| These are some of the selected questions sent by visitors to this malaria
web site since January 1999. The identity of the questioners has not been revealed.
Q: From N., Nairobi
I have visited your Malaria
web site. I am writing from Nairobi. Malaria and HIV are rampant in this region. What are
the complications of Malaria in AIDS patients, particularly if it goes untreated?
A: (B.S.K.)
Studies on the association
of malaria and AIDS have been conducted at various hospitals in Zaire, Tanzania, Nigeria,
Zambia and other African countries where both these diseases are prevalent. The following
are the important observations from these studies
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There is no difference in the incidence of
malaria in HIV infected and non-infected populations. Malaria does not occur as an
opportunistic infection in these patients
-
Due to the immunodeficiency state in AIDS,
the clinical symptoms of malaria may be atypical in AIDS
-
It has been observed that cerebral malaria
and mortality on that account are less among patients with AIDS compared to non-HIV
population, despite high parasitemia in these patients. This has been attributed to low
tumor necrosis factor (a chemical released by the white cells in response to
infection/inflammation, which mediates many of the host responses) in patients with AIDS
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Mass screening for malaria by finger
pricking for blood smears may carry a risk of HIV transmission
-
Malaria can cause severe anemia and
treatment of such patients with blood transfusion can also transmit HIV infection
-
Chloroquine is known to suppress the
effects of interferons and this may result in faster viral replication and may be one of
the factors responsible for higher transmission of HIV in African countries where
chloroquine is used for treating the epidemic of malaria
-
AIDS associated and endemic Kaposi's
sarcoma are highly prevalent in Africa and this may have some relationship to malaria or
arthropod vectors
-
Serological tests for malaria may not be
reliable in patients with HIV infection
Q: C.H., Singapore
Are there instances of
Plasmodium infection in pigs or wild boars? If there are, what is the species?
Is Plasmodium known to
cross-infect from humans to animals?
A: (B.S.K.)
I have no information to
suggest that malaria can occur in pigs and wild boars. It has been reported in different
species of monkeys, birds and rodents. And very rarely these can infect man. P.
cynomolgi, P. cynomolgi bastianellii, P.simium, P. brasilianum, P. inui,
P. shortti, P. knowlesi are examples for malaria in monkeys. P. berghei, P.
yeolii, P. vinckei and P. chabaudi are rodent species and P. gallinaceum,
P. cathemerium, P. circumflexum etc are species in birds. Human malaria
can be transmitted to animals. P. vivax can occur in chimpanzees, and Aotus
monkeys, but rhesus monkeys are immune. P. ovale can infect chimpanzees. P.
malariae has been reported in chimpanzee, and other animals. P. falciparum
can infect mice, gibbons, Aotus monkeys, howler monkeys, chimpanzee etc.
Q: Dr. M., Florida
Could you explain how both
sickle cell anemia and thalassemia are protective mechanisms against the development of
malaria?
It has been observed that
certain inborn defects in the blood hemoglobin offer some sort of a protection against
either clinical attacks of malaria or its complications. The exact mechanism of this
protection is not well understood. However, many possibilities have been suggested.
-
People of West African origin are
strikingly non-susceptible to P. vivax infections. It has been found that P.
vivax merozoites penetrate the red cells after binding to the Fya and Fyb
receptors, which are the Duffy blood group antigen alleles. In the West African
population, this blood group antigen is an extreme rarity and this explains the
phenomenon.
-
The sickle cell trait (heterozygous state)
has been found to confer protection against the complications of P. falciparum
malaria (at a ratio of 1:10 compared to non-sickle cell children, in a controlled study).
Decreased availability of oxygen in the presence of abnormal hemoglobin, faster clearance
of sickled cells by the spleen, decrease in the intracellular pH, leakage of potassium,
rigidity of cell membrane in the presence of Hb S may all contribute to the resistance.
-
Hemoglobin F also has protective effects
against severe malaria. In beta thalassemia, fetal hemoglobin levels are high.
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In Melanasian ovalocytosis, the rigid
membrane of the red cells prevents entry of the parasites.
Q: R.S.
By the way, is the major
vector in your area Anopheles stephensi? If so, Anopheles stephensi is rather unique
in that, in the literature, I have seen that it breeds in containers like water tanks,
cisterns, old tires? etc. If An. stephensi is the vector in the area, have you
thought about coordinating the community in a source reduction effort?
A: B.S.K.
A. stephensi is the
major vector for urban malaria in India. In fact, malaria has made a dramatic comeback in
India since early 1990 mainly in the urban areas like Mangalore, Bombay, Calcutta, Madras,
Goa and others. This has been attributed mainly to increase in movement of rural workforce
(may be carriers of malaria) to the cities and to tremendous increase in construction
activities in the cities since 1990. This helped in water logging at construction sites-
breeding of the vector-and the rural workers at these sites provided the parasites. As you
have rightly said, malaria cannot be controlled without the active participation of the
public. The page on Malaria in Mangalore also gives the information on the initiative
taken by some of us in organizing a mass campaign for malaria control. This has now become
a role-model for the National Malaria Eradication Programme in India. Although the
committee had some problems of ego of some of its senior members and is not functioning as
actively as before, the work has already started showing results with significant
reduction in the incidence of malaria this year.
Q: K.K., Research
Engineer
Is the jaundice a symptom of
the hemolytic icterus. I always thought a hemolytic icterus wouldn't result in yellow eyes
and urine because the bilirubin in the blood isn't conjugated.
A: (B.S.K.)
Yellowish discoloration of
the sclera of the eye is seen in any type of jaundice. Increase in either unconjugated or
conjugated or both types of bilirubin results in yellowish discoloration of the sclera. In
hemolytic jaundice, it is generally a lemon yellow tinge whereas in conjugated
hyperbilirubinemia, it can be deeper and even greenish yellow. Yellowish discoloration of
the urine is seen only when the conjugated bilirubin levels are high in the serum.
Unconjugated bilirubin being insoluble in water, it is not excreted in the urine. In
situations where the unconjugated bilirubin levels are greatly increased, naturally the
conjugated bilirubin levels are also increased to facilitate excretion. In malaria,
jaundice could be due to hemolysis of infected red cells and/or malarial hepatitis.
Therefore it is common to see unconjugated and/or conjugated hyperbilirubinemia.
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