Parasitic Infections

Gustavo C. Román

INTRODUCTION

Parasitic infections are a tremendous public health burden in tropical and subtropical regions. Parasitic tropical diseases of the nervous system can be found anywhere in the world due to the exponential increase in international travel, tourism, and migration. One important factor is the disregard of tourists and business travelers for the prophylactic measures recommended before traveling to parts of the world where potential exposure to endemic parasitic diseases may occur. When travel history precedes the onset of the disease, neurologists should have a high index of suspicion based on basic knowledge of the most common parasitic neurologic diseases (Table 65.1) in order to diagnose and treat these exotic conditions.

TABLE 65.1 Parasitic Infections of the Nervous System

Name	Agent	Reservoir	Transmission
Metazoan Infections
Neurocysticercosis	Taenia solium	Pigs, humans	Human Taenia carriers
Gnathostomiasis	Gnathostoma spinigerum	Fish, poultry, dogs, cats	Undercooked fish, poultry
Hydatid cysts	Echinococcus species	Dogs, foxes, sheep, cows	Dogs’ feces
Larva migrans	Toxocara canis, Toxocara cati, Ascaris species	Dogs, cats	Dogs’ and cats’ feces
Baylisascariasis	Baylisascaris procyonis	Raccoon (Procyon lotor)	Raccoons’ feces
Paragonimiasis	Paragonimus westermani	Fresh water crustaceans, snails	Eating uncooked crustaceans
Schistosomiasis/bilharziasis	Schistosoma species	Fresh water snails	Skin penetration by larval forms (cercariae) in infected water
Sparganosis	Spirometra mansoni	Reptiles, amphibians	Eating uncooked frogs or snakes
Strongyloidiasis	Strongyloides stercoralis	Human	Infected soil contact
Trichinosis	Trichinella spiralis	Pigs	Eating undercooked pork
Protozoan Infections
African trypanosomiasis Sleeping sickness	Trypanosoma brucei	Ungulates	Tsetse flies (Glossina)
American trypanosomiasis Chagas disease	Trypanosoma cruzi	Opossum, dogs	Triatomine bugs
Amebiasis	Entamoeba histolytica	Human	Ingestion of food contaminated with feces
Primary amebic meningoencephalitis	Naegleria species	Warm fresh water ponds	Nasal route while swimming
Granulomatous amebic encephalitis	Acanthamoeba species	Fresh and brackish water	Nasal route while swimming
Cerebral malaria	Plasmodium falciparum	Human	Anopheles mosquitoes
Toxoplasmosis	Toxoplasma gondii	Cat	Cats’ feces in contaminated soil or vegetables

Parasitic diseases are divided into protozoan infections caused by unicellular organisms (malaria, trypanosomiasis, amebiasis) and metazoan infections caused by worms (helminths), mainly cestodes or tapeworms (cysticercosis), nematodes or round worms (larva migrans, baylisascariasis, gnathostomiasis, strongyloidiasis), and trematodes or flukes (paragonimiasis). Not included in this chapter are neurologic diseases transmitted by ectoparasites, such as ticks and other arthropods, including Lyme disease (a spirochetal infection caused by Borrelia burgdorferi) (see Chapter 64); other forms of borreliosis presenting as relapsing fevers transmitted to humans by lice or ticks (see Chapter 64); and gram-negative bacterial infections, such as the Rickettsial typhus group (caused by Rickettsia prowazekii and Rickettsia typhi, transmitted respectively by the body louse Pediculus humanus and the rat flea Xenopsylla cheopis), as well
as the spotted fevers transmitted by ticks and caused by Rickettsia rickettsii (see Chapter 63). Toxoplasma gondii infection is discussed in the context of HIV infection (see Chapter 67).

PROTOZOAN INFECTIONS OF THE NERVOUS SYSTEM

CEREBRAL MALARIA

Cerebral malaria is an acute encephalopathy caused by Plasmodium falciparum, the most virulent of the four Plasmodium species that infect humans when a female Anopheles mosquito inoculates the protozoan parasites through the skin. Parasites are carried to the liver where they mature and multiply to enter the red cells in the bloodstream.

According to the Centers for Disease Control and Prevention (CDC), malaria causes 660,000 deaths each year, mainly among young children in sub-Saharan Africa. In 2011, the number of malaria cases reported in the United States was the largest since 1971, representing a 48% increase from 2008. Most malaria infections occurred among travelers to regions with active malaria transmission.

Clinical Features

Malaria presents with typical bouts of intermittent fever with chills, rigors, and anemia. Cerebral malaria may be heralded by headache, vomiting, and a clinical picture of encephalopathy developing over days in a febrile patient, accompanied by confusion, decreased responsiveness, and somnolence rapidly progressing to stupor and coma. Psychomotor agitation and psychiatric manifestations may precede cerebral malaria. Focal findings are uncommon, except when stroke occurs. In children, tonic-clonic seizures occur, followed by postictal unresponsiveness.

In adults, cerebral malaria may occur in the setting of severe malaria presenting with acute respiratory distress; pulmonary edema; acute renal failure and hemoglobinuria (“blackwater fever”); jaundice and liver failure; severe anemia; thrombocytopenia; disseminated intravascular coagulation; and bleeding complications, including intracranial hemorrhages. Severe hypoglycemia must be assumed to be present in children with cerebral malaria and should be treated promptly and aggressively.

Retinal hemorrhages and exudates are usually seen on funduscopic examination and reflect the cerebral small-vessel vasculopathy. Meningeal signs do not occur and cerebrospinal fluid (CSF) is normal; however, spinal tap is mandatory to exclude other causes of encephalopathy. Brain imaging may show evidence of brain swelling and herniation or small hemorrhages.

Treatment

The drugs of choice for treatment of cerebral malaria are the derivatives of artemisinin, such as artesunate, artemether, or arteether. Quinine is an equivalent alternative for cerebral malaria. Development of drug resistance to artemisinin derivatives has occurred and combination therapy for P. falciparum malaria with other antimalarial drug is recommended. Cerebral malaria is a critical condition and requires intensive care treatment; complications such as hypoglycemia, respiratory distress syndrome, and acute renal and liver failure must be promptly recognized and treated. Severe anemia or bleeding diathesis may require blood transfusions. Steroids are not recommended in cerebral malaria. Despite treatment, the mortality is over 25%, but survivors usually recover without sequelae; however, residual hemiplegia, extrapyramidal symptoms, blindness, psychiatric symptoms, and epilepsy may occur.

There is intensive research on the immune mechanisms of cerebral malaria leading to vascular occlusion by parasitized erythrocytes, vasoconstriction, and alterations of the blood-brain barrier with decreased cerebral blood flow, edema, demyelination, ischemia, hypoxia, acidosis, and death. Potential therapies based on nitric oxide bioavailability, high levels of endothelin-1, and angiopoietin dysfunction appear promising.

Malaria prevention relies on avoiding exposure to mosquitoes using repellents and insecticide-treated bed nets and prophylactic use of antimalarial drugs prior to, during, and after travel to endemic malaria regions. A viable malaria vaccine is yet to succeed.

Only gold members can continue reading. Log In or Register to continue