vector born disease for b.sc. nursing.pptx

VECTOR BORN DISEASES
Presented by –
Debdatta Mandal
Associate Professor

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.

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

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.

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

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

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.

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.

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

 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

Life cycle of malaria parasite

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

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

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

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.

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

Incubation period
Type of malaria Incubation period
P. vivax 14 days
P. falciparum 12days
P. quartun 28 days
P. ovale 17 days

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

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.

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

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

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

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

Complications
P. Falsiparum
 Cerebral malaria
 Acute renal failure
 Liver damage
 Black water fever
Other 3 types
 Anemia
splenomegaly
 Herpes
 Liver enlargement

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)

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

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

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.

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

AGENT: DENGUE VIRUS
WHY SECOND INFECTION IS
MORE DANGEROUS??
SENSITIZATION
OF IMMUNE
SYSTEM
PATIENT
FIRST
INFECTION
SECOND INFECTION WITH
DIFFERENT SEROTYPE
IMMUNOLOGICAL
CATASTROPHY

AEDES MOSQUITO
 Asmall (5mm), black mosquito with white
stripes.
 Adult life span:15 days,
 Flight range – 400 meters (average).

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.

AEDES MOSQUITO
Life cycle: 7 – 10 days

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

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

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

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.

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

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

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

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,

FEBRILE PHASE
 Day 1 – 4
 Fever with Positive tourniquet test

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.

CRITICAL / HAEORRHAGIC PHASE
 Whenthetemperaturedrops to37.5-38°Cor
less,andremainsbelowthis level, usuallyon days4-
7ofillness,
 Anincreasein capillary permeability in parallel with
increasing haematocritlevels mayoccur.
 This marksthebeginning ofthecritical phase.
 Theperiodofclinicallysignificant plasmaleakage
usuallylasts 24-48 hours.

 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.

 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.

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

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

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.

RECOMMENDED TESTS
IgG (FIRST)
IgG (SECOND)
IgM
NS-1
VIRUS

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.

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

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

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

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

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.

Culex mosquito
Disease manifestation -
 None to both acute & chronic
 Not fatal
 Responsible for considerable suffering, deformity
& disability.
Mansonia mosquito

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.

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

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)

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

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

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

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

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

The breeding of Mansonia is
associated with certain aquatic
plant – Pista stratiotes.

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

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

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

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.

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

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.

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.

 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

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

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

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

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

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

b. Filaria control in the community
Filaria control
in the
community
Mass therapy
Selective
treatment
DEC
medicated
salt

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.

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

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

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

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

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.

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.

PERSONAL PROTECTION MEASURES
Protective clothing mats
coils
Insecticide treated nets
Permethrin treated clothing
Repellent sprays
(DEET)
Electric Raquete

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.

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.

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.

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)

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

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

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

Epidemiology
• Mode of transmission
• Incubation period – 4 – 7 days

Sign & symptoms
• High fever (400 C / 1040 F), chills
• Joint pain
• Joint swelling
• Anorexia
• Lumbago
• Conjunctivities
• Adenopathy
• 60 – 80% patient have morbilliform rash, occasionally with purpura
• Cutaneous eruption may recur every 3. - 7 days
• arthropathy

Diagnosis
• Serology
• ELISA, may confirm the presence of IgM and IgG anti – chikungunya
anti bodies
• RT - PCR

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.

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

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