WEEK 13

HEPATITIS HA: Infectious hepatitis, Catarrhal- HB: Serum Hepatitis HC: Post-transfusion hepatitis
jaundice hepatitis
MOT: percutaneous, sexual, MOT: percutaneous, sexual
MOT: fecal-oral, oral-anal sex mother- child. intercourse

Clinical Manifestations
Preicteric phase Icteric “Yellowish” phase Post icteric phase
- anorexia - dark urine (increase bilirubin) - malaise
- nausea - pruritus - fatigue
- RUQ pain - clay-colored stools: due to - hepatomegaly (several weeks)
- malaise decrease excretion of conjugated
- headache bilirubin in intestine
- low grade fever - enteric jaundice (scleral
jaundice)

COMPLICATION Nursing Interventions: PREVENTION HB: MEDS

- chronic hepatitis 1. Bed rest - HB vaccination (0, Antivirals:
- cirrhosis 2. SFF, high CHO 6, 14 weeks 0.5 cc lamivudine,
3. Avoid alcohol and OTC drugs IM) interferon
NX DIAGNOSIS 4. Implement Standard -
- Hepatitis Profile precaution
- Liver function test
- Liver UTZ
CHOLERA Violent Dysentery Cholera
“BLUE DEATH” CAUSATIVE: CLINICAL MANIFESTATIONS
Vibrio coma or vibrio cholera ➢ Mild diarrhea → becomes voluminous
(dying of cholera may ➢ Rice-watery stool (pathognomonic sign)
lose so many body Incubation Period of ➢ Washer woman’s hands
fluids that their skin Period Communicability ➢ Effortless vomiting
turns bluish gray) few hrs- 5 days As long as mo are ➢ Cramping of the extremities (hypokalemia)
(ave. of 3 days) present in bowel ➢ Sx of severe dehydration; SUNKEN EYEBALL
Filippo Pacini excreta ➢ Acidosis
discovered of Vibrio ➢ shock
cholera. Diagnostic Exams (3 DEFICITS)
- Stool or vomitus culture - Severe dehydration & ECF volume deficit
Waldemar Haffkine - Serum electrolytes - Hypokalemia
1st cholera vaccine - Dark field or Phase Microscopy - Metabolic acidosis
(July 1892); Russian-
Jewish bacteriologist NX MANAGEMENT
MED MANAGEMENT - Assess patient for signs of dehydration and
Dr. John Snow - Correction of dehydration & fluid imbalance complications
1 of the founding - Antibiotics: Tetracycline (DOC) - Observe enteric precautions
fathers of modern - Increase oral fluid intake
epidemiology and
discovered how Bacillary Dysentery “Shigelosis” Amoebic Dysentery “Amoebiasis”
cholera was spread in Shigella dysenteriae Entamoeba histolitica
London ➢ +/- fever ➢ +/- fever
➢ +/- vomiting ➢ +/- vomiting
➢ Abdominal pain (colicky or cramping) ➢ Abdominal pain
➢ Diarrhea with tenesmus ➢ Diarrhea with tenesmus
➢ Mucus and Blood streaked stool ➢ Muco-purulent blood streaked stool

Tx: Cotrimoxazole Tx: Metronidazole

TYPHOID FEVER CAUSATIVE: Clinical Manifestations

Almroth Edward Salmonella Gradual onset
Wright ➢ A-norexia and abdominal pain
1st effective vaccine for Incubation Period of ➢ B-radycardia
typhoid was developed Period Communicability ➢ C-onstipation
by & introduced for Variable; 1- 3 As long as bacilli ➢ D-iarrhea, D-evelop skin eruptions on abdomen, back &
military use in 1896. wks (ave: 2wks) appears in excreta chest (ROSE SPOTS)
Diagnostic Exams ➢ E-nlarged spleen
Georg Gaffky - CBC ➢ F-ever and chills
(pathologist) - Widal test: agglutination test (H & O) ➢ G-eneralized body weakness
confirmed bacillus - Typhidot exam: detecting Antibodies G&M ➢ H-eadache
Eberthella typhi - Blood culture (3) cardinal signs of Pyrexial stage “DEF”
(Salmonella enterica) - Urine and stool culture Dev skin eruption; Enlarged spleen (Splenomegaly); Fever
Mary Mallon (Typhoid MOT
Mary) - Fecal – oral route
Irish cook; - Ingestion of contaminated food and water
asymptomatic carrier - 5 F’s – fingers, feces, flies, food, fomites
causes typhoid fever;
spreading the disease
to multiple people,
leading to several
outbreaks early 20th
century

MED MANAGEMENT NX MANAGEMENT

- Antibiotics: chloramphenicol (DOC) - Enteric isolation
- IVF to correct dehydration or fluid imbalance - VS: recorded accurately
- Paracetamol: fever - I &O: accurately measured
- Oral therapy rehydration (oresol, hydrites) - Concurrent disinfection
- Isolation
- Increase oral fluid intake
RED TIDE POISONING Explosions or “Blooms”
“RED TIDE”: harmful Coastal phenomena Factors favorable for growth are:
algal bloom (HAB); ➢ caused by environmental conditions which 1. Warm surface temperatures;
colonies of algae promote the explosive growth of 2. High-nutrient content;
(simple plants that live microorganisms. 3. Low salinity and calm seas; and
in the sea & freshwater) 4. Rainy days followed by sunny weather
grow out of control SHELLFLISH
while producing toxic ➢ prone to contamination as they feed by DOES IT REALLY COLOR THE WATER?
effects on people, fish, filtering microscopic food out of the water ➢ water in the coastal areas can be colored red
shellfish, marine ➢ filter feeders → accumulate toxins produced by the algae, thus, the term red tide.
mammals, birds. by microscopic algae dinoflagellates &
diatoms LOBSTER, CRABS, SHRIMPS, FISH
“Population Explosion” ➢ do not accumulates toxins
of toxic, naturally Quahogs, Soft Shell clams, Oysters, Mussels, ➢ safe to eat even if they are from affected
occuring microscopic Scallops, Moon snails waters.
phytoplanktons, PATHOPHYSIOLOGY
specifically a subgroup Paralytic shellfish poisoning (PSP) TOXINS RESPONSIBLE FOR SHELLFISH
“dinoflagellates” POISONING CHARACTERISTICS
➢ caused by saxitoxin (produced by: A. catanella)
- one of the most potent toxins known ➢ water-soluble
- blocking sodium movement in muscle tissue ➢ heat-and acid stable
*Conduction block primarily occurs in the neurons and ➢ not inactivated by ordinary
muscles. cooking
➢ Nervous System: immed. affected after ingestion - Cooking or freezing
- Sx: within 30 minutes does not destroy red
- Severity: depends on amount of toxins consumed tide toxin.

4 SYNDROMES OF SHELLFISH CLINICAL MANIFESTATIONS

POISONING “PDAN” ➢ INITIAL SX: tingling of the lips & tongue → spreads to the face,
neck, fingertips and toes
1. Paralytic Shellfish Poisoning ➢ Headache, dizziness & nausea (mistaken as drunken condition)
2. Diarrheal Shellfish Poisoning - aggravated by alcohol consumption
3. Amnesic Shellfish Poisoning
➢ SEVERE: muscular paralysis & DOB may occur in 5 -12 hrs due
4. Neurologic Shellfish Poisoning
to paralysis of the diaphragm (aid of a respirator)
➢ Fatalities from respiratory arrest have been reported
 MODALITIES OF TREATMENT PREVENTION & CONTROL
1. induced to vomit 1.All shellfish-producing have monitoring program to test water,
2. Charcoal hemoperfusion: sediments, shellfish for contamination.
- pumping arterial blood through 2. Department of Environmental Quality Engineering (DEQE) is
an activated charcoal filter to responsible for year-round testing of shellfish & shellfish-growing
remove the toxin. area.
3. Alkaline fluids (sodium 3. When blooms subside, shellfish has purifies themselves of the
bicarbonate): helpful because toxin and when testing indicates a return to safe levels, the areas
the toxins in unstable in alkaline
are reopened.
condition. 4. If accidental ingestion of toxic shellfish is suspected, seek medical
4. Artificial respiration is attention immediately
required if the patient exhibits 5. Recreational shellfish gatherers should look for posted warnings
respiratory stress. and pay close attention to local media announcements
LEPROSY “HANSEN’S Causative Agent TYPES
DISEASE” Mycobacterium Leprae Multibacillary (MB) Paucibacillary (PB)
Chronic disease of the ➢ More infectious, ➢ hypopigmented
skin, peripheral nerves malignant macule
MOT
and nasal mucosa ➢ Numerous macules,
a. Intimate skin to skin contact
papules, nodules
b. Droplet Infection
“Living dead”
perceived to be caused
LATE MANIFESTATIONS DIAGNOSTIC: Slit Skin smear
by sin
Leonine face: Pathognomonic ➢ to demonstrate M. leprae
➢ Lagophthalmos: inability to close eyelids (-) in all site = Paucibacillary
Nursing Diagnosis
➢ Madarosis: loss of eyebrows (+) in all sites = Multibacillary
➢ Altered body
➢ Sinking of bridge of the nose Number of lesions
image
➢ Contractures (clawing of fingers and toes) ▪ 2-5 PB
➢ Social stigma
➢ Gynecomastia for males ▪ 5 MB

TREATMENT HEALTH EDUCATION

Multi drug therapy (MDT) RA 4073 ➢ Dapsone: cutaneous eruptions, iritis, orchitis
A. Paucibacillary: Rifam,Dapsone ➢ Lamprine: Brownish black skin discoloration,
- Rifampicin(600mg) /once a month dryness, flakiness
- Dapsone (100mg) OD (6-9 mos) ➢ Skin care: Prevent injury

B. Multibacillary: Rifampicin, dapsone, lamprine Preventive

- Day 1: R-600 D-100 C-300 once month ➢ BCG: at birth
- Day 2-28: D-100 OD, Clofazimine (Lamprine) 50
mg
TETANUS “LOCKJAW” Causative Agent INCUBATION PERIOD
CLOSTRIDIUM TETANI ADULT: 3 days- 3 wks
Nursing Diagnosis - TETANOSPASMIN: causes spasm NEWBORN: 3-30 days
➢ Ineffective - TETANOLYSIN: RBC destruction
breathing pattern MOT SOURCES OF INFECTION
rt muscles spasm - Through breaks in the skin and mucous - Soil
and neurologic membranes - Street dust
impairment. - Animal and human feces
➢ Risk for injury rt - Rusty materials
muscle spasms. CLINICAL MANIFESTATIONS
NEONATES ADULT
➢ Malaise Risus sardonicus (sardonic smile): pathognomonic
➢ High fever ➢ Trismus: lock jaw
➢ Difficulty in sucking ➢ Opisthotonus
➢ Excessive of crying ➢ Muscular spasm
➢ Stiffness of jaw ➢ Low grade fever, diaphoresis

CLASSIFICATION OF SEVERITY
I: MILD Mild Trismus, General Spasticity; NO RESPI EMBARRASMENT, SPASMS &
DYSPHAGIA
II: MOD Moderate Trismus, Rigidity, short Spasms, Mild dysphagia, No respi involvement,
RR > 30
III: SEVERE Severe Trismus, Generalized Spasticity, prolonged spasms, RR > 40, Apnoiec
Spells, PR > 120
IV: V. SEVERE Grade 3 Plus severe autonomic disturbances involving Cardio sys
 *DECORTICATE: flexion
*DECEREBRATE: extension
DIAGNOSTIC EXAM MANAGEMENT
- Clinical manifestations Equine tetanus antitoxin
- History of wound ➢ should no longer be used, as there
MED MANAGEMENT is a risk of hypersensitivity and
- ATS (ANTI T. SERUM): both preventing and curing Tetanus serum sickness.
- TAT (T ANTITOXIN) ➢ It should be replaced by human
- TIG (T. IMMUNOGLOBULIN) tetanus immunoglobulin
- Pen G, Metronidazole
- Diazepam (cover from sunlight) ATS
- Muscle relaxant ➢ purified antibodies prepared from
Equine Blood (Horse)
NX MANAGEMENT ➢ Skin test is needed
➢ Keep the room dim and quiet. ➢ temporary passive immunity
➢ Avoid stimuli of spasm against tetanus for 2 weeks
➢ Avoid unnecessary handling ➢ 1500 IU: single dose
➢ Close monitoring of v/s & muscle tone ➢ 3000 IU: if > 24 hours has elapsed.
➢ Provide adequate airway ➢ admin as soon as possible after
injury, along with tetanus vaccine,
PREVENTION in a separate syringe and injection
➢ Immunization with tetanus toxoid for adults site.
➢ DPT for babies and children

POLIOMYELITIS Causative Agent MOT

LEGIO DEBILITANS - fecal-oral: through saliva, vomitus and feces
- TYPE 1 BRUNHILDE: permanent immunity; most - Direct contact from one person to another
paralytogenic - Ingestion through of contaminated food (fecal-
- TYPE 2 LANSING: Tempo immunity oral route)
- TYPE 3 LEON: Tempo immunity INCUBATION PERIOD
PREDISPOSING FACTORS 7 – 14 days
➢ Age: 60% of patient 10 yo PERIOD OF COMMUNICABILITY
➢ Sex. Males more prone than females. Death - Not accurately known
rate is proportionately higher in males. - Polio virus can be found in throat secretions as
➢ Heredity. Not heredity early as 36 hours and in the feces 72 hours after
➢ Environment and hygienic condition: rich are exposure to infection.
more often - Risk of spreading the microorganism is highest
➢ Excessive work, strain & marked overexertion during the prodromal period
are also factors causing the disease
SIGNS AND SYMPTOMS
Inapparent/ Abortive (Minor Major Illness Stage
Subclinical Stage Illness Stage) A. NON-PARALYTIC/ PREPARALYTIC or MENINGITIC TYPE
asymptomatic - Fever Tightness and spasm of hamstring: Pathognomonic
stage (90-95%) - Sore throat - Recurrence of fever
- GI symptoms - Poker spine (stiffness of the back)
- Low lumbar - Hypersensitiveness of the skin
backache/ cervical - Deep reflexes are exaggerated
stiffness on ante- - Paresis
flexion of spine B. PARALYTIC
- With paralysis depending on the part affected
- Positive hoyne’s sign: head drop
- (+) kernig’s and brudzinki signs:
➔ Kernig: Raise (K)nee → Head will also raise
➔ Brudzinki: Head towards chest (B)aba → leg will
also raise
 TYPES OF PARALYSIS
BULBAR SPINAL BULBOSPINAL
Respiratory paralysis Paralysis of the upper and lower Involvement of neurons both in
extremities and intercostal brainstem and the spinal cord
muscles

DIAGNOSTIC EXAM TREATMENT

- Blood and throat culture - Pain relievers (like ibuprofen)
- Lumbar tap (pandy’s test) - ventilator (a device that helps breathing)
- EMG - Physical therapy: help keep the muscles working.
- Stool exam - Bed rest and fluids for flu-like symptoms.
- Antispasmodic medications to relax muscles.
NURSING MANAGEMENT - Antibiotics for urinary tract infections.
- Heating pad for muscle aches and spasms.
- Strict isolation, enteric precaution
- CBR / Firm and non-sagging bed
VACCINES: 2 TYPES
- ROM exercises Oral Polio Vaccine (OPV)
- Analgesics / Hot moist compress Inactivated Polio Vaccine (IPV)
- Protective devices ➢ Philippines still using OPV, IPV does not
- Hand roll – claw hand replace the OPV vaccine, but is used
- Trochanter roll – outer (rotation of the femur) with OPV to strengthen a child's immune
- Footboard system & protect from polio.

IPV (Salk) - Jonas OPV (Sabin) – Albert Bruce

Killed formulized virus
➢ Given SC or MI
➢ Include circulating antibodies but not local
(intestinal immunity)
➢ Prevents paralysis but does not prevent re-
infection
➢ Difficult to manufacture and costly
➢ Not useful with controlling epidemic
Live attenuated virus
➢ Given orally
➢ Immunity is both humoral and intestinal.
Induces antibody quickly.
➢ Prevents paralysis and prevent re-infection
➢ Easy to manufacture and cheaper
➢ Can be effectively use in controlling
epidemics

MENINGITIS/ Causative Agent MOT

CEREBROSPINAL FEVER Neisseria meningitides - Respiratory droplets through nasopharyngeal
Streptococcus pneumonia mucosa
H. influenza - Direct invasion through otitis media
Streptococcus agalactae - May result after a skull fracture, penetrating
Listeria monocytogenes head wound
INCUBATION PERIOD PERIOD OF COMMUNICABILITY
3-6 days As long as the microorganism is present in the
discharges
CLINICAL MANIFESTATIONS
➢ Fever ➢ Signs of meningeal irritation
➢ Petecchial/purpuric rashes - Kernig’s sign
➢ Signs of increased ICP - Nuchal rigidity – pathognomonic sign
- Severe frontal headache
- Opisthotonus
- Altered level of consciousness
- Restlessness - Brudzinski’s sign
- Projectile vomiting ➢ Late Signs
- Blurring of vision; papilledema; diplopia - Decerebration
- Bulging fontanel in infants - Decortication
 DIAGNOSTIC COMPLICATIONS
➢ Blood C & S. - Bronchitis
➢ CSF Analysis/ Lumbar Puncture/ Lumbar Tap - Pneumonia
- Otitis media/ Mastoiditis
- Blindness
- Hydrocephalus

MED TREATMENT
➢ Antibiotic
▪ Penicillin G- DOC
▪ Chloramphenicol: Alternative

➢ Osmotic Diuretic
▪ Mannitol: Decrease Cerebral Edema
NURSING MANAGEMENT ➢ CNS stimulant
➢ Respiratory Isolation: 24 hours after onset of ▪ Pyrentinol/Encephabol
antibiotic therapy
➢ Provide non-stimulating environment ➢ Anticonvulsant
➢ Initiate seizure precaution ▪ Diazepam.
➢ Avoid factors that increase ICP ▪ Phenytoin (Dilantin): SE Gingival
Hyperplasia
PREVENTIVE
➢ Vaccination: Hib- for children ➢ Corticosteroid
➢ Avoid MOT ▪ Prednisone
➢ Rifampicin: prophylactic treatment ▪ Dexamethasone
➢ Ciprofloxacin: Alternative

LEPTOSPIROSIS/ Causative Agent MOT

WEIL’S DISEASE LEPTOSPIRA (LEPTOSPIRA - Ingestion or contact with skin & mucous
Adolf Weil of INTERROGANS) membrane of infected urine or carcasses of wild
Heidelberg and domestic animals.
- Spirochete
reported the clinical - Through the mucous membrane of eyes, nose,
INCUBATION PERIOD
entity of fever, mouth; through a break on skin.
6-15 days
jaundice, hemorrhage, - Direct human to human transmission is rare
PERIOD OF COMMUNICABILITY
renal failure in 1886.
Leptospira is found in the urine between 10- 20
AKA
days after the onset
➢ Canicola Fever
CLINICAL MANIFESTATIONS
➢ Mud Fever
SEPTIC STAGE IMMUNE/ TOXIC STAGE CONVALESCENT
➢ Hemorrhagic
- marked with febrile lasting for - Iritis (sclera discoloration: yellow-orange) STAGE
jaundice
4-7 days - Headache - relapse may
➢ Swineherd’s
- Abrupt onset of remittent - Meningeal manifestations occur during
Disease
fever ▪ Disorientation the 4th- 5th
- chills ▪ Convulsions week
- headache ▪ CSF findings of aseptic meningitis.
- anorexia - Oliguria & anuria with progressive renal failure
- abdominal pain - Shock, coma
- severe prostration - CHF are also seen in severe cases
- respiratory distress
- fever subsides by lysis
 COMPLICATIONS DIAGNOSTIC TEST
- Meningitis - BUN and urea
- Respiratory Distress - Enzyme Link Immuno-sorbent Assay (Elisa)
- Renal interstitial tubular necrosis that result to - Leptospira Antigen-antibody test (LAAT)
renal failure (Weil’s disease) - Leptospira Antibody Test (LAT)
- Cardiovascular problems - Liver function test

MED MANAGEMENT NX MANAGEMENT

➢ Suppressing causative agent ➢ Isolate the patient; urine (properly disposed
➢ Fighting possible complications of)
▪ Penicillin G – drug of choice ➢ Darken patient’s room.
▪ Ampicillin, Amoxicillin: Alt ➢ Observe meticulous skin care
▪ Doxycycline: prophylaxis ➢ Keep clients under close surveillance.
➢ Peritoneal Dialysis ➢ Home Care: clean near dirty places, pools,
▪ Administration of fluid and electrolyte stagnant water.
and blood as indicated. ➢ Facilitate health education on MOT of
disease.
➢ Encourage oral fluid intake
PREVENTION AND CONTROL
➢ Sanitation in homes, workplaces, farms (must) ➢ Animals must be vaccinated
➢ proper drainage system & control of rodents ▪ Cattle
(40- 60% infected) ▪ Dogs
▪ cats
▪ pig
ENCEPHALITIS Causative Agent MOT
“BRAIN FEVER” FLAVIVIRUS - Direct infection to brain by virus, bacteria,
Acute inflammation (mosquito vector) fungus; when immune sys respond to prev.
(swelling) of brain Culex Tritaenorhynchus infection
resulting from Culex vishnui - Immune sys mistakenly attacks brain tissue
VIRAL INFECTION OR Culex gelidus
AUTOIMMUNE - Most common cause of viral infection INCUBATION PERIOD
(own immune sys. - Brain inflamed: result of body’s attempt 4-21 days
Attacking brain tissue) to fight off virus
- 1 in every 1k of measles cases
SOUTHEAST ASIA
& FAR EAST PRIMARY SECONDARY
Most prevalent Virus directly infects brain & Spinal C. Infection starts elsewhere in body then travels
3-MAIN CATEGORIES to brain
Can be Life-threatening ➢ Common Viruses ➢ Cause by: Complication of Viral Infection
but is rare ➔ HSV (herpes simplex V.) ➢ Sx: appears days or wks after initial
➔ EBV (Epstein- Barr V.) infection
➢ Measles & Mumps: childhood viruses ➢ Px immune sys: treats healthy brain cells
➢ Arboviruses: by mosquitos, ticks, other insects as foreign orgs & attacks them
➔ Japanese E.
➔ West Nile E.
➔ Tick-borne E.
JAPANESE E. CLINICAL MANIFESTATIONS
Generally begins w/ Sx rapidly worsen, with s/s of:
- Fever, Nausea, chills, Headache, - Rigidity
Vomiting - Ataxia
- STIFFNESS & NEUROLOGIC - Speech difficulties
manifestations within 24 hrs - Ocular palsy
- Dizziness, conjunctivitis, athralgia, - Flaccid paralysis
Myalgia - Seizures
- Decreased IQ - Confusion
- Serious Brain Damage - Loss of consciousness
- coma

MORTALITY DEPENDS ON MORE LIKELY TO AFFECT

➢ Severity of disease ➢ Children
➢ Age ➢ Older Adults
- Younger: recover without many ongoing ➢ W/ weaken Immune System
health issues ➢ People lives where mosquitos and ticks that
- Older:  risk for complications & spread specific virus are common
mortality
 LABORATORY DIAGNOSIS TREATMENT
- Serum: Detection of Antigen ➢ No specific treatment
- CSF: detect Virus Specific igM antibodies within 7 ➢ Supportive Care
days of onset MED MANAGEMENT
- Compliment fixation Test:: antibodies for ➢ SSS: Self limiting, Symptomatic, Supportive
infection ➢ Focus: Alleviating sx
- Neutralization Test: presence of virus infection ➢ W/ Mild Sx:
- Immunofluorescence Assay: antigen & antibodies ➔ Rest, plenty of fluids
Tentative Definitive ➔ Tylenol (paracetamol): Fever, Headaches
➢ ELISA: antibody titer ➢ Virus ➢ Antiviral (Aclovyr): Herpes Simplex
➢ In Serum/ CSF: JE- Isolation: CSF *success is limited for most infection
sepcific IgM sample, Brain

OTHER MED MANAGEMENT NX MANAGEMENT

➢ Corticosteroids: reduce
brain inflammation (esp:
post-infectious secondary
encephalitis)
➢ Anticonvulsants: seizures
(Dilantin: check WBC →
may cause
agranulocytosis)
➢ Sedatives: for seizures,
restlessness, irritability
SEVERE: MECHANICAL
VENTILATION
➔ Help breathe
➔ Supportive Tx
➢ PROVIDE COMFORT
➔ keep in quiet, well-ventilated room
➔ encourage oral hygiene & bed bath
➢ PREV. COMPLICATION
➔ turn q 2 hrs
➔ encourage  oral fluid intake;  cal diet
➔ moisten lips w/ Mineral Oil
➢ MONITOR I & O
PREVENTION & CONTROL
➢ Prev: identification of vectors and eliminating breeding grounds,
desctructon of larvae, screening homes, use repellants
➢ Personal protective measures; mosquito elimination (most
important)
➢ Travellers going to Endemic areas → consider Vaccination

DF MOSQUITO: Aedes Aegypti MALARIA MOSQUITO: Anopheles

- Day Biting - Night Biting
- Breeds in stagnant water - Breeds in clear, flowing, shaded streams
- Dotted mosquito - Brown Colored & bigger in size
- Bite a person in motion - Do not bite person in motion
DENGUE/ BREAKBONE/ Causative Agent INCIDENCE
DANDY FEVER GROUP B ARBOVIRUS (I, II, III, IV): most ➢ AGE: at any age; peak: 4-9 yo
OTHER NAME: widespread arthropod-borne viruses ➢ SEX: both sexes affected
➢ Infectious FLAVIVIRUS ➢ SEASON: more freq. during rainy season; cases
Thrombocytopenic all year round
purpura CHIKUNGUNYA VIRUS ➢ LOCATION: most prevalent in urban than rural
➢ H-fever ZIKA VIRUS
INCUBATION MOT
CYCLICAL 3-14 DAYS ➢ AEDES AEGYPTI’s BITE: Female mosquito that
VARIATION carries virus
CLINICAL MANIFESTATION
# of cases  towards Grade I: Symptomatic and Supportive Grade II: Manifestations of grade I plus spontaneous
the end of rainy season ➢ Fever, Headache, Malaise, Anorexia, Chills bleeding (BED REST)
➢ Pain (Abdominal, Bone and Joint, Ocular) ➢ Epistaxis; Gingival Bleeding; Petechiae/ ecchymosis
➢ Rashes ➢ Gastrointestinal bleeding
FEVER BEFORE ➢ + Herman’s Sign: Flushing of skin → ➢ Ground coffee colored vomitus
CHILLS Pathognomonic ➢ Hematemesis
▪ Flushing in extremities: rapture of ➢ Melena
fragile small veins ➢ Hematochezia
➢ + Tourniquet Test (Rumple Leeds Test) → Grade III: Manifestations of Grade II plus Beginning
20 or more petichae symptoms of circulatory failure
➢ Monitor V/S
➢ Watch out for complication of shock
➢ Hypotension & narrowing of pulse pressure.
Pulse pressure difference fr systole & diastole
➔ < 40: narrowing
➔ > 60: widening (px w/ meningitis;  ICP)
➢ Weak and thready pulse
➢ Cold, clammy skin
➢ Restlessness
GRADE IV: Manifestations of Grade III
+ Shock (PROPER POSITIONING)
➢ Undedected BP and pulse
Note: Wait: 5-15 (not > 15 mins)

Mild DHF
➢ slight fever
➢ with or without
petechial hemorrhage
CLASSIFICATION OF DHF
Moderate DHF Severe DHF
➢ high fever ➢ frank type: flushing, sudden high fever
➢ less hemorrhage ➢ severe hemorrhage
➢ no shock ➢ followed by sudden drop of temperature
➢ shock
➢ terminating in recovery or death

DIAGNOSTIC TEST COMPLICATIONS

➢ Tourniquet Test- Presumptive dx; detects ➢ SHOCK → DEATH
capillary fragility
MEDICAL TREATMENT
➢ Platelet Count: Confirmatory test!! ➢ Antipyretic/ Analgesic
➔ Result: < 100, 000 CELLS/ mm3 ➔ Do not administer NSAID for Fever

➢ Hemoconcentration-  20% Hematocrit Count ➢ Intravenous Fluid Therapy

➔ NO SHOCK = IVF Crystalloids
➢ Dengue NS1 Ag (nonstructural protein 1) ▪ D5LR
➔ Intro in 2006 ▪ D5 0.9 NaCl
➔ rapid detection on 1st day of fever, before ▪ PLR at 5-7 ml/kg/hr
antibodies appear some 5 or more days
later (Should be performed within 5 days of ➔ SHOCK= IVF Crystalloids
fever onset) ▪ PLR.
➔ Through enzyme-linked immunosorbent ▪ P 0.9 NSS at 20ml/KBW IV bolus in
assay (ELISA) < 20mins
➔ Accuracy: high w/ sensitivity 55%-82%
➔ Specificity: 97%-100% ➔ if NO IMPORVEMENT
➔ (+) NS1: confirms dengue virus infection ▪ Colloids- Dextran, Haemacel, Haesteril at
➔ (-) NS1: does not rule-out infection → 10ml/kg bolus in < 10 mins
should be detested for presence of dengue
igM antibodies (Dengue Duo) to determine ➔ STILL NO IMPROVEMENT
possible recent dengue exposure. ▪ Fresh Frozen Plasma at 15cc/kg in 2 hours
▪ start inotropes Dopamine 7-15 ug/kg/m
➢ Dengue Duo
5’ S
RESULTS ➢ Search and destroy (sustain vector control
IgG & IgM measures)
(+) (-) RECENT PRIMARY ➢
Self protection
INFXN ➢
Seek early consultation
(+) (+) RECENT SECONDARY ➢
Say no to indiscriminate fogging (but support
INFEXN fogging, spraying, misting in hot spot areas)
(-) (+) RECENT SECONDARY ➢
Sustain hydration
INFEXN
(-) (-) NO RECENT INFXN
MALARIA/ AGUE SPECIES INCUBATION PERIOD (LIVER CYCLE)
King of Tropical and P. FALCIPARUM : malignant tertian (fatal); 1 only in PH 7-14 days
Sub-tropical Diseases P. VIVAX : Benign tertian 12-17 days (w/ relapse up to 3 yrs)
P. OVALE : Ovale Tertian 9-18 days (w/ relapse up to 20 yrs)
Charles Louis Alphonse P. MAlARIAE : Quartan 13-40 days
Laveran VECTOR: Anopheles mosquito
protozoan parasite in MOT CLINICAL MANIFESTATION
1880 - Bite of infected female anopheles mosquito ➢ 3- STAGES
(Discovered the cause) (during their pregnancy) ➔ COLD STAGE: severe recurrent chills
- Through blood transfusion ➔ HOT STAGE: fever 4-6 hrs
CHILLS BEFORE FEVER - Contaminated needles and syringes ➔ WET STAGE: profuse sweating 2-4 hrs
- Congenital transmission (rare) (note: in dengue → Hot, Cold, Wet)

DIAGNOSTIC EXAM ➢ Early signs of anemia: repeated chronic

➢ Malarial smear: Confirmatory test; detects symptoms CBQ (destruction of RBC)
malaria parasite ➔ Pallor
- best done during the height of fever ➔ Easy fatigability
➔ (quantitative) thick blood smear: presence ➔ Dizziness
and percentage of parasite in the blood, ➢ Malaise
➔ (qualitative) thin blood smear: specific ➢ Splenomegaly
species in blood ➢ Hepatomegaly
➢ Quantitative Buffy Coat (QBC)/ Rapid
Diagnostic Test (RDT)
➔ Detects malarial antigen
➔ taken anytime; faster test
 COMPLICATIONS MED MANAGEMENT
➢ CEREBRAL MALARIA ➢ PREGNANCY “quine”
➔ most severe neurological complication of infection - Chloroquine
with Plasmodium falciparum malaria - amodiaquine
➔ clinical syndrome characterized by seizures and coma - quinine
- azithromycin
➢ BLACKWATER FEVER “Malarial Hemoglobinuria” - sulfadoxine-pyrimethamine
➔ one of the less common yet most dangerous - mefloquine
complications of malaria. - dapsone-chlorproguanil
➔ The distinctive color of the urine (dark) → large - artemisinin derivatives
amounts of hemoglobin, released during extensive - atovaquone-proguanil
destruction of RBC by malarial parasites that leads to - Lumefantrine
kidney failure. *EXCEPT: AMOXCILLIN

PREVENTION (when going to malaria endemic area) CLASSIFICATION

➢ CHEMOPROPHYLAXIS ➢ 1ST line
- DOXYCYCLINE: 1 day before going; 4 wks after leaving ➔ Artemether-lumefantrine
- CHLOROQUINE: 1 wk before; 4 wks after combination tablet
- MEFLOQUINE: 2-3 wks before; 4 wks after
➢ 2ND line:
➢ ZOOPROPHYLAXIS ➔ Chloroquine
- Typing of domestic animals to divert attention of ➔ Primaquine
mosquitos (ex: carabao, Tilapia-fishes) ➔ Pyrimethamine & Sulfadoxine

➢ NO VACCINE ➢ Complicated Malaria (Multi drug

resistant Falciparum):
➢ “CLEAN” ➔ Artemether 20mg/ Lumefantrine
Chemically treated mosquito nets 120mg (C0-Artem)
Larvae-eating fish
Environmental Sanitation ➢ Erythrocyte Exchange Transfusion
Anti-mosquito soap
Natural anti-mosquito plant
FILARIASIS Causative Agent MOT
“ELEPHANTIASIS” WUCHERERIA BANCROFTI ➢ Bite of Aedes Poecilius
BRUGIA MALAYI
BRUGIA TIMORI INCUBATION
LOA LOA (the only 1 for animal; esp. flies) 8- 16 MONS

MANIFESTATIONS DIAGNOSTIC EXAM

Acute Stage: ➢ Nocturnal blood exam
➢ Lymphadenitis ➢ Immunochromatographic test (ICT)
➢ Lmphangitis
➢ Funiculitis, orchitis, epididymitis MED MANAGEMENT: DOC
Chronic Stage: ➢ Diethlycarbamazine citrate (Hetrazan)
➢ H-ydrocele ➔ “DEC”
➢ E-lephantiasis
➢ L-ymphedema