‫بسم الله‬

‫‪malaria‬‬‫الرحمن‬
‫الرحيم اشراف‬
‫‪:‬‬
‫د‪.‬عثما‬
‫ن‬
‫اعداد‬
‫‪:‬وتقديم‬
‫الزبير‬
‫ضحى‬
‫معتصم‬
‫غيداء‬
Objectives:
1-history.
2-epidemiology and
malaria in sudan.
3-life cycle.
4- relation of
clinical picture to
life cycle.
5-investigations.
6-management.
7-prevention.
 Malaria in
sudan
 75% of
population is at risk of
developing malaria.

 In 2015, 586,827
confirmed cases were
reported from public
health facilities out
of the estimated
1,400,000 cases
 The reported malaria
cases represent 8.7%
and 12.2% of the total
outpatient attendance
and of
hospital admissions
respectively.
 Mortality was
4.3% in
2015 putting
malaria as one of
the main causes of
death in Sudan.
 Survey in 2016
showed an overall
prevalence of 5.9%

 The prevalence
correlates with age,
children are 3 times
more likely to get
malaria than adults.
 The main species is
the P. falciparum
representing
87.6% of cases.

 The main
vector species is
Anopheles arabiensis
besides An. Gambia
and An. funestus.
 The low
economic class
is at higher risk.

 Internally
displaced people
and refugee
camps reported
prevalence
doubled that in
rural areas and 3
times higher than
that in urban
areas.
Plasmodium vivax
PLASMODIUM SPECIES WHICH
(tertian) 8,1%
Plasmodium ovale INFECT
(tertian) HUMANS
Plasmodium falciparum
(tertian) 87,6%
Plasmodium malariae
(quartan)
Mixed vivax and
falciparum 5%
[Link]
[Link] :- tropics in West ,
Central and parts of East Africa
ALSO in Middle East and Eastern
Asia
[Link]:- in tropics & subtropics +
some temperate regions ,
predominant form in Middle East
and Eastern Asia
[Link]:- tropics in Africa , India
and South America
Completely eradicated :- in Europe
& North America
COUNTRIES AFFECT BY MALARIA
Stable malaria :- repeated infections
ENDEMICITY OF MALARIA
and the population has high degree of
immunity
Unstable M :- transmission is
intermittent (seasonal) epidemic liable
to occur
Intensity of transmission :-can be
estimated in numbers of ways:-
parasite rate , spleen rate , age group&
entomological inoculation to
(holoendemic , hyperendemic ,
hypoendemic and mesoendemic areas
 LOW INCIDENCE OF MALARIA
1)Sickle cell disease IN:-

2)G6PDD
3)Thalassaemia
4)Neonate
 MODE OF TRANSMISSION
[Link] of sporozoites by
contaminated female mosquito
into the host blood ( main route
of infection (
[Link] transfusion
[Link] needles
[Link] (congenital
mode)
LIFE CYCLE
 HUMAN STAGE:-
EXO-ERYTHROCYTIC (TISSUE) PHASE
Blood is infected with sporozoites about 30
minutes after the mosquito bite ( [Link] )
The sporozoites are rapidly disappear from
blood stream where are implanted within the
hepatic cells and multiply (pre-erythrocytic
schizogeny)
P. vivax and P. ovale sporozoites form parasites
in the liver called hypnozoites which remain
dormant for months (relapsing malaria)
P. malariae or P. falciparum sporozoites
do not form hypnozites, develop directly
into pre-erythrocytic schizonts in the liver
Pre-erythrocytic schizogeny takes 6-16
days post infection
Schizonts(infected liver cells containing
up to 40,000 merozoites)rupture, releasing
merozoites which invade red blood cells
(RBC)
These are asexual forms
 ERYTHROCYTIC PHASE
Pre-patent period – interval between date of
infection and detection of parasites in peripheral
blood ( 6-16 days )
Incubation period – time between infection and
first appearance of clinical symptoms (10-21days)
Merozoites from liver invade peripheral RBCs
(give appearance of ring form) , replicated and
mature to trophozaites
RBC is rupture and releasing merozoites that
repeated the cycle and some developed to
gametocyte sexual form of parasite that are suck
by anopheles
 MOSQUITOES STAGE
Gametocytes go to mosquito
intestine and fertilization occur to
form the zygote that is devolpe to
oocytes (content thousands of
sporozoites released when ruptures)
which migrate to salivary glands and
then injected into host's tissues
This cycle take about 10 days
 REMEMBER ABOUT RECURRENCE
Recrudescence :- symptoms recur after symptom
free period due to parasites surviving in blood after
inadequate or ineffective treatment
Relapse :- symptoms reappear between 2-28w seen
in [Link] & [Link]
Reinfection :- due to new parasite infection usually >2
weeks after treatment
 CLINICAL FEATURES
The clinical picture depends mainly on the
type of parasite ,process of parasite's
invasion and multiplication within and
rupturing of the host's RBCs
[Link] and [Link] retculocytes
 [Link] normoblast
[Link] any age
Also depends on the Host
factors:-
1. Age
[Link] status
3. General health condition and
nutritional status
4. Chemoprophylaxis or
chemotherapy use
 UNCOMPLICATED MALARIA

[Link] stage :- cold skin , pale ,

tachycardia , rigors , posterior orbital
headache,muscle or joint pain
[Link] stage :- high grade intermittent
fever ( due to release of pyrogens from
rupture RBCs lasts about 15m to one
hour) , flushing , hypotension ,loss of
appetite ,N/V are common
[Link] stage :- here c° slowly subsides
and Pt begins to feel comfortable and go
to deep sleeping , it last 1-4 h , the cycle
Gradual hepato-splenomegaly
occurs :- due to liberated
parasites and pigment being
engulfed by the
reticuloendothelial cells
Anaemia may develop :- due
to immunological factors and
destruction of the RBCs ,
normocytic normochromic
form , reach serious proportion
• P. falciparum parasite displays adhesive proteins
on the surface of the infected blood cells, causing
the blood cells to stick to the walls of small blood
vessels, thereby sequestering the parasite from
passage through the general circulation and the
spleen
 SEVERE MALARIA
Defined as malaria due to [Link] mainly or
[Link] infection that is sufficiency serious to be an
immediate threat to life
Categories have higher risk:-
[Link] women ( esp primigravidae )
[Link] returning to endemic areas after a few years
absence
[Link] from non endemic areas
[Link] < 5years
[Link] individuals
[Link] malaria :- defused cerebral edema due to
RBCs sequestration and cytoadherent , obstruction of
micro vessels , ischemia ,edema presented by :-
confusion ,headache ,delirium , meningism ,
convelsion , coma and other neurological S/S should
be differentiated from meningitis and encephalitis
[Link]:- because parasites feed on glucose ,
fasting , may affect the liver and the quinine
treatment
[Link] acidosis :- respiratory distress
4 non cardiogenic pulmonary edemia
5 Acute renal impairment
6 GI malaria :- bilious remittent M (from severe hepatic &
biliary affection acute epigastric pain & typhoid like
state characteristic remittent fever,stool watery contain
B B , may reach jaundice and hepatomegaly choleric M
( acute watery diarrhoea) OR dysenteric M (bloody
mucoid diarrhoea )
7 algid M :- shock due to gram -ve septicemia
8 black water fever :- intravascular hemolysis of RBCs ,
release of Hb which go to the kidney and executed as
dark urine DD G6PDD
9) hyperpyrexia :- unknown mechanism , Pt become
disoriented & may pass to coma , incontinence of
U/S are common , D/D heat stroke and meningitis
ACCORDING TO TYPES OF PARASITE
General features : malaise , N/V , loss of
appetite , diarrhoea , back pain , joint pain and
headache , rapid pulse and degree of hypotension
In acute a take spleen is usually enlarge & tender ,
rupture may occur in minor trauma
 [Link]
i. Severe hemolysis -> anemia
[Link] -> due to pre mature red cell
destruction -> thrombocytopenia
[Link] adhere to the lining of the capillaries
of the organs and with uninfected blood cells by
the formation of ‘knob’
proteins -> congested of the vessels -> hypoxia
to organs tissues + release toxins that cause
damage of these organs
IV . Immunity is impaired in pregnancy
and the parasite can preferentially bind
to a placental protein known as
chondroitin sulphate A. Abortion and
intrauterinegrowth retardation from
parasitisation of the maternal side of
the placenta are frequent.
 [Link] & [Link]
I. the illness starts with several
days of continued fever before the
development of classical bouts of
fever on alternate days
[Link] develops slowly
[Link] hypersplenism
[Link] malaria
 [Link]
I. Usually mild symptoms
[Link] may persist for many
years, with the occasional
recrudescence of feveror without
producing any symptoms
[Link] P. malariae infection causes
glomerulonephritis and long term
nephrotic syndrome in children.
 TROPICAL SPLENOMEGALY
SYNDROME
1In endemic area
2Huge splenomegaly
3Increase in Igm antibody
4Good response to chloroquine
5Presinosiodal lymphocytosis in
liver biopsy
Investigation
s:
 specific:

Parasite based
diagnosis
blood smear
preparation
(thick and thin
films)

Antigen based
diagnosis:

immunochromatographic
 blood film report
components:
 Presence of
malaria parasite
(seen or unseen)

 Parasite species
(pf, pv, po, pm and
p knowlesi)
 Stages of the parasite
(ring stage,
trophozoite, schizont
and
gametocytes)

 Parasite count
Reporting of parasite
count:
Two methods are
commonly used in
reporting blood smear
results, the parasite
per micro-litre and the
“plus” system.
[Link]
[Link]
[Link]
E
rasite per microlitre of blood:

(Parasite count per µl of blood) = (Number

of parasites × 8000 WBC) ÷ (Number of
leucocytes counted
3-DNA detection
(PCR) :useful for
determining whether
a patient has
a recru-
descence of the
samemalaria parasite
or a re-
infection with a new
parasite.
General
investigation:-

 Cbc:
*Hb%
*wbc (super
added infection)

 RBG(severe
malaria)
 RFT(severe
malaria)
manageme
nt
CLASSIFICATION of antimalarial drugs
 Schizontocidal drugs:- act
against asexual erythrocytic of
all species of malaria parasites
[Link] , quinine
 Gametocytcidal drugs:- active
against sexual form of all species
of malaria [Link] ,
quinine and quinocide
 Sporontcidal drugs:- inhibited
the development of parasite in
mosquito [Link] and
quinocide
 Anti-relapse:- act on pre-
erythrocytic forms e.g.
 Uncomplicated malaria
Fist line treatment :-
 in Sudan is Artemether-
lumefantrine [AL]
tablets(CoArtem)
Highly effective fixed dose
combination antimalarial drugs
 Six doses twice / day for 3 days
20mg A , 120mg L for children
AL 80/480 for adult
SE: nausea and vomiting, pruritus ,
no serious adverse reaction and no
risk of cardiotoxiaty

Contraindications :-
hypersensitivity to AL & 1st
Second line treatment :-

Treatment failure :consider

when fever and parasitemia
persist or recurs within 4weeks
after initial treatment
 Dihydroartemisinin +
piperaquine ( DHAP ) 3 dose
over 3 days one daily at same
time
20/160 mg DHAP -> paediatric
40/329mg -> adult
Third line :-
In case of non-response
to DHAP or not
available
Oral quinine
(dihydrochloride ,
hydrochloride or
sulphate )
Dose 10mg salt/kg 8
hourly for 7 days
Treatment of
uncomplicated vivax
malaria:-

 First line treatment is AL

followed by primaquine
Primaquine is used in all
cases of [Link],except:
pregnant women , infant
<6months , breastfeeding
mothers and known people
of G6PDD
Dose 15mg daily for 14 days
-> adult
,25 mg/kg 14 days ->
children
Management of severe malaria
 SM should be managed at
hospital
 The health care providers on
duty at any level of health care
services should consider the
following ( 8+8+4) points
 Do the following 8 immediate
measures:-
• 1- ABCs
• 2-Establish IV line
• 3-Make thick blood smear or
RDTs
• 4-Classify the degree of
• 5-Control fever : tepid sponge ,
fanning and oral or rectal
paracetamol
• 6-Control convulsion :
diazepam ( rectal ,5mg/kg
or ,3mg/kg IV maximum 10mg
• 7-Detect & treat
hypoglycaemia :- if blood
glucose < 40mg/dl give 1ml/kg
of 50% dextrose
• 8-Start quinine IV or
artesunate IV OR IM
Look and deal with the following 8
complications:
1. Shock, algid malaria
Correct hemodynamic disturbances. Treat with: 30ml/kg 0.9%
Saline IV in
1hour, then, reassess.

2. Consider the need for blood transfusion

(no palor, some palor or severe palor)

3. metabolic acidosis: Exclude and treat hypoglycaemia,

hypovolaemia and gram negative septicaemia.
4. If spontaneous bleeding and
coagulopathy: Transfuse screened fresh whole
blood or clotting factors; give vitamin K 10 mg IV
per day for adult, Vitamin K should be given SC or
IV.

5. Acute renal failure: maintain strict fluid

balance; carry out dialysis if indicated
.
6. Malarial hemoglobinuria (black-water
fever): Continue with suitable
anti-malarial treatment; transfuse screened fresh
blood if needed
[Link] pulmonary
oedema: Prevent by
avoiding excessive
rehydration.

[Link] common
infections/conditions that
present like severe
malaria
Monitor considering
the following 4
points:-

Level of
consciousness :- if
there is an alter in
consciousness level used
Glasgow scales every 6h

Fluid input/output:-
detect dehydration and avoid
overload
Vital signs :- every 6h to
3. Vital signs: Monitor vital signs
every 6 hours to detect complications of
severe malaria. If pulmonary oedema
develops (rapid respiratory rate and
deep laboured breathing) stop all IV
fluids except quinine.

4. Level of parasitaemia:
Determine the parasite count daily to
monitor the
therapeutic effect of treatment.
Specific treatment of SM
1-quinine IM (10mg salt/kg
dilution with NS ) OR

2-artesunate
suppositories (for paediatric
pt only 10mg/kg)

If after 24h the pt has

not been referred to
hospital and is still
unable to take oral
medication , second
dose should be
repeated
1-IV Quinine :- by 3 ways
depending on pt conditions and
health facility:

 Quinine for 7 days :- 10mg

quinine in 5% glucose or Dx+NS
infusion ( 8 hourly over 4h ) for at
least 2 days & shift to oral quinine

 Quinine IM:- same dose and

shift when pt can take orally

 Oral Quinine for at least 3days

& then first line: it's observed that
compliance to oral quinine
sometime is not good.
Quinine side
effects:
Rapid intravenous
administration of
Quinine can precipitate
hypoglycaemia,
hypotension and fatal
cardiovascular toxicity.
Treatment with IV
artesunate:-
 Short acting that clear [Link]
more rapid than other antimalarial ,
it acts against both sexual and
asexual stage

 Available at 30 , 60 , 120 mg
 Side affects :- hypersensitivity
reaction , GI disturbances , cough ,
rash , arthralgia and dizziness , the
most significant SE clinically is
hemolysis which has been reported
up to week after treatment
What is special about
malaria in pregnancy?

The mortality and morbidity

of MIP is higher than in non-
pregnant women.
The risk is even more
increased in primigravidae.

Reduced immunity to
malaria in pregnancy leads
to more relapses of malaria
and more parasitaemia and so
worsens clinical
manifestations.
Malaria in pregnancy:
Uncomplicated M first trimester
-> oral quinine 7days

Uncomplicated M second & third

trimester -> AL , DHAP or
Quinine

Severe M first trimester ->

quinine infusion 3 days shift to
oral

Severe M second & third ->

quinine or IV artesunate
Prevention:
 Control the reservoir
and vector.

 Protect against
disease by
prophylaxis , nets ,
proper clothing ,
spraying and
improving the
environment
groups are at
higher risk to malaria
infection:
1- Travellers from
malaria free areas
(visitors).
2- People with sickle
cell disease.
3-Splenectomised
individuals.
4-Children on
steroids or
immunosuppressive
Prophylaxis for pregnant
travellers: Mefloquine is
the agent of choice in
chloroquine-resistant
areas,

The dose is 250 mg

orally once a
week after the main
meal. Start 1 to 2 weeks
before arrival and
continue
for 4 weeks after leaving