Power point presentation

1. Toxoplasma gondii and its
pathogenicity
Presenter: GANIYU SAMSON OLUWASEUN
139094009
DEPARTMENT OF MEDICAL MICROBIOLOGY AND
PARASITOLOGY
COLLEGE OF MEDICINE, UNIVERSITY OF LAGOS.

2. CONTENTS
 INTRODUCTION
 LIFE CYCLE
 PATHOGENICITY AND VIRULENCE FACTORS
 CLINICAL PRESENTATION AND TREATMENT
 CONCLUSION AND RECOMMENDATION
 REFERENCES

3. INTRODUCTION
 T.gondii was first discovered in 1908 in Tunis within
the tissue of the North African rodent, Ctenodactylus
gondii, in the same year it was also described in Brazil
in rabbits by Nicolle and Manceaux .
 Rediscovered in 1935 in the brain tissue of guinea pigs.
 In 1939 it was found as the cause of encephalitis in a 31
day old infant.
 In 1969 infective cysts were detected in the stools of
cats.
 A member of Apicomplexa related to Plasmodium,
Isospora and others

4.  Toxoplasma gondii is a single-celled, intracellular
protozoan that causes the parasitic disease known
as toxoplasmosis.
 Found in animals: birds, humans etc but the
essential reservoir host is the common house cat
and other felines.
 Is cosmopolitan and occurs in areas where cat are
many and where low hygiene holds sway.
 Infection is high where meat is eaten raw or
partially cooked.
 Infection is common but diseases is rare.

5. MORPHOLOGY
 Are ovoid or crescent shaped
 4-6µm in length and 2-3micron in width
 One of the end is bluntly pointed or rounded
 When stained with Giemsa, the cytoplasm appears
blue and the nucleus red.
 Occurs in 2 forms: tachyzoite (trophozoites) which is
slender shaped. On maturity, they develop into cysts
which contain 50-thousands of growing organisms. .
 The growing forms are called the bradyzoites (slow
growing forms)
 Tachyzoites are highly infective and develop from the
oocyst

7. EPIDEMIOLOGY
 It is generally assumed that approximately 25 to 30% of
the world's human population is infected by
Toxoplasma (Montoya and Liesenfeld, 2004).
 Found worldwide, it is capable of infecting virtually all
warm blooded animals (Linday and Dubey, 2013).
 In humans, it is one of the most common parasites,
serological studies estimate that up to a third of the
global population has been exposed to and may be
chronically infected with T. gondii, although infection
rates differ significantly from country to country
(Pappas et al., 2009).

8. TRANSMISSION
According to Tenter et al. (2000) infection in humans
and other warm-blooded animals can occur:
 by consuming raw or undercooked meat containing T.
gondii tissue cysts
 by ingesting water, soil, vegetables, or anything
contaminated with oocysts shed in the feces of an
infected animal
 from blood transfusion or organ transplant
 transplacental transmission from mother to fetus,
particularly when T. gondii is contracted during
pregnancy
 Reactivation of infection( Immunocompromised e.g
AIDS or Immunosuppressed e.g Drugs)

9. LIFE CYCLE
DEFINITIVE HOST INTERMEDIATE HOST
 Mainly domestic and
wild cats.
 Human, birds, pigs,
rodents, and sheep.

10. Toxoplasma gondii

11. PATHOGENICITY AND VIRULENCE FACTORS
 Its has ability to invade a wide variety of host cells which is
an active process relying on parasite motility and the
sequential secretion of proteins from secretory organelles,
the micronemes, the rhoptries, and the dense granules.
 Attachment of the parasite to the host cell membrane
involves secretion of micronemes protein (MIC2).
 Cell invasion involves a process called gliding motility;
promoted by actin-myosin interaction and dynamic
rearrangement of the parasite cytoskeleton.
 Formation of tight relationship occur between apical end
and host cell membrane called moving joint.
 Internalization of the parasite into parasitophorus vacoule
(PV).

12.  The moving joint around the invading parasite
requires the distribution of apical membrane antigen
(AMA1) and Rhoptry(ROP) neck protein.
 Parasitophorous vacoule membrane (PVM)is formed
which requires the secretion of protein from ROPs (
ROP18, ROP16).
 Dense granular protein also contribute to the
formation of PVM during the 1st hour of invasion.
 Replication is by endodyogeny and the tachyzoites
divide during 6-9h cycle.
 They exit the cell usually after 64-128 parasites have
accumulated in the PV.
 The parasite avoid destruction by preventing fusion of
phagosome with the lysosome.

13.  The parasite is able to
cause infection by
modulating the host
immune response by
using the heat shock
protein (TgHSP70)
 It induces interleukin -12
linked immune response
which serve to control
abundance of active
tachyzoites in the host.

14. CLINICAL PRESENTATION
 In Healthy Individual or Immunocompetent
Individual
 Fever, malaise, night sweats, and myalgias
 Retinochoroiditis is reported
 In Immunocompromised Individuals
Acute toxoplasmosis in hosts who do not have AIDS but are immunodeficient
 Seizure, dysequilibrium, cranial nerve deficits, altered mental
status, focal neurologic deficits, headache
 Patients may have encephalitis, meningoencephalitis, or mass
lesions
 Hemiparesis and seizures have been reported
 Patients may report visual changes

15. Clinical manifestations of toxoplasmosis in patients with
AIDS
 Altered mental state, Seizures, Weakness, Cranial
nerve disturbances, Sensory abnormalities, Cerebella
signs, Meningismus, Movement disorders,
Neuropsychiatric manifestations
 Most commonly, hemiparesis and/or speech
abnormality is the major initial manifestation
 Pulmonary toxoplasmosis may be clinically
indistinguishable from Pneumocystis (carinii) jiroveci
pneumonia and the mortality rate, even when treated
appropriately, may be as high as 35% (Murat et al.,
2014).

16.  PREGNANCY-ASSOCIATED INFECTION
(Congenital Toxoplasmosis)
 Miscarriage, still birth, hydrocephaly,
mental disability, Yellowing of the skin
and whites of the eyes (jaundice)
hearing loss or other severe neurologic
sequelae and seizures later in life
 Retinochoroiditis, hearing loss e.t.c.

17. LABORATORY DIAGNOSIS
 Serology: ELISA, IFAT
 PCR
 Histologic diagnosis
TREATMENT AND CONTROL
 Sulfadoxine and pyrimethamine are two drugs widely used to treat
toxoplasmosis in humans.
 Patients allergic to sulfa drugs may take Clindamycin,
Clarithromycin, Azithromycin
 Hands should be washed after contact with raw meat or in contact with
soil.
 Vegetables should be washed well .
 Avoid undercooked meats.
 If you own a cat
– Keep it inside if possible.
– Don’t feed it raw meat.
–Avoid cat for pregnant women

18. CONCLUSION AND RECOMMENDATION
 Toxoplasmosis is a disease that is caused by an intestinal coccidium
Toxoplasma gondii that affect humans and virtually all warm blooded animals.
It is capable of breaking down the host immune system through its various
pathogenic means and its virulence factor.
 Toxoplasma gondii causes congenital toxoplasmosis, cerebral toxoplasmosis
and ocular toxoplasmosis.
 Research work should carried out on the production of Toxoplasma gondii
heat shock protein 70 which is a virulence factor used by the parasite in
destroying the host defence mechanism and how its production can be
inhibited in the host.
 Pregnant women especially during the first trimester period should be
screened for Toxoplasma gondii and if positive, should be treated on time to
avoid congenital toxoplasmosis.
 The health sector and Government should sensitize the people on how the
disease is been transmitted and the role cats play in the transmission of the
parasite especially for pregnant women and people living with HIV and AIDS.

19. REFERENCES
Lindsay, D.S. and Dubey, J.P. (2011). Toxoplasma gondii: the
paradigm of congenital toxoplasmosis. Parasitology. 22:1-3.
Montoya, J.G. and Liesenfeld O. (2004). Toxoplasmosis.
Lancet. 363:1965–1976.
Pappas, G., Roussos, N. and Falagas, M.E. (2009).
Toxoplasmosis snapshots: global status of Toxoplasma
gondii seroprevalence and implications for pregnancy and
congenital toxoplasmosis. International Journal for
Parasitology 39 (12): 1385–94.
Tenter, A.M., Heckeroth, A.R. and Weiss, L.M. (2000).
Toxoplasma gondii: from animals to humans. International
Journal for Parasitology 30 (12–13): 1217–58.

20. THANK YOU