Typhlohepatitis and Amyloidosis Associated with High Mortality in Chukar Partridges (Alectoris chukar).

Twelve chukar partridges (Alectoris chukar) from a farm experiencing poor uniformity and increased mortality of up to 65% were submitted for diagnosis. Several birds had mild to moderate multifocal white foci or multifocal petechial hemorrhages throughout the liver. Livers and spleens of older birds were moderate to severely diffusely enlarged. In addition, some birds had caseous cores mixed with blood within the ceca as well as segmentally thickened cecal walls. Histopathology showed acute, multifocal, severe, often coalescing foci of necrosis with accumulation of fibrin and/or fibrinosuppurative inflammation in livers and spleens. Scattered within exudate were protozoa that were spherical or round and measured 12-20 µm in diameter. In the ceca, acute necrosis of the mucosa was observed, often with ulceration and fibrinosuppurative inflammation. Immunohistochemistry using an antiserum against Tritrichomonas foetus revealed round protozoa in ceca, small intestines, liver, spleen, and lung. Quantitative PCR to detect DNA of Histomonas meleagridis was negative. Non-species-specific PCRs amplifying the partial rDNA, the internal transcribed spacer (ITS) region, and the partial beta-tubulin gene yielded products of the expected size. Sequences of the PCR products had the highest homology to sequences of Tetratrichomonas gallinarum and less homology to sequences of H. meleagridis. In addition there was accumulation of amyloid in the space of Disse in the liver, splenic sinuses, and walls of the blood vessels. The typhlohepatitis and other inflammatory processes that were diagnosed might be the underlying cause of the amyloidosis. Other findings were clusters of Clostridium perfringens associated with the lesions in the ceca; multifocal granulomas in the lungs, occasionally associated with fungal hyphae; hyperkeratosis associated with bacteria and Candida sp. cells in the crop; mild infection of the bursal mucosa with Cryptosporidium.

Tiflohepatitis y amiloidosis asociadas con alta mortalidad en perdices chukar (Alectoris chukar). Doce perdices chukar (Alectoris chukar) de una granja con baja uniformidad y alta mortalidad de hasta el 65% se presentaron para diagnóstico. Varias aves presentaron áreas blancas multifocales de leves a moderadas o hemorragias petequiales multifocales en todo el hígado. Los hígados y los bazos de las aves con mayor edad estuvieron agrandados de tamaño de manera difusa y de moderado a severo. Además, algunas aves tenían contenidos caseosos mezclados con sangre dentro de los ciegos, así como paredes cecales engrosadas de manera segmentaria. La histopatología mostró focos de necrosis agudos, multifocales, graves, a menudo coalescentes con acumulación de fibrina y/o inflamación fibrinosupurativa en hígados y bazos. Dispersos dentro del exudado se encontraban protozoarios que eran esféricos o redondos y que medían de 12 a 20 µm de diámetro. En el ciego, se observó necrosis aguda de la mucosa, a menudo con ulceración e inflamación fibrinosupurativa. La inmunohistoquímica con un antisuero contra Tritrichomonas foetus reveló protozoarios redondos en el ciego, intestino delgado, hígado, bazo y pulmón. El método de PCR cuantitativo para detectar el ADN de Histomonas meleagridis fue negativo. Los métodos de PCR no específicos de especie que amplifican parcialmente al rDNA de la región espaciadora transcrita interna (ITS) y el gene parcial de la beta-tubulina dieron productos del tamaño esperado. Las secuencias de los productos de PCR tuvieron la mayor similitud con las secuencias de Tetratrichomonas gallinarum y menos similitud con las secuencias de H. meleagridis. Además, se observó acumulación de amiloide en el espacio de Disse en el hígado, en senos esplénicos y paredes de los vasos sanguíneos. La tiflohepatitis y otros procesos inflamatorios que se diagnosticaron pueden ser la causa subyacente de la amiloidosis. Otros hallazgos incluyeron grupos de Clostridium perfringens asociados con las lesiones en el ciego; granulomas multifocales en los pulmones, ocasionalmente asociados con hifas fúngicas; hiperqueratosis asociada a bacterias y Candida spp. en el buche, e infección leve de la mucosa bursal con Cryptosporidium.

Post mortem findings and their relation to AA amyloidosis in free-ranging Herring gulls (Larus argentatus).

Since the late 1990s, high mortality and declining populations have been reported among sea birds including Herring gulls (Larus argentatus) from the Baltic Sea area in Northern Europe. Repeated BoNT type C/D botulism outbreaks have occurred, but it remains unclear whether this is the sole and primary cause of mortality. Thiamine deficiency has also been suggested as a causal or contributing factor. With this study, we aimed to investigate gross and microscopic pathology in Herring gulls from affected breeding sites in Sweden in search of contributing diseases. Herring gulls from Iceland served as controls. Necropsies and histopathology were performed on 75 birds, of which 12 showed signs of disease at the time of necropsy. Parasites of various classes and tissues were commonly observed independent of host age, e.g. oesophageal capillariosis and nematode infection in the proventriculus and gizzard with severe inflammation, air sac larid pentastomes and bursal trematodiasis in pre-fledglings. Gross and microscopic findings are described. Notably, amyloidosis was diagnosed in 93 and 33% of the adult birds from Sweden and Iceland, respectively (p<0.001), with more pronounced deposits in Swedish birds (p<0.001). Gastrointestinal deposits were observed in the walls of arteries or arterioles, and occasionally in villi near the mucosal surface. Amyloid was identified within the intestinal lumen in one severely affected gull suggesting the possibility of oral seeding and the existence of a primed state as previously described in some mammals and chickens. This could speculatively explain the high occurrence and previously reported rapid onset of amyloidosis upon inflammation or captivity in Herring gulls. Amyloid-induced malabsorbtion is also a possibility. The Herring gull SAA/AA protein sequence was shown to be highly conserved but differed at the N-terminus from other avian species.

Myopathy in a patient with systemic AA amyloidosis possibly induced by psoriasis vulgaris: An autopsy case.

INTRODUCTION: Amyloid myopathy is a rare manifestation of primary systemic amyloid light-chain (AL) amyloidosis, but it has not been reported to occur in secondary amyloid A (AA) amyloidosis. METHODS: We describe a 46-year-old man with psoriasis vulgaris who presented with idiopathic upper and lower limb weakness and was eventually diagnosed with hypertrophic cardiomyopathy. Muscle biopsy findings were compatible with mild inflammatory myopathy. He died of cardiopulmonary arrest, and an autopsy was performed. RESULTS: The autopsy revealed amyloid plaques immunopositive for AA (but not AL or transthyretin) in the perimysial, perivascular, and endomysial regions of the iliopsoas muscle. The final diagnosis was systemic AA amyloidosis with muscle amyloid angiopathy, possibly induced by psoriasis vulgaris. CONCLUSION: This is an extremely rare autopsy case of myopathy in a patient with systemic AA amyloidosis. The reason for the unusually large amount of amyloid deposition in muscle blood vessel walls remains unclear.

Leishmania (Leishmania) amazonensis: experimental cutaneous leishmaniasis associated with systemic amyloidosis in mice.

We infected Swiss and C57BL/6 female mice in the left hind footpad with 10(4)Leishmania (L.) amazonensis promastigotes in stationary phase. The macroscopic examination showed a nodular non-ulcerated lesion at the site of inoculation and hepatic and spleenic enlargement. Histopathologically, the primary lesion showed an extensive liquefactive necrosis and inflammatory infiltrate, mainly consisting of macrophages filled with amastigotes, and rare lymphocytes. The inflammatory reaction in liver, spleen and kidney showed amyloid deposits. Additionally, C57BL/6 had accentuated amyloidosis in both ovarian cortical and medullar region and inflammatory infiltrates in the pancreas and adrenal gland.

Schistosoma-induced amyloidosis in hamsters is gender-dependent.

BACKGROUND: A high serum level of female protein (FP), found to be a constituent of Syrian hamster amyloid was associated with enhanced amyloidosis. In this work, we studied the sex-limited factors in the induction of amyloidosis in Syrian hamsters infected with either Schistosoma mansoni or S. hematobium cercariae. METHODS: Hamsters were infected with different species of schistosome cercariae and sacrificed after different time periods of infection. Kidney and liver specimens were processed in paraffin, stained with Congo-red and examined by ordinary light and polarized light microscopy. RESULTS: Statistical analysis showed a significant difference in intensity of kidney and liver amyloid deposits (P<0.002 & <0.007 respectively) between females and male hamsters with extensive deposits in the former. Amyloid deposits were correlated significantly to the duration of infection (P<0.001) than the load of worm recovered. CONCLUSION: From this study, we conclude that, in hamster model, Schistosoma-induced amyloidosis is enhanced in females than male hamsters. This may be due to the high serum level of FP that is normally detected in females. As an experimental model for schistosomal nephropathy, we recommend to use male hamsters instead of females to minimize the effect of amyloid deposits, which may mask other pathological changes associated with schistosomal infection.

[Amyloidosis in infected Didelphis marsupialis]. / Amiloidosis en Didelphis marsupialis infectado experimentalmente con Leishmania chagasi.

A male opossum, Didelphis marsupialis, captured in Teruel (Huila), Colombia, was inoculated intraperitoneally with 1 x 10(6) promastigotes of Leishmania chagasi (MHOM/CO/84/CL044B). The animal died 5 weeks after inoculation. Autopsy revealed signs of visceral leishmaniasis along with amastigote parasite form in Kupffer cells and spleen macrophages. Amyloid deposits in liver and spleen were demonstrated by histological staining and electron microscopy. The rapid death was considered a consequence of a secondary, reactive amyloidosis.

Hepatic lesions caused by excretory and secretory products of Ascaris lumbricoides in golden hamster.

OBJECTIVE: To ascertain the role of excretory and secretory (ES) products of Ascaris lumbricoides in liver damage. METHODS: The ES products of A lumbricoides were collected in vitro and their SDS-PAGE analysis was done. Feeding and subcutaneous injection of ES products were done in hamsters. Estimation of serum proteins, alkaline phosphatase and alanine aminotransferase and histology of liver were carried out. Control animal experiments were done concurrently. RESULTS: The ES products of A lumbricoides contained several proteins ranging in molecular weight from 14 to 205 Kd. Prolonged feeding of ES products caused elevation of ALT and amyloid deposition in the liver, whereas short term feeding or subcutaneous challenge caused focal cell necrosis and granuloma formation in the liver. CONCLUSION: ES products of A lumbricoides can produce liver damage.

Amyloidosis in experimental tegumentary leishmaniasis in mice.

Renal and hepatosplenic amyloidosis was found in chronic cutaneous leishmaniasis in mice infected with 10(6) purified amastigotes from lesions produced by the H21 strain of Leishmania mexicana amazonensis. After 1 year a progressive lesion leading to metastasis was observed in most animals.