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03 January 2011 Inflammatory and Immunologic (Communicable Diseases) Belinda Capistrano/Alex Bitanghol TERMINOLOGIES

illness caused by an infection agent or its toxic products transmitted directly/indirectly to a well-person through direct sexual contact indirect airborne, contaminated food INFECTION implantation and successful replication of an organism in the host as a result: signs and symptoms inflammatory response microorganisms injures the person by: competing the host cell metabolism cellular damage produced by microbes (necrosis = cell death) intracellular multiplication (hyperplasia) ex. AIDS, viruses patterns of occurrence and distribution: sporadic diseases occur occasionally and irregularly with no specific pattern (tetanus, gas gangrene) epidemic diseases occur in a greater number than what is expected in a specific area over a specific time (dengue, malaria) pandemic diseases an epidemic that affects several countries/continents (HIV/AIDS, SARS, AH1N1) endemic diseases present in a population or community at times, few people involve during a specific period CARRIER individual who harbors the microorganism and is capable of transmitting to a susceptible host types of carriers: incubatory is capable of transmitting a pathogen during the incubation period convalescent harbors and can transmit a particular pathogen while recovering from an infectious disease (convalescent period) intermittent CONTACT person or animal that is in close association with an infected person, animal, or freshly soiled material CONTAGIOUS DISEASE easily transmitted from one person to another through direct/indirect means not all infectious are contagious but all contagious are infectious DISINFECTION destruction of pathogenic microorganisms outside the body through direct physical/chemical means

types: concurrent disinfection immediately after the infected individual discharges infectious material/secretion it is done while the px is still the source of infection terminal disinfection px is no longer the source of infection (either died/discharged) everything used materials, room are disinfected INFLAMMATORY RESPONSE reaction of the body to microbial invasion 5 cardinal signs of infection: pain (dolor) heat (calor) redness (rubor) swelling (tumor) disordered function HABITAT place where organism lives/usually found HOST person, animal or plan on which a parasite depends for its survival INFECTIOUS DISEASE transmitted not only through ordinary contact but also requires direct inoculation of the organism through skin/mucus membrane QUARANTINE limitation of the freedom of movement of persons or animals exposed to a communicable disease for a period of time equivalent to the longest incubation period of that disease RESERVOIR animal/plant in which an infectious agent lines and reproduces in such a manner that it can be transmitted to man PATHOGENECITY microbes ability to cause pathogenic change or disease (rabies, virus) VIRULENCE degree of a microbes pathogenecity (mycobacterium avium intracellulare) TOXICOGENECITY r/t virulence, refers to a microbes potential to damage host tissues by producing and releasing toxins (diphtheria and tetanus) SPECIFICITY attraction to a microbe to a specific host/range of hosts (rubeola measles for humans) VIABILITY ability of a microbe to survive outside the body viability = survival = infection ANTIGENECITY degree to which a microbe can induce a specific immune response varies among microbes ISOLATION separation from other person of an individual suffering from a communicable disease

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7 categories recommended in isolation: strict prevent highly contagious/virulent infections (handwashing, proper waste disposal, masks, gowns, gloves, etc) contact prevent infection that spreads primarily by close/direct contact respiratory prevent transmission of infectious disease over short distances through air TB isolation for px with active TB enteric spread through direct contact with feces drainage/secretion precaution direct/indirect contact with purulent materials or drainage from an infected body universal handling bloody/bodily fluids (HIV, HBC, blood-borne pathogens, semen, vaginal secretions, etc) CHAIN OF INFECTIONS Epidemiologic triad

Causative agent


agent microbe capable of producing disease Bacteria simple, one-celled microbe with double cell membrane that protects them from harm shape (cocci, bacillus, spirillae) need for oxygen (aerobic, anaerobic) response to staining (gram positive, negative or acid fast) motility (motile/non-motile) tendency to capsulate (encapsulated, capsulated) capacity to form spores (spore forming, non-spore forming)

Spirochete flexible, slender, endulating, spiral rods that process cell walls triponema leptospira borilia Virus smallest known microbe cannot replicate independently of hosts cell; rather, invade and stimulate the cell to participate in the formation Rickettsia small, gram negative microbes that can induce life threatening infection transmitted through the anthropod carnivores (lice, ticks, etc) Chlamydiae smaller than rickettsia but larger than viruses produce common infection of the urethra , bladder, fallopian tubes, prostate gland through sexual contact Fungi almost everywhere on earth thrive either inside/outside the body and may be harmful/beneficial beneficial in terms of manufacturing of certain products and drugs Protozoa much larger than bacteria simplest single-celled organism of the animal kingdom absorb nutrients from the body of the host Parasites live on inside other organisms (host) at the expense of those organisms doesnt kill the host but only take the nutrition they need Reservoir of infection human frank cases/very ill sub-clinical/ambulatory carrriers incubating carrier convalescent carrier intermittent occasionally sheds chronic/sustained has the infectious organism in his/her system animals non-living things Portal of exit respiratory system GIT GUT skin and mucus membranes placenta (in transplacental transmission) Mode of transmission contact most common; usually 24 hrs

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direct person-person indirect susceptible to contamination droplet contact with respiratory secretions through coughs, sneeze, talks airborne fine microbial particles or dust particles remain suspended in the air for a prolonged period infectious disease spread by air current and can be inhaled by susceptible host vehicle through articles/substances that harbor the organism until it is ingested by or inoculated into the host vector-borne immediate carriers, fleas, flies, and mosquitoes transfer the microbes to another Portal of entry venue through which the organism gains entrance microbes use the same venues when they exit from reservoir Susceptible host if the human defenses are good, no infection takes place weakened hosts, microbes take place INFECTION CONTROL MEASURES: universal precaution standard precaution LEVELS OF PREVENTIVE CARE: Primary true prevention clients considered physically/mentally healthy aims at health promotion includes health education generalized health promotion and specific protection against health problems ex. immunizations, exercise, healthy lifestyle, breast exam Secondary experiencing health problem/illness who are at risk for developing complications reducing severity and enabling the client to return to a normal level of health as possible focuses on early detection of health problems ex. executive health check-up, screening procedures (cholesterol screening) Tertiary permanent disability/irreversible minimizing the effect of long-term disability focuses on restoration and rehabilitation with the goal of returning an individual to an optimum level of functioning ex. cardiac rehabilitation, physical therapy TYPES OF IMMUNITY: Natural passive placental transfer

active recovery from a certain disease

(measles, mumps, chickenpox, german measles) Artificial passive administration of anti-toxin antiserum, convalescent serum/gammaglobulins active administration of vaccine and toxoid (BCG, DPT, Polio, Hepa-B) Sub-clinical constant exposure to a particular disease or organism TYPES OF ANTIGEN: Inactivated (killed organism) not long lasting multiple doses needed booster doses needed ex. pertussis, typhoid, pneumonia Attenuated (live organism) single dose long lasting immunity ex. polio, measles

HISTORY: obtain details about chief complaint investigate the px history for factors that may contribute to infection to influence the outcome of treatment observe the px for clues to his/her health status and nutritional status level of consciousness history focuses on the following potential exposure risk factor (pollution, dust) medical history (chemotherapy, immunocompromised) previous infection immunization complaints GENERAL ASSESSMENT: behavior and appearance listen to px nonspecific complaints monitor temp and VS o monitor temp, PR, RR and BP q4 to detect fever and systemic responses to fever monitor for flushing and diaphoresis associated with fever (compensatory mechanism) exam of lymph nodes inspect and palpate lymph nodes in the region where localized infection is suspected examine all lymph nodes for systemic infection = pulmonary edema (complication with obstructive lymphatic system) REVIEW OF SYSTEMS: skin (eythema, jaundice, etc) eyes (edema, excessive lacrimations) ears (tenderness, swelling, nodules) nose and sinuses (discharge, swelling) mouth and throat (lesions, edema) thorax (RR, expansions, breath sounds, etc) heart (heart sounds, murmurs) endpoint of all CD, the heart is the one that can be destroyed

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abdomen (bowel sounds, organ enlargement cholera, amoebiasis) peripheral vascular (absent/diminished, homans sign) musculoskeletal (swelling, erythema) CNS ( LOC, emotional response) GU (costovertebral angle for tenderness, lab analysis) rectal (inflammation, lesions, signs of parasites) DIAGNOSTIC PROCEDURES: Urine, Secretion, Sputum, Fecal Specimen direction in getting specimen privacy to avoid embarrassment obtain during acute stage of infection and before antibiotic therapy, if possible specimen must be representative of the infection adequate amount of specimen proper collection instruments and containers label container for proper identification avoid environment organism to enter to the obtained specimen open container when necessary discard while obtaining specimen wash hands wear gloves wrap securely protect form needle stick injury (prick) clean up spilled specimen make sure that the environment will not be contaminated Sputum to obtain sputum put hands at the back breathe in and out 3 times release sputum on sterile container specimen should be from LRT expectoration most common secretion from LRT with infection contains mostly WBC Urine normally sterile catheterization direct method clean catch and midstream best method results: < 10,000ml = no infection 10,000 100,000 = require second specimen 100,000 = UTI Fecal culture organism not part of the normal bowel flora WBC contains 95% anaerobes EENT must be collected with a sterile polyester swab (not a cotton swab) Blood cultures, microscope studies, serologic tests CI: coagulation disorders done before antibiotic therapy

3 blood samples over 24hr period or 3 blood

samples part/3 specimens CSF specimen infection in CNS through lumbar tap (between 3rd-4th lumbar vertebra) CI: uncooperative px, severe spinal disorders, infection nursing responsibility informed consent 3 sterile vials materials needed gloves cotton balls towel ice Wound and Decubiti specimen Geniuretheral and Rectal specimen Rectal specimen Genital specimen Microscopic exam Gram staining bacteria that do not grow in culture and some anaerobes results: gram (+) = remains purple gram (-) = loses purple; turns red or pink in color Other stains Acid-fast physical property of some bacteria referring to their resistance to decoloration by acids during staining procedures Cultures Immunologic tests Agglutination test performed with the use of antigens to specific organisms and their reaction (agglutination) with antibodies in the clients blood serum performed to identify cold agglutinins, antibodies that result from pneumonia infection Enzyme-linked immunosorbent Assay (ELISA) biochemical technique used mainly immunology to detect the presence of an antibody or a antigen in a sample Radioimmunoassay Neutralizing test Hematology test Antibody test AGAR test Tube dilution



aka Asiatic Cholera or Epidemium Cholera acute bacterial enterotoxin mediated GI infection ETIOLOGIC AGENT: Vibrio cholera/Vibrio coma

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curved rod (comma-shaped), gram negative,

and motile with polar flagellum penicillin PATHOGENIC SIGN: rice water stools hypermotility of stomach INCUBATION PERIOD: ranges from few hours to 5 days; usually 1-5 days PERIOD OF COMMUNICABILITY: during stool (+) stage, usually few days after recovery note: occasionally, carrier may have the organism for several months (hemorrhaging) MODE OF TRANSMISSION: fecal transfer water, milk, and food flies, soiled hands, and utensils also served to transmit the infection ingestion of food or water contaminated with the stools or vomitus of a px FOCUS INTERVENTION: fluids and electrolytes PATHOGENESIS AND PATHOLOGY: fluid loss is attributed to the enterotoxin elaborated by the organism as it lies in opposition with the lining cells of the intestines toxin stimulates adenyltae cyclase, which results in the conversion of ATP to cyclic adesine monophosphate (cAMP) mucosal cells are stimulated to secretion of chloride; the secretion is associated with water and bicarbonate loss toxin acts upon the intact epithelium on the vasculature of the bowel, thus resulting in the outpouring of intestinal fluids fluid loss of 5-10% of the body weight results in dehydration and metabolic acidosis if treatment is delayed or inadequate, acute renal failure and hypokalemia become secondary problems PRINCIPAL PATHOGENIC EVENTS IN CHOLERA: passage of Vibrio cholerae into small intestines multiplication of bacteria in small intestines production of enterotoxin by the bacteria secretion of isotonic fluid by the intestinal epithelium in response to the production of enterotixin cones CLINICAL MANIFESTATIONS: acute, profuse, watery diarrhea with no tenesmus (feeling of having to defecate) or intestinal cramping initially, stool is brown and contains fecal material, but soon becomes pale gray and rice water-like in appearance, with an inoffensive, slightly fishy odor vomiting often occurs after diarrhea has been established diarrhea causes fluid loss accounting to 1-30L/day, owing to subsequent dehydration and electrolytes loss poor skin turgor, sunken eyes into the orbits cold skin, wrinkled fingers and toes = washerwomans hand imperceptible radial pulses and unobtainable BP

cyanotic hoarse voice then lost, px speaks in whispers (aphonia) rapid and deep breathing (loss of O2) peripheral circulation oliguria and even anuria temp N at the onset , subN in later stages (shock) death may come 4hrs after onset, usually on the 1st2nd day PRINCIPAL DEFICITS: extracellular volume (ECV) in the loss of intestinal fluid that can lead to: severe dehydration with the appearance of washerwomans hand, restlessness and excessive thirst circulatory collapse, or shock metabolic acidosis d/t loss of a large volume of bicarbonate-rich stools, w/c results in rapid respiration with intervals of apnea (Kussmaul respiration) hypokalemia d/t massive loss of potassium through the stools px may manifest abdominal distention that could be attributed to paralytic ileus renal failure consequence of prolonged, untreated shock or unrelieved hypokalemia convulsions and tetany caused by loss of magnesium hypoglycemia untreated children who have been in stupor for several days corneal scarring stuporous px who has lost wink reflex acute pulmonary edema may follow hydration in cases of uncorrected metabolic acidosis DIAGNOSTIC EXAM: rectal swab dark field/phase microscopy (for gram positive/ negative) stool exam (for growth of bacteria) MEDICAL MANAGEMENT: treatment aims to: correcting the basic abnormalities without delay IV treatment by rapid infusion of an alkaline saline solution containing Na, K, Cl, and bicarbonate ions in proportions to the water-stools oral therapy rehydration (oresol, hydrites) unless contraindicated or if the px is not vomiting maintenance of volume of fluids and electrolytes (careful intake of I&O) antibiotics o tetracycline 500mg, q6 (adults); 125mg/kg o o body wt q6 for 72 (children) o furazolidone 100mg (adults); 125mg/kg q6 for o 72 (children) o chloramphenicol 500mg (adults); 18mg/kg q6 o for 72 (children) o cotrimoxazole 8mg/kg for 72

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NURSING MANAGEMENT: medical aseptic protective care enteric isolation VS accurately I&O accurately must be done every hour and every time px passes stool, let px drink careful personal hygiene proper disposal of excreta concurrent disinfection (using zonrox, etc) food must be properly prepared appropriate diet according to stage of recovery PREVENTION: food and water supply must be protected from fecal contamination water must be boiled/chlorinated milk should be pasteurized sanitary disposal of human excreta sanitary supervision is important COMMON NURSING DIAGNOSES: altered nutrition: less than body requirements altered tissue perfusion activity intolerance risk for fluid volume deficit diarrhea impaired skin integrity

during 2nd week, they form sloughs which are often bile-colored during 3rd week, the sloughs seprate and leave an ulcerated surface hemorrhage and perforation may occur d/t growth of the lesion and the continuous erosion of the epithelial of the small intestines since the toxin is absorbed into the bloodstream, almost all organs of the body are affected, but most commonly the heart, liver, and spleen; mesenteric lymph are red and swollen PATHOPHYSIOLOGY:
ingestion of food or water multiply in the deep mucosal layers of the stomach and small intestine lodging in the lamina propia inflammatory resoponse mesenteric lymph node edematous Peyers patches edema and superficial ulceration stimulates mononuclear leukocytes reaction (may contain into the area/it facilitates early hematogenous dissemination) enteric fever invasion to other organs lesion formation with disease manifestations endocarditis, meningitis, pneumonia, pylenonephritis, osteomyelitis, cholecystitis, hepatitis (from invasion of Salmonella)

bacterial infection transmitted by contaminated water, milk, shellfish, and other food affecting lymphoid tissues of the small intestine called Peyers patches (the one responsible for neutralizing bacteria in food, absorption) ETIOLOGIC AGENT: Salmonella typhosa/typhi gram negative, motile, and non-spore forming INCUBATION PERIOD: 5-40 days; mean of 10-20 days PERIOD OF COMMUNICABILITY: variable as long as px is capable of excreting microorganisms SOURCE OF INFECTION: recovered from the disease/has recently taken cared of a person with typhoid fever and was infected (considered carrier) ingestion of shellfish stool/vomitus MODE OF TRANSMISSION: fecal-oral transmission can be transmitted through 5Fs (flies, food, fingers, feces, formites) ingestion of contaminated water and milk PATHOGENESIS: organism gains access to the bloodstream through the bowels, principally through infected Peyers patches in the lymphoid tissues during the first week these lymph nodes are swollen; necrosis of the lymph nodes follows, caused by progressive edema and eventual vascular obstruction from the center to the periphery of the node, resulting in an oval ulcer along the long axis of the small intestine

CLINICAL MANIFESTATIONS: Onset headache, chilly sensation and aching all over body n/v, diarrhea 4th-5th day: sx at worst fever is high in the AM than the PM (regulated by the hypothalamus) accelerated breathing, furned tongues, skin is dy and hot, distended and tender abdomen 7th-9th day: rose spots appear on the abdominal wall 2nd week: sx become more aggravated and stable temp, rose spots more prominent Typhoid state decline of sx tongue protrudes dry and brown teeth and lips dirty brown in collection of dried mucus and bacteria staring blankly (coma vigil) twitching of tendons especially in wrist (subsultus tendonum) mutters deliriously and carphologia(picks up aimlessly at bedclothes with his fingers in a continuous fashion) tendency to slip down to the foot part of the bed severe cases, numbling delirium ending in death COMPLICATIONS: hemorrhage or perforation (most dreaded complication) perotinitis

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bronchitis/pneumonia meteorism or excessive distention of the bowels (tympanites) thromboembolism early HF typhoid spine neuritis septicemia Reiters syndrome (joint pain, eye irritation, and painful urination that can lead to chronic arthritis) DIAGNOSTIC EXAM: typhidot (blood procedure) confirmatory ELISA Widal test rectal swab MEDICAL MANAGEMENT: Chloramphenicol (drug of choice) Ampicilin Co-triamoxazole Ciprofloxacin/Citriaxone No response to Chloramphenicol = 3rd-4th generation drugs NURSING MANAGEMENT: medical aseptic technique restore fluid monitor VS prevent further injury (if with typhoid psychosis) personal hygiene and mouth care cooling measure WOF intestinal bleeding terminal and concurrent disinfection PREVENTION: sanitation excreta supervision of food handlers enteric isolation adequate amount of safe drinking water detection and monitoring education about mode of transmission POSSIBLE NURSING DIAGNOSES: fluid volume deficit hyperthermia increase risk to surgery (psychosis) self-care deficit constipation anxiety knowledge deficit

2 developmental stages

trophozoites/vegetative form found in parasitized tissues and liquid colonic contents cyst passed out with formed or semiformed stools and is resistant to environmental conditions considered as infective stage in the life cycle PATHOPHYSIOLOGY:
ingestion of entamoeba cysts develop to trophozoites penetrates into mucosa and submucosa of the large intestine through mechanical and proteolytic activity producing an edema fibrin formation and necrosis (creating lesions extending to submucosa area) fish-like appearance lesions appear primarily in something in cecal area, sigmoid colon and rectum hematogenous dissemination may occur to liver ulceration gangrene toxemia

Amoebic dystentry protozoal infection of human beings involves the colon, may spread to soft tissues commonly to liver and lungs by contiguity, hematogenous or lymphatic dissemination ETIOLOGIC AGENT: Entamoeba hystolica prevalent in unsanitary areas common in warm climates acquired by swallowing cysts survives a few days outside of the body cyst passes to the large intestine and hatches into a throphozoite; it passes into the mesenteric veins, the portal vein, and finally to the liver where it causes amoebic liver abscess

INCUBATION PERIOD: severe infection 3 days sub-acute and chronic form several months average cases 3-4 weeks PERIOD OF COMMUNICABILITY: entire duration of the illness MODE OF TRANSMISSION: fecal-oral direct contact sexual, orogenital, oroanal, and proctogenital sexual act indirect contact through foods uncooked leafy vegetables, food containing E. histolyca food or drinks may be contaminated through pollution of water supply, exposure to flies, use of night soil for fertilizing vegetables, and through unhygienic practices of food handlers CLINICAL MANIFESTATIONS: acute amoebic dysentry slight attack of diarrhea, periods of constipation with tenesmus diarrhea, watery, foul-smelling stools often containing blood-streaked foods colic and gaseous distention lower abdomen nausea, flatulence, abdominal distention and tenderness right iliac region chronic amoebic dystentry several days usually preceded by constipation tenesmus anorexia weight loss and weakness, liver may be enlarged stool first is semi-solid, later watery, bloody and mucoid

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abdominal distress, flatulence, constipation or irregular bowel movement constant fatigue, mild oxemia, lassitude abdomen loses its elasticity when picked up between fingers scattered ulcerations with whitish and erythematous borders gangrene type (fatal large sloughs if intestinal tissues in the stool with hemorrhage) extraintestinal forms hepatic pain RUQ tenderness on liver jaundice intermittent fever loss of weight/anorexia abscess lungs, px coughs anchovysauce sputum DIAGNOSTIC EXAM: stool exam blood exam protoscopy-sigmoidoscopy MEDICAL MANAGEMENT: Metronidazole (Flagyl) 800mg, TID x 5 days o Tetracycline 250mg, q6 Ampicillin, Quinolone, Sulfadiazine Streptomycin sulfate, Chloramphenicol fluid and electrolytes replacement NURSING MANAGEMENT: isolation and enteric precaution health education about food and water management boil water for drinking or use purified water avoid washing food with water from open drums or pails cover leftover food wash hands after defecation and before eating avoid eating ground vegetables (lettuce, carrots, etc) proper collection of stool specimen never give paraffin or any oil preparation for at least 48 hours prior to the collection of specimen instruct px to avoid mixing urine with stools if whole stools cannot be sent to the lab, select as large portions containing blood and mucus as possible send specimen immediately to laboratory; stools that are not fresh are nearly useless for examination label specimen properly skin care cleanliness and freedom from wrinkles on the sheet will be helpful with all the usual precautionary measures against pressure sores mouth care optimum comfort px should be kept warm; dysenteric px should never be allowed to feel cold, even for a moment diet during acute stage, fluids should be enforced


in the beginning of an attack, cereals and

strained meat broths without fat should be given chicken and fish may be added when convalescence is established bland diet without cellulose or bulk-producing foods should be maintained for a long time POSSIBLE NURSING DIAGNOSES: altered bowel elimination altered nutrition: less than body requirements increase risk of infection PREVENTION: health education sanitary disposal of feces food and water management detection and treatment of carriers fly control (they can serve as vectors)

a rare but serious paralytic illness caused by a potent neurotoxin ETIOLOGIC AGENT: Clostridium botulinum gram positive, spore-forming, anaerobic organism whose natural habitat is soil spore can withstand boiling for several hours most potent toxin MODE OF TRANSMISSION: foodborne (classical) results from ingestion of inadequately cooked contaminated food, especially those with low acid content wound botulism (cutaneous botulism) formation of ulcers with sharply demarcated edges and a membranous base as a result of deposition of toxin in the area infant botulism afflict infants aged 3-20 weeks produces hypotonic (floppy) infant syndrome, manifested by constipation, feeble cry, depressed gag reflex, and inability to suck can cause death to infant by weakening or paralyzing the muscles of the tongue and pharynx which are innervated by CN 9-12 PATHOGENESIS: all 3 forms produce disease via a final common pathway; the toxin is disseminated to peripheral cholinergic synapses and blocks acetylcholamine, causing impaired autoimmune and voluntary neuromuscular transmission PATHOPHYSIOLOGY:
ingestion of toxin disseminated to peripheral cholinergic synapses blocks acetylcholine impaired autonomic and voluntary neuromuscular transmission

CLINICAL MANIFESTATIONS: flaccid paralysis first affects and descends via the bulbar musculature

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somatic musculature is next affected and px may have generalized weakness paralysis is almost invariably displays symmetry as it descends neurological symptoms diplopia and double vision ptosis, dry mouth, dysphagia, and dysarthria classic symptoms diplopia and double vision, drooping eyelids slurred speech, difficulty swallowing, and dry mouth muscle weakness infants appear lethargic, feed poorly and are usually constipated weak cry and poor muscle tone if untreated, these symptoms may cause paralysis of the arms, legs, trunk, and respiratory muscles in foodborne botulism, symptoms usually begin 18-36 hours after eating contaminated food sx may continue to cause paralytic ileus with severe constipation and lead to body paralysis respiratory muscles are affected, which may cause death d/t respiratory failure COMPLICATIONS: pneumonia urinary tract infection pulmonary embolism decubitus ulcer flexion contractures MEDICAL MANAGEMENT: supportive care (nutritional and respiratory) in foodborne botulism, emetics and gastric lavage are recommended in wound botulism, exploration and debridement of the site need to be undertaken PREVENTION: health education through instruction on proper preparation of food, especially on home canning is necessary infant botulism can be prevented by not giving infants food with honey, as it is known to contain Colstridium botulinum promptly report suspected cases or an outbreak of foodborne botulism POSSIBLE NURSING DIAGNOSES: impaired physical mobility potential impairment of skin integrity alteration in bowel elimination pain and discomfort altered nutrition: less than body requirements anxiety

high-nutrient content low salinity and calm seas rainy days followed by sunny weather SOURCE OF INFECTION: shellfish quahogs soft shell clamps oysters mussels scallops moon snails PATHOPHYSIOLOGY:
ingestion of shellfish toxin conduction block in neurons and muscles saxitoxin blocks sodium movement in muscle tissue

CLINICAL MANIFESTATIONS: tingling of the lips and tongue which spreads to the face, neck, fingertips and toes headache, dizziness, and nausea follow, sx which may be mistaken as being d/t drunken condition aggravated by alcohol consumption in severe cases, muscular paralysis and breathing difficulty may occur in 5-12hours d/t paralysis of the diaphragm respiratory arrest MEDICAL MANAGEMENT: induced to vomit charcoal hemoperfusion (pumping the arterial blood through an activated charcoal filter to remove the toxin) alkaline fluids such as sodium bicarbonate (toxins are unstable in alkaline condition) artificial respiration for respiratory arrest PREVENTION: all shellfish-producing areas should have a monitoring program to test water sediments, and shellfish for contamination when blooms subside, shellfish has purified themselves of the toxins and when testing indicates a return to safe levels, the areas are re-opened if accidental ingestion of toxic shellfish is suspected, seek medical attention immediately recreational shellfish gatherers should look for posted warnings and pay close attention to local media announcements

slowly progressive disease caused by blood flukes chronic wasting disease common among farmers and their families in certain parts of the Philippines ETIOLOGIC AGENT: Schistosoma japonicum parasitic worm with 3 major types of organism Schistosoma japonicum infects intestinal tract oriental schistosomiasis

caused by a population explosion of toxic, naturally occurring microscopic phytoplanktons ETIOLOGIC AGENT: Alexandrium sp. environmental conditions which promote the explosive growth of microorganisms: warm surface temperature

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Schistosoma mansoni affects intestinal tract but occurs in Africa Schistosoma haematobium affects urinary tract can be found in Middle East INCUBATION PERIOD: at least 2 months SOURCES OF INFECTION: feces of infected persons dogs, pigs, carabaos, cows, monkeys, and wild rats have been found to be infected and also serve as hosts MODE OF TRANSMISSION: ingestion of contaminated water skin pores intermediary host, a tiny snail called Oncomelania quadrasi thrives best along riverbanks, freshwater streams, creeks, canals, and swamps found clinging to water hyacinths, grasses, decaying leaves and pieces of rotting wood, bamboo, and coconut husks sandy-loamy soil PATHOPHYSIOLOGY:
larvae penetrate the skin or mucous membrane work their way to the livers venous portal circulation eggs are filtered in the liver small lesions and granulomas are formed granulomas replaced by fibrous tissue ulceration in intestines are healed and scar formation occurs liver enlarges due to increasing fibrosis flow of blood is interrupted in intrahepatic portion portal hypertension

CLINICAL MANIFESTATIONS: pruritic rash, swimmers itch (develops at site of penetration) low-grade fever, myalgia, cough abdominal discomfort d/t hepatomegaly, splenomegaly, and lymphadenopathy bloody-mucoid stools, similar to those in dysentery, that comes on and off for weeks icteric and jaundice later, px belly becomes big because of inflamed liver, resulting from the accumulation of eggs in liver after some years, the px becomes weak and pale with marked muscle wasting when parasites reach the brain, severe headaches, dizziness, convulsions COMPLICATIONS: liver cirrhosis and portal hypertension cor pulmonale and pulmonary hypertension heart failure ascites hematemesis as a result from rupture of esophageal varices

renal failure cerebral schistosomiasis eggs already crossed blood-brain barrier manifested by ICP with focal neurological signs PATHOGENESIS: several aspects of the pathogenesis of cerebral schistosomiasis are unknown, although available evidence suggests that: starts with cercariae penetrating the human skin and entering the venous circulation schistosomulae migrate to the lungs and the liver they then mature into mating pairs, and settle in the mesenteric veins eggs may reach the brain through the valveless venous plexus of Batson, which joins the deep iliac veins and the inferior vena cava with the veins of the spinal cord and the brain alternately, the eggs may migrate to the brain via the pulmonary arteriovenosus or the portalpulmonary arteriovenosus shunts once, the worms have entered the cerebral veins, they lay eggs directly at the ectopic sites, which could be the cerebrum, cerebellum, meninges or the brainstem DIAGNOSTIC PROCEDURES: fecalysis or direct stool exam Kato-Katz technique liver and rectal biopsy ELISA circumoval precipitin test (COPT) confirmatory diagnostic test MEDICAL MANAGEMENT: Praziquantel tablet for 6 months; 1 tab BID for 3 mos, 1 tab OD for 3 mos Fuadin injection, IM/IV, 360mg for entire treatment continuously reinfected and retreated to those in endemic areas POSSIBLE NURSING DIAGNOSES: body image disturbance impaired skin integrity altered role function altered urinary elimination social isolation self-esteem disturbance PREVENTION: have stool examinations reduce snail density by: clearing vegetation, thus exposing snails to sunshine constructing a drainage system (canals) to dry the areas where the snails thrive improve farming through proper irrigation and drainage, crop rotation and removal of weeds; thus, disturbing the living condition of the snail diminish infection rate proper waste disposal control of stray animals prohibition of people, especially children, from bathing in infected streams construction of footbridges over snail-infessted areas

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provision of an adequate water supply for

bathing and laundering and safe water for drinking providing health education on the disease process, mode of transmission and prevention

also known as Shigellosis acute bacterial infection of the intestines characterized by diarrhea and fever and is associated with the passing out of bloody mucoid stools accompanied by tenesmus ETIOLOGIC AGENT: Shigella group gram negative, non-motile bacteria 4 serologic groups Shigella flexneri Shigella boydii Shigella connei Shigella dysentriae most infections habitat is exclusively the GIT of man develop resistance against antibiotics rarely invade bloodstream INCUBATION PERIOD: 7 hours to 7 day; average of 3-5 days PERIOD OF COMMUNICABILITY: capable of transmitting the microorganism during the acute infection until the feces are negative of the organism some remain carriers for 1-2 years MODE OF TRANSMISSION: ingestion of contaminated food, water or milk transmitted by flies or through other objects contaminated by feces of px fecal-oral transmission PATHOGENESIS/PATHOLOGY: after the incubation period, the organism invades the intestinal mucosa and causes inflammation dirty, green, fibrinous sloughing areas or ulcers are formed within a few days, the stool may contain pus, mucus, and blood CLINICAL MANIFESTATIONS: fever (especially in children) tenesmus, n/v, and headache colicky or cramping abdominal pain associated with anorexia and body weakness diarrhea with bloody-mucoid stools that are watery at first rapid dehydration and loss of weight COMPLICATIONS: rectal prolapse (particularly in undernourished children) respiratory complications (cough and pneumonia) non-suppurative arthritis and peripheral neuropathy DIAGNOSTIC PROCEDURES: fecalysis or microscopic examination of stools isolation of the causative organism from rectal swab or culture peripheral blood examination blood culture

sheets of polymorphonuclear leukocytes seen in staining with methylene blue MEDICAL MANAGEMENT: Ampicillin, Tetracycline, Co-trimoxazole may be useful in several cases but use of antibiotics are of question in treating IV may be infused with normal saline (with electrolytes) to prevent dehydration low-residue diet is recommended anti-diarrheal drugs is contraindicated because they delay fecal excretion that can lead to prolonged fever NURSING MANAGEMENT: maintain fluid and electrolyte balance to prevent profound dehydration keep the px warm and comfortable restrict food until n/v subsides isolation can be carried out through medical aseptic technique personal hygiene must be maintained proper disposal of excreta concurrent and terminal disinfection return to normal activities must be gradual because relapse may occur as a result of fatigue POSSIBLE NURSING DIAGNOSES: pain and discomfort fear alteration in bowel elimination altered nutrition: less than body requirement anxiety altered body temperature high risk for infection PREVENTION: sanitary disposal of human feces sanitary supervision of processing, preparing, and serving of food, particularly those eaten raw adequate provision of safe washing facilities fly control and protection against fly contamination isolation of px during acute stage protection and purification of public water supply persons known to be infection should be excluded from handling food for public consumption

infection caused by a parasitic roundworm ETIOLOGIC AGENT: Ascaris lumbricoides elongated, cylindrical worms that are tapered at the oral portion and pointed at the anal end creamy and pinkish yellow when fresh can grow as thick as a pencil and live for 1-2 years female worm can produce up to 240,000 eggs per day, which are then discharged into the feces and incubated in the soil for weeks MODE OF TRANSMISSION: contaminated fingers put into the mouth ingestion of food and drinks contaminated with embryonated eggs

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EPIDEMIOLOGY: most common in tropical regions, especially in poorly sanitized areas and in farms where night soil is used as fertilizer mostly affects children who are 4-12 years old considered the most prevalent form of parasitism in the Philippines children with poor nutritional status show a high incidence of positive ascaris in stool examination; they get infected more easily because they usually put things into their mouth and children also have poorer hygiene than adults pigs can be infected with another species of ascaries; pig ascaris infection can spread to humans; this occurs when infective eggs found in the soil and manure are ingested or if infected pig manure is used to fertilized crops, especially vegetables PATHOGENESIS: after ingestion of contaminated water or raw vegetables, ascaris lumbricoides hatches and releases larvae, which penetrate the intestinal wall and reach lungs through the bloodstream; after 10 days in the pulmonary capillaries and alveoli, the larvae migrate to the bronchioles, the bronchi, trachea and epiglottis; they are then swallowed and returned to the intestine where they mature and mate CLINICAL MANIFESTATIONS: Embryonated ova soil contamination with human excreta contamination of food, water and other objects ingested to intestine Larval stage larvae penetrate the walls of the intestine (duodenum) nausea and vomiting, poor appetite larvae are picked up by lymphatics or bloodstream periumbilical pain carried to the liver RUQ pain sometimes larvae may reach the heart sometimes they are carried to the biliary tract they may reach stomach, esophagus, and then the URT may stay in the capillaries of the lungs, and then reach the alveoli, where they grow and molt for 10 days cough, fever, rales, blood-tinged sputum nasal pruritus if larvae reach the nose from alveoli, they migrate to bronchioles, bronchi, trachea, and epiglottis ascaris in the larvae stage may be swallowed or ingested Adult stage adult ascaris stays in the small intestine colicky, periumbilical pain aggravated by cold stimulation (Nakamura sign) at times they become erratic they go to the stomach to the esophagus, and sometimes to the common bile duct and the gallbladder

intestinal obstruction may be caused by a bolus of entangled worms which may be palpable severe abdominal pain associated with vomiting in the GIT, they copulate; the female lays eggs about 2-3 months after embryonated eggs are ingested DIAGNOSTIC EXAM: stool for ova demonstration of fertilized or unfertilized eggs in the stools (Kato-Katz technique) abdominal x-ray densed shadow of adult ascaris which looks like strands of spaghetti (dot sign) routine blood counts significant eosinophilia MEDICAL MANAGEMENT: Albendazole/Mebendazole (15cc as a single dose) Piperazine citrate (75mg/kg, BID, PO) Pyrantel pamoate (1mg/kg as a single dose, PO) infection with ascaris is not an emergency; pregnant woman gets infected, treatment is postponed until after delivery COMPLICATIONS: biliary tract obstruction; develops cholestatic jaundice hepatic abscess and cholangitis intestinal obstruction, perforation, perotinitis malnutrition d/t damage of the intestinal mucosa, which impairs the absorption of nutrients NURSING MANAGEMENT: isolation is not needed preventive measures in each home and in the community should be enforced all members of the family must be taught on sanitary practices such as washing of hands before handling food, washing of all fruits and vegetables that are eaten raw, and effective sewage disposal availability of toilet facilities must be ensured importance of personal hygiene should be explained proper disposal of diapers should be emphasized to mothers POSSIBLE NURSING DIAGNOSES: self-care deficit altered nutrition: less than body requirements alteration in bowel elimination fear pain and discomfort high risk for infection PREVENTION: improved sanitation and hygienic practices improved nutrition deworming may be advised when travelling to areas where sanitation and hygiene are poor, avoid water or food that may be contaminated


an infection that occurs primarily in herbivores can be potential use for biological warfare or bioterrorism ETIOLOGIC AGENT: Bacillus anthracis

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large, aerobic, spore-forming, gram-positive,

rod-shaped microorganism, capsulated and non-motile can survive for years in dry soil but can be destroyed by boiling for 10 minutes SOURCE OF INFECTION: domestic herbivores (cattle, sheep, horses, goats) wild herbivores TYPES OF HUMAN CASES: agricultural cases result most often from contact with animals that are infected (skinning, butchering, or dissecting), from bites of contaminated or infected flies, and from consumption of contaminated meat industrial cases associated with exposure to contaminated hides, goat hair, or bones INCUBATION PERIOD: 9 hours to 2 weeks; average of 2-7 days MODES OF TRANSMISSION: direct contact with infected animals or contaminated animal products indirect animal bites and ingestion of contaminated meat airborne inhalation of contaminated or polluted air CLINICAL MANIFESTATIONS(ACCORDING TO TYPE): cutaneous anthrax 2nd-3rd day: small pimple/macule appears 4th day: ring of vesicle develops around the papule, vesicular fluid may exude marked edema develops; unless there is secondary infection, there is no pus and the lesion is not painful, although painful lymph adenitis may occur in the inguinal area 5th-7th day: original papule ulcerates to form the characteristic eschar (a necrotic mass of tissue) edema extends to some distance from the lesion sx are severe if lesions are located on the face, neck or chest in more severe forms, clinical findings are high fever, toxemia, regional painful lymphadenopathy, and extensive edema; shock and death may occur inhalational anthrax (woolsorters disease) presenting sx resemble those of severe viral respiratory distress after 1-3 days of acute phase, fever, dyspnea, stridor, hypoxia, and hypotension occur, usually leading to death within 24hrs organisms are directly deposited into the alveoli, producing hemorrhagic necrosis of the nodes associated with hemorrhagic mediastinitis gastrointestinal anthrax (ingestion of inadequatelycooked meat from animals with anthrax) primary infection is initiated in the intestines where lesions are formed, accompanied by hemorrhagic lymphadenitis sx include: fever, n/v, abdominal pain, bloody diarrhea, rapidly developing ascitis

COMPLICATIONS: anthrax meningitis intense inflammation of the meninges of the brain and spinal cord marked by elevated CSF pressure with bloody CSF; followed by rapid loss of consciousness and death fatality rate is almost 100% anthrax sepsis develops after the lymphohematogenous spread of B. anthracis from the primary lesion clinical features: high fever, toxemia, shock with death following in a short time MEDICAL MANAGEMENT: o Parenteral Penicillin G, 2M units q6 until edema subsides with subsequent administration of oral penicillin for 7-10 days Erythromycin, Tetracycline, Chloramphenicol (for px allergic to penicillin) NURSING MANAGEMENT: careful history taking thorough physical examination skin care, psychological and emotional support supportive measures are geared toward the type of anthrax exposure any type of anthrax must be reported to health authorities POSSIBLE NURSING DIAGNOSES: anxiety altered nutrition altered body temperature impaired physical mobility alteration in bowel elimination altered nutrition: less than body requirement

acute viral infectious disease affecting the respiratory system ETIOLOGIC AGENT: myxoviruses types A, A-prime, B,C RNA-containing INCUBATION PERIOD: 24-48 hours PERIOD OF COMMUNICABILITY: until the 5th day of illness (up to 7th day in children) MODE OF TRANSMISSION: airborne spread among crowded populations direct contact with the infected droplet influenza virus persists for hours in dried mucus PATHOPHYSIOLOGY:
influenza virus invades respiratory mucosa damages ciliated epithelium of the tracheobronchial tree the patient becomes vulnerable to secondary infection other organisms give rise to severe reactions, producing edema of the respiratory tree serosanguinous discharge complications

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CLINICAL MANIFESTATIONS: onset is sudden and is marked by chilly sensation, hyperpyrexia, malaise, sore throat, coryza, rhinorrhea, myalgia, and headache severe aches and pain, usually at the back, associated with severe sweating may manifest sometimes there are gastrointestinal sx and vomiting worst sx usually last from 3-5 days before condition begins to improve may occasionally cause severe dse, but most people recover COMPLICATIONS: directly related to primary viral infection hemorrhagic pneumonia encephalitis and other neurologic syndromes Reyes syndrome (acute encephalopathy and fatty degeneration of the liver associated with epidemic influenza B infection) myocarditis which may lead to HF sudden infant death syndrome myoglobinuria (myoglobin/muscle fibers in the urine) superimposed bacterial infections d/t Strep pneumonia, Haemophilus influenza, Strep pyogenes and Staphy aureus otitis media sinusitis pneumonia DIAGNOSTIC EXAM: blood examination is usually normal but leukopenia may be noted virus may be cultured from oropharyngeal washings or swabs during the first few days of illness viral serology complement fixation test hemo-agglutination test neutralization test NURSING MANAGEMENT: there has been no specific treatment for influenza let px stay at home drink plenty of fluids take following to relieve fever and headache paracetamol aspirin, unless contraindicated (should not be given to children below 16 y/o) ibuprofen or other anti-inflammatory drugs sponge down with tepid water isolate px to risk of infecting others (respiratory infection) limit strenuous activity specially in children watch out for complications, especially among people at risk POSSIBLE NURSING DIAGNOSES: impaired physical mobility activity intolerance fluid volume deficit ineffective airway clearance nutrition: less than body requirement alteration in comfort PREVENTION:

immunization avoidance of crowded places educate public and health care personnel regarding the basic personal hygiene advised that people belonging to the ff categories should receive vaccine annually: elderly people who have poor immunity with DM and lung, kidney, heart, or liver dse


was first reported in China in Nov 2002 with over 8,300 cases and 812 death reported by the beginning of July 2003 CAUSATIVE AGENT: novel coronavirus CLINICAL CRITERIA: asymptomatic or mild illness with a temp of o o >100.4 F (>38 C) one/more clinical findings of respiratory illness (ex. cough, shortness of breath, difficulty in breathing or hypoxia) EPIDEMIOLOGIC CRITERIA: travel (including transit in airport) within 10 days of the onset of sx to an area with current or previously documented or suspected community transmission of SARS close contact within 10 days of the onset of sx with a person known or suspected to have SARS MODE OF TRANSMISSION: direct mucous membranes (especially eye, nose, mouth) are always involved contact with infectious respiratory droplets and/or through exposure to fomites transmission through casual and social contact occasionally occurs as a result of intense exposure to a case of SARS (in workplaces, in vehicles) or in highrisk transmission settings, such as health care and household settings contamination of inanimate materials or objects by infectious respiratory secretions or body fluids (saliva, tears, urine, and stools) which have been found to contain the virus SOURCE OF INFECTION: virus is stable in urine and feces at room temperature for at least 1-2 days and in stools from px with diarrhea for up to 4 days survives on paper, on a plastered wall after 36 hrs, on a plastic surface or stainless steel after 72 hrs and on a glass slide after 96 hrs hospital envt samples from a number of sites, including walls and ventilation systems, have tested positive for SARS virus virus loses its infectivity after exposure to different commonly used disinfectants and fixatives; heat at o 56 C rapidly kills the virus other risk factors: household contact with a probable case of SARS increasing age male sex

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presence of co-morbidities CLINICAL MANIFESTATIONS: sudden onset of high-grade fever, usually greater o than 38 C headache and overall feeling of discomfort and bodyaches mild respiratory sx at the onset; after 2 days, dry cough and respiratory difficulty MEDICAL MANAGEMENT: no specific treatment recommendations can be made at this time; treatment choices may be influenced by the severity of the illness it is difficult to decide on the appropriate time to discharge SARS px SARS appears to have lingering after-effects once the acute phase of the disease ends the psychosocial aspects of this illness should not be underestimated PREVENTION: consult a doctor promptly if there are respiratory symptoms such as fever, malaise, chills, headache, joint pain, dizziness, rigors, cough, sore throat, and runny nose; early treatment is the key build up good body immunity; proper diet, getting regular exercise and adequate rest, reducing stress and avoiding smoking practice good personal hygiene; cover nose and mouth when sneezing or coughing wear a mask if you develop a runny nose, sore throat or cough wear protective mask in public areas, computer rooms, public transport, etc. wash hands properly and keep them clean; use liquid soap for handwashing and disposable towels for drying hands

rarely is the disease transmitted through skin


chronic, sub-acute or acute respiratory disease commonly affecting the lungs characterized by the formation of tubercules in the tissues which tend to undergo caseation, necrosis and calcification ETIOLOGIC AGENT: Mycobacterium tuberculosis and M. africanum in humans and M. bovis in cattle rod-shape organisms INCUBATION PERIOD: 2-10 weeks PERIOD OF COMMUNICABILITY: px is capable of discharging the organism all throughout his/her life if he/she remains untreated; disease is highly communicable during its active phase MODE OF TRANSMISSION: deliberate inoculation of the microorganism respiratory droplets inhalation of organisms directly into the lungs from contaminated air direct or indirect contact with infected persons, usually by discharges from the respiratory tract by means of coughing, sneezing, or kissing contact with contaminated eating or drinking utensils

lesions SOURCES OF INFECTION: sputum blood from hemoptysis nasal discharge saliva QUANTITATIVE CLASSIFICATION OF PTB: Minimal characterized by small lesions without demonstrable excavation that are confined to a small part of one or both lungs Moderately advanced one or both lungs may be involved volume affected should not extend to one lobe total diameter of the cavity should not exceed four centimeters Advanced characterized by lesions that are more extensive than moderate CLINICAL CLASSIFICATION: Inactive TB symptoms of TB are absent sputum is negative for tubercle bacilli after repeated examination no evidence of cavities on chest x-ray Active tuberculin test is positive x-ray of chest is generally progressive symptoms d/t lesions are usually present sputum and gastric contents are positive for tubercle bacilli Activity not determined activity has not been determined from a suitable period of observation or adequate laboratory and x-ray studies CLINICAL MANIFESTATIONS: afternoon rise in temperature night sweating body malaise and weight loss dry to productive cough dyspnea and hoarseness of voice hemoptysis (considered pathognomonic of the disease) occasional chest pains sputum positive for AFB PATHOPHYSIOLOGY:
organism penetrates the lining of the respiratory tract lodges and produces the first lesion, the tubercle in the parenchyma of lungs (Ghons tubercle) structural changes in the tissue bacilli will establish themselves in the alveoli of the lungs, walls of blood vessels, lymph channels or walls of bronchi bacteria replicate within the macrophages for 2-3 weeks before spreading throughout the body

DIAGNOSTIC EXAM: sputum analysis for AFB (confirmatory) chest x-ray tuberculin testing Mantoux test (PPD)

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tine test (OT) heaf test (LT)

supervised treatment ensures that patient take

MEDICAL MANAGEMENT: short course chemotherapy consisting of isoniazid (INH), rifampicin, pyrazinamide (PA) and ethambutol may be given for a period of 6 months px with drug resistance may be given second-line drugs such as capreomycin, streptomycin, cycloserine, amikacin, and quinolone WHO recommends the directly observed treatment, short-course (DOTS) to prevent noncompliance. The health worker ensures that the px takes his/her drugs if the medicine is taken incorrectly, the px becomes resistant to anti-TB drugs. This is very dangerous because if the disease recurs it becomes hard to treat the second time around relapsing px usually become resistant to individual drugs (INH, rifampicin, ethambutol, and PZA), they are given a combination of the abovementioned drugs ASSOCIATED DISEASES WITH PTB: older age groups DM chronic alcoholism psychiatric px hematologic disorder HIV infection NURSING MANAGEMENT: maintain respiratory isolation until the px responds to treatment or until he/she is no longer contagious administer medicines as ordered always check the sputum for blood or purulent expectoration encourage questions and conversation so that the px can air his/her feelings teach or educate the px about PTB encourage the px to stop smoking teach the px to cough or sneeze onto tissue paper and dispose of secretions properly advise the px to get plenty of rest and eat balanced meals be alert for signs of drug reaction if the px is receiving ethambutol, WOF optic neuritis; if it develops, discontinue the drug if the px is receiving rifampicin (Rifampin), WOF hepatitis and purpura; observe px for other complications like hemoptysis emphasize the importance of regular follow-up examination and instruct the px and his/her family about the s/sx of recurring TB ELEMENTS OF DOTS: political commitment with increased and sustained financing case detection through quality-assured bacteriology bacteriology remains to be a confirmatory diagnostic test for TB; properly equipped laboratories and trained personnel are necessary for quality-assured sputum smear microscopy standardize treatment with supervision and px support

their drugs regularly and completely; particular attention should be given to the poorest and most vulnerable groups an effective drug supply and management system an uninterrupted and sustained supply of quality assured anti-TB drugs is fundamental to TB control. Anti-TB drugs should be available free of charge to all TB patients, especially the poor, because treatment has benefits that extend to society. The use of anti-TB drugs by all providers should be strictly monitored. monitoring and evaluation system, and impact measurement this requires the standardized recording of individual patient data, including information on treatment outcomes, which are then used to compile quarterly treatment outcomes in cohorts of patients. these data when compiled and analyzed, can be used: facility level to monitor treatment outcomes district level to identify local problems as they arise provincial or national level to ensure consistency high-quality TB control nationally and internationally evaluate the performance of each country regular programmed supervision should be carried out to verify the quality of information and to address performance problems POSSIBLE NURSING DIAGNOSES: sleep pattern disturbance body image disturbance altered nutrition: less than body requirements fatigue self-care deficit alteration in comfort knowledge deficit ineffective airway clearance PREVENTION: submit all babies for BCG immunization avoid overcrowding improve nutritional and health status advise persons who have been exposed to infected persons to receive the tuberculin test, and if necessary, chest x-ray and prophylactic isoniazid


infectious disease characterized by repeated attacks of spasmodic coughing which consists of a series of explosive expirations, typically ending in a long-drawn forced inspiration which produces a crowing sound, the whoop, and is usually followed by vomiting coughing is initiated by the direct toxic effect of the organism on the CNS CAUSATIVE AGENT: Bordetella pertussis an infection that is more serious when it occurs in infants non-motile, gram-negative bacillus

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easily destroyed by light, heat, and drying INCUBATION PERIOD: 7-14 days PERIOD OF COMMUNICABILITY: 7 days after exposure to 3 weeks after typical paroxysms MODE OF TRANSMISSION: direct contact and droplet indirectly through spoiled linens and other articles contaminated by respiratory secretions SOURCES OF INFECTION: secretions from the nose and throat of infected persons contain the causative organism; it is extremely contagious in non-immune cases INCIDENCE: infants are highly susceptible one attack usually produces lifetime immunity second attack may be d/t other microorganisms causing whooping cough syndrome PATHOLOGY: after incubation period, large number of B. pertussis are confined to the tracheobronchial mucosa, entangled in the cilia where it produces progressively tenacious mucus this mucus is irritating to the mucosa and initiates coughing; cough is spasmodic because the tenacious material is not readily expelled whooping cough follows a classic 6-day course of 3 stages, each of which lasts about 2 weeks it is believed that coughing is initiated by direct toxic effect of the organism on the CNS CLINICAL MANIFESTATIONS: Catarrhal stage non-specific symptomatology where there is mucoid rhinoria, sneezing, lacrimation and dry bronchial cough cough becomes irritating, hacking and nocturnal and more severe during this stage that the disease is most communicable lasts for about 1-2 weeks Paroxysmal stage occurs on the 7th-14th day; lasts from 4-6 weeks cough becomes spasmodic and recurrent with excessive, explosive outbursts in a rapid series of 5-10 rapid coughs in one expiration each cough characteristically ends in a loud, crowing, inspiratory whoop, and chocking on mucus that causes vomiting paroxysmal coughing may induce nosebleeding, venous pressure, periorbital edema, conjunctival hemorrhage and hemorrhage of the anterior chamber of the eye during paroxysm, the face becomes cyanotic, veins on the face, and neck become distended, the eyes appear to bulge or pop out of the eyeballs, and tongue protrudes violent coughing is usually accompanied by profuse sweating, involuntary urination, lethargy and exhaustion cough is usually provoked by crying, eating, drinking or physical exertion

convulsions may occur as a result of intracranial

between paroxysms, the child appears well and

no physical signs can be observed Convalescent stage marked by a gradual in the paroxysms of coughing both in frequency and severity; vomiting ceases after about 6 weeks from onset, the attack subsides COMPLICATIONS: tissues around the bronchioles become inflamed and interstitial pneumonia occurs air passages become obstructed by mucus plugs; this results in atelectasis (lung collapse) convulsions d/t lack of oxygen on the tissues umbilical hernia otitis media bronchopneumonia (the most dangerous complication) severe malnutrition and starvation, d/t persistent vomiting, sleep and rest DIAGNOSTIC EXAM: nasopharyngeal swabs sputum culture CBC (leukocytosis) MEDICAL MANAGEMENT: supportive therapy fluid and electrolyte replacement adequate nutrition oxygen therapy antibiotics, such as erythromycin and ampicillin, are helpful in eliminating infection and to shorten the period of communicability hyperimmune convalescent serum or gammaglobulin has been found effective NURSING MANAGEMENT: objective: to prevent complications isolation and medical asepsis should be carried out during a paroxysm, the patient should not be left alone; suctioning equipment should be ready at all time for emergency use to avoid obstruction of the airways sunshine and fresh air are important, but the patient should be protected from drafts child should be kept as still and quiet as possible since activity and excitement precipitate paroxysm provide warm baths and keep the bed dry and free from soiled linens intake and output should be closely monitored POSSIBLE NURSING DIAGNOSES: ineffective airway clearance altered nutrition: less than body requirement risk for infection/complication sleep pattern disturbance alteration in comfort PREVENTION: any case of pertussis should be reported at once previously immunized children should be given reinforcing injection/immunization

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patients should be isolated 4-6 weeks from the onset of illness effective control measures should include efforts to locate subclinical or unreported cases public education for active immunization and early diagnosis, together with reporting of all cases, should be encouraged


acute and chronic parasitic disease transmitted by the bite of infected mosquitoes and is confined mainly to tropical and subtropical areas causes more disability and heavier economic burden than any other parasitic disease ETIOLOGIC AGENT: Protozoa of genus plasmodia plasmodium falciparum (malignant tertian) most serious malarial infection because of the development of high parasitic densities in the blood (RBC) tend to cause agglutination = microembolus formation most common in Philippines Plasmodium vivax (benign tertian) non-life threatening, except for the very young and the very old manifested by chills every 48 hours on the third day onward, especially if untreated Plasmodium malariae (quartan) less frequently seen than the first two types non-life threatening fever and chills usually occur every 72 hours, usually on the 4th day after onset Plasmodium ovale rare type of protozoan species VECTOR: female Anopheles mosquito breeds in clear, flowing, and shaded streams, usually in the mountains bigger in size than ordinary mosquitoes brown in color night-biting mosquito usually does not bite a person in motion o assumes a 36 position when it alights on walls, trees, curtains and the like INCUBATION PERIOD: 12 days for P. falciparum 14 days for P. vivax and ovale 30 days for P. malariae PERIOD OF COMMUNICABILITY: any untreated or insufficiently treated px may be the source of mosquito infection for more than 3 years in P. malariae, one or two years in P. vivax and not more than one year on P. falciparum MODE OF TRANSMISSION: mechanically transmitted through the bite of an infected female Anopheles mosquito parenterally transmitted through blood transfusion shared contaminated needles (rare occasions)

transplacental transmission of congenital malaria (rare case) CLINICAL MANIFESTATIONS: paroxysms with shaking chills may last for 12 hours and may attack daily or every 2 days rapidly rising fever with severe headache profuse sweating myalgia (muscle pain) with feelings of well-being in between splenomegaly, hepatomegaly orthostatic hypotension in children fever maybe continuous convulsions and GI symptoms are prominent splenomegaly is present in cerebral malaria severe headache, vomiting and changes in sensorium Jacksonian or grand mal seizure may occur PATHOPHYSIOLOGY:
Anopheles mosquito gets parasites from the blood of an infected person parasites multiply in the mosquito parasites invade the salivary glands of mosquito mosquito bites a human and, thus, injects the parasites parasites invade the RBCs, where they grow old and undergo asexual reproduction RBCs rupture or burst, releasing tiny organisms (merozoites) merozoites invade a new batch of RBCs to start another schizonic cycle indefinite malaise and slow-rising fever occur for several days there are shaking, a rapidly-rising temperature, and profuse sweating

coagulation defect

anemia shock

liver and renal failure

pulmonary and cerebral edema coma DEATH

DIAGNOSTIC EXAM: Malarial smear a film of blood is placed on a slide, stained and examined microscopically Rapid diagnostic test (RDT) blood test for malaria that can be conducted outside the laboratory and in the field results within 10-15 minutes done to detect malarial parasite antigen in the blood MEDICAL MANAGEMENT: Anti-malarial drugs Chloroquine (all species except for P. malariae) Quinine

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Sulfadoxine (for resistant P. falciparum) Primaquine (relapses of P. vivax and ovale)

erythrocyte exchange transfusion for rapid production of high levels of parasites in blood NURSING MANAGEMENT: patient must be closely monitored intake and output should be closely monitored to prevent pulmonary edema daily monitoring of px serum bilirubin (liver), BUN creatinine, and parasitic count if px exhibits respiratory and renal sx, determine the arterial blood gas (ABG) and plasma electrolyte during the febrile stage, tepid sponges, alcohol rubs and an ice cap on the head bring help the temperature down application of external heat and hot drinks during the chilling stage are helpful provide comfort and psychological support encourage to take plenty of fluids as the temp falls and sweating begins, warm sponge baths may be given the bed and clothing should be kept dry watch for neurologic toxicity (quinine infusion) like muscular twitching, delirium, confusion, convulsion and coma evaluate degree of anemia watch for any signs, especially abdominal bleeding consider severe malaria as medical emergency that requires close monitoring of VS POSSIBLE NURSING DIAGNOSES: altered body temperature activity intolerance knowledge deficit altered nutrition: less than body requirements PREVENTION: all malaria cases should be reported thorough screening of all infected person from mosquitoes is important breeding places of mosquitoes must be destroyed homes should be sprayed with effective insecticides that have residual actions on the walls mosquito nets should be used, especially in infected areas insect repellants must be applied to the exposed portion of the body people living in malaria-infested areas should not donate blood for at least 3 years blood donors should be properly screened

small viruses what contain single-stranded RNA Arboviruses group B MODE OF TRANSMISSION: bite of an infected mosquito, principally the Aedes aegypti Aedes aegypti is a day-biting mosquito (they appear 2 hours after the sunrise and 2 hours before onset) breeds in areas of stagnant water has limited, low-flying environment has fine white dots at the base of the wings and white bands on the legs Aedes albopictus may contribute to the transmission of the dengue virus in rural areas other contributory mosquitoes: aedes polymensis aedes scutellaris simplex INCUBATION PERIOD: 3-14 days (commonly 7-10 days)

PERIOD OF COMMUNICABILITY: a day before the febrile period to the end of it mosquito becomes infective day 8-12 after the blood meal and remains infective throughout its life SOURCES OF INFECTION: infected persons the virus is present in the blood of patients during the acute phase of the disease and will become a reservoir of the virus, sucked by mosquitoes, which may then transmit the disease standing water any stagnant water in the household and its premises are usual breeding places of these mosquitoes INCIDENCE: age dengue fever may occur at any age, but it is common among children and peaks between 4-9 years old sex both sexes can be affected season more frequent during rainy season location more prevalent in urban communities PATHOPHYSIOLOGY:
infectious virus is deposited in the skin initial replication occurs at the site of infection and in local lymphatic tissues viremia (viruses on blood) occurs within a few days (lasting until 4th-5th day after onset of symptoms) at the site of petechial rash, non-specific changes are notes, which include endothelial swelling, perivascular edema, and extravasation of blood marked in vascular permeability, hypotension, hemoconcentration, thrombocytopenia with platelet agglutination and/or moderate DIC permeability to vascular endothelium and loss of plasma from the intravascular space pathophysiological abnormality like hypovolemia

acute afebrile disease caused by infection with one of the serotypes of dengue virus, which is transmitted by mosquito genus Aedes refers to a benign form of disease with systemic symptoms: fever and often ash associated with pain and in the joints, bones, and behind the eyes severe, sometimes fatal manifestation of the dengue virus infection characterized by a bleeding, diathesis (susceptibility to diseases), and hypovolemic shock ETIOLOGIC AGENT: Flaviviruses 1,2,3,4, and a family of Togaviridae

CLINICLA MANIFESTATIONS: dengue fever prodromal (onset) symptoms characterized by: malaise and anorexia up to 12 hours

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fever and chills accompanied by severe frontal headache, ocular pain, myalgia with severe backache, and arthralgia nausea and vomiting fever is non-remitting and persists for 3-7 days rash is more prominent on the extremities and the trunk; it may involve the face in some isolated cases petechiae usually appears near the end of the febrile period and most commonly on the lower extremities dengue hemorrhagic fever (DHF) severe form of dengue virus infection is manifested by fever, hemorrhage, diathesis, hepatomegaly, and hypovolemic shock PHASES OF ILLNESS: initial febrile phase lasting from 2-3 days o fever (39-40 C) accompanied by headache febrile convulsions may appear palms and sole are usually flushed positive tourniquet test anorexia, vomiting, myalgia maculopapular or petechial rash may be present and usually starts in the distal portion of the extremities (sparing the axilla and chest); the skin appears purple, with blanched areas of varying size (Hermans sign, considered pathognomonic to the disease) generalized or abdominal pain hemorrhagic manifestations like positive tourniquet test, purpura, epistaxia, and gum bleeding may be present circulatory phase fall of temperature accompanied by profound circulatory changes usually on the 3rd-5th day restless with cool, clammy skin cyanosis profound thrombocytopenia accompanies the onset of shock bleeding diathesis may become more severe and lead to GIT hemorrhage shock may occur d/t loss of plasma from the intravascular space; hemoconcentration with markedly elevated hematocrit is present pulse is rapid and weak; pulse pressure becomes narrow and blood pressure may drop to an unobtainable level untreated shock may result in coma; metabolic acidosis and death may occur within 2 days with effective therapy, recovery may follow in 2-3 days CLASSIFICATION (ACCORDING TO SEVERITY): Grade I fever with accompanied non-specific constitutional symptoms and the only hemorrhagic manifestation is positive in tourniquet test Grade II all signs of grade I, plus spontaneous bleeding from the nose, gums and GIT are present

Grade III presence of circulatory failure as manifested by weak pulse, narrow pulse pressure, hypotension, cold, clammy skin and restlessness Grade IV profound shock, and undetectable blood pressure and pulse COMPLICATIONS: dengue fever epistaxis, menorrhagia (excessive bleeding during menstruation) GI bleeding concomitant GI disorder (peptic ulcer) DHF metabolic acidosis hyperkalemia tissue anoxia hemorrhage into the CNS or adrenal glands uterine bleeding may occur myocarditis severe manifestations dengue encephalopathy is manifested by restlessness, apprehension/anxiety, disturbed sensorium, convulsions, spacity, and hyporeflexia DIAGNOSTIC TESTS: tourniquet test screening test, done by occluding the arm veins for about 5 minutes, to detect capillary fragility platelet count confirmatory test hemoconcentration an of at least 20% in the hematocrit or a steady rise in the hematocrit occult blood hemoglobin determination MEDICAL MANAGEMENT: there is no effective antiviral therapy for dengue fever; treatment is entirely symptomatic analgesic drugs other than aspirin may be required for relief from headache, ocular pain and myalgia initial phase may require IV infusion to prevent dehydration and replacement of plasma blood transfusion for severe bleeding oxygen therapy for shock sedatives may be needed to allay anxiety and apprehension NURSING MANAGEMENT: patient should be kept in mosquito-free environment to avoid further transmission of infection keep patient at rest during bleeding episodes VS must be promptly monitored in cases of nose bleeding, keep the patients trunk elevated; apply ice bag to the bridge of nose and to the forehead observe for signs of shock, such as slow pulse, cold, clammy skin, prostration (lie facing downward), and fall of BP restore blood volume by putting the patient in Trendelenburg position to provide greater blood volume to the head part patient with dengue is not infectious; isolation is not required

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POSSIBLE NURSING DIAGNOSES: altered body temperature fear anxiety knowledge deficit activity intolerance PREVENTION: health education early detection and treatment of cases will not worsen the victims condition treat mosquito nets with insecticides house spraying is advised eliminate vector by: changing water and scrubbing sides of flower vases once a week destroying the breeding places of mosquitoes by cleaning the surroundings keeping the water containers covered avoid hanging too many clothes inside the house case finding

mosquito bites a person with lymphatic filariasis microscopic worms circulating the persons blood enter and infect the mosquito microscopic worms enter lymph vessels where they grow into adults adult worm lives for 7 years in lymph vessels; they mate and release into bloodstream millions of microscopic worms (microfilaria) the worms in the blood are picked up by the biting mosquito and is transmitted to another person via the larvae many mosquito bites over several months to years before filariasis takes place adult worms die = first symptoms occur damages kidney and lymph system fluid collects and causes swelling in the arms, breasts, legs, and for men, the genital area swelling and decreased function of lymphatic system make it difficult for the body to fight the infection more bacterial infections in the skin, thus skin hardens and thickens (elephantiasis) worms can obstruct the vessels causing the surrounding tissues to enlarge in conjunctival filariasis, larvae migrate to the eyes and can sometimes be seen beneath the conjunctiva blindness (onchocerciasis)

parasitic disease caused by the microscopic, threadlike African worm. The adult worm can live only in the human lymphatic system. The disease is an extremely debilitating and stigmatizing and affects men, women and children. It affects the poor in both rural and urban areas. The disease is rarely fatal; however, it can causes extensive disability, gross disfigurement, and untold suffering in millions of men, women and children ETIOLOGIC AGENT: Wuchereria bancrofti causative agent for filariasis threadworm 4-5cm long and affects the lymph nodes and vessels of the legs, arms, vulva, and breasts Brugia malayi shows manifestations resembling that of the bancroftin, but swelling of the extremities is confined to the areas below the knees and below the elbows Brugia timori rarely affects the genitals Loa loa another filarial parasite in humans transmitted by deer fly MODE OF TRANSMISSION: person-to-person by mosquito bites persons having circulating microfilariae are outwardly healthy but transmit the infection to others through mosquito bites persons with chronic filarial swellings suffer severely form the disease but no longer transmit the infection

CLINICAL MANIFESTATIONS: symptoms vary depending on the type of parasitic worm involved, but all infections usually begin with on-and-off chills, headache, and fever that lasts between 3 months and 1 year after the insect bite there may also be swelling, redness and pain in the arms, legs, or scrotum areas if abscesses may appear as a result of dying worm or a secondary bacterial infection DIAGNOSTIC EXAM: circulating filarial antigen (CFA) performed on a finger-prick blood droplet taken anytime of the day; results are available in a few minutes larvae can also be found in the blood, but mosquitoes which spread the disease are active at night; larvae are usually found between about 102am patients history must be taken and on the pattern of inflammation and signs of lymphatic obstruction must be observed MEDICAL MANAGEMENT: Ivermectin, Albendaole, Diethylcarbamazine (DEC) are used in treatment and act by: eliminating the larvae impairing the adult worms ability to reproduce actually killing the adult worms the above medications are started at low doses to prevent immunologic reactions triggered by the large number of dying parasites

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surgery may be performed to remove surplus tissue and provide a way to drain the fluid around the damaged lymphatic vessels; surgery may also be used to minimize massive enlargement of the scrotum elephantiasis of the legs can also be eased by elevating the legs and providing support with elastic bandages DEC-fortified salt is helpful NURSING MANAGEMENT: health education and information dissemination as to the mode of transmission must be carried out environment sanitation and the destruction of breeding places of mosquitoes must be emphasized psychological and emotional support to client and the family are necessary personal hygiene must be encouraged the course of the disease must be explained to the client and his/her family POSSIBLE NURSING DIAGNOSES: impaired physical mobility knowledge deficit impaired skin integrity activity intolerance body image disturbance altered health maintenance PREVENTION: mosquiroes that carry the microscopic worms usually bite between the hours of dusk and dawn; it is advised that people living in an area with filariasis should: sleep under a mosquito net use mosquito repellant in the hours between dusk and dawn take yearly dose of medicine that kills the worms circulating in the blood


zoonotic infectious bacterial disease carried by animals, both domestic and wild infected urine contaminates water or food, which causes disease when ingested or inoculated through skin ETIOLOGIC AGENT: Leptospira (Leptospira interrogans) spirochete chiefly saprophytic aquatic organisms which are found in river and lake waters, sewage and in the sea there are 150 serotypes divided among 18 serogoroups; some species are pathogenic to man and animals Weils disease is specifically caused by the serovar icterohaemorrhagiae INCUBATION PERIOD: 6 15 days PERIOD OF COMMUNICABILITY: found in urine between 10-20 days after disease onset SOURCE OF INFECTION: comes from contaminated food and water and infected wildlife and domestic animals, especially rodents

L. icterohaemorrhagiae source of Weils disease frequently observed among mine, sewer and abattoir workers L. bataviae that attacks rice field workers dogs L. ccanicola among veterinarians, breeders and owners of dogs mice L. grippotyphosa farmers MODE OF TRANSMISSION: ingestion or contact with skin or mucous membranes of infected urine or carcasses if either wild or domestic animals mucous membranes of the eyes nose and mouth and through breaks in the skin enters blood to cause damage, and thereafter, in the kidneys, the liver, meninges, and conjunctiva semen of infected animals common among water sports enthusiasts in certain areas as prolonged immersion in water is known to promote the entry of bacteria occupations at risk include veterinarians, slaughter workers, farmers and sewer workers human-to-human transmission is rare CLINICAL MANIFESTATIONS: range in severity from asymptomatic to fatal clinical course is generally biphasic and majority of cases are unicteric (non-liver related) 3 stages: septic stage marked by febrile lasting from 4-7 days abrupt onset of remittent fever, chills, headache, anorexia, abdominal pain, and severe prostration (weakness) respiratory distress fever subsides with lysis immune/toxic stage can be with/without jaundice and lasts for 4-30 days iritis, headache, meningeal manifestations like disorientation, and convulsions with CSF findings of aseptic meningitis oliguria and anuria with progressive renal failure shock, coma, and CHF are also seen in severe cases death may occur between 9th-16th days convalescence relapse may occur during the 4th-5th weeks LABORATORY EXAM: Blood urea-nitrogen and creatinine ELISA liver function tests usually are slightly to moderately elevated aspartate aminotransferase (AST) alanine aminotransferase (ALT) gamma-glutamyltransferase (GGT) Leptospira antigen-antibody test (LAAT) Leptospira antibody test (LAT)

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cattle, swine and other livestock dogs rodents, wild animals

contact with contaminated water and soil entry through the eyes, mouth and broken skin


PREVENTION: sanitation in homes, workplaces and farms is a must if there is a need for proper drainage system and control of rodents (40-60% infected) animals (cattle, dogs, cats, and pigs) must be vaccinated infected humans and pets should be treated information dissemination campaign must be conducted effectively

ORGANS OF THE BODY INVADED BY ORGANISM: after organism gains entrance into the body, it multiplies in the bloodstream and invades the liver, resulting in jaundice in kidneys, the presence of the organism causes inflammation of the nephrons and tubular necrosis, resulting in renal failure leptospira may affect the muscles, resulting in pain and sometimes edema organism also invades the eyes, resulting in conjunctivitis; in addition, d/t liver involvement, the patient becomes icteric, thereby giving an orangecolored sclera COMPLICATIONS: meningitis respiratory distress renal interstitial tubular necrosis that results in renal failure (Weils disease) CV problems MEDICAL MANAGEMENT: suppressing the causative agent fighting possible complications Aetiotropic drugs Penicillin, Doxycycline, Ampicillin, Amoxicillin for prophylaxis, doxycycline 100mg, PO, o q12 for 1 week peritoneal dialysis administration of fluid and electrolytes and blood, as indicated NURSING MANAGEMENT: isolate the patient; urine must be properly disposed of darken the room because light is irritating to the patients eyes observe meticulous skin care to ease pruritus keep clients under close surveillance keep homes clean regularly replace water in pools, vases, acquaria, etc. prevent stagnation eradicate rats and rodents provide health education on the modes of transmission of the disease encourage oral fluid intake POSSIBLE NURSING DIAGNOSES: body image disturbance high risk for injury anxiety altered nutrition: less than body requirements impaired physical mobility impaired skin integrity knowledge defict

specific, acute viral infection communicated to man by the saliva of an infected animal ETIOLOGIC AGENT: Rhabdovirus bullet-shaped filterable virus with a strong affinity for the CNS organism is sensitive is sensitive to sunlight, ultraviolet light, either, formalin, mercury, and nitric acid; resistant to phenol, merthiolate, and common antibacterial agents INCUBATION PERIOD: 1 week 7 1/2 months in dogs 10 days 15 years in human incubation period depends on the following factors: distance of the bite to the brain extensiveness of the bite species of the animal richness of the nerve supply in the area of the bite resistance of the host PERIOD OF COMMUNICABILITY: 3-5 days before onset of symptoms until the entire course of illness MODE OF TRANSMISSION: an infected animal carries the rabies virus in its saliva and transmits it to humans by biting; in some cases, the virus spreads when the saliva comes in context with the persons mucous membranes, such as those of mouth and eyelids, or broken skin like in cuts, scratches or open wounds PATHOGENESIS: from the site of the bite, the organism proceeds to the CNS through the exoplasm of the peripheral nerves experimental studies have shown that the virus stays for some time in the inoculation site and that the multiplication of the virus occurs in the myocytes it has been observed that the period between inoculation and nerve invasion is the only time when prophylactic vaccine is effective once the virus infects the individual, the spread is both centripetal and centrifugal after infection of the CNS, the virus spreads through the peripheral nerves to the salivary glands and other organs, such as the lungs, adrenals, kidneys, bladder, and testicles (priapism) PATHOLOGY: rabies virus causes the widespread changes throughout the CNS

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histologic findings include neural necrosis and mononuclear cellular infiltration, especially in the thalamus, hypothalamus, and medulla the cranial nerve nuclei are extremely damaged neural changes are present in the spinal cord, especially in the posterior horn negri bodies are most abundant in the degenerating neurons of the salivary glands (pathologic sign for rabies) CLINICAL MANIFESTATIONS: Prodromal/Invasion phase characterized by fever, anorexia, malaise, sore throat, copious salivation, lacrimatiom, perspiration, irritability, hyperexcitability, apprehensiveness, restlessness, drowsiness (sometimes), mental depression, melancholia and marked insomnia pain at the original site of the bite; headache and nausea may be present patient becomes sensitive to light, sound, and temperature pain and aches in different parts of the body anesthesia, numbness, and tingling, burning, and cold sensation may be felt along the peripheral nerves involved and the site of the bite mild difficulty in swallowing Excitement/Neurological phase characterized by marked excitation and apprehension; terror may even occur delirium associated with nuchal rigidity, involuntary twitching, or generalized convulsions may exhibit maniacal behavior; eyes are fixed and glossy and the skin is cold and clammy severe and painful spasms of the muscles of the mouth, pharynx and larynx on attempt to swallow water or food or even at the mere sights of them aerophobia or intense fear or dislike of air profuse drooling tonic/clonic contractions of the muscles death may occur during the episode of spasms or from cardiac/respiratory failure if patient survives this phase, he/she deteriorates rapidly and enters the terminal phase Terminal/Paralytic phase quiet and unconscious loss of bowel and urinary control spasms cease and there is progressive paralysis tachycardia and labored irregular respiration death occurs d/t respiratory paralysis, circulatory collapse, or heart failure DIAGNOSTIC PROCEDURES: virus isolation from the patients saliva/throat fluorescent rabies antibody (FRA) provides the most definitive diagnosis presence of negri bodies in the dogs brain MEDICAL MANAGEMENT: thoroughly wash the wounds from the bite and scratches with soap and running water for at least 3 mins

check the patients immunization status; give tetanus toxoid if needed give tetanus antiserum infiltrated around the wound or intramuscularly after a negative skin test give anti-rabies vaccine, both passive and active, depending on the site and size of the bite, as well as the health condition of the biting animal NURSING MANAGEMENT: isolate the patient give emotional and spiritual support provide optimum comfort and prevent injury, especially during hyperactive episodes darken the room and provide a quiet environment patient should not be bathed and there should not be any running water in the room or within the hearing distance of the patient if IV fluid has to be given, it should be wrapped; needle should be securely anchored to the vein to avoid dislodging in times of restlessness concurrent and terminal disinfection should be carried out POSSIBLE NURSING DIAGNOSES: altered nutrition: less than body requirements fluid volume deficit anxiety knowledge deficit altered thought process anticipatory grieving PREVENTION: primary preventive measure is the interruption in the mode of transmission vaccination of all dogs enforcement of regulations for the pick-up and destruction of stray dogs 10-14 day confinement of any dog that has bitten a person availability of laboratory facilities for observation and diagnosis providing public education, especially to children, on the avoidance and reporting of all animals that appear sick

chronic systemic infection characterized by progressive cutaneous lesions ETIOLOGIC AGENT: Mycobacterium leprae acid-fast baccilus that attacks cutaneous lesions and peripheral nerves, producing skin lesions, anesthesia, infection and deformities not highly contagious and actually has low inefectivity INCUBATION PERIOD: 5 1/2 months 8 years MODE OF TRANSMISSION: respiratory droplets inoculation through skin break and mucous membranes may also be a mode of transmission DISTINCT FORMS: Lepromatous leprosy (multibacillary) most serious type and is considered to be the most infectious

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causes damage to the respiratory tract, eyes

and testes, as well as the nerves and the skin lepromin test is negative but the skin lesion contains large amounts of Hansens bacillus gradual thickening of the skin with the development of a granulomatous condition lesions frequently appear as macules and become nodular in character (leproma) slow involvement of the peripheral nerves, with some degree of anesthesis and loss of sensation and gradual destruction of the nerves atrophy of the skin, and muscles and eventual melting or absorption of small bones, primarily those of the hands and feet there is ulceration of the mucous membrane of the nose because of the melting or absorption of small bones and ulcerations, natural amputation may occur Tuberculoid leprosy it affects the peripheral nerves and sometimes the surrounding skin, especially on the face, eyes and testes, as well as the nerves on the skin lepromin test is positive, but the organism is rarely isolated from the lesions macules are elevated, with clearing at the center, and are more clearly defined than in the lepromatous form anesthesia is present, and involvement of the peripheral nerves occurs more rapidly than in the lepromatous form Borderline (dimorpous) leprosy characteristics of both lepromatous and tuberculoid leprosy skin lesions of this type of leprosy are diffused and poorly defined PATHOLOGY: M. leprae attacks the peripheral nerves, especially the ulnar, radial, posterior-popliteal, anterior-tibial and facial nerves when the bacilli damage the skins fine nerves, they cause anesthesia, anhidrosis and dryness if they attack a large nerve trunk, motor nerve damage, weakness and pain occur, followed by peripheral anesthesia, muscle paralysis and atrophy CLINICAL MANIFESTATIONS: Neural involvment earliest manifestations are caused by nerve damage atrophy of the muscles of the hands which extends to the thenar, hypothenar, and the forearm muscles, resulting in clawhand nerves often involved are the ulnar, median, radial, lateral popliteal and facial paralysis and peripheral anesthesia can occur either independently or concurrently secondary consequences of nerve involvement include malperforant, clawhand and ocular complications

incident to corneal paralysis of the eyelids Skin



lepromatous and tuberculoid leprosy differ

greatly in their cutaneous manifestations lepromatous disease, early lesions are multiple, symmetrical ad erythematous, sometimes appearing as macules or papules with smooth surfaces later, these lesions enlarge and form plaques or nodules on the earlobes, nose, eyebrows and forehead, giving the patient a leonine appearance eventually, there is loss of eyebrows and eyelashes loss of function of the sweat and sebaceous glands makes affected skin appear dry and hairless tuberculoid leprosy may be purely neural or may simultaneously affect the skin raised, large erythematous plaques appear on the skin with clearly defined boarder; as they grow, they become rough, hairless and hypopigmented, leaving an anesthetic scar Eye
specific ocular manifestations are found only in

lepromatous and borderline leprosy

conjunctiva, sclera, cornea, and iris are infected,

sparing the retina and optic nerve

photophobia, conjunctivitis and iridocyelitis

frequently occur; opacity of the cornea, insensitivity, and ulceration can lead to blindness Upper respiratory tract nose, mouth, pharynx, larynx, trachea, and esophagus are often involved in lepromatous leprosy epistaxis, ulceration of the uvula and tonsils, septal perforation and nasal collapse are also present Visceral leprosy apart from skin and nerves, the heaviest concentration of lesions is in the organs representing the reticuloendothelial system, the lymph system and liver testicular damage occurs in almost all moderately advanced cases of lepromatous leprosy DIAGNOSTIC EXAM: identification of signs and symptoms tissue biopsy tissue smear blood tests show RBC and ESR; serum Ca, albumin and cholesterol levels MEDICAL MANAGEMENT: Sulfone therapy rehabilitation, recreational and occupational therapy multiple drug therapy (MDT) combination of rifampicin, clofazimine, and dapsone for multibacillary leprosy; rifampicin and dapsone for paucibacillary type

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among these, rifampicin is the most anti-

leprosy drug and is therefore included in the treatment of both types of leprosy treatment with only 1 anti-leprosy drug will always result in the development of drug resistance treatment with dapsone or any anti-leprosy drug used as monotherapy should be considered as an unethical practice for multibacillary leprosy, rifampicin 600mg is given once a month; dapsone 100mg daily; clofazimine 50mg daily for a 12-month duration paucibacillary leprosy, give rifampicin 600mg once a month; dapsone once daily; duration of treatment is 6 months Clofazamine causes brownish black discoloration and dryness of the skin; however, this disappears within a few months after topping treatment; this should be explained to patients starting the MDT regimen for MB leprosy MB and PB patients should have fixed-duration reatment, which means: MB patients after taking 12 monthly doses of MDT, the person is considered cured and should be removed from the register PB patients after taking 6 monthly doses of MDT, the person is considered cured and should be discharged NURSING MANAGEMENT: if the patient is admitted to the hospital, isolation and medical sepsis should be carried out moral support and encouragement are necessary diet should be full, wholesome, and nutritious special attention should be given to personal hygiene terminal disinfection should be carried out POSSIBLE NURSING DIAGNOSES: impaired skin integrity social isolation ineffective coping knowledge deficit anxiety impaired body image PREVENTION: report all cases and suspects of leprosy newborn infants should be separated from leprous mothers BCG vaccine may be protective if given during the first 6 months of life health education should be given, with particular focus on the mode of transmission

most common vector-borne disease in United States and Europe occurs from 2 to 88 years onset of illness is during summer (June-July), associated with camping, hiking, and residence in wooded, rural, or coastal areas RESERVOIR: ticks that feed on deer, wild rodents MODE OF TRANSMISSION: tick bite or contact with tick feces adult ticks usually feed on deers and occasional hosts to horses, dogs, other larger mammals and birds rodents and small mammals are the natural host of the larval and nymphal stages of the causative agent INCUBATION PERIOD: 3-32 days PATHOPHYSIOLOGY:

B. bugdorferi is injected into skin by the bite of an infected ixodes tick spirochetes multiply and migrate outward within the dermis appearance of characteristic EM lesion activation of inflammatory response to bacteria spirochetes avoid the immune response by expression of surface proteins, which may interfere with the function of immune factors neutrophils fail to appear in the developing EM lesion permitting bacteria to survive and eventually spread throughout the body spirochetes spread via the bloodstream to the joints, heart, nervous system and distant skin sites

joints subjective joint pain, arthritis


heart AV block (first degree, Wenckebach, complete heart block) myopericarditis, chronic cardiomyopathy, pericardial effusion

induce astrocytes to undergo astroliosis (proliferation followed by apoptosis natural death of neurons)

spirochetes may induce host cells to secrete products toxic to nerve cells fatigue and malaise chronic secretion of stress hormones tryptrophan in CNS dysregulation of hormones

neurological dysfunction

multi-system illness caused by a tick-borne spirochete this illness closely mimics other rheumatic diseases ETIOLOGIC AGENT: Borrelia bugdorferi INCIDENCE: occurs in temperate regions of North America, Europe, Asia

COMPLICATIONS: Aseptic meningitis or encephalitis Cerebellar ataxia Chorea Cranial or peripheral neuropathies Heart block Congestive heart failure Congenital infection DIAGNOSTIC FINDINGS: Positive culture from Erythema Migrans (EM) lesion

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Blood tests antibody titers enzyme-linked immunosorbent assay Western blot assay (to confirm ELISA findings) Serology tests mild anemia ( Hmg) erythrocyte sedimentation rate (ESR), WBC, IgM level, aspartate aminotransferase CSF analysis presence of antibodies to B. burgdorferi CLINICAL MANIFESTATIONS: according to stages: [Early infection] Stage 1: Localized infection occurs during first several days of onset erythema migrans skin lesions; commonly seen during early stage annular skin lesion that expands over a period of days to weeks and develops central clearing warm to touch but not painful may be accompanied with fatigue, fever, chills, generalized achiness, headache and regional lymphadenopathy [Early infection] Stage 2: Disseminated infection may occur within several days to weeks of onset multiple annular secondary skin lesions generally smaller, migrate less, and lack indurated center usually fade within 3-4 weeks neurologic abnormalities meningitis, encephalitis, cranial neuritis (bilateral facial palsy) in children, optic nerve may be affected by inflammation or increased ICP which may lead to blindness Bannwarths syndrome most common neurologic manifestation neuritic pain, lymphocytic pleocytosis without headache and sometimes cranial neuritis cardiac involvement AV block (first-degree, Weneckebach or complete heart block) migratory musculoskeletal pain common in tendons, joints, burse, muscle or bones conjunctivitis (most common eye abnormality in Lyme disease) [Late infection] Stage 3: Persistent infection months after the onset of illness intermittent attacks of joint swelling primarily in large joints, especially the knee or one or two joints at a time attacks of arthritis generally last from a few weeks to months separated by periods of complete remission chronic neurologic manifestations months to years after onset of disease

spinal radicular pain or distal paresthesias chronic encephalomyelitis (ataxia, cognitive impairment, bladder dysfunction, cranial neuropathy 7th/8th nerve) MEDICAL MANAGEMENT: Drugs of choice First choice Doxycycline, 100mg, BID, PO (for penicillin allergy: 100mg, BID, IV) Amoxicillin, 500mg, TID, PO Ceftriaxone, 2000mg daily, IV Second choice Clarithromycin, 500mg, BID, PO (for penicillin allergic too) Azithromycin, 500mg, daily, PO and IV (for penicillin allergic too) Cefuroxime, 500mg, BID, PO o Cefotaxime, 2000mg at 8 interval, IV o Penicillin G, 5 million IU at 6 interval, IV Pediatric considerations Amoxicillin, 50mg/kg/day, PO Ceftriaxone, 75mg/kg/day, IV Penicillin G, 300,000IU/kg/day, IV NURSING MANAGEMENT: possible nursing diagnosis: Anxiety related to knowledge deficit of disease progression, treatment, and prevention nursing interventions: collaborative administer oral antibiotics or IV antibiotics fever is treated with antipyretics and cooling blankets independent manage fever with cool sponge baths and limited bedding maintain a cool temperature in the environment if possible maintain fatigue with promotion of rest and comfort ice bags are effective for headache for arthralgia: immobilization of painful joint, warm moist applications, and other pharmacologic measures to control pain assist patient with ROM exercises and activities to strengthen muscles and joints, being careful not to overexert the patient explain reason for mental status changes to patient and significant others, and answer any questions about the long-range complications of the disease prevention and health teachings teach patient strategies to prevent tick bites by wearing protective clothing, such as long sleeves and long pants (pant legs should be tucked inside of socks) in at-risk areas, full cover shoes (not sandals), and light-colored

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clothing to make identification of the tiny dark ticks easier vaccination of A recombinant vaccine against Lyme disease, based on the outer surface protein A (OspA) of B. burgdorferi (developed by GlaxoSmithKline) use chemical repellants (such as DEET), but note they may cause respiratory distress if too much is used, especially in children; they are only used in occasional hike in the woods stay on cleared paths and avoid wandering through grass and woods inspect the body daily with attention to the prime locations for bites if a tick is attached to the skin, remove it carefully to avoid causing it to regurgitate saliva and spirochetes into the host. Use tweezers close to skin to pull the head or jaw out of the skin. Clean the site with antiseptic agents. do not try to burn off the tick or smother it with kerosene/petroleum jelly emphasize that the client should finish the entire course of antibiotics even if he/she is asymptomatic

an old-age skin infection caused by an itch mite, which penetrates the skin, forming burrows (tiny thread-like projections ranging from 2-6mm long that appear as thin, gray, brown or red lines in affected areas ETIOLOGIC AGENT: Sarcoptes scabiei mite is yellowish-white and can barely be seen by unaided eye female parasite burrows beneath the epidermis to lay her eggs; this causes intense irritation the males are smaller and reside on the surface of the skin scabies occur worldwide and is predisposed by overcrowding and poor hygiene parasite does not survive more than 3-4days away from skin INCUBATION PERIOD: itch mite may burrow under the skin and lay ova within 24 hours PERIOD OF COMMUNICABILITY: for the entire period that the host is infected MODE OF TRANSMISSION: direct through an infected individual sleeping on an infested bed or wearing infested clothing anyone may become infected or re-infected infestation with mites may also result from contact with dogs, cats, and other small animals scabies on dogs is called mange; when canine or feline mites land on human skin, they fail to thrive and produce only a mild itch that eventually disappears

human scabies gets worse and worse unless the condition is treated PATHOLOGY/PATHOGENESIS: female mite burrows into the skin to lay her eggs with larvae emerge to copulate and re-burrow under the skin while any part of the body may be infected, the itch mite is commonly found in the interdigital spaces of the fingers or in warm folds in the skin areas of friction, such as the crotch, axillae, the belt line, around the nipple in women and the periumbilical region are sites of predilection external genitalia are most frequently involved in adult males lesions are slightly elevated, straight or twitching burrows, thread-like and are either brown or black in color; they measure 5-6mm in length severe inflammation, with the development of papules, blisters, pustules and crusts, may occur as a result of infection from scratching in infants, burrows may appear on the head and neck the disease may become fully developed in 2 weeks, the eggs hatch in about 6 days and the parasite grows very rapidly; it may persist for months or even years if not recognized or properly treated CLINICAL MANIFESTATIONS: invariably accompanied by itching, characteristically more pronounced at night, when the patient has retired, since the warmth of the skin has a stimulating effect on the parasite for the 1st week, the itch is subtle; it gradually becomes more intense that after a month or two, sleep becomes almost impossible secondary lesions like vesicles, papules, pustules, excoriations and crusts may be found on the affected side bacterial superinfection may result from constant excoriation of burrows ad papules DIAGNOSTIC EXAM: a drop of mineral oil placed over the burrow, followed by superficial scraping and examination of expressed material under a low-power microscope, may reveal mites, ova or mite feces MEDICAL MANAGEMENT: application of a pediculicide, such as permthrin cream or lindane lotion, as a thin layer over the entire skin surface, left on for 10 12 hrs Crotamiton cream is applied for 5 consecutive nights Neosporin ointment is rubbed onto the affected skin 4-5 times a day Eurax and Kwell lotion also prove effective in some patients Antihistamines, like diphenhydramine (Benadryl) can be useful in giving relief from the itch all clothes used before and during the treatment should be disinfected by dry cleaning or boiling NURSING MANAGEMENT: instruct to apply cream at bedtime, from the neck down to the toes, covering the entire body contaminated clothing or bedclothes should be drycleaned or boiled advise the patient to report any skin irritation

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suggest that family members and other close contacts of the patient be checked for possible symptoms and treated if necessary if the patient is hospitalized, practice good handwashing technique or use gloves while performing nursing procedure terminal disinfection should be carried out after the discharge of the patien POSSIBLE NURSING DIAGNOSES: alteration in comfort: itchiness impaired skin integrity altered role performance knowledge deficit social isolation body image disturbance PREVENTION: good personal hygiene avoid contact with infected persons all members of the household, including close contacts, should be treated after treatment, beddings and clothing worn next to skin should be properly laundered

three varieties of liceflattened, wingless insects commonly attack man, although some infest lower forms of animals and may become temporarily deposited on human hosts ETIOLOGIC AGENT: Pediculus humanos var. capitis (head lice) Pediculus humanos var. corporis (body lice) Phthirus pubis or pubice lice (crab lice) these lice feed on human blood and lay their eggs (nits) in body hair and clothing fibers after the nits hatch, the lice must feed within 24 hrs; otherwise, it will die they mature in about 2-3 weeks when a louse bites, it injects toxins into the skin that produces mild irritation and a purpuric spot repeated bites causes sensitization to the toxin, leading to more serious inflammation CLINICAL MANIFESTATIONS: head louse more common in females than in males; it infects more children than adults itching is the first and predominant symptom when neglected, varying degree of irritation, excoriation and crusting ensue and a foulsmelling mass consisting of matted hair, nits, ova, pus, crusts and pediculi is produced (plica plonica) body louse body louse is a gray-white active insect about 34mm long; the female is a little longer than the male both sexes are equipped with mouth parts adapted to sucking blood and legs adapted to grasping hair lifespan of the female is about 1 mo, during which she lays about 8-10 eggs/day, cementing

then firmly to the base of the hair to a fiber in the hosts clothing eggs (nits) are hatched in 8 days, releasing nymphs that require about 8 days to mature initial lesions are minute red spots spots swells , much like mosquito bite, and a secondary crust and excoriation is formed on the surrounding skin as a result of scratching head lice and body lice are closely related, interbreedable variants of the same species, despite their different habits crab lice a rounder, stubbier insect, 2-3mm long, more sedentary in its habits, translucent and difficult to see unless filled with blood from a recent meal 4 of its 6 legs terminate in its sturdy crab-like claws, hence the name, crab lice lifespan is 3-4 weeks and the female lays a maximum of 3 eggs a day, securely cementing them to the base of the hair where they incubate 6-8 days before hatching unusual, persistent itching in the pubic region and in the other affected areas is the chief symptom because they are difficult to see, their presence may be unsuspected, until nits become apparent on the hair, or until the louse becomes detached from its feeding ground and is seen on the fingers used for scratching the head or on the bed sheet grayish pigmented spots (maculae caeuleae) are found on the surfaces of the inner thighs or the abdomen and are of varying size from that of a pea to that of a small coin MEDICAL MANAGEMENTS: head louse dusting the scalp with 1% malathion powder is a reliable and convenient method thoroughly massage gamma-benzene hexachloride shampoo in the scalp for 4 mins, then rinse body louse launder (dry clean) or boil the clothing and beddings good body hygiene must be observed always crab lice apply Kwell or Gamene (lindane) cream or lotion wet the affected area and apply a sufficient amount of shampoo to cover it add a small amount of water from time to time, working the hair and skin thoroughly until a good lather forms for 4 mins rinse thoroughly and dry briskly rub crotamiton (Eurax, Geigy) onto the affected area repeat the application of crotamiton after 1 week simultaneously treat a person who has had sexual contact with the patient remove remaining nits mechanically

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infestations in the eyelids of children can be

treated with yellow oxide of mercury; apply it to the eyelids twice daily for a few days, after which lice and nits can be tweezed out easily COMPLICATIONS: pigmentation and honey crust of secondary pyoderma Vagabondia combination of extensive excoriation, hypo- and hyperpigmentation associated with lichenification enlargement of the nuchal and cervical nodes, with febrile episodes that can lead to micrococcal infection blepharitis POSSIBLE NURSING DIAGNOSES: alteration in comfort impaired skin integrity body image disturbance risk for infection sleep disturbance PREVENTION: good personal hygiene avoiding contact with persons suffering from pediculosis


acute viral disease manifested by the swelling of one or both parotid glands, with occasional involvement of other glandular structures, particularly the testes in males ETIOLOGIC AGENT: Paramyxovirus group usually found in the saliva of an infected person man is the only natural reservoir INCUBATION PERIOD: 14-25 days (average is 18 days) PERIOD OF COMMUNICABILITY: 6 days before and 9 days after the onset of parotid gland swelling; the 48-hour period immediately preceding the onset of swelling is considered the time of highest communicability PATHOLOGY: mumps is a generalized disease that affects glandular structures, as well as renal and nervous tissues virus gains entry into the system through droplet infection and multiplies in the URT and localizes in the salivary glands the glands become edematous and the ducts are obstructed because of the swelling of the epithelial lining on some occasions, necrosis may occur in the acinar cells CLINICAL MANIFESTATIONS: first symptoms of mumps may be sudden headache, earache, loss of appetite, fever and swelling of parotid glands, which are located in front of and below the ears pain is r/t the extent of swelling of the gland, which usually reaches its peak in about 2 days and continuous for 7-10 days

temperature usually remains moderately elevated, o but may reach 40 C during the acute stage of the disease one gland may be affected at first; 1-3 days later, the other side may become involved occasionally, enlargement of the glands may be the only symptom noted COMPLICATIONS: orchitis (most notorious complication) testicular involvement usually occurs several days after the onset of parotid swelling. Orchitis is often accompanied by elevation of temperature. Pain is often excruciating and is aggravated by movement. The testes are swollen and are tender to palpate. oophiritis may occur in women and manifests pain and tenderness of the abdomen mastitis has also been reported to accompany mumps CNS involvement has been reported to complicate mumps as manifested by headache, elevation of CS protein concentration and cell count changes nuchal rigidity associated with lethargy, headache, convulsions or delirium deafness as a result of mumps has been reviewed and studied meningoencephalitis (common complications of mumps) pancreatitis manifests as epigastric pain, vomiting, chills, and prostration transverse myelitis, ataxia, thrombocytopenia, myocarditis, arthritis, nephritis (rare complications) DIAGNOSTIC EXAM: compliment fixation test shows a presumptive evidence of infection hemoagglutination inhibition test is used to determine immune status neutralization test determines immunity to mumps viral culture or the isolation of virus from the pharynx a few days before and at least 5 days after parotid swelling is done serum amylase determination is the most useful test in making an early presumptive diagnosis for mumps MEDICAL MANAGEMENT: anti-viral drugs relief of pain from parotid swelling can be afforded by the application of a hot or cold pack, whichever is preferred by the patient NURSING MANAGEMENT: medical aseptic protective care patient should be cared for in a singleoccupancy room susceptible individuals must use masks and must wash hands regularly terminal disinfection is desirable oral care and overall personal hygiene are a must

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general management of the disease bed rest is encouraged by some physicians to avoid complications diversion activities are recommended for the less ill patient diet no restriction of food is necessary, except during the acute stage, when the patient may find it very difficult and painful to chew and swallow soft and semisolid food are easily managed acidic foods, like fruit juices, may increase discomfort POSIBLE NURSING DIAGNOSES: social isolation pain body image disturbance impaired swallowing altered nutrition: less than body requirements knowledge deficit potential for infection PREVENTION: active immunization (MMR) reporting of cases to health authorities isolation of patient

after initial inhalation of contaminated respiratory droplets viral proliferation in regional lymph nodes of the upper respiratory tract a second round of viral replication occurs in the bodys internal organs, the liver and the spleen this second viremia is characterized by diffused viral invasion of capillary endothelial cells and the epidermis VZV infection of cells of the Malphigian layer produces both intercellular and intracellular edema resulting in the characteristic vesicle

acute and highly contagious disease of viral etiology that is characterized by vesicular eruptions on the skin and mucous membrane with mild constitutional symptoms ETIOLOGIC AGENT: Herpesvirus varicellae DNA-containing virus human beings are the only source of infection this is closely related or identical to herpes zoster virus INCUBATION PERIOD: 10 21 days or may be prolonged after passive immunization against chickenpox MODE OF TRANSMISSION: direct contact with a patient who sheds the virus from the vesicles indirect contact, through linens or fomites airborne or spread by aerosolized droplets from the nasopharynx of ill individuals high viral titers are found in the vesicles of chickenpox; thus, viral transmission may also occur through direct contact with these vesicles, although the risk is lower following primary infection there is usually lifelong protective immunity from further episodes of chickenpox PERIOD OF COMMUNICABILITY: a day before eruption of the first lesion up to about 5 days after the disappearance of the last crop DIAGNOSTIC EXAM: determination of the V-Z virus through the complement fixation test determination of the V-Z virus through electron microscopic examination of vesicular field

CLINICAL MANIFESTATIONS: pre-eruptive manifestations are mild fever and malaise eruptive stage rash starts on the trunk (unexposed area), then spreads to other parts of the body initial lesions are distinctively red papules whose contents become milky and pus-like within 4 days in adults and bigger children, the lesions are more widespread and more severe rapid progression so that transition is completed in 6-8 hours vesicular lesions are very pruritic all stages are present simultaneously before all are covered with scabs, leading to the appearance known celestial map the stages are characterized as follows: macule is a lesion that is not elevated above the skin surface papule is a lesion that is elevated above the skin surface with a diameter of about 3mm vesicle is a pop-like eruption filled with fluid; the thin-walled vesicle easily bursts and dries up in 3-5 days pustule is a vesicle that is infected or filled with pus; if the lesion becomes infected the scar may be big and wide crust is a scab or eschar; this is a secondary lesion caused by the secretion of vesicle drying on the skin; the scars are superficial, depigmented and take time to fade out COMPLICATIONS: rarely fatal, although it is generally more severe in adults than in children pregnant women and those with a suppressed immune system are the highest risk of serious complications the most common late complication of chicken pox is shingles, caused by reactivation of the varicella zoster virus decades after the initial episode of chickenpox secondary infection of the lesions furuncles, cellulitis, skin abscess, erysipelas pneumonia sepsis

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MEDICAL MANAGEMENT: oral acyclovir 800 mg 3x/day for 5 days must also be given oral antihistamine can be taken to symptomatic pruritus calamine lotion eases itchiness salicylates must not be given antipyretic might be given for fever antihistamine must be given NURSING MANAGEMENT: respiratory isolation is a must until all vesicles have crusted prevent secondary infection of the skin lesions through hygiene care of patient attention should be given to nasopharyngeal secretions and discharges; linens must be disinfected under the sunlight or through boiling cut fingernails short and wash hands more often to minimize bacterial infections that may be introduced by scratching a child must wear mittens provide activities to keep child occupied to lessen pruritus observe oral and nasal care as rashes may appear in the buccal cavity PREVENTIVE MEASURES: active immunization with live, attenuated varicella vaccine is necessary avoid exposure as much as possible to infected persons patient must be isolated to avoid transmission of organism to other members of the family

acute bacterial disease that can infect the body in two areas: the throat (respiratory diphtheria) and the skin (skin or cutaneous diphtheria) ETIOLOGIC AGENT: Corynebacterium diptheriae Klebs-Leoffler bacillus toxin-producing organism that manufactures an exotoxin which is responsible for major pathologic changes gram-positive, non-sporulating, and generally aeobic the bacilli invade the superficial tissues with very limited extension beyond the mucous membrane, but soluble toxin is capable of producing severe fatal sequelae unstable and easily destroyed by light, heat, and aging capable of damaging muscles and especially the kidneys, liver, and cardiac nerves, and other tissues 3 strains of organisms Gravis (severe) is the strain that produces the most severe and greatest number of fatal cases in Europe Mitis (mild) is the strain that produces lesions extending to the larynx and lungs but it is rarely a cause of death

Intermedius (intermediate) is related to gravis but results in a tendency to bleed INCUBATION PERIOD: 2-5 days PERIOD OF COMMUNICABILITY: varies; more than 2-4 weeks in untreated patients and 1-2 days in treated patients SOURCE OF INFECTION: discharges of nose, pharynx, and eyes or lesions on other parts of the body of infected persons MODE OF TRANSMISSION: contact with a patient or a carrier, or with articles soiled with discharges of infected persons PREDISPOSING FACTORS: an operation in an area of the nose and throat economic status lack of proper nutrition overcrowding PATHOGENESIS/PATHOLOGY: toxin is absorbed into the mucous membranes and causes destruction of the epithelium and superficial inflammatory response takes place necrotic epithelium becomes embedded in exuding, fibrin so that a grayish pseudomembrane is formed by leukocytes, fibrin, and necrotic tissues; microorganisms that adhere to the underlying tissues leave a raw bleeding when detached; the size of the pseudomembrane reflects the amount of toxin produced (the larger the pseudomembrane, more toxins are present in the blood stream and in the tissues) the microorganisms are commonly seen over the tonsils, pharynx, or larynx so that any attempt to remove the pseudomembrane, exposes and tears the capillaries and results in bleeding the bacilli within the pseudomembrane continue to actively produce toxins that result in distant damage, particularly parenchmatous degeneration, fatty infiltration, and necrosis in the muscles of the heart and in the liver, kidney and adrenals, sometimes accompanied by gross hemorrhage toxins also produce nerve damage, resulting in paralysis of the soft palate, eye muscles, or extremities TYPES: Nasal with foul-smelling serosanguinous secretions from the nose Tonsilar which has a low fatality rate; the lesions are confined to the tonsils but tend to spread over the pillars and into the soft palate and uvula Facial Nasopharyngeal (more severe type) cervical lymph nodes are swollen nose tissues are edematous, resulting in the appearance of a bulls neck marked degree of toxemia breath is usually fetid (nauseating) Laryngeal most commonly found in children ages 2-5 years old considered as the most severe and most fatal type d/t anatomical reason

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respiration is increased because less air is

brought to the lungs d/t the narrowing of the air passages moderate hoarseness, the voice is diminished until it is finally absent Wound o cutaneous diptheria affects the mucous membrane and any absent CLINICAL MANIFESTATIONS: onset of the disease is insidious, marked by a feeling of fatigue, malaise, slight sore throat, and elevation o of temperature usually not exceeding 38 C inflammatory reaction is initiated by the body; exudates consisting of leukocytes, RBC, and necrotic tissues begin to form the exudates forming the membrane are grayish in appearance as they begin to form; as they thicken, they become dull white cervical adenitis with tenderness of the glands occurs there is the presence of body malaise, weakness and apathy, with a rapid pulse rate that becomes disproportionate to the low-grade fever in severe cases, the entire neck becomes swollen, with edema extending to the chest swelling of the neck was given the name, bulls neck form if the membrane forms in the larynx, it may extend to the trachea, resulting in respiratory problem, in which case, tracheostomy may be necessary after administration of the antitoxin, the membrane beings to curl at the edges, separate and flake off in large pieces other common symptoms if respiratory diphtheria include: breathing difficulty husky voice HR stridor (a shrill-breathing sound heard on inspiration) nasal drainage/secretions (serosanguinous with a foul smell) swelling of the palate low-grade fever symptoms of skin or cutaneous diphtheria are usually milder and may include yellow spots or sores (similar to impetigo) on the skin COMPLICATIONS: myocarditis caused by action of diphtheria toxin on the heart muscles polyneuritis that includes paralysis of the soft palate, the ciliary muscles of the eyes, pharynx, larynx or extremities airway obstruction may lead to death through asphyxiation (suffocation) cervical adenitis otitis media bronchopneumonia DIAGNOSTIC EXAM: swab from nose and throat or other suspected lesions Virulence test Schick test Molony test

Leoffler test MEDICAL MANAGEMENT: overall health and medical history extent of the condition tolerance for specific medications, procedures and therapies Penicillin is usually effective in treating respiratory diphtheria before it releases toxins in the blood antitoxin can be given in combination with Penicillin skin testing is necessary before administration of anti-toxin fractional doses are given in positive cases, with the following schedule 0.05 ml (1:20 dilution) = SQ 0.05 ml (1:10 dilution) = SQ 0.10 ml undiluted = SQ 0.20 ml undiluted = SQ 0.50 ml undiluted = IM 0.10 ml undiluted = IV the above doses are given at 15-minute intervals if no reaction is noted Erythromycin, 40mg/kg bw in 4 doses x 7-10 days supportive therapy maintenance of adequate nutrition maintenance of adequate fluid and electrolyte balance bed rest oxygen inhalation in the presence of laryngeal obstruction, tracheostomy and is usually done NURSING MANAGEMENT: patient must be advised to take full bed rest for at least 2 weeks; patient must not be permitted to bathe by himself; the patient must avoid exertion during defecation in order to conserve energy and decrease cardiac workload soft diet is recommended; small, frequent feedings are advised patient must be encouraged to drink fruit juices rich in Vitamin C to maintain the alkalinity of the blood and his/her resistance ice collar must be applied to the neck nose and throat must be taken care of POSSIBLE NURSING DIAGNOSES: ineffective airway clearance risk for activity intolerance poor tissue perfusion fear anxiety PREVENTION: cases of diphtheria must be mandatorily reported patients should be isolated for a minimum of 14 days from the onset of the disease until 3 cultures from the nose and throat are reported negative patient should avoid contact with children and refrain from handling food until bacteriologic examination of cultures is reported negative children under 5 years old should be given booster doses of diphtheria tetanus vaccine DPT immunization of babies is mandatory

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WHO SHOULD AND SHOULD NOT RECEIVE THE VACCINE: children with moderate or severe fever can be vaccinated as soon as they have recovered children with minor illnesses, such as URTI, with or without fever, can be vaccinated persons on immunosuppressive therapy given for cancer or other treatments may not develop the same response as a normal person; therefore, if immunosuppressive therapy is to be d//c shortly, it is reasonable to defer immunization until the patient has been off the therapy for at least 1 month; if the therapy is to be d/c, then proceed with the immunization those who are infected with HIV may receive a diphtheria toxoid-containing immunization, such as DPT or DT persons who have experienced an immediate lifethreatening allergic reaction, requiring medical attention after a dose of diphtheria toxoidcontaining vaccine, should not receive additional doses of the vaccine persons who develop encephalitis within 7 days of DPT immunization should not receive additional immunizations containing the pertussis vaccine; the immunization series should be completed using the DT vaccine; it may be desirable, however, to postpone further doses of diphtheria-tetanus doses until the childs neurologic status becomes clear a family history of convulsions or other CNS disorder does not justify withholding diphtheria immunization; decision not to immunize should be made by the doctor who is familiar with the patients history and circumstances

acute, contagious and exanthematous (skin rashes) disease that usually affects children who are susceptible to URTI this may be one of the most common and most serious of all childhood diseases ETIOLOGIC AGENT: filtrable virus genus Morbilivirus of the family paramyxoviridae is the agent of measles rapidly inactivated by heat, UV light, and extreme degrees of acidity and alkalinity INCUBATION PERIOD: 10-12 days (longest is 20 days and the shortest is 8 days) a single attack conveys lifelong immunity PERIOD OF COMMUNICABILITY: 9-10 days from the beginning of the prodromal syndromes to the fading of the rash 4 days before and 5 days after the appearance of rashes most communicable at the height of the rash SOURCES OF INFECTION: patients blood secretions from the eyes, nose and throat MODE OF TRANSMISSION: direct contact with droplets spread through coughing/sneezing

indirectly through articles or fomites freshly contaminated with respiratory secretions of infected patients PATHOGNOMONIC SIGN: Kopliks spots inflammatory lesions of the buccal mucous glands with superficial necrosis they appear on the mucosa of the inner cheek opposite to the second molars, or near the junction of the gum and the inner cheek usually appear 1-2 days before the measles rash CLINICAL MANIFESTATIONS: Pre-eruptive stage fever catarrhal symptoms (rhinitis, conjunctivitis, photophobia, coryza) respiratory symptoms start from common colds to persistent coughing Enanthem sign (Kopliks spot, Stimsons line) Eruptive stage a maculo-papular rash usually starts to appear late on the 4th day maculo-papular rash appears first on the cheeks, bridge of the nose, temples, earlobes or along the hairline rash is fully developed by the end of the 2nd day and all symptoms are at their most severe at this time high-grade fever comes on and off anorexia and irritability abdominal tympanism, pruritus and lethargy throat is red and often extremely sore fever subsides, coughing may diminish, but more often it hangs on for a week or two and becomes looser and less metalic Stage of convalescence rashes fade away in the same manner as they erupted when fever subsides as rashes start to fade when the rashes have faded, desquamation (peeling of skin) begins symptoms subside and appetite is restored DIAGNOSTIC EXAM: nose and throat swab urinalysis blood exams (CBC, leucopenia, leukocytes) complement fixation or hemogglutinin test MEDICAL MANAGEMENT: anti-viral drugs (Isoprinosine) antibiotics if with complication supportive therapy (oxygen inhalation, IV fluids) COMPLICATIONS: bronchopneumonia otitis media pneumonia/bronchitis nephritis encephalitis; encephalomyelitis blindness (seldom) UNFAVORABLE SIGNALS: violent onset with high-grade fever fading eruption with rising fever

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hemorrhagic or black measles persistence of fever for 10 days or more slight eruptions accompanied by severe symptoms, especially those of encephalitis NURSING MANAGEMENT: isolation of the patient is necessary (the room must be quiet, well-ventilated, subdued light) control of the patients high temperature with warm or tepid sponges skin care is utmost importance; the patient should have a daily cleansing bed bath; the water should be comfortably warm oral and nasal hygiene is a very important aspect of the nursing care of a patient with measles care of the eyes is necessary; the patient is sensitive to light; position the patient in such a way that direct glare of light is avoided; keep eyes free from secretions care of the ears is also important; it is the responsibility of the nurse to be on the alert for any signs of early mastoid infections daily elimination is important; this can be accomplished with a mild laxative, as prescribed by physician during the febrile stage, limit the diet to fruit juices, milk, and water; if the patient is vomiting, give frequent, small servings of iced juices the patients position should be changes every 3-4 hrs Penicillin or other prescribed meds are usually given in cases where there is complication POSSIBLE NURSING DIAGNOSES: ineffective airway clearance altered nutrition: less than body requirements impaired skin integrity activity intolerance knowledge deficit body image disturbance alteration in comfort sleep pattern disturbance altered body temperature PREVENTION: immunization anti-measles at the age of 9 months, as a single dose; the first dose of the MMR vaccine is given at 15 months old, with the 2nd dose at 11-12 years old; measles vaccine should not be given to pregnant women or to persons with active TB, leukemia or lymphoma, or those with depressed immune system avoid overcrowded places to lessen the chances of contracting the virus


acute contagious disease characterized by mild constitutional symptoms and a rose-colored macular eruption which sometimes resemble measles and at other times, scarlet fever causes mild, feverish illness associated with rashes and aches in joints; it has teratogenic effect on the fetus rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40; the older the person is, the more severe the symptoms

are likely to be; up to 1/3 of older girls/women experience joint pain or arthritic type symptoms with rubella ETIOLOGIC AGENT: Rubella virus family Togaviridae genus -- Rubivirus INCUBATION PERIOD: 14-21 days from exposure to the appearance of rash PERIOD OF COMMUNICABILITY: 1 week before and 4 days after the onset of the rash, but is at its worst when the rash is at its peak highly communicable with infants with congenital rubella may shed virus for months after birth MODE OF TRANSMISSION: direct contact with nasopharyngeal secretions air droplets transplacental transmission in congenital rubella infants with congenital rubella she large quantities of virus through their pharyngeal secretions and urine, which serve as sources of infection to other contacts CLINICAL MANIFESTATIONS: Prodromal period low-grade fever headache malaise mild coryza conjunctivitis post-auricular, sub-occipital, and posterior cervical lymphadenopathy which occurs on the 3rd-5th days after onset Eruptive period a pinkish rash on the soft palate (Forchheimers spot), an exanthematous rash that appears first on the face, spreading to the neck, the arms, trunk, and legs eruption appears after the onset of adenopathy children usually present less or no constitutional symptoms the rash may last for 1-5 days and leaves no pigmentation nor desquamation testicular pain in young adults transient polyarthralgia and polyarthritis may occur in adults and occasionally in children MEDICAL MANAGEMENT: very little treatment is necessary; treatment is essentially asymptomatic COMPLICATIONS: encephalitis neuritis arthritis arthralgia Rubella syndrome microencephaly mental retardation cataract deaf-mutism heart disease RISK OF CONGENITAL MALFORMATION: 100% when maternal infection occurs on the 1st trimester of pregnancy or 1st month of gestation

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4% -- in the 2nd and 3rd trimester of pregnancy 90% of congenital rubella cases excrete the virus at birth and are therefore infectious 10% -- the virus remains contagious until the first year of age of the infected child PATHOGENESIS:
maternal viremia placental infection fetal viremia disseminated infection involving many fetal organs

prevent spread of infection by minimizing contact with visitors


sexual-transmitted bacterial disease involving the mucosal lining of the genitourinary tract, the rectum, and pharynx ETIOLOGIC AGENT: Neisseria gonorrhoeae or gonococcus gram negative coccus found in pairs coccus is non-spore former and non-motile fragile and does not survive long outside the body readily killed by drying, sunlight, and UV light may be killed by ordinary disinfectants INCUBATION PERIOD: 3-21 days and averages from 3-5 days PERIOD OF COMMUNICABILITY: varies; as long as the organisms are present in secretions and discharges MODE OF TRANSMISSION: contact with exudates from the mucous membranes of infected persons, usually as a result of a sexual activity may occur in utero upon the rupture of membranes, as observed in infants delivered by CS after the membrane ruptures direct contact with contaminated vaginal secretions of the mother as the baby comes out of the birth canal may be acquired through sexual contact (orogenital, anogenital) between opposite sexes, as well of the same sex fomites PATHOLOGY: after infection, gonococci become adherent to the urethral epithelium penetration of the mucosa usually elicits an acute inflammatory response consisting mainly of polymorphonuclear leukocytes in the submucosa inflammatory edema of the gland ducts or plugs of debrit obstruct drainage to form microabscesses that may coalesce to form large abscesses infection tends to spread along mucosal surfaces and may involve the fallopian tubes and the endometrium and eventually enter the peritoneal cavity of women scarring from this abscess formation or total or tubal involvement may lead to structures and sterility similar mechanism, epididymitis, and, therefore, possible sterility may occur in men CLINICAL MANIFESTATIONS: Females burning sensation and frequent urination yellowish purulent vaginal discharge redness and swelling of the genitals burning sensation and itching of the vaginal area urinary frequency and pain on urination urethritis or cervicitis occurs initially a few days after exposure

CLINICAL MANIFESTATIONS: Classical congenital rubella syndrome intrauterine growth retardation; infants has low birth weight all manifestations of congenital rubella syndrome thrombocytopenic purpura known as blueberry muffin skin lethargy and hypothermia Intrauterine infection may result in spontaneous abortion birth of a live child who may have 1 or multiple birth anomalies such as: cleft palate, hare lip, talipes, and eruption of teeth cardiac defects (PDA, aterial septal defect) eye defects (glaucoma, retinopathy, micrpthalmia, unequal-shaped eyeballs) ear defects (deafness usually bilateral, abnormally-shaped ears) neurologic (microcephaly, mental retardation, psychomotor retardation, behavioral disturbances, vasomotor instability) NURSING MANAGEMENT: patient isolation advise patient to rest in bed until fever subsides room must be darkened to avoid photophobia take a mild liquid but nourishing diet eyes should be irrigated with warm normal saline to relieve irritation ears must be take care of; do not apply heat or cold compress unless ordered good ventilation is necessary spread of infection must be prevented occurrence of complications must also be prevented encourage OFI POSSIBLE NURSING DIAGNOSES: impaired social interaction knowledge deficit impaired physical mobility impaired skin integrity pain high risk for infection PREVENTION: administration of live attenuated vaccine (MMR) pregnant women should avoid exposure to patients infected with the rubella virus administration of immune serum globulin 1 week after exposure to rubella

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endometritis salpingitis or pelvic perotinitis are

symptoms of uterine invasion which may lead to infertility; there is the presence of early signs of pelvic infection like fever, n/v, and abdominal pain/tenderness pregnant women with gonorrhea may infect the eye of her baby during the tenderness pregnant women with gonorrhea may infect the eye of her baby during the passage through the birth canal Males after 3-6 days of incubation period, the ff occurs: dysuria with purulent discharge (gleet) from the urethera 2-7 days after exposure rectal infection is common in homosexuals inflammation of the urethra can cause strictures which can prevent the passage of the urine prostatitis urethritis pelvic pain and fever OTHER CLINICAL FEATURES VARY ACCORDING TO SITE INVOLVED: urethra dysuria urinary frequenc and incontinence purulent discharge itching red and edematous meatus vulva occasional itching burning and pain d/t exudates from the adjacent infected area vulval symptoms are more severe before puberty and after menopause vagina engorgement, redness and swelling profuse purulent discharge pelvis severe pelvic and lower abdominal pain muscle rigidity, tenderness and abdominal distention tachycardia may develop in patients with PID and salpingitis liver RUQ pain other possible symptoms include pharyngitis, tonsillitis, rectal burning COMPLICATIONS: sterility and pelvic inflammatory disease in women epididymitis arthritis endocarditis conjunctivitis meningitis DIAGNOSTIC EXAM: in females culture of specimen takes from the cervix and anal canal(inoculation of specimen on Thayer-Martin medium; the medium contains antibiotic that inhibits growth of microorganisms) in males graim stain

MEDICAL MANAGEMENT: for uncomplicated gonorrhea in adults Ceftriaxone 125-250mg, IM, single dose; Doxycycline 100mg PO BID for 7 days for pregnant womenCeftriaxone 125-250mg, IM, single dose, plus erythromycin, 500mg orally for 7 days Aqueous procaine penicillin4M units injected IM, after a negative skin test recommended initial regimen for disseminated gonococcal infection in adults and adolescents is 1g o Ceftiaxone IM/IV q24 , or for patients allergic to o beta-lactam antibioticsm 2g spectinomycin Im q12 o all regimen should be continued for 24-48 after improvement begins, then therapy may be switched to the following regimens to complete one full week of antimicrobial therapy 400mg Cefixime PO BID or 500mg Ciprofloxacin PO BID; Ciprofloxacin is contraindicated for children, adolescents, pregnant and lactating women treatment for gonococcal conjunctivitis requires 1g single dose of Ceftriaxone IM and irrigation of infected eye with PNSS NURSING MANAGEMENT: before treatment, ask patient whether he/she has drug sensitivities and watch closely for adverse effects during therapy explain to the patient that until cultures prove negative, he/she is still infectious and can transmit gonococcal infection practice standard precautions all information concerning the patient is confidential; there should be no discussion concerning the patient and the laboratory reports the patient should be isolated until he/she recovers from the disease for a patient with gonococcal arthritis, apply moist heat to relieve pain on the affected site infant born to mothers positive for gonorrhea should be instilled with 1% silver nitrate or any recommended ophthalmic prophylaxis onto both eyes at the time of birth report all gonorrheal cases to health authorities, and for gonorrhea in children to child abuse authorities encourage patient to inform sexual contacts so that they can seek treatment; advice them to refrain from sexual intercourse until treatment is completed SIGNS OF GONOCOCCAL OPTHALMIA NEONATORIUM: lid edema bilateral conjunctival edema abundant purulent discharge 2-3 days after birth untreated gonococcal conjunctivitis can progress to corneal ulceration and blindness POSSIBLE NURSING DIAGNOSES: altered sexuality pattern social isolation knowledge deficit altered urinary isolation risk for infection

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PREVENTION: sex education, not only in schools, but also in the community, must emphasize the mode of transmission and the source of the infection case finding, contact tracing incidence of gonorrhea must be reported so that health authorities may be notified and contacts can be treated

chronic, infectious, sexually transmitted disease that usually begins in the mucous membranes and quickly becomes systemic caused by a spirochete and is acquired through sexual contact; it may also be congenital in nature ETIOLOGIC AGENT: Treponema pallidum has no other host but man from a fresh smear taken from a lesion, it appears as a shiny, twirling thread twisting its way in a wave-like corkscrew motion through the debris in the smear believed that the spirochete can pass through the mucosa even though a crack on its surface may not be visible at the site of entry organism is also able to pass through the placenta and infect the developing fetus within the body of a syphilitic mother spirochete does not withstand drying, but withstands considerable temperature variation based on studies, the organism has been found alive in a drinking glass a half-hour after the glass has been rinsed with cold water SOURCES OF INFECTION: discharges from obvious or concealed lesions of the skin or mucous membranes semen, blood, tears and urine of infected persons mucous discharges from the nose, eyes, genital tract or bowels surface lesions contain spirochetes in very high numbers INCUBATION PERIOD: 10-90 days (average of 3 weeks) PERIOD OF COMMUNICABILITY: variable and indefinite MODE OF TRANSMISSION: direct transmission which occurs through any kind of intimate contact with an infected person; mucus or glandular secretions from an infected individual is transmitted to the skin or mucous surface of any one with whom he comes in contact indirect contact (articles from freshly soiled with discharges or blood containing the organism) congenitally through the placenta of a syphilitic mother accidentally, the disease can be transmitted from a syphilitic baby to a wet nurse or to anyone carelessly handling diapers

CLINICAL MANIFESTATIONS: Primary syphilis starts with one/more chancres (painless ulceration) that erupt in the genitalia, anus, nipples, tonsils or eyelids usually painless, start as papule and then erode endurated, raised edges and clear bases disappear after 3-6 weeks even without treatment usually associated with lymphadenopathy that is either unilateral or bilateral in women, it is often overlooked because they often develop on internal surfaces, such as cervix and vaginal wall Secondary syphilis development of mucocutaneous lesions and generalized lymphadenopathy signifies the onset of secondary phase, which usually occurs from a few days to about 8 weeks after the onset of the initial chancre rash can be macular, papular, postular or nodular lesions are of a uniform size, well-defined and generalized macules often erupt between rolls of fat on the trunk and on the arms, palms, soles, face and scalp in warm, moist areas of the body, such as the perineum, vulva and rolls of fats in the scrotum, the lesions enlarge and erode, producing highly contaminated pink or grayish-white lesions (condylomata lata) mild constitutional symptoms in the 2nd stage (headache, anorexia, malaise, weight loss, n/v, sore throat, and possibly slight fever) alopecia may occur, but it is temporary nails become brittled and pitted Latent syphilis no clinical symptoms occur in latent syphilis test, but a serologic test will prove reactive approximately 2/3 of patients remain asymptomatic until death Late syphilis considered as destructive but non-infectious stage late syphilis has 3 subtypes: late, benign syphilis develops between 1-10 years after the infection typical lesion is the gumma (chronic, superficial nodule, or a deep granulomatous lesion that is solitary, asymmetric, painless and endurated) may appear on skin, bones, mucous membranes, upper respiratory tract, liver or stomach gummas can be found in any bone, particulary the long bones of the legs late syphilis involves the liver; can cause epigastric pain, tenderness, a enlarged spleen and anemia

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if it affects the upper respiratory tract, it can cause perforation of the nasal septum or the palate in severe cases, the disease causes the destruction of bones and other organs, which may lead to death cardiovascular syphilis develops about 10 years after the initial infection may appear asymptomatic but may suffer from aortic regurgitation and aneurysm Congenital syphilis once treponeme enters the fetal circulation, dissemination to all the tissues occur at one; the treponeme multiplies and infects many organs fetus may be overwhelmed by the infection and die; fetus will then be expelled by the uterus, leading to either miscarriage or stillbirth, depending on the stage of pregnancy syphilitic stillborn may have a macerated appearance, with a collapsed skull and a protuberant (unusual prominent convexity) abdomen skin is of a livid red color; on its surface may be seen a number of bullae filled with hemorrhagic fluid on autopsy, the spleen and the liver are found to be enlarged, with intense pancreatitis and thickening of the intestines if treponemal infection does not prove fatal, it may still show alterations in fetal development at various stages CLINICAL MANIFESTATIONS: Early congenital syphilis lesions of the skin and mucous membranes bullous rash, sometimes called syphilitic pemphigus, may be present at birth; the bullae are approximately 3 cm in diameter, rounded and contain serous to seropurulent fluid swarming with treponemes loss of weight may produce wrinkling of the skin especially on the face, giving what has been called the old man look syphilitic papules may involve the skin at the base of the nails and extend to the nail beds; the nails may be loosened and shed (syphilitic nonychia) mucous patches may also be found on the lips, mouth, throat and nasal passages; nasal discharges may be slightly mucoid or abundant and mucopurulent or purulent; sometimes they are blood-stained and contain large numbers of T. pallidum, rendering them highly infectious liver and spleen infants abdomen is protuberant, owing to the enlargement of the liver and spleen; liver cells tend to be immature and imperfectly formed; hepatic insufficiency results in the failure of protein metabolism

Late congenital syphilis interstitial keratitis is the most common late lesion may begin at any age from 4-30 years or even later appears as circumcorneal vascularization of the sclera followed by vascular infiltration extending from the sclera into the deep layers of the cornea; it usually affects one eye at first and eventually affects the other eye from a few weeks to many years severe lesions are likely to cause corneal scarring, giving rise to opacities which may cause slight impairment of vision or even complete blindness COMPLICATIONS: severe damage to several organs and the nervous system heart disease, insanity and brain damage severe illness or death in newborn DIAGNOSTIC EXAM: dark field illumination is the most effective if moist lesions are present fluorescent treponemal antibody absorption test, in which the specimen consists of exudates from a lesion VDRL slide test and rapid plasma reagent test CSF analysis MEDICAL MANAGEMENT: for early syphilis, treatment consists of the administration of Penicillin G benzathine IM (2-4M units) syphilis of more than a year duration is treated with Penicillin G benzathine, 2.4M units/wk for 3 weeks non-pregnant patients who develop an allergy to Penicillin may be treated with oral tetracycline or doxycycline for 15 days for early syphilis and for 30 days for late infections; tetracycline is contraindicated in pregnant women patients who are receiving treatment must abstain from sexual contact until the infection is completely healed NURSING MANAGEMENT: stress to the client the importance of completing the treatment even after symptoms subside instruct infected individuals to inform their partner that they should be tested and if necessary, treated practice universal precaution in secondary syphilis, keep the lesions dry as much as possible; if they are draining, dispose contaminated materials properly in CV syphilis, check for signs of cardiac output ( sensorium and urine output and hypoxia) and pulmonary congestion in neurosyphilis, regularly check the level of consciousness, mood and coherence; WOF signs of ataxia encourage the patient to undergo VDRL testing after 3,6,12, and 24 months to detect any possible relapse

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be sure to report all cases of syphilis to local public health authorities; refer to the patient and his/her partners for HIV testing POSSIBLE NURSING DIAGNOSES: altered sexual pattern self-esteem disturbance social isolation knowledge deficit impaired skin integrity anxiety PREVENTION: report cases to DOH control prostitution require sex workers to have regular check-ups proper sex education should be given in early life at home, in schools and in the community look for cases of syphilis infection contact tracing



AIDS it is acquired, which means it is neither hereditary nor inborn. It involves an immune deficiency. When a persons immune system breaks down, he/she becomes susceptible to many infections, which eventually lead to death. It is a syndrome, a combination of signs and symptoms that form a distinct clinical picture of disorder. HIV virus which causes AIDS. It is a retrovirus belonging to the family of lentiviruses, which are sometimes called slow viruses. They are described as such because the time between infection and the appearance of symptoms tends to be much longer, allowing greater opportunity for these microorganisms to be transmitted to other hosts. The period between infection and appearance of AIDS can take from 7-12 years. PATHOPHYSIOLOGY: human beings produce antibodies against specific infections. When HIV infection takes place, anti-HIV antibodies are produced but they do not become detectable immediately (window effect). In some cases however, antibodies to HIV become detectable 4-6 weeks after infection. When HIV is in circulation, it invades several types of cellsthe lymphocytes, macrophages, Langerhans cells, and neurons within the CNS HIV attacks the bodys immune system. The organism attaches to a protein molecule called CD4, which is found on the surface of T4 cells. Once the virus enters the T4, it inserts its genetic materials into the T4 cells nucleus, taking over the cell to replicate itself. Eventually, the T4 cell dies after having been used to replicate HIV. the virus mutates rapidly, making it more difficult for the bodys immune system to recognize invaders. HIV infection progresses through several stages. clinical course of HIV begins when a person becomes infected through sexual contact with an infected person injection of infected blood or blood products perinatal or vertical transmission

MODIFIED CLASSIFICATION (STAGES): Clinical Stage I: Asymptomatic asymptomatic/acute HIV infection characterized by general lymphadenopathy Clinical Stage II: Early (mild) weight loss greater than 10% of body weight minor mucocutaneous manifestations: seborrhic dermatitis fungal nail infection recurrent oral ulceration angular cheilitis recurrent respiratory infection (rhinitis, tonsilopharyngitis) Clinical Stage III: Intermediate (moderate) weight loss greater than 10% chronic unexplained diarrhea for more than 1 month oral candidiasis (thrush) oral hairy leukoplakia severe bacterial infection (pneumonia) Clinical Stage IV: Late (severe) HIV wasting syndrome pneumocystitis carinii pneumonia toxoplasmosis of the brain cryptosporidiosis with diarrhea for more than 1 month herpes simplex virus infection progressive multifocal leukoencephalopathy disseminated endemic myocosis CLINICAL MANIFESTATIONS: a person may remain asymptomatic, feeling and appearing healthy for years and even though he/she is infected with HIV while he/she does not exhibit AIDS, the immune system started to be impaired. neurological symptoms such as memory loss, altered gait, depression, sleep disorders and gastrointestinal symptoms (chronic diarrhea) often called AIDS complex complex (ARC) as the symptoms progresses, the patient becomes an AIDS patient normal CD4 count ranges from 500-1500; CD count is criterion that determines whether the client is HIV-positive or whether the illness is already categorized as AIDS a viral load of less than 10,000 is considered low, and a viral load of more than 100,000 is high. The higher the viral load, the faster the CD4 T-cells are killed by HIV. Thus, a CD4 count of 230 with a viral load of 350,000 would be considered a serious risk for disease progression to AIDS and HIV ad treatment is absolutely indicated MINOR SIGNS: persistent cough for 1 month generalized pruritic dermatitis recurrent herpes zoster infection oropharyngeal candidiasis chronic disseminated herpes simplex infection generalized lymphadenopathy MAJOR SIGNS: loss of weight 10% of body weight chronic diarrhea for more than 1 month prolonged fever for one month

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TOP 10 SYMPTOMS OF HIV/AIDS: depression diarrhea thrush weight loss lipodystrophy (fat redistribution syndrome) sinus infection fatigue n/v lactic acidosis lactic builds up in the clients body d/t damage in the mitochondria burning and tingling of the feet and hands (peripheral neuropathy) COMMON OPPORTUNISTIC INFECTION: Bacterial MACmycobacterium avium complex, a TB-like manifestation that usually occurs when the patients CD4 count is below 50 TB salmonillosis Viral herpes hepatitis genital warts CMV (cryptomegalovirus) can cause retinitis, pain on swallowing and numbness of the legs. This can be transmitted through semen, vaginal secretions, blood and breast milk Molluscum contagiosum a disease of the skin and mucous membrane characterized by domeshaped papules that usually occur on the face, trunk, and extremities Fungal candidiasis cryptococcal meningitis Histoplasmosis small lesions that appear on the skin usually transmitted by direct contact it is autoinoculable the organism is resistant to treatment when the CD4 count falls below 200, lesions tend to proliferate and start to spread other symptoms: fever, adenopathy, cough, SOB, weight loss Pneumonias bacterial pneucystis carinii pneumonia (PCP) atypical type of pneumonia Cancers Kaposis sarcoma cancerous lesion caused by overgrowth of blood vessels. KS typically appears as painless pink or purple spots or nodules on the surface of the skin or oral cavity. It can also occur internally, especially on the intestine, lymph nodes and lungs. The cancer can spread and can also attack the eyes. Cervical dysplasia and cancer researcher found out that women with HIV have higher rates of this type of cancer; cervical carcinoma is associated with HPV Non-Hodgkins lymphoma cancerous tumor of lymph nodes; this is usually late manifestation

Parasitic toxoplasmosis parasitic disease that causes neurologic symptoms cryptosporidiosis caused by the microscopic parasite Cryptosporidium (commonly known as crypto) can also cause severe illness if CD4 is >200, crypto may cause symptoms for a long time if CD4 is <200, symptoms may only appear only for 1-3 weeks crypto spreads by having contact with feces containing crypto; not transmitted by contact with blood; there is no drug cure for crypto; however, anti-retrovirals can or get rid of symptoms signs and symptoms: watery diarrhea abdominal cramps low-grade fever weight loss d/t persistent diarrhea preventive measures against crypto: wash hands thoroughly after contact with feces practice safe sex be careful not to swallow water when swimming wash and/or cook food properly drink safe water MODE OF TRANSMISSION: sexual intercourse blood transfusion and sharing of infected syringes and needles among IV drug users vertical or perinatal transmission (from pregnant woman to the fetus during pregnancy, child delivery, or breastfeeding) several ways of receiving infected blood: blood transfusion sharing of unsterilized syringes and needles used for IV injections transmission during pregnancy transplacental greater risk of transmission when the mother has developed advanced AIDS organ donation accidental exposure in hospitals or clinics DIAGNOSTIC EXAM: EIA or ELISA particle agglutination (PA) test western blot analysis confirmatory diagnostic test immunofluorescent test radio immune-precipitation assay (RIPA) HIV antibody test when HIV antibodies are not detectable in blood at the time of examination, it is considered a negative antibody test when HIV antibodies are present in the blood in the positive antibody test, the person is considered HIV positive MEDICAL MANAGEMENT: AIDS drugs works by inhibiting reproduction of virus

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used to treat but not cure HIV infection; drugs

are sometimes referred to as antiretroviral/anteroviral drugs 2 groups: Reverse transcriptase inhibitors inhibit enzyme called reverse transcriptase, which is needed to copy information for the virus to replicate these drugs are: Zedovudine (ZDV) Retirvir Zalcitabine Havid Stavudine Zerit Lamivudine Epivir Nevirapine Viramune Didanosine Videx Protease inhibitors work by inhibiting the enzyme protease which are needed for the assembly of viral particles these drugs are: Saquinavir Invarase Ritonavir Norvir Indinavir Crixivan NURSING MANAGEMENT: health education give practical advice inform the client of the disease process and the mode of transmission emphasize the AIDS awareness program avoid judgmental and moralistic messages be consistent and concise in giving instructions, especially those about taking medications use positive statement encourage client to trace or identify previous contacts for proper management practice universal/standard precaution there is a need for a thorough medical hand washing after every contact with each patient and after removing the gown and gloves, and before leaving the room of an AIDS suspect or known AIDS patient use of universal barriers or personal protective equipment (PPE) cap, gloves, mask, CD gown, face shield/goggles, is very necessary prevention care should be taken to avoid accidental pricks from sharp instruments with potentially infectious materials from an AIDS patient gloves should be worn when handling blood specimens and other body secretions, as well as surfaces, materials and objects exposed to them blood and other specimens should be labeled with a special warning such as AIDS precaution blood spills should be cleaned immediately using common household disinfectant such as chlorox needles should not be bent after use, but should be disposed into a puncture-resistant container personal articles, like razors or razor blades and toothbrushes, should not be shared with other members of the family; razor blades may be disposed in the same manner as needles

patients with active AIDS should be isolated clients considered at risk for HIV should not be

allowed to donate blood or any organ of the body encourage monogamous relationships HIV-infected pregnant women should go into regular prenatal, interpartal, and postpartal care speak openly with partners about safer sex techniques and HIV status POSSIBLE NURSING DIAGNOSES: knowledge deficit social isolation risk for infection anxiety self-esteem disturbance altered role performance FOUR Cs IN THE MANAGEMENT OF HIV/AIDS: Compliance making sure that the client sticks with the program Counseling/education giving instructions about the treatment disseminating information about the disease providing guidance on how to avoid contacting STD again sharing facts about HIV and AIDS Contact tracing tracing and providing treatment to partners Condoms promoting the use of condoms by giving away samples and providing information on their proper use

viral disease characterized by the appearance of sores and blister anywhere on skin; these sores usually occur either around the mouth and nose, or on the genitals and buttocks (thus the nickname virus of love) related to the viruses that cause infectious mononucleosis (Eipstein-Barr virus), chickenpox, and shingles ETIOLOGIC AGENT: Herpes simplex virus (HSV) Type 1 virus can cause cold sores that usually infect during infancy and childhood sore is characterized by tiny, clear, fluidfilled blisters sore most commonly affects the lips, mouth, nose, chin, or cheeks and occurs shortly after exposure; it may also develop on wounds on the skin may barely notice the symptoms or need medical attention for relief of pain disease can be transmitted by kissing and sharing kitchen utensils and towels usually catch the infection from family members or friends who carry the virus sores of the primary infection appear 2-20 days after contact with an infected person and usually last from 7-10 days

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Type 2 virus

causes genital sores, affecting the buttocks, penis, vagina or cervix and lasts 2-20 days most people get infection from sexual contact with an infected person affects about 20% of sexually active individuals can also spread by touching an unaffected part of the body after touching the herpes lesion manifestations include minor rash or itching and painful sores, fever, muscular pain and burning sensation during urination PATHOGENESIS: before blisters appear, the skin may itch or become very sensitive lesions are limited to the epidermisor superficial mucous membrane blister may break as a result of injury, allowing the fluid of the blister to ooze and crust crust falls off, leaving slightly red, healing skin; however, the virus remains in the body; it then infects nerve cells, where it remains in a resting state infection may recur in either the same location or in a nearby site; infection may recur every few weeks or less frequently subsequent infections tend to be milder than the primary infection; this can be set off by a variety of factors, including fever, sun exposure and menstrual period; for many, the recurrence is unpredictable and has no recognizable cause CLINICAL MANIFESTATIONS: mild to moderate oral herpes gingivostomatitis in young children is the most common clinical manifestation of the initial infection with HSV vesicular and ulcerative lesions occur in the buccal mucosa and may involve the tongue inflammation of the gums, cervical adenopathy and fever are present excessive salivation results from pain on swelling in infants and young children feeding is painful and fluid intake is poor labial herpes lips may occasionally be involved in the primary infection; in such cases, it is commonly known as cold sores or fever blisters; lesions then crust and heal within 3-10 days; subsequent recurrences are usually close to the original site ocular herpes herpetic keratitis is a major medical problem that potentially leads to loss of vision primary keratitis may be accompanied by conjunctivitis and pre-auricular lymphadenopathy conjunctivitis alone may also be a manifestation of primary infection

recurrent keratitis is usually unilateral, but 2-6% of cases may be bilateral more serious disease occur if the stroma is involved or if iridocyclitis occurs cutaneous herpes HSV may affect the skin or any part of the body primary cutaneous infection may be accompanied by deep, burning pain, fever, skin edema, ascending lymphagitis and regional lymphadenopathy majority of samples isolated from above the waistline is type 1 and those isolated from below the waistline is type 2 herpes multiforme allergic reaction of the skin is sometimes a complication of HSV infections HSV lesions sometimes appear as a zosteriform distribution that mimics herpes zoster genital herpes considered one of the most common sexually transmitted diseases severe to fatal disease newborns neonatal herpetic infection is usually acquired from maternal infection at the time of delivery eczema varicelliform eruption occurs most commonly in individuals with atopic dermatitis occasionally occurs in patients with other skin disorders, such as seborrheic dermatitis and diaper rash fatality rate ranges from 5-10%; death is usually d/t disseminated viremia to the brain and visceral organs or a superimposed bacterial infection encephalitis considered as one of the most common non-epidemic forms of herpes infection in the US and other countries may be observed in infected patients of any age, even among those who already have circulating HSV in the blood MEDICAL MANAGEMENT: oral anti-viral drugs such as Acyclovir, Famciclovir, or Valacyclovir personal hygiene restoration of fluid and electrolyte balance isolation of clients, especially those with eczema herpeticum or neonatal herpes practice of universal precaution and thorough handwashing

commonly known as shingles, is caused by the same virus responsible for chickenpox; after the initial exposure, herpes zoster lies dormant in certain nerve fibers; it may become active as a result of many factors such as aging, stress, suppression of the immune system, and certain medications ETIOLOGIC AGENT: Varicella-zoster (V-Z) virus to cause 2 disease, varicella and herpes zoster

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occurs in partially immune individuals d/t

previous varicella infection INCUBATION PERIOD: unknown but believed to be 13-17 days PERIOD OF COMMUNICABILITY: a day before the appearance of the first rash until 56 days after the last crust disappears MODE OF TRANSMISSION: direct contact, specifically, through droplet infection and airborne spread indirect contact (articles freshly soiled by secretions and discharges from an infected person) PATHOGENESIS: after the primary infection, the varicella zoster virus may persist in a dormant state in the dorsal nerve root ganglia the virus may later emerge from the site, either spontaneously or in association with immunosuppression, to cause herpes zoster produces localized vesicular skin lesions confined to a dermatome and severe neurologic pain in the peripheral areas innervated by the nerves arising in the inflamed root ganglion infection usually occurs in adults CLINICAL MANIFESTATIONS: any part of the trunk may be affected, but the thoracic segment is commonly involved other areas may be affected are the extremities and branches of the 5th and 7th cranial nerves the virus affects the ganglion of the posterior nerve roots or the extramedullar cranial nerve ganglion erythematous base of the skin lesions appears first, it is followed by the appearance of the vesicles within 24 hours; a cluster of vesicles appears to form patches, which coalesce to form an irregular band-like distribution along the course of involved dermatomes; eruptions are unilateral and never cross the midline of the body; vesicles become pustular, break down, and form crusts; lesions may last for 1-2 weeks pain of varying intensity is a presenting symptom in about 2/3 of patients; pain occurs from 1-5 days prior to the development of rash and is neuralgic and paroxysmal in type; the pain may described as burning or stabbing; patient may complain of pruritus; the pain is usually worse at night and is intensified by movement fever, malaise, anorexia and headache occur for one or more days regional lymph nodes are involved in the early stage of the disease when the ophthalmic (5th) nerve is affected, corneal anesthesia may occur, and the condition is known as Gasserian ganglionitis paralysis of the facial nerve and vesicles in the external auditory canal affects the 7th cranial nerve (Ramsay-Hunt syndrome) DIAGNOSTIC EXAM: characteristic skin rash may be diagnostic tissue culture technique virus may be isolated from fluid taken from newly developing vesicles smear of vesicle fluid

microscopy COMPLICATIONS: encephalitis paralytic ileus, bladder paralysis ophthalmic herpes, which may lead to blindness MEDICAL MANAGEMENT: symptomatic antiviral drugs analgesics to control pain anti-inflammatory NURSING MANAGEMENT: keep patient comfortable; maintain meticulous hygiene keep patient in strict isolation apply cool, wet dressings with NSS to pruritic lesions efforts should be made to prevent secondary infection prevent entrance of microorganisms into the lesions, especially if they are broken assess the degree of pain; to avoid neuralgic pain, do not delay the administration of pain relievers as prescribed encourage sufficient bed rest and provide supportive care to promote proper healing of lesions provide the patient with a diversionary activity to take his mind off the pain and the pruritus POSSIBLE NURSING DIAGNOSES: pain alteration of comfort body image disturbance risk of infection impaired physical mobility impaired skin integrity altered role performance PREVENTION: immunization against chickenpox avoid exposure to a patient suffering from either varicella or herpes zoster patients immune resistance


inflammation of the meninges of the brain and spinal cord as a result of viral or bacterial infection; such inflammation may involve the 3 meningeal membranesdura mater, arachnoid membrane and pia mater ETIOLOGIC AGENT: can be caused by several kinds of organism: Pneummococcus, Staphylococcus, Streptococus and tubercle bacillus Neisseria meningitides (meningococcus) most epidemics of meningitis INCUBATION PERIOD: varies; extreme limits being set from 1-10 days MODE OF TRANSMISSION: respiratory droplets through the nasopharyngeal mucosa direct invasion through otitis media after a skull fracture, a penetrating head wound, lumbar puncture or ventricular shunting procedures

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DIAGNOSTIC EXAM: CSF analysis through lumbar puncture, the purpose of which are: diagnostic procedure obtaining the CSF specimen taking x-rays of the spinal canal and cord therapeutic purposes reducing the intracranial pressure introducing serum and other medications injecting an anesthetic agent gram staining smear and blood culture smear from petechiae urine culture CLASSIFICATIONS: Acute meningococcemia meningococci invade the bloodstream without involving the meninges onset is characterized nasopharyngitis, followed by a sudden attack of high-grade fever with chills, nausea, vomiting, malaise and headache petechial, purpuric or ecchymotic hemorrhages scatter over the entire body and mucous membranes adrenal lesions start to bleed into the medulla, extending to the cortex combination of meningococcemia and adrenal medullary hemorrhage is known as Waterhouse-Friderichsen syndrome (rapid development of petechiae that become purpuric and ecchymotic spots in association with shock) condition runs a short course and is usually fatal; this frequently occurs in the fulminant type Aseptic meningitis benign syndrome characterized by headache, fever, vomiting and meningeal symptoms o begins suddenly with a fever of up to 40 C, alterations in consciousness (drowsiness, confusion and stupor), and neck and spine stiffness, which is slight at first characteristic signs of meningeal irritation: stiff neck and nuchal rigidity opisthotonos (body is held in abnormal posture, usually rigid back and severe arching of back with head thrown backward) (+) Brudzinskis sign (an involuntary flexion of the hip and knee when the neck is passively flexed) (+) Kernigs sign (inability to completely extend the leg when sitting or lying with the thigh flex upon the abdomen; when in dorsal decubitus position, the leg can be easily and completely extended) exaggerated and symmetrical deep tendon reflexes sinus arrhythmia, irritability, photophobia, diplopia, and other visual symptoms delirium, deep stupor and coma signs of ICP bulging fontanels in infants n/v (projectile)

severe frontal headache blurring of vision alteration in sensorium COMPLICATIONS: subdural effusion hydrocephalus deaf-mutism blindness of either one or both eyes otitis media and mastoiditis pneumonia or bronchitis MEDICAL MANAGEMENT: if meningitis is left untreated it has a mortality rate of 70-100% treatment includes appropriate antibiotic therapy and vigorous supportive care IV antibiotics are usually given for 2 weeks and are followed by oral antibiotics such as: ampicillin cephalosporins (Ceftriaxone) aminoglycosides digitalis glycoside (Digoxin) is administered to control arrhythmias an anticonvulsant or sedative is needed to reduce restlessness and convulsions acetaminophen is helpful in relieving headache and fever NURSING MANAGEMENT: assess for neurologic signs often; observe the patients level of consciousness and check for ICP (signs include plucking at bedcovers, vomiting, seizures, and changes in motor functions and VS) WOF deterioration of the patients condition, which may signal in impending crisis monitor fluid balance; maintain adequate fluid intake to avoid dehydration, but avoid fluid overload because of the danger of cerebral edema; measure CVP and I&O WOF any adverse reaction to the antibiotics and/or other drugs; avoid infiltration and phlebitis position the patient carefully to prevent joint stiffness and neck pain; turn the patient often to avoid pressure sores and respiratory complication; assist with ROM maintain adequate nutrition and elimination ensure the patients comfort provide reassurance and support to the patient and family follow strict aseptic technique when treating patients with head wounds or skull fractures isolation is necessary, especially if nasal culture is positive POSSIBLE NURSING DIAGNOSES: altered cerebral perfusion altered nutrition: less than body requirement high risk for injury altered sensory perception fluid volume deficit knowledge deficit altered body temperature PREVENTION: several vaccines are available to protect against certain types of meningitis

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teach clients with chronic sinusitis or other chronic infections the importance of proper and prompt medical treatment give rifampicin as prophylaxis, as ordered by physician implement the universal precaution

infectious disease which produces a potent exotoxin with prominent systemic neuromuscular effects such as generalized spasmodic contractions of the skeletal musculator fatal in up to 60% of unimmunized persons, with death occurring usually within 10 days of onset; when develop within 3 days, the prognosis is poor ETIOLOGIC AGENT: Clostridium tetani anaerobic, gram positive, with a round terminal spore and a slender body, giving it a drumstick appearance organism comes in two forms, spore-forming and vegetative releases 2 types of toxin: tetanospasmin, responsible for muscle spasms tetanolysin, responsible for destruction of RBCs INCUBATION PERIOD: 3 days 3 weeks in adults and 3-30 days in newborn (tetanus neonatorum) SOURCES OF INFECTION: animals and human feces (organism are found in the intestinal wall of herbivorous animals, including man) soil and dust Plaster of Paris, unsterile sutures, pins, and scissors; rusty materials MODE OF TRANSMISSION: normally it is through punctured wounds contaminated by dust, soil, or animal excreta rugged, traumatic wounds and burns umibilical stump of the newborn, especially if delivered at home and thus have faulty cord dressings babies delivered to mothers without TT immunization unrecognized wounds (cleaning of the ears with sharp materials) dental extraction, circumcision and pear piercings PATHOGENESIS: when Cl. tetani enters the body, it causes local infection and extensive tissue destruction local multiplication of microorganisms occurs more frequently when the wound has healed; while reproducing, Cl. tetani also releases toxins that are absorbed by the bloodstream and lymphatics or directly by peripheral motor nerves; these eventually spread into the CNS the toxin has a high affinity for CNS tissues and spinal motor ganglia; it induces hyperexcitability of

the motor neurons by interfering with the release of an inhibitory transmitter other tissues exhibit effects of toxic degeneration, inanition (lethargy), and non-specific complications CLINICAL MANIFESTATIONS: Neonate newborn infants have feeding and sucking difficulties infant may cry excessively; most of the time, however, the cry is short, mild and voiceless an attempt to suck results in spasm and cyanosis there is fever d/t infection and dehydration jaw becomes so stiff that the baby cannot suck or swallow tonic/rigid muscular contractions, spasms or convulsions are provoked by stimuli cyanosis and pallor develop severe cases may end in flaccidity, exhaustion and finally, death Older children and adults if tetanus remains localized, signs of onset are spasm and muscle tone near the wound if it becomes systemic or generalized it includes: hypertonicity, hyperactive deep tendon reflexes, tachycardia, profuse sweating, low-grade fever and painful involuntary muscle contractions neck and facial muscle rigidity (trismus) grinning expression (risus sardonicus) considered pathognomonic of the disease board-like abdomen/abdominal rigidity opisthonos intermittent convulsions lasting for several minutes which may result in cyanosis and sudden death d/t asphyxiation in severe cases, laryngospasm is followed by accumulation of secretions in the lower airways, resulting in respiratory distress d/t involvement of respiratory muscles fracture of the vertebrae may occur during severe spasms, yielding coma and death in mild cases, after a period of weeks, spasms gradually diminish in frequency and severity, with trismus being the last symptom to disappear in fatal cases, death usually occurs during the first 10 days of the disease COMPLICATIONS: results of laryngospasm and involvement of the respiratory muscle hypostatic pneumonia hypoxia d/t laryngospasm and oxygen atelectasis and pneumothorax traumatic glossitis (inflammation of tongue) and microglossia (abnormal smallness of tongue) changes r/t sympathetic nervous system transitory hallucinosis hypersalivation, diaphoresis, and unusual tachycardia, especially with the use of aerosolized bronchodilators

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standstill and bradycardia (high mortality) d/t trauma laceration of the tongue and buccal mucosa IM hematoma fracture of the spine and ribs septicemia MEDICAL MANAGEMENT: specific within 72 hrs after a punctured wound, he patient should receive ATS, TAT or TIG, especially if the patient does not have any previous immunization tetanus toxoid, .5cc IM, given on standard schedule Pen G Na, to control infection muscle relaxant to muscle rigidity and spasm non-specific oxygen inhalation NGT feeding tracheostomy adequate fluid, electrolytes and caloric intake NURSING MANAGEMENT: maintain an adequate airway provide cardiac monitoring maintain an IV line for medication and emergency care if necessary carry out efficient wound care avoid stimulation; warn visitors not to upset or overly stimulate the patient prevent contractures and pressure sores WOF urinary retention closely monitor VS and muscle tone provide optimum comfort measures PROGNOSIS: the highest fatality rate occur at the extremes of life (very young and very old) local tetanus usually offers favorable prognosis, except in the dysphagic form of cephalic tetanus absence of convulsions favors the prognosis, especially in patients 20 years old and below apnea occurs after a prolonged spasm and is a critical factor in sudden death acute respiratory obstruction and oversedation may lead to early death; response to anticonvulsant therapy is relevant to the prognosis POSSIBLE NURSING DIAGNOSES: altered nutrition: less than body requirement impaired physical mobility activity intolerance sensory perceptual alteration high risk for infection/complication hyperexcitability knowledge deficit PREVENTION: active immunization with tetanus toxoid for adults and pregnant women (in the latter, to prevent the occurrence of tetanus neonatorum) DPT for babies and children


acute infectious disease characterized by changes in the CNS which may result in pathologic reflexes, muscle spasms, and paresis or paralysis disease of the lower motor neurons; there in anterior horn involvement ETIOLOGIC AGENT: Legio debilitans filterable virus, polio virus 3 strains of virus Brunhilde Lansing Leon INCUBATION PERIOD: 7-21 days for paralytic cases with a repeated range of 3-35 days PERIOD OF COMMUNICABILITY: 1st 3 days 3 months most contagious during the first few days of active disease and possibly from 3-4 days before onset of symptoms MODE OF TRANSMISSION: direct contact with infected oropharyngeal secretions and feces healthy carriers indirectly through flies and contaminated food, water, utensils and other articles PREDISPOSING CAUSES: Age about 60% of patients are under 10 years of age Sex males are more prone to the disease than females, with a ratio of 3:2; death rate is proportionately higher in males Heredity poliomyelitis is not hereditary Environment and hygienic condition rich are often spared than the poor; excessive work, strain and marked overexertion are also factors causing the disease TYPES: Abortive (does not invade the CNS) headache and sore throat slight or moderate fever occasional vomiting low lumbar pain patient usually recovers within 72 hours accounts for about 4-8% non-paralytic all signs of abortive type are observed types and spasm of the muscles of the hamstring changes in deep and deep superficial reflexes pain in the neck, back, arms, legs and abdomen inability to place the head in between the knees (+) Pandys test (CSF with elevated proteins) transient paresis may occur usually lasts for about a week, meningeal irritation persisting for about 2 weeks paralytic signs and symptoms listed under abortive and non-paralytic type are observed present paralysis occurs less tendon reflexes

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(+) Hoynes sign (the head fall back limply when

the head is turned to the side of bed when in lying position) weakness of the muscles hypersensitivity to touch usually there is urine retention, constipation, and abdominal distention spinal paralytic paralysis occurs in muscles innervated by the motor neurons of the spinal cord characterized by asymmetry and scattered flaccid paralysis on one or both lower extremities autonomic involvement manifested by excessive sweating respiratory difficulty bulbar type of paralysis usually develops rapidly and is more serious motor neurons in the brainstem are attacked, affecting the medulla; this weakens the muscles supplied by the cranial nerves, especially the 9th and 10th facial, pharyngeal and ocular muscles are paralyzed cardiac irregularities and respiratory failure hypothalamic dysfunction (impaired temperature regulation) encephalitic manifestations such as facial weakness, dysphagia, difficulty in chewing, inability to swallow or expel saliva, regurgitation of food through the nasal passages and dyspnea, are observed in about 30% of patients bulbospinal there is an involvement of the neurons both in brainstem and spinal cord PATHOLOGY: organism usually enters the body through the alimentary tract and multiplies in the oropharynx and lower intestinal tract organisms spread to the regional lymph nodes and the blood in the spinal type, there is evidence of gross inflammation in the anterior horn of the gray matter in the cord that often extends into the arachnoid membrane of the nerve roots in the cerebral type, the lesions are indistinguishable from other brain inflammations, although there seems to be predilection for the medulla and basal ganglia there seem to be subsequent congestion, edema and necrosis in the area lesions are found mainly in the anterior horn cells at the following sites: spinal cord vestibular nuclei of the medulla and cranial nerves roof and dermis of the cerebellum gray matter of the midbrain

motor cortex COMPLICATIONS: respiratory failure circulatory collapse electrolyte imbalance bacterial infection urinary problems r/t retention or paralysis of the urinary bladder abdominal distention DIAGNOSTIC EXAM: isolation of the virus from throat washings or swab early in the disease stool culture throughout the course of the disease culture from the CSF MEDICAL MANAGEMENT: analgesics are helpful in easing headaches, back pain and leg spasms; morphine is contraindicated because of the danger of additional respiratory suppression moist heat application may reduce muscle spasm and pain bed rest is necessary paralytic polio requires rehabilitation using physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery NURSING MANAGEMENT: carry out enteric isolation observe patient closely for signs of paralysis and other neurologic damage perform neurologic assessment at least once a day, but dont demand any vigorous muscular involvement check blood pressure regularly, especially in bulbar poliomyelitis WOF fecal impaction d/t dehydration and immobility; to prevent this, give sufficient fluid to ensure adequate daily output prevent the occurrence of pressure sores; provide good skin care; reposition the patient frequently and keep the bed dry to prevent spread of disease, wash hands every after contact with patient apply hot packs on the affected limb to relieve pain and muscle shortening dispose excreta and vomitus properly provide emotional support both to the patient an his/her family maintain good personal hygiene, particularly oral care and skin care POSSIBLE NURSING DIAGNOSES: impaired mobility anxiety pain high risk for injury body image PRVENTION: immunization: oral polio vaccine (OPV) proper disposal of GIT secretions isolation implementation of standard precaution sanitation of the premises and proper food handling should be strictly observed to avoid contamination health

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