Respiratory Viral Diseases

Respiratory viral infections cause acute local and systemic illnesses. The common cold, influenza, pharyngitis, laryngitis (including croup), and tracheobronchitis are common.

An acute, usually afebrile, viral infection of the respiratory tract, with inflammation in any or all airways, including the nose, paranasal sinuses, throat, larynx, and sometimes the trachea and bronchi.

Etiology and Epidemiology

Picornaviruses, especially rhinoviruses and certain echoviruses and coxsackieviruses, cause the common cold. About 30 to 50% of all colds are caused by one of the > 100 serotypes of rhinoviruses.

Symptoms and Signs

Clinical symptoms and signs are nonspecific.

After an incubation period of 24 to 72 h, onset is abrupt, with a burning sensation in the nose or throat, followed by sneezing, rhinorrhea, and malaise.

Characteristically, fever is not present, particularly with a rhinovirus or coronavirus. Pharyngitis usually develops early; laryngitis and tracheobronchitis vary by person and causative agent. Nasal secretions are watery and profuse during the first days, but become more mucoid and purulent.

Cough is usually mild but often lasts into the 2nd wk.

Osteopetrosis (Albers-Schönberg disease or marble bone disease) 

is a group of rare genetic disorders characterized by reduced osteoclast-mediated bone resorption and therefore defective bone remodelling. The bones are solid and heavy with no medullary canal, long ends are bulbous, small neural foramina compress nerves. The affected bone is grossly dense but fractures occur readily like a piece of chalk. 

Patients frequently have cranial nerve compressions by the surrouding bone, and recurrent infections. The latter is attributable to diminished hematopoiesis resulting from reduced marrow space with impressive hepatosplenomegaly due to extramedullary hematopoiesis 
 
a. Caused by abnormal osteoclasts. This results in defective bone remodeling (i.e., abnormally low bone resorption) and increased bone density, which may invade into bone marrow space.
b. Causes severe defects in infants, including:
(1) Anemia and infections—caused by decreased bone marrow.
(2) Blindness, deafness, paralysis of facial muscles—caused by the narrowing of cranial nerve foramina.
(3) Is life-threatening.
(4) Oral findings include delayed eruption of teeth.
c. Disease is less severe in adults

Glomerulonephritis

Characterized by inflammation of the glomerulus.

Clinical manifestations:
Nephrotic syndrome (nephrosis) → Most often caused by glomerulonephritis.

Laboratory findings:
(i) Proteinuria (albuminuria) and lipiduria—proteins and lipids are present in urine.
(ii) Hypoalbuminemia—decreased serum albumin due to albuminuria.
(iii) Hyperlipidemia—especially an increase in plasma levels of low-density lipoproteins and cholesterol.

Symptoms

severe edema, resulting from a decrease in colloid osmotic pressure due to a decrease in serum albumin.

Pulmonary embolism

A pulmonary embolism (thromboembolism) occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.

Clinical presentation

Signs of PE are sudden-onset dyspnea (shortness of breath, 73%), tachypnea (rapid breathing, 70%), chest pain of "pleuritic" nature (worsened by breathing, 66%), cough (37%), hemoptysis (coughing up blood, 13%), and in severe cases, cyanosis, tachycardia (rapid heart rate), hypotension, shock, loss of consciousness, and death. Although most cases have no clinical evidence of deep venous thrombosis in the legs, findings that indicate this may aid in the diagnosis.

Diagnosis

The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography

An electrocardiogram may show signs of right heart strain or acute cor pulmonale in cases of large PEs

In massive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure.

Treatment

Acutely, supportive treatments, such as oxygen or analgesia

In most cases, anticoagulant therapy is the mainstay of treatment. Heparin or low molecular weight heparins are administered initially, while warfarin therapy is given

Graves disease 

Graves disease is an organ-specific autoimmune disorder that results in thyrotoxicosis due to overstimulation of the thyroid gland by autoantibodies. 
- It is the most common form of thyrotoxicosis, females being affected more than males by 8: 1. 
- It is usually associated with a diffuse enlargement of the thyroid.

Pathogenesis
 
IgG-type immunoglobulins bind to TSH membrane receptors and cause prolonged stimulation of the thyroid, lasting for as long as 12 hours 
(cf. 1 hour for TSH). The autoantibody binds at a site different to the hormone-binding locus and is termed the TSH-receptor autoantibody (TRAb); 95% of Graves’ disease patients are positive for TRAbs

Gross features 
- The thyroid gland is diffusely and moderately enlarged
- It is usually smooth, soft, and congested  

Histologically
- the gland shows diffuse hypertrophy and hyperplasia of acinar epithelium, reduction of stored colloid and local accumulations of lymphocytes with lymphoid follicle formation.

Clinical features

- Exophthalmos (protrusion of the eyeballs in their sockets)—due to the infiltration of orbital tissues by fat, mucopolysaccharides and lymphocytes. May cause compression of the optic nerve, hence blindness. However, only about 5% of Graves’ patients show signs of exophthalmos.
- Thyroid acropachy—enlargement of fingernails. 
- Pretibial myxoedema—accumulation of mucoproteins in the deep dermis of the skin.

Treatment is as for thyrotoxicosis.

FUNGAL INFECTION

Aspergillosis

Opportunistic infections caused by Aspergillus sp and inhaled as mold conidia, leading to hyphal growth and invasion of blood vessels, hemorrhagic necrosis, infarction, and potential dissemination to other sites in susceptible patients.

Symptoms and Signs: Noninvasive or, rarely, minimally locally invasive colonization of preexisting cavitary pulmonary lesions also may occur in the form of fungus ball (aspergilloma) formation or chronic progressive aspergillosis.

Primary superficial invasive aspergillosis is uncommon but may occur in burns, beneath occlusive dressings, after corneal trauma (keratitis), or in the sinuses, nose, or ear canal.

Invasive pulmonary aspergillosis usually extends rapidly, causing progressive, ultimately fatal respiratory failure unless treated promptly and aggressively. A. fumigatus is the most common causative species.

 Extrapulmonary disseminated aspergillosis may involve the liver, kidneys, brain, or other tissues and is usually fatal. Primary invasive aspergillosis may also begin as an invasive sinusitis, usually caused by A. flavus, presenting as fever with rhinitis and headache