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Contact-transmitted infections

Invasion of the skin or mucous membranes by a pathogenic organism or parasite.

Infection in which entrance of the pathogenic organism (or the parasite) occurs through the skin or mucus membranes.

Some infectious agents can invade the intact (undamaged) skin or mucous membranes, but the majority needs injured surfaces in the form of abrasions, scratches, wounds or ulcers.

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Contact-transmitted infections

  1. 1. CONTACT – TRANSMITTED INFECTIONS Dr. Dalia El-Shafei Assist.Prof., Community Medicine Department, Zagazig University http://www.slideshare.net/daliaelshafei
  2. 2.  Invasion of the skin or mucous membranes by a pathogenic organism or parasite.  Infection in which entrance of the pathogenic organism (or the parasite) occurs through the skin or mucus membranes.  Some infectious agents can invade the intact (undamaged) skin or mucous membranes, but the majority needs injured surfaces in the form of abrasions, scratches, wounds or ulcers.
  3. 3. Viral AIDS Hepatitis “B&C” Rabies Bacterial Anthrax Gas gangrene Gonorrhea Leprosy Tetanus Parasitic Ancylostomiasis Schistosomiasis Spirochetes Syphilis
  5. 5. Viral AIDS Hepatitis “B&C” Rabies Bacterial Anthrax Gas gangrene Gonorrhea Leprosy Tetanus Parasitic Ancylostomiasis Schistosomiasis Spirochetes Syphilis
  6. 6. HBV, HCV and HDV are transmitted mainly percutaneous “contact infections”. HAV is transmitted mainly by faeco-oral transmission )food borne disease(. HDV & HFV are similar to HBV. HEV is similar to HAV. HGV is similar to HCV. Other viruses cause acute hepatitis e.g. cytomegalovirus, Epstein-Barr virus.
  7. 7. EPIDEMIOLOGY OF VIRAL HEPATITIS • Usually the disease is self-limited, however some cases show massive or chronic hepatic necrosis & chronic hepatitis. • Virus B and C may be complicated by liver cirrhosis & hepatocellular carcinoma. • An estimated 248 million people have chronic HBV infection globally. In Egypt the prevalence is < 2%.
  8. 8. Viral hepatitis C is a major health problem in Egypt.
  9. 9. • Egypt is one of the countries most affected by HCV. • The Egypt Demographic and Health Surveys (EDHS) measured antibody prevalence among the adult population aged 15–59 years at 14.7% in 2009 & at 10.0% in 2015 substantially higher than global levels. • Egypt developed a national strategy for HCV control & established HCV prevention & treatment programs. • Following successful negotiations for 99% discounted direct-acting antivirals (DAAs) prices, Egypt launched an ambitious national HCV treatment program aiming to treat over 250,000 chronically infected individuals per year, with the goal of achieving a national chronic infection prevalence of < 2% by 2025. • Despite this progress, existing evidence suggests ongoing HCV transmission in Egypt, with higher incidence levels relative to other countries.
  10. 10. Hepatitis B Hepatitis C CausativeAgent • Hepatitis B Virus (HBV) • DNA virus • Contains: HBsAg, HBcAg, HBeAg • It is more resistant than virus A to heat & disinfectants and can retain infectivity for at least 1 month at room temperature. • Hepatitis C Virus (HCV). • RNA virus, • There are 6 known genotypes and 50 or more subtypes of HCV • Types 1,2 and 3 are worldwide while type 4 is found in North Africa and Middle East, type 5 in south Africa, 6 in Asia • About 90% of HCV in Egypt belongs to subtype 4b which has less response to interferon therapy.
  11. 11. HCVHBV Cases, carriersCases, carriersReservoir 1-2 w before symptoms, clinical course So long is HBs AG (+ve) appear 30-60 days after infection Period of communicability 1- Percutaneous exposure to infective body fluid 2-Insufficient sterilized needles, syringes, razors, toothbrushes, surgical & dental instruments, blood transfusion (Blood borne pathogens “BBP”). 3- Maternal fetal transmission 4- Organ transplantation 5- Sexual transmission Mode of transmission
  12. 12. HCVHBV 2-12 weeks (average 6 weeks)60-150 days (average 90 days)IP 1-Asymptomatic or mild symptoms. 2.Low grade fever, fatigue, N,V , Rt. sided abdominal pain, 3.Jaundice. 4.Self-limiting infection after 3-6 months. No jaundice. 5.Chronic infection “80%”: weakness, pain in Rt. upper abdomen. 1-Nonspecific prodroma of malaise, fever, headache, myalgia. 2- Dark urine, jaundice. 3-Asymptomatic or have illness not specific for hepatitis B “50%”. C/P Liver cirrhosis “25%”, liver failure, Cancer liver, Renal disorders, formation of auto- antibodies, DM Fulminant hepatitis, Chronic hepatitis, Liver cirrhosis, Causes up to 80% of hepatocellular carcinoma. Complications
  13. 13. HCVHBV -C/P: ↑ liver enzymes- detection of AB by ELISA +VE ELISA: PCR test -Liver biopsy - Genotyping of HCV -Serum fibrosis markers C/P- ↑ liver enzymes- markers: HBsAb: active or past infection HBsAg: disease or chronic carrier state- HBcAB:recent infection Diagnosis
  14. 14. HCVHBV No specific preventive measures1- HBV, 3 Doses,0.5 ml each at 0, 1,6 months (for who?). Give 95% protection for 7 years. 2- Ig, 0.1ml/kg, 2 doses 1 month apart given at once after exposure (for who?) not > 48hs 3- Combined vaccine+ Ig 1ry (specific) Prevention 1- Screening & testing blood, plasma and organ tissue donors. 2- Health education. 3- Sterilization of surgical instruments & use of disposable syringes. 4- Prevention of drug abuse & needle shared injections. 5- Prevention of tattooing, prevention of use of common razors or scissors. 6- Surgeons should use thick protective gloves. 7- Proper handling & disposal of sharp instruments and needles. 8- Quarantine measures: some countries prevent HCV patients from entrance. 1ry (general) Cases: case finding- notification-isolation-disinfection-HE-treatment (antiviral, antioxidants). Contact: enlistment- examination-HE-specific protection in case of HBV (vaccination, seroprophylaxis) 2ry Rehabilitation of liver failure or cancer liver cases. 3ry
  15. 15. TREATMENT • HCV TTT continues to evolve rapidly. • Since 2014, several new all-oral direct-acting antiviral agents have been approved for use. • Egyptian MOH proposed a new national strategy to control the HCV epidemic with a greater capital fund & with support from the WHO as well as other institutes. • This scheme was entitled “The Plan of Action for the Prevention, Care and Treatment of Viral Hepatitis 2014–2018” & promoted sofosbuvir (Sovaldi™) as its 1ry ttt.
  16. 16. The scheme aims to treat 300,000 patients annually MOH 38% HIO 51% Private payments 3% Patients 8% TTT Cost
  17. 17. REMMEBER Risk of infection & required post exposure prophylaxis for the 3 most commonly transmitted pathogens
  18. 18. RABIES
  19. 19. Definition: acute viral zoonosis, transmitted to man by bite of an infected animal & causing acute encephalomyelitis illness. Causative organism: Rabies virus, RNA rhabdovirus with 5 genetically related viruses.
  20. 20. Reservoir: Domestic & wild animals “dog, cat, fox, wolf, rats, bat, etc”. Exit: in saliva of rabid animals. Modes of transmission: Infection is transmitted with saliva through the bite of an infected animal usually or when saliva gets on an injured skin by lick. No man to man infection.
  21. 21. IP: - Depends on the distance between the site of bite & brain. - Usually 2-8 weeks, but up to 1 year. PATHWAY OF RABIES VIRUS
  22. 22. Clinical picture: History of animal bite. Non-specific manifestation: e.g. FHMA. Specific manifestations: Paraesthesia Aerophobia Hydrophobia Difficult swallowing Convulsions Death: 1-2 weeks Convulsions Respiratory paralysis
  23. 23. Diagnosis C/P following a history of an animal bite. Detection of virus particles in saliva, C.S.F or urine Detection of viral antigen in skin biopsy using direct fluorescent antibody technique. Rising antibody titers in blood or C.S.F.
  24. 24. Control: Measures for animals: Destruction of stray dogs. Vaccination of domestic animals: inactivated rabies vaccine every 2 years & giving license. Quarantine of imported animals
  25. 25. MEASURES FOR MAN (A) Pre-exposure vaccination: vaccination of at risk e.g. night guards & zoo workers. 3 inactivated types of rabies vaccines are used: I.M., 3 doses, 1 ml each, in deltoid region on days 0, 7, and 21 or 28. Booster dose every 2 years if risk of exposure continues. Human diploid cell vaccine (HDCV) Rabies vaccine adsorbed (RVA) Duck embryo vaccine (DEV)
  26. 26. MEASURES TO THE WOUND (BITE) • Immediate local ttt of animal bite & scratches through repeated flushing & cleaning of wound with soap & water. • A rabies immunoglobulin (20 IU/kg) or antiserum (40 IU/kg) is infiltrated locally around the wound (half the dose). The other half is given I.M. • Wound should not be sutured then wound is dressed. • Give tetanus prophylaxis & antibacterial treatment.
  27. 27. Measures for cases Notification to LHO. Isolation. Disinfection of saliva & soiled articles. Treatment: only symptomatic Measures of contacts: No specific measures, as there is no man to man transmission; however, avoid contamination of skin wound or mucous membrane by patient's saliva.
  28. 28. A life threatening clinical condition that represent the late clinical stage of infection with HIV which results in progressive damage to the immune and other organ systems specially CNS. Acquired Immunodeficiency Syndrome (AIDS) Causative agent:  Human immune deficiency virus (HIV): DNA retrovirus.  2 serologically & geographically distinct types with similar epidemiological characteristics:HIV-1 & HIV-2.
  29. 29. Specific affinity to T-helper lymphocyte cells causing their depletion.
  30. 30.  Reservoir: man  Exit: in blood and body fluids e.g. semen, vaginal secretion, saliva and tears.  Period of communicability: so long the infected person is alive.  IP: variable, but 50% of those infected develop AIDS about 10 years after infection.
  31. 31. Non-specific manifestations:
  32. 32. Specific indicator diseases: Opportunistic infections • Pneumocystis carinii pneumonia • Chronic cryptosporidiosis • CNS toxoplasmosis. Neurologic diseases • Dementia • Sensory neuropathy. Cancers • Kaposi sarcoma • Hodgkin's lymphoma. Others • T.B.
  33. 33. HIV CONTROL Preventive measures: 1ry (HE - ↑ religious roots - disposable syringe - testing blood donors - no tattooing or acupuncture) 2ry Measures for cases: Case finding – Notification - Isolation is unnecessary - Disinfection - ttt of opportunistic infections, Antiretroviral ttt. Measures for contacts: Notification – Screening – HE - No vaccination or chemoprophylaxis).
  34. 34. No vaccination is available yet. Pre-exposure prophylaxis (PrEP) • Highly effective in preventing HIV infection. • 2 oral antiretroviral “ARV” medications (tenofovir & emtricitabine) • Co-formulated as a single pill (Truvada) that is taken once daily. Post-exposure prophylaxis (PEP) • 2014 WHO guidelines • Irrespective of exposure source • As soon as possible to be effective • Within 72 hours (3 days) after a possible exposure • 3 or more ARV medicines every day for 28 days.
  35. 35. N .B. WHO recommends immunization of asymptomatic HIV infected children with the EPI (Expanded program Immunization) vaccines; those who are symptomatic should not receive BCG vaccine. Live Measles-Mumps-Rubella (MMR) & polio vaccines are recommended for all HIV-infected
  37. 37. Viral AIDS Hepatitis “B&C” Rabies Bacterial Anthrax Gas gangrene Gonorrhea Leprosy Tetanus Parasitic Ancylostomiasis Schistosomiasis Spirochetes Syphilis
  38. 38. CAUSATIVE AGENT Clostridium tetani
  39. 39. PERIOD OF COMMUNICABILITY It is the only vaccine-preventable disease that is infectious but not contagious from person to person. IP.: 6-8 days
  40. 40. Mode of infection Surgical (postoperative) tetanus Puerperal tetanus Contamination of wounds Neonatal tetanus
  41. 41. SYMPTOMS - Tetanic seizures (painful, powerful bursts of ms. contraction) - Ms. spasms of larynx or chest wall: asphyxiation - Stiffness of abdominal & back ms.: resus sardonicus
  42. 42. The back muscles are more powerful, thus creating the arc backward “Oposthotonus” Baby has neonatal tetanus with complete rigidity.
  43. 43. Newborn showing risus sardonicus & generalized spasticity
  44. 44. TYPES OF TETANUS: A- MOST COMMON TYPES Generalized tetanus - descending pattern: lockjaw  stiffness of neck  difficulty swallowing  rigidity of abdominal and back muscles. - Spasms continue for 3-4 weeks, and recovery can last for months - Death occurs when spasms interfere with respiration. Neonatal tetanus: - Form of generalized tetanus that occurs in newborn infants born without protective passive immunity because the mother is not immune. - Usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with an unsterile instrument.
  45. 45. B-Uncommon types: • Local tetanus: persistent muscle contractions in the same anatomic area as the injury, which will however subside after many weeks; very rarely fatal; milder than generalized tetanus, although it could precede it. • Cephalic tetanus: occurs with ear infections or following injuries of the head; facial muscles contractions.
  46. 46. DIAGNOSIS OF TEATANUS History C/P Lab diagnosis: Difficult
  47. 47. CONTROL OF TEATANUS Measures Preventive General Special forms Neonatal Surgical Puerperal Specific measures Active immunization Infant Pregnant High risk Injury Wound Immunization Control
  48. 48. GENERAL MEASURES 1.Community development & cleanliness of the environment. 2. Control of animal reservoir e.g. segregation of stables & animal sheds from residential areas, replacing animal carts with mechanical vehicles. 3. Health education about the disease & importance of environmental sanitation.
  49. 49. MEASURES FOR SPECIAL FORMS OF TETANUS • Aseptic cutting & dressing of the umbilical cord • Training & health education of birth attendants for sound health behavior. • Pre-conceptional or prenatal active immunization of mothers in high risk areas. Neonatal tetanus • Proper sterilization of catgut & instruments and asepsis in care of surgical wounds. • Clean hospital environment & surrounding. Surgical infection • Active immunization of pregnant in high risk areas. • Proper asepsis & sterilization in labor or abortion. • Chemoprophylaxis after labor or abortion. Puerperal infection
  50. 50. SPECIFIC MEASURES: A-ACTIVE IMMUNIZATION BY TETANUS TOXOID VACCINE 1. Infants: DPT compulsory, at 2, 4 & 6 months, 0.5 ml, I.M., then booster dose at 18 months. DT is used instead of DPT after 4 years.
  51. 51. A-ACTIVE IMMUNIZATION BY TETANUS TOXOID VACCINE 1st • 1st contact with the health service (in 1st pregnancy). 2nd • At least 4 weeks after 1st dose. 3rd • 6-12 months after 2nd dose or during subsequent pregnancy. 4th • 5 years after 3rd dose or during subsequent pregnancy. 5th • 10 years after 4th dose or during subsequent pregnancy. 2. Pregnant mothers: to prevent neonatal tetanus. 5 doses of tetanus toxoid:
  52. 52. 3 doses are given as follows 1st dose (0.5ml) 2nd dose (0.5 ml) 3rd dose (1 ml) 3-High risk groups: e.g. Military forces, soldiers, farmers, night guards and pregnant. “Immunity for 10 years, so booster dose is given every 10 years”. 4 ws 6 months
  53. 53. B-MANAGEMENT OF INJURED PERSONS Prevent further toxin production by: Cleaning & local debridement of the wound by removing foreign matters & necrotic tissues, then application of local antiseptic solution. Suturing & dressing of the wound. Chemoprophylaxis: Antibiotic (e.g. penicillin or tetracycline) & metronidazole.
  54. 54. TetanusImmunization No record of immunization or > 10 years 1st dose TT + HIG 2nd dose after 4 ws 3rd dose after 6 months Within 10 years Booster dose TT
  55. 55. II-CONTROL MEASURES FOR CASES: Notification to the LHO. Isolation in a quiet room. Treatment: Human immunoglobulin (3000-6000 I.U.) or equine antitoxin (30,000 I.U.) I.M. with precautions for serum reaction. Surgical care of the wound. Chemoprophylaxis (e.g. penicillin & metronidazole). Sedatives to avoid stimuli. Tracheostomy is performed if needed. Active immunization should be initiated concurrently with therapy.
  56. 56. NICE TO KNOW The Maternal and Neonatal Tetanus elimination initiative was launched by UNICEF, WHO in 1999, revitalizing the goal of MNT elimination as a public health problem - defined as less than one case of neonatal tetanus per 1000 live births in every district of every country
  57. 57. GAS GANGRENE
  58. 58. GAS GANGRENE It is a severe form of wound infection characterized by destruction of tissues and muscles (with production of gas) and toxaemia.
  59. 59. Causative organisms: Two groups of anaerobic spore-forming clostridia: 2ry Invaders Proteolytic & Facilitate growth of the 1ry organisms. Cl. histolyticum, Cl. sporogenes & others. 1ry Organisms Saccharolytic & Toxigenic. Cl. welchii, Cl. oedematients, & Cl. septicum.
  60. 60. Modes of transmission: Contamination of deep lacerated wounds with spores of causative organisms. Infection of the uterus following septic abortion. Postoperative infection may occur due to contamination and deficient sterilization of skin.
  61. 61. SYMPTOMS High fever Shock Massive tissue destruction Blackening of skin Severe pain around a skin of wound Blisters with gas bubbles near the infected area Tachycardia & tachypnea Toxemia & Death I/P: 1-7 days
  62. 62. CONTROL OF GAS GANGRENE Prevention • Surgical care of injuries, removal of any foreign matter and excision of damaged tissues. • Aseptic techniques in surgery and chemoprophylaxis with antibiotics. • Emergency care of abortion to prevent puerperal infection. • Sero-prophylaxis by polyvalent antitoxin I.M. Measures for cases • Early diagnosis and surgical management. • Penicillin in massive doses • Sero-therapy in proper dose. • Sterilization of any used object or material.
  63. 63. ANTHRAX
  64. 64. Source of infectionAgent - Domestic animals: Cattle, goat, horse, pigs, sheep. - In blood, hair, stool, meat - No man to man infection except in pneumonic anthrax Bacillus anthracis spore forming bacilli (zoonotic disease) IP: 2-7 days Anthrax (wool sorter’s disease) Malignant pustule
  65. 65. Cutaneous: “most common, benign” pruritic vesicle at contact site as face, neck. Ulcer, black scar. Gastrointestinal: GE, intest. oedma, obstruction, death Inhalation (pneumonic): “most serious form” cough, fever, massive oedma of neck & chest, death within 48hs
  66. 66. Modes of transmission Cutaneous anthrax • Contamination of skin abrasions through contact with diseased animals or handling infected tissues or organs. • Using unsterilized shaving brushes made of natural bristles. Intestinal anthrax • Ingestion of contaminated milk or insufficiently cooked meat of diseased animals. Pneumonic anthrax • Inhalation of spores with dusty air of raw wool during the process of wool sorting (wool sorter's disease). • Droplet infection from pneumonic anthrax case to a contact.
  67. 67. Diagnosis History & clinical picture Gram stained smears from skin lesions. Blood cultures.
  68. 68. Prevention Protection of people at risk Control of source of infection Control Measures for cases Measures for contacts Specific prevention
  69. 69. Protection of people at risk • Health education. • Disinfection of raw wool & hair. • Quarantine measures for raw wool & hair. • Vaccination with anthrax vaccine for occupational exposure. Control of reservoir (sources) of infection • Eradication of anthrax in animals: • 1- Sanitary clean environment. • 2- Veterinary care. • 3-Vaccination “annual”: all domestic animals at risk in endemic areas. • Control of diseased animals: • 1- Isolation of diseased animals. • 2- Disinfection of discharges. • 3-Carcasses of dead animals: incinerated or buried in a deep pit.
  70. 70. • Notification to LHO. • Isolation at hospital or special place. • Disinfection of discharges from lesions & soiled articles. • Chemotherapy: Penicillin. Tetracyclines, Erythromycin and Chloramphenicol are also effective. The U.S. military recommends parenteral ciprofloxacin or doxycycline for inhalation anthrax. Measures for cases • Contacts of respiratory cases are isolated for 7 days. Measures for contacts
  71. 71. LEPROSY (Hansen's disease)
  72. 72. Chronic granulomatous disease Mycobacterium leprae Primarily affecting skin, mucous membranes of upper respiratory tract & peripheral nerves
  73. 73.  Causative agent: Mycobacterium leprae, acid-fast, gram-positive bacillus.  Reservoir: 1 - Humans (the main reservoir). 2 - Wild armadillos, mangabey monkeys & Chimpanzee: naturally infected with M.leprae.
  74. 74. Modes of transmission: • Humans are the only significant reservoirs. • The disease is in all likelihood transmitted from the nasal mucosa of a patient to the skin and respiratory tract of another person. Transmission requires close contact.
  75. 75. IP: 9 months to 20 years (average 4-8 years).
  76. 76. Indeterminate leprosy • Hypo-pigmented maculae with ill-defined borders; if untreated, it may progress to tuberculoid, borderline or lepromatous disease. Lepromatous (multibacillary) leprosy • Symmetrical & bilateral nodules, papules, macules & diffuse infiltrations “numerous & extensive”. • Involvement of the nasal mucosa: crusting, obstructed breathing & epistaxis. • Ocular involvement: iritis & keratitis. Tuberculoid (paucibacillary) leprosy • Skin lesions: single or few, sharply demarcated, anesthetic or hypo-anesthetic. • Bilateral asymmetrical involvement of peripheral nerves tends to be severe. Borderline leprosy • Features of both polar forms and is more labile.
  77. 77. DIAGNOSIS OF LEPROSY: Characteristic skin lesions (↓or lost sensation, thickened peripheral nerves). Skin smear stained with Ziel-Neelsen stain: most important method. Nasal scrapping: assessing the infectiousness of a patient. Nerve biopsy: when there is no skin lesion. PCR to detect M. leprae DNA. Lepromin test
  78. 78. Lepromin test • Not diagnostic test but measures the degree of cell-mediated immunity. • Used for classification. • -ve in lepromatous type & strongly +ve in tuberculoid type. • Useful to assess susceptibility of population in community surveys.
  79. 79. PREVENTIVE MEASURES: General measures • Improvement in general hygiene, better housing & prevent overcrowding. • Health education. Specific measures • BCG immunization gives considerable reduction in the incidence of tuberculoid leprosy.
  80. 80. CONTROL MEASURES Measures for cases • Case finding e.g. surveys in endemic areas. • Notification to LHO. • Isolation: “stigmatization”. No restrictions in employment or attendance at school are indicated. • Disinfection. • Specific treatment: • Combined chemotherapy to avoid resistance. • Rifampicin 600 mg once monthly + dapsone 100 mg/ day + clofazimine 50 mg once a day and 300 mg once a month. • Minimum duration of ttt is 12 months or moreuntil skin smears are negative. • Release: after becoming bacteriological free. Measures for contacts • Enlistment • Initial examination then periodically at 12 months intervals for at least 5 years after last contact with an infectious case. • Chemoprophylaxis with dapsone is not recommended because of limited effectiveness and danger of resistance.
  82. 82. Viral AIDS Hepatitis “B&C” Rabies Bacterial Anthrax Gas gangrene Gonorrhea Leprosy Tetanus Parasitic Ancylostomiasis Schistosomiasis Spirochetes Syphilis
  83. 83. A parasitic disease caused by a trematode infecting venous system & transmitted by water contact. It is an endemic disease in Egypt.
  84. 84. Schistosoma hematobium • Urinary tract • Bullinus trancutus snail • Egypt Schistosoma mansoni • Large intestine • Biomphilaria alexandrina snail • Egypt Schistosoma japonicum • Large intestine • Oncomelania snails e.g. Oncomelaniahupensis • China
  86. 86.  Mode of transmission: Cercaria in polluted water penetrates skin of new host during bathing or irrigating lands.  IP.: 5-8 ws (1-2 ms) from penetration of skin by cercaria till appearance of eggs in stool or urine.  Infective stage: Cercaria “lives 24-72 hs (1-3 ds) in water then dies”.
  87. 87. Clinical picture: Itching Dermatitis “Cercaria penetration ” General weakness Anemia Terminal hematuria or blood in faeces Cystitis Urethritis Stone formation Colitis Liver cirrhosis Portal HPN Esophageal varices & bleeding Cancer
  88. 88. DIAGNOSIS • Suggestive in endemic areas. • e.g. terminal haematuria or dysentery C/P • (a) Microscopic exam.: ova in urine & stools. • (b) Immunologic tests: • Complement fixation test: +ve few ws after infection & persists for many ys. • Intradermal test: injection of Ag. prepared from adult worms. Reading is taken within 15 min. +ve reaction signifies infection (past or present). Lab examination
  89. 89. Spread of schistosomiasis in Egypt After construction of High Dam Upper Egypt: S. hematobium is more prevalent (5-14%) & increased south of Assuit. Lower Egypt: S. mansoni is more prevalent (18-43%) & almost totally replaced S. hematobium. Before construction of High Dam S. hematobium: all over Egypt + low prevalence south of Assuit. S. mansoni: Nile delta & Giza Gov.
  90. 90. Change of basin irrigation to perennial irrigation ……...change in velocity & volume of water flow + decreased silt in water……….affected snail distribution.
  91. 91. ECOLOGY (ENDEMICITY) Environment • Unsanitary environment. • Lack of safe water supply for bathing & washing. • Unavailable latrines. • Suitable climate (temp.+humidity) for development of cercaria & snails. Agent • Continuous flow of snail intermediate host from Nile resources. • Perennial irrigation favors development of snails. • Cercaria characts. (big No., survive 2-3 ds, thermotropic, have great affinity to man). Host • Age: 10-20 ys (swimming in infected canals in summer). • Sex: males (farming & irrigation). • Education:↓in educated persons (avoid polluted water & seek medical care early). • Occupation: farmers & fishermen. • Habits & Behavior: defecation & urination in canal water. • Underutilization or reluctance to seek medical care.
  92. 92. CONTROL 1ry prevention • 1. Sanitary water supply &waste disposal e.g. sanitary latrines. • 2. Mechanization of agriculture, irrigation & drainage system. • 4. Provision of recreation places in rural areas. • 5. Snail control: • Periodic drying of canals. • Clearance from vegetation. • Trapping snails. • Manual collection of snails. • Molluscicides to kill snails. Protection of susceptible host • Health education for: • 1. Mode of transmission. • 2. Role of defecation & urination in canal water. • 3.Drying of skin after water contact to kill cercaria before entering skin. • 4.Wearing PPE on water contact e.g. gloves & boots. • 5. Seek medical ttt early when infected.
  93. 93. Secondary prevention: Measures for cases • Early case finding by routine stool & urine examination for S. eggs at any occasion of health appraisal, such as: • (a) Health appraisal of school children. • (b) Examination of army recruits. • (c) Periodic checkup. • (d) Pre-placement examination. • (e) All attendants of health services. • ttt of discovered cases. • Re-examination to be sure of cure. • Health education for preventing re- infection. Measures for contacts • No special measures as there is no man to man infection; but the following are recommended: • Stool & urine examination for early detection of cases. • Health education to avoid infection. • Mass treatment controls reservoir of infection & limits spread of disease. Praziquantel (non-antimonial drug) “orally in a single dose, 30 mg/Kg BW with a max. of 2400 mg (4 tablets)”.
  94. 94. TREATMENT OF SCHISTOSOMIASIS Praziquantel (non-antimonial drug) • Orally in a single dose, 30 mg/Kg BW with a max. of 2400 mg (4 tablets). • Tablets 600 mg as: Distocide tab., Biltricide tab., Praziquantel tab. • Suspension 600 mg/5 ml as: epiquantel susp. Commiphora Mukul extract • Mirazid 300 mg, 2 caps daily on an empty stomach.
  95. 95. ANCYLOSTOMIASIS (Hookworm disease)
  96. 96. • Endemic parasitic helminthic disease which is prevalent in underdeveloped countries. • More prevalent in Upper than in Lower Egypt. • Declining due to community development of rural areas & availability of health services.
  97. 97. Contact of bare skin with moist contaminated soil Attached to mucosa by mouth capsule. continuously sucking blood & laying eggs Ancylostoma duodenale
  98. 98. Period of communicability: untreated cases remain infective for years. IP: 6 ws from penetration of skin to appearance of eggs in stool. Reservoir of infection: Man: infected person who discharges eggs in faeces
  99. 99. Clinical picture: May be asymptomatic. Ground itch • Local dermatitis at site of entry of larvae. Respiratory manifestations • Migrating larvae • Patchy lung consolidation, Upper respiratory catarrh. Anaemia • Microcytic hypochromic “chronic blood loss by worm sucking blood”. General manifestations • Retarded physical growth & mental development of children.
  100. 100. DIAGNOSIS: Suggestive but not diagnostic. C/P Stool exam: 4-cell eggs Laboratory
  101. 101. ECOLOGY OF ANCYLOSTOMIASIS Environment • Unsanitary environment. • Lack of safe water supply for bathing & washing. • Unavailable latrines. • Suitable climate (temp. & humidity) for eggs to hatch & continue life cycle. Host • Age: children of underdeveloped areas. • Occupation: farmers & agriculture workers. • Habits & behavior: Promiscuous defecation in field & vicinity of houses. • Bare foot & getting in contact with contaminated soil. • Reluctance of cases to seek medical ttt & repeated exposure.
  102. 102. CONTROL I- Prevention: Community development: safe water supply & sanitary latrines. Health education: Avoid promiscuous defecation & contamination of soil. Not to walk bare footed or sit on the soil. Upgrading of health services. II. Measures for cases: as bilharzioasis III. Measures for contacts: non as there is no man to man transmission.
  104. 104. Viral AIDS Hepatitis “B&C” Rabies Bacterial Anthrax Gas gangrene Gonorrhea Leprosy Tetanus Parasitic Ancylostomiasis Schistosomiasis Spirocheteal Syphilis
  105. 105. • Spirochaete, treponema pallidum. • Delicate & is rapidly killed by: Causative organism Drying High temperature Disinfectants Soap & water
  106. 106. Reservoir: Man: untreated case is infectious during the 1ry & 2ry stages of disease, usually for 2-4 years. Exit: • Exudates of skin & mucous membranes. • Blood & body fluids (semen, saliva, vaginal & cervical discharge). IP: About 3 weeks • Worldwide disease affecting mainly age group from 15-39 • Recently it was found to be increasing.
  107. 107. TRANSMISSION Contact with open lesion • Sexuel contact (Most important mode). • Kissing. • Contact with baby having congenital syphilis. • Contact with contaminated articles. Congenital infection • Trans-placental from 4th month till delivery (not before as treponema can’t pass BPB). Inoculation infection • Contaminated blood & body fluids (contaminated syringes & needles & blood transfusion).
  108. 108. Primary syphilis: • Chancre at portal of entry: firm, indurate, painless & highly infectious ulcer. • Enlarged lymph nodes. • Spontaneously disappears without treatment after 4-6 weeks.
  109. 109. Secondary: • Generalized skin rash “Patchy lesions of mucous membranes especially mouth”. • Involvement of other parts of body. • Spontaneously disappears within weeks or months followed after a latent period (years) by the 3rd stage.
  110. 110. Late symptomatic syphilis:  Reappearance of symptoms.  Characterized by occurrence of neuro & cardiovascular syphilis & characteristic lesions involving different parts of body.
  111. 111. History & c/p Lab investigations • Dark field microscopic exam • Serologic testing: • 1-Non-treponemal test (non-specific): for screening e.g. Wassermann Reaction (WR) & Venereal Disease Research Laboratory test (VDRL) “↑false +ve”. • 2-Treponemal tests (specific test): Use treponema Ag. e.g. fluorescent treponema antibody absorption test. DIAGNOSIS
  112. 112. PREVENTION A. General measures: B. Specific: Chemoprophylaxis: 1 dose of 2.4 million units of long acting penicillin I.M. soon after exposure. Avoidance of sexual promiscuity. Health education to increase awareness. Religious & social guidance especially of youth. Convenient family life & supervision of youth. Suitable places for leisure time & development of hobbies. Socioeconomic development & provide facility for marriage.
  113. 113. A. Cases: 1. Early case finding: during survey & on health appraisal: • Premarital & prenatal examination. • Exam of food handlers, blood donors, army recruits, child nurses. • Suspected attendants of medical services. • Diagnosis of congenital syphilis when mother is syphilitic. 2. Measures for cases: • Notification confidentially to LHO. • Isolation: not needed but avoid sexual contact till elimination of infectivity. • Disinfection: non but precautions with blood & body fluids.
  114. 114. SPECIFIC TREATMENT: • Long acting penicillin 2.4 million units in a single dose I.M. • Penicillin sensitive patients: doxycycline 100 mg twice daily for 14 days. • Re-examination after treatment.
  115. 115. B. Contacts: • Tracing & Enlistment. • Examination. • Health education. • Surveillance. • Chemoprophylaxis: 1 dose of 2.4 million units of long acting penicillin I.M. C. Congenital syphilis: • Serologic testing & ttt. • Proper handling of baby with congenital syphilis with caution to avoid infection.