Pseudomembrane Formation Research Articles

TERMINAL ILEUM PERFORATION SECONDARY TO Clostridium difficile ENTERITIS

Pseudomembranous colitis occurs in patients in whom the normal balance of colonic flora has been disturbed, allowing the overgrow of Clostridium difficile (C. diff). The distribution of pseudomembrane formation is generally restricted to the colon with abrupt termination at the ileocecal valve. Pseudomembrane formation involving the small bowel is extremely unusual. We present two cases of patients with intestinal perforation secondary to C. diff enteritis and compare them with seven cases reported in the literature in the last ten years. Small bowel C. diff enteritis is a rare entity. Presenting symptoms are similar to those of C. diff colitis, but may be more severe, with higher mortality rate. The majority of patients, in this review, were older, with prior gastrointestinal surgery. Although rare, C. diff enteritis should be part of the differential diagnosis in any septic patient with persistent severe diarrhea, despite correct antibiotic therapy and colectomy for C. diff colitis.

Fatal necrotic enteritis associated with Clostridium perfringens in wild crows (Corvus macrorhynchos)

Sporadic outbreaks of fatal enteritis occurred among free-living wild crows (‘large billed’ or ‘wok’ crow; Corvus macrorhynchos) in an open-air park in Japan in 2002. Eight crows were found dead during February, followed by two more in September, and five of the eight were examined histopathologically. At necropsy, all cases showed a markedly dilated small intestine, especially the jejunum and ileum, with large amounts of gas, and dark red to greenish–brown soft content. The necrotic intestinal wall was markedly thickened with multifocal haemorrhages. All cases had multifocal white foci in the liver, and four cases showed marked splenomegaly. Histologically, there was severe necrotic enteritis characterized by extensive mucosal necrosis and multifocal haemorrhages, as well as inflammatory cell infiltrations. A prominent pseudo-membrane formation was noted in the affected intestine. Severe adhesive peritonitis was also observed in three cases. Gram-positive bacilli were present in large numbers in the lumen, and in and around necrotic lesions in the affected intestine. The bacilli were positive for Clostridium perfringens enterotoxin type A by immunohistochemistry, and were also positive for C. perfringens type A using the immunofluorescence method. C. perfringens was isolated by anaerobic culture from the intestinal contents. The present enteritis was thought to be induced by proliferated C. perfringens in the intestine, and to be the cause of death.

Subcutaneous pseudomembranous fat necrosis: new observations.

Pseudomembranous fat necrosis is a peculiar manifestation of necrosis of adipose tissue characterized by formation of pseudocystic cavities lined by crenulated membranes. The underlying mechanism for the formation of pseudomembranes is unknown and numerous hypotheses have been proposed. Despite divergent interpretations, most authors consider necrotic fat cells to be the anatomic substrate for the formation of pseudomembranes. A total of 341 panniculitides were reviewed for the presence of pseudomembranous fat necrosis. The specific diagnoses were established after correlation of all available clinical and laboratory data with the histopathology. Special attention was given to the time in the evolution of the disease when the biopsy was taken. Additional immunohistochemical studies were performed in 12 cases. Thirty of 341 cases of different types of panniculitides were found to show pseudomembranous fat necrosis, namely: 10 of 15 cases of sclerosing panniculitis (lipodermatosclerosis), 6 of 95 cases of erythema nodosum, 7 of 34 cases of traumatic panniculitis, 1 of 7 cases of lupus panniculitis, 1 of 20 cases of erythema induratum Bazin (nodular vasculitis), 1 of 9 cases of necrobiosis lipoidica, 1 of 4 cases of sclerotic lipogranuloma, 1 of 9 cases of infectious panniculitis (erysipelas), 1 of 2 cases of pancreatic panniculitis, and 1 of 4 cases of subcutaneous sarcoidosis. Pseudomembranous fat necrosis labelled strongly for the histiocytic markers CD68 and lysozyme. Our series provides data suggesting that pseudomembranous fat necrosis represents a dynamic process that varies according to the evolution of the lesion at the time of the biopsy. In biopsies taken from early foci of panniculitides pseudomembranes show vescicular or picnotic nuclei. Later, pseudomembranes retain their crenulated appearance but lack nuclear elements. Furthermore, we present histopathologic, histochemical, and immunohistochemical evidence that pseudomembranous fat necrosis results from the interaction of residual products of disintegrated fat cells and macrophages. Histiocytic markers such as CD68 and lysozyme may be used as reliable tools in order to detect pseudomembranes in panniculitides.

Bupropion-Induced Erythema Multiforme

Bupropion-Induced Erythema Multiforme

Pathology of shell disease in the blue crab, Callinectes sapidus Rathbun, (Decapoda: Portunidae)

Blue crabs affected with shell disease displayed a wide array of pathologies in response to this very common affliction. Grossly, shell disease lesions most commonly presented as variably sized brown to black foci. Such lesions ranged from very small (1 mm2) to locally extensive (up to 200 mm2 in area). The larger of the melanized lesions sometimes appeared ulcerated. The most severe lesions observed (Pamlico River shell disease-PRSD) resulted in loss of up to 25% of the entire carapace. A diverse bacterial flora consisting of aeromonads, vibrios and five other genera were isolated as the predominant organisms from shell disease lesions. Fungi were rarely observed in larger lesions. Protozoa and algae were also rarely observed on the surface of some lesions. Histologically, lesions ranged from mild erosion of the epicuticle and outermost layers of the calcified endocuticle to more extensive endocuticle erosion with accompanying inflammation. In the most severe cases, there was total loss of the endocuticle and epidermis, with pseudomembrane formation, intense haemocyte infiltration, and involvement of adjacent viscera. There was no apparent relationship between the size of gross lesions and their histological severity (as defined by the extent of tissue damage), suggesting that gross examination of shell disease lesions is not a reliable method for assessing the damage to affected blue crabs.

The pathology of diphtheria.

Diphtheria is an acute, communicable disease caused by Corynebacterium diphtheriae. The disease is generally characterized by local growth of the bacterium in the pharynx with pseudomembrane formation or, less commonly, in the stomach or lungs; systemic dissemination of toxin then invokes lesions in distant organs. Acute disease of the upper respiratory tract usually involves one or more of the following: tonsillar zones, larynx, soft palate, uvula, and nasal cavities. A recent epidemic in Russia emphasized the role of vaccination in reducing disease in children and adults.

Diagnosis and management of pseudomembranous colitis and clostridium difficile- associated disease

Clostridium difficile-associated disease results in a wide spectrum of clinical manifestations, ranging from mild diarrhea to colitis, with or without pseudomembrane formation, to toxic megacolon, intestinal perforation, and death. This disease is considered primarily a nosocomial infection that is transmitted in an oral-fecal manner. Colonization with this anaerobic bacteria is often asymptomatic, but disease can result in those patients whose normal colonic flora has been altered by either antibiotics or antineoplastic agents. C difficile is responsible for virtually all cases of pseudomembranous colitis and 15–20% of cases of antibiotic-associated diarrhea without colitis. The treatment of choice for the majority of cases is oral metronidazole. Relapses occur and may require additional courses of oral antibiotics and other medications. Rapid diagnosis with either laboratory studies or endoscopy is necessary to avoid progression to life-threatening complications. Prevention is of utmost importance in order to curb the spread of this largely nosocomial pathogen and involves hygienic policies as well as antibiotic control programs.

Endoscopic diagnosis of lower intestinal lesions of leukaemia and malignant lymphoma.

There have been only a few endoscopic studies with respect to lower intestinal lesions of leukaemia and malignant lymphoma, although there have been many autopsy studies of these lesions. The aim of this study was to clarify these lesions using endoscopy. Colonoscopy was performed on 11 of 341 patients with leukaemia and on 32 of 105 patients with malignant lymphoma for frequent diarrhoea, anal bleeding or abnormal findings on barium enema examination, between April 1984 and September 1994. In eight of the 11 patients with leukaemia on whom endoscopy was performed, nine lesions were found; aphthoid ulcers, small ulcers or large tumours due to leukaemic infiltration were found in five, and colorectal adenoma was found in only one patient. Antibiotic-associated haemorrhagic colitis or pseudomembranous colitis was found in one patient each. In 10 of the 32 patients with malignant lymphoma, 11 lesions were found. The following were found in one patient each: large lymphomatous tumours, a large lymphomatous ulcer, multiple small polypoid lesions, multiple lymphomatous polyposis; and colorectal cancer or adenoma in six patients. However, the autopsy findings in patients with both diseases were mostly pseudomembrane formation or ulcers due to fungal and/or bacterial infection. It is concluded that accurate endoscopic diagnosis of lower intestinal lesions in patients with leukaemia or malignant lymphoma is essential for staging and treatment of these diseases and for determining their prognosis. Most lesions in leukaemia are aphthoid and small ulcers are due to leukaemic infiltration or antibiotics; most lesions in malignant lymphoma are elevated lesions such as cancer, adenoma or lymphomatous lesions as determined by endoscopy. This is in contrast to pseudomembrane formation or ulcers due to fungal and/or bacterial infection which are detected at autopsy.

Cytomegalovirus colitis complicated by perianal fistula: report of one case

Although gastrointestinal cytomegalovirus (CMV) disease most frequently occurs in adults with immune deficiency, such as the acquired immunodeficiency syndrome (AIDS), organ transplantation, cancer chemotherapy, and steroid therapy, it can occur in persons with normal immune function.1-3 Many manifestations of gastrointestinal CMV infection, including ulcerative lesions, perforation, hemorrhagic proctocolitis, inflammatory pseudotumor, lesions mimicking neoplasia, appendicitis, toxic megacolon, pseudomembrane formation, and pneumonitis intestinalis, have been observed.1-3 We describe a patient who developed a perianal fistula that was presumed to be due to CMV infection. To our knowledge, this is the first reported case of CMV colitis complicated by perianal fistula formation. CASE REPORT

Ligneous conjunctivitis: a clinicopathologic study of 3 cases.

The clinical, histopathologic features, and treatment outcomes in 3 patients with ligneous conjunctivitis are described. Bilateral, idiopathic membranes occurred in the palpebral conjunctiva in 2 patients. In 1 patient, unilateral conjunctival changes occurred in the bulbar conjunctiva, at the site of pterygium excision. Treatment included topical hyaluronidase, chymotrypsin, heparin, and cyclosporine and surgical excision with limited or no success. In one patient, conjunctival autografting from the normal fellow eye resulted in pseudomembrane formation at the donor site in the previously unaffected eye. Histopathological evaluation of excised membranes revealed the presence of amorphous eosinophilic hyaline material and chronic inflammatory cells. Immunohistochemical study revealed a predominance of T-lymphocytes. This case series confirms the recalcitrant clinical course of ligneous conjunctivitis. Conventional treatment modalities described in literature were not useful in the management of this condition. Surgical manipulation of the unaffected fellow eye in patients with unilateral disease can result in pathologic conjunctival changes, and is best avoided.

Cleaning up Clostridium difficile infection

Clostridium difficile infection affects mainly the elderly, among whom reported cases increased almost eight-fold between 1990 and 1994 in England and Wales. Here C difficile was the most commonly reported cause of intestinal infection in the elderly in 1994, ahead of both salmonella and campylobacter (figure). 1 Djuretic T Ryan MJ Fleming DM Wall PG Infectious intestinal disease in elderly people. Commun Dis Rep CDR Rev. 1996; 6: R107-R112 PubMed Google Scholar Elderly individuals may have impaired resistance to colonisation by C difficile, 2 Borriello SP Barclay FE An in-vitro model of colonisation resistance to Clostridium difficile infection. J Med Microbiol. 1986; 21: 299-309 Crossref PubMed Scopus (89) Google Scholar which in turn can lead to symptomless carriage, diarrhoea, or colitis (with or without pseudomembrane formation). C difficile is the commonest infective cause of hospital-acquired diarrhoea, but the true incidence of community-acquired C difficile infection is unknown because many laboratories do not routinely look for the bacterium or its toxin(s) in faecal specimens from general practice.

Clostridium difficile infection.

The spore-forming anaerobe Clostridium difficile has become a serious enteropathogen. Changes in the composition of natural intestinal flora, mainly due to antibiotic therapy, permit its colonization of, and multiplication in, the colon. The disease is caused by (entero)toxin A and (cyto)toxin B, and infection ranges from asymptomatic carrier state and mild diarrhea to pseudomembranous colitis. The clinical diagnosis is made by observing inflammatory, sometimes bloody, diarrhea and by the colonoscopic detection of epithelial necrosis, ulceration, and, in the advanced state, pseudomembrane formation. The laboratory supports the diagnosis by detecting toxin A and/or B by an enzyme-linked immunoassay with high specificity, but sometimes less sensitivity than with the cytotoxin assay in tissue culture cells. Fecal leukocytes or fecal lactoferrin may be found. Culture for the isolation and identification of toxigenic C. difficile is time consuming but necessary for epidemiological studies. Polymerase chain reaction (PCR) tests have been tested for detection of the toxin B gene directly in stool. Therapy consists of stopping all systemic antibiotic treatment and the use of oral metronidazole or vancomycin. There may be more relapses after vancomycin therapy, and the increasing vancomycin resistance of Enterococcus is worrisome. Prevention, especially of nosocomial spread, requires isolation and enforced handwashing. For epidemiological studies, the bacteria can be typed by molecular DNA analyses, including PCR, protein electrophoresis, and immunological tests.

Effect of epidermal growth factor on tympanic membranes with chronic perforations: A clinical trial

Epidermal growth factor is an important modulator of cell growth, and its role in normal wound healing is well documented. Epidermal growth factor receptors have been identified in tympanic membranes of different animals. The ability of epidermal growth factor to promote healing of tympanic membrane perforations has recently been shown in experimental animals. We performed a double-blind, placebo-controlled study of the effect of epidermal growth factor applied locally on the tympanic membrane for 1 week in patients with chronic perforations. Seventeen adult patients took part in the study, eight in the epidermal growth factor group and nine in the placebo group. Three placebo-treated patients were later treated with epidermal growth factor, and five patients received repeated epidermal growth factor treatment. Perforation size was measured as a percentage of the tympanic membrane area before and at least 1 month (mean, 2.6 months) after treatment. One perforation in the placebo group healed completely, but none of the epidermal growth factor-treated perforations closed. Perforations became slightly smaller in both groups (mean decrease, 0.3% and 2.7% for epidermal growth factor and placebo, respectively), but these changes in size were not statistically significant for either group. At otomicroscopy, a proliferation reaction with thickening of the tympanic membrane and pseudomembrane formation at the perforation edge could be seen in some ears. Histologically, a sample from one epidermal growth factor-treated ear demonstrated signs of hypertrophic epithelium when compared with the morphology of a placebo-treated tympanic membrane. The only complications were two mild infections in the placebo group. Hearing remained stable after epidermal growth factor treatment. (OTOLARYNGOL HEAD NECK SURG 1995;113:375-9.)

Effect of Epidermal Growth Factor on Tympanic Membranes with Chronic Perforations: A Clinical Trial

Epidermal growth factor is an important modulator of cell growth, and its role in normal wound healing is well documented. Epidermal growth factor receptors have been identified in tympanic membranes of different animals. The ability of epidermal growth factor to promote healing of tympanic membrane perforations has recently been shown in experimental animals. We performed a double-blind, placebo-controlled study of the effect of epidermal growth factor applied locally on the tympanic membrane for 1 week in patients with chronic perforations. Seventeen adult patients took part in the study, eight in the epidermal growth factor group and nine in the placebo group. Three placebo-treated patients were later treated with epidermal growth factor, and five patients received repeated epidermal growth factor treatment. Perforation size was measured as a percentage of the tympanic membrane area before and at least 1 month (mean, 2.6 months) after treatment. One perforation in the placebo group healed completely, but none of the epidermal growth factor-treated perforations closed. Perforations became slightly smaller in both groups (mean decrease, 0.3% and 2.7% for epidermal growth factor and placebo, respectively), but these changes in size were not statistically significant for either group. At otomicroscopy, a proliferation reaction with thickening of the tympanic membrane and pseudomembrane formation at the perforation edge could be seen in some ears. Histologically, a sample from one epidermal growth factor-treated ear demonstrated signs of hypertrophic epithelium when compared with the morphology of a placebo-treated tympanic membrane. The only complications were two mild infections in the placebo group. Hearing remained stable after epidermal growth factor treatment.

Candidiasis caused by Candida glabrata in the forestomachs of a calf

A female Japanese black calf suffering from diarrhoea was treated with six different antibiotics for 9 days. The diarrhoea worsened and the calf was killed when 17 days old. At necropsy, the mucosal surface of the forestomachs showed diffuse haemorrhagic necrosis and pseudomembrane formation. Candida glabrata infection was diagnosed histologically, immunohistochemically, and by isolation and examination of the yeast. The intensive antibiotic treatment was considered to have been a predisposing or exacerbating factor. This is the first report of C. glabrata infection of the bovine forestomachs.

Antibiotic-Associated Pseudomembranous Enteritis Due to Clostridium difficile

Although pseudomembranous colitis is relatively common following antibiotic exposure, there have been few reported cases of pseudomembrane formation involving the small intestine. Herein we report a case of pseudomembranous enteritis of the small and large intestine that occurred after antibiotic exposure. The etiologic organism appears to be Clostridium difficile, as evidenced by the characteristic pseudomembranous lesions and a positive ELISA for toxin A in an ileal tissue specimen.

Pseudomembranous colitis in sickle cell disease responding to exchange transfusion

We report a case of ischemic colitis with pseudomembrane formation in a 6 1/2-year-old boy with sickle cell disease that responded to medical management including exchange transfusion. This case was not associated with Clostridium difficile infection but with an elevation of serum levels of tumor necrosis factor alpha. This rare complication of sickle cell disease has been reported only in adults.

Pathologic Cuticular Changes of Winter Impoundment Shell Disease Preceding and During Intermolt in the American Lobster, Homarus americanus.

Cuticular lesions from twenty-four market sized lobsters (Homarus americanus) with winter impoundment shell disease were examined. Histological descriptions of cuticular lesions were correlated with the substage of molt for each lobster, because cuticle components and inflammatory mechanisms vary in each. A lesion severity grading system was developed and applied to four specific substages of the five-stage (A-E) molting cycle. Lesions present in substage C4, in which the membranous layer is deposited, and D0 (passive premolt) were divided into five grades, ranging from mild erosions (Grade I) to severe ulceration (Grade V) of the cuticle. Cuticular lesions from lobsters in C4/D0 were compared with cuticular lesions from lobsters in substages C2/C3. Defensive mechanisms exhibited by animals in all substages were epicuticle deposition, melanization, inflammatory cell infiltration, and pseudomembrane formation. In addition, animals in C4 and D0 showed proliferation of the membranous layer in affected foci. The lesion grading scheme presented in this paper can be used to describe and compare both inter- and intraspecies crustacean shell lesions.

The Morphology of Smoke Inhalation Injury in Sheep

Pulmonary injury resulting from inhalation of chemical and particulate products of incomplete combustion is one of the principal determinants of mortality following burn injury. In this study, the histopathology of inhalation injury was examined in sheep. Mild, moderate, or severe smoke injury was produced in anesthetized sheep by insufflation with various doses of ambient temperature smoke, generated by burning polyethylene, wood pulp, and nonwoven cellulose pads. A total of 64 sheep were exposed and evaluated at times ranging from 15 minutes to 4 weeks after exposure. Morphologic changes in the lungs were studied using light microscopy and both transmission and scanning electron microscopy. The primary, dose-responsive injury observed was acute cell membrane damage in the trachea and bronchi leading to edema, progressive necrotic tracheobronchitis with pseudomembrane formation, and airway obstruction. These inflammatory and occlusive effects were followed by congestion, alveolar space edema, atelectasis, and bronchopneumonia. Morphologic changes occurring in the alveolar epithelium following high smoke dosage included intracellular edema in type-I cells, changes in the membrane-bound vacuoles of type-II cells, and septal thickening caused by interstitial edema. No capillary endothelial changes were observed.

Bacterial Tracheitis: Report of Eight New Cases and Review

Bacterial tracheitis, previously referred to as nondiphtheritic laryngitis with marked exudate, was commonly discussed in pediatric textbooks before 1940. It seemed to disappear as a clinical entity after that time, but it has been recorded with increasing frequency in the pediatric literature since 1979. We describe eight new cases and review 110 previously described cases. The clinical course consists of a prodromal upper respiratory illness with stridor, fever, and a variable degree of respiratory distress. Unlike patients with croup, patients with bacterial tracheitis do not respond to aerosolized racemic epinephrine. Most patients require endotracheal intubation; some require tracheostomy. Reported complications include pneumonia, pneumothorax, formation of pseudomembranes, toxic shock syndrome, and cardiopulmonary arrest. Bacterial tracheitis is a secondary bacterial infection following a primary viral respiratory infection. The most common preceding viral infection is parainfluenza. Staphylococcus aureus and Haemophilus influenzae are the predominant causes of bacterial tracheitis. Secondary bacterial infection may occur as a result of tracheal mucosal injury or impairment of normal phagocytic function due to viral infection.