Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment

Parasitic Infections:
Clinical Manifestations,
Diagnosis and Treatment
www.freelivedoctor.com
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
Case1
42-yr-old previously healthy, UF professor
6-week history of intermittent diarrhea, flatus
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
Case 1
His 8-yr-old son had had a mild
course of watery diarrheaascribed
to viral gastroenteritis by general
practitioner
Stool smearno pus cells
However, wet preps showed
Diagnosis?
Giardiasis (G. lamblia)
Should be suspected in prolonged diarrhea

Contaminated water often implicated
outbreaks
Campers who fail to sterilize mountain
stream water
Person-person in day care centers
MSM
Symptoms usually resolve spontaneously in
4-6 weeks
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
Case 2
40 y/o male vicar returned from 2 years of
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
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
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
Case 2
Diagnosed with ulcerative colitis
Started on corticosteroids
Temperature rose to 40C
Abdomen distension increased and
worsening of symptoms
Emergency laparotomy for toxic
megacolon
Diagnosis?
Entamoeba histolytica
One of 7 amoebae commonly found in humans
Only one that causes significant disease
Causes intestinal (diarrhea and dysentery) and
extraintestinal (liver primarily) disease

In US
Institutionalized patients
MSM
Tourists returning from developing countries
Patients with depressed cell mediated
immunity
Trophozoites with ingested RBC
Trophozoites in colon tissue (H & E stain)
Cyst (wet mount)
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
Amoebiasis: Clinical Manifestations
Can be mistaken for ulcerative colitis

Steroids can dramatically worsen and
precipitate toxic megacolon
Amebic liver abscesses
RUQ pain, pain referred to right shoulder
High fever
Hepatomegaly (50%)
Amoebic abscess
remember
Can occur in lung, brain, spleen
Amoebic Abscess
Liquefaction of liver cells

Do not contain pus
Anchovy paste sauce
Culture of contents usually sterile
Liver affected:
53%-right lobe
8%-left lobe
Remember
That stool is merely a convenient
vehicle passing by
Amoebae live the bowel wall
Direct observation preferable to mere
examination of stool
Trophozoites best seen in direct
scrapings of ulcers
Amoebiasis
Treatment
Most respond to metronidazole

Open surgical drainage should be
avoided, if at all possible
Case 3
Previously healthy 3-year-old girl

Attends day-care center
7 day history of watery diarrhea
Nausea
Vomiting
Abdominal cramps
Low-grade fever
Case 4
34 year-old AIDS patient

Debilitating, cholera-like diarrhea
Severe abdominal cramps
Malaise
Low-grade fever
Weight loss
Anorexia
Diagnosis?
Case 3 & 4
Three cysts stained pale red are seen in the center

with this acid fast stain
Modified acid-fast stain of stool showing red oocysts of

Cryptosporidium parvum against the blue background of
coliforms and debris www.freelivedoctor.com
Cryptosporidium parvum
Causes secretory diarrhea: 10 liter/day

Significant cause of death in HIV/AIDS
Animal reservoirs
Incubation period: 5-10 days
Cryptosporidium parvum
Infants & young children in day-care

Unfiltered or untreated drinking water
Farming practices: lambing, calving, and
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)

Best diagnosed by stool exam
No known effective treatment
Nitazoxamide shortens duration of
diarrhea
Case 5
Mr. & Mrs. R. were sailing with their 3
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
Case 5
Two days later, Mr. R. became
jaundiced and passed dark urine
He progressively worsened, became
comatose and died
In the meantime, Mrs. R. was
transferred to SUF for liver transplant
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.
Falciparum vs. Vivax
Location: Falciparum confined to
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
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
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

Febrile paroxysms have 3 classic stages
Cold stage
Pt feels cold and has shaking chills
15-60 mins. prior to fever
Hot stage
39-41C
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

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)
Always suspect malaria in travelers

from developing countries who
present with:
Influenza-like illness
Jaundice
Confusion or obtundation
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
Differences in strains
P. falciparum
No dormant phase in liver
Multiple signet ring trophs per cell
High percentage (>5%) parasitized
RBCs considered severe
P. vivax and ovale
Dormant liver phase
Single signet ring trophs per cell
Schuffners dots in cytoplasm
Low percent (< 5%) of parasitized
RBCs
P. malariae
No dormant stage
Single signet ring trophs per cell
Very low parasitemia
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).
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)
Treatment
Severe malaria
Drug options
Quinidine gluconateonly
approved parenteral agent in US
Artemisin
Prevention
Mefloquine
Doxycycline
Nets
30-35% DEET
Permethrin spray for clothing and nets
And dont forget baggage

malaria!
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
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
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
Diagnosis?
An intact macrophage practically filled with

amastigotes (arrows),
Leishmaniasis
Tropical areas where phlebotomine

sandfly is common: South America,
India, Bangladesh, Middle East, East
Africa
Sandfly introduces flagellated
promastigote into human ingested
by macrophages develops into
nonflagellated amastigote
Leishmaniasis
Cutaneous
Most common among farmers, settlers,
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
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
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
Hepatosplenomegaly
Splenic aspirate
Most satisfactory method

Spleen must be at least 3cm below
LCM
Aspirate stained with Giemsa
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
Remember..
The factors determining the form of
leishmaniasis:
Leishmanial species
Geographic location
Immune response of the host
Case 7
38-year-old businessman
Previously fit
2-week history of fever since returning from
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
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
Cases 7 & 8
What parasite could
cause this picture?
AIDS Patient
AIDS Patient
Toxoplasma gondii cyst in brain

tissue with H & E stain (100x)
For the businessman

Toxoplasma serology was positive at
a very high titer
Responded to treatment with
sulphonamide + pyrimethamine
No relapse
Transmission
Eating oocysts excreted by cats
harboring sexual stages of parasite
Outbreaks traced to inadequately
cooked meat of herbivores (raw beef)
Mutton
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
Toxoplasma gondii:
Immunocompetent hosts
Latent infection (persistence of cysts)
is generally asymptomatic
Cervical lymphadenopathy (10-20%)
Mono-like presentation (<1% of all
mono-like illnesses)
Chorioretinitis
Very rare: myocarditis, myositis
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,
cranial nerve abnormalities, cerebellar signs,

Can present as acute hemiparesis/language
deficit
Usually multiple ring-enhancing lesions on
CT/MRI
Pneumonitis
Chorioretinitis
Toxoplasma gondii:
Clinical manifestations
Immunocompromised hosts
Non-AIDS (transplants, hematologic
malignancies)
CNS
75%
Myocardial 40%
Pulmonary 25%
Toxoplasma gondii:
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
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
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
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
Case 22
25-year-old Caucasian woman presented
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
Thick smear
Thin smear
Maltese cross
Diagnosis??
Babesiosis
Babesiosis caused by
hemoprotozoan parasites of the
genus Babesia
>100 species reported
Few actually cause human
infection
Babesiosis
Babesia microti
Life cycle involves two hosts:
Deer tick, Ixodes dammini, (definitive
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
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
Babesiosis
Clindamycin* plus quinine
Atovaquone* plus azithromycin*
Exchange transfusion in severely ill
patients with high parasitemia
* Approved by FDA
Case 9
6-year-old son of seasonal farm
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
Diagnosis?
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
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)
Ascaris lumbricoides
Diagnosis
Characteristic eggs on direct smear
examination
If treating mixed infections, treat Ascaris first
Mebendazole
Pyrantel
Control:
Periodic mass treatment of children,
health education, environmental
sanitation
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
Diagnosis?
Enterobius (Pinworm)
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
Case 11
69-year-old male was admitted to VA
Hospital
Far East Prisoner of War (FEPOW)
COPD--steroids for 3 years
2-month history of nausea, vomiting
and anorexia
25 pounds weight loss
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
Diagnosis
Strongyloides: Crucial Aspects

of Life Cycle
Infection acquired through penetration
of intact skin
Infection may persist for many years via
autoinfection
In immunocompromised patients, there
is risk of dissemination or hyperinfection
Hyperinfection syndrome
Disseminated Strongyloidiasis
High mortality75%
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
SummaryClinical Findings
Defective cell-meditated immunity:
steroids, burns, lymphomas, AIDS (?)
Gl symptoms in about two-thirds:
Abdominal pain
Bloating
Diarrhea
Constipation
hemoptysis
Wheezing, SOB,
SummaryClinical 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
Summary-Clinical Findings
Eosinophilia 60-95%
Less if on steroids
Case 12
57 year old farmer from Dixie County
Presents with profound SOB
Physical examination: anemic otherwise
unremarkable
Laboratory examination reveals a profound
anemia (hct 24) with aniso and poikilocytosis
Remainder of laboratory examination normal.
Diagnosis?
Hookworm
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
Mebandazol
Pyrantel pamoate
Case 13
8-yr-old schoolgirl visiting the U.S. from
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
Diagnosis?
Trichuris trichiura (Whipworm)
Common in Southeast U.S.

Frequently coexists with ascaris
Entirely intraluminal life cycleeggs 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
Case 14
18-year-old trailer park handyman seen
in ER
Worked under trailers wearing shorts
and no shirt
Developed intensely pruritic skin rash
Unable to sleep
WBC 18,000
65% eosinophils.
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.
Diagnosis ?
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
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.

(creeping eruption)
Usually not associated with
systemic symptoms

(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
Visceral Larva Migrans
Infection with dog or cat round worms

Toxocara canis; Toxocara catis
Underdiagnosed based on seroprevalence
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
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
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.
Chronic intestinal schistosomiasis

Case 17
The patient was treated with
praziquantel and did not have

relapse of symptoms at 2-year
follow-up
AEC=250
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).
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
Schistosomiasis: Clinical manifestations

Three stages of disease, corresponding to life
cycle within human hosts

Swimmers 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
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
Schistosomiasis:
Detection of characteristic eggs in stool, urine
or tissue biopsy is diagnostic

Urine is best between 12N and 2Pm,
passed through 10 m filter to concentrate
eggs
Antibody tests are available, but limited by
sensitivity, specificity
Praziquantel is the drug of choice
S. mansoni
Stool
S. haematobium
Urine
S. japonicum
Case 18
15-yr-old girl
Fever, rash, swelling around the eye and 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
Diagnosis?
Investigations
Blood films
Lumbar puncture
Blood smear
African trypanosomiasis
Trypanosoma brucei gambiense
Tsetse fly
Treatment
Suramin
Melasoprol
Case 19
6-yr-old boy recently arrived from Brazil

Swelling around the eye
Conjunctivitis
Fever
Enlarged lymph nodes
Hepatosplenomegaly
Had stayed in a hoteladobe style with
thatched roof
Diagnosis?
Blood smear
Reduviid bug
(assassin bug)
Chagas disease:
Local edema is followed by fever, malaise,
anorexia
More rarely: myocarditis, encephalitis
Years later: chronic Chagas Disease (10-30%)
Heart: primary target
Cardiomyopathy associated with CHF,
emboli, arrythmias
GI tract: mega-esophagus, megacolon
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
Chagas Disease
Public health implications in the US
Chronic
Cardiomyopathy
Megaesophagus
Megacolon
Blood transfusion
Transplant
Solid organ
Musculoskeletal allograft tissue
Case 20
20-yr-old male
Abdominal pain and nausea for several 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
Diagnosis?
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.
Beef Tapeworm
Treatment
Praziquantel
Albendazole
Niclosamide
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
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
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.
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
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
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.
Cysticercosis
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
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
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
Case 21
He was not treated with praziquantel or
albendazole
He continued to receive dilantin for
seizures and was treated with
corticosteroids for edema
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
General rules of treatment
Protozoa: require species-specific

treatment
Metozoa: species-specific
General rules of treatment of metazoa

Nematodes
Intestinal
Mebendazole or
Albendazole
Tissue
Albendazole
Filiariae
Ivermectin, doxycycline
Cestodes
Praziquantel, Albendazole,
Niclosamide
Trematode
Praziquantel
Ectoparasites
Permethrin, Ivermectin
This is just the beginning of a great

adventure in infectious diseases
Sine qua non:
history and physical examination
Thank you
Lennox K. Archibald, MD, PhD, FRCP
lka1@ufl.edu

Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment

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Parasitic Infections: Clinical Manifestations, Diagnosis and Treatment

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Parasitic Infections:

Ascaris (1: 4 persons on earth)

and abdominal cramps

Giardiasis (G. lamblia)

Should be suspected in prolonged diarrhea

missionary work in South Africa

Multiple punctate bleeding sites

extraintestinal (liver primarily) disease

Trophozoites with ingested RBC

Trophozoites in colon tissue (H & E stain)

Cyst (wet mount)

Amoebiasis: Clinical Manifestations

Symptoms depend on degree of bowel

Amoebiasis: Clinical Manifestations

Can be mistaken for ulcerative colitis

Can occur in lung, brain, spleen

Liquefaction of liver cells

Most respond to metronidazole

Previously healthy 3-year-old girl

34 year-old AIDS patient

Three cysts stained pale red are seen in the center

Modified acid-fast stain of stool showing red oocysts of

Causes secretory diarrhea: 10 liter/day

Infants & young children in day-care

Diagnosis and Treatment

Falciparum vs. Vivax

Location: Falciparum confined to

tropics and subtropics; vivax more

Malaria: Genetic susceptibility

Two genetic traits associated with

Malaria: Clinical manifestations

Malaria: Clinical manifestations

Malaria: Clinical manifestations

of parasitemia profound hemolysis

Malaria: Clinical manifestations

Always suspect malaria in travelers

Non- P. falciparum malaria rarely

Widespread drug resistance dictates

P. vivax, ovale, malariae, chloroquinesusceptible falciparum

And dont forget baggage

An intact macrophage practically filled with

Tropical areas where phlebotomine

troops and tourists in Mid East (L. major

Biopsy and Giemsa stain with amastigotes

Most satisfactory method

Brazil business trip

Toxoplasma gondii cyst in brain

For the businessman

Latent infection (persistence of cysts)

cranial nerve abnormalities, cerebellar signs,

sequelae that develop at various times after

Toxoplasma gondii: diagnosis

Toxoplasma gondii: Treatment

Toxoplasma gondii: Treatment

with 1-week history of fever, chills, sweating,

host) introduces sporozoites into

In GI tract, few symptoms in light infections

Effects of Adult Ascaris Worms

Depends on worm load

18 million infections in U.S.

On the day of admission

Strongyloides: Crucial Aspects

American and Old World)