Leishmaniasis is caused by protozoan parasites of the genus Leishmania. It occurs in three main forms: visceral leishmaniasis, cutaneous leishmaniasis, and mucocutaneous leishmaniasis. It is transmitted by sand flies and affects millions of people worldwide. The document discusses the causative parasites, geographical distribution, transmission and life cycle, clinical features of the different forms of the disease, diagnostic methods, and treatment options.

1. Leishmaniasis

2. Leishmaniasis
• Leishmaniasis is:
• a disease caused by protozoan parasites that are
obligate intrcellular, different species in the genus
Leishmania
• Leishmaniasis disease occurs in the form of Visceral
Leishmaniasis (VL), Cutaneous Leishmaniasis,
• and Mucocutaneous Leishmaniasis.
• Leishmaniasis is still a major public health problem
and the burden is increasing.
• WHO estimates the number of persons at risk of
infection to be around 310 million and the number

3. • of Leishmaniasis cases to be 1.3 million
throughout the world except in Australia, Pacific
Islands, and Antarctica
• Over 90% of Visceral Leishmaniasis (VL) cases
occur in six countries: Bangladesh, Brazil, Ethiopia,
India, South Sudan and Sudan.
• The majority of Cutaneous Leishmaniasis cases
occur in Afghanistan, Algeria, Brazil, Colombia,
• Iran, Pakistan, Peru, Saudi Arabia and Syrian.
• Almost 90% of Mucocutaneous Leishmaniasis
cases occur in Bolivia, Brazil and Peru

4. Transmission and Life cycle of
Leishmania

5. • Different mammals: - Primates, Rodents,
Canids, Edentates, Marsupials, Procyonids,
and Ungulates
• serve as potential reservoir hosts of the
parasites and as sources for human infection.
• There are 31 sand fly insect vectors in Genus
Phlebotomus (in the ‘Old World’) and in
Genus Lutzomyia
• (in the ‘New World’) that transmit Leishmania
parasites.

6. • Majority of human infections in many areas
are acquired from reservoir animals (both wild
and domestic)
• via the insect vector.
• However, in some parts of the world
transmission cycle is maintained among
people (human—sand fly—
• human), this type of transmission is called
anthroponotic. e.g. L. donovani

7. List of Leishmania parasites that cause
human infection
• L. donovani complex- L. donovani, L. infantum, L.
chagasi
• L. tropica complex - L. tropica, L. Killick
• L. mexicana complex- L. mexicana, L. amazonensis, L.
venezuelensis, L. garnhami, L. pifanoi
• L. braziliensis complex- L. braziliensis, L. peruviana ,
L. guyanensis, L. panamensis, L. shawi
• L. aethiopica
• L. major
• L. naiffi
• L. lainsoni

8. Geographical Distribution of
Leishmaniasis
• . Visceral leishmaniasis
• Visceral leishmaniasis is mainly caused by
Leishmania donovani Complex
• • Leishmania donovani (India, Pakistan, sub-
Saharan Africa, North Africa)
• • Leishmania infantum (Mediterranean Basin,
Middle East)
• • Leishmania chagasi (South America & Central
America)

9. Cutaneous leishmaniasis
• In the `Old World `skin leishmaniasis is due to the
following Leishmania spp
• • L. tropica (Southern Europe or Mediterranean
basin, Middle East). Causes frequently dry lesions
• • L. major (Middle East, Sub-Saharan Africa).
Causes frequently moist lesions
• • L. aethiopica (Ethiopia, Kenya). Causes diffuse
cutaneous leishmaniasis (DCL) and sometimes also
• affects mucosal tissue

10. • In the ‘New World’ skin leishmaniasis is caused
by L. mexicana Complex & L. braziliensis
Complex (in
• South and Central America, Southern USA)
• • L. mexicana complex: L. mexicana, L.
venezuelensis, L. amazonensis , L. pifanoi
• • L. braziliensis complex: L. braziliensis, L.
peruviana, L. guyanensis, L. panamensis, L
shawi

11. Mucocutaneous leishmaniasis
• Occurs in the ‘New World’ in South and Central
America due to L. braziliensis, L. panamensis and
L. guyanensis
• Diseases / Pathological features of Leishmania
sis in Human
Leishmaniasis may occur as asymptomatic carrier
state, mild or severe cutaneous lesions, as severe
mucocutaneous disease, visceral disease and death.

12. (A) Cutaneous leishmaniasis (CL),
usually caused by the Leishmania tropica complex, L. major, L.
aethiopica and all species of the L. mexicana complex
• Cutaneous leishmaniasis is the most common form of
Leishmaniasis. It usually produces ulcers on
the exposed parts of the body, such as the face, arms and
legs.
• Cutaneous leishmaniasis is frequently self-healing in the ‘Old
World’, but lesions can be multiple
sometimes up to 200 – which can cause serious disability and
leave life-long scars.
• The most severe form of CL is due to L. tropica, which is
called recidivans and very difficult to treat,
long-lasting (chronic), destructive and disfiguring.

13. (B) Diffuse cutaneous leishmaniasis
(DCL),
• caused by L. aethiopica or L. amazonensis
• • DCL occurs in individuals with a defective
cell-mediated immune response.
• • Its severity is due to disseminated nodular
lesions, resembling those of lepromatous
leprosy.
• • It is subject to relapse after treatment with
any of the currently available drugs.

14. (C)Mucocutaneous leishmaniasis
(MCL),
• is usually caused by L. braziliensis, but also less
frequently
• by L. panamensis and L. guyanensis
• • MCL causes extensive destruction of oral, nasal
and pharyngeal cavities (surrounding tissues)
with
• disfiguring lesions resulting mutilation of the lips
and nose.
• • Mucosal leishmaniasis is the less common form
of leishmaniasis.

15. (D)Visceral leishmaniasis (VL) (also
called kala -azar),
• usually caused by species of the L. donovani
• Complex.
• It is the most severe disease nearly always
fatal within 2 years if left untreated.
• Parasites invade vital organs spleen, liver,
bone marrow, lymph nodes and sometimes
can infect the
• kidneys, lungs, CNS, intestinal mucosa.

16. • VL is characterized by undulating fever,
substantial weight loss, splenomegaly,
hepatomegaly,
• lymphadenopathy, anaemia, leukopenia, and
thrombocytopenia.
• • VL causes large-scale of epidemics with a high
fatality rate, Th1 response (IL-1, IFN-ɣ) is
protective,
• whereas Th2 response (IL-4) results susceptibility.
• • VL has emerged as an important opportunistic
infection associated with HIV.

17. • A co-infection of HIV with asymptomatic VL
increases the risk of developing active VL by 100
• times and even more.
• • The two diseases are mutually reinforcing:- HIV-
infected people are particularly vulnerable to VL,
• while VL accelerates HIV replication and
progression to AIDS.
• • In co-infected individuals risk of treatment
failure for VL is high, there is relapse and
eventually

18. • patients die unless they are given antiretroviral
therapy (ART).
• • In southern Europe, up to 70% of cases of
visceral leishmaniasis in adults are associated
with HIV
• infection. In Ethiopia there are significant number
of HIV/VL co-infection cases (reports being
• 23%, even up to 40%)
• • To date, as many as 35 countries throughout
the world have reported cases of VL/HIV co-
infection.

19. (E) Post-kala-azar dermal leishmaniasis
(PKDL)
• is a complication of visceral leishmaniasis (VL) in
• areas where Leishmania donovani is endemic. It
is characterized by a hypopigmented macular,
• maculopapular, and nodular skin rash in patients
who have recovered from VL caused by L.
donovani.
• It usually appears 6 months to 1 year or more
after apparent cure of the VL. PKDL heals
• spontaneously in the majority of cases in Africa
but rarely in patients in India.

20. Diagnostic Methods
• Microscopy examination
• The confirmatory diagnosis of leishmaniasis is
microscopic detection of amastigotes in samples
• Samples are aspirates by FNA or biopsies from bone
marrow, spleen, lymph nodes, liver, and nodular
• skin lesions. Other samples peripheral blood, skin
scrapping from ulcerated lesion.
• • The sample smear can be stained with Giemsa stain,
or Hemotoxyline Eosine (H & E) stain on glass
• slide, where amastigotes are clearly seen under
microscope with 1000x magnification.

21. Direct agglutination test (DAT)
• DAT is a highly specific and sensitive test and
simple to perform for both field and laboratory
use.
• The test can be carried out on plasma or serum
from patient against Promastigotes in suspension
• Enzyme-linked immunosorbent assay (ELISA)
• ELISA is most sensitive test for the serodiagnosis
of visceral leishmaniasis

22. • ELISA can be performed with various antigens
such as whole soluble antigen (cytoplasmic SA),
• purified antigens , synthetic peptides,
recombinant proteins, L. donovani antigen (Ld-
ESM),
• L. major gene B protein (rGBP), recombinant
protein (rORFF) of L. infantum
• • ELISA test using these antigens was found to
be highly sensitive and specific against patient
• antibodies.

23. Rapid antibody or antigen detection
methods
• Two rapid tests are developed for antibody
detection in patient serum using commercially
available
• antigens (Lc-rK39 antigen and Ld-rKE-16 antigen)
coated on membrane.
• For antigen detection in patient sample, a latex
agglutination test (KATEX) is used for the
detection
• of leishmanial antigens from urine of VL patients.

24. Leishmanin skin test (LST)
• It is Dermal Delayed Hypersensitivity Reaction
also known as the Montenegro reaction ,where
• Leishmania antigen is injected into the skin to
observe hypersensitivity reaction.
• LST is used as an indicator of the prevalence of
cutaneous and mucocutaneous leishmaniasis
and to
• evaluate successful cure of the visceral
leishmaniasis.

25. Treatment (Chemotherapy)
• Cutaneous and Mucocutaneous Leshmaniasis
– Direct therapy:
– Local therapy (intralesional antimonials), Topical
paromomycin in 10% urea or 12%
methylbenzethonium chloride
– Oral Chemotherapy:
– Azoles (Fluconazole, Ketoconazole, Itraconazole),
Miltefosine, Dapsone, Allopurinol
– Parenteral Chemotherapy:

26. • Pentavalent Antimonials (Sodium stibogluconate
or Meglumine antimoniate)
• Pentamidine isethionate
• Amphotercin B (second-line treatment for sever
infection)
• For mucosal treatment Pentavalent Antimonial
drugs are best options or Amphtericin B
• Physical therapy :
• Cryotherapy:- weekly treatment of two freeze /
thaw cycles until cure

27. • Thermotherapy:- 1-3 applications of
radiofrequency waves at 50°C for 30 Seconds. Its
use depends on number and size of lesions.
• Visceral Leishmaniasis
• • There must be effective and rapidly active
therapy for VL , because it is fatal if left
untreated.
• • Pentavalent antimonials (Sodium
stibogluconate or Meglumine antimoniate) with
IFN-γ.

28. • • Second line chemotherapy is Lipid
formulation of Amphotericin B.
• • Alternative drugs are Miltefosine,
Paromomycin sulphate, or Pentamidine
isethionate.
• • Immunotherapy:- 5% imiquimod, which
induces the production of cytokines that
stimulate a Th1 Response.

29. Malaria
• Plasmodium species are the causes of a disease known as
Malaria. The genus Plasmodium comprises
• more than 200 species that infect reptiles, birds, and
different mammals
• • Human malaria is caused by Plasmodium falciparum, P.
malariae, P. ovale, P. vivax, and P. knowlesi.
• • Human infection was documented occasionally by other
Plasmodium species such as P. cynomolgi,
• P. bastianelli, P. simiovale, P. brasilianum, P. schwetzi, P. inui,
P. simium.
• • There are about 460 species of Anopheles mosquito, but
only 30-40 transmit malaria parasites as
• vectors to human.

30. • In Ethiopia malaria transmission is by Anopheles
arabiensis Patton in the intermediate highlands,
• Anopheles funestus Giles is the second most
important malaria vector, and Anopheles nili
Theobald is an important local malaria vector in low
land regions of south-west Ethiopia.
• P. knowlesi, is a malaria parasite species that
commonly infects long-tailed and pig-tailed
macaque monkeys (Macaca fascicularis and Macaca
nemestrina, respectively) in Southeast Asia.

31. • Recently, a number of human infections are
being detected in Southeast Asia countries
(Cambodia,
• Laos, Myanmar, Thailand, Vietnam, Peninsular
Malaysia, Indonesia…), but not reported from
other countries.
• Hence, P. knowlesi is now recognized as the
fifth species of Plasmodium infecting humans
with public health importance.

33. • It is a major public health problem in 97 countries
mostly in Africa and Asia.
• • An estimated 3.3 billion people are at risk of
acquiring malaria.
• • WHO reported in 2014, 128 million cases of
malaria occurred worldwide (estimated cases
were
• 198 million) and 78% of these in Africa, followed
by 15% in Southeast Asia, the rest in Central, &
• South America.

34. • Approximately 7,000 imported malaria cases
were recorded in Europe.
• • In the year 2014 about 584,000 deaths were
registered, 90% of death occurred in Africa.
• • About 78% of the global death toll
comprises children under 5 years of age (75%
in Africa)
• • Almost all deaths are caused by P. falciparum
(over 95%)

35. • Between the year 2000 and 2013 malaria
incidence is reduced by 30 % globally and 34%
in Africa
• (in same period mortality decreased 47%
globally, and 54% in Africa)
• • Malaria in Ethiopia is caused by four human
malaria species: P. falciparum, P. vivax, P. ovale
and P. malariae.

36. • P. falciparum and P. vivax malaria in Ethiopia
takes a significant share of about 60% and 40 %,
• respectively
• • P. malariae is found sporadically in some areas
and P. ovale was reported rarely in Ethiopia.
• • In Ethiopia an estimated 75% of the total area
of the country with altitudes below 2000m is
malarious

37. • About 50 million people (65-68% of the population)
live in these areas
• • The peak of malaria incidence occurs between
September-December each year after the main rainy
• season, but there is heterogeneous pattern all over
the country
• • There is also increasing frequency and magnitude
of unstable malaria epidemics in highland areas
• with altitude up to 2500 meter.
• In Ethiopia generally malaria is associated with
altitude, rainfall, humidity and population
• movement

38. Aetiology and Pathogenesis of Malaria
• Malaria occurs as either mild (uncomplicated) disease or
severe (fatal) disease.
• Pathogenesis depends on virulence of the parasite isolate
and a variety of host related factors such as host’s immunity,
genetic make-up, physiology.
• All the clinical symptoms associated with malaria are caused
by the asexual erythrocytic or blood
• stage parasites. When the parasites develop in the
erythrocytes, numerous known and unknown
• waste substances such as hemozoin pigment and other toxic
factors accumulate in the infected red
• blood cells. These are dumped into the bloodstream when
the infected cells lyse and release
• invasive merozoites.

39. • The waste/toxic substances released into the blood
due to rupture of infected erythrocytes
• contribute to pathogenesis and symptoms by
stimulating macrophages and other cells to produce
• cytokines and other inflammatory soluble factors
which act to produce fever, rigors and other
• malaria related symptoms.
• • Some of these waste/toxic substances are red blood
cell membrane products, hemozoin pigment,
• plasmodial DNA, antigens & toxic factors such as
glycosylphosphatidylinositol (GPI).

40. • The cytokines and inflammatory mediators are
TNF, IFN-γ, IL-1, Il-6, IL-8, macrophage
colonystimulating factor, lymphotoxin,
superoxide, nitric oxide (NO) and hemozoin
are released and Hemozoin is linked to the
induction of apoptosis (cell death) in
developing erythroid cells in the bone marrow
that contributes to anaemia.

41. • Severe malaria is often caused by Plasmodium
falciparum
• P. f infected erythrocytes, particularly those with
mature trophozoites, adhere to the vascular
• endothelium of venular blood vessel walls and do
not freely circulate in the blood.
• • When this sequestration of infected erythrocytes
occurs in the vessels of the brain it is believed to
• be a factor in causing the severe disease syndrome
known as cerebral malaria, which is associated
• with high mortality.

42. • Severe malaria in addition involves pathogenesis
mechanisms such as rosetting, cytoadherence,
and
• sequestration of infected erythrocytes in the vital
organs.
• • These mechanisms contribute to blocking of
blood flow, local oxygen supply, mitochondrial
ATP
• synthesis, and stimulating cytokines production
resulting in various organ dysfunctions.

44. Uncomplicated (Mild) Malaria
• Can be caused by all five human malaria Plasmodium
species
• Can be caused by all five human malaria Plasmodium
species
• Symptoms of uncomplicated malaria are nonspecific and
acute
• A febrile illness (fever) with headache, tiredness (fatigue),
muscle pain, joint aches, abdominal pains,
• rigors (severe shivering), perspiration, nausea, anorexia,
vomiting and diarrhea.
• Mild anaemia, jaundice, splenomegaly, hepatomegaly

45. B. Severe (Fatal) Malaria
• Clinical signs:
• Deep coma due to CM, multiple convulsions,
acute renal failure, pulmonary edema, hepatic
• dysfunction, disseminated intravascular
coagulation, haemoglobinuria, retinal oedema,
lack of retinal reflex, circulatory shock
• • Severe vivax malaria is defined as for
falciparum malaria but with no parasite density
thresholds.
• • Severe knowlesi malaria is defined as for
falciparum malaria but with two differences:

46. • P. knowlesi hyperparasitemia: parasite density > 100
000/μL
• • Jaundice and parasite density > 20 000/μL.
• • In children, malaria has a shorter course, often rapidly
progressing to severe malaria. Children are
• more likely to present with hypoglycemia, seizures, severe
anemia, and sudden death, but they are
• much less likely to develop renal failure, pulmonary
edema, or jaundice.
• • Cerebral malaria results in neurologic sequelae in 9-26%
of children, but of these sequelae,
• approximately one half completely resolve with time.

47. Cerebral Malaria (CM)
• Due to cytoadherence, rosetting, rigidity of infected
erythrocytes (IE), elevated TNF-α, IL-5, IFNγ, NO
• in the brain
• • There is seizure, coma, retinal hemorrhage,
subconjuctival hemorrhage.
• • Duration of coma is 48 – 72 hrs.
• • Brainm becomes swollen with multiple petechial
hemorrhages in white matter, with mid-zonal necrosis.
• • Parasite sequestration is higher in comatous pts.

48. • Long term sequelae:- heparesis, cerebellar
ataxia, blidness, mental retardation,
encephalopathy, and others
• Liver
• Sequestration occurs, perivenous ischaemia,
necrosis, hepatomegaly, becomes gray color,
• • Elevated hepatic enzymes, decreased serum
albumin, lactic acidosis, increased bilirubin,
jaundice

49. • Spleen
• Splenomegaly, occasionally ruptures, color grey to
black, congested with IE & Non-IE,
• reticuloendothelial hyperplasi
• Kidneys
• May swell, sequestration in glomeruli, capillaries with
malaria pigment, tubular necrosis with acute
• renal failure, immune complex deposition in glomeruli.
• GIT
• Sequestration of IE & Non- IE in mucosa, gut ischaemia,
malaria pigment, haemorrhage, dyspepsia, epigastric
pain, diarrhea.

50. • Placenta
• Massive sequestration in sinusoids with IE, becomes
black, perivillous fibrin deposition, macrophage
infiltration, thickning
• Bone Marrow
• Sinusoids congested with IE, becomes hyperaemic,
abnormality in erythrpoesis leading to anaemia.
• Shock (`Algid Malaria`)
• Due to hypovolaemia or septicaemia, endotoxemia,
hypoglycaemia, lactic acidosis, haemorrhage in organs.

51. • Metabolic Acidosis
• Lactic acidosis rapidly fatal, due to renal failure
for H+ ion retention, increased anaerobic
glycolysis
• of the parasite & hepatic gluconeogenesis
• Coagulopathy
• Disseminated intravascular coagulation
• Blackwater fever
• Black or dark brown-red urine, due to massive
haemolysis, with high mortality.

52. • Malaria in Pregnant Mother
• Pregnant women, especially primigravidae
women, are up to 10 times more likely to
contract malaria
• than nongravid women. Gravid women who
contract malaria also have a greater tendency to
develop
• severe malaria commonly with P falciparum and
there is also high risk developing severe malaria
with P
• vivax infection.

53. • • For these reasons, it is especially important that
nonimmune pregnant women in endemic areas
use the
• proper pharmacologic and non-pharmacologic
prophylaxis.
• • In susceptible mothers there can be intense
placental parasitaemia, more susceptible to
hypoglycaemia,
• pulmonary oedema, haemolytic anaemia.
• • There is risk of abortion, still birth, premature
labour, low-birth-weight infant, fetal distress.

54. • Congenital Malaria
• Parasitaemia is found frequently in infants born from
non -immune mothers in endemic areas.
• • Malaria symptoms are rare in the new born if
maternal antibodies are transferred and give
protection.
• • Most antimalarial drugs are very effective and safe in
children, provided that the proper dosage is
• administered. Children commonly recover from
malaria, even from severe disease, much faster than
• adults.

55. Labratory Diagosis
Microscopy methods
• A. Light Microscope
• Thin and thick blood smear on glass slide stained with
Giemsa is used to detect parasites (ring stage)in infected
erythrocytes.
• B. Dark field microscopy
• This method to parasites based on the light refracted from
malaria pigment
• C. Fluorescent microscope
• Fluorochrome stains (acridine orange,
benzothiocarboxypurine) are used on thick smear to detect
• parasite with Fluorescent microscope.

56. Immunodignostic methods
• A. Antigen capture assay
• • Polyclonal or monoclonal antibodies adsorbed
on to a solid chromatographic surface are used to
• detect specific parasite antigens from patient
blood.
• • Such a method is used as rapid diagnostic test
(RDT) to detect antigens, histidine rich protein- II
• (PfHRP-II) from P. falciparum actively secreted
from IE and Lactic dehydrogenase (LDH) secreted
• form P. vivax.

57. • B. Antibody Detection
• Serological tests that detect antibodies from
patient’s serum are Immunoprecipitation,
Indirect haemagglutination test, Indirect
fluorescent antibody (IFA) test, ), ELISA test.

58. Laboratory and Physical Indicators of
Severe Malaria
• Sever anaemia- -Hct < 15%
• • Renal failure- -No urine or < 400ml in 24 hr or
12ml/kg/24 hr after rehydration
• or serum creatinine n> 265 μmol/l (> 3 mg/dl)
• • Hypoglycaemia- -Blood suger < 2.2mmol/l (40ml/dl)
• • Shock- -Systolic BP < 70mmHg in adult or <50mmHg
in children
• • Acidosis- -Arterial PH < 7.25 or plasma HCO
• -3 < 15
• More than 3X elevation in serum enzymes
(aminotransferases)
• • Increased plasma TNFα (tumor necrosis factor α )

59. • Peripheral schizontaemia -Presence of schizontes in
peripheral blood
• • Peripheral blood PMNL - > 12 000/ µl
• • Malaria pigment- -In > 5% of polymorphonuclear
leucocytes
• • High plasma lactate- - >6 mmol/l
• Hyperparasitaemia- - > 5% in non-immune, or >100,000/ µl
for low to moderate
• transmission area or >200, 000 / µl for high transmission
area
• • Mature pigmented parasites in peripheral blood (>20% of
parasites)
• • Hyperpyrexia- T° > 40

60. Treatment
• There are different classes of antimalarial drugs
with different biological activities.
– 1) 4-Aminoquinolines- (Chloroquine, Amodiaquine,
Piperaquine) with blood schizonticide activity
– (2) Arylaminoalcohols- (Quinine, Quinidine,
Mefloquine, Halofantrine, Lumefantrine) with
blood schizonticide activity

61. • Currently artemisinin based combination therapy (ACT) drugs:-
Artemether/Lumefantrine,
• Artesunate/Amodiaquine, Artesunate/Mefloquine,
Artesunate/Sulfadoxine-pyrimethamine and
• Dihydroartemisinin/Piperaquine are potent for the treatment of
uncomplicated P. falciparum malaria
• • The target for Artemisinin drugs has been shown to be PfATPase6
enzyme, which is the molecule
• responsible for refilling of calcium ion into the endoplasmic
reticulum (ER) stores of the parasite.
• • Artemether/Lumefantrine (AL), a fixed dose in a 1:6 ratio
(20mg/120mg) approved as Coartem®,
• now comprises nearly 75% of the 100 million or so ACT oral
treatments in endemic countries for P.
• falciparum including Ethiopia.

62. • Severe falciparum malaria is treated with IV Quinine or IV
Artesunate and other supportive therapies
• towards all kinds of organ and system complications.
• • Treat adults and children with severe malaria (including
infants, pregnant women in all trimesters and
• lactating women) with intravenous or intramuscular
artesunate for at least 24 h and until they can
• tolerate oral medication. Once a patient has received at
least 24 h of parenteral therapy and can
• tolerate oral therapy, complete treatment with 3 days of an
ACT.
• • Plasmodium vivax uncomplicated malaria is treated with
oral Chloroquine

63. Malaria Control/Prevention Methods
• By eliminating or reducing mosquitoes
• • Killing of larva, pupa, adult by chemicals--- DDT, Pyrethrum, Pyrethrins,
Pyrethroides,
• Malathaion,Temephos, Propoxur and Copper acetoarsenite, Petroleum oils
and derivatives on water
• surface where mosqiutoes breed.
• • Protection of people with Impregnated bed nets, repellents, clothing,
good house with insect screen. By eliminating or reducing mosquitoes
• • Killing of larva, pupa, adult by chemicals--- DDT, Pyrethrum, Pyrethrins,
Pyrethroides,
• Malathaion,Temephos, Propoxur and Copper acetoarsenite, Petroleum oils
and derivatives on water
• surface where mosqiutoes breed.
• • Protection of people with Impregnated bed nets, repellents, clothing,
good house with insect screen.

64. • By making human dwellings away from mosquito
breeding area.
• • Environmental managment– Filling in ditches,
clearing vegetation, cover water containers or pits.
• • Biological control of mosquito by using hostile
bacteria (Bacillus sphaericus & B. thuringiensis),
• growing plants that inhibit mosquito breeding.
• • Early diagnosis , effective and prompt treatment of
malaria patients.
• • Early detection or forecasting of malaria epidemics
(e.g. by remote sensing methods).