This section includes viruses not included in the previous sections which are important to know for USMLE. You need to know about oncogenic viruses and their mechanisms also which will be covered in 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. It mediates binding of 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. The virus spreads from the site of bite to the local nerves and via their axons to the spinal cord and brain. It forms eosinophilic cytoplasmic inclusions in the neurons. It multiplies in the neurons and then transmits down the peripheral nerves to salivary glands. It is shed in the saliva, milk and urine. Incubation period varies from 2 weeks to 6 months or more. It initially presents as fever, headache, anorexia proceeding to neuritic pain, fasciculations , tingling at the site of the bite followed by cerebral symptoms of encephalitis. Patients characteristically show hydrophobia as they are unable to swallow water as it precipitates 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 neck. 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 also called German Measles. It presents as fever and maculopapular rash starting on the face which spreads down to the extremities. The rash is not seen on the palms and soles. There is posterior auricular lymphadenopathy. Polyarthritis may be caused. Congenital rubella is seen in infants born to infected mothers. Earlier the stage of pregnancy at the time of infection, more is the damage to the fetus. The syndrome presents as 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.
It 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. Apart from being transmitted by 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. It is 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 gets in through broken skin or mucous membranes in the eyes, nose, or mouth. The virus can also spread to people 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 as 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 Arenavirus family. It is endemic in mice. It is transmitted to humans by food or water infected with mice urine or feces and by infected organ transplant. It clinically presents as a biphasic febrile illness. The initial phase, which may last as long as a week, 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. Virus can be detected by PCR or virus isolation in the CSF during the acute stage of illness.
They are infectious particles without any detectable nucleic acids. So technically, they are not viruses or microbes as such. They are proteinaceous particles that induce abnormal folding of specific, normal cellular proteins called prion proteins that are found most abundantly in the brain. The abnormal folding of the prion proteins leads to brain damage and the characteristic signs and symptoms of Prion diseases. They cause Prion diseases or 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 inflammatory response.
Sign up for free to take 2 quiz questions on this topic