Eric L. Nuermberger
In previous editions, Richard G. Bennett, MD, contributed to this chapter.
Gastroenteritis is an inflammation of the stomach and/or small intestine. Acute symptoms of gastroenteritis may follow the ingestion of a wide variety of infectious and chemical agents. Ingestion may occur because of direct person to person contact, contact with fomites or, more commonly, via contaminated food or water. Although viral enteropathogens may spread by aerosol transmission (1), these other routes are more common. With several important exceptions, the acute illnesses caused by these agents are characterized by prominent nausea and vomiting, often with systemic symptoms (fever, chills, malaise, myalgia) and diarrhea. Diarrhea, defined as an increase in the number or volume of bowel movements, which are usually fluid, is the primary manifestation of infectious colitis. Ingestion of select agents however, may result in diverse symptoms such as abdominal pain or cramping, neurologic symptoms, or respiratory difficulty. All of these symptoms usually begin abruptly and the hour of onset can typically be documented by the patient. With few exceptions, these illnesses are self-limited and terminate within 1 to 5 days.
Tables 35.1 (infectious agents) and 35.2 (chemical agents) summarize the etiologic agents, pathophysiology, clinical and epidemiologic features, and principles of diagnosis and treatment for conditions that may occur in the United States.
Epidemiology
Incidence and Distribution
The incidence of the conditions listed in Tables 35.1 and 35.2 varies from year to year, and the true incidence is never known because a large proportion of cases are not reported to physicians or health authorities. A national population-based laboratory surveillance system, the Centers for Disease Control and Prevention (CDC) Emerging Infections Program Foodborne Diseases Active Surveillance Network (FoodNet, http://www.cdc.gov/foodnet), has helped establish more precise incidence rates for foodborne illnesses. Current estimates are that 211 million persons become ill, more than 900,000 are hospitalized, and more than 6,000 die each year in the United States related to acute diarrheal illness (2). Much of the burden (78 million illnesses, 325,000 hospitalizations, and 5,000 deaths) is attributed to eating contaminated food (2). Of 239 foodborne outbreaks reported nationally in 2004, the cause was established for only 152 (64%) (3). However, the number of outbreaks for which the causative pathogen is identified is increasing. This reflects improvements in diagnostic capabilities, particularly for identifying noroviruses and other viral enteropathogens. In fact, noroviruses now account for as much as 67% of foodborne illnesses for which the causative agent is identified (Table 35.3) (2). Bacterial pathogens, in particular Campylobacter and Salmonella, account for another 24%. Studies of outbreaks of viral gastroenteritis in adults have shown that the symptoms it produces overlap with the symptoms produced by the common bacterial pathogens.
FoodNet data obtained from 1996 through 2004 document a substantial decline in the incidence of many foodborne infections (3). For example, the incidence of Campylobacter infection declined by 31%. Most notably, the incidence of infection with E. coli O157:H7, one strain that produces the potent Shiga-like toxin responsible for hemolytic uremic syndrome (HUS), increased between 1988 and through 1996, but has decreased by 42% since 1996. These improvements no doubt relate to improved safety practices in the beef and poultry industries and in fast-food restaurants, which now always cook hamburgers until well done, as well as to increased education of consumers about safe food-handling.
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TABLE 35.1 Characteristics of Acute Illness Caused by Ingestion of Infectious Agents |
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Sources and Modes of Transmission
Tables 35.1 and 35.2 summarize the sources and modes of transmission of the etiologic agents causing foodborne illness. The features of four of the most well recognized etiologic agents illustrate the diverse ways that foodborne disease is acquired:
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intact shells can also be infected (e.g., from a salmonella abscess in the ovary of a hen). Only hard-cooked eggs and pasteurized eggs are absolutely safe; raw egg dishes (e.g., homemade salad dressings, eggnog, ice cream) and undercooked eggs (e.g., scrambled and soft-cooked eggs) should be avoided, particularly by immunocompromised and elderly people (5,6).
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diarrhea and hemolytic uremic syndrome (7). The mortality among patients with the latter syndrome can be high. Recently, natural environmental contamination of nonmeat products (e.g., produce and apple juice) has resulted in outbreaks (8,9).
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TABLE 35.2 Characteristics of Acute Illness Caused by Ingestion of Chemical Agents |
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Thus, most episodes of foodborne illness follow the ingestion of normally safe foods that have been rendered unsafe by one or more of the following factors: failure to refrigerate foods properly or to heat foods thoroughly, preparing foods a day or more before they are served, allowing
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foods to remain at warm temperatures, failure to reheat or cook foods at temperatures that kill vegetative bacteria, incorporating raw (contaminated) ingredients into foods that receive no further cooking, failure to clean and disinfect kitchen or processing plant equipment, and contamination by infected food handlers who practice poor personal hygiene. The complexity of the world's food distribution system and the difficulty in controlling food safety even at a national level are exemplified by an outbreak of salmonellosis in Finland and the United States resulting
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from contaminated alfalfa sprouts grown from seeds supplied by a Dutch shipper (10) and an outbreak of cyclosporiasis in North America related to raspberries from Guatemala (11).
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TABLE 35.3 Burden of Foodborne Illness, United States, 1999 |
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Some foodborne illnesses are caused by the ingestion of foods that are always unsafe because of the presence of toxins that cannot be rendered innocuous by cooking or other means (e.g., histamine or scombrotoxin, ciguatoxin, Amanita mushroom toxins, paralytic shellfish toxin, and heavy metals) (12). A recent report of histamine poisoning associated with eating tuna burgers highlights the increasing recognition of scombroid poisoning (named for the type of fish most often associated with this illness), which is characterized by flushing, vomiting, and profuse watery diarrhea (13).
Not all gastroenteritis and diarrheal disease is foodborne. Waterborne outbreaks may result from contaminated drinking water or recreational water sources. Crypto-sporidium is a common cause of waterborne outbreaks because it is chlorine-resistant. A large outbreak of cryptosporidiosis in 1993 resulted from contamination of the public water supply in Milwaukee, Wisconsin, affecting over 400,000 people (14). Recreational water illnesses are on the rise and are caused largely by swallowing contaminated water while swimming.Cryptosporidium, Giardia, Shigella, and E. coli are the most common pathogens.
Outbreaks unrelated to contaminated food or water are commonly caused by noroviruses and other viral enteropathogens, especially within institutional settings (e.g., day care centers, nursing homes, and assisted living facilities) and during the winter. A viral cause is more likely when secondary cases develop in a household or institution, a pattern that suggests person-to-person spread rather than one-time exposure to a common food.
More serious forms of diarrheal disease resulting from animal exposures are increasingly recognized. These include infection withenterohemorrhagic E. coli while visiting farms or petting zoos (15,16) and salmonellosis associated with pet reptiles or amphibians (17). In both cases, children have borne the brunt of the morbidity and mortality.
Populations at Risk
For many of the conditions listed in Tables 35.1 and 35.2, people are at risk at all ages, and a single episode may not confer protective immunity against a later episode. Although most cases of acute diarrhea occur in children, older adults are at increased risk of dying from gastrointestinal illnesses. Of 28,538 diarrhea-related deaths in the United States between 1979 and 1987, 78% occurred in adults aged 55 and older versus 11% in children younger than 5 years old (18). A particularly high rate of diarrheal illness also occurs in people of all ages who travel to developing countries. For older adults who are commonly prescribed cardiovascular medications that can block normal physiologic responses to volume depletion, special counseling is advisable. Patients with cirrhosis are at increased risk for complications of acute hepatitis A infection and infection with Vibrio vulnificus and should be counseled to avoid consuming raw or partly cooked shell-fish.
Immunocompromised persons are also at greater risk for gastrointestinal (GI) infections and their associated morbidity and mortality. The diagnosis of HIV infection must be considered in patients with unusual diarrheal syndromes. Protracted diarrhea can herald the progression of HIV infection, and a number of enteropathogens can cause not only acute illness but also prolonged symptoms of diarrhea in patients with advanced HIV disease. Cryptosporidium infection, usually a benign self-limited diarrheal illness in children and healthy adults, may cause a prolonged and life-threatening illness (19). Isospora belli, usually not thought of as a diarrheal pathogen, may also cause diarrheal illness in these patients. Diarrheal illnesses caused by Salmonella and Campylobacter jejuni, which are usually self-limited normal hosts, may be prolonged in HIV-infected patients. (See Chapter 39 for additional discussion of infection in HIV-infected patients.)
Pathogenesis
As indicated in Tables 35.1 and 35.2, most of the etiologic agents produce symptoms by causing inflammation of the GI tract or through the physiologic effects of toxins.
The common bacterial diarrheal syndromes can be separated into invasive and enterotoxigenic syndromes (Table 35.4), and this becomes important when antibiotic
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treatment is considered. In invasive disease, the etiologic agent invades the intestinal mucosa and diarrhea results from destruction of mucosal cells that occurs due to inflammation. This usually involves the large bowel and produces systemic symptoms (particularly fever), local symptoms (tenesmus, abdominal discomfort), and frequent small amounts of stool that contain pus cells and often blood. Shigellosis is the prototype of this syndrome. In enterotoxigenic diarrhea, the organisms do not invade tissue but colonize and multiply on the small bowel mucosal surface. During this process they produce enterotoxins, which act as chemical mediators and cause net secretion of fluid and electrolytes into the small bowel lumen. Little tissue damage is produced, and inflammation of the mucosa is minimal. Symptoms consist of watery diarrhea (which may be voluminous), accompanied by minimal systemic signs, unless dehydration becomes significant. The prototypes of this syndrome are diarrheas caused by Vibrio cholerae and by enterotoxigenic E. coli (20).
Unfortunately, not all enteric diseases caused by bacteria fit into this simple dichotomy. Enteroaggregative strains of E. coli do not invade mucosal cells, but tightly adhere to the mucosal surface and induce an inflammatory diarrhea, at least in part through the production of one or more enterotoxins. These strains produce diarrhea primarily in small children, HIV-infected patients, and travelers, and many belong to the classic enteropathogenic serotypes (21). In addition, Clostridium difficile, a cause of pseudomembranous colitis, produces two toxins: an enterotoxin (toxin A), which causes secretion of fluid into the gut lumen, and a potent cytotoxin (toxin B), which damages the gut epithelium and leads to inflammation (22).
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TABLE 35.4 Characteristics Distinguishing Invasive and Enterotoxigenic Diarrhea |
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Patient Evaluation
Historical Information
In addition to a history of the specific symptoms, the clinical history should include items that may suggest the most likely pathogens (Table 35.5). The most useful information is as follows:
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onset within 24 to 48 hours suggests Salmonella infection, and onset of symptoms 1 week or more after exposure suggests a less common problem, such as giardiasis.
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TABLE 35.5 Evaluation of Acute Gastroenteritis or Diarrhea: Using the Clinical History to Suggest Probable Pathogens |
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Physical Examination
The physical examination is usually of minimal help in establishing a cause. Fever or significant abdominal tenderness in association with diarrhea suggests an invasive organism as the etiologic agent. Poor skin turgor and postural hypotension suggest significant salt and water deficits (uncommon in adults with diarrhea in the United States). Rare conditions in which the physical findings may be helpful are botulismand other neurotoxic forms of food poisoning and trichinosis (Tables 35.1 and 35.2).
Laboratory Studies
In most outpatients with acute GI illness, no laboratory studies are indicated (25) unless a common source outbreak is suspected. In such cases, the physician should notify local and/or state health authorities since special cultures and assays for viral pathogens, as well as tests for toxins in stools and in food, may be obtained for epidemiologic purposes.
Diarrhea lasting >1 day, especially if accompanied by fever, bloody stools, systemic illness, recent antibiotic use, day care center attendance, recent hospitalization, or dehydration should prompt consideration of the following laboratory studies (25):
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Shiga-like toxin on routine stool samples, but most laboratories have adopted this practice. Unfortunately, other bacteria (e.g., Vibriospp.) and most viral agents are not identified in routine laboratory workups and testing must be specifically requested.
Testing for norovirus infection is usually unnecessary in routine clinical practice, although tests based on nucleic acid amplification are increasingly available. Examination of stool for ova and parasites should not be added routinely to the evaluation of diarrhea of less than 2 weeks’ duration. In suspected cases, the laboratory should be asked to examine the stool microscopically for Giardia lamblia, Entamoeba histolytica, or Cryptosporidium (Table 35.1). For the diagnosis of giardiasis, stools may need to be examined repeatedly. E. histolyticatrophozoites are best identified in fresh or freshly preserved stool specimens or from the mucus taken from the base of ulcerations seen at proctoscopy. Acid-fast staining of the stool enhances the detection of Cryptosporidium.
For patients who develop new diarrhea after 3 or more days in the hospital, ordering a C. difficile test alone is the most cost-effective approach, as stool cultures and ova and parasite examinations are usually unrevealing (26). Chapter 45 provides information about the laboratory evaluation of patients with chronic diarrhea.
Management
In all patients with acute gastroenteritis or diarrheal disease, symptomatic treatment is of primary importance. In addition, some patients may require antibiotics, usually indicated on the basis of the history and physical examination. Most illnesses are self-limited, lasting 1 to 2 days, but occasionally symptoms last 5 to 10 days. Resolution of illness is thought to be caused by the local secretory immune response of the GI tract.
Symptomatic Treatment
Fluid Therapy
With the exception of giardiasis, amebiasis, C. difficile colitis, and the more severe cases of shigellosis, salmonellosis, and campylobacter infection, practically all acute diarrheal disease seen commonly in the United States can be treated with only symptomatic therapy, the mainstay of which is the replacement of fluids and electrolytes lost in the stool. Because in most patients the disease is mild and the amount of stool is small, replacement is simple. Young healthy patients should be encouraged to drink plenty of fluids, to avoid spicy foods, and otherwise to eat what they like. Foods with complex carbohydrates (e.g., cereals, rice, toast), but not foods with concentrated simple sugars (most sweet foods), may facilitate fluid reabsorption at the brush border of the intestinal mucosa and help to limit duration of diarrhea (27).
In patients who have a very large loss of stool, those who experience weakness and lassitude (with or without signs of volume depletion), and older adults (who are at increased risk for hypoperfusion of vital organs with even moderate dehydration because of silent atherosclerosis), replacement should consist of fluids containing electrolytes and glucose. Oral glucose–electrolyte or carbohydrate–electrolyte replacement solutions (e.g., Pedialyte, CeraLyte) and packets containing pre-measured salts and sugars that must be dissolved in water (e.g., Oral Rehydration Salts) are available commercially (27). These products have been developed primarily for treating children but are adequate for adults. Most have sodium concentrations of 50 to 75 mEq/L and substitute citrate for bicarbonate. A less complete replacement fluid can be made using constituents available at home: one pint (500 mL) water, 1/2 teaspoon table salt, and four rounded teaspoons of table sugar.
Because of their sugar and salt contents, none of the following beverages is satisfactory for fluid replacement in patients whose diarrhea is causing moderate to severe fluid loss: nondietetic soft drinks (hyperosmolar sugar solution), dietetic soft drinks (inadequate amount of simple sugars needed to facilitate intestinal fluid reabsorption), and sports drinks such as Gatorade that are designed to replace the hypotonic fluids lost with perspiration (inadequate amount of salts for replacement of intestinal fluid losses).
Patients should be instructed to replace estimated fluid losses roughly on a 1:1 basis. Typically, 1 to 2 L should be drunk in the first 1 to 2 hours after diarrhea commences and an additional 1 to 2 L a day until symptoms resolve. Hydration is judged adequate if dilute urine is passed every 3 to 4 hours.
Patients experiencing severe diarrhea or vomiting that precludes easy replacement with oral replacement fluids and those who have evidence of moderate to severe salt and
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water depletion should receive initial intravenous saline replacement. This can be accomplished in ambulatory settings, in the patient's home (see Chapter 9), or in the hospital depending on the availability of resources and the severity and duration of the patient's illness.
Other Symptomatic Measures
Several types of medications are commonly used to treat diarrhea symptomatically. Diphenoxylate with atropine (Lomotil) and loperamide(Imodium or generic, nonprescription) are agents that cause a decrease in intestinal motility and stool frequency; they may be useful to the patient at times when frequent defecation would be inconvenient or embarrassing. These drugs do not alter the natural course of the disease and are potentially harmful if invasive pathogens such as Shigella are causing the diarrhea. These medications should also be avoided in persons at risk for infection with enterohemorrhagic E. coli (absence of fever, presence of bloody diarrhea, high white blood cell count) or C. difficile (antibiotic exposure, recent hospitalization or nursing home residence) because they may promote retention of toxin and precipitate hemolytic uremic syndrome or severe colitis and toxic megacolon.
Kaolin and pectin mixtures (Kaopectate or generic, nonprescription) add to the bulk of the stool and thus the stools become less watery; actual fluid loss, however, is not affected by these agents. Bismuth subsalicylate (Pepto-Bismol or generic, nonprescription) has been demonstrated to decrease the volume of stools in patients with diarrhea caused by enterotoxigenic organisms and to be safe in a variety of diarrheal illnesses (28). This compound has antibacterial activity as well. It may be taken in either liquid or tablet form. The dosage is two tablets or 30 mL every half to 1 hour, as needed, up to a maximum of eight doses per 24 hours. Patients should be advised that this compound causes black stools and sometimes a blackened tongue.
In patients with protracted vomiting, which may occur with staphylococcal food poisoning, the antiemetic drug prochlorperazine (Compazine) may be helpful, given as a 25-mg rectal suppository two or three times daily to healthy adults and at lower dosages for the elderly.
Specific Treatment
In patients in whom shigellosis is strongly suspected or from whom the organism has been cultured in the stool, appropriate antibiotic treatment should be given because this will shorten the illness from 3 to 7 days to 1 to 2 days. A fluoroquinolone antibiotic (e.g., ciprofloxacin 500 mg or norfloxacin 400 mg, twice daily) for 3 days is the current drug of choice if susceptibility results are not available (29). An alternative therapy is trimethoprim-sulfamethoxazole, one double-strength tablet every 12 hours for 5 days (30).
If Salmonella is isolated from diarrheal stool, patients should not routinely receive antibiotics. In nonsevere infections, antibiotic treatment does not speed resolution of illness (31). Moreover, routine treatment of Salmonella gastroenteritis with antibiotics may prolong the carrier state (32). Even without antibiotic treatment, patients may excrete Salmonella in the stool for several weeks to months after their acute illness has terminated. If severe disease is present (high fever, more than eight stools per day, or need for hospitalization) or if the patient is immunocompromised, the same antibiotics listed above for shigellosis should be prescribed, but the duration of therapy should be 3 to 7 days. Ceftriaxone or cefotaxime are additional options when parenteral therapy is required.
Patients infected with Campylobacter may benefit from antibiotic therapy, but controlled studies indicate only modest reductions in symptom resolution in most cases (33). Increasing resistance to fluoroquinolones among Campylobacter isolates is a worldwide problem; infection with these strains has been associated with longer duration of illness and greater risk of invasive disease and death (34,35). Azithromycin, 500 mg once followed by 250 mg daily for 4 additional days, and erythromycin 500 mg four times a day for 5 days are generally active against increasingly prevalent fluoroquinolone-resistant Campylobacter and represent the treatments of choice (29).
In patients who develop significant diarrhea related to antibiotics, the antibiotic should be stopped whenever possible, and another substituted only if antibiotic therapy must be continued. C. difficile causes approximately 20% of antibiotic-associated diarrhea in hospitalized patients but is almost always responsible for severe cases of antibiotic-associated diarrhea accompanied by fever and abdominal pain. The diarrhea usually begins during antibiotic treatment or within 2 weeks of stopping antibiotics; occasionally it begins weeks to months later (23). If C. difficile is strongly suspected, bismuth subsalicylate (see Symptomatic Treatment) often helps, particularly in patients with mild-to-moderate diarrhea without significant systemic symptoms. Metronidazole, 250 mg by mouth four times a day for 10 to 14 days, shortens the illness in most patients and is indicated when severe diarrhea and other symptoms occur (e.g., low-grade fever and mild abdominal pain) (22). For the 20% of patients with relapsing infection (36) or for those with severe diarrhea and systemic manifestations of illness such as high fever, abdominal pain, or elevated blood leukocyte count indicative of pseudomembranous colitis, the much more expensive antibiotic vancomycin should be given in an oral dosage of 125 mg four times daily for 7 to 14 days (22).
Although antibiotics are useful in shortening the duration of traveler's diarrhea, most of which is caused by enterotoxigenic E. coli (seeChapter 41), there is no evidence that antibiotics are useful in patients infected with enterohemorrhagic E. coli. In fact, due to some evidence
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that antibiotic treatment of diarrhea caused by E. coli O157:H7 infection is associated with an increased risk of hemolytic uremic syndrome (37,38), most experts recommend against antibiotic treatment of this infection (25).
Patients with giardiasis and amebiasis require appropriate antimicrobial therapy. For giardiasis, treatment options include metronidazole, 250 mg three times a day for 5 days, or the newly approved drugs tinidazole, in a single dose of 2 g, or nitazoxamide in a dose of 500 mg two times a day for three days. (Quinacrine hydrochloride, an earlier recommended treatment, is no longer available in the United States.) For moderate to severe amebic dysentery, metronidazole (750 mg three times a day for 10 days) or tinidazole (2 g once daily for 3 days) should be administered, followed by an agent active against the luminal cyst form, such as paromomycin (10 mg per kg three times a day for 5 to 10 days) or iodoquinol (650 mg three times a day for 3 weeks) (39).
Trichinosis is treated with mebendazole (200 to 400 mg three times daily for 3 days and then 400 to 500 mg three times daily for 10 days) or albendazole (400 mg twice daily for 10 to 15 days). High dosages of prednisone (e.g., 40 to 60 mg/day) should be given simultaneously, if symptoms are pronounced, for 3 to 5 days, and then tapered.
Patients with suspected botulism should be hospitalized in an intensive care unit immediately and should be given polyvalent antitoxin, which must be obtained through the local health department. Patients with mushroom poisoning caused by Amanita muscaria should be treated with atropine and hospitalized (Table 35.2).
Chapter 39 describes the treatable opportunistic organisms that cause diarrheal illnesses in patients with HIV infection.
Patient's Role in Therapy
Acute gastroenteritis, like the common cold, is often diagnosed and handled by the patient without contacting a physician. In some instances, patients contact their physician by telephone and a working diagnosis and plan of therapy can be established without an office visit. This is particularly true for healthy patients with typical symptoms of staphylococcal food poisoning or viral gastroenteritis. In all situations, whether the patient is examined or not, it should be stressed that care of gastroenteritis requires taking of sufficient fluids, at times supplemented by an oral electrolyte solution (see Symptomatic Treatment), and by oral antibiotics if prescribed. Patients should be advised to contact their physician if diarrhea becomes worse or if they develop fever or protracted vomiting. A followup visit is not needed unless symptoms persist beyond 2 to 3 days or unless stool cultures have been taken and reveal that antibiotic therapy is indicated. Limitation of activity should be dictated by how the patient feels and by proximity of toilet facilities.
Course of Illness
The dehydrated patient feels almost immediate improvement when adequate oral replacement fluids are given. When the patient is given antimicrobial therapy for an invasive pathogen, diarrhea and fever should decrease notably within 24 to 36 hours.
An atypical course occasionally occurs after initial diagnosis and treatment. After being initially seen, any patient may develop an increase in diarrhea that could result in unanticipated significant dehydration. An increase in severity of symptoms could also occur if the patient develops antibiotic-associated colitis. The occasional patient infected with an antibiotic-resistant bacterial pathogen may not respond to initial therapy, indicating the need for an alternative drug. The enteric fever syndrome caused by S. typhi (typhoid fever), some otherSalmonella species, and some Yersinia species typically begins with constipation, fever, headache, and abdominal pain, but diarrhea may develop. The progressive course and abdominal tenderness (at times suggesting acute appendicitis) are features that suggest these causes and the need for both stool and blood cultures (40). An initial episode of ulcerative colitis (bloody diarrhea) or an initial episode of Crohn disease (pain with nonbloody intermittent diarrhea that does not remit) could be misdiagnosed as shigellosis. With inflammatory bowel diseases, fluids or antibiotic therapy would not lead to resolution of symptoms.
Rarely, a patient's diarrheal symptoms may persist for more than a week. In this case, the patient should return for further evaluation, particularly repeated stool examinations, which may be necessary to confirm the diagnosis of parasitic infections.
Prevention
Primary Prevention
Primary prevention of the diseases discussed above can theoretically be accomplished by the following measures:
Regulations governing sewage treatment, water purification, and food processing, packing, and preparation provide the principal protective barriers to foodborne disease outside the home. Unfortunately, this is often inadequate, as evidenced by the observation that as many as 70% of poultry carcasses sold commercially in supermarkets are contaminated with Salmonella or Campylobacter (41,42). In coming years, the use of food irradiation may become more widespread, and this could drastically improve food
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safety (43), but thus far the consumer demand for irradiated meat has been weak.
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TABLE 35.6 Measures to Prevent Foodborne Disease in the Home |
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In the home, almost all forms of foodborne disease can be prevented if several measures are followed routinely (Table 35.6). Many people do not realize that some of the food they prepare each day is contaminated before cooking and that proper cooking and storing, not absence of contamination, is the way in which most food is rendered safe to eat. Whenever food known to be contaminated is eaten raw, the risk of foodborne disease is present. This is particularly important with respect to shellfish, which concentrate microbial organisms from the waters in which they are grown.
Despite routine testing of water by public health authorities for contamination by enteric pathogens, the number of cases of illness related to consumption of raw seafood continues to increase. Illnesses arise from bacteria such as Shigella and Vibrio, particularly Vibrio vulnificus, viruses such as hepatitis A and noroviruses, and unusual parasites in sushi (44). Some experts suggest that the risks associated with eating raw seafood are now unacceptable (45), and people at risk for GI infections or severe complications, such as patients with cirrhosis, should be instructed to avoid eating uncooked seafood.
Secondary Prevention
After an outbreak of an acute enteric illness, appropriate measures should be taken to prevent additional cases. In the household, any foods suspected of transmitting illness should be thrown away. (In the event that an epidemiologic investigation is warranted, a sample should be submitted to the local health department.) An error in storage or cooking of the suspected food is often evident; the patient's physician should point out this error and, most important, review the standard precautions listed in Table 35.6 to prevent repeated episodes of foodborne illness. When a member of a household has an enteric infection that is transmissible from person to person (Table 35.1), this person should be instructed to wash his or her hands frequently, especially before preparing food for others.Food service employees should not work until the symptoms of infectious gastroenteritis resolve. Those with shigellosis or salmonellosis should not work until two consecutive stool cultures obtained not less than 24 hours apart (and not less than 48 hours after discontinuation of antibiotics if antibiotics were given) are negative.
Secondary prevention of norovirus infection in the home should be focused on adequate hand hygiene and disinfection of contaminated surfaces. It should be recognized that the organism can be transmitted in emesis as well as in stool. Norovirus outbreaks in institutional settings require scrupulous attention to infection control procedures, including hand hygiene, barrier precautions, proper disposal or sterilization of contaminated material, and surface decontamination. Cohorting of patients may also be beneficial.
When exposure outside the home is suspected, the problem should be reported immediately to the local health department; it is the responsibility of the health department to undertake an epidemiologic investigation to protect others. Each year, investigations of 400 to 500 outbreaks of foodborne illness are reported to the CDC, and many lead to measures that interrupt potentially widespread outbreaks of diseases, some of them particularly hazardous, such as botulism.
Specific References
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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