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Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
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Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
Waterborne & foodborne diseases
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Waterborne & foodborne diseases

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  • Rabies is a serious disease. Each year, it kills more than 50,000 people and millions of animals around the world. Rabies is a big problem in Asia, Africa, and Central and South America. In the United States, rabies has been reported in every state except Hawaii. Any mammal can get rabies. Raccoons, skunks, foxes, bats, dogs, and cats can get rabies. Cattle and humans can also get rabies. Only mammals can get rabies. Animals that are not mammals -- such as birds, snakes, and fish -- do not get rabies. Rabies is caused by a virus. An animal gets rabies from saliva, usually from a bite of an animal that has the disease.
  • Virus – minute organism not visible with ordinary light microscopy. It is parasitic in that it is entirely dependent on nutrients inside cells for its metabolic and reproductive needs. Can only be seen by use of eclectron microscopy. Consists of DNA or RNA covered with a protein covering called capsid.Neurotropic – viruses that reproduce in nerve tissueFilterable virus – virus causing infectious disease, the essential elements of which are so tiny that they retain infectivity after passing through a filter of the Berkefeld type.Berkefeld filter – a filter of diatomaceous earth designed to allow virus-size particles to pass throughDiatomaceous earth – substance composed of diatoms, a group of unicellular microscopic algae that possess a siiceous or calcium-containing cell wall.
  • You get rabies from the saliva of a rabid animal, usually from a bite. The rabies virus is spread through saliva. You cannot get rabies by petting an animal. You may get rabies from a scratch if the animal, such as a cat, was licking its paw before it scratched you. (Remember that the rabies virus is found in the saliva of an animal).
  • Transcript

    • 1. Amoebiasis • Entamoeba Hystolitica –protozoan (parasite) • MOT = 5 F’s, fecal oral route • IP = 2-4 weeks • IMMUNITY = xxx
    • 2. • Dx microscopic stool exam or rectal secretions • (tetra nucleated cyst and trophozoites) • Diarrhea and constipation (non dysenteric) • Blood streaked, diarrhea and watery mucoid, abd’l cramps (dysenteric) • Extra amoebiasispenile, vagina, spleen, liver, anal, lungs and meninges • Metronidazole (Flagyl)
    • 3. Typhoid Fever • • • • Salmonella typhosa (bacteria) MOT = same with amoebiasis (5 F’s) IP = 1-3 weeks IMMUNITY • Active = vaccine • Passive = xxx • Natural = lifetime immunity
    • 4. Pathophysiology • Oral ingestion • Bloodstream • Reticuloendothelial system (lymph node, spleen, liver) • Bloodstream • Gallbladder • Peyer’s patches of SI • necrosis and ulceration
    • 5. • 1st week step ladder (BLOOD) • 2nd week rose spot and fastidial • typhoid pyschosis (URINE & STOOL) • 3rd week (complications) intestinal bleeding, • perforation, peritonitis, encephalitis, • 4th week (lysis) decreasing S?SX • 5th week (convalescent)
    • 6. • Blood (typhi dot) 1st week after • Stool and urine 2nd week after • Chloramphenicol
    • 7. • Rose spot (abdominal rashes) • Step ladder fever to fastidial (peak of fever) typhoid psychosis • Peyer’s patches of small intestine • May stay in the gallbladder (hiding area)
    • 8. BACKGROUND Cholera, is a Greek word, which means the gutter of the roof. It is caused by bacteria: Vibrio cholerae, which was discovered in 1883 by Robert Koch during a diarrheal outbreak in Egypt. V. cholerae has 2 major biotypes: classical and El Tor, which was first isolated in Egypt in 1905. Currently, El Tor is the predominant cholera pathogen worldwide.
    • 9. EPIDEMIOLOGY/3 • Crowding & gathering of people during religious rituals (e.g. Muslims pilgrimage to Mecca or Hindu swimming festivals in holy rivers) enhance the spread of infection. • Index cases when travelled back to their homes may pass the organism to at risk individuals leading to secondary epidemic or small scale infection.
    • 10. PATHOGENESIS V cholerae cause clinical disease by producing an enterotoxin that promotes the secretion of fluid and electrolytes into the lumen of the gut. The result is watery diarrhea with electrolyte concentrations isotonic to those of plasma. The enterotoxin acts locally & does not invade the intestinal wall. As a result few WBC & no RBC are found in the stool.
    • 11. PATHOGENESIS/2 Fluid loss originates in the duodenum and upper jejunum; the ileum is less affected. The colon is usually in a state of absorption because it is relatively insensitive to the toxin. The large volume of fluid produced in the upper intestine, however, overwhelms the absorptive capacity of the lower bowel, which results in severe diarrhea.
    • 12. TRANSMISSION Cholera is transmitted by the fecal-oral route through contaminated water & food. Person to person infection is rare. The infectious dose of bacteria required to cause clinical disease varies with the source. If ingested with water the dose is in the order of 103-106 organisms. When ingested with food, fewer organisms are required to produce disease, namely 102-104.
    • 13. TRANSMISSION/2 V. cholerae is a saltwater organism & it is primary habitat is the marine ecosystem. Cholera has 2 main reservoirs, man & water. Animals do not play a role in transmission of disease. V. cholerae is unable to survive in an acid medium. Therefore, any condition that reduces gastric acid production increases the risk of acquisition.
    • 14. HOST SUSCEPTIBILITY The use of antacids, histamine-receptor blockers, and proton-pump inhibitors increases the risk of cholera infection and predisposes patients to more severe disease as a result of reduced gastric acidity. The same applies to patients with chronic gastritis secondary to Helicobacter pylori infection or those who have had a gastrectomy.
    • 15. AT RISK GROUPS All ages but children & elderly are more severely affected. Subjects with blood group “O” are more susceptible; the cause is unknown. Subjects with reduced gastric acid.
    • 16. CLINICAL PICTURE Incubation period is 24-48 hours. Symptoms begin with sudden onset of watery diarrhea, which may be followed by vomiting. Fever is typically absent. The diarrhea has fishy odor in the beginning, but became less smelly & more watery over time.
    • 17. CLINICAL PICTURE/2 The classical textbook “rice water” diarrhea, which describes fluid stool with very little fecal material, appears within 24h from the start of the illness. In severe cases stool volume exceeds 250 ml /kg leading to severe dehydration, shock & death if untreated.
    • 18. CHOLERA IN CHILDREN Breast-fed infants are protected. Symptoms are severe & fever is frequent. Shock, drowsiness & coma are common. Hypoglycemia is a recognized complication, which may lead to convulsions. Rotavirus infection may give similar picture & need to be excluded.
    • 19. TREATMENT The primary goal of therapy is to replenish fluid losses caused by diarrhea & vomiting. Fluid therapy is accomplished in 2 phases: rehydration and maintenance. Rehydration should be completed in 4 hours & maintenance fluids should replace ongoing losses & provide daily requirement.
    • 20. PUBLIC HEALTH ASPECTS Isolation & barrier nursing is indicated Notification of the case to local authorities & WHO. Trace source of infection. Resume feeding with normal diet when vomiting has stopped & continue breastfeeding infants & young children.
    • 21. PREVENTION Education on hygiene practices. Provision of safe, uncontaminated, drinking water to the people. Antibiotic prophylaxis to house-hold contacts of index cases. Vaccination against cholera to travellers to endemic countries & during public gatherings.
    • 22. CHOLERA VACCINES The old killed injectable vaccine is obsolete now because it is not effective. Two new oral vaccines became available in 1997. A Killed & a live attenuated types. Both provoke a local immune response in the gut & a blood immune response. Cholera vaccination is no more required for international travellers because risk is small.
    • 23. BLOOD BORNE DISEASES
    • 24. What Is Hepatitis? • Hepatitis means inflammation of the liver • Hepat (liver) + itis (inflammation)= Hepatitis • Viral hepatitis means there is a specific virus that is causing your liver to inflame (swell or become larger than normal)
    • 25. Inflammation Walls of scar tissue begin to form Healthy liver cells become trapped by a wall of scar tissue
    • 26. Viral Hepatitis 5 types: A: fecal-oral transmission B: sexual fluids & blood to blood C: blood to blood D: travels with B E: fecal–oral transmission Adapted from Corneil, 2003 Vaccine Preventable
    • 27. Hepatitis C • Affects each person differently • No vaccine available • Many people have the virus and do not even know it • Approximately 1 out of 100 Canadians infected Overall cure rate with new treatment is 55% Service 2003 *BC Hepatitis *
    • 28. Factors Affecting Progression • 30yrs or longer if: • Young at time of infection • Healthy liver at time of infection • Female • 20yrs or less if: • Drinking alcohol • Co-infection (HIV, Hep B) • Damaged liver before infection Adapted from Bigham, BC Hepatitis Services 2002
    • 29. Signs and Symptoms • Individuals may have one or more of the following symptoms, while others experience no symptoms: –Tiredness –Nausea –Muscle or joint pain –Trouble sleeping –Loss of appetite –Weight loss –Abdominal pain –Itchiness –Depression –Dark urine (pee)
    • 30. Signs and Symptoms • A few may have specific liver related symptoms initially: • Pale stool (poo) • Jaundice (yellowing of the skin or eyes)
    • 31. Prevention • Never share drug equipment • Straws, bills, needles, syringes, water, filter, cooker, pipes etc… • Never share tooth brushes/razors or any personal hygiene articles that have blood on them (even tiny amounts). • Practice safer sex
    • 32. Prevention • Always make sure new & sterilized equipment is being used for tattooing & piercing • Make sure ink for tattooing is not being shared • Do not touch dirty needles without proper equipment or following proper procedures
    • 33. Dirty Needle Precautions 1. Handle only if you have proper equipment • Sturdy pair of gloves, tongs or pliers and a puncture proof container (heavy plastic or metal) 2. Place needle in puncture proof container • Do not touch needle with bare hands and do not try to recap needle if cap present 3. Can dispose container in garbage but better if it is taken to health clinic or needle exchange 4. At school, notify custodian, teacher, nurse or police liaison officer
    • 34. Needle Prick 1. Do not “milk” prick site 2. Wash the area with soap and water 3. Go to nearest emergency department for assessment and treatment
    • 35. HEPATITIS A
    • 36. PREVENTION • If already infected with HAV 1. Wash your hands thoroughly every time you use the bathroom, before touching or preparing food, and before touching others. Wash carefully with soap and warm water and dry thoroughly. 2. Contaminated surfaces should be cleaned with household bleach to kill the virus. 3. Heat food or water to 185°F or 85°C to kill the virus. NOTE: Strict personal hygiene and hand washing help prevent transmission of HAV to others.
    • 37. PREVENTION… • If NOT yet Infected with HAV 1. Wash your hands carefully with soap and warm water several times a day, including every time you use the bathroom, every time you change a diaper, and before preparing food. 2. Do not eat raw or undercooked seafood or shellfish such as oysters from areas of questionable sanitation (just about everywhere). 3. Travelers to developing countries should not drink untreated water or beverages with ice in them. Fruits and vegetables should not be eaten unless cooked or peeled.
    • 38. Vaccines that Work against HAV • Havrix and VAQTA • contain no live virus and are very safe • given in a series of 2 shots. The second is given 6-18 months after the first. • protection starts about 2-4 weeks after the first shot. The second dose is necessary to ensure long-term protection. • thought to protect from infection for at least 20 years • must be given before exposure to the virus
    • 39. Groups Recommended to have the HAV Vaccine • All children older than 2 years who live in communities where the number of HAV infections is unusually high or where there are periodic outbreaks of hepatitis A • People who are likely to be exposed to HAV at work • . Travelers to developing countries (it must be given at least 4 weeks before travel) • Men who have sex with men • People who use illegal drugs • people with impaired immune systems or chronic liver disease • People with blood-clotting disorders who receive clotting factors
    • 40. MEDICAL TREATMENT • No specific medicines to cure infection with hepatitis A • immune globulin- given to people who are likely to be exposed to someone who is infected with HAV
    • 41. MEDICAL TREATMENT … 1. Bed rest during the acute stage and a diet that is both acceptable to the patient and nutritious are part of the treatment and nursing care. 2. During the period of anorexia, the patient should receive frequent small feedings, supplemented, if necessary, by IV fluids with glucose. 3. If dehydration occurs, IV fluids are being prescribed to help the patient feel better.
    • 42. MEDICAL TREATMENT… 4. Medicines are being prescribed by the physician to control nausea and vomiting. 5. People whose symptoms are wellcontrolled can be cared for at home. If dehydration or other symptoms are severe, then the patient is managed at the hospital. 6. Gradual but progressive ambulation seems to hasten recovery, provided the patient rests after activity and does not participate in activities to the point of fatigue.
    • 43. Dietary Management 1. 2. 3. 4. Recommend small, frequent meals. Provide intake of 2,000 to 3,000 kcal/day during acute illness. Although early studies indicate that a high-protein, high-calorie, diet may be beneficial, advise patient not to force food and to restrict fat intake. Carefully monitor fluid balance.
    • 44. Dietary Management 5. 6. 7. If anorexia, nausea and vomiting persist, enteral feedings may be necessary. Instruct patient to abstain from alcohol during the acute illness and for 6 months after recovery. Advise patient to avoid substances (medication, herbs, illicit drugs and toxins) that may affect liver function.
    • 45. NURSING MANAGEMENT • The patient is usually managed at home unless symptoms are severe. • The nurse assists the patient and family in coping with temporary disability and fatigue that are common in hepatitis and instructs them to seek additional health care if the symptoms persist or worsen
    • 46. Self-Care at Home 1. Take it easy; curtail your normal activities and spend time resting at home. 2. Drink plenty of clear fluids to prevent dehydration. 3. Avoid medicines and substances that can cause harm to the liver such as acetaminophen (Tylenol) and preparations that contain acetaminophen.
    • 47. Self-Care at Home… 4. Avoid alcoholic beverages, as these can worsen the effects of HAV on the liver. 5. Avoid prolonged, vigorous exercise until symptoms start to improve. 6. Call your health care provider if symptoms worsen or a new symptom appears. 7. Be very careful about personal hygiene to avoid fecal-oral transmission to other members of the household.
    • 48. HEPATITIS B
    • 49. PREVENTION • immune globulin (BayHep B, NabiHB) • given along with the hepatitis B vaccine to unvaccinated people who have been exposed to hepatitis B • Engerix-B, Recombivax HB • safe and works well to prevent the disease • a total of 3 doses of the vaccine are given over several months • recommended for all children younger than 19 years
    • 50. Groups Recommended to have the HBV Vaccine 1. All children younger than 18 years, including newborns-especially those born to mothers who are infected with HBV. 2. All health care and public safety workers who may be exposed to blood 3. People who have hemophilia or other blood clotting disorders and receive transfusions of human clotting factors 4. People who require hemodialysis for kidney disease
    • 51. Groups Recommended to have the HBV Vaccine… 5. Travelers to countries where HBV infection is common - This includes most areas of Africa, Southeast Asia, China and central Asia, Eastern Europe, the Middle East, the Pacific Islands, and the Amazon River basin of South America. 6. People who are in prison 7. People who live in residential facilities for developmentally disabled persons
    • 52. Groups Recommended to have the HBV Vaccine… 8. People who inject illegal drugs 9. People with chronic liver disease such as hepatitis C 10. People who have multiple sex partners or have ever had a sexually transmitted disease 11. Men who have sex with men
    • 53. Other ways to protect yourself from HBV infection • Safe Sex • Don't share needles or other sharp equipments such as razors • Health care workers should follow standard precautions and handle needles and sharps safely • Think about the health risks if you are planning to get a tattoo or body piercing
    • 54. MEDICAL TREATMENT • Acute hepatitis B infection • • • If dehydration occurs, IV fluids are being prescribed to help the patient feel better. Medicines are being prescribed by the physician to control nausea and vomiting. People whose symptoms are wellcontrolled can be cared for at home. If dehydration or other symptoms are severe, then the patient is managed at the hospital NOTE: No treatment can prevent acute HBV infection from becoming chronic
    • 55. MEDICAL TREATMENT… • Chronic hepatitis B infection • Regularly measuring the amount of HBV DNA in the blood gives a good idea of how fast the virus is multiplying • Treatment: antiviral drugs • not appropriate for everyone with chronic HBV infection. It is reserved for people whose infection is most likely to progress to chronic hepatitis B.
    • 56. Medications • Interferon alfa-2b (Intron A) - was the standard treatment of chronic hepatitis B for several years • Lamivudine (Epivir) - an alternative for people who cannot or do not want to take interferon • Adefovir dipivoxil (Hepsera) works well even in people whose disease is resistant to lamivudine • Entecavir (Baraclude) - newest medication approved for chronic hepatitis B
    • 57. Surgery and Other Therapy • No herbs, supplements, or other alternative therapy is known to work as well as antiviral medication in slowing HBV replication and promoting liver healing in hepatitis B. • no surgical therapy for hepatitis B • If liver damage is severe enough, the only treatment that will help is liver transplant
    • 58. NURSING MANAGEMENT • nurse identifies psychosocial issues and concerns, particularly the effects of separation from family and friends if the patient is hospitalized during acute and infective stage. • Follow-up visits by a home care nurse may be needed to assess the patient’s progress and answer the family members’ questions about disease transmission • reinforces previous instructions
    • 59. Self-Care at Home 1. Drink plenty of fluids to prevent dehydration. Water is fine; broth, sports drinks, Jello, frozen ice treats (such as Popsicles), and fruit juices are even better because they provide calories. 2. Avoid medicines and substances that can cause harm to the liver, such as acetaminophen (Tylenol). 3. Avoid drinking alcohol until your health care provider OKs it. If your infection becomes chronic, you should avoid alcohol for the rest of your life.
    • 60. Self-Care at Home… 4. 5. Avoid using drugs, even legal drugs, without consulting your doctor. Hepatitis can change the way drugs affect you. If you take prescription medications, continue taking them unless your health care provider has told you to stop. Do not start any new medication (prescription or nonprescription), herbs, or supplements without first talking to your health care provider. Try to eat enough for adequate nutrition. Eat foods that appeal to you, but try to maintain a balanced diet. Many people with hepatitis have the greatest urge to eat early in the day.
    • 61. Self-Care at Home… 6. Take it easy. Your activity level should match your energy level. 7. Avoid prolonged, vigorous exercise until symptoms start to improve. 8. Call your health care provider for advice if your condition worsens or new symptoms appear. 9. Avoid any activity that may spread the infection to other people
    • 62. HEPATITIS C
    • 63. PREVENTION • no vaccine for the prevention of HCV transmission • best means of preventing transmission of HCV is to prevent contact with infected blood and organs and to avoid high-risk sexual behavior such as multiple partners and anal contact. • Avoiding alcohol and drugs that can damage the liver may help slow the rate of progression of the disease.
    • 64. MEDICAL TREATMENT • pegylated interferon alpha (Pegasys, PEG-Intron) - often combined with an antiviral drug called ribavirin (Virazole)
    • 65. Certain medical conditions preclude the use of interferon • • • • • Depression and certain other mental and neurologic disorders Active alcohol or drug abuse Autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, or psoriasis Low blood hemoglobin level (anemia) or blood cell counts Cirrhosis that is severe enough to cause symptoms such as jaundice, wasting, fluid retention that causes swelling, or mental disturbances
    • 66. Medication • Interferon alpha (Intron A) pegylated type (Pegasys, PEGIntron) • Interferon is a protein that the body makes naturally in response to viral infections in order to fight the infection. Pegylation describes a chemical process that makes the interferon last longer in the body. • Ribavirin (Virazole) • has little effect on HCV, but interferon increases its potency
    • 67. Surgery and Other Therapy • For end-stage liver disease, the only treatment is liver transplantation • Alternative therapies has not been proven to work in any scientific study • most promising complementary therapy is milk thistle • licorice and ginseng • ginger (to reduce nausea) and St. John's wort (to relieve depression) may be taken as complementary therapy to help relieve the side effects of interferon
    • 68. NURSING MANAGEMENT • Same as Hepatitis B
    • 69. Patient Instruction • • • • • Eat a varied, healthy diet, take part in some physical activity daily, and get plenty of rest. Drink plenty of water and other noncaffeinated fluids to stay well hydrated. Avoid alcoholic beverages and medicines such as nonsteroidal antiinflammatory drugs (like Brufen, Aleve, Advil) that can be harmful in people with liver disease. If you have symptoms, avoid prolonged or vigorous physical exercise until your symptoms improve. If symptoms worsen at any time, contact
    • 70. Self-Care at Home 1. Take it easy; get plenty of rest. 2. Drink plenty of fluids to prevent dehydration. 3. Do not drink alcohol of any kind, including beer, wine, and hard liquor. 4. Avoid medicines and substances that can cause harm to the liver such as acetaminophen (Tylenol) and other preparations that contain acetaminophen. 5. Avoid prolonged, vigorous exercise until symptoms start to improve
    • 71. RABIES
    • 72. CONTENTS:
    • 73. What is rabies? (DEFINITION & ETIOLOGY) • • Is an acute infectious disease of warmblooded animals and humans characterized by an involvement of the nervous system resulting in death. It is caused by the RABIES VIRUS, a rhabdovirus of the genus lyssavirus.
    • 74. The Rabies Virus RV – a neurotropic filterable virus present in the saliva of rabid animals. It has a preferrence for nerve tissues. Rod-shaped rabies viruses colored for effect RHABDOVIRUS: any group of rod-shaped RNA viruses with 1 important member, rabies virus, pathogenic to man. The virus has a predilection for tissue of mucus-secreting glands and the Central Nervous System. All warm-blooded animals are susceptible to infection with these viruses. Parts of the rabies virus A rhabdovirus of the genus lyssavirus. RHABDO: from Greek rhabdos, "rod" LYSSA: Greek – frenzy, rage, fury, canine madness This is a photograph of the virus under electron microscope
    • 75. How do you get rabies? (MODE & MEDIA OF TRANSMISSION, IMMUNITY) •All warm-blooded mammals are susceptible. Natural immunity in man is unknown. •You get rabies through the saliva of an infected animal by an exposure to an open break in the skin such as bites, open wound or scratch and inhalation of infectious aerosols such as from bats. •In some cases, it is transmitted through organ transplants (corneal transplant), from an infected person. •The virus gets transmitted through saliva, tears, semen, some liquor (amniotic fluid, CST) but not blood, urine or stool.
    • 76. How do you know if an animal has rabies? • Animals with rabies may act differently from healthy animals. • Some signs of rabies in animals are:      • • changes in an animal’s behavior general sickness (fever, restlessness) problems swallowing increased drooling aggression (biting at inanimate objects, aimless running) Wild animals may move slowly or may act as if they are tame. Some wild animals (foxes, raccoons, skunks) that normally avoid porcupines, may even try to bite these prickly rodents. A pet that is usually friendly may snap at you or may try to bite.
    • 77. How do you know if one has rabies? (DIAGNOSIS) •There is yet no way of immediately knowing who had acquired rabies virus. No tests are available to diagnose rabies in humans before the onset of clinical disease. •The most reliable test for rabies in patients who have clinical signs of the disease is a DIRECT IMMUNOFLUORESCENT STUDY of a full thickness biopsy of the skin taken from the back of the neck above the hair line. •The RAPID FLUORESCENT FOCUS INHIBITION TEST is used to measure rabies-neutralizing antibodies in serum. This test has the advantage of providing results within 24 hours. Other tests of antibodies may take as long as 14 •days.
    • 78. EPIDEMIOLOGY RABIES INCIDENCE: WORLDWIDE:35, 00050, 000 cases/ year (WHO)
    • 79. EPIDEMIOLOGY PHILIPPINES: 350-450 cases/ year 5-7 per million population DOG BITE INCIDENCE: 140, 000- 560, 000/ year 200-800 per 100, 000 population/ year AGE MOST AFFECTED: 5-14 year age group (53% of cases) BITING ANIMALS: (SLH STUDY 1982- 2002) DOGS: 98% PET: 88% STRAY: 10% CATS: 2%
    • 80. • Based on the report from NCDPC (2004), the six regions with the most number of rabies cases are Western Visayas, Central Luzon, Bicol, Central Visayas, Ilocos and Cagayan Valley • Data shows that 53.7 percent of animal bite patients are children • Dogs remain the principal animal source of rabies
    • 81. STAGES OF RABIES INFECTION Rabies virus Entry into the body INCUBATI0N PERIOD (20 – 90 days) INVASION (0 – 10 days) EXCITEMENT (2 – 7 days) PARALYTIC COMA (5 – 14 days) DEATH
    • 82. RABIES CLASSIFICATION ANIMAL RABIES • There are two common types of rabies. One type is "furious" rabies. Animals with this type are hostile, may bite at objects, and have an increase in saliva. In the movies and in books, rabid animals foam at the mouth. In real life, rabid animals look like they have foam in their mouth because they have more saliva. The second and more common form is known as paralytic or "dumb" rabies. The dog pictured below has this type. An animal with "dumb" rabies is timid and shy. It often rejects food and has paralysis of the lower jaw and muscles. • Another two types of rabies. One type is “urban” rabies. The type of rabies in domestic dogs and cats. The other type is called “ sylvatic” rabies. These type came from wild animals such as bats, weasels, skunks and moles & voles.
    • 83. HUMAN RABIES • Humans also have a “furious” type, the classic foaming of the mouth, aggression, apprehension & hydrophobia, and the “dumb” type, progressive paralysis of the body until they couldn’t breathe anymore.
    • 84. DIFFERENT STAGES OF RABIES INFECTION C A T S D O G S B A T S VIRUS IN SALIVA INHALED AEROSOLS VIRUS IN SALIVA INVASION PHASE INVASION PHASE PARALY SIS EXCITEMENT PARALY SIS DEATH DEATH
    • 85. INVASION STAGE • Also called PRODOME PERIOD; • • Prodrome – symptom indicative of an approaching disease 2-10 DAYS Sensory changes on the site of entry. Pain: dull, constant pain referable to the nervous pathways proximal to the location of the wound or itching, intermittent, stabbing pains radiating distally to the region of inoculation. In general, sensitivity is the early symptom which may be ascribed to the stimulative action of the virus affecting groups of neurons, esp. sensory system. Though there is apt to be decreased sensitivity to local pain e.g. needle introduction, patient may complain bitterly of drafts & bed clothes which produce a general stimulation Tick me!
    • 86. • Fever,headache malaise sore throat anorexia increased sensitivity (bright lights, loud noises) increased muscle reflex irritability, tics and muscle tone • Overactive facial expression
    • 87. EXCITATION STAGE • • • • • • • • • Also called ACUTE NEUROLOGICAL PHASE; hyperactivity 2 – 10 DAYS Imminent thoraco-lumbar involvement (SNS): pupillary dilation, lacrimation increased thick saliva production / foaming of mouth, excessive perspiration, increased HR Anxiety: increased nervousness, insomnia, apprehension; a strong desire to be up, wandering aimlessly about, and Fear: a sense of impending doom Hydrophobia (perhaps, SNS stimulation: depresses GI activity > inhibits esophageal, gastric & intestinal function) > violent expulsion of fluids, drooling (in attempt not to swallow) > dehydration and parched mouth & tongue Pronounced muscular stimulation & general tremor Mania (tearing of clothes & bedding, cases of biting & fighting rare but may occur) and Hallucinations with lucid intervals (normal mental function in which patient is well-oriented & answers questions intelligently) Convulsions( besides r/t pronounced muscular stimulation, further precipitated by sensory stimuli – sight, sound, name of water > throat spasms > choking > apnea, cyanois, gasping > death, but if patient survive excitement phase… Tick me Tick me 1st! next! Sympathetic nervous system Parasympathetic nervous system
    • 88. Tick me!
    • 89. PARALYTIC STAGE -also called DEPRESSION PHASE • Gradual weakness of muscle groups • muscle spasms cease • OCULAR PALSY – strabismus, ocular incoordination, nystagmus, diplopia, central type partial blindness > responds poorly to light, @ times pupil is constricted or unequal (parasympathetic involvement) • Oro-facial: FACIAL & MASSETER PALSY > difficulty closing eyes & mouth, face expressionless • Oral: Weakness of muscles of phonation > hoarsness & loss of voice • Loss of tendon reflexes, always precedes weakness of extremity • Corneal reflex decreased or absent, dry
    • 90. • Ears: VERTIGO . Middle ear disease . Early symptom, but may develop @ any period • Neck stiffness • (+) Babinski [lesions of pyramidal tract], ( - ) Kernig’s ( - ) Brudzinski’s • Cardiac: shifts from tachycardia (100 – 120bpm) @ bed rest to bradycardia (40 -60 bpm) • Respi: Cheyne-Stokes > breathing pattern characterized by a periodic 10 – 6- sec of apnea followed by gradual increasing depth and frequency of respiration • Local sensation (pin prick, heat, cold) diminished • Incoordination
    • 91. • Hydrophobia and aerophobia gone, but still has some difficulty swallowing • General arousal (PNS stimulation) • Bladder & intestinal retention and obstipation (damage to to innervation of the musculature of intestine & bladder)(SNS damage) in some cases, patient shows period of recovery, this apparent remission is followed by progressive • Ascending, flaccid paralysis of extremities until it reaches the respiratory muscle • Apathy, stupor • Complications: Pneumothorax, thrombosis, secondary infections
    • 92. MANAGEMENT NURSING INTERVENTIONS • HIGH RISK FOR INFECTION TRANSMISSION • provide patient isolation • handwashing. Wash hands before and after each patient contact and following procedures that offer contamination risk while caring for an individual patient. Handwashing technique is important in reducing transient flora on outer epidermal layers of skin. • Wear gloves when handling fluids and other potential
    • 93. • KNOWLEDGE DEFICIT (about the disease, cause of infection and preventive measures) • assess patient’s and family’s level of knowledge on the disease including concepts, beliefs and known treatment. • Provide pertinent data about the disease: • organism and route of transmission • treatment goals and
    • 94. • ALTERED BODY TEMPERATURE: FEVER RELATED TO THE PRESENCE OF INFECTION. Since fever is continuous, provide other modes to reduce discomfort. • If patient is still well oriented, Inform the relation of fever to the disease process. The presence of virus in the body … • Monitor temperature at regular intervals • Provide a well ventilated environment free from drafts and wind.
    • 95. • DEHYDRATION related to refusal to take in fluids secondary to throat spasms and fear of spasmodic attacks. • Assess level of dehydration of patient. • Maintain other routes of fluid introduction as prescribed by the physician e.g. parenteral routes • Moisten parched mouth with cotton or gauze dipped in water but not dripping.
    • 96. IMMUNIZATION ACTIVE IMMUNIZATION - induce antibody and T-cell production in order to neutralize the rabies virus in the body. It induces an active immune response in 7-10 days after vaccination, which may persist for one year or more provided primary immunization is completed. TYPES: a. PVRV (Purified Vero Cell Rabies Vaccine) b. PCEVC (Purified Chick Embryo Cell Vaccine)
    • 97. PASSIVE IMMUNIZATION - RIG (Rabies Immune Globulins) - provide the immediate availability of antibodies at the site of exposure before it is physiologically possible for the pt.to begin producing his own antibodies after vaccination. - Important for pts. w/ Cat III exposures Types: a. HRIG (Human Rabies Immune Globulins) b. Highly Purified Antibody Antigen Binding fragments c. ERIG (Equine Rabies Immune Globulins)
    • 98. VACCINATION (Intradermal Schedule) Day of Immunization PVRV/PCECV Site DAY 0 0.1 ml L & R deltoids/ anterolateral thighs of infants DAY 3 0.1 ml L & R deltoids/ anterolateral thighs of infants DAY 7 0.1 ml L & R deltoids / anterolateral thighs of infants DAY 28/30 0.1 ml L & R deltoids/ anterolateral thighs of infants
    • 99. Intramuscular Schedule Day of Immunization PVRV PCECV Site Day 0 0.5 ml 1.0 ml One deltoid/ anterolateral thigh of infants Day 3 0.5 ml 1.0 ml Same Day 7 0.5 ml 1.0 ml Same Day 14 0.5 ml 1.0 ml Same Day 28 0.5 ml 1.0 ml same
    • 100. MANAGEMENT OF RABIES PATIENT • Once symptoms start, treatment should center on comfort care, using sedation & avoidance of intubation & life support measures once diagnosis is certain 1. a. b. c. MEDICATIONS Diazepam Midazolam Haloperidol + Dipenhydramine
    • 101. 2. SUPPORTIVE CARE - Pts w/ confirmed rabies should receive adequate sedation & comfort care in an appropriate medical facility. a. Once rabies diagnosis has been confirmed, invasive procedures must be avoided b. Provide suitable emotional and physical support c. Discuss & provide important info. to relatives concerning transmission of dse. & indication for PET of contacts d. Honest gentle communication concerning prognosis should be provided to relatives of pt
    • 102. 3. INFECTION CONTROL a. Patient should be admitted in a quiet, draftfree, isolation room b. HLCR workers & relatives in contact w/ pt should wear proper personal protective equipment (gown, gloves, mask, goggles) 4. DISPOSAL OF DEAD BODIES
    • 103. Tetanus
    • 104. • Tetanus • Clostridium tetani • MOT = wound setting • IP = 3 -21 days • IMMUNITY • Active = TT • Passive = TAT and TIG • Natural = active none, passive (+)
    • 105. • Wound Infection • FATAL INFECTION OF THE CNS • TOXIN-NEUROTOXIN
    • 106. • PATHOPHYSIOLOGY: • SETTING OF WOUND ---- ENTRANCE OF C.T. ---- RELEASES TETANUS TOXIN ---- TETANOSPASMIN (CNS), TETANOLYSIN (BLOOD) ---ABSORBED BY MOTOR NERVE ENDINGS ---- SYNAPSE (CONNECTION BETWEEN NEURONS) ---- MYONEURAL JUNCTION ---- ACETYLCHOLINE DISTURBANCE IN THE TRANSMISSION OF NERVE IMPULSE
    • 107. • • • • Trismus – lock jaw Risus sardonicus - maskface Risorius - grinsmile Dx wound and blood extraction (non specific)
    • 108. • Immunization • DPT (0.5 ml IM) 1 – 1 ½ months old 2 after 4 weeks 3 – after 4 weeks • 1 st booster – 18 mos • 2 nd booster – 4-6 yo • subsequent booster – every 10 yrs thereafter • TT (0.5 ml IM) TT1 - 6 months within preg TT2 - one month after TT1 TT3 to TT5 - every succeeding preg or every year • TAT (horse) and TIG (human)
    • 109. • Management • 1. Anticonvulsant, muscle relaxants, • antibiotics, wound cleansing and debridement, hyperbaric chamber • 2. Active-DPT and tetanus toxoid • 3. Passive-TIG and TAT, placental immunity

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