Colonic Angiodysplasia with a Huge Submucosal Hematoma in the Sigmoid Colon.

Colonic angiodysplasia (AD) with bleeding as a comorbidity in the aging population is being increasingly reported. However, to our knowledge, there is no report on colonic AD accompanied by a huge hematoma. Herein, we report a case of colonic AD with a huge submucosal hematoma. A 75-year-old man with sudden melena was referred to our hospital. Helical computed tomographic angiography (CTA) revealed bleeding from the sigmoid colon. Additionally, colonoscopy showed a huge submucosal hematoma with bleeding in the sigmoid colon. As endoscopic hemostasis was difficult, sigmoidectomy was performed. The pathological diagnosis was colonic AD. The present case indicates that colonic AD should be considered in the differential diagnosis for melena. In addition, the case shows that helical CTA, which is a noninvasive imaging modality, is useful for the diagnosis of colonic AD and is as effective as colonoscopy and angiography for diagnosis.

Clinicopathological subclassification of biliary cystic tumors: Report of 4 cases with a review of the literature.

Biliary cystic tumors are rare hepatic neoplasms, and knowledge regarding the origin and pathology of these tumors remains vague. They should be analyzed in more detail. In our institution, 4 biliary cystic tumor surgeries were performed between December 1999 and March 2010. Pathological evaluation of resected specimens was performed to evaluate the characteristics of the intracystic epithelium and to determine the presence or absence of interstitial infiltrate, ovarian mesenchymal stroma (OMS), luminal communication between the cystic tumor and the bile duct, and mucin (MUC) protein expression. We evaluated the following 4 cases: case 1, a 21-year-old woman with a biliary cystadenoma who underwent extended right hepatectomy; case 2, a 39-year-old woman with a biliary cystadenoma who underwent left hepatectomy; case 3, an 80-year-old man with a biliary cystadenoma who underwent left hepatectomy; and case 4, a 61-year-old man with a biliary cystadenocarcinoma revealing papillary proliferation of atypical epithelium and interstitial infiltrates who underwent left hepatectomy. Case 3 had papillary proliferation of the intracystic atypical epithelium but showed interstitial infiltrates. Luminal communication with the bile duct, centrally or peripherally, was found in all 4 cases. Only case 2 showed OMS. Immunohistochemical staining revealed the following findings: cases 1 and 2, MUC1-/MUC2-; case 3, MUC1+/MUC2-; and case 4, MUC1+/MUC2+. It is important to gather information on more cases of biliary cystic tumors because atypical cases were observed, where both OMS and luminal communication with the bile duct were present or absent.

Prototheca cutis sp. nov., a newly discovered pathogen of protothecosis isolated from inflamed human skin.

A strain of a novel pathogenic, achlorophyllic alga belonging to the genus Prototheca was isolated from the inflamed skin of a patient with protothecosis in a Japanese hospital. The pathogen was detected and isolated in biopsy specimens by histopathology and culture-based examination. Analyses of the nuclear 18S rDNA gene and 26S rDNA gene D1/D2 domain sequences and chemotaxonomic studies indicated that this strain represents a novel species with a close phylogenetic relationship to Prototheca wickerhamii and Auxenochlorella protothecoides. This strain grew well at 28-30 degrees C, showed slow and weak growth at 37 degrees C, and no growth at 40 degrees C. This strain grew in vitamin-free medium and assimilated acetate (pH 5.1), l-arabinose and soluble starch as a carbon source. The taxonomic description of Prototheca cutis sp. nov. is proposed (type strain JCM 15793(T) =CBS 11262(T) =DSM 22084(T)) as a pathogen of dermatitis.

[A case of Streptococcus suis endocarditis, probably bovine-transmitted, complicated by pulmonary embolism and spondylitis].

Streptococcus suis, a major global porcine pathogen, is an emerging zoonosis in Southeast Asia that triggered a 2005 outbreak in China. S. suis causes meningitis, sepsis, and endocarditis in both pigs and humans and involves significant mortality. We report the case of a previously healthy 50-year-old dairy farmer who developed S. suis type 2 endocarditis complicated by pulmonary embolism and spondylitis. He experienced a high fever, chills, fatigue, and worsening low back pain in the 6 weeks prior to admission. On physical examination, he had lumbar spine tenderness and weakness of the left leg. Blood culture identified penicillin-sensitive S. suis type 2. Echocardiography showed vegetation on the tricuspid valve, and magnetic resonance imaging (MRI) showed signs of spondylitis. The man reported sudden chest pain several days after admission, which computed tomography (CT) showed what was diagnosed as a septic pulmonary embolism. He was treated with penicillin G for 4 weeks and gentamicin for the first 2 weeks, followed by 2 weeks of oral amoxicillin, after which his symptoms gradually improved. The infection source was probably his dairy herd, since calves often bit his fingers while feeding and S. suis was found in their oral mucus. Over 400 cases of human S. suis infection have been reported globally, but this is, to our knowledge, the first known case of bovine transmission. All of Japan's 8 other cases involved occupational swine exposure, 5 of whom had injuries to their fingers. This emerging situation should be made known to all possibly involved in unprotected direct contact with swine and cattle, particularly when the skin could be compromised by cuts or abrasions.

Group A streptococcal cysteine protease degrades C3 (C3b) and contributes to evasion of innate immunity.

A relative lack of neutrophils around Streptococcus pyogenes is observed in streptococcal toxic shock syndrome (STSS). Because the bacteria spread rapidly into various organs in STSS, we speculated that S. pyogenes is equipped with molecules to evade the host innate immune system. Complement C3b opsonizes the pathogen to facilitate phagocytosis, and a complex of C3b converts C5 into anaphylatoxin. Because we found that C3 (C3b) is degraded in sera from patients with STSS, we investigated the mechanism of C3 (C3b) degradation by S. pyogenes. We incubated human C3b or serum with recombinant SpeB (rSpeB), a wild-type S. pyogenes strain isolated from an STSS patient or its isogenic DeltaspeB mutant and examined the supernatant by Western blotting with anti-human C3b. Western blot and Biacore analyses revealed that rSpeB and wild-type S. pyogenes rapidly degrade C3b. Additionally, C3 (C3b) was not detected in sera collected from infected areas of STSS patients. Furthermore, the survival rate in human blood and in mice was lower for the DeltaspeB mutant than the wild-type strain. Histopathological observations demonstrated that neutrophils were recruited to and phagocytosed the DeltaspeB mutant, whereas with the wild-type strain, few neutrophils migrated to the site of infection, and the bacteria spread along the fascia. We observed the degradation of C3 (C3b) in sera from STSS patients and the degradation of C3 (C3b) by rSpeB. This suggests that SpeB contributes to the escape of S. pyogenes from phagocytosis at the site of initial infection, allowing it to invade host tissues during severe infections.

[One case with Erysipelothrix rhusiopathiae endocarditis].

We report case of a 67-year-old alcoholic fisherman who developed infective endocarditis caused by Erysipelothrix rhusiopathiae. The initial manifestations were fever and back pain of approximately three months' duration. Auscultation of the heart revealed a loud systolic murmur at the apex and a diastolic murmur over the aortic valve area. Echocardiographic studies showed vegetations on both the aortic valve and mitral valve. Blood cultures grew Erysipelothrix rhusiopathiae, and it was sensitive to aminobenzyl penicillin. No other bacteria grew aut. A diagnosis of infective endocarditis caused by the Erysipelothnx rhusiopatniae was made, and the patient was treated with aminobenzyl penicillin 12g/day for 6 weeks. His clinical course was complicated by heart failure, multiple cerebral embolism, and renal infarctions. However, he recovered without valve replacement. Although the exact route of infection remains unknown, erosions of the skin, of his palms at the time of tho initial examination appeared to be one possible source of the systemic infection in this case. The serotype of the bacteria was Ib. To our knowledge this is the first case of serotyping of bacterium that caused endocarditis in humans.

[Epidemiological study on Streptococcus pyogenes strains isolated from the patients with streptococcal toxic shock syndrome (STSS) in Japan in 1992-2001].

To investigate clinical and microbiological features of streptococcal toxic shock syndrome (STSS), clinical, epidemiological, and bacteriological data obtained from 250 patients between 1992 and 2001 were analyzed. Among these 250 cases, 16 cases were excluded from the study because the causative microorganism were not Streptococcus pyogenes. 234 strains of S. pyogenes obtained from the aforementioned 234 cases were tested for T-type by a serological method, and for streptococcal pyrogenic exotoxin (SPE) by in vitro productivity of the toxin as well as molecular genetic methods. The number of patients was 141 (56.4%) for males, and 107 (42.8%) for females. The highest frequency of STSS was observed in those patients in their sixties in both sexes. The overall mortality rate was 43.2%. The mortality rate for male was 36.9%, and 52.3% for female. Bacteriological studies revealed that most common T types were T1 and T3. These strains consisted 54.3% of the strains collected. Among strains of T1 type, 98.8% possessed genes of spe A, and 46.1% were shown to produce SPE A in vitro. Among strains of T3 type, 82.9% possessed spe A gene, and all of these strains were shown to produce the toxin in vitro. It is concluded that certain strains of S. pyogenes, such as those with T1, or T3 type, and those with spe A gene or in vitro production of SPE A, are the most frequent cause of STSS. Although infections caused by such bacteria are quite common, STSS rarely occurs in most such patients. Additional factors, such as host factors, may play a crucial role in the pathogenesis of STSS.