Protozoan Diseases of the Nervous System

Only a few species of protozoa are important central nervous system pathogens for humans. One interesting example, Naegleria fowleri, causes primary amebic meningoencephalitis after penetrating the skull along the nerves responsible for the sense of smell. The protozoan occurs worldwide, but less than 200 cases have been reported, almost all rapidly fatal. The disease is usually acquired by swimming in or being splashed with warm fresh water, with or without chlorine, but apparently it can also be contracted by inhaling dust laden with cysts of the protozoa. For every case of Naegleria meningoencephalitis, many millions of people are exposed to the organism without harm. Naegleria fowleri can exist in three forms: ameba, flagellate, and cyst (see

25 mm

Figure 26.22 Trypanosoma brucei in the Blood Smear of an Individual with African Sleeping Sickness (African Trypanosomiasis)

Pathogenesis

During the bite of an infected tsetse fly, the protozoan enters the bite wound in the fly's saliva. The organism multiplies at the skin site and within a few weeks enters the lymphatics and blood circulation. The patient responds with fever and production of IgM antibody against the protozoa, and symptoms improve. Within about a week and at roughly weekly intervals thereafter, however, there are recurrent increases in the number of parasites in the blood. Each of these bursts of increased parasitemia, meaning parasites in the circulating blood, coincides with the appearance of a new glycoprotein on the surface of the trypanosomes. More than a thousand genes, each coding for a different surface gly-coprotein, are present in the protozoan chromosome. Only one of these genes is activated at a time, and the patient's immune system must respond to each gene product with production of a new antibody. The recurrent cycles of parasitemia and antibody production continue until the patient is treated or dies.

In T. brucei rhodesiense infections, the disease tends to progress rapidly, with the heart and brain invaded within 6 weeks of infection. Irritability, personality changes, and mental dullness result from brain involvement, but the patient usually dies from heart failure within 6 months. With T. bruceigambiense, progression of infection is much slower, and years may pass before death occurs, often from secondary infection. Much of the damage to the host is due to immune complexes formed when antibody reacts with complement and high levels of protozoan antigen. ■ immune complexes, p. 448

Epidemiology

African sleeping sickness occurs on the African continent within about 15° ofthe equator, with 10,000 to 20,000 new cases each year, including a number of American tourists. The occurrence of the disease is determined by the distribution of the tsetse fly vectors. The main reservoirs of the severe Rhodesian form of the disease are wild animals; for the milder Gambian form, humans are the main reservoir, and human-to-human transmission is more common than animal-to-human. Bites of the infected tsetse fly transmit the disease, but less than 5% of the flies are infected. ■ reservoir, p. 486

Prevention and Treatment

Preventive measures directed against tsetse fly vectors include insect repellents and protective clothing to prevent bites, traps containing bait and insecticides, and clearing ofbrush that provides breeding habitats for the flies. Populations can be screened for T. brucei infection by examining blood specimens. Treatment of infected people helps reduce the protozoan's reservoir. A single intramuscular injection of the medication pentamidine prevents the Gambian form of the illness for a number of months, although it will not necessarily prevent an infection that could progress at a later time. As with other eukaryotic pathogens, treatment is problematic because of toxic side effects of the available medications. Suramin can be used if the disease has not progressed to involve the central nervous system; melarsoprol and eflornithine cross the blood-brain barrier and can be used when the central nervous system is involved. ■ antiprotozoan medications, p. 528

26.6 Transmissible Spongiform Encephalopathies

Table 26.10 African Sleeping Sickness

Symptoms

Tender nodule at site of tsetse fly bite; fever, enlargement of lymph nodes; later, involvement of the central nervous system, uncontrollable sleepiness, headache, poor concentration, unsteadiness, coma, death

Incubation period

Weeks to several years

Causative agent

Trypanosoma brucei, a flagellated protozoan

Pathogenesis

The protozoa multiply at site of a tsetse fly bite, then enter blood and lymphatic circulation; as new cycles of parasites are released, their surface protein changes and the body is required to respond with a new antibody

Epidemiology

Bites of infected tsetse flies transmit the trypanosomes through fly saliva; wild animal reservoir for T. brucei rhodesiense

Prevention and treatment

Protective clothing, insecticides, clearing of brush where flies breed, pentamidine.Treatment: suramin; when central nervous system is involved, melarsoprol or eflornithine

The main characteristics of African sleeping sickness are presented in table 26.10.

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  • Semret Tesfay
    What is the causative agent for protozoan?
    3 years ago
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    HOW TO Causative tsetsefly?
    3 years ago

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