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Shigellosis is an infectious disease caused by a group of bacteria called Shigella. Humans are the only natural host for Shigella (Giannella, 2010). Although less common than infection with Salmonella or Campylobacter, Shigella infection is still a significant cause of foodborne disease in the United States (Taege, 2010). In fact, Shigella causes between 10 and 20% of cases of bacterial foodborne illness every year in the United States (Taege, 2010).
Infection with Shigella, which causes bacillary dysentery, is not a new phenomenon. Hippocrates, an ancient Greek physician born sometime around 460 B.C., used the term “dysentery” to describe frequent passage of bloody, mucous-containing stool accompanied by straining, painful defecation (DuPont, 2010). Though the two distinct forms of dysentery were not accurately separated until the late 1800s, due to the lack of liver complications, much of the dysentery in older historical writings is considered to have been caused by Shigella bacteria (DuPont, 2010).
In discussing Shigella, perhaps the greatest historical consideration is the influence that bacillary dysentery has had on military campaigns. Almost every extended siege and long campaign has been associated with epidemics of bacillary dysentery, particularly when food sources and sanitation could not be controlled adequately (DuPont, 2010). A heavier toll was ascribed to bacillary dysentery than to war-related injuries in numerous battles during the Peloponnesian War, the 18th century campaigns by the British, Napoleon’s campaigns, the American Civil War, the Franco-Prussian War, and the Sino Japanese War (DuPont, 2010).
Presently, an estimated 165 million cases of shigellosis occur annually across the globe (Kumar, 2009). In countries where Shigella is endemic, the bacteria is responsible for about 10% of all cases of pediatric diarrheal disease, and up to 75% of diarrheal deaths (Kumar, 2009).
Shigella is the name for a family of bacteria that can cause diarrhea in humans. Shigella are microscopic living creatures that pass from person to person. They were discovered in 1906 by a Japanese scientist who conclusively demonstrated that a bacterium was present in the stool of many dysentery patients (DuPont, 2010; CDC, 2009). The bacteria is named after the scientist, who was named Shiga (CDC, 2009).
Shigella was first isolated during the Japanese red diarrhea epidemic of 1897 (Kumar, 2009). Since then, shigellosis has become virtually synonymous with bacterial dysentery (Adachi et al., 2007). Today, we know of four species, or groups, of the Shigella bacteria:
Group A Shigella, or Shigella dysenteriae, is comprised of 10 serotypes (Giannella, 2010). One of those serotypes, S. dysenteriae 1 (Shiga bacillus), can cause epidemics of dysentery and is most common in developing countries (CDC, 2009; Adachi et al., 2007). Epidemics of S. dysenteriae type 1 have occurred in Central America and Africa, and have been associated with case fatality rates of 5-15% (CDC, 2009). For example, an outbreak that occurred in Central America in the late 1960s and early 1970s was associated with the deaths of over 10,000 individuals, most of whom were young children (Giannella, 2010). In recent years, this organism has continued to cause outbreaks in many developing countries (Giannella, 2010). The mortality rate in cases where S. dysenteriae type 1 is left untreated is as high as 25% in developing countries (Adachi et al., 2007). However, the mortality rate drops to less than one percent with adequate microbial therapy (Adachi et al., 2007).
Group B Shigella, or Shigella flexneri, contains bacteria with 14 distinct serotypes (Giannella, 2010). Between 1926 and 1938, S. flexneri became more prevalent than Group A Shigella in the developing world (DuPont, 2009). It remains the major type of Shigella in those areas today (DuPont, 2010). S. flexneri is responsible for almost all cases of non-Group D of shigellosis in the United States (CDC, 2009).
There are 18 different serotypes present in Group C Shigella, or Shigella boydii (Giannella, 2010). Shigella boydii is seen mostly in the Indian subcontinent (Lima and Guerrant, 2010).
Group D Shigella, or Shigella sonnei, has only one serotype (Giannella, 2010). Of the four groups of Shigella, the serotype in this group produces the mildest illness (Giannella, 2010). Infection with S. sonnei generally causes high-volume watery diarrhea with relatively few other systemic signs (Craig and Zich, 2009). S. sonnei has become the major cause of bacillary dysentery in the United States and Europe (DuPont, 2010), and is responsible for 72% of shigellosis cases in the US (CDC, 2009).
The major attack site for the Shigella bacteria is the colon (Giannella, 2010). In essence, the bacteria use specific mechanisms to penetrate the surface of the colon (Giannella, 2010). Once inside the epithelial cells, the organisms multiply (Giannella, 2010). The infection spreads by cell-to-cell transfer of the bacilli (Giannella, 2010). However, the bacteria rarely penetrate beyond the intestinal mucosa, and generally do not invade the bloodstream (Giannella, 2010). However, bacteremia (which occurs when bacteria do invade the bloodstream) can occur in malnourished children and immunocompromised individuals who ingest the bacteria (Giannella, 2010).
The majority of individuals infected with Shigella develop stomach cramps, diarrhea, and fever 24 to 48 hours (one to two days) after they ingest the bacteria (Craig and Zich, 2010; CDC, 2009). The incubation period may, however, be as long as four days in rare cases (Kumar, 2009). Often, the diarrhea is bloody (CDC, 2009). Illness typically resolves in five to seven days (CDC, 2009).
Other possible symptoms include fever, abdominal pain, tenesmus (a feeling of incomplete evacuation), bloody stools, and nausea. Fever occurs in over 57% of cases (Craig and Zich, 2010). At least 75% of people infected with Shigella bacteria experience abdominal pain, and tenesmus occurs in somewhere between 55 and 96% of infections (Craig and Zich, 2010). Somewhere between 46 and 73% of infected individuals have blood in their stool, and nausea is present in over 62% of cases (Craig and Zich, 2010).
A significant proportion of infected individuals are asymptomatic (experience no adverse symptoms associated with infection), or experience only mild, watery diarrhea with few, if any, constitutional symptoms (Craig and Zich, 2010). People who are infected but asymptomatic may still pass the bacteria to others (CDC, 2009).
Generally, shigellosis is self-limiting (Craig and Zich, 2010). Patients typically are afebrile (no longer have a fever) after three to four days (Craig and Zich, 2010). Abdominal cramping and diarrhea generally disappear within one week (Craig and Zich, 2010). However, unless the infection is treated by antibiotics, about 10% of patients will experience a relapse, or return of symptoms (Craig and Zich, 2010). Additionally, some cases may persist for weeks (Adachi et al., 2007).
A significant number of infected individuals, when not treated with antibiotics, will continue to shed Shigella bacteria in their stool for two or more weeks (Craig and Zich, 2010).
A period of watery diarrhea that lasts anywhere from a few hours to a few days typically precedes the development of a true case of dysentery (Craig and Zich, 2010). Patients with dysentery have both grossly bloody diarrhea (diarrhea with blood visible to the naked eye) and tenesmus (Craig and Zich, 2010). Constitutional symptoms – such as headache, myalgias, vomiting, fever, and nausea – are also present (Craig and Zich, 2010). When symptoms are severe enough, the infected individual may become profoundly dehydrated, and circulatory collapse may occur (Craig and Zich, 2010).
Many different kinds of germs can cause diarrhea, so establishing the cause help to guide treatment (CDC, 2009). Determining that Shigella is the cause of the illness depends on laboratory tests that identify Shigella in the stools of an infected person (CDC, 2009; Ashkenazi and Cleary, 2008). Prompt testing is critical. Stool culture results from samples obtained during the first three days of illness are positive in more than 90% of cases (Craig and Zich, 2010). On the other hand, cultures obtained more than one week after the onset of diarrhea test positive in only 75% of cases (Craig and Zich, 2010). The laboratory can also do special tests to determine which antibiotics, if any, would be best to treat the infection (CDC, 2009).
Treatment of shigellosis generally involves correction of fluid and electrolyte imbalances (Craig and Zich, 2010). Fluid losses generally can be replaced by oral intake because the diarrhea that is associated with bacillary dysentery is not normally associated with profound fluid and electrolyte depletion (DuPont, 2010). However, when vomiting or extreme toxemia occurs, particularly in the very young or very old, intravenous fluid replacement may be appropriate and necessary (DuPont, 2010).
Persons with mild infections usually recover quickly without antibiotic treatment. However, appropriate antibiotic treatment kills Shigella bacteria, and may shorten the illness by a few days (CDC, 2009). Antibiotic treatment often eradicates Shigella from the stool, often within 48 hours (Craig and Zich, 2010). The antibiotics commonly used for treatment are ampicillin, trimethoprim/sulfamethoxazole (also known as Bactrim or Septra), ceftriaxone (Rocephin), or, among adults, ciprofloxacin (Cipro) (CDC, 2009). In cases where antibiotics are appropriate, antibiotic treatment is generally required for only three days (Craig and Zich, 2010). However, in immunocompromised patients, antibiotic treatment is often extended to 7-10 days (Craig and Zich, 2010).
Some Shigella bacteria have become resistant to antibiotics, which means that some antibiotics might not be effective for treatment (CDC, 2009). In the United States, more than 80% of Shigella organisms are resistant to ampicillin, and 47% are resistant to TMP-SMX, which are antibiotics that were historically administered to treat shigellosis (Craig and Zich, 2010; Ashkenazi and Cleary, 2008). The CDC cautions that using antibiotics to treat shigellosis can sometimes make the germs more resistant (CDC, 2009). Therefore, when many persons in a community are affected by shigellosis, antibiotics are sometimes used to treat only the most severe cases (CDC, 2009). The appropriateness of antibiotic treatment may also be evaluated based on the patient’s clinical condition and the feasibility of sanitary control (Craig and Zich, 2010).
Antidiarrheal and antimotility agents such as loperamide (Imodium) or diphenoxylate with atropine (Lomotil) can make the illness worse and should be avoided (CDC, 2009). Use of such agents may prolong fever, diarrhea, and shedding of Shigella bacteria in the stools (Craig and Zich, 2010). Occasionally, use of antidiarrheal drugs such as diphenoxylate (Lomotil) worsens bacillary dysentery, and may play a role in the development of toxic dilation of the colon (DuPont, 2010). In dysenteric diarrhea caused by Shigella bacteria, some studies indicate that antimotility drugs may be safe when used simultaneously with antibiotics (Craig and Zich, 2010; DuPont, 2010).
Persons with diarrhea usually recover completely, although it may be several months before their bowel habits are entirely normal. However, there are some rare complications associated with shigellosis.
Severe anemia (deficiency of red blood cells or hemoglobin) and hypoalbuminemia (low levels of albumin in blood serum) can result from blood and protein losses (Adachi et al., 2007). Additionally, a severe leukemoid reaction (elevated white blood cell count), with a white blood cell count of up to 50,000, may result after it appears the infected individual has experienced marked clinical improvement (Adachi et al., 2007).
Children younger than two years of age may experience adverse neurological manifestations associated with Shigella infection (Craig and Zich, 2010). These neurologic symptoms may precede the onset of diarrhea, and can sometimes suggest central nervous system infection (Ashkenazi and Cleary, 2008). The most common associated neurological condition is seizures; however, lethargy and frank coma have been known to develop in a small number of infected patients (Craig and Zich, 2010). Additionally neurological symptoms may include lethargy, confusion, hallucinations, and severe headache (Ashkenazi and Cleary, 2008). Though the exact mechanism responsible for causing seizures is unclear (Ashkenazi and Cleary, 2008; Pigott, 2008), they may be related to metabolic alterations or a rapid rate of temperature elevation (CDC, 2009). Most children experience a complete recovery with no residual neurologic deficit (Ashkenazi and Cleary, 2008).
About 2% of persons who are infected with Shigella flexneri later develop arthritis (pains in their joints), conjunctivitis (irritation of the eyes), and urethritis (painful urination) (CDC, 2009; Kumar, 2009; Ashkenazi and Cleary, 2008). This is called post-infectious arthritis, also known as reactive arthritis or Reiter’s syndrome (Pigott, 2008). A disproportionate number of individuals who develop reactive arthritis are males between 20 and 40 years old, and the syndrome is particularly common among those with the genetic marker HLA-B27 (CDC, 2009; Kumar, 2009). The majority of individuals who develop reactive arthritis are adults (Ashkenazi and Cleary, 2008). The condition can last for months or years, and can lead to chronic arthritis.
S. dysenteriae type 1 infections are associated with hemolytic uremic syndrome (HUS), a potentially fatal type of kidney failure (Craig and Zich, 2010). Complications of HUS include thrombocytopenia (abnormally low platelet count), hemolytic anemia (insufficient number of red blood cells), and acute renal failure. Seizures, strokes, and other neurological sequelae may also later occur as a result of the disease (Taege, 2009).
Septicemia (presence of pathogenic organisms in the blood stream, often leading to sepsis) occurs in less than 5% of Shigella infections, and metastatic abscesses (abscessed formed by the transport of bacteria in the bloodstream) occurred with even less frequency (Adachi et al., 2007).
Once someone has contracted shigellosis, they are not likely to become infected with that specific bacteria again for at least several years. This is because temporary immunity to that specific strain of Shigella follows natural infection (Adachi et al., 2007). However, they can still become infected with other types of Shigella.
Shigella are present in the diarrheal stools of infected persons while they are sick and for up to a week or two afterwards (CDC, 2009). Most Shigella infections are the result of the bacterium passing from stools or soiled fingers of one person to the mouth of another person. This happens when basic hygiene and handwashing habits are inadequate and can happen during certain types of sexual activity CDC, 2009).
During acute infection, a single gram of stool can contain as many as 1,000,000,000 bacteria (Kumar, 2009). This is particularly relevant given the fact that as few as 10-200 Shigella bacilli can cause infection (CDC, 2009; Pigott, 2008). In fact, no other enteric pathogen is as efficient as Shigella at producing overt disease in humans (Craig and Zich, 2010). The low infectious dose is likely related to the fact that Shigella are resistant to the harsh acidic environment of the stomach (Kumar, 2009).
Shigella infections may be acquired from eating contaminated food (CDC, 2009). Contaminated food usually looks and smells normal (CDC, 2009). Vegetables, fruits, and shellfish are foods commonly associated with Shigella infection (Taege, 2010). Additionally, dramatic epidemics related to ingestion of milk, ice cream, and occasionally even water have occurred (Giannella, 2010). Shigella bacteria can survive for up to 30 days in foods such as whole eggs, flour, milk, oysters, and shrimp (Ashkenazi and Cleary, 2008). Food may become contaminated by infected food handlers who forget to wash their hands with soap after using the bathroom (CDC, 2009). Vegetables can also become contaminated if they are harvested from a field with sewage in it (CDC, 2009). Finally, flies can breed in infected feces and then contaminate food (CDC, 2009).
Additionally, Shigella infections can then be acquired by drinking, swimming in, or playing with the contaminated water (CDC, 2009). Water may become contaminated with Shigella bacteria if sewage runs into it, or if someone with shigellosis swims in or plays with it (especially in splash tables, untreated wading pools, or shallow play fountains used by daycare centers) (CDC, 2009). In fact, over the past few years, a number of large outbreaks have been associated with recreational water venues including swimming pools, water parks, fountains, hot tubs, and spas (Craig and Zich, 2010). Dysentery strains of Shigella can be recovered from room-temperature water samples for up to six months (DuPont, 2010). Proper chlorination of water may remove the risk of such infections (DuPont, 2010).
Some groups of people are at increased risk of shigellosis, including:
(Craig and Zich, 2010; CDC, 2009).
Children under the age of 5 account for approximately 30% of Shigella infections (Craig and Zich, 2010). Shigellosis is particularly likely to occur among toddlers who are not fully toilet-trained. Over the past few years, several outbreaks of multidrug-resistant Shigella infection have been reported in day care centers located in the United States (Pigott, 2008). In these cases, transmission was thought to be a result of inadequate handwashing and hygiene practices (Pigott, 2008).
Further, dysentery occurs most frequently in children (Giannella, 2010). The age group at highest risk for shigellosis is children between 1 and 4 years old – at particular risk are 2- and 3-year-olds – followed by children between 5 and 9 years old (Ashkenazi and Cleary, 2008). However, dysentery is rarely seen in infants under six months old (Giannella, 2010). This may be due to the fact that specific antibodies present in the breast milk of women living in endemic areas decrease the severity of infection in infants (Ashkenazi and Cleary, 2008). Additionally, disease tends to be less severe in children than in adults (Giannella, 2010).
In addition to children in daycare centers, shigellosis is common in other confined populations, including those in mental and penal institutions, nursing homes, and Native American Indian reservations (Craig and Zich, 2010). The high rate of Shigella infections on Native American Indian reserves may result not from a somewhat confined population, but instead from lack of sanitary facilities and water (Adachi et al., 2007).
Many cases of dysentery in industrialized regions of the world result from person-to-person transmission, and widespread epidemics have occurred in military and civilian populations and among cruise ship passengers who have ingested contaminated food or water (DuPont, 2010). An increased incidence has been documented in AIDS patients (Craig and Zich, 2010).
Although research into live-attenuated Shigella vaccines is ongoing, there is currently no vaccine to prevent shigellosis (Pigott, 2008). However, the spread of Shigella from an infected person to other persons can be stopped by frequent and careful handwashing with soap. Handwashing among children should be supervised by an adult in daycare centers and homes with children who have not been fully toilet trained.
If a child in diapers has shigellosis, everyone who changes the child’s diapers should be sure the diapers are disposed of properly in a closed-lid garbage can, and should wash his or her hands and the child’s hands carefully with soap and warm water immediately after changing the diapers. After use, the diaper changing area should be wiped down with a disinfectant such as diluted household bleach, Lysol or bactericidal wipes. When possible, young children with a Shigella infection who are still in diapers should not be in contact with uninfected children.
Basic food safety precautions and disinfection of drinking water prevents shigellosis from food and water. However, people with shigellosis should not prepare food or drinks for others until they have been shown to no longer be carrying the Shigella bacterium, or if they have had no diarrhea for at least 2 days. At swimming beaches, having enough bathrooms and handwashing stations with soap near the swimming area helps keep the water from becoming contaminated. Daycare centers should not provide water play areas.
Simple precautions taken while traveling to the developing world can prevent shigellosis. Drink only treated or boiled water, and eat only cooked hot foods or fruits you peel yourself. The same precautions prevent other types of traveler’s diarrhea.
In 2005, a total of 10,484 cases of shigellosis were documented in the United States (Craig and Zich, 2010). This represents approximately 3.5 cases per every 100,000 individuals living in the country (Craig and Zich, 2010). There are generally about 14,000 laboratory confirmed cases of shigellosis in the United States and 20-50,000 in the United Kingdom annually (CDC, 2009; DuPont, 2010). However, because many milder cases are not diagnosed or reported, the actual number of infections may be twenty times greater. In fact, the CDC estimates that there are actually approximately 450,000 cases of shigellosis in the United States annually (CDC, 2009).
Shigellosis is particularly common and causes recurrent problems in settings where hygiene is poor and can sometimes sweep through entire communities. Children, especially toddlers aged 2 to 4, are the most likely to get shigellosis. Many cases are related to the spread of illness in child-care settings, and many are the result of the spread of the illness in families with small children.
In recent years, there have been shifts in the prevalence of specific serotypes and the incidence of dysentery (Giannella, 2010). In the tropics, S. flexneri is the most common Shigella serotype, and dysentery occurs mostly in the late summer (Giannella, 2010). Flies are thought to be important in the transmission of bacillary dysentery, particularly in the tropics, and scientific studies have shown that flies can occasionally be shown to test positive for Shigella bacteria (DuPont, 2010). This theory is supported in part by the fact that dysentery in warm countries is most prevalent at the same time that the fly population reaches its peak (DuPont, 2009).
On the other hand, in developed countries like the United States and many countries in Europe, dysentery cases are now most frequently seen during the winter months (Giannella, 2010). S. sonnei is the most common serotype in these developed countries (Giannella, 2010). For example, between 60 and 80% of bacillary dysentery cases in the United States are caused by S. sonnei (Gianella, 2010). Shigella flexneri causes the vast majority of the remaining cases, as the two remaining groups – Shigella boydii and Shigella dysenteriae – are responsible for fewer than 2% of cases in the United States (Craig and Zich, 2010).
Additionally, epidemics of bacillary dysentery are cyclic; each cycle lasts between 20 and 50 years (DuPont, 2010). For example, in Europe during the first 25 years of the 20th century, dysentery was generally caused by S. dysenteriae 1 (DuPont, 2010). Between 1926 and 1938, S. flexneri strains became more prevalent than S. dysenteriae 1 in the developing world, and remains the major type of Shigella bacteria present in still-developing countries (DuPont, 2010). Today, S. sonnei has become the major cause of bacillary dysentery in both the United States and Europe (DuPont, 2010).
To prevent the spread of shigellosis, individuals should:
(DuPont, 2010; CDC, 2009)
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Taege, Alan. “Foodborne Disease.” Current Clinical Medicine. Ed. William D. Carey. 2nd ed. Philadelphia: Saunders Elsevier. 2010. 730-734.
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Lima, Aldo A. M., and Richard L. Guerrant. “Inflammatory Enteritides.” Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. Ed. Gerald M. Mandell, John E. Bennett, and Ralph Dolin. 7th ed. Vol. 1. Philadelphia: Churchill Livingstone Elsevier, 2010. 1389-1398. 2 vols.
Craig, Sandy A., and David K. Zich. “Gastoenteritis.” Rosen’s Emergency Medicine: Concepts and Clinical Practice. Ed. John A. Marx, et al. 7th ed. Vol. 1. Philadelphia: Saunders Elsevier, 2010. 1200-1226. 2 vols.
Pigott, David C. “Foodborne Illness.” Emergency Medicine Clinics of North America 26.2 (2008): 475-497.