COMMUNICABLE DISEASE
Disease caused by an infectious agent that are transmitted directly or indirectly to a well person through an agency, vector or inanimate objectCONTAGIOUS DISEASE
Disease that is easily transmitted from one person to another INFECTIOUS DISEASE
Disease transmitted by direct inoculation through a break in the skinINFECTION
-Entry and multiplication of an infectious agent into the tissue of the host
INFESTATION
- Lodgement and development of arthropods on the surface of the body
ASEPSIS
- Absence of disease – producing microorganisms SEPSIS
- The presence of infection MEDICAL ASEPSIS
-
Practices designed to reduce the number and transfer of pathogens-
Clean techniqueSURGICAL ASEPSIS
-
Practices that render and keep objects and areas free from microorganisms-
Sterile technique
CARRIER – an individual who harbors the organism and is capable of transmitting it without showing manifestations of the disease
CASE – a person who is infected and manifesting the signs and symptoms of the disease
SUSPECT – a person whose medical history and signs and symptoms suggest that such person is suffering from that particular disease
CONTACT – any person who had been in close association with an infected personHOST
- A person, animal or plant which harbors and provides nourishment for a parasite
RESERVOIR
- Natural habitat for the growth, multiplication and reproduction of microorganism
ISOLATION
- The separation of persons with communicable diseases from other persons
QUARANTINE
- The limitation of the freedom of movement of persons exposed to communicable diseases
STERILIZATION – the process by which all microorganisms including their spores are destroyed
DISINFECTION – the process by which pathogens but not their spores are destroyed from inanimate objects
CLEANING – the physical removal of visible dirt and debris by washing contaminated surfacesCONCURRENT
- Done immediately after the discharge of infectious materials / secretions
TERMINAL
- Applied when the patient is no longer the source of infection BACTERICIDAL
- A chemical that kills microorganisms BACTERIOSTATIC
- An agent that prevents bacterial multiplication but does not kill microorganisms
CHAIN OF INFECTION
INFECTIOUS AGENT
Any microorganism capable of producing a disease RESERVOIR
Environment or object on which an organism can survive and multiplyPORTAL OF EXIT
The venue or way in which the organism leaves the reservoir MODE OF TRANSMISSION
The means by which the infectious agent passes from the portal of exit from the reservoir to the susceptible hostPORTAL OF ENTRY
Permits the organism to gain entrance into the host SUSCEPTIBLE HOST
A person at risk for infection, whose defense mechanisms are unable to withstand invasion of pathogensSTAGES OF THE INFECTIOUS PROCESS
Incubation Period – acquisition of pathogen to the onset of signs and symptoms
Prodromal Period – patient feels “bad” but not yet experiencing actual symptoms of the disease
Period of Illness – onset of typical or specific signs and symptoms of a disease
Convalescent Period – signs and symptoms start to abate and client returns to normal healthMODE OF TRANSMISSION CONTACT TRANSMISSION
Direct contact – involves immediate and direct transfer from person-to-person (body surface-to-body surface)
Indirect contact – occurs when a susceptible host is exposed to a contaminated objectDROPLET TRANSMISSION
Occurs when the mucous membrane of the nose, mouth or conjunctiva are exposed to secretions of an infected person within a distance of three feetVEHICLE TRANSMISSION
Transfer of microorganisms by way of vehicles or contaminated items that transmit pathogensAIRBORNE TRANSMISSION
Occurs when fine particles are suspended in the air for a long time or when dust particles contain pathogensVECTOR-BORNE TRANSMISSION
Transmitted by biologic vectors like rats, snails and mosquitoes TYPES OF IMMUNIZATION
ACTIVE – antibodies produced by the bodyNATURAL – antibodies are formed in the presence of active infection in the body; lifelong
ARTIFICIAL – antigens are administered to stimulate antibody production
PASSIVE – antibodies are produced by another sourceNATURAL – transferred from mother to newborn through placenta or colostrum
ARTIFICIAL – immune serum (antibody) from an animal or human is injected to a person
SEVEN CATEGORIES OF ISOLATION
STRICT- prevent highly contagious or virulent infections
Example: chickenpox, herpes zoster
CONTACT – spread primarily by close or direct contact
Example: scabies, herpes simplex
RESPIRATORY – prevent transmission of infectious distances over short distances through the air
Example: measles, mumps, meningitisTUBERCULOSIS – indicated for patients with positive smear or chest x-ray which strongly suggests tuberculosis
ENTERIC – prevent transmission through direct contact with feces Example: poliomyelitis, typhoid fever
DRAINAGE – prevent transmission by direct or indirect contact with purulent materials or discharge
Ex. Burns
UNIVERSAL – prevent transmission of blood and body-fluid borne pathogens
Example: AIDS, Hepatitis B
CENTRAL NERVOUS SYSTEM
MENINGO-COCCEMIA
MENINGITIS
ENCEPHALITIS
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSION - Inflammation of the brain - Inflammation of the meninges - Acute infection of the bloodstream and developing vasculitis - Arboviruses - Streptococcus - Staphylococcus - Pneumococcus - Tubercle bacillus - Neisseria meningitides5-15 days 1-10 days 3-4 days
Bite of infected
mosquito Respiratory droplets
SIGNS AND SYMPTOMS OF ENCEPHALITIS
Virus enters neural cells
Perivascular
congestion
Disruption in
cellular
functioning
Inflammatory
reaction
Lethargy
Convulsions
Seizures
Headache
Photophobia
Vomiting
Stiff neck
Fever
Sore throat
SIGNS AND SYMPTOMS OF MENINGITIS
THREE SIGNS OF MENINGEAL IRRITATION OPISTHOTONUS
State of severe hyperextension and spasticity in which an individual’s head, neck and spinal column enter into a complete arching position BRUDZINSKI’S SIGN
Place the patient in a dorsal recumbent position and then put hands behind the patient’s neck and bend it forward.
If the patient flexes the hips and knees in response to the manipulation, positive for meningitis
KERNIG’S SIGN
Place the patient in a supine position, flex his leg at the hip and knee then straighten the knee; pain and resistance indicates meningitis
SIGNS AND SYMPTOMS OF MENINGOCOCCEMIA
URTI:
cough, sore
throat,
fever,
headache,
nausea and
vomiting
Vasculitis:
petechial
rash in the
trunk and
extremities
DIC
Micro-thrombosis
Purpura
Hypotension
Shock
Death
MENINGO-COCCEMIA
MENINGITIS
ENCEPHALITIS
SIGNS AND SYMPTOMS
INCIDENCE
5-10 years old
< 5 years old
6 months–5
years old
Stiff neck
Photophobia
Lethargy
Convulsions
Nuchal rigidity
Opisthotonus
Brudzinski’s
Kernig’s sign
Vasculitis
Waterhouse-Friderichsen
syndrome
Petechiae with
the development
of hemorrhage
DIAGNOSTIC EXAM Informed consent Empty bowel and bladder Fetal, shrimp or “C” position Spinal canal, subarachnoid space between L3-L4 or L4- L5 After: bedrest
Flat on bed to prevent spinal headache
MENINGO-COCCEMIA
MENINGITIS
ENCEPHALITIS
TREATMENT MODALITIES PREVENTION1. Japanese
encephalitis
VAX
1. HiB vaccine
Dexamethasone
Mannitol
Anticonvulsants
Antipyretics
Ceftriaxone
Penicillin
Chloramphenicol
Rifampicin
Ciprofloxacin
MENINGO-COCCEMIA
MENINGITIS
ENCEPHALITIS
NURSING MANAGEMENT 1. Comfort: quiet, well-ventilated room 2. Skin care: cleansing bath, change in position 3. Eliminate mosquito breeding sites: CULEX mosquito 1. Respiratory isolation 24-72 hours after onset of antibiotic therapy 2. Room protected against bright lights 3. Safety: side-lying position and raised side rails1. Side boards 2. Close contacts H – ouse I – nfected person kissing S – ame daycare center S – hare mouth instruments 3. Antibiotics as prophylaxis
TETANUS
RABIES
POLIOMYELITIS MAIN PROBLEM ETIOLOGIC AGENT Acute infection of the CNS – muscle spasm, paresis and paralysisAcute viral disease of the CNS – by saliva of infected animals
Acute infectious disease with systemic neuromuscular effects Legio debilitans Rhabdovirus Bullet-shaped Affinity to CNS Killed by sunlight, UV light, formalin Resistant to antibiotics Clostridium tetani Anaerobic Gram positive Drumstick appearance
TETANUS
RABIES
POLIOMYELITIS INCUBATION PERIOD MODE OF TRANSMISSION 7-21 days 2-8 weeks Adult: 3 days-3 weeks Distance of bite to brain- Direct contact with infected feces Bite of an infected animal Direct inoculation through a broken skin Extensiveness of the bite Resistance of the host Neonate: 3-30 days
- Direct contact with respiratory secretions - Indirect with soiled
linens and articles
TETANUS
RABIES
POLIOMYELITIS
SIGNS AND SYMPTOMS
1. Abortive type
1. Prodromal /
invasion
phase
R – isus sardonicus
3. Paralytic type
2. Pre-paralytic
or meningetic
type
3. Terminal /
paralytic type
2. Excitement /
neurological
phase
O – pistothonus
T – rismus
C – onvulsions
H – eadache
I – rritability
L – aryngeal
spasm
POLIO ABORTIVE TYPE Does not invade the CNS Headache
Sore throat
Recovery within 72 hours and the disease passes by unnoticed PRE-PARALYTIC OR MENINGETIC TYPE Slight involvement of the CNS Pain and spasm of muscles Transient paresis
(+) Pandy’s test (increased protein in the CSF) PARALYTIC TYPE
CNS involvement
Flaccid paralysis Asymmetric Affects lower extremities Urine retention and constipation
(+) HOYNE’S SIGN (when in supine position, head will fall back when shoulders are elevated)
RABIES
PRODROMAL/INVASION PHASE Fever
Anorexia Sore throat
Pain and tingling at the site of bite Difficulty swallowing
EXCITEMENT OR NEUROLOGICAL PHASE Hydrophobia (laryngospasm)
Aerophobia (bronchospasm) Delirium
Maniacal behavior Drooling
TERMINAL OR PARALYTIC PHASE Patient becomes unconscious Loss of urine and bowel control Progressive paralysis Death
TETANUS
RABIES
POLIOMYELITIS COMPLICATION ISOLATION PRECAUTION DIAGNOSTIC PROCEDURES Paralysis of respiratory muscles RESPIRATORY FAILURE DEATH1. Stool culture 1. Throat washings 1. Blood exam
Enteric isolation Respiratory isolation 2. CSF culture 2. Flourescent rabies antibody (FRA) 3. Negri bodies
TETANUS
RABIES
POLIOMYELITIS TREATMENT MODALITIES1. Analgesics
1. Local
treatment of
wound
1. Tetanus immune globulin (TIG)2. Morphine
3. Moist heat
application
4. Bed rest
5. Rehabilitation
2. Active
immunization
Lyssavac
Imovax
Antirabies vax
2. Passive
immunization
2. Tetanus antitoxin (TAT) 3. Penicillin G 4. Tetracycline 5. Diazepam 6. Phenobarbital 7. Tracheostomy 8. NGT feedingTETANUS
RABIES
POLIOMYELITIS
NURSING MANAGEMENT
1. Enteric isolation 1. Isolation 1. Adequate airway 2. Proper disposal
of secretions 3. Moist hot packs 4. Firm / nonsagging bed 5. Suitable body alignment 6. Comfort and safety 2. Optimum comfort 3. Restful environment 4. Emotional support 5. Concurrent and terminal disinfection 2. Quiet, semi-dark environment 3. Avoid sudden
stimuli and light
TETANUS
RABIES
POLIOMYELITIS PREVENTIONSalk vaccine
- Inactivated
polio vaccine
- Intramuscular
1. If the dog is healthy1. Aseptic
handling of
umbilical cord
Sabin vaccine
- Oral polio
vaccine
- Per orem
2. If the dog dies or shows signs suggestive of rabies 3. If dog is not available for observation 4. Have domestic dog 3 months to 1 year old immunized
2. Tetanus toxoid
immunization
3. Antibiotic
prophylaxis
- Penicillin
- Erythromycin
- Tetracycline
RESPIRATORY SYSTEM
SARS
BIRD FLU
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSIONFlu infection in birds that affects humans
A new type of atypical pneumonia that infects the lungs
Avian influenza virus, H5N1 Corona virus
3-5 days 2-8 days
Inhalation of feces and discharge of an infected bird
Respiratory droplets
SARS
BIRD FLU
SIGNS AND SYMPTOMS
Body weakness or muscle
pain
High fever >38’Celsius
Chills
Cough
Difficulty breathing
Episodes of sore throat
Fever
SARS
BIRD FLU
COMPLICATIONS
Severe viral pneumonia
Acute respiratory distress
syndrome
Hypoxemia
Fluid accumulation in
alveolar sacs
Severe breathing difficulties
Multiple organ failure
DEATH
Severe viral
pneumonia
Respiratory failure
SARS
BIRD FLU
TREATMENT MODALITIES- Generic flu drugs
1. No definitive treatment
for SARS
1. Amantadine/Rimantadine
- H5N1 developed resistance
2. Oseltamivir (TAMIFLU)
Zanamavir (RELENZA)
- Primary treatment
- Within 2 days at onset of
symptoms
- 150 mg BID x 2 days
2. Antiviral drugs
(normally used to treat
AIDS)
- RIBAVIRIN
3. Corticosteroids
SARS
BIRD FLU
PREVENTION1.Culling – killing of
sick or exposed
birds
1.Quarantine
2. Banning of
importation of
birds (Executive
order # 280)
3. Cook chicken
thoroughly
2. Isolation
3. WHO alert
on SARS
(March 12,
2003)
NURSING MANAGEMENT
BIRD FLUWHAT TO DO WITH A PERSON SUSPECTED TO HAVE BIRD FLU
• Isolation
•
Face mask on the patient•
Caregiver: use a face mask and eye goggles/glasses•
Distance of 1 meter from the patient•
Transport the patient to a DOH referral hospital REFERRAL HOSPITALS•
National Referral Center – Research Institute for Tropical Medicine (RITM) (Alabang, Muntinlupa)•
Luzon – San Lazaro Hospital (Quiricada St., Sta. Cruz, Manila)•
Visayas – Vicente Sotto Memorial Medical Hospital (Cebu City)•
Mindanao – Davao Medical Center (Bajada, Davao City) S A R SSUSPECT CASE
1. A person presenting after 1 November 2002 with a history of:
High fever >38 0C AND
One or more of the following exposures during the 10 days prior to the onset of symptoms:
Close contact , with a person who is a suspect or probable case of SARS
History of travel , to an area with recent local transmission of SARS
Residing in an area with recent local transmission of SARS2. A person with an unexplained acute respiratory illness resulting in death after 1 November 2002, but on whom no autopsy has been performed :
AND
One or more of the following exposures during the 10 days prior to the onset of symptoms:
Close contact , with a person who is a suspect or probable case of SARS
History of travel , to an area with recent local transmission of SARS
Residing in an area with recent local transmission of SARSPROBABLE CASE
1. A suspect case with radiographic evidence of infiltrates consistent with pneumonia or respiratory distress syndrome on Chest x-ray. 2. A suspect case of SARS that is positive for SARS coronavirus by one or more assays.
3. A suspect case with autopsy findings consistent with the pathology of SARS without an identifiable cause.
PERTUSSIS
DIPHTHERIA
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSIONAcute bacterial disease characterized by the elaboration of an exotoxin
Repeated attacks of spasmodic coughing
Corynebacterium diphtheriae or
Klebs-Loeffler bacillus Bordetella pertussis
2-5 days 7-14 days
1. Respiratory droplets
2. Direct contact with respiratory secretions 3. Indirect contact with articles
PERTUSSIS
DIPHTHERIA
SIGNS AND SYMPTOMS
Types:
1.Nasal
2.Tonsilopharyngeal
3.Laryngeal
4.Wound or
cutaneous
Stages:
1. Catarrhal
2. Paroxysmal
3. Convalescent
NASAL DIPHTHERIA• Bloody discharge from the nose • Excoriated nares and upper lip TONSILOPHARYNGEAL DIPHTHERIA
• Low grade fever • Sore throat
• Bull-neck appearance
•
Pseudomembrane- Group of pale yellow membrane over tonsils and at the back of the throat as an inflammatory response to a powerful necrotizing toxinsLARYNGEAL DIPHTHERIA • Hoarseness • Croupy cough • Aphonia
•
Membrane lining thickens à airway obstruction • Suffocation, cyanosis or deathWOUND OR CUTANEOUS DIPHTHERIA • Yellow spots or sores in the skin PERTUSSIS
CATARRHAL STAGE
•
Lasts for 1 to 2 weeks•
Most communicable stage•
Begins with respiratory infection, sneezing, cough and fever•
Cough becomes more frequent at night PAROXYSMAL STAGE• Lasts for 4 to 6 weeks
•
Aura: sneezing, tickling, itching of throat•
Cough, explosive outburst ending in “whoop”•
Mucus is thick, ends in vomiting•
Becomes cyanotic•
With profuse sweating, involuntary urination and exhaustion CONVALESCENT STAGE • End of 4th-6th week • Decrease in paroxysmsPERTUSSIS
DIPHTHERIA
DIAGNOSTIC PROCEDURESSCHICK’S TESTS
CBC – increase in
lymphocytes
- Susceptibility and immunity todiphtheria
-ID of dilute diphtheria toxin (0.1 cc)
(+) local circumscribed area of redness, 1-3 cm
MALONEY’S TEST -Determines hypersensitivity to diphtheria anti-toxin
-ID of 0.1 cc fluid toxoid -(+) area of erythema in 24 hours
PERTUSSIS
DIPHTHERIA
COMPLICATIONS
Toxins in the bloodstream
Myocarditis (epigastric or chest pain) Peripheral paralysis (tingling, numbness, paresis) Broncho-pneumonia (fever, cough) Heart failure Decreased in respiratory rate Respirat ory arrest DEATH
C
onvulsions (brain
damage from
asphyxia)
O
titis media
(invading
organisms)
B
ronchopneumonia
(most dangerous
complication)
PERTUSSIS
DIPHTHERIA
TREATMENT MODALITIES1. Diphtheria anti-toxin 1. Erythromycin – drug of choice
- Requires skin testing - Early administration
aimed at neutralizing the toxin present in the circulation before it is absorbed by the tissues
2. Antibiotic therapy - Penicillin G - Erythromycin 2. Ampicillin – if resistant to erythromycin 3. Betamethasone (corticosteroid) – decrease severity and length of paroxysms 4. Albuterol
PERTUSSIS
DIPHTHERIA
NURSING MANAGEMENT 1. Isolation: 14 days (until
2-3 cultures, 24 hours apart)
1. Isolation: 4-6 weeks from onset of illness
2. Bedrest for 2 weeks 3. Care for nose and
throat (gentle swabbing) 4. Ice collar (decrease pain
of sore throat) 5. Diet (soft food, small
frequent feedings)
2. Supportive measures (bedrest, avoid
excitement, dust, smoke and warm baths) 3. Safety (during
paroxysms, patient should not be left alone) 4. Suctioning (kept at
bedside for emergency use)
MUMPS
MAIN PROBLEMAn acute contagious disease, with swelling of one or both of the parotid glands
ETIOLOGIC AGENT
Filterable virus of paramyxovirus group INCUBATION PERIOD
12-26 days
MODE OF TRANSMISSION Respiratory droplets
PERIOD OF COMMUNICABILITY
6 days before and 9 days after onset of parotid swelling SIGNS AND SYMPTOMS
PRODROMAL PHASE F-ever (low grade) H-eadache M-alaise PAROTITIS F-ace pain E-arache
S-welling of the parotid glands COMPLICATIONS
•
Orchitis – the most notorious complication of mumps•
Oophoritis – manifested by pain and tenderness of the abdomen•
CNS involvement – manifested by headache, stiff neck, delirium, double vision•
Deafness as a result of mumps NURSING MANAGEMENT1. Prevent complications
− Scrotum supported by suspensory − Use of sedatives to relieve pain
− Treatment: oral dose of 300-400 mg cortisone followed by 100 mg every 6 hours
− Nick in the membrane 2. Diet
- Soft or liquid diet
- Sour foods or fruit juices are disliked 3. Respiratory isolation
4. Comfort: ice collar or cold applications over the parotid glands may relieve pain
5. Fever: aspirin, tepid sponge bath
6. Concurrent disinfection: all materials contaminated by these secretions should be cleansed by boiling
7. Terminal disinfection: room should be aired for six to eight hours
GASTROINTESTINAL TRACT
SHIGELLOSIS
AMOEBIASIS
MAIN PROBLEM
ETIOLOGIC AGENT Protozoal infection of the large intestine
Acute infection of the lining of the small intestine
Entamoeba histolytica
Shigella group - Prevalent in areas with illsanitation
-Acquired by swallowing - Trophozoites: vegetative form
- Cyst
: infective stage1. Shigella flesneri – most common in the Philippines 2. Shigella connei
3. Shigella boydii
4. Shigella dysenterae – most infectious type
SHIGELLOSIS
AMOEBIASIS
SIGNS AND SYMPTOMS
1. Acute amoebic dysentery
Fever
- Diarrhea alternated withconstipation
- Tenesmus
2. Chronic amoebic dysentery
- Bloody mucoid stools
- Enlarged liver
- Large sloughs of intestinal
tissues accompanied by hemorrhage
Abdominal pain
Diarrhea and
tenesmus
Bloody mucoid
stool
SHIGELLOSIS
AMOEBIASIS
DIAGNOSTIC TESTS 1. Stool exam TREATMENT MODALITIES1. Metronidazole – drug
of choice
1. Cotrimoxazole – drug
of choice
2. Blood exam 3. Sigmoidoscopy2. Tetracycline
3. Chloramphenicol
SHIGELLOSIS
AMOEBIASIS
NURSING MANAGEMENT1.Enteric isolation
2. Boil water for
drinking
3. Handwashing
4. Sexual activity
5. Avoid eating
uncooked leafy
vegetables
TYPHOID FEVER
CHOLERA
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSIONAcute bacterial disease of the GIT characterized by profuse secretory diarrhea
An infection affecting the Peyer’s patches of the small intestines
Vibrio cholerae Salmonella typhi
1 to 3 days 1 to 3 weeks
1. Fecal-oral transmission 2. 5 F’s
TYPHOID FEVER
CHOLERA
SIGNS AND SYMPTOMS
Rice-water stool
Fever (ladder-like)
Abdominal cramps
Vomiting
Intravascular
Dehydration
Shock
Rose spots
Diarrhea
TYPHOID STATE
Sordes
Subsultus Tendinum
Coma vigil
Carphologia
TYPHOID FEVER
CHOLERA
TREATMENT MODALITIES1.Lactated Ringer’s
solution
1.Chloramphenicol –
drug of choice
2. Oral rehydration
therapy
3. Antibiotic therapy
- Tetracycline – drug
of choice
- Cotrimoxazole
- Chloramphenicol
2. Ampicillin/
Amoxicillin – for
typhoid carriers
3. Cotrimoxazole – for
severe cases with
relapses
TYPHOID FEVER
CHOLERA
NURSING MANAGEMENT
1. Maintain and restore the fluid
and electrolyte balance
2. Enteric isolation
3. Sanitary disposal of excreta
4. Adequate provision of safe
drinking water
5. Good personal hygiene
INTEGUMENTARY SYSTEM
HERPES ZOSTER
CHICKENPOX
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSIONA highly contagious disease characterized by vesicular eruptions on the skin and mucous membranes
An acute viral infection of
the sensory nerve
Varicella zoster virus
10-21 days 13-17 days 1. Droplet method 2. Direct contact 3. Indirect contact
HERPES ZOSTER
CHICKENPOX
SIGNS AND SYMPTOMS PERIOD OF COMMUNICABILITY
One day before eruption
of 1
stlesion and five days
after appearance of last
crop
One day before eruption
of 1
strash and five to six
days after the last crust
PRODROMAL
PERIOD
- Fever (low-grade)
- Headache
- Malaise
HERPES ZOSTER
CHICKENPOX
SIGNS AND SYMPTOMS
•
Rashes : Centrifugal
distribution
•
Rashes
-Unilateral, band-like
distribution
•Rash stages: macule
papule vesicle
pustule crust
• Pruritus
-Dermatomal
- Erythematous base
- Vesicular, pustular or
crusting
•Regional
lymphadenopathy
•Pruritus
•Pain – stabbing or
burning
HERPES ZOSTER
CHICKENPOX
COMPLICATIONSSCARRING – most common complication; associated with staphylococcal or streptococcal infections from scratching NECROTIZING FASCIITIS – most severe complication REYE SYNDROME – abnormal accumulation of fat in the liver plus increase of pressure in the brain resulting to coma, therefore leading to DEATH
RAMSAY-HUNT
SYNDROME -Involvement of Involvement of the facial nerve in herpes zoster the facial nerve in herpes zoster with facial paralysis, hearing with facial paralysis, hearing loss, loss of taste in half of the loss, loss of taste in half of the tongue
tongue GASSERIAN GANGLIONITIS –
Involvement of the optic nerve resulting to corneal anesthesia ENCEPHALITIS – acute inflammatory condition of the brain
HERPES ZOSTER
CHICKENPOX
TREATMENT MODALITIES
1. Antihistamines –
symptomatic relief of itching Ex. Diphenhydramine (Benadryl)
2. Analgesics and antipyretics Ex. Acetaminophen
3. Antiviral agents – for patient to experience less pain and faster resolution of lesions when used within 48 hours of rash onset
Ex. Acyclovir (Zovirax)
4. Corticosteroids – anti-inflammatory and decreased pain Ex. Prednisone
HERPES ZOSTER
CHICKENPOX
NURSING MANAGEMENTS
trict isolationP
revent secondary infection (cut fingernails short, wear mittens)E
liminate itching: calamine lotions, warm baths, baking soda pasteE
ncourage not going to school: usually 7 daysD
isinfection of clothes and linen with nasopharyngeal discharges by sunlight or boilingGERMAN MEASLES
MEASLES
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSION A contagious exanthematous disease with chief symptoms to the upper respiratory tractA benign communicable exanthematous disease caused by rubella virus 1. Droplet method Rubella virus 10-12 days 14-21 days Filterable virus of paramyxoviridae
2. Direct contact with respiratory discharges 3. Indirect with soiled linens and articles
GERMAN MEASLES
MEASLES
PERIOD OF COMMUNICABILITY
SIGNS AND SYMPTOMS
4 days before and 5 days after the appearance of rashes
One week before and four days after the appearance of rashes
PRE-ERUPTIVE STAGE PRE-ERUPTIVE STAGE
C
oughC
oryzaC
onjunctivitisF
ever (high-grade)P
hotophobiaF
everH
eadacheM
alaiseC
oryzaC
onjunctivitisKOPLIK’S SPOT (Rubeola)
- Bluish white spots surrounded by a red halo
- Appear on the buccal mucosa opposite the premolar teeth FORCHEIMER’S SPOTS (Rubella)
- small, red lesions
- Soft palate to mucus membrane
GERMAN MEASLES
MEASLES
SIGNS AND SYMPTOMS 2. ERUPTIVE STAGE
ERUPTIVE STAGE Rashes
- Elevated papules
- Begin on the face and behind the ears
- Spread to trunk and extremities
Color: Dark red – purplish hue – yellow brown
3. Stage of Convalescence - Desquamation
- Rashes fade from the face downwards
1. Rash
- pinkish, maculopapular - Begins on the face - Spread to trunk or limbs - No pigmentation or
desquamation 2. Posterior auricular and
suboccipital lymphadenopathy
GERMAN MEASLES
MEASLES
COMPLICATIONSP
neumonia
1. EncephalitisO
titis media
S
evere diarrhea (leading
to dehydration)
E
ncephalitis
2. Congenital rubella syndrome - Spontaneous abortion - Intrauterine growth retardation
(IUGR)
- Thrombocytopenia purpura “blueberry muffin skin” - Cleft lip, cleft palate, club foot - Heart defects (PDA, VSD) - Eye defects (Cataract,
glaucoma)
- Ear defects (Deafness) - Neurologic (microcephaly,
mental retardation, behavioral disturbances
GERMAN MEASLES
MEASLES
TREATMENT MODALITIES
1.Vitamin A – helps
prevent eye damage
and blindness
1.Aspirin – help reduce
inflammation and
fever
2. Antipyretics – for
fever
3. Penicillin – given
only when secondary
infection sets in
GERMAN MEASLES
MEASLES
NURSING MANAGEMENT
1. Darkened room to relieve photophobia 2. Diet: should be liquid but nourishing 3. Warm saline solution for eyes to relieve
eye irritation
4. For fever: tepid sponge bath and anti-pyretics
5. Skin care: during eruptive stage, soap is omitted; bicarbonate of soda in water or lotion to relieve itchiness
6. Prevent spread of infection: respiratory isolation
SCABIES
MAIN PROBLEMInfestation of the skin produced by the burrowing action of a parasite mite resulting in skin irritation and formation of vesicles and pustules ETIOLOGIC AGENT
INCUBATION PERIOD Within 24 hours MODE OF TRANSMISSION Direct contact Indirect contact Sarcoptes scabiei
1. Yellowish white in color 2. Barely seen by the unaided eye
3. Female parasite burrows beneath the epidermis to lay eggs 4. Males are smaller and reside on the surface of the skin SIGNS AND SYMPTOMS
•
T hin, pencil-mark lines on the skin•
Itching, especially at night•
Rashes and abrasions on the skin PRIMARY LESIONSNODULAR LESIONS SECONDARY LESIONS TREATMENT MODALITIES
• SCABICIDE : Eurax ointment (Crotamiton) • PEDICULICIDE : Kwell lotion (Gamma Benzene
Hexachloride) – contraindicated in young children and pregnant women
• Topical steroids
• Hydrogen peroxide : cleanliness of wound • Lindane Lotion
NURSING MANAGEMENT
• Apply cream at bedtime, from neck to toes • Instruct patient to avoid bathing for 8 to 12 hours • Dry-clean or boil bedclothes
• Report any skin irritation
• Family members and close contact treatment • Good handwashing
• Terminal disinfection
SEXUALLY TRANSMITTED DISEASES
SYPHILIS
AIDS
MAIN PROBLEM
ETIOLOGIC AGENT
INCUBATION PERIOD Final and most serious stage of HIV disease, which causes severe damage to the immune system
Infectious disease caused
by a spirochete
Retrovirus – Human T-cell lymphotropic virus III (HTLV-3)
Treponema pallidum
3 to 6 months to 8 to 10 years 10-90 days
SYPHILIS
AIDS
MODE OF TRANSMISSION
•
Sexual contact – oral, anal or
vaginal sex
•Blood transfusion
•Mother-to-child
•Indirect contact through soiled
articles
SYPHILIS
AIDS
SIGNS AND SYMPTOMS OPPORTUNISTIC INFECTIONS 1. Pneumocystis carinni pneumonia 2. Oral candidiasis 3. Toxoplasmosis 4. Acute/chronic diarrhea 5. Pulmonary tuberculosis MALIGNANCIES 1. Kaposi’s sarcoma 2. Non-Hodgkin’s lymphoma
SYPHILIS
AIDS
SIGNS AND SYMPTOMS 1. PRIMARY SYPHILIS - CHANCRE: small, painless,
pimple-like ulceration on the penis, labia majora, minora and lips
- May erupt in the genitalia, anus, nipple, tonsils or eyelids - Lymphadenopathy
SYPHILIS
AIDS
SIGNS AND SYMPTOMS 2. SECONDARY SYPHILIS - Skin rash
- Mucous patches - Hair loss
- CONDYLOMATA LATA: coalescing papules which form a gray-white plaque frequently in skin folds
SYPHILIS
AIDS
SIGNS AND SYMPTOMS 3. TERTIARY SYPHILIS - 1 to 10 years after infection - Appear on the skin, bones,
mucus membrane, URT, liver and stomach
- GUMMA: chronic, superficial nodule or deep
granulomatous lesion that is solitary, painless, indurated
SYPHILIS
AIDS
DIAGNOSTIC PROCEDURES
1.ELISA
1.Dark Field
Illumination test
2. Western blot
3. RIPA
4. PCR
2. Flourescent
Treponemal
Antibody
Absorption Test
3. VDRL
SYPHILIS
AIDS
TREATMENT MODALITIES1. Antivirals
- Shorten the clinical
course, prevent
complications, prevent
development of
latency, decrease
transmission
- Example: Zidovudine
(Retrovir)
1. Penicillin G Benzathine - Disease < 1 year: 2.4 M unitsonce in two injection sites - Disease > 1 year: 2.4 M units
in 2 injection sites x 3 doses 2. Doxycycline – if allergic to penicillin 3. Tetracycline - if allergic to penicillin - Contraindicated for pregnant women
GONORRHEA
CHLAMYDIA
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIOD MODE OF TRANSMISSIONPurulent inflammation of mucous membrane surfaces
Sexually transmitted disease caused by a bacteria
Chlamydia trachomatis Neisseria gonorrhea
2-3 weeks (males) 2-10 days
Sexual contact: Oral, vaginal or anal sex Asymptomatic (females)
GONORRHEA
CHLAMYDIA
SIGNS AND SYMPTOMS
Women
Abdominal or pelvic pain Bleeding after intercourse and in-between menses
Unusual vaginal discharge
Women
Bleeding after intercourse Burning sensation during urination
Yellow or bloody vaginal discharge
Men
Burning with urination Swollen, painful testicles Discharge from the penis
White, yellow or green pus from the penis
GONORRHEA
CHLAMYDIA
COMPLICATIONS Women Pelvic inflammatory disease Ectopic pregnancy Sterility Men Epididymitis Sterility Newborn Conjunctivitis Otitis media Pneumonia Newborn Gonococcal ophthalmiaGONORRHEA
CHLAMYDIA
TREATMENT MODALITIES1. Azithromycin
(Zithromax)
1. Cefixime
- Drug of choice because
of single-dose treatment
effectiveness and lower
cost
2. Doxycycline
- Secondary drug of
choice
- Drug of choice
because of oral
efficacy, single dose
2. Ciprofloxacin
3. Ceftriaxone
4. Erythromycin
HERPES SIMPLEX
CANDIDIASIS
MAIN PROBLEM ETIOLOGIC AGENT INCUBATION PERIODMild superficial fungal
infection
A viral disease
characterized by the
appearance of sores and
blisters on the skin
Candida albicans
Herpes simplex virus
types 1 and 2
2-3 weeks
2-12 days
HERPES SIMPLEX
CANDIDIASIS
MODE OF TRANSMISSION1. Rise in glucose as in
diabetes mellitus
2. Lowered body
resistance as in cancer
3. Increase in estrogen
level in pregnant women
4. Broad-spectrum
antibiotics are used
TYPE 1
- Respiratory droplets
- Direct exposure to
infected saliva
- Kissing and sharing
utensils
TYPE 2
- Sexual or genital
contact
SIGNS AND SYMPTOMS (Candidiasis) ONYCHOMYCOSIS
• Red, swollen darkened nailbeds • Purulent discharge
• Separation of pruritic nails from nailbeds DIAPER RASH
• Scaly, erythematous, papular rash • Covered with exudates
• Appears below the breasts, between fingers, axilla, groin and umbilicus
THRUSH
• Cream-colored or bluish-white patches on the tongue, mouth or pharynx
• Bloody engorgement when scraped MONILIASIS
• White or yellow discharge • Pruritus
• Local excoriation
• White or gray raised patches on vaginal walls with local inflammation
HERPES SIMPLEX
CANDIDIASIS
TREATMENT MODALITIES1. Antifungals
- Fluconazole (Diflucan)
- Ketoconazole (Nizoral)
- Imidazole (Nystatin)
- Used for oral thrush
- 48 hours until
symptoms disappear
- Cotrimoxazole
1. Antivirals
VECTOR-BORNE DISEASES
MALARIA
DENGUE
MAIN PROBLEM
ETIOLOGIC AGENT
An acute febrile disease An acute and chronic parasitic disease
The most common arboviral
illness transmitted globally The most deadly vector-borne disease in the world
Dengue virus types 1, 2, 3 and 4 Chikungunya virus
O’nyong’nyong virus West Nile virus
Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae
MALARIA
DENGUE
INCUBATION PERIOD MODE OF TRANSMISSION P. Falciparum – 12 days P. Vivax – 14 days P. Ovale – 14 days P. Malariae – 30 days 3-14 daysBite of an infected mosquito
Blood transfusion, contaminated syringe or needle Trans-placentally
MALARIA
DENGUE
VECTOR Aedes aegypti (Aedes albopictus) White stripes on the back and legs (Tiger mosquito)Day biting (2 hours after sunrise and 2 hours before sunset) Breeds on clear stagnant water Urban-based
Anopheles flavirostris
Brown in color
Night biting (9 PM-3 AM) Breeds on clear, flowing and shaded streams
Rural-based
MALARIA
DENGUE
SIGNS AND SYMPTOMS
FEVER
CHILLS
PROFUSE SWEATING
FEVER
HEADACHE
MALAISE
RASH
EPISODES OF
BLEEDING
MALARIA
DENGUE
DIAGNOSTIC PROCEDURES 1. TORNIQUET TEST- Screening test for dengue - A test for the tendency for blood
capillaries to break down or produce petechial hemorrhage
- Performed by examining the skin of the forearms after the arm veins have been occluded for 5 minutes - To detect unusual capillary fragility
1. CLINICAL DIAGNOSIS
- Based on triad symptoms, 50% accuracy
2. PLATELET COUNT
- Confirmatory test for dengue - Decreased count is confirmatory
2. BLOOD SMEAR
- Definitive diagnosis of infection is based on demonstration of malaria
parasites in blood film 3. RAPID DIAGNOSTIC TEST
- Uses immunochromatographic methods to detect Plasmodium-specific antigens
- Takes about 7 to 15 minutes - Sensitivity and specificity > 90%
MALARIA
DENGUE
TREATMENT MODALITIES 1. Analgesics and antipyretics - acetaminophen
2. Volume expanders
- Used in the treatment of
intravascular volume deficits
- Example: Lactated Ringers
3. Blood transfusion – for severe bleeding 4. Oxygen therapy 5. Sedatives 1. Chloroquine 2. Primaquine 3. Pyrimethamine 4. Sulfadoxine 5. Quinine 6. Quinidine
LEPTOSPIROSIS
SCHISTOSOMIASIS
MAIN PROBLEM ETIOLOGIC AGENT A slowly progressive diseasecaused by a blood fluke A zoonotic infectious disease
1. SCHISTOSOMA JAPONICUM
- Intestinal tract, endemic in the Philippines
2. SCHISTOSOMA MANSONI
- Africa
3. SCHISTOSOMA HAEMATOBIUM
- Middle East countries like Iran and Iraq
Leptospira interrogans
LEPTOSPIROSIS
SCHISTOSOMIASIS
INCUBATION PERIOD
MODE OF TRANSMISSION
At least 2 months 7 to 19 days
Ingestion Skin penetration Contact with the skin
LEPTOSPIROSIS
SCHISTOSOMIASIS
VECTOR
Oncomelania quadrasi 1. Thrives in fresh water stream
2. Clings to grasses and leaves 3. Greenish brown in color 4. Size is as big as the smallest grain of palay
LEPTOSPIROSIS
SCHISTOSOMIASIS
SIGNS AND SYMPTOMS ACUTE STAGE 1. Cercarial dermatitis (swimmer’s itch) 2. Katayama syndrome C - ough
H – eadache and fever A – norexia and lethargy R – ash
M - yalgia
Septic or Leptospiremic Stage F – ever (remittent H – eadache M – yalgia N – ausea V – omiting C – ough C – hest pain
LEPTOSPIROSIS
SCHISTOSOMIASIS
SIGNS AND SYMPTOMS CHRONIC STAGE 1. Hepatic: pain, abdominal distension, hematemesis, melena 2. Intestinal: fatigue, abdominal pain, dysentery
3. Urinary: dysuria, urinary frequency, hematuria
4. Cardiopulmonary: palpitations, dyspnea on exertion
5. CNS: seizures, headache, back pain and paresthesia
Immune or Toxic Stage - Lasts for 4 to 30 days - Iritis, headache, meningeal manifestations
- Oliguria, anuria with renal failure
- Shock, coma and congestive heart failure
LEPTOSPIROSIS
SCHISTOSOMIASIS
DIAGNOSTIC PROCEDURES 1. Fecalysis 2. Kato-Katz Technique3. Cercum ova precipitin test (COPT)
- Confirmatory test for schistosomiasis
LEPTOSPIROSIS
SCHISTOSOMIASIS
TREATMENT MODALITIES 1. Praziquantel (Biltricide) - Taken for 6 months - 1 tablet BID for 3 months - 1 tablet OD for 3 months
1stline drugs
1. Penicillin G – drug of choice 2. Doxycycline 2ndline drugs 3. Ampicillin 4. Amoxicillin
FILARIASIS
MAIN PROBLEMA parasitic disease caused by an African eye worm ETIOLOGIC AGENT Wuchereria bancrofti Brugia malayi Brugia timori INCUBATION PERIOD 8 to 16 months MODE OF TRANSMISSION Person-to-person by mosquito bites ACUTE STAGE
•
Lymphadenitis (inflammation of lymph nodes)•
Lymphangitis (inflammation of lymph vessels)• Male genitalia affected leading to funiculitis, epididymitis and orchitis (redness, painful and tender scrotum) CHRONIC STAGE
• Develop 10-15 years from onset of first attack
•
Hydrocele (swelling of the scrotum)•
Lymphedema (temporary swelling of the upper and lower extremities)•
Elephantiasis (enlargement and thickening of the skin of the upper and lower extremities, scrotum and breast LABORATORY EXAMINATIONS•
Nocturnal blood examination (NBE) – taken at patient’s residence/hospital after 8PM•
Immunochromatographic test (ICT) – rapid assessment method; an antigen test done at daytimeTREATMENT
•
Diethylcarbamazine Citrate (DEC) or HETRAZAN – an individual treatment kills almost all microfilaria and a good proportion of adult worms.PREVENTION AND CONTROL
• Measures aimed to control vectors