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Listeria monocytogenes peritonitis
Abstract
Listeria monocytogenes peritonitis in a patient with cirrhosis and simultaneous soft tissue infection is reported. Six previously documented cases are reviewed. All seven patients were bacteremic, suggesting hematogenous seeding to the peritoneum as the pathogenic mechanism. Clinical and laboratory characteristics of L. monocytogenes peritonitis are compared with peritonitis of other bacterial etiologies.
... There was a total of 35 instances of possible neonatal crossinfection which occurred between 1971 and 2012: ten episodes have been described previously as case reports [12][13][14][15][16][17][18][19][20][21]. ...
Neonatal listeriosis is rare and detecting more than one case together would be unlikely without a causal link. Thirty-five instances of neonatal listeriosis where cross-infection occurred in the UK and Ireland were reviewed together with 29 other similar episodes reported elsewhere. All instances comprised an infant who was ill at or within one day of delivery and who had direct or indirect contact with a second infant, or in the minority, two or more infants, who then usually developed meningitis 6 to 12 days later. In most instances, the infants were nursed on the same day in obstetric units or new-born nurseries and consequently, staff and equipment were common: hence, the likely route of transmission was via direct or indirect neonate to neonate contact. In one instance, a stethoscope was used on both infants nursed in different parts of the same hospital. In a further incident, the mother of the early-onset infant cuddled a baby from an adjacent bed who developed meningitis 12 days later. The largest outbreak occurred in Costa Rica where nine neonatal listeriosis cases resulted after bathing in mineral-oil shortly after birth which had been contaminated from the early-onset index case.
... 22 Using PubMed and Google Scholar with key words "Listeria" and "peritonitis," we performed a further search revealing 23 additional cases, [9][10][11][12][13][14][15][16][17][18][19][20] with just five of these cases reported after 2011. 10,13,14,19,20 Of the cases of SBP reported in the United States, those due to Listeria are relatively rare. 1 The 11 cases of Listeria peritonitis in the United States that, to our knowledge, have been published to date are summarized in Table 2. 9,12,17,20,[23][24][25][26][27][28] Interestingly, approximately 60% of the reported cases of Listeria peritonitis worldwide have been from Spain. 10 Possible explanations for the increased number of reports of Listeria peritonitis coming from Spain include a diet richer in unpasteurized cheese and delicatessen meats, although the incidence of listeriosis in general (i.e., manifesting as other clinical syndromes) is not increased in Spain. 29,30 The index of suspicion for Listeria SBP may be appropriately elevated in travelers from Spain. ...
Spontaneous bacterial peritonitis (SBP) is a frequent and potentially deadly complication of ascites in patients with end-stage liver disease. Unlike other pathogens more commonly implicated in SBP, Listeria monocytogenes is a nonenteric organism that may be acquired either sporadically or in the setting of foodborne outbreaks. Listeria is an unusual cause of SBP that presents particular management challenges because of the organism's intrinsic resistance to first-line and empiric SBP treatment that would otherwise include third-generation cephalosporins. We present here a case of Listeria SBP in a 68-year-old man with previously unidentified cirrhosis. His infection occurred in the context of a nationwide fruit recall for Listeria contamination, prompting an epidemiologic investigation. After describing the case, we then review the extant literature on Listeria peritonitis. To date, no case studies on Listeria SBP have systematically described risk factors for Listeria acquisition. As incidence of Listeria SBP is increasing, however, knowledge of patient risk factors, especially foodborne exposure risks, may be important in preventing future episodes of Listeria SBP, and in accurately monitoring foodborne outbreaks.
Although
Listeria monocytogenes
has been isolated from the gastrointestinal tract, it is an infrequent cause of bacterial peritonitis. Since 1963 only 23 cases of peritonitis caused by listeria have been reported. This report describes another case in a patient with cirrhosis and chronic renal failure and presents a review of the literature. Most (16) of the previous cases were cirrhotic while six were undergoing chronic ambulatory peritoneal dialysis. Eight patients were on immunosuppressive therapy. Blood cultures were positive in fewer than half (42%) of the cases and Gram stain of peritoneal fluid was positive only twice. The peritoneal fluid protein concentration was relatively high compared with other causes of bacterial peritonitis. Ampicillin was the drug most commonly used for treatment, and the majority of patients survived the acute infection.
Spontaneous bacterial peritonitis (SBP) is a common and often serious complication of long standing ascites in the presence of advanced liver disease.1 We report a case of a 51- year-old man with alcoholic cirrhosis admitted to our department with jaundice, ascitis and lower limbs edema. A diagnosis of spontaneous bacterial peritonitis was made and empiric therapy with cefotaxime was prescribed with no response. Three days later Listeria monocytogenes was detected in peritoneal fluid culture and amoxicillin was initiated according to in vitro sensibility test. Despite adequate antibiotic therapy, the patient died one week later.
Background:
Spontaneous bacterial peritonitis (SBP) is a serious complication in cirrhotic patients. Gram (-) (E. coli, Klebsiella pneumoniae), and Gram (+) (Streptococci, Staphylococci) bacteria are most frequently cultured from patients'ascites. Listeria monocytogenes (Lm) is scarcely reported as a causative agent.
Objective:
Our objective is to describe Lm peritonitis as a clinical entity, including its presentation, clinical features, treatment, and the potential factors that might affect survival outcome.
Material and methods:
Data sources:
MEDLINE, Scholar.Google, Scopus databases, including English, Spanish, French, and German language papers published between 1966 and June 2011, and reference lists.
Data extraction:
investigators abstracted details about medical history, disease presentation, laboratory data, treatment and outcome.
Data synthesis:
One-hundred and twenty-eight cases with known survival outcome--eighty-six cirrhotics, seventeen individuals undergoing continuous ambulatory peritoneal dialysis and another twenty-five with other or no underline condition were reviewed. An additional number of twenty-five cases with unknown outcome were searched in Listeria studies published from 1990 to 2009 and were only used for calculating worldwide distribution.
Conclusion:
Cirrhotics, mostly alcoholics, presented with fever and abdominal pain. Those who succumbed had significantly higher peripheral WBC count (15622 vs. 8155 cells/mm(3), p = 0.01) and (%) polymorphonuclear cells in differential count (83.3 vs. 71%, p = 0.001). Higher mortality was experienced in those with comorbidities, and those who presented with encephalopathy. Lower mortality was experienced in patients on continuous ambulatory peritoneal dialysis. Ascites was neutrocytic in 86% of the samples. In the sum of the cases mortality was 27.3%, with significantly highest rates in the elderly, in patients with bacteremia, immunosuppression, hematological malignancies, and lowest rates in those who presented with abdominal pain and in diabetics (type I or II). The latter observation was surprising and could be considered a single fortuitous fact. Initial appropriate treatment was associated with significantly better outcome (p = 0.002) than inappropriate; combination therapy with an aminoglycoside was superior to monotherapy (p = 0.038).
Listeria monocytogenes has been increasingly implicated in spontaneous bacterial peritonitis in patients with cirrhosis. This bacterium can be mistaken for diphtheroids and gram-positive cocci if special attention is not paid to the motility pattern and specific biochemical tests. Although the sensitivity of ascitic fluid Gram stain is low, we describe a case in which the Gram stain of the ascites fluid was positive. This issue is now pertinent given recent recommendations of third-generation cephalosporin antibiotics as empiric therapy for spontaneous bacterial peritonitis;Listeria is resistant to cephalosporin agents. A positive Gram stain could affect the empiric antibiotic therapy. We review the clinical presentation and outcome in nine other cases ofListeria peritonitis occurring in cirrhotic patients.
Infections with Listeria monocytogenes can present clinically with a wide range of different organ manifestations such as gastroenteritis, meningoencephalitis or osteomyelitis, posing a serious threat, particularly to immunocompromised patients. We present the case of a 76-year-old female patient with advanced liver disease due to underlying haemochromatosis, who was admitted to the hospital with increasing abdominal pain. She was diagnosed with spontaneous bacterial peritonitis caused by infection with Listeria monocytogenes, which she had acquired after consuming contaminated cheese from a local supermarket chain. To the best of our knowledge, this is the first case to describe Listeria-induced spontaneous bacterial peritonitis in a patient with haemochromatosis. Both end-stage liver disease and hereditary haemochromatosis on their own impair the local and systemic immune response, thereby representing predisposing factors for acquiring Listeria monocytogenes infection. This case demonstrates a rare organ manifestation of Listeria monocytogenes infection, which can be life-threatening if not diagnosed and treated adequately, and underlines the need to identify possible sources of infection in order to apply measures to prevent the further spread of the contaminated food.
Two new cases of spontaneous bacterial peritonitis (SBP) caused by Listeria monocytogenes are reported. Listeria monocytogenes was recovered from the ascitic fluid but not from the blood cultures of two adult diabetic inpatients with hepatic cirrhosis and SBP that had been treated empirically with cefotaxime. These two cases add to the 17 cases of Listeria monocytogenes SBP reported previously, stressing the relevance of this microorganism to this clinical condition. The recovery of Listeria monocytogenes from blood has been achieved in only half of the cases reported, suggesting the possibility of a direct translocation mechanism. Combinations of amino- or ureidopenicillins with beta-lactamase inhibitors or carbapenems might be more effective as empiric therapy of SBP in cirrhotic patients.
The influence of various factors on the fate of Listeria monocytogenes on cut leaves of broad‐leaved endive has been studied. Factors considered were temperature, characteristics of the leaves (age, quantity and quality of the epiphytic microflora) and characteristics of the L. monocytogenes inoculum (concentration, strain). The increases in numbers of L. monocytogenes were lower than those of the aerobic mesophilic microflora at 3°, 6°, 10° and 20°C. Doubling times of the populations of L. monocytogenes were in the same order of magnitude as those of aerobic bacteria at 10° and 20°C, but longer at 3° and 6°C. There were positive significant correlations between growth of L. monocytogenes and populations of aerobic bacteria, and between growth of L. monocytogenes and extent of spoilage on the leaves.
Of 225 bacteria isolated from the leaves, 84% were identified as fluorescent pseudomonads; there was no difference in the species isolated from leaves that showed a low growth of L. monocytogenes and leaves that showed a high growth of L. monocytogenes. Populations of L. monocytogenes increased faster during the first 2 and 4 d of storage at 10°C on leaves inoculated with 10–10 ³ cfu g ‐1 than on leaves inoculated with about 10 ⁵ cfu g ‐1 , but the population reached after 7 d was lower. The behaviour of L. monocytogenes was similar among the three strains tested.
We aimed to assess the incidence, demographic data, clinical features, and outcome of peritoneal infections due to Listeria monocytogenes in individuals with cirrhosis.
During a 10-yr study period, 153 cases of invasive listeriosis were recorded in a prospective population-based surveillance project carried out in Barcelona, Spain.
Thirteen cases were of spontaneous bacterial peritonitis by L. monocytogenes. Ages of the patients ranged between 29 and 85 yr. In addition to cirrhosis, underlying conditions included diabetes mellitus in four and malignancy in three. Bacteremia was present in six cases (46%). Only one patient with bacteremia developed meningitis. Analysis of the peritoneal fluid showed a mean (SD) protein content of 21.5 (9.6) g/L and leukocyte count of 7,273 (9,171) cells/ml. L. monocytogenes serotype 4b was the serogroup predominantly isolated (61%). The mortality rate was 30.7%. Eight patients received empirical antibiotic treatment with cephalosporins.
In geographical areas with a high incidence of listeriosis, L. monocytogenes should be suspected as a causative pathogen of spontaneous bacterial peritonitis in cirrhosis. Early adjustment of antibiotic therapy is essential to reduce mortality.
Central nervous system involvement often follows bacteremia because of Listeria monocytogenes. Meningitis is clinically the most common manifestation, while brain abscess occurs in about 1% of patients. Brain abscess is usually solitary but in recent years, probably in part because of the availability of computerized tomography and magnetic resonance imaging, several reports have described two or more separate supratentorial abscesses.
We have described three patients with listerial brain abscesses and reviewed the North American and European literature of brain abscess(es) because of L. monocytogenes through December 2001. We have evaluated the role of underlying diseases and therapeutic immunosuppression on the development of solitary or greater than one brain abscess.
In contrast to meningitis, where immunosuppression does not predispose either to disease incidence or to higher mortality, patients with solitary and particularly those with more than one supratentorial abscess usually are immunosuppressed either by disease or by therapy. Corticosteroids in particular are significant predisposing factors, especially in those patients with two or more brain abscesses. Mortality resulting from listerial brain abscess, whether solitary or multiple, is nearly three times higher than nonlisterial brain abscess, probably in part because of both underlying diseases and immunosuppressive therapy.
Therapy with high-dose ampicillin in combination with gentamicin appear to be the drugs of choice, followed by trimethoprim/sufamethoxazole and vancomycin. In general, antimicrobial therapy appears to be satisfactory treatment without surgical intervention.
To assess the risk of development of spontaneous bacterial peritonitis in relation to the ascitic fluid total protein concentration, routine admission abdominal paracentesis was performed on a group of 107 patients during 125 hospitalizations. The paracentesis was repeated if evidence of peritonitis developed during hospitalization. Twenty-one episodes of spontaneous peritonitis (or its culture-negative variant) were documented in 17 patients. The ascitic fluid protein concentration in the spontaneous peritonitis group (0.72 ± 0.53 g/dl) was significantly lower (p < 0.001) than that in the group of patients with sterile portal hypertension-related ascites (1.36 ± 0.89 g/dl) and was significantly lower than that of patients with ascites due to miscellaneous causes. Of the patients whose initial sterile ascitic fluid protein concentration was ≤1.0 g/dl, 7 of 47 (15%) developed spontaneous peritonitis during their hospitalization; whereas only 1 of 65 (1.5%) patients who had an initial sterile ascitic fluid protein concentration >1.0 g/dl developed spontaneous peritonitis. This difference in risk of development of peritonitis in relation to initial ascitic fluid protein concentration was also significant (p < 0.01). Low-protein-concentration ascitic fluid predisposes to spontaneous bacterial peritonitis.
Ascites is the most common complication of cirrhosis and is also a frequent indication for hospitalization. In the past there has been much confusion and perpetuation of traditional, non-data-supported concepts regarding the evaluation and treatment of patients with ascites. Currently we know a great deal about this condition. The newer concepts of differential diagnosis and management of patients with ascites will be discussed here. Also the diagnosis, prevention, and management of complications of ascites will be presented.
Listeria monocytogenes is a Gram-positive bacillus that is pathogenic in both the normal and compromised host. We describe Listeria peritonitis and cerebritis in a patient with cirrhosis due to non-A, non-B hepatitis, and review the 11 other cases of Listeria peritonitis reported in the English-language literature. Listeria is a rare cause of peritonitis in debilitated, older patients, with two-thirds of the cases occurring in patients with chronic liver disease. Listeria peritonitis may also occur in patients undergoing peritoneal dialysis, or in those with malignancy. Peritonitis due to Listeria is clinically similar to spontaneous bacterial peritonitis, and is associated with fever, variable abdominal pain, and neutrocytic ascites; bacteremia commonly accompanies Listeria peritonitis. This syndrome can be successfully treated with antimicrobial drugs, although the third-generation cephalosporins commonly used in the therapy of spontaneous bacterial peritonitis are not recommended. Ampicillin may be the drug of choice, with combination therapy with an aminoglycoside reserved for cases that do not respond to ampicillin alone.
Spontaneous bacterial peritonitis is an infection of the ascitic fluid of patients who, in general, have severe chronic liver disease. Several variants of this disease exist including bacterascites, culture-negative neutrocytic ascites, and secondary bacterial peritonitis. Spontaneous bacterial peritonitis is frequently manifested by signs and symptoms of peritonitis although the findings may be subtle; however, occasionally it may be completely without clinical manifestation. The clinician must have a high index of suspicion in order to make this diagnosis at a relatively earlier stage of infection. An abdominal paracentesis is required to make the diagnosis of spontaneous bacterial peritonitis. This paracentesis should be performed on all patients who are admitted to the hospital for ascites and should be repeated if there is any manifestation of bacterial infection during the hospitalization. Patients with severe intrahepatic shunting--as manifested by marked redistribution of activity from the liver to the spleen and to the bone marrow on liver-spleen scan as well as patients with an ascitic fluid total protein concentration of less than 1 g/dl--appear to be particularly susceptible to bacterial infection of their ascites. In order to optimize the yield of ascitic fluid culture, it is probably appropriate to inject blood culture bottles with ascites at the bedside immediately after the abdominal paracentesis. The mortality of spontaneous bacterial peritonitis continues to be very high. Perhaps routine admission paracentesis and prompt empiric antibiotic therapy with a third-generation cephalosporin will decrease the mortality of this infection if the Gram stain of the ascitic fluid demonstrates bacteria or the ascitic fluid neutrophil count is greater than 250 cells/cu mm. Repeating the paracentesis after 48 hours of treatment to reculture the fluid and reassess the ascitic fluid neutrophil count appears to be the best way to assess efficacy of treatment. After 48 hours of treatment the ascitic fluid neutrophil count should be less than 50% of the original value if the antimicrobial therapy is appropriate. The optimal duration of antibiotic treatment is unknown; however, until controlled trials provide data regarding duration of treatment it is appropriate to treat with parenteral antibiotics for 10 to 14 days. Research is also needed to determine if there are measures which can be taken to prevent the development of spontaneous peritonitis.
A retrospective analysis of 22 patients whose ascitic fluid had been analyzed prior to the onset of spontaneous bacterial peritonitis, during infection and/or after treatment of peritonitis revealed that neither the ascitic fluid total protein nor the absolute ascitic fluid glucose changed during the infection or after treatment of the infection although the ascitic fluid/serum glucose ratio did decrease (p less than 0.001) with infection. The ascitic fluid lactate dehydrogenase increased significantly (p less than 0.05) during infection compared to the baseline value. Contrary to the typical findings in infected body fluids, the total protein content and absolute glucose content of "spontaneously" infected ascitic fluid do not measurably change.
The opsonic activity of 60 ascitic fluids from 47 patients was measured using a standard opsonophagocytic assay. Curve analysis of the opsonic activity compared to the ascitic fluid concentration of total protein, total hemolytic complement, C3 and C4 yielded correlation coefficients of 0.84 (p less than 0.001), 0.84 (p less than 0.001), 0.94 (p less than 0.001) and 0.92 (p less than 0.001), respectively. There appeared to be a threshold of concentration for each protein below which there was no killing of bacteria. Cirrhotic ascites had significantly (all p less than 0.001) lower concentrations of total protein and complement and less opsonic activity than noncirrhotic ascites (including malignant, cardiac and miscellaneous types). Perhaps it is the dilution of crucial antimicrobial proteins below a threshold which predisposes to spontaneous bacterial peritonitis.
Listeria monocytogenes peritonitis in cirrhotic patients value of ascitic fluid gram stain and a review of literature
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Nguyen MH, Yu VL: Listeria monocytogenes peritonitis in cirrhotic patients value of ascitic fluid gram stain and a review of literature. Dig Dis Sci 39:215-218, 1994