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Toxoplasmosis Clinical Presentation

  • Author: Murat Hökelek, MD, PhD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 20, 2015
 

History

Only 10-20% of toxoplasmosis cases in adults and children are symptomatic. Toxoplasmosis is a serious and often life-threatening disease in immunodeficient patients. Congenital toxoplasmosis may manifest as a mild or severe neonatal disease, with onset during the first month of life or with sequelae or relapse of a previously undiagnosed infection at any time during infancy or later in life. Congenital toxoplasmosis has a wide variety of manifestations during the perinatal period.

Acute toxoplasmosis in immunocompetent persons

See the list below:

  • Approximately 80-90% of patients are asymptomatic. Symptomatic disease may be characterized as follows:
  • Patients may have cervical lymphadenopathy with discrete, usually nontender, nodes smaller than 3cm in diameter
  • Fever, malaise, night sweats, and myalgias have been reported
  • Patients may have a sore throat
  • Retroperitoneal and mesenteric lymphadenopathy with abdominal pain may occur
  • Retinochoroiditis is reported

Acute toxoplasmosis in hosts who do not have AIDS but are immunodeficient

The disease in these patients may be newly acquired or a reactivation. It may be characterized as follows:

  • CNS toxoplasmosis occurs in 50% of patients - 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
  • They may have signs and symptoms similar to those observed in immunocompetent hosts.
  • Patients may have flulike symptoms and lymphadenopathy
  • Myocarditis and pneumonitis are reported.
  • Toxoplasmic pneumonitis can occur - Typical symptoms of a pulmonary infection, mirroring in particular P ( carinii) jiroveci, including nonproductive cough, dyspnea, chest discomfort, and fever

Symptoms associated with reactivation toxoplasmosis are dependent on the tissue or organ affected.

Clinical manifestations of toxoplasmosis in patients with AIDS

Brain involvement (ie, toxoplasmic encephalitis), with or without focal CNS lesions, is the most common manifestation of toxoplasmosis in individuals with AIDS.

Clinical findings include the following:

  • Altered mental state
  • Seizures
  • Weakness
  • Cranial nerve disturbances
  • Sensory abnormalities
  • Cerebellar signs
  • Meningismus
  • Movement disorders
  • Neuropsychiatric manifestations

The characteristic presentation is usually a subacute onset, with focal neurologic abnormalities in 58-89% of cases. However, in 15-25% of cases, the clinical presentation is more abrupt, with seizures or cerebral hemorrhage. Most commonly, hemiparesis and/or speech abnormality is the major initial manifestation.

Brainstem involvement often produces cranial nerve lesions, and many patients exhibit cerebral dysfunction with disorientation, altered mental state, lethargy, and coma.

Less commonly, parkinsonism, focal dystonia, rubral tremor, hemichorea-hemiballismus, panhypopituitarism, diabetes insipidus, or syndrome of inappropriate antidiuretic hormone secretion may dominate the clinical picture.

In some patients, neuropsychiatric symptoms such as paranoid psychosis, dementia, anxiety, and agitation may be the major manifestations.

Diffuse toxoplasmic encephalitis may develop acutely and can be rapidly fatal; generalized cerebral dysfunction without focal signs is the most common manifestation, and CT scan findings are normal or reveal cerebral atrophy.

Spinal cord involvement manifests as motor or sensory disturbances of single or multiple limbs, bladder or bowel dysfunctions, or both and local pain. Patients may present with clinical findings similar to those of a spinal cord tumor. Cervical myelopathy, thoracic myelopathy, and conus medullaris syndrome have been reported.

Pulmonary toxoplasmosis (pneumonitis) due to toxoplasmosis is increasingly recognized in patients with AIDS who are not receiving appropriate anti-HIV drugs or primary prophylaxis for toxoplasmosis. The diagnosis may be confirmed by demonstrating T gondii in bronchoalveolar lavage fluid.

Pulmonary toxoplasmosis occurs mainly in patients with advanced AIDS (mean CD4+ count of 40 cells/µL ±75 standard deviation) and primarily manifests as a prolonged febrile illness with cough and dyspnea. Pulmonary toxoplasmosis may be clinically indistinguishable from P (carinii) jiroveci pneumonia, and the mortality rate, even when treated appropriately, may be as high as 35%.

Extrapulmonary toxoplasmosis develops in approximately 54% of persons with toxoplasmic pneumonitis.

Ocular toxoplasmosis, ie, toxoplasmic retinochoroiditis, is relatively uncommon in patients with AIDS; it commonly manifests as ocular pain and loss of visual acuity. Funduscopic examination usually demonstrates necrotizing lesions, which may be multifocal or bilateral. Overlying vitreal inflammation is often present and may be extensive. The optic nerve is involved in as many as 10% of cases.

Other, uncommon manifestations of toxoplasmosis in patients with AIDS include the following:

  • Panhypopituitarism and diabetes insipidus
  • Multiple organ involvement, with the disease manifesting as acute respiratory failure and hemodynamic abnormalities similar to septic shock
  • Syndrome of inappropriate antidiuretic hormone secretion and possibly orchitis
  • Gastrointestinal system invasion of T gondii may result in abdominal pain, diarrhea, and/or ascites (due to involvement of the stomach, peritoneum, or pancreas)
  • Acute hepatic failure
  • Musculoskeletal involvement
  • Parkinsonism
  • Focal dystonia
  • Rubral tremor
  • Hemichorea-hemiballismus

Congenital toxoplasmosis

This is most severe when maternal infection occurs early in pregnancy. Approximately 15-55% of congenitally infected children do not have detectable T gondii –specific IgM antibodies at birth or early infancy. Approximately 67% of patients have no signs or symptoms of infection.

Retinochoroiditis occurs in about 15% of patients, and intracranial calcifications develop in about 10%. Cerebrospinal fluid (CSF) pleocytosis and elevated protein values are present in 20% of patients.

Infected newborns have anemia, thrombocytopenia, and jaundice at birth. Microcephaly has been reported. Affected survivors may have mental retardation, seizures, visual defects, spasticity, hearing loss or other severe neurologic sequelae.

The prevalence of sensorineural hearing loss is as high as 28% in children who do not receive treatment.[43]

Ocular toxoplasmosis

Patients develop retinochoroiditis (focal necrotizing retinitis). They have a yellowish white, elevated cotton patch with indistinct margins. The lesions may occur in small clusters. Congenital disease is usually bilateral and acquired disease is usually unilateral.

Symptoms include the following:

  • Impaired vision - Either sudden or gradual, depending on the site of infection
  • Blurred vision
  • Scotoma
  • Pain
  • Photophobia
  • Floaters
  • Red eye
  • Metamorphopsia
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Physical Examination

The acquired infection is usually subclinical and asymptomatic. In 10-20% of cases that become symptomatic, the patient develops a flulike illness characterized by fever, lymphadenopathy, malaise, myalgias, and a maculopapular skin rash that spares the palms and the soles.[44] In individuals who are immunocompetent, the disease is benign and self-limited. Hepatosplenomegaly can also occur. Infrequently, patients develop myocarditis, polymyositis, pneumonitis, hepatitis, or encephalitis

The most common form of symptomatic acute toxoplasmosis in immunocompetent individuals is lymphadenopathy. The typical presentation is painless, firm lymphadenopathy that is confined to 1 chain of nodes, most commonly cervical.

Ophthalmologic examination reveals multiple yellow-white cottonlike patches with indistinct margins located in small clusters in the posterior pole.

A flare-up of congenitally acquired retinochoroiditis is often associated with scarred lesions juxtaposed to the fresh lesion.

Ocular toxoplasmosis (retinochoroiditis)

Symptoms of retinochoroiditis include the following[45] :

  • Decreased visual acuity - Other deficits depend on the location of the lesion
  • White focal lesions with inflammation of the vitreous humor (the classic "headlight in the fog" appearance) seen on ophthalmoscopic examination
  • Recurrent lesions at the border of the retinochoroidal scars

Immunocompromised individuals (AIDS CD4 count < 100 cells/microL)

Host immune function plays an important role in the pathogenicity of toxoplasmosis. Symptoms depend largely on the organ system and tissue involved and may be gradual in onset over a few weeks. They include the following:

  • CNS toxoplasmosis - Seizure, mental status change, focal motor deficits, cranial nerve disturbances, sensory disturbances, cerebellar abnormalities, movement disorders, neuropsychiatric findings
  • Retinochoroiditis (similar to that seen in immunocompetent individuals)
  • Pneumonitis - More common in patients who have undergone bone marrow transplantation and in patients with AIDS; nonproductive cough, blood-tinged sputum, hypoxia (symptoms indistinguishable from P [ carinii] jiroveci)
  • Septic shock–like presentation

Multifocal, bilateral, and relentlessly progressive lesions characterize the ocular involvement. Because of their immunosuppression, these patients often have problems mounting an inflammatory reaction, which makes the formation of a retinochoroidal scar difficult. Often, the serologic diagnosis is also difficult.

Congenital toxoplasmosis

The classic clinical triad of retinochoroiditis, cerebral calcifications, and convulsions defines congenital toxoplasmosis. Other findings include the following:

  • Hydrocephalus
  • Microcephaly
  • Organomegaly
  • Jaundice
  • Rash
  • Fever
  • Psychomotor retardation
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Contributor Information and Disclosures
Author

Murat Hökelek, MD, PhD Professor, Department of Clinical Microbiology, Istanbul University Cerrahpasa Medical Faculty, Turkey

Murat Hökelek, MD, PhD is a member of the following medical societies: American Society for Microbiology, Turkish Society for Parasitology

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Joseph U Becker, MD Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Mark L Plaster, MD, JD Executive Editor, Emergency Physicians Monthly

Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

Amar Safdar, MD, FACP, FIDSA Associate Professor of Medicine, Consulting Staff, Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, University of Texas

Amar Safdar, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International Immunocompromised Host Society, New York Academy of Sciences, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Joseph Sciammarella, MD, FACP, FACEP Major, Medical Corps, US Army Reserve; Attending Physician, Emergency Medicine, Weatherby Locums; President and Director of Education, Health Training/Consulting, Inc

Joseph Sciammarella, MD, FACP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Deepika Singh, MD Staff Physician, Department of Emergency Medicine, Lawrence and Memorial Hospital, New London, CT

Deepika Singh, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Nurses Association, Emergency Medicine Residents Association, and Sigma Theta Tau International

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Toxoplasmosis. Toxoplasma gondii tachyzoites (Giemsa stain).
Toxoplasmosis. Toxoplasma gondii tachyzoites in cell line.
Toxoplasma gondii in infected monolayers of HeLa cells (Giemsa stain).
Ophthalmic toxoplasmosis. Used with permission of Anton Drew, ophthalmic photographer, Adelaide, South Australia.
Macular scar secondary to congenital toxoplasmosis. Visual acuity of the patient is 20/400
Papillitis secondary to toxoplasmosis, necessitating immediate systemic therapy.
Acute macular retinitis associated with primary acquired toxoplasmosis, requiring immediate systemic therapy
Peripapillary scars secondary to toxoplasmosis
Perimacular scars secondary to toxoplasmosis
Inactive retinochoroidal scar secondary to toxoplasmosis
 
 
 
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