MIM 34 Enteric Protozoa-Hamrick-2024.pdf

MIM 34 Enteric Protozoa...

MIM 34 Enteric Protozoa Terri S. Hamrick, PhD Office #167 (910) 893-1705 [email protected] The copyrighted materials available in this class are for educational use only. One copy per student is permitted for educational purposes. Redistribution is not permitted. MIM –Block 1 Fall 2024 https://www.grc.org/biology-of-spirochetes-conference/2024/  Readings 1. Lippincott’s Illustrated Reviews: Microbiology, Cornelissen, NA and Hobbs, MM (editors) 2019, 4th ed. Wolters Kluwer. Chapter 21 2. W. Levinson, 2022, Review of Medical Microbiology and Immunology 18th Ed., Chapter 51. Learning objectives 1. Describe the general clinical manifestations of gastrointestinal infectious etiologies. 2. Identify the common intestinal protozoal infections. 3. Explain the life cycle of Entamoeba histolytica and Balantidium coli, and identify their pathogenic, transmissible, and diagnostic forms. 4. Describe the pathogenesis, clinical manifestations, and epidemiology of E. histolytica amebiasis. 5. Describe and contrast the clinical significances, pathobiology, transmission, and risk factors of giardiasis, cryptosporidiosis, cyclosporiasis. 6. Identify the infectious and diagnostic forms of Cryptosporidium, Giardia, and Cyclospora. 3 Presentation Outline Introduction to ID in GI and Protozoal Gastroenteritis Entamoeba histolytica Cryptosporidium, Giardia lamblia, Cyclospora: small intestine  Infections and GI Disorders Infectious: Viral, Bacterial, or Parasitic? GI Disorders Nausea/ Vomiting Non-GI Non-Infectious Disorders  Tips: connect what Infections and GI Disorders the pathogen does with the pts’ presentation Infectious Watery Non- Bacterial? infectious Viral? parasitic? Diarrhea Fatty Infectious Clues? Inflammatory Non- infectious  Clinical Presentations of “Food-Borne” Gastrointestinal Disease: diarrhea or dysentery, nausea and vomiting, and abdominal cramping Infection Ingestion of preformed toxin: Early onset of Small intestine: Large intestine: nausea, vomiting, dysentery (small and diarrhea, but watery diarrhea fecal volume with (usually) no fever and vomiting mucus and blood)  Overview of Protozoal Gastroenteritis Fecal–oral route transmission: acquired by ingestion of cysts in contaminated food or water Entamoeba histolytica (amoeba) and Balantidium coli (ciliate) Cause colonic ulcerations and dysentery Giardia lamblia (flagellate); Cryptosporidium and Cyclospora (sporozoan): Infect the small intestine Cause noninflammatory, watery diarrhea  Protozoa: single-celled 9 Presentation Outline Introduction to ID in GI and Protozoal Gastroenteritis Entamoeba histolytica Cryptosporidium, Giardia lamblia, Cyclospora: small intestine 11  Entamoeba histolytica: Amebiasis Lippincott’s Illustrated Reviews: Microbiology Fecal –Oral Anal-Oral (human to human only)  Life Cycle of E. histolytica Humans acquire amebic infection by oral ingestion of the cyst The parasite excysts after passing through the stomach, replicates asexually, and transforms to the pathogenic trophozoite form. When conditions in the gastrointestinal tract are unfavorable, trophozoites transform into cysts, which can remain dormant for long periods of time in the host and the environment. Trophozoites cause amebic dysentery in the colon and can spread to the liver (most often), lung, and brain  Pathobiology of Amebiasis Flask-shaped ulcers in the colonic mucosal epithelium. Can produce abscesses in the liver (less commonly in the lung, brain, or other organs). Cell-mediated immunity is the most important line of defense. a typical flask-shaped ulcer of intestinal amebiasis (CDC)  Epidemiological Considerations Transmission: Patients with diarrhea shedding mainly active growing trophozoites (labile) are minor threats. Asymptomatic carriers are the greatest danger of transmission. (shedding cysts) Prevalence: not restricted to warm climates 50% of the population in some areas (world-wide) are infected (average prevalence, 10% to 15%) U.S. prevalence is 4% to 5%  Management of Amebiasis Lab Diagnosis Microscopic identification of trophozoites and cysts in freshly passed dysenteric stool or in scrapings from colonic ulcers most useful Stool immunoassay (for E. histolytica antigen), PCR Serological diagnosis is useful in the US (no endemic) Treatment The drug of choice for active amebic Cysts infection is metronidazole.  Microscopic Morphology A trophozoite with six A cyst ingested red blood cells RBCs Four nuclei might be seen if the cyst is mature CDC  Microscopic Morphology Iodine Wet Mount Image Source: CDC image library  Summary: Amebiasis As the cyst matures nuclear division produces four nuclei 20  Balantidium coli: Balantidiasis The only known pathogenic ciliated protozoan for humans. Life cycle: § Ingestion of infectious cysts and invasion of trophozoites into the mucosal lining of the large intestine; rarely disseminated to distant organs § Infective cysts found in contaminated water and not inactivated by chlorination. § Pigs are the natural reservoirs.  Balantidiasis Clinical Manifestation: ranging from asymptomatic carriage to abdominal discomfort and mild diarrhea to acute dysentery; disease similar to amebiasis in causing intestinal ulceration. Cysts are not inactivated by chlorine Laboratory Diagnosis: a large organism compared with other intestinal protozoa; readily detectable in fresh, wet microscopic preparations. Treatment: tetracyclines or metronidazole.  Balantidium coli Lab Diagnosis https://www.cdc.gov/dpdx/balantidiasis/index.html Trophozoite: very large; surface covered with cilia; with prominent internal structure including a macronucleus, two pulsating contractile The cyst is smaller, surrounded vacuoles. by a clear refractile wall, and has a single nucleus in the cytoplasm. Presentation Outline Introduction to ID in GI and Protozoal Gastroenteritis Entamoeba histolytica Cryptosporidium, Giardia lamblia, Cyclospora: small intestine Giardia lamblia (duodenalis/ intestinalis): Giardiasis A flagellate!!  Life Cycle of Giardia lamblia § Cysts are hardy and can survive several months in cold water. § Transmission: ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites, person-to-person possible) § Excystation of ingested cyst releases trophozoites in the small intestine. § Trophozoites multiply and remain in the lumen of the proximal small bowel. § Encystation occurs as the parasites transit toward the colon. § Both cysts and trophozoites can be found in the feces (diagnostic stages)  Pathogenesis of Giardiasis Mild but persistent diarrheal disease: Mechanism: Submucosal infiltration of chronic inflammatory cells and effacement of the normal intestinal villi Giardia attach to the wall, but not invade– they damage the mucosa ®malabsorption of fats (associated with greasy, foul-smelling stools) Deficiencies of fat-soluble vitamins (i.e. A, D, E, and K) and weight loss. Presentation: Non-bloody diarrhea (local infection only) Scanning electron micrograph of Giardia lamblia A. G. lamblia adhering to the gastrointestinal epithelium using its ventral sucking disk. B. The organisms often leave a clear impression on the microvillous surface (upper circles).  Epidemiology of Giardiasis qGiardia cysts are resistant to chlorine. qWaterborne outbreaks associated with ingestion of water contaminated by feces from animal carriers. qGiardia cysts are highly resistant in the environment and are found in ostensibly “pure” mountain streams contaminated by the feces of infected animals or humans. qTransmitted in cold or warm climate qDiarrhea can be prolonged (a week or more) qSex: reduce contact with feces Giardia and pets Dogs and cats can carry giardia, but you are unlikely to get it from pets (not usually the same type) Animals that can spread giardia to people: Chinchillas, beavers, birds, opossums, and monkeys Sometimes called beaver fever, although no fever 30  Management of Giardiasis Microscopic identification of parasites (difficult; excretion of Giardia occurs in “showers”; 3 daily samples required) Antigen detection assay Treatment: Metronidazole and others G. lamblia cyst. Iodine stain (L) G. lamblia Trophozoite (R) flagellated  Cryptosporidium Intracellular protozoan Cryptosporidium parvum GI illness Cryptosporidium hominis Diarrhea and biliary tract disease Chlorine resistance (unless really high) Excretion after resolution of symptoms Cryptosporidium causes over half of the waterborne disease outbreaks associated with public swimming pools, hot tubs, and splash pads 32  Cryptosporidium parvum and C. hominis: Cryptosporidiosis Within the intestine, the Food-borne: less common oocyst produces trophozoites that cause diarrhea Millions of parasites can be released in a bowel movement  Highlights of Cryptosporidiosis § Infectious oocyst forms produced in the intestine and spread to other animals. § Oocysts are highly resistant to chlorine. § Transmission: contact with animals; person to person; contaminated water. § Outbreaks associated with drinking water, food, or swimming pools.  Oocysts of C. parvum Wet Mount Acid-fast Stain Sporozoites are visible inside the oocysts Image: CDC Epidemiology of Cryptosporidiosis § Worldwide § ~ 748,000 cases/year in the US § Reported in a wide variety of animals (mammals) § Transmission: oZoonotic origin: animal reservoirs to humans oPerson-to-person: fecal-oral and oral-anal routes § High-risk population: veterinary personnel, animal handlers, children, MSM, and immunocompromised individuals Clinical Considerations of Cryptosporidiosis qClinical manifestations: § In immunocompetent hosts: asymptomatic or a single episode of watery diarrheal disease that lasts 2 weeks. § In immunocompromised patients: persistent and intractable watery diarrhea; dissemination possible qLab identification: acid-fast cysts in the stool and stool antigen detection assay. qManagement: Nitazoxanide  Cyclospora cayetanensis: Cyclosporiasis (Sai-ko-spo-ra sai-ye-te-nan-sis) §A single species identified so far §An increasingly recognized cause of epidemic chronic diarrhea in US.  Transmission and Epidemiology of C. cayetanensis Humans: only natural host The oocysts (also acid-fast) are not infectious when freshly excreted in feces (need a few days to mature) Usually not killed by chemical disinfection or sanitization New infections are acquired by ingestion of contaminated food or water (not person-person)  Cyclosporiasis Clinical Significances, Diagnosis, and Treatment § Watery diarrhea most common § The illness may last for only a few days or for a month or longer; relapses are common. § High rate of recurrence and biliary tract infection in Diagnostic Cyclospora oocysts immunocompromised pts. from fresh stool stained using a modified acid-fast stain. The oocysts § Treatment with trimethoprim- are variably acid fast, ranging from sulfamethoxazole relieves unstained to light pink to deep red. symptoms and shortens the course Image: CDC (DPDx). of infection.  Summary of Major Intestinal Protozoa Diagnosis- CLINICAL ORGANISM infectious Forms Transmission MANIFESTATIONS Entamoeba Bloody diarrhea (dysentery), distant histolytica abscesses (especially liver), (amebiasis) asymptomatic intestinal infection Balantidium coli (Balantidiasis) Giardia lamblia Watery diarrhea; may also cause (giardiasis) steatorrhea and malabsorption Cryptosporidium Watery diarrhea; massive outbreak; parvum intractable diarrhea in people with (cryptosporidiosis) AIDS Cyclospora cayetanensis (Cyclosporiasis)  MAJOR REFERENCES Lippincott’s Illustrated Reviews: Microbiology, Cornelissen, NA and Hobbs, MM (editors) 2019, 4th ed. Wolters Kluwer. Review of Medical Microbiology and Immunology by Warren Levinson, 18th Ed. 2024, McGraw Hill. UpToDate: Giardiasis: Epidemiology, clinical manifestations, and diagnosis. Updated May 01, 2024. Cyclospora infection. Authors: Peter F Weller, Karin Leder. Updated 10/23, 2023. Cryptosporidiosis: Epidemiology, clinical manifestations, and diagnosis. Authors: Karin Leder, Peter F Weller. Updated June 13, 2024 Balantidium coli infection. Authors: Peter F Weller, Karin Leder. Updated October 23, 2024