Parasitic Infestations

Parasitic Infestations
Basim Asmar, M.D. Wayne State University School of Medicine Children’s Hospital of Michigan Division of Infectious Diseases

Parasitic Infestations
Parasitic diseases: Caused by protozoa or helminths Parasitic protozoa & helminths: Referred to as animal parasites to distinguish them from bacteria, fungi & viruses Endoparasitic protozoa: A diverse group of >10,000 eukayotic unicellular animals Endoparasitic helminths of humans: Two phyla – (1) Platyheminths (flatworms) (2) Nematoda (round-worms)

Intestinal Parasitic Infestations Protozoa
Giardia lamblia (Giardiasis) A flagellated protozoan Infects the duodenum and upper part of the small intestine Infection is often asymptometic but can be associated with a variety of intestinal manifestations

Giardia lamblia

Giardia lamblia - Life Cycle
Infection occurs by the ingestion of cysts in contaminated water or food. In the small intestine, excystation releases trophozoites that multiply by longitudinal binary fission. The trophozoites remain in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk. Encystation occurs when the parasites transit toward the colon, and cysts are the stage found in normal (non diarrheal) feces. The cysts are hardy, can survive several months in cold water, and are responsible for transmission. Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.

Giardia lamblia

In wet mounts, cysts show the typical ovoid ellipsoid shape measuring from 8-19 mm (range 11-14 mm)

Giardia trophozoite (Trichrome stain x 1000)

Giardia lamblia 10-25 cysts sufficient to initiate infection
Colonization  morphologic damage to intestinal epihelial cells and brush border may result in normal microvilli or subtotal atrophy Disaccharidase deficiencies (usually lactase) Malabsorption affecting protein & fat-soluble vitamines Decreased intestinal absorption of antibiotics

Giardia lamblia Cysts viable for 3 months in water at 4o C
Freezing does not eliminate infectivity completely Heating, drying and sea water are likely to do so Human milk is lethal to Giardia trophozoites through the action of fatty acids Duodenal fluid is also lethal to Giardia Survival in hostile environment is attributed to the protective effect of human mucus

Giardia lamblia Anti-Giardia IgG is found in >80% of patients during symptomatic infection Anti-Giardia IgG tends to persist, thus limiting usefulness in distinguishing current from past infection Serum anti-Giardia IgM antibodies increase early in infection and decrease rapidly after 2-3 weeks Human milk protection against Giardia correlates with anti-Giardia serum IgA

Giardiasis Epidemiology
Occurs worldwide Age-specific prevalence: Highest in children 0-5 years Followed by years old Most cases reported in late summer and early fall Transmission is common in certain high risk populations: Children and employees in DCC’s Consumers of contaminated water Travelers to certain areas of the world Those exposed to domestic and wild animals (dogs, cats, cattle deer, and beaver)

Giardiasis Epidemiology
Major reservoir/vehicle for spread: Water contaminated with cysts Major risk for hikers: Drinking untreated mountain stream water Person-to-person spread: Frequent in areas of low hygienic standards/crowding Person-to-person spread occurs in: Childcare centers Families of children with diarrhea

Giardiasis Clinical Manifestations Symptom Percent Diarrhea 64-100
Malaise. Weakness Abdominal distension Flatulance Abdominal cramps Nausea Foul-smelling, greasy stools 15-79 Anorexia Weight loss Vomiting Fever Constipation

Giardiasis Clinical Manifestations Symptoms vary with age
Profuse watery stools  greasy, foul smelling, buoyant Blood, mucus & fecal leukocyte are absent Varying degrees of malabsorption can occur Abnormal stool patterns can alternate with constipation and normal bowel movements Infrequent associations: reactive arthritis, urticaria

Giardiasis Clinical Manifestations
Asymptomatic carriers in USA: %-7% (up to 20% in southern regions) Prevalence studies in DCC children <36 months: 21% Asymptomatic infection is well tolerated Testing of case contacts/treatment of asymptomatically infected individuals is NOT indicated routinely Humoral immunodeficienies (hypo-, agammaglobulinemia) predispose to chronic symptomatic giardiasis

Giardiasis Diagnosis Definitive Diagnosis: Stool specimens:
Detection of trophzoites, cysts or antigens in stool or duodenal fluid Stool specimens: Examined within 1 hour after being passed or should be stored in vials containing polyvinyl alcohol (PVA) or 10% formalin Trophozoites are more likely to be found in unformed stools (rapid transit time) Cysts, but not trophozoites, are stable outside the GI tract Duodenal Specimens: Aspirate/Biopsy  Trophozoites can be seen on direct wet mount

Giardiasis Diagnosis Microscopy: Antigen Detection:
Diagnostic: 70% of patients with single exam 85% with a second exam Antigen Detection: (Polyclonal antisera or monoclonal antibodies) EIA: 87%-100% sensitivity / 100% specificity DFA: 100% sensitivity/specificity Giardiasis is NOT associated with eosinophilia

Giardiasis Treatment Oral Antimicrobial Therapy for Giardiasis
Agent Pediatric Dose Adult Dose Metronidazole mg/k/d divided in 3 doses X 5d mg tid X 5d (Flagyl) Furazolidone mg/k/d divided in 3-4 doses X 10d mg tid X 10d (Furoxone) Albendazole mg/day X 5d mg/day X 5d (Albenza) Quinacrine mg/k/d divided in 3 doses X 5d mg tid X 5d (Atabrine) Nitazoxanide mo: 100 mg bid X 3d N/A (Alinia) yrs: 200 mg bid X 3d (100 mg/5 ml)

Giardiasis Prevention Strict hand washing after contact with feces
Purification of public water supplies Chlorination Sedimentation Filtration Avoid swallowing: recreational water, water from shallow wells, lakes, rivers, streams, ponds & springs Travelers to endemic areas: avoid drinking untreated water & uncooked foods that have been grown, washed or prepared in potentially contaminated water Purification of drinking water: Heating (55o C X 5 min) or use filter (pore size < 1 um)

Cryptosporidium parvum
Human disease caused by Cryptosporidiun was first described in 1976 The AIDS epidemic fueled interest in cryptosporidiosis Improved detection of oocysts in feces  infection is common cause of diarrhea in immunocompetent & immunocompromised hosts 2- to 6-um coccidian parasite that infects the epithelial cells lining the digestive and respiratory tract of vertebrates (fish, reptiles, and mamals, & humans)

Life cycle of Cryptosporidium parvum
Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces (1). Transmission of Cryptosporidium parvum occurs mainly through contact with contaminated water (e.g., drinking or recreational water) (2). Occasionally food sources, such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum occur through exposure to infected animals or exposure to water contaminated by feces of infected animals . Following ingestion (and possibly inhalation) by a suitable host (3), excystation occurs (a). The sporozoites are released and parasitize epithelial cells (b,c) of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) (d, e, f) and then sexual multiplication (gametogony) producing microgamonts (male) (g) and macrogamonts (female) (h). Upon fertilization of the macrogamonts by the microgametes (i), oocysts (j, k) develop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host (j), and the thin-walled oocyst (k), which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct& immediate fecal-oral transmission.

Cryptosporidium parvum

Cryptosporidium parvum Epidemiology
Crptosporidiosis is associated with diarrheal illness worldwide Transmission to humans: Close association with infected animals (calves, rodents, puppies, kittens) Person-to-person (DCC, Traveler’s diarrhea) Environmentally contaminated water ~130 oocysts can cause infection in immunocompetent

Cryptosporidium parvum Epidemiology
Outbreaks have been associated with contaminated community water supplies Waterborne outbreak in Milwaukee, WI (1985): ,000 cases of diarrhea 4400 were hospitalized Total cost: $96.2 million Swimming pool water & water from decorative fountains have been linked with outbreaks of crptosporodiosis

Cryptosporidiosis Epidemiology
More prevalent in underdeveloped countries & in children <2 years of age Most cases are not recognized Infection rates surveys in selected populations: Developed countries: 0.6%-20% Underdeveloped countries: up to 32% Difference is due to: Poor sanitation, lack of clean water, crowded living conditions, close association with animals

Cryptosporidiosis Clinical Manifestations
Incubation period: 2-14 days Diarrhea: Profuse watery diarrhea + mucus Rarely contains WBC’s or RBC’s Crampy abdominal pain, nausea, vomiting (50%) Fever is uncommon Infection may be asymptomtic, self-limited or protracted

Cryptosporidiosis Clinical Manifestations
Severity is linked with immunosuppression Most immunocompetent hosts: self-limited illness (10-14 days) Immunocompromised (HIV, malignancy): prolonged debilitating disease Oocysts shedding: up to 2 weeks after clinical improvement Biliary tract disease may occur in immunocompromised hosts (15%): Fever RUQ pain N,V,D Jaundice & elevated LFT’s can occur

Cryptosporidiosis Laboratory Diagnosis
Identification of oocysts in (1) stools or (2) along epithelial surface of biopsy tissue Highest concentration in jejunum Histology: villous atrophy, blunting, epithelial flattening Stool specimens for oocysts identification: Put in fixative (to prevent infection in lab workers) 3 specimens in immunocompetent 2 specimens in immunocompromised Auramine & rhodamine stain – most sensitive/expensive Acid fast stain – commonly used Not detected by routine O & P

Cryptosporidiosis Cryptosporidia are usually identified in stool specimens by a modified acid-fast stain. The left panel shows numerous red staining oocysts. In more difficult cases, a biopsy of small bowel or colon leads to the diagnosis. In the right panel, numerous basophilic cryptosporidia stud the surface of the enterocytes. Note the lack of inflammation.

Cryptosporidiosis – Small spherical organisms (red arrow) attached to the brush border of absorptive intestinal epithelial cells

Oocysts of Cryptosporidium visualized with Acid-fast stain

Oocysts of Cryptosporidium parvum

Cryptosporidiosis Treatment
In most immunocompetent: Self-limited; no therapy except adequate hydration In severe cases/immunocompromised hosts: A variety of agents have been used without consistent results Until recently the mainstay of treatment was supportive care Newly effective/FDA-approved agent: Nitazoxanide (Alinia): 12-47 mo: 100 mg bid X 3d 4-11 yrs: 200 mg bid X 3d (Concentration: 100 mg/5 ml)

Cryptosporidiosis Prevention
Hand washing: prevent person-to-person transmission Enteric precautions for hospitalized patients Cohort infected patients in hospital Immunocompromised hosts should take special precautions around animals Avoid swallowing recreational water Avoid drinking water from shallow wells, lakes, rivers, streams, ponds and springs

Entamoeba histolytica
Amebiasis Entamoeba histolytica Pseudopod-forming, non-flagellated protzoa Most invasive parasite of the Entamoeba group Only member that causes: Amebic colitis & liver abscess Life Cycle consists of: (1) Infectious cyst (2) Invasive trophzoite Trophozoites adhere to colonic mucin and epithelial cells  kill host epithelial & immune cells  tissue destruction

Entamoeba histolytica Entamoeba histolytica mature cyst
Amebiasis Entamoeba histolytica trophozoite Entamoeba histolytica mature cyst

Amebiasis Cysts are passed in feces(1). Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands (2). Excystation occurs in the small intestine(3)  trophozoites released  migrate to the large intestine (4). Trophozoites multiply by binary fission and produce cysts (5) passed in the feces. Cysts (protected by their cell walls) can survive days to weeks in the external environment and are responsible for transmission. In many cases, trophozoites remain confined to the intestinal lumen (noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients trophozoites invade the intestinal mucosa (intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease), with resultant pathologic manifestations. Invasive and noninvasive forms represent two separate species (E. histolytica & E. dispar respectively), however not all persons infected with E. histolytica will have invasive disease. These two species are morphologically indistinguishable. Transmission can also occur through fecal exposure during sexual contact (cysts, & also trophozoites could prove infective).

Trophozoites of Entamoeba histolytica (Trichrome stain)
Trophozoites of Entamoeba histolytica (Trichrome stain). Two diagnostic characteristics: Two of the trophozoites have ingested erythrocytes, and the nuclei have typically a small, centrally located karyosome, as well as thin, uniform peripheral chromatin.

Entamoeba histolytica Epidemiology
Greatest morbidity/mortality in the developing countries of Central & South America, Africa, and India Disease more severe in: The very young Elderly Pregnant women Worldwide: million symptomatic infections/year 100,000 deaths annually In Dhaka, Bangladesh, 50% of children have serologic evidence of E. histolytica infection by 5 years Groups at increased risk of amebiasis in developed nations: Immigrants from endemic areas Long-term visitors to endemic areas Institutionalized individuals

Entamoeba histolytica Clinical Manifestations
Amebic colitis Sign or Symptom % of Patients Affected Symptoms > 1 wk Most patients Diarrhea Dysentery Abdominal pain Weight loss Fever >38oC 10 Heme (+) stool Immigrant from or traveler to endemic area >50 Prevalence (male/female) /50

Amebic colitis Patients with chronic, non-dysenteric intestinal amebiasis may complain for months to years of abdominal pain, flatulence, intermittent diarrhea, mucus in the stools, and weight loss Chronic non-dysenteric intestinal amebiasis has been mistakinly diagnosed as ulcerative colitis

Amebic Colitis: Severe dysentery with multiple ulcers in the large bowel, and a bloody diarrhea

Entamoeba histolytica trophozoites in section of intestine (H&E)

Acute Fulminant or Necrotizing Colitis Unusual (about 0.5% of cases) A complication that occurs more frequently in patients inappropriately treated with corticosteroid Abdominal pain, distension, and rebound tenderness are present in most patients Indications for surgery: Failure of response to anti-amebic drugs after intestinal perforation/abscess formation Persistence of abdominal distention after institution of anti-amebic Rx Toxic megacolon

Histopathology of a typical flask-shaped ulcer of intestinal amebiasis

Ameboma Segmented mass of granulation tissue in the cecum or ascending colon Occurs in 0.5% to 1.5% of patients with intestinal amebiasis Tender palpable abdominal mass Concuurent amebic dysentery present in 2/3 of patients “Apple-core” lesions on barium enema study Lesions resolve with anti-amebic chemotherapy Intestinal constriction occurs in the colon in <1% of patients

Amebic Liver Abscess Develops in about 10% of patients with invasive E. histolytica infections Few patients have concurrent dysentery – most report dysentery within the preceding year Occurs in any age group Patients with a more chronic illness (2-12 weeks of symptoms) commonly present with hepatomegaly and weight loss

Amebic Liver Abscess Sign or Symptom % of Patients Affected Symptoms > 4 wks Fever Abdominal tenderness Hepatomegaly Jaundice Diarrhea Weight loss Cough Immigrant from or traveler to endemic area >50 Prevalence (male/female) /50 in children; 90/10 in adults

Gross pathology of liver containing amebic abscess

Gross pathology of amebic abscess of liver
Gross pathology of amebic abscess of liver. Tube of "chocolate" pus from abscess.

Entamoeba histolytica Laboratory Findings and Diagnosis
Differential Diagnosis of Amebic Dysentery: IBD Ischemic colitis Other infectious causes of bloody diarrhea Diagnostic Tests: EIA is best for specific diagnosis of amebiasis (Sensitivity & specificity of assay on stool >95%) Colonoscopy remains important to evaluate for other causes Serology for antibodies: IHA Positive in: 88% amebic dysentery, 70-80% liver abscess, % of general population

Entamoeba histolytica Laboratory Findings and Diagnosis
Differential Diagnosis of Amebic Liver Abscess: Pyogenic abscess Echinococcal cyst Hepatoma Diagnostic Tests: Ultrasonography CT MRI None differentiate amebic from pyogenic abscess Diagnosis is frequently a diagnosis of exclusion IHA: Acutely, E. Histolytica antibody can be detected in serum in 70-80% of cases EIA: Can detect E. histolytica antigen in serum in ~96% of patients with abscess

Amebic liver abscesses

Entamoeba histolytica Treatment
Asymptometic amebiais: Luminal agent (paromomycin, diloxanide furate, or iodohydroxyquin) Amebic Colitis: Metronidazole & a luminal agent Amebic Liver Absces: Metronidazole & a luminal agent

Entamoeba histolytica Prevention
Prevention of E. hisolytca transmission requires disruption of the fecal-oral spraed of amebic cysts Individuals should be advised regarding: Risk of traveling to endemic areas Safeguards to prevent ingesting colonic organisms Because humans and primates are the only known reservoirs of E. histolytica, a successful vaccine Could potentially eliminate this disease

Intestinal Nematodes Round Worms
The most common parasitic infections in humans; affect one quarter of the world population Remain a major cause of physical growth delay, cognitive delay, and malnutrition throughout the world In certain endemic populations, children are disproportionately affected Being increasingly encountered in the developed world In the USA, groups at increased risk include: international travelers, recent immigrants, refugees, and international adoptees

Ascaris lumbricoides The most common helminthic infection in humans
1.2 billion infected worldwide 51 million children are currently estimated to be infected Commonly affects children living in economically disadvantaged communities Ascariasis still occurs frequently in the USA as an imported infection in recent immigrants from Latin America and Asia & internationally adopted children Young children seem to be affected more severely than adults (larger worm burden, parasite-induced malnutrition)

Ascaris lumbricoides Adult worms live in the lumen of the small intestine (1). A female may produce approximately 200,000 eggs per day, which are passed with the feces (2) . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks(3) , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed (4) , the larvae hatch (5), invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs (6) . The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat (7), and are swallowed . Upon reaching the small intestine, they develop into adult worms (1) . Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.CDC

Ascaris lumbricoides Clinical Manifestations
Larvae migration through the lung parenchyma  mechanical and immune-mediated damage: Pulmonary microhemorrhages Inflammation & exudation of fluid Pulmonary infiltrates Cough, dyspnea, wheeezing, mild hemoptysis (Loffler pneumonia) Adult ascaris worms in the small bowel Epigastric pain Diffuse abdominal discomfort Heavy infestation  intestinal obstruction Chronic infection  malnutrition due partly to malabsorption (proteins, fat & vitamin A)

Ascaris lumbricoides

Ascaris lumbricoides Laboratory Findings/Diagnosis
Diagnosis is established by stool examination for characteristic ova. Each adult female produces so many eggs that a single stool specimen is adequate Migration of larvae through the lungs is assocaited with peripheral eosinophilia and pulmonary infiltrates on chest radiograph In endemic areas, any child presenting with signs suggestive of intestinal obstruction should be evaluated for Ascariasis

Ascaris lumbricoides Characteristic fertilized egg: Bile stained, mammillated thick external layer, unembryonated (55-75 um x um) Characteristic unfertilized egg: elongated & larger than fertile egg, thin shelled (85-95 um x um)

Ascaris lumbricoides Treatment
Mebendazole (100 mg twice daily X 3 days) or Albendazole (400 mg as a single dose) (The above are not generally given to children < 1 yr) Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days) In cases of partial bowel obstruction caused by Ascaris: alternative therapy with piperazine citrate, which paralyzes the worms may abrogate the need of surgical intervention

Ascaris lumbricoides Prevention
Elimination of contact with soil contaminated by egg-containing feces. In tropical areas, poor sanitation is responsible for infection rates approaching 100% Diagnosis, effective treatment, improved sanitation practices In endemic areas (infection rate is >50%), antihelmenthic agents administration to school-age children has been recommended as part of a targeted deworming program Sustained economic growth is most effective means of long-term parasite control

Hookworms Approximately 1 billion people harbor hookworms in their gastrointestinal tract A leading cause of iron deficiency anemia in the developing world Children are particularly vulnerable to the morbid effects of hookworms infections (often because dietary intake fails to compensate for intestinal losses of iron and serum proteins)

The two most common hookworms that infect humans: (1) Ancylostoma duodenale (2) Necator americanus Adult females:10-13 mm (A. duodenale), 9-11 mm (N. americanus) Adult males: 8-11 mm (A. duodenale), 7-9 mm (N. americanus) A smaller group of hookworms infecting animals can invade and parasitize humans (A. ceylanicum) or can penetrate the human skin (causing cutaneous larva migrans), but do not develop any further (A. braziliense, Uncinaria stenocephala).

Life Cycle: A. duodenale & N. americanus
Eggs are passed in the stool (1), and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil (2), and after 5 to 10 days (and two molts) they become become filariform (third-stage) larvae that are infective (3). These infective larvae can survive 3-4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed (4). The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host (5). Most adult worms are eliminated in 1 to 2 years, but longevity records can reach several years.

Geographic distribution of Ancylostoma duodenale

Geographic distribution of Necator americanus

Hookworms In the bowel, adults attach by their mouth to the intestinal mucosa and begin to feed Equipped with teeth, cutting plates or both, powerful esophageal muscles, and hydrolytic enzymes, the hookworm digests the plug of tissue within its buccal capsule Potent anticoagulants and inhibitors of platelet function are released and cause profound bleeding from lacerated capillaries in the lamina propria Adult worms mate in the small intestine, and the females deposit fertilized eggs in the lumen

Hookworms The heads of these worms look like some monster out of a horror movie The mouth parts of these nematodes are designed to bite onto the lining of the intestine, abrade the surface and suck the patients blood Horrific as this sounds many people who are infected show no outward symptoms of disease The presence and severity of the disease depends on the number of worms per individual, the nutritional state of the patient and the species of hookworm (A. duodenale suck greater volumes of blood than N. americanus and so it requires fewer worms to produce disease).

Necator americanus Ancylostoma duodenale
Anterior: Note the ventral teeth in the buccal capsule of A.duodenale. N. americanus has ventral cutting plates. Male Posterior: The copulatory bursa is used by the males for grasping the female during mating.Females lack a copulatory bursa.

Hookworms Clinical Manifestations
Skin penetration by third stage larvae  an intensely pruritic dermatitis called ground itch (localized to site of hookworm entry) Adult hookworms in intestine: Nonspecific GI tract symptoms Blood loss secondary is proportional to worm burden and develops weeks after infection A. duodenale infection is usually associated with greater loss than occurs with N. amricanus Hookworm anemia results when blood loss exceeds the host’s iron reserve and dietary intake Occasionally, severe hookworm anemia leads to heart failure

Hookworms Laboratory Findings and Ddiagnosiss
Characteristic rash of ground itch occurs on any skin surface and can be erythematous, papular, or vesicular Intense prtutitis can lead to scratching, excoriation, and secondary bacterial infection In contrast to Ascaris, pulmonary symptoms are usually not severe Intestinal hookworm infection is detected by identifying the characteistic egg in feces The eggs of Ancylostoma & Necator amerianus are similar under light microscope & cannot be easily distinguished by morphology

Ancylostoma duodenale & Necator americanus
Although the adult form of these intestinal nematodes can be distinguished, the diagnostic form in humans, the ova, are essentially identical. The ova are oval and measure about 60 X 40 µm. There is typically a clear space between the embryo and the thin shell. This is unstained wet-prep.

Hookworms Treatment Mebendazole (100 mg twice daily X 3 days) or
Albendazole (400 mg as a single dose) Mebendazole is poorly absorbed and may not eradicate developmentally arrested Ancylostoma larvae residing in extraintestinal issues. Therefore periodic follow up stool examination may be necesessary Alternate Treatment: Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days) Re-infection in endemic areas occur so commonly that the effect of single course of treatment is of questionable benefit Iron supplementaion reverses mild to modertae hookworm anemis

Hookworms Prevention No evidence of naturally acquired resistance
Children in endemic areas are constantly exposed to infective third-stage larvae Interest in development of a vaccines aimed at preventing hookworm infection/disease in children in the developing world Most promising vaccine candidates: family of proteins called ASP’s (Ancylostoma–secreted proteins) which are secreted by the infective larval stage Immunization with recombinant hookworm ASP has been shown to prevent tissue migration in a murine model of ancylostomiasis

Tapeworms Taenia saginata and Taenia solium
Segmented worms, called tape worms, cause human illness in either of two stages in their life cycle: Adult stage: Cause gastrointestinal symptomatology Larval stage: Causes signs and symptoms referable to enlarging larval cysts in a variety of tissues Humans are the only definitive hosts for T. saginata (the beef tapeworm) and T. solium (the pork tapeworm)

Life cycle of Taenia saginata and Taenia solium
Humans are the only definitive hosts for Taenia saginata and Taenia solium. Eggs or gravid proglottids are passed with feces (1); eggs can survive for days to months in the environment Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids (2). In the animal's intestine, the oncospheres hatch(3), invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal Humans become infected by ingesting raw or undercooked infected meat (4). In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex(5) and reside in the small intestine (6). Length of adult worms is usually <5 m for T. saginata (may reach up to 25 m) and m for T. solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (~6 per day T. saginata adults usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T. saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively. CDC

Taenia saginata - The Beef Tapeworm

Taenia solium - The Pork Tapeworm

Taenia saginata & Taenia solium Epidemiology
T. saginata: Widespread in cattle breeding areas of the world. Prevalence >10% in some independent states of the former Soviet Union, in Near East, and in central and eastern Africa. Lower rates in Europe, Southeast Asia, & South America T. solium: Prevalent in Mexico, Central and South America, Africa, Southeast Asia,and the Philippines Infections in USA and Canada are found in immigrants from areas where taeniasis is endemic, and in travelers who consume undercooked meats in endemic areas

Taenia saginata & Taenia solium Clinical Manifestations
Cysticercosis occurs in humans after the ingestion of T. solium eggs Embryonic metacestode migrates from the intestine and can lodge in a number of tissue sites such as the brain, muscle, and eyes with proclivity for the brain The clinical course largely depends on the endurance of the parasite inside the tissue and on the ensuing inflammation In the brain parenchyma, the intruding cysticercus might be destroyed within a few days by host immune mechanisms or remain viable in the brain for > 10 years

Cysticercosis can affect humans at any age Most common during the 3rd and 4th decades of life About 10% occur in children In infants initial signs of cysticecosis in infants is generalized seizure CT with contast or T2-weighted MRI  isolated cystic lesion in the brain parenchyma Typically the lesion disappears spontaneously 2-3 months later, but in some  granuloma  cacification (permanent sequela) Isolated lesion is most common; some children have two-several cysts Cystcercotic encephalitis is a severe form of CNS cystcercosis that occasionally occurs in children, particularly adolescent girls

In adults neurocysticercosis is quite different: Multiple brain cysticerci, variable immune response, chronic inflammation, chronic persistence of many active cysts, vasculitis and protean clinical picture Epilepsy occurs in 50% of cases; intracranial hypertension in 30% Occular Cysticercosis: Subretinal area or vitreous chamber Muscular cystcercosis: Rare in both children and adults; usually benign course

Taenia saginata & Taenia solium Laboratory Findings/Diagnosis
CT and MRI are the most relaible tools for the diagnosis of neurcysticercosis Serologic tests are unreliable (cross reactivity with antigens of other parasites) Serology is highly specific for CNS inection when tests are performed on CSF

Taenia saginata & Taenia solium Treatment
Intestinal T. solium infection: Praziquantel - (5-10 mg/kg once) Neurocysticercosis: Albendazole - 15 mg/kg/day (maximum, 800 mg/day) divided into two doses X 8 days Two months later, if repeat imaging studies show cysts: Praziquantel in a total dose of 75mg/kg divided in three doses for 15 days. Repeat imaging studies in two months

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