Chain of InfectionSusceptible hostPortal of EntryEtiologic Agent (microorganism)ReservoirMethod of transmission from reservoir to (Source) susceptible hostPortal of exit
Pathogens• Bacteria – Aerobic – Anaerobic• Viruses - intracellular parasite capable of reproducing outside of a living cell.• Mycoplasma – similar to bacteria and have no cell wall – resistant to antibiotics that inhibit cell wall synthesis• Rickettsiae & Chlamydia - rigid cell wall; with some feature of both bacteria and viruses. – Chlamydia- transmitted by direct contact – Rickettsiae- infect cells of arthropods and are transmitted by these vectors.• Fungi - self-limited, affecting the skin and subcutaneous tissue.• Parasites
Reservoir -where the pathogen lives and multiplies – Endogenous – Exogenous• Mode of Transmission – Direct contact – Indirect contact• Vector – Droplet or airborne transmission
Host Factors• Factors that enable a host to resist infections: • Physical barriers • Hostile environment created by stomach acid secretions, urine & vaginal secretions. • Antimicrobial factors e.g. saliva, tears • Respiratory defenses • Specific and nonspecific immune responses to pathogenic invasion. • Age • Nutrition
Portal of Entry• Respiratory Tract• GI Tract• Genitourinary Tract• Skin and mucous membrane• Bloodstream
Stages of Infectious Process• Incubation period – period begins with active replication but with no symptoms• Prodromal stage – Symptoms first appear• Acute phase – proliferation and dissemination of pathogens• Convalescent stage - containment of infection and pathogens are eliminated• Resolution – total elimination of pathogens without residual manifestationNosocomial infection– Infection acquired in a health care setting.– Typically manifest after 48 hrs.– UTI most common type
FACTORS AFFECTING RISK OF INFECTION• AGE• HEREDITY• LEVEL OF STRESS• NUTRITIONAL STATUS• CURRENT MEDICAL THERAPY• PRE-EXISTING DISEASE• IMMUNIZATION STATUS
Standard precautions• Blood• All body fluids, secretions, excretions,• Non-intact skin• Mucous membranes• Essential elements: • Use barrier protection • Prevent inadvertent percutaneous exposure, dispose of needles • Immediate and thorough hand washing
Infection Control in In-Patient Health Care Agencies• Hand Hygiene• Patient Placement• Protective Equipment• Proper disposal of Soiled Equipment
Infection Control In Community – Based Setting• Sanitation• Proper Disposal of Waste• Food Preparation• Report CD Occurrence
Pharmacology• Check for: – History of hypersensitivity. – Age and childbearing status of the client. – Renal function – Hepatic function – Site of infection• Classification of antimicrobial preparations: – Bacteriostatic – Bactericidal
COMMUNICABLE DISEASE – Is any disease that can be transmitted directly or indirectly from one person to another
INFECTION – Is a condition caused by the entry and multiplication of pathogenic microorganisms within the host body. – It is also an invasion of an organisms (bacteria, helminths, fungi, parasite, ricketsia and prion)
ISOLATION– It is necessary when a person is known or suspected to be infected with pathogens that can be transmitted by direct or indirect contact.– The principle behind isolation technique is to create a physical barrier that prevents the transfer of infectious agents. To do this you have to know how the organisms are transmitted.
AIRBORNE– PRIVATE ROOM– NEGATIVE AIR PRESSURE– VENTILATION SAFEGUARDS air from room is not recirculated to other areas– DOOR SHOULD BE KEPT CLOSED– BARRIER TO SMALL PARTICLES masks HEPA high efficiency particulate air– COVER MOUTH OF PATIENT WITH MASK DURING TRANSPORT
DROPLET• – PRIVATE ROOM – WEAR MASK IF WORKING WITHIN 3 FEET – WEAR MASKS UPON ENTRY INTO THE ROOM – COVER MOUTH OF PATIENT WITH MASK DURING TRANSPORT
CONTACT– PRIVATE ROOM– WEAR GLOVES– GLOVES ARE REMOVED BEFORE EXITING FROM THE ROOM– HANDS ARE WASHED THOROUGHLY– NOTHING IS TOUCHED BEFORE EXITING THE ROOM– GOWN IS WORN WHEN ENTERING THE ROOM– REMOVE GOWN CAUTIOUSLY BEFORE LEAVING THE ROOM– PATIENT CARE ITEMS SHOULD BE RESTRICTED TO SINGLE PATIENT
AFB ISOLATION – VISITORS REPORT TO NURSES’ STATION BEFORE ENTERING ROOM • MASKS ARE TO BE WORN IN THE PATIENT’S ROOM • GOWNS ARE INDICATED TO PREVENT CLOTHING CONTAMINATION • GLOVES ARE INDICATED FOR BODY FLUIDS AND NON- INTACTSKIN • HANDWASHING-after touching the patient or potentially contaminated articles and after removing gloves • articles should be discarded, cleaned or sent for decontamination and reprocessing • room is to remain closed • patient is to wear mask during transport
STRICT ISOLATION– VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM– PRIVATE ROOM-necessary, door must be kept closed– GOWNS-must be worn by all persons entering the room– MASKS- must be worn by all persons entering the room– HANDS-must be washed on entering and leaving room– GLOVES-must be worn by all persons entering the room– ARTICLES-must be discarded, or wrapped before being sent to CENTRAL SUPPLY for disinfection or sterilization
RESPIRATORY ISOLATION – VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM – PRIVATE ROOM-necessary, door must be kept closed – GOWNS-gowns not necessary – MASKS- must be worn by all persons entering the room if susceptible disease – HANDS-must be washed on entering and leaving room – GLOVES-not necessary – ARTICLES-those contaminated with secretions must be disinfected – CAUTION-all persons susceptible to the specific disease should be excluded from the area, susceptibles must wear masks
WOUND AND SKIN PRECAUTIONS– VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM– PRIVATE ROOM-desirable– GOWNS-must be worn by all persons having direct contact with the patient– MASKS- during dressing changes– HANDS-must be washed on entering and leaving room– GLOVES-must be worn by all persons having direct contact with infected area– ARTICLES-instruments, dressing, linens
ENTERIC PRECAUTIONS– VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM– PRIVATE ROOM-necessary FOR CHILDREN ONLY– GOWNS- must be worn by all persons having direct contact with the patient– MASKS- not necessary– HANDS-must be washed on entering and leaving room– GLOVES-must be worn by all persons having direct contact with patient or articles contaminated with fecal material– ARTICLES-special precautions necessary for articles contaminated with urine and feces, must be disinfected or discarded
PROTECTIVE ISOLATION– VISITORS-REPORT TO NURSES’ STATION BEFORE ENTERING ROOM– PRIVATE ROOM-necessary, door must be kept closed– GOWNS- must be worn by all persons entering room– MASKS- - must be worn by all persons entering room– HANDS-must be washed on entering and leaving room– GLOVES-must be worn by all persons having direct contact with patient
Diphtheria– Corynebacterium diphtheriae– Klebsloeffler’s bacillus (bacteria)– MOT = droplets and airborne • HIGHLY CONTAGIOUS– IP 2-5 days– IMMUNITY • Active = DPT • Passive = DAT • Natural = xxx
– Dx = throat swab, MOLONEY, SCHICK– Pseudomembrane, Bullneck– Penicillin or erythromycin– Resp Acidosis with hypoxemia– Cx: myocarditis, septicemia
Nursing Considerations:– OBSERVE CNS, CARDIAC AND KIDNEY COMPLICATIONS– PSEUDOMEMBRANOUS MAY LEAD TO RESP. OBSTRUCTION– ISOLATION UNTIL 2 NEGATIVE CULTURE AT 24 HOUR INTERVAL– F&E RESUSCITATION– PARENTS OR SIBLINGS WHO HAVE NEVER IMMUNIZED SHOULD RECEIVE A DOSE OF DIPH. ANTI-TOXIN– ATTENTION TO NASOPHARYNGEAL DISCHARGE– ANTIBIOTICS-PENICILLIN, ERYTHROMYCIN IF ALLERGIC TO PENICILLIN
Diphtheria KEY POINTS!– Highly contagious– Pseudomembrane and bullneck– Immunization best intervention PREVENTION– Obstruction and myocarditis– Isolation technique
Measles, Rubeola, 7 Day Fever, Hard Red Measle– Paramyxo virus– MOT = droplets and airborne • PC 4 days before and 5 days after rash • HIGHLY CONTAGIOUS– IP 7-14 days– IMMUNITY • Active = measles vaccine, MMR • Passive = measles Ig • Natural = lifetime
– Rashes:– Maculopapular– Cephalocaudal– With desquamation– Pruritus
• Rashes: maculopapaular, cephalocaudal (hairline and behind the ears to trunk and limbs), confluent, desquamation, pruritus
German Measles, Rubella, Rotheln Disease, 3 Day Measles– RNA rubella virus– MOT = droplets and airborne • PC 5 days before and 5 days after rash • HIGHLY CONTAGIOUS– IP = 10-21 days– IMMUNITY • Active = MMR • Passive = rubella Ig • Natural = lifetime
– Rashes:– Maculopapular– Diffuse– No desquamation
– Rashes: Maculopapular, Diffuse/not confluent, No desquamation, spreads from the face downwards•
Chicken Pox, Varicella– Herpes Zoster Virus– Varicella Zoster Virus– MOT = droplets and airborne • PC one day before rash and 6 days after first crop of vesicles • HIGHLY CONTAGIOUS– IP 14-21 days– IMMUNITY • Active = varicella vaccine • Passive = xxx • Natural = lifetime
– Rashes: Maculopapulovesicular (covered areas), Centrifugal, starts on face and trunk and spreads to entire body– Leaves a pitted scar (pockmark)
– Dx = Tzanck smear (scraping of ulcer for staining)– Rashes: • Maculopapulovesicular (covered areas) • Centrifugal • Leaves a pitted scar (pockmark)– CX furunculosis, erysipelas, meningoencephalitis– Dormant: remain at the dorsal root ganglion and may recur as shingles
Meningitis Menigococcemia– Neisseria meningitides (bacteria)– MOT = droplets– IP = 1-2 days– IMMUNITY = xxx
What is rabies? (DEFINITION & ETIOLOGY)• Is an acute infectious disease of warm-blooded animals and humans characterized by an involvement of the nervous system resulting in death.• It is caused by the RABIES VIRUS, a rhabdovirus of the genus lyssavirus.Rabies is a serious disease. Each year, it kills more than50,000 people and millions of animals around the world.Rabies is a big problem in Asia, Africa, and Central and SouthAmerica. In the United States, rabies has been reported inevery state except Hawaii. Any mammal can get rabies.Raccoons, skunks, foxes, bats, dogs, and cats can get rabies.Cattle and humans can also get rabies. Only mammals can getrabies. Animals that are not mammals -- such asbirds, snakes, and fish -- do not get rabies. Rabies is causedby a virus. An animal gets rabies from saliva, usually from abite of an animal that has the disease.
The Rabies VirusRV – a neurotropic filterable virus present in thesaliva of rabid animals. It has a preferrence for Rod-shapednerve tissues. rabies viruses colored for Virus – minute organism not visible effect with ordinary light microscopy. It is parasitic in that it is entirely dependent on nutrients inside cells for its metabolic and reproductive needs. Can only be seen by use of eclectron microscopy. Consists of DNA or RNA covered with a protein Parts of the rabies covering called capsid. A rhabdovirus virus of the genus lyssavirus. Neurotropic – viruses that reproduce in nerve tissue Filterable virus – virus causing RHABDOVIRUS: any group of rod-shaped infectious disease, the essential This is a RNA viruses with 1 important member, elements of which are so photograph of tiny that rabies virus, pathogenic to man. The they retain infectivity aftervirus under the virus has a predilection for tissue of RHABDO: from Greek passing through a filter of the electron mucus-secreting glands and the Central rhabdos, "rod" Berkefeld type. microscope Nervous System. All warm-blooded
How do you get rabies? (MODE & MEDIA OF TRANSMISSION, IMMUNITY)•All warm-blooded mammals are susceptible. Natural immunity in man isunknown.•You get rabies through the saliva of an infected animal by an exposure toan open break in the skin such as bites, open wound or scratch andinhalation of infectious aerosols such as from bats.•In some cases, it is transmitted through organ transplants (cornealtransplant), from an infected person.•The virus gets transmitted through saliva, tears, semen, some liquor(amniotic fluid, CST) but not blood, urine or stool. You get rabies from the saliva of a rabid animal, usually from a bite. The rabies virus is spread through saliva. You cannot get rabies by petting an animal. You may get rabies from a scratch if the animal, such as a cat, was licking its paw before it scratched you. (Remember that the rabies virus is found in the saliva of an animal).
How do you know if an animal has rabies?• Animals with rabies may act differently from healthy animals.• Some signs of rabies in animals are: changes in an animal’s behavior general sickness (fever, restlessness) problems swallowing increased drooling aggression (biting at inanimate objects, aimless running)• Wild animals may move slowly or may act as if they are tame. Some wild animals (foxes, raccoons, skunks) that normally avoid porcupines, may even try to bite these prickly rodents.• A pet that is usually friendly may snap at you or may try to bite.
How do you know if one has rabies? (DIAGNOSIS)•There is yet no way of immediately knowing who had acquiredrabies virus. No tests are available to diagnose rabies in humansbefore the onset of clinical disease.•The most reliable test for rabies in patients who have clinical signsof the disease is a DIRECT IMMUNOFLUORESCENT STUDY of afull thickness biopsy of the skin taken from the back of the neckabove the hair line.•The RAPID FLUORESCENT FOCUS INHIBITION TESTis used to measure rabies-neutralizing antibodies inserum. This test has the advantage of providing resultswithin 24 hours. Other tests of antibodies may take aslong as 14•days.
EPIDEMIOLOGYPHILIPPINES: 350-450 cases/ year 5-7 per million populationDOG BITE INCIDENCE: 140, 000- 560, 000/ year200-800 per 100, 000 population/ yearAGE MOST AFFECTED: 5-14 year age group (53% of cases)BITING ANIMALS: (SLH STUDY 1982- 2002) DOGS: 98% PET: 88% STRAY: 10% CATS: 2%
• Based on the report from NCDPC (2004), the six regions with the most number of rabies cases are Western Visayas, Central Luzon, Bicol, Central Visayas, Ilocos and Cagayan Valley• Data shows that 53.7 percent of animal bite patients are children• Dogs remain the principal animal source of rabies
STAGES OF RABIES INFECTIONRabies virus Entry into the body INCUBATI0N PERIOD (20 – 90 days) INVASION (0 – 10 days) EXCITEMENT (2 – 7 days) PARALYTIC COMA (5 – 14 days) DEATH
RABIES CLASSIFICATIONANIMAL RABIES• There are two common types of rabies. One type is "furious" rabies. Animals with this type are hostile, may bite at objects, and have an increase in saliva. In the movies and in books, rabid animals foam at the mouth. In real life, rabid animals look like they have foam in their mouth because they have more saliva. The second and more common form is known as paralytic or "dumb" rabies. The dog pictured below has this type. An animal with "dumb" rabies is timid and shy. It often rejects food and has paralysis of the lower jaw and muscles.• Another two types of rabies. One type is “urban” rabies. The type of rabies in domestic dogs and cats. The other type is called “ sylvatic” rabies. These type came from wild animals such as bats, weasels, skunks and moles & voles.
HUMAN RABIES• Humans also have a “furious” type, the classic foaming of the mouth, aggression, apprehension & hydrophobia, and the “dumb” type, progressive paralysis of the body until they couldn’t breathe anymore.
DIFFERENT STAGES OF RABIES INFECTION C B A A T TD S SOGS VIRUS IN SALIVA INHALED AEROSOLS VIRUS IN SALIVA INVASION PHASE INVASION PHASE PARALY SIS EXCITEMENT PARALY SIS DEATH DEATH
INVASION STAGE• Also called PRODOME PERIOD; Prodrome – symptom indicative of an approaching disease• 2-10 DAYS• Sensory changes on the site of entry. Pain: dull, constant pain referable to the nervous pathways proximal to the location of the wound or itching, intermittent, stabbing pains radiating distally to the region of inoculation. In general, sensitivity is the early symptom which may be ascribed to the stimulative action of the virus affecting groups of neurons, esp. sensory system. Though there is apt to be decreased sensitivity to local pain e.g. needle introduction, patient may complain bitterly of drafts & bed clothes which produce a general stimulation Tick me!
EXCITATION STAGE• Also called ACUTE NEUROLOGICAL PHASE; hyperactivity• 2 – 10 DAYS• Imminent thoraco-lumbar involvement (SNS): pupillary dilation, lacrimation increased thick saliva production / foaming of mouth, excessive perspiration, increased HR• Anxiety: increased nervousness, insomnia, apprehension; a strong desire to be up, wandering aimlessly about, and Fear: a sense of impending doom• Hydrophobia (perhaps, SNS stimulation: depresses GI activity > inhibits esophageal, gastric & intestinal function) > violent expulsion of fluids, drooling (in attempt not to swallow) > dehydration and parched mouth & tongue• Pronounced muscular stimulation & general tremor• Mania (tearing of clothes & bedding, cases of biting & fighting rare but may occur) and Hallucinations with lucid intervals (normal mental function in which patient is well-oriented & answers questions intelligently)• Convulsions( besides r/t pronounced muscular stimulation, further precipitated by sensory stimuli – sight, sound, name of water > throat spasms > choking > apnea, cyanois, gasping Sympathetic nervous system• > death, but if patient survive excitement phase… Tick me Parasympathetic nervous system Tick me 1st! next!
PARALYTIC STAGE-also called DEPRESSION PHASE• Gradual weakness of muscle groups – muscle spasms cease – OCULAR PALSY – strabismus, ocular incoordination, nystagmus, diplopia, central type partial blindness > responds poorly to light, @ times pupil is constricted or unequal (parasympathetic involvement) – Oro-facial: FACIAL & MASSETER PALSY > difficulty closing eyes & mouth, face expressionless – Oral: Weakness of muscles of phonation > hoarsness & loss of voice• Loss of tendon reflexes, always precedes weakness of extremity• Corneal reflex decreased or absent, dry
• Ears: VERTIGO . Middle ear disease . Early symptom, but may develop @ any period• Neck stiffness• (+) Babinski [lesions of pyramidal tract], ( - ) Kernig’s ( - ) Brudzinski’s• Cardiac: shifts from tachycardia (100 – 120bpm) @ bed rest to bradycardia (40 -60 bpm)• Respi: Cheyne-Stokes > breathing pattern characterized by a periodic 10 – 6- sec of apnea followed by gradual increasing depth and frequency of respiration• Local sensation (pin prick, heat, cold) diminished• Incoordination
• Hydrophobia and aerophobia gone, but still has some difficulty swallowing• General arousal (PNS stimulation)• Bladder & intestinal retention and obstipation (damage to to innervation of the musculature of intestine & bladder)(SNS damage) in some cases, patient shows period of recovery, this apparent remission is followed by progressive• Ascending, flaccid paralysis of extremities until it reaches the respiratory muscle• Apathy, stupor• Complications: Pneumothorax, thrombosis, secondary infections
MANAGEMENTNURSING INTERVENTIONS• HIGH RISK FOR INFECTION TRANSMISSION » provide patient isolation » handwashing. Wash hands before and after each patient contact and following procedures that offer contamination risk while caring for an individual patient. Handwashing technique is important in reducing transient flora on outer epidermal layers of skin. » Wear gloves when handling fluids and other potential contaminated articles. Dispose of every after patient care. Gloves provide effective barrier protection. Contaminated gloves becomes a potential vehicle for the transfer of organisms.
• KNOWLEDGE DEFICIT (about the disease, cause of infection and preventive measures) »assess patient’s and family’s level of knowledge on the disease including concepts, beliefs and known treatment. »Provide pertinent data about the disease: »organism and route of transmission »treatment goals and process »community resources if necessary »allow opportunities for questions and discussions
• ALTERED BODY TEMPERATURE: FEVER RELATED TO THE PRESENCE OF INFECTION. Since fever is continuous, provide other modes to reduce discomfort. »If patient is still well oriented, Inform the relation of fever to the disease process. The presence of virus in the body … »Monitor temperature at regular intervals »Provide a well ventilated environment free from drafts and wind.
• DEHYDRATION related to refusal to take in fluids secondary to throat spasms and fear of spasmodic attacks. »Assess level of dehydration of patient. »Maintain other routes of fluid introduction as prescribed by the physician e.g. parenteral routes »Moisten parched mouth with cotton or gauze dipped in water but not dripping.
IMMUNIZATION ACTIVE IMMUNIZATION- induce antibody and T-cell production in order to neutralize the rabies virus in the body. It induces an active immune response in 7-10 days after vaccination, which may persist for one year or more provided primary immunization is completed.TYPES: a. PVRV (Purified Vero Cell Rabies Vaccine) b. PCEVC (Purified Chick Embryo Cell Vaccine)
PASSIVE IMMUNIZATION- RIG (Rabies Immune Globulins)- provide the immediate availability of antibodies at the site of exposure before it is physiologically possible for the pt.to begin producing his own antibodies after vaccination.- Important for pts. w/ Cat III exposuresTypes: a. HRIG (Human Rabies Immune Globulins) b. Highly Purified Antibody Antigen Binding fragments c. ERIG (Equine Rabies Immune Globulins)
VACCINATION (Intradermal Schedule) Day of PVRV/PCECV SiteImmunization DAY 0 0.1 ml L & R deltoids/ anterolateral thighs of infants DAY 3 0.1 ml L & R deltoids/ anterolateral thighs of infants DAY 7 0.1 ml L & R deltoids / anterolateral thighs of infants DAY 28/30 0.1 ml L & R deltoids/ anterolateral thighs of infants
Intramuscular ScheduleDay of PVRV PCECV SiteImmunizationDay 0 0.5 ml 1.0 ml One deltoid/ anterolateral thigh of infantsDay 3 0.5 ml 1.0 ml SameDay 7 0.5 ml 1.0 ml SameDay 14 0.5 ml 1.0 ml SameDay 28 0.5 ml 1.0 ml same
MANAGEMENT OF RABIES PATIENT• Once symptoms start, treatment should center on comfort care, using sedation & avoidance of intubation & life support measures once diagnosis is certain1. MEDICATIONSa. Diazepamb. Midazolamc. Haloperidol + Dipenhydramine
2. SUPPORTIVE CARE- Pts w/ confirmed rabies should receive adequate sedation & comfort care in an appropriate medical facility. a. Once rabies diagnosis has been confirmed, invasive procedures must be avoided b. Provide suitable emotional and physical support c. Discuss & provide important info. to relatives concerning transmission of dse. & indication for PET of contacts d. Honest gentle communication concerning prognosis should be provided to relatives of pt
3. INFECTION CONTROL a. Patient should be admitted in a quiet, draft- free, isolation room b. HLCR workers & relatives in contact w/ pt should wear proper personal protective equipment (gown, gloves, mask, goggles)4. DISPOSAL OF DEAD BODIES
• Immunization – DPT (0.5 ml IM) 1 – 1 ½ months old 2 - after 4 weeks 3 – after 4 weeks – 1 st booster – 18 mos – 2 nd booster – 4-6 yo – subsequent booster – every 10 yrs thereafter – TT (0.5 ml IM) TT1 - 6 months within preg TT2 - one month after TT1 TT3 to TT5 - every succeeding preg or every year – TAT (horse) and TIG (human)
• Management – 1. Anticonvulsant, muscle relaxants, – antibiotics, wound cleansing and debridement, hyperbaric chamber – 2. Active-DPT and tetanus toxoid – 3. Passive-TIG and TAT, placental immunity
IINTRODUCTION: Philippine Hemorrhagic Fever was first reported in 1953. In 1958, hemorrhagic became a notifiable disease in the country and was later reclassified as Dengue Hemorrhagic Fever.What is DengueHemorrhagic Fever? • A severe mosquito transmitted viral illness endemic in the tropics. • It is characterized by increased vascular permeability, hypovolemia and abnormal blood clotting mechanisms.
WHO case definition for DHF:• fever or history of recent fever• thrombocytopenia (platelet count equal to or less than 100 x 10 /cu mm)• hemorrhagic manifestations such as petechiae or overt bleedingphenomena, and• evidence of plasma leakage due to increase vascular permeabilityInfectious Agent / Etiologic Agent: Flaviviruses; Dengue Virus Types 1, 2, 3, and 4
Occurrence: Dengue occurrence is sporadic throughout the year. Epidemic usually occurs during the rainy seasons June – November. Peak months are September and October. DHF are observed most exclusively among children of the indigenous population under 15 years of age. Occurrence is greatest in the areas of high Aedis Aegypti prevalence.
Notifiable Diseases and Deaths by Cause in the Philippines (2001 – 2004) 2001 2002 2003 2004Notifiable Diseases Reported Reported Reported Reported Cases Deaths Cases Deaths Cases Deaths Cases Deaths Dengue Fever 23,235 13,187 18,039 15,838 Source: National Statistics Office
INCIDENCE OF DENGUE HEMORRHAGIC FEVER IN CEBU CITY (YEAR 2007) Selected Number of New Cases Number of Deaths YearCommunicable Disease: total male female total male femaleDengue / DHF 43, 350 … … 416 … … 2007 Source: Department of Health Region VII
• The DOH reported 70,204 dengue cases for week ending September 10, 2011. This was over 24,000 cases less or 25.87% lower than for the same period last year. In addition, the number of cases in July and August (the peak months for dengue) was 52% lower than last year. A total of 396 deaths were reported for this year, which is lower than last year’s number of 620.
Reservoir / Source of Infection: • Some source is a vector mosquito, the Aedes Aegypti or the common household mosquito • The infected person
Mode of Transmission: Mosquito bite (Aedis Aegypti)Incubation Period: Probably 6 days to one weekPeriod of Presumed to be on the 1st week of illness – when virus is stillCommunicability: present in the bloodSusceptibility and All persons are susceptible. Both sexes are equally affected. The ageresistance: groups predominantly affected are the preschool age and school age. Adults and infants are not exempted. Peak age affected 5-9 years. Susceptibility is universal. Acquired immunity may be temporary but usually permanent.
Diagnostic Test: 1.) Tourniquet Test (Rumpel Leads Tests) • Inflate the blood pressure cuff on the upper arm to a point midway between the systolic and diastolic pressure for 5 minutes • Release cuff and make an imaginary 2.5 cm square or 1 inch just below the cuff, at the antecubital fossa • Count the number of petechiae inside the box • A test is (+) when 2 or more petechiae per 2.5 cm square or 1 inch square are observed 2.) A con firmed diagnosis is established by culture of the virus, polymerase-chain-reaction (PCR) tests, or serologic assays.
Clinical Manifestations (Public Health Nursing inthe Philippines, 2007):An acute febrile infection of sudden onset with 3 stages:• 1st-4th day (febrile or invasive stage)-high fever, abdominal pain and headache; later flushing whichmay be accompanied by vomiting, conjunctiva infection andepistaxis.• 4th-7th day (toxic or hemorrhagic stage)-lowering of temperature, severe abdominal pain, vomiting andfrequent bleeding from gastrointestinal tract in the form ofhematemesis or melena. Unstable blood pressure, narrow pulsepressure and shock. Death may occur. Tourniquet test which may bepositive may become negative due to low or vasomotor collapse.
• 7th-10th day (convalescent or recovery stage) -generalized flushing with intervening areas of blanching, appetite regained and blood pressure already stable.• Dengue shock syndrome is defined as denguehemorrhagic fever plus:*Weak rapid pulse,*Narrow pulse pressure (less than 20 mm Hg) or,*Cold, clammy skin and restlessness
Grading of Dengue Fever:The severity of DHF is categorized into four grades:• grade I, without overt bleeding but positive for tourniquet test• grade II, with clinical bleeding diathesis such as petechiae, epistaxis andhematemesis• grade III, circulatory failure manifested by a rapid and weak pulse withnarrowing pulse pressure (20 mmHg) or hypotension, with the presence ofcold clammy skin and restlessness; and• Grade IV, profound shock in which pulse and blood pressure are notdetectable. It is note-worthy that patients who are in threatened shock orshock stage, also known as dengue shock syndrome, usually remainconscious.* Grade III and IV are considered to be Dengue Shock Syndrome
• Promote rest• Medication –Paracetamol – for fever and muscle pains. –Analgesic – for headache –DON’T GIVE ASPIRIN
• Rapid replacement of body fluids is the most important treatment – Give ORESOL to replace fluid as in moderate dehydration at 75ml/kg in 4-6 hours or up to 2-3L in adults. Continue ORS intake until paient’s condition improves. – Intravenous fluid
• For hemorrhage – Keep patient at rest during bleeding periods – For epistaxis – maintain an elevated position of trunk and promote vasoconstriction in nasal mucosa membrane through an ice bag over the forehead. – For melena – ice bag over the abdomen.
• Provide support during the transfusion therapy• Diet – Low fat, low fiber, non- irritating, non-carbonated – Noodle soup may be given• Observe signs of deterioration (shock) such as low pulse, cold clammy perspiration, prostration.
• Eliminate vector by: –Changing water and scrubbing sides of lower vases once a week –Destroy breeding places of mosquito by cleaning surroundings –Proper disposal of rubber tires, empty bottles and cans –Keep water containers covered
OTHER PRECAUTIONS:• When outdoors in an area where dengue fever has been found –Use a mosquito repellant –Dress in protective clothing-long- sleeved shirts, long pants, socks, and shoes
• Keeping unscreened windows and doors closed• Keeping window and door screens repaired• Use of mosquito nets
MALARIA• Malaria, King of Tropical – P. VIVAX AND OVALE Disease MAY HAVE RECCURENCE OF SYMPTOMS – Protozoan plasmodium • tertian-febrile paroxysm • plasmodium ovale - q24H-48H dormant (liver) • quartan-febrile paroxysm • plasmodium vivax - q48H-72H benign • plasmodium malariae - mild but resistant • plasmodium falciparum - malignant (cerebral malaria)
– MOT • Bite from infected anopheles mosquito or minimus flavire (night biting) • Blood Transfusion • Sexual cycle – sporogony (mosquito) – gametes is the infective stage • Asexual cycle – schizogony (human)– IP (Incubation Period) 5-6 days
– Nursing Considerations– Dx: • blood extraction (extract blood at the height of fever)– Fever, chills, profuse sweating-convulsion– Anemia and fluid and electrolytes imbalance, hepatomegaly, splenomegaly, rigor, headache and diarrhea.– Chloroquine and Primaquine drug of choice– Chloroquine for pregnant women– For resistant plasmodium-use chemo drug– RBC is being attack
– Nursing Considerations– IV FLUIDS AND ELECTROLYTES– Blackwater Fever – hemolysis and hemoglobinuria– Sickle Cell Trait – provides natural resistance– DECREASE FLUIDS IN CEREBRAL EDEMA– ASSISTED VENTILATION IN PULMONARY EDEMA– DIALYSIS IN RENAL FAILURE– BT IN ANEMIA
– TRAVELERS TO MALARIA ENDEMIC area SHOULD FOLLOW PREVENTIVE MEASURES- (CHEMOPROPHYLAXIS CHLOROQUINE MAY BE TAKEN 1 WEEK BEFORE ENTERING ENDEMIC AREA)– SOAKING OF MOSQUITO NET IN AN INSECTICIDE SOLUTION– BIO PONDS FOR FISH– ON STREAM CLEARING (TO EXPOSE THE BREEDING STREAM TO SUNLIGHT)– VECTORS PEAK BITING AT NIGHT 9PM-3AM– PLANTING OF NEEM TREE (REPELLENT EFFECT)– ZOOPROPHYLAXIS (DEVIATE MOSQUITO BITES FROM MAN TO ANIMALS)– INFECTED MOTHER CAN STILL CONTINUE BREAST FEEDING
Filariasis, Elephantiasis, Human Lymphatic Filariasis– CAUSATIVE AGENT-NEMATODE PARASITE • MICROFILARIAE OR FILARIAL WORMS • WUCHERERIA BRONCOFTI • BRUGIA MALAYI • BRUGIA TIMORI– MOT • Bite from aedes poecilius (night biting) • Invade the lymph vessel, obstructing the lymphatic channel-leads to edema and may infiltrate the reproductive organs.– IP 8-16 months
CLINICAL MANIFESTATIONS:– ASYMPTOMATIC STAGE • (+) MICROFILARIAE IN THE BLOOD– NO CLINICAL S/SX– ACUTE STAGE • LYMPHADENITIS (LYMPH NODES) • LYMPHANGITIS (LYMPH VESSELS) • GENETALIA-FUNICULITIS, EPIDYDIMITIS, ORCHITIS– CHRONIC STAGE • HYDROCOELE • LYMPHEDEMA (UPPER AND LOWER EXTREMITIES) • ELEPHANTIASIS
– INCIDENCE-REGION 5,8,11 AND CARAGA, MARINDUQUE, SARANGGANI– Drug: Diethyl Carbamazine Citrate or Hetrazan 6mg/KgBW one dose every year– Dx: • NBE nocturnal blood exam (night) • ICT immunochromatographic test (day)
Nursing Considerations– MASS TREATMENT-DOSE IS 6mg/KBW, SINGLE DOSE PER YEAR.– ENVIRONMENTAL SANITATION– PERSONAL HYGIENE– MOSQUITO NETS– LONG SLEEVES, LONG PANTS AND SOCKS– INSECT REPELLENT– SCREENING OF HOUSES– HEALTH EDUCATION
Schistosomias, Snail Fever, Takayama – Blood fluke – Schistosoma japonicum – S. hematobium – S. mansoni – MOT skin entry (cercaria) travel in to the blood stream where they will infiltrate the liver, from liver to intestines
– Cycle: Egg-larvae (miracidium)-intermediary host (oncomelania quadrasi-tiny snail)-cercaria– Itchiness at the site– RUQ pain (hepatomegaly)– Intestine infiltration-abd’l cramps, diarrhea with blood– Praziquantel– Dx COPT (stool exam)
HIV and AIDS– Retrovirus (HIV1 & HIV2)– Attacks and kills CD4+ lymphocytes (T-helper)– Capable of replicating the lymphocytes undetected by the immune system– Immunity declines and opportunistic microbes sets in
HIGH RISK GROUP– Homosexual or bisexual– Intravenous drug users– BT recipients before 1985– Sexual contact with HIV+– Babies of mothers who are HIV+
MOT– Sexual intercourse (oral, vaginal and anal)– Exposure to contaminated blood, semen, breast milk and other body fluids– placenta
HIV TEST– Elisa– Western Blot– Rapid hiv test • Suds hiv-1 • Results are obtained in less than 10 minutes • Color indicator similar to pregnancy test • Positive result needs a confirmatory test
How to Diagnose– HIV+ 2 consecutive positive ELISA and 1 positive Western Blot Test– AIDS+ HIV+ CD4+ count below 500/ml Exhibits one or more of the ff: (next slide)– Full blown AIDS CD4 is less than 200/ml
– Exhibits one or more of – Weight loss the ff: – Severe diarrhea– Extreme fatigue – Apathy and depression– Intermittent fever – PTB– Night sweats – Kaposis sarcoma– Chills – Pneumocystis carinii– Lymphadenopathy – AIDS dementia– Enlarged spleen– Anorexia
• HIV CLASSIFICATION – CATEGORY 1 – CD4+ 500 OR MORE – CATEGORY 2 – CD4+ 200-499 – CATEGORY 3 – CD4+ LESS THAN 200
• Management – Prevention of spread (safe sex) – Universal precautions – Health Education – Symptomatic intervention – No known cure – Prevent CD4 reduction
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