EPIDEMIOLOGY OF COMMUNICABLE DISEASES

transmission of guineaworm disease is water infested with ( b ) dengue haemorrhagic fever without shock, or (c) dengue

cyclops. The risk of transmission exists where such cyclops­ haemorrhagic fever with shock. The manifestations of the

infested water-sources are frequented by infected persons. dengue syndrome are as shown in Fig. 1 .

Season : The seasonal variations in the incidence of the
Dengue fever is a self-limiting disease and represents the
disease are marked. Where the step-wells are the source of
majority of cases of dengue infection. A prevalence of Aedes
water supply, peak transmission occurs during the dry
aegypti and Aedes albopictus together with the circulation of
season (March-May) when the contact between open cases
dengue virus of more than one type in any particular area
of gunieaworm disease and the drinking water is the
tends to be associated with outbreaks of DHF/DSS ( 1 ) .
greatest; and there is little transmission when the wells are

full during and after rains. Where the ponds are used, Problem statement
transmission appears to be confined to June-September,
Dengue fever (OF) and its severe forms – dengue
when the ponds contain water (4, 5). Temperature : The
haemorrhagic fever (DHF) · and dengue shock syndrome
larvae develop best between 25 and 30 deg C, and will not
(DSS) – have become major international public health
develop below 19 deg C. Therefore, the disease is limited to
concerns. Over the past three decades, there has been
tropical and subtropical regions ( 6 ) .
dramatic global increase in the frequency of dengue fever,

DHF and DSS and their epidemics. It is found in tropical
M o d e of transmission
and subtropical regions around the world, predominantly in
The disease is transmitted entirely through the
urban and semi-urban areas, and are now spreading to
consumption of water containing cyclops harbouring the
rural areas.
infective stages of the parasite. Guineaworm disease is a
Some 2.5 billion people i.e. two fifth of the world’s
totally water-based disease and does not have an alternate
population in tropical and subtropical countries are at risk of
pathway of transmission.
the disease. An estimated 50 million dengue infections occur

Treatment worldwide annually and about 5 0 0 , 0 0 0 people with DHF

require hospitalization each year. Approximately 90 per cent
No drug cures the infection but metronidazole and
of them are children aged less than five years, and about 2 . 5
mebendazole are sometimes used to limit inflammation and
per cent of those affected die. Epidemics of dengue are
facilitate worm removal. Wet compresses may relieve
· increasing in frequency. During epidemics, infection rate
discomfort. Occlusive dressings improves hygiene and limit
among those who have not been previously exposed to the
shedding of infectious larvae. Worms are removed by
virus are often 40 to 50 per cent, but can also reach 80 to 90
sequentially rolling them out over a small stick. When
per cent (2). Cocirculation of multiple serotypes/genotypes is
available simple surgical procedure can be used to remove
evident.
worm. Topical antibiotics may limit bacterial superinfection.
Dengue and DHF is endemic in more than 100 countries
Eradication in the WHO regions of Africa, the Americas, Eastern

Mediterranean, South-East Asia and Western Pacific. The
Guineaworm disease is amenable to eradication. The

eradication strategy comprises the following elements : South-East Asia and Western Pacific regions are most

seriously affected. Detection of all four serotypes has now
i) Provision of safe drinking water (e.g., piped water,
rendered the countries hyperendemic. The countries of
installation of hand pumps).
South-East Asia region are divided into 3 categories (2).
ii) Control of cyclops (see C h a p . 1 2 ) .
Category A (Bangladesh, India, Indonesia, Maldives,
iii) Health education of the public in matters relating to
Myanmar, Sri Lanka, Thailand and Timor-Leste)
boiling or sieving drinking water through a double­

thickness cotton cloth for personal protection, and a. Major public health problem;

prevention of water contamination by infected persons. b. Leading cause of hospitalization and death among

iv) Surveillance : Active search for new cases, and children;

c. Hyperendemicity with all 4 serotypes circulating in
Guineaworm Eradication Programme
urban areas; and
Refer to chapter 7 for details.
d. Spreading to rural areas.

References Category B (Bhutan, Nepal)

1. WHO ( 2 0 1 4 ) , Fact Sheet No. 359, March 2 0 1 4 . a. Endemicity uncertain;
2. WHO (2000), Weekly Epidemiological Record 2nd June 2000 No. 22.
b. Bhutan reported first outbreak in 2004; and
3. WHO ( 1 9 7 9 ) . Techn. Rep. Ser., No. 6 3 7 .
c. Nepal reported first indigenous case in 2004.
4. Muller, R. ( 1 9 7 9 ) . Bull WHO, 57 ( 5 ) 683.

5. WHO ( 1 9 8 0 ) . WHO Chr., 34 (4) 1 5 9 .
Category C (DPR Korea)

6. National Guineaworm Eradication Programme, National Health No evidence of endemicity.
Programme series 2, National Institute of Health and family welfare,

New Mehrauli Road, New Delhi.
INDIA

In India, the risk of dengue has shown an increase in
Ill. ARTHROPOD-BORNE INFECTIONS recent years due to rapid urbanization, lifestyle changes and

deficient water management including improper water

storage practices in urban, peri-urban and rural areas,

THE DENGUE SYNDROME leading to proliferation of mosquito breeding sites. The

disease has a seasonal pattern i.e. the cases peak after

Dengue viruses are arboviruses capable of infecting monsoon, and it is not uniformly distributed throughout the

humans, and causing disease. These infections may be year. However, in the southern states and Gujarat the

asymptomatic or may lead to (a) “classical” dengue fever, or transmission is perennial (3).
THE DENGUE SYNDROME

Dengue is endemic in 3 1 states/UTs. During 2 0 1 3 , about the two most important vectors of dengue. They both carry

74,168 cases were reported with 168 deaths. The case high vectorial competency for dengue virus, i.e., high

fatality rate was 0.22 per cent. As seen from Table 1, the susceptibility to infecting virus, ability to replicate the virus

highest number of cases were reported from Punjab and ability to transmit the virus to another host. Aedes

followed by Tamil Nadu, Gujarat, Kerala and Andhra aegypti is a highly domesticated, strongly anthropophilic,

Pradesh (5). nervous feeder ( i . e . , it bites more than one host to complete

one blood meal) and is a discordant species {i.e., it needs
All the four serotypes i . e . dengue 1 , 2 , 3 and 4 have been
more than one feed for the completion of the gonotropic
isolated in India but at present DENV-1 and DENV-2
cycle). This habit results in the generation of multiple cases
serotypes are widespread (4).
and the clustering of dengue cases in the cities. On the

contrary, Ae. albopictus partly invades peripheral areas of
E p i d e m i o l o g i c a l determinants
urban cities. It is an aggressive feeder and concordant

Agent factors species, i . e . , the species can complete its blood meal in one

go on one person and also does not require a second blood
( a ) AGENT : The dengue virus form a distinct complex
meal for the completion of the gonotropic cycle.
within the genus flavivirus based on antigenic and biological

characteristics. There are four virus serotypes which are
Transmission of d i s e a s e
designated as DENV-1, DENV-2, DENV-3 and DENV-4.
The Aedes mosquito becomes infective by feeding on a
Infection with any one serotype confers lifelong immunity to
patient from the day before onset to the 5th day (viraemia
that virus serotype (6). Although all four serotypes are
stage) of illness. After an extrinsic incubation period of 8 to
antigenically similar, they are different enough to elicit cross­
10 days, the mosquito becomes infective, and is able to
protection for only a few months after infection by any one
transmit the infection. Once the mosquito becomes infective,
of them. Secondary infection with dengue serotype 2 or
it remains so for life. The genital tract of the mosquito gets
multiple infection with different serotypes lead to severe
infected and transovarian transmission of dengue virus
form dengue DHF/DSS (2). The first infection probably
occurs when virus enters fully developed eggs at the time of
sensitizes the patient, while the second infection with
oviposition.
different serotype appears to produce immunological

catastrophy.
Environmental factors
The pathogenesis of severe syndrome involves pre­
The population of Aedes aegypti fluctuates with rainfall
existing dengue antibody. It is postulated that virus
and water storage. Its life span is influenced by temperature
antibodies are formed within a few days of the second
and humidity, survives best between 16°C-30°C and a
dengue infection and that the non-neutralizing enhancing
relative humidity of 60-80 per cent. It breeds in the
antibodies promote infection of higher numbers of
containers in and around the houses. Being a domestic
mononuclear cells, followed by the release of cytokines,
breeder, it is a endophagic and endophilic. However, even
vasoactive mediators, and procoagulants, leading to the
with a 2 ° C increase in temperature the extrinsic incubation
disseminated intravascular coagulation seen in the
period of DENV will be shortened and more infected
haemorrhagic fever syndrome ( 7 ) .
mosquitoes are available for a longer duration. Besides that

All four serotypes have been associated with epidemics of the mosquitoes will bite more frequently because of

dengue fever (with or without DHF) with varying degree of dehydration and thus increase man-mosquito contact (2, 4 ) .

severity.
The failure of urban authorities to provide civil amenities

(b) VECTOR : Aedes aegypti and Aedes Albopictus are and poor public health infrastructure raises the potential for

TABLE 1

Dengue I DHF situation in I n d i a 2 0 1 0 – 2 0 1 3

2010 2011 2012 2013
State
Cases Deaths Cases Deaths Cases Deaths Cases Deaths

Andhra Pradesh 776 3 1,209 6 2,299 2 990 1

Assam 237 2 0 0 1,058 5 4,526 2

Delhi 6,259 8 1,131 8 2,093 4 5,574 6

Chandigarh 29 5 186 33 2,255 6 7,132 6

Goa 175 1 50 0 239 6 1,255 9

Gujarat 2,568 1 1,693 9 3,067 6 6,170 15

Haryana 866 20 267 3 768 2 1,751 4

Karnataka 2,285 7 405 5 3,924 2 6,408 12

Kera la 2,597 17 1,304 10 4,172 15 7,911 25

Maharashtra 1,489 5 1,138 25 2,931 59 5,432 48

Punjab 4,012 15 3,921 33 770 9 4,114 11

Rajasthan 1,823 9 1,072 4 1,295 10 3,160 8

Tamil Nadu 2,051 8 2,501 9 12,826 66 6,122 0

Uttar Pradesh 960 8 155 5 342 4 1,409 5

West Bengal 805 1 510 0 6,456 1 5,920 6

I Total 28,292 110 18,860 169 50,222 242 74,168 168

Source: (5)
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

the vector to breed at high level and makes the environment 500 fold risk of DHF compared with primary infection. For

transmission conducive. The rural spread of the vector is the DENV-3/DENV-2 sequence the risk was 150-fold, and a

relatively recent occurrence associated with the DENV-4/DENV-2 sequence had a 50-fold risk of DHF. There

development of rural water supply schemes, improved is no time-limit to sensitization after a primary infection. The

transport systems, scarcity of water and lifestyle changes (4). 1997 Santiago de Cuba epidemic clearly demonstrated that

with the introduction of DENV-2, DHF had occurred 16-20
Dengue in the community (2)
years after the primary infection with DENV-1.

A number of factors that contribute to initiation and
High risk patients (2)
maintenance of an epidemic include: (i) the strain of the

virus, which may influence the magnitude and duration of The following host factors contribute to more severe

the viraemia in humans; (ii) the density, behaviour and disease and its complications :

vectorial capacity of the vector population; (iii) the
1. infants and elderly ;
susceptibility of the human population (both genetic factors
2. obesity;
and pre-existing immune profile); and (iv) the introduction
3. pregnancy;
of the virus into a receptive community.
4. peptic ulcer disease;

DF!DHF syndrome 5. women who are in menstruation or have abnormal

DF/DHF is characterized by the “iceberg” or pyramid bleeding;

p h e n o m e n o n . At the base of the pyramid, most of the cases 6. haemolytic disease such as G-6PD, thalassemia and

are symptomless, followed by DF,DHF and DSS. Clusters of other haemoglobinopathies;

cases have been reported in particular households or 7. congenital heart disease;

neighbourhoods due to the feeding behaviour of the vector. 8. chronic diseases such as diabetes mellitus, hypertension,

asthma, ischaemic heart disease, chronic renal failure,
Affected population
liver cirrhosis; and

The population affected varies from one outbreak to 9. patients on steroid or NSAID treatment.
another. Actual estimates can be made by obtaining clinical/
C l i n i c a l mainfestations
subclinical ratios during epidemics. In a well-defined

epidemic study in North Queensland, Australia, with primary · Dengue virus infection may be asymptomatic or may
infection, 20% to 50% of the population was found affected. cause undifferientiated febrile illness (viral syndrome),

dengue fever(DF), or dengue haemorrhagic fever (DHF)
Severity of the disease
including dengue shock syndrome (DSS) as shown in Fig.l

The serotype that produces the secondary infection and, in

particular, the serotype sequence are important to ascertain 1 . Undifferentiated fever

the severity of the disease. All the four serotypes are able to
Infants, children and adults who have been infected with
produce DHF cases. However, during sequential infections,
denuge virus, especially for the first time (i.e. primary
only 2% to 4% of individuals develop severe disease.
dengue infection), may develop a simple fever

Studies in Thailand have revealed that the DENV-1/ indistinguishable from other viral infection. Maculopapular

DENV-2 sequence of infection was associated with a rashes may accompany the fever or may appear during

Dengue virus infection

Asymptomatic Symptomatic

Undifferentiated Dengue fever Dengue haemorrhagic Expanded dengue syndrome/

fever (DF) fever (DHF) Isolated organopathy

(viral syndrome) (with plasma leakage) (unusual manifestation)

Without With unusual DHF DHF with shock

haemorrhage haemorrhage non-shock Dengue shock

syndrome (DSS)

FIG. 1

Manifestations of the dengue virus infection

S o u r c e : (2)
THE DENGUE SYNDROME

defervescence. Upper respiratory and gastrointestinal 1 . Febrile phase
symptoms are common.
Following an incubation period of four to six days, the

illness commonly begins abruptly with high fever
2 . C l a s s i c a l dengue fever
accompanied by facial flushing and headache. Anorexia,
All ages and both sexes are susceptible to dengue fever. vomiting, epigastric discomfort, tenderness at the right costal
Children usually have a milder disease than adults. The margin and generalized abdominal pain are common.
illness is characterized by an incubation period of 3 to 10 During the first few days the illness usually resembles
days (commonly 5-6 days). The onset is sudden, with chills classical OF, but maculopapular rash usually rubelliform
and high fever, intense headache, muscle and joint pains, type, is less common. It may appear early or late in the
which prevent all movement. Within 24 hours retroorbital course of the illness. Occasionally, the temperature may be
pain, particularly on eye movements or eye pressure and 40°C to 41 °C and febrile convulsions may occur particularly
photophobia develops. Other common symptoms include in infants (1).

extreme weakness, anorexia, constipation, altered taste
The major pathophysiologic changes that determine the
sensation, colicky pain and abdominal tenderness, dragging
severity of disease in DHF and differentiate it from OF are
pain in inguinal region, sore throat and general depression.
plasma leakage and abnormal haemostasis, as manifested
Fever is usually between 39°C and 40°C. Fever is typically
by a rising haematocrit value and moderate to marked
but not inevitably followed by a remission of a few hours to
thrombocytopenia. These two clinical laboratory changes
2 days (biphasic curve). The skin eruptions appear in 80 per
are distinctive and constant findings.
cent of cases during the remission or during second febrile

phase, which lasts for 1-2 days. The rash is accompanied by A positive tournicate test is the most common

similar but milder symptoms. The rash may be diffuse haemorrhagic phenomenon. The test is performed by

flushing, mottling or fleeting pin-point eruptions on the inflating a blood pressure cuff to a a mid point between

face, neck and chest during the first half of the febrile period systolic and diastolic pressure for 5 minutes. The test is

and a conspicuous rash, that may be maculopapular or considered positive when 10 or more petechiae per

scarlatiniform on 3rd or 4th day. It starts on the chest and 2 . 5 x 2 . 5 cm ( 1 inch square) are observed. In DHF, the test

trunk and may spread to the extremities and rarely to the usually gives a definite positive with 20 petechiae or more (4).

face. It may be accompanied by itching and hyperaesthesia.

The rash lasts for 2 hours to several days and may be
2. Critical phase (9)

followed by desquamation ( 1 ) . Fever lasts for about 5 days, Around the time of defervescence, when the temperature
rarely more than 7 days after which recovery is usually drops to 37 .5-38°C or less, and remains below this level,
complete although convalescence may be protracted (8). usually on days 3- 7 of illness, an increase in capillary
The case fatality is exceedingly low. permeability in parallel with increasing haematocrit levels

may occur. This marks the beginning of the critical phase.
3 . Dengue haemorrhagic fever
The period of clinically significant plasma leakage usually

Dengue haemorrhagic fever (DHF) is a severe form of lasts 24-48 hours.

dengue fever. The course of dengue illness can be divided
Progressive leukopenia followed by a rapid decrease in
into three phases-febrile phase, critical phase and recovery
platelet count usually precedes plasma leakage. At this point
phase, as shown in Fig. 2 (9).
patients without an increase in capillary permeability will

improve, while those with increased capillary permeability

Days of illness 1 2 3 4 5 6 7 8 9 1 0 may become worse as a result of lost plasma volume. The

degree of plasma leakage varies. Pleural effusion mostly on

right side and ascites may be clinically detectable depending
Temperature
on the degree of plasma leakage and the volume of fluid

therapy. Gall bladder oedema has been found to precede

plasma leakage. Hence chest X-ray and abdominal

ultrasound can be useful tools for diagnosis. The degree of
Dehydration Reabsorption
increase above the baseline haematocrit often reflects the
fluid overload
Potential severity of plasma leakage.
clinical issues
Shock occurs when a critical volume of plasma is lost
Organ impairment
through leakage. It is often preceded by warning signs of

abdominal pain or tenderness, persistent vomiting, clinical
Platelet
fluid accumulation, mucosa! bleeding, lethargy, restlessness,
Laboratory

changes liver enlargement more than 2 cm. and oliguria. The body

temperature may be subnormal when shock occurs. With

prolonged shock, the consequent organ hypoperfusion

lgM/lgG results in progressive organ impairment, metabolic acidosis

and disseminated intravascular coagulation. This in turn
Serology
leads to severe haemorrhage causing the haematocrit to
and virology
decrease in severe shock. Instead of the leukopenia usually

seen during this phase of dengue, the total white cell count
Course of L—“—-=’-‘————‘
may increase in patients with severe bleeding. In addition,
dengue illness : Febrile Critical Recovery phases
severe organ impairment such as severe hepatits,

encephalitis or myocarditis and/or severe bleeding may also
FIG.2
develop without obvious plasma leakage or shock.
The course of dengue illness

Source: (9) Those who improve after defervescence are said to have
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

non-severe dengue. Some patients progress to the critical combination with thrombocytopenia, hypoxia and acidosis,

phase of plasma leakage without defervescence and, in can lead to multiple organ failure and advanced

these patients, changes in the full blood count should be disseminated intravascular coagulation. Massive bleeding

used to guide the onset of the critical phase and plasma may occur without prolonged shock in instances when

leakage. Those who deteriorate will manifest with warning acetylsalicylic acid (aspirin), ibuprofen or corticosteriods

signs. This is called dengue with warning signs. Cases of have been taken.

dengue with warning signs will probably recover with early
. Unusual manifestations, including acute liver failure and
intravenous rehydration. Some cases will deteriorate to
encephalopathy, may be present, even in the absence of
severe dengue.
severe plasma leakage or shock. Cardiomyopathy and

encephalitis are also reported in a few dengue cases.
3. Recovery phase
However, most deaths from dengue occur in patients with
If the patient survives the 24-48 hour critical phase, a profound shock, particularly if the situation is complicated by
gradual reabsorption of extravascular compartment fluid fluid overload.
takes place in the following 48-72 hours. General well-being

improves, appetite returns, gastrointestinal symptoms abate, CRITERIA FOR CLINICAL DIAGNOSIS (2, 4)
haemodynamic status stabilizes and diuresis ensues. Some
A summary of clinical diagnosis of OF and DHF is as
patients may have a rash of “isles of white in the sea of red”.
follows:
Some may experience generalized pruritus. Bradycardia and

electrocardiographic changes are common during this stage.
Dengue fever
The haematocrit stabilizes or may be lower due to the

dilutional effect of reabsorbed fluid. White blood cell count Probable diagnosis

usually starts to rise soon after defervescence but the Acute febrile illness with two or more of the following;
recovery of platelet count is typically later than that of white
– headache,
blood cell count.
retro-orbital pain,
Respiratory distress from massive pleural effusion and
– myalgia,
ascites will occur at any time if excessive intravenous fluids
· arthralgia/bone pain,
have been administered. During the critical and/or recovery
– rash,
phases, excessive fluid therapy is associated with pulmonary

oedema or congestive heart failure. – haemorrhagic manifestations,
3
– leucopenia (wbc $ 5000 cells/mm ),

4. Severe dengue 3
– thrombocytopenia (platelet count < 150,000 cells/mm ),

Severe dengue is defined by one or more of the following : – rising haematocrit ( 5 – 1 0 % ) ;
(i) plasma leakage that may lead to shock (dengue shock)
and at least one of following :
and/or fluid accumulation, with or without respiratory

distress, and/or ( i i ) severe bleeding, and/or (iii) severe organ – supportive serology on single serum sample: titre z 1280

impairment. with haemagglutination inhibition test, comparable lgG

titre with enzyme-linked immunosorbent assay, or
As dengue vascular permeability progresses,
testing positive in lgM antibody test, and
hypovolaemia worsens and results in shock. It usually takes
– occurrence at the same location and time as
place around defervescence, usually on day 4 or 5 (range
confirmed cases of dengue fever.
days 3- 7) of illness, preceded by the warning signs. During

the initial stage of shock, the compensatory mechanism
Confirmed diagnosis
which maintains a normal systolic blood pressure also
Probable case with at least one of the following :
produces tachycardia and peripheral vasoconstriction with

reduced skin perfusion, resulting in cold extremities and – isolation of dengue virus from serum, CSF or autopsy
delayed capillary refill time. Uniquely, the diastolic pressure samples.
rises towards the systolic pressure and the pulse pressure – fourfold or greater increase in serum lgG (by
narrows as the peripheral vascular resistance increases. haemagglutination inhibition test) or increase in lgM
Patients in dengue shock often remain conscious and lucid. antibody specific to dengue virus.
The inexperienced physician may measure a normal systolic
– detection of dengue virus or antigen in tissue, serum or
pressure and misjudge the critical state of the patient.
cerebrospinal fluid by immunohistochemistry,
Finally, there is decompensation and both pressures
immunofluorescence or enzyme-linked immunosorbent
disappear abruptly. Prolonged hypotensive shock and
assay.
hypoxia may lead to multi-organ failure and an extremely
– detection of dengue virus genomic sequences by
difficult clinical course.
reverse transcription-polymerase chain reaction.

The patient is considered to have shock if the pulse

pressure is $20 mm Hg in children or he/she has signs of Dengue haemorrhagic fever
poor capillary perfusion (cold extremities, delayed capillary
All of following :
refill, or rapid pulse rate). In adults, the pulse pressure of
– acute onset of fever of two to seven days duration.
$20 mm Hg may indicate a more severe shock. Hypotension

is usually associated with prolonged shock which is often – haemorrhagic manifestations, shown by any of the

complicated by major bleeding. following; positive tourniquet test, petechiae,

ecchymoses or purpura, or bleeding from mucosa,
Patients with severe dengue may have coagulation
gastrointestinal tract, injection sites, or other
abnormalities, but these are usually not sufficient to cause
locations.
major bleeding. When major bleeding does occur, it is
3
– platelet count s, 1 0 0 , 0 0 0 cells/mm
almost always associated with profound shock since this, in
THE DENGUE SYNDROME

– objective evidence of plasma leakage due to increased which consists of RNA, can be detected by reverse

vascular permeability shown by any of the following : transcriptase polymerase chain reaction (RT -PCR) assay

– Rising haematocrit/haemoconcentration � 20% and real time RT-PCR. In recent years, a number of

from baseline or evidence of plasma leakage such RT -PCR assays have been reported for detecting dengue

as pleural effusion, ascites or hypoproteinaemia/ virus. They offer better specificity and sensitivity compared

albuminaemia. to virus isolation with a much more rapid turnaround time.

3. Immunological response and serological tests :
Dengue shock syndrome
Following tests are available for diagnosis of dengue
Criteria for dengue haemorrhagic: fever as above with infection :
signs of shock including :
a. Haemagglutination – inhibition assay (HIA);
– tachycardia, cool extremities, delayed capillary refill,
b. Complement Fixation ( C F ) ;
weak pulse, lethargy or’ restlessness, which may b e . a
c. Neutralization test (NT);
sign of reduced brain perfusion. ·
d. IgM capture enzyme-linked immunosorbent assay
– pulse pressure � 20 mmHg with increased diastolic
(MAC-ELISA);
pressure, e . g . 100/80 mmHg.

– hypotension by age, defined as systolic pressure <80 e. Indirect IgG- ELISA, and

mmHg for those aged <5 years, or 80 to 90 mmHg for f. IgM/lgG ratio

older children and adults.
4. Viral antigen detection : ELISA and dot blot assays

directed against the envelop/membrane (EM) antigens and
Laboratory diagnosis (2, 4)
nonstructural protein 1 (NS 1 ) can be detected in both
Rapid and accurate dengue diagnosis is of a paramount
patients with primary and secondary dengue infection upto
importance f o r : ( 1 ) clinical management; (2) epidemiological
6 days after the onset of the illness. Commercial kits for the
surveillance; (3) research; and (4) vaccine trials.
detection of NSl antigens are now available; however, these
Epidemiological surveillance requires early determination of
kits do not differentiate between the serotypes. Besides
dengue virus infection during the outbreak for urgent public
providing an early diagnostic marker for clinical
health action towards control, as well as at sentinel sites for
management, it may also facilitate the improvement of
detection of circulating serotypes/genotypes during the inter­
epidemiological surveys of dengue infection.
epidemic period for use in forecasting possible outbreak. The

following laboratory tests are available to diagnose dengue 5. Rapid diagnostic test (RDT) : A number of commercial

fever and DHF : rapid format serological test-kits for anti-dengue lgM and

IgG antibodies have become available in the past few years,
1 . Virus isolation : Isolation of dengue virus from clinical
some of these producing results within 15 minutes.
specimens is possible provided the specimen is taken during
Unfortunately, the accuracy of most of these tests is
the first six days of illness and processed without delay.
uncertain since they have not yet been properly validated.
Specimen that are suitable for virus isolation are – acute

phase serum, plasma or washed buffy coat from the 6. Analysis of haematological parameters : Standard

patient,autopsy tissue from fatal case (especially liver, spleen, haematological parameters such as platelet count and

lymph nodes and thymus), and mosquitoes collected from the haematocrit are important and are part of the diagnosis of

affected areas. dengue infection. They should be closely monitored.

2. Viral nucleic acid detection : Dengue viral genome, The diagnostic tests are summarized in Table 2 .

TABLE 2

Dengue diagnostics and sample characteristics

-. Clinical sample Diagnostic method Methodology . – Time to results

Mosquito or.mosquito cell One week or more
Viral isolation
culture inoculation

Virus Acute serum
RT-PCR and real time 1 or 2 days
detection (1-5 days of fever) Nucleic acid detection
RT-PCR
and its and

components necropsy tissues NS 1 Ag rapid tests Minutes

Antigen detection NSl Ag ELISA 1 day

lmmuno-histochernistry 2-5 days

Paired sera (acute serum from ELISA 1-2 days
lgM or lgG
1-5 days and second HIA
seroconversion
serum 15-21 days after)
Neutralization test Minimum 7 days
Serological

response
ELISA 1 or 2 days
lgM detection

(recent infection)
Rapid tests Minutes
Serum after day

5 of fever lgG ELISA 1 or 2 days
lgG detection
HIA

ELISA = enzyme-linked immunosorbent assay; HIA = haemagglutination inhibition assay; lgG = immunoglobulin G ;

lgM = immunoqlobulin M; NSl Ag = non-structural protein 1 antigen; RT-PCR = reverse transcriptase polymerase chain reaction.

Source : (10)
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

CLINICAL MANAGEMENT acid (aspirin), ibuprofen or other non-steroidal anti­

inflammatory agents (NSA!Ds) as these drugs may
Grading of the severity of dengue infection aggravate gastritis or bleeding. Acetylsalicylic acid

To decide where to treat the patient, it is important to (aspirin) may be associated with Reye’s Syndrome.

classify the severity of dengue infection. The presence of (3) Instruct the care-givers that the patient should be brought to

thrombocytopenia with concurrent haemoconcentration hospital immediately if any of the following occur; no clinical

differentiates grade I and grade II DHF from OF. Table 3 improvement, deterioration around the time of

shows gra�ing of dengue infection. defervescence, severe abdominal pain, persistent vomiting,

cold and clammy extremities, lethargy or irritability/
G u i d e l i n e s for treatment
restlessness, bleeding (e.g. black stools or coffee-ground

A full blood count of the patient should be done at the first vomiting), not passing urine for more than 4-6 hours.

visit. A haematocrit test in the early febrile phase establishes Patients who are sent home should be monitored daily by
the patient’s own baseline haematocrit. A rapidly decreasing health care providers for temperature pattern, volume of
platelet count in parallel with a rising haematocrit compared fluid intake and losses, urine output (volume and frequency),
to the baseline is suggestive of progress to the plasma warning signs, signs of plasma leakage and bleeding,
leakage/critical phase of the disease. In the absence of the haematocrit, and white blood cell and platelet counts.
patients baseline, age specific population haematocrit levels

could be used as a surrogate during the critical phase. 2 . Management of DHF (Febrile Phase) (4)

The management of febrile phase is similar to that of OF.
1 . Management of dengue fever
Paracetamol is recommended to keep the temperature below
These are patients who are able to tolerate adequate 39°C. Copious amount of fluid should be given orally, to the
volumes of oral fluids and pass urine at least once every six extent the patient tolerates, oral rehydration solution {ORS),
hours, and do not have any of the warning signs, such as those used for the treatment of diarrhoeal disesases
particularly when fever subsides. Those with stable and/or fruit juices are preferable to plain water. IV fluid may
haematocrit can be sent home after being advised to return be administered if the patient is vomiting persistently or
to the hospital immediately if they develop any of the refusing to feed.
warning signs, and to adhere to the following action plan :
Patients should be closely monitored for the initial signs
( 1 ) Encourage intake of oral rehydration solution (ORS), of shock. The critical period is during the transition from the
fruit juice and other fluids containing electrolytes and febrile to the afebrile stage and usually occurs after the third
sugar to replace losses from fever and vomiting. day of illness. Serial haematorcrit determinations are
Adequate oral fluid intake may be able to reduce the essential guide for treatment, since they reflect the degree of
number of hospitalizations. (Caution : fluids containing plasma leakage and need for intravenous administration of
sugar/glucose may exacerbate hyperglycaemia of fluids. Haematocrit should be determined daily from the
physiological stress from dengue and diabetes mellitus.) third day until the temperature has remained normal for one

(2) Give paracetamol for high fever if the patient is or two days. If haematocrit determination is not possible,

uncomfortable. The interval of paracetamol dosing haemoglobin determination may be carried out as an

should not be less than six hours. Tepid sponge if the alternative. The details of IV treatment when required for

patient still has high fever. Do not give acetylsalicylic patients are given in Fig. 3.

TABLE 3

WHO classification and grading of the severity of dengue infection

DF/DHF Grade . Symptoms/signs · Laboratory flndings

OF Fever with two or more of following – Leucopenia (WBC � 5000 cells/cu.mm),

– Headache – Thrombocytopenia (platelet count < 150,000 cells/cu.mm),

– Retro-orbital pain – Rising haernatocrit (5-10 per cent)

– Myalgia

– Arthralgia

– Rash

– Haemorrhagic manifestations

– No evidence of plasma leakage

Above criteria for DF and haemorrhagic manifestaion Thrombocytopenia : Platelet count < 100,000/cu.mm.
IDHF
plus positive tourniquet test, evidence of plasma leakage Haematorcit rise 20% or more ·

DHF II Above signs and symptoms plus some evidence of Thrombocytopenia platelet c o u n t < 100,000/cu.mm.

spontaneous bleeding in skin or other organs Haematocrit rise 20% or more

(black tarry stools, epistaxis, bleeding from gums, etc)

and abdominal pain

DHF Ill Above signs and symptoms plus circulating failure Thrombocytopenia : Platelet count < 100,000/cu.mm.

(weak rapid pulse, pulse pressure a 20 mm Hg or high Haematocrit rise more than 20%

diastolic pressure, hypotension with the presence ·of

cold clammy skin and restlessness)

DHF IV Signs as grade Ill plus profound shock with undetectable Thrombocytopenia : Platelet count < 100,000/cu.mm.

blood pressure or pulse Haemotocrit rise more than 20%
I

I DHF I l l and IV are Dengue Shock Syndrome

Source : (2, 4)
THE DENGUE SYNDROME

Haemorrhagic (bleeding) tendencies, Thrombocytopenia

Initiate IV therapy – 6 ml/kg/hr crystalloid solution for 1-2 hrs.

l
l
lmp+m,nt No improvement

IV therapy by crystalloid successively Increase IV – 10 ml/kg/h crystalloid – duration 2 hrs

reducing from 6 to 3 ml/kg/hr

l

Further improvement
Improvement No improvement

unstable vital signs

Discontinue IV

after 24 hrs Reduce IV to 6 ml/kg/hr

crystalloid with further

reduction to 3 ml/kg/hr
l
discontinue after 24-28 hrs Haematocrit

falls*

IV Colloid Dextran (40) Blood transfusion

1 0 ml/kg/hr duration 1 hr. 10 ml/kg/hr duration 1 hr

* Suspected internal haemorrhage

Improvement Haernatocrtt falls, pulse rate and
‘—–.i•I Improvement I�
blood pressure stable, urine output rises
r
No improvement Haematocrit or pulse rises, pulse pressure
IV therapy by crystalloid successively reducing
falls below 20 mmHg, Urine output falls
the flow from 10 to 6 and 6 to 3 ml/kg/hr
Unstable vital signs : Urine output falls, signs of shock discontinue after 24-48 hrs.

FIG.3

Volume replacement flow chart for patients with DHF Grades I & II

Source: (4)

3 . Management of D H F Grade I and II haematocrit is decreasing, fresh whole blood transfusion

10 ml/kg/hour should be given.
Any person who has dengue fever with

thrombocytopenia and haemoconcentration and presents However, in case of persistent shock when, after initial

with abdominal pain, black tarry stools, epistaxis, bleeding fluid replacement and resuscitation with plasma or plasma

from the gums and infection etc needs to be hospitalized. All expanders, the haematocrit continues to decline, internal

these patients should be observed for signs of shock. The bleeding should be suspected. It may be difficult to recognize

critical period for development of shock is transition from and estimate the degree of internal blood loss in the

febrile to abferile phase of illness, which usually occurs after presence of haemoconcentration. It is thus recommended to

third day of illness. A rise of haemoconcentration indicates give fresh whole blood in small volumes of 10 ml/kg/hour for

need for IV fluid therapy. If despite the treatment, the patient all patients in shock as a routine precaution. Oxygen should

develops fall in BP, decrease in urine output or other be given to all patients in shock. The detailed graphical

features of shock, the management for Grade III/IV DHF/ presentation of the treatment for patients with DHF Grades

DSS should be instituted. III and IV is given in Fig. 4.

Oral rehydration should be given along with antipyretics
I n d i c a t i o n s of red c e l l transfusion
like paracetamol, sponging, etc. as described above. The
1. Loss of blood ( overt blood) – IO per cent or more of total
detailed treatment for patients with DHF Grade I and II is
blood volume – preferably give whole blood or
given in Fig. 3.
components to be used.

4 . Management of DHF Grade I I I and IV 2. Refractory shock despite adequate fluid administration

and declining haematocrit.
Common signs of complication are observed during the
3. Replacement volume should be 10 ml/kg body weight at
afebrile phase of DHE Immediately after hospitalization, the
a time and coagulogram should be done.
haematocrit, platelet count and vital signs should be

examined to assess the patient’s condition and intravenous 4. If fluid overload is present packed cells are to be given.

fluid therapy should be started. The patient requires regular
I n d i c a t i o n s of platelet transfusion
and sustained monitoring. If the patient has already received

about 1000 ml of intravenous fluid, it should be changed to In general there is no need to give prophylactic platelet

colloidal solution preferably Dextran 40/haemaccele or if even at < 20,000/cu.mm.
•
, EPIDEMIOLOGY OF COMMUNICABLE DISEASES _

UNSTABLE VITAL SIGNS

Urine output falls, signs of shock

Immediate rapid volume replacement : initiate IV therapy

10-20 ml/kg/hr crystalloid solution for 1 hour

Improvement No Improvement

IV therapy by crystalloid Oxygen

successively reducing from 20 to 10,

10 to 6 and 6 to 3 l
l l l
Haematocrit Haematocrit falls rapidly
Further improvement
rises (due to haemorrhage)

Discontinue IV
IV colloid (dextran (40) or Blood transfusion
after 24 hrs
plasma 10 ml/kg/hr ( 1 0 ml/kg/hr)

as intravenous bolus

(repeat if necessary)

I �1 Improvement

l
..
IV therapy by crystalloid successively reducing

the flow from 10 to 6 and 6 to 3 ml/kg/hr.

Discontinue after 24-48 hrs.

Serial platelet and haematocrit determinations : drop in platelets and rise in haematrocrit are

essential for early dignosis of DHE

Cases of DHF should be observed every hour for vital signs and urinary output.

FIG. 4

Volume replacement flow chart for patients with DHF Grades III & IV

Source: (4)

1. Prophylactic platelet transfusion may be given at level of CONTROL MEASURES
< 10,000/cu.mm. .

1 . Mosquito control
2. Prolonged shock; with coagulopathy and abnormal

coagulogram. The vectors of DF and DHF ( e . g . , A aegypti} breed in and

around houses and, in principle can be controlled by individual
3. In case of systemic massive bleeding, platelet transfusion
and community action, using antiadult and antilarval
may be needed in addition to red cell transfusion.
measures. These measures are outlined in chapter 12.

Criteria for discharge of patients
2 . Vaccines
1. Absence of fever for atleast 24 hours without the use of
So far, there is no satisfactory vaccine and no immediate
anti-pyretic drugs.
prospect of preventing the disease by immunization.
2. Return of appetite.
3 . Other measures
3. Visible clinical improvement.
Isolation of the patient under bed-nets during the first few
4. Good urine output.
days; individual protection against mosquitoes.
5. Minimum of 2-3 days after recovery from shock.
The personal prophylactic measures are wearing of full

6. No respiratory distress from pleural effusion or ascites. sleeves shirts and full pants; use of mosquito repellent

creams, liquids, coils, mats etc.; use of bed-nets for sleeping
7. Platelet count > 50,000/cu.mm.
infants and young children during day time to prevent

D i s e a s e notification mosquito bite.

The environmental measurements are detection and
In dengue-endemic countries, cases of suspected,
elimination of mosquito breeding places, management of
probable and confirmed dengue should be notified as soon
roof tops, porticos and sunshades, proper covering of stored
as possible so that appropriate health measures can be
water, observation of weekly dry day.
initiated.
——-
MALARIA Ill
G l o b a l strategy for dengue prevention and affected. In 2 0 1 3 , 97 countries and territories had ongoing

control 2 0 1 2 – 2 0 2 0 ( 1 1 ) malaria transmission.

Dengue is a global threat that requires a global response The specific risk groups for malaria includes the following

population (1) :
involving all possible partners. The global strategy promotes

co-ordination and collaboration among multisectoral 1. young children in stable transmission areas who have
partners on integrated vector management approach and not yet developed protective immunity against the
sustained control measures at all levels. The goals are : most severe forms of the disease;

a. to reduce dengue mortality by at least 50 per cent by 2. non-immune pregnant women as malaria causes high

2020; rates of miscarriage and can lead to maternal death;

b. to reduce dengue morbidity by at least 25 per cent by 3. semi-immune pregnant women in areas of high

2020;and transmission. Malaria can result in miscarriage and

c. to estimate the true burden of the disease by 2015. low birth weight, especially during first and second

pregnancies;

References 4. semi-immune HIV-infected pregnant women in stable

1. WHO (1993), Monograph on Dengue/Dengue Haemorrhagic Fever, transmission areas, during all pregnancies. Women
Compiled by Prasert Thongchroen, Regional Publication, SEARO with malaria infection of the placenta also have a
No.22.
higher risk of passing HIV infection to their newborns;
2. WHO (2011), Comprehensive Guidelines for Prevention and Control
5. people with HIV/AIDS;
of Dengue and Dengue Haemorrhagic Fever, Revised and expanded

edition, Regional office of SEAR. 6. international travellers from non-endemic areas

3. Govt. of India (2012), Annual Report 2011-2012, DGHS, Ministry of because they lack immunity.
Health and Family Welfare, New Delhi.
7. immigrants and their children living in non-endemic
4. Govt. of India (2008), Guidelines for Clinical Management of Dengue
areas and returning to their home countries to visit
Fever, Dengue Haemorrhagic Fever and Dengue Shock Syndrome,
friends and relatives are similarly at risk because of
Ministry of Health and Family Welfare, New Delhi.
waning or absent immunity.
5. Govt. of India (2014), National Health Profile 2013, DGHS, Ministry

of Health and Family Welfare, New Delhi. · ·
Malaria affects mainly · poor, underserved and
6. WHO (2012), Weekly Epidemiological Record, No. 8, 24th Feb., 2012.
marginalized populations in remote rural areas which are
7. Jawetz, Melnick and Adelberg’s Medical Microbiology, 24th
characterized by inadequate control measures and limited
International Ed. (2007), A Lange Medical Publication.
access to health care – . Higher malaria prevalence has been
8. Internet, Govt. of India (2006), National Vector Borne Disease Control
reported among ethnic and tribal groups living in remote
Programme, Ministry of Health and Family Welfare, New Delhi.
forested and border areas, as well as among mobile and
9. WHO (2009), Dengue, Guidelines for Diagnosis, treatment,

Prevention and Control, New edition, 2009. migrant populations.

10. WHO (2012), Handbook for clinical management of dengue.
The childhood deaths result mainly from cerebral malaria
11. WHO (2012), Global Strategy for Dengue Prevention and Control,
and anaemia. Fatality rates of 10-30 per cent have been
2012-2020.
reported among children referred to hospital with severe

malaria. However, these rates are even higher in rural and
: I
remote areas where patients have restricted access to

adequate treatment. Malaria also contributes indirectly to

Malaria is a protozoa! disease caused by infection with illness and deaths from respiratory infections, diarrhoeal

parasites of the genus Plasmodium and transmitted to man disease and malnutrition. Deaths from malaria in countries

by certain species of infected female Anopheline mosquito. outside Sub-Saharan Africa occur principally in non­

A typical attack comprises three ·distinct stages : cold stage, immune people who become infected with P. falciparum.

hot stage and sweating stage. The clinical features of malaria Underreporting of malaria cases and deaths remain a
vary from mild to severe, and complicated, according to the major challenge. Drug-resistant parasites, poor treatment­
species of parasite present, the patient’s state of immunity, seeking behaviour and the presence of counterfeit
the intensity of the infection and also the presence of antimalarial drugs further hinder control efforts. Resistance
concomitant conditions such as malnutrition or other of P. [alciparum to the 4-aminoquinolines and sulfadoxine­
diseases. The febrile paroxysms occur with definite pyrimethamine is widespread in almost all countries of
intermittent periodicity repeating every third or fourth day SEAR, with varying levels of severity. Resistance to
depending upon the species of the parasite involved. mafloquine was reported from Myanmar and Thailand.

Quinine has reduced susceptibility in Thailand. With
Problem statement progress from mono-to-multidrug resistance, all malaria­

endemic countries that have falciparum malaria adopted
WORLD
the highly effective artemisinin – based combination

According to the latest estimates, there were about 198 therapy (ACT).

million (124-283 million) cases of malaria in the year 2013
The coverage of indoor residual spraying with insecticides
and an estimated 584,000 deaths (367,000-755,000).
(IRS) remains low (42 per cent). Insecticide-treated nets have
Malaria mortality rates have fallen by 47 per cent globally
been introduced in almost all countries to supplement IRS
since year 2000, and by 54 per cent in the WHO African
efforts, but the coverage remains extremely low.
Region. Most deaths occur among children living in Africa,

where a child dies every minute from malaria (lA). INDIA

Approximately half of the world’s population is at risk of Malaria continues to pose a major public health

malaria. Most malaria cases and deaths occur in sub­ threat in India, particularly due to Plasmodium

Saharan Africa. However, Asia, Latin America, and to a falciparum which is prone to complications. In India about

lesser extent the Middle East and parts of Europe are also 2 1 . 9 8 per cent population lives in malaria high transmission
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

(� 1 case/1000 population) areas and about 67 per cent in localities and mysorensis form is present in rural areas (it is

low transmission ( 0- 1 case/1000 population) areas (2). not a vector ); ( 3 ) An. fluviatilis is the main vector in hilly

About 92 per cent of malaria cases and 97 per cent of deaths areas, forests and forest fringes in many states, especiall y in

due to malaria is reported from North-eastern states, the east; (4) An. minimus is the vector in the foot hills of

Chhattisgarh, Jharkhand, Madhya Pradesh, Orissa, Andhra North-Eastern states; (5) An. dirus is an important forest

Pradesh, Maharashtra, Gujarat, Rajasthan, West Bengal and vector in the North-East; and ( 6) An. epiroticus is now

Karnataka. However, the other states are also vulnerable restricted to the Andaman and Nicobar Islands (5).

with local and focal outbreaks of malaria. Much of these

areas are remote and inaccessible, forest or forest fringed Prevalent major epidemiological types of

with operation difficulties and predominantly inhabited by malaria in I nd i a (6)

tribal population (3).
In the course of the stratification exercise, various problems

The countrywide malaria surveillance data for the period and constraints responsible for the slow progress of malaria

from 1995 to 2 0 1 3 is as shown in Table 1 . control have been identified. An analysis of these factors has

The API has been steadily declining in India from 3.29 in resulted in the identification of malaria priority areas.

1995 to 0.88 in 2 0 1 2 . When interpreting API, it is important TRIBAL MALARIA : The population of tribal areas are

to evaluate the level of surveillance activity indicated by the contributing about 50 per cent of P. falciparum cases of the

Annual Blood Examination Rate (ABER). At low levels of country (5). Infants, young children and pregnant women
surveillance, the Slide Positivity Rate (SPR) is a better
have been identified as malaria high risk groups followed by

indicator. The SPR has also shown a decline in the country
mobile tribal population engaged in forest-related activities.
from 3.51 in 1995 to 0.51 in 2013. The Pf cases have
Limited health infrastructure and lack of drugs at village
declined from 1 . 1 4 million in 1995 to 0.44 million cases in
level are the factors responsible for high morbidity and
2 0 1 3 . However Pf% has gradually increased from 38.8% in
mortality due to malaria.
1995 to nearly 66.9% in 2013, which may indicate
RURAL MALARIA : These include irrigated areas of arid
increasing resistance to chloroquine (4).
and semiarid plains. Malaria is of moderate to low
India is predominantly characterized by unstable malaria
endemicity. An. culicifacies is the main vector and P. vivax is
transmission. Transmission is seasonal with increased
predominant during lean period and P.falciparum during
intensity related to rains. Due to the low and unstable
periodic exacerbation. In these the health infrastructure is
transmission dynamics, most of the population has no or little
moderately developed.
immunity toward malaria. As a result, the majority of Indians
URBAN MALARIA : 15 major cities including 4
living in malarious areas are at risk of infection with all age
metropolitans account for nearly 80 per cent of malaria
groups affected. However, surveys have shown that in some
cases covered under urban malaria control scheme. The
foci, mainly in forested areas, transmission is intense and the
health infrastructure is well developed. In peri-urban areas
disease burden is to a large extent concentrated in children.

malaria situation is influenced by poor sanitary conditions
There are six primary vectors of malaria in India :
and low socio-economic groups living in unplanned
( 1 ) An. culicifacies is the main vector of rural and peri-urban
settlements prone to periodical epidemics.
areas and is widespread in peninsular India. It is found in a

variety of natural and man-made breeding sites. It is highly MALARIA IN PROJECT AREAS : Project areas are those

zoophilic. Species A is an established vector for P. Vivax and areas where construction and developmental activities are

P. falciparum, whereas species B i s completely refractory to taken up and temporary tropical aggregation of labourers

P. Vivax and partially refractory to P. falciparum. It has been takes place bringing in different strains of malaria parasite

demonstrated that species B, however, may play a role as a and non – immu n e population. T his results in disturbance in

vector of P. falciparum in areas where the cattle population is eco-system, prolific increase in vector breeding places and

very low or absent; ( 2) An. stephensi is responsible for increased man-mosquito contact favouring high malaria

malaria in urban and industrial areas. The type form is found tr ansmission. These pockets contribute a large num b er of

in urban areas; intermediate form in urban and semi-urban malaria cases which are highly disproportionate to the

TABLE 1

C ountr yw ide ma l aria surve i llance data ( 1995 – Apr i l 2 0 1 4 )

Deaths.due
SPR .. SFR
to’ malaria

1995 888,143. 2.93 1.14 38.84 3.29 3.51 1,151

2008 l,119,624 9.73 1.52 0.77 50.81 1.36 1.57 0.80 1,055

2009 1,150,113 10.33 1.56 0.84 53.72 1.36 1.51 0.81 1 , 1 44

2010 1,151,788 10.60 .1.60 0.83 52.12 1.37 1.41 0.74 1,023

2011 1,210,000 10.93 1.31 .0.66 50.30 1.10 1.20 0.61 754

2012 1,211,509 10.89 1.06 0.53 50.01 0.88 0.98 0.49 516

March 2013 23.40 0.8 0.44 66.93 0.51 0.34 379

j to April 2014

Pf – Plasmodium falciparum BSE – Blood Smear Examined

API – Annual Parasite Incidence SFR – Slide Falciparum Rate

SPR – Slide Positivity Rate

Source: (4)
MALARIA

relatively small population groups inhabitating the area. worldwide incidence of infection caused by a specific agent;

One or more major vectors are involved in malaria applies to a particular malaria parasite species. Intervention

transmission. Limited health facilities for prompttreatment is measures are no longer needed once eradication has been

invariably associated with chloroquine resistant malaria achieved.

parasite. Hence specific control strategy is required for such

areas. E p i d e m i o l o g i c a l determinants

BORDER MALARIA : These are the high malaria Agent factors
transmission belts along the international borders and state
(a)AGENT
borders. These areas have their own problems in regard to

malaria control because of mixing of population and poor Malaria in man is caused by four distinct species of the

administrative control. malaria parasite – P. vivax, P. falciparum, P. malariae and

P. ovale. Plasmodium vivax has the widest geographic
Some definitions (2)
distribution throughout the world. In India, about 50 per

Malaria control : reducing the malaria disease burden to a cent of the infections are reported to be due to P. falciparum

level at which it is no longer a public health problem. and 4-8 per cent due to mixed infection and rest due to

P. vivax. P. maloriae has a restricted distribution and is said
Malaria elimination : the interruption of local mosquito­
to be responsible for less than 1 per cent of the infections in
borne malaria transmission; reduction to ‘zero’ of the
India. The largest focus of P. malariae in India is reported to
incidence of infection caused by human malaria parasites in
be in Tumkur and Hassan districts in Karnataka. P. ovale is a
a defined geographical area as a result of deliberate efforts;
very rare parasite of man, mostly confined to tropical Africa.
continued measures to prevent re-establishment of
It has also been reported in Vietnam. The severity of malaria
transmission are required.
is related to the species of the parasite.
Certification of malaria elimination : can be granted by

WHO after it has been proven beyond reasonable doubt that Life history

the chain of local human malaria transmission by Anopheles
The malaria parasite undergoes 2 cycles of development
mosquitoes has been fully interrupted in an entire country
– the human cycle (asexual cycle) and the mosquito cycle
for at least 3 consecutive years.
(sexual cycle). Man is the intermediate host and mosquito

Malaria eradication : permanent reduction to ‘zero’ of the the definitive host (Fig. 1 ) .

EXOGENOUS PHASE (IN MOSQUITO) ENDOGENOUS PHASE (IN HUMAN)

Sexual cycle (sporogony) Asexual cycle (schizogony)

Sporozoites Sporozoites Exoerythrocytic
pass through body in saliva from mosquito multiplication in liver
cavity, injected into human host parenchymal cells
reach salivary glands

I SPOROGONY SCHIZOGONY
Oocyst grows (multiple

division stage: cyst bursts

to release sporozoites) l
/Mem,o;�,�

Mature schizont (E t d )
11
(Segmentes) n er re ce s

(Penetrates to outer layer

of stomach wall of Erythrocytic cycle
mosquito and encysts) CLINICAL MALARIA

Immature schizont Ring trophozoite

f
� /
Ookinete (motile zygote)

Mature trophozoite
GAMETOGENY

Human
Microgamete Microgametocyte
blood
Zygote …______ (fertilization) —–­ ( differentiation)
‘ � Macrogamete
enters
Macrogametocyte
mosquito

FIG.1

Lifecycle of the malaria parasite.

Source: (10)
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

(i) Asexual cycle: The asexual cycle begins when an 10-20 days depending upon favourable conditions of

infected mosquito bites a person and injects sporozoites. A atmospheric temperature and humidity. This period is also

considerable amount of new knowledge about the parasite’s referred to as the “extrinsic incubation period”.

life cycle has become available in recent years, concerning
(b) RESERVOIR OF INFECTION
almost all phases of the cycle (7). A brief description is as

follows – four phases are described in the human cycle: With the possible exception of chimpanzees in tropical

(a) HEPATIC PHASE: The sporozoites disappear within Africa, which may carry the infection with P. malariae, no

60 minutes from the peripheral circulation (8). Many of other animal reservoir of human plasmodia is known to exist

· them are destroyed by phagocytes, but some reach the liver (9). A human reservoir is one who harbours the sexual forms

cells. After 1-2 weeks of development (depending upon the (gametocytes) of the parasite. A patient can be a carrier of

species), they become hepatic schizonts, which eventually several plasmodial species at the same time. Children are

burst releasing a shower of merozoites. The number of more likely to be gametocyte carriers than adults. The child is

merozoites produced from a single sporozoite varies thus epidemiologically a better reservoir than the adult.

considerably with the infecting species. A single Certain conditions must be met before a person can serve as

P. falciparum sporozoite may form as many as 40,000 a reservoir: ( i ) the person must harbour both the sexes of the

merozoites, whereas sporozoites from other species of gametocyte in his blood. If the person harbours only male or

plasmodia produce only 2 , 0 0 0 to 15,000 merozoites (8). In female gametocytes, further development cannot take place

the case of P. falciparum, the intrahepatic schizonts rupture in the mosquito vector, ( i i ) the gametocytes must be mature;

almost simultaneously and there is no persistent tissue phase immature forms do not undergo further development. It may

(the so-called exo-erythrocytic phase). On the contrary, the take 2-4 days for the gametocytes to attain maturity after

intrahepatic schizonts of the other plasmodia do not burst all their appearance in the blood , ( iii) the gametocytes must be

at the same time. Some hepatic forms persist and remain viable, i.e., if the patient receives an antimalarial drug, the

dormant in the hepatocytes for considerable periods before gametocytes lose their viabili ty or infectivity to mosquitoes

they begin to grow and undergo pre-erythrocytic (iv) the gametocytes must be present in sufficient density to

schizogony, thus liberating merozoites into the blood stream infect mosquitoes. The number of gametocytes necessary to

causing relapses of these infections. P. vivax and P. ovale infect mosquitoes is not definitely known, but it is thought by

may continue to relapse for 2 to 3 years and P. malariae may some that there must be at least 12 per cubic mm of blood.

persist for 10 to 20 years or more. Once the parasites

enter the RBC, they do not reinvade the liver.
(c) PERIOD OF COMMUNICABILITY

(b) ERYTHROCYTIC PHASE: Many of the merozoites are Malaria is communicable as long as mature, viable

quickly destroyed, but a significant number attach to specific gametocytes exist in the circulating blood in sufficient

receptor sites on the RBC. The merozoites then penetrate densi ty to infect vector mosquitoes. In vivax infections,

the RBC and pass through the stages of trophozoite and gametocytes appear in blood 4-5 days after the appearance

schizont. The erythrocytic phase ends with the liberation of of the asexual parasites; in falciparum infections, they do

merozoites, which infect fresh red blood cells. The cycle is not appear until 10-12 days after the first appearance of

repeated over and over again until it is slowed down by the asexual parasites. Gametocytes are t h e . most numerous

immune response of the host (9). The duration of the during the early stages of the infection when their density

erythrocytic cycle is constant for each species of malaria may exceed 1 , 0 0 0 per cubic mm of blood. They also tend to

parasite- 48 hours for P. falciparum, P. vivax and P. ovale; occur in waves in peripheral blood.

and 72 hours for P. malariae. (c) GAMETOGENY: In all
RELAPSES: It is usual for vivax and ovale malaria to
species of malaria some erythrocytic forms do not divide but
relapse more than 3 years after the patient ‘ s first attack.
become male and female gametocytes. These are the sexual
Recurrences of falciparum malaria usually disappear within
forms of the parasite which are infective to mosquito.
1-2 years. P. malariae has a tendency to cause prolonged

(ii) Sexual cycle: The mosquito cycle (sporogony) begins low-level, asymptomatic parasitaemia (11). The infection is

when gametocytes are ingested by the vector mosquito known to persist for 40 years or more. It is probable that

when feeding on an infected person. The gametocytes persons harbo u ring such infections are at least occasionally

continue further development in the mosquito. The first infective to mosquitoes.

event to take place in the stomach of the mosquito is
It is now considered more likely that vivax and ovale
exflagellation of the male gametocyte; 4-8 thread-like
relapses are derived from original, sporozoite-induced, liver
filaments called “micro-gametes” are developed. The female
schizonts which have lain latent long before bursting. In
gametocyte undergoes a process of maturation and becomes
P. falciparum and P. malariae infections latent liver schizonts
a female gamete or “macrogamete”. By a process of
do not appear to occur. Relapses in these species, most
chemotaxis, microgametes are attracted towards the female
authorities maintain, are due to a chronic blood infection,
gamete, and one of which (microgamete) causes fertilization
i.e., erythrocytic schizogony persisting at a low level.
of the female gamete. The resulting zygote is at first a

motionless body, but within 18-24 hours, it becomes motile.
Host factors
This is known as Ookinete, which penetrates the stomach
The main variables of the human element that have an
wall of the mosquito and develops into an oocyst on the
influence on malaria epidemiolo gy include the following :
outer surface of the stomach. The oocyst grows rapidly and

develops within it numerous sporozoites. When mature, the (a) AGE : Malaria affects all ages. N ewborn infants have

oocyst bursts and liberates sporozoites into the body cavity considerable resistance to infection with P. falciparum. This

of mosquito. Many of the sporozoites migrate to the salivary has been attributed to the high concentration of foetal

glands of the mosquito, and the mosquito now becomes haemoglobin during the first few months of life, which

infective to man. The period of time required for the suppresses the developmen t of P. falciparum (12). ( b ) SE X:

development of the parasite from the gametocyte to Males are more frequently exposed to the risk of acquirin g

sporozoite stage in the body of the mosquito is about malaria than females because of the outdoor life they lead .
MALARIA •
———‘—–
Further, females in India are usually better clothed than (b) TEMPERATURE: Temperature affects the life cycle of the

males. (c) RA C E : Individuals with AS haemoglobin (sickle­ malaria parasite. The optimum temperature for the

cell trait) have a milder illness with falciparum infection than development of the malaria parasite in the insect vector is

do those with normal (AA) haemoglobin (8). Persons whose between 20 deg. to 30 deg.C (68 deg. to 86 deg.F). The

red blood cells are “Duffy negative” (a genetic trait) are parasite ceases to undergo development in the mosquito if

resistant to P. uiuax infection. (d) PREGNANCY: Pregnancy the mean temperature is below 16 deg.C (60.8 deg.F).

increases the risk of malaria in women. Malaria during Temperatures higher than 30 de g .C are lethal to the

pregnancy may cause intrauterine death of the foetus; it may parasite. (c ) H UMIDITY: The atmospheric humidi ty has a

also cause premature labour or abortion. Primigravid direct effect on the length of life of the mosquito, although it

women are at greatest risk (13). (e) SOCIO-ECONOMIC has no effect on the parasite. A relative humid i ty of 60 per

DEVELOPMENT Malaria has demonstrated the cent is considered necessary for mosquitoes to live the i r

relationship between health and socio-economic no r mal span of life. W hen the relative humidi ty is hi g h ,

development. It is generally accepted that malaria has mos q uitoes are more active and they feed more voraciously.

disappeared from most developed countries as a result of If the humidity is low, mosquitoes do not live lon g.

socio-economic development (13). (f) HOUSING: Housing ( d) RAINFALL : Rain in general provides opportunities for

plays an important role in the epidemiology of malaria. The the breeding of mosquitoes and may give rise to epidemi c s

ill-ventilated and ill-lighted houses provide ideal indoor of malaria. Rain increases the atmospheric humidity which is

resting places for mosquitoes. Malaria is acquired in most necessary for the survival of mos q uitoes. H owever, heavy

instances by mosquito-bites within the houses. The site, rain may have an adverse affect in flushing out the breeding

type of construction, nature of the walls, etc. influence the places. Paradoxically in some areas, ( e . g . , Sri Lanka) severe

selection of control measures (14). (g) POPULATION epidemi cs of malaria followed years of drought. It was

MOBILITY : People migrate for one reason or other from because, the lesser monsoon rains led to the formation of

one country to another or from one part of a country to small p ools of water in river beds, which served as active

another. Labourers connected with various engineering, breeding places for malaria vectors. The relationship

irrigation, agricultural and other projects and periodic b etween rainfall (total and its distri b ution) and mosquito

breeding is of fundamental importance ( 1 5 ) . (e) ALTITUDE:
migration of nomads and wandering tribes are outstanding
As a rule, Anophelines are not found at altitudes above
examples of internal migration. Some of them may import
2000-2500 metres, due to unfavourable climatic conditions.
malaria parasites in their blood and reintroduce malaria into
(f) MAN-MADE MALARIA: Burrow pits, garden pools,
areas where malaria has been controlled or eliminated.
irrigation channels and engineering pr ojects like
Imported malaria has become quite a public health problem
construction of hydroelectric dams, roads, bridges have led
in Europe, North America, and other temperate parts of the
to the breeding of mosquitoes and an increase in malaria.
world, owing to the rising tide of air travel, tourism and
Malaria consequent on such human undertakings is called
migration (10). (h) OCCUPATION Malaria is
” man – made malaria”.
predominantly a rural disease and is closely related to

agriculture practices. (i) HUMAN HABITS : Habits such as
Vector of malaria
sleeping out of doors, nomadism, refusal to accept spraying

of houses, replastering of walls after spraying and not using Out of about 45 species of anopheline mosquitoes in

measures of personal protection (e.g. bed nets) influence India , only a few are regarded as the vectors of p rimary

man-vector contact, and obviously the choice of control importance. These are: An. cuiicijacies, An. fluviatilis,

measures. (j) IMMUNITY: The epidemic of malaria is An. stephensi, An. m r rn m u s , An. philippinensis,

influenced by the immune status of the population. An. sundaicus, and An. maculatus. The vectors of major

Immunity to malaria in humans is acquired only after importance are An culicifacies in rural areas and

repeated exposure over several years. Thus in endemic An. siephensi in urban areas.

malarious areas a state of collective immunity becomes In the absence of a vaccine, vector control is the only
established slowly, so that infants, young children, migrants practical approach to malaria control. A k nowledge of
and travellers from non-endemic areas suffer most from the ano p heline biology is essential for understanding the
disease. Those, however, who survive to the adult age show epidemiology of malaria and its prevention . The main
less evidence of adverse effects to the attenuated infection. factors which determine the vectorial importance of
Infants born of immune mothers are generally protected mos q uitoes are: (a) DENSITY : To be an effective vector, a
during the first 3-5 months by maternal lgG antibody; species must be present in adequate density in or near
infants born of semi-immune mothers are only partially h u man habitations. A sudden increase in density of vectors ,

protected. Active immunity is species-specific, that is, may be a cause of epidemic outbreaks . . For each vector,
immunity against one strain does not protect against there is what is k nown as ” critical density ” below which
another. People living in endemic areas exposed continually effective transmission cannot be maintained in a community.
to malaria develop considerable degree of resistance to This level varies with different s p ecies . In the case of An.

clinical disease, but their partial immunity to malaria culicifacies a high density is re q uired for the propagation of
declines with time after they leave their endemic countries. malaria; in the case of An. fluviatilis which is very efficient

Semi-immune individuals may harbour malaria parasites vector, a much lower density would suffice. (b) LIFE SPAN:

without presenting any symptoms of disease. Both humoral The k ey factor in the transmission of malaria is the life span

and cellular factors play a role in this protection ( 1 ) . of the vector. The vector mosquito must live for at least

10 – 12 days after an infective blood meal to become
Environmental factors
infective. The strategy in malaria eradication is to shorten

India’s geographic position and climatic conditions had the life span of mosquitoes to less than 1 0 days by

been, for long, favourable to the transmission of malaria. insecticides. ( c) C HOICE OF HOST : Some m o squitoes

(a) S EA S O N : Malaria is a seasonal disease. In most parts of prefer human blood , some animal blood , and so m e show

India, the maximum prevalence is from July to November. great variation in their feeding habits. The percentage of
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

human blood feeds in the case of An. culicifacies, an C l i n i c a l features
important vector in India, has been found to vary from 2-80
The primary fever is marked by paroxysms whic h
per cent (8). In contrast, An. fluviatilis is a highly
correspond to the development of the parasites in the red
anthrophilic species. The anthrophilic species, i.e., those
blood cells. The peaks of the fever coincide with the release
that have a high preference for human blood are better
into the blood stream of successive broods of merozites.
vectors of malaria than zoophilic species. (d) RESTING
The typical attack comprises three distinct stages, i . e . , the
HABITS : After a blood meal, some mosquitoes rest indoors
cold stage, the hot stage and the sweating stage. These are
on the walls for quite sometime. This behaviour pattern is
followed by an afebrile period in which the patient feels
known as “endophily”. But there are some species which
greately relieved.
rest outdoors (exophily). A knowledge of the resting habits

(which must be under constant surveillance) is the basis for COLD STAGE : The onset is with lassitude , headache,

organizing rational anti-adult measures. In fact, the concept nausea and chilly sensation followed in an hour or so by

of malaria eradication is based on endophilism (indoor rigors. The temperature rises rapidly to 39-41 ° C. Headache

resting habits) of most malarial vectors. (e) BREEDING is often severe and commonly there is vomiting. In early part

HABITS: The breeding habits of mosquitoes vary of this stage, skin feels cold; later it b ecomes hot. Parasites

considerably. Some breed in moving water (An. fluviatilis), are usually demonstrable in the blood. The pulse is rapid

some in brackish water (An. sundaicus) and some in wells, and may be weak. This stage lasts for 1/4-1 hour.

cisterns, fountains and overhead tanks (An. stephensi). A
HOT STAGE : The patient feels b urning hot and casts off
knowledge of the breeding habits is required for conducting
his clothes. The skin is hot and dry to touch. Headache is
anti-larval operations. (f) TIME OF BITING : The majority
intense but nausea commonly diminishes. The p ul se is full
of Indian mosquitoes bite at night excepting the Aedes
and respiration rapid. This stage lasts for 2 to 6 hours.
mosquitoes. Anophiline mosquitoes have nocturnal feeding
SWEATING STAGE : Fever comes down with profuse
habits, between dusk and dawn. (g) VECTORIAL
sweating. The temperature drops rapidly to normal and skin
CAPACITY : The term vectorial capacity refers to the
is cool and moist. The pulse rate becomes slower, patient
combined effect of the density of the vector population, its
feels relieved and often falls asleep. This stage lasts for 2-4
susceptibility to infection, life span and probability of
hours.
feeding on man. It is distinct from physiological capacity to

transmit infection. (h) RESISTANCE TO INSECTICIDES : A The febrile paroxysms occur with definite intermittent

knowledge of the status of vector resistance to insecticides is periodicity repeating every third or fourth day depending

also necessary. On this depends the choice of insecticides to upon the species of the parasite involved. The classical 3

be used. When an insect vector is resistant to a given stages (cold, hot and sweating) may not always be observed

insecticide, alternative insecticides have to be used. due to maturation of generations of parasite at different

times. Periods of latency may last several weeks or months
Mode of t r a n s m i s s i o n
(8, 19). The disease has a tendency to relapse and is

(a) VECTOR TRANSMISSION: Malaria is transmitted by characterized by enlargement of the spleen and secondary

the bite of certain species of infected, female, anopheline anaemia. Febrile herpes is common in all malarial patients.

mosquitoes. A single infected vector, during her life time,
In patients with P. falciparum infection the primary fever
may infect several persons. The mosquito is not infective
in its first few days is usually irregular or even continuous
unless the sporozoites are present in its salivary glands.
and then the classical 48 hour periodici ty becomes
(b) DIRECT TRANSMISSION: Malaria may be induced
established or the fever may continue to be irregular and the
accidentally by hypodermic intramuscular and intravenous
hot and cold stages, so typical of other malarial infections
injections of blood or plasma, e.g., blood transfusion,
are less clearly separated from one another. In persons w ith

malaria in drug addicts (16, 1 7 ) . Blood transfusion poses a
poor immunity the paroxysms are associated with marked
problem because the parasites keep their infective activity
prostration. H eadache, nausea and vomiting are usually
for at least 14 days in blood bottles stored at – 4 deg.C (16).
more severe, and there is greater tendency towards the
Persons who have lived in an endemic area (including those
development of delirium, haemolytic jaundice and anaemia.
who have been taking antimalarials prophylactically) and
The mortality is much greater than in other forms of malaria.
anyone who has had malaria should not be accepted as
With P. vivax infection, symptoms are same but are
blood donor until 3 years afterwards (18). (c) CONGENITAL
usually milder and more regularly divided into “hot” and
MALARIA: Congenital infection of the newborn from an
“cold” stages than in P. falciparum infections.
infected mother may also occur, but it is comparatively rare.
P. ovale infections differ little from that of P. · vivax.

Incubation period However, they tend to be milder than P. vivax and cease

after a few paroxysms even if no treatment is given.
This is the length of time between the infective mosquito

bite and the first appearance of clinical signs of which fever Clinically, P. malariae attacks resemble those of P. vivax

is most common. This period is usually not less than 10 but the cycle is of 72 hours instead of 48 hours. The

days. tendency for long-term relapses to occur is marked.

The duration of the incubation period varies with the The complications of P. falciparum malaria are cerebral

species of the parasite, and in natural infections (in malaria, acute renal failure, liver damage, gastro-intestinal

mosquito-transmitted malaria) this is 12 (9-14) days for symptoms, dehydration, collapse, anaemia, blackwater fever

falciparum malaria, 14 (8-17) days for vivax malaria, _28 etc. The complications of P. vivax, P. ovale and P. malariae

(18-40) days for quartan malaria and 1 7 ( 1 6 – 1 8 ) days for infections are anaemia, splenomegaly, enlargement of liver,

ovale malaria. With some strains of P. vivax, the incubation herpes, renal complications etc.

period may be delayed for as long as 9 months; this may
Diagnosis
also occur with other species in persons who have been

taking suppressive antimalarial drugs (8). The diagnosis of malaria depends on demonstration of
MALARIA

the parasite in the blood. Suspicion of the diagnosis is population. Only the positive slides are included in the

aroused by epidemiological and clinical evidence. denominator (8). (e) INFANT PARASITE RA T E : It is defined

as the percentage of infants below the age of one year

1 . Microscopy showing malaria parasites in their blood films. It is regarded

as the most sensitive index of recent transmission of malaria
Two types of blood films are useful in searching for and
in a locality. If the infant parasite rate is zero for 3
identification of malaria parasite. The “thin film” and the
consecutive years in a locality, it is regarded as absence of
“thick f i l m ” . It is recommended that both types of film be
malaria transmission even though, the Anopheline vectors
prepared on a single microscope glass slide. The thick film is
responsible for previous transmission may remain.
more reliable in searching for parasite, as large volume of
(f) PROPORTIONAL CASE RATE : Since the morbidity rate
blood is examined under each microscope field. When
is difficult to determine, except in conditions when the
scanty, parasite may be found about 20 times more rapidly
diagnosis and reporting of each case is carried to perfection,
in thick slide than in thin slide. The thin slide is more
proportional case rate is used (8). It is defined as the
valuable for identifying the species of the parasite present. In
number of cases diagnosed as clinical malaria for every 100
. it they are seen more clearly.
patients attending the hospitals and dispensaries. This is a
The advantage of microscopy are : The sensitivity is high.
crude index because the cases are not related to their time/
It is possible to detect malarial parasite at low densities. It
space distribution.
also helps to quantify the parasite load; It is possible to

distinguish the various species of malaria parasite and their
ERADICATION ERA (current incidence levels)
different stages.
During the eradication era, the microscopic diagnosis of

malaria cases became the main method of diagnosis. The
2. Serological test
parameters used for the measurement of malaria were
The malarial fluorescent antibody test usually becomes
mostly parasitological in nature; the commonly used
positive two weeks or more after primary infection, by which
parameters were API, ABER, SPR and SFR. The same
time the infection may have been cured. A positive test is
parameters are being used at the present time. These
therefore, not necessarily an indication of current infection.
parameters are unlikely to reveal the true epidemiological
The test is of the greatest value in epidemiological studies
picture, unless the case detection machinery is fully
and in determining whether a person has had malaria in the
supervised and very efficient. The following parameters are
past (20).
in use at present :

3. Rapid diagnostic test (RDT) a. Annual parasite incidence (API)

b. Annual blood examination rate (ABER)
Rapid Diagnostic Tests are based on the detection of

circulating parasite antigens with a simple dipstick format. c. Annual falciparum incidence (AFI)

Several types of RDTs are available. Some of them can only d. Slide positivity rate (SPR)
detect P falciparum while others can detect other parasites
e. Slide falciparum rate (SFR).
also. The latter kits are expensive and temperature sensitive.

RDTs are produced by different companies, so there may be a. A n n u a l parasite incidence (AP!)
differences in the contents and in the manner in which the

test is done. The users manual should always b e · read API is given by the formula :

properly to avoid false negative results ( 2 1 ) .
Confirmed cases during one year
AP!= x 1000
Measurement of malaria Population under surveillance

API is a sophisticated measure of malaria incidence in a
PRE-ERADICATION ERA
community. It is based on intensive active and passive
In the pre-eradication era, the magnitude of the malaria
surveillance, and cases are confirmed by blood examination.
problem in a country used to be determined mostly from the
Areas with API � 2 per 1000 population per year have been
reports of the clinically diagnosed malaria cases. The
classified as high risk areas in India, and thereby eligible for
classical malariometric measures are spleen rate, average
vector control.
enlarged spleen, parasite rate etc. In a control programme,

the case detection machinery is weak. Therefore, the b. A n n u a l blood examination rate (ABER)
classical malariometric measures may provide the needed
ABER is given by the formula :
information, i . e . the trend of the disease.

Number of slides examined
(a) SPLEEN RATE : It is defined as the percentage of
ABER= x 100
children between 2 and 10 years of age showing Population

enlargement of spleen. Adults are excluded from spleen
ABER is an index of operational efficiency. The annual
surveys, because causes other than malaria frequently
parasite incidence (API) depends upon the annual blood
operate in causing splenic enlargement in them. The spleen
collection and examination rates. A sufficient number of
rate is widely used for measuring the endemicity of malaria
blood slides must be systematically obtained and examined
in a community. (b) AVERAGE ENLARGED SPLEEN: This
for malaria parasite to work out accurately annual parasite
is a further refinement of spleen rate, denoting the average
incidence ( A P I ) .
size of the enlarged spleen (22). It is a useful malariometric

index. (c) PARASITE RATE : It is defined as the percentage At present, about 100 million fever cases are screened

of children between the ages 2 and 10 years showing every year in India. The aim is to screen 10 per cent of the

malaria parasites in their blood films. (d) PARASITE population even though the disease transmission is expected

DENSITY INDEX : It indicates the average degree of to reduce. The surveillance system has not undergone any

parasitaemia in a sample of well-defined group of the change (5).
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

c. A n n Lia[ falciparum incidence (c) Epidemic preparedness and early response

Since the emergence of P. falciparum problem in India, (d) Supportive interventions

data are collected separately for total malaria cases and ( 1 ) Capacity building

P. falciparum cases. ( 2 ) Behavioural change communication

(3) lntersectoral collaboration
d. Others
(4) Monitoring and Evaluation
The slide positivity rate and slide falciparum rate are
(5) Operational research and applied field research.
useful parameters. They provide information on the trend of

malaria transmission. Early diagnosis and treatment of malaria aims at :

Slide positivity rate : slide positivity rate is the percentage (1) C omplete cure ;

of slides found positive for malarial parasite, irrespective of (2) Prevention o f progression of uncomplicated m alaria to

the type of species. severe disease ;

(3) P revention of deaths ;
Slide falciparum rate : It is the percentage of slides

positive for P. falciparum parasite. ( 4 ) Interruption of transmission ; and

(5) Minimizing risk of selection and spread of drug resistant
VECTOR INDICES . malaria parasite. .

A malaria survey is not complete unless it includes

investigations relating to the insect vector. Some of the G U I D E L I N E S FOR DIAGNOSIS AND
important vector indices are: (a) HUMAN BLOOD I N D E X : It TREATMENT OF MALARIA IN I N D I A – 2 0 1 3 (23)
is the proportion of freshly-fed female Anopheline

mosquitoes whose stomach contains human blood. It According to the revised drug policy 2013, there is no

indicates the degree of anthrophilism. (b) SPOROZOITE scope of presumptive treatment in malaria control. The

RATE : It is the percentage of female anophelines with recommended guidelines are as follows :

sporozoites in their salivary glands. (c) MOSQUITO

DENSITY : It is usually expressed as the number of mosquitoes Treatment of U n c o m p l i c a t e d Malaria

per man-hour-catch. (d) MAN-BITING RATE (Biting All fever cases diagnosed as malaria by microscopy or
density) : It is defined as the average incidence of anopheline ROT should promptly be given effective treatment.
bites per day per person. It is determined by standardized

vector catches on human bait (e) INOCULATION RATE: The TREATMENT OF P. VIVAX CASES .
man-biting rate multiplied by the infective sporozoite rate is
Positive P. uiuax cases should be treated with chloroquine
called the inoculation rate. All these rates are employed in the
in full therapeutic dose of 25 mg/kg divided over three days.
quantitative assessment of malaria and in building up a
Vivax malaria relapses due to the presence of hypnozoites in
composite epidemiological picture of malaria.
the liver. The relapse rate in vivax malaria in India is around

30%. or its prevention, primaquine may be given at a dose
F

APPROACHES AND STRATEGIES OF
of 0 .25 mg/kg daily for 14 days under supervision.
MALARIA CONTROL
Primaquine is contraindicated in G6 PD deficient patients,

infants and pregnant w omen. C aution should be exercised
As the concept of control replaces that of eradication in
before administering primaquine in areas k nown to have
many national programmes, a reordering of priorities in the
high prevalence of G 6 PD deficiency. Primaquine can lead to
selection of control methods must occur. These priorities and
haemolysis in G 6 PD deficiency. Patient should be advised to
approaches must be based on epidemiological
stop primaquine immediately if he develops symptoms li k e
considerations, adverse effects on health, economy, technical
dark coloured urine, yello w con j unctiva, bluish
feasibility, functional resources, human resources and
discolouration of lips , abdominal pain, nausea, vomiting etc.
community participation. Recently WHO stressed a number
and should report to the doctor immediately.
of points relevant to future strategy of malaria control. The

main emphasis is on the need to base it on an epidemiological
TREATMENT OF P. FALCIPARUM CASES
approach. These aspects are discussed below.

Artemisinin Combination Therapy (ACT) (Artesunate
APPROACHES TO MALARIA CONTROL
3 days + sulphadoxine – pyrimethamine 1 day) should be

Strategic Action Plan for malaria control in India, 2007- given to all confirmed P. falciparum cases found positive by

2012, and more recently 2012-2017 were developed by microscopy or ROT. This is to be accompanied by single

Directorate of National Vector Borne Disease Control dose of primaquine (0. 75 mg/kg body weight) on Day 2.

Programme.
However, considering the reports of resistance to SP drug

The strategies for prevention and control of malaria and in North Eastern states, the Technical Advisory Committee

its transmission are (5) : has reco m mended to use · the coformulated tablet of

Artemether ( 2 0 mg) + Lumefantrine ( 1 2 0 mg) as per age­
(a) Surveillance and case management
specific dose schedule for the treatment of Pf cases in North
( 1 ) Case detection (passive and active)
Eastern states. This drug is not recommended during the first
(2) Early diagnosis and complete treatment
tri m ester of pregnancy and for children w eighing < 5 k g.
(3) Sentinel surveillance.
Production and sale of A rtemisinin monoth e rapy has b e en

( b ) Integrated vector management banned in India, as it can lead to development of parasite

( 1 ) Indoor residual spray (IRS) resistance to the drug.

(2) Insecticide treated bed-nets (ITNs) and long lasting
TREATMENT OF MALARIA IN PREGNANCY
insecticidal nets( (LLINs)

(3) Antilarval measures including source reduction. ACT should be given for treatment o f · P. falciparum
MALARIA •
——–
malaria in second and third trimesters of pregnancy, while oral quinine with tetracycline/doxicycline. These instances

quinine is recommended in the first . trimester. P. vivax should be reported to concerned District Malaria/State

malaria can be treated with chloroquine. Primaquine is Malaria Officer/ROHFW for initiation of therapeutic efficacy

contraindicated in pregnant woman. studies.

TREATMENT OF MIXED INFECTIONS Diagnosis and treatment of malaria (23)

Mixed infections with P. falciparum should be treated as All fever cases diagnosed as malaria by either ROT or
falciparum malaria. microscopy should be promptly given effective treatment.

Resistance should be suspected if inspite of full treatment The medicines chosen will depend upon whether the patient

with no history of vomiting, diarrhoea, patient does not has vivax malaria or falciparum malaria. The flow charts in

respond within 72 hours, clinically and parasitologically. different settings for diagnosis and drug selection for the

Such cases not responding to ACT, should be treated with treatment of malaria are shown in Fig. 2, 3 and 4.

A. Where microscopy result is available within 24 hours

-. Suspected malaria case
I I

,J,.

Take slide arid send for microscopic examination
I I

,J,.
I I
Result?
I I

I

�- 1 Jr …
Positive for Positive for Positive for Negative

P. vivax P. [alciparum mixed infection
No anti-

Treat with: In North-Eastern states: Treat with In. North-Eastern states:Treatwith malarial

C Q 3 days+ age-specific ACT-AL for 3 days + age-specific ACT-AL for 3 days + . treatment

PQ 0.25 rrig PQ single dose on second day . . Primaquine 0 . 2 5 mg per kg body
Treat as per
per kg body wejght daily for 14 days.
In other stdtes: Treat with: ACT-SP·for clinical
weight
3 days + PQ single dose on second Iri other states: SP-ACT 3 days + diagnosis
daily for
day Primaquine 0.25 mg per kg body
14 days
.··
weight daily for 14 days .

ACT-AL – Artemisinin-based combination therapy – Artemether – Lumefantrine CQ – Chloroquine

ACT-SP – Artemisinin-based combination therapy (Artesunate + Sulfadoxine-Pyrimethamine) PQ – Primaquine

FIG. 2

B. Where microscopy result is not available within 24 hours and monovalent RDT is used

Suspected malaria case
I I

J,.
..1… ..1…

Where TfR 2: 1 %, and Pf%> 30% in any of last 3 years In other areas, if patient not at high-risk of Pf
I I

.L .L

Do ROT for detection of Wait for slide result. Give CQ 25 mg/kg over 3 days

malaria & prepare slide only if high suspicion of malaria
I I

..J.. . ..J..

J.. J.. J.. ..L

Positive for RDT negative: Wait for slide Positive for Positive for

P. falciparum result. Give CQ 25 mg/kg over P. vivax P. falciparum

3 days, if high suspicion of malaria
1n North-Eastern states: Treat with Give CQ if In North-Eastern states: Age-

age-specific ACT-AL for 3 days + not already specific ACT-AL for 3 days + PQ

PQ single dose on second day 1 given+ single dose on second day

PQ 0,25 mg/kg
In other states: Treat with ACT-SP If confirmed as Po, give CQ if not In other states: Treat with:
single dose
for 3 days -i- PQ single dose on already given PQ 0.25 mg/kg/ ACT-SP for 3 days + PQ single
for 14 days
second day day over 14 days dose on second day

TfR = Test falciparum rate

Note : If a patient has severe symptoms at any stage, then immediately refer to a nearest PHC or other health facility with indoor patient

management or a registered medical doctor.

FIG.3
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

C. Where microscopy result is not available within 24 hours and bivalent RDT is used

Suspected malaria case
I I

l
Do blood test with RDT
I I

l

-.r … … ….. …. …

Positive for Positive for Positive for Negative

P vivax P falciparum mixed infection
No anti-

Discard slide Discard slide Discard slide malarial

treatment
Treat with: In North-Eastern states: Treat with In North-Eastern states: Treat with

C Q 3 days age-specific ACT-AL for 3 days + PQ age-specific ACT-AL for 3 days + Primaquine

+ PQ 14 single dose on second day 0.25 mg per kg body weight daily for 14 days.

days
In other states; Treat with: ACT-SP for In other states: SP-ACT 3 days + Primaquine

3 days + PQ single dose on second 0.25- mg per kg body weight daily for 14 days.

day

Note: (a) If a patient has severe symptoms at any stage, then immediately refer to a nearest PHC or other health facility with indoor patient

management or a registered medical doctor.

(b) PQ is contra-indicated in pregnancy and in children under 1 year (Infant).

FIG. 4

Treatment of vivax malaria (23) Treatment of Jalciparum malaria (23)

Diagnosis of vivax malaria may be made by the used of Diagnosis of falciparum malaria may be made by the use

ROT (Bivalent) or microscopic examination of the blood of ROT (monovalent or bivalent) or microscopic
smear. On confirmation, following treatment is to be given : examination of the blood smear. It is imperative to start

the treatment for falciparum malaria immediately on
Drug schedule for treatment of P vivax malaria:
diagnosis. The treatment for falciparum malaria is as

1. Chloroquine: 25 mg/kg body weight divided over follows:

three days i . e .
In other states (other than North-Eastern states):
10 mg/kg on day 1 ,
1. Artemisinin based combination therapy (ACT-SP)*
10 mg/kg on day 2 and
Artesunate (AS), available as 50 mg tablets are given for
5 mg/kg on day 3 .
three days, and Sulfadoxine-Pyrimethamine (S-P)
2. Primaquine: 0.25 mg/kg body weight daily for 14 days.
tablets, containing 500 mg Sulfadoxine and 25 mg

Primaquine is contraindicated in infants, pregnant pyrimethamine are given for one day, as shown in the

women and individuals with G6PD deficiency. dosage chart below.

14 day regimen of Primaquine should be given under All tablets for a day should be taken together, swallowed

supervision. with water.

In addition, Primaquine (PQ large) tablets should be
Dosage chart for treatment of vivax malaria
given on the second day.

Day 1 Day2 Day3 Day4
Dose schedule for treatment of uncomplicated
to 14

Age CQ PQ CQ PQ CQ PQ PQ P falciparum cases:

(150 (2.5 (150 (2.5 (150 (2.5 ( 2 . 5 mg)
1. Artemisinin based combination therapy (ACT-SP) *
mg mg) mg mg) mg mg)

base) base) base) Artesunate 4 mg/kg body weight daily for 3 days, plus

Less than 1
1 2 0 1
1 2 0 % 0 0 Sulfadoxine (25 mg/kg body weight) – Pyrimethamine

1 yr ( 1 . 2 5 mg/kg body weight) on first day.

1-4 years 1 1 1 1 112 1 1
* ACT is not to be given in 1st trimester of pregnancy.
5-8 years 2 2 2 2 1 2 2
2. Primaquine * : 0. 75 mg/kg body weight on day 2.
9-14 years 3 4 3 4 l1h 4 4
With the introduction of different coloured blister packs
15 yrs 4 6 4 6 2 6 6
for different age groups, treatment by the field level staff
or more*
has been made easy. The colour code for different age
Pregnancy 4 0 4 0 2 0 0
groups for packing of tablet ACT +SP has been given as

Note : CQ 250 mg tablet is having 150 mg base follows:
MALARIA

Dosage chart for treatment of falciparum malaria Primaquine (PQ) prevents transmission of falciparum

with ACT-SP malaria to others by its ability to kill gametocytes. PQ tablets

should .be taken after a meal; not on an empty stomach.
Age group 1st day 2nd day 3rd day
Children less than the age of one year and pregnant women
(Years) AS SP AS PQ AS should not be given primaquine. As pregnant women having

falciparum malaria require different medicines, they should
0-1 * 1 1 1 Nil 1

Pink (25 mg) (250+ (25 mg) 25 (mg) be directed to go to the nearest PHC or hospital

blister 1 2 . 5 mg) immediately, without delay.

1-4 1 1 1 1 1

Yellow (50mg) (500+25 (50 mg) ( 7 . 5 mg (50mg) Treatment of mixed infections
blister mg each) base) (.P. vivax + .P. falciparum) cases (23)
5-8 1 1 1 2 1
All mixed infections should be treated with full course of
Green ( 1 0 0 mg) (750+37.5 ( 1 0 0 mg) ( 7 . 5 mg ( 1 0 0 mg)
ACT and Primaquine 0 . 2 5 mg per kg body weight daily for
blister mg each) base each)
14 days.
9-14 1 2 1 4 1

Red ( 1 5 0 mg) (500+25 ( 1 5 0 mg) ( 7 . 5 mg ( 1 5 0 mg) In North-Eastern states: Treat with: Age-specific ACT-AL
blister mg each) base each) for 3 days + Primaquine 0 . 2 5 mg per kg body weight daily
1 5 & above 1 2 1 6 1 for 14 days.
White (200 mg) (750+37.5 (200 mg) ( 7 . 5 mg (200 mg)
In other states: ACT-SP 3 days + Primaquine 0 . 2 5 mg per
blister mg each) base each)
kg body weight daily for 14 days.

* SP is not to be prescribed for children <5 months of age and

should be treated with alternate ACT Dosage chart for treatment of mixed

* ACT-AL is not to be prescribed for children weighing less than (vivax and falciparum) malaria with ACT-SP
5 kg.

Age Day 1 Day 2 Day3 Day

4-14

In North-Eastern states (NE states): AS SP PQ AS PQ AS PQ PQ

tablet tablet (2.5 tablet (2.5 tablet (2.5 (2.5
1. ACT-AL co-formulated tablet of Artemether (20 mg) –
(50 mg) mg) (50 mg) mg) (50 mg) mg) mg)
Lumefantrine ( 1 2 0 mg)

Less than ‘/2 ’12 0 2
‘1 0 ’12 0 0
(Not recommended during the first trimester of
1 year
pregnancy and for children weighing <5 kg)
1-4 years 1 1 1 1 1 1 1 1

Recommended regimen by weight and age group 5-8 years 2 1% 2 2 2 2 2 2

The packing size for different age groups 9-14 years 3 2 4 3 4 3 4 4

based on Kg body weight.
1 5 years 4 3 6 4 6 4 6 6

or more
Co-formulated 5-14 kg 15-24 kg 25-34 kg > 3 4 kg

tablet ACT-AL (>5 months ( > 3 to 8 ( > 9 to 14 ( > 1 4 years)

to < 3 years) years) years)
Treatment of .P. ovale and .P. malariae

Total dose of 20 mg/ 40 mg/ 60 mg/ 80 mg/
In India these species are very rarely found in few places.
ACT-AL 1 2 0 mg 240mg 360 mg 480 mg
P. ova/e should be treated as P. vivax and P. malariae should
twice daily twice daily twice daily twice daily

for 3 days for 3 days for 3 days for 3 days be treated as P. falciparum.

Pack size
General r e c o m m e n d a t i o n s for the management
No. of tablets 6 12 18 24 of u n c o m p l i c a t e d malaria
in the packing
1. Avoid starting treatment on an empty stomach. The first
Give 1 tablet 2 tablets 3 tablets 4 tablets
dose should be given under observation. Dose should be
twice daily twice daily twice daily twice daily

for 3 days for 3 days for 3 days for 3 days
repeated if vomiting occurs within 15 minutes by

opening a new blister pack (discard what remains of old
Colour of Yellow Green Red White

the pack pack). If the patient vomits the first dose again, it is

considered a severe case of malaria and refer the patient

immediately to the nearest Block PHC/CHC/Hospital.

2. Primaquine * : 0. 75 mg/kg body weight on day 2 Special precaution should be taken in case of a child

under-5 years of age, and in pregnant woman.
Treatment of uncomplicated P. falciparum cases in
2. Explain to the patient or caretaker that : (a) if the
pregnancy:
treatment is not completed as prescribed, the disease
1st trimester : Quinine salt 10 mg/kg 3 times daily for may manifest again with more serious features and more
7 days. difficult to treat; ( b ) to come back immediately, if there is

Quinine may induce hypoglycaemia; pregnant women no improvement after 24 hours, if the situation gets

should not start taking quinine on an empty stomach and worse or the fever comes back; and (c) that regular use

should eat regularly, while on quinine treatment. of a mosquito net (preferably insecticide treated net) is

the best way to prevent malaria.
2nd and 3rd trimester : Area-specific ACT as per dosage

schedule given above i.e. ACT-AL in North-Eastern states, 3. Patient should also be examined for concomitant

ACT-SP in other states. illness.
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

R e s i s t a n c e to anti-malarial drugs Treatment of severe malaria

Resistance can be defined as either the ability of a
CLINICAL FEATURES (23)
parasite strain to survive and/or multiply despite the

administration and absorption of a drug given in doses equal Severe manifestations can develop in P falciparum

to or higher than those usually recommended, but within the infection over a span of time as short as 12-24 hours and

limits of tolerance of the patient. may lead to death, if not treated promptly and adequately.

Severe malaria is characterized by one or more of the
Drug resistance is a complex phenomenon, where, by
following features:
genetic mutation, a parasite acquires the ability to resist,
(1) Impaired consciousness/coma
partly or fully, the effects of one or more anti-malarial drugs.

When the resistant parasites are exposed to the drug, they (2) Repeatd generalized convulsions

multiply selectively. If parasites are resistant to the drug
(3) Renal failure (Serum Creatinine > 3 mg/di)
being used, the patient may not respond to treatment. One
(4) Jaundice (Serum Bilirubin > 3 mg/di)
of the commonest reasons for the development of drug

resistance is that the parasites are exposed to insufficient (5) Severe anaemia (Hb < 5 g/dl)

amount of the drug due to low prescription dosage, lesser (6) Pulmonary oedema/acute respiratory distress
amount of drug dispensed, incomplete treatment taken by syndrome
the patient, drug vomited out or low absorption of drug due
(7) Hypoglycaemia (Plasma glucose <40 mg/di)
to any other reason e . g . , diarrhoea, poorly stored drug, poor
(8) Metabolic acidosis
quality drug when supplied or expiry date medicine. In such

cases, most of the sensitive parasites are killed by even these (9) Circulatory collapse/shock (Systolic BP<80 mm Hg,

small doses, but resistant parasites survive, multiply and < 50 mm Hg in children)

spread to other people by mosquitoes. The new patient then
(10) Abnormal bleeding and disseminated intravascular
gets infection from the resistant malaria parasites and does
coagulation.
not respond to the drug at all, or responds only partly.
(11) Haemoglobinuria
Meanwhile, the earlier patient may appear cured because

most of the parasites were killed by the drug, and the (12) Hyperthermia (Temperature > 1 0 6 ° F or 42°C)

symptoms abated. (13) Hyperparasitaemia ( <5% parasitized RBCs in low

It should be kept in mind that the patient might have had endemic and > 1 0 % in hyperendemic areas)

a fresh reinfection, or in the case of vivax malaria, there
Foetal and maternal complications are more common in
might have been a relapse of malaria (23).
pregnancy with severe malaria; therefore, they need prompt

attention.
Treatment failure (24)

Microscopic evidence may be negative for asexual
After treatment patient is considered cured if he/she does
parasites in patients with severe infections due to
not have fever or parasitaemia till day 28th. Some patients
sequestration and partial treatment. Efforts should be made
may not respond to treatment which may be due to drug
to confirm these cases by RDT or repeat microscopy.
resistance or treatment failure, specially in falciparum
However, if the symptoms clearly point to severe malaria
malaria. If patient does not respond and presents with
and there is no alternative explanation, such a case should
following, he/she should be given alternative treatment.
be treated accordingly.
Early treatment failure (ETF) : Development of danger
Criteria for immediate referral are as follows:
signs or severe malaria on Day 1 , 2 or 3 , in the presence of
(a) Persistence of fever after 24 hours of initial treatment;
parasitaemia; parasitaemia on Day 2 higher than on Day 0,
(b) Continuous vomiting and inability to retain oral drug;
irrespective of axillary temperature; parasitaemia on Day 3
(c) Headache continues to increase; ( d ) Severe dehydration
with axillary temperature >37.5°C; and parasitaemia on
(dry, parched skin, sunken eyes etc.); (e) Too weak to
Day 3 , > 25% of count on Day 0.
walk in the abscence of any other obvious reason;

Late clinical failure (LCF) : Development of danger signs (f) Change in sensorium e . g . confusion, drowsiness, blurring

or severe malaria in the presence of parasitaemia on any of vision, photophobia, disorientation; (g) Convulsion or

day between Day 4 and Day 28 in patients who did not muscle twitchings; (h) Bleeding and clotting disorder;

previously meet any of the criteria of early treatment failure; (i) Suspicion of severe anaemia; (j) Jaundice; and

and presence of parasitaemia on any day between Day 4 (k) Hypothermia (23).

and Day 28 with axillary temperature >37.5°C in patients
Treatment of severe malaria cases (23)
who did not previously meet any of the criteria of early

treatment failure. Severe malaria is an emergency and treatment should be

given as per severity and associated complications which
Late parasitological failure (LPF) Presence of
can be best decided by the treating physicians. Before
parasitaemia on any day between Day 7 and Day 28 with
admitting or referring patients, the attending doctor or
axillary temperature < 37 .5 °C in patients who did not
health worker, whoever is able to do it, should do RDT and
previously meet any of the criteria of early treatment failure
take blood smear, give a parenteral dose of artemisinin
or late clinical failure.
derivative or quinine in suspected cerebral malaria cases

Such cases of falciparum malaria should be given and send case sheet, details of treatment history and blood

alternative ACT or quinine with Doxycycline. Doxycycline is slide with patient. Parenteral artemisinin derivatives or

contraindicated in pregnancy, lactation and in children upto quinine should be used irrespective of chloroquine

8 years. Treatment failure with chloroquine in P vivax resistance status of the area with one of the following

malaria is rare in India. options:
MALARIA

Chemotherapy of severe and complicated malaria

Initial parenteral treatment for at least 48 hours: Follow-up treatment, when patient can take oral·

Choose one of following four options medication following parenteral treatment

Q u i n i n e : 20 mg quinine salt/kg body weight on admission Q u i n i n e 10 mg/kg three times a day with: doxycycline

(IV infusion or divided IM injection) followed by maintenance 100 mg once a day OR clindamycin in pregnant

dose of 10 mg/kg 8 hourly; infusion rate should not exceed women and children under 8 years of age.

5 mg/kg per hour. Loading dose of 20 mg/kg should not – to complete 7 days of treatment.

be given, if the patient has already received q u i n i n e .

Artesunate: 2 . 4 mg/kg IV or IM given on admission Full oral course of area-specific ACT:

(time=D), then at 12 h a n d 24 h, then once a day. In North-Eastern states: Age-specific ACT-AL for

3 days + PQ single dose on second day

OR

Artemether: 3 . 2 mg/kg bw IM given on admission In other states: Treat with: ACT-SP for 3 days +

then 1 . 6 mg/kg per day. PQ single dose on second day

OR

Arteether: 150 mg daily IM for 3 days in adults only

(not recommended for children).

Note : The parenteral treatment in severe malaria cases should be given for minimum of 24 hours once started (irrespective

of the patient’s ability to tolerate oral medication earlier than 24 h o u r s ) .

After parenteral artemisinin therapy, patients will receive reports of teratogenicity in experimental animals, most

a full course of area-specific oral ACT for 3 days. Those authorities accept that pyrimethamine can safely be taken

patients who received parenteral Quinine therapy should alone during pregnancy (25). The teratogenic effect of

receive oral Quinine 10 mg/kg body weight three times a day pyrimethamine in man is not proved. In regard to

for 7 days (including the days when parenteral Quinine was primaquine, although in recommended doses, no serious

administered) plus Doxycycline 3 mg/kg body weight once a toxic manifestations have been encountered so far in India.

day, or Clindamycin 10 mg/kg body weight 12-hourly for 7 It is useful to bear in mind the likely toxic symptoms, which

days (Doxycycline is contraindicated in pregnant women may be of three types : (a) Plasmocid types : this is a rare

and children under 8 years of age) or area-specific ACT as toxic manifestation involving the CNS, (b) Gastrointestinal :

described. cramps, nausea and vomiting, (c} Cardiovascular : This is

probably the most serious toxic manifestation which is to be
Note:
carefully observed during the administration of the drug.
Pregnant women with severe malaria in any trimester
Even the first dose may bring about the warning sign of
can be treated with artemisinin derivatives, w h i c h , in
cyanosis. The surveillance worker/MPW must carefully check
contrast to qumme, do not risk aggravating
for all possible toxic symptoms before he administers the
hypoglycaemia.
daily dose of p r i m a q u i n e . In the case of appearance of any
The parenteral treatment should be given for of the toxic symptoms . discussed above, primaquine
minimum of 24 hours. treatment should be stopped immediately (26).

Once the patient can take oral therapy; give:
Chemoprophylaxis
Quinine 10 mg/kg three times a day with doxycycline

100 mg once a day or clindamycin in pregnant Chemoprophylaxis against malaria has, with the

women and children under 8 years of age, to development of drug resistance, become unreliable. Experts

complete 7 days of treatment, in patients started on disagree on whether well-conducted prophylaxis gives an

parenteral q u i n i n e . additional benefit if effective treatment is readily available.

Full course of ACT to patients started on artemisinin However, experts feel that it can play a useful role in

derivatives. reducing the risk of fatal disease ( 2 7 ) .

Use of mefloquine should be avoided in cerebral Chemoprophylaxis is recommended for travellers from

malaria due to neuropsychiatric complications non-endemic areas and, as a short term measure for
associated with it. soldiers, police and labour forces serving in highly endemic

areas. Chemoprophylaxis should be complemented by
Some don’ts in severe malaria case management
personal protection where feasible and by other methods of

Do not use corticosteroids, do not give intravenous vector control (27).

mannitol, do not use heparin as anticoagulant, do not
The recommendations for short-term chemoprophylaxis
administer adrenaline or do not overhydrate.
(less than 6 weeks) are as follows (27) :

( 1 ) Dosing schedules for the children should be based on
Toxic hazards of drugs
body weight.
Chloroquine has few side-effects. Nausea, vomiting,
( 2 ) Antimalarials that have to be taken daily (e.g.
blurring of vision and headaches may occur, but they are
Doxycycline) should be started the day before arrival in
mild and transient. Cases of retinal damage have been
the risk area.
reported but only in persons exposed to large cumulative

doses over many years. It is important to remember that ( 3 ) Weekly chloroquine should be started 1 week before

chloroquine should not be given on empty stomach. Despite arrival.
EPIDEMIOLOGY OF COMMUNICABLE DISEASES
•
——
(4) Weekly mefloquine should preferably be started 2-3 TABLE 2

weeks before departure, to achieve higher pre-travel Drug regimens for prophylaxis of malaria

blood level and to allow side-effects to be detected before

travel so that possible alternative can be considered.

(5) All prophylactic drugs should be taken with unfailing

regularity for the duration of the stay in the malaria risk

area, and should be continued for 4 weeks after the last
Chloroquine” ··Arale� : . 100 or
· 300 mg (base) = 3
possible exposure to infection, since parasites may still
•. Avlochlor · . 150mg ..tabletsdlOOmg .:
emerge from the liver during this period.
-‘, > Nivaquine . (base) ·. or 2 tablets. of

The recommendations for the long-term .; .Resochin . 1 5 0 m g oncea

chemoprophylaxis (more than 6 weeks) are as follows: ;: week, oh. the same

•.· day each week
( 1 ) The risk of serious side-effects associated with long-term
OR
prohylactic use of chloroquine and proguanil is low.
_ . •. lOOmg (base) = 1
However, anyone who has taken 300 mg of chloroquine
· ··• tabletof 100 mg
weekly for over five years and requires further daily for six days

prophylaxis should be screened twice-yearly for early ‘: perweek

retinal changes. If daily dose of 100 mg chloroquine have
Proguanil” ·. Paludrine 100 !119 200 ing == 2 tablets
been taken, screening should start after three years (27).
once a day .
. .
(2) Data indicate no increased risk of serious side-effects
Mefloquine” · Larlarn Eloquin 250 mg 250 mg c= 1 tablet
with long-term use of mefloquine if the drug is tolerated
•… Mephaquin •i onceaweek,
. .on:

in the short-term, as mefloquine does not accumulate .• the same.day . .

during long-term intake. each week

(3) Available data on long-term chemoprophylaxis with Doxycycline” Vibramycin 100 mg · 100 m g = l capsule

doxycycline is limited. once a day

a. Also available as suspension.
Mefloquine is contraindicated in cases with history of
b. Recommended only in association with chloroquine.
convulsions, neuropsychiatric problems and cardiac
c. The use of the higher treatment dose regimen is recommended
conditions.
for infections acquired in areas on the Thailand/Cambodia
and Thailand I Myanmar borders only.
Chemoprophylaxis is still desirable for pregnant women
d. There is relatively little experience with this drug, and
living in areas where transmission is very intense and leads to
knowledge of its efficacy and toxicity is limited.
parasitaemias, causing low birth weight and anaemia, or to a

high risk of life-threatening malaria attacks. However, the Source : (27)

choice of safe drugs is becoming increasingly narrow, and it
1 . STRATIFICATION OF THE PROBLEM
may be necessary to replace chemoprophylaxis by prompt

treatment of clinical episodes or periodic treatments during Malaria is a complex disease, and its distribution and
pregnancy. While the choice of strategy should be guided by intensity vary from place to place. Stratification of the
the national malaria control policy, its implementation problem has become an essential feature for the planning
should normally be part of antenatal care (28). and development of a sound control strategy to maximize

the utilization of available resources. It can also provide
The recommended regimens for chemoprophylaxis are as
guidelines as to which strategy could be most suited and
given in Table 2 .
economical under the existing conditions. For details please

refer to page 416 chapter 7 .
ACTIVE INTERVENTION MEASURES

Neither chemotherapy nor chemoprophylaxis will be able 2 . VECTOR CONTROL STRATEGIES

to reduce significantly the malaria prevalence or
Vector control is still one of the primary weapons to
transmission. It can be obtained only when proper anti­
control malaria in endemic areas. The methods used are as
mosquito measures are introduced.
shown in Table 3.

TABLE 3

Malaria vector control measures

0

Reduction of h uman-mosquito Insetticide-treated nets, repellents, Insecticide-treated nets

contact · ,.Pf<!tectivedothini;i, screening of houses zooprophylaxis

I D�str�ction of ad�lt . . “‘ · .· Insecticide-treated nets, indoor residual spraying,

space spraying, ultra low-volume sprays
I

I z�:::·�;..,o,�·”;,1�;; · ‘ ·.• t>elao.;; “;;.”;,�,io; es Larviciding ofwater surfaces; intermittent irrigation,

sluicing, biological control
I

I Source}:ductlwf_’;. .: . ·–· . . · ‘·s��l!0;cile d��iilag� . . . Environmental sanitation, water management, drainage I

Social �-a_ rt-.ic1.·;�ti�n . ·.· . . ·- Motiv at on i for pe r
so nal and Health education,· community participation

_ fam ily p rotection
I

Source : (29)
(a) Anti-adult measures interventions. Vector resistance to insecticides has

necessitated the use of more expensive pyrethroid, thereby
{i) Residual spraying : The discovery of DDT in 1940s
limiting the coverage. Malaria control added impetus as
and followed by other insecticides revolutionized malaria
Roll Back Malaria initiative was launched by WHO,
control. The spraying of the indoor surfaces of houses with
UNICEF, UNDP and the World Bank in 1998.
residual insecticides (e.g., DDT, malathion, fenitrothion) is

still the most effective measure to kill the adult mosquito. It

has been observed that discontinuation of spraying has very
THE GLOBAL POLICY FOR DIAGNOSIS AND

often led to the resurgence of malaria. This implies that TREATMENT OF MALARIA, INCLUDING

spraying once applied may need to be continued for an PREVENTIVE TREATMENT (33)

indefinite period. If indoor spraying is to have any effect,
The government of every country affected by malaria has
then exhaustive coverage is needed. Indoor house spraying
a national malaria control policy covering prevention and
reduces the longevity of the vector.
case-management.
Malathion and fenitrothion are organophosphate
The objectives of an antimalarial treatment policy are to :
insecticides which are being used with increasing frequency

for malaria control following the development of vector ensure rapid cure of the infection; reduce morbidity and

mortality, including malaria-related anaemia; prevent the
resistance to DDT (30).
progression of uncomplicated malaria into severe and
{ii) Space application : This is a major anti-epidemic
potentially fatal disease; reduce the impact of malaria
measure in mosquito-borne diseases. It involves the
infection on the fetus during pregnancy; reduce the reservoir
application of pesticides in the form of fog or mist using
of infection; prevent the emergence and spread of drug
special equipment. The ultra-low-volume method of
resistance; and prevent malaria in travellers.
pesticide dispersion by air or by ground equipment has
The launch of Roll Back Back Malaria (RBM) in 1998, the
proved to be effective and economical. Outdoor space
United Nations Millenium Declaration in 2000, the Abuja
sprays reduce vector population quickly.
Declaration by African Heads of State in 2000 (part of the
(iii) Individual protection : Man-vector contact can be
African Summit on Roll Back Malaria), the World Health
reduced by other preventive measures such as the use of
Assembly in 2005, and the RBM global strategic plan 2005-
repellents, protective clothing, bed-nets· (preferably
2015 have all contributed to the establishment of goals,
impregnated with safe, long-acting repellent insecticides),
indicators and targets for malaria control.
mosquito coils, screening of houses etc. The methods of
With the publication in 2005 of the Roll Back Malaria
personal protection are of great value when properly
global strategic plan for 2005-2015, WHO and RBM set
employed. However, they have rarely been used on a large
targets to be achieved by the year 2 0 1 0 and 2 0 1 5 . The goals
scale because of cost.
established by World Health Assembly and the Roll Back

(b) Anti-larval measures Malaria partnership is to reduce the number of malaria cases

and deaths recorded in 2000 by 50 per cent or more by the
(i) Larvicides : During the first half of the 20th century,
end of 2010 and by 75 per cent or more by 2015. In
anti-larval measures such as oiling the collections of standing
September 2008, RBM launched the Global Malaria Action
water or dusting them with paris green effectively controlled
Plan that defines the steps required to accelerate
malaria (but the measures were eclipsed at the end of World
achievement of the partnership’s 2 0 1 0 and 2 0 1 5 targets for
War I I ) . With the increase in insecticide resistance, the older
malaria control and elimination (34).
methods of mosquito control have now become promising.

Some modern larvicides such as temephos which confer long Malaria v a c c i n e s
effect with low toxicity are more widely used. However
Vaccination against malaria is a burning issue today.
larviciding must be repeated at frequent intervals and for this
Over the past decades, there has been significant progress in
reason it is a comparatively costly operation.
malaria vaccine development, yet many valid candidate
{ii) Source reduction : Techniques to reduce mosquito
vaccines have been slow to enter clinical trial and an
breeding sites (often called source reduction) which include
effective vaccine is thought to be still 10 years away. Several
drainage or filling, deepening or flushing, management of
vaccine candidates are now being tested in Africa, Asia and
water level, changing the salt content of water and
the United States.
intermittent irrigation are among the classical methods of

malaria control to which attention is being paid again (31). References

Whenever practicable, measures for the improvement of the 1. WHO ( 2 0 1 4 ) , Fact Sheet Malaria, No. 94, March 2 0 1 4 .
environment by the permanent reduction of sources should lA. WHO ( 2 0 1 4 ) , Fact Sheet on World Malaria Report 2014, December

be instituted. 2014.

2. WHO ( 2 0 1 3 ) , World Malaria Report 2013.
{iii) Integrated control : In order to reduce too much
3. Govt. of India ( 2 0 1 3 ) , A n n u a l Report 2012-2013, Ministry of Health
dependance on residual insecticides, increasing emphasis is
and Family Welfare, New Delhi.
being put on “integrated” vector control methodology which
4. Govt. of India ( 2 0 1 4 ) , Malaria, Magnitude of the problem NVBDCP,
includes bioenvironmental and personal protection measure DGHS, Ministry of Health and Family Welfare, New Delhi.

(32). This approach is important because there is no single 5. Govt. of India ( 2 0 1 4 ) , Strategic Action Plan for Malaria Control in India

and simple method that would ensure control of transmission. 2012-2017, DGHS, Ministry of Health and Family Welfare, New D e l h i .

6. National Malaria Control Strategy ( 1 9 9 5 ) , Malaria Research Centre,
By mid 1995 all malaria endemic countries in the region
22 Sham Nath Marg, New Delhi.
had adopted the revised malaria control strategy to reduce
7. WHO ( 1 9 8 0 ) . Summary of Scientific Progress in the Field of Malaria
morbidity and mortality and to reduce its area of published during the last Five Years, MAP/80.1 VBC/80.2, WHO

distribution, particularly of multidrug resistant malaria. The Geneva.

use of stratification approach by the majority of anti-malaria 8. Youmans, G. P. et al (1980). The Biological and Clinical Basis of

programmes in the Region has led to more cost-effective Infectious Diseases, 2nd ed. Saunders. ·
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

9. Bruce-Chwatt, LJ. (1980). Essential Malariology, William About 95 per cent of cases of lymphatic filariasis are
Heinemenn, London.
caused by infection with W. bancrofti; other related parasites
10. Jawetze et.al, Medical Microbiology, 24th Ed, 2007, A Lange Medical
that infect humans are Brugia malayi in South-East Asia and
Book.
B . timori in Indonesia.
11. Hall, A. P. ( 1 9 7 6 ) Brit. Med. J., 1 : 323.

12. Pasrol, G . e t a ! ( 1 9 7 6 ) Lancet, 1 , 1269. The formal goal of the global lymphatic filariasis

13. WHO ( 1 9 8 6 ) . Techn. Rept. Ser. 735. programme is to eliminate the disease “as a public health

14. WHO ( 1 9 7 9 ) . Tech Rep. Ser. No. 640. problem” and 2020 is the informal target date for

15. W H O ( 1 9 9 5 ) , Tech. Rep. Ser., No. 857. interrupting transmission. The strategy to interrupt

16. Lariviere, M . ( 1 9 7 7 ) . Children in the Tropics No. 1 0 6 , p. 9 . transmission of the disease calls for mass administration of a
17. WHO ( 1 9 8 4 ) . Techn. Rep.Ser. No.712. 2-drug regimen (ivermectin or DEC plus albendazole)
18. WHO ( 1 9 9 5 ) , World Health, March-April, 1 9 9 5 . administration as a single dose annually for 4-6 years.
19. Council for International Organization of Medical Sciences (1973).
Between 2 0 0 0 – 2 0 1 1 , the global programme provided a
Communicable Diseases, Provisional Nomenclature, CIOMS/WHO,

Geneva. cumulative total of nearly 4 . 4 billion treatments to at least

20. WHO ( 1986). The clinical Management of Acute Malaria, SEARO, SEA 984 m i l l i o n people. It represents about 7 3 . 2 per cent of the

Ser. No. 9. New Delhi. 1 . 4 billion people at risk (2).
21. Govt. of India (2009), Guidelines for Diagnosis and Treatment of
The current hypothesis is that reducing the prevalence of
Malaria in India 2009, NVBDCP Division, Ministry of Health and

Family Welfare, New Delhi.
microfilaraemia in humans to <1 per cent will stop

22. WHO ( 1 9 6 1 ) Techn.Rep.Ser. No.205. transmission. One provisional set of guidelines for stopping

23. Govt. of India (2013), National Drug Policy on Malaria 2013, treatment would require � 5 annual rounds of MDA with

Directorate of NVBDCP, Ministry of Health and Family Welfare, New coverage of z 65 per cent of the total population (3).
Delhi.
Lymphatic filariasis is a public health problem in India.
24. Govt. of India (2011), Guidelines for Diagnosis and Treatment of

Malaria in India 2011, NVBDCP, National Institute of Malaria
The disease is endemic all over India, except in Jammu and

Research, New Delhi. Kashmir, Himachal Pradesh, Punjab, Haryana, Delhi,

25. Editorial ( 1 9 7 6 ) . Lancet, 2 :1005. Chandigarh, Rajasthan, Nagaland, Manipur, Tripura,

26. Department of Family Welfare, Ministry of Health, Govt. of India Meghalaya, Sikkim, Arunachal Pradesh, Mizoram, and
(1977). Role of Medical Officer of PHC in Malaria Control, Mass
Dadra and Nagar Haveli. However, surveys carried out
Mailing Unit.
during the past two decades indicate that areas previously
27. WHO ( 2 0 1 0 ) , International travel and health.
known to be free from filariasis are showing evidence of low
28. WHO ( 1 9 9 3 ) , Tech. Rep. Ser., N o . 8 3 9 .
degrees of transmission. Heavily infected areas are found in
29. WHO (2006), Tech. Rep. Ser. No. 936.
Uttar Pradesh, Bihar, Jharkhand, Andhra Pradesh, Orissa,
30. WHO Bull ( 1 9 8 5 ) 63 ( 2 ) 353.
Tamil Nadu, Kerala and Gujarat .
31. WHO ( 1 9 9 1 ) , World Health, Sept-Oct 1 9 9 1 .

32. WHO ( 1 9 8 3 ) . Techn. Rep.Ser. No.688. An estimated 600 m i l l i o n people are at risk of lymphatic

33. WHO (2008), World Malaria Report, 2008. filariasis infection in 250 endemic districts in 20 states/UTs in

34. WHO ( 2 0 1 1 ) , World Malaria Report 2 0 1 1 . I n d i a . Mapping was carried out using epidemiological data

supplemented by data from filaria control units, filaria

clinics, and survey units under the national filaria control
·.·. LYMPHATIC flLARIASIS

programme. Morbidity surveys (upto 2 0 1 2 ) of filaria cases in

the states/UTs revealed 8 lacs cases of lymphoedema and

The term “lymphatic filariasis” covers infection with three 4 lacs cases of hydrocele (4). The microfilaria survey reports

closely related nematode worms – W. bancrofti, B. malayi received from 205 districts revealed microfilaria rate of

a n d B. t i m o r i . All three infections are transmitted to man by about 0.45 per cent (4).

the bites of infective mosquitoes. All three parasites have Mass drug administration (MDA) is being implemented in
basically similar life cycles in man-adult worms living in India since year 2004. In 2007 India changed its strategy
lymphatic vessels whilst their offspring, the microfilariae from delivery of DEC alone to delivery of DEC plus
circulate in peripheral blood and are available to infect albendazole; since that time, the number of people treated
mosquito vectors when they come to feed (1). The disease with combination therapy has increased steadily. In 2012,
manifestations range from none to both acute and chronic about 87 per cent people at risk were treated with
manifestations such as lymphangitis, lymphadenitis, combination drug (4). India has reduced the prevalence of
elephantiasis of genitals, legs and arms or as a microfilaria to less than 1 per cent i n · 192 out of 250
hypersensitivity state such as tropical pulmonary implementation units. In implementation units in Nalganda

eosinophilia or as an atypical form such as filarial arthritis. in Andhra Pradesh, the prevalence of microfilaria

Though not fatal, the disease is responsible for considerable was reduced from 17 per cent in 2004 to 0.8 p e r cent in

suffering, deformity and disability. 2009 ( 5 ) .

Problem statement E p i d e m i o l o g i c a l determinants

Filariasis is a global problem. It is a major social and
Agent factors
economic scourage in the tropics and subtropics of Africa,

Asia, Western Pacific and parts of the Americas, affecting There are at least 8 species of filarial parasites that are

over 73 countries. More than 1 . 4 billion people live in areas specific to man (6). These are shown in Table 1. The first

where there is a risk of infection, of whom 120 million are three worms are responsible for lymphatic filariasis; and the

infected and in need of treatment, including 40 million rest for “non-lymphatic filariasis”. The parasites causing

people with overt d i s e a s e . This includes 15 million people non-lymphatic filariasis will not be described as they are not

with lymphoedema and 25 million men with urogenital found in India. Table 2 shows the differences between the

swelling principally scrotal hydrocele (2). microfilariae (Mf) of W. bancrojti and B. malavi.
LYMPHATIC FILARIASlS

TABLE 1 development take place in the vector : ( a) Exsheathing : The

Human filarial infections larva comes out of the sheath in which it is enclosed, within

1 to 2 hours of ingestion. This is known as exsheathing

which takes place in the stomach of the mosquito. (b) First

1. Wuchereria bancrofti : Culex Mosquitoes Lymphatic fllariasis stage larva : After exsheathing, the larva is able to penetrate
__ __ __ __
., ,,

2. Brugia malayi · Mansonia –“– the stomach wall of ‘the mosquito which it does in 6 to 12

3. Brugia timori . Anopheles –“– —
II

— —
II

— hours and migrate to the thoracic muscles where it grows

· Mansonia –‘.’– and develops into a sausage-shaped (short, thick) form.

(c) Second stage larva : The larva moults and increases in
4. Onchocercc uoluu/us Simulum flies Subcutaneous;

nodules; length (long, thick form) with the development of an

River blindness alimentary canal, but is relatively inactive. (d) Third stage

5. Loaloa .- Chrysops flies Recurrent, transient larva : There is a final moult to the third stage or infective
subcutaneous · · larva (long, thin form) which may be found in any part of
swellings
the insect. It is highly active or motile. When it migrates to
6. T. perstans Culicoides — Probably rarely any the proboscis of the mosquito, it is ready to be transmitted to
.clinical illness
a new host, and the mosquito is said to be infective. Under
7. T. streptocerca –”-:- —:-11-:–

__ __.,
optimum conditions of temperature and humidity, the
8. Mansonella ozzardi -”�-
duration of mosquito cycle (extrinsic incubation period) is

between 10 and 14 days. In the human host, the infective
TABLE 2
larvae develop into adult male and female worms.
Differences between Mf of W. bancrofti and B. malayi

RESERVOIR OF INFECTION
. < ‘. : : < · : , -. : . , , > � )i1J.::w:?�drici-0itr::;::TrJii. �;Ji}1q�i : ,-i ,\
Although filarial infections occur in animals, human
1 . General appearance Graceful, sweepirig Crinkled, secondary
filariasis is not usually a zoonosis (sub-periodic B. malayi and
·curves curves
T perstans are exceptions). Animal reservoirs of Brugia are
2 . Length 244 to 2 9 6 µ 1 7 7 to 230 µ
present in monkeys, cats and dogs (7); these animals are
3 . Fee cephalic As long as broad Nearly twice as long
believed to acquire their infections from man, and they are
space as broad
not regarded as important sources of infection to man (1).
4. Excretory pore Not prominent · Prominent
There is no evidence that W. bancrofti has animal reservoirs
5. Caudal end Uniformly tapering Kinkled and two
in India.
to a delicate point, terminal nuclei

No terminal nuclei present In humans the source of infection is a person with
present circulating Mf in peripheral blood. In filarial disease (late
6. Nuclear column Nuclei discrete Smudged obstructive stages) Mf are not found in the blood.

The minimum level of Mf which will permit infection of
PERIODICITY
mosquitoes is not known. It was reported that a man with
The Mf of W. bancrofti and B. malayi occurring in India one Mf per 40 cu. mm of blood was infective to 2 . 6 per cent
display a nocturnal periodicity, i.e., they appear in large of the mosquitoes which fed on him (9). On the other hand,
numbers at night and retreat from the blood stream during when mosquitoes were fed on carriers having as many as 80
the day. This is a biological adaptation to the nocturnal or more Mf per 20 cu. mm of blood, the heavily infected
biting habits of the vector mosquitoes. The maximum mosquitoes did not survive when a number of Mf began to
density of Mf in blood is reported between 10 pm and 2 am. reach maturity ( 1 0 ) .
When the sleeping habits of the host are altered, a reversal

in periodicity has been observed. Host factors

In most parts of the world, Mf are nocturnally periodic Man is a natural host. ( a ) AGE: All ages are susceptible to

but in the South Pacific islands and in limited foci in the infection. In endemic areas, filarial infection has been found

Nicobar islands, Thailand and Vietnam, W. bancrofti Mf are even in infants aged less than 6 months. Infection rates rise

non-periodic (sub-periodic), being detectable throughout with age up to the age of 20-30 years and then level off.

the 24 hours with a slight peak during day or night. Sub­ After a few years at this plateau level, Mf rates may decline

periodic B. malayi is found in parts of Malaysia and in middle and old age. Filarial disease appears only in a

Indonesia. small percentage of infected individuals, commonly in the

age group over 10 years (11), although there may be
LIFE CYCLE exceptions. (b) SEX : In most endemic areas the Mf rate is

Man is the definitive host and mosquito the intermediate higher in men. (c) MIGRATION : The movement of

host of Bancroftian and Brugian filariasis. The adult worms people from one place to another has led to the extension

are usually found in the lymphatic system of man. The males of filariasis into areas previously non-endemic.

are about 40 mm long and the females 50 to 1 0 0 mm long. (d) IMMUNITY : Man may develop resistance to infection

The females are viviparous. They give birth to as many as only after many years of exposure (7). The immunological

50,000 Mf per day (7) which find their way into blood basis of this resistance is not known (12). (e) SOCIAL

circulation via the lymphatics. The life span of the Mf is not FACTORS : Lymphatic filariasis is often associated with

exactly known, probably up to a year or more. The adult urbanization, industrialization, migration of people,

worms may survive for 15 years or more ( 7 ) . There is a case illiteracy, poverty and poor sanitation.

on record of a woman, in whom live Mf were present 40

years after she left an endemic area (8). Environmental factors

The mosquito cycle begins when the Mf are picked up by (a) CLIMATE : Climate is an important factor in the

the vector mosquito during feeding. The following stages of epidemiology of filariasis. It influences the breeding of
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

mosquitoes, their longevity and also determines the (ii) Asymptomatic microfi/araemia : A considerable

development of the parasite in the insect . vector. The proportion of people are asymptomatic, although their

maximum prevalence of Cu/ex quinquefasciatus (previously blood is positive for Mf. They may remain without any

known as C. fatigans) was observed when the temperature symptoms for months – in some instances for years. They

was between 22 to 38 deg. C and optimum longevity when are an important source of infection in the community.

the relative humidity was 70 per cent. (b) DRAINAGE: These carriers are usually detected by night blood

Lymphatic filariasis is associated with bad drainage. The examination.

vectors breed profusely in polluted water. (c) TOWN
{iii) Stage of acute manifestations : In the first months and
PLANNING : Inadequate sewage disposal and lack of town
years there are recurrent episodes of acute inflammation in
planning have aggravated the problem of filariasis in India
lymph glands and vessels. The clinical manifestations
by increasing the facilities for the breeding of
comprise filarial fever, lymphangitis, lymphadenitis,
C. quinquefasciatus (C. fatigans). The common breeding
lymphoedema of the various parts of the body and of
places are cesspools, soakage pits, ill-maintained drains,
epididymo-orchitis in the male.
septic tanks, open ditches, burrow pits, etc.
(iu) Stage of chronic obstructive lesions : The chronic

Vectors of lymphatic f i l a r i a s i s stage usually develops 10-15 years from the onset of the

first acute attack. This phase is due to fibrosis and
All three infections (W. bancrofti, B. malayi a n d B. timori)
obstruction of lymphatic vessels causing permanent
are transmitted to man by the bites of infective mosquitoes.
structural changes.
No less than 5 genera are involved in different areas of the

world – Cu/ex, Anopheles and Aedes serve as vectors for In chronic Bancroftian filariasis, the main clinical features
W. bancrofti; and Mansonia, Anopheles and Coqui/lettidia are hydrocele, elephantiasis and chyluria. Elephantiasis may
serve as the vectors of the Brugia species. affect the legs, scrotum, arms, penis, vulva and breasts,

The main vectors in India are : C. quinquefasciatus usually in that order of decreasing frequency. The

(C. fatigans) for Bancroftian filariasis, and Mansonia prevalence of chyluria is usually very low.

(Mansonoides) mosquitoes (e.g., M. annulifers and The Brugian filariasis is generally similar to Bancroftian
M. uniformis) for Brugian filariasis. The breeding of filariasis, but strangely the genitalia are rarely involved,
Mansonia mosquitoes is associated with certain aquatic
except in areas where Brugian filariasis occurs together with
plants such as Pistia stratiotes. In the absence of these
Bancroftian filariasis.
plants, these mosquitoes cannot breed.
Not all elephantiasis is caused by lymphatic filarial

Mode of transmission infection. Even in endemic areas, a small proportion of cases

may be due to other causes – i.e., due to obstructions
Filariasis is transmitted by the bite of infected vector
following infections (such as tuberculosis), tumours, surgery
mosquitoes. The parasite is deposited near the site of
or irradiation ( 1 3 ) . In Ethiopia, endemic leg elephantiasis is
puncture. It passes through the punctured skin or may
caused by silica in the iliac lymph glands ( 1 4 ) .
penetrate the skin on its own and finally reach the lymphatic

system. The dynamics of transmission depends upon the
2 . OCCULT FILARIASIS
man-mosquito contact ( e . g . , infective biting rate).

The term occult or cryptic filariasis refers to filarial
I n c u b a t i o n period infections in which the classical clinical manifestations are

The time interval between inoculation of infective larvae not present and Mf are not found in the blood. Occult

and the first appearance of detectable Mf is known as “pre­ filariasis is believed to result from a hypersensitivity reaction

patent period”. Direct information on the duration of the to filarial antigens derived from Mf. The best known example

prepatent period is lacking ( 1 3 ) . is tropical pulmonary eosinophilia.

T h e time interval from invasion of infective larvae to the
Lymphoedema management (15)
development of clinical manifestations is known as the

“clinical incubation p e r i o d ” . This period, most commonly, is The recommended management of lymphoedema in

8 to 16 months. This period may, however, be longer ( 1 3 ) . areas where lymphatic filariasis is endemic involves simple

activities that have demonstrated their effectiveness in
C l i n i c a l manifestations significantly improving the quality of life of patients. These

Only a small proportion of infected individuals exhibit activities include providing early detection of lymphoedema,

clinical signs. The disease manifestations can be divided into caring for the skin by washing and drying the affected limb

two distinct clinical types : ( a ) lymphatic filariasis caused by or area, preventing and treating entry lesions and providing

the parasite in the lymphatic system, and ( b l occult filariasis lymph drainage by elevating the limb and exercising. These

caused by an immune hyper-responsiveness of the human are the minimum activities that need to be undertaken, and

host ( e . g . , tropical pulmonary e o s i n o p h i l i a ) . there is a standard care beyond this that can be accessed

where available.
1 . LYMPHATIC FILARIASIS
Since the prevention and management of disability
The following stages have been described (13):
caused by lymphatic filariasis is now viewed as public health

(i) Asymptomatic amicrofilaraemia : In all endemic areas a issue, the guidelines for the first level care worker developed

proportion of population does not show Mf or clinical by WHO to manage acute dermato-lymphangioadenitis

manifestations of the disease although they have the same (ADLA) are as follows:

degree of exposure to infective larvae as those who become
1 . TREATMENT FOR UNCOMPLICATED ADLA
infected. With presently available diagnostic procedures it is

not possible to determine whether persons in this group have a. Give analgesic such as paracetamol (lg given 3-4

detectable infections or whether they are free from infection. times a day);
LYMPHATIC FILARIASIS

b. Give oral antibiotic such as amoxicillin (1.5g in 1 . MASS BLOOD SURVEY
3 divided doses or oral p e n i c i l l i n ) for at least 8 days.
The definitive diagnosis of lymphatic filariasis depends
In case of allergy to penicillin, oral erythromycin
upon the demonstration of living parasites in the human
( l g , given 3 times a day) can be used;
body. This calls for a night blood survey.
c. Clean the limb with antiseptic;
(i) The thick film : The thick film made from capillary
d. Check for any wounds, cuts, abscesses and interdigital blood is still the most commonly used method for
infection (especially between the toes). Clean with epidemiological assessment. 20 cu. mm of blood is collected
antiseptic, if any present. If local superficial skin by a deep finger prick between 8 . 3 0 pm and 12 mid-night. A
infection is found give antibiotic cream, apply thick smear is prepared on a glass slide, and the slide is dried
antifungal cream if interdigital infection is present; and serially numbered. The age, sex and other host factors

are recorded on the survey card or register. On the next day
e. Give advice about prevention of chronic
or so, the blood films are dehaemoglobanised, stained, dried
lymphoedema caused by lymphatic filariasis;
and examined for Mf under low power. The usual technique
f. Do not give antifilarial medicine.
for enumeration of Mf on slides is to start at one end of the
g. Home management includes drinking plenty of water, smear and work across to the other end, moving the slide
rest, elevation of the limb, wriggling the toes, cooling field by field till the smear is covered.

the limb with cold water and washing the limb if the
(ii) Membrane filter concentration (MFC) methods : The
patient can do it; and
most sensitive method currently available for detecting low­

h. Follow-up after 2 days at home. If situation does not density ni.icrofilaraemia in the blood is by concentration

improve, then refer the patient to physician. techniques. It requires collection of blood by venepuncture

and filtering large volumes of blood. Although MFC is the
2. MANAGEMENT OF SEVERE ADLA
most sensitive method available, some very-low-density

a. Refer the patient to physician immediately to receive carriers will still not be detected ( 1 3 ) .

recommended antibiotic treatment
(iii) DEC provocation test : Mf can be induced to appear
Intravenous benzylpenicillin (Penicillin G) 5 million in blood in the daytime by administering diethylcarbamazine
units given 3 times a day or intramuscular procain (DEC) 100 mg orally. Mf begin to reach their peak within 15
benzylpenicillin 5 million units given 2 times/day minutes and begin to decrease 2 hours later. The blood may
until fever subsides, then give oral be examined one hour after administration of DEC.
phenoxymethylpenicillin (penicillin V) 750 mg

(1.2 million units) to lg. (1.6 million units) given 2 . CLINICAL SURVEY

3 times/day. The minimum total treatment is atleast At the same time when blood is collected, the people are
for 8 days. examined for clinical manifestations of filariasis which

– In case of allergy to penicillin give IV erythromycin should be recorded in the suggested schedule.

lg 3 times/day until fever subsides, then give oral
3 . SEROLOGICAL TESTS
erythromycin lg given 3 times/day or give other

antibiotic according to local situation. Serological tests to detect antibodies to Mf and adults

using immunofluorescent and complement-fixing techniques
b. Give analgesic I antipyretic such as paracetamol;
cannot distinguish between past and present infection, and
c. Do not give any antifilarial medicine.
heavy and light parasite loads in the human hosts (17).

Recent interest has focussed on the direct detection of
Hydrocele management
parasite antigens in patient’s blood or urine ( 1 3 ) .
In the management of hydrocele, the objective of any

lymphatic filariasis disability prevention programme should 4. XENODIAGNOSIS
be to increase access to hydrocelectomy. One of the first
The mosquitoes are allowed to feed on the patient, and
activities of the programme should be to detect scrotal
then dissected 2 weeks later (8). Where other techniques
swelling using an existing community survey (such as
may fail, this may succeed in detecting low-density
enumeration of mass drug administration or other health
microfilaraemia.
initiatives). Individuals with scrotal swelling should be

referred to a facililty for diagnosis, and if necessary for
5 . ENTOMOLOGICAL SURVEY
surgery.
This comprises of general mosquito collection from

houses, dissection of female vector species for detection of
FILARIA SURVEY
developmental forms of the parasite, a study of the extent

and type of breeding places and other bionomics of
The size of the sample to be examined in a filaria survey
mosquitoes.
varies with the type of survey, whether it is a routine survey or

survey for evaluation. The NICO (National Institute of The data are assembled, analyzed and the results are

Communicable Diseases, Delhi) standard is to examine 5- 7 expressed in terms of certain parameters ( clinical,

per cent of the population for routine surveys, and at least parasitological and entomological) as described below.

20 per cent for evaluation studies. The sample must be

random, representative and cover all ages and both sexes. ASSESSMENT OF FILARIA CONTROL
Statistical advice should be obtained when surveys are being
PROGRAMMES
planned. A standardized schedule for conducting filaria

surveys is given in a WHO Expert Committee Report on The effect of filariasis control can be assessed using

Filariasis (16). A filaria survey comprises the following clinical, parasitological and entomological methods. These

elements: are:
EPIDEMIOLOGY OF COMMUNICABLE DISEASES

1 . CLINICAL PARAMETERS circulation. It is effective in killing Mf. The effect of the drug
on the adult worm is uncertain. It has probably no effect on
The clinical parameters measured are the incidence of
the infective stage larvae.
acute manifestations (adeno-lymphangitis, epididymo­

orchitis, etc), and the prevalence of chronic manifestations Toxic reactions : DEC may produce severe side reactions.

(lymphoedema, elephantiasis, hydrocele, chyluria, etc). The reactions may be of two kinds : (a) those due to the drug

itself, e . g . , headache, nausea, vomiting, dizziness, etc, These

2 . PARASITOLOGICAL PARAMETERS reactions are observed a few hours after the first dose of

DEC and generally do not last for more than 3 days, and
These are : (a) MICROFILARIA RATE : It is the percentage
(b) those which are allergic reactions due to destruction
of persons showing Mf in their peripheral blood (20 cu. mm)
of microfilariae and adult worms, e.g., fever, local
in the sample population, one slide being taken from each
inflammations around dead worms, orchitis, lymphadenitis,
person. Specify the species of the parasite. (b) FILARIAL
transient lymphoedema and hydrocele. The local reactions
ENDEMICITY RATE : It is the percentage of persons
tend to occur later in the course of treatment and to last
examined showing microfilariae in their blood, or disease

manifestation or both. (c) MICROFILARIAL DENSITY : It is longer. If the drug is given in spaced doses, systemic

the number of Mf per unit volume (20 cu. mm) of blood in reactions are much less frequent and less intense after the

samples from individual persons. It indicates the intensity of second dose and are rare after subsequent doses. These

infection. (d) AVERAGE INFESTATION RATE : It is the reactions disappear spontaneously and interruption of

average number of Mf per positive slide, each slide being treatment is not necessary.

made from 20 cu.mm of blood. It indicates the prevalence of
b. Fi/aria control in the community
microfilaraernia in the population.

There are three reasons why filariasis never causes

3 . ENTOMOLOGICAL PARAMETERS explosive epidemics : (a) the parasite does not multiply in

the insect vector, (b) the infective larvae do not multiply in
These comprise : (a) vector density per 10 man-hour
the human host, and (c) the life cycle of the parasite is
catch ( b ) percentage of mosquitoes positive for all stages of

development (c) percentage of mosquitoes positive for relatively long, 15 years or more. These factors favour the

infective (stage III) larvae (d) the annual biting rate – for success of control programme ( 1 3 ) .

assessment of transmission (e) types of larval breeding The administration of DEC can be carried out in various
places, etc. ways:

The above parameters help to measure the conditions
(i) Mass therapy
existing before and after control procedures began, and also

to measure the progress of the control campaign against In this approach, DEC is given to almost everyone in the

vectors from time to time. community irrespective of whether they have

microfilaraemia, disease manifestations or no signs of

CONTROL MEASURES infection except children under 2 years, pregnant women and

seriously ill patients. The dose recommended is 6 mg/kg body
The current strategy of filariasis control is based on :
weight. In some countries it is used alone and some countries

1. Chemotherapy with albendazole or ivermectin. Mass therapy is indicated in

highly endemic areas (13). For mass chemotherapy to be
2. Vector control
accepted, a good rapport must be established with the
Many years of experience with DEC chemotherapy has
community before the treatment begins. This requires
shown that, even after the full regimen of treatment, some
intensive health education of the general public.
microfilariae still persist in the body. Due to this and other

reasons (e.g., toxic effects), it has not been possible to (ii) Selective treatment
prevent the spread of filariasis by the administration of DEC
DEC is given only to those who are Mf positive. It is
alone. Chemotherapy must, therefore, be supplemented by
generally accepted that selective treatment may be more
an effective vector control programme, if the disease
suitable in areas of low endemicity than in highly endemic
transmission has to be effectively prevented.
areas.

1 . Chemotherapy In India the current strategy is based on detection and

treatment of human carriers and filaria cases. The
a. Diethylcarbamazine
recommended dose in the Indian programme is 6 mg DEC
Diethylcarbamazine (DEC) is both safe and effective. The per kg of body weight daily for 12 doses, to be completed in
dose of DEC that is most generally accepted for the 2 weeks ( i . e . , 6 days in a week). In endemic areas, treatment
treatment of Bancroftian filariasis is 6 mg/kg body weight per must be repeated at specified intervals, usually every 2
day orally for 12 days, given preferably in divided doses years. This is partly because, despite remarkable
after meals. This amounts to a total of 72 mg of DEC per kg antimicrofilarial properties, expected microfilaria clearance
of body weight as a full treatment. For Brugian filariasis, with DEC is incomplete at times even after adequate
recommended doses range from 3 to 6 mg of DEC/kg body treatment (18). The other reason is that people living in
weight per day, up to a total dose of 36- 72 mg DEC/kg body
endemic areas are exposed to reinfection.
weight as a full treatment ( 1 3 ) .

DEC is rapidly absorbed after oral administration, (iii) DEC-medicated salt

reaching peak blood levels in 1-2 hours. It is also rapidly
The use of DEC-medicated salt is a special form of mass
excreted – the blood half-life is only 2-3 hours in alkaline
treatment using very low doses of the drug over a long
urine and about 10-20 hours in acid urine.
period of time. Common salt medicated with 1-4 g of DEC

DEC causes rapid disappearance of Mf from the per kg has been used for filariasis control in some endemic
LYMPHATIC FILARIASIS

areas of W. bancrofti and B. malayi, particularly after an vector mosquito has developed resistance to many of these

initial reduction in prevalence has been achieved by mass or chemicals. The frequency of application is once weekly on

selective treatment of Mf carriers. Treatment should be all breeding places.

continued for at least 6 to 9 months. In the Lakshadweep
(2) REMOVAL OF PISTIA PLANT : In the case of
islands, this regimen has been shown to be safe, cheap and
Mansonia mosquitoes, breeding is best controlled by
effective ( 1 3 ) .
removing the supporting aquatic vegetation such as the

The combination of the long life of the adult parasite for pistia plant from all water collections and converting the

several years and infectiousness of a patient with low ponds to fish or lotus culture. Alternatively, certain

parasitaemia represents a serious obstacle to control herbicides such as phenoxylene 30 or Shell Weed Killer D

programmes based on chemotherapy alone ( 1 9 ) . may be used for destroying the aquatic vegetation.

(3) MINOR ENVIRONMENTAL MEASURES : Larvicidal
c. Ivermectin
operations are complemented by minor engineering

Ivermectin is a semisynthetic macrolide antibiotic with a operations such as filling up of ditches and cesspools,

broad spectrum of activity against a variety of nematodes drainage of stagnant water, adequate maintenance of septic

and ectoparasites. The dose is 150-200 µg/kg of body tanks and soakage pits, etc. Environmental management is

weight the most efficient approach to the problem of controlling

mosquito breeding.
Ivermectin is not used in India. It is used in the region of

Africa.
II. Anti-adult measures
There is no drug toxicity in normal persons. However, in
The vector mosquitoes of filariasis have become resistant
microfilaraemic patients there may be a variety of reactions
to DDT, HCH and dieldrin. The use of these compounds for
as a result of inflammatory response triggered by the cleared
indoor residual spraying, tried earlier, has been
and dying microfilariae.
discontinued. Pyrethrum, as a space spray, still holds

promise. It is useful as a temporary means of personal
2 . Vector control
protection, but has no practical value in present-day vector
Where mass treatment with DEC is impracticable, the control programmes.
control of filariasis must depend upon vector control. Vector

control may also be beneficial when used in conjunction III. Personal prophylaxis

With mass treatment. The most important element in vector
The most effective preventive measure is avoidance of
control is the reduction of the target mosquito population in
mosquito bites (reduction of man-mosquito contact) by
order to stop or reduce transmission quickly. The techniques
using mosquito nets. Screening of houses can substantially
for controlling mosquitoes are given in chapter 12. Briefly
reduce transmission, but it is expensive.
they are :

Integrated vector control
I. Antilarval measures
None of the above vector control measures applied alone
The ideal method of vector control would be elimination
is likely to bring about sustained control of filariasis vectors.
of breeding places by providing adequate sanitation and An integrated or combined approach is needed to control
underground waste-water disposal system. This involves filariasis using all the above strategies and approaches in
considerable expenditure amounting to several crores of optimum combination.
rupees. Because of financial constraints, this may not be
In filariasis four major breakthroughs have occurred. The
feasible in developing countries such as India in the near
first of these is the development of safe, single dose, annual
future. For the time being, therefore, vector control must be
drug treatment. Trials have proved that a single dose of DEC is
based on temporary or recurrent methods.
very effective even two years after treatment. A single dose of
The current approach in India is to restrict the antilarval ivermectin has proved to be equally effective.
measures to urban areas, because it is operationally difficult A combination of single dose of both drugs reduced
and very costly to cover the vast rural areas of the country.
microfilaraemia more than 95 per cent, 2 years after
The urban areas include an extra 3-km peripheral belt
treatment. Secondly, intensive local hygiene on the affected
because the flight range of Cu/ex quinquefasciatus
limb, with or without the use of antibiotic and antifungal
(C. fatigans) is about 3 km.
creams, has shown to have dramatic effects by halting the

The anti-larval activities comprise the following (20). progression of, or even reversing elephantiasis and

lymphoedema. Thirdly, DEC-medicated tablet or cooking salt
( 1 ) CHEMICAL C O N T R O L : (a) Mosquito larvicidal o i l :
has been introduced in India. The carefully controlled
Mosquito larvicidal oil (MLO) is active against all preadult
addition of very low concentration of DEC has long been
stages. It has. been the main chemical used to control
recognized as an effective means of eliminating lymphatic
C. quinquefasciatus for some time. Since it has proved to be
filariasis infections in communities. However, the addition
less efficient under field conditions and more expensive than
increases the price of the salt. During 1994, the first
other chemical preparations, it is being replaced by
commercially prepared DEC salt went on sale in India, at
pyrethrum oil, temephos and fenthion. (b) Pyrosene oil- E :
about twice the price of ordinary salt. Finally, there has been
This is a pyrethrum-based emulsifiable larvicide. The
the development of insecticide sprays and polystyrene beads
emulsion concentrate contains O . 1 to O .2 per cent pyrethrins
to seal latrines and roof-top water-storage tanks, to eliminate
by weight and is required to be diluted with water before
or reduce populations of urban Culex mosquitoes ( 2 1 ) .
use. The emulsion is diluted in the ratio of 1 :4,

(c) Organophosphorus /arvicides : During the past 1 0 years,
National Filaria Control Programme
organophosphorus larvicides (e.g., temephos, fenthion)

have been widely used with successful results. However, the See chapter 7, page 421 for details.