Parasitic Infestations Basim Asmar, M.D. Wayne State University School of Medicine Children’s...

Parasitic Infestations

Basim Asmar, M.D.Wayne State University

School of MedicineChildren’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 InfestationsProtozoa

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

GiardiasisEpidemiology

• Occurs worldwide

• Age-specific prevalence:– Highest in children 0-5 years– Followed by 31-40 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)

GiardiasisEpidemiology

• 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 72-97Abdominal distension 42-97Flatulance 35-97Abdominal cramps 44-81Nausea 14-79Foul-smelling, greasy stools 15-79Anorexia 41-73Weight loss 53-73Vomiting 14-35Fever 0-28Constipation 0-17


• 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


• Asymptomatic carriers in USA: 3%-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

GiardiasisDiagnosis

Definitive Diagnosis: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:

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 15 mg/k/d divided in 3 doses X 5d 250 mg tid X 5d (Flagyl)

Furazolidone 6 mg/k/d divided in 3-4 doses X 10d 100 mg tid X 10d (Furoxone)

Albendazole 400 mg/day X 5d 400 mg/day X 5d (Albenza) Quinacrine 6 mg/k/d divided in 3 doses X 5d 100 mg tid X 5d (Atabrine)

Nitazoxanide 12-47 mo: 100 mg bid X 3d N/A (Alinia) 4-11 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 parvumEpidemiology

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 parvumEpidemiology

• Outbreaks have been associated with contaminated community water supplies

• Waterborne outbreak in Milwaukee, WI (1985): 403,000 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

CryptosporidiosisEpidemiology

• 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

CryptosporidiosisClinical 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

CryptosporidiosisClinical 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

CryptosporidiosisLaboratory 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

CryptosporidiosisCryptosporidia 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

CryptosporidiosisTreatment

• 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)

CryptosporidiosisPrevention

• 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

AmebiasisEntamoeba 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 tissuedestruction

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).

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 histolyticaEpidemiology

• 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: 40-50 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 histolyticaClinical Manifestations

Amebic colitis Sign or Symptom % of Patients Affected Symptoms > 1 wk Most patients Diarrhea 94-100

Dysentery 94-100Abdominal pain 12-80Weight loss 44Fever >38oC 10Heme (+) stool 100

Immigrant from or traveler to endemic area >50

Prevalence (male/female) 50/50


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 21-51 Fever 85-90

Abdominal tenderness 84-90Hepatomegaly 30-50Jaundice 6-10Diarrhea 20-33

Weight loss 33-50 Cough 10-30 Immigrant from or traveler to endemic area >50

Prevalence (male/female) 50/50 in children; 90/10 in adults

Gross pathology of liver containing amebic abscess

Gross pathology of amebic abscess of liver.

Tube of "chocolate" pus from abscess.

Entamoeba histolyticaLaboratory 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, 50% of general population

Entamoeba histolyticaLaboratory 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 casesEIA: Can detect E. histolytica antigen in serum in ~96% of

patients with abscess

Amebic liver abscesses

Entamoeba histolyticaTreatment

Asymptometic amebiais:Luminal agent (paromomycin, diloxanide

furate, or iodohydroxyquin)

Amebic Colitis: Metronidazole & a luminal agent

Amebic Liver Absces: Metronidazole & a luminal agent

Entamoeba histolyticaPrevention

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 knownreservoirs of E. histolytica, a successful vaccine

Could potentially eliminate this disease

Intestinal NematodesRound 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)


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 lumbricoidesClinical 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 lumbricoidesLaboratory 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 lumbricoidesCharacteristic fertilized egg:Bile stained, mammillated thick external layer, unembryonated (55-75 um x 35-50 um)

Characteristic unfertilized egg: elongated & larger than fertile egg, thin shelled (85-95 um x 43-47 um)

Ascaris lumbricoidesTreatment

• 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 lumbricoidesPrevention

• 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.

HookwormsClinical 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 10-20 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

HookwormsLaboratory 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

HookwormsPrevention

• 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

soliumSegmented worms, called tape worms, cause

human illness in either of two stages in their life cycle:

(1) Adult stage: Cause gastrointestinal symptomatology

(2) 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 2 - 7 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,

SoutheastAsia,and the Philippines

Infections in USA and Canada are found in immigrantsfrom 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

remainviable in the brain for > 10 years


Cysticercosis can affect humans at any age Most common during the 3rd and 4th decades of lifeAbout 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 cystcercosisthat occasionally occurs in children, particularly adolescent girls


In adults neurocysticercosis is quite different:

Multiple brain cysticerci, variable immune response, chronicinflammation, 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

Parasitic Infestations Basim Asmar, M.D. Wayne State University School of Medicine Children’s...

Documents

Transcript of Parasitic Infestations Basim Asmar, M.D. Wayne State University School of Medicine Children’s...