2. MALARIA
• Malaria is a protozoal disease and mosquito – borne disease that affects
human.
• Malaria is an infection of liver and RBCs.
• Transmitted through the bite of infected anopheles mosquito
• Infected mosquitoes carry the plasmodium parasite.
• When this mosquitoes bite human, the parasite is released into the blood
stream.
3. Epidemiological determinant
• Agent factors:
Agent – Plasmodium Vivax, Plasmodium falciparum, Plasmodium
Malariae and P. Ovale.
Reservoir infection:
1. Chimpanzees in tropical Africa
2. Human
3. Children – Gametocytes carrier
4. Life cycle of malaria parasite
The malaria parasite undergoes 2 cycles of
development -
1. Human cycle (asexual cycle)
2. Mosquito cycle (sexual cycle)
Man is the intermediate host and mosquito
the definitive host.
5. 1. Asexual cycle
The asexual cycle begins when an infected
mosquito bites a person and injects sporozoites.
Four phases in the asexual cycle are –
1. Hepatic phase
2. Erythrocytic phase
3. Gametogeny
6. 1. Hepatic phase
• Sporozoites disappear within 60min from peripheral
circulation
• Many – destroyed by phagocytes, some reach the liver cells
• After 1-2wks, they become hepatic schizonts, which burst -
releasing shower of merozoites.
• P. falciparum - form 40,000 merozoites
• & other species may form 2,000to 15,000merozoites (do not
burst all at same time, they persist & remains dormant in
hepatocytes causing relapse of infection.)
• P. vivax & P. ovale - relapse for 2-3 yrs
• P. malariae – 10-20 yrs or more
7. 2. Erythrocytic phase
Many merozoites are destroyed and significant number of
merozoites are attached to RBC
Merozoites penetrate RBC & passes through the stages of
trophozoites & schizonts
The erythrocytic phase ends with the liberation of merozoites ,
which infect red blood cells
The cycle is repeated over & over again until it is slowed
down by immune response of the host
Duration of erythrocytic cycle –
P. falciparam, P. vivax & P.ovale – 48hrs
P. Maleriae – 72 hrs.
8. 3. Gametogeny
Some erythrocytic form do not divide but
become male & female gametocytes
These are sexual forms of the parasite which
are infective to mosquito.
9. Sexual cycle (in mosquito)
Vector mosquito feed on infected person
Gametocytes ingested by mosquito
Development in mosquito
In mosquito stomuch – exflagellation of male
gametocyte –- micro-gamates are formed
Female gametocyte undergoes a process of maturation
& become female gamete or macrogamete
By process of chemotaxis, microgametes are attached
towards female gamete & one of microgamete causes
fertilization of female gamete.
Zygote formation – motionless body
Within 18-24hrs – becomes motile known as Ookinete
10. Ookinete penetrate stomach wall of mosquito
Develops into an oocyst
Oocyst grows rapidly & develops within it
numerous sporozoites
When mature, oocyst burst & liberates
sporozoites into the body cavity of mosquito and
the mosquito becomes infective to man
Extrinsic incubation period - Time required for
development of the parsite from the gametocyte
to sporozoite stage - 10-20dys
12. Period of communicability
• Malaria is communicable as long as mature, viable gametocytes
present in blood
• Gametocytes in sufficient density
• Vivax infection – 4 to 5 days
• Falciparum infection – 10 to 12 days
13. Relapse
• P. Vivax & Ovale - >3 yrs. after patient first attack
• P. Falciparum – disappear within 1 – 2 yrs.
• P. Malariae – tendency to cause prolonged low level asymptomatic
parasitemia. Infection may persist for more than 40 yrs or more.
• Vivax & Ovale relapse – sporozite induced (latent)
• P. falciparum malariae – due to chronic blood infection
14. Host Fsctors
• Age : all age (Except Newborn and Infant)
• Sex: Males are more exposed
• Race: Sickle cell trait (AS Hb) milder illness with falciparum infection
• Pregnancy : increase risk of malaria. Primi – greatest risk
• Socio – economic status
• Housing
• Population mobility
• Occupation
• Human habits
• Immunity
15. Environmental factors
• Season : In India July to November
• Temperature : 20 – 300 C
• Humidity: 60% necessary for mosquito life
• Rainfall: provides opportunities of mosquito breeding and may give
rise to epidemic of malaria.
• Altitude : Anophelines are not found at altitude above 2000 – 2500
meters, due to unfavorable condition
• Man made malaria: Burrow pits, garden pools, irrigation channels and
engineering projects etc.
16. Mode of transmission
1. Vector transmission – transmitted by the bite of certain species of
infected , female, anopheline mosquitoes
2. Direct transmission - malaria may be induced by hypodermic
intramuscular and intravenous injections of blood or plasma, e.g.,
blood transfusion, malaria in drug addicts.
3. Congenital - rare
17. Incubation period
Type of malaria Incubation period
P. vivax 14 days
P. falciparum 12days
P. quartun 28 days
P. ovale 17 days
18. Clinical features
• The typical attack comprises 3 stages. These are –
1. Cold stage
2. Hot stage
3. Sweating stage
These are followed by an afebrile period in which patient feels greatly
relieved
19. 1. Cold stage
Onset with lassitude, Headache,
Nausea & Chilly sensation
Temp rises rapidly 39-410C
Severe headache & vomiting
Early phase – skin cold, later hot
Pulse rapid & weak
Parasite demonstrate in the blood
Pulse – rapid, weak
This stage lasts for ¼-1hour.
20. 2. Hot stage
Patient feels burning
hot & cast off his cloths
Intense headache
Skin hot & dry
Nausea diminish
Pulse full
Respiration rapid
Lasts for 2-4hrs
21. 3. Sweating stage
Fever comes down
with profuse sweating
Temperature normal
Skin cool & moist
Pulse rate slow
Patient feels relieved
& falls asleep
Lasts for 2-4hrs
22. Febrile peroxysms
Occurs with definite intermittent periodicity
Every 3rdor 4th day – depend on species of
parasite
Tendency of relapse – month to yrs
1. P. Falsiparum
Fever irregular/ continuous
Classical 48hrs periodicity
Hot & cold stage
23. 2. P. Vivax
Symptoms are like p. falsiparum but mild
Regularly divide into hot & cold stage
3. P. Ovale
Milder than vivax
Ceases after few paraxymus
4. P. Malariae
Resembles P. Vivax
But 72 hrs periodicity
Tendency for long term relapse
24. Complications
P. Falsiparum
Cerebral malaria
Acute renal failure
Liver damage
Black water fever
Other 3 types
Anemia
splenomegaly
Herpes
Liver enlargement
25. Diagnosis
1. Microscopy
2 Types of film on single slide
a. Thick film – searching of parasite
b. Thin film – identification of parasite
2. Serological test
After 2 wks +ve --- treatment /cure
3. Rapid diagnostic test (RDT)
26.
27. Guidelines for diagnosis & treatment of
Malaria -2013
Treatment of uncomplicated Malaria
Diagnosis by RDT /microscopy
a. Treatment of P. vivax
1. Chloroquine 25mg/kg body wt for 3 days
2. Primaquine 0.25mg/
kgbody wt for 14 days
28. b. Treatment of P. falciparum
a. In other states – ACT-SP x 3days
1.Artemisinin combination therapy (ACT)
( Artesunate 50mg x 3days
Sulphadoxine-pyrimethamine x1 day)
2. Primaquine 0.75mg /kg body wt on day 2
b. NE states - ACT-AL (age specific)
Artemether 20mg +Lumefantrine 120mg x 3days
Primaquine single dose on 2ndday
29. DENGUE
Most rapidly spreading mosquito-borne viral
disease in the world.
The infection causes flu-like illness,
⚫ and occasionally develops into a potentially lethal
complication – dengue shock syndrome.
Incidence of dengue has grown dramatically
around the world in recent decades.
There is under-reporting & misclassification.
30. Epidemiological determinant
• Agent factors
Agent - DENV – 1, DENV – 2, DENV – 3 & DENV - 4
Vector - Aedes aegypti and Aedes Albopictus
- High susceptibility to infecting virus
- Highly domesticated , strongly anthropophilic, nervous feeder (i.e. it
bites more than one host to complete one blood meal)
- Discordant species
31. AGENT: DENGUE VIRUS
WHY SECOND INFECTION IS
MORE DANGEROUS??
SENSITIZATION
OF IMMUNE
SYSTEM
PATIENT
FIRST
INFECTION
SECOND INFECTION WITH
DIFFERENT SEROTYPE
IMMUNOLOGICAL
CATASTROPHY
32. AEDES MOSQUITO
Asmall (5mm), black mosquito with white
stripes.
Adult life span:15 days,
Flight range – 400 meters (average).
33. AEDES MOSQUITO
FEEDING HABITS:
Usually a Day biter,
preferably bites on the ankles and elbows.
⚫ (Peak : within 2 hours after dawn and before
sunset.)
Is strongly anthropophilic.
Known to be a nervous feeder
⚫ it bites more than one host to complete one meal.
⚫ This feeding habit results in the generation of
multiple cases and the clustering of dengue cases
in the cities.
35. TRANSMISSION OF DISEASE
TheAedes mosquito becomes infective by feeding on a
patient from the day before onset to the 5th day (viraemia
stage) of illness.
After an extrinsic incubation period of 8 to 10 days, the
mosquito becomes infective, and is able to transmit the
infection.
Once the mosquito becomes infective, it remains so for
life.
The genital tract of the mosquito gets infected and
transovarian transmission of dengue virus occur.
K.Parks.Park’s Textbook of Preventive and social medicine. Epidemiology of communicable
diseases.24rd edition.Jabalpur india:M/s Banaridas Bhanot;2017:page-264
37. ENVIRONMENTAL FACTORS
The population of Aedes aegypti fluctuates with
rainfall and water storage.
Its life span is influenced by
⚫ temperature (160C -300C) and humidity (60-80 %).
Even with a 20 increase in temperature,
⚫ The extrinsic incubation period of DENV will be
shortened
⚫ and more infected mosquitoes are available for a
longer duration.
K Park , 24th ed; 2017,p 262
38. High risk factors
• Infant and elderly
• Obesity
• Pregnancy
• Peptic ulcer diseases
• Women who are in menstruation or have abnormal bleeding
• Hemolytic diseases such as G – 6PD, thalassemia and other
haemoglobinopathies
• Congenital heart disease
• Chronic diseases
• Patient on steroid or NSAID treatment
39. CASE DEFINITION
Suspected:
⚫ Acase compatible with the clinical description.
Probable:
⚫ Acase compatible with the clinical description with
one or more of the following:
⚫ Supportive serology.
⚫ Occurrence at same location and time as other
confirmed cases of dengue fever.
Confirmed:
⚫ Acase compatible with the clinical description that is
laboratory confirmed.
41. Clinical manifestation
• Undifferentiated fever
- primary dengue infection
- simple viral fever
- maculopapular rashes with fever or may appear during defervescence
- upper respiratory and gastrointestinal symptoms are common
• Classical dengue fever
- all ages and both sexes
- incubation period 3 to 10 days
- onset is sudden with chills and high fever, intense headache, muscle
and joint pain
- retroorbital pain and photophobia
42. Cont…
• Classical dengue fever
- all ages and both sexes
- incubation period 3 to 10 days
- onset is sudden with chills and high fever, intense headache, muscle
and joint pain
- retroorbital pain and photophobia
43. Cont…..
• Other common symptoms
- extreme weakness
- anorexia
- constipation
- altered taste sensation
- colicky pain and abdominal tenderness
- dragging pain in inguinal region
- Sore throat
- General depression
44. Cont….
• Dengue hemorrhagic fever (DHF)
Asevere form of dengue fever.
The course of dengue illness can be divided into three phases-
⚫ febrile phase,
⚫ critical phase and
⚫ recovery phase,
47. TOURNIQUET TEST
Goal of the test :-
Toasses fragility of capillary walls
T
oidentify thrombocytopenia
In DHF grade 1, a positive
tourniquet test serves as the only
indicator of haemorrhagic tendency
• ≥20 petechiae
per 1 square
inch.
49. CRITICAL / HAEORRHAGIC PHASE
Shock occurs when a critical volume of
plasma is lost through leakage.
It is often preceded by warning signs of
⚫ Abdominal pain or tenderness,
⚫ Persistent vomiting,
⚫ Clinical fluid accumulation,
⚫ Mucosal bleeding,
⚫ Lethargy,
⚫ Restlessness,
⚫ Liver enlargement more than 2 cm. and
⚫ Oliguria.
50. CRITICAL / HAEORRHAGIC PHASE
With prolonged shock, the consequent organ
hypoperfusion results in progressive organ
impairment, metabolic acidosis and disseminated
intravascular coagulation.
This in turn leads to severe haemorrhage causing the
haematocrit to decrease in severe shock. Instead of the
leukopenia usually seen during this phase of dengue, the
total white cell count may increase in patients with severe
bleeding.
In addition, severe organ impairment such as severe
hepatitis, encephalitis or myocarditis and/or severe
bleeding may also develop without obvious plasma leakage
or shock.
51. RECOVERY PHASE
After critical phase, 48-72 hours of reabsorption
of extravascular fluid
Well-being, appetite improves
Bradycardia common
Hemodynamic status improves
GI symptoms abate
Blood counts normalize (RBC>WBC>Plt)
Diuresis occurs
Prolonged convalescence
52. RECOMMENDED TESTS
GOI recommends use of ELISAbased antigen
detection test (NS1) for diagnosing the cases
from 1st day onwards.
Antibody detection test IgM Capture ELISA
(MAC ELISA) for diagnosing the cases after
5th day of onset of disease for confirmation of
Dengue infection
53. RECOMMENDED TESTS
NVBDCPhad been using MAC- ELISAfor
diagnosis of dengue infection in the network of
Diagnostic Centers established/ identified in the
Sentinel Surveillance Hospitals (SSHs) and
Apex Referral Laboratories (ARLs) across
the country.
55. RAPID TEST COMBO KIT
Most of the studies have
shown that detection of
both the NS1 Antigen
and the anti-dengueIgm
together yields
satisfactory clinical
results, instead of sole
NS1 antigen detection.
56. MANAGEMENT OF DENGUE FEVER
MANAGED AT HOME
BED REST
COLD/TEPID SPONGING
PARACETAMOL
WARNING SIGNS SHOULD BE EXPLAINED
ADVISED TO REPORT TO HOSPITAL IF WARNING
SIGNSAPPEAR
57. WARNING SIGNS
RECURRET VOMITING
BLEEDING FROM DIFFERENT SITES:
GUM BLEEDING
BLOOD IN SPUTUM
BLOOD IN VOMIT OR STOOL
INCREASED MENSTRUAL FLOW
ABDOMINAL PAIN OR DISCOMFORT
COLD CLAMY SKIN
PALPITAION BREATHLESSNESS
58. MANAGEMENT OF DHF
ALLCASES TO BEADMITTED
ENCOURAGE ORAL FLUIDS:ORS,JUICES
START I.V. FLUIDS
PARACETAMOL
DAILYHEMATOCRIT DETERMINATION
MONITOR URINE OUTPUT, B.P. AND OTHER VITALSIGNS
Platelet concentrate :
if the platelet count is < 50,000 / mm3 with bleeding.
In the absence of bleeding :counts <10,000/ mm3
59. MANAGEMENT OF DSS
All of the following 6 criteria must be met before a
patient is discharged from the hospital :
1. Visible improvement in clinical picture
2.Absence of fever for 24 hours & return of appetite
3.Three days after recovery from shock
4.Stable hematocrit
5.Platelet count greater than 50,000/mm3 and rising
6.No respiratory distress
60. Lymphatic filariasis
The term lymphatic filariasis covers infection with three
closely related nematode worms -
• W. bancrafti, B. malayi and B. timori.
Transmitted to man by bite of infected mosquito
All three parasites have Similar life cycle in man-adult worm
living in lymphatic vessels with their offspring, the
microfilariae circulate in peripheral blood and are available to
infect mosquito vectors when they come to feed.
61. Culex mosquito
Disease manifestation -
None to both acute & chronic
Not fatal
Responsible for considerable suffering, deformity
& disability.
Mansonia mosquito
62. Periodicity
1. W. Bancrafti and B. malayi (India )
Nocturnal periodicity ( appear in large numbers at
night and retreat from blood stream during day.
Maximum density of Mf – 10pm to 2am
If sleeping habit of the host is altered – reversal
periodicity
2. In south Pacific islands & limited foci in Nicobar
islands Thialand, Viatnam - W. bancrafti micrifilaria
are not periodic (subperiodic) and detectable
throughout 24hrs with slight peak during day or
night.
3. B. malayi – subperiodic in Malaysia & Indonesia.
63. Life cycle
Man – definite host
Mosquito – intermediate host
The adult worm found in the lymphatic system of
man
Male – 40mm long
Female – 50 -100mm long
Viviparous – gives birth to as many as 50000Mf per
day which find their way into blood circulation via
lymphatics
Life span of Mf is not known, probably upto year or
more.
Adult worm may survive for 15 years
64. Life cycle
• Mosquito cycle begins when the Mf are picked up
by the vector mosquito during feeding.
• The following stages of development takes place in
the vector
a. Exsheathing – larva comes out of sheath – within 1-
2hr of ingestion. It occurs in stomach of mosquito.
b. First stage larva- larva is able to penetrate the
stomach wall of mosquito (6-12hrs) and migrate to
thoracic muscle where it grows & develops into a
sausage shaped form ( short, thick)
65. c. Second stage larva
Larva moults and increase in length (long, thick)
with the development of an alimentary canal, but is
relatively inactive.
d. Third stage larva
Final moult to third stage larva or infective larva
(long, thin) which may be found in any part of the
insect. It is highly active or motile.
When it migrates to proboscis of the mosquito, it is
ready to be transmitted to new host and mosquito is
said to be infective.
Extrinsic incubation period – 10-14days
In human host, infective larva develops into adult
male & female worms
66. Reservoir of infection
1. Animal –
Brugia – monkey, cat, dog
Bancrafti – no animal reservoir
2. Human –
Circulating Microfilaria in peripheral blood
Filarial disease last stage – Microfilaria not
found in blood
67. Host factors
1. Age – infects all age
Infection rate rise with age of 20-30yrs
Decrease in middle & older age
2. Sex – Higher in men
3. Migration
4. Immunity – Man may develop resistance to
infection only after many years of exposure.
5.Social factors – associated with industrialization,
poverty, literacy, poor sanitation
68. Environmental factors
1. Climate –Climate influences the breeding of
mosquitoes, their longevity and also determines
the development of the parasite in the insect
vector. The maximum prevalence of C. fatigans
was observed when the temperature was
between 22 to 38 deg. C and optimum longevity
when the relative humidity was 70 %.
2. Drainage –
Associated with bad drainage, polluted water
Vector breed profusely in polluted water
3. Town planning- Lack of town planning,
inadequate sewage disposal
69. Vectors
Culex, Anaphelus, Ades serves as vectors for
W. Bancrafti
Mansonia, Anophelus serves as vector for
Brugia
Main vector in India
1.Culex fatigans – Bancraftian filariasis
2. Mansonia – Brugian filariasis
70. The breeding of Mansonia is
associated with certain aquatic
plant – Pista stratiotes.
71. Mode of transmission
Filariasis is transmitted by-
Bite of infected vector mosquito
Parasite deposited near the site of puncture
Punctures skin/penetrate skin
Reach to lymphatic system
72. Incubation period
The time interval from invasion of infective
larvae to the development of clinical
manifestations is known as the clinical
incubation period.
This period is 8 to 16 months or longer
73. Clinical manifestation – 2 clinical
types
A. Lymphatic filariasis
Caused by the parasite in the
lymphatic system
Stages in lymphatic filariasis
are -
1. Asymptomatic amicrofilaria
2. Asymptomatic microfilaria
3. Stage of acute manifestation
4. Stage of chronic obstructive
lesion
• B.Occult filariasis
Caused by immune
• hyper
responsiveness of
human host
• Ex. Tropical
pulmonary
esinophilia
74. Lymphatic filariasis
1. Asymptomatic amicrofilaria
In endemic areas –proportion of population does not
shows Mf or clinical manifestation of disease –
although they have same degree of exposure.
2. Asymptomatic microfilaria
Asymptomatic but blood positive for Mf
microfilaria.
They may remain without any symptoms for
many months or years.
Important source of infection in the community.
Carrier detected by night blood exam.
75. 3. Stage of acute manifestation
In first month & years –there arerecurrentepisode
of acute inflammation in lymph glands & vessels.
Clinical manifestation-
Filarial fever
Lymphangitis, lymphadenitis, lymphoedema of
various part of the body
Male – epidymo-orchitis
76. 4. Stage of chronic obstructive lesions
It develops 10-15years from onset first acute attack.
This phase is due to fibrosis & obstruction of
lymphatic vessels causing permanent structural
damage.
In chronic Bancraftian filariasis, the main clinical
features are hydrocele, elephantitis and chyluria.
Elephantitis may affect the legs, scrotum, arm, penis,
vulva& breast usually in order of decreasing
frequency.
Prevalence of Chyluria is usually very low.
Brugian filariasis – similar to Bancraftian fileriasis,
but genitalia are rarely involved.
77.
78.
79. Lymphoedema treatment
1. Treatment for uncomplicated ADLA
(Acute dermato lymphangioadenitis)
Give analgesic such as paracetamol
Give oral antibiotic such as amoxicillin for at
least 8 days.
Clean the limb with antiseptic.
Check for any wounds, cuts, abscesses and
interdigital infection (especially between the
toes) and Clean with antiseptic.
If local superficial skin infection is found
give antibiotic cream, apply antifungal cream
if interdigital infection is present.
80. Give advice about prevention of chronic
lymphoedema caused by lymphatic filariasis;
Do not give antifilarial medicine.
Home management includes drinking plenty
of water, rest, elevation of the limb, wriggling
the toes, cooling the limb with cold water and
washing the limb if the patient can do it; an
Follow-up after 2 days at home.
If situation does not improve, then refer the
patient to physician
81. Management of severe ADLA
Refer the patient to physician immediately to
receive following antibiotic treatment-
Benzylpenicillin (Penicillin G) 5 million units
given 3 times a day
Phenoxymethylpenicillin (penicillin V) 750 mg to
1gm given 3 times/day.
In case of allergy to penicillin, give IV
erythromycin1g 3 times/day until fever subsides,
then give oral erythromycin 1g given 3times/day
Give analgesic /antipyretic such as paracetamol
Do not give any antifilarial medicine
82. Filaria survey
Routine survey -5-7%population
Evaluation survey – 20% population
1. Mass blood survey
2. Clinical survey
3. Serological tests - to detect antibodies to Mf
4. Xenodiagnosis
5. Entomological survey
83. Mass blood survey/night blood survey
Diagnosis depends on demonstration of living
parasite in human body.
a. Thick film – capillary blood – 8:30pm to 12 am
b. Membrane filter concentration (MFC)
Venepuncture – filtering large volume of blood
For detection of low density Mf
c. DEC provocation test
Administration of DEC 100mg orally
Mf begins to reach their peak 15 minutes and
begin to decrease 2 hours later.
Blood may be examined 1 hr after administration
of DEC
84. Control measures
The current strategy of filariasis control is
based on –
1. Chemotherapy
a. Diethylcarbamazine
b. Filaria control in the community
c. Ivermectin
2. Vector control
85. 1. Chemotherapy
a. Diethylcarbamazine (DEC)
Effective in killing Mf
Safe
Oral – rapidly absorbed
Reaches peak blood level within 1-2hrs
Rapidly excreted
Type of filariasis DEC dose
Bancrafian filariasis 6mg/Kg body weight for 12 days
Brugian filariasis 3-6mg/Kg body weight
86. b. Filaria control in the community
Filaria control
in the
community
Mass therapy
Selective
treatment
DEC
medicated
salt
87. i. Mass therapy
DEC is given to almost everyone in the
community irrespective of whether they have
microfilaraemia, disease manifestations or no
signs of infection
Contraindication - children under 2 years,
pregnant women and seriously ill patients.
Dose - 6 mg/kg body weight
Indicated in highly endemic areas.
88. ii. Selective treatment
For Mf positive
Indicated in low endemic areas
Dose – 6mg/Kg per body weight for 12days In
endemic areas, treatment must be repeated at
specified intervals; usually every 2yrs.
iii. DEC medicated salt
Common salt medicated with 1-4gm of DEC per Kg
for 6-9months
89. c. Ivermectin
Ivermectin is a semisynthetic macrolide
antibiotic with a broad spectrum of activity
against a variety of nematodes and ectoparasites
Dose - 150-200 µg/kg of body weight
Not used in India, used in Africa
90. 2. Vector control
Vector control may be beneficial, when used in
conjunction with mass treatment.
The most important element in vector control is
the reduction of target mosquito population in
order to stop or reduce transmission quickly.
It consist of
i. Anti larval measures
ii. Anti adult measures
iii. Personal prophylaxis
91. Mosquito control measures
1. Antilarval measures
a. Envirnmental measures
b. Chemical
c. Biological
2. Anti-adult measures
a. Space spray -application of pesticides in the form
fog or mist
b. IRS – indoor surface of houses – DDT, malathion
c. Genetic control
3. Legislative control - Civil, laws
4. Protection against mosquito bite - Bed net, Repellent,
screening
96. ENVIRONMENTAL CONTROL
Don’t allow water to remain stagnant
in and around your house.
Fill the ditches.
Clean the blocked drains.
Empty the room air coolers and flower vases completely
at least once in seven days and let them dry.
Dispose off old containers, tins and tyres etc. properly.
Keep the water tanks and water containers tightly
covered so that the mosquitoes can not enter them and
start breeding.
97. ENVIRONMENTAL CONTROL
Wherever it is not possible to completely drain the water
off from room cooler, water tanks etc., it is advised to put
about two tablespoons (30 ml.) of petrol or kerosene
oil into them for each 100 litres of water.
This will prevent mosquito breeding.
Repeat it every week.
Keep the surroundings of your house clean.
Don’t allow wild herbs etc. to grow around
your house. They act as hiding and resting
places for mosquitoes.
99. INDOOR SPACE SPRAYING
Commercial formulation of 2% pyrethrum
(deltamethrin) extract is diluted with kerosene
in the ratio one part of 2% pyrethrum extract
with 19 parts of kerosene (volume/volume).
One liter of ‘formulation is sufficient to cover
20 households, each household having 100
cubic meters of indoor space.
100. OUTDOOR SPACE SPRAYING
Usually carried out in early morning or late afternoon
For narrow roads: the spray should be directed backwards
from the vehicle.
For wide roads: the spray should be directed at a right angle
(downward) to the road.
1. Ultra Low Volume (ULV) Spray(cold fog):
⚫ Malathion TECHNICAL is the insecticide used for this
purpose.
⚫ Remain suspended in air and driven under the influence of
wind.
⚫ Since no diluent is used, the technique is more cost-
effective than thermal fogging.
⚫ But it does not generate a visible fog.
101. OUTDOOR SPACE SPRAYING
2. Thermal Fogging
⚫ Water based
⚫ Oil based(m/c used)
Technique is based on the principle that insecticide is
vaporized, which condenses to form a fine cloud of droplets
on contact with cooler air when it comes out of the
machine.
Insecticide of choice for fogging is
malathion/pyrethrin.
102. LARVICIDES
Cycle : 2-3rounds /year
Both internal and external walls of container should
be sprayed and up to 60cm of height.
LARVICIDES
FOR POTABLE WATER FOR NON-POTABLE WATER
TEMEPHOS (1mg/L)
METHOPRENE(1mg/l)
TEMEPHOS (1mg/L)
Bacillus thuringiensis israelensis
(bio-chemical)
103. BIOLOGICAL CONTROL
Larvivorous Fish
Advantages
Environmental friendly
Easy to introduce
Self propagating & self sustainable
User friendly
Helps build community participation &
intersectoral collaboration
Cost-Effective - no recurrent costs
Gambusia affinis
Lebister reticularis
104. BIOLOGICAL CONTROL
Larvivorous Fish
Limitations
Extremes of temperatures and pollution
Suitable for some types of breeding sources only
Needs proper planning with mapping of
breeding sources & promotional efforts
Biolarvicide:
Bacillus thuringiensis iserailensis (Bti)-Endotoxin
: 2.5% suspension, 1 lit/50 m2, once every 2
Aphanius dispar
106. CHIKUNGUNYA
• A dengue like disease caused by a group A virus
• It was first isolated in 1953 in Tanzania.
• During 2006, there was a large outbreak of Chikungunya in India.
• It is an RNA virus.
• Transmitted by Aedes mosquito
• Chikungunya means “ to become contorted”
• As the affected person walks in a stooped posture because of joint
pain
110. Treatment of Chikungunya
• No specific antiviral drug treatment
• Usually self - limiting
• Analgesics, antipyretic along with fluid supplementation are
recommended.
• No commercial chikungunya vaccines till date.
111. Prevention of chikungunya
• Vector control
• Biological control
• Using insect repellent
• Wearing bite proof long sleeves and trousers
• Securing screens on window and door at house
