TRIPASS XR تري باس

 However, these tests are not routinely used, nor are the reagents commercially available.

Therapy:

Clinical improvement has been seen in adults receiving tetracycline, and symptomatic relief has been observed

in children receiving diiodohydroxyquin, metronidazole, or tetracycline.

Prevention:

Fecal-oral transmission has not been documented; therefore, it is difficult to speculate about preventive

measures. However, if transmission does occur from ingestion of certain helminth eggs, the appropriate hygiene

and sanitary measures to prevent contamination with fecal material are appropriate.

Figure 15Trophozoites of Dientamoeba fragilis

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Pentatrichomonas hominis:

 P. hominis is probably the most commonly identified flagellate, other than G. lamblia and D. fragilis. P. hominis has

been recovered from all parts of the world, in both warm and temperate climates, and is considered nonpathogenic and

noninvasive. It is not known to have a cyst stage P. hominis trophozoites live in the cecum and feed on bacteria. The

trophozoite measures 5 to 15 μm long and 7 to 10 μm wide. It has a pyriform membrane, which aid identification of the

organism. The undulating membrane extends the entire length of the body, in contrast to that seen in the pathogen T.

vaginalis (on which the membrane extends halfway down the body).

Epidemiology:

Because P. hominis is not known to have a cyst stage, transmission probably occurs in the trophic form. If

ingested in a substance such as milk, these organisms apparently can survive passage through the stomach and

small intestine in patients with achlorhydria.

Pathogeneis and Spectrum of Disease:

P. hominis is considered nonpathogenic and does not cause disease.

Laboratory Diagnosis:

P. hominis trophozoites can sometimes be seen on a permanent stained smear, but definitive identification can

be difficult. However, it is important to report the presence of the organism if seen.

Therapy:

Specific treatment is not recommended for this nonpathogen.

Prevention:

Prevention depends on adequate disposal of human excreta and improved personal hygiene, preventive

measures that apply to most of the intestinal protozoa.

CILIATES:

The class Ciliata, or ciliates, includes species that move by means of cilia, or short extensions of cytoplasm that

cover the surface of the organism. The ciliates also have two different types of nuclei, one macronucleus and

one or more micronuclei. This group includes only one organism that infects humans, Balantidium coli, which

infects the intestinal tract and may produce severe symptoms.

Balantidium Coli:

General Characteristics:

The life cycle of B. coli includes both the trophozoite and cyst stages (Figures 16).

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 The cyst form is the infective stage. After ingestion of the cysts and excystation, trophozoites secrete

hyaluronidase, which aids the invasion of the colonic tissue.The trophozoite is quite large, oval, and covered

with short cilia. It measures approximately 50 to 150 μm long

and 40 to 70 μm wide. The organism can be seen wet preparation on lower power. The anterior end is

somewhat pointed and has a cytostome (primitive mouth opening); in contrast, the posterior end is broadly

rounded. The cytoplasm contains many vacuoles with ingested bacteria and debris. The trophozoite has two

nuclei: one very large, bean-shaped macronucleus and a smaller, round micronucleus. The organisms live in the

large intestine. The trophozoites have a rapid, rotatory, boring motion because of the movement of the cilia.

The cyst is formed as the trophozoite moves down the intestine. Nuclear division does not occur in the cyst;

therefore, only two nuclei are present, the macronucleus and the micronucleus. The cysts measure 50 to 70 μm

in diameter.

Epidemiology:

B. coli is widely distributed in hogs, particularly in warm and temperate climates, and in monkeys in the

tropics. Human infection is found in warmer climates, sporadically in cooler areas, and in institutionalized

groups with low levels of personal hygiene.

Pathogenesis and Spectrum of Disease:

Some individuals with B. coli infection are asymptomatic, whereas others have severe dysentery, similar to that

seen in patients with amebiasis. Symptoms include diarrhea or dysentery, tenesmus, nausea, vomiting, anorexia,

and headache. Insomnia, muscular weakness, and weight loss also have been reported. Diarrhea may persist for

weeks to months, with or without subsequent development of dysentery. Tremendous fluid loss may occur,

with diarrhea similar to that seen in cholera or in some coccidial or microsporidial infections. B. coli can invade

tissue. It may penetrate the mucosa on contact, with cellular infiltration in the area of the developing ulcer.

Some of the abscess formations may extend to the muscular layer. The ulcers may vary in shape, and the ulcer

bed may be full of pus and necrotic debris. Although the number of cases is small, extraintestinal disease

(peritonitis, urinary tract infection, inflammatory vaginitis) has been reported

Figure 16 A, Balantidium coli trophozoite. B, B. coli trophozoite.

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Laboratory Diagnosis:

Routine stool examinations, particularly wet preparation examinations of fresh and concentrated material,

demonstrate the presence of organisms. Organism recognition and identification on a permanent stained smear

is usually difficult. These protozoa are large and stain very darkly, which obscures any internal morphology. B.

coli organisms may be confused with helminth eggs or debris because of their size.

Therapy:

Tetracycline is the drug of choice for treating B. coli infection, although it is considered investigational for this

infection. Iodoquinol or metronidazole may be used as an alternative. Nitazoxanide, a broad-spectrum

antiparasitic drug, may be another alternative.

Prevention

In areas where pigs are raised, the incidence of human infection can be quite high in pig farmers and

slaughterhouse workers. Human infection is fairly rare in temperate areas, although infections can develop into

an epidemic, particularly in areas of poor environmental sanitation and personal hygiene. This situation has

been seen in mental hospitals in the United States. Preventive measures involve increased attention to personal

hygiene and sanitation measures, because the mode of transmission is ingestion of infective cysts through

contaminated food or water.

Sporozoa (APICOMPLEXA):

 All the Apicomplexa are unicellular and have an apical complex. These structures can be seen in electron

microscopy studies and are used to help classify the various organisms. Genera that develop in the

gastrointestinal tract of vertebrates throughout their entire life cycle include Isospora, Cyclospora, and

Cryptosporidium. Genera capable of or requiring extraintestinal developmentare referred to as cyst-forming

coccidia; they include Sarcocystis and Toxoplasma spp. The genera that cause disease in humans include

Cryptosporidium, Cyclospora, Isospora, Sarcocystis, and Toxoplasma .

Cryptosporidium SPP.:

General Characteristics

Cryptosporidium spp. are intracellular parasites that primarily infect epithelial cells of the stomach, intestine,

and biliary ducts. The organism previously called Cryptosporidium parvum, thought to be the primary

Cryptosporidium species infecting humans, now is classified as two species, C. parvum (mammals, including

humans) and C. hominis (primarily humans). Differentiation of these two species based on oocyst morphology

is not possible. Currently, more than 20 established Cryptosporidium species have been identified in

vertebrates, and more than 10 Cryptosporidium spp. have been reported in humans. Cryp

Cryptosporidium species infecting humans, now is classified as two species, C. parvum (mammals, including

humans) and C. hominis (primarily humans). Differentiation of these two species based on oocyst morphology

is not possible. Currently, more than 20 established Cryptosporidium species have been identified in

vertebrates, and more than 10 Cryptosporidium spp. have been reported in humans. Cryptosporidium infections

begin with ingestion of viable oocysts. Upon contact with gastric and duodenal fluid, each oocyst releases four

sporozoites, which invade.

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Figure 17 Life cycle of Cryptosporidium. (a) Sporulated oocyst infeces. (b) Excystation in intestine. (c) Free

sporozoite in intestine. (d)Type I meront (six or eight merozoites). (e) Recycling of type I merozoite.(f) Type II meront

(four merozoites). (g) Microgametocyte withapproximately 16 microgametes. (h) Microgamete fertilizes

macrogamete(i) to form zygote (j). Approximately 80% of the zygotes form thick-walled oocysts (k), which sporulate

within the host cell. About 20% of the zygotes do not form an oocyst wall; their sporozoites are surrounded only by a

unit membrane (l). Sporozoites in “autoinfective,” thin-walled oocysts (l) are released into the intestinal lumen (m) and

reinitiate the endogenous cycle (at c).

Figure 18 Cryptosporidium. A, Oocysts recovered from a Sheather’s sugar flotation; organisms measure 4 to

6 μm. B, Scanning electron microscopy view of organisms at brush border of epithelial cells.

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the epithelial cells and develop into trophozoites surrounded by a parasitophorous vacuole (layers of

endoplasmic reticulum around an intracellular parasite). In the epithelial cells, trophozoites undergo two or

three generations of asexual amplification, called merogony, leading to the formation of different types of

meronts containing four to eight merozoites. The merozoites differentiate into sexually distinct stages in a

process called gametogony. New oocysts are then formed in the epithelial cells in a process called sporogony.

About 20% of the oocysts are thin walled and may excyst in the digestive tract of the host, leading to the

infection of new cells (autoinfection). The remaining 80% of the oocysts are excreted into the environment; are

resistant to low temperature, high salinity, and most disinfectants; and can initiate infection in a new host.

Cryptosporidium oocysts in humans measure 4 to 6 μm in diameter.

Epidemiology:

Humans can acquire cryptosporidiosis through several transmission routes, such as direct contact with infected

people or animals or consumption of contaminated water (drinking or recreational) or food. The interval

between ingestion of infective oocysts to completion of the life cycle and excretion of new oocysts usually is 4

to 10 days. The only extracellular stage in the Cryptosporidium life cycle is the oocysts; these are the

environmental stage of the parasite and are immediately infectious when passed in the stool.

Cryptosporidiosis is common in immunocompromised individuals, such as those with AIDS or primary

immunodeficiency and cancer and transplant patients undergoing immunosuppressive therapy.

Pathogenesis and Spectrum of Disease:

Immunocompetent Individuals: Clinical symptoms include nausea, low-grade fever, abdominal cramps, anorexia, and five

to 10 watery, frothy bowel movements per day, which may be followed by constipation. Some patients may have diarrhea,

and others may have few symptoms, particularly later in the course of the infection.

Immunocompromised Individuals. Hemodialysis patients with chronic renal failure and renal transplant patients

Figure 19 Cryptosporidium oocysts and Giardia cysts stained with monoclonal antibody–conjugated

fluorescent reagent.

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with cryptosporidiosis can have chronic, life-threatening diarrhea. In individuals infected with the human

immunodeficiency

virus (HIV), cryptosporidiosis increases as the CD4+ lymphocyte count falls, Cryptosporidium infections are not always

confined to the gastrointestinal tract; additional symptoms (respiratory problems, cholecystitis, hepatitis, and pancreatitis)

have been associated with extraintestinal infections.

Laboratory Diagnosis:

Oocysts in clinical specimens are difficult to see without special staining techniques, such as the modified acid-fast,

Kinyoun’s, or Giemsa method, or the newer immunoassay methods. The four sporozoites may be seen in the oocyst wall

in some of the organisms, although they are not always visible in freshly passed specimens.

Antigen Detection.Immunoassays are very helpful, because they are a more sensitive method of detecting organisms in

stool specimens. A direct fluorescent antigen (FA) procedure with excellent specificity and sensitivity has been developed

and results in a significantly increased detection rate over conventional staining and microscopy methods. Some of these

reagents, particularly the combination direct FA product used to identify both Giardia spp. cysts and Cryptosporidium

spp. oocysts, are being widely used in water testing and outbreak situations. Most antibodies in commercial direct

fluorescent antibody (DFA) kits react with oocysts of almost all Cryptosporidium species, making identification to the

species level impossible. Enzyme immunoassay (EIA) tests also provide excellent specificity and sensitivity for

laboratories using this approach, as do the immunochromatographic cartridge rapid test formats. It is important to

remember that if a patient is in the carrier state or undergoing self-cure, the number of oocysts may drop below the

sensitivity levels of these kits, producing a false-negative result.

Nucleic Acid-Based Methods. Molecular techniques, especially polymerase chain reaction (PCR) and PCRrelated

methods, have been used to detect and differentiate Cryptosporidium spp., and a few of the PCR assays are commercially

available. Several genus-specific PCRrestriction fragment length polymorphism–based genotyping tools have been

developed for detecting and differentiating Cryptosporidium organisms at the species level. Other genotyping techniques

are designed mostly for differentiation of C. parvum and C. hominis and cannot detect and differentiate other

Cryptosporidium spp. Or genotypes.

Histology.In the examination of histologic preparations, developmental stages (sporozoites, trophozoites, merozoites, and

oocysts) in the life cycle of Cryptosporidium spp. can be found at all levels of the intestinal tract, with the jejunum being

the most heavily infected site. Routine hematoxylin and eosin staining is sufficient to demonstrate these parasites. Under

regular light microscopy, the organisms are visible as small, round structures (about 1 to 3 μm in diameter) aligned along

the brush border. They are intracellular but extracytoplasmic and are found in parasitophorous vacuoles. In clean wet

mounts, Cyclospora organisms are seen as nonrefractile spheres, which are difficult to recognize as parasites. Unless a

high number of oocysts are present, they may easily be mistaken for artifacts. They are acidfast variable with the modified

acid-fast stain; those that are unstained appear as glassy, wrinkled spheres (wrinkledcellophane). The oocysts are twice the

size of those of Cryptosporidium spp. and measure 8 to 10 μm in diameter. Because it takes 10 days to 2 weeks for the

oocysts to sporulate, no internal structures are visible (sporozoites), as can be seen in Cryptosporidium organisms.

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Therapy:

 Oral or intravenous rehydration and antimotility drugs are used whenever severe diarrhea is associated with

cryptosporidiosis. Nitazoxanide is the only drug approved by the U.S. Food and Drug Administration (FDA) for the

treatment of cryptosporidiosis in immunocompetent individuals. This drug can shorten the clinical disease and reduce the

number of parasites present.

Cyclospora cayetanensis

 These organisms are acid-fast variable and have been found in the feces of immunocompetent travelers to developing

countries, immunocompetent individuals with no travel history, and patients with AIDS.

The life cycle of C. cayetanensis involves only humans as hosts. Oocysts are passed in the feces unsporulated , At room

temperature (23° to 25°C), small numbers of oocysts may sporulate within 10 to 12 days. In clean wet mounts,

Cyclospora organisms are seen as nonrefractile spheres, which are difficult to recognize as parasites. Unless a high

number of oocysts are present, they may easily be mistaken for artifacts. They are acidfast variable with the modified

acid-fast stain; those that are unstained appear as glassy, wrinkled spheres (wrinkled cellophane). The oocysts are twice

the size of those of Cryptosporidium spp. and measure 8 to 10 μm in diameter. Because it takes 10 days to 2 weeks for the

oocysts to sporulate, no internal structures are visible (sporozoites), as can be seen in Cryptosporidium organisms.

Epidemiology:

Transmission of C. cayetanensis is thought to be by the fecal-oral route. However, direct person-to-person transmission

has not been well documented and may not be a factor, because sporulation takes a number of days. Outbreaks linked to

contaminated water and various types of fresh produce (raspberries, basil, baby lettuce leaves, and snow peas) have been

reported. Information on reservoir hosts is not well defined; however, in some areas humans appear to be the only host.

Pathogenesis and Spectrum of Disease:

Although some patients are asymptomatic, others report a flulike illness, marked by nausea, vomiting, anorexia, weight

loss, and explosive diarrhea lasting 1 to 3 weeks.

The incubation period is not yet known. However, the onset of symptoms after infection generally averages 7 to 8 days,

and the symptoms last 2 to 3 weeks. Oocyst shedding in the feces is highly variable and may range from 7 days to several

months. Indigenous infections are confined primarily to tropical, subtropical, or warm temperate regions of the world.

Outbreaks occur in other areas of the world as a result of contaminated

foodstuffs.

In immunocompromised and immunocompetent patients, C. cayetanensis infection can be associated with biliary disease.

With light and transmission electron microscopy developmental stages have been seen in the gallbladder epithelium of

AIDS

Laboratory Diagnosis:

Special Stains. With modified acid-fast stains, the oocysts appear light pink to deep red, and some contain granules or

have a bubbly appearance (described as wrinkled cellophane).

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Flow Cytometry. Flow cytometry is another diagnostic option. This approach appears to be a useful alternative to

microscopy, particularly for screening large numbers of clinical specimens for Cyclospora oocysts in an outbreak

situation. However, it is not commonly used. Other Diagnostic Methods. Although culture, antigen detection, nucleic acid

detection, and serologic tests for antibody have been developed, none of these methods is routinely available for most

clinical laboratories.

Therapy:

Patients have been treated symptomatically with antidiarrheal preparations and have obtained some relief; however, the

disease appears to be self-limiting within a few weeks. Trimethoprim (TMP-SMX), currently the drug of choice, is given

orally twice daily for 7 days. Elimination of parasites, a decrease in diarrhea, and diminished abdominal pain occur within

2 to 3 days after treatment. Patients with AIDS may need higher doses and long-term maintenance treatment. However,

more than 40% of patients have a recurrence of symptoms in 1 to 3 months after treatment.

Prevention:

Individuals in endemic areas should wear gloves when gardening to prevent exposure to oocysts of C. cayetanensis

Thorough washing of produce may help remove oocysts. Most of the produce items implicated in the transmission of C.

cayetanensis are consumed raw; thus cooking as a means of prevention is not relevant.

ISOSPORA (CYSTOISOSPORA) BELLI

General Characteristics:

 Although isosporiasis is found worldwide, certain tropical areas in the Western Hemisphere have specific

locations where endemic infections occur. These organisms infect both adults and children, and intestinal

involvement and symptoms are generally transient unless the patient is immunocompromised. I. belli has also

been implicated in traveler’s diarrhea. However, unlike with Cryptosporidium spp. and C. cayetanensis, large

outbreaks of isosporiasis have not been reported I. belli oocysts are passed in the stool. They are long and

oval, measuring 20 to 33 μm long by 10 to 19 μm wide. Usually the oocyst contains one immature sporont, but

two may be present. Continued development occurs outside the body, with the development of two mature

sporocysts, each containing four sporozoites, which can be recovered from the fecal specimen. The sporulated

oocyst is the infective stage that excysts in the small intestine, releasing the sporozoites, which penetrate the

mucosal cells and initiate the life cycle.

Epidemiology

I. belli oocysts are passed in the feces unsporulated or partially sporulated. Oocysts complete sporulation

within72 hours, although it may take longer, depending on the temperature. The time required for unsporulated

oocysts to appear in the feces after ingestion of sporulated oocysts is 9 to 17 days. Oocyst shedding is variable

and depends on the immune status of the infected individual. Oocysts can be found for 30 to 50 days in

immunocompetent patients, and immunosuppressed patients may continue to shed oocysts for 6 months or

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longer. Chronic infections can occur, and oocysts can be shed for months to years. In one particular case, an

immunocompetent individual had symptoms for 26 years, and I. belli was recovered in stool a number of times

over 10 years. I. belli is thought to be the only species of Isospora that infects humans, and no other reservoir

hosts are recognized

for this infection. Transmission occurs through ingestion of water or food contaminated with mature, sporulated

oocysts. Sexual transmission by direct oral contact with the anus or perineum also occurs, although this mode

of transmission is probably much less common.

 The oocysts are very resistant to environmental conditions and may remain viable for months if kept cool and

moist; oocysts usually mature within 48 hours after stool passage and are then infectious. Pathogenesis and

Spectrum of Disease Symptoms include diarrhea (most common), weight loss, abdominal colic, and fever.

Stools (usually six to 10 per day) are watery to soft, foamy, and offensive smelling, suggesting a malabsorption

process. Many patients have eosinophilia, recurrences are quite common, and the disease is more severe in

infants and young children. Patients who are immunosuppressed, particularly those with AIDS, often present

with profuse diarrhea associated with weakness, anorexia, and weight loss. Biopsies reveal an abnormal mucosa

with short villi, hypertrophied crypts, and infiltration of the lamina propria with eosinophils, neutrophils, and

round cells. Physicians should consider I. belli in AIDS patients with diarrhea who have immigrated from or

traveled to Latin America, are Hispanics born in the United States, are young adults, or who have not received

prophylaxis with TMP-SMX for Pneumocystis infection. It has also been recommended that patients with AIDS

traveling to Latin America and other developing countries be advised of the waterborne and food-borne

transmission of I. belli and that chemoprophylaxis should be considered.

Extraintestinal infections in patients with AIDS have been reported. At autopsy, microscopic findings

associated with I. belli infection were seen in the lymph nodes and walls of the small and large intestines,

mesenteric and mediastinal lymph nodes, lymphatic channels, liver, and spleen. I. belli infections in the

gallbladder epithelium and endometrial epithelium have also been reported, and oocysts have been recovered in

bile specimens.

Laboratory Diagnosis:

 Examination of fresh material, either as the direct smear or as concentrated material, is recommended rather

than the permanent stained smear. The oocysts are very pale and transparent and can easily be overlooked. The

light level should be reduced, and additional contrast should be obtained with the microscope for optimal

examination conditions. On the permanent stained smear, the organisms may take up excess stain and resemble

helminth eggs or artifacts.

 It is possible to have a positive biopsy specimen but not recover the oocysts in the stool because of the small

numbers of organisms present. The oocysts are acid-fast and can also be demonstrated by using auramine

rhodamine stains. Organisms tentatively identified by using auramine rhodamine stains should be confirmed by

wet smear examination or acid-fast stains, particularly if the stool contains other cells or excess artifact material

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(more normal stool consistency). Currently, there are no commercially available nucleic acid-based methods for

the detection of I. belli. However, PCR assays have been developed for the detection of the organism in stool

samples.

Histology:

Developmental stages of I. belli have been reported for intestinal biopsy specimens of the duodenum, jejunum,

and occasionally ileum. Intestinal development tends to occur in epithelial cells, although developing stages are

occasionally reported from the lamina propria or submucosa. Extraintestinal infections in patients with AIDS

have been reported; the organisms become dormant as cysts in a variety of tissues, including the intestine,

mesenteric lymph nodes, liver, and spleen;

these cysts are called unizoite cysts. In histologic sections, these cysts are thick walled and measure 12-22 × 8-

10 μm, and each contains a single dormant sporozoite/merozoite of about 8-10 × 5 μm. As immunity declines,

these cysts can reactivate patent infections.

Therapy:

The drug of choice to treat I. belli infection is trimethoprimsulfamethoxazole, which is given two to four times

a day for 10 to 14 days. With this approach, the parasites are

eliminated, the diarrhea stops, and the abdominal pain decreases within a few days.

Prevention:

Because transmission occurs through the infective oocysts, prevention includes improved personal hygiene

measures and sanitary conditions to eliminate possible fecal-oral transmission from contaminated food, water,

and possibly environmental surfaces.

Sarcocystis spp.:

General Characteristics:

 Two well-described Sarcocystis species include S. bovihominis (cattle) and S. suihominis (pigs). (Some

publications refer to S. bovihominis as S. hominis.) When uncooked meat from these infected animals is

ingested by humans, gamogony (fission resulting in the production of sporozoan gametes) can occur in the

intestinal cells, with eventual production of the sporocysts in stool. Sarcocystis spp. have an obligatory twohost life cycle. Intermediate hosts (herbivores and omnivores) become infected through ingestion of sporocysts

excreted in the feces of the definitive hosts (carnivores and omnivores).

The definitive hosts become infected through ingestion of mature cysts found in the muscles of the intermediate

hosts. In some intermediate hosts, such as cattle and sheep, all adult animals may be infected. Extraintestinal

human sarcocystosis is rare, with a much lower incidence than is seen with the intestinal infection. Humans

who have ingested meat containing the mature sarcocysts serve as the definitive hosts. Fever, severe diarrhea,

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abdominal pain, and weight loss have been reported in immunocompromised hosts, although the number of

patients with these symptoms has been quite small.

 The sporocysts found in the stool are broadly oval and slightly tapered at the ends. They measure 9 to 16 μm

long and contain four mature sporozoites and the residual body . Normally, the oocyst contains two sporocysts

(similar to I. belli); however, in Sarcocystis infections, the sporocysts are released from the oocyst and normally

are seen singly. These sporocysts tend to be larger than Cryptosporidium oocysts that contain four sporozoites,

so they look totally different. The oocysts are fully sporulated when passed in the stool.

Pathogenesis and Spectrum of Disease:

 When humans (intermediate host) ingest oocysts from other animal stool sources, the sarcocysts that develop

in human muscle are 7 to 16 μm long and cause few, if any, problems. Basically, no inflammatory response to

these organisms occurs in the muscle, and no evidence of pathogenicity is seen. Patients demonstrate symptoms

related to the disintegration of the sarcocysts and death of intracystic bradyzoites. Painful muscle swellings

measuring 1 to 3 cm in diameter are associated with erythema of the overlying skin; these occur periodically

and last 2 days to 2 weeks. Symptoms also include fever, diffuse myalgia, muscle tenderness, weakness,

eosinophilia, and bronchospasm. Different types of skeletal and cardiac muscle sarcocysts have been found in

humans. No specific therapy is required for this type of infection. Corticosteroids can reduce allergic

inflammatory reactions.

Infections in humans can manifest primarily as intestinal disease if infected meat is ingested or as muscular

disease if sporocysts are ingested. Intestinal disease occurs within a few hours after consumption of infected

meat and is characterized by nausea, abdominal pain, and diarrhea. However, in both situations patients may be

infected and asymptomatic.

Laboratory Diagnosis:

 A presumptive diagnosis of intestinal disease may be based on the patient’s symptoms, particularly with

documented ingestion of raw or poorly cooked meat. Confirmation of the diagnosis may depend on finding

human fecal specimens containing sporocysts, which are passed in the stool 11 to 18 days after ingestion of

beef or pork.

 Sporocysts of the two Sarcocystis species are very difficult to differentiate. A muscle biopsy is appropriate for

suspected symptomatic intramuscular infection in a patient with a history of travel to or residence in a tropical

location. Sarcocysts in biopsy specimens can be identified by microscopy on routine histologic sections stained

with hematoxylin and eosin. Most sarcocysts in humans have been found inskeletal and cardiac muscle

however, muscles in the larynx, pharynx, and upper esophagus have also been involved. No molecular assays

are currently available for the detection of sarcocystis in humans. However, several amplification methods have

been used to detect sarcocystis in intermediate hosts.

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Therapy:

No known treatment or prophylaxis is available for intestinal infection, myositis, vasculitis, or related lesions

caused by human sarcocystosis. Supportive therapy for patients with severe diarrhea is indicated. It is also

unclear whether immunosuppressives are effective at reducing the inflammatory reactions seen in vasculitis or

myositis. Without more definitive data, no course of therapy currently can be recommended.

Prevention:

Cooking meat to an internal temperature higher than 67°C kills Toxoplasma gondii tissue cysts in meat; this

temperature should also kill Sarcocystis tissue cysts in meat.

Preventing cattle, buffalos, and swine from consuming human feces shedding infective oocysts also prevents

animal infection. Most cases of human muscular Sarcocystis

infection have been reported from the Far East. When humans are intermediate hosts, preventive measures

involve careful disposal of animal feces that may contain the infective sporocysts. This may be impossible in

wilderness areas, where wild animals may serve as reservoir hosts for many Sarcocystis spp.

Microsporidia:

 Microsporidia are obligate intracellular, spore-forming parasites. More than 140 microsporidial genera and

1200 species have been identified. To date, seven genera (Anncaliia, Encephalitozoon, Enterocytozoon,

Nosema, Pleistophora, Vittaforma, and Trachipleistophora) and unclassified microsporidia (Microsporidium)

have been identified as causing human infections.

 Although the microsporidia are true eukaryotes, they also have molecular and cytologic characteristics of

prokaryotes. Microsporidia evolved from the fungi and are most closely related to the Zygomycetes. Features

shared with fungi include the presence of chitin and trehalose, similarities in cell cycles, and certain gene

organizations.

 Microsporidia are now considered highly derived fungi that underwent genetic and functional losses, resulting

in one of the smallest eukaryotic genomes known.

However, the life cycle of microsporidia is unique and unlike that of any fungal species. At this point, clinical

and diagnostic issues and responsibilities may remain with the parasitologists, and we may be in a transition

stage, similar to that seen with Pneumocystis jirovecii as it was moved from the parasites to fungi in terms of

classification status.

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General characteristics:

 Human microsporidial infections have been documented worldwide. The spore, the only life cycle stage able

to survive outside the host cell, is the infective stage (see Figures 20).

Infection occurs with ingestion or inhalation of the infective spores, from which the infective sporoplasm (spore protoplasm)

enters the host cell through the polar tubule. The microsporidia multiply extensively in the host cell cytoplasm; the life

cycle includes repeated divisions by binary fission (merogony) or multiple fission (schizogony) and spore

production (sporogony). Both merogony and sporogon

can occur in the same cell at the same time. During sporogony a thick spore wall is formed, providing environmental

protection for the spore. Microsporidial spores measure 0.7 to about 4 μm in diameter. Mature spores contain a tubular

extrusion apparatus (polar tube or tubule) for injecting infective spore contents (sporoplasm) into the host cell.

Epidemiology:

Transmission possibilities include human-to-human and animal-to-human routes. Many questions relating to

reservoir hosts and possible congenital infections are still unanswered. Primary infection occurs through

inhalation or ingestion of spores from environmental sources or by zoonotic transmission. The presence of

Encephalitozoon intestinalis has been confirmed in tertiary sewage effluent, surface water, and groundwater;

Figure 20 Life cycle diagram of the microsporidia. A to G, Asexual development of sporoblasts. H, Release of spores.

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 Arranged by Sarah Mohssen

SectionIII– Parasitology By Nada Sajet

Enterocytozoon bieneusi has been confirmed in surface water; and Vittaforma corneae has been confirmed in

tertiary effluent.

This study represents the first confirmation, to the species level, of human-pathogenic microsporidia in water,

indicating that these parasites are probably waterborne pathogens. Ingestion of the environmentally highly

resistant spores is probably the normal mode of

transmission. E. bieneusi, an intestinal pathogen, serves as an example of infection potential. The spores are

released into the intestinal lumen and are passed in the stool. These spores are environmentally resistant and can

be ingested by other hosts. Zoonotic transmission of microsporidia infecting humans has not been verified but

appears likely, because many microsporidial species can infect both humans and animals.

Pathogenesis and spectrum of disease:

 Microsporidia were recognized as causing disease in animals as early as the 1920s but were not recognized as

agents of human disease until the AIDS pandemic began in the mid-1980s. Before then, several earlier human

cases had been reported but were thought to be very unusual.

Enterocytozoon bieneusi:

A number of cases of E. bieneusi infection have been reported in patients with AIDS. Chronic intractable

diarrhea, fever, malaise, and weight loss are symptoms of E. bieneusi infections, and these symptoms mimic

those seen with cryptosporidiosis or isosporiasis.