Hepatitis D is a defective RNA that appears to replicate only with the hepatitis B virus. It requires HbsAg to replicate.

It occurs along with Hepatitis B or may superinfect a chronic HBV carrier. It cannot outlast a Hepatitis B infection. It may be acute or chronic. Its mode of transmission and incubation period are the same as that of HBV.Its occurrence in the United States is primarily among IV drug users and among recipients of multiple blood transfusions. It causes about 50% of fulminant hepatitis, which has a high mortality. Clinical Manifestations: Similar to Hepatitis B but more severe and chronic active hepatitis and cirrhosis With superinfection of chronic HBV carriers, it causes sudden worsening of condition and rapid progression of cirrhosis. Diagnostic evaluation: 1. Elevated serum transferase levels ALT, AST 2. Anti-delta antibodies in the presence of HBsAg or the detection of IgM in acute disease and IgG in chronic disease.
Prevention: 1. Always screen blood and blood products for blood-borne diseases. 2. Always practice safe sex. 3. Never re-use needles for injections. Always open a new sterile syringe and discard properly after use. 4.Wash hand thoroughly right after direct contact with body fluids of patients with Hepatitis D. 5. Never use the personal belongings of persons with Hepatitis D, such as toothbrush, eating utensils, razor, etc.

Medical Management: 1. Targeting the causative agent of Hepatitis B may also kill the causative agent of Hepatitis D. 2. Interferon is under investigation as a specific treatment for Hepatitis D. 3. Acyclovir, ribavirin, lamivudine and synthetic analogues of thymosin have proved ineffective. Nursing Management: 1. Inform the patient and family members about the nature of the disease if the patient is taken care at home. 2. Assist is paracentesis if indicated. 3. Patients with cirrhosis could be in deep pain and discomfort, use of analgesics should be administered with great caution since it can worsen the liver damage. 4. Diversionary therapy and non-pharmacological approach should be applied in managing pain. 5. Ongoing monitoring of vital signs, abdominal girth and reminding for the routine checkup must be emphasized for effective management.Photo credits: www.google.com.ph

Hepatitis C (HCV) was formerly called non-A, non-B hepatitis and is an RNA virus. It is not related to any virus that cause hepatitis. Usual mode of transmission is through blood and blood products, including: 1. 2. 3. 4.

IV drug users and renal dialysis patients Sexual intercourse Theoretically, through contaminated piercing and tattooing tools and ink Sharing a razor or nail-clipper with the patient that is infected. Incubation period varies from 1 week to several months. About 35,000 new cases of Hepatitis C are reported in the United States each year. HCV is the most common reason for liver transplantation. Approximately 50% of HCV develop to chronic liver disease and at least 20% progress to cirrhosis

Clinical Manifestations: 1. Similar to Hepatitis B, but usually less severe 2. Symptoms usually occur 6-7 weeks after transfusion but may be attributed to another viral infection Diagnostic Evaluation: 1. Elevated serum transferase levels ALT, AST 2. Hepatitis C antibody may not be detected for 3 to 6 months after onset of HCV illness. Prevention: 1. Always screen blood and blood products for blood-borne diseases. 2. Always practice safe sex. 3. Never re-use needles for injections. Always open a new sterile syringe and discard properly after u se. 4. Educate adolescents about the risk of piercing and tattooing in transmission of HCV. Medical Management: 1. Combination therapy of interferon (Intron-A) and ribavirin (Rebetol) is effective for treating relapses. 2. Alcohol and hepatotoxic drugs should be avoided. 3. Close monitoring is imperative. Nursing Management: 1. Encourage verbalization of feelings of anxiety of family members as well as the patient when the disease is diagnosed.

2. Always observe standard precautions in handling blood and body fluids. 3. Always instruct patient and care givers to properly dispose used needles in a puncture resistant container. 4. Emphasize proper nutrition, a high-calorie, low-fat diet is small frequent feedings should be given. 5. Always monitor the vital signs as well as markers if the disease progresses. Complication:

Hemolytic anemia from combination therapy.

Staphylococcal food poisoning is caused by staphylococcal enterotoxin produced by some strains of Staphylococcal aureus, a gram positive bacteria.It can cause a wide variety of diseases such as bacteremia, pneumonia, osteomyelitis, skin infections and food poisoning. This discussion is focused on food poisoning only. This is the leading cause of gastroentiritis. The organism is often an inhabitant of the nasal passages from which it contaminates the hands. It is also a frequent cause of skin lesions on the hands. From these sources, it can readily enter food. If the microbes are allowed to incubate in the food, a situation called temperature abuse, or reproduction and release of enterotoxin into the food. The incubation period is 1 to 7 days. Events which may lead to outbreaks of staphylococcal intoxication: 1. Cooking foods rich in protein 2. Food handlers have staphylococcal growth on bare hands which may be transmitted to the food 3. Organisms incubate in the food long enough to form and release toxins *Reheating will eliminate staphylococci but not the toxin. The toxin is heat stable and can survive up to 30 minutes of boiling. Therefore, once the toxin is formed, it is not destroyed when the food is reheated, although the bacteria will be killed. 4. Food with the toxin is ingested. 5. Intoxication occurs in one to six hours or days Pathophysiology: Once the toxin has been ingested, it quickly triggers the brains vomiting reflex center; abdominal crapms and usually diarrhea then happens. Physical Findings: 1. 2. 3. 4. diarrhea abdominal cramping excessive salivation nausea

Diagnosis: 1. Physical examination according to presenting signs ans symptoms. Short incubation time characteristic of intoxication. 2. Blood, sputum, vomitus, feces and spinal fluid 3. Contaminated food (usually contaminated are custards, pastries, salads, ham and other foods rich in carbohydrates and protein) Medical Management:

1. Use of Penicillin G drug of choice; cephalosporin as substitute drug 2. Culture and sensitivity test is done for cases with resistance to Penicillin-resistant strains Nursing Management: 1. Administer prescribed medications, which include antipyretics and antibiotics. 2. Provide health education as well as encourage compliance to the whole course of antibiotics 3. Practice proper hand washing regularly 4. Observe good personal hygiene 5. Teach clients to refrain from eating left over foods, especially foods rich in carbohydrates and protein Staphylococcal food poisoning is caused by staphylococcal enterotoxin produced by some strains of Staphylococcal aureus, a gram positive bacteria.It can cause a wide variety of diseases such as bacteremia, pneumonia, osteomyelitis, skin infections and food poisoning. This discussion is focused on food poisoning only. This is the leading cause of gastroentiritis. The organism is often an inhabitant of the nasal passages from which it contaminates the hands. It is also a frequent cause of skin lesions on the hands. From these sources, it can readily enter food. If the microbes are allowed to incubate in the food, a situation called temperature abuse, or reproduction and release of enterotoxin into the food. The incubation period is 1 to 7 days. Events which may lead to outbreaks of staphylococcal intoxication: 1. Cooking foods rich in protein 2. Food handlers have staphylococcal growth on bare hands which may be transmitted to the food 3. Organisms incubate in the food long enough to form and release toxins *Reheating will eliminate staphylococci but not the toxin. The toxin is heat stable and can survive up to 30 minutes of boiling. Therefore, once the toxin is formed, it is not destroyed when the food is reheated, although the bacteria will be killed. 4. Food with the toxin is ingested. 5. Intoxication occurs in one to six hours or days Pathophysiology: Once the toxin has been ingested, it quickly triggers the brains vomiting reflex center; abdominal crapms and usually diarrhea then happens. Physical Findings: 1. diarrhea 2. abdominal cramping

3. excessive salivation 4. nausea Diagnosis: 1. Physical examination according to presenting signs ans symptoms. Short incubation time characteristic of intoxication. 2. Blood, sputum, vomitus, feces and spinal fluid 3. Contaminated food (usually contaminated are custards, pastries, salads, ham and other foods rich in carbohydrates and protein) Medical Management: 1. Use of Penicillin G drug of choice; cephalosporin as substitute drug 2. Culture and sensitivity test is done for cases with resistance to Penicillin-resistant strains Nursing Management: 1. Administer prescribed medications, which include antipyretics and antibiotics. 2. Provide health education as well as encourage compliance to the whole course of antibiotics 3. Practice proper hand washing regularly 4. Observe good personal hygiene 5. Teach clients to refrain from eating left over foods, especially foods rich in carbohydrates and protein Staphylococcal food poisoning is caused by staphylococcal enterotoxin produced by some strains of Staphylococcal aureus, a gram positive bacteria.It can cause a wide variety of diseases such as bacteremia, pneumonia, osteomyelitis, skin infections and food poisoning. This discussion is focused on food poisoning only. This is the leading cause of gastroentiritis. The organism is often an inhabitant of the nasal passages from which it contaminates the hands. It is also a frequent cause of skin lesions on the hands. From these sources, it can readily enter food. If the microbes are allowed to incubate in the food, a situation called temperature abuse, or reproduction and release of enterotoxin into the food. The incubation period is 1 to 7 days. Events which may lead to outbreaks of staphylococcal intoxication: 1. Cooking foods rich in protein 2. Food handlers have staphylococcal growth on bare hands which may be transmitted to the food 3. Organisms incubate in the food long enough to form and release toxins *Reheating will eliminate staphylococci but not the toxin.

The toxin is heat stable and can survive up to 30 minutes of boiling. Therefore, once the toxin is formed, it is not destroyed when the food is reheated, although the bacteria will be killed. 4. Food with the toxin is ingested. 5. Intoxication occurs in one to six hours or days Pathophysiology: Once the toxin has been ingested, it quickly triggers the brains vomiting reflex center; abdominal crapms and usually diarrhea then happens. Physical Findings: 1. 2. 3. 4. diarrhea abdominal cramping excessive salivation nausea

Diagnosis: 1. Physical examination according to presenting signs ans symptoms. Short incubation time characteristic of intoxication. 2. Blood, sputum, vomitus, feces and spinal fluid 3. Contaminated food (usually contaminated are custards, pastries, salads, ham and other foods rich in carbohydrates and protein) Medical Management: 1. Use of Penicillin G drug of choice; cephalosporin as substitute drug 2. Culture and sensitivity test is done for cases with resistance to Penicillin-resistant strains Nursing Management: 1. Administer prescribed medications, which include antipyretics and antibiotics. 2. Provide health education as well as encourage compliance to the whole course of antibiotics 3. Practice proper hand washing regularly 4. Observe good personal hygiene 5. Teach clients to refrain from eating left over foods, especially foods rich in carbohydrates and protein

Erythema infectiosum or the Fifth Disease is an infectious disorder that affects children aging 2-12 years of age. The term fifth disease was based on the classification system for childhood rashes decades ago. Generally, the five frequent childhood rashes are the following: 1. 2. 3. 4. 5. Measles (rubeola) Chickenpox (vaicella) German measles (rubella) Roseola Erythema Infectiosum (Parvovirus B19)

Because erythema infectiosum is the fifth disease that causes rashes in children, thus, the term has been used by most people. The prevalence of the illness is more commonly seen during spring and winter period and studies show that females are often affected than males. Parvovirus B19, sometimes called as erythrovirus B19 is a part of the genus Parvoviridae. It was accidentally detected in 1975 by an Australian virologist Yvonne Cossart. Fifth Disease Related Data

Causative Agent: Parvovirus B19 Incubation period: 6-14 days Mode of transmission: droplet (respiratory secretions transmitted by cough and sneeze) Period of communicability: uncertain Signs and symptoms

Fifth disease produces symptoms that are benign and go away on their own. The following are most likely observed:

Fever, headache, coryza, abdominal pain, sore throat and malaise on the first week.

Rashes appear a week after, erupting in three sequential phases:

Face Bright red rash coalesces at the cheeks forms a slapped face appearance. (Hallmarksign) Extensor surface of extremities(outer arm) Rashes are expected to scatter on the extremities (extensor surface) a day after the facial rash develops. (Extensor surfaces refers to the part of the skin that do not touch when the joints are bend) Flexor surfaces of extremities and trunk Rash invasion in these areas are observed a day after it appeared on the extensor surfaces (inner arm and leg).

The eruptions will last for a week or more. Rashes start to fade from the center outward (a lace-like appearance will be observe due to this manner of disappearance)

Management

Home care:

1. Adequate fluid intake 2. Frequent hand washing. 3. Acetaminophen (Tylenol) is given to decrease body temperature. Aspirin (acetylsalicylic acid) is not recommended as it is related to the occurrence of Reye syndrome.

Droplet precautions should be implemented if the child is hospitalized. (wearing mask,gloves, eyewear, spacing client in single room) Avoid contact to pregnant women. Parvovirus B19 is teratogenic. It causes severe anemia with congestive heart failure to the fetus. A child may resume school as soon as the rash appears. (the disease is no longer contagious at this time)

Chlamydial Infection

Is a common sexual transmitted disease that occurs in women and men, particularly in adolescents and young adults. Women are asymptomatic or present with cervicitis. Men are commonly asymptomatic but may present with urethritis. Untreated chlamydial infections can lead to epididymitis, salphingitis, pelvic inflammatory disease and eventually sterility.

Mode of Transmission 1. The disease is transmitted through vaginal or rectal intercourse. 2. The disease is also transmitted through oral-genital contact with an infected person. 3. Conjunctivitis, otitis media, and pneumonia may develop to children born to mothers with chlamydial infection passed through birth canal. Clinical Manifestations 1. May be asymptomatic or have vaginal discharge may be clear mucoid to creamy discharge. 2. May have dysuria and mild pelvic disorder. 3. Cervix may be covered by thick mucopurulent discharge and be tender, erythematous, edematous, and friable. Diagnostic Evaluation 1. DNA detection test on cervical smear or urine sample (by DNA amplification method). 2. Chlamydia culture from cervical exudate. 3. Screening urinalysis in males for leukocytes; if positive result, confirmed by DNA detection test. 4. ELISA 5. Direct fluorescent anti-body test.

6. The Centers for Disease Control and Prevention (CDC) recommends annual screening for all sexually active adolescents women as well as young women, ages 20 to 24, and older women at high risk (multiple sex partners or new partner). Complications 1. Pelvic Inflammatory Disease. 2. Ectopic pregnancy or infertility secondary to untreated or recurrent pelvic inflammatory diseases. 3. Transmission to neonate born through infected birth canal. Treatment 1. Doxycycline oral for several days. 2. Azithromycin in single dose. Nursing Interventions 1. Advice abstinence from sexual intercourse until treatment has been completed. No follow-up culture is necessary to ensure cure; however, re-screening is recommended 3 to 4 months after treatment to detect reinfection, particularly in adolescents and young women. 2. Ensure that the partner is treated at the same time; recent partners should receive treatment despite lack of symptoms and negative Chlamydia result. 3. Report case to local public health department (Chlamydia is a reportable infectious disease). 4. Ensure that the patient begins treatment and will have access to prescription follow up. 5. Explain mode of transmission, complications, and the risk for other STDs. 6. Teach about all STDs and their symptoms. 7. Explain the treatment regimen to patient and advise her of adverse effects. 8. Encourage abstinence, monogamy, or safer sex methods, such as female or male condom. 9. Stress the importance of follow-up examination and testing to eradication of infection. Recurrence rates are highest in young patients.

Scabies
A communicable disease of the skin caused by Sarcopte Scabiei and characterized by the eruptive lesions produced from the burrowing of the parasite into the skin

Etiologic Agent 1. The mite is yellowish-white and can barely be seen by unaided eye. 2. The female parasite burrows beneath the epidermis to lay her eggs and sets up an intense irritation. 3. The males are smaller and reside at the surface of the skin. 4. Scabies occurs worldwide, and is predisposed by overcrowding and poor hygiene. Incubation

It occurs within 24 hours from the original contact, the length of time required from itch mite to (burrow) or infected skin lay ova.

Period of Communicability

The disease is communicable for the entire period that the host is infected.

Signs and Symptoms 1. Itching 2. When secondarily infected the skin may feel hot and burning but this is a minor discomfort. 3. When large areas are involved and secondary infection is severe there will be fever, headache and malaise. Secondary dermatitis is common. Mode of Transmission 1. The disease is transmitted by direct transmission of infected individuals. 2. The disease is also be transmitted through sleeping in an infected bed or wearing infected clothing. 3. Anyone may become infected or re-infected. 4. Infestation with mites may also result from contact with dogs, cats, and small animals. Pathology 1. The female mite burrows into the skin to lay her eggs, from which larvae emerge to copulate and re-burrow under the skin. 2. While any part of the body maybe infected, the itch mite maybe found in the interdigital spaces of the fingers or in warm folds in the skin.

3. Areas of friction, such as the crotch, axillae, or the belt line, around the nipple in women and the periumbilical region are sites of predilection. 4. The external genitalia are most frequently involved in adult males. 5. The lesions are slightly elevated, straight or twitching burrows, thread like that are either brown or black in color, that are about 5 to 6 mm in length. 6. Severe inflammation with the development of the papules, blisters, pustules, and crusts may come as a result of infection from scratching. 7. In infants, burrows may appear on the head or neck. 8. The disease may become fully developed into two weeks; the eggs hatch in about 6 days, and the parasite grows very rapidly. It may persist for month or even years if not recognized or properly treated. Diagnosis 1. Appearance of lesion, and intense itching and finding of the causative mite. 2. Scraping from its burrow with a hypodermic needle or curette, and then examined under low power of the microscope or by hard lens. Treatment 1. The whole family should be examined before undertaking treatment, as long as a member of family remains infected, other members will get the disease 2. Treatment for scabies consists of application of pediculicide, like permethrin cream of lindane lotion in thin layer over the entire skin surface and is left for ten to twelve (10-12) hours. 3. Crotamiton cream applied for five consecutive nights. 4. Neosporin ointment rubbed into the affected skin four to five times a day. 5. Eurax and kwell lotion also prove effective to some patients. 6. All clothes used before and during the treatment period should be disinfected by dry cleaning or boiling. Nursing Interventions 1. Instruct patient to apply the cream at bedtime, from neck down to toes, covering the entire body. 2. Advise patient to report any skin irritation. 3. Suggest the family members and other close contact of the patient be checked for possible symptoms and be treated if necessary. 4. If patient is hospitalized, practice good handwashing technique, or use gloves while performing nursing procedure. 5. Terminal disinfection should be carried out after discharge of patient. Prevention and Control 1. Good personal hygiene daily bath; washing the hands before and after eating, and after using the toilet; cutting off fingernails.

2. Regular changing of clean clothing beddings and towels. 3. Eating the right kind of food like rich in Vitamin A and Vitamin C such as green leafy vegetable and plenty of fruits and fluids. 4. Keeping the house clean. 5. Improving the sanitation of the surroundings.

Anthrax

Is a serious infection caused by the gram-positive, spore-forming bacteria, Bacillus anthracis. In industrialized nations, infection in human was all but nonexistent until the threat of bioterrorism became apparent in late 2001. Infection occurs through contact with infected animals, products from infected animals, and intentionally tainted materials. Anthrax is potential biologic weapon because spores can be distributed easily through the mail or other means. People exposed to airborne particles may develop cutaneous, inhalation, or G.I. anthrax, based on the route of exposure. Complications include meningitis, circulatory collapse, and death.

Modes of Transmission 1. Direct transmission through contact with infected animals or contaminated animal products. 2. Indirect transmission through animal bites and ingestion of contaminated meat. 3. Airborne transmission through inhalation of contaminated or polluted air. Assessment 1. Cutaneous anthrax: After incubation period of 1 to 12 days, a papule develops and progresses to vesicle and, ultimately, to necrotic ulcer; fever, malaise, headache, and lymphadenopathy may also occur. 2. Inhalation anthrax: After an incubation period of several days to 60 days, a brief prodrome of fever, cough, fatigue, and mild chest discomfort occurs and may rapidly progress to severe respiratory distress, diaphoresis, stridor, cyanosis, and signs of meningitis (nuchal rigidity, headache, photophobia, altered mental status); may proceed to shock and death within 24 to 36 hours. 3. GI anthrax: Approximately 1 to 7 days after ingestion of tainted material or undercooked contaminated meat, nausea, anorexia, fever, severe abdominal pain, hematemesis, and bloody diarrhea may occur; the oropharyngeal form may also occur, characterized by lesions at base of tongue, dysphagia, fever, and cervical lymphadenopahy. Diagnostic Evaluation

1. Nasal swab testing may be conducted on several people to detect contamination by anthrax in the environment, but this does not confirm infection by anthrax in an individual. 2. Testing to confirm disease in an individual includes blood, tissue, and spinal fluid cultures (before antibiotics); polymerase chain reaction testing; and x-ray to identify mediastinal widening in inhalation anthrax. Pharmacologic Interventions 1. Antibiotic prophylaxis after exposure to spores is warranted, and 60 days therapy is advised. Drug recommendations include: o Ciprofloxacin 500 mg bid for adults: 10 to 15 mg/kg bid for children. o Doxycycline 100 mg bid for those weighing 99 pounds (45kg) and over; 2.2 mg/kg bid for children at least age 8 but weighing 99 pounds or less. o Amoxicillin 500 mg bid for adults; 80 mg/kg divided into three doses for children (if penicillin sensitivity of organism is confirmed). 2. Treatment of cutaneous anthrax involves 60 days treatment using antibiotics, however, signs of systemic involvement, including lesions of the head and neck and extensive edema, require I.V. treatment with multiple drugs as for inhalation anthrax. 3. I.V. corticosteroids may be given to adjunct therapy in severe cases. 4. Symptomatic treatment includes analgesics, antiemetics, and emergency drugs for circulatory collapse. 5. An anthrax vaccine has been available for veterinarians (not routinely used due to low incidence of animal disease). Complications 1. Antrax meningitis is the intense inflammation of the meninges of the brain and spinal cord. o This is marked by elevated CSF pressure pressure with bloody CSF followed by rapid loss of consciousness and death. o The case fatality rate is almost 100 percent. 2. Anthrax sepsis - develops after the lymphohematogenous spread of B. anthracis from primary lesion. Nursing Interventions 1. 2. 3. 4. Monitor vital signs and hemodynamic parameters closely for circulatory collapse. Monitor temperature for response to antibiotic therapy. Auscultate chest for crackles, indicating need for better secretion mobilization. Monitor oxygen saturation and arterial blood gases periodically to determine oxygenation status and acid-base balance. 5. Monitor level of consciousness and for meningeal signs such as nuchial rigidity. 6. Provide supplemental oxygen or mechanical ventilation, as needed. 7. Position for maximum chest expansion and reposition frequently to mobilize secretions.

8. Suction frequently and provide chest physiotherapy to clear airways, prevent atelectasis, and maximize oxygen therapy. 9. Administer I.V. fluids to encourage oral fluid intake to replace the fluid lost through hyperthermia and tachypnea. 10. For G.I. anthrax, maintain G.I decompression, monitor emesis and liquid stool output, and medicate for abdominal pain, as needed. 11. Advice the patient and family that anthrax is not transmitted person to person; one must come in contact with the spores to contact infection.

Herpes Zoster (Shingles)

Herpes Zoster also known as Shingles is an acute viral infection of the sensory nerve caused by a variety of chickenpox virus. It is an inflammatory skin condition in which the varicella zoster virus produces a painful vesicular eruption along the nerve tracks leading from one or more dorsal root ganglia. After a primary chickenpox infection, the virus persists in a dormant state in the dorsal ganglia. The virus may then become active again in later years, either spontaneously or in association with immunosuppression, to cause the eruptions. Herpes zoster may progress too chronic pain syndrome (postherpetic neuralgia), characterized by constant aching and burning pain or intermittent lancinating pain or hyperesthesia of affected skin after healing. Herpes zoster is communicable a day before the appearance of the first rash until five to six days after the last crust.

Assessment 1. Eruption may be accompanied or preceded by fever, malaise, headache, and pain. Pain may be burning, lancilating, stabbing or aching. 2. Inflammation usually unilateral, involving the cranial, cervical, thoracic, lumbar, or sacral nerves in a bandlike configuration. 3. After 3 to 4 days, patches of grouped vesicles appear on erythematous, edematous skin. 4. Early vesicles contain serum, these later rupture and form crusts. Scarring usually does not occur unless the vesicles are deep and involve in the dermis. 5. Patient may have a painful eye if ophthalmic branch of the facial nerve is involved. 6. Lesions usually resolve in 2 to 3 weeks.

Diagnostic Evaluation 1. Culture of varicella zoster virus from lesions or detection by fluorescent antibody techniques, including monoclonal antibodies. Pharmacologic Interventions 1. Antivirals, such as acyclovir or valacyclovir, interfere with viral replication; may be used orally in all cases but especially for the treatment of immunosuppressed or debilitated patients (I.V route). Antivirals are most effective if started within 48 hours of onset of symptoms. 2. Corticosteroids early in illness for severe herpes zoster if symptoms measures fail; given for anti-inflammatory effect and relief of pain. 3. Aspirin, acetaminophen, nonsteroidal anti-inflammatory drugs, or opiiods to manage pain during the acute stage; good pain control may reduce the incidence of postherpetic neuralgia. Nursing Interventions 1. Asses the patients level of discomfort and medicate as prescribed. 2. Teach the patient to apply wet dressings and calamine lotion for soothing and cooling effect on inflamed tissue. 3. Encourage diversional activities. 4. Teach relaxation techniques, such as deep breathing, progressive muscle relaxation, and imagery, to help control pain. 5. Apply anti-bacterial ointments (after acute stages) as prescribed to soften and separate adherent crusts and prevent secondary infection. 6. Teach the patient to use proper hand-washing techniques to avoid spreading herpes zoster virus. 7. Advise the patient not to open the blister to avoid a secondary infection and scarring. 8. Reassure the patient that shingles is a viral infection of the nerves. Assessment 1. Eruption may be accompanied or preceded by fever, malaise, headache, and pain. Pain may be burning, lancilating, stabbing or aching. 2. Inflammation usually unilateral, involving the cranial, cervical, thoracic, lumbar, or sacral nerves in a bandlike configuration. 3. After 3 to 4 days, patches of grouped vesicles appear on erythematous, edematous skin. 4. Early vesicles contain serum, these later rupture and form crusts. Scarring usually does not occur unless the vesicles are deep and involve in the dermis.

5. Patient may have a painful eye if ophthalmic branch of the facial nerve is involved. 6. Lesions usually resolve in 2 to 3 weeks. Diagnostic Evaluation 1. Culture of varicella zoster virus from lesions or detection by fluorescent antibody techniques, including monoclonal antibodies. Pharmacologic Interventions 1. Antivirals, such as acyclovir or valacyclovir, interfere with viral replication; may be used orally in all cases but especially for the treatment of immunosuppressed or debilitated patients (I.V route). Antivirals are most effective if started within 48 hours of onset of symptoms. 2. Corticosteroids early in illness for severe herpes zoster if symptoms measures fail; given for anti-inflammatory effect and relief of pain. 3. Aspirin, acetaminophen, nonsteroidal anti-inflammatory drugs, or opiiods to manage pain during the acute stage; good pain control may reduce the incidence of postherpetic neuralgia. Nursing Interventions 1. Asses the patients level of discomfort and medicate as prescribed. 2. Teach the patient to apply wet dressings and calamine lotion for soothing and cooling effect on inflamed tissue. 3. Encourage diversional activities. 4. Teach relaxation techniques, such as deep breathing, progressive muscle relaxation, and imagery, to help control pain. 5. Apply anti-bacterial ointments (after acute stages) as prescribed to soften and separate adherent crusts and prevent secondary infection. 6. Teach the patient to use proper hand-washing techniques to avoid spreading herpes zoster virus. 7. Advise the patient not to open the blister to avoid a secondary infection and scarring. 8. Reassure the patient that shingles is a viral infection of the nerves.

Definition:

Bird flu or Avian Influenza (A1) is a contagious disease of bird raging from mild to serve form of illness. Some forms of bird flu infections can cause illness to humans. Bird flu is caused by an influenza A virus. The outbreaks affecting some Asian countries have been caused by influenza A/H5N1 virus. It can also cause severe infection in humans.

History:

First identified in Italy in 1878, highly pathogenic avian influenza is characterized by sudden onset of severe disease, rapid contagion, and a mortality rate that can approach 100% within 48 hours. Human deaths from avian influenza were unknown until 1997, when six people in Hong Kong died from the particularly virulent H5N1 strain. In January 2004, a new major outbreak of H5N1 avian influenza surfaced again in Vietnam and Thailands poultry industry, and within weeks, spread to ten countries and religions in Asia including Indonesia, South Korea, Japan, and China. In February 2004, avian influenza virus was detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. Fresh outbreaks in poultry were confirmed in Ayutthaya and Pathumthani provinces of Thailand, and Chaohu city in Anhui, China, in July 2004. In North America, the presence of avian influenza was confirmed at several poultry farms in British Columbia in February 2004. In August 2004 avian flu was confirmed in Kampung Paris, Kelantan, Malaysia. Two chickens were confirmed to be carrying H5N1.

Etiologic Agent:

The causative agent is the avian influenza (A1) virus. A1 viruses all belong to the influenza virus, a genus of the Orthomyxoviridae family and are negative-stranded, and segmented.

Modes of Transmission: 1. Avian influenza spreads in the air and in manure. Wild fowl often acts as resistant carrier spreading it to more susceptible domestic stocks. 2. It can also be transmitted through contaminated feeds, water, equipment, and clothing; however, there is no evidence that the virus can survive in well cooked meat. 3. Cats are also thought to be possible infection vectors for H5N1 strains of avian flu. 4. While avian influenza spreads rapidly among birds, it does not infect humans easily, and there is no confirmed evidence of human-to-human transmission. Of the 15 subtypes known, only subtypes H5 and H7 are known to be capable of crossing the species barrier. Incubation Period:

The incubation period is three to five days.

Signs and Symptoms: 1. Symptoms in animals vary, but virulent strains can cause death within a few days. 2. The symptoms of avian influenza in humans following exposure to bird flue infected chicken patient develops:

fever, body weakness or muscle pain, sore throat, cough, sore eyes, may have difficulty of breathing in severe cases

Prevention and Treatment: Avian influenza in humans can be detected reliably with standard influenza tests. Antiviral drugs are clinically effective in both preventing and treating the disease. Vaccines, however, taken at least four months to produce and must be prepared for each subtype. 1. Wash hands thoroughly with soap and water before and after handling live and dressed chicken. 2. Cook chicken thoroughly. 3. Do not sell live chickens and other birds in the market while there is a threat of bird flu. 4. Do not let chickens roam freely. Keep them in cages or pens. 5. Do not place chicken, ducks and pigs together in one area, cage or pen. 6. Do not catch, get near or keep in captivity wild birds. 7. Report to the nearest agricultural/veterinary office any unusual death or illness of chickens and other birds. 8. Report to the nearest local health centers any case of respiratory illness with history of exposure to sick or dead chickens and other birds. 9. Individuals at risk are those directly exposed to sick chicken and other birds. The government thereby advises prospective travelers to countries affected with bird flu not to go to bird parks, poultry farms and markets where live chicken and other birds are sold.

Definition:

Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the Human Immunodeficiency Virus (HIV) This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. The time between infection and the appearance of symptoms tends to be much longer, allowing more opportunities for these microorganisms to be transmitted to other hosts. The period between infection and the appearance of AIDS can take from 7 to 12 years. AIDS is now a pandemic. In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people, including 330,000 children.

History:

Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified in the early 1980s.

Pathophysiology of HIV/AIDS

Signs and Symptoms

The symptoms of AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems Most of these conditions are infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the elements of the immune system that HIV damages. A person may remain asymptomatic, feel, and appear healthy for even years even though he or she is infected with HIV. While he or she does not exhibit AIDS, the immune system starts to be impaired. The person may exhibit neurological symptoms such as memory loss, altered gait, depression, sleep disorders or chronic diarrhea. This set of symptoms is often called AIDS-related Complex (ARC) by clinicians. As the symptom progress, the patient becomes an AIDS patient.

Minor Signs: 1. 2. 3. 4. 5. 6. Persistent Cough for one month Generalized pruritic dermatitis Recurrent herpes zoster Oropharyngeal candidiasis Chronic disseminated herpes simplex Generalized lymphadenopathy

Major Signs: 1. Loss of weight 10 percent of body weight 2. Chronic diarrhea for more than one month

3. Prolonged fever for one month Common Opportunistic Infections 1. 2. 3. 4. Pneumocystis carinii pneumonia Oral candidiasis Toxoplasmosis of the CNS Chronic diarrhea/wasting syndrome 5. Pulmonary/extra-pulmonary tuberculosis 6. Cancers a. Kaposis sarcoma affects small blood vessels and internal organs b. Cervical dysplasia and cancer. Researchers found out that women with HIV have higher rates of this type of cancer. Cervial carcinoma is associated with Human Papilloma Virus (HPV). c. Non-Hodgkins lymphoma cancerous tumor of the lymph nodes. This is usually a late manifestation of HIV infection. Mode of Transmission: 1. Sexual intercourse 2. Blood transfusion and sharing of infected syringes and needles among intravenous drug users 3. Vertical or perinatal transmission (from a pregnant woman to the fetus during pregnancy, child delivery or breast-feeding) There are several ways of receiving infected blood: 1. Blood transfusion 2. Sharing of unsterilized syringes and needles used for intravenous injections 3. Transmission during pregnancy a. Maybe transplacental b. There is greater risk of transmission when mother has developed advanced AIDS 4. Organ donation 5. Accidental exposure in hospitals or clinics Diagnostic Examination:

1. 2. 3. 4. 5.

ELA or ELISA Enzyme link immunosorbent assay Particle agglutination (PA) test Western blot analysis confirmatory diagnostic test Immunofluorescent test Radio immuno-precipitation assay (RIPA) Many people are unaware that they are infected with HIV. HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results.

Treatment Modalities:

AIDS Drugs are medicines used to treat but not to cure HIV infection. These drugs are sometimes referred to as anteroviral drugs. These work by inhibiting the reproduction of the virus. There are two groups of anteroviral drugs: 1. Reverse trancriptase inhibitors they inhibit the enzyme called reverse transcriptase which is needed to copy information for the virus to replicate. These drugs are: a. Zedovudine (ZDV) Retirvir b. Zalcitabine Havid c. Stavudine Zerit d. Lamivudine Epivir e. Nevirapine Viramune f. Didanosine Videx 2. Protease inhibitors. They work by inhibiting the enzyme protease which are needed for the assembly of viral particles. These drugs are: a. Saquinavir Invarase b. Ritonavir Norvir c. Indinavir Crixivan

Nursing Management: 1. Health education The healthcare worker must: a. Know the patient b. Avoid fear tactics c. Avoid judgmental and moralistic messages d. Be consistent and concise e. Use positive statement f. Give practical advice 2. Practice universal/standard precaution a. There is a need for a thorough medical handwashing after every contact with patient and after removing the gown and gloves, and before leaving the room of an AIDS suspect or known AIDS patient. b. Use of universal barrier or Personal Protective Equipment (PPE) e.g., cap, mask, gloves, CD gown, face shield/goggles are very necessary. 3. Prevention a. Care should be taken to avoid accidental pricks from sharp instruments contaminated with potentially infectious materials form AIDS patient. b. Gloves should be worn when handling blood specimens and other body secretions as well as surfaces, materials and objects exposed to them. c. Blood and other specimens should be labeled with special warning AIDS Precaution. d. Blood spills should be cleaned immediately using common household disinfectants, like chlorox. e. Needles should not be bent after use, but should be disposed into a punctureresistant container. f. Personal articles like razor or razor blades, toothbrush should not be shared with other members of the family. Razor blades may be disposed in the same manner as needles are disposed. g. Patients with active AIDS should be isolated. The Four Cs in the Management of HIV/AIDS
1. Compliance giving of information and counseling the client which results to the clients successful treatment, prevention and recommendation. 2. Counseling/education a. Giving instruction about the treatment b. Disseminating information about the disease c. Providing guidance on how to avoid contracting STD again d. Sharing facts about HIV and AIDS 3. Contact tracing a. Tracing out and providing treatment or partners 4. Condoms a. Promoting the use of condom, giving instructions about its use, and giving away available condoms

Hepatitis B is the inflammation of the liver caused by hepatitis B virus. This is considered to be more serious than hepatitis A due to the possibility of severe complications such as massive damage and hepatocarcinoma of the liver. Hepatitis B is a viral infection that attacks the liver and can cause both acute and chronic disease.About 2 billion people worldwide have been infected with the virus and about 350 million live with chronic infection. An estimated 600 000 persons die each year due to the acute or chronic consequences of hepatitis B. About 25% of adults who become chronically infected during childhood later die from liver cancer or cirrhosis (scarring of the liver) caused by the chronic infection. The hepatitis B virus is 50 to 100 times more infectious than HIV. Hepatitis B virus is an important occupational hazard for health workers. Hepatitis B is preventable with a safe and effective vaccine.

Etiologic Agent: The disease is caused by Hepatitis B virus 1. This virus has very limited tissue tropism 2. HBV infects the liver and possibly the pancreas. 3. HbsAg appears in the blood 30 to 60 days after exposure and persists for variable periods of time. Incubation Period: The incubation period is 50 to 189 days or two to five months with a mean equal to 90 days. Period of Communicability: The patient is capable of transmitting the virus during the latter part of the incubation period and during the acute phase. The virus may persist in the blood for many years. Mode of Transmission: 1. Hepatitis B can be directly transmitted by person to person contact via infected body fluids. 2. It can be transmitted though contaminated needles and syringes. 3. Transmission can occur through infected blood or body fluids introduced at birth.

4. It can also be transmitted through sexual contact. HBV transmission does not occur. 1. by fecal-oral route 2. by food-borne or water-borne transmission 3. by arthropod (mosquito) transmission. Pathogenesis: 1. HBV can cause acute or chronic hepatitis. 2. Production of virus and high level of HbsAg is continuous and the particles are found in the blood until the infections is resolved. 3. The virus must be delivered into the liver to establish infection. 4. The virus replicates and large amount of HbsAg is released into the blood. 5. Initiation of virus replication may be as short as three days from acquisition, but symptoms may not be observed for 45 days or much longer. 6. Replication of the virus is not cytopathic and proceeds to relatively long periods without causing liver damage. 7. During the acute phase of infection, the liver parenchyma shows degenerative changes consisting of cellular swelling and necrosis, especially in hepatocytes. Clinical Manifestations: 1. Prodormal period o Fever, malaise, and anorexia. o Nausea, vomiting, abdominal discomfort, fever and chills. o Jaundice, dark urine, and pale stools. o Recovery is indicated by a decline of fever and improved appetite. 2. Fulminant hepatitis may be fatal and manifested by severe symptoms like ascitis and bleeding. Diagnostics Procedures: 1. 2. 3. 4. 5. 6. 7. Compliment fixation test Radio-immunoassay-hemaglutinin test Liver function test Bile examination in blood and urine Blood count Serum transaminase SGOT, SGPT, ALT HbsAg

Prevention: 1. Blood donors must be screened to exclude carriers.

2. Caution must be observed in giving care to patients with known HBV. 3. Hands and other skin areas must be washed immediately and thoroughly after contact with body fluids. 4. Avoid injury with sharp objects or instruments. 5. Use disposable needles and syringes only once and discard properly. 6. Avoid sharing of toothbrush, razor, and other instruments that may be contaminated with blood. 7. Observe safe sex. 8. Have adequate rest, sleep, and exercise and eat nutritious food. 9. Hepatitis B vaccine is recommended for pre-exposure. 10. Hepatitis Immune Globulin (HBIg) should be administered within 72 hours to those exposed directly to hepatitis B virus either by ingestion, by prick or by inoculation.

Hepatitis A is a liver disease caused by the hepatitis A virus. This is an inflammation of the liver that is not really very severe and runs an acute course. This generally starts within two to six weeks after contact with the virus, and lasts no longer than two months. It is known as infectious hepatitis because it spreads relatively easy from those infected to close contact. Incubation Period: The incubation period for hepatitis A ranges from 15-60 days or three to five weeks; with a mean incubation period of 30 days. Period of Communicability: The infected patient is capable of transmitting the organism a week before and a week after the appearance of symptoms. Mode of Transmission: 1. Hepatitis A virus is transmitted by ingestion of contaminated drinking water or ice, uncooked fruits and vegetable, and fruits and vegetables grown in or washed with contaminated water. 2. It is also transmitted through fecal-oral pathway. 3. The virus is transmitted also by infected food handlers. Groups who are at risk for Hepatitis A Virus: 1. Children in Day Care Centers can transmit the infection through diapers and toys.

2. Troops living under crowded conditions at military camps or in the field are at great risk. 3. Homosexual men are increasingly at risk of HAV infection from oral-anal sexual contact. 4. People who live in areas with breakdown sanitary conditions, such as after flood and other natural disaster. Clinical Manifestations: 1. 2. 3. 4. 5. 6. Flu-like illness with chills and high fever Diarrhea, fatigue and abdominal pain Loss of appetite Nausea, diarrhea and fever Jaundice and dark-colored urine. The infection in young children is often mild and asymptomatic.

Complications: 1. Progressive encephalopathy characterized by drowsiness and cerebral edema 2. GIT bleeding progressing to stupor and later coma. Bleeding is not responsive to parenteral Vitamin K administration. 3. Clonus and hyperflexia are later replaced by loss of deep tendon reflexes. 4. Edema and ascitis 5. Aplastic anemia. 6. In late course of the disease, loss of corneal and papillary reflexes, elevated arterial blood, respiratory failure, to cerebrovascular collapse may be present. Diagnostic Procedure: 1. HAV and HBV complement fixation rate 2. Liver function test to determine the presence and extent of liver damage and to check the progress of the liver 3. Bile examination in stool and urine 4. SGOT serum glutamix oxaloacetic transaminase 5. SGPT serum glutamic pyruvic transaminase 6. ALT serum alanine transaminase 7. IgM level Treatment Modalities: 1. 2. 3. 4. 5. There is no specific treatment, although bed rest is essential. Diet must be high in carbohydrate, low in fat, and low in protein. Patient must take vitamin supplement especially the B complex group. Intravenous therapy is occasionally necessary. Isoprinosine (methisoprenol) may enhance the cell-mediated immunity of the Tlymphocytes. 6. Alkalies, belladonna and anti-emetics should be administered to control dyspepsia and malaise.

Nursing Management: 1. 2. 3. 4. 5. 6. 7. The patient must be isolated (enteric isolation). Patient should be encouraged to rest during acute or symptomatic phase. Improve nutritional status. Utilize appropriate measures to minimize spread of the disease. Observe the patient for melena and check stool for the presence of blood. Provide optimum skin and oral care. Increase in ability to carry out activities. a. Encourage the patient to limit activity when fatigued. b. Assist the client in planning periods of rest and activity. c. Encouraged gradual resumption of activities and mild exercise during recovery.

Prevention Control: 1. 2. 3. 4. 5. Hands should be washed thoroughly every after use of toilet. Travelers should avoid water and ice if unsure of their purity. Food handlers should carefully be screened. Safe preparation and serving of food must be practiced. The public should be educated on the mode of transmission of the disease.

Hepatitis A Vaccines:

The vaccine protects against the virus in more than 95% of cases for 10 years. It contains inactivated Hepatitis A virus providing active immunity against a future infection. The vaccine was first phased in 1996 for children in high-risk areas, and in 1999 it was spread to areas with elevating levels of infection. The vaccine is given in two doses in the muscle of the upper arm. The first dose provides protection two to four weeks after initial vaccination; the second booster dose, given six to twelve months later, provides protection for up to twenty years.

Nursing Care Plan Hepatitis A More About Hepatitis