Ulcer bacterial

Complications of pressure sores are not uncommon and may be life-threatening. Infection is one of the most serious and most frequently encountered complications of pressure ulcers. Bacterial colonization must be differentiated from true bacterial infection. While most pressure sore wounds are colonized, the majority of these eventually heal. When the tissue is infected, there is bacterial invasion of previously healthy tissue. Without treatment, an initial small, localized area of ulceration can progress rapidly to 5 to 6 cm within days. The visible ulcer is just a small portion of the actual wound up to 70% of the total wound is below the skin. A pressure-gradient phenomenon is created by which the wound takes on a conical nature the smallest point is at the skin surface, and the largest portion of the defect is at the base of the ulcer (Fig. 108-1). 

GI diseases ulcerative coHtis and anorectal disorders Bacterial meningitis... 

Deoxyribonuclease (DNAase), an enzyme that degrades deoxyribonucleic acid, has been used in patients with chronic bronchitis, and found to produce favorable responses presumably by degrading the DNA, contributed by cell nuclei, to inflammatory mucus (213). Lysozyme [9001 -63-2] hydrolyzes the mucopeptides of bacterial cell walls. Accordingly, it has been used as an antibacterial agent, usually in combination with standard antibiotics. Topical apphcations are also useful in the debridement of serious bums, cellulitis, and dermal ulceration. 

In extreme cases irritant chemicals can have a corrosive action. Corrosive substances can attack and weaken materials of construction, as mentioned in Chapter 3. They can also attack living tissue (e.g. to cause skin ulceration and in severe cases chemical burns), kill cells and possibly predispose to secondary bacterial invasion. Thus while acute irritation is a local and reversible response, corrosion is irreversible destruction at the site of the contact. The outcome is influenced by the nature of the compound, the concentration, duration of exposure, the pH (see Figure 4.1) etc. Thus dilute mineral acids may be irritant whereas at higher concentrations they may cause corrosion. 

Various conditions such as perforated peptic ulcer, cholecystitis, common bile duct and intestinal obstruction, trauma to the abdomen inducing pancreatitis and ruptured ectopic pregnancy may cause an elevated serum amylase but the levels are usually not as high as those found in acute pancreatitis. Mumps and bacterial parotitis, which block the secretion of salivary amylase are associated with mild elevations of serum amylase. 

Treat acute bacterial conjunctivitis with broad-spectrum antibiotics. Although the condition is usually self-limiting, antibiotic treatment decreases the spread of disease to other people and prevents extraocular infection. Additionally, treatment may help decrease the risk of corneal ulceration or other complications that affect sight. Finally, treatment speeds recovery.14... 

Bacterial keratitis is a broad term for a bacterial infection of the cornea. This includes corneal ulcers and corneal abscesses. The cornea in a healthy eye has natural resistance to infection, making bacterial keratitis rare. However, many factors predispose a patient to bacterial infection by compromising the defense mechanisms of the eye (Table 60-5).19... 

Cellulitis and erysipelas are bacterial infections of the skin. Although separate entities, there is some clinical difficulty in distinguishing the two. 0 Cellulitis is a bacterial infection of the dermis and subcutaneous tissue, whereas erysipelas is a more superficial infection of the upper dermis and superficial lymphatics. Although both can occur on any part of the body, about 90% of infections involve the leg.8,9 Another 7.5% of cases involve the arm or face. Erysipelas is most common in the young and the elderly. Typically, both infections develop after a break in skin integrity, resulting from trauma, surgery, ulceration, burns, tinea infection, or other skin disorder. 

Peritonitis may be classified as primary, secondary, or tertiary. Primary peritonitis, also called spontaneous bacterial peritonitis, is an infection of the peritoneal cavity without an evident source of bacteria from the abdomen.1,2 In secondary peritonitis, a focal disease process is evident within the abdomen. Secondary peritonitis may involve perforation of the gastrointestinal (GI) tract (possibly because of ulceration, ischemia, or obstruction), postoperative peritonitis, or posttraumatic peritonitis (e.g., blunt or penetrating trauma). Tertiary peritonitis occurs in critically ill patients and is infection that persists or recurs at least 48 hours after apparently adequate management of primary or secondary peritonitis. 

Pitcher MCL, Cummings JH. 1996. Hydrogen sulphide A bacterial toxin in ulcerative colitis Gut 39 1-4. 

Triclosan (10.279) kills a wide range of bacteria that cause food poisoning, dysentery, cholera, pneumonia, tetanus, meningitis, tuberculosis and sore throats. It also prevents the development of bacterially related odours and kills the yeasts responsible for Candida ulcers... 

Brummer RJ, Stockbruegger RW Effect of nizatidine 300 mg at night and omeprazole 20 mg in the morning on 24-hour intragastric pH and bacterial overgrowth in patients with acute duodenal ulcer. Dig Dis Sci 1996 41 2048-2054. 

Greenlee HB, Vivit R, Paez J, Dietz A Bacterial flora of the jejunum following peptic ulcer surgery. Arch Surg 1971 102 260-265. 

Investigations performed in rats with experimental acute pancreatitis [196] or ulcerative colitis [197] have shown that both rectal and oral administration of rifaximin decreased colonic bacterial translocation towards mesenteric lymph nodes. In the model of ANP [196] not only was the intra-abdominal spread of enteric bacteria (fig. 8) significantly reduced but also the pancreatic damage was lessened by rifaximin treatment. 

Minimal effects on intestinal flora were seen with rifaximin administration [9, 35]. In an early study, performed on healthy volunteers who received a short-term (5 days) rifaximin treatment, the observed changes in bowel flora returned to baseline levels within 1-2 weeks [9]. In a recent investigation fecal samples of patients with ulcerative colitis given three 10 day courses of the antibiotic were cultured and the different microbial species quantitated. Despite the high dose (i.e. 1800 mg daily) of rifaximin used there was only a minor change in bacterial counts which reverted back to pre-treatment values during the washout period [35]. It appears therefore that administration of this antibiotic does not disrupt intestinal microbial ecology. 

Pitcher MCL, Beatty ER, Cummings JH Salicylates inhibit bacterial sulphide production within the colonic lumen in ulcerative colitis. Gut 1995 37 A15. 

Helicobacter pylori to human gastric epithelium.26 Clinical studies have identified H. pylori as a causative agent in gastric and duodenal ulcers.27 Considerable evidence exists to suggest that carbohydrate-based treatments could be an effective means to combat infection.28 Since bacterial attachment is a prerequisite to infection,29 soluble Leb oligosaccharides may serve as therapeutic alternatives to broad-spectrum antibiotics. 

In mice exposure to 9 ppm caused a 50% decrease in respiratory rate. Lesions included ulceration and necrosis of the respiratory epithelium and moderate damage to lung tissue. Rats administered, via oral gavage, 10, 20, 40, or 80mg/kg for 10 consecutive days or 32 mg/kg for 90 consecutive days had inflammation, necrosis, acantholysis, hyperkeratosis, and epithelial hyperplasia of the forestomach. Chloropicrin was genotoxic in bacterial test systems."... 

M/sce//aneons - Asthenia, back pain, bacterial infection, chest pain, fever, flu-like symptoms, flushing, hot flushes, intermittent claudication, leg ulcer, malaise, moniliasis, ptosis, rigors, varicose vein, viral infection. 

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