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Malar ia10
1. Malaria
Paludisme, Paludismo,
Малария
Malaria is the world’s most important
parasitic disease.
2. Distribution
• Malaria-endemic countries
- more than 100 countries in
Africa, Asia, Oceania, South
and Central America, some
of the Caribes.
Malaria-endemic countries
are among the poorest in the
world.
• More than a third of the
world’s population (about 2
billion people) live in
malaria-endemic areas and 1
billion people are estimated
to carry parasites at any one
time.
Mortality
• In Africa alone, there are • Annual malaria mortality range from 0.5 to 3 million people.
an estimated 200-450
million cases of fever in Malaria-related mortality is particularly difficult to measure
children with malaria each because the symptoms of the disease are non-specific
year. and most deaths occur at home.
• Despite global economic development, more people die from
malaria
nowadays than 40 years ago.
3. World situation
• During the “eradication era”, half a century
age, malaria was eliminated or effectively
suppressed in many parts of the world,
particularly subtropical regions.
• Malaria is now on the rise again;
since it is appearing in areas where it had
disappeared, it is classified by some as a re-
emerging disease.
• WHO dates: Malaria in Europe region - 10
countries:
Тurkey, Аzerbaijan, Аrmenia, Таdjekistan,
Grusia, Uzbekistan, Каzakhstan, Кyrgystan,
Тurkmenistan, Russia
• Use of ineffective drugs for a potentially
lethal disease will inevitably result in an
increase in mortality. Development of
resistance to antimalarial drugs had resulted
in a four to eight fold increase in mortality.
4. Etiology and pathogenesis
Four species of the genus Plasmodium cause nearly all infections in
humans. These are Plasmodium vivax, Plasmodium ovale, Plasmodium
malariae, and Plasmodium falciparum.
P. falciparum predominates in Africa, New Guinea, and Haiti;
P. vivax is more common in Central America and the Indian
subcontinent. The prevalence of these two species is approximately
equal in South America, eastern Asia, and Oceania.
P. malariae is found in most endemic areas, especially throughout
sub-Saharan Africa, but is much less common.
P. ovale is relatively unusual outside Africa.
6. Vector
Various species of anopheline
mosquitoes
are definitive hosts of
malarial parasites
• An. Maculipenis,
• An. Superpictus,
• An. Elutus ets.
7. Bilogical Cycle of
parasites
Human infection
begins when a
female anopheline
mosquito
inoculates
plasmodial
sporozoites from
its salivary gland
during a blood
meal
8. When the female
mosquito bites
an infected
person, she
draws into her
stomach blood
that may
contain
gametocytes –
male end female.
• In mosquito
glend of the
developmental
cycle depends
not only on the
species of
Plasmodium,
but on the
particular
mosquito host
and the ambient
temperature
(more than
16ºC).
9. • These microscopic forms of the
malarial parasite are carried
rapidly via the bloodstream to the
liver, where they invade hepatic
parenchymal cells and begin a
period of asexual reproduction.
• By this amplification process
(known as intrahepatic or
prerythrocytic schizogony or
merogony), a single sporozoite
eventually produces thousands of
daughter merozoites.
• The swollen liver cell eventually
bursts, discharging motile
merozoites into the bloodstream;
at this point the symptomatic
stage of the infection begins.
• These microscopic forms of the
malarial parasite are carried
rapidly via the bloodstream to the
liver, where they invade hepatic
parenchymal cells and begin a
period of asexual reproduction.
• By this amplification process
(known as intrahepatic or
prerythrocytic schizogony or
merogony), a single sporozoite
eventually produces thousands of
daughter merozoites.
10. • By the end of the 48-h intraerythrocytic life cycle (72 h for P.
malariae), the parasite has consumed nearly all the hemoglobin and
grown to occupy most of the red cell. Multiple nuclear divisions take
place (schizogony or merogony), and the red cell ruptures to release
6 to 30 daughter merozoites, each capable of invading a new red cell
and repeating the cycle.
The disease in human beings is caused by the direct effects of red
cell invasion and destruction by the asexual parasite and the host's
reaction. During this process, some parasites develop into
morphologically distinct sexual forms (gametocytes, still within the
erythrocytes), which are long-lived.
11. • Thus the infected erythrocytes sequester
inside the small blood vessels.
• At the same stage, these P. falciparum-infected
red cells may also adhere to uninfected red
cells to form rosettes. The processes of
cytoadherence and rosetting are central to the
pathogenesis of falciparum malaria. They
result in the sequestration of red cells
containing mature forms of the parasite in
vital organs (particularly the brain and heart),
where they interfere with microcirculatory flow
and metabolism. only the younger ring forms
of the asexual parasites are seen in the
peripheral blood in falciparum malaria.
• In the other three "benign" malarias,
sequestration does not occur, and all stages of
the parasite's development are evident on
peripheral blood smears. Whereas P. vivax, P.
ovale, and P. malariae show a marked
predilection for either old red cells or
reticulocytes and produce a level of
parasitemia seldom exceeding 2 percent, P.
falciparum can invade erythrocytes of all ages
and may be associated with very high levels of
parasitemia.
12. Clinical features
Incubating period - 9 до 60 days
P. vivax – 10 - 21 days, 8–14 months (P. vivax hibernans)
P. ovale – 11 - 16 days
P. falciparum – 9 - 16 days
P. malariae – 28 - 60 days
The first symptoms of malaria are nonspecific – the lack of
a sense of well-being, headache, fatigue, abdominal
discomfort, and muscle aches, anorecia, subfebril
period, in children diarrhea , followed by fever are all
similar to the symptoms of a minor viral illness.
This Prodromal period is 3-5 days.
In some instances, a prominence of headache, chest pain,
abdominal pain, arthralgia, myalgia, or diarrhea may
suggest another diagnosis.
13. Clinical features
Malarial paroxysm
1. Fever - trembelling, tachicardia (1/2 - 2 hours);
2. Febrile period - 38 - 41 С, 4-6
hours, nausea, headache, tahipnoea, myalgia, a
rthralgia, convulsions, lose consciousness
3. Sweating - after fast fall of temperature (1-2 h)
14. • Start of malarial fever - on day ( 09 - 15 h)
- Ovale malaria - usually evening
• Periodicity:
- 48 h – invasion with P. vivax и P.ovale
- 36- 48 h, or every day – invasion with P. falciparum
- 72 h – P. malariae
• The classic malarial paroxysms, in which fever spikes,
chills, and rigors occur at regular intervals, suggest
infection with P. vivax or P. ovale.
• The fever is irregular at first (that of falciparum malaria
may never become regular). The temperature of
nonimmune individuals and children often rises above
40ºC in conjunction with tachycardia and sometimes
delirium.
• Liver enlargement – in first days of desease
15. • Splenic enlargement, mild
jaundice may develop in
patients with otherwise -
uncomplicated falciparum
malaria and usually resolves
over 1 to 3 weeks.
Severe Falciparum malaria
Cerebral malaria
• Coma is a characteristic and
ominous feature of falciparum
malaria and, despite treatment,
is associated with death rates of
approximately 20 % among
adults and 15 among children.
• - Cerebral malaria manifests as
diffuse symmetric
encephalopathy; focal
neurologic signs are unusual.
16. • Cerebral malaria manifests as diffuse symmetric encephalopathy; focal neurologic signs are
unusual. Although some passive resistance to head flexion may be detected, signs of
meningeal irritation are lacking. Approximately 15 % of patients have retinal hemorrhages.
Fewer than 5 % have significant bleeding
Convulsions usually generalized and often repeated, are common, particularly among
children with cerebral malaria. Whereas adults rarely suffer neurologic sequelae,
approximately 10 % of children surviving cerebral malaria especially those with
hypoglycemia, severe anemia, repeated seizures, and deep coma have some residual
neurologic deficit when they regain consciousness.
• Pulmonary Edema (Noncardiogenic) Adults with severe falciparum malaria may develop
noncardiogenic pulmonary edema even after several days of antimalarial therapy. Mortality is
over 80 %. This condition can be aggravated by overly vigorous administration of intravenous
fluid.
Renal Impairment Renal impairment is common among adults with severe falciparum
malaria but rare among children. The pathogenesis of renal failure is unclear but may be
related to parasitized-erythrocyte sequestration interfering with renal microcirculatory flow
Mortality in the initial phase of hypercatabolic acute renal failure is high; in survivors, urine
flow resumes in a median of 4 days, and serum creatinine levels return to normal in a mean
of 17 days Dialysis considerably enhances the likelihood of a patient's survival.
• Hematologic Abnormalities Anemia results from accelerated red cell destruction and
removal by the spleen in conjunction with ineffective erythropoiesis. In severe malaria in
nonimmune individuals and in areas with unstable transmission, anemia can develop rapidly
and transfusion is often required. In many areas of Africa, children may develop severe
anemia due to repeated malarial infections. This is a common consequence of continued
infection resulting from treatment with chloroquine (or other drugs) to which the parasites
are resistant.
17. • In Pregnancy Falciparum malaria is an important cause of fetal death. In hyper- and
holoendemic areas, malaria in primigravida and secundigravida is associated with
infected mothers remain asymptomatic despite intense parasitization of the placenta
due to sequestration of parasitized erythrocytes in the placental microcirculation.
• Congenital malaria occurs in fewer than 5 % of newborns whose mothers are
infected and is related directly to the parasitic density in maternal blood and in the
placenta.
• Malaria In Children Most of the estimated 1 to 3 million persons who die of
falciparum malaria each year are young African children. Convulsions, coma,
hypoglycemia, metabolic acidosis, and severe anemia are relatively common among
children with severe malaria, whereas deep jaundice, acute renal failure, and acute
pulmonary edema are unusual.
• Chronic complications of malaria
• Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly) Chronic or
repeated malarial infections produce hypergammaglobulinemia; normochromic,
normocytic anemia; and in certain situations splenomegaly.
• Some residents of malaria - endemic areas in tropical Africa and Asia exhibit an
abnormal immunologic response to repeated infections that is characterized by
massive splenomegaly, hepatomegaly marked elevations in serum titers of IgM and
malarial antibody
18. • Quartan Malarial Nephropathy
Chronic or repeated infections with P. malariae may cause soluble immune-complex injury to
the renal glomeruli, resulting in the nephrotic syndrome. Other, unidentified factors must
contribute to this process since only a very small proportion of infected patients develop renal
disease.
• Recrudescens of malaria develops in:
• - Patients with P. falciparum without radical Therapy
• - Resistent P. falciparum to 4-AQ
• - Patients with P. vivax and P. ovale without Primaquine Th
R Relapses are: short-time – after 1 month; late – after 2 or more mths
• Asimptomic carrier
19. DIAGNOSIS
• The diagnosis of malaria rests on the demonstration of asexual forms of
the parasite in peripheral blood smears subjected to Romanovsky
staining. Giemsa at pH 7.2 is preferred.
• Both thin and thick blood smears should be examined.
• The level of parasitemia is expressed as the number of parasitized
erythrocytes among 1000 cells. The relation between parasitemia and
prognosis is complex; in general, patients with more than 105 parasites
per microliter are at increased risk of dying, but nonimmune patients may
die with much lower counts.
• A poor prognosis is indicated by a predominance of more mature P.
falciparum parasites (i.e., more than 20 percent of parasites with visible
pigment) or circulating schizonts in the peripheral blood film or by the
presence of phagocytosed malarial pigment in more than 5% of
neutrophils.
20.
21. Laboratory Findings
• Normochromic, normocytic anemia is usually
documented.
• The leukocyte count is generally low to normal, although
it may be raised in very severe infections.
• The platelet count is usually reduced to about 105 per
microliter. Severe infections may be accompanied by
prolonged prothrombin and partial thromboplastin times
and by especially severe thrombocytopenia
• Findings in severe malaria may include metabolic
acidosis,
• with low plasma concentrations of:
• glucose, sodium, bicarbonate, calcium, phosphate, and
albumin together with elevations in lactate, blood urea
creatinine, urate, muscle and liver enzymes, and
conjugated and unconjugated bilirubin.
22. Treatment
1. Blood schizonticides
2. Tissue schizonticides of P. vivax и P. ovale
3. Gametocyticides
1. Blood schizonticides
1. 4-aminoquinolines (4-АQ):
diphosphates - Chloroquin, Arthrochin, Resochin, Delagil, Aralen
sulphates - Nivaquin
Chloroquine – total doses 25-30 mg./kg., 1,5 g. 3 days, 1 day - 0,900 g. (I-st dose
0,600 g., after 6-8 h 0,300 g.), 2 и 3-ти day – x 0,300 g. Children – total dose: 25
mg/kg, 1 days 10 mg/kg, after 6-8 h 5 mg/kg, 2 и 3-th day x 5 mg/kg.
2. Pyrimethamine (Tindurin, Daraprim) tb. 25 mg, 2 / day
3. Sulfonamides - Sulfadoxin tb. 0,250 g, Sulfalene tb 0,250 g
4. Quinoline methanols - Mefloquine (Lariam) tb 0,250 g
5. Phenanthrine ethanols - Halfan (Halophantrin)
6. Antibiotics – Tetracycline, Doxycycline (Vibramycin)
7. Combined medicine:
• Fansidar (Sulfadoxin + Pyrimethamin) tb. 0,5 g. 3 tb. eднокр.,
• Fansimef (Sulfadoxin+Mefloquine+Pyrimethamine) tb.0,775 g, 3 tb.
8. Artemisin (Qinghaosu) 10 mg/kg, 3 days, Artemether, Paluther, Artesunat
9. Sinthetic – Pyronaridine и др.
23. The drug of choice for treatment of Resistant falciparum malaria are:
- Quinine (sulphuricum/dihydrochloricum ) tb.0,200 g.
600 mg every 8 ч., 7 days + Tetracycline 250 mg/6h, 7 days, Children- 10 mg/kg
every 8 h, 3-7 days;
- Mefloquin tb. 0,250 gr, 15 mg/kg. immune person and 25 mg/kg non-immune,
max. dose 1 g, in 2 dose after 6 h.
Therapy in patients who are unable to take the oral drug:
I.V. - Chloroquine (diphosphate или sulfate) 10 mg/kg в 10 ml/kg isotonic fluid
(or amp. 5% sol. Chloroquine diphosphate – 0,2 ml/kg), very slow - for 4 h,
second dose 5 mg/kg after 8 h, total dose 25 mg/kg
I.M. - Chloroquine 2,5 mg/kg every 4 h or subcutan - 3,5 mg/kg every 6 h till
total dose 25 mg/kg.
I.V. - Chininum dihydrochloridum amp 2 ml. 300 mg base in 1 ml in adults and
children: 10 mg/kg in 10 ml/kg 5% Glucose for 4 h, second infussion after 8-
12 h. In pregnancy – the risk to the fetus of severe falciparum malaria greatly
outweighs the possible risk of quinine therapy
2. Tissue schizonticides of P. vivax и P. ovale (effective against tissue
schisonts)
• 8-aminoquinolines (8-АQ) – Primaquine 15 mg / day, 14 days, per os; in G-
6-PD deficient - 7,5 mg/kg/ week, 8 weeks
• in patients with deffisancy of G6PD develop intravasals hemolisis
• Children > 1 years – 0,25 mg/kg/day, 14 days.
3. Gametocyticides - Primaquine for all species of human malarial paracites
• Chloroquine and amodiaquine – effective against the gametocytes of p. vivax,
p. ovale, p. malariae but do not affect p. falciparum
24. PREVENTION
In most of the tropics, the eradication of malaria is
not feasible because of the widespread
distribution of Anopheles breeding sites, the great
number of infected persons, and inadequacies in
resources, infrastructure, and control programs.
• Where is possible, the disease is contained by
judicious use of insecticides to kill the mosquito
vector, rapid diagnosis and appropriate patient
management, and administration of
chemoprophylaxis to high-risk groups.
• No safe, effective, long- acting vaccine is likely to
be available for general use in the near future.
25. Personal Protection Against malaria
•Simple measures to reduce the frequency of mosquito bites in malarious areas are very
important. These measures include the avoidance of exposure to mosquitoes at their peak
feeding times (usually dusk and dawn) and the use of insect repellents, suitable clothing,
and insecticide-impregnated bed nets. Widespread use of bed nets, particularly those
treated with permethrin (a residual pyrethroid), often reduces the incidence of malaria
and has recently been shown to reduce mortality in western and eastern Africa.
•Antimalarial prophylaxis. Travelers should start taking antimalarial drugs at least 1
week before departure so that any untoward reactions can be detected and therapeutic
antimalarial blood concentrations will be present when needed. Antimalarial prophylaxis
should continue for 4 weeks after the traveler has left the endemic area.
•Mefloquine has become the antimalarial prophylactic agent of choice for much of the
tropics because it is usually effective against multidrug-resistant falciparum malaria and
is reasonably well tolerated.
•Chloroquine 300 mg, деца 5 mg/kg./week, 1 week before travel
•Fansidar – 1 tb./ 1 week before travel, 4-6 weeks after coming back x 2 tb./2 weeks
•Mefloquine - x 1 tb./ week for adults and children above 45 kg
•Proguanil ( Paludrin ) tb. 100 mg. (in pregnancy) - 200 mg/day, in children: <1 years -25
mg, 1-4 years - 50 mg, 5-8 years -100 mg, 9-14 years -150 mg/day
•Pyrimethamine - 2 tb./ week
