blood)
  • 13. Period of communicability• As long as mature, viable gametocytes exist in circulating blood in sufficient density
  • 14. Mode of transmission• Vector transmission• Direct transmission• Congenital malaria
  • 15. Incubation period• Falciparum – 12 (9-14)• Vivax – 14 (8-17)• Ovale – 17 (16-18)• Malariae – 28 (18-40)
  • 16. Clinical features• Signs and symptoms• Complications – Cerebral malaria – Dehydration – ARF – Collapse – Liver damage – Anemia – GI symptoms – Blackwater fever
  • 17. • Anemia• Splenomegaly• Enlargement of liver• Herpes• Renal complications
  • 18. MALARIAGLOBAL SCENARIO
  • 19. Every minute 2 people die of malaria. Bythe time we will finish this lecturemalaria would have killed180 morepeople.
  • 20. MALARIASOUTH-EAST ASIA REGION
  • 21. MALARIAPREVENTION & CONTROL
  • 22. A. Malaria Vector Control• Integrated Vector Management (IVM)• Indoor Residual Spraying (IRS) Integrated vector management (IVM) is a•rational decision-making process for the Insecticide Treated Nets (ITNs)•optimal use of resources in the management Other methods of – Larviciding vector populations, so as to reduce or – Environmental management approaches to interrupt transmission of vector-borne vector control diseases. – Personal protection measures (includes ITNs) – Fogging or area spraying
  • 23. INSECTICIDESOrgano-Chlorines DDTOrgano- Malathion,Abate, FentPhosphates hion, ChlorpyrifosCarbamates Propoxur, CarbarylSynthetic Tetramethrin, Resmethpyrethroids rin, Allethrin
  • 24. B. Diagnosis• Direct Microscopy• RDTs (Rapid diagnostic tests)
  • 25. • Histidine-rich protein-2 (HRP2)• Parasite-specific lactate dehydrogenase (pLDH)
  • 26. C. Treatment CQ Chloroquine 25 mg/Kg over 3days PLUS Sensitive Primaquine 0.25 mg/kg BW daily for 14 days Vivax CQ ACT PLUS Resistant Primaquine 0.25 mg/kg BW daily for 14 days ACTFalciparum PLUS Primaquine 0.75 mg/kg BW single doseSevere Parenteral Artemesinin Followed by fullMalaria derivatives/Quinine course of ACT
  • 27. • Plasmodium vivax cases – Day 0: T. Chl 10 mg/kg BW (600 mg adult dose) – Day 1: T. Chl 10 mg/kg BW (600 mg adult dose) – Day 2: T. Chl 5 mg/kg BW (300 mg adult dose) PLUS T. Primaquin 0.25 mg/kg BW daily for 14 days
  • 28. ACT (Artesunate Combination Therapy)T. Artesunate 4mg/kg BW daily X 3days PLUST. Sulphadoxine 25 mg/kg BW and T.Pyrimethamin 1.25 mg/kg BW on the first dayResistance to Chloroquine and ACTOral Quinine 10 mg/kg BW and T.Doxycycline 100 mg daily for 3 daysTHEREAFTER T. Primaquin 0.75 mg/kg BWsingle dose
  • 29. 1.Artesunate 2.4 mg/Kg BW IV or IM at 0, 12 & 24 hrs, then daily2.Artemether 3.2 mg/Kg BW at 0, then 1.6 mg.Kg BW per day3.Quinine 20 mg salt/Kg BW at 0 (IV infusion), then 10 mg/Kg BW every 8 hrs
  • 30. D. Intermittent Preventive Treatment
  • 31. E. Malaria vaccines
  • 32. • Pre-erythrocytic vaccines• Blood-stage vaccines• Transmission-blocking vaccines – Pfs25• Cocktail vaccines – SPf66
  • 33. F. Chemoprophylaxis• Travelers from non-endemic areas• Soldiers serving in highly endemic areas• Migrant labourers• Should be complemented by personal protection and environmental measures• Intermittent preventive treatment in pregnancy
  • 34. • For short-term prophylaxis (< 6 weeks) – Doxycycline 100 mg X OD in adults or 1.5 mg/kg BW for children >8 years old. – Started 2 days before travel and continued for 4 weeks after leaving the malarious area. – Contraindicated in pregnant females and children <8 years.• For long-term prophylaxis (>6 weeks) – Mefloquine 5 mg/kg BW (upto 250 mg) weekly – Started 2 weeks before travel and continued till 4 weeks of leaving the malarious area. – Contraindicated in cases with H/O convulsions, neuropsychiatric problems and cardiac conditions.
  • 35. MALARIAINDICATORS
  • 36. • Eradication era – Annual parasite incidence (API) – Annual blood examination rate (ABER) – Annual falciparum incidence (AFI) – Slide positivity rate (SPR) – Slide falciparum rate (SFR)
  • 37. LYMPHATIC FILARIASIS
  • 38. • The term “lymphatic filariasis” covers infection with three closely related nematode worms – Wuchereria bancrofti – Brugia malayi – Brugia timori
  • 39. • Transmitted to man by the bites of infective mosquitoes.• Adult worms live in the lymphatic vessels; their offspring-the microfilariae-circulate in peripheral blood and are available to infect mosquito vectors when they come to feed.
  • 40. FILARIA ENDEMIC DISTRICTS250 Endemic districts in 20 States/UTs Population: 600 Million
  • 41. Agent factorsOrganism VectorsW. bancrofti CulexB. malayi Mansonia, AedesB. timori Anopheles
  • 42. • The Mf display nocturnal periodicity. They appear in large numbers at night and retreat from the blood stream during the day.• The maximum density of Mf in blood is reported between 10 pm and 2 am.
  • 43. Mf W. bancrofti Mf B. malayiGeneral Graceful, Crinkled,appearance sweeping curves secondary curvesLength 244 to 296 µ 177 to 230 µExcretory pore Not prominent ProminentCaudal end Uniformly Kinkled and two tapering to a terminal nuclei delicate point; present no terminal nuclei presentNuclear column Nuclei discrete Smudged
  • 44. The typical vector for Brugia malayi filariasis are mosquito species from thegenera Mansonia and Aedes. During a blood meal, an infected mosquitointroduces third-stage filarial larvae onto the skin of the human host, wherethey penetrate into the bite wound . They develop into adults thatcommonly reside in the lymphatics . The adult worms resemble those ofWuchereria bancrofti but are smaller. Female worms measure 43 to 55 mmin length by 130 to 170 μm in width, and males measure 13 to 23 mm inlength by 70 to 80 μm in width. Adults produce microfilariae, measuring177 to 230 μm in length and 5 to 7 μm in width, which are sheathed andhave nocturnal periodicity. The microfilariae migrate into lymph and enterthe blood stream reaching the peripheral blood . A mosquito ingests themicrofilariae during a blood meal . After ingestion, the microfilariae losetheir sheaths and work their way through the wall of the proventriculus andcardiac portion of the midgut to reach the thoracic muscles . There themicrofilariae develop into first-stage larvae and subsequently into third-stage larvae . The third-stage larvae migrate through the hemocoel to themosquitos prosbocis and can infect another human when the mosquitotakes a blood meal .
  • 45. • Reservoir of infection: – There is no evidence that W. bancrofti has animal reservoirs in India – Animal reservoirs of Brugia are present in monkeys, cats and dogs• Source of infection: – A person with circulating Mf in peripheral blood – In late obstructive stages Mf are not present in the blood
  • 46. Vectors of lymphatic filariasis• Main vectors in India are: – C. quinquefasciatus for Bancroftian filariasis – Mansonia mosquitoes for Brugian filariasis
  • 47. • Modes of transmission: – Bite of infected vector mosquitoes• Incubation period: – 8-16 months
  • 48. Clinical manifestations• Asymptomatic microfilaraemia• Acute adenolymphangitis (ADL)• Chronic lymphoedema/Elephentiasis• Tropical pulmonary eosinophilia (TPE)
  • 49. Diagnosis• Demonstration of Mf in peripheral blood – Blood collected between 8:30 pm to 12:00 am• DEC provocation test – Blood examined one hour after administration of 100 mg DEC given orally
  • 50. • Antigen detection assays• Serological assays to detect antibodies to Mf and adults using IF and CF techniques – Do not distinguish between past and present infection
  • 51. Parasitological parameters• Microfilaria rate – % of persons showing Mf in their peripheral blood• Filarial endemicity rate – % of persons examined showing Mf in their blood, or clinical manifestations, or both• Microfilarial density – Number of Mf per unit volume (20cumm) of blood• Average infestation rate – Average number of Mf per positive slide
  • 52. Control measures• Chemotherapy – DEC (Diethylcarbamazine) • Selective treatment (6 mg/kg X 12 days) • Mass therapy (MDA) – Ivermectin• Vector control
  • 53. DENGUE(Breakbone fever)
  • 54. WHAT IS DENGUE?• Viral disease (Flavivirus)- four serotypes• Transmitted by the infective bite of Aedes aegypti/Aedes albopictus• Man develops disease after 5-6 days of being bitten by an infective mosquito• Occurs in two forms – Dengue Fever and – Dengue Haemorrhagic Fever(DHF)
  • 55. World-wide dengue distribution, 2006. Red: Epidemic dengue. Blue: Aedes aegypti
  • 56. DISTRIBUTION OF DENGUE/DHF IN INDIA
  • 57. • Disease is prevalent throughout India in most of the metropolitan cities and towns• Outbreaks have also been reported from rural areas of Haryana, Maharashtra & Karnataka
  • 58. CASESDEATHS
  • 59. TRANSMISSION CYCLE OF DENGUE Man-Mosquito-Man
  • 60. VECTOR OF DENGUE/DENGUE HAEMORRHAGIC FEVER• Aedes aegypti• Extrinsic IP= about 7 to 8 days• Feeding Habit – Day biter – Mainly feeds on human beings in domestic and peridomestic situations – Bites repeatedly
  • 61. • RESTING HABIT – Rests in the domestic and peridomestic situations – Rests in the dark corners of the houses, on hanging objects like clothes, umbrella, etc. or under the furniture• BREEDING HABITS – Aedes aegypti mosquito breeds in any type of man made containers or storage containers having even a small quantity of water – Eggs of Aedes aegypti can live without water for more then one year
  • 62. • FAVOURED BREEDING PLACES – Desert coolers, Drums, Jars, Pots, Buckets, Flower vases, Plant saucers, Tanks, Cisterns, Bottles, Tins, Tyres, Roof gutters, Refrigerator drip pans, Cement blocks, Cemetery urns, Bamboo stumps, Coconut shells, Tree holes and many more places where rainwater collects or is stored
  • 63. • PERIOD OF COMMUNICABILITY – Infected person with Dengue becomes infective to mosquitoes 6 to 12 hours before the onset of the disease and remains so upto 3 to 5 days• AGE & SEX GROUP AFFECTED – All age groups & both sexes are affected – Deaths are more in children during DHF outbreak
  • 64. SIGNS & SYMPTOMS OF DENGUE FEVER• Abrupt onset of high fever• Severe frontal headache• Pain behind the eyes which worsens with eye movement• Muscle and joint pains• Loss of sense of taste and appetite• Measles-like rash over chest and upper limbs• Nausea and vomiting
  • 65. SIGNS & SYMPTOMS OF DENGUE HAEMORRHAGIC FEVER AND SHOCK SYNDROME• Symptoms similar to dengue fever• Severe continuous stomach pains• Skin becomes pale, cold or clammy• Bleeding from nose, mouth & gums and skin rashes
  • 66. • Frequent vomiting with or without blood• Sleepiness and restlessness• Patient feels thirsty and mouth becomes dry• Rapid weak pulse• Difficulty in breathing
  • 67. DIAGNOSIS• Tourniquet test (look for the petechiae)• Low platelet count (<100,000/mm3)• Hemoconcentration (Hematocrit increased by 20% or more of the baseline value)
  • 68. MANAGEMENT OF DENGUE CASE• Early reporting• Management of dengue fever is symptomatic & supportive• In dengue shock syndrome, the following treatment is recommended: – Replacement of plasma losses – Correction of electrolyte and metabolic disturbances – Blood transfusion
  • 69. Control of Dengue/ DHF• No drug/vaccine available• Control of Aedes aegypti only method of choice
  • 70. • Vector control measures: – Environmental management & source reduction – Biological control – Chemical control – Personal protection measures – Health education – Community participation
  • 71. DO’S AND DON’TS• Remove water from coolers and other small containers at least once in a week• Use aerosol during day time to prevent the bites of mosquitoes• Do not wear clothes that expose arms and legs• Children should not be allowed to play in shorts and half sleeved clothes• Use mosquito nets or mosquito repellents while sleeping during day time
  • 72. JAPANESE ENCEPHALITIS (JE)
  • 73. What is Japanese Encephalitis?• A viral disease- Flavivirus• Transmitted by infective bites of female mosquitoes mainly belonging to Culex tritaeniorhynchus, Culex vishnui and Culex pseudovishnui group• JE virus is primarily zoonotic in its natural cycle and man is an accidental host• JE virus is neurotorpic and arbovirus and primarily affects central nervous system
  • 74. PROBLEM STATEMENT• Leading cause of viral encephalitis in Asia with 30-50,000 cases reported annually• Fewer than 1 case/year is reported in U.S. civilians and military personnel traveling to and living in Asia
  • 75. • Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination • China Korea • Japan Taiwan • Thailand• Countries that still have periodic epidemics • Viet Nam Cambodia • Myanmar India • Nepal Malaysia
  • 76. JE endemic areas
  • 77. Extent of problem of JE in India• JE viral activity has been widespread in India. The first evidence of presence of JE virus dates back to 1952.• First case was reported in 1955• Outbreaks have been reported from different parts of the country.• During recent past (1998-2004), 15 states and Union Territories have reported JE incidence
  • 78. 7000 6000Number of cases 5000 4000 6061 3000 3024 1124 3003 2000 2320 1030 1000 0 2003 2004 2005 2006 2007 2008 AP Assam Bihar Haryana Karnataka Kerala Maharashtra TN UP WB
  • 79. 1800 1600 1400Number of deaths 1200 1000 1500 800 645 600 237 400 528 536 228 200 0 2003 2004 2005 2006 2007 2008 AP Assam Bihar Haryana Karnataka Kerala Maharashtra TN UP WB
  • 80. JE affected districts in India
  • 81. TRANSMISSION CYCLE•Culex- Vector•Pigs- Amplifier host•Ardeid birds (Cattle egret, Pond heron)- Naturalhosts•Man- Dead end (Mosquitoes do not get infectionfrom JE patient)
  • 82. CATTLE EGRET POND HERONReintroduction of infectedmosquitoes or TRITAENORHYNCUS vertebrates PIG Viral CULEX amplification Vertical transmission Infected vertebrate reservoir
  • 83. • Japanese encephalitis outbreaks are usually circumscribed and do not cover large areas• They usually do not last more than a couple of months, dying out after the majority of the pig amplifying hosts have become infected
  • 84. Epidemiological features• Incubation period: – Usually 5 to 15 days• Mortality rate: – Case-fatality rates range from 0.3% to 60% (Usually 20-40%)
  • 85. • Who is at risk for getting Japanese encephalitis? – Residents of rural areas in endemic locations – Active duty military deployed to endemic areas – Expatriates who visit rural areas• Japanese encephalitis does not usually occur in urban areas
  • 86. Clinical features• Febrile illness of variable severity associated with neurological symptoms ranging from headache to meningitis or encephalitis• Ratio of overt disease to inapparent infection varies from 1:300 to 1:1000• Headache, fever, meningeal signs, stupor, disorientation, coma, tremors, paralysis (generalized), hypertonia, loss of coordination
  • 87. • Prodromal stage: – Abrupt (1-6 hours) – Acute (6-24 hours) – Subacute (2-5 days)- more common – Fever, headache, malaise
  • 88. • Acute encephalitic stage: – Usually lasts for a week – Convulsions – Alteration of sensorium – Behavioural changes – Motor paralysis – Involuntary movement – Focal neurological deficit
  • 89. • Convalescent phase: – Prolonged; may vary from a few weeks to several months – Those who survive may fully recover through steady improvement or suffer with residual neurological deficit• JE virus infection presents classical symptoms similar to any other virus causing encephalitis. Clinically it is difficult to differentiate between JE and other viral encephalitis
  • 90. Diagnosis• Clinical• Laboratory – Antibody detection • HI, CF, ELISA for IgG (paired) and IgM (MAC) antibodies – Antigen Detection • RPHA, IFA • Immunoperoxidase • Genome Detection – RTPCR • Isolation – Tissue culture, Infant mice, etc• In view of the limitations associated with various tests, IgM ELISA is the method of choice provided samples are collected 3-5 days after the infection
  • 91. Prevention and control• Vector control: – reducing the vector density – role of insecticides is limited – reduction in mosquito breeding (eco- management; source reduction) – personal protection against mosquito bites – using insecticide treated mosquito nets
  • 92. • Vaccination:Three types of vaccines available – Mouse brain-derived, purified and inactivated, freeze dried vaccine (Nakayama strain) – Cell culture-derived inactivated vaccine (Beijing strain) – Cell culture-derived live attenuated vaccine (SA 14-14-2 strain)
  • 93. Mouse brain-derived inactivated vaccine• Has been used globally • Multiple doses ( 3 Primary successfully to control + Booster) JE • High cost• Safe, efficacious • Low availability • Limited duration of induced• Manufactured in India protection and used in many • CRI may also close down states since 70s the production
  • 94. • Immunization schedule – 2 primary doses 4 weeks apart – Booster after 1 year – Subsequent boosters every 3 years till 10-15 years of age• Route of administration – SUBCUTANEOUS• Dose – 0.5ml (<3 years) – 1 ml (>3 years)
  • 95. SA14-14-2 Live attenuated JE Vaccine• Has been used since 1988 in China• Over 200 million children vaccinated• Safe and efficacious• High immunogenicity following single dose (booster after 1 year)• Licensed in Nepal and South Korea and Thailand – Following this the vaccine has been licensed in India for use in public health programs and is in the final stages of licensing in Sri Lanka• Special cost of vaccine for public program in GAVI eligible countries – Approximately 13 children could be vaccinated with the SA14-14-2 vaccine with the cost of vaccinating one child with the inactivated m-b derived vaccine
  • 96. “A proven immunization strategy for JEcontrol seems to be to initiate a pre
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