PARASITOLOGY

Dr. Shanae Gill

Medical parasitology: the study and
medical implications of parasites that
infect humans

What is a Parasite?


Definitions
Parasite: a living organism that acquires
some of its basic nutritional requirements
through its intimate contact with another
living organism.

Parasites may be simple unicellular
protozoa or complex multicellular
metazoa.

Definitions
Host: the organism in, or on, which the parasite lives
and causes harm

Definitive host: the organism in which the adult or
sexually mature stage of the parasite lives

Intermediate host: the organism in which the
parasite lives during a period of its development only

Vector: a living carrier (e.g.an arthropod) that
transports a pathogenic organism from an infected to
a non-infected host. A typical example is the female
Anopheles mosquito that transmits malaria

Epidemiology
Although parasitic infections occur
globally, the majority occur in tropical
regions, where there is poverty, poor
sanitation and personal hygiene

Often entire communities may be infected
with multiple, different organisms which
remain untreated because treatment is
neither accessible nor affordable


Common Medically Important Parasites
CLASSIFICATION OF MEDICALLY
IMP. PARASITES
PARASITES
PROTOZOA
(Single celled)
SARCODINA
(AMEBAS)
SPOROZOA
(SPOROZOANS
)
MASTIGO
PHORA
(FLAGELLATES)
CILIATA
(CILIATES)
METAZOA
(HELMINTHS)
Muliticellular
PLATI HELMINTHE S
(FLAT WORMS)
TREMATODA
(FLUKES)
CESTODA
(TAPE
WORMS)
NEMATHELMINTHES
(ROUND WORMS &
NEMATODES)
INTESTINAL AND
UROGENITAL
PROTOZOA
Amebae
Primitive unicellular organisms
Simple life cycle
Trophozoite (Ameoboid form)
Motile
Reproducing (binary fission or production of trophozoites)
Metabolically active
Cyst
Resistant
Metabolically inactive
Usually infective
Recovered patient has cyst in the stool and they are more
infectious than protozoa.
If person have antibodies and the person ingest the cyst then the
antibodies protect them.
Amebae (cont.)
Avirulent organisms
which signal ingestion of
fecal contamination
Entamoeba coli
E. hartmanni
E. dispar (avirulent E.
histolytica)
E. gingivalis
Endolimax nana
Iodamoeba
butschlii
Blastocystis
hominis
Pathogen = Entamoeba histolytica
Case 1
CC:
A 28-year-old male from India complains
of gradual-onset, intermittent, crampy
abdominal pain with 1-4 foulsmelling,
frothy loose stools daily.

HPI:
His stools sometimes contain blood and mucus.
He also complains of flatulence, tenesmus, and,
at times, alternating diarrhea and constipation.
PE:
Slight tenderness during palpation of cecum and ascending
colon; no hepatomegaly.
Labs:
CBC: mild leukocytosis; no eosinophilia. Fresh stool
examination reveals presence of Entamoeba histolytica cysts
and motile hematophagous trophozoites; serology for
antiamebic antibodies is positive.
Imaging:
Colonoscopy: multiple colonic mucosal ulcers that are slightly
raised and covered with shaggy exudate; mucosa between
ulcers normal.
Micro pathology:
Biopsy specimens reveal lesions extending
under adjacent intact mucosa to produce
classical "flask-shaped" ulcers; amebic
trophozoites demonstrated at base of
ulcer.
Case 2
CC:
A 45-year-old male Peace Corps volunteer who
recently spent two years in rural Mexico complains of a
spiking fever, malaise, headache, and right upper
quadrant abdominal pain.
HPI:
He admits to having had bloody diarrhea with mucus
(DYSENTERY) and tenesmus that disappeared with
some pills that he took several months ago.
Case 2
PE:
VS: fever (39.6 C). PE: pallor; slight jaundice;
tender 3+ hepatomegaly with no rebound
tenderness; pain on fist percussion of right
lower ribs.
Labs
CBC: leukocytosis with neutrophilia. Amebic
cysts in stool specimen (not concurrent with
abscess); positive serology for antibodies to
Entamoeba histolytica.
Case 2
Imaging:
CXR: elevation of right hemidiaphragm; small right pleural
effusion. CT/US: cavitating lesion in right lobe of liver (due
to abscess).

Gross pathology:
Multiple mucosal ulcers, slightly raised and covered with
shaggy exudate; enlarged liver with one large abscess on
right lobe containing chocolate-colored pus; abscess may
rupture and spread to lungs, brain, or other organs.
Micro pathology:
Sterile pus; ameba may be obtained from periphery of lesion.
Entamoeba histolytica Epidemiology
Distribution world-wide

Prevalence highest in tropical/subtropical areas,
poor sanitation, contaminated water

In areas of high endemicity 30-50% prevalence

In US/Canada 1-2% seroprevalence

Trophozoites cant survive passage through
stomach. Therefore only the cyst that is infectious.
Form/transmission:
Fecal-oral transmission--- water, fresh
fruits, and vegetables
Asymptomatic carrier (shedding cysts) is
much more important than symptomatic
patient who is shedding trophozoites.

Life cycle
Entamoeba histolytica Clinical
Syndrome
Disease can range from inapparent carriage
to intestinal amebiasis to extraintestinal
amebiasis (moved from the GI tract to blood
and cause infection of other parts of the body
especially liver).

Intestinal amebiasis
Symptoms = abdominal pain with cramping and colitis
with diarrheae
Inverted flask shaped lesions in large intestine
Severe disease pass several bloody stools per day (cause
ulcerations in GI tract).
May be dehydrated with electrolyte imbalance
May be fatal in malnourished pregnant women,
immunocompromised, or infants
Amebic liver abscess
Tube of "chocolate"
pus from abscess.

Anchovy Paste
consistency
E. histolytica Clinical Syndrome
(cont.)
Extraintestinal amebiasis
Systemic signs fever, chills, leukocytosis (WITHOUT
eosinophilia), usually follows colitis. They will have history of colitis.
Eosinophilia is only associated with worms not amoeba.
Usually primary involvement of liver WHY?
Frequently abscesses form in liver
Pain
Hepato-splenomegaly with elevation of the diaphragm
Abscess may rupture and erode through diaphragm -> pleural space or lung
parenchyma
Aspiration of the liver abscess yields brownish-yellow pus with the
consistency of anchovy-paste
E. histolytica Pathogenesis
Infectious form = cysts
Cysts become trophozoites after passing
through stomach
Trophozoites produce an adhesin, once
adhered
Probably cytotoxin-mediated cytolysis
Tissue necrosis
Some of the damage may be host-mediated
Trophozoites may invade deep mucosa and get
to the liver
E. histolytica Lab. Diagnosis
Microscopic Ova & Parasite (O&P) Exam is
diagnostic
Must be differentiated from avirulent colonizers (Entamoeba coli,
etc.)
Dont order O&P on every patient with diarrhea! Because
the prevalence is so low. Patient have been back from
endemic place that has E. histolytica then you will order
the test.
Many hospitals wont do O&P on inpatient without special request
Serology can be very helpful especially in extra
intestinal disease
Antibody
Antigen
E.Histolytica treatment
The treatment of choice for symptomatic
intestinal amebiasis or hepatic abscess is
metronidazole followed by iodoquinal or
paromomycin
Flagellates
Giardia lamblia
Trophozoite and cyst
forms
Diaentamoeba fragilis
Trophozoite form only,
no cyst
Trichomonas vaginalis
Trophozoite form only,
no cyst. Do not need to
go through the GI.
Case 3
CC:
A 4-year-old female is brought to the pediatrician
because of lack of appetite; nausea and
vomiting; chronic, foulsmelling diarrhea; and a
bloated sensation.
HPI:
She has been in several day-care centers over the
past three years.
PE:
Low weight and height for age; mild epigastric
tenderness.
Labs:
Binucleate, pear-shaped, flagellated
trophozoites (GIARDIA LAMBLIA) on freshly
passed stool; cysts found on stool exam.
Giardia lamblia Epidemiology
Distribution world-wide
Urban daycare centers, poor sanitation
Fecal-oral route
Oral-anal sex
Contaminated water
Contaminated fruit/vegetables
Often epidemic!
Sylvatic beavers, muscrats (hiking and camping in the
Rocky Mountains!)
Must boil water, resistant to regular chlorine concentrations
If you drink contaminant you will get infected.
Life cycle
G. lamblia Clinical Disease
50% of those infected are asymptomatic
Symptoms can range from mild diarrhea to
severe malabsorption syndrome
Incubation = 1-4 weeks (avg. 10 days)
Symptoms
Foul-smelling, watery diarrhea, cramping
Blood/pus rarely present (usually no tissue destruction)
The more chronic stage is associated with vitamin B
12

malabsorption, disaccharidase deficiency and lactose
intolerance.
Usually recover in 2-3 weeks
Chronic in pts with IgA deficiency or diverticulae
G. lamblia Laboratory Diagnosis
O&P exam obsolete
Look for trophozoites and/or cysts
Falling leaf motility
If the microscopic examination of the stool is
negative ,the string test should be performed
A string test involves swallowing a string to
obtain a sample from the upper part of the small
intestine. The sample is then tested to detect the
presence of intestinal parasites. Rarely used in the
United States.
Giardia antigen test
Much more sensitive than O&P
Replaces O&P for inpatients in many
hospitals
Treat with metronidazole

Dientamoeba fragilis Epidemiology
Distribution world-wide
Transmitted fecal-oral
May be transmitted by worm-egg vehicle!
Therefore the patient is already infected with
worms and D. fragilis is spread through the
worm eggs.
Remember no cyst form
Included with amebae until recently
D. fragilis Clinical Disease
Majority of infections asymptomatic
colonization of caecum/colon

Occasionally diarrhea, anorexia,
weight loss

No invasion of tissue mucosa

Diagnosis O & P exam
Remember, not always clinically significant!
Trichomonas vaginalis - Epidemiology
Urogenital, not intestinal
Distribuiton world-wide
Primarily sexually transmitted
Prevalence US/Canada
5-20% of women
2-10% of men
T. vaginalis

T. vaginalis Clinical Disease
A common cause of vaginitis in women
Some are asymptomatic carriers
Many have symptoms
Thin watery frothy discharge
Mild to severe inflammation
Itching, burning, painful urination
Strawberry cervix
Men
Primarily asymptomatic carriers
Occasionally urethritis, prostatitis
Diagnosis wet prep (hanging drop)
Treatment metronidazole

End of Part 1

Balantidium coli A Ciliate
Distribution world-wide,
swine reservoir
Transmitted fecal-oral, poor
sanitation
Trophozoite and cyst form
Surrounded by cilia and use it
to move.
A pig farmer who has
diarrhea and laboratory see
this enormous ciliated
organism.
Trophozoite Cyst


B. coli Clinical Disease
Some carriers are asymptomatic
Symptoms pain, nausea, anorexia, watery
stools with blood and pus.
Organism invade and GI tract will bleed.
Does not usually cause extraintestinal
disease.
Sometimes ulceration of intestinal mucosa
Rarely extraintestinal
B. coli Laboratory Diagnosis
Microscopic O&P exam
LARGE ciliate
No serology
Isospora belli Epidemiology
Distribution world-wide
Spread fecal-oral
Complex life cycle
Oocyst ingested
Releases sporozoites (replicate in intestinal mucosa)
Sexual forms develop and produce oocyst
Oocyst passed and matures outside the host
Life Cycle

I.belli Clinical Disease
Many carriers are asymptomatic
Symptomatic like Giardia disease
Not uncommon in AIDS patients!
Diagnosis O&P exam
Specify Isospora
Organism is acid-fast
Most labs will send sample externally for
testing
Case 3
CC:
A 30-year-old man with AIDS presents with chronic,
recurrent profuse, nonbloody, watery diarrhea.
HPI:
The diarrhea has recurred over the past two months with
intermittent cramping, and previous treatments have not
been effective.
PE:
V5: no fever. PS: moderate dehydration; thin; generalized
lymphadenopathy.
Labs:
Acid-fast staining demonstrates oocysts
of Cryptosporidium in fresh stool.
Cryptosporidium parvum
Distribution world-wide, many
animal hosts

Associated with contaminated
water supplies

Epidemic associated with
contaminated water and
undercooked meat

Often seen in farmers and
veterinarians, daycare centers
Cryptosporidium

C. parvum Clinical Disease
Carriage may be asymptomatic
Symptoms usually mild, self-limiting
Watery diarrhea (no invasion = no
blood)
Can be chronic (and very serious) in
AIDS patients
Very difficult to treat (keep them hydrated)
Mostly supportive
C. parvum Laboratory Diagnosis
O&P exam
Acid fast oocysts in stool
Biopsy shows dots in intestinal glands
Antigen test by EIA
Cyclospora cayatenensis
Distribution world-wide, endemic in
Nepal, India
Prevalence where endemic = 2-18%
Prevalence in US/Canada = 0.1-0.5%

Many animal hosts

Spread via contaminated water
C. cayatenensis Clinical Disease

Probably many asymptomatic infections

Symptoms, cramping, nausea, anorexia,
watery diarrhea

Usually self-limited

Can be serious and chronic in AIDS patients

Diagnosis O&P exam, specify
Cyclospora
Microsporidia Epidemiology
Obligate intracellular parasites
Six different genera
Infectious = spores
Life cycle
Ingestion of spore
Spore lodges intracellularly in small intestine
Multiplies by binary fission
Eventually kills cell
Mature spores released
Microsporidia Clinical disease
Symptoms variable
Diarrhea
Can infect several different organ
systems
Can be a serious infection of AIDS
patients
Diagnosis histology
Treatment none
Blood and Tissue Protozoans
Plasmodium sp. (Malaria)
Babesia (Babesiosis)
Toxoplasma (Toxoplasmosis)
Sarcocystis (Sarcocystosis)
Free-living amebae
Leishmania (Leishmaniasis)
Trypanosoma (Sleeping Sickness and
Chagas Disease)
Case 4
CC:
A 40-year-old male diagnosed with AIDS
presents with a severe headache.

HPI:
He suffered a grand mal seizure two hours
before his arrival in the emergency room. He
denies any past history of seizures and adds that
he has many pets, including cats.
PE:
Generalized lyrnphadenopathy; bilateral
papilledema; leftsided hemiparesis with
hyperactive deep tendon reflexes on left side;
positive Babinski's sign on left side.
Labs:
Positive indirect fluorescent antibody test for
toxoplasmosis; positive SabinFeldman dye test.
Imaging:
MR/CT-Head: single or multiple rounded mass lesions
with ring or nodular enhancement.
Gross pathology:
Large brain abscesses with concomitant focal neurologic
abnormalities, seizures, or altered mental status.
Micro pathology:
Parasites appear in tissue as tachyzoites or encysted
bradyzoites; aggregates of nonencapsulated organisms
constitute pseudocysts.
CT Brain

Toxoplasma gondii
Obligate intracellular parasite
Found in many birds and animals, especially cats.
Cats that eat mice have it.
Pregnant women avoid cat faeces!

Infective oocysts develop (3-4 days) in passed
cat feces
Man is a dead-end host
Rodents are a great intermediate host
T. gondii

Cyst

T. gondii Epidemiology
Distribution world-wide
Man can be infected in two ways
Consumption of improperly cooked meat
Ingestion of infectious oocyte from feces

Transplacental infection = serious fetal
infection

Immunocompromised are especially
susceptible (AIDS)
T. gondii Clinical Disease
Most infections are asymptomatic
Symptoms chills, fever, myalgias, headache, fatigue
If chronic, lymphadenitis, rash, hepatitis,
encephalomyelitis, myocarditis, choreoretinitis
In AIDS or immunocompromised frequently
neurologic
Encephalopathy
Meningoencephalitis
Cerebral mass lesions usually multifocal
Lesion in head with no respiratory symptoms then its
T. gondii , if see lesion in the head and respiratory
problems the its Nocardia.
Congenital Infection
Congenital infection of the fetus occurs
only when the mother is infected during
pregnancy.

If she infected before the pregnancy, the
organism will be in the cyst form and
there will be no trophozoites to pass
through the placenta
Congenital Infection
Congenital infection can result in abortion, still
birth, or neonatal disease with encephalitis,
chorio retinitis, and hepato megaly.

Intracranial calcifications are also seen.

Congenital infection with Toxoplasma is one of
the leading cause of blindness in children
T. gondii Lab. Diagnosis
Serology sensitive and specific
Must document four-fold rise
EIA also available for IgM

Histology identification of trophozoites is
definitive.
Can use monoclonal antibodies to do direct fluorescence

Culture not done

PCR available at reference labs

Treatment with combination of sulfadiazine and
pyrimethamine
Questions??

Sarcocystis lindemanni
Coccidian related to T. gondii and I. belli
World-wide pathogen of animals
Humans infected accidentally
Usually asymptomatic
Very rare invasive disease
Free-Living Amebae
Includes Naeglaria and Acanthamoeba
Live in fresh water and soil
People contract while swimming/diving
Sometimes isolated from contact lens
solutions (Acanthamoeba)
Free-Living Amebae (cont.)
Meningitis (usually Naeglaria)
Enters through nasal mucosa -> cribiform plate -> brain
Get it by diving into freshwater lakes
Rapidly fatal after infection of the brain
Can see motile amebae in CSF

Granulomatous amebic encephalitis (usually Acanthamoeba)
encephalitis with brain abscess(es), its much slower takes a
month for granulomas to grow.

Keratitis (usually Acanthamoeba)
Associated with improper contact lens care
Can disseminate in AIDS patients systemic disease.

Diagnosis - microscopy and culture
Naegleria fowleri

End