A case report on death from acute bacterial cholangitis accompanied by von Meyenburg complexes: Use of 16S rRNA gene sequencing to identify pathogenic microbes from postmortem formalin-fixed, paraffin-embedded tissue.

RATIONALE: In some cases, autopsy is the first opportunity to find a previously unrecognized critical infection. Pathogens are identified by various methods, such as microscopic examination, special stains, culture tests, and immunohistochemistry. Here, we report a case of 16S ribosomal RNA (rRNA) gene sequencing using a postmortem formalin-fixed, paraffin-embedded (FFPE) tissue, which was useful for identifying pathogenic microbes. PATIENT CONCERNS: Autopsy was performed on an 87-year-old man who had chronic renal failure and had developed sepsis from a central venous catheter infection 10 days before his death. Prior to these events, von Meyenburg complexes (VMCs) were also found during regular checkups. DIAGNOSIS: Postmortem microscopic examination revealed acute purulent cholangitis with numerous microabscesses, accompanied by VMCs. Gram-negative rods were observed in some microabscesses, which were considered causative pathogens. INTERVENTIONS: 16S rRNA gene sequencing using postmortem FFPE tissue. OUTCOMES: Pseudomonas aeruginosa was identified, different from the one detected in the central venous catheter culture while alive. LESSONS: 16S rRNA gene sequencing is a useful tool for identifying pathogenic microbes in postmortem FFPE tissues. This technique may be useful for amplicon sizes of approximately 100 bp or less.

Brunner's Gland Hyperplasias and Hamartomas in Association with Helicobacter pylori.

Background: The proliferative lesions of the Brunner's glands (BGs) are hyperplasia and hamartomas, and they are usually asymptomatic and very rarely diagnosed. The aetiology of these lesions is not yet clear. The aim of this study is to evaluate the clinical presentations of patients with BG hyperplasia and hamartomas and to assess the pathological features of these lesions in association with Helicobacter pylori (H. pylori). Methods: Our retrospective study included patients who underwent upper gastrointestinal system endoscopy between 2010 and 2015. The hospital records of 18 patients diagnosed with hyperplasia or hamartoma of BG were reviewed for the clinical and pathological findings. Data from patients with BG lesion were compared with 37 patients who had nonspecific duodenitis as the control group. Results: Female/male ratio in our study sample was 1/1. The age range was between 16 and 85 years with a mean age of 48.61. BG hyperplasia and hamartomas were found in 72.22 and 27.78% of the patients, respectively. The rate of H. pylori in gastric mucosa was 43.2% in the control group and 66.7% in the BG lesion group. In the BG lesion group, the rate of H. pylori was higher. H. pylori was identified in 60% of BG hamartomas and in 69.2% of hyperplastic BGs. Conclusion: Our study demonstrated that H. pylori may play an important role in the development of BG hyperplasia and hamartomas in association with chronic gastritis and duodenitis. This is probably due to chronic irritation.

Endobronchial hamartoma with obstructive pneumonia due to Nocardia asiatica.

A 60-year-old man who had diabetes had a history of hospitalization for pneumonia in the right lower lobe at the age of 57 years. He visited our facility complaining of fever and cough. He was admitted owing to pneumonia in the right lung. Computed tomography and bronchoscopy performed after admission revealed a tumor in the right basal bronchus. Nocardia asiatica was detected in a sputum culture. Complete resection of the bronchial tumor could not be achieved with a high-frequency snare, although the patient was preoperatively diagnosed as having hamartoma. The patient subsequently underwent resection of the right lower lobe due to his deteriorated clinical condition. The postoperative course was favorable, and there has been no recurrence of nocardiosis or bronchial hamartoma for 3 years.

A comparative ultrastructural and molecular biological study on Chlamydia psittaci infection in alpha-1 antitrypsin deficiency and non-alpha-1 antitrypsin deficiency emphysema versus lung tissue of patients with hamartochondroma.

BACKGROUND: Chlamydiales are familiar causes of acute and chronic infections in humans and animals. Human pulmonary emphysema is a component of chronic obstructive pulmonary disease (COPD) and a condition in which chronic inflammation manifested as bronchiolitis and intra-alveolar accumulation of macrophages is common. It is generally presumed to be of infectious origin. Previous investigations based on serology and immunohistochemistry indicated Chlamydophila pneumoniae infection in cases of COPD. Furthermore, immunofluorescence with genus-specific antibodies and electron microscopy suggested involvement of chlamydial infection in most cases of pulmonary emphysema, but these findings could not be verified by PCR. Therefore, we examined the possibility of other chlamydial species being present in these patients. METHODS: Tissue samples from patients having undergone lung volume reduction surgery for advanced alpha-1 antitrypsin deficiency (AATD, n = 6) or non-alpha-1 antitrypsin deficiency emphysema (n = 34) or wedge resection for hamartochondroma (n = 14) were examined by transmission electron microscopy and PCR. RESULTS: In all cases of AATD and 79.4% of non-AATD, persistent chlamydial infection was detected by ultrastructural examination. Intra-alveolar accumulation of macrophages and acute as well as chronic bronchiolitis were seen in all positive cases. The presence of Chlamydia psittaci was demonstrated by PCR in lung tissue of 66.7% AATD vs. 29.0% non-AATD emphysema patients. Partial DNA sequencing of four positive samples confirmed the identity of the agent as Chlamydophila psittaci. In contrast, Chlamydophila pneumoniae was detected only in one AATD patient. Lung tissue of the control group of non-smokers with hamartochondroma was completely negative for chlamydial bodies by TEM or chlamydial DNA by PCR. CONCLUSIONS: These data indicate a role of Chlamydophila psittaci in pulmonary emphysema by linking this chronic inflammatory process to a chronic infectious condition. This raises interesting questions on pathogenesis and source of infection.

Low prevalence of Helicobacter pylori infection in patients with hamartomatous fundic polyps.

Helicobacter pylori infection of the gastric mucosal surface was investigated in patients with hamartomatous fundic polyps or hyperplastic polyps and in patients without endoscopic evidence of disease (healthy subjects). Presence of H. pylori infection was determined by culture, histologic examination, and the endoscopic phenol red test. Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral biopsy specimens. Both prevalence of H. pylori infection (P < 0.001) and H. pylori adherence (P < 0.05) were less in patients with hamartomatous fundic polyps than in healthy subjects and patients with hyperplastic polyps. However, the percentages of plasma cells in gastric mucosa that contained IgA and of gastric epithelial cells that expressed Lewis b did not differ significantly among the three groups. These findings suggest that defense mechanisms against the attachment of H. pylori other than IgA or Lewis b antigen are present in patients with hamartomarous fundic polyps.