Pathological Changes of the Rumen in Small Ruminants Associated with Indigestible Foreign Objects

The use of agriculture by-products is highly demanded for livestock nutrition. However, the employment of certain non-degradable materials could potentially induce concretions and lesions in ruminants’ forestomach. Thus, the aim of this study was to determine the morphological lesions showed in rumen containing indigestible foreign objects, named foreign bodies, in small ruminants. Twenty-two animals (12 goats and 10 ewes) presenting foreign bodies (2.750 ± 1.577 kg) were included in this study. Rumenotomies were performed to remove the foreign bodies, and rumen samples were taken for further morphological evaluations. Rumen samples from healthy small ruminants (n = 24) were also taken at slaughterhouses as controls. Morphologically, the rumen from affected animals showed a significant reduction of the ruminal papillae length (1.243 vs. 3.097), hyperplasia of the squamous epithelium, mononuclear infiltration in the subepithelial spaces and, less consistently, vacuolization of keratinocytes, presence of intraepithelial leukocytes and vascular changes of the lamina propria. It can be concluded that indigestible foreign bodies would cause ruminal lesions that would be able to trigger inflammatory and/or degenerative lesions. Our study demonstrates morphological lesions because of the presence of intraruminal foreign bodies, but further studies on the functional activity of the rumen in these cases are required. The avoidance of the presence of indigestible materials in agriculture exploitations is highly recommended in order to prevent the accumulation of indigestible foreign objects in small ruminants.

Histopathological findings in Dalmatian pelicans (Pelecanus crispus) naturally infected with avian influenza subtype A H5N1 in Bulgaria

The aim of this study is to estimate the histopathological changes in visceral organs of naturally infected with the avian influenza virus (AIV) subtype A H5N1 dalmatian pelicans in Bulgaria. The identified gross lesions are: haemorrhagic small intestine, sparse content in gizzard and proventriculus, well defined hyperemia of the tracheal mucosa associated with petechiae, as well as meningeal and brain congestion. The infected birds exhibited the following histopathological changes: edema of the tracheal mucosa with loss of mucosal glands, mild to moderate congestion with focal necrosis and multifocal non suppurative encephalitis and gliosis, mononuclear infiltration in the cecum, and diffuse mononuclear infiltration in the submucosa of the small intestine. The virus was detected by virus isolation (VI) and RT-PCR from tissue samples (lung, trachea, small intestine, brain, proventriculus, cloaca) from the infected birds.

Importin-α7 Is Required for Enhanced Influenza A Virus Replication in the Alveolar Epithelium and Severe Lung Damage in Mice

ABSTRACTInfluenza A viruses recruit components of the nuclear import pathway to enter the host cell nucleus and promote viral replication. Here, we analyzed the role of the nuclear import factor importin-α7 in H1N1 influenza virus pulmonary tropism by using variousex vivoimaging techniques (magnetic resonance imaging, confocal laser scanning microscopy, and correlative light-electron microscopy). We infected importin-α7 gene-deficient (α7−/−) mice with a recombinant H1N1 influenza virus and compared thein vivoviral kinetics with those in wild-type (WT) mice. In WT mice, influenza virus replication in the bronchial and alveolar epithelium already occurred a few days after infection. Accordingly, extensive mononuclear infiltration and alveolar destruction were present in the lungs of infected WT mice, followed by 100% lethality. Conversely, in α7−/−mice, virus replication was restricted mostly to the bronchial epithelium with marginal alveolar infection, resulting in significantly reduced lung damage and enhanced animal survival. To investigate the host immune response during alveolar virus replication, we studied the role of primary macrophages in virus propagation and clearance. The ability of macrophages to support or clear the virus infection, as well as the host cellular immune responses, did not significantly differ between WT and α7−/−mice. However, cytokine and chemokine responses were generally elevated in WT mice, likely reflective of increased viral replication in the lung. In summary, these data show that a cellular factor, importin-α7, is required for enhanced virus replication in the alveolar epithelium, resulting in elevated cytokine and chemokine levels, extensive mononuclear infiltration, and thus, severe pneumonia and enhanced virulence in mice.IMPORTANCEInfluenza A viruses are respiratory pathogens that may cause pneumonia in humans. Viral infection and replication in the alveoli of the respiratory tract are believed to be crucial for the development of the acute respiratory distress syndrome associated with fatal outcomes in influenza virus-infected patients. Here, we report the requirement of a cellular factor, importin-α7, for efficient virus replication in the alveolar epithelium of mice. Using complementaryex vivoimaging approaches, we show that influenza virus replication is restricted to the bronchial epithelium, followed by enhanced survival in importin-α7-deficient mice. In contrast, the presence of this gene results in enhanced virus replication in the alveoli, elevated cytokine and chemokine responses, mononuclear infiltration, alveolar destruction, and 100% lethality in wild-type mice. Taken together, our results show that importin-α7 is particularly required for virus replication in the alveolar epithelium in association with severe pneumonia and death in mice.

A Histochemical Study of Changes Observed in the Mouse Diaphragm after Organophosphate Poisoning

A sublethal dose of sarin (GB, isopropyl methylphosphonofluoridate) was administered to mice. The animals were killed up to 28 d after dosing and frozen sections were made of the excised diaghragms which were stained using haematoxylin and eosin and a modified Gomori trichrome method. Muscle fibre degeneration and mononuclear infiltration were seen, notably at 24 h and 3 d. A number of histochemical procedures were carried out, including the GBHA procedure for ionized calcium. Calcium accumulation, seen at 4 h, was the earliest abnormality observed. All changes were rapidly regressing by 5 d and histological appearances were normal by 14 d. It was concluded that sarin produced myopathic changes preceded by calcium accumulation.