This section covers a few important viruses (and prions) that weren’t included earlier but are commonly tested on the USMLE. You should also know the major oncogenic viruses and their mechanisms; those are covered in more detail in Immunology and Oncology.
It belongs to the family Rhabdoviridae. It is a bullet-shaped, enveloped RNA virus. It has knob-like spikes made of glycoprotein G, which mediates binding of the virus to acetylcholine receptors in neural tissue. It has RNA-dependent RNA polymerase.
It is transmitted by the bite of rabid wild animals such as bats, skunks, raccoons, dogs, and cats. Exposure to aerosols of infected bats or corneal implants has also been known to cause rabies.
After inoculation at the bite site, the virus spreads to local nerves and then travels via axons to the spinal cord and brain. It forms eosinophilic cytoplasmic inclusions in neurons. It multiplies in neurons and then travels down peripheral nerves to the salivary glands. It is shed in saliva, milk, and urine.
The incubation period varies from 2 weeks to 6 months or more. It initially presents with fever, headache, and anorexia, progressing to neuritic pain, fasciculations, and tingling at the bite site, followed by cerebral symptoms of encephalitis. Patients characteristically show hydrophobia because they are unable to swallow water; attempts precipitate choking and laryngeal spasms. Seizures, paralysis, and coma are terminal findings.
Diagnosis is by fluorescent antibody staining of corneal smears or skin biopsy from the nape of the neck. The virus can be isolated from saliva, brain tissue, or CSF by animal inoculation and cell cultures. RT-PCR or dot blot hybridization can be used for nucleic acid detection. Antibodies can be detected in CSF or serum by ELISA. Corneal scrapings and postmortem brain biopsy from the hippocampus, brainstem, and cerebellum show characteristic intracytoplasmic, eosinophilic inclusions called Negri bodies.
It belongs to the family Togavirus. It is an enveloped, spherical RNA virus. The envelope has haemagglutinin peplomers. It is transmitted by respiratory droplets and transplacentally.
It causes rubella (German measles). It presents with fever and a maculopapular rash starting on the face that spreads down to the extremities. The rash is not seen on the palms and soles. Posterior auricular lymphadenopathy is typical. Polyarthritis may occur.
Congenital rubella is seen in infants born to infected mothers. The earlier the stage of pregnancy at the time of infection, the greater the fetal damage. The syndrome presents with cardiac defects like PDA, cataracts, mental retardation, deafness, hepatosplenomegaly, purpura, and growth retardation.
Laboratory diagnosis is done by antibody detection by ELISA and haemagglutination inhibition, and by isolation of the virus by cell culture.
Zika virus is a Flavivirus transmitted by Aedes mosquitoes. It is endemic in areas of Africa, South America, and Asia. In the USA, Florida and Texas reported local transmission of Zika virus by mosquitoes in 2016-17.
In addition to mosquito bites, perinatal, in utero, and possible sexual and transfusion transmission can occur. Symptoms are generally mild and include fever, rash, conjunctivitis, muscle and joint pain, malaise, or headache.
Zika virus infection during pregnancy can cause infants to be born with microcephaly and other congenital malformations, known as congenital Zika syndrome. Infection is associated with a risk of Guillain-Barré syndrome, neuropathy, and myelitis. As an arboviral disease, Zika virus is a nationally notifiable condition.
Laboratory diagnosis is made by nucleic acid amplification tests (NAAT) like RT-PCR and by Zika virus immunoglobulin IgM and IgG antibody testing. Plaque reduction neutralization tests (PRNT) are quantitative assays that measure virus-specific neutralizing antibody titers and are used as a confirmatory test.
Ebola virus was first discovered in 1976 near the Ebola River in what is now the Democratic Republic of Congo. It causes outbreaks mainly in African countries. Bats act as sources of Ebola virus.
Ebola virus spreads to people through direct contact with bodily fluids of a person who is sick or has died from the disease. The virus enters through broken skin or mucous membranes in the eyes, nose, or mouth. It can also spread through direct contact with the blood, body fluids, and tissues of infected fruit bats or primates. It can be transmitted through sexual contact.
The virus can persist in semen, breast milk, ocular (eye) fluid, and spinal column fluid. Clinically, it presents with fever, headache, myalgia, fatigue, diarrhea, vomiting, stomach pain, and bleeding tendencies with hemorrhages.
Laboratory diagnosis can be made by RT-PCR, rapid tests for Ebola protein antigen, or by ELISA for IgG and IgM. Remember that a related virus called Marburg virus causes a clinically similar syndrome.
It belongs to the Arenavirus family. It is endemic in mice. It is transmitted to humans by food or water infected with mouse urine or feces, and by infected organ transplant.
Clinically, it presents as a biphasic febrile illness.
The initial phase may last as long as a week and typically begins with any or all of the following symptoms: fever, malaise, lack of appetite, muscle aches, headache, nausea, and vomiting. Other symptoms appearing less frequently include sore throat, cough, joint pain, chest pain, testicular pain, and parotid gland pain.
During the second phase of illness, meningitis (fever, headache, stiff neck, etc.), encephalitis (drowsiness, confusion, sensory disturbances, and/or motor abnormalities such as paralysis), or meningoencephalitis (inflammation of both the brain and meninges) and acute hydrocephalus may occur. Long-term sequelae like deafness and arthritis can be seen.
Intrauterine infection can cause vision problems, mental retardation, and hydrocephalus in the newborn.
Laboratory diagnosis is usually made by detecting IgM and IgG antibodies in the CSF and serum. The virus can be detected by PCR or virus isolation in the CSF during the acute stage of illness.
Prions are infectious particles without any detectable nucleic acids, so technically they are not viruses or microbes. They are proteinaceous particles that induce abnormal folding of specific normal cellular proteins called prion proteins, which are found most abundantly in the brain.
Abnormal folding of prion proteins leads to brain damage and the characteristic signs and symptoms of prion diseases. They cause prion diseases (transmissible spongiform encephalopathies), which present as progressive neurodegenerative disorders with long incubation periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce an inflammatory response.
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