Parasites occur in two distinct forms: single-celled protozoa and multicellular metazoa called

helminths or worms. They can be classified by morphology:

P r o t o z oa
Amoebas - Sarcodina
Entamoeba histolytica

Flagellates- Mastigophora
Trichomonas
UGT

Ciliated
Balantidium.

Sporozoa - Apicomplexa
In blood/tissue
GI tract

Naegleria species

Giardia lamblia GIT

Plasmodium

Cryptosporidium

Acanthamoeba species

Leishmania
(hemoflagellates)
Trypanosoma.
(hemoflagellates)

Toxoplasma

Isospora

Babesin

Protozoa are free-living, singled, eukaryotic cells with a cytoplasmic membrane and cellular
organelles, including 1 or 2 nuclei, mitochondria, food vacuoles and ER, and they come in many sizes
(5 m - 2 mm).
They reproduce either asexually (undergoing a DNA replication, followed by division into 2 cells) or
sexually (fusion of 2 cells so called Zygote, DNA exchange, and separation into 2 cells again).
Protozoa ingest solid pieces of food through a small mouth,
called cytostome.
When exposed to new environments, they can secrete a
protective coat and shrink into a round armored, non-motile
form, called cyst, which is infective when ingested in humans.
Following ingestion it converts back to the mobile form, called
trophozoite.
This process is reversible: Cyst to Trophozoite = Excystati on, and Trophozoite to cyst = Encystation
Metazoa (worms)
Flat worms (Platyhelminthes):
Trematodes (flukes) - Fasciola, Fasciolopsis, Paragonimus, Clonorchis,
Schistosoma.
Cestodes (tapeworms) - Diphyllobothrium, Hymenolepis, Taenia, Echinococcus.
Round worms: Necator, Enterobius, Wuchereria, Ascaris, Ancylostoma, Toxocara, Trichuris,
Trichinella, Onchocerca, Dracunculus, Loa, Strongyloides.
The hosts are classified as:
- Intermediate host in which larval ( ) stages develop.
- Definitive host in which the adult parasite reaches sexual maturity.
Vectors are living transmitters (such as flies) of disease and may be:
- Mechanical, which transport the parasite but there is no development of the parasite
in the vector.
- Biologic, in which some stages of the life cycle occur.

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Some important basics about protozoas life cycles

Parasitic stages of protozoans may be intercellular or intracellular occupants of host tissues, or occupy
space within the lumen of various organs. There is not a common life cycle or sequence of
morphological stages to represent this group. However, most of the parasitic protozoans exhibit one of
three broad patterns.
The first pattern, common among many Apicomplexa (the Sporozoans
Plasmodium , Toxoplasma , Cryptosporidium, Isospora)
Incorporates an alternation between asexual and sexual reproductive stages. Cycles of schizogony in
host tissues increase the population asexually, but at some point individuals undergo the sexual process
of gametogony to produce gametes. The gametes unite and divide in the asexual process
of sporogony to produce sporozoites which can infect a new host. Some species complete their life
cycle in a vertebrate host, and transmit from host to host via cysts, containing sporozoites, which are
passed externally. Other species use two hosts, a vertebrate host in which schizogony and gametogony
occur, and an invertebrate vector in which gametes unite in the lumen of the gut and sporogony takes
place in the tissues. In the two host life cycles, the parasite has no free-living stage and usually
transmits between hosts by a blood-feeding vector.(plasmodium)
The second pattern, common among flagellates
Trichomonas, Leishmania, Giardia, Trypanosoma
Involves asexual reproduction almost exclusively. Various morphological transformations may occur,
but all reproduce by binary fission. Some species complete their life cycle in a vertebrate host, and
transmit from host to host via cysts, containing trophozoites, which are passed externally. Other species
use two hosts, a vertebrate host in which some morphological forms occur in the tissues, and an
invertebrate vector in which other morphological forms reside in the tissues. In the two host life cycles,
the parasite has no free-living stage and usually transmits between hosts by a blood-feeding vector.
The third pattern, common among Amoebas
E.Histolitica, Acanthamoeba, Naegleria
Also involves asexual reproduction almost exclusively. A single host is used, which
harbors trophozoites that live in the lumen of the gut and multiply by binary fission. Trophozoites may
be stimulated to encyst and within the cyst they undergo nuclear division. The cyst is ingested by
another host and after liberation from the cyst the parasite undergoes cytokinesis to produce new
trophozoites.

Glossary:
Schizogony -a form of asexual reproduction characterized by multiple mitoses and cytokineses that form numerous
daughter cells.
Schizont- a cell undergoing schizogony in which the cytokineses are not complete.
Gamete- a mature reproductive cell, usually haploid, which fuses with another gamete of the opposite sex to form
a diploid zygote. (fork-tailed)
Gametocyte- the sexual stage of Sporozoa.
Gametogony -cell division resulting in the formation of gametes.
Spore- small, non-motile transmission stage containing a single infective organism; resistant to environmental
conditions.
Sporoblast- a cell that produces a spore.
Sporocyst- an early developmental stage capable of asexual reproduction:
in sporozoans it is usually enclosed within an oocyst; in digeneans it is an intramolluscan stage lacking a gut.
Sporogony- multiple fission of a zygote that forms large numbers of sporozoites.
Sporozoite- a daughter cell resulting from sporogony within an oocyst.

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Entamoeba histolytica
Diseases:
1. Amoebiasis (amoebic dysentery), same as E. coli and shighella,
2. Liver abscess
1. Pseudo appendicitis.
Transmission and epidemiology: fecal-oral route, by infective cysts. No animal reservoir. Spread
mainly in tropical areas.
Rarely, in a risk group population, it seems to have a
sexual transmission.
Life cycle:
1. The cysts are ingested with food or water that is
contaminated with human fecal material.
2. The cysts than reach the small intestine and
undergo excystation resulting as trophozoites
(active state), that tend to colonize the large
intestine.
3. They reproduce by simple division (asexual).
4. Their colonization can be asymptomatic or it
can result in symptoms (colitis, diarrhea...).
5. The trophozoites can than either reach faeces as
cysts (undergoing encystation), or invade the
large vessels of the large intestine and be
transported to other organs in the body (such as
brain, liver, lungs).

Morphology:

The Cyst

The Trophozoite

Is non-motile, spherical, found in lesions and

diarrhoea. It is 10-18 m in size. It can be
eliminated by boiling, but is resistant to Cl-. It has
4 nuclei (more in non-pathogenic), which later
can forms 8 trophozoites.
It can sometimes have a glycogen retractile mass
(chromidial bar).

Is motile due to pseudopods, found mostly in

normal stool. It is 12-30 m in size. It has 1 small
central nucleus with a prominent nucleolus and
even lining of peripheral chromatin
It is haematophagus (feeding on blood) when
aggressive stage, containing RBC
Not all stains are pathogen.

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Pathogenesis: trophozoites invade the colonic epithelium (primary location) and secrete enzymes that
cause localized necrosis, and a little inflammation occurs at the site.
The lesion reaches the muscularis layer, forming a "flask-shaped" ulcer, which can destroy large areas
of the intestinal epithelium, causing amoebic dysentery with bloody and mucous diarrhea.
Progression of trophozoites into the submucosa leads to their invasion of the portal circulation and to
different organs. This is called the secondary location.
The most frequent site is the liver, where amoebic liver abscesses (ALA) are formed.
It is impossible to have a secondary location in the absence of a primary one, either the digestive
event is remarked by the patient, or not.
Manifestations:
Amoebic dysentery usually appears as insidious onset and not as an abrupt onset.
The incubation period is 7 days to several months (presence of diarrhea), containing 6-12 bloody, pus
and mucous stools on 24 hours, accompanied by an abdominal pain and tenesmus (
). Fever or malaises are rarely present.
It lasts for a few weeks (usually up to 6) and then gradually diminishes in intensity.
The appearance of the attacks is irregularly, for several years, simulating a non-specific ulcerative
colitis.
In the absence of re-infection, the disease may be self-limiting over a period of 3-5 years.
Chronic cases include occasional diarrhea, weight loss, and fatigue, sleep disorders, skin and ocular
allergies, decreased mental activity.
90% remain asymptomatic carriers.
Amebic liver abscess (ALA) appears several months up to years following the bowel lesion.
An intermediate amebic hepatitis can take place before the real abscess formation.
The living amoebas are in the peripheral zone of the abscess, nearby the surrounding normal liver
tissue, where they can actively multiply and invade the liver parenchyma. There is no inflammatory
reaction or capsule surrounds the abscess.
The liver can enlarge and invade to the pleural cavity, the peritoneal cavity (causing peritonitis.
ALA is characterized by painful hepatomegaly, fever, tenderness of the liver, localized edemas or
tenderness of the skin when the abscess approaches the surface, dullness to percussion with reduced
breath sounds.
Aspiration of the liver abscess yields brownish-yellow pus with the consistency of anchovy-paste.
Generally, parasites in small intestine cause acute diarrhea with many non-bloody stools, while
parasites in the large intestine cause fewer stools with blood and mucosa.
Complications:
Local: bleeding, ulceration, fulminating amoebiasis, amoeboma chronic inflammation (around an
abscess mainly in ileocecal area, associating a secondary infection, presenting a carcinoma-like aspect.
Rarely evolution can determine bowel occlusion), post dysenteric colitis (strictures, or stool looseness,
presenting a progressive evolution). It can penetrate the portal circulation by invading the submucosa,
causing general complications.
General: amoebic liver abscess (blood metastasis of amoebic trophozoites, via portal vein, finally
concretized as a pink or pinkish-brown viscous fluid amoebic pus), lung abscesses (from the liver, or
by blood metastasis), pleural cavity, pericardium, brain, kidney, or pancreatic secondary locations,
cutaneous amoebiasis (bowel abscess involving all the abdominal layers, up to the skin, or to the
deeper tissues perianal and/or perineal destruction).
In ALA, cyst rupture can lead to: amoebic empyema, hepatobronchial fistula, amoebic peritonitis,
amoebic pericarditis, cutaneous dissemination. Other complications are jaundice, anemia and distance
hematogenous metastasis (brain).
Diagnosis:
Antibodies are formed against trophozoite antigens in invasive amebiasis, but they are not protective,
as previous infection does not prevent reinfection. The antibodies are useful, however, for serologic
diagnosis.
Amoebic dysentery
Direct diagnosis-

|Page4

- Direct stool examination (bloody or mucous fragments of the specimen): trophozoites during the
acute phase, and cysts in the chronic and infection, or asymptomatic carriers. At least 3 specimens
needed as cysts are passed intermittently.
- Culture: on spleen medium or Loeffler.
- Large bowel biopsy (iron hematoxylin stain).
Indirect diagnosis- Serum specific anti E. histolytica antibodies (IFAT, IHA). Only 40% of the
asymptomatic patients are serologically positive.
- Stool antigen detection (useful in the field).
Amebic liver abscess
Direct diagnosisAbscess aspiration (not very useful for diagnosis because of spillage of the trophozoites).
Recommended when suspect drug resistance or imminence of rupture.
Indirect diagnosis- Copro-antigens (antigen prepared from fecal sample of infected animal) IFAT, ELISA.
- Antibodies: immune-electrophoresis, ELISA, agglutination.
Complementary diagnosis
- Hematology: leukocytosis (PMNs - neutrophils), anemia, inflammation
(high ESR, Fg and CRP).
- Stool examination: mainly in endemic areas, where the disease presents a chronic
evolution with cysts excretion.
- Imagery: X-ray (raised hemi-diaphragm), US (one or more areas of discontinuity of
the liver), CT, MRI, isotope (lacunars areas).
Free living amobae

Are amoebae which present a non-parasitic life in stagnant water, but which, under
certain conditions, can be infective for humans.

Naegleria (N.fowlery, N.grubery)

Disease: primary amoebic encephalitis (PAE). Present
in north and South America, Europe, Australia, Newzealand, Africa.
Transmission: nasal route. Found in warm freshwater
pools, moist soils, streams, lakes.
Life cycle:
1. The cyst becomes an amoeboid trophozoide
via excystation (in his external environment).
2. Then it becomes flagellated trophozoide and
becomes motile.
3. It is then inspired by a human nasal route
4. Migrate via the olfactory nerve and becomes
an amoeboid trophozoide once again and
multiply in the CNS causing PAE.

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Morphology:
The Cyst

The Trophozoite

Is round, 9 m in diameter, and is present only in

culture, in small numbers. It can be spread on dust

Is 227 m in size. It is mobile in water through

its anterior pseudopodia. It multiplies by binary
fission.
The flagellate intermediate stage develops under
improper living conditions.

Pathogenesis: penetrate the nasal mucosa; pass to the cribriform plate, and into the brain and spinal
fluid, causing meningoencephalitis. At the same time is spread also through the respiratory system,
causing pneumonia. There is no exit route for the parasite.
Manifestations: primary amoebic encephalitis appears in healthy, young, immune competent persons,
causing an acute disease, followed by death in a few days. Infection is most common in children. The
incubation period is 3-7 days. The disease is usually rapidly fatal. The onset is sudden, with a flu-like
symptoms (sore throat, rhinitis, fever, headache, vomiting), neck stiffness, convulsions, photofobia,
loss of smell, coma. The status of the patient gets worse, until death.
Complications: pneumonia, myocarditis, otitis, skin ulcers.
Diagnosis: examination of the CSF reveals characteristics of bacterial meningitis, but in microscopic
examination, pus-like CSF has no bacteria.
Direct diagnosis- Direct examination: Amoebas are recognized by their slug-like movement.
- Chemical examination: high level of albumin with normal or low glucose levels.
- Cytological examination: local increase in leucocyte levels with increased
polymorphonuclear neutrophils.
- Immunofluorescence staining on tissue sections (retrospective diagnosis).
Indirect diagnosis- local or serum antibodies. This method is possible but is less useful because of
the rapid evolution of the disease.

Acantamoeba
Acanthamoeba spp. have been found in soil; fresh, brackish, and sea water; sewage; swimming pools;
contact lens equipment; medicinal pools; dental
treatment units; dialysis machines; heating,
ventilating, and air conditioning systems;
mammalian cell cultures; vegetables; human
nostrils and throats; and human and animal
brain, skin, and lung tissues. Unlike N. fowleri,
Acanthamoeba has only two stages, cysts and
trophozoites, in its life cycle. No flagellated
stage exists as part of the life cycle. The
trophozoites replicate by mitosis (nuclear
membrane does not remain intact). The
trophozoites are the infective forms, although
both cysts and trophozoites gain entry into the
body through various means. Entry can occur
through the eye, the nasal passages to the lower
respiratory tract, or ulcerated or broken skin

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Disease:
- In immune competent host - keratitis after trauma or contact lance manipulation, chronic
granulomatous skin lesions.
- In immunosuppressed host - chronic granulomatous encephalitis in the CNS through a hematogenous
spread.
Transmission: through mucous, skin and eyes (cornea).
Life cycle: the infection can be done by both trophozoites and cysts. (Look at the figure, up)
Morphology:
The Cyst

The Trophozoite

Is 13-19 m in size, it has an external

polygonal shape layer and an internal
wrinkled layer with pores. It has 1
nucleus. Dry cysts can survive for years.
The cysts can be isolated from dust or
air.
No free living stage.

Is 30 m in size, it has a rough exterior

with several projections (achanthopoda).
It has 1 nucleus with a big cariosoma. It
represent the infective stage for humans.

Pathogenesis: the parasite enters through respiratory route, skin ulcer or the eyes. It spreads to the
respiratory system and migrates throughout the body by blood.
In immunosuppressed host it may cause encephalitis, skin nodules, pneumonia, and may affect the
kidney, uterus and prostate.
Manifestations: incubation period of 7-10 days.
1. Acantamoeba keratitis
Not related to the progressive brain disease. Almost always related to a history of
local trauma. Red, painful eye, foreign body sensation, tears. Ophthalmologic
examination is negative at first, but rapidly followed by a progressive keratitis.
The progressive corneal ulcer can even destroy the eye.
2. Chronic granulomatous encephalitis
Can produce a progressive brain disease with focal brain damage and death after weeks or months in
immune compromised people due to drug administration.
Single or multiple brain abscess, accompanied by headache, fever, focal epileptiform attacks.
Diagnosis:
CSF shows a mononuclear pleocytosis with rarely present amoebae.
Parasite

Naegleria

Disease

primary amoebic encephalitis

Habitat

Swimming pools, lakes, ponds,

thermal water

Host immune
status

Immune-competent

Entrance gate

Nasal mucosa olfactive nerve

Symptoms
Diagnosis clue

Acanthamoeba
Keratitis, chronic amoebic
meningoencephalitis
Normal water, even cold.
Opportunistic amoeba
Diabetes, burns, sterolds or
other immune-suppressed
factors, radiotherapy, HIV
Skin, respiratory, then
hematogenous

Acute hemorrhagic
Chronic or subacute
meningoencephalitis, followed
granulomatous encephalitis
by death in 3-7 days
CSF - trophozoite
CSF - trophozoite (rarely), cysts

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Giardia duodenalis (G. Intestinalis, G. lamblia)

Disease: giardiasis. Locate at the upper small bowel, causing diarrhea.
The pathogenic strains for humans are: G. duodenalis, G. muris, G. agilis.
Transmission and epidemiology: animal and human reservoirs. The transmitted disease is contagious:
1. Person to person, by fecal-oral route (cysts).
2. Contaminated drinking water and food (cysts).
The disease is more common in children. In adults, following the repeated infections, certain immunity
is developed. In immune competent host the disease is self-limited.
About 200 million symptomatic people and 500.000 new cases each year.
Life cycle:
1. The cysts from the contaminated food and
water are ingested, passing through the
mouth as cysts.
2. The cyst has reached the duodenum where
it becomes a trophozoite via excystation.
(the mature, motile form)
3. Eventually reaching the stool both as cysts
and trophozoites.
4. From the stool it may reach again to the
contaminated food and water, beginning
another cycle.
The cyst stage is both infective and diagnostic
stages, while the trophozoite stage is only a
diagnostic stage. (Via duodenal juice
examination)

Morphology:

The Cyst

The Trophozoite

Is 8-145-10 m, oval, double coated,

with 4 nuclei. It also has a refractive
axostile inside (an axial rod present in
many parasitic flagellates, used for
locomotion or support).
It is infective for the environment, but is
destroyed by temperature higher than
50C, or by desiccation. It does not
destroyed by chlorine. It has resistance
for 8 days at 21C in water.

Is flatten, pear-like or kite shape,

1593 m.
It has 4 pairs of flagella, which allows its
locomotion. The ventral face is concave
and is attached to the intestinal mucosa,
through a sucking disc. The dorsal face is
convex and it is the active face of the
vegetative form. It multiplies by binary
fission.

|Page8

Pathogenesis: after ingestion the cyst converts to the trophozoite form, cruises down and adheres and
coats the small intestine wall. There they multiply, blocking and interfering with intestinal absorption.
They decrease the level of brush border enzymes (lactase, maltase, surcease, saccharine), causing a
decreased digestion and malabsorption of glucose and lipids.
This may lead to milk intolerance, fatty stools (steatorea), flatulence, borgorygmi (GI noises) and
fermentation of unabsorbed glucose.
It is possible that neurotoxin responsible for intellectual and behavior disturbances in sick children.
Associated allergic signs may appear in the skin, digestive, respiratory, ocular.
Giardia does not invade the intestinal wall - therefore there is no blood in the stool.
Manifestations: incubation period of 1-2 weeks, including anorexia, vomiting and loss of appetite. The
onset of the disease can be either insidious or sudden.
The disease can be:
- Asymptomatic - infective dose dependent, host immune response, strain infectivity.
- Acute - accompanied by signs and symptoms mentioned during the stage phase.
- Chronic - with or without signs, symptoms.
About 50% of the infected people are asymptomatic carriers for years. It is more common in
children, and is self-limited in immune-competent, which gives them certain immunity.
Stage of the disease:
- Diarrhea: 5-10 stools/day, pale, bulky, smelly and fatty diarrhea. accompanied by flatulence. There is
no blood or mucus, and no fever.
- Abdominal cramps (months to years).
- Urgent call to stool.
- Abdomen distension, bloating, borgorygmi.
- Milk intolerance (mainly in children).
Complications:
- Malabsorption: fat, glucoses, proteins, A, B12 vitamins, folic acid.
- Milk intolerance: consecutive to the insufficient synthesis of brush border enzymes, mainly lactases.
- Chronic, or recurrent: loose of appetite, painful abdomen, and diarrhea. skin / respiratory or ocular
allergies, sleeping disorders, decrease in mental or physical activities.
Diagnosis:
Morphology:
- Of trophozoites - from stool, duodenal liquid, duodenal biopsy. Can be done by direct
examination, entero-test (string test), duodenum juice, endoscopic isolates.
- Of cysts - from stool. Can be done by direct examination (Lugol), smear (Giemsa stain),
cultures. In asymptomatic patients we will find only cysts.
Immunology:
- Copro-antigens - related to the active stage of the disease.
- Serum antibodies - ELISA. Has no clinical importance, and is not related to the clinical
evolution or cure.
At least 3 examinations, separated by 7-10 days free interval, are recommended in order to
perform a correct diagnosis and monitoring following the treatment.

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Trichomonas vaginalis
Disease: trichomoniasis.
It is the cause of acute vaginitis in 5-50% of cases, and is the most common STD in the world.
There are several types of Trichomonas: T. vaginalis (urinary-genital), T. tenax (bucalis), and T.
hominis (intestinalis). (T. vaginalis is the only pathogen specie in humans.)

The normal vaginal flora includes:

- Lactobacilli - predominant bacteria in the vaginal tract, regulator of normal vaginal flora; it makes
lactic acid which maintains the normal vaginal pH of 3.8-4.5, and it inhibit the adherence of bacteria to
vaginal epithelial cells.
60% of lactobacilli strains produce hydrogen peroxide which inhibits the growth of bacteria
and destroys HIV in vitro.
- Other bacteria - streptococcal species, gram-negative bacteria, Gardenella vaginalis, anaerobes.
- Estrogen - improves lactobacilli colonization by enhancing vaginal epithelial cells production of
glycogen into glucose and acts as substrate for bacteria.

Typical features of Vaginites:

Condition
Bacterial vaginitis

Candidiasis

Trichomoniasis

Symptoms/ signs Findings on examination pH

Wet mount
Increased discharge
Thin, whitish-grey >4.5
Clue cells
(white, thin) Increased homogenous discharge,
Shift in flora
odor
sometime frothy
Amine odor after
adding K hydroxide

Comments
Greatly decreased
lactobacilli
Greatly increased
cocci, bacilli, small
curved rods
Increased discharge Thick curdy discharge , <4.5 Hyphae* or spores Can be mixed infection
(white, thick) Pruritus,
Vaginal erythema
with bacterial
Dysuria
vaginosis, T.vaginalis
or both and have a
higher pH
Increased discharge Yellow frothy discharge >4.5
Mobile
More symptoms at
(yellow frothy)
with or without vaginal
Trichomonas
higher vaginal pH
Increased odor
or cervical erythema
Increased WBC
Pruritus, Dysuria

* hypha - is a long, branching filamentous structure of a fungus

Transmission and epidemiology: the source of infection is humans. The disease can be transmitted by
sexual intercourse STD, indirectly by poor hygiene or from mother to baby during birth (causing
conjunctivitis).
Symptomatic disease is most common among sexually active female in their 30s, the least - in
postmenopausal women. It is common in 20-25% of the women in the U.S.

| P a g e 11

Life cycle: No Cyst!

1. The infective stage is the trophozoite stage, which has
short life span, since temperatures above or fewer than
37C are destroying the parasite.
2. They are water resistance, staying on towels and in
urines for about 40 minutes.
3. The parasite passes from person to person and infects
during sexual intercourse in its trophozoite form,
which is also its diagnostic stage, as it is detectable in
urine and vaginal and prostatic secrations. It then
multiplies by binary fission in the
vagina or the urethra.
Morphology: the trophozoite is 203010-202-3 mm in size, pear- like
shape. It has 4 anterior flagella and a recurrent one embedded in an undulating
membrane, over 2/3 body length, originate in blepharoplast (basal body in
certain flagellated protozoans that consists of a minute mass of chromatin
embedded in the cytoplasm at the base of the flagellum).
It contains cytoskeleton bodies: axostyl, which curves around the nucleus,
extending posterior, and a costa - intracytoplasmatic, corresponding to the
undulating membrane.
It is actively phagocytic and has an active motility.
The cyst form does not exist.
Pathogenesis: Trichomonas vaginalis has some adherence factors that allow cervico-vaginal epithelium
colonization in women.
Manifestations: incubation period of 3-30 days (most frequent up to 10 days).
The disease includes liquid, foamy, greenish-yellow vaginal discharge, which appears 2-3 days after
the infective contact. The area is itching and burning; forming a typical appearance of "strawberry
cervix" (erythema due to the infection).
These symptoms increase before and after periods, accompanied by an intense pruritus, burning,
chafing, sometimes by the inability to consume the sexual intercourse, and by dysuria (increased
frequency of urination).
There are both symptomatic cases (chronic or acute vulvo-vaginitis) and aymptomatic cases.
In asymptomatic cases the great majority are carriers, while in symptomatic cases, there is a
persistent, recurrent urethritis involvement of seminal vesicles, prostate and the higher part of the
urinary-genital tract. This may lead to dysuria, nycturia, local discomfort, pruritus, epididymitis,
enlarged tender prostate, urethral discharge containing parasites.
Urethral discharge has 2 phases:
- Acute phase - important quantity for a few days.
- Chronic phase - daily small quantity, noticed in the morning, before the first leak.
Complications: cystitis, salpingitis (inflammation of the fallopian tubes, which may lead to infertility),
anexitis (inflammation of the pelvic).
Chronic vaginal mucous inflammation (the local lesions plus discharge) can hide a local cell tumor
process.
Diagnosis: Local examination can reveal a red punctuates
lesions.
Morphology: trophozoites can be detected in genital
discharges or urine by direct examination (saline wet
preparation), phase contrast microscopy, permanent stains
(Giemsa), cultures (different media).
Immunology: antigens detection in genital discharges.

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Leishmaniasis
Disease: Leishmaniasis.
There are 3 main forms of leishmaniasis, each caused by a different species:
Cutaneous (old world) - involving the skin at the site of a sand fly bite.
Caused by:
L. tropica - present in Northwest India, Pakistan Afghanistan, Mediterranean areas, West
Africa)
L. major - present USSR, Afganistan Iran, Arabia, North Africa, Sudan, Senegal, Niger.
Visceral - involving liver, spleen, and bone marrow.
Caused by:
L. donovani complex - Present around the Mediterranean Basin, tropical Africa, parts of
South America, Central and Eastern Asia.
Muco-cutaneous (new world) - involving mucous membranes of the mouth and nose after
dissemination from a nearby cutaneous lesion (very rare).
Caused by:
L. brasiliensis complex - present in South America, Belize, Guyanas, Venezuela, Brasil,
Panama, other parts of South America
L. mexicana complex - present in Belize, Venezuela, Brazil, other parts of South America).
Transmission and epidemiology: transmitted by sand flies bite, and is found in parts of at least 88
countries including the Middle East.
There are about 1.5 million new cases/year of cutaneous leishmaniasis in the world, and 500,000 new
cases/year of visceral leishmaniasis each year.
The transmission can be done by:
1. Vector inoculation- Phlebotomus spp, female sand fly (old world), Lutzomyia (new world).
1. Blood transfusion.
2. Laboratory infections (accidentally).
3. Infected discharges (sexual).
4. Congenital (extremely rare).
5. Digestive (under the discussion in man).
Only L. donovani has human as infection
source, the others leishmania species has an
animal reservoir: dogs, rodents (zoonosis).
Life cycle and pathogenesis: involves the
sandfly as the vector and a variety of
mammals such as dogs, foxes, and rodents as
reservoirs. Only the female sand-fly bites, as
she needs the blood to feed her eggs.
1.
2.

3.

4.
5.
6.

The sand-fly injects the promastigote

form of the parasite into the skin.
The promastigotes are phagocytized by
macrophages and transform into the nonmotile amastigotes inside the
macrophages.
The amastigotes can remain in the
cytoplasm of macrophages because they
can prevent fusion of the vacuole with lysosomes.
They multiply inside the macrophages, and the infected cells die and release progeny amastigotes that
infect other macrophages and reticuloendothelial cells.
This way the amastigotes can reach to various tissues and also migrate into the pharynx. These phases
are the diagnostic phases.
Another bite of the sandfly leads to its ingestion of macrophages with amastigotes, which are then
transform into the promastigotes stage, and are ready to be injected in the next bite.

| P a g e 12

The different diseases caused depend on the invasiveness of the species, as well as the host's immune
response. The life cycle is the same, but the local evolution, or the infection blood spreading is
consequent to the involved specie. This cycle lasts for 10 days.

Morphology: both visceral and cutaneous forms are morphologically identical. Differences consist in
the enzymatic profile - zymodemes.
The Amastigote

The Proamastigote

Cell or unicellular organism that does

not have any flagella or cilia. Is an
intracellular form, 2-4 mm in diameter,
roughly spherical structure. It has 2
distinct pieces of nuclear
chromatin: nucleus (the large piece) and
kynetoplast (the small
one). It is present in the vertebrate host.

is the elongated form, 12-141.5-3 mm,

and has an anterior flagella, 1 nucleus,
kynetoplast, and is present in invertebrate
host and culture media NNN.

Manifestations:
Visceral leishmaniasis L. donovani complex
Incubation period of 3-18 months. L. donovani complex- human reservoir
There are both asymptomatic cases (strong local tissue response, leading to the death of the parasite,
and their complete elimination) and symptomatic cases (including both a local reaction Leishmanoma, following promastigotes inoculation, and the formation of a small nodule, or the
hematogenous phase).
The symptoms may include:
Irregular, intermittent fever, rigors, sweating. When the cell mediated immune response is poor,
amastigotes multiply rapidly, the parasitized local macrophages are destroyed and the parasites are
taken up by farther phagocytic cells of the reticulo-endothelial system, leading to the visceral stage.
In contrast with the high fever (39-40C), the patient feels relatively well continuing to eat and to
work until the advanced stage of the disease is coming.
Increase of the mass of reticulo-endothelial tissues (spleen, liver,
lymph nodes):
- Splenomegaly - enormous, up to several kilos, reaching to the iliac
margin. When painful, it can lead to splenic infarcts.
- Hepatomegaly - palpation of the inferior margin is interrupted low
albumin synthesis and increased globulins vitamin K deficiency
(leading to hemorrhages hemostasis cascade is vit-K dependent).
- Bone marrow invasion reduced activity. Trombocytopaenia,
anemia and finally
leucopaenia, due to the very active turnover of macrophages.
- Lymphadenopaty - less constant feature depending on the strain
and geographic areas (very prominent in the African type).
Jaundice - present in advanced stages of the disease.
Emaciation (), loose of appetite, together with the damaged liver
functions and micro nodular cirrhosis.

| P a g e 13

Cutaneous leishmaniasis Old world

The most important cause of chronic ulcer in tropical areas.
They are usually zoonoses, although in some, the animal reservoir was not identified.
L. major and L. tropica are the most common species In the Middle East. L. major causes skin
infections and L. tropica causes skin and visceral infections.
L. tropica is present in urban areas and is considered as the "dry form". It has an incubation period of
20 days to 6-8 months, and it probably has only human reservoir.
In immune competent patients recovery occurs in a couple of months.
It causes a solitary, painless skin ulcer, few cm in diameter, with no inflammation surrounding, very
well defined and raised edges and no satellite lymph nodes enlarged. It is present very often on face
and extremities, and it heals without complications within a few months in immune competent host.
L. major spreads in rural areas (country side) and is considered as the "humid form". It has an
Incubation period of 10- 45 days, and it has both human and animal reservoirs.
It causes many, painless skin ulcers, few cm in diameter, important inflammation surrounding, quite
well defined edges and satellite lymph nodes enlarged. It heals with a skin scar within several months
in immune competent host.
Lesions predictive for bad prognosis:
- Big lesions (greater than 2 cm in size).
- Many lesions (3 or more).
- Sores on the face.
- Sores on the hands and feet.
- Sores over joints.
If cell-mediated immunity does not develop, the lesions can spread to
involve large areas of skin and contain enormous numbers of
organisms.
Muco-cutaneous leishmaniasis- New world
Very rarely associated with L. tropica which is found in the Middle East. It affects mostly forestry and
construction workers.
It causes cutaneous lesion on the face, which spreads to involve the nose or mouth and leading to
granulomatous inflammation. Mucosal involvement may occur if a skin lesion near the mouth or nose
is not treated. Ulcerating lesions destroy nasal cartilage but not adjacent bone. It heals slowly, if at all.
Death can occur from secondary infection. The disease can occur months to years after original skin
lesion.
It is hard to confirm diagnosis as few parasites are in the lesion, and the lesions can be very disfiguring.
This disease is caused by 2 complexes of parasits:
L. brasiliense complex, which causes:
- Espundia - by L. Br. Brasiliense, causing humid, muco-cutaneous
lesions. These are the most destructive lesions, probably greatly enhanced
by the secondary infections with aerobic and anaerobic bacteria.
The first appearance is like L. tropica ulcer, but after the apparent
healing, in a few months, a lot of new elements appear, involving the
muco-cutaneous junction of the nose, and spread inwards to destroy
the adjacent tissues in several years.
- Uta - by L. br. Panamensis, causing dry muco-cutaneous lesion, face
ulcer, having several years evolution, able to invade the surrounding tissues.
- Pean bois - by L. br.guyanensis, L. aethiopica, L. mexicana
amasonensis,
L. mexicana pifanoi, causing muco-cutaneous lesions.
L. mexicana complex, which causes:
Chicleros ulcer - by L. m. Mexicana. After the healing of the first lesion
there are 2 or 3 relapses following each bite and all together realize a
chronic ulcer aspect. Diffuse cutaneous lesions are very often associated.
This disease is quite frequent in Mexico.

Espundia

Chicleros ulcer

| P a g e 14

Complications:
Post Kala-azar syndrome (common in India & Sudan; 1-2 years after spontaneous or treated recovery)
presenting painless infective skin nodules on face, neck & arms; destructive lesions of nasal mucosa;
infiltration of the small intestine. L. tropica may also cause visceral infection. Death may occur from
secondary infections of the visceral leishmaniasis:
Infection of the nasal mucosa - localized destructive lesion resembling espundia.
The small intestinal mucosa - show marked infiltration with parasitized macrophages.
Death - weeks to years, mainly by inter-current infections of the respiratory or digestive tract.
Opportunistic infection - immune compromised patients (HIV).

Diagnosis:
Visceral leishmaniasis
Morphology: Amastigotes can be detected by puncture of the liver, spleen or bone marrow (Giemsa
stain), animal inoculation (impression smear) and cutaneous biopsy In PKDL.
Promastigotes can be detected in cultures (Novy, Mc Neal, Nicolle medium - NNN).
Immunology: specific antibodies by screening tests (HA, IFAT, ELISA) and confirmation tests (WB).
It is done mainly when spleen or liver puncture is forbidden to be done (risk for hemorrhages, PLT
count under 50,000).
Cross reactions with malaria, toxoplasmosis, disseminated TB may occur.
Circumstantial diagnosis: weakness, enlargement of liver and spleen, anemia,
hyperglobulinemia - monitoring marker after an appropriate treatment (back to normal of the
modified protein electrophoresis).
Differential diagnosis: malaria, trypanosomiasis, aleukaemic leukaemia, aplastic
anaemia, brucellosis, disseminated TB, histiocytic medullary reticulocytosis.
Muco-cutaneous leishmaniasis
Morphology: by smear (using a wide bore needle the material to be examined is collected from the
active edge - Giemsa stain, or skin-slit smear - Giemsa stain), biopsy, culture medium NNN or animal
inoculation.
Immunology: not very useful, due to the cross reactivity with lepromatous leprosy.
Leishmanin test (Montenegro test) detects a delayed sensitivity (48 hours) reaction to killed
promastigotes intradermal inoculated.
High concentration of IgG is neither specific nor protective. It is an indicative of infection, and is not
diagnostic.

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Trypanosomiasis
T.b.gambiense and T.b. rhodesiense
Disease: African trypanosomiasis (sleeping sickness).
Transmission and epidemiology: T. brucei gambiense is present is central and west Africa, and T.
brucei rhodesiense is present in east Africa. (You gamble in the west and eat rodent in the east)
This is an insect transmitted disease, by the species of the Glosina fly. Both
sexes are feeding on blood.
Reservoir of infection for T.b gambiense is only human, and for T.b rhodesiense
both, human and herbivorous (plants eating) animals.
The infective trypo-mastigote is found in salivary glands 20 days after the
initial blood meal, but the fly remains infective all his life (months).
The Glossina species that use as vectors include 22 species; they live in a shady
Glosina fly.
habitat (20-30C). They are viviparous (producing living young offspring
instead of eggs) - 12 offspring, they are diurnal feeders (eat during daytime) and
the parasite development inside of them lasts 10-14 days.
The risk population includes 50 millions, < 20% is under surveillance. There are 20,000 new
cases/year.
T. gambiense
reservoir

Humans

Virulence
vector
Zoonotic

Less
G. palpalis
Less
West Africa - water
regions

Distribution

T. rhodesiense
Both domestic animals (especially cattle)
and wild animals (e.g., antelopes)
More
G. mortisans
More
East Africa - dry regions

Life cycle:
1. Lasts for 3 weeks. Trypomastigotes
are taken up by the Glossina
(Tsetse) fly from the infected host.
2. The Trypomastigotes multiply in
the fly gut and migrate to the
salivary glands, where they
transform into epimastigotes
(changes include the kinetoplast
lining just in front to the nucleus).
3. They are than forming the infective
form in saliva - the metacyclic
trypanosome.
4. Metacyclic trypanosome in the
saliva of the fly is injected into the
infected person. Primary chancre
containing trypomastigotes
develops at the site of the bite.
5. The trypomastigotes migrate and multiply in the bloodstream.
6. When the fly bites again, it acquires an infection from the infected blood.
7. The fly is infectious for its entire life (2-3 months).
8. The amastigotes form is rare (does not have a visible external flagella or cilia).

| P a g e 16

Morphology:

Flattened, elongated in shape, like slender pointed leaves.

They are 12-351.5-3.5 mm in size, actively motile.
They have 1 nucleus, kinetoplast, undulating membrane
( ) and flagellum.

Trypomastigot
Are specific form in human, in which the flagellum arises from a
posteriorly located kinetoplast (a disk-shaped mass of circular DNA inside a large mitochondrion that
replicates independently) and emerges from the side of the body, with an undulating membrane
running along the length of the body. They multiply in the vertebrate host by simple fission. Their
general configuration is variable: they can be short and sturdy (stumpy forms) or long, slender
(gracile).
Pathogenesis: trypanosomes exhibit remarkable antigenic variation of their surface glycoproteins,
with hundreds of antigenic types helping it evading the immune system. The antigenic variation occurs
every 8-10 days. This variation is due to sequential movement of the glycoprotein genes to a
preferential location on the chromosome, where only that specific gene is transcribed into mRNA.
The constant antigenic variation leads to fever.
The parasites spread through the blood into lymph nodes, and to the brain, causing inflammation and
direct CNS damage. Because of the antigenic variation, antibodies have no protective role.
3-4 days post infection is present a strong IgM response. VSG (variable surface glycoprotein) specific
IgG appears, but is not relevant. IgM response is often greater than IgG. After several cycles VSG
antibodies vanish, but antibodies to invariant antigens remain elevated.
The immunology response also includes hypocomplementemia (decreased complement regulation
proteines - CRP), and immune suppression.
Trypanosome elimination is antibody mediated, and includes destruction by Kupffer cells. Splenic
macrophages have a minor role. Trypanosomes are destroyed within minutes. C mediated lysis is not
important. The trypanosomes disappear within hours.
It is necessary for the immune system to be regulated:
- There is no secondary response to VSGs unless cured by chemotherapy.
- Failure of primary or secondary response occurs prior to death.
- Suppresser macrophages.
- Failure of antigen presentation.
- Nonspecific polyclonal activation.
- Anti idiotype responses.
Manifestations: incubation period of 5-20 days.
T.b.gambiense is better adapted to the human host, which leads to sub-acute or chronic infection (up to
2 years).
T.b Rhodesiense has pronounced toxic effects, severe incapacity and
a rapid course of the disease (few months).
The early stage lasts several months up to 2 years. It includes a
painful trypanosomal chancre which appears about 5 days after the
bite. It increases in size during the following 2-3 weeks and can
affect the local lymph glands. It than slowly regress.
The hematogenous phase includes:
Fever - very early, sometimes accompanied by headache or cutaneous
edemas.
Undulant fever is the expression of antigenic variation, rarely becomes
chronic.
Skin maculo-papular rush - circinate erythema like, following the antigenic
variation, accompanied by generalized pruritus.
A characteristic thickening of the facial tissue, changing the face aspect.
Enlarged lymph nodes symmetrically, non-suppurating (no pus), not very
painful,

Winterbottoms sign

| P a g e 17

Lateral cervical or occipital location - Winterbottoms sign.

In T.br. rhodesiense the axillar and epitrochlear glands are involved.
Splenomegaly is variable.
Hepatocellular jaundice, mild anemia, mainly in T.br. rhodesiense.
Serous effusions especial into the pleural and pericardial spaces.
Myocarditis may occur, mainly in T.br. rhodesiense.
Genital or urinary signs: loose of urine, sterility, amenorrhea (the absence of a menstrual period), and
abortion.
Neurological signs (announcing the next stage): muscles cramps during the night,
Cutaneous hyperesthesia (When a non-noxious stimulus causes the sensation of pain the area will be
termed hyperaesthetic ) and paraesthesia.(numbness)
Rapid toxemic evolution, followed by death even before the CNS involvement mainly in T.br.
rhodesiense, and rarely in T. br. Gambiense.
The late stage includes:
Changes in behavior, having a psychiatric presentation: violent and excitable state, Delusions, or
simulate schizophrenia.
Sleep disorders - the patient sleeping badly at night, but falls asleep during the day.
Later on it will be very difficult to awake him up, the sleeping periods, are longer and longer, finally
most of the day, even fall asleep while eating.
Spasticity, choreiform movements, fits are not very common signs.
Following a firm pressure on the tissues overlying the bones, there is a definite delay before the
patient shows any sign of pain- Karandels sign. (Delayed sensation to pain)
Neuro-endocrine disturbances - body temperature changes, thyroid disturbances, sterility, loose of
periods or sexual appetite, etc.
Diagnosis:

Morphology:
1. Thin and thick blood film, wet or Gimsa, Romanowsky stained (T.b.
Rhodesiense).
2. Concentration methods (buffy coat following centrifugation).
3. Gland puncture - the most useful method for (T.b. rhodesiense).
4. Bone marrow aspiration - the most useful method in early stages for T.b.
gambiense infection).
5. CSF examination - Giemsa stained smear, after centrifugation (Late T.b.
rhodesiense & T.b. gambiense), serology.
6. Aspirate from the chancre.
Immunology:
1. Antibodies detection by IFAT, ELISA, CATT (Card Agglutination Test for
Trypanosomes - test of choice in T. brucei infection).
It presents cross reactivity with some protozoa and bacteria.
2. Antigens detection - useful for the diagnosis.
Animal inoculation.
Circumstantial diagnosis:
1. High total and specific IgM level, lasting as long as the infection is active
(Marker for case management during the treatment).
2. If CNS is involved - an increase in cells and/or proteins and CNS IgM.
Differential diagnosis:
- Fever.
- Lymphadenopaty.
- Cerebral malaria - negative thin and thick blood film.
- Cerebral meningoencephalitis - CSF culture negative.

| P a g e 18

Trypanosomiasis
T.Cruzi
Disease: American trypanosomiasis (Chagas disease).
Transmission and epidemiology: transmitted by the Reduviid bug vector. This is a
zoonotic (passes from animals) and stercoraric (transmitted by contamination
through the feces of the insect vector) disease. The parasite infective stage is the
presence of epimastigote in bug feces.
Reduviid bug
The vectors include the entire family of reduviidae, the subfamily of triatominae,
mainly Triatoma infestans and Rhodnius prolixus.
The source of infection can be either animal (domestic cats and dogs, rat, wild species such as the
armadillo, raccoon) or human.
The transmission can be:
1. Vector - skin contamination of trypanosomes, then skin penetration by the metacyclic infective
forms. They bite mostly around the mouth and eyes (kissing bugs). Vectors have blood meal during
all stages, but only adults bugs are transmitting the disease.
2. Conjunctiva - infective metacyclic stage - Romana's sign.
3. Vertical transmission.
4. Blood transfusion.
Present in South American continent, rural (country-side) or suburban areas. 15-20 millions are
infected.
Life cycle:
1. Trypomastigotes are present in the blood of the
reservoir host, and are ingested by the bug from
their blood as they are bitten.
2. The trypomastigotes multiply in the insects
gut, differentiate first into epimastigotes and
then into metacyclic trypomastigotes.
3. The metacyclic trypomastigotes than enter via
bite site on the skin or mucosa and penetrate
various cells, where they transfom into
amastigoites.
4. The amastigoites multiply by binary fission in
the cells of the infected tissue.
5. The intracellular amastigoites than transform
into trypomastigotes, than burst out of the cell
and enter the blood stream.
6. The parasite has a short haematogenous life, as the trypomastigotes can infect other cells (prefer
myocardium, glial cells and reticuloendothelial cells) and result clinical manifestations.
When the fly bites again, it acquires an infection from the infected blood.
Pathogenesis: the Amastigotes kill cells and cause inflammation, formed mainly by mononuclear cells.
Cardiac cell is most frequently and severely affected tissue.
Neuronal damage leads to cardiac arrhythmias and loss of tone in the colon (megacolon) and esophagus
(megaesophagus).
During the acute phase, there are both trypomastigotes in the blood and amastigotes
intracellularly in the tissues.
During the chronic phase, the organism persists in the amastigote form only.
Manifestations:
1. Congenital Chagas disease - can cause multiple CNS or visceral malformations, often
incompatible with a normal life. Death usually occurs within the first 2 years of life.
2. Chronic stage Parasite penetration site:
- Chagoma - painful skin edema at the insect bite site.
- Romanas sign - conjunctiva hyperemia, pre-auricular and sub-mandibular lymph nodes
enlargement, orbital and facial edemas.

Romanas sign

| P a g e 19

 Toxaemic stage: lymphadenopaty, spleen and liver enlargement.

- Death can occur during this stage mainly in children, by meningoencephalitis or myocarditis.
- Long latent period with an intermittent low parasitemia and a continuous intracellular replication
of amastigotes - most frequently.
3. Asymptomatic forms.
Complications: after many years:
Cardiac involvement - Cardiomegaly (destruction of myocardial fibres and ganglion cells).
- Arrhythmias.
- Cardiac failure (cardiac fibers changes and autoimmune disturbances).
- Sudden death.
Visceral involvement - due to the destruction of the mienteric or intramural plexus.
- Mainly colonic (chronic constipation and abdominal distension).
- Esophagomegaly (often followed by aspiration pneumonia), some other "mega" disorders as in
small bowel and ureter.
Usually people having one complication (like cardiac) extremely rare present in some other
(digestive one).
Diagnosis:
Morphology:
1. Blood examination (different concentration techniques) - to prove trypanosome presence.
2. Xenodiagnosis (useful to detect very low parasitemia):
- Laboratory bugs, free of parasites are fed on the patients. 2-4 weeks later, insects are killed and
their gut examination makes evident the metacyclic infective stage.
- Muscle biopsy - intacellular amastigates (rarelly used).
- Blood culture on NNN medium - epimastigotes appearance in positive cases.
Immunology:
1. Complement fixation test (CFT).
2. Immuno fluorescent antibodies test (IFAT) - the earliest to become positive.
3. Enzyme Linked Immunosorbent Assay (ELISA).
In acute disease trypomastigotes are detectable in thick or thin blood film (wet & stained). In chronic
disease there are few trypomastigotes in the blood, so it is more difficult to detect them, therefore
we will use more xenodiagnoses* and serologic tests.
* Xenodiagnosis - is a process to diagnose an infectious disease by exposing tissue to a vector and then examining the vector for
the presence of a microorganism or pathogen

Thick and Thin Blood film preparation

| P a g e 21

Toxoplasma gondii
Disease: Toxoplasmosis.
A cosmopolite tissue coccidia presenting high infectivity rate in humans. It includes various clinical
spectrums depending on: infective dose, infective strain, immune status of the host, type of
transmission.
Transmission and epidemiology: infects a wide variety of mammals and birds, and it grows on almost
any mammalian cell in culture.
Source of infection can be cats. Rodents and birds maintain the cycle as IH (intermediate host),
containing tissue cysts - when the DH (definite host) eats them.
Transmission can occur by:
1. Contact with cats or their feces.
2. Digestive - improperly meat or milk cooking (tissue cysts containing bradyzoites) or
contaminated vegetables with cats oocysts (containing sporozoites).
3. Blood transfusion (trophozoites).
4. Organs transplantation (cysts).
5. Laboratory infections (cysts, trophozoites).
6. Vertical transmission (mother to child).
Life cycle:
1. Cat is the definitive host. The parasite
reproduces schizogony (asexual type of
reproduction by fission) in the cats gut epithelial
cells becoming gametocytes, than gametes, than
zygotes and eventually becoming oocysts.
2. Oocysts are shed in the cats feces. It takes 1-5
days for the oocysts to sporulate (produce and
release spores) in the environment and become
sporozoites - the infective form.
3. Intermediate hosts in nature (including birds and
rodents) become infected after ingesting soil,
water or plant material contaminated with
oocysts.
4. Shortly after ingestion, the oocysts in the small
intestine release parasites that invade the gut wall and are ingested by macrophages, forming
the tachyzoites (trophozoites). They rapidly multiply by binary fission, spread to tissues and
kill the infected cells as well as other cells. This killing process is usually limited by the
immunity.
5. These tachyzoites are localized mostly in neural and muscle tissue, and also in the liver, lungs
and eyes, where they develop into tissue cyst bradyzoites (slow-growing).
6. Cats become infected after consuming intermediate hosts tissue cysts, or by directly ingestion
of sporulated oocysts.
7. Animals used for human consumption may also become infected with tissue cysts after
ingestion of sporulated oocysts in the environment.
8. In the human host, the parasites form tissue cysts, most commonly in skeletal muscle,
myocardium, brain, and eyes. These cysts may remain throughout the life of the host.

| P a g e 21

Morphology:
The trophozoite is found in both indirect and direct hem-agglutination. They are 4-72-4 mm in
size. They have a crescent form with round end, containing the nucleus, and a pointed end containing
the apical complex (responsible for the intracellular penetration of the parasite). They multiply rapidly
by binary fission.
The tissue cyst is found in indirect hem-agglutination. It is 100-200 mm in size, spherical. It is a
modified host cell, usually macrophage, containing hundreds of parasites in a latent stage, as
bradyzoites. They are usually located in brain or muscles.
The oocysts are found only in indirect hem-agglutination and in feces. It is 9-1111-14 mm in size,
oval. It contains 2 sporocysts, having 4 sporozoites each.
Direct Agglutination
Direct agglutination reactions, test patients serum for
the presence of antibodies against large, cellular
antigens.
Direct agglutination reactions can be used to determine
antibody titer.

For oocysts and trophozoite

Indirect Agglutination
To test patient serum for the presence of antibodies
against soluble antigens serum is mixed with latex
spheres with the soluble antigens attached.
Antibodies will then cause visible agglutination of the
latex spheres with the soluble antigens attached.
Alternatively, antibodies may be attached to the latex
spheres to test for the presence of soluble antigens in
patient serum.

For oocysts only

Pathogenesis: limited by cell-mediated immunity. Parasites can be killed with help of antibodies.
If the cell mediated immunity is good, tachyzoites develop into cyst and the cell multiply slower
(bradyzoites). Therefore most of the diseases are asymptomatic at first.
In immune compromised patients, however, cyst breaks and the disease start to be symptomatic.
Manifestations: in an immune competent host most infections are asymptomatic (except pregnancy,
where special care because of a risk of vertical transmission) or containing a few flu-like symptoms.
In an immune compromised host, a new infection involves many organs. Reactivation of an old
infection may occur in patients with defective CMI, HIV, organ transplantation and malignancies.
1. Immune competent host:
Asymptomatic forms - positive serology, hazardously discovered in persons without any sign of
disease.
Acute, benign toxoplasmosis - (15-20% of cases) mostly lymphadenopatic or
cutaneous form. The disease lasts about 4-12 months with no inflammation signs. Symptoms
include:
- Cervical lymphadenopaty (preferential), axils, groin.
- Fever (in 50% of cases) - moderate, daily appearance, lasting for few days to
several weeks (flue like syndrome).
- Asthenia (abnormal physical weakness or lack of energy) - sometimes important, lasts several
weeks after lymphadenopathy disappearance.
- Skin, migratory rash, or maculo-papular eruption - sole/hand.
- Ocular locations (extremely rare).
2. Congenital toxoplasmosis (30-50% of cases with risk pregnancies):
Lesions appearance is related to the age of pregnancy, being more important
when the disease is acquired during the first 3 months, when the organogenesis process is very
active.
Sero-conversion appears during pregnancy. (is the development of detectable specific antibodies
to microorganisms in the blood serum as a result of infection or immunization)
Newborns from previously infected mothers - parasitemia due to
immunosuppression:
- HIV infection.
- Iatrogenous (immunosuppressive medication).
- Following surgery (splenectomy).
Seroconversion appears 2-3 months before the conception.
Ancient infections (the reactivation of tissue cysts in myometer).

| P a g e 22

 Severe congenital toxoplasmosis

During the first 3-4 months is the appearance of Sabins signs:
microcephaly,
Hydrocephaly (blocked CSF circulation), cerebral calcifications,
Chorioretinitis (sometimes associated with microphtalmia, strabismus,
cataract and glaucoma), nistagmus, retinal haemorrhages.
After first 3-4 months - severe infectious syndrome of the neonate,
including
Jaundice, hepatosplenomegaly, haemorrhagic syndrome, ocular or CNS
involvement.
Benign congenital toxoplasmosis
Including microphtalmia, cerebral calcifications, strabismus,
chorioretinitis, cataract, seizures, transient jaundice, hepatomegaly.
Latent congenital toxoplasmosis
Any positive serology results a compulsory to be followed up during the
first 12 months after birth. Symptoms may include hydrocephaly,
seizures, transient jaundice, ocular involvement, retard in development.
Complications include cataract, glaucoma, retinal haemorrhages, optic
nerve atrophy, and chronic iridocyclitis.

Hydrocephaly

Brain Calcifications

Chorioretinitis

3. Immune compromised host (HIV, malignancies, immune suppressive

medication):
Acquired infection on this condition: febrile, generalized, severe disease with
Multi-visceral involvement (lung, heart, liver, bone marrow, bones).
Reactivation of a previous infection:
- Cerebral form: cerebral abscess aspect, or toxoplasmic acute encephalitis (mostly in HIV patients).
- Ocular form: multi-focal active retinal lesions with concomitant vitreous and nterior segment
reaction.
- Isolated locations: skin, pancreas, kidney, urinary bladder, lymph nodes, muscles, cavum (Body
cavities), heart, lung, liver, etc.
Diagnosis:
Morphology:
1. Smear examination - Giemsa stain - blood, CSF, placenta, vaginal discharges, and ganglia. In a
positive result intra and extracellular trophozoites are seen, as well as cysts.
2. Cells culture or fibroblasts. It can be either a direct (appearance of pseudo-cysts in a positive
diagnosis) or rapid (intra and extracellular trophozoites are seen) examination.
3. Mouse intra-cerebral or peritoneal inoculation. Cerebral cysts are seen in a positive diagnosis.
In congenital toxoplasmosis a microscopical examination of the amniotic fluid, blood and placenta is
performed Amniocentesis
In toxoplasmosis in immune compromised patients, an examination is done of the blood, CSF and
biopsy is taken.

Immunology:
1. Antibodies:
IgA and IgE persist for about 4-6 months, IgM
for up to a year and IgG for 10 years and more.
Using figurate antigens - Dye test (Sabin and Feldman) - The test is
based on the presence of certain antibodies that
prevent methylene blue dye from entering
the cytoplasm of Toxoplasma organisms. Patient serum is treated with Toxoplasma
trophozoites and complements as activator, and then incubated. After incubation, methylene
blue is added. If anti-Toxo antibodies are present in the serum, because these antibodies are

| P a g e 23

activated by complements and lyse the parasite membrane, Toxoplasma trophozoites are not
stained (positive result); if there are no antibodies, trophozoites with intact membrane are
stained and appear blue under microscope (negative result)
- IFAT (Indirect Fluorescent Antibodies Test) - formalin treated tachyzoides fixed on the
slide, in contact with serum dilutions, are linking antibodies. It emphasize Ag/Ab complexes
after adding the marked anti immune globulins antibody. It results with the higher dilution
producing indirect fluorescent.
It is specific to IgM and IgG detection. Its disadvantages are the false positive reactions if
the serum contains antinuclear Ab, the false negative reactions when IgG are very high,
blocking IgA access, and the fact that it requires a special device.
- Direct agglutination.
Using soluble antigens - ELISA (Enzyme Linked Immuno Sorbent Assay) - with IgE, IgA, IgM, IgG specific
antibodies.
Antibody is fixed on a solid phase (polystyrene), incubation with suspect serum, wash with
anti IgG conjugate and add enzyme substrate. Color reaction measured by
spectrophotometer.
- ISAGA (Immuno-Sorbent Agglutination Assay) - with specific IgM, IgA,
IgG detection.
Anti IgM MAB fixed are on the wells, diluted sera according to ELISA results,
Toxoplasma formalin suspension. In the absence of specific IgM antibodies Toxo parasites
determine a precipitate in the wells, estimated from 0 to ++++.
- Hem-agglutination - agglutination of sheep RBC coated with Toxo antigen, with
successive sera dilutions: double-treated and non-treated sera (for IgM inactivation).
Reading after 2-8 hours incubation.
- Latex agglutination test - detection of total antibodies. Antigen is fixed on
latex particules, and undergoes an agglutination reaction. It is a simple reaction which uses
as a screening test, but it has no quantification of antibodies level, and there might be false
positive and false negative reactions on sera with very high IgG titers.
- Western blot - electrophoresis of T. gondii antigens. The antigen is fixed on a
nitrocellulose paper, incubation with serum samples, proving antibodies and analyzing the
profile.
- Avidity tests - checks how strong the Ag/Ab complexes, which determines how old the
infection is and can estimate the risk for pregnancy.Weak complexes in recent infections and
very strong and stable complexes in old infections.
Avidity is measured using indirect ELISA and a supplementary wash step with urea
solution, able to dissociate the already formed Ag/Ab complexes.
- ELIFA (Enzyme Linked Immuno Filtration Assay) - identification of precipitation arcs by
counter immunelectrophoresis, in the presence of an enzymatic substrate, using soluble
antigens.This test can be performed on couple of sera (mother and cord blood).
2. Circulating antigens in blood.
3. Molecular diagnosis: PCR.

Circumstantial diagnosis:
- Moderate leukocytosis or leucopoenia.
- Mononucleosis - like syndrome.
- Low hypereosinophilia (up to 10%).
- Lymphadenopathy.

| P a g e 24

Cryptosporidium
C.parvum C.muris
Disease: cryptosporidiosis ("travellers diarrhea").
Transmission and epidemiology:
The disease is transmitted through the GI tract by:
1. Eating - food contaminated with oocysts.
2. Drinking - contaminated water with infective oocysts.
3. Oral-anal sexual intercourse.
4. Laboratory - accidental infections, by oocysts aspiration.
The source of infection can be either human or zoonotic reservoir (calf, pigs, sheep).
The disease is present all over the world, and in about 1-9% of the diarrheal diseases in developing
countries.
It has a special high frequency in tropical countries and in immune compromised patients (mainly due
to HIV infection).
The risk population includes:
- AIDS patients or other immune compromised patients.
- People taking care on sick animals.
- Nurses manipulating the infected samples.
- Children under 6 months (their immune system is unable to produce sufficient antibodies), or
malnourished children.
- Risk travelers.
Life cycle:
The life cycle of Cryptosporidium parvum consists of an
asexual stage and a sexual stage.[1]
1.

2.

3.
4.

5.

6.

After being ingested, the oocysts excyst in the

small intestine. They release sporozoites that
attach to the microvilli of the epithelial cells of the
small intestine.
From there they become trophozoites that
reproduce asexually by multiple fission, a process
known as schizogony.
The trophozoites develop into Type 1 meronts that
contain 8 daughter cells.
These daughter cells are Type 1 merozoites,
which get released by the meronts. Some of these
merozoites can cause autoinfection by attaching to
epithelial cells. Others of these merozoites
become Type II meronts, which contain 4 Type II
merozoites.
These merozoites get released and they attach to
the epithelial cells. From there they become either macrogamonts or microgamonts. These are
the female and male sexual forms, respectively. This stage, when sexual forms arise, is called
gametogony.
Zygotes are formed by microgametes from the microgamont penetrating the macrogamonts.
The zygotes develop into oocysts of two types. 20% of oocysts have thin walls and so can
reinfect the host by rupturing and releasing sporozoites that start the process over again. The
thick-walled oocysts are excreted into the environment. The oocysts are mature and infective
upon being excreted. They can survive in the environment for months.

| P a g e 25

Morphology:
sporozoite
Is 2-5 mm in diameter, located in the brush border
of the intestinal mucosa. It is located under the
membrane, but extracytoplasmatic and inside of
parasitophorous vacuolae.

cyst
Is 4-5 mm in diameter, round form. It contains
4 sporozoites and Tyzzer body.
Mature cyst - thick coat (5 layers), represents the
infective
stage in nature, resistant to environment
conditions.
Immature cyst: thin layer, allows the spread of
the parasite to the mucous level.

Pathogenesis: during the excystation of oocyst in small intestine, the sporozoites attach to gut wall
without invasion, mostly in jejunum. They are located under the membrane, but not in cytoplasm. They
have no toxin, but they cause problems in the cellular pumps (similar to bacteria).
C. parvum is able to spread into the whole digestive segment, while C. muris is located only in the
initial part if the intestine.
Manifestations: the incubation period is about 2-10 days, averaging a week.
The disease has different effects on immune competent and immune compromised hosts.
Immune competent host can present both asymptomatic disease and a symptomatic disease. The
symptomatic cases include:
- Common gastroenteritis, lasting for 3-12 days, followed by a spontaneous cure.
- 3-10 liquid, non-bloody daily stools, brown-green, rarely containing mucus.
- Abdominal pain, nausea, vomiting - rarely associated.
- Chronic diarrhea, followed by malabsorption in malnourished children.
Immune compromised host present symptomatic disease:
- AIDS - very severe infection (CD4 lymphocyte less than 100/ml).
- In 50% of cases - relevant for the full clinical picture of AIDS, when opportunistic infections are
characteristic.
- Liquid, no bloody, cholera-like stools, about 10-20 /day, soon followed by dehydration.
- No morphological changes of the intestinal mucous.
- Migration of the biliary tree, gall bladder and the respiratory tract (invading the ciliated cells,
followed by interstitial pneumonia, making evident the parasite in BAL).
Diagnosis:
Morphology:
- Stool examination: wet preparation is usually useless.
- Smear, Ziehl Neelsen modified by Herricksien and Pohlentz stain method.
Results in red purple elements, about 4-5 mm in diameter, with, or without
structure details (sporozoytes and Tyzzer bodies), on the green scale.
- Kynioun or Giemsa stain methods are rarely used, because of the weak contrast.
Ziehl Neelsen smear
Immunology:
- Copro-antigens detection by IFAT- monoclonal antibodies.
- Specific IgM or IgG (antibodies ELISA technique /IFAT).
Molecular diagnosis:
1. Fecal microscope analysis - limit 50,000 oocysts per gram of stool.
2. PCR - amplifies ~ 400 base pair sequence from feces - sensitivity to 6 oocysts per gram of
stool.
Differential diagnosis:
Cholera, Giardiasis, Any cause of watery diarrhea produced by bacteria, fungal, parasites, viruses,
- travellers' diarrhea.

| P a g e 26

Isospora belli
Disease: Isosporidiasis.
Transmission and epidemiology: the disease is transmitted through the GI tract by ingestion of
contaminated food or water with human feces, containing oocysts. It can be also transmitted by
travelers' diarrhea agent.
The disease is present all over the world. A high incidence in the US and tropical areas, mainly Asia
and Africa. Low incidence in Europe.
In immune compromised patients the infection is common in areas where PCP (Pneumocystis Carinii
Pneumonia) prophylaxis is not routinely used.
Life cycle:
1. At time of excretion, the immature oocyst contains
usually one sporoblast. In further maturation after excretion, the
sporoblast divides in two.
2. The sporoblasts secrete a cyst wall, thus becoming
sporocysts, and the sporocysts divide twice to produce 4
sporozoites each.
3. Infection occurs by ingestion of sporocysts-containing
oocysts: the sporocysts excysts in the small intestine and release
their sporozoites, which invade the epithelial cells and initiate
schizogony.
4. Upon rupture of the schizonts, the merozoites are
released, invade new epithelial cells, and continue the cycle of
asexual multiplication.
5. Trophozoites develop into schizonts which contain
multiple merozoites.
6. The entire multiplication cycle is taking place in human
intestinal mucous.
7. After a minimum of one week, the sexual stage begins
with the development of male and female
gametocytes. Fertilization results in the development of oocysts
that are excreted in the stool.

Morphology:
The trophozoite is similar to Cryptosporidium. The oocyst is is 20-3012-16 mm in size, oval shape,
very resistant in environmental conditions.
Immature oocyst contains 2
undeveloped sporocysts, becoming
rapidly infective.
Mature cyst contains 2 sporocysts, each
containing 4 sporozoites inside.
Manifestations: - Incubation period of 9-15 days.
The disease has different effects on immune competent and immune compromised hosts.
Immune competent host can present both asymptomatic disease and a symptomatic disease. The
asymptomatic cases were discovered by coprology.
The symptomatic cases include:
- Non-invasive enteritis - self-limiting, usually lasting for 7-10 days, rarely can lasts for few
months.
- Fever, asthenia, nausea, vomiting, abdominal pain, diarrhoea, flatulence.
- The elimination of oocysts in faeces, during the stage of the disease, is followed by clinical
improvement.
Immune compromised host present symptomatic disease: chronic diarrhea associated with
malabsorption due to the mucous lesions.

| P a g e 27

Fever, asthenia, nausea, vomiting, abdominal pain, diarrhea, flatulence rapidly followed by
dehydration and worsened condition.
In AIDS (CD4 less than 100/ml) - undulant evolution with bloody and mucus stools, weakness,
malabsorption, sometimes followed by extraintestinal dissemination (lymph nodes).

Diagnosis:
Morphology:
1. Stool examination:
- Direct stool examination - useful for the diagnosis.
- Concentration methods (Ritchie), in order to emphasize the immature
oocysts containing 2 undivided sporocysts.
- Modified Ziehl-Neelsen stain, on smear, permanent preparation - purple
oocysts on the green slide.
2. Enterotest: duodenal liquid examination.
3. Culture: 2-3 days in water containing bicarbonate, at 25-300C, temperature
Ziehl Neelsen smear
allows to emphasize sporocysts segmentation and the differential diagnosis
with Eimeria spp.
Immunology: useless, not developed.
Histopathology:
- Duodenal villous atrophy.
- Local eosinophilic infiltrate in lamina propria depending on the parasitic burden.
- Rarely - blood eosinophilia.
Differential diagnosis
1. Giardiasis
2. Oocists in transit - Eimeria spp. from the rabit liver or meat, mackerels, sardines, herrings. The
recommendation is to avoid of consuming these products before copro-logical examination.
3. Travelers' diarrhea (giardiasis, intestinal amoebiasis, cryptosporidiasis).

Pneumocystis carinii
Disease: Pneumocystis Carinii Pneumonia (PCP), Plasmocytic Infiltrative Pneumnia (PIP),
Pneumocystosis.
Transmission and epidemiology: the disease is transmitted directly by inhalation, person to person, oral
transmission.
The disease geographical distribution is worldwide.
The parasite is usually found in domestic animals such as horses and sheeps, and in a variety of
rodents, but it is thought that these animals are not a reservoir for human infection. Each mammalian
species is thought to have its own species of Pneumocystis.
Life cycle:
1. The asexual phase includes replication by mitosis of the trophic
forms.
2. The sexual phase occurs: The trophozoite is present extracellularly,
attached to the type I pneumocytes, covered by the alveolar
surfactant.
3. It is than becomes a precyst, and after 1-2 hours a cyst is formed.
4. After 4 hours it becomes spherical and contains 8 peripheral
sporozoites.
5. The sporozoites are than braking of coat, than get free as
trophozoite.
6. The trophozoite is attached after 2 hours by the pneumocytes.
Morphology: the trophozoite is 1-10 mm in diameter; it has a thin coat and a central nucleus. It
presents filopodia (fixed to the alveolar epithelia). Usually, many parasites are clustered inside alveoli.
The cyst is 6-8 mm in diameter. It has 8 intracystic bodies - the mature stage, and it represents the
infective stage.

| P a g e 28

Pathogenesis: the parasite has a major surface glycoprotein that exhibits significant antigenic variation
in a manner similar to that of Trypanosoma brucei. Pneumocystis species have multiple genes encoding
these surface proteins, but only one is expressed at a time.
Inhalation of the cyst causes inflammatory response involving mainly plasma cells. It than causes
exudates that block oxygen exchange, but the organism does not invade the parenchyma.
Manifestations:
1. Epidemic form:
In newborn, premature, malnourished children, aged between 2 weeks up to 6 months:
The disease includes loose of appetite, weakness, dry cough, dyspnea, frequent, inefficient
breathing, cyanosis, fever (no more than 38-38.5C, not always) and spontaneous pneumothorax.
In contrast to the clinical signs and symptoms, having as climax the respiratory distress syndrome,
there are few objective elements to help us for the right diagnosis.
2. Sporadic form:
In immune compromised adult patient, mainly due to HIV infection (CD4 bellow 100/ml, or less
than 20% of the total lymphocytes). The incubation period is short (few days).
The disease in this case includes dyspnoea, productive cough, cyanosis, worsening of the physical
condition, progressive respiratory distress syndrome, decreasing O2 partial pressure and increasing
CO2 partial pressure (dyspnoea, cyanosis).
Complications: in immune compromised patients may occur some complications of the eye (retinal),
cutaneous (vasculitis), pneumothorax, pneumomediastin, subcutaneous emphysema and even a
progressive evolution to death.
Diagnosis:
Morphology:
On sputum, induced sputum, BAL, lung biopsy.
1. Giemsa stain which is difficult in reading and is time consuming, but is
compulsory to be made, as it is the only method allowing to make evident
both: cysts - 8 violet peripheral sporozoites coat, does not fix the stain and
trophozoites - violet, like a bunch, having the nucleus more intense colored.
2. Orto blue toluidine - violet, spherical or oval cysts, without internal
Giemsa stain arrow- cyst
details structure. It is easy to be performed and to be red.
3. Grocott (silver methenamine) - dark brown cysts, without any structure
details, on the green background.
Immunology:
1. Antibodies detection by IFAT, ELISA.
2. Antigen detection in sputum (perspective).
Pathology:
1. Lympho-plasmocytic interstitial infiltrate.
2. Alveolus are filled with honey comb material, enlarged intra alveolar septum, due to the
lymphocytes and plasmocytes infiltrates.
Imagery:
1. X ray - reveals opacities in both lungs (in babies) and lobar pneumonic aspect in adult,
spontaneous pneumothorax, bronchopneumonia, reticular-nodular opacities.
2. CT scan, using radio isotopes (early diagnosis).
Circumstantial diagnosis:
- In children: leucocytosis, hypercalcemia.
- In adults: leucopoenia, elevated CO2 and LDH, clinical signs can be announced few weeks ago,
by radiological changes.
Differential diagnosis:
- Flu.
- Bacterial or viral (CMV) pneumonia.

| P a g e 29

Plasmodium spp
P.vivax (benign tertian malaria), P.ovale (ovale tertian malaria), P.malariae (quartan malaria),
P.falciparum (malignant tertian malaria)
Disease: Malaria
Plasmodium spp. Are parasites invading the RBC cells, Malaria causes symptoms that typically
include fever and headache, which in severe cases can progress to coma or death.
The disease is widespread in tropical and subtropical regions the most important source of transmission
is the vector Anopheles. It is the most frequent cause of tropical fever in tropical areas.
there are about 300-400 million sick people estimated and about 1-2 million cases of
death/year.
More than 1 milliard people live in endemic areas.
Geographical distribution:
P.falciparum is widely distributed in many tropical countries, but rarely also in temperate
region.
P.vivax has a very large distribution and may be transmitted in tropical regions and in
temperate ones as well.
P.ovale is rarely present in areas outside Africa and usually appears in mixed infection with
P.vivax or P.falciparum
P.malariea is much less common than P.vivax/falciparum
Transmittion:

1.
2.
3.

4.
5.

Tropical Areas
Vector Anopheles spp. tropical and
subtropical areas below 2,000 2,500 m
Vertical (mother to child mostly P.
falcilprum)
Blood transfusion - mostly in countries where
blood transfusion is a commercial transaction
Infectivity: P. falciparum lasts for 1 year
P.ovale and P. vivax last for 3- 5 years (in
hepatocytes)
P. malariae lasts for up to 50 years (in RBC)
Intravenous drug users (accidentally by syringe
or needles)
Therapeutic impaludation (history - cerebral
syphilis, in order to kill
the spirochetes)

6.

7.

8.

Temperate areas
Post transfusion (compulsory surveillance
of blood donors)
definitely forbidden to make a donation
less than 4 months after coming back
from an endemic area !
Airport malaria - mosquitoes from endemic
areas are transported by plains in other not
impaludated zones plains disinfection
(Roissy 1994, seven cases) Imported
malaria cases increasing
Accidental malaria (by syringe) or
congenital, mainly P.Vivax

| P a g e 31

Life cycle:
- Sexual phase -sporogony in the female Anopheles gut
- Asexual phase schizogony tissue phase or pre-eritrocityc schizogony (in the liver)
- eritrocytic phase or eritrocytic schizogony Diagnosis stage!
1.

In the life cycle of Plasmodium, a female Anopheles mosquito (the definitive host) transmits a
motile infective form called the sporozoite to a vertebrate host such as a human (the secondary
host), thus acting as a
transmission vector.

2.

A sporozoite travels through the

blood vessels to liver cells
(hepatocytes), where it
reproduces asexually
(tissue schizogony), producing
thousands of merozoites

3.

They infect new red blood cells

and initiate a series of asexual
multiplication cycles (blood
schizogony) that produce 8 to 24
new infective merozoites,

4.

At which point the cells burst

and the infective cycle begins anew.

5.

Other merozoites develop into immature gametocytes, which are the precursors of male and
female gametes. When a fertilized mosquito bites an infected person, gametocytes are taken
up with the blood and mature in the mosquito gut.

6.

The male and female gametocytes fuse and form a ookinetea fertilized, motile zygote.

7.

Malaria life cycle Ookinetes develop into new sporozoites that migrate to the insect's salivary
glands, ready to infect a new vertebrate host. The sporozoites are injected into the skin, in the
saliva, when the mosquito takes a subsequent blood meal.

Only female mosquitoes feed on blood; male mosquitoes feed on plant nectar, and thus do not
transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at night. They
usually start searching for a meal at dusk, and will continue throughout the night until taking a meal
Morphology:
Sporozoites elongated formations, crescent shape, having a central nucleus 10X1
um in length, life span 30 minutes.
Merozoites inside the hepatocytes / RBC

| P a g e 31

Pathogenesis:
-

RBCs lysis by release of merozoites in the circulation and in the spleen

(splenomegaly)
Antibodies provide partial immunity (a few years) & prevent merozoites from
invading RBCs.
P. falciparium can infect all RBCs (5-30% invasion) and may cause capillary
occlusion by aggregates of invaded RBCs results in haemorrhage & necrosis, esp. in
brain (cerebral malaria) & kidney haemoglobinurea (blackwater fever). G6PD
deficit protects against severe effects.
P. malariae (much less common than the others) infects only mature RBCs;
P. vivax & ovale reticulocytes, via Duffy antigen (absent in most West Africans
resistant).

Manifestations: after 2 weeks, abrupt onset:

1. Cold --1 hr, temp. rise with pale skin & shivering
2. Hot -6-8 h, fever with flushed skin
3. Sweating stage- if not caught from transfusion, at the beginning the fever may be
continuous. Btw the fever episodes the patient usually feels well. Anaemia & jaundice (severe
with P. falciparum); splenomegaly in most; hepatomegaly in ~1/3. Non-falciparum malaria is
usually self-limiting.
For all the species - common clinical features, related to the liberation of fever producing substances
especially during schizogony because every RBC containing a trophozoite will be destroyed within 4872 hours
Paroxysm of malaria:
Cold stage - 30-60 minutes: the patient shivers or has a frank rigor, the temperature rises sharply, pale
skin, piloerection, skin hyperaesthesia
Hot stage 6-8 hours usually (except P. falciparum, when it can be longer): high temperatures
sustained for few hours, flushed skin, tachypnea, and rapid full pulse
Sweating stage the patient sweats freely, the temperature rapidly decrease, he remains a little dizzy,
falling asleep
The rhythmicity of the access is fixed, related to the species and the eritrocytic schizogony:

Quatrain malaria
P. malariae

Disease Cycle
Tertian malaria
benign - P. vivax, P.
malignant P. falciparum
ovale

72 h

48 h

24-48 h

Signs and symptoms:

1. Fever: often irregular during the first 1-2 weeks following the insect bite, than becomes
periodic, depending on synchronized schizogony
- It appears regular from the very beginning only in cases acquired after blood
transfusion
2. Anemia: a hemolytic type, due to the breakdown of parasite-invaded red blood cells Except
P. falciparum, when the rate of infected RBC is up to 30 %, in all the cases about 1-4 % of
RBC are infected. In P. falciparum anemia is more severe and often complicated with
autoimmune reactions and spleen increasing activity (splenomegaly)
- The expected reticulocytosis is often absent, probably due to bone marrow
suppression by some toxins of parasitic provenience
- Bone marrow aspirate phagocyted RBC either containing parasites or not, can be
seen dys-erithropoiesis
3. Splenomegaly
- common feature in all the species - during the acute phase; it follows the febrile attack
(variable in size) and during the chronic stage, an enormous spleen exists, often leading to
secondary hypersplenism. This feature also aggravates the existing anemia (spleen

| P a g e 32

Increasing activity - hypersplenism)

4. Jaundice
- mild jaundice due to hemolysis - all type of malaria
- sever jaundice is noticed in P. falciparum infection due to specific liver
involvement

P. vivax and P. ovale

Are the most common clinical

forms
Irregularly, periodically relapses
can occur over a period of up to 5
years, when liver (hepatocytes)
hypnozoites awake from dormancy

P. malariae
There is a longer incubation period
weeks following the first
exposure
Enlarged liver and spleen together
with an important anemia

The recrudescence can appear after

years (even more than 30 years),
due to the persistence of intraerythrocytic forms
Patients should be monitored for
up to 5 years, following the first
attack when they have fever

P. falciparum
Is more serious disease in both
morphological and clinical point
of view - different than the other
species
Following the first attack, in a
non-immune person, the death
can appear very often, or they
can survive, developing a degree
of anemia
The blood forms last no longer
than a year, so that the
recrudescence due to the
persistence of blood forms
appear during the first year post
infection
There are no liver dormancy
hipnozoites, so that in spite the
disease is very severe, it is not
necessary for the patient to be
followed up longer than one year
The immunity is rapidly lost and
in the absence of Reinfection
The infected RBC are arrested in
small blood vessels and do not
escape to the peripheral blood.
Except those containing young
trophozoites stages so there is a
lot of misdiagnosed cases.

Complications of P. falciparum
1.
2.

3.
4.
5.
6.
7.
8.

Hypoglycemia - mainly in children and pregnant women (glycogen depletion), in patients

treated with quinine and/or in untreated cases
Black water fever - consequence of intravascular haemolysis together with haemoglobinuria
and renal failure mostly in people using irregular quinine as prophylaxis or having a Gl-6PD
deficiency
Anaemia important & complex in P.falciparum malaria increased % of destroyed RBC
hypersplenism
dys-eritropoesis
autoimmune disorders
Tropical Splenomegaly Syndrome (TSS)- enlarged and firm splenomegaly
Cerebral malaria in non-immune patients present loose of consciences, focal
neurological signs, and rearly cerebral edema.

Malaria in pregnancy
All type of malaria infection can lead to abortion, but P. falciparum is quite a rule
In P. falciparum, woman either immune, or not, present a sever course of the disease.
Microcirculatory arrest of infected RBC in placenta may cause fetal death, prematurity.
Progressive haemolytic anemia in a child who is failing to thrive

| P a g e 33

Immunity in malaria
Related to the parasite species: i.e. people having P. ovale infection, can get P. malariae too
Lasts for a few years in absence of reinfection: that is why people living in endemic areas for
long time have to get chemoprophylaxis when they return to endemic areas
Is related to the human species: the infective species for rodents, P. berghei, are not dangerous
in man
Non-immune protective factors
Red cells lacking the Duffy blood group antigen are resistant to infection with P. vivax
Individuals having hemoglobin genotype AS (carriers for sickle cell anemia) are resistant to
sickle cell RBC have low ATPase activity and cannot produce sufficient energy to support the
growth of the parasite.
the lethal P. falciparum infection
Malnutrition protects against the lethal P. falciparum infection
Diagnosis:
Morphology:
Thin blood film Giemsas stain, or Leishman, Romanovski allows a detailed study of the parasite
morphology and the specie identification.
The diagnosis is difficult when there is low parasitemia
It needs more time for reading (at least 30/slide)
At least 3 thin blood films, sampled in different times, should be examined before infirming
malaria
Thick blood film - Fields, or Giemsas stained
A concentration method allowing confirming the disease; it can be considered as a screening
method
Because of the RBC haemolysis it is difficult to appreciate the plasmodial species
It should be completed with the thin blood film
Both thin and thick blood films by finger prick is needed to be performed in suspected cases:
During irregular fever 3-4 samples should be taken at 8 hours interval
During there is a regular, rhythmic fever, samples should be taken immediately after the
onset of febrile attack

Immunology:

Antigen detection available for each species

Specific antibodies detection- Useless for the diagnosis of acute attack
It depends on finding specific antibodies and most methods are unable in distinguishing between
antibodies of different species of parasite. Antibodies may be detectable for several years after the last
attack of malaria
Most common tests: IFAT, ELISA
The benefit: In endemic area - The Screening of blood donors
In non-endemic areas
The Retrospective diagnosis in a febrile access modified by Inappropriate treatment, with low
parasitemia (military)
Febrile people coming back from an endemic area, without positive blood tests (thin and thick
blood films)
Cross reactions between the different species
There is about 1 week between the antibodies appearance and malaria attack following the first
infection
Western blot confirmation test
Molecular diagnosis: Polymerize chain reaction - PCR
Circumstantial diagnosis: Anaemia, leukopenia or leucocytosis. Thrombopenia,
hyperglobulinemaia, Fever, Jaundice, Neurological signs

| P a g e 34

Differential diagnosis of malaria parasites:

Parasite

P.vivax

P.malariea

P.ovale

P.falciparum

Schizogonic cycle
RBC

48 hours
Reticulocyte ,
enlarged 1-4%

72 hours
Mature RBC, normal 14%

Young trophozoite

Thick ring, 1
chromatin dot

Thick ring, 1 chromatin

dot (bird eye)

48 hours
Reticulocyte , RBC
enlarged with
irregular edges 14%
Thick ring, 1
chromatin dot

24-48 hours
Both mature RBC
and Reticulocyte
sometime irregular
10-30%
Fine, multiple rings
1-2 chromatin dots

Mature trophozoite

Irregular,
amoeboid

Round with central

chromatin and band
forms, pigment distinct

Round, Compact

Ring enlarged
slightly irregular

Schizont

12-24 merozoites
Irregularly
arranged

6-12 merozoites,
arranged as rosette,
pigment in centre
daisy form

4-14 merozoites,
not as regularly as
P.malariea

Rarely seen in
peripheral blood 832

Stippling-

Present, small
yellow-brown
intracytoplasmic
Schuffners dots

Present. Extremely rare

in eritrocytic cytoplasm,
but sometime evident in
band form Ziemann's
stippling

Always present,
like Schuffners
dots James dots

Sometimes present
few large black
spots Maurers
dots

Gametocyte

Male round or
oval, central,
diffuse chromatin.
Female reddish
eccentric, triangle
shape contained in
a typical RBC

Male round or oval,

central, diffuse
chromatin.
Female reddish
eccentric, triangle shape
contained in a typical
RBC

Male round or
oval, central,
diffuse chromatin.
Female reddish
eccentric, triangle
shape contained in
a typical RBC

Male crescent
reddish with
diffused chromatin,
pointed endings
Female Bluish
with compact
chromatin

female
Peripheral blood

All the described

stages

All the described stages

All the described

stages

Only young
trophozoite and
gametocytes

Differential diagnosis
-

Tropical fever: dengue, haemorrhagic fever

Digestigve troubles: typhoid

| P a g e 35

Metazoa (multi-cellular organisms -worms)

Flat worms (Platyhelminthes):
Are bilaterally symmetrical and triploblastic (composed of three fundamental cell layers).
Flatworms have no body cavity other than the gut (and the smallest free-living forms may
even lack that!) and lack an anus.
The same pharyngeal opening both takes in food and expels waste. Because of the lack of any
other body cavity, in larger flatworms the gut is often very highly branched in order to
transport food to all parts of the body.
The lack of a cavity also constrains flatworms to be flat; they must respire by diffusion, and
no cell can be too far from the outside, making a flattened shape necessary.
2 main pathological spp:
Trematodes (flukes) - Fasciola, Fasciolopsis, Paragonimus, Clonorchis, Schistosoma.
Cestodes (tapeworms) - Diphyllobothrium, Hymenolepis, Taenia, Echinococcus.

Round worms (Nematodes)

are slender worms, The smallest nematodes are microscopic, while free-living species can
reach as much as 5 cm (2.0 in), and some parasitic species are larger still, reaching over a
meter in length. The body is often ornamented with ridges, rings, bristles, or other distinctive
structures.
The head of a nematode is relatively distinct. Whereas the rest of the body is bilaterally
symmetrical, the head is radially symmetrical, with sensory bristles ( (and, in many cases,
solid 'head-shields' radiating outwards around the mouth. The mouth has either three or six
lips, which often bear a series of teeth on their inner edges. An adhesive 'caudal gland' is often
found at the tip of the tail.
The oral cavity opens into a muscular, sucking pharynx. Digestive glands are found in this
region of the gut, producing enzymes that start to break down the food.
There is no stomach, with the pharynx connecting directly to a muscleless intestine that forms
the main length of the gut. This produces further enzymes, and also absorbs nutrients through
its single cell thick lining. The last portion of the intestine is lined by cuticle, forming
a rectum, which expels waste through the anus just below and in front of the tip of the tail.
Movement of food through the digestive system is the result of body movements of the worm.
The intestine has valves or sphincters at either end to help control the movement of food
through the body.

Round worms: Necator, Enterobius, Wuchereria, Ascaris, Ancylostoma, Toxocara, Trichuris,

Trichinella, Onchocerca, Dracunculus, Loa, Strongyloides.

The hosts are classified as:

- Intermediate - host in which larval ( ) stages develop.
- Definitive - host in which the adult parasite reaches sexual maturity.

Vectors are living transmitters (such as flies) of disease and may be:
- Mechanical, which transport the parasite but there is no development of the parasite
in the vector.
- Biologic, in which some stages of the life cycle occur inside the vector.

| P a g e 36

Platyhelminthes: Cestoda
Taenia solium (pork tapeworm)
Diseases: adult -taeniasis, larvae cysticercosis.
T.solium infection is less common than T.saginata, but is more important due to his
ability to cause more severe diseases in humans.
Epidemiology Basically its cosmopolitan but more common in Asia, South
America, East Europe. Destroyed at 56 C, resists 40 hrs at -10 C, 40 days at 4 C.
Morphology: Adult
Scolex ( Head)
body

Proglotis

Genital pore

(4 suckers; 20-

Contains ( a mature stage worm)

Young Immidietly following the scolex, they

Irregularly

50 hooks on a

a chain (strobili) of 800-1000

wider than longer.

placed on each

short pigmented

measuring more then 4-6m

Mature thet become longer than wider, containing

side

rostellum)

inside the uterus when gravid, each has 5-10

primary uterine branches with 30,000- 50,000
fertilized eggs (Gravid segment)
1.
2.
3.
4.
5.

The Gravid segment can break the strobili and reaching the stool and passively discharge.
Eggs are round/oval with a thick membrane.
Adult worm lives for 15-20 years.
Grows by adding new proglottids from its germinal center adjacent to scolex
The oldest proglottids (at the distal end) are gravid.

Life cycle: Remember Human can be IH or DH

1. Humans infected from raw/undercooked pork with cysticerci
cellulosae (larvae, pea-sized fluid-filled vesicle with
invaginated scolex); those attach to small intestine.
2. In ~ 3 months - adult worms (up to 5 m) that daily shed gravid
terminal proglottids (eggs) passed in stool & ingested by pigs
(IH).
3. In the pigs intestine egg - oncosphere (6-hooked embryo)
to blood vessels to muscle, develop into cysticerci.
4. Raw meat eaten by humans (IH or DH). Or: humans ingest
eggs from food/water, or fecal-anal, or from self
(autoinfection), those hatch into oncospheres in small intestine
to blood form cysticerci C. cellulosae 5-15 mm in
muscle, ~10x5 mm in parenchyma; C. racemosus branched,
no scolex, develop in brain (subarachnoid).
Pathogenesis: adult worm usually asymptomatic may cause anorexia
& diarrhea.
The larval stage Cysticerus cellulosae

Invaginated scolex in a vesicle full of liquid

Swallowing the infective eggs containing oncosphere
It hatches in the Pigs gut (accidentally in humans)
From the gut it become larvae and carried in the blood stream to the
striated muscles there it develop some cyst formations. ( may be also
locate at adipose tissue, eyes and CNS)
Easly visible in the naked eye.

| P a g e 37

Eggs Round or oval shape with a thick membrane, Embryonated eggs have 6 hooklets inside
oncosphera and infective when it discharged to the environment ( usually in the feces)
Cysticercosis is a parasitic tissue infection caused by larval cysts of the pork tapeworm. These larval
cysts infect brain, muscle, or other tissue, and are a major cause of adult onset seizures in most lowincome countries. An individual acquires cysticercosis from ingesting eggs excreted by a person who
has an intestinal tapeworm. People living in the same household with a tapeworm carrier have a much
higher risk of getting cysticercosis than others.
Cysticercosis is not acquired by eating undercooked pork -- rather, it is the tapeworminfection that is
acquired by eating undercooked pork containing the larval cysts. Pigs become infected by ingesting
tapeworm eggs in the feces of the human tapeworm carrier
C.racemosus

C.cellulosae

Branched, no scolex!

Spherical / ovoid shape vesicle

Anarchic development ,

Inward collagen fibers , microvillisities

under-arachnidan space development or inside

3 muscle layers

the ventricles.

Scolex 4 suckers, rostellum and hooklets

His liquid content is immunogenic, allergenic

Cysticercosis - Pathogenesis:

Brain (60-90% cases) form space-occupying lesions headache, vomiting, seizures;

pyramidal signs; mental disturbances;

Eyes (2-7% cases) painful, may cause papillary, lid & corneal edema, uveitis, conjunctivitis;
exophthalmia blindness.

Muscle myalgia, calcification, dead cysticerci can cause inflammatory response.

Adipose tissue painless subcutaneous nodules on thorax, legs & arms that become painful
from inflammatory reaction after the larvae die.

Diagnosis: proglottids in stool (rarely identified); eggs (Ziehl Neelsen dark blue); cysts in tissues,
usually seen on CT (up to 10 years after; peripheral contrast cerebral edema). Cysticercosis can be
diagnosed by immunological assays (e.g. ELISA and WB) of serum, CSF, aqueous humor.
Transient eosinophilia of 10-20% (cysts during migration).
Differential Diagnosis: other intestinal parasites, allergy, T. saginata; alimentary debris.

| P a g e 38

Taenia saginata (beef tapeworm)

Taenia saginata, also known as the beef tapeworm, is part of the order Cyclophyllidea and is
a parasite of both cattle and humans, causing taeniasis in humans. Taenia saginataoccurs
where cattle are raised by infected humans maintaining poor hygiene, human feces are improperly
disposed of, meat inspection programs are poor, and where meat is eaten without proper cooking.
Distribution & resistance similar to T.solium.

Scolex ( Head)

body

Proglotis

Genital pore

4 suckers, NO

Contains ( a mature stage worm)

Young Immidietly following the scolex, they

Irregularly

hooks - will fix

a chain (strobilia) of 1000-2000

wider than longer.

placed on each

on the upper 1/3

proglottis (usually 800-1000)

Mature they become longer than wider,

side

of the intestinal

measuring more then 4-6m

containing inside the uterus when gravid, each has

mucosa

15-25 primary uterine branches

Life cycle:
1.

2.

3.

4.

Humans infected from raw/undercooked

beef with cysticerci that attach to small
intestine.
In ~ 3 months adult worms (up to 10 m)
that shed gravid terminal proglottids passed
in stool & ingested by cattle (IH).
In the cattle: the egg oncospheres to
blood vessels migrate to muscle, develop
into cysticerci eaten by humans (DH).
Cysticerci will fix on the upper 1/3 of the
intestinal mucosa of the small intestine.

Pathogenesis: worm causes little damage; may cause

GI disturbances; neural signs (impaired attention,
insomnia, seizures); malaise; appetite disturbances;
pruritus. Proglottids may appear in stools & protrude from anus. Migration of mature proglottids may
cause appendicitis. Cysticercosis is extremely rare in humans (may occur in muscle).

Diagnosis: gravid proglottids (usually on clothes, rarely in stool); eggs are very rare in stools. Eggs of
T. saginata, T. solium & Echinococcus look alike. We can differentiate them by staining the eggs Egg
with Ziehl Neelsen : T. saginata RED, T. solium BLUE. Scotch (Graham) test from perianal
region.

| P a g e 39

Hymenolepis nana (dwarf tapeworm)

Disease: Hymenolepidosis
Hymenolepis infection or infection with the dwarf tapeworm is found worldwide. It is most often seen in children
in countries in which sanitation and hygiene are inadequate. Although the dwarf tapeworm infection rarely causes
symptoms, it can be misdiagnosed for pinworm infection.

Scolex ( Head)

Proglotis

Genital pore

Subglobular

About 100-200 proglottids

Marginal and

Well-developed

The ones that placed immiditly under the neck are

placed near

retractable rostellum

shorter than the distal proglottis

the anterior

Single crown with 20-

Wider than longer

border.

30 hooklets

The gravid proglottides are broader than longer

4 globular suckers

The adult can reach 3-5 cm in length

Maturate 4 weeks post infection

The larvae- Cysticercoid is located inside the intestinal villus (about 7 days)
The eggs

oval and globular

One cover contain 2 membranes:

o

The inner shell - 2 poles with 4-8 fillaments

External layer smooth

Oncosphere inside- Hexacanth embryo 6 hooklets

The egg is the infective stage

H.nana egg

Life cycle:
1.

2.
3.

4.

Within 4 weeks in duodenum eggs

cysticercoids larvae adult worm.
Gravid proglottids (80-200 eggs in
each segment) detach & release
fertilized eggs that pass into stool or
reinfect the host (autoinfection);
100s of H. nana worms can be found
in a host.
Eggs directly infectious (can develop
into adult worms in a human without
an intermediate host, unlike other
tapeworms).
Transmitted by direct contact or fecaloral route.

Pathogenesis: asymptomatic (few parasites) or symptomatic mostly often in children that have high
number of parasites causing vomiting, anorexia, diarroea followed by Malabsorption, abdominal
discomfort and allergic reactions.
in immunocompromised opportunistic infection importand diarrhea, Malabsorption,
malnourishment and sometimes the larvae can migrate via blood circulation to some other organs.
Diagnosis: eggs in stool, Clinical story + eosinophilia.

| P a g e 41

Diphyllobothrium latum (fish tapeworm)

Disease: Diphyllobotheriasis

It is the largest tapeworm reach up to 10-12m

Locate in the small intestine
Can live for 29 years and rarely may discharged spontaneously

Scolex ( Head)

Proglotis

Genital pore

3mm in diameter

About 3,000-4,000 segments

The genital pore (tochostoma) in the

2 slits longitudinal

Broader than longer

middle a continuous discharged

grooves

og the eggs (about 36,000 1

No rostellum no

million /day)

suckers

Larvae Plerocercoid, encysted in the fishs viscera or muscle, after swallowing the larvae,
it develops into adult stage within 4-5 weeks. It resistant for kippering or ordinary smoking
Eggs Operculated (having an operculum Arrow in the picture*) with a brown shell, having a
pointed carena/knob on the opposite pole. No embryo inside not infective! Need water for
development
Life cycle:

D.latums Egg

1.

Humans (definitive host) infected from raw/undercooked fish with larvae

(plerocercoids).
2. Those attach to gut wall & develop into adult
worms in 4-5 weeks.
3. Gravid proglottids release into stools fertilized
eggs (up to 1 million/day) that are not infective
& must be deposited in fresh water for
continuation of the cycle.
4. Eggs turn in the water into embryos eaten by
Copepod Crustacea (1st IH), in which the
embryos procercoid larvae (not infective).
5. Copepod is eaten by fish (2nd IH), in which the
larvae plerocercoids, Located in small
intestine, usually several worms at the same
time; lives for ~ 29 years.
Pathogenesis: may be asymptomatic. When it is
symptomatic- may cause digestive complaints
epigastric or generalized abdominal pain, nausea, vomiting loose of appetite constipation and diarrhea.
Some general signs also : asthma and lose of weight and allergic signs. neuro-psychiatric signs (loss of
attention, insomnia, paresthesia);
Complications influence the uptakes vit. B12 and thus may cause deficiency with megaloblastic
anemia (more common in tall & slim with yellow hair & blue eyes :S );
Diagnosis: Direct coprology - eggs (different from those of other tapeworms) in stool + macrocytic
anemia, eosinophilia, leucopenia.

| P a g e 41

Echinococcus granulosus (dog tapeworm)

E. granulosus, also called the Hydatid worm or Dog Tapeworm, is a cyclophyllid cestode that
parasitizes the small intestine of canids ( (as an adult, but which has important intermediate
hosts such as humans, where it causes cystic echinococcosis, also known as hydatid disease. The
adult tapeworm ranges in length from 3 mm to 5.8 mm and has 3-8 proglottids.
Scolex ( Head)

Proglotis

Genital pore

Piriform scolex,

3-5 proglottides, the distal one

The genital pore located at

having a projected

is larger. A mature gravid

alternative sides

rostellum armed with

proglotis contain up to 5000

2 raws of hooks.

eggs

4 suckers

Egg

Present in the dogs faeces,

2 shells, the inner one is thicker
The oncosphere inside contain 3 pairs of hooklets
Infective when it is discharged

Larvae The oncosphera (An embryonic form of a tapeworm ) develops a hydatic cyst:
Ectocyst fibrous layer produced by the host
Endocyst
Internal germinal layer producing broad capsule, liquid and protoscolices.
The broad capsule evaginates to form a protective cup for the growing scrolex
-Hydatic sand = scolices and daughter cyst
-Sterile Immunogenic liquid inside
External layer cover the inner one

Lifecycle:
1.

In a dog (DH) worms release eggs which

ingested by cattle or humans (IH)

2.

The oncosphere embryos develop in the

small intestine & migrate mostly to liver,
also to lungs, bones & brain and develop
cysts.

3.

Dogs infected by ingesting cysts from

sheep, buffalos or camels (each of those
carries a different strain).

| P a g e 42

Pathogenesis: cyst fluid contains antigens that can cause anaphylaxis if its ruptured(secondary
hydatidosis). Swallowing infective eggs causes primary hydratidosis; hematogenic spread of
protoscolices when a cyst breaks secondary. Cyst grows ~ 1 cm/year; infection is often asymptomatic
for years. 40-50% are diagnosed accidentally (seeing cysts by imaging), others after complications.
General symptoms: 50% of the paitens: asthenia, sweating, rigor, subfebrile temperature. Other
symptoms depend on location.

Organ Signs
Liver

Lungs:

Brain

Bones

Other

60% in right lobe, slow

in 20% cases; rapid

1-2% cases; more

2% cases; mostly in long

Spleen: 8% of

progression; can cause

progression; may cause

in children.

bones. External layer

cases

cholestasis with jaundice,

cough, dyspnoea and pain

Headache, nausea,

(ectocyst) not formed due to

(splenomegaly);

portal hypertension; liver

in thorax; as the cyst

movement/sensory

the limitations of the bone.

kidney 3%

abscess

grows lung abcess;

disturbances

Painless, causes tumor-like

(hematuria);

broken cyst hemoptysis

lesions with bone fractures.

thyroid.

& vomica with cysts

Bad prognosis, cysts in bones

content

dont respond to medication

and are difficult to remove
surgically. May require
lifetime treatment by
antiparasitic medications

Diagnosis: by clinical signs, imaging (MRI, X-ray); protoscolices in secretions; immunological tests
(ELISA, Western Blot, PCR); circumstantial eosinophilia. Cyst puncture forbidden -not to cause
anaphylaxis. Surgical removal indicated for large cysts, single superficial cysts. Alternative: PAIR
(puncture, aspiration, injection of alcohol, re-aspiration). Skin test Cassoni.

Echinococcus multilocularis (alveolar echinococcosis): similar to E. granulosus, but fox is the

definitive host. Humans infected by contact with food contaminated by fox feces (hunters); in the liver
larvae form multiloculated cysts with few protoscoleces. No outer fibrous capsule, so a cyst produces
hundreds of daughter cysts on its external layer. Manifested by jaundice & weight loss. 97-100%
produces antibodies.

Polycystic echinoccoccosis: caused by E. vogeli (definitive host bush dog, intermediate paca
(wild rabbit)) & E. oligarthrus (definitive felines, intermediate agouti). Daughter cysts grow inside
& outside of the cyst membrane, usually in the liver.

| P a g e 43

Trematoda- Flukes
Adult flukes are leaf-shaped flatworms. Prominent oral and ventral
suckers help maintain position in situ. Flukes are hermaphroditic
except for blood flukes, which are bisexual. They are
internal parasites of molluscs and vertebrates. Most trematodes have
a complex life cycle with at least two hosts. The primary host,
where the flukes sexually reproduce, is a vertebrate. The
intermediate host, which is the agent of dispersal, is usually a snail.

Fasciola hepatica (sheep liver fluke)

Fasciola hepatica, also known as the sheep liver fluke, is a parasitic flatworm of the
class Trematoda, phylum Platyhelminthes that infects the livers of various mammals, including
humans. The disease caused by the fluke is called fascioliasis (also known
as fasciolosis). F. hepatica is distributed worldwide, and causes great
economic losses in sheep and cattle. It has been known as an important
parasite of sheep and cattle for hundreds of years. Because of its size and
economic importance, it has been the subject of many scientific
investigations and may be the best known of any trematode species.
Hyperendemic regions in Peru, Bolivia, Egypt, Iran, Chile, Cuba
Morphology: Adult - 3X1.5cm brownish in color (one of the largest fluke
in the world), Leaf shaped .
Eggs large, ovoid and Unembrionated = non infective and need water for development.
Transmission: mainly by digestion by ingestion of cercaria (in water) or metacercarie in vegetables
(watercress)
Lifecycle:
1. Metacercariae (larvae) excyst in
duodenum of cattle (esp. sheep)
or humans (DH), penetrate gut
wall & migrate to liver, where
they mature into (hermaphroditic)
adults that occupy bile ducts &
produce eggs excreted in stool.
2. Eggs are not infective, need fresh
water to hatch into miracidia.
3. Miracidia than penetrate snails
(IH), and develops into cercariae.
4. Cercariae released back into the
water & encyst into
5. Metacercariae on water plants.
Infection can be transmitted by
metacercariae from water plants
or cercariae from water.
Pathogenesis: due to biliary tract obstruction, often asymptomatic. We may divide the pathogenesis of
the disease into 3 stages:
Abdominal stage pain, rarely diarrhea, nausea; sometime this stage is not recognizable.
Migratory stage fever, urticaria, eosinophilia, right hypochondrial pain, nausea;
liver stage eosinophilia, hepatomegaly. After months or years can cause obstructive jaundice. Adult
flukes (from raw sheep liver) cause halzoun painful pharyngitis.
Diagnosis: eggs in stool or in biliary fluid; advice not to eat sheep or cattle liver a few days before
stool examination to avoid false positives. Stool examination would be negative during migratory
stage, when diagnosis can be made by serology (immunological testing).

| P a g e 44

For the best accuracy do US (moving larvae in the bile) +CT+signs and symptoms + lab results
(elevated liver function, high ESR, anemia, leukocytosis and eosinophilia)

Paragonimus species (lung fluke)

Paragonimus is a lung fluke (flatworm) that infects the lungs of humans after eating an infected raw or
undercooked crab or crayfish. Less frequent, but more serious cases of paragonimiasis occur when the
parasite travels to the central nervous system.
Geographical distribution: P.westermanii - Far east, South East Asia ( Korea, China, Philippines,
Laos) South and Central America. P.africanus Parts of west Africa (Cameroon, Nigeria)
P.americanus Parts of central America (Peru, Ecuador, Mexico)
Morphology:
Adults - small in size not more than 1.5 cm (hermaphrodites) have ventral & oral suckers;
live for 10-20 yrs. Their main location is in the lung cavities.
Eggs - are operculated, non-infective & need water for hatching. Unembryonated= non
infective
Transmission Humans gets
accidently infected by eating raw fresh
water crustaceans (crabs, crayfish)
Metacercaria .
Lifecycle:
1.

2.

3.

4.

Humans infected from

raw/undercooked crabs with
metacercariae (encysted
larvae)
excyst in small intestine,
penetrate the well & migrate
thru the diaphragm into lung
parenchyma,
There they differentiate into
hermaphroditic adults that
release eggs, which are
coughed or swallowed.
Eggs are not infective, need fresh water to hatch into miracidia and enter to the snails (1st IH),
differentiate into sporocyst radiae (larvae) then into free-swimming cercariae that infect
crabs (2nd IH). Have animal reservoir (e.g. domestic animals).

Pathogenesis: from ectopic migration of adults; granuloma formation from eggs.

Digestive stage hours to days post-infection: abdominal pain, cramps, nausea, vomiting diarrhea.
Migration stage: fever, skin allergy, subcutaneous nodules from migrating flukes (eosinophilia) .
Lung stage: dyspnea, chest pain, hemoptysis, fever, night sweats; without ant TB signs and symptoms.
Ectopic migration: pain; peritoneal irritation; diarrhea; tender lymphadenopathy; may migrate to eyes
( blindness), testis ( inflammation) or brain (common in Korean flukes seizures).
Diagnosis: eggs in sputum and/or stool or abscess fluid; eosinophilia; chest X-ray (radiological aspect
of Olympic rings) . Differential diagnosis from TB, hydratid cysts, lung cancer.

| P a g e 45

Schistosoma (blood flukes) S.haematobium, S.mansoni, S.japonicum,

S.intercalatum, S.mecongi
A genus of trematodes, Schistosoma, commonly known as blood-flukes, are parasitic flatworms which
are responsible for a highly significant group of infections in humans termed schistosomiasis.
Schistosomiasis is considered by the World Health Organization as the second most socioeconomically
devastating parasitic disease, (after malaria), with hundreds of millions infected worldwide.
Adult flatworms parasitize mesenteric blood vessels. They are unique among trematodes and any other
flatworms in that they are dioecious with distinct sexual dimorphism between male and female.

Geographical distribution & disease

S.haematobium

S.mansoni

S.mecongi

S.intercalatum

S.japonicum

Urinary

Intestinal

Intestinal

Lower Bowel

Bowel and liver schistomiasis

schistomiasis

schistomiasis

schistomiasis

schistomiasis

Africa, Parts of

Africa, Madagascar,

East border of

West africa

Arabia

South America,

Thailand

China, Japan, Philippines

Caribbean, Arabia

Morphology: 1-2 cm, separate sexes (unlike other trematodes); Female is

protected in the males schist (gynecophoric groove), the male
continuously fertilizes the females eggs. The female is slender and longer
than male.
The male has 1/3 anterior part round and 2 suckers (ventral and anterior.
The female has 2 suckers placed inside the gynicoporic cancal
Eggs: all of them are oval in shape, thin and transparent shell with motile miracidium inside but not
infective.
S. mansoni
eminent lateral spine- in

S.japonicum
flat lateral spine in feces

feces

S.haematobium
terminal spine in urine or
feces

Cercariae the infective stage: 200um long, separated sexes with forked (bifid) tail, derived from
snails this larvae will die if he will not find a DH in 48 hours.
Transmission Active penetration of the bifid cercariae
through the skin immersed into the fresh water.

| P a g e 46

Lifecycle:
1.

Humans infected by freeswimming cercariae that

actively penetrate the skin &
differentiate to schistosomula
(larvae).

2.

Carried by veins into arterial

circulation. Larvae that reach
superior mesenteric arteries
pass by portal circulation into
the liver.

3.

There they turn into adult

flukes.

4.

The female lay fertilized eggs that penetrate the vascular endothelium & enter the intestinal or
bladder lumen.

5.

Eggs than eliminated by urine or stool and must enter fresh water for hatching into ciliated
larvae (miracidia).

6.

Than - penetrate snails, in which they produce cercariae released into fresh water; cercariae
die in 48 h if they dont encounter a definitive host (human)
REMEBER cercaria & miracidia in water; schistosomula, schistosomes & eggs in humans;
sporocysts in snails. Only S. japonicum, found only in Asia, has significant animal reservoirs
(cattle, pigs).

Clinical Picture:

Skin penetration :
- Local reaction caused by schistomulums presence called swimmers itch or
fishman itch - popular rash, pruritus, urticaria can be for several hours or days
piquina a Puerto rico. Very common in immune compromised patients and very
rare in people that lives in endemic areas even children are immunized transplacental.
Invasion phase lasts for 2-4 month obvious in S.mansoni and S.japonicum infection and less
in S. haematobium:
- Allergic and toxic phenomena: fever, urticaria, hypereosinophilia, cough and
wheezing, hepatomegaly, splenomegaly
- Katayma fever common in S.japonicum (usually the fever appears 1-2 month after
the exposure to the infected water) .
Chronic phase due to the eggs retention (eggs stay in the tissue)
- Granuloma formation- epithelia giant cells, lymphocytes and eosinophils arranged in
concentric layers surrounding the eggs.

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The cellular content diminishes and replaced by fibrosis and collagen fibers and
leaving a small scar that lasts for 2-3 months.

Pathogenesis:
The organ signs depend on the Schistosoma species: In light infections the clinical signs appear 4 to 25
years post infection while in heavy infections it will be much sooner 18 months. Thats why the
pathology is due to eggs retention and the intensity and time for the clinical signs is due to the time
exposure.
S. haematobium: The ova are initially deposited in the muscularis propria which leads to ulceration of
the overlaying tissue. Infections are characterized by pronounced acute inflammation, squamous
metaplasia, blood and reactive epithelial changes. Granulomas and multinucleated giant cells may be
seen. Early painless hematuria & bladder polyps; later urinary tract obstruction, thickening/rigidity
of bladder wall, kidney stones, reversible nephrotic syndrome due to deposition of immune complexes;
granulomas & fibrosis that may lead to bladder carcinoma. Also co-infection with Salmonella typhi.

S.mansoni : liver and intestinal schistosomiasis - In intestinal schistosomiasis, eggs become lodged in
the intestinal wall and cause an immune system reaction called a granulomatous reaction. This immune
response can lead to obstruction of the colon and blood loss. The infected individual may have what
appears to be a potbelly. Eggs can also become lodged in the liver, causing Symmer's fibrosis leading
to high blood pressure through the liver, enlarged liver and spleen, the buildup of fluid in the
abdomen, and potentially life-threatening dilations or swollen areas in the esophagus or
gastrointestinal tract that can tear and bleed profusely (esophageal varices). Rarely, the central
nervous system is affected. Individuals with chronic active schistosomiasis may not complain of typical
symptoms.
S.japonicum Early aspects Katayama fever is very well clinicaly expressed, and the late aspect of
the disease is very close to S.mansoni infection.
-

-small bowel ulcers (at the sup.mesenteric vein territory )

Bloody and mucus diarrhea
liver granuloma

Extra info about S.japonicum for better understanding

Once the parasite has entered the body and begun to produce eggs, it uses the hosts' immune system
(granulomas) for transportation of eggs into the gut. The eggs stimulate formation of granuloma around
them. The granulomas, consisting of motile cells, carry the eggs to the intestinal lumen. When in the
lumen, granuloma cells disperse leaving the eggs to be excreted within feces. Unfortunately, about twothirds of eggs are not excreted, instead they build up in the gut. Chronic infection can lead to
characteristic Symmer's fibrosis . S. japonicum is the most pathogenic of the schistosoma species
because it produces up to 3,000 eggs per day, ten times greater than that of S. mansoni..
As a chronic disease, S. japonicum can lead to Katayama fever, liver fibrosis, liver cirrhosis, liver
portal hypertension, splenomegaly, and ascites. Some eggs may pass the liver and enter lungs, nervous
system and other organs where they can adversely affect the health infected individual.
Genital schistosomiasis: hematospermia, hydrocele.

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Diagnosis: colonoscopy (not relevant in field conditions); eggs in feces (all species) or urine (only
S.hematobium); biopsy of rectal, bladder or liver tissue;
-

serology ELISA, hemagglutination or IFAT;

pathology: adult parasites in portal system or eggs in tissues;

imaging (ultrasound or radiography).

Differential diagnosis with tropical fever/diarrhea; bladder pathology; cirrhosis;

swimmers itch can be caused by cercariae of non-human schistosomes.

Nematodes
Are roundworms with cylindrical body covered by a cuticle () .
Have a complete digestive tract, mouth & anus. Most females are larger than
males; and males have a coiled tail. 2 categories: intestinal & tissue.
Nematodes during their migrating phase thru the tissues cause significant
eosinophilia.

Intestinal:
-

Enterobius, Tricuris, Ascaris are transmitted by eggs.

Hookworms - Necator, Ancylostoma, small roundworm

Strongyloides & Trichinella by larvae.

Larvae have 2 forms: rhabditiform (1st & 2nd stage) are

non-infectious feeding forms and filariform (3rd stage) are
infectious, non-feeding. Adults live only in humans,
except Strongyloides that can also live in soil.

Tissue (filariasis): Wuchereria, Onchocerca, Loa produce microfilariae motile embryos that
circulate in blood & tissue fluids.
-

Have a vector: mosquitoes or flies. Dracunculus larvae live in copepods and are
transmitted in drinking water.

Larva migrans: cannot maturate to adults in humans, but their migrating larvae can cause
disease visceral (Toxocara) or cutaneous (Ancylostoma). VLM visceral larva migrans,
OLM ocular larva migrans, CLM cutaneous larva migrans.

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Ascaris Lumbricoides
Ascaris lumbricoides is the giant roundworm of humans, belonging to the phylum Nematoda. An ascarid
nematode, it is responsible for the disease ascariasis in humans, and it is the largest and most
common parasitic worm in humans. One-sixth of the human population is estimated to be infected by
Ascaris lumbricoides or another roundworm. Ascariasis is prevalent worldwide and more so in tropical
and subtropical countries. It can reach a length of up to 35 cm.
Geographical distribution: Cosmopolitan very often found on moist wormed climate, mainly in rural areas
and in children .

Morphology - adult:

Largest intestinal nematodes ~ 25 cm or more.

Life span 1-2 years.
Female is longer than male and lye 200K to 250K eggs daily.
The head has 3 ant lips carrying some teeth on their margins.
Thick and smooth cuticle covers the strong somatic muscle layer.

F
M

Morphology - Eggs
Fertilized

Non-fertilized

Ovoid unembryonated, 2 shells: internal one thin

vitelin membrane covered by a thicker one translucent
surrounded by irregular albuminous coat. Need soil
development for 3-4 weeks

Non homogenous content and irregular external coat

The eggs are very resistant to the environmental stress

They can survive in moist soil for 3-5 years
They resistant to cold heat aand antiseptic

Transmission Ingestion of embryonated eggs

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Lifecycle:
1.

Humans infected

by eggs

that

contaminate soil
2.

The eggs hatch in small intestine,

larvae migrate thru gut wall
bloodstream lungs alveoli
bronchi

trachea; swallowed

larvae become adults.

3.

They do not attach to the wall, feed

on ingested food. Lay 200-250K
eggs/day;

4.

The eggs are excreted in stool and

need to be embryonate in warm & moist soil for 3-4 weeks, are very resistant & can survive in
soil for 3-5 years.

Pathogenesis:
damage mostly from larval migration (Loefflers syndrome) or ectopic worms. Low parasitic burden
usually asymptomatic, heavy may lead to malnutrition, intestinal obstruction, cholangitis, liver abscess
or granuloma, appendicitis, peritonitis.
Adult phase: Abdominal pain, nausea, vomiting, diarrhea may be spontaneous discharge of the adult
worm, allergic reactions and loose of apetite.
Complications: Intestinal obstruction (in heavy infections), ectopic migrations appendix, biliary tree,
pancreatic duct. Liver granuloma- female release their eggs in the liver.
Loefflers: fever, cutaneous/respiratory allergic reaction, cough, bronchospasm.
Diagnosis: eggs (oval with irregular surface) in stool. 1-2 years post-infection adult worms
spontaneously expelled in stool. Sometimes larvae can be identified in gastric secretions or sputum.
Also imaging methods X-ray , Endoscope examination .

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Toxocara T.canis T.cati

Disease: Toxocariasis, Visceral larva migrans VLM, Ocular larva migrans OLM

Toxocariasis is an illness of humans caused by a larvae (immature worms) of either the

dog roundworm(Toxocara canis), the cat roundworm (Toxocara cati) or the fox (Toxocara canis).
Toxocariasis is often called visceral larva migrans (VLM). Depending on geographic location, degree
of eosinophilia, eye and/or pulmonary signs the terms ocular larva migrans (OLM), Weingarten's
disease, Frimodt-Moller's syndrome, and eosiniphilic pseudoleukemia are applied to Toxocariasis.
Other terms sometimes or rarely used include nematode ophthalmitis, toxocaral
disease, toxocarose, and covert toxocariasis.
Geographic Distribution: Cosmopolitan mainly in areas with lots of dogs and cats
feces
Morphology: adults worms is similar to Ascaris; larvae smaller in size than Ascaris
can disappear in tissue, where they become encapsulated & die.
Eggs similar to Ascaris in size but has a pitted surface, Unembryonated and
unfertilized. Need soil for development and NEVER FOUND IN HUMAN FECES!
Toxocaras egg
Lifecycle: is not complete in humans
1. Dogs (definitive host) hosting adult worms that produce eggs that pass in stool.
2. the eggs need soil for hatching.
3. Humans infected by ingestion of
fertilized eggs that hatch to larvae in
the small intestine. Transmitted
congenitally to puppies.
Pathogenesis: larvae migrate to organs,
mainly to the liver, brain & eyes, forming
granulomas (delayed hypersensitivity reaction
to larval proteins). Children are at higher risk
of infection.
Manifestations: heavy VLM infection
mostly in children till 5 yr. pruritus,
abdominal pain, nausea, pruritus
hepatosplenomegaly, fever, cough with
dyspnea; may penetrate the heart
(myocarditis) or brain (seizures). Latent
toxocariasis lymphadenopathy, asthenia,
myalgia, pruritus, prolonged fever. May be
asymptomatic with marked eosinophilia.
Migration to eyes (OLM) can cause
endophtalmitis blindness, usually in
children over 5 years or adults.

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Risk factors for VLM and OLM

Diagnosis:

Host associated risks

Clinical signs and symptoms.

Environmental risks

Viceral larva migrans

Visualizing larvae in tissues;

-globulins & eosinophilia,

Children

Low socio-economic status

Other inflammation markers;

Black race >white

Rural residence

Serology (e.g. ELISA, but larval antigens are

Pica/Geographic

Contact with puppies at home

not standardized); larvae in tissue biopsy.

location

Contact with contaminated soil

Cant be found in stool.

Consumption of raw liver

Lab tests: WBS,RBC, Liver enzymes,

GGT(Gamma-glutamyl transpeptidase),ECP
(Eosinophilic cationic protein)
Imagery: X-ray, US, CT

Children

Contact with puppies at home

Pica/Geographic

Contact with contaminated soil

Pica disorder -

location

Ocular larva migrans

http://en.wikipedia.org/wiki/Pica_(disor
der)
VLM certain diagnoisis 1. Liver biopsy central zone abscess with PMNs and Ne in old infections and
Eo/Charcot-Leiyden crystals in recent. Necrotic area surrounding and peripheral
granuloma, giant cells.
2. Immunological diagnosis precipitation reactions, agglutination reactions, skin tests,
IFAT test, CFT complement fixation test.

Trichuris (whipworm)
An estimated 604-795 million people in the world are infected with whipworm. Whipworm,
hookworm, and Ascaris are known as soil-transmitted helminths (parasitic worms). Together, they
account for a major burden of disease worldwide.
Whipworms live in the large intestine and whipworm eggs are passed in the feces of infected persons.
If the infected person defecates outside (near bushes, in a garden, or field) or if human feces as used as
fertilizer, eggs are deposited on soil. They can then mature into a form that is infective. Whipworm
infection is caused by ingesting eggs. This can happen when hands or fingers that have contaminated
dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully
cooked, washed or peeled.
People infected with whipworm can suffer light or heavy infections. People with light infections
usually have no symptoms. People with heavy symptoms can experience frequent, painful passage of
stool that contains a mixture of mucus, water, and blood. Rectal prolapse can also occur. Children with
heavy infections can become severely anemic and growth-retarded.

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Geographical distribution cosmopolitan but more common in South East

Asia.
Morphology:
Adult - 35-50 mm, anterior part thin & elongated, posterior fleshy &
bulbous. The adult is usually found in cecum and the large bowel. The
female is longer than the male
Eggs are brownish & transparent; non embyonated non-infective, need soil
for hatching (~3 weeks).

Lifecycle: lasts for 3 months

1.

Humans infected by ingesting fertilized eggs from soil.

2.

The eggs hatch in small intestine larvae penetrate the

gut mucosa for a week immature adults, then migrate to
the colon where it matures & produce daily 1000s of eggs
released in stool.

3.

Eggs embryonate in soil.

Pathogenesis: most are asymptomatic; may cause dysenteric

syndrome diarrhea (bloody and mucus) & nausea vomiting; rarely
Complications: rectal prolapse, anemia, appendicitis.Death in
malnourished patients.
Diagnosis: eggs (barrel-shaped, with a plug at each end) in stool.
Circumstantial diagnosis: Anemia,Hypereosinophilia, Chronic abdominal pain .
Endoscopical diagnosis.

Enterobius (pinworm)
Pinworm infection is caused by a small, thin, white roundworm
called Enterobius vermiculari causing Enterobiasis. Although pinworom
infection can affect all people, it most commonly occurs among children,
institutionalized persons, and household members of persons with
pinworm infection. Pinworm infection is treatable with over -the-counter
or prescription medication, but reinfection, which occurs easily, should be
prevented.
Geographical distribution mainly in temperate regions than tropical
ones, mainly in children populations.
MorphologyAdult: round, yellowish, with muscular esophagus. Female is longer than
male .
Eggs Double transparent shell, embryonated, infective infective larvae
are already developed.

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Transmission: Humans are the source of infection transmission by digestive:

-ingestion of own infective eggs
- retro-infection (skin penetration of larvae hatching from the eggs at the anal region)
-hetero-infection.

Lifecycle: only in humans;

1.

Humans are infected by eggs ingestion

(hetero-infection) that hatches in small
intestine.

2.

The adults than migrate to colon & mates.

3.

At night the female migrate to the perianal

region and release 1000s of eggs on
perianal skin.

4.

Eggs are infective (larvae develop in 5-6

hrs after laying) can cause retroinfection (larvae return) or autoinfection
(ingestion of eggs after scratching the
area).

Pathogenesis: manifested mostly by perianal pruritus (predisposes to secondary infections).

Asymptomatic with less than 10 parasites; may cause abdominal pain, insomnia, Cutaneous larva
migrans CLM, vaginitis or urethritis.
Complications: appendicitis, peritonitis, migration to urinary tract.
Diagnosis: macroscopically adult worms in stool; eggs in stool in only 15% cases; Graham (scotch)
test from perianal area.

Trichinella (8 species known, all pathogenic)

T.spiralis is by far the most common known as pathogenic and

spread in humans. Distribution is cosmopolitan.

Morphology: species divided into encapsulated & non-encapsulated.

But we need to focus only on T.spiralis:
Adult round worm male is a bit smaller than female. After mating, the female give birth to new
larvae! NO EGGS!!
Hosts are animals, especially pigs, rats, bears. Larvae die if frozen

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Transsmition by consumption of row or improperly cooked meat of the definitive hosts: Pigs (most
common), wild bear, horse, fox etc
The severity of the disease is depends on: The quantity of infective larvae that has ingested. Trichnella
species, the immune status of the host.

Lifecycle:
1. Trichinellosis is acquired by ingesting meat

2.

3.

4.

5.
6.

containing cysts (encysted

larvae) of Trichinella.
After exposure to gastric acid and pepsin,
the larvae are released from the cysts and
invade the small bowel mucosa where they
develop into adult worms ( life span in the
small bowel: 4 weeks).
After 1 week, the females release
larvae that migrate to the striated muscles
where they encyst. (Trichinella
pseudospiralis, however, does not encyst).
Encystment is completed in 4 to 5 weeks
and the encysted larvae may remain viable
for several years.
Ingestion of the encysted larvae perpetuates
the cycle.
Rats and rodents are primarily responsible
for maintaining the endemicity of this
infection. Carnivorous/omnivorous
animals, such as pigs or bears, feed on infected rodents or meat from other animals.

Pathogenesis: after incubation period (may last 2-50 days, depending on former infection &
immune status of the host; its length is predictive of the severity) .
Enternal (digestive phase):

2-4 days following the ingestion of the infected meat

Abdominal cramps, diarrhoa (10-15 stools/day)
Fever,lossof apetite, vomiting
Self limiting after migration phase start.
Can last ~ 30 days or more.
Influenced by corticosteroids administration

Acute phase:
-

Can co-exist with the enteric phase

NBL (new born larvae) migrate via lymphatic vessels and invading the muscle cells.
Sudden onset of general weakness, chills, headache, fever and sweating, tachycardia.
Symmetrical eyelid and periorbital edema .
Coetaneous allergy pruritus rash
Muscle pain and restrict motility
Hemorrhage of the nail beds
Conjunctival chemosis ( seen in the picture)

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Can co-exist with digestive. Ocular involvement also possible. Migration stage may be
accompanied by Loeffler syndrome (dyspnea, wheezing, cough).
Loeffler's syndrome is a disease in which eosinophils accumulate in the lung in response to
a parasitic infection.

Diagnosis: larvae in muscle biopsy; serology positive 3 weeks post-infection; circumstantial

eosinophilia, imbalance of muscle enzymes, electrolytes & proteins.

Hookworms
The parasite: Amcylostoma duodenale, Necator americanus.
An estimated 576-740 million people in the world are infected with hookworm. Hookworm was once
widespread in the United States, particularly in the southeastern region, but improvements in living
conditions have greatly reduced hookworm infections. Hookworm,Ascaris, and whipworm are known
as soil-transmitted helminths (parasitic worms). Together, they account for a major burden of disease
worldwide.
Hookworms live in the small intestine. Hookworm eggs are passed in the feces of an infected person. If
the infected person defecates outside (near bushes, in a garden, or field) of if the feces of an infected
person are used as fertilizer, eggs are deposited on soil. They can then mature and hatch, releasing
larvae (immature worms). The larvae mature into a form that can penetrate the skin of humans.
Hookworm infection is mainly acquired by walking barefoot on contaminated soil. One kind of
hookworm can also be transmitted through the ingestion of larvae.

Morphology - Adult:
- Inhabit the small intestine of humans.
- Slender, cylindrical, about 1 cm long.
- Mouth and esophagus are fixed in the anterior part to the intestinal mucosa
by suction.
- -life span several years.
Eggs:
- Ovoid, thin, transparent shell allowing to the mature larvae to escape.
- 4-8 cell stage when discharge
- Fertilized but not infective
Larvae
- 1st stage- hatch out of the egg during the first 24-48 hrs.
- 2nd stage rhabditoid esophagus, not infective
- 3rd stage infective, filariform esophagus

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Life cycle: humans infected by filariform larvae from soil that penetrate skin (usually of
legs) & are carried by blood to lungs up the trachea swallowed; develop into adults
in small intestine, feed on blood from intestinal villi. Lay 1000s eggs/day that are passed
in shit (1) larvae hatch in 24-48 h (2) non-infective, feeding rhabditiform (
) larvae (3) infective, non-feeding filariform ( ) larvae.
Pathogenesis: (1) skin penetration ground itch, an itching vesicle; (2) invasion
usually asymptomatic, may cause rash & eosinophilia; lung migration may cause Loeffler
syndrome; (3) enteric phase abdominal pain, bloody diarrhea followed by microcytic
anemia from blood loss (worms also release anticoagulants), up to 0.3 mL/day/worm.
Fe deficiency anemia, its extent depends on Fe intake/demand and the parasitic burden.
Heavy parasitic burden can also cause protein malabsorption.
Diagnosis: eggs in stool (Harada-Mori on paper strip; on charcoal); occult blood;
eosinophilia.

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