Review Articles Neuroinvasions Caused by Parasites
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Annals of Parasitology 2017, 63(4), 243–253 Copyright© 2017 Polish Parasitological Society doi: 10.17420/ap6304.111 Review articles Neuroinvasions caused by parasites Magdalena Dzikowiec 1, Katarzyna Góralska 2, Joanna Błaszkowska 1 1Department of Diagnostics and Treatment of Parasitic Diseases and Mycoses, Medical University of Lodz, ul. Pomorska 251 (C5), 92-213 Lodz, Poland 2Department of Biomedicine and Genetics, Medical University of Lodz, ul. Pomorska 251 (C5), 92-213 Lodz, Poland Corresponding Author: Joanna Błaszkowska; e-mail: [email protected] ABSTRACT. Parasitic diseases of the central nervous system are associated with high mortality and morbidity. Many human parasites, such as Toxoplasma gondii , Entamoeba histolytica , Trypanosoma cruzi , Taenia solium , Echinococcus spp., Toxocara canis , T. cati , Angiostrongylus cantonensis , Trichinella spp., during invasion might involve the CNS. Some parasitic infections of the brain are lethal if left untreated (e.g., cerebral malaria – Plasmodium falciparum , primary amoebic meningoencephalitis (PAM) – Naegleria fowleri , baylisascariosis – Baylisascaris procyonis , African sleeping sickness – African trypanosomes). These diseases have diverse vectors or intermediate hosts, modes of transmission and endemic regions or geographic distributions. The neurological, cognitive, and mental health problems caused by above parasites are noted mostly in low-income countries; however, sporadic cases also occur in non-endemic areas because of an increase in international travel and immunosuppression caused by therapy or HIV infection. The presence of parasites in the CNS may cause a variety of nerve symptoms, depending on the location and extent of the injury; the most common subjective symptoms include headache, dizziness, and root pain while objective symptoms are epileptic seizures, increased intracranial pressure, sensory disturbances, meningeal syndrome, cerebellar ataxia, and core syndromes. Many early symptoms of CNS invasion are often nonspecific therefore a diagnosis can be difficult. This article presents the epidemiology, pathophysiology and clinical manifestations of selected parasitic neuroinfections. Key words: parasite, central nervous system, neuroinvasion, encephalitis, meningoencephalitis Introduction from different taxonomic groups that cause neuroinfections in humans. Some examples of Infection of the central nervous system (CNS) by endemic neuroparasitic infections are malaria, a parasite is considered a serious complication. angiostrongylosis, gnathostomosis, loaosis, baylisa - Generally, while species specific to humans, except scariosis, alveolar echinococcosis, paragonimosis and Plasmodium falciparum and Taenia solium , occur cysticercosis, while the most common cosmopolitan mainly accidentally in CNS (ectopic locations), a parasitoses are toxoplasmosis, toxocarosis, cystic relatively large number of animal parasites have echinococcosis and trichinellosis. The signs o f CNS been found in the human brain or spinal cord (e.g. invasion depend upon the number and location Toxoplasma gondii , Toxocara canis , T. cati, parasites, and the host immune response. The epide - Echinococcus spp., Angiostrongylus cantonensis , miology, pathophysiology and clinical presentation Trichinella spp.). Some parasitic infections of the for selected parasitic neuroinfections are reviewed brain are lethal if left untreated (e.g., Plasmodium in this article. Some issues related to parasites fal cipa rum , Naegleria fowleri , African trypano - involved in CNS disorders in humans were somes), but others can be controlled by the host presented during the 56th Clinical Day of Medical immune response and can remain for many years as Parasitology – 56. DKPL (Lodz, 2nd June 2017). a chronic infection (e.g., Toxoplasma gondii , Try pa - no soma cruzi ). Table 1 summarizes a list of par asites 244 M. Dzikowiec et al. Protozoa infections of the CNS erythrocyte membrane protein 1) and MESA (the mature parasite-infected erythrocyte surface antigen). Plasmodium falciparum The intracellular adhesion molecule ICAM-1 is the The World Health Organization reports that in major cellular ligand which conditions the 2015, 212 million new cases of malaria were sequestration erythrocytes in cerebral vessels. It has reported worldwide, of which around 90% were been recently demonstrated that the binding of the caused by Plasmodium falciparum ; there were parasite to the endothelial protein C receptor (EPCR) 429,000 deaths from malaria globally. Cerebral is associated with severe malaria [5]. In addition, malaria (CM) is the most severe complication, infected erythrocytes tend to connect with the ABO affecting up to 7% of all P. falciparum malaria blood group antigens (particularly group A), receptor cases, and is one of the most common causes of 1 (CR1), heparan-sulfate proteoglycans (HSPG) and CNS infection in the world [1]. In the course of CM, other membrane antigens of uninfected erythrocytes, mortality is estimated to range from 30% to 50%, forming rosettes that clog the capillaries. Moreover, with higher values observed in the pediatric capillary obstruction is caused by the massive population. CM is defined as a febrile and mainly accumulation of immune complexes with the diffuse encephalopathy, with impairment of participation of complement components of C3 and consciousness being a prominent feature. C4 [1]. Unarousable coma may be preceded by severe headache, confusion, drowsiness and in many Toxoplasma gondii instances, convulsions. WHO guidelines require the It is estimated that antibodies against Toxo plas - following criteria to be fulfilled for a diagnosis of ma gondii can be identified in 30% of all humans; CM to be confirmed: the coma is not attributable to this rate varies greatly from 6 to 90% worldwide, any other encephalopathy, it is awarded a Glasgow depending on the local population. The incidence of Coma Scale score <11 and that it should persist for primary neurotoxoplasmosis (NT) in immuno - at least 30 minutes after a generalized convulsion. competent individuals is very low, i.e. below 0.02% Brain swelling, intracranial hypertension and brain [6]. NT can often develop or reactivate in immuno - stem signs are commonly observed [2]. compromised patients, such as those with AIDS, The typical pathological features of this disease neoplastic diseases and organ transplants. Cerebral include adhesion and sequestration of P. falciparum- toxoplasmosis is an opportunistic parasitic infected red blood cells in brain microvessels, ring infection, and is a frequent complication of AIDS hemorrhages and Dürck’s granulomas. Adult when the lymphocyte CD4+ cell count drops below patients with CM demonstrate the presence of 100 cells/mm 3. In Europe, the prevalence of axonal injury and blood-brain barrier dysfunction. encephalitic toxoplasmosis in HIV-positive patients Extracerebral manifestations aggravating the is reported to be 30–40%, with a mortality rate of encephalopathy typically include anemia- 20%. NT is found in 10 to 34% of autopsies on hypoxemia-hypoxia, thrombocytopenia, renal and patients with HIV/AIDS. The most common hepatic failure, pulmonary edema, hypotension and presenting symptom of NT is headache, which is bleeding and clotting disturbances [3]. One often accompanied by fever, motor weakness, altered presentation at the 56th Clinical Day of Medical mental status, speech and visual disturbances, Parasitology (N. Nowak, Ł. Pielok, J. Stefaniak, seizures and cranial nerve abnormalities. The most UM P oznan) presented a severe case of malaria commonly affected areas in the CNS include the caused by P. falciparum in a 60-year-old patient who basal ganglia and cortico medullary junction. Tissue returned after a one-week stay in Burkina Faso; in the cysts (with bradyzoites) in the brain are often first days after admission to the clinic, blood spheroidal and usually range in size from 5–50 µm parasitemia was 2%, and – the neurological in diameter; however, in rare cases, they can reach symptoms were accompanied by acute renal failure. over 1 cm [7]. Cerebral toxoplasmosis is Disseminated intravascular coagulation (DIC) is seen characterized by multiple masses of lesions with in <5% of patients with severe P. falciparum malaria surrounding vasogenic edema; hemorrhages are and is relatively often observed in cerebral malaria occasionally present in the periphery of the lesion. [4] . Infection of red blood cells by P. falciparum leads Congenital infection (CT) occurs predominantly to changes in cell surface proteins and the expression after primary infection of a pregnant woman and is of new proteins, such as PfEMP-1 (P. falciparum usually asymptomatic in the newborn period (75% Neuroinvasions 245 of infected newborns). CT has a broad spectrum of hyperplasia, astrocylial proliferation and formation nonspecific clinical manifestations; the classic triad of microglial nodules are visible. Very characteristic of signs (chorioretinitis, intracranial calcifications, of infection are morular (mulberry-like) cells or hydrocephalus) occurs in 5 to 10% of CT cases. Mott cells; these bear a small peripherally-located Congenital infection is estimated to be 0.5 of 10,000 nucleus and eosinophilic inclusions (Russel body) live births in the United States, and 2.9 of 10,000 in the cytoplasm, with IgM immunoglobulin on live births in France; however, the incidence of their surface [10,12]. Trypomastigota are rarely acute infection among Toxoplasma -seronegative observed in the