IMPORTANT VECTOR BORNE diseases

1. IMPORTANTVECTOR
BORNE
DISEASES AND VECTOR
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2. 2
At theendof thischapter,thestudentswill be learn:
Definition of vector
Typesof vectorsthat are of public health
importance
Vector-borne disease transmission mechanisms
Classification of vectors
Measuresthat canbe usedto controlvectors
Objectives of the topic
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3. 3
• Vectorsare an organism, typically a biting insect or tick,
that transmits a disease or parasite from one animal or
plant to another
• Vectors are living organisms that can transmit
infectious diseases between humans or from animals
to humans.
• Many of these vectors are bloodsucking insects, which
ingest disease-producing microorganisms during a
blood meal from an infected host(human or animal) and
later inject it into a new host during their subsequent
blood meal.
Introduction
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4. 4
Introduction….
• Vectors are found within or close to human habitation; some
breed in open water that may be found around homes and
othersbreedinside thehome.
• The burden of these diseases is highest in tropical and
subtropical areas and they disproportionately affect the
poorest populations.
• Since 1970s, there has been a world wide resurgence of
vector-borne diseases, malaria, yellow fever, and Zika virus,
louse-borne typhus, leishmaniasis, sleeping sickness, have
afflicted populations, claimed lives and overwhelmed health
systems in many developing countries, particularly Sub-
SaharanAfrica and SoutheastAsia
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• Reasonsfor the emergenceor resurgenceof vector-borne
diseases include
– Thedevelopment of insecticideand drug resistance;
– Decreased resourcesfor surveillance, prevention and
controlof vectorbornediseases;
– Deterioration of the public health infrastructure required
to deal with these diseases;
– Unprecedented population growth and uncontrolled
urbanization and
– Changesin agricultural practices,deforestation; and
increased travel.
Introduction….
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Key facts about vector
 Vector-borne
diseases
infectious diseases,
annually.
accoun
t causing
for
mor
e more
than
than 17% of all
700 ,000 deaths
 More than 3.9 billion people in over 128 countriesare at riskof
contractingdengue,with 96 million casesestimated per year.
 Malaria causes more than 400, 000 deaths every year
globally, mostof themchildren under 5 years of age.
• The discovery of the insecticide Dichlorodiphenyl
trichloroethane (DDT) wasa major breakthrough in the control of
vector borne diseases
 Many of thesediseasesare preventablethroughinformed
protective measures. Source, WHO, 2017
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7. Public health importance of
vectors
Disease transmission
Malaria, yellow fever,
Typhusfever, Rabies
Onchocerciasis, leishmaniasis,
Schistosomiasis
• Three-quarters of the country is an area of malaria
transmission and two-thirds of the Ethiopian
population isat riskfrommalaria
Are all communicable
diseasesthat are
prevalent in Ethiopia.
All of theseare
transmittedby vectors.
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8. 8
Public health
importance……..cont
diarrhoea, dysentery, typhoid fever)
• A number of diarrhoeal diseases (acute watery
can also be
transmitted by vectors
Fooddestruction/ damage:rodentsand insects.
Interference with human comfort: buzzing mosquitos,
biting of lice, bed bugs,rodentsand other insects.
• A barrier to development. Irrigation and dam workers
will not be productive if they get malaria or
schistosomiasis(bilharzia or snail fever).
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Why vector control?
Diseases transmitted by vectors account for around
17% of the estimated global burden of communicable
diseases.
Mosquitoes:-transmit malaria, dengue,lymphatic filariasis,
yellow fever and Zika amongother diseases;
Flies:- transmit leishmaniasis, onchocerciasis and sleeping
sickness; and
Bugs or ticks:- transmit Chagas disease, borreliosis (L
yme
disease), typhusand encephalitis.
 Formost,prevention by targeting vectorsisthe first and best
approach.
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10. Vector-BorneDisease
Transmission Mechanisms
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11. Transmission
Mechanisms
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• Thereare two waysthat vector-bornediseasesare transmitted:
1. Mechanical transmission takes place when a vector simply carries
pathogenic microorganisms on their body and transfers them to
food, whichwethenconsume.
– Fliesandcockroachesare in this category
• Flies like to rest on faecal matter and then may move on to fresh
food.
• Theycancarry infectiousagentsthrough their mouthand on their
legsand otherbody parts.
• They deposit these agents on ready-to-eat foods and the recipient
gets infected if they consumethe contaminated food.
– Example-Trachoma
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2.Biological transmission: involves the multiplication and
growth of a disease-causing agent inside the vector’s
body.
 Malaria isa good example of biological transmission.
 The female mosquitoes take the malaria infectious agent
(Plasmodium) from an infected person with a blood meal. After
sexual reproduction in the gut of the mosquito, the infectious
agent migrates into the salivary gland of the insect, where it
grows in size, matures and becomes ready to infect humans.
When the mosquito next bites a human the saliva is injected into
the skinand transfers the infection in doing so.
Transmission Mechanisms
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13. Important vectors and disease
transmission
mechanisms.
13
Vector Diseases Mechanism
Housefly Diarrheal diseases, TB, polio,
worms, food poisoning,
infective hepatitis
Mechanical
Mosquito Malaria, yellow fever, filariasis,
dengue fever
Biological
Louse Typhus fever, relapsing fever, dermatitis Biological
Mite Scabies, Biological
Flea Flea Plague, murine typhus/endemic typhus Biological
Sand-fly Leishmaniasis Biological
Blackfly Onchocerciasis Biological
Dog Rabies Biological
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Environmental Factors Affecting The
Distribution Of Vector Borne
Diseases
1. Climate:Altitude, rainfall, and temperature
2. Overcrowding:
• Determined by theair ventilation, air spaceper capita
and # of rooms/ dwellings.
• Substandard housingin all aspectsexit inEthiopia;
3. Poor housing:
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Environmental Factors …….
Cont
4 Temperaturedependencefor breeding:
Example:Housefly life cycle:7-16 days in
tropical areas, 12-30 days in cold areas;
Plasmodiumbetter develops in the intermediate host
(anopheles):150C -7 days; 200C-18 days; 24-
270C-14.5 days.
5. Human activities:
Irrigation, urbanization, displacement due to war,
famine, and natural calamities: intensifies disease
transmission.
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Main vectors and diseases they
transmit
Vectors are living organisms that can transmit infectious
diseasesbetween humansor from animalsto humans.
Many of these vectors are bloodsucking insects, which
ingest disease-producing microorganisms during a
blood meal from an infected host(humanor animal) and
later inject it into a new host during their subsequent
blood meal.
Mosquitoesare the bestknowndiseasevector.
Others include ticks, flies, sandflies, fleas, bugs and
somefreshwater aquatic snails.
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17. 1. Arthropods
• The large group of animals called arthropods includes three
main types of organism that are important for the
transmissionof diseases:
• Insects(flies, mosquitoes,bed bug, cockroach); arachnids
(ticks,mites);and crustacean (Cyclopes)
• Now we will focus on insects, because they cause major public
health problems.
• Flies: different varieties: stable fly, deer fly horse fly, black fly,
tsetse fly, sand fly, anthropogenic (aggressive biters); house
flies.
• Of these house flies are the most important for human
diseasestransmissionin Ethiopia.
Classification of vectors and their life
cycles
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18. 18
Housefly
• We are all familiar with this small creature that disturbs
us in and around the household and in workplaces. The
female lays 200–250 eggs at a time on organic
matter.
• The organic matter could be human faeces, decaying
animal and vegetable matter, fresh food or dung Eggs
are white and about 1 mm long. Within 8 to 48 hours
the eggs hatchinto tiny larvae.
• These maggots feed voraciously and pass through the
three larval stages rapidly; then after four to eight
days they pupate.
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Mosquitoes
• There are three main mosquito groups: Anopheles,
Culexand Aedes.
• Anopheles mosquitoes breed in stagnant, relatively
clean water bodies; Culex breed in polluted water;
andAedeslike relatively clean water.
• Eggs are laid in a group (150–200 for Anopheles,
200–500 for Culex) on the water surface and hatch
into larvae within a few hours.
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MALARIA
Malaria isa major public health problem in warm
climates especially in developing countries.
•It isa leading causeof diseaseand death among
children under five years, pregnant womenand non-
immune travellers/immigrants.
Affect1 billion personsworldwide and causing
between 1 and 3 million deaths each year.
Children under 5 are the major at risk group in
malarious regions. Inset:AnAnophelesmosquito
taking a blood meal
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23. What is malaria ?
Definition: Malaria isa diseasecausedby the
protozoan parasites of the genusPlasmodium.
Etiology:Fivespeciesof the genusplasmodia
P
.Falciparum
P
.Vivax
P
.Ovale
P
.Malariae
P
.Knowlesi
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24. Species Major features
P.
falciparum
Themostimportant speciesasit isresponsible for 50% of
all malaria casesworldwide and nearly all morbidity and
mortality from severe malaria
 Foundin the tropics & sub-tropics
P.vivax  Themalaria parasite with the widest geographical
distribution
 Seenin tropical and sub-tropical areas
 Estimated to cause43% of all malaria casesin theworld
P.ovale  Thisspeciesisrelatively rarely encountered
Primarily seenin tropical Africa, especially, the westcoast,
but hasbeen reported in SouthAmerica and Asia
P.malariae
24-Dec-22
 Responsiblefor only 7% of malaria cases
 Occursmainly in sub-tropical climates
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Endemicity
Endemicityrefers to the amountor severity of malaria inanarea
or community. Malaria issaid to be endemicwhenthere isa
constant incidence of casesover a period of manysuccessive
years.
 Endemicmalaria may be present in various degrees. Recognised
categories of endemicity include :
A.Hypoendemicity(<10%) - little transmissionand the diseasehas
little effect onthepopulation.
B.Mesoendemicity(11–50%) - varying intensity of transmission;
typically found in the small,rural communitiesof the sub-tropics.
C. Hyperendemicity(51–75%) - intensebut seasonaltransmission;
immunityis insufficient to prevent the effects of malaria onall
age groups.
D. Holoendemicity(>75%); - intensetransmissionoccursthroughout
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26. How is malaria transmitted?
• Malaria parasites are transmitted from
one person to another by the bite of a
female anopheles mosquito.
• The female mosquito bites during dusk
and dawn and needs a blood meal to
feed her eggs.
• Thereare about 400 speciesof
anophelesmosquitobut only about 60
are able to transmit malaria.
• Likeall mosquitoes,anophelesbreed in
water - henceaccumulationof water
favours the spread of the disease.
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How does infection develop ?
• Plasmodiuminfects the humanand insecthostalternatively and several
phasesof the parasite life cycle are described.
• During feeding, saliva from the mosquitoisinjected into the human
blood stream. If the mosquitoiscarrying malaria, the saliva contains
primitive stagesof malaria parasites called sporozoites.
• Hepatic, tissueorpre-erythrocytic phase:Sporozoitesinvade and
develop in liver cells.Theinfected hepatocyte ruptures to release
merozoites.
• Erythrocyticphase:Merozoites theninvade red blood cells.Thered
cellslyse and thiscausesboutsof fever and the other symptomsof the
disease.Thiscycle repeats asmerozoites invade other red cells.
• Sexualphase:Sexualforms of the parasites develop and are ingested
whenanother female anophelesmosquitofeeds. Thesedevelop into
sporozoites in the gut of the insecthostand travel to its salivary glands.
Thenthe cyclestarts again…
• Thelife cycleof the malaria parasite isshownonthe next slide
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28. The Malaria Parasite Life
Cycle
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29. 29
The clinical course of P.
falciparum
• Following a bite by an infected mosquito,many
people do notdevelop any signsof infection.
• If infection doesprogress,the outcomeisoneof three
depending onthe hostand parasite factors
enumerated in the previous slides:
A. Asymptomaticparasitaemia (“clinical immunity”)
B. Acute,uncomplicatedmalaria
C. Severe malaria
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A. Asymptomatic
parasitaemia
• This is usually seen in older children and adults who
have acquired natural immunity to clinical disease as a
consequence of living in areas with high malaria
endemicity.
• There are malaria parasites in the peripheral blood
but no symptoms. These individuals may be important
reservoirs for disease transmission.
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B. Simple, uncomplicated
malaria
• This can occur at any age but it is more likely to be
seen in individuals with some degree of immunity to
malaria.
• The affected person, though ill, does not manifest life-
threatening disease.
• Feveristhe mostconstantsymptomof malaria. It may
occurin paroxysmswhenlysisof red cellsreleases
merozoitesresulting in fever, chills and rigors
(uncontrollable shivering).
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The periodicity of malaria
fever
Erythrocyticschizogonyisthe time taken for trophozoites to
mature into merozoitesbefore release whenthe cell ruptures.
It isshortestinP
.falciparum (36 hours),intermediate in P
.
vivax and P
.ovale (48 hours)and longest in P
.malariae (76
hours).
Typicalparoxysmsthusoccurevery
•2nd day or morefrequently inP
.falciparum (“sub-tertian”
malaria)
• 3rd day inP
.vivax and P
.ovale(“tertian” malaria)
• 4th day inP
.malariae infections, (“quartan” malaria)
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33. Other features of simple,
uncomplicated malaria
include:
33
o Vomiting
o Diarrhoea
o Convulsions– commonly
seenin young children.
Malaria isthe leading
causeof convulsionswith
fever in African children.
o Pallor(mild anemia)
o Jaundice(Mild)– mainly
due to haemolysis.
Malaria is a multisystem disease.
Other
common clinical features are:
o Anorexia
o Cough
o Headache
o Malaise
o Muscle aches
o Spleenomegaly
o Tender hepatomegaly
These clinical features occur in
“mild” malaria. However, the
infection requires urgent
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C. Severe Falciparum Malaria
• Nearly all severediseaseand deathsfrom malaria are
due to P
.falciparum.
• Althoughseveremalaria isboth preventable and
treatable, it isfrequently a fatal disease.
• Thefollowing are 8 important severemanifestations of
malaria:
1. Cerebral malaria
2. Severe malaria
anaemia
3. Hypoglycaemia
4. Metabolic acidosis
5. Acuterenal failure
6. Pulmonary oedema
7
. Circulatory collapse, shockor “algid
malaria”
8. Blackwater fever
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Diagnosis
Malaria isa multisystemdisease.It presentswith a wide variety of
non-specific clinical features: there are nopathognomonic
symptomsor signs.Many patients havefever, general aches and
pains and malaise and are initially misdiagnosed ashaving
“flu”.
P
.falciparum malaria canbe rapidly progressive and fatal.
Promptdiagnosis saveslives and relies onastuteclinical
assessment:
• A goodhistory&Physicalexamination
– History of fever (maybe paroxysmal in nature)
– Non-specific clinical features suchasvomiting, diarrhoea, headache,
malaise
– Fever,pallor, jaundice,splenomegaly
– Excludeother possible causesof fever (viral and bacterial infections)
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36. Investigations
• BloodFilmExamination
• Thickand thinblood films (or “smears”) have
remained the gold standard for the diagnosis
of malaria. Thefilms are stained and examined
by microscopy.
• Thick blood film - Usedfor detecting malaria:
a larger volumeof blood isexamined allowing
detection of evenlow levelsof parasitaemia.
Alsousedfor determining parasite density and
monitoring the responseto treatment.
• Thinbloodfilm – Givesmoreinformation
about the parasite morphology and, therefore,
isusedto identify the particular infecting
speciesof Plasmodium.
Show
Me
Show
Me
36
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37. Appearance of P. falciparum in thin
blood films
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Treatment: Malaria
Known chloroquine-sensitive
• Chloroquine (10 mg of base/kg stat followed by 5
mg/kg at 12, 24, and 36 h or by 10 mg/kg at 24 h
and 5 mg/kg at 48 h)
or
• Amodiaquine(10–12 mgof base/kg qd for 3 days)
RadicaltreatmentforP
.vivax orP
.ovale infection
• primaquine(0.5 mgof base/kg qd) shouldbe given
for 14 days to prevent relapse.
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Multidrug-resistant P. falciparum
malaria
• Eitherartemether-lumefantrinec(1.5/9 mg/kg bid
for 3 days with food)
or
• Artesunatec(4 mg/kg qd for 3 days)
plus
• Mefloquine(25 mgof base/kg—either 8 mg/kg qd
for 3 days or 15 mg/kg onday 2 and then10
mg/kg onday 3)
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40. Coartem 20/120mg formulations,
dosage
5-14 kg (3m-2
years)
15-24 kg (3-7
years)
25-34 kg (8-10
years)
35+ (>10 years)
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Management of Complications
AcuteRenal Failure
–Adequate rehydration
–Hemofiltration and hemodialysis
AcutePulmonaryEdema
–bed at a 45° elevation and given oxygen and IV
diuretics
Hypoglycemia
–slow injection of 50% dextrose (0.5 g/kg) should be
followed by an infusion of 10% dextrose (0.10 g/kg
per hour)
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Management….. Cont.
• Severeanemia- packed RBCtransfusion
• Spontaneousbleedingshouldbe given freshblood
and IV vitamin K.
• Convulsionsshouldbe treated with IV or rectal
benzodiazepines
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Prevention
Personal Protection
• Avoidanceof exposureto mosquitoesat their peak
feeding times
• Useof insectrepellentscontaining
• Suitable clothing, and insecticide-impregnated bed nets
Chemoprophylaxis
• Atovaquone/proguanil (Malarone)
• Doxycycline
• Mefloquine
• Primaquine
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44. Leishmaniasis
William Leishmani
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45. Leishmania
sis
Introduction
Agroup of diseasedueto infection with genusleishmaniaand
primarily affects the host'sreticuloendothelial system
Leishmaniaspeciesproduce widely varying clinical syndromes
ranging from self-healing cutaneousulcersto fatal visceral disease
Presentin different forms
Zoonotic form, dogs as main reservoir, occurs most in the
Mediterranean basin, China, the Middle East, and South-
America; causeisL.infantum
The anthroponotic form, humans as reservoir, is caused by
L.donovani;prevalent in EastAfrica and the Indian subcontinent
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46. Etiology
Infectious Agents:
L.tropica, L.braziliensis, L.major, & L. aethiopica:
Cutaneous(CL)
L.braziliensis,L.aethiopica: Mucocutaneous (MCL)
L.donovani, L. infantum, L.chagasi: Visceral(VL)
Vector:Sandfly(phlebotamine)
Livesin humidand hot areas, cracks, mudor straw
houses
Only mosquitonetswith fine meshworkhold themoff
Abite from justoneinfected sandfly canresult in
infection of the disease
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47. A variety of species and species
complexes causes disease in
humans
Visceral Leishmaniasis
Leishmania donovani
Leishmania infantum
Leishmania chagasi
Cutaneous Leishmaniasis
Leishmania tropica
Leishmania major
Leishmania aethiopica
Mucocutaneous Leishmaniasis
Leishmania brazieliensis
Leishmania mexicana
Leishmania amazoniensis
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48. Epidemiology
Leishmaniaisworldwide diseaseaffecting 98 countriesof
mostof themdeveloping (tropical and temperate regions)
Twomillion casesoccurannually, of which1–1.5 million
are CLand 500,000 are VL
India and neighboring Nepal, Bangladesh,Sudan,and
Brazil are the four largest foci of VLand accountfor 90%
of the world's VLburden, with India theworst affected
Inthe Hornof Africa, Sudan,Ethiopia, Kenya,Uganda,
and Somalia report VL
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49. Epidemiology…….. Cont.
Lowlandsof Ethiopia with varying endemicity
N. West:Metema and Humera,Wolkayit, Libo/Fogera
N. East:Ethio-DjiboutiAwashValley
S.West:Segen,Dawa, Genale, Woito,Konso,Omo,
Gambella Sudan border
Main risk factor: population migration
Estimatedannual VL:4500-5000people
VLcause:by speciesof the Leshmaniadonovani complex - L.
Donovani
Thesandfly: Phlebotomusorientalis, Phlebotomusmartini and
Phlebotomus celiae
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50. Life Cycle
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51. Life cycle of Leishmaniasis
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52. Clinical Spectrum of Disease
Depends on
Parasiticproperties (Infectivity, pathogenicity and
Virulence)
Hostfactors and hostresponses
Manifestation range from asymptomatic, self healing
cutaneousleishmaniasisto diffuse cutaneousand
visceral disease
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53. Visceral Leishmaniasis
Presentation
The most common presentation of VL is an abrupt onset
of moderate- to high-grade fever associated with rigor
and chills
Thespleen may be palpable by the secondweek of
illnessand, depending onthe duration of illness,may
becomehugelyenlarged
Hepatomegaly (usually moderate in degree) soon
follows
Lymphadenopathy iscommon
Night sweats,weight loss
Cachexia, pallor
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54. Visceral Leishmaniasis…
Darkening of theskin/ashen grey appearance
Pancytopenia(Anemia,Thrombocytopenia,
Leukopenia, Neutropenia)
Bleeding 20 to thrombocytopenia
Susceptibility to 20 infection
Untreated, the disease isfatal in mostpatients,
including 100% of thosewith HIV co-infection
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55. Diagnosis
Demonstration of amastigotes in tissue aspirates
Diagnostic sensitivity
Spleen 95%
Bonemarrow  70%
L
ymph nodes  50%
Serology
Theindirect immunofluorescentantibody test (IFAT)are
usedin sophisticated laboratories
Culture
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56. Treatment
• Pentavalent antimonial (SSG)isthe drug of choicein most
endemicregions of the world
SodiumStibogluconate (SSG)20mg/kg iv/im for 30 days
Alternative:
Amphotericin B1mg/kg every other day for 30
days/total 15 doses
AmBisome4mg/kg for 5-7 doses:1-5days, 10th, 14th
AmBisome4mg/kg: 1-5 days, 10th, 17th, 24th, 31st and
38th in HIV-VL coinfection
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57. Cutaneous and mucosal
disease
Start asa papule at thesite of insectbite and evolve
to nodules,ulcer, plaque
It maycomplicaté with regional adenopathy,
sporotrichoid subcutaneousnodules,lesionpain or
pruritis, 20 bacterial infection
Manifestation and chronicity of the lesiondepends on
Theinfecting spps
Thelocation of lesionand
Thehostimmuneresponse
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58. Cutaneous…..cont.
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59. Diagnosis & Treatment
Visualization of amastigotes in Giemsa-Stained thin
smearfrom dermal scraping /biopsy specimen
One or a few smalllesionsdue to "self-healing species"
canbe treated with topical agents
Indication for systemic therapy
Persistentlesion( > 6 months)
Lesions that are located over the face, handsand joints
Multiple lesions(> 5 to10 innumber)
Large lesions(> 4-5cm)
CLwith the potential for developmentof ML
CLin HIVco-infected patients
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60. Mucosal leishmaniasis
20% of infected patients develop ulcers of the oral
and nasal mucosa if a skin lesion near the mouth or
noseisnottreated
Progressionof the ulceration isslowbut steady,
ultimately destroying all soft parts of the nose,the
lips, and the soft palate
Erythemaandulceration of thenares Nasal
septal perforation and destructive inflammatory lesion
 obstructionof pharynx/larynx and remarkable
disfigurement
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61. Mucosal Leishmaniasis
Treatment
IV/IM SSGtherapy
Amphotericin B
Miltifoseine
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62. Prevention and Control
Measures
Preventive Measures
Casedetection and treatment
Apply insecticides periodically
Screening usingimpregnated bed nets(fine mesh
screen)
Insectrepellents onexposedskins
Limitoutdoor activity at duskand during evening(when
the sandfly ismostactive)
Eliminate rubbish heap and other breading places
Control of reservoirs
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63. FILARIAL INFECTIONS
Filarial wormsare nematodesthat dwell in the
subcutaneoustissuesand thelymphatics
Filarial parasites, whichinfect an estimated 170
million personsworldwide, are transmitted by specific
speciesof mosquitoesor other arthropods
Eightfilarial speciesinfect humans;of these,four—
Wuchereria bancrofti, Brugia malayi, Onchocerca
volvulus,and Loaloa—are responsiblefor most
seriousfilarial infections
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64. Cont…
Usually,infection isestablished only with repeated,
prolonged exposuresto infective larvae
Sincethe clinical manifestations of filarial diseases
develop relatively slowly, theseinfections shouldbe
considered to inducechronicdiseaseswith possible
long-term debilitating effects
Characteristically, filarial disease ismoreacuteand
intensein newly exposed individuals than in natives of
endemic areas
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65. 65
Organism Periodicity Distribution Vector Location of
adult
Microfilari
al location
Wuchereria
bancrofti
Nocturnal
Subperiodic
Worldwide Culex,Anopheles
Aedes
Lymphatic
tissue
Blood
Brugia
malayi
Nocturnal
Subperiodic
Southeast Asia,
Indonesia, India
, SoutheastAsia
Mansonia,
Anopheles
Lymphatic
tissue
Blood
B. timori Nocturnal Indonesia Anopheles Lymphatic
tissue
Blood
Loa loa Diurnal West and Central
Africa
Chrysops
(deerflies)
Subcutaneous
tissue
Blood
Onchocerca
volvulus
None South and
Central
America,Africa
Simulium
(blackflies)
Subcutaneous
tissue
Skin, eye
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66. Lymphatic Filariasis
Definition: a chronicdebilitating disease of the
lymphaticscausedby different filarial nematodes
Etiology
Infection with 3 closely related nematodes
Wuchereria bancrofti
Brugia malayi
Brugia timori
Modeof transmission:by the bite of infected
mosquito
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67. Definitive host
Humansare the definitive
hostfor the wormsthat cause
lymphatic filariasis
Thereare noknownanimal
reservoirs for W.bancrofti
B.malayihasbeen found in
macaques,leaf monkeysand
cats
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68. Intermediate host
W.bancrofti is
transmitted by Culex,
Aedes,and Anopheles
species
B.malayiistransmitted
by Anophelesand
Mansonia species
Aede
s
Cule
x
Mansoni
a
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69. 69
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70. 70
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71. LIFE CYCLE
Biteof mosquitoes
Mosquitoesdeposit third-stage infective larvae into the
skin
Theselarvae travel throughthe dermis and enter local
lymphatic vessels
Over a period of approximately ninemonths,these larvae
undergo a seriesof moltsand develop into mature adult
worms
Theysurvivefor approximately five years (occasionally
up to 12 to 15 years), during whichtime male and
females wormsmate and produce
microfilariae(embryonic or first stage larvae)
71
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72. Cont….
NB:Femaleparasites canrelease morethan
10,000 microfilariae per day into the bloodstream
Mosquitoes,whichbite infected individuals, cantake
up thesecirculatingmicrofilariae
Within the mosquito,theseembryoniclarvae develop
into secondthenthird stage larvae over a period of
10 to 14 days
Themosquitoisthenready to bite and infect a new
human host
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73. Clinical manifestations
Initially asymptomatic
Symptomsdevelop with increasing numbersof worms
Lessthan 1/3 of infected individuals haveacute symptoms
Clinical Coursehas3phases:
Asymptomatic Microfilaremia
Acutedisease:Adenolymphangitis (ADL)and Filarial
fever
Chronic/Irreversible lymphedema: Superimposed upon
repeated episodes of ADL
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74. Acute disease
AcuteAdenolymphangitis (ADL)
ADLcharacteristically presentswith the suddenonsetof fever and
painful lymphadenopathy
Often there isretrogradelymphangitis
ADListhoughtto occurbecauseof immune-mediatedresponsesto
dying adult worms
Commonlyinvolved nodesare the inguinal nodes&lower limbs
Theinflammation tendsto resolve spontaneously after four to seven
days, but recurrencesare frequent
Typically seenoneto four timesper year
Butthe numberof attacks increaseswith increasingseverity of
lymphedema
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75. Cont…
Filarial fever
Filarial fever ischaracterized by acute,self-limited
episodesof fever, often in the absenceof
lymphangitis or lymphadenopathy
Chills,myalgias, and headache
Becauseof the lack of associated features, this
syndromeisfrequently confusedwith other causesof
fever in the tropics, suchasmalaria
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76. Tropical pulmonary
eosinophilia
Characterized by dry hacking coughand nocturnal
wheezing
Causedby an immunehyperresponsivenessto
microfilariae trapped in the lungs
Occursfour to seventimesmorefrequently in males
than in females
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77. Chronic manifestations
Chronicmanifestationsof lymphatic filariasis include
lymphedema,renal involvement,and secondary infection
Lymphedema
Mostly affects the lower extremities and inguinal, but canaffect
upper extremities and breast
Initially pitting edema, with gradual hardening of tissues
When the lymph vesselsin the inguinal region are involved,
swelling of the lower limb(s) ensues
When axillary lymph nodesare involved, swelling of the upper
limb(s)results& involvementof the breast
When lymphedema issevere elephantiasis
GenitaliaHydroceles
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78. Chronic manifestations…
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79. Chronic manifestations…
Renal involvement
Intestinal lymphmay be intermittently discharged into
the renal pelvis, causinglymphfluid to be passedin
the urine
Thisisknownaschyluria, and it resultsin a milky
appearance to the urine
Since large amounts of fat and protein can be lost in the urine
in individuals with chyluria, this condition can lead to nutritional
deficiencies suchasanemia and hypoproteinemia
Secondary infection
Secondary bacterial/fungal infections of the skin
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80. Urine sample with chyluria
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81. DIAGNOSIS
Thediagnosis of lymphatic filariasis isbased uponclinical and
epidemiologic cluestogether with laboratory evaluation
Nonspecifictestabnormalities: Eosinophiliaup to 3000/microL
Bloodexamination for detection of microfilariae shouldbe
performed in all individuals in whomthe Dx is suspected
Bancroftianand Brugianfilariasis tend to shownocturnal
periodicity
Blood shouldbe drawn between 10 p.m.and 2 a.m.
becausethe greatest numberof microfilariae canbe found
in blood during thispeak biting time of the mosquito
Ultrasound
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82. TREATMENT
Diethylcarbamazine citrate 2mg/kg po tid for 10-21
days isthedrug of choice
Ivermectin50-200 microgram/kg every 6 month
Studieshaveestablished that a single doseof
ivermectin reducesmicrofilaremia by ≈ 90% one
year after Rx
Albendazole hasalso been usedin filarial infections
Doxycycline: Hasgood activity against Wolbachia,
leads to sterility of adult worms
Surgery
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83. Prevention and control
Useof personal protective barriers against mosquito
bite
Casetreatment
Mass treatment
83
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84. 84
Malaria Control Strategies
1. Early caseDetectionandPromptTreatment(EDPT)
• EDPT is the main strategy of malaria control –
radical treatment is necessary for all the cases of
malaria to prevent transmissionof malaria.
• is the main anti-malaria drug for uncomplicated
malaria.
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85. 85
2. Vector Control:
(i) Chemical Control
 Use of Indoor R
esidual Spray (IR
S) with insecticides
recommendedunder the programnme
 Useof chemicallarvicides like Abate in potable water
 Aerosol spacespray during day time
 Malathion fogging during outbreaks
Malaria Control Strategies
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86. 86
Cont…
(ii) Biological Control
 Useof larvivorous fish in pond, ornamental tanks,fountains etc.
 Use of biocides-(a substance that is poisonous to
living organisms,suchasa pesticide).
(iii)Personal Prophylatic Measures that individuals/communities
cantakeup
 Useof mosquitorepellent creams,liquids, coils,mats etc.
 Screeningof the houseswith wire mesh
 Useof bed netstreated withinsecticide
 Wearing clothesthat covermaximumsurface area of the body
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87. 4. Community Participation
 Sensitizing and involving the communityfor detection of
 Anophelesbreeding places and their elimination
 Involving NGOs in programme strategies
 Collaboration with CII/ASSOCHAM/FICCI
5. EnvironmentalManagement&SourceReductionMethods
 Sourcereduction i.e. filling of the breeding places
 Proper covering of stored water
 Channelization of breeding source
6. Monitoring andEvaluationof the programme
 Monthly ComputerizedManagement Information System (CMIS)
 Field visitsby State and National Programme Officers
Malaria Control
Strategies
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88. 88
Vector management and control
• Vectorscanbecontrolledusingvariousmethods.
– Elimination or reduction of environment that facilitates breeding
and harborage(places where vectorsfind refuge or shelter).
– Elimination of all possible breeding places for insects, the
prevention of stagnation of water to limit the breeding of
mosquitoes, and proper solid waste management and use of a
latrine to control the breeding of houseflies.
– The use of clean water from protected sources for drinking
preventsthe transmissionof guinea worm.
– R
ats are controlled by starving them and eliminating
breeding places.
– Personalhygiene contributes to the control of lice.
their
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89. 89
1. The general vector management and control
methods?
2. Classification of vectorsandtheirlifecycles?
Home Reading Assignment
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90. 90
Summary
• A vector is a non-human carrier of communicable diseases.
Arthropods such as insects, and mammals such as rats, play major
roles.
• The public health importance of vectors is related to disease
transmission, damage to food and property, and acting as a
barrier to development.
• There are mechanical and biological methods of disease
transmissionby vectors.
• Insects are identified by their body structure and the presence of
three pairs of legs. Insects go through three or four stages to
complete their life cycles.
• Rats are vectors that inhabit and breed inside a house. They are
involved in the transmission of diseases, destroying materials and
damaging food. Thereare different methodsto control them.
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91. 91
• Vectors can be managed using simple control methods
such as sanitation and also physical, biological and
chemicalmethodsof control.
• An integrated approach using sanitation in combination
with others is the best option in order to effectively
reducethevector population.
• Planning activities for vector management on an annual
basisisonemajor taskof thehealth practitioner.
Summary
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92. 92
References
1. AntenehFikrie.IntroductionT
oEnvironmentalHealth and Ecology
Handout for health Sciences students, Pharma Health
Science CollegeHawassa, Departmentof Public Health
March, 2018.
2. Federal Democratic Republic of Ethiopia Ministry of Health.
Hygiene and Environmental Health, Part 2, Blended Learning
Modulefor theHealth Extension Programme.
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93. Questions?
93
Questions?
Questions?
Questions?
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