The patient was a 35-year-old man who consulted his physician because of upper abdominal pain.The pain was described as a steady burning or gnawing sensation, like a severe hunger pain. Usually it came on 1 1/2 to 3 hours after eating, and sometimes it woke him from sleep. Generally, it was relieved in a few minutes by food or antacid medicines.
On examination, the patient appeared well, without evidence of weight loss.The only positive finding was tenderness slightly to the right of the midline in the upper part of the abdomen.
A test of the patient's feces was positive for blood. The remaining laboratory tests were normal.
Endoscopy, a procedure which employs a long flexible fiber-optic device passed through the mouth, showed a patchy redness of parts of the stomach lining. A biopsy was taken.The endoscopy tube was passed through the pylorus and into the duodenum. About 2 cm into the duodenum, there was a lesion 8 mm in diameter that lacked a mucous membrane and appeared to be "punched out."The base of the lesion was red and showed adherent blood clot. After the endoscopy, a biopsy portion was placed on urea-containing medium.Within a few minutes, the medium began to turn color, indicating a developing alkaline pH.
1. What is the patient's diagnosis?
2. What would you expect microscopic examination and culture of the gastric mucosa biopsy to show?
3. Outline the pathogenesis of this patient's disease.
4. Why did it take so long for doctors to accept that this condition had an infectious etiology?
1. This patient had a duodenal ulcer.The ulcer had penetrated deeply beyond the mucosa, involving small blood vessels and causing bleeding.This was apparent from the clot that was visualized at endoscopy and the positive test for blood in the stool.
2. Microscopic examination of the biopsy showed curved bacteria, confirmed by culture to be Helicobacter pylori.
3. Helicobacter pylori enters the gastrointestinal tract by the fecal-oral route. In the stomach, they escape the lethal effect of gastric acid because they produce urease. Highly motile, they enter the gastric mucus and follow a gradient of acidity ranging from pH 2 in the gastric juices to pH 7.4 at the epithelial surface. Mutant strains that lack the ability to produce urease are only infectious if they are introduced directly into the mucus layer. Multiplication occurs just above the epithelial surface, but some of the bacteria attach to the epithelial cells and cause a loss of microvilli and thickening at the site of attachment. An inflammatory reaction develops beneath the affected mucosa.Two genes, vacA and cagA, correlate with virulence.The gene product VacA is a toxin similar to the adenylate cyclase of Bordetella pertussis.The bacteria inject
CagA into host cells causing the cells to elongate and spread out. CagA also provokes a strong immune response. Once established, H. pylori infections persist for years and often for a lifetime. It is not known why some people develop gastric or duodenal ulcers and others do not. Both host and bacterial factors are almost certainly involved. For example, strains of H. pylori isolated from peptic ulcer patients tend to be more virulent than those from patients who just have gastritis; patients with blood group O have more receptors for the bacterium and a higher incidence of peptic ulcers than do other people. Stomach acid and peptic enzymes probably play a role in ulcer formation by acting on damaged epithelium unprotected by normal mucus. Claude Bernard, a scientist of Pasteur's time, put it this way: "It is that which we do know which is the greatest hindrance to our learning that which we do not know." In 1983, when Dr. Barry J. Marshall proclaimed before an international gathering of infectious disease experts that a bacterium caused stomach and duodenal ulcers, everyone "knew" it could not be true because no organism was known to exist that could survive stomach acidity and enzymes. Indeed, almost everyone already "knew"the cause of ulcers to be psychosomatic.There is much still to be learned about the cause of ulcers, however, and Bernard's statement remains true.
ear DNA. There are two types of the virus, HSV-1 and HSV-2. Most oral infections are due to HSV-1; HSV-2 usually causes genital infections. ■ genital herpes simplex, p. 653
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