Avian Malaria.docx

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Avian Malaria

Introduction

Malaria is a protozoal disease caused by members of the genus

Plasmodium. Infections may occur in both humans and animals.Approximately 350-500 million people are infected annually,with 1.3 million deaths. It is endemic to parts of Asia, Africa,Central and South America, and certain Caribbean islands. Thereare four species ofPlasmodium that cause disease in people: P.falciparum, P. vivax, P. ovale, P. malariae. Plasmodium sp. mayalso infect primates, rodents, reptiles, and birds. Many birds canserve as a definitive host for these parasites. Plasmodium can bepathogenic to penguins, domestic poultry, ducks, canaries,falcons, and pigeons, but is most commonly carried

asymptomatically by passerine birds. Avian malaria has aworldwide distribution and is of great economic significance is tothe poultry industry. Organisms such as P. gallinaceum, P.juxtanucleare and P. durae may cause up to 90% mortality inpoultry. Incidentally, birds with avian malaria have been used asmodel systems for studying the pathogenesis and treatment ofmalaria in humans.

Clinical Signs

Infected birds are often weak, depressed, dyspneic andanorexic. Birds may have abdominal protrusion (due tohepatosplenomegaly) and ocular hemorrhage. Central nervoussystem ischemia may occur with P. gallinaceum due to occlusionof capillaries by exoerythrocytic schizonts in heavily parasitizedendothelial cells. Hemolytic anemia, often accompanied byleukocytosis, lymphocytosis, and hemoglobinuria, may also bepresent. Coma and death may occur quickly when the parasiteburden is high. However, many birds, especially passerines, donot become ill and play an important role as asymptomatic

carriers of the parasite.

Life Cycle

Plasmodium may exploit several genera of mosquitoes (Culex,Anopheles, Culiceta, Mansonia, and Aedes) as vectors andintermediate hosts. The mosquito inoculates the bird withsporozoites that enter the birds reticuloendothelial system. Eachsporozoite develops into thousands of merozoites (pre-erythrocytic cycle) (Figure 1). These merozoites rupture theirhost cell and invade endothelial cells or other cells of the

reticuloendothelial system to complete another cycle ofreplication. The merozoites then rupture that host cell and enter


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erythrocytes in the blood stream. This initiates theintraerythrocytic cycle. Merozoites multiply in the RBC, forming aschizont (shizogony). The schizont will rupture, killing the RBCand releasing the merozoites to infect more RBCs. Duringschizogony, the parasites feed on the RBC cytoplasm, ingesting

hemoglobin which produces brown pigment granules. The intra-erythrocytic cycles continue until the host dies or the parasitesare suppressed by host immunity. After the initial cycles inerythrocytes, a few merozoites develop into sexual cells(microgametes and macrogametes) with each new cycle. Thesexual cells are maintained in the RBC until they are consumedby a mosquito with its blood meal.

Figure 1: Liver impression smear froma Penguin. Two macrophagescontaining numerous Plasmodiummerozoites.

The sex cells are released in the mosquitos midgut. Fertilizationand zygote formation occurs when a microgamete encounters amacrogamete. The zygote matures into an elongated mobile cellthat crosses the midgut wall. This cell is called an ookinete. Theookinete forms an oocyst on the outer wall of the midgut. Thenucleus of the oocyst divides into thousands of spindle shapedsporozoites. The oocyst then bursts and releases thesporozoites, some of which migrate to the salivary gland wherethey are injected into a bird during the mosquitos blood meal.

While most avian infections occur through the bite of amosquito, it is possible for a direct bird-to-bird transmission to


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occur. Schizogony occurs in the RBC and, therefore, blood-to-blood transfer without the intermediate host can result ininfection. The life cycle of avian malaria is very similar to thatseen in infected human beings. However, birds (unlikemammals) suffer from repeated cycles of pre-erythrocytic

merogony with reinvasion of reticuloendothelial cells byerythrocytic forms.

Clinicopathologic Features and Diagnosis

Experimental infection of domestic fowl resulted in peakparasitemia six days post-infection in most birds. The birds werefebrile and anemic (hematocrit


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The intraerythrocytic gametocytes ofPlasmodium can easily beconfused with those ofHaemoproteus because they both containrefractive yellow to brown pigmented granules (Figures 3 and4).

Figure 3: Plasmodiumgametocytes in avianblood. Note the smallersize when compared toHemoproteus organisms.

Figure 4:Hemoproteus inavian blood. Typicallylarger than Plasmodiumgametocytes and oftenhave a characteristiccanoe shape that wrapsaround the erythrocytenucleus.

Features that can help distinguish between the two infectionsinclude:

Plasmodium gametocytes are smaller in size thanHaemoproteus organisms, usually occupying less than one-halfof the host cell cytoplasm

Some Plasmodium gamonts displace the RBC nucleus(Haemoproteus does not)

Plasmodium may undergo schizogony in the peripheral blood(Haemoproteus does not)

Plasmodium parasites can be found in cells other thanerythrocytes (thrombocytes, leukocytes, and endothelial cells).


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In birds that die peracutely, organisms may be few to sparse inthe blood. In these cases, schizonts can be found in capillariesby examining impression smears of brain, lung, liver, andspleen.

PCR has also been used to diagnose Plasmodium. However, thisdiagnostic test is most often used in a research setting.

Treatment

Note: Treatment of animals should only be performed bya licensed veterinarian. Veterinarians should consult thecurrent literature and current pharmacologicalformularies before initiating any treatment protocol.

Affected flocks can be treated with Chloroquine (5-10mg/kg)potentiated with primaquine (0.3mg/kg). Chloroquine can alsobe added to the drinking water at a dose of 250mg/120ml.Grape or orange juice may be needed to override the bitter tasteof the medication. Quinacrine at a dose of 1.6 mg/kg given IMfor 5 days is another treatment possibility. Additional treatmentsinclude sulfonamides combined with trimethoprim,pyrimethamine, and chlorguanil. Due to strain differences insusceptablity, different anti-malarial drugs can be tried. It is

important to remember that malaria can be prevented byscreening chicken houses to prevent contact with the mosquitovectors.

References

Aiello SE (ed): The Merck Veterinary Manual, 8th ed. NationalPublishing, Philadelphia, PA, 1998

Barriga O: Parasitology for Practitioners , 2nd ed. InternationalGroup, Minnesota, 1997.

Campbell T: Avian Hematology and Cytology. Iowa StateUniversity Press, Ames, 1998.

Kaufmann J: Parasitic Infections of Domestic Animals: ADiagnostic Manual, Birkhauser Verlag, 1996.

Richie B, Harrison G, Harrison L: Avian Medicine: Principles andApplications. Wingers Publishing, Lake Worth FL, 1997.

Slater LB. Malarial Birds: Modeling Infectious Human Disease inAnimals. Bull. Hist. Med., 2005, 79: 261-294.


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Williams RB: Avian Malaria: clinical and chemical pathology ofPlasmodium gallinaceum in the domesticated fowl Gallus gallus.Avian Pathology February 2005 34(1), 29-47.

Acknowledgement

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Avian Malaria.docx