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MAHALAKSHMI.R
II-M,Sc MICROBIOLOGY
SYNOPSIS:
 Introduction
 Causative agents
 Structure of Wuchereria bancrofti.
 Epidemiology
 Transmission
 Risk factor
 Incubation period
 Lifecycle
 Pathogenesis and its clinical diseases
 Diagnosis, Treatment and Prevention.
INTRODUCTION:
LYMPHATIC FILARIASIS:
 Commonly known as elephantiasis-painful and
profoundly disfiguring disease.
 Caused by infection with parasites-nematodes-
transmitted through bites of infected mosquitoes.
 Mosquito transmitted larvae are deposited on skin –
enters the body.
 Larvae migrates to lymphatic vessels-develops into
adult worms and continuous its lifecycle.
 It affects and survive in human lymphatic system.
CAUSATIVE AGENTS:
 Causative agents of lymphatic filariasis are mosquito
borne filarial nematodes Wuchereria bancrofti, Brugia
malayi,B.timori.
 W.bancrofti causes 90% of LF cases.
 It is named after physician Otto wucherer and
parasitologist Joseph bancroft.
 STRUCTURE:
ADULT WORMS:
 W.bancrofti exhibits sexual dimorphism.
 Filiform shape with ends tapering.
 They are minute ,long hair like transparent nematodes
and creamy in color.
 Head end terminating in a slightly round swelling &
surrounded by two rows of 10 sessile papillae.
 Posterior end-anus and life span is long-5-10 yrs.
 Male worms -2.5 to 4 cm in length with 0.1mm in
thickness.
 Tail end is curved ventrally and has 2 spicules of
unequal length.
 Female worm-longer than male,8-10 cm length with
0.2-0.3 mm in thickness.
 Its tail end is narrow and abruptly pointed and they are
ovo-viviparous.
 The adults obtain their nourishment from lymph.
MICROFILARIAE(EMBRYOS):
 First stage of larvae called microfilaria.
 Appears as colorless and transparent bodies with blunt
heads and pointed tails.
 Measures about 290mm in length by 6-7mm in breadth.
 When dead and stained with romanowsky stain can
observe following features:
a)Hyaline sheath: Sac like envelope-359mm.
 Remains as membrane around larva.
 Cuticle: Lined by subcuticular cells and can seen only
with vital stains.
 Somatic cells or nuclei: Nuclei appears as granules
in central axis of body & extend from head to tail end.
 Space at anterior end-devoid of granules called
cephalic space.
 Life span in human body-70 days.
 Infective larvae(third stage of larva): L3 larva is
infective form of parasite found only in mosquito.
 Elongated,filariform measures 1.4-2cm in length and
18-23cm in breadth.
EPIDEMIOLOGY:
 W.bancrofti occurs in Africa, Southeast asia,Indian
subcontinent and many of pacific islands.
 B.malayi-China,India,Malaysia,Phillipines and
Indonesia.
 B.timori-Timors island of Indonesia.
 LF affects over 120 million people in 73 countries-
tropics and subtropics of Asia, Western pacific and
parts of Caribbean and south America.
 India – heavily infected areas are
UP,AP,TN,Bihar,Jharkhand,Orissa,Kerala and
Gujarat.
TRANSMISSION:
 Transmitted to person thru bites from mosquitoes that
has larvae which bites at night.
 Infected larva-deposit near puncture site, gets
attracted by warmth body temperature penetrates skin
on its own and enters lymphatic system thru
capillaries.
WHO IS AT RISK FOR INFECTION:
 Repeated mosquito bite over several months-years.
 People-in tropical or subtropical area-disease is
common are at greatest risk of infection.
 Short-term tourists have low risk.
INCUBATION PERIOD:
Extrinsic incubation period:
 Time interval for MF is develop inside mosquito to 3rd
stage of infective larvae(10-14 days).
Pre-patent period:
 Time interval between introduction of infective larvae
and first appearance of detectable MF in peripheral
blood(12-18 months).
Clinical incubation period:
 Time interval from invasion of infective larvae to
development of clinical manifestations(8-16 months).
LIFECYCLE OF W.BANCROFTI
 DEFINITE HOST: MAN.
 INTERMEDIATE HOST: MOSQUITOES
(Anopheles, Aedes and Culex).
 INFECTIVE FORM:THIRD STAGE LARVA.
LIFE CYCLE IN MAN: Known as human phase.
 Process of copulation takes place in lymphatic system
of human.
 Male and female worms copulate when present in
lymph gland.
 Female worms-ovoviviparous-produce eggs hatch
within the female body without obtaining nourishment
 Numerous microscopic juvenile larvae called
Microfilarae released into lymph.
 Each MF is about 0.2-0.3mm in length surrounded by
loose cuticular sheath called egg membrane.
 Surface of larvae is covered by flattened epidermal
cells.
 MF after being released into lymphatic vessels enters
blood vessels and circulate with blood.
 Then migrates to visceral organs and reside in deeper
blood vessels of thorax region.
 In this region, larvae do not undergo any development
changes and it will happen in intermediate host.
 These larvae migrates to peripheral blood vessels
during night b/w 10pm-4am undergoing for feeding
habit for mosquito called nocturnal periodicity.
 During day time, these larvae live in large deep seated
blood vessels but during night they migrate to
peripheral blood vessels. Hence MF showing day and
night periodicity known as diurnal periodicity.
 This MF will die if not transferred to mosquito within
70 days, So MF is a infective stage to mosquitoes.
LIFE CYCLE IN MOSQUITO: Known as mosquito
phase.
 When female mosquitoes like Anopheles,Aedes and
Culex sucks blood from Wuchereria infected
person,MF from peripheral blood enters midgut of
mosquito.
 In midgut, shed their protective sheath within 6hrs.
 After, shedding they penetrate stomach wall and
migrates to thoracic muscles where growth and
metamorphosis takes place.
 Initially, they metamorphose into flat sausage shaped
larva called L1 or first stage larva.
 Later this larvae undergoes first moulting and grows
into slender elongated L2 or second stage larvae.
 finally, second stage larva undergoes second moulting
transforming into long infective stage called L3 or
third stage larvae.
 These all will takes place within 10-20days.
 Final third stage larva migrates to labium(proboscis)
and it can be transferred to definite host.
 In man,filarial larva first enters blood circulation thru
bite of mosquito and then it enters into lymphatic
vessels that undergoes 3rd & 4th moulting and
transforms into adult.
 Adult male and female copulate and delivers MF.
PATHOGENESIS AND ITS CLINICAL
DISEASE:
 Pathogenic effects seen in wuchereriasis are produced
by adult worms.
 Three following stages occurs sequentially in
pathogenesis of LF:
a) Dilation of lymphatic vessels.
b) Infection of lymphatics.
c) Obstruction of lymph nodes.
Diseases are of two types:
a) lymphatic/classical filariasis b) occult filariasis.
 LYMPHATIC/CLASSICAL FILARIASIS: Caused
by adult worm.
 Example: Lymphangitis,Elephantiasis,Lymphedema
etc.
 OCCULT FILARIASIS: Caused by MF/embryos.
 Example: Eosinophilia,hepatosplenomegaly.
MANIFESTATIONS(LYMPHATIC FILARIASIS):
 ASYMPTOMATIC STAGE: Characterized by
presence of MF in peripheral blood.
 No clinical signs and symptoms of the disease.
 Some infected person-remains asymptomatic for yrs
or some instances in life.
 Others leads to acute and chronic stages.
 ACUTE STAGE: Starts when they have already
manifestations like Lymphangitis, Lymphadenitis and
Filarial fever.
 In some cases, male genitalia is affected leading to
funiculitis, epidydimitis and orchitis.
 Also results in headache, nausea and urticaria.
 LYMPHANGITIS: An inflammation or an infection
of lymphatic vessels and lymphatic channels that
occurs as a result of infection at a site distal to the
channel.
 LYMPHADENITIS: An inflammation or infection in
one or more lymph nodes.
 FILARIAL FEVER: High fever of sudden onset
leading for 2-3 days with temp of 103-104 degree.
 Temperature comes down by profuse sweating.
 Associated with localized sign of inflammation of
lymphatic vessels.
 Blood examination-transient leukocytosis,Increased
neutrophils and presence of MF.
 CHRONIC STAGE: Develops 10-15 years from
onset of first attacks.
 Manifestations like Hydrocele, Lymphedema,
Elephantiasis and Chyluria.
 HYDROCELE: Accumulation of fluid occurs as a
result of obstruction of lymph vessels of spermatic
cord and also due to exudation from inflamed testis
and epididymis.
 Clear and straw colored and sometimes milky, cloudy
or hemorrhagic.
 Occasionally, Hydrocele on enormous amount with
elephantiasis of scrotum.
 Fluid filled balloon like enlargement of sac around
testes.
 LYMPHEDEMA: Abnormal accumulation of lymph
in tissues causing swelling of arms, breasts or
genitals.
 Caused by fluid collection because of improper
functioning of lymph node system results in swelling.
 Swelling caused by lymphatic system blockage which
is a part of immune and circulatory system.
 ELEPHANTIASIS: Caused by mechanical blocking
of lumen of lymph vessels.
 Excessive fibrosis of lymphatic vessels.
 Commonly also affects limbs, genitals and breasts.
 Disabling and disfiguring Lymphedema of limbs,
breasts and genitals accompanied by marked
thickening of skin.
 Causes hardening and thickening of skin.
 Swelling and decreasing function of lymph system
makes body difficult to fight against infection and
germs.
 Results in decrease of blood flow due to worms inside
blood vessels.
 Chances of heart failure, breathing
difficulty,Eosinophilia and kidney damage.
 CHYLURIA: Due to rupture of varicose chyle vessels
thru mucous membrane of urinary tract.
 Lymph fluid in urine.
 Appears as milk white in color and contains fat
particles , albumin and fibrinogen.
 Microscopic examination- MF, few RBCS and
Lymphocytes.
 LYMPHANGIOVARIX: Dilation of lymph vessels in
inguinal, scrotal and abdominal regions.
 LYMPHORRHAGIA: Rupture of lymph vessels
results in release of lymph/chyle.
 Results in lymph scrotum, lymphocele, Chyluria,
chylous diarrhoea, chylous ascites and chyothorax.
 OCCULT FILARIASIS: Called as meyers-
kouwenaar syndrome.
 Clinical conditions not due to lymphatic involvement
but due to hypersensitivity reactions to filarial
antigens.
 Characterized by lymph node enlargement,
Hepatosplenomegaly, pulmonary symptoms and
absence of MF in blood.
 MF not reaches peripheral blood as they are destroyed
by tissues.
 Results in Eosinophil granuloma.
 TROPICAL PULMONARY EOSINOPHILIA:
Characterized by low fever, weight loss, paroxysmal
cough with scanty sputum and hepato-splenomegaly.
 Total serum IgE and anti- filarial antibody titres will
rises.
 Responds well to treatment, if not treated-progressive
pulmonary damage occurs.
 Eosinophil count in peripheral blood exceeds 450/mul
but in usual condition less than 7% in circulate
leukocytes.
DIAGNOSIS:
 BLOOD MICROSCOPY:
A) Direct wet mount
B) Thick blood smear
C) DEC provocation test.
 Using concentration of blood
 Intradermal test
 Urine microscopy.
 Antigen and antibody detection assay.
 ELISA, HA TEST, CF, IMMUNOBLOTTING.
 Direct immunofluorescent antibody
 PCR
 X-ray
 Ultra sound/Ultrasonography.
 Examination of biopsy.
TREATMENT:
 Diethylcarbamazine: Drug is effective in killing MF
rapidly and adult worms slowly –can be given orally
in dosage of 2-6mg/kg for 12 days.
 Ivermectin: Taken as single oral dose 200ug/kg is
highly effective.
 Surgical treatment – small lymphatics are anatomized
to large central vein. Produce marked reduction in
limb size.
 General treatment: Rest, Antibiotics, Physiotherapy
and bandaging.
 Para methyl phenyl stibonate against infective larvae.
 Arsenical preparation against adult worms.
 In US , combination of albendazole with Ivermectin.
 DEC and albendazole is also effective against MF.
 In 2003, common antibiotic-Doxycycline was
suggested for treating elephantiasis to kill adult worm
with dosage of 200mg/day for 4-6 weeks.
PREVENTION:
 Avoid mosquito bites.
 Sleep under mosquito nets.
 Use of mosquito repellants cream on skin.
 Public awareness.
 Destruction of breeding sites of vectors by
insecticides.
 Environmental sanitation should be maintained.
 Adult mosquitoes can be controlled by spraying
insecticides like DDT and BHC in homes.
 Spraying of kerosene pyrethrum oil on sewage gutters
and ditches –effective to kill mosquito larvae.
 Biological control using larvivorous fish like
GAMBUSIA is much safer to kill larvae.
Thank you…..

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Filariasis (WUCHERERIA BANCROFTI)

  • 2. SYNOPSIS:  Introduction  Causative agents  Structure of Wuchereria bancrofti.  Epidemiology  Transmission  Risk factor  Incubation period  Lifecycle  Pathogenesis and its clinical diseases  Diagnosis, Treatment and Prevention.
  • 3. INTRODUCTION: LYMPHATIC FILARIASIS:  Commonly known as elephantiasis-painful and profoundly disfiguring disease.  Caused by infection with parasites-nematodes- transmitted through bites of infected mosquitoes.  Mosquito transmitted larvae are deposited on skin – enters the body.  Larvae migrates to lymphatic vessels-develops into adult worms and continuous its lifecycle.  It affects and survive in human lymphatic system.
  • 4. CAUSATIVE AGENTS:  Causative agents of lymphatic filariasis are mosquito borne filarial nematodes Wuchereria bancrofti, Brugia malayi,B.timori.  W.bancrofti causes 90% of LF cases.  It is named after physician Otto wucherer and parasitologist Joseph bancroft.  STRUCTURE: ADULT WORMS:  W.bancrofti exhibits sexual dimorphism.  Filiform shape with ends tapering.
  • 5.  They are minute ,long hair like transparent nematodes and creamy in color.  Head end terminating in a slightly round swelling & surrounded by two rows of 10 sessile papillae.  Posterior end-anus and life span is long-5-10 yrs.  Male worms -2.5 to 4 cm in length with 0.1mm in thickness.  Tail end is curved ventrally and has 2 spicules of unequal length.  Female worm-longer than male,8-10 cm length with 0.2-0.3 mm in thickness.
  • 6.
  • 7.  Its tail end is narrow and abruptly pointed and they are ovo-viviparous.  The adults obtain their nourishment from lymph. MICROFILARIAE(EMBRYOS):  First stage of larvae called microfilaria.  Appears as colorless and transparent bodies with blunt heads and pointed tails.  Measures about 290mm in length by 6-7mm in breadth.  When dead and stained with romanowsky stain can observe following features: a)Hyaline sheath: Sac like envelope-359mm.  Remains as membrane around larva.
  • 8.  Cuticle: Lined by subcuticular cells and can seen only with vital stains.  Somatic cells or nuclei: Nuclei appears as granules in central axis of body & extend from head to tail end.  Space at anterior end-devoid of granules called cephalic space.  Life span in human body-70 days.  Infective larvae(third stage of larva): L3 larva is infective form of parasite found only in mosquito.  Elongated,filariform measures 1.4-2cm in length and 18-23cm in breadth.
  • 9. EPIDEMIOLOGY:  W.bancrofti occurs in Africa, Southeast asia,Indian subcontinent and many of pacific islands.  B.malayi-China,India,Malaysia,Phillipines and Indonesia.  B.timori-Timors island of Indonesia.  LF affects over 120 million people in 73 countries- tropics and subtropics of Asia, Western pacific and parts of Caribbean and south America.  India – heavily infected areas are UP,AP,TN,Bihar,Jharkhand,Orissa,Kerala and Gujarat.
  • 10. TRANSMISSION:  Transmitted to person thru bites from mosquitoes that has larvae which bites at night.  Infected larva-deposit near puncture site, gets attracted by warmth body temperature penetrates skin on its own and enters lymphatic system thru capillaries. WHO IS AT RISK FOR INFECTION:  Repeated mosquito bite over several months-years.  People-in tropical or subtropical area-disease is common are at greatest risk of infection.  Short-term tourists have low risk.
  • 11. INCUBATION PERIOD: Extrinsic incubation period:  Time interval for MF is develop inside mosquito to 3rd stage of infective larvae(10-14 days). Pre-patent period:  Time interval between introduction of infective larvae and first appearance of detectable MF in peripheral blood(12-18 months). Clinical incubation period:  Time interval from invasion of infective larvae to development of clinical manifestations(8-16 months).
  • 12. LIFECYCLE OF W.BANCROFTI  DEFINITE HOST: MAN.  INTERMEDIATE HOST: MOSQUITOES (Anopheles, Aedes and Culex).  INFECTIVE FORM:THIRD STAGE LARVA. LIFE CYCLE IN MAN: Known as human phase.  Process of copulation takes place in lymphatic system of human.  Male and female worms copulate when present in lymph gland.
  • 13.  Female worms-ovoviviparous-produce eggs hatch within the female body without obtaining nourishment  Numerous microscopic juvenile larvae called Microfilarae released into lymph.  Each MF is about 0.2-0.3mm in length surrounded by loose cuticular sheath called egg membrane.  Surface of larvae is covered by flattened epidermal cells.  MF after being released into lymphatic vessels enters blood vessels and circulate with blood.  Then migrates to visceral organs and reside in deeper blood vessels of thorax region.
  • 14.  In this region, larvae do not undergo any development changes and it will happen in intermediate host.  These larvae migrates to peripheral blood vessels during night b/w 10pm-4am undergoing for feeding habit for mosquito called nocturnal periodicity.  During day time, these larvae live in large deep seated blood vessels but during night they migrate to peripheral blood vessels. Hence MF showing day and night periodicity known as diurnal periodicity.  This MF will die if not transferred to mosquito within 70 days, So MF is a infective stage to mosquitoes.
  • 15.
  • 16. LIFE CYCLE IN MOSQUITO: Known as mosquito phase.  When female mosquitoes like Anopheles,Aedes and Culex sucks blood from Wuchereria infected person,MF from peripheral blood enters midgut of mosquito.  In midgut, shed their protective sheath within 6hrs.  After, shedding they penetrate stomach wall and migrates to thoracic muscles where growth and metamorphosis takes place.  Initially, they metamorphose into flat sausage shaped larva called L1 or first stage larva.
  • 17.  Later this larvae undergoes first moulting and grows into slender elongated L2 or second stage larvae.  finally, second stage larva undergoes second moulting transforming into long infective stage called L3 or third stage larvae.  These all will takes place within 10-20days.  Final third stage larva migrates to labium(proboscis) and it can be transferred to definite host.  In man,filarial larva first enters blood circulation thru bite of mosquito and then it enters into lymphatic vessels that undergoes 3rd & 4th moulting and transforms into adult.  Adult male and female copulate and delivers MF.
  • 18. PATHOGENESIS AND ITS CLINICAL DISEASE:  Pathogenic effects seen in wuchereriasis are produced by adult worms.  Three following stages occurs sequentially in pathogenesis of LF: a) Dilation of lymphatic vessels. b) Infection of lymphatics. c) Obstruction of lymph nodes. Diseases are of two types: a) lymphatic/classical filariasis b) occult filariasis.
  • 19.  LYMPHATIC/CLASSICAL FILARIASIS: Caused by adult worm.  Example: Lymphangitis,Elephantiasis,Lymphedema etc.  OCCULT FILARIASIS: Caused by MF/embryos.  Example: Eosinophilia,hepatosplenomegaly. MANIFESTATIONS(LYMPHATIC FILARIASIS):  ASYMPTOMATIC STAGE: Characterized by presence of MF in peripheral blood.  No clinical signs and symptoms of the disease.  Some infected person-remains asymptomatic for yrs or some instances in life.
  • 20.  Others leads to acute and chronic stages.  ACUTE STAGE: Starts when they have already manifestations like Lymphangitis, Lymphadenitis and Filarial fever.  In some cases, male genitalia is affected leading to funiculitis, epidydimitis and orchitis.  Also results in headache, nausea and urticaria.  LYMPHANGITIS: An inflammation or an infection of lymphatic vessels and lymphatic channels that occurs as a result of infection at a site distal to the channel.  LYMPHADENITIS: An inflammation or infection in one or more lymph nodes.
  • 21.  FILARIAL FEVER: High fever of sudden onset leading for 2-3 days with temp of 103-104 degree.  Temperature comes down by profuse sweating.  Associated with localized sign of inflammation of lymphatic vessels.  Blood examination-transient leukocytosis,Increased neutrophils and presence of MF.
  • 22.  CHRONIC STAGE: Develops 10-15 years from onset of first attacks.  Manifestations like Hydrocele, Lymphedema, Elephantiasis and Chyluria.  HYDROCELE: Accumulation of fluid occurs as a result of obstruction of lymph vessels of spermatic cord and also due to exudation from inflamed testis and epididymis.  Clear and straw colored and sometimes milky, cloudy or hemorrhagic.  Occasionally, Hydrocele on enormous amount with elephantiasis of scrotum.
  • 23.  Fluid filled balloon like enlargement of sac around testes.  LYMPHEDEMA: Abnormal accumulation of lymph in tissues causing swelling of arms, breasts or genitals.  Caused by fluid collection because of improper functioning of lymph node system results in swelling.  Swelling caused by lymphatic system blockage which is a part of immune and circulatory system.  ELEPHANTIASIS: Caused by mechanical blocking of lumen of lymph vessels.
  • 24.  Excessive fibrosis of lymphatic vessels.  Commonly also affects limbs, genitals and breasts.  Disabling and disfiguring Lymphedema of limbs, breasts and genitals accompanied by marked thickening of skin.  Causes hardening and thickening of skin.  Swelling and decreasing function of lymph system makes body difficult to fight against infection and germs.  Results in decrease of blood flow due to worms inside blood vessels.
  • 25.  Chances of heart failure, breathing difficulty,Eosinophilia and kidney damage.  CHYLURIA: Due to rupture of varicose chyle vessels thru mucous membrane of urinary tract.  Lymph fluid in urine.  Appears as milk white in color and contains fat particles , albumin and fibrinogen.  Microscopic examination- MF, few RBCS and Lymphocytes.  LYMPHANGIOVARIX: Dilation of lymph vessels in inguinal, scrotal and abdominal regions.
  • 26.  LYMPHORRHAGIA: Rupture of lymph vessels results in release of lymph/chyle.  Results in lymph scrotum, lymphocele, Chyluria, chylous diarrhoea, chylous ascites and chyothorax.  OCCULT FILARIASIS: Called as meyers- kouwenaar syndrome.  Clinical conditions not due to lymphatic involvement but due to hypersensitivity reactions to filarial antigens.  Characterized by lymph node enlargement, Hepatosplenomegaly, pulmonary symptoms and absence of MF in blood.
  • 27.  MF not reaches peripheral blood as they are destroyed by tissues.  Results in Eosinophil granuloma.  TROPICAL PULMONARY EOSINOPHILIA: Characterized by low fever, weight loss, paroxysmal cough with scanty sputum and hepato-splenomegaly.  Total serum IgE and anti- filarial antibody titres will rises.  Responds well to treatment, if not treated-progressive pulmonary damage occurs.  Eosinophil count in peripheral blood exceeds 450/mul but in usual condition less than 7% in circulate leukocytes.
  • 28.
  • 29. DIAGNOSIS:  BLOOD MICROSCOPY: A) Direct wet mount B) Thick blood smear C) DEC provocation test.  Using concentration of blood  Intradermal test  Urine microscopy.  Antigen and antibody detection assay.  ELISA, HA TEST, CF, IMMUNOBLOTTING.
  • 30.  Direct immunofluorescent antibody  PCR  X-ray  Ultra sound/Ultrasonography.  Examination of biopsy.
  • 31. TREATMENT:  Diethylcarbamazine: Drug is effective in killing MF rapidly and adult worms slowly –can be given orally in dosage of 2-6mg/kg for 12 days.  Ivermectin: Taken as single oral dose 200ug/kg is highly effective.  Surgical treatment – small lymphatics are anatomized to large central vein. Produce marked reduction in limb size.  General treatment: Rest, Antibiotics, Physiotherapy and bandaging.
  • 32.  Para methyl phenyl stibonate against infective larvae.  Arsenical preparation against adult worms.  In US , combination of albendazole with Ivermectin.  DEC and albendazole is also effective against MF.  In 2003, common antibiotic-Doxycycline was suggested for treating elephantiasis to kill adult worm with dosage of 200mg/day for 4-6 weeks. PREVENTION:  Avoid mosquito bites.  Sleep under mosquito nets.  Use of mosquito repellants cream on skin.
  • 33.  Public awareness.  Destruction of breeding sites of vectors by insecticides.  Environmental sanitation should be maintained.  Adult mosquitoes can be controlled by spraying insecticides like DDT and BHC in homes.  Spraying of kerosene pyrethrum oil on sewage gutters and ditches –effective to kill mosquito larvae.  Biological control using larvivorous fish like GAMBUSIA is much safer to kill larvae.