Infectious Diseases Transmissed by Skin and Mucosa. Cuneyt Mirzanli Istanbul gelişim University

Transcription

1 Infectious Diseases Transmissed by Skin and Mucosa Cuneyt Mirzanli Istanbul gelişim University 1

2 Pediculosis Infestation of human parasitic lice, which feed exclusively on human blood and lay eggs (nits) on body hairs or clothing. Pediculosis capitis (head lice): confined to scalp and occasionally, eyebrows, eyelashes and beard. Pediculosis corporis (body lice): found next to skin in clothing seams; move to the host only to feed on blood. Pediculosis pubis (crab lice): found primarily in pubic hairs. 2

3 Pathophysiology Lice attach superficially to the epidermis and hair, survive by ingesting blood from the human host. Bite injects a toxin into the skin. Mild irritation and purpuric spot result. Repeated bites cause sensitization to the toxin, leading to more serious inflammation. In severe cases, sensitization causes a rash on the trunk. Scratching may result in secondary bacterial infection. 3

4 Causes Pediculosis capitis Pediculosis corporis Pediculosis pubis 4

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6 Risk factors: Poor hygiene Overcrowded living conditions Incidence: P. capitis is more common in children. P. pubis is more common in adults. 6

7 Complications: Skin breakage Secondary bacterial infections Hyperpigmentation or residual scarring 7

8 Assessment History: Exposure to causative organism Headache Fever Malaise Pruritus Cutaneous changes 8

9 Physical findings Pediculosis capitis: Visible lice Skin excoriation on the scalp and neck Matted, lusterless hair (in severe cases) Occipital and cervical lymphadenopathy Oval, gray-white nits visible on hair shafts 9

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11 Pediculosis corporis: Red papules or macules, usually on the shoulders, trunk or buttocks Excoriations from scratching Nits on clothing seams 11

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13 Pediculosis pubis: Visible brownish-gray lice Erythematous papules Small macules on the thighs, buttocks or lower abdomen. 13

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15 Diagnosis Direct inspection with hand lens shows visible lice or nits. 15

16 Treatment General: Hair-washing with ordinary shampoo Laundering of potentially contaminated clothing and bed linen Bathing with soap and water Petroleum jelly applied to eyebrows or eyelashes. 16

17 Medications Permethrin Pediculicide cream Pediculicide shampoo 17

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19 Nursing Considerations Nursing diagnoses: Acute pain Disturbed body image Impaired skin integrity Risk for infection 19

20 Nursing Interventions Give prescribed drugs. Use personal protective equipment when administering treatment. Notify the school if infestation occurs in a child. Encourage the patient to express feelings about the infestation. 20

21 Patient teaching General: Be sure to cover: how to inspect for lice, eggs and lesions how to decontaminate infestation sources how to apply insecticidal agents removal of nits and lice importance of not sharing personal articles adverse reactions to treatment, including when to notify the practitioner. 21

22 Scabies Transmissible skin infestation with Sarcoptes scabiei. Characterized by burrows, severe pruritus and excoriations. 22

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24 Pathophysiology Mites burrow into the skin on contact, progressing 2 to 3 mm per day. Females live about 4 to 6 weeks and lay about 40 to 50 eggs, which hatch in 3 to 4 days. Pruritus occurs only after sensitization to the mite develops. With initial infestation, sensitization requires several weeks. With reinfestation, sensitization develops within 24 hours. Dead mites, eggs, larvae and their excrement trigger an inflammatory eruption of the skin in infested areas. 24

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26 Causes Direct (skin to skin) contact or contact with contaminated articles for up to 48 hours. 26

27 Risk factors: Overcrowded living conditions Poor hygiene Day-care or institutional settings 27

28 Incidence Scabies is common in children, young adults, elderly and debilitated patients. It occurs worldwide. It can be endemic. 28

29 Complications Excoriations Secondary bacterial infection Abscess formation Septicemia 29

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31 Assessment History: Predisposing risk factors May not produce symptoms initially. Intense pruritus that's more severe at night. 31

32 Physical Findings Characteristic gray-brown, threadlike burrows (0.5 to 1 cm long) with tiny papule or vesicle at one end. Common sites: flexor surfaces of wrists, elbows, axillary folds, waistline, nipples in females and genitalia. 32

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35 Diagnosis Wound culture demonstrates secondary bacterial infection. Punch biopsy may help to confirm the diagnosis. 35

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37 Treatment General: Bathing with soap and water Performing skin care Decontaminating environment and clothing Medications: Scabicides 6% to 10% sulfur solution Systemic antibiotics Antipruritics 37

38 Nursing Considerations Nursing diagnoses: Acute pain Disturbed body image Impaired skin integrity Ineffective therapeutic regimen management Risk for infection 38

39 Nursing Interventions Trim patient's fingernails short. Give prescribed drugs. Isolate the patient until treatment is completed. Practice meticulous hand washing. Sterilize blood pressure cuffs in a gas autoclave before using on other patients. Decontaminate linens, towels, clothing and personal articles. Disinfect the patient's room after discharge 39

40 Nursing Interventions (Contd.) If the patient is a child, notify his school of the infestation. Encourage verbalization of feelings. Observe wound and skin precautions for 24 hours after treatment with a scabicide. 40

41 Patient Teaching General: Be sure to cover: the disorder, diagnosis, and treatment identification of characteristic lesions modes of transmission mite resistance to scabicides assessment of close personal contacts for infestation. successful treatment for infestation with good hygiene and scabicides. 41

42 Patient Teaching (Contd.) prevention of transmission and recurrence proper application of the prescribed scabicide. 42

43 Rabies An acute central nervous system (CNS) infection usually transmitted by animal bite. Incubation period usually 20 to 90 days. Vaccinations have reduced transmission from dogs. Almost always fatal if symptoms occur, although prompt treatment may prevent fatal CNS invasion. 43

44 Pathophysiology The rabies virus is transmitted through the bite of an infected animal that introduces the virus through the skin or mucous membrane. The virus begins to replicate in the striated muscle cells at the bite site. It then travels up the nerves to the CNS and replicates in the brain. Finally, it moves through the nerves into other tissues, including the salivary glands. 44

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46 Causes: Bite from a rabid animal. Risk factors: Occupation with exposure to potentially rabid animals. Travel to areas with poor rabies control. can affect anyone at any age. 46

47 Complications: Paralysis Coma Death 47

48 Assessment History: Animal bite Fever Malaise ( general feel of illness) 48

49 Physical findings Burning at wound site Tachycardia Excessive salivation Shallow respirations Dilated pupils and photophobia 49

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52 Diagnosis Virus is isolated from the patient's saliva or throat; examination of blood shows fluorescent rabies antibody (FRA). White blood cell count is elevated with increased polymorphonuclear and large mononuclear cells. Urinary glucose, acetone and protein levels are elevated. 52

53 Treatment General: Immediate wound treatment Medications: Tetanus prophylaxis, if needed Passive immunization with rabies immune globulin and active immunization with human diploid cell vaccine as soon as possible (if not previously immunized) Vaccine booster (if already immunized) 53

54 Nursing Considerations Nursing diagnoses: Anxiety Decreased cardiac output Hyperthermia Imbalanced nutrition Impaired swallowing Impaired tissue integrity Ineffective breathing pattern Risk for deficient fluid volume Risk for infection 54

55 Nursing Interventions When injecting the rabies vaccine, rotate injection sites on the upper arm or thigh. Cooperate with public health authorities to determine the animal s vaccination status. If the animal is proven rabid, help identify others at risk. Provide aggressive supportive care (even after onset of coma). Follow standard precautions. Provide emotional support. 55

56 Patient Teaching General: Be sure to cover: the need for vaccination of household pets that may be exposed to rabid wild animals. importance of not touching wild animals, especially if they appear ill. 56

57 Tetanus An acute exotoxin-mediated infection Usually systemic, but possibly localized Up to 60% fatal in unimmunized patients 57

58 Pathophysiology After the organism enters the body, local infection and tissue necrosis result. Toxins enter the bloodstream and lymphatics, eventually spreading to central nervous system tissues. The incubation period is 3 to 21 days. 58

59 Causes Anaerobic, spore-forming, gram-positive bacillus Clostridium tetani. Transmission through puncture wounds, burns or minor wounds, contaminated by soil, dust or animal excreta containing C. Tetani. 59

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61 Incidence Tetanus occurs worldwide but is more prevalent in agricultural regions and developing countries that lack mass immunization programs. Tetanus is one of the most common causes of neonatal deaths in developing countries. 61

62 Pneumonia Airway obstruction Respiratory arrest Heart failure Fractures Cardiac arrhythmias Rhabdomyolysis Death Complications 62

63 Assessment History: Inadequate immunization Recent wound or burn Pain or paresthesia at the site of injury Complaints of difficulty chewing or swallowing food. 63

64 Physical Findings Spasm and increased muscle tone near the wound (local infection). Irregular heartbeat and tachycardia Marked muscle hypertonicity Hyperactive deep tendon reflexes Profuse sweating, low-grade fever Painful, involuntary muscle contractions 64

65 Physical Findings (Contd.) Rigid neck and facial muscles, resulting in lockjaw. Rigid somatic muscles causing arched back rigidity (opisthotonos) Intermittent tonic seizures 65

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69 Diagnosis Blood cultures and tetanus antibody tests are negative in tetanus patients. Wound culture is positive in one-third of all tetanus patients. 69

70 Treatment General: Airway maintenance Diet: Enteral or parenteral feeding Activity: Bed rest until recovery 70

71 Treatment (Contd.) Medications: Tetanus immune globulin Tetanus antitoxin Tetanus toxoid immunization Muscle relaxants Neuromuscular blockers Antibiotics 71

72 Nursing considerations Nursing diagnoses: Acute pain Imbalanced nutrition: Less than body requirements Impaired physical mobility Ineffective airway clearance Ineffective breathing pattern Ineffective tissue perfusion: Cerebral, peripheral Risk for deficient fluid volume Risk for injury 72

73 Nursing Interventions Debride and clean the injury site. Check the immunization history. Maintain an adequate airway and ventilation. Keep emergency airway equipment on standby. Administer I.V. therapy as prescribed. Minimize stimulation. Perform range-of-motion exercises. 73

74 Patient Teaching General: Be sure to cover: the disorder, diagnosis, and treatment importance of getting a booster dose of tetanus toxoid every 10 years. importance of tetanus prophylaxis in case of a skin injury or burn. importance of avoiding external stimulation (evokes muscle spasms) and to keep the room dark and quiet. 74

75 Anthrax An acute bacterial infection occurring most commonly in animals, the natural resistance of humans to anthrax is greater than that of these animals. Human cases classified as either agricultural or industrial. In humans, occurs in three forms, depending on the mode of transmission: Cutaneous, İnhalation, and GI. 75

76 Cutaneous anthrax most common form. Without treatment, mortality from cutaneous anthrax 20%; mortality less than 1% with treatment. Even with treatment, inhalation anthrax usually fatal. With treatment, mortality from GI anthrax 25% to 60%. No screening test available. 76

77 Pathophysiology Bacillus anthracis is an encapsulated, chainforming, aerobic, grampositive rod that forms oval spores; spores are hardy and can survive for years under adverse conditions. 77

78 Pathophysiology (Contd.) B. anthracis, an extracellular pathogen, evades phagocytosis, invades the bloodstream and multiplies rapidly. 78

79 Pathophysiology (Contd.) In cutaneous anthrax, spores enter the body through a broken skin or by biting flies, the spores germinate within hours, the vegetative cells multiply and anthrax toxin is produced. 79

80 Pathophysiology (Contd.) In inhalation anthrax, spores are deposited directly into the alveoli and phagocytized by macrophages, some are carried to and germinate in mediastinal nodes. This may result in overwhelming bacteremia, hemorrhagic mediastinitis, and secondary pneumonia. 80

81 Pathophysiology (Contd.) In GI anthrax, primary infection can be caused in the intestine by organisms that survive passage through the stomach; acute inflammation of the intestinal tract results. 81

82 Causes Bacterial infection with B. anthracis Human cases: Contact with infected animals or contaminated animal products Ingestion Inhalation Insect bites 82

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84 Agricultural cases: Bites of contaminated or infected flies Consumption of contaminated meat Contact with animals that have anthrax 84

85 Industrial cases: Animal hides Bones Goat's hair Wool 85

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89 Laboratory and industrial workers at risk for occupational exposure. Anthrax occurs worldwide. The disease is most common in developing countries. Anthrax is most common in sheep, cattle, cow, horses and goats, An estimated 20,000 to 100,000 cases of anthrax occur per year. (Approximately 95% of human anthrax cases are the cutaneous form; about 5% are the inhalation form; GI anthrax is rare.) 89

90 Complications Septicemia Hemorrhagic mediastinitis Pneumonia Respiratory failure Hemorrhagic thoracic lymphadenitis Meningitis Death 90

91 Assessment History: Cutaneous anthrax: Contact with animals or animal products, Painless ulcer Mild or no constitutional symptoms. 91

92 Inhalational anthrax: Initial prodromal flulike symptoms Malaise; dry cough Mild fever; chills Headache; myalgia Severe respiratory distress Chest pain 92

93 GI anthrax: Nausea; vomiting Decreased appetite Fever Abdominal pain Vomiting blood Severe bloody diarrhea 93

94 Physical Findings Cutaneous anthrax: Initially, a small, papular, pruritic lesion that resembles an insect bite. Lesion that develops into a vesicle in 1 to 2 days. Lesion that finally becomes a small, painless ulcer with a necrotic center, surrounded by edema. 94

95 Cutaneous Anthrax (Contd.) Lesions that are generally located on exposed areas of the skin Painful, regional, nonspecific lymphadenitis. 95

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99 Inhalational anthrax: Increasing fever Dyspnea Hypoxia Hypotension 99

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101 GI anthrax: Fever Rapidly developing ascites 101

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103 Diagnosis Gram stain, direct fluorescent antibody staining, and culture show presence of B. anthracis. Blood cultures show presence of B. anthracis. Cerebrospinal fluid analysis reveals presence of B. anthracis. Complete blood count shows polymorphonuclear leukocytosis in severe disease. Serum antibody tests reveal the specific antibody to B. Anthracis. 103

104 Imaging: Chest X-ray shows symmetric mediastinal widening in hemorrhagic mediastinitis. 104

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106 Treatment General: Initiated as soon as exposure to anthrax is suspected Diet: No restrictions Adequate fluid intake Activity: As tolerated Medications: Antibiotics Oxygen as needed 106

107 Nursing Considerations Nursing diagnoses: Anxiety Diarrhea Fear Imbalanced nutrition: Less than body requirements Impaired physical mobility Ineffective breathing pattern Risk for deficient fluid volume 107

108 Nursing Interventions Give prescribed drugs. Maintain patent airway and adequate ventilation. Report any case of anthrax in either livestock or humans to the local board of health. Maintain standard precautions. Encourage verbalization of fears and concerns. 108

109 Nursing Interventions (Contd.) Provide adequate hydration. Provide a well-balanced diet. Assist the patient in the development of effective coping mechanisms. Provide adequate rest periods. 109

110 Patient Teaching General: Be sure to cover: the disorder, diagnosis, and treatment medications and potential adverse reactions when to notify the practitioner anthrax prevention. 110