karyosome, similar to that found in N. fowleri. This morphologic characteristic can be seen on a wet preparation.

The cysts are usually round with a single nucleus, also having the large karyosome as in the trophozoite nucleus. The

double wall is usually visible, with the slightly wrinkled outer cyst wall and what has been described as a polyhedral inner

cyst wall. This cyst morphology is identifiable in organisms cultured on agar plates.

Pathogenesis and spectrum of disease :

GAE (granulomatous amebic encephalitis):

Meningoencephalitis caused by Acanthamoeba spp. May present as an acute suppurative inflammation of the brain and

meninges similar to N. fowleri infection. The incubation period of GAE is unknown; several weeks or months are

probably necessary to establish disease. The clinical course tends to be subacute or chronic and is usually associated with

trauma or underlying disease, not as a result of swimming. GAE may present with symptoms of confusion, dizziness,

drowsiness, nausea, vomiting, headache, lethargy, stiff neck, seizures, and sometimes hemiparesis. Unlike PAM caused by

N. fowleri, both trophozoites and cysts are found throughout the tissue. Also, dissemination to other tissues such as the

liver, kidneys, trachea, and adrenals can occur in immunocompromised individuals; or additional unusual sites also

include the ear and necrotic bone from a bone graft of the mandible. Some patients, especially those with AIDS, can

develop erythematous nodules, chronic ulcerative skin lesions, or abscesses. Keratitis Acanthamoeba spp. also cause

keratitis and corneal ulceration. Clinicians need to consider acanthamoebic infection in the differential diagnosis of eye

infections that are not responding to bacterial, fungal, or viral therapy.

These infections are often due to direct exposure of the eyes to contaminated materials or solutions. Use of

contact lenses is the leading risk factor for keratitis. Conditions that are linked with disease include the use of home-made

saline solutions, poor contact lens hygiene, and corneal abrasions. A contact lens can act as a mechanical vector for

Figure 29 Naegleria fowleri in brain tissue. Hematoxylin and eosin stain.

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transport of amebae present in the storage case onto the cornea. Subsequent multiplication and invasion of the tissue may

occur.

Laboratory diagnosis :

 Routine Methods:

Tissue stains are effective, and cysts isolated from cultures can be stained with Gomori’s silver methenamine, periodic

acid-Schiff, and calcofluor white. Identification of Acanthamoebae in ocular samples and other tissues can be difficult,

even for trained laboratory professionals; in histologic preparations, the organisms appear similar to keratoplasts, as well

as neutrophils and monocytes. It has been estimated that up to 70% of clinical Acanthamoeba keratitis cases are

misdiagnosed as viral keratitis. Also, the average time to diagnosis of keratitis attributable to Acanthamoeba infection can

average 2.5 weeks longer for non–contact lens wearers than for contact lens users.

 Other Methods :

CSF or bronchoalveolar lavage fluid cytospin preparations can be used to look for amebae in patients with

GAE or respiratory symptoms.

Organisms have also been found in the adrenal gland, brain, eyes, kidneys, liver, pancreas, skin,

spleen, thyroid gland, and uterus.

In infections caused by Acanthamoeba spp., periodic acid-Schiff stains the cyst wall red and methenamine silver stains the

cyst black.

Therapy :

Disseminated Infections

Trophozoites and cysts of Acanthamoeba isolates vary in their sensitivity to antimicrobial agents. They are sensitive in

vitro to ketoconazole, pentamidine, hydroxystilbamidine, paromomycin, 5-fluorocytosine, polymyxin, sulfadiazine,

trimethoprim-sulfamethoxazole, azithromycin, and extracts of medicinal plants, especially, to combinations of these

drugs. In vitro testing confirms strain and species differences in sensitivity.

Balamuthia mandrillaris

Pathogenesis and spectrum of disease

The disease is very similar to GAE caused by Acanthamoeba spp. The clinical presentation is subacute or chronic and is

usually not associated with swimming in freshwater. No characteristic clinical symptoms, laboratory findings, or

radiologic indicators have been found to be diagnostic for GAE. Whether single or multiple, the lesions in the brain

involve mainly the cerebral cortex and subcortical white matter. Symptoms include headache, nausea, vomiting, fever,

visual disturbances, dysphagia, seizures, and hemiparesis. The clinical course ranges from a few days to several months.

In immunocompetent hosts, an inflammatory response occurs; however, with rare exceptions, these patients also tend to

die with severe CNS disease.

Laboratory diagnosis :

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these organisms can be cultured in mammalian cell cultures using monkey kidney cells ,Although serum antibodies have

been identified in infections, laboratory testing is notroutinely available.

Therapy :

In vitro studies indicate that B. mandrillaris is susceptible to pentamidine isethiocyanate and that patients may

benefit from this treatment.

Trichomonas vaginalis:

General characteristics:

 Infection is acquired primarily through sexual intercourse, hence the need to diagnose and treat asymptomatic

males. The organism is capable of survival for extended periods in a moist environment such as damp towels and

underclothes; however, this mode of transmission is thought to be very rare. Trichomoniasis is the primary nonviral sexually transmitted disease worldwide. Infection with T. vaginalis has major health consequences for

women, including complications in pregnancy, association with cervical cancer, and predisposition to HIV

infection.

The life cycle of T. vaginalis has a single trophozoite stage, and is very similar in morphology to other

trichomonads. The trophozoite is 7 to 23 μm long and 5 to 15 μm wide. The axostyle is usually obvious and

protrudes through the bottom of the organism, whereas the undulating membrane ends halfway down the side

ofthe trophozoite. There are a large number of granules evident along the axostyle.

Pathogenesis and spectrum of disease:

 Growth of the organism results in inflammation and large numbers of trophozoites in the tissues and the

secretions. As the acute infection becomes more chronic, the purulent discharge diminishes, with a decrease in the

number of organisms. Symptoms such as vaginal or vulval pruritus and discharge are often sudden and occur

during or after menstruation as a result of the increased vaginal acidity. Symptoms include vaginal discharge

(42%), odor (50%), and edema or erythema (22% to 37%). Complaints also include dysuria and lower abdominal

pain.

Figure 30 : Trichomonas, Giemsa stain

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From 25% to 50% of infected women may be asymptomatic and have a normal vaginal pH of 3.8 to 4.2 and normal

vaginal flora. Even in the carrier form, about 50% of women will become symptomatic during the following 6

months.

Although vaginitis is the most common finding in women with trichomoniasis, other complications include

distention of a fallopian tube with pus, endometritis, infertility, low birth weight, and cervical erosion. There is also

an increased association with HI transmission and cervical dysplasia.

Dysuria, often the earliest symptom, occurs in about 20% of women with vaginal trichomoniasis. Infected males

may be asymptomatic, or the infection may be selflimited, persistent, or result in recurring urethritis. In nonspecific

urethritis, T. vaginalis has been detected in 10% to 20% of subjects and in 20% to 30% of those whose sexual

partners had vaginitis. Once established, the infection persists for an extended period in females but only for about

10 days or less in males. T. vaginalis is the cause of 11% of all cases of non–gonococcal urethritis in males.

Respiratory distress has been reported in a full-term, normal male infant with T. vaginalis with severe respiratory

problems following delivery. A wet preparation of thick, white sputum demonstrated few leukocytes and motile

flagellates, which were identified as T. vaginalis.

This study supports previous data confirming that the organism may cause neonatal pneumonia.

Laboratory diagnosis:

 Humans are the only natural host for T. vaginalis, and organisms reside in the vagina and prostate; they usually

do not survive outside the urogenital tract. The parasites feed on the mucosal surface of the vagina, where bacteria

and leukocytes are abundant. The preferred pH for good

parasitic growth in females is slightly alkaline or acidic (6.0 to 6.3 optimal), not the normal pH (3.8 to 4.2) of the

healthy vagina. The organisms can also be recovered in urine, in urethral discharge, or after prostatic massage.

Often, the organisms are recovered in centrifuged urine sediment from both male and female patients.

Wet mounts:

 The identification of T. vaginalis is often based on the examination of wet preparations of vaginal and urethral

discharges, urine, and prostatic secretions. This examination must be performed within 10 to 20 minutes after

sample collection; if not, organisms lose motility and may not be identified. Several specimens may need to be

examined for detection of the organisms. The sensitivity associated with wet mount examinations varies between

40% and more than 80%. Often, the percent detection from this procedure is quite low with limited sensitivity and

specificity.

Stained Smears:

 Giemsa or Papanicolaou stain can be used. However, atypical cellular changes can be misinterpreted, particularly

on the Papanicolaou smear. The organisms are routinely missed on Gram stains. The number of false-positive and

false-negative results reported on the basis of stained smears strongly suggests that confirmation should be

accomplished by observation of motile organisms either from the direct wet mount or from appropriate culture

media.

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Culture:

 A convenient plastic envelope method has been developed, which allows immediate examination and culture in

one self-contained system. This system is serves as the specimen transport container, the growth chamber during

incubation, and the “slide” durin microscopy. Once it is inoculated, it requires no opening for examination, and

positive growth will occur within 5 days. The sensitivity of this system is reported to be superior to those of othe

available culture methods.

Antigen Detection:

 Several diagnostic tests have been developed, including the XenoStrip-Tv and the OSOM Trichomonas Rapid

Test both of which are more sensitive than the wet mount.

Molecular Diagnostics:

 The use of polymerase chain reaction (PCR) methods has led to improvements in T. vaginalis detection;

nonviable organisms and cells and target sequences can also be detected.

Therapy:

 Metronidazole is recommended for the treatment of urogenital trichomoniasis. Tinidazole has also been used for

therapy.

Pentatrichomonas hominis:

 Pentatrichomonas hominis derives its name on the basis of the morphologic structure of the trophozoite. The

organism has five anterior flagella and a parabasal body. The organism is recovered worldwide and is considered to

be nonpathogenic although it has been isolated from patients with diarrhea.

General characteristics:

 There is no known cyst stage. The trophozoite resides in the large intestine where it feeds on bacteria. The

organism resembles Trichomonas vaginalis, measuring 5 to 15 μm in length and 7 to 10 μm in width with an

undulating membrane and an axostyle. The organism’s undulating membrane extends the entire length of the body,

differentiating it from Trichomonas vaginalis.

Pathogenesis and spectrum of disease:

 Although the organism is considered nonpathogenic, it is the most commonly identified flagellate other than G.

lamblia and Dientamoeba fragilis. The organism may be associated with infections in warm climates.

Laboratory diagnosis:

 Similar to Trichomonas vaginalis, the wet preparation is commonly used to identify motile trophozoites.

However, permanent stained smears provide the greatest sensitivity and specificity.

Therapy:

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 Because the organism is nonpathogenic, it is important to differentiate it from Trichmonas vaginalis. However, if

identified, no treatment is necessary.

TOXOPLASMA GONDII:

Toxoplasma gondii is a protozoan parasite that infects most species of warm-blooded animals, including humans.

Members of the cat family, Felidae, are the only known definitive hosts for the sexual stages of T. gondii and serve

as the main reservoirs of infection. Cats become infected with T. gondii through carnivorism or by ingestion of

oocysts. After tissue cysts or oocysts are ingested by the cat, organisms are released and invade epithelial cells of

the cat small intestine, where they undergo an asexual cycle followed by a sexual cycle with the formation of

oocysts, which are excreted in the feces. The uninfective oocyst takes 1 to 5 days after excretion to become

infective.

Cats shed oocysts for 1 to 2 weeks and large numbers may be shed, often more than 100,000 per gram of feces.

Oocysts survive in the environment for several months to more than 1 year and are resistant to disinfectants,

freezing,and drying. However, they are killed by heating to 70° C for 10 minutes. The life cycle in the cat takes

approximately 19 to 48 days after infection with the oocysts but only 3 to 10 days after the ingestion of meat

infected with cysts (e.g., a mouse) .

General characteristics:

There are three infectious stages of T. gondii: the tachyzoites(in groups or clones), the bradyzoites (in tissuecysts),

and the sporozoites (in oocysts from cat feces).

Tachyzoites rapidly multiply in any cell of the intermediate host and in epithelial cells of the definitive host (cats).

Bradyzoites are found within the tissue cysts and usually multiply very slowly; the cyst may contain few to

hundreds of organisms, and intramuscular cysts may reach 100 μm in size. The tissue cysts can be found in visceral

organs such as the lungs, liver, and kidneys; however, they are more prevalent in the brain, eyes, and skeletal and

cardiac muscle. Intact tissue cysts can persist for the life of the host and do not cause an inflammatory response.

Tachyzoites are crescent-shaped and are 2 to 3 μm wide by 4 to 8 μm long . One end tends to be more rounded than

the other. Giemsa is the stain of choice; the cytoplasm stains pale blue, and the nucleus stains red and is situated

toward the broad end of the organism.

Cysts are formed in chronic infections, and the bradyzoites within the cyst wall are strongly periodic acid-Schiff

positive. During the acute phase, there may be groups of tachyzoites that appear to be cysts; however, they are not

strongly periodic acid-Schiff positive and have been

termed pseudocysts.

Pathogenesis and spectrum of disease:

As the tachyzoites actively grow, increase in number, and eventually rupture from the cell, they invade adjacent

cells. This process creates additional lesions. Once the cysts are formed, the process becomes quiescent, with little

or no multiplication and spread. In the immunocompromised or immunodeficient patient, a cyst rupture Tachyzoites

or primary exposure to the organisms often leads to lesions. The organisms can be disseminated via the lymphatic

system and the bloodstream to other tissues.

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Toxoplasmosis can be categorized into four groups: (1) acquired in the immunocompetent patient; (2)acquired or

reactivated in the immunodeficient patient; (3) congenital; and (4) ocular.

Laboratory diagnosis:

The most common method of diagnosis for toxoplasmosis is serologic testing for T. gondii– specific

antibodies.Other procedures include PCR; examination of biopsy

specimens, buffy coat cells, or cerebrospinal fluid; orisolation of the organism in tissue culture or in laboratory

animals.The serologic diagnosis of toxoplasmosis a number of additional procedures include enzyme

immunoassays, enzymelinked immunosorbent assays (ELISAs), direct agglutination, an immunosorbent

agglutination assay, an indirect immunofluorescence assay (IFA), immunocapture, and immunoblot tests.

Therapy:

 Treatment is recommended for the following conditions: clinically active disease, diagnosed congenital

toxoplasmosis in newborns, pregnant women with infection during gestation, patients with chorioretinitis, and

disease in symptomatic compromised patients. Therapy is also recommended for preventive or suppressive

treatment in HIV-infected persons. The currently recommended drugs work primarily against the actively

dividing tachyzoite form of T. gondii and do not eradicate encysted organisms (bradyzoites).

The most common drug combination used to treat congenital toxoplasmosis consists of pyrimethamine and a

sulfonamide , plus folinic acid in the form of leucovorin calcium to protect the bone marrow from the toxic

effects of pyrimethamine. Spiramycin is recommended for pregnant women with acute toxoplasmosis when

fetal infection has not been confirmed in an attempt to prevent transmission of T. gondii from the mother to the

fetus.

In immunosuppressed persons with toxoplasmosis, the combination of pyrimethamine and sulfadiazine plus

leucovorin is the preferred treatment. Clindamycin, in combination with other antiparasitic medications, is

frequently used for the treatment .

Intestinal Nematodes (Roundworms):

Helminths Nematodes Intestinal (roundworms):

Ascaris lumbricoides

Enterobius vermicularis (pinworm)

Strongyloides stercoralis (threadworm)

Trichostrongylus spp.

Trichuris trichiura (whipworm)

Capillaria philippinensis (hookworms)

Ancylostoma duodenale (Old World)

Necator americanus (New World)

 There are more than 60 species of nematodes known to infect humans. Nematodes are nonsegmented,

elongate, cylindrical worms with a well-developed digestive tract and reproductive system. The adult worms

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have separate sexes, with the male generally smaller than the female. Most nematodes are diagnosed by finding

the characteristic eggs in the stool. The infective stage of the nematodes varies with species; for example,

transmission may occur through the ingestion of eggs, whereas others burrow through the skin and migrate to

the intestine.

The nematodes have very diverse life cycles providing different routes of transmission as well as disease

symptoms.

ASCARIS LUMBRICOIDES:

General characteristics:

Ascaris lumbricoides is the most common and the largestroundworm. The parasite with higher prevalence in

the tropical regions. Eggs are ingested and hatch in the duodenum, penetrate the intestinal wall, and migrate to

the hepatic portal circulation.

The adult worms live and reproduce in the lumen of the small intestine. The ovum is a thick, oval mammillated

(outer protrusions) and embryonated egg. The eggs are passed in the feces and become infective 2 to 6 weeks

following deposition, depending on the environment.

Epidemiology:

Transmission is through the fecal-oral route, usually through the ingestion of eggs on contaminated material.

Ascaris eggs are capable of survival within harsh environmental conditions, including dry or freezing

temperatures.

Pathogenesis and spectrum of disease:

Many A. lumbricoides infections are asymptomatic. The presentation of symptoms correlates with the length of

infection, the number of worms present, and the overall health of the host. Intestinal symptoms range from mild

to severe intestinal obstruction. Some patients will develop pulmonary symptoms and present with immunemediate hypersensitivity pneumonia. The worms may cause an immune condition known as Lِ ffler’s syndrome

characterized by peripheral eosinophilia.

Figure 31 Bile-stained mammillated A. lumbricoides

ovum.

Figure 32 A. lumbricoides adult male worm. Note the

curvedposterior end

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Laboratory diagnosis:

 Female worms have an extremely high daily output of eggs, making diagnosis relatively easy through the

identification of eggs in feces. The large, broadly oval mammillated

ova are typically stained brown from bile (Figure 31). Some eggs will be decorticated, or lacking the

mammillated outer cover. Infertile eggs may be oval or irregular shaped with a thin shell and containing

internal granules. Adult worms may also be identified in feces.

The male is smaller (15 to 31 cm) with a curved posterior end (Figure 32) and contains three well-characterized

lips. Larvae may be found in sputum or gastric aspirates as a result of larval migration during development

within the human host.

Therapy:

Anthelmintic treatment is recommended for all infections.Preferred therapy includes oral albendazole,

mebendazole, or pyrantel pamoate.

Prevention:

Prevention is managed through proper sanitation and good hygiene.

Enterobius vermicularis:

General characteristics:

 Enterobius vermicularis (pinworm) is distributed worldwide and commonly identified in group settings of

children ages 5 to 10 years. The life cycle is considered direct; transmission occurs from an infected host to

another individual , During the night, the mature female worm migrates out of the anus of the infected host and

lays eggs in the perianal region. The embryonated eggs will mature and a third-stage larva stage develops,

resulting in infectivity within hours. Transmission occurs by ingestion or inhalation of eggs. Reinfection may also

occur when the eggs hatch and larvae return to the intestine where they mature.

Epidemiology:

 Pinworm is more prevalent in school-age children up to about 14 years of age. Infections are associated with

institutional crowding and are familial. Transmission is also associated with an increased rate of reinfection

within agroup or autoinfection from hatched larvae.

Pathogenesis and spectrum of disease:

 Infections with E. vermicularis are typically asymptomatic. The most common complaint is perianal pruritus

(itching) and resultant restless sleep. Occasionally, the parasite may migrate to other nearby tissues, causing

pelvic, cervical, or peritoneal granulomas.

Laboratory diagnosis:

Diagnosis is typically by microscopic identification of the characteristic flat-sided ovum (Figure 33).

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The eggs are collected using a sticky paddle or cellophane tape pressed against the perianal region. Eggs are not

typically identified in feces, although they may occasionally

be found in a stool specimen. Although adult pinworms may be visible, they can be easily confused with small

pieces of thread. The female worm measures 8 to 13 mm long with a pointed “pin” shaped tail. In gravid

females, almost the entire body will be filled with eggs (Figure 34). The males measure only 2 to 5 mm in

length, die following fertilization, and may be passed in feces.

Therapy:

Anthelmintic therapy is generally effective with one of the following agents: albendazole, mebendazole,

pyrantel pamoate, or ivermectin.

Prevention:

Regular good personal hygiene is the major factor for prevention of continued reinfection and autoinfection.

Strongyloides stercoralis:

General characteristics:

 Infection with Strongyloides stercoralis is less common than other intestinal nematodes.

S. stercoralis, commonly referred to as the threadworm, may inhabit the intestine or exist as a free-living

organism in the soil. The life cycle can be classified as direct, indirect (free-living phase), or autoinfective ,The

filariform (infective larvae) penetrate the skin and migrate via the circulatory system to the heart and lungs.

The organism enters the bronchial tree and then is swallowed, where it lives in the digestive tract and matures

into an adult worm. In the intestine the filariform larvae may also penetrate the mucosa, resulting in

autoinfection.

The female worm produces eggs by parthenogenesis (a form of asexual reproduction where growth and

development occur without fertilization), because parasitic adult male worms are nonexistent. Within the

indirectlife cycle, the rhabditiform (noninfective) larvae develop into mature males and egg-producing females

(Figure 35).

Figure 33: Enterobius vermicularis eggs Figure 34: Enterobius vermicularis gravid female.

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Epidemiology:

 S. stercoralis is transmitted via direct penetration in endemic areas. Person-to-person transmission occurs

within institutionalized groups, in day care centers, and among homosexual men.

Pathogenesis and spectrum of disease:

Infections may be asymptomatic or consist of a variety of disseminated strongyloidiasis syndromes.

Reinfection is more commonly associated with immunocompromised patients. Acute infections may develop a

localized pruritic, erythematous papular rash. Some patients develop a macropapular or urticarial (red and

raised) rash on the buttocks, perineum, and thighs. The migration of larvae may cause epigastric pain, nausea,

diarrhea, and blood loss. Hyperinfection, an increased worm burden within the lungs and intestines, may occur.

Disseminated infections may also result in larvae within the central nervous system, kidneys, and liver.

A second species, Strongyloides fuelleborni, a primate parasite, has been isolated from humans in Africa and

causes a severe life-threatening condition called “swollen belly syndrome.”

Laboratory diagnosis:

The rhabditiform larva is the primary diagnostic stage for strongyloidiasis in humans through microscopic

examination of stool. The larvae are 250 to 300 μm long with

a short buccal capsule, a large bulb on the esophagus, and a prominent genital primordium ,The filariform

larvae are larger (up to 500 μm) and have a notched tail with an esophageal to intestinal ratio of 1 : 1.

The eggs, which are rarely identified, are segmented with a thin shell. S. stercoralis larvae are the most

common found in human stool specimens.

 Although not available in routine laboratories, realtime polymerase chain reaction (PCR) methods have been

developed that amplify the small subunit of the rRNA gene. The assay is used to detect DNA in fecal samples

and has a demonstrated sensitivity and specificity of 100%. A high throughput multiplex assay has also been

developed that includes primer and probe pairs for S. stercoralis as well as other intestinal nematodes and

protozoa.

Figure 35 Strongyloides stercoralis rhabditiform larva, iodine stain

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Additional specimens such as sputum, body fluids, and tissues may be used for the diagnosis of

hyperinfections.

Therapy:

Ivermectin is the recommended treatment for uncomplicated infections. Albendazole is an alternative.

Prevention:

Immunocompromised individuals and patients taking immunosuppressive medications should avoid

contaminated beaches and other areas.

Trichostrongylus spp.:

General characteristics:

 Although commonly found in mammals and birds worldwide, approximately 10 different species of

Trichostrongylus have been found in human infections. The worms are small and live in the mucosa of the

small intestine. The adult worm has no visible buccal capsule.

Pathogenesis and spectrum of disease:

Following ingestion of the larvae, the larvae mature and migrate through the lungs. Symptoms are related to

the worm burden and the amount of damage within the intestine.

Laboratory diagnosis:

 Laboratory diagnosis includes identification of eggs or hatched larvae in the stool. The eggs are oval and

resemble hookworm eggs except they are slightly longer and more pointed (Figure 36). Larvae should be

differentiated from hookworm and S. stercoralis .

Therapy:

Anthelmintic agents are recommended including mebendazole and pyrantel pamoate. Albendazole is the

treatment of choice.

Figure 36 Trichostrongylus sp. egg.

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Prevention:

 Thorough washing of plant material, including cultivated vegetables, before handling or ingestion is

recommended.

Trichuris trichiura:

General characteristics:

 Trichuris trichiura, whipworm, has a worldwide distribution. Unlike other intestinal nematodes there is no

tissue migration phase within the life cycle of T. trichiura.

Epidemiology:

 Humans are infected by ingestion of the eggs. Larvae are released in the intestine ,where they mature into

adult worms. Eggs are then passed in the feces and deposited in the soil. The eggs require a warm, moist

environment for embryonation in order to become infective to another host.

Pathogenesis and spectrum of disease:

Pathogenesis and severity of the disease are closely related to the worm burden. The lack of symptoms is

related to the life cycle that does not include a tissue migration stage, as is seen in other nematode

infections.Infections range from mild, very low worm burden, to severe infections with bleeding and weight

loss in heavy worm infestations. The characteristic whiplike worm buries its threadlike anterior into the

intestinal mucosa and feeds on tissue secretions, causing an inflammatory reaction and peripheral eosinophilia.

Laboratory diagnosis:

 Diagnosis is typically from the identification of eggs and rarely the adult worm within the feces.

(Figure37,38).

Therapy:

Anthelmintics such as albendazole are recommended when necessary.

Figure 37 Trichuris trichiura egg. Note the clearly evident

polar hyaline plugs.

Figure 38 Adult female Trichuris trichiura.

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Prevention:

 Prevention includes practicing proper hygiene and sanitation as well as the disposal of dirt or soil

contaminated with feces.

Capillaria philippinensis:

General characteristics:

 Human infection is thought to occur from the ingestion of uncooked fish harboring infective larvae. The

people ingest a large spectrum of raw seafood, including fish, shrimp, crabs, and snails.

Pathogenesis and spectrum of disease

Symptoms vary with the level of worm burden. The larvae are ingested and reside in the small intestine where

they burrow into the mucosa. Because of the mechanical insertion into the intestinal wall, patients lose weight

rapidly as a result of malabsorption and fluid loss. Long term infections lasting weeks to months may result in

death attributable to a severe loss of electrolytes, particularly potassium (hypokalemia), and associated organ

Laboratory diagnosis:

 Diagnosis is typically from the identification of eggs, adult worms, or larvae in stool specimens. The eggs

resemble those produced by T. trichiura. They are somewhat smaller with a thick, striated shell and less

prominent polar plugs. Female worms produce the characteristic thick-shelled eggs as well as thin-shelled and

free larvae.

Therapy

Anthelmintic agents including albendazole and mebendazole are recommended.

Prevention

Adequate preparation and cooking of seafood, including fish, snails, crabs, and shrimp in endemic areas, are

encouraged.

Hookworms:

 Hookworms are known to have a worldwide distribution with two species known to infect humans,

Ancylostoma duodenale (Figure 39) and Necator americanus . They are the second most common helmintic

infection reported in humans. The eggs and rhabditi- form larvae of the two species are indistinguishable.

Differentiation of the species is based on the morphology of the buccal capsule and the adult male copulatory

bursa (see Figure 40)

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.

The parasites, infective filariform larvae, penetrate the skin and enter the circulation where the larvae are

capable of breaking through the capillaries and entering the lungs of the host. The larvae migrate up the

bronchial tree, over the epiglottis, and are swallowed. Upon entering the digestive system, the hookworms

attach to the mucosa of the small intestine. Here they secrete anticoagulants and ingest blood as their source of

nourishment.

The worms mature and eggs are passed in the feces and deposited in soil where they mature into rhabditiform

larvae. The noninfective rhabditiform larvae will then mature into filariform.

Ancylostoma duodenale:

General characteristics

 The adult male tends to be larger than the adult male of N. americanus. They attach to the intestinal mucosa by

well-developed mouthparts, especially teeth (see Figure 39).

Pathogenesis and spectrum of disease :

A. duodenale is capable of maturation within the intestine without migrating through the lungs of the host.

Necator americanus:

General characteristics

N. americanus, New World hookworm, attach to the intestinal mucosa by well-developed cutting plates (see

Figure 40).

Figure 39: A, Ancylostoma duodenale head. B, Tail; note the appearance of the pointed tail

 Figure 40 A, Necator americanus head; note the clearly evident rounded cutting plates protruding from the head. B,

Copulatory bursa.

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Pathogenesis and spectrum of disease

 Skin-associated symptoms as described for hookworms Eosinophilia peaks in approximately 2 months in

gastrointestinal phase.

Laboratory diagnosis

 Hookworms are typically diagnosed by the presence of eggs or rhabditiform larvae found in stool specimens.

The eggs and larvae of the two species are indistinguishable.

The eggs are oval and thin-shelled and contain a clearly visible four- to eight-cell stage embryo. There is a characteristic

clear space between the shell and the developing embryo (see figure 40). Recovery and identification of eggs on direct smear

or from concentration methods is recommended. Eggs may appear distorted on permanently stained smears. The

rhabditiform larvae are typically 250 to 300 μm with a long buccal capsule and an inconspicuous genital primoridum

(Figures 41 and 42). The larger filariform larvae are approximately 500 μm, with a pointed tail and a esophageal to intestinal

ratio of 1 : 4. Both the rhabditiform and filariform larvae must be differentiated from S. stercoralis.

Fresh stool stored at room temperature may result in continued maturation and hatching of larvae.

Therapy:

Anthelmintic agents including albendazole, mebendazole, and pyrantel pamoate are indicated.

Prevention

Avoid contaminated soil and beaches. Wear appropriate footwear such as enclosed shoes in potentially contaminated areas.

Tissue Nematodes (Roundworms):

Figure 41: Hookworm egg, iodine stain. Figure 42 Hookworm rhabditiform larvae.

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Helminths Nematodes (Roundworms) Tissue:

Trichinella spiralis

Visceral larva migrans (Toxocara canis or Toxocara cati)

Ocular larva migrans (Toxocara canis or Toxocara cati)

Cutaneous larva migrans (Ancylostoma braziliense or Ancylostoma

caninum)

Dracunculus medinensis

Parastrongylus (Angiostrongylus) cantonensis

Parastrongylus (Angiostrongylus) costaricensis

Gnathostoma spinigerum

 Tissue nematodes have life cycles similar to those of intestinal nematodes, consisting of five distinct stages

including adult male and female worms and four larval stages. These organisms are distributed worldwide,

predominantly in the tropics and subtropics. The organisms are transmitted by three routes: biting and

subsequent blood-feeding arthropods (filarial worms), ingestion of small freshwater crustaceans; and ingestion

of contaminated meat. In most cases, adult worms do not multiply and develop within the human host. Clinical

symptoms are dependent on the number of infecting parasites, the tissue invaded, and the host’s general health

and immune response. Diagnosis is typically by th microscopic visualization of the organisms in tissue when

appropriate.

Trichinella spiralis:

General characteristics:

The family Trichinellidae contains 11 recognized species including Trichinella spiralis, Trichinella nativa,

Trichinella nelsoni, T. murrelli, T. papuae, T. zimbabwensis, T. pseudospiralis, and T. britovi, all capable of

causing trichinosis.

However, T. spiralis is the most common human pathogen. The organism is unique in comparison to other

helminths in that all stages of development, including the adult and larval stages, occur within a single host.

Epidemiology

Trichinella occurs worldwide with the cycle maintained in several different mammalian species. The mammal

serves as the definitive host for the adult worm and the intermediate host for the encysted larvae. Humans

acquire the infection by eating undercooked meat that contains the infective encysted larvae. Although this is

typically transmitted in pork, human cases have been associated with ingestion of bear, walrus, horsemeat, and

other mammals.

The encysted larvae are ingested. When the undercooked meat is digested in the stomach, the larvae are

resistant to the gastric pH and pass to the intestine, where they invade the mucosa. In about 1.5 days, the larvae

mature and mate, and the female worm begins to

release motile larvae. These larvae then migrate to the lymphatic system or mesenteric venules and become

distributed throughout the body. The larvae then deposit

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in the striated muscle tissue, where they can continue development, coil, and encyst, becoming infective. The

larvae encyst in the active striated muscle including the

diaphragm, larynx, tongue, jaws, neck, ribs, biceps, and gastrocnemius.. The larvae may remain viable within

the cyst for several years. The larvae eventually die and the

encysted capsules become calcified.

Pathogenesis and spectrum of disease

Trichinosis is a disease of the muscle caused by infection with the encysted larval form of Trichinella spp.

(Figure 43). The adult stages reside in the human intestine.

The disease ranges from mild to severe dependent on the number of parasites present. The intestinal stage lasts

approximately 1 week and typically includes mild symptoms of nausea, abdominal discomfort, diarrhea, and/or

constipation. Diarrhea may last as long as 14 weeks with no apparent muscle involvement. The migration of the

larvae results in an intense inflammatory response causing periorbital edema, fever, muscle pain or

tenderness, headache, and myalgia. A marked peripheral eosinophilia is often present. If the parasitic infection

is low, eosinophilia may be the only diagnostic sign evident.

Occasionally, splinter hemorrhages may be present below the nails.

In addition to the typical infection of the active striated muscle as previously indicated, occasionally larvae will

migrate into the brain, meninges, and myocardium.

However, the larvae will not encyst in these tissues. Brain and meningeal infections will result in neurologic

symptoms, and infection of the myocardium may result in myocarditis and dysrhythmias leading to sudden

death.

Laboratory diagnosis :

 Diagnosis may be difficult, because the symptoms may resemble a variety of flulike illnesses. A thorough

patient history is required to assist the physician in diagnosing the condition in a timely fashion. Identification

of encysted larvae through muscle biopsy provides definitive diagnosis. However, based on location, some

Figure 43: Trichinosis. Encysted larvae within tissue.

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tissues may be difficult to access and therefore the condition may not be diagnosed until the postmortem

examination.

Histologic examination of formalin-fixed or paraffin-imbedded tissue may be used to visualize encysted larvae.