The Common Cold

1. The common cold is a viral illness

2. The symptoms of rhinorrhea and nasal
obstruction are prominent;
3. myalgia and fever are absent or mild.
4. It is often termed rhinitis but includes self-
limited involvement of the sinus mucosa and
is more correctly termed rhinosinusitis
 Etiology
ASSOCIATION PATHOGEN RELATIVE FREQUENCY
Agents primarily Rhinoviruses Frequent
associated with colds
Coronaviruses Occasional
Agents primarily Respiratory syncytial Occasional
associated with other viruses
clinical syndromes that Human Occasional
also cause common metapneumovirus
cold symptoms
Influenza viruses Uncommon
Parainfluenza viruses Uncommon
Adenoviruses Uncommon
Enteroviruses Uncommon
 EPIDEMIOLOGY
• Rhinovirus infection : august– October & April–May
• Parainfluenza viruses : between December and April
• Respiratory syncytial virus: January, February, or
march
• Influenza viruses : colder months of the year in
temperate climates December and April
 Age
• Young children have an average of 6–8 colds per year but
10–15% of children have at least 12 infections per year.
• The incidence of illness decreases with age, with 2 to 3
illnesses per year by adulthood.
• Children in out-of-home daycare centers during the 1st
year of life have 50% more colds than children cared for
only at home.
• minimum 3/year as per ARI program
• Attack rate is 100%
 PATHOGENESIS
• Rhinoviruses and RSV: direct contact
transmission by large-particle aerosols
• Influenza viruses: spread by small-particle
aerosols.
• Repeated infections due to:
1. Large number of distinct serotypes of each virus.
2. Protective immunity to some viruses does not
develop after an infection
3. The severity of subsequent illness is moderated by
pre-existing immunity
 Pathology
1. Infection of the nasal epithelium is associated with
release of a variety of inflammatory cytokines and
infiltration of the mucosa by inflammatory cells.

2. Inflammation can obstruct the sinus ostium or

eustachian tube and predispose to bacterial sinusitis
or otitis media
 CLINICAL MANIFESTATIONS
1. 1–3 days after viral infection:
1. Sore or “scratchy” throat,
2. Nasal obstruction
3. Rhinorrhea.
2. The sore throat usually resolves quickly & nasal
symptoms predominate.
3. Cough in > 30% of pts
4. Influenza viruses, RSV, and adenoviruses are more
likely to have fever
5. The usual cold persists for about 1 wk, although 10%
last for 2 wk
 The physical findings
1. Increased nasal secretion is frequently
obvious to the examiner.
2. A change in the color or consistency of the
secretions is common
3. Examination of the nasal cavity may reveal
swollen, erythematous nasal turbinates,
 Diagnosis and DD
CONDITION DIFFERENTIATING FEATURES

Allergic rhinitis Prominent itching and sneezing; Nasal eosinophils

Unilateral, foul-smelling secretions; Bloody nasal
Foreign body
secretions
Presence of fever, headache or facial pain, or
Sinusitis periorbital edema or persistence of rhinorrhea or
cough for >14 days
Streptococcosis Nasal discharge that excoriates the nares

Pertussis Onset of persistent or severe cough

Congenital Persistent rhinorrhea with onset in the 1st 3 mo of
syphilis life
 LABORATORY FINDINGS
1. Routine laboratory studies are not necessary for the
diagnosis
2. A nasal smear for eosinophils for allergic rhinitis
3. polymorphonuclear leukocytes in the nasal does not
indicate bacterial superinfection.
4. The viral pathogens associated with the common cold
can be detected by culture, antigen detection,
polymerase chain reaction (PCR), or serologic methods.
5. Bacterial cultures or antigen detection
 TREATMENT
1. The management is symptomatic
2. Antiviral Treatment.
1. Rhinovirus: nil; pleconaril is under evaluation
2. RSV : ribavirin
3. Influenza : neuraminidase inhibitors oseltamivir
and zanamivir
4. For treatment of rhinovirus infections
3. Antibacterial therapy is of no benefit in the
treatment of the common cold.
 Symptomatic Treatment
1. Fever is infrequent and antipyretic treatment is not indicated.

2. NASAL OBSTRUCTION.

1. xylometazoline, oxymetazoline, or phenylephrine are

available as either intranasal drops or nasal sprays

2. they are not approved for use in children <2 yr old.

3. Systemic absorption has very rarely been associated

with bradycardia, hypotension, and coma.

4. Prolonged use may lead to rhinitis medicamentosa

• RHINORRHEA.

1. The first-generation antihistamines reduce rhinorrhea by

25–30%.

2. Rhinorrhea can also be treated with ipratropium

bromide, a topical anticholinergic agent.

• SORE THROAT.

1. The sore throat is treated with mild analgesics

2. Aspirin should not be given to children with respiratory

infections because of the risk of Reye syndrome
 COUGH
1. Cough suppression is generally not necessary
2. For cough due to postnasal drip, treatment with a first-
generation antihistamine may be helpful.
3. Cough due to virus-induced reactive airway disease may have
cough for days to weeks and may benefit from inhaled steroids
and bronchodilator therapy.
4. Codeine or dextromethorphan hydrobromide has no effect on
cough from colds.
5. Expectorants such as guaifenesin are not effective antitussive
agents.
 Ineffective Treatments
1. Vitamin C, guaifenesin, and inhalation of warm,
humidified air are no more effective than placebo
for the symptomatic treatment of colds.

2. Zinc has no clinically significant impact on common

cold symptoms in children.

3. Echinacea is a popular herbal treatment for the

common cold. But echinacea is not effective as a
common cold treatment in children.
 COMPLICATIONS
1. Otitis media: in 5–30% of children and treatment
with oseltamivir may reduce the incidence of otitis
media in patients with influenza.
2. Sinusitis: fever, facial pain, or facial swelling
develop
3. Exacerbation of asthma
4. Inappropriate use of antibiotics leads to increasing
antibiotic resistance of pathogenic respiratory
bacteria.
 Prevention
1. Chemoprophylaxis or immunoprophylaxis is not available
2. Immunization or chemoprophylaxis against influenza may be
useful
3. Vitamin c and echinacea do not prevent the common cold.
4. Isolation: interrupting the chain involved in the spread of
virus by direct contact may prevent colds.
5. Personnel wearing protective face shields to prevent hand-
to-eye or hand-to-nose contact.
6. Good handwashing by the infected individual and/or the
susceptible contact.
 WHO classification of ARI
• No pneumonia: • Severe Pneumonia:
– Normal breathing – Chest retraction
• Pneumonia: – Grunting
– Increased respiratory • Severe disease:
rate: – Cyanosis
• > 60 infants – Unconsciousness
• > 50 2-12 months – convulsions
• > 40 1-5 years
 Definitions
• Acute respiratory tract infection: infection of R.S for
less than 14 days
• URI: upto epiglottis including middle ear
• LRI: from trachea to pleura
• Pneumonia: Inflammation of parenchyma of lungs;
often focal involving some lobes
• Bronchopneumonia : acute inflammation of the walls
of the bronchioles with peri bronchial inflammation of
lung parenchyma; bilateral and symmetrical
involvement
 Etiology of Pneumonias
1. Infection: viral, bacterial, fungal, parasitic
2. Aspiration: food; gastric juice
3. Foreign body
4. Hydrocarbons
5. Lipoid substance
6. Hypersensitivity : airy and grain products, animal
dander and protein
7. Drugs: anticancer drugs
8. Radiation
 Leading Etiologic Agents of Pneumonia Infants and Children
Age Bacterial pathogens Viral Pathogens Other

-Neonate Group B Streptocaccus RSV

Gram-negative bacilli( Herpes simplex
E.coli,K.pneumoniae,Pr virus
oteus spp.,others) CMV
S.aureus Adenovirus

1-3 mo. S.pneumoniae RSV C.trachomatis

H.Infuenzae type b
4 mo.-5 yrs S.pneumoniae Parainflenza
H.Influenzae type b virus1 and 3,
Adenovirus
Influenza viruses A
and B
5 yrs and older S.pneumoniae M.pneumoniae
C.pneumoniae
Common pathogens
 Pathogenesis

• Lower respiratory tract is sterile

• Immune defense by leukocytes and Ig.A

• Mucous coat

• Ciliary clearance

• Cough
 Viral pneumonias
1. Spreads along the airways
2. Infects epithelium
3. Cell injury
4. Edema
5. Exudation
6. Cellular debris
7. Airway narrowing
8. Airway obstruction
9. Atelectasis
10. Ventilation perfusion mismatch
11. Hypoxia
Bacteriral pneumonias
Viral infection

Surface defense
knocked down

Altered secretions

bacterial invasion

Inflammation
 Pathogenesis
1. Streptococcus peumoniae: Focal often lobar
pneumonia

2. G.A. Streptococcus: Diffuse often involves pleura

3. Staphylococcus: Unilateral ; extensive;

hemorrhagic necrosis; cavitation; pneumatoceles;
empyema

4. Mycoplasma: Patchy; edema; airway obstruction

 Pathology
1. Congestion (1-2 days)

2. Red hepatization (2nd-4th day)

3. Gray hepatization (4th-6th day)

4. Resolution (8th-9th day)

All 4 phases may be seen in different parts of

the same lung.
 Recurrent pneumonia
1. 2 episodes in a year
2. 3 episodes in life time
3. Causes:
1. Cystic fibrosis
2. HIV
3. Immunodeficiency
4. Immotile cilia syndrome (Kartagener syndrome)
5. Foreign body
6. Sequestration
7. Con emphysema
8. TEF
9. Bronchiectasis
10. Neuromuscular incoordination
 Clinical features
1. Starts as upper 1. Chest retraction
respiratory catarrh 2. Working of accessory
2. Fever muscles of respiration
3. Chills 3. Crackles and wheeze
4. Tachypnoea
4. Restlessness
5. Grunt
5. Delirium
6. Cyanosis
6. Pleuritic pain
 Infants

1. Diarrhea

2. Vomiting

3. Abdominal distension

4. Incessant cry
 WHO classification
1. No pneumonia: 4. Severe disease:
1. Normal breathing 1. Cyanosis
2. Pneumonia: 2. Unconsciousness
1. Increased respiratory 3. convulsions
rate:
1. > 60 infants
2. > 50 2-12 months
3. > 40 1-5 years
3. Severe Pneumonia:
1. Chest retraction
2. Grunting
 Diagnosis
Lab: CXR:

• TC normal in viral – Sun ray appearance

increased in bacterial – Airbronchogram

– Lobar consolidation
• Lymphocytosis in viral
– Perbronchial cuffing
• CRP increased
– Silhouette sign
• ESR increased
 Treatment
1. Amoxicillin Poor response:
2. Cloxacillin 1. Antibiotic
3. Cefuroxim axitil resistance
4. Azithrocyn 2. Viral
5. Levofloxacin
3. Aspiration
6. Gatrifloxacin
4. Immunodeficiency
7. Aminoglycosides
5. Cystic fibrosis
 Complications
1. Septicemia
2. Meningitis
3. Osteomyelitis
4. Metastasis
5. Empyema
6. Pericarditis
7. suppurative arthritis

8. Death due to: resp.failure and other complications

 Staph pneumonia
1. Coagulase positive Staphylococci produce
abscess formation
2. Panton-Valentine leukocidin (PVL) is an exotoxin
causes leukocyte destruction and tissue
necrosis
3. They produce B-lactamase which inactivates
most penicillins
4. Methycillin resistant staphylococcus aureus
(MRSA) are becoming more prevalent
 Clinical features
1. Abdominal distention, high fever, respiratory
distress, and toxemia.
2. Occurs without predisposing factors or after
minor skin infections.
3. The organism is necrotizing, producing
bronchoalveolar destruction.
4. Pneumatoceles, pyopneumothorax, and
empyema are frequently encountered.
5. Rapid progression of disease is characteristic
 Treatment
– Community acquired staph pneumonia:
• Co Trimoxazole
• Clindamycin
– Methicillin sensitive Staph aureus:
• Penicillinase resistant antibiotics such as:
– Oxacillin } 100-150 mg /kg/day/IV in 4 divided doses
– Nafcillin }
– Methicillin 200-300 mg /kg/day/IV in 4 divided doses
• Cephalosporins:
– Cefazolin 100-150 mg /kg/day/IV in 4 divided doses
– Cephalexin 50-100 mg /kg/day/orally in 4 divided doses
• For methicillin resistant staph. Aureus:
• Vancomycin 40 mg mg /kg/day/IV in 4
divided doses
• Linozolid is a recent drug
• Rifampin may be added to vancomycin
• Othyer measures:
– Inter costal drainage of empyema
Thymic shadow
Sail sign
Mild bronchopneumonia
Severe Bronchopneumonia
Bronchiolitis
Bow sign
Pneumonitis
Pneumonitis
Pneumonia with air bronchogram
Silihoutte sign
Friedlander Pneumonia
bulging fissure sign
Klebsiella
Staphylococcal pneumonia
Empyema
Pyopneumothorax
Mycoplasma pnumonia