Pneumonia, Bacterial

Introduction

Background

Medical practitioners have known of pneumonia since ancient times. Hippocrates indoctrinated his students about "peripneumonia," which, for the ancient healers, had a connotation of an acute illness either with pain in the side or with severe dyspnea. The term acquired a more punctilious meaning as the study of morbid anatomy and physical diagnosis progressed over the last few centuries. Morgagni contributed the concept of solidification of the lung. Laennec, the father of pulmonary medicine, described pathological stages of the disease and showed how to diagnose them using auscultation.

Rokitansky's graphic narration helped distinguish lobar from lobular or bronchial pneumonia. Pasteur discovered Streptococcus pneumoniae in 1880, and before long, this organism was proved to be a cause of lobar pneumonia. The contemporary physicians of the 19th century were well aware of lobar pneumonia. Coope described lobar pneumonia as that "which consists of a series of changes by which the spongy pulmonary tissue is rapidly converted into a solid mass, returning afterwards, in cases that recover, to its normal condition." The modern physician, who is more adept with the x-ray viewing box than the autopsy room, has acquired sufficient familiarity with this common malady as knowledge and wisdom has been acquired over the centuries.

Pneumonia is defined as inflammation and consolidation of the lung tissue due to an infectious agent. Pneumonia that develops outside the hospital setting is considered community-acquired pneumonia. Pneumonia developing 72 hours or more after admission to the hospital is termed nosocomial or hospital-acquired pneumonia. Community-acquired pneumonia is caused most commonly by bacteria that traditionally have been divided into 2 groups, typical and atypical. Typical organisms include S pneumoniae (pneumococcus) and Haemophilus and Staphylococcus species. Atypical refers to pneumonia caused by Legionella, Mycoplasma, and Chlamydia species.

The most common atypical pneumonias are caused by 3 zoonotic pathogens, Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever), and 3 nonzoonotic pathogens, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella pneumoniae. These atypical community-acquired pneumonias (CAPs) often cause systemic manifestations and are helpful in clinically differentiating from typical CAPs by the pattern of extrapulmonary organ involvement, which is characteristic for each atypical CAP. While zoonotic pneumonias may be eliminated from diagnostic consideration with a negative contact history, the atypical pneumonias are infrequent (approximately 15% of CAPs are atypical), difficult to diagnose, and unresponsive to beta-lactam therapy.

A definitive laboratory diagnosis of Legionella is usually based on investigations such as direct fluorescent antibody (DFA) or indirect fluorescent antibody (IFA). Antibiotics used against Legionella include macrolides, doxycycline, rifampin, quinolones, and telithromycin. Treatment is usually continued for 2 weeks although morbidity and mortality is high.

Pathophysiology

Pathogenesis of typical pneumonia

S pneumoniae generally resides in the nasopharynx and is carried asymptomatically in approximately 50% of healthy individuals. Invasive disease may occur upon acquisition of a new epithelium serotype. A strong association exists with viral illnesses, such as influenza. Viral infections increase pneumococcal attachment to the receptors on activated respiratory epithelium. Once aerosolized from the nasopharynx to the alveolus, pneumococci infect type II alveolar cells. The pneumonic lesion progresses as pneumococci multiply in the alveolus and invade alveolar epithelium. Pneumococci spread from alveolus to alveolus through the pores of Kohn, thereby producing inflammation and consolidation along lobar compartments.

A recent multivariate analysis showed an independent association between pneumococcal CAP and alcoholism. Current alcohol abuse was associated with severe CAP. No significant differences were found in mortality, antibiotic resistance of S pneumoniae, and other etiologies.

Pathogenesis of atypical infection

After aspiration or inhalation, the atypical organisms attach to the respiratory epithelial cells by a variety of mechanisms. The presence of pili on the surface of Legionella species facilitates attachment. Once adhered, the organisms cause injury to the epithelial cells and their associated cilia. Many of the pathogenetic mechanisms may be immune-mediated rather than due to direct injury by the bacteria. A host defense is mounted via cell-mediated and humoral immunity. Infection caused by atypical organisms often spreads beyond the lobar boundaries and frequently is bilateral.

Pathogenesis of nosocomial pneumonia

Aspiration plays a central role in the pathogenesis of nosocomial pneumonia. Approximately 45% of healthy subjects aspirate during sleep, and an even higher proportion of severely ill patients aspirate routinely. Depending on the number and virulence of the pathogenic organisms reaching the lower respiratory tract and on the host defense factors, pneumonia may develop. The oropharynx of hospitalized patients may become colonized with aerobic gram-negative bacteria within a few days of admission. Therefore, nosocomial pneumonia is caused predominantly by the gram-negative bacilli. However, the incidence of Staphylococcus aureus lower respiratory tract infection is increasingly common in the hospitalized and institutionalized patient and must now be considered a possible pathogen for nosocomial pneumonia.

Frequency

United States

Community-acquired pneumonia remains a common illness. Approximately 4.5 million cases of community-acquired pneumonia occur annually, and 20% result in hospitalization. Estimates of incidence of nosocomial pneumonia range from 4-7 episodes per 1000 hospitalizations. Approximately 25% of patients in intensive care units (ICUs) develop pneumonia. Overall incidence of community-acquired pneumonia is reported to be 170 cases per 100,000 persons. With advancing age, the incidence increases from 94 cases per 100,000 persons in patients aged 44 years to 280 cases per 100,000 persons in those older than 65 years. Pneumonia as a cause of hospitalization increased from 36 to 48 cases per 100,000 persons between 1984 and 1995.

Mortality/Morbidity

Pneumonia is the sixth leading cause of death in the United States and is the most common infectious cause of death. The mortality rate is reported to be 1% in the outpatient setting but may increase to up to 25% in those requiring hospital admission. In a patient with preexisting respiratory disease, onset of bacterial pneumonia may result in deterioration of respiratory status, leading to respiratory failure and death.

• Nosocomial pneumonia is the leading cause of death among hospital-acquired infections. Recent studies have shown that nosocomial pneumonia causes excessive risk of death, and the mortality rates range from 20-50%.
• Although less common in the antibiotic era, bacterial pneumonia may lead to bronchiectasis. However, lower respiratory infection with pneumococci, staphylococci, and Klebsiella species may result in bronchiectasis, especially if treatment is delayed. The damaged alveoli and small- to medium-sized airways are replaced by dilated saccules that are filled with purulent material. Ongoing chronic inflammation may gradually destroy the surrounding lung tissue.
• In patients with community-acquired pneumonia, daily activities were restricted for 24.8 days per 100 persons. Lost days of work were 8.9 days per 100 adult employees. The annual cost to treat patients with community-acquired pneumonia in the United States was 9.7 billion dollars in 1994; 92% of these costs were secondary to hospitalization. A substantial difference in cost exists between inpatient and outpatient therapy for pneumonia (US $7517 vs $264).

Sex

Incidence is greater in males than in females.

Age

Advanced age increases the incidence of pneumonia and the mortality from pneumonia.

• Elderly persons have weaker immune responses, higher risk of aspiration, and other comorbidities.
• In a 20-year US study, the mortality rate from pneumococcal pneumonia with bacteremia was 20.3%, overall. However, a higher mortality rate (37.7%) occurred in elderly patients.

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Pulmonary Eosinophilia

Introduction

Background

Pulmonary diseases associated with tissue and/or blood eosinophilia are a heterogeneous group of disorders. Various nosologies have been offered, but this article classifies these syndromes as extrinsic or intrinsic in origin. Some syndromes overlap, but this approach is convenient from the diagnostic standpoint.

Inhaled or ingested extrinsic factors, including medications and infectious agents (eg, parasites, fungi, mycobacteria), may trigger an eosinophilic immune response. This may be mild and self-limited, as in Loeffler syndrome.

Intrinsic pulmonary eosinophilic syndromes are generally idiopathic in nature. They include a diverse group of autoimmune and idiopathic syndromes ranging from blood dyscrasias to vasculitis. This group includes acute eosinophilic pneumonia (AEP), chronic eosinophilic pneumonia (CEP), idiopathic hypereosinophilic syndrome (IHES), Churg-Strauss syndrome (CSS), and eosinophilic granuloma (EG; pulmonary histiocytosis X or Langerhans cell granulomatosis).

Eosinophilia and pulmonary infiltrates have been reported in patients with AIDS, lymphoma, a variety of inflammatory lung diseases, and collagen vascular diseases (see Causes).

Asthma may manifest with marked eosinophilia, with or without infiltrates.

For additional information, see the following:

• Asthma
• Churg-Strauss Syndrome
• Pneumonia, Bacterial
• Pneumonia, Fungal
• Pneumonia, Viral
• Medscape's Pneumonia Resource Center

Pathophysiology

Tissue pathology is largely related to the release of toxic eosinophil products. These products include major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin, which damage the respiratory epithelium, induce ciliastasis, and influence mucus production. Tissue injury may also be caused by the release of reactive oxygen species. The release of platelet-activating factor and leukotrienes contributes to bronchospasm. In some syndromes, such as tropical pulmonary eosinophilia (TPE) and CEP, interstitial fibrosis may result from chronic inflammation. Commonly, lung parenchyma is affected, but in certain extrinsic and intrinsic syndromes, other organs may be affected.

Extrinsic eosinophilic syndromes

• Loeffler syndrome: The pathogenesis of Loeffler syndrome is unknown but presumably reflects a hypersensitivity response to an ingested or inhaled antigen from food, medication, or an infectious agent. Many of the original cases of Loeffler syndrome were thought to be related to Ascaris infection.
• Parasitic infections: Migrating parasites traversing the lungs may cause bronchospasm, dyspnea, and pulmonary infiltrates. Embolization of microfilariae or eggs, which degenerate and expose antigens to the local immune system, leads to granuloma formation. Local elaboration of chemokines and cytokines plays a role in T-cell recruitment and granuloma formation. Persistent inflammation may lead to parenchymal necrosis and fibrosis.
• Schistosomiasis: The most common pulmonary complication is pulmonary hypertension from chronic embolization of ova.
• TPE: These patients have marked immune responses to filariae, while other individuals infected with Wuchereria bancrofti or Brugia malayi have suppressed parasite-specific immune responses. Patients with TPE rarely have signs of lymphatic filariasis. Elevated immunoglobulin E (IgE) and immunoglobulin G (IgG) levels in patients with TPE reflect polyclonal B-cell activation.
• Strongyloidiasis: Patients who are immunocompromised, including those recently prescribed systemic corticosteroids, may develop hyperinfection syndrome, in which large numbers of recently released larvae burrow through the intestine and migrate to the lungs. Sepsis and respiratory failure may result from accompanying enteric bacteremia.
• Fungal causes: Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic response to Aspergillus antigens in the airways of individuals with obstructive lung disease. Both IgE-mediated and immune complex–mediated hypersensitivity responses are active. Chemokines recruit CD4+ T helper 2 antigen-specific cells to the lung. The inflammatory responses lead to airway reactivity, mucus hypersecretion, epithelial damage, bronchiectasis, eosinophilic pneumonia, and parenchymal injury and fibrosis. Aspergillus proteases likely also contribute to airway damage. Other fungi have also been found to cause a similar disorder, prompting some to suggest renaming this disorder allergic bronchopulmonary mycosis.
• Bronchocentric granulomatosis: This idiopathic condition, in which the mucosal epithelium is supplanted by epithelioid histiocytes and then by granuloma formation, is often associated with ABPA.

Intrinsic eosinophilic syndromes

• AEP: This is not associated with any history of medication usage or infection. Many patients have engaged in dusty outdoor activities, suggesting a hypersensitivity response to inhaled antigens. Eosinophilic alveolitis may be extensive, and profound hypoxemia with respiratory failure may result.
• CEP: The pathogenesis is unknown. CEP may occur in isolation and/or in association with polyarteritis nodosa, rheumatoid arthritis, scleroderma, ulcerative colitis, breast carcinoma,¹ and histiocytic lymphoma. Most patients have evidence of asthma and atopy. Although not a prominent feature, microgranulomata are occasionally seen on biopsy specimens, suggesting that an antigen-driven, T-cell–mediated process is active.
• IHES: Some patients display overproduction of chemokines,² proeosinophilic factors, including interleukin (IL)–4 and IL-5 by clonally expanded differentiation clusters 3 and 4 (CD3⁺ and CD4⁺) and Th2-like lymphocytes. These patients also have evidence of polyclonal hypergammaglobulinemia. Other patients have increased numbers of stem cells committed to the eosinophil lineage. Pulmonary involvement is manifested as wheezing, coughing, pulmonary edema, and pleural effusions. Pulmonary emboli result from a hypercoagulable state. Multiple organ systems may be affected, resulting in gastrointestinal tract dysfunction, skeletal muscle weakness (which may lead to respiratory failure), endomyocardial fibrosis, myocarditis, congestive heart failure, and/or valvular disease.
• CSS: The pathogenesis is unknown. Inhaled or ingested antigens have been proposed as causative agents in susceptible individuals. Recent reports linking the syndrome with the leukotriene inhibitors zafirlukast and montelukast in the setting of steroid withdrawal suggest these agents unmask preexisting CSS rather than suggesting that CSS is a direct causal effect of these agents. Vasculitis may affect the sinuses, central and peripheral nervous systems, gastrointestinal tract, kidneys, and heart.
• EG: The cause is unknown, but the reactive histiocytic proliferation suggests a reactive process, perhaps to an unknown antigen. Patients develop reticulonodular interstitial and cystic disease. EG is strongly associated with cigarette smoking. This may affect the lungs, bones (including the skull, resulting in diabetes insipidus), and other organs. Tissue and peripheral eosinophilia are generally not prominent features of this condition.

Frequency

United States

Intrinsic syndromes are uncommon. Regarding extrinsic syndromes, medication- or food-related syndromes are sporadic. Occasionally, outbreaks are related to contaminated food or medication, eg, L-tryptophan and toxic oil syndrome.

• Strongyloidiasis is the most common infection in the United States and is usually observed in individuals from the south, southeast, and Caribbean areas.
• Schistosoma mansoni infection is observed in the Caribbean.
• Toxocariasis (visceral larva migrans) is usually found in the southeast region of the country.
• Ascariasis, because it is prevalent worldwide, is likely to be observed in the United States.
• Among the hookworms, Necator americanus is endemic to the southeastern United States.
• Occasionally, international visitors or recent immigrants may present with other parasitic infections such as TPE and paragonimiasis.
• For fungal causes, ABPA is relatively common, with some estimates indicating that 5-10% of people who are steroid-dependent and have asthma meet the criteria. Of persons with cystic fibrosis, 10% have ABPA. Coccidioidomycosis is found predominantly in the southwestern part of the United States or among individuals with a relevant travel history.

International

Intrinsic syndromes are uncommon. Regarding extrinsic syndromes, in much of the world, parasitic infections are endemic.

• Ascaris is likely the most prevalent nematode infecting humans worldwide but tends to occur in tropical or subtropical areas.
• Ancylostoma duodenale is commonly found in the Eastern Hemisphere.
• Visceral larva migrans is found throughout the world.
• Strongyloidiasis, which usually occurs in warmer climates, has a worldwide prevalence of approximately 50-100 million individuals.
• Schistosomiasis is common in Africa, Asia, Latin America, and South America. Paragonimiasis and clonorchiasis are common in Asia.
• TPE is often observed in southern Asia, Southeast Asia, and South America. Most reported cases have occurred in ethnic Indians, while it is uncommon in Chinese persons. TPE is actually observed in a minority of patients infected with the causative filariae.

Mortality/Morbidity

• With the exception of Loeffler syndrome and drug-induced disease, these syndromes may be associated with significant morbidity. While most are responsive to corticosteroids, recognition of infection and institution of an appropriate therapy are important in preventing chronicity of symptoms and, in some cases, respiratory failure.
• Patients with IHES may develop congestive heart failure, pulmonary emboli, and multiorgan-system dysfunction. Mortality in cases of IHES has been improving with increasing therapeutic options; now, 80% of patients are surviving at 5 years and 40% are surviving at 10-15 years.
• The mortality rate in cases of CSS has been decreasing, with approximately 75% of patients surviving 5 years.

Race

• No clearly defined racial predispositions have been identified in these syndromes.
• Parasitic infections are endemic in many geographic areas, but they reflect public health conditions rather than racial predispositions.

Sex

• No sexual predilection has been noted for extrinsic eosinophilic syndromes, with the exception of TPE, which has been reported to have a male predominance at a male-to-female ratio of 4:1.
• Among the intrinsic syndromes, differences are noted. AEP is more common in men than in women, unlike CEP. CEP is twice as common in women as in men, but this sexual disparity declines with increasing age. For IHES, approximately 90% of cases are found in men and 10% are found in women. For CSS, no sexual predisposition has been reported. For EG, no sexual predominance is described. The older literature suggests a male predominance, but more recent data suggest equal distribution between sexes, possibly reflecting the changing demographics of cigarette smoking, which is thought to be etiologic.

Age

• Extrinsic syndromes tend to affect adults, but exceptions exist. Toxocariasis tends to occur in children and is often associated with geophagia. Ascariasis tends to occur in children. ABPA usually occurs in adults but may occur in children, including some patients with cystic fibrosis.
• Intrinsic syndromes generally affect adults. AEP usually occurs in persons in their third decade of life. CEP peak incidence is in the fourth decade of life. IHES usually occurs in people aged 20-50 years; however, it has also been infrequently reported in children. Most cases of CSS have been reported in adults. EG may affect individuals ranging in age from infancy to old age, but it most frequently affects patients in their second to third decade of life.

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Syringoma

Introduction

Background

Syringoma is a benign adnexal neoplasm formed by well-differentiated ductal elements. Its name is derived from the Greek word syrinx, which means pipe or tube.

Pathophysiology

Syringoma is a benign neoplasm, which is traditionally considered to differentiate along eccrine lines.

Enzyme immunohistochemical tests demonstrate the presence of eccrine enzymes such as leucine aminopeptidase, succinic dehydrogenase, and phosphorylase. The immunohistochemical pattern of cytokeratin expression indicates differentiation toward both the uppermost part of the dermal duct and the lower intraepidermal duct (ie, sweat duct ridge). However, sometimes distinguishing between eccrine and apocrine ducts is difficult and many tumors that were traditionally thought to be eccrine have recently been shown to have apocrine differentiation. Electron microscopy demonstrates ductal cells with numerous short microvilli, desmosomes, luminal tonofilaments, and lysosomes. The histogenesis of syringomas is most likely related to eccrine elements or pluripotential stem cells.

Some investigators have suggested that cases of eruptive syringoma may represent a hyperplastic response of the eccrine duct to an inflammatory reaction rather than a true adnexal neoplasm. In this setting, they propose the term syringomatous dermatitis for such cases. Likewise, the scalp "syringomas" seen in scarring alopecia represent a reactive proliferation in response to the fibrosis.

Frequency

International

Syringomas are fairly common lesions.

Mortality/Morbidity

These benign tumors are largely of cosmetic significance.

Sex

Females are affected more often than males.

Age

These tumors usually first appear at puberty; additional lesions can develop later.

Clinical

History

• The lesions are asymptomatic.
• Rarely, the patient may have a family history of similar lesions. Rarely, syringomas may be associated with the Brooke-Spiegler syndrome, an autosomally dominant disease characterized by the development of multiple cylindromas, trichoepitheliomas, and occasional spiradenomas.
• Syringomas may be associated with Down syndrome.

Physical

Appearance of lesions

• Syringomas are skin-colored or yellowish, small, dermal papules (see Media File 1).
• Sometimes, the lesions may appear translucent or cystic.
• The surface can be rounded or flat-topped.
• The lesions are usually smaller than 3 mm in diameter.
• Eruptive syringomas commonly appear as hyperpigmented papules on the chest or penile shaft.

Distribution of lesions

• The lesions are usually multiple, arranged in clusters, and symmetrically distributed.
• Most commonly, lesions are limited to the upper parts of the cheeks and lower eyelids.
• Other common sites include the axilla, chest, abdomen, penis, and vulva.
• In the variant of eruptive syringoma, multiple lesions appear simultaneously, typically on the chest and lower abdomen.
• Rarely, syringomas appear as unilateral linear nevoid lesions.

Differential diagnoses and related conditions

• In rare instances, scalp syringomas can produce scarring alopecia.
• On occasion, syringomas can be associated with milia and vermiculate atrophoderma.
• Clinically, syringomas on the face are must be distinguished from trichoepitheliomas and basal cell carcinomas.
• Lesions on the eyelids may be confused with xanthelasma.
• Eruptive syringomas on the trunk can resemble disseminated granuloma annulare.

Causes

• Syringomas are frequently incidental, although some familial cases may occur.
• Eruptive syringomas (see Media File 2) are more common in African Americans and Asians than in other patients.
• Syringomas can be associated with Down syndrome.
• Clear-cell syringomas may be associated with diabetes mellitus.

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Huntington's disease

Definition

Huntington's disease is a disorder passed down through families in which nerve cells in the brain waste away, or degenerate.

Alternative Names

Huntington chorea

Causes

American doctor George Huntington first described the disorder in 1872.

Huntington's disease is caused by a genetic defect on chromosome #4. The defect causes a part of DNA, called a CAG repeat, to occur many more times than it is supposed to. Normally, this section of DNA is repeated 10 to 35 times. But in persons with Huntington's disease, it is repeated 36 to 120 times.

As the gene is passed on from one generation to the next, the number of repeats - called a CAG repeat expansion - tend to get larger. The larger the number of repeats, the greater your chance of developing symptoms at an earlier age.

There are two forms of Huntington disease. The most common is adult-onset Huntington's disease. Persons with this form usually develop symptoms in their mid 30s and 40s.

Early-onset form of Huntington disease is less common and begins in childhood or adolescence. Symptoms may resemble those of Parkinson's disease with rigidity, slow movements, and tremor.

If one of your parents has Huntington's disease, you have a 50% chance of getting the gene for the disease. If you get the gene from your parents, you will develop the disease at some point in your life, and can pass it onto your children. If you do not get the gene from your parents, you cannot pass the gene onto your children.

Symptoms

• Abnormal and unusual movements
  • Head turning to shift eye position
  • Facial movements, including grimaces
  • Slow, uncontrolled movements
  • Quick, sudden, jerking movements of arms, legs, face, and other body parts
  • Unsteady gait
• Behavior changes
  • Antisocial behaviors
  • Hallucinations
  • Irritability
  • Moodiness
  • Restlessness or fidgeting
  • Paranoia
  • Psychosis
• Dementia that slowly gets worse, including
  • Loss of memory
  • Loss of judgment
  • Speech changes
  • Personality changes
  • Disorientation or confusion

Additional symptoms that may be associated with this disease:

• Anxiety, stress, and tension
• Difficulty swallowing
• Speech impairment

In children:

• Rigidity
• Slow movements
• Tremor

Exams and Tests

The doctor will perform a physical exam. The doctor may see signs of dementia and abnormal movements. Reflexes may be abnormal. The gait is often "prancing" and wide. Speech may be hesitant or enunciation poor.

A head CT scan may show loss of brain tissue, especially deep in the brain.

Other tests that may show signs of Huntington's disease include:

• Head MRI scan
• PET (isotope) scan of the brain

DNA marker studies may be available to determine if you carry the gene for Huntington's disease.

Treatment

There is no cure for Huntington's disease, and there is no known way to stop the disease from getting worse. The goal of treatment is to slow down the course of the disease and help the person function for as long and as comfortably as possible.

Medications vary depending on the symptoms. Dopamine blockers may help reduce abnormal behaviors and movements. Drugs like tetrabenazine and amantadine are used to try to control extra movements. There has been some evidence to suggest that co-enzyme Q10 may also help slow down the course of the disease.

Depression and suicide are common among persons with Huntington's disease. It is important for all those who care for a person with Huntington's disease to monitor for symptoms and treat accordingly.

There is a progressive need for assistance and supervision, and 24-hour care may eventually be needed.

Support Groups

Huntington's Disease Society of America - www.hdsa.org

Outlook (Prognosis)

Huntington's disease causes progressive disability. Persons with this disease usually die within 15 to 20 years. The cause of death is often infection, although suicide is also common.

It is important to realize that the disease affects everyone differently. The number of CAG repeats may determine how the severity of symptoms. Persons with few repeats may have mild abnormal movements later in life and slow disease progression, while those with large repeats may be severely affected at a young age.

Possible Complications

• Loss of ability to care for self
• Loss of ability to interact
• Injury to self or others
• Increased risk of infection
• Depression
• Death

When to Contact a Medical Professional

Call your health care provider if symptoms of this disorder develop.

Prevention

Genetic counseling is advised if there is a family history of Huntington's disease. Experts also recommend genetic counseling for couples with a family history of this disease who are considering having children.

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Diseases of gums can cause barreness

The Israeli doctors have established possible communication between the bacteria causing diseases of gums, with barreness at men.

Doctor Avigdor Klinberg specializing on gingival diseases in stomatologic branch of hospital, sampled at patients of branch on treatment of barreness.

The research which is spent within three years, has shown, that at 65 % of men whose spermogram had unsatisfactory parameters, diseases of gums also have been detected, informs Rol.ru. However, at 48 % of patients with sick gums, parameters of spermogram were in the full order.

According to doctors, barreness is caused by order 500 types of the bacteria which are being a mouth, and they are capable to get into blood system and to harm to various internal bodies.

Also 50 % of men were revealed, that, in whose sperm in general are absent sperm cells, have chronic illness of gums, and bacteria causing it, also have been found in the sperm.

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Nerve Compression Syndromes

Common nerve compression syndromes include carpal tunnel syndrome, cubital tunnel syndrome, and radial tunnel syndrome. Compression of nerves often causes paresthesias; these paresthesias can often be reproduced by tapping the compressed nerve, usually with the examiner's fingertip (Tinel's sign). Suspected nerve compression can be confirmed by testing nerve conduction velocity and distal latencies, which accurately measure motor and sensory nerve conduction. Initial treatment is usually conservative, but surgical decompression may be necessary if conservative measures fail or if there are significant motor or sensory deficits.

Carpal Tunnel Syndrome

Carpal tunnel syndrome is compression of the median nerve as it passes through the carpal tunnel in the wrist. Symptoms include pain and paresthesias in the median nerve distribution. Diagnosis is suggested by symptoms and signs and is confirmed by nerve conduction velocity testing. Treatments include ergonomic improvements, analgesia, splinting, and sometimes corticosteroid injection or surgery.

Carpal tunnel syndrome is very common and most often occurs in women aged 30 to 50. Risk factors include RA or other wrist arthritis (sometimes the presenting manifestation), diabetes mellitus, hypothyroidism, acromegaly, amyloidosis, hemodialysis, and pregnancy-induced edema in the carpal tunnel. Activities or jobs that require repetitive flexion and extension of the wrist may contribute, but rarely. Most cases are idiopathic.

Symptoms and Signs

Symptoms include pain of the hand and wrist associated with tingling and numbness, classically distributed along the median nerve (the palmar side of the thumb, the index and middle fingers, and the radial half of the ring finger) but possibly involving the entire hand. Typically, the patient wakes at night with burning or aching pain and with numbness and tingling and shakes the hand to obtain relief and restore sensation. Thenar atrophy and weakness of thumb opposition and abduction may develop late.

Diagnosis

• Clinical evaluation
• Nerve conduction testing

The diagnosis is strongly suggested by Tinel's sign, in which median nerve paresthesias are reproduced by tapping at the volar surface of the wrist over the site of the median nerve in the carpal tunnel. Reproduction of tingling with wrist flexion (Phalen's sign) is also suggestive. However, clinical differentiation from other types of peripheral neuropathy may sometimes be difficult. If symptoms are severe or the diagnosis is uncertain, nerve conduction testing should be done on the affected arm for diagnosis and to exclude a more proximal neuropathy.

Treatment

• Splinting
• Sometimes corticosteroid/anesthetic injection
• Sometimes surgical decompression

Changing the position of computer keyboards and making other ergonomic corrections may occasionally provide relief. Otherwise, treatment includes wearing a lightweight neutral wrist splint (see Fig. 4: Hand Disorders: Neutral wrist splint.), especially at night, and taking mild analgesics (eg, acetaminophen, NSAIDs). If these measures fail to control symptoms, a corticosteroid (eg, a mixture of 1.5 mL dexamethasone, 4 mg/mL, and 1.5 mL 1% lidocaine) should be injected into the carpal tunnel at a site just ulnar to the palmaris longus tendon and proximal to the distal crease at the wrist. If bothersome symptoms persist or recur or if hand weakness and thenar wasting develop, the carpal tunnel can be surgically decompressed by using an open or endoscopic technique.

Cubital Tunnel Syndrome

(Ulnar Neuropathy)

Cubital tunnel syndrome is compression or traction of the ulnar nerve at the elbow.

The ulnar nerve is commonly irritated at the elbow or, rarely, the wrist. Cubital tunnel syndrome is most often caused by leaning on the elbow or by prolonged and excessive elbow flexion. It is less common than carpal tunnel syndrome. Baseball pitching (particularly sliders), which can injure the medial elbow ligaments, confers risk.

Symptoms and Signs

Symptoms include numbness and paresthesia along the ulnar nerve distribution (in the ring and little fingers and the ulnar aspect of the hand) and elbow pain. In advanced stages, weakness of the intrinsic muscles of the hand and the flexors of the ring and little fingers may develop. Weakness interferes with pinch between the thumb and index finger and with hand grip.

Diagnosis

Diagnosis is often possible clinically. However, if clinical diagnosis is equivocal and when surgery is being considered, nerve conduction studies are done. Cubital tunnel syndrome is differentiated from ulnar nerve entrapment at the wrist (in Guyon's canal) by the presence of sensory deficits (on sensory testing or with Tinel's sign) over the ulnar dorsal hand and by the presence of ulnar nerve deficits proximal to the wrist on muscle testing or nerve conduction velocity testing.

Treatment

Treatment involves splinting at night, with the elbow extended at 45°, and use of an elbow pad during the day. Surgical decompression can help if conservative treatment fails.

Radial Tunnel Syndrome

(Posterior Interosseous Nerve Syndrome)

Radial tunnel syndrome is compression of the radial nerve in the proximal forearm.

Compression at the elbow can result from trauma, ganglia, lipomas, bone tumors, or radiocapitellar (“elbow”) synovitis.

Symptoms and Signs

Symptoms include lancinating pain in the dorsum of the forearm and lateral elbow. Pain is precipitated by attempted extension of the wrist and fingers and forearm supination. Sensory loss is rare because the radial nerve is principally a motor nerve at this level. This disorder is sometimes confused with backhand tennis elbow (lateral epicondylitis). When weakness of the extensor muscles is the primary finding, the condition is referred to as posterior interosseus nerve palsy.

Diagnosis

Lateral epicondylitis can cause similar tenderness around the lateral epicondyle but does not cause Tinel's sign or tenderness along the course of the radial nerve.

Treatment

Splinting allows avoidance of the forceful or repeated motion of supination or wrist dorsiflexion, reducing pressure on the nerve. If wristdrop or weakened digital extension develops, or conservative treatment fails to provide relief after 3 mo, surgical decompression may be needed.

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OHSU finds association between Epstein-Barr virus, inflammatory diseases of the mouth

2008 NOV 24 -- Researchers at Oregon Health & Science University's School of Dentistry (www.ohsu.edu/sod) have found that a significant percentage of dental patients with the inflammatory diseases irreversible pulpitis and apical periodontitis also have the Epstein-Barr virus. The Epstein-Barr virus is an important human pathogen found in more than 90 percent of the world population. It is associated with many diseases, including infectious mononucleosis, malignant lymphomas, and naspharyngeal carcinoma.

The findings are published online (www.jendodon.com/article/S0099-2399(08)00879-0/abstract) in the Journal of Endodontics, one of the leading peer-reviewed endodontology journals. The study also is expected to be published in the December 2008 (volume 34, issue 12) issue of the Journal of Endodontics.

Although the number of studies examining the role of herpesviruses in oral disease has been increasing, the majority of studies have focused on periodontitis, with no systematic attempt to examine herpesvirus in endodontic patients with varying inflammatory diseases. The OHSU study assessed the presence of human cytomegalovirus (HCMV), Epstein-Barr virus (EPV), herpes simplex virus (HSV-1), and Varicella zoster virus (VZV) in 82 endodontic patients, including patients with irreversible pulpitis and apical periodontitis, and compared them with 19 healthy patients. The goal of the study was to determine the potential association of herpesvirus with clinical symptoms, including acute pain and size of radiographic bone destruction.

Using a variety of methods, the OHSU team found the Epstein-Barr virus DNA and RNA in significantly higher percentages (43.9 percent and 25.6 percent respectively) compared with healthy patients (0 percent). Human cytomegalovirus DNA and RNA were found in measurable numbers in both endodontic patients (15.9 percent and 29.3 percent respectively) and in healthy patients (42.1 percent and 10.5 percent respectively). Herpes simplex virus DNA was found in low percentages of endodontic patients (13.4 percent) and only one patient showed the presence of Varicella zoster virus.

While a previous study examined the incidence of herpes viruses in apical periodontitis, "this is the first time irreversible pulpitis has been analyzed for the presence of herpes viruses and associated with Epstein-Barr virus," noted Curt Machida, Ph.D., OHSU professor of integrative biosciences and principal investigator, whose lab was host for the study. "The incidence of irreversible pulpitis and apical periodontitis, caused by bacteria and possibly the latent herpes virus, is painful and can greatly impair the body's natural immune system. Studies such as ours could someday lead to more effective treatments of inflammatory diseases of the mouth."

Keywords: Carcinoma, Chickenpox, Chronic Fatigue Syndrome, Cytomegalovirus, Dentistry, EBV, Endodontics, Epstein-Barr Virus, HSV-1, Hematology, Herpes Zoster Virus, Herpesvirus, Infectious Disease, Infectious Mononucleosis, Lymphoma, Oncology, Periodontitis, Pulpitis, Varicella Zoster, Varicella-Zoster Virus, Viral Research, Virology, Oregon Health & Science University.

This article was prepared by Clinical Oncology Week editors from staff and other reports. Copyright 2008, Clinical Oncology Week via NewsRx.com.

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