1. RESPIRATORY SYSTEM lecture 3&4

2. THE LUNG
LECT-3&4

3. Normal Lung

4. Normal Lung

5. Infectious Disease Nose & upper respiratory tract (most common)
95%, very wide spread in children, general public
Lower respiratory tract (pneumonias)
5%, often affecting elderly, immune compromised, drug addicts, alcoholics, hospitalized individuals (secondary pneumonia)
75% of all diagnosed human infections are respiratory

6. Upper Respiratory Infections
Common cold (most common)
Most caused by viruses (no treatment, no correlation to “cold”)
Seasonal epidemics
Increased incidence in individuals with other health problems (physical exhaustion, depression, immune diseases, old age, poor nutrition, stress)
Self-limiting except for possible bacterial superinfections

7. Upper Respiratory Infections
Pathology
Inflammation of mucosa: congestion, edema
Bacterial superinfection: appearance of whitish-yellow membranes on tonsils & throat
Clinic
Rhinorrhea, congestion, throat pain, sneezing…..
Streptococcal superinfection may lead to severe complications (rheumatic fever, acute glomerulonephritis

8. Middle Respiratory Infections
Larynx, trachea, extrapulmonary bronchi
Common in children through spread from upper tract
Whooping cough (Pertussis) rare today due to immunization against Bordetella pertussis
Croup: Acute, potentially life-threatening laryngitis

9. Middle Respiratory Infections: Croup
Spasm of vocal cords
Barking cough
Parainfluenza virus
Possible suffocation due to swelling of larynx (intubation)
Mostly affects children <3 years

10. Middle Respiratory Infections: Epiglottitis
Haemophilus influenza
High school-aged children, young adolescents
Sudden loss of voice, hoarseness
Antibiotic therapy
(acute cases: Intubation)

11. Middle Respiratory Infections: Bronchiolitis
Very common viral infection in young children
Affect bronchi and/or bronchioles (not reaching alveoli  pneumonia)
Epidemics from fall – spring
Self-limiting unless accompanied by bacterial superinfection

12. Pathology of Pneumonia
Department of pathology and forensic medicine- TUCOM.

13. Introduction: Daily 10,000 liters of air - filtered..!
Normal lungs are sterile
Pneumonia: Inflammation of lung.
Respiratory tract infections – commonest in medical practice.
Enormous morbidity & mortality.

14. Patterns of infections:
Airway
Bronchitis, Bronchiectasis, Bronchiolitis.
Parenchyma
Pneumonia
Lung abscess TB
Pleura:
Pleural effusion.

15. definition
Exudative solidification (consolidation) of the pulmonary tissue as a result of bacterial invasion.
Vary according to specific etiologic agent, host reaction, and extent of involvement.
1- etiologic: pneumococcal, staphylococcal.
2- host reaction: suppurative, fibrinous.
3- gross anatomic distribution (lobar, bronchopneumonia).

16. Etiology and pathogenesis:
Decreased resistance - General/immune
Virulent infection - Lobar pneumonia
Defective Clearing mechanism
Cough Reflex – Comatose, paralysis, sick.
Mucosal Injury – smoking, toxin aspiration
Low Alveolar defense - Immunodeficiency
Pulmonary edema – Cardiac failure, emboli.
Obstructions – foreign body, tumors

17. Etiologic Types: Viral – Interstitial Bacterial -
Mycoplasmal - atypical
Fungal – chronic..

18. Complications:
1- Tissue destruction and necrosis, abscess, formation seen especially in type 3 pneumococci or klebsiella.
2- Spread of infection to pleura, empyema.
3- organization of exudate.
4- bacteremic dissemination to heart valves, pericardium, brain, kidney, spleen and joints.

19. Morphologic Types: Bronchopneumonia - Patchy Lobar Pneumonia - Lobe
Bacterial, viral, TB, Fungal etc.
Lobar Pneumonia - Lobe
Streptococcal pneumonia
Interstitial Pneumonia – diffuse
Viral & Mycoplasma
Special Types
Immunocompromised, Pneumocystis, Candida, aspergillus – diffuse both lungs.

20. Bronchopneumonia Staph, Strep, Pneumo & H. influenza
Patchy consolidation – not limited to lobes.
Suppurative inflammation, in a form of neutrophil rich exudate fill bronchi, bronchioles and adjacent alveoli.
Usually bilateral
Lower lobes common
Complications:
Abscess
Empyema
Dissemination
Pleural effusion

21. Broncho -pneumonia

22. Broncho -pneumonia

23. Broncho -pneumonia

24. Abscess formation

25. Bronchopneumonia:

26. Abscess formation

27. Bronchopneumonia - CT

28. Bronchopneumonia

29. Lobar Pneumonia: Fibrinosuppurative consolidation – whole lobe
Rare due to antibiotic treatment.
~95% - Streptococcus pneumoniae
Four stages:
Congestion - vasodilatation
Red Hepatization – hemorrhage RBC
Gray Hepatizaiton - Macrophages
Resolution – Normal – few macrophages

30. Morphology contd: Congestion: gross: the lung is heavy and red.
Micro: vascular engorgement, intra-alveolar fluid and few neutrophils, numerous bacteria.
Red Hepatization: gross: red, firm and airless lobe with liver like consistency.
Micro: massive exudate, red cells, neutrophils, and fibrin filling the alveoli.
Gray Hepatizaiton: gross: grayish-brown colour with dull surface.
Micro: disintegration of RBCs, and persistence of Fibrinosuppurative exudate.
Resolution: digestion of exudate, into granular semifluid debris, resorbed and digested by macrophages or coughed up.
The pleura if involved either resolved or end with organization and fibrous thickening and adhesions.

31. Lobar Pneumonia:

32. Lobar Pneumonia – Gray hep…

33. Viral and Mycoplasma pneumonia (primary atypical pneumonia)
It is an acute respiratory disease characterized by patchy inflammation of the lungs mainly confined to the alveolar septa and pulmonary interstitium with absence of exudate (atypical).
Etiology: Mycoplasma pneumoniae, Influenza virus type A and B, respiratory syncytical virus, adenovirus, rhinovirus, Varicella, Chlamydia (Psittacosis), Coxiella burnetii (Q fever).
Predisposing causes: malnutrition, alcoholism & debilitating illnesses.

34. Morphology: Gross: patchy, or whole lobes, bilateral or unilateral.
Red blue congested areas.
No obvious consolidation.
Pleura smooth (pleuritis infrequent).
Micro: interstitial inflammatory reaction, localized to alveolar walls.
Contains lymphocytes, histiocytes and occasionally plasma cells.
Alveolar space is free and in some patients intra alveolar proteinaceous material with acellular exudate and hyaline membrane.
Sometimes superadded bacterial infection, or necrosis.
Epithelial giant cells with intranuclear or intracytoplasmic inclusions.

35. Clinical features: Extremely varied.
May present as upper respiratory tract infections or cold, without localizing symptoms.
Cough may be absent.
Fever, headache and myalgia.
Positive cold agglutinin in 50% of MP and 20 % of adenovirus and negative in other viruses.
Sporadic cases are mild but may run in epidemics with severe disease and high mortality as in highly fatal pandemic in 1915 and 1918 and other smaller epidemics since then. Secondary staphylococcal and streptococcal infections are common.

36. Bird flu: important type:
There are three types of influenza virus: A, B and C. Type A can infect humans, other mammals and birds and can spread fast and affect many people.
Types B and C affect only humans and type C causes only a mild infection.
Influenza type A viruses are sub-typed into categories based on their H and N surface antigens. The virus uses the H protein molecule to latch on to the host's cell and uses the N protein molecule to break away and spread the infection.
Types A and B continue to evolve genetically, and thus prevent the hosts from enjoying any prolonged protection against the virus.

37. Influenza virus showing Neuramindase and Hemagglutinin projecting from the surface

38. Symptoms Very sudden - 1-2 hours healthy to prostrate
Fevers: degrees
General weakness
Eyes burn
Severe aches in muscles, joints, backs, heads
As if they had “been beaten all over by a club”
High fever caused hair to fall out for survivors

39. Face turns a dark brownish purple Cough up blood Feet turn black
Death
Face turns a dark brownish purple
Cough up blood
Feet turn black
Gasp for breath
Blood-tinged saliva
Drown
lungs fill with reddish fluid

40. SARS Severe Acute Respiratory Syndrome Corona virus Pneumonia
Unknown etiology
Contagious, infect health care personnel and family members and close contacts
No response to antibiotics or antiviral drugs
Most of the infected HCW were admitted in ICU with respiratory failure. Those who died were previously healthy without underlying diseases.
It spreads out to other countries in Asia, Europe and North America from traveling.
Man to man transmission and capable to travel

41. Clinical features Fever (>38 C) and
One or more signs and symptoms of respiratory illness including cough, shortness of breath, difficulty breathing, hypoxia, radiographic finding of pneumonia, or respiratory distress and
History of travel to an area with recent local transmission of SARS within 10 days of symptom onset or
Close contact with persons with SARS within 10 days of onset of symptoms or
Residing in an area with recent local transmission of SARS

42. A suspect case with radiographic evidence of infiltrates consistent with pneumonia or respiratory distress syndrome on chest X-ray.
A suspect case of SARS that is positive for SARS corona virus by one or more assays.
A suspect case with autopsy finding consistent with the pathology of RDS without an identifiable cause

43. Lung Abscess:
Definition: Focal suppuration with necrosis of lung tissue
Etiology and pathogenesis:
Strep, Staph & Gram negative & anaerobes
Mechanism:
Aspiration of infective material in coma, alcoholism, anesthesia, sinusitis, gingivo-dental sepsis, and debilitation. Also in aspiration of gastric contents.
Post pneumonic: especially in staph. aureus, Klebsiella and type 3 pneumococci.
Septic embolism
Neoplasms (post-obstruction pneumonia)
Miscellaneous: direct traumatic penetration, spread from adjacent infection as spine, or hematogenous.

44. Clinical features: Productive Cough foul smell, fever.
Clubbing of fingers, and toes.
Associated with carcinoma in 10-15%.
Complications: extension to pleura, hemorrhage, Systemic spread, brain abscess and meningitis and reactive secondary amyloidosis (type AA).

45. Morphology:
Gross: It is vary in size from few mm to large cavities about 5-6 cm, affect any part of the lungs, and can be single or multiple. The cavity may or may not be filled by suppurative debris, with superadded saprophytic infections, seen as large fetid, green to black.
Microscopy: There is suppurative debris (neutrophils & necrotic material). The lung parenchyma is destructed with central cavitations, and in chronic cases the wall of the abscess is fibrotic with 4 layers.

46. Lung Abscess:

47. Lung Abscess:

48. Lung Fungal Abscess: Candida