3 rd march.2015.physiology module dr jalees khalid khan pathology deptt. kemu. lahore

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An overview of bacterial and viral infections of the upper respiratory tract.Injury to mucociliary apparatus 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

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Page 1: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

An overview of bacterial and viral infections of the upper respiratory

tract.Injury to mucociliary apparatus

3rd March.2015.Physiology moduleDr Jalees Khalid Khan

Pathology Deptt. KEMU. Lahore

Page 2: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Upper respitaory infections

Upper respiratory tract infections are the most common human affliction.Major share of time lost from work and school.Most common cause of antibiotic abuse.

Page 3: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Figure 21.1

Page 4: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

• Generally limited to the upper respiratory tract• Gram-positive bacteria (streptococci and

staphylococci) very common• Disease-causing bacteria are present as

normal biota; can cause disease if their host becomes immunocompromised or if they are transferred to other hosts (Streptococcus pyogenes, Haemophilus influenza, Streptococcus pneumonia, Neisseria meningitides, Staphylococcus aureus)

• Normal biota perform microbial antagonism

Normal flora of respiratory tract

Page 5: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

• Most common place for infectious agents to gain access to the body

• Upper respiratory tract: mouth, nose, nasal cavity, sinuses, pharynx, epiglottis, larynx

• Lower respiratory tract: trachea, bronchi, bronchioles, lungs, alveoli

• Defences– Nasal hair– Cilia– Mucus– Involuntary responses such as coughing, sneezing, and

swallowing– Macrophages– Secretory IgA against specific pathogens

Respiratory tract

Page 6: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

InfluenzaEpiglottitisSinusitisThe Common ColdDiphtheria

Diseases

Page 7: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Nosocomial infections-indisciminate use of drugs by doctors and quacks.

Drug resistance-causes Cell wall alteration, Plasmid, ESBL,Efflux

pump etc Lysogenic strains MRSA and others

The significance in relationship with antibiotic abuse

Page 8: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Pandemics Worldwide - antigenic shift

Epidemics Local - antigenic drift Endemic Sporadic Seasonal Winter months - abrupt Age Infection: children

>adultsMortality: adults >children

Epidemiology

Page 9: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Virus replication: 24 - 72 hours

Virus excretion: 3 - 7 days

Antibodies to HA, NA subtypes

Pathogenesis

Page 10: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

S. pneumoniae

H. influenzae

S. aureus - Toxin Shock Syndrome

Secondary bacterial pathogens

Page 11: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Post influenza B Encephalopathy Hepatic dysfunction Elevate NH3, LFTs, CPK Children:Streptococcus pneumoniae

◦ Most common cause outside of neonatal period◦ Nasopharyngeal colonization – 50% of kids◦ >90 serotypes – majority of invasive disease caused by 10

serotypes◦ Bacteremia in 25-30% of kids◦ Gram stain – gram positive lancet shaped diplococci (“gram

positive cocci in pairs”)

Reye’s syndrome

Page 12: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Adults – lobar pneumonia

Kids – lobar or bronchopneumonia

Age differences

Page 13: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Classically a lobar consolidation on CXR Raise suspicion of staph

◦ Pneumatoceles◦ Pleural effusion◦ Air fluid levels◦ Necrosis

Diagnosis

Page 14: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Changes in alveolar epithelial-ciliated columnar to pseudostratified/columnar epithelium

Inefficiency of cilia to expel the debris,contaminants,carbon etc inhaled from atmosphere

Emphysema, COPD, Bronchiectasis,Carcinoma of lung

The effect of cigarette smoke or gaseous inhalation on respiratory tract

Page 15: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Influenza Vaccine

Trivalent vaccineA/Beijing/262/95-like (H1N1)A/Sydney/5/97-like (H3N2)B/Harbin/07/94

Page 16: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Elderly (age>65) High-risk* Household contacts Health-care personnel Pregnant women after 14th week

High-risk: institutionalized, chronic heart or lung disease, diabetes,

renal dysfunction, immunosuppressed, children on aspirin

Indications for Vaccine

Page 17: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Killed vaccines Live vaccines Live vaccines are long acting while short acting

are killed vaccines Immunization

◦ Measles – Pneumonia is what they die of – often super-infection World-wide coverage rate – 76% in 2004 Still having 30-40 million cases a year

◦ HemophilusInfluenzae B – 2-3 million cases of severe disease a year In 2003, developed world coverage – 92% Developing world – 42% Least developed countries – 8%

The significance of vaccination,the target groups that should be vaccinated, frequency and side effects

Page 18: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Influenza Vaccine

Timing: October - Mid-November

Duration of immunity:

start 1-2 weeks end 4-6 months

Page 19: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Prozone phenomenon Serum sickness Fever, lymphadenopathy Severe anaphylactic reation Defective vaccine production-NIH DPT-not properly killed

Side effects

Page 20: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Diagnosis

*Viral culture – tissue culture *Fluorescent-labeled murine monoclonal Ab - shell viral cell culture - viral Ag*PCR*CF - at onset and 2 weeks 4-fold-rise in Ab titre

Page 21: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Control of outbreaks in institutions Adjunct to late vaccination Immunodeficient - AIDS Vaccine contraindicated Home caregivers of high risk

Prophylaxis of Influenza A

Page 22: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Epidemiology: ◦ most common in children 3-7 yrs.◦ decreased incidence because of Hib conjugate

vaccine-stable rate in adults Rate:

◦ 1 in 1000-2000 pediatric admissions◦ 1 in 100,000 adult admissions

Epiglottitis

Page 23: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Peritonsillar abscess◦ sore throat, drooling, hoarseness, trismus, asymmetric

tonsillar enlargement Epiglottitis

◦ Children: high fever, toxic, drooling, absence of cough ◦ Adult: severe sore throat, dyshagia, fever

Infectious mononucleosis◦ tonsillar enlargement, exudative tonsillitis, pharyngeal

inflammation, lymphadenopathy, splenomegaly, maculopapular rashes, petechial anathema

Parapharyngeal space infection◦ neck swelling after a sore throat

D/Diagnosis

Page 24: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Haemophilus influenzae type b, S. pneumoniae, S. aureus, H. influenzae type non-b, H. parainfluenzae

Inflammation and edema of the epiglottis, arytenoids, arytenoepiglottic folds, subglottic area

Epiglottis pulled down into larynx and occludes the airway

Epiglottitis - Pathogenesis

Page 25: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Visualization of epiglottis - “cherry red” Laternal neck x-rays: “thumb sign” WBC count > 15,000 left shift Blood cultures

Prophylaxis: Rifampin - 20 mg/kg for 4 days

All household contacts if children under 4 Daycare and nursery school contacts Patient before discharge

Epiglottitis - Pathogenesis

Page 26: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Sinusitis-clinical signs

*Viral URI, fever (50%), purulent nasal discharge, swelling, facial pain worse on percussion, headache, nasal obstruction, loss of smell*Children: facial pain, swelling, malodorous breath (50%), cough (80%), nasal discharge (76%), fever (63%), sore throat (23%)

Page 27: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Nasal swabs not helpful Transillumination of maxillary and frontal

sinuses Sinus x-rays: air-fluid level, complete

opacity, mucosal thickening CT scan not indicated - unless chronic

infection, immunocompromised, suspected intracranial or orbital complication

Direct sinus aspiration

Diagnosis

Page 28: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Impaired mucociliary functionObstruction of sinus ostiaImmune defectsIncreased risk of microbial invasion

Factors predisposing to sinusitis

Page 29: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

PREVALENCE MEAN (RANGE)Adults Children

MICROBIAL AGENT (Bacteria) (%) (%)Streptococcus pneumoniae 31 (20-35) 36Haemophilus influenzae 21 (6-26) 23

(nonencapsulated)S. pneumoniae and H. influenzae 5 (1-9) --Anaerobes (Bacteroides, Fusobacterium, 6 (0-10) --

Peptostreptococcus, Veillonella)Staphylococcus aureus 4 (0-8) --Streptococcus pyogenes 2 (1-3) 2Branhamella (Moraxella) catarrhalis 2 19 Gram-negative bacteria 9 (0-24) 2 Fugal causes in immunocompromised

Microbial causes

Page 30: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

PREVALENCE MEAN (RANGE)AdultsChildren

MICROBIAL AGENT (%) (%)Viruses

Rhinovirus 15 --Influenza virus 5 --Parainfluenza virus 3 2

Adenovirus -- 2

Microbial causes

Page 31: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Complication Clinical Signs Meningitis Headache, fever, stiff neck

lethargy, rapid death

Osteomyelitis Pott’s puffy tumor Epidural abscess Headache, fever Subdural empyema Headache, seizures

hemiplegia, rapid death Cerebral abscess Convulsions, headache,

personality change Venous sinus thrombosis Picket-fence fever, rapid

death Cavernous sinus Orbital edema, ocular palsies

Complications of Sinusitis

Page 32: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Virus type SerotypesAndenoviruses 41Coronaviruses 2Influenza viruses 3Parainfluenza viruses 4Respiratory syncytial virus 1Rhinoviruses 100+Enteroviruses 60+

VirologyOver 200 viruses

Page 33: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

May-Aug - Enteroviruses Sept-Dec - Mycoplasma, Rhinoviruses,

Parainf. 1+2, RSV Jan-Feb - Adenoviruses, Influenza,

Coronaviruses Mar-Apr - Parainf. 3,

Rhinoviruses

Seasonal variation

Page 34: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Direct contact with infected secretions Hand - to - hand Hand - to environmental surface - to hand Spread by aerosoles Complications:Bacterial superinfection

◦ Otitis media◦ Sinusitis◦ S. pneumoniae, H. influenzae, B. catarrhalis

Guillain-Barre Syndrome Asthma attacks

Transmission

Page 35: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore

Aspirin - prolonged excretion of rhinoviruses, influenza virus

Children - aspirin associated with Reye’s syndrome

Prevention:Vaccines◦ influenza A/B◦ adenoviruses types 4,7

Intranasal interferon ◦ rhinoviruses◦ nasal obstruction, bloody discharge

Aspirin and influenza

Page 36: 3 rd March.2015.Physiology module Dr Jalees Khalid Khan Pathology Deptt. KEMU. Lahore