Coccidia of several different types occur in birds although the majority belong to two genera. These differ mainly in whether they produce oocysts or eggs containing four smaller cysts, or whether the oocysts contain two sporocysts: the former parasites belong to the genus Eimeria and the latter to Isospora. The two genera show a different distribution in their bird hosts. The genus Eimeria favours birds in the orders Galliformes, Columbiformes, and Anseriformes, but also occurs in Gruiformes, Pelecaniiformes, Psittaciformes and Charadriiformes. The genus Isospora is more widespread, infecting birds mainly in the Order Passeriformes, but also the Struthioniformes, Falconiformes, Galliformes, Coraciiformes, Charadriiformes, Psittaciformes, Strigiformes and Piciformes. Unlike Eimeria spp. there is virtually no evidence that species of Isospora are pathogenic. Several species of Eimeria, however, produce disease in domestic poultry, various species of game birds such as pheasants and in peafowl.
Most species of coccidia occur in different areas of the intestines and penetrate the mucous lining. According to the species of bird and coccidia, the parasites occur at different sites, extending from the duodenum to the cloaca, including the caeca if present. Coccidia, including Eimeria, may infect the kidneys in some species of swans, geese, ducks and owls. Oocysts become mature and infective within one to three days after being passed in the droppings. If these oocysts are then swallowed by a susceptible bird, the stages known as sporoziotes are liberated in the gut by digestion of the oocyst wall. Here the parasites undergo rapid and complicated stages of asexual multiplication at various depths in the gut epithelium. Finally two dissimilar types of offspring unite to form an organism capable of producing further oocysts. The entire cycle takes from one to two weeks depending upon the species of coccidia.
CLINICAL SIGNS: During the life cycle the parasites may cause inflammation of varying severity in the gut wall according to species of bird and coccidia, the number of oocysts swallowed and the general health and age of the bird. The disease causes all stages of ill-health from mild diarrhoea to fatal dysentery. Signs include depression, anaemia, loss of weight, thirst, unthriftiness and watery, slimy greenish, or bloody diarrhea. The disease may be an acute or a lingering chronic process with or without fatalities. Rapid loss of weight leading to emaciation and dehydration precede death, particularly in young stock. Death is lingering in some birds with extreme depression and weakness. Tremors, convulsions or lamenesses are occasionally seen. A mild or moderate infection in a fairly resistant bird results after a time, in immunity to further infection.
DIAGNOSIS: Diagnosis depends on microscopical examination and finding oocysts in the droppings. It is unlikely that epidemics of the magnitude seen in poultry will be encountered in cage or aviary birds. In most establishments a few birds harbour coccidia but show no signs of disease.
SPREAD AND CONTROL: The concentration of oocysts builds up most rapidly where birds are kept in overcrowded conditions, where food or water is readily contaminated with droppings and where litter is moist, warm, or not removed daily. Under these circumstances young stock which has not yet developed any immunity to the disease is particularly vulnerable. Attempts to rear birds in coccidia-free surroundings are almost bound to be followed by failure, but, if successful, leave the birds highly prone to the first oocysts which come their way. A light infection is probably preferable therefore, to a coccidia-free environment. Good hygiene therefore should prevent the disease causing any significant trouble. Removal of soiled food and wet litter will usually prevent serious outbreaks.
TREATMENT: Numerous drugs have been used for the treatment of poultry. However, sulphonamides, especially sulphadimidine, sulphaquinoxaline, and also furazolidone are still among the most effective drugs. Certain other drugs are also used for poultry.
Trichomoniasis: (Canker, Frounce or Diptheria)
Trichomonas gallinae is a fragile protozoan which can swim actively by means of its five whip-like flagella and it possesses a wavy fin-like membrane down one side. It is the most important trichomonad of cage birds and it is especially pathogenic to pigeons. Trichornonas gallinae affects various pigeons, doves, quail, falcons and hawks and occasionally other birds, including some of the smaller finches, Java sparrows and the canary. In the pigeon and dove family (Columbidae) it can cause severe epidemics. Wild species and feral pigeons frequently harbour the organisms and can be a source of infection.
CLINICAL SIGNS: In pigeons, the disease usually affects one to two week old squabs or sometimes older youngsters (squeakers), and less frequently adults. Characteristic lesions are sticky, creamy white or cheesy deposits in the mouth, pharynx, inner nares and oesophagus. As a general rule the wet, sticky type of exudate is seen mainly in the acute disease and the hard cheesy type in more chronic infections. The lesions sometimes extend to the crop, into the upper parts of the respiratory tract and even onto the outside of the beak. As the result of such lesions, eating and drinking become difficult, food is refused or merely picked at, and respiration is often noisy. Lesions may occasionally extend down the alimentary tract, and cause cheesy, necrotic spots in the liver, spleen, lung of on the surface of the gut. Depression precedes early death in acute cases. In older or more resistant birds, great loss of weight occurs prior to death, and this may take up to three weeks or even longer. The disease is similar in diurnal birds of prey, such as falcons, hawks and eagles, and in these species it is often called "frounce". It is believed that birds of prey usually contract the infection by eating affected pigeons. The disease may be confused with candidiasis and vitamin A deficiency.
TREATMENT: Treatment with dimetridazole is most effective against the organism provided the bird can swallow. The apparent success of tetracyclines and sulphadimidine is probably mainly due to the susceptibility of secondary bacterial invaders which flourish in the exudates. Recovery from mild attacks produces an immunity to more virulent strains of T. gallinae. Severely infected birds should be destroyed, for even if they recover, they are likely to remain debilitated. As trichomonads are susceptible to drying, heat and chemicals, it is perhaps surprising that they can be such a scourge. They are mainly spread by direct contact from beak to beak, especially when parent birds are feeding young. Indirect transmission, especially via the drinking water, also probably occurs. Direct spread is very difficult to control in a colony of birds. It must be remembered that trichomonads can be harboured in small numbers by certain birds without producing clinical signs.
Giardia infects mainly mammals and is a rare parasite of birds but has been recorded in a parakeet, passerine, toucan and a few other hosts. The organism is shaped like a tennis racket without a handle and has eight flagella by means of which it swims about in the intestinal contents. It forms cysts and in this form is passed out in the faeces and transmitted to other hosts by ingestion. Diagnosis is based on the identification of the motile organisms and/or cysts in the excreta on microscopical examination.
CLINICAL SIGNS: Loss of condition, diarrhoea and death have been attributed to the parasite.
TREATMENT: Strict attention should be paid to hygiene, especially avoiding faecal contamination of food. Drugs used for the treatment of malaria should prove effective.
Histomoniasis Blackhead or Infectious Enterohepatitus:
This is one of the most important diseases of turkeys and more detailed information is available in books on diseases of poultry. The disease also infects the domestic fowl, pheasants, partridges, quail, peafowl and probably all species of gallinaceous birds. Birds in other Orders are not naturally infected. The parasites are carried in the ova of the caecal worm Heterakis gallinae in which they can survive for long periods. Birds become infected by swallowing the infected worm eggs. The protozoa are released into the caeca when the worm eggs hatch and they then attack the caecal walls whilst some are carried in the blood to the liver. In the caeca other worms become infected and produce further ova infected with Histomonas.
CLINICAL SIGNS: The name "blackhead" is extremely misleading because this is not a characteristic sign of the disease. The usual clinical signs are drowsiness, increasing weakness, drooping wings and tail and ruffled plumage. Diarrhoea is a constant feature, the faeces usually being yellowish in colour. Occasionally the skin of the face and head of infected turkeys becomes a deep reddish-black. Young birds of all susceptible species are most commonly infected. In young turkeys mortality may reach almost 100 per cent.
DIAGNOSIS: Although the disease can be suspected from the clinical signs, the presence of the infection can be confirmed only at post-mortem examination by finding the typical lesions in the liver and caeca. Large, round, pale grey areas of necrosis occur in the liver. At least part of the walls of the caeca are thickened and their epithelial lining is ulcerated.
TREATMENT AND PREVENTION: Usually the disease can be prevented by incorporating drugs such as dimetridazole or furazolidone in the food at low dosages as recommended by the manufacturers. For actual treatment of those infected and birds in contact in the same flock, these drugs are also used, but at higher dosage rates. Domestic fowls are less susceptible to histomoniasis than turkeys and some other species of gallinaceous birds and can be apparently healthy carriers. It is unwise therefore, to keep such birds as peafowl and ornamental pheasants on the same land as poultry or on land which has been used for that purpose. As Histomonas meleagridis is carried by the caecal worm, the disease can be controlled by preventing infestation with these parasites.
Avian Malaria (Plasmodium infections):
Plasmodium causes malaria in man, other mammals and birds. The organisms are parasites of red blood cells. At this stage of its lifecycle, the parasite may produce fever and is also infective to the intermediate hosts which are various species of mosquitoes. In these insects further multiplication occurs until a stage is reached in the salivary glands when the parasites are again infectious to birds. When the bloodsucking female mosquito bites a bird, it introduces the parasites into the blood; these do not remain in the bird's circulation at this stage but invade certain cells of the liver, spleen, kidney and other organs. They reappear later, to produce attacks of the disease during which multiplication occurs in the red blood cells. Numerous species of bird can contract malaria, both in tropical and temperate climates. Several species of Plasrnodium exist and infect several species and families of birds. The canary is particularly susceptible to certain species of Plasmodium, especially P. cathemerium, and is used for experimental purposes in malaria research. Although numerous species can be infected, the organisms are usually pathogenic only to penguins and the domestic fowl when these birds are kept in warm climates. Young birds are more susceptible to malaria than adults.
CLINICAL SIGNS: In most species the parasites appear to be harmless under normal conditions. Heavy infections may result in a febrile disease showing as depression, ruffled feathers and incoordination, but most Plasmodium spp. only produce a mild illness.
DIAGNOSIS: The presence of pigmented reproductive forms of the parasite in the peripheral blood on microscopical examination of blood smears. Only red blood cells are infected.
TREATMENT AND PREVENTION: Mepacrine hydrochloride and other anti-malarial drugs are usually effective. Untreated birds which have recovered, may still harbour the parasites. Mosquitoes (Culex, Aedes and Anopheles spp.) must be controlled and if necessary, the birds should be protected by mosquito-proof netting.
Haemoproteus (Parahaemoproteus infections):
These genera are closely related to Plasmodium but differ in two important respects from that parasite by not multiplying in the circulating blood and by not being transmitted by mosquitoes. Multiplication is restricted to special cells in blood vessels, especially in the lungs. In the case of Haemoproteus the parasites are transmitted by louse flies (Hippoboscids), whilst Parahaemoproteus is carried by midges of the genus Culicoides. Plasmodium parasites of both genera infect red blood cells and can seldom be identified and differentiated by examination of blood forms alone. A very wide variety of birds may be infected with the parasites which are widespread in distribution.
CLINICAL SIGNS: Under ordinary circumstances the parasites are harmless and rarely cause disease. In ornate lorikeets they have been reported as the cause of anaemia and congestion of the lungs leading eventually to asphyxia and there are a few indications of pathogenicity in other birds.
DIAGNOSIS: The infection can be suspected by the presence of pigmented parasites showing no evidence of reproductive forms on microscopic examination of blood smears. Only the red blood cells are infected.
TREATMENT AND PREVENTION: This is the same as that recommended for malaria.
Trypanosomiasis (Trypanosome infections):
Trypanosomes are elongated, flagellated blood parasites, some of which cause sleeping sickness and other diseases of man and domestic stock in tropical countries. Avian trypanosomes have an almost world-wide distribution, but parasites in birds are of little significance. Numerous species of birds, but especially passerines, have been found infected. Louse flies, red mites, mosquitoes and simuliids (black flies or buffalo gnats) have all been implicated as carriers.
CLINICAL SIGNS: There is virtually no evidence that the parasites are pathogenic to birds, with the possible exception of canaries.
DIAGNOSIS: The presence of the parasites in the peripheral blood on microscopical examination of blood smears.
TREATMENT AND PREVENTION: This is unlikely to be necessary.
Leucocytozoonosis (Leucocytozzon infections):
These blood parasites which are confined to birds, are similar to Plasmodiurn, Haemoproteus and Parahaernoproteus spp. except that they do not contain pigment granules derived from the haemoglobin of the red cells. Leucocytozoon and Akiba spp. also occur in blood cells, but characteristically in the leucocytes, and unlike Plasmodium do not multiply in the circulating blood. Leucocytozoon spp. are transmitted by simuliid flies, and Akiba spp. by Culicoides midges. The life histories of the parasites with few exceptions are unknown and there is no other way of differentiating between the two genera. It is believed that the genus Leucocytozoon is the commoner of the two. Both organisms reproduce in various organs, including liver, heart, brain, lung and spleen. The parasites have an almost world-wide distribution and occur in a wide variety of species, including ducks, geese, turkeys, domestic fowl, game birds, owls and other birds of prey, numerous passerines and parakeets (excluding budgerigars).
CLINICAL SIGNS: Leucocytozoon is pathogenic to young birds of many species, especially ducks, geese, turkeys, parakeets, certain passerines such as weaver birds and probably many others. Clinical signs are not diagnostic and include anaemia. Mortality may be high and in parakeets the parasite's presence in the cardiac muscle may cause heart failure. In temperate zones the disease is seasonal, occurring when the insect carriers are active.
DIAGNOSIS: The presence of non-pigmented parasites in the leucocytes or red blood cells on microscopical examination of blood smears and the presence of cysts in the heart and gizzard musculature or skeletal muscles.
TREATMENT AND PREVENTION: Sulpha drugs as used for coccidiosis may be effective. The disease is most likely to occur in warm weather when the vectors are active and therefore at these times, birds should be protected if possible from the insects by keeping them indoors.
Lankesterellosis (Lankesterella infections):
Lankesterella was previously called Atoxoplasma. So far as is known it occurs only in birds and amphibia, inhabiting lymphocytes and monocytes. The parasites reproduce in the spleen, bone marrow, liver, lungs and kidneys. At least one species, namely, L. garnhami, is believed to be transmitted by the red mite Dermanyssus gallinae. Lankesterella is widespread and particularly common in house sparrows in Great Britain. Canaries are commonly infected and the parasite has been reported in several other passerines. Young birds of all species are most susceptible.
CLINICAL SIGNS: Infected canaries become listless, have ruffled feathers and show loss of appetite. The distended liver may produce a visible swelling behind the sternum. L. garnhami is also pathogenic to house sparrows.
DIAGNOSIS: The presence of non-pigmented parasites in lymphocytes and monocytes of the peripheral blood. A prolonged examination may, however, be necessary because the organisms are usually scarce. They can most easily be found at post-mortem examination in impression smears of the spleen.
TREATMENT AND PREVENTION: There appears to be no specific treatment for the parasite. If red mites really do transmit the infection, then it should be possible to prevent the disease by controlling these ectoparasites. Some parasitologists, however, believe that the organism may be a stage in the life-cycle of the coccidian parasite known as Isospara.
Other Protozoan Infections:
There are a few other protozoan infections which have not been included, because most of them are rare and virtually nothing is known about their pathogenicity--at least in non-domesticated birds. These include infections by Sarcocystis spp. toxoplasmosis, hexamitiasis and infections by coccidia belonging to the genera Dorisiella, Wenyonella and Tyzzeria.
[ GO BACK ]
Hamilton & District Budgerigar Society Inc.