COMMUNICABLE

DISEASES
PREPARED BY: Abigail E. Tan BSN IV C (Group 14)

TOPICS TO BE DISCUSS:

POLIOMYELITIS RABIES TETANUS

POLIOMYELITIS
Other Name: Infantile Paralysis; Heine Medin Disease DEFINITION: An acute infectious disease characterized by changes in the central nervous system which may result in pathologic reflexes, muscle spasm and an paresis or paralysis. It is a disease of the lower neurons, and it is because of the anterior horn involvement that it is named Anterior Poliomyelitis.

 ETIOLOGIC AGENT: Caused by filterable virus. Polio virus, Legio debilitans There are 3 strains of viruses and as far as it is known, the disease affects man alone. Brunhilde Lansing Leon INCUBATION PERIOD: 7-21 days for paralytic cases with a repeated range of 335 days. PERIOD OF COMMUNICABILITY: Capable of transmitting the disease during the first 3 days to 3 months of illness. The disease is most contagious during the first few days of active disease, and is possibly for 3-4 days before that.

MODE OF TRANSMISSION: Direct contact with contaminated oropharyngeal secretions and feces Person to person transmission through healthy carriers Indirectly, through contaminated articles and flies-contaminated water, food and utensils. PREDISPOSING CAUSES OF POLIOMYELITIS: AGE: 60% of patients are under 10 years of age. SEX: males than females (ratio of 3:2) death is proportionately higher in males. HEREDITY: poliomyelitis is not hereditary. ENVIRONMENTAL AND HYGIENIC CONDITION: The rich are more often spared than the poor. Excessive work, strain, marked overexertion are also factors that cause the disease. TYPES OF POLIOMYELITIS ABORTIVE TYPE accounts to about 4 8 % of all cases.
Does not invade the CNS HA and sore throat Slight or moderate fever Occasional vomiting Low lumbar pain The patient usually recovers within 72 hours and in most cases, the disease passes unnoticed.

 PRE PARALYTIC OR MENINGETIC TYPE:

All the above signs Patient manifests higher temperature, more severe ha, restlessness, vomiting, anorexia and lethargy. Pain and spasm in the muscles of the hamstring, pain at the neck and back. Changes in deep and superficial reflexes. Pain in the neck, back, arms, legs and abdomen. Inability to place the head in between the knees. Positive PANDYS SIGN. Transient paresis may occur. Usually lasts for about a week, with meningeal irritation persisting for about 2 weeks.

 PARALYTIC
The above signs and symptoms Positive HOYNES SIGN Paralysis occurs Less tendon reflexes. Positive KERNIGS and BRUDZINSKIS SIGN Weakness of the muscles. Hypersensitivity to touch There is usually urine retention, constipation and abdominal distention.

SPINAL PARALYTIC:
Paralysis occurs in muscles innervated by motor neurons of the spinal cord. Characterized by asymmetry, scattered flaccid paralysis on one or both lower extremities. Autonomic involvement manifested by excessive sweating and respiratory difficulty.

 BULBAR:
Usually has a rapid development and more serious type. Motor neuron in the brainstem are attacked, affecting the medulla Weakens the muscles supplied by the CN especially the 9th (Glossopharyngeal) and the 10th (Vagus). Paralysis of the facial, pharyngeal and ocular muscles. Respiratory failure and cardiac irregularities Hypothalamic dysfunction as manifested by impaired temperature regulation.

BULBOSPINAL:
Involvement of the neurons both the brainstem and the spinal cord.

 PATHOGENESIS: (PHASES) INTESTINAL PHASE: The organism enters the body through the alimentary tract, multiplies in the oropharynx, proceed to the intestine where they lodge and multiply. VIREMIC PHASE: the organisms are spread to the regional lymph nodes and the bloodstream. NEURAL PHASE: The microorganisms migrate to the CNS. In SPINAL TYPE, there is a gross evidence of inflammation in the ant. Horns of the gray matter of the cord, often extending in the arachnoid membrane of the nerve roots. - in CEREBRAL TYPE, the lesions are indistinguishable from other brain inflammations.
The lesions are found mainly in the anterior horn cells at the ff. sites.
Spinal cord The vestibular nuclei of the medulla and the cranial nerve The roof and the dermis of the cerebellum Gray matter of the midbrain The motor cortex.

COMPLICATIONS: Respiratory failure Circulatory collapse Electrolyte imbalance Bacterial infection Urinary problems related to retention or paralysis of the urinary bladder. Abdominal distention

 DIAGNOSTIC PROCEDURES:
Isolation of the virus from throat washing or swab early in the disease. Stool culture throughout the disease. Culture from the Cerebrospinal fluid (CSF).

MODALITIES OF TREATMENT:
Analgesics to ease headache, back pain and leg spasms. MORPHINE IS CONTRAINDICATED BECAUSE OF THE DANGER OF ADDITIONAL RESPIRATORY SUPPRESSION. Moist heat application may reduce muscle spasm and pain. Bed rest is necessary. PARALYTIC POLIO requires rehabilitation using physical therapy, braces, corrective shoes, and in some cases, orthopedic surgery.

 NURSING MANAGEMENT:
CARRY OUT ENTERIC ISOLATION. Observe the patient carefully for signs of paralysis and other neurologic damage. Perform a neurologic assessment at least once a day, but dont demand any vigorous muscular activity. Check blood pressure regularly in BULBAR POLIOMYELITIS. Watch for signs of fecal impaction due to dehydration and immobility. To prevent this, give sufficient fluids and high fiber diet to ensure an adequate daily output. Prevent the occurrence of pressure sores. Provide good skin care. Reposition the patient frequently, and keep the bed dry. To prevent the spread of the disease, wash hands every after contact with patient. Apply hot packs to affected limb to relieve pain and muscle shortening. Dispose excreta and vomitus properly. Provide emotional support both to patient and family. Maintain good personal hygiene, particularly oral and skin care.

 PREVENTION AND INFECTION CONTROL MANAGEMENT:

Immunization. Oral Polio Vaccine (OPV). PROPER DISPOSAL of GIT secretions. Enteric isolation. Implementation of standard precaution. Sanitation of the premises and proper food handling to avoid contamination by flies should be strictly observed. Avoid overcrowding.

RABIES
Other Name: Hydrophobia; Lyssa DEFINITION:
A specific acute, viral infection communicated to man by the saliva of an infected animal.

ETIOLOGIC AGENT:
RHABDOVIRUS
A bullet-shape filterable virus with strong affinity to the CNS. Sensitive to sunlight, ultraviolet light either, formalin, mercury and nitric acid. The organism is resistant to phenol, merthiolate and common antibacterial agents.

 INCUBATION PERIOD:
1 week to 7 months in dogs. 10 days to 15 years in human. Incubation period depends upon the ff. factors:
Distance of the bite to the brain. Extensiveness of the bite. Specie of the animal. Richness to blood supply. Resistance of the host.

PERIOD OF COMMUNICABILITY:
The patient is communicable 3-5 days before the onset of symptoms until the entire course of the disease.

 PATHOGENESIS:
From the site of the bite, the organism proceeds to the CNS through the exoplasm of the peripheral nerves. Experimental studies have shown that the virus stay for sometime in the inoculation site, and the multiplication of the virus occurs in the myocytes. It has been observed that the period between inoculation and nerve invasion is the ONLY time when the prophylactic vaccine is effective. Once the virus infects the individual, the spread is both centripetal and centrifugal. After infection of the CNS, the virus spread through the peripheral nerves, to the salivary glands, and also to other organs such as lungs, the adrenals, the kidneys, the bladder, and the testicles (priapism).

 PATHOLOGY:
RABIES VIRUS causes widespread changes throughout the CNS. This consist the neural necrosis and mononuclear cellular infiltration especially in the thalamus, hypothalamus, pons and medulla oblongata. The Cranial nerve nuclei are extensively damaged. Neural changes are present in the spinal cord especially in the posterior horns. Negri bodies are most abundant in the hypocampus, basal ganglia, pons and medulla, and are found in the degenerating neurons of the salivary glands. (PATHOLOGIC SIGN FOR RABIES).

CLINICAL MANIFESTATIONS: (3 PHASES)

PRODROMAL/ INVASION PHASE: - Characterized by fever, anorexia, malaise, sore throat, copious salivation, lacrimation, perspiration, irritability, hyper-excitability, apprehensiveness, restlessness, sometimes drowsy, mental depression, melancholia and marked insomnia. -Pain or tingling sensation at the original site of the bite, headache and nausea. -Sensitive to light, sound and temperature. -Pain and aches in different parts of the body. -Anesthesia, numbness, tingling, burning, and cold sensation maybe felt along the peripheral nerves involved and the site of the bite. -Mild difficulty in swallowing.

 EXCITEMENT OR NEUROLOGICAL PHASE: -Characterized by marked excitation, apprehension, and even terror may occur. -Delirium associated with nuchal rigidity, involuntary twitching or generalized convulsions. -Maniacal behavior, eyes are fixed and glossy, skin is cold and clammy. -Severe and painful spasm of the muscles -Aerophobia -Difficulty in swallowing causes frothy saliva to drool from the patients mouth. -DEATH may occur during the episode of spasm or from cardiac or respiratory failure. -If patient survive during this phase, the patient deteriorates rapidly and enters in the terminal phase.

3. TERMINAL / PARALYTIC PHASE: -Patient becomes quiet and unconscious. -Loss of bowel and urinary control -Spasm ceases with progressive paralysis. -Tachycardia, labored, irregular respiration. -DEATH occurs d/t respiratory paralysis, circulatory collapse of heart failure. DIAGNOSTIC PROCEDURES:
Virus isolation from the patients saliva or throat. Flourescent Rabies Antibody (FRA) provides the most definitive diagnosis. Presence of negri bodies in the dogs brain.

 MODALITIES OF TREATMENT:
Thoroughly wash the bite wounds and scratches with soap and running water for at least 3 minutes as first aid. Check the patients immunization status. Give Tetanus Toxoid if needed. Tetanus anti serum infiltrated around the wound or given intramuscularly after a negative skin test. Anti- rabies vaccine, both passive and active, depending upon the site and extensiveness of the bite as well as the health condition of the biting animal.

 NURSING MANAGAMENT:
Isolate the patient. Emotional and spiritual support to the patient and the family to help them to cope with the patients symptoms and probable death. Provide optimum comfort. Darken the room, provide quiet environment. Patient should not be bathed and there should not be any running water in the room or within the hearing distance of the patient. If an IV fluid has to be given it should be wrapped and needle should be securely anchored in the vein to avoid dislodging in times of restlessness. Concurrent and terminal disinfection should be carried out. Continuously monitor cardiac and respiratory function.

 PREVENTION AND INFECTION CONTROL AND MANAGEMENT:

The eradication of rabies should be on global scale and should include measures to prevent and control the disease in animals and wildlife. Vaccinations of all dogs. Enforcement of regulations and pick up destruction of astray dogs. Confinement for 10 14 days of any dog that has bitten a person. Laboratory facilities for observation and diagnosis. Public education, especially children, in avoiding and reporting all animals that appear sick.

TETANUS
Other Name: Lock Jaw DEFINITION:
An infectious disease caused by CLOSTRIDIUM TETANI which produces potent exotoxin with prominent systemic neuromuscular efforts manifested by generalized spasmodic contractions of the skeletal musculator. TETANUS is fatal up to 60 % of unimmunized persons, usually within 10 days of onset. When symptoms develop within 3 days, the prognosis is poor.

INCUBATION PERIOD:
3 days to 3 weeks in adult; 3 30 days in neonate.

 ETIOLOGIC AGENT:
The causative organisms of the disease os Cl. Tetani with the following characteristics:
Anaerobic, gram (+) with round terminal spore with slender body giving a drumstick appearance. The organism comes in two forms, spore forming and the vegetative form. The organism releases 2 types of toxin: 1. TETANOSPASMIN that is responsible for muscle spasm 2. TETANOLYSIN responsible for destruction of the RBC.

SOURCES OF INFECTION:
Animal and human feces. The organisms are found in the intestinal wall of herbivorous animals, including man. Soil and dust. Plaster of Paris, unsterile sutures, pins, rusty materials and scissors.

MODE OF TRANSMISSION:
Direct inoculation of microorganism through punctured wound that is contaminated by dust, soil, animal excreta containing Cl. Tetani.

 AVENUES FOR ENTRANCE OF THE ORGANISM: Rugged traumatic wounds and burns. Umbilical stump in newborn especially for babies delivered at home with faulty cord dressing; babies delivered to mothers without tetanus toxoid immunization. Unrecognized wounds (cleaning of the ears with sharp materials). Dental extraction, circumcision and ear piercing.

 CLINICAL MANIFESTATIONS: NEONATE:

Feeding and sucking difficulty. Excessive crying, most of the time voiceless crying. An attempt to suck results in spasm and cyanosis. Fever due to infection and dehydration. The jaw becomes so stiff that the baby cannot suck or swallow. Tonic or rigid muscular contraction, spasm or convulsions provoked by stimuli. Cyanosis and pallor. May end with flaccidity, exhaustion and finally DEATH.

 OLDER CHILDREN AND ADULT:

If tetanus remains localized, signs of onset are spasm and increase muscle tone near the wound. If it becomes systemic or generalized, indications include:
Hypertonicity, hyperactive deep tendon reflexes, tachycardia, profuse sweating, low grade fever and painful involuntary muscle contractions. Neck and facial muscle rigidity (trismus). Grinning expression (risus sardonicus) considered pathognomonic sign of the disease. Board like, rigid abdomen Opisthotonos Intermittent tonic convulsions lasting for several minutes which may result in cyanosis and sudden death due asphyxiation. In severe cases, laryngospasm followed by the accumulation of secretions in the lower airway resulting to respiratory distress d/t involvement of respiratory muscles. Fracture of the vertebrae may occur during severe spasm, yielding to coma and death. In fatal cases, death usually occurs during the 1st 10 days of the disease.

 COMPLICATIONS:
Resulting from laryngospasm and involvement of the respiratory muscles. Due to trauma Septicemia or generalized infection.

MODALITIES OF TREATMENT:
SPECIFIC:
Within 72 hours after the punctured wound, the patient should receive ATS, TAT, or TIG especially if he dont have any previous immunization. Tetanus toxoid 0.5 ml intramuscular is given in standard schedule. Pen G Na to control infection. Muscle relaxant to decrease muscle rigidity and spasm.

 NON SPECIFIC:
Oxygen inhalation Feed thru NGT. Tracheostomy set Adequate fluid, electrolyte and caloric intake. Good nursing care:
Avoidance of external stimulation. Prevention from further injury. Maintain adequate airway. Provide cardiac monitoring. Maintain an IV line for medication and emergency care as necessary. Carry out efficient wound care. Avoid contractures and pressure sores. Watch out for urinary retention. Close monitoring on vital signs and muscle tone. Provision of optimum comfort measures.

PREVENTION AND INFECTION CONTROL AND MANAGEMENT: Active immunization with Tetanus toxoid for adult. DPT for babies and children. Early consultation and adequate wound care after an injury.