CHICKEN POX

Varicella

CHICKENPOX

Chickenpox is an acute and highly contagious disease of viral etiology that is characterized by vesicular eruptions on the skin and mucous membrane with mild constitutional symptoms. In unimmunized populations, most people contract chickenpox by age 15, the majority between ages 5 and 9, but all ages can contract it. Chickenpox is usually more severe in adults and very young infants than children. Winter and spring are the most common times of the year for chickenpox to occur. Chickenpox is very highly contagious. It is easily passed between members of families and school classmates through airborne particles, droplets in exhaled air, and fluid from the blisters or sores. It also can be transmitted indirectly by contact with articles of clothing and other items exposed to fresh drainage from open sores. Patients are contagious up to five days (more commonly, one to two days) before and five days after the date that their rash appears. When all of the sores have crusted over, the person is usually no longer contagious.

CHICKENPOX

INFECTIOUS AGENT

Herpesvirus varicellae a DNA-containing virus Humans are the only source of infection. Closely related or identical to herpes zoster virus. Incubation period is 10 to 21 days or may be prolonged after passive immunization against chickenpox.
Period of Communicabilty A day before the eruption of the first lesion up to about five days after the appearance of the last crop

MODE OF TRANSMISSION

Direct with a patient who sheds the virus from the vesicles Indirect contact, through linens or formites Airborne, or spread by aerosolized droplets from the nasopharynx of ill individuals High viral titers in the vesicles of chickenpox; thus, viral transmission may also occur through direct contact with these vesicles, although the risk is lower. Following primary infection there is usually lifelong protective immunity from further episodes of chickenpox

PATHOPHYSIOLOGY

initial inhalation of contaminated respiratory droplets viral proliferation in regional lymph nodes of the upper respiratory tract a second round of viral replication occurs in the bodys internal organs, the liver and the spleen this secondary viremia is characterized by diffused viral invasion of capillary endothelial cells and the epidermis VZV infection of cells of the Malphigian layer produces both intercellular and intracellular edema Resulting in the characteristic vesicle

CLINICAL MANIFESTATIONS

1. Pre-eruptive manifestations are mild fever and malaise. 2. Eruptive stage Rash starts on the trunk spreading to the other parts of the body Initial lesions are distinctively red papules whose contents become milky and pus-like within four days In adults and bigger children, the lesions are more widespread and more severe There is rapid progression so that transition is completed in six to eight hours Vesicular lesions are very pruritic. All stages are present simultaneously before all are covered with scabs, leading to the appearance known as celestial map

The stages are characterized as follows:

Macule = not elevated above the skin surface

Papule = elevated above the skin surface with a diameter of about 3 mm.
Vesicle = pop-like eruption filled with fluid Pustule = a vesicle that is infected or filled with pus Crust = a scab or an eschar.

LESIONS

Macule

Pa p u l e

LESIONS

Ve s i c l e

Pustule

DIAGNOSTIC TESTS

Determination of the V-Z virus

Complement fixation test Electron microscopic examination of vesicular fluid

COMPLICATIONS

Rarely fatal, although generally more severe in adults than in children Pregnant women and those with suppressed immune systems are at the highest risk. Most common late complication is shingles, caused by reactivation of varicella zoster virus decades after the initial episodes of chicken pox Secondary infection of the lesions- furuncles, cellulitis, skin abscess, erysipelas. Meningoencephalitis Pneumonia Sepsis

TREATMENT MODALITIES

Oral acyclovir 800mg TID for 5 days Oral antihistamine for pruritus Calamine lotion for itchiness Salicylates must NOT be given Antipyretics for fever

NURSING MANAGEMENT AND PREVENTIVE MEASURES

Respiratory isolation is a must. Hygienic care Diversional activities to lessen pruritus in children Oral and nasal care

Active immunizations Isolation

DENGUE FEVER
Breakbone Fever/ Hemorrhagic Fever/ Dandy Fever/ Infectious Thrombocytopenic Purpura

DENGUE FEVER

Dengue fever is a disease caused by a family of viruses that are transmitted by mosquitoes. It is an acute illness of sudden onset that usually follows a benign course with symptoms such as headache, fever, exhaustion, severe muscle and joint pain, swollen glands (lymphadenopathy), and rash. The presence (the "dengue triad") of fever, rash, and headache (and other pains) is particularly characteristic of dengue. Other signs of dengue fever include bleeding gums, severe pain behind the eyes, and red palms and soles.
Dengue (pronounced DENG-gay) strikes people with low levels of immunity. Because it is caused by one of four serotypes of virus, it is possible to get dengue fever multiple times. However, an attack of dengue produces immunity for a lifetime to that particular serotype to which the patient was exposed. Dengue Fever is an acute febrile disease caused by infection with one of the serotypes of dengue virus, which is transmitted by mosquito genus Aedes.

DENGUE

ETIOLOGIC AGENTS AND MODE OF TRANSMISSION

Flaviviruses 1, 2, 3, 4, a family of Togaviridae, are small viruses that contain single-stranded RNA. Arboviruses group B
Bite of an infected mosquito: Principally, the Aedes aegypti
Day-biting (2 hours after sunrise and before sunset) Breeds in stagnant water Has limited, low-flying movement Has fine white dots at the base of the wings and white bands on the legs

Aedes albopictus (rural areas) Aedes polynensis Aedes scutellaris simplex

AEDES AEGYPTI

The bite of an infected mosquito transmits the disease.

Incubation Period Three to fourteen days; commonly seven to ten days Period of Communicability Patients are usually infective to the mosquito from a day before the febrile period to the end of it. The mosquito becomes infective for day 8 to 12 after the blood meal and remains infective throughout its life. Sources of Infection Infected persons the virus is present in the blood of patients during the acute phase of the disease and will become a reservoir of the virus, sucked by mosquitoes, which may then transmit the disease. Standing water any stagnant water in the household and its premises are usual breeding places of these mosquitoes.

INCIDENCE

Age may occur at any age, but is common among children and peaks between four to nine years old. Sex- both sexes can be affected Season more frequent during the rainy season Location more prevalent in urban communities

PATHOGENESIS AND PATHOLOGY

The infectious virus is deposited in the skin by the vector and initial replication occurs at the site of infection and in local lymphatic tissues. Within a few days, viremia occurs, lasting until the 4 th or 5th day after the onset of symptoms. Evidence indicates that macrophages are the principal site of replication. At the site of petechial rash, non-specific changes are noted, which include endothelial swelling, perivascular edema, and extravasation of blood. There is marked increase in vascular permeability, hypotension, hemoconcentration, thrombocytopenia with increased platelet agglutinability, and or moderate disseminated intravascular coagulation. The most serious pathophysiological abnormality is hypovolemic shock resulting from the increased permeability of the vascular endothelium and loss of plasma from the intravascular space.

CLINICAL MANIFESTATIONS

Dengue Fever
Prodromal symptoms characterized by: Malaise and anorexia up to 12 hours Fever and chills accompanied by severe frontal headache, ocular pain, myalgia with severe backache and arthralgia Nausea and vomiting Fever is non-remitting and persists for three to seven days Rash is more prominent on the extremities and the trunk. It may involve the face in some isolated cases Petechiae usually appears near the end of the febrile period and most commonly on the lower extremities.

Dengue Hemorrhagic Fever

Fever, hemorrhagic diathesis, hepatomegaly and hypovolemic shock.

PHASES OF THE ILLNESS

Initial Febrile phase lasting from two to three days

Fever (39-40 Celsius) accompanied by headache Febrile convulsions may appear Palms and soles are easily flushed Positive tourniquet test Anorexia, vomiting, myalgia Maculopapular or petechial rash may be present and usually starts in the distal prtion of the extremities. The skin appears purple, with blanched areas of varying site (Hermans sign, considered pathognomonic to the disease)

Generalized or abdominal pain

Hemorrhagic manifestations like (+) tourniquet test, purpura, epistaxis, and gum bleeding may be present.

PETECHIAL RASH

A sign of dengue positive tourniquet test

PHASES OF THE ILLNESS

Circulatory Phase
There is a fall of temperature accompanied by profound circulatory changes, usually on the 3rd to 5th days. Patient becomes restless, with cool, clammy skin. Cyanosis is present.

Profound thrombocytopenia accompanies the onset of shock.

Bleeding diathesis may become more severe and lead to GIT hemorrhage. Shock may occur due to loss of plasma from the intravascular spaces; hemoconcentration with markedly elevated hematocrit is present.

Pulse is rapid and weak; pulse pressure becomes narrow and blood pressure may drop to an unobtainable level.
Untreated shock may result in coma; metabolic acidosis and death may occur within two days. With effective therapy, recovery may follow in two to three days.

CLASSIFICATION ACCORDING TO SEVERITY (HALSTEAD AND NIMMANITYA)

Grade I Fever accompanied with non-specific constitutional symptoms and the only hemorrhagic manifestation is a (+) tourniquet test. Grade II All signs of Grade I plus spontaneous bleeding from the nose, gums and GIT are present. Grade III There is the presence of circulatory failure, as manifested by a weak pulse, narrow pulse pressure, hypotension, cold, clammy skin and restlessness. Grade IV There is profound shock and undetectable blood pressure and pulse.

COMPLICATIONS

Dengue Fever
Epistaxis, menorrhagia GI bleeding Concomitant GI disorder

DHF
Metabolic acidosis Hyperkalemia Tissue anoxia Hemorrhage into the CNS or adrenal glands Uterine bleeding may occur

Myocarditis

Severe manifestations
Dengue encephalopathy is manifested by increasing restlessness, apprehension or anxiety, disturbed sensorium, convulsions, spacity and hyporeflexia.

DIAGNOSTIC TESTS AND TREATMENT MODALITIES

Diagnostic Tests Tourniquet test Platelet count Hemoconcentration Occult blood Hemoglobin determination Treatment modalities asymptomatic only Analgesic drugs Intravenous infusion to prevent dehydration and for replacement of plasma Blood transfusion for severe bleeding Oxygen therapy for patients in shock Sedatives may be needed to allay anxiety and apprehension

Because dengue fever is caused by a virus, there is no specific medicine or antibiotic to treat it. For typical dengue, the treatment is purely concerned with relief of the symptoms (symptomatic). Rest and fluid intake for adequate hydration is important. Aspirin and nonsteroidal anti-inflammatory drugs should only be taken under a doctor's supervision because of the possibility of worsening hemorrhagic complications. Acetaminophen (Tylenol) and codeine may be given for severe headache and for the joint and muscle pain (myalgia). Typical dengue is fatal in less than 1% of cases. The acute phase of the illness with fever and myalgias lasts about one to two weeks. Convalescence is accompanied by a feeling of weakness (asthenia), and full recovery often takes several weeks.

NURSING MANAGEMENT

Keep patient in a mosquito-free environment to avoid further transmission. Keep patient at rest during bleeding episodes Monitor vital signs. In cases of bleeding, act quickly. Observe for signs of shock.

PREVENTION AND CONTROL

Health education Early detection and treatment Eliminate vectors by removing their breeding grounds Case finding

ANTHRAX

ANTHRAX

Anthrax is an infection caused by Bacillus anthracis that occurs primarily in herbivores.

Etiologic Agent Bacillus anthracis It is a large, aerobic, spore-forming, Gram (+), rod-shaped microorganism that is capsulated and non-motile. Can survive for years in dry soil but can be destroyed by boiling for 10min. Treatment is done by oxidizing agents such as KMnO 4 hydrogen peroxide, or diluted formaldehyde. Most are susceptible to penicillin.

ANTHRAX

An anthrax victim

ANTHRAX

Anthrax occurs worldwide and is most prevalent among domestic herbivores. Human cases are more resistant to anthrax than herbivorous animals.
Human cases are classified as: Agricultural cases, which result most often contact with animals that are infected. Industrial cases, which are associated with exposure to contaminated hides, goat hair, wool or bones.

MODE OF TRANSMISSION

Direct through contact with infected animals or contaminated animal products. Indirect through animal bites and ingestion of contaminated meat. Airborne through inhalation of contaminated or polluted air.

TYPES OF ANTHRAX

Cutaneous anthrax approximately 95% of human cases The incubation period ranges from nine hours to two weeks. a small pimple or macule appears two to three days after the entrance of the microorganism. A ring of vesicles develops around the papule. Vesicle fluid may exude Marked edema starts to develop. Unless there is no secondary infection, there is no pus and the lesion is not painful, although painful lymph adenitis may occur in the inguinal area. The original papules ulcerated to form the characteristic of eschar on the 5 th to 7th days. Edema extends to some distance of the lesion Clinical symptoms may be severe if the lesions are located on the face, neck or chest. High fever, toxemia, regional painful lymphadenopathy, and extensive edema. Shock and death may also ensue.

CUTANEOUS ANTHRAX

TYPES OF ANTHRAX

Inhalational anthrax (woolsorters disease) 5% of cases Symptoms resemble those of severe viral respiratory disease. After 3 days, increasing fever, dyspnea, stridor, hypoxia and hypotension occur, usually leading to death within 24 hours. Organisms are deposited into the alveoli or into alveolar ducts, producing hemorrhagic necrosis of nodes associated with hemorrhagic mediastinitis. Gastrointestinal anthrax results from ingestion of inadequately cooked meat from animals with anthrax. Occurs in the intestines where lesions are formed, accompanied by hemorrhagic lymphadenitis. Fever, nausea and vomiting, abdominal pain, bloody diarrhea and sometimes rapidly developing ascitis.

ANTHRAX

Inhalational

Gastrointestinal

COMPLICATIONS

Anthrax meningitis is the intense inflammation of the meninges of the brain and spinal cord. Elevated CSF pressure with bloody CSF, followed by rapidly loss of consciousness and death. Fatality rate is almost 100 percent.
Anthrax sepsis develops after the lymphohematogenous spread from the primary lesion. High fever, toxemia and shock, with death following in a short time.

TREATMENT AND MANAGEMENT

Parenteral penicillin G 2 million units every 6 hours, until edema subsides, with subsequent administration of oral penicillin for a 7 to 10 course. Patients who are sensitive to penicillin can be treated with erythromycin, tetracycline, or chloramphenicol.
Nursing management Careful history taking Thorough physical examination Skin care, psychological, and emotional support Supportive measures are geared toward the type of anthrax exposure Any type of anthrax should be reported to health authorities.

PERSONAL PROTECTIVE EQUIPMENTS

PPE

Personal protective equipment (PPE) is used by healthcare providers to protect themselves from injury or infection. There is personal protective equipment to keep rescuers safe from physical injuries, from chemical hazards, and from infection. Lay rescuers should follow their professional counterparts by practicing universal precautions and using PPE to provide protection from infection when assisting victims in an emergency.

HAND CLEANERS

The best way to prevent the spread of disease is to wash hands with soap and warm water after every contact with a medical victim. Unfortunately, soap and water are not always available. Make sure your medical supplies include a form of waterless hand cleaner.

GLOVES

Exam gloves come in three common types: latex, nitrile, and vinyl. Many people develop allergies to the protein found in latex. Nitrile and vinyl are much more hypoallergenic. Find out more about exam gloves.

CPR MASKS

Many lay rescuers do not want to perform the rescue breathing part of CPR because of the close contact required with the victim. The best way to avoid that squeamish feeling is to be prepared. CPR masks provide an important barrier between rescuer and victim.

FACE MASKS

Blood or other potentially infectious material sprayed or splashed in the face of a rescuer can enter the mouth or nose and spread an infection. Use a face mask whenever blood or other body fluids may become airborne.

EYE PROTECTION

Protect your eyes from injury as well as infection by obtaining the correct type of eye protection. Rescuers can choose from combination mask and eye protection that does not provide protection from injury, or they can choose more robust protection. Pick the correct eye protection for you.

SHARPS CONTAINER

Contaminated sharps must be deposited into a puncture-proof container. These containers protect sanitation workers from injury as well as other rescuers.

GOWNS

Full-body gowns are not used very often outside of the hospital. There is no good reason for this, it is just common practice across the country. Put the correct gown in your first aid kit and avoid the need to dispose of your favorite shirt or blouse.

BIOHAZARDOUS WASTE

Contaminated waste should be placed into a red, bio-hazardous waste container to distinguish it from regular garbage. When working with an ambulance, it is common for the ambulance crew to allow lay rescuers to dispose of their contaminated items in the ambulance's bio hazard container.

PREVENTION IS BETTER THAN CURE. Desiderius Erasmus

THANK YOU!
Caberte, Mae Lyn M., Group 20