Foodborne illnesses are a group of conditions produced by ingestion of food and are caused by a broad range of chemical contaminants, bacteria, viruses, parasites and biotoxins, and are often referred as neglected diseases. On a global scale, they constitute important public health issues due to their incidence, serious sequelae and mortality, new forms of transmission, vulnerable population groups, increased resistance of causative agents to antimicrobial compounds, as well as the negative effects on the economy attributable to costs in health services, productivity, demands and consumer´s confidence (Marin et al., 2020; Sander et al., 2020).
According to the World Health Organization (WHO) parasitic diseases, resulted in 48.4 million cases and n 59,724 deaths annually, resulting in 8.78 million Disability Adjusted Life Years (DALYs), and it is estimated that 48 % of these parasitic diseases were food-borne (Torgerson et al., 2015).
The zoonotic potential of foodborne pathogens and their ability to cause several diseases or even death is sufficient to recognize the seriousness of the situation (Heredia & García, 2018)
For a foodborne illness to occur, the pathogen must be present in the food. However, the mere presence of the pathogen does not mean that the disease will occur. In most cases of foodborne parasitic illnesses (OPS/WHO, 2014):
The parasite must be present in sufficient quantities to cause infection.
The parasite must be able to subsist on the food. That is, the food must have intrinsic characteristics that keeps the agent under favorable conditions.
Food must remain at an appropriate temperature long enough for the parasite to survive.
Enough (portion) of the food containing the pathogen must be ingested so that the individual’s immunological response is surpassed.
Rates of parasitic contamination differ from one country to another, and even between regions within the same country. The increase of human population and urbanization, the globalization, cultural preferences and eating habits have led to an increase in zoonotic infections incidence. Nowadays, there is a worldwide increase in the consumption of raw or slightly cooked vegetables, which also increases the risk of foodborne infections (Berrouch et al., 2020; Trevisan et al., 2019; Heredia & García, 2018). Millions of people contract foodborne diseases daily. Parasites can be present in food and water and can cause illness. They range in size from small, single-celled organisms to worms visible to the naked eye. Their life cycles also vary. While some parasites use a permanent host, other parasites go through a series of developmental stages using different hosts, whether humans, or other animals. These parasitosis can cause a wide variety of illnesses, from uncomfortable symptoms to debilitating disorders and possibly death (USDA, 2017).
The tropical climate of many developing countries favors the proliferation of pests and naturally occurring toxins, as well as the risk of contracting parasitic diseases, including worm infestations. Parasitic diseases often result in high burdens of disease in low- and middle-income countries and are frequently transmitted to humans via contaminated food. These parasitosis are often chronic, with long-term sequelae (Trevisan et al., 2019; Torgerson et al., 2015)
Water usage in the food industry include activities such as: irrigation, washing of fresh produce, and processing. Water scarcity means increased utilization of wastewater for these previous activities, increasing the chance of fresh produce contamination (Trevisan et al., 2019).
The climate of the neotropics (which extends from Mexico to southern Brazil, encompassing all Central America, the Caribbean, and almost all South America), favors the presence of a great diversity of food-borne parasitic diseases. The scarcity of studies carried out in this geographical region prevents the exact epidemiology of these diseases from being established. In addition, it is not mandatory to notify public health authorities about most parasitic diseases, for which the real prevalence or incidence of the diseases is not known (WHO, 2018). In the present work we focus on nine of the most important neotropic foodborne parasites:
The eggs of
Life cycle takes place when pigs ingest human stools containing
Intestinal taeniasis is usually asymptomatic, while cysts in the nervous system produce neurocysticercosis (NCC) which is the most common clinical manifestation. This manifestation varies depending on the number of cysts, location, size and stage of the parasite, as well as the inflammatory response of the host. Parasitic larvae located in the parenchyma of the brain most frequently manifest with seizures (Garcia et al., 2014). NCC diagnosis is based on tests detecting antibodies against
Some commercial anthelmintics have shown efficacy in the treatment of taeniasis, including albendazole, praziquantel and niclosamide (Haby et al., 2020). In the pig host, vaccines are available including TSOL18, alongside anthelmintic treatment using oxfendazole (CystiTeam Group, 2019).
Human echinococcosis is a zoonotic disease result from infection with the larval stage of several species of the genus
It should be noted that exists two indigenous neotropical species:
Echinococcosis has a cosmopolitan distribution and represents a major public health problem in some regions. In South America is endemic in parts of Argentina, Bolivia, Brazil, Chile, Peru, and Uruguay (Larrieu & Zanini, 2012). It is prevalent in low-income, livestock-raising communities. The prevalence of cystic echinococcosis increases with age, and women are affected more frequently than men; this might be related to domestic activities that bring them in closer contact with dogs through feeding, herding, or milking livestock (Agudelo et al., 2016).
Cystic echinococcosis is usually asymptomatic unless complications occur. The rate at which symptoms appear typically depends on the location of the cyst. Rupture with resultant infection or anaphylaxis, fistula development with adjacent structures (e.g., in the biliary tract, intestine, and bronchus) or mass effect on neighboring structures are the major mechanisms by which a cyst usually becomes symptomatic. Most patients (40 % to 80 % of cases) have a single cystic lesion located in a single organ. The liver is affected in 70 % of the cases, the right lobe more commonly than the left. The lung is the next most frequently affected organ and is affected in about 20 % of the cases (Agudelo et al., 2016).
Imaging techniques are essential for diagnosis, with the relatively inexpensive and portable ultrasound (US) widely used to diagnose CE or AE liver lesions; X-ray is used for lung cysts. Serologic tests are available, including the enzyme linked immune transfer blot (EITB) test, which apparently offers greater sensitivity and specificity than do the enzyme-linked immunosorbent assay (ELISA) and arc-5 double-diffusion assay (DD5). Serologic differentiation between cystic and alveolar echinococcosis, involving recombinant larval antigens has also been used (Garcia, 2007).
Several options are available for treatment of echinococcosis, including surgery, puncture-aspiration injection-respiration (PAIR), and chemotherapy (benzimidazoles). Surgery is generally considered the treatment of choice for a complete cure. In cases where multiple cysts are present in several different sites or in patients with a high surgical risk, PAIR and chemotherapy are considered appropriate options, either together or separately. Long-term follow-up with imaging is required to evaluate the efficacy of treatment, as serology results may remain positive for years even after successful treatment (Agudelo et al., 2016; Garcia, 2007).
Toxoplasmosis is present in every country and seropositivity rates range from less than 10 % to over 90 %. The annual incidence of congenital toxoplasmosis worldwide was estimated to be 190,100 cases (Togerson & Mastroiacovo, 2013). In the United States and the United Kingdom, it is estimated that between 16 % and 40 % of the population is infected, while in Central America, South America and continental Europe, infection estimates range between 50 % and 80 % (Hill & Dubey, 2002). Brazil has a very high rate of
Studies of genotypes of
There are three infectious stages of
In most adults the disease is asymptomatic, but it can cause blindness and mental retardation in children with congenital infection, this occurs when a woman becomes infected during pregnancy. Infections during the first trimester are more serious than those acquired in the second and third trimester. At first there is a generalized infection in the fetus, later, the infection clears the visceral tissues and can be localized to the central nervous system (Wang et al., 2017). Mild disease may consist of slightly impaired vision, while severely ill children may have the full tetrad of signs: retinochoroiditis, hydrocephalus, seizures, and intracerebral calcification. Of these, hydrocephalus is the least common, but most dramatic lesion of toxoplasmosis. The most common sequela of congenital toxoplasmosis are eye conditions. Toxoplasmosis could be a devastating disease in immunosuppressed individuals, in which encephalitis is the most dangerous manifestation of the disease.
Concentration methods (eg, flotation in a high-density sucrose solution) are often used as detection methods because of the number of
Although there are many drugs available, the treatment of choice is the combination of pyrimethamine with sulfadiazine, which can control the rapid replication phase (acute phase of the disease) but does not influence cysts. For cysts treatments with hydroxynaphthoquinone (atovaquone) and azithromycin seem to be the treatment of choice (Zamora et al., 2020).
It is an enteric protozoan parasite that can be transmitted to humans from animals, other humans, contaminated food, or water, and tends to cause waterborne outbreaks (Vanathy et al., 2017).
An initial macroscopic examination should be done to look for the consistency of the stool, where flotation and concentration techniques are used (Sheather’s sucrose, zinc sulfate, and saturated sodium chloride). Specific anti-
Chemotherapy treatments include macrolide antibiotic, aminoglycoside paromomycin, ionophores such as maduramycin, rifaximin, octreotide, as well as immunotherapy. Nitazoxanide is found to be useful in immunocompetent patients and it is a licensed drug (Rousseau et al., 2018).
Amebiasis or amoebic dysentery is a common parasitic enteral infection, which is caused by any of the pathogenic species of the genus Entamoeba (Zulfiqar et al., 2020), whose pathogenesis is mainly characterized by cytotoxicity, inflammation, and tissue invasion (Shirley et al., 2020). Most infections are asymptomatic, but invasive intestinal disease can occur. Likewise, disseminated extraintestinal disease can also occur, such as liver abscess, pneumonia, purulent pericarditis and even cerebral amebiasis (Kantor et al., 2018).
Currently, amebiasis is the third main cause of disease and the fourth main cause of death from protozoan infections worldwide (Kantor et al., 2018; Debnath, 2015). It is estimated that approximately 500 million people are infected by the parasite worldwide, of which 10 % have invasive amebiasis (Ximénez et al., 2010), with around 100,000 patients dying per year due to clinical complications of the disease (Shirley et al., 2020). Amebiasis is a disease of global importance that occurs mainly in developing countries, where hygiene and access to sanitation are inadequate (Shirley et al., 2018). The areas with the highest infection rate, in which the disease is endemic, include Central and South America, Africa, and Asia (Kantor et al., 2018). In developing countries, the exact burden of amoebiasis is difficult to quantify. Reports can be affected by geographic region, study design, sample size, incubation, severity of symptoms, and the sensitivity of the diagnostic tools used (Shirley et al., 2018).
The life cycle of
Amebiasis can be asymptomatic, known as luminal amebiasis; or it can lead to the development of a serious infection with amoebic colitis and amoebic liver abscess (Shirley et al., 2018). Approximately 90 % of people will remain asymptomatic after ingestion of the infectious amoebic cyst and most will eventually clear the parasite (Shirley et al., 2020), the other 10 % progress to develop a symptomatic infection (Shirley et al., 2018). Symptoms can develop after an incubation period that can be as short as 2 to 4 weeks. Diarrhea is the most common manifestation of the disease, followed by dysentery and very rarely can progress into extraintestinal abscess (Shirley et al., 2020).
Intestinal amebiasis presents as a spectrum of diseases ranging from acute amoebic dysenteric colitis to more chronic non-dysenteric colitis that presents sub acutely with non-specific watery diarrhea (Shirley et al., 2020). Amoebic colitis generally has a subacute onset, with symptoms that can range from mild diarrhea to severe dysentery, with abdominal pain and watery or bloody diarrhea, and weight loss (Shibayama et al., 2015; Kantor et al., 2018; Shirley et al., 2018). Unusual but serious complications can occur, such as fulminant necrotic colitis, whose fatality ranges from 40 % to 89 % (Shirley et al., 2018), toxic megacolon, and fistulizing perianal ulcers, especially when diagnosis and treatment are not timely. Exclusion of inflammatory intestinal disease is exceptionally important, since misdiagnosis and corticosteroid treatment can lead to these serious complications (Kantor et al., 2018). Amebic liver abscess can occur in the presence or absence of intestinal symptoms, and is the most common extraintestinal manifestation of amebiasis, which develops when trophozoites spread to the liver. Onset can be insidious, subacute, or acute. Symptoms include fever, cough, respiratory symptoms, epigastric pain, pleuritic pain, hepatomegaly with pinpoint liver tenderness, prominent weight loss with less fever and abdominal pain (Shirley et al., 2018; Shirley et al., 2020). Pleuropulmonary amebiasis is the most common complication of amoebic liver abscess (Kantor et al., 2018) and can present in the form of pneumonitis, lung abscess or broncho hepatic fistula (Shirley et al., 2020). Occasionally, trophozoites can also spread via bloodstream to the central nervous system (Shirley et al., 2018) causing cerebral amebiasis, which has an abrupt onset and rapidly progresses to death over 12 to 72 hours without adequate therapy (Shirley et al., 2020).
Differential diagnosis in amoebiasis is extremely important for two aspects: 1) to differentiate amoebic colitis from a bacterial enteric infections, such as those caused by S
Since there is currently no vaccine against amebiasis, current therapy for clinical disease requires treatment with two types of drugs: 1) tissue amebicides, such as metronidazole and tinidazole (Nagaraja & Ankri, 2019), which are very effective in eliminating invading trophozoites and remain the recommended therapy for amoebic colitis and amoebic liver disease (Shirley et al., 2018); and 2) luminal amebicides such as paromomycin, to eliminate intraluminal cysts (Kantor et al., 2018), and prevent invasion and transmission (Shirley et al., 2018). However, concerns about adverse effects and the possible appearance of
The species of the parasite nematode of the genus
Trichinellosis is a parasitic disease characterized by having a wide range of hosts and geographic distribution (Gottstein et al. 2009). According to the World Health Organization (WHO) until 2009, more than 65,000 cases of trichinellosis were registered around the world, with more than 42 fatal cases (Berger, 2017) in the regions of America, Africa, South Asia, and Europe (Pozio & Zarlenga, 2013). However, it is estimated that currently 11 million humans in the world are infected with
On the other hand, some authors mention that the importance of
The severity of the clinical disease is strongly dependent and directly correlates with the number of L1 ingested, as well as host’s age, sex, nutritional, hormonal condition, immunity, and tissue invaded. Likewise, the infection can lead to a wide spectrum of clinical forms, ranging from being an asymptomatic infection to even cause death (Gottstein et al., 2009). The clinicopathology of trichinellosis can be divided based on the phases of the life cycle and/or stages of
Early clinical diagnosis of trichinellosis is quite difficult due to the lack of pathognomonic symptoms and signs, likewise, chronic forms of the disease are not easy to diagnose (Gottstein et al., 2009). When the infection occurs on its epizootic or outbreak form, its diagnosis is easier, however, low-level, or sporadic infections are difficult to diagnose since the clinical features are often common to many other enteric diseases. This calls for a differential diagnosis technique (Bruschi & Murrell, 2002; Gottstein et al., 2009). The identification of
Currently there is no specific therapy for trichinellosis, however, the pharmacotherapy used includes the use of antiparasitic drugs such as benzimidazoles, mainly albendazole and mebendazole, which are directed against the parasite, and the use of steroidal anti-inflammatory drugs, such as glucocorticoids, whose purpose is to treat the symptoms produced by the disease (Muñoz-Carrillo et al., 2017a). Recently, studies have reported that treatment with resiniferatoxin (RTX), a vanilloid agonist of the transient receptor potential vanilloid (TRPV)-1 (Carnevale & Rohacs, 2016) has the potential to down-regulate the production of proinflammatory mediators and cytokines, such as NO, PGE2, IFN-γ, IL-12, IL-1β and TNF-α in the intestinal phase of
Approximately one billion people in the world are infected with
Infection occurs when the host ingests eggs from stool-contaminated soil. Once in the duodenum, larvae are released and enter the circulation via the enteric mucosa. Once in the capillaries (venous, arterial, or lymphatic), it reaches the liver via the portal vein and then the lungs within the first week. In the lung, they damage the alveolar membrane and mature in the alveolus. Eventually, the larvae are expectorated and swallowed re-entering the gastrointestinal tract. Once in the small intestine lumen, the larvae mature to adult worms in approximately 20 days. When the adult female and male worms are present, they copulate, and the female can produce up to 200,000 eggs per day, which are later eliminated in the feces to the soil. If appropriate moist, shady, and warm environmental conditions are present, the eggs mature to infective form in two to eight weeks and remain viable for up to 17 months. They can be ingested and restart the infective cycle (De Lima & Horrall, 2020).
Patients infected with ascariasis can be asymptomatic, only showing long-term manifestations of growth retardation and malnutrition. If symptoms are present, abdominal pain, bloating, nausea, vomiting, anorexia, intermittent diarrhea are the most common manifestations. If the number of larvae passing through the lung is significant, pneumonitis and eosinophilia can be seen (also known as Loeffler syndrome). Symptoms include wheezing, dyspnea, cough, hemoptysis, and fever. In superinfection, adult worms can migrate to tubular structures like the biliary and pancreatic system causing cholecystitis, cholangitis, pancreatitis, small bowel obstruction, volvulus, appendicitis, and intussusception. Children are more susceptible to complications than adults (De Lima & Horrall, 2020).
The best diagnostic test is still the stool exam for ova and parasites, searching for large oval brown trilayered eggs with a mamillated coat. Stool exam can be negative, while the worm migrates and matures (approximately one month). A complete blood count can show eosinophilia during the active migration phase from the intestine to the lungs and larvae can be found in the sputum. Abdominal x-rays can be sensitive but not specific when a whirlpool sign is present. Ultrasound and CT scan can be used to identify worms in the biliary duct and gallbladder (De Lima & Horrall, 2020). Albendazole 400 mg as a single dose is the drug of choice. The second choice of treatment is mebendazole 100 mg twice a day for three days or ivermectin 100 microgram/kg to 200 microgram/kg once. In pregnancy, piperazine 50 mg/kg/day for five days is the drug of choice. Treatment should be repeated after one to three months (de Lima & Horrall, 2020).
Chagas disease (CD) is a potentially fatal disease caused by the protozoan
Although, Transmission was traditionally considered almost exclusively vectorborne, other transmission routes have been observed, including foodborne, where the vector is still essential. This transmission occurs when food get contaminated with metacyclic trypomastigotes from either the feces of triatomines or from the whole insect, which are then ingested by humans. Generally, metacyclic trypomastigotes are inactivated by drying or by low moisture content, so drinks such as fruit juices are the most common foodborne transmission vehicles (Robertson et al., 2016).
More than 100 years after its discovery and despite technological advances and socio-demographic changes, this disease continues to be a challenge for health experts, highlighting its existence as a neglected tropical disease (Molina et al., 2016).
The WHO estimated that in 2020 between 6 and 7 million individuals are infected with
Within the host cells, the trypomastigote becomes amastigote, a vegetative state that is characterized by a rounded shape and no flagellum, its size is approximately 1.5 to 4 μm and it usually agglomerates forming tissue nests or also called pseudocysts. Within its life cycle there is an intermediate morphological form called epimastigote, its size is slightly smaller than that of trypomastigote, only 5 – 7 μm, it has a fusiform appearance, a small undulating membrane and does not have a flagellum. According to its genetic diversity,
In the wild, it can infect arthropods and many mammalian species (domestic and wild). When the vector feeds from the blood of an infected mammal, it also ingests the circulating parasite. In the the intestinal lumen it multiplies and develops into meta-cyclic trypomastigotes (infective forms) that come out along with the excretions, pass through the skin or mucous membranes and infect the new host. In the new host, they access circulation as blood trypomastigotes and later as amastigotes on its intracellular form, multiplying by longitudinal binary fission within cells of the mononuclear phagocytic system, lymphoid, muscular or nervous tissue and the cycle is completed when the blood trypomastigotes are ingested by the vector (triatomids). The infection in humans is acquired mainly by the transcutaneous penetration of the parasite present in the excreta of infected hematophagous insects (Salaza-Schettino et al., 2016).
It has been identified three phases of this disease: acute, indeterminate, and chronic. The acute phase occurs when the parasite has been inoculated for the first time, it is generally asymptomatic, although it can cause fever and body ache in 5 % of patients. It is believed that 50 % of infected patients will remain in an indeterminate and asymptomatic phase for life, without complications. After a decade or more, 20 to 30 % will present cardiovascular disease with heart failure, arrhythmias, and thrombus embolism, 15 % to 20 % will present mega esophagus and megacolon. When this disease occurs in the mother and child, the repercussions can be catastrophic for both. For vertical transmission, placental infection can occur before the 22nd week of gestation, and/or the baby can be infected during childbirth with the blood of the infected mother. Factors such as intensity of the parasitemia, parasite virulence, maternal and fetal ability to mount a specific immune response and the functionality of the placental barrier have been mentioned important for congenital infection to develop (Ceballos et al., 2017). Currently the diagnostic methods for trypanososmiasis are based on detecting the parasite in tissue or blood, as well as the detection of antibodies or secretory products of the parasite. In the acute phase, the parasite is rarely detected unless symptoms are severe (WHO, 2012). Microscopy observation is possible since the parasite can be found in blood, cerebrospinal fluid, and tissue, this can be achieved by giemsa staining or fresh.
Since 1990, thiazole compounds, inhibitors of the biosynthesis of ergosterol, which is part of the protozoan membrane, have shown promise results since the parasite requires specific sterols (lipopeptidylphosphoglycerol) for its survival and proliferation. Posaconazole showed parasitological cure in murines in both the acute and chronic phases of CD. Other compounds such as posaconnaitoquinones, diamines, nitromidazoles, ruthenium derivatives and complexes have been evaluated, which showed high toxicity. Over the year’s consortia have been formed for the discoveries against Chagas. Among the clinical trials carried out in humans for the development of new drugs, we highlight: “Clinical trial for the treatment of chronic Chagas disease whit posaconazole and benzinmidazole (BNZ) (Chagazol®) and E1224, studies that evaluated posaconazole and ravuvonazole”, in this study, it was concluded that these drugs are not effective as single-agent drugs. In 2011, the pediatric formulation of nezinidazole was approved, with a dosage that will allow its administration to young children, reducing side effects (Belaunzaran, 2015). The WHO in 2020 mentions that BNZ and nifurtimox are 100 % effective if administered in the acute phase of the disease (WHO, 2020). The only drugs prescribed are nifurtimos (NF) (lampit®) and benzimidazole (BNZ), (Ragomil®), ROchagan®; Ranadil®) (Murillo, 2018).
Human fascioliasis is a reemerging disease, found in more than 70 countries, there is little information on fascioliasis in humans and its geographical distribution, however it is estimated that there are 17 million people affected by this parasite in the world (Mas-Coma et al., 2018). In Latin America estimations are up to 2.39 million people infected, which 50 % of cases resides in Bolivia, Ecuador and Peru affecting mainly children (Mas-Coma et al., 2020). The principal disease is caused by
Biological cycle is characterized by four stages (miracidium, sporocyst, cercariae and metacercariae) and takes place in two hosts: a gastropod mollusk and a mammal. Infecting metacercariae enter the digestive tract through consumption of contaminated water or raw vegetables. Then penetrate through the oral cavity and lose their covering in the stomach, releasing a small parasite that crosses the intestinal wall, falls into the peritoneum, and migrates towards the liver, feeding on hepatocytes and causing hemorrhagic necrosis, to finally locate in the bile ducts. Two weeks later the parasites reach sexual maturity and begin to egg laying. The non-embryonic eggs pass from the bile ducts to the intestine and exit through the feces (Valero et al., 2006; Mas-Coma et al., 2018). Symptomatology depends on the number of parasites ingested, and in some cases the person can remain asymptomatic. Infection can be acute or chronic, and is characterized by 30 – 40 % eosinophilia, fever, diarrhea, vomiting, painful hepatomegaly, biliary obstruction, intestinal tenderness, urticaria, irregular fever, and diarrhea (Walker et al., 2006; WHO, 2008).
Confirmatory diagnosis results from egg observation in a stool sample, which must be repeated three times with ten days separation in between analysis. Other signs useful in diagnosis are: Immunological reactions: intradermal reaction, hemagglutination and gel precipitation; Alteration of the hemogram: eosinophilia of 40 to 80 % in initial state that later decreases; And elevated concentration of bilirubin and alkaline phosphatase in cases of bile duct obstruction (Estrada et al., 2020).
Treatments used for several years were: emetine hydrochloride, dihydroemetine and bithionol, which are already withdrawn from the market. Triclabendazole is the most common treatment today. The dose is 10 – 12 mg. / kg. weight of 1 to 2 doses (Estrada et al., 2020; Walker et al., 2006; WHO, 2018).
The diseases described here are caused by parasitic species and are foodborne infections, resulting from the ingestion of fecal contaminated food or water. Their main carriers are water, fresh fruits, and vegetables, therefore, good hygiene in their manipulation is key to control and eradicate these diseases. Unfortunately, most of the countries located in the Neotropic area are underdeveloped, which accounts for higher poverty numbers, limited education, and the lack of an adequate health system, these impact negatively not only life quality, but also the control and eradication of these important pathologies. Generally, parasitic diseases are asymptomatic, when symptoms appear, they usually present as gastroenteric diseases, making it particularly difficult to have an accurate diagnose and statistics. Although not all these parasitosis are fatal, the biggest problem of the high prevalence of these pathologies is the negative impact on the quality of life. The annual incidence of the main parasitic diseases transmitted by food has been estimated by the Pan American Health Organization (PAHO) to be up to 10 % of the population, with tropical countries being the most affected. Prevention and control measures are fundamental, being pillars the provision of safe water and the sanitary disposal of excreta, in addition to health education: such as hygienic habits and hygienic handling of food.
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