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Ancylostoma Duodenale

Ancylostoma duodenaleis an S-shaped worm because of its flexure at the frontal end. The worm

is pinkish-white. Adult male hookworms range in size from 8-11 mm long, whereas adult females

range in size from 10-13 mm long. This species is dimorphic, with the males having bursa

characteristics and needle-like spicules with small tips, which are distally fused. Females have a

vulva located approximately one-third of the body length from the posterior end. Both male and

female hookworms have two powerful ventral teeth in the adult forms of the parasite, one along

each side of the buccal capsule; smaller pairs of teeth are located deeper in the capsule.Hookworm

eggs have a thin shell and the larvae possessamphids, large paired sensilla on each side of the

mouth, which allow them to locate their host. The larvae are rod-shaped and are about 0.004 cm.

It is a parasitic nematode worm and commonly known as Old World hookworm.It is small

cylindrical worm, greyish-white in color.. The average lifespan of Ancylostoma duodenale is one

year.When a filariform larva (infective stage) penetrates the intact skin, the larva enters the blood

circulation. It is then carried to the lungs, coughed up, and swallowed back into the small

intestine. The larva later matures into an adult in the small intestine and female worms can lay

25,000 eggs per day. The eggs are released into the feces and reside on soil. Embryonated eggs on
http://animaldiversity.ummz.umich.edu/accounts/Ancylostoma_duodenale/http://animaldiversity.ummz.umich.edu/accounts/Ancylostoma_duodenale/http://animaldiversity.ummz.umich.edu/collections/contributors/biodidac/nematodanter/http://animaldiversity.ummz.umich.edu/collections/contributors/biodidac/nematodanter/http://animaldiversity.ummz.umich.edu/collections/contributors/biodidac/nematodanter/http://animaldiversity.ummz.umich.edu/collections/contributors/biodidac/nematodanter/http://animaldiversity.ummz.umich.edu/accounts/Ancylostoma_duodenale/


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soil will hatch into juvenile 1 stage (rhabditiform or noninfective stage) and mature into filariform

larvae. The filariform larvae can then penetrate another exposed skin and begin a new cycle of

infection. Ancylostoma duodenale is prevalent in southern Europe, northern Africa, India, China,

and southeast Asia, small areas of United States, the Caribbean islands, and South America.

Transmission of Ancylostoma duodenale is by contact of skin with soil contaminated with larvae.

Light infection causes abdominal pain, loss of appetite and geophagy. Heavy infection causes

severe protein deficiency or iron deficiency anemia. Protein deficiency may lead to dry skin,

edema and potbelly, while iron deficiency anemia might result in mental dullness and heart

failure. The eggs of Ancylostoma duodenale and Necator americanus cannot be distinguished.

Larvae cannot be found in stool specimen unless they are left at ambient temperature for a day or

more.Education, improved sanitation and controlled disposal of human feces are important.

Wearing shoes in endemic areas can reduce the prevalence of infection as well.

Ancylostoma duodenale can be treated with albendazole, mebendazole and benzimidazoles.

Pyrantel pamoate is an alternative. In severe cases of anemia, blood transfusion may be necessary.
http://en.wikipedia.org/wiki/Geophagyhttp://en.wikipedia.org/wiki/Geophagy


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Necator Americanus

Necator americanus has a cylindrical body, and a cuticle with three main outer layers made of

collagen and other compounds, secreted by the epidermis. The cuticle layer protects the nematode

so it can invade digestive tracts of animals. Eggs range in size from 65-75 micrometers x 36-40

micrometers and are virtually indistinguishable from those ofAncylostoma duodenale, another

common hookworm.Necator americanus has four larval stages. The first stage is referred to as

rhabditiform larvae because the esophagus has a large bulb separated from the rest of the

esophagus by a region called the isthmus. The third stage is referred to as filariform larvae

because the esophagus has no bulb. Adult females range in size from 9 mm to 11 mm while the

smaller males range in size from 7 mm to 9 mm. The mouth of the adults has two pair of cutting

plates, one dorsal and the other ventral. The males of the species are characterized by fused

spicules found on the bursa. The common name "hookworm" comes from the dorsal curve at the

anterior end. This worm starts out as an unembryonated egg in the soil. After 2448 hours under

favorable conditions, the eggs become embryonated and hatch. This first juvenile stage 1 is

known as 'rhabditiform'. The rhabditiform larvae grow and molt in the soil, transforming into a

juvenile stage 2. The juvenile stage 2 molts once more until reaching the juvenile 3 stage, which
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is also called 'filariform'; this is also the infective form. The transformation from rhabditiform to

the filariform usually takes five to 10 days. This larval form is able to penetrate human skin,

travel through the blood vessels and heart, and reach the lungs. Once there, they burrow through

thepulmonary alveoli and travel up the trachea, where they are swallowed and are carried to the

small intestine, where they mature into adults and reproduce by attaching themselves to the

intestinal wall, causing an increase of blood loss by the host. The eggs end up on the soil after

leaving the body through the feces. On average, most adult worms are eliminated in one to two

years. When adult worms attach to the villi of the small intestine, they suck on the host's blood,

which may cause abdominal pain, diarrhea, cramps, and weight loss that can lead to anorexia.

Heavy infections can lead to the development ofiron deficiency and hypochromic microcytic

anemia. This form of anemia in children can give rise to physical and mental retardation.

Infection caused by cutaneous larvae migrans, a skin disease in humans, is characterized by skin

ruptures and severe itching.The most common technique used to diagnose a hookworm infection

is to take a stool sample, fix it in 10% formalin, concentrate it using the formalin-ethyl acetate

sedimentation technique, and then create a wet mount of the sediment for viewing under a

microscope. However, the eggs of A. duodenale and N. americanus cannot be distinguished; thus,

the larvae must be examined to identify these hookworms. An infection of N. americanus

parasites can be treated by using benzimidazoles,albendazole, and mebendazole. A blood

transfusion may be necessary in severe cases of anemia.
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Ancylostoma Ceylanicum

Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae

hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil , and after

5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective . These

infective larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with

the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart

and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the

pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature

into adults. Adult worms live in the lumen of the small intestine, where they attach to the

intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1 to 2

years, but the longevity may reach several years. Necator americanus predominates in the

Americas and Australia, while only.Iron deficiency anemia (caused by blood loss at the site of

intestinal attachment of the adult worms) is the most common symptom of hookworm infection,

and can be accompanied by cardiac complications. Gastrointestinal and nutritional/metabolic

symptoms can also occur. In addition, local skin manifestations ('ground itch') can occur during

penetration by the filariform (L3) larvae, and respiratory symptoms can be observed during

pulmonary migration of the larvae.Treatment: albendazole, Mebendazole, or pyrantel pamoate.
http://wiki.medpedia.com/Iron_Deficiency_Anemiahttp://wiki.medpedia.com/Clinical:Mebendazole_(Mebendazole)http://wiki.medpedia.com/Iron_Deficiency_Anemiahttp://wiki.medpedia.com/Clinical:Mebendazole_(Mebendazole)


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Ancylostoma Braziliense

Males measure 7.5 to 8.5 mm. Females measure 9 to 10.5 mm. The buccal capsule has one pair of

small medium teeth and one of larger outer teeth.

Hosts: Definitive: dog (Canis Familiaris), Cat (Felis catus).Eggs are passed in feces. Larvae

develop in soil to the L3 infective stage and then are ingested by the host or they enter the

host through cutaneous contact and then the larvae migrate to the lungs, and then on to the

intestinal tract of the host. In the intestinal tract, the larvae develop into adults. Eggs are then

expelled in feces and the cycle continues.Eggs are found infecal flotation,Eggs are 60 x 40

um.

Puppies and kittens: Anemia, diarrhea, weight loss, weakness, poor growth, occasionally death.

Adults: Usually asymptomatic but any of the above symptoms may be present.

Treatment: Febantel, Febantel/Pyrantel embonate, Fenbendazole, Ivermectin,Mebendazole,

Milbemycin oxime, Pyrantel Pamoate
http://cal.vet.upenn.edu/projects/dxendopar/techniques/comfecal.htmlhttp://cal.vet.upenn.edu/projects/dxendopar/techniques/comfecal.htmlhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/febantel.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/fenbendazole.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/ivermectin.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/mebendazole.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/milbemycin_oxime.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/pyrantel_pamoate.htmhttp://cal.vet.upenn.edu/projects/dxendopar/techniques/comfecal.htmlhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/febantel.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/fenbendazole.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/ivermectin.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/mebendazole.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/milbemycin_oxime.htmhttp://cal.vet.upenn.edu/projects/dxendopar/drug%20pages/pyrantel_pamoate.htm


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Ancylostoma caninum

Ancylostoma caninum is usually gray, but appears reddish if there is blood in its alimentary canal.

The body is covered by a non-living cuticle that sheds at molts allowing for growth of the

nematode. A male is 10 to 12 mm long and 0.36 mm wide; a female is 14 to 20 mm long by 0.5

mm wide and has a pointed tail. The anterior end is bent dorsally so that the arrangement of the

hookworm's ventral and dorsal sides are reversed. In the head of the hookworm is an area called

the buccal capsule which contains one the mouth and teeth. Ventrally, there is one pair of teeth,

each with three points. In the depth of the capsule there is a pair of triangular dorsal teeth and a

pair of ventro-lateral teeth. At its posterior end, a male A. caninum has a prominent bursa. The

rays inside the bursa are used in identifying species of hookworms, so A. caninum has a particular

arrangement of rays in its bursa. The female reproductive organ, the vulva, is found near the

junction of the second and last thirds of the body.
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Hosts:Definitive: Dog (Canis familiaris) Paratenic: Rodents

The larval stage penetrates the skin and makes it way through the circulatory system into the

digestive tract, where adult forms lay eggs that are passed through the feces. Common symptoms

include anemia and diarrhea. The parasite can also affect humans. It occasionally develops into an

adult to cause eosinophilic enteritis in people, and their invasive larvae can cause an itchy rash

called cutaneous larva migrans.Vaccination may soon be possible. Parasites are dioecious, with

male and female organs in separate individuals.Following copulation, female lays her eggs in the

hosts intestine. Eggs are passed out in the host feces.Usual daily output of eggs for a single female

hookworm is between 10,000 and 30,000 eggs. In favorable conditions of moisture, temperature,

and oxygen, eggs develop in the soil and hatch when they reach maturity. They release a

rhabditiform larva which feeds for a short time and molts twice before becoming an infective

filariform larva.Larva enters the host either by being swallowed or by burrowing into the skin

through hair follicles. In the case of pregnant bitches, larvae may enter the fetus and infect

prenatally.When it reaches the small intestine of the host, the larva molts a fourth and final time

and develops to maturity in about five weeks.
http://en.wikipedia.org/wiki/Anemiahttp://en.wikipedia.org/wiki/Diarrheahttp://en.wikipedia.org/w/index.php?title=Eosinophilic_enteritis&action=edit&redlink=1http://en.wikipedia.org/wiki/Cutaneous_larva_migranshttp://en.wikipedia.org/wiki/Vaccinationhttp://en.wikipedia.org/wiki/Anemiahttp://en.wikipedia.org/wiki/Diarrheahttp://en.wikipedia.org/w/index.php?title=Eosinophilic_enteritis&action=edit&redlink=1http://en.wikipedia.org/wiki/Cutaneous_larva_migranshttp://en.wikipedia.org/wiki/Vaccination


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Plasmodium Falciparum

The preferred method to diagnose malaria and determine which species of Plasmodium is causing

the infection is by examination of ablood film under microscope in a laboratory. Each species has

distinctive physical characteristics that are apparent under a microscope. In P. falciparum, only

early (ring-form) trophozoites and gametocytes are seen in the peripheral blood. On occasion,

faint, comma-shaped, red dots called "Maurer's dots" are seen on the red cell surface. The comma-

shaped dots can also appear as pear-shaped blotches. Malaria is carried by Anopheles mosquitoes.

Of the over 400 Anopheles species, only 3040 can transmit malaria. The infection starts, when a

female mosquito injects (in her saliva) "sporozoites" (one form of P. falciparum) into human skin

while taking a blood meal. A sporozoite travels (in the bloodstream) into the liver where it

invades a liver cell. It matures into a "schizont" (mother cell) which produces 3000040000

"merozoites" (daughter cells) within six days. The merozoites burst out and invade red blood

cells. Within two days one merozoite transforms into a trophozoite, then into a schizont and
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finally 824 new merozoites burst out from the schizont and the red cell as it ruptures. Then the

merozoites invade new red cells. P. falciparum can prevent an infected red cell from going to the

spleen (the organ where old and damaged red cells are destroyed) by sending adhesive proteins to

the cell membrane of the red cell. The proteins make the red cell to stick to small blood vessel

walls. This poses a threat for the human host since the clustered red cells might create a blockage

in the circulation system.

A merozoite can also develop into a "gametocyte" which is the stage that can infect a mosquito.

There are two kinds of gametocytes: males (microgametes) and females (macrogametes). They

get ingested by a mosquito, when it drinks infected blood. Inside the mosquito's midgut, male and

female gametocytes merge into "zygotes" which then develop into "ookinetes." The motile

ookinetes penetrate the midgut wall and develop into "oocysts." The cysts eventually release

sporozoites, which migrate into the salivary glands where they get injected into humans. The

development inside a mosquito takes about two weeks and only after that time can the mosquito

transmit the disease. P. falciparum cannot complete its life cycle at temperatures below 20 C.

After being bitten by an infected mosquito, symptoms usually begin within 1030 days.

Malaria is usually diagnosed by examining a blood sample under a microscope.

Treatment: artemesinin,atovaquone-proguanil,chloroquine,doxycycline,mefloquine,quinine


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Plasmodium vivax

The infection of Plasmodium vivax takes place in human when an infected female anopheles

mosquito sucks blood from a healthy person. During feeding, the mosquito injects saliva to

prevent blood clotting (along with sporozoites), thousands of sporozoites are inoculated into

human blood; within a half-hour the sporozoites reach the liver. There they enter hepatic cells,

transform into the tropozoite form and feed on hepatic cells, and reproduce asexually. This

process gives rise to thousands of merozoites (plasmodium daughter cells) in the circulatory

system and the liver. The P. vivax sporozoite enters a hepatocyte and begins its exoerythrocytic

schizogony stage. This is characterized by multiple rounds of nuclear division without cellular

segmentation. After a certain number of nuclear divisions, the parasite cell will segment and

merozoites are formed. The parasite uses the Duffy blood group antigens (Fy6) to penetrate red

blood cells. This antigen does not occur in the majority of humans in West Africa .As a result P.

vivax occurs less frequently in West Africa. The parasitised red blood cell is up to twice as large

as a normal red cell and Schffner's dots (also known as Schffner's stippling or Schffner's

granules) is seen on the infected cell's surface, the spotted appearance of which varies in color
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from light pink, to red, to red-yellow, as coloured with Romanovsky stains. The parasite within it

is often wildly irregular in shape (described as "amoeboid"). Schizonts of P. vivax have up to

twenty merozoites within them. It is rare to see cells with more than one parasite within them.

Plasmodium Malariae

\

The primary mode of transmission from host to host by these four species uses a female

Anopheles mosquito as a vector. The life cycle is initiated when the mosquito vector injects

sporozites into the human hosts during a blood-meal. The sporozites then migrate to the liver,

where they reproduce asexually and produce merozites. These merozites then enter the

bloodstream and infect erythrocytes, becoming trophozoites. The period of time that the

trophozoites are enlarging is called the trophic period, and this ends when several divisions occur,

but none of these cycles go through the cytokinesis stage, forming what is called a schizont. The

erythrocyte then lyses, introducing new merozites into the blood cycle and starting the cycle over

again, until an uninfected Anopheles mosquito takes a blood-meal from the infected host, and

transmits the infection to another host. The main physical manifestations of malaria in a human

host are febrile attacks that are known as malarial paroxysms. These symptoms appear during the

blood stage of the life cycle; no symptoms will appear during other stages. The severity of the

infection depends on the infecting species of Plasmodium and the health of the host prior to
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infection.The preferable method for diagnosis of P. malariae is through the examination of

peripheral blood films stained with Giemsa stain.P. malariae is the only human malaria parasite

that causes fevers that recur at approximately three-day intervals (therefore occurring evey fourth

Plasmodium Ovale

While it is frequently said that P. ovale is very limited in its range being limited to West Africa,

the Philippines, eastern Indonesia, and Papua New Guinea., it has been reported from Bangladesh,

Cambodia,India,Thailand and Vietnam..The P. ovale sporozoite enters a hepatocyte and begins

its exoerythrocytic schizogony stage. This is characterized by multiple rounds of nuclear division

without cellular segmentation. After a certain number of nuclear divisions, the parasite cell will

segment and merozoites are formed. There are situations where some of the sporozoites do not

immediately start to grow and divide after entering the hepatocyte, but remain in a dormant,

hypnozoite stage for weeks or months. The duration of latency is variable from one hypnozoite to

another and the factors that will eventually trigger growth are not known; this explains how a

single infection can be responsible for a series of waves of parasitaemia or "relapses".While

similar to P. vivax, P. ovale is able to infect individuals who are negative for the Duffyblood

group, which is the case for many residents of sub Saharan Africa. This explains the greater

prevalence of P. ovale (rather than P. vivax) in most of AfricaThe prepatent period in the human
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ranges from 12 to 20 days. Some forms in the liver have delayed development and relapse may

occur after periods of up to 4 years after infection. Standard treatment is concurrent treatment

with chloroquine andprimaquine.
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