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

Staphylococcal Infection

Staphylococci, including pathogenic strains, are normal inhabitants of the nose and skin of most healthy people
Virulence factors include coagulase (which clots blood), hemolysin, and protein A (which ties up Fc portions of antibodies). Although we have antibodies against staphylococci, they are of limited usefulness. 

Staphylococci (and certain other microbes) also produce catalase, which breaks down H2O2, rendering phagocytes relatively helpless against them. 

The coagulase-positive staphylococcus (Staphylococcus pyogenes var. aureus) is a potent pathogen. It tends to produce localized infection
It is the chief cause of bacterial skin abscesses. Infection spreads from a single infected hair (folliculitis) or splinter to involve the surrounding skin and subcutaneous tissues

Furuncles are single pimples
carbuncles are pimple clusters linked by tracks of tissue necrosis which involve the fascia.

Impetigo is a pediatric infection limited to the stratum corneum of the skin -- look for honey-colored crusts

Staphylococcal infections of the nail-bed (paronychia) and palmar fingertips (felons) are especially painful and destructive

These staph are common causes of wound infections (including surgical wounds) and of a severe, necrotizing pneumonia. Both are serious infections in the hospitalized patient.

Staph is the most common cause of synthetic vascular graft infections. Certain sticky strains grow as a biofilm on the grafts

Staph aureus is pathogenic, β-hemolytic, and makes coagulase.
Staph epidermidis are non-pathogenic strains that don’t make coagulase.  Often Antibiotics resistant, and     can become opportunistic infections in hospitals.

Staph aureus is normal flora in the nose and on skin, but can also colonize moist areas such as perineum.  Causes the minor infections after cuts.  Major infections occur with lacerations or immune compromise, where large number of cocci are introduced.

While Staph aureus can invade the gut directly (invasive staphylococcal enterocolitis), it is much more common to encounter food poisoning due to strains which have produced enterotoxin B, a pre-formed toxin in un-refrigerated meat or milk products

Staph epidermidis (Coagulase-negative staphylococci)
Universal normal flora but few virulence factors.  Often antibiotic resistant.
Major cause of foreign body infections such as prosthetic valve endocarditis and IV line sepsis.

Staph saprophyticus
Common cause of UTI in women.

Pathogenicity
Dominant features of S. aureus infections are pus, necrosis, scarring.  The infections are patchy.  Serious disease is rare because we are generally immune.  However, foreign bodies or necrotic tissue can start an infection.  Staph infections include wound infections, foreign body sepsis, pneumonia, meningitis.
Occassionally, S. aureus can persist within cells.

Major disease presentations include:
    --Endocarditis
    --Abscesses (due to coagulase activity)
    --Toxic Shock
    --Wound infections
    --Nosocomial pneumonia

Prevention of Staph aureus infections
S. aureus only lives on people, so touching is the main mode of transmission.  Infected patients     should be isolated, but containment is easy with intense hand washing.
 

Lymphomas

A. Hodgkin’s disease

1. Characterized by enlarged lymph nodes and the presence of Reed-Sternberg cells (multinucleated giant cells) in lymphoid tissues.

2. Disease spreads from lymph node to lymph node in a contiguous manner.

3. Enlarged cervical lymph nodes are most commonly the first lymphadenopathy observed.

4. The cause is unknown.

5. Occurs before age 30.

6. Prognosis of disease depends largely on the extent of lymph node spread and systemic involvement.

B. Non-Hodgkin’s lymphoma

1. Characterized by tumor formation in the lymph nodes.

2. Tumors do not spread in a contiguous manner.

3. Most often caused by the proliferation of abnormal B cells.

4. Occurs after age 40.

5. Example: Burkitt’s lymphoma

a. Commonly associated with an EpsteinBarr virus (EBV) infection and a genetic mutation resulting from the translocation of the C-myc gene from chromosome 8 to 14.

b. The African type occurs in African children and commonly affects the mandible or maxilla.

c. In the United States, it most commonly affects the abdomen.

d. Histologically, the tumor displays a  characteristic “starry-sky” appearance.

HYPERPLASIA
It is the increase in the size of an organ or tissue due to increase in the number of its constituent cells. This is seen in organs made up of labile and stable cells.

Causes
I. Increased demand:
- Bone marrow in hypoxia and haemolytic states.
- Thyroid gland in puberty

2. Persistant Trauma:
- Acanthosis of the epidermis in chronic inflammations and in warts.
- Hyperplasia of oral mucosa due tooth and denture trauma.
- Mucosa at the edges of a gastric ulcer.

3. Endocrine target organ:
- Pregnancy hyperplasia of breast.
- Prostatic hyperplasia.

4. Compensatory:

Hyperplasia of kidney when the other kidney has been removed.

5. Idiopathic:
Endocrine organs like thyroid, adrenals, pituitary etc. can undergo hyperplasia with no detectable stimulus. .
 

Rickets and Osteomalacia 

Rickets in growing children and osteomalacia in adults are skeletal diseases with worldwide distribution. They may result from
1. Diets deficient in calcium and vitamin D
2. Limited exposure to sunlight (in heavily veiled women, and inhabitants of northern climates with scant sunlight)
3. Renal disorders causing decreased synthesis of 1,25 (OH)2-D or phosphate depletion 
4. Malabsorption disorders.

Although rickets and osteomalacia rarely occur outside high-risk groups, milder forms of vitamin D deficiency (also called vitamin D insufficiency) leading to bone loss and hip fractures are quite common in the elderly.

Whatever the basis, a deficiency of vitamin D tends to cause hypocalcemia. When hypocalcemia occurs, PTH production is increased, that ultimately leads to restoration of the serum level of calcium to near normal levels (through mobilization of Ca from bone & decrease in its tubular reabsorption) with persistent hypophosphatemia (through increase renal exretion of phosphate); so mineralization of bone is impaired or there is high bone turnover.

The basic derangement in both rickets and osteomalacia is an excess of unmineralized matrix. This complicated in rickets by derangement of endochondral bone growth.

The following sequence ensues in rickets:
1. Overgrowth of epiphyseal cartilage with distorted, irregular masses of cartilage
2. Deposition of osteoid matrix on inadequately mineralized cartilage
3. Disruption of the orderly replacement of cartilage by osteoid matrix, with enlargement and lateral expansion of the osteochondral junction
4. Microfractures and stresses of the inadequately mineralized, weak, poorly formed bone
5. Deformation of the skeleton due to the loss of structural rigidity of the developing bones 

Gross features
• The gross skeletal changes depend on the severity of the disease; its duration, & the stresses to which individual bones are subjected.
• During the nonambulatory stage of infancy, the head and chest sustain the greatest stresses. The softened occipital bones may become flattened. An excess of osteoid produces frontal bossing. Deformation of the chest results from overgrowth of cartilage or osteoid tissue at the costochondral junction, producing the "rachitic rosary." The weakened metaphyseal areas of the ribs are subject to the pull of the respiratory muscles and thus bend inward, creating anterior protrusion of the sternum (pigeon breast deformity). The pelvis may become deformed.
• When an ambulating child develops rickets, deformities are likely to affect the spine, pelvis, and long bones (e.g., tibia), causing, most notably, lumbar lordosis and bowing of the legs .
• In adults the lack of vitamin D deranges the normal bone remodeling that occurs throughout life. The newly formed osteoid matrix laid down by osteoblasts is inadequately mineralized, thus producing the excess of persistent osteoid that is characteristic of osteomalacia. Although the contours of the bone are not affected, the bone is weak and vulnerable to gross fractures or microfractures, which are most likely to affect vertebral bodies and femoral necks.

Microscopic features

• The unmineralized osteoid can be visualized as a thickened layer of matrix (which stains pink in hematoxylin and eosin preparations) arranged about the more basophilic, normally mineralized trabeculae.

Histopathological techniques

Histopathological examination studies tissues under the microscope. During this study, the pathologist looks for abnormal structures in the tissue. Tissues for histopathological examination are obtained by biopsy. Biopsy is a tissue sample from a living person to identify the disease. Biopsy can be either incisional or excisional.

Once the tissue is removed from the patient, it has to be immediately fixed by putting it into adequate amount of 10% Formaldehyde (10% formalin) before sending it to the pathologist.

The purpose of fixation is:

1. to prevent autolysis and bacterial decomposition and putrefaction

2. to coagulate the tissue to prevent loss of easily diffusible substances

3. to fortify the tissue against the deleterious effects of the various stages in the preparation of sections and tissue processing.

 4. to leave the tissues in a condition which facilitates differential staining with dyes and other reagents.