PubMed Health⌕ Search

Biomedical subjects

A J Marco

Publications and source records attributed to A J Marco.

15 recordsLinked to original sources
PubMed2003

Anemia, myopathy, and pansteatitis in vitamin E-deficient captive marmosets (Callithrix spp.).

Five young adult pet marmosets (Callithrix spp.) were presented with weight loss (5/5); fecal retention (3/5); diarrhea (2/5); impaired locomotion (3/5); anemia (4/4); hypoproteinemia or hypoalbuminemia (3/4); elevations of creatine phosphokinase, lactic dehydrogenase, and alanine aminotransferase (3/4); and renal failure with hypercholesterolemia (2/4). All anemic marmosets had low serum vitamin E levels. The anemia responded to vitamin E and selenium therapy in two marmosets. One of the five marmosets died before presentation, and two others died despite therapy. The two marmosets necropsied had degenerative myopathy, pyogranulomatous pansteatitis, and increased erythrophagocytosis and hemosiderosis. The striated muscle and adipose tissue of both marmosets were negative for coxsackievirus ribonucleic acid by in situ hybridization. These findings suggest that vitamin E deficiency may be involved in the development of anemia, myopathy, and steatitis in callitrichids; however, in some marmosets, underlying diseases such as chronic colitis may have influenced the development of anemia and impaired vitamin E status.

Adipose Tissue↗
PubMed2000

Critical role of neutrophils in eliminating Listeria monocytogenes from the central nervous system during experimental murine listeriosis.

Neutrophils are the main inflammatory cell present in lesions involving the central nervous system (CNS) during human and murine listeriosis. In this study, administration of the neutrophil-depleting monoclonal antibody RB6-8C5 during experimental murine listeriosis facilitated the multiplication of Listeria monocytogenes in the CNS. These data suggest that neutrophils play a key role in eliminating bacteria that gain access to the CNS compartment. In addition, we provide evidence that their migration into the CNS may be necessary for the subsequent recruitment of macrophages and activated lymphocytes.

Animals↗
PubMed1999

Expression of E-selectin, P-selectin, and intercellular adhesion molecule-1 during experimental murine listeriosis.

The expression of adhesion molecules E-selectin, P-selectin, and intercellular adhesion molecule-1 (ICAM-1) was immunohistochemically investigated during the course of experimental murine listeriosis. Infection was monitored by microbiological count of blood, liver, and spleen. After an early generalized expression of P-selectin and ICAM-1, a later regulation occurred specifically to areas of inflammation. Expression of E-selectin was faint and inconstantly detected in all of the studied organs. In the liver, typical lesions of murine listeriosis were related to the expression of ICAM-1 on sinusoidal endothelial cells and the biliary system and to the de novo expression of P-selectin in hepatic portal vessels. Inflammation in the spleen was related to the expression of ICAM-1 on red pulp sinusoidal cells, especially in the marginal sinus. High endothelial venules of inflamed lymph nodes also expressed P-selectin and ICAM-1. Lesions in the central nervous system appeared on day 3 after infection as a pyogranulomatous leptomeningitis associated with an intense expression of P-selectin and ICAM-1 in meningeal vessels, especially those in the hippocampal sulcus, suggesting a way through which inflammation initially reach the central nervous system during experimental murine listeriosis. Leptomeningitis was followed by the presence of ventriculitis, which was related to the up-regulation of ICAM-1 on choroid plexus epithelial cells, periventricular vessels and ependymal cells. Up-regulation of P-selectin and ICAM-1 during experimental murine listeriosis could play an important role in the recruitment of leukocytes, especially to the liver, lymphoid organs, and central nervous system.

Animals↗
PubMed1998

Fatal acute toxoplasmosis in three golden lion tamarins (Leontopithecus rosalia).

Fatal acute toxoplasmosis was diagnosed in three golden lion tamarins (Leontopithecus rosalia), a breeding pair and their male offspring, by histology and immunohistochemistry. The distribution and severity of lesions differed among the animals, but the small intestine and the pancreaticoduodenal lymph nodes were especially affected. Protozoal organisms consistent with Toxoplasma gondii tachyzoites, often clustered, were seen in all lesions and were specifically immunostained with a T. gondii polyclonal antibody. The infection was probably acquired orally. Several breeding groups of golden lion tamarins have succumbed to toxoplasmosis both in North American and European zoos, so this disease should be considered an important problem in this endangered species. Toxoplasma gondii can cause latent infections in New World primates and therefore could potentially induce abortions or congenital infections in wild golden lion tamarins born from latently infected reintroduced females.

Acute Disease↗
PubMed1997

Prolonged persistence of Listeria monocytogenes after intragastric infection in corticosteroid-treated mice.

In an attempt to obtain a model more closely resembling natural listeriosis, we studied the course of infection in mice inoculated by the intragastric route with Listeria monocytogenes. Corticosteroid-treated, and untreated mice both developed subclinical infection without mortality, but faecal shedding and persistence of bacteria in the liver and spleen of corticosteroid-treated mice were significantly more protracted than in untreated mice. Untreated mice cleared the bacteria from their livers and spleens by day 5 postinfection (PI), whereas treated mice did not clear the organisms until 8-9 days PI. In untreated mice faecal shedding lasted 5 days PI, whereas in treated mice the organisms were recovered at significantly higher levels until day 9 PI. The only intestinal lesions observed were mild pyogranulomatous changes in the dome area of some Peyer's patches in treated mice.

Animals↗
PubMed1997

Penetration of Listeria monocytogenes in mice infected by the oral route.

In this study, it is suggested that the Peyer's patches are the most important point of entry of Listeria monocytogenes in the host after subclinical infection by the oral route. Microbiological, histopathological and ultrastructural evidence of infection was obtained in mice inoculated with a sublethal dose of 10(9) cfu. No mortality was observed. L. monocytogenes was isolated from the mesenteric lymph nodes from 6 hours post infection (hpi) through day 7 p.i. and from the liver and spleen from 24 h p.i. until days 5 and 7 p.i. respectively. Lesions were mainly restricted to the dome area of Peyer's patches and consisted of a purulent to pyogranulomatous inflammatory reaction. Scarce and minor lesions were also observed in the mesenteric lymph nodes and liver. L. monocytogenes was detected by immunohistochemistry in the Peyer's patches from 12 h p. i. to day 6 p.i. Ultrastructural study of Peyer's patches showed that the majority of Listeria cells were free within the cytoplasm of neutrophils and macrophages, not surrounded by a phagosomal membrane, and some of them were dividing.

Animals↗
PubMed1997

Epizootic disseminated toxoplasmosis in captive slender-tailed meerkats (Suricata suricatta).

Fatal disseminated toxoplasmosis was diagnosed in seven captive slender-tailed meerkats (Suricata suricatta) according to clinicopathologic findings and immunohistochemistry. Five of nine meerkats died during an outbreak in late 1994. These included four kits (2.5 to 4.5 months old) and a 4-year-old meerkat. Two other meerkats, both adults, died in 1992 and 1995. Respiratory insufficiency (4/7) and incoordination (3/7) were the most consistent clinical signs. although two of seven meerkats died unexpectedly. At necropsy, the lungs were reddened and noncollapsed (6/7), and had multiple pale round foci (4/7). Yellow foci of necrosis in mesenteric lymph nodes (4/7), splenomegaly (3/7), and hydropericardium (3/7) were other common gross findings. Microscopically, interstitial pneumonia was present in all seven meerkats, being acute to subacute in six of them. Type 2 pneumocyte hyperplasia, aggregates of foamy macrophages, and giant cells were consistently seen. Multifocal to locally extensive necrosis of mesenteric lymph nodes (4/7), mild to severe multifocal necrotizing hepatitis (5/6), and mild nonsuppurative encephalitis (4/6) were also seen. Toxoplasma-like organisms were consistently associated with these lesions and were stained by the avidin biotin peroxidase procedure with an antiserum that does not cross-react with Neospora caninum. Meerkats were most likely infected after an oral, primary exposure to Toxoplasma. Several observations indicate that meerkats may be highly susceptible to toxoplasmosis.

Animals↗
PubMed1992

A microbiological, histopathological and immunohistological study of the intragastric inoculation of Listeria monocytogenes in mice.

The course of murine infection after intragastric inoculation of L. monocytogenes was investigated by immunocytochemical, histopathological and microbiological techniques. L. monocytogenes antigen was observed in epithelial cells of intestinal mucosa overlying Peyer's patches, but not in mucosa devoid of them. This suggests that penetration of L. monocytogenes into the host organism may take place through epithelium overlying Peyer's patches. The efficiency of bacterial penetration appeared to be low, as shown by the small amounts of L. monocytogenes antigen detected and the low counts of bacteria in organs. Gross or histopathological lesions in the intestinal tract were not observed. The presence of L. monocytogenes in spleen, liver and in maxillary and mesenteric lymph nodes, confirmed that the systemic course of infection by this route of inoculation is similar to that of the parenteral routes. The results emphasize the subclinical character of murine listeriosis by the oral route.

Administration, Oral↗
PubMed1992

Pathologic and immunocytochemical studies of morbillivirus infection in striped dolphins (Stenella coeruleoalba).

Hundreds of striped dolphins (Stenella coeruleoalba) died along the Spanish Mediterranean coast during the second half of 1990. We necropsied 58 dolphins. Partial collapse of the lungs with patchy atelectasis, subcutaneous edema, icterus, and stomatitis were the most prominent gross morphologic changes. Histologically, a bronchiolo-interstitial pneumonia was the most frequent lesion (72% of the animals). It was characterized by hyperplasia of alveolar epithelial type II cells and formation of multinucleate syncytia in alveolar and bronchiolar lumina. Other prominent lesions were encephalitis (69%), lymphoid depletion, and formation of multinucleate syncytia in the cortex of lymph nodes. The distribution of morbillivirus antigen was investigated in 23 well-preserved dolphins using a monoclonal antibody against the hemagglutinin glycoprotein of phocine distemper virus. Positive immunostaining was found in brain (77%), in lung (70%), and in mesenteric (61%), mediastinal (47%), and prescapular (45%) lymph nodes. Phocine distemper virus antigen was demonstrated less frequently in trachea, stomach, biliary epithelium, intestine, kidney, and mammary gland. Necrotizing-hemorrhagic pneumonia and encephalitis due to Aspergillus fumigatus were seen in three dolphins, whereas two animals had lesions of toxoplasmosis. Changes in our dolphins were similar to those caused by distemper in seals and porpoises. The origin of the dolphin virus and the relationships among dolphin, seal, and porpoise morbilli viruses are unknown.

Animals↗
PubMed1992

Lymphatic drainage of Listeria monocytogenes and Indian ink inoculated in the peritoneal cavity of the mouse.

The lymphatic drainage of the peritoneal cavity has been investigated by intraperitoneal inoculation of an intracellular bacterium (Listeria monocytogenes) and an inert marker (Indian ink). The results reveal that both agents are transported, either after phagocytosis by intraperitoneal macrophages or in suspension in the lymph, towards the cranial sternal lymph nodes (Lymphonodi sternales craniales) of the ventral thoracic lymphocentrum (Lymphocentrum thoracicum ventrale) and to the lymph nodes of the mediastinal lymphocentrum (Lymphocentrum mediastinale), prior to systemic dissemination. This mechanism of peritoneal lymph drainage has relevance on experimental studies involving the inoculation of pathogens, and on the investigation of metastatic diffusion of neoplasms from the peritoneum.

Animals↗
PubMed1991

Pathogenesis of lymphoid lesions in murine experimental listeriosis.

Adult female Swiss albino mice were infected intraperitoneally or subcutaneously with Listeria monocytogenes Serovar 4b or 1/2a and killed at intervals. Thymus, spleen, Peyer's patches and a variety of lymph nodes, including the jejunal (mesenteric), mediastinal, lumbar, mandibular and superficial inguinal, were examined by histopathology and by immunocytochemistry for detection of L. monocytogenes antigen. Similar results were obtained with both Serovars and by both routes of inoculation used. In the spleen, L. monocytogenes was detected, by immunoperoxidase staining, as soon as 4 h after inoculation, inside phagocytic cells located predominantly in the marginal zone of the white pulp. This was followed by inflammation, necrosis and depletion of lymphoid cells, which extended in extreme cases to the whole organ. Inflammatory lesions diminished progressively at 5 to 6 days after inoculation. In animals dying of the infection, a severe necrotizing splenitis was present. Depletion of lymphoid cells and inflammatory changes were widespread in the lymph nodes and to a lesser extent in the Peyer's patches. An extensive necrotizing lymphadenitis was the prominent lesion in severely affected nodes. Inflammatory lesions and detection of L. monocytogenes antigen started around the venules of high endothelium. A thymus depletion, not associated with the multiplication of bacteria in the organ, was also a constant feature of the infection. This study suggests that L. monocytogenes (1) is transported to the spleen and to the lymph nodes by phagocytes, entering the organs by the marginal sinus in the spleen and by the venules of high endothelium in the lymph nodes; (2) multiplies in these cells as well as in neutrophilic granulocytes (the latter rapidly migrate to the affected zones); and (3) induce a splenitis and lymphadenitis, involving predominantly T cell-dependent areas, with a necrotizing component in severe cases. From our observations it is concluded that infection of the lymphoid system is a major feature in the pathogenesis of murine listeriosis.

Animals↗
PubMedDate not supplied

Metastatic Listeria monocytogenes infection of the peritoneum in mice with cyclosporine a-induced peritonitis.

Inoculation of mice with Listeria monocytogenes intragastrically or by parenteral routes has not been reported to cause peritonitis. In this study, however, severe listerial peritonitis was induced in mice infected subcutaneously and treated intraperitoneally with cyclosporin A (Cs A) in an oil carrier. In both uninfected and listeria-infected mice, intraperitoneal administration of Cs A consistently produced overexpression of P-selectin in the peritoneal microvasculature and pyogranulomatous inflammation of the peritoneum, suggesting that Cs A causes endothelial damage. We suggest that in listeria-infected mice the non-specific irritant peritonitis induced by the intraperitoneal administration of Cs A results in transfer of listeria-infected phagocytes from the liver and spleen to the peritoneal microvasculature, producing metastatic infection.

Animals↗