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Title: Parasitic Infestations


1
  • Parasitic Infestations
  • Basim Asmar, M.D.
  • Wayne State University
  • School of Medicine
  • Childrens Hospital of Michigan
  • Division of Infectious Diseases

2
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 gt10,000 eukayotic
    unicellular animals
  • Endoparasitic helminths of humans
  • Two phyla (1) Platyheminths (flatworms)
  • (2) Nematoda (round-worms)

3
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

4
Giardia lamblia
5
Giardia lamblia
6
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.

7
Giardia lamblia
8
In wet mounts, cysts show the typical ovoid
ellipsoid shape measuring from 8-19 mm (range
11-14 mm)
9
Giardia trophozoite
(Trichrome stain x 1000)
10
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

11
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

12
Giardia lamblia
  • Anti-Giardia IgG is found in gt80 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

13
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 DCCs
  • Consumers of contaminated water
  • Travelers to certain areas of the world
  • Those exposed to domestic and wild animals (dogs,
    cats, cattle deer, and beaver)

14
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

15
Giardiasis
  • Clinical Manifestations
  • Symptom Percent
  • Diarrhea 64-100
  • Malaise. Weakness 72-97
  • Abdominal distension 42-97
  • Flatulance 35-97
  • Abdominal cramps 44-81
  • Nausea 14-79
  • Foul-smelling, greasy stools 15-79
  • Anorexia 41-73
  • Weight loss 53-73
  • Vomiting 14-35
  • Fever 0-28
  • Constipation 0-17

16
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

17
Giardiasis
  • Clinical Manifestations
  • Asymptomatic carriers in USA
    3-7 (up to 20 in southern regions)
  • Prevalence studies in DCC children lt36 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

18
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

19
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

20
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

21
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 lt 1 um)

22
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)

23
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.

24
Cryptosporidium parvum
25
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, Travelers diarrhea)
  • Environmentally contaminated water
  • 130 oocysts can cause infection in
    immunocompetent

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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

28
CryptosporidiosisEpidemiology
  • More prevalent in underdeveloped countries in
    children lt2 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

29
CryptosporidiosisClinical Manifestations
  • Incubation period 2-14 days
  • Diarrhea Profuse watery diarrhea mucus
  • Rarely contains WBCs or RBCs
  • Crampy abdominal pain, nausea, vomiting (50)
  • Fever is uncommon
  • Infection may be asymptomtic, self-limited or
    protracted

30
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 LFTs can occur

31
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

32
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.

33
Cryptosporidiosis Small spherical organisms
(red arrow) attached to the brush border of
absorptive intestinal epithelial cells
34
Oocysts of Cryptosporidium visualized with
Acid-fast stain
35
Oocysts of Cryptosporidium parvum
36
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)

37
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

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39
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

40
Amebiasis
  • Entamoeba histolytica
  • trophozoite
  • Entamoeba histolytica mature cyst

41
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).

42
Trophozoites of Entamoeba histolytica (Trichrome
stain).Two diagnostic characteristicsTwo of
the trophozoites have ingested erythrocytes, and
the nuclei have typically a small, centrally
located karyosome, as well as thin, uniform
peripheral chromatin.
43
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

44
Entamoeba histolyticaClinical Manifestations
  • Amebic colitis
  • Sign or Symptom of Patients Affected
  • Symptoms gt 1 wk Most patients
  • Diarrhea 94-100
  • Dysentery 94-100
  • Abdominal pain 12-80
  • Weight loss 44
  • Fever gt38oC 10
  • Heme () stool 100
  • Immigrant from or traveler
  • to endemic area gt50
  • Prevalence (male/female) 50/50

45
Entamoeba histolyticaClinical Manifestations
  • 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

46
Amebic ColitisSevere dysentery with multiple
ulcers in the large bowel, and a bloody
diarrhea
47
Entamoeba histolytica trophozoites
in section of intestine (HE) 
48
Entamoeba histolyticaClinical Manifestations
  • 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

49
Histopathology of a typical flask-shaped ulcer of
intestinal amebiasis
50
Entamoeba histolyticaClinical Manifestations
  • 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
    lt1 of patients

51
Entamoeba histolyticaClinical Manifestations
  • 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

52
Entamoeba histolyticaClinical Manifestations
  • Amebic Liver Abscess
  • Sign or Symptom of Patients Affected
  • Symptoms gt 4 wks 21-51
  • Fever 85-90
  • Abdominal tenderness 84-90
  • Hepatomegaly 30-50
  • Jaundice 6-10
  • Diarrhea 20-33
  • Weight loss 33-50
  • Cough 10-30
  • Immigrant from or traveler
  • to endemic area gt50
  • Prevalence (male/female) 50/50 in
    children 90/10 in adults

53
Gross pathology of liver containing amebic
abscess 
54
Gross pathology of amebic abscess of liver. Tube
of "chocolate" pus from abscess. 
55
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
    gt95)
  • 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

56
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 cases
  • EIA Can detect E. histolytica antigen in serum
    in 96 of patients with abscess

57
Amebic liver abscesses
58
Amebic liver abscesses
59
Entamoeba histolyticaTreatment
  • Asymptometic amebiais
  • Luminal agent (paromomycin, diloxanide furate, or
  • iodohydroxyquin)
  • Amebic Colitis Metronidazole a luminal agent
  • Amebic Liver Absces Metronidazole a luminal
    agent

60
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 known
  • reservoirs of E. histolytica, a successful
    vaccine
  • Could potentially eliminate this disease

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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

63
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)

64
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

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66
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)

67
Ascaris lumbricoides
68
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

69

Ascaris lumbricoidesCharacteristic fertilized
eggBile 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)
70
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 lt
    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

71
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 gt50),
    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

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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)

74
The two most common hookworms that infect humans
(1) Ancylostoma duodenale(2) Necator
americanusAdult females10-13 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).
75
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.

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Geographic distribution of Ancylostoma duodenale
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Geographic distribution of Necator americanus
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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

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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).

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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.

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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 hosts iron reserve and dietary intake
  • Occasionally, severe hookworm anemia leads to
    heart failure

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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

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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.

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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

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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 ASPs (Ancylostomasecreted
    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

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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)

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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 lt5 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

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Taenia saginata - The Beef Tapeworm
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Taenia solium - The Pork Tapeworm
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Taenia saginata Taenia solium Epidemiology
  • T. saginata
  • Widespread in cattle breeding areas of the world.
    Prevalence gt10
  • 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

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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 gt 10 years

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Taenia saginata Taenia solium Clinical
Manifestations
  • 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

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Taenia saginata Taenia solium Clinical
Manifestations
  • 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

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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

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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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