PBL 3:

Dengue Fever/Dengue Haemorrhagic Fever

Malaria
Chikungunya
Japanese Encephalitis
Leptospirosis
1. Status of incidence and prevalence of
the disease in Malaysia and the world

UMA, DURGA, THAMARAI

 Dengue fever
The incidence of dengue has grown dramatically around the world
in recent decades. The actual numbers of dengue cases are
underreported and many cases are misclassified. One recent
estimate indicates 390 million dengue infections per year (95%
credible interval 284528 million), of which 96 million (67136
million) manifest clinically (with any severity of disease). Another
study, of the prevalence of dengue, estimates that 3.9 billion people,
in 128 countries, are at risk of infection with dengue viruses.2

Member States in 3 WHO regions regularly report the annual

number of cases.. The number of cases reported increased from 2.2
million in 2010 to 3.2 million in 2015. Although the full global
burden of the disease is uncertain, the initiation of activities to
record all dengue cases partly explains the sharp increase in the
number of cases reported in recent years.
 Before 1970, only 9 countries had experienced severe dengue
epidemics. The disease is now endemic in more than 100
countries in the WHO regions of Africa, the Americas, the
Eastern Mediterranean, South-East Asia and the Western
Pacific. The America, South-East Asia and Western Pacific
regions are the most seriously affected.
Cases across the Americas, South-East Asia and Western
Pacific exceeded 1.2 million in 2008 and over 3.2 million in
2015(based on official data submitted by Member States).
Recently the number of reported cases has continued to
increase. In 2015, 2.35 million cases of dengue were reported
in the Americas alone, of which 10 200 cases were diagnosed
as severe dengue causing 1181 deaths.
 In 2012, an outbreak of dengue on the Madeira islands of
Portugal resulted in over 2 000 cases and imported cases were
detected in mainland Portugal and 10 other countries in
Europe. Among travellers returning from low- and middle-
income countries, dengue is the second most diagnosed cause
of fever after malaria.
In 2013, cases have occurred in Florida (United States of
America) and Yunnan province of China. In Asia, Singapore has
reported an increase in cases after a lapse of several years
and outbreaks have also been reported in Laos. In 2014,
trends indicate increases in the number of cases in the
People's Republic of China, the Cook Islands, Fiji, Malaysia and
Vanuatu, with Dengue Type 3 (DEN 3) affecting the Pacific
Island countries after a lapse of over 10 years. Dengue was
also reported in Japan after a lapse of over 70 years.
 The year 2015 was characterized by large dengue outbreaks
worldwide, with the Philippines reporting more than 169 000
cases and Malaysia exceeding 111 000 suspected cases of
dengue, representing a 59.5% and 16% increase in case
numbers to the previous year, respectively.
Brazil alone reported over 1.5 million cases in 2015,
approximately 3 times higher than in 2014. Also in 2015, Delhi,
India, recorded its worst outbreak since 2006 with over 15 000
cases.
The Island of Hawaii, United States of America, was affected by
an outbreak with 181 cases reported in 2015 and ongoing
transmission in 2016. The Pacific island countries of Fiji, Tonga
and French Polynesia have continued to record cases.
An estimated 500 000 people with severe dengue require
hospitalization each year, a large proportion of whom are
children. About 2.5% of those affected die.
Reference:http://www.who.int/denguecontrol/epidemiology/Average_number_susp
ected_confirmed_dengue_cases_reported
 INCIDENCE MORTALITY
RATE RATE

http://www.moh.gov.my/images/gallery/stats/heal_fact/healthfact-P_2009.pdf
 Malaria
Malaria transmission occurs in five WHO regions. Globally, an
estimated 3.2 billion people in 95 countries and territories are at
risk of being infected with malaria and developing disease
(map), and 1.2 billion are at high risk (>1 in 1000 chance of
getting malaria in a year). According to the World Malaria Report
2015, there were 214 million cases of malaria globally in 2015
(uncertainty range 149303 million) and 438 000 malaria deaths
(range 236 000635 000) , representing a decrease in malaria
cases and deaths of 37% and 60% since 2000, respectively.
The burden was heaviest in the WHO African Region, where an
estimated 90% of all malaria deaths occurred, and in children
aged under 5 years, who accounted for more than two thirds of
all deaths.
Reference:http://www.who.int/gho/malaria/malaria_003.jpg?ua=1
Reference:www.who.int/malaria/publications/country-profiles/profile_mys_en.pdf
 Chikungunya
From the early 2000s, major outbreaks of chikungunya virus
infection were reported in Southeast Asian, South Asian and
Indian Ocean island countries, including Indonesia, Malaysia,
Reunion, Seychelles, and India. An increased number of
chickungunya outbreaks worldwide has resulted in numerous
reports of imported infections among travellers recently
returned from these and other countries.

Chikungunya virus infection became a notifiable disease in

Western Australia in May 2008. Between 2008 and 2012, an
average of 6 chikungunya cases were notified per year (range: 2
10 cases), with infection acquired in a number of countries,
mostly in Southeast Asia
 Prior to 2013, chikungunya virus outbreaks had been identified
in countries in Africa, Asia, Europe, and the Indian and Pacific
Oceans.
In late 2013, the first local transmission of chikungunya virus in
the Americas was identified in Caribbean countries and
territories. Local transmission means that mosquitoes in the
area have been infected with the virus and are spreading it to
people.
Since then, local transmission has been identified in 45
countries or territories throughout the Americas with more
than 1.7 million suspected cases reported to the Pan American
Health Organization from affected areas
 Malaysia experienced the first outbreak of chikungunya (CHIK) in Klang
in late 1998 due to CHIK virus of Asian genotype. The CHIK virus of
Asian genotype reemerged causing outbreak in Bangan Panchor, Perak
in March 2006. CHIK virus of Central/East African genotype was first
detected from a patient who returned from India in August 2006.
In December 2006, CHIK virus of Central/East African genotype was re-
introduced into Malaysia from India and caused an outbreak in Kinta
district, Perak but was successfully controlled following an early
detection and institution of intensive vector control measures.
In late April 2008, CHIK virus of Central/East African genotype was
laboratory confirmed as the cause of CHIK outbreak in Johore which
spread to other parts of Malaysia by August 2008.
Phylogenetic analysis based on the 254-bp fragment of the virus
envelope protein gene as the genetic marker showed that three
different strains of CHIK virus of Central/East African genotype were
introduced into Malaysia on three separate occasions from 2006 to
2008. The strain that was introduced into Johor state was responsible
for its subsequent spread to other parts of Malaysia, inclusive of
Sarawak
Reference:https://www.cdc.gov/chikungunya/geo/index.html
Reference:https://www.cdc.gov/chikungunya/geo/index.h
tml
http://medcraveonline.com/MOJPH/MOJPH-02-00043.pdf
 Leptospirosis
Leptospirosis occurs worldwide but is most common in tropical
and subtropical areas with high rainfall. The disease is found
mainly wherever humans come into contact with the urine of
infected animals or a urine-polluted environment.
The number of human cases worldwide is not known precisely.
According to currentlyavailable reports, incidences range from
approximately 0.11 per 100 000 per year in temperate climates
to 10100 per 100 000 in the humid tropics.
During outbreaks and in high-exposure risk groups, disease
incidence may reach over 100 per 100000
 It is estimated that 100-200 Leptospirosis cases are identified
annually in the United States. About 50% of cases occur in
Hawaii.
The largest recorded U.S. outbreak occurred in 1998, when 775
people were exposed to the disease. Of these, 110 became
infected.
Although incidence in the United States is relatively low,
leptospirosis is considered to be the most widespread zoonotic
disease in the world.
Significant increases in incidence have been reported from
Peru and Ecuador following heavy rainfall and flooding in the
spring of 1998. Thailand has also reported a rapid increase in
incidence between 1995 and 2000.
Reference:http://www.infectionlandscapes.org/2013/06/leptospirosis.html
Figure 1.Reported leptospirosis cases in Ministry of Health hospitals, Malaysia, between 2004
and 2012
Figure 2: The map shows the sites of reported human leptospirosis outbreaks in
Malaysia
 Japanese encephalitis
The annual incidence of clinical disease varies both across and
within endemic countries, ranging from <1 to >10 per 100 000
population or higher during outbreaks.
A literature review estimates nearly 68 000 clinical cases of JE
globally each year, with approximately 13 600 to 20 400
deaths. JE primarily affects children. Most adults in endemic
countries have natural immunity after childhood infection, but
individuals of any age may be affected.
 The global incidence of JE is unknown because the intensity
and quality of JE surveillance and the availability of diagnostic
laboratory testing vary throughout the world. Countries that
have implemented high-quality childhood JE vaccination
programmes have seen a dramatic decline in JE incidence.
Although JE is reportable to the World Health Organization
(WHO) by its Member States, reporting is highly variable and
incomplete. In the late 1980s, Burke and Leake estimated that
50 000 new cases of JE occurred annually among the 2.4 billion
people living in the 16 Asian countries considered endemic at
the time (approximate overall annual incidence: 2 per 100 000).
In the intervening two decades, despite major population
growth, urbanization, changes in agricultural practices and
increased use of the JE vaccine in many countries, this figure
has been widely quoted, including very recently..
 In 2000, assuming an annual, age-group-specific
incidence of 25 cases per 100 000, Tsai estimated that
in the absence of vaccination 175 000 cases of JE
would occur annually among Asian children aged 0
14 years living in rural areas.14 The current study
used more recent, published, local or national
incidence estimates and current population data to
produce an updated estimate of the annual global
incidence of JE
 Although information is scarce regarding the national JE
epidemic in Malaysia, three JE outbreaks were recorded in 1974,
1988, and 1999, with 154 reported JE cases (42 laboratory
confirmed cases) and 56 deaths in the 1999 outbreak.
Most of the patients were adult males who worked on pig
farms.
The JE vaccine was introduced to children under 15 years of age
in July 2001.
According to a hospital-based surveillance study focused on
cases in Sarawak, the estimated JE incidence rate decreased
from 9.8 to 4.3 cases per 100,000 children under 12 years of age
Reference:https://www.cdc.gov/japaneseencephalitis/maps/index.html
2. The National Epidemiological
Surveillance

OH WENG KIN
 Dengue fever/ Dengue Hemorrhagic
fever
The most significant arthropodborne viral disease worldwide. It
occurs in over 100 countries and territories and threatens the
health of over 2500 million people in tropical and subtropical
regions.
Dengue fever is a severe disease with high epidemic potential. An
estimated 500 000 patients, 90% of them below the age of 15, are
hospitalized with DHF / DSS every year.

http://www.who.int/csr/resources/publications/surveillance/whocdscsrisr992.pdf
 The geographical distribution of the disease and the
number of cases has increased dramatically in the past
40 years.
A pandemic in 1998, in which 1.2 million cases of dengue
fever and dengue hemorrhagic fever were reported from
56 countries, was unprecedented.
It is estimated that each year 50 million infections occur
with 500,000 cases of dengue hemorrhagic fever and at
least 12,000 deaths, mainly among children although
fatalities could be twice as high.
 In 2008 the South-East Asia region and Western Pacific
Region accounted for 70% of the global burden of
DF/DHF.
High burden countries in the South-East Asia Region were
Indonesia, Thailand and Myanmar, with India,
Bangladesh and Sri Lanka also reporting frequent
outbreaks Bhutan and Nepal reported their first cases in
2004 and 2006 respectively.
During 2000, SEAR reported about 190,000 cases with
1600 deaths.
 Malaria
In 2008, there were an estimated 243 million (190-
311million) cases of malaria worldwide.
About 85 per cent, were in African followed by the South-
East Asia Region (10 %) and East Mediterranean (4 %).
Malaria accounted for an estimated 863,000 (708-1003
million) deaths, of which 89 percent were in African
Region, followed by the Eastern Mediterranean (6%) and
the South-East Asia Region (5%).
 In 2008, the reported cause specific mortality rate for
malaria was 17 per lakh(100,000) population worldwide.
African Region reported about 104 per lakh population.
Eastern Mediterranean about 3 per lakh population
South-East Asia Region about 1 per lakh population.
About 8 per cent of total under-5 years mortality was due
to malaria, with maximum deaths from African Region
(16 per cent of total under 5 years mortality) and 3 per
cent from Eastern Mediterranean Region. SEAR
accounted for 1 per cent.
 The childhood deaths result mainly from cerebral malaria
and anemia.
Fatality rates of 10-30 per cent have been reported among
children with severe malaria. However, these rates are even
higher in rural and remote areas where patients have
restricted access to adequate treatment.
Malaria also contributes indirectly to illness and death from
respiratory infections, diarrhoeal diseases and malnutrition.
Death from malaria in countries outside Sub-Saharan Africa
occur principally in non-immune people who become
infected with Plasmodium falciparum.
 Malaria affects mainly poor, undeserved and marginalized
populations in remote rural areas which are characterized
by inadequate control measures and limited access to
health care.
Higher malaria prevalence has been reported among ethic
and tribal groups living in remote forested and border
areas, as well as among mobile and migrant populations.
Drug-resistant parasites, poor treatment-seeking behavior
and the presence of counterfeit antimalarial drugs further
hinder control efforts.
 Chikungunya fever
WHO- Chikungunya has been identified in over 60
countries in Asia, Africa, Europe and the Americas.
An outbreak of this disease in Kolkata(in India) in 1963-
1964 and another in Chennai in 1965, which gave rise to
300,000 cases in Chennai city alone.
According to reports, the virus has not been active since
1965.
Reappeared after 41 years. In 2006, there was a large
outbreak of chikungunya in India, with 1,39 million
officially reported cases spread over 16 states.
In 2007, up until 12th Oct, a further 37683 cases had been
reported by the Govt. of India.
 In recent decades, mosquito vectors of chikungunya have
spread to Europe and the Americas.
In 2007, disease transmission was reported for the first
time in a localized outbreak in north-eastern Italy.
Outbreaks have since been recorded in France and
Croatia.
 Japanese encephalitis
The leading cause of viral encephalitis in Asia and occurs in
almost all Asian countries.
Largely as a result of immunizations, its incidence has been
declining in Japan, the Korea peninsula and in some
regions of China, but the disease is increasingly reported
from Bangladesh, India, Nepal, Pakistan, northern Thailand
and Viet Nam.
Transmission occurs principally in rural agriculture location
where flooding irrigation is practiced. Transmission is
seasonal and mainly related to the rainy season in South-
East Asia Region.
Flood irrigation
 Rare in other parts of the world, and when seen, is
generally associated with travelers returning from endemic
areas.
An estimated 50,000 cases of JE occur globally each year,
with 10,000 deaths and nearly 15000 disabled.
The vast majority of cases (about 85 per cent), occur
among children less than 15 years of age.
Nearly 10 per cent of the cases are among those over 60
years, perhaps reflecting waning protective immunity.
 Leptospirosis
Most widespread of the disease transmissible from animal
to man.
It has high prevalence in warm humid tropical countries.
Outbreaks mostly occur as a result of heavy rainfall and
consequent flooding.
Reports indicate that it is fairly widespread throughout
India.
An outbreak of leptospirosis in Orissa after the super
cyclone of 29th Oct 1999, and in the month of August
2000, there were cases of leptospirosis in Gujarat, Kerala,
Maharashtra, and Andaman and Nicobar.
 WHO-Leptospirosis is reported in a number of countries
of the South-East Asia Region from time to time.
The magnitude of the leptospirosis problem differs from
country to country and depends on awareness and
attitude of public heath care decision makers.
Most human cases have been reported from India,
Indonesia, Thailand and Sri Lanka during the rainy
season.
 Major outbreaks in South-East Asia were reported in the
past in Jakarta (2003), Mumbai (2005) and Sri Lanka
(2008).
Seasonal outbreaks are reported in northern Thailand and
in Gujarat, India following heavy rainfall and flooding.
A few human cases have been reported from Maldives.
According to currently available reports, incidences range
from approximately 0.110 per 100,000 per year globally.
During outbreaks and in high-exposure risk groups,
disease incidence may reach over 50 per 100 000.
3. The causative organisms, types and
their modes of transmission

I. Dengue Fever
Viruses
II. Chikungunya
III. Japanese encephalitis
IV. Malaria Parasite

V. Leptospirosis Bacteria

KELVIN SOON
 Arboviruses(Arthropod-born viruses)

group of viruses that are transmitted by arthropod vectors

Classification:
Group A:Alphavirus
Group B:Flavivirus
Group C :Group C serogroup of genus Old classification
Orthobunyavirus
Group D:Guama serogroup of genus
Orthobunyavirus
 Base on biological classification:

4 common families of viruses:

Family of Flaviviridae-(JEV,DEN 1-4)
Family of Togaviridae-(Chikungunya virus)
Family of Bunyaviridae-
Family of Reoviridae-
Diseases Causative agents Vector Mode of
transmission
s
Dengue Fever Flaviviridae Aedes aypti
(Flavivirus genus- Aedes albopictus
Dengue virus:1,2,3,4)
Japanese Flaviviridae Culex
encephalitis (Flavivirus genus-JEV) tritaeniorhynchus
Culex vishnui Vector-
Culex gelidus borne
Aedes anophelines
Chikungunya Togavirus family Aedes aegypti
fever (alpha virus genus- ) Aedes albopictus
Aedes
africanus(K.park)
Aedes furcifer-taylori
group
Aedes luteocephalus.
Disease Causative agents Vector Mode of
transmission

Malaria Plasmodium vivax Aedes anopheles Vector borne

Plasmodium
ovale
Plasmodium
falciparum
Disease Causative
Plasmodium
agent Reservoirs Mode of
malariae transmission

Leptospirosis Leptospira genus Domestic Water borne

(L.interrogans- animals- Injured skin
pathogenic) rodents(rats,mice Mucous
,and voles) membrane
Drinking
(Cattle, buffaloes, contaminated
horses, sheep, goat, water
pigs and dogs are
also considered )
4. Mention the phases in the life cycle of
the causative agents
 DENGUE
Dengue Mosquito borne infection caused by a flavivirus (
Aedes aegypti) that is characterized by fever ,muscle pain,
rash and lymphadenopathy.
a)Classic dengue fever
b)Dengue hemorrhagic fever
-Increased vascular permeability
and leakage of plasma &
thrombocytopenia
Malaria life cycle
 the life cycle in human begins with introduction of
sporozoites into blood from saliva of the bitting
mosquito
sporozoites are taken up by liver and it started to
multiply and differentiate into merozoites
merozoites released from the liver cells and infect
red blood cells
the cycle repeated when mosquito takes a blood
meal. During release of the merozoites a person
can have typical recurrent symptoms of chills, fever
and sweat.
 Female mosquitoes lay their eggs on the inner,
wet walls of containers with water.

Larvae hatch (picture 1)when water inundates

the eggs as a result of rains or the addition of
water by people.

The larvae (picture 2) will feed on

microorganisms and particulate organic matter,
shedding their skins three times to be able to
grow from first to fourth instars then changing
the larva into a pupa (picture 3).
(Aedes Pupae do not feed; they just change in form until
aegypti) the body of the adult, flying mosquito is formed.

Then, the newly formed adult emerges from the

water after breaking the pupal skin (picture 4)

The entire life cycle lasts 8-10 days at room

temperature
Chickungunya fever
Sudden onset of high fever and joint pains ( wrist and ankles), stiffness
of the joints and maculopapular rash over the body is common
It transmitted by Aedes aegypti and albopictus ( species of aedes
mosquitoes)

Aedes Albopictus (Tiger mosquitoes)

Tiger mosquitoes are several closely related species from the same
genus:

The Asian tiger mosquito,Aedes albopictus (Stegomyia albopicta)

The yellow fever mosquito, also dengue mosquito or Egyptian tiger

mosquito, Aedes aegypti (Stegymyia aegypti)

The Polynesian tiger mosquito, Aedes polynesiensis (Stegomyia

polynesiensis).
Japanese Encephalitis life cycle
Leptospirosis life cycle
 leptospira interrorgans is the the cause of
leptospirosis
leptospiras infect various animals such as rats and
other rodents
animals excrete leptospiras in urine which
contaminates water and soil.
Therefore, swimming in contaminated water or
consuming food or drinks can infect human
miners, farmers, and people who work in sewers have
high risk. Urban poor people also have the highest risk
of infection
5. Seasonal variations
 Dengue fever/DHF
The pattern of dengue transmission is influenced by climate and
weather.
Climatic factors responsible for epidemics either alone or in
combination (rainfall, variation in temperature sometimes
humidity.)
Widespread in regions with higher or increasing surface
temperature, more in rainy and post rainy season.
It is sensitive to weather for several reasons:
a warm ambient temperature is critical to adult dengue vectors
feeding behavior and gonotrophic cycle, as well as the rate of
larval development and speed of virus replication; and
rainfall-induced standing water are necessary for dengue
vectors to breed.
 Malaria
Its transmission is usually associated with topography,climate and socio-
economic conditions. The problem of the disease is aggravated by
changing climate,poverty and lack of efficient controlling mechanisms.

In a study, the frequency of plasmodium vivax and plasmodium falciparum

were analysed during different seasons of the year.

The results showed 32.60% presented in the autumn season (vivax:33.58%

falciparum:66.42%) 9% in winter season (Vivax:32.4 falciparum:67.6%)
18.49% in spring season (vivax:93.4 and falciparum 6.6%) and 39.9% during
summer season (vivax:89.6% falciparum:10.4%)

This shows that plasmodium falciparum reached its highest frequency in

autumn and winter seasons while plasmodium vivax reached its peak
frequency in spring and summer seasons

There are many reasons why plasmodium favours certain seasons such as
rain fall, climatic change and behaviour of different vectors
 Chikungunya
In the present study, the Chikungunya cases occurred
in the months of November and December - Post
monsoon season.
This artificial water collection is the source of breeding
of the Aedes mosquito.
In other studies, most of the cases occurred between
March to April, thus showing a seasonal variation
 Japanese encephalitis
In temperate areas of Asia, transmission is seasonal, and
human disease usually peaks in summer and fall.

In the subtropics and tropics, seasonal transmission varies

with monsoon rains and irrigation practices and may be
prolonged or even occur year-round.
 Leptospirosis
Leptospirosis is a worldwide zoonotic infection with a much
greater incidence in tropical regions

It has now been identified as one of the emerging infecttious

disease

The epidemiology of leptospirosis has been modified by changes

in animal husbandry (the science of breeding and caring for
farm animals ), climate, and human behavior.

We found that the amount of rainfall was correlated to

leptospirosis cases in both regions of interest, namely the
northern and northeastern region of Asia, while the temperature
played a role in the northeastern region only.
 6. The susceptible population
Identify the at-risk groups or target groups (according to the
defined criteria)
Direct appropriate action to them first (Risk approach)
Risk approach is a managerial device for increasing the efficiency
of health care services within the limits of existing resources.
Something for all, but more for those in need in
proportion to the need.

WONG YONG JIN

Guidelines for defining at-risk
population
 Herd immunity
Immunity plays a crucial role in the dynamics of disease transmission.
The more people are immune, the less likely it is that a pathogen will
find a susceptible person. If enough people are immune, the chance
of the pathogen causing an infection becomes so small that
transmission stops, even though there are still susceptible people.
This is called herd immunity. With poliomyelitis, for example, if 80 to
85 per cent of the entire population is immune, the virus will
disappear. A population can lose its herd immunity through births,
migration of susceptible people into the population, or waning
immunity in the population over time.
 Two important points can be deduced from Figure 3.1:
The immunity in a population is the result of people either
overcoming the infection or being immunised (vaccinated).
The susceptibility of the population in an area increases
through the influx of non-immune people, birth, and from
people losing their immunity (through time or another reason,
such as HIV infection).
 infected people enter a non-immune population, in an environment
favourable to transmission (e.g. infected refugees or migrants enter a
non-endemic area);
susceptible people move into an endemic area (e.g. non-immune
refugees or migrants enter an endemic area; people enter an area
where a zoonosis occurs in an animal population)
the population has lost its resistance or immunity, and the pathogen
is reintroduced (e.g. peoples immunity has diminished over time;
babies have been born; or people are suffering from disease or
malnutrition)
the environment has changed, and has become more favourable to
transmission (e.g. construction of a dam has produced an
environment favourable to mosquitoes (a malaria vector) or snails
(the intermediate host of schistosomiasis)).
 Factors contribute to initiation and
maintenance of an epidemic:
The strain of the virus, which may influence the magnitude and
duration of the viraemia in humans
The density, behaviour and vectorial capacity of the vector
population
The susceptibility of the human population (both genetic
factors and pre-existing immune profile)
The introduction of virus into a receptive community
Dengue Fever/Dengue
Haemorrhagic Fever
Population At Risk (Biological Factor)
 Physical and Socioeconomic Situation
An estimated 500,000 cases of DHF require hospitalization each
year, of which a very large population are children
At least 2.5% of cases die without proper treatment
(Socioeconomic factors income, education, occupation and
political policies)
Living in endemic areas of tropics (or warm, moist climates such
as the southern United States) where the vector mosquito thrives
is an important risk factor for infection
Increased air travel easily transport infectious diseases between
population.
 Rural population (sanitation, access to healthcare resources and etc.)
Household water storage is common and where solid waste disposal
services are inadequate. (Applicable to both the rural and urban slum
population.)

HOWEVER,
Poorly planned rapid urbanization combined with explosive global
population growth brings mosquito and the human host in close
proximity.
A rapid rise in urban population is bringing greater numbers of
people into contact with this vector, especially in areas that are
favourable for mosquitoes breeding. For example, SLUM
Leptospirosis
 Host Factors
1. Age
2. Occupation
3. Socioeconomic status
4. Immunity
 Environmental factors
1. Sanitation
2. Poor housing
3. Limited water supply
4. Inadequate method of waste disposal
Malaria
 Biological factors
1. Age
2. Sex
3. Genetic (Sickle cell anemia)
4. Physiological state: pregnant mother
5. Immunity level/ state
 Socioeconomic factors
Income related to housing issues
Occupation
Education
Political policies on Healthcare resources and
intervention
 Some population groups are at considerable higher risk of contracting
malaria than others
These includes pregnant mothers, infants, children under 5 years of
age and patients with HIV/AIDS as well as non-immune migrants,
mobile populations and travellers
Malaria in pregnant mother women increases the risk of maternal
and fetal anemia, stillbirth and neonatal death.
Malaria in infants born to mother living in endemic areas are more
vulnerable to malaria from three months of age when immunity
acquired from mothers starts to wane.
Malaria in children under 5 years of age are most vulnerable. In 2015
69% of malaria deaths occurred in children under 5 years worldwide.
Malaria in HIV/AIDS patients co-infect and interact between these 2
diseases. HIV infection increases malarial infection while malaria may
results in worsening of clinical AIDS.
Malaria in migrants and mobile populations often lack the partial
immunity and have limited access to prevention an treatment.
Chikungunya Fever
 The susceptible populations
1. Living in endemic regions
2. Age (young and elderly)
3. Occupation (agricultural labour vs white collar)
4. Socioeconomic status (influence on the housing urban vs
rural)
5. Immunity
6. Behaviours (vector-borne disease, stagnant water promote
breeding of mosquitoes)
 Chikungunya is generally spread through bites from Aedes aegypti
mosquitoes, but the chikungunya virus strains in the 2005-2006
Reunion Island outbreak contained a mutation that facilitated
transmission by Aedes albopictus (Tiger mosquito). Enhanced
transmission of chikungunya virus by Aedes albopictus could
mean an increased risk for chikungunya outbreaks in other areas
where the Asian tiger mosquito is present. A recent epidemic in
Italy was likely perpetuated by Aedes albopictus. Currently,
chikungunya fever has been identified in more than 50 countries
Japanese Encephalitis
 Host factors
1. Age (20 to 40 years)
2. Sex (male engage more in outdoor activity)
3. Occupation
4. Socioeconomic status (education, income,
occupation and political policies)
7. Susceptible (sensitive) localities and the
methods employed to recognize the
locations

SHOBENI SELVARAJAH,
NERASHINI TAMILARASAN,
YOGESWARAN MANIAM
Dengue fever/dengue
haemorrhagic fever
 Incidence
rate in 2014

Burden of
dengue in SE Asia
 The first epidemic of dengue hemorrhagic fever (DHF) was described in
Southeast Asia, Manila in 1953. After that, outbreaks of dengue
fever became more common. In the 1950s, 9 countries reported dengue
outbreaks. Epidemic dengue has become more common since the 1980s. By
the late 1990s, dengue was the most important mosquito-borne disease
affecting humans after malaria, with around 40 million cases of dengue
fever and several hundred thousand cases of dengue hemorrhagic fever
each year. Significant outbreaks of dengue fever tend to occur every five or
six months. DHF epidemics occur yearly, with major outbreaks occurring
approximately every 3 years. This pattern has repeated itself as dengue
fever has spread to new regions.

Initial epidemics were located in urban areas, increased dengue spread has
involved suburban and rural locales in Asia and Latin America. The only
continents that do not experience dengue transmission include Europe and
Antarctica. Dengue transmission spread from Southeast Asia into
surrounding subtropical and tropical Asian countries, southern China and
southern Taiwan, the Indian subcontinent and Sri Lanka, and down the
island nations of Malaysia, the Philippines, New Guinea, northeastern
Australia, and several Pacific islands, including Tahiti, Palau, Tonga, and the
Cook Islands .Nepal has not reported dengue transmission. Hyperendemic
transmission is reported in Vietnam, Thailand, Indonesia, Pakistan, India,
Malaysia, and the Philippines. Dengue continues to extend its range.
 Dengue fever has been endemic in Malaysia since 1901 and reached
epidemic proportions in 1973. In 1982, Malaysia experienced a major
dengue/dengue hemorrhagic fever outbreak, which has affected all
states in Peninsular and East Malaysia. Since then, dengue has
became a major public health problem especially among the highly
urbanized states in Malaysia.

Most vulnerability mapping of dengue has been done in small local

hotspot areas, e.g. in Subang Jaya, Selangor (Nazri et al. 2009; Dom et
al. 2013) and Hulu Langat District, Selangor (Er et al. 2010). There is
still a lack of evidence for dengue risk in a larger area including
Selangor, Kuala Lumpur and Putrajaya. Hassan et. al. (2012) for
example, conducted vulnerability mapping in Selangor and Kuala
Lumpur, but only for an aggregated district level. Moreover, to our
knowledge, there is no study that compares the disease clustering
pattern on different geographical scales, e.g. at sub-district and
address level.
 Malaria
Figure 1
Malaria is one of the most important public health problem in term of morbidity and
mortality, causing more than 200 million cases and 655.000 deaths every year.1

According to the World Health Organization (WHO) Malaria Report 2011, a total of 106
countries in the world are at risk of transmission of malaria infection.( Figure 1)

A total of 216 million estimated malaria cases occurred in 2010, 81% of which were
reported in the African Region, followed by South East Asia (13%) and Eastern
Mediterranean Region (5%). The total number of malaria deaths was estimated to be
655.000 in 2010; 91% of whom occurred in the African Region, 6% in South-East Asia
and 3% in Eastern Mediterranean Region. (Table 1)

Absolute number of people at risk for malaria infection increased from 0.8 billion in
1900 to 3.3 billion in 2010, as a consequence of the absolute increase of the
population living in malaria-endemic regions.

However, between 2005 and 2010 malaria cases decreased from 244 million to 216
million; moreover, malaria mortality rates showed a global reduction of 26% between
2000 and 2010
Table 1

WHO region Malaria cases (%) Malaria deaths (%)

African Region 81 91
South East Asia 13 6
Eastern Mediterranean
5 3
Region
Others 1 <1
Malaria cases in Malaysia have been on the decline from 12,705 cases in 2000 to 4,725 cases in
2012. The incidence rate declined from 0. 55 per 1,000 population in 2000 to 0.16 per 1,000
populations in 2012. For the past decade (2000 2012), malaria cases has reduced from 3,918
cases to 1,097 cases in Peninsular Malaysia, from 3,011 cases to 1,571 cases in Sarawak and
from 5,776 cases to 2052 cases in Sabah. There has also been a reduction in the number of
malaria deaths from 35 in 2000 and to 16 deaths in 2012. The Case Fatality Rate of malaria has
been around 0.3 to 0.5 per 100,000 population since 2006.

In 2012, of the 4,725 reported cases, 61.6% were human malaria infection and a significant
proportions (38.4%) were zoonotic. Among human malaria infection, P. vivax accounted for
50.2%, followed by P. falciparum (30.7%), P. malariae (16.7%) and mixed infection (2.2%). Of the
human malaria, 2051 cases (70.4%) were indigenous cases and a small proportion of 861 cases
(29.6%) were imported.

Of the indigenous malaria 74.0% were reported from Sabah followed by 15.9% from Sarawak
and 10.1% from Peninsular Malaysia. Of the zoonotic malaria, 56.9% were reported from
Sarawak followed by 23.3% from Peninsular Malaysia and 19.8% from Sabah. In Peninsular
Malaysia, Selangor, Pahang, Kelantan and Perak reported more than 100 cases throughout the
year 2012. A big proportion (78.2%) of the cases were among male with only 21.8% among
female. About 8.5% of the female patients were pregnant.

Children below the age of 5 accounted for 2.5% of all cases whilst those mostly affected were in
the age group of 20 29 years (25%). About 61.9% of the cases were between the ages of 20 to
49 years.
CHIKUNGUNYA
 Chikungunya likely originated in Africa (see also section History of
Chikungunya), where the virus is spread via a sylvatic cycle in which
the virus largely resides in other primates in between human
outbreaks. In 1952, the first outbreak of chikungunya was reported in
the Makonde Plateau. The first significant urban outbreaks of
chikungunya were reported in the early 1960s in Bangkok and from
1963 through 1973 in India. The chikungunya virus was detected
mainly in the Indian cities Calcutta, Maharashtra and Yellore. Minor
outbreaks periodically occurred over the next 30 years, but no major
outbreaks were recorded. In 1969, chikungunya was detected in Sri
Lanka and in 1975 the disease was reported in Vietnam and
Myanmar. Another outbreak was reported in Indonesia in 1982.
 As of January 2015 at least one major city (Medelln) in Colombia has
issued sanitary alerts due to the expanding epidemic. By January
2015 the epidemic is considered to be in the initial expansion phase
and it is expected by the Colombian National Health Institute
(Instituto Nacional de Salud - INS) that the total number of cases will
reach around 700,000 by the end of 2015 due to the in-country
massive travel of tourists to and from regions where cases of the
disease have been confirmed and the vector is indigenous. It is
expected that the disease will become endemic and sustain itself,
with a pattern of outbreaks similar to dengue fever, due to the fact
that both vector and natural reservoirs are indigenous in large areas
of the country.
On 24 September 2015, the Ministry of Health and Social Protection
of Colombia officially declared the country free of Chikungunya.
There were 441,000 reported cases but the government stimated the
infected to reach the 873,000.
Japanese encephalitis
JE virus is the most common vaccine-preventable cause of encephalitis
in Asia, occurring throughout most of Asia and parts of the western
Pacific (Map 3-08). Local transmission of JE virus has not been detected
in Africa, Europe, or the Americas. Transmission principally occurs in
rural agricultural areas, often associated with rice cultivation and flood
irrigation. In some areas of Asia, these ecologic conditions may occur
near, or occasionally within, urban centers. In temperate areas of Asia,
transmission is seasonal, and human disease usually peaks in summer
and fall. In the subtropics and tropics, seasonal transmission varies with
monsoon rains and irrigation practices and may be prolonged or even
occur year-round.

In endemic countries, where adults have acquired immunity through

natural infection, JE is primarily a disease of children. However, travel-
associated JE can occur among people of any age. For most travelers to
Asia, the risk for JE is extremely low but varies based on destination,
duration, season, and activities.
From 1973 through 2013, 68 JE cases among travelers or expatriates from
nonendemic countries were published or reported to CDC. From the time JE
vaccine became available in the United States in 19932013, only 8 JE cases
among US travelers were reported to CDC.

The overall incidence of JE among people from nonendemic countries traveling

to Asia is estimated to be <1 case per 1 million travelers. However, expatriates
and travelers who stay for prolonged periods in rural areas with active JE virus
transmission are likely at similar risk as the susceptible resident population (5
50 cases per 100,000 children per year). Travelers on even brief trips might be
at increased risk if they have extensive outdoor or nighttime exposure in rural
areas during periods of active transmission. Short-term (<1 month) travelers
whose visits are restricted to major urban areas are at minimal risk for JE. In
some endemic areas there are few human cases among residents because of
natural immunity among older people or vaccination; however, JE virus is
usually still maintained in these areas in an enzootic cycle between animals
and mosquitoes. Therefore, susceptible visitors may be at risk for infection.
Japanese encephalitis virus (JEV) is an important encephalitis virus in
Asia, but there are few data on Malaysia.

A hospital-based surveillance system for Japanese encephalitis (JE) has

been in operation in
Sarawak, Malaysia, for the last 10 years.

JEV is endemic in Sarawak, with cases occurring throughout the year

and a seasonal peak in the last quarter (one-way anova, P < 0.0001).

Ninety-two per cent of 133 cases were children aged 12 years or

younger; the introduction of JE vaccination in July 2001 reduced the
number of JE cases .

After implementation of the programme, the mean age of infected

children increased from 6.3 to 8.0 years
Leptospirosis
 Leptospirosis occurs worldwide but is most common in tropical and
subtropical areas with high rainfall.
The actual incidence of Leptospirosis in Hawaii is estimated to be
double the reported incidence.
A study in Peru demonstrates high levels of under-diagnosis of
Leptospirosis and under-recognition of severe complications
especially in urban areas.
A study from Gabon shows that over 15% of people in slum
communities show evidence of infections with Leptospira.
Unusual flooding in Bangladesh, India, and Sri Lanka caused
overflowing of rodent-infested sewers exposing inhabitants to
Leptospirosis infection.
Leptospirosis soared across Central America following Hurricane
Mitch (1998).
Global travel to high-risk areas increases the exposure of individuals
to Leptospirosis.
 Leptospirosis is an emerging disease, especially in countries with a
tropical climate such as Malaysia. A dramatic increase in the number
of cases has been reported over the last decade; however,
information on the epidemiological trends of this disease is lacking.
The objective of this study is to provide an epidemiological
description of human leptospirosis cases over a 9-year period (2004-
2012) and disease relationship with meteorological, geographical,
and demographical information.
 8. Prevention, promotion and control
measures
Dengue
Malaria
Chikungunya
Japanese Encephalitis
Leptospirosis

WHO website; K park textbook LIM YIN YEE

 Dengue
1. Mosquito control
Consists of anti-larval and anti-adult measures
Break the channel of transmission
Eg: flower-vase and air coolers must be periodically emptied
and kept dry at least for a day before they are refilled, a
measure not adopted and predisposed for epidemic.

2. Vaccines
One dengue vaccine has been licensed,
Dengvaxia (CYD-TDV)
What is Dengvaxia (CYD-TDV)?

first dengue vaccine to be licensed.

It was first licensed in Mexico in December 2015 for use in

individuals 9-45 years of age living in endemic areas.

CYD-TDV is a live recombinant tetravalent dengue vaccine.

Given as a 3-dose series on a 0/6/12 month schedule.

 preventing mosquitoes from accessing egg-laying habitats by
environmental management and modification
disposing of solid waste properly and removing artificial man-made
habitats
covering, emptying and cleaning of domestic water storage
containers on a weekly basis
applying appropriate insecticides to water storage outdoor
containers
using of personal household protection such as window screens,
long-sleeved clothes, insecticide treated materials, coils and
vaporizers;
applying insecticides as space spraying during outbreaks as one of
the emergency vector-control measures
active monitoring and surveillance of vectors should be carried out
to determine effectiveness of control interventions.
 Malaria
*Long-lasting insecticidal nets (LLINs) and indoor residual
spraying (IRS).

LLINS
-Sleeping under a net treated with an effective insecticide can reduce
contact between mosquitoes and humans by providing both a physical
barrier and an insecticidal effect.
- Current WHO-recommended LLINs contain pyrethroid insecticides
only.

Indoor residual spraying (IRS).

- -Sprayed typically once or twice a year
- -Sprayed on indoor walls and ceilings where malaria vectors are likely
to rest after biting.
Breaking the Channel of Transmission

This measure consists of control of vectors.

The different methods of control of vectors are:
a. Anti-adult measures
b. Anti-larval measures
(a) Anti-adult measures
(i) Residual spraying: Dichlorodiphenyltrichloroethane (DDT)
-Melathion and fenitrothoin are organophospate insecticides which
are being use with increasing frequency for malaria control following
the development of vector resistance to DDT.

(ii)Space application: application of pesticides in form of mist or fog.

(iii) Individual protection: repellents, bed nets, protective clothings,

mosquito coils
(b) Anti-larval measures
(i) Larvicides: Temephos -confer long effect with low toxicity
-larvicides must be repeated at frequent intervals.

(ii)Source reduction: Reduce mosquito breeding sites eg: drainage or

filling, flushing, management of water level, change salt content of
water and intermittent irrigation.

(iii)Integrated control: bioenvironmental and personal protection

-this is to reduce dependence on residual insecticides
 Chikungunya
(a) Vector control
-A.aegypti; keep water storage containers free of mosquitoes,
eliminate other breeding places around house.
-Organophosphate: Abate is being used as larvicides and can prevent
breeding up to 3 months when applied in sand granules. It does not
harm man and does not alter the taste of water.
-Aerosal spray of ultra low volume (ULV) quantities of malathion or
sumithion (250ml/hectare) is also effective.

(b) Vaccine
-No suitable vaccine has yet been developed
 Japanese Encephalitis
Vector Control:
- Aerial or ground fogging with ULV insectides such as malathion
and fenitrothion. Uninfected villages 2km-3km radius away of
infected villages should also receive spraying as preventive
measure.
-Use of mosquito nets.

Vaccination:
There are 4 main types of JE vaccines currently in use:
inactivated mouse brain-derived vaccines
inactivated Vero cell-derived vaccines
live attenuated vaccines
live recombinant vaccines
-In Sarawak, JE vaccination is given to babies at 9m
and booster in 18/21m
 Leptospirosis
Prevention:
prevent swimming in water that might be contaminated with
animal urine.
eliminate contact with potentially infected animals.
protective clothing or footwear should be worn
Antibiotics
Penicillin is the DOC but tetracycline or doxycycline are also effective.
Dosage of penicillin is 6 millions units daily IV.
Doxycycline is reported to give some degree of protection to exposed
individuals from non-endemic areas. However, even if it does not
always prevent infection, it can reduce the severity of the disease and
thus mortality and morbidity.

Vaccination
Human vaccines are available only in a few countries, such as China.
Animal vaccines only cover a few strains of the bacteria. Dog
vaccines are effective for at least one year.
Source of Reference:
-WHO website: http://www.who.int/en/
-K Park Textbook of Preventive and Social
Medicine
9. Management the illness
Dengue
Malaria
Chikungya
Japanese Encephalitis
Leptospirosis

ONG YU KI
 Dengue
Clinical features of dengue are rather non-specific and mimcs
many other diseases.
Disease notification
All suspected dengue cases from private and public health
facilities must be notified to the nearest health of centre
within 24 hours of diagnosis.
Failure to notify is liable to be compounded under the
Prevention and Control of Infectious Diseases Act, 1988 (Act
342).
 TYPE OF TESTS FOR DENGUE DIAGNOSIS

Type of test Technique When To Test Sensitivity

i (%) Specificty (%
)

1. Antibody IgM Detection 4 days after onset of 61.5-100 52.0-100

Detection symptoms and up to 3
months in primary dengue.
3 days after onset of
symptoms and sometimes
hindered by large scale
IgG production in
secondary dengue

IgG Detection 10 days after onset of 46.3-99.0 80.0-100

symptom in primary
dengue and 3 days after
onset of symptoms in
secondary dengue

Rapid IgM 5 days after onset of 20.5-97.7 76.6-90.6

Detection symptoms and up to 2
(Strips) months
2.Antigen/ NS1 and IgM As this is a combo test, 89.9-92.9 75.0 100
Antibody Combo Kit useful in early stage of
Combined infection (day 3 onwards)
Detection and up to sero conversion
period (up to 2 weeks)
NS1 and IgM/ As this is a combo test, 93.0 100
IgG Combo kit useful in early stage of
infection (day 3 onwards)
and up to sero conversion
period (up to 2 weeks
onwards). In the event
of both NS1 and IgM are
non reactive and IgG is
reactive, case can be
interpreted as secondary
dengue.
3. Viral Virus Isolation 1-5 days of onset of 40.5 100
Detection (cell culture) symptoms in Primary
Dengue and 1-4 days
after onset of symptoms in
secondary dengue

Virus Isolation - same as above- 71.5-84.2 100

(mosquitoes)

Viral RNA - same as above- 48.4-100 100

RT-PCR
(Conventional)

Viral RNA - same as above- 58.9-100 100

RT-PCR (Real
Time)

Viral Antigen 1-7 days of onset of 54.2-93.4 92.5-100

(NS1) symptoms in Primary
Dengue and 1-5 days
after onset of symptoms in
secondary dengue
TYPE OF DENGUE TESTS RECOMMENDED BASED ON CLINICAL HISTORY

Clinical Test Result Interpretation

History
History of Dengue NS1 Ag Positive Acute dengue infection.
fever less or RCT
than 5 Negative Dengue infection still cannot rule out.
days Suggest to send second sample for
Dengue IgM after day 5 of fever
History of Dengue IgM Positive Presence of detectable IgM antibody.
fever more Suggestive of recent dengue infection
than 5
days Indeterminate Advice to repeat the test.

Negative The result does not rule out dengue

infection. Advice to send repeat sample
for dengue IgM after day 7 of fever or ask
for Dengue IgG test.
History of Dengue IgG Positive Elevated IgG levels are seen in acute or
fever more past infections.
than 5 A titre of equal or more than 1:2560 is
days and consistent with acute secondary infection.
Dengue
IgM and /or Indeterminate Advice to repeat the test if clinically
NS1 was indicated.
negative
Negative No detectable elevated IgG antibody. The
absence of elevated IgG is presumptive
evidence that the patient does not have
secondary dengue infection.
 Diagnostic Tests
Rapid combo Test
can detect the presence of virus as well as antibodies
simultaneously
useful during the early phase of onset when there is
viraemia as well as at a later stage when antibodies against
dengue begin to rise
 Dengue Antigen and Serology Tests by
ELISA
Non-structural Protein-1 (NS1 Antigen)
Secretion of the NS1 protein is a hallmark of flavivirus infecting mammalian
cells and can be found in dengue infection as well as in yellow fever and West
Nile virus infection. False positive results have been reported in chronic diseases
and haematological malignancies.
The presence of NS1 detection after day 5 may predict severe dengue.

Dengue IgM test

most widely used serological test
antibody titre is significantly higher in primary infections compared to
secondary infections
primary dengue infection detected in 80% after 5 days, 93-99% in day 6-10
secondary dengue infections - detected in 78% after day 7

Dengue IgG test

Detected in 100% of patients after day seven of onset of fever
 False positive dengue serology

Serological tests for dengue have been shown to cross-react

with:
other flavivirus Japanese Encephalitis
non- flavivirus malaria, leptospirosis, toxoplasmosis,
syphilis
connective tissue diseases rheumatoid arthritis
 Dengue Viral RNA Detection (Real
time RT-PCR)
molecular method that utilises reagents that will target
specfic genome of the virus to enable amplification and
detection of the target
useful only during the viraemic stage of the disease and can
detect the viral RNA target up to 5 days after onset of the
symptoms
useful for determination of circulating dengue serotypes in
the country.
 Plan of management
1. Dengue assessment checklist must be filled by the attending
doctor
2. Notify the district health of centre (refer to Chapter 4 on disease
notification) followed by disease notification form
3. If admission is indicated (refer to admission criteria)
Stabilise the patient at primary care before transfer (intravenous
fluid regime)
Communicate with the receiving hospital/Emergency Department
before transfer
4. If admission is not indicated
Daily follow up is necessary especially from day 3 of illness
onwards until the patient is afebrile for at least 24-48 hours
without antipyretics.
Provide the patient with Outpatient Dengue Monitoring Record
and Home Care Advice Leaflet for Dengue Patients
 Disease monitoring tests
White cell count (WCC) and Platelet count:
In the early febrile phase WCC and platelet count are usually normal but will
decrease rapidly as the disease progresses. The decrease in WCC is
accompanied by platelet reduction.
There is no correlation between disease severity and platelet count and it is not
predictive of bleeding. In recovery phase, the WCC normalises followed by
platelet.

Haematocrit (HCT):
A rising HCT is a marker of plasma leakage in dengue infection. The median
values of normal HCT level among Malaysian populations are: 33
male < 60 years 46%
male > 60 years 42%
Female (all age groups) 40%

Other important blood tests in disease monitoring are LFT, RP, coagulation
profile, lactate and blood gases.
 Parameters for Frequency of monitoring
monitoring Febrile phase Critical phase Reabsorption
phase
Clinical Parameters

General well being Daily or more At least twice a day Daily or more
Appetite / oral intake frequently towards late and more frequently as frequently as indicated
Warning signs febrile phase indicated

Haemodynamic
status
CCTVR
BP
Pulse pressure 2-4 hourly depending
on clinical status
Respiratory status 4-6 hourly depending
RR on clinical status In shock 4-6 hourly
SpO2 Every 15-30 minutes till
stable then 1-2 hourly
Neurological Status
conscious level
restlessness
seizures

Urine output 4 hourly 2-4 hourly 4-6 hourly

In shock : Hourly
 Parameters for Frequency of monitoring
monitoring Febrile phase Critical phase Reabsorption
phase
Laboratory Parameters and Imaging

All investigations done at ED must be reviewed immediately upon ward admission

4-12 hourly depending

on clinical status

FBC Daily or more In shock Daily

frequently as indicated Repeated before i and
after each flud
resuscitation and as
indicated

At least daily or more

BUSE/Creatinine frequently as indicated
LFT + AST As clinically indicated As clinically
RBS In shock indicated
Creatine Kinase Crucial to monitor ABG
and lactate closelye

ABG, lactate As clinically indicated As clinically indicated As clinically indicated

Coagulation profil
CRP
Troponin or CKMB
Fibrinogen, LDH,
ferritin,
triglyceride
ECG
Echocardiogram
Ultrasound
 In non shock dengue patients, increased oral fluid intake may
be sufficient in those who are haemodynamically stable and
not vomiting. Inappropriate IV fluid therapy had been shown
to prolong hospitalisation with a tendency to develop more
fluid accumulation
 Dengue fever IV management
In non shock dengue patients, increased oral fluid intake may be sufficient
in those who are haemodynamically stable and not vomiting. Inappropriate
IV fluid therapy had been shown to prolong hospitalisation with a tendency
to develop more fluid accumulation
In dengue patients without co-morbidities who can tolerate orally,
adequate oral fluid intake of two to three lit. daily should be encouraged.
These patients may not require IV fluid therapy.
IV fluid should be instituted in dengue patients with:
vomiting, unable to tolerate oral fluids or severe diarrhoea
increasing haematocrit (with other signs of ongoing plasma leakage)
despite increased oral intake
In patients with persistent warning signs with increasing or persistently high
HCT, the graded fluid bolus may be initiated with caution.
Crystalloids solution should be the fluid of choice for non-shock dengue
patients.
Calculation for maintenance of IV fluid
Table 7 : Calculations for maintenance of intravenous flud inf usi on
infusion
Non-obese patients

1.2 to 1.5 ml/kg/hour

Adapted : National Clinical Guideline Centre (UK). Intravenous Fluid

Therapy: Intravenous Fluid Therapy in Adults in Hospital
[Internet]. London: Royal College of Physicians (UK); 2013 Dec.
i Available from http://www.ncbi.nlm.nih.gov/books/NBK247761/

Obese patients (BMI

i >27.5 kg/m2)*

Maintenance flud can be cal cul at ed based on adj ust ed body we i ght

Adjusted bodyweight (ABW) can be calculated using the

formula.
o ABW = IBW + 0.4 (actual weight - IBW)**

o Ideal bodyweight (IBW) can be estimated based on the

following formula. 72, level III
Female: 45.5 kg + 0.91(height in cm -152)
Male: 50.0 kg + 0.91(height in cm -152)
 adjusted according to clinical response. Use of volumetric
pumps is encouraged, especially in patients requiring close
i
flud mo ni tor ing.

Table 8 : Graded Fluid Bolus Regime

Obtain a baseline
i HCT before flud ther apy .
Give crystalloids solution (such as 0.9% saline).
Start with 5 ml/kg/hour for 12 hours, then reduce to 3 ml/kg/hr for 24
hours, and then reduce to 2 ml/kg/hr or less according to the clinical
i response.
If the clinical parameters are worsening and HCT is rising, increase the
rate of infusion.
Reassess the clinical
i status, repeat the HCT and review flud inf usi on
rates accordingly.
 Management of dengue shock
syndrome
Dengue shock syndrome is a medical emergency. Recognition
of shock in its early stage (compensated shock) and prompt
fluid resuscitation will give a good clinical outcome but failure
to recognise the phase of compensated shock will ultimately
lead to decompensated (hypotensive) shock with a more
complicated disease course and organ failures.
All patients with dengue shock should be managed in high
dependency or intensive care units.
Following initial resuscitation there maybe recurrent episodes
of shock because capillary leakage can continue for 24-48
hours.
 IV fluid therapy is the mainstay of treatment for dengue
shock.
The volume of initial and subsequent fluid resuscitation
depends on the degree of shock and can vary from 10-20
ml/kg adjusted body weight.
Patients with DSS who do not respond to initial crystalloid
resuscitation should receive colloids as the second fluid bolus.
In DSS with persistent shock, other causes of shock should be
aggressively looked for and treated accordingly.
Table 9 : Fluid Responsiveness Parameters

A. Clinical response parameters

Improvement of general well being/mental state
Warm peripheriesl
Capillary refil tim
e <2sec
BP stable
Improving pulse pressure
Reducing tachycardia
Improving urine output
Less tachypnoea
B. Laboratory parameters
Appropriate decrease in HCT
Improvement in metabolic acidosis and lactate clearance
C. Imaging parameters (recommended but not mandatory)

Improvement of IVC collapsibility index (spontaneous breathing patient)

IVC expiratory diameter IVC inspiratory diameter

X 100 = Caval index (%)
IVC expiratory diameter
* Caval index close to 100% is indicative of almost complete collapse, therefore
volume depletion and 0% suggests
i minimal collapse i.e. likely volume overload.
>40% collapse
m will be flud responsi ve. 72

Adapted : Goldfla K, Saul T and Lewiss R. Focus on: inferior vena cava
ultrasound. ACEP News 6. 2011. pp 24-25. (available at : http://www.acep.org/
Content.aspx?id=80791 )

CAUTION : IVC assessment should be performed by trained personnel and not

to be interpreted in isolation.
 ALGORITHM A - FLUID MANAGEMENT IN COMPENSATED SHOCK ALGORITHM C - FLUID MANAGEMENT IN DECOMPENSA TED SHOCK
ALGORITHM B - FLUID MANAGEMENT IN DECOMPENSA TED SHOCK
(WITH PRESENCE OF BLEEDING & LEAKING OR OTHER CAUSES OF SHOCK)
DECOMPENSATED SHOCK
COMPENSATED SHOCK Fluid resuscitation with 20 ml/kg colloid / crystalloid within 15 - 30 minutes
(systolic pressure maintained but has signs of reduced perfusion) HAEMATOCRIT REMAIN UNCHANGED AFTER
Obtain HCT/FBC, RP, LFT, RBS, PT/APTT, CK, Lactate/HCO i 3
, GXM1 before flud
Fluid resuscitation with isotonic crystalloid 5-10 ml/kg/hr for 1 hour
l resuscitation. FIRST FLUID RESUSCITATION
Obtain FBC, HCT, RP, LFT, RBS, PT/APTT, CK, Lactate/HCO i 3
, GXM1 before flud
resuscitation.
IMPROVEMENT*
YES NO
Consider other causes of shock

Review HCT

IMPROVEMENT* Crystalloid/colloid 10ml/

YES NO kg/hr for 1 hour, then
continue with:

Check HCT IV crystalloid HCT or HCT HCT unchanged Bleeding and leaking at Severe metabolic
5-7 ml/kg/hr for same time acidosis with
IV crystalloid 5-7 ml/kg/hr for 1-2 hours; then hyperlactataemia (liver
1-2 hours, then: Administer 2 nd
i Consider a REFER TO Look for source of bleeding + multiorgan failure)
reduce to 3-5 bolus of flud significnt ALGORITHM C
ml/kg/hr for 2-4 (eg. OGDS)
reduce to 3-5 ml/kg/hr (colloid)^ occult/overt
hours; then
10-20 ml/kg bleed Vasopressor
for 2-4 hours; then Evidence of leaking (USG,
over to 1 hour Initiate transfusion +
reduce to 2-3
ml/kg/hr for 2-4 with packed red chest X-ray)
reduce to 2-3 ml/kg/hr
for 2-4 hours hours cells and /or blood Supportive care
components Check for coagulopathy
HCT or high HCT If patient continues to +
If patient continues to improve,
i flud can be
improve,
i flud can be further Transfuse packed red cells Continuous renal replacement
further reduced. YES and blood components therapy (CRRT)
reduced.
Monitor HCT 4 hourly IMPROVEMENT*
Monitor HCT 4-6 hourly. Administer 2 nd bolusi Consider significnt or more frequent as NO
of flud (col loi d) ** occult/overt bleed indicated.
If the patient is not stable, 10-20 ml/kg/hr for 1 hour Initiate transfusion with Repeat 2nd HCT
If the patient is not
act according to HCT packed red cells and/or Septic shock Cardiac dysfunction Cytokine storm
stable, act according
levels: blood components to HCT levels:

if HCT increases, if HCT increases, Vasodilated state Noradrenaline

i
consider bolusi consider and fluds
flud administration bolus
i flud HCT or high HCT Noradrenaline
or increase
i flud NO administration titrated to MAP Check for disease
or increase
i flud
administration IMPROVEMENT* administration; 65 mmHg markers of
haemophagocytic
if HCT decreases, if HCT syndrome
Administer 3 rd bolusi of
consider transfusion YES decreases,
flud (col loi d) 10- 20 ml /kg Low CO : High CO :
with packed red consider
over 1 hour
cells and/or blood transfusion with Inotrope Vasodilated shock with
components packed red cells (eg. dobutamine/
If patient improves, reduce to adrenaline) myocardial dysfunction
7-10 ml/kg/hr for 1-2 hours Consider to stop
Consider to stop IV i flud at NO
IV i flud at 48 hours Inotropes + vasopressor
48 hours of plasma leakage/ of plasma leakage/ Repeat
a
Then reduce further IMPROVEMENT* (eg. noradrenaline +
defervescence. defervescence. 3rd HCT
dobutamine /adrenaline)

* Reassess the patients clinical condition, vital signs, pulse volume, capillary refil YES
time, urine output and temperature of extremities. * Reassess the patients clinical condition, vital signs, pulse volume, capillary
l refil time All the above types of shocks need to be supported by echocardiography and non-
and temperature of extremities. invasive cardiac output monitoring and treatments tailor to each patient.
** Colloid is preferable if the patient has already received previous bolus of crystalloid ^ Colloid is preferable if the patient has already received previous bolus of crystalloid.
IV = intravenous ; HCT = haematocrit IV = intravenous ; HCT = haematocrit HCT = haematocrit ; MAP = mean arterial pressure ; CO = cardiac output;
= increased ; = decreased = increased ; = decreased OGDS = oesophagogastroduodenoscopy USG = ultrasonography
1
1
GXM: emergency cross-match GXM: emergency cross-match
 Metabolic acidosis
Compensated metabolic acidosis is an early sign of shock due
to leakage or bleeding. Lactic acidosis due to tissue hypoxia
and hypoperfusion is the most common cause of metabolic
acidosis in dengue shock.
Monitoring of blood lactate levels in severe dengue. A lactate
level of <2 mmol/L in a critically ill patient generally implies
that the patient has adequate tissue perfusion, although
higher levels are not necessarily the result of tissue hypoxia
Correction of shock and adequate fluid replacement will
correct the metabolic acidosis.
 ABG

ABG- frequently done (2-4 hourly) in patients with shock

mainly for detection of worsening acidosis by looking at base
excess, bicarbonate, CO2 and lactate.
Mixed respiratory alkalosis with metabolic acidosis (CO2 lower
than expected) commonly seen in liver failure, dengue
encephalitis and sepsis. This is seen in patients with pleural
effusion and moderate ascites as they are tachypnoeic.
Hypoxaemia is a guide to warn us of fluid overload, pleural
effusion and interstitial oedema.
Electrolyte and acid-base imbalances
All patients with severe dengue should be monitored for
electrolytes imbalances such as hyponatraemia and
hyperkalaemia.
Presence of hyponatraemia is a common observation in
severe dengue and a marker of disease severity
Other electrolytes that need to be monitored are :-
serum calcium
serum phosphate
serum magnesium
 Malaria
Giemsa-stained blood smear
Thick smear provide efficient evaluation of large volumes of
blood
Thin smear are better for discrimination of parasite species
Single smears are usually +ve for infected individuals
Diagnostic is rapid diagnostic test to identify circulating
plasmodial antigens with simple dipstick format
Serologic treatment indicate h/o disease but not useful for
diagnosis of acute infection
PCR and molecular tests (eg LAMP) are high sensitivity but not
available routinely .
 Treatment
Non-falciparum Malaria
First line : Chloroquine
But due to increasing resistance , Artemisinin-bases
combination therapy (ACTs)
P vivax / P. ovale eradication of erythrocytic parasites
with chloroquine should be acc. by treatment of
primaquine (after evaluatiing G6PD defi.) to eradicate
dormant liver stages (hypnozoites) which may lead to
relapse with recurrent erthrocytic infection and malaria
symptoms
Tafenoquine related to primaquine offer similarity
efficacy with simpler dosing , but engenders potential
toxicity in G6PD defi.
 Treatment
Uncomplicated Falciparum
Malaria
P. falciparum is resistance to
chloroquine and sulfadoxine
pyrimethamine in most areas
ACTs are first line treatment
WHO recommends 6 ACTs to
treat falciparum malaria
 Treatment
Severe malaria (medical emergency)
IV artesunate - 4 doses of 2.4mg/kg over 3 days , every 12
hours on day 1 and then daily
If unavailable, intrarectal administration of artemether /
artesunate
If IV quinine / quinidine cardiac monitoring
If QTc prolongation >25% baseline , infusion rate should
be reduced
Monitor blood glucose every 4-6 h & 5-10% dextrose may be
co-adminstered to decrease likehood of hypoglycemia
Appropriate care : maintenance of fluids and electrolytes ,
respiratory and haemodynamic supports , consideration of
blood transfusion , anticonvulsants, antibiotics for bacterial
inf. And hemofiltration or hemodialysis
Chemoprohylaxis
 Japanese encephalitis
Clinical laboratory findings
moderate leukocytosis, mild anemia, and hyponatremia.
Cerebrospinal fluid (CSF) typically has a mild to moderate
pleocytosis with a lymphocytic predominance, slightly elevated
protein, and normal ratio of CSF to plasma glucose.
Magnetic resonance imaging (MRI) of the brain is better than
computed tomography (CT) for detecting JE virus-associated
abnormalities such as changes in the thalamus, basal ganglia,
midbrain, pons, and medulla. Thalamic lesions are the most
commonly described abnormality; although these can be highly
specific for JE in the appropriate clinical context, they are not a very
sensitive marker of JE.
EEG abnormalities may include theta and delta coma, burst
suppression, epileptiform activity, and occasionally alpha coma.
 Japanese encephalitis Diagnostic
Testing
Test of serum or cerebrospinal fluid (CSF) to detect virus-specific
IgM antibodies. JE virus IgM antibodies are usually detectable 3 to 8
days after onset of illness and persist for 30 to 90 days, but longer
persistence has been documented. Therefore, positive IgM
antibodies occasionally may reflect a past infection or vaccination.
Serum collected within 10 days of illness onset may not have
detectable IgM, and the test should be repeated on a convalescent
sample. For patients with JE virus IgM antibodies, confirmatory
neutralizing antibody testing should be performed. In fatal cases,
nucleic acid amplification, histopathology with
immunohistochemistry, and virus culture of autopsy tissues can
also be useful.
Diagnostic testing for JE virus IgM antibodies is commercially-
available. Confirmatory testing is only available at CDC and a few
specialized reference laboratories.
 Japanese encephalitis
Treatment
No specific treatments have been found to benefit patients with
JE, but hospitalization for supportive care and close observation
is generally required.
Treatment is symptomatic. Rest, fluids, and use of pain relievers
and medication to reduce fever may relieve some symptoms.
Patients often require feeding, airway management, and
anticonvulsants for seizure control.
 Inactivated Vero cell culture-derived Japanese
encephalitis (JE) vaccine
JE vaccine is recommended for travelers who plan to spend 1 month or more in
endemic areas during the JE virus transmission season. This includes long-term
travelers, recurrent travelers, or expatriates who will be based in urban areas but
are likely to visit endemic rural or agricultural areas during a high-risk period of JE
virus transmission.
Vaccine should also be considered for the following:
Short-term (less than1 month) travelers to endemic areas during the transmission
season, if they plan to travel outside an urban area and their activities will increase
the risk of JE virus exposure. Examples of higher-risk activities or itineraries include:
1) spending substantial time outdoors in rural or agricultural areas, especially
during the evening or night; 2) participating in extensive outdoor activities (such as
camping, hiking, trekking, biking, fishing, hunting, or farming); and 3) staying in
accommodations without air conditioning, screens, or bed nets.
Travelers to an area with an ongoing JE outbreak.
Travelers to endemic areas who are uncertain of specific destinations, activities, or
duration of travel.
JE vaccine is NOT recommended for short-term travelers whose visits will be
restricted to urban areas or times outside a well-defined JE virus transmission
season.
 Management of Chikungunya

CPG Malaysia and K park

 Laboratory diagnosis
The confirmation of Chikungunya fever is through any of the
followings:
o Isolation of virus
o PCR
o Detection of IgM antibody (ELISA)
o Demonstration of rising titre of IgG antibody

IgM antibodies demonstrable by ELISA may appear within two weeks.

It may not be advisable to do the antibody test in the first week. In
some persons it may take six to twelve weeks for the IgM antibodies
to appear in sufficient concentration to be picked up in ELISA.

If a serologic test for IgG was done, remember to draw a second

blood sample after a gap of 2-4 weeks.
 No significant pathognomonic hematological finding is seen.
o Leucopenia with lymphocyte predominance is the usual
observation.
o Thrombocytopenia is rare.
o Erythrocyte sedimentation rate is usually elevated.
o C-Reactive Protein is increased during the acute phase and
may remain elevated for a few weeks.
o A small proportion of patients have tested positive for
rheumatoid factor during and after clinical episode.
 Clinical Management
There is no specific antiviral drug against CHIK virus.
Treatment is entirely symptomatic.
Paracetamol is the drug of choice with use of other analgesics if
paracetamol does not provide relief. (up to two 500mg tablets four
times daily), in persons with no preexisting liver or kidney disease.
If the case has already been treated with paracetamol/ other
analgesics, start one of the NSAIDS (as per standard
recommendations). Monitor for any adverse side effects of NSAIDS.
During the acute stage of the disease, steroids are not usually
indicated because of the adverse effects.
Aspirin is preferably avoided for fear of gastrointestinal and other
side effects like Reyes syndrome.
 Cutaneous manifestations can be managed with topical or systemic
drugs.
Use hydroxychloroquine 200 mg orally once daily or chloroquin
phosphate 300 mg orally per day for a period of four weeks in
cases where arthralgia is refractory to other drugs. Before using
chloroquine or related compounds in these doses, the peripheral
blood smear examination must be done at least twice to rule out
malaria.
Assess the disability and recommend rehabilitative procedures.
Mild forms of exercise and physiotherapy are recommended in
recovering persons.
Treatment should be instituted in all suspect cases without waiting
for serological or viral confirmation.
 All suspected cases should be kept under mosquito nets during the
febrile period.
Adequate rest in a warm environment; avoid damp surroundings.
Heat may increase/worsen joint pain and is therefore best to avoid
during acute stage.

Cold compresses may help in reducing joint damage

Consume plenty of water with electrolytes (approximately 2 litres of

home available fluids with salt in 24 hours).

All persons should be assessed for dehydration and proper

rehydration therapy (preferably oral) instituted quickly.
 Refer cases with any of the following to a higher healthcare centre:
o pregnancy,
o oliguria/anuria,
o refractory hypotension,
o bleeding disorders,
o altered sensorium,
o meningo- encephalitis,
o hemodynamic instability (frequent syncopal attacks, hypotension
with a systolic BP less than 100 mmHg or a pulse pressure less
than 30 mmHg), persistent fever of more than one weeks
duration,
o not responding or having persistent joint pain or disabling arthritis
even after three days of symptomatic treatment
o extremes of age - persons above sixty years and infants (below one
year of age).
 CURB 65 scoring system may be used for deciding on referrals.
CURB-65 is a clinical prediction rule that has been validated for
predicting mortality in community-acquired pneumonia and infection
of any site.
The score is an acronym for each of the risk factors measured. Each
risk factor scores one point, for a maximum score of 5:
o Confusion
o Urea greater than 7 mmol/l (Blood Urea Nitrogen > 19)
o Respiratory rate of 30 breaths per minute or greater
o Blood pressure less than 90 systolic or diastolic blood pressure 60
or less
o age 65 or older
 Management of Leptospirosis

CPG Malaysia and K park

 Laboratory diagnosis

1. Microscopic Agglutination Test (MAT) Gold standard

For single serum specimen - titre 1:400
For paired sera - four fold or greater rise in titre
Positive after 7 to 10 days of illness and peak at 3 4 weeks and
may persist at high levels for several years.
Second serum samples must be taken to detect fourfold or
greater rise in titre

2. Positive PCR
Samples should be taken within 10 days of disease onset
3. The ELISA/other rapid tests
Detect IgM antibodies as early diagnosis.
The presence of IgM antibodies may indicate current or recent
leptospirosis.
A patients serum may be positive 5 to 10 days after onset of
symptoms but not usually before this.
***IgM-class antibodies may remain detectable for several years.

4. Positive culture
blood samples should be taken within 7 days of onset and urine
sample after the 10th day
Culture takes 1 6 weeks to be positive
Organism may grow from urine from 10th day to 6 weeks.

5. Rapid test kit for Leptospira

any leptospirosis rapid test kit to be used must be
validated/approved by IMR.
 Treatment
Early treatment with antibiotics is essential.
Severe cases are usually treated with high doses of IV C-penicillin (2
M units 6 hourly for 5-7 days).
Less severe cases treated orally with antibiotics such as doxycycline (2
mg/kg up to 100 mg 12-hourly for 5-7 days), tetracycline, ampicillin
or amoxicillin.

Third generation cephalosporins, such as ceftriaxone and cefotaxime,

and quinolone antibiotics may also be effective.
***Jarisch-Herxheimer reactions may occur after the start of
antimicrobial therapy.

Monitoring and supportive care as appropriate, e.g. dialysis,

mechanical ventilation.
10. How would you manage an outbreak
of the disease as an health officer
11. Prevention and control of pest
Mosquitoes (all types)
Rats
Flies
Cockroach
 PEST CONTROL
Pests are unwanted plants, animals, insects, germs or other
organisms that interfere with human activity. They may bite,
destroy food crops, damage property or otherwise make our
lives more difficult.

Effective pest control requires some knowledge about the pest

and its habits. The first step is to identify the pest correctly; the
second step is to learn about its lifestyle. After that, you can
evaluate strategies to control your pest.
 MOSQUITO
Mosquitoes are small, midge-like flies that constitute the
family Culicidae. Females of most species are ectoparasites,
whose tube-like mouthparts pierce the hosts' skin to consume
blood.
Types of mosquitos :1) AEDES
2) MARSH MOSQUITOS
3) YELLOW FEVER MOSQUITOS
4)ASIAN TIGER MOSQUITO
5) MANSONIA
 BITING HOURS
Although mosquitoes may bite at any time of day,
peak biting activity for vectors of some diseases
(such as dengue and chikungunya) is during daylight
hours. Vectors of other diseases (such as malaria) are
most active in twilight periods (dawn and dusk) or in
the evening after dark.
 MOSQUITOS AND DISEASES
Annoyance pest: A mosquito bite may induce local
dermatitis or even systemic reaction in senstive
people.

Parasitic diseases: Malaria and filariasis.

Viral diseases : Japanese Encephalitis B.

PREVENTION OF MOSQUITOS
 CONTROL OF MOSQUITOS
Use mosquito-eating fish in ponds(guppy fish)
Repair window screens.
Wear repellents and protective clothing.
Spray in populated areas.
PREVENTION AND CONTROL OF
RATS
Prevention and control
1. Rodent inspections
2. Sanitation
3. Exclusion
4. Population reduction
Trapping programs
Baiting programs
Predation
Cultural practices
Sign of rats infestation

Dropping
Gnawing damage
Burrows
Urine stains
Sounds and odor of rats
SANITATION
Proper removal of trash and garbage piles
Removal of grass, weed and undesirable
vegetation
Elimination of potential rodent harborages
Proper storage practices to allow cleaning
inspection
EXCLUSION

Seal all the opening greater than for rats

Use coarse steel wool, sheet metal, hardware
cloth, mortar for sealing openings
Use 12 inches of 24 gauge sheet metal at the
bottom of doors
POPULATION REDUCTION

1. Traps
Cage traps, wooden traps, wire traps, snap
traps
The traps should be cleaned by water after
each installation and fresh and attractive bait
materials like breads, fruits should be used.
2.POISON BAITING PROGRAMS

This group is generally used to kill the rats

with various rodenticides
Single dose poison, this can kill the rats by
single exposure to poison baits, example zinc
phosphate
Multiple dose poison effective only after the
multiple feeding of poison baits by rats,
example warfarin and ratanfin.
Effective control by poison baits
Installation of fresh baits and baits points in rodents highly
active area
Placement of enough bait points to ensure better access of
rodents to poison baits

Factors affecting baiting programs

Availability of other foods
Insufficient number
Poor maintenance
3. Cultural practices

Soil cultivation
Irrigation
Debris removal
Grazing management
FLIES
 WHAT IS FLY ?
The housefly (also house fly, house-fly or common housefly),
Musca domestica, is a fly of the suborder Cyclorrhapha.

It is believed to have evolved in the Cenozoic era, possibly in the

Middle East, and has spread all over the world.

It is the most common fly species found in habitations.

Adult insects are grey to black with four dark longitudinal lines on
the thorax, slightly hairy bodies and a single pair of membranous
wings.

They have red eyes, and the slightly larger

female has these set further apart than the male.
 PREVENTION AND CONTROL MEASURES
Sanitation
The key to managing all filth flies is sanitation.

Eliminating fly breeding sites, i.e., the material to which they are attracted to and
on which they lay eggs, is usually sufficient to eliminate and prevent fly
infestations.

Conversely, without thorough sanitation, other control methods are largely

ineffective.

Therefore, trash should be kept in sealed containers (in trash bags and/or cans with
tight-fitting lids). Dumpsters should be kept as clean as possible, emptied regularly
and kept as far away from buildings as is practical. Manure and other decaying
plant and animal material should be promptly removed. Also, eliminate areas of
excessive moisture.
Inspection

Just as sanitation is the key to successful filth fly

management, inspection is the key to sanitation.

To eliminate fly breeding sites, one must first locate the

attracting material. Often this can only be accomplished by
conducting a thorough inspection of the premises, and by
knowing what to look for and where to look.

First, identify the flies involved, inspect for material that

attracts that species and then eliminate the material.
Exclusion

Another important step in fly management is to exclude them

from the premises. This is done by keeping doors, windows and
vents closed as much is practical, and by screening and sealing
around these and other fly entry points.

Automatic door closing devices and air curtains that blow air
away from doorways also can be installed to supplement an
integrated fly management program.
Mechanical Control

In addition to fly swatting, mechanical fly control includes

trapping. Sticky fly paper is one type of fly trap.

Ultraviolet light traps are another, often used to supplement fly

control in commercial buildings. To be effective light traps must
be properly placed.

This type of trap should be placed where it cannot be seen from

outside the building, no more than 5 feet above the floor
(where most flies fly), and away from competing light sources
and food preparation areas.

Bulbs should be changed at least once per year.

Chemical Control
While the use of pesticides is usually not the best means of managing filth fly problems,
sometimes chemical control can be a valuable component of an integrated fly management
program.

Pesticide-releasing fly strips can be placed in attics and smaller, unoccupied enclosed rooms
where filth flies are a problem.

Contact (non-residual) pesticides labeled for fly control can be applied as a space treatment
(fogged) to kill adult flies.

This type of control provides only temporary relief, however, and cannot be relied upon to
eliminate the problem.

Residual pesticides those that remain active for some time can be applied to outdoor
surfaces where flies rest, such as the outside surfaces of barns, stables, restaurants and
houses.

Some pesticide bait formulations are also available for outdoor fly control, including use
around dumpsters.
COCKROACHES
 WHAT IS A COCKROACH ?
Cockroaches are insects of the order Blattodea, which
also includes termites. About 30 cockroach species out
of 4,600 are associated with human habitats.

About four species are well known as pests.

TYPES OF COCKROACHES
 PREVENTION AND CONTROL MEASURES
Leave no food for cockroaches

Keep premises, especially kitchen, dry and clean

Store food properly and remove pet food completely after

feeding

Put all refuse and food remnants into a bin with well-fitting
lid. Contents of the dustbin must be emptied completely at
least daily. Refuse bags should be tied up before disposal to
prevent spilling
Eliminate Harbourage for Cockroaches

Clean up unused articles especially old

newspapers and magazines at homes

Inspect at least quarterly the bottom and back of

furniture and concealed places like false ceilings,
air ducts and wire ducts

Seal any cracks and crevices at ceilings and on

walls and floor
Stop Cockroaches from entering premises

Install drain covers (without openings) which can be opened for the
discharge of the drainage water. Replace them if they are found damaged

Seal all openings on external walls, floors and roofs through which pipes
and wires pass or left by installation of split-type air-conditioners

Apply a band of petroleum jelly at least 10 cm in width around dry drain

hole to prevent cockroach from passing through the hole

Install wire mesh of 2mm at drain holes for preventing entry of

Periplaneta americana.
Trapping
Use sticky traps at places frequented by cockroaches. Whenever
possible, place traps either against a wall or in a corner of a floor, a
shelf or a drawer

Poisoning
Use insecticide with residual effect for killing the pest by contact

Set poisonous bait to kill cockroaches. The bait will not only kill those
cockroaches consuming the bait but also those in the harbourage
indirectly

Caution must be taken when using insecticides. Follow strictly the

application instructions on the label to avoid harming people and
animals.
Handling of dead cockroaches

Wear gloves when handling dead cockroaches.

Areas or equipment including the gloves having

contacted with cockroaches should be washed
and disinfected with household disinfectant as
soon as possible
10. How to Manage An Outbreak
(As a Health Officer)
 Outbreak

An outbreak or an epidemic exists when there are more cases of a

particular disease than expected in a given area, or among a specific
group of people, over a particular period of time.

Minor outbreak - could be defined as one that can be dealt with

within existing routine arrangements.

Major outbreak - A situation where a large number of patients are

involved, wards closed to all admissions, and other hospitals are
required to accept the patients (requires convening of major
outbreak control team)
 An outbreak and an epidemic essentially mean the
same thing to an epidemiologist

But the term epidemic has a more serious

connotation than outbreak and is used less
frequently to avoid the perception of a crisis situation

A pandemic refers to a disease epidemic that is

widespread and often global.
 How Outbreaks are Recognized
Outbreaks of disease come to the attention of public health
officials in various ways:
Clinical/Laboratory (astute clinician, infection control nurse,
or clinical laboratory worker)
Routine surveillance (analysis from Public Health
Department)
General public (from patient or someone close to the
patient)
Media (local newspaper or television news)
 Why Manage Outbreaks?

Objective of outbreak management of

communicable/infective diseases is to interrupt transmission
as quickly as possible and thus prevent further cases
To achieve this:
- recognize a potential or actual outbreak
- eliminate the source
- stop further spread
- prevent recurrence
- ensure satisfactory communication between all concerned
- disseminate lessons learnt
 Outbreak Control Plan
Each health facility should have a facility-specific outbreak control plan (OCP)
OCP should be reviewed periodically at least every two years & after an outbreak
OCP should include:
- a description of the roles and extent of the responsibilities and accountabilities of
each of the organiations and individuals
- arrangements for informing and consulting those who need to be aware of an
outbreak situation
- arrangements for creating an outbreak control team (OCT) to investigate and control
a major disease outbreak, the support which will be available to the group and what
its duties are
- resources required to manage an outbreak
- staff issues
- training for all staff involved in investigating communicable disease outbreaks
- ensuring staff are familiar with requirements for completing and disseminating the
final outbreak report
- Criteria for when an outbreak is considered over
 Outbreak Control Team
A multi-disciplinary group which will work together to investigate an
outbreak. The core team is responsible for planning and coordinating the
investigation
Decision to convene an OCT will be made by relevant personnel, such as the
chairperson of the infection control committee
Following factors should be considered:
- number of cases and the demographics of the population at risk
- organism/agent, its clinical severity, likely mode of transmission and
communicability/transmissibility
- extent of the outbreak
- likely source
- potential impact on service delivery
- public concern
- media interest
- the potential public health risk
 OCT Membership
coordinator of the OCT will usually be the infection control committee
chairperson
- Hospital and Health Service (HHS) executive member or delegate
- chairperson infection control committee
- infection control practitioner
- manager/clinician representatives from the relevant area
- infectious diseases physician, microbiologist and/or Public Health
Physician
- media relations officer
- other relevant stakeholders e.g. occupational health and safety,
support services, food services, sterilizing services, pharmacy etc as
required
- other individuals, including representatives of other agencies involved
in the outbreak may be co-opted as necessary
 The investigation and control of an
outbreak
Outbreak management tends to fall into four
distinct phases:
- Detection
- Investigation
- Response
- Evaluation of response

In practice there is considerable overlap between

the phases
 Outbreak detection
timely identification of an outbreak
Basic steps to help identify if an outbreak exists includes:
- assessing what is happening e.g. symptoms observed
- determining the timeline since symptoms first observed /
notified
- define the area where it is happening
- determining the likely transmission routes (e.g. human,
animal, vector, environmental, food or other factors)
- determine likely numbers affected
- determine characteristics of individuals affected (e.g.
age, sex, health status)
 Outbreak Investigation
First establish a case definition

formed by using a standard set of criteria to decide whether,

in this investigation, an individual should be classified as
having the disease or health condition under investigation

4 components:
- clinical information about the disease
- characteristics about the people who are affected
- information regarding the location or place
- specification of time during which the outbreak occurred
 Steps of Outbreak Investigation

1) Prepare for field work

2) Establish the existence of an outbreak
3) Verify the diagnosis
4) Define and identify cases
5) Line listing method for cases
6) Describe Outbreak/ Descriptive Epidemiology
7) Develop hypotheses
8) Evaluate hypotheses
9) Refine hypotheses and carry out additional studies
10) Implement control and prevention measures
11) Communicate findings
1. Prepare for field work
Research the disease and gather the supplies and equipment
needed.
Get local contacts.
Make a necessary administrative and personal arrangement.

2. Establish existence of an outbreak

Determine the expected number of cases for the area in the
given time frame. Then observe number of cases which
exceeds the expected number
if the current number of reported cases exceeds the expected
number, the excess may not necessarily indicate an outbreak.
Changes in local reporting procedures,
Changes in the case definition
Increased interest because of local or national awareness
Improvements in diagnostic procedures
3. Verify diagnosis
Confirm the diagnosis by means of: signs, symptoms, test results
(ex: NS1 is a glycoprotein - dengue serotypes and can be used to
detect either primary or secondary infections in the earliest
stages. Serology testing for dengue virus-specific antibodies,
types IgG and IgM, can be useful in confirming primary or
secondary diagnosis )

4. Define & Identify Cases

When case definition has been established, additional persons
who meet the case definition should be identified 1) more
accurate estimate of the magnitude of the outbreak, 2) reduces
the likelihood of bias which may occur by only focusing on cases
detected early in the investigation and 3) increases the sample
size.
 Outbreak response
Characterized by hypothesis-forming and the implementation
of relevant control measures
Primary goal = control & prevention
Control measures should be considered at all stages of the
investigation and implemented ASAP

These measures directed at:

- Controlling the source (ex: fogging malaria & dengue,
destroy rodent nests leptospirosis)
- Controlling the spread (ex: isolation of cases & contacts,
screening & monitoring, protection of contacts by
chemoprophylaxis or immunization)
 Define & identify cases (cont.)
A structured questionnaire should be used to collect
detailed information regarding cases. Information to be
collected from each case includes:
- identifying information
- demographic information
- clinical information (date/time of onset, signs and
symptoms, hospitalisation, death etc)
- laboratory information
- risk factor information (contact with known case,
environmental exposures etc)
- contact with individuals with similar symptoms.
Case definition:
A definition of a disease that allows a simple, uniform way to
identify cases
Distinguishes cases from unaffected members of population
Develop a SPECIFIC CASE DEFINITION using:-
1. Symptoms, signs and lab results
2. Time period
3. Location need to be specific enough not to include endemic
disease
Categories of Cases:
Possible/Suspected:
Symptoms reported but not confirmed
No lab/epidemiologic link
Probable:
Symptoms confirmed
No lab/epidemiologic link
Confirmed:
Symptoms characteristic of the agent
Lab test
Epidemiologic link
 5. Line Listing
Traditionally data are collected on a standard case
report form, questionnaire or data abstraction form.
Then the critical items are selected on a form called a
line listing for analysis, manipulation or cross-
tabulation and further use in the investigation.

includes important variables, such as name, ID, age,

sex, case classification etc. New cases are added to a
line listing as they are identified. Thus; a line listing
contains key information on every case, and can be
scanned and updated as necessary.
Example:
6. DESCRIBE OUTBREAK/ DESCRIPTIVE
EPIDEMIOLOGY
3 aspects to consider
Person:
Define by personal characteristics: age, sex, ethnicity etc
Define by exposure to risk factors: occupation, diet

Place:
Where were they infected?

Time:
When were they infected?
Determine type of outbreak (point source, propagated)
7. Develop Hypotheses
Form a hypothesis regarding:
Type of epidemic: point source or propagated
Source of the epidemic: common source, multiple
exposure etc.
Reservoir
Mode of spread and risk factors
Details of the illness with date of onset, duration, time of
exposure, incubation period and severity of symptoms.

8. Test Hypotheses
Cohort & Case-Control Study
9. REFINE HYPOTHESES AND CARRY OUT ADDITIONAL STUDIES
Microbiological, Environmental, Veterinarian investigations

10. IMPLEMENT CONTROL AND PREVENTION MEASURES

Vaccination, medication or prophylaxis
PPE respirator, glasses, mask, gown, latex gloves etc.
Isolation/quarantine
Educate/Communication
May implement earlier for effectiveness
11. Communicate findings
- Identify a single member of the investigation team to interact with media and communicate progress
and findings
- Summarize investigation and disseminate report to all participants
- Publish
 Evaluation of outbreak response
Helps bring about continuous improvements in practice
Aim: 1) determine if the incident objectives were met and 2) identify
positive outcomes and document areas for improvement
Criteria that helps guide the evaluation:
- preparedness for this type of investigation (includes resources,
guidelines, questionnaires, databases, etc)
- coordination of outbreak meetings, communication (including media
management)
- Organisation
- record keeping (responsibility)
- Epidemiology
- investigation processes and control initiatives implemented
 Writing Outbreak Report
Should contain the following:
1. Background (geographic, socioeconomic etc)
2. Historical Data (previous outbreak, related diseases
etc)
3. Methodology of investigation (type of survey,
questionnaire etc)
4. Analysis of data (clinical, epidemiological data)
5. Interpretation of data (formulation & testing
hypotheses)
6. Implement control measures (define & evaluate)
Finally:
Prepare written report
Communicate public health messages
Influence public health policy
Evaluate performance
 References
https://www.publichealthontario.ca/en/LearningAndDevelopment/
Events/Documents/Retirement%20Homes%20darlene.pdf

https://www.nhmrc.gov.au/book/australian-guidelines-prevention-
and-control-infection-healthcare-2010/b3-2-2-infection-control

http://www.rdash.nhs.uk/wp-
content/uploads/2014/05/Management-of-Outbreak-of-Infection-
Policy-approved-CASG-29.11.2011-V6.pdf

http://www.gosh.nhs.uk/health-professionals/clinical-
guidelines/infection-management-outbreaks-including-diarrhoea-
and-vomiting