CD Part 2 - Communicable Diseases With Pics (1) Con

Infection process: Immunodeficiency (opportunistic infections, unusual cancer).
Autoimmunity (lymphoid interstitial pneumonitis, arthritis, hypergammaglobulinemia and production of autoimmune antibodies.) Neurologic dysfunction (AIDS dementia complex,HIV encepalopathy and peripheral neuropathies) Signs and symptoms: Mononucleosis-like syndrome. (flu like symptoms which may remain asymptomatic for years.) Persistent adenopathy Non specific symptoms: weight loss, fatigue, weakness, pallor, anorexia, diarrhea, night sweats, fever, enlarged lymph gland.) Respiratory symptoms: dyspnea, cyanosis, pain in respiration, persistent unexplained cough and colds
Fundamentals of Nursing
Incubation Period:
Adults: years, about 5 yrs before the first identifiable symptom occurs.) Children: shorter time of appearance of synptoms; like-bacterial infections- otitis media, sepsis, mycobacterium avium complex, chronic salivary gland enlargement, pneumocystis carinii.
Diagnosis:
One or more indicators coexisting with laboratory evidences: HIV infected people with CD4+ T-cell count of 200/L and associated with prolonged illness without ready explanation. Antibody test indicates HIV infection by revealing HIV antibodies. Screening of blood products with enzyme-linked immunosorbent assay (ELISA). Test should be repeated, if positive; should be confirmed with an alternate method such as; Western blot immunoflourescent assay.
Treatment:
No cure has been found or developed, however, primary therapy for HIV infections include (HAART) - Highly Active Antiretroviral Therapy: 3 different types of Antiretroviral agents: 1. Protease inhibitor (PIs) i.e. amprenavir, ritonavir, indinavir and saquinavir. Nucleoside reverse transcriptase inhibitors (NRTI) i.e. zidovudine(AZT), didanosine, zalcitabine, lamivudine, abacavir/ stavudine. Non-nucleoside reverse transcriptase (NNRTI). i.e. efavirenze, nevirapine, delavirdine.
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These agents are designed to inhibit HIV replication.
Other potential therapies: Immunomodulary agents designed to boost the weakened immune system. Anti infective and anti neoplastic agents to combat opportunistic infection and associated cancers. (Some are used prophylactically to help patients resist opportunistic infections) **Under investigation and testing= are vaccines for HIV.
Treatment protocols: combination of 2 or more medication agents & treatment in an effort to gain maximum benefits with fewest adverse reaction.
Special Considerations:
Be sure to use precaution in all situations that risk exposure to blood, body fluids and secretions. Combination of antiretroviral therapies aims to maximize the suppression of HIV replication, thereby improving survival. Poor drug compliance results to resistance and treatment failure. Immuno suppression caused by HIV disease makes patients vulnerable to additional infections and complications. Recognize that the diagnosis of AIDS is profoundly distressing because of its social impact, and discouraging prognosis. Coping with altered body image, the emotional burden of serious illness and the threat of death may overwhelm the patient. Prevention of HIV infection should include: risk reduction counseling particularly information on safe sex
Nursing Diagnoses:
Impaired gas exchange related to respiratory infection. Altered nutrition (less than body requirements) related to anorexia, weight loss and possible GI manifestation. Infection related to immunocompetence. Activity intolerance related to weakness and air hunger. Fear and Anxiety related to outcome of the disease. Impaired body image related to Kaposis Sarcoma. Body image disturbance related to body weight loss. Social isolation related to possible rejection by peers due to infectious state of illness
Nursing Management:
1. Proper assessment. Understanding and acceptance of the present manifestations of the disease; client to enter a disease and drug program. Emphasis in Health education, Disease information and counseling. (covers sexual orientations and attitudes) Medical management. Activity and Rest balance. Care for physical as well as environment. Balanced Nutrition. Prevention of complications and contaminations. Generous emotional support
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COMMON COLD
Acute, usually afebrile viral infection, causes inflammation of the upper respiratory tract. It is self-limiting. Cold stems from a viral infection of the upper respiratory passages and consequent mucous inflammation. Occasionally it results from mycoplasma infection.
Causative agents / Transmissions:

Rhinovirus, corona virus, myxovirus, adenovirus, coxsackievirus, and echovirus.
Airborne, droplet nuclei infection, contact with contaminated objects, hand to hand transmission.
Signs and Symptoms;

4-day incubation period/ communicable:2-3 days after onset Pharyngitis Nasal congestion, stuffiness that persists for a week, Burning watery eyes Rhinitis headache. Fever, sometimes chills Myalgia, arthralgia, Malaise, lethargy Hacking non productive cough or nocturnal coughs After a day, symptoms will be; fullness with copious nasal discharge.
Treatment and Management:
Supportive and Preventive:

Analgesics or Acetamenophen (eases myalgia and relieves headache) Fluids, Bed rest (loosens respiratory secretions, rehydration, regain energy, combat fatigue and weakness.) Decongestants / Antihistamines / lozenges, anti tussives Steam inhalations Vitamin C and Zinc.
CONJUNCTIVITIS
Hyperemia of the conjunctiva, from infection, allergy or chemical reaction. Highly contagious, but self limiting.
Causative Agents: Bacterial staphylococcus aureus, streptococcus pneumoniae, neisseria gonorrheae, neisseria meningitides. Viral adenovirus, herpes simplex virus. Chlamydial chlamydia trachomatis.
Signs and Symptoms:
Teary eyed, with discharges. Pain and Photophobia. Redness of the eye pink eye Swelling of orbital area Burning and Sensation of foreign body in the eye.
Diagnosis
PE reveals peripheral injection of the bulbar conjunctival vessels. Lymphocytes predominant if caused by virus. Polymorphonuclear cells (neutrophils) if caused by bacteria Eosinophils if its allergy related. Culture sensitivity tests identify the causative bacterial organism.
Treatment
Topical broad spectrum antibiotic Trifluridine drops Vidarabine ointment or oral acyclovir Corticosteroid eye drops as necessary, followed by cromolyn sulfate. Cold compress to relieve itching and warm compress is necessary too during swelling of eyelids. Antihistamines as necessary.
HAEMOPHILUS INFLUENZAE
(A small, gram negative, pleomorphic aerobic bacillus) causes disease in many organ system but frequently attacks respiratory Provokes a characteristic tissue response = acute suppurative inflammation. (mucosal edema and thick exudate) Most common as a secondary disease of existing immunocompromised client. Incidence greatest in alcoholics, elderly, clients in chronic care facilities and nursing homes, clients with debilitating conditions and children less than 5 yrs old.
Signs and Symptoms

Onset is insidious associated with upper respiratory tract infection Fever Chills Productive cough Mucosal edema and thick exudates found in clients with infection of the larynx, trachea and bronchial tree. Pain and difficulty in swallowing. Diagnosis: Blood culture Polymorphonuclear leukocytosis (15000 30000/ul) Leukopenia (2000-3000/ul) in young children with infection. H.I bacteremia found frequently in clients with meningitis.
Treatment and Management

1. Antibiotic therapy Ampicillin 2 weeks course of 1500mg/day. (30% of strains are resistant.) Ceftriaxone, Cefotaxime Chloramphenicol is used concurrently until sensitivities are identified. Rifampin should be given before discharge to assure treatment success. Maintain adequate respiratory function through clients proper positioning, humidification and suctioning as necessary Monitor rate and type of respiration. Watch for signs of cyanosis and dyspnea, which necessitate intubation or tracheotomy. Check the clients history for drug allergies. And for home treatment; suggest clients need for use of humidifier.
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Monitor complete blood count for signs of bone marrow depression Monitor intake (including IV infusions) and output.watch for signs of dehydration Preventive measures; H.Influenzae vaccine to children ages 2-6yrs old. Maintain respiratory isolation Observe proper handwashing technique. Proper disposal of respiratory secretions, placing soiled tissues in a container for disposal and decontamination of all equipments in contact with the clients.
INFLUENZA (La Grippe)

Acute, highly contagious infection of respiratory tract. Popularly called flu
Onset is sudden
Causative agent:
Myxovirus influenzae usually during cold months. Peak 2-3 weeks in epidemics. 1. Type A most prevalent, strikes every year with new serotypes (epidemics q 3 years.) 2. Type B also strikes yearly but causes epidemics q 4-6 years. 3. Type C is endemic, causes only in sporadic cases.
Incubation Period: 24- 48 hours, flu symptoms starts to appear. Period of Communicability: until the 5th day of illness.
Signs and Symptoms:

1. 2. 3. 4. 5. 6. Sudden onset of chills Rise in temperature 38.3 C 40 C. Headache Malaise, myalgia (arms,legs,back), easy fatigability Nonproductive cough, laryngitis, hoarseness of voice Conjunctivitis, Rhinitis, Rhinorrhea.
Symptoms usually subside in about 5 days, fever persists more than 5 days indicates presence of a complication. The absence of the manifestations after 3-5 days, patient will still feel fatigue and weakness with anorexia, generalized malaise.
Three distinct types:

1. Respiratory type high fever, PR-rapid and weak in toxic cases, increase RR and profuse sweating. Catarrhal symptoms cough which becomes hacking and annoying, moist rales in lungs, sore throat, tachycardia and enlarged lymph nodes. Intestinal type nausea and vomiting, fever, abdominal pain, constipation, or diarrhea (which may lead to dehydration, as secondary condition/infection.) Neurologic type headache, fever, joint pain, lumbar back pain, eye ache and frontal headache. Common complication is Meningitis or Encephalitis.
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Most Common Complication : Pneumonia

Other Complications: Encephalitis, Sudden Infant Death
syndrome, Myocarditis. Treatment: Uncomplicated is treated/ managed with; 1. Bed rest 2. Adequate fluid intake 3. Nutritious food intake 4. Acetamenophen, Expectorants, or Prophylactic Antibiotic (when necessary, as prescribed.)
Special Consideration on Management:

Vaccination Anti viral therapy and Chemoprophylaxis. Isolation and CBR Health Education / Health Information. Watch out for signs of Complication. Prevention is important!
PNEUMONIA
Acute infection of the lung parenchyma associated with exudates in alveoli, resulting to consolidation of lung tissues. Causative Agents: Viral Bacterial *Pneumococcus *Streptococcus, Staphylococcus aureus, Haemophilus influenzae,Pseudomonas, Klebsiellae(Freid Lander bacillus), Legionella, Mycoplasma, and Chlamydial. Other opportunistic microorganisms: Pneumocystis carinii, Aspergillus fumigatus, Mycobacterium TB
Classifications:
Microbiological etiology : Viral, Bacterial, Fungal, Protozoal, Mycobacterial, Mycoplasmal, Rickettsial. Location: bronchopneumonia involves distal airways and alveoli; lobular involves part of the lobe; lobar involves an entire lobe. Types: 1. Primary Pneumonia results from direct cause/ aspiration of the pathogens, with predisposing and contributory factors. 2. Secondary Pneumonia- arising from lung damage from noxious chemicals and other insults (superinfection) or maybe result of hematogenous spread of the bacteria from distant focus, with predisposing and contributory factors.( old age, debilitating disease,ngt, impaired gag reflex, decreased level of consciousness.) Incubation Period: 1-3 days, sudden onset.
Mode of Transmission: droplet infection direct/indirect. Signs and Symptoms: Five Cardinal symptoms of early bacterial Pneumonia: 1. Coughing 2. Sputum production 3. Pleuritic chest pain 4. Shaking chills 5. High fever (rapid rise) Other Signs: Body Malaise Difficulty in breathing/ marked tachypnea with respiratory grunting and flaring of nares Rapid bounding pulse Flushed cheeks, lip blisters Diaphoresis, Anxiety, Delirium in acute stage. Fundamentals of Nursing
Stage of Lung engorgement dark red in color; blood tinge, frothy sputum. 2. Stage of Red Hepatization 3. Stage of Gray Hepatization 4. Stage of Resolution exudates and secretions expectorated and liquefied. ***Exudates consists of coagulated fibrin containing red and white corpuscles epithelial cells and some embedded bacterias. Exudates in the alveoli is protein rich fibrinous edema fluid; polymorphonuclear and mononuclear cells found in it. 1.
Widely Used Classifications of Major Pneumonias
Four Categories
Typical Atypical Cavitary/Anaerobic Oppurtunistic
CAP (Community Acquired Pneumonia Pneumonia in Immunocompromised Host Aspiration Pneumonia Hospital Acquired (Nosocomial Pneumonia)
Diagnosis:
History Physical Examination and Assessment Sputum culture/tests Blood and Serologic exams Nuefeld-Quelling test test for capsular swelling/serologic typing Complications: Pleurisy Empyema / pleural effusion Pericarditis/Endocarditis with effusion Pneumococcal Meningitis Otitis Media Hyperstatic Edema and Hyperemia Rare complications such as: arthritis, lung abscess, gangrenous lung, pulmonary emboli, atelectasis.
Treatment:
Antimicrobial therapy Supportive measures: humidified oxygen therapy for hypoxia, mechanical ventilation for respiratory failure. Patients may require positive end-expiratory pressure to facilitate adequate oxygen. High caloric diet, adequate fluid intake, bed rest, analgesics to relieve pleuritic pain.
Special Consideration/Management:
Maintain patent airway and adequate oxygenation, measure arterial blood gas level (administer supplemental oxygen if partial pressure of arterial 02 is less than 60mmHg. Give oxygen cautiously. Elevate head and shoulders if necessary to aid in respiration. Teach patient how to cough and perform deep breathing exercises to clear secretions. Endotracheal tubing for severe pneumonia. Respiratory care, suction often using sterile technique. Obtain sputum specimen Administer antibiotic, record response to medications. Fever and dehydration requires IV fluids and electrolyte replacement Maintain adequate nutrition to replace high caloric utilization secondary to infection. High caloric, high protein, soft diet.
Supplemental oral feedings with NGT, Parenteral nutrition. Measure I & O, Monitor fluids and I & O. Absolute bed rest but with passive activities to prevent other complications arising from immobility. Provide quiet, calm environment. Keep patient warm especially in the lower extremities to maintain vasodilation. To avoid aspiration during NGT fedings, elevate head, check tubesposition, and administer formula slowly, if client is in endotracheal tube, inflate the tube cuff. Keep clients head elevated for at least 30 minutes after the feeding. Check for residual formula at 4-6 hour interval.
PULMONARY TUBERCULOSIS (Kochs Disease 1882)

-is a bacterial infection caused by Mycobacterium tuberculosis. Transported by the blood or lymphatic system, the TB bacilli can infect almost any part of the body, most commonly affecting lymph glands, joints, kidneys and bone extra-pulmonary TB. Bacterium resembles fungus - multiplies slowly and characterized as AF aerobic organism - can be eliminated by heat, sunshine, drying and UV light. - reservoir is clients sputum
Most common and most contagious type of active tuberculosis. Characterized by pulmonary infiltrates, formation of granulomas in the tissues of tubercles that undergo caseation and necrosis or fibrosis and cavitation.
Pathophysiology
Susceptible pax inhales the airborne droplets l Bacilli traverse URT and bronchi to reach alveoli l Alveolar macrophages takes up the bacilli,holding some in the lungs and transporting others throughout the body. l Immune response limits further multiplication and spread of the bacilli. (cell-mediated immunity to myobacteria,w/c develops 3-6wks later) ____________l_____________ Some clients go into active disease Others maybe able to contain the l infection.
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some may eliminate all bacteria/in many, bacilli remain dormant & viable l latent TB infection (usually + TB skin test but have no symptoms & are not contagious.)
*Etiology
Small areas in the lung infected with the bacilli
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gradually merge to form a bigger lesion

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filled with infected material that has a cheese-like consistency

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This material can become liquid,

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then is coughed out leaving a cavity in the lung.

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process continues causing extensive damage to the lung tissue and its blood vessels,
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Generates more infectious material and inflammation.
The damage to the blood vessels can result in Some patients coughing up blood (hemoptysis )
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healing may occur in parts of the lung l resulting in scar tissue.
Leading cause of morbidity and mortality with 8 10 million new cases/yr. 5% exposed and infected develop the disease within the year
The immune system usually controls the tubercle bacillus by killing it, walling it up in a tiny nodule (tubercle) bacillus may lay dormant within the tubercle for years, later reactivated and spreads. Incubation period: 2-10 weeks (ave.4-8 wks) Factors that contribute to the development of the disease: 1. Poverty and Overcrowded homes 2. Malnutrition 3. Vitamin deficiencies (A,D,C) 4. Decrease in clients resistance due to existing infections (that threatens their immune system). 5. Children below 5yrs old who are prone to infections due to factors found above.
Mode of Transmission:
Airborne, transmitted thro droplet nuclei, suspended in the air for a prolong time and is inhaled by a susceptible host.expelled by carriers and active clients through coughing, sneezing or just plain talking. Person to person. In pulmonary, common route is respiratory tract. Patients with cavity lesion are particularly infectious because their sputum usually contains 1M 10M bacilli/ml. Two most common Mode of Entry: 1. Inhalation microbes found in the sputum, spread thro coughing, sneezing, talking via droplets suspended in the air. 2. Ingestion bacteria can be ingested in form of droplet secretions. Bacilli maybe swallowed, reach intestinal mucosa producing early lesions in the mesenteric nodes.
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Risk of exposure : history of TB, personally or amongst friends and extended family; migration from places/country or history of travel to an area with high incidence of TB; Urban areas where people live, travel, work in cramped condition; Other social habits, behaviors (communal drug taking) Risk of infection : (depends on) number of mycobacterium inhaled; duration of exposure; virility of bacilli; strength of persons immune system. Risk of developing active TB : 10% risk of developing active TB in their lifetime; greatest risk during the first two years after infection; Others smoking, Vitamin D deficiency, malnutrition, alcohol/substance abuse, poverty. Risk of developing MDR-TB : 4% of new cases is MDR-TB; improper use of anti TB agents; need to develop adequate laboratory capacity to diagnose these new cases. Risk of Death : 1.7 M deaths every yrworldwide. Inadequate Tx; HIV infection; Malnutrition; Severe pulmonary disease.
Signs and Symptoms:

Early symptoms vague, often attributed to other conditions and remains undetected for sometime. General symptoms: - Fever - Night sweats - Weight loss - Fatigue - Loss of appetite Other prominent S&S: Pulmonary symptoms Extra pulmonary symptoms Dry productive cough localized pain/swelling (depenChest pain -ding on site of disease) Shortness of breathe signs arising specific to area Haemoptysis affected.
Laboratory / Diagnosis
These processes, initial infiltration, lesions and cavities, can all be seen on x-ray. However, to confirm active disease, the patients sputum must be examined for the presence of acid-fast bacilli (AFB), so called because of their staining characteristics when sputum is prepared for microscopic examination. Mycobacteria may also be isolated and identified by means of: 1. Sputum culture. 2. Sputum test : AFB (acid fast bacillus) = stained bright red stands against blue background. Ziehl-Neelsen stain technique Other: auramine-rhodamine stain : flourescence microscopy Mantoux test (PPD skin test) tuberculin skin test
Diagnostic Help
Auscultation detects crepitant rales, bronchial breathe sounds, wheezes and whispered pectoriloquy. Chest percussion detects dullness over the affected area indicating consolidation or pleural fluid. Chest X-rays shows nodular lesions, patchy infiltrates(mainly upper lobes), cavity formation, scar tissue, calcium deposits. Will not distinguish active from inactive stage of tuberculosis. Treatment : 1. Antitubercular therapy: isoniazid 5mg/kg daily, rifampicin10mg/, pyrazinamide25mg/, streptomycin15mg, ethanbutol15mg/. To be taken for six months. (after 2-6 wks, client is no longer infectious.) 2. For client who are Drug resistant are being given second linedrugs : capreomycin, streptomycine, para aminosalisylic acid, cycloserine & quinolone drugs.
To prevent non compliance, inadequate or incomplete teatment of patients, DOTS (direct observed therapy system) is being employed to patients in treatment of anti TB drugs. Anti-TB drugs have 3 main actions: bactericidal activity; sterilizing activity, and ability to prevent resistance. Management/ Special considerations: 1. Isolate the infectious client in a quiet, well ventilated room. 2. Teach client to cough and sneeze through a tissue or a handkerchief, and proper disposal of secretion infected things 3. Instruct client to wear mask when outside his room. Visitor and hospital personnel should likewise wear mask when inside clients room. 4. Sufficient rest. Well balanced diet. Record weight weekly. 5. Be alert for adverse reaction of medications and watch for signs of complication. 6. Be firm on clients drug/medication compliance.
FUNGAL INFECTION: CANDIDIASIS

Most commonly called: Moniliasis. Infects nails (onychomycosis), skin (diaper rash), mucous membrane especially oropharynx (thrush), vagina (moniliasis), esophagus and GITract.
Caused by Candida Albicans , these fungi is part of a normal flora of GIT and mouth, vagina and skin. Causes infection only when body permits their proliferation; - rise in glucose level as in diabetes mellitus, lowered resistance/immunocompromised from disease (cancer), immunosuppressive drugs, radiation, aging, human immune deficiency virus (HIV)infection, elevated estrogen levels during pregnancy, IV or urinary catheters, drug abuse, hyperalimentation or surgery.
Most common predisposing factor: -use of broad spectrum antibiotics! The incidence increases especially because of wider use of IV therapy and greater number of HIVpatients.
Signs and Symptoms: Corresponds to the following sites of infection: SKIN : scaly, erythematous, papular rash sometimes covered w/exudates, appearing below the breasts, between the fingers, axilla, groin, and umbilicus; in diaper rash, papules appear in the edges of the rash. NAIL : red swollen, darkened nailbed; sometimes purulent discharge and the separation of the pruritic nail from the nailbed. OROPHARYNGEAL : (thrush) cream colored or bluish-white patches of exudates on the tongue, mouth or pharynx that reveal bloody engorgement when scraped. ESOPHAGEAL MUCOSA : dysphagia, retrosternal pain, regurgitation and occassional scales in mouth and throat.
VAGINAL MUCOSA : white or yellow discharge cheese like, pruritus with local excoriation, white-grayish raised patches on vaginal walls with local inflammation with dyspareunia. Systemic infections produces : chills, high spiking fever, hypotension, occasional rash. Specific symptoms according to site: Pulmonary system : hemoptysis, fever, cough. Renal system : fever, flank pain, dysuria, hematuria, pyuria. Brain : headache,nuchal rigidity, seizures, focal neurologic deficits. Endocardium: systolic and diastolic murmurs, fever, chest pain, embolic phenomena. Eye : endophthalmitis, blurred vision, orbital or periorbital pain, scotoma exudates.
Treatment and Management:

Aim to improve the underlying condition that predisposes the patient to candidiasis: - control of DM, discontinuation of antibiotic or catheter or cleaning and change of NGTubing. Nystatin effective antifungal superficial medication. Chlotrimazole, fluconazole, ketoconazole, miconazole are effective antifungals in mucous membrane and vaginal candidiasis. Systemic tx is IV of Fluconazole or IV of Amphotericin B with or without Fluorocytocin. 1. 2. 3. 4. 5. 6. 7. Swab Nystatin on oral mucosa for infant with thrush. Instruct patient to swish Nystatin solution around mouth before swallowing. Non-irritating mouth wash. Soft tooth brush to prevent mucal irritation. Topical anesthesia (lidocaine) 1 hour before meals. Soft diet. Cornstarch or dry padding in intigenous areas for obese patient to prevent irritation.
MENINGITIS
Inflammation of the meninges of the brain and spinal cord, usually as a result of bacterial, viral. Can follow a skull fracture, a penetrating head wound, lumbar puncture, or ventricular shunting procedure. Causative Agents: Meningococcus Other bacterias and viruses arising from diseases like : pneumonia, empyema, osteomyelitis, endocarditis, sinusitis, otitis media, mastoiditis encephalitis, myelitis, or brain abscess Usually caused by: Neisseria Meningitides, haemophilus influenzae, streptococcus pneumoniae, and eschirichia coli.
Signs and Symptoms

Cardinal Signs: Infection fever, chills, malaise Increased Intracranial Pressure headache, vomiting, and (rarely) papilledema. Meningeal Irritation : Nuchal rigidity, (+) brudzinskis and kernigs sign Opisthotonous, a spasm in which the back and extremities arch backward, the body rests on heels and head. Other manifestations: sinus arrythmia, irritability, photophobia, diplopia, and other visual problem, delirium, deep stupor, coma.
Meningitis
KERNIGS & BRUDZINSKI SIGN
Diagnosis
1. 2. Lumbar puncture (tap) Blood and urine culture, nose and throat as well. Blood test reveals leukocytosis and serum electrolyte abnormalities. 3. CAT scan 4. Chest X ray, ECG ALERT: Meningitis if left untreated has a 70 - 100% mortality Treatment: Antibiotic IV: Penicillin (ampicillin, piperacillin), or Cephalospherins (ceftriaxone sodium, cefotaxime sodium) Vancomycin hydrochloride alone or in combination with Rifampin for resistant strain. Dexamethasone- as adjunct therapy, given 15-20 minutes before first dose of antibiotic and every 6hrs x 4 days.improves the outcome of Tx in adult and does not increase the risk of gastrointestinal bleeding
Dilantin (Phenytoin) controls seizure that occurs early part of the disease. Management: Supportive treatment Fluid Volume expanders for Dehydration and Shock IV fluid replacement (care is given to prevent overload) Supportive care clients prognosis depends on this. Assess neurologic status/functions & vital signs continuously Pulse oximetry and arterial blood gases basis to identify the need for respiratory support, as increasing ICP compromises the brain stem. Monitor body weight, serum electrolytes, urine volume, specific gravity and osmolality. Position client carefully to prevent joint stiffness and neck pain. Turn often and Assist in ROM.
Protect client from injury secondary to seizures or altered level of consciousness. Prevent complications specially associated with immobility. Institute droplet precautions until 24 hrs after initiation of antibiotic therapy (oral and nasal discharge is considered infectious). Watch of adverse reaction of medications Keep and ensure clients comfort. Provide generous emotional support and Health education Follow strict Aseptic technique.
MENINGOCOCCEMIA
Occurs as simple bacteremia. Infection occurs sporadically or in epidemics. Virulent infections maybe fatal within a matter of hours.
Incubation period : 2 10 days Two major meningococcal infections: 1. Meningitis 2. Meningioma. - caused by gram negative bacteria Neisseria meningitides which also causes primary pneumonia, purulent conjunctivitis, endocarditis, sinusitis and genital infection.
Meningococcemia occurs as simple bacteremia, fulminant meningococcemia and (rarely) chronic meningococcemia. It often accompanies meningitis.
Signs and Symptoms: 1. Sudden spiking fever, chills, headache 2. Sore throat, cough 3. myalgia, (back and legs), arthralgia 4. Tachycardia, tachypnea, mild hypotension. 5. Petechial nodular maculopapular rash, enlargement of skin lesions 6. Extreme prostration 7. Disseminated intravascular coagulation (DIC), Shock.
Alert: unless treated promptly, fulminant meningococcemia results to death within 24 hours.
Treatment and Special Considerations:

Large dose of Aqueos Penicillin G. ; Ampicillin; Cephalosphorin; for clients allergic to penicillin, give Chloramphenicol*iv Therapy includes: IV Heparin for DIC Mannitol for cerebral edema Dopamine for shock Digoxin or diuretic if heart failure develops Strict Isolation and Observance of Standard precaution. Supportive therapy: Fluid and Electrolyte balance; Proper ventilation (room and good patent airway and oxygen); CVP line to monitor cardiovascular status. Bed rest Chemophrophylaxis with Rifampin, Minocycline temporarily eradicates infection in carriers. Health education
ENCEPHALITIS
A severe inflammation of the brain, usually caused by mosquito-borne or arthropod-borne virus (Arbovirus); herpes simplex virus (HSV); and fungal infection. It can also be transferred through ingestion of infected goats milk. Clinical manifestation: 1. Intense lymphocytic infiltration of the brain tissues and leptomeninges causing cerebral edema. 2. Degeneration of brains ganglion cells 3. Diffuse nerve cell destruction
Causative agents:
Herpes simplex virus (HSV)- most common cause of acute encephalitis in US. Mumps virus; HIV; Adenovirus also demyelinating disease such as Measles, Varicella,Rubella or post vaccination. Arbovirus (primary vector is mosquito) occurs during summer and fall and common in north america. 4 types: 1. LaCrosse encephalitis - most common pediatric encephalitis 2. St. Louis encephalitis affects adults over 50 years old. 3. Western equine encephalitis pediatric encephalitis but less prevalent. 4. Eastern equine encephalitis non specific. Fungus related to compromised immune system
ENCEPHALITIS
Signs and Symptoms/ Clinical Manifestations:

All viral forms have similar clinical features although there are certain differences: Acute illnesses starts with: Sudden onset of fever, headache, vomiting and progresses to signs of meningeal irritation (stiff neck & back) and neuronal damage (drowsiness, coma, paralysis, seizures, ataxia, and organic psychoses), ICP. In arbovirus: necrotizing disease flu-like prodrome, seizures In herpes virus: spreads thro trigeminal nerve. Inflammation and necrosis of the temporal lobe, frontal lobe and limbic system. Symptoms include also confusion and behavioural (changes) abnormalities, focal seizures(focal symptoms present within 7days of infection and progress for 14-21 days), dysphasia, hemiparesis, altered level of consciousness. In Fungal: common symptoms with lethargy, mental status changes, vascular changes (arteritis or cerebral infarction)
Diagnosis and Laboratory Based on clinical findings and clients history Identification of causative agent in the CSF or Blood CSF elevated, WBC and Protein level elevated, glucose level- normal to low(HSV), normal glucose level(Arbovirus), Polymorphonuclear leukocytic pleocytosis. Serologic studies shows rising titers of complementfixing antibodies. EEG reveals abnormalityCAT scan and MRI is ordered to rule out cerebral hematoma reveals reveal lesions in basal ganglia and thalamus.

Acyclovir (Zorivax)- drug of choice for HSV enceph. (to inhibit viral DNA replication) to prevent relapse, tx should continue for up to 3weeks, slow adm over 1 hr to prevent crystallizationof the meds in urine. If client is resistant , Foscarnet sodium is given No specific meds for arbovirus enceph. Medical mgmt is aimed in controlling seizures and increase in ICP. Seizures are controlled by antiseizure medications Increased ICP is controlled by repeated lumbar punctures or shunting Antifungal agents are given for a specific period of time to cure infection of client with competent immune system. Amphotericin B is used for tx, dose must be high enough to penetrate the BBB without causing renal toxicity. Fluconazole (Diflocan) or Flucytosine may be administered in conjunction with ampho.[S.E. of Fluco nausea, abd pain, headache, dizziness, rashes, reversible alopecia, increase in liver enzymes. S.E.of Flucy- bone marrow suppression, therefore leukocyte and platelet monitored twice a wk.]
Other drug therapy : Phenytoin given thro IV Glucocorticoids cerebral edema/swelling. Furosemide or Mannitol Sedatives for restlessness Aspirin/acetamenophen-headache & fever Supportive care Adequate fluids and electrolyte: avoid fluid overload, Measure and record I & O. Antibiotic for associated infection Adequate nutrition, small but frequent feedings.NGT or parenteral feeding Assess neurologic functions often (assessment should focus on early changes in intracranial dynamics. Cranial nervecompression is due to swelling. Monitor signs of herniation pattern: flaccidity, decerebration, decortication, noxious to stimuli Watch for cranial nerve involvement (ptosis, strabismus, diplopia), abnormal sleep pattern, behavioral changes. Fundamentals of Nursing
GUILLIAN BARRE SYNDROME

Autoimmune attack of the peripheral nerve myelin. = acute, rapid segmental demyelination of peripheral nerves and some cranial nerves producing ascending weakness with Dyskinesia (inability to execute voluntary movements) and Paresthesias (numbness) Myelin is complex substance that covers nerves, provides insulation and speeds the conduction of impulses from cell body to dendrites. (The cell that produces myelin is Schwann cell.) Predisposing factors: Respiratory or gatrointestinal infections Post vaccination Pregnancy Surgery
Pathophysiology
Cell mediated immune attack on peripheral nerve myelin protein
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By infectious microorganism that mimics peripheral nerve Myelin protein

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Immune system unable to distinguished between the two protein and attacks.
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Destroys peripheral nerve myelin

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Inflammation and Destruction Axon unable to support nerve conduction.

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Posterior(sensory) and Anterior(motor) nerve roots

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Signs of sensory and motor losses occurs simultaneously Symptoms of muscle weakness and diminished reflexes
Clinical Manifestation:
Muscle weaknesses (symmetric weakness, ascending). 24-72hrs Diminished reflexes Cranial nerve demyelination: Optic nerve= blindness; Bulbar muscle weakness related to demyelination of glossopharyngeal and vagus nerves= inability to swallow or clear seretions. Vagus nerve demyelination= autonomic dysfunction- tachy/bradycardia, hypertension, orthostatic hypotension. Progressive sensory symptoms an atypical axonal destruction and the Miller-Fisher variant includes paralysis and ocular muscles, ataxia, areflexia. Rapid progression and neuromuscular respiratory failure
GB is a life threatening disease, / is a medical emergency therefore requires an intensive care unit management. is an infectious polyneuritis. Fundamentals of Nursing
Clinical course: 1. Initial phase- first symptom to 1-3 wks later. 2. Plateau phase several days to 2 wks. 3. Recovery phase coincide with remyelination and axonal process regrowth. 4-6 wks, but may take up until 2years to recover.
Treatment and Management: Respiratory therapy or mechanical ventilation Adequate Oxygenation Anticoagulant Thigh-high elastic compression stockings preventions of thrombosis and pulmonary emboli. Continuous ECG monitoring Short acting alpha adrenergic blocking agent for cardiovascular symptoms To treat and manage hypotension, increase in the administration of IVFluids.
Nursing Diagnoses
Ineffective breathing pattern and Impaired gas exchange related to rapidly progressive weakness and impending respiratory failure. Impaired physical mobility related to paralysis. Imbalanced nutrition, less than body requirements related to inability to swallow. Impaired verbal communication related to cranial nerve dysfunction. Fear and Anxiety related to loss of control and paralysis. Nursing Management: Primarily Supportive: endotracheal intubation (clear secretions) Incentive spirometry monitors vital capacity and negative inspiratory force key to early intervention for neuromuscular respiratory failure.
Mechanical ventilation needed if vital capacity falls (spontaneous breathing impossible andtissue oxygenation inadequate) Trial dose of Prednisone Watch for ascending sensory loss (precedes motor loss) Obtain arterial blood gases measurement (because neuromuscular disease results hypoventilation with hypoxemia and hypercapnia, partial pressure of arterial oxygen (Pao2) below 70mmHg results to respiratory failure. Auscultate for breathe sounds, turn or reposition patient regularly and encourage coughing and deep breathing. Skin care to prevent skin break and contractures. Passive ROM
DIPHTHERIA
Acute, highly contagious toxin mediated infection Causative agent : corynebacterium diphtheriae, a gram positive rod that usually infects the respiratory tract primarily the tonsils, nasopharynx and larynx. Characterized by local inflammation and fibrin formation (pseudomembrane) or sometimes called membranous pharyngitis. Referred to as : Klebs Loffler bacterium. Mode of transmission : airborne, droplet infection, or direct intimate contact.. More prevalent in cold months. Humans are the only known reservoir of the bacteria. Incubation Period : 1-7 days
Diphtheria
Communicability period : toxins released and accumulates at the membrane and is released to the system. By culture; finds Ca, streptococci, pneumococcous found in membrane that tends to affect the heart and peripheral nerves. Signs and symptoms : 1. Tonsils/Pharynx- formation of thin fibrin of fibrinous membrane that rapidly increases to thick patchy, grayish-green membrane over the mucous membrane of the pharynx, larynx, tonsils, soft extends to palate and uvula. 2. swelling of Neck glands- bull-neck appearance due to edema rather than gland enlargement. 3. Rasping / barking cough 4. Husky / hoarseness of voice 5. Stridor 6. Breathe-characteristic odor; FETID-due to necritic cells/tisues If membrane causes airway obstruction, as in laryngeal diptheria;
7. Retraction of sternum 8. Cyanosis, rapid weak pulse rate, tachycardia, tachypnea, and suffocation follows due to much obstruction of brochial tree. 9. Coma, Death follows because of Asphyxiation. 10.Attempts to remove membrane can cause bleeding. 11.In cutaneous diptheria, skin lesion resemble impetigo 12.muco-sanguinous discharge 13.marked excoriation of upper lips and nasi.

1. CBR 2. Strict Isolation 1. Keep patient quiet and in cool protected room 2. Keep visitors to the minimal and wear of gown, mask and gloves is advised for prevention of contamination and cross infection.
3. Infection Control 4. Tracheostomy 5. Suction 6. Croup tents 7. Care of the nose and throat
Maintain infection precaution, until after 3 consecutive negative culture of at least 24 hours apart. 3. Proper disposal of Nasopharyngeal secretions 4. If airway obstruction is present. Nasal gavage is done for feeding. Monitor respirations. 5. The presence of discharges that client is unable to expel. 6. For steam inhalation, in aid for dificulty in breathing due to mucus discharges. 7. Gentle swabbing of liquid albolene after cleaning to prevent from dying. Anoint petroleum jelly on skin and lips. Warm irrigation of NaHCO3. Ice collar to reduce pain. Supportive meds, as prescribed
Treatment must not wait for confirmation by culture.

8. Medications, Immunization Diptheria antitoxin 8. Immunization should be given during convalescence. ThroIM or IV. But this doesnt confer immunity. Because mortality increases directly with the delay. In antitoxin administration, antitoxin is given before laboratory confirmation of diagnosis if sensitivity test is negative. Be alert for anaphylaxis Keep ephinephrine 1:1000 and resuscitation equipment handy. Pts who receive erythromycin, watch for thrombophlebitis.
Antibiotics: Penicillin, Erythrocin 9. Preventions;
10. Nutrition
To eliminate microbes from upper respiratory tract and other sites. To terminate carrier state 9. ECG should be performed twice weekly 4-6 wks. Monitor for signs of shock. Monitor respirations, watch for airway obstruction and resistance. Obtain cultures as needed. Be aware of peripheral neuritis, may not develo 2-3 months after onset of illness. Be alert for the development of myocarditis; heart murmurs, vetricular fibrillation 10. Soft diet, small but frequent feeding. Fruit juices to maintain alkalinity. Nourishment maybe given by rectum, hypodermoclysis or intravenously
Complications : maybe due to C.Diptheriae or other superinfecting microbes. 1. Paralysis 2. Respiratory involvement : Bronchpneumonia 3. Myocarditis with the ff symptoms; abdominal pain, vomiting, restlessness, irregular weak pulse, decrease blood pressure, heart murmurs. 4. Thrombocytopenia 5. Neurologic involvement (motor fibers, sensory neurons) 6. Renal involvement Diagnosis : 1. Throat culture or culture of other lesions. Special consideration : Serial ECGs should be performed twice weekly for 4-6 weeks to watch for myocarditis. Be alert for the signs of developing myocarditis. Ventricular fibrillation is a common cause of a sudden death in diptheria patients.
POLIOMYELITIS
Commonly referred to as infantile paralysis. This is an acute communicable disease caused by a virus ranging from inapparent infection to fatal paralytic illness. Discovered in 1840. But vaccine was only developed in early 50s called Salk vaccine. Mostly in infants and children but now known to have occur in 15 years old and above.
Causative agent: Piconavirus (Piconaviridae family)- An RNA virus and are resistant to ether or chloroform, but can be inactivated by formaldehyde./ multiplies in GIT but particularly neurotropic. Classified to 3 genera; Entero virus, Rhino virus, Calcifi virus. Entero virus is the polio virus because the behavior of virus is affected by climate(temperature), season(summer), age, and socio-economic status.
Incubation period : 5 35 days. (Ave of 9-12 days) Mode of transmission : droplet infection / fecal-oral route Portal of entry : oral / upper respiratory tract.
*Virus enters the body through alimentary tract, l infiltrates mucosa and lymphoid tissues from pharynx to gut, l (multiplies in the oropharynx and lower intestinal tract), l spreads to regional lymph nodes and the blood (hematologic spread, then becomes neurotropic), l infects motor neurons (anterior horn cells and brain stem) l causing inflammation of perivascular cells and diffuse infiltration of mononuclear cells of the meninges, testicles, skin, and the heart. l Development of flaccid paralysis which may be: Bulbar or Spinal in distribution.
Bulbar poliomyelitis is associated with the highest rate of complication and mortality. Spinal poliomyelitis follows. Abortive recovers with significant sequelae. Manifest in 4 different forms differentiated in; Phases/Stages in the progress of the disease and its corres- ponding Signs and Symptoms. 1. Inapparent infection 90-95% of cases, frequently asymptoma-tic 2. Abortive Phase- few hours to days only. 5-10% of cases, with history of: Anorexia, vomiting, abdominal pain Presence of: Fever, headache, muscle pain, sorethroat, pharyngitis and listlessness. (duration of illness is less than 5 days). Patient normally recovers after 72 hrs. 3. Non paralytic phase- more toxic than abortive. Symptoms in abortive disease is present, and; Meningeal irritation(asceptic meningitis) persists to about 2wks :Stiffness of neck, increased headache, higher temperature.
4. Frank paralysis phase(Paralytic disease)- contains 1% of all viruses Biphasic course;-minor illness (viremia,1-3 days / 2-5 days asymptomatic. Non paralytic symptoms meningeal symptoms with chills and rigors. Systemic manifestations mortality associated with respiratory failure due to respiratory arrest (paralysis). Major polio involves CNS : paralytic and non paralytic; Non Paralytic: Nuchal rigidity, Lethargy, irritability, pains in the neck, back, arms, legs, and abdomen and sometimes hamstring and other muscles. Paralytic: 5-7 days of the onset of the fever;- compromised motor neurons localized or widespread.-
Paralytic; 5-7 days of the onset of the fever; Asymmetrical weakness of various muscles, Loss of superficial and deep reflexes, Paresthesia, hypersensitivity to touch, Urine retention, Contipation and abdominal distention Extent of paralysis depends on the level of spinal lesions; cervical, thoracic, or lombar Resistance to neck flexion = patient will tripod (extends his arm behind him for support when he sits up) Patient displays Hoynes sign- head will fall back when he is in supine position and shoulders are elevated, when in supine position he wont be able to raise his legs a full 900 Also positive for Kernigs and Brudzinskis signs. Recovery maybe complete, partial or absent.
POLIOMYELITIS
Other signs and symptoms :

Facial weakness Diplopia, dysphagia, inability to swallow or expel saliva Difficulty in chewing, regurgitation of food through nasal passages Dyspnea, abnormal respiratory rate, depth, rhythm = respiratory arrest 1. Vaccines : a. Oral Polio vaccine (OPV)- oral attenuated polio vaccine (1960) it induces mucosal immunity, providing appropriate herd immunity increasing vaccine uptake because it is taken orally and cost effective. But is associated with Vaccine Associated Paralytic Poliomyelitis (VAPP). - given on 2 mos, 4, 6 mos with booster dose @4 yrs. VAPP occurs frequently after the 1st dose, but may occur anytime after. b. 8-10 cases/year of polio is associated with vaccine virus. As an alternative to prevent rising cases of these development), an All Inactivated Poliovirus Vaccine (IPV) was instituted and is administered parenterally. This is the 1st polio vaccine available, but this does not induce mucosal immunity. The present IPV was enhanced to suit the need.
Treatment and Management :
c. New Monovalent Oral Poliovirus type 1 Vaccine (mOPV1) Introduced in India in 2005. Vaccine targets to eliminate some polio virus reservoir and eradicate wild poliovirus. 2. Supportive- prescribe meds for headache, back pains, muscle spasms and other pains. Analgesia for myalgias and aches Morphine is contraindicated because of danger of respiratory suppression Moist heat application to reduce muscle spasm and pain Laxatives for fecal impaction frequent in paralytic cases. 3. Mechanical ventilation is needed in patients with bulbar paralysis. Tracheostomy care often needed in patients requiring long term ventilatory support. 4. Bed rest./ Diet rich in fiber. More fluid intake. 5. Physical therapy for long term rehabilitation - Frequent mobilization to avoid development of decubitus ulceration - Active/Passive motion exercises during convalescent 6. Isolation 7. Prevention of complications
Complications : 1. Respiratory failure 2. Aspiration Pneumonia 3. Pulmonary Edema 4. Viral Myocarditis 5. GI hemorrhage 6. Paralytic ileus and 7. Gastric dilatation 8. Paralysis 9. Shock 10. and other CNS involvement conditions. Laboratory: Specimen from CSF, stool and throat for viral culture Acute and Convalescent serum for antibody concentration against 3 polioviruses. 4 fold increase in immunoglobulin G antibody titers or a positive anti Immunoglobulin M (IgM) titers during the acute stage.
Special considerations : Observe for signs of paralysis and other neurologic damage Practice strict aseptic technique specially during suctioning, sterile solution for nebulize medication. To control poliomyelitis, wash hands properly and often Check BP frequently specially on bulbar poliomyelitis, which can cause HPN or shock because of its effect on the brain stem. Watch for signs of fecal impaction-(due to dehydration and intestinal inactivity) give sufficient fluids to ensure adequate, well balanced diet Provide good skin care to prevent pressure ulcers. Reposition patient often and keep dry Apply high top sneakers or use a top board to prevent foot drop. To alleviate discomfort, use foam rubber pads and sandbags as needed, and light splints, as ordered. Provide emotional support to patients, family, community. Help setup an interdisciplinary rehab program- which includes physical, occupational therapists, physicians and if necessary a psychiatrist to help manage emotional stability. Fundamentals of Nursing
MUMPS (Acute Parotitis)

Causative Agent :myxovirus Acute viral contagious disease characterized by inflammation of parotid glands and tendency to involve the testes. Inflammation confined largely to interstitial tissue/parenchyma slightly affected Incubation Period: 14-21 days (2-3 weeks) Mode of transmission : direct, person-person contact, droplet nuclei Period of Communicability : 2 days before symptoms appear, immediately when swelling starts and 6 days after swelling ends Recovery : about 10-12 days. It takes about 1 week (7days) for the swelling to subside.
Prodromal Signs : 1. malaise, headache, lassitude, sore throat 2. Pain at the region of both parotids & ear for a few days 3. Stiffness and pain at angle of jaw 4. Swelling of parotids- tender and diffuse lasts for 7-10 days 5. Anorexia and Dysphagia 6. Moderate fever- sometimes absent
Severe if c secondary illness Mouth- congestion, redness (Stensens duct)
Clinical Manifestations and Complications Meningo encephalitis- frequent complication of the disease or post infectious encephalitis with demyelination- usually occurs 10 days after the parotitis. Orchitis (epididymo-orchitis) : High-fever, shaking chills and headache
: Nausea and Vomiting : Abdominal pain (mistaken for appendicitis.) : General prostration : Swollen testes- tender Atrophy later
Acute pancreatitis : Abdominal pain with nausea and vomiting, chills Deafness and Optic Neuritis Oophoritis- pelvic pain Nephritis Thyroiditis Myocarditis- pericardial pain, bradycardia, fatigue and depression of S-T segment in the ECG.
Nursing Care/ Management 1. Comfort: Rest in bed (duration of swelling) - Isolation (until all swelling and until 5 days after) - Analgestics for pain and steroid for orchitis - Hot & cold compress - Care of nose and throat - Mouth wash w/ Na Perborate (cinnamon or nut meg)
2. Diet: -Soft bland: CHO, no milk low fats 3. Protection for the exposed clients: Stage after puberty- live attenuated mumps virus vaccine or attenuated lyophilized vaccine (protective in 98% of susceptible vaccines.) Contraindications: patients allergic to eggs, those that are taking immunosuppressive drugs or the presence of immune deficiencies. This is not recommended either to children less than 1 years old. 4. Control Measures: Immunization and Disinfections of contaminated articles (Infection control) Vaccines given alone or part of MMR. Usually given to children 12-15 months of age. 2nd dose given 4-6 yrs of age, should be no later than 11-12 years of age.
MEASLES (Rubeola/ Morbelli)

Causative Agent : paramyxovirus
Incubation Period:21 days (ave 14 days) *acute onset, characterized by fever and catarrhal symptons involving URT and with typical eruptions in skin and mucous membrane Stages: 1. Incubation Period/ Prodromal stage; (4-5 days)- coryza, cough, fever, malaise
2. Invasive / Pre-eruptive stage; (3-6 days)- photophobia, fever of 40O40.5O, buccal mucous appearance of koplicks spots (after18O, spots fades/ disappear). Fever falls when rash appears, and then rises again 6 days after kopliks spots. Excessive lacrimation and edema of eyelids. 3. Eruptive stage; Rash, Enanthem (mucous membrane) then exanthem (7-10 days) Reddish inflammation maculopopular eruptions from post auricular to face and extremities to trunk (behind ears, along neck, forehead, along hairline, arms, legs, trunk) it takes 3 days for the rash to cover the entire body. Then desquamation starts extend to 1 week. 4. Covalescent stage; rashes fades the same way as it appears. Fever subsides. This is the stage wherein complication starts (if there is negligence in management of the disease) severe form of measles called black measles- hemorrhagic rashes, epistaxis, melena and marked toxicity are some of the manifestations, may occur.
MEASLES
Complications : 1. Bronchopneumonia (usually after rash) *failure of the temperature to decrease during this stage, indicates Pneumonia (viral involvement of the lungs/ interstitial, often complicated by bacterial infection)= dry cough, increase respiratory/ dilation of alaenasi, increase pulse rate, cyanosis. 2. Otitis Media; earache, foul smell coming from the ears, pus exudates/ mucous dripping out of ear/ears. 3. Catarrhal inflammation of conjunctiva, corneal ulceration. 4. Diarrhea/ Abdominal pain 5. Membraneous laryngitis (rare) 6. Encephalitis- acute usually occurs in the 2nd week of illness but may occur in the prodromal stage or after rash appears. 7. (Paralysis of three cranial nerves)- occulomotor. 8. Pulmonary Tubercolosis 9. Bacterial super infection- patient should be monitored for this, wherein this should be treated with appropriate antibiotics basing on the clinical and laboratory findings.
Treatment and Management : 1. Provide client comfort; Rest- Activity balance 2. Keep client warm and dry 3. Care of the skin, eyes, ears, mouth and nose Neosilvol 5% solution, 4grams- (instill1-2 gtts directly into each of the eye daily 5 gtts in each nostrils od.) Vaseline- applied at the eyelids, to moisturize area around 4. Isolation until 5th day of/with rash 5. Bed rest till fever subsides 6. Medications: Promotive, Preventive / Symptomatic and Supportive= Antipyretic, antitussives, TSB, cool mint vaporizer. Antibiotic- only if infection sets in according to clinical evaluation and confirmed by laboratory tests. 7. Increased fluid intake 8. Vaccines and immunoglobins for prophylaxis, though this is of no value once the illness is in progress
9. Care for the exposed person : Measles Hyperimmune Globulin, IM- 0.04-ml/kg body wt. is given within 5 days after exposure; beyond 5 days after exposure, client should receive 0.1-ml/kg body wt. In place of MHG, standard immune serum globulin should be given IM immediately after exposure. - Previously healthy unvaccinated children, 0.25-ml/kg body wt. 8 weeks thereafter, child should be vaccinated with live attenuated measles virus vaccine. - Unvaccinated children with malignancy/ or immuno deficiency disorder or those that are receiving immunosuppressive drugs= 0.05ml/kg body wt (max 0.15) Prophylaxis: Active Immunity: *Natural acquired, after infection confers a limited time of immunity *Artificially acquired; live attenuated virus vaccine- 5ml subcutaneous (arm) single dose to 9-12 mos. Old baby (not to give a patient with leukemia / lymphoma or pregnant)
Passive immunity : *Natural acquired- infants acquire a temporary transplacental immunity *Artificially acquired- 0.25ml/kg gamma globulin or killed virus vaccine given within 5 days after exposure, 250-750 mg IM given to young children exposed to the disease and in poor health. Special Consideration : Prevent client from developing complications, by watching out for signs of secondary infections, and giving prescribed medications and good, appropriate nursing management. Report case of measles to public health office for continuing community care.
GERMAN MEASLES (Rubella)

-acute onset but mild disease, characterized by fever, enanthem and retoauricular and sub occupital adenopathy and which is found to have a teratogenic effect on a pregnant womans fetus Causative agents: sheroidal RNA containing virus. (human amnion cells infected by the virus presents a round clumping of nuclear chromatin and eosinophilic intranuclear inclusions) Mode of transmission: direct contact (droplet as well as respiratory secretions, and may also be found in blood, stools and urine. Incidence: symptoms are often missed or are misdiagnosed as an allergy, or mild measles Incubation Period: 10-21 days, an average of 14 days (2 weeks) Period of Communicability: rash stage Fundamentals of Nursing
Signs and Symptoms: 1. Low grade fever 2. Mild catarrhal symptoms 3. Malaise, headache, mild conjunctivitis, sore throat, stifness of the neck and anorexia 4. Small red lesions at the palate called(forecheimers spot) this is not a pathognomonic sign 5. Minimal rashes that can be diagnose as an allergy. -Pinkish, maculopapular rash which begins on the first day with or without fever. Starts on the face, then on the neck, followed by the arms (exposed part of the body), eventually the trunk and legs, spreads very rapid that it may progressively fade away within 48-72 hours (with some cases, within 24 hrs. only) 6. Lymphadenopathy (swelling of posterior auricular & sub occupital nodes) appears before the rashes are apparent and lasts about 3-5 days.
GERMAN MEASLES
7. Splenomegaly 8. Pain and swelling of the wrist, fingers, and knees, which are most marked during period of rashes and persists to about 14 days after all other symptoms disappear. Polyarthralgia and Poly arthritis 9. Testicular pain in young adult Diagnosis: 1. No Pathognomonic sign 2. Virus isolation, identification; changes in Ab titers 3. C-fixationtest, ELISA (enzymes link immunosorbent assay), RIA (radioimmunoassay), SRH (single radial hemolysis) 4. Hemaglutination Inhibitation (HI) antibody test- the most useful for diagnosing german measles.
Treatment : Purely symptomatic and suuportive Management : 1.Relief of discomfort; care of skin, eyes, ears and mouth & nose 2. Isolation 3. Good Ventilation and Environment 4. Prevention of complication (for the fetus is Congenital Rubellaretardation, eyes and ear defects, neurological abnormalities and CHD) 5. Proper Nutrition and Good Diet
CHICKEN POX (Varicella)

-Acute, highly contagious disease. A DNA carrying virus characterized by mild constitutional symptoms and generalized eruptions of papules and vesicles, which appears in crops- drying up and leaving a superficial crust. Causative Agent: herpes virus varicella zoster (v-z) Mode of transmission: direct contact (droplet, and respiratory secretions and vesicular content) Incubation period: 14 days, 2-3 weeks vary Period of communicability: 1 day before rash and until vesicles is fully crusted. Virus present in mouth, in vesicular fluids (moist lesions) on the skin, infectious 24O hours prior to appearance of eruptions and till fully crusted. Fundamentals of Nursing
Signs and Symptoms: 1. Rash maculopapulo-vesicular eruptions : highly pruritic, presence of Pocks (main lesion) then, formation of scabs/ crust. 2. Prodromal stage- initially with slight fever (chicken pox doesnt manifest increase in temperature.), malaise, anorexia, coryza within 24 hrs of rash. vesicles continue to appear 3-4 days after prodromal signs, all forms are present. 7 9 days after, most pocks have dried up. Complications: Infection (skin abscess) Myocarditis Encephalitis Pneumonia Other minor complications: furuncles, erysipelas, cellulites.
CHICKEN POX
Diagnosis:
Virus can be isolated in 3-4 days after rash. Geimsa strain distinguishes V-Z from vaccinia variola viruses. Serum contains antibody 7 after onset. Fluorescent antibody to membrane antigen (FAMA) for identification of antibody Complement Fixation test Treatment and Management: 1. Strict Isolation 2. Supportive and preventive measure Care of the Skin : > provide mittens to prevent infection due to scratches. > Local / systemic antipruritic agents. > Equal parts of boric acid, zinc oxide and talcum powder
Comfort: > Calamine lotion, Cool bicarbonate of soda baths. > Antihistamine dipenhydramine > Olive oil, Warm bath. Prevention of Infection: > Antibiotics: penicillin ointments. > Acyclovir may slow vesicle formation, speed skin healing and control systemic spread of infection. *** Salicylates are contraindicated!
3.
Health Education
HERPES ZOSTER
-an acute unilateral, and segmental inflammation of the dorsal root ganglia caused by infection of herpes virus varicella which also causes chicken pox. Also called Shiingles Causes: - Reactivation of varicella virus that has lain dormant in the cerebral ganglia (extramedullary ganglia of the cranuial nerves) Signs and Symptoms : 1. Skin lesions runs in a typical course 2. begins with fever and malaise 3. 2-4 days severe deep pain, pruritus 4. paresthesia and hyperesthesia develop
HERPES ZOSTER
5.
2 wks after the first symptom, small, red, nodlar skin lesions erupt on the painful areas; spread unilaterally around the thorax or vertically over the arms or legs.. nodular that turns to vesicles filled with clear fluids or pus 6. 10 days after, vesicles dry up and form scabs 7. When it involves cranial nerve, trigeminal, geniculate ganglia, occulomotor nerve Diagnosis : 1. Positive diagnosis isnt possible until the characteristic skin lesions develop 2. Pain mimics that of appendicitis, pleurisy 3. Diagnostic test;
V. fluid and infected tissues- shows eosinophilic intranuclear inclusion and varicella virus Lumbar puncture shows increased CSF pressure; csf shows increased protein levels, possibly pleocytosis Staining antibodies from v. fluid, under fluorescent light differentiaties zoster from simplex
No Specific Treatment Primary goal is supportive tx relieve itching and neuralgic pain with calamine lotion and antipruritic Collodion or tincture of benzoin applied to unbroken lesions Analgesics Systematic antibiotic Instillation of antiviral agent Systematic cortecosteroid to reduce inflammation and to deal with post herpetic neuralgia Tranquilizers, or sedatives, tricyclic antidepressants with phenothiazines Acyclovir therapy maybe administered through IV- this prevents dessiminated life threatening disease in some patients.- this shortens the duration of the pain and symptoms in normal adult.
Special Considerations : Keep patient comfortable, maintain cleanliness and good hygiene to prevent infection
During acute phase encourage rest and promote proper healing of lesions
Apply calamine lotion
DIARRHEAL DISEASES
In developing countries, infectious diarrhea kills about 4 million people/year. In Industrial countries like United States, children under 5 years old are most affected
Portal of Entry:
oral ingestions. (high acidity of the stomach, and antibody-producing cells of small bowel serves to decrease potential of pathogens.)
Specific causes: Viral, Bacterial, Parasitic. ** Rotavirus most significant viral cause of diarrhea in young children. ** Bacterial - Escherichia Coli - Salmonella - Shigella Nursing Process: - most important element is : Assessment is to determine hydration status. Goal of rehydration: To correct dehydrationimmediately! Assessment includes: Thirst Oral mucous membrane dryness Sunken eyes Weakened pulse Loss of skin turgor
Health history check for recent travel - whether client was recently treated of antibiotics - whether client has been in contact with anyone who has recently had diarrheal disease. - recent food intake. Nursing Diagnosis: Deficient fluid volume related to fluid loss due to diarrhea. Deficient knowledge about infection and risk of transmis-sion to others related to specific personal status. Nursing Intervention / Management: Correcting dehydration associated with diarrhea. Fluid infusion and oral rehydration Measure I & O, weigh regularly Assess physical signs of dehydration.
Prevent spread of infection: - Proper Sanitation & Sewerage, Clean Water. - Screening Practice standard precaution with enteric precaution Isolation Medications: Antibiotic and other supportive medications. Monitoring and managing potential complications. CBR, proper management of Diet and Nutrition Maintain Fluid and Electrolyte balance.
ESCHIRICHIA COLI /GASTROENTERITIS

Aerobic, gram negative bacilli. Causes local and nosocomial infection. Non-invasive, enterotoxin-producing E.Coli infections, a major cause for diarrheal illness. these toxins interact with intestinal juices and promote excessive loss of chloride and water. The invasive form directly invades the intestinal mucosa without producing enterotoxins= local irritations, inflammation and diarrhea Transmissions : -directly from infected person, or indirectly by ingestion of contaminated food or contact with contaminated utensils.
Signs and Symptoms : depends on the causative toxins; 1. Abrupt onset of loose watery diarrhea 2. Abdominal cramping, pain 3. Chills & fever 4. Changes in consistency=yellow to green stools, mucoid or blood tinged 5. Vomiting, listlessness, irritability 6. Anorexia 7. In severe illness- fever, severe dehydration, acidosis and shock Diagnosis : - Culturing is of little value since E.Coli resides in GI tract. Therefore clinical observation is most appropriate. Identification procedures : bioessay- which rules out shigellosis, and salmonellosis
Treatment and Management : 1. Isolation 2. Correction of fluid and electrolyte imbalance 3. IV of antibiotics to the appropriate case 4. Bismuth subsalicylate 5. Keep an accurate intake and output records. Monitor volume of stool and note of the presence of blood or mucous 6. Prevent the spread of infection: screen all personnel and staff of diarrhea, proper hand-washing technique, discard used bottles, irrigating tubes etc. 7. Report cases to public health, boil water and wash raw foods before intake
SALMONELLOSIS / (SALMONELLA
THYPOSA)
A common infection usually caused by non-spore forming, gram negative bacilli, motile and ferments lactose, sucrose and glucose. Most severe form of salmonellosis.
Causative agent : Salmonella typhosa Incubation period : 7-14 days with (innoculum size 3-60 days) Mode of transmission: direct / indirect. Food to humans through a vehicle with 5 Fs. Reservoir : only humans.
Sources of infection: 1. Carriers patients who have recovered from fever but whose stools or urine may carry the bacilli for years. 2. Ingestion of infected food or water. 3. Certain drug substances of animal origin Salmonella produce disease only if hosts resistance is impaired and an increase in the virulence of the organism. Progress of the Disease ST enters the body through alimentary tract
l
GI tract (localized in the reticulo-endothelial system)

l
invades the bloodstream via lymphatics (there is hyperplasia and hypertrophy of the lymph nodes)
l
Setting up intracellular sites infection sets in including gallbladder and affects the billiary tract
Intestinal seeding of millions of bacilli; penetrates and involve lymphoid tissues (peyers patches in the ileum)
l
Enlarged, ulcerated and necrosed tissue.

l
Hemorrhage Symptoms are due to the effect of endotoxins and other bacterial products.
Signs and Symptoms: First week > gradual increase in temperature, starts with low grade fever > myalgia, malaise, anorexia > headache, slow pulse ( which is disproportion to presence of high temperature) with distinct dicrotic wave.
Second week >remittent fever up to 40 C usually in the evening, lasts for 4-6 weeks. > chills, diaphoresis, weakness, delirium > abdominal pain and distention (tympanites) and tenderness at the right quadrant (hepatomegaly) and left (spleenomegaly) > diarrhea and constipation. > cough, moist crackles > maculopapular rash especially in the abdomen and chest. Third week > persist fever, increasing fatigue and weakness. Subsides on the 3rd week. > relapse or complications occur. Carrier state bacteria present in at least a year in the fecal matter; gallbladder is a site of persistent intestinal infection (asymptomatic)
Complications: 1. Intestinal hemorrhage due to perforation 2. Myocarditis 3. Abcesses, bone marrow suppression 4. Localized infection 5. Meningitis, thrombophlebitis, cerebral thrombosis 6. Pneumonia, osteomyelitis, acute circulatory failure.
Treatment: Specific: Ampicillin IV or PO 100mg/kg body wt/day Amoxicillin PO 4g/day

Trimethoprim(320-640mg) combined with Sulfametazole (1600-3200mg/day) given in 2 divided doses is given to clients resisting to chloramphenicol.
Chloramphenicol IV or PO 50mg/kg/day given in 4 divide doses or 100mg/kg/day given in 4 divided doses. Total dose should not exceed 2grams *Recommended duration of therapy : 2 weeks. Non-specific: Acetaminophen Steroid (prednisone) 1-2 mg/kg/day in 3-4 divide doses orally for 3days in severe delirious client For blood loss give plasma expanders. Diagnostic tests: Stool exams McConkeys agar (differntial agar positive for organism after the 1st week and throughout the course. Serologic test positive for organism after 1 week. Widals tests agglutination or clamping of organism on clients serum; (+) in the 10thday or end of 2ndwk.
shows rising titer in the 2nd-3rd wk of the disease recommended time of test on the 8th-10thday and repeat by the 4thwk Bone marrow puncture or culture to determine presence of microorganism. Management: Isolation of client enteric precaution, care for the exposed persons, avoidance of further contact. Supportive care with CBR Antibiotics and prescribed medications given cautiously. Environmental sanitation Vaccine, immunization for prevention Diet : avoid gas forming foods Fluid and Electrolyte (oral rehydration or IVF ) Most important: determine hydration state of the client I&O should be measured High caloric, high protein, cho, low fats and low residue diet with Vit B. Watch altered state and other signs of complications.
CHOLERA
is an enterotoxin-mediated GI infection, causing severe gastrointestinal symptoms resulting to generalized physiological imbalance. Causative agent: Vibrio Cholerae gram negative motile, aerobic bacillus.
Mode of transmission: humans as carriers, host and victims. ** transferred through contaminated food and water by infected feces/stools. Infectd stools, unsanitary environment- dirty surroundings, water and preparation of food
Signs and Symptoms Acute, painless, profuse watery diarrhea Stools white fleck mucous. (rice watery stools) Effortless vomiting. Intense thirst due to massive diarrhea and vomiting Fluid and Electrolyte imbalance Fluid loss is as much as 1L/hour. =(hypovolemic shock, metabolic acidosis, and death if treatment is delayed.) Specific Symptoms: Rice watery stools Vomiting Generalized weakness. Poor skin turgor. Sunken eyes, pinched facial expression Muscle cramps, especially the extremities. Cyanosis, Oliguria, Tachycardia, Tachypnea Thready or absent peripheral pulses, falling blood pressure. Inaudible, hypoactive bowel sound. Fever and body malaise.
3% of clients who recover continue to carry V.cholerae in their gallbladder, however, most of the clients are free from infection after about 2 weeks. Incubation period: several hours to 5 days. Treatment and Management: If treatment is delayed or inadequate, Cholera may lead to metabolic acidosis, uremia and possibly coma and death. Antibiotic therapy. (is not proven to have shorten the course of infection, but is given to prevent complication.) Doxycycline (tetracycline) given through IV, especially if symptoms persists despite replacement of Fluids and Electrolytes
IV infusion of large amount of isotonic saline solution (50-100ml/min.) alternating with isotonic sodium bicarbonate or sodium lactate. Potassium replacement added to IV solution. Oral glucose electrolyte solution. Improved Sanitation and Administration of Cholera vaccine. Community health education.
A cholera patient requires enteric precautions, Supportive care and close observation.
Wear gloves and gown in handling feces contaminated articles. Proper hand washing and avoidance of contact with infected materials. Monitor intake and output, including volume of stools and fluid replacements. Protect clients family by giving prophylactic oral medications of tetracycline. Proper boiling of water and cooking of food as preventions Avoid areas where there is an endemic case of Cholera.
AMOEBIASIS
Also known as amebic dysentery. Acute or Chronic protozoa infection caused by: Entamoeba Histolytica Most common in the tropics, produces varying degrees of illness, mild to severe fulminant dysentery. Extraintestinal amebiasis can induce Hepatic abscess, infections of the lungs, pleural cavity pericardium, peritoneum but rarely the brain.
Incidence higher in gay men and lesbian women and institutionalized people in whom fecaloral contamination is common. Prognosis: Good, but with some common complications Causes: Entamoeba Histolytica exists in 2 forms : A Cyst (survives outside the body). A Trophozoite (cannot survive outside the body) Mode of transmission: fecal oral route / contaminated food and water Ingested cysts pass through to the intestine l Digestive secretions break down the cyst and liberates the motile trophozoites within l Trophozoites multiply, then invades and ulcerate the mucosa of large intestine l Or simply feeds on the bacterias l As these are carried slowly towards the rectum, it is encysted and then excreted with the feces/stool.
Signs and Symptoms: Sudden rise in temperature(40 C) and chills Abdominal pain and cramping Profuse bloody, mucoid diarrhea with tenesmus Diffuse abdominal tenderness due to extensive rectosigmoid ulcers, tenderness over the cecum and ascending colon (indicates hepatomegaly) Foul smelling mucoid and blood tinged stools daily Weight loss Chronic amebic dysentery: intermittent diarrhea, 1-4 weeks, recurs several times a year. Partial or complete bowel obstruction due to complication of granuloma.
Diagnosis: Isolating E.Histolytica from feces or aspirated fluids from abscesses, ulcers or tissues confirms Amebic Dysentery. Sigmoidoscopy detects recto-sigmoid ulceration, biopsy maybe helpful. X-rays, Stool exams, Cecum palpation. Indirect Hemagglutination test (+) with current & previous infection Complement fixation usually (+) only during active phase of disease. Barium studies rule out non-amebic causes of diarrhea such as polyps and cancer. Complications: Amebic granuloma commonly mistaken as cancer. Acute appendicitis due to toparasitic and bacterial invasion of the appendix. Perforation of the intestinal wall, causing spread to the liver and diaphragm. Perforation of the lungs, pleural cavity and sometimes the brain. Treatment : Drugs Metronidazole - Iodoquinol, Diloxamide, Paronomycin *** advise clients with Amebic Dysentery to avoid drinking alcohol when taking metronidazole, the combination causes nausea, vomiting and headache.
HEPATITIS
A common systemic disease, marked by hepatocellular destruction, necrosis and autolysis leading to anorexia, jaundice, hepatomegaly. Some patients hepatic cells regenerate. Prognosis is poor if edema and end stage liver disease develops
Types of hepatitis :
1. Type A (infectious or short incubation hepa.) rising among homosexuals and people with immunosuppression related to human immunodeficiency virus (HIV) infection. Usually self-limiting. Highly contagious, usually transmitted by fecal-oral route. Usually results from ingestion of contaminated food, milk, or water. Often ingestion seafood from polluted water. At risk: IV drug abusers and recipients of multiple blood product transfusions. Type B (serum or long incubation hepa.) is now considered sexually transmitted disease. Transmitted by contact with human secretions and stool passed or recipients of plasma derived products or hemodialysis patients. Also during sexual contact or perinatal transmission.
2.
VIRAL HEPATITIS A
HEPATITIS B
3.
Type C accounts for 20% of all viral hepatitis. Usually obtained from tattooing. Transmitted through transfused blood from asymptomatic donors. Associated with high rate of chronic liver disease(chronic hepatitis, cirrhosis, increased risk of hepatocellular carcinoma) Type D (delta hepa.) responsible for 50% of all fulminant hepatitis, high mortality causes unremitting liver failure with encephalopathy, progresses to coma and death. People who are frequently exposed to blood and blood products. Transmitted parenterally, less frequent in sexually frequent H-B illness. Type E (non-A or non-B hepatitis)- water borne. Fecal oral route. Detection is difficult.
4.
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Signs and Symptoms : 1. Prodromal stage (pre icteric) : weight loss, malaise, depression, headache, weakness, arthalgia, myalgia, photophobia, nausea and vomiting. Vital signs; 37.9OC-38.9O 1-5 days before jaundice stage. Dark colored urine and clay-colored stools Clinical stage (icteric) : jaundice stage, pruritus, abdominal pain, tenderness, anorexia, jaundice of sclerae, mucous membranes and skin, lasts for 1-2 wks. Indicates liver damage is unable to remove bilirubin from blood, rashes, erythematous patches, urticaria occasionally, splenomegaly and cervical adenopathy Recovery stage (post icteric) : patients symptoms decrease. Lasts for 2-12 weeks although sometimes it lasts longer.
2.
3.
Diagnosis : - Serumaspartate aminotransferase and serum alanine aminotransferaselevels are increased in acute viral hepa. - Serum alkaline phosphatase are slightly increased - Serum bilirubin levels elevated - Prothrombin time- prolonged (more than 3 seconds longer indicates liver damage) - WBC reveals transient neutropenia and lymphocytosis - Liver biopsy done only if diagnosis is questionable. Treatment and Management : 1. No specific drug therapy except on type c which is successfully responding to interferon alfa-2b. 2. Rest is strongly recommended 3. Small frequent feedings in high protein, largest meal should be in the morning.
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5. 6. 7.
Protein reduce if there is sign of lethargy, confusion and mental changes Antiematic Parental nutrition Anti pruritic resin cholestyramine
Enteric precaution Thorough and proper hand washing; Strict isolation; Provide rest periods; importance of activity pacing Health education and restrictions emphasized to prevent recurrence Administer supplemental vitamins and feedings Monitor patients weight daily, record intake and output Watch for signs of fluid shift such as fluid gain and orthostasis Watch signs of hepatic coma, maintain electrolyte balance Watch out for signs of complications In fulminant hepatitis, maintain F7E balance, patent airway, prevent infections and control bleeding, control hypoglycemia
Non viral hepatitis, classified as toxic or drug induced inflammation of the liver, most clients recover but some develops fulminating hepatitis or cirrhosis. Causes : Alcohol overuse Direct hepatotoxicity liver cell damage due to toxins, also dose dependent, usually caused by acetamenophen overdose Idiosyncratic hepatotoxicity sensitivity to medications such as; isoniazid, methyldopa, mercaptopurine, lovastatin, pravastatin, dipyridamole, and halothane. Cholestatic reactions lack of bile excretion, direct damage from oral contraceptives or anabolic steroids. Hypersensitivity to phenothiazine derivatives such as chlorpromazine, antibiotics, thyroid meds, antidiabetic drugs and cytotoxic drugs.
Metabolic and autoimmune disorders acute exacerbations of other liver disease.

Infectious agents systemic virus such as cytomegalovirus, mononucleosis or Epstein-Barr virus, measles virus, varicella zoster, adenovirus, herpes simplex, coxsackievirus, and human immune deficiency virus; spirochetes such as syphilis and leptospirosis.
Diagnostic Evaluation : Hermatologic and Liver function test; CBC, hematocrit, hemoglobin level, prothrombin time, AST, ALT, LDH, alkaline phosphatase, total protein, albuminglobulin levels, fasting blood glucose, bilirubin levels. Anemia commonly results from decreased red blood cell life Enzymes will show elevation 4-10 times normal due to liver cell necrosis Protein and serum A/G levels, abnormally low Serum bilirubin levels, elevated. Urinalysis - elevated bilirubin levels - Proteinuria and hematuria maybe present
Chest X-Ray and ECG : this determines the condition of the respiratory and cardiac tissues. Liver Biopsy : shows local or diffuse, widespread necrosis Serum studies for hepatitis B surface antigen (HBsAg): confirms the diagnosis if antigen is present. Nursing Diagnosis : Altered nutrition (less than body requirements) related to anorexia Fluid volume deficit related to nausea, vomiting, and diarrhea. Impaired physical mobility related to bed rest Impaired skin integrity related to pruritus Social isolation related to bed rest and separation from peers Depression due to anxiety related to knowledge deficit Planning and Goals Client recovers from hepatitis w/out life threatening sequel Regain adequate nutritional and fluid through intake Learn how to prevent infection Fundamentals of Nursing
Nursing care 1. Assist client to comfortable positions in bed; provide padding to lessen pressure over bony prominences; provide skin care
2.
Monitor vital signs and weight.
Nursing Rationale 1. Bed rest is necessary until the diagnosis is clearly established (client have limited mobility for 5-10 days or until liver enlargement decreases) Because of weight loss, his skin and bony prominences may be vulnerable to injury 2. Clients temperature may fluctuate and weight continue during the acute stage of the disease 3. Maximum precautions help prevent infecting others with the clients equipment and utensil
3.
Maintain infectious disease precaution to prevent spread of hepatitis. Promote gradual intake of high biologic value protein with vitamins and minerals; encourage fluid intake, measure I & O.
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4.
Although anorexia may be pronounced, clients appetite will slowly improve as he recovers. HBV protein contains all essential amino acids.
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Refrain from administering medications not ordered by the physician. Assist client with ROM exercises, as needed.
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Teach client about the disease methods of transmission and preventive measures. Provide activities to induce positive mood and self concept. Prepare for home care.
9.
10. Contact community health care providers.
A dysfunctioning liver cant metabolize medications, the client may develop toxicity. 6. Bed rest and fatigue may prevent client from maintaining satisfactory muscle mass or function. Hepatitis-B has a 6month recovery period. 7. Knowledge deficit can be associated with clients deteriorating condition. 8. Fatigue and depression may hinder the client in investing full interest or participation. 9. Discharge when condition improves sufficient for him to continue recovery at home. 10. Follow up care at home is vital to the health and safety of the client and those in contact with him.
Vector Borne Diseases And Other Zoonotic common Infectious disease
VECTOR-BORNE DISEASES viral * bacterial * parasitic
MALARIA
An acute infectious disease caused by a protozoa of genus Plasmodium. Literally means bad air It is transmitted by the bite of female Anopheles mosquitoes, which proliferates in humid swampy areas.
Types: Plasmodium Falciparum Plasmodium Vivax Plasmodium Malariae, and Plasmodium Ovale Etiology:
Infected mosquito bites injects a Plasmodium sporozoites in a host l Sporozoites goes with the blood circulation l Invades parenchymal cells of the liver l Forms cyst-like structures containing thousands of Merozoites
Merozoites are released in the circulation, each merozoite invades an erythrocyte and feeds on hemoglobin l Eythrocyte rupture, releasing malaria pigments, cell debris and more merozoites, (which if not destroyed will destroy more erythrocytes) Infected person becomes the reservoir l non infected mosquito gets infected blood from reservoir. l Same cycle begins.
Hepatic parasites P.vivax, P.ovale, P.malariae persists in the liver for years chronic carriers
Signs and Symptoms: Specific: Chills, fever, headache, myalgia (with periods of well being) In acute attacks: 3 stages when erythrocytes rupture: Cold stage 1-2 hours : chills to extreme shaking. Hot stage 3-4 hours : high fever (107.F / 41.C) Wet stage 2-4 hours : profuse sweating Paroxysms every 48-72 hrs (P.Malariae) Every 42-50 hrs (P.vivax or P.ovale) Hepatospleenomegaly Hemolytic anemia Persistent high fever, orthostatic hypotension, RBC sludging w/c leads to capillary obstruction at various sites found in P.Falciparum which the most life threatening form of Malaria.
MALARIA
Signs and symptoms of obstruction of the capillaries in specific sites Cerebral hemiplegia, seizures, delirium, coma. Pulmonary coughing, hemoptysis Splanchnic vomiting, abdominal pain, diarrhea, melena. Renal oliguria, anuria, uremia Diagnosis: Blood test indirect fluorecent serum antibody (but can be unreliable in acute phase because antibodies cant be detected 2wks after onset) - decreased hemoglobin level - normal decreased leukocyte count (as low as 3,000/ul) - reduced number of platelets (20,000-50,000/ul) - prolonged prothrombin time (18-20 sec.) - prolonged partial thromboplastin time (60-100 secs) - decreased plasma fibrinogen. Urine presence of protein and leukocyte.
Treatment: Chloroquine therapy oral for comatose, pt is given thru IM Oral Quinine ( for chloroquine resistant malaria) for 10 days Pyrimethamine and Sulfonamide (Sulfadiazine) or Tetracycline. In hepatic stage; Primaquine phosphate is given daily for 14 days. (induces hemolytic anemia) Preventions/ Prophylaxis: Oral Chloroquine should be taken weekly 2wks before the trip and 6 wks after for those staying less than 3 wks in a malaria infested areas. Chloroquine and Sulfadoxine-Pyrimethamine (Fansidar) for those staying longer than 3 weeks in the area. with severe adverse reaction for drug combination
Special Considerations/ Management: Obtain a detailed patient history, noting any recent travel, foreign residence, blood transfusion, or drug addiction. Record symptom pattern, fever, type of malaria, and any systemic sign. Proper assessment of patient upon admission; Enforce bed rest. Fluid and Electrolyte watch and balance, strict record of I & O Monitor IV fluids closely and avoid fluid overload. Protect patient from secondary bacterial infection. Practice standard precaution and Aseptic techniques. Proper and frequent hand washing. Discard used needles, syringe and contaminated objects. Double bag these items Supportive care Preventive care Watch for signs of Complications. Community care with health education.
Leptospirosis
A group of bacterial diseases caused by antigenetically distinct members of the bacteria which is aerobic, motile, gram-negative spirochete tightly coiled around axial filament bent at one or both ends producing hook-like appearance. Also known as Red Water disease in cattle (primarily an animal pathogen, zoonotic in origin). Weils or Swineherds in humans. Mutated as human pathogen Thrives in kidney / urine.
Causative agent: leptospira interrogans Organism is released through urination, transmission from humans to animals and vice versa. Can survive several weeks outside the body/host in a moist, alkaline soil or stagnant slow moving slightly alkaline water. Portal of entry: Mucous membranes of the eye, nose, mouth as well as abraded/break in the skin. Signs and Symptoms: Exposure and manifestation of first clinical symptoms: 2days to 4weeks. First phase / Initial signs are: Abrupt onset of: fever, headache, vomiting, muscle aches, weakness, conjunctivitis, diarrhea, abdominal pain, jaundice, hemorrhagic rash. Symptoms usually lasts 4-7 days, sometimes asymptomatic. Disease is Biphasic, Second phase is more severe with the ff symptoms: 1. Kidney or Liver failure. 2. Vasculitis 3. Meningitis, which complicates recovery this phase is called Weils disease
Diagnosis: Wharthin-Starry or Geimsa stains can reveal leptospire. Flourescent antibody and microscopic andm macroscopic agglutination tests are serologic methods of detection. Blood, Cerebrospinal fluid, urine, and tissues can be cultured. Treatment and Management: Antibiotics Doxycycline, Penicillin, Streptomycin during acute phase. For severe cases; Penicillin IV is recommended. Fluid therapy to prevent dehydration In severe cases: Dialysis and life support measures Phrophylactic therapy: Doxycycline 200mg once a week, beginning in the week prior to anticipated exposure.
Special Consideration: Although human to human infection has not been documented, wear gloves in handling fluids. Proper hand washing. Maintain Fluids and Electrolyte balance. Monitor I & O accurately. Laboratory tests should be done, Monitor BUN, Creatine, Liver function test and Bleeding time. Community involvement for prevention and awareness. Patients who have been infected of leptospira should not donate blood for at least 12 months after recovery.
Hemorrhagic Fever
(H-Fever ; Dengue)
Condition arising from infection due to virus transmitted by specific mosquitoes carrying disease that can sometimes cause internal bleeding which can be life threatening due to shock. Causative Agent: Aedes mosquitoes (Aedes Aegypti) Four serotypes of Viruss that rely on mosquitoes and other organisms to complete their life cycle. Mode of Transmission: through a bite of the virus carrying mosquito (daytime mosquito, more prevalent by dawn, around 4am or early morning till sunrise)
Dengue Hemorrhagic Fever
Incubation period: 2 5 days (sometimes 24 hours) after the bite of an infected mosquito. Forms of H-Fever: 1. Mild 2. Severe Signs and symptoms: Sudden onset of headache Fever (with the characteristic of 3 days elevated, and plateau after the 3rd day.) Flu-like symptoms; patient complaint od sorethroat, cough, groin pain photophobia Retro orbital pain Backache, bone and joints / weakness Malaise
Hyperpigmented rashes Flushing of the face Conjunctivitis Anorexia Abdominal pain, Nausea or vomiting Lymphadenopathy Hepatomegaly may occur. Diagnostic tests: (Tourniquet test is done initially) Complete blood count Platelet count Clotting time
Pathophysiology:
Bite of a virus carrying aedes mosquito l Mosquito injects fluid into victims skin And virus enters the blood stream. l Infects cells and generate cellular response (as in any viral infection, virus enters the cells and initiates cell activity to survive) l Initiates immune reponse (stimulates release of cytokines) l In the process the cytokines (release to destroy the virus),it also destroys the cell membrane and cell wall. l (viral antigens found in monocytes) Fluid shift
l when treated early with doctor prescribed Medications and managed to prevent the Appearance of other symptoms. l IVFs and Electrolyte replacements and preventions. l Patient recovers
l when illness becomes severe l > damage cells due to both cytokines & and virus l > fluid shifts from ICF to ECF l Manifests evanescent rashes, (indicating there is bleeding) and rashes in several areas of the body. l may have bloody vomitus, urine and stool. l this precedes circulatory collapse that will result to SHOCK = Death.
Management: IVF (intravenous fluids) specially to patients with dehydration and hemoconcentration. Electrolyte replacements Blood plasma / platelet transfusion Oxygen inhalation Sedatives and other medications deem necessary according to the evaluation of the attending physician.
Health Teachings on: Awareness Instructions and education, Behavior modification Avoidance.. Precaution and Prevention Good nursing care
Diseases / Conditions that affects Brain and Spinal Cord

BOTULISM (Food Poisoning)

-results from exotoxin produced by gram positive anaerobic bacillus
Clostridium Botulinum occurs as food poisoning.
Causes:
- ingesting inadequately cooked contaminated food, especially those that with low acid content, i.e. home canned fruits and vegetables, sausages, smoked or preserved fish or meat, Honey or corn syrup may contain C.Botulinum spores and should not be fed to infants.
Signs & Symptoms:

- disease presents 12 to 36 hours after ingestion of infected food. - Dry mouth, sore throat, weakness, vomiting and diarrhea.
Diagnosis:
-Identification of toxins in the patients serum, stool and gastric content. -Electromyogram - must rule out other disease often confused with botulism i.e. Guuillain Barre syndrome, Myasthenia gravis, Cerebro Vascular accident, staphylococcal food poisoning, tick paralysis, chemical intoxications, carbon monoxide poisoning, fish poisoning, trichinosis and diphtheria.
Treatment:
- IV or IM adminsitration of botulinum antitoxins. Antibiotics and aminoglycosides should be avoided because the risk of neuromuscular blockade. They should be used only for the secondary infections.
Management:
- observe careful history of the patients food intake for the past several days. Check for the presence of symptoms with the other members of the family. - Observe carefully for abnormal neurologic signs. Signs for : weakness, blurred visions, and slurred speech. - if ingestion occurred within several hours only, induced vomiting, begin gastric lavage and give enema to purge any unabsorbed toxin from the bowel. - Bring the patient to intensive care unit. - Administer botulinum antitoxin, as required to neutralize any circulating toxins. - Obtain accurate history of allergies, especially with horses, perform skin test. - Serum sample should be collected to identify the toxins before the antitoxins are administered.
1. 2. 3. 4. 5. 6. 7. 8.
After administration of antitoxins, watch for anaphylaxis or other hypersensitivity, and serum sickness. Keep Epinephrine 1:1000 (subcutaneous) and emergency airway equipment available. Closely observe and accurately record neurologic function, bilateral motor status (reflexes, ability to move legs and arm). Give IV fluids as needed. Turn patient often, encourage deep breathing exercises, assisted respiration required. Isolation required. Because botulism is fatal, keep patient and family informed of the progress of the disease. Immediately notify community/ public health authorities of all cases of botulism.
To help prevent botulism ; encourage patients to observe proper techniques in processing, preserving and storing foods. Warn them not to taste food from bulging can, or one with peculiar odor. Sterilize by boiling any utensils that comes in contact with suspect food.
TETANUS
Infectious disease characterized by generalized spasmodic contractions of skeletal muscles. It is an acute exotoxin mediated infection caused by Clostridium Tetani. Usually infection is systemic, less often localized. Tetanus is fatal in 60% of unimmunized persons, usually within 10 days of onset. If symptoms develop in 3 days after exposure, prognosis is poor.
Causitive Agent: Clostridium Tetani an anaerobic, spore forming gram

positive rod shaped (drumstick appearance) bacteria. Release potent exotoxin that affects nerves and destroys blood components.
Incubation Period: 3-36 days (an average of 10 days) depending on the area
of infection and history of vaccines/immunization of the patient.
Mode of Transmission
Wounds (deep punctured) contact of an article or contaminated soil, dust or animal excreta harboring the anaerobic bacteria, clostridium tetani. Burns Accessed through contaminated instruments/umbilical stump, circumcision or ear piercing or tattooing. In rare cases, GIT = causes local infection and tissue necrosis. Exotoxins released by Clostridium Tetani on the site of the wound normally travels through neural path and through blood stream. Along the way it will destroy red and white blood cells (tetanolysin) causing a deadly effect on the patient. The toxin will affect nerves as well causing localized spasm and pain. When it reaches the CNS it will affect both Spinal Cord and the Brain creating now combination of dangerous symptoms arising from the effect of toxins.
Signs and Symptoms / Clinical Manifestations

1. Lockjaw when there is spasm of the mastoid muscles that causes difficulty and pain in opening and closing of the mouth that it tends to lock in a certain movement. Trismus painful spasm of the mastoid muscles that is caused by the affected trigeminal nerve. Muscle hypertonicity. Risus Sardonicus facial nerve is affected. (patient appears to have a permanent smile). Opisthotonous hyperextension and arching of the back, due to the spasm and rigidity of the back muscles. Hyperactive deep tendon reflex. Specific signs onset is insidious.
- muscular spasm and cramp like pain - irritability and restlessness with progressively increasing stiffness of the voluntary muscles within 24-48 hours. Rigidity and convulsions. - headache, profuse sweating, dysphagia. - anxiety and apprehension (sensorium). - urinary incontinence - difficulty of breathing.
2. 3. 4. 5.
TETANUS
Complications
1. 2. 3. 4. 5. 6. 7. Hypostatic pneumonia respiratory (secretion) obstruction due to patients poor position. Atelectasis collapse of the lungs, due to pneumonia. Pulmonary emboli Acute gastric ulcers Intramuscular hematomas Laceration of tongue or buccal cavity. Fractures of the spine or some other bones that is subjected to violent muscular spasm direct trauma due to spasm and convulsion. /Flexion Contractures. Cardiac Arrythmias Septicemia uncontrolled bacteremia (microorganisms in the blood and in the circulation) that causes septic shock.
8. 9.
Despite pronounced neuromuscular symptoms, cerebral and sensory functions remain normal.
Diagnosis
is based on clinical manifestation and clinical features and a history of trauma and no previous tetanus immunization. Tetanus antibody tests are often negative; only 1/3rd of patients have positive wound culture. CSF normal; CSF pressure may rise above normal. Blood exam normal to slightly elevated WBC Diagnosis should rule out meningitis, rabies, phenothiazine or strychnine toxicity and other conditions that mimic tetanus.
Treatment
1. Tetanus Immune Globulin (TIG) 3,000-6,000 units, IM or Tetanus antitoxin (TAT) or tetanus horse serum antitoxin to confer a temporary protection 50,000-100,000 units IV and the rest can be given through IM (newborn=1,500-5,000 units only). *skin testing is imperative! *a patient who has not received any tetanus immunization within 5 years should be given a booster injection of tetanus toxoid.
If tetanus develops despite immediate post injury treatment, patient will need airway maintenance and muscle relaxant to decrease muscle rigidity and spasm; if muscle relaxant is ineffective then patient should be given neuromuscular blocker. 2. Patient needs a high dose of antibiotics: Penicillin G 200,000 units/kg/24 hours in 6 divided doses for ten days. In neonates, PenG 100,000 units/kg/day in 3 doses, IV for 10-14 days Tetracyclines NOT recommended. But if patient is sensitive to penicillin, give tetracyclines with caution and not more than 2 grams (40 mg/kg/day in 4 divided doses for 10-14 days.
3.
4.
Other drugs: for control of spasm:

a) b) c) d) e) Diazepam 0.2 mg/kg/dose every 3-4 hours IV (higher dose can be used but not more than 8 mg/kg/day (infants) and 10 mg/kg/day for adults. Chlorpromazine (thorazine) 2mg/kg/day in divided doses. Chloral hydrate (valium, axionil, trazepam) Paraldehyde and Avertin maybe used Phenobarbital = 0.1-2.0 gr every 6 hours, useful for newborn Mephenesin muscle relaxant 1-3 ml of 2% solution IV or 175 mg/kg PO. 3-5 doses in mild cases.
Nursing Management 1. Prevention of respiratory and cardiovascular complications. 2. Wound care. 3. Supportive treatment and intervention. 4. Adequate nutrition and proper diet. 5. Health education.
RABIES
Acute viral disease of warm blooded animal, causing a central nervous system infection caused by a ribonucleic acid virus, Rhabdoviridae (filterable virus with strong affinity to CNS cells, it can be destroyed with high temperature heat as well as UV light. Characterized by extreme excitation and delirium, uncontrolled manic behavior, with violent and painful spasms of the muscles and tissues.
Mode of Transmission: virus transmitted to humans through a bite of an infected animal that is introduced through skin or mucous membrane. / present in the saliva of a rabid animals for several days before onset of clinical signs of illness Rabies is always almost fatal. 2 Forms of Rabies: vary in nature of presentation. 1. Furious form common in humans with classic symptoms of paresthesia at the site of the bite , hypersalivation and hydrophobia including spasms and contractions of neck muscles 2. Dumb rabies - paralytic form Both progress to paralysis of pharyngeal and respiratory muscles,seizures and coma with death in 1-3 weeks.
RABIES
3 days for dog, 1 day for cat, and 10 days for insectivorous bats
Rhabdo
l
Remains in site (innoculates)

l
Replication occurs in muscles (striated cells)

l
Spreads up through the nerves to CNS and replicates in the brain (deposited negri bodies)
l
Causes neuronal necrosis affecting the spinal cord including the (sympathetic ganglia and dorsal root) and mononuclear infiltration causing demyelination and degeneration of the axis cylinder
l
Causing the damage and cranial nerve nuclei destruction

l
Moves through the nerves into the tissues including the salivary glands (unless inactivated by natural or induced immune mechanism)
l
Enters periheral nervous system.
Physical Symptoms; Localized extent of the wound, tissue distruction. Evidence of secondary complications such as bacterial super infection. Neurologic examination presents altered mental status, anxiety, hyperactivity and bizarre behaviour with interspersed calm periods. Autonomic instability HPN, hypersalivation, hyperthermia, hyperventilation
Signs and Symptoms: Progressive stage of Invasive phase : > local, radiating, burning pain > sensation of cold, pruritus and tingling in the bite site > prodromal signs- slight elevation in temperature 37.5-39.5C, headache, anorexia, nausea and sore throat. > marked nervousness, agitation, restlessness. > photophobia, sensitivity to noise, papillary dilation, excessive salivation and perspiration
2 10 days after prodromal symptoms, Stage of Excitation : characterized by marked excitation, restlessness & hypersensitivity > cranial nerve dysfunction occular palsies, strabismus, constriction, absence of corneal reflexes. > hypersensitivities to light, noise, touch and hearing > fear of water, light and air. > painful spasm, involuntary twitching and uncontrolled salivation > becomes violent and delirious > tachycardia or bradycardia and a cyclic respiration with urinary retention. Temperature is elevated to 39.C and up to 3days, during which client suffers from tonic and clonic contraction of muscles. > hydrophobia / difficulty of swallowing > cyanosis, then client condition deteriorates rapidly and enters the terminal stage
Terminal stage or Paralytic phase : > client becomes quiet and unconscious > loss of bowel and urine control. > labored and irregular respiration. > steady rise in temperature > spasm ceases, progressive increase in paralytic condition > respiratory distress due to paralysis of respiratory muscles.
Treatment: Wound treatment > Thoroughly wash the bite wounds and scratches with soap and water. Quantenary ammonium compound may be used to cleansed the wound, but all forms of soap should be thoroughly washed out before applying. > Apply 1% solution of Benzalconium chloride (Zephiran) or Povidone Iodine. Suturing of wound if necessary Fundamentals of Nursing
Take measures to control infection and prevention of complications. Administer Tetanus-Diphtheria prophylaxis and antibacterial medications. Immunization (after exposure) with : > Passive : Human Rabies immune globulin (HRIg)- given to person not previously vaccinated against rabies in a dose of 20 iu/kg body wt.- apply as much as possible at the injury site and the remainder given deep IM / gluteal. (HRIg is produced from individuals who have been vaccinated and Equine Rabies Immunoglobulins (ERIg) is produced from immunized horses) > Active : 3 different Inactivated Rabies Vaccines 1. Human diploid cell vaccine (HDCV, Imovax)- intradermal preparation only as a pre exposure prophylaxis. Regular dose given IM only.
2. Rabies Vaccine Absorbed (RVA) IM only 3. Purified Chick Embryo Cell Vaccine (PCECV, Rabavert) IM only. Dose of all vaccines for post exposure prophylaxis = 1 ml IM, deltoid or upper thigh for Infants. 5 doses schedule is the same for all 3 vaccines product as follows: Day 0, day 3, day 7, day 14, & day 28 post exposure. Post exposure prophylaxis for patient NOT previously vaccinated: Local wound cleansing with soap and water. HRIg (HumanRabies Immunoglobulin) 20 iu/kg with full dose injected to the site and remainder administered /IM Vaccine administered: HDCV, RVA 1 ml @deltoid. Days 0, 3, 7, 14 & 28.
Complications :
Myocarditis Neurological : - increase ICP, cerebral edema, hypothalamic involvement ( inappropriate secretions of ADH.) Autonomic dysfunction: - HPN, Hypotension, hypothermia, and seizures, cardiac arrythmia (atrial premature contraction, sinus bradycardia) causing cardiac arrest. Arterial and Veinal thrombosis Secondary bacterial infection of lungs and Urinary tract and GIT > pneumothorax > paralytic ileus > urinary bladder paralysis Diagnosis: Flourescent rabies antibody (FRA) most definitive diagnosis. WBC count increase polymorphonuclear cells and large mononuclear cells.
Sellers May-Grunwald and Mann strains- used for microscopic exam of the characteristics of Negri bodies in the brain tissue samples and saliva of the infected animal.
Special Consideration / Nursing management Provide comfort to the patient Isolation of the patient : dark, quiet, cool environment Prevention of complication. Studying and eradicating cause. Control spread of rabies infection. Monitor Cardiac and Pulmonary functions. Proper diet and nutrition, with maintenance of balanced fluid and electrolyte. Community care includes animal management as well as community education and protection.
New Diseases /Conditions with Global Threat
SEVERE ACUTE RESPIRATORY SYNDROME (Sars-CoV)

-
Was first recognized during a global outbreak of severe and highly contagious infectious atypical pneumonia in 2003. Zoonotic in origin (emerged from animal reservoir and adapted to efficient human-to-human transmission.) Is characterized by diffuse alveolar damage (DAD), hemophagocytosis, occasional lesions.
Can be detected extra-pulmonary sites.
Causative/ Etiologic agent: SARS-corona virus. Viral peak load : 7-10 days (incubation period) w/c accounts for high risk of nosocomial outbreaks.
Confronting this outbreak required understanding the etiology, modes of transmission and pathogenesis, specific diagnostic tests and effective infection control! Mode of Transmission: Airborne, Droplet (Respiratory) Signs and Symptoms: High fever Flu-like illness Shortness of breathe, with or without non-productive cough, (which progressed to acute respiratory failure in absence of medical attention.) Specific Signs of extra-pulmonary organs affected: hematological system, gastrointestinal and liver. Severe cytokine dysregulation has been demonstrated.
Treatment:
There is no optimal treatment for SARS,, different forms of experimental pharmacotherapies are in place and most of them are seen to have improved outcomes of the disease. Antiviral, Immunotherapy, and others. Lopinvair, Ritonavir plus ribavirin Interferon alphacon-1 Other Protease inhibitors, interferons, pentaglobin, hyperimmune globulin Monoclonal antibodies and RNA interference Management and Care: Early detection and identification of the disease. Quarantine suspected patient and all those who were in close contact. Manage client as pneumonia case and other care necessary. Ventilatory care for patient in acute stage. Prevention of complication. Health teaching to patient, family and community. Fundamentals of Nursing
Meticulous attention has to be made to infection control measures to reduce nosocomial spread of SARS among hospital patients and healthcare workers.
AVIAN INFLUENZA A (Bird Flu)

Caused by H5N1 Influenza virus, that exists primarily in birds. (H5N1 virus is a potent inducers/stimulant for cytokine responses) Originated in Asia-Pacific region and is carried throughout the world by infected migratory birds.
Mode of Transmission: Airborne (through pulverized particles) virus present in particles blown by wind. Droppings and respiratory secretions of infected bird, that have dried up, pulverized then is carried by the wind and is inhaled by host (humans and other birds). Fundamentals of Nursing
Signs and Symptoms:

Body malaise / general weakness Headache, Dizziness Fever, cough and dyspnea Myalgia Abdominal pain/and vagueness / Diarrhea Respiratory distressed syndrome high fatality rate. Autonomic dysfunction: vital signs becomes erratic Some symptoms related to involvement of CNS. Organ failure or dysfunction Management: No known specific cure but patient is treated as symptom is presented** Symptomatic and Supportive care Preventive care: effective Infection control Strict Isolation
Treatment:
1. Antiviral medications: Oseltamivir for three days (dosage depend on Physicians assessment.) Empiric broad spectrum antibiotic for community acquired pneumonia. Pennicillin, Ceftriaxone, or Doxycycline Systemic steroids for complicated condition of ARDS. Prednisone
2. 3.
Laboratory finds: CBC mild to moderate leukopenia, lympophenia and thrombocytopenia. Respiratory specimens of patients (+)for H5 virus. Serum test - High level of chemokines (confirms cytokine dysregulation)
Sexually Transmitted Disease

CHLAMYDIAL INFECTION
Most common sexually transmitted disease. Causative agent: Chlamydia Trachomatis Mode of Transmission: Vaginal / Rectal intercourse oral, genital contact with infected persons. Signs and Symptoms: Appears very late in the course of the disease and vary with the specific type of Chlamydial infection and determined by the organisms route of transmission to susceptible tissue. both Male and Female are asymptomatic if symptoms appear..:
Female: Cervicitis cervical erosions, pelvic pain, dyspareunia, mucopurulent discharge, Endometritis or Salphingitis experienced signs of PID, pain and tenderness of the abdomen, cervix, uterus & lymphnodes: chills, fever, bleeding after intercourse, vaginal discharge. Urethral syndrome dysuria, pyuria, urinary frequency. Male: Urethritis dysuria, erythema, tenderness of urethral meatus, urinary frequency, pruritus. Epididymitis scrotal swelling and urethral discharge. Prostatitis lower back pain, urinary frequency, dysuria, nocturia, painful ejaculation. Proctitis diarrhea, tenesmus, pruritus, bloody or mucopurulent discharge and diffuse or discrete ulceration of the rectosigmoid colon.
If left untreated, this leads to: Complications: 1. Acute Epididymitis 2. Salphingitis 3. PID 4. Sterility
Diagnosis: Swabbing the site of infection (urethra, cervix or rectum) establishes urethritis, cervicitis, salphingitis, endometritis, or proctitis. Culture of aspirated materials establishes epididymitis. Nucleic acid probe using polymerase chain reactions are diagnostic method of choice. Antigen detection method :Enzyme link immunosorbent assay(ELISA) Direct fluorescent antibody test. Tissue cell cultures more specific and sensitive.
Treatment: Drug therapy Oral Doxycycline 200mg for 7 days Azithromycin (Zithromax) single dose - treatment of choice. Special Consideration: 1. Practice universal precaution. 2. Patient should fully understand the importance of medication and dosage requirement. 3. Record and report 4. Patient and partner should be treated for the disease and submit for HIV testing. 5. Community care and health education.
HERPES SIMPLEX / GENITALIS

This is a widespread, recurrent viral infection. Affect skin and mucous membranes and commonly produces cold sores and fever blisters. Causes and MOT: 1. Herpes Type 1 HVH (herpes virus hominis) typically affects oral mucous membranes, and is transmitted by oral, respiratory secretions. 2. Herpes Type 2 HSV (herpes simplex virus) primary affects the genital area and is transmitted by sexual contact. Cross infection may result from orogenital sex. Saliva, stool, Urine, Skin lesions, Purulent eye exudates are potential sources of infection.
IP: 2 12 days / Signs and Symptoms : aslo effect the eye; herpetic keratoconjunctivitis, blepharitis, edema and excessive lacrimation 85% are subclinical localized lesions and systematic reaction Generalized infection; 4 10 days, virus reactivation causes cold sores. 1. Onset of infection begins with: fever, pharyngitis, erythema, and edema 2. Brief prodromal itching and tingling. Primary lesion erupt as vesicles on an erythematous base, ruptures and becomes painful ulcers with yellowish crust, healing begins 7 10 days after onset. Completed in 3 weeks 3. Clinical features: Herpetic Stomatitis vesicles in oral mucosa; tongue, gingival, cheeks With: submaxillary lymphadenopathy, increase salivation , halitosis, anorexia and high temperature of 40.6 C.
Herpetic Keratoconjunctivitis and other local eye symptoms; blepharitis, vesicles on eyelids, excessive lacrimation, chemosis, photophobia, edema. Herpetic Whitlow an HVH finger infections: finger tingles then it becomes swollen, red and painful. Vesicles with red halo, erupts and ulcerates.
Localized infection; usually affects adolescents and young adults. 4. Typically very painful 5. Both types can cause acute sporadic encephalitis = causes altered level of consciousness, personality changes and seizures. 6. Smell and taste hallucination 7. Neurologic abnormalities- aphasia 8. Other effect; satellite vesicles, fever, chills, malaise, and red streak up the arm.
DX: Isolation of virus in specialized culture tubes to identify and confirm the type of virus
Treatment and Management: 1. Supportive therapy; analgesic antipyretics. 2. Anesthetic mouthwash viscous lidocaine ( may reduce pain of gingivo stomatitis). 3. Topical lidocaine for vulvovaginal pain. 4. Eyedrops such as trifluridine, vidarabine, idoxoridine are given for eye infections. (topical steroid contraindicated in active infection). 5. Acyclovir oral, ointment and intravenous. To reduce duration of episodes. 6. Warm compress, hot sitz bath several times a day for relief 7. Increased fluid intake. 8. Avoid unprotected intercourse during active stage of disease, or avoidance of sexual intercourse. 9. No sharing of towel or utensils with others. 10. Standard precaution.
Herpes Genitalis (Genital Herpes) is an acute inflammatory disease of the genitalia. - self limiting but may cause painful local/ systematic disease. - is usually caused by infection with herpes simplex virus type2 and type1 MOT: - through sexual intercourse, orogenital sexual activity, kissing, and hand to body contact. Incubation Period: - 3 7 days Sign and Symptoms: 1. Fluid filled vesicles, usually cervix (primary site of infection). Labia, perianal skin, vulva or vagina in female. 2. In male, at the glans penis, foreskin, penils shaft 3. Extra genital lesions mouth, anus 4. Painless, initially; when the lesions rupture, it develops into extensive, shallow, painful ulcers, with redness, marked edema, tender inguinal lymphnodes 5. Fever, malaise, dysuria and leukorrhea Fundamentals of Nursing
Complications: 1. Herpetic Keratitis- may lead to blindness. 2. Herpetic encephalitis fatal Diagnosis/ Diagnostic test : 1. PE and Pts history 2. Laboratory data's; increased antibody titers 3. Smears of genital lesions show atypical cells and cytologic preparations (Tzanck test) reveals giant cells 4. Tissue culture or antigen test that identify specific antigens Treatment and Management: Medical management: Acyclovir oral to first time infection or recurrent outbreaks. IV administration to those with severe infection and those who are immunocompromised and have potential life threatening infection. 2. Record and Report. 3. Hygiene, health and cleanliness. 4. Practice standard precaution 5. Papanicolaou test is recommended to females
GONORRHEA
- This is a common sexually transmitted disease. It is infection of genitourinary tract (especially urethra and cervix) and occasionally rectum, pharynx and eyes. - When untreated spreads through the blood and joints, meninges or the endocardium.
Causative Agent: Neisseria Gonorrheae MOT and POE: Sexual intercourse/ activity, through genital/ oral or rectal. Incubation period: 3 6 days after contact.
In Female: leads to PID and sterility.( Usually Asymptomatic) But may develop inflammation in the cervix with greenish yellow mucupurulent discharge to some. In Male: lead to Epididymitis and Sterility. 1. Urethritis, dysuria, purulent urethral discharge, redness and swelling at the site of infection. Clinical features: vary according to site involved. 1. Urethra: dysuria, urinary frequency/incontinence, purulent discharge, itching, redness and edematous meatus. 2. Vulva: occasional itching, burning and pain due to exudates from adjacent infected area. (severe before puberty and after menopause.) 3. Vagina: most common site in children over 1 = engorgement, redness and swelling and profuse purulent discharges.
4.
Pelvis: severe pain of pelvis and lower abdominal, muscle rigidity, tenderness and abdominal distention. As infection spreads, patient presents; nausea and vomiting, fever, tachycardia for patients with salpingitis or PID. 5. Liver: right upper quadrant pain in patients with perihepatitis. Other symptoms: tonsillitis, pharyngitis, rectal burning and itching, bloody, mucopurulent discharges. Gonococcal septicemia: more common in females than in male: tender papillary skin, with lesions (maybe purulent, hemorrhagic or necrotic) on hands and feet. Gonococcal opthalmia neonatorium = lid edema, bilaterla conjunctival infection, with abundant mucupurulent discharge 2- 3 days after birth.
Diagnosis: Tissue culture on site of infection; using Thayer Martin or Transgrow medium establishes the diagnosis by isolating the microorganism. DNA probe analysis (can also detect chlamydia) Complement fixation Immunoflourescent assay Treatment and Management: For uncomplicated gonorrhea caused by non penicillinase N.G. is: Single dose 125mg of Ceftriaxone IM. Or Single dose Cefixime 400mg PO. Or Single dose Ciprofloxacin 500mg PO. or Single dose Ofloxacin 400mg.
For presumptive treatment with concurrent chlamydia trachomatis infection: Doxycycline 100mg. PO 2x daily x 7days. Or Single dose Azithromycin(Zithromax) 1g. PO.
For pregnant patients and those allergic to penicilline: Single dose of Ceftriaxone and Erythromycin x 7 days.
For recommended initial regimen for disseminated gonococcal infection, adults and adolescents: Ceftriaxone 1g IM or IV q24hrs./ for patients allergice to beta-lactam antiboitics: Spectinomycin2g IM q12hrs. (All regimens should be continued 24- 48hrs after improvement begins, then may switch to one of the ff. to complete 1 whole week of antimicrobial therapy.) Cefixime 400mg PO 2xdaily or Azithromycin 1g single dose
Special considerations: 1. Practice standard precaution 2. Urge patient to inform sexual partner/s of the infection and encourage to seek medical treatment. 3. Before treatment, establish drug sensitivity. 4. Record and report. 5. Routinely instill 2 gtts. 1% silver nitrate or erythromycin ointment or tetracycline ointment in the eyes of the neonates immediately after birth. ** Safe sex should be advised to clients, use of condom to decrease incidence of transmission and to avoid sharing washcloth or douche equipment.
GENITAL WARTS
Also called venereal warts and condylomata acuminata. Consists of papillomas with fibrous tissue overgrowth from the dermis and thickened epithelial lining. Causes: infection with one of the more than 60 strains of HPV (human papilloma virus) uncommon before puberty or before menopause. MOT sexual contact wart grows rapidly in heavy perspiration, poor hygiene and pregnancy, or accompany other genital infections. IP 1 6 months (usually 2 months)
Signs and Symptoms: 1. Develops in moist area: in men, on supra preputial sac, within urethral meatus, penile shaft. In women, on the vulva, vagina or cervical wall. 2. Genitalwarts may develop years after the first contact. 3. Papilloma spreads to perineum, and peri anal area. 4. Painless wart, which started as a tiny pink or red swelling (about 10 cm). For multiple swellings give them a cauliflower- like appearance. 5. If infected, becomes malodorous. 6. Few complains of itch or pain
Diagnosis/ Diagnostic tests: 1. Dark field examination scrapings from wart cells- vascularization of epidermal cells which differentiates wart from condylomata lata of syphillis.
2. 3.
Histologic exams of biopsies of wart- for classification and assess cancer risk. Applying 5% acetic acid (white vinegar) turns the wart to white.
Treatment & Management:- to remove exophatic wart and to ameliorate S&S 1. Topical drug therapy; trichloroacetic acid 85% applied to the external areas. 2. Podophyllum resin maybe applied topically, weekly (contraindicated for pregnancy) 3. Carbon dioxide laser treatment for warts larger than 2.5cm. 4. Cryosurgery or electrocautery 5. Interferon (intralesional) 6. Podofilox (patient applied)
7. 8. 9. 10. 11.
Imiquimod (patient applied) Combined laser and interferon therapy. Use standard precaution Recommend abstinence of sexual intercourse till healing Encourage sexual partner to be checked for HPV and HIV and other STDs
Relapse is common, recommend annual paps smear test, and male be examined by urologist, because cancer of the penis may develop.
TRICHOMONIASIS / TRICHOMONAS
VAGINALIS
Protozoa infection of genitourinary tract (A & C) *Risk minimized when sexual partners are treated. Female: infects vagina, urethra & endocervix, bladder, bartholins or skins Male: lower urethra, prostrate gland, seminal.
Trichomonas Vaginale: grows best when vaginal mucosa is alkaline, than normal (normal 5.5- 5.8) Cause: oral contraceptives, pregnancy, bacterial overgrowth, exudative cervical or vaginal lesions, frequent douches w/c disturbs lactobacilli.
Signs & Symptoms: Male: asymptomatic/ mild to moderate urethritis dysuria. Female: gray to greenish yellow & possibly profuse & frothy malodorous vaginal severe itch. (redness, swelling, tenderness), dysparunia, dysuria, urinary frequency. Occasional post coital spotting, mennorhagia, dysmenorrhea. Diagnosis: Direct micrscopic examination of vaginal or seminal fluid. Physical examination
Treatment and Management: - Single dose of oral Metronidazole given to both partners. - Alternative treatment is 500mg of oral metronidazole 2x daily for 7 days, - not safe during pregnancy. - Hot sitz bath to relieve symptoms. Instruct client to refrain from douching before being examined for trichomoniasis. Abstain from sexual intercourse until client is cured and both partners are treated Warn client to abstain from alcohol while being treated with metronidazole. PREVENTION TIP: Tell client she can reduce genitourinary bacterial growth by wearing loose fitting, cotton underwear which allows ventilation. Bacteria flourishes in warm, dark, moist environment.
SYPHILIS
Chronic, infectious, sexually transmitted disease. Begins in the mucous membrane, quickly becomes systematic, spreading to nearby lymphnodes and the bloodstream. This disease is characterized by progressive stages Serologic test developed by August Von Wasserrmann in 1906 Paul Ehrlich discovered the drug salvarsan (606)
Causitive agent: Treponema Pallidum MOT: primarily through sexual contact. Prenatal transmission from an infected mother to her fetus.
Incubation period: 3- 6 weeks before there are evidences of the disease (90 days maximum) ** Treponema Pallidum loses viability upon exposure to air and sunlight, 48 720 congenital or acquired, 94% genital, 6% extra genital. Stages of disease progression with specific Signs and Symptoms: 1. Primary- appearance of a pimple like on infected spot, a small fluidfilled lesions called Chancre usually painless and start as papules and then erode, they have indurated, raised edges and clear bases, no itch found on the genitalia, anus, prepuse, glans, fingers, lips, tongue, nipples, tonsils, eyelids. In women, often it is overlooked since it appears in the cervix or vagina, labia minora. Disappears after 3-6 weeks even when untreated. Associated with lymphadenopathy. 2. Secondary development of symetrical mucocutaneous lesions and general lymphadenopathy. Develops within the few days or up to 8weeks after onset of initial chancre.
Rash can be maculopapular, pustular or nodular lesions are uniform in size, well defined edges, surface covered with necrotic membrane. Lesions enlarged and eroded producing highly contagious pink, or grayish-white lesions called Condylomata lata often erupt between rolls of fat on the trunk, arms, palms, soles, face, scalp, and in warm moist areas (perineum, scrotum, vulva). May disappear spontaneously. Symptoms: headache, malaise, anorexia, weight loss, nausea & vomiting, sorethroat, slight fever, nails are brittle and pitted. Alopecia may occur. 3. Tertiary or Latent no clinical symptoms, but it produces a reactive serologic test. Infectious mucocutaneous lesions may reappear. Gumma usually mistaken as sebaceous cyst, 2/3s of patients are asymptomatic in late latent stage until death.
Late Syphilis noninfectious but final and destructive. Late benign syphilis, cardiovascular syphilis (develops in about 10years), neurosyphilis (develops in about 5-35 yrs after infection. Lesions of benign syphilis develops in 1-10 yrs after infection, may appear in skin, bones, mucous membranes, upper respiratory tract, liver or stomach. This typical lesion is same with latent stage, this can be found in the bones, particularly in long bones of the leg, or in the organ. Gumma, a chronic superficial nodule, deep granulomatous lesion that is solitary, asymmetric, painless and indurated.
Treatment and Management: Administration of Penicillin IM drug of choice for early syphilis. Single injection of Penicillin G benzathine IM (2.4 million units). Syphilis of more than 1year duration should be treated with the same but given per week for three weeks.
Communicable Disease Nursing
Antibiotics with Arsenicals (2 injections/wk x 10wks)IM with Bismuth (1 injection/wk x 10 wks) Oral Tetracyclines or Doxycycline for 15 days for those that are allergic to Penicillin. Note: tetracycline is contraindicated in pregnant women. Stress importance of completing the course of therapy even after symptoms subsides. Control of the disease. Check history of drug sensitivity. Practice universal precaution. Keep lesions dry and clean. Dispose contaminated materials properly. Promote comfort and healing. Check for signs of complications arising from and indicative of the subtypes of syphilis; decreased CO, hypoxia, decreased sensorium, pulmonary congestion. Check for leel of consciousness, mood, coherence, ataxia. Urge patient to seek VDRL testing. 3,6,12,24 months to detect possible relapse. Blood test at 6 months interval x 2yrs.
Report all cases of syphilis to local health authorities. Refer patient and partner for treatment and for HIV testing. Health teachings for client, family and community. Laboratory / Diagnosis: 1. Darkfield exam. special condenser identifies T.Pallidum from a moist lesion in primary, secondary and prenatal syphilis. 2. Serologic reaction: Wassermann test (10days 3weeks) Kahn precipitation reacton Nelson test treponema fixation test which rules out false (+) reaction. VDRL slide test and rapid plasma reantgen (RPR)- detects nonspecific antibodies (4-5 wks after infection) TPI & FTAA (identifies antigen in tissues, CSF, secretions) 3. CSF exams identify neurosyphilis when total protein level is above 40mg/100ml, and when VDRL slide test is reactive and CSF cell count exceeds 5 mononuclear cells/ul

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Infection process: Immunodeficiency (opportunistic infections, unusual cancer).

These agents are designed to inhibit HIV replication.

Causative agents / Transmissions:

Signs and Symptoms;

Treatment and Management:

Supportive and Preventive:

Signs and Symptoms:

Signs and Symptoms

Treatment and Management

INFLUENZA (La Grippe)

Signs and Symptoms:

Three distinct types:

Most Common Complication : Pneumonia

Special Consideration on Management:

Widely Used Classifications of Major Pneumonias

PULMONARY TUBERCULOSIS (Kochs Disease 1882)

gradually merge to form a bigger lesion

filled with infected material that has a cheese-like consistency

This material can become liquid,

then is coughed out leaving a cavity in the lung.

Generates more infectious material and inflammation.

healing may occur in parts of the lung l resulting in scar tissue.

Signs and Symptoms:

FUNGAL INFECTION: CANDIDIASIS

Treatment and Management:

Signs and Symptoms

KERNIGS & BRUDZINSKI SIGN

Treatment and Special Considerations:

Signs and Symptoms/ Clinical Manifestations:

Treatment and Management

GUILLIAN BARRE SYNDROME

By infectious microorganism that mimics peripheral nerve Myelin protein

Destroys peripheral nerve myelin

Inflammation and Destruction Axon unable to support nerve conduction.

Posterior(sensory) and Anterior(motor) nerve roots

Treatment and Management

Treatment must not wait for confirmation by culture.

Antibiotics: Penicillin, Erythrocin 9. Preventions;

Other signs and symptoms :

Treatment and Management :

MUMPS (Acute Parotitis)

MEASLES (Rubeola/ Morbelli)

GERMAN MEASLES (Rubella)

CHICKEN POX (Varicella)

Apply calamine lotion

ESCHIRICHIA COLI /GASTROENTERITIS

GI tract (localized in the reticulo-endothelial system)

Enlarged, ulcerated and necrosed tissue.

Treatment: Specific: Ampicillin IV or PO 100mg/kg body wt/day Amoxicillin PO 4g/day

Metabolic and autoimmune disorders acute exacerbations of other liver disease.

Monitor vital signs and weight.

10. Contact community health care providers.

Vector Borne Diseases And Other Zoonotic common Infectious disease

VECTOR-BORNE DISEASES viral * bacterial * parasitic

Dengue Hemorrhagic Fever

Diseases / Conditions that affects Brain and Spinal Cord

BOTULISM (Food Poisoning)

Signs & Symptoms:

Causitive Agent: Clostridium Tetani an anaerobic, spore forming gram

Signs and Symptoms / Clinical Manifestations

Other drugs: for control of spasm:

Remains in site (innoculates)