Immunohistochemical Detection of Listeria Antigens in the Placenta in Perinatal Listeriosis

Parkash, Anand; Ra, Morotti; Joshi,; Cartun, R. A.; Ca, Rauch; Ab, West

doi:10.1097/00004347-199810000-00008

Cited by 31 publications

(19 citation statements)

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“…This is achieved by several mechanisms, including low lytic ability (12), unique receptor repertoire (9,11), and the presence of ligands such as HLA-G, -C, and -E, on EVT cells, interacting with inhibitory receptors on NK cells (5-7). However, if local bacterial (28) or viral (29) infection occurs, it may lead to decidual lymphocyte activation. This might result in changes in the composition, cytotoxicity, and cytokine profile (30) of decidual lymphocytes that might eventually damage fetal tissue (31).…”

Section: Discussionmentioning

confidence: 99%

Pivotal role of CEACAM1 protein in the inhibition of activated decidual lymphocyte functions

Markel¹,

Wolf²,

Hanna³

et al. 2002

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Pivotal role of CEACAM1 protein in the inhibition of activated decidual lymphocyte functions

Markel¹,

Wolf²,

Hanna³

et al. 2002

J. Clin. Invest.

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“…This occurs via induction of neutrophil chemoattractant synthesis by the trophoblast (251a). In humans, placental infection is characterized by numerous microabscesses and focal necrotizing villitis (502,582). Colonization of the trophoblast layer followed by translocation across the endothelial barrier would enable the bacteria to reach the fetal bloodstream, leading to generalized infection and subsequent death of the fetus in utero or to premature birth of a severely infected neonate with miliary pyogranulomatous lesions (the above-mentioned granulomatosis infantiseptica) ( Fig.…”

Section: Pathogenesismentioning

confidence: 99%

ListeriaPathogenesis and Molecular Virulence Determinants

et al. 2001

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The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research

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“…13 Although immunohistochemistry was used to localize the pathogen in this foal, the placenta had been discarded and was unavailable for examination, so in utero infection cannot be completely ruled out. 11,13 Immunohistochemistry may be beneficial both retrospectively and prospectively in potential cases of perinatal listeriosis where bacterial cultures have been equivocal or reported as contaminated.…”

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confidence: 99%

Listeria MonocytogenesSepticemia in a Thoroughbred Foal

et al. 2000

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Listeria monocytogenes septicemia was diagnosed in a 6-day-old Thoroughbred foal. Primary clinical signs included fever, depression, diarrhea, and respiratory distress. Hematologic abnormalities included leukopenia, neutropenia, degenerative left shift, and hyperfibrinogenemia. Clinical chemistry and blood gas abnormalities included metabolic acidosis, hypoxemia, hypocapnia, hypoglycemia, and hyponatremia. Despite aggressive therapeutic intervention and intensive care, the foal died within 12 hours of admission. A postmortem examination was performed, and the primary gross lesion was bilaterally severe, focally extensive bronchopneumonia. Histopathology revealed severe subacute multifocal suppurative bronchopneumonia with necrotizing vasculitis and intralesional coccobacilli. Cultures of blood collected at admission and immediately prior to death were positive for L. monocytogenes, as were cultures obtained from lung and liver at necropsy. Immunohisto-chemical examination of formalin-fixed tissues revealed abundant intra- and extracellular L. monocytogenes antigen within the lung and intravascularly in multiple organs.

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Immunohistochemical Detection of Listeria Antigens in the Placenta in Perinatal Listeriosis

Cited by 31 publications

References 0 publications

Pivotal role of CEACAM1 protein in the inhibition of activated decidual lymphocyte functions

Pivotal role of CEACAM1 protein in the inhibition of activated decidual lymphocyte functions

ListeriaPathogenesis and Molecular Virulence Determinants

Listeria MonocytogenesSepticemia in a Thoroughbred Foal

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