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.

Pyelonephritis

- A bacterial infection that affects the renal tubules, interstitium, and renal pelvis.
- One of the most common renal diseases. 
- Usually caused by gram-negative, rod-shaped bacteria that are part of the normal flora of the enteric tract. Most commonly caused by Escherichia coli, followed by Proteus, Klebsiella, and Enterobacter.
- The infecting bacteria are usually from the patient’s own enteric flora an example of an endogenous infection.
- Usually associated with a urinary tract infection (acute pyelonephritis) or involved with another precipitating condition, such as obstruction (chronic pyelonephritis).

Diseases from Str. pyogenes (Group A strep)

1.  Streptococcal pharyngitis.  Most frequent Group A infection.  Throat has gray-white exudate.  Infection may become systemic into blood, sinuses, jugular vein, meninges.  In less than a week the M-protein and capsule production decrease, and transmission declines.

2.  Skin infections, such as impetigo.  Especially in children.  Different M-proteins than in pharyngitis.  Skin infections associated with edema and red streaking (characteristic).

3.  Necrotizing fasciitis/myositis.  Infection of deeper tissue advances despite antibiotics.

4. Scarlet fever.  Caused by phage-associated erythrogenic toxin-producing strains.  Toxins cause cardiac, renal, and other systemic failures.  Rash is very red with a sand-papery feel and shedding of superficial skin.

5.  Toxic Shock Syndrome.  Parallels the toxic shock caused by TSST-carrying Staph. aureus.

6.  Non-suppurative, post-infection diseases. 

Rheumatic fever (myocarditis, cardiac valve disease, polyarthralgia, rashes.  Occurs two  weeks after a pharyngeal infection)

Glomerulonephritis (Occurs two weeks after pharyngeal or skin infections.  Often due to immunologic reaction to M-protein type 12)

Bronchitis

Bronchitis is an obstructive pulmonary disease characterized by inflammation of the bronchi of the lungs

Signs and symptoms

persistent cough that produces sputum

shortness of breath (dyspnea) on exertion

hypercapnia

insufficient oxygenation of the blood hypoxemia leading to cynosis

Severe chronic bronchitis will commonly lead to cor pulmonale and heart failure.

Pathology

an increase in the number of goblet cells with mucus blocking the airway clusters of pigmented alveolar macrophages

the presence of inflammatory cells (e.g. neutrophils) scarring (fibrosis) of the walls of the bronchioles

Diagnosis

• decreased intensity of breath sounds (rhonchi) and extended expiration.
• a sputum culture has pathogenic microorganisms
• a chest x-ray that reveals hyperinflation and increased bronchovascular markings
• a pulmonary function test that shows an increase in the lung's residual volume and a decreased vital capacity

Pathophysiology

• The initiating event in developing bronchitis appears to be chronic irritation due to inhalation of certain chemicals
• earliest clinical feature of bronchitis is increased secretion of mucus by submucousal glands of the trachea and bronchi
• Damage caused by irritation of the airways leads to inflammation and infiltration of the lung tissue by neutrophils
• The neutrophils release substances that promote mucousal hypersecretion
• As bronchitis persists to become chronic bronchitis, a substantial increase in the number of goblet cells in the small airways is seen
• The role of infection in the pathogenesis of chronic bronchitis appears to be secondary.

Treatment

Quit smoking, Oxygen therapy, bronchodilator drugs

Prognosis

Pulmonary hypertension, cor pulmonale, and chronic respiratory failure are possible complications of chronic bronchitis

In severe chronic bronchitis is poor

Hepatitis

Hepatitis viruses—this group of viruses causes hepatitis, a disease affecting the liver.
1. General characteristics of hepatitis.
a. The general presentation of hepatitis is the same regardless of the infecting virus; however, the time and severity of symptoms may differ.
b. Symptoms of hepatitis include fever, anorexia, malaise, nausea, jaundice, and brown-colored urine.
c. Complications of a hepatitis infection include cirrhosis, liver failure, and hepatorenal failure.

Haemolytic anaemia 

Anemia due to increased red cell destruction (shortened life span)

Causes:

A. Corpuscular defects:

1.Membrane defects:

    - Spherocytosis.
    - Elliptocytosis.

2. Haemoglobinopathies:

    - Sickle cell anaemia.
    - Thalassaemia
    - Hb-C, HBD, HbE.
    
3. Enzyme defects .deficiency of:

    - GIucose -6 phosphate dehydrogenase (G6-PD)
    - Pyruvate kinase
    
4. Paroxysmal nocturnal haemoglobinuria.

B. Extracorpusular mechanisms 

1. Immune based:
    - Autoimmune haemolytic anaemia.
    - Haemolytic disease of new born.
    - Incompatible transfusion.
    - Drug induced haemolysis
    
2. Mechanical haemolytic anaemia.
3. Miscellaneous due to :

    - Drugs and chemicals.
    - Infections.
    - Burns.

features of haemolytic anaemia

- Evidence of increased Hb breakdown:

    -> Unconjugated hyperbilirubinaemia.
    -> Decreased plasma haptoglobin.
    -> Increased urobilinogen and stercobilinogen.
    -> Haemoglobinaemia, haemoglobinuria and haemosiderinuria if Intravascular haemolysis occurs.

- Evidence or compensatory erythroid hyperplasia:

    -> Reticulocytosis and nucleated RBC in peripheral smear.
    -> Polychromasia and macrocytes 
    -> Marrow erythroid hyperplasia
    -> Skull and other bone changes.

- Evidences of damage to RBC:

    -> Spherocytes and increased osmotic fragility
    -> Shortened life span.
    -> Fragmented RBC.
    -> Heinz bodies.