Urinary tract infection
Most often caused by gram-negative, rod-shaped bacteria that are normal residents of the enteric tract, especially Escherichia coli.

Clinical manifestations: 

frequent urination, dysuria, pyuria (increased PMNs), hematuria, and bacteriuria.

May lead to infection of the urinary bladder (cystitis) or kidney (pyelonephritis).

Q Fever

An acute disease caused by Coxiella burnetii (Rickettsia burnetii) and characterized by sudden onset of fever, headache, malaise, and interstitial pneumonitis.

Symptoms and Signs

The incubation period varies from 9 to 28 days and averages 18 to 21 days. Onset is abrupt, with fever, severe headache, chills, severe malaise, myalgia, and, often, chest pains. Fever may rise to 40° C (104° F) and persist for 1 to > 3 wk. Unlike other rickettsial diseases, Q fever is not associated with a cutaneous exanthem. A nonproductive cough and x-ray evidence of pneumonitis often develop during the 2nd wk of illness.

In severe cases, lobar consolidation usually occurs, and the gross appearance of the lungs may resemble that of bacterial pneumonia

About 1/3 of patients with protracted Q fever develop hepatitis, characterized by fever, malaise, hepatomegaly with right upper abdominal pain, and possibly jaundice. Liver biopsy specimens show diffuse granulomatous changes, and C. burnetii may be identified by immunofluorescence.

HERPES ZOSTER (Shingles)

An infection with varicella-zoster virus primarily involving the dorsal root ganglia and characterized by vesicular eruption and neuralgic pain in the dermatome of the affected root ganglia.

caused by varicella-zoster virus

Symptoms and Signs

Pain along the site of the future eruption usually precedes the rash by 2 to 3 days. Characteristic crops of vesicles on an erythematous base then appear, following the cutaneous distribution of one or more adjacent dermatomes

Eruptions occur most often in the thoracic or lumbar region and are unilateral. Lesions usually continue to form for about 3 to 5 days

Geniculate zoster (Ramsay Hunt's syndrome) results from involvement of the geniculate ganglion. Pain in the ear and facial paralysis occur on the involved side. A vesicular eruption occurs in the external auditory canal, and taste may be lost in the anterior two thirds of the tongue

Salivary gland pathology

Inflammation 

a. Sialolithiasis produces a secondary inflammatory reaction  to obstruction and the resultant enlargement of ducts by stones. It may be complicated by actual infection with mouth flora. 

b. Sialadenitis is a primary inflammatory reaction, but it is not always infectious. It may be part of an autoimmune disease  (e.g., Sjogren's syndrome), or the result of bacterial or virals (e.g., mumps) infection. 

Sjögren’s syndrome

a. An autoimmune disease of the salivary and lacrimal glands.
b. Autonuclear antibodies (ANAs) against salivary ducts may be seen.
c. Triad of symptoms include:
(1) Xerostomia—from decreased saliva production.
(2) Keratoconjunctivitis sicca (dry eyes)—from decreased tear production.
(3) Rheumatoid arthritis.
(4) Enlargement of the salivary or lacrimal glands, known as Mikulicz syndrome, may also be observed. 

d. Histologically, a dense infiltration of the gland by lymphocytes is observed.

Tumors

The parotid gland accounts for more than three-quarters of these tumors, most of which are benign. Of the remainder, more occur in the submandibular gland than in the sublingual, and most of these are malignant. Many are surgically, cured, but local recurrence is common. 

a. Pleomorphic adenoma is generally benign and accounts for approximately three-quarters of all salivary gland tumors. If  is composed of multiple epithelial and mesenchymal cell types. Complications may arise due to involvement of cranial nerve VII. 

(a) The most common salivary gland tumor.
(b) Is benign.
(c) Prognosis is good after proper surgical excision.

b. Warthin's tumor (adenolymphoma) is also benign, occuring almost exclusively in the parotid gland. It is grossly cystic.

Microscopic examination reveals cell types suggestive of branchial cleft origin embedded in a lymphoid matrix. 

c. Mucoepidermoid tumors also occur primarily in the parotid and have a high rate of malignant transformation.The malignant component is usually squamous cell.  Prognosis of tumor depends on grade and stage of disease.

d. Cylindroma (adenoid cysticc. Mucoepidermoid tumors carcinoma) is more common in the minor salivary glands found in the oral mucosa, and metastases are more common than in other tumors of the salivary glands. Facial nerve complications are frequent. 
(1) Grossly, the tumor forms multiple lobules surrounded by a capsule. 
(2) Microscopically, small cells form glands containin mucoid material 

Polycystic kidney disease

Characterized by the formation of cysts and partial replacement of renal parenchyma.
Genetic transmission: autosomal dominant.
Clinical manifestations:

 hypertension, hematuria, palpable renal masses, and progression to renal failure. Commonly associated with berry
aneurysms. 

PNEUMONIAS  

Pneumonia is defined as acute inflammation of the lung parenchyma distal to the terminal bronchioles which consist of the respiratory bronchiole, alveolar ducts, alveolar sacs and alveoli. The terms 'pneumonia' and 'pneumonitis' are often used synonymously for inflammation of the lungs, while 'consolidation' (meaning solidification) is the term used for macroscopic and radiologic appearance of the lungs in pneumonia.

 PATHOGENESIS. 
 The microorganisms gain entry into the lungs by one of the following four routes: 
 1. Inhalation of the microbes. 
 2. Aspiration of organisms. 
 3. Haematogenous spread from a distant focus. 
 4.  Direct spread from an adjoining site of infection.

Failure of defense mechanisms and presence of certain predisposing factors result in pneumonias. 
 
 These conditions are as under: 
 1. Altered consciousness. 
 2. Depressed cough and glottic reflexes. 
 3. Impaired mucociliary transport. 
 4. Impaired alveolar macrophage function. 
 5. Endobronchial obstruction. 
 6. Leucocyte dysfunctions. 
 
 
 CLASSIFICATION. On the basis of the anatomic part of the lung parenchyma involved, pneumonias are traditionally classified into 3 main types: 
 
 1. Lobar pneumonia. 
 2. Bronchopneumonia (or Lobular pneumonia). 
 3. Interstitial pneumonia. 
 
BACTERIAL PNEUMONIA  

Bacterial infection of the lung parenchyma is the most common cause of pneumonia or consolidation of one or both the lungs. Two types of acute bacterial pneumonias are distinguished—lobar pneumonia and broncho-lobular pneumonia, each with distinct etiologic agent and morphologic changes. 
 
  1.    Lobar Pneumonia  
 Lobar pneumonia is an acute bacterial infection of a part of a lobe, the entire lobe, or even two lobes of one or both the lungs. 
 
 ETIOLOGY. 
 Following types are described: 
 1.  Pneumococcal pneumonia. More than 90% of all lobar pneumonias are caused by Streptococcus pneumoniae, a lancet-shaped diplococcus. Out of various types, type 3-S. pneumoniae causes particularly virulent form of lobar pneumonia. 
 
 2. Staphylococcal pneumonia. Staphylococcus aureus causes pneumonia by haematogenous spread of infection. 
 
 3.  Streptococcal pneumonia, β-haemolytic streptococci may rarely cause pneumonia such as in children after measles or influenza. 
 
 4.  Pneumonia by gram-negative aerobic bacteria. Less common causes of lobar pneumonia are gram-negative bacteria like Haemophilus influenzae, Klebsiella pneumoniae (Friedlander's bacillus), Pseudomonas, Proteus and Escherichia coli. 
 
 MORPHOLOGY. Laennec's original description divides lobar pneumonia into 4 sequential pathologic phases: 
 
 1.   STAGE OF CONGESTION: INITIAL PHASE 
 The initial phase represents the early acute inflammatory response to bacterial infection and lasts for 1 to 2 days. 
 
The affected lobe is enlarged, heavy, dark red and congested. Cut surface exudes blood-stained frothy fluid. 
 
Microscopic Examination 
 i) Dilatation and congestion of the capillaries in the alveolar walls. 
 ii)   Pale eosinophilic oedema fluid in the air spaces.
 iii)  A few red cells and neutrophils in the intra-alveolar fluid. 
 iv) Numerous bacteria demonstrated in the alveolar fluid by Gram's staining. 
 
  2.   RED HEPATISATION: EARLY CONSOLIDATION  
 This phase lasts for2 to 4 days. The term hepatisation in pneumonia refers to liver-like consistency of the affected lobe on cut section. 
 
 The affected lobe is red, firm and consolidated. The cut surface of the involved lobe is airless, red-pink, dry, granular and has liver-like consistency. 
 
Microscopic Examination   
 i) The oedema fluid of the preceding stage is replaced by strands of fibrin. 
 ii)   There is marked cellular exudate of neutrophils and extravasation of red cells. 
 iii)  Many neutrophils show ingested bacteria. 
 iv) The alveolar septa are less prominent than in the first stage due to cellular exudation. 
 
 3.   GREY HEPATISATION: LATE CONSOLIDATION This phase lasts for4 to 8 days. 
The affected lobe Is firm and heavy. The cut surface is dry, granular and grey in appearance with liver-like consistency. The change in colour from red to grey begins at the hilum and spreads towards the periphery. Fibrinous pleurisy is prominent. 
 
Microscopic Examination   
 i) The fibrin strands are dense and more numerous. 
 ii)   The cellular exudate of neutrophils is reduced due to disintegration of many inflammatory cells. The red cells are also fewer. The macrophages begin to appear in the exudate. 
 iii) The cellular exudate is often separated from the septal walls by a thin clear space. 
 iv) The organisms are less numerous and appear as degenerated forms. 
 
  COMPLICATIONS. Since the advent of antibiotics, serious complications of lobar pneumonia are uncommon. However, they may develop in neglected cases and in patients with impaired immunologic defenses.

 These are as under: 
 1.  Organisation. In about 3% of cases, resolution of the exudate does not occur but instead it is organised. There is ingrowth of fibroblasts from the alveolar septa resulting in fibrosed, tough, airless leathery lung tissue. 
 2.  Pleural effusion. About 5% of treated cases of lobar pneumonia develop inflammation of the pleura with effusion. 
 3.   Empyema. Less than 1% of treated cases of lobar pneumonia develop encysted pus in the pleural cavity termed empyema. 
 4.   Lung abscess. A rare complication of lobar pneumonia is formation of lung abscess. 
 5.   Metastatic infection. Occasionally, infection in the lungs and pleural cavity in lobar pneumonia may extend into the pericardium and the heart causing purulent pericarditis, bacterial endocarditis and myocarditis. 
 
 
 CLINICAL FEATURES. The major symptoms are: shaking chills, fever, malaise with pleuritic chest pain, dyspnoea and cough with expectoration which may be mucoid, purulent or even bloody. The common physical findings are fever, tachycardia, and tachypnoea, and sometimes cyanosis if the patient is severely hypoxaemic. There is generally a marked neutrophilic leucocytosis. Blood cultures are positive in about 30% of cases. Chest radiograph may reveal consolidation. 
 
 II.   Bronchopneumonia (Lobular Pneumonia)  
  Bronchopneumonia or lobular pneumonia is infection of the terminal bronchioles that extends into the surrounding alveoli resulting in patchy consolidation of the lung. The condition is particularly frequent at extremes of life (i.e. in infancy and old age), as a terminal event in chronic debilitating diseases and as a secondary infection following viral respiratory infections such as influenza, measles etc, 
 
  ETIOLOGY.

The common organisms responsible for bronchopneumonia are staphylococci, streptococci, pneumococci, Klebsiella pneumoniae, Haemophilus influenzae, and gram-negative bacilli like Pseudomonas and coliform bacteria. 
 
 Bronchopneumonia is identified by patchy areas of red or grey consolidation affecting one or more lobes, frequently found bilaterally and more often involving the lower zones of the lungs due to gravitation of the secretions. On cut surface, these patchy consolidated lesions are dry, granular, firm, red or grey in colour, 3 to 4 cm in diameter, slightly elevated over the surface and are often centred around a bronchiole. These patchy areas are best picked up by passing the fingertips on the cut surface. 
 
Microscopic Examination 

i) Acute bronchiolitis, ii) Suppurative exudate, consisting chiefly of neutrophils, in the peribronchiolar alveoli, iii) Thickening of the alveolar septa by congested capillaries and leucocytic infiltration, iv) Less involved alveoli contain oedema fluid. 
 
 COMPLICATIONS. 
 
 The complications of lobar pneumonia may occur in bronchopneumonia as well. However, complete resolution of bronchopneumonia is uncommon. There is generally some degree of destruction of the bronchioles resulting in foci of bronchiolar fibrosis that may eventually cause bronchiectasis.
 
 CLINICAL FEATURES. The patients of bronchopneumonia are generally infants or elderly individuals. There may be history of preceding bed-ridden illness, chronic debility, aspiration of gastric contents or upper respiratory infection. 
 
  VIRAL AND MYCOPLASMAL PNEUMONIA (PRIMARY ATYPICAL PNEUMONIA)  
 
 Viral and mycoplasmal pneumonia is characterised by patchy inflammatory changes, largely confined to interstitial tissue of the lungs, without any alveolar exudate. Other terms used for these respiratory tract infections are interstitial pneumonitis, reflecting the interstitial location of the inflammation, andprimary atypical pneumonia, atypicality being the absence of alveolar exudate commonly present in other pneumonias. Interstitial pneumonitis may occur in all ages. 
 
ETIOLOGY. Interstitial pneumonitis is caused by a wide variety of agents, the most common being respiratory syncytial virus (RSV). Others are Mycoplasma pneumoniae and  many viruses such as influenza and parainfluenza viruses, adenoviruses, rhinoviruses, coxsackieviruses and cytomegaloviruses (CMV). 
 
 Depending upon the severity of infection, the involvement may be patchy to massive and widespread consolidation of one or both the lungs. The lungs are heavy, congested and subcrepitant. Sectioned surface of the lung exudes small amount of frothy or bloody fluid. 
  
Microscopic Examination 

 I) Interstitial Inflammation: There is thickening of alveolar walls due to congestion, oedema and mononuclear inflammatory infiltrate comprised by lymphocytes, macrophages and some plasma cells. illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
 ii)  Necrotising bronchiolitis: This is characterised by foci of necrosis of the bronchiolar epithelium, inspissated secretions in the lumina and mononuclear infiltrate in the walls and lumina. 
 
 iii) Reactive changes: The lining epithelial cells of the bronchioles and alveoli proliferate in the presence of virus and may form multinucleate giant cells and syncytia in the bronchiolar and alveolar walls. 
 
 iv) Alveolar changes: In severe cases, the alveolar lumina may contain oedema fluid, fibrin, scanty inflammatory exudate and coating of alveolar walls by pink, hyaline membrane similar to the one seen in respiratory distress syndrome. 
 
 COMPLICATIONS. 
 
 The major complication of interstitial pneumonitis is superimposed bacterial infection and its complications. Most cases of interstitial pneumonitis recover completely.
 
 CLINICAL FEATURES. 
 
 Majority of cases of interstitial pneumonitis initially have upper respiratory symptoms with fever, headache and muscle-aches. A few days later appears dry, hacking, non-productive cough with retrosternal burning due to tracheitis and bronchitis. Chest radiograph may show patchy or diffuse consolidation.  
 
  C. OTHERTYPES OF PNEUMONIAS  
 
 I.     Pneumocystis carinii Pneumonia  
 
 Pneumocystis carinii, a protozoon widespread in the environment, causes pneumonia by inhalation of the organisms as an opportunistic infection in neonates and immunosuppressed people. Almost 100% cases of AIDS develop opportunistic infection, most commonly Pneumocystis carinii pneumonia. 
 
 II.     Legionella Pneumonia 

 Legionella pneumonia or legionnaire's disease is an epidemic illness caused by gramnegative bacilli, Legionella pneumophila that thrives in aquatic environment. It was first recognised following investigation into high mortality among those attending American Legion Convention in Philadelphia in July 1976. The epidemic occurs in summer months by spread of organisms through contaminated drinking water or in air-conditioning cooling towers. Impaired host defenses in the form of immunodeficiency, corticosteroid therapy, old age and cigarette smoking play important roles. 
 
 III. Aspiration (Inhalation) Pneumonia  
 
 Aspiration or inhalation pneumonia results from inhaling different agents into the lungs. These substances include food, gastric contents, foreign body and infected material from oral cavity. A number of factors predispose to inhalation pneumonia which include: unconsciousness, drunkenness, neurological disorders affecting swallowing, drowning, necrotic oropharyngeal tumours, in premature infants and congenital tracheo-oesophageal fistula. 
 
 1.   Aspiration of small amount of sterile foreign matter such as acidic gastric contents produce chemical pneumonitis. It is characterised by haemorrhagic pulmonary oedema with presence of particles in the bronchioles. 
 
 2.    Non-sterile aspirate causes widespread bronchopneumonia with multiple areas of necrosis and suppuration. 
 
IV. Hypostatic Pneumonia 

 Hypostatic pneumonia is the term used for collection of oedema fluid and secretions in the dependent parts of the lungs in severely debilitated, bedridden patients. The accumulated fluid in the basal zone and posterior part of lungs gets infected by bacteria from the upper respiratory tract and sets in bacterial pneumonia.

 V. Lipid Pneumonia  Another variety of noninfective pneumonia is lipid pneumonia. It is of 2 types: 
 
 1.   Exogenous lipid pneumonia. This is caused by aspiration of a variety of oily materials. These are: inhalation of oily nasal drops, regurgitation of oily medicines from stomach (e.g. liquid paraffin), administration of oily vitamin preparation to reluctant children or to debilitated old patients. 
 
 2.   Endogenous lipid pneumonia. Endogenous origin of lipids causing pneumonic consolidation is more common. The sources of origin are tissue breakdown following obstruction to airways e.g. obstruction by bronchogenic cancer, tuberculosis and bronchiectasis.