Catastrophic gastrointestinal injury due to battery acid ingestion.

BACKGROUND: Acids account for 20% of all chemical exposures through various routes. Caustic acids such as hydrochloric and sulfuric acid are common ingredients in many household and industrial products. Due to the corrosive properties of these substances, tissue injury caused by oral exposure can lead to severe esophageal and gastrointestinal burns. CASE REPORT: We report a case of a patient presenting with severe acidosis, who required multiple laparoscopic evaluations to assess various gastrointestinal tract injuries and who ultimately underwent total gastrectomy. The diagnosis was made primarily based on the arterial blood gas and esophagogastroduodenoscopy findings, as well as the pathological examinations of various biopsied and resected tissues showing hemorrhagic necrosis of the esophagus, stomach, and small bowel. This patient eventually admitted to having ingested an unspecified amount of battery acid. CONCLUSIONS: Collaborative efforts by Emergency Medicine, Pathology, and General Surgery services are required for timely diagnosis, treatment, and management of patients after caustic acid exposures.

IL-4 production by CD8+ lymphomatoid papulosis, type C, attracts background eosinophils.

There are two subsets of CD8+ T cells: Tc1 and Tc2. INF-gamma production by Tc1 cells causes granulomatous inflammation. IL-4 production by Tc2 cells attracts eosinophils. A 76-year-Caucasian female presented with CD8+ lymphomatoid papulosis (LyP), type C. We hypothesized that the LyP cells belonged to the Tc2 subset because of abundant background eosinophils. Hematoxylin and eosin and immunohistochemical stains were carried out on tissue sections from a skin punch biopsy. Antibodies for immunohistochemical stains included CD3, CD4, CD5, CD7, CD8, CD30, CD56, ALK-1, clusterin and IL-4. There was involvement of the dermis by a dense lymphoid infiltrate composed of large atypical cells and numerous eosinophils. The LyP cells expressed CD5, CD8, CD30 and IL-4. Keratinocytes showed a membranous pattern of immunoreactivity for IL-4. IL-4 production by CD8+ LyP, type C indicates that it belongs to the Tc2 subset. The cytokine milieu produced by the LyP cells attracted eosinophils. The IL-13R complex on keratinocytes bound IL-4 and produced a membranous staining pattern. Although CD8+ LyP is rare, we believe that this CD30+ lymphoproliferative disorder should be included in the World Health Organization-European Organization for Research and Treatment of Cancer classification of cutaneous T-cell lymphomas.

Decreased neutrophil response in a model of chronic intraperitoneal Klebsiella infection.

BACKGROUND: Previously, we developed an infection model by intraperitoneal (IP) injection of Klebsiella pneumoniae. The high early mortality rate prompted a study of the effect of gentamicin on the disease course. METHODS: Infection was induced in Balb/c mice by IP inoculation of 10(3) colony-forming units (cfu) of K. pneumoniae serotype 2. Mice then received either saline or gentamicin twice daily at 5 mg/kg/day. Survival and weight loss were determined daily over 14 days. Leukocyte counts (WBC) were performed on peritoneal lavage fluid (PL) and peripheral blood. Bacterial counts in blood, lung homogenate, and PL were determined by culture. RESULTS: A significant survival benefit was seen in the gentamicin group by 48 h (p < 0.05), which persisted at 14 days. Weight loss of 2 g (p < 0.05) occurred in all mice by day three, with recovery seen only in the gentamicin-treated mice. Mice that did not regain their weight by day seven or lost more than 4 g (20%) died. All animals had peritoneal bacteria recovered at all time points. The gentamicin group showed fewer bacteria at one day in lung, blood, and PL, the difference being significant for the PL. Gentamicin did not clear peritoneal bacteria, and counts remained at inoculum concentration (10(3) cfu), but elicited no significant neutrophil influx. Whereas there was a progressive increase in total lavage WBC over time, the gentamicin group showed no significant neutrophil influx in PL or lung until bacterial counts exceeded 10(5) cfu. CONCLUSIONS: Despite persistent intra-abdominal infection, gentamicin treatment significantly prolonged survival in this uniformly lethal model. Although antibiotic treatment did not suppress bacteremia, it did diminish bacterial spread from the blood to the lung. This procedure produced a clinically relevant, novel model of antibiotic-treated chronic intraperitoneal infection, which will allow future study of specific host defense mechanisms.

Antibiotic modulation in a clinically relevant model of chronic intraabdominal infection.

Continuous and twice-daily cefoxitin dosing was used in a highly lethal model of acute peritonitis in mice using intraperitoneal (IP) Klebsiella pneumoniae (Kpn). The purpose was to use antibiotics to create a model of chronic infection. Male Balb/c mice (averaging 20 g body weight) were inoculated IP with 10(3) colony-forming units (CFU) Kpn serotype 2. Controls received subcutaneous saline either twice daily or continuously. Antibiotic groups received 300 mg/kg per day of cefoxitin either twice daily or continuously. Survival and daily weight losses were determined. Another group was inoculated with 10(3) Kpn given twice daily saline or cefoxitin and harvested at 24 hours. Leukocyte counts were performed on peritoneal exudate cells (PEC) and peripheral blood. Cultures determined Kpn counts in blood, lung, and PEC. By 24 hours, saline-treated animals had lost more weight than cefoxitin mice (1 g vs. 2 g, P < 0.05). Continuous cefoxitin showed significant advantage with 50 per cent mortality at 5 days. Kpn levels were not significantly altered by cefoxitin. Cefoxitin treatment extended chronicity by preventing weight loss and increasing survival in a highly lethal, monomicrobial peritonitis model. This model will allow future study of specific host defense mechanisms over a prolonged time period.

Interleukin-10 suppresses natural killer cell but not natural killer T cell activation during bacterial infection.

Interleukin (IL)-10 is an anti-inflammatory cytokine known to modulate the outcome of sepsis by decreasing pro-inflammatory cytokine production, including IL-12, a main activator of natural killer (NK) cells. We hypothesized that neutralization of IL-10 would increase NK and natural killer T (NKT) cell activation through increased IL-12 in a mouse model of bacterial peritonitis. NK and NKT cell activations were measured by CD69 expression on NK1.1+/CD3- and NK1.1+/CD3+ cells after cecal ligation and puncture (CLP). NK cells were significantly more activated in mice treated with anti-IL-10 antibodies, whereas no such effect was observed in NKT cells. Similarly, intracellular interferon gamma (IFN-gamma) levels were increased in NK cells of anti-IL-10-treated mice, but not in NKT cells. IL-12 and IL-18 levels were increased in both CLP groups, but in anti-IL-10-treated mice, early IL-12 and late IL-18 levels were significantly higher than in controls. Survival at 18 h after CLP was lower in anti-IL-10 mice, which was associated with increased liver neutrophil accumulation. In summary, these data show an activating effect of IL-10 on NK, but not on NKT cells after CLP, which corresponded with decreased survival, higher IFN-gamma production, and increased remote organ neutrophil accumulation. These effects were not mediated by IL-12 and IL-18 alone, and reinforce a role for NK cells in remote organ dysfunction following peritonitis.