Enteric Protozoal and Bacterial Infections by ravenms


									Newer Enteric Protozoan and Bacterial Pathogens
David Kramer, M.D.

I.   Cyclosporiasis

     A.   The infectious agent is Cyclospora cayetanensis. Newly recognized as a protozoan
          parasite causing illness in humans, although earlier reports had suggested other
          identities for this pathogen, including blue-green algae (eg, Cyanobacteria-like
          bodies) or other protozoan forms.

     B.   Epidemiology.

          1.   Parasite is widely distributed geographically, including the U.S., Latin America
               and Asia.

          2.   Waterborne transmission and food-borne transmission occur; whether other
               modes of transmission exist remains to be defined. Oocysts when passed in stool
               are not immediately infectious and require sporulation over days to weeks.
               Consequently, direct person-to-person spread of infection is not likely. In US
               associated with widespread outbreaks of diarrheal illness due to contaminated
               raspberries imported from Guatemala.

     C.   Pathophysiology

          1.   Parasite invades epithelial cells as detectable in small bowel biopsies.

          2.   Mechanism of pathogenesis not understood, but the absence of fecal leukocytes
               and blood suggests that disease is due to a noninvasive mechanism.

     D.   Clinical

          1.   Immunocompetent hosts: Incubation period is usually about seven days. Patients
               experience diarrhea, flu-like symptoms and symptoms common to other small
               bowel pathogens, such as flatulence and burping. May have a single self-limited
               episode, but prolonged diarrhea, anorexia and upper GI symptoms often occur.
               Pronounced fatigue and malaise have been frequent symptoms with weight loss
               experienced by some.

          2.   Immunocompromised hosts: Recognized in ADS, but nature of intestinal illness
               due to Cyclospora in immunocompromised hosts not yet defined.

     E.   Diagnosis
           1. Oocysts in stool (8-10 µm in diameter) are acid-fast and can be detected with
           acid-fast stains of stool. Thus, must be distinguished from Cryptosporidium,
           Cyclospora oocysts are not found on routine stool O + P exams; rather specific acid-
           fast stains must be requested.

      F.   Treatment

           1.   Trimethoprim-sulfamethoxazole 1 double strength tablet bid for 7 days is
                effective. Alternative therapies for those unable to take TMP-SMX are not

II.   Cryptosporidiosis

      A.   Agent - Cryptosporidium parvum

      B.   Epidemiology

           1.   Parasite infects humans and a variety of veterinary animals. Oocysts passed in
                human or animal feces are infectious and ingestion leads to acquisition of

           2.   Infection may spread via:

                • waterborne transmission:
                      both drinking water and recreational water (pools, slides, etc)

                • food-borne spread - oocyst contamination after any cooking

                • direct person-to-person transmission (amongst male homosexuals,
                      within day-care centers, within hospitals)

                • animal to person spread (from calves, lambs, ?dogs/cats)

      C.   Pathophysiology

           1.   Parasite invades epithelial cells and exists within a parasitophorous
                vacuole, which is intracellular but extra-cytoplasmic. Parasite replicates.

           2.   Mechanism of pathogenesis not understood. Diarrhea appears to be a
                secretory process and infection does not cause disruption of bowel
                epithelium. In addition to small bowel, parasites may be found in
                colon, rectum and esophagus in some patients. Oocysts have been
                recovered from pulmonary secretions: ? 20 to aspiration or due to
                infection of bronchial epithelium. Also may spread into biliary tract to
                cause disease.
     D.    Clinical

           1.     Immunocompetent hosts: Incubation period of about 6 days (3-12 days range).
                  Watery, non-bloody diarrhea; less commonly, abdominal discomfort, anorexia,
                  fever, nausea and weight loss. Usually self-limited, lasting 3-14 days, only
                  occasionally for months. Malabsorption can develop. Asymptomatic carriage is

           2.     Immunocompromised hosts: Chronic, unremitting, profuse, watery diarrhea. In
                  AIDS, worse with CD4 count < 180/ul.

     E.    Diagnosis

           1.     Oocysts in stool are small (4-5 µm diameter) and may be missed on
                  conventional stool O + P exams. Oocysts, however, are acid-fast and
                  can be detected with acid-fast stains of stool or more sensitively with a
                  specific fluorescent antibody stain. For low numbers of oocysts, can
                  use modified sucrose flotation method. Parasites may also be found
                  along luminal surface of biopsied intestinal epithelium.

     F.    Treatment

           1.     For immunocompetent, illness is self-limited and no therapy, other than
                  possible supportive fluid and electrolyte replacement, is needed.

           2.     For immunocompromised, therapy is needed, but none has been found
                  to be effective. Limited and not uniform successes with paromomycin.

III. Isoporosis

     A.    Agent - lsospora belli

     B.    Epidemiology

           1.     Modes of transmission and sources of human infections not defined.

     C.    Pathophysiology

           1.     Parasite infects the intestinal tract, but underlying pathogenic
                  mechanisms uncertain.

     D.    Clinical

           1.     Immunocompetent hosts: Usually abrupt in onset with fever and
                  malaise followed by abdominal pain, diarrhea and weight loss. Most
                infections self-limited, although some may last for weeks to months.

          2.    Immunocompromised hosts: Chronic, unremitting, profuse, watery
                diarrhea, indistinguishable for cryptosporidiosis.

     E.   Diagnosis

          1.    Oocysts are acid-fast and can be detected with acid-fast stains of stool.
                For low numbers of oocysts, can use zinc sulfate concentration method.
                Parasites may also be found along luminal surface of biopsied intestinal

     F.   Treatment

           1. Trimethoprim-sulfamethoxazole double-strength tablets qid for 10 days and then
     bid for 3 weeks. For those with AIDS, relapses are frequent and maintenance therapy is
     needed with one double strength trimethoprim-sulfamethoxazole tablet three times/week.

IV. Escherichia coli O157

     A.   Escherichia coli O157 produces amounts of
          two types of Shiga toxins. A cause of diarrheal illness and the hemolytic-
          uremic syndrome.

     B.   Epidemiology O157 is a non-pathogenic gut bacterium in cattle.

          1.    Beef is the food source most likely to harbor O 157.

          2.    Milk, fruit, vegetables that have contacted bovine feces may also
                become contaminated.

          3.    Heating (70EC for 2 mins) kills O157; thus undercooked meat or
                non-pasteurized cider may efficiently spread infection.

     C.   Pathophysiology

           1. O157 adheres to intestinal epithelial cells. Shiga-like toxins I and II, encoded by
     a bacteriophage, may be elaborated and act:

                •     locally to cause intestinal epithelial ulceration and diarrhea, and

                •     systemically to damage small blood vessels, eg in the kidney, causing acute
                      renal failure, hemolytic anemia and thrombocytopenia (hemolytic uremic
     D.      Clinical Diarrhea, bloody diarrhea and abdominal cramps are common.

     E.      Diagnosis

             1.   A history of bloody diarrhea and/or having visible blood in stools is very
                  common, but one third of isolates are from non-bloody samples. Fecal
                  leukocytes may be present.

             2.   Culture; toxin immunoassay and gene probes.

     F.      Treatment

             1.   Fluoroquinolones, eg ciprofloxacin 500 mg bid or norfloxacin 400 mg bid, for 3-
                  5 days.

             2.   TMP/SMX double strength tabs bid for 3-5 days.


I. Cyclospora

1.   Herwaldt BL, Ackers ML. An outbreak in 1996 of cyclosporiasis associated with imported
     raspberries. The Cyclospora Working Group. N Engl J Med. 336:1548, 1997.

2.   Ortega YR, Sterling CR, Gilman RH, Cama VA, Diaz F. Cyclospora species - a new
     protozoan pathogen of humans. N Engl J Med. 328:1308, 1993.

3.   Huang P, Weber JT, Sosin DM et al. The first reported outbreak of diarrheal illness
     associated with Cyclospora in the United States. Ann Intern Med 123:409, 1995.

4.   Pape JW, Verdier RI, Boncy M, Boncy J, Johnson WD Jr. Cyclospora infection in
     adults infected with HIV. Clinical manifestations, treatment, and prophylaxis. Ann Intern
     Med 121:654, 1994.

5.   Hoge CW, Shlim DR, Ghimire Met al. Placebo-controlled trial of co-trimoxazole for
     Cyclospora infections among travelers and foreign residents in Nepal. Lancet 345:691,

6.   Outbreaks of pseudo-infection with Cyclospora and Cryptosporidium - Florida and New
     York City, 1995. MMWR Morb Mortal Wkly Rep 46:354, 1997.

7.   Gascon J Corachan M Bombi JA Valls ME Bordes JM. Cyclospora in patients with
     traveller's diarrhea. Scand J Infect Dis 27:511, 1995.

II. Cryptosporidiosis
1.   Goldstein ST, Juranek DD, Ravenholt O, et al. Cryptosporidiosis: an outbreak associated
     with drinking water despite state-of-the-art water treatment. Ann Intern Med 124:459,

2.   Chappell CL, Okhuysen PC, Sterling CR, DuPont HL. Cryptosporidium parrum: intensity

     of infection and oocyst excretion patterns in healthy volunteers. J Infect Dis 173:232,

3.   McAnulty JM, Fleming DW, Gonzalez AH. A community-wide outbreak of
     cryptosporidiosis associated with swimming at a wave pool. JAMA 272:1597, 1994.

4.   Millard PS, Gensheimer KF, Addiss DG, et al. An outbreak of cryptosporidiosis from
     fresh-pressed apple cider. JAMA 272:1592, 1994.

5.   Vakil NB, Schwartz SM, Buggy BP, et al. Biliary cryptosporidiosis in HIV-infected
     people after the waterborne outbreak of cryptosporidiosis in Milwaukee. N Engl J Med
     334:19, 1996.

6.   Addiss DG, Pond RS, Remshak M, et al. Reduction of risk of watery diarrhea with
     point-of-use water filters during a massive outbreak of waterborne Cryptosporidium
     infection in Milwaukee, Wisconsin, 1993. Am J Trop Med Hyg 54:549, 1996.

7.   Hashmey R, Smith NH, Cron S, Graviss EA, Chappell CL. White AC Jr.
     Cryptosporidiosis in Houston, Texas. A report of 95 cases. Medicine (Baltimore) 76:118,

III. Isospora

1.   DeHovitz JA, Pape JW, Boncy Met al. Clinical manifestations and therapy of lsopsora
     belli infection in patients with the acquired immunodeficiency syndrome. N Engl J Med
     315:87, 1986.

2.   Pape JW, Verdier R-I, Johnson WD Jr. Treatment and prophylaxis of Isospora belli
     infection in patients with the acquired immunodeficiency syndrome. N Engl J Med
     320:1044, 1989.

3.   Sorvillo FJ, Lieb LE, Seidel J, Kerndt P, Turner J, Ash LR. Epidemiology of
     isosporiasis among persons with acquired immunodeficiency syndrome in Los Angeles
     County. Am J Trop Med Hyg 53:656, 1995.

IV. Escherichia coli 0157

1.   Outbreaks of Escherichia coli O157:H7 infection and cryptosporidiosis associated with
     drinking unpasteurized apple cider--Connecticut and New York, October 1996. MMWR
     Morb Mortal Wkly Rep 46:4, 1997.

2.   Slutsker L, Ries AA, Greene KD, Wells JG, Hutwagner L, Griffin PM. Eschereicha coli
     0157:H7 diarrhea in the United States: Clinical and epidemiologic features. Ann Int Med
     126:505, 1997.

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