Download MALARIA

MALARIA
,
AL- Abbasi A.M.,
MD, PhD, FRCP DCN, DTM&H
Professor of Infectious
Diseases&
Clinical Immunology
A mosquito-borne infectious disease of
humans and other animals
caused by parasitic unicellular protozoon
microorganism of the genus Plasmodium.
Transmitted via a bite from
an infected female
Anopheles mosquito.
WHO
has estimated in 2010, 219 million documented cases of
malaria.
That year, the disease killed between 1.2 million
people, many of whom were children in Africa.
Actual number of deaths is not known with certainty, as
accurate data is unavailable in many rural areas, and many
cases are undocumented.
Malaria is associated with poverty and economic
development.
Malaria is prevalent in tropical and subtropical regions
because rainfall, warm temperatures, and stagnant waters
provide habitats ideal for mosquito larvae.
Five species of Plasmodium can infect and be
transmitted by humans.
The vast majority of deaths are caused
by P. falciparum, its prevalence 75%,
P. vivax prevalence 20%, most common outside Africa.
P. ovale, and P. malariae cause a milder form of
malaria, rarely fatal.
The zoonotic species P. knowlesi, prevalent in Southeast
Asia, causes malaria in macaques but can also cause
severe infections in humans.
Life cycle
Female Anopheles mosquito (the definitive host)
motile infective form (sporozoite)
a human (the secondary host).
(hepatocytes), asexually (tissue schizogony),
producing thousands of merozoites.
infect new red blood cells and initiate a series of asexual
multiplication cycles (blood schizogony)
that produce 8 to 24 new infective merozoites, at which point the
cells burst and the infective cycle begins a new.
Some merozoites
immature gametocytes,
precursors of male and female gametes.
mature in the mosquito gut.
The male and female gametocytes fuse and form a ookinete—a
fertilized, motile zygote.
Ookinetes develop into new sporozoites
migrate to the insect's salivary glands, ready to infect a new
vertebrate host.
sporozoites injected into the skin, in the saliva, when the mosquito
takes a subsequent blood meal.
Only female mosquitoes feed on blood;
male mosquitoes feed on plant nectar, and do
not transmit the disease.
Females of the Anopheles genus of mosquito
prefer to feed at night.
Malaria parasites can also be transmitted
by blood transfusions, although this is rare.
In the blood, the protests' travel to the liver to mature and reproduce
Genetic resistance
• Several genetic factors provide some resistance to it
including sickle cell trait, thalassemia traits, G6PD deficiency, and
the absence of Duffy antigens on red blood cells.
• Sickle cell trait causes a defect in the hemoglobin molecule in the
blood. Instead of retaining the biconcave shape of a normal RBC,
the cell to sickle or distort into a curved shape.
• Infection causes red cells to sickle more, and so they are removed
from circulation sooner.
• This reduces the frequency with which malaria parasites
complete their life cycle in the cell.
Signs and symptoms
Symptoms typically begin 8–25 days
following infection, or later if anti malarial
medications are taken for prevention.
Initially flu-like symptoms,
but can resemble septicemia,
gastroenteritis, and viral diseases.
The presentation may include headache, fever, shivering, joint
pain, vomiting, hemolytic anemia, jaundice, hemoglobin
urea, retinal damage, and convulsions.
The classic paroxysm
a cyclical occurrence
of sudden coldness,
shivering and then fever
and sweating,
occurring every two days
(tertian fever) in P. vivax
and P. ovale infections,
and every three days
(quartan fever) for
P. malariae.
P. falciparum infection can cause recurrent fever every
36–48 hours or a less pronounced and almost continuous
fever.
Severe malaria is usually caused by falciparum malaria
which arise 9–30 days after infection.
Individuals with cerebral
malaria frequently exhibit
neurological symptoms,
including abnormal posturing,
nystagmus, opisthotonus,
seizures, or coma.
Ring-forms and gametocytes of Plasmodium
falciparum in human blood
Complications
Respiratory distress, up to 25% of adults and 40% of
children with severe P. falciparum malaria.
Possible causes include respiratory compensation
of metabolic acidosis,
Non cardiogenic pulmonary oedema,
Severe anemia.
ARDS may develop in 5–25% in adults and up to 29% of
pregnant women but rare in young children.
Co infection of HIV with malaria increases mortality.
Renal failure is a feature of black water fever.
P. falciparum may result in cerebral malaria,
It is associated with retinal whitening, distinguishing
malaria from other causes of fever.
Splenomegaly, severe headache, hepatomegaly,
hypoglycemia,
hemoglobinuria,
renal failure may occur.
Malaria in pregnant women with stillbirths, infant
mortality and low birth weight,
Recurrent malaria
Symptoms of malaria can recur after varying symptom-free
periods. Either recrudescence, relapse, or re infection.
Recrudescence:
Symptoms return after a symptom-free period, caused by
parasites surviving in the blood as a result of inadequate or
ineffective treatment.
Relapse:
symptoms reappear after the parasites have been eliminated
from blood but persist as dormant hypnozoites in liver cells.
Relapse commonly occurs between 8–24 weeks and is commonly
seen with P. vivax and P. ovale infections.
Re infection
Means the parasite that caused the past infection was
eliminated from the body but
a new parasite was introduced.
Re infection cannot readily be distinguished from
recrudescence,
although recurrence of infection within two weeks of
treatment for the initial infection is typically
attributed to treatment failure.
Diagnosis
Clinical
microscopic examination of
blood films
antigen-based rapid diagnostic tests (RDT)
PCR
Treatment
For P. falciparum artemisinins in combination with other
antimalarials
(artemisinin-combination therapy, or ACT),
to decreases resistance to any single drug component.
Additional anti malarials
amodiaquine, lumefantrine, mefloquin or
sulfadoxine/pyrimethamine.
Another recommended combination
dihydroartemisinin and piperaquine.
ACT is about 90% effective when used to treat
uncomplicated malaria.
To treat malaria during pregnancy,
WHO recommends the use of
Quinine plus clindamycin early in the pregnancy (1st
trimester),
and ACT in later stages (2nd and 3rd trimesters).
In the 2000s (decade), malaria with partial resistance
to artemisins emerged in Southeast Asia.
Treatment of P. vivax requires both treatment of blood
stages (with chloroquine or ACT) as well as clearance of
liver forms with primaquine.
Severe malaria needs IV use of anti malarial drugs.
For severe malaria, artesunate is superior to quinine in
both children and adults.
Severe malaria needs supportive measures in ICU.
Monitor
high fevers
seizures
poor breathing effort
low blood potassium.
Malaria prophylaxis
• Chloroquine may be used where the parasite is still
sensitive.
In resistant malaria:
one of three medications
mefloquine (Lariam),
doxycycline or the combination of
atovaquone and proguanil hydrochloride (Malarone).
• Doxycycline and the atovaquone and proguanil
combination are the best tolerated.
• Mefloquine is associated with death, suicide, and
neurological and psychiatric symptoms.
The protective effect does not begin immediately, usually
start taking the drugs one to two weeks before arriving
and continue taking them for four weeks after leaving
(with the exception of atovaquone/proguanil, which only
needs to be started two days before and continued for
seven days afterward).
The use of preventative drugs where malaria-bearing
mosquitoes are present may encourage the development
of partial resistance.
Preventative drugs is seldom practical for those who
reside in areas where malaria exists, and their use is
usually only in short-term visitors and travelers.
Due to the cost of the drugs, side effects, difficulty in
obtaining anti-malarial drugs outside of wealthy nations.