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Clinical Features:
The classical malarial fever has 3 stages.
Cold stage(Shivering) lasting for 2 hours
Hot stage lasting for 3-4 hours
Sweating lasting for 2-4 hours
These symptoms occur at regular intervals i.e show periodicity. Periodicity becomes apparent only after the first few days of illness and depending upon the species it could be tertian (every 2nd day for vivax, falciparam and ovale) or quartan (every 4th day for malariae)
However, these clinical symptoms are not present in many patients who have the infection.
Malaria especially caused by P.falciparam is a very variable diseases mimicking many other conditions such as typhoid, meningitis, gastroenteritis etc., Symptoms due to malaria depend opon the age, immune status, intensity of transmission and prevalent species of malarial parasite.
In those living in non-endemic areas, symptoms are very vague because, most of the people are non immune. The disease often presents like flu. Presence of rigors and a rapid increase in temperature should alert the physician to the possibility of malaria.
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In those living in endemic areas, the attacks are modified by immunity. Fever is often intermittent and may have periodicity.
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In children fever due to malaria is variable and has no periodicity.It is mostly irregular, may be high and continous or low grade.
Othere manifestations in children are pallor, nausea, vomiting, refusal of feeds, lethargy, restlesness, headache, diarrhoea and unproductive cough.
Severe forms of malaria are seen with P.falciparam species. Some of the manifestations are severe vomiting and diarrhoea, cerebral malaria, algid malaria, hepato renal syndrome, black water fever and malaria shock lung.
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Diagnosis
Microscopic Diagnosis
- Malaria is diagnosed by making blood smears stained with
Giemsa and examining through microscope using 100x oil immersion objective.
- Microscopy is sensitive, can detect densities as low as
5-10 parasites /ul blood.
- When parasites are found, their species and
circulating stage can be found.
Treatment:
The Best approach in malaria treatment is diagnosis and treatment on the same day.
A.In High Risk Areas (Pf.Predominant And Drug Resistance Areas)
i)Presumptive Treatment of all Suspected clinical Malaria Cases:
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Day 1 |  |
Tab.Chloroquine - 10 mg/kg body weight (bw) (600 mg adult dose) |
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Tab.Priomaquine - 0.75 mg/kg bw 45 mg adult dose) |
Day 2 Tab.Chloroquine - 10 mg/kg bw (600 mg adult dose)
Day 3 Tab.Chloroquine - 5 mg/kg bw (300 mg adult dose)
ii)Radical Treatment after Microscopic confirmation of Species:
P.vivax - Tab.Primaquine 0.25 mg/kg bw (15 mg adult dose) daily for 5 days.
P.falciparam - No further treatment required.
iii)In Chloroquine Resistant P.falciparam Cases/Area
Single dose of 25 mg/kg bw tab.Sulfalenes/Sulfadoxine and 1.25 mg/kg bw Pyrimethamine combination
(3 tabs adult) with tab.Primaquine 0.75 mg/kg bw
B. In Low Risk Areas
i) Presumptive Treatment
Day1 Tab.Chloroquine 10 mg/kg body weight (bw) (600 mg adult state dose)
ii)Radical Treatment after Confirmation of Species
P. vivax Tab.Chloroquine 10 mg/kg bw single dose and tab.Primaquine 0.25 mg/kg bw daily for 5 days
P.faliciparam- Tab.Chloroquine 10 mg/kg bw plus tab.Primaquine 0.75 mg/kg bw single dose
C. Severe & Compicated Malaria Cases to be Hospitalized for the Treatment
i) Choice of antimalarial is quinine injection preferably, 10 mg per kg bw i/v drip in 5% dextrose saline
to be run over 4 hours, 8 hourly. Switch over to oral dose as early as possible and total duration of treatment
should be 7 dyas.
ii) Injectable form of artemisinin derivatives may be used for severe and complicated malaria only.
D.Other information:
i) Tab.Mefloquine is to be used only in Pf cases having proven resistance to chloroquine. Drug may be obtained from drug depots
after producing prescription given by registered medical specialist and lab report confirming of having blood slide
positive for asexual stage of Pf.parasite.
ii) Sulfa-Pyrimethamine combination is not effective in P.vivax cases.
Note:Primaquine is not to be given to pregnant women, infants and Glucose 6 Phosphate Deficient Persons
Source:NAMP
Parasite
There are four species of plasmodium causing four different types
of malaria.
- Plasmodium vivax - Vivax malaria
- Plasmodium falciparam - falciparam malaria
- Plasmodium ovale - Ovale malaria
- Plasmodium malariae - Quartan malaria
Life cycle of malaria
parasite
Comprises
- The exogenous sexual phase (sporogony) in female anophelene mosquitoes, and
- An endogenous asexual
phase
(schizogony) in human host.
 Malaria parasite in mosquito.
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When a female anophele mosquito bites a human host harbouring
maria parasite, it ingests malaria parasites along with the blood meal.
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The asexual forms are digested, while the mature forms called
gametocytes undergo further development.
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In the male gamatocytes the nucleus divides into 4-8 nuclei,
each forming thread like structures called microgametes.
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Female gamatocytes undergo maturation process and form
macrogametes.
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In the mosquito stomach, microgamete fuses with the
macrogamete (fertilization) resulting in a product called a zygote.
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Within 18-24 hrs, zygote develops into a long mobile worm
like form called the Ookinete. (18-24u)
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The Ookinete passes between epithelial cells to the outer surface of the mosquito stomach and becomes rounded up into a
small sphere called an Oocyst.
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The Oocyst increases in size and the nucleus divides repeatedly to form (40 to 80u) Sporoblast.
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The divided nuclei of sporoblast form elongated sporozoites (10-15u) and are released into the body cavity.
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These sporozoites migrate to the salivary gland of the mosquito and are now ready for transmission to human host.
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When the mosquito feeds on blood sporozoites are released into the bloodstream of the human host.
Malaria parasite in Human Host.
Endogenous asexual phase includes
Exo-erythrocytic schizogony or tissure phase (sporozoites in the parenchyma cells of the liver.) Erythrocytic schizogony (Development of sporozoites in the red corpuscles in the blood)
Exo-erythrocytic schizogony or tissure phase.
Sporozoites inoculated by a mosquito into the human host circulate for about half an hour and many are destroyed by the phagocytes.
Some sporozoites enter the parenchymal cells of the liver and undergo a process of development known as Pre-erythrocytic schizogony.
During pre-erthrocytic schizogony (In P.falciparam and P. malariae,) sporozoites develop into schizonts.
In P.ovale and P.vivax, within 40-48 hrs, after an infective bite, sporozoites shrunk and form narrow cytoplasmic rim structures called hypnozoites
Hypnozoites remain dormant in hepatocytes and then grow into schizonts.(Delayed Schizogony)
After about 6 to 16 days from the time of infection, mature schizonts (30 to 70u) enlarge and burst to release thousansands of merozoites(1 um) into the blood.
Merozoites re-enter fresh liver cells and repeat the process of schizogony, thus causing relapses of infection during the secondary exo erythrocytic schizogony.
Erythrocytic schizogony
- Initial recognition and attachment
Formation of juction
Creation of vacuole memberane continous with the red cell memberane
Entry into the vacoule through the moving junction
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And Sealing of the erythrocytes after entry.
After entering the eyrthocytes merozoites assume rounded form.
These youngest stage of parasites in red blood cells are rounded bodies with annular appearance called as ring forms.
The ring forms grow into irregular shapes called trophozoites.
The parasite lives on cytoplasm of the RBC, absorbing haemoglobin and leaves a product of digestion a pigment called haemozoin(combination of haematin with protein)
After a period period of growth, trophozoites divide asexually forming schizonts by a process known as erythrocytic schizogony.
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Mature schizonts divide into small round forms (merozoites)
When the process of schizogony is completed the red blood cell bursts, releasing the merozoites into the blood stream.
Merozoites invade fresh erythrocytes and repeat the erythrocytic schizogony cycle.
After several rounds of erythrocytic schizogony, some merocytes develop into sexual forms, the gamaetocytes.
The number of gametocytes increase with increasing number of erythrocytic schizogony.
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