Left Ventricular Apical Aneurysm in a Cat With Primary Cardiomyopathy.

A 13-year-old female Persian cat died suddenly after severe respiratory distress. At necropsy, the changes were compatible with congestive heart failure. The heart was enlarged with a flabby and puckered sac-like aneurysm at the apex of the left ventricle. The apical zone showed a thin muscular wall arising from the free wall of the left ventricle connected to a bulged saccular area through a wide communication. Microscopically, the wall of the aneurysm was composed of fibrous connective tissue with neovascularization and sparse atrophied myocardial cells at the margins. A few isolated cardiomyocytes in the lesion stained positively for desmin, and the inner lining of the aneurysm had immunoreactivity to von Willebrand factor and CD31. Mature fibrous connective tissue was interspersed with degenerated and disorganized cardiomyocytes elsewhere in the myocardium, and many small myocardial arteries were tortuous and thickened. In this case of sudden death, the diagnosis was primary cardiomyopathy, with formation of a left ventricular apical aneurysm within an area of marked myocardial fibrosis and cardiomyocyte atrophy.

Disseminated paracoccidioidomycosis in a Southern two-toed sloth (Choloepus didactylus).

A Southern two-toed sloth (Choloepus didactylus), originally acquired from French Guiana, died while maintained in quarantine in a pet store in Monterrey, Mexico. Large yeast cells with multiple buds compatible with Paracoccidioides brasiliensis were observed in disseminated granulomatous lesions in the lungs, liver, spleen and kidney. Transmission electron microscopical examination supported the diagnosis. This is the first report of paracoccidioidomycosis in a two-toed sloth.

Chlorella infection in a sheep in Mexico and minireview of published reports from humans and domestic animals.

Algal infections are rare in humans and domestic animals. Prototheca spp. and Chlorella spp. are among the most commonly reported. Herein, we present a brief review on Chlorella spp. infections and related pathologies and discuss this information including a natural case in a sheep in Mexico with a disseminated form of the disease.

First report of Oxyspirura sp. from a captive fulvous owl (Strix fulvescens) in Mexico.

Nematodes similar to Oxyspirura sp. were recovered from the cornea and nictitating membrane of a fulvous owl (Strix fulvescens). The bird had been captive for several months, but died suddenly. It had no clinical history of prior diseases, including ocular lesions.

Does Cry1Ab protein affect learning performances of the honey bee Apis mellifera L. (Hymenoptera, Apidae)?

Genetically modified Bt crops are increasingly used worldwide but side effects and especially sublethal effects on beneficial insects remain poorly studied. Honey bees are beneficial insects for natural and cultivated ecosystems through pollination. The goal of the present study was to assess potential effects of two concentrations of Cry1Ab protein (3 and 5000 ppb) on young adult honey bees. Following a complementary bioassay, our experiments evaluated effects of the Cry1Ab on three major life traits of young adult honey bees: (a) survival of honey bees during sub-chronic exposure to Cry1Ab, (b) feeding behaviour, and (c) learning performance at the time that honey bees become foragers. The latter effect was tested using the proboscis extension reflex (PER) procedure. The same effects were also tested using a chemical pesticide, imidacloprid, as positive reference. The tested concentrations of Cry1Ab protein did not cause lethal effects on honey bees. However, honey bee feeding behaviour was affected when exposed to the highest concentration of Cry1Ab protein, with honey bees taking longer to imbibe the contaminated syrup. Moreover, honey bees exposed to 5000 ppb of Cry1Ab had disturbed learning performances. Honey bees continued to respond to a conditioned odour even in the absence of a food reward. Our results show that transgenic crops expressing Cry1Ab protein at 5000 ppb may affect food consumption or learning processes and thereby may impact honey bee foraging efficiency. The implications of these results are discussed in terms of risks of transgenic Bt crops for honey bees.

Long-term effects of meloxicam in the treatment of respiratory disease in fattening cattle.

The long-term effects of a single dose of meloxicam (Metacam 20 mg/ml; Boehringer Ingelheim Vetmedica) in conjunction with antibiotic therapy in cattle with clinical signs of bovine respiratory disease (BRD) was evaluated in a blind, controlled, randomised study. Two hundred animals with clinical signs of brd received a single subcutaneous injection of 20 mg/kg oxytetracycline; 100 of them also received a subcutaneous injection of 0.5 mg/kg meloxicam, and the other 100 received an injection of isotonic saline. The animals were weighed before they were treated and seven, 35, 70 and 105 days later, and finally before they were slaughtered. The mean bodyweight of the meloxicam-treated animals was significantly higher from day 70 until slaughter, and the mean average daily weight gain until slaughter and the mean carcase weight of the animals treated with meloxicam were significantly higher. In the animals with lung lesions, significantly less lung tissue was affected in those that had been treated with meloxicam.

Mast cell density during initiation and progression of the local Shwartzman reaction.

OBJECTIVE AND DESIGN: To quantify the number of mast cells in the skin of rabbits during initiation and progression of the local Shwartzman reaction. MATERIALS: Thirty New Zealand rabbits were divided in two groups (n = 15/group). One group was subjected to the Shwartzman reaction and the other group served as control. Subsequently, animals were further subdivided in six groups of five animals each according to time of euthanasia. TREATMENTS: The local Shwartzman reaction was induced by two inoculations of Salmonella typhimurium lipopolysaccharide. Preparatory inoculation was given intradermally and, 24 h later, the provocative injection was administered intravenously. Controls were subjected to the same procedure but received saline. After provocative injection animals were killed at 1, 8, and 15 days. METHODS: Skin samples were fixed in Carnoy's solution and mast cells were identified employing a low pH toluidine blue stain. Numbers of mast cells were determined per square millimetre and, subsequently, those cells degranulated were identified and quantified to obtain absolute values. A Student's t test was initially used to compare Shwartzman versus controls at each time point. Subsequently, an ANOVA test employing a factorial experiment was used to assess a possible interaction between time of euthanasia and treatments. RESULTS: The values were transformed (natural logarithms) for appropriate statistical comparisons. Independent comparisons at each time point showed that Shwartzman groups had higher numbers of mast cells than controls at 1 and 8 days, but not at 15 days (5.71 +/- 1.00 Vs. 2.40 +/- 0.58, P < 0.005; 3.77 +/- 0.90 Vs. 2.33 +/- 0.56, P < 0. 025, and 2.61 +/- 0.25 Vs. 2.39 +/- 0.39, P > 0.05, respectively). Degranulated cells were numerous in Shwartzman groups, particularly at day 1 (3.48 +/- 0.78) and less obvious at day 8 (0.72 +/- 0.50), but were scarce by day 15 (-0.67 +/- 0.99) as well as controls (-0.68 +/- 0.91). The factorial experiment demonstrated that the Shwartzman reaction and time of euthanasia were independently significant (P < 0.005) but their interaction at day 1 was the major contributor (P < 0.005). Tukey's w pairwise comparisons of means confirmed that the Shwartzman group killed at day 1 was significantly different from the others (P < 0.05). CONCLUSIONS: Mast cells significantly increase in the early stages of the local Shwartzman reaction. Thus, mast cells are a highly dynamic cell population, which have a prominent role during the acute phase of this lipopolysaccharide-induced inflammatory reaction but not during healing.

Mast cell density and substance P-like immunoreactivity during the initiation and progression of lung lesions in ovine Mannheimia (Pasteurella) haemolytica pneumonia.

To determine the density of mast cells (MCs) and the extent of substance P (SP) immunoreactivity during initiation and progression of pneumonic pasteurellosis (PP), 18 lambs were inoculated intrabronchially with Mannheimia (Pasteurella) haemolytica or saline, and lung tissue was collected at 1, 15 and 45 days post-inoculation (n=3, each group). Additionally, the left (non-inoculated) contralateral lungs in bacteria-inoculated animals were collected as controls. At 1 day after bacterial inoculation the lungs had typical M. haemolytica lesions. These pneumonic lesions had fewer numbers of MCs and reduced histamine content. Macrophages infiltrating some of the inflamed areas were strongly immunoreactive for SP. At 15 days, MCs remained scarce at sites where lung damage persisted, i.e. pyogranulomatous foci, but were increased in number in areas of interstitial damage. Pulmonary ganglion neurons were strongly immunoreactive for SP. By 45 days the fibrosing changes became more defined as pleural fibrosis, fibrosing alveolitis, alveolar epithelial hyperplasia and bronchiolitis obliterans. These lungs had increased numbers of MCs, but histamine content was not different from saline- and non-inoculated left lungs. Substance P immunoreactivity occurred only in nerves and was scarce and mild. This work demonstrates that MC density decreases initially with PP, but increases with progression of PP. SP fibres tend to be decreased during the initiation and at 45 days of PP, but other cells, such as macrophages and neuronal ganglion cells, produce substance P during progression of PP and thereby constitute an additional source of substance P.

Dihydrocapsaicin treatment depletes peptidergic nerve fibers of substance P and alters mast cell density in the respiratory tract of neonatal sheep.

In the present study we administered dihydrocapsaicin (DHC) to neonatal lambs to deplete C-fibers of neuropeptides. We measured the density of substance P (SP)-fibers in nasal septum to assess the effectiveness of the treatment at 3, 9, and 21 days. The numbers of mast cells in the upper and lower respiratory tract were determined at the same time points and histamine content was determined from lung tissue. DHC treatment depleted SP-fibers for up to the 21 day time point. This depletion was estimated as 85% in comparison with controls. In vehicle-treated lambs, the density of SP-fibers decreased progressively with age, but not to the degree of DHC-treated lambs whose SP-fibers were depleted from the initial 3-day measurement. In both, vehicle- and DHC-treated lambs, numbers of mast cells increased progressively with time; however, the density of mast cells was augmented in the entire respiratory tract of DHC-treated animals. Apparently, DHC treatment exerts a single and initial effect in increasing mast cells whereas time maintains a continuous influence; both factors exert their influence independently. Despite large numbers of mast cells in DHC-treated animals, histamine content in the lung had similar levels as controls. Our study provides fundamental data for a better understanding of conditions that may influence defense mechanisms dependent on the mast cell-nerve axis in the respiratory tract.

Reduction of pulmonary mast cells in areas of acute inflammation in calves with Mannheimia (Pasteurella) haemolytica pneumonia.

Mast cells in the left cranial pulmonary lobe of colostrum-deprived neonatal calves were quantified 2 and 6 h after intrabronchial inoculation with Mannheimia (Pasteurella) haemolytica A1. The mast cells were detected (1) immunohistochemically with a mouse anti-human mast cell tryptase monoclonal antibody, and (2) by metachromatic staining with low pH toluidine blue. A greater number of mast cells was demonstrated by the second method than by the first. At 6 h after inoculation, but not at 2 h, the number of mast cells was significantly reduced at the site of the main lesions. Treatment of calves with a sialyl Lewis mimetic (TBC1269) did not appreciably affect the results at 6 h.

The potential role of the Arthus and Shwartzman reactions in the pathogenesis of pneumonic pasteurellosis.

Pneumonic pasteurellosis (PP) is an economically important disease in cattle, sheep, and goats. Pasteurella haemolytica is commonly isolated from the severe fibrinopurulent pneumonia that characterize this respiratory syndrome. During infection, the bacteria produce leukotoxin (LKT) and lipopolysaccharide (LPS), both potent inducers of inflammation. Nonetheless, it has also been demonstrated that an exacerbated host's inflammatory response is responsible for the severe lung damage. Despite research in this field, the pathogenesis of PP is still incomplete. Two classical models of acute inflammatory response induced in laboratory animals, the Arthus and Shwartzman reactions, could explain the pathogenesis of the severe lung lesions that characterize PP.

Is Brucella abortus a facultative intracellular pathogen with mitochondria-like activity?

Brucella abortus is the agent of bovine brucellosis, a zoonotic disease of worldwide importance. In latently infected humans and animals, acute disease may recur under conditions that decrease the host resistance. This bacterium is considered to be a facultative intracellular pathogen. However, its pathogenic attributes appear reduced in comparison with other Gram-negative pathogens. It has been recognized that B. abortus and other Brucella species reach their intracellular location inside the rough endoplasmic reticulum (RER) of placental trophoblasts and other nonphagocytic epithelial cells. This location is the limiting step for their replication and is in contrast to their intraphagosomal survival and growth in macrophages. To reach the RER, Brucella may be handled as another cellular organelle, like mitochondria. Furthermore, because of its inherent morphological and physiological characteristics, this alpha Proteobacteria may display here some mitochondria-like functions. Finally, external signals mediated by the host hormones and/or cytokines may turn this weak endosymbiotic relationship into a pathological one.

Influence of immunization on the pulmonary inflammatory response of rabbits induced by Pasteurella haemolytica A1 lipopolysaccharide.

Immune complex formation has long been thought to play a role in the pathogenesis of Pasteurella haemolytica pneumonia. This study in laboratory rabbits was designed to investigate immune-mediated damage in respiratory tissue caused by lipopolysaccharide (LPS). Severe lesions were induced by the intratracheal (IT) injection of P. haemolytica A1 LPS (50 micrograms) into rabbits previously immunized with P. haemolytica killed whole cells emulsified with Freund's incomplete adjuvant (FIA); these lesions included perivascular oedema and polymorphonuclear leucocyte (PMN) infiltration of the subintima, with degeneration and necrosis of the media. Smaller vessels were occluded by PMNs in various stages of degranulation. PMN counts in bronchoalveolar lavage (BAL) fluid were significantly elevated (P < 0.05). Lesions were also induced by the IT injection of LPS (50 micrograms) into rabbits pretreated with an emulsion consisting merely of FIA and formol-saline; these lesions included moderate to severe congestion, interstitial oedema, alveolar serofibrinous exudation and PMN infiltration. PMNs were also present in BAL fluid. Rabbits pretreated with FIA in formol-saline and given a later IT injection of saline, and rabbits pretreated with bovine serum albumin (BSA) in FIA and given a later IT injection of BSA, were included as negative and positive control groups. Cutaneous lesions were also induced by the intradermal injection of LPS into rabbits immunized against P. haemolytica and of BSA into rabbits immunized with BSA. Overall, the pulmonary and cutaneous lesions induced in vaccinated rabbits by antigen administration were more severe than those seen in non-vaccinated rabbits. The lesions in rabbits, which were similar to those seen in natural cases of P. haemolytica pneumonia in cattle, were characterized by a fibrinopurulent inflammatory process with extensive interstitial oedema, fibrinous exudate, and PMNs. This model may help to elucidate the pathogenesis of pneumonic pasteurellosis in immunized animals.

[Pathogenesis of lung damage caused by Pasteurella haemolytica]. / Patogénesis del daño pulmonar provocado por Pasteurella haemolytica.

Pneumonic pasteurellosis is the major economic problem of the cattle industry in North America. This disease is characterized by an acute, severe, fibrinonecrotic pleuropneumonia. Pasteurella haemolytica A1 is commonly isolated from these pneumonic lesions. It has been demonstrated that stress or viral infection compromises defense mechanisms of the upper respiratory tract and lung, predisposing to an initial multiplication of bacteria in the nasopharynx and, subsequently, lungs are deluged with large numbers of bacteria. Once multiplication in the alveoli has begun, virulence factors exert their influence to induce an excessive host inflammatory response that results in severe tissue damage. Despite a large number of studies conducted to explore the complex interaction between P. haemolytica and the host response, there still remains a lack of detailed understanding. This review discusses evidence of the role of the main virulence factors of P. haemolytica on the pathogenesis of pulmonary damage.