Great Britain Border Breeders Visit Dr. Peter Coutteel Belgium Part 2 Diseases: Circovirus, Macrorhabdosis, Coccidial

CIRCOVIRUS

A disease called “black spot” by European canary breeders has been proven to be caused by a circovirus. The disease is observed in hatchlings and nestlings and has a high mortality. Signs include abdominal enlargement and congestion of the gall bladder (visible as a black spot through the skin) Feather loss and lethargy in finches also have been associated with circovirus. Diagnosis is based on recognizing inclusion bodies on histopathology of the bursa of Fabricius or the presence of 18-nm viral particles on electron microscopy. PCR techniques for psittacine circovirus (psittacine beak and feather disease— PBFD virus) fail to demonstrate viral presence, indicating that the canary circovirus differs genetically from the PBFD virus. Nucleotide sequencing showed the virus to be more closely related to the Columbid circovirus than to the PBFD virus. Differential diagnoses include Atoxoplasma, Isospora, E. coli and other causes of mortality in nestlings. The use of GROG from day of hatch is recommended.

MACRORHABDOSIS

Classically known as a common disease in Canaries (“going light”), this organism was previously termed

“Megabacteria” or “avian gastric yeast”. Observation has been made of this organism in a wide range of passerine species. Historically described as “megabacteriosis” during the last 20 years, there has been frequent debate on the description of this as a large gram-positive bacterium. Recent investigations in Germany proved that the so-called megabacteria are indeed fungi, and Phalen has now renamed the pathogen, Macrorhabdus ornithogaster. Clinical Disease Chronic depression and weight loss are typical of macrorhabdosis. Birds are always hungry and stay close to the food bowl, eating large quantities of soft food. Regurgitation is not a clinical sign in passerines. Droppings often contain undigested seeds. The patient may be anemic with pale muscles. The liver becomes visible due to the proventricular dilatation.
 

Other diseases that either may have triggered macrorhabdosis or developed as secondary diseases following macrorhabdosis must be considered. Diagnosis is based on microscopic examination of a fecal sample. The organism is easily recognized on a wet mount or following a Gram’s stain using a 1000 magnification. Failure to find Macrorhabdus organisms does not prove that the bird is not infected,

as shedding begins only after a certain stage of disease and then may occur irregularly. Microscopic examination of sequential fecal samples will increase the sensitivity. Pooled fecal samples from an aviary will give good information on the status of infection within a group of birds. The organism appears in proventricular scrapings after necropsy. Note that routine fungal culture will not yield growth of this fastidious organism

COCCIDIAL DISEASES

Atoxoplasma

The taxonomy of Atoxoplasma is controversial. This disease is also called “Lankesterella” or “big liver disease”. The species affecting canaries has been named Atoxoplasma or Isospora serini. Unlike other Eimeriidae species, the asexual life cycle of Atoxoplasma takes place in internal organs and not in

the intestinal mucosa.59 The life cycle of the organism begins with the host’s oral ingestion of oocysts.81

Oocysts  excyst the sporozoites within the intestinal tract.  Sporozoites penetrate the intestinal wall and spread in lymphocytes and macrophages to parenchymal organs. Affected organs include lung, liver, spleen, pancreas, pericardium and intestinal epithelium. Several generations of asexual schizogony in these organs produce merozoites. Merozoites migrate back to the intestinal mucosa. Gametogony (sexual cycle) of the merozoites produce oocysts. Oocysts are excreted with the faeces. This is a common flock disease in canaries but only occasionally diagnosed in exotic finches

Clinical Disease

Typically, this is a disease of young canaries aged 2 to 9 months. The affected bird will appear fluffed up and will be debilitated and anorectic. It will have diarrhea and a red, swollen vent. Hepatomegaly is visible through the abdominal wall caudal to the sternum. Mortality is variable, but up to 80%. Occasionally, a patient will exhibit neurologic signs, such as epileptiform seizures and intermittent weakness. It may exhibit respiratory distress.

Diagnosis

Definitive antemortem diagnosis is difficult because after the acute phase, only a few Atoxoplasma oocysts are excreted. Fecal flotation shows oocysts with 2 sporocysts, each containing 4 sporozoites. Microscopic differentiation from Isospora is not easy: Atoxoplasma serini oocysts = 20.1 x 19.2 μm, Isospora canaria oocysts = 24.6 x 21.8 μm. A PCR assaye has been developed that will detect an DNA fragment of Atoxoplasma species in faeces, blood and tissues of infected birds.

Necropsy

Necropsy reveals severe splenomegaly, hepatomegaly and dilated bowel loops. Intracytoplasmic inclusion bodies will appear in mononuclear cells in impression smears or on histopathology of the lung, liver and spleen.

Prophylaxis

Sound husbandry practices must be observed: avoid overcrowding, practice good hygiene and provide

proper nutrition. Newly acquired birds must be quarantined and screened with multiple fecal flotations for the presence of Atoxoplasma. Adult canaries can be asymptomatic carriers and will shed oocysts

 sporadically. In collections with recurrent disease, consider annual coccidial treatment prior to the breeding season.

Treatment

Clinically diseased individuals usually die before they respond to treatment. Anticoccidial drugs such as

toltrazuril, sulfachloropyridazine (Esb3 30%) or other sulfonamides may be given. Atoxoplasmosis is considered resistant to treatment; however, Esb3 30% at 150mg/L of drinking water 5 days a week every week from the moment of diagnosis until after moulting has proven to stop production of oocysts, although it will not influence the intracellular stages.

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