Virology-paramyxoviruses | quick Revision Notes for NEET-PG

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Mumps

MC cause of parotid gland enlargement in children

Pathogenesis

Transmission is through the respiratory route via droplets, saliva, and fomites———–> virus causes primary infection in nasal and upper respiratory mucosa————–>infects mononuclear cells and regional lymph nodes————->spills over to bloodstream————-> causes viremia————> dissemination————> mumps virus has special affinity for glandular epithelium of salivary glands, testes, pancreas, mammary gland, ovaries, and CNS.

Clinical manifestations

  1. IP period- 2-3 weeks
  2.  UP TO 50% of patients(adults>children) are either asymptomatic or present with fever, myalgia, anorexia, and other inapperent symptoms.
  3.  UP TO 90 % of cases present with non-suppurative bilateral(rarely unilateral) parotid gland enlargement.
  4. Unilateral(rarely bilateral) epididymo-orchitis- infertility following this is rare as only one side of the organ is affected
  5. Self- limiting aseptic meningitis
  6. Oophoritis
  7. Pancreatitis

LAB Dx

  1. Buccal/oral swab(most ideal-massage the parotid gland for the 30s prior to swabbing), saliva, CSF, urine, seminal fluid, blood———->innoculate the specimen directly onto monkey kidney cell lines———->wait for 1-2 weeks————–>viral growth can be demonstrated by the CPE/hemadsorption———>viral antigen detection by direct IF
  2. RT- PCR is used to detect mumps-specific PCR(specific and sensitive)
  3. Detection of IgM antibody(present up to 60 days after infection ) and rise in IgG titer using ELISA(most widely used assay)
 

Measles(rubeola virus)

Measles is an acute highly contagious disease of childhood characterized by fever and respiratory symptoms followed by a typical maculopapular rash

Pathogenesis

Transmission via resp. Tract through inhalation of droplet/aersols———->virus multiplies locally in the respiratory tract————>spreads to regional lymph nodes—–>enters into the bloodstream———>infects monocytes——>further multiplies in RES———–>spills over to blood(sec. Viremia)———–> disseminates to various sites———-> goes to target sites-epithelial surfaces of body like skin, resp. Tract and conjunctiva.

Clinical manifestations

IP- 10 days (average)

The disease can be divided into 3  stages

Prodromal stage

Eruptive stage

Post measles stage

10th-14th day

14th day of infection

After acute infection

    1. Fever on the 10th day of infection
    2. Koplik’s spot on the 12th day of infection which is characterized by white to a bluish spot of 1mm size surrounded by erythema which appears 1st on the buccal mucosa and spreads to involve the entire buccal mucosa and then fade with the onset of rashes
    1. Maculopapular dusky red rashes appear on the 14th day of infection which appears behind the ears then face, arm, trunk, legs and fade away in the same order in next 4 days
    1. It is characterized by it. Loss and weakness
    1. Nonspecific symptoms included redness of eye, diarrhea, cough, vomiting, etc
    1. Rashes are typically absent in HIV infected individuals
    1. Failure to recover can lead to gradual deterioration into a chronic illness.

Complications

Otitis media

Bronchopneumonia

Worsening of underlying Tb

Diarrhea leading to malnutrition

Giant-cell pneumonitis

Post-measles encephalomyelitis

Subacute sclerosing panencephalitis

LAB Dx

  1. Nasopharyngeal swab/conjunctival swab/blood/resp. Secretions/urine———->innoculate the specimen directly onto human kidney cell line/Vero cell line coated with measles-specific hSLAM receptor——> wait for 7-10 days————–>viral growth can be demonstrated by the CPE characterized by multinucleated giant cells k/a WARTHIN-FINKELDAY cells containing both intranuclear and intracytoplasmic inclusion bodies/hemadsorption———>viral antigen detection by direct IF
  2. RT- PCR is used to detect measles RNA(specific and sensitive)
  3. Detection of measles-specific IgM antibody(present up to 60 days after infection ) and 4 fold rise in IgG titer between acute and convalescent phase using ELISA(most widely used assay) using capture ELISA(IgM) and indirect ELISA(IgG) respectively is the most recommended test.
 

Respiratory syncytial virus

  1. Major respiratory pathogen of young children
  2. MC cause of lower respiratory infection in infants(below 1yrs of age)

Pathogenesis

Transmission of RSV via direct contact/droplet inhalation————>RSV replicates locally in the epithelial cells of nasopharynx———–>may spread to lower resp. Tract to cause bronchiolitis and pneumonia

Lymphocytes in large no. Migrate to the site of infection and secretes several cytokines which cause the following changes-

  1. Peribronchial infiltration of inflammatory cells
  2. Submucosal edema
  3. Necrosis of bronchial epithelium
  4. Formation of a plug(containing mucus, fibrin, cellular debris) occluding the lumen of smaller bronchioles

CLINICAL manifestation

  1. IP period- 3-5 days
  2. MC cause of lower respiratory infection in infants(below 1yrs of age) causing bronchiolitis, pneumonia, and tracheobronchitis
  3. Symptoms include running nose, fever, cough, wheezing, dyspnea, etc
  4. X-ray shows peri-bronchial thickening, diffuse interstitial infiltration, and lobar consolidation.
  5. RSV in adults produces symptoms like upper-rep influenza such as common cold, running nose, sore throat, and cough.
  6. It can cause worsening of asthma/COPD
  7. Recurrent infection is common but milder

LAB Dx

  1. Nasopharyngeal swab/conjunctival swab/blood/resp. Secretions/urine———->innoculate the specimen directly onto HeLa or Hep cell line———->wait for 10 days————–>viral growth can be demonstrated by the CPE–syncytium formation(multinucleated giant cell) appear and shell vial technique can be used to enhance viral replication so that viral growth can be detected within 1-2 days———>viral antigen detection by direct IF or ELISA
  2. RT- PCR is used to detects viral RNA(specific and sensitive)
  3. Detection of antibody using ELISA.

 

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