Psoriasis
1. Characterized by skin lesions that appear as scaly, white plaques.
2. Caused by rapid proliferation of the epidermis.
3. Autoimmune pathogenesis; exact mechanism is unclear.

Immunodeficiency

This may be :- 
- Congenital (Primary)
- Acquired (Secondary)

Features : Complete or near complete lack of T & B lymphoid tissue. Fatal early in life Even with marrow grafting, chances of graft versus host reaction is high.

T Cell Defects :

- Thymic dysplasia
- Digeorge’s syndrome
- Nazelof’s syndrome
- Ataxia teltngiectaisa
- Wiscott Aldrich’s syndrome

These  lessons show predominantly defective cell mediated immunity. But they may also show partial immunoglobulin defects cell mediated immunity. But they may also show partial immunoglobulin defects due to absence og T-B co-operation.

C. Humoral immunity defects.
Bruron type- aggammaglobulinaemia.
- Dysgammaglobulinaemias-variable immunodeficiency’s of one or more classes.

Acquired deficiency

A. Immuno suppression by :
- Irradiation.
- Corticoids.
- Anti metabolites.
- Anti lymphocyte serum.

B. Neaplasia  of lymphoid system :

- Hodgkin's and Non Hodgkin's lymphomas.
- Chronic lymphocytic leukaemia..
- Multime myeloma and other paraproteinaemias (normal immunoglobulins reduced in spite of hyperglobulinaemia).

c. excessive protein loss.
- Nephrotic Syndrome.
- Protein losing enteropathy.

Chickenpox (varicella)
 - primarily a childhood disease (70%)
 - incubation period 14-16 days; highly contagious; infectious 2 days before the vesicles until the last one dries.
 - present with generalized, intensely pruritic skin lesions starting as macules vesicles pustules (MVP-most valuable player) usually traveling centrifugally to the face and out to the extremities; unlike smallpox vesicles, chickenpox vesicles appear in varying stages of development as successive crops of lesions appear; intranuclear inclusions similar to HSV.
 - pneumonia develops in 1/3 of adults; MCC death in chickenpox.
 - association with Reye's syndrome if child takes aspirin. 

Vitiligo is an autoimmune destruction of melanocytes resulting in areas of depigmentation.
 - commonly associated with other autoimmune diseases such as pernicious anemia, Addison's disease, and thyroid disease.
 - common in the Black population

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.
 

Congenital heart defect
Congenital heart defects can be broadly categorised into two groups,
o    acyanotic heart defects ('pink' babies) :

 An acyanotic heart defect is any heart defect of a group of structural congenital heart defects,  approximately 75% of all congenital heart defects.
 It can be subdivided into two groups depending on whether there is shunting of the blood from the left vasculature to the right (left to right shunt) or no shunting at all.

Left to right shunting heart defects include 
- ventricular septal defect or VSD (30% of all congenital heart defects),
- persistent ductus arteriosus or PDA, 
- atrial septal defect or ASD, 
- atrioventricular septal defect or AVSD.

Acyanotic heart defects without shunting include 
- pulmonary stenosis, a narrowing of the pulmonary valve, 
- aortic stenosis 
- coarctation of the aorta.

cyanotic heart defects ('blue' babies). 
obstructive heart defects

 cyanotic heart defect is a group-type of congenital heart defect. These defects account for about 25% of all congenital heart defects. The patient appears blue, or cyanotic, due to deoxygenated blood in the systemic circulation. This occurs due to either a right to left or a bidirectional shunt, allowing significant proportions of the blood to bypass the pulmonary vascular bed; or lack of normal shunting, preventing oxygenated blood from exiting the cardiac-pulmonary system (as with transposition of the great arteries).

Defects in this group include 
hypoplastic left heart syndrome,
tetralogy of Fallot, 
transposition of the great arteries, 
tricuspid atresia, 
pulmonary atresia, 
persistent truncus arteriosus.