Nursing Lecture on Communicable Disease

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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)

FACTORS AFFECTING RISK OF INFECTION
AGE
HEREDITY
LEVEL OF STRESS
NUTRITIONAL STATUS
CURRENT MEDICAL THERAPY
PRE-EXISTING DISEASE
IMMUNIZATION STATUS

IMMUNITY
THE QUALITY OF BEING INSUSCEPTIBLE TO OR UNAFFECTED BY A PARTICULAR DISEASE.

TYPES OF IMMUNITY
INNATE = within the HOST Immune System
ACQUIRED = inoculation and disease Active Passive

IMMUNE SYSTEM PROTECTION AGAINST ANTIGEN OR DISEASES BY A SYSTEM OF ANTIBODY PRODUCTION
ANTIBODY PRODUCED BY LYMPHOCYTES IN RESPONSE TO ANTIGEN.
ANTIGEN TRIGGERING AGENT OF THE IMMUNE SYSTEM

IMMUNOGLOBULINS
IgG MOST PREVALENT ANTIBODY 80%, PRODUCE LATER IN THE IMMUNE RESPONSE, ONLY Ig THAT CAN CROSS THE PLACENTA
IgA FOUND IN COLOSTRUM , TEARS, SALIVA, SWEAT
IgM PRINCIPAL ANTIBODY OF BLOOD, QUICKLY PRODUCED IN RESPONSE TO AN ANTIGEN, RESPONDS TO ARTIFICIAL IMMUNIZATION
IgE ALLERGIC REACTION
IgD UNKNOWN, ANTIGEN RECEPTOR, FOUND IN THE SURFACE OF B CELLS

IMMUNIZATION
A PROCESS BY WHICH RESISTANCE TO AN INFECTIOUS DISEASE IS INDUCED OR AUGMENTED.
ACTIVE AND PASSIVE IMMUNIZATION

EPI
Hepa b 3 shots, 0-1-6 mo, im, 0.5 ml, vas. lateralis
Bcg 1 at birth, id, 0.05 ml, right arm
Bcg 2 at 6 y/o, id, 0.1 ml, left arm
Dpt 3 shots, 6 weeks old, 4 weeks interval im, 0.5 ml, vas. lateralis
Opv 3x, same with dpt, oral gtts, 2-3 months
Measles 1x, 9 mo, sq, 0.5 ml, right arm

Active Immunity
ANTIBODIES ARE PRODUCED BY THE BODY IN RESPONSE TO INFECTION. ANTIGEN IS INTRODUCED, LONG DURATION
EXAMPLE:
NATURAL ACTIVE = DISEASE
ARTIFICIAL ACTIVE = VACCINES

ARTIFICIAL ACTIVE
ANTIGENS (VACCINES OR TOXOIDS) ARE ADMINISTERED TO STIMULATE ANTIBODY PRODUCTION. REINFORCED BY BOOSTER DOSE TO INCREASE IMMUNITY.
KILLED VACCINES PERTUSSIS VACCINE, TYPHOID VACCINE
LIVE VACCINES ATTENUATED, WEAKENED SABIN, MEASLES
TOXOID INACTIVATED BACTERIAL TOXIN-TETANUS, DIPHTHERIA

Artificial Active

PASSIVE IMMUNITY
ANTIBODIES ARE PRODUCED BY ANOTHER SOURCE. ANTIBODIES ARE INTRODUCED, SHORT DURATION
Example:
NATURAL PASSIVE = MOTHER
ARTIFICIAL PASSIVE = GLOBULINS

ARTIFICIAL PASSIVE
IMMUNE SERUM (ANTIBODY) FROM ANIMAL OR HUMAN IS INJECTED. PROVIDE IMMEDIATE PROTECTION (DIPHTHERIA ANTITOXIN, TETANUS ANTITOXIN) SKIN-TESTING IS A MUST.

CONDITIONS BEFORE AN INFECTION DEVELOPS
Sufficient number of microorganisms
Virulence of microorganisms
Resistance of the of the host
Immunity of the host
Cycle of infection must be completed

THE INFECTION PROCESS CYCLE
Agent (bacteria or virus)
Reservoir (fomites or living things)
Portal of Exit
Mode of Transmission (direct or indirect)
Portal of Entry
The Host

STAGES OF AN INFECTIOUS PROCESS
INCUBATION PERIOD
PRODROMAL PERIOD
ILLNESS PERIOD (PATHOGNOMONIC SIGN)
CONVALESCENT PERIOD

Terminologies
ETIOLOGY
EPIDEMIOLOGY
INCIDENCE
PREVALENCE
ENDEMIC
EPIDEMIC
PANDEMIC
SPORADIC

FUNDAMENTALS OF STANDARD PRECAUTION
HANDWASHING
GLOVES
MASKS, GOGGLES, FACE SHIELDS
AIR FILTERS
GOWNNS
ISOLATION
STRICT ISOLATION
CONTACT ISOLATION
RESPIRATORY ISOLATION
TUBERCULOSIS ISOLATION
ENTERIC PRECAUTION
DRAINAGE/SECRETION PRECAUTION
BLOOD/BODY FLUIDS PRECAUTION

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

OTHER TYPE OF ISOLATION
AFB ISOLATION
STRICT ISOLATION
WOUND AND SKIN ISOLATION
ENTERIC ISOLATION
PROTECTIVE OR REVERSE ISOLATION

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

GOWNS-gowns not necessary
MASKS- must be worn by all persons entering the room if susceptible disease
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
PRIVATE ROOM-desirable
GOWNS-must be worn by all persons having direct contact with the patient
MASKS- during dressing changes
GLOVES-must be worn by all persons having direct contact with infected area
ARTICLES-instruments, dressing, linens

ENTERIC PRECAUTIONS
PRIVATE ROOM-necessary FOR CHILDREN ONLY
GOWNS- must be worn by all persons having direct contact with the patient
MASKS- not necessary
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
GOWNS- must be worn by all persons entering room
MASKS- - must be worn by all persons entering room
GLOVES-must be worn by all persons having direct contact with patient

DIAGNOSTIC TOOLS
COLLECTION OF SPECIMEN
PRINCIPLES
TYPES OF SPECIMEN COLLECTION
BLOOD
URINE
STOOL
SPUTUM
WOUNDS
THROAT

LABORATORY TESTS
MICROSCOPY
CULTURE
ANTIBIOTIC SUSCEPTIBILITY TESTING
WHITE BLOOD CELL COUNT
IMMUNOLOGIC TEST

DISORDERS
CNS DISEASES
GIT DISEASES
RESPIRATORY DISEASE
BLOOD BORNE DISEASES
ERUPTIVE FEVER DISEASES
CONTACT DISEASE
SEXUALLY TRANSMITTED DISEASES
TORCHS
HIV AND AIDS
HEPATITIS

Tetanus
Clostridium tetani
MOT = wound setting
IP = 3 -21 days
IMMUNITY
Active = TT
Passive = TAT and TIG
Natural = active none, passive (+)

Tetanus
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)

3 types of patients w/ skin wounds post exposure prophylaxis
(+) immunization as a child w/ boosters but last shot > 10 yrs – give TT
2. (-) immunization - TT + TIG/TAT
3. (+) tetanus – TIG/TAT + TT + Abx + wound cleansing + supportive therapy

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

Rabies/Lyssa (Zoonotic)
Rhabdovirus/filterable virus
MOT = Bite from warm blooded animals
Canine (human) and sylvatic (animals)
IP = 10 days to several years
IMMUNITY
Active = rabies vaccine
Passive = HRIG, ERIG
Natural = active none, passive none

Hydrophobia (fear of choking)
Aerophobia (laryngospasm)
Bite from warm blooded animals
Encephalitis/meningitis/respiratory paralysis

Category of bites
I – intact skin (lick)
II – mucosal, non bleeding wounds, abrasions
III – bleeding bites and above neck, stray dogs, laceration, multiple bites

Observe dog for maniachal s/sx
Active-rabies vaccine
Passive-rabies immunoglobulin
Dx
History taking
Quarantine the dog
Staining of brain tissue (dog) (+) Negri bodies

AFTER THE BITE
WASH WITH SOAP AND WATER
GIVE ANTIBIOTICS AND ANTITETANUS
OBSERVE DOG FOR 14 DAYS, IF IT DIES CONSULT DOCTOR
IF DOG SHOWS SUGGESTIVE OF RABIES, KILL THE DOG IMMEDIATELY AND BRING HEAD FOR LAB EXAM (+) NEGRI BODIES SUBMIT FOR IMMUNIZATION WHILE WAITING FOR RESULTS
IF DOG IS NOT AVAILABLE FOR OBSERVATION SUBMIT FOR IMMUNIZATION

Immunization
Rabies vaccine (5 shots) IM (2 ml deltoid) 0, 3, 7, 14, 28 days ID (0.1 ml deltoid) 0, 3, 7 days (0.1 ml deltoid 2 shots) 30, 90 days (0.1 ml deltoid single shot)
Rabies immunoglobulin (HRIG and ERIG) IM (0.2 x kg) single shot wound 40% deltoid 60%

4 STAGES
1. prodrome - fever, headache, paresthesia,
2. encephalitic – excessive motor activity, hypersensitivity to bright light, loud noise, hypersalivation, dilated pupils
3. brainstem dysfunction – dysphagia, hydrophobia, apnea
4. death/recovery

RESPONSIBLE PET OWNERSHIP
HAVE PET IMMUNIZED AT 3 MONTHS AND EVERY YEAR AFTER
NEVER ALLOW PETS TO ROAM IN THE STREET
LEASHED YOUR DOG
YOUR PET ACTION IS YOUR RESPONSIBILITY

Poliomyelitis Infantile Paralysis
Polio virus, Legio debilitans
Legio brunhilde (fatal)
Legio lansing
Legio leon
MOT = Fecal oral route (common) and droplets
IP = 7-12 days
IMMUNITY
Active = OPV
Passive = none
Natural = active (+), passive none

Assymetrical paralysis
Hayne’s sign - head drop
Poker’s sign - opisthotonus
Landry’s sign - ascending paralysis
Pandy’s Test – increased in CSF CHON

I – abortive or inapparent
II – meningitis (non-paralytic)
III – paralytic (anterior horn of spinal cord)
IV – bulbar (encephalitis)

Meningitis Menigococcemia
Neisseria meningitides (bacteria)
MOT = droplets
IP = 1-2 days
IMMUNITY = xxx

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

Menigococcemia
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

Menigococcemia
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

Encephalitis
Arbo virus (arthropod borne virus)
MOT = bite from mosquito (St. Louise)
IP = xxx
IMMUNITY = xxx

Encephalitis
S/sx: fever, abdominal pain, sore throat, respiratory symptoms, headache, meningeal signs, photophobia, Seizure (lacrosse), SIADH w/ hypoNa (St Louis)
Dx: CSF analysis
r/o other CNS disease, CT scan, MRI
Mgmt: nonspecific; control seizures

Leprosy
Mycobacterium Leprae, Hansen’s Bacillus
MOT = (unknown)
may be due to prolonged skin-skin contact (common)
or droplets
IP = years to decades
IMMUNITY
Active = BCG
Passive = none
Natural = none

Leprosy
EARLY
Skin lesion and paresthesia
LATE
Lagopthalmos
Madarosis
Gynecomastia
Saddle Nose
Contractures

Leprosy

Leprosy
Dx:
Lepromin Test – ID injection
Slit Skin Smear
Dapsone-Lamprene-Rifampicin
Dapsone-don’t give to anemic
Lamprene-dry skin, hyperpigmentation (lasting)
Rifampicin-renal and liver toxicity

Leprosy
MDT-RA 4073 (home meds)
Paucibacillary - 6-9 months 1. Dapsone
2. Rifampicin
Multibacillary- 12-24 months
1. Dapsone – mainstay; hemolysis, agranulocytosis
2. Clofazimine – reddish skin pimentation, intestinal toxicity
3. Rifampicin – bactericidal; renal and liver toxicity

Leprosy
MDT- two or more drugs
RA 4073 (home meds)
Paucibacillary.- 6-9 months
Multibacillary.- 12-24 months
Tuberculoid – high resistant, less severe (+LT)
Lepromatous – most severe, low resistant (-LT)

Leprosy
Non - communicable
After 1 week of medication
Considered cured
After completing the course of treatment

Red Tide Poisoning
Pyromidium Bahamense
Exotoxin
Dinoflagellates
Plankton
Algae
MOT = Ingestion of contaminated bi-valve shellfish
IP = within 30 minutes
IMMUNITY = xxx

Red Tide Poisoning
Dx gastric siphoning
EARLY
Circumoral numbness
nausea and vomiting
LATE
Bulbar paralysis and metabolic acidosis
Mgmt: emesis/gastric lavage + activated charcoal, supportive

CLINICAL MANIFESTATIONS:
NUMBNESS OF THE FACE ESPECIALLY AROUND THE MOUTH
VOMITING, DIZZINESS, HEADACHE
TINGLING SENSATION, WEAKNESS
RAPID PULSE, DIFFICULTY OF SPEECH (ATAXIA), DYSPHAGIA, RESPI PARALYSIS, DEATH.

MANAGEMENT AND CONTROL MEASURES:
NO DEFINITE MEDICATIONS
INDUCE VOMITING (EARLY INTERVENTION)
DRINKING PURE COCONUT MILK (WEAKENS TOXIC EFFECT) DON’T GIVE DURING LATE STAGE IT MAY WORSEN THE CONDITION.
NaHCO3 SOLUTION (25 GRAMS IN ½ GLASS OF WATER)
RESPIRATORY SUPPORT
AVOID USING VINEGAR IN COOKING SHELLFISH AFFECTED BY RED TIDE (15X virulence)
TOXIN OF RED TIDE IS NOT TOTALLY DESTROYED IN COOKING.
AVOID TAHONG, TALABA, HALAAN, KABIYA, ABANIKO. WHEN RED TIDE IS ON THE RISE.

Botulism
Clostridium Botulinum (bacteria)
Endotoxin
MOT
canned foods
Ingestion of contaminated foods)
IP = 12-36H canned food, 4-14 days wound
IMMUNITY
Active = xxx
Paiive = botulinum antitoxin
Natural = xxx

Botulism
Dx = gastric siphoning
EARLY
VISUAL DIFFICULTY, DYSPHAGIA, DRY MOUTH
LATE
VOMITING, CONSTIPATION/DIARRHEA
DESCENDING SYMMETRICAL FLACCID
BULBAR PARALYSIS

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

Amoebiasis
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)

Bacillary Dysentery Shigellosis
Shiga bacillus (bacteria)
s. dysenterae (fatal)
s. flexneri (common in the Philippines)
s. boydii
s. sonnei
MOT = same with amoebiasis
IP = 1-7 days
IMMUNITY = xxx

Bacillary Dysentery Shigellosis
Dx stool exam
Watery mucoid, bloody with pus feces
Tenesmus = rectal prolapse
Chloramphenicol, Tetracycline

Cholera, El Tor
Vibrio Coma (inaba, ogawa, hikojima)
Vibrio Cholerae
Vibrio El Tor (bacteria)
MOT = same with amoebiasis
IP = few hours to 5 days
IMMUNITY
Active = cholera vaccine
Passive = none
Natural = none

Cholera, El Tor
Dx stool exam
Rice watery stool with fishy odor
Washerwoman’s appearance
Severe dehydration
Chloramphenicol

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

Typhoid Fever
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)

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

Typhoid Fever
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)

Hookworm (Roundworm)
Necator Americanus, Ancylostoma Duodenale
Skin entry (sole of the feet to blood steam then into the lungs then ascends to the pharynx where it is swallowed and attached into the intestinal mucosa and subsists on the blood of the host)
Anemia, abd’l cramps, abd’l distention, perforation to peritinotis to septicemia

IP few weeks to months
Dx microscopic exam (stool exam)
Pyrantel Pamoate and Mebendazole
Note: don’t give drug without (+) stool exam members of the family must be examined and treated also.

Nursing Consideration
FOLLOW-UP EXAMINATION OF THE STOOL 2 WEEKS AFTER THERAPY
NUTRITION COUNSELING AND IRON SUPPLEMENTS
FAMILY MEMBERS AND CLOSE CONTACTS SHOULD BE EXAMINED AND TREATED FOR PARASITES
EDUCATE PUBLIC ABOUT DANGERS OF CONTAMINATED SOIL
IMPORTANCE OF WEARING SHOES
DEWORMING

Ascariasis (Roundworm)
Ascaris Lumbricoides
MOT ingestion of food contaminated by ascaris lumbricoides GIT to LUNGS and other ORGANS

MOT: ingestion of food contaminated by ascaris eggs larvae in large intestine penetrate wall towards lung where larvae grow and coughed up intestine larvae mature and passed out in feces

Ascariasis (Roundworm)
Coughing, wheezing and hemoptysis
IP same with hookworm
Drug: same with hookworm
Dx same with hookworm

Tapeworm
Taenia Saginata (cattle)
Taenia Solium (pigs)
MOT fecal oral route (ingestion of food contaminated by the agent)
Dx: Stool Exam
S/Sx diarrhea, abdominal discomfort, anemia

Pinworm
Enterobiasis (nocturnal animation/alive)
Vermicularis Enterobius
MOT fecal oral route
S/sx Itchiness at the anal area (eggs of the agent causes the itchiness)
Dx tape test at night time (agents release their eggs during night time)

Thread worm – storgyloidiasis
Whip worm – trichoniasis voracious eating abdominal pain weight loss
Flat worm - paragonimiasis

QUIZ
1. hookworm a. taenia s.
2. ascariasis b. vermicularis enterobius
3. pinworm c. ascaris lumbricoides
4. tapeworm d. necator americanus

5. Common s/sx of worm infestation?
6. single most important nursing consideration prior to DEWORMING?
7. MOT of hookworm infestation?
8. distinct s/sx of PINWORM infestation?
9. WHIPWORM infestation s/sx?
10. LUNG FLUKE infestation?

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

Schistosomias, Snail Fever, Takayama
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)

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

Mumps
Mumps virus/filtrable virus
MOT = droplets and airborne
HIGHLY CONTAGIOUS
IP 12-16 days
IMMUNITY
Active = MMR
Passive = mumps Ig
Natural = active =lifetime

Mumps
Unilateral or bilateral parotitis
Ice collar
Stimulating foods cause severe pain
Bilateral orchitis and oophoritis
Active spermatogenesis
Sterility
Steroids
Supporter

Respiratory System

Diphtheria
Corynebacterium diphtheriae
Klebsloeffler’s bacillus (bacteria)
HIGHLY CONTAGIOUS
IP 2-5 days
IMMUNITY
Active = DPT
Passive = DAT
Natural = xxx

Diphtheria
Dx = throat swab, MOLONEY, SCHICK
Pseudomembrane, Bullneck
Penicillin or erythromycin
Resp Acidosis with hypoxemia
Cx: myocarditis, septicemia

Diphtheria
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

S/sx: sore throat, fever, “Bull-neck” (Pseudomembrane- gray exudate, foul breath, massive swelling of tonsils and uvula, thick speech, cervical lymphadenopathy, swelling of submandibular and anterior neck), obstruction of respiratory tract
Dx: Schick test - susceptibility to diphtheria toxin
Moloney - sensitivity to diphtheria toxoid
Throat swab (K tellurite and Loeffler’s coagulated blood serum)
Mgmt: Diphtheria antitoxin (Skin test), Penicillin,erythromycin, rifampicin, clindamycin

Diphtheria KEY POINTS!
Highly contagious
Pseudomembrane and bullneck
Immunization best intervention PREVENTION
Obstruction and myocarditis
Isolation technique

Whooping Cough, Pertussis
Bordetella pertussis (bacteria)
B. parapertussis
B. bronchiseptica
Hemophilus bacillus
HIGHLY CONTAGIOUS
IP 3-21 days
IMMUNITY
Active = DPT
Passive = xxx
Natural = xxx

Manifestations:
CATARRHAL (HIGHLY CONTAGIOUS)
1-2 WEEKS, CORYZA, SNEEZING, DRY COUGH, FEVER, ANOREXIA
PAROXYSMAL
4-6 WEEKS, SEVERE VIOLENT COUGHING ATTACKS IN CLUSTERS, THAT ENDS IN WHOOP (NOISY SPASM OF INSPIRATION) RESULTING TO CYANOSIS, VOMITING, EXHAUSTION.

Ferrous iodide to liquefy thicky secretions
Erythromycin or Ampicillin
Bordet gengao (agar for culture)
Catarrhal stage (highly contagious)
Clusters of cough that ends with a whoop
Prostration

PERTUSSIS key points!
Highly contagious
Thick secretions
Cluster of cough
Extreme exhaustion
HYPOXIA
PREVENTION is still the BEST intervention
IMMUNIZATION

PTB, Koch’s Pulmonary
Mycobacterium tubercle
Tubercle bacillus (bacteria)
MOT: Airborne/droplets
INCUBATION-DEPENDS ON HOST RESISTANCE
RISK FACTORS: DECREASED BODY RESISTANCE MALNUTRITION, POVERTY, OVERCROWDING, STEROID THERAPY, CHEMOTHERAPY

PTB
Pathogenesis:
Transmission into the lungs
Immune response macrophage (bacilli) creating a lesion
Tubercle formation scar or spot
Dissemination
EPTB

PTB, Koch’s Pulmonary
Manifestation:
EARLY WEIGHT LOSS, LISTLESSNESS, VAGUE CHEST PAIN, PLEURISY, ANOREXIA, FEVER, NIGHT SWEATS
LATE PULMONARY HEMORRHAGE, EXPECTORATION OF PURULENT SPUTUM, DYSPNEA, HEMOPTYSIS (CAVITARY SPREAD)

PTB
Dx:
PPD-exposure
0-4 mm (negative)
5 mm variable
> 10 mm (positive)
Chest xray-cavitary lesion
Sputum-confirmatory

PTB
MDT
r-orange urine
i-neuritis and hepatitis
p-hyperuricemia
e-impairment of vision
s-8th cranial nerve damage

PTB
CGFNS and NCLEX
Usual Dose RIE – 9 months to 12 months 2-4 weeks non infectious
Drug Resistant Tuberculosis RIE+ (2 nd line drug) STREPTOMYCIN PYRAZINAMIDE CAPREOMYCIN PARA-AMINOSALICYLIC ACID CYCLOSERINE

PTB
2 weeks after medications – non communicable
3 successive negative sputum-non communicable
rifampicin-prophylactic

PTB
category I (new PTB (+) sputum)
category II (relapsed)
category III (PTB case (-) sputum)
short course – 6-9 months
long course – 9-12 months
DOTS- direct observe treatment short course
Case finding
Home meds (members of the family)
Referrals
Follow-up

TREATMENT:
CATEGORY 1 NEW PTB, (+) SPUTUM GIVE RIPE 2 MONTHS, MAINTENANCE OF RI 4 MONTHS
CATEGORY 2 PREVIOUSLY TREATED WITH RELAPSES GIVE RIPES 1ST 2 MONTHS, REPS 1 MONTH, MAINTENANCE RIE 5 MONTHS
CATEGORY 3 NEW PTB (-) SPUTUM FOR 3X GIVE RIP 2 MONTHS, MAINTENACE RI 2 MONTHS

Pneumonia
Typical
Community Acquired
Streptococcus pneumoniae
Hospital Acquired
Staphylococcus aureus, Pseudomonas aeruginosa
Elderly
Hemophilus influenzae type B

Pneumonia
Atypical
Pneumocystis carinii (fungal)
Aspergillosis (fungal) Azole,
SARS

Pneumonia
s/sx chest pain, fever with chills,
Dx:
C&S and XRAY
Productive cough pneumococcal – purulent, rusty sputum staphylococcal – yellow, blood streaked klebsiella species – red, gelatinous sputum mycoplasmal – non productive, mucoid sputum
ABG
Pulse Oximetry

Pneumonia
CARI-health teachings
Watchout for complications
Respiratory distress
In 24 hours death will occur RESPIRATORY SUPPORT!

Pneumonia
Cx:
pleural effusion
Empyema
consolidation Diminished Lung Sound: egophony CHANGE IN VOICE bronchophony CLARITY OF VOICE whispered pectoriloquy AUSCULTATE

Severe Acute Respiratory Syndrome
Coronavirus
Severe acute respiratory syndrome
IP: 2-7 days
MOT: respiratory droplet/person to person contact
Risk Factors:
History of recent travel to
China
Hong Kong
Taiwan
Close contact
w/ ill persons
with a hx of recent travel to such areas
Health workers

SARS
Dx: sputum C&S CLINICAL
MANIFESTATIONS:
FEVER-38 C AND ABOVE CONTINUOUS FOR 7-10 DAYS
CHILLS HEADACHE, GENERAL FEELING OF DISCOMFORT, BODY ACHES, DRY PRODUCTIVE COUGH WITH HYPOXEMIA (RESP. ACIDOSIS)
DYSPNEA RELATED TO LOSS OF AERATING SURFACE

SARS
NURSING CONSIDERATIONS:
NO SPECIFIC TREATMENT
ANTIVIRAL AGENT-OSELTAMIVIR OR RIBAVIRIN
CLOSE SUPERVISION/OBSERVATION
PROPHYLACTIC ANTIBIOTIC
AVOID INFECTED AREAS IDENTIFIED BY WHO (HONGKONG, GUANDONG, SHANXI, CHINA, HANOI, VIETNAM, TORONTO, CANADA, SINGAPORE)

SARS
NURSING CONSIDERATIONS:
SEEK IMMEDIATE MEDICAL ATTENTION IF YOU SUSPECT SARS
WEAR FACE MASK N95, BRA MASK (HONGKONG),
DON’T GO TO WORK OR SCHOOL
OBSERVE PERSONAL HYGIENE
HANDWASHING (5 MINUTES)
BUILD UP BODY RESISTANCE (PROPER DIET)
DIET (HIGH IN CHON, CHO, VIT C, D , E , A, MINERAL ZINC (INCREASE BODY RESISTANCE)

BLOOD BORNE DISEASES

Dengue Fever, H-Fever, Dandy Fever, Breakbone Disease
Acute Febrile Disease
CAUSATIVE AGENT-FILTRABLE VIRUS
DENGUE VIRUS TYPE 1,2,3,4,
CHIKUNGUNYA VIRUS
MOT (Mode of Transmission) bite from:
Aedes aegypti
Aedes albopictus
Culex fatigans
IP (Incubation Period) 1 week

Hyperpyrexia without focal of infection
TRIAD: fever, rashes and muscle pain
Bleeding to hypovolemic shock
ASA (Aspirin) is contraindicated
Watchout for bleeding
PLATELET is being attack

Dx:
ACUTE FEBRILE ILLNESS WITH NO IDENTIFIABLE FOCUS OF INFECTION
Internal and external sign of bleeding
Torniquet Test or Rumpel Lead Test
Platelet count
PT (Prothrombin Time)
APTT (Activated Partial Thromboplastin Time)
Bleeding time
Coagulation time

TRIAD (FEVER, RASH, SEVERE HEADACHE/BACKACHE/MYALGIA)
1ST STAGE, FIRST 4 DAYS HIGH FEVER, ABDOMINAL PAIN, HEADACHE, FLUSHING, VOMITING, EPISTAXIS
2ND STAGE, 4-7 DAYS TOXIC OR HEMORRHAGIC STAGE LOWERING OF BODY TEMP., SEVERE ABDOMINAL PAIN, VOMITING, GIT BLEEDING-HEMATEMESIS, MELENA, NARROW BP, SHOCK
3RD STAGE, 7-10 DAYS
CONVALESCENT OR RECOVERY STAGE SIGN OF PLASMA LEAKAGE PLEURAL EFFUSION, ASCITES, HYPOPROTEINEMIA HERMAN’S SIGN

GRADE 1 (+) TORNIQUET TEST, NO BLEEDING
GRADE 2 SPONTANEOUS BLEEDING, (+) GRADE 1
GRADE 3 CIRCULATORY FAILURE,,DECREASED BP, RAPID WEAK PULSE, NARROWING OF PULSE PRESSURE, COLD CLAMMY SKIN, RESTLESSNESS
GRADE 4 PROFOUND SHOCK, UNDETECTABLE BP AND PULSE

Nursing Considerations
ANY CONDITION ASSOCIATED WITH BLEEDING IS ENOUGH CAUSE FOR ALARM
FOR FEVER DON’T GIVE ASA
RAPID REPLACEMENTS OF FLUIDS IS THE MOST IMPORTANT TREATMENT
GIVE ORESOL/HYDRITE
VIT C TO PROMOTE CAPILLARY INTEGRITY

BLOOD TRANSFUSION
IV CRYSTALLOIDS (PLAIN LRS, PLAIN 0.9 NSS)
DEXTRAN (COLLOIDS)
PLATELETS
FRESH FROZEN PLASMA
CRYOPRECIPITATE
WHOLE BLOOD
NO KNOWN IMMUNIZATION (VACCINE CURRENTLY UNDERWAY)

Dengue KEY POINTS
Day biting aedes aegypti, stagnant
Fever with no focal of infection
Bleeding is imminent when fever subsides
Fluid replacement
BT
platelets

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

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

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

MALARIA key points
Night biting anopheles, running water
Falciparum – fatal
Ovale and vivax – exacerbate
Sporogony – sexual – mosquito
Schizogony – asexual – human
Chloroquine
Seizure, fluid and elec loss
Rbc and liver

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)

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

Filariasis KEY POINTS
Night biting aedes poecilius, plants
Chronic, lymphedema
HETRAZAN
ICT and NBE
Lymphatic vessel obstruction

Leptospirosis, Weil’s Disease (Zoonotic)
Spirochete-leptospira interrogans
IP 5-6 days
MOT (Mode of Transmission)
Skin penetration = flood
INGESTION OF CONTAMINATED FOOD
SKIN, MUCUS MEMBRANE, ABRADED SKIN, CONJUNCTIVA
INHALATION
AFTER PENETRATION LEPTOSPIRES ENTER THE BLOOD STREAM AND ARE CARRIED TO ALL PARTS OF THE BODY INCLUDING
Liver, kidneys and CSF

Leptospirosis, Weil’s Disease (Zoonotic)
Dx:
CULTURE OF MICROORGANISMS
BLOOD AND CSF EXAMINATION (FIRST WEEK)
URINE EXAM- AFTER 10 DAYS
MICROSCOPIC AGGLUTINATION TEST (MAT) A RISE IN ANTIBODY TITER

CLINICAL MANIFESTATIONS
EARLY = fever and headache
LEPTOSPIREMIC PHASE = vasculitis
HEPATITIS, JAUNDICE, SKIN HEMORRHAGE, FEVER, CHILLS, RENAL FAILURE, MENINGITIS WITH MENTAL STATUS CHANGE, MUSCULAR PAIN, NAUSEA AND VOMITING, COUGH AND CHEST PAIN
IMMUNE PHASE
APPEARANCE OF CIRCULATING IgM

NURSING CONSIDERATIONS
PENICILLIN OR DOXYCYCLINE (IMMEDIATELY)
ERYTHROMYCIN IF ALLERGIC TO PENICILLIN
FLUID AND ELECTROLYTE BALANCE
ENSURE ADEQUATE RENAL PERFUSION TO PREVENT ARF
IF AZOTEMIA IS SEVERE OR PROLONGED (CONSIDER DIALYSIS)
DISEASE IS USUALLY SHORT LIVED AND MILD BUT SEVERE INFECTION CAN DAMAGE KIDNEYS, LIVER, CNS AND RESPIRATORY SYSTEM
MOST SERIOUS FORM IS CALLED WEIL’S DISEASE
PRIMARILY A DISEASE OF DOMESTICATED AND WILD ANIMALS

PREVENTION AND CONTROL
AVOIDANCE OF EXPOSURE TO URINE AND TISSUES FROM INFECTED ANIMALS (FLOOD)
RODENT CONTROL
VACCINATION OF ANIMALS
HYGIENIC CONDITIONS IN SLAUGHTERHOUSES, FARM YARD BUILDINGS AND BATHING POOLS
USE OF PROTECTIVE CLOTHING AND BOOTS
CHEMOPROPHYLAXIS (DOXYCYCLINE 200 mg PO ONCE A WEEK
SUPPORTIVE MANAGEMENT
ALL PATIENT SUSPECTED TO HAVE LEPTO, MILD OR SEVERE SHOULD BE ADMITTED

LEPTOSPIROSIS key points
Spirochette, rat, urine and feces
Skin penetration, ingestion
Fever and headache
Liver, kidneys and CSF
Doxycycline

ERUPTIVE FEVER

Measles, Rubeola, 7 Day Fever, Hard Red Measle
Paramyxo virus
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
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

PS forschheimer’s
Characteristic: cervical lymphadenopathy
Fever: low grade fever
CX rare
CX to pregnant women:
1st tri-congenital anomalies
2nd tri-abortion
3rd tri-pre mature delivery

Chicken Pox, Varicella
Herpes Zoster Virus
Varicella Zoster Virus
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

Small Pox, Variola
Pox virus
PC until all crust disappear
HIGHLY CONTAGIOUS
IP 1-3 weeks
ERADICATED
BIOLOGIC WEAPON

Small Pox, Variola
Rashes
Maculopapulovesiculopustular
Centripetal
CX same with chicken pox
Differential Dx
Paul’s test - instilling of vesicular fluid of small pox into the cornea if keratitis develops its small pox

CONTACT

Pediculosis
Blood sucking lice
Pediculus humanus
p. capitis-scalp
p. palpebrarum-eyelids and eyelashes
p. pubis-pubic hair
p. corporis-body
Drugs: Lindane (Kwell) topical
Permethrin (Nix) topical
CX impetigo to AGN, RHD, SLE
MOT skin contact

Scabies
Sarcoptes scabie
Pruritus (excreta of mites)
Mites come-out from burrows to mate at night
Drugs: Permethrin (Nix) cream
Sulfur soap
Linens: wash with hot water
MOT skin contact

Conjunctivitis
Children
Viral-hygiene and rest
Bacterial-yellow, green or white pus, photophobia-antibiotic eyedrops or ointment
Chlamydial –cough, history of maternal infection-antibiotic
Herpetic-pain, photophobia, skin lesions-antiviral agents
Allergic-itching, watery discharge-antihistamine
S/Sx
From mild pruritus to severe drainage, burning, hyperemia and chemosis (edema)
Pink eye-infectious conjunctivitis
MOT direct contact with eye secretions

Gonorrhea (bacteria)
Neisseria gonorrheae (gram positive)
IP 3 -7 days
Asymptomatic in women
Mucopurulent discharge
Painful urination
DX:
gram stain of cervical secretions
Drugs: single dose only
Ceftriaxone (Rocephin) 125 mg IM
Ofloxacin (Floxin) 400 mg orally
CX:
PID, ectopic pregnancy and infertility
Ophthalmia neonatorum and sepsis (infant) vaginal birth

Syphilis (bacteria)
Treponema pallidum (spirochete)
IP 10-90 days
Painless, clean chancre
DX:
Non specific VDRL
Confirmed by-antitreponemal antibody tests
Dark-field examination of lesion

Primary – painless chancre Secondary – generalized rash Tertiary - gumma

Syphilis (bacteria)
Primary-chancre-most infectious
Secondary-generalized macular papular rash including palms and soles (condylomata lata)
Tertiary-neurosyphilis-permanent damage (insanity) (gumma)
Drugs:
Primary and secondary
Pen G
Tertiary
IV Pen G

Chlamydia (bacteria)
Chlamydia trachomatis
IP 2-10 days
Maybe asymptomatic
Gray white discharge
Burning and itchiness at the urethral opening
DX:
Antigen detection test on cervical smear
Urinalysis

Drugs:
Azithromycin (Zithromax) 1 g orally one dose
Erythromycin and Ofloxacin
CX:
PID
Ectopic pregnancy
Fetus transmittal (vaginal birth)

Herpes Genitalis (virus)
HSV 2
Painful sexual intercourse
Painful lesion (cervix, vagina, perineum, glans penis)
DX:
Viral culture
Pap smear (shows cellular changes)
Tzanck smear (scraping of ulcer for staining)
Drugs:
Anti viral-acyclovir (zovirax)
CX:
Meningitis
Neonatal infection (vaginal birth)

Genital Warts, Condyloma Acuminatum (virus)
HPV type 6 & 11, papilloma virus
Single or multiple soft, fleshy painless growth of the vulva, vagina, cervix, urethra, or anal area
Vaginal bleeding, discharge, odor and dyspareunia
DX:
Pap smear-shows cellular changes (koilocytosis)
Acetic acid swabbing (will whiten lesion)
Management:
Laser treatment is more effective
CX:
Neoplasia
Neonatal laryngeal papillomatosis (vaginal birth)

Genital Warts, Condyloma Acuminatum (virus)
Mgmt:
Laser treatment is more effective
CX:
Neoplasia
Neonatal laryngeal papillomatosis (vaginal birth)

Candidiasis, Moniliasis
Yeast or fungus
Cheesy white discharge
Extreme itchiness
DX:
KOH (wet smear indicate positive result)
Drugs:
Monistat
Diflucan
CX:
Oral thrush to baby (vaginal birth)

Trichomoniasis
Parasite
Trichomona vaginalis
Yellow gray frothy vaginal discharge
Foul smelling
Drugs: Metronidazole (Flagyl)
CX: PROM

Prevention
A abstinence
B be faithful
C condom
D do it yourself
“ One stick one hole”
Both partners must be treated

TORCHS
T toxoplasmosis
O others Papilloma virus - STD Gonorrhea - STD Varicella zoster – chicken pox Hepa B HIV Measles Mumps
R rubella
C cytomegalovirus – hemolytic anemia, hydro/microcephalus
H herpes genitalis - STD
S syphilis - STD

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

DRUGS
1. Nucleoside Reverse Transcriptase Inhibitors NRTI’s
INTERFERES WITH DNA CHAIN
Zidovudine (AZT)
SE – NEUROPATHY AND RASH

DRUGS
2. Non-nucleoside Reverse Transcriptase Inhibitors NNRTI’s
- BINDS TO REVERSE TRANSCRIPTASE AND BLOCKS RNA AND DNA REPLICATION
Ritonavir (Norvir)
SE – RASH, HEPATOTOXICITY, BONE MARROW DEPRESSION

DRUGS
3. Protease Inhibitors PI
BLOCK VIRUS ABILITY TO BREAK DOWN LARGER PROTEIN MOLECULES
Indinavir (Crixivan)
SE – HEPATOTOXICITY, NV, ABDOMINAL PAIN, RENAL CALCULI

Hepatitis

Types of Hepatitis
Hepa A – fecal oral route
Hepa B – body fluids
Hepa C – non A non B, BT, body fluids
Hepa D – hypodermic, body fluids
Hepa E – fecal oral route, fatal and common among pregnant women
Hepa G – body fluids (HIV)

Hepatitis A
Hepa A virus
Infectious hepa
Fecal oral route
Short incubation (3-5 weeks)
Poor sanitation
Worldwide distribution
Spread from person-person
Food handlers, contaminated water
Mortality 1%, with full recovery
Enteric precautions
Active Immunity (Havrix)
Passive Immunity (HAIg)
(+) ANTI HAV – INFECTED
(+) Igm ANTI HAV – RECENT INFECTION (ANTIBODY)

Hepatitis B
Hepa B virus
Serum hepa
Blood recipients, hemodialysis, IV drug users, sexually active homosexual, tattoing and health care workers (high risk)
Blood and other body fluids route
Long incubation (2-5 months)
Worldwide distribution
Main cause of liver cirrhosis and liver cancer
(+) HBsAg indicates acute, chronic and carrier
Active Immunity (hevac-B)
Passive Immunity (HBIg)
85% full recovery, 15% lifetime carrier

DX
Elevated AST or SGPT (specific) and ALT or SGOT
Increased IgM during acute phase
HBsAg (+) or REACTIVE = INFECTED maybe acute, chronic or carrier
HBeAg (+) = highly infectious
HBcAg found only in the liver cells
Anti-HBc (+) = acute infection
Anti-HBe (+) = reduced infectiousness
Anti-HBs (+) = with antibodies (FROM vaccine or disease)
Blood Chem. Analysis (to monitor progression)
Liver biopsy (to detect progression to CA)

Manifestations:
Stage I pre-icteric for 1-21 days Anorexia, nausea and vomiting, LBM, weight loss RUQ pain, fatty food intolerance, fever, chills and headache
Satge II icteric for 2-6 weeks Jaundice, pruritus, weight gain, ascites, dark-tea colored urine (urobilirubin) ADEK deficiency
Stage III pre coma NH3 level increases with decreasing LOC Flapping tremors or asterixis
Stage IV recovery

jaundice

Manifestations
CHO – fatigue
CHON – toxicity (latent phase)
Fats – bile, fat intolerance, ADEK
Bilirubin – jaundice, kernicterus (children)
Deamination – NH3 increases
Synthesis CHON – immunocompetent
Cirrhosis and Cancer - complications

Management:
Rest
Diet: - high CHON 75-100 g/day - high CHO – energy - low fat - high calorie 2,500-3,000 cal/day - increase vit A, E if there is steatorrhea
Bile sequestrants – to reduce pruritus Cholestryamine (Questran)
Avoid hepatotoxic drugs Acetaminophen, Sedatives, ASA
Give Antiviral and Interferon

Other diseases

Lyme disease
Named for the Connecticut town, 1975
Appears in summer or early fall
Spirochete, Borrelia burgdorferi
Carried by “deer ticks”
Pahogenesis:
Tick injects spirochete-laden saliva into the blood stream or deposits fecal matter on the skin
disseminate to other skin sites or travel into the blood stream and lymphatic system

s/sx: may take years to fully develop
*Skin lesion “erythema chronicum migrans”
Early localized (Stage 1) = lesion with bright red outer rim with white center, itchy, may sting or burn; fatigue, headache, chills, fever, sore throat and muscle joint pain
Early disseminated (Stage 2) = meningitis, extreme neck flexion and cranial nerve palsy, cardiac symptoms, brief attacks of arthritis
Late (Stage 3) = Chronic arthritis, Behavioral changes, depression and psychosis
Cardiac, neurologic, arthritis (complications)

Lyme disease
Dx: – biopsy, antibody titer, ELISA, Western Blot
Mgmt:
symptomatic
14-28 day oral tetracycline or doxycycline
Children – oral Penicillin
Late stage: IV or IM antibiotics
Vaccine – Immulyme, Lymerix

Toxoplasmosis ZOONOTIC
Toxoplasma gondii, parasite
Affects birds, mammals ie cats
Infected person may carry the organism for life (reactivation is possible)
Pathogenesis:
ingestion of cyst from uncooked meat / fecal oral route from infected cats (feces)
Quickly multiply in the GIT
Distributed to CNS, lymphatic tissue, skeletal muscle, myocardium, retina and placenta

S/sx: Toxoplasmosis
Malaise, fever, myalgia, headache, fatigue, sore throat, lymphadenopathy
Fulminant = vomiting, cough and dyspnea, hyperpyrexia, delirium and seizures, encephalopathy, meningitis
Infants = hydrocephalus and microcephalus, seizure, jaundice later strabismus, blindness, epilepsy, mental retardation

Toxoplasmosis
Dx: serology, CT scan
Mgmt:
4-6 weeks of sulfonamide and pyrimethamine (take folic acid to counteract drug’s adverse effects)

TORCHS
T toxoplasmosis
O others Papilloma virus - STD Gonorrhea - STD Varicella zoster – chicken pox Hepa B HIV Measles Mumps
R rubella
C cytomegalovirus – hemolytic anemia, hydro/microcephalus
H herpes genitalis - STD
S syphilis - STD

Ebola ZOONOTIC
Filoviruses, 1960
Unknown reservoir
Viral replication takes place in almost all organs
90% mortality, recovery is often prolonged
BIOLOGICAL WEAPON
IP: 3-9 days
MOT: direct contact w/ blood, vomitus, urine, stool, semen
probably aerosol transfer during later stages

Ebola
S/sx: frontal and temporal headache, malaise, myalgia, nausea, vomiting, fever, conjunctivitis, watery diarrhea (3 rd day), lethargy, nonpruritic maculpapular rash, desaquammation, hemorrhagic manifestations (5 th day)
Dx: history
Report suspected EBOLA case
Health workers = advised to wear cap, goggles, mask, gown, gloves and shoe covers

Bird Flu ZOONOTIC
Avian influenza, virus
Occur naturally among birds (intestines)
but some types very contagious among birds
Influenza A (H5N1) virus– deadly to birds and has caused human illness and death in Asia
Person to person transmission rare

Bird Flu
MOT:
saliva, nasal secretions, and feces
direct contact with infected waterfowl or other infected poultry
contact with surfaces (such as dirt or cages) or materials (such as water or feed) contaminated with virus

Bird Flu
S/sx: Influenza-like symptoms
Fever, Cough, sore throat,
muscle aches, eye infections,
Pneumonia
Mgmt:
* resistant to amantadine and rimantadine – comon influenza drugs
* oseltamavir and zanamavir - under study

Foot and Mouth Disease ZOONOTIC
Aphthovirus
Hosts - cattle, buffaloes,
sheep, goats, swine
IP: 2-4 days
MOT: contact w/ infected animals
Ingestion of unprocessed milk or dairy products from infected animals
Humans act as transmitter to animals
Harbor virus in respiratory tract for 1-2 days
Contaminated boots, clothing, vehicles
Spread to susceptible animals

Foot and Mouth Disease
s/sx: Very rarely develop mild clinical signs
malaise, fever, vomiting, red ulcerative lesions of oral tissues, vesicular lesions skin
Dx: Virus isolation or antibody identification required for diagnosis
Mgmt: supportive care

Infectious Mononucleosis
3 hallmarks fever sore throat swollen cervical lymph nodes
(+) heterophil antibodies
No major complications
Self limiting
“ Kissing Disease”
Incubation period is 10-50 days

EBV
Caused by EBV epstein-barr virus
Or cytomegalovirus
Lodges in the salivary glands
Spread via oropharyngeal route
Kissing (intimate)
Contagious before symptoms start until fever subsides

EBV
Virus invades the B cells of lymphoid tissue
As the B cells die virus is released in the blood
Causing fever and other symptoms
Antiviral antibodies in the blood fights the virus
They disappear in the blood and lodges in to the salivary glands

EBV
Diagnostic WBC count abnormally high (+) heterophil antibodies Indirect immunoflourescent (+) EBV (specific)

EBV
Management
Symptomatic
ASA
Steroids

Gas Gangrene
Clostridium perfringens welchii novyi
Deep wound (bronzed or blackened wound)
Necrosis of muscle tissue
Pain and Anemia

Gas Gangrene
CS
Incision and Drainage
Debridement
Hyperbaric oxygenation
Amputation
SEPSIS

Anthrax (Zoonotic)
Bacillus anthracis (gram negative)
Cattle, sheep, goat and pig
Biological weapons

Anthrax
Inhalation- URTI-fever-3-5 days-lower infection (alveoli)-metabolic acidosis-hypoxia
GIT- ingestion of contaminated carcasses-severe gastroenteritis-bloody stools-perforation-peritoniitis-septicemia
Skin- most common-direct/indirect-itchiness-papule-vesicle-depressed black eschars-painless-septicemia-death

Lyme Disease
Named for the Connecticut town, 1975
Appears in summer or early fall
Skin lesion “ erythema chronicum migrans ”
Cardiac, neurologic, arthritis (complications)

Lyme Disease
Caused by spirochete borrelia burgdorferi
Carried by “deer ticks”
Tick injects spirochete-laden saliva into the blood stream or deposits fecal matter on the skin
Spirochetes disseminate to other skin sites or travel into the blood stream and lymphatic system

Lyme Disease
Signs and symptoms may take years to fully develop
Stage 1 = site, red lesion, it may itch, sting or burn lesion has white center, bright red outer rim rash is accompanied with fatigue, headache, chills, fever, sore throat and muscle joint pain severe headache may suugest meningeal irritation

Lyme Disease
Stage 2 = meningitis and cranial nerve palsy also cardiac symptoms may appear extreme neck flexion
Stage 3 = Chronic arthritis
Note: may change the behavior, depression and psychosis

Lyme Disease
Diagnostic antibody titer ELISA Western Blot IgM AST WBC ESR

Lyme Disease
Management
14-28 day oral tetracycline or doxycycline
Children – oral Penicillin
Late stage: IV or IM antibiotics
symptomatic

Toxoplasmosis (Zoonotic)
Toxoplasma gondii
Affecting birds and mammals
Transmitted to humans by ingestion of uncooked meat and fecal oral route from infected cats (feces)
Quickly multiply in the GIT
Disseminate to the CNS, lymphatic tissue, skeletal muscle, myocardium, retina and placenta

Toxoplasmosis
Malaise, fever, myalgia, headache, fatigue and sore throat
Fulminant = vomiting, cough and dyspnea, hyperpyrexia, delirium and seizures
Infants = hydrocephalus and microcephalus, seizure, jaundice later strabismus, blindness, epilepsy, mental retardation
Infected person may carry the organism for life (reactivation is possible)

Toxoplasmosis
Management
4-6 weeks of sulfonamide and pyrimethamine (take folic acid to counteract drug’s adverse effects)

Ebola and Marburg Viruses (Zoonotic)
Filoviruses, 1960
Biological weapons
Extreme virulence
Reservoir not yet confirmed
Exposure to unrecognized host
Insect bites
Asia and Africa (animals)

Ebola
MOT not known
Diagnosis = febrile and hemorrhagic fever from Asia and Africa (travellers)
Health workers = advised to wear cap, goggles, mask, gown, gloves and shoe covers

Ebola
Rapid onset of symptoms profound hemorrhage organ failure and shock
90% mortality, recovery is often prolonged
No known antiviral drugs
Report suspected EBOLA case

Bird Flu (Zoonotic)
Avian influenza
Infection caused by avian (bird) influenza (flu) viruses.
Occur naturally among birds
Wild birds worldwide carry the viruses in their intestines, but usually do not get sick from them
However, avian influenza is very contagious among birds and can make some domesticated birds, including chickens, ducks, and turkeys, very sick and kill them.

Bird Flu
MOT = saliva, nasal secretions, and feces
direct contact with infected waterfowl or other infected poultry, or through contact with surfaces (such as dirt or cages) or materials (such as water or feed) that have been contaminated with the virus.

Bird Flu
Low and high extremes of virulence
The “low pathogenic” form may go undetected and usually causes only mild symptoms (such as ruffled feathers and a drop in egg production)
The highly pathogenic form spreads more rapidly through flocks of poultry. This form may cause disease that affects multiple internal organs and has a mortality rate that can reach 90-100% often within 48 hours.

Bird Flu
Human infection with avian influenza viruses
There are many different subtypes of type A influenza viruses. These subtypes differ because of changes in certain proteins on the surface of the influenza A virus (hemagglutinin [HA] and neuraminidase [NA] proteins). There are 16 known HA subtypes and 9 known NA subtypes of influenza A viruses. Many different combinations of HA and NA proteins are possible. Each combination represents a different subtype. All known subtypes of influenza A viruses can be found in birds.

Bird Flu
Usually, “avian influenza virus” refers to influenza A viruses found chiefly in birds
Infections with these viruses can occur in humans
The risk from avian influenza is generally low to most people, because the viruses do not usually infect humans
However, confirmed cases of human infection from several subtypes of avian influenza infection have been reported since 1997
Most cases of avian influenza infection in humans have resulted from contact with infected poultry (e.g., domesticated chicken, ducks, and turkeys) or surfaces contaminated with secretion/excretions from infected birds
The spread of avian influenza viruses from one ill person to another has been reported very rarely, and transmission has not been observed to continue beyond one person.

Bird Flu
“ Human influenza virus” usually refers to those subtypes that spread widely among humans.
There are only three known A subtypes of influenza viruses (H1N1, H1N2, and H3N2) currently circulating among humans.
It is likely that some genetic parts of current human influenza A viruses came from birds originally.
Influenza A viruses are constantly changing, and they might adapt over time to infect and spread among humans.

Bird Flu
During an outbreak of avian influenza among poultry, there is a possible risk to people who have contact with infected birds or surfaces that have been contaminated with secretions or excretions from infected birds.

Bird Flu
Influenza-like symptoms
Fever
Cough
sore throat
muscle aches
eye infections
Pneumonia
severe respiratory diseases

Bird Flu
Avian Influenza A (H5N1)
Avian influenza A (H5N1) in Asia and Europe
Influenza A (H5N1) virus – also called “H5N1 virus” – is an influenza A virus subtype that occurs mainly in birds, is highly contagious among birds, and can be deadly to them.

Bird Flu
Outbreaks of avian influenza H5N1 occurred among poultry in eight countries in Asia (Cambodia, China, Indonesia, Japan, Laos, South Korea, Thailand, and Vietnam) during late 2003 and early 2004. At that time, more than 100 million birds in the affected countries either died from the disease or were killed in order to try to control the outbreaks. By March 2004, the outbreak was reported to be under control. Since late June 2004, however, new outbreaks of influenza H5N1 among poultry were reported by several countries in Asia (Cambodia, China [Tibet], Indonesia, Kazakhstan, Malaysia, Mongolia, Russia [Siberia], Thailand, and Vietnam). It is believed that these outbreaks are ongoing. Influenza H5N1 infection also has been reported among poultry in Turkey and Romania and among wild migratory birds in Croatia.

Bird Flu
Human cases of influenza A (H5N1) infection have been reported in Cambodia, China, Indonesia, Thailand, and Vietnam. For the most current information about avian influenza and cumulative case numbers

Bird Flu
Human health risks during the H5N1 outbreak
H5N1 virus does not usually infect people, but more than 130 human cases have been reported by the World Health Organization since January 2004. Most of these cases have occurred as a result of people having direct or close contact with infected poultry or contaminated surfaces; however, a few cases of human-to-human spread of H5N1 have occurred.

Bird Flu
No one can predict when a pandemic might occur. However, experts from around the world are watching the H5N1 situation in Asia and Europe very closely and are preparing for the possibility that the virus may begin to spread more easily and widely from person to person.

Bird Flu
Treatment and vaccination for H5N1 virus in humans
The H5N1 virus that has caused human illness and death in Asia is resistant to amantadine and rimantadine, two antiviral medications commonly used for influenza. Two other antiviral medications, oseltamavir and zanamavir, would probably work to treat influenza caused by H5N1 virus, but additional studies still need to be done to demonstrate their effectiveness.

Bird Flu
Treatment and vaccination for H5N1 virus in humans
There currently is no commercially available vaccine to protect humans against H5N1 virus that is being seen in Asia and Europe. However, vaccine development efforts are taking place. Research studies to test a vaccine to protect humans against H5N1 virus began in April 2005, and a series of clinical trials is under way.

Foot and Mouth Disease (Zoonotic)
Picornaviridae, genus Aphthovirus
One of the most contagious animal diseases, with important economic losses
Low mortality rate in adult animals, but often high mortality in young due to myocarditis

Hosts
Bovidae (cattle, zebus, domestic buffaloes, yaks), sheep, goats, swine, all wild ruminants and suidae. Camelidae (camels, dromedaries, llamas, vicunas) have low susceptibility

Transmission
Direct or indirect contact (droplets)
Animate vectors (humans, etc.)
Inanimate vectors (vehicles, implements)
Airborne, especially temperate zones (up to 60 km overland and 300 km by sea)

Sources of virus
Incubating and clinically affected animals
Breath, saliva, faeces, and urine; milk and semen (up to 4 days before clinical signs)
Meat and by-products in which pH has remained above 6.0
Carriers: particularly cattle and water buffalo; convalescent animals and exposed vaccinates (virus persists in the oropharynx for up to 30 months in cattle or longer in buffalo, 9 months in sheep). African Cape buffalo are the major maintenance host of SAT serotypes

Occurrence
FMD is endemic in parts of Asia, Africa, the Middle East and South America (sporadic outbreaks in free areas)
Incubation Period
2-14 days

Sanitary prophylaxis
Protection of free zones by border animal movement control and surveillance
Slaughter of infected, recovered, and FMD-susceptible contact animals
Disinfection of premises and all infected material (implements, cars, clothes, etc.)
Destruction of cadavers, litter, and susceptible animal products in the infected area
Quarantine measures ( Code Chapter 2.1.1.)

Medical prophylaxis
Inactivated virus vaccine containing an adjuvant. Immunity: 6 months after two initial vaccinations, 1-month apart, depending on the antigenic relationship between vaccine and outbreak strains

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Nursing Lecture on Communicable Disease

by 1nurses on Oct 03, 2009

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Nursing Lecture on Communicable Disease — Presentation Transcript