Parasites

Question 1

Helminth - Hookworm

Answer 1

Hookworms may persist for many years in the host and impair the physical and intellectual development of children and the economic development of communities
Females release thousands of eggs into stool daily; in sandy moist soil, eggs hatch and must molt twice before developing into third-stage larvae.
Third-stage larvae are 500-700 µm long and are capable of rapid penetration into normal skin, most commonly of the feet
Transmission occurs after > 5 of skin contact with soil that contains viable larvae
Ground itch at the site of penetration is more common withAncylostomaspecies than withNecator
They puncture and feed on mucosal capillaries in the jejunum.
Larvae burrow into venules and embolize the lungs, where they break into alveoli

Question 2

Helminth - Hookworm Etiology

Answer 2

Hookworm infection is acquired through skin exposure to larvae in soil contaminated by human feces

Question 3

Helminth- Hookworm Epidemiology

Answer 3

Hookworms represent a widespread; clinically important human nematode infection
Prevalence figures indicate that the roundworms Ancylostoma duodenale & Necator americanusinfect 576-740 million people and that they causeanemia in approximately 10% of those infected

Question 4

Hookworm- Workup

Answer 4

Direct microscopic stool examination for ova and parasites usually reveals oval, 60-µm X 40-µm eggs with thin colorless shells that can be seen 2 months after exposure
Anemia is confirmed by CBC count and peripheral blood smear results that demonstrate signs typical of iron deficiency anemia
Eosinophilia is usually present during the migratory phase before stool findings are positive (may be due to adult worms to the intestinal mucosa with peak eosinophil counts are 1,350-3,828 cells/µL at 5-9 weeks after experimental human exposure to 45-50 infective larvae
Eosinophilia can be a clue to hookworm, as well asStrongyloidesinfestation, in chronically infected patients

Question 5

Hookworm Treatment

Answer 5

Albendazole (single dose) or mebendazole (3 day course) is the drug of choice for hookworm infection (short-term cure in 90-95% of children, with up to a 99% reduction in egg counts)
Quarterly retreatment resulted in improved anemia and malnutrition after one year
Concomitant iron supplementation in a recent study in Kenya did not improve final hemoglobin concentrations in children or adults
Rapid hookworm reinfection is common in endemic areas and is made particularly problematic by the high prevalence and worm burden in adults who are untreated and who continue to contaminate soil

Question 6

Infections of RoundwormAscaris lumbricoides

Answer 6

Lumbricoidesis the largest of the intestinal nematodes affecting humans, measuring 15-35 cm in length in adulthood
Infection begins with the ingestion of embryonated (infective) eggs in feces-contaminated soil or foodstuffs
Once ingested, eggs hatch, usually in the small intestine, releasing small larvae that penetrate the intestinal wall
Larvae migrate to the pulmonary vascular beds and then to the alveoli via the portal veins usually 1-2 weeks after infection, during which time they may cause pulmonary symptoms (eg, cough, wheezing)
During the time frame of pulmonary symptoms, eggs are not being shed, and thus diagnosis via stool ovas and parasites is not possible
Eggs are not shed in stool until roughly 40 days after the development of pulmonary symptoms
After migrating up the respiratory tract and being swallowed, they mature, copulate, and lay eggs in the intestines
Adult worms may live in the gut for 6-24 months, where they can cause partial or complete bowel obstruction in large numbers, or they can migrate into the appendix, hepatobiliary system, or pancreatic ducts and rarely other organs such as kidneys or brain

Question 7

Roundworm Epidemiology

Answer 7

US, ~ 4 million people are believed to be infected
High-risk groups include international travelers, recent immigrants (especially from Latin America and Asia), refugees, and international adoptees
Ascariasis is indigenous to the rural southeast, where cross-infection by pigs with the nematode Ascaris suummay occur

Question 8

Roundworm Presentation in the Early Phase (4-16 days)

Answer 8

Fever
Nonproductive cough
Dyspnea
Wheezing
respiratory symptoms result from the migration of larvae through the lungs

Question 9

Roundworm Presentation in the Late phase (6-8 weeks)

Answer 9

Passage of worms (from mouth, nares, anus)
Diffuse or epigastric abdominal pain
Nausea, vomiting
Pharyngeal globus, “tingling throat”
Frequent throat clearing, dry cough
Complications - Biliary and intestinal obstruction, appendicitis, pancreatitis

Question 10

Roundworm Workup

Answer 10

Early infection (larval migration)
Complete blood count (CBC) may show eosinophilia
Sputum analysis may reveal larvae or Charcot-Leyden crystals (collections of crystalloid composed of eosinophilic proteins)
Stool examination findings are typically normal in absence of previous infection (during the first 40 d)
Ascarisspecific antibodies (not useful in acute infection and not protective)
Increases in IgE and later IgG
Established infection (adult phase)
Stool examination findings include characteristic eggs
Adult females lay about 200,000 eggs per day, aiding microscopic identification of characteristic eggs

Question 11

Roundworm Treatment- Early Infection

Answer 11

Inhaled beta-agonists may be indicated
Steroids for pulmonary symptoms are controversial
Whether anthelmintic therapy is effective against larval stages is unclear. (Stool ova microscopy will likely be negative at this phase).
Because infection in the early phase is rarely serious, generally treatment is delayed until definitive diagnosis can be made.

Question 12

Roundworm Treatment- Established Infection (Adult)

Answer 12

Benzimidazoles - mainstay of treatment of symptomatic and asymptomatic infections; low toxicity as they are poorly systemically absorbed
Bowel obstruction treated with intravenous hydration, nasogastric suctioning, electrolyte monitoring, and laparotomy, colonoscopyand esophagogastroduodenoscopy (EGD) to remove obstructing masses of worms
Piperazine citrate, a helminth paralytic, in cases of obstruction; no longer commercially available in the United States
Hepatobiliary ascariasis typically responds to similarly conservative therapy, but it may require invasive intervention (e.g. ERCP) should this fail, or if there are coexisting stones or strictures; also indicated in cases of pyogenic cholangitis and acute pancreatitis.

Question 13

Tapeworms

Answer 13

Tapeworms are long, segmented worms of the class Cestoda, which comprise 1 of 3 classes of parasitic worms (worms that require a host within which to mature)
Other classes are Nematoda and Trematoda
The worms lack an intestinal tract and instead can absorb nutrients through their integument
The adult consists of a head (scolex), where the worms attach to the mucosa of the intestine; a neck; and a segmented body that contains both male gonads and female gonads (proglottids)

Question 14

Tapeworms - Pathophysiology

Answer 14

Typically, a cestode requires one or more intermediate hosts in their life cycle. The life cycle is as follows:
Eggs are passed into the environment from the primary host
Eggs are ingested by an intermediate host in which they hatch
Larvae enter the tissues of the intermediate host and encyst
Primary host ingests the cysts in the flesh of the intermediate host
When humans are the primary hosts (ingest cysts), the adult cestode is limited to the intestinal tract
When humans are the intermediate hosts (ingest eggs), the larvae are within the tissues, migrating through the different organ systems

Question 15

Echinococcus and Diphyllobothrium

Answer 15

Cysticercosis is a clinical syndrome of expanding embryonal cysts that occurs withT solium; cysticerci can be found anywhere; but mainly occur in the central nervous system (neurocysticercosis) and skeletal muscles
Diphyllobothriumspecies absorb and interfere with absorption by ileum of vitamin B-12, pernicious anemia
Echinococcuspenetrate intestinal mucosa after ingestion; enter the portal circulation to invade other organs, liver (60%) and lungs (25%); remains asymptomatic until the cysts cause a mass effect on the organ, which can be 5-20 years after the initial infestation

Question 16

Treatment of Intestinal tapeworm infestation

Answer 16

Effectively treated with praziquantel or niclosamide (rates of 85-98%)
Vitamin B-12 if vitamin B-12 deficiency with Diphyllobothriuminfections

Question 17

Treatment of Echinococcosis

Answer 17

Echinococcosis is treated with albendazole and surgery or albendazole and PAIR (puncture, aspiration, injection, re-aspiration)
lbendazole is recommended for 1-3 months before surgical intervention

Question 18

Treatment of Sparganosis and coenurosis

Answer 18

Treatment involves surgical excision for localized infections

Question 19

Cysticercosis

Answer 19

If the patient is asymptomatic with calcified soft tissue or neural lesions, no treatment is required
In neurocysticercosis, neurologic manifestations indicate the need for antiepileptics and antihelminths: albendazole or praziquantel These agents can provoke an inflammatory response in the central nervous system; patient must be started on dexamethasone
Therapy effect monitored via radiographic imaging; active lesions should decrease within 3-6 months
Some patients require surgery in addition to treatment with albendazole, praziquantel, and dexamethasone

Question 20

Malaria Epidemiology

Answer 20

• • 25-30 million people travel to tropical areas annually; 10,000-30,000 US and European travelers acquire malaria
• • Almost all US cases of malaria are imported from patients traveling from endemic areas
• • infections in individuals who have not traveled have occurred near airports (so-called airport malaria)
• –*responsible for approximately 1-3 million deaths per year, typically in children in sub-Saharan Africa infected withP falciparum: individuals at increased risk for mortality due to malaria include primigravida individuals, travelers without immunity, and young children aged 6 months to 3 years who live in endemic areas
• –Worldwide, 300-500 million cases occur annually
• –*Most prevalent in rural tropical areas below elevations of 1000 m (3282 ft) but is not limited to these climates (climate change)

Question 21

Malaria Complications (most caused byP falciparum)

Answer 21

Cerebral malaria, defined as coma, altered mental status, or multiple seizures withP falciparumin the blood; most common cause of death in patients with malaria; lethal is untreated; 15% of children and 20% of adults who develop cerebral malaria die

Seizures – 2nd to hypoglycemia or cerebral malaria
Renal failure - 30% of nonimmune adults suffer acute renal failure

Hemoglobinuria (blackwater fever) - Blackwater fever is the passage of dark urine, described as Madeira wine colored; hemolysis, hemoglobinemia, and the subsequent hemoglobinuria and hemozoinuria

Noncardiogenic pulmonary edema – esp. pregnant women w/ death in 80%

Profound hypoglycemia – malaria metabolizes glucose 70 times faster than RBC; hypoglycemia often occurs in young children and pregnant women; diagnosis difficult as adrenergic signs are not always present & stupor already may have occurred

Lactic acidosis – malarial metabolic glucose use; microvasculature also becomes clogged withP falciparum; if the venous lactate level reaches 45 mg/dL, a poor prognosis is very likely

Hemolysis resulting in severe anemia and jaundice
Bleeding (coagulopathy)

Question 22

Malaria Presentation

Answer 22

Arthralgia
Myalgia
Paroxysm of fever, shaking chills, and sweats (every 48 or 72 hours, depending on species)
Headache, virtually all patients with malaria
Cough
Fatigue
Malaise
Shaking chills
excessive diaphoresis

Question 23

Malaria Workup

Answer 23

In returning travelers from endemic areas, malaria is suggested by the triad that should prompt malarial smear
Thrombocytopenia
Elevated lactate dehydrogenase (LDH) levels
Atypical lymphocytes
Blood cultures should be drawn in a febrile patient; patients from tropical areas may have more than 1 infection; to be considered when patients do not respond to antimalarials
Hemoglobin (decreased in 25% of patients, often profoundly in young children), platelet counts (thrombocytopenia in 50-68% of patients), and liver function (results abnormal in 50% of patients)
If consideringprimaquine, a G-6-PD level should be obtained because primaquine can result in severe hemolysis
If the patient has cerebral malaria, need blood glucose level to rule out hypoglycemia as a cause of mental-status changes
Microhematocrit centrifugation is a more sensitive method of detection of malaria infection, do not allow the identification of the species ofPlasmodium
Fluorescent dyes/ultraviolet indicator tests may not yield speciation information
Polymerase chain reaction assay (PCR) is specific and sensitive means of determining if species ofPlasmodiumare present in the blood

Question 24

Malaria Treatment

Answer 24

P falciparummalaria - Quinine-based therapy is with quinine (or quinidine) sulfate plus doxycycline or clindamycin or pyrimethamine-sulfadoxine; alternative therapies are artemether-lumefantrine, atovaquone-proguanil, or mefloquine
P falciparummalaria with known chloroquine susceptibility (only a few areas in Central America and the Middle East) - Chloroquine
P vivax, P ovalemalaria - Chloroquine plus primaquine
P malariaemalaria - Chloroquine
P knowlesimalaria – Recommendations same as those forP falciparummalaria.

Question 25

Malaria - Deterrence and Prevention

Answer 25

Avoid mosquitoes by limiting exposure during times of typical blood meals (i.e. dawn, dusk)
Long-sleeved clothing and using insect repellants may also prevent infection
Avoid wearing perfumes and colognes
Adult-dose 95% DEET lasts up to 10-12 hours, and 35% DEET lasts 4-6 hours. In children, use concentrations of less than 35% DEET; use sparingly and only on exposed skin; remove DEET when the skin is no longer exposed to potential mosquito bite
Bed nets that are treated with permethrin (increasing incidence of pyrmethrhoid resistance inAnophelesspp)
Chemoprophylaxis with antimalarials in patients traveling to endemic areas; drug of choice is determined by the destination of the traveler and any medical conditions the traveler may have that contraindicate the use of a specific drug, consult theMalaria and Traveler’s Web siteof the CDC to determine the most appropriate chemoprophylaxis

Question 26

Pinworm, orEnterobius vermicularis is Prevalent where?

Answer 26

prevalent throughout the temperate regions of the world and is the most common helminthic infection in the US

Question 27

E vermicularis- Pinworm

Answer 27

E vermicularisis a white slender nematode with a pointed tail
In humans, they reside in the caecum, appendix, and ascending colon
Female pinworms (8-13 mm long) are larger than their male counterparts (2-5 mm long)
Pinworm infection is generally asymptomatic; some infected individuals experience sharp prickling pains or intense itching in the anal area, especially at night (e.g. pruritis ani, bruxism)
Transmission can occur via direct contact with contaminated furniture, bedclothes, bedding, towels, toilets, doorknobs, or other objects. The parasite can also be transmitted during sexual contact

Question 28

Pinworm Workup

Answer 28

Use a perianal cellophane swab or cellophane tape to detect eggs; adult female pinworm dies after ovideposition
Egg detection is associated with 5-11% false-positive rate and a 70-95% false-negative rate
One report found that a single cellophane-tape examination yielded a sensitivity of 50%, 3 examinations yielded a sensitivity of 90%, and 5 examinations yielded a sensitivity of 99%
Repeated examinations 1-2 days later produce more accurate results

Question 29

Pinworm Treatment

Answer 29

Anthelmintics are active againstE vermicularis
Reinfection withE vermicularisimmediately after the completion of drug therapy is common; some young pinworms may be resistant to drugs
Pinworm eggs remain infective in the environment for 2 weeks after deposition
Reinfection from other persons who test positive for eggs is common
Tests for pinworms carry a high false-negative rate. Therefore, successful eradication requires at least 3 doses of medication, separated by 3 weeks
The recommended treatment regimen for pinworm infection is as follows:
Simultaneously treat all family members and/or classmates who are infected
Prescribe drugs at least 3 times at 3-week intervals
Personal and group hygiene must be improved; individuals must wash their hands before eating; discourage children from activities such as finger-sucking
Mebendazole (Vermox)
Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell
Pyrantel pamoate (Pin-Rid, Pin-X)
Depolarizing neuromuscular blocking agent. Inhibits cholinesterases, resulting in spastic paralysis of the worm
Albendazole (Albenza)
Decreases ATP production in worm causing energy depletion, immobilization, and, finally, death
Pre-existing neurocysticercosis may be uncovered in patients treated w/ albendazole for other conditions, apparent by neurological symptoms (eg, seizures, increased intracranial pressure, focal signs); promptly treat w/ corticosteroid & anticonvulsant therapy

Question 30

Toxoplasmosis

Answer 30

Toxoplasmosis is caused by infection with the protozoanToxoplasma gondii,an obligate intracellular parasite
Infection produces a wide range of clinical syndromes in humans, land and sea mammals, and various bird species
T gondiiinfects a large proportion of the world’s population (perhaps 1/3) but uncommonly causes clinically significant disease
Certain individuals are at high risk (fetuses, newborns, and immunologically impaired patients) for severe or life-threateningtoxoplasmosis

Question 31

Toxoplasmosis – Congenital Infection

Answer 31

10-20% of pregnant women infected withT gondiibecome symptomatic
Most common signs of infection are lymphadenopathy and fever
If the mother was infected prior to pregnancy, there is virtually no risk of fetal infection, as long as she remains immunocompetent
When a mother is infected withT gondiiduring gestation, the parasite may be disseminated hematogenously to the placenta & infection may be transmitted to the fetus transplacentally or during vaginal delivery
10% of prenatal T gondiiinfections result in abortion or neonatal death
67-80% of prenatally infected infants, the infection is subclinical and can be diagnosed using only serological and other laboratory methods.
Although these infants appear healthy at birth, they may develop clinical symptoms and deficiencies later in life

Question 32

1st Trimester Toxoplasmosis – Congenital Infection

Answer 32

untreated, the risk of infection to the fetus is approximately 14-17%, and toxoplasmosis in the infant is usually severe

Question 33

3rd Trimester Toxoplasmosis – Congenital Infection

Answer 33

untreated, the risk of fetal infection is approximately 59-65%, and involvement is mild or not apparent at birth; transmission rate most likely related to placental blood flow, the virulence and amount ofT gondiiacquired, and the immunologic ability of the mother to restrict parasitemia
The most significant manifestation of toxoplasmosis in the fetus is encephalomyelitis, may be severe

Question 34

Acute toxoplasmosis in immunocompetent persons

Presentation

Answer 34

80-90% of patients are asymptomatic
Symptomatic disease:
Cervical lymphadenopathy with discrete, usually nontender, nodes smaller than 3cm in diameter
Fever, malaise, night sweats, and myalgias
Sore throat
Retroperitoneal and mesenteric lymphadenopathy with abdominal pain
Retinochoroiditis

Question 35

Acute toxoplasmosis in hosts who do not have AIDS but are immunodeficient
(Presentation)

Answer 35

CNS toxoplasmosis occurs in 50% of patients - seizure, dysequilibrium, cranial nerve deficits, altered mental status, focal neurologic deficits, headache
Patients may have encephalitis, meningoencephalitis, or mass lesions
Hemiparesis and seizures have been reported
Patients may report visual changes
They may have signs and symptoms similar to those observed in immunocompetent hosts
Patients may have flulike symptoms and lymphadenopathy
Myocarditis and pneumonitis are reported
Toxoplasmic pneumonitis can occur - Typical symptoms of a pulmonary infection, mirroring P(carinii)jiroveci, including nonproductive cough, dyspnea, chest discomfort, fever

Question 36

Clinical manifestations of toxoplasmosis in patients with AIDS
(Presentation)

Answer 36

Brain involvement (ie, toxoplasmic encephalitis), with or without focal CNS lesions, is the most common manifestation of toxoplasmosis in AIDS

Altered mental state
Seizures
Weakness
Cranial nerve disturbances
Sensory abnormalities
Cerebellar signs
Meningismus
Movement disorders
Neuropsychiatric manifestations

Question 37

Congenital toxoplasmosis (Presentation)

Answer 37

Severity correlates with earlier gestational age of maternal infection
15-55% of congenitally infected children do not have detectableT gondii–specific IgM antibodies at birth or early infancy
67% of patients have no signs or symptoms of infection
Retinochoroiditis occurs in about 15% of patients, and intracranial calcifications develop in about 10%
CSF pleocytosis and elevated protein values are present in 20% of patients
Infected newborns have anemia, thrombocytopenia, andjaundiceat birth
Affected survivors may have microcephaly, mental retardation, seizures, visual defects, spasticity, or other severe neurologic sequelae

Question 38

Direct Detection of Toxiplasmosis

Answer 38

Diagnosis of toxoplasmosis is confirmed with the demonstration ofT gondii organisms in blood, body fluids, or tissue (isolated from the blood via either inoculation of human cell lines or mouse inoculation)
PCR assay is capable of detectingT gondii deoxyribonucleic acid (DNA)
Tachyzoites may be demonstrated in tissues or smears obtained from biopsy
Indirect detection
IgG is possible within 2 weeks of infection using the enzyme-linked immunosorbent assay (ELISA) test
Skin tests that show delayed skin hypersensitivity toT gondiiantigens may be useful as a screening test

Question 39

Treatment of Toxiplasmosis

Answer 39

Treatment is usually unnecessary in asymptomatic hosts, except in children younger than 5 years
Symptomatic patients should be treated until immunity is ensured
Outpatient care is sufficient for acquired toxoplasmosis in immunocompetent hosts and for persons with ocular toxoplasmosis
Inpatient care is appropriate initially for persons with CNS toxoplasmosis and for acute toxoplasmosis in immunocompromised hosts

Question 40

Treatment for Patients with AIDS and Toxiplasmosis

Answer 40

Patients with AIDS who have a CD4 count of less than 100 cells/μL should be commenced on suppressive therapy forT gondiiuntil they undergo immune reconstitution
Medications act primarily against the tachyzoite form ofT gondii; thus, they do not eradicate the encysted form (bradyzoite)
Pyrimethamine is the most effective agent and is included in most drug regimens, regimen usually 6 weeks
Leucovorin (i.e. folinic acid) should be administered concomitantly to prevent bone marrow suppression
Unless circumstances preclude using more than 1 drug, a second drug (e.g. sulfadiazine, clindamycin) should be added

Question 41

Giardiasis

Answer 41

Flagellate protozoanGiardia intestinalis­­(previously known asG lamblia), its causative agent, is the most commonly identified intestinal parasite in the United States and the most common protozoal intestinal parasite isolated worldwide
G intestinaliscan cause asymptomatic colonization or acute or chronic diarrheal illness
Organism has been found in as many as 80% of raw water supplies from lakes, streams, and ponds and in as many as 15% of filtered water samples
Giardia intestinalishas been isolated from the stools of beavers, dogs, cats, and primates
Ingestion of as few as 10 Giardiacysts may be sufficient to cause infection, giardiasis is common in daycare center attendees and institutionalized patients in developed countries

Question 42

Symptoms of Giardiasis

Answer 42

Predisposing factors to symptomatic infection: malnutrition, hypochlorhydria, immune system deficiencies, blood group A
Diarrhea is the most common symptom of acuteGiardiainfection, occurring in 90% of symptomatic subjects, also abdominal cramping, bloating, and flatulence occur in 70-75% of symptomatic patients
Symptoms of chronic infection include chronic diarrhea, malaise, nausea, and anorexia

Question 43

Diagnosis of Giardiasis

Answer 43

Giardia intestinalis trophozoites or cysts in the stool via a stool ova and parasite (O&P)
Ideally, 3 specimens from different days should be examined because of potential variations in fecal excretion of cysts; G intestinalisis identified in 50-70% of patients after a single stool examination; > 90% after 3 stool examinations
Stool antigen enzyme-linked immunosorbent assays have a sensitivity of 88-98% ; a specificity of 87-100%

Question 44

Treatment of Giardia

Answer 44

Metronidazole is the most commonly prescribed antibiotic for this condition
Appropriate fluid and electrolyte management is critical, particularly in patients with large-volume diarrheal losses
Treat children with acute or chronic diarrhea who manifest a failure to thrive, malabsorption, or other GI tract symptoms in whomGiardiaorganisms have been identified

Question 45

Treatment of Asymptomatic Giardia

Answer 45

Generally, do not treat asymptomatic persons who excrete the organism, except:
To prevent household transmission (e.g. from toddlers to pregnant women or to patients with hypogammaglobulinemia or cystic fibrosis) and
To permit adequate treatment in individuals with possibleGiardia intestinalis–associated antibiotic malabsorption who require oral antibiotic treatment for other infections
Routine treatment of infected persons in highly endemic areas where water supplies continue to be contaminated is of questionable value because reinfection may readily occur, but treat all infected persons who are in nonendemic areas

Question 46

Cryptosporidium- Waterborne Disease

Answer 46

Screening for the parasite has shown a relatively high prevalence, oocysts were detected in 27% of 66 drinking water samples (from 14 states and one Canadian province)
Most individuals presenting with Cryptosporidium have a nonspecific gastrointestinal infection with severe diarrhea and abdominal cramps (mean duration - 12 days, range of 1 to 55 days; 19 watery diarrhea stools per day at the peak of the illness)
Typically they may not seek medical care for their symptoms nor would they be specifically tested for the organism if seen

Question 47

Concerns with Cryptosporidium- Waterborne Disease

Answer 47

Most concerning with regards to Cryptosporidium is the microbe’s resistance to chlorination and filtration (due to very small size) As an oocyte, Cryptosporidium may not be routinely detectable by checking effluent BOD levels, as BOD measures active microbial metabolism
Specific testing with PCR has become available which allows for both clinical evaluation and detection of the parasite in other specimens, making detection of Cryptosporidium more reliable and allows for more practical screening of exposures and detection of infection