Positive Mesenteric Lymph Node Cultures Research Articles

Assessment of Post-Resuscitation Intestinal Injury and Timing of Bacterial Translocation in Swine Anaesthetized With Propofol-Based Total Intravenous Anaesthesia.

Introduction and objectivesBacterial translocation (BT) is the passage of viable bacteria or endotoxins from the gastrointestinal lumen to extra-luminal tissues and is usually observed after intestinal ischaemia-reperfusion injury. The aim of this study was to investigate post-resuscitation BT after cardiac arrest and resuscitation in a swine anaesthetized with propofol-based total intravenous anaesthesia.Materials and methodsEighteen female Landrace/Large White piglets were randomly divided into control (CON), cardiac arrest (CA) and cardiac arrest-cardiopulmonary resuscitation (CA-CPR) groups. In the CON group, the animals were only monitored for two hours. In the CA group, the animals were not resuscitated and underwent necropsy immediately after cardiac arrest. In the CA-CPR group, the animals were resuscitated until the return of spontaneous circulation (ROSC) and were monitored for two hours. The animals of the CON and CA-CPR groups underwent necropsy 24 hours later. Bacterial translocation was assessed by blood and tissue cultures and endotoxin measurement in the portal and systemic circulation. Malondialdehyde content calculation and histological analysis of the intestine were performed in order to estimate ischemia and reperfusion (I/R) tissue damage.Results Malondialdehyde content, an indicator of oxidative stress, was significantly higher in the CA-CPR group compared to the CA in homogenized ileum (p=0.016). Malondialdehyde content in homogenized colon revealed significantly higher levels in the CA-CPR group compared to the CON (p=0.004) and the CA group (p=0.016). We found significantly higher levels of portal endotoxin in the CA-CPR group compared to the CON (p=0.026) and the CA group (p=0.026). The number of positive mesenteric lymph nodes cultures for E. coli was greater in the CA-CPR group, followed by the CA and CON groups, although the difference was not significant (67%, 33%, and 33%, respectively; p=0.407).ConclusionsMalondialdehyde content and portal endotoxin levels do not increase during the cardiac arrest interval, but only after CPR and ROSC. Although the number of positive MLNs cultures was greater in the CA-CPR animals, no statistically significant differences were observed between the three groups due to the short monitoring period.

Cirrhotic rats with bacterial translocation have higher incidence and severity of hepatopulmonary syndrome

Bacterial translocation, that is, extra-intestinal dissemination of gut bacteria, occurs in approximately 50% of humans and rats with cirrhosis and plays a significant role in enhanced tumor necrosis factor-alpha (TNF-alpha) production. The authors' previous studies have indicated that prevention of bacterial translocation with norfloxacine or inhibition of TNF-alpha with pentoxifylline treatment decreased both the incidence and severity of hepatopulmonary syndrome by attenuating the induction of pulmonary intravascular macrophages in cirrhotic rats. In the present study the hypothesis was tested that the cirrhotic rats with bacterial translocation had higher TNF-alpha production, higher level of sequestration of macrophages in pulmonary vessels, and increased incidence and severity of hepatopulmonary syndrome. Rats were studied 5 weeks after common bile duct ligation or sham operation. Bacterial translocation was defined by positive mesenteric lymph node cultures. Hepatopulmonary syndrome was assessed by measurements of alveoloarterial oxygen difference (AaPO(2)) and intrapulmonary shunt. The TNF-alpha concentration in plasma was measured by ELISA. Pulmonary intravascular macrophage sequestration was assessed by lung morphometric analysis. Bacterial translocation occurred in 48% of cirrhotic rats. Plasma concentrations of TNF-alpha and the percentage of vessels with pulmonary intravascular macrophages were higher in the cirrhotic rats with bacterial translocation. Rats with bacterial translocation also had a higher incidence (9% vs 63%, P < 0.01) and severity of hepatopulmonary syndrome, as indicated by higher levels of both AaPO(2) and intrapulmonary shunt. These results suggest that bacterial translocation may play a role in the pathogenesis of hepatopulmonary syndrome by inducing pulmonary intravascular macrophages through TNF-alpha upregulation.

Gut Bacterial Translocation and Postoperative Infections: A Prospective Study in Schistosomotic Patients

Bacterial translocation (BT) across the intact intestinal mucosal barrier has been postulated as a source of sepsis in susceptible patients, including those with cirrhosis and portal hypertension. This condition has not been studied in hepatosplenic schistosomiasis, wherein portal hypertension and the presence of an immune deficiency state associated with the parasitic disease could predispose to BT into mesenteric lymph nodes (MLN). A study was conducted to determine the prevalence of aerobic bacteria in MLN (bacterial translocation) of patients with hepatosplenic schistosomiasis, and establish a possible association with postoperative infections. In a series of 51 patients submitted to surgical treatment of schistosomotic portal hypertension with splenectomy and gastric devascularization, MLN were obtained from each patient at the beginning (MLN1) and at the end (MLN2) of the surgical procedure, and sent for bacteriological analysis. Prospective patient evaluation during the postoperative period correlated positive MLN cultures with infectious complications. The prevalence of aerobic bacteria was 17.6% at MLN1 and 27.5% at MLN2, however, this difference was non-significant (p = 0.24). Bacterial translocation to all MLN was 22.5%. Escherichia coli was the most frequent organism (26.1%, 6/23). The overall incidence of postoperative infections was 19.6% (10/51), with a significant association with the presence of positive cultures of MLN (p = 0.043). The findings of this study suggest that the presence of aerobic bacteria on MLN as a consequence of BT may play a role in the development of postoperative infectious complications, particularly in schistosomotic patients.

Whole gut washout ameliorates the progression of acute experimental pancreatitis

Background: Septic complications are mainly responsible for deterioration of a patient with acute pancreatitis. Intestinal tract is accepted as the main source of pancreatic or peripancreatic infection. Material andmethods: Acute pancreatitis was induced in 40 Sprague-Dawley rats by ligation of the main biliopancreatic duct. Animals were divided into two groups. The first group of animals (n = 20) received high volume polyethylene glycol-3500 (GoLYTELY) for 6 hours through a silastic catheter introduced into the proximal part of the jejunum from a puncture gastrostomy during the initial laparotomy. The second group animals (n = 20) did not receive any treatment. Half of the animals from each group were sacrificed 72 hours later and tissue samples were taken from mesenteric lymph nodes, pancreas, spleen, and liver for bacteriologic cultures. Cecum cultures were also prepared. Blood samples at 72 hours were obtained for the measurement of amylase, lactic dehydrogenase (LDH), lactic acid, alanine aminotransferase (ALT), glucose, calcium, arterial pH, base excess, partial oxygen pressure, bicarbonate, leucocyte count, and hematocrit levels. The pancreas was examined histopathologically. The remaining half of the animals from each group were allowed to survive until death. Results: The levels of amylase, LDH, ALT, lactic acid, pH, pO 2, bicarbonate and base excess for the rats in group I were significantly lower when compared with the rats in group II ( P <0.05). Positive mesenteric lymph node cultures were detected in 30% of group I animals whereas they were positive in 90% of group II animals ( P = 0.0198). Distant organ cultures were positive in 8 animals (liver 5, spleen 2, pancreas 1) in group II, whereas only one positive distant organ culture (liver) was established in group I ( P >0.05). Histopathological scoring observed in the pancreas were less severe for the rats in group I when compared with the rats in group II ( P = 0.012). The rats in group I survived longer than the rats in group II (median survival 6.8 days versus 17.3 days, P <0.001). Conclusions: Whole gut washout with high-volume polyethylene glycol in pancreatitis reduced the blood levels of enzymes and increased the survival. Whole gut washout for acute pancreatitis appears effective to ameliorate the prognostic factors in blood and this modality may be a promising treatment method in acute pancreatitis.

Bacterial dissemination, rather than translocation, mediates hypermetabolic response in endotoxemic rats.

To study the pathogenesis of the host response during bacterial translocation, a rat model was designed for prolonged follow-up after injury. A prospective, controlled animal study. Animal laboratory. Young male Wistar rats. Antibiotic decontamination of rats was performed 4 days before intragastric inoculation with a selected Escherichia coli strain (10(10) bacteria/kg of body weight). Two days later, the rats received a lipopolysaccharide injection or not (control group) and were observed for 3 days. They were then killed. A reference group (pair-fed healthy animals) was studied in parallel. During observations, urinary total nitrogen loss and 3-methylhistidine excretion were determined daily. When the rats were killed, mesenteric lymph nodes (MLNs), spleen, and liver were aseptically removed and cultured. Colonies identified as translocated E. coli were counted in each organ. Intracellular amino acid free pools were measured in extensor digitorum longus and anterior tibialis. Endotoxin induces bacterial translocation of bacteria from gut lumen to MLNs (100% vs. 59% in the lipopolysaccharide-untreated control group; p < .05) and dissemination to spleen and liver (65% and 45% of positive cultures after endotoxemia, respectively, vs. 6% and 12% in the control groups). No translocation occurred in the reference group. Evidence for the hypermetabolic response was seen in lipopolysaccharide-treated and infected rats, but protein catabolism was more closely related to the occurrence of bacterial dissemination to spleen and liver than to translocation alone (e.g., the cumulative 3-methylhistidine excretion during the observation period was 4.07+/-0.18 micromol in uninfected rats, 4.48+/-0.29 in rats with positive MLN cultures alone and 6.17+/-0.30 in MLN, spleen, or liver infected rats; 1 vs. 2, NS; 3 vs. 1, and 3 vs. 2, p < .05). Gut barrier failure is associated with a deep excessive catabolic response in the host. The mechanism by which the metabolic state affects the resistance to infection apparently involves amino acid metabolism.

Does large-bowel enema reduce septic complications in acute pancreatitis?

BACKGROUND: The source of septic complications in acute pancreatitis was unknown until recent years. The pathogenesis of bacterial translocation from the gut has been accepted as the main source of pancreatic or peripancreatic infection. This study was designed to investigate the role of large bowel enema during acute pancreatitis in preventing bacterial translocation. MATERIALS AND METHODS: Twenty-four Spraque-Dawley rats were used in this study. The rats were divided into two groups. Group I animals received biliopancreatic duct ligation plus colon cleansing by rectal enemas; group II animals received only biliopancreatic duct ligation. Rectal enemas were applied to the first group of animals three times, at 6, 24, and 48 hours after the operation using 10 cc sodium hydrogen phosphate solutions. All animals were sacrificed 72 hours later, and tissue samples were taken from mesenteric lymph nodes, pancreas, spleen, and liver for bacteriologic cultures via a midline laparatomy. Blood and cecum cultures were also prepared. RESULTS: Positive mesenteric lymph node cultures were found in all 12 animals in group II but in only 3 of 11 animals of group I ( P <0.05). Distant organ cultures were positive in 9 of group II, but the only infected distant organ culture found in group I was the positive liver culture ( P <0.05). CONCLUSION: As a result of this study, we believe that large bowel enema can reduce the frequency of septic complications in acute pancreatitis by reducing bacterial translocation.

Effects of Growth Hormone and Insulin-Like Growth Factor-I on Radiation Enteritis

The effect of growth hormone (GH) and insulin-like growth factor-I (IGF-I) on intestinal mucosal integrity and bacterial translocation after abdominal radiation was studied in rats. Animals were divided into the following groups: I (control), II (radiation), III (radiation plus GH) and IV (radiation plus IGF-I). Radiation (1,100 cGy) was administered on the 1st day to groups II, III and IV. GH [0.25 mg/kg body weight (BW) s.c. once daily] was administered on days 1, 2 and 3 to group III, and IGF-I (0.1 mg/kg BW s.c. twice daily) was given on days 1, 2 and 3 to group IV. On day 4, animals were sacrificed. Cultures of the mesenteric lymph nodes (MLN) and blood cultures from aorta and portal vein were performed. The number of villi per centimeter (V/cm), the villus height (Vh), mitoses per crypt (M/C) and protein and DNA contents of the mucosa were evaluated in samples from the terminal ileum. Radiation increased the number of positive MLN cultures, while treatment with GH and IGF-I reduced them significantly. V/cm, Vh, M/C, protein and DNA contents were significantly increased in all irradiated animals treated with GH and IGF-I. In conclusion both GH and IGF-I are not only capable of improving the mucosal integrity but also to reduce the bacterial translocation that follows intestinal radiation. In small doses IGF-I could reproduce the effects of GH and in some parameters the effects were more pronounced, although not statistically significant. This suggests that the effects of GH on intestine could be mediated through the local and systemic generation of IGF-I.

Orall-2-Oxo-4-thiazolidine Reduces Bacterial Translocation after Radiation in the Fischer Rat

Glutathione (GSH) is important in protecting rapidly dividing intestinal cells against free radicals generated following radiation.l-2-Oxo-thiazolidine (OTZ) promotes GSH synthesis through increased cysteine delivery. We hypothesize that oral supplementation with OTZ will augment GSH levels and decrease the incidence of bacterial translocation after abdominal radiation, and these effects will be abrogated by treating with a blocker of GSH synthesis, buthionine sulfoximine (BSO). Fischer rats received by oral gavage either OTZ (OTZ/rad), OTZ plus BSO (OTZ/BSO/rad), or saline (sal/rad) 4 hr prior to and 18 hr after radiation. One group underwent saline gavage and no radiation (ctl/sal). On Day 4, animals were sacrificed and mesenteric lymph nodes (MLN) were cultured. Liver and jejunum were removed for GSH analysis by HPLC. Nonradiated, ctl/sal had higher levels of hepatic and jejunal GSH than ctl/rad (13.0 ± 1.2 vs 9.7 ± 1.5, 11.2 ± 1.0 vs 7.8 ± 2.5 μmol/g dry wt,P< 0.05). Supplementation with OTZ (OTZ/rad) increased hepatic and jejunal GSH levels but treatment with OTZ and BSO (OTZ/BSO/rad) eliminated this benefit (12.0 + 2.6 vs 9.5 + 1.7, 10.1 + 2.4 vs 5.9 + 1.3 μmol/g dry wt,P< 0.05). Ctl/rad had a high rate of positive MLN cultures (80%) compared to ctl/sal and OTZ/rad (10 and 30%,P< 0.05). Treatment with OTZ and BSO (OTZ/BSO/rad vs OTZ/rad, 70 and 30%,P< 0.05) reversed the benefit of OTZ supplementation. This study demonstrated whole abdominal radiation depleted both hepatic and jejunal levels of GSH. Uniquely, OTZ supplementation restored hepatic and jejunal levels of GSH and decreased rate of bacterial translocation.

Bacterial translocation to mesenteric lymph nodes is increased in cirrhotic rats with ascites

Background/Aims: Cirrhotic patients are predisposed to develop spontaneous bacteremias and/or peritonitis, mainly caused by enteric bacteria. The aim of this study was to investigate if bacterial translocation, which is the passage of bacteria from the intestinal lumen to regional lymph nodes and/or the systemic circulation, is increased in a rat model of cirrhosis. Methods: Rats were studied after 12–16 weeks of CCl 4 inhalation, when samples of mesenteric lymph nodes, blood, liver, and spleen for standard bacteriologic cultures and a fragment of colon and liver for histology were obtained. Immunostaining of the cecum was performed using a polyclonal anti- Escherichia coli antibody. Results: A significantly greater proportion of rats with cirrhosis and ascites (5 of 9; 56%) had positive mesenteric lymph node cultures compared with cirrhotics without ascites (0 of 9) and normal controls (0 of 12) ( P < 0.01). In one cirrhotic rat, E. coli was isolated from both mesenteric lymph nodes and ascites. Rats with cirrhosis and ascites had significantly greater cecal submucosal edema and inflammation than rats with no ascites and controls. Immunoreactivity with E. coli was present in the cecal wall in 3 of 5 animals with E. coli translocation to mesenteric lymph nodes. Conclusions: In cirrhotic rats, bacterial translocation is increased after the development of ascites and may be a major factor in the development of spontaneous infections in cirrhosis.

Bacterial Translocation in Acute and Chronic Portal Hypertension

Patients with cirrhosis are predisposed to develop spontaneous bacteremias and peritonitis, mainly by enteric bacteria. Portal hypertension, by producing congestion and edema of the bowel wall, could increase the passage of bacteria from the intestinal lumen to regional lymph nodes to the systemic circulation or to both, a process termed bacterial translocation. The aim of this study was to investigate bacterial translocation at two stages of experimental portal hypertension: (a) acute (when shunting is minimal); and (b) chronic (when shunting is extensive and mimics the portal hypertension of cirrhosis). Rats were killed 2 days (acute) or 15 days (chronic) after partial portal vein ligation or control surgeries. Samples of mesenteric lymph nodes, blood, liver and spleen for standard bacteriological cultures and a fragment of ileum for histological examination were obtained. Two days after surgery, a significantly greater proportion of rats with acute portal hypertension (12 of 13 or 92%) had positive mesenteric lymph node cultures compared with both control groups: sham-operated (4 of 13 or 31%) and inferior vena cava-ligated (3 of 10 or 33%) animals (p < 0.01). However, 15 days after surgery no differences in translocation to mesenteric lymph nodes were found between rats with chronic portal hypertension (3 of 15 or 20%) and sham-operated controls (3 of 11 or 27%). In neither the acute nor the chronic rats were bacteria isolated from blood, spleen or liver. Rats with acute portal hypertension had significantly greater mesenteric inflammation than rats with chronic portal hypertension and control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial translocation in mesenteric ischemia-reperfusion injury: Is dysfunctional motility the link?

The authors previously reported that mesenteric ischemia and reperfusion ( I R ) in a chronic newborn piglet model creates dysfunctional intestinal motility. Whether this leads to inadequate bacterial clearance and translocation (BT) through the gastrointestinal tract remains unclear. To test this hypothesis the authors used their chronic piglet model (weight, 3.5 ± 0.3 kg; age, 18 ± 4 days; on formula feeding); nonocclusive mesenteric ischemia was induced via reversible pericardial tamponade. Mesenteric flow (SMA Doppler measurement via the retroperitoneal approach) was decreased to 25% ± 5% of baseline for 300 minutes in the ischemia group (n = 7) and followed by 14 hours of reperfusion in the I R group (n = 6). Control subjects had a sham operation (n = 7). Mesenteric lymph nodes (MLN), liver (L), spleen (S), ileum, peritoneum, and blood were harvested for blind quantitative microbial analysis. Subjects in the control group had no cultures positive for growth. Eighty-five percent of animals in the ischemia group had positive MLN cultures only ( P < .05 v control). All piglets in the I R group had positive MLN cultures ( P < .05 v control), and one third of them manifested bacteremia. Histological examination did not show mucosal disruption in any group. The validity of this model is confirmed by the negative cultures in the control group and by the presence of normal ileal flora in all animals. In the ischemia and I R groups, MLN cultures were consistently positive with gram-negative bacilli ( Escherichia coli and/or Klebsiella pneumoniae). When subjects of the I R group had more than 1,000 colonies in the MLN, bacteremia with the translocating organisms was also identified. The overall solid organ (L&S) translocation rate was 17% in the I R group but absent in the ischemia-only group. Variables known to contribute to BT were eliminated in our model. The peritoneal cavity was not violated, subjects were studied without the influence of any drugs or anesthesia, and mesenteric ischemia was accomplished without mechanical manipulation of the SMA or hypovolemic shock. To our knowledge, this is the first report of an infant animal model that demonstrates the occurrence of enteric BT following ischemia and I R injury. We suggest that BT is mediated by the dysfunctional motility induced by I R , an abnormality that may be operant in many critically ill infants.

Inhibition of bacterial translocation in obstructive jaundice by muramyl tripeptide phosphatidylethanolamine in the rat

Obstructive jaundice is frequently associated with septic complications and enteric bacteria have been isolated from both the infectious focus and bile in jaundiced patients. The present study aimed to evaluate bacterial translocation and the influence of a macrophage-stimulant (muramyl tripeptide phosphatidylethanolamine) on bacterial translocation in obstructive jaundice. Male Sprague-Dawley rats were subjected to sham operation (n = 10) or common bile-duct ligation and transection (n = 35). Two weeks later, jaundiced animals received either physiological saline (n = 15), muramyl tripeptide phosphatidylethanolamine liposomes (n = 10) or placebo (empty) liposomes (n = 10) orally, while sham-operated rats received physiological saline, 48 h prior to evaluation of enteric bacterial translocation. Blood, bile and caecal contents were collected and cultured aerobically and anaerobically, as were tissue samples from the liver, spleen and mesenteric lymph nodes. Positive mesenteric lymph node cultures in animals with jaundice + saline (7/15; 47%) and jaundice + placebo liposomes (4/10; 40%) significantly differed (p < 0.05) from sham-operated animals (1/10; 10%) and muramyl tripeptide phosphatidylethanolamine treated animals (0/10). Caecal counts (CFU/g) of Escherichia coli, Lactobacilli and aerobic and microaerobic bacteria did not differ statistically among the groups, although the number of E. coli tended to be higher in jaundiced animals. Thus, liposomal muramyl tripeptide phosphatidylethanolamine inhibits bacterial translocation, probably by activating mucosal macrophages and enhancing reticuloendothelial system function in rats with biliary obstruction.

Bacterial translocation in acute and chronic portal hypertension

Patients with cirrhosis are predisposed to develop spontaneous bacteremias and peritonitis, mainly by enteric bacteria. Portal hypertension, by producing congestion and edema of the bowel wall, could increase the passage of bacteria from the intestinal lumen to regional lymph nodes to the systemic circulation or to both, a process termed bacterial translocation. The aim of this study was to investigate bacterial translocation at two stages of experimental portal hypertension: (a) acute (when shunting is minimal); and (b) chronic (when shunting is extensive and mimics the portal hypertension of cirrhosis). Rats were killed 2 days (acute) or 15 days (chronic) after partial portal vein ligation or control surgeries. Samples of mesenteric lymph nodes, blood, liver and spleen for standard bacteriological cultures and a fragment of ileum for histological examination were obtained. Two days after surgery, a significantly greater proportion of rats with acute portal hypertension (12 of 13 or 92%) had positive mesenteric lymph node cultures compared with both control groups: sham-operated (4 of 13 or 31%) and inferior vena cava-ligated (3 of 10 or 33%) animals (p &lt; 0.01). However, 15 days after surgery no differences in translocation to mesenteric lymph nodes were found between rats with chronic portal hypertension (3 of 15 or 20%) and sham-operated controls (3 of 11 or 27%). In neither the acute nor the chronic rats were bacteria isolated from blood, spleen or liver. Rats with acute portal hypertension had significantly greater mesenteric inflammation than rats with chronic portal hypertension and control animals. Results suggest that portal hypertension alone may not be a major factor in the development of spontaneous infections in cirrhosis and that other mechanisms, such as a defective immune system, may be more important. (Hepatology 1993;17:1081-1085.)

Bacterial translocation after major hepatectomy in patients and rats.

Bacterial infections are frequent complications after liver resection. Of 138 patients who underwent major hepatectomy, 11 patients (8%) developed intra-abdominal sepsis in the postoperative period. Seven bacterial strains of gut origin were isolated from the abdominal cavity. Eight patients had multiple bacteria cultured. In the experimental studies on rat models, positive mesenteric lymph node cultures were seen 2 hours after removal of 70% and 90% of the total weight of the rat liver, and 12 hours after 50% hepatectomy, persisting for 3 and 4 days after 50% and 70% hepatectomy, respectively. The incidences of bacteremia 2 and 4 hours after 90% hepatectomy were 80% and 100%, respectively; 6 hours after 70% liver resection, the incidence of bacteremia was 33%. Blood cultures were positive in only 6% of the rats following 50% hepatectomy, and in none of the controls. Thus, bacterial translocation occurs in the early course after hepatectomy, the incidence being proportional to the amount of liver tissue removed.

Neurotensin reduces microbial translocation and improves intestinal mucosa integrity after abdominal radiation.

The effect of neurotensin (NTN) on preventing microbial translocation and preserving intestinal mucosal integrity after abdominal radiation was studied in rats. Animals were divided into the following groups: I (control), II (radiation control) and III (radiation and NTN). Radiation (1,100 cGy) was administered on the 1st day to groups II and III. NTN (300 micrograms/kg) was given intraperitoneally to group III animals, once daily for 3 days. On the 4th day, mesenteric lymph nodes (MLN) were obtained and cultured. Villi per centimeter (V/cm), villus height (Vh) and mitoses per crypt (M/c) were evaluated from ileal mucosa. Radiation increased positive MLN cultures, while treatment with NTN reduced them significantly. V/cm and Vh also returned to normal levels after NTN treatment, while M/c were increased in all irradiated animals. It was shown that NTN reduces bacterial translocation after abdominal radiation. Examination of ileal mucosa indicates that this can be attributed to the improvement of the mucosal integrity, due to the trophic effect of the hormone on the gut.

Cytomegalovirus Infection Promotes Bacterial Translocation in Thermally Injured Mice

Thermally injured mice that were given intraperitoneal injections of murine cytomegalovirus (MCMV) appeared to be clinically septic and to have increased mortality rates. To evaluate the possible role of MCMV infection in promoting bacterial translocation in burned mice, mesenteric lymph nodes were cultured from two strains of mice (BALB/c and CBA) that were given thermal injuries alone, MCMV alone, or both. BALB/c mice injected with 5 X 10(5) plaque-forming units MCMV following a 15% to 16% total body surface area scald injury had increased incidence of positive mesenteric lymph node cultures compared with other groups. No intestinal mucosal histologies, mucosal dry weights, or wet-to-dry weight ratios in any animals were abnormal. Differences in cecal bacterial concentrations were not observed. Murine cytomegalovirus infection appears to enhance bacterial translocation in this model.