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.

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.

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.

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.

Disseminated intravascular coagulation in a novel porcine model of severe Staphylococcus aureus sepsis fulfills human clinical criteria.

Sepsis is a common and often fatal complication in human patients in intensive care units. Relevant and well characterized animal models of sepsis may provide valuable information on pathophysiological mechanisms and be a mean of testing new therapeutic strategies. Large animal models of Staphylococcus aureus sepsis are rare, even though S. aureus increasingly affects human patients. Sepsis changes the haemostatic balance and leads to endothelial cell (EC) activation, coagulopathy and, in severe cases, disseminated intravascular coagulation (DIC). The aim of this study was to characterize the haemostatic and vascular alterations in a novel porcine model of severe S. aureus sepsis, investigating whether the changes fulfill the human clinical criteria for DIC. Five pigs were inoculated intravenously with S. aureus and two control animals were sham-inoculated. Blood samples were collected for thromboelastography (TEG) and assessment of plasma-based haemostatic parameters. Tissue was collected for histopathology and reverse transcriptase quantitative real-time polymerase chain reaction for measurement of mRNA encoding EC markers. All infected animals developed DIC; including procoagulant activation represented by hypercoagulable TEG profiles and prolonged clotting time. Histologically, numerous pulmonary thrombi were present in one pig. Inhibitor consumption was represented by decreasing antithrombin levels in infected pigs. Hyaline globules were found in three infected pigs, confirming fibrinolytic activation. EC activation was identified by expression of von Willebrand factor in small vessels together with elevated mRNA encoding activated EC markers. Severe haemostatic and vascular changes fulfilling the human criteria for DIC were therefore seen in all infected pigs. A tendency towards uncompensated DIC was seen in two animals.

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.

Pathology and biofilm formation in a porcine model of staphylococcal osteomyelitis.

A porcine model was used to examine the potential of human and porcine Staphylococcus aureus isolates to induce haematogenously spread osteomyelitis. Pigs were inoculated in the right femoral artery with one of the following S. aureus strains: S54F9 (from a porcine lung abscess; n = 3 animals), NCTC-8325-4 (a laboratory strain of human origin; n = 3 animals) and UAMS-1 (a human osteomyelitis isolate; n = 3 animals). Two pigs were sham inoculated with saline. At 11 or 15 days post infection the animals were scanned by computed tomography before being killed and subjected to necropsy examination. Osteomyelitis lesions were present in the right hind limb of all pigs inoculated with strain S54F9 and in one pig inoculated with strain NCTC-8325-4. Microscopically, there was extensive loss of bone tissue with surrounding granulation tissue. Sequestrated bone trabeculae were intermingled with colonies of S. aureus as demonstrated immunohistochemically. By peptide nucleic acid fluorescence in situ hybridization bacterial aggregates were demonstrated to be embedded in an opaque matrix, indicating that the bacteria had formed a biofilm. Development of experimental osteomyelitis was therefore dependent on the strain of bacteria inoculated and on the formation of a biofilm.

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.

Expression of matrix metalloproteinase-9 and -12 in porcine lung infections.

Matrix metalloproteinases (MMPs) play a variety of roles during organogenesis, in the immune response and during acute and chronic diseases as well as in tissue remodelling. During the last decade, the pig has become used increasingly as a model for human diseases; however, studies on the expression of porcine MMPs are limited. In the present study species-specific antibodies were produced to investigate the expression of MMP-9 and MMP-12 immunohistochemically in lungs from pigs infected with Actinobacillus pleuropneumoniae, Pasteurella multocida and Staphylococcus aureus. The immunolabelling of lung tissues (one infected and one control pig representing each infection) was evaluated for cellular distribution and intensity, which was scored semiquantitatively. When compared with healthy, non-infected controls, the expression of both MMP-9 and MMP-12 was higher in infected lungs. The highest expressions were seen in the alveolar epithelium (MMP-9) and alveolar macrophages (MMP-12). These results are in accordance with studies of human lungs.

Host response to porcine strains of Escherichia coli in a novel pyelonephritis model.

The initial pathology and pathogenesis of pyelonephritis and the influence of different strains of Escherichia coli were investigated in a novel porcine model. Nine female pigs were divided into three groups (A, B and C) and inoculated repeatedly into one renal pelvis with porcine pyelonephritis E. coli strain LK67 (P fimbriae PapG(I)), LK76 (type 1 fimbriae) or LK82 (type 1 fimbriae and P fimbriae PapG(II/III)), respectively. The contralateral kidneys were inoculated with saline and served as controls. Pigs were killed 6h post-inoculation (hpi). Differential leucocyte counts, serum biochemical analyses and measurement of serum concentrations of proinflammatory cytokines and acute phase proteins were carried out at 0, 3 and 6 hpi. Bacteriological evaluation of urine, kidneys, spleen, liver, abdominal swabs and blood samples and gross and histopathological evaluation of kidneys, renal lymph nodes, liver and spleen were performed by quantitative, semiquantitative and/or descriptive methods. Immunohistochemistry was used to identify cells expressing L1 antigen, CD3ɛ, CD4, CD8, CD79αcy and lysozyme, and to identify E. coli and Tamm-Horsfall protein (THP). E. coli was re-isolated from all inoculated kidneys. Gross and microscopical lesions of acute pyelonephritis were demonstrated in all but one kidney inoculated with E. coli, but in none of the control kidneys. Renal parenchymal infiltration with both neutrophils and mononuclear cells, primarily CD3+ T lymphocytes, was observed at 6 hpi. Most T lymphocytes were CD8+. Pigs in group C had the highest mean pathology scores. Neutrophils were the dominant renal leucocyte in this group, while the number of mononuclear cells was at least equal to the number of neutrophils in the lesions of pigs from groups A and B. Kidneys with a high number of E. coli had severe lesions. Systemic spread of E. coli was observed in five pigs. THP was observed interstitially in 89% of the E. coli-inoculated kidneys. In all groups, increased numbers of neutrophils and decreased numbers of lymphocytes and monocytes were shown by differential leucocyte count at 6 hpi, and from 3 to 6 hpi there was a significant increase in C-reactive protein concentration.

Endocarditis-associated brain lesions in slaughter pigs.

Left-sided valvular endocarditis (LSVE) is a common finding in slaughter pigs. The lesion is often associated with renal thromboembolism, but information on embolization to other organs is sparse. This study focuses on the presence and type of endocarditis-associated brain lesions (EABLs). The brains of 20 slaughter pigs with spontaneously arising LSVE and 11 controls were examined by sectioning half of a formalin-fixed brain into 4mm slices for histological examination. The aetiology of the endocarditis was determined by bacteriological and, in some cases, by fluorescence in-situ hybridization examinations. These examinations identified 11 cases of Streptococcus suis, six cases of Erysipelothrix rhusiopathiae, one Streptococcus spp. and two cases that remained aetiologically undetermined. One of the S. suis cases had a dual infection with S. suis in the aortic valve lesions and Streptococcus dysgalactiae subsp. equisimilis in the atrioventricular valve lesions. Renal infarcts were present in eight cases. Focal encephalitis was found in 12 cases, with the number of lesions ranging from one to 11. Most pigs had less than four microscopical lesions. Acute lesions were characterized by focal microabscesses without observable bacteria. Chronic lesions were characterized by astrocytosis and focal accumulation of mononuclear leucocytes. An infarct was observed in one animal. Perivascular inflammation was seen in 14 cases, mostly as two or three lesions, while focal leptomeningitis was found in eight cases. EABLs are therefore common in slaughter pigs with LSVE. The number of lesions per animal is small, which may explain the limited attention paid to this sequela of LSVE. EABLs have rarely been reported in domestic animals and mostly in patients with neurological signs. The frequent occurrence of EABLs in slaughter pigs suggests that this pathology should be investigated in other animal species with LSVE.

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.

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.

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.

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.