Segmental Arterial Mediolysis in Pigs Presenting With Renal Infarcts.

Segmental arterial mediolysis, a rare arteriopathy first reported in humans, is described in the kidneys of 36 pigs slaughtered in an abattoir in Jutland, Denmark. The kidney changes presented themselves macroscopically as one or more cortical wedge-shaped hemorrhagic or pale lesions. The arterial lesions involved the interlobar and arcuate arteries and exhibited injurious and reparative phases of development. Two types of injurious lesions occurred: (1) a tearing separation of the outer media from the adventitia with fibrin, erythrocytes, and edema fluid filling the formed space, causing collapse of the arterial wall, and (2) outer and mid-medial foci showing irregularly bordered cytoplasmic vacuolar change containing membranous and organelle debris or smooth muscle shrinkage with nuclear loss. In the reparative phase, granulation tissue filled and expanded tear sites and zones of arterial medial muscle loss and extended into the adventitia and through the intima into the arterial lumen. Sequelae, including dissecting hematomas and arterial occlusions causing renal infarcts, were found. Although repartitioning agents widely used in animal husbandry in many countries may potentially cause segmental arterial mediolysis, no such link could be identified. The causation of segmental arterial mediolysis in these pigs is currently unknown but is being further investigated.

Porcine melanotic cutaneous lesions and lymph nodes: immunohistochemical differentiation of melanocytes and melanophages.

Porcine melanomas have proven interesting in a wider biological perspective due to a common phenomenon of spontaneous regression, which is characterized by infiltration of macrophages, among others. Separation of neoplastic melanocytes from pigment-laden macrophages may, however, be challenging as the morphology of melanocytes varies considerably and sometimes resembles macrophages. The aim of this study was correspondingly to characterize and differentiate the cells in 20 porcine melanocytomas and regional lymph nodes by histologic examination and immunohistochemistry for melan A, PNL2, S100, lysozyme, alpha-1-antitrypsin, and ionized calcium binding adaptor molecule 1 (Iba1). Grossly, the melanocytomas were divided into 2 distinct types: pigmented maculae (n = 7) and raised tumors (n = 13). In the maculae, the pigmented cells were mainly melanocytes reactive for melan A, PNL2 and S100. In contrast, the majority of the cells in the raised tumors were melanophages, which expressed Iba1, alpha-1-antitrypsin, and lysozyme. Yet, cells histomorphologically indistinguishable from the melanophages expressed melan A and PNL2. These cells were Iba1 and S100 negative, and ultrastructurally, they were devoid of lysosomal bodies and filled with stage III and IV melanosomes. In the regional lymph nodes, melanocytes were present in the trabecular sinuses. In focally or diffusely black lymph nodes, pigmentation was, however, mainly due to aggregates of melanophages, which were confined to the trabeculae, deep cortex, and peripheral lymphoreticular tissue. Normal and neoplastic porcine melanocytes express melan A and PNL2, and immunohistochemical staining for melan A, PNL2, and Iba1 was found useful to identify and distinguish melanocytes and melanophages in porcine melanotic lesions.

Distribution and histopathological changes induced by cysts of Taenia solium in the brain of pigs from Tanzania.

Neurocysticercosis (NCC) caused by Taenia solium cysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore, T. solium cysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.

Distribution and histopathological changes induced by cysts of Taenia solium in the brain of pigs from Tanzania.

Neurocysticercosis (NCC) caused by Taenia solium cysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore, T. solium cysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.

Histologic and immunohistochemical classification of 41 bovine adrenal gland neoplasms.

Tumors of the adrenal glands are among the most frequent tumors in cattle; however, few studies have been conducted to describe their characteristics. The aim of this study was to classify 41 bovine adrenal neoplasms from 40 animals based on macroscopic and histologic examination, including electron microscopy and immunohistochemistry for melan A, synaptophysin, chromogranin A, vimentin, pan-cytokeratin, 2',3'-cyclic nucleotide-3'-phosphohydrolase (CNPase), and Ki-67. The tumors were classified as 23 adrenocortical adenomas, 12 adrenocortical carcinomas, 2 schwannomas, 2 pheochromocytomas (1 malignant), and 1 ganglioneuroma. Five histologic features were characteristic of metastasizing adrenocortical tumors: invasion of the capsule, vascular invasion, diffuse growth pattern, spindle-cell morphology, and nuclear pleomorphism. Adrenocortical tumors with at least 3 of these features were classified as malignant. Immunohistochemically, adrenocortical tumors expressed melan A (16/19), vimentin (14/26), cytokeratin (11/26), and chromogranin A (9/27), whereas pheochromocytomas expressed chromogranin A (2/2), synaptophysin (2/2), and vimentin (1/2). Both schwannomas expressed CNPase. An immunohistochemistry panel consisting of antibodies against melan A, synaptophysin, and CNPase was considered most useful to classify bovine adrenal tumors. However, the distinction between benign and malignant adrenocortical tumors was based on histologic features as in human medicine.

The impact of Staphylococcus aureus concentration on the development of pulmonary lesions and cytokine expression after intravenous inoculation of pigs.

Acute respiratory distress syndrome is a common complication in severe sepsis. In pigs, the lungs play an important role in clearing systemic bacterial infections due to pulmonary intravascular macrophages found specifically in pigs. However, this increases the exposure of the porcine lungs to pathogens and potential injury. The authors propose that increasing the concentration of the inoculum without changing the bacterial dose will lead to severe sepsis with pronounced pulmonary lesions. This could potentially create a risk of cytokine spillover to the circulation, leading to an increased systemic response. Eight Danish Landrace pigs, approximately 10 weeks old, were inoculated twice with a low or once with a high concentration of Staphylococcus aureus. Three pigs were sham-inoculated. The animals were grouped based on macro- and microscopic lung lesions. The mRNA expression of local pulmonary inflammatory markers was compared to protein levels of systemic inflammatory markers. The most severe pulmonary lesions were observed in animals receiving the high S. aureus concentration, indicating that severity of lesions is dependent on inoculum concentration rather than total numbers of bacteria. Furthermore, local mRNA expression of inflammatory cytokines appeared to be dependent on the magnitude and severity of tissue destruction, including the ability to confine the lesions. Increasing mRNA levels of serum amyloid A could be a confident marker of severity of pulmonary lesions. Since no correlation was observed between local and systemic levels of inflammatory cytokines, this finding could indicate an ability of the porcine lung to compartmentalize the local inflammatory response and thus restrict systemic contribution.

Immunohistochemistry for 2',3'-cyclic nucleotide-3'-phosphohydrolase in 63 bovine peripheral nerve sheath tumors.

To establish a simple and uniform classification of bovine peripheral nerve sheath tumors (PNSTs), 63 tumors from 44 cattle were examined histologically and immunohistochemically with antibodies against S100 protein and 2',3'-cyclic nucleotide-3'-phosphohydrolase (CNPase). Immunohistochemically, all the tumors were positive for S100 protein, CNPase, or both. Four types of PNST were recognized: 35 schwannomas, 9 neurofibromas, 14 hybrid (neurofibroma-schwannoma) tumors, and 5 malignant PNSTs. Axons were identified by immunohistochemistry for neurofilament in a proportion of tumors of each type of PNST. In conclusion, bovine PNSTs commonly have both schwannomatous and neurofibromatous areas. Moreover, the Schwann cell markers S100 protein and CNPase, in combination with antibodies against neurofilament, are valuable diagnostic tools to classify bovine PNSTs.

The immune response in Taenia solium neurocysticercosis in pigs is associated with astrogliosis, axonal degeneration and altered blood-brain barrier permeability.

Immunohistochemistry was used to examine the immuno-pathological changes and the extent of neuronal damage caused by either viable or dead Taenia solium cysticerci during porcine neurocysticercosis. Thirty pig brains with cerebral cysticercosis and 5 brains from T. solium free pigs were used in this study. Results revealed extensive astrogliosis, neuronal and mostly axonal damage in both early (grade I) and late (grades III and V) lesions as evidenced by an increased expression of glial fibrillary acidic protein (GFAP) and neurofilament protein (NFP). In many late lesions, astrocyte end-feet formed glial scars that surrounded the dead parasite. Rapid angiogenesis resulted in blood vessels lacking astrocyte end-feet suggesting loss of blood-brain barrier (BBB) hence allowing an influx of peripheral blood immune cells such as eosinophils, macrophages, CD3+ T cells, B lymphocytes and plasma cells into lesions. This study showed that porcine NCC was associated with severe nervous tissue damage, the host response of which is a collaborative effort between the local and peripheral immune responses comparable to that observed in human NCC. Results further implied that porcine NCC could be a useful model for understanding the course of NCC in human as well as provide useful information for therapeutic and/or immune strategies.

Host-cell apoptosis in Taenia solium-induced brain granulomas in naturally infected pigs.

To assess whether apoptosis occurs in pig brain granulomas due to Taenia solium cysticerci, brain tissues from 30 pigs naturally infected with T. solium cysticercosis were evaluated by terminal deoxynucleotidyl transferase-end labelling (TUNEL) staining. In addition, tissues were stained with CD3 marker to identify T lymphocytes. Examination of TUNEL-stained tissues showed apoptotic cells in early lesions that contained viable cysticerci. Apoptotic cells were primarily found interspersed with normal cell types, and were mostly located in the inflammatory infiltrate. Late or advanced granulomas with disintegrated scolices did not show TUNEL-positive cells. CD3+ cells were found in both early and advanced lesions and apoptosis mainly co-localized with CD3+ T lymphocytes. This suggests that these cells are constantly undergoing apoptosis and thus die as soon as they arrive at the site of infection. Apoptosis indeed may be one way by which T. solium cysticerci down-regulate the host's cellular immune response in early cysticercosis. Therefore, further research is needed to establish if other cells besides T-lymphocytes are also a target for destruction by cysticerci in early cysticercosis as well as studies to assess if cysteine protease is expressed by viable cysticerci in situ.

Taenia solium porcine cysticercosis: viability of cysticerci and persistency of antibodies and cysticercal antigens after treatment with oxfendazole.

The aim of this study was to assess the effect of treating Taenia solium infected pigs with oxfendazole (OFZ) on viability and clearance of cysticerci and the corresponding persistence of specific antibody isotypes (IgG(total), IgG1, IgG2 and IgA) and circulating cysticercal antigen (CCA). Antibody isotypes and CCA responses were measured by antibody-ELISA (Ab-ELISA) and antigen ELISA (Ag-ELISA), respectively. Correlations were made between antibodies, CCA and the total number of cysticerci enumerated at necropsy. Forty pigs with cysticercosis were randomly allocated into two groups: Treatment group (n=20) was treated with OFZ at 30 mg/kg orally while the treatment control group (n=20) was not treated. Five uninfected pigs served as negative controls. Pigs were killed at 1, 4, 8 and 26 weeks post-treatment (wkpt). Overall, the mean total cyst count in treated pigs was 2904+/-5397 (mean+/-S.D.) while in the controls it was 6235+/-6705. Mean cyst viability was 5+/-11% (mean+/-S.D.) and 97+/-4% in treated and control pigs, respectively. Results showed that OFZ killed muscular cysticerci over a period of 4 weeks but failed to kill cerebral cysticerci. Antibodies, CCA responses and clearance of dead cysts from the meat, depended on the cyst intensity of individual pigs at time of treatment since both antibody and CCA correlated with intensity of cysticerci at necropsy (r=0.441, P=0.005; r=0.654, P<0.001), respectively. IgG1 responses were the best indicator of treatment efficacy because they were predominant in both infected treated and control pigs and disappeared early after treatment. Both Ab/Ag-ELISA failed to detect cysts in the brain. Though dead cysticerci took some time (26 wkpt) to clear from the meat, treatment of porcine cysticercosis with OFZ should, in combination with other intervention measures be considered as an important, cost-effective measure in the control of taeniosis/cysticercosis.

Nonstrangulating intestinal infarctions associated with Strongylus vulgaris: Clinical presentation and treatment outcomes of 30 horses (2008-2016).

BACKGROUND: Strongylus vulgaris is re-emerging in horses kept under surveillance-based parasite control regimens. Information on nonstrangulating intestinal infarction associated with S. vulgaris is needed to improve recognition of the condition. OBJECTIVE: To describe the typical clinical presentation, laboratory findings, gross pathology, treatment and outcome of horses with nonstrangulating intestinal infarction. STUDY DESIGN: Retrospective case series. METHODS: Nonstrangluating intestinal infarction was diagnosed in 30 horses with a localised intestinal infarction with concurrent signs of S. vulgaris migration and no signs of intestinal strangulation or enterocolitis. Data were obtained from medical records in the period 2008-2016. Long-term follow-up information was obtained by telephonic interviews. Levels of S. vulgaris-specific antibodies were retrospectively assessed. Associations between nonstrangulating intestinal infarction and selected variables were evaluated using Fisher's exact and Mann-Whitney U tests. RESULTS: The most consistent findings at admission were mild colic of >24 h duration without signs of shock or strangulated intestine, increased peritoneal fluid WBC (>5 × 109 /L), increased serum amyloid A (SAA) concentration and a positive S. vulgaris-specific antibody titre. Medical treatment was attempted in nine horses with none surviving. Exploratory laparotomy was performed in 21 horses. Eleven horses were subjected to euthanasia intraoperatively due to the presumed poor prognosis. Of the nine horses, three (33%) undergoing intestinal resection survived to discharge. The surviving horses were alive and returned to athletic function for at least 2 years following discharge. MAIN LIMITATIONS: Only nine of the 30 horses underwent resection of the infarcted intestine, and the prognosis for surgical intervention in nonstrangulating intestinal infarction is, therefore, difficult to estimate. CONCLUSIONS: In areas where S. vulgaris is prevalent, nonstrangulating intestinal infarction should be considered as a differential diagnosis in horses presenting with mild colic and peritonitis. Survival of nonstrangulating intestinal infarction is possible in cases where surgical intervention with resection of the infarcted intestine is feasible. The summary is available in Spanish - see Supporting Information.

Hepatic changes in congenital Schistosoma japonicum infections in pigs.

The inflammatory response in liver tissue from piglets congenitally infected with Schistosoma japonicum was examined at two different timepoints after infection. The piglets, which were the offspring of three sows infected with 9000 S. japonicum cercariae in the 10th week of gestation, were allocated into two groups (n=9 and 17) killed 5 or 11 weeks after birth, respectively. All piglets developed a low level infection,with no significant difference between the groups. Inflammatory lesions in the liver consisted mainly of granulomas in portal areas, often obliterating the portal veins, and frequently with central eggs or egg remnants. The granulomatous reaction consisted of epithelioid cells and occasional giant cells surrounded by layers of lymphocytes, eosinophils, plasma cells, and various amounts of collagen and fibroblasts. Mild to moderate infiltration of portal and septal connective tissue with eosinophils and lymphocytes was common, but the connective tissue was generally not increased. At the two timepoints, slight differences were observed in the numbers of eosinophils and lymphocytes in the granulomas and in the size of the granulomatous reaction. The same pattern of immunohistochemical labelling was seen in both groups. CD79alpha(+) B cells were scarce except in granuloma-associated lymphoid follicles;the majority of lymphocytes in granulomas and at other sites were CD3epsilon(+) T cells. The granulomatous reaction in the livers of piglets to schistosoma eggs from prenatal S. japonicum infection was similar to that seen in postnatal infection. Signs of immunomodulation of granulomas between the two timepoints of infection were not demonstrable.

Immunoreactivity of bovine schwannomas.

Thirty schwannomas from 22 cows were examined immunohistochemically. All were positive for vimentin and Ki-67 but negative for pancytokeratin, neurofilament, and desmin. S-100 immunolabelling varied between and within lesions. The numbers of tumours giving positive results for S-100, neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP) were 16, 30 and 25, respectively. It was concluded that vimentin-positive tumours suspected to be schwannomas should also be immunolabelled for NSE and GFAP to confirm the diagnosis.

Histology of selected immunological organs in polar bear (Ursus maritimus) from East Greenland in relation to concentrations of organohalogen contaminants.

Samples of lymph nodes (axillary, n = 54 and inguinal, n = 45), spleen (n = 60), thymus (n = 11) and thyroid tissue (n = 5) from a total of 82 polar bears (Ursus maritimus) collected in East Greenland 1999-2002 were examined histologically. The purpose was to relate histology to concentrations of organohalogen contaminants (OHCs) [i.e., sum (Sigma)PCBs, SigmaDDTs, SigmaHCHs, SigmaCHLs, HCB, Dieldrin and SigmaPBDEs] determined in adipose tissue, as studies on polar bears have indicated that some OHCs act as immunosuppressive agents. Secondary follicle counts were evaluated in spleen and lymph nodes, and semiquantitively divided into four groups (0: few/absent to 3: high). In the spleen, a high secondary follicle count was found in 21% of the cases (12/60), and this was significantly higher in subadults (p < 0.01) compared to adults of both sexes. Also in the lymph nodes a high secondary follicle count was found in 20% of the cases (20/99), and in the axillary lymph nodes changes were significantly higher in subadults (p < 0.05) compared to adults of both sexes. Significantly weak correlations between concentrations of OHCs and the amount of secondary follicles in lymph nodes was found, but probably occurred as a consequence of other multiple stress factor(s) (all: p < 0.05) and also one significant, but modest positive correlation was found between SigmaPBDE concentrations and secondary follicle counts (p < 0.01; r = 0.41). In spleen, a significant relation between low concentrations of OHCs in adipose tissue and few/absent secondary follicles was found with respect to SigmaCHLs, SigmaHCHs, HCB and Dieldrin. No histopathological observations (e.g., neoplasia) were found in spleen or lymph nodes, nor in thymus or thyroid. In conclusion, the present data suggest that the exposure concentrations of OHCs to polar bears are unlikely to have resulted in adverse effects on the tissues in question, although SigmaCHLs, SigmaHCHs, HCB and Dieldrin were related to increased secondary follicle counts in the spleen.

Enlarged clitoris in wild polar bears (Ursus maritimus) can be misdiagnosed as pseudohermaphroditism.

A 23-year-old female polar bear (Ursus maritimus) killed in an Inuit hunt in East Greenland on July 9, 1999 had a significantly enlarged clitoris resembling, in size, form and colour, those of previously reported 'pseudohermaphroditic' polar bears from Svalbard. It has been suggested that an enzyme defect (21-hydroxylase deficiency), androgen producing tumour or high exposure to organochlorines during the foetal stage or early development could be the reason for the supposed pseudohermaphroditism observed for Svalbard bears. Except for the enlarged clitoris, all dimensions of the external and internal reproductive organs of the present were similar to a reference group of 23 normal adult female polar bears from East Greenland collected in 1999-2002. The aberrant bear was a female genotype, and macroscopic examination of her internal reproductive organs indicated that she was reproductively functional. A histological examination of the clitoral enlargement in the present East Greenland specimen allows a first-time histological evaluation of the earlier macroscopic field diagnosis from Svalbard. This examination revealed intense chronic ulcerative and perivascular clitoriditis similar to "acral lick dermatitis" frequently seen in domestic dogs (i.e., we did not find any signs of pseudohermaphroditic hyperplasia of clitoral tissue due to androgenic or antiestrogenic endocrine disruption). The levels of organohalogens and TEQ values were lower than concentration thresholds of toxicological risk. It is hence possible that the previously reported adult female polar bear pseudohermaphrodites from Svalbard are in fact misdiagnoses. Therefore, future studies examining pseudohermaphroditism in wildlife should consider that certain occurrences are natural events, e.g., enlarged clitoris in the present East Greenland polar bear. Furthermore, caution should be exercised in suggesting linkages of such inflammatory abnormalities with correlations to anthropogenic pollutant exposures.

Serotonin markers show altered transcription levels in an experimental pig model of mitral regurgitation.

Serotonin (5-hydroxytryptamine, 5-HT) signalling is implicated in the pathogenesis of myxomatous mitral valve disease (MMVD) through 5-HT1B receptor (R), 5-HT2AR and 5-HT2BR-induced myxomatous pathology. Based on increased tryptophan hydroxylase-1 (TPH-1) and decreased serotonin re-uptake transporter (SERT) in MMVD-affected valves, increased valvular 5-HT synthesis and decreased clearance have been suggested. It remains unknown how haemodynamic changes associated with mitral regurgitation (MR) affect 5-HT markers in the mitral valve, myocardium and circulation. Twenty-eight pigs underwent surgically induced MR or sham-operation, resulting in three MR groups: control (CON, n = 12), mild MR (mMR, n = 10) and severe MR (sMR, n = 6). The gene expression levels of 5-HT1BR, 5-HT2AR, 5-HT2BR, SERT and TPH-1 were analysed using quantitative PCR (qPCR) in the mitral valve (MV), anterior papillary muscle (AP) and left ventricle (LV). MV 5-HT2BR was also analysed with immunohistochemistry (IHC) in relation to histological lesions and valvular myofibroblasts. All 5-HTR mRNAs were up-regulated in MV compared to AP and LV (P <0.01). In contrast, SERT and TPH-1 were up-regulated in AP and LV compared to MV (P <0.05). In MV, mRNA levels were increased for 5-HT2BR (P = 0.02) and decreased for SERT (P = 0.03) in sMR vs. CON. There were no group differences in 5-HT2BR staining (IHC) but co-localisation was found with α-SMA-positive cells in 91% of all valves and with 33% of histological lesions. In LV, 5-HT1BR mRNA levels were increased in sMR vs. CON (P = 0.01). In conclusion, these data suggest that MR may affect mRNA expression of valvular 5-HT2BR and SERT, and left ventricular 5-HT1BR in some pigs.

Typing of Pasteurella multocida from haemorrhagic septicaemia in Danish fallow deer (Dama dama).

Isolates of Pasteurella multocida ssp. multocida (n = 31) from a Danish population of fallow deer which succumbed to haemorrhagic septicaemia during 1992 1993 and isolates from the palatine tonsils of apparently healthy fallow deer from the same area (n=6) were typed and compared with P. multocida from other sources. Plasmids were net observed in the fallow deer strains and one unique pattern was observed by ribotyping using HindIII and by pulsed-field gel electrophoresis using SanlI as restriction endonuclease. All Danish fallow deer isolates belonged to serotype B:3,4. On restriction endonuclease analysis using HhaI as restriction endonuclease, all had a profile identical to that of a fallow deer isolate from the United Kingdom: profile 0033 of Wilson et al. On restriction endonuclease analysis using HpaII as restriction endonuclease, the Danish fallow deer isolates had a unique profile, designated 0062, which differed slightly from that of a fallow deer isolate from the United Kingdom. P. multocida from other animal species were genotypically different from the fallow deer isolates. It is concluded that a specific clone of P. multocida was responsible for the outbreak of haemorrhagic septicaemia among Danish fallow deer. A carrier rate of 27% was demonstrated among apparently normal animals from the same population.

Cadmium toxicity to ringed seals (Phoca hispida): an epidemiological study of possible cadmium-induced nephropathy and osteodystrophy in ringed seals (Phoca hispida) from Qaanaaq in Northwest Greenland.

The Greenland marine food chains contain high levels of cadmium, mercury and selenium. Concentrations of cadmium in the kidney of ringed seals (Phoca hispida) from the municipalities of Qaanaaq and Upernavik (Northwest Greenland) are among the highest recorded in the Arctic. The purpose of the study was to determine whether cadmium-induced damage in the kidneys and the skeletal system could be detected among 100 ringed seals from Northwest Greenland. The cadmium concentrations in the kidney cortex ranged from 0 to 248 microg/g wet weight (mean=44.5, N=100) in the 99 kidneys examined. Experience from cadmium-poisoned humans and laboratory mammals indicates that concentrations above 50-200 microg/g wet wt. may induce histopathological changes. Overall, 31 of the ringed seals had cadmium concentrations in the kidney cortex above 50 microg/g wet wt., 11 had concentrations above 100 and one had a concentration above 200 microg/g wet wt. Obvious histopathological changes (categorised mainly as glomerulonephritis) were found in 10 of the seals; however, none of these changes could be attributed to cadmium-induced renal damage (mainly tubulopathy) as described for other species. Damage to the proximal kidney tubules is known to induce demineralisation of the skeletal system (Fanconi's syndrome). Therefore, the three lowest lumbar vertebrae were scanned in 91 seals to measure the content of calcium. The 10 cases of nephropathy could neither be linked to the degree of mineralisation of the skeleton nor to the cadmium concentrations. Furthermore, the degree of mineralisation of the skeleton was not correlated with the cadmium concentration, age or sex. It can therefore be concluded that despite high levels of cadmium, none of the ringed seals showed any signs of cadmium-induced nephropathy or osteodystrophy. This might be explained by the composition of the ringed seals diet, which contains high levels of vitamin D, calcium, phosphorus, zinc, selenium and protein. These elements are all likely to counteract cadmium-induced damage. It is speculated that ringed seal are not particularly vulnerable to osteodystrophy, due to their continuous growth (bone mineralisation) throughout life and the oestrogen hormonal activity of females throughout life.

Pathogenesis of congenital infection with Schistosoma japonicum in pigs.

To elucidate aspects of pathogenesis of congenital infections with Schistosoma japonicum, 5 Danish crossbred sows were infected during late pregnancy with a Chinese isolate of S. japonicum, and 17 of their offspring (fetuses and piglets) were examined 7, 20. 34, 54, and 69 days postinfection (PI). Organ samples were collected for histopathological examination with emphasis on liver and lung. Samples of the corresponding placenta were also collected from fetuses at postmortem examinations. Perfusions were performed on some of the fetuses to recover schistosomes, and in addition, amniotic fluid was examined for schistosomes. A schistosomulum was found in a 99-day-old fetus 3 wk PI. Eggs were found in meconium from 109-day-old fetuses 34 days after infection of the dam, showing that the prepatent time was the same as in postnatal infections. Piglets examined 54 and 69 days PI had inflammatory reactions in their livers, and progression toward healing and repair of the inflammatory reaction occurred from 54 to 69 days PI. This pilot study is one of the bases for the model of congenital schistosomiasis used currently at the Danish Centre for Experimental Parasitology.

Pulmonary intravascular macrophages in the pathogenesis of bovine pulmonary lesions caused by Actinomyces pyogenes.

Rabbit antisera raised against somatic antigens from two strains of Actinomyces pyogenes reacted specifically in a peroxidase anti-peroxidase technique which was developed for the location of the bacteria in formalin-fixed tissues. The technique was applied on experimental murine and spontaneous bovine lesions caused by A. pyogenes. By electron microscopy and immunohistochemistry it was demonstrated that pulmonary intravascular macrophages play a role in the uptake of A. pyogenes from the blood, and in the production of pyaemic pulmonary lesions.