Diseases Associated with Ingestion of Food and Water Flashcards
Amebiasis Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Distributed worldwide, particularly in the tropics; more common in areas of poor sanitation. Long-term travelers (duration >6 months) are significantly more likely than short-term travelers (duration <1 month) to develop E. histolytica infection. People at higher risk for severe disease are those who are pregnant, immunocompromised, or receiving corticosteroids; associations with diabetes and alcohol use have also been reported.
Prevention:
Food and water precautions
Symptoms:
Most patients have a gradual illness onset days or weeks after infection. Symptoms include cramps, watery or bloody diarrhea, and weight loss and may last several weeks. Occasionally, the parasite may spread to other organs (extraintestinal amebiasis), most commonly the liver. Amebic liver abscesses may be asymptomatic, but most patients present with fever and right upper quadrant abdominal pain, usually in the absence of diarrhea.
Treatment:
For symptomatic intestinal infection and extraintestinal disease, treatment with metronidazole or tinidazole should be followed by treatment with iodoquinol or paromomycin. Asymptomatic patients infected with E. histolytica should also be treated with iodoquinol or paromomycin, because they can infect others and because 4%–10% develop disease within a year if left untreated.
Brucellosis Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
High-risk regions include the Mediterranean Basin, South and Central America, Eastern Europe, Asia, Africa, and the Middle East.
Prevention Avoid unpasteurized dairy products and undercooked meat.
Transmission Most commonly through consumption of contaminated dairy products. Brucella can enter the body via skin wounds, mucous membranes, or inhalation. Person-to-person transmission is rare.
Symptoms: Incubation period is 2–4 weeks (range, 5 days to 5 months). Initial presentation is nonspecific, including fever, muscle aches, fatigue, headache, and night sweats.
Treatment: Doxycycline, rifampin, and trimethoprim-sulfamethoxazole have been used in various combinations for treatment. Sometimes surgery is required.
Cholera Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Since 1961, the seventh pandemic of cholera, caused by V. cholerae serogroup O1, biotype El Tor, has spread from Indonesia through most of Asia into Eastern Europe and Africa, and from North Africa to the Iberian Peninsula. In 1991, an extensive epidemic began in Peru and spread to neighboring countries in the Western Hemisphere. Although few cases of cholera occur in South or Central America, V. cholerae O1 remains endemic in much of Africa and South and Southeast Asia. V. cholerae O139 spread rapidly through Asia in the early 1990s but has since remained localized to a few areas in Asia. In October 2010, a cholera epidemic began in Haiti, just 10 months after a devastating earthquake destroyed the Haitian capital of Port-au-Prince and surrounding areas.
Prevention: Vaccine Safe food and water precautions and frequent handwashing are critical in preventing cholera Transmission Toxigenic V. cholerae O1 and O139 are free-living bacterial organisms found in fresh and brackish water, often in association with copepods or other zooplankton, shellfish, and aquatic plants. Cholera infections are most commonly acquired from drinking water in which V. cholerae is found naturally or into which it has been introduced from the feces of an infected person. Other common vehicles include contaminated fish and shellfish. Other foods, including produce, are less commonly implicated. Direct transmission from person to person, even to health care workers during epidemics, has been reported but is not frequent.
Symptoms: Cholera infection is most often asymptomatic or results in a mild gastroenteritis. Severe cholera is characterized by acute, profuse watery diarrhea, described as “rice-water stools,” and often nausea and vomiting, leading to volume depletion. Signs and symptoms include tachycardia, loss of skin turgor, dry mucous membranes, hypotension, and thirst. Additional symptoms, including muscle cramps, are secondary to the resulting electrolyte imbalances. If untreated, rapid loss of body fluids can lead to severe dehydration, hypovolemic shock, and death within hours. With adequate and timely rehydration, CFRs are <1%. Most people infected with toxigenic V. cholerae will be asymptomatic or have mild diarrhea.
Treatment:
Rehydration is the cornerstone of cholera treatment. Oral rehydration solution and, when necessary, intravenous fluids and electrolytes, if administered in a timely manner and in adequate volumes, will reduce CFRs to well under 1%. Antibiotics reduce fluid requirements and duration of illness. Antimicrobial therapy is indicated for moderate and severe cases, which can be treated with doxycycline, tetracycline, erythromycin, azithromycin, or ciprofloxacin. Whenever possible, antimicrobial susceptibility testing should inform treatment choices. Zinc supplementation reduces the severity and duration of cholera and other diarrheal diseases in children in resource-limited areas.
Cryptosporidiosis Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Distributed worldwide. Cryptosporidium caused only a small proportion (6%) of cases of travelers’ diarrhea in North American travelers to Mexico.
Prevention: Food and water precautions and handwashing. Cryptosporidium is extremely tolerant to halogens (such as chlorine or iodine), and alcohol-based hand sanitizers are not effective against the parasite.
Transmission: Oral-fecal, primarily through contaminated food or water, including water swallowed while swimming, or through contact with an infected person or animal, most notably pre-weaned calves.
Symptoms: Symptoms usually begin 7–10 days (range, 2–26 days) after infection and are generally self-limited. The most common symptom is watery diarrhea. Other symptoms can include abdominal cramps, vomiting, weight loss, fever, decreased appetite, fatigue, joint pain, and headache. In immunocompetent people, symptoms most frequently resolve within 2–3 weeks; patients might experience a recurrence of symptoms after a brief period of recovery before complete symptom resolution. Clinical presentation of cryptosporidiosis in HIV-infected patients varies with level of immunosuppression, ranging from no symptoms or transient disease to relapsing or chronic diarrhea or cholera-like diarrhea, which can lead to life-threatening wasting and malabsorption. Extraintestinal cryptosporidiosis (in the biliary or respiratory tract or rarely the pancreas) has been documented in people who are immunocompromised.
Treatment: Most immunocompetent patients will recover without treatment. Diarrhea should be managed with fluid replacement. Nitazoxanide is approved to treat cryptosporidiosis in immunocompetent patients and is available for those aged ≥1 year. Nitazoxanide has not been shown to be an effective treatment of cryptosporidiosis in HIV-infected patients. However, dramatic clinical and parasitologic responses have been reported in these patients after the immune system has been reconstituted with active combination antiretroviral therapy. Protease inhibitors might have direct anti-Cryptosporidium activity
Cyclosporiasis Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Most common in tropical and subtropical regions where outbreaks are frequently seasonal (such as during summers and rainy season in Nepal). Outbreaks in the United States and Canada have been linked to imported fresh produce.
prevention: Food and water precautions
Transmission Ingestion of infective Cyclospora oocysts, such as in contaminated food or water.
Symptoms: Incubation period averages 1 week (range, 2 days to >2 weeks). Onset of symptoms is often abrupt but can be gradual; some people have an influenzalike prodrome. The most common symptom is watery diarrhea, which can be profuse. Other symptoms can include anorexia, weight loss, abdominal cramps, bloating, nausea, body aches, vomiting, and low-grade fever.
Treatment: Trimethoprim-sulfamethoxazole; no highly effective alternatives have been identified.
Giardiasis Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Transmission occurs worldwide, most commonly diagnosed in travelers returning from south Asia, the Middle East, and South America. Risk of infection increases with duration of travel.
Prevention: Food and water precautions Transmission: By ingesting fecally contaminated food or water, including water swallowed while swimming; through contact with fecally contaminated environmental surfaces; or through person-to-person contact, such as caring for an infected person or sexual contact.
Symptoms: Symptoms typically develop 1–2 weeks after infection and generally resolve within 2–4 weeks. Signs and symptoms include diarrhea (often with foul-smelling, greasy stools), abdominal cramps, bloating, flatulence, fatigue, anorexia, and nausea. Typically, a patient presents with the gradual onset of 2–5 loose stools per day and gradually increasing fatigue. Sometimes upper gastrointestinal symptoms are more prominent. Weight loss may occur over time. Fever and vomiting are uncommon. Reactive arthritis, irritable bowel syndrome, and other chronic symptoms sometimes occur after infection with Giardia
Treatment: Tinidazole, metronidazole, nitazoxanide, paromomycin, furazolidone, and quinacrine are known to be effective in treating giardiasis. Because making a definitive diagnosis is difficult, empiric treatment can be used in patients with the appropriate history and typical symptoms.
Hepatitis A Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Common throughout the developing world, where infections most frequently are acquired during early childhood and are usually asymptomatic or mild. In these countries, a high proportion of adults in the population are immune to HAV, and epidemics of hepatitis A are uncommon. In developed countries, infection is less common, but communitywide outbreaks may occur. Hepatitis A is one of the most common vaccine-preventable infections acquired during travel. In the United States the most frequently identified risk factor for hepatitis A is international travel. Risk is highest for those who live in or visit rural areas, trek in backcountry areas, or frequently eat or drink in settings of poor sanitation. However, cases of travel-related hepatitis A can also occur in travelers to developing countries with “standard” tourist itineraries, accommodations, and eating behaviors.
Prevention: Vaccination or immune globulin (IG), and food and water precautions.
Transmission: Through direct person-to-person contact; contaminated water, ice, or shellfish harvested from sewage-contaminated water; or from contaminated raw fruits, vegetables, or other foods. HAV is shed in the feces of infected people. The virus reaches peak levels 1–2 weeks before onset of symptoms and diminishes rapidly after liver dysfunction or symptoms appear, which is concurrent with the appearance of circulating antibodies to HAV. Infants and children, however, may shed virus for up to 6 months after infection.
Symptoms: Incubation period averages 28 days (range, 15–50 days). Infection may be asymptomatic or may range in severity from a mild illness lasting 1–2 weeks to a severely disabling disease lasting several months. Clinical manifestations include the abrupt onset of fever, malaise, anorexia, nausea, and abdominal discomfort, followed within a few days by jaundice. The likelihood of having symptoms with HAV infection is related to the age of the infected person. In children aged 50 years.
Treatment: Supportive care only.
Hepatitis E Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Waterborne outbreaks (often large, involving hundreds to thousands of people) have occurred in South and Central Asia, tropical East Asia, Africa, and Central America Clinical attack rates are highest in young adults aged 15–49 years. In outbreak-prone areas, interepidemic disease is sporadically encountered. In these areas, pregnant women—whether infected sporadically or during an epidemic—are at risk of progressing to liver failure and death after infection. Miscarriages and neonatal deaths also commonly occur as a result of HEV infection. Sporadic disease also occurs in regions that are not prone to outbreaks, such as the Middle East, temperate East Asia (including China), North and South America, and Europe. Symptomatic disease is observed most frequently in adults aged >50 years. Primary infection acquired by people who are immunosuppressed, particularly solid-organ transplant recipients, may progress to chronic infection. People living in the United States are at risk of HEV infection when they travel to areas where epidemics have occurred. When traveling in Japan and Europe, eating raw or inadequately cooked venison, boar meat, pig liver, or food products derived from these, is a risk factor for infection.
Prevention: No vaccine is available, nor are drugs for preventing infection. Travelers should avoid drinking unboiled or unchlorinated water and beverages that contain unboiled water or ice. Travelers should eat only thoroughly cooked food, including seafood, meat, offal, and products derived from these
Transmission: HEV is transmitted primarily by the fecal-oral route. In regions with poor sanitation and limited access to safe drinking water, epidemics and interepidemic occurrences of hepatitis E are largely waterborne. Transmission to fetuses and neonates by women infected during pregnancy is common. In Japan, sporadic disease can be zoonotic and foodborne, associated with eating meat and offal (including liver) of deer, boars, and pigs. In France, disease can be acquired from eating figatellu, a sausage delicacy prepared from raw pig liver. Sporadic disease is also observed in other temperate countries, including the United States, but its cause is generally unknown. Shellfish can transmit HEV. Disease from blood transfusion has been reported, although rare.
Symptoms:
The incubation period is 2–9 weeks (mean 6 weeks). Signs and symptoms of disease during primary infection include jaundice, fever, loss of appetite, abdominal pain, and lethargy. Acute hepatitis E is frequently self-limited. Pregnant women (particularly those infected during the second or third trimester) may present with or progress to liver failure, and the fetus is at risk for spontaneous abortion and premature delivery. People with preexisting chronic liver disease may undergo further hepatic decompensation when infected with HEV. Recipients of organ transplants may have no symptoms when infected by HEV but can occasionally develop neurologic deficits.
Treatment: Treatment is supportive.
Norovirus Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Seroprevalence studies in the Amazon, southern Africa, Mexico, Chile, and Canada have shown that norovirus infections are common throughout the world, and most children will have experienced ≥1 infection by the age of 5 years. Norovirus infections can occur year round, but in temperate climates, norovirus activity peaks during the winter. In the United States, norovirus is the leading cause of sporadic cases and outbreaks of gastroenteritis, estimated to cause 21 million illnesses a year and approximately 50% of all foodborne outbreaks. Noroviruses are common in both developing and developed countries. Norovirus is a cause of travelers’ diarrhea; prevalence ranges from 3% to 17% of travelers returning with diarrhea. However, coinfection and asymptomatic infection with norovirus are common, so focused studies are needed to determine exactly how frequently norovirus is the cause of disease. Risk for infection is present anywhere food is prepared in an unsanitary manner and may become contaminated, or where drinking water is inadequately treated. Of particular risk are “ready-to-eat” cold foods, such as sandwiches and salads. Raw shellfish, especially oysters, are also a frequent source of infection, because virus from contaminated water concentrates in the gut of these filter feeders. Contaminated ice has also been implicated in outbreaks. Large norovirus outbreaks are associated with settings where people live in close quarters and can easily infect each other, such as hotels, cruise ships, camps, and hospitals. Viral contamination of inanimate objects (fomites) may persist during outbreaks and be a source of infection. On cruise ships, for instance, such environmental contamination has caused recurrent norovirus outbreaks on successive cruises with newly boarded passengers. Transmission of norovirus on airplanes has been reported during both domestic and international flights and likely results from contamination of lavatories or from symptomatic passengers in the cabin.
Prevention: No vaccine is currently available, although vaccine development efforts are advancing. Noroviruses are common and highly contagious, but the risk for infection can be minimized by frequent and proper handwashing and avoiding possibly contaminated food and water. Washing hands with soap and water for at least 20 seconds is considered the most effective way to reduce norovirus contamination; alcohol-based hand sanitizers (containing ≥60% alcohol) might be useful between handwashings but should not be considered a substitute for soap and water. In addition to handwashing, measures to prevent transmission of noroviruses between people traveling together include carefully cleaning up fecal material or vomit and disinfecting contaminated surfaces and toilet areas. Products should be approved by the Environmental Protection Agency for norovirus disinfection; alternatively, a high concentration of domestic bleach (5–25 tablespoons bleach per gallon of water) may be used. Soiled articles of clothing should be washed at the maximum available cycle length and machine-dried at high heat
Transmission: Transmission occurs primarily through the fecal-oral route, either through direct person-to-person contact or indirectly via contaminated food or water. Norovirus is also indirectly spread through aerosols of vomitus and contaminated environmental surfaces and objects.
Symptoms: Infected people usually have an acute onset of vomiting with nonbloody diarrhea. The incubation period is 12–48 hours. Other symptoms include abdominal cramps, nausea, and occasionally a low-grade fever. Illness is generally self-limited, and full recovery can be expected in 1–3 days. In some cases, dehydration, especially in patients who are very young or elderly, may require medical attention.
Treatment Supportive care, especially oral or intravenous rehydration. Antimotility agents should be avoided in children aged
Poliomyelitis Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
As of March 2012, WPV circulation has never been interrupted in only 3 countries: Afghanistan, Nigeria, and Pakistan. In 3 African countries (Angola, Chad, and Democratic Republic of the Congo), WPV transmission has been reestablished after importations and outbreaks in 2008 and 2009. In spite of progress made in eradicating WPVs globally, countries are still at risk for imported cases. In 2010 and 2011, WPV outbreaks from importations occurred in 18 countries in Africa, Eastern Europe, and Asia. Because of polio eradication efforts, the number of countries where travelers are at risk for polio has decreased dramatically. The last documented case of WPV-associated paralysis in a US resident traveling abroad occurred in 1986 in a 29-year-old vaccinated adult who had been traveling in South and Southeast Asia. In 2005, an unvaccinated US adult traveling abroad acquired VAPP after contact with an infant recently vaccinated with OPV.
Prevention: Vaccine
Transmission: Fecal-oral or oral transmission. Acute infection involves the oropharynx, gastrointestinal tract, and occasionally the central nervous system.
Symptoms: Clinical manifestations of poliovirus infection range from asymptomatic (most infections) to symptomatic, including acute flaccid paralysis of a single limb to quadriplegia, respiratory failure, and rarely, death. Treatment: Only treatment for symptoms is available, ranging from pain and fever relief to intubation and mechanical ventilation for patients with respiratory insufficiency.
Seafood Poisoning/Toxins - Ciguatera Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Ciguatera fish poisoning occurs after eating reef fish contaminated with toxins such as ciguatoxin or maitotoxin. These potent toxins originate from small marine organisms (dinoflagellates) that grow on and around coral reefs. Dinoflagellates are ingested by herbivorous fish. The toxins are then concentrated as they pass up the food chain to large carnivorous fish (usually >6 lb, 2.7 kg) and finally to humans. Toxins are concentrated in fish liver, intestinals, roe, and head. Gambierdiscus toxicus, which produces ciguatoxin, may proliferate on dead coral reefs more quickly than other dinoflagellates. The risk of ciguatera is likely to increase as more coral reefs die because of climate change, ocean acidification, construction, and nutrient runoff. Risk for Travelers More than 50,000 cases of ciguatera poisoning occur globally every year. The incidence in travelers to highly endemic areas has been estimated as high as 3 per 100. Ciguatera is widespread in tropical and subtropical waters, usually between the latitudes of 35°N and 35°S; it is particularly common in the Pacific and Indian Oceans and the Caribbean Sea. The incidence and geographic distribution of ciguatera poisoning are increasing. Newly recognized areas of risk include the Canary Islands, the eastern Mediterranean, and the western Gulf of Mexico. Fish that are most likely to cause ciguatera poisoning are carnivorous reef fish, including barracuda, grouper, moray eel, amberjack, sea bass, or sturgeon. Omnivorous and herbivorous fish such as parrot fish, surgeonfish, and red snapper can also be a risk.
Prevention: Travelers can take the following precautions to prevent ciguatera fish poisoning: Avoid or limit consumption of the reef fish listed above. Never eat high-risk fish such as barracuda or moray eel. Avoid the parts of the fish that concentrate ciguatera toxin: liver, intestines, roe, and head. Remember that ciguatera toxins do not affect the texture, taste, or smell of fish, and they are not destroyed by gastric acid, cooking, smoking, freezing, canning, salting, or pickling.
Symptoms: Typical ciguatera poisoning results in a gastrointestinal illness and may also cause neurologic symptoms. Although very rare, cardiovascular collapse may result. The first symptoms usually appear 1–3 hours after eating contaminated fish and include nausea, vomiting, diarrhea, and abdominal pain. Neurologic symptoms usually appear 3–72 hours after the meal and include paresthesias, pain in the teeth or the sensation that the teeth are loose, itching, metallic taste, blurred vision, or even transient blindness. Cold allodynia (dysesthesia when touching cold water or objects) is characteristic, though there can be acute sensitivity to both hot and cold. Neurologic symptoms usually last a few days to several weeks. Chronic neuropsychiatric symptoms resembling chronic fatigue syndrome may be disabling, last several months or longer, and include malaise, depression, headaches, myalgias, and fatigue. Cardiac manifestations include bradycardia, other arrhythmias, and hypotension. The overall death rate from ciguatera poisoning is approximately 0.1% but varies according to the toxin dose and availability of medical care to deal with complications. The diagnosis of ciguatera poisoning is based on the clinical signs and symptoms and a history of eating fish that are known to carry ciguatera toxin.
Treatment: There is no specific antidote for ciguatoxin or maitotoxin. Treatment is generally for specific symptoms and includes supportive care. Intravenous mannitol has been reported to reduce the severity and duration of neurologic symptoms, particularly if given within 48 hours of the appearance of symptoms.
Seafood Poisoning/Toxins - Scomboid Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Scombroid, one of the most common fish poisonings, occurs worldwide in both temperate and tropical waters. The illness occurs after eating improperly refrigerated or preserved fish containing high levels of histamine, and often resembles a moderate to severe allergic reaction. Fish typically associated with scombroid have naturally high levels of histidine in the flesh and include tuna, mackerel, mahimahi (dolphin fish), sardine, anchovy, herring, bluefish, amberjack, and marlin. Histidine is converted to histamine by bacterial overgrowth in fish that has been improperly stored after capture. Histamine and other scombrotoxins are resistant to cooking, smoking, canning, or freezing.
Prevention: Fish contaminated with histamine may have a peppery, sharp, salty, or “bubbly” feel but may also look, smell, and taste normal. The key to prevention is to make sure that the fish is properly iced, refrigerated, or immediately frozen after it is caught (<38°F, <3.3°C). Cooking, smoking, canning, or freezing will not destroy histamine in contaminated fish.
Symptoms:Symptoms of scombroid poisoning resemble an acute allergic reaction and usually appear 10–60 minutes after eating contaminated fish. They include flushing of the face and upper body (resembling sunburn), severe headache, palpitations, itching, blurred vision, abdominal cramps, and diarrhea. Untreated, symptoms usually resolve within 12 hours. Rarely, there may be respiratory compromise, malignant arrhythmias, and hypotension requiring hospitalization. Diagnosis is usually clinical. A clustering of cases helps exclude the possibility of fish allergy.
Treatment:
Scombroid poisoning usually responds well to antihistamines (H1-receptor blockers, although H2-receptor blockers may also be of benefit).
Seafood Poisoning/Toxins - SHELLFISH POISONING Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
Several forms of shellfish poisoning may occur after ingesting filter-feeding bivalve mollusks (such as mussels, oysters, clams, scallops, and cockles) that contain potent toxins. The toxins originate in small marine organisms (dinoflagellates or diatoms) that are ingested and concentrated by shellfish. Risk for Travelers Contaminated shellfish may be found in temperate and tropical waters, typically during or after dinoflagellate blooms called harmful algal blooms (HABs). One example of a HAB is the Florida red tide caused by Karenia brevis.
Prevention: Shellfish poisoning can be prevented by avoiding potentially contaminated bivalve mollusks. This is particularly important in areas during or shortly after algal blooms, which may be locally referred to as “red tides,” “brown tides,” etc. Travelers to developing countries should avoid eating all shellfish, because they carry a high risk of viral and bacterial infections. Marine shellfish toxins cannot be destroyed by cooking or freezing.
Symptoms: Poisoning results in gastrointestinal and neurologic illness of varying severity. Symptoms typically appear 30–60 minutes after ingesting toxic shellfish but can be delayed for several hours. Diagnosis is usually one of exclusion and is usually made clinically in patients who recently ate shellfish.
- Paralytic Shellfish Poisoning This is the most common and most severe form of shellfish poisoning. Symptoms usually appear 30–60 minutes after eating toxic shellfish and include numbness and tingling of the face, lips, tongue, arms, and legs. There may be headache, nausea, vomiting, and diarrhea. Severe cases are associated with ingestion of large doses of toxin and clinical features such as ataxia, dysphagia, mental status changes, flaccid paralysis, and respiratory failure. The case-fatality ratio averages 6% and is dependent on the availability of modern medical care, including mechanical ventilation. The death rate may be particularly high in children.
- Neurotoxic Shellfish Poisoning Neurotoxic shellfish poisoning usually presents as gastroenteritis accompanied by minor neurologic symptoms, resembling mild ciguatera poisoning or mild paralytic shellfish poisoning. Inhalation of aerosolized toxin in the sea spray associated with a Florida red tide (Karenia brevis bloom) can induce bronchoconstriction and may cause acute, temporary respiratory discomfort in healthy people. People with asthma may experience more severe and prolonged effects.
- Diarrheic Shellfish Poisoning This produces chills, nausea, vomiting, abdominal cramps, and diarrhea. No deaths have been reported. Amnesic Shellfish Poisoning This is a rare form of shellfish poisoning that has been reported to produce gastroenteritis and neurologic symptoms that may be severe. There are little data on this type of poisoning.
Treatment: Treatment is symptomatic and supportive. Severe cases of paralytic shellfish poisoning may require mechanical ventilation.
Travellers’ Diarrhea Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
The most important determinant of risk is travel destination, and there are regional differences in both the risk for and etiology of diarrhea. The world is generally divided into 3 grades of risk: low, intermediate, and high.
- Low-risk countries include the United States, Canada, Australia, New Zealand, Japan, and countries in Northern and Western Europe.
- Intermediate-risk countries include those in Eastern Europe, South Africa, and some of the Caribbean islands.
- High-risk areas include most of Asia, the Middle East, Africa, Mexico, and Central and South America.
TD occurs equally in male and female travelers and is more common in young adult travelers than in older travelers. In short-term travelers, bouts of TD do not appear to protect against future attacks, and >1 episode of TD may occur during a single trip. A cohort of expatriates residing in Kathmandu, Nepal, experienced an average of 3.2 episodes of TD per person in their first year. In more temperate regions, there may be seasonal variations in diarrhea risk. In south Asia, for example, much higher TD attack rates are reported during the hot months preceding the monsoon. In environments where large numbers of people do not have access to plumbing or outhouses, the amount of stool contamination in the environment will be higher and more accessible to flies. Inadequate electrical capacity may lead to frequent blackouts or poorly functioning refrigeration, which can result in unsafe food storage and an increased risk for disease. Inadequate water supplies can lead to the absence of sinks for handwashing by restaurant staff, as well as direct contamination of foods, such as fruits and vegetables washed in contaminated water. Poor training in handling and preparation of food may lead to cross-contamination from meat, and inadequate disinfection of food preparation surfaces and utensils. In destinations in which effective food handling courses have been provided, the risk for TD has been demonstrated to decrease. However, some pathogens that cause TD, such as Shigella sonnei, are not unique to developing countries. The risk of TD is associated with the water, sanitation, and hygiene environment and practices in specific destinations, as well as the handling and preparation of food in restaurants in developed countries.
Prevention Vaccine Food and beverage Pepto Bismol Prophylactic antibiotics
Transmission: Food and water
Symptoms: Bacterial diarrhea presents with the sudden onset of bothersome symptoms that can range from mild cramps and urgent loose stools to severe abdominal pain, fever, vomiting, and bloody diarrhea. Viral enteropathogens present in a similar fashion to bacterial pathogens, although with norovirus vomiting may be more prominent. Protozoal diarrhea, such as that caused by Giardia intestinalis or E. histolytica, generally has a more gradual onset of low-grade symptoms, with 2–5 loose stools per day. The incubation period of the pathogens can be a clue to the etiology of TD: Bacterial and viral pathogens have an incubation period of 6–48 hours. Protozoal pathogens generally have an incubation period of 1–2 weeks and rarely present in the first few weeks of travel. An exception can be Cyclospora cayetanensis, which can present quickly in areas of high risk. Untreated bacterial diarrhea lasts 3–5 days. Viral diarrhea lasts 2–3 days. Protozoal diarrhea can persist for weeks to months without treatment. An acute bout of gastroenteritis can lead to persistent gastrointestinal symptoms, even in the absence of continued infection (see Chapter 5, Persistent Travelers’ Diarrhea). Other postinfectious sequelae may include reactive arthritis and Guillain-Barré syndrome.
Treatment: Antibiotics are the principal element in the treatment of TD and are effective in cases caused by bacterial pathogens that are susceptible to the particular antibiotic prescribed. Adjunctive agents used for symptomatic control may also be recommended. Antibiotics As bacterial causes of TD far outnumber other microbial causes, empiric treatment with an antibiotic directed at enteric bacterial pathogens remains the best therapy for TD. The benefit of treating TD with antibiotics has been proven in numerous studies. The effectiveness of a particular antimicrobial depends on the etiologic agent and its antibiotic sensitivity. Both as empiric therapy or for treatment of a specific bacterial pathogen, first-line antibiotics include those of the fluoroquinolone class, such as ciprofloxacin or levofloxacin. Increasing microbial resistance to the fluoroquinolones, especially among Campylobacter isolates, may limit their usefulness in some destinations, such as Thailand, where Campylobacter is prevalent. Increasing cases of fluoroquinolone resistance have been reported from other destinations and in other bacterial pathogens, including Shigella and Salmonella. A potential alternative to the fluoroquinolones in these situations is azithromycin. Rifaximin has been approved to treat TD caused by noninvasive strains of E. coli. However, since it is often difficult for travelers to distinguish between invasive and noninvasive diarrhea, and since they would have to carry a back-up drug in the event of invasive diarrhea, the overall usefulness of rifaximin as empiric self-treatment remains to be determined. Single-dose or 1-day therapy for TD with a fluoroquinolone is well established, both by clinical trials and clinical experience. The best regimen for azithromycin treatment is not yet established. One study used a single dose of 1,000 mg, but side effects (mainly nausea) may limit the acceptability of this large dose. Azithromycin, 500 mg per day for 1–3 days, appears to be effective in most cases of TD. Antimotility Agents Antimotility agents provide symptomatic relief and serve as useful adjuncts to antibiotic therapy in TD. Synthetic opiates, such as loperamide and diphenoxylate, can reduce bowel movement frequency and enable travelers to ride on an airplane or bus while awaiting the effects of antibiotics. Loperamide appears to have antisecretory properties as well. The safety of loperamide when used along with an antibiotic has been well established, even in cases of invasive pathogens. Antimotility agents are not generally recommended for patients with bloody diarrhea or those who have diarrhea and fever. Loperamide can be used in children, and liquid formulations are available. In practice, however, these drugs are rarely given to small children (aged < 6 years old)
Oral Rehydration Therapy
Fluids and electrolytes are lost in cases of TD, and replenishment is important, especially in young children or adults with chronic medical illness. In adult travelers who are otherwise healthy, severe dehydration resulting from TD is unusual unless vomiting is prolonged. Nonetheless, replacement of fluid losses remains an adjunct to other therapy and helps the traveler feel better more quickly. Travelers should remember to use only beverages that are sealed, treated with chlorine, boiled, or are otherwise known to be purified. For severe fluid loss, replacement is best accomplished with oral rehydration solution (ORS), prepared from packaged oral rehydration salts, such as those provided by the World Health Organization, which are widely available at stores and pharmacies in most developing countries. ORS is prepared by adding 1 packet to the indicated volume of boiled or treated water—generally 1 liter. Travelers may find most ORS formulations to be relatively unpalatable, due to their saltiness. In less severe cases, rehydration can be maintained with any palatable liquid (including sports drinks), although overly sweet drinks, such as many sodas, can cause osmotic diarrhea if consumed in quantity.
Children who accompany their parents on trips to high-risk destinations may be expected to have TD as well. There is no reason to withhold antibiotics from children who contract TD. In older children and teenagers, treatment recommendations for TD follow those for adults, with possible adjustments in the dose of medication. Macrolides such as azithromycin are considered first-line antibiotic therapy in children, although some experts now use short-course fluoroquinolone therapy (despite its not being FDA-approved for this indication in children) for travelers aged <18 years. Rifaximin is approved for use in children aged ≥12 years.
Infants and younger children with TD are at higher risk for developing dehydration, which is best prevented by the early use of ORS. Breastfed infants should continue to nurse on demand, and bottle-fed infants can continue to drink their formula. Older infants and children may eat a regular diet, depending on the level of their appetite while they are ill. Infants in diapers are at risk for developing a painful, eczematous rash on their buttocks in response to the liquid stool.
Typhoid and Paratyphoid Fever Geographic risk, prevention, transmission, possible symptoms and appropriate referral/triage of:
An estimated 22 million cases of typhoid fever and 200,000 related deaths occur worldwide each year; an additional 6 million cases of paratyphoid fever are estimated to occur annually. Each year in the United States, approximately 400 cases of typhoid fever and 100 cases of paratyphoid fever are reported, most in recent travelers. The risk of typhoid fever is highest for travelers to southern Asia (6–30 times higher than for all other destinations). Other areas of risk include East and Southeast Asia, Africa, the Caribbean, and Central and South America. The risk of infection with S. enterica serotype Paratyphi A is also increased among travelers to southern and Southeast Asia. In certain regions, the risk of typhoid fever is decreasing. Travelers to southern Asia are at highest risk for infection with typhoid and paratyphoid strains that are nalidixic acid–resistant or multidrug-resistant (resistant to ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole). Travelers who are visiting friends and relatives (VFRs) are at increased risk. ravelers who are visiting friends and relatives (VFRs) are at increased risk (see Chapter 8, Immigrants Returning Home to Visit Friends and Relatives [VFRs]). Although the risk of acquiring typhoid or paratyphoid fever increases with the duration of stay, travelers have acquired typhoid fever even during visits of <1 week to countries where the disease is endemic.
Prevention:
Safe food and water precautions and frequent handwashing are important in preventing typhoid and paratyphoid fever . Although vaccines are recommended to prevent typhoid fever, they are not 100% effective; therefore, even vaccinated travelers should follow recommended food and water precautions. These precautions are the only prevention method for paratyphoid fever, as no vaccines are available.
Vaccine
Symptoms:
The incubation period of typhoid and paratyphoid infections is 6–30 days. The onset of illness is insidious, with gradually increasing fatigue and a fever that increases daily from low-grade to as high as 102°F–104°F (38°C–40°C) by the third to fourth day of illness. Headache, malaise, and anorexia are nearly universal. Hepatosplenomegaly can often be detected. A transient, macular rash of rose-colored spots can occasionally be seen on the trunk. Fever is commonly lowest in the morning, reaching a peak in late afternoon or evening. Untreated, the disease can last for a month. The serious complications of typhoid fever generally occur after 2–3 weeks of illness and may include intestinal hemorrhage or perforation, which can be life threatening.
Treatment:
Specific antimicrobial therapy shortens the clinical course of typhoid fever and reduces the risk for death. Empiric treatment in most parts of the world uses a fluoroquinolone, most often ciprofloxacin. However, resistance to fluoroquinolones and nalidixic acid is highest in the Indian subcontinent and increasing in other areas. Injectable third-generation cephalosporins are often the empiric drug of choice when the possibility of fluoroquinolone nonsusceptibility is high. Azithromycin is increasingly used to treat typhoid fever or paratyphoid fever because of the emergence of multidrug-resistant strains.
Patients treated with an antibiotic may still require 3–5 days for fever to subside completely, although the height of the fever decreases each day. Patients may actually feel worse during the several days it takes for the fever to end. If fever does not subside within 5 days, alternative antimicrobial agents or other foci of infection should be considered.
