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Bronchitis and bronchiolitis inflammatory processes of tracheobronchial tree that donot involve the pulmonary alveoli . Acute bronchitis seen in all ages Common in young and old Also called-acute tracheobronchitis Bronchiolitis –disease of the infants ? Chronic bronchitis Differentiation between bronchitis in healthy patients and those with underlying structural lung disease Patients with chronic obstructive pulmonary (related to smoking)may have excessive sputum production known as chronic bronchitis Leads to acute exacerbation of chronic bronchitis(AECB) Clinical diagnosis of AECB made on patient’s iincreased sputum, cough,increased sputum purulence,increased shortness of breath. Presence of two f the three symptoms, -gives bacterial aetiologycontroversial But with antibiotics-improvement A 34 yr old physician developed symptoms of cough, myalgias and headache made worse by coughing, substernal chest pain and high fever. She suspected influenza because an outbreak was in progress and she had recently cared for several patients with similar symptoms, During the next 3 days, she was bed ridden because of weakness and temp of 38,9c. The symptoms gradually resolved over the next few days without treatment After 10 days,,she resumed her usual activities. A viral throat culture she took on first day of illness confirmed the diagnosis of influenza. Do most cases of tracheobronchitis resolve on their own or are antibiotics usually required? Causative agents of bronchitis: RhinoV,CoronaV( URT) InfluenzaV,AdenoV,M pneumonae(LRT S pneumoniae, H influenzae –sec inf Chlamydia pneumoniae-5% B pertussis, S typhi, Measles V,S pyogenes- bronchitis may be part of symptoms. Seen after URT inf with extension into the bronchial tree Common in winter months Predisposing factors in children-poor nutrition,allergy,deficiences in IgG subclasses. Older predisposed have emphysema or chronic resp dis like TB Manifestations: Malaise,head ache, coryza ,sore throat Nonproductive cough –with time mucopurulent Substernal pain,moderate fever diagnosis: differentiation between bronchitis, viral or mycoplamsal pneumonias – possible from Roentgenograminfiltrates with atypical pneumonias If fever elevated,bacterial bronchitis In young & old with predisposing conditions,Atelectasis, bronchiectasis and pneumonia seen Treatment: symptomatic and supportive unless Sputum is purulent and fever present demonstration of bacteria- antibiotics Prevention: no measures An Influenza virus and B pertussis vaccine available. Chronic bronchitis Inf is only one component Cough and excessive mucus secretion Cigaratte smoking,inhalation of dust or fumes S pneumoniae, unencapsulated H influenzae –isolated-significance not known Bronchiolitis Acute viral self limiting infection Seen mostly in infants < two yrs 75% -RSV Influenza,AdenoV,Rhino,Parainfluenza (type 3), M pneumoniae No predisposing factors Extension of inf from URT to the bronchioles Inflammation of the lining cells of the bronchioles restricts air passage to and from the alveoli. Following URT inf, coryza and cough. Moderate fever, disease progresses to dyspnea,cyanosis,suprasternal and intercoastal retractions during inspiration seen,wheezing (musical crackles) Diagnosis: Demonstartion of Ag in sputum or in cultures, serological tests RESPIRATORY SYNCYTIAL VIRUS ARI & Pneumonia –deaths of4 million children < 5yrs of age-world-wide every year (WHO) Imp cause of bronchiolitis &pneumonia in infants and young children 25% of paediatric hospitalisations due to respiratory disease Paramyxovirus- Group A , Group B PATHOGENESIS: replicates in ep cells of nasopharynxspread to LRT bronchiolitis,Pneumonia lymphocyte migration resulting in peribronchiolar infiltration,submucosal tissues become edematous,plugs of mucus,celluar debris,fibrin occlude smaller bronchioles Viral ags detected in URT &shed epi cells In plugs Incub period: 3-5 days,viral shedding for 1-3 wks in infants & young children .In adults -1-2 days Patients with impaired CMI may be more infected Clinical findings: Ranges from inapparent inf to common cold through pneumonia in infants to bronchiolitis in very young babies 1/3rd of LRT inf by RSV needs med attention 2% of inf babies need hospitalisation Peak mortality at 3 months of age Mortality has reduced –paed ICU If RSV imposed on CHD,cystic fibrosis-mortality high Reinf common in children ,adults-URT RSV infs account for 1/3rd of resp infs in bone marrow transplant patients Pneumonia in half of infected immunocompromised children & adults.-mortality 20-80% Infs in elderly in long care – Pneumonia in 5-10% among 10-20% infected-mortality 2-5% Children who suffered with RSV – bronchiolitis,Pneumonia as infantswheeze for many yrs. RSV causes otitis media . Immunity: Maternal Neutralising abs protective first several months Severe RSV seen in infants 2-4 months Primary &reinfection occur in presence of neutralising abs. Serum & secretory(IgA,IgG) abs are produced as response to RSV inf. CMI is imp in recovery from inf. Viral lab diagnosis: Isolation of virus –less common detection of ag (IF or ELISA – smears of exfoliative cells obtained from nasopharyngeal lavage) PCR for viral RNA treatment: supportive Ribavirin-LRT inf aerosol 3-6 days Vaccines: ??? hope WHOOPING COUGH ( B pertussis) Acute & serious inf of the LRT in childhood. Worldwide with 1 million deaths in underdeveloped countries Confined to only Man Spreads by airborne droplets Bordet-gengou medium +Penicillin G Pathogenesis: Number of toxic factors Filamentous haemagglutinin –adherence to ciliated ep cells of URT Pertussis toxin promotes lymphocytosis,sensitisation to histamine,enhanced insulin secretion,disrupts signal transduction to host cells Adenylate cyclase toxin brings about inhibition of chemotaxis,phagocytosis and bactericidal killing by neutrophils Tracheal cytotoxin inhibits DNA synthesis in ciliated cells. Hemolysin ,dermonecrotic toxins &lipopolysaccharide in the cell wall cause damage to ep cells of URT Organism adheres,multiples on ep cells of trachea & bronchi. Blood not invaded Bacteria liberate toxins that irritate surface cells causing cough&lymphocytosis Necrosis of epi,PMN infiltration with peribronchial inflammation and interstitial pneumonia Sec invaders Staph or H influenzae – bact pneumonia Obstruction of bronchioles by mucus plugs –atelectasis +diminished Oxygenation of blood-responsible for convulsions in infants clinical manifestations: Incub period 1-3 wks Catarrhal illness-mild cough,sneeze-urt Highly infectious – lasts for 1 week Paroxysmal stage- series of short coughs with copious mucus, followed by ‘whoop’– characteristic sound produced by an inspiratory gasp of air.This leads to exhaustion with vomiting,cyanosis ,convulsions WBC count is high(16,00030,000/microlitre)-with lymphocytosis Complications-segmental or lobar collapse of lungs,CNS anoxia,sec pneumonia due to invasion of damaged resp tract by other pathogens. Diagnosis suspected only during this stage . This stage blends into convalescent phase for months Diagnosis: Saline nasal wash,nasopharyngeal swab,cough plate method IF staining for bordetella/aggln with antiserum PCR Prognosis: Dependent on age,state of health,supportive care available US-children-pneumonia-20%,seizures2.5%,death-0.7% Treatment: Supportive care Admission to hospitals to infants at greater risk-, <1 yr old Erythromycin-paryoxsmal stage-reduce severity +duration+infectivity in throat Erythromycin to close contacts –control spread of inf Prevention: Whole cell vaccine(killed) –DPT Side effects: fever,malaise,pain at the site-20% infants Convulsions-0.5% of vacinees Encephalopathy & permanent neurologic damage- <0.01% Acellular vaccines: 5 antigens-5 doses -inactivated pertussis toxin+filamentous haemagglutinin- DTaP Prophylactic Erythromycin-5 days to unimmunised infants or heavily exposed adults. Schedule in US: Birth– Hep B 2-6 months-polio,diphtheria,pertussis,tetanus,Hib 12-18months Measles,mumps, rubella,varicella,pneumococcal vaccine 10-16yrs tetanus, diphtheria 0ver 50 yrs influenza(> 50yrs) Pneumococcal vaccine( > 65 yrs) PARAINFLUENZA Croup, LRT, Pneumonia in children Paramyxoviruses-4 types Surface spikes composed of HA+neuraminidase –one type of spike fusion proteins –on another spike Spread by droplets Para 1-3 cause pharyngitis,croup,otitis media,bronchiolitis,Pneumonia Type 4 –mild common cold INFLUENZA Orthomyxovirus fly Segmented single stranded RNA,helical nucleocapsid,outer lipoprotein,RNA dependent RNA polymerase Two glycoprotein spikes-H,N Based on internal ribonucleoprotein(RNP) – Grp specific antigen– A B C Types A –epidemics,occassionally pandemics Reservoir in birds B- only epidemics-no animal hosts C – only minor respiratory illness changes in antigenicity of HA and NA Proteins contributes to their capacity to cause devastating worldwide epidemics Ag drifts:AND Ag shifts Group specific ags-RNP– A B C types Type specific ags- HA & NA Abs against HA neutralises infectivity of virus and prevents disease but Abs against RNP does not Abs against NA doesnot neutralise but reduces disease. Influenza A –also found in animals aquatic birds,chickens, swine, horses Act as a source of RNA segments that code the ag shift variants that cause epidemics among man. Eg: if avian and human influenza V infect the same cell(RT) of a farmerreassortment occurs and a new variant of human A virus with avian virus HA may appear. Epidemic flu is cyclic –type A or type B Type A epidemics- occur every 2-3 yrs Type B epidemics- occur every 4-6yrs Epidemics seen during late autumn to early spring Mortality is 1% Complications like pneumonia seen in very young,very old,pregnant women,persons with underlying cardiopulmonary,metabolic,renal diseases Terminology: A/Ann Arbor/1/86 All mammalian Influenza viruses are derived from birds(avian) H1N1 & H3N2 – most common and included in the current vaccine. Pathogenesis: Droplets inhaled virus attaches to ep cells of tracheobronchial tree->desquamation of ciliated ep,edema,congestion,increased secretions Pneumonic complications due to sec inf with bacteria( S aureus) Incub period- 1-4 days Adults –infectious for 5 days Children->= 10days Young children<= 6 days Immunocompromised –wks to months Abrupt onset with fever, chilliness,rigors, head ache, congested conjunctiva,myalgia in the back and limbs,nonproductive cough Among children,otitis media,nausea, Vomiting Fever subsides in 3-4 days –recovery in a week Cough and malaise -2 wks In debilitated-persistent fever,cough with rales,pneumonia (sec bacterial-S aureus, H influenzae,Strepto pyogenes,Strepto pneumoniae. Diagnosis: Confused with other RTinfs. --common cold –afebrile with coryza --ARdisease by adenoV-difficult to differentiate --Atypical pneumonia from influenza pneumonia- here its rapid in onset based on isolation of virus/serological tests,flourescent ab test Prognosis: Uncomplicated –recovery complete Complicated in patients with underlying diseases.pregnant women Pneumonia and death Influenza is related to underlying med conditions ( pul or cardiac)and lead to sec bacterial or primary influenza pneumonia. Assoc with encephalopathy,Reye syndrome,myositis,myocarditis Antipyretics and analgesics Amantadine,zanamivir-antiviral drugs prevention: Vaccination – 2 A’s ,1B+ antiviral drug in high risk group persons aged > 50 yrs Residents of nursing homes and other chronic care that house persons of any age who have chronic medical conditions adults ,children who have chronic disorders of pul or cardiovas systems including asthma Adults, children who have reqd regular medical followup or hospitalisation during preceding yr because of chronic metabolic diseases(including diabetes mellitus) ,renal dysfunction,hemoglobinopathies,or immunosuppression Children and teenagers (6 mths 18yrs) receiving long term aspirinand therefore might be at risk of developing Reye syndrome after influenza inf Women who will be in the second or third trimester of pregnancy during influenza season.
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