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Case History: A syndrome of acute neurological dysfunction with increased mortality was observed in lambs of 10 dairy sheep flocks and adult animals in one flock in Central and Northern Greece. Each farmer completed a questionnaire regarding the management and feeding of their flocks. In seven of the 11 flocks the affected animals were grazing pasture, while in the remaining four flocks (5, 8, 9, 10) the animals were fed alfalfa hay (Medicago sativa) and concentrates indoors. A follow-up study of the affected flocks was conducted during the next 12 months., Clinical Findings: Of 42 sheep with acute coenurosis that were examined, the most prominent neurological abnormalities were ataxia, depression, blindness, scoliosis, coma and dysmetria. Except for the four sheep that were comatose, all other animals had normal body temperatures and their appetites remained normal or were slightly decreased. Haematological findings of 15 examined sheep were within normal limits. The affected sheep were subject to euthanasia. A histopathological examination was performed in 13 cases. Faecal samples from dogs associated with these flocks were negative for taeniid infections. During the following 12 months cases of chronic coenurosis in these flocks were observed., Pathological Findings: In the 42 animals that were necropsied, the main gross findings were cystic formations between 0.5-1 cm in diameter with translucent walls that were seen lying free on the leptomeninges or partly penetrating the brain tissue, sterile microabscecess and brain necrosis. Histopathological evaluation of tissue sections of 13 brains showed multifocal purulent or pyogranulomatous meningoencephalitis, accompanied by eosinophilic infiltrations. No bacteria were isolated following bacterial culture of brain tissue Parasitological examination of the cysts from five cases revealed whitish specks on the transparent cyst wall and germination membrane representing the scolices., Diagnosis: Acute coenurosis was diagnosed in all cases studied., Clinical Relevance: Acute coenurosis can be one of the causes of acute encephalopathy mainly in lambs, but also in adult sheep. This condition is incurable, but can be controlled by changing the feeding regime. Cases of chronic coenurosis may be seen a few months later in the same flock.

Case History: A 5-day-old red deer calf was submitted with tachypnoea and dyspnoea, and was reluctant to move., Clinical Findings: Muscular damage was established via elevated creatinine phosphokinase (CPK) activities (5,000 U/L), while concentrations of Se in whole blood were low (24.8 nmol/L). The animal died despite treatment with penicillin and streptomycin and 0.1 mg/kg Se/vitamin E administered by S/C injection., Diagnosis: Necropsy and histological examination of cardiac and skeletal muscle confirmed the presumptive diagnosis of congenital white muscle disease (WMD). Prophylactic administration of a Se/vitamin E commercial preparation (as above) to another calf born in the same herd one month later was associated with good health and apparently normal growth and development., Clinical Relevance: Congenital WMD due to Se deficiency can be fatal in red deer calves. However, prophylactic administration of Se and vitamin E to neonatal calves may be beneficial for neonatal red deer calves.

In 2002, postweaning multisystemic wasting syndrome (PMWS) was diagnosed in a European female wild boar (Sus scrofa), based on the detection of porcine circovirus 2 (PCV2) DNA in various organs, including the uterus, and on histopathologic lesions. This is the first detection of PCV2 DNA in the uterus of a wild boar. Three years later (2005), a wild boar < 6-8 mo of age was found moribund. It presented wasting and dyspnea and finally died. PCV2 DNA was detected in tissue samples, and histopathologic lesions consistent with PMWS were observed. Both wild boars were from neighboring hunting areas in central Greece. Two PCV2 strains from the wild boars were genetically characterized and compared to other reported PCV2 sequences from wild boars and domestic pigs. The PCV-2 sequences from the wild boars in this study were closely related to each other and were grouped with two isolates from wild boars from Hungary. The phylogenetic analysis revealed that the virus might be transmitted between hunting areas. In addition, PCV2 may spread from domestic pigs to wild boars and vice versa.

From 1999 to mid-2003, 97 European brown hares (Lepus europaeus) found dead throughout Greece were examined by necropsy, histopathology, and reverse-transcription polymerase chain reaction (RT-PCR) for the presence of European brown hare syndrome (EBHS) and EBHS virus (EBHSV), respectively. Hare losses were sporadic, starting in the cold season and lasting for many months (December to May). The most prominent gross lesions were observed in the liver and included swelling and discoloration; congestion and hemorrhages were present mainly in lungs and tracheal mucosa. Necropsy findings were suggestive of EBHS, which was confirmed by histopathology and RT-PCR. This study documents, for the first time, EBHS in Greece.

A total of 216 local crossbred sheep from 16 scrapie-affected Greek flocks and 210 purebred sheep of the milk breeds Chios and Karagouniko from healthy flocks were analysed for scrapie-linked polymorphisms in the prion protein (PrP) gene. Of the 216 sheep in this case-control study, 96 sheep were clinical cases, 25 subclinical cases (asymptomatic at the moment of euthanasia but positive by histopathology and/or ELISA detecting proteinase-resistant PrP) and 95 healthy controls (negative by all evaluations). Polymorphisms at codons 136, 154 and 171 were determined by denaturing gradient gel electrophoresis, followed by RFLP and sequencing. Scrapie, both clinical and subclinical, was associated with the genotypes ARQ/ARQ (88 of 110 sheep of that genotype), ARQ/TRQ (9 of 13), ARQ/AHQ (15 of 38) and VRQ/VRQ (9 of 17). Histopathological lesions were more severe in the clinical cases. Genotypes ARQ/ARR (26 sheep), ARQ/ARK (seven sheep), AHQ/ARR (one sheep), ARH/ARH (one sheep) and ARR/ARH (three sheep) were detected exclusively in healthy control sheep. In the purebred survey, four genotypes were present in the Chios sheep (ARQ/ARQ, ARQ/TRQ, ARQ/AHQ and ARQ/ARR) and four in the Karagouniko sheep (ARQ/ARQ, ARQ/AHQ, ARQ/ARR and ARQ/ARH).

A total of 51 goats, including seven clinical cases, from the first herd in Greece reported to have scrapie was examined to discern an association between scrapie susceptibility and polymorphisms of the gene encoding the prion protein (PrP). Each animal was evaluated for clinical signs of the disease, histopathological lesions associated with scrapie, the presence of detectable protease-resistant PrP in the brain and PrP genotype. Eleven different PrP genotypes encoding at least five unique predicted mature PrP amino acid sequences were found. These genotypes included the amino acid polymorphisms at codons 143 (H-->R) and 240 (S-->P) and 'silent' nucleotide alterations at codons 42 (a-->g) and 138 (c-->t). Additionally, novel caprine amino acid polymorphisms were detected at codons 21 (V-->A), 23 (L-->P), 49 (G-->S), 154 (R-->H), 168 (P-->Q) and 220 (Q-->H) and new silent mutations were found at codons 107 (g-->a) and 207 (g-->a). The following variants were found in scrapie-affected goats: VV(21), LL(23), GG(49,) SS(49), HH(143), HR(143), RR(154), PP(168), PP(240), SP(240) and SS(240). All scrapie-affected animals carried the HH(143)RR(154) genotype, with the exception of two goats (HR(143)), both of which had detectable protease-resistant PrP but showed no clinical signs or histopathological lesions characteristic of scrapie.

The first cases of scrapie were detected in Greece in a flock of sheep in October 1986. All the animals of the affected flock and all sheep in two flocks that were in contact were killed and buried. A systematic investigation of all available cases with signs indicating a neurological disease started in sheep and goats in late 1986, as well as in cattle in 1989. The investigation was based on clinical examination, necropsy or macroscopical examination of the brain and viscera, and histological examination of the brain in all animals except those with coenurosis. Histological examinations of specimens from the spinal cord and other tissues, and if considered necessary bacteriological, toxicological and serological examinations were also carried out. In October 1997, scrapie was diagnosed in sheep of a second flock (a mixed flock of sheep and goats), grazing in a pasture close to the place where scrapie was initially detected. All animals of the second flock were also killed and buried. Diagnosis in the first flock was based on clinical signs and histological lesions, and in the second immunoblotting was also used. Distinctive lesions of scrapie were found in the brain and/or the spinal cord of eight sheep with clinical signs from the two flocks. The lesions were revealed in the brain stem and/or in the cervical spinal cord, and tended to be symmetrical. In one sheep, severe lesions in the cortex of cerebral hemispheres and of the cerebellum were also found. In the brain of two sheep from the second flock the pathological isoform of PrP protein was detected. Despite the eradication scheme applied, scrapie in sheep reappeared after 11 years in a place close to where it occurred initially. This may indicate that the effectiveness of the eradication scheme implemented was not adequate and additional approaches may be needed.

Thirteen susceptible piglets, aged 40 days, were divided into two groups and were experimentally infected either with a Greek (myocardial) or a Belgian (reproductive) encephalomyocarditis virus (EMCV) strain (total dose 5 x 10(6) TCID50, intramuscularly and intranasally). Six piglets were placed in the same rooms, 24 h later, as contact controls. The following criteria were studied: ante mortem: clinical signs, serum cardiac isoenzyme activities (CK-MB and LD-1), viraemia, nasal and faecal virus excretion and serological response. Post mortem (after death or euthanasia): gross lesions, virus isolation from tissues, RT-PCR, as well as histopathological and immunohistochemical findings. The Greek strain was more pathogenic, producing mortality, with high cardiac isoenzyme activities and pronounced macroscopic myocardium lesions. The Belgian strain was able to induce mild heart lesions, as detected only by cardiac isoenzyme activity and histopathologically. All contact pigs were infected, within the first 1-2 days of their introduction, that coincided with the period of viral excretion by the experimentally infected pigs (up to the 3rd day post infection). Disease was mild, with no mortality.