By Levi Clancy for Student Reader on
Parainfluenza virus (PIV)
It has only one RNA segment, meaning all genetic information is in one long RNA strand. It is an enveloped virus, which makes it very unstable. These envelopes are part of the cell membrane of the mamallian cell. The wall is unstable and easily dissolved, unlike polio which has a protein capsid and is very stable in the environemnt. Enveloped viruses tend to be very unstable because the bilayer is easily degraded. The viral attachment protein extends through the envelope, and without the envelope the virus is left with a very stable capsid that is uninfectious. It is unable to infect the mamallian cell because it lacks the viral attachment proteins in the bilayer.
Transmission Parainfluenza is transmitted via sneezing, virus shedding, and contact with eyes and nose. It gets into upper respiratory tracts and the trachea swell, resulting in croup. There is no vaccine for parainfluenza virus. It is mostly a pediatric virus.
Respiratory syncytial virus
Respiratory syncytial virus fuses membranes together to make enormous cells (fused aggregates). These aggregates get into alveoli of the lower respiratory tract, and the patient has trouble breathing out. It is more invasive than parainfluenza virus, as it goes deeper into the lungs, and is responsible for a lot of infant pneumonia. There is no vaccine.
Mumps virus is a member of the genus Paramyxovirus. It causes distinctive and generally benign system infections characterized by fever and parotitis (parotid inflammation, a salivary gland below the ear).
Epidemiology It is a disease of school-aged children worlwide. In unvaccinated populations, 92% of children have antibodies by age 15. A mumps vaccine was licensed in the U.S. in 1967, and it has reduced mumps infections to only 1,500 cases annually. Mumps is highly contagious. The virus infects epithelial cells of the upper respiratory tract, then spreads to regional lymphnodes. A viremia (bloodborne virion) spreads the virus to glandula and neural tissues.
Clinical Manifestations Up to 30% of mumps are asymptomatic. Symptoms include fever, malaise, and headache. After an 18 day replication phase of local replication and viremia, patients complain of ear pain and swollen salivary glands. CNS involvement is the most common extra-salivary manifestation, and occurs 10-30% of cases. It is 3-4 times more likely to occur in males than females for unknown reasons. Mumps CNS presents with high fever, vomiting, and headache lasting 48-96 hours. Maternal mumps infections during the first trimester of pregnancny may increase likelihood of spontaneous abortion.
Complications Mumps can effect gonads of both sexes. Testis inflammation (orchitis) is usually unilateral. Patients with mumps orchitis prsent with severe testicular pain and swelling, accompanied by high fever, nausea, vomiting, and headache. Testicular atrophy may follow orchitis in 35-50% of cases, but impotence or sterility is rare. Ovarian inflammation (oophoritis) occurs in 5% of postpubertal women with mumps. Patients typically report fever, nausea, and vomiting. Sequellae are uncommon, but impaired fertility can occur.
Prevention Children with mumps are usually isolated for 1 week after appearance of parotitis, even though this has dubious benefit since the virus is shed via respiratory secretions for several days before onset of clinical symptoms. In the U.S., the Jeryl-Lynn B strain of live virus is used for vaccination, following attenuation by serial passage in embryonated eggs. The mumps vaccine is a component of the MMR vaccine (measles, mumps, rubella).
Measles virus is a member of the genus Morbillivirus within the family Paramyxovirus. Measles virus differes from other members of the family in that it lacks neuraminidase. There is only one measles serotype, so recovery from natural infection confers lifelong immunity. Measles is one of five childhood exanthems, the others being rubella, varicella, roseola and fifth disease. Humans are the only known host for measles virus.
Epidemiology Measles is one of the most contagious human diseases. Vaccination has reduced the global incidence of measles, yet the World Health Organization reports there are still 45 million cases annually and 1.2 million deaths.
Transmission The principal mode of transmission is via large droplets of infected respiratory secretions inhaled during face-to-face exposure with coughing and sneezing individuals. This occurs during the catarrhal stage of the disease.
Pathogenesis Natural infection is initiated when measles virus reaches epithelial cells in the respiratory tract, oropharynx, or conjuctivae. During the first 2-4 days, the virus replicates locally and spreads via macrophages to draining lymph nodes, where further replication occurs. The virus then enters the bloodstream, producing a 1Âº viremia that spreads the virus throughout the reticuloendothelial system. Lymphoid hyperplasia occurs, and giant cells form due to cell fusion promoted by viral proteins. Further replication at these sites occurs, producing a secondary viremia of increasing magnitude that begins 5-7 days post-infection and spreads the virus to tissues throughout the body. During this 2 viremia, the virus is carried within leukocytes, more than 5% of which may be infected.
Clinical Manifestations Measles virus infection is rarely subclinical. The initial incubation period is clinically silent. Slight fever, malaise, and faint rash may occur in primary viremia. The prodromal stage of measles begin 8-12 days post-infect with fever, malaise, and anorexia followed by coryza (acute nasal congestion caused by secretion of mucus), conjunctivitis, sneezing, and cough. Catarrhal symptoms increase in intensity on or about the 5th day. Coryza is intense, with profuse mucopurulent nasal discharge. There is palpebral conjuctivitis with lacrimation (abnormal and abundant shedding of tears). Severe coughing with a brass, barky quality ensues. 2-3 days before onset of rash, Koplik's spots appear on inside of mouth. Kolplik describe them as 1-3 mm small irregular bright red spots with a minute bluish white speck at center. The rash begins 3-4 days after prodromal symptoms. The lesions appear behind the ear, on the forehead and on the upper part of the neck. They spread downward over the face, neck, and extremities, reaching the feet by the 3rd day.
Clinical Diagnosis Measles can be diagnosed by isolates virus in cell culture from respiratory secretions, nasopharyngeal and conjuctiva swabs, PBMC, and urine as well as tissue biopsies. One can see giant cells characteristic of measles virus infection, or use specific antisera RT-PCR of the RNA.
Treatment Treatment of uncomplicated measles is symptomatic and includes bed rest, hydration, and antipyretics as needed. There is no antiviral therapy. The MMRV viaccine or a monovalent MV vaccine is used.
Composition: Live attenuated virus.
Measles: Schwartz or Moraten substrains of Edmonston B strain.
Mumps: Jeryl Lynn strain.
Rubella: RA/27-3 strain.
Vaccination schedule: at 12-15 months and again at 4-6 years or before middle school.
Efficiency: 95% lifelong immunization with a single dose.