Communicable diseases immunologic

INFECTIONS

Chain of Infection

Susceptible host Portal of Entry Etiologic Agent (microorganism)ReservoirMethod of transmission from reservoir to

(Source) susceptible host Portal 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 manifestation

Nosocomial 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 and Prevention

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.

Transmission-Based Precautions

–Airborne–Droplets–Contact

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

Airborne Diseases

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

– PS koplik’s spot– Characteristic: stimsons, photophobia (typical

complaint)– Fever: high fever– CX pneumonia, meningitis

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

– Immunocompetent are susceptible– Petechiae (volar/palm of hands) EARLY– Opisthotonus MENIGEAL IRRITATION– Brudzinski MENINGEAL IRRITATION– Kernigs MENINGEAL IRRITATION– Increased ICP BRAIN– Seizure BRAIN

– S/sx:– Meningococcemia – spiking fever, chills, arthralgia,

petechial rash– Fulminant Meningococcemia (Waterhouse

Friderichsen) – septic shock; hypotension, tachycardia, enlarging petecchial rash, adrenal insufficiency

• Meningitis – most common; nuchal rigidity, brudzinski, kernigs, Photophobia, confusion

– Dx: CT/ MRI, CSF analysis, CSF gram stain, CSF and blood culture

– Mgmt: antibiotics (Pen G, ceftriaxone), steroids, anticonvulsants, Rifampin for close contacts of meningococcemia

Amoebiasis

– Entamoeba Hystolitica –protozoan (parasite)– MOT = 5 F’s, fecal oral route– IP = 2-4 weeks– IMMUNITY = xxx

– Dx microscopic stool exam or rectal secretions– (tetra nucleated cyst and trophozoites)– Diarrhea and constipation (non dysenteric)– Blood streaked, diarrhea and watery mucoid, abd’l

cramps (dysenteric)– Extra amoebiasis-penile, vagina, spleen, liver, anal,

lungs and meninges– Metronidazole (Flagyl)

Typhoid Fever

– Salmonella typhosa (bacteria)– MOT = same with amoebiasis (5 F’s)– IP = 1-3 weeks– IMMUNITY

• Active = vaccine• Passive = xxx• Natural = lifetime immunity

Pathophysiology

– Oral ingestion– Bloodstream– Reticuloendothelial system (lymph node, spleen,

liver)– Bloodstream– Gallbladder– Peyer’s patches of SI– necrosis and ulceration

– 1st week step ladder (BLOOD)– 2nd week rose spot and fastidial

• typhoid pyschosis (URINE & STOOL)

– 3rd week (complications) intestinal bleeding,• perforation, peritonitis, encephalitis,

– 4th week (lysis) decreasing S?SX– 5th week (convalescent)

– Blood (typhi dot) 1st week after– Stool and urine 2nd week after– Chloramphenicol

– Rose spot (abdominal rashes)– Step ladder fever to fastidial (peak of fever)

typhoid psychosis– Peyer’s patches of small intestine– May stay in the gallbladder (hiding area)

BLOOD BORNE DISEASES

RABIES

CONTENTS:

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 than 50,000 people and millions of animals around the world. Rabies is a big problem in Asia, Africa, and Central and South America. In the United States, rabies has been reported in every 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 get rabies. Animals that are not mammals -- such as birds, snakes, and fish -- do not get rabies. Rabies is caused by a virus. An animal gets rabies from saliva, usually from a bite of an animal that has the disease.

The Rabies VirusRV – a neurotropic filterable virus present in the saliva of rabid animals. It has a preferrence for nerve tissues.

Virus – minute organism not visible 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 covering called capsid.Neurotropic – viruses that reproduce in nerve tissueFilterable virus – virus causing infectious disease, the essential elements of which are so tiny that they retain infectivity after passing through a filter of the Berkefeld type.Berkefeld filter – a filter of diatomaceous earth designed to allow virus-size particles to pass throughDiatomaceous earth – substance composed of diatoms, a group of unicellular microscopic algae that possess a siiceous or calcium-containing cell wall.

RHABDOVIRUS: any group of rod-shaped RNA viruses with 1 important member, rabies virus, pathogenic to man. The virus has a predilection for tissue of mucus-secreting glands and the Central Nervous System. All warm-blooded animals are susceptible to infection with these viruses.

RHABDO: from Greek rhabdos, "rod"LYSSA: Greek – frenzy, rage, fury, canine madness

A rhabdovirus of the genus lyssavirus.

This is a photograph of the virus under electron microscope

Parts of the rabies virus

Rod-shaped rabies viruses colored for effect

How do you get rabies? (MODE & MEDIA OF TRANSMISSION, IMMUNITY)

•All warm-blooded mammals are susceptible. Natural immunity in man is unknown.•You get rabies through the saliva of an infected animal by an exposure to an open break in the skin such as bites, open wound or scratch and inhalation of infectious aerosols such as from bats.•In some cases, it is transmitted through organ transplants (corneal transplant), 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?

•There is yet no way of immediately knowing who had acquired rabies virus. No tests are available to diagnose rabies in humans before the onset of clinical disease.

•The most reliable test for rabies in patients who have clinical signs of the disease is a DIRECT IMMUNOFLUORESCENT STUDY of a full thickness biopsy of the skin taken from the back of the neck above the hair line.

•The RAPID FLUORESCENT FOCUS INHIBITION TEST is used to measure rabies-neutralizing antibodies in serum. This test has the advantage of providing results within 24 hours. Other tests of antibodies may take as long as 14 •days.

(DIAGNOSIS)

RABIES INCIDENCE:

WORLDWIDE:35, 000- 50, 000 cases/ year(WHO)

EPIDEMIOLOGY

EPIDEMIOLOGY PHILIPPINES: 350-450 cases/ year

5-7 per million population

DOG BITE INCIDENCE: 140, 000- 560, 000/ year200-800 per 100, 000 population/ year AGE 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 INFECTION

Rabies virus Entry into the body INCUBATI0N PERIOD(20 – 90 days)

INVASION(0 – 10 days)

PARALYTIC

EXCITEMENT(2 – 7 days)

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

INVASION PHASE

VIRUS IN SALIVA

EXCITEMENT

INHALED AEROSOLS

INVASION PHASE

VIRUS IN SALIVA

DEATH DEATH

PARALYSIS

PARALYSIS

DOGS

CATS

B A T S

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!

• Fever,headache malaise sore throat anorexia increased sensitivity (bright lights, loud noises) increased muscle reflex irritability, tics and muscle tone

• Overactive facial expression

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

• > death, but if patient survive excitement phase…Tick me next!

Sympathetic nervous system

Parasympathetic nervous systemTick me 1st!

Tick me!

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.

» Practice isolation techniques. To prevent self-contamination and spread of disease.

• 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

fragmentsc. ERIG (Equine Rabies Immune Globulins)

VACCINATION(Intradermal Schedule)

Day of Immunization

PVRV/PCECV Site

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 Schedule

Day of Immunization

PVRV PCECV Site

Day 0 0.5 ml 1.0 ml One deltoid/ anterolateral thigh of infants

Day 3 0.5 ml 1.0 ml Same

Day 7 0.5 ml 1.0 ml Same

Day 14 0.5 ml 1.0 ml Same

Day 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 certain

1. 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 CONTROLa. Patient should be admitted in a quiet, draft-

free, isolation roomb. HLCR workers & relatives in contact w/ pt

should wear proper personal protective equipment (gown, gloves, mask, goggles)

4. DISPOSAL OF DEAD BODIES

Tetanus

• Tetanus– Clostridium tetani– MOT = wound setting– IP = 3 -21 days– IMMUNITY

• Active = TT• Passive = TAT and TIG• Natural = active none, passive (+)

– Wound Infection– FATAL INFECTION OF THE CNS– TOXIN-NEUROTOXIN

• PATHOPHYSIOLOGY:– SETTING OF WOUND ---- ENTRANCE OF C.T. ----

RELEASES TETANUS TOXIN ---- TETANOSPASMIN (CNS), TETANOLYSIN (BLOOD) ---- ABSORBED BY MOTOR NERVE ENDINGS ---- SYNAPSE (CONNECTION BETWEEN NEURONS) ---- MYONEURAL JUNCTION ---- ACETYLCHOLINE DISTURBANCE IN THE TRANSMISSION OF NERVE IMPULSE

– Trismus – lock jaw– Risus sardonicus - maskface– Risorius - grinsmile– Dx wound and blood extraction (non specific)

• 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

VECTOR-BORNE DISEASES

DENGUE HEMORRHAGIC FEVER

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.

IINTRODUCTION:

What is Dengue Hemorrhagic 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 bleeding phenomena, and

• evidence of plasma leakage due to increase vascular permeability

Infectious 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.

  2001 2002 2003 2004

Notifiable Diseases Reported Reported Reported Reported

  Cases Deaths Cases Deaths Cases Deaths Cases Deaths

Dengue Fever

23,235   13,187  

18,039  

15,838  

Notifiable Diseases and Deaths by Cause in the Philippines (2001 – 2004)

Source: National Statistics Office

Selected Number of New Cases Number of Deaths Year

Communicable              

Disease: total male female total male female  

Dengue / DHF 43, 350 … … 416 … … 2007

INCIDENCE OF DENGUE HEMORRHAGIC FEVER IN CEBU CITY (YEAR 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 week

Period of Communicability:

Presumed to be on the 1st week of illness – when virus is still present in the blood

Susceptibility and resistance:

All persons are susceptible. Both sexes are equally affected. The age 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 in the 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 which may be accompanied by vomiting, conjunctiva infection and epistaxis.

• 4th-7th day (toxic or hemorrhagic stage)

-lowering of temperature, severe abdominal pain, vomiting and frequent bleeding from gastrointestinal tract in the form of hematemesis or melena. Unstable blood pressure, narrow pulse pressure and shock. Death may occur. Tourniquet test which may be positive 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 dengue hemorrhagic 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 and hematemesis

• grade III, circulatory failure manifested by a rapid and weak pulse with narrowing pulse pressure (20 mmHg) or hypotension, with the presence of cold clammy skin and restlessness; and

• Grade IV, profound shock in which pulse and blood pressure are not detectable. It is note-worthy that patients who are in threatened shock or shock stage, also known as dengue shock syndrome, usually remain conscious.

* Grade III and IV are considered to be Dengue Shock Syndrome

MANAGEMENT

• 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.

PREVENTION

• 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 Disease– Protozoan plasmodium

• plasmodium ovale - dormant (liver)

• plasmodium vivax - benign

• plasmodium malariae - mild but resistant

• plasmodium falciparum - malignant (cerebral malaria)

– P. VIVAX AND OVALE MAY HAVE RECCURENCE OF SYMPTOMS

• tertian-febrile paroxysm q24H-48H

• quartan-febrile paroxysm q48H-72H

– 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)

– Egg– miracidium– snail– cercaria- human– Itchiness – liver – intestines– Praziquantel– COPT– PREVENTION– Samar and Leyte

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 the ff:

– Extreme fatigue– Intermittent fever– Night sweats– Chills– Lymphadenopathy– Enlarged spleen– Anorexia

– Weight loss– Severe diarrhea– Apathy and depression– PTB– Kaposis sarcoma– Pneumocystis carinii– AIDS dementia

• 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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