Definition: o Acute bacterial enteric disease of the GIT characterized by diarrhea, vomiting, massive loss of fluid and electrolytes, which can lead to hypovolemic shock, acidosis and death o Acute bacterial enterotoxin (Responsible for secretion of electrolytes from the cell out into the intestinal lumen) Host: Children, squatters, crowded, uneducated, poor economic level Reservoir: Contaminated water BOIL! Portal of Entry: GIT Portal of Exit: GIT (Feces) Etiologic Agent: Vibrio cholerae / Vibrio coma o Curved (Comma-shaped) o Gram-negative o Motile with polar flagellum Pathognomonic Sign: Rice-water Stool = Odorless, colorless appearance of stools with mucoid appearance like slime Incubation Period: o Ranges from A FEW HOURS to FIVE DAYS o Usually ONE to THREE DAYS
PERIOD of Communicability During the stool-positive stage and usually a few days after recovery Note: Occasionally, carrier may have the organism for several months
MODE of TRANSMISSION (Water-borne Transmission) 1. Fecal transmission (Water, milk, food) 2. 5 Fs (Fomites, Finger, Food, Flies, Feces) 3. Flies, soiled hands, utensils also serve to transmit the infection
*** Life THREATENING! - 24 48 Hours may kill client Topics Discussed Here Are: 1. GIT Infectious Diseases a. Cholera (El Tor) / Asiatic Cholera, Epidemic Cholera b. Typhoid Fever c. Amoebiasis (Amoebic Dysentery) d. Botulism e. Red Tide f. Schistosomiasis (Bilharziasis / Snail Fever) g. Bacillary Dysentery (Shigellosis / Bloody Flux) 2. Skin Diseases a. Leprosy (Hansens Disease / Hansenosis) b. Scabies c. Pediculosis (Phthiriasis) 3. Respiratory Infective Diseases a. Pulmonary Tuberculosis (PTB) b. Severe Acute Respiratory Syndrome (SARS) c. Pneumonia d. Anthrax e. Influenza (La Grippe) f. Influenza A (H1N1) Virus g. Pertussis (Whooping Cough) h. Paragonimiasis (Lung Fluke) LOOKY HERE
jcmendiola_Achievers2013 PATHOGENESIS
CLINICAL MANIFESTATIONS 1. Acute, profuse, watery diarrhea 2. Initially, stool is brown; Later, becomes pale gray and rice water-like in appearance with an inoffensive slightly fishy odor 3. Vomiting occurs after diarrhea 4. Complication: Dehydration = 1 30 Liters/day of fluid from diarrhea 5. Poor skin turgor, sunken eyes into orbits 6. Cold skin, wrinkled fingers and toes washerwomans hand 7. Imperceptible radial pulses and unobtainable blood pressure 8. Cyanosis 9. Hoarse voice, then is lost, patient speaks in whispers (Aphonia) 10. Rapid and deep breathing 11. Diminished peripheral circulation 12. Oliguria and even Anuria 13. Temperature could be normal at the onset, subnormal in later stages 14. DEEP SHOCK = Diarrhea STOPS! 15. Death may come four hours after onset, usually on the first or the second day
PRINCIPAL Deficits 1. Extracellular Volume = Loss of intestinal fluid due to enterotoxin adenylate cyclase, cAMP 2. Metabolic Acidosis = Due to loss of a large volume of HCO 3
3. Hypokalemia = Due to massive loss of potassium 4. Renal Failure = Decreased urine output 5. Convulsions and Tetany = Due to loss of magnesium 6. Hypoglycemia = Due to rapid loss of sugar 7. Corneal Scarring = Lost the wink reflex 8. Acute pulmonary Edema = Due to rapid infusion of IV
MODALITIES OF TREATMENT Treatment Aims To: Correcting the basic abnormality without delay 1. IV Treatment 2. Oral Therapy (ORESOL, HYDRITES) Unless contraindicated
jcmendiola_Achievers2013 3. Maintenance of fluid and electrolyte volume 4. Antibiotics o Tetracycline 500 mg q6 hours (Adults) 125 mg/kg body weight q6 hours for 72 hours (Children) o Furazolidone 100 mg (Adults) 125 mg/kg q6 hours for 72 hours (Children) o Chloramphenicol 500 mg (Adults) 18 mg/kg q6 hours for 72 hours (Children) o Cotrimoxazole 8 mg/kg for 72 hours
NURSING MANAGEMENT 1. Medical Aseptic Protective Care (Handwashing!) 2. Enteric isolation 3. VS recorded accurately 4. I&O accurately measured 5. Careful personal hygiene 6. Proper disposal of excreta 7. Concurrent disinfection 8. Food must be properly prepared 9. Environmental sanitation 10. Weighing the client 11. Appropriate diet is given according to stage of recovery
PREVENTION 1. Food and water supply must be protected from fecal contamination by boiling at least 20 minutes 2. Water should be boiled or chlorinated 3. Milk should be pasteurized 4. Sanitary disposal of human excreta 5. Sanitary supervision is important
COMMON NURSING DIAGNOSES High risk for fluid volume deficit Impaired skin integrity Altered nutrition: Less than body requirements Altered tissue perfusion Knowledge deficit Diarrhea
Typhoid Fever Bacterial infection transmitted by contaminated water, milk, shellfish and other foods affecting the lymphoid tissues of the small intestines called Peyers Patches Pathognomonic Sign: Rose spots appear on the abdominal wall (7 th 9 th Day)
INCUBATION PERIOD: 5 40 Days (With a mean of 10 20 Days)
PERIOD OF COMMUNICABILITY: Variable, as long as the patient is excreting the microorganism, he is capable of infecting others
jcmendiola_Achievers2013 SOURCES OF INFECTION: 1. Person who just recovered from the disease or has recently taken care of a diseased patient with typhoid 2. Ingestion of shellfish (oysters) from contaminated waters 3. Stool / Vomitus (Reptile feces)
MODE OF TRANSMISSION 1. Fecal-oral Transmission 2. Through the 5 Fs 3. Contaminated food, water and milk
PATHOGENESIS
CLINICAL MANIFESTATIONS 1. Onset a. Headache, chilly sensation and aching all over the body Body reacting b. N/V, diarrhea c. All symptoms are WORST 4 th and 5 th Day d. Fever is higher in the morning than in the afternoon e. Breathing is accelerated, furred tongue, hot and dry skin, distended and tender abdomen f. 7 th 9 th Day Rose spots appear on the abdominal wall g. 2 nd Week: Symptoms become more aggravated. Temperature becomes stable, rose spots are more prominent due to massive hemorrhage / apposes DENGUE IS DIFFERENT 2. Typhoid State a. Decline of symptoms b. Tongue protrudes, dry and brown Dehydration and wrinkles c. Teeth and lips are dirty-brown, collection of dried mucus (Sordes) d. Staring blankly (Coma vigil) e. Twitching of tendons, especially those of the wrist (Subsultus tendinum) f. Mutters deliriously (Carphologia) g. Tendency to slip down to the foot part of the bed h. Severe Cases: Rambling delirium ending in DEATH
jcmendiola_Achievers2013 COMPLICATIONS 1. Hemorrhage or Perforation [Secretin III Secretion] = Most dreaded complications 2. Peritonitis 3. Bronchitis and Pneumonia 4. Meteorism or Excessive distention of the bowels (tympanites) 5. Thrombosis and embolism 6. Early heart failure 7. Typhoid Spine or neuritis 8. Septicemia 9. Reiters Syndrome Joint pain, eye irritation, painful urination can lead to chronic arthritis
DIAGNOSTIC PROCEDURE 1. Typhidot Confirmatory (Injection of antigen of typhoid 2. ELISA 3. Widal Test 4. Rectal Swab 5. Mouse Bioassay
MODALITIES OF TREATMENT 1. Chloramphenicol (DRUG OF CHOICE!) 2. Ampicillin 3. Co-trimoxazole 4. Ciprofloxacin or Ciftriaxone 5. Does not respond to Chloramphenicol, 3 rd and 4 th Generation Drugs are used
NURSING MANAGEMENT 1. Medical aseptic technique 2. Restore F&E by small quantities at frequent intervals 3. Monitor VS 4. Prevent further injury (If with typhoid psychosis) 5. Personal hygiene and mouth care 6. Cooling measures 7. WOF: Intestinal bleeding 8. Terminal and concurrent disinfection
PREVENTION and CONTROL 1. Boil water up to 40C , COOK it, PEEL it/Forget it 2. Supervision of food handlers 3. Enteric isolation 4. Adequate amounts of safe drinking water 5. Reporting of cases 6. Detection and monitoring 7. Education on the mode of transmission
COMMON NURSING DIAGNOSES Fluid volume (Diarrhea) Hyperthermia Self-care deficit Constipation Anxiety Knowledge deficit High risk for injury (Typhoid psychosis)
jcmendiola_Achievers2013 Amoebiasis (Amoebic Dysentery) - Protozoal infection of human beings which involves the colon, spreading to the soft tissues commonly to the liver and lungs by contiguity or hematogenous / lymphatic dissemination - Host: People who commonly eat STREET FOODS
ETIOLOGIC AGENT Entamoeba histolytica o Has two Developmental Stages 1) Trophozoites / Vegetative Form Cant survive in tropical environment 2) Cyst Infective stage of E. histolytica INCUBATION PERIOD Severe infection: 3 Days Sub-acute and Chronic Form: Several Months Average Cases: Varies from 3 4 Weeks (For life Amoebiasis)
PERIOD OF COMMUNICABILITY: Entire Duration of the ILLNESS
MODE OF TRANSMISSION 1. Fecal-oral Transmission 2. Direct contact: Sexual contact by orogenital, oroanal and proctogenital sexual activity 3. Indirect Contact: Uncooked leafy vegetables, foods contaminated with fecal material
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS 1. Acute Amoebic Dysentery a. Slight attack of diarrhea, period of constipation accompanied by Tenesmus Abnormal contraction of anal sphincter b. Diarrhea, watery and foul-smelling stools often containing blood-streaked mucus c. Colic and gaseous distention of lower abdomen Bloated / Inflamed d. Nausea, flatulence, abdominal distension and tenderness in the right iliac region over the colon 2. Chronic Amoebic Dysentery a. Several days, usually succeeded by constipation b. Tenesmus
jcmendiola_Achievers2013 c. Anorexia, weight loss, and weakness d. Liver may be enlarged If protozoa e. First are semifluid, but soon become water, bloody and mucoid f. Vague abdominal distress, flatulence, constipation or irregularity of bowel movement g. Mild toxemia, constant fatigue and lassitude Feeling of exhaustion h. Abdomen loses its elasticity when picked up between the fingers i. Scattered ulceration with whitish/yellowish and erythematous borders j. Gangrenous Type (Fatal), large sloughs of intestinal tissues in the stools, accompanied by hemorrhage 3. Extraintestinal Forms HEPATIC a. Pain in upper right quadrant with tenderness of the liver b. Jaundice c. Intermittent fever d. Loss of weight or anorexia e. Abscess through the lungs; patient coughs anchovy-sauce sputum
TREATMENT MODALITIES 1. Metronidazole (Flagyl) 800 mg TID x 5 days 2. Tetracycline 250 mg q6 hours 3. Ampicillin, Quinolone, Sulfadiazine 4. Streptomycin SO 4 , Chloramphenicol 5. F&E replaced
NURSING MANAGEMENT 1. Isolation and enteric precaution 2. Health education: Food and water management 3. Proper collection of stool specimen As long as client has diarrhea, NO TO ANTI- DIARRHEAL DRUGS and NO TO DAIRY PRODUCTS 4. Skin Care 5. Mouth Care 6. Provide optimum comfort 7. Diet Forced fluids
METHODS OF PREVENTION 1. Health education 2. Sanitary disposal of feces 3. Protect, chlorinate, and purify drinking water 4. Observe scrupulous cleanliness in food preparation and food handling 5. Detection and treatment of carriers 6. Fly control (Can serve as vectors)
Botulism A rare but serious paralytic illness caused by a potent neurotoxin
ETIOLOGIC AGENT: Clostridium botulinum o Gram-positive, spore-forming, anaerobic organism
jcmendiola_Achievers2013 Three Human Forms of Botulism 1) Foodborne Ingestion of inadequately cooked contaminated food, low acid content 2) Wound Botulism (Cutaneous Botulism) Ulcers with sharply demarcated edges 3) Infant Botulism Aged 3 20 weeks. Hypotonic (floppy) infant syndrome
PATHOPHYSIOLOGY
CLINICAL CHARACTERISTICS 1. Flaccid paralysis and descends via the bulbar musculature 2. Somatic musculature is the next part which will result in generalized weakness 3. Neurological Symptoms: a. Diplopia and blurred vision b. Ptosis, dry mouth, dysphagia and Dysarthria 4. Classic Symptoms: a. Double vision, blurred vision, drooping eyelids b. Slurred speech, difficulty swallowing and dry mouth c. Muscle weakness d. Infants: i. Lethargic appearance, feed poorly, usually constipated due to peristalsis of smooth muscles ii. Weak cry and poor muscle tone e. If untreated, can cause paralysis of arms, legs, trunk and respiratory muscles f. Foodborne Botulism: i. Symptoms usually begin 18 36 hours after eating contaminated food ii. Symptoms continue to cause paralytic ileus with severe constipation and to body paralysis iii. Respiratory muscles are affected, DEATH (Respiratory failure)
TREATMENT / MANAGEMENT 1. Supportive care especially to respiratory and nutritional needs Clostridium botilinum enters the body through the wound Wound Botulism Produces toxins in traumatized and necrotic tissue Formation of ulcers with sharply demarcated edges and a membranous base from the deposition of toxin Ingestion of C. Botulinum (Improper processed canned foods, inadequate cooked contaminated foods) Food Borne Produces toxins to the bowel lumen Hematogenously disseminated to peripheral cholinergic synapses (Irreversible bond) Blocks acetylcholine ACh Produces impaired autonomic and voluntary neuromuscular transmission and muscular paralysis
jcmendiola_Achievers2013 2. Food Borne Botulism: Emetics and gastric lavage is recommended 3. Wound Botulism: Exploration and debridement
PREVENTION and CONTROL 1. Health education on proper preparation of food, especially on home canning 2. Infant Botulism can be prevented by NOT giving infants HONEY 3. Promptly report Foodborne botulism outbreak
COMMON NURSING DIAGNOSES Impaired physical mobility Potential impairment of skin integrity Alteration in bowel elimination Pain and discomfort Altered Nutrition: Less than body requirements Anxiety
Red Tide Caused by a population explosion of toxic, naturally occurring microscopic phytoplanktons (toxin), specifically a subgroup known as Dinoflagellates
ETIOLOGIC AGENT Gonyaulax, Protogonyaulax, and Gessnerium. Presently, known by the accepted name Alexandrium sp. 1. Alexandrium tamarense = Atlantic Coast 2. Alexandrium catanella = Pacific West Coast 3. Ptychodiscus brevis = Gulf of Mexico, West Florida Coast
TYPES OF SHELLFISH THAT ARE PRONE FOR TOXIC ACCUMULATION 1. Quahogs 2. Soft Shell Clamps 3. Oysters 4. Mussels 5. Scallops 6. Moon Snails
FOUR SYNDROMES OF SHELLFISH POISONING 1. Paralytic shellfish poisoning 2. Diarrheal shellfish poisoning 3. Amnestic shellfish poisoning 4. Neurologic shellfish poisoning FIRST TARGET
PATHOPHYSIOLOGY
REMEMBER: Toxic shell fish taste and appear no different from non- toxic shellfish!! Cooking DOES NOT destroy the organism
jcmendiola_Achievers2013 CLINICAL MANIDESTATIONS 1. Initial Sign: Tingling of the lips and tongue which spreads to the face, neck and fingertips and toes 2. HA, dizziness and nausea follow (May be mistaken as being a drunken condition) 3. Symptoms are aggravated by alcohol consumption 4. In severe cases, muscular paralysis and difficulty of breathing in 5 12 hours due to paralysis of the diaphragm, can only survive with the aid of a respirator 5. Fatalities have been reported due to respiratory arrest
MODALITIES OF TREATMENT 1. Induced to vomit 2. Charcoal hemoperfusion 3. Alkaline fluids (Na HCO 3 ) 4. Artificial respiration
PREVENTION and CONTROL 1. Monitoring program for all shellfish-producing areas 2. Year-round testing of shellfish and shellfish-growing areas 3. Seek medical attention if accidental ingestion of toxic shellfish is suspected 4. Pay close attention if hot season, look for posted warnings about red tide
Schistosomiasis (Bilharziasis / Snail Fever) Slowly, progressive disease caused by blood flukes of class Trematoda A chronic wasting disease common among farmers and their families in certain parts of the Philippines
ETIOLOGIC AGENT Schistosoma japonicum o Three Major Types 1) Schistosoma japonicum Infects the intestinal tract (Katayama disease) Also known as oriental schistosomiasis 2) Schistosoma mansoni Also affects the intestinal tract 3) Schistosoma haematobium Affects the urinary tract
INCUBATION PERIOD: At least two months
SOURCES OF INFECTION 1. Feces of infected persons 2. Dogs, pigs, carabaos, cows, monkeys and wild rats serve as hosts
MODE OF TRANSMISSION 1. Ingestion of contaminated water 2. Skin pores 3. Through an intermediary host, a tiny snail called Oncomelania quadrasi
jcmendiola_Achievers2013 PATHOPHYSIOLOGY
CLNICAL MANIFESTATIONS Signs and Symptoms depend on the site of infection, but these are common 1. Pruritic rash, swimmers itch At the site of penetration 2. Low-grade fever, myalgia and cough 3. Abdominal discomfort due to Hepatomegaly, Splenomegaly and Lymphadenopathy 4. Bloody-mucoid stools 5. Icteric and jaundice (Obstructive jaundice) 6. Later, belly becomes big because of an inflamed liver, from the accumulation of eggs in the organ 7. Chronic disease: Weak and pale and marked muscle wasting 8. When parasites reach the brain, victim experiences severe HA, dizziness, and convulsions
COMPLICATIONS 1. Liver cirrhosis and portal hypertension 2. Cor pulmonale and pulmonary hypertension
jcmendiola_Achievers2013 3. Heart failure 4. Ascites 5. Hematemesis as a result from rupture of esophageal varices 6. Renal failure 7. Cerebral schistosomiasis Crossed the Blood Brain Barrier
DIAGNOSTIC PROCEDURES 1. Fecalysis or direct stool exam 2. Kato-Katz Technique 3. Liver and rectal biopsy 4. Enzyme-linked Immunosorbent Assay (ELISA) 5. Circumoval precipitin test (COPT) Confirmatory diagnostic test
MODALITIES OF TREATMENT Treatment is effective when given EARLY in the course of the disease 1. Praziquantel tablet for 6 months o 1 tab BID for 3 months, then o 1 tab a day for another 3 months 2. Fuadin injection given either IM or IV, should consume 360 mg for entire treatment
PREVENTION and CONTROL To prevent Schistosomiasis , one must know: - How the disease spreads - How to interrupt the life cycle of the worm - How to protect people from infection 1. Stool examination 2. Reduce snail density 3. Diminish infection rate 4. Health education on the disease process, mode of transmission and prevention
COMMON NURSING DIAGNOSES Body image disturbance Impaired skin integrity Altered role function Altered urinary elimination (S. hematobium) Social isolation Self-esteem disturbance Knowledge deficit Risk for infection
Bacillary Dysentery (Shigellosis / Bloody Flux) - Acute bacterial infection of the intestines characterized by diarrhea, fever and associated with passing out of bloody-mucoid stools accompanied by tenesmus
ETIOLOGIC AGENT E Shigella group - Short, non-motile, gram-negative organism - Four Serologic Groups: 1. Shigella flexneri (Group B) 2. Shigella boydii 3. Shigella connei 4. Shigella dysenteriae
INCUBATION PERIOD: 7 HOURS to 7 DAYS (With an average of 3 5 DAYS)
jcmendiola_Achievers2013 PERIOD OF COMMUNICABILITY: During the acute infection until negative feces
MODE OF TRANSMISSION 1. Ingestion of contaminated food or water or milk 2. Flies or through other objects contaminated by the feces 3. Fecal-oral
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS 1. Fever, specially in children 2. Tenesmus, nausea, vomiting and headache 3. Colicky or cramping abdominal pain with anorexia and body weakness 4. Diarrhea with blood-mucoid stools that are watery at first 5. Rapid dehydration
COMPLICATIONS 1. Rectal prolapse (Particularly in undernourished children) 2. Respiratory Complications (Cough and pneumonia) 3. Non-suppurative arthritis and peripheral neuropathy
DIAGNOSTIC PROCEDURE 1. Fecalysis or microscopic examination of stools 2. Isolation of the causative organism from rectal swab or culture 3. Peripheral blood examination 4. Blood culture 5. Sheets of polymorphonuclear leukocytes seen in staining with methylene blue
MODALITIES of TREATMENT 1. Ampicillin, tetracycline and Cotrimoxazole may be useful in severe cases 2. F&E Management (Prevent dehydration with NSS) 3. Low-residue diet is recommended 4. Anti-diarrheal drugs are CONTRAINDICATED = They delay fecal excretion can lead to prolonged fever (Also dairy products are contraindicated)
NURSING MANAGEMENT 1. Maintain F&E balance 2. Keep client warm and comfortable 3. Restrict food until N/V subsides 4. Isolation 5. Personal hygiene maintained 6. Proper disposal of excreta 7. Concurrent and terminal disinfection should be employed
jcmendiola_Achievers2013 8. Return to normal activities must be gradual, relapse may occur
METHODS of PREVENTION and CONTROL 1. Sanitary disposal of human feces 2. Sanitary supervision of processing, preparation and serving of food particularly those eaten raw 3. Adequate provision of safe washing facilities 4. Fly control and protection 5. Isolation of client during acute stage 6. Protection and purification of public water supply 7. Persons known to be infected should be excluded from handling food for public consumption
Skin Diseases Leprosy (Hansens disease / Hansenosis) 1. Chronic disease that mainly affects the skin, peripheral nerves, eyes, and mucosa of the upper respiratory tract and eventually producing deformities - Host - Immune response, crowded places, related to tuberculosis, poverty, malnutrition - Agent: Mycobacterium leprae - Reservoir Nasal secretions of infected persons - Portal of Entry Respiratory / skin - Portal of Exit Respiratory / skin - Mode of Transmission Droplet / direct contact 2. Pathognomonic Sign: Weakness
MODE OF TRANSMISSION 1. Droplets 2. Inoculation through skin breaks and mucous membranes
THREE DISTINCT FORMS 1. Lepromatous Leprosy (Multibacillary) a. Most serious type, most infectious b. Damage to the respiratory tract, eyes and testes as well as the nerves and the skin c. Lepromin test is negative but the skin lesion contains large amounts of Hansens bacillus d. Gradual thickening of the skin with development of a granulomatous condition e. Lesions appear as macules and become nodular (Leproma) f. Slow involvement of the peripheral nerves, with some degree of anesthesia, loss of sensation and gradual destruction of the nerves g. Atrophy of the skin and muscles, melting or absorption of small bones, primarily hands and feet h. Ulceration of the mucous membrane of the nose i. Due to melting or absorption of small bones and ulceration, natural amputation may occur 2. Tuberculoid Leprosy a. Affects the peripheral nerves and sometimes surrounding skin (face, eyes, and testes), nerves, skin b. Lepromin test is positive but the organism is rarely isolated from the lesions The concentration is in the blood! NOT in the tissues c. Elevated macules, with clearing at the center, more clearly defined than in the lepromatous form d. Anesthesia is present, involvement of the peripheral nerves occurs more rapidly than in the lepromatous form 3. Borderline (Dimorphous) Leprosy a. Has characteristics of both Lepromatous and Tuberculoid leprosy b. Diffused and poorly defined
jcmendiola_Achievers2013
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS 1. Neural Involvement The earliest manifestations (Nerve Damage) a. Atrophy of muscles of the hands which extends to the thenar, hypothenar and forearm muscles, resulting in clawhand b. Nerves involved are: Ulnar, median, radial, lateral popliteal and facial c. Paralysis and peripheral anesthesia d. Secondary consequences of nerve involvement include: Malperforant, clawhand, ocular complications incident (corneal insensitivity or paralysis of the eyelids) 2. Skin Lepromatous and Tuberculoid leprosy differ greatly in their Cutaneous manifestations: a. Lepromatous Leprosy: o Multiple early lesions, symmetrical, and erythematous, macules or papules with smooth surfaces o Later, enlarged lesions and forms plaques or nodules on the earlobes, nose, eyebrows and forehead (Leonine appearance) o Loss of eyebrows and eyelashes o Loss of function of sweat and sebaceous glands makes skin dry and hairless b. Tuberculoid Leprosy o Purely neural or may simultaneously affect the skin o Raised, large erythematous plaques appear on the skin 3. Eye a. Ocular manifestations Found only in LEPROMATOUS and BORDERLINE Leprosy b. Conjunctiva, sclera, cornea and iris are affected, sparing the retina and optic nerve c. Photophobia, conjunctivitis and iridocyclitis frequently occurs, opacity of the cornea, insensitivity and ulceration can lead to blindness 4. Upper Respiratory Tract a. Nose, mouth, pharynx, larynx, trachea, and esophagus involved in LEPROMATOUS LEPROSY b. Epistaxis, ulceration of the uvula and tonsils, septal formation and nasal collapse 5. Visceral Leprosy a. Heaviest concentration of lesions in the organs representing the reticuloendothelial system, the lymph system and liver M. leprae attacks peripheral nerves Nerves of Ulnar, radial, posterior popliteal, anterior-tibial and facial nerves When bacilli damage the skins fine nerves, they cause anesthesia, anhydrosis and dryness If they attack a large nerve trunk, Motor nerve damage, weakness and pain occur, Followed by peripheral anesthesia, muscle paralysis and atrophy
jcmendiola_Achievers2013 b. Testicular damage occurs in almost all moderately advanced cases of Lepromatous Leprosy
DIAGNOSTIC PROCEDURES 1. Identification of the Signs and symptoms 2. Tissue biopsy Confirmatory 3. Tissue smear Confirmatory (+) M. leprae 4. Blood tests (Increased RBC and ESR, Decreased Serum Ca, Albumin and Cholesterol levels)
MODALITIES of TREATMENT 1. Sulfone Therapy 2. Rehabilitation, recreational and occupational therapy 3. Multiple Drug Therapy (MDT) a. Combinations of: i. Rifampicin (600 mg once a month) ii. Clofazimine (50 mg daily) iii. Dapsone (100 mg daily) For Multibacillary Leprosy iv. And Rifampicin and Dapsone Pausibacillary Type b. Among these, Rifampicin is the most important ant-leprosy drug and is therefore included in the treatment of both types of leprosy c. Treatment of leprosy with only one anti-leprosy drug will always result in the development of DRUG RESISTANCE d. Treatment of leprosy with Dapsone or any anti-leprosy drug used as monotherapy should be considered as an UNETHICAL PRACTICE e. For Multibacillary Leprosy: i. Rifampicin 600 mg is given once a month ii. Dapsone 100 mg is given daily iii. Clofazimine 50 mg daily for 12 months f. For Paucibacillary Leprosy: i. Give Rifampicin 600 mg once a month ii. Dapsone once daily iii. Duration of treatment is 6 months g. Clofazimine causes black discoloration and dryness of skin (Disappears within a few months after treatment) h. MB and PB patients should have fixed-duration treatment, which means: i. MB Px: After 12 monthly doses of MDT (Cured and removed from register) ii. PB Px: After 6 monthly doses of MDT (Cured and discharged)
NURSING MANAGEMENT 1. Respiratory isolation and medical asepsis 2. Moral support and encouragement 3. Diet full! WHOLESOME and NUTRITIOUS! 4. Terminal disinfection
PREVENTION 1. Report suspects of leprosy 2. Newborn infants should be separated from leprous mothers 3. BCG protective if given during 1 st 6 months of life 4. Health education on mode of transmission
COMMON NURSING DIAGNOSES Impaired skin integrity Social isolation Ineffective coping
jcmendiola_Achievers2013 Knowledge deficit Anxiety Impaired body image
Scabies An age-old skin infection caused by a female itch mite, which penetrates the skin, forming burrows
ETIOLOGIC AGENT Sarcoptes scabiei
INCUBATION PERIOD: Itch mite may burrow under the skin and lay ova within 24 hours of the original contact
PERIOD OF COMMUNICABILITY: Entire period that the host is infected
MODE of TRANSMISSION 1. Direct Through infected individual 2. Sleeping on an infested bed or wearing infested clothing 3. Anyone can become infected or re-infected 4. Contact with dogs, cats, and other small animals 5. Scabies on dogs is called mange 6. But human scabies gets worse and worse if untreated
PATHOPHYSIOLOGY
SIGNS and SYMPTOMS 1. Itching, more pronounced at night when the client has retired (Since the increased warmth of the skin has a stimulating effect on the parasite) 2. The itch is subtle for the first week, gradually becomes more intense after a month or two (Sleep becomes almost IMPOSSIBLE) 3. Secondary lesions like vesicles, papules, pustules, excoriations and crusts may be found on the affected site 4. Bacterial superinfection results from constant excoriation
DIAGNOSTIC PROCEDURE A drop of mineral oil placed over the burrow, followed by superficial scraping and examination of expressed material under a low-power microscope
jcmendiola_Achievers2013 MODALITIES of TREATMENT 1. Application of pediculicide, such as permethrin cream or lindane lotion left on for 10 12 hours [Miticide Drugs] 2. Crotamiton Cream for 5 consecutive nights 3. Neosporin ointment (Rubbed onto the affected skin 4 5 times a day) 4. Eurax and Kwell lotion (Prove effective in some patients) 5. Antihistamines like diphenhydramine (Benadryl) Relief from the itch 6. All clothes used before and during the treatment period should be disinfected (Dry cleaning or boiling)
NURSING MANAGEMENT 1. Instruct the patient to apply the cream at bedtime, neck down to the toes (Covering the entire body) 2. Dry cleaned or boil contaminated clothing or bedclothes 3. Report any skin irritation 4. Close contacts of the patient be checked for possible symptoms 5. Handwashing technique or use gloves while performing nursing procedures 6. Terminal disinfection
PREVENTION and CONTROL 1. Good personal hygiene 2. Avoid contact with infected persons 3. Household members and close contacts should be treated 4. After treatment, beddings and clothing should be properly laundered
COMMON NURSING DIAGNOSES Alteration in comfort; itchiness / risk for infection Impaired skin integrity Altered role performance Knowledge deficit Social isolation Body image disturbance
Pediculosis (Phthiriasis) Infestation of the hairy parts of the body / clothing with eggs; larvae / adult lice
Direct contact Lice feed on the blood Lice stay close to skin for moisture, food, and warmth Fertilized female louse lays about 10 eggs/day for upto a month until it dies Eggs (nits) attached to the hair shafts are close to the skin surface where the temperature is optimal for incubation Eggs hatch after about 7 14 days of incubation
ETIOLOGIC AGENT 1. Pediculus humanos var. capitis Head lice 2. Pediculus humanos var. corporis Body lice 3. Phthirus pubis or pubic lice Crab lice a. Feed on human blood and lay eggs in hairs and clothing fibers b. After hatching, lice must feed within 24 hours or else it will die c. Mature in about 2 3 weeks d. When a louse bites, it injects toxins into the skin (Producing mild irritation and a purpuric spot) e. Repeated bites cause sensitization to the toxin, leading to more serious inflammation
PATHOPHYSIOLOGY
jcmendiola_Achievers2013 CLINICAL MANIFESTATIONS 1. The Head Louse a. Common in females, more in children than adults b. Itching is the predominant symptom c. If neglected, irritation, excoriation and crusting ensue, foul-smelling mass (Matted hairs, nits, ova, pus, crusts and pediculi) Plica polonica 2. Body Louse a. Gray-white active insect 3 4 mm long b. Mouth parts (adapted to sucking blood), Leg parts (Adapted to grasping hair) c. Lifespan of females is about 1 month, she lays about 8 10 eggs per day d. Eggs hatch in 8 days, releasing nymphs that will mature in 8 days e. Initial lesions are minute red spots f. Spot swells much like a mosquito bite g. Head and body lice are closely related, interbreedable variants of the same species 3. Crab Lice a. Rounder, stubbier insect, 2 3 mm long, difficult to see unless filled with blood from a recent meal b. 4 of its 6 legs terminate in its sturdy crab-like claws c. Lifespan: 3 4 weeks, female lays a maximum of 3 eggs/day d. Unusual, persistent itching in the pubic region and in the other affected areas is the chief symptom e. Presence is unsuspected, until nits become apparent on the hair, or until detached and seen on fingers due to scratching f. Grayish pigmented spots (Maculae caeruleae) found on the surface of inner thighs or the abdomen
TREATMENT 1. Head Louse a. Dusting the scalp with 1% malathion powder b. Thoroughly massage gamma-benzene hexachloride shampoo in the scalp for 4 minutes then rinse 2. Body Louse a. Launder (dry clean) or Boil the clothing and beddings b. Good body hygiene 3. Crab Louse a. Apply Kwell or Gamene (Lindane) cream or lotion b. Rub crotamiton (Eurax, Geigy) onto affected area c. Repeat after one week d. Treat a person who has had sexual contact with the patient e. Remove remaining nits mechanically f. Infestations in the eyelids of children treated with yellow oxide of mercury, apply to eyelids BID for a few days
COMPLICATIONS Pigmentation and honey crusts of secondary pyoderma Vagabondia Combination of extensive excoriation, hypo- and hyper pigmentation with lichenification Enlargement of the Nuchal and cervical nodes with febrile episodes which can lead to micrococcal infection Blepharitis
PREVENTION 1. Good personal hygiene 2. Avoiding contact with persons suffering from pediculosis
COMMON NURSING DIAGNOSES Alteration in comfort Impaired skin integrity Body image disturbance Risk for infection Sleep disturbance
jcmendiola_Achievers2013 Respiratory Infective Diseases Refer to OLD NOTES on RESPI Pulmonary Tuberculosis (PTB) Severe Acute Respiratory Syndrome (SARS) Pneumonia
Anthrax 1. An infection caused by Bacillus anthracis that occurs primarily in herbivores 2. Use in biological warfare or bioterrorism
ETIOLOGIC AGENT Bacillus anthracis o Large, aerobic, spore-forming, gram (+), rod-shaped microorganism that is capsulated and non motile o Can be destroyed by boiling in 10 minutes, but can survive for years in the dry soil
HUMAN CASES are CLASSIFIED AS: 1. Agricultural Cases a. Contact with animals that are infected b. Consumption of contaminated meat 2. Industrial Cases a. Exposure to contaminated hides, goat hair, wool or bones
MODES of TRANSMISSION 1. Direct Contact with infected animals or contaminated animal products 2. Indirect Animal bites and ingestion of contaminated meat 3. Airborne Inhalation of contaminated or polluted air
TYPES 1. Cutaneous Anthrax a. Incubation period is 9 hours 2 weeks (2 7 days)
Entrance of Bacillus anthracis 2 3 Days Pimple or Macule appears Ring / Vesicle develops around the papule 4 th Day Edema!! Painful lymph adenitis may occur in inguinal area Papules ulcerate and form Eschar 5 th 7 th Day Edema extends from lesion SEVERE CASES Face, neck or chest High fever Toxemia Regional painful lymphadenopathy Extensive edema Shock/death
jcmendiola_Achievers2013 2. Inhalation Anthrax (Woolsorters Disease) a. Resembles those of severe viral respiratory diseases
3. Gastrointestinal Anthrax a. Inadequately-cooked meat from animals with anthrax
COMPLICATIONS 1. Anthrax Meningitis Intense inflammation of the meninges of the brain and spinal cord a. CSF Pressure with bloody CSF, with loss of consciousness b. 100% Fatality rate 2. Anthrax Sepsis a. Develops after lymphohematogenous spread of B. anthracis from primary lesion b. Clinical features: High fever, toxemia and shock, with DEATH following in a short time
TREATMENT 1. Parenteral Penicillin G 2 million units q6 hours until edema subsides Subsequent administration of oral penicillin for 7 10 days 2. Patients who are sensitive to penicillin can be treated with erythromycin, tetracycline or chloramphenicol
NURSING MANAGEMENT 1. History taking 2. Physical examination 3. Skin care, psychological and emotional support 4. Supportive measures and geared toward the type of anthrax exposure 5. Report to health authorities any type of anthrax
jcmendiola_Achievers2013 COMMON NURSING DIAGNOSES - Anxiety - Altered nutrition - Altered body temperature - Impaired physical mobility - Alteration in bowel elimination - Altered nutrition: less than body requirements
Influenza (La Grippe) 1. Generalized, acute, febrile disease associated with upper and lower infection
ETIOLOGIC AGENT RNA-containing myxoviruses, types A, A-prime, B and C
INCUBATION PERIOD: 24 48 Hours
PERIOD of COMMUNICABILITY: Until 5 th Day of illness (Up to 7 th day in children) MODE of TRANSMISSION 1. Airborne 2. Direct contact with infected droplet 3. Persists for hours in dried mucus
CLINICAL MANIFESTATIONS 1. Chilly sensation, hyperpyrexia, malaise, sore throat, coryza, Rhinorrhea, myalgia and HA 2. Severe aches and pain, associated with severe sweating 3. Sometimes GI symptoms and vomiting 4. Worst Symptoms: 3 5 days before the condition improves 5. Most people recover
COMPLICATIONS 1. Directly related to primary viral infection a. Hemorrhagic pneumonia b. Encephalitis and other neurologic syndromes c. Reyes Syndrome d. Myocarditis can lead to Cardiac failure e. SIDS f. Myoglobinuria 2. Superimposed bacterial infections due to Streptococcus pneumoniae, Haemophilus influenzae, Streptococcus pyogenes and Staphylococcus aureus a. Otitis media b. Sinusitis c. Pneumonia
jcmendiola_Achievers2013 a. Complement fixation test b. Hemo-agglutination test c. Neutralization test
MANAGEMENT Advice the client to: 1. Stay home 2. Drink plenty of fluids 3. Medications to relieve fever and HA a. Paracetamol b. Aspirin (Unless contraindicated) c. Ibuprophen or other anti-inflammatory drugs 4. Sponge down with tepid water Also, make sure to: 1. Isolate 2. Limit strenuous activity 3. WOF Complications
PREVENTIVE MEASURES 1. Immunization 2. Avoidance of crowded places 3. Educate the public and health care personnel regarding personal hygiene 4. Vaccine annually: a. Elderly b. Poor immunity c. People with diseases such as diabetes, and lung, kidney, heart or liver disease
Influenza A (H1N1) Virus New virus Almost all people are susceptible More contagious than seasonal influenza - 22 33% Attack rate vs. 5 15% Mild illness in healthy people (Except in Mexico) Younger age group are affected
WHAT IS the INFLUENZA AH1N1 VIRUS THAT HAS BEEN CAUSING RECENT OUTBREAKS GLOBALLY? ` The specific type of H1N1 virus causing illness now is new/novel ` This virus is able to infect humans and be passed from person to person ` Caused by a novel virus that resulted from the triple reassortment of pigs, humans, and avian influenza A strain ` Characteristics: - RNA Virus -
Two Surfaces Protein of the Virus e Haemagglutinin (H) o Glycoprotein enables virus to attach to host cell o 15 exists in water o H1H2 and H3 most commonly associated with human infection e Neuraminidase (N) o Glycoprotein enzyme essential for virus replication o N1 and N2 most commonly associated with human infection
Fighting of bacteria: Stimulates Sympathetic Nervous System o Releases cortisol (Immunosuppressant) o Stimulates Catechol
jcmendiola_Achievers2013 Antigenic Shift + Type A Infective virus undergo frequent change in their surface antigen / protein enabling the virus to cause epidemics / pandemics
What Should I know About HIV? L They spread through infected droplets from breathing passages o Droplets are expelled by talking, spitting, coughing, sneezing L Droplet spread about 1 meter (3 feet) from the infected person, either direct L Virus can live for several hours in hard surfaces / on a cloth / paper L If healthy people touch infected hands, doorknobs, keys, telephones etc. L Virus can spread through the air L An infected person is most likely to spread the virus when he/she has a cough and fever L It is possible that a person can transmit during the incubation period
Individuals at HIGH RISK For Hospitalization / Death Elderly greater than 65 years old Children less than 2 years old Certain chronic diseases Pregnant women
PATHOPHYSIOLOGY ` Similar to influenza System Signs and Symptoms Respiratory System Cough / runny nose, sneezing Respiratory failure Circulatory System Fever / Extensive cold GI System N/V Musculoskeletal System Fatigue, sore joints EENT Loss of smell Nasal coughs Sire throat Reddened eyes Skin, mouth, throat
Signs and Symptoms Fever Chills Lethargy
INCUBATION PERIOD : Although the precise incubation period has not been established for H1N1, Influenza A infection is 1 week
Case Defense A confirmed case of Influenza A Virus An acutely febrile respiratory illness and lab confidence origin infection
1) Real Time Reverse Transcriptase Polymeric Chain Reaction (rRT PCR) 2) Viral Culture
A Probable Case of Influenza A (H1N1) Virus infection is defined as: Acute febrile respiratory illness in a person who is positive for influenza A
INFECTIOUS PERIOD Confirmed diagnosis
jcmendiola_Achievers2013 Close Contact History with a convention with a person positive for A H1N1 Within 6 feet of an ill person Acute Respiratory Illness o Not confirmed but has symptoms
WHAT IS THE DIFFERENCE BETWEEN SEASONAL and PANDEMIC INFLUENZA ? LOL
MEDICAL MANAGEMENT Supportive care Strict isolation Quarantine Drugs of Choice o Oseltamivir Pills o Inhaled Zanamivir
NURSING DIAGNOSES : Impaired gas exchange : Risk for infection
NURSING INTERVENTIONS W Nursing History o Recent contact within 24 hours with someone known to have W Onset of any cold / flu type symptom W Physical Assessment o Check VS o Palpate: Cervical lymph nodes o Percussion o Auscultate: Presence of rales, crackles W Improve Gas Exchange W Monitor breath sounds, rate and dyspnea W Manage rest and avoid exhaustion
PREVENT TRANSMISSION of INFECTION 1. Universal Precaution and droplet precaution 2. Basic Infection Control a. Hand hygiene b. Appropriate use of masks c. Cough etiquette d. General measures
Pertussis (Whooping Cough) Infectious disease characterized by repeated attacks of spasmodic coughing which consists of a series of explosive expirations Ending in a long-drawn forced inspiration producing a crowing sound Whoop and is usually followed by vomiting (Client coughs 5 10 times before inspiration)
ETIOLOGIC AGENT Bordatella pertussis o Non-motile, Gram-negative bacillus o 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
jcmendiola_Achievers2013 MODE of TRANSMISSION 1. Direct Contact and Droplet 2. Indirectly soiled linens and other articles contaminated
SOURCES of INFECTION Secretions from nose and throat of infected persons
INCIDENCE Infants are highly susceptible One attack produces lifetime immunity Second attack may be due to other microorganisms causing whooping cough syndrome
PATHOPHYSIOLOGY
COMPLICATIONS l Interstitial pneumonia Inflamed bronchioles l Atelectasis Due to mucus plugs l Convulsions Due to lack of O 2
l Umbilical hernia l Otitis media l Bronchopneumonia MOST DANGEROUS COMPLICATION l Severe malnutrition and starvation Due to persistent vomiting
CLINICAL MANIFESTATIONS 1. Catarrhal Stage a. Non-specific symptomatology, there is mucoid rhinorrhea, sneezing, Lacrimation and dry bronchial cough b. Cough is irritating, hacking, nocturnal and more severe c. Stage where disease is MOST COMMUNICABLE d. Lasts about 1 2 Weeks 2. Paroxysmal Stage a. Occurs on the 7 th 14 th Day b. Cough is spasmodic and recurrent with excessive explosive outbursts in a rapid series (5 10 rapid coughs in one expiration) c. Ends in a loud, crowing Inspiratory whoop, and choking on mucus that causes vomiting d. Paroxysmal coughing induces nose bleeding, venous pressure, periorbital edema, conjunctival hemorrhage and hemorrhage of the anterior chamber of the eye e. During a paroxysm, face becomes cyanotic, veins of face and neck are distended, eyes bulge or pop out of the eyeballs, tongue protrudes f. Profuse sweating, involuntary urination, lethargy and exhaustion g. Cough provoked by crying, eating, drinking or physical exertion h. Convulsions occur due to intracranial hemorrhage i. Between paroxysms, no physical signs and seems well j. Stage lasts from 4 6 Weeks 3. Convalescent Stage (Recovery Stage) a. Gradual decrease in the paroxysms of coughing, vomiting ceases b. Attack subsides after about 6 weeks from the onset
MODALITIES of TREATMENT 1. Supportive therapy a. F&E Replacement b. Adequate nutrition c. O 2 Therapy 2. Erythromycin and Ampicillin 3. Hyperimmune convalescent serum or gammaglobulin
NURSING MANAGEMENT Major Objective: Prevent complications Isolation and medical asepsis During a paroxysm, patient should NOT be LEFT ALONE (Suctioning equipment should be ready) Sunshine and fresh air Kept as still and quiet as possible Warm baths and keep bed dry (Free from soiled linens) I&O closely monitored
PREVENTION and CONTROL 1. Report at once any case of pertussis 2. Immunize children 3. Isolated 4 6 weeks from onset of illness 4. Public education for active immunization and early diagnosis
COMMON NURSING DIAGNOSES Ineffective airway clearance Altered nutrition: Less than body requirements Risk for infection / complication Sleep pattern disturbance Alteration in comfort
Paragonimiasis Lung Fluke o Chronic parasitic infection contracted by the consumption of fresh water crabs or crayfish
INTERMEDIATE HOST in PHILIPPINES: Antemelenia asperata
INCUBATION PERIOD: 9 12 Weeks
PERIOD of COMMUNICABILITY: May persist for 20 years for humans
MODE OF TRANSMISSION: Ingestion of raw or insufficiently cooked crabs Contamination of foods / utensils with Metacercariae Inadequately cooked meal of animal reservoir Drinking of contaminated water with infected larvae (Metacercariae)
jcmendiola_Achievers2013 PATHOPHYSIOLOGY
General Intervention > Treatment of infected persons > Disinfection > Sanitary disposal of excreta > Anti-mollusk campaigns > Health education on mode of transmission > Avoid infected foods > Avoid bathing in infected water
CLINICAL MANIFESTATIONS Acute Phase o Invasion and migration o Diarrhea, abdominal pain, fever, cough, urticaria, hepato-splenomegaly Chronic Phase o Pulmonary manifestations Cough, expectoration of discolored sputum, hemoptysis and chest radiography abnormality
MEDICAL MANAGEMENT 1. Drugs a. Praziquantel (Biltricide) DRUG of CHOICE! b. Bithionol (Bitin) Alternative 2. Surgical removal for heterotrophic cases DIAGNOSTIC TESTS ` Sputum Examination ` Immunology ` Cerebral Paragonimiasis Fluke in CNS ` Effusion fluid test / Biopsy