• Infective foodborne illnesses are innumerable and are caused by various microorganisms. Some microorganisms are established agents, several others are emerging pathogens, and the pathogenicity of the remainder is still under speculation.
• Classification of these illnesses is best done according to their incubation periods, the symptoms they produce, or both.
• Nausea and vomiting predominate in illnesses with short incubation periods caused by preformed toxins, whereas diarrhea predominates in those with long incubation periods caused by toxins produced in the intestine.
• Undercooked charcuterie, meat, poultry, and seafood account for a majority of foodborne illness, but dairy products, salads, pastries, fruits, and vegetables can also cause illness.
• Contaminated water acts as a vehicle in almost all instances.
• The majority of infective foodborne illnesses with symptoms confined to the gastrointestinal tract, although apparently alarming, are self-limiting and need only supportive measures including replacement of water and electrolytes.
• Antimicrobial agents are indicated only in certain patients, including those with systemic illnesses, extremes of age, immunocompromised and malnourished states, and severe life- threatening illness.
• Antitoxin is useful in botulism poisoning.
• Vaccines are available against Vibrio cholerae, Salmonella typhi, hepatitis A virus, and rotavirus, but their effectiveness and cost- effectiveness are debatable.
The Centers for Disease Control and Prevention (CDC) estimates that each year roughly one in six Americans (about 48 million people) gets sick from foodborne illnesses; 128,000 are hospitalized, and 3000 die. These figures are higher in developing nations, and many cases are not brought to light because they occur in remote villages. The 2011 estimates provide the most accurate picture of infective foodborne illnesses, of which bacteria, viruses, and parasites account for the majority. Processing of ready-to-eat foods increases the risk of acquiring foodborne illness because of increased food handling, leading to introduction and growth of pathogens. Increased international travel and migration have also resulted in a greater risk because travelers are at high risk for developing foodborne gastroenteritis caused by pathogens to which they have not been exposed at home.
Classification of Foodborne Illnesses
Agents causing foodborne diseases may be classified in several ways. The most common scheme is a taxonomic combined with a classification based on mode of action (Tables 1 to 3).
Classification of Foodborne Illnesses
Common Organisms Implicated in Infective Foodborne Illness
Abbreviation: GI = gastrointestinal.
Rare and Emerging Infections
Species of Aeromonas are ubiquitous and autochthonous in aquatic environments, more so after the tsunami that followed the Indonesian earthquake in December 2004. These aeromonads share many biochemical characteristics with members of the Enterobacteriaceae.
The mesophilic species Aeromonas caviae, Aeromonas hydrophila, and Aeromonas veronii are principally associated with gastroenteritis; A. caviae particularly infects children younger than 3 years.
Transmission is documented as occurring from a contaminated piped water source, as seen in community-based outbreaks, especially among children. The probability of occurrence of Aeromonas infection increased significantly when the mean seasonal temperature exceeded 14 °C (57°F), and this was exacerbated where the mean free chlorine concentration fell below 0.1 mg/L.
Aeromonas species are potential food-poisoning agents. A. hydrophila is psychrotrophic and has been associated with spoilage of refrigerated animal products including chicken, beef, pork, lamb, fish, oysters, crab, and milk.
The incubation period for Aeromonas-associated traveler’s diarrhea is 1 to 2 days. It usually causes a sporadic illness. Usually a mild to moderate but self-limiting diarrhea occurs, but it can be severe enough in children to require hospitalization. Aeromonas gastroenteritis can occur as a nondescript enteritis, as a more-severe form accompanied by bloody stools, as the etiologic agent of a subacute or chronic intestinal syndrome, as an extremely rare cause of cholera-like disease, or in association with episodic traveler’s diarrhea. By far the most common presentation of Aeromonas gastroenteritis is watery enteritis. The most serious complication resulting from Aeromonas gastroenteritis is hemolytic uremic syndrome.
Mesophilic Aeromonas spp. can express a range of virulence factors, including attachment mechanisms and production of a number of toxins. Toxins include aerolysin (a pore-forming cytolysin that attaches to cell membrane, leading to leakage of cytoplasmic contents) and a cytotonic enterotoxin with activity similar to that of cholera toxin. Strains of A. hydrophila produce lectins and adhesins, which enable adherence to epithelial surfaces and gut mucosa.
Samples are best transported using Cary-Blair medium. Aeromonas forms a bull’s-eye–like colony on the selective medium cefsulodin irgasan novobiocin (CIN) agar owing to fermentation of D-mannitol. Ampicillin blood agar has an advantage over CIN agar in that hemolytic colonies can readily be tested for oxidase. Aeromonas species produce hemolysis on sheep blood agar.
In Aeromonas infections, ciprofloxacin (Cipro)1 500 mg PO or 400 mg IV twice daily is the antimicrobial treatment of choice. Piperacillin- tazobactam (Zosyn)1 4.5 g IV three times daily or ceftazidime (Fortaz)1 2 g IV daily may be added in severe infections. The organism is also susceptible to aminoglycosides and carbapenems. Resistance is now becoming a problem because Aeromonas can produce β-lactamases and carbapenemases. Therefore, it is preferable to initiate therapy with a fluoroquinolone when the organism is isolated.
Bacillus cereus is found abundantly in the environment and vegetation. It is known to produce two forms of food poisoning, emetic and diarrheal. The emetic (short-incubation) type of illness is associated with contaminated fried rice that is not refrigerated. The organism is present in uncooked rice, and the spores survive boiling. The illness is usually self-limiting, with recovery in a day. It is mediated by a heat- stable, preformed enterotoxin resembling that of Staphylococcus aureus.
The first major outbreak of Bacillus cereus food poisoning was in 1971 in England. The diarrheal (long-incubation) type of illness is produced by a heat-labile diarrheal enterotoxin formed in the intestine, which activates adenylate cyclase, causing intestinal fluid secretion, similar to Escherichia coli LT toxin and the toxin of Clostridium perfringens.
During the slow cooling of cooked rice, spores germinate and vegetative bacteria multiply; then they sporulate again. Sporulation is also associated with toxin production. The toxin is heat stable and can easily withstand the temperatures used to cook fried rice.
The disease is diagnosed by the isolation of B. cereus from the incriminated food (emetic type) or from stool and food (diarrheal type). Isolation from stools alone is not sufficient because gastrointestinal colonization with B. cereus occurs in many persons.
B. cereus food poisoning may be symptomatically managed with replacement of fluids and electrolytes. Antimicrobials have no role in treatment. B. cereus is also known to produce a variety of ocular and systemic infections such as meningitis, osteomyelitis, pneumonia, and endocarditis. These are usually not foodborne, and it is in this situation that vancomycin (Vancocin)1 becomes the drug of choice, with clindamycin (Cleocin)1 and carbapenems being the alternative drugs, both being used along with aminoglycosides for synergistic action.
Campylobacter jejuni are harbored in the reproductive and alimentary tracts of some animals. Other than gastrointestinal symptoms, the patient has malaise and headache. The organism may be shed in the patient’s stool for up to 2 months. Bacteremia is observed in a small minority of cases. The disease is usually self-limiting. Guillain-Barré syndrome and Reiter’s syndrome are recognized sequelae.
As few as 500 organisms can cause enteritis. The organism is invasive but generally less so than Shigella. Campylobacter produces adenylate cyclase–activating toxins resembling E. coli LT and cholera toxin.
The feces may be inoculated in enrichment medium or on selective media such as Campy-BAP or Skirrow’s medium.
Indications for antibiotic therapy in C. jejuni infections are prolonged fever, severe diarrhea, dysentery, and persistent symptoms for more than a week. Therapy of Campylobacter infection with ciprofloxacin (Cipro 500 mg orally twice daily for 7 days) early in the course of the illness shortens its duration. Unfortunately, this has led to the emergence of fluoroquinolone-resistant Campylobacter infections.
Erythromycin eradicates carriage of susceptible C. jejuni and might shorten the duration of illness if given early in the disease.
Erythromycin (Ery-Tab)1 250 mg PO four times daily is the drug of choice in Campylobacter enteritis. Azithromycin (Zithromax)1 is also useful and has the advantage of shorter duration of therapy.
Gentamicin (Garamycin), carbapenems, amoxicillin-clavulanate (Augmentin),1 and chloramphenicol1 are useful in systemic infections. The usual duration of treatment is 2 weeks. The therapy is prolonged in immunocompromised persons and in patients with endovascular infections.
Clostridum botulinum is widely distributed in soil, in sediments of lakes and ponds, and in decaying vegetation. C. botulinum elaborates the most potent toxin known in humans. When the toxin is ingested, paralysis occurs, often requiring prolonged artificial ventilation. Common signs and symptoms include vomiting, thirst, dry mouth, constipation, ocular palsies, dysphagia, dysarthria, bulbar paralysis, and death due to respiratory paralysis. Coma or delirium occurs in some. Infants present with lethargy, poor feeding, loss of head control, and sometimes sudden infant death syndrome (SIDS).
The incriminated foods are corn syrup, home-canned or bottled meat, fruits, fish, vegetables, herb-infused oils, and cheese sauce. Infant botulism is associated with consumption of honey; honey should not be given to infants younger than 1 year.
Not all strains of C. botulinum produce botulinum toxin. Toxigenic types of the organism, designated A, B, C1, D, E, F, and G, produce immunologically distinct forms of botulinum toxin. Lysogenic phages encode toxin C and D serotypes.
Foodborne botulism is not an infection but an intoxication because it results from the ingestion of foods that contain the preformed clostridial toxin. If contaminated food has been insufficiently heated or canned improperly, the spores can germinate and produce botulinum toxin. The toxin is released only after cell lysis and death. The toxin resists digestion and is absorbed by the upper gastrointestinal tract and enters the blood. The toxin blocks release of acetylcholine by binding to receptors at synapses and neuromuscular junctions and causes flaccid paralysis.
Spoilage of food or swelling of cans or presence of bubbles inside the can indicate growth of C. botulinum. Food is homogenized in broth and inoculated in Robertson cooked meat medium and blood agar or egg-yolk agar, which is incubated anaerobically for 3 to 5 days at 37°C. The toxin can be demonstrated by injecting the extract of food or culture into mice or guinea pigs intraperitoneally.
Hospitalization in an intensive care unit with immediate administration of botulinum antitoxin is vital in the management of botulism. The antitoxin neutralizes only toxin molecules unbound to nerve endings and does not reverse the paralysis. It should be given within 24 hours after the diagnosis is made. Penicillin is the antimicrobial of choice. Intubation and mechanical ventilation are needed for respiratory failure. If swallowing difficulty persists, intravenous fluids or alimentation should be given through a nasogastric tube.
C. perfringens is heat resistant and elaborates two toxins that can induce specific pathology in the human intestinal tract. It is the third leading cause of foodborne illnesses in United States, after norovirus and cereus. It is present abundantly in the environment, vegetation, sewage, and animal feces.
Human diseases caused by this organism are the more common C. perfringens type A food poisoning and the less common, but more serious, C. perfringens type C food poisoning producing necrotic enteritis. Necrotic enteritis is characterized by vomiting, severe abdominal pain, and bloody diarrhea. The incubation period is 2 to 5 days. Progression to necrosis of the jejunum and death occur.
Spores in food can survive cooking and then germinate when the food is improperly stored. When these vegetative cells form endospores in the intestine, they release enterotoxins. Food poisoning is mainly caused by type A strains, which produce alpha and theta toxins. The toxins result in excessive fluid accumulation in the intestinal lumen.
Because the bacterium is present normally in intestines, isolation from feces might not be sufficient to implicate it as the cause of the illness.
Similarly, isolation from food, except in large numbers (> 109/g), might not be significant. The homogenized food is diluted and plated on selective medium as well as Robertson cooked meat medium and subjected to anaerobic incubation. The isolated bacteria must be shown to produce enterotoxin.
Food poisoning due to Clostridium perfringens is managed conservatively with hydration and replacement of electrolytes. C. perfringens is susceptible to benzylpenicillin (penicillin G), which may be useful in managing severe infections (1 mU IV every 4 hours).
Vancomycin,1 clindamycin,1 cefoxitin (Mefoxin), and metronidazole (Flagyl) are alternatives. C. perfringens type C toxoid vaccine2 (two doses, 4 months apart) is preventive in pigbel.
Cronobacter sakazakii causes neonatal meningitis or necrotizing enterocolitis and bacteremia, which results in an alarming mortality rate. Surviving patients sometimes develop ventriculitis and cerebral abscess. C. sakazakii has been isolated from infant formulas.
Enterobacter species are generally resistant to the cephalosporins, except cefepime (Maxipime),1 but are responsive to carbenicillin (Geocillin),1 piperacillin (Pipracil),1 ticarcillin (Ticar),1 amikacin (Amikin),1 and tigecycline (Tygacil).1
Enterohemorrhagic Escherichia coli
Many serogroups of E. coli, including O4, O26, O45, O91, O111, O145, and O157, are pathogenic, but the most common pathogenic serotype is O157:H7. Cattle are the main sources of infection; most cases are associated with the consumption of undercooked beef burgers and similar foods from restaurants and delicatessens.
Enterohemorrhagic E. coli (EHEC) strains can produce one or more types of cytotoxins, which are collectively referred to as Shiga-like toxins because they are antigenically and functionally similar to Shiga toxin produced by Shigella dysenteriae. (Shiga-like toxins were previously known as verotoxins.) The toxins provoke cell secretion and kill colonic epithelial cells, causing hemorrhagic colitis and hemolytic-uremic syndrome (HUS), leading occasionally to disseminated intravascular coagulation (DIC). A fibrin layer forms in the glomerular capillary bed, and acute renal failure occurs due to DIC. These are most likely to occur in children, elderly patients, and pregnant women. The young recover fully, but at times dialysis is warranted.
Laboratory diagnosis is performed by culturing the feces on McConkey’s agar or sorbitol McConkey’s agar. Strains can then be identified by serotyping using specific antisera. Shiga-like toxins can be detected by enzyme-linked immunosorbent assay (ELISA), and genes coding for them can be detected by DNA hybridization techniques.
Hydration with electrolyte replacement is the mainstay of treatment in E. coli O157:H7 infection, and patients should be monitored closely and constantly for the development of HUS, which requires management in an intensive care setting with blood transfusion and dialysis. Although dysentery is self-limiting, the use of rifaximin (Xifaxan), a nonabsorbable agent, is recommended in those who are increasingly susceptible to infections. In the absence of dysentery, early institution of drugs like ciprofloxacin (Cipro) or azithromycin (Zithromax),1 especially in traveler’s diarrhea, decreases the duration of illness.
Enterotoxigenic Escherichia Coli
Enterotoxigenic E. coli (ETEC) is now ubiquitous in nature. Wild animals and cattle act as reservoirs of the organism. E. coli is carried normally in the intestine of humans and animals. Some specific serotypes harbor plasmids that code for toxin production. This bacterium is responsible for a majority of traveler’s diarrhea. The disease is self-limiting and resolves in few days.
The bacteria colonize the gastrointestinal tract by means of fimbriae, attaching to specific receptors on enterocytes of the proximal small intestine. Enterotoxins produced by ETEC include the LT (heat-labile) toxin and the ST (heat-stable) toxins. LTs are similar to cholera toxin in structure and mode of action, consisting of A and B subunits. The B (binding) subunit of LTs binds to specific ganglioside receptors (GM1) on the epithelial cells of the small intestine and facilitates the entry of the A (activating) subunit, which activates adenylate cyclase.
Stimulation of adenylate cyclase causes an increased production of cyclic adenosine monophosphate (cAMP), which leads to hypersecretion of water and electrolytes into the lumen and inhibition of sodium reabsorption.
The sample of feces is cultured on McConkey’s agar. The ETEC stains are indistinguishable from the resident E. coli by biochemical tests.
These strains are differentiated from nontoxigenic E. coli present in the bowel by a variety of in vitro immunochemical, tissue culture, or DNA hybridization tests designed to detect either the toxins or the genes that encode for these toxins. With the availability of a gene probe method, foods can be analyzed directly for the presence of ETEC in about 3 days. LTs can be detected by ligated rabbit ileal loop test and by observing morphological changes in Chinese hamster ovary cells and Y1 adrenal cells. ELISA, immunodiffusion, and coagglutination are also used in diagnosis.
Listeria monocytogenes is quite hardy and resists the deleterious effects of freezing, drying, and heat remarkably well for a bacterium that does not form spores. It is capable of growing at 3 °C and multiplies in refrigerated foods.
L. monocytogenes invades the gastrointestinal epithelium. Once the bacterium enters the host’s monocytes, macrophages, or neutrophils, it is bloodborne and can grow. Its presence in phagocytes also permits access to the brain and transplacental migration to the fetus in pregnant women. Granulomatosis infantisepticum is a feature of listeriosis. The pathogenesis of L. monocytogenes centers on its ability to survive and multiply in phagocytic host cells.
The diagnosis of listeriosis is most commonly made by isolation of L. monocytogenes from a normally sterile site. β-Hemolytic colonies, which test negative for catalase, hydrolyze hippurate, and have a positive cAMP reaction, form on blood agar. Serologic testing is not useful in diagnosing acute invasive disease, but it can be useful in detecting asymptomatic disease and gastroenteritis in an outbreak or in other epidemiologic investigations. Stool testing is not commercially available.
Ampicillin1 (2 g IV every 4 hours) is the drug of choice in Listeria monocytogenes infections. Aminoglycosides are added for synergistic effect. Trimethoprim-sulfamethoxazole (TMP-SMX)1 (Bactrim, 20 mg of trimethoprim/day IV every 6 hours) is an alternative for patients allergic to penicillin. Ampicillin and TMP-SMX may be used in combination. Vancomycin (Vancocin),1 linezolid (Zyvox),1 carbapenems, macrolides, and tetracyclines are also effective.
Cephalosporins are ineffective in the treatment of listeriosis and should not be used. The duration of therapy is highly variable depending on the clinical situation and is 14 days for bacteremia, 21 days for meningitis, 42 days for endocarditis, and 56 days for neurologic infections. Patients whose disease is promptly diagnosed and treated recover fully, but permanent neurologic sequelae are common in patients with cerebral illnesses. Consuming only pasteurized dairy products and fully cooked meats, meticulously cleaning utensils, and thoroughly washing fresh vegetables before cooking will prevent foodborne listerial infections. Pregnant women and others at risk should avoid soft cheeses and thoroughly reheated ready-to-serve and charcuterie foods.
Nontyphoidal salmonellosis consists of several causative organisms classified under the family Enterobacteriaceae; one such organism is Salmonella enteritidis. It does not occur normally in humans, but several animals act as reservoirs.
The diarrhea may be watery, with greenish, foul-smelling stools.
This may be preceded by headache and chills. Other findings include prostration, muscle weakness, and moderate fever.
The organism penetrates and passes through the epithelial cells lining the terminal ileum. Multiplication of bacteria in lamina propria produces inflammatory mediators, recruits neutrophils, and triggers inflammation. Release of lipopolysaccharides and prostaglandins causes fever and also loss of water and electrolytes into the lumen of the intestine, resulting in diarrhea.
Culture in selenite F broth and then subculture on deoxycholate citrate agar isolates the organisms. Plates are incubated at 37°C overnight, and growth is identified by biochemical and slide agglutination tests.
The antibiotics recommended for gastroenteritis due to nontyphoidal salmonellosis are ciprofloxacin (Cipro)1 500 mg PO twice daily, and ceftriaxone (Rocephin) 2 g IV daily, for 3 to 7 days. Amoxicillin (Amoxil)1 and TMP-SMX1 are also effective. Therapy is prolonged in bacteremia, endocarditis, or meningitis.
Shigella species belong to the family Enterobacteriaceae. Bacillary dysentery is caused by Shigella flexneri, Shigella boydii, Shigella dysenteriae, and Shigella sonnei. S. flexneri is most common in developing countries where hygiene is poor and clean drinking water is unavailable; S. sonnei is most common in developed countries. The watery diarrhea that is present initially becomes bloody after a day or two owing to spread of infection from the ileum to the colon. The illness is caused by exotoxin acting in the small bowel.
Extraintestinal manifestations are recognized, including HUS, Reiter’s syndrome, meningitis, Ekiri syndrome (reported in Japanese children and consisting of a triad of encephalopathy due to cerebral edema, bizarre posturing, and fatty degeneration of liver), vaginitis, lung infections, and keratoconjunctivitis. Toxic megacolon, pneumatosis coli, perforation, and rectal prolapse are recognized complications.
Tossed salads, chicken, and shellfish are the commonly incriminated foods. Person-to-person spread by anal intercourse or oral sex also occurs. Prepared food acts as vehicle of transmission. Spread of infection is also linked to flies.
Children are at high risk during the weaning period, and increasing age is associated with decreased prevalence and severity. Children in daycare centers, persons in custodial institutions, migrant workers, and travelers to developing countries are also at high risk.
The virulence factor is a smooth lipopolysaccharide cell wall antigen, which is responsible for the invasive features, and the Shiga toxin, which is both cytotoxic and neurotoxic. Shigellae survive the gastric acidity and invade and multiply within the colonic epithelial cells, causing cell death and mucosal ulcers, and spread laterally to involve adjacent cells but rarely invade the bloodstream.
Shigellosis can be correctly diagnosed in most patients on the basis of fresh blood in stool. Neutrophils in fecal smears strongly suggest infection. Any clinical diagnosis should be confirmed by cultivation of the etiologic agent from stools. Cary-Blair medium is the transport medium of choice, and MacConkey agar or deoxycholate citrate agar (DCA) as well as a highly selective medium such as xylose-lysin deoxycholate (XLD), Hektoen enteric (HE), or Salmonella-Shigella (SS) agar are also used.
Ciprofloxacin (Cipro, 500 mg PO twice daily for 3 days) is the antibiotic of choice for shigellosis. Alternative agents are pivmecillinam (Selexid),2 ceftriaxone (Rocephin),1 and azithromycin (Zithromax).1
A notable incident of staphylococcal food poisoning occurred in February 1975 when 196 of 344 passengers and one flight attendant aboard a jet from Tokyo to Copenhagen via Anchorage contacted a gastrointestinal illness characterized by nausea, vomiting, and abdominal cramps. The flight attendant and 142 passengers were hospitalized. Symptoms developed shortly after a ham and omelet breakfast had been served. S. aureus was incriminated as the offending agent and ham as the vehicle of the outbreak. The source was traced to a cook with pustules on his fingers.
S. aureus is ubiquitous in environment. Only strains that produce enterotoxin cause food poisoning. Food is usually contaminated by infected food handlers.
If food is stored for some time at room temperature, the organism can multiply in the food and produce enterotoxin. Most food poisonings are caused by enterotoxin A, and the isolates commonly belong to phage type III. These are heat stable, and ingestion of as little as 23 µg of enterotoxin can induce symptoms. The toxin acts on the receptors in the gut, and sensory stimulus is carried to the vomiting center in the brain by vagus and sympathetic nerves.
Because the ingested food contains preformed toxin, the incubation period is very short. In severe illness, profound hypotension occurs.
Death is known to occur at extremes of age and in the malnourished.
The presence of a large number of S. aureus in food can indicate poor handling or sanitation; however, it is not sufficient evidence to incriminate the food as the cause of food poisoning.
Staphylococcal food poisoning can be diagnosed if staphylococci are isolated in large numbers from the food and their toxins are demonstrated in the food or if the isolated S. aureus is shown to produce enterotoxins. Dilutions of food may be plated on Baird- Parker agar or mannitol salt agar. Enterotoxin may be detected and identified by gel diffusion.
Therapy is mainly supportive. Antibiotics have no role in the treatment because they are not antitoxins. Intravenous fluids and electrolyte replacement are imperative in the severely dehydrated patient.
The Yersinia species that cause food poisoning are commonly Yersinia enterocolitica and rarely Yersinia pseudotuberculosis. Pigs and other wild or domestic animals are the hosts, and humans are usually infected by the oral route. Serogroups that predominate in human illness are O:3, O:5, O:8, and O:9.
Yersiniosis is common in children and occurs most often in winter.
Y. enterocolitica is associated with terminal ileitis and Y. pseudotuberculosis with mesenteric adenitis, but both organisms can cause mesenteric adenitis and symptoms that cause a clinical picture resembling appendicitis, resulting in surgical removal of a normal appendix. Rarer strains of Y. enterocolitica are likely to cause systemic infections, especially in patients with diabetes or in iron overload states. In Japan, a form of vasculitis, called Izumi fever, occurs, and in Russia a scarlet fever–like illness has been reported.
Yersinia organisms can survive and grow during refrigerated storage. Strains that cause human yersiniosis carry a plasmid that is associated with a number of virulence traits. Ingested bacteria adhere and invade M cells or epithelial cells.
Suspect food is homogenized in phosphate-buffered saline and inoculated into selenite F broth and held at 4°C for 6 weeks. The broth is subcultured at weekly intervals on deoxycholate citrate (DCA) or Yersinia-selective agar plates. This is termed cold-enrichment technique.
Antibiotics are not recommended for gastroenteritis caused by Yersinia enterocolitica and the less-common Yersinia pseudotuberculosis, but bacteremia and extraintestinal infections require treatment with ciprofloxacin1 (500 mg PO or 400 mg IV twice daily for 2 weeks).
Third-generation cephalosporins (cefotaxime1 [Claforan]), amoxicillin1 (Amoxil), TMP-SMX1 (Bactrim), amoxicillin-clavulanate1 (Augmentin), carbapenems, and gentamicin (Garamycin) are also effective agents in therapy.
Noroviruses (formerly called Norwalk or Norwalk-like viruses and small round structured viruses [SRSV]) and sapoviruses belong to the family Caliciviridae and are the most common cause of gastroenteritis. They account for about 90% of epidemic nonbacterial outbreaks of gastroenteritis around the world. Norovirus infection often affects people during the winter months and is therefore sometimes called winter vomiting disease; however, people may be affected at any time of the year. After a norovirus infection, immunity lasts only for 14 weeks and is incomplete. Persons with blood group O are more susceptible to infection, whereas those with groups B and AB are partially protected. Norovirus infection outbreaks more commonly occur in closed or semiclosed communities, such as prisons, dormitories, cruise ships, schools, long-term care facilities, and overnight camps—places where infection can spread rapidly from human to human or through tainted food and surfaces. Infection outbreaks can also result from food handled by an infected person.
Outbreaks have often been linked to consumption of cold foods, including salads, sandwiches, and bakery products. Salad dressing, cake icing, and oysters from contaminated waters have also been implicated in gastroenteritis outbreaks. Weight loss, lethargy, low- grade fever, headache, and (rarely) ageusia occur. Vomiting is more likely with infections caused by norovirus than sapovirus.
Norovirus strains that infect humans are found in genogroups I, II, and IV. GII.4 strains are more commonly associated with person-to- person transmission, and GI strains are identified more commonly in shellfish-associated outbreaks.
Noroviruses were shown to differentially bind to histo-blood group antigens, and the binding pattern correlates with susceptibility to infection and illness. A number of enzymes are important in the synthesis of histo-blood group antigens, including fucosyl transferase- 2 (FUT-2, secretor enzyme), FUT-3 (Lewis enzyme), and the A and B enzymes. The glycan produced by FUT-2 H type 1, serves as a viral receptor for noroviruses.
The virus can be recovered from the infected person’s stool and vomitus during illness for about 2 weeks. Electron microscopy and reverse-transcriptase polymerase chain reaction (RT-PCR) antigen- detection assays are performed on stool samples. Serologic assays are not available for clinical use. However, infection can be diagnosed by identifying a fourfold or greater increase in antibody titer between acute and convalescent sera using norovirus virus-like particles as antigen.
There is no specific treatment for norovirus infection. Hydration is generally adequate for most patients. In developing countries, oral rehydration therapy is the treatment of choice. Effective hand washing, careful food processing, and education of food handlers along with chlorination of water are important preventive measures. A vaccine for norovirus is in clinical trials.
Among the seven rotavirus species (A to G), rotavirus A, B, and C can cause disease in humans. Rotavirus A is the most common and is the major cause of waterborne outbreaks in humans. Infections are referred to as infantile diarrhea, winter diarrhea, or acute viral gastroenteritis. Children 6 months to 2 years of age, premature infants, the elderly, and the immunocompromised are particularly prone to more-severe symptoms caused by infection with group A rotavirus.
Rotavirus can survive in water for days to weeks, depending on water quality and temperature. Waterborne outbreaks are most common, followed by spread by fomites. Rotaviruses infect intestinal enterocytes; diarrhea may be caused by malabsorption secondary to the destruction of enterocytes, villus ischemia and activation of the enteric nervous system, and intestinal secretion stimulated by the action of rotavirus nonstructural protein 4 (NSP4), a novel enterotoxin and secretory agonist with pleiotropic properties.
Outbreaks caused by group B rotavirus, also called adult diarrhea rotavirus, have also been reported in the elderly and adults. Such infections are rare and usually subclinical. Group C rotavirus has been associated with rare and sporadic cases of diarrhea in children in many countries. Subclinical infection to severe gastroenteritis leading to life-threatening dehydration can occur. The illness has an abrupt onset, with vomiting often preceding the onset of diarrhea. Up to one third of patients have fever of about 39 °C. The stools are characteristically watery and only occasionally contain red or white cells. Symptoms generally resolve in a week.
Respiratory and neurologic features in children have been reported. Rotavirus infection has been associated with other clinical conditions including sudden infant death syndrome (SIDS), necrotizing enterocolitis, Kawasaki’s disease, and type 1 diabetes.
Electron microscopy, direct antigen detection assays (ELISA, immunochromatography, latex agglutination), and nucleic acid detection (e.g., RT-PCR, polyacrylamide gel electrophoresis [PAGE]), are used mainly in epidemiologic studies during outbreaks.
Dehydration due to group A rotavirus infection is treated with early institution of oral and intravenous fluids. The role of probiotics,7 bismuth subsalicylate (Pepto Bismol),1 inhibitors of enkephalinase, and nitazoxanide (Alinia)1 are not clearly defined. Antimicrobials and antimotility agents should be avoided. A marked fall in deaths from childhood diarrhea following introduction of rotavirus vaccines (Rotarix, RotaTeq) has been reported from various parts of the world, and surveillance information has not revealed an association of any serious adverse reactions with the vaccine.
Transmission of Cryptosporidium is usually by the fecal-oral route, often through food and water contaminated by livestock mammal feces. Persons most likely to be infected by Cryptosporidium parvum are infants and young children in daycare centers; those whose drinking water is unfiltered and untreated; those involved in farming practices such as lambing, calving, and muck-spreading; people engaging in anal sexual practices; patients in a hospital setting (from other infected patients or health care workers); veterinarians; and travelers.
Cryptosporidium spp. are believed to be noninvasive. Malabsorption resulting from the intestinal damage caused by prolonged protozoal infection can be fatal. Although host cells are damaged in cryptosporidiosis, the means by which the organism causes damage is not known. Mechanical destruction and the effects of toxins, enzymes, or immune-mediated mechanisms, working alone or together, may be instrumental. In the immunocompromised, the illness is much more debilitating, with cholera-like diarrhea.
Traditionally, cryptosporidiosis is diagnosed by microscopic observation of developmental stages of the organism in an intestinal biopsy specimen. Oocysts can be recovered from stool samples by formalin-concentration techniques, staining with a modified Ziehl- Neelsen acid-fast stain. Serologic tests (ELISA, immunofluorescence antibody, PCR) are of added value.
Nitazoxanide (Alinia, 500 mg PO twice daily for 3 days) is recommended with antiretrovirals for HIV-positive patients. Fluid replacement and antidiarrheal agents are also given.
Trichinosis is due to Trichinella spiralis infection, commonly as a result of consuming improperly cooked pork. The parasite lodges in the extraocular muscles, deltoid, biceps, intercostals, diaphragm, tongue, or masseter and produces severe weakness with pain, fever, and cough along with splinter hemorrhages and eosinophilia.
Moderate T. spiralis infection is treated with mebendazole (Vermox 200–400 mg PO three times daily for 3 days) or albendazole1 (Albenza 400 mg PO twice daily for 7–14 days). For severe infections, prednisone is added in a dose of 1 mg/kg/day for 5 days.
Neurocysticercosis is caused by Taenia saginata infection, commonly as a result of consuming improperly cooked pork or contaminated raw vegetables and water. The parasite lodges in the central nervous system and skeletal muscle and presents as intracranial calcifications and ring-enhancing lesions on radioimaging studies. Other than leukocytosis, eosinophilia, and raised erythrocyte sedimentation rate, antibodies to species-specific antigens of T. solium can be detected by immunosorbent assay and complement fixation-tests. Treatment is aimed at controlling seizures and relief of hydrocephalus.
Albendazole (15 mg/kg/day for 8–28 days) or praziquantel (50– 100 mg/kg/day in three divided doses for a month) are given for parenchymal cysticerci with glucocorticoids to suppress the inflammatory response around the dying parasites. Surgery may be required to reduce intracranial pressure.
Dinoflagellates, a very large and diverse group of eukaryotic algae in the marine ecosystem, are the major group producing toxins that impact humans. Dinoflagellate toxins are structurally and functionally diverse, and many present unique biological activities. Five major seafood poisoning syndromes caused by toxins have been identified from the dinoflagellates (Table 4): paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), amnesic shellfish poisoning (ASP), diarrheic shellfish poisoning (DSP) and ciguatera fish poisoning (CFP). Symptoms include allergic manifestations, neurologic including paresthesia of the extremities, headache, ataxia, vertigo, cranial nerve palsies, and paralysis of respiratory muscles as well as gastrointestinal. Symptomatic treatment and antihistamines are the mainstay of treatment.
Seafood Poisoning Caused by Neurotoxins Identified from Marine Dinoflagellate Species
It is a neurotoxin concentrated in the skin and viscera of puffer fish, and other fishes of the order Tetraodontiformes and in some amphibian, octopus, and shellfish species. Human poisonings occur when the flesh and/or organs of the fish are improperly prepared and eaten. Tetrodotoxin acts by blocking the conduction of nerve impulses along nerve fibers and axons and interferes with the transmission of signals from nerves to muscles. Onset of symptoms usually is 30–40 min but may be as short as 10 min; it includes lethargy, paraesthesia, emesis, ataxia, weakness, and dysphagia; ascending paralysis occurs in severe cases with high mortality (1-2 mg is lethal). Management is symptomatic.
Group B Sreptococcus (GBS)
GBS bacteria is found in 15%–30% of adult human intestines and urinary tract. Rarely implicated in infections of skin, joints, heart and brain, a recent outbreak of food-borne illness caused by the Type III GBS ST283 strain was reported in Singapore during the period of January – July 2015. It is the largest of its kind and first association to food-borne transmission of GBS to people via consumption of “yusheng-style” raw fresh water fish. The primary case presented with giddiness and suffered bouts of vomiting and diarrhoea. Further studies are ongoing to establish the link between increase in cases of Group B streptococcus (GBS) infection to consumption of raw fish. Treatment is symptomatic.
Many other organisms are implicated in foodborne and waterborne illnesses (Box 1). Some are discussed elsewhere in this book.
Amebiasis, brucellosis, cholera, hepatitis A and E, giardiasis, typhoid fever, and other foodborne intestinal nematodes and cestodes are covered in the infectious diseases section of this text and are not covered in this section.
|Miscellaneous Organisms Implicated in Foodborne and Waterborne Illnesses|
|Adenovirus 40, 41
Enterococcus faecalis, E. faecium
Taenia solium, T. saginata
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1 Not FDA approved for this indication.
2 Not available in the United States.
7 Available as dietary supplement.