Human listeriosis in Britain, 1967–85, a summary of 722 cases: 1. Listeriosis during pregnancy and in the newborn

McLauchlin, James

doi:10.1017/s0950268800059343

Cited by 173 publications

(133 citation statements)

References 26 publications

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“…In both instances, the predominant clinical forms correspond to disseminated infection or to local infection in the central nervous system (CNS). Listeriosis is usually a very severe disease-in fact, one of the most deadly bacterial infections currently known-with a mean mortality rate in humans of 20 to 30% or higher despite early antibiotic treatment (422,423,554,594).…”

Section: Clinical Featuresmentioning

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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Section: Clinical Featuresmentioning

confidence: 99%

ListeriaPathogenesis and Molecular Virulence Determinants

et al. 2001

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“…monocytogenes has a striking predilection for invading the CNS in humans. Reviews published in the past 40 years show that CNS infection is present in 28 to 79% of cases of invasive listeriosis in nonpregnant adults (229,277,358) and in 13 to 44% of neonates (119,251,278,348,377). In contrast to extracellular bacteria that commonly cause CNS infection, i.e., S. pneumoniae, N. meningitidis, and H. influenzae, L. monocytogenes infection results in a variety of CNS manifestations including meningitis, meningoencephalitis, rhombencephalitis, cerebritis, and brain abscess.…”

Section: Listeria Monocytogenesmentioning

confidence: 99%

Invasion of the Central Nervous System by Intracellular Bacteria

2004

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Infection of the central nervous system (CNS) is a severe and frequently fatal event during the course of many diseases caused by microbes with predominantly intracellular life cycles. Examples of these include the facultative intracellular bacteria Listeria monocytogenes, Mycobacterium tuberculosis, and Brucella and Salmonella spp. and obligate intracellular microbes of the Rickettsiaceae family and Tropheryma whipplei. Unfortunately, the mechanisms used by intracellular bacterial pathogens to enter the CNS are less well known than those used by bacterial pathogens with an extracellular life cycle. The goal of this review is to elaborate on the means by which intracellular bacterial pathogens establish infection within the CNS. This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens

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“…In the UK between 1967 and 1985, 248 out of 722 cases of human listeriosis (34%) were associated with pregnancy of which 42 cases resulted in intrauterine deaths (19%) and 47 in neonatal deaths (35%), with an overall case fatality rate of 50% [4].…”

Section: Introductionmentioning

confidence: 99%

Neonatal listeriosis in the UK 2004–2014

Sapuan

Kortsalioudaki

Anthony

et al. 2017

Journal of Infection

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ObjectiveTo define the clinical features and outcomes of neonatal listeriosis, and identify the maternal risk factors to seek scope for improvement. MethodsNeonatal listeriosis was identified prospectively from a United Kingdom neonatal infection surveillance network (neonIN) between 2004 and 2014. The participating neonatal units completed a study-specific proforma. ResultsThe incidence of neonatal listeriosis was 3.4 per 100,000 live births. Of the 21 cases identified, 19 were confirmed with a median gestational age of 33 weeks and a median birth weight of 1960g. The majority had clinical features (95%, 18/19), presented within the first 24 hours (95%, 18/19), and received penicillin empirically (94%, 18/19). The neonatal casefatality rate was 21% (24% if probable cases were included). A proportion of mothers were investigated (60%, 12/18) and diagnosed with listeriosis (58%, 7/12); 32% (6/19) were treated with antibiotics but only 33% (6/12) included penicillin. DiscussionDespite its rarity and the prompt and appropriate use of antibiotics neonatal listeriosis has a high case-fatality rate. There is room for improvement in the adherence to the national guidance in the choice of empiric antibiotics for puerperal sepsis, which would target listeriosis. Strategies should be in place to prevent pregnancy-associated listeriosis in higher risk population.

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Human listeriosis in Britain, 1967–85, a summary of 722 cases: 1. Listeriosis during pregnancy and in the newborn

Cited by 173 publications

References 26 publications

ListeriaPathogenesis and Molecular Virulence Determinants

ListeriaPathogenesis and Molecular Virulence Determinants

Invasion of the Central Nervous System by Intracellular Bacteria

Neonatal listeriosis in the UK 2004–2014

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