1. TOXOPLASMOSI S Leo Francis Pacquing June 24, 2013
2. TOXOPLASMOSIS Toxoplasmosis is a systemic disease caused by
the organism Toxoplasma gondii. Both Humans and Animals can be
infected Most patients have no recognizable symptoms and develop
immunity to the organism An infection could show non-constitutional
signs and symptoms may reach the posterior segment of the eye
through the bloodstream, leading to formation of cysts within the
retinal tissue, or they may cause localized, relentless destruction
of the retina Congenital or Acquired
3. TOXOPLASMOSIS Toxoplasmosis is the most common cause of
infectious retinochoroiditis in both adults and children. It is
caused by the parasite Toxoplasma gondii, a single- cell obligate
intracellular protozoan parasite. Cats are the definitive hosts
Humans and a variety of other animals serve as intermediate
hosts.
4. TOXOPLASMA OOCYST, or soil form TACHYZOITE, or infectious
form BRADYZOID or TISSUE CYST, or latent form
5. TRANSMISSION Ingestion of undercooked, infected meat
containing Toxoplasma cysts; contaminated water, fruit, or
vegetables or unpasteurized goat milk from a chronically infected
animal Inadvertent contact with cat feces, cat litter, or soil
containing oocysts transplacental transmission with primary
infection during pregnancy Introduction of tachyzoites through a
break in the skin blood transfusion or organ transplantation
6. PENETRATION & INVASION Toxoplasma organisms then invade
intestinal mucosal cells and initiate the infection. Tachyzoits are
found in the circulatory system and in nearly all tissues of the
body. In Immunocompetent states, the replication of the tachyzoits
eventually ceases and most organisms are removed, although some may
remain as dormant bradyzoits within intercellular tissue cyst.
7. EPIDEMIOLOGY Geographic area, age, and socioeconomic factors
influence the prevalence of the disease. The prevalence is highest
in tropical regions and lowest in cold regions of the world. The
reported seropositivity rates among healthy adults vary
considerably throughout the world. 70% and 80% of women of
childbearing age in the United States lack antibodies to T gondii,
however, the incidence of toxoplasmosis acquired during pregnancy
is only 0.2%- 1%. In southern Brazil, where the prevalence of
toxoplasmosis is extremely high, 1/770 births; Higher prevalence of
ocular involvement.
8. EPIDEMIOLOGY Disease acquired early in pregnancy often
results in spontaneous abor- tion, stillbirth, or severe congenital
disease, whereas that acquired later in gestation may produce an
asymptomatic, normal-appearing infant with latent infection.
Besides the ingestions of the raw, uncooked meat, several ways of
transmission were also reprted: Transconjunctival Puppies-
Inhilation of the oocyts Food Consumed by humans may be
contaminated by Insects and cockroaches.
9. EPIDEMIOLOGY TOXOPLASMIC RETINOCHOROIDITIS It had been
believed that most cases of toxoplasmic retinochoroiditis
represented a recrudescence of a congenital disease. But it is also
more recognized at present are cases of Acute Toxoplasmic
Retinochoroiditis = After Systemic Acquired Toxoplasmosis
10. CLINICAL MANIFESTATIONS Clinical Entities of Toxoplasmosis
1. Congenital Toxoplasmosis 2. Acquired Systemic Toxoplasmosis 3.
Toxoplasmosis in the Immunocompromised Host 4. Acquired or
Reactivation of Latent Infection 5. Ocular Toxoplasmosis * 1.
Congenital 2. Acquired Systemic
11. The prevalence of congenital toxoplasmosis has been
estimated to vary between 1:1000 and 1:10,000 The Disease is
Bilateral in 65-85% of cases and involves the macula in 58%
Toxoplasmic infection in consecutive siblings is rare, but
congenital ocular toxoplasmosis has been described in siblings. The
classic presentation of congenital toxoplasmosis includes
retinochoroiditis, hydrocephalus, and intracranial calcification
CONGENITAL TOXOPLASMOSIS
12. CONGENITAL TOXOPLASMOSIS Retinochoroiditis, which occurs in
up to 80% of cases, is the MOST COMMON abnormality in patients with
congenital infections and is BILATERAl in approximately 85% of
affected individuals, with a predilection for the posterior pole
and macula. Varying degrees of retinitis Hepatosplenomegaly
Intracranial calcifications Microcephaly Developmental delay
13. CONGENITAL TOXOPLASMOSIS Retinitis, sometimes with
associated choroiditis, iritis, and anterior uveitis The active
area of retinal inflammation is usually thick- ened and cream-
colored with an overlying vitritis. So called Satellite Lesion
14. CONGENITAL TOXOPLASMOSIS Diagnosis PRIMARILY CLINICAL in
nature based on the characteristic retinal lesion. Supported by
ELISA for Toxoplasma AB Lack of antibody essentially rules out the
diagnosis. Maternal IgM does not cross the placenta
15. CONGENITAL TOXOPLASMOSIS Vision can be compromised by the
location of the reactivation adjacent to the macula or optic nerve
or by significant vitritis. Most practitioners recommend treatment
if the macula or optic nerve is involved or if massive vitritis
threatens vision. Systemic treatment involves the use of 1or more
antimicrobial drugs with or without oral corticosteroids.
Pyrimethamine and sulfadiazine
16. TREATMENT
17. TREATMENT Other antibiotic treatment:
Trimethoprim/sulfamethoxazole (Bactrim) Clindamycin +pyrimethamine
is the regimen of choice for the PROPHYLAXIS against and TREATMENT
of Toxoplasmosis Azithromycin
18. ACQUIRED TOXOPLASMOSIS Adult acute acquired toxoplasmosis
presents as an acute febrile illness associated with cervical
lymphadenopathy. Hilar and submental lymph node enlargement also
may occur. Hepatosplenomegaly, lymphocytosis with the presence of
atypical forms of lymphocytes, and hilar lymphadenopathy may occur.
Acquired toxoplasmosis may present as fever of unknown origin with
or without abdominal pain. The clinical manifestations of
toxoplasmosis may mimic many diseases, including Hodgkin's disease
and infectious mononucleosis
19. APPEARANCE A unifocal area of acute-onset inflammation
adjacent to an old chorioretinal scar is virtually pathognomonic
for toxoplasmic chorioretinitis.
20. APPEARANCE Classically, Ocular toxoplasmosis appears as a
focal, white retinitis with overlying moderate vitreous
inflammation ("headlightin the fog"), often adjacent to a pigmented
chorioretinalscar
21. APPEARANCE Retinal vessels in the vicinity of an active
lesion may show perivasculitis with diffuse venous sheathing and
segmental Arterial sheathing (Kyrieleis arteriolitis)
22. OCULAR FINDINGS Toxoplasma gondii is the most common cause
of infection of the RETINA. Ocular findings include involvement of
the retina, choroid, retinal vessels, macula, optic nerve,
vitreous, and anterior uvea.
23. OCULAR FINDINGS Typical Manifestations Focus of retinitis
surrounded by fuzzy retinal edema Pigmented atrophic
retinochoroiditic scar adjacent to the lesion or elsewhere in the
fundus Vitreous cells and exudates Focal retinal vasculitis
Hyperemia of the optic nerve head Cells and flare in the anterior
chamber (rarely, mutton-fat keratic precipitates) In patients with
recurrent ocular toxoplasmosis: anterior segment findings,
including posterior synechiae, secondary cataract, and secondary
glaucoma
24. OCULAR FINDINGS Necrotizing Retinitis focus of Toxoplasma
retinitis close to healed retinochoroiditic scars
25. Typical punched-out Toxoplasma retinochoroiditic scar
surrounded by pigmentation. Macular retinochoroiditic scar in a
6-year-old child with healed congenital ocular toxoplasmosis
26. OCULAR FINDINGS Optic Nerve The CNS is frequently involved
in toxoplasmosis. The optic nerve may present with optic neuritis
or papillitis associated with edema. The diagnosis may be hard to
make when patients present with severe papillitis and no evidence
of active retinal lesion. Vitreous Toxoplasma gondii is an obligate
intracellular parasite and, therefore, the organism does not invade
the acellular vitreous cavity. PVD- Posterior Segment Inflammation
Anterior Uvea Anterior uveitis (granulomatous or nongranulomatous)
may be associated with Toxoplasma retinochoroiditis In
immunocompetent patients- anterior uveal inflammation
28. OCULAR COMPLICATIONS Severe inflammatory changes within the
globe secondary to toxoplasmosis may lead to several complications.
Fuchs' heterochromic iridocyclitis- Unclear Periphreal Anterior
Synechia Subretinal neovascularization RRD, SRD Cataract CME
29. TOXOPLASMOSIS AMONG AIDS PATIENTS One of the most common
parasitic infections in patients with AIDS is toxoplasmosis. This
may occur in the retina or elsewhere in the body. Toxoplasmic
encephalitis is a fatal disorder if not treated early or promptly.
Neuroimaging is warranted in AIDS patients presenting with these
findings because intracranial toxoplasmic lesions have been
reported in up to 29% of these patients who have toxoplasmic
chorioretinitis.
30. CEREBRAL TOXOPLASMOSIS CT scan will show Ring Enhancing
Lesions with darker areas of Surounding edema that are typical of
your toxoplasmosis.
31. TOXOPLASMOSIS IN IMMUNOSUPPRESSED Toxoplasmosis is becoming
an important cause of mortality and morbidity in patients. Patients
with impaired immunity such as those with lymphoma, leukemia,
malignancies, and AIDS. Patients may present with fever,
encephalitis, myocarditis, and pneumonitis, which are the most
common and serious of the clinical manifestations. Retinal Tears
(rhegmatogenous)
32. NOTE Focal retinitis in the absence of chorioretinal
scarring should raise the suspicion of acquired disease or another
cause for the necrotizing retinitis Retinochoroiditis developing in
immunocompromised and older patients may present with atypical
findings including large, multiple, and/or bilateral lesions, with
or without associated chorioretinal scars. Other ATypical
Presentations Unilateral neuroretinitis Punctate outer retinal
toxoplasmosis (PORT) Small , multifocal lesions at the level of the
deep retina with scant overlying vitreous inflammation Unilateral
Pigmentary retinopathy simulating retinitis pigmentosa
33. DIAGNOSIS In most instances, the diagnosis of Toxoplasmic
retinochoroiditis is made clinically, on the basis of the
appearance of the characteristic Lesion. Serologic Evaluation
through Indirect Fluorescent Antibody testing. (ELISA) to confirm
the diagnosis (to detect specific Anti T. Gondii antibodies is
commonly used to confirm exposure to the parasite ) IgG First 2
weeks after infection, Remain detectable for life, Does cross
placenta IgM Rise early During Acute Disease, typically detectable
in less than a year, Does not cross Placenta PCR
