MALARIA: Disease, Life Cycle,Distribution, Prevention and cure drugs treatment

MALARIA: Disease, Life Cycle, Distribution
Definition:

Malaria is both an acute and chronic disease caused by protozoa of the genus Plasmodium. Four species cause human malaria: P. falciparum, P. vivax, P. malariae, and P. ovale. The protozoa are transmitted to humans by female mosquitoes of the genus Anopheles. (Transmission can also occur by direct inoculation of infected red blood cells via transfusion, needles, or congenitally). Some signs and symptoms of the illness are high fever, chills, headache, anemia, and splenomegaly. Most serious and fatal complications are caused by P.falciparum.

MALARIA PREVENTION AND CURE

Life Cycle:
The life cycle of malaria is complex (see Fig. 1-1) with developmental stages and corresponding symptoms differing according to the Plasmodium species involved (see Table 1-1). Sporozoites, the infective stage of plasmodia, are injected from the salivary glands of infected mosquitoes during feeding. Following inoculation, the sporozoites disappear from the blood within 30 minutes. Many are destroyed by white blood cells, but some enter liver cells.

Exoerythrocytic Phase of Malaria

Erythrocytic Phase: Released merozoites invade red blood cells (erythrocytes), where they develop into trophozoites. After a period of growth, the trophozoites divide and develop, eventually forming 8-24 merozoites in each red blood cell. When this process is complete, the host red blood cells rupture, releasing mature merozoites. The symptoms associated with malaria occur at this
point. The merozoites then invade fresh erythrocytes and another generation of parasites develops in the same manner. This process occurs repeatedly during the course of infection and is called eryrthrocytic schizogony. The length of this development cycle differs according to the species of parasite, varying from 48 hours in vivax, ovale, and falciparum malaria, to 72 hours in P. malariae infections. In the early stages of infection there is no characteristic periodicity as groups of parasites develop at different times. The febrile episodes
caused are inconsistent. Later, the erythrocytic schizogony development cycle becomes synchronized, and the febrile paroxysms become more consistent. Some merozoites differentiate into sexual forms (female macrogametocytes, male microgametocytes) and develop in invaded red blood cells. 

Vector Phase:  Anopheles mosquitoes feeding on infected hosts ingest sexual forms developing in red blood cells. The 7 female macrogametocytes and male microgametocytes mature in the mosquito’s stomach and combine forming a zygote that undergoes mitosis. The products of mitosis are ookinetes, which force themselves between the epithelial cells to the outer surface of the stomach, and form into small spheres called oocysts. The oocysts enlarge as the nucleus divides, eventually rupturing and releasingthousands of motile sporozoites into the body cavity. The sporozoites migrate to the salivary glands, making the female mosquito infective.
The vector phase of the life cycle, called sporogony, is complete in 8 to 35 days depending on species and environmental conditions.

Environmental Factors

Environmental Factors:
Anopheles mosquitoes are essential for
development, multiplication, and spread of plasmodia. Therefore, any area harboring Anopheles mosquitoes may be at risk for
Table 1-1. Selected Characteristics of the Four Species of
Human Malaria

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Selected Characteristics of the Four Species of
Human Malaria

Malaria Life Cycle

Malaria Life Cycle:

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Malaria Life Cycle

 malaria transmission. Specific environmental conditions optimal for
anopheline mosquito vector and parasite development include
temperature between 200 and 300C and a mean relative humidity of
60%. The sporogony phase requires temperatures between 160 and
330C. High relative humidity increases mosquito life-span, thereby
increasing the probability of mosquitoes becoming infective. Areas
with high rainfall have increased malaria incidence because of an
increase in breeding sites. The accompanying high humidity
increases survival rates of female anopheline mosquitoes. Elevation,
along with cooler temperatures and lower humidity, is also a factor as
transmission rarely occurs above 2000-2500 meters.
Distribution. The worldwide distribution of malaria is illustrated by the
map in Fig 1-2. This is a general representation and not intended for
threat assessment or countermeasure planning. Country-specific
information can be obtained from the Medical Environmental Disease
Intelligence and Countermeasures (“MEDIC”) compact disc, and the
11
Navy Environmental and Preventive Medicine Unit responsible for a
particular world area. (Further intelligence can be obtained from the
agencies listed in Appendix One).
Malaria transmission occurs in more than 100 countries.
Regions include Africa, Asia, islands of the South, west, and central
Pacific Ocean, Latin America, certain Caribbean islands, and Turkey.
These areas, all between 450 N and 400 S latitude (see Fig. 1-2),
possess tropical or

PREVENTION OF MALARIA:

Prevention of  Malaria:
Systematic applications of four tactics are essential to planning
and carrying out disease and injury prevention in field and combat
operations. Listed in order, they are applicable for prevention of
malaria (or any other threat):
1) Determine disease and injury threats in the area of operation
before deployment.
2) Identify or develop countermeasures to reduce threats to an
acceptable level.
3) Educate personnel regarding threats and train in correct use of
countermeasures.
4) Command enforcement of countermeasures.
The next three sections of this chapter review effective malaria
countermeasures available. Preventive countermeasures are divided
into three sections: Personal Protective Measures,
Chemoprophylaxis, and Unit Protective Measures. Medical
personnel must seek information to answer the questions outlined
below and determine which countermeasures to employ, and make
recommendations for the same to commanders:
1) What type(s) of malaria is(are) present?
2) Which countermeasures will be effective in the area and
situations the unit will encounter?
3) How will the unit obtain the necessary supplies, personnel, and
equipment needed?
4) Do unit personnel know how to apply the countermeasures
chosen? Will they apply them? What training is needed?
5) Does the entire chain of command understand its role and
accountability in enforcing the countermeasures?

HIV/AIDS and Antiretroviral Therapy

HIV/AIDS and
Antiretroviral Therapy

The risk of transmitting HIV/AIDS depends on the mode of transmission, the infectiousness of the person with HIV, and the susceptibility of the person exposed (table 3.1). Despite these relatively limited modes of transmission, few countries have slowed or reversed the growing HIV/AIDS epidemic. NACO estimates that 84 percent of new HIV infections occur through heterosexual transmission. Reduction of transmission through vaginal intercourse should therefore have the greatest impact on epidemic dynamics.
Strategies to reduce sexual transmission in India would involve:

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•Reducing the probability of HIV transmission during each sexual contact
by increasing condom use.

• Reducing the number of sexual partners through behavioral interventions

for commercial sex workers and the general population.
• Reducing the level and duration of infectiousness through medical interventions,
including treatment of sexually transmitted infections and use of antiretroviral therapy.

Infectiousness depends on the concentration of HIV in genital secretions and on the strain of virus a person carries (Dyer and others 1997; Hart and others 1999). Studies of couples in which one partner is infected and the other is not (so-called “discordant” couples) have shown that the risk to the uninfected partner rises dramatically with the concentration of virus in blood plasma (Gray and others 2001). When the plasma viral load is less than 1,500 copies per cubic millimeter, no transmission is observed. Therisk of infection increases to 1 per 10,000 episodes of intercourse at a plasma viral load level of 3,500 copies per cubic millimeter and to 1 per 200 episodes at a plasma viral load greater than 50,000 copies per cubic millimeter.
By increasing viral shedding, increasing the number of cells receptive to HIV and the number of HIV receptors per cell, the presence of a classic sexually transmitted disease, such as chancroid or gonorrhea, may
increase the risk of HIV transmission for both men and women by a factor of as much as 10, accelerating the spread of the epidemic (Holmes and others 1998; Over and Piot 1993). Different types of HIV may have different capacities for infection. Subtype C, the subtype most commonly found in India, is believed to be the
most infectious. Drug-resistant strains of the virus that are emerging in all parts of the world in response to antiretroviral therapy may be either more or less infectious than strains of the virus that have never been subjected toselection pressure from antiretroviral therapy.

Toxicity, Adherence, and the Development of Resistance as a Result of Antiretroviral Drug Therapy

Antiretroviral Drug (

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Toxicity, Adherence, and the Development of Resistance
as a Result of Antiretroviral Drug Therapy
The advent of antiretroviral drugs in the late 1980s began a revolution in the
management of HIV/AIDS, a revolution that may eventually be seen as analogous
to the use of penicillin for treating bacterial infections in the 1940s.
Antiretroviral treatment strategies seek to suppress viral replication, which
leads to restoration of the immune system. The goal is to slow or halt disease
progression, prevent drug resistance, and improve quality of life.
Three groups of antiretroviral drugs interrupt viral replication. The use
of a single drug or two-drug combinations has been shown to promote rapid
development of resistant strains of HIV and consequent ineffectiveness of
therapy. In the past five years compelling epidemiological and clinical evidence
has shown that with strict adherence, the use of three drugs in combination
achieves sustained viral suppression for several years.1
Since the introduction of antiretroviral therapy, three issues—toxicity,
adherence, and resistance—have tempered initial enthusiasm that HIV/
AIDS could be successfully controlled and that people with HIV/AIDS could