Prepared by:

Dr. kholoud Baraka

Lecturer of Microbiology and Immunology.
Faculty of Pharmacy, Damanhour University.
 V- Tissue sporozoa
TOXOPLASMA GONDII
 Is the causative agent of toxoplasmosis.
 Of those who are infected, very few have symptoms because a
healthy person's immune system usually keeps the parasite from
causing illness. However, pregnant women and individuals who have
compromised immune systems should be cautious; for them, a
Toxoplasma infection could cause serious health problems.
 It infects a wide spectrum of warm-blooded vertebrate species (for
example humans, sheep, pigs, cattle, horses, dogs, cats, wild
mammals, and bird species).
 There are three infectious stages of T. gondii: the tachyzoites (in
groups or clones), the bradyzoites (in tissue cysts), and the
sporozoites (in oocysts). These stages are linked in a complex life
cycle.
1.Tachyzoites (endozoites): The term “tachyzoite” (tachos =
speed in Greek). They are proliferative forms that reproduce
rapidly in host cells by means of endodyogeny (budding).
* The conoid and the polar ring complex contribute to parasite
penetration into host cells. Polar ring is a thickening of the inner
membrane complex at the anterior end of the tachyzoite, which
encircles a cylindrical cone called the conoid, which consists of
six to eight
microtubules.
2. Bradyzoites (cystozoites): The term “bradyzoite” (brady = slow in
Greek) describing the slow multiplication of the organism by endodyogeny
within a tissue cyst. The cysts develop intracellularly in various tissues, and
can contain up to several thousand bradyzoites. They have a long lifespan in
the host.

An oocyst containing sporozoites

3. Oocysts: are rounded and encysted stages of the organism. They are
the final product of a sexual reproductive cycle in the intestinal
epithelial calls. They are shed in feces. Sporulation takes place
producing two sporocysts and each sporocyst contains four sporozoites.
Life cycle:
 The only known definitive hosts for Toxoplasma gondii are members of
family Felidae (domestic cats and their relatives).
 Large numbers of oocysts are usually shed for 1-2 weeks in cats feces.
Oocysts take 1-5 days to sporulate in the environment and become
infective.
 Intermediate hosts in nature (including birds and rodents) become
infected after ingesting soil, water or plant material contaminated with
oocysts.
 The parasite enters macrophages in the intestinal lining and is distributed
via the blood stream or lymph to various organs and multiplies in somatic
cells. Endodyogenic cycles are repeated and the host cells burst producing
tachyzoites. Generalization of the infection can lead to colonization of the
placenta and, infection of the fetus.
 These tachyzoites localize in neural and muscle tissue and develop into
tissue cyst bradyzoites. The reproductive bradyzoites form cysts mainly
in the tissues of the brain, the skeletal and heart muscles as well as in the
retina, the uterine wall and other organs. Since the parasites are inside
cells, they are safe from the host's immune system. Oocysts are shed in
the feces and the cycle is repeated.
a- Development in the definitive host (cat):
Intestinal phase with production of sexual forms: (1) Toxoplasma
that has penetrated into a small intestine epithelial cell; (2) asexual
reproductive stage with merozoites (can continue for several
generations). (3) Production of sexual forms (gamogony) and
formation of the zygote; (4) oocyst.
b- External phase with sporogony:
(5) unsporulated oocyst, shed in cat feces; (6) sporulated oocyst
with two sporocysts each containing four sporozoites.
c- Development in an intermediate host (mammals,
birds, humans):
Extraintestinal phase with only asexual multiplication of parasites: (7)
sporozoite released in organism following oral ingestion of oocysts; (8a) human
infection; (8b) infection of various animal species; (9) asexual reproductive
stages (tachyzoites) in a somatic cells; (10) free tachyzoite; (11) cyst with
bradyzoites in musculature; (12a) infection of a dog with Toxoplasma cysts in
animal meat; (12b) infection of a human with Toxoplasma cysts; (13) infection
of cat with infective stages of cysts in meat or with oocysts.
Transmission
 Cats become infected after consuming intermediate hosts harboring
tissue cysts or directly by ingestion of sporulated oocysts.
 Humans can become infected by any of several routes:
 Eating undercooked meat of animals harboring tissue cysts.
 Consuming food or water contaminated with cat feces or by
contaminated environmental samples (such as fecal-contaminated
soil when changing the litter box of a pet cat) containing oocysts.
 Transplantation of infected organs to uninfected recipients.
 Transplacentally from mother to fetus.
Immunity
• Various Toxoplasma antigens induce immune responses which,
following a primary infection, result in antibody production and
inhibition of tachyzoite multiplication. Toxoplasmas then “escape”
from the immune defense system by encysting (immunoevasion). This
enables them to persist in a latent state for many years in their hosts.
 Clinical manifestations
Primary infection in immune-competent persons:
* Approximately 80-90% of patients are asymptomatic. Symptomatic
disease (acute toxoplasmosis) may be characterized by: influenza-like
symptoms: swollen lymph nodes, muscle aches and pains that last for a
month or more.
Primary infection in immunosuppressed persons:
 CNS toxoplasmosis occurs in 50% of patients: Seizures, cranial nerve
deficits, altered mental status, and headache.
 Patients may have encephalitis, meningoencephalitis, or mass lesions.
 Necrotizing interstitial pneumonia, hepatosplenomegaly, mycocarditis,
eye damage, and other manifestations.
Primary infection during pregnancy:
* Thismay cause prenatal infection of the fetus. Infected newborns may
have anemia, thrombocytopenia, and jaundice at birth. Microcephaly has
been reported. Affected survivors may have mental retardation, seizures,
visual defects, hearing loss or other severe neurologic sequelae. Clinically
severe cases: brain damage and perinatal deaths.
Diagnosis
 In immunocompetent adults:
Serologically by detection of parasite-specific IgG and IgM
antibodies.
 IgM antibodies can be detected as early as one week after
the primary infection, peak within two to four weeks.
IgG antibodies appear later, peak after two to four months
and persist for many years. A high or rising IgG titer with
simultaneous detection of IgM indicates an acute primary
infection.

 In prenatal diagnostics: PCR is used for direct

detection of pathogenic genetic material in the amniotic fluid.
 Treatment
 Sulfadiazine: an antibiotic used in combination with pyrimethamine
and folic acid to treat toxoplasmosis .Combination therapy is most
useful in case of HIV patients.
 Clindamycin.
 Spiramycin: an antibiotic used most often for pregnant women to
prevent the infection of their children.

Prevention
 Toxoplasma cysts remain viable and infectious in meat for up to three
weeks at 4 °C. However, deep-freezing to –20 °C kills bradyzoites
within three days and heating to 70 °C is lethal to them within a few
minutes.
 Pregnant women should eat only meat that has been thoroughly
heated or deep-frozen and avoid close contact with cats .
 Prevention of prenatal toxoplasmosis by serological monitoring, with
one check per trimester and early treatment is introduced if required.
 2- Nematodes
or roundworms
 2- Nematodes or roundworms
Phylum: Nemathelminthes Class: Nematoda
 The nematodes (nema: thread) are threadlike, non-segmented
parasites.
 Length: a few mm to 1m in length.
 Sex: separated sexes. The males are usually smaller than the females.
 Development from egg includes four larval stages to be adult.
 Some species require an intermediate host to complete development.
 They possess a digestive tract and reproductive system.
 Nematodes are classified according to the habitat of adult worm in
human into:
A- Intestinal nematodes.
B- Tissue and vascular nematodes (e.g. Filariae, Trichinella
spiralis).
 A- Intestinal nematodes

*Some of them inhabit the small intestine; however others inhabit

the large intestine.

*Nematodes of small intestine:

 Ascaris lumbricoides (large roundworm).
 Ancylostoma species & Necator americanus (hookworms).
 Strongyloides stercoralis (dwarf threadworm).
*Nematodes of large intestine:
 Trichuris trichiura (whipworm).
 Enterobius vermicularis (pinworm).
 Ascaris lumbricoides
(Large Roundworm)

 Is the causative agent of ascariasis.

 It is the largest and most common parasitic worm in humans
(reservoir host).
 Ascariasis is prevalent worldwide, especially in tropical and
subtropical countries.
 The adult worm lives in the small intestine and is very large in
size (15–40 cm in length).
 The sexually mature females produce as many as 200,000 eggs
per day, which are shed with feces in the unembryonated state
and can remain viable for years in a moist environment (soil).
 The round-to-oval fertilized egg has a thick, brownish shell
and an uneven surface. In case of optimum temperatures of
20–25 °C with sufficient moisture and oxygen, an infective
larva develops in the egg.
(Egg larvated egg (rhabditiform) larva adult).

Adult worm Egg

 Life cycle
 Humans are infected when ingesting a fertilized egg that will
become a larval worm penetrating the wall of the duodenum
and entering the blood stream.
 From there, it is carried to the liver and heart, enters the
pulmonary circulation and reaches the alveoli, where it grows.
 In three weeks, the larva passes from the respiratory system to
be coughed up, swallowed, and thus returned to the small
intestine, where it matures to an adult male or female worm.
Fertilization can now occur and the female produces as many as
200,000 eggs per day for a year.
 These fertilized eggs become infectious after two weeks in soil;
they can persist in soil for 10 years or more. The eggs have a
lipid layer which makes them resistant to the effects of acids
and alkalis, as well as other chemicals. This resistance helps to
explain why this nematode is such a ubiquitous parasite.
Transmission
 Fecally contaminated food, water or hands containing embryonated eggs .
 Inhalation of embryonated eggs.
Clinical manifestations
 Mild infections frequently remain asymptomatic .
 In severe infections, in the early phase, respiratory symptoms
result from the migration of larvae through the lungs causing
eosinophilic pneumonia (Löffler syndrome).The symptoms are:
Fever, non-productive cough, dyspnea, wheezing, hemoptysis
(expectoration with blood stained sputum) and blood eosinophilia.
 In the late phase, gastrointestinal symptoms may occur and are
more typically related to the mechanical effects of the high load of
the adult parasites).The symptoms are: passage of worms from the
anus, diffuse or epigastric abdominal pain, nausea, vomiting,
diarrhea, loss of appetite, malnutrition and impairment of growth
in children.
 Complications: Biliary and intestinal obstruction, appendicitis and
pancreatitis.
 Diagnosis
 Microscopic detection of unembryonated eggs by direct
examination of feces or following concentration techniques.
However, eggs do not appear in stool for at least 40 days after
infection; thus, early diagnosis cannot be made by this
diagnostic method.
 Microscopic detection of migrating larvae in sputum or in
gastric lavage.
 Serological antibody detection.
 Eosinophilia (↑ No. of eosinophiles in blood), particularly during
the phase of larval migration through the lungs.
 Ultrasound examination can help to diagnose hepatobiliary or
pancreatic ascariasis.
Treatment
 Pyrantel pamoate, mebendazole, albendazole, and
nitazoxanide are highly effective against the intestinal
stages of Ascariasis. Migratory larvae are not affected by
these drugs, only adult worms are affected; thus, the
treatment should be repeated after two to three weeks to
ensure that no eggs are detectable.
 Symptomatic treatment: in addition to specific
anthelminthic therapy, supportive therapy may be
required, including: inhaled bronchodilators and systemic
corticosteroids.
 Surgical or endoscopic interventions for complications (e.g.
intestinal and/or biliary obstruction).
Prevention
 Stool should not be used as fertilizer unless being
treated by chemicals or high temperature to kill eggs.
 Good food hygiene practices (washing fruits and
vegetables, cooking foods).
 Health education.
 Regular anthelminthic treatment of infected persons
in endemic areas.