Infections of upper respiratory tract

Kauser Jabeen Assistant Professor Pathology and Microbiology

Objectives
Normal flora of respiratory tract Host defense mechanisms of respiratory tract Membranous pharyngitis (Diphtheria) Common cold Sinusitis Otitis media Mastoiditis

Microbiology of Respiratory Tract

Common residents: >50% of normal population
Neisseria spp., Streptococcus viridians, Candida spp., Haemophilus spp., Bacteroides spp., Fusobacterium spp.

Occasional residents: <10% of normal population

Streptococcus pyogenes, Streptococcus pneumoniae, Niesseria meningitidis

Uncommon residents: <1% of normal population

Corynebacterium diphtheriae, Klebsiella pneumoniae

Host Defense Mechanisms

Presence of normal flora Ciliated epithelium

Phagocytes
Lysozymes Secretary IgA

Sites of upper respiratory infections

Diphtheria
Corynebacterium diphtheriae Occurs primarily in non immunized patients Gram positive rod (Chinese figures) Strains may be toxigenic or nontoxigenic (Role of bacteriophages)

Exotoxin required for disease Mode of action

Diphtheria
Epidemiology Humans are the only reservoir Spread by respiratory secretions Infectivity lasts 2-6 weeks if untreated If treated, communicability usually lasts less than 4 days

Bull Neck of Diphtheria

Pseudomembrane in Diphtheria

Diagnosis
Gram stain and culture Specimen from under membrane or membrane itself Inform lab Lofflers or tellurite selective media (Tindales agar) Test strains for toxigenicity

Diphtheria
Complications Obstruction of respiratory tract by pseudomembrane Myocarditis Polyneuritis (bulbar and peripheral) Mortality 10-30%

Diphtheria
Complications Obstruction of respiratory tract by pseudomembrane Myocarditis Polyneuritis (bulbar and peripheral) Mortality 10-30% usually due to cardiac damage

Treatment
Antibiotic Equine antitoxin + penicillin G (erythromycin if PCN allergy)

Aims: Decrease toxin production Decrease local inflammation Decrease carrier state

Prevention
Immunization with formalin inactivated toxin Chemoprophylaxis Strict isolation of patients

Infectious rhinitis
2nd most common diagnosis

Huge economic burden

Viruses associated with the common cold

Virus group Rhinoviruses Corona virus Antigenic type 100 types 3 or more types % of cases 30-40 10-15

Para influenza virus Respiratory syncytial virus

Influenza Adenovirus

4 types
2 types 3 types 47

5%
5% 25-30% 5-10%

FACTS: the common cold

Transmission:
Most efficient = direct contact
virus can survive for 2 hours on human skin

Also aerosol

NOT via saliva (In 90% of people with colds, no detectable virus in saliva)

Common cold

Pathogenesis
Viral invasion :
Through upper respiratory tract Incubation = 24-72 hours

Relation with winter season:

NO evidence that cold climate increases susceptibility to respiratory illness
Increase crowding indoors of population during colder months

Relative humidity may be important variable that controls prevalence of different virus families Viral excretion is maximum during acute clinical illness Self limited illness

Secondary Bacterial Infections

Infectious sinusitis
Sinuses have small orifices (ostia) which open into recesses (meati) of the nasal cavities. Maxillary and ethmoid sinuses are most frequently involved. Persistence of URI symptoms >10 days without improvement.

 Usually follows rhinitis, which may be viral or allergic. Change in nasal flora Continuous nose blowing propels flora including bacteria , viruses and inflammatory mediators Inflammation and edema of mucous membranes cause obstruction This provides for an opportunistic bacterial infection Postnasal drainage causes obstruction of nasal passages and an inflamed throat

How Does infectious Sinusitis Develop?

Etiology of Sinusitis
70% of bacterial sinusitis is caused by: Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Other causative organisms are: Staphylococcus aureus Streptococcus pyogenes Gram-negative bacilli Respiratory viruses

S.pneumoniae
Most common bacterial cause of RTIs Small gram positive diplococci Alpha hemolytic Most are encapsulated (> 80 distinct types) Colonizes the nasopharynx in 5-10% of adults and 20-40% of children Incidence increases in winter months

Pneumococcal Capsule

Respiratory Tract Infections

Antibiotic resistance to Penicillin resistance major concern

Vaccine 23 different serotypes, account for 90% of invasive strains, protection wanes with time and age

H.influenzae
Small pleomorphic Gram negative bacilli requires X and V factors for growth chocolate agar (5% CO2), may be encapsulated Historically, type b (Hib) responsible for majority of invasive disease, Hib vaccine reduced Hib

Complications of Sinusitis
Orbital cellulitis or abscess Meningitis Brain abscess Intractable wheezing in children with asthma Cavernous sinus thrombosis Subdural empyema

Clinical Presentations of Sinusitis

Periorbital edema Cellulitis Nasal mucosa is reddened or swollen Percussion or palpation tenderness over a sinus Nasal discharge, thick, sometimes yellow or green Postnasal discharge in posterior pharynx Swelling of turbinates Boggy pale turbinates Antimicrobials-treat for 10-14 days, depending upon severity

Acute invasive Aspergillus rhinosinusitis

Occours in immunocompromised individual:
Organ and bone marrow Transplant Prolonged and profound neutropenia (<100 neutophils/l Corticosteroides Other immunosupressive therapy

Immunocompetent (rare)

Host defense for aspergillus

Mucociliary propulsion leads to failure of deposition of conidia 2nd to this is macrophages which engulf resting conidia before germination If it doesnt work and germination to hyphae took place Then third line is neutrophils act extracellularly kill both swollen conidia and hyphae

Diagnosis
Fever, cough , epiataxis, sinus discharge and headaches Clinical signs, ulcarative nasal lesion with an eschar or non sensitive area may be a clue Mortality is high Plain radiograph are not diagnostic CT scan of sinus are useful for establishing extent of infection and local tissue invasion Hyphal growth and tissue invasion are hallmark features of invasive aspergillosis

ZYGOMYCOSIS
Causative agents Rhizopus, Rhizomucor, Mucor... Natural reservoir Air, water, soil Risk factors Diabetic ketoacidosis, immunosuppression Pathogenesis Inhalation of sporangiospores Infected tissue vascular invasion, thrombus, infarct, bleeding

Invasive fungal sinusitis

Treatment Surgical debridement Amphotericin B

***High mortality rate

Otitis Media
Inflammation of the middle ear May also involve inflammation of mastoid, petrous apex, and perilabyrinthine air cells

EPIDEMIOLOGY
Peak incidence in the first two years of life (esp. 6-12 months) 50% of children 1 yr of age will have at least 1 episode. 1/3 of children will have 3 or more infections by age 3 90% of children will have at least one infection by age 6. Occurs more frequently in the winter months

Eustachian tube
Protection from nasopharyngeal sound and secretions clearance of middle ear secretions ventilation (pressure regulation) of middle ear Usually closed Opens during swallowing, yawning, and sneezing Opening involves cartilaginous portion

Otitis media: Pathogenesis

Microbiology
S. pneumoniae - 30-35% H. influenzae - 20-25% M. catarrhalis - 10-15% Group A strep - 2-4% Infants with higher incidence of gram negative bacilli RSV - 74% of middle ear isolates Rhinovirus Parainfluenza virus Influenza virus

Complications
Intra temporal hearing loss TM perforation CSOM mastoiditis petrositis Labyrinthitis facial paralysis Intra cranial meningitis extradural abscess subdural empyema focal encephalitis brain abscess lateral sinus thrombosis

Treatment
Antimicrobial agents Prevention:
Chemoprophylaxis Vaccine

Mastoiditis
Infection secondary Close proximity to brain and venous sinuses Fever, hearing loss, otalgia Redeness and tenderness over pinna Complications are brain abscess or septic thrombosis of venous sinuses Antimicrobial agnets; sometimes mastoidectomy

Thank you