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110 PROTOZOAL INFECTIONS

110 PROTOZOAL INFECTIONS
Harrison’s Manual of Medicine

110

PROTOZOAL INFECTIONS

Amebiasis
Malaria
Leishmaniasis
Trypanosomiasis

Chagas’ Disease

Sleeping Sickness
Toxoplasmosis
Protozoal Intestinal Infections

Giardiasis

Cryptosporidiosis

Isosporiasis

Cyclosporiasis

Microsporidiosis
Bibliography

AMEBIASIS
EPIDEMIOLOGY   Amebiasis is the third leading cause of death from parasitic disease worldwide. The areas of highest incidence include most developing countries in the tropics, particularly Mexico, India, and the nations of Central and South America, tropical Asia, and Africa. The main groups at risk in developed countries are travelers, recent immigrants, homosexual men, and residents of institutions. Entamoeba histolytica, the intestinal protozoan that causes amebiasis, is acquired by ingestion of viable cysts from fecally contaminated water, food, or hands. Food-borne exposure is most common. Less common modes of transmission include oral and anal sexual practices; rare cases are transmitted by direct rectal inoculation through colonic irrigating devices.
PATHOGENESIS   After ingestion, cysts release trophozoites (the only form that invades tissue) into the lumen of the small intestine. While cysts can persist in a moist environment for several weeks, trophozoites are killed rapidly by exposure to air. In most pts trophozoites are harmless commensals, but in some they invade the bowel mucosa, causing symptomatic colitis. In yet other pts, trophozoites invade the bloodstream, causing distant abscesses of the liver, lungs, or brain. Numerous virulence factors, including extracellular proteinase, have been linked to the ability of amebas to invade through interglandular epithelium.
CLINICAL MANIFESTATIONS   Intestinal Amebiasis   The most common type of amebic infection is asymptomatic cyst passage. Symptomatic amebic colitis develops 2–6 weeks after ingestion of infectious cysts. Lower abdominal pain and mild diarrhea develop gradually and are followed by malaise, weight loss, and diffuse lower-abdominal or back pain. Cecal involvement may mimic appendicitis. In full-blown dysentery, pts may daily pass 10–12 stools consisting of blood and mucus but little fecal material. Virtually all pts have heme-positive stools; <40% are febrile. Rarely (most often in children), a more fulminant form occurs, with high fevers, severe abdominal pain, and profuse diarrhea. Pts may develop toxic megacolon. Pts receiving glucocorticoids are at risk for more severe amebiasis. Uncommonly, pts develop a more chronic form of amebiasis, which can be confused with inflammatory bowel disease. Amebomas are inflammatory mass lesions due to chronic intestinal amebiasis.
Amebic Liver Abscess   Extraintestinal amebic infection frequently involves the liver. Most pts develop symptoms within 5 months. The majority of these pts are febrile and have RUQ pain, which may be dull or pleuritic and may radiate to the shoulder. Point tenderness of the liver and right pleural effusion are common; jaundice is rare. Fewer than one-third of pts have accompanying diarrhea. In some pts, especially those who are older, the illness can have a subacute course with weight loss and hepatomegaly. Only about one- third of pts with chronic presentations are febrile. Amebic liver abscess must be considered in the differential diagnosis of fever of unknown origin, as 10– 15% of pts present with fever only. Complications of amebic liver abscesses include pleuropulmonary involvement in 20–30% of pts with sterile effusions, contiguous spread from the liver, and frank rupture into the pleural space, the peritoneum, or the pericardium. Rupture of an amebic abscess, which may occur during medical therapy, usually requires drainage.
Other Extraintestinal Sites   Besides the liver, extraintestinal sites of amebiasis include the genitourinary tract (with painful genital ulcers) and the cerebrum (in <0.1% of pts).
DIAGNOSIS   The definitive diagnosis of amebic colitis relies on the demonstration of trophozoites of E. histolytica on wet mount, iodine-stained concentrates of stool, or trichrome stains of stool or concentrates. A combination of these procedures is positive in 75–95% of cases. At least three fresh stool specimens should be examined. Experience in distinguishing E. histolytica from Entamoeba hartmanni, Entamoeba coli, and Endolimax nana is important as the latter parasites do not cause clinical disease and do not need to be treated. Commercially available serologic tests are positive in >90% of cases of invasive disease, including colitis. A positive test suggests active infection, since serologies usually revert to negative in 6–12 months. Liver scans, ultrasound, CT, and MRI are all useful for the detection of liver abscess. Barium enemas and sigmoidoscopy with biopsy are potentially dangerous in acute amebic colitis because of a risk of perforation.

TREATMENT
Asymptomatic cyst carriers should be treated with a luminal amebicide that is poorly absorbed. Two luminal drugs are available in the U.S.—iodoquinol (650 mg PO tid for 20 d) and paromomycin (500 mg PO tid for 10 d). Pts with colitis or liver abscess should receive a tissue amebicide and a luminal agent. Metronidazole (750 mg PO or IV tid for 5–10 d) is used for the treatment of amebic colitis or liver abscess. Clinical response occurs within 72 h in >90% of pts with liver abscesses. Except in the case of rupture, amebic liver abscesses rarely require drainage. Indications for abscess aspiration include (1) the need to rule out a pyogenic process, (2) failure to respond to therapy in 3–5 d, (3) the threat of imminent rupture, and (4) the need to prevent left-lobe abscess rupture into the pericardium.

MALARIA
ETIOLOGY   Four species of the genus Plasmodium infect humans: P. vivax, P. ovale, P. malariae, and P. falciparum. This last species is responsible for most deaths due to malaria.
EPIDEMIOLOGY   Malaria is the most important parasitic disease of humans, causing 1–3 million deaths annually. The disease is found throughout the tropical regions of the world. P. falciparum predominates in Africa, New Guinea, and Haiti. P. vivax is more common in Central America and the Indian subcontinent, but P. falciparum has been found with increasing frequency in India over the past decade. P. falciparum and P. vivax are equally prevalent in South America, eastern Asia, and Oceania. P. malariae is less common but is found in most areas (especially sub-Saharan Africa). P. ovale is uncommon outside of Africa. Malaria is transmitted by the bite of the female anopheline mosquito.
PATHOGENESIS   Human infection begins with the transfer of sporozoites from the mosquito’s salivary glands to the bloodstream during a blood meal. After a period of asexual reproduction of the parasite in liver cells, the swollen cells rupture, releasing merozoites into the bloodstream and initiating the symptomatic phase of infection. In P. vivax and P. ovale infection, some intrahepatic forms remain dormant for months and can cause relapses after treatment. Merozoites attach to specific erythrocyte surface receptors and then invade the cell. In P. vivax infection, this receptor is related to the Duffy group antigen, whose absence in most West Africans renders them resistant to this form of malaria. After invading the erythrocyte, the parasite grows progressively, consumes and degrades intracellular proteins (principally hemoglobin), and alters the cell membrane.
Host defense also plays a role in malaria. In the nonimmune individual, infection triggers nonspecific host defense mechanisms such as splenic filtration. When parasitized erythrocytes that have evaded splenic filtration rupture, the material released activates macrophages, which release proinflammatory cytokines that cause fever and exert other pathologic effects. The distribution of malaria before the introduction of mosquito control programs paralleled the distribution of sickle cell disease, thalassemia, and G6PD deficiency. These diseases may confer protection against death due to falciparum malaria, as has been demonstrated with the sickle cell trait. With repeated exposure to malaria, a specific immune response develops and limits the degree of parasitemia. Over time, pts are rendered immune to disease but remain susceptible to infection.
CLINICAL MANIFESTATIONS   The first symptoms are nonspecific and include malaise, headache, fatigue, abdominal discomfort, and muscle aches, followed by fever and chills. Nausea, vomiting, and orthostatic hypotension are common. The classic malaria paroxysms, in which fever spikes, chills, and rigors occur at regular intervals, suggest infection with P. vivax or P. ovale. Most often, the fever is irregular at first. In uncomplicated malaria, mild anemia and a palpable spleen may be the only clinical abnormalities identified. The complications of falciparum malaria include cerebral malaria (obtundation, delirium, or gradual or sudden onset of coma, with seizures common as well), hypoglycemia, lactic acidosis, noncardiogenic pulmonary edema, renal impairment (seen mainly in adults and resembling acute tubular necrosis), hematologic abnormalities (anemia, coagulation defects, DIC in pts with cerebral malaria, and so-called blackwater fever, in which massive hemolysis causes hemoglobinemia, black urine, and renal failure), and aspiration pneumonia.
DIAGNOSIS   The diagnosis of malaria rests on the demonstration of the asexual form of the parasite in thick or thin smears of peripheral blood. Giemsa is the preferred staining method. The level of parasitemia, which can be determined from either type of smear, is expressed as the number of parasitized erythrocytes per 1000 cells; this figure is then used to derive the number of infected erythrocytes per microliter of blood. A thick smear concentrates the parasites and increases diagnostic specificity but should be interpreted with care as artifacts are common. Smears should be examined every 12 h for 2 d before a diagnosis of malaria is excluded. It is important to diagnose probable or possible P. falciparum infection. Features on smear suggestive of falciparum malaria include double-chromatin dots, multiple infected erythrocytes of normal size, banana-shaped gametocytes, and a parasitemia level of >5%. P. vivax infection is characterized by the presence of Schüffner’s dots in enlarged erythrocytes; P. ovale infection is typified by Schüffner’s dots in minimally enlarged erythrocytes that are slightly oval in shape and may have fringed edges. A simple, sensitive, and specific diagnostic test that detects P. falciparum histidine-rich protein 2 in fingerprick blood samples has been introduced.

TREATMENT
Table 110-1 summarizes malaria therapy. Severe falciparum malaria constitutes a medical emergency. The antiarrhythmic agent quinidine gluconate is as effective as quinine in these cases and is more readily available; thus quinidine infusion can be used with cardiovascular monitoring (acceptable QTc, <0.65; acceptable QRS widening, <25% of baseline). In addition to anti- malarial agents, the pt should be given phenobarbital (a single dose of 5–20 mg/kg) to prevent seizures. In comatose pts, the blood glucose level should be measured every 4–6 h; those with levels <40 mg/dL should receive IV dextrose. Exchange transfusion is indicated for vital organ dysfunction and a parasitemia level of >15% and should be considered for pts with parasitemia levels of 5–15%. Glucocorticoids, urea, heparin, and dextran are of no value.

Table 110-1 Recommended Therapeutic Doses of Antimalarial Drugs

PREVENTION   Table 110-2 summarizes malaria prophylaxis.

Table 110-2 Prophylaxis for Malaria

LEISHMANIASIS
EPIDEMIOLOGY   Leishmaniasis is spread by female phlebotomine sandflies. Rodents, small mammals, and canines are the common reservoir hosts of Leishmania spp; humans are incidental hosts.
CLINICAL MANIFESTATIONS   Visceral Leishmaniasis (Kala-Azar)   Visceral leishmaniasis is most often caused by Leishmania donovani. Visceral infection may remain subclinical or become symptomatic, with an acute, subacute, or chronic course. The incubation period usually ranges from weeks to months but can be years. In some settings, inapparent infections far outnumber clinically apparent ones; malnutrition is a risk factor for the development of disease. The term kala-azar refers to the classic image of the profoundly cachectic, febrile pt who is heavily parasitized and has life-threatening disease. Splenomegaly is typically more impressive than hepatomegaly and can be massive. Peripheral lymphadenopathy may also be detected. With advanced disease, pancytopenia, hypergammaglobulinemia, and hypoalbuminemia may develop.
Visceral leishmaniasis is becoming an important opportunistic infection in HIV pts from Leishmania-endemic areas; most dual infections have been reported from southern Europe. Such cases may represent newly acquired or reactivated infections. In these hosts, even relatively avirulent leishmanial strains may disseminate to the viscera. The CD4 cell count is usually <200/µL when disease becomes clinically evident.
Cutaneous Leishmaniasis   Cutaneous leishmaniasis has traditionally been classified as New World (American) or Old World. New World leishmaniasis occurs from southern Texas to northern Argentina; it is usually caused by the L. mexicana complex or the Viannia subgenus but can also be attributable to L. major–like organisms and L. chagasi. Old World disease is caused by L. tropica, L. major, L. aethiopica, L. infantum, and L. donovani. The incubation period ranges from weeks to months. The lesion usually begins as a single papule at the site of a sandfly bite and evolves to a nodular and then an ulcerative form, with a central depression surrounded by a raised indurated border. Multiple primary lesions, satellite lesions, regional lymphadenopathy, sporotrichoid subcutaneous nodules, lesional pain or pruritus, and secondary bacterial infection are variably present. Spontaneous resolution of the lesions may require weeks, months, or years; reactivation may occur. Diffuse cutaneous leishmaniasis (DCL) develops in the context of Leishmania-specific anergy and manifests as chronic nonulcerative skin lesions. Leishmaniasis recidivans, a hyperergic variant with scarce parasites, manifests as a chronic solitary lesion on the cheek that expands slowly despite central healing.
DIAGNOSIS   The diagnosis of leishmaniasis requires demonstration of amastigotes by smear or culture of aspirates or biopsy specimens (e.g., spleen, liver, bone marrow, or lymph node for visceral disease). Organism density on histologic exam decreases as the lesion ages. Serologic testing shows elevated antibody titers only in pts with DCL. In contrast, skin testing is usually positive in simple cutaneous or recidivans leishmaniasis but not in DCL. The sensitivity of antibody testing is only ~50% in pts with visceral disease who are coinfected with HIV.

TREATMENT
Drug regimens for treatment of leishmaniasis are listed in Table 110-3. Local or topical therapy (paromomycin ointment, intralesional Sbv, heat therapy, or cryotherapy) should be considered only for infections that do not have the potential to disseminate.

Table 110-3 Drug Regimens for Treatment of Leishmaniasisa

TRYPANOSOMIASIS
Chagas’ Disease
EPIDEMIOLOGY   Chagas’ disease (American trypanosomiasis) is a zoonosis caused by Trypanosoma cruzi, a parasite found only in the Americas. The disease is transmitted to humans primarily by infected reduviid bugs, which are spottily distributed from the southern U.S. to southern Argentina. Infection can also be transmitted by transfusion of infected blood as well as vertically from mother to fetus. Human T. cruzi infection is a health problem primarily among the rural poor of Central and South America.
CLINICAL MANIFESTATIONS   The first signs of acute Chagas’ disease begin at least 1 week after infection. An indurated area of erythema and swelling (the chagoma), accompanied by lymphadenopathy, may appear. Romaña’s sign (unilateral painless palpebral and periocular edema) occurs when the conjunctiva is the portal of entry. Local signs are followed by fever, anorexia, and edema of the face and lower extremities. Severe myocarditis is a rare but potentially fatal complication. Acute symptoms resolve spontaneously, after which pts enter the asymptomatic or indeterminate phase of chronic T. cruzi infection. Symptomatic, chronic Chagas’ disease develops years or even decades later, with manifestations attributable principally to cardiac and/or GI involvement. Cardiomyopathy, rhythm disturbances, or thromboemboli may occur. RBBB is the most common ECG abnormality. GI manifestations include megaesophagus (causing dysphagia, odynophagia, chest pain, and regurgitation) and megacolon (leading to abdominal pain, chronic constipation, obstruction, perforation, septicemia, and even death).
DIAGNOSIS   The diagnosis of acute Chagas’ disease requires the detection of parasites, which may be found by examination of fresh blood or buffy coat or of thick or thin blood smears. Mouse inoculation and culture of blood in special media can be attempted if efforts at direct visualization are unsuccessful. Chronic disease is diagnosed by serology. CF, immunofluorescence, and ELISA are all available, but their utility is limited by false-positive results. For this reason, it is recommended that positivity in one assay be confirmed by two other tests.

TREATMENT
Nifurtimox, the only drug active against T. cruzi that is available in the U.S., reduces the duration and severity of acute disease, but its efficacy in eradicating parasites is low, with only ~70% of acute infections parasitologically cured. Treatment should be started as early as possible at a daily dose of 8– 10 mg/kg for adults, 12.5–15 mg/kg for adolescents, and 15–20 mg/kg for children 1–10 years of age. Treatment is given orally in four divided doses each day for 90–120 d. Nifurtimox may be obtained from the CDC (tel. no. 770-639-3670). Although the point has been debated for years, it is currently recommended that pts infected with T. cruzi be treated, regardless of their clinical status or the duration of infection.

Sleeping Sickness
EPIDEMIOLOGY   Sleeping sickness (African trypanosomiasis) is caused by parasites of the Trypanosoma brucei complex and is transmitted to humans by tsetse flies.
CLINICAL MANIFESTATIONS   A painful chancre may appear at the site of inoculation. The disease is divided into stages. Stage I, during which hematogenous and lymphatic dissemination occurs, is characterized by fever, lymphadenopathy, pruritus, and circinate rash. Stage II (CNS invasion) is characterized by the insidious development of neurologic manifestations, such as daytime somnolence, halting speech, extrapyramidal signs, and ataxia, and by progressive CSF abnormalities. Neurologic impairment eventually ends in coma and death. East African trypanosomiasis (caused by T. brucei rhodesiense) follows a more acute course than West African trypanosomiasis (caused by T. brucei gambiense).
DIAGNOSIS   Definitive diagnosis requires detection of the parasite in expressed fluid from the chancre, thin or thick blood smear, buffy coat, lymph node aspirates, bone marrow biopsies, or CSF. CSF examination is mandatory in all pts in whom African trypanosomiasis is suspected. Serology is variably sensitive and specific and is most useful for epidemiologic surveys.

TREATMENT
Drugs for the treatment of this infection include suramin (1 g IV on days 1, 3, 7, 14, and 21 after a test dose of 100–200 mg), eflornithine (400 mg/kg qd in four divided doses for 2 weeks), or pentamidine (4 mg/kg qd IM or IV for 10 d). Suramin and eflornithine are available through the CDC. The choice of regimens is based on the stage of disease and the parasite subspecies.

TOXOPLASMOSIS
EPIDEMIOLOGY   Cats are the definitive host for Toxoplasma gondii, which is transmitted to humans by ingestion of contaminated oocysts from the soil or of bradyzoites in undercooked meat. In the U.S., mutton and pork are far more likely to be contaminated than is beef. The seroprevalence of antibody to T. gondii varies by geographic location and population age. Transplacental transmission occurs overall in about one-third of cases in which the mother acquires infection during pregnancy. The risk of transmission and the potential consequences for the fetus vary according to the time in pregnancy at which maternal infection occurs. Only ~15% of women infected in the first trimester transmit infection, but neonatal disease is most severe in these cases; 65% of women infected in the third trimester transmit infection, but the infant is usually asymptomatic at birth.
CLINICAL MANIFESTATIONS   Immunocompetent Patients   Acute infection is usually asymptomatic and may go unrecognized in 80–90% of children and adults who acquire infection postnatally. Acute toxoplasmosis is characterized by lymphadenopathy, which, while most often cervical, is generalized in 20–30% of symptomatic pts. Headache, malaise, fatigue, and fever develop in 20–40% of pts with lymphadenopathy. Symptoms usually resolve within several weeks. Lymphadenopathy may persist for months.
Ocular Infection   T. gondii causes 35% of cases of chorioretinitis in the U.S. and Europe. Most such infections are acquired congenitally.
Immunocompromised Patients   Pts who have AIDS or who are receiving chemotherapy for a lymphoproliferative disorder are at greatest risk for acute infection. More than 95% of toxoplasmosis cases in AIDS pts represent reactivated latent infection. Encephalitis occurs in most of these cases, typically when CD4 cell counts are <100/µL. Manifestations referable to CNS disease occur in >50% of immunocompromised hosts with acute toxoplasmosis. Symptoms and signs include altered mental status (75%), fever (10–72%), seizures (33%), headaches (56%), and focal neurologic abnormalities (60%) and are attributable to encephalopathy, meningoencephalitis, and/or mass lesions.
Congenital Infection   Each year in the U.S., 400 to 4000 infants are born with congenital toxoplasmosis. Although many of these transplacentally infected infants are asymptomatic at birth, reactivation of infection years or even decades later can result in disease and disabilities that are often relatively severe and include chorioretinitis, strabismus, epilepsy, and psychomotor retardation. Appropriate treatment (see below) is followed by normal development in upwards of 70% of children.
DIAGNOSIS   Serologic testing is the routine diagnostic method. The Sabin-Feldman dye test, the indirect fluorescent antibody test, and the ELISA all satisfactorily measure circulating IgG antibody, which can appear as early as 2–3 weeks after infection and persists for life. Simultaneous testing for IgM antibody is necessary to determine the timing of infection; the methods used are double-sandwich IgM-ELISA and IgM-immunosorbent assay. The former is more sensitive for detecting fetal and neonatal infections. In AIDS pts, a positive IgG serology and compatible neuroradiographic findings are sufficient for a presumptive diagnosis. On CT or MRI, pts with Toxoplasma encephalitis have focal or multifocal lesions, usually in the basal ganglia or at the corticomedullary junction; these lesions are usually ring-enhancing on CT. These findings are not pathognomonic of Toxoplasma infection since 40% of CNS lymphomas are multifocal and 50% are ring-enhancing. If presumptive therapy for toxoplasmosis fails to result in early radiologic improvement, a brain biopsy should be considered. The persistence of IgG antibody or a positive IgM titer after the first week of life is suggestive of congenitally acquired infection. However, up to 25% of infected newborns may be seronegative and have normal routine physical exams. Thus, specific end-organ assessment (eye, brain) may be necessary to establish the diagnosis.

TREATMENT
Immunocompetent pts with lymphadenopathy due to toxoplasmosis generally do not require therapy. For immunocompromised pts, the preferred regimen is pyrimethamine (a 200-mg PO loading dose followed by 50–75 mg/d) plus sulfadiazine (4–6 g/d PO, divided qid), along with leucovorin (10–15 mg/d). Hypersensitivity develops in up to 20% and toxicity in 40% of pts given this dual regimen. Pyrimethamine (75 mg/d) plus clindamycin (450 mg tid) is an alternative. Glucocorticoids are often used to treat intracerebral edema. After 4–6 weeks (or when radiographic improvement becomes evident), the pt may be switched to chronic suppressive therapy with pyrimethamine (25–50 mg/d) plus sulfadiazine (2–4 g/d) or pyrimethamine (75 mg/d) plus clindamycin (450 mg tid); pyrimethamine alone (50–75 mg/d) may be sufficient. Pts with ocular infection can be treated for 1 month. Congenitally infected neonates are treated with daily pyrimethamine (0.5–1 mg/kg) and sulfadiazine (100 mg/kg) for 1 year. A variety of other regimens are available for pts in whom long-term therapy is limited by toxicity. Dapsone may be substituted for sulfadiazine. For pts with AIDS and Toxoplasma encephalitis, pyrimethamine (25–75 mg/d) plus clindamycin (300–1200 mg IV qid) is effective, as is pyrimethamine plus clarithromycin. Atovaquone (750 mg tid or qid) is an optional agent. For prophylaxis in AIDS pts with CD4 counts of <100/µL, TMP-SMZ alone or the combination of pyrimethamine, dapsone, and leucovorin may be used.

PROTOZOAL INTESTINAL INFECTIONS
Giardiasis
EPIDEMIOLOGY   Giardiasis is one of the most common parasitic infections worldwide and is the most common cause of waterborne epidemics of gastroenteritis in the U.S. Infection follows ingestion of the cyst form of Giardia lamblia. Person-to-person transmission may take place (e.g., among children in day-care centers, among residents of institutions where fecal hygiene is poor, and during sexual contact). Food-borne transmission has also been documented.
CLINICAL MANIFESTATIONS   Manifestations may range from asymptomatic infection to fulminant diarrhea and malabsorption. The usual incubation period is 1–3 weeks; symptoms may develop suddenly or gradually. Early symptoms include diarrhea, abdominal pain, bloating, belching, flatus, nausea, and vomiting. Diarrhea is common, but upper intestinal manifestations may predominate. The duration of acute symptoms is usually >1 week; diarrhea may abate earlier. In chronic giardiasis, diarrhea may not be prominent, but increased flatus, loose stools, sulfurous burping, and (in some cases) weight loss occur. Fever is uncommon, as is the presence of blood or mucus in the stool.
DIAGNOSIS   Giardiasis is diagnosed by the identification of cysts in the feces or of trophozoites in the feces or small intestine. Repeat examinations of stool or examination of aspirated duodenal fluid or of tissue from a small- intestinal biopsy may be required. A sensitive and specific alternative is to test for parasitic antigen in stool.

TREATMENT
Metronidazole (250 mg PO tid for 5 d) is curative in >80% of cases. Furazolidone (100 mg PO qid for 7–10 d) is somewhat less effective but more palatable to children. Pts in whom initial treatment fails can be re-treated with a longer course. Those who remain infected should be evaluated for reinfection through close personal contacts or environmental sources and for hypogammaglobulinemia. In particularly refractory cases, prolonged treatment with metronidazole (750 mg PO tid for 21 d) has been successful. Paromomycin can be used in pregnant pts with symptomatic giardiasis.

Cryptosporidiosis
EPIDEMIOLOGY   Cryptosporidiosis is acquired by ingestion of oocysts. Water is the primary source in outbreaks; the oocysts are resistant to killing by routine chlorination. Cryptosporidial infection may cause symptomatic diarrhea in immunocompetent hosts, but pts with immunodeficiencies (especially AIDS) are at greatest risk.
CLINICAL MANIFESTATIONS   The diarrhea of cryptosporidiosis characteristically is watery, nonbloody, and profuse. Abdominal pain, nausea, anorexia, fever, and weight loss may occur. In immunocompetent hosts, diarrhea resolves in 1–2 weeks. In immunocompromised hosts, especially AIDS pts, diarrhea may be chronic and profuse and may cause significant fluid and electrolyte losses. Stool volumes may reach 25 L/d.
DIAGNOSIS   The diagnosis is made by the demonstration of oocysts in stool. Concentration methods as well as modified acid-fast or immunofluorescent staining enhance detection. Small-intestinal biopsy may also be useful.

TREATMENT
There is no effective therapy for this infection, although paromomycin (500–750 mg qid) may be partially effective for some HIV-infected pts. Supportive treatment is used, including fluid and electrolyte replacement and the administration of antidiarrheal agents.

Isosporiasis
CLINICAL MANIFESTATIONS   Acute infection with Isospora belli begins abruptly with fever, abdominal pain, and watery nonbloody diarrhea and may last for weeks or months. In AIDS and other immunocompromised pts, the infection may not be self-limited but rather may resemble cryptosporidiosis, with chronic profuse watery diarrhea. Eosinophilia, not found in other enteric protozoan infections, may develop.
DIAGNOSIS   The diagnosis is made by the demonstration in stool of large oocysts revealed by modified acid-fast staining. Repeated stool examinations, sampling of duodenal contents by aspiration or a string test, or even small- bowel biopsy may be required.

TREATMENT
I. belli does respond to treatment. TMP-SMZ (160/800 mg PO qid for 10 d, then bid for 3 weeks) has proved effective. Pyrimethamine (50–75 mg/d PO) may be used in pts with sulfonamide intolerance. Relapses can occur in AIDS pts, necessitating maintenance therapy with TMP-SMZ (160/800 mg) three times a week or with sulfadoxine (500 mg) plus pyrimethamine (25 mg) once a week.

Cyclosporiasis
CLINICAL MANIFESTATIONS   Cyclospora cayetanensis is globally distributed. Waterborne transmission is one means of its acquisition by humans. Infection may be asymptomatic or may manifest as diarrhea, a flulike illness, flatulence, and burping. The illness may be self-limited, may wax and wane, or may persist for >1 month.
DIAGNOSIS   The diagnosis can be made by detection of spherical 8- to 10-µm oocysts in the stool. The oocysts are refractile, are variably acid-fast, and fluoresce under UV light.

TREATMENT
Cyclosporiasis is effectively treated with TMP-SMZ (160/800 mg PO bid for 7 d). HIV-infected pts may require suppressive maintenance therapy.

Microsporidiosis
ETIOLOGY AND CLINICAL MANIFESTATIONS   Microsporidia are obligate intracellular spore-forming protozoa that have recently been recognized as agents of human disease, especially among people infected with HIV. Six genera are recognized. Enterocytozoon bieneusi and Encephalitozoon intestinalis cause chronic diarrhea and wasting in AIDS pts; these organisms are found in 10–40% of pts with chronic diarrhea. Disseminated disease due to E. intestinalis may also occur, with fever, diarrhea, sinusitis, cholangitis, and bronchiolitis.
DIAGNOSIS   The diagnosis of tissue infection may require electron microscopy, although intracellular spores (0.5–2 µm × 1–4 µm) may be seen in tissue sections stained with hematoxylin and eosin, Giemsa, or Gram’s stain.

TREATMENT
Definitive therapies for microsporidial infections remain to be established.

Bibliography

For a more detailed discussion, see Reed SL: Amebiasis and Infection with Free-Living Amebas, Chap. 213, p. 1199; White NJ, Breman JG: Malaria and Babesiosis: Diseases Caused by Red Blood Cell Parasites, Chap. 214, p. 1203; Herwaldt BL: Leishmaniasis, Chap. 215, p. 1213; Kirchhoff LV: Trypanosomiasis, Chap. 216, p. 1218; Kasper LH: Toxoplasma Infection, Chap. 217, p. 1222; and Weller PF: Protozoal Intestinal Infections and Trichomoniasis, Chap. 218, p. 1227, in HPIM-15.

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One comment on “110 PROTOZOAL INFECTIONS

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