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Summary Hearing represents the major sense in harbour porpoises (Phocoena phocoena) and impairment of hearing has a great impact on the survival of these animals. In this communication, some anatomical and histological aspects of the tympanoperiotic complex of harbour porpoises are presented. In addition, the ears of 21 incidentally bycaught or stranded freshly dead harbour porpoises of different age groups and sex were investigated histologically. At the entrance to the middle ear cavity, mucosa-associated lymphoid tissue was present that was often hyperplastic in juvenile (9/10) and adult individuals (7/8). Solitary lymphoid follicles were additionally found in the corpus cavernosum and adjacent to the stapedius muscle in single porpoises. The nematode Stenurus minor represented the most common pathogen observed in the middle ear cavity of juvenile and adult harbour porpoises and the parasite was associated with chronic inflammation with metaplastic and hyperplastic epithelial changes. An unusual bone formation at the attachment of the corpus cavernosum to the perioticum was a common finding, even in young individuals. Whether this represents a normal structure or a metaplastic change remains undetermined. Acute haemorrhages in the cochlea and/or the tympanic cavity occurred in all animals and were most likely agonal changes. Single porpoises suffered from purulent otitis media, mycotic otitis media with osteolysis or chronically fractured tympanic bones, likely causing impairment of hearing that may have contributed to by-catch. There was no evidence that stranding in five porpoises was associated with the aural changes. Histological examination of the ears in harbour porpoises is a valuable part of the assessment of their health status. Damage to hearing structures may explain starvation due to impaired ability to catch prey or unusual behaviour such as stranding or entanglement in nets.

Toxoplasmosis is a parasitic disease that affects man and animals worldwide. The primary hosts and major reservoir for Toxoplasma gondii are felids and the intermediate hosts are most warm-blooded animals including man. This report describes fatal toxoplasmosis in three different rodent species in Germany: a female red squirrel (Sciurus vulgaris) and a male Swinhoe's striped squirrel (Tamiops swinhoei), both kept as pets, and a female New World porcupine (Erethizontidae sp.) from a zoo. All three animals had multifocal necrotizing hepatitis. Additional findings included lymphohistiocytic and necrotizing myocarditis in the New World porcupine and the Swinhoe's striped squirrel, lymphohistiocytic encephalomyelitis in the New World porcupine and suppurative lymphadenitis in the red squirrel. Numerous tachyzoites were identified associated with the lesions. The diagnosis was confirmed by Toxoplasma. gondii immunohistochemistry and electron microscopy. This is the first report of toxoplasmosis in a New World porcupine and a Swinhoe's striped squirrel.

Within 4 weeks, five cats with skin lesions affecting the hindlimbs and mainly consisting of oedema, hyperaemia and plaque-like alterations were presented to the same veterinary clinic. The cats were suffering from lameness, trauma, renal insufficiency or complicated tail amputation. Although the lesions seemed unusual for a poxvirus infection, microscopical examination of biopsy samples or specimens taken during necropsy examination revealed ballooning degeneration of keratinocytes with eosinophilic, cytoplasmic inclusion bodies indicative of an orthopoxvirus infection. Cowpox virus infection was verified using immunohistochemistry and virus isolation. Molecular analysis revealed identical haemagglutinin gene sequences in four cases and spatiotemporal circumstances in some cases pointed to hospital-acquired transmission. Unusual manifestations of feline cowpox may have an unexpected risk for human infection.

A 9-year-old by-caught harbour porpoise (Phocoena phocoena) was subject to routine post-mortem examination. Major findings included parasitic infection (Stenurus minor) of the left middle ear and severe mycotic infection of the right middle ear. The morphological appearance of the causative organism was consistent with Aspergillus fumigatus. These pathological findings were likely to have impaired echolocation in this animal and this may have contributed to the by-catch. The ears of marine mammals should be examined routinely during post-mortem investigations.

Neurolymphomatosis is a rare manifestation of lymphoma and is characterized by neoplastic infiltration of the peripheral nervous system. The present report describes neoplastic infiltration of peripheral nerves in three horses with multicentric lymphoma. Immunohistochemistry revealed the presence of CD79a(+) lymphoblastic cells and well-differentiated CD3(+) T cells, characteristic of T-cell-rich B-cell lymphoma in all cases. Nerve infiltration by lymphoma is rare, but should be considered as a differential diagnosis for peripheral neuropathy in horses with lymphoma.

Multiple sclerosis (MS), one of the most frequent central nervous system (CNS) diseases in young adults, is a chronic demyelinating disease of unknown etiology and possibly multifactorial causes. Due to clinical and pathological similarities, Theiler’s murine encephalomyelitis (TME) represents a commonly used infectious animal model for the chronic-progressive form of human MS. Inadequate viral clearance in susceptible SJL mice leads to persistent infection of the CNS and immune mediated spinal cord demyelination. In contrast resistant C57BL/6 mice eliminate the virus from the CNS by specific cellular immunity, including effective CD8-mediated cytotoxicity. Previous studies have demonstrated that regulatory T cells (Treg) reduce antiviral immune responses in TME in susceptible mice strains. However, the function of Treg in resistant C57BL/6 mice remains undetermined. Thus the aim of the present study was to investigate the impact of in vivo-expansion of Treg by interleukin-2 immune complexes (Treg-expansion) and antibody-mediated CD8+ T cell depletion (CD8-depletion) upon TME virus-induced disease progression in C57BL/6 mice to get further insights into role of Treg and their interaction with other leukocyte subsets in persistent viral infections. Results of the present study confirmed the central role of antiviral cytotoxicity for TME virus elimination in resistant C57BL/6 mice. In agreement with previous reports simple manipulation of the Treg-compartment showed only minor effect upon the disease course in resistant mice, though Treg-expansion exerted profound inhibitory responses in an CD8-reduced environment. Flow cytometric analyses revealed an increased percentage of Foxp3+ Treg in the blood and spleen of C57BL/6 mice following Treg-expansion and CD8-depletion (combined treated animals) associated with an increased CD4/CD8 ratio. Furthermore, a prolonged effect of Treg-expansion was observed in combined treated mice, indicative of an inhibitory effect of CD8+ T cells upon Treg. Peripheral phenotypical changes were associated with an enhanced recruitment of lymphocytes to the brain and spinal cord of TME virus-infected C57BL/6 mice as determined by histology. Real time polymerase chain reaction confirmed chronic brain infection at 42 days post infection (dpi) in combined treated C57BL/6 mice. Immunohistochemistry revealed a predominent infection of hippocampal neurons and significant infiltrations of CD3+ T cells, CD45R+ B cells and CD107b+ microglia/macrophages till 14 dpi in the cerebrum. Foxp3+ Treg were found in the hippocampus also during the late phase (42 dpi), potentially attributed to termination of inflammatory responses. In the spinal cord CD8-depletion and combined treatment led to prolonged infection and leukomyelitis in mice. Immunohistochemistry revealed a significant loss of myelin basic protein expression at 42 dpi in combined treated mice. Moreover, spinal cord demyelination was associated with an increase of β-amyloid precursor protein-postitive axons predominetely in combined treated mice, indicative of axonal damage. Inflammatory responses in the spinal cord white matter were dominated by CD3+ T cells and CD107b+ macrophages/microglia, suggestive of T cell-mediated immunopathology. In addition, significant numbers of Foxp3+ Treg and CD45R+ B cells were found in the spinal cord white matter during the late phase in combined treated C57BL/6 mice. In conclusion, the present project demonstrates synergistic effects of combined Treg-expansion and CD8-depletion to efficiently reduce antiviral immune responses in TME virus-infected C57BL/6 mice, which renders them susceptible to develop chronic infection, leukomyelitis and myelin loss. In addtion to the well described inhibitory effect of Treg upon CD8+ T cells, also regulatory effects of cytotoxic cells upon Treg or bidirectional interaction of these two T cell subsets, respectively, may occur in infectious CNS disoders. C57BL/6 mice are widely used for genetic modification and several transgenic mice with this genetic background have been established for the use as animal models. Thus, findings will potentially support the development of novel therapeutic strategies for chronic inflammatory disorders and provide a base for future studies upon virus-induced immunopathology using transgenic mice.