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