General information

Encephalitozoon cuniculi

The pathogen Encephalitozoon cuniculi causes encephalitozoonosis (also called torticollis, wry neck, head tilt) in rabbits. Approximately 80% of healthy rabbits carry the pathogen without showing any clinical signs. Mature infectious spores are mainly excreted intermittently in the urine, so that transmission takes place orally and nasally by eating infected food or sniffing at food and litter. However, infected pregnant female hares can also transmit the pathogen to their young in the womb. Faecal shedding of pathogens was detected but seems to be of little importance.

The pathogen has also been found in many other animal species such as dogs, foxes, rodents and some bird species and even in humans. Especially in immunocompromised persons, infection can be relevant.

Apart from head tilt, the clinical picture in rabbits is mainly characterised by ataxia, nystagmus, seizures or cramps. As the disease can also take a milder course, it is recommended to test for E. cuniculi in case of any neurological sign.

Encephalitozoon pogonae

Encephalitocoon pogonae has been described in bearded dragons (Pogona spp.; Agamidae) and is a member of the phylum Microsporidia. Microsporidia are single-celled, intracellular, spore-forming fungi reclassified from the group of protozoa. Due to similar morphology and genetic similarities, the pathogen was first identified as Encephalitozoon cuniculi. Since 2016 it has been classified as independent species.

Infections can be associated with non-specific signs such as lethargy, anorexia, weight loss and polydipsia. Multiplication takes place in macrophages of different organs, especially the kidneys, but also the gastrointestinal tract, liver, ovaries, spleen, lungs, the vascular endothelium and ventricular ependymal cells of the brain are affected, and granulomas are formed. Co-infections with agamid adenovirus 1 and coccidia have been described and may lead to a more severe clinical picture.
Faecal excretion can occur and transmission is likely via the faecal-oral route. Diagnosis is made by PCR and/or histopathology of the affected tissue or by PCR from a cloacal swab or faeces.