Intracytoplasmic Crystalline Inclusions in the Hepatocytes of an Antelope

This case report describes intracytoplasmic crystalline inclusions in the hepatocytes of a 13-year-old female Thomson's gazelle. Histologically, multifocal to coalescing areas of many hepatocytes contained large cytoplasmic vacuoles filled with pale eosinophilic homogeneous material and rare fine basophilic granules. Von Kossa staining showed the presence of calcium within cytoplasm, mainly in the inclusions, of hepatocytes. Transmission electron microscopy, scanning electron microscopy, energy dispersive X-rays analyses, and infrared spectroscopy on the liver showed the hepatocellular material consistent with protein and carbohydrate with secondary accumulation of calcium and phosphorus. It was concluded that crystalline inclusions may have been derived due to failure of normal physiological hepatocellular clearance associated with a severe chronic disease. To the authors' knowledge this is the first reported case of hepatocellular crystalline inclusions in an antelope

Interleukin-12p40 Modulates Human Metapneumovirus-Induced Pulmonary Disease in an Acute Mouse Model of Infection

The mechanisms that regulate the host immune response induced by human metapneumovirus (hMPV), a newly-recognized member of the Paramyxoviridae family, are largely unknown. Cytokines play an important role in modulating inflammatory responses during viral infections. IL-12p40, a known important mediator in limiting lung inflammation, is induced by hMPV and its production is sustained after the resolution phase of infection suggesting that this cytokine plays a role in the immune response against hMPV. In this work, we demonstrated that in mice deficient in IL-12p40, hMPV infection induced an exacerbated pulmonary inflammatory response and mucus production, altered cytokine response, and decreased lung function. However, hMPV infection in these mice does not have an effect on viral replication. These results identify an important regulatory role of IL-12p40 in hMPV infection

Image Challenge in Veterinary Pathology.

Klossiella muris is a sporadic apicomplexan protozoan pathogen of mice. In this case, the mouse was a pet. Contemporary infections in laboratory mice are rare. Sporocysts are shed in the urine and thus transmitted to naive animals by ingestion. Ensuing hematogenous spread facilitates localization to the glomerular capillaries where schizogony occurs. The renal tubular epithelial cells are the site of gametogony and sporogony. Infiltrates of lymphocytes and plasma cells can sometimes accompany infection, which is usually asymptomatic. Renal klossiellosis may also be seen in horses (Klossiella equi), guinea pigs (Klossiella cobayae), and other specie

Bilateral seminoma with hepatic metastasis in a cockatiel (Nymphicus hollandicus)

Abstract: An 18-year-old, intact male cockatiel (Nymphicus hollandicus) presented with a clinical history of dyspnea, lethargy, and reluctance to perch. Coelomic ultrasonographic examination revealed hypoechoic nodules in the proximity of, and within, the liver. The bird did not respond to supportive care and was euthanatized. At necropsy, the testes were bilaterally enlarged, whitish-tan, firm, and multilobulated. The right hepatic lobe contained a mass that had a similar color and consistency to those in the testes. On histologic and ultrastructural examinations, the diagnosis was bilateral testicular seminoma with hepatic metastasis. To our knowledge, this is the first case of a metastatic bilateral testicular seminoma reported in a cockatiel

Opportunistic Fungal Infections in Small Animals

Opportunistic fungal infections have long been recognized as rare causes of disease in immunocompetent dogs and cats. Recently, the escalating use of multiagent immunosuppression protocols (especially those that include cyclosporine) has resulted in an increased number of patients with opportunistic fungal infection encountered by small animal practitioners and has altered the typical case phenotype. Based on histologic and cytologic features such as pigmentation, hyphal diameter, and distribution in tissue, these opportunistic mycoses can be placed into categories such as phaeohyphomycosis, hyalohyphomycosis, and eumycotic mycetoma. This review aims to summarize the clinical presentations, methods for diagnosis, treatment recommendations, and prognosis for both immunocompetent and immunosuppressed patients with opportunistic fungal infections. An example case description is included to illustrate the most common current clinical presentation

Both TRIF- and MyD88-dependent signaling contribute to host defense against pulmonary Klebsiella infection

Klebsiella pneumoniae causes extensive lung damage. TLR signaling involves adaptors TRIF and MyD88. However, the relative contribution of TRIF and MyD88 signaling in host defense against pulmonary K. pneumoniae infection has not been elucidated. Therefore, we investigated the role of TRIF and MyD88 in K. pneumoniae pneumonia. TRIF(-/-) mice infected with K. pneumoniae showed impaired survival and reduced bacterial clearance, neutrophil influx, histopathologic evidence of inflammation, and TNF-alpha, IL-6, KC, MIP-2, but not LIX, expression in the lungs. In addition, K. pneumoniae-induced late NF-kappaB activation and phosphorylation of MAPKs was attenuated in the lungs of TRIF(-/-) mice. However, MyD88(-/-) mice infected with K. pneumoniae showed a much more remarkable phenotype, including impaired survival and reduced bacterial clearance, histopathology, and TNF-alpha, IL-6, KC, MIP-2, and LIX expression with almost no neutrophil influx in the lungs. In MyD88(-/-) mice, K. pneumoniae-induced early NF-kappaB and MAPK activation in the lungs was also reduced. Furthermore, the role of MyD88 is dominant over TRIF because TRIF/MyD88 double knockout mice displayed a more pronounced phenotype than TRIF(-/-) mice. Moreover, human alveolar macrophages pretreated with MyD88 blocking peptide showed attenuated TNF-alpha, IL-6, and IL-8 expression. Also, C57BL/6 mice pretreated with MyD88 blocking peptide exhibited attenuation in K. pneumoniae-induced neutrophil influx and enhanced bacterial burden in the lungs and dissemination. Overall, this investigation provides new insights into the TRIF and MyD88 signaling triggered by pulmonary K. pneumoniae infection in the lungs and demonstrate the therapeutic potential of MyD88 in reducing excessive neutrophil influx in human disease during Gram-negative bacterial pneumonia

NLRC4 inflammasome-mediated production of IL-1β modulates mucosal immunity in the lung against gram-negative bacterial infection

Bacterial flagellin is critical to mediate NLRC4 inflammasome-dependent caspase-1 activation. However, Shigella flexneri, a nonflagellated bacterium, and a flagellin (fliC) knockout strain of Pseudomonas aeruginosa are known to activate NLRC4 in bone marrow-derived macrophages. Furthermore, the flagellin-deficient fliC strain of P. aeruginosa was used in a mouse model of peritonitis to show the requirement of NLRC4. In a model of pulmonary P. aeruginosa infection, flagellin was shown to be essential for the induction of NLRC4-dependent caspase-1 activation. Moreover, in all P. aeruginosa studies, IL-1β production was attenuated in NLRC4(-/-) mice; however, the role of IL-1β in NLRC4-mediated innate immunity in the lungs against a nonflagellated bacterium was not explored. In this article, we report that NLRC4 is important for host survival and bacterial clearance, as well as neutrophil-mediated inflammation in the lungs following Klebsiella pneumoniae infection. NLRC4 is essential for K. pneumoniae-induced production of IL-1β, IL-17A, and neutrophil chemoattractants (keratinocyte cell-derived chemokines, MIP-2, and LPS-induced CXC chemokines) in the lungs. NLRC4 signaling in hematopoietic cells contributes to K. pneumoniae-induced lung inflammation. Furthermore, exogenous IL-1β, but not IL-18 or IL-17A, partially rescued survival, neutrophil accumulation, and cytokine/chemokine expression in the lungs of NLRC4(-/-) mice following infectious challenge. Furthermore, IL-1R1(-/-) mice displayed a decrease in neutrophilic inflammation in the lungs postinfection. Taken together, these findings provide novel insights into the role of NLRC4 in host defense against K. pneumoniae infection

EFFECTS OF DOXYCYCLINE HYCLATE, ONE PERCENT POLIDOCANOL, AND ABSOLUTE ETHANOL ON THE CUTANEOUS AND SUBCUTANEOUS TISSUES OF CHICKENS () AND THE POTENTIAL IMPLICATIONS IN TREATING CERVICOCEPHALIC DIVERTICULA RUPTURE

The objective of this pilot study was to examine the histologic effects associated with three known sclerosing agents and their ability to induce fibrosis in the subcutaneous space between the cervicocephalic air sac and skin. In the future, these drugs may prove useful in treating birds experiencing cervicocephalic diverticula rupture. The agents used were 1% polidocanol, absolute ethanol, and doxycycline hyclate. Twelve healthy adult chickens () were used in this study. The chickens were randomly allocated into three groups denoting day of euthanasia (day 4, 7, or 14). On day 0, all agents were injected (0.2 ml) subcutaneously, in a four-point grid fashion, in both the cervical and pectoral region of each bird. After euthanasia, the skin and subcutaneous tissues corresponding to the injection sites were harvested for histologic assessment. Tissue sections were assessed for fibrosis and lymphocytic and histiocytic inflammation. A scoring system was established to rank sclerosing agents by fibrosing and inflammatory ability. In the cervical region of chickens, 1% polidocanol induced the greatest inflammatory changes by day 7. Data suggest that doxycycline hyclate may produce the greatest cutaneous and subcutaneous fibrosis overall among all groups of birds. No adverse reactions were associated with any injection. Sterile saline produced the least amount of inflammation when assessed with the scoring system. Further investigation is needed to determine the safety of injections of larger volume with these chemicals and whether these findings can be extrapolated to birds with disease