FUNGAL INFECTION

Histoplasmosis

A disease caused by Histoplasma capsulatum, causing primary pulmonary lesions and hematogenous dissemination.

Symptoms and Signs

The disease has three main forms. Acute primary histoplasmosis is usually asymptomatic

Progressive disseminated histoplasmosis follows hematogenous spread from the lungs that is not controlled by normal cell-mediated host defense mechanisms. Characteristically, generalized involvement of the reticuloendothelial system, with hepatosplenomegaly, lymphadenopathy, bone marrow involvement, and sometimes oral or GI ulcerations occurs, particularly in chronic cases

Progressive disseminated histoplasmosis is one of the defining opportunistic infections for AIDS.

Chronic cavitary histoplasmosis is characterized by pulmonary lesions that are often apical and resemble cavitary TB. The manifestations are worsening cough and dyspnea, progressing eventually to disabling respiratory dysfunction. Dissemination does not occur

Diagnosis

Culture of H. capsulatum from sputum, lymph nodes, bone marrow, liver biopsy, blood, urine, or oral ulcerations confirms the diagnosis

Paroxysmal nocturnal haemoglobinuria (PNH).

Feature:

• Acquired RBC rnembrane defect rendering it susceptible  to complement lysis.
• Features of intravascular haemolysis.
• Blood picture of haemolysis anemais with pancytopenia.
• Ham’s acid serum test (lysis at 37COin acid pH) + ve

Hyperparathyroidism 

Abnormally high levels of parathyroid hormone (PTH) cause hypercalcemia. This can result from either primary or secondary causes. Primary hyperparathyroidism is caused usually by a parathyroid adenoma, which is associated with autonomous PTH secretion. Secondary  hyperparathyroidism, on the other hand, can occur in the setting of chronic renal failure. In either situation, the presence of excessive amounts of this hormone leads to significant skeletal changes related to a persistently exuberant osteoclast activity that is associated with increased bone resorption and calcium mobilization. The entire skeleton is affected. PTH is directly responsible for the bone changes seen in primary hyperparathyroidism, but in secondary hyperparathyroidism additional influences also contribute. In chronic renal failure there is inadequate 1,25- (OH)2-D synthesis that ultimately affects gastrointestinal calcium absorption. The hyperphosphatemia of renal
failure also suppresses renal α1-hydroxylase, which further impair vitamin D synthesis; all these eventuate in hypocalcemia, which stimulates excessive secretion of PTH by the parathyroid glands, & hence elevation in PTH serum levels. 

Gross features
• There is increased osteoclastic activity, with bone resorption. Cortical and trabecular bone are lost and replaced by loose connective tissue. 
• Bone resorption is especially pronounced in the subperiosteal regions and produces characteristic radiographic changes, best seen along the radial aspect of the middle phalanges of the second and third fingers.

Microscopical features

• There is increased numbers of osteoclasts and accompanying erosion of bone surfaces.
• The marrow space contains increased amounts of loose fibrovascular tissue.
• Hemosiderin deposits are present, reflecting episodes of hemorrhage resulting from microfractures of the weakened bone.
• In some instances, collections of osteoclasts, reactive giant cells, and hemorrhagic debris form a distinct mass, termed "brown tumor of hyperparathyroidism". Cystic change is common in such lesions (hence the name osteitis fibrosa cystica). Patients with hyperparathyroidism have reduced bone mass, and hence are increasingly susceptible to fractures and bone deformities.

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.
 

PERTUSSIS (Whooping Cough)

An acute, highly communicable bacterial disease caused by Bordetella pertussis and characterized by a paroxysmal or spasmodic cough that usually ends in a prolonged, high-pitched, crowing inspiration (the whoop).

Transmission is by aspiration of B. pertussis

Symptoms and Signs

The incubation period averages 7 to 14 days (maximum, 3 wk). B. pertussis invades the mucosa of the nasopharynx, trachea, bronchi, and bronchioles, increasing the secretion of mucus, which is initially thin and later viscid and tenacious. The uncomplicated disease lasts about 6 to 10 wk and consists of three stages: catarrhal, paroxysmal, and convalescent.

German measles (rubella)
 - sometimes called "three day measles".
 - incubation 14-21 days; infectious 7 days before the rash and 14 days after the onset of the rash.
 - in adults, rubella present with fever, headache, and painful postauricular Lymphadenopathy 1 to 2 days prior to the onset of rash, while in children, the rash is usually the first sign.
 - rash (vasculitis) consists of tiny red to pink macules (not raised) that begins on the head and spreads downwards and disappears over the ensuing 1-3 days; rash tends to become confluent.
 - 1/3rd of young women develop arthritis due to immune-complexes.
 - splenomegaly (50%)