Epidemiology of Malaria

13,497 views 41 slides Mar 07, 2022
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About This Presentation

This ppt contains all the information about the epidemiology of Malaria. It is useful for students of the medical field learning Preventive and social medicine, Swasthavritta (Ayurved), and everyone who is interested in knowing about it


Slide Content

Malaria
Dr. ShubhangiS. Kshirsagar
Assistant professor
Department of Swasthvritta& Yoga
[email protected]

Malaria
▪Malariaisaprotozoaldiseasecausedby
infectionwithparasitesofthegenus
Plasmodiumandtransmittedtomanbycertain
speciesofinfectedfemaleAnophelinemosquito.
▪Atypicalattackcomprisesthree·distinctstages–
1.Coldstage
2.Hotstage
3.Sweatingstage

Agent factors
a. Agent
▪Malaria is caused by 4 distinct species of
maleriaparasite -P. vivax, P. falciparum, P.
malariaeand P. ovale
▪P. vivax–widest geographic distribution
throughout the world
▪In India
✓P. Falciparum-50% infections
✓Mixed infection -4-8%
✓P. Malariaerest ( 42%)
✓P. Ovale

Life cycle of malaria parasite
▪The malaria parasite undergoes 2 cycles of
development -
1.Human cycle (asexual cycle)
2.Mosquito cycle (sexual cycle)
▪Man is the intermediate host and mosquito
the definitive host.

1. Asexual cycle
▪The asexual cycle begins when an infected
mosquito bites a person and injects sporozoites.
▪Four phases in the asexual cycle are –
1.Hepatic phase
2.Erythrocyticphase
3.Gametogeny

1.Hepatic phase
•Sporozoitesdisappear within 60min from peripheral
circulation
•Many –destroyed by phagocytes, some reach the liver cells
•After 1-2wks, they become hepatic schizonts, which burst -
releasing shower of merozoites.
•P. falciparum-form 40,000 merozoites
•& other species may form 2,000 to 15,000 merozoites(do not
burst all at same time, they persist & remains dormant in
hepatocytescausing relapse of infection.)
•P. vivax& P. ovale-relapse for 2-3 yrs
•P. malariae–10-20 yrs or more

2. Erythrocyticphase
Many merozoitesare destroyed and significant number of
merozoitesare attached to RBC
Merozoitespenetrate RBC & passes through the stages of
trophozoites& schizonts
The erythrocyticphase ends with the liberation of merozoites,
which infect red blood cells
The cycle is repeated over & over again until it is slowed
down by immune response of the host
Duration of erythrocyticcycle –
✓P. falciparam, P. vivax& P.ovale–48hrs
✓P. Maleriae–72 hrs.

3. Gametogeny
▪Someerythrocyticformdonotdividebut
becomemale&femalegametocytes
▪Thesearesexualformsoftheparasitewhich
areinfectivetomosquito.

Sexual cycle (in mosquito)
▪Vector mosquito feed on infected person
▪Gametocytes ingested by mosquito
▪Development in mosquito
▪In mosquito stomuch–exflagellationof male
gametocyte –-micro-gamatesare formed
▪Female gametocyte undergoes a process of maturation
& become female gamete or macrogamete
▪By process of chemotaxis, microgametesare attached
towards female gamete & one of microgamete causes
fertilization of female gamete.
▪Zygote formation –motionless body
▪Within 18-24 hrs –becomes motile known as Ookinete

▪Ookinetepenetrate stomach wall of mosquito
▪Develops into an oocyst
▪Oocystgrows rapidly & develops within it
numerous sporozoites
▪When mature, oocystburst & liberates
sporozoitesinto the body cavity of mosquito and
the mosquito becomes infective to man
▪Extrinsic incubation period -Time required for
development of the parsitefrom the gametocyte
to sporozoitestage -10-20dys

Life cycle of malaria parasite

Reservoir of infection
1.Animal reservoir –Chimpanzees in tropical
Africa
2.Human reservoir
Conditions to serves as a reservoir
a.Both sexes of gametocytes in blood
b.Gametocytes musts be mature
c.Gametocytes musts be viable
d.Gametocytes must be present in sufficient
density ( at least 12/cubic mm of blood.
3. Children as reservoir –gametocytes carrier

Period of communicability
▪Malaria is communicable as long as mature,
viable gametocytes present in blood
▪Gametocytes in sufficient density
▪Vivaxinfection –4-5days
▪Falciparuminfection –10-12 days

Relapse
▪P. Vivax& ovale->3yrs after patient first attack
▪P. Falciparum–disappear within 1-2yrs
▪P. Maleriae–tendency to cause prolonged low
level asymptomatic parasitemia. Infection may
persist for more than 40 yrs or more.
▪Vivax& ovalerelapse –sporozoiteinduced (latent)
▪P. falciparum& malariae–due to chronic blood
infection

Host factors
1.Age –all age
✓Newborn infants have considerable resistanceto
infection with P. falciparum
✓Due to high concentration of foetalHb during
first few months of life, which suppresses the
development of P. falciparum
2. Sex –males are more exposed
3. Race –Sickle cell trait ( AS Hb) milder illness with
falciparuminfection
4. Pregnancy –increases risk of malaria
Primi–greatest risk
May cause IUD, premature labouror abortion

5.Socio-economicstatus
6.Housing–illventilated&illlightedhouses
provideidealindoorrestingplacesfor
mosquito
7.Populationmobility
✓Onecountrytoanotheror1partofcountryto
anotherpart
✓Importedmalaria

8. Occupation –related to agriculture
9. Human habits
✓Sleeping out of doors
✓Refusal to accept spraying houses
✓Not using measures of personal protection
10. Immunity
Acquired after repeated exposure
Endemic areas –collective immunity

Environmental factors
1.Season–seasonal disease, max prevalence in
India from July to Nov
2.Temperature –optimum temperature for
development of malaria parasite 20-30
0
C.
Temp higher than 30
0
C is lethal to the parasite.
3. Humidity –60% necessary for mosquito life.
> 60% -more active & feed voraciously
< 60% -not live long
4. Rainfall –provides opportunities of mosquito
breeding & may give rise to epidemic of malaria.

5. Altitude –
Anophelinesare not found at altitude above
2000-2500 meters, due to unfavorable
conditions
6. Man –made malaria
Burrow pits, garden pools, irrigation channels
and engineering projects like construction of
hydroelectric dams, roads, bridges have led to
the breeding of mosquitoes and an increase in
malaria.

Mode of transmission
1. Vector transmission -Malaria is transmitted by
the bite of certain species of infected, female,
anophelinemosquitoes.
2. Direct transmission -Malaria may be induced
accidentally by hypodermic intramuscular and
intravenous injections of blood or plasma, e.g.,
blood transfusion, malaria in drug addicts .
3. Congenital –rare

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

Clinical features
▪The typical attack comprises 3 stages. These are
-
1.Cold stage
2.Hot stage
3.Sweating stage
These are followed by an afebrileperiod in
which patient feels greatly relieved.

1. Cold stage
▪Onset with lassitude, Headache,
Nausea & Chilly sensation
▪Temp rises rapidly 39-41
0
C
▪Severe headache & vomiting
▪Early phase –skin cold, later hot
▪Pulse rapid & weak
▪Parasite demonstrate in the blood
▪Pulse –rapid, weak
▪This stage lasts for ¼-1hour.

2. Hot stage
▪Patient feels burning
hot & cast off his cloths
▪Intense headache
▪Skin hot & dry
▪Nausea diminish
▪Pulse full
▪Respiration rapid
▪Lasts for 2-4hrs

3. Sweating stage
▪Fever comes down
with profuse sweating
▪Temperature normal
▪Skin cool & moist
▪Pulse rate slow
▪Patient feels relieved
& falls asleep
▪Lasts for 2-4hrs

Febrile peroxysms
▪Occurs with definite intermittent periodicity
▪Every 3
rd
or 4
th
day –depend on species of
parasite
Tendency of relapse –month to yrs
1. P. Falsiparum
▪Fever irregular/ continuous
▪Classical 48hrs periodicity
▪Hot & cold stage

2. P. Vivax
▪Symptoms are like p. falsiparumbut mild
▪Regularly divide into hot & cold stage
3. P. Ovale
▪Milder than vivax
▪Ceases after few paraxymus
4. P. Malariae
▪Resembles P. Vivax
▪But 72 hrs periodicity
▪Tendency for long term relapse

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

Diagnosis
1.Microscopy
2 Types of film on single slide
a. Thick film –searching of parasite
b. Thin film –identification of parasite
2. Serological test
After 2 wks +ve---treatment /cure
3. Rapid diagnostic test (RDT)

Guidelines for diagnosis &
treatment of Malaria -2013
Treatment of uncomplicated Malaria
Diagnosis by RDT / microscopy
a. Treatment of P. vivax
1.Chloroquine25mg/kg body wt for 3 days
2.Primaquine0.25mg/kgbodywt for 14 days

b. Treatment of P. falciparum
a. In other states –ACT-SP x 3days
1. Artemisinincombination therapy (ACT)
( Artesunate50mg x 3days
Sulphadoxine-pyrimethaminex1 day)
2. Primaquine0.75mg /kg body wt on day 2
b. NE states -ACT-AL (age specific)
Artemether20mg +Lumefantrine120mg x 3days
Primaquinesingle dose on 2
nd
day

Treatment

Mosquito control measures
Mosquito
control
measures
Antilarval
measures
1. Environmental
2. Chemical
3. Biological
Anti-adult
measures
1. Space spray
2. IRS
3. Genetic control
Legislative
control
Civil laws
Protection
against
mosquito bite
1. Bed net
2. Repellent
3. Screening

Mosquito control measures
1. Antilarvalmeasures
a.1. Envirnmentalmeasures
b.2. Chemical
c.3. Biological
2. Anti-adult measures
a.Space spray -application of pesticides in the form
fog or mist
b.IRS –indoor surface of houses –DDT, malathion
c.Genetic control
3. Legislative control -Civil, laws
4. Protection against mosquito bite -Bed net, Repellent,
screening

Anti adult measures

Insecticide residual spray

Smog

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