Clinical Parasitology Board Review

Clinical Parasitology
Protozoa and Helminth

The occurrence of protozoan parasites in
the body
Location, transmission and disease cause by
medically important protozoa
LOCATION MODE OF TRANSMISSION DISEASE
Intestinal tract Ingestion of cysts in food or Amebiasis

water Giardiasis
Cryptosporidiosis
Isosporiasis
Cyclosporiais
Microsporidiosis
Urogenital tract Sexual Trichomoniasis
Blood and tissue Bug or fly Trypanosomiasis, Chagas

disease
Sleeping sickness
Sand fly Leishmaniasis visceral or
cutaneous
Anopheles mosquito Malaria
Ingestion of cysts in raw Toxoplasmosis

meat, contact with soil
contaminated with cat feces,
vertical transmission )
How helminth parasites enter the body
Helminth- Worms
Tapeworms (Cestodes)
No digestive system
Acquired by eating undercooked or raw meal containing larval
stages
Flukes (Trematodes)
The most important cause Schistosomiasis or Bilharzia
Indirect life cycle involving stages of larval development in the
body of a snail.
Roundworms (Nematodes)
Autoinfection: eggs hatched in the intestine releasing infective
larvae which re-invade the body
Transmitted person to person, via arthropod vector or as a
zoonosis
Infectious Disease transmitted by arthropods
Etiologic agents Disease Arthropod vector
Viruses
Arboviruses Dengue fever Mosquitoes
Yellow fever Mosquitoes
Encephalities Mosquitoes, ticks
Hemorhragic fevers Ticks, mosquitoes
Bacteria
Yersinia pestis Plague Fleas
Borrelia recurrentis Relapsisng fever Soft ticks
Borrelia bugdorferi Lyme disease Hard ticks
Ricketsias
R prowazeki Epidemic typhus Lice, ticks
R mooseri Endemic typhus Fleas
R rickettsia Spotted fever Ticks
R akari Rickettisial pox Mites
Protozoa
Trypanosoma cruzi Chagas disease Reduviid bugs
Trypanosoma rhodesiense Sleeping sickness Tsetse flies
Trypanosoma gambiense Sleeping sickness Mosquitoes
Plasmodium spp. Malaria Sandflies
Leishmania spp. Leishmaniasis
Worms
Wuchereria and Brugia Lymphatic filariasis Mosquitoes
Onchocerca Onchocerciasis Simulium flies
Key concepts
Infections vs disease
Infection: Presence of parasites without
lesion or damage
Asymptomatic Carrier
Disease: Presence of parasites with
damage or symptoms
Key concepts
Parasite
pathogen that simultaneously injures and
derives sustenance from its host.
Zoonoses
Acquired by exposure to birds, reptiles or
other mammals
Dead end-host
The parasite do not have a developmental
stage in the host nevertheless can infect
Key concepts
PREVALENCE
measure of the frequency of a disease or
condition at a particular point in time,
usually expressed as the number of cases per
100 people examined
INCIDENCE
number of deaths or new cases of a
condition, symptom, or injury that arises
during a specific period of time, such as a
year
CLINICAL SIGNS
INFECTION
DETECTION
OF PARASITE
Incubation
Period
Patent
Period
Prepatent Period
TIME
Key concepts
Life cycle
Determines which developmental stages of a
parasite occur in which host
Important for diagnosis because certain forms
of the parasite can be found in human
samples
Eggs of hookworms in feces
Larvae of Strongyloides in feces
Whole Enterobius or eggs in perianal region (only
early in the morning)
Key concepts
Vectors
Transmits the parasite in a developmental stage
Usually are arthropods
Their presence correlate with the endemism of the
parasite
Host
receives the parasite
Tissue tropism
Determines the organs or tissue that supports
any stage of the parasite
Types of host
Definitive
Host has the parasite in adult state or sexual
reproduction
Intermediate
Host has the parasite in larvae state or
asexual reproduction
Transporter
Host has the parasite in larvae state, Non
developed
Types of parasites: protozoa
One cell-eukaryotes
Protozoan diseases range from very mild to life-
threatening
Includes medically important agents
Plasmodium (malaria)
Giardia
Cryptosporidium
Leishmania
Trypanosomes
Some have intracellular life cycles, some
extracellular
Types of parasites: protozoa
Transmitted by arthropods
Two basic life stages
Trophozoite
Replicate by binary fission
Cyst
Dormant
Highly resistant to desiccation
Can be transmitted via fecal-oral
Trophozoite and Cyst
Types of protozoa
Amebas
Flagellates
Ciliates
Apicomplexans
Types of protozoa: amebas
Entamoeba histolitica
Move by pseudopods
Intestinal parasite, low protein diet may favor its
virulence and growth)
Alternate between trophozoite and non motil cysts
(infectious stages). Bloody diahrrea, liver abcess
Fecal oral by water (cysts in water)
Dx: wagon wheel like nuclei and ingested WBCs
and RBCs in stools
Tx: Metronidazole or Iodoquinol for asymptomatic
passers
Entamoeba histolytica
Trophozoite in stool (arrow)

Entamoeba histolytica
Cyst (arrow) in stool

iodine preparation
Examples of amebas
Acanthamoeba sp
free-living amebas that inhabit soil and water
Cyst stages can be airborne entering through
lungs or eyes
Serious eye-threatening corneal ulcers in
individuals who use contact lenses,
Dx: Granulomatous amebic encephalitis
Trophozoites and wrinkled cyst in CSF; keratitis
with severe ocular pain may led to loss of eyesight
The parasites presumably are transmitted in
contaminated lens-cleaning solution.
Examples of amebas
Naegleria fowleri
inhabit bodies of fresh water
responsible for almost all cases of the usually
fatal disease primary amebic
meningoencephalitis
Dx: Trophozoites (slug-like amebas and smooth
walled cysts in CSF)
Tx: Amphotericin B
Enter the body from water that is splashed onto
the upper nasal tract during swimming or
diving.
Types of protozoa: Ciliates
Extremely unusual; associated with individuals who
raise pigs or who work in slaughterhouses
Small projections or cilia cover their bodies with a
macronucleus both in trophozoites and cysts.
Balantidium coli is the largest intestinal protozoan
of humans causing dysenteria
Cysts are ingested
Trophozoites descend colon and feed on bacteria
and fecal debris
Cysts can be secreted in feces
Tx: Tetracycline
Balantidium coli
Balantidium coli
Cyst Trophozoite
Types of protozoa
Flagellates
Intestinal and blood protozoa
Locomotion through flagella
Medical important members include:
Giardia
Trichomonas
Trypanosoma - Hemoflagelates
Leishmania - Hemoflagelates
Flagellates: Giardia
Most common pathogenic flagellate Dx in USA
Its found in the duodenum and jejunum of humans
causing diarrhea with mal absorption, bloating
flatulence, foul-smelling. Late onset diarrhea gets
fatty(steatorrhea); severe pain on ingestion of dairy is
common
Cysts are found in the stools in great numbers (even if
asymptomatic) or even trophozoites
Dx: cysts in stool and pyriform motile trophozoites.
Fecal Ag test is more sensitive
Three or more stool examinations are needed
Tx: Tinidazole, Nitazoxamide,Metronidazole
Giardia lamblia
Giardia lamblia
Cyst
Trophozoite
Flagellates: Giardia
Flagellates: Trichomonas
Three species are important
T. tenax- mouth
T. hominis- intestine
T. vaginalis- genitourinary tract, sexual contact
Can affect both, men usually asymptomatic
Dx: vaginal and urethral discharge associated
with burning or itching should be examined
microscopically
Motile trophozoite with ondulant membrane and
excessive neutrophils, foul smeling greenish
discharge or vaginitis
Treatment: metronidazole or tinidazole for both
sexual partners
Flagellates: Trichomonas
Trichomonas infection
Trichomonas vaginalis-
protozoan parasite
Metronidazole; if pregnant
acetic acid douche
Cause vaginitis with copious

creamy discharge
Rarely symptomatic in men
Sexual partner and

symptomatic women have to
be treated at the same time to
prevent re-infection (ping
Dx: flagellates moving in wet
35
pong relapses)
prep of vaginal secretion
Flagellates: Trypanosoma
Two representative:
African species T. brucei brucei (T. b. gambiense
and T. b. rhodesiense)
T. cruzi
Mammals are infected with trypomastigotes
hemoflagellate noted for antigenic variation
Human African trypanosomiasis, also known as
sleeping sickness
In their cells specially heart, liver, brain
develops the amastigotes, that will eventually
release by bursting the cell the
trypomastigotes
Transmitted to humans by tsetse fly
Mother-to-child infection: the trypanosome
can cross the placenta and infect the fetus.
Mechanical transmission through other blood
sucking insects is possible.
Accidental infections have occurred in
laboratories due to pricks from contaminated
needles.
Human African trypanosomiasis
Two disease stages
First stage: restricted to subcutaneous
tissues, blood and lymph. Symptoms are
fever, headaches, joint pains and itching.
Second stage: parasites cross the blood-
brain barrier to infect the central nervous
system. This is known as the neurological
phase. Symptoms are changes of behavior,
confusion, sensory disturbances and poor
coordination.
Trypanosoma: Chagas disease
Infection is lifelong travel or residence in
poor areas of South America. T. cruzi
Complications of chronic Chagas disease may
include: heart failure with enlarged heart ,
cardiomyopathy, megacolon, mega esophagus
Dx: Chagas disease can be made by
observation of the parasite amastigotes in
heart tissue or trypomastigostes in blood early
Dx: sleeping sickness can be made by seen
trypomastigostes in blood or CSF and
hypergammaglobulinemia
Trypanosoma cruziamastigote colonies (arrows) in heart
muscle. Amastigotes are 13um in diameter in tissue
sections.
Triatomine bug
Romaa's sign
The trypanosomiases, Barrett, et al

The Lancet, Volume 362, Issue 9394, Pages 1469-1480
Radiographs of pathological findings of Chagas' disease(A)
Enlarged heart, (B) megaoesophagous, and (C) megacolon.
The trypanosomiases, Barrett, et al

The Lancet, Volume 362, Issue 9394, Pages 1469-1480
Trypanosomiasis causative agents
Trypansoma
cruzi trypomastigotes
that measure 12 to 30
m in length. They
contain a membrane
and a flagellum.
Trypanosomiasis causative agents
Diagnostic
Fresh blood can detect actively motile
trypanosomes
CSF can also be examined
Theres an available ELISA
Treatment for
African trypanosomiasis is suramin sodium
(Germanin) or pentamidine isethionate
(Lomidine)
American trypanosomiasis is Nifurtimox
Flagellates: Leishmania
Promastigotes are not found in human tissue;
this stage occurs in the mid-gut of the sand fly
Replicate within macrophages
Amastigote
The two most common forms are visceral and
cutaneous leishmaniasis.
There are about 500000 newvisceral
leishmaniasis (kala azar)cases each year.
More than 90 % of the visceral leishmaniasis
infections take place in Bangladesh, Brazil,
India, Nepal and Sudan
Leishmaniasis Etiology
Organisms are transmitted by

phlebotomine sandflies of the genus
Phlebotomusin the Asia, Africa, and
Europe and the genusLutzomyiain the
the Americas
Leishmaniasis distribution
The disease develops a few months after
the sandfly bite and symptoms include:
anemia
enlarged liver and spleen
fever
weaker inflammatory response (due to the
loss of phagocytes)
weight loss
Diagnostic:
For skin lesions a biopsy from the margin of the
lesion can be examined in the microscope to
look for amastigotes
Lymph node aspirates, blood , and spleen, liver
or bone marrow puncture are important for
visceral kala-azar
Treatment:
Single lesions can be cleaned and left to heal
For other large lesions, sodium gluconate is the
drug of choice
PostKala-Azar DermalLeishmaniasis
PostKala-Azar DermalLeishmaniasis
Cutaneousleishmaniasis
Localized cutaneous leishmaniasis:
volcano sign
CL: crusted erythematous plaque and
nodule
CL: chiclero ulcer. A deep ulcer on the helix
at the site of a sandfly bite
Leishmaniasis diagnosis
The diagnosis is based on history and clinical
findings, PCR is more sensitive than microscopy
and culture and allows identification of the specie
Giemsa staining will show amastigotes within
macrophages
For CL,biopsies should be taken from the raised border
of a skin lesion. For MLdiagnosis is done by detecting
amastigotes in scrapings, biopsy preparations, or
aspirated tissue fluid
Montenegro test
Bone marrow biopsy specimen from a patient with visceral
leishmaniasis showing a macrophage containing
Leishmaniaamastigotes. CDC photo.
Leishmaniaspp. amastigotes; touch-
prep stained with Giemsa.
Histologic examination (hematoxylin and eosin).A.Acute cutaneous leishmaniasis. Moderately dense
lymphohistiocytic infiltrate with numerous parasitized macrophages containing amastigotes (Leishman
bodies).B.Chronic cutaneous leishmaniasis. Tuberculoid granulomatous dermatitis. Note the presence of
multinucleated giant cells, the surrounding lymphoplasmacytic infiltrate, and the absence of parasites.
Types of protozoa: Apicomplexans
Named also sporozoa
Important pathogens
All have intracellular replication
Locomotion is by gliding that permits forced
entry to host cell
Clinical important members include
Plasmodium, Toxoplasma,
Cryptosporidium, Cyclospora, Isospora,
Babesia
Apicomplexans: Plasmodium
Causative agent of malaria
Transmission is by the bloodsucking bite of
female anopheles mosquitoes
Transmits the sporozoite
These will invade liver cells and develop into
merozoites
These will rupture and leave the liver cells
and enter the bloodstream to invade
erythrocytes
Anopheles distribution
Kiszewksi et al., 2004. American Journal of Tropical Medicine and Hygiene 70(5):
486-498
http://www.cdc.gov/malaria/about/biology/mosquitoes/
Species:
Falciparum
Most dangerous, multiply quickly causing severe
blood loss , can clog blood vessels, tropical
distribution
Malariae
Ovale
Vivax
Malaria lifecycle
Pulmonary malaria:
Plasmodium vivax,Plasmodium falciparum, Plasmodium ovale
Malaria is caused by the obligate

intraerythrocytic
Humans get infected upon female
Anophelesmosquitoes bite
The parasites grow and multiply first in the
liver cells and then in the red cells of the blood
Incubation period in most cases varies from 7 to
30 days
General symptoms
Fever
Chills
Sweats
Headaches
Nausea and vomiting
Body aches
General malaise
Pulmonary malaria:

Acute respiratory distress syndrome
(ARDS)
inflammatory reaction in the lungs that
inhibits oxygen exchange, which may occur
even after the parasite counts have
decreased in response to treatment
Acute pulmonary edema is usually a fatal
complication of severe falciparum malaria
with more than 50% mortality.
Diagnostic:
Thick blood film stained with Giemsa
Treatment
Chloroquine is the drug of choice
Malaria treatment
chloroquine
atovaquone-proguanil (Malarone)
artemether-lumefantrine (Coartem)
mefloquine (Lariam)
quinine
quinidine
doxycycline (used in combination with quinine)
clindamycin (used in combination with quinine)
Apicomplexans: Toxoplasma
Infects a wide range of animals
Cause of brain abcess in HIV, congenital toxoplasmosis
=classic triad of chorioretinitis, hydrocephalus and
intracranial calcifications
Cyst in meat or cat feces, crosses placenta (pregnant
women should avoid cats
T cell compromised patients, fever with
lymphadenopathy and pneumonia; often changes in
mental status, symptoms resemble mononucleosis
Pulmonary toxoplasmosis:
Toxoplasma gondii
Important opportunistic infection in HIV
Pts
Disease is transmitted to other host species
by the ingestion of oocysts passed in the
feces of infected felines
The parasite can cause lymphadenopathy,
encephalitis, myocarditis, and pneumonitis
Can infect and replicate in all mammalian
cells, and provoke cytotoxicity by rupture
Invasive trophozoite forms
Cyst manifestation
Toxoplasmosis pathology
Can cause cell death and focal necrosis due to
replicating tachyzoites
Induce an intense mononuclear inflammatory
response
Interstitial pneumonitis can develop in neonates
and immunocompromised patients.
Thickened and edematous alveolar septa
infiltrated with mononuclear and plasma cells
are apparent. This inflammation may extend to
the endothelial walls.
Diagnosis of toxoplasmosis
Immunofluorescent staining with parasitic
antigenspecific antibodies can reveal
either the organism itself or evidence of
antigen.
Culture is difficult and requires
subinoculation into mice
Other involves PCR or serology (detection
of the simultaneous presence ofIgGand
IgM antibodies toToxoplasmain serum)
Treatment of toxoplasmosis
Pyrimethamine (Daraprim)
It's a folic acid antagonist
Sulfadiazine
antibiotic is used in combination with
pyrimethamine
An alternative to sulfadiazine is
clindamycin (Cleocin)
Diagnostic:
Blood (buffy cot of heparinized sample),
sputum, bone marrow and CSF can be
examined under the microscope (stained with
Giemsa)
Treatment:
pyrimethamine + sulfadiazine or spiramycin
(drug of choice to use during pregnancy)
Cryptosporidium parvum
Related to Isospora
Self-limiting in normal patients (Pts) but
serious in immunocompromised Pts
Incubation period is an average of 7 days
In immunocompetent Pts, symptoms are
usually short lived (1 to 2 weeks ) and
primary cause a mild gastroenteritis
In immunocompromised Pts
Watery diarrhea is the most frequent symptom
In addition Pts can suffer dehydration, weight
loss, abdominal pain, fever, nausea and
vomiting
Found worldwide
Transient diarrhea in healhy person;
severe in the immunocompromised persons
Infection occurs by ingestion of cysts

(chlorine resistant). When the excystation
occurs the sporozoites are released and
parasitize epithelial cells of the
gastrointestinal tract.
Then the parasites undergo asexual
multiplication and then sexual multiplication
Diagnosis includes detection of oocysts by
immunofluorescence microscopy
Infective dose are 30 organisms

Treatment to immunocompromised
includes Spyramycin and cessation of
immunosuppressant's (if they are taken)
For immunocompetent Nitazoxanide was
approved by FDA ((500 mg twice daily for
3 days)
For HIV Pts only supportive therapy is
available
Immunofluorescence image of Cryptosporidium parvum oocysts, purified from

murine fecal material. (Same field of view) Oocysts were stained with
commercially available immunofluorescent antibodies. Oocysts should have an
intense apple green fluorescence on the periphery of their oocyst wall, and
measure 4 to 6 microns in diameter. Scale bar is 10 microns.
Fluorescence image of Cryptosporidium parvum oocysts, purified from

murine fecal material. Oocysts were stained with 4,6-diamidino 2-phenyl-
indole dihydrochloride (DAPI). DAPI interacts with nucleic acids and stains
the nucleus of each sporozoite within the oocyst. There should be 4
sporozoites each with 1 nucleus, or 4 stained nuclei in each oocyst.
Isospora belli
Infection is acquired by the consumption
of oocysts
Parasite invades intestinal epithelial cells
and undergoes both sexual and asexual
cycles of development.
Oocysts excreted in stool are not
immediately infectious but must undergo
further maturation.
Isospora belli
Inhabits the small intestine
Incubation period is 1 week
Symptoms in immunocompetent Pts are
low-grade fever, lassitude, malaise, mild
diarrhea, and vague abdominal pain
Usually self-limiting
Worldwide distribution, especially in
tropical and subtropical areas.
Isospora belli
In immunocompromised Pts such HIV+,
infections often are not self-limited
Resemble cryptosporidiosis, with chronic,
profuse watery diarrhea.
Eosinophilia, which is not found in other
enteric protozoan infections, may be
detectable
Isospora belli
Treatment:
Trimethoprim-sulfamethoxazole (TMP-
SMX, 160/800 mg four times daily for 10
days
HIV-infected patients(TMP-SMX, 160/800
mg three times daily for 3 weeks)
Isospora belli
Isospora belli
Oocyst of C. belli in an unstainedOocyst of C. belli stained with

wet mount safranin
Isospora belli
Oocysts of C. belli in the epithelial cells of a

mammalian host, stained with H&E (yellow arrows)
Cyclospora
Life cycle as (Isopora and
Cryptosporidium) involves epithelial cell
of the mucosa
Disease can be self-limited
It can involve prolonged diarrhea, anorexia,
and upper gastrointestinal symptoms, with
sustained fatigue and weight loss
Diarrheal illness may persist for >1 month.
Cyclospora
Many has reported the parasite including
USA and Canada, but is most common in
tropical and subtropical areas
There is absence of fecal blood and
leukocytes indicating there is no
destruction of the small-bowel mucosa
Cyclospora
Diagnosis can be made by detection of
spherical oocysts in the stools
three or more specimens at 2- or 3-day
intervals may be required
concentration procedures should be used to
maximize recovery of oocysts
Cyclospora
Treatment includes TMP-SMX (160/800 mg
twice daily for 7 days).
HIV-infected patients may experience
relapses after such treatment and thus
may require longer-term suppressive
maintenance therapy
Cyclospora
Cyclospora oocysts appear

as round organisms, 7-10
m in diameter, with a
distinct oocyst wall
Cyclospora
UV fluorescence microscopy, where the oocysts autofluoresce

under ultraviolet light. Cryptosporidium spp. oocysts do not
autofluoresce to any extent. Cycloospora belli do fluoresce, the
walls of the oocysts fluoresce brightly
Cyclospora
Apicomplexan:Babesia
Babesia microti,B. divergens,Babesia
duncani
Two host prior humans, a rodent and tick
Humans (dead-end-host) are definite
host, however we can infect ither humans
Symptoms includes ever, chills, sweating,
myalgias, fatigue, hepatosplenomegaly,
and hemolytic anemia
Pulmonary babesiosis:
Babesia microti,Babesia divergens
Protozoans are obligate parasites of red blood
cells (RBCs)
is endemic in southeastern Massachusetts,
coastal Rhode Island and Connecticut, central
New Jersey, Wisconsin, and Minnesota
Deer tickIxodes scapularisis the primary vector
Severe symptoms can include: anemia, acute
respiratory distress syndrome, disseminated
intravascular coagulation, congestive heart
failure, and renal failure
Babesiosis diagnosis
Should be considered for any patient who
presents with flu-like symptoms and has
recently resided in or traveled to an
endemic area or received a blood
transfusion
Presents with symptoms of or has been
diagnosed with Lyme disease
Babesiosis diagnosis
Diagnosed by microscopic examination of
Giemsa-stained thin blood smears, on
which they appear as round or pear-
shaped organisms. The ring form is most
common and lacks the central brownish
deposit (hemozoin)
Absence of schizonts and gametocytes
Occasionally presents tetrads known as
Maltese crosses
Babesia
Maltese crosses
Treatment
Helminths
Multicellular animals
Reproduce sexually (although some can be
hermaphroditic)
Some macroscopic
Extracellular
Impermeable cuticle that protect them
Several hosts
Types of helminths
Roundworms (nematode)
Circular in cross section
Necator, Enterobius,Buchereria,Brugia, Ascaris,
Anculostoma,Trichinella, Trichuris, Toxocara, Onchocerca,
Dracunculus,Loa loa and Strongyloides
No body segmentation
Flatworms (cestode)
Asymmetric in cross section
Taenia, Diphilobotrium, Hymenolepsis,Dipilydium, Cysticercosis
and Echinococcus
Tapeworms (cestodes)
Ribbon-like segmented bodies , each segment called strobila
Flukes (trematode)
Leaf-shaped
Schistosoma
Vectors and reservoirs
Vectors
Transmitter of disease
Most are arthropods
Are also involved in the parasite life cycle
Containing their multiplication, you often
control the disease spread
Reservoirs
Source of parasites
Humans serve as parasite reservoirs
Pork for T. solium and cattle for T. saginata
Pathologic mechanisms
Parasite produce toxic products that
mediate tissue damage and contribute to
deregulation of immune system
These includes:
Toxic products
Direct tissue damage
Immunopathology

Pathologic mechanisms: Toxic products
Hydrolitic enzymes
Schistosomes, strongyloides, hookworms,
Entamoeba histolytica, African trypanosome
and Plasmodium falciparum
Mechanical tissue damage
Blockage (Ascaris), Pressure atrophy
(Echinococcus sp, Cysticercus sp)
Immunopathology
Hypersensitivities (a type of pneumonia)
Parasite Ports of entry
ROUTE EXAMPLES
Ingestion
Giardia sp, Entamoeba histolytica,

Crypstosporidium sp, cestodes, nematodes
Direct penetration
Arthropod bite Malaria, Babesia, filaria, Leishmania spm,
Trypanosomes
Transplacental Toxoplasma gondii

Organisms-direct Hookworms, Strongyloides sp,
Schistosomes
Role of immunity in parasitic infections
Many intracellular parasite such as

Leishmania are difficult to eliminate
because they are not exposed to the
immune system
Plasmodium often changes they protein
expression making the antibodies
produced in a previous infection,
unhelpful
Hypersensitivities
Type 1
Antigen +IgE mediates histamine release, occurs
in helminthes infections
Type 2
Cytotoxic, lysis of cells bearing parasite Ags, T.
cruzi infection
Type 3
Immune complexes, inflammation (plasmodium)
Type 4
Cell-mediated, sensitized T cells become
activated and activates macrophages
(granuloma)
Helminths: flukes
Typically leaf-shaped with a pair of suckers
Members include
Fasciola hepatica
Schistosoma mansoni, haematobium and
japonicum
Snails are host, cercaria penetrates the skin
of humans causing urticarial, dysentery, liver
granulomas, fibrosis and inflammation.
Chronic infection of squamous cells cause
carcinoma of the bladder.
Flukes: Schistosoma
Diagnostic is the presence of differentiated eggs in
feces or in urine
Treatment of choice is Praziquantel (for Fasciola is
bithionol)
Heavy infestation may cause fever, chills, lymph
node enlargement, and liver and spleen
enlargement.
Swimmer's itch
Dx: Egg with lateral spine in feces
Tx: Intestinal: Praziquantel
Schistosomiasis Etiology
Eggs are pass in the feces or urine

These eggs hatch and release miracidia,
that swim and penetrate specific snail
intermediate hosts.
Snail releases the cercariae.This infective
cercariae swim, penetrate the skin of the
human host,shed their forked tail,
becoming a schistosomulae
From there travel to veins
Manifestations include fever, cough,

abdominal pain, diarrhea,
hepatosplenomegaly, and eosinophilia
Pulmonary schistosomiasis:
Schistosoma haematobium, Schistosoma mansoni
Schistosoma japonicum
Symptoms include fever, cough,

abdominal pain, diarrhea,
Treatment is praziquantel
Intestinal and visceral schistosomiasis
Diagnosis is done by microscopic

identification of eggs in stool or urine
Urine recommended time for collection:
between noon and 3 PM
The preferred treatment to all the
Schistosomaspecies is praziquantel
Infection occurs when infective cercariae

swim penetrates the human skin
Geographical distribution
S. mansoniis found in parts of South America
and the Caribbean, Africa, and the Middle
East
S. haematobiumin Africa and the Middle East
S. japonicumin the Far East
Blood trematodes
S. japonicumfrequently found in the
superior mesenteric veins that drains the
small intestine
S. mansonifound in the superior mesenteric
veins draining the large intestine
S. haematobium most often lives in the
venous plexus of bladderor in the rectal
venules
Females (size 7 to 20 mm; males slightly

smaller) deposit eggs in the small venules
The eggs of S. mansoniandS. japonicum
are moved toward the lumen of the
intestine and are excreted in feces
The eggs of S. haematobium travel to the
bladder and ureters, and are eliminated
with the urine
Katayama's fever (acute schistosomiasis by S.

mansoniandS. japonicum) include fever,
cough, abdominal pain, diarrhea,
Prolonged infections can cause
granulomatous reactions and fibrosis
Maniestation S. mansoni S. japonicum S. haematobium
colonic polyposis with

bloody diarrhea

portal hypertension
and splenomegaly

cystitis and ureteritis*

pulmonary
hypertension

Cercarial dermatitis
Localized erythema develops

Can progress to pruritic maculopapular
rash persisting for days
Can be caused by human schistosomes
and, in nontropical areas, by bird
schistosomes that cannot complete their
life cycle in humans (swimmer's itch)
Schistosomiasis distribution
Schistosoma mansoniis found in parts of

South America and the Caribbean, Africa,
and the Middle East
S. haematobiumin Africa and the Middle
East
S. japonicumin the Far East
Schistosomiasis mechanisms
Acuteschistosomiasiscauses an itchy rash

(swimmer's itch) that occurs within an
hour after cercariae penetrate the skin
Other symptoms are headache, chills,
fever, diarrhea, and eosinophilia (known
as snail fever or Katayama fever) 212
weeks after exposure (Salvana and King,
2008)
Schistosoma mansoni
S. japonicum
S. haematobium
Flukes : Fasciola hepatica
Tapeworms
Taenia saginata (beef)
Taenia solium (pork)
Diphyllobotrium latum (fish)
Hymenolepsis nana (humans and rodents)
Dipilydium caninum (Dog and Cats)
Helminths: flukes
Helminths: Tapeworms
Ribbon-like segments or strobila
Each contains a male and female
system
Contains the scolex, a hold-fast organ
that consists of suckers and hooks to
maintain worm in position
Members include
Taenia solium: human ingest cysticerci, that
releases worms
Taenia saginata: infects only humans
Diagnostic:
Several stool specimens over several days for
microscopic examination
CT or X-ray if neurocysticercosis is suspected
Treatment: Praziquantel
Taenia Infx Transmission
Ingestion of larvae encysted in under
cooked meal
Ingestion of eggs
Taenia Disease
Intestinal Infection: Tx: Praziquantel
Cysticercosis: Tx: Praziquantel
Neurocystecercosis: Tx: Praziquantel-

bendazole
Tapeworms (Taenias)
Pork tapeworm (T. solium), Beef
tapeworm (T. saginata)
Main cause of human cysticercosis
Worldwide distribution
pigs and cattle are intermediate hosts of the
parasites, completion of the life cycle occurs
in regions where humans have contact with
rare meat
No direct gastrointestinal symptoms
Tapeworms (Taenias)
T. saginata(may reach up to 25 m) and 2
to 7 m forT. solium
Inhabits the human jejunum and are long-
lived
It can be distinguished by its (suckers) and
proglottid (egg-filled terminal segments)
Can be seen in feces
Tapeworms (Taenias)
Symptoms are associated with the
involved tissues
decrease visual acuity with
ophthalmocysticercosis
headache, nausea, vomiting, mental
disturbances, and seizures caused by
encysted cysticerci in the brain
(neurocysticercosis)
Treatment is Praziquantel
Tapeworms (Taenias)
Taenia solium
Several cysticerci (larval forms) encysted in muscle.

Taenia solium
A single cysticercus
seen in a magnetic
resonance imaging
scan of the brain.
Tapeworms (Taenias)
Eggs are indistinguishable from each other

Tapeworms (Taenias)
Scolex of T. saginata. Scolex of T. solium. Contains

Contains four large suckers four large suckers and
and lack of rostellum and rostellum containing two
rostellar hooks. rows of hooks.
Tapeworms (Taenias)
Mature proglottids Mature proglottids

of T. saginata of T. solium
Diphyllobothrium latum
Ingestion of larvae from raw freshwater fish
Vitamin B12 deficiency by competition causes

anemia
Ingestion of late larvae
Dx: Proglotids and eggs in stools
Tx: Praziquentel
Echinococcus
Pulmonary hydatid disease:
Echinococcus granulosus,
Echinococcus multilocularis
Humans become infected when they swallow
eggs in contaminated food with dog feces.
The infection is carried to the liver,
wherecystsform.
Cysts can also form in the brain, bones, kidney,
lungs, skeletal muscles and spleen
Echinococcus sp. Life cycle
Pulmonary hydatid disease
Pain in the upper right part of the
abdomen
Bloody sputum
Chest pain
Cough
Fever
Severe skinitching
Treatment
Treatment includes albendazole or
mebendazole.
for up to 3 months
Praziquantel can be combined with
albendazole or mebendazole
The cysts may be removed with surgery
A 14 cm hydatid cyst from a
splenectomized patient
Roundworms: hookworms
Ancyslostoma duodenale and Necator
americanus
Eggs are released in stools
Larva develops and can penetrate skin
(Ground-itch)
BothN. americanusandA. duodenaleare
found in Africa, Asia and the Americas.
Microscopic identification of eggs in the stool
is the most common method for diagnosing
Roundworms: hookworms
Practically unrecognizable unless genetic
testing is done
Severe infection includes intestinal blood
loss, anemia, and protein malnutrition
Humans are the definitive hosts
A. brazilienseandA. caninum
Treatment: Albendazole and
Mebendazole
Hookworms (Ancylostoma / Necator)
Larva hatches from the egg within a day

or two and can survive in moist soil for
several weeks
Can invade and parasitize humans or can
penetrate the human skin (causing
cutaneous larva migrans)
Second most common human helminthic
infection (after ascariasis)
Femalehookwormsare 10 mm in length
and males are slightly smaller
Have a characteristic copulatory bursa
(broadened posterior end), which is used
to mate with females.
Females can release more than 10,000
eggs per day into the feces
Worldwide distribution mostly in areas

with moist, warm climate.
Necator americanusis found
predominantly in Americas and Australia.
A. duodenaleis found in the Middle East,
North Africa and southern Europe.
Symptoms include:
Iron deficiency anemia (caused by blood loss at
the site of intestinal attachment of the adult
worms)
Gastrointestinal and nutritional/metabolic
symptoms can also occur
Skin manifestations ('ground itch') can occur
during penetration by the filariform (L3) larvae,
and respiratory symptoms can be observed
during pulmonary migration of the larvae.
Pulmonary ancylostomiasis:
Ancylostoma duodenale,
Necator americanus
Diagnosis is made by presence of eggs in

stools
Treatment includes albendazole and
mebendazole

identification of eggs in the stool
cannot distinguish betweenN.
americanusandA. duodenale
Treatment
Albendazole, mebendazole or pyrantel
pamoate
Hookworms
Hookworms (Ancylostoma)
Hookworms
Longitudinal section of an adu

hookworm worm in a bowel
biopsy, stained with H&E. No
the oral cavity (OC) and stron
muscled esophagus (ES).
Ancylostoma duodenale. Necator americanus. Anterior end

Anterior end is depicted showing showing mouth parts with cutting
cutting teeth. plates.
Watch out, I can bite!!
Roundworms: Enterobius vermicularis
Known as the pin worm

Humans are the only hosts
Most typical symptom is perianal
pruritus, especially at night in young
children
Diagnostic is by microscopic
identification of eggs collected in the
perianal area
Enterobius vermicularis
Nematode (roundworm)Enterobius
vermicularis
Only hosts
Acquired by person-to-person, by handling
of contaminated clothes or bed linens,
curtains, carpets. Some small number of
eggs may become airborne and inhaled.
Worldwide distribution but is more
frequent in school- or preschool-children
Symptoms include perianal pruritus,
vulvovaginitis, irritability, and abdominal
pain
identification of eggs collected in the
perianal area
Treatment is done with pyrantel
pamoateandmebendazole
Eggs of E. vermicularis in a Eggs of E. vermicularis viewed

cellulose-tape preparation under UV microscopy.
Roundworms: Enterobius vermicularis
Filariasis
Filariasis is caused by nematodes

(roundworms)
Eight main species infect humans.
Three of these are responsible for most of
the morbidity due to
filariasis:Wuchereria bancroftiandBrugia
malayicause lymphatic filariasis,
andOnchocerca volvuluscauses
onchocerciasis (river blindness)
Filariasis
The other five species areLoa

loa,Mansonella perstans,M.
streptocerca,M. ozzardi, andBrugia
timori. (The last species also causes
lymphatic filariasis.)
Roundworms: Wuchereria bancrofti
Larva is injected when mosquitoes are sucking
blood
Culex, Anopheles, Aedes, Mansonia
Some patients develop lymphatic dysfunction
causing lymphedema and elephantiasis
(frequently in the lower extremities)
Diagnostic:
Blood smear
Treatment: depends on filiaria. For W. bancrofti
the recommended is Diethylcarbamazine
Roundworms: Wuchereria bancrofti
Pulmonary filariasis:
Wuchereria bancrofti, Brugia malayi
Known also as tropical pulmonary

eosinophilia
Caused by an immune
hyperresponsiveness to microfilariae
trapped in the lungs
Treatment includes ivermectin and
albendazole alone or in combination
Ascaris lumbricoides
Largest round worm that infects humans
Adult females: 20 to 35 cm; adult male:
15 to 30 cm
Worldwide distribution but high
prevalence in tropical and subtropical
regions, and places with poor sanitation
Infection occurs after eggs are ingested
Larvae hatch in the duodenum, penetrate
through the mucosa, migrate in the
circulatory system, lodge in lung
capillaries, penetrate the alveoli, and
migrate from the bronchioles to the
trachea and pharynx; larvae are
swallowed and return to the intestine and
mature into adults
No acute symptoms.
Symptoms are related with high worm
burdens
These includes abdominal pain, intestinal
obstruction.
Migrating adult worms may cause
mechanical obstruction of the bowel and
bile and pancreatic ducts
During the lung phase of larval migration,
pulmonary symptoms can occur (cough,
dyspnea, hemoptysis, Loefflers
syndrome)
Treatment of choice for treatment of is
albendazole
Worms tend to migrate if drugs such as
anesthetics or steroids are given, leading
to bowel perforation and peritonitis, anal
passage of worms, vomiting, and
abdominal pain.
Ascaris lumbricoides, obstruction, appendix

Mass of adult worms recovered from infant at autopsy

Bowel obstruction
Largest round worm that infects humans
Adult females: 20 to 35 cm; adult male:
15 to 30 cm
Worldwide distribution but high
prevalence in tropical and subtropical
regions, and places with poor sanitation
Infection occurs after eggs are ingested
Larvae hatch in the duodenum, penetrate
through the mucosa, migrate in the
circulatory system, lodge in lung
capillaries, penetrate the alveoli, and
migrate from the bronchioles to the
trachea and pharynx; larvae are
swallowed and return to the intestine and
mature into adults
No acute symptoms.
Symptoms are related with high worm
burdens
These includes abdominal pain, intestinal
obstruction.
Migrating adult worms may cause
mechanical obstruction of the bowel and
bile and pancreatic ducts
During the lung phase of larval migration,
pulmonary symptoms can occur (cough,
dyspnea, hemoptysis, Loefflers
syndrome)
Treatment of choice for treatment of is
albendazole
Worms tend to migrate if drugs such as
anesthetics or steroids are given, leading
to bowel perforation and peritonitis, anal
passage of worms, vomiting, and
abdominal pain.
Roundworms: Ascaris
Bowel obstruction
Roundworms: Ascaris
Ascaris lumbricoides, obstruction, appendix

Mass of adult worms recovered from infant at autopsy

Pulmonary ascariasis
Largest nematode (roundworm) parasitizing
the human intestine
Adult females: 20 to 35 cm; adult male: 15 to 30
cm
Cough are due to migration of the worms
through the body
Diagnosis is mad by presence of eggs in stools
Treatment includes albendazole and
mebendazole
Roundworms: Ascaris
Ascariasis is the most common intestinal worm
infection.
Infection occurs by ingestion of eggs, these hatch
and release immature larvae within the small
intestine and then migrate to lung
In the lungs the larvae may produce an uncommon
form of pneumonia called eosinophilic pneumonia.
Once they are back in the small intestine, the
larvae mature into adult roundworms.
Adult worms live in the small intestine where they
lay eggs that are present in feces. They can live 10
24 months.
Roundworms: Ascaris
Diagnostic:
Presence of typical eggs in feces
Treatment:
Albendazole
Mebendazole
Loeffler Syndrome
Simple pulmonary eosinophilia is
inflammation of the lungs associated with
an increase in eosinophils
Causes
Most cases of simple pulmonary eosinophilia
are due to an allergic reaction, either from a
drug, such as sulfonamide, or infection with a
fungus or parasite, including Ascaris
lumbricoides.
Pulmonary trichinellosis:
Trichinella spiralis
Symptoms start within 2 weeks after
eating contaminated meat, and last up to
8 weeks. These include:
Muscle pain
Fever
Swelling of the face, particularly the eyes
Weakness or fatigue, headache, Chills
Cough, itchy skin or rash, diarrhea
Constipation
Trichinella life cycle
Pulmonary trichinellosis:
Trichinella spiralis
Diagnosis ofTrichinellainfection is most
often made by aTrichinellaantibody test
Additionally a muscle biopsy may be
performed
Treatment can include
mebendazole or
albendazole
Roundworm: Trichuris
Called the human whipworm
Causes primary gastrointestinal
problems (abdominal pain, diarrhea,
rectal prolapse) and possibly growth
retardation
Treatment ?
Diagnosis: characteristic eggs in stools
Trichuris trichiura
Third most common round worm of humans
Heavy infections can cause gastrointestinal
problems (abdominal pain, diarrhea, rectal
prolapse)
identification of whipworm eggs in feces
Treatment is done with Mebendazole and
albendazole
Trichuris trichiura
Female can produce up to 10,000 oval
eggs each day
The adults inhabit cecum and release
eggs to lumen
These pass out the body with the feces, but
are not infective
Must developed in soil (10 days) before
become infective
Long-lived (adult live 4 to 8 years)
Trichuris trichiura
Worldwide distribution but is more
frequent in areas with tropical weather
and poor sanitation practices
It is estimated that 800 million people are
infected worldwide.
Trichuriasis occurs in the southern United
States.
Treatment is done with Mebendazole and
Albendazole
Trichuris trichiura
Trichuris trichiura
Terminal ileum
covered with
adult Trichuris
trichiura
Trichuris trichiura
Posterior end of an
adult T. trichiura, taken
during a colonoscopy.
Image courtesy of Duke
University Medical Center.
Trichuris trichiura
Cutaneous larva migrans Etiology
The filariform form penetrates the skin

The larvae cannot mature further in the human
host, and migrate aimlessly within the
epidermis, sometimes as much as several
centimeters a day.
Some larvae may persist in deeper tissue after
finishing their skin migration
Cutaneous larva migrans
causative agents
Ancylostoma caninum(dog hookworm)

andAncylostoma braziliense(cat
hookworm) and Uncinaria stenocephala.
OccasionallyA. caninumlarvae may
migrate to the human intestine, causing
eosinophilic enteritis
Toxocara canis / Toxocara catis
Visceral larva migrans (toxocariasis)
Cutaneous larva migrans
mechanims
The larvae penetrate the skin andmigrate

through subcutaneous tissue,causing an
inflammatory response.
Lesions called creeping eruption" are
extremely pruritic
Visceral larva migrans:
Toxocara canis, Toxocara cati
Caused by worms (parasites) that infect the
intestines of dogs and cats
Symptoms include abdominal pain, cough,
fever, irritability, itchy skin (hives),
shortness of breath, wheezing
Blood tests to detect antibodies toToxocara
Treatment includes mebendazole,
thiabendazole, and corticosteroids,
Roundworm: Strongyloides stercoralis
Mostly asymptomatic
Some experience gastrointestinal symptoms
identification of larvae (rhabditiform and
occasionally filariform) in the stool or
duodenal fluid
Re-infection do occur
Pulmonary strongyloidiasis:
Strongyloides stercoralis
Pulmonary symptoms (including Loefflers
syndrome) can occur during pulmonary
migration of the filariform larvae
Diagnosis is stools analysis, but larvae can
be detected in sputum
Treatment can include ivermectin with
albendazole
Roundworm: Strongyloides stercoralis
Nematode (roundworm)
Adult females (about 2 mm long) inhabit
the intestine are parthenogenic
they do not need to mate with male worms to
reproduce
They lay eggs within the intestine
Larvae hatch from the eggs
Eggs are released and are passed out into the
feces
Larvae penetrate the intestine and using
the circulatory system can migrate to the
lungs, heart
Found predominantly in tropical and
subtropical areas
Gastrointestinal symptoms include severe
diarrhea, abdominal pain, gastrointestinal
bleeding, nausea, and vomiting
Immunosuppressed patients can suffer
from diseminated strongyloidiasis
Symptoms are abdominal pain, distension,
shock, pulmonary and neurologic
complications and septicemia, and is
potentially fatal.
Blood eosinophilia is generally present during
the acute and chronic stages
Diagnosis is dine by microscopic
identification of larvae (usually the
rhabditiform and occasionally filariform)
in the stool
Rhabditoid larva of
S. stercoralis in an
unstained wet mount of
stool. Notice the
prominent genital
primordium (blue arrow),
rhabditoid esophagus (red
arrow) and short buccal
canal (green arrow).
Filariform (L3) larvae

of S. stercoralis in a
sputum specimen,
stained with Giemsa.
Notice the
characteristic notched
tail
Cutaneous larva migrans diagnosis and
treatment
Diagnosis is made clinically

Thiabendazole (10% aqueous suspension) can
be applied topically three times daily for 5
or more days
Systemic therapy withalbendazole(400 mg
orally once or twice daily for 35 days)
orivermectin(200 mcg/kg orally single
dose) is highly effective
Onchocerciasis etiology
River blindness is caused byOnchocerca

volvulus
Over 99% of infections are in subsaharan
Africa
Transmitted by blackflies
Microfilariae ofO. volvulusfrom a skin nodule
of a patient from Zambia, stained with H&E.
After the bite the larvae are

deposited in the skin
Adults develop over 612 months
Adult worms live in subcutaneous
connective tissue or muscle for a
decade or more.
Microfilariae are released from the

nodules and migrate through
subcutaneous and ocular tissues.
Disease is due to responses to worms
Symptoms include severe pruritus; skin
excoriations, thickening, depigmentation,
subcutaneous nodules.
Conjunctivitis progressing to blindness
40- to 60-cm thread-like female adults lie,

together with their diminutive male partners, in
coiled masses within fibrous subcutaneous and
deep tissue nodules
Females can give birth to more than 2000
microfilariae each day of her 15-year lifespan
Nodules are firm, freely movable, and measure
1 to 3 cm in diameter. Unless the nodule is
located over a joint, pain and tenderness are
unusual.
Onchocercal dermatitis.Onchocerca volvulus microfilaria are
concentrated in the dermal papillae, which makes them
particularly available when the vector black flies bite and feed.
Onchocerciasis diagnosis
Is made by demonstrating the

microfilariae in a thin skin snips taken
from an involved area.
When the eye is involved, the organism
may sometimes be seen in the anterior
chamber with the help of a slit lamp.
Onchocerciasis treatment
Treatment is ivermectin with a single oral

dose of 150 mcg/mL
Loa loa
Eye worm
Swelling in skin worm in conjunctiva
Transmitted by deer fly, horse fly, mango
fly
Tx: Diethylcarbamazine
ECTOPARASITES: Scabies
Caused by infestation with theSarcoptes

scabieimite
The female burrows into the skin to
deposit eggs
4 to 6-week incubation period after
exposure
Adult females ofSarcoptes scabieimites are
0.30-0.45 mm long by 0.25-0.35 mm wide
Scabies symptoms
In older children and adults include:

generalized eruption with linear
burrows
Papules
Pustules
Lesions show a proclivity for the hands,
feet, and groin
Severe pruritus is the most common
symptom
Scabies
Scabies
Scabies: diagnosis
Diagnosis is made on history and physical

alone
However scrapings of lesions may reveal
mites on microscopy
Scabies
Scabies is caused by infestation with

theSarcoptes scabieimite. The female
burrows into the skin where eggs are
deposited and larvae hatch, resulting in
the severe pruritus that characterizes the
disease. There is typically a 4- to 6-week
incubation period after exposure
Scabies: treatment
Topical treatment consists of

permethrin(brand names Elimite or
Nix) cream applied from the neck down
(avoiding the mucous membranes) and
left on for 8 to 12 hours before washing
off
Lindane can be used in the same fashion
but is contraindicated in young children
due to neurotoxicity.
Scabies: treatment
For severe infestations, oral treatment can

include a single dose ofivermectin, 200 ug/kg
All bed clothing must be washed in hot water
Treatment should include all family members
Antipruritics such asdiphenhydramine(1 mg/
kg/dose every 6 to 8 hours)
Pediculosis
Head lice, or pediculosis capitis, common

worldwide infestation
Occurs in children ages 3 to 11 years
Caused by the louse, calledPediculus
capitis
Lice need a blood meal every 4 to 6 hours
and live for 30 days while laying many
eggs
Pediculosis
Transmission occurs by head-to-head

contact as well as by brushes and combs
Intense pruritus is the main characteristic
Permethrincream, 1%-5%, applied to the
hair and left on overnight followed by
neutral shampoo is effective
Pyrethrin cream is applied for 10 minutes
and then rinsed out. Retreatment is
advised in 1 to 2 weeks
Pediculosis
Pediculosis
http://www.pestid.msu.edu

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Clinical Parasitology

Protozoa and Helminth

Intestinal tract Ingestion of cysts in food or Amebiasis

Urogenital tract Sexual Trichomoniasis

Blood and tissue Bug or fly Trypanosomiasis, Chagas

Anopheles mosquito Malaria

Ingestion of cysts in raw Toxoplasmosis

Trophozoite in stool (arrow)

Cyst (arrow) in stool

Cause vaginitis with copious

Rarely symptomatic in men

Sexual partner and

The trypanosomiases, Barrett, et al

The trypanosomiases, Barrett, et al

Organisms are transmitted by

Malaria is caused by the obligate

Infection occurs by ingestion of cysts

Infective dose are 30 organisms

Immunofluorescence image of Cryptosporidium parvum oocysts, purified from

Fluorescence image of Cryptosporidium parvum oocysts, purified from

Oocyst of C. belli in an unstainedOocyst of C. belli stained with

Oocysts of C. belli in the epithelial cells of a

Cyclospora oocysts appear

UV fluorescence microscopy, where the oocysts autofluoresce

Giardia sp, Entamoeba histolytica,

Transplacental Toxoplasma gondii

Many intracellular parasite such as

Eggs are pass in the feces or urine

Manifestations include fever, cough,

Symptoms include fever, cough,

Intestinal and visceral schistosomiasis

Diagnosis is done by microscopic

Infection occurs when infective cercariae

Females (size 7 to 20 mm; males slightly

Katayama's fever (acute schistosomiasis by S.

colonic polyposis with

cystitis and ureteritis*

Localized erythema develops

Schistosoma mansoniis found in parts of

Acuteschistosomiasiscauses an itchy rash

Cysticercosis: Tx: Praziquantel

Neurocystecercosis: Tx: Praziquantel-

Several cysticerci (larval forms) encysted in muscle.

Eggs are indistinguishable from each other

Scolex of T. saginata. Scolex of T. solium. Contains

Mature proglottids Mature proglottids

Vitamin B12 deficiency by competition causes

Dx: Proglotids and eggs in stools

Larva hatches from the egg within a day

Worldwide distribution mostly in areas

Diagnosis is made by presence of eggs in

Diagnosis is done by microscopic

Longitudinal section of an adu

Ancylostoma duodenale. Necator americanus. Anterior end

Known as the pin worm

Eggs of E. vermicularis in a Eggs of E. vermicularis viewed

Filariasis is caused by nematodes

The other five species areLoa

Known also as tropical pulmonary

Ascaris lumbricoides, obstruction, appendix

Mass of adult worms recovered from infant at autopsy

Ascaris lumbricoides, obstruction, appendix

Mass of adult worms recovered from infant at autopsy

The filariform form penetrates the skin