Vector borne diseases

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Vector-borne diseases-Malaria, Filariasis, Dengue, JE, YF, Chikungunya, KFD, Leishmaniasis and the national program against vector-borne diseases NVBDCP.

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Vector borne diseases

  1. 1. MALARIA
  2. 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. 3. MALARIATHE PARASITE
  4. 4. • Plasmodium falciparum• Plasmodium vivax• Plasmodium ovale – Tropical Africa• Plasmodium malariae – Karnataka
  5. 5. MALARIATHE VECTOR
  6. 6. Some species• An. culicifacies• An. fluviatilis• An. stephensi• An. minimus• An. philippinensis• An. sundaicus• An. maculatus
  7. 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. 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. 9. MALARIATHE DISEASE
  10. 10. Reservoir of infection• Human reservoir – Harbors the sexual forms (gametocytes) of the parasite• P. malariae – Chimpanzees in tropical Africa
  11. 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. 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. 13. Period of communicability• As long as mature, viable gametocytes exist in circulating blood in sufficient density
  14. 14. Mode of transmission• Vector transmission• Direct transmission• Congenital malaria
  15. 15. Incubation period• Falciparum – 12 (9-14)• Vivax – 14 (8-17)• Ovale – 17 (16-18)• Malariae – 28 (18-40)
  16. 16. Clinical features• Signs and symptoms• Complications – Cerebral malaria – Dehydration – ARF – Collapse – Liver damage – Anemia – GI symptoms – Blackwater fever
  17. 17. • Anemia• Splenomegaly• Enlargement of liver• Herpes• Renal complications
  18. 18. MALARIAGLOBAL SCENARIO
  19. 19. Every minute 2 people die of malaria. Bythe time we will finish this lecturemalaria would have killed180 morepeople.
  20. 20. MALARIASOUTH-EAST ASIA REGION
  21. 21. MALARIAPREVENTION & CONTROL
  22. 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. 23. INSECTICIDESOrgano-Chlorines DDTOrgano- Malathion,Abate, FentPhosphates hion, ChlorpyrifosCarbamates Propoxur, CarbarylSynthetic Tetramethrin, Resmethpyrethroids rin, Allethrin
  24. 24. B. Diagnosis• Direct Microscopy• RDTs (Rapid diagnostic tests)
  25. 25. • Histidine-rich protein-2 (HRP2)• Parasite-specific lactate dehydrogenase (pLDH)
  26. 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. 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. 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. 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. 30. D. Intermittent Preventive Treatment
  31. 31. E. Malaria vaccines
  32. 32. • Pre-erythrocytic vaccines• Blood-stage vaccines• Transmission-blocking vaccines – Pfs25• Cocktail vaccines – SPf66
  33. 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. 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. 35. MALARIAINDICATORS
  36. 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. 37. LYMPHATIC FILARIASIS
  38. 38. • The term “lymphatic filariasis” covers infection with three closely related nematode worms – Wuchereria bancrofti – Brugia malayi – Brugia timori
  39. 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. 40. FILARIA ENDEMIC DISTRICTS250 Endemic districts in 20 States/UTs Population: 600 Million
  41. 41. Agent factorsOrganism VectorsW. bancrofti CulexB. malayi Mansonia, AedesB. timori Anopheles
  42. 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. 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. 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. 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. 46. Vectors of lymphatic filariasis• Main vectors in India are: – C. quinquefasciatus for Bancroftian filariasis – Mansonia mosquitoes for Brugian filariasis
  47. 47. • Modes of transmission: – Bite of infected vector mosquitoes• Incubation period: – 8-16 months
  48. 48. Clinical manifestations• Asymptomatic microfilaraemia• Acute adenolymphangitis (ADL)• Chronic lymphoedema/Elephentiasis• Tropical pulmonary eosinophilia (TPE)
  49. 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. 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. 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. 52. Control measures• Chemotherapy – DEC (Diethylcarbamazine) • Selective treatment (6 mg/kg X 12 days) • Mass therapy (MDA) – Ivermectin• Vector control
  53. 53. DENGUE(Breakbone fever)
  54. 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. 55. World-wide dengue distribution, 2006. Red: Epidemic dengue. Blue: Aedes aegypti
  56. 56. DISTRIBUTION OF DENGUE/DHF IN INDIA
  57. 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. 58. CASESDEATHS
  59. 59. TRANSMISSION CYCLE OF DENGUE Man-Mosquito-Man
  60. 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. 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. 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. 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. 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. 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. 66. • Frequent vomiting with or without blood• Sleepiness and restlessness• Patient feels thirsty and mouth becomes dry• Rapid weak pulse• Difficulty in breathing
  67. 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. 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. 69. Control of Dengue/ DHF• No drug/vaccine available• Control of Aedes aegypti only method of choice
  70. 70. • Vector control measures: – Environmental management & source reduction – Biological control – Chemical control – Personal protection measures – Health education – Community participation
  71. 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. 72. JAPANESE ENCEPHALITIS (JE)
  73. 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. 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. 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. 76. JE endemic areas
  77. 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. 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. 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. 80. JE affected districts in India
  81. 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. 82. CATTLE EGRET POND HERONReintroduction of infectedmosquitoes or TRITAENORHYNCUS vertebrates PIG Viral CULEX amplification Vertical transmission Infected vertebrate reservoir
  83. 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. 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. 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. 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. 87. • Prodromal stage: – Abrupt (1-6 hours) – Acute (6-24 hours) – Subacute (2-5 days)- more common – Fever, headache, malaise
  88. 88. • Acute encephalitic stage: – Usually lasts for a week – Convulsions – Alteration of sensorium – Behavioural changes – Motor paralysis – Involuntary movement – Focal neurological deficit
  89. 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. 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. 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. 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. 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. 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. 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. 96. “A proven immunization strategy for JEcontrol seems to be to initiate a preventivecampaign in high risk areas and age groupsfollowed by introduction of vaccine into theroutine EPI programme”
  97. 97. JE Vaccination Strategy for India• Vaccinate all children between the age group of 1-15 years with a single dose of live attenuated SA14-14-2 JE vaccine in a one time campaign• Integration into the routine immunization in the district to cover the new cohort of 1- 2 years
  98. 98. • Control of piggeries: – Vaccination of swine – Live/killed vaccines available – Maintaining vaccination coverage is difficult because their population is renewed very rapidly – Piggeries may be kept away (4-5 kms) from human dwellings
  99. 99. CHIKUNGUNYA FEVER
  100. 100. • Dengue like disease• Flavivirus• Aedes aegypti (Culex?, Mansonia?)• Sub- Saharan Africa, India, Asia• 151 districts in 8 states/UTs have reported cases between Feb 2006 & Oct 2006• South & central India• Karnataka & Maharashtra
  101. 101. • Incubation period: – 4-7 days• Clinical features: – Fever, chills, headache, backache – Adenopathy – Rash on trunk and limbs – Arthropathy • Adults • Metacarpophalangeal, wrists, elbow, shoulder, knee, an kle, metatarsal • Can persist for months or even years
  102. 102. • No deaths have been reported• Diagnosis by serology (ELISA to detect IgM)• No vaccine available• No specific treatment• Control – Vector control
  103. 103. VIRAL HEMORRHAGIC FEVERS
  104. 104. • Arenaviridae – Lassa fever• Filoviridae – Marburg hemorrhagic fever, Ebola HF• Flaviviridae – Dengue HF, Yellow fever, KFD• Bunyaviridae – HF with renal syndrome (Hantaan virus), Rift valley fever
  105. 105. YELLOW FEVER
  106. 106. • Zoonotic disease caused by an arbovirus (Flavivirus, ssRNA)• Viral hemorrhagic fever• Tropical & subtropical regions of Africa & Americas• Historically, accompanied travelers during European colonial period
  107. 107. Problem Statement
  108. 108. • ETHIOPA – 1 lakh cases, 30000 deaths• GAMBIA – 2.5% prevalence of severe infection, with a CFR of 19%• NIGERIA – 18735 cases, 4522 deaths
  109. 109. • No cases reported from Asia where Dengue, a closely related disease is endemic• Dengue immunity ? Cross-protection against yellow fever- Yellow fever immunization does not protect against dengue• INDIA – Population unvaccinated & susceptible to YF – Aedes aegypti is abundant – Climatic conditions are favorable for transmission – Indian monkey (Macacus) is susceptible to YF – ? Missing link-Virus is not present in India
  110. 110. Agent factors• AGENT – Flavivirus, ssRNA• RESERVOIR OF INFECTION – Forest areas- Monkeys, Forest mosquitoes – Urban areas- Man, Aedes aegypti• PERIOD OF COMMUNICABILITY – Man- 1st 3-4 days of illness – Mosquitoes- 8-12 days Extrinsic IP – Transovarian transmission documented
  111. 111. Host factors• AGE & SEX – All ages & both sexes susceptible• OCCUPATION – Contact with forests (wood cutters, hunters)• IMMUNITY – One attack gives life-long immunity
  112. 112. Environmental factors• CLIMATE – >24⁰C, 60% RH- required fro multiplication of virus in the mosquito• SOCIAL FACTORS – Urbanization – Forest encroachment – Expanding population – Travel- frequency and speed
  113. 113. Modes of transmission Three types of transmission cycle for yellow fever• Sylvatic (or Jungle) yellow fever – Monkeys• Intermediate yellow fever – Monkeys & humans• Urban yellow fever – Humans
  114. 114. • Sylvatic (or Jungle) yellow fever- Africa & America – Occurs in monkeys infected by wild mosquitoes (Haemagogus in America; Aedes africanus in Africa) in tropical rainforests – Infected monkeys pass the virus to mosquitoes during feeding – Infected wild mosquitoes bite humans entering the rainforest (accidental infection)- Sporadic cases – The majority of cases are young men working in the forest (logging, etc) – On occasion, the virus spreads beyond the affected individual
  115. 115. • Intermediate yellow fever- Africa – Small-scale epidemics that occur in humid or semi-humid grasslands of Africa – Separate villages experience simultaneous infections transmitted by semi-domestic mosquitoes that infect both monkey and human hosts – Most common type of outbreak in Africa – It can shift to a more severe urban-type epidemic if the infection is carried into a suitable environment (with the presence of domestic mosquitoes and unvaccinated humans)
  116. 116. • Urban yellow fever- Africa & America – Large epidemics occurring when the virus is introduced into high human population areas by migrants – Domestic mosquitoes of one species (Aedes aegypti) transmit the virus from person to person – Monkeys are not involved in transmission – Outbreaks spread from one source to cover a wide area
  117. 117. Incubation period• 3-6 days• SIX days recognized for International Health Regulations
  118. 118. Clinical features• Mild, undifferentiated fever to severe illness• Hemorrhagic, hepatic & renal manifestations predominate• Jaundice- develops after 4-6 days of illness• Renal Tubular Necrosis- during 2nd week• Albuminuria, Anuria• Hemoptysis, Melena, Epistaxis• Death between 5th & 10th day of illness
  119. 119. Prevention & Control1. Treatment – No specific treatment for yellow fever – ORS and paracetamol for dehydration and fever – An appropriate antibiotic(s) for any superimposed bacterial infection – Intensive supportive care may improve the outcome for seriously ill patients, but is rarely available in poorer, developing countries
  120. 120. 2. Vaccination – Type of vaccine • Live attenuated freeze dried chick embryo • 17D vaccine – Dose • One dose of 0.5 ml subcutaneously – Schedule • Routine immunization with measles vaccine at nine months of age
  121. 121. – Booster • International health regulations require a booster every 10 years– Contraindications • Egg allergy • Immune deficiency from medication or disease • Symptomatic HIV infection • Hypersensitivity to previous dose • Pregnancy*
  122. 122. – Special pecautions • Do not give before six months of age • Avoid during pregnancy • Cholera & YF vaccines should be given at least 3 weeks apart– Adverse effects • Hypersensitivity to egg • Rarely, encephalitis in the very young • Hepatic failure • Yellow fever vaccine-associated viscerotropic disease; among older recipients
  123. 123. – Storage • Between +5 & -30 deg C, preferably below ZERO deg C • Saline diluent • Discarded if not used within half an hour of dilution • Kept on ice away from sunlight
  124. 124. – Validity • The validity of yellow fever vaccination certificate begins 10 days after the date of vaccination and extends up to 10 years– India requires vaccination of infants too
  125. 125. 3. Vector control – Anti-adult measures – Anti-larval measures – “Source reduction”- Elimination of breeding places – Personal protection – Health education- for community involvement
  126. 126. 4. Surveillance – Clinical – Serological – Histopathological – Entomological – “Aedes aegypti Index” • The percentage of houses & their premises, in a limited well-defined area, showing actual breeding of Aedes aegypti larvae • This index should not be more than 1% in towns & seaports in endemic areas
  127. 127. 5. International measures – “Yellow fever receptive area”- An area in which YF is does not exist, but where conditions would permit its development if introduced – Valid international YF vaccination certificate for travelers to endemic areas or traveling through such areas – If not present, QUARANTINE for 6 days – Aerosol spraying of ships & aircraft from endemic areas – AEI kept below 1% at airports & seaports (kept free from breeding places over 400 m area around their perimeters)
  128. 128. KAYASANUR FOREST DISEASE (KFD)
  129. 129. • Viral hemorrhagic fever• Arboviral; Flavivirus• Transmitted to man by bite of infective ticks (Haemaphysalis)• Karnataka in 1957• 2167 cases & 69 deaths in 1983-84• 306 cases & 11 deaths in 2003
  130. 130. Epidemiological determinants• AGENT – Tick-borne flavivirus• NATURAL HOSTS & RESERVOIR – Main reservoirs- Rats & squirrels – Amplifying host- Monkeys – Man is an incidental or dead-end host – Cattle- Provide blood meals for ticks; important in maintaining tick populations
  131. 131. • VECTORS – Haemaphysalis spinigera, H turtura – Nymph stages – January to June- Highest number of infections; peak nymphal activity of ticks• HOST FACTORS – Age- 20-40 years – Sex- Males>Females – Occupation- involving forest visits – Human activity- Forest activity; Jan to June
  132. 132. • MODE OF TRANSMISSION – Transmission cycle involves monkeys and ticks – No evidence of man to man transmission• INCUBATION PERIOD – 3-8 days
  133. 133. Clinical features• Sudden onset fever, headache and severe myalgia• Acute phase for 2 weeks• GI disturbances and hemorrahges• SECOND PHASE – Mild meningoencephalitis after an afebrile period of 7-21 days• CFR= 5-10%
  134. 134. Diagnosis• Presence of virus in blood• Serology
  135. 135. CONTROL• CONTROL OF TICKS – Carbaryl/Fenthion/Propoxur – Carried out in “hot spots” ( areas where monkey deaths have been reported) – Restriction of cattle movement
  136. 136. • PERSONAL PROTECTION – Adequate clothing – Insect repellents (DEET) – Remove ticks from body and clothing at the end of the day – Discourage lying down or sitting on ground• VACCINATION – Killed vaccine
  137. 137. Leishmaniasis
  138. 138. • A group of protozoal diseases caused by parasites of the genus Leishmania, and transmitted to man by the bite of female phlebotomine sandfly• Majority of leishmaniasis are zoonoses involving wild or domestic mammals (rodents, canines)• Indian kala-azar is considered to be a non- zoonotic infection
  139. 139. • Visceral leishmaniasis (VL)• Cutaneous leishmaniasis (CL)/Oriental sore• Muco-cutaneous leishmaniasis (MCL)
  140. 140. Problem statement• Visceral leishmaniasis Bangladesh India Brazil Sudan• Cutaneous leishmaniasis Afghanistan Iran Brazil Peru Saudia Arabia Syria• Muco-cutaneous leishmaniasis Brazil Bolivia Peru
  141. 141. • Endemic in 88 countries• Co-infection of VL & AIDS is emerging due to spread of the AIDS pandemic particularly in southern Europe, where 25-70% of adult VL cases are related to HIV infection, & 1.5-9% of AIDS patients suffer from newly acquired or reactivated VL
  142. 142. Indian scenario• Kala-azar (VL) Bihar Jharkhand West Bengal Uttar Pradesh (eastern)• Cutaneouos Leishmaniasis North-western India (Rajasthan)
  143. 143. • Both cutaneous and visceral diseases occur in India• Kala-azar is the most important leishmaniasis in India
  144. 144. Epidemiological determinants• AGENT: – VL (Kala-azar) • Leishmania donovani – CL (Oriental sore) • L. tropica • L. major – MCL • L. braziliensis
  145. 145. • Sandfly injects the promastigote stage into skin• Promastigotes transform into amastigotes (LD bodies) inside the macrophages (human)• Sandfly ingests amastigotes• Amastigotes transform into promastigote stage inside the sandfly midgut, divide & migrate to proboscis
  146. 146. • RESERVOIRS OF INFECTION: – Rodents, dogs, jackals, foxes etc – Indian kala-azar is considered to be a non- zoonotic infection with man as the only reservoir
  147. 147. • HOST FACTORS: – Kala-azar can occur in all age groups. Peak age in India is 5-9 years – Males are affected twice as often as females – Population movement can result in spread of infection from non-endemic to endemic areas – Lower socio-economic class – Farming practices, forestry, mining, fishing etc are risk occupations
  148. 148. • ENVIRONMENTAL FACTORS: – Kala-azar is mostly confined to the planes; does not occur in altitudes over 2000 feet – Generally there is a high prevalence during & after rains – Generally confined to rural areas – Overcrowding – Ill-ventilation – Accumulation of organic matter in the environment
  149. 149. Vector• Kala-azar – Phlebotomus argentipes• CL – P. papatasi – P. sergenti• New world – Lutzomyia species
  150. 150. • Sandflies breed in cracks and crevices in the soil & buildings, tree holes, caves etc• They have nocturnal habits• Only females bites
  151. 151. Mode of transmission• Bite of the female phlebotomine sandfly (P. argentipes/papatasi/sergenti)• By contact when the insect is crushed during the act of feeding• Extrinsic IP = 6-9 days• Transmission of kala-azar has also been recorded by blood transfusion
  152. 152. Incubation period• 1 to 4 months (10 days to 2 years)
  153. 153. Clinical features• Kala-azar: – Fever – Splenomegaly – Hepatomegaly – Anaemia – Weight loss – Darkening of skin (face, hands, feet, abdomen)
  154. 154. • PKDL (Post-kala-azar Dermal Leishmaniasis): – Common in India – Occurs one to several months after apparent cure of kala-azar – Multiple nodular infiltrations of the skin – Numerous parasites in the skin lesions; important in disease transmission
  155. 155. • Cutaneous leishmaniasis: – Painful ulcers in areas of skin exposed to sandfly bite (legs, arms, face)• Muco-cutaneous leishmaniasis: – Ulcers around mouth & nose – Can mutilate the face
  156. 156. Laboratory diagnosis• Demonstration of the parasite LD bodies (Leishman-Donovan body) in the aspirates of spleen, liver, bone marrow, LNs, or in the skin (in CL)
  157. 157. • Napier’s Aldehyde test – 1-2 ml of serum + 40% formalin – White opacity within 2-20 min = strongly positive – Becomes positive 2-3 months after onset of disease, & reverts to negative 6 months after cure – Non-specific• Serology – ELISA
  158. 158. • Leishmanin test (Montenegro test) – Leishmanin is a prepration of 106 per ml washed promastigotes of leishmania suspended in 0.5% phenol – An intradermal injection of 0.1 ml on the flexor aspect of forearm is given and examined after 48- 72 hours
  159. 159. – An induration of 5 mm or more is considered positive– The test is usually positive 4-6 weeks after onset in case of CL and MCL– Usually negative in the active phases of kala-azar & becomes positive in 75% cases within one year of recovery
  160. 160. • Haematological findings: – Leucopenia – Anaemia – Reversal of A:G ratio – Decreased WBC:RBC ratio (1:1500 or more) – Increased ESR
  161. 161. Control measures• Control of reservoir• Sandfly control• Personal protection
  162. 162. Control of reservoir• Man – Active & passive case detection – Treatment of those found to be infected (including PKDL) • Sodium stibogluconate – 20mg/kg (max 850 mg) IM/IV X 20 days • Pentamidine – (3mg/kg) IV X 10 days • Amphotericin B • Miltefosine
  163. 163. Sandfly control• Insecticides – DDT – Spraying should be undertaken in human dwellings, animal shelters, & all other resting places up to a height of 6 feet from floor level
  164. 164. • Sanitation measures – Elimination of breeding places (cracks in mud or stone walls, rodent burrows, removal of firewood, rubbish around the house) – Location of cattle sheds & poultry at a fair distance from human dwellings – Improvement of housing & general sanitation
  165. 165. Personal protection• Avoiding sleeping on floor• Using fine-mesh nets around the bed• Insect repellents• Health education• There are no drugs for personal prophylaxis
  166. 166. NVBDCP (National Vector Borne Diseases Control Program)
  167. 167. • Malaria• Filariasis• Kala-azar• Japanese encephalitis• Dengue• Chikungunya
  168. 168. Three pronged strategy:• Disease management – Early case detection and complete treatment – Strengthening of referral services – Epidemic preparedness and rapid response
  169. 169. • Integrated vector management – Indoor residual spraying – Insecticide treated bed nets – Larvivorous fish – Source reduction and minor environmental engineering
  170. 170. • Supportive interventions – Behavior change communication – Public private partnership & intersectoral convergence – Human resource development – Operational research – Monitoring and evaluation
  171. 171. MALARIA
  172. 172. • National Malaria Control Program – 1953• National Malaria Eradication Program – 1958• Modified Plan of Operations (MPO) – 1977• National Anti-Malaria Program – 1999
  173. 173. • Objectives of MPO: – Consolidation of the achievements already made in the containment of malaria – Prevention of malaria mortality and reduction of malaria morbidity – Maintenance of agricultural and industrial productivity by intensive operations in the labor- intensive endemic areas
  174. 174. • Organization and implementation: – Integration of the malaria organization with the state health system – Reinforcement • District Malaria Officer • Malaria laboratory in every PHC • Fever Treatment Depots (FDT) - (Smear+Drugs) • Drug Distribution Centers (DDC) - Drugs
  175. 175. • Operational details: – For API 2 or more areas • Regular insecticidal spraying – 2 DDT (1g/sq m) OR 3 Malathion (2 g/sq m) OR 2 Synthetic pyrethroids (0.25g/sq m) • Entomological assessment • Surveillance (active & passive) • Treatment of cases
  176. 176. – For API less than 2 areas • Focal spraying around Pf cases detected • Surveillance • Treatment • Follow-up • Epidemiological investigation
  177. 177. • Area-based initiatives: – Enhanced Malaria Control Project (EMCP) • Tribal population • 100 districts in 8 states • 100% assistance through World Bank support • 1997 – 2005 • 48 districts achieved an API of less than 2
  178. 178. – Intensified Malaria Control Project • Launched in 2005 with assistance from ‘Global Fund for AIDS, Tuberculosis, and Malaria’ • Increase access to rapid diagnosis & treatment through community participation • Use of ITNs • Vector control by larvivorous fish • NGO & private sector participation
  179. 179. – Assistance to NE states • 100% central assistance to NE states
  180. 180. • Activity-based initiatives: – Indoor Residual Spraying – Insecticide-treated bed-nets – Larvivorous fish use – Case detection and treatment
  181. 181. • Present strategies for prevention and control of malaria1. Early case Detection and Prompt Treatment (EDPT)2. Vector control3. Community Participation4. Environmental Management & Source Reduction Methods5. Monitoring and Evaluation of the program
  182. 182. • Annual parasite incidence (API)• Annual blood examination rate (ABER)• Annual falciparum incidence (AFI)• Slide positivity rate (SPR)• Slide falciparum rate (SFR)
  183. 183. MALARIA CONTROL
  184. 184. Two different approaches to malaria control• Management of malaria cases in the community• Active intervention to control or interrupt malaria transmission with community participation
  185. 185. Management of malaria cases in the community• Case detection• Treatment – Uncomplicated malaria • Plasmodium vivax • Plasmodium falciparum – Severe and complicated malaria• Chemoprophylaxis
  186. 186. Case detection• Active and passive case detection• Fever cases presumed to be suffering to be suffering from malaria, unless proved otherwise• In case laboratory diagnosis is not immediately available, differential diagnosis on clinical grounds should be made
  187. 187. Treatment• Any fever in endemic areas during transmission season without any other obvious cause should be considered as malaria and investigated and treated accordingly• Drug resistance are present in country, but chloroquine is still safe and effective• The best approach in malaria control is diagnosis and treatment on the same day
  188. 188. Treatment: Uncomplicated malaria• 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• Plasmodium falciparum cases • Chloroquin sensitive areas – 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) THEREAFTER T. Primaquin 0.75 mg/kg BW single dose
  189. 189. Treatment: Uncomplicated malaria• Plasmodium falciparum cases • Chloroquin resistant areas • Give ACT (Artesunate Combination Therapy) • T. Artesunate 4mg/kg BW daily X 3days PLUS • T. Sulphadoxine 25 mg/kg BW and T. Pyrimethamin 1.25 mg/kg BW on the first day (Contraindicated in pregnant females) THEREAFTER T. Primaquin 0.75 mg/kg BW single dose • Resistance to Chloroquine and ACT • Oral Quinine 10 mg/kg BW and T. Doxycycline 100 mg daily for 3 days THEREAFTER T. Primaquin 0.75 mg/kg BW single dose
  190. 190. Treatment: In severe and complicated malaria• Cases should be hospitalized for treatment – Quinine – Artesunate Followed by full – Artemether course of ACT – Artether – Use of Mefloquin alone or in combination with artesunate should be avoided in cerebral malaria due to neuro-psychiatric complications associated with it.
  191. 191. 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
  192. 192. Chemoprophylaxis• 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.
  193. 193. Active intervention measures• Stratification of the problem• Vector control strategies – Anti-adult measures – Anti-larval measures• Malaria vaccines
  194. 194. Stratification of the problem• For planning and development of a sound control strategy to maximize the utilization of available resources• Stratification is based on API – Areas with API<2 – Areas with API>2
  195. 195. Vector control strategies• Anti-adult measures – Residual spraying – Personal protection measures • ITN • LLITN • Repellents • Protective clothing • Screening of houses
  196. 196. • Anti-larval measures – Source reduction – Larvicides • Oils • Paris green • Insecticides (Temephos) – Integrated control
  197. 197. Malaria vaccines• Pre-erythrocytic vaccines• Blood-stage vaccines• Transmission-blocking vaccines – Pfs25• Cocktail vaccines – SPf66
  198. 198. FILARIASIS
  199. 199. • National Filaria Control Program – 1955 – Implemented through • Filaria control units Endemic • Filaria clinics urban towns • Survey units • Though PHc system in rural areas – Filaria control strategy • Vector control • Detection & treatment of microfilaria carriers • Morbidity management • IEC
  200. 200. • WHA resolution of 1997 – global elimination of lymphatic filariasis• Elimination of filariasis by 2015 – Revised filaria control strategy • Annual MDA – Single dose DEC (6mg/kgBW) for 5 years or more to ‘at risk population’ excluding pregnant females, children <2 years of age, seriously ill patients • Case management • Capacity building • Social mobilization
  201. 201. Kala-azar
  202. 202. • Strategies for Kala-azar elimination are: – Enhanced case detection and complete treatment (including rapid diagnostic kits, miltefosine) – Vector control – BCC and intersectoral convergence – Capacity building – Monitoring, supervision and evaluation – Research
  203. 203. • In may 2005, a tripartite MoU between India, Nepal & Bangladesh; to reduce the annual incidence of Kala-azar to <1/10000 population at sub-district level by 2015.• National Health Policy envisages Kala-azar elimination by 2010.
  204. 204. Dengue and Chikungunya
  205. 205. • Case management – Health personnel training- upgrading clinical skills and diagnostic competence• Health education – Community is informed on the characteristic features of the disease and the facilities available for their clinical management• Vector control – Elimination of vector breeding sites – Disposing of all the junk material that collects water & encourages vector breeding – Keeping all water containers and storage facilities tightly covered – Cleaning the water coolers at least once a week before refilling• Monitoring and surveillance
  206. 206. JAPANESE ENCEPHALITIS
  207. 207. • Operational strategy: – Early case detection and prompt management – Vector density reduction by adulticidal and larvicidal measures – IEC campaigning for community participation – Immunization of high-risk population groups
  208. 208. 233

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