cd eco

COMMUNICABLE DISEASE NURSING Jeremiah B. Eco, R.N. Clinical Instructor DEFINITIONS OF TERMS COMMUNICABLE DISEASE an illness due to an infectious agent or its toxic products w/c is transmitted directly or indirectly to a well person or animal or through an agency of an intermediate animal host, vector of the inanimate environment RESERVOIR natural habitat of the organism that is where it resides and multiplies SOURCE site from w/c the organism passes immediately to a host MODE OF TRANSMISSION it indicates the potential of the disease; conveyance of the agent to the host it can be by common source transmission, contact source, air-borne and vector borne HOST a person or animal or plant upon w/c a parasite depends for its survival (Patient, Carrier) ISOLATION (vs. REVERSE ISOLATION) the separation of persons suffering from communicable disease or carriers of the infecting organism from other persons and placing them under such conditions that direct or indirect transmission to susceptible person is prevented UNIVERSAL PRECAUTIONS are infectious control measures designed to protect health workers form exposure to diseases INCUBATION PERIOD the time between exposure to a pathogenic organism and the onset of symptoms of a disease ETIOLOGY all factors that may be involved in the development of a disease PROPHYLAXIS prevention of or protection against disease, often involving the use of a biologic chemical or mechanic agent to destroy o prevent entry of infectious disease PERIOD OF COMMUNICABILITY refers to a frame of time that a disease is contagious or transmissible by direct or indirect means SEQUELAE any abnormal conditions that follows and is the result of a disease, treatment or an injury PROGNOSIS a prediction of the provable outcome of a disease based on the condition of the person and the usual course of the disease as observed in similar situation PATHOGENICITY is the ability of a microorganism to produce disease. PATHOGENS microorganisms that cause diseases in humans are called. VIRULENCE is the degree of pathogenicity of an infection’s microorganism. Power to cause infection. INFECTION is an invasion and multiplication of microorganisms in body tissue that results in cellular injury. these microorganisms are called infectious agents. COLONIZATION is the multiplication of microorganisms on or within a host that does not result in cellular injury. FLORA are the vegetation of microorganisms on the human body. Resident flora   microorganisms which are always present on skin can be reduced through hand washing, but not totally removed microorganisms that are picked up by the skin from another person or object attach themselves to the skin and then may be transmitted to a susceptible host Transient flora   CONTAGIOUS vs. INFECTIOUS CONTAGIOUS applied to disease that are easily spread directly transmitted from person-to-person INFECTIOUS are those disease not transmitted by ordinary contact, but require a direct inoculation through a break in the previously intact skin or mucous membrane all contagious diseases are infectious “ALL CD ARE INFECTIOUS BUT SOME ARE CONTAGIOUS” INFECTION PROCESS Chain of Infection INFECTIOUS AGENT SUSCEPTABLE HOST RESERVOIR or SOURCE PORTAL OF ENTRY INTO HOST PORTAL OF EXIT FROM RESERVOIR MODE OF TRANSMISSION Infectious Agent Agents that produce infections can consist of       The ability of a microorganism to infect a client is related to:  Pathogenicity ability to cause disease bacteria viruses fungi protozoa rickettsia chlamydia  Virulence disease severity  Invasiveness ability to enter and move through the tissue  Infective Dose number of organisms needed to initiate infection  Organism Specificity host preference  Susceptibility of the Host Source or Reservoir Required for the microorganism to survive while awaiting a host. May allow the organism to multiply, making it more dangerous.   The human body is the most common reservoir. Food, plants, animals, and feces are other common reservoirs. Infectious Agent Route of Transmission Contact Transmission  Vehicle Route  Airborne Transmission  Vectorborne Transmission  Contact Transmission direct contact person to person indirect contact usually an inanimate object droplet contact from coughing, sneezing, or talking by an infected person Vehicle Route food salmonellosis water shegellosis, legionellosis drugs bacteremia resulting from infusion of a contaminated infusion product blood hepatitis B, or non-A non-B hepatitis Airborne Transmission droplet nuclei residue of evaporated dust particles air containing the infectious agent organisms shed into environment from skin hair wounds or perineal area Vector Transmission via contaminated or infected arthropods such as; flies mosquitoes ticks, etc. Mode of Escape from Reservoir 1. 2. 3. 4. 5. Respiratory tract GI tract GU tract Open lesion Mechanical escape bites from insects 6. Blood Mode of Entry into Human Body Respiratory tract 2. GI tract 3. GU tract 4. Mucous membrane or skin 1. Susceptible Host A person with a reduced immune response has increased susceptibility. The immune response is the body’s natural defense against infection. Factors Influencing Production of an Infectious Disease 1. 2. 3. 4. 5. 6. Age Heredity Stress Surgery Nutrition Health Status Factors Influencing Production of an Infectious Disease Age The elderly and children under two years of age are at greatest risk. Heredity Conditions or diseases resulting in the absence of or inability to form immune defenses. Stress Increase in metabolic rate which results in using up stored energy Elevation of blood cortisol, decreasing anti-inflammatory responses Continued stress produces exhaustion, further depleting ability to ward off infection. Factors Influencing Production of an Infectious Disease Surgery Eliminates primary barrier of infection. Predisposes clients to surgical site infections. Localized infection at wound site can progress to a systemic infection. Additional risks include catheters and tubes. Nutrition Insufficient protein consumption reduces antibody production and inhibits the body’s ability to ward off infection. Health Status Clients w/ disease of their immune system are at greater risk. Chronic diseases can predispose the client to infection. Four Stages of Infection Incubation the time between exposure to a pathogenic organism and the onset of symptoms of a disease Prodromal earliest phase of the developing disease condition Illness Convalescence period of recovery after an illness DISEASE ACQUIRED THROUGH THE SKIN TETANUS RABIES MALARIA DENGUE LEPTOSPIROSIS SCHISTOSOMIASIS LEPROSY Acquired through contact Tetanus TETANUS (Lockjaw) Tetanus is an acute disease caused by Clostridium tetani w/c produces a potent exotoxin w/ prominent systemic neuromuscular effects manifested by generalized spasmodic contractions of the skeletal musculature commonly found in soil, particularly if contaminated with animal or human feces Epidemiology Mortality rates reported vary from 40% to 78%. In recent years approximately 11% of reported tetanus cases have been fatal. The highest mortality rates are in unvaccinated persons and persons over 60 years of age. Tetanus occurs worldwide but is more common in hot, damp climates with soil rich in organic matter. Tetanus – particularly the neonatal form – remains a significant public health problem in non-industrialized countries. There are about one million cases of tetanus reported worldwide annually, causing an estimated 300,000 to 500,000 deaths each year. Tetanus Toxoid Immunization Percent of surviving children 0 to 59 months of age who were protected at birth against neonatal tetanus by residence, Philippines: 2002 and 2004 2004 FPS 64.5 2002 MCHS 67.7 65.1 62.2 61.0 58.8 Total Urban Rural Source: National Statistics Office, 2002 Maternal and Child Health Survey and 2004 Family Planning Survey Mode of Entry Clostridium tetani is found throughout the world in the soil and in animal and human intestines. Contaminated wounds are the sites where tetanus bacteria multiply. Deep wounds or those with devitalized tissue are particularly prone to tetanus infection. Puncture wounds such as those caused by nails or splinters are favorite locations of entry for the bacteria. Mode of transmission Thru break in the skin and mucus membrane Toxins: Tetanolysin and Tetanospasmin  by tetanospasmin, a neurotoxin produced by the Gram-positive, obligate anaerobic bacterium Clostridium tetani Tetanus is the only vaccine-preventable disease that is infectious but is not contagious. Clostridium Tetani The toxin migrates across synapses to presynaptic terminals where it blocks the release of inhibitory neurotransmitters This leads to muscle contraction and spasm Incubation Period 3 days to 3 weeks 10 days – average In general, the further the injury site is from the central nervous system, the longer the incubation period Pathophysiology Tetanus begins when spores of Clostridium tetani enter damaged tissue The spores transform into rod-shaped bacteria and produce the neurotoxin tetanospasmin This toxin is inactive inside the bacteria, but when the bacteria dies, it is released and activated by proteases during replication the bacteria produce a potent neurotoxin, tetanospasmin, which blocks neurotransmitter release the toxin binds to peripheral neurons, enters the axon, and is transported to the nerve-cell body in the brain stem by retrograde interneuronal transport in both the motor and sympathetic nervous systems RELEASE OF TOXINS TETANOSPASMIN •affects nerves specially myoneural junction of muscle w/c causes localized spasm & pain BLOOD STREAM CENTRAL NERVOUS SYSTEM TETANOLYSIN •deadly effect by lysis or destruction of RBC and WBC SPINAL CORD •lockjaw •Trismus – painful spasm of masticatory muscle due to trigeminal involvement •Risus Sardonicus – facial nerve are affected •Opisthotonus – arching of the back BRAIN •irritable •headache •laryngeal/pharyngeal spasms •causes general rigidity •convulsions Muscle Spasm Other Manifestations In Neonatal 1. 2. 3. In Children & Adults 1. 2. 4. 5. 6. 7. fever inability to suck & swallow spasms & convulsions occurring spontaneously or provoked by stimuli such as noise or light exaggerated deep tendon reflex cry cyanosis or pallor may end w/ flaccidity, anorexia, exhaustion & finally DEATH 3. 4. 5. 6. 7. 8. 9. Jaw – trismus or lockjaw Neck & Back – opisthotonus Face – risus sardonicus Board like abdomen Extremities are stiff and extended Respiration – laryngeal spasm followed by accumulation of secretions fracture of the vertebral bodies can occur during spasm headache & profuse bleeding coma and DEATH Diagnosis The diagnosis is based on the presentation of tetanus symptoms spatula test - touching the posterior mpharyngeal wall with a sterile, soft-tipped instrument, and observing the effect. PREVENTION Avoiding contamination of the organism 1. 2. 3. 4. aseptic technique in handling neonatal umbilical stump & other wound active immunization of TT to pregnant mother on the last trimester to give rise to protective titers in newborn active immunization of women of child bearing age supervision of unlicensed wives Preventing its multiplication & pathogenecity 1. 2. 3. Active Immunization Passive Immunization Antibiotic Prophylactic Therapy  Penicillin, Erythromycin & Tetracyclines kills clostridium before they multiply if given w/in 4 hours post injury TREATMENT Tetanus Immune Globulin / Human Hyperimmune Globulin (TIG) 3,000 – 6,000 units, IM Tetanus Antitoxin (TAT) 50,000 – 100,000 units, ½ IV and the rest IM 1,500 – 5,000 units in newborn Penicillin G 200,000 units/kg/day in 6 divided doses, IV, for 10 days 100,000 units/kg/day in 3 doses, IV, for 10 – 14 days, in neonates Tetracycline, not recommended to neonate Tetracycline if hypersensitive to Penicillin given at 30 – 40 mg/kg/day (not > 2 gms) in 4 divided doses, IV, for 10-14 days TREATMENT Control of Muscular Spasms Drugs 1. 2. 3. 4. 5. 6. Diazepam Chlorpromazine (Thorazine) Chloral Hydrate (Valium, Anxionil, Trazepam) Phenobarbital Mephenesin Barbiturates-Diazepam (tetanus neonatorum) Keep patient in a dark, quiet room Avoid unnecessary handling TREATMENT Cleaning and extensive debribement of necrotic tissue after administration of TIG or antitoxin and antibiotic Oxygen Feed through NGT Tracheostomy Adequate fluid, electrolytes and caloric intake NURSING INTERVENTION Prevention of respiratory & cardiovascular complications 1. Maintain adequate Airway 2. Provide cardiac monitoring 3. Keep vein open Wound & systemic care 1. Give TIG, TT and antibiotic 2. Debribe and irrigate wound NURSING INTERVENTION Ongoing assessment & support 1. Give diazepam and neuromuscular blocking agents 2. Place client in a quiet, semi-dark environment to avoid stimulating reflex spasms 3. Avoid fractures and pressure sores 4. Observe for urinary retention Prevention and health education 1. Immunization 2. Prevention of injury and safety handling RABIES Rabies is an infectious disease of animals caused by virus present in animals (Hydrophobia, Lyssa, Le rage) Most rabies viruses belong to genus Lyssavirus and the family Rhabdoviridae. Incubation period:    5 days to 1 year 20-90 day, AVERAGE In some cases, the incubation period has been thought to be significantly longer than 1 year Examples: Rabies Virus Mode of Transmission saliva of rabid dog and infected person virus cannot be acquired in utero; doesn’t cross the placenta Period of Communicability 3 to 5 days Pathogenesis virus spread from the site bite to CNS through peripheral nerves and multiplies spread from CNS to salivary glands & lungs Diagram showing the transmission of rabies virus PATHOLOGY Infection causes widespread changes throughout the CNS neuronal and mononuclear cellular infiltration in the thalamus, hypothalamus, substantia nigra, pons, medulla extensive damage of cranial nerve nuclei demyelinization and degeneration of the white matter neuronal changes in spinal cord presence of negri bodies CLINICAL MANIFESTATIONS Divided in 3 Stages 1. STAGE OF INVASION characterized by;    Prodromal Phase or Stage of Invasion (Invasive Stage) 2. Stage of Excitement ( Hydrophobia)     3. Terminal Phase or Paralytic Stage  fever & malaise anorexia & salivation sore throat & difficulty swallowing perspiration irritability & restless hyper excitability sensitive to light, sound and changes in temperature numbness and tingling sensation on the area of bite CLINICAL MANIFESTATIONS STAGE OF EXCITEMENT characterized by          marked excitation, apprehension & even terror delirium w/ nuchal stiffness, involuntary twitching and convulsion maniacal behavior alternate w/ depression sensitive to light, noise & faint odors eyes are fixed & glossy skin is cold & clammy Hydrophobia-pathognomonic sign aerophobia     violent, severe & painful spasm of muscle of the mouth, pharynx & larynx attacks precipitated even by mild stimuli fever of 1 to 3 days w/ tonic & clonic contraction of the muscle death during episode of spasm or from cardiac respiratory failure within 1 to 3 days, pt deteriorates and enter the terminal phase CLINICAL MANIFESTATIONS PARALYTIC STAGE patient becomes quiet & unconscious loss of bowel & bladder control tachycardia & irregular respiration spasm cease and paralysis progresses circulatory collapse or heart failure coma or death due to respiratory paralysis DIAGNOSIS definite history of exposure like bite or close contact to animal onset of hydrophobia 3. Laboratory Exams 1. 2. presence of negri bodies on microscopic examination Fluorescent Rabies Antibody (FRA) Intra cerebral inoculation from the animal that bit the person (Negri bodies) Observation of the animal within 10 days PREVENTION Eliminate exposure to rabid animals Pre-exposure prevention After exposure wash wound w/ soap and water tetanus prophylaxis and antibacterial therapy   Human Diploid Cell Rabies Vaccine (HDCV) Rabies Immune Globulin (RIG) Management of Biting Animal Capture the dog or animal that inflicted the bite and keep under veterinary surveillance. Healthy animal for 10 days is assumed not infective Dog that has been killed after biting a person should be decapitated and the head packed in ice or glycerin for examination for negri bodies TREATMENT No specific treatment Care of patient is symptomatic and supportive directed towards alleviation of spasm. Continuing cardiac and pulmonary monitoring. Evaluation of animal observe animal for 5 to 10 days nonavailability is best taken as an indication for vaccination Treatment of wound clean site w/ soap and water a portion of the antirabies serum should be infiltrated around the wound tetanus prophylaxis and antibiotics TREATMENT Antirabies Serum Heterologous Serum Homologous Rabies Immunoglobulin or Human Origin (HRIG) Rabies Vaccines The Fermi Type  prepared in nerve tissue and inactivated w/ phenol nerve tissue of adult animals brain tissue of suckling animals duck embryo human diploid cell Inactivated Vaccines - produced w/ fixed virus in any of the ff;     TREATMENT Active Immunization   administered 3 years duration for lower extremities bites both active and passive immunization is given if bites is in the head part of the body LYSSAVAC (IM or SQ) 1. 2. Lyssavac N – no need for skin testing Lyssavac Plain – need skin testing 3 doses – if dog didn’t die 6 doses – w/ dog death given into abdominal wall SQ for 14 days IMOVAX (IM)   ANTI-RABIES VACCINE  TREATMENT Passive Immunization administered for 3 months  Rabuman, IM  Hyper Rab, IM  Imogam, IM  NURSING INTERVENTION Isolation of patient throughout the course of treatment Provide comfort for the patient padding of bedside or use restraints use gloves to prevent contamination do not bathe patient wipe saliva or provide sputum jar Provide a restful environment minimal noise or very quiet environment no faucets or running water should be heard no site of water and electric fans should be seen room should be semi-dark and close NURSING INTERVENTION Diet and medication fluid are given rectally administer morphine as ordered Provide assurance and emotional support to the members of the family stay w/ family members encourage family members to receive vaccination especially those members who are exposed to rabies Local and treatment of wound Hyperimmune serum must be given w/in 72 hours SCHISTOSOMIASIS SYNONYMS Blood Flukes Bilharziasis Snail Fever SPECIES Schistosoma Haematobium Schistosoma Mansoni Schistosoma Japonicum   found in Asian countries also known as Oriental Schistosomiasis INCUBATION PERIOD at least 2 months LIFE CYCLE Adult Male & Female in Copula in portal vessels Eggs escape into Intestinal Lumen Become adults in 24 days and start laying eggs Schistosomulae carried in circulation and reach portal veins Eggs pass out w/ female hatch upon contact w/ water & liberate Miracidia Penetrate snail host (Oncomelania Quadrasi) Penetrate skin of definitive host in 3-5 minutes Development w/in snail (4-8 weeks) Primary Sporocysts Secondary Sporocysts Developing Sporocysts Cercarial escape into water 1-3 days CLINICAL MANIFESTATIONS Incubation Period    minute lesions with needling pain cough liver enlargement diarrhea dysenteric stools liver disturbance jaundice and ascites portal hypertension secondary infection CNS involvement – signs & symptoms will depend on the site of egg deposition Period of Egg Deposition & Extrusion    Period of Tissue Repair & Proliferation     DIAGNOSIS Identification of Eggs in the stool    Direct Fecal Smear Kato Katz Technique Concentration Technique Intradermal Test Liver & Rectal Biopsy Immunodiagnostic Test   Circumoval Precipitin Test Cercarial Envelope Reactions COMPLICATIONS PROGNOSIS Pulmonary Hypertension Cor Pulmonale Myocardial Damage Portal Cirrhosis good if treated early TREATMENT Trivalent Antimony Tartar Emetic  via vein given IM Stibophen  Praziquantel (Biltricide)  given orally Niridazole  given orally PREVENTION Avoidance of endemic areas Washing clothes or bathing in streams reduces exposure Proper sanitary disposal of human feces Destruction of snail host – Oncomelania Quadrasi Construction of irrigation system to prevent formation of breeding places Schistosoma Japonicum Schistosoma Mansoni Schistosoma Hematobium Oncomelania Quadrasi