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Inhalation – Virus laden droplets Incubation 2-8 days (nasopharyngeal epithelium) Further 1-3 days – Spread through tracheobronchial tree Both upper and lower RTI Viremia is uncommon in immunocompetent hosts Infants/children more commonly affected
Airway inflammation Necrosis/sloughing of epithelium Oedema/excessive mucous production Croup (PIV1,2) Peaks between 1-2 yrs of age Swelling of vocal cords, larynx, trachea, bronchi Obstruction of inflow of air (Stridor) LRTI (PIV3) Alveolar filling Interstitial infiltration
Maternal antibodies usually not protective Neutralizing antibodies (protective humoral immunity) HN & F May not protect against re-infection 21 epitopes in PIV1 HN 20 epitopes in PIV3 F Repeated infections needed for full protection (implications in vaccine development)
Specimens: All used successfully Throat swab nasopharyngeal swab nasal wash nasal aspiratesTransport Swab/2-3ml washings VTM (2-3ml) (MEM with 0.5% BSA + antibacterials/antifungals) 4 °C If delay (Frozen – If delayed >24 hrs)
Serological diagnosis ELISA/RIA/HI/CFT/WB Drawback – cross reactivity among different PIV types CFT – least cross reactions (max specificity) but least sensitive ELISA – Most sensitive but least specific 4 fold rise to any PIV type – significant (even if heterologous antibodies +ve) – can not tell the subtypeAntigen detection Direct immunofluorescence Rapid but less sensitive than viral isolation Highly specific immune reagents (MAbs)required for serotype identification
Culture/Isolation Cell culture Primary monkey Kidney cells (best) Cynomolgus cell line CPE – 4-7 days – syncytia & roundening Identification & typing – IF – most rapid & accurate EGGS - Poor medium - Many repeated blind passages needed
Supportive Prevent secondary bacterial infectionsIn vitro trials with antivirals Neuraminidase inhibitor – Zanamivir Protein synthesis inhibitor – Puromycin Ascorbic acid Calcium enolateNovel approach Inhibitors of syncytia formation (synthetic peptides against F protein) Several immunostimulators tried (no significant outcome)
Respiratory syncytial virus is the most important cause of lower respiratory tract illness in infants and young children, usually outranking all other microbial pathogens as the cause of bronchiolitis and pneumonia in infants under 1 year of age.
RNA ss, unsegmented, negative sense 3 surface proteins G – Attachment (No HA & NA activity) F – Fusion 2 matrix proteins M, M2 3 Nucleocapsid proteins N, P & L F & G – Neutralizing Abs – Imp for vaccine development
Most common cause of bronchiolitis May also cause – Pneumonia/croup/pharyngitis/common cold Bronchiolitis Predominantly in infants Peak age – 2-6 months >80% cases in 1st year of life Often starts with rhinitis After 2-3 days – LRT symptoms appear Wheezing – Hallmark of bronchiolitis Flaring of nostrils, use of accessory muscles. Elevated respiratory rate – 50-80breaths / min. 1/3rd may be afebrile – fever does not indicate the severity
Cell culture Nasal swab, throat swab, tracheal aspirates nasopharyngeal aspirates – All tested for efficiency Nasal washes/aspirates – better than swabs Cell lines Human epithelial (HEp-2) – 8-10 days Human lung fibroblast (WI-38 or MRC 5) – 14 days Rhesus monkey kidney – 7 days CPE - Distinct syncytia formation - Balled up syncytia become detached & float freely Identification by – IFA (most common)
Antigen detection ELISA/IF assays Several kits available commercially IF -Best results with pool of antibodies to Fusion & Nucleoproteins - 91 % sensitivity ELISA - 79% sensitivityAntibody detection CFT/ELISA Poor sensitivity in infants
Bacterial superinfections infrequent – routine antibiotics not warranted Supportive care – fluids/electrolyte monitoring Bronchodilators- Conflicting reports, no beneficial role. Antivirals – Ribavirin - initial reports showed benefit - findings not confirmed - considered primarily in severe cases RSV-IGIV (RespiGam) - Passive transfer of specific antibodies - Prophylactic (premature, congenital heart disease)
100-150 nm RNA ss, negative sense Outer envelope proteins H –Attachment (CD46, CD150) F – Fusion M - Matrix
Natural infection only in humans Age : 6 months to 5 years old (maternal antibodies are protective) Air-borne transmission Highly contagious (90% attack rate in susceptible individuals) Permanent immunity acquired after disease – single serotype
Virus gains access via respiratory tract It multiplies locally Spreads to regional lymphoid tissue Further multiplication occurs Primary viremia disseminates the virus Then replicates in the reticuloendothelial system. A secondary viremia seeds the epithelial surfaces of the body where focal replication occurs skin respiratory tract conjunctiva. Multinucleated giant cells with intranuclear inclusions are seen in lymphoid tissues throughout the body
Characterized by Fever URT catarrhal koplik’s spots Maculopapular rash Seuence:behind the ear→along thehairline→face→neck→chest→back→abdomen→ limbs→hand and feet(palm,sole)
Antigen Detection Directly in epithelial cells in respiratory secretions and urine Nucleoprotein detection- The most abundant viral protein in infected cellsSerological Diagnosis fourfold rise in antibody titer between acute-phase and convalescent-phase sera Specific IgM antibody in a single serum specimen drawn between 1 and 2 weeks after the onset of rash ELISA, HI, and Nt tests all may be used
Isolation and Identification of Virus Samples Nasopharyngeal and conjunctival swabs Blood Respiratory secretions Urine Cell lines Monkey or human kidney cells Lymphoblastoid cell line (B95-a) Detection Cytopathic effects (multinucleated giant cells containing both intranuclear and intracytoplasmic inclusion bodies) take 7–10 days to develop Fluorescent antibody staining to detect measles antigens in the inoculated cultures.
General therapy: rest, nursing and diet Symptomatic therapy: fever and cough Support therapy : Vitamin A Treatment of complications Active immunization Lived attenuated measles vaccine.
Humans are the only natural hosts Acute contagious disease More than one-third of all mumps infections are asymptomatic. Primary replication occurs in nasal or upper respiratory tract epithelial cells. Viremia then disseminates the virus to the salivary glands and other major organ systems. Mumps is a systemic viral disease with a propensity to replicate in epithelial cells in various visceral organs.
The incubation period -2 weeks to 4 weeks A prodromal period of malaise and anorexia Rapid enlargement of parotid glands as well as other salivary glands. Hallmark - Nonsuppurative enlargement salivary glands. Virus is shed in the saliva from about 3 days before to 9 days after the onset of salivary gland swelling. Infected individuals who do not exhibit obvious symptoms (inapparent infections) are equally capable of transmitting infection. Mostly causes a mild childhood disease, but in adults complications including meningitis and orchitis are fairly common.
Central nervous system involvement – Aseptic meningitis (10-30% cases) Testes and ovaries may be affected, especially after puberty. Pancreatitis is reported in about 4% of cases
Immunity is permanent after a single infection. There is only one antigenic type of mumps virus It does not exhibit significant antigenic variation Antibodies against the HN antigen correlate well with immunity.(Protective )
Serology Fourfold or greater rise in antibody titer is evidence of mumps infection. Specific IgM in serum drawn early in illness strongly suggests recent infection The ELISA or HI test is commonly used
Isolation and Identification of Virus Samples Saliva Cerebrospinal fluid Urine Cell line – Monkey Kidney cell line Detection Cytopathic effects typical of mumps virus consist of cell rounding and giant cell formation Immunofluorescence
There is no specific therapy Supportive/symptomatic treatment Immunization with attenuated live mumps virus vaccine is the best approach