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19.6: Protozoan Infections of the Gastrointestinal Tract - Biology

19.6: Protozoan Infections of the Gastrointestinal Tract - Biology


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skills to develop

  • Identify the most common protozoans that can cause infections of the GI tract
  • Compare the major characteristics of specific protozoan diseases affecting the GI tract

Like other microbes, protozoa are abundant in natural microbiota but can also be associated with significant illness. Gastrointestinal diseases caused by protozoa are generally associated with exposure to contaminated food and water, meaning that those without access to good sanitation are at greatest risk. Even in developed countries, infections can occur and these microbes have sometimes caused significant outbreaks from contamination of public water supplies.

Giardiasis

Also called backpacker’s diarrhea or beaver fever, giardiasis is a common disease in the United States caused by the flagellated protist Giardia lamblia, also known as Giardia intestinalis or Giardia duodenalis ([link]). To establish infection, G. lamblia uses a large adhesive disk to attach to the intestinal mucosa. The disk is comprised of microtubules. During adhesion, the flagella of G. lamblia move in a manner that draws fluid out from under the disk, resulting in an area of lower pressure that promotes its adhesion to the intestinal epithelial cells. Due to its attachment, Giardia also blocks absorption of nutrients, including fats.

Transmission occurs through contaminated food or water or directly from person to person. Children in day-care centers are at risk due to their tendency to put items into their mouths that may be contaminated. Large outbreaks may occur if a public water supply becomes contaminated. Giardia have a resistant cyst stage in their life cycle that is able to survive cold temperatures and the chlorination treatment typically used for drinking water in municipal reservoirs. As a result, municipal water must be filtered to trap and remove these cysts. Once consumed by the host, Giardia develops into the active tropozoite.

Infected individuals may be asymptomatic or have gastrointestinal signs and symptoms, sometimes accompanied by weight loss. Common symptoms, which appear one to three weeks after exposure, include diarrhea, nausea, stomach cramps, gas, greasy stool (because fat absorption is being blocked), and possible dehydration. The parasite remains in the colon and does not cause systemic infection. Signs and symptoms generally clear within two to six weeks. Chronic infections may develop and are often resistant to treatment. These are associated with weight loss, episodic diarrhea, and malabsorption syndrome due to the blocked nutrient absorption.

Diagnosis may be made using observation under the microscope. A stool ova and parasite (O&P) exam involves direct examination of a stool sample for the presence of cysts and trophozoites; it can be used to distinguish common parasitic intestinal infections. ELISA and other immunoassay tests, including commercial direct fluorescence antibody kits, are also used. The most common treatments use metronidazole as the first-line choice, followed by tinidazole. If the infection becomes chronic, the parasites may become resistant to medications.

Cryptosporidiosis

Another protozoan intestinal illness is cryptosporidiosis, which is usually caused by Cryptosporidium parvum or C. hominis. (Figure (PageIndex{1})) These pathogens are commonly found in animals and can be spread in feces from mice, birds, and farm animals. Contaminated water and food are most commonly responsible for transmission. The protozoan can also be transmitted through human contact with infected animals or their feces.

In the United States, outbreaks of cryptosporidiosis generally occur through contamination of the public water supply or contaminated water at water parks, swimming pools, and day-care centers. The risk is greatest in areas with poor sanitation, making the disease more common in developing countries.

Signs and symptoms include watery diarrhea, nausea, vomiting, cramps, fever, dehydration, and weight loss. The illness is generally self-limiting within a month. However, immunocompromised patients, such as those with HIV/AIDS, are at particular risk of severe illness or death.

Diagnosis involves direct examination of stool samples, often over multiple days. As with giardiasis, a stool O&P exam may be helpful. Acid fast staining is often used. Enzyme immunoassays and molecular analysis (PCR) are available.

The first line of treatment is typically oral rehydration therapy. Medications are sometimes used to treat the diarrhea. The broad-range anti-parasitic drug nitazoxanide can be used to treat cryptosporidiosis. Other anti-parasitic drugs that can be used include azithromycin and paromomycin.

Figure (PageIndex{1}): Immunofluorescent staining allows for visualization of Cryptosporidium spp. (credit: modification of work by EPA/H.D.A. Lindquist)

Amoebiasis (Amebiasis)

The protozoan parasite Entamoeba histolytica causes amoebiasis, which is known as amoebic dysentery in severe cases. E. histolytica is generally transmitted through water or food that has fecal contamination. The disease is most widespread in the developing world and is one of the leading causes of mortality from parasitic disease worldwide. Disease can be caused by as few as 10 cysts being transmitted.

Signs and symptoms range from nonexistent to mild diarrhea to severe amoebic dysentery. Severe infection causes the abdomen to become distended and may be associated with fever. The parasite may live in the colon without causing signs or symptoms or may invade the mucosa to cause colitis. In some cases, the disease spreads to the spleen, brain, genitourinary tract, or lungs. In particular, it may spread to the liver and cause an abscess. When a liver abscess develops, fever, nausea, liver tenderness, weight loss, and pain in the right abdominal quadrant may occur. Chronic infection may occur and is associated with intermittent diarrhea, mucus, pain, flatulence, and weight loss.

Direct examination of fecal specimens may be used for diagnosis. As with cryptosporidiosis, samples are often examined on multiple days. A stool O&P exam of fecal or biopsy specimens may be helpful. Immunoassay, serology, biopsy, molecular, and antibody detection tests are available. Enzyme immunoassay may not distinguish current from past illness. Magnetic resonance imaging (MRI) can be used to detect any liver abscesses. The first line of treatment is metronidazole or tinidazole, followed by diloxanide furoate, iodoquinol, or paromomycin to eliminate the cysts that remain.

Cyclosporiasis

The intestinal disease cyclosporiasis is caused by the protozoan Cyclospora cayetanensis. It is endemic to tropical and subtropical regions and therefore uncommon in the United States, although there have been outbreaks associated with contaminated produce imported from regions where the protozoan is more common. This protist is transmitted through contaminated food and water and reaches the lining of the small intestine, where it causes infection. Signs and symptoms begin within seven to ten days after ingestion. Based on limited data, it appears to be seasonal in ways that differ regionally and that are poorly understood.

Some individuals do not develop signs or symptoms. Those who do may exhibit explosive and watery diarrhea, fever, nausea, vomiting, cramps, loss of appetite, fatigue, and bloating. These symptoms may last for months without treatment. Trimethoprim-sulfamethoxazole is the recommended treatment. Microscopic examination is used for diagnosis. A stool O&P examination may be helpful. The oocysts have a distinctive blue halo when viewed using ultraviolet fluorescence microscopy (Figure (PageIndex{2})).

Figure (PageIndex{2}): Cyclospora cayetanensis are autofluorescent under ultraviolet light. (credit: modification of work by Centers for Disease Control and Prevention)

Exercise (PageIndex{1})

Which protozoan GI infections are common in the United States?

Key Concepts and Summary

  • Giardiasis, cryptosporidiosis, amoebiasis, and cyclosporiasis are intestinal infections caused by protozoans.
  • Protozoan intestinal infections are commonly transmitted through contaminated food and water.
  • Treatment varies depending on the causative agent, so proper diagnosis is important.
  • Microscopic examination of stool or biopsy specimens is often used in diagnosis, in combination with other approaches.

Multiple Choice

Which protozoan is associated with the ability to cause severe dysentery?

A. Giardia lamblia
B. Cryptosporidium hominis
C. Cyclospora cayetanesis
D. Entamoeba histolytica

D

Which protozoan has a unique appearance, with a blue halo, when viewed using ultraviolet fluorescence microscopy?

A. Entamoeba histolytica

C

The micrograph shows protozoans attached to the intestinal wall of a gerbil. Based on what you know about protozoan intestinal parasites, what is it?

(credit: Dr. Stan Erlandsen, Centers for Disease Control and Prevention)

A. Entamoeba histolytica

Fill in the Blank

Chronic _________ infections cause the unique sign of disease of greasy stool and are often resistant to treatment.

giardia

Short Answer

What is an O&P exam?

Contributor

  • Nina Parker, (Shenandoah University), Mark Schneegurt (Wichita State University), Anh-Hue Thi Tu (Georgia Southwestern State University), Philip Lister (Central New Mexico Community College), and Brian M. Forster (Saint Joseph’s University) with many contributing authors. Original content via Openstax (CC BY 4.0; Access for free at https://openstax.org/books/microbiology/pages/1-introduction)


High Frequency of Enteric Protozoan, Viral, and Bacterial Potential Pathogens in Community-Acquired Acute Diarrheal Episodes: Evidence Based on Results of Luminex Gastrointestinal Pathogen Panel Assay

Infectious diarrhea is endemic in most developing countries. We aimed to investigate the protozoan, viral, and bacterial causes of acute diarrhea in Taif, Saudi Arabia. A cross-sectional prospective 1-year study was conducted on 163 diarrheal patients of various ages. Stool samples were collected, 1 per patient, and tested for 3 protozoa, 3 viruses, and 9 bacteria with the Luminex Gastrointestinal Pathogen Panel. Overall, 53.4% (87/163) of samples were positives (20.8% protozoa, 19.6% viruses, 2.8% bacteria, and 9.8% mixed). Rotavirus (19.6%), Giardia duodenalis (16.5%), and Cryptosporidium spp. (8.5%) were the mostly detected pathogens. Adenovirus 40/41 (4.2%), Salmonella (3%), Shiga toxin-producing Escherichia coli (3%), and Entamoeba histolytica (2.4%) were also detected. Norovirus GI/II, Vibrio cholerae, Yersinia enterocolitica, and Clostridium difficile toxin A/B were not detected in any patients. All pathogens were involved in coinfections except E. histolytica. Giardia (5.5%) and rotavirus (3%) were the most commonly detected in co-infections. Enterotoxigenic E. coli (2.4%), Campylobacter spp. (2.4%), E. coli 0157 (1.8%), and Shigella spp. (1.2%) were detected in patients only as co-infections. Infections were more in children 0-4 years, less in adults <40 years, and least >40 years, with statistically significant differences in risk across age groups observed with rotavirus (P<0.001), Giardia (P=0.006), and Cryptosporidium (P=0.036) infections. Lastly, infections were not significantly more in the spring. This report demonstrates the high burden of various enteropathogens in the setting. Further studies are needed to define the impact of these findings on the clinical course of the disease.

Keywords: Cryptosporidium Entamoeba histolytica Giardia duodenalis co-infection diarrhea enteropathogen mono-infection xTAG™ GPP.


Staphylococcal Food Poisoning

Staphylococcal food poisoning is one form of food intoxication. When Staphylococcus aureus grows in food, it may produce enterotoxins that, when ingested, can cause symptoms such as nausea, diarrhea, cramping, and vomiting within one to six hours. In some severe cases, it may cause headache, dehydration, and changes in blood pressure and heart rate. Signs and symptoms resolve within 24 to 48 hours. S. aureus is often associated with a variety of raw or undercooked and cooked foods including meat (e.g., canned meat, ham, and sausages) and dairy products (e.g., cheeses, milk, and butter). It is also commonly found on hands and can be transmitted to prepared foods through poor hygiene, including poor handwashing and the use of contaminated food preparation surfaces, such as cutting boards. The greatest risk is for food left at a temperature below 60 °C (140 °F), which allows the bacteria to grow. Cooked foods should generally be reheated to at least 60 °C (140 °F) for safety and most raw meats should be cooked to even higher internal temperatures (Figure 19.10).

Figure 19.10 This figure indicates safe internal temperatures associated with the refrigeration, cooking, and reheating of different foods. Temperatures above refrigeration and below the minimum cooking temperature may allow for microbial growth, increasing the likelihood of foodborne disease. (credit: modification of work by USDA)

There are at least 21 Staphylococcal enterotoxins and Staphylococcal enterotoxin-like toxins that can cause food intoxication. The enterotoxins are proteins that are resistant to low pH, allowing them to pass through the stomach. They are heat stable and are not destroyed by boiling at 100 °C. Even though the bacterium itself may be killed, the enterotoxins alone can cause vomiting and diarrhea, although the mechanisms are not fully understood. At least some of the symptoms may be caused by the enterotoxin functioning as a superantigen and provoking a strong immune response by activating T cell proliferation.

The rapid onset of signs and symptoms helps to diagnose this foodborne illness. Because the bacterium does not need to be present for the toxin to cause symptoms, diagnosis is confirmed by identifying the toxin in a food sample or in biological specimens (feces or vomitus) from the patient. Serological techniques, including ELISA, can also be used to identify the toxin in food samples.

The condition generally resolves relatively quickly, within 24 hours, without treatment. In some cases, supportive treatment in a hospital may be needed.

E. coliInfections

The gram-negative rod Escherichia coli is a common member of the normal microbiota of the colon. Although the vast majority of E. coli strains are helpful commensal bacteria, some can be pathogenic and may cause dangerous diarrheal disease. The pathogenic strains have additional virulence factors such as type 1 fimbriae that promote colonization of the colon or may produce toxins. These virulence factors are acquired through horizontal gene transfer.

Extraintestinal disease can result if the bacteria spread from the gastrointestinal tract. Although these bacteria can be spread from person to person, they are often acquired through contaminated food or water. There are six recognized pathogenic groups of E. coli, but we will focus here on the four that are most commonly transmitted through food and water.

Enterotoxigenic E. coli(ETEC), also known as traveler’s diarrhea, causes diarrheal illness and is common in less developed countries. In Mexico, ETEC infection is called Montezuma’s Revenge. Following ingestion of contaminated food or water, infected individuals develop a watery diarrhea, abdominal cramps, malaise (a feeling of being unwell), and a low fever. ETEC produces a heat-stable enterotoxin similar to cholera toxin, and adhesins called colonization factors that help the bacteria to attach to the intestinal wall. Some strains of ETEC also produce heat-labile toxins. The disease is usually relatively mild and self-limiting. Diagnosis involves culturing and PCR. If needed, antibiotic treatment with fluoroquinolones, doxycycline, rifaximin, and trimethoprim-sulfamethoxazole (TMP/SMZ) may shorten infection duration. However, antibiotic resistance is a problem.

Enteroinvasive E. coli(EIEC) is very similar to shigellosis, including its pathogenesis of intracellular invasion into intestinal epithelial tissue. This bacterium carries a large plasmid that is involved in epithelial cell penetration. The illness is usually self-limiting, with symptoms including watery diarrhea, chills, cramps, malaise, fever, and dysentery. Culturing and PCR testing can be used for diagnosis. Antibiotic treatment is not recommended, so supportive therapy is used if needed.

Enteropathogenic E. coli(EPEC) can cause a potentially fatal diarrhea, especially in infants and those in less developed countries. Fever, vomiting, and diarrhea can lead to severe dehydration. These E. coli inject a protein that attaches to the surface of the intestinal epithelial cells and triggers rearrangement of host cell actin from microvilli to pedestals. The protein also happens to be the receptor for a surface protein produced by EPEC, thereby allowing E. coli to “sit” on the pedestal. As with ETEC, diagnosis involves culturing and PCR. Treatment is similar to that for ETEC.

The most dangerous strains are enterohemorrhagic E. coli(EHEC), which are the strains capable of causing epidemics. In particular, the strain O157:H7 has been responsible for several recent outbreaks. Recall that the O and H refer to surface antigens that contribute to pathogenicity and trigger a host immune response (“O” refers to the O-side chain of the lipopolysaccharide and the “H” refers to the flagella). Similar to EPEC, EHEC also forms pedestals. EHEC also produces a Shiga-like toxin. Because the genome of this bacterium has been sequenced, it is known that the Shiga toxin genes were most likely acquired through transduction (horizontal gene transfer). The Shiga toxin genes originated from Shigella dysenteriae. Prophage from a bacteriophage that previously infected Shigella integrated into the chromosome of E. coli. The Shiga-like toxin is often called verotoxin.

EHEC can cause disease ranging from relatively mild to life-threatening. Symptoms include bloody diarrhea with severe cramping, but no fever. Although it is often self-limiting, it can lead to hemorrhagic colitis and profuse bleeding. One possible complication is HUS. Diagnosis involves culture, often using MacConkey with sorbitol agar to differentiate between E. coli O157:H7, which does not ferment sorbitol, and other less virulent strains of E. coli that can ferment sorbitol.

Antibiotic therapy is not recommended and may worsen HUS because of the toxins released when the bacteria are killed, so supportive therapies must be used. Table 19.1 summarizes the characteristics of the four most common pathogenic groups.


Infections of the Gastrointestinal Tract

All regions of the gastrointestinal tract (GIT) are subject to infection. Saliva traps and removes many pathogens and these can also be killed by stomach acid . Unfortunately new ones are constantly introduced through breathing and eating.


Infections of the oral cavity (Figure 3.6) differ in type and symptoms to those of the stomach and intestines. Inflammation of oral tissues caused by fungal infection, actinomycosis, often occurs following injuries, such as an accidental bite to the lining of the mouth or fracture of the jaw. Immunosuppression resulting from viral infections, AIDS, cancer treatment or treatment with broad spectrum antibiotics can all allow the yeast Candida albicans (Figure3.10) to invade and colonize the mucous membrane, eventually producing athick layer of yeast cells called candidiasis or thrush.


Some bacteria can resist removal by saliva and become immobilized by binding to surface receptors of cells in the mouth, eventually forming biofilms and microcolonies. Oral streptococci, such as Streptococcus sanguis and Streptococcus mutans (Figure 3.11), secrete glycosyltransferases that mediatetheir adhesion to extracellular carbohydrates on tooth surfaces leading to the formation of dental plaque, which is a complex mixture of bacteria and extracellular materials. These bacteria, together with Actinomyces species, can cause caries by forming plaque on the tooth enamel, where they catabolize sugars to produce acid that demineralizes enamel and allows the dentine to be eroded. Abscesses of the roots of teeth can also be caused by mixed bacterial infections.


Periodontal (gum) diseases are inflammatory conditions that attack the gums, bone, and other supporting structures of the teeth. The extent of the inflammatory response depends upon the types of pathogens involved and the effectiveness of the immune response. However, they are major causes of tooth loss in adults. Gingivitis is the earliest form of periodontal disease and occurs when plaque accumulates on the teeth near the gums, which become inflamed and bleed easily. If detected and treated early, gingival tissues will return to normal without long-lasting damage. Untreated gingivitis progresses to periodontitis, which is also known as pyorrhea. Plaque hardens and extends from the gum line to the tooth root causing the gums to detach from the teeth and form pockets. Periodontal pockets create room for greater bacterial activity, particularly of facultative and obligate anaerobic bacteria leading to a progressive cycle of tissue damage until eventually the bone supporting the teeth is destroyed resulting in their loss.

Stomach and intestinal infections are caused by viruses, bacteria, protozoa and worms, all of which may be transmitted in food, contaminated drinking water or by fecal–oral contact. The need for strict personal hygiene is emphasized because these are the most frequent infections of children under five years of age. Approximately 40% of cases of diarrhea in children are caused by rotaviruses (Figure 3.12). In the very young this is potentially lethal and the WHO has estimated that out of the nearly two billion annual diarrhea diseases worldwide, three million end fatally.


Figure 3.13 indicates a number of pathogens that can infect the GIT. Theacidic environment and proteolytic enzymes of the stomach kill most


ingested microorganisms. However, the motile bacterium, Helicobacterpylori has specific receptors enabling it to bind to the gastricepithelium. It secretes urease, which catalyzes the hydrolysis of urea releasing ammonia that neutralizes stomach acid, and cytotoxins that damage the cells. This causes chronic inflammation of the gastric mucosal membrane and can lead to stomach and duodenal ulcers . The partially digested food (chyme) in the stomach is made alkaline in the small intestine by secretions of the gut and pancreas and by bile salts . In the ileum and jejunum, nonenveloped viruses, such as rotaviruses and adenoviruses, may infect enterocytes and damage the intestinal mucous membrane with disruption of water and electrolyte resorption. This can result in intestinal cramps, vomiting, watery diarrhea and a raised temperature. Enteropathogens, such as Vibrio cholerae and forms of Escherichia coli that are enterotoxic (ETEC) or enteropathogenic (EPEC) all have similar effects. The protozoan parasites Giardia lamblia and Cryptosporidium parvum are water-borne parasites that can infect the GIT. Giardia lamblia (Figure 3.14) frequently causes chronic disease, with watery diarrhea and, in some cases, a subfebrile temperature leading to malnutrition in children as a result of malabsorption. Cryptosporidium parvum can adhere to the epithelium of the small intestine and cause a shortening of the villi, which may be the cause of the diarrhea.


The lower portion of the ileum has areas of lymphoid tissue called Peyer’s patches (Figure 3.13) composed of so-called M (microfold) cells, rather than the usual enterocytes and goblet cells . These cells are able to translocate materials directly to the lymph follicles found beneath the mucosal surface. Invasive bacteria such as Campylobacter jejuni (Figure 3.15), Salmonellae and Yersiniae can use M cells to enter the submucosal area. Here they can multiply and destroy the adjacent epithelium, form abscesses and spread through the lymph and blood systems into the mesenteric lymph nodes, spleen and liver. The infection can also spread into the colon, causing inflammation of the colon or colitis. The ileum and colon can also be attacked by the bacteria Yersinia enterocolitica, Salmonella enterica and Campylobacterjejuni resulting in abdominal cramps, vomiting, watery, occasionally bloody,diarrhea and fever. Shigella dysenteriae and Escherichia coli pathotypes, EHEC (enterohemorrhagic) and EIEC (enteroinvasive) can cause a hemorrhagic colitis with bloody stools and subfebrile to febrile temperatures. The pathogenic protozoan Entamoeba histolytica is thought to infect 50 million people and kill about 100 000 per year worldwide due to amebic liver abscesses. Lastly, Clostridium difficile, a normal inhabitant of the gut, is an opportunistic pathogen. It is especially common in older people in hospitals and nursing homes and has been implicated in iatrogenic infections following medical interventions, such as antibiotic therapy. Infection with Clostridium difficile is now recognized as the major causative agent of colitis and diarrhea, which may occur following antibiotic intake and can be fatal in older patients.


Amoebiasis (Amebiasis)

The protozoan parasite Entamoeba histolytica causes amoebiasis, which is known as amoebic dysentery in severe cases. E. histolytica is generally transmitted through water or food that has faecal contamination. The disease is most widespread in the developing world and is one of the leading causes of mortality from parasitic disease worldwide. Disease can be caused by as few as 10 cysts being transmitted.

Signs and symptoms range from nonexistent to mild diarrhoea to severe amoebic dysentery. Severe infection causes the abdomen to become distended and may be associated with fever. The parasite may live in the colon without causing signs or symptoms or may invade the mucosa to cause colitis. In some cases, the disease spreads to the spleen, brain, genitourinary tract, or lungs. In particular, it may spread to the liver and cause an abscess. When a liver abscess develops, fever, nausea, liver tenderness, weight loss, and pain in the right abdominal quadrant may occur. Chronic infection may occur and is associated with intermittent diarrhoea, mucus, pain, flatulence, and weight loss.

Direct examination of faecal specimens may be used for diagnosis. As with cryptosporidiosis, samples are often examined on multiple days. A stool O&P exam of faecal or biopsy specimens may be helpful. Immunoassay, serology, biopsy, molecular, and antibody detection tests are available. Enzyme immunoassay may not distinguish current from past illness. Magnetic resonance imaging (MRI) can be used to detect any liver abscesses. The first line of treatment is metronidazole or tinidazole , followed by diloxanide furoate , iodoquinol , or paromomycin to eliminate the cysts that remain.


Pinworms (Enterobiasis)

Enterobius vermicularis, commonly called pinworms, are tiny (2–13 mm) nematodes that cause enterobiasis. Of all helminthic infections, enterobiasis is the most common in the United States, affecting as many as one-third of American children. 2 Although the signs and symptoms are generally mild, patients may experience abdominal pain and insomnia from itching of the perianal region, which frequently occurs at night when worms leave the anus to lay eggs. The itching contributes to transmission, as the disease is transmitted through the fecal-oral route. When an infected individual scratches the anal area, eggs may get under the fingernails and later be deposited near the individual’s mouth, causing reinfection, or on fomites, where they can be transferred to new hosts. After being ingested, the larvae hatch within the small intestine and then take up residence in the colon and develop into adults. From the colon, the female adult exits the body at night to lay eggs (Figure 3).

Infection is diagnosed in any of three ways. First, because the worms emerge at night to lay eggs, it is possible to inspect the perianal region for worms while an individual is asleep. An alternative is to use transparent tape to remove eggs from the area around the anus first thing in the morning for three days to yield eggs for microscopic examination. Finally, it may be possible to detect eggs through examination of samples from under the fingernails, where eggs may lodge due to scratching. Once diagnosis has been made, mebendazole, albendazole, and pyrantel pamoate are effective for treatment.

/>Figure 3. (a) E. vermicularis are tiny nematodes commonly called pinworms. (b) This micrograph shows pinworm eggs.​​

E. coli Infections

​The gram-negative rod Escherichia coli is a common member of the normal microbiota of the colon. Although the vast majority of E. coli strains are helpful commensal bacteria, some can be pathogenic and may cause dangerous diarrheal disease. The pathogenic strains have additional virulence factors such as type 1 fimbriae that promote colonization of the colon or may produce toxins (see Virulence Factors of Bacterial and Viral Pathogens). These virulence factors are acquired through horizontal gene transfer.

Extraintestinal disease can result if the bacteria spread from the gastrointestinal tract. Although these bacteria can be spread from person to person, they are often acquired through contaminated food or water. There are six recognized pathogenic groups of E. coli, but we will focus here on the four that are most commonly transmitted through food and water.

Enterotoxigenic E. coli (ETEC), also known as traveler’s diarrhea, causes diarrheal illness and is common in less developed countries. In Mexico, ETEC infection is called Montezuma’s Revenge. Following ingestion of contaminated food or water, infected individuals develop a watery diarrhea, abdominal cramps, malaise (a feeling of being unwell), and a low fever. ETEC produces a heat-stable enterotoxin similar to cholera toxin, and adhesins called colonization factors that help the bacteria to attach to the intestinal wall. Some strains of ETEC also produce heat-labile toxins. The disease is usually relatively mild and self-limiting. Diagnosis involves culturing and PCR. If needed, antibiotic treatment with fluoroquinolones, doxycycline, rifaximin, and trimethoprim-sulfamethoxazole (TMP/SMZ) may shorten infection duration. However, antibiotic resistance is a problem.

Enteroinvasive E. coli (EIEC) is very similar to shigellosis, including its pathogenesis of intracellular invasion into intestinal epithelial tissue. This bacterium carries a large plasmid that is involved in epithelial cell penetration. The illness is usually self-limiting, with symptoms including watery diarrhea, chills, cramps, malaise, fever, and dysentery. Culturing and PCR testing can be used for diagnosis. Antibiotic treatment is not recommended, so supportive therapy is used if needed.

Enteropathogenic E. coli (EPEC) can cause a potentially fatal diarrhea, especially in infants and those in less developed countries. Fever, vomiting, and diarrhea can lead to severe dehydration. These E. coli inject a protein (Tir) that attaches to the surface of the intestinal epithelial cells and triggers rearrangement of host cell actin from microvilli to pedestals. Tir also happens to be the receptor for Intimin, a surface protein produced by EPEC, thereby allowing E. coli to “sit” on the pedestal. The genes necessary for this pedestal formation are encoded on the locus for enterocyte effacement (LEE) pathogenicity island. As with ETEC, diagnosis involves culturing and PCR. Treatment is similar to that for ETEC.

The most dangerous strains are enterohemorrhagic E. coli (EHEC), which are the strains capable of causing epidemics. In particular, the strain O157:H7 has been responsible for several recent outbreaks. Recall that the O and H refer to surface antigens that contribute to pathogenicity and trigger a host immune response (“O” refers to the O-side chain of the lipopolysaccharide and the “H” refers to the flagella). Similar to EPEC, EHEC also forms pedestals. EHEC also produces a Shiga-like toxin. Because the genome of this bacterium has been sequenced, it is known that the Shiga toxin genes were most likely acquired through transduction (horizontal gene transfer). The Shiga toxin genes originated from Shigella dysenteriae. Prophage from a bacteriophage that previously infected Shigella integrated into the chromosome of E. coli. The Shiga-like toxin is often called verotoxin.

EHEC can cause disease ranging from relatively mild to life-threatening. Symptoms include bloody diarrhea with severe cramping, but no fever. Although it is often self-limiting, it can lead to hemorrhagic colitis and profuse bleeding. One possible complication is HUS. Diagnosis involves culture, often using MacConkey with sorbitol agar to differentiate between E. coli O157:H7, which does not ferment sorbitol, and other less virulent strains of E. coli that can ferment sorbitol.

Serological typing or PCR testing also can be used, as well as genetic testing for Shiga toxin. To distinguish EPEC from EHEC, because they both form pedestals on intestinal epithelial cells, it is necessary to test for genes encoding for both the Shiga-like toxin and for the LEE. Both EPEC and EHEC have LEE, but EPEC lacks the gene for Shiga toxin. Antibiotic therapy is not recommended and may worsen HUS because of the toxins released when the bacteria are killed, so supportive therapies must be used. Table summarizes the characteristics of the four most common pathogenic groups.

​Some Pathogenic Groups of E. coli

  • ​Compare and contrast the virulence factors and signs and symptoms of infections with the four main E. coli groups.​

Cholera and Other Vibrios

The gastrointestinal disease cholera is a serious infection often associated with poor sanitation, especially following natural disasters, because it is spread through contaminated water and food that has not been heated to temperatures high enough to kill the bacteria. It is caused by Vibrio cholerae serotype O1, a gram-negative, flagellated bacterium in the shape of a curved rod (vibrio). According to the CDC, cholera causes an estimated 3 to 5 million cases and 100,000 deaths each year. [4]

Because V. cholerae is killed by stomach acid, relatively large doses are needed for a few microbial cells to survive to reach the intestines and cause infection. The motile cells travel through the mucous layer of the intestines, where they attach to epithelial cells and release cholera enterotoxin. The toxin is an A-B toxin with activity through adenylate cyclase (see Virulence Factors of Bacterial and Viral Pathogens). Within the intestinal cell, cyclic AMP (cAMP) levels increase, which activates a chloride channel and results in the release of ions into the intestinal lumen. This increase in osmotic pressure in the lumen leads to water also entering the lumen. As the water and electrolytes leave the body, it causes rapid dehydration and electrolyte imbalance. Diarrhea is so profuse that it is often called “rice water stool,” and patients are placed on cots with a hole in them to monitor the fluid loss (Figure 4).

Cholera is diagnosed by taking a stool sample and culturing for Vibrio. The bacteria are oxidase positive and show non-lactose fermentation on MacConkey agar. Gram-negative lactose fermenters will produce red colonies while non-fermenters will produce white/colorless colonies. Gram-positive bacteria will not grow on MacConkey. Lactose fermentation is commonly used for pathogen identification because the normal microbiota generally ferments lactose while pathogens do not. V. cholerae may also be cultured on thiosulfate citrate bile salts sucrose (TCBS) agar, a selective and differential media for Vibrio spp., which produce a distinct yellow colony.

Cholera may be self-limiting and treatment involves rehydration and electrolyte replenishment. Although antibiotics are not typically needed, they can be used for severe or disseminated disease. Tetracyclines are recommended, but doxycycline, erythromycin, orfloxacin, ciprofloxacin, and TMP/SMZ may be used. Recent evidence suggests that azithromycin is also a good first-line antibiotic. Good sanitation—including appropriate sewage treatment, clean supplies for cooking, and purified drinking water—is important to prevent infection (Figure 4)

Figure 4. (a) Outbreaks of cholera often occur in areas with poor sanitation or after natural disasters that compromise sanitation infrastructure. (b) At a cholera treatment center in Haiti, patients are receiving intravenous fluids to combat the dehydrating effects of this disease. They often lie on a cot with a hole in it and a bucket underneath to allow for monitoring of fluid loss. (c) This scanning electron micrograph shows Vibrio cholera. (credit a, b: modification of work by Centers for Disease Control and Prevention credit c: modification of work by Janice Carr, Centers for Disease Control and Prevention)

V. cholera is not the only Vibrio species that can cause disease. V. parahemolyticus is associated with consumption of contaminated seafood and causes gastrointestinal illness with signs and symptoms such as watery diarrhea, nausea, fever, chills, and abdominal cramps. The bacteria produce a heat-stable hemolysin, leading to dysentery and possible disseminated disease. It also sometimes causes wound infections. V. parahemolyticus is diagnosed using cultures from blood, stool, or a wound. As with V. cholera, selective medium (especially TCBS agar) works well. Tetracycline and ciprofloxacin can be used to treat severe cases, but antibiotics generally are not needed.

Vibrio vulnificus is found in warm seawater and, unlike V. cholerae, is not associated with poor sanitary conditions. The bacteria can be found in raw seafood, and ingestion causes gastrointestinal illness. It can also be acquired by individuals with open skin wounds who are exposed to water with high concentrations of the pathogen. In some cases, the infection spreads to the bloodstream and causes septicemia. Skin infection can lead to edema, ecchymosis (discoloration of skin due to bleeding), and abscesses. Patients with underlying disease have a high fatality rate of about 50%. It is of particular concern for individuals with chronic liver disease or who are otherwise immunodeficient because a healthy immune system can often prevent infection from developing. V. vulnificus is diagnosed by culturing for the pathogen from stool samples, blood samples, or skin abscesses. Adult patients are treated with doxycycline combined with a third generation cephalosporin or with fluoroquinolones, and children are treated with TMP/SMZ.

Two other vibrios, Aeromonas hydrophila and Plesiomonas shigelloides, are also associated with marine environments and raw seafood they can also cause gastroenteritis. Like V. vulnificus, A. hydrophila is more often associated with infections in wounds, generally those acquired in water. In some cases, it can also cause septicemia. Other species of Aeromonas can cause illness. P. shigelloides is sometimes associated with more serious systemic infections if ingested in contaminated food or water. Culture can be used to diagnose A. hydrophila and P. shigelloides infections, for which antibiotic therapy is generally not needed. When necessary, tetracycline and ciprofloxacin, among other antibiotics, may be used for treatment of A. hydrophila, and fluoroquinolones and trimethoprim are the effective treatments for P. shigelloides.

Think about It


Summary

Background

HIV infection continues to pose a serious challenge to global health by predisposing patients to opportunistic infections. A cross-sectional study was conducted from December 2012 to February 2013 to assess the enteric protozoan infection status among individuals living with HIV/AIDS in Felegehiwot Referral Hospital, Bahir Dar, northwest Ethiopia.

Methods

Stool specimens from 399 HIV-positive individuals were examined for the presence of trophozoites, cysts, and oocysts using direct wet mount, formol–ether sedimentation and modified Ziehl–Neelsen techniques. In addition, CD4+ T-cell counts were measured to evaluate the immune status of the study subjects.

Results

An overall prevalence of 30.6% enteric protozoan infections was recorded. Pre-ART (antiretroviral treatment) individuals were more infected than patients on ART, although this was not statistically significant (p > 0.05). The highest prevalence of enteric protozoan infection was due to Entamoeba histolytica/E. dispar (19.3%), followed by Cryptosporidium spp (5.8%), Giardia lamblia (4.3%), and Isospora belli (1.3%). A CD4+ T-cell count of <200 cells/μl and status of being diarrhoeic were significantly associated with the overall prevalence of enteric protozoan infection.

Conclusions

A relatively high prevalence of enteric protozoan infection was observed among individuals living with HIV/AIDS. Routine stool and CD4+ T-cell examinations should be conducted to monitor the status of HIV/AIDS patients.


Conclusion

In this study, the prevalence of intestinal parasites was found lower than WHO annual or biannual population treatment level. Child food freshness, regular trimming fingernails, Children playground cleanliness, and family use of toilet were significantly associated with intestinal parasitic infection. Thus, strengthening of health education about food, personal and environmental hygiene of both children and mothers/guardians is crucial. Besides, improving mothers/guardian awareness about the mode of intestinal parasites transmission is necessary.


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