Blood born parasites are organisms that's some or most of its life cycle is lived in the blood streams of humans. Most of these parasites pose great challenges to health in most part of the world, with most of the incidence in the tropics. Blood born parasites cause some of the worlds highest mortality rates in women and children across the world1.
Blood born parasites can be transmitted majorly be vector insects from one individual to another or from some other animals to man. They can also be transmitted from one individual to another through blood transfusion of infected blood or organ transplant and by sharing sharps from infected individuals to those not infected2.
TYPES OF BLOOD BORN PARASITES
There are various types of human parasitic organisms but only few are seen to be blood born parasites across the geographical distribution of the world. These are; Leishmania, Babesia, and Plasmodium that causes that malaria fever.
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Leishmania infection is the infection with the pormatigotes of the genus Leishmania. This type of infection is called, Leishmaniasis. This is often spread by the bite of Phlebotomus sand flies. These parasitic diseases found in the Tropics, subtropics and in southern Europe. They are found to affect human internal organs especially the bone marrow, liver, and the spleen3. Leishmania are of various types namely;
The life cycle of this infection is illustrated in the diagram (figure 1) below.
[Fig.1] . Life cycle of leishmaniasis.
Diagnosis of Leishmaniasis.
Leishmaniasis is diagnosed in the laboratory by a smear preparation of Buffy-coat form freshly collected venous blood, or by bone marrow of spleen aspirate smear preparation. The smear is then stained by the use of Giemsa's Staining technique for 20 minutes at a PH of 7.2.
The below figure 2 shows a bone marrow film picture of Leishmania indicated with the arrows.
[Fig. 2] 4 A Giemsa's stained bone marrow film showing Leishmaniasis.
Treatment of Leishmaniasis.
Leishmaniasis is often treated with the use of a drug called Amphotericin B deoxycholate. This is usually by alternate days infusions of 1mg/kg for a period of 30 days5.
This is a parasite that causes an infection called Babesiosis. This infection is spread by the vector insect called Ixodes Scapularis Tick. It can also be transmitted by blood transfusion and organ transplant. The parasite is an intraerythrocytic organism just like Malaria parasite. It is a protozoon of the genus Babesia6 .
Types of Babesia;
There are about a hundred (100) types of Babesia but only four types has been identified as causing infection in humans these are;
Babesia incidence is particularly common in the Northeast and upper Midwest of America and usually common during warm periods of the year7.
Symptoms: Patients with Babesiosis often show clinical signs after three weeks of a bite by an infective tick. These parasites invade the erythrocytes, where they proliferate and invade more cells. This sequence of red cell invasion subsequently leads to increasing red cell rupturing, which in turn lead to anaemia8. Other symptoms may include fatigue, headache, nausea, vomiting, and excess sweating.
The figure 38a below shows the diagrammatic illustration of Babesia.
[Fig 3] Babesia life circle
Diagnosis of Babesiosis.
Babesia can be diagnosed by identification of the parasites on a peripheral blood film stained with a Romanosky Stain and viewed under a light microscope Figure 4 below is a Romanosky Stained film, showing Babesia in red cells with the arrow.
[Fig.4] A blood film of Showing Babesia in red blood cells.
Genetic analysis like the PCR methods is also used to detect Babesia DNA in the blood. Fluorescent In-situ Hybridisation (F ISH) assays is also used to detect ribosomal RNA of Babesia in human blood. Besides antibody testing for Babesia antibodies is also used. These various tests are better ran along side with controls9.
This is another blood born parasitic protozoa flagellate organism that causes a diseased condition called Trypanosomiasis popularly called sleeping sickness or African Trypanosomiasis. The other form of Trypanosomiasis is mostly seen in the South American region. It is called the Chagas diseases.
Types of Trypanosome
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African Trypanosome: these are unicellular single flagellated protozoan's of two types and they a transmitted by the bite of a vector fly called the Tsetse fly (Figure 5.1 below) 10 . This is common in the Sub-Saharan Africa and said to cause sleeping sickness. Figures 5.2, 5.3 below shows a blood film and the life cycle of African Trypanosomes respectively.
Trypanosoma Brucei Rhodesiense
Trypanosoma Brucei Rhodesiense,
[fig 5.1] Tsetse Fly
[fig 5.2]A blood film showing African Trypanosome.
Fig 5.3 illustrative life cycle of African trypanosome
American Trypanosome: These are also flagellated protozoan organism, and are called Trypanosoma Cruzi ( shown in Figure 6.1 below). They cause the disease called Chagas disease which was discovered in 1909 by a Brazilian scientist called Carlos Chagas. T. Cruzi is transmitted by an insect vector called the Triatomine bugs (kissing bugs) 11. The Triatomine bugs (Figure 6.2 below) infect human with the T Cruzi through their faeces during a blood meal on human's skin as illustrated on the life cycle shown in figure 6.3below.
[Fig.6.1] A blood film of T. Cruzi.
Fig. 6.2 Triatomine bugs11a
[Fig 6.3] Above is an illustrative life cycle chat of T. Cruzi.
Diagnosis and treatment of Trypanosomiasis
Trypanosomiasis can generally be diagnosed in the laboratory by the preparation of thin and think blood film and staining with a Romanosky Stain. Both Figures 5.2 and 6.1 shown above are demonstrating thin films of T. Rhodesiense and T Cruzi respectively.
Aspirates from body fluids or biopsy of a chancre can also be collected for laboratory investigation microscopically. There are several serological method of diagnosis for Trypanosomiasis, but they are not widely used because of the straight forward nature of the laboratory microscopic methods12. A cerebrospinal fluid examination is important to ascertain the stage of infection in patients with evidence of infection in peripheral blood or other body fluids and to know the type of treatment that can be administered.
Treatment type depends on the stage of the infection. The drugs used in the early stages of the infection is easier to use and less toxic than the once used at the neurological late stages. That is why it is essential to ascertain the stage of the infection before the onset of treatment.
Pentamidine and Suramin are used for the first stage of infection in T. b. gambiense and T.b. rhodesiense respectively; While Malasoprol and Eflonithine are use for the second stages respectively13. Benznidazole or Nifurtimox on the other hand has shown to be almost 100% curative drugs for T cruzi14.
This is an intra-erythrocytic protozoa organism which is the causative organism of the disease called Malaria. This organism was first proven to be transmissible in 1897 by Sir Ronald. Plasmodium was first visualised in red blood cells stained blood film, by a scientist named Lavern in the year 1980 in Algeria 15. Mosquitoes are of about 2,500 known species, only about 50 to 60 are known to be capable of plasmodium transition 16. Plasmodium is basically transmitted by a vector known as the Anopheles Mosquitoes. Plasmodium is of over 200 types, but only about five types are known to infect humans 17, namely;
Plasmodium Falciparum, (most Virulent)
Of all the species of plasmodium, Falciparum is the most virulent. According to the WHO 2008 World Malaria Report, Falciparum accounted for about 98% of all reported 247 million human malaria fever infection cases in sub-Saharan Africa. Of all the death caused by malaria in the same geographical region, 90% were reported cases of Falciparum infection.
Plasmodium Falciparum can be transmitted by any of these Anopheles species; Gambiae, albimanus, freebomi, maculatus and stephensi. But Gambiae popularly called the female Anopheles Mosquito is the known principal vector of Falciparum 18.
The life cycle of plasmodium Falciparum is relatively complicated in human infection. This starts with a bite by an infected female anopheles mosquito then followed by the release of the sporozoites from the salivary glands of the mosquito into the bloodstream of the human during the mosquito's blood meal. This sequence if followed by the invasion of the hepatocytes (liver cells) within 30 minites. The liver cell stage of this invasion is a crucial stage for P. Falciparum development in human; this is because, in the next 14 days, the parasites undergo a series of asexual multiplication and development into thousands of merozoites. These merozoites busts and invade red cells and go through another round of multiplication to produce about 12 - 16 merozoites within a schizont.
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The following sequences if shown in the diagrammatic illustrative figure 7.0 below.
[Fig7.0]The Malaria infection stages in this cycle is of three main stages, which are the, A. Exo- Erythrocytic Stage (Human Liver Stage); B. Erythrocytic stage (Human Blood Stage);C. Sporogenic Stage (Mosquito stage)19
Pathogenesis of P. falciparum.
The severity of Malaria cause by P. falciparum is more them other forms. This is because during the 48-hour asexual blood stage, the developed forms alter the membrane of the red cells. This membrane alteration causes the red cells to adhere to the epithelia cells of the blood vessels and subsequently lead to an occlusion of microcirculation. This process is called Cytoadherence. If this process is not arrested on time, it could lead to multiple dysfunctions of organs. This is what happens in cerebral malaria 20.
Plasmodium Falciparum genome.
The Malaria genome project (MGP) was set up in 1995 to sequence the genome of P. falciparum. This was able to report the genome of the mitichonrion of the parasite in the same year, them the Plastid in 1996. This project was also able to report the sequence of the first nuclear chromosome 2 in 1998 them chromosome 3 in 1999. The entire genome was reported in October 2 2002. This project explains that the genome contains 14 chromosomes which encodes tor about 5,300 genes. This genome was also found be rich in (A+T) regions more than any genome till date. This genome was also found to consist of an antigenic subtelomeric region which varies from other eukaryotic microbes. This project also opened up a new ground for exploits in the search for drugs and vaccines in the fight against malaria because it said a lot about the molecular biology and metabolic processes of plasmodium falciparum 21.
In 1948 Dr Beet who was working in Zimbabwe stated that sickle cell disease could exhibit some level of defence mechanism against P. falciparum. In 1949 J.B.S Haldane also said that Thalassaemia could do the same.
Glucose-6-dehydrogenase deficiency has also been proven to form some form of resistance to P falciparum Malaria. This was published in a journal called 'PolS Medicine' by the US National Institute of Allergy and infectious diseases. Their studies showed that children with G6PD deficiency in Mali showed a level of protection against severity of P Falciparum Malaria 22.
Sickle cell anaemia poses a level of resistance to P falciparum. This happens in the erythrocytic stage of the parasite's cycle. The parasite is not able to bind to the haemoglobin in order to form a sticky knob. Without the formation of this sticky knob complex which is P. falciparum main element of action, the red cells no not stick to the endothelia walls of vessels. These processes tend to shield infected individuals from the severity of the infection to the level of cerebral malaria 23.
DIAGNOSIS AND TREATMENT OF PLASMODIUM FALCIPARUM.
The diagnosis of Plasmodium entails the identification of the parasite's antigen or products in the blood of infected individuals. This may sound simple but the quality of the diagnosis is largely dependent on various critical factors. This ranges from the stages the parasite in the erythrocytes, the endemicity of the disease, the skilfulness of the personnel handling the diagnosis, drug resistance and so many other factors.
The diagnosis can basically be classified into the Microscopic and non- Microscopic methods.
Under the microscopic diagnostic method we have the;
Peripheral blood smear,
Quantitative Buffy coat test.
In the microscopic method of diagnosis, a thin and thick blood film is made and stained with Romanosky staining technique. Figure 7.1 24 below shows a blood film of P. falciparum with various stages indicate with an arrow.
[Fig7.1]. A blood film with ring form to the right side arrow, the Schizont, the centre arrow and the trophozoite, the arrow to the left side.
The non Microscopic Methods include
rapid dipstick immunoassays, Polymerase Chain reaction assays, enzyme immunoassays,