Toxoplasmosis in HIV infection: An overview

Toxoplasmosis in HIV infection: An overview

Keywords: CD4 counts, HIV infection, toxoplasmosis

Introduction
u Toxoplasma gondii- protozoan causing major opportunistic infections in HIV
infected.
u Most cases CMI develop after an infection and resolve but not eradicated.
u In latent phase, it persist in tissues like brain, skeletal muscles and cardiac
muscles
u Symptomatic disease occur due to reactivation of latent infection
u Its most common opportunistic infection in 3rd world countries especially
encephalitis
u Infection is by ingestion of oocyte contaminated food and water or infected
meat
u Also toxoplasma pneumonia occour by respiratory route, vertical transmission
or nosocomial route.
Morphology
u T. gondii has 3 morphological forms; oocyst, tachyzoites and tissue cysts having bradyzoites.
u Cats are the definitive hosts infecting humans with oocyst.
u After ingestion, sporozoites in oocyst develop to tachyzoites which is the invasive form
u They infect nucleated cells and multiply massively and get transported to the other body parts
u Inflammatory response transforms the tachyzoites into tissue cyst, a dormant form of
bradyzoites
Pathogenesis
u Tachyzoites invades the cells, multiply rapidly causing cell necrosis.
u This forms a necrotic focus surrounded by an inflammation.
u This activates the CMI
u Tcells , macrophages and type 1 cytokines; IL-12 and IF-ɤ are responsible of T. gondii inactivity
u In HIV/AIDS people, depletion of CD4ᶧ reduces the expression of CD154 protein (CD40 Ligand)
impairing activation of cytotoxic T cell activity
u Dormant T. gondii cysts gets activated to tachyzoites
Clinical manifestation of toxoplasmosis
u Mainly encephalitis, choriotinitis and pneumonitis or disseminated infections according to immune
status.
u It is sub-acute in onset with focal neurological signs associated with fever, poor concentration and
headache.
u Cerebellar, sub-cortical, or cortical lesions is present - 50% of cases resulting in hemiparesis,
ambulatory gait, and speech abnormalities.
u people with encephalitis can also present with neuropsychiatric disorders like psychosis and
personality disorders.
u Can also present extra-cerebrally affecting eyes and lungs
Epidemiology
u Prevalence is dependent with geographical areas, population and age group.
u Nigeria-75.4%, Tunisia-58.4%, benin-28.5%, Senegal- 40.2%, brazil-74.5%, paris-63.7% Czech 30%
u In US, a third of HIV infected tests positive for anti T. gondii
u Another study showed 68% prevalence in immunocompromised as compared to 30.9% in
immunocompetent.
u Other studies showed higher prevalence in women than men
u Some studies showed highest prevalence at 3rd and 4th decade of life.
Association with CD4 cells
u Different studies have showed an association of CD4 cell count with toxoplasmosis prevalence
u Toxoplasma igG antibodies were present in 75% of Patients with CD4 cells count between 50-100
cells/mm3 (without any neurological signs).
u 79.4% of HIV positive with CD4 cell count <100 cells/mm3 (without any neurological signs)
u A study in France showed a 79% in patient with CD4<150 cells/mm3 and showing neurological signs
u There are other studies which linked low CD4 count with high seropositivity of the infection.
diagnosis
u Diagnosis could be either presumptive or definitive but this depend on the manifestation of the
infection. Include -
Clinical diagnosis
HIV positive patients with CD4 cells<100 and presenting with compatible focal neurological
lesions.
Serological diagnosis
u Anti-T. gondii IgG antibodies starts to increase after 1-2weeks of infection reaching a peak at
6-8 weeks.
u Gradually decline in 1-2 years
u Demonstration of high titers of anti-T. gondii IgG antibodies with high IgG avidity is an
evidence of secondary reactivation.
Radiological diagnosis
u CT and MRI should be used to diagnose cerebral toxoplasmosis if hypodense lesions are observed
with ring enhancing and peri- lesional edema.
u 20% of patients will present hypodense lesions without ring enhancing.
u Other newer techniques such as positron emission tomography can be used to enhance precision
to rule out other CNS lesions like lymphoma.
Biopsy
u Biopsy where tissue cysts form gives a definitive diagnosis.
Molecular diagnosis
u direct detection of T. gondii DNA in biological samples provide perfect results
PREVENTION
u Testing for all HIV positive patient for anti. T. gondii IgG to determine latent infection
u Counselling people about transmission.
u Avoiding raw or under cooked meat
u Proper handwashing.
u Washing vegetables and fruits before eating raw.
u Proper handling of cat litter.
u Feeding pet cat with cooked or canned food
Treatment of cerebral toxoplasmosis
Primary prophylaxis regimen for toxoplasmosis
Maintenance treatment for toxoplasmosis
conclusion
u T. gondii is one of the most causative agents of opportunistic infections in HIV/AIDS
patients.
u Its association with HIV-infected patients has been reported worldwide
u In HIV infection due to immunosuppression, there is reactivation of chronic latent
infection resulting in Toxoplasma encephalitis
u The risk of infection is more when the CD4 counts are <100 cells/μL
u Due to the high rate of reactivation in HIV-positive patients, all HIV-positive
patients must be tested for the presence of T. gondii antibodies

 Full Text

 Author : Anuradha Basavaraju
CITATION:
Basavaraju A. Toxoplasmosis in HIV infection: An overview. Trop Parasitol
2016;6:129-135
Date accepted : 30-aug-2016
Date published: 19-sep-2016
Cited 5 times

MOST IMPORTANT REFERENCES
u Luft BJ, Brooks RG, Conley FK, McCabe RE, Remington JS. Toxoplasmic
encephalitis in patients with acquired immune deficiency syndrome. JAMA.
1984;252:913–7
u Falusi O, French AL, Seaberg EC, Tien PC, Watts DH, Minkoff H, et al.
Prevalence and predictors of toxoplasma seropositivity in women with and at
risk for human immunodeficiency virus infection. Clin Infect Dis.
2002;35:1414–7
u Eliaszewicz M, Lecomte I, Da SA. Relation between decreasing series CD4
lymphocyte count and outcome of toxoplasmosis in AIDS patients: A basis for
primary prophylaxis. Int Conf AIDS. 1990;6:20–3