Transcript P. falciparum

Parasitic Infections:
Clinical Manifestations,
Diagnosis and Treatment
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The Reality
• 1.3 billion persons infected with
Ascaris (1: 4 persons on earth)
• 300 million with schistosomiasis
• 100 million new malaria cases/yr
• At UCLA, 38% of pediatric and
dental clinic children harbored
intestinal parasites
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Case1
• 42-yr-old previously healthy, UF professor
• 6-week history of intermittent diarrhea, flatus
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and abdominal cramps
Diarrhea: x8/day; pale; no blood or mucus
No tenesmus
Illness began slowly during camping trip to
Colorado with loose stools
Spontaneously remission for 5-6 days at a
time, then recur
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Case 1
• His 8-yr-old son had had a mild
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course of watery diarrhea—ascribed
to viral gastroenteritis by general
practitioner
Stool smear—no pus cells
However, wet preps showed…
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Diagnosis?
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Giardiasis (G. lamblia)
• Should be suspected in prolonged diarrhea
• Contaminated water often implicated—
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outbreaks
Campers who fail to sterilize mountain
stream water
Person-person in day care centers
MSM
Symptoms usually resolve spontaneously in
4-6 weeks
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Giardiasis
Tests of choice
• Examination of concentrated stools for
cysts (90% yield after 3 samples)
– Usually no PMNs
• Stool ELISA, IF Antigen (up to 98%
sensitive/90-100% specific)
• Consider aspiration of duodenal
contents--trophozoites
• Treatment: Metronidazole for 5-7 days
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Case 2
• 40 y/o male vicar returned from 2 years of
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missionary work in South Africa
Excellent health throughout stay there
3 months after returning to U.S.
– Suddenly ill with abdominal distension
– Fever
– Periumbilical pain
– Vomiting
– Blood-tinged diarrheal stools
Denied arthritis /known exposure to parasites
Family history of “inflammatory bowel
disease”
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Case 2
• Physical examination:
– Acutely ill
– Distended abdomen
– No hepatomegaly or splenomegaly
– Decreased bowel sounds
– Stool exam
Gross blood present
No pus cells
Negative for O&P, one negative C&S
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Sigmoidoscopy revealed…
• Multiple punctate bleeding sites
at 7 to 15 cm with normal
appearing mucosa between sites
• This mucosa easily denuded
when pressure applied to it,
leaving large areas of bleeding
submucosa
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Case 2
• Diagnosed with ulcerative colitis
• Started on corticosteroids
• Temperature rose to 40°C
• Abdomen distension increased and
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worsening of symptoms
Emergency laparotomy for toxic
megacolon
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Diagnosis?
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Entamoeba histolytica
• One of 7 amoebae commonly found in humans
• Only one that causes significant disease
• Causes intestinal (diarrhea and dysentery) and
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extraintestinal (liver primarily) disease
In US
– Institutionalized patients
– MSM
– Tourists returning from developing countries
– Patients with depressed cell mediated
immunity
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Trophozoites with ingested RBC
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Trophozoites in colon tissue (H & E stain)
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Cyst (wet mount)
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Amoebiasis: Clinical Manifestations
• Symptoms depend on degree of bowel
invasion
– Superficial: watery diarrhea and
nonspecific GI complaints
– Invasive: gradual onset (1-3 weeks) of
abdominal pain, bloody diarrhea,
tenesmus
• Fever is seen in minority of patients
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Amoebiasis: Clinical Manifestations
• Can be mistaken for ulcerative colitis
• Steroids can dramatically worsen and
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precipitate toxic megacolon
Amebic liver abscesses
–RUQ pain, pain referred to right
shoulder
–High fever
–Hepatomegaly (50%)
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Amoebic abscess—
remember…
• Can occur in lung, brain, spleen
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Amoebic Abscess
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Liquefaction of liver cells
Do not contain pus
Anchovy paste sauce
Culture of contents usually sterile
Liver affected:
– 53%-right lobe
– 8%-left lobe
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Remember…
• That stool is merely a convenient
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vehicle passing by
Amoebae live the bowel wall
Direct observation preferable to
mere examination of stool
Trophozoites best seen in direct
scrapings of ulcers
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Amoebiasis
Treatment
• Most respond to metronidazole
• Open surgical drainage should be
avoided, if at all possible
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Case 3
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Previously healthy 3-year-old girl
Attends day-care center
7 day history of watery diarrhea
Nausea
Vomiting
Abdominal cramps
Low-grade fever
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Case 4
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34 year-old AIDS patient
Debilitating, cholera-like diarrhea
Severe abdominal cramps
Malaise
Low-grade fever
Weight loss
Anorexia
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Diagnosis?
Case 3 & 4
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Three cysts stained pale red are seen in the center
with this acid fast stain
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Modified acid-fast stain of stool showing red oocysts of
Cryptosporidium parvum against the blue background of
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Cryptosporidium parvum
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Causes secretory diarrhea: 10 liter/day
Significant cause of death in HIV/AIDS
Animal reservoirs
Incubation period: 5-10 days
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Cryptosporidium parvum
• Infants & young children in day-care
• Unfiltered or untreated drinking water
• Farming practices: lambing, calving, and
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muck-spreading
Sexual practices: oral contact with stool of an
infected individual
Nosocomial setting with other infected
patients or health-care employees
Veterinarians: contact with farm animals
Travelers to areas with untreated water
Living in densely populated urban areas
Owners of infected household pets (rare)
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Diagnosis and Treatment
• Best diagnosed by stool exam
• No known effective treatment
• Nitazoxamide shortens duration of
diarrhea
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Case 5
• Mr. & Mrs. R. were sailing with their 3
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children in Jamaica
Living primarily on the boat with several
day trips to a small coastal island
On island, ate several types of tropical fruit
Both became suddenly ill with fevers,
chills, muscle aches, and loss of appetite.
Sought treatment locally, and were
diagnosed with hepatitis, likely due to
ingestion of toxic fruit
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Case 5
• Two days later, Mr. R. became
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jaundiced and passed dark urine
He progressively worsened, became
comatose and died
In the meantime, Mrs. R. was
transferred to SUF for liver transplant
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Case 5
• None of the children were sick despite
having eaten the same fruits and other
foods.
• The family had taken chloroquine
prophylaxis against malaria, but the
parents stopped the medicine 2 weeks
prior to becoming ill because of side
effects.
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Falciparum vs. Vivax
• Location: Falciparum confined to
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tropics and subtropics; vivax more
temperate
Falciparum infects RBC of any age;
others like reticulocytes
Falciparum-infected RBCs stick to
vascular endothelium causing
capillary blockage
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Malaria: Genetic susceptibility
• Two genetic traits associated with
decreased susceptibility to malaria
• Absence of Duffy blood group antigen
blocks invasion of Plasmodium vivax
– Significant number of Africans
• Persons with sickle cell hemoglobin are
resistant to P. falciparum
• Sickle cell disease and trait
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Malaria: Clinical manifestations
• Non-specific, flu-like illness
• Incubation
– P. falciparum: 9-40 days
– Non-P. falciparum: may be prolonged
P. vivax: 6-12 months
P. malariae and ovale: years
• Fever is the hallmark of malaria
– Classically, 2-3 day intervals in P. vivax and
malariae
– More irregular pattern in P. falciparum
• Fever occurs after the lysis of RBCs and release
of merozoites
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Malaria: Clinical manifestations
• Febrile paroxysms have 3 classic stages
– Cold stage
Pt feels cold and has shaking chills
15-60 mins. prior to fever
– Hot stage
39-41°C
Lassitude, loss of appetite, bone and joint
aches
Tachycardia, hypotension, cough, HA, back
pain, N/V, diarrhea, abdo pain, altered
consciousness
– Sweating stage
Marked diaphoresis followed by resolution of
fever, profound fatigue, and sleepiness
2-6 hours after
onset of hot stage
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Malaria: Clinical manifestations
• Other symptoms depend on malaria strain
• P. vivax, ovale and malariae: few other sxs
• P. falciparum:
– Dependent upon host immune status
– No prior immunity/splenectomy  high levels
of parasitemia  profound hemolysis
– Vascular obstruction and hypoxia
Kidneys: renal failure
Brain: (CNS) ― hypoxia, coma, seizures
Lungs: pulmonary edema
– Jaundice & hemoglobinuria (blackwater fever)
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Malaria: Clinical manifestations
• Always suspect malaria in travelers
from developing countries who
present with:
–Influenza-like illness
–Jaundice
–Confusion or obtundation
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Diagnosis
• Giemsa-stained blood smear
– Thick and thin smears
• P. falciparum:
– Best just after fever peak
• Others:
– Smears can be performed at any time
• Examine blood on 3-4 successive days
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Differences in strains
• P. falciparum
–No dormant phase in liver
–Multiple signet ring trophs per cell
–High percentage (>5%) parasitized
RBCs considered severe
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Differences in strains
• P. vivax and ovale
–Dormant liver phase
–Single signet ring trophs per cell
–Schuffner’s dots in cytoplasm
–Low percent (< 5%) of parasitized
RBCs
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Differences in strains
• P. malariae
–No dormant stage
–Single signet ring trophs per cell
–Very low parasitemia
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Treatment
• P. falciparum malaria can be fatal if not
promptly diagnosed and treated
• Non- P. falciparum malaria rarely
requires hospitalization
• Widespread drug resistance dictates
regimen (www.cdc.gov/travel; CDC
malaria hot line: 770-488-7788).
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Treatment
Uncomplicated malaria
• P. vivax, ovale, malariae, chloroquinesusceptible falciparum
– Chloroquine
– Primaquine for dormant liver forms
• Chloroquine-resistant falciparum
– Quinine plus doxycycline
– Mefloquine
– Atovaquone plus proguanil (AP)
– Artemisins (common in SE Asia due to
multi-drug resistance)
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Treatment
Severe malaria
• Drug options
–Quinidine gluconate—only
approved parenteral agent in US
–Artemisin
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Prevention
• Mefloquine
• Doxycycline
• Nets
• 30-35% DEET
• Permethrin spray for clothing and nets
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And don’t forget baggage
malaria!
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Case 5
• Mrs. R. was treated with IV quinidine
and improved rapidly.
• In retrospect, Mr. R. had died from
untreated blackwater fever
– Few parasites in peripheral blood
– Acute renal failure
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Case 6
• A 24-year-old white male army officer
• Referred to the VA ID clinic with a 3-month
history of a lesion on his right leg,
developing approximately 2 weeks after
returning from Iraq
• Recent travel history: 1 month in Kuwait and
2 months traveling between Kuwait and Iraq
• Recalled being bitten numerous times by
small flying insects and other nasty “bugs”
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Case 6
Physical examination essentially normal
except for:
• Non-tender (20 × 15 mm) scaly
erythematous plaque with a moist
central erosion of the left popliteal area.
• There was no lymphadenopathy and no
mucosal lesions were noted
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Diagnosis?
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An intact macrophage practically filled with
amastigotes (arrows),
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Leishmaniasis
• Tropical areas where phlebotomine
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sandfly is common: South America,
India, Bangladesh, Middle East, East
Africa
Sandfly introduces flagellated
promastigote into human  ingested
by macrophages  develops into
nonflagellated amastigote
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Leishmaniasis
• Cutaneous
– Most common among farmers, settlers,
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troops and tourists in Mid East (L. major
and tropica), Central and South America
(L. mexicana, braziliensis, amazonensis,
and panamensis)
– L. mexicana reported in Texas
Visceral (kala azar)
– Anemia, leukopenia, thrombocytopenia,
hypergammaglobulinemia common
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Leishmaniasis: Diagnosis
• Biopsy and Giemsa stain with amastigotes
• Species most prevalent in different places
• L. donovani – India
• L. infantum – Mid East
• L. chagasi – Latin America
• L. amazonensis -- Brazil
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Visceral Leishmaniasis
• Dissemination of amastigotes
throughout the reticulendothelial system
of the body
– Spleen
– Bone marrow
– Lymph nodes
• Opportunistic infection in AIDS patients
• Ineffective humeral response
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Hepatosplenomegaly
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Splenic aspirate
• Most satisfactory method
• Spleen must be at least 3cm below
LCM
• Aspirate stained with Giemsa
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Leishmaniasis: treatment
• Only drug approved in US is
Amphotericin B
• Treatment of cutaneous disease
depends on anatomic location
• Many spontaneously heal and do not
require treatment
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Remember..
• The factors determining the form of
leishmaniasis:
– Leishmanial species
– Geographic location
– Immune response of the host
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Case 7
• 38-year-old businessman
• Previously fit
• 2-week history of fever since returning from
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Brazil business trip
Flu-like symptoms and myalgia
Had consumed steak tartare in Brazil
Results all unremarkable---normal WBC and
ESR; negative smears; CXR and urine OK
Continued to have fever, tachycardia and
myalgia
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Case 8
• A 29-yr-old man with AIDS (CD4
count=59) presents with a 2 week
history of headache, fevers and new
onset seizures
• He had not been taking any
antiretroviral medications
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Cases 7 & 8
What parasite could
cause this picture?
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AIDS Patient
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AIDS Patient
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Toxoplasma gondii cyst in brain
tissue with H & E stain (100x)
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For the businessman…
• Toxoplasma serology was positive at
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a very high titer
Responded to treatment with
sulphonamide + pyrimethamine
No relapse
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Transmission
• Eating oocysts excreted by cats
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harboring sexual stages of parasite
Outbreaks traced to inadequately
cooked meat of herbivores (raw beef)
Mutton
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Toxoplasma gondii
• Worldwide distribution
• Human infection
– Ingestion of cysts in undercooked meat of
herbivores
– Water/food contaminated with oocysts
– Congenitally
– Infected organs, blood (less common)
• Prevalence of latent infection in US about 10%;
France about 75%
– Generally higher in less-developed world
– 50% in AIDS patients; up to 90% of AIDS
patients in developing world
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Toxoplasma gondii:
Immunocompetent hosts
• Latent infection (persistence of cysts)
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is generally asymptomatic
Cervical lymphadenopathy (10-20%)
Mono-like presentation (<1% of all
mono-like illnesses)
Chorioretinitis
Very rare: myocarditis, myositis
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Toxoplasma gondii:
Immunocompromised hosts
• Often life-threatening
• Almost always reactivation of latent infection
• AIDS
– Encephalitis most common manifestation
– Usually subacute onset/focal (if CD4< 200)
– Mental status changes, seizures, weakness,
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cranial nerve abnormalities, cerebellar signs,
– Can present as acute hemiparesis/language
deficit
– Usually multiple ring-enhancing lesions on
CT/MRI
Pneumonitis
Chorioretinitis
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Toxoplasma gondii:
Clinical manifestations
• Immunocompromised hosts
– Non-AIDS (transplants, hematologic
malignancies)
CNS
75%
Myocardial 40%
Pulmonary 25%
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Toxoplasma gondii:
Clinical manifestations
• Congenital
• Acute infection asymptomatic in mother
• Clinical manifestations range: no sequelae to
sequelae that develop at various times after
birth
– Chorioretinitis
– Strabismus
– Blindness
– Epilepsy, mental retardation, pneumonitis,
microcephaly, hydrocephalus,
spontaneous abortion, stillbirth
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Toxoplasma gondii: diagnosis
• Clinical suspicion crucial
• Serology is primary method of diagnosis
– IgM, IgG
• Histopathology
– Tachyzoites in tissue sections or body
fluid (difficult to stain)
– Multiple cysts near necrotic,
inflammatory lesions
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Toxoplasma gondii: Treatment
• Immunocompetent adults are usually
not treated unless visceral disease is
overt or symptoms are severe and
persistent
• Immunodeficient patients
– Latent disease: not treated
– Active disease: pyrimethamine +
sulfadiazone + folinic acid
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Toxoplasma gondii: Treatment
• Congenital:
– Treatment of acute infected pregnant
women decreases but does not eliminate
transmission
Spiramycin
– If fetal infection is documented, treat with
pyrimethamine + sulfadiazone + folinic acid
– Postnatal treatment: pyrimethamine +
sulfadiazone + folinic acid
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Case 22
• 25-year-old Caucasian woman presented
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with 1-week history of fever, chills,
sweating, myalgias, fatigue
No travel abroad
Had gone cranberry picking in
Massachusetts approx 3 weeks earlier
PE: anemic, hepatosplenomegaly
Blood workup: hemolytic anemia, reduced
platelets
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Thick smear
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Thin smear
Maltese
cross
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Diagnosis??
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Babesiosis
• Babesiosis caused by
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hemoprotozoan parasites of the
genus Babesia
>100 species reported
Few actually cause human
infection
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Babesiosis
• Babesia microti
• Life cycle involves two hosts:
– Deer tick, Ixodes dammini, (definitive
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host) introduces sporozoites into
white-footed mouse
Once ingested by an appropriate tick
gametes unite and undergo a sporogonic
cycle resulting in sporozoites
Humans enter cycle when bitten by
infected ticks
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Babesiosis
Deer are the hosts upon which the
adult ticks feed and are indirectly part
of the Babesia cycle as they influence
the tick population
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Babesiosis
• Clindamycin* plus quinine
• Atovaquone* plus azithromycin*
• Exchange transfusion in severely ill
patients with high parasitemia
* Approved by FDA
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Case 9
• 6-year-old son of seasonal farm
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worker
Presents with cough and fever,
wheeze
CXR reveals a lobar pneumonia
Admitted for initial therapy
After 2 days of antibiotics, with good
defervescence, a worm is found in his
bed
Stool exam reveals …
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Diagnosis?
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Ascaris lumbricoides
• In GI tract, few symptoms in light infections
– Nausea
– Vomiting
– Obstruction of small bowel or common
bile duct.
• Pulmonary: symptoms due to migration
– Alveoli (verminous pneumonia)—cough,
fever wheeze, dyspnea, X-ray changes,
eosinophilia
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Effects of Adult Ascaris Worms
• Depends on worm load
• Effects
– Mechanical: obstruction, volvulus,
intussusception, appendicitis,
obstructive jaundice, liver
abscesses, pancreatitis, asphyxia
• Toxic and Metabolic
– Malnutrition (complex)
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Ascaris lumbricoides
Diagnosis
• Characteristic eggs on direct smear
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examination
If treating mixed infections, treat Ascaris
first
– Mebendazole
– Pyrantel
Control:
– Periodic mass treatment of children,
health education, environmental
sanitation
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Case 10
• 11-year-old female
• Doing poorly in school
• Not sleeping well
• Anorectic
• Complains of itching in rectal region
throughout the day
• A Scotch-tape test reveals…
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Diagnosis?
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Enterobius (Pinworm)
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18 million infections in U.S.
Incidence higher in whites
Preschool and elementary school most often
Mostly asymptomatic
Nocturnal anal pruritis cardinal feature due to
migration and eggs
May have insomnia, possible emotional
symptoms
DS-eggs or adults on perineum {scotch tape}
Mebendazole 100 mg. Repeat in 2 weeks.
Pyrantel pamoate 11 mg/kg; repeat 2 weeks
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Case 11
• 69-year-old male was admitted to VA
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Hospital
Far East Prisoner of War (FEPOW)
COPD--steroids for 3 years
2-month history of nausea, vomiting
and anorexia
25 pounds weight loss
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On the day of admission…
• Fever, confusion, and not able to get
out of bed---transported to the hospital
• Initial blood work:
– Elevated WBC
– Raised eosinophil count 4 times
normal
• Underwent UGI endoscopy
• Duodenal biopsy obtained
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Diagnosis
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Strongyloides: Crucial Aspects
of Life Cycle
• Infection acquired through
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penetration of intact skin
Infection may persist for many years
via autoinfection
In immunocompromised patients,
there is risk of dissemination or
hyperinfection
–Hyperinfection syndrome
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Disseminated Strongyloidiasis
• High mortality75%
• Penetration of gut wall by infective
larvae
• Gut organisms carried on the surface of
larvae results in polymicrobial sepsis,
meningitis
• Larvae disseminate into all parts of
body: CNS, lungs, bladder, peritoneum
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Summary—Clinical Findings
• Defective cell-meditated immunity:
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steroids, burns, lymphomas, AIDS (?)
Gl symptoms in about two-thirds:
–Abdominal pain
–Bloating
–Diarrhea
–Constipation
Wheezing, SOB, hemoptysis
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Summary—Clinical Findings
• Skin rash or pruritis in ~ one-third
–Larva currens (racing larva)
–Intensely pruritic
–Linear or serpiginous urticaria
with flare that moves 5-15 cm/hr
–Usually buttocks, groin, and trunk
–In dissemination, diffuse
petechiae and purpura
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Summary-Clinical Findings
• Eosinophilia 60-95%
• Less if on steroids
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Case 12
• 57 year old farmer from Dixie County
• Presents with profound SOB
• Physical examination: anemic otherwise
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unremarkable
Laboratory examination reveals a profound
anemia (hct 24) with aniso and poikilocytosis
Remainder of laboratory examination normal.
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Diagnosis?
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Hookworm
• Hookworm responsible for development
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of USPHS
Caused by two different species (North
American and Old World)
Very similar to strongyloides in life cycle
Attaches to duodenum, feeds on blood
Elaborates anticoagulant, attaches and
reattaches many times
Loss of around 0.1 ml/d of blood per
worm
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Case 13
• 8-yr-old schoolgirl visiting the U.S. from
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Malaysia
1 week history of epigastric pain,
flatulence, anorexia, bloody diarrhea
No eosinophilia noted
Clinical diagnosis of amoebic dysentery
made
However, microscopy of stool prep…
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Diagnosis?
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Trichuris trichiura (Whipworm)
• Common in Southeast U.S.
• Frequently coexists with ascaris
• Entirely intraluminal life cycle—eggs are
•
•
•
•
•
ingested
Frequently asymptomatic
Severe infections: diarrhea, abdominal
pain and tenesmus
Rectal prolapse in children
DS-eggs in stool
Mebendazole 100 mg bid x 3 days
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Case 14
• 18-year-old trailer park handyman seen
•
•
•
•
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in ER
Worked under trailers wearing shorts
and no shirt
Developed intensely pruritic skin rash
Unable to sleep
WBC 18,000
65% eosinophils.
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Case 15
• An 8 year old boy
• Presents with skin lesions and itching
after spending the summer at a beach
condo in St. Augustine with his family
(mother, father, younger sister, dog and
cat).
• Legs show several raised, reddened,
serpiginous lesions that are intensely
pruritic.
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Diagnosis ?
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Cutaneous Larva Migrans
• Caused by filariform larvae of dog or cat
•
•
•
•
•
•
•
hookworm (Ancylostoma braziliense or
Ancylostoma duodenale
Common in Southeast U.S.
Red papule at entry with serpiginous tunnel
Intense pruritis
Self limiting condition
Diagnosis clinical
Topical or oral thiabendazole 25 mg/kg bid for 35 days
May use ethyl chloride topically
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Cutaneous larva migrans
(creeping eruption)
• More common in children
– Larvae penetrate skin and cause
•
•
tingling followed by intense itching.
Eggs shed from dog and cat bowels
develop into infectious larvae outside the
body in places protected from
desiccation and extremes of temperature
Shady, sandy areas under houses, at
beach, etc.
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Cutaneous larva migrans
(creeping eruption)
Usually not associated with
systemic symptoms
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Cutaneous larva migrans
(creeping eruption)
•
•
•
•
•
Diagnosis and treatment
Skin lesions are readily recognized
Usually diagnosed clinically
Generally do not require biopsy
–Reveal eosinophilia inflammatory infiltrate
–Migrating parasite is generally not seen
Stool smear will reveal eggs
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Visceral Larva Migrans
• Infection with dog or cat round worms
• Toxocara canis; Toxocara catis
• Underdiagnosed based on seroprevalence
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•
•
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surveys
Heavy infections associated with fever, cough,
nausea, vomiting, hepatomegaly, and
eosinophilia
Uncommon in adults
Ocular type more common in adults
Diagnosis-ELISA
Thiabendazole: 25 mg/kg bid X 5 days
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Case 17
• A 34 yr-old woman from Saudi Arabia
• Radiation and cyclophosphamide, adriamycin,
vincristine and prednisone for diffuse large B cell
lymphoma of the neck.
• Mild eosinophilia (AEC=500) at the time of
diagnosis
• 4 months after initiation of chemo, c/o intermittent
diffuse abdominal pain, bloating, constipation
and occasional rectal bleeding.
• Absolute eosinophil count: 1000
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Case 17
• No evidence of lymphoma found on re•
•
•
staging
Completed chemo, was deemed to be in
complete remission, but had persistence of GI
complaints.
Upper endoscopy was unrevealing.
Colonoscopy and biopsy revealed
granulomatous inflammation, prominent
eosinophilic infiltrate, surrounding a collection
of eggs.
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Chronic intestinal schistosomiasis
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Case 17
• The patient was treated with
•
praziquantel and did not have
relapse of symptoms at 2-year
follow-up
AEC=250
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Schistosomiasis: Epidemiology
and life cycle
• Cercariae in fresh water penetrate
human skin.
• Cercariae mature to schistosomulae,
which enter the bloodstream, liver and
lung.
• Mature worms migrate to the venous
system of the small intestine (S.
japonicum), large intestine (S. mansoni)
or bladder venous plexus (S.
haematobium).www.freelivedoctor.com
Schistosomiasis: Epidemiology
and life cycle
• Worms release eggs for many years into stool
•
•
•
•
or urine, resulting in fresh water contamination.
Freshwater snails are infected by miracidia and
are necessary for the production of cercariae
and human infection.
S. mansoni
– South America, Caribbean, Africa, Mid East
S. japonicum
– China and Philippines
S. haematobium
– Africa, Mid East
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Schistosomiasis: Clinical manifestations
• Three stages of disease, corresponding to life
cycle within human hosts
• Swimmer’s itch
– Within 24 hours of cercariae penetration
• Serum sickness syndrome (Katayama fever)
– 4 to 8 weeks later when worms mature and
release eggs
Fever, headache, cough, chills, sweating,
lymphadenopathy, hepatosplenomegaly 
usually resolves spontaneously
Elevated IgE and eosinophils
Most common with S. japonicum
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Chronic Schistosomiasis
• Granulomatous reaction to egg deposition in
•
•
intestine, liver, bladder, lungs
S. mansoni, japonicum
– Chronic diarrhea, abdominal pain, blood loss,
portal hypertension, hepatosplenomegaly,
pulmonary hypertension
– Eosinophilia is common
– Liver function tests are usually normal
S. Haematobium
– Hematuria, bladder obstruction, hydronephrosis,
recurrent UTIs, bladder cancer
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Schistosomiasis:
Diagnosis and Treatment
• Detection of characteristic eggs in stool, urine
•
•
or tissue biopsy is diagnostic
– Urine is best between 12N and 2Pm,
passed through 10 µm filter to concentrate
eggs
Antibody tests are available, but limited by
sensitivity, specificity
Praziquantel is the drug of choice
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S. mansoni
Stool
S. haematobium
Urine
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S. japonicum
Case 18
• 15-yr-old girl
• Fever, rash, swelling around the eye and
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hands, severe headaches
Fatigue, aching muscles and joints
Swollen lymph nodes on the back of neck
Weight loss
Progressive confusion, personality changes
Sleeping for long periods of the day
Insomnia
Had been on a safari with parents to West
Africa
Dusky red lesion developed within 1 week
Vaguely remembered being bitten by a fly
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Diagnosis?
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Investigations
• Blood films
• Lumbar puncture
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Blood smear
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African trypanosomiasis
Trypanosoma brucei gambiense
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Tsetse fly
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Treatment
• Suramin
• Melasoprol
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Case 19
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•
•
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6-yr-old boy recently arrived from Brazil
Swelling around the eye
Conjunctivitis
Fever
Enlarged lymph nodes
Hepatosplenomegaly
Had stayed in a hotel—adobe style with
thatched roof
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Diagnosis?
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Blood smear
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Reduviid bug
(assassin bug)
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Chagas disease:
Clinical manifestations
• Local edema is followed by fever, malaise,
•
anorexia
– More rarely: myocarditis, encephalitis
Years later: chronic Chagas Disease (1030%)
– Heart: primary target
Cardiomyopathy associated with CHF,
emboli, arrythmias
– GI tract: mega-esophagus, megacolon
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Chagas disease: Diagnosis
and treatment
• Acute disease is diagnosed by seeing
•
•
trypomastigotes on peripheral blood
smear
Chronic disease is diagnosed by
ELISA detecting IgG antibody to T.
cruzi
Treatment slows the progression of
heart disease
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Chagas Disease
• Public health implications in the US
• Chronic
– Cardiomyopathy
– Megaesophagus
– Megacolon
• Blood transfusion
• Transplant
– Solid organ
– Musculoskeletal allograft tissue
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Case 20
• 20-yr-old male
• Abdominal pain and nausea for several
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•
•
•
•
•
months
More common in the morning
Relieved by eating small amounts of food
Some diarrhea and irritability
Weight loss
Pruritus ani
Passage of white “bits”
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Diagnosis?
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Taenia saginata
• Ingestion of raw or poorly cooked beef
• Cows infected via the ingestion of human
•
•
•
•
waste containing the eggs of the parasite
Cows contain viable cysticercus larvae in
the muscle
Humans act as the host only to the adult
tapeworms
Up to 25 meters in the lumen of intestine
Found all over the world, including the U.S.
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Beef Tapeworm
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Treatment
• Praziquantel
• Albendazole
• Niclosamide
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Tapeworms (Cestodes)
• Adult worms inhabit GI tract of definitive vertebrate
host
• Larvae inhabit tissues of intermediate host
• Humans
– Definitive for T. saginata
– Intermediate for Echinococcus granulosus
(hydatid)
– Both definitive and intermediate for T. solium
• Adult worms shed egg-containing segments in stool
ingested by intermediate host
larval form in
tissues
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Case 21
• A 33 year-old Indian man was admitted
with a grand mal seizure
• 2 yrs PTA, he had vertigo and CT revealed
an enhancing calcified lesion in left
temporal-parietal region
• FHx: Brother had grand mal seizure
several years earlier
• Throughout his life, he has eaten a diet
heavy in pork
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Case 21
• Difficulty speaking and loss of consciousness
while on the phone
• Co-workers noticed generalized tonic-clonic
seizures lasting 10 minutes.
• CT revealed new localized edema around the
previously identified lesion and a second
contiguous ring enhancing lesion.
• He received phenytoin (Dilantin, an antiseizure
med) and 5 days of corticosteroids.
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Case 21
• ELISA titer was positive for antibodies
against Taenia solium.
• The neurosurgeons tell you that
resection is impossible because of the
extent and location of the lesion
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Cystercercosis
• Human infected with the larval stage of Taenia
solium
• Humans can serve as definitive or intermediate
host
• Eggs are ingested, or possibly get to stomach by
reverse peristalsis
• Probably much more common than is reported,
since most infections are asymptomatic
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Cystercercosis
• Symptoms depend on location of cysts, but
•
frequently include motor spasms, seizures,
confusion, irritability, and personality change
In the eye, often subretinal or in vitreous.
Movement may be seen by the patient. Pain,
amaurosis, and loss of vision may occur.
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Cysticercosis
• Clinical manifestations
– Adult worms rarely cause sxs
– Larvae penetrate intestine, enter blood, and
eventually encyst in the brain.
Cerebral ventircles  hydrocephalus
Spinal cord  compression, paraplegia
Subarachnoid space  chronic meningitis
Cerebral cortex  seizures
– Cysts may remain asymptomatic for years, and
become clinically apparent when larvae die
– Larvae may encyst in other organs, but are rarely
symptomatic
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Cysticercosis
• Diagnosis
– CT and MRI preferred studies
Discrete cysts that may enhance
Usually multiple lesions
– Single lesions especially common in cases
from India
Older lesions may calcify
– CSF
Lymphs or eos, low glucose, elevated protein
– Serology
Especially in cases with multiple cysts
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Cysticercosis
• Treatment
– Complex and controversial
– Praziquantel and albendazole may kill
cysts, but death of larvae can increase
inflammation, edema and exacerbate sxs
– When possible, surgical resection of
symptomatic cyst is preferred
– Corticosteroids vs. edema and
inflammation; antiseizure meds
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Case 21
• He was not treated with praziquantel or
albendazole
• He continued to receive dilantin for
seizures and was treated with
corticosteroids for edema
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Classification of Parasitic Diseases
•
•
Protozoa: amoeba; flagellates; ciliates
Metazoa (two phyla)
1) Helminths (worms)
 Nematodes
– Intestinal
– Extra-intestinal
 Flatworms (platyhelminths)
– Cestodes (tapeworms)
– Trematodes (flukes)
2) Arthopods (ectoparasites): scabies, lice, fly
larvae
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General rules of treatment
• Protozoa: require species-specific
treatment
• Metozoa: species-specific
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General rules of treatment of metazoa
Nematodes
Cestodes
Intestinal
Tissue
Mebendazole or
Albendazole
Albendazole
Filiariae
Ivermectin, doxycycline
Trematode
Praziquantel, Albendazole,
Niclosamide
Praziquantel
Ectoparasites
Permethrin, Ivermectin
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This is just the beginning of a great
adventure in infectious diseases
Sine qua non:
history and physical examination
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Thank you
Lennox K. Archibald, MD, PhD, FRCP
[email protected]
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