Health Articles

Salmoncllae are gram-negative, non-spore-form ing bacilli that belong lo the family of Knterobacleriaceae. Three species exist: Salmonella typhi, Salmonella choleraesuis, and Salmonella enteritidis. S. enteritidis typhimttrium is Ihe serotype most commonly causing inl’eclion in humans. It invades mucosal cells and multiplies within them, elicil-ing a polymorphonuclear leukocyle response. Fluid accumulation within the intestinal lumen is related lo the elaboration of heat-labile and heat-stable enterotoxins.
Gastroenteritis caused by Salmonella is found more frequently in patients > 60 yr. partially because of reduced gastric acidity. Salmonella bacteremia also occurs more often in the elderly lhan in young adults wilh Salmonella gastroenteritis and is potentially more harmful because it tends to colonize the endothelial surfaces of atherosclerotic aortic aneurysms. An outbreak in a long-term care facility may cause a local epidemic.
Symptoms and Signs
The initial clinical manifestations of S. enteritidis typhimurium in the elderly include nausea, vomiting, and a chill followed by colicky abdominal pain, diarrhea, and vomiting. The diarrhea ranges from a few loose stools lo as many as 30 bowel movements daily. Characteristically, the stools are walery. green, and malodorous, wilh varying amounts of mucus. Some patients present with high fever and bloody, mucoid diarrhea, suggesting significant colonic involvement. The illness may last only a week or as long as 3 mo. The average course is 3 wk. The main complications are bleeding, toxic megacolon, and overwhelming sepsis.
Diagnosis and Treatment
Microscopic examination of methylene bine-stained specimens reveals moderate numbers of polymorphonuclear leukocytes. Stool should be cultured on selective or differential media.
Usually, antimicrobial therapy is nol used for Salmonella gastroenteritis. However, elderly patients—especially Ihose with underlying malignancies, lymphoproliferative disorders, cardiovascular diseases, aneurysms, and vascular grafts—should he given ampicitlin 50 to 100 mg/kg/day in divided doses orally or parenterals for 10 to 14 days. Based on the incidence of relapse, such therapy may be continued for up to 21 days. Alternatively, TMP-SMX is given at a dosage of 10 mg/kg/day TMPand 50 mg/kg/day SMX to a maximum of 4 tablets/day (320 mg and 1600mg)for 2 wk. Other alternatives include ciprofloxacin and several other third-generation cephalosporins.

Shigellae are a group of gram-negalive enteric organisms. Four major subgroups exist: group A-serotypcs of Shigella dysenteriae, group B-serotypes of Shigella flexneri, group C-serotypes of Shigella boydii, and group D-serotypes of Shigella sonnet- The most common serotype is S. sonnet, which is responsible for 60% to 80% of Shigella dysentery in the USA.
Symptoms and Signs
The illness is characterized by lower abdominal pain, rectal burning, tenesmus, and diarrhea. In about 33% of patienls. dysentery stool contains blood and mucus; in about 40%, fever occurs. Severe disease causes toxicity, and patients are highly febrile. The duration of symptoms is variable, bul in the elderly, the average is 7 days.
Diagnosis and Treatment
Microscopic examination of fecal samples reveals multiple polymorphonuclear leukocytes and RBCs. Stool should be cultured, and antibi olic sensitivily testing should be performed. Sigmoidoscopy and biopsy are generally not performed.
Therapy consisls of rehydration with oral and IV fluids for high-volume diarrhea and excessive vomiting. Opiate and atropine derivatives should be avoided because an inhibition of peristalsis prevents the removal of the pathogen and can exacerbate the gastroenteritis. Moderate lo severe cases require ampicillin 500 mg orally qid or I gm IVq6h. In communities where isolates are known to be resistant lo ampicillin. TMP-SMX at a dosage of 10 mg/kg/day TM P and 50 mg/kg/day SMX for 5 days should be prescribed. Alternatively, TMP-SMX 960 mg (TMP 160 mg, SMX 800 mg) orally or IV q 12 h for 5 days may be given.

The principal pathogens include Shigella, Salmonella, Campylobacter, and Yersinia. The latter two are seen predominantly in children and young adults. These four invasive pathogens involve the distal ileum and colon, producing mucosal ulceration.

At least five types of Escherichia coli can cause GI infections, including enterotoxigenic, enteropathogenic, enteroinvasive. enterohemorrhagic, and enteroadhercnt E. colt. Enterotoxigenic E. colt comes from contaminated waler and causes a subacute illness with a 24- Lo 72-h incubation period. This illness is associated wilh diffuse, mild abdominal pain; foul-smelling, profuse watery diarrhea; and occasional vomiting. The duration of the illness is less than a week.
Diagnosis is based on the clinical picture. Treatment primarily con-sisls of fluid replacement. In severe cases, oral tetracycline 250 my qid for 2 days may be given. When enterotoxigenic E. colt is the causative pathogen in traveler’s diarrhea, rehydration should be provided immediately. Bismuth subsalicyate 30 to 60 niL (or 2 tablets) qid significantly reduces diarrhea. In severe cases associated wilh nausea, vomiting, abdominal cramps, fever, or bloody stool, antibiotics can be used to reduce the duration of the illness. Trimethoprim-sulfamethoxazole (TMP-SMX) 960 mg (TMP 160 mg, SMX 800 me) should be administered bid for 3 to 5 days. Ciprofloxacin 500 mg bid for 5 days and norfloxacin 400 mg bid /or 5 days are also effective.
Klderly patients, especially those in nursing homes, are more susceptible toE.coJi0157:H7 infection, which has high morbidity and mortality rates. The incubation period is about 8 days. The clinical picture is hemorrhagic colitis, which begins with watery diarrhea; hours to days later, the stool becomes grossly bloody. The diarrhea is accompanied by abdominal cramps and vomiting; fever is not a prominent feature. Risk factors include reduced gastric acidity, antacid and hh-receplor antagonist use, and antibiotic therapy. The development of fever and leukocytosis may herald complications including hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, and dealh. Fatality rales in two nursing home outbreaks were 16% and 35%. (By contrast, the rale among younger persons is typically 5% lo 10%.)
Diagnosis is established by stool culture for F.. coli 0157:H7 in the first 4 days of the illness; stool filtrates should be tested for verotoxin activity. Treatment is supportive with IV fluid replacement.

Bacillus cereus, a frequent cause of food poisoning, is usually associated with contaminated retried rice or vegetables. This type of poisoning is characterized by two clinical syndromes: short-incubation emesis syndrome and long-incubation diarrheal syndrome. The emesis syndrome mimics Staphylococcus aureus poisoning; vomiting associated with abdominal pain and diarrhea begins about 6 h after the ingestion of the contaminated food. The diarrheal syndrome mimics Clostridium perfringens poisoning, occurring 8 to 16 h after the ingestion of contaminated food; it is not associated with vomiting, but nausea occasionally occurs. This syndrome includes abdominal pain with some tenesmus and profuse, foul-smelling watery diarrhea. In one long-incubation B. cereus outbreak involving elderly patients in a chronic disease hospital, the mean duration of illness was 2.3 days; in one patient the illness lasted 10 days.
Diagnosis is made by finding 10s CFU/gm of the organism in Ihe stool. Treatment is supportive; both forms of the illness subside in 12 to 24 h.
CLOSTRİDİUM PERFRINGENS FOOD POISONING
Clostridium perfringens is a gram-positive, spore-forming bacillus producing a potent thermolabile exotoxin. It exerls its effect on the proximal small intestine by activating adenylate cyclase, producing increased intestinal fluid secretion and decreased reabsorption. C. perfringens poisoning is associated with contaminated beef, beef products, and poultry and is characterized by the sudden onset of unusually foul-smelling diarrheal stools without blood or mucus, moderately severe colicky abdominal pain, and no vomiting. The self-limited disorder usually lasls less than 24 h.
Diagnosis is established by finding > 103 CFU/gm of the organism in food or stool. Treatment is supportive.

Staphylococcus aureus food poisoning is caused by heat-stable enlerotoxin R that is preformed by a toxigenic strain of S. aureus growing in contaminated food. The onsel is explosive, generally wilhin 2 lo (S h after ingesting a contaminated food, such as cream pastries, coleslaw, or potato salad. Severe vomiting precedes the passage of loose, foul-smelling stools. Moderate to diffuse abdominal cramps occur without tenesmus and fever. The self-limited clinical course usually resolves in 12 to 24 h. Diagnosis is made on the characteristic clinical picture, a finding of > 10s colony-forming units (CFUl/gm of staphylococci in the food, and a test identifying enlerotoxin Et. Treatment is supportive. Antimicrobial Iherapy is not indicated.

Toxigenic diarrheas are caused by several microorganisms that usually produce an enterotoxin or enlerotoxin-likc substance. These microorganisms include Staphylococcus aureus. Bacillus cereus, Clostridium perfringens, Escherichia coli. Vibrio choleras, Clostridium boluliiiutn, Clostridium difficile, and Vibrio parahaemolyiicus.

The exact incidence of infectious diarrhea in the elderly is unknown, but it is higher than in younger adults and has a higher mortality. Age-related anatomic and physiologic changes, chronic illnesses, and increased drug use make the elderly more susceptible lo gastrointestinal infections. Gastric acidity, which helps inactivate ingested bacteria, is generally decreased because of mucosal atrophy, frequent use of Hi-receptor blockers and antacids, and in some cases, gastric resection. Intestinal motility, another defense mechanism, is also decreased secondary to intrinsic neuronal degeneration, vascular ischemia, diabetes mellitus, and frequent use of anticholinergic drugs or narcotics. As a result, pathogenic organisms and their loxins can remain in the gut for an extended period and thus may overgrow. Intestinal mucosal immunity (ie. IgA secretion) is also believed to be decreased, although such a decrease has not been proved.
Viruses responsible for infectious diarrhea include the Norwalk virus-like agents and. less commonly, rotavirus. The exact pathogenetic mechanism is unclear. Diarrhea is caused by Norwalk virus throughout the year, whereas rotavirus infection occurs more often in the cooler months. Both agents have caused epidemic diarrhea in nursing homes and are easily spread by the fecal-oral route.

Osmotic Diarrhea
In the elderly, osmotic diarrhea is caused by the ingestion of poorly absorbable solutes such as magnesium sulfate, sodium sulfate, laxatives containing citrate, antacids containing magnesium hydroxide and mannitol, and sorbitol (chewing gum and diet candy). Disaccharidase deficiencies, especially lactase deficiency, can cause osmotic diarrhea. About 80% of the world population has primary lactase deficiency. Although it begins in childhood, people do nol outgrow it. The highest incidence of lactase deficiency occurs in black Americans and .lews. Osmotic diarrhea also occurs after a gastrectomy or vagotomy, in dumping syndrome, in short bowel syndrome, and with chronic small intestinal ischemia.
The diarrhea begins abruptly and is characterized by increased stool volume and an absence of blood and fat in the stool. Nausea, vomiting, and crampy abdominal pain do not occur in osmotic diarrhea. The diarrhea stops when the patient fasts or stops ingesting the poorly absorbable solute.
Diagnosis
The history of symptoms after ingestion of milk or milk products is essential. Inpatients with lactase deficiency, the stool pH is usually 4 to 6 (normal is > 6) with an associated increase in short-chain fatty acids. A lactose-hydrogen breath lest reveals breath hydrogen > 20 ppm within 3 h after lactose ingestion. Measuring magnesium (normal is <    12 mmol), sulfate (normal is < 5 tnmol) and phosphate (normal is
<12 mmol) in stool water may be necessary, especially in cases of sur
reptitious laxative abuse, a problem more common in elderly women.
Treatment
Treatment consists of having the patient avoid the offending solute and explaining why this is necessary. Lactase deficiency is treated by having the patient avoid foods wilh lactose and drugs with lactose fillers. Low-lactose milk or milk with lactase added are recommended. Lactase caplets can be prescribed, but they are expensive.

An Increase in the frequency of defecation (more than
three stools per day) associated with increased stool
volume (> 300 mL), increased fluidity, and abnormal
sensations such as urgency and pain.
Diarrhea can be classified on the basis of pathophysiologic processes and disorders. A simple classification uses six general processes: (1) osmotic diarrhea secondary to ingestion of osmotically active ingredients in foods and drugs; (2) infectious diarrhea including toxigenic diarrhea from infection caused by bacteria or viruses, which elaborate toxins that cause the intestinal epithelial cells to secrete water and electrolytes into the intestinal turncn, and invasive diarrhea caused by invasive pathogens affecting the distal ileum and colon; (3) maldigestive diarrhea secondary to pancreatic exocrine insufficiency (especially lipase deficiency) and bile acid insufficiency and bacterial overgrowth syndromes; (4) malabsorptive diarrhea encountered in celiac disease, tropical sprue, giardiasis, and Whipple’s disease; (5) diarrhea secondary to increased secretion of hormones, peptides, or biogenic amines from tumors, including carcinoid tumors, medullary carcinoma of the thyroid, islet-cell tumor of (he pancreas (vipoma), gastrinoma (Zollinger-Ellison syndrome), parathyroid adenoma, and small cell carcinoma of the lung: and (6) colonic diarrhea secondary to ulcerative colitis.
Crohn’s disease, ischemic colitis, carcinoma of the colon, villous adenoma, radiation colitis, and resection of < 100 cm of the distal ileum (bile-acid-induced diarrhea).
Supportive Treatment
Elderly persons with acute, nonspecific diarrhea should reduce their activity. To prevent pressure sores, they should change position frequently and get out of bed for meals. For the first 24 h, clear liquids (such as ginger ale, decaffeinated cola, decaffeinated tea, broth, and Gatorade) and gelatin should be given. The patient should consume 2 to 3 L of fluid because most diarrhea-associated complications result from fluid and electrolyte loss. After 24 h. the patient should eat bland foods, such as cooked cereals, rice, soup, bread, crackers, baked potatoes, eggs, and applesauce. Fruits, vegetables, fried or spicy foods, bran, candy, and caffeinaled and alcoholic beverages should be avoided. After 2 or 3 days, patients can progress to their regular diet.
Non-antimicrobial agents used to treat acute diarrhea include bismuth subsalicylate (effective for traveler’s diarrhea), tincture oi” opium, diphenoxylate with atropine, and loperamide (highly effective at a daily dose of 8 me). Both diphenoxylate with atropine and loperamide should be avoided in patients with fever or blood in the stool.