Parasitic Infestations

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

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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)

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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

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Giardia lamblia
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Giardia lamblia
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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.

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

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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

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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

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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)

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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

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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

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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

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Giardiasis

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

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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

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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

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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

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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)

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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)

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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.

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Cryptosporidium parvum
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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

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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

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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

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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

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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

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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.

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

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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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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

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Amebiasis

• Entamoeba histolytica
• trophozoite

• Entamoeba histolytica mature cyst

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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).

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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.
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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

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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

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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

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

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Histopathology of a typical flask-shaped ulcer of
intestinal amebiasis
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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

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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

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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

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

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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

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Amebic liver abscesses
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Amebic liver abscesses
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Entamoeba histolyticaTreatment

• Asymptometic amebiais
• Luminal agent (paromomycin, diloxanide furate, or
  
• iodohydroxyquin)
• Amebic Colitis Metronidazole a luminal agent
• Amebic Liver Absces Metronidazole a luminal
  agent

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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

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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)

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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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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)

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Ascaris lumbricoides
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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

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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)
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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

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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)

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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).
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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