Chapter 159: Food and Waterborne Illnesses

INTRODUCTION AND EPIDEMIOLOGY

Foodborne illness occurs after consumption of a food contaminated with bacteria, viruses, parasites, chemicals, or biotoxins. As one example, in 2008, melamine-contaminated dairy products in China affected over 50,000 children. The World Health Organization estimates that more than two million children die every year from exposure to unsafe water or food.¹ Outbreaks from contaminated food are often widespread, and foodborne disease is a public health concern. International travel contributes to foodborne illnesses as travelers are exposed to new pathogens, and migrants may introduce diseases.¹

The Centers for Disease Control and Prevention (CDC) estimates that foodborne diseases cause 1 in 6 Americans to get sick, leading to 128,000 hospitalizations and 3000 deaths in the United States each year.^2,3 Children have the highest frequency of foodborne illness. Viruses are the most common cause of foodborne disease, with the norovirus causing more than half of all cases and 26% of all admissions.² Other viral sources of infection include rotavirus, astrovirus, and enteric adenovirus.

Bacterial causes tend to be more severe, with nontyphoidal Salmonella triggering the most cases requiring admission or resulting in fatality.³ Other common bacterial causes of foodborne illness include Clostridium perfringens, Campylobacter spp., Toxoplasma gondii, Shigella, Staphylococcus aureus, and Shiga toxin–producing Escherichia coli. Over the past decade, there has been little change in the overall incidence of foodborne pathogens aside from Campylobacter, which has been steadily increasing since 2001.³ The most common foods associated with outbreaks reported in the United States are poultry, leafy vegetables, and fruits/nuts.^2,3

PATHOPHYSIOLOGY

There are three basic mechanisms by which microbes cause illness. First, some pathogens such as S. aureus, Bacillus cereus, and Clostridium botulinum (botulism) produce toxins capable of causing illness. These preformed toxins are present in the food before ingestion and result in the rapid onset (1 to 6 hours) of symptoms. Preformed toxins such as staphylococcal enterotoxin exert their effect by stimulating the host immune system to release inflammatory cytokines within the intestine.⁴ These cytokines are responsible for the accompanying nausea and vomiting.

The second method involves toxin production after ingestion, which interacts with intestinal epithelium as seen with Vibrio, Shigella, and Shiga toxin–producing E. coli. These cause diarrhea and lower GI symptoms (cramping and sometimes bloody diarrhea), with onset at approximately 24 hours after exposure. Some toxins produced by Vibrio and enterotoxigenic E. coli alter chloride and sodium transport across intestinal mucosal surfaces without destroying cells.⁵ The resulting osmotic gradient produces a large fluid shift into the intestinal lumen, which overwhelms the absorptive capacity of the colon, causing watery diarrhea. Other toxins produced after ingestion by organisms such as Shigella and Shiga toxin–producing E. coli disrupt host cell protein production, which causes death of the intestinal epithelium, resulting in bloody diarrhea and extraintestinal symptoms.⁶

Finally, direct invasion of the intestinal epithelium is a common mechanism for the enteric viruses, Salmonella, enteroinvasive E. coli, and Campylobacter. These pathogens enter host cells and destroy intestinal epithelium.⁷ This causes diarrhea due to transient malabsorption that is frequently bloody and accompanied by systemic symptoms such as fever. These viruses require ingestion of just a few viral particles to cause disease. The upper and lower GI symptoms from invasive organisms last from 24 hours to weeks (Table 159-1).

The normal human digestive tract has physiologic defenses against foodborne diseases. The low gastric pH of 1 to 3 kills many ingested pathogens, while the normal intestinal flora competitively inhibits pathogens and secretes bactericidal fatty acids and other chemicals.^8,9 Normal intestinal motility prevents pathogens from having prolonged contact with mucosal surfaces and mixes organisms with mucous-containing protective glycoproteins. Immunologic tissues are also present in the GI tract to directly attack pathogens attempting transmural migration.⁹

Alteration of these protective mechanisms can increase susceptibility to foodborne disease. For example, proton pump inhibitors, histamine-2 (H₂) blockers, and antacids reduce gastric acid production. Recent antibiotic use, chemotherapy or radiation therapy, and recent surgery alter the intestinal flora. Decreased intestinal motility from narcotics, antiperistaltic drugs, and surgery may encourage pathogen growth and migration.⁹

CLINICAL FEATURES

Suspect a foodborne disease when two or more people in a household or close association (e.g., the same workplace or communal eating arrangement) simultaneously develop GI symptoms. The most common symptoms are nausea, vomiting, diarrhea, and abdominal cramping. Systemic symptoms of fever, dehydration, and malaise are also common in patients with severe foodborne infections.

Question patients about the types of food they have recently ingested, frequency of restaurant meals, consumption of public-vended or street-vended foods, ingestion of seafood, and consumption of raw foods. Additional questions include recent travel or camping, contact with food handlers, and diaper changing. Children who attend day care centers and residents of long-term care facilities are at increased risk for foodborne diseases. People working in the food industry are also frequent victims or sources; ask them about their personal hygiene and food-handling practices. Finally, seek a history of comorbidities or influencing therapies, including human immunodeficiency virus (HIV) infection or immunosuppressive drug use.

On exam, look for dehydration and a toxic appearance. Another priority is the identification of blood in the stool and the exclusion of alternative causes of symptoms such as appendicitis. The clinical features of specific foodborne infections are summarized in Table 159-2.

DIAGNOSIS

Most patients with foodborne diseases do not require diagnostic testing; illnesses are often self-limited. Routine testing for stool ova and parasites or cultures is not indicated.¹⁰ However, electrolytes and a CBC are helpful in toxic patients or those with prolonged symptoms. Stool tests are obtained in the following clinical situations^10,11:

• Watery diarrhea with signs of hypovolemia

• Bloody diarrhea

• Fever ≥38.5^oC (101.3^oF)

• Prolonged duration of illness >1 week

• Severe abdominal pain or tenderness

• Hospitalized patients or recent antibiotic use

• Elderly (≥70 years of age) or the immunocompromised

• Pregnant women or those with comorbidities such as inflammatory bowel disease

Routine stool cultures will identify Salmonella, Campylobacter, and Shigella. A single sample is usually sufficient, but be aware of local laboratory limitations. For example, most laboratories do not routinely culture enterotoxigenic E. coli, vibrios, and viruses. In 2009, the Centers for Disease Control and Prevention recommended that clinical laboratories culture all submitted stool specimens for Shiga toxin–producing E. coli and perform toxin assays for Shiga toxin.¹²

Testing for ova and parasites is indicated for the immunocompromised, patients with symptoms lasting longer than 2 weeks, community waterborne outbreaks, or men who have sex with men.^10,13 Because parasite excretion may not be continuous, three specimens separated by at least 24 hours may be needed to identify the causative pathogen.

Testing for fecal leukocytes has historically been performed to predict the presence of an invasive cause for acute diarrhea and increase stool culture yield. Unfortunately, several studies have shown that fecal leukocytes are neither sensitive nor specific for invasive disease, and they are a poor a predictor of response to antimicrobial therapy.^14,15 The neutrophil marker lactoferrin is a more sensitive, but less widely available, screening test for inflammatory cells in stool. If positive, fecal lactoferrin also increases the likelihood of positive stool cultures.^16,17 Direct antigen detection panels are available for specific viruses such as rotavirus, bacteria, and parasitic pathogens in many clinical laboratories.

TREATMENT

Most episodes of acute gastroenteritis require only adequate hydration and supportive care. The World Health Organization recommends initial therapy with a glucose-containing fluid (i.e., Pedialyte or equivalent) for oral rehydration.¹⁸ Parenteral rehydration is recommended for patients with severe dehydration or continued vomiting and inability to tolerate oral fluids. Antiemetics may reduce vomiting, emergency department length of stay, and need for admission.^19,20 Antimotility medications, such as loperamide, may decrease illness duration for mild to moderate nonbloody diarrhea in adults without fever but are generally avoided in young children and patients with dysentery (fever and bloody diarrhea) due to concerns of prolonging the illness.²¹

Empiric antibiotics do not appear to dramatically alter the course of illness since most cases are viral or self-limited bacterial in origin. The 2001 Infectious Diseases Society of America guidelines recommend empiric treatment for patients with moderate to severe traveler's diarrhea, those with symptoms for more than 1 week, patients requiring hospitalization due to volume depletion, and immunocompromised hosts.¹⁰ A common bacterial enteritis regimen is oral ciprofloxacin 500 milligrams twice daily or levofloxacin 500 milligrams once a day, each for 3 to 5 days. Azithromycin 500 milligrams once daily for 3 days is an alternative regimen.¹⁰ Antibiotics and antimotility agents are contraindicated in patients with Shiga toxin–producing E. coli O157:H7 infection due to increased risk of hemolytic-uremic syndrome, especially in children and the elderly.²² See Tables 159-3, 159-4, 159-5, and 159-6 for more detailed treatment recommendations.

DISPOSITION AND FOLLOW-UP

Patients who appear toxic or have systemic symptoms, significant comorbidities, or severe dehydration with inability to tolerate oral fluids are admitted. Discharged patients should receive instructions on proper hygiene, notably frequent hand washing, to protect family members and contacts who are not ill. Patients discharged with pending stool culture or other studies should have a clear plan for follow-up.

SPECIAL POPULATIONS

Elderly patients, young children, and the immunocompromised are more likely to have severe illness, atypical presentations, and long-term sequelae. Patients with human immunodeficiency virus or other immunocompromised states can rapidly develop life-threatening symptoms. Thus, test more liberally and admit at a lower threshold. Pregnant patients have increased risk of complications, especially with Listeria infection, and may require further monitoring.¹⁰

SPECIAL CONSIDERATIONS

Enterohemorrhagic E. coli and Hemolytic-Uremic Syndrome Enterohemorrhagic E. coli that produces Shiga toxin is the most common cause of hemolytic-uremic syndrome in the United States.²² The Shiga toxin–producing E. coli strain O157:H7 is most commonly associated with pediatric hemolytic-uremic syndrome, but other strains such as O104:H4 and O111 are associated with adult hemolytic-uremic syndrome–like illnesses. The Shiga toxin produced by these organisms halts protein synthesis in renal glomerular cells as the precipitating event in hemolytic-uremic syndrome. Toxin binding to the glomerular endothelium produces a thrombogenic environment leading to microangiopathic hemolysis through multiple cellular mechanisms.^23,24 Antibiotics may promote Shiga toxin release, which increases the incidence of hemolytic-uremic syndrome, and are avoided when this is suspected or identified. In addition, avoid antimotility agents. Treatment of hemolytic-uremic syndrome is supportive, with plasma infusion and exchange therapy showing some benefit. Approximately 50% of pediatric patients with hemolytic-uremic syndrome will require dialysis, and dehydration at the time of admission increases the frequency and duration of renal support.²⁵

Scombroid and Ciguatera Poisoning Scombroid fish poisoning occurs after ingestion of fish of the family Scombridae (tuna, mackerel, and bonito). Other non-Scombridae fish such as mahi-mahi, bluefish, herring, and sardines are also implicated. The disease occurs when histidine is metabolized by bacteria into histamine and other bioactive amines. Improper temperature control allows high concentrations of these substances to accumulate in the fish. Symptoms usually begin 30 minutes to 24 hours after ingestion and include flushing, headache, abdominal cramping, vomiting, and diarrhea. Symptoms are usually self-limited for 12 to 48 hours. However, severe cardiac and respiratory symptoms may occur in the elderly or patients with comorbid conditions. Treatment is with antihistamines (H₁ and H₂ blockers) such as diphenhydramine and cimetidine. Laboratory testing is not needed in most cases.²⁶

Ciguatera poisoning is caused by eating reef fish contaminated with the dinoflagellate Gambierdiscus toxicus, which produces ciguatoxin. The toxin is heat resistant and accumulates in large predatory fish such as grouper, snapper, amberjack, and barracuda. Ciguatoxin acts on sodium channels resulting in membrane depolarization. Nausea, vomiting, and diarrhea occur 1 to 24 hours after ingestion, followed by hypesthesias, paresthesias, numbness, malaise, generalized weakness, and sensitivity to temperature extremes. The latter is often described as a reversal of heat and cold sensation. Bradycardia and hypotension are also described.²⁷ The GI symptoms typically resolve over a few days, whereas the neurologic symptoms may persist in a waxing and waning pattern for 3 months to years.²⁸ Acute treatment is supportive. Mannitol has been used to treat severe cases, but the evidence is conflicting.^29,30

Chronic Sequelae of Foodborne Illness About 2% to 3% of patients with foodborne diseases have chronic sequelae thought to be related to autoimmunity.^31,32 Protein virulence factors (superantigens) present in a number of foodborne pathogens can initiate extreme immune responses. Salmonella, Shigella, and Campylobacter have been associated with a seronegative reactive arthritis in about 2% of those infected.³³ Campylobacter infection is associated with Guillain-Barré syndrome with a reported rate as high as 30.4 per 100,000 cases.³² Symptoms of Guillain-Barré syndrome typically occur 7 to 21 days after the GI symptoms resolve.^31,32 Other autoimmune disorders thought to be associated with superantigens from foodborne pathogens include multiple sclerosis, rheumatoid arthritis, psoriasis, and Graves' disease.³² Infections with Salmonella, Yersenia, and Campylobacter may increase short- and long-term risk of death even after accounting for comorbid diseases.³³

Prevention and Surveillance The Centers for Disease Control and Prevention tracks foodborne infections in the United States through FoodNet. The U.S. Food and Drug Administration and U.S. Department of Agriculture provide the Centers for Disease Control and Prevention with data about the origin and distribution of food products, which allows investigators to determine the source of a foodborne outbreak.

The Food Safety Modernization Act was passed into law in 2011 to address the rise in foodborne diseases by preventing, rather than responding to, outbreaks of foodborne illness. The law gives the U.S. Food and Drug Administration broad regulatory authority to oversee how food is harvested and processed.³⁴

INTRODUCTION AND EPIDEMIOLOGY

Waterborne illnesses occur from ingestion or contact with contaminated water found in swimming pools, hot tubs, spas, and naturally occurring fresh and salt water during recreational use.³⁵ Numerous species of bacteria, viruses, and protozoans are introduced into the water by fecal contamination and are capable of causing waterborne infections. However, some species of bacteria are indigenous aquatic organisms such as Pseudomonas aeruginosa, Vibrio, Aeromonas, nontuberculous Mycobacterium, and Legionella. Schistosomiasis is common among children in Africa, Asia, and South America, because they are likely to play in infected water. There is concern about the relationship between pediatric urogenital or intestinal schistosomiasis (often acquired in childhood) and human immunodeficiency virus risk.³⁶

There were 81 recreational waterborne disease outbreaks in the United States reported to the Centers for Disease Control and Prevention in 2009–2010, which resulted in at least 1326 cases of disease and 62 hospitalizations.³⁵ The vast majority of these outbreaks were from treated water sources such as swimming pools and water fountains. Approximately two thirds of the waterborne illnesses were gastroenteritis, and 25% were dermatologic diseases or chemical exposures. The most common pathogen associated with these outbreaks was Cryptosporidium, which accounted for half of all cases.³⁵ The most common noninfectious source of waterborne disease was exposure to pool chemicals.

BACTERIA AND WATERBORNE ILLNESS

Implementation of water disinfection and filtration treatments has significantly reduced waterborne outbreaks from enteric bacteria.³⁷ Waterborne infections from Vibrio cholerae and Salmonella typhi are now extremely rare in the developed world, but both remain a major cause of illness in developing nations.³⁷

Several enteric bacteria are commonly implicated in waterborne disease outbreaks in the United States. Campylobacter is found in virtually all surface waters due to contamination from wild bird feces and is the most common bacteria associated with recreational waterborne disease outbreaks.^35,38 Several outbreaks of human campylobacteriosis have been reported from contaminated drinking water.³⁹ Shiga toxin–producing E. coli can also be transmitted from ingestion or contact with water contaminated by farm animal feces.⁴⁰ Shigella species, Salmonella species, and Yersinia enterocolitica are other enteric bacteria that can cause waterborne outbreaks.³⁶ Most enteric bacteria, including E. coli O157:H7 and Campylobacter, are susceptible to chlorination.

Although V. cholerae is an enteric organism acquired from water with fecal contamination, many Vibrio species are endemic in marine and estuarine waters. The cholera epidemic began in Haiti in October 2010 and continues, with over 600,000 cases and nearly 8000 deaths. Environmental reservoirs have been identified in Haiti, with concern that transmission could occur to the Dominican Republic and other parts of the Caribbean.⁴¹ Vibrio species can cause diarrheal illnesses or skin infections. Vibrio vulnificus is associated with life- and limb-threatening necrotic wound infections. The organism is found predominantly along the Gulf Coast and is acquired by patients with open wounds that are exposed to seawater. The wound infections are associated with a high rate of sepsis and amputation. Cirrhosis and high iron levels are associated with worse outcome.⁴²

Found in fresh and marine waters, Aeromonas species can cause gastroenteritis and wound infections.⁴³ The majority of wound infections are simple cellulitis, but necrotizing infections and septic arthritis occur.^44,45 In addition, immunocompromised patients may progress to develop peritonitis, cholangitis, and meningitis.⁴³

P. aeruginosa is an opportunistic pathogen found in fresh water. Immunocompromised patients are at risk from waterborne disease due to Pseudomonas. In normal hosts, Pseudomonas can cause otitis externa, keratitis in contact lens wearers, and folliculitis.⁴⁶ Although Pseudomonas can contaminate drinking water, it does not appear to cause a diarrheal illness in normal hosts.⁴⁷

Nontuberculous Mycobacterium are found in salt and fresh water and can cause illness.⁴⁸ Mycobacterium marinum is associated with granulomatous skin infections (Figure 159-1).⁴⁹ Mycobacterium avium complex is associated with GI, pulmonary, or disseminated disease in immunocompromised patients, particularly patients with human immunodeficiency virus.³⁶

Legionella is a common inhabitant of fresh water, including water that meets the standards for drinking.³⁶ Infection occurs from inhalation of contaminated aerosols, resulting in one of two syndromes: Legionnaires' disease or Pontiac fever. Pontiac fever is a flulike illness contracted by breathing mist that comes from a water source (such as air conditioning cooling towers, whirlpool spas, and showers) contaminated with the bacteria. For further discussion of Legionnaires' disease, refer to the chapter 65, "Pneumonia and Pulmonary Infiltrates."

PROTOZOA AND WATERBORNE ILLNESS

Giardia lamblia is a common protozoal cause of waterborne disease in the United States that accounts for 20,000 cases of diarrheal disease annually.^36,50 It is frequently found in surface waters from mountain streams to municipal reservoirs and is resistant to the levels of chlorination typically used in water treatment. Infected animals such as beavers may contribute to contamination of natural waters, which explains the term "beaver fever" used to describe giardiasis. Backpackers, campers, and travelers to disease-endemic areas are at high risk for waterborne giardiasis, as are children under 5 years of age.^50,51 Community outbreaks often start out as a waterborne disease, but subsequent transmission commonly occurs from person to person. Giardia is associated with acute and chronic forms of gastroenteritis, although many patients infected with Giardia remain asymptomatic.

Cryptosporidium is an intracellular protozoan parasite that is another common cause of waterborne illness in the United States.⁵² The Centers for Disease Control and Prevention estimates that 748,000 cases of cryptosporidiosis occur each year and result in hospital admissions costing $45.8 million.⁵² The inoculum required to cause infection is low, and large numbers of oocysts are excreted in the feces of infected hosts.⁵³ Standard doses of chlorine and zonation used in water treatment are not effective against Cryptosporidium, which explains its association with recreational water sources.⁵² Water filtration reduces the number of oocysts, but occasionally enough remain to be infective. Infection with Cryptosporidium in a normal host results in a self-limited diarrheal illness, and many exposures are asymptomatic. Immunocompromised patients may experience chronic diarrhea or life-threatening complications.^51,53 Cyclospora, Isospora, and Microspora are other protozoan parasites that can cause severe disease in immunocompromised patients.^54,55

Entamoeba histolytica is a protozoa that causes intestinal amebiasis. It is a significant waterborne pathogen in developing countries, but in the United States, it is most commonly seen in migrants, travelers to endemic areas, men who have sex with men, and institutionalized patients.^56,57 Symptoms range from asymptomatic infection to severe dysentery.⁵⁶ Fulminant colitis with bowel necrosis and perforation occurs in <1% of cases but has a mortality rate of >40%.⁵⁸ Seeding of the liver can occur, particularly in men with underlying liver disease, resulting in the formation of amoebic hepatic abscesses.^56,59

ENTERIC VIRUSES AND WATERBORNE INFECTION

Enteric viruses are an important cause of waterborne disease. More than 100 enteric viruses pathogenic in humans have been reported, many of which can be transmitted via drinking water and recreational water.⁶⁰ Several enteric viruses, including the Norwalk virus and rotaviruses, are relatively chlorine resistant. Outbreaks have been associated with contamination of private wells and community water systems.⁶⁰

Hepatitis A and E are associated with epidemic and sporadic infections from contaminated water. Infection from the hepatitis A virus typically results in an acute self-limited hepatitis that rarely develops into fulminant hepatic failure. The incidence of hepatitis A infections has decreased in the United States due to implementation of vaccination in high-risk adults and all children.⁶¹ Hepatitis E is mostly confined to tropical and subtropical regions but is often complicated by cholestasis, and it causes significant morbidity and mortality in pregnant women.⁶²

Noroviruses, including the Norwalk virus, are the leading cause of acute gastroenteritis across all age groups.⁶³ Outbreaks have been linked to contaminated drinking and recreational water, including on cruise ships.⁶⁴ Rotavirus and enteric adenoviruses are other important waterborne enteric viruses. Noroviruses, rotaviruses, and enteric adenoviruses typically cause a self-limited gastroenteritis, although dehydration from these infections can be severe in children.³⁶

CLINICAL FEATURES

The majority of patients with waterborne disease present with nausea, vomiting, and diarrhea. Think of this cause in symptomatic patients with recent travel, outdoor activities such as camping or backpacking, recent recreational water use, or those using a private drinking water supply rather than municipal drinking water or bottled water. Patients with severe or chronic gastroenteritis symptoms may have immune deficiency such as human immunodeficiency virus or immunosuppressive drugs. In patients with bloody diarrhea, suspect invasive enteric bacteria as the cause.¹¹ Giardia and other protozoan parasites are suspected in patients with diarrhea lasting 2 or more weeks.¹⁰

Physical examination should focus on identifying signs of dehydration and any open skin wounds acquired in fresh or marine waters. Waterborne skin infections can range in severity from simple cellulitis to necrotizing fasciitis. Patients with V. vulnificus present after recent exposure to salt water and hemorrhagic bullae or signs of necrotizing infection (Figure 159-2).⁴³ Clinical features of waterborne pathogens are summarized in Table 159-7.

DIAGNOSIS

Diagnostic testing is usually not needed. Viral antigen tests for rotavirus may be helpful in children with severe or persistent symptoms to distinguish viral from bacterial pathogens. Testing of stool for ova and parasites is indicated in patients with recent travel to endemic countries, immunocompromised status, or diarrheal illness of 2 or more weeks; during community-wide waterborne outbreaks; or in men who have sex with men.^10,13 Because parasite excretion may not be continuous, three specimens separated by at least 24 hours may be needed to identify the causative pathogen.

The diagnosis of waterborne skin infections is based primarily on the patient's physical examination findings and history of water exposure. Identification of the causative agent can be attempted by Gram stain and wound culture (acid-fast staining if M. marinum is suspected). Blood cultures are best reserved for systemically ill patients.

TREATMENT

In most cases of acute gastroenteritis from waterborne pathogens, treatment is limited to rehydration. Empiric antibiotic therapy is used for patients with moderate to severe disease, recent travel history, or symptoms lasting more than 1 week; those needing hospitalization; and immunocompromised hosts.¹⁰ Avoid antibiotics in cases of suspected E. coli O157:H7 due to an increased risk of development of hemolytic-uremic syndrome. Appropriate antibiotics include 3 to 5 days of oral ciprofloxacin 500 milligrams twice daily, levofloxacin 500 milligrams once daily, or double-strength trimethoprim-sulfamethoxazole twice daily.¹⁰ Azithromycin 500 milligrams orally once daily for 3 to 5 days is recommended for pregnant women, children, and patients with travel to areas with fluoroquinolone-resistant Campylobacter (Thailand).¹⁰

Antimotility agents can be given to patients or children >3 years old without signs of invasive bacterial infection (bloody stools or fever).^21,22 Probiotics, such as lactobacilli, may shorten the duration of diarrheal illnesses in adults and children.⁶⁵

Infections from Giardia and Entamoeba are typically treated with metronidazole (Table 159-5). Paromomycin is an alternative to metronidazole in pregnant women.⁶⁶ Other alternatives for Giardia and Entamoeba treatment include tinidazole and nitazoxanide.⁶⁶ Albendazole is also effective for giardiasis, but not amebiasis. Infections from Cryptosporidium are generally self-limited and usually do not require specific treatment in immunocompetent patients. However, antimicrobial treatment with nitazoxanide or paromomycin is used in patients with prolonged infections, children, and the immunocompromised.⁶⁷ For immunocompromised patients with Cryptosporidium, nitazoxanide or paromomycin alone or in combination with azithromycin is used. Initiation of highly active antiretroviral therapy is the first priority for Cryptosporidium treatment in patients with human immunodeficiency virus.⁶⁸

Treatment of waterborne skin infections includes empiric antibiotic administration (Table 159-8) and tetanus vaccination if needed. Consensus is that initial empiric antibiotic therapy should be broad spectrum, including clindamycin in combination with a fourth-generation cephalosporin, an extended-spectrum fluoroquinolone (i.e., moxifloxacin), or an antipseudomonal penicillin (i.e., piperacillin-tazobactam).^69,70 If V. vulnificus is suspected, treat with doxycycline and a fourth-generation cephalosporin.⁴² Clarithromycin or doxycycline is indicated for most M. marinum infections, but severe cases require added rifampin or ethambutol.⁴⁹ Patients with evidence of necrotizing infections need immediate surgical consultation for operative debridement.⁶⁹

DISPOSITION AND FOLLOW-UP

Most episodes of acute gastroenteritis secondary to waterborne pathogens are benign and self-limited. Patients with systemic symptoms, severe dehydration, significant comorbidities, or inability to tolerate oral fluids should be considered for admission. Patients with waterborne skin infections should be admitted for systemic illness, suspected necrotizing infections, or comorbidities such as immunocompromised states.

PREVENTION AND SURVEILLANCE

The U.S. Safe Water Drinking Act of 1974 authorizes the Environmental Protection Agency to set national standards for U.S. public drinking water systems. The agency has set standards for 90 chemical, microbiologic, radiologic, and physical contaminants.⁷¹ These include coliform counts, the presence of human enteric viruses, Cryptosporidium, and Giardia.

All public drinking water is required to be disinfected, which typically involves treatment with chlorine and ozone.⁷¹ Enteric bacteria such as E. coli and Campylobacter are susceptible to these disinfection measures. However, pathogens such as protozoans and some enteric viruses are less susceptible to chlorine, and despite filtration, these pathogens may be present in sufficient quantities to cause disease.

Several recently developed vaccines are available to prevent waterborne infection from hepatitis A virus. An aggressive vaccination campaign in high-risk adults and all children has resulted in a decline in cases in the United States.⁶¹