Parasitic CNS Infections
CNS parasitic involvement is associated with high morbidity and mortality. • Depending on the infection stage, location, and host immunization, CNS parasitic infections can cause local or widespread damage
- Parasitic infections present systemically, including in the central nervous system (CNS).
CNS parasitic involvement is associated with high morbidity and mortality.
- Depending on the infection stage, location, and host immunization, CNS parasitic infections can cause local or widespread damage.
- Clinical CNS associations are encephalitis, meningitis, myelitis, cerebral cysts, and cerebral calcification.
- Parasites enter the body directly through the 2 most common pathways:
- Gastrointestinal tract
- Other parasites can enter through insect bites.
- Parasites invade CNS mostly through the blood
- After entering the body → circular blood → blood-brain barrier → brain.
- In some cases, the parasite invades the olfactory neuroepithelium → subarachnoid space/neural skulls foramina → the brain.
- Parasitic CNS infections are generally classified into two groups
- Single-celled (protozoa)
- Multicellular helminth (metazoa).
The most common CNS infection is cysticercosis.
- Less frequent infections are toxoplasmosis, echinococcosis, schistosomiasis, paragonimiasis, malaria, toxocariasis, onchocerciasis, and Chagas disease (American trypanosomiasis), sleeping sickness (African trypanosomiasis), and angiostrongyliasis.
Mode of transmission
Fecal-oral; Eggs ingestion
Worldwide, mostly in Sub-Saharan Africa and Asia
Contaminated water/food, contact with infected animals
Middle East, Europe, Pacific, Latin America; Inuit populations in North America
Tropical and sub-tropical regions; mostly in Africa, Asia, and Latin America.
Oral-fecal: Oocytes/cysts ingestion from cat’s feces, undercooked meat Transplacentally
Worldwide, mostly in Sub-Saharan Africa and Asia
Tropics from Sub-Saharan Africa, Latin America, Asia, and Oceania
Primary amoebic meningoencephalitis
Olfactory penetration through swimming, bathing, diving
Insect bite: triatomine bug
Insect bite: Tsetse fly
Derived from Carpio, A., Romo, M. L., Parkhouse, R. M., Short, B., & Dua, T. (2016). Parasitic diseases of the central nervous system: lessons for clinicians and policymakers. Expert review of neurotherapeutics, 16 (4), 401–414. https://doi.org/10.1586/14737175.2016.1155454
- Intraparenchymal NCC
- Common: seizure, headache
- Less common: altered vision, focal neurologic signs, and meningitis.
- Extraparenchymal NCC
- Appears in ventricles, subarachnoid space, spine, and/or the eye
- Elevated intracranial pressure: headache, nausea, and vomiting.
- Accompanied by altered mental status.
- Extraparenchymal NCC occurs in >60% of cases while intraparenchymal NCC carries higher complications than extraparenchymal NCC.
- Extraneural cysticercosis: Asymptomatic nodule 0.5-2cm in diameter, calcified cysts in muscular and subcutaneous tissues.
- Cerebral toxoplasmosis subtype
- Immunocompetent: Asymptomatic
- Immunocompromised: Altered mental status, seizure, weakness, cranial nerves deficits, sensory abnormalities.
- Congenital infection
- Hepatosplenomegaly, jaundice
- Rash, petechia
- Developmental delay
- Ruptured or super-infected cysts can cause severe infection.
- Associated with the space-occupying lesion, increase intracranial pressure: headache, nausea, vomiting, and seizures.
- Some Echinococcus can secondarily infect the CNS from either the liver or lungs.
- Swimmer itch
- Localized dermatitis: pruritic papular or urticarial rash at the larva’s entry site after swimming in freshwater
- Acute Schistosomiasis syndrome (Katayama syndrome)
- Appears 3-10 weeks after infection, associated with swimming, bathing, diving, skiing in freshwater.
- Sudden onset of fever, urticaria, angioedema, chills, myalgias, arthralgias, dry cough, diarrhea, abdominal pain, and headache.
- Severe infection can cause acute myelopathy, encephalitis
- Chronic infection
- Symptoms depend on the infected organs: intestinal, liver, lung, urinary tract, and CNS.
- Spinal cord involvement
- Lower limb pain, lower motor dysfunction
- Bladder paralysis
- Bowel dysfunction.
- Brain involvement
- Delirium, loss of consciousness
- Dysphasia, visual field impairment
- Focal motor deficits
- Uncomplicated malaria
- Mild symptoms of malaria and absence of severe malaria
- Symptoms of mild malaria
- Tachycardia, tachypnea
- Chills, malaise, fatigue, diaphoresis
- Anorexia, nausea, vomiting, abdominal pain, diarrhea
- Arthralgias, myalgias
- Anemia, and palpable spleen.
- Complicated malaria
- Altered consciousness
- Respiratory distress, circulatory collapse
- Metabolic acidosis, hypoglycemia
- Renal failure, hemoglobinuria
- Hepatic failure
- Coagulopathy, severe anemia, or massive intravascular hemolysis.
- Cerebral malaria
- Onset: gradual or sudden following a convulsion
- Symptoms: impaired consciousness, delirium, and/or generalized seizures; focal neurologic signs are unusual
- Acute hemorrhagic meningoencephalitis
- High fever
- Severe headache, photophobia, nausea, vomiting, meningeal signs
- Behavioral abnormalities, smell and taste abnormalities
- Cranial nerve palsy
- Altered mental status, seizures
- Rapid progression and high mortality rate: rapid, profound alter mental status, severe cranial hypertension → herniation, and death in a few days.
- Acute phase
- Generalized lymphadenopathy
- Swelling at the bite site
- Unilateral painless edema of eyelids and periocular tissue.
- Chronic phase: mainly involved in cardiomyopathy, gastrointestinal tract.
- CNS involvement in a small percentage of patients in the acute phase. In the chronic phase, CNS involvement mainly presents as meningoencephalitis.
- Hemolymphatic phase
- Intermittent fever
- Painless cervical lymphadenopathy in the posterior triangle of the neck (Winterbottom’s sign)
- Cutaneous symptoms: erythematous, targetoid, nodular, ulcer
- Anemia, facial edema.
- Neurologic phase
- Behavioral changes: apathy, psychosis, confusion
- Daytime somnolence, nighttime insomnia
- Ataxia, rigidity
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