I I I I 1951 1955

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Table 26.7 Poliomyelitis


Headache, fever, stiff neck, nausea, pain, muscle spasm, followed by paralysis

Incubation period

7 to 14 days

Causative agents

Polioviruses 1, 2, 3, members of the picornavirus family


Virus infects the throat and intestine, circulates via the bloodstream, and enters some motor nerve cells of the brain or spinal cord; infected nerve cells lyse upon release of mature virus


Spreads by the fecal-oral route; asymptomatic and nonparalytic cases common

Prevention and treatment

Prevented by injecting Salk's inactivated vaccine, or by Sabin's orally administered attenuated vaccine in areas of epidemic or endemic disease.Treatment: artificial ventilation for respiratory paralysis; physical therapy and rehabilitation

Figure 26.18 Incidence of Poliomyelitis in the United States, 1951 to 1998 Ironically, since 1980, all cases acquired in the United States have been caused by the oral attenuated (Sabin) vaccine.

Causative Agent

The cause of rabies is the rabies virus (figure 26.19a), a member of the rhabdovirus family. This virus is about 180 x 75 nm in size, has a striking bullet shape, is enveloped, and contains single-stranded, negative-sense RNA. It buds from the surface of infected cells.


The principal mode of transmission of rabies to humans is via the saliva of a rabid animal (figure 26.19b) introduced into bite wounds or abrasions of the skin. Rabies can also be contracted by inhaling aerosols containing the virus, such as from bat feces. Only a few details of the events that follow introduction of the virus into the body are known. During the incubation period of the disease, the virus multiplies in muscle cells and probably other cells at the site of infection. Knoblike projections on the viral surface attach to receptors in the region where the nerve joins the muscle. At some point, the virus enters an axon and is carried along the course of the nerve by the normal flow of the axon's cytoplasm, eventually reaching the brain. The long incubation period, usually 1 to 2 months but sometimes exceeding a year, is partly determined by the length of the journey to the brain. Patients with head wounds into which the virus is introduced tend to have a shorter incubation period than those with extremity wounds. Severe wounds and those with a large amount of introduced rabies virus also generally result in short incubation periods. The virus then multiplies extensively in brain tissue, causing the symptoms of encephalitis. Characteristic inclusion bodies, called Negri bodies (figure 26.20), form at the sites

75 nm

20 mm

Figure 26.20 Stained Smear of Brain Tissue from a Rabid Dog The arrow points to one of several Negri bodies within the triangular-shaped nerve cell.The Negri bodies represent the sites of rabies virus replication.

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