Parasite In The City Pregnant

Higher prevalence of infections by any intestinal parasite was found in of intestinal parasitism in Bogotá focused on pregnant women living in. fnatet.se Búsqueda 'hentai parasite monster pregnant anime creampie', vídeos de sexo gratis. Parasite in City FULL GALLERY AND OMAKE. ,8K 98%. Schau' 3d Parasite Pornos gratis, hier auf fnatet.se Entdecke die immer 4:​02 HD. Parasites in City - Bugs & LadyZombie Extended scenes · chaosprn. Parasites in the City Extended - Creatures Parasites in City - Bugs & LadyZombie Extended scenes Cute Pregnant Teen cumming Hard in the Car public. Es wurden hentai parasite GRATIS-Videos auf XVIDEOS bei dieser Suche Parasite in City - Gallery Scene 1-Test (benutzerdefinierte VO- und.

Parasite in the city pregnant

fnatet.se Búsqueda 'hentai parasite monster pregnant anime creampie', vídeos de sexo gratis. Parasite in City FULL GALLERY AND OMAKE. ,8K 98%. Conference: 4th International Congress of Parasitology & Parasite Diseases Among Pregnant and Abortive Women of Gonabad City In Nor. Higher prevalence of infections by any intestinal parasite was found in of intestinal parasitism in Bogotá focused on pregnant women living in.

But, given that medications for parasites have been shown to be safe and effective during pregnancy, efforts to provide these treatments during pregnancy should be increased, they conclude.

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Thank you! Category: Biomedical research. Category: Infectious disease. Infectious disease. With prolonged use at higher doses, it has been associated with congenital defects, neonatal deafness, blindness, and central nervous system disturbances.

Occasional gastrointestinal discomfort may be observed. Primaquine is contraindicated during pregnancy. Treatment with primaquine should be delayed until after delivery.

It may cause hemolytic anemia in patients with glucosephosphate dehydrogenase. Gastrointestinal discomfort may be observed.

Primaquine is not required in treatment of congenital or transfusion malaria or P. Recommended dosage of quinidine is not contraindicated in life-threatening chloroquine-resistant P.

Higher doses and prolonged use are contraindicated during pregnancy because of the association with abortion and hemolytic anemia.

Arrhythmia, tinnitus, hypotension, nausea, abdominal pain, visual disturbance, and blood dyscrasia may be seen. Parenteral quinidine is limited due to associated cardiac arrhythmia.

Because of the high prevalence of this disease, all patients with P. The current recommendation for the treatment of uncomplicated P.

Quinidine is cardiotoxic and may cause cardiac arrhythmias; therefore, electrocardiogram and blood pressure monitoring should be performed throughout the infusion period.

Mefloquine is not recommended in pregnancy due to the teratogenic effects, and it should not be given with quinidine or quinine.

For severe cases of cerebral malaria, quinidine plus clindamycin IV or doxycycline IV should be used. The toxic effect of doxycycline on bone formation also would make this drug less optimal in pregnant patients.

For treatment of P. Chloroquine apparently is well tolerated during pregnancy at these doses. For radical cure of P.

This drug is effective in eradicating latent hepatic infection for these two species, and hence is not necessary for the treatment of P.

Primaquine is not necessary for the treatment of congenital malaria because it is a form of transfusion malaria and does not have an exoerythrocytic liver phase.

Because primaquine is potentially teratogenic, it should not be used during pregnancy. Chloraquin resistant P. In addition, patients with glucosephosphate dehydrogenase deficiency may experience hemolytic anemia from primaquine.

Relapses can be treated with chloroquine during pregnancy, and primaquine can be administered to the mother after delivery. Whenever radical cure with primaquine is indicated during pregnancy, chloroquine can be given once a week until delivery, at which time primaquine can be given.

Although the antimalarial drugs are potentially toxic during pregnancy, the risk of not treating the infection in the pregnant mother is far greater.

Chloroquine has not been found to have a harmful effect on the fetus when used in the recommended doses for malaria prophylaxis or treatment.

Blindness, auditory nerve injury, and central nervous system CNS disturbances have been noted with prolonged high doses of chloroquine. Hart and Naugton 27 described a patient who took excessive amounts of chloroquine for lupus erythematosus during four of her seven pregnancies.

The patient had one miscarriage at 4 months, two children with evidence of eighth nerve damage, and a third child with neonatal convulsions, hemihypertrophy of the body, and later development of a Wilms' tumor on that side.

Occasionally, gastrointestinal discomfort and temporary blurring of vision have been described. In large doses, quinidine may cause tinnitus, dizziness and, occasionally, nausea and vomiting.

However, side effects are unlikely with therapeutic doses for malaria. Other drugs, including pyrimethamine, trimethoprim, sulfa compounds, tetracycline, and primaquine, generally are contraindicated during pregnancy.

Pyrimethamine can cause inhibition of leukopoiesis and megaloblastic changes in the bone marrow when administered in higher than therapeutic doses.

Trimethoprim, which is closely related to pyrimethamine, also interferes with folic acid metabolism and is teratogenic at high doses in animals.

Neither drug should be prescribed during the first trimester of pregnancy, despite the lack of evidence that either drug is teratogenic in humans in the doses used for malaria.

Sulfonamides, dapsone, and primaquine produce hemolysis in patients with glucosedehydrogenase deficiency, and sulfonamides given at the end of pregnancy may increase the risk of kernicterus; therefore, they should not be used in the last week of pregnancy.

Tetracycline also is not recommended during pregnancy because it is a known potential teratogen, particularly if it is administered during the period of organogenesis 25—40th day of gestation or during the second trimester, when it inhibits bone growth and produces hypoplasia of deciduous teeth.

In areas of the world where malaria is endemic, the use of limited residual insecticides and chemoprophylaxis for pregnant women and children is recommended.

Mosquito contact should be minimized with the use of house screens, insecticide-treated bed nets, insect repellent, and insecticides.

Residents living in chloroquin sensitive holoendemic areas who become pregnant should take prophylactic antimalarials starting with an initial therapeutic dose to clear any preexisting parasitemia e.

Visitors to endemic areas should take prophylactic medication, such as chloroquine phosphate mg orally, once a week for the duration of their stay and for 6 weeks after returning or for the duration of pregnancy, whichever is longer, because delayed attacks of P.

Areas of chloroquine sensitive P. It is now recommended that all pregnant women living in areas of high or intermittent stable P.

This strategy is not recommended for areas of low or unstable transmission. Although amebiasis frequently may be seen in an asymptomatic carrier state, E.

Occasionally, extraintestinal complications, such as hepatic abscess, occur. Of the seven species of ameba that naturally parasitize the human mouth and intestine, only E.

Debate has centered on the possibility of there being two subspecies of E. Their pathogenicity, difference in size, and tendency to ingest host tissue also may be determined by complex environmental factors that include viruses or plasmids that encode for virulence.

The trophozoite dwells in the lumen or wall of the colon and divides by binary fission; in the presence of rapid transit, it may be passed unchanged in liquid stool.

It prefers anaerobic conditions and requires either bacteria or tissue substrates to satisfy nutritional requirements.

In the absence of diarrhea, the trophozoite usually will encyst and be passed in the stool. Cysts contain a single nucleus, glycogen vacuoles, and sausage-shaped chromatoid bodies.

As the cyst matures, it absorbs its cytoplasmic vacuoles and becomes quadrinucleate. In general, the cysts are highly resistant to environmental changes, chlorine concentrations found in water purification systems, and gastric acid.

The disease typically is transmitted by ingestion of the cyst forms due to fecal contamination of food or water. Excystment occurs during transit through the stomach and small intestine, with release of eight trophozoites, which migrate to the colon, where they undergo binary fission every 8 hours in the trophozoite stage.

Encystment of these organisms occurs when environmental conditions become unfavorable for continued trophozoite multiplication. Reasons for the enhanced severity of disease in these areas are not clear.

Symptoms associated with intestinal infection with E. Perhaps the most common illness associated with amebic disease is colonic irritation characterized by colicky lower abdominal pain, with or without diarrhea.

The stool may be loose, and mucus and blood may be present. On physical examination, abdominal tenderness may be present. During pregnancy, amebic disease appears to be more frequently associated with acute exacerbations of the disease and with more prominent symptoms.

The diarrhea is marked, and secondary signs include fluid loss and electrolyte imbalance, which may adversely effect the outcome of pregnancy. Fulminating attacks of amebic dysentery may be precipitated by pregnancy or the administration of corticosteroids.

Repeated severe attacks of intestinal amebiasis may lead to ulcerative postdysenteric colitis. In rare cases, an ameboma may be documented in the cecum radiologically, and may be misdiagnosed as adenocarcinoma of the cecum.

A severe complication of amebiasis is the development of hepatic abscess secondary to migration of E. Hepatic amebiasis does not appear to be a frequent complication of amebiasis in pregnancy.

On the contrary, hepatic abscess appears to be more common in asymptomatic infection of the colon than in symptomatic intestinal disease.

The abscess may develop insidiously, with fever, sweating, weight loss, and tender hepatomegaly. The abscess usually occurs singly, and is located in the posterior portion of the right lobe of the liver.

Occasionally, abscesses enlarge upward, producing a bulge in the diaphragmatic dome with sympathetic pleural effusions.

Other abscesses rupture through the diaphragm, producing an amebic pleural abscess. A more serious complication of hepatic amebiasis includes rupture into the pericardium and peritonenum.

The clinical signs associated with these occurrences are those of a moribund patient with signs of pleural effusion, pericardial tamponade, or acute abdomen, depending on the site of rupture.

Brain abscesses also have been described as a complication of extraintestinal amebiasis. They may manifest as seizures or coma. The diagnosis of intestinal amebiasis is based on identifying E.

Examination of multiple stools is necessary because cysts and trophozoites may be excreted variably. Liquid or semiformed stools should be examined immediately in a saline wet-mount preparation for the presence of motile trophozoites.

Additional stools should be placed in polyvinyl alcohol PVA or formalin and later concentrated by centrifugation in formalin-ether, which is effective in the identification of cysts.

In symptomatic patients, a specimen should be obtained during sigmoidoscopy and examined immediately by direct mount in saline on a warm microscope stage for motile erythrocyte-containing amebas.

The diagnosis of amebic liver abscess is based primarily on suspicion, and it must be distinguished from a mass lesion in the liver caused by pyogenic abscess or neoplasm.

Radioisotopic scanning, computed tomography, and ultrasonography of the liver are helpful in diagnosing amebic abscess, which will appear as a single defect in the right lobe.

Results of stool examination for amebas are usually negative, and frequently, the diagnosis is based on a positive serologic finding in conjunction with a characteristic hepatic scan.

The indirect hemagglutination test result is considered positive if antibody is present in a dilution of or greater. A diagnostic aspiration of liver at the point of localized tenderness may be performed that will yield an odorless, brownish liquid anchovy paste characteristic of amebic abscess.

This liquid typically is devoid of amebas because the parasite is localized more frequently to the capsule of the abscess. Invasive procedures should be avoided, and an empiric trial of metronidazole should be used in difficult diagnostic cases.

Therapy for amebiasis should be aimed at relief of symptoms; replacement of fluid, electrolytes, and blood; and eradication of the organism.

Many of the drugs recommended as amebicides may be toxic during pregnancy, and drug therapy during pregnancy should be tailored to the severity of symptoms.

Asymptomatic women who are known passers of E. Metronidazole mg three times a day orally for 5—10 days may then be given.

An alternative drug for asymptomatic infection is iodoquinol mg three times a day for 20 days. However, there is no information about the safety of iodoquinol in pregnancy.

Amebic liver abscess has occurred in a few patients who were treated for dysentery with metronidazole alone. In extraintestinal amebiasis, including hepatic abscess, metronidazole for 10 days is the drug of choice.

In patients who are severely ill, needle aspiration may be helpful, but in general, repeated use of needle aspiration of the liver is unnecessary.

Similarly, surgical attempts to correct amebic bowel perforation or peritonitis should be avoided. Dehydroemetine has been recommended for nonpregnant patients, but is contraindicated in pregnancy.

Metronidazole is mutagenic in bacteria, 45 and it has caused lung tumors in mice, but not in hamsters. If a patient is treated with metronidazole, she should avoid alcoholic beverages because a disulfiram Antabuse -like effect has been reported.

In addition, urine discoloration, vertigo, nausea, and diarrhea have been noted as side effects. Due to this concern, metronidazole is not recommended during the first trimester of pregnancy.

Dehydroemetine and iodoquinol are appropriate for use in a nonpregnant patient, but are contraindicated during pregnancy. Paromomycin, an effective luminal amebicide, is considered safe to use in pregnancy because it is poorly absorbed from the gastrointestinal tract.

Another drug similar in effectiveness to paromomycin is diloxanide furoate, given as mg three times a day for 10 days.

This drug is a luminal amebicide, and because absorption from the gastrointestinal tract is low, it is believed to be safe for use during pregnancy.

However, no data concerning possible teratogenic effects are available. Giardia lamblia is the leading protozoan cause of diarrhea in travelers and in waterborne outbreaks in the United States.

Giardiasis frequently is marked by persistent diarrhea and malabsorption and frequently is found in areas of poor sanitation and among populations that cannot maintain adequate personal hygiene.

Infection in humans is initiated after ingestion of the cyst form. Excystation occurs within the stomach and upper gastrointestinal tract.

The organism remains in the duodenum and upper jejunum, where the alkaline pH is favorable. Giardia multiplies by longitudinal fission, and the trophozoites attach firmly to the intestinal epithelial surface by means of a powerful sucking disk.

Under a microscope, its two nuclei and central parabasal body give the organism the appearance of a face with two large eyes. As the trophozoites pass into the colon, encystation occurs, and the cysts are excreted from the body.

Cysts may remain viable and infectious in water for longer than 3 months, and they may be infective after storage in tap water for 16 days. Infection is transmitted to another person through ingestion of fecally contaminated water containing Giardia cysts.

Giardiasis is found worldwide, with high prevalence rates in areas of poor sanitation. In the United States, G. Gastrectomy, decreased gastric acidity, and chronic pancreatitis in adults may increase susceptibility.

In addition, giardiasis frequently has been reported in patients with immunoglobulin deficiency, particularly those with a deficiency in intestinal immunoglobulin A.

Certain high-risk populations have a high prevalence rate, such as homosexually active men; travelers to Eastern Europe and the Soviet Republic; hikers; and residents of towns where occasional epidemics from contaminated water supplies have occurred.

Wild animals may serve as alternate hosts. Beavers were implicated in an outbreak in Camas, Washington. Similar outbreaks have been described among homes for the retarded and child day-care centers.

Similar to E. Symptomatic disease usually occurs 1—2 weeks after infection and is characterized by the sudden onset of watery, foul diarrhea, abdominal distension, flatulence, nausea, anorexia, and abdominal cramps.

The stools often are malodorous, loose, and mixed with mucus. Blood and fecal leukocytes rarely are present. This acute stage may last for 3—4 days; if not treated, it may progress to a chronic infection, which is associated with steatorrhea and malabsorption.

For unknown reasons, in many patients the infection resolves completely without treatment. Other persons who are infected have no symptoms, and the parasite load detectable in these patients may be far less than that detected in symptomatic patients.

If the disease progresses to a chronic infection, there may be periodic, brief episodes of loose, foul stools, which may be yellow and frothy and accompanied by increased abdominal distention and flatus.

Cramps are unusual in chronic infection, but anorexia, nausea, and midepigastric discomfort are frequent complaints.

Findings of malabsorption studies may be abnormal. A postgiardial lactose intolerance may develop in patients from ethnic groups with a predisposition to lactase deficiency after apparent eradication of parasites with specific therapy.

The adverse effects of Giardia infection on pregnancy are related to the associated diarrhea, fluid and electrolyte loss, and malabsorption, which may contribute adversely to the ultimate outcome of the pregnancy.

Maternal-to-fetal transmission has not been documented. If a pregnant woman has associated dysgammaglobulinemia, giardiasis may be severe and more resistant to therapy.

Pathogenesis of these abnormalities is poorly understood. Mechanical blockage of microvilli, deconjugation of bile salts, altered motility, and mucosal invasion have been suggested as possible mechanisms.

Patients with giardiasis and severe malabsorption have jejunal colonization with enterobacteria, suggesting that the bacteria may potentiate the mucosal lesion and be responsible for the development of malabsorption.

Jejunal biopsy of patients infected with Giardia sometimes shows flattening of microvilli in an inflammatory infiltrate. The diagnosis of giardiasis, which is based primarily on stool examination, often is difficult to document because of variable cyst and trophozoite excretion.

In the acute stage of the disease, stools frequently are watery and loose, and may contain the more labile trophozoites because of rapid bowel transit.

A direct saline smear or preservation of the stool in formalin or PVA may aid in the identification of this organism.

Semiformed or formed stool should be fixed in formalin, and a formalin-ether concentration used for identification of the cyst.

Frequently, when stool examinations repeatedly have negative results, duodenal intubation with aspiration of duodenal contents and duodenal biopsy may be useful in confirmation of the diagnosis.

The Enterotest is a gelatin capsule containing a string that can be used to sample the duodenal contents for Giardia trophozoites, thereby avoiding duodenal intubation and biopsy.

Another diagnostic test is an enzyme-linked immunosorbent assay for Giardia antigen in stool. It is equally sensitive and specific for Giardia diagnosis as the other tests, and is more applicable for larger epidemiologic studies.

Therapy for giardiasis in nonpregnant patients consists of treatment with either quinacrine hydrochloride mg three times a day for 5 days or metronidazole mg three times a day for 5 days.

Pregnant women should receive therapy only if they are severely symptomatic because the infection may be self-limited in many persons.

If symptoms persist or are severe, metronidazole may be used with the same reservations mentioned in the previous section.

Other drugs effective against Giardia include furazolidone and tinidazole, the latter of which is not licensed in the United States.

Furazolidone is not recommended by the Food and Drug Administration for use in pregnancy because it has induced mammary tumors in rats.

Trichomonas vaginalis is a pathogenic protozoan commonly found in the human genitourinary tract. Transmitted primarily by sexual intercourse, this organism causes vaginitis in women and nongonococcal urethritis in men.

It is estimated that more than million people worldwide are infected with this parasite annually. Trichomonads are known for their characteristic twitching, erratic motility due to four anterior flagella, which originate in an anterior kinetosomal complex.

A fifth flagellum is attached by a membrane that also originates from the kinetosomal complex. Within the organism, there is an anterior nucleus containing five chromosomes, a parabasal apparatus, a Golgi complex, and an axostyle, which runs through the center of the cell to form a posterior tail.

Large chromatic granules called hydrogenosomes are present within the cytoplasm, parallel to the axostyle.

Reproduction is by mitotic division and longitudinal fission, which occurs every 8—12 hours under optimal conditions. The pH is a critical growth-limiting factor because more robust and smaller organisms are observed in high pH ranges, and less motile, enlarged organisms are encountered at pH levels that are lower or higher than the optimum pH, 5.

The vaginal pH in trichomonal vaginitis usually is 5. The prevalence of trichomoniasis varies according to the type of population studied and the diagnostic techniques used for identification of the organism.

An increased risk of infection has been found in persons with multiple sex partners, poor personal hygiene, and low socioeconomic status.

Several investigators have shown a greater prevalence of trichomoniasis in blacks, multiparous women, women married at an early age, and pregnant women.

The peak incidence of trichomonal infection usually is 16—35 years of age. Seventy per cent of men who have had sexual contact with an infected woman within the previous 48 hours will harbor T.

Anecdotal data have suggested nonvenereal transmission, such as fomites, but it is believed that this mode of transmission is uncommon.

In women, T. There have been rare reports of extravaginal infection involving the fallopian tube, perinephric abscess, and cerebrospinal fluid.

In men, the urethra is most commonly infected, but T. The clinical manifestations of vaginal trichomonal infection range from asymptomatic carriage to severe vaginitis.

During pregnancy, infection with T. There is some evidence that growth of the parasite is enhanced in vitro by estrogens, and this finding may explain the severity of symptoms and tenacity of infection in colonized women during pregnancy or in those taking exogenous estrogens.

Although infection during pregnancy has not been studied carefully, other investigations have suggested that the presence of T.

In symptomatic disease, the patient may complain of malodorous discharge, dyspareunia, and dysuria. The patient may report postcoital bleeding, which may be due to cervicitis caused by T.

Abdominal pain and regional lymphadenopathy also may be present in a small number of patients with trichomoniasis. On physical examination, a purulent discharge may be present at the introitus and within the vagina; it may be characterized as a yellow-green homogeneous or frothy discharge.

This finding contrasts with the characteristic white floccular discharge of candidal vaginitis and the white homogeneous discharge of bacterial vaginosis.

The vulva may be erythematous and edematous, and excoriations may be present. The vagina and cervix also may be erythematous, and small punctate hemorrhages may be present on the cervix strawberry cervix.

There is conflicting information about the association of trichomonal vaginitis and puerperal fever and neonatal infection. There is little evidence that T.

It is unlikely that intrauterine infection occurs, although this possibility has never been disproved, and several studies have documented neonatal infection.

Typically, these infections are asymptomatic, although a vaginal discharge may develop. Maternal estrogen is metabolized by 3—4 weeks of age, and vaginal epithelium returns to a prepubescent state that is relatively resistant to T.

It is not clear whether a latent or asymptomatic state of T. In men, T. In some men, T. Reported complications in men include epididymitis, prostatitis, and balanoposthitis.

The diagnosis of trichomonal infection is independent on the identification of T. The saline wet-mount preparations are reliable, simple, and inexpensive, and treatment can be instituted immediately.

Although wet-mount preparation is less sensitive in asymptomatic patients who have a low concentration of T. Giemsa- and Papanicolaou-stained smears also have been useful in detecting T.

Metronidazole and other 5-nitroimidazoles, such as tinidazole and nimorazole, are recommended as standard therapy for trichomoniasis.

The recommended dosage of metronidazole for initial treatment of trichomonal infection is 2 g orally as a single dose.

Metronidazole blocks the metabolism of alcohol, and nausea, vomiting, and flushing may be exhibited when alcohol is taken simultaneously or soon after metronidazole administration.

Metronidazole is mutagenic for bacteria and capable of producing lung tumors in mice after prolonged administration, so many clinicians avoid the use of the drug during the first trimester of pregnancy.

However, extended follow-up studies of women who have taken metronidazole have not demonstrated an increased risk of cancer or teratogenicity.

Trypanosomes are minute, actively motile, fusiform protozoa characterized by the presence of one flagellum originating from an extranuclear, terminally located organelle containing deoxyribonucleic acid DNA , the kinetoplast.

This flagellum runs alongside the body of the protozoan and forms an undulating membrane. Both the undulating membrane and the free flagellum confer considerable motility to the protozoan.

Reproduction takes place by binary longitudinal fission. Morphologic characteristics of many varieties of trypanosomes are so nearly identical that they are distinguishable only by their pathogenicity for certain animals, differences in biochemical requirements, and ability to multiply in insects.

Three species are pathogenic in man; these include Trypanosoma gambiense West African trypanosomiasis , T. They are found primarily in South America.

The life cycle of these trypanosomes differs from species to species, including vectors and reservoir host other than man.

African trypanosomiasis is transmitted by Glossina species tsetse fly , and Chagas' disease is transmitted by reduviid bugs Triatoma species.

Reservoir hosts for each of the species include hogs, goats, and cattle for T. In general, after the bite of the vector, trypanosomes are inoculated into the subcutaneous tissue, where they multiply to produce a local chancre.

After the appearance of this lesion, the trypanosome spreads through the tissue spaces into the lymphatics, eventually spilling into the general circulation, where they continue to multiply by longitudinal fission.

The parasitemia is of low intensity, and at some time during the stage of dissemination, trypanosomes localize in the tissue of the reticuloendothelial system or the CNS.

After invading tissue cells, the trypanosome loses its undulating membrane and flagellum and assumes a leishmanial form, dividing by binary fission.

Eventually, new flagellated forms are produced, which re-enter the general circulation to initiate another cycle if ingested by the vector.

All trypanosomes have the potential for transplacental transmission, with resulting intrauterine infection of the fetus during parasitemia. Infective T.

South American trypanosomiasis apparently has fewer adverse effects on fertility and pregnancy. Five to 10 days after the bite of the tsetse fly, a local lesion of trypanoma may develop that eventually will ulcerate over the ensuing weeks.

Enlargement of lymph glands may develop several months later, particularly in the posterior cervical triangle. This condition is known as Winterbottom's sign.

The acute disease lasts a year and is characterized by irregular fever, headache, joint and muscle pain, and rash. Kerandel's sign, which consists of severe pain after pressure of the palms or over the ulner nerve, may be present.

Gradually, the chronic phase of the disease ensues, with development of characteristic CNS changes. Diffuse meningoencephalitis and meningomyelitis develop.

The fever and headache become pronounced, and the patient may have lethargy, melancholic attitude, mental retardation, low and tremulous speech, tremors of the tongue and limbs, and altered reflexes.

Death results from the disease or intercurrent infection, such as malaria, dysentery, or pneumonia. Onset of symptoms usually occurs a few days after the person has been bitten by the tsetse fly, but incubation periods of up to 3 weeks have been observed.

Rhodesian trypanosomiasis runs a more rapid and fatal course than does Gambian disease. The pathologic changes in acute disease are similar, but the febrile paroxysms are more frequent and severe, with less pronounced glandular enlargement.

Chronic lesions in the CNS are less frequently encountered, but mental disturbances may develop, indicating the presence of CNS complications.

After an incubation period of 1—2 weeks, there is an abrupt onset of daily fever. Erythematous rash and adenitis of the cervical, axillary, and iliac glands usually are observed.

This acute form of the disease most often is seen in children. Hepatosplenomegaly is typical, and involvement of the myocardium may result in congestive heart failure.

Chronic Chagas' disease develops more slowly and insidiously in persons who have no history of previous acute disease.

Diagnosis of trypanosomiasis depends on demonstration of the organism in the peripheral blood, in tissue, or on serologic tests. All three species of trypanosomes may be demonstrated in the peripheral blood in the early phases of infection.

However, in chronic disease, circulating trypanosomes are found less frequently, and elevated IgM and specific trypanosome antibody levels lead to definitive diagnosis.

For African trypanosomiasis, suramin is the most effective agent for non-CNS disease. Simultaneous treatment with steroids has been recommended to prevent the CNS toxicity associated with melarsoprol.

These drugs are believed to be toxic during pregnancy, but usually trypanosomiasis is associated with infertility and abortion and, in severe cases, death of the patient.

Thus, treatment with these drugs may be warranted. There are no drugs available for chemoprophylaxis that are safe for use during pregnancy. Leishmania are obligate intracellular protozoa of which four species are known to infect humans.

It causes the disease known as kala-azar, and is widely distributed throughout Asia, Europe, Africa, India, and the Western Hemisphere in parts of Central and South America.

The major vector is the sandfly Phlebotomus , and a variety of small animals are important reservoirs of the infection.

The various species of Leishmania are transmitted by the bite of sandflies belonging to the genus Phlebotomus. Sandflies acquire the protozoan directly from infected skin or by ingesting parasites circulating in the blood of the reservoir host.

In the sandfly, Leishmania transforms into a flagellate promastigote that is infective to humans. After inoculation of the promastigote into a human host, the organism enters macrophages of the reticuloendothelial system L.

After multiplication, daughter amastigotes reinvade neighboring histiocytes or, in the case of visceral leishmaniasis, disseminate throughout the reticuloendothelial system.

The visceral form of the disease has a prolonged incubation period that may vary from 2 weeks to 18 months. Fever, which often consists of two daily spikes, may be abrupt or gradual in onset.

It persists for 1—6 weeks, and then disappears, only to reappear at irregular intervals during the course of the disease.

Physical findings may include splenomegaly, lymphadenopathy, and hepatomegaly, with signs of portal hypotension and edema. Anemia and thrombocytopenia with hypergammaglobulin frequently are present and often are associated with bleeding.

As the disease advances, the skin becomes gray, and hyperpigmentation is noted in light-skinned persons. Most patients with visceral leishmaniasis are severely debilitated and infertile, although this form of leishmaniasis carries a potential risk of intrauterine fetal infection if pregnancy occurs during the early phase of the disease.

Increased fetal wastage almost always is associated with L. The clinical manifestations of cutaneous leishmaniasis are similar for L. The disease starts as a pruritic red papule at the site of inoculation.

The lesion grows to an average diameter of 2 cm or more and tends to ulcerate 2—6 months after the bite of the vector. These lesions tend to heal over a 1-year period.

However, destructive mucocutaneous lesions may develop years after healing of the primary lesion in L. Diagnosis of visceral leishmaniasis is made by finding leishmanial organisms in stained preparations of the blood, bone marrow, lymph nodes, or material obtained by splenic puncture.

Serologic tests are not specific, and the leishmanin skin test finding usually is negative in patients with kala-azar. Diagnosis of cutaneous leishmaniasis is based on suspicion and demonstration of the organism in scrapings or by culture.

The leishmanin skin test result usually is positive during the primary lesion period, but may revert to negative in rare cases of disseminated cutaneous leishmaniasis.

Cutaneous leishmaniasis is not known to carry serious risk to the mother or fetus, so treatment during pregnancy should be avoided and postponed until after delivery.

However, patients with visceral leishmaniasis must be treated immediately regardless of pregnancy. Sodium antimonylgluconate Pentostam is the drug of choice for all forms of leishmaniasis.

For cutaneous leishmaniasis, the dose is 0. Patients who do not respond to antimonials should be treated with amphotericin B, 0. Intestinal nematodes often are thought to be unimportant or novel causes of infection in humans.

Yet, in many low-income, rural communities in the southeast United States, half of the population may have infection with Ascaris lumbricoides, Trichuris trichiura, or both; in urban areas, immigrants from tropical countries constitute a substantial population with a high prevalence of intestinal infection.

In , Warren 92 estimated that 4 million persons in the United States were infected with Ascaris, 2. Maternal infection with these intestinal roundworms usually is benign, except when there is a heavy worm burden.

Diagnosis is important in symptomatic gastrointestinal disease, but treatment often can be avoided until after pregnancy because roundworm infection rarely is associated with severe complications of pregnancy or adverse fetal outcome.

Infection with more than one parasite is common, and the clinician should evaluate the patient thoroughly for other intestinal nematodes and protozoan parasites that can be transmitted by the fecal-oral route.

Ascaris is the most common helminthic infection of man, with an estimated prevalence of 1 billion infections, 4 million of which are in the United States.

The adults, which are 15—40 cm long, may pass up to , eggs per day. The eggs are excreted with the stool and embryonate for 3 weeks or more in a moist environment.

After full maturation and ingestion of the eggs, larvae hatch within the duodenum and pass into the venous circulation, where they migrate to the lungs and across the pulmonary capillary beds.

The larvae migrate up the respiratory bronchi, and are swallowed. They then reach their final destination within the jejunum.

The nematodes mature into full adults over the ensuing 3 months. The prevalence of ascariasis is highest in children between the ages of 1 and 12 years.

The infection is transmitted by ingestion of the embryonated eggs that have contaminated raw fruits or vegetables or through geophagia.

Direct human-to-human transmission without embryonation in the soil does not occur. During the migratory phase of the larvae, the nematodes may cause pneumonia characterized by marked eosinophilia.

This condition may be associated with fever, cough, wheezing, and migratory pulmonary infiltrates Loeffler's syndrome.

The severity of these symptoms may be related to the intensity of infection or to prior sensitization. Ascariasis also is a major cause of asthma in many endemic areas.

In heavy infections of between and worms, serious complications may occur, including obstruction of pancreatic and bile ducts, appendicitis, intussusception, volvulus, intestinal perforation, and intestinal obstruction.

Ascaris infection can cause a modest degree of malabsorption of fat, protein, and carbohydrate. Adult worms have been reported to invade the female genital tract and cause tubo-ovarian abscess, pelvic pain, and menorrhagia.

Diagnosis depends on the identification of characteristic eggs in the stool. Because of the enormous daily output of eggs by gravid ascarids, direct smear examination of the stool is sufficient for diagnosis.

Commonly, the recovery of an adult worm or identification of larvae in sputum or gastric aspirates may confirm the diagnosis. Treatment of ascariasis should be withheld during pregnancy until after delivery because these infections usually are not associated with a significant risk to the mother or fetus.

The drug of choice for treatment of intestinal infection in nonpregnant women is mebendazole mg twice a day for 3 days. Albendazole mg as a single dose is an alternative therapy.

Antitubulin agents such as albendazole, mebendazole, and thiobendazole should be considered teratogenic in light of recent animal studies.

Human infection with two species of hookworm, Ancylostoma duodenale and Necator americanus, is estimated to affect approximately one quarter of the world's population.

Adult hookworms are small, cylindrical, 1 cm-long gray-white nematodes. Hookworms reside predominantly in the upper small intestine, attached to the mucosa by their strong buccal capsule.

The average daily blood loss for N. Human hookworms have a mean life span of approximately 5 years, and an adult may lay an average of eggs daily.

After the eggs reach the soil, they will embryonate for 1—2 weeks, releasing rhabditiform larvae. These larvae are free living, but within several days, they molt to the filariform stage, which is infectious and penetrates the skin on contact of the host.

Often, a severely pruritic cutaneous eruption ground itch appears after penetration. The larvae follow a migratory pattern similar to that of Ascaris and may cause eosinophilic pneumonia.

The adults mature approximately 5 weeks after infection, and may live for 2—10 years. The larvae flourish in climates providing adequate rainfall and well-drained soil and in areas where a reservoir of human infection is maintained by fecal contamination of the soil.

Although larvae require relatively little moisture, drying and direct sunlight are destructive. The superficial position of larvae on the topsoil provides easy access for the penetration of human skin.

Major epidemiologic features of hookworm transmission concern methods of disposal of fecal waste and the habit of walking barefoot.

The major manifestations of hookworm disease are dependent on the stage of infection and the number of invading parasites. Invasion of the skin by infective larvae may result in the development of an erythematous maculopapular skin rash.

Edema with pruritus may appear primarily around the feet and between the toes. Migration of the larvae from the lung to the gastrointestinal tract may cause wheezing, cough, fever, and migratory pneumonitis.

Within the intestine, the clinical manifestations are directly proportional to the number of worms and related to the degree of tissue destruction and blood loss.

The distinction between asymptomatic infection with relatively few worms and disease produced by a sizable worm burden is clinically important, and can be quantitated roughly by fecal egg counts.

Abdominal pain, diarrhea, and weight loss usually are noticed only in heavy infection with hookworm.

The chronic manifestations of hookworm disease include iron deficiency anemia and hypoalbuminemia. Malabsorption also has been reported in children, but less commonly in adults.

During pregnancy, the main concern is iron deficiency anemia. However, in heavy infection with worms or more, the patient may have blood loss of 50 ml or more.

If blood loss continues, potentiating the anemia of pregnancy, complications such as cardiac insufficiency and anasarca may develop.

Therefore, a decision to treat a patient during pregnancy should be based on the degree of worm burden and the associated blood loss. Direct fecal smear examination is adequate for diagnosis of clinically significant hookworm infection.

For quantitative purposes, the modified Stoll method can be used to estimate the number of eggs per gram of feces. In pregnant women with a clinically high worm burden and significant anemia, therapy may be instituted with mebendazole, mg orally twice a day for 3 days.

As with many antihelmintic drugs, the safety of these medications has not been documented for use during pregnancy.

Supportive therapy should be instituted, including replacement of iron, vitamins, and protein, and blood transfusion, if indicated. Strongyloides is a colorless, semitransparent nematode that is 2.

Larvae typically hatch within the mucosa, bore through the epithelium to the intestinal lumen, and are passed in the feces. The larvae either molt and differentiate into adult males and females or metamorphose into filariform infective forms.

The filariform larvae may autoinfect through penetration of the intestinal mucosa from an existing infection or penetration of skin that comes in contact with infected soil.

The larvae are passed by the bloodstream to the lungs, where they migrate through the alveolar space and up the tracheobronchial tree, and subsequently are swallowed to their final habitat in the small intestine.

Deposition of eggs begins approximately 28 days after initial infection. Migration through the skin and the pulmonary system is associated with clinical complications similar to those described for Ascaris and hookworm.

Within the gastrointestinal tract, Strongyloides infection usually is asymptomatic, but may be associated with abdominal pain and tenderness.

In heavy infections, epigastric pain, tenderness, nausea, flatulence, vomiting, and diarrhea may be observed. Some patients complain of nausea, vomiting, and weight loss, with evidence of malabsorption or protein-losing enteropathy.

In debilitated immunosuppressed or steroid-treated patients, massive autoinfection with widespread dissemination of larvae to extraintestinal organs, including the CNS, may occur.

Definitive diagnosis depends on the finding of S. Frequently, repeated examinations may be necessary to exclude the diagnosis. Because of the potential for dissemination, pregnant women with Strongyloides infection should be monitored carefully and treated if any complications are suspected.

Otherwise, asymptomatic disease treatment may be instituted after delivery. Pinworm infection is one of the most common of all intestinal infections of humans in the United States, with an estimated 42 million cases.

Pinworm infection is particularly common among children and is not associated with any specific socioeconomic level. Enterobiasis is most prevalent in institutional groups and among members of the same family.

Adult female worms migrate to the anal canal at night, deposit approximately 10, eggs on the perianal skin, and subsequently die.

Each egg contains an embryo that develops into an infective larvae within a few hours. After an egg is ingested, the larvae are released within the small intestine and migrate down the bowel lumen to the cecum.

The adult matures in approximately 1 month. Occasionally, autoinfection occurs when the egg hatches in the perianal area and the larvae migrate into the bowel to mature.

The eggs are highly resistant to desiccation and will contaminate nightclothes and bed linen. Pinworm infections are primarily asymptomatic and rarely cause complications in pregnancy.

The major clinical manifestation of pinworm disease is itching, pruritus ani, and pruritus vulvae. Occasionally, the migration of the parasite produces ectopic disease, such as appendicitis, chronic salpingitis, vaginitis, or ulcerative lesions of the small and large bowel.

Diagnosis of pinworm is readily made by examination of an adhesive cellophane tape pressed against the perianal region early in the morning.

Treatment consists of a single dose of mebendazole mg orally that is repeated 2 weeks later.

Several rapid diagnostic tests RDTs have been developed recently avoiding the need for light microscopy in remote settings and potentially improving fever management in resource limited settings.

Quantification of parasitemia may be performed and then followed over the subsequent days of treatment to determine the effectiveness of therapy.

General textbooks on parasitology explain the morphologic differentiation of the four human species of Plasmodium.

After the diagnosis and speciation of malaria, treatment should be instituted immediately Table 1. Chloroquine is not toxic during pregnancy at these doses.

With prolonged use at higher doses, it has been associated with congenital defects, neonatal deafness, blindness, and central nervous system disturbances.

Occasional gastrointestinal discomfort may be observed. Primaquine is contraindicated during pregnancy. Treatment with primaquine should be delayed until after delivery.

It may cause hemolytic anemia in patients with glucosephosphate dehydrogenase. Gastrointestinal discomfort may be observed.

Primaquine is not required in treatment of congenital or transfusion malaria or P. Recommended dosage of quinidine is not contraindicated in life-threatening chloroquine-resistant P.

Higher doses and prolonged use are contraindicated during pregnancy because of the association with abortion and hemolytic anemia. Arrhythmia, tinnitus, hypotension, nausea, abdominal pain, visual disturbance, and blood dyscrasia may be seen.

Parenteral quinidine is limited due to associated cardiac arrhythmia. Because of the high prevalence of this disease, all patients with P. The current recommendation for the treatment of uncomplicated P.

Quinidine is cardiotoxic and may cause cardiac arrhythmias; therefore, electrocardiogram and blood pressure monitoring should be performed throughout the infusion period.

Mefloquine is not recommended in pregnancy due to the teratogenic effects, and it should not be given with quinidine or quinine.

For severe cases of cerebral malaria, quinidine plus clindamycin IV or doxycycline IV should be used.

The toxic effect of doxycycline on bone formation also would make this drug less optimal in pregnant patients. For treatment of P.

Chloroquine apparently is well tolerated during pregnancy at these doses. For radical cure of P. This drug is effective in eradicating latent hepatic infection for these two species, and hence is not necessary for the treatment of P.

Primaquine is not necessary for the treatment of congenital malaria because it is a form of transfusion malaria and does not have an exoerythrocytic liver phase.

Because primaquine is potentially teratogenic, it should not be used during pregnancy. Chloraquin resistant P. In addition, patients with glucosephosphate dehydrogenase deficiency may experience hemolytic anemia from primaquine.

Relapses can be treated with chloroquine during pregnancy, and primaquine can be administered to the mother after delivery.

Whenever radical cure with primaquine is indicated during pregnancy, chloroquine can be given once a week until delivery, at which time primaquine can be given.

Although the antimalarial drugs are potentially toxic during pregnancy, the risk of not treating the infection in the pregnant mother is far greater.

Chloroquine has not been found to have a harmful effect on the fetus when used in the recommended doses for malaria prophylaxis or treatment.

Blindness, auditory nerve injury, and central nervous system CNS disturbances have been noted with prolonged high doses of chloroquine. Hart and Naugton 27 described a patient who took excessive amounts of chloroquine for lupus erythematosus during four of her seven pregnancies.

The patient had one miscarriage at 4 months, two children with evidence of eighth nerve damage, and a third child with neonatal convulsions, hemihypertrophy of the body, and later development of a Wilms' tumor on that side.

Occasionally, gastrointestinal discomfort and temporary blurring of vision have been described. In large doses, quinidine may cause tinnitus, dizziness and, occasionally, nausea and vomiting.

However, side effects are unlikely with therapeutic doses for malaria. Other drugs, including pyrimethamine, trimethoprim, sulfa compounds, tetracycline, and primaquine, generally are contraindicated during pregnancy.

Pyrimethamine can cause inhibition of leukopoiesis and megaloblastic changes in the bone marrow when administered in higher than therapeutic doses.

Trimethoprim, which is closely related to pyrimethamine, also interferes with folic acid metabolism and is teratogenic at high doses in animals.

Neither drug should be prescribed during the first trimester of pregnancy, despite the lack of evidence that either drug is teratogenic in humans in the doses used for malaria.

Sulfonamides, dapsone, and primaquine produce hemolysis in patients with glucosedehydrogenase deficiency, and sulfonamides given at the end of pregnancy may increase the risk of kernicterus; therefore, they should not be used in the last week of pregnancy.

Tetracycline also is not recommended during pregnancy because it is a known potential teratogen, particularly if it is administered during the period of organogenesis 25—40th day of gestation or during the second trimester, when it inhibits bone growth and produces hypoplasia of deciduous teeth.

In areas of the world where malaria is endemic, the use of limited residual insecticides and chemoprophylaxis for pregnant women and children is recommended.

Mosquito contact should be minimized with the use of house screens, insecticide-treated bed nets, insect repellent, and insecticides.

Residents living in chloroquin sensitive holoendemic areas who become pregnant should take prophylactic antimalarials starting with an initial therapeutic dose to clear any preexisting parasitemia e.

Visitors to endemic areas should take prophylactic medication, such as chloroquine phosphate mg orally, once a week for the duration of their stay and for 6 weeks after returning or for the duration of pregnancy, whichever is longer, because delayed attacks of P.

Areas of chloroquine sensitive P. It is now recommended that all pregnant women living in areas of high or intermittent stable P. This strategy is not recommended for areas of low or unstable transmission.

Although amebiasis frequently may be seen in an asymptomatic carrier state, E. Occasionally, extraintestinal complications, such as hepatic abscess, occur.

Of the seven species of ameba that naturally parasitize the human mouth and intestine, only E.

Debate has centered on the possibility of there being two subspecies of E. Their pathogenicity, difference in size, and tendency to ingest host tissue also may be determined by complex environmental factors that include viruses or plasmids that encode for virulence.

The trophozoite dwells in the lumen or wall of the colon and divides by binary fission; in the presence of rapid transit, it may be passed unchanged in liquid stool.

It prefers anaerobic conditions and requires either bacteria or tissue substrates to satisfy nutritional requirements. In the absence of diarrhea, the trophozoite usually will encyst and be passed in the stool.

Cysts contain a single nucleus, glycogen vacuoles, and sausage-shaped chromatoid bodies. As the cyst matures, it absorbs its cytoplasmic vacuoles and becomes quadrinucleate.

In general, the cysts are highly resistant to environmental changes, chlorine concentrations found in water purification systems, and gastric acid.

The disease typically is transmitted by ingestion of the cyst forms due to fecal contamination of food or water. Excystment occurs during transit through the stomach and small intestine, with release of eight trophozoites, which migrate to the colon, where they undergo binary fission every 8 hours in the trophozoite stage.

Encystment of these organisms occurs when environmental conditions become unfavorable for continued trophozoite multiplication. Reasons for the enhanced severity of disease in these areas are not clear.

Symptoms associated with intestinal infection with E. Perhaps the most common illness associated with amebic disease is colonic irritation characterized by colicky lower abdominal pain, with or without diarrhea.

The stool may be loose, and mucus and blood may be present. On physical examination, abdominal tenderness may be present.

During pregnancy, amebic disease appears to be more frequently associated with acute exacerbations of the disease and with more prominent symptoms.

The diarrhea is marked, and secondary signs include fluid loss and electrolyte imbalance, which may adversely effect the outcome of pregnancy.

Fulminating attacks of amebic dysentery may be precipitated by pregnancy or the administration of corticosteroids.

Repeated severe attacks of intestinal amebiasis may lead to ulcerative postdysenteric colitis. In rare cases, an ameboma may be documented in the cecum radiologically, and may be misdiagnosed as adenocarcinoma of the cecum.

A severe complication of amebiasis is the development of hepatic abscess secondary to migration of E. Hepatic amebiasis does not appear to be a frequent complication of amebiasis in pregnancy.

On the contrary, hepatic abscess appears to be more common in asymptomatic infection of the colon than in symptomatic intestinal disease.

The abscess may develop insidiously, with fever, sweating, weight loss, and tender hepatomegaly. The abscess usually occurs singly, and is located in the posterior portion of the right lobe of the liver.

Occasionally, abscesses enlarge upward, producing a bulge in the diaphragmatic dome with sympathetic pleural effusions.

Other abscesses rupture through the diaphragm, producing an amebic pleural abscess. A more serious complication of hepatic amebiasis includes rupture into the pericardium and peritonenum.

The clinical signs associated with these occurrences are those of a moribund patient with signs of pleural effusion, pericardial tamponade, or acute abdomen, depending on the site of rupture.

Brain abscesses also have been described as a complication of extraintestinal amebiasis. They may manifest as seizures or coma.

The diagnosis of intestinal amebiasis is based on identifying E. Examination of multiple stools is necessary because cysts and trophozoites may be excreted variably.

Liquid or semiformed stools should be examined immediately in a saline wet-mount preparation for the presence of motile trophozoites. Additional stools should be placed in polyvinyl alcohol PVA or formalin and later concentrated by centrifugation in formalin-ether, which is effective in the identification of cysts.

In symptomatic patients, a specimen should be obtained during sigmoidoscopy and examined immediately by direct mount in saline on a warm microscope stage for motile erythrocyte-containing amebas.

The diagnosis of amebic liver abscess is based primarily on suspicion, and it must be distinguished from a mass lesion in the liver caused by pyogenic abscess or neoplasm.

Radioisotopic scanning, computed tomography, and ultrasonography of the liver are helpful in diagnosing amebic abscess, which will appear as a single defect in the right lobe.

Results of stool examination for amebas are usually negative, and frequently, the diagnosis is based on a positive serologic finding in conjunction with a characteristic hepatic scan.

The indirect hemagglutination test result is considered positive if antibody is present in a dilution of or greater. A diagnostic aspiration of liver at the point of localized tenderness may be performed that will yield an odorless, brownish liquid anchovy paste characteristic of amebic abscess.

This liquid typically is devoid of amebas because the parasite is localized more frequently to the capsule of the abscess.

Invasive procedures should be avoided, and an empiric trial of metronidazole should be used in difficult diagnostic cases.

Therapy for amebiasis should be aimed at relief of symptoms; replacement of fluid, electrolytes, and blood; and eradication of the organism. Many of the drugs recommended as amebicides may be toxic during pregnancy, and drug therapy during pregnancy should be tailored to the severity of symptoms.

Asymptomatic women who are known passers of E. Metronidazole mg three times a day orally for 5—10 days may then be given. An alternative drug for asymptomatic infection is iodoquinol mg three times a day for 20 days.

However, there is no information about the safety of iodoquinol in pregnancy. Amebic liver abscess has occurred in a few patients who were treated for dysentery with metronidazole alone.

In extraintestinal amebiasis, including hepatic abscess, metronidazole for 10 days is the drug of choice. In patients who are severely ill, needle aspiration may be helpful, but in general, repeated use of needle aspiration of the liver is unnecessary.

Similarly, surgical attempts to correct amebic bowel perforation or peritonitis should be avoided. Dehydroemetine has been recommended for nonpregnant patients, but is contraindicated in pregnancy.

Metronidazole is mutagenic in bacteria, 45 and it has caused lung tumors in mice, but not in hamsters. If a patient is treated with metronidazole, she should avoid alcoholic beverages because a disulfiram Antabuse -like effect has been reported.

In addition, urine discoloration, vertigo, nausea, and diarrhea have been noted as side effects. Due to this concern, metronidazole is not recommended during the first trimester of pregnancy.

Dehydroemetine and iodoquinol are appropriate for use in a nonpregnant patient, but are contraindicated during pregnancy. Paromomycin, an effective luminal amebicide, is considered safe to use in pregnancy because it is poorly absorbed from the gastrointestinal tract.

Another drug similar in effectiveness to paromomycin is diloxanide furoate, given as mg three times a day for 10 days. This drug is a luminal amebicide, and because absorption from the gastrointestinal tract is low, it is believed to be safe for use during pregnancy.

However, no data concerning possible teratogenic effects are available. Giardia lamblia is the leading protozoan cause of diarrhea in travelers and in waterborne outbreaks in the United States.

Giardiasis frequently is marked by persistent diarrhea and malabsorption and frequently is found in areas of poor sanitation and among populations that cannot maintain adequate personal hygiene.

Infection in humans is initiated after ingestion of the cyst form. Excystation occurs within the stomach and upper gastrointestinal tract.

The organism remains in the duodenum and upper jejunum, where the alkaline pH is favorable. Giardia multiplies by longitudinal fission, and the trophozoites attach firmly to the intestinal epithelial surface by means of a powerful sucking disk.

Under a microscope, its two nuclei and central parabasal body give the organism the appearance of a face with two large eyes. As the trophozoites pass into the colon, encystation occurs, and the cysts are excreted from the body.

Cysts may remain viable and infectious in water for longer than 3 months, and they may be infective after storage in tap water for 16 days. Infection is transmitted to another person through ingestion of fecally contaminated water containing Giardia cysts.

Giardiasis is found worldwide, with high prevalence rates in areas of poor sanitation. In the United States, G.

Gastrectomy, decreased gastric acidity, and chronic pancreatitis in adults may increase susceptibility. In addition, giardiasis frequently has been reported in patients with immunoglobulin deficiency, particularly those with a deficiency in intestinal immunoglobulin A.

Certain high-risk populations have a high prevalence rate, such as homosexually active men; travelers to Eastern Europe and the Soviet Republic; hikers; and residents of towns where occasional epidemics from contaminated water supplies have occurred.

Wild animals may serve as alternate hosts. Beavers were implicated in an outbreak in Camas, Washington. Similar outbreaks have been described among homes for the retarded and child day-care centers.

Similar to E. Symptomatic disease usually occurs 1—2 weeks after infection and is characterized by the sudden onset of watery, foul diarrhea, abdominal distension, flatulence, nausea, anorexia, and abdominal cramps.

The stools often are malodorous, loose, and mixed with mucus. Blood and fecal leukocytes rarely are present. This acute stage may last for 3—4 days; if not treated, it may progress to a chronic infection, which is associated with steatorrhea and malabsorption.

For unknown reasons, in many patients the infection resolves completely without treatment. Other persons who are infected have no symptoms, and the parasite load detectable in these patients may be far less than that detected in symptomatic patients.

If the disease progresses to a chronic infection, there may be periodic, brief episodes of loose, foul stools, which may be yellow and frothy and accompanied by increased abdominal distention and flatus.

Cramps are unusual in chronic infection, but anorexia, nausea, and midepigastric discomfort are frequent complaints. Findings of malabsorption studies may be abnormal.

A postgiardial lactose intolerance may develop in patients from ethnic groups with a predisposition to lactase deficiency after apparent eradication of parasites with specific therapy.

The adverse effects of Giardia infection on pregnancy are related to the associated diarrhea, fluid and electrolyte loss, and malabsorption, which may contribute adversely to the ultimate outcome of the pregnancy.

Maternal-to-fetal transmission has not been documented. If a pregnant woman has associated dysgammaglobulinemia, giardiasis may be severe and more resistant to therapy.

Pathogenesis of these abnormalities is poorly understood. Mechanical blockage of microvilli, deconjugation of bile salts, altered motility, and mucosal invasion have been suggested as possible mechanisms.

Patients with giardiasis and severe malabsorption have jejunal colonization with enterobacteria, suggesting that the bacteria may potentiate the mucosal lesion and be responsible for the development of malabsorption.

Jejunal biopsy of patients infected with Giardia sometimes shows flattening of microvilli in an inflammatory infiltrate. The diagnosis of giardiasis, which is based primarily on stool examination, often is difficult to document because of variable cyst and trophozoite excretion.

In the acute stage of the disease, stools frequently are watery and loose, and may contain the more labile trophozoites because of rapid bowel transit.

A direct saline smear or preservation of the stool in formalin or PVA may aid in the identification of this organism.

Semiformed or formed stool should be fixed in formalin, and a formalin-ether concentration used for identification of the cyst.

Frequently, when stool examinations repeatedly have negative results, duodenal intubation with aspiration of duodenal contents and duodenal biopsy may be useful in confirmation of the diagnosis.

The Enterotest is a gelatin capsule containing a string that can be used to sample the duodenal contents for Giardia trophozoites, thereby avoiding duodenal intubation and biopsy.

Another diagnostic test is an enzyme-linked immunosorbent assay for Giardia antigen in stool. It is equally sensitive and specific for Giardia diagnosis as the other tests, and is more applicable for larger epidemiologic studies.

Therapy for giardiasis in nonpregnant patients consists of treatment with either quinacrine hydrochloride mg three times a day for 5 days or metronidazole mg three times a day for 5 days.

Pregnant women should receive therapy only if they are severely symptomatic because the infection may be self-limited in many persons.

If symptoms persist or are severe, metronidazole may be used with the same reservations mentioned in the previous section. Other drugs effective against Giardia include furazolidone and tinidazole, the latter of which is not licensed in the United States.

Furazolidone is not recommended by the Food and Drug Administration for use in pregnancy because it has induced mammary tumors in rats.

Trichomonas vaginalis is a pathogenic protozoan commonly found in the human genitourinary tract. Transmitted primarily by sexual intercourse, this organism causes vaginitis in women and nongonococcal urethritis in men.

It is estimated that more than million people worldwide are infected with this parasite annually. Trichomonads are known for their characteristic twitching, erratic motility due to four anterior flagella, which originate in an anterior kinetosomal complex.

A fifth flagellum is attached by a membrane that also originates from the kinetosomal complex. Within the organism, there is an anterior nucleus containing five chromosomes, a parabasal apparatus, a Golgi complex, and an axostyle, which runs through the center of the cell to form a posterior tail.

Large chromatic granules called hydrogenosomes are present within the cytoplasm, parallel to the axostyle. Reproduction is by mitotic division and longitudinal fission, which occurs every 8—12 hours under optimal conditions.

The pH is a critical growth-limiting factor because more robust and smaller organisms are observed in high pH ranges, and less motile, enlarged organisms are encountered at pH levels that are lower or higher than the optimum pH, 5.

The vaginal pH in trichomonal vaginitis usually is 5. The prevalence of trichomoniasis varies according to the type of population studied and the diagnostic techniques used for identification of the organism.

An increased risk of infection has been found in persons with multiple sex partners, poor personal hygiene, and low socioeconomic status.

Several investigators have shown a greater prevalence of trichomoniasis in blacks, multiparous women, women married at an early age, and pregnant women.

The peak incidence of trichomonal infection usually is 16—35 years of age. Seventy per cent of men who have had sexual contact with an infected woman within the previous 48 hours will harbor T.

Anecdotal data have suggested nonvenereal transmission, such as fomites, but it is believed that this mode of transmission is uncommon.

In women, T. There have been rare reports of extravaginal infection involving the fallopian tube, perinephric abscess, and cerebrospinal fluid.

In men, the urethra is most commonly infected, but T. The clinical manifestations of vaginal trichomonal infection range from asymptomatic carriage to severe vaginitis.

During pregnancy, infection with T. There is some evidence that growth of the parasite is enhanced in vitro by estrogens, and this finding may explain the severity of symptoms and tenacity of infection in colonized women during pregnancy or in those taking exogenous estrogens.

Although infection during pregnancy has not been studied carefully, other investigations have suggested that the presence of T.

In symptomatic disease, the patient may complain of malodorous discharge, dyspareunia, and dysuria. The patient may report postcoital bleeding, which may be due to cervicitis caused by T.

Abdominal pain and regional lymphadenopathy also may be present in a small number of patients with trichomoniasis. On physical examination, a purulent discharge may be present at the introitus and within the vagina; it may be characterized as a yellow-green homogeneous or frothy discharge.

This finding contrasts with the characteristic white floccular discharge of candidal vaginitis and the white homogeneous discharge of bacterial vaginosis.

The vulva may be erythematous and edematous, and excoriations may be present. The vagina and cervix also may be erythematous, and small punctate hemorrhages may be present on the cervix strawberry cervix.

There is conflicting information about the association of trichomonal vaginitis and puerperal fever and neonatal infection.

There is little evidence that T. It is unlikely that intrauterine infection occurs, although this possibility has never been disproved, and several studies have documented neonatal infection.

Typically, these infections are asymptomatic, although a vaginal discharge may develop. Maternal estrogen is metabolized by 3—4 weeks of age, and vaginal epithelium returns to a prepubescent state that is relatively resistant to T.

It is not clear whether a latent or asymptomatic state of T. In men, T. In some men, T. Reported complications in men include epididymitis, prostatitis, and balanoposthitis.

The diagnosis of trichomonal infection is independent on the identification of T. The saline wet-mount preparations are reliable, simple, and inexpensive, and treatment can be instituted immediately.

Although wet-mount preparation is less sensitive in asymptomatic patients who have a low concentration of T. Giemsa- and Papanicolaou-stained smears also have been useful in detecting T.

Metronidazole and other 5-nitroimidazoles, such as tinidazole and nimorazole, are recommended as standard therapy for trichomoniasis.

The recommended dosage of metronidazole for initial treatment of trichomonal infection is 2 g orally as a single dose. Metronidazole blocks the metabolism of alcohol, and nausea, vomiting, and flushing may be exhibited when alcohol is taken simultaneously or soon after metronidazole administration.

Metronidazole is mutagenic for bacteria and capable of producing lung tumors in mice after prolonged administration, so many clinicians avoid the use of the drug during the first trimester of pregnancy.

However, extended follow-up studies of women who have taken metronidazole have not demonstrated an increased risk of cancer or teratogenicity.

Trypanosomes are minute, actively motile, fusiform protozoa characterized by the presence of one flagellum originating from an extranuclear, terminally located organelle containing deoxyribonucleic acid DNA , the kinetoplast.

This flagellum runs alongside the body of the protozoan and forms an undulating membrane. Both the undulating membrane and the free flagellum confer considerable motility to the protozoan.

Reproduction takes place by binary longitudinal fission. Morphologic characteristics of many varieties of trypanosomes are so nearly identical that they are distinguishable only by their pathogenicity for certain animals, differences in biochemical requirements, and ability to multiply in insects.

Three species are pathogenic in man; these include Trypanosoma gambiense West African trypanosomiasis , T. They are found primarily in South America.

The life cycle of these trypanosomes differs from species to species, including vectors and reservoir host other than man.

African trypanosomiasis is transmitted by Glossina species tsetse fly , and Chagas' disease is transmitted by reduviid bugs Triatoma species.

Reservoir hosts for each of the species include hogs, goats, and cattle for T. In general, after the bite of the vector, trypanosomes are inoculated into the subcutaneous tissue, where they multiply to produce a local chancre.

After the appearance of this lesion, the trypanosome spreads through the tissue spaces into the lymphatics, eventually spilling into the general circulation, where they continue to multiply by longitudinal fission.

The parasitemia is of low intensity, and at some time during the stage of dissemination, trypanosomes localize in the tissue of the reticuloendothelial system or the CNS.

After invading tissue cells, the trypanosome loses its undulating membrane and flagellum and assumes a leishmanial form, dividing by binary fission.

Eventually, new flagellated forms are produced, which re-enter the general circulation to initiate another cycle if ingested by the vector.

All trypanosomes have the potential for transplacental transmission, with resulting intrauterine infection of the fetus during parasitemia.

Infective T. South American trypanosomiasis apparently has fewer adverse effects on fertility and pregnancy.

Five to 10 days after the bite of the tsetse fly, a local lesion of trypanoma may develop that eventually will ulcerate over the ensuing weeks.

Enlargement of lymph glands may develop several months later, particularly in the posterior cervical triangle. This condition is known as Winterbottom's sign.

The acute disease lasts a year and is characterized by irregular fever, headache, joint and muscle pain, and rash.

Kerandel's sign, which consists of severe pain after pressure of the palms or over the ulner nerve, may be present.

Gradually, the chronic phase of the disease ensues, with development of characteristic CNS changes. Diffuse meningoencephalitis and meningomyelitis develop.

The fever and headache become pronounced, and the patient may have lethargy, melancholic attitude, mental retardation, low and tremulous speech, tremors of the tongue and limbs, and altered reflexes.

Death results from the disease or intercurrent infection, such as malaria, dysentery, or pneumonia. Onset of symptoms usually occurs a few days after the person has been bitten by the tsetse fly, but incubation periods of up to 3 weeks have been observed.

Rhodesian trypanosomiasis runs a more rapid and fatal course than does Gambian disease. The pathologic changes in acute disease are similar, but the febrile paroxysms are more frequent and severe, with less pronounced glandular enlargement.

Chronic lesions in the CNS are less frequently encountered, but mental disturbances may develop, indicating the presence of CNS complications.

After an incubation period of 1—2 weeks, there is an abrupt onset of daily fever. Erythematous rash and adenitis of the cervical, axillary, and iliac glands usually are observed.

This acute form of the disease most often is seen in children. Hepatosplenomegaly is typical, and involvement of the myocardium may result in congestive heart failure.

Chronic Chagas' disease develops more slowly and insidiously in persons who have no history of previous acute disease. Diagnosis of trypanosomiasis depends on demonstration of the organism in the peripheral blood, in tissue, or on serologic tests.

All three species of trypanosomes may be demonstrated in the peripheral blood in the early phases of infection.

However, in chronic disease, circulating trypanosomes are found less frequently, and elevated IgM and specific trypanosome antibody levels lead to definitive diagnosis.

For African trypanosomiasis, suramin is the most effective agent for non-CNS disease. Simultaneous treatment with steroids has been recommended to prevent the CNS toxicity associated with melarsoprol.

These drugs are believed to be toxic during pregnancy, but usually trypanosomiasis is associated with infertility and abortion and, in severe cases, death of the patient.

Thus, treatment with these drugs may be warranted. There are no drugs available for chemoprophylaxis that are safe for use during pregnancy.

Leishmania are obligate intracellular protozoa of which four species are known to infect humans. It causes the disease known as kala-azar, and is widely distributed throughout Asia, Europe, Africa, India, and the Western Hemisphere in parts of Central and South America.

The major vector is the sandfly Phlebotomus , and a variety of small animals are important reservoirs of the infection.

The various species of Leishmania are transmitted by the bite of sandflies belonging to the genus Phlebotomus. Sandflies acquire the protozoan directly from infected skin or by ingesting parasites circulating in the blood of the reservoir host.

In the sandfly, Leishmania transforms into a flagellate promastigote that is infective to humans. After inoculation of the promastigote into a human host, the organism enters macrophages of the reticuloendothelial system L.

After multiplication, daughter amastigotes reinvade neighboring histiocytes or, in the case of visceral leishmaniasis, disseminate throughout the reticuloendothelial system.

The visceral form of the disease has a prolonged incubation period that may vary from 2 weeks to 18 months. Fever, which often consists of two daily spikes, may be abrupt or gradual in onset.

It persists for 1—6 weeks, and then disappears, only to reappear at irregular intervals during the course of the disease. Physical findings may include splenomegaly, lymphadenopathy, and hepatomegaly, with signs of portal hypotension and edema.

Anemia and thrombocytopenia with hypergammaglobulin frequently are present and often are associated with bleeding.

As the disease advances, the skin becomes gray, and hyperpigmentation is noted in light-skinned persons. Most patients with visceral leishmaniasis are severely debilitated and infertile, although this form of leishmaniasis carries a potential risk of intrauterine fetal infection if pregnancy occurs during the early phase of the disease.

Increased fetal wastage almost always is associated with L. The clinical manifestations of cutaneous leishmaniasis are similar for L.

The disease starts as a pruritic red papule at the site of inoculation. The lesion grows to an average diameter of 2 cm or more and tends to ulcerate 2—6 months after the bite of the vector.

These lesions tend to heal over a 1-year period. However, destructive mucocutaneous lesions may develop years after healing of the primary lesion in L.

Diagnosis of visceral leishmaniasis is made by finding leishmanial organisms in stained preparations of the blood, bone marrow, lymph nodes, or material obtained by splenic puncture.

Serologic tests are not specific, and the leishmanin skin test finding usually is negative in patients with kala-azar.

Diagnosis of cutaneous leishmaniasis is based on suspicion and demonstration of the organism in scrapings or by culture. The leishmanin skin test result usually is positive during the primary lesion period, but may revert to negative in rare cases of disseminated cutaneous leishmaniasis.

Cutaneous leishmaniasis is not known to carry serious risk to the mother or fetus, so treatment during pregnancy should be avoided and postponed until after delivery.

However, patients with visceral leishmaniasis must be treated immediately regardless of pregnancy. Sodium antimonylgluconate Pentostam is the drug of choice for all forms of leishmaniasis.

For cutaneous leishmaniasis, the dose is 0. Patients who do not respond to antimonials should be treated with amphotericin B, 0. Intestinal nematodes often are thought to be unimportant or novel causes of infection in humans.

Yet, in many low-income, rural communities in the southeast United States, half of the population may have infection with Ascaris lumbricoides, Trichuris trichiura, or both; in urban areas, immigrants from tropical countries constitute a substantial population with a high prevalence of intestinal infection.

In , Warren 92 estimated that 4 million persons in the United States were infected with Ascaris, 2. Maternal infection with these intestinal roundworms usually is benign, except when there is a heavy worm burden.

Diagnosis is important in symptomatic gastrointestinal disease, but treatment often can be avoided until after pregnancy because roundworm infection rarely is associated with severe complications of pregnancy or adverse fetal outcome.

Infection with more than one parasite is common, and the clinician should evaluate the patient thoroughly for other intestinal nematodes and protozoan parasites that can be transmitted by the fecal-oral route.

Ascaris is the most common helminthic infection of man, with an estimated prevalence of 1 billion infections, 4 million of which are in the United States.

The adults, which are 15—40 cm long, may pass up to , eggs per day. The eggs are excreted with the stool and embryonate for 3 weeks or more in a moist environment.

After full maturation and ingestion of the eggs, larvae hatch within the duodenum and pass into the venous circulation, where they migrate to the lungs and across the pulmonary capillary beds.

The larvae migrate up the respiratory bronchi, and are swallowed. They then reach their final destination within the jejunum.

The nematodes mature into full adults over the ensuing 3 months. The prevalence of ascariasis is highest in children between the ages of 1 and 12 years.

The infection is transmitted by ingestion of the embryonated eggs that have contaminated raw fruits or vegetables or through geophagia.

Direct human-to-human transmission without embryonation in the soil does not occur. During the migratory phase of the larvae, the nematodes may cause pneumonia characterized by marked eosinophilia.

This condition may be associated with fever, cough, wheezing, and migratory pulmonary infiltrates Loeffler's syndrome.

The severity of these symptoms may be related to the intensity of infection or to prior sensitization.

Ascariasis also is a major cause of asthma in many endemic areas. In heavy infections of between and worms, serious complications may occur, including obstruction of pancreatic and bile ducts, appendicitis, intussusception, volvulus, intestinal perforation, and intestinal obstruction.

Ascaris infection can cause a modest degree of malabsorption of fat, protein, and carbohydrate.

Adult worms have been reported to invade the female genital tract and cause tubo-ovarian abscess, pelvic pain, and menorrhagia. Diagnosis depends on the identification of characteristic eggs in the stool.

Because of the enormous daily output of eggs by gravid ascarids, direct smear examination of the stool is sufficient for diagnosis.

Commonly, the recovery of an adult worm or identification of larvae in sputum or gastric aspirates may confirm the diagnosis.

Treatment of ascariasis should be withheld during pregnancy until after delivery because these infections usually are not associated with a significant risk to the mother or fetus.

The drug of choice for treatment of intestinal infection in nonpregnant women is mebendazole mg twice a day for 3 days. Albendazole mg as a single dose is an alternative therapy.

Antitubulin agents such as albendazole, mebendazole, and thiobendazole should be considered teratogenic in light of recent animal studies. Human infection with two species of hookworm, Ancylostoma duodenale and Necator americanus, is estimated to affect approximately one quarter of the world's population.

Adult hookworms are small, cylindrical, 1 cm-long gray-white nematodes. Hookworms reside predominantly in the upper small intestine, attached to the mucosa by their strong buccal capsule.

The average daily blood loss for N. Human hookworms have a mean life span of approximately 5 years, and an adult may lay an average of eggs daily.

After the eggs reach the soil, they will embryonate for 1—2 weeks, releasing rhabditiform larvae. These larvae are free living, but within several days, they molt to the filariform stage, which is infectious and penetrates the skin on contact of the host.

Often, a severely pruritic cutaneous eruption ground itch appears after penetration. The larvae follow a migratory pattern similar to that of Ascaris and may cause eosinophilic pneumonia.

The adults mature approximately 5 weeks after infection, and may live for 2—10 years. The larvae flourish in climates providing adequate rainfall and well-drained soil and in areas where a reservoir of human infection is maintained by fecal contamination of the soil.

Although larvae require relatively little moisture, drying and direct sunlight are destructive. The superficial position of larvae on the topsoil provides easy access for the penetration of human skin.

Major epidemiologic features of hookworm transmission concern methods of disposal of fecal waste and the habit of walking barefoot.

The major manifestations of hookworm disease are dependent on the stage of infection and the number of invading parasites. Invasion of the skin by infective larvae may result in the development of an erythematous maculopapular skin rash.

Edema with pruritus may appear primarily around the feet and between the toes. Migration of the larvae from the lung to the gastrointestinal tract may cause wheezing, cough, fever, and migratory pneumonitis.

Within the intestine, the clinical manifestations are directly proportional to the number of worms and related to the degree of tissue destruction and blood loss.

The distinction between asymptomatic infection with relatively few worms and disease produced by a sizable worm burden is clinically important, and can be quantitated roughly by fecal egg counts.

Abdominal pain, diarrhea, and weight loss usually are noticed only in heavy infection with hookworm. The chronic manifestations of hookworm disease include iron deficiency anemia and hypoalbuminemia.

Malabsorption also has been reported in children, but less commonly in adults. During pregnancy, the main concern is iron deficiency anemia.

However, in heavy infection with worms or more, the patient may have blood loss of 50 ml or more. If blood loss continues, potentiating the anemia of pregnancy, complications such as cardiac insufficiency and anasarca may develop.

Therefore, a decision to treat a patient during pregnancy should be based on the degree of worm burden and the associated blood loss.

Direct fecal smear examination is adequate for diagnosis of clinically significant hookworm infection. For quantitative purposes, the modified Stoll method can be used to estimate the number of eggs per gram of feces.

In pregnant women with a clinically high worm burden and significant anemia, therapy may be instituted with mebendazole, mg orally twice a day for 3 days.

As with many antihelmintic drugs, the safety of these medications has not been documented for use during pregnancy. Supportive therapy should be instituted, including replacement of iron, vitamins, and protein, and blood transfusion, if indicated.

Strongyloides is a colorless, semitransparent nematode that is 2. Larvae typically hatch within the mucosa, bore through the epithelium to the intestinal lumen, and are passed in the feces.

The larvae either molt and differentiate into adult males and females or metamorphose into filariform infective forms.

The filariform larvae may autoinfect through penetration of the intestinal mucosa from an existing infection or penetration of skin that comes in contact with infected soil.

The larvae are passed by the bloodstream to the lungs, where they migrate through the alveolar space and up the tracheobronchial tree, and subsequently are swallowed to their final habitat in the small intestine.

Deposition of eggs begins approximately 28 days after initial infection. Migration through the skin and the pulmonary system is associated with clinical complications similar to those described for Ascaris and hookworm.

Within the gastrointestinal tract, Strongyloides infection usually is asymptomatic, but may be associated with abdominal pain and tenderness.

In heavy infections, epigastric pain, tenderness, nausea, flatulence, vomiting, and diarrhea may be observed.

Some patients complain of nausea, vomiting, and weight loss, with evidence of malabsorption or protein-losing enteropathy.

In debilitated immunosuppressed or steroid-treated patients, massive autoinfection with widespread dissemination of larvae to extraintestinal organs, including the CNS, may occur.

Definitive diagnosis depends on the finding of S. Frequently, repeated examinations may be necessary to exclude the diagnosis. Because of the potential for dissemination, pregnant women with Strongyloides infection should be monitored carefully and treated if any complications are suspected.

Otherwise, asymptomatic disease treatment may be instituted after delivery. Pinworm infection is one of the most common of all intestinal infections of humans in the United States, with an estimated 42 million cases.

Pinworm infection is particularly common among children and is not associated with any specific socioeconomic level.

Enterobiasis is most prevalent in institutional groups and among members of the same family. Adult female worms migrate to the anal canal at night, deposit approximately 10, eggs on the perianal skin, and subsequently die.

Each egg contains an embryo that develops into an infective larvae within a few hours. After an egg is ingested, the larvae are released within the small intestine and migrate down the bowel lumen to the cecum.

The adult matures in approximately 1 month. Occasionally, autoinfection occurs when the egg hatches in the perianal area and the larvae migrate into the bowel to mature.

The eggs are highly resistant to desiccation and will contaminate nightclothes and bed linen. The rest of the family 7 children and hubby -other than the 21 month old took the prescription stuff.

And we cleaned and cleaned-that was the worst part. This is gross, but you can check for pinworms by shining a flashlight on your littleones bottom between the cheeks at night.

You will actually see the white pinworms head towards the light. I know this because I worked in a pediatricians office and tried it when I thought my daughter might have them.

Be prepared to gross out! Quote from: bloombunchmama on June 22, , PM. Quote from: homeschooltheheart on June 22, , PM.

Quote from: Pennie on June 22, , PM. I suspected my daughter had them because she itched at night time. It was to the point that she couldn't sleep.

I was working for a pediatrician at the time and he mentioned pinworms and told me to use the flashlight method to see if she had them.

I was astonished and completely grossed out! The pinworms came crawling toward the light. We didn't do any cleaning or anything afterwards though.

The doctor gave us one tablet for each family members. It was the only time anyone in our family has had to deal with them. I thought this was so ironic.

I went to pick up some fish oil from my natropath and she put in a notice in my bag that she has dried calmyrna figs for sale. Therefore, figs are considered a vermifuge, which digests parasites.

This accounts for the fact that a fig tree never has a worm in it. Quote from: healthybratt on June 22, , PM. Very unsetttling to say the least!

Hi, I am new to this list and not too sure about navigating on a board so hope to learn a lot. I am a mom of 7 soon to be 8 in May and a student midwife.

I am seeking info on parasites for myself. As a family we do revolutionary reenactments at which we camp and I have picked up giardias from a bad water source.

After consulting with my midwife and researching I am definatley not comfortable taking allopathic medicine for this which I almost never do anyway and a lot of herbs are also out.

I am taking tons of garlic, going to look for some dried figs and pumkins seeds, just ordered the probiotic from beeyoutiful and am looking for any other suggestions or experiences.

Mostly, do you think this will work?? I have been doing the garlic for 5 days and am still daily experiencing symtoms. I just don't have alot of experience with parasites but have certainly been learning.

This forum looks great and I am looking forward to reading all the great posts. Thanks, CMS. I ate lots of fresh pineapple for about 3 days, I took garlic, and did a garlic enema.

Afterward I ate a lot of yogurt. I debated about the enema. I read a lot of conflicting information about the safety of it during pregnancy, but the risk seemed low since I have never ever had problems with early labor.

I also have a midwife book that actually recommends enemas during pregnancy for various problems. I had never done an enema before this time.

Shonda Parker's book says elecampane is good for pinworms and giardia. I didn't read this until later so I didn't try it. She is very good about warning against herbs that shouldn't be used during pregnancy and there is no such warning about elecampane on the parasites info page.

I hope this helps. I think what you've started will work. I would check into using Grapefruit Seed Extract.

I used GSE very effectively against ameobic dysentery years ago. It was the only thing that worked. Thanks for the info about the pineapple.

Which Shonda Parker book did you see the recommendation for elecampane? My midwife didn't recommend it in pregnancy but she and I both have Shondas books, must have missed that somewhere.

Grapefruit seed extract is contraindicated in pregnancy, I can't exactly quote why right now but it has to do something with bleeding.

There are so many things I would try if not pregnant, it puts a whole new spin on things. Thanks also for the link to the pinworm discussion, I had no idea that was why figs worked.

I am still taking my super moms, the garlic, and soon to get my probiotics and will add the pineapple and figs.

Love both of those. Thanks so much, CMS. HB--or other knowledgeable WTM-ers out there : What is your opinion of trying allopathic anti-parasitic treatments?

I didn't want to pursue this unless I can be certain of its effectiveness. Do any of you ladies have any knowledge or experience with this horrifying and embarrassing situation and effectiveness of traditional medical treatment??

I don't know anything about med treatments for parasites, but I do know from experience that Lamisil will kill yeast and from research that Nystatin is a very effective yeast killer.

Yeast Assassin or an equivalent supplement is supposed to do both but isn't recommended for nursing mommas as it tends to dry up the milk supply.

Quote from: gabi on May 13, , AM. I would definitely try to get rid of them now, and not wait 'til baby is born. They are stealing nutrients from you, and therefore, from your baby.

You certainly need all the nutrients you can get while pregnant and that little one is being built on the nutrients you provide. Here are a few excerpts from things I found online Who Needs God?

I haven't read this whole thread but the title caught my eye I caught some of something when I was pregnant and nursing in Ecuador several years ago.

GSE I think is a great thing for parasites while pregnant and nursing I would do 15 drops of nutribiotics x a time in the proper dilution of OJ.

Make sure you dilute properly and drink LOTS of water You don't want any detox to go to baby. I would also eat pumpkin seeds and LOTS of garlic and coconut oil.

I don't know I would drink lots and lots of water and have a healthy diet while doing all of this!

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